This this actually does NOT line up. Before I get into why this does not matter, and also how to answer this easily, let's Break this down... First they ignored the differences. Humans have much fewer Olfactory receptor (OR) pseudogenes. That's right, primates have almost twice as many!
Now remember, evolutionists believe in something called neutral theory, where all things evolve (mutate) at the same rate. Therefore since the split, humans and chimps have existed for the same amount of time and have undergone the same amount of evolution. Therefore, a constant rate of mutations should have caused humans and chimps to have the same amount of pseudogenes right?
Well let's read this study; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC546523/ "In agreement with previous reports based on a small number of ORs, we find that humans have a significantly higher proportion of OR pseudogenes than chimpanzees. Moreover, we can reject the possibility that humans have been accumulating OR pseudogenes at a constant neutral rate since the divergence of human and chimpanzee."
They literally refuted their own evolutionary theory and didn't realize it! Evolution theory hinges on neutral theory.
This study states; "Humans have >1,000 OR genes, of which only ∼40% have an intact coding region and are therefore putatively functional. In contrast, the fraction of intact OR genes in the genomes of the great apes is significantly greater (68%–72%)". This study resequenced 20 OR genes in 16 humans, 16 chimpanzees, and one orangutan. We compared the variation at the OR genes with that at intergenic regions."
So humans have almost twice as many intact Olfactory receptor (OR) than other primates and way more than monkeys but much more pseudogenes. What does that mean? Less is broken, it's more functional.
They even admitted; "the observation that humans have more pseudogenes than apes remains statistically significant." So they notice this matters but remember they will always discount any differences and only look to similarities. Remember, they are always thinking in an evolutionary mindset. So the fact this is reversed means everything. We should have less intact since there are more pseudogenes, but we find the opposite! If mutations are breaking up these intact coding regions to make pseudogenes, then why do we have more than apes? If neutral theory was true we should have the same if not less than apes literally have twice as fast generation times.
Now, this is where they try to validate this proves evolution... "14 OR loci from one gene cluster on human chromosome 17 in humans and apes (9). Although three to five of these 14 OR loci were found to carry coding region disruptions in one or more ape species, all 14 OR genes were inferred to be intact in the common ancestor of all apes". Of the 5 total max that are in the protein coding regions of some primates alive today, only a few of those match down the line. And when we actually compare humans and chimps in this area what do we see? Well darn look at that. "The comparison of the two repertoires reveals two chimpanzee-specific OR subfamily expansions and three expansions specific to humans." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC546523/ So we find 3 that are different and specific to humans that do not align with chimps at all and 2 in chimps that are specific to only chimps. So the whole, "but they have mutations in the same spot" argument doesn't matter at all. Yes they have the same genes, but the gene's mutation rate is in reverse order!
If humans and chimps have existed the same amount of time, then chimps who would have had double the amount of generations would have many more pseudogenes than humans today. They only have 2 of these protein coding genes and humans have 3 (1 more than them). So even if evolutionists wanted to claim that neutral theory was true and that they mutate at the same rate, well that fails them as well. So either way they have nothing but storytelling at this point to try and prove common ancestry, this is why they will hand wave all of that away and focus on just mutations that are in the same spot of a gene.
But that is easily answered as there are mutation hot spots in every region of the genome, so of course there are going to be matching mutations in some regions. It's like looking at tires on vehicles and wondering why they wear down faster than other parts of the vehicle. Well they should! Consider this. Mutations that end up being bad, what happens to them? Well, if you get cancer you die. You are no longer going to pass that mutation on. Therefore, most mutations that get passed on are ones that selection cannot remove because its not harmful enough for selection to remove.
When you drive does it matter if you turn left or right to wear your tires down? Of course not. Damage is damage, and it looks the same. The same goes for the genome. at each gene site you have 4 possible outcomes. One you were born with, odds are most likely beneficial. 2 possible outcomes are bad and one of those will most likely cause a huge health problem and selection most likely will remove or you will die. The other will cause another health problem but not as bad. That only leaves one more option. So it should not be surprising there are shared mutations.
What is the magical rescue device they use for all of this nonsense? Selection must have done it. JUST ADD TIME! Shocking I know (Sorry for the sarcasm, but how many times I have read, co-option, convergence and selection at this point it's getting annoying.) Imagine if every article I wrote I said, and God did it, and then a miracle happened, then God did that. Well, that's all I am reading, it's a God of the gaps argument for evolutionists to fill in all the problems and not address them. Its "evolution must be true so fill in the gaps anyway you chose, just make it sound scientific."
Here is the real question; Why do evolutionists ignore everything that does not line up? Here are some examples; HERV-K GC1 is found in chimps, bonobos, and gorillas, but not in humans? https://www.mdpi.com/1999-4915/6/11/4140 It's clear that since humans are related and in the last line of ancestry we would have inherited this right? Yet we did not. So like any hypothesis, if this was in court and a jury wanted just one piece of evidence to prove if evolution was guilty or innocent of starting with the assumption of shared common ancestry using inheritable variants and never considering design, then it would be found guilty. Remember we only need one piece of evidence to prove common ancestry is not true and it all breaks down. We have that, but let's look at more shall we? Endogenous retrovirus PtERV1 is present in chimps and other great apes, but NOT in humans and orangutans. DOI:https://doi.org/10.1016/S0960-9822(01)00227-5 So wait a minute, the orangutan came first. It never attracted the virus, then a gorilla got infected and when it speciated into the next ancestor it passed it on, then then this common ancestor produced the ancestors of both the human and chimp line it just forgot to pass it onto the human line? Comon, this is nonsense. These are germline inheritable only things, they cannot just not get passed on. Every proceeding lineage should have it down the line if evolution was true. The fact that multiple examples from genes, ERVs, mutations, chromosomes, etc... all do not follow common descent shows us that evolution is not true. This is why when you look at cytochrome C vs Cytochrome B they both falsify each other. Yet, they should both make the same tree if evolution was true. Yet they form different trees. Why is that? Read for yourself what evolutionists themselves have even admitted when they discovered this!
As one article in Trends in Ecology and Evolution stated: "The mitochondrial cytochrome b gene implied... an absurd phylogeny of mammals, regardless of the method of tree construction. Cats and whales fell within primates, grouping with simians (monkeys and apes) and strepsirrhines (lemurs, bush-babies and lorises) to the exclusion of tarsiers. Cytochrome b is probably the most commonly sequenced gene in vertebrates, making this surprising result even more disconcerting."
French evolution biologist François Jacob states “The cytochrome C phylogeny disagrees with the traditional [evolutionary] one in several instances,” https://eric.ed.gov/?id=EJ194813
Even another evolutionary biologist Francisco Ayala at UCI reluctantly concedes, “including the following: the chicken appears to be related more closely to the penguin than to ducks and pigeons; to the turtle. a reptile, appears to be related more closely to birds than to the rattlesnake, and man and monkeys diverge from the mammals before the marsupial kangaroo separates from the placental mammals.”
They never consider design differences. A study on this very subject admitted this when comparing genetic similarity...
That is the problem! Wrong starting points draw the wrong conclusions. It's the paradigm driving the conclusions. Evolution MUST be true because evolution IS true. Evolution is not bad science, it is not science at all.
To start we must first examine the most controversial scripture which is Acts 13:19-20, I have seen many articles trying to reconcile this time by adding Moses and Joshua as Judges, stretching and shortening different time periods and all of them without a satisfactory outcome.
If we take Acts 13:19-20 that the Judges should span 450 years AFTER the death of Joshua (Joshua 24:29) we run into big problems. We can only assume how old Joshua was before God sentenced the Israelites to wander 40 years, the most common answer is around 20 years old, add 40 years of wandering and this places Joshua around 60 years old. There was a long period of peace (Joshua 23:1) after Joshua’s 7 year conquest of the land of Canaan, Joshua died at 110 years old which leaves a time of peace of around 43 years. In Judges 2:16 God declares raising up Judges after Joshua’s death, which means that the combined time of the Judges (including the oppression years) is 450 years (without Samuel’s Judgeship because we do not know when he started nor the age he died, much of that must be inferred). This far exceeds both Acts and 1 Kings, what is the solution?
After quite a bit of research it became clear that the passage in Acts was translated improperly, besides the KJV and NKJV all other Bible translations state:
“The God of this people Israel chose our fathers and made the people great during their stay in the land of Egypt, and with an uplifted arm He led them out from it. For a period of about forty years He put up with them in the wilderness. When He had destroyed seven nations in the land of Canaan, He distributed their land as an inheritance -- all of which took about four hundred and fifty years. After these things He gave them judges until Samuel the prophet”
Essentially, all Bible versions (except KJV and NKJV) and the oldest manuscripts say that since the fathers were chosen to the distribution of land (during Joshua’s time) took about 450 years AND then he gave them Judges until Samuel. So Acts 13:19-20 is not referring to the time of the Judges as being 450 years but from the fathers (Abraham, Isaac and Jacob) to just after Joshua’s 7 year conquest. From Abraham at 100 years old (Isaacs birth) to the exodus is 400 years (400 year sojourn mentions), 40 years of wandering with 7 years of conquest is 447 years, which fits Acts 13:19-20.
Reconciling Acts 13:19-20 sources
http://www.christianlibrary.
https://apologeticspress.org/
As stated above, the time of the Judges with the years of oppression is 450 years not including Samuel’s time because Samuel was a Judge his whole life. Adding to that we must have the 40 years of wandering, 7 years of conquest, an unknown time for Joshua’s peace/rest (average estimates are ~40 years), Saul and David’s reigns over the monarchy of Israel which is 40 years for Saul and 40 years for David, ending with the fourth year of Solomon’s reign in 976 BC. This should be 480 years (1 Kings 6:1), but it is not; it adds up to 617 years not including Samuel’s time. (I dropped the fourth year into Solomon’s reign, throughout this post I do not include it but will conclude with ‘give or take four years’)
The most disturbing is when I see articles say we must rework 1 Kings 6:1, basically many do not want to read the context of Judges and 1 & 2 Samuel. Context is key, either the Bible is right or it is wrong, we don’t substitute our presuppositions or other peoples opinions. I have thoroughly read Judges and 1 & 2 Samuel, written out a timeline with minimal commentary which I will link but I do not hold to their timeline 100% because many of the explanations are invalid based on a faulty synchronism with Egypt and conclusions they didn’t explain. (Linked below)
https://www.bible.ca/
Any asterisks ** are places I made inferences and they are places where the age and death can be potentially shifted or judgeship.
Moses 80 years old at the Exodus - 1450 BC
Wandering of 40 years - 1450 - 1410 BC
Joshua’s Conquest 7 years - 1410 - 1403 BC
**Joshua’s time of rest/peace - unknown
**Joshua’s death 110 years old (if 20 years old at Exodus) 1360 BC
-(Note, Joshua is called a young man in Exodus 33:11 while Caleb is known to be past the age of 20 and not under the condemnation of God in Numbers 14:24 & 30. In Joshua 14:10 Caleb says he was 40 years old at the Exodus and 85 when speaking in that verse. We cannot have Joshua too old because scripture says he was young, he could be older than 20 years old but not by much)
Judges 2:16 - God raised up Judges over Israel
3:8 Cushan oppression 8 years 1361 - 1353 BC
3:11 Othniel 1st Judge 40 years 1353 - 1312 BC
3:14 Eglon of Moab oppression 18 years 1312 - 1294 BC
3:14 Ehud 2nd Judge 80 years 1294 - 1214 BC
-(Note: these cannot be split up or modified or have co-reigns, it is very clearly laid out in scripture they each Judged one after another)
*4:3 Jabin & Sisera 20 years 1214 - 1194 BC
**6:1 Midianites 7 years 1201 - 1194 BC
**5:31 Deborah 3rd Judge & 8:28 Gideon 4th Judge 1194 - 1154 BC (40 years)
-(Note: The article linked above shows the synchronism between Deborah and Gideon. Both had the same length of rest, both had the same tribes refuse to join them and the same tribes join them. They fought their battles in different parts of Israel (Deborah north and Gideon central))
**Eli born 1185 BC - this is an assumption on my part which will be explained later on
9:22 Abimelech (not called a Judge) 3 years 1154 - 1151 BC
10:2 Tola 5th Judge 23 years 1151 - 1128 BC
10:3 Jair 6th Judge 22 years 1128 - 1106 BC
-(Note: Many articles suggested combing these two but scripture is clear, one verse to the next, they followed each other so closely there isn’t a verse separating them)
10:7 “And the anger of the LORD was hot against Israel, and he sold them into the hands of the Philistines, and into the hands of the children of Ammon”
**10:8 Ammonite oppression 18 years 1106 - 1088 BC
**13:1 Philistine oppression 40 years 1106 - 1066 BC
-(Note: Here and moving forward is where I diverge from the previous article listed. Judges 10:7 indicates Israel was attacked on two fronts and can be readily implied from 1 Samuel 7:14 this was probably the case. Judges could be contemporary is implied in 1 Samuel 12:9-12)
**15:20 Samson 11th Judge 20 years in the days of the Philistines
-(Note: We do not know when Samson began is Judgeship nor when he died)
**Samuel’s birth 1099 BC
-(Note: This is my assumption, he more than likely was born before this but I am placing him here because the contemporary thought is that Samuel was 12 when God called him in 1 Samuel 3, with the cute story of God calling Samuel but Samuel thought it was Eli but by verse 20 we see he is established throughout Israel as a prophet)
11:26 300 year occupation mention by Jephthah, his Judgeship begins right after this mention at the end of the 18 year Ammonite oppression
12:7 Jephthah 7th Judge 6 years 1088 - 1082 BC
**1 Samuel 4:15-18 Eli’s death 98 years old & 40 years Judge 1087 BC
**1 Samuel 6:1 Ark of God in Philistine hands 7 months
**1 Samuel 7:1-4 Ark of God in Kirjathjearm 20 years 1087 - 1066 BC
-(Note: I place Eli’s death here and subsequently his birth 98 years prior as stated during Deborah and Gideon’s time. It is clear from scripture Eli died when the Ark of God was taken and Samuel was obviously born and old enough to be called ‘old’ in 1 Samuel 8:1. In 1 Samuel 12:2 Samuel calls himself ‘old and greyheaded’ which seems to imply greater age than in 1 Samuel 8:1. This also could mean I need to push Samuel’s birth date back but old is a subjective term, Moses was 120 and was not called old but hearty and hale, Caleb was 85 and not called old but still had strength as a warrior; each person experiences age differently)
12:9 Ibzan 8th Judge 7 years 1082 - 1075 BC
12:11 Elon 9th Judge 10 years 1075 - 1065 BC
12:4 Abdon 10th Judge 8 years 1065 - 1057 BC
**7 year gap for Samuel and his activities, meeting with Saul and anointing him captain. This also gives time for the events from Judges 17 to 21 to happen, there are no more Judges raised up after chapter 17
1 Samuel 11:15 Saul is King 1050 - 1010 BC
**Samuel’s death 1011 BC
-(Note: 1 Samuel 25:1 & 1 Samuel 28:3 records his death but within a short timeframe Saul calls on a witch in 1 Samuel 28:7 to bring Samuel back since God had abandoned him. Within days it seems Saul dies, that is my interpretation of 1 Samuel 29:10 when David departs, then in 1 Samuel 30:1 it had been only three days for David and his men, so the rest of chapter 30 could be seen in a short period, a week to a few weeks. In 1 Samuel 31 we have the death of Saul and three of his sons, so I place Samuel’s death during the last year and regnal year of Saul)
2 Samuel 5:3-5 David is King, reigning 7 years over Judah and then 33 years over Judah and Israel 1010 - 970 BC
**2 Samuel 2:10 Ishbasheth, Saul’s son who is 40 years old in this passage reigned after Saul (contemporary with David, potentially) for 2 years over Israel.
-(Note: 1 Samuel 13:1 has missing numbers for Saul’s reign, there is much contention over this but most Hebraic scholars think his Kingship was between 22-42 years with the majority saying it is 32 years. This whole verse is omitted in the LXX, Syriac and Vulgate have two different translations and the MS has 1 & 2 numbers and some copies with a 30 added, meaning 32 years. Saul reigning for 32 years could make sense in light of his son Ishbasheth being 40 years old and ruling the last years after his father died but it contradicts Acts 13:21 that says Saul’s reign was 40 years. Whatever the puzzle is here, it is not enough to shift the chronology more than 10 years at most, so very insignificant and a minor scribal error)
To conclude we have 40 years of wandering, 7 years of conquest, Judges and oppression years 302 years, Saul and David 80 years of Kingship which equals 429 years. 1 Kings 6:1 says 480 years so minus 429 years which is 51 years that we can place during Joshua’s time of peace/rest as mentioned in Joshua 23:1 “And it came to pass a long time after that the LORD had given rest unto Israel from all their enemies round about, that Joshua waxed old and stricken in age”
Descriptions of the Judges - Fun article to read, simple condensed biographies
]]>This study is vitally important because the conclusion will revolutionize how mankind views their past. Right now history is portrayed as though man slowly progressed over deep time and evolved the ability of language. This data will show you that the statistical probability of this occurring with human language is highly improbable, to the point where you could say it never happened. The implications of my research will have a profound impact on society and how we view our historical past. With new insight never before considered, you are about to witness the collapse of an old system and the rise of a new one.
They tell us man grunted language into existence. But who are “they”? Scientists, that's right. Not linguists who actually study and specialize in language. Are you going to take some paleontologists, zoologists or anthropologists idea’s for human language development from people who know nothing about the subject nor has never studied it? That is not logical. So before I get into why this is impossible developmentally, neurologically, mathematically and statistically that language can not arise on its own. I want you to ask yourself, “why would man wait hundreds of thousands of years before using the same skills of today to record history?”
Speech IS a fundamental part of evolution, even Darwin himself said: “Speech is 95 percent plus of what lifts man above animals!” So no one can say that language has nothing to do with evolution, it most certainly does. And Linguistics requires intelligence"- Where does it come from? "Language as a code only comes from an intelligence". Although Darwin attempts to explain the rise of language as a part of the evolutionary process in The Descent of Man, he fails miserably. As a result, in the entire debate over the Evolution of man, language—was abandoned, thrown down the memory hole and forgotten. This is why today, language origin is ignored by evolutionists and they so quickly SCREAM, THAT HAS NOTHING TO DO WITH EVOLUTION. But if tomorrow a monkey started talking it would be front-page news and proof of evolution. You need to see the double standard bias these people really have.
So now, let's get into the details of language; What I have noticed from studying stochastic models (a tool for estimating probability distributions of potential outcomes by allowing for random variation in one or more inputs over time), is that human language could not have arisen on its own, and the numbers required for it to have, don't come even close to telling the real story. Anyone can take a look for themselves at ANY of the stochastic models and notice the same. As all of them take into account possibilities of human populations anywhere from as low as 10,000 (as assumed by the world population average 200,000 years ago (World_population_estimates) to as high as 1 million (a high over-estimate).
I am not talking about communication, I am talking specifically about language! Huge Difference.
Keep this in mind, Epoch 1 has nothing whatsoever to do with geology, paleontology or time. It is a period used to denote the transition from non-language (epoch 0) to language (epoch 1). An epoch is a period that represents a state. epoch 0 has no grammar and therefore no language. Epoch 1 is the first use of grammar and accordingly the first use of language. The period between epoch 0 and epoch 1 is not a day, a week, or a year. It is any period, and gradations required for the transition between the states. That is why it's called an epoch and not a year.
Reviewing all possible stochastic models associated with the age of complexity constraints of language acquisition, it is clear that there were not enough people and that human mental development could never have allowed humans to invent language. These models are what have helped me determine this information to be a fact, that no evolutionary theory or debate can get around. I will get into more detail, but for now, I think this first lesson on the Markov processes is far more important to help you understand how this process can be used to show a transition between states (No language to Language) “epochs”.
Draw 2 bubbles side by side. In the left bubble put the letter A. In the right bubble put the letter B. Your bubbles represent states: State A and State B. If we further define the states, we can say that State A represents an epoch of no language and state B represents an epoch of language. We begin with our entire world population in bubble A. They can only move to B if they can pass the burdens associated with the age and complexity constraints which are based on more than 300 years of medical, psychiatric, and linguistic observation. At epoch 0 there aren't enough people in bubble A to overcome the burdens and move to bubble B. And it is not even remotely close. There are a lot of definitions and math associated with the full explanation which I will elaborate a little bit on below, but I do not want this to be boring and get lost on you. In a nutshell, it is a population problem, where language cannot arise on its own. There weren't enough people at epoch 0 to overcome the burdens of the constraints. And people don't get to graduate to bubble B for free. They have to (overcome) pass the constraints. If there weren't enough people to overcome the burdens at epoch 0, then language is not a byproduct of nature. If language is not a byproduct of nature, then language came from somewhere else. If language came from somewhere else, then evolution is false. And because it only takes ONE piece of evidence to falsify the theory of evolution, I have done just that with this irrefutable evidence.
I guess the next best way for me to describe this model is by looking at multiple cases of feral children or totally neglected/isolated children. Specifically let’s look at the data from Genie Wiley's case, mostly because I like this one.
Using Dr. Eric Lenneberg and Professor Susan Curtiss’s work regarding the age and complexity constraints of language acquisition and then applying that data to a small world population (hint all world populations were small until agriculture began), then it forms an infinite no language loop (parent to child to parent to child over and over). And there is no natural exit from the loop. Studies found once a human is in the loop they are trapped. There aren't enough people to overcome the statistical burdens, it's not even remotely close even in a larger population. If it was even in the ballpark, then I would give evolution the benefit of the doubt. But it isn't, and that means there is no natural path to language acquisition. One would need a population size that is sufficient to meet the burdens that are imposed on the population. Language came from somewhere else it seems and nature had nothing to do with it.
You were raised normally which means that you were provided with language stimuli and you met the standards for language fluency before you turned 5 years old. The defining difference between a Language acquisition (L1) and a Second-language acquisition (L2), is the age of the person who learned the language. For example, linguist Eric Lenneberg used second language to mean a language consciously acquired or used by its speaker after puberty. Language is only learned for L2. L1 is not learned. L1 is acquired. And there is a huge difference between learning a language and acquiring a language. Genie was a prime example of that difference. We are not talking about communication here, we are talking about language.
You can use your L1 for the rest of your life to learn any new abstract concepts or for gradations to learn a new language (L2). That is not a challenge. Before there was language, there was no language. The challenge was not to get primitive man to use his L1 (to learn new abstract words). Primitive man would have been like Genie Wiley (no language at all) https://en.wikipedia.org/wiki/Genie_(feral_child). She had no L1, nor did primitive man. Dr. Eric’s challenge would have been to create grammar because none existed. So you can't compare primitive man's challenges to your ability to use your L1 to learn new abstract things. I have noticed from all the research that abstract words can not be learned after puberty because abstract concepts cannot be learned. The information I have gathered comes from the work of Dr. Lenneberg, and his book “Biological foundations of language” and more than 300 years of medical observations. I am just taking it to the next level and combining it with others’ work and have concluded there is a major problem that is greatly overlooked because the research itself wasn't trying to figure out where language came from, but rather how to teach these poor feral children how to communicate. Which in the end was futile because it's an impossibility.
Nativist Noam Chomsky suggested that acquiring language could not be fully explained by learning alone. Instead, he proposed that children are born with a language acquisition device (LAD), an innate ability to understand the principles of language. Once exposed to language, the LAD allows children to learn the language at a remarkable pace. Linguist Eric Lenneberg suggests that like many other human behaviors, the ability to acquire language is subject to critical periods. A critical period is a limited span of time during which an organism is sensitive to external stimuli and capable of acquiring certain skills. According to Lenneberg, the critical period for language acquisition lasts until around age 13. After the onset of puberty, he argued, the organization of the brain becomes set and no longer able to learn and utilize language in a functional manner.
Again, I'm not saying that people with an L1 can not learn new abstract words. Humans have an L1, so they can learn any new abstract words. Primitive pre-language man did not have an L1 according to the theory of evolution. I'm saying that there is a time limit for homo sapiens to acquire L1 which science has found to be age 13. If they miss that window, no amount of time, money, skills, technology, resources, education, or effort can fix it. If you were language deprived for the first 13 years of your life it can't be fixed, no matter how much time and effort are thrown at the problem you will never learn human language. Language deprived post-pubescent homo sapiens can never become fluent. The ability is forfeited if not acquired before puberty. Primitive man would have had the same limitations but with a much smaller world population. And it would have been statistically impossible for them to exit the loop.
Trying to argue that a certain number of people are not needed to form the first language, only proves that they have never heard of HJ Eysenck and his work with the rarity of creativity (hint creativity is extremely rare. Most people are not creative at all). Most are unfamiliar with the work of Dr. Lenneberg and Professor Susan Curtiss regarding these age and complexity constraints as well. The results are devastating to the theory of evolution of man grunting language into existence.
Sadly today public teachers just irrationally say “all primitive homo sapiens must have been creative”, even though all the evidence says only a tiny percentage are or could have been in the past. I have found that in the academic world they ignore the 300 years of evidence surrounding the age constraints culminating in Dr. Lenneberg's book and they just say “there is no age limit, any language deprived person of any age can acquire L1”. Even though the evidence shows that to be unequivocally wrong. In today's world of the unchallenged theory of evolution, we ignore Professor Curtiss’s work on complexity constraints and just pretend that grammar formation would not have been an immensely complex task for language deprived primitive man. We also ignore that writing worldwide seems to have developed at the same time, farming at the same time, calendars, math, and inventions all just arose out of seemingly nowhere worldwide all at the same time.
When it comes to language, the only way to get around this is to ignore every bit of scientific evidence in this field. Again there is no cutoff point for humans to learn new meanings to words that describe physical objects that can be seen (nouns). However, there IS A HARD CUTOFF POINT for language deprived people to learn abstract words (grammar). That is why no language deprived post-pubescent person has ever been able to achieve fluency.
Words without grammar are just vocabulary. Fluency can not be achieved without grammar. Grammar is what can't be learned by language deprived people after puberty or after 13 years of age. There is a huge difference in a post-puberty person's ability to learn the difference between the words cat vs rain or dog vs yesterday. The words for physical objects are capable for them to learn. But the words for anything abstract are impossible if they are over 13 and language deprived. This same limitation would have had a huge negative effect on primitive man.
Think about this; You can see nouns. You can point to nouns and say the word to teach a language deprived person what a noun is. You can't point at abstract things. Genie Wiley was taught the meanings of hundreds of nouns by James Kent and Susan Curtiss. She never learned the meaning of a single word of grammar. So it's obvious the problem is with the abstract words and thought. The evidence shows that grammar for L1 must be learned before you turn 13. If it is not learned before 13 then you will never learn L1. Noam Chomsky said they threw millions of dollars and spent years trying to teach genie grammar and the most brilliant minds in the world couldn't do it because it is not possible. If it is not possible then when looking for candidates to form the first grammar by primitive man, you have to eliminate everyone over the age of 13 from the model.
The evidence shows that this is an impossibility, man had to have been taught language, exactly what the Bible says. Again people can learn nouns but can contribute nothing to the formation of grammar. And that is 75% of the people NOT including the elimination for complexity. Over 75% are just the people that are too old to contribute. There also has to be elimination based on the evidence of complexity/creativity. Complexity constraints wipes out everybody else. There is no one left that is qualified to be a candidate to form the first language. There were not enough people. Not even close. Logically, mathematically and scientifically this destroys evolution's theory of language formation. Especially considering 100,000 years is the time frame origin of language that these renowned experts like Noam Chomsky, Susan Curtiss, and other leading professional linguists used to calculate this phenomenon. It doesn't matter if it was 2,000 years ago, 200,000 years ago, or 200,000,000 years ago. The characteristics of the problem forms an infinite loop from parent to child that contains no natural exit. It is not possible to transition from non-language to language naturally because there is no natural exit from the loop. It is impossible for homo sapiens to transition from non-language to language. Humans have always had a much higher density in our lower jaw, as compared with the top teeth, and this is consistent with spoken language. So we apparently always have had that ability since humans were created. Even secular scientists agree and they hate Creationism.
Without abstract words, grammar doesn't exist. Without grammar, language doesn't exist. And that cutoff occurs around puberty. This single constraint wipes out approximately 75% of the pre-language world and renders them incapable of contributing to the formation of the first language. And unfortunately, that is not the only encumbrance to the formation of the first language. The 2nd constraint wipes out everybody. There are no candidates left to form the first language after the constraints are applied. There weren't enough people, that is the main problem and a fact of the situation. Even if you add 1 billion people to the model, it wouldn't be enough. It’s not about time, either, 900 million years it still wouldn't matter, it's all about population size.
Wolves don't have a language, they have primitive communication techniques. Fish don't have a language. They have primitive communication techniques. No professional linguist would say that wolves possess a language or that fish do because non-humans do not communicate by using language. To be classified as a formal language, grammar must be present. Wolves and dolphins, for example, have no grammar, even my friend’s bird who can pronounce words has no language. Only humans have grammar. So all known fish, birds, primates and wolves can't talk about yesterday or tomorrow or past activities or future activities. They can only make sounds about current activities or base nouns. Only human children possess the ability to learn grammar for L1. Adults then can take their knowledge of L1 and use translations to learn an L2, but no language deprived adult can ever learn grammar without L1. If a person has been deprived of language for the first 13 years of life then it is over.
Other study results found that anatomically speaking, apes and monkeys are perfectly well equipped for humanlike speech even compared with a human! The simulated monkey’s voice sounds flat and gravelly, but the words are clear and comprehensible. They even share the same broca and wernicke regions of the brain responsible for speech and language called area 44 and F5 https://carta.anthropogeny.org/moca/topics/brocas-and-wernickes-areas. Then why can’t they speak? Because their brain is not the same as ours! Not the so-called larynx location vocal cords & larynx muscles which they have been lying to you about. We were created differently and nothing can change that. They can never reach L1, their brains are only able to comprehend basic epoch 0 (nouns). The same applies to apes and sign language. They tell you that apes can talk to us easily using sign language. Well, the best to ever live and the most popular ape “Koko”, does not have attributes that any linguists would say is language. There is a big leap between "communication" and "language." There is no evidence that her signs used consistent syntactic rules. She seemed not to be able to talk about the past or future or things that were not present. She strung words together, and Dr. Patterson would rephrase them to be coherent, or simply say what she believed Koko meant. Koko would communicate about food by, for example, pointing to something in Dr. Patterson's pocket and signing about eating. Koko's use of words were the exact same as Genie, the girl who was raised until about 13 without language, and who learned words but not the other aspects of language. Like Koko, she would string words together to get some meaning across without actually creating sentences. In reality, Koko was the best ape in history at sign language and in those experiments, she only mastered 50-100 words, though they taught her 2,000 and to sign 1000.
Koko and other apes signing is not truly linguistic. For example, when shown a picture of a swan, Koko is reported to have said "water bird". The researchers claim that this is the "name" Koko gave to what she was seeing. However, with the new research proving L1 is not achievable, it actually just proves that Koko was simply describing what she saw in the picture: water and a bird. Much of the research results appear to be the result of confirmation bias (what the researchers WANT to see is interpreted as being so) rather than actual evidence that these animals are not producing true linguistic forms at all.
It is significant as well that almost every Deaf person involved in this research with animal sign language has left this work, because most deaf people refuse to ascribe linguistic capability to uncertain evidence, and are almost always overruled by non-native Hearing supervisors of this research in order to justify their research. Of course, in the movies, TV and tabloids, signing apes are always portrayed as being more linguistically competent than they really are in life, which gives the general public a misunderstanding of what is truly happening with this research. In reality, even the most gifted of apes (such as Koko) have never mastered ASL beyond the level of an infant. Whether it is in sign language, or in your theoretical vocal transplant, the apes have not, and never will, master human language.
They begrudgingly admit this “Talking birds and signing apes rank among the most fantastic claims in the literature on language evolution, but examination of the evidence shows fundamental differences between child language acquisition and nonhuman species’ use of language and language-like systems. For instance, dogs can respond to a few hundred words, but only after thousands of hours of training; children acquire words rapidly and spontaneously generalize their usage in a wide range of contexts. Similarly, Nim Chimpsky, the chimpanzee that produced the only public corpus of data in all animal language studies, produced signs considerably below the expected degree of combinatorial diversity seen in two-year old children, and with no understanding of syntactic structure or semantic interpretation. Though these studies are of potential interest to understanding the acquisition of specialized, artificial skills — akin to our learning a computer language — they do not inform understanding of language evolution.”
They conclude: “For now, the evidence from comparative animal behavior provides little insight into how our language phenotype evolved. The gap between us and them is simply too great to provide ANY understanding of evolutionary precursors or the evolutionary processes (e.g., selection) that led to change over time.”
I feel like I should mention that most Deaf people find the use of signed language with primates to be insulting. This is because since the middle of the 1800s, Oralists (people against the use of signed languages in the education of Deaf people) have justified Oralism by stating, among other things, that the use of sign language is an evolutionary throwback to when humans (cavemen, Neanderthals, etc) did not communicate through speech, and used gestures. Modern-day Oralists will often use the research on primates to assert a claim that if "monkeys can learn sign language, then that goes to show signed languages are not true languages, since language (meaning spoken language) is what separates humans from animals". Of course, this is far from the truth, but it brings up a painful history that we are still trying (without much success) to overcome.
Remember, it is not about communication, we can communicate with a dog. It’s about language formation, not simple communication skills. To argue and say early man primates had nouns, and all they had to do was add verbs is now proven wrong! And to argue that children could have formed the first language is also wrong because the cut off was age 13, maximum. Man had to be taught language, and the Bible says exactly that. And considering ancient Paleo Hebrew “Adam’s language” which has all mathematical, pictorial, descriptive and diverse to the highest degree of all languages, it is not logical that apes nor children developed this. http://www.ancient-hebrew.org/language_edenics.html
To argue that Numbers have nothing to do with it is also 100% wrong. The number of people has everything to do with it because you need a population size that is sufficient to meet the burdens that are imposed on the population. How many people there are on earth affects the probability of everything we do. Consider this logic. A world with 3 billion people is statistically far better odds to send a man to the moon than a world with only 3 million people. A world with 3 million people is far more likely to have knowledge of mathematics than a world with only 3,000 people, etc.. Saying that there aren't enough people also doesn't mean zero probability. It means extremely low probability. For zero probability you can throw all the people that ever existed at a problem and it won’t change the fact that it is still zero probability. If you had ever taken a stats course then you would know this. With words, we know statistics play a huge factor as well because its an empirical law under Zipfian distribution called power-law probability distributions. The amazing thing about this law is that it shows no matter what language humans speak, “the” “of” and “and” are the 3 most used words in existence.
Another good thing about language is that we actually have specific detailed data based on more than 300 years of medical observations (not theory) that we can use to build a Markov process and then apply that process to the population size that evolutionary biologists believe existed back then. The Markov process shows there weren't enough people. And it isn't even remotely close. Even if we add 1 billion people to the model, it fails completely… https://www.cs.cmu.edu/~roni/papers/survey-slm-IEEE-PROC-0004.pdf. So again, Nouns are still able to be learned, but grammar becomes an impossibly heavy lift that no language deprived teenager or adult has ever been able to lift. If the evidence shows this to be an impossible task for any language deprived person that is over 13 years old, then all people that are over 13 must be eliminated from pre-human language models because the evidence shows that it would have been impossible for them to contribute to the formation of the first grammar. But the problem doesn't stop there. The children that are below 13 have to pass the constraints to be candidates to form the first grammar. If you wanted to see how many people in a group can bench press 1,000 lbs you would look at empirical evidence to determine how common of an event this would be. You would then take your discovered evidence and apply it to the group in question to make a prediction about how many could bench press 1,000 lbs. You wouldn't just say “well my test group has 1,000 people in it, so I think all of them can bench press 1,000 pounds.” If bench pressing 1,000 lbs is a rare event, that fewer than 1 out of every 10,000,000 people can perform, then you would need a very large test population to find the 1 person to make the lift. If you only had a test group of 20 people, you wouldn't expect the lift to be successful. It would be extremely statistically improbable for a random test group of size 20 to produce someone capable of performing the lift. This is analogous to the language "lift" you are imposing on the small world population at epoch 1 (Early Earth's population). It is a statistical extreme improbability that contradicts all of the available scientific and mathematical evidence. There weren't enough people and it’s not even close.
The SPECIFIC problems that language has arising on its own, make it impossible for homo sapiens to transition from non-language to formal language because an infinite loop is formed that contains no natural exit. And that infinite loop is caused by very specific problems. The model even uses a 100,000 years ago base, as the origin of language because that is when renowned experts like Noam Chomsky, Susan Curtiss, and other leading professional linguists believe it began. The amazing part is, when it actually began doesn't matter. It doesn't matter if it was 200,000 years ago or if it was 6,000 years ago. The characteristics of the problem forms an infinite loop from parent to child that contains no natural exit. It is not possible to transition from non-language to language naturally because there is no natural exit from the loop. Once humans are in the loop they are trapped there. There is no natural way out of the loop.
RECAP; All of the evidence above is paired from medical observations of isolated, abused, neglected, and feral children worldwide, with population estimates from evolutionary biologists, which shows that there is a huge mathematical problem. Without abstract words, grammar doesn't exist. Without grammar, language doesn't exist. And that cutoff occurs before, or at puberty (age 13). This single constraint wipes out approximately 75% of the pre-language world population and renders them incapable of contributing to the formation of the first language. And unfortunately, that is not the only encumbrance to the formation of the first language. The 2nd constraint wipes out everybody. There are no candidates left to form the first language after the constraints are applied. The case files of Genie Wiley alone contain objective evidence that destroys evolution theory. And to say this doesn't qualify as evolution, it absolutely does, both the evolution of language and on humans themselves as homo-sapiens are the focus of the study.
At epoch 0 (Let’s give it approximately 100,000 years ago for the benefit of the doubt) there were not enough people on earth to overcome the burdens of the age and complexity constraints and out of hundreds of years and thousands of cases of neglected, abused, traumatized and feral children. Since observations and study began in 1644, not a single case of a child over the age of 13 has ever been able to learn language. And that is not based on creationism or any religious belief. This is all based on medical observations over the past 250+ years. Based on the accepted criteria for falsifying evolution theory by professional scientists, this problem meets that criteria, because for evolution to be true, there has to be a natural path to everything that all species possess.
Knowing all of this, imagine now the idea that propagates today that humans unconnected worldwide all managed to form language independently and roughly at the same time without knowledge of one another. Utter nonsense and this falsifies the concept that language arose on its own and that man grunted it into existence. Evolution falsified once again with observable facts.
Demonstrating a failure in heritability, selection, variation or Quantitative linguistics (QL) is a sub-discipline of general linguistics and, more specifically, of mathematical linguistics... QL is empirically based on the results of language statistics by itself disproves evolution. Darwinists don’t realize or want to acknowledge this. Most actually think that to disprove evolution requires disproving just the supporting evidence. But real scientists know that to disprove the theory only requires a single successful challenge against it and then the theory becomes untenable.
As you should know now, even Darwin himself acknowledged language is the major factor in human evolution and I have given verifiable, testable, provable, observable evidence that has 100% falsified the theory of evolution. Considering evolution predicts everything so that it can never be falsified, that's pretty incredible, wouldn't you say? For those of you who think this doesn't and it's too trivial, you are wrong. Falsifying something is basically evidence to prove the current concept wrong. Something small and seemingly insignificant will also do the trick. If someone is accused of a crime, all it takes is a single piece of evidence, no matter however small and seemingly insignificant, which proves the person's innocence or guilt to nullify the thousands of other pieces of evidence.
Highly trained police officers and highly experienced police detectives are forever at risk of falling victim to their belief bias when it comes to evaluating evidence that proves a suspect's guilt; just as the general population and scientists themselves are forever at risk of falling victim to their belief bias when it comes to evaluating evidence for evolution. They go in already assuming evolution is true and then look for evidence to prove it to continue getting grant money. That's not science, that is a joke.
We can look at the Beginning of this research and find that ten such children all the way back in 1735 and a few even back in the 1600s have helped us conclude that the cut off for being able to ever learn language is 12 to 13, it could be even younger (since puberty range is 8-13) but we so far have no one younger to study, and let’s hope it stays that way for the children's sake. https://linguistics.ucla.edu/people/curtiss/1974%20-%20The%20development%20of%20language%20in%20Genie.pdf
Marc D. Hauser et al puts it perfectly in their study titled; The mystery of language evolution. When stated “Understanding the evolution of language requires evidence regarding origins and processes that led to change. In the last 40 years, there has been an explosion of research on this problem as well as a sense that considerable progress has been made. We argue instead that the richness of ideas is accompanied by a poverty of evidence, with essentially no explanation of how and why our linguistic computations and representations evolved. We show that, to date, (1) studies of nonhuman animals provide virtually no relevant parallels to human linguistic communication, and none to the underlying biological capacity; (2) the fossil and archaeological evidence does not inform our understanding of the computations and representations of our earliest ancestors, leaving details of origins and selective pressure unresolved; (3) our understanding of the genetics of language is so impoverished that there is little hope of connecting genes to linguistic processes any time soon; (4) all modeling attempts have made unfounded assumptions, and have provided no empirical tests, thus leaving any insights into language's origins unverifiable. Based on the current state of evidence, we submit that the most fundamental questions about the origins and evolution of our linguistic capacity remain as mysterious as ever, with considerable uncertainty about the discovery of either relevant or conclusive evidence that can adjudicate among the many open hypotheses. We conclude by presenting some suggestions about possible paths forward.”
Since science deals with p-value which is statistical hypothesis testing, of what the probability value is for a given statistical model, the probability that, when the null hypothesis is true - the statistical summary would be greater than or equal to the actual observed results. That said, all evidence shows that human language formation cannot arise on its own and because of p-value, stochastic models have all falsified the theory of evolution regarding language formation. Thus by the criteria put forth by science which is capable of falsifying a theory. Then scientifically, human language evolution is falsified and the Bible is correct again.
All 6 known theories of human language origin (https://mentalfloss.com/article/48631/6-early-theories-about-origin-language) have just been dispelled. With actual testable, repeatable, observable science in well over 300 years. Man never grunted language into existence and it’s impossible for primates to ever learn language. If you were able to prove any of this work wrong, then you’re in line for a Nobel Prize, because it would change everything! This is why I said in the beginning, I won't hold my breath for you to debunk me. No one has, and no one can.
The Creation story tells us that Adam was Created by God, and Adam’s mind would have been like an empty child's. Notice what Scripture tells us what God let Adam do “Adam gave names to all the livestock, the birds in the sky and all the wild animals.” Gen 2:20. Notice Adam was using nouns, perhaps this is how God even taught Adam eventual Grammar.
Special Thanks Dr. Eric Lenneberg & Professor Susan Curtiss for this current research into language development http://webcache.googleusercontent.com/search?q=cache:TPonawWuW8gJ:cbsd.org/cms/lib010/PA01916442/Centricity/Domain/2100/Genie%2520Wiley%2520Reading%2520and%2520Documentary%2520Questions%2520-%2520Copy.docx+&cd=13&hl=en&ct=clnk&gl=us
The mystery of language evolution Marc D. Hauser,1 et al. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4019876/]]>In 2015, Young-Earth Creationist (YEC) Dr. Nathaniel T. Jeanson predicted the mutation rate of mtDNA in humans and 3 different animal “kinds”.
Since that time, those predictions based on a YEC timeline, have come to confirm YEC. This confirmation has demonstrated that we can explain the diversity we see today based on the fast observable mutation rates we find in some pedigree studies.
Regarding the Y chromosome, however, we have recently discovered that the observable mutation rate is also extremely fast, far beyond evolutionary expected predictions, and far outside their time frame. This was discovered by Dr. Jeanson in 2019 when he was reading the Poznik et al. 2016 technical paper and noticed that they obtained a much higher mutation rate than they published. They hid it under the supplemental section of their study (probably to keep grant money coming in since it falsified the very theory they were paid to confirm). Dr. Jeanson published these findings of the fast mutation rate gathered from their results and demonstrated that the rate can explain all the genetic diversity we see in the world today with the exception of Africans.
Jeanson’s 2019 paper shows the root position on the far left. The fast rate captures nearly all known haplogroups (even many Africans if accounting for the highest rate), with the exception of the deepest A00 branch length belonging to a subset of Africans. Since he has yet made any future predictions on the Y chromosome, I will focus this study on that. Specifically, and using the YEC timeline predicts what we will find when southern African pedigree studies are finally published.
Back to the Jeanson and Holland 2019) paper. They found that the Y chromosome mutation rate was much higher than that which the evolutionary model assumed to be true. Once again the phylogenetic mutation rate charts they invented failed miserably to real-world observation. Rather, results fell in line with the expectations of YEC after comparisons were derived from low coverage vs high coverage Y chromosome sequences (Poznik et al. 2016). The high coverage Y chromosome test results finally gave the data we have needed to observe an actual mutation rate rather than infer one. The results implied that the total timescale for the human Y chromosome tree was only a few thousand years. That’s right! A mutation rate so fast that even the slowest mutation rate obtained from the slowest mutating people could not possibly push humanity back even 10,000 years!
The actual mutation rate for Europeans was 2 to 3 base pairs per generation, on average. Keep in mind these results were not from African people (no African father-son pedigrees were part of either the Karmin et al. 2015 and Maretty et al. 2017 studies), who of course biblically are Ham’s line. As Ham inherited all of Africa according to scripture.
The mutation rate for Japheth’s line tells us a few things. 1:) Europeans are known to have the slowest mutation rate of all people groups. The Amish for example mutate 7% - 14% SLOWER than even other Europeans, because of their high generation times, and cold regions where they live (in our opinion). Therefore, if we know the slowest mutation rate of the Y chromosome, and it can explain the diversity of all people groups on earth except for one, then we do not have much of a problem on our hands as YEC’s. Evolution on the other hand, has a substantial problem. You see, all that we as YECs have to do is account for a single people group (Africans) having a slightly faster mutation rate (people who have yet to be tested). Evolutionists however, needed the observable mutation rate to be exponentially slower than what has been discovered in even the slowest mutation rate studies.
This slow mutation rate found in the Amish (January 21, 2020, in PNAS) was so shocking to the evolutionary community who believe in Neutral theory (That all things in nature, including humans, mutate at the same rate), stated; “It really looks like environmental differences might actually [have] the most significant effect on the number of mutations that you pass on to your offspring, rather than . . . there being some sort of gene causing mutations”, says Aylwyn Scally, a geneticist at the University of Cambridge.
You see, the 59 Amish families were a perfect group of people to test since they have been genetically isolated from other populations since the 1700s and all descended from about 700 individual founders. They had a seven-percent-lower mutation rate compared with the other populations.
Timothy O’Connor from the University of Maryland and co-author of the study stated; “We were pretty surprised,” Initially the team thought the lower mutation rate had to be a mistake from the sequencing or analysis. “We did basically everything we could to try and figure out what kind of artifact would be causing it, and we couldn’t find one.” So far the group has speculated that environmental factors are probably the cause for this slower mutation rate phenomenon. You will notice though, that they made no predictions based on this. Yet we have because our model tells us, so we have a hypothesis to start out with to make predictions based on.
Parsons actually already discovered this slower mutation rate back in the ’90s. You can see in the chart near the bottom. He noted that the Amish mutated 14% slower than the average European.
Considering he was looking at de novo mutations of the cell lines in both hypervariable regions of the D-loop, and substitutions. you would expect the same rate as other people groups, but that is not what he found. They have a slower mutation rate and this has now been confirmed in separate studies decades apart.
Most have forgotten about his work, but the FBI still uses his mutation rate to this day and this new study confirms his previous work, which of course points to Eve living 6,500 years ago as his work concluded.
Parsons original 1997 study
Parsons in 1997 studied 167 independent mtDNA lineages (33 Sweden, 73 US mixed ancestry, 5 England, 40 Amish, & 16 people from Utah). Then in 1998 after working on the tsar's DNA case, Parsons conducted another large study along with Holland, about the same size as his first 1997 study. The results confirmed earlier results, humanity mtDNA mutation rates go back around 6,500 years on average.
Based on genetic diversity and the Biblical timeline, Dr. Jeanson has predicted the mtDNA mutation rate in the African Khoisan people would be twice as fast as rates in other people groups. Therefore I will predict the mutation rate of the Y chromosome, using scripture to devise a hypothesis that the reason we see more mutations in Ham’s paternal Y chromosome, is because of a combination of younger generation times, smaller population sizes over time, with more generations total, including warmer weather and lack of migration.
These factors will allow for an explanatory prediction to be made as long as we have a timeframe to start with. Dr. Jeanson uses the Masoretic texts which place’s Noah's flood sometime around 4,365 years ago. I personally view the other bobcat text’s chronology as superior as all other ancient texts place the age of the flood between 5,190-5,320 years ago. So my mutation rate will be rooted around that date, not Dr. Jeanson’s.
The top mutation rate is what we already have evidence for…
3 mutations per generation average (5320 years, 25 years generation time = 212 generations) 212 x 3 = 424 mutations. This number captures the genetic diversity in the Asian and European haplogroups.
Using only the mutation rate from Europeans in the pedigree study, we get up to 1,122 mutations which explains the genetic diversity in basically all the other people groups. Is this true? Yes, we notice most mutations are somewhere around 450. So this observable mutation rate discovery easily explains the genetic diversity we see in all people groups around the earth but one, Africans.
Now, My Future Predictions are based on a Biblical timeline...
4-7 mutations per generation for most Africans (Paternal Haplogroup A2, A3 & B). With the highest mutation per generation being 9.73 mutations per generation in the African San’s people. (5,320 years, with an 18 year generation time over 295 generations = 2,870 mutations over time since the flood.
Now for the African people groups. If the average mutation rate of 3 per generation in Europeans, then what should we expect to find in the average African population? Predictions were based on Ham’s line and since his inheritance was that of Africa. Migration into the land took place right after Babel. So we have around 4,800 years of isolation in the continent, giving the average African between 5-7 mutations per generation. Essentially double the rate of Europeans. The more mutations in Africans is the reason people believe in the Out of Africa theory in the first place. They believe since everybody mutates at the same rate, then Africans must be the oldest because they have more mutations. I have already shown you that even within the European lineage Amish people mutate 7% -14% slower than the rest of their brethren, so we already know the neutral theory is wrong even by looking at just humans.
Although the new observable rapid rate of the Y chromosome literally destroys evolutionism, we like to have not just a better model with more predictions and all the answers, but also have repeatable in-your-face data that cannot be cherry-picked and twisted like evolutionary theory loves to do. We can explain this fast rate in our model, just as we can with the mtDNA fast rates as well. Evolutionists have to invent more desperate rescue devices and ad nauseam storytelling. This includes invoking that we YECs should be using the evolutionary non-observable phylogenetic mutation rates that are based on deep-time evolution being true. This is the one of their most embarrassing arguments to date, because clearly as YECs, we do not buy into deep-time, and universal common ancestry. Therefore, why would we start with the assumption that the very thing in question is true in the first place? It makes no logical sense just like the rest of their horrible arguments against the observable data. This argument is actually very fallacious as it demonstrates the circular reasoning of the evolutionist. The fact that mutations occurred every generation in the Y chromosome study implies that the Y chromosome could record changes in human population size at every generation in human history. This makes the Y chromosome rate far superior to mtDNA mutation rates for reaching a conclusion, as mtDNA is much harder to count as they are less than ½ a mutation per generation.
Dr. Jeanson discovered that pedigree-based mutation rates from high-coverage sequence runs are hidden in the evolutionary literature. They are forced to hide this information because the data falsifies their entire theory (not that it hasn’t already been falsified multiple times over again).
But they know, if they lose mutations, they lose it all. Evolution is a house of cards built on a foundation of mutations. Since they cannot explain the diversity of life we see even regarding mutations, then they have lost and lost they have and the entire concept implodes. We already know they cannot make any predictions because they have already admitted that they can’t since evolution can theoretically do anything, thus also proving evolution is not science. This tells us and everyone with even half a brain that evolution is finished since evolutionary theory hinges on mutations to explain the diversity of life we see. Since not only is the maternal mtDNA mutation rate extremely fast, which points to YEC being true, we also know that the Y chromosome (which is not only much more clear and easier to read than the mtDNA), but is also mutating faster. You will only find the most stiff-necked anti-science atheists refusing to accept the obvious conclusion of the data at this point.
It has no predictive power, it explains nothing since it claims to be able to do everything, and it’s unfalsifiable since no matter what happens it's just proof of evolution. If the data doesn’t match the story it is discarded and something else is invented and put in its place.
The truth is, Evolution only hangs on because it's protected by law and does not allow alternative theories to conflict with it whatsoever. This theory is as anti-science as you can get and it’s all kids are allowed to learn. The observable evidence tells us that the only viable model is YEC and it is ironic that it is the one they mock the most because they know deep down it destroys their theory. Everyone knows that deep down if there’s nothing to worry about then what’s the fear of teaching something else alongside the other? The only reason you would restrict somebody from learning an alternative model would be because you don’t want them to see the truth. If evolution theory was really true then they should be confident as it would be repeatedly confirmed decade after decade. In essence, it would have nothing to worry about. Yet, they protect it by law and disallow any alternative theory. But if you’re reading this, you know as well as I know that the books we studied in school are all in the garbage now, and everything that is in them was wrong. Just like every textbook that is in kids’ hands right now will also be in the trash in 10 years from now.
If you believe in evolution after reading this article, you either 1:) Do not understand what you just read, 2:) You are an atheist and facts do not matter anyway. 3:) You want to keep on the majority side at all costs and toss away real science and evidence to fit in with the majority so you can allow scripture to meld with pagan ideas.
Since evolution Theory is based around one thing, mutations. And evolution can’t make any predictions based on mutations in theory really cannot explain anything and it’s just that, a story. And not even a good one at that. They can’t even explain the diversity that we see in the world today which is all they have claimed from the beginning to do. Yet, it is the young-earth creationist making the predictions based on the observable testable and repeatable science and it confirmed biblical creation.
Either way, none of those are valid reasons. Become a YEC today and watch your life change as you become rooted into the foundation of faith that scripture is based on.
Resources;
Parsons 1997 DOI: 10.1038/ng0497-363
Dr. Nathaniel T. Jeanson Human mtDNA mutation rate; Answers Research Journal 8 (2015): 375–378
mtDNA mutation rate in separate “kinds” https://answersresearchjournal.org/origin-mitochondrial-genes-metazoan/
Dr. Nathaniel T. Jeanson and Ashley D. Holland Answers Research Journal 12 (2019): 393–404. Published on December 4, 2019. Y chromosome pedigree-based mutation rates from high-coverage sequence runs are hidden in the evolutionary literature.
Dr. Nathaniel T. Jeanson; Answers Research Journal 12 (2019): 405–423. human population growth should be reflected in most of the branches of the Y chromosome tree.
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CHAPTER 3
Adam and Eve—The First Couple
By D. Joseph (Standing For Truth)
Featured in THE INDEPENDENT ORIGINS HANDBOOK
The evidence for the literal Adam and Eve is so overwhelming that it's even challenging to pick out a couple lines of evidence to discuss here in this handbook on Independent Origins. The vast amount of evidence and data confirming separate ancestry and a literal Adam and Eve is exactly why I have written so many books on the topic. This includes very technical books written specifically to refute the best arguments put forth by the critics of Biblical creation, as well as books specifically meant to be more basic, and that are not really meant to address every single objection the critic could resort to. The best evidence is almost certainly the fact that we have actually discovered the first couple in genetics. For example, we have discovered both mitochondrial Eve and Y chromosome Adam. There is no disputing the fact that there is one single Y chromosome ancestor, and one mitochondrial DNA ancestor. Every single Y chromosome on this planet is nearly identical, and we have very little variation in the Y chromosome. Our Y chromosome is also incredibly dissimilar to the chimpanzee Y chromosome (less than 35% dissimilar when we consider overall gene content, and overall architecture). The evolutionary community were shocked at the massive differences between human and chimpanzee Y chromosomes. Proponents of human evolution have had to invoke all sorts of rescue devices and hypotheses to explain the incredible discrepancy.
Source: Jennifer F. Hughes, et al., “Chimpanzee and human Y chromosomes are remarkably divergent in structure and gene content,” Nature 463 (January 28, 2010): 536-539.
We know that the Y chromosome mutates a lot faster than ever predicted or expected by the evolutionary community. The number of DNA differences separating men from the Y chromosomal Adam sequence is only a few, and since there is incredibly low variation in the male Y chromosome, this chromosome must be young! You cannot have a rapidly changing Y chromosome with incredibly low variation, and at the same time this chromosome is purported to be old. No—what we see in terms of this uni-parentally inherited DNA compartment is exactly what we would expect to find if Biblical creation were true. To be specific, the male Y chromosome has about 4500 years’ worth of mutation accumulation—which means that our last Y chromosomal ancestor would actually be Noah—and not Adam. This is fascinating news! By invoking a rapidly changing Y chromosome to explain the incredible dissimilarity in human and chimpanzee Y chromosomes only adds more problems for those who want to so desperately believe that humans evolved from ape-like ancestors. We should find some highly divergent Y chromosome sequences on the planet today, and yet we do not. All the data we have suggests that this male specific chromosome is young. The data we have from the Y chromosome strongly supporting separate ancestry has even led to some amazing testable predictions made by Dr. Nathaniel Jeanson of Answers In Genesis.
Please see: Jeanson, N. T. and A. D. Holland. 2019. Evidence for a Human Y Chromosome Molecular Clock: Pedigree-Based Mutation Rates Suggest a 4,500-Year History for Human Paternal Inheritance. Answers Research Journal. 12 (2019) 393-404.
Jeanson, Nathaniel T. 2019. “Testing the Predictions of the Young-Earth Y Chromosome Molecular Clock: Population Growth Curves Confirm the Recent Origin of Human Y Chromosome Differences.” Answers Research Journal 12: 405–423.
The mitochondrial DNA also has extremely low variation as well. Before I continue, I want to take a moment to go over some genetics basics to fully understand the importance of this evidence that points directly to our first parents, Adam and Eve. In genetics, the man passes down the Y chromosome and the woman passes down the mitochondrial DNA. These are the uni-parentally inherited DNA compartments. We can make some seriously good predictions using these DNA compartments. If the Bible’s account of human origins is true, we should be able to look at the mitochondrial DNA and the Y chromosome and trace them back to two common ancestors—two individuals. The data we have did not have to be true if evolution were true, but this did have to be true if the Bible were true. The Bible predicted this. The evolutionary community did not predict the genetic data that suggests we came from just two people in the not so distant past—mitochondrial Eve and Y chromosome Noah (coined Y chromosome Adam by the evolutionary community). Focusing in on mitochondrial DNA, and specifically, Eve the mother of us all—the mitochondrial DNA turns out to be exactly what we would expect if the Genesis account of human origins were true. Remember—this was not predicted by the evolutionary community. There is every reason to believe that if ape-to-man evolution were true, there would be multiple mitochondrial lines with many even being shared with the chimpanzee (human and chimpanzee mitochondrial DNA sequences are immensely different). Remember—the evolutionists did not predict this. They have decided to retrofit the data into their evolutionary story. Proponents of universal common ancestry are constantly having to invoke storytelling and rescue devices. Again—there was every possible reason to have discovered that this mitochondrial DNA ancestor was not so unique. We can construct some very revealing family trees with the mitochondrial DNA. Additionally, we can develop some very intriguing family trees with the Y chromosome as well. I will discuss both. First off, mitochondrial trees grow in branching like patterns. This is due to mutations (changes in the nucleotide sequence of DNA). Basically, we can reverse the clock back to the point where we would find Eve. We could also start with Eve; she would have children, and her children would have children. Every time a child is born, there is the chance that the child would have a mutation, and over time, due to mutations, the family tree gains more and more branches. The next step would consist of backing this process up to where we discover the woman of whom we have all descended from. We know the mitochondrial DNA mutates fast, and we know that there are only a few DNA differences separating any two people on the planet today. This all confirms that we have all descended from Eve—the mother of us all. Proponents of evolution cannot explain why there is such low genetic variation in the mitochondrial DNA, nor can they explain why there are such few DNA differences in this non-recombining DNA compartment. This is precisely why they do not like observed mutation rates. Pedigree based mutation rates where we can measure mutation rates in the present support the model of Independent Origins. And since there are only a few DNA differences in the mitochondrial DNA, with many generations since creation, we can still account for plenty of purifying selection.
Let us now focus on a Y chromosome phylogenetic tree derived by Dr. Robert Carter.
(Figure 2)
This is a tree—a Y chromosome phylogenetic tree (Figure 2). Dr. Robert Carter took all the Y chromosomes and made a Y chromosome family tree. This tree is remarkable, because what we are seeing is exactly what we would expect if separate ancestry and biblical creation were true. Visually, you will notice an explosion from a central point. This is an explosion essentially from Noah—the last Y chromosomal ancestor of us all. But the most important aspect of this tree I want the reader to notice is the length of the branches. This is essentially all a reflection of DNA differences—a reflection of mutations over time. What should be noticed is that when we focus on the length of the branches, we realize that this is an incredibly easy number of mutations to account for in the biblical time frame. This reflects far too few mutations if deep time evolutionary history were true. The reader will remember this was the same problem we covered when discussing mitochondrial DNA. We are not looking at 10s of thousands of mutations here—we are looking at just a few hundred mutations—as would be expected if the Bible’s account of independent origins were true. This data did not have to be true—and yet it is. Evolutionists are constantly having to retrofit the data into their evolutionary story. They did not predict low genetic diversity in humans today, they did not predict the one Y chromosomal line, nor did they predict the one mitochondrial DNA line. One last thing to consider is the fact that the length of some of these branches indicate that some people can pick up more mutations in the exact same amount of time. It is difficult to look at the branch lengths and conclude a definitive amount of time that has passed. Therefore, the pattern, and the overall data is what is so significant.
Source for Y chromosome phylogenetic tree: Carter, R., Patriarchal drive in the early post-Flood population, Journal of Creation 33(1):110-118, April 2019. https://creation.com/patriarchal-drive
“Figure 1. An unrooted neighbour-joining phylogenetic tree of the Y chromosomes, based on the Simons Genome Diversity Project (SGDP) data (from Carter, Lee, and Sanford 2018). SGDP attempted to sample from a wide range of peoples. The result is a tree that is a good representation of total worldwide Y chromosome diversity. Note the clear central ‘starburst’, and the irregular branches that display more mutations than close kin. In this ‘unrooted’ tree, branches are allowed to spread out naturally. The evolutionary root would be located midway along the ‘A1’ branch. Forcing a root at that point would produce the squared-off ‘stairstep’ tree perhaps more familiar to the majority of readers, with long spidery branches leading to a few rare African lineages. But this unrooted representation allows for a more natural reading of the data.”
Also, please see: Carter, R.W., Lee, S.S., and Sanford, J.C., An overview of the independent histories of the human Y-chromosome and the human mitochondrial chromosome. In Proceedings of the Eighth International Conference on Creationism, ed. J.H. Whitmore, pp. 133–151. Pittsburgh, Pennsylvania: Creation Science Fellowship, 2018.
Sanford, J.C., and R. Carter. 2014. In light of genetics…Adam, Eve, and the creation/fall. Christian Apologetics Journal 12, no. 2:51–72.
This is a mitochondrial DNA phylogenetic tree.
(Figure 3)
This photo is also from Dr. Robert Carter. He took this from the 1000 genomes project. This is a family tree of all the mitochondrial genomes in the world. Just like with the Y chromosome phylogenetic tree, I want the reader to notice the obvious, and incredible pattern. This is typically where proponents of ape-to-man evolution close their eyes. This pattern is exactly what we would expect if biblical creation were true. We see an explosive pattern—explosive growth from a single person. In fact, there is history on this tree. We can see geography. For example, there are African specific groups, European specific groups, Asian specific groups, and so on. Not only is this fascinating data that confirms separate ancestry, but it is also empirical. When we focus on the pattern, we quickly recognize that this explosive growth starts from a center point. The Bible claims to be the history book of the universe. Genesis tells us God created two people, Adam, and Eve. Humans were supernaturally created by God and made in His image. The Bible gives no indication that we are related to chimpanzees, or any other form of life. We should be able to test these claims to modern scientific data. As you have seen in both the Y chromosome and the mitochondrial DNA, the claims made in Genesis pertaining to human origins have been confirmed by empirical scientific data. Modern science has discovered Adam (Noah being our last Y chromosome ancestor) and Eve. In addition to the overall pattern, I want the reader to pay close attention to the branches and the lengths of them. As with the Y chromosome family tree, we see these branches have different lengths. For example—have a look at the haplogroup in Europe, the H/V/R haplogroup. These differences in branch lengths indicate that various people groups have happened to pick up twice as many mutations as their cousin. Just like we have seen with Y chromosome DNA phylogenetics, this creates massive problems for the assumptions behind the evolutionary molecular clock. If people can pick up twice as many mutations as other people, then we clearly cannot make assumptions as to when humans and chimpanzees split from a hypothetical common ancestor. We cannot look at the genetic differences between humans and chimpanzees and use those DNA differences to make assumptions as to when they split resulting in a very slow unobservable mutation rate. Remember—proponents of human evolution never question their basic assumptions pertaining to universal common ancestry. They assume that humans and chimpanzees are related through common ancestry. What we are looking at in this phylogenetic tree is essentially random mutations in populations over periods of time. It is important to remember that with both the Y chromosome and the mitochondrial DNA, we see a pattern that fits the biblical based model of ancestry. In regard to the mitochondrial DNA family tree in Figure 3, we see evidence for one woman who lived recently. And so once again, and most importantly, this tree is an obvious reflection of only thousands of years as compared to hundreds of thousands of years as the proponents of human evolution would have everybody believe. These family trees do not have a lot of mutations, and without any preconceived ideas about ape-to-man evolution, and evolutionary molecular clocks riddled with assumptions, the clear conclusion is that this tree (and the Y chromosome tree in Figure 2) is young. Remember—this is one female ancestor from whom we have all descended from, and she is nothing like the chimpanzee. Once again—Independent Origins is confirmed.
Source for mitochondrial DNA family tree: Carter, R.W., Lee, S.S., and Sanford, J.C., An overview of the independent histories of the human Y-chromosome and the human mitochondrial chromosome. In Proceedings of the Eighth International Conference on Creationism, ed. J.H. Whitmore, pp. 133–151. Pittsburgh, Pennsylvania: Creation Science Fellowship, 2018.
Please see references for further reading: Carter, R. W. (2007) Mitochondrial diversity within modern human populations. Nucleic Acids Research, 35(9), 3039–3045.
Carter, R. W., D. Criswell, and J. Sanford. 2008. The "Eve" Mitochondrial Consensus Sequence. In Proceedings of the Sixth International Conference on Creationism. Snelling, A. A, ed. Pittsburgh, PA: Creation Science Fellowship and Dallas, TX: Institute for Creation Research, 111-116.
Jeanson, N.T. 2015b. “A Young-Earth Creation Human Mitochondrial DNA ‘Clock’: Whole Mitochondrial Genome Mutation Rate Confirms D-Loop Results.” Answers Research Journal 8: 375–378.
Nathaniel T. Jeanson, “On the Origin of Human Mitochondrial DNA Differences, New Generation Time Data Suggest a Unified Young-Earth Creation Model and Challenge the Evolutionary Out-of-Africa Model,” Answers Research Journal 9 (2016): 123-130, https://answersingenesis.org/genetics/mitochondrial-dna/origin-human-mitochondrial-dna-differences-new-generation-time-data-both-suggest-unified-young-earth/.
Tomkins, J. P. 2015. “Empirical Genetic Clocks Give Biblical Timelines.” Journal of Creation 29 (2): 3–5.
Tomkins, J. P., and J. Bergman, J. 2015. “Evolutionary Molecular Genetic Clocks—A Perpetual Exercise in Futility and Failure.” Journal of Creation 29 (2): 26–35.
Howell, N., I. Kubacka, and D. A. Mackey. 1996. How rapidly does the human mitochondrial genome evolve? American Journal of Human Genetics 59, no. 3:501–509.
Howell, N., C. B. Smejkal, D. A. Mackey, P. F. Chinnery, D. M. Turnbull, and C. Herrnstadt. 2003. The pedigree rate of sequence divergence is the human mitochondrial genome: There is a difference between phylogenetic and pedigree rates. American Journal of Human Genetics 72, no. 3:659–670.
Parsons T. J., D. S. Muniec, K. Sullivan, N. Woodyatt, R. Alliston-Greiner, M. R. Wilson, D. L. Berry et al. 1997. A high observed substitution rate in the human mitochondrial DNA control region. Nature Genetics 15, no. 4:363–368.
The Independent Origins Handbook - https://www.amazon.com/dp/B08ZW6N7V4
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Do Neanderthals provide evidence for human evolution or Independent Origins (the separate special creation of Adam and Eve):
https://www.youtube.com/watch?v=jLEltauyDL0&t=2s
Man is presently degenerating due to mutation accumulation (Genetic Entropy). The accumulation of low-impact nearly neutral deleterious mutations puts shelf lives on genomes. This indicates that species cannot be old. This also refutes universal common ancestry:
https://www.youtube.com/watch?v=eOU8B7O97Z4&t=425s
Dr. John Sanford lecture on Human Deterioration (Upload from Standing For Truth):
https://www.youtube.com/watch?v=2Mfn2upw-O8
Standing For Truth (D. Joseph) discussion/debate with atheist critic (Andrew Coming known as A Rational Empiricist on Youtube):
https://www.youtube.com/watch?v=xsoPDrGC8_4&t=2712s
What about the fossil record? Does the fossil record provide supporting evidence for ape-to-man evolution? This video dismantles the best evolutionary icons:
https://www.youtube.com/watch?v=WM2T3o0FWfI&t=244s
Don't forget to check out Team Standing For Truth's MANY books on the topic of ancestry!
https://creationistclothing.com/collections/books
KINDLE VERSION for The Independent Origins Handbook now available:
https://www.amazon.com/INDEPENDENT-ORIGINS-HANDBOOK-Standing-Truth-ebook/dp/B09BQ1K1FM/ref=tmm_kin_swatch_0?_encoding=UTF8&qid=&sr=
NEW BOOK COMING SOON (THE HUMAN EVOLUTION HANDBOOK).
SERIES: Debunking Low-Quality and Low-Confidence Science (The Fossil Record) -
https://www.youtube.com/playlist?list=PLeROpayG6Sh3UwTW61omUzj2aXocbMnZE
Michael J. Oard is a leading Global Flood Researcher--and has done fantastic work in not only demonstrating how overwhelming the evidence is for a worldwide flood--but also in answering challenges put forth by the critics.
"Michael has a Masters Science degree in Atmospheric Science from the University of Washington and is now retired after working as a meteorologist with the US National Weather Service for 30 years. He has researched and speaks on the compelling evidence for Noah’s Flood and the Ice Age that followed, and how the incredible wooly mammoth connects to biblical history. Michael has published many papers in his field in widely recognized journals and has written An Ice Age Caused by the Genesis Flood, Ancient Ice Ages or Gigantic Submarine Landslides?, The Missoula Flood Controversy and the Genesis Flood and The Frozen Record. He is also author of Frozen in Time, The Weather Book and Life in the Great Ice Age.
He serves on the board of the Creation Research Society, USA and lives in Montana."
https://creation.com/michael-j-oard
We at Team Standing For Truth have been blessed to have Michael J. Oard on the channel 4 times where he presented undeniable evidence for the Global Flood of Noah. This overwhelming evidence demonstrating the reliability of Genesis, and the validity of a worldwide flood has gone unchallenged by the critics. They cannot refute the data.
Not only has Michael J. Oard blessed us with multiple MUST-WATCH presentations that provided astounding evidence for the Global Flood of Noah--Mike has been generous enough with his time to answer many of the most-common and difficult challenges against the Genesis Flood. In addition to these presentations--we have hours worth of questions and answers. If you are interested in both the evidence for a Worldwide Flood and answering challenges to Flood Geology--then you do not want to miss this series on Team Standing For Truth with Mike Oard.
Amazing Evidence for the Worldwide Flood: The Receding Floodwaters (Plus Audience Q&A) - https://www.youtube.com/watch?v=-zj6tOzEKvo&list=PLeROpayG6Sh1roTdTdR7qxTmkV4U2KcVC&index=1&t=6053s
Frozen in Time: The Ice Age (Plus Audience Q&A) - https://www.youtube.com/watch?v=AP0wOsGnVvQ&list=PLeROpayG6Sh1roTdTdR7qxTmkV4U2KcVC&index=2
Refuting Objections and Answering Challenges (Plus Audience Q&A) - https://www.youtube.com/watch?v=b4YW7U4E8aA&list=PLeROpayG6Sh1roTdTdR7qxTmkV4U2KcVC&index=3&t=3037s
Flood Geology, Refuting the Critics, and Answering Challenges (Plus Audience Q&A) - https://www.youtube.com/watch?v=M4p7M_8nePk&list=PLeROpayG6Sh1roTdTdR7qxTmkV4U2KcVC&index=4
Enjoy--and make sure to share around! The truth is important. It's 2021 and it's a great time to be a Young Earth Creationist!
GENETIC DEGENERATION—EVIDENCE FOR INDEPENDENT ORIGINS
By D. Joseph (Standing For Truth)
Featured in SPECIAL CREATION: DISMANTLING EVOLUTION AND CONFIRMING INDEPENDENT ORIGINS
In this chapter, I am going to focus on genetic degeneration and why it not only presents an unsolvable challenge to evolutionary theory—but also confirms independent origins. Are we evolving or devolving? Do any proponents of ape-to-man evolution actually believe that humans are getting better genetically? We are accumulating far too many mutations per generation. This means natural selection is incapable of filtering out all the new mutations that are pouring into our genetics every single generation. We now know that the genome is both poly-functional and poly-constrained. We also know that the genome has multiple overlapping messages. What is actually happening on the molecular level is science fiction. Try to picture a chapter in a book, and embedded within that chapter (in addition to the obvious meanings in the chapter) are additional meanings. Even in the same sentences there may be several other messages embedded. We write books—but we do not write books that can be read both forwards and backwards—DNA can do this. This is Data compression on the most sophisticated level. In his article “Critic ignores reality of Genetic Entropy: The author of a landmark book on genomic decay responds to unsustainable criticisms”, Dr. John Sanford points out that mutations are even more damaging due to the existence of these multiple overlapping codes within the genomes of life:
“Genomes are the genetic specifications that allow life to exist. Specifications are obviously inherently SPECIFIC. This means that random changes in specifications will disrupt information with a very high degree of certainty. This has become especially clear ever since the publication of the ENCODE results, which show that very little of our genome is actually ‘junk DNA’.10 The ENCODE project also shows that most nucleotides play a role in multiple overlapping codes, making any beneficial mutations which are not deleterious at some level vanishingly rare (https://doi.org/10.1142/9789814508728_0006).” Source: Sanford, J., Critic ignores reality of Genetic Entropy: The author of a landmark book on genomic decay responds to unsustainable criticisms. 7 March 2013.
In the abstract of the paper titled “Multiple Overlapping Genetic Codes Profoundly Reduce the Probability of Beneficial Mutation”, the authors describe why these overlapping genetic codes present a profoundly serious challenge to evolutionary theory:
“There is growing evidence that much of the DNA in higher genomes is poly-functional, with the same nucleotide contributing to more than one type of code. Such poly-functional DNA should logically be multiply-constrained in terms of the probability of sequence improvement via random mutation. We describe a model of this relationship, which relates the degree of poly-functionality and the degree of constraint on mutational improvement. We show that: a) the probability of beneficial mutation is inversely related to the degree that a sequence is already optimized for a given code; b) the probability of beneficial mutation drastically diminishes as the number of overlapping codes increases. The growing evidence for a high degree of optimization in biological systems, and the growing evidence for multiple levels of poly-functionality within DNA, both suggest that mutations that are unambiguously beneficial must be especially rare. The theoretical scarcity of beneficial mutations is compounded by the fact that most of the beneficial mutations that do arise should confer extremely small increments of improvement in terms of total biological function. This makes such mutations invisible to natural selection. Beneficial mutations that are below a population's selection threshold are effectively neutral in terms of selection, and so should be entirely unproductive from an evolutionary perspective. We conclude that beneficial mutations that are unambiguous (not deleterious at any level), and useful (subject to natural selection), should be extremely rare.” Please see: https://www.worldscientific.com/doi/abs/10.1142/9789814508728_0006
In terms of genetics, what we have is a huge genome of 3 billion letters. We know that the mutation rate is extremely high. There are approximately 100 new mutations per person per generation—and it also turns out we have 3 new mutations every cell division in our body. This is astounding. Mutations are essentially alterations in the DNA sequence. Harmful mutations vastly outweigh truly beneficial mutations. This means that harmful deleterious mutations are accumulating in the genomes of living organisms, without any type of mechanism that can filter out so many harmful mutations entering the genomes of living organisms each generation. In addition to this problem for evolutionary theory, beneficial mutations are incredibly rare, and most mutations are deleterious. Ultimately, this means that large-scale evolution cannot be true. We are all more and more mutant every day. We are adding 3 new mutations per cell per day. All these mutations are coming in and they are having tiny effects. The next time somebody tells you that you do not look like yourself—please tell them “of course not, this is the most mutant that I’ve ever been!” In his article titled “Genetic entropy and simple organisms”, Dr. Robert Carter explains exactly why this problem of mutation accumulation leads to a downward spiral that becomes unsolvable for the evolutionary community:
“When living things reproduce, they make a copy of their DNA and pass this to their progeny. From time to time, mistakes occur, and the next generation does not have a perfect copy of the original DNA. These copying errors are known as mutations. Most people think that ‘natural selection’ can dispose of harmful mutations by eliminating individuals that carry them. But ‘natural selection’ properly defined simply means ‘differential reproduction’, meaning some organisms leave more progeny than others based on the mutations they carry and the environment in which they live. Moreover, reproductive success is only affected by mutations that have a significant effect. Unless mutations cause a noticeable reduction in reproductive rates, the organisms that carry them will be just as successful in leaving offspring as all the others. In other words, if the mutations aren’t ‘bad’ enough, selection can’t ‘see’ them, cannot eliminate them, and the mutations will accumulate. The result is ‘genetic entropy’. Each new generation carries all the mutations of previous generations plus their own. Over time, all these very slightly harmful mutations build up to a point that, in combination, they start to have serious effects on reproductive fitness. The downward spiral becomes unstoppable, because every member of the population has the same problem: natural selection can’t choose between ‘fit’ and ‘less fit’ individuals if every member of the population is, more or less, equally mutated. The population descends into sickness and finally becomes extinct. There’s simply no way to stop it.” Source: Carter, R., Genetic entropy and simple organisms: If genetic entropy is true, why do bacteria still exist? 25 October 2012.
This clearly puts shelf lives on genomes. This strongly indicates that man could not have evolved from an ape-like ancestor. Mutations are the destroyer and not the creator. Evolutionists look to mutations as the source for all genetic variation—but mutations are destructive to the genomes of living organisms. If you were to change 1 letter in a genome of 3 billion (we get three billion letters from our mothers and 3 billion letters from our fathers), you are not going to have a huge effect. The effect will be exceedingly small and very subtle. But nonetheless, we have still lost a little bit of information. And if this process is not stopped, you are going to eventually destroy all the information. It is important to note that the majority of mutations are effectively neutral and the typical mutation has too small of an effect on fitness to actually be measurable. Natural selection cannot see these mutations—they are virtually unselectable and invisible to ‘mother nature.’ Selection can of course act on the worst and most damaging of mutations. We have some mutations where you can see an effect of course. For example, 1 letter change can possibly cause disease that would lead to death—but the typical mutation is not detectable in any way. Remember, selection acts on phenotype—not genotype. Selection happens for the whole individual. We are 100 trillion cells, and, in every cell, there are 6 billion nucleotides.‘Mother nature’ has to decide if my body is going to be selected or not. There is much in the genome that selection cannot see. Therefore, selection may not even work at all. Selection chooses the whole genome—and at the organism level, there is either reproduction or non-reproduction. What type of mechanism can the proponents of evolution present us with that can filter out so many new mutations that are pouring into our genomes? Paul Price from Creation Ministries International points out the limitations of natural selection in his article “Genetic entropy: The silent killer”.
“Evolutionists will sometimes try to rebut these ideas by saying things like, “If a mutation is damaging, it will be weeded out by natural selection.’ This oversimplified view of selection is drilled into biology students relentlessly in classrooms all over the world—and it is greatly misleading, because for most mutations, it is totally wrong!”
Notice the unsophisticated thinking of the evolutionist when it comes to countering the clear data that indicates life is degenerating due to the accumulation of low-impact deleterious mutations. Paul Price continues:
“Natural selection (NS)—a straightforward, real process—essentially just means ‘differential reproduction’; some members of a population will reproduce more than
others. Therefore, the traits that are possessed by the ones reproducing the most are going to become the most common in the population over time.
The power of NS has been carefully measured.14 For selection to be able to ‘see’ the mutation, it must be strong enough to affect reproduction (e.g. by killing the individual before it can reproduce, or by causing sterility or a significant decline in fertility).
Thus, NS cannot ‘see’ a nearly-neutral mutation because, on its own, the negative effect of the individual mutation is very tiny—far too small to cause any appreciable difference in reproduction. As errors accumulate with each generation, eventually their collective effect is very damaging (see ‘Racing cars and error catastrophe’ p. 50).
It is easy to see that selection does not weed out most mutations. We all have hundreds of mutations our ancestors did not have—yet most people have no trouble becoming parents and passing on their genes (along with many mistakes, both old and new).” Source: Price, P., Genetic entropy: The silent killer: A devastatingly powerful argument against evolution. October 2019.
The best natural selection can do is slow down this process of genetic degeneration. I mentioned how selection acts on phenotype and not genotype. This is an especially important point to understand as it creates a major problem for actually being capable of solving the problem of genetic entropy. Paul Price explains this even further in the same article cited above:
“Forced to acknowledge that NS is blind to nearly-neutral mutations, a common evolutionist response is, ‘Once the accumulating damage from the mutations becomes significant, NS will start to remove them.’ But this fails to understand the problem. Natural selection can only weed out individual mutations as they happen. Once mutations have accumulated enough to be a real, noticeable problem, they are then a problem in the entire population, not just in an individual here or there. The whole population cannot be ‘selected away’—except by going extinct!”
In my book “The First Couple: Adam and Eve – Independent Origins”, I also point out that when we look to the genotype—we see that these changes we see in living organisms are mostly downhill and reductive.
“Evolutionists often look at the phenotype and proclaim what is occurring at the phenotypic level (the physical features) is evidence for evolution, when in fact, the real evidence is what happens on the genotype level. Let us explore a few examples when it comes to looking to the genotype as compared to looking to the phenotype. We need to look under the hood to see what is really going on. Malaria resistance in humans is often pointed to as evidence of a truly beneficial mutation. The disease sickle cell anemia results in an immunity to Malaria. Is this the type of change necessary for large-scale evolution? This benefit is due to a broken cell and a loss of information. This is not beneficial because this change was at the expense of a pre-existing protein! To be more specific, people who have this damaging mutation that causes sickle cell anemia have a broken gene. This broken gene makes a broken protein. This broken hemoglobin protein then causes deformed red blood cells and these deformed red blood cells will clot. This would lead to inadequate oxygen supply and as a result, causes anemia. It turns out that two doses of this gene will cause one to die prematurely. This is deleterious and destructive and clearly not an improvement. Why would anybody say this is beneficial? For people who have this broken gene and broken protein, the red blood cells are defective to the point where malaria cannot thrive in the person with this condition. Therefore, they are more resistant to malaria. The sickness associated with the disease results in a resistance to the malaria parasite. This is reductive and a clear loss of net information. All examples of so-called beneficial mutations have been shown to either be a loss of information (degradative), or general organismal adaptation (epigenetic). Oftentimes a mutation will inactivate a pre-existing regulatory system! This is not taking things forward. What about antibiotic resistance? We have heard the example of a “beneficial” mutation repeatedly. We have a population of bacteria and in the presence of an antibiotic, there may be a small portion of that population that is resistant. This can be due to the moving of genes around (horizontal gene transfer) or the result of mutations that cause loss of enzyme activity, and a loss of regulatory proteins. As you should be able to see by now, there is a trend. We should be seeing that these changes are all the result of reduction! There is no real significant benefit to be had. Adaptation yes. Forward evolution no! Breaking down pre-existing systems
for adaptive purposes is not going to take a single-celled ancestor into a whale over billions of years.”
The types of changes we observe are exactly what a biblical creationist would expect to find. These changes are not going to explain the biodiversity of life. When the critics of biblical creation assert that there is no evidence for genetic degeneration—they are not understanding, or acknowledging the fact that most mutations, when observed on a genotypic level, are reductive, and damaging. This is evidence for genetic degeneration. This is all downhill. This is all evidence of a once perfect creation going downhill.
Going back to the reality of genetic entropy, the critics of biblical creation have desperately attempted to fight the data with some incredibly unimpressive arguments. I deal with several of these objections in the same book cited above:
“Critics of biblical creation and genetic entropy have attempted several rescue devices. They have proposed that rare beneficial mutations can counterbalance the damage. Of course, this damage is due to the continuous accumulation of deleterious mutations over time. As we know, the best beneficial mutations are reductive and are not taking things forward. We went over this earlier in some detail. We also know that beneficial mutations are roughly one in a million. We have learned this from the Lenski experiment. Therefore, the rare beneficial mutation, even if hugely beneficial, cannot counterbalance the accumulating genetic load. Even if there is a beneficial mutation that increases fitness, it would only be increasing fitness in a very narrow sense. Since the best definition of fitness is total functionality, most beneficial mutations cannot resolve the issue of net gain versus net loss. This means that although there may be adaptive gains, the gain is severely outweighed by all the incredible loss. For example, Lenski’s bacterial populations have been observed to adapt to their environment. There have been some genuinely interesting adaptations observed. But overall, the bacterial populations have shrunk in functional genome size. They have adapted in a narrow sense, but they are losing genes short term for adaptive purposes. This is all long-term degeneration. Bacteria are known to lose genes for short term adaptation. Breaking down a functional system can oftentimes be beneficial, but this in no way is going to take a fish-to-fisherman.”
The critics have also attempted to grant natural selection with unlimited abilities in removing deleterious mutations. I point out in “The First Couple: Adam and Eve – Independent Origins” that creationists do not ignore the role of selection—we simply understand that selection has limitations and cannot act upon that which it cannot see.
“Advocates of evolution have resorted to arguing against a strawman. They have proposed that biblical creationists ignore the important role of natural selection. This reveals a strong misunderstanding and misrepresentation of what genetic entropy really means. Nobody argues against natural selection. And nobody argues against mutations and adaptation. These are all basics. We can only begin to address the real challenges of genetic degeneration once we acknowledge the roles that mutations, natural selection, and adaptation play in functional biological systems. Of course, natural selection occurs. I have said it numerous times that selection keeps species as strong as they can be. Natural selection comes down to reproduction. Who is reproducing more? And who is passing on their genes the most? A better term for natural selection would be differential reproduction. Natural selection can even amplify the best possible beneficial mutations. This can lead to adaptive episodes. These are much more rare than deleterious mutations. Natural selection can even remove the most damaging of mutations. This is because these types of detrimental mutations can be seen by selection. It is the effectively neutral mutations that are the biggest problem when it comes to the degeneration of biological systems. These are the types of mutations that have exceedingly small effects on fitness that they are invisible to selection. How can these types of mutations be stopped if selection cannot see them? Once again, we can see why the apologists of evolution have failed to address the key issue. This is all a lot like rust on a car. The rust builds up unnoticeably until it becomes too late. We can take our cars for regular servicing. We can change the brakes. We can change the oil. We can do everything in our power to ensure the longevity of our automobiles but eventually the car will rust out.”
The critics of genetic entropy have also looked to a trade-off in explaining how the damage in the genome can be counterbalanced. I address this in the very next paragraph of the same book cited above (found in chapter 2 titled Evolution or Devolution?).
“Another rescue device constantly repeated by the evolutionist is that there is a trade off. Beneficial mutations, as we know, are context dependent. A mutation that is beneficial may be positive in one environment and negative in another. The bigger question to ask is whether this trade off is sustainable? What we know about the rarity of beneficial mutations means that this trade off is not sustainable. While so many mutations are pouring into our genomes generation after generation, a single beneficial mutation may pop up that proves to be adaptive to its host, but it will not be great enough to stop that which has been accumulating relentlessly from one generation to the next. Although a few nucleotide sites may be improving, there are far too many sites being degraded. All this will do is result in a shrinking functional genome size. If I wanted to get better gas mileage in my car for only a short period of time, I could start tearing things off of the car. I could remove the doors. I could remove the seats. I could do everything in my power to remove as much weight from the car as possible. Yes, this will temporarily improve gas mileage, but it would be due to degradation and damage. Once again, it is clear, the trade off is not sustainable. Evolutionists need to stop using this rescue device as it is just as bad as the rest of them. Proponents of evolution would have us believe that you can throw out tons of information from a multitude of nucleotide sites while making up for all the loss by simply invoking one single beneficial point mutation. This is not reality. This is not science. All population geneticists would agree that man is presently degenerating. Is there anyone out there that would suggest man is getting better? Is man improving? Of course not!”
In the article “In Light of
Genetics… Adam, Eve, and the Creation/Fall”, Dr. John Sanford and Dr. Robert Carter point out the fact that leading population geneticists recognize the reality of mutation accumulation:
“Every time a human cell divides, a few new mutations arise. These mutations are, literally, copying errors in the instruction book of life. Such errors are consistently destructive—they systematically destroy biological information. Almost all bad mutations must be removed over time in order for forward evolution to be feasible. Yet leading human geneticists agree that in mankind deleterious (bad) mutations are accumulating faster than they are being selected away, and so the human genome is degenerating. It is acknowledged that this has been going on through most of recorded history. Numerous leading evolutionists like Crow,8 Kondrashov,9 and Lynch, 10 among others, have written extensively on this problem.” Source: Sanford, J.C., and R. Carter. 2014. In light of genetics…Adam, Eve, and the creation/fall. Christian Apologetics Journal 12, no. 2:51–72. This article can also be found at: https://www.logosra.org/adam--eve
The critics will very frequently make the uninformed argument that there is no evidence for genetic entropy, and they will insist that genetic degeneration has not been demonstrated. In the same article, Dr. John Sanford and Dr. Robert Carter make it clear that genetic entropy has been demonstrated through numerous published studies and numerical simulations:
“We, along with other collaborating scientists, have studied the problem of deleterious mutation accumulation in great depth, going deeper than anyone before us. We agree with the current assessment that the human genome is degenerating, but we are convinced the problem is much worse than is generally acknowledged. The theoretical evidence of this is described in depth in the book Genetic Entropy. 11 In addition, we, along with our collaborators, have produced a long series of published scientific papers, which show experimental evidence of pervasive and systematic genetic degeneration. These papers employ a form of scientific analysis called “numerical simulation,” and they show that, given realistic circumstances, over 90% of deleterious mutations fail to be selected away, even with intense natural selection.12,13,14,15,16,17,18,19,20 Lastly, we have carefully documented the reality of genetic entropy in living biological systems such as the influenza virus,21 human mitochondria,22 and long-term E. coli populations.23 The case for human genetic degeneration is compelling on the scientific level. The most fundamental reason why most deleterious mutations are not removed over time is because most of such mutations are extremely subtle (they are technically called “nearly-neutral”) and so are invisible to natural selection. A second basic problem is that mutations in the human genome are occurring at an alarming rate—much faster than they can conceivably be selected away. We have been extensively studying this problem for the last 10 years and have published a long series of scientific publications supporting the reality of genetic entropy (above).”
It is not only the scientific evidence that demonstrates man is presently degenerating. It is also the biblical data that confirms genetic entropy. The scientific evidence and data corroborate the biblical account of human origins. What we would expect based on the fall of man is exactly what we have observed in genetics and especially mutation accumulation. In the same article cited above, the authors (Dr. John Sanford and Dr. Robert Carter) point out how consistent the genetic data is with the biblical data:
“In addition to many scientific evidences, there is strong historical evidence, as recorded in the Bible, which indicates that man is degenerating. This evidence comes directly from the Old Testament, which records the age of death of all of the first 23 patriarchal generations, followed by data on scattered additional generations. Figure 3 plots generation time versus the lifespans from Noah to David, with a final data point showing the average lifespan in the Roman Empire at the time of Jesus.24 While most of the first ten Patriarchs lived to be over 900 years old, lifespans declined rapidly after the Flood, following a classic biological decay curve. This is almost impossible to explain except in terms of genetic degeneration. The nature of this historical decay curve is extremely informative. The remarkable consistency of the rate of decline over so many generations powerfully argues that the data and the curve are very real. Because the individual data points come from different parts of the Bible, and because the ancients would not have had a clear idea of either exponential decay or genetics, we can rule out the notion that the data resulted from any type of ancient scientific fabrication, or arose as a type of ancient allegory. The data are highly consistent. The coefficient of determination (matching the curve to the data) is very high: 0.96. Due to the consistency of the decay rate, we can also rule out the idea that there were hundreds (or thousands) of missing generations that were not recorded. We conclude that the genealogical record must either be complete or very nearly complete. This validation of the genealogical record very powerfully points to the historicity and reliability of the book of Genesis. The precipitous decline in lifespan after the time of the biblical Flood strongly suggests that the flood was indeed a pivotal event in the history of the world. Why was there such a dramatic decline in life-expectancy at that time? It is feasible this cataclysmic event may have been associated with elevated levels of radiation. 25 Some have suggested that the historic decline in longevity after the flood might be attributed to the effects of inbreeding. We know that marriage between close relatives can lead to what is referred to as “inbreeding depression,” which can cause severe decline in intelligence, fertility, and longevity. However, this hypothesis is not viable because a single-generation bottleneck episode followed by rapid population regrowth would not result in a continuous long-term decline in viability – it would result in a momentary dip in fitness followed by stabilization.”
I am still shocked that the proponents of evolution have such a difficult time understanding the difference between absolute fitness, or total functionality, and reproductive fitness. A good example of this difference would be sickle cell anemia. This disease is due to the corruption of genetic functionality. It is essentially due to a broken cell and protein. Of course, this is not a good change—and yet even though this trait hurts people, it still helps them to survive. Overall, it's not good for humanity, but it's beneficial enough that if you live in places where malaria is prevalent, you will be at an advantage. The problem is that fitness is so subjective since people with this bad trait can still have children. They can live to adulthood and they can pass on their genes. Therefore, there may be an increase in fitness in a very narrow sense, but in the sense of absolute fitness, we have an overall decrease. Selection acts on phenotype and not genotype as we have talked about earlier—which means that although we may get a few local examples of an increase in fitness—but it is the absolute fitness and total functionality that is always decreasing. The question comes down to a net gain versus a net loss and there is no way to counterbalance the damage done by the accumulating mutational load. We always pass on the good and the bad. The critics have not sufficiently addressed the reality of genetic entropy. Once again, the evidence is incredibly consistent with Special Creation.
Countless critics have attempted to deny the reality of genetic entropy. Many of these criticisms have been directly addressed by Dr. Robert Carter, Dr. John Sanford, and Paul Price in a recent article titled Responding to supposed refutations of genetic entropy from the ‘experts’. One common argument utilized by the more militant critics of YEC and genetic entropy have erroneously purported that if enough nearly neutral mutations accumulate, there will be enough damage that natural selection will be able to work efficiently. This objection is dealt with sufficiently in the article cited above:
“Claim: Natural selection will kick in after a certain amount of near-neutral mutations have accumulated. Effectively neutral mutations may well accumulate, but once they start to create enough damage to cause reproductive problems, they are no longer effectively neutral. At this point, they become selectable and NS will prevent further accumulation (again, leading to an equilibrium).
This was stated by Stern Cardinale,7 by Dr. Stephen Schaffner,8 population geneticist and computational biologist at the Broad Institute of MIT and Harvard,9 and (possibly less clearly) by Felsenstein.10
Answer: This is essentially the ‘mutation count’ hypothesis. It has already been answered.11 But Stern Cardinale also claimed, “Dr. Sanford’s model requires mutation accumulation without purifying selection…” The near-neutral mutations do add up and are a factor in reproductive success. But since a near-neutral on its own does little to influence reproduction, they end up acting as if they were completely neutral and thus are only affected by genetic drift. And yet, as we will see in point #3 below, these adversaries want to invoke as many positive near-neutral mutations as there are deleterious near-neutral mutations, which is entirely odd. How can random changes to an information system be good for that system as often as they are bad? That’s like saying spelling errors are as likely to improve this article as they are to detract from it. Also, appeals to natural selection preserving the “least bad” genotypes are missing the mark. The point of genetic entropy is that the “least bad” in one generation is actually a little “more bad” than in the generation before. As slight mutations build up, the fitness of all organisms in the population should decline.”
In addition to the comments above, Dr. John Sanford provide some very helpful feedback:
“They have not carefully thought through what they are saying. The nature of near-neutral mutations is such that they are not only un-selectable due to environmental noise, but they are also un-selectable because they are ‘noise’ to each other. Thus, as the number of neutral mutations accumulate, selection gets worse, not better. If an individual carries just one near-neutral mutation, it might be very weakly selectable (but probably not, as environmental noise will override its tiny effect, so there will be little or no selection at all). If each individual has 10,000 near-neutrals, selection has to try and select for (or select against) all 10,000 conflicting mutational fitness effects simultaneously. Ten thousand independent mutational fitness effects (usually bad ones, vanishingly few good) will not just be pulling in different directions with each other, they will all act as ‘noise’, blotting out the fitness effects of each other. Haldane makes it clear that only a few mutations can be effectively selected for simultaneously. Trying to select for too many mutations at once totally overwhelms any type of selection. Indeed, selection interference not only prevents selection for countless near neutrals, it even interferes with selection for the more impactful mutations that are also accumulating.” Source: Price, P., Carter, R., Sanford, J., Responding to supposed refutations of genetic entropy from the ‘experts’, Creation Ministries, 1 December 2020. https://creation.com/genetic-entropy-defense
I highly recommend reading through the entire article refuting the critics to see just how unsophisticated the arguments really are against genetic degeneration.
Also please see:
Carter, R.W. More evidence for the reality of genetic entropy, J Creation 28(1):16–17, 2014; creation.com/evidence-for-genetic-entropy.
Carter, R.W. More evidence for the reality of genetic entropy—update, J Creation 33(1):3–4, 2019; creation.com/evidence-for-genetic-entropy-update.
Carter, R.W. and Sanford J.C., A new look at an old virus: patterns of mutation accumulation in the human H1N1 influenza virus since 1918, Theor. Biol. Med. Model 9:42, 2012; tbiomed.com/content/9/1/42.
It is also very important to once again note that the best arguments the critics have offered have all been dealt with using numerical simulations. This cannot be emphasized enough. The best that these mechanisms and rescue devices can do is slow down the degeneration. There is no resolution to mutation accumulation and the reality of genetic entropy points us to our first couple—Adam and Eve. Dr. Robert Carter has pointed out in his article titled “A successful decade for Mendel’s Accountant” that there have been no successful rebuttals to the technical papers that have come out from Mendel’s Accountant falsifying the rescue devices employed by the critics.
“A Google search for Mendel’s Accountant will bring up multiple hits that criticize the program and the conclusions being drawn from its discoveries. Essentially none of these attacks are substantive, and many are highly misleading. It is clear that most people commenting on Mendel have not read either the documentation or the background papers. Thus, many evolutionists arguing against it don’t seem to understand their own theory. This is probably due to the anonymous nature of the internet, and the level of expertise required to make comments online (i.e. no understanding required). However, one anti-creationist blogger (not trained in either biology or genetics, and it shows) tried to build a credible case against the genetic entropy thesis, and thus tangentially attacking Mendel’s Accountant. John Sanford has rebutted that review in an important article on creation.com.32 We are unaware of any peer-reviewed paper that attempts to refute the methods or conclusions of Mendel. After a decade of established work, there should be something. Their silence is telling.” Source: Carter, R. A successful decade for Mendel’s Accountant, J Creation 33(2):51-56, August 2019
The critics have failed in every way to address the actual data confirming genetic entropy and Special Creation.
See these sources for more on Mendel’s Accountant:
Sanford, J., Baumgardner, J., Brewer, W., Gibson, P., and ReMine, W., Mendel’s Accountant: a biologically realistic forward-time population genetics program, SCPE 8(2):147–165, 2007.
Sanford, J., Baumgardner, J., Brewer, W., Gibson, P., and ReMine, W., Using computer simulation to understand mutation accumulation dynamics and genetic load; in: Shi, Y. et al. (Eds.), ICCS 2007, Part II, LNCS 4488, 2007.
Baumgardner, J., Sanford, J., Brewer, W., Gibson, P., and, ReMine, W., Mendel’s Accountant: a new population genetics simulation tool for studying mutation and natural selection; in: Snelling, A.A. (Ed.), Proceedings of the Sixth International Conference on Creationism, Creation Science Fellowship, Pittsburgh, PA, and Institute for Creation Research, Dallas, TX, pp. 87–98, 2008.
Sanford, J., Baumgardner, J., Brewer, W., Gibson, P., and ReMine, W., Using numerical simulation to test the validity of neo-Darwinian theory; in: Snelling, A.A. (Ed.), Proceedings of the Sixth International Conference on Creationism, Creation Science Fellowship, Pittsburgh, PA, and Institute for Creation Research, Dallas, TX, pp. 165–175, 2008.
Sanford, J. and Nelson, C.W., The next step in understanding population dynamics: comprehensive numerical simulation; in: Carmen Fusté, M. (Ed.), Studies in Population Genetics, InTech, chap. 7, pp. 117–135, 2012.
Also see:
Brewer, W., Baumgardner, J., Gibson, P., and Sanford, J., Can purifying natural selection preserve biological information? in: Marks II, R.J., Behe, M.J., Dembski, W.A., Gordon, B., and Sanford, J.C. (Eds), Biological Information—New Perspectives, World Scientific, Singapore, pp. 232–263, 2013.
anford, J., Baumgardner, J., and Brewer, W., Selection threshold severely constrains capture of beneficial mutations; in: Marks II, R.J., Behe, M.J., Dembski, W.A., Gordon, B., and Sanford, J.C. (Eds.), Biological Information—New Perspectives, World Scientific, Singapore, pp. 264–297, 2013.
Nelson, C.W. and Sanford, J.C., Computational evolution experiments reveal a net loss of genetic information despite selection; in: Marks II, R.J., Behe, M.J., Dembski, W.A., Gordon, B., and Sanford, J.C. (Eds.) Biological Information—New Perspectives, World Scientific, Singapore, pp. 338–368, 2013.
Brewer, W., Baumgardner, J., and Sanford, J., Using numerical simulation to test the ‘Mutation-Count’ hypothesis; in: Marks II, R.J., Behe, M.J., Dembski, W.A., Gordon, B., and Sanford, J.C. (Eds.), Biological Information—New Perspectives, World Scientific, Singapore, pp. 298–311, 2013.
Baumgardner, J., Brewer, W., and Sanford, J., Can synergistic epistasis halt mutation accumulation? Results from numerical simulation; in: Marks II, R.J., Behe, M.J., Dembski, W.A., Gordon, B., and Sanford, J.C. (Eds.), Biological Information—New Perspectives, World Scientific, Singapore, pp. 312–337, 2013.
Brewer, W., Smith, F.D., and Sanford, J.C., Information loss: potential for accelerating natural genetic attenuation of RNA viruses; in: Marks II, R.J., Behe, M.J., Dembski, W.A., Gordon, B., and Sanford, J.C. (Eds.), Biological Information—New Perspectives, World Scientific, Singapore, pp. 369–384, 2013.
Sanford, J., Brewer, W., Smith, F., and Baumgardner, J., The waiting time problem in a model hominin population, Theoretical Biology and Medical Modelling 12:18, 2015.
Sanford, J., Carter, R., Brewer, W., Baumgardner, J., Potter, B., and Potter, J., Adam, Eve, designed diversity, and allele frequencies; in: Whitmore, J.H. (Ed.), Proceedings of the Eighth International Conference on Creationism, Creation Science Fellowship, Pittsburgh, PA, pp. 200–216, 2018.
The critics of Special Creation have a lot of work to do before they think they can go up against the empirical data.
Don’t forget to read:
https://creation.com/genetic-entropy-defense
https://creation.com/fitness
]]>The Biblical model of origins has opposite predictions compared to the popular view of universal common ancestry. The popular view, which is taught in schools, purports that all of life shares relationships through common descent. This includes banana plants, humans, monkeys, and dogs. They say everything on earth is shared through interconnectedness. The model of separate ancestry would imply there exists a boundary when it comes to ancestry. God created groupings of creatures. This would be the idea of kinds. I give what I believe is the best definition of kinds on page 103 of my book “Universal or Separate Ancestry? The Biblical Model of Origins Made Easy”:
“Biblical creationists do not believe in species fixity. Species are not static, and neither are their genomes. Species can change and adapt, and they can do this through various mechanisms. Scripture tells us that God creates kinds. How do we define kinds? I highly encouraged creationists to define kinds in terms of gene pools. Since genetics is the only direct way to determine what is related and what is not related, the original genomes of the biblical kinds are what should be in focus. This means that groups of organisms belong to the same kind if they descend from an original gene pool. As a result, to determine the kind boundaries we would need to determine which organisms can be grouped into separate original gene pools. We can also make good inference as to what is related and what may not be related by simply standing back and looking at the organism. For example, we can infer with pretty good certainty that dogs, wolves, coyotes and foxes all go back to an original ancestral gene pool, but we cannot scientifically infer that dogs, wolves and pine trees go back to an original ancestral gene pool. Ultimately, the answers are going to come from genetics though.
The Bible is clear that God did not create one universal common ancestor that evolved into all the lifeforms that have ever existed on this planet. This would indicate that there are independent ancestries. We can already demonstrate that not all life is related, and that life arose recently by the secularist’s own literature. This is because their own research has demonstrated that 90% of all life has the same level of genetic diversity. This means that almost all life on earth is the same age. This is exactly what would be expected given the separate ancestry model.”
This simply means that there is no universal common descent. Therefore, both models have very distinct and unique predictions. What are the types of genetic requirements that would take a single-celled ancestor billions of years ago into all the lifeforms we see today? The types of changes and requirements for large-scale evolution are opposite of the types of changes necessary for biblical creation. Ancestry is fundamentally a genetics question. Darwin knew nothing about genetics. This was not his fault since genetics was not a field back in his day. Darwin proposed evolution without knowing anything about genetics. There was no genetics to hold him back from suggesting that banana plants and birds are related through common ancestry. Darwin was just a product of the knowledge of his day. Today, there is no excuse.
Does the theory of evolution have real empirical scientific evidence backing it up? In my books, I have examined all the various lines of evidence for evolution and have demonstrated how to sufficiently refute them. My goal is not to just refute evolution and universal common descent; but to also reveal why the biblical model of ancestry and origins is the far better explanation! Modern scientific data confirms biblical creation! It confirms a literal Adam and Eve. If you have read my previous books, and if you have made it this far into the book, you have seen much of this evidence presented already. For those who are new to creation and evolution, you will find this evidence fascinating. Some may find it overwhelming and others may wonder why they have never heard of all this evidence before.
Evolutionists will say mutations are the driving mechanism behind evolutionary change. These genetic mistakes took a simple organism into a complex organism. Any change to the nucleotide sequences is the common definition for mutation. A mutation will change the sequence of DNA. This is much like changing a letter on the page of a book. Changing the informational content may lead to a change in the story. And so, an evolutionist will suggest that mutations can lead to some type of increase in complexity. The mutation may have a detectable effect that will make an organism bigger, better, and stronger. To change from a fish to some type of amphibian and an amphibian to a reptile, and eventually into a mammal and a human, would require mutations that are beneficial to the point where there is added novel and meaningful information to the genome. These changes would need to have a positive effect on the organism. The accumulation of these beneficial mutations would have to drive the changes necessary to take a fish to a fisherman.
Evolutionists often look at the phenotype and proclaim what is occurring at the phenotypic level (the physical features) is evidence for evolution, when in fact, the real evidence is what happens on the genotype level. Let us explore a few examples when it comes to looking to the genotype as compared to looking to the phenotype. We need to look under the hood to see what is really going on. Malaria resistance in humans is often pointed to as evidence of a truly beneficial mutation. The disease sickle cell anemia results in an immunity to Malaria. Is this the type of change necessary for large-scale evolution? This benefit is due to a broken cell and a loss of information. This is not beneficial because this change was at the expense of a pre-existing protein! To be more specific, people who have this damaging mutation that causes sickle cell anemia have a broken gene. This broken gene makes a broken protein. This broken hemoglobin protein then causes deformed red blood cells and these deformed red blood cells will clot. This would lead to inadequate oxygen supply and as a result, causes anemia. It turns out that two doses of this gene will cause one to die prematurely. This is deleterious and destructive and clearly not an improvement. Why would anybody say this is beneficial? For people who have this broken gene and broken protein, the red blood cells are defective to the point where malaria cannot thrive in the person with this condition. Therefore, they are more resistant to malaria. The sickness associated with the disease results in a resistance to the malaria parasite. This is reductive and a clear loss of net information. All examples of so-called beneficial mutations have been shown to either be a loss of information (degradative), or general organismal adaptation (epigenetic). Oftentimes a mutation will inactivate a pre-existing regulatory system! This is not taking things forward. What about antibiotic resistance? We have heard the example of a “beneficial” mutation repeatedly. We have a population of bacteria and in the presence of an antibiotic, there may be a small portion of that population that is resistant. This can be due to the moving of genes around (horizontal gene transfer) or the result of mutations that cause loss of enzyme activity, and a loss of regulatory proteins. As you should be able to see by now, there is a trend. We should be seeing that these changes are all the result of reduction! There is no real significant benefit to be had. Adaptation yes. Forward evolution no! Breaking down pre-existing systems for adaptive purposes is not going to take a single-celled ancestor into a whale over billions of years.
Proponents of evolution often ask what are the limits exactly? I think it should be obvious by now that the limit has to do with the type of change observed. How can anybody expect any type of real evolutionary advancement when nearly all changes observed are reductive and involve the breaking down of pre-existing functional systems? Is there any real question as to whether this is all sustainable? Where did all this pre-existing information and these pre-existing systems come from for them to be broken down in the first place? Organisms will lose information and break pre-existing systems for adaptive purposes. I have demonstrated this repeatedly. It is uncontested. This is all simply short-term adaptation, and oftentimes long-term degeneration. Even the famous Lenski experiment (a long-term experiment on bacteria) has demonstrated nothing more than reductive evolution. We touched on this in the introduction chapter. Lenski attempted to identify mechanisms in the genome that could provide evidence for large-scale evolution. Numerous proponents of evolution have jumped all over the famous Lenski experiment to show biblical creationists why we are all wrong about universal common ancestry. Richard Dawkins is one of these proponents. But what is really going on in the famous Lenski experiment? Is this truly evidence for evolution that cannot be denied? What they are finding is that most of the time the bacteria are knocking out pre-existing genes and pre-existing functional systems for the purposes of short-term adaptation. Remember the trend? This is all genetic degeneration. Nothing new has been observed to be added to the genome that could ever possibly lead to a novel phenotype. Where did these genes come from? Evolutionists constantly offer these types of examples in a desperate attempt to demonstrate evolutionary philosophy. Let us pretend we wanted to make the dining room in our homes larger and we decided to do this by knocking out the interior wall. Would we then say that we built the house by knocking down walls? No of course not! According to the common examples of beneficial mutations that evolutionists provide, it appears that this is exactly how an evolutionist would say the house itself was built! Evolutionists are looking at the phenotype when they need to look at the genotype! We gained a bigger room by knocking out a pre-existing wall. But this is not how we built the wall and the house! We can get some genuinely nice changes by knocking out genes and functional systems, but this is all a downhill process. The biblical creation model suggests that we started at the top and we have been going down ever since. This is all we have ever observed. Dr. Robert Carter goes over a few of these examples of degradation that proponents of evolution claim are the types of changes necessary for large-scale evolution:
“There are abundant examples in the evolutionary literature where genetic degradation has been used in an attempt to show an increase in information over time. Examples include sickle cell anemia (which confers a resistance to the malaria parasite by producing deformed hemoglobin molecules),40 aerobic citrate digestion by bacteria (which involves the loss of control of the normal anaerobic citrate digestion),41 and nylon digestion by bacteria (which involves a loss of substrate specificity in one enzyme contained on an extra-chromosomal plasmid).42 Since they all involve decay of prior information, none of these examples are satisfactory evidence for an increase in biological complexity over time.” Please see: Carter, R., Can mutations create new information? J. of Creation 25(2):92–98, August 2011.
As you can see, there is a trend that cannot be emphasized enough. When evolutionists propose beneficial mutations to change a single celled organism to a whale over billions of years of incremental changes, they are more than likely citing examples of degradation and loss of information or loss of function.
Natural selection is a fine-tuning mechanism that keeps biological organisms as resilient as they can be. Sadly, for champions of evolution, natural selection is utterly useless when it comes to effectively neutral (nearly neutral) mutations. These are the types of mutations natural selection cannot see. The types of mutations have only very subtle impacts on the genotypes of living organisms. Proponents of evolution struggle to explain the distinction between neutral (mutations that have zero effect on genotype and phenotype) mutations and effectively neutral mutations. They mistakenly think that most mutations have absolutely no effect on genotype. Now it is true that many mutations may be neutral to the perspective of the organism’s phenotype, but nearly all mutations must have some effect on the organism’s genotype. These nearly neutral mutations are what gradually degrade the information systems of living organisms. Since they are invisible to selection, they build up over time with only marginally deleterious effects. The fact that most mutations are damaging means that the claimed operating force of evolution (evolutionists claim that mutations are the definitive source for all genetic variation) cannot build genomes. Genetic mistakes cannot take a single-celled like ancestor into a whale over billions of years. Not only are the majority of mutations deleterious and harmful to living systems, the so-called best examples of beneficial mutations are reductive. This means that not even beneficial mutations can rescue evolution from the continuous deterioration of genetic information by low-impact and slightly deleterious mutations. Even the evolutionist would be forced to admit that there is a better chance of a mutation doing something harmful than something constructive. It is much easier to break a system than to make one better. Mutations are essentially alterations to functional systems. Mutations are akin to typographical errors in a text. Spelling mistakes are far more likely to ruin the message rather than improving the message.
Critics of biblical creation and genetic entropy have attempted several rescue devices. They have proposed that rare beneficial mutations can counterbalance the damage. Of course, this damage is due to the continuous accumulation of deleterious mutations over time. As we know, the best beneficial mutations are reductive and are not taking things forward. We went over this earlier in some detail. We also know that beneficial mutations are roughly one in a million. We have learned this from the Lenski experiment. Therefore, the rare beneficial mutation, even if hugely beneficial, cannot counterbalance the accumulating genetic load. Even if there is a beneficial mutation that increases fitness, it would only be increasing fitness in a very narrow sense. Since the best definition of fitness is total functionality, most beneficial mutations cannot resolve the issue of net gain versus net loss. This means that although there may be adaptive gains, the gain is severely outweighed by all the incredible loss. For example, Lenski’s bacterial populations have been observed to adapt to their environment. There have been some genuinely interesting adaptations observed. But overall, the bacterial populations have shrunk in functional genome size. They have adapted in a narrow sense, but they are losing genes short term for adaptive purposes. This is all long-term degeneration. Bacteria are known to lose genes for short term adaptation. Breaking down a functional system can oftentimes be beneficial, but this in no way is going to take a fish-to-fisherman. On page 22 of “Universal or Common Ancestry? The Biblical Model of Origins Made Easy”, I point out the importance of natural selection in removing deleterious mutations if living organisms have any chance at countering genome-wide degradation:
“Genesis is backed up by science. The question the opponents of creation must ask themselves is: what type of selection could eradicate so many mutations that are entering into the human population? Selection ought to somehow thwart the accumulation of huge numbers of minor mutations. If there is no type of selection that can remove so many deleterious mutations entering the human population and the populations of all living organisms, the species will rapidly decline. Higher genomes will eventually degenerate to the point of extinction.”
Advocates of evolution have resorted to arguing against a strawman. They have proposed that biblical creationists ignore the important role of natural selection. This reveals a strong misunderstanding and misrepresentation of what genetic entropy really means. Nobody argues against natural selection. And nobody argues against mutations and adaptation. These are all basics. We can only begin to address the real challenges of genetic degeneration once we acknowledge the roles that mutations, natural selection, and adaptation play in functional biological systems. Of course, natural selection occurs. I have said it numerous times that selection keeps species as strong as they can be. Natural selection comes down to reproduction. Who is reproducing more? And who is passing on their genes the most? A better term for natural selection would be differential reproduction. Natural selection can even amplify the best possible beneficial mutations. This can lead to adaptive episodes. These are much more rare than deleterious mutations. Natural selection can even remove the most damaging of mutations. This is because these types of detrimental mutations can be seen by selection. It is the effectively neutral mutations that are the biggest problem when it comes to the degeneration of biological systems. These are the types of mutations that have exceedingly small effects on fitness that they are invisible to selection. How can these types of mutations be stopped if selection cannot see them? Once again, we can see why the apologists of evolution have failed to address the key issue. This is all a lot like rust on a car. The rust builds up unnoticeably until it becomes too late. We can take our cars for regular servicing. We can change the brakes. We can change the oil. We can do everything in our power to ensure the longevity of our automobiles but eventually the car will rust out.
Another rescue device constantly repeated by the evolutionist is that there is a trade off. Beneficial mutations, as we know, are context dependent. A mutation that is beneficial may be positive in one environment and negative in another. The bigger question to ask is whether this trade off is sustainable? What we know about the rarity of beneficial mutations means that this trade off is not sustainable. While so many mutations are pouring into our genomes generation after generation, a single beneficial mutation may pop up that proves to be adaptive to its host, but it will not be great enough to stop that which has been accumulating relentlessly from one generation to the next. Although a few nucleotide sites may be improving, there are far too many sites being degraded. All this will do is result in a shrinking functional genome size. If I wanted to get better gas mileage in my car for only a short period of time, I could start tearing things off of the car. I could remove the doors. I could remove the seats. I could do everything in my power to remove as much weight from the car as possible. Yes, this will temporarily improve gas mileage, but it would be due to degradation and damage. Once again, it is clear, the trade off is not sustainable. Evolutionists need to stop using this rescue device as it is just as bad as the rest of them. Proponents of evolution would have us believe that you can throw out tons of information from a multitude of nucleotide sites while making up for all the loss by simply invoking one single beneficial point mutation. This is not reality. This is not science. All population geneticists would agree that man is presently degenerating. Is there anyone out there that would suggest man is getting better? Is man improving? Of course not!
More and more mutation related diseases enter the database every single year. Mutations are destroying us. Mutations are the destroyer and not the creator. Both evolutionists and biblical creationists would agree that natural selection happens. As I stated earlier, natural selection will only remove the worst deleterious and detrimental mutations. And it will only amplify the absolute best beneficial mutations. What do these facts indicate? The accumulating damage is largely invisible and undetectable. Not even the rare beneficial duplication can offset the accumulating damage!
I have debated Dr. Stefan Frello (Master of Science in Mathematics and Molecular Biology, and a PhD in Botany) on the popular debate channel Modern Day Debate. One of his main criticisms against the reality of genetic entropy was bacteria. Dr. Stefan Frello is not the only critic that attempts to use the existence of bacteria to refute genetic entropy. As we touched on earlier, even bacteria are subject to genetic degeneration. We have seen this in the Lenski experiment. But do we really expect bacteria to be the first organisms to go extinct due to genetic entropy? Dr. Robert Carter addresses this objection very thoroughly in his article “Genetic entropy and simple organisms: If genetic entropy is true, why do bacteria still exist?” He sums it up perfectly in the conclusion of this article. If genetic entropy is true, why do we still have bacteria?
“It is sufficient to say, however, that bacteria, of all the life forms on Earth, are the best candidates for surviving the effects of GE over the long term. Their simpler genomes, high population sizes, short generation times, and lower overall mutation rates combine to make them the most resistant to extinction.” See: Carter, R., Genetic entropy and simple organisms: If genetic entropy is true, why do bacteria still exist? 25 October 2012.
It should be obvious that bacteria would not be the first biological organism to go extinct due to genetic entropy. As you should be able to see, there are numerous reasons why bacteria and other simple organisms should be the most resistant to genome degradation and eventual extinction. Of course, as I iterated earlier, this does not mean bacteria are excluded from the negative effects of mutations and genetic entropy. Dr. John Sanford himself has a few things to say about the Lenski experiment in his article “Critic ignores reality of Genetic Entropy: The author of a landmark book on genomic decay responds to unsustainable criticisms.”
“Scott makes a big deal about Lenski’s long-term bacterial experiments, but these actually support my thesis. Although a very trivial adaptation happened (optimal growth on a given medium), his bacteria shrank in genome size (the functional genome decreased). Evidently the more rapid growth was largely accomplished through genetic degeneration. Many useful genes not essential in that artificial environment were apparently lost. When transferred to a natural environment, those highly degenerated bacteria would essentially be dead-on-arrival.” See: Sanford, J., Critic ignores reality of Genetic Entropy: The author of a landmark book on genomic decay responds to unsustainable criticisms. 7 March 2013.
There are two specific rescue mechanisms that have been invoked to halt genome degradation. Both mechanisms have been thoroughly falsified. The first mechanism is called synergistic epistasis. What is synergistic epistasis? Basically, as deleterious mutations accumulate, they will also amplify each other’s deleterious effects.
It is then claimed that the deleterious effects should become so intense and noticeable that selection is now able to see these effects. This means that the amplified effects of these deleterious mutations would result in improved selection. It turns out that by introducing synergistic epistasis you are only making the problem worse. The second mechanism invoked is called mutation count mechanism.
This artificially contrived mechanism would say that as mutations accumulate, mother nature is somehow capable of counting the number of mutations per person. Eventually, mother nature will select the higher number individuals. This is another way proponents of evolution have attempted to improve selection. Simulations have also disproven this. Dr. John Sanford has pointed out that the mutation count mechanism is not even biologically real since this model does not even remotely resemble reality. He has also demonstrated that even if all mutations are made equal in effect, this mechanism still fails whenever realistic probability selection is operational.
Extensive numerical simulations have falsified both these rescue mechanisms. As a matter of fact, even when the most generous of settings is employed, the mutation count mechanism fails to halt deleterious mutation accumulation. Please see: “Wesley H. Brewer, et al., “Using numerical simulation to test the ‘mutation-count’ hypothesis,” in Biological Information: New Perspectives, ed. Robert J. Marks III, et al. (Hackensack, NJ: World Scientific Publishing, 2013), 298-311.” Also see: “John Baumgardner, et al., “Can synergistic epistasis halt mutation accumulation? Results from numerical simulation,” in Biological Information: New Perspectives, ed. Robert J. Marks III, et al. (Hackensack, NJ: World Scientific Publishing, 2013), 312-337.”
On Page 23 of “Universal or Separate Ancestry? The Biblical Model of Origins Made Easy”, I make it evident that the more functional our genome is, the more of a problem genetic degeneration becomes:
“The problem is even worse for the evolutionist since we now know that there is strong evidence that the human genome is near-fully functional. This means the human species will degenerate even faster than ever expected. A near-fully functional genome is not only strong confirmation of the created genetic diversity hypothesis but also strong evidence for the rapid deterioration of living organisms as expected, given the fall in Genesis. The next time a critic complains about the functionality of our genome and wants to assert that the vast majority of our genome is junk (junk DNA has been proven wrong), tell them that even if the human genome were only 10% functional, that still means 10 new mutations per person per generation are accumulating that are deleterious and need to be removed by natural selection. Even a genome that is only 10% functional is fatal to evolutionary theory!”
It should be clear by now. Mutations are not going to build a genome. What we observe in mutations is exactly what a biblical creationist would expect. We live in a fallen world and mutations are an aspect of this fallen world. As Christians, we have a hope and that hope is in Christ.
Real world examples actually prove this wrong. But before I provide that evidence let’s tackle the other critic’s argument.
Those that do know the model do not use that above argument, instead they try and use the argument that because there were only four sets of chromosomes in Eden, all variants would have had an initial frequency of either 25%, 50%, or 75%. And since today, most allelic variants have frequencies in the range of 0–10%, then this proves we could not have come from just 2 people. This logical fails.
Dr. John Sanford, Dr. Rob Carter and Dr. John Baumgardner has actually run the numbers and the simulation proves that allelic variation could have easily come from just two people in the recent past.
Why would Adam and Eve have Heterogeneous genomes? You really wouldn't expect a creation that is biological to be formed empty without the ability to have genetic diversity would you? I mean it's like saying, why didn't God not create Adam only homozygous with 1 allele option? Well because that would be a disaster obviously. Since Adam was created with genetic diversity built in (remember God told Adam be fruitful and multiply) then how much diversity had to be built-in to Adam? The first human couple could have been designed with millions of variable genetic sites because God obviously knew they would have to intermarry to populate and fill the World in the beginning since that was his very command to do.
Traditionally it has been assumed that genetic variation only comes from mutations, giving rise to mutational variants (“mutational alleles”). However, given a miraculous creation, there could be a very different class of created variants (“designed alleles”). Mutational alleles and designed alleles would be different in several important respects. Mutational alleles need time to accumulate, while designed alleles can exist from the beginning. Mutational alleles are essentially random typographical errors in the genome and so are typically harmful, while designed alleles would logically be created to be beneficial. While mutational alleles always arise in a population as a single isolated copy, designed alleles would logically be created at higher frequencies.
It is widely understood that a mutational allele arises as a single copy – which is, therefore, on the verge of its own extinction. When a new mutation enters a population, its frequency is just one copy in a population of 2n (with n being the population’s size). Therefore, most mutational alleles are rapidly lost due to genetic drift within just a few generations (Rupe and Sanford 2013). While mutational alleles are typically very rare, designed alleles would typically be expected to be abundant, in accord with the nature of their function, and in accord with their initially designed frequencies.
The smallest possible unit of genetic variation involves a single letter difference in the genome. Population geneticists call these single nucleotide variants (SNVs). If the minor allele is found at a frequency greater than 1%, such a variant allele is also called a single nucleotide polymorphism (SNP). For simplicity, and in keeping with the final report from the 1000 Genomes Project (1000 Genomes 2015), we will use the term “SNP” for all single nucleotide variations, regardless of their allelic frequency.The 1000 Genomes Project detected 84 million SNPs within the human population (1000 Genomes 2015). The vast majority of these are very rare alleles (about 64 million of the observed SNPs had allele frequencies of less than 0.5%). However, this is still a serious underestimate of how many rare human alleles exist. Given our current population size and mutation rate, every nucleotide site in the human genome should mutate many times every generation somewhere on this planet. Therefore, the number of existing SNPs should be roughly the size of the genome (3 billion). But most of these variants are so rare that they are not detectable, due to limited sampling size. Most rare human alleles are unique to a single people group or sub-population. This indicates that most of these rare variants have arisen via mutation in the relatively recent past.
Excluding rare alleles, a large fraction of currently observed human genetic diversity might have arisen from designed genetic variants that were built into Adam and Eve when they were first created "The Designed Diversity Model" (Sanford and Carter) & The Created Heterozygosity Model (Dr. Jeanson). The latest analysis of the human genome (1000 Genomes 2015), indicates that there are only 8 million SNPs with allele frequencies of 5% or more. In our model most of these common alleles could be designed alleles.
The average person living today carries 4–5 million SNP alleles (Levy et al. 2007). Therefore, a single human today accounts for a large fraction (approximately 30%) of all common genetic variation (Carter 2018). The African people groups tend to have slightly higher rates of polymorphism (Gurdasani et al. 2014; 1000 Genomes 2015). Since there are only about 8 million common SNPs in the human population, and since most of the SNPs in a single person are common SNPs,this means that any given person carries a very significant percentage of all the common genetic variants found across the world (Carter 2018). A single modern couple should carry most of the 8 million common SNPs that are ubiquitous in the human population. Obviously, the genomes of Adam and Eve could have contained this amount of diversity and much more (Sanford and Carter 2015a, 2015b). Some fraction of the pre-Flood genetic diversity would be lost due to the genetic bottleneck of the biblical Flood. However, population geneticists have known for decades that even the most extreme bottleneck (i.e., two people) can capture a significant amount of a population’s pre-bottleneck diversity, assuming the bottleneck only lasts for one or just a few generations and is followed by rapid population re-growth (Nei et al. 1975). This has also been demonstrated using computer simulation. Therefore, there is no problem with the Flood scenario in terms of preserving most of the originally designed variants, even though there would be some loss of diversity.
For example, if Noah’s three daughters-in-law were distantly related, the Ark-borne population could have carried up to 80% of the pre-Flood diversity (Carter and Powell 2016). Even in a worst-case scenario (where Shem, Ham and Japheth married their sisters), nearly 60% of the pre-Flood diversity would still have been retained (Carter 2018). Thus, while some created diversity would be lost at the Flood, Noah’s family could have easily carried millions of polymorphic alleles.
In addition to the 8 million common alleles (most of which may be designed alleles), the 1000 Genomes Project identified another 64 million rare SNPs (most of which can be assumed to be mutational alleles). How many generations would it take for 64 million mutations to accumulate? Given a mutation rate of roughly 100 mutations per person per generation, and assuming our current population of over 7 billion people, it would require less than one generation to accumulate 64 million mutations in the human population. Even for a human population of just 10,000, it would only take about 80 generations. While most new mutational alleles usually drift out of a population, the rate of loss of mutational alleles would be greatly reduced in a population that is continuously growing rapidly. In light of all this, the blanket claim, “There is no way Adam and Eve could have given rise to so much diversity,” is not reasonable.
FOR A TECHNICAL ANSWER TO "Adam and Eve could not possibly account for the specific patterns of allele frequencies that we see in the modern human population.” Make sure to check out the simulation run in the study below.
https://digitalcommons.cedarville.edu/icc_proceedings/vol8/iss1/8/
Also be sure to see Henry Dalcke's work on the subject = https://bit.ly/3fCrn1r
You can learn about variation potential found in the human race.
Here's the link to his website, you will need translator for its in German: www.kreationeum.de
Regarding examples of 2 animals left on an island and doing just fine would be In 1957 a single pair of Mouflon sheep were left on one of the Kerguelen islands near the Antarctic circle. In 1977 when they had returned, the number had grown to 700 sheep! https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1766376/ That's just 20 years stuck on a small island and male sheep are nomadic travelers by nature, so the conditions were not even suitable for them! Given that the population began with only two individuals, has experienced cyclical changes in the population size, and was isolated on an island, the researchers (because of their belief in Evolution) predicted this would not have occurred, yet it did. This is just 1 of many examples of their utter failure to grasp that something outside of the theory of evolution is true, even when confronted with real-world outcomes that defy the theory and portray the Biblical Model.If all this is not bad enough, we have mapped Eve's sequence and since the majority allele were found in at least 90% of the individuals using over 800 available sequences. It became easy to trace and easy to verify. Given the high mutation rate within mitochondria and the large geographic separation among the individuals within their dataset, they did not expect to find the original human mitochondrial sequence to be so well preserved within modern populations. With the exception of a very few ambiguous nucleotides, the consensus sequence clearly represents Eve's mitochondrial DNA sequence. This tells us that because so little has changed in our genome that not a lot of time has passed because mutation rates of change are so rapid. So the fact we have much little change within us today with such a rapid rate of change occurring in mtDNA is total validation of YEC. Make sure to read the study here; https://bit.ly/31DfBvz
Next we must look at how we know Eve’s mitochondrial sequence.
The lack of diversity within human mtDNA worldwide with less than 83% of the mitochondrial genome invariant but in over 99% of the variable positions, the majority allele were found in at least 90% of the individuals when using over 800 available genome sequences. On average, the individuals in our dataset differed from the Eve consensus by only 21.6 nucleotides. Given the high mutation rate within mitochondria and the large geographic separation among the individuals within our dataset, we did not expect to find the original human mitochondrial sequence to be so well preserved within modern populations. With the exception of a very few ambiguous nucleotides, the consensus sequence clearly represents Eves mitochondrial DNA sequence.
So here is the thing. We have fast observable mutation rates occurring but not a lot of diversity. This unequivocally tells us that not a lot of time has passed since Eve lived. For technical information see https://bit.ly/31DfBvz
Now, was Eve a clone from Adam? No.
We see she was made from his rib, but she was considered a separate creation by God and the last of God’s created works on Day six. The reason God took Adams rib was so that we would know women are equal to men. If God chose a hair from Adam people would interpret this to mean women are above men and the head of men. If God took a toe nail then people would intrepid this to mean mean are above woman and they are beneath us.
When we look at Eve, we find that God took the rib/side (Hebrew: tsela), but built a new person—with new DNA and all just for Adam and companionship. Someone he can unite with and fill (populate) the Earth with. Iit is obvious that Eve wasn’t a clone because she was female. She had different sex chromosomes (XX) as opposed to Adam’s XY.
If she had the same DNA, they would have both been males. So, God stepped in and specially created Eve—as well as her DNA—just like he did when creating Adam and she was just as unique as Adam. This means they were both special creations and we can see this when looking at the original root words in Hebrew.
The uniqueness of her creation is reflected in the different verb used: banah (בָּנָה). This means to ‘build’, ‘construct’, and even to ‘fashion’, as befitting God’s last creative act of Creation Week.
“Build” applies to the fashioning of a structure of some importance; it involves constructive effort. Both of these factors are verbal evidence in the case of the independent creation of women. Thus, God ingrained into Adam and Eve the vast majority of information that appears in various people groups today—right from the start.
Some people next claim that its impossible that Adam and Eve could have even had enough children to have a population.
Well considered a recognized recorded number of children born to just a single mother is 69, to the first wife of Feodor Vassilyev (1707-1782) of Shuya, Russia. Between 1725 and 1765, in a total of 27 confinements, she gave birth to 16 pairs of twins, seven sets of triplets, and four sets of quadruplets. 67 of them survived infancy. Considering this is today's standard with women only able to really have kids up till 45 or so safely, yet Adam and Eve lived over 900 years. It's obviously possible many children could have come from Adam and Eve alone.
If all of this isn't bad enough for evolution, let’s really validate our genetic data with historical data shall we? We have genealogical records that if we follow back a single family line of royal blood going back to the oldest in history, what do we find? Well below is the British Kings list which shows an unbroken royalty lineage going all the way back to Adam himself.
Remember, blood lines are very important and always have been. Today we can prove relation through genetics, but before that, it was all in the details written down. This list goes through the ancestors of Queen Elizabeth II of England and goes back through the kings of Wessex to one Sceaf, “a son of Noah born in the Ark,” and then to father Adam. The original text is on display in the British museum of History and dated as authentic. So evidence in genealogy also validates these mutation rates and YEC.
But this is not the only genealogical discovery, others have been found as well. One of these traces through Irish royalty back to one Tamar Tephi, a daughter of King Zedekiah, who was king of Judah when Lehi left Jerusalem in 600 B.C. Another traces back through one Anna, a daughter of Joseph of Arimathea, who was a kinsman of Christ and the one who provided the Savior’s burial place. There are also others.
All the time frames are perfectly in line with the Y.E.C model.
Ironic how all these timelines fit in a Y.E.C time frame, while completely missing the evolutionary one. yet the critic will gloss over this without a thought.
Cain got his wife?
When I got to the section entitled, “Cain and Abel, Sons of Adam,” I read,
After that [when God put a mark on Cain, (probably Vitiligo in my opinion), Cain went out from the presence of the Lord, and dwelt in the land of Nod, to the east of Eden.
And later in the land of Nod, Cain took a wife and she gave birth to a son who was named Enoch.
This paraphrased account of Scripture highlights a very common misconception related to where Cain got his wife.
First, let’s read the actual words of Genesis 4:16–17, which The Golden Children’s Bible attempted to paraphrase:
Then Cain went out from the presence of the Lord and dwelt in the land of Nod on the east of Eden. And Cain knew his wife, and she conceived and bore Enoch. And he built a city, and called the name of the city after the name of his son—Enoch.
The Bible does not say that Cain went to Nod and later found a wife there. Rather, the implication in Scripture is that he already had a wife when he went to Nod. The event that took place in Nod was that he “knew” his wife—had sexual relations with her—and she conceived and gave birth to a son.
If Cain didn’t marry someone living in the land of Nod, we still have the question, “Where did Cain get his wife?” or, “Whom did Cain marry?” Again, we need to look to Scripture for the answer. Genesis 5:4 makes it clear that they had multiple sons and daughters:
After he begot Seth, the days of Adam were eight hundred years; and he had sons and daughters.
In addition, Genesis 3:20 states,
And Adam called his wife’s name Eve, because she was the mother of all living.
Scripture is clear that every human being is descended from Adam and Eve.
Acts 17:26 states, “And He has made from one blood every nation of men to dwell on all the face of the earth, and has determined their preappointed times and the boundaries of their dwellings.”
The Bible only follows 2 of Adams liniages in detail from start to end. Yet we know that Adam had many other kids. These other lineages were not as important because they do not lead to the theme of the Bible which is salvation and sin. This is why the Bible traces only the 2 lineages (Seth to Jesus and Cain to Tubal-cain).
When God curses Cain for his sin, Cain replies: “Today you are driving me from the land, and I will be hidden from your presence; I will be a restless wanderer on the earth, and whoever finds me will kill me." (Genesis 4:14, NIV)
The phrase "whoever finds me" implies there were other people already besides Adam, Eve, and Cain. By the time Adam fathered his third son, Seth, a replacement for Abel, Adam was already 130 years old. Several generations had been born in that time.
Genesis 5:4 states: "After Seth was born, Adam lived 800 years and had other sons and daughters."
Here is something else I want to add. The word “Nod” literally translates as "fugitive or wanderer" in Hebrew. Bible scholars believe Nod was not a literal place, but a state of roaming, without roots or commitment that was East from Edens location.
Intermarriage Was expected and obviously Part of God's Plan at creation. This is why He would have obviously built in a large diverse enough genome to be compatible with such a thing till long after the Flood.
It was at this early point in human history, intermarriage with relatives was not only necessary but was sanctioned by God. Although Adam and Eve had been tainted by sin, genetically they were pure and their descendants would have been genetically pure for many generations.
Those marriage combinations would have paired the same dominant genes, resulting in healthy, normal children. Today, after thousands of years of mixed gene pools, a marriage between a brother and sister could result in recessive genes combining, producing abnormalities.
The same problem would have occurred after The Flood. All of the people would have descended from Ham, Shem, and Japheth, the sons of Noah, and their respective wives. Following the Flood, God commanded them to be fruitful and multiply.
Much later, after the Jews had escaped slavery in Egypt, God handed down laws forbidding incest, or sex between close relatives. By then the human race had grown so much that such unions were no longer necessary and would be harmful.
Resources;
A Young-Earth Creation Human Mitochondrial DNA “Clock”: Whole Mitochondrial Genome Mutation Rate Confirms D-Loop Results
https://assets.answersingenesis.org/doc/articles/pdf-versions/arj/v8/mitochondrial-dna-clock-d-loop-results.pdf
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3145720/
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M. Nailor, D. Joseph
ABSTRACT
Using the scriptural based Created Heterozygosity Model and calculating factors regarding physiological, environmental, and rates of geographical expansion. Predictions regarding mutation rates are made on Hominidae (humans and primates), Canid (Wolf, dogs), Vulpes (foxes), Felidae (cats). The implications of rapid mutation changes and increases in diversity has implications in molecular biology, genetics and medicine. Phylogenetic methods are put to the test against pedigree methods for accuracy, and determination of when the last bottleneck in animal life is also discussed.
The worldwide pattern of limited variation among all animal life, tells us that something physically happened in the recent past that reset all mitochondrial diversity at the same time. What was this? When exactly was this? Is genetic diversity still increasing today? Is a Universal molecular clock that is explained by neutral theory really the best explanation for all the diversity we see in life today and can it explain the patterns observed in nature? Are evolutionary phylogenetic mutation rates more valid than pedigree mutation rates? Can future predictions be made regarding different mutation rate models? These questions demand attention, as many paradoxes exist regarding these controversial topics.
INTRODUCTION
In this study, I puzzle together empirical studies with other theoretical concepts that can help us build connections between that which connects mutation to diversification. First, we must consider the different ways in which mutation rates vary between related species. Then we will consider how mutation rates affect substitutions via population size, demographic dispersal rate, geographic range size, migration, and reproductive isolation. Since the diversification rate today is measured from phylogenetic analyses based on evolutionary assumption. When phylogenies are reconstructed based on nucleotide sequences, such variation is typically accounted for by only using a relaxed molecular clock, which, however, is just a statistical distribution of mutation rates without any underlying biological mechanism. Without using this “relaxed” clock evolutionarily, many more discrepancies arise.
Current studies attempting to reconstruct the evolutionary phylogeny of a clade often discover that the sequence data in no way support the assumption of a strict molecular clock in Neutral theory, which is that of a constant substitution rate across lineages governed by generation time. For these types of problematic cases, evolutionists created phylogenetic inference software called “relaxed molecular clock models.” (Lepage et al 2007; Drummond et al 2006). These are nothing more than ad-hoc solutions to resolve an unresolvable problem in the evolutionary model and save neutral theory from falsification. What they have done by implementing this new relaxed clock is essentially allow an inconsistent clock in their neutral ticking only clock theory, to capture known contradictions and place them back into the phylogenetic evolutionary branches they need. Basically they have made a circle wide enough to capture everything that does not fit the evolutionary model and the data is now force fitted to agree even when it clearly disagrees. They have done this same shady move in paleontology and geology by saying that evolution is a slow process described by Darwin known as Gradualism. However when contradictions were abundant they allowed for stasis, punctuated equilibrium, and Saltationism. Basically allowing the theory of gradualism unfalsifiable nonsense, just as they have now done using neutral theory. Carl Woese, the father of evolutionary molecular systematics states: "Phylogenetic incongruities can be seen everywhere in the universal tree, from its root to the major branchings within and among the various taxa to the makeup of the primary groupings themselves."
For these reasons, I propose an alternative idea that uses a more logical approach and resolves these problems using observation, testing, and predictions as the basis for this study taken directly from the Created Heterozygosity model - CHM (Jeanson 2015).
Here, I present a more explicit biological explanation for differences in mutation rates across the Created bush of life; I propose that variation in accumulated mutations may be explained by many different mechanisms and factors like population size, geographical expansion, population growth and partly explained by reproductive isolation, hybridization, speciation and inbreeding. I will be critically evaluating the empirical evidence for these differences, focusing on the mutational pedigree methodology v.s. The phylogenetic methodology regarding neutral theory. The aim of this hypothesis and theory study is to explain that pattern of diversity through mutation rates is predictable using the CHM, and how a phylogenetic evolutionary universal molecular clock makes no testable predictions and cannot account for the patterns we observe in nature. We will be investigating how different factors shape the number and type of mutations that cause diversity and why some become fixed features of the genome while others do not.
Even though there are other factors of genetic change that may be drivers of diversification, such as regulatory changes, chromosomal rearrangement, and epigenetic modification. We will be focusing on recombination, gene flow, and point mutations since mutation alone is what is used as a marker for all diversity. This has been done from the start of the theory, as evolution believes that all diversity is the cause of mutation. The relationship between species has been documented by only comparing gene sequences between lineages. Therefore I will be confining our discussion to mutations that change nucleotide sequences and also making predictions on that subject as well.
The evolutionary rate of speciation is derived from the distribution of branching events in a phylogeny (Pagel et al 2006), and differences in the net diversification rate are estimated by comparing the number of extant species per lineage (Bromham et al 2015). Another problem with these phylogenetic measures of diversification rates do not map to the process being considered in speciation models. The CHM model suggests that genetic drift and recombination are the main drivers of speciation and diversity and occurs rapidly.
Phylogenetic estimates of diversification are not actually direct measures of time to reach reproductive isolation as predicted by studies on speciation (Wiens 2004). It’s even been discovered that previously isolated populations can also rejoin and fuse after they had already speciated (Coyne and Orr 2004), and physically or spatially distinct forms may actually be connected by interbreeding populations (Irwin et al 2001). These factors are overlooked in phylogenetic mutation rates.
Synonymous mutations are point mutations, meaning they are just a miscopied DNA nucleotide that only changes a single base pair. For a mutation to be detected as a consistent difference in the DNA sequences sampled from different animal populations, it must clear several hurdles. First, if a new mutation arises it then must be copied from the genome it occurred in (parent) and passed on to that individual’s offspring (child), in order to enter a new generation. If the newly arising mutation is included in one or more offspring in the next generation, then each of those individuals has a chance to reproduce and pass the mutation to their offspring. While the mutation is new and at low frequency in the population and depending on the population size. There is a chance of the mutation being lost by chance if those few individuals fail to reproduce. If it increases in representation in the population, the mutation becomes established as a polymorphism, carried by some but not all members of the population. Eventually, it may rise in frequency until it replaces all other variants in the population, so now all new individuals born in that population will carry a copy of that mutation. At this point, we call the mutation a substitution and say that it has been fixed in the population. So a point mutation can make its way through the population, and depending on the population size and growth rate will determine the substitution rate. This is why pedigree studies are so important, as they can catch newly arising mutations, and since selection has no effect on the region then it ultimately is the best way to determine a species age. Overall the rate of mutation is what we need to focus on because this will determine the mutation rate clock per species and is a much better indicator of time than substitution rates because population size can change over time. Effective population size does not have a significant effect on the neutral substitution rate. Only the rate at which fixation is reached. This brings me to the region of the mitochondria I will be focusing on, the Cytochrome c oxidase I (Co1) gene fragment. Since out of all regions in the mitochondria this is the highest conserved of them all.
The Co1 gene fragment is a segment of the mitochondrial that is 658 base pairs (bp) long in all life (longer in some). It is going to be the focus of my predictions and the focal point of discussion from this point on. The sequence of this region is often referred to as “DNA barcode” (Ratnasingham and Hebert 2003 & 2013). DNA barcoding is based on the premise that Co1 sequence divergence is higher between species than within species (Hebert, Ratnasingham & DeWaard, 2003). Thus far all Co1 gene studies regarding mutation rates come from fossil record based calibrations on the geologically oldest fossils (Peter B Marko 2002).
The reason I am focusing my attention on the Co1 gene is the fact that it is highly conserved across all species, it non-recombining, a bottleneck would entirely reset this region, all mutations that do arise are neutral therefore selection doesn’t alter the region and the gene itself is part of the mitochondria - which itself mutates fast and clear rates of change can be observed in real-time rather than mere ad hoc speculation.
Differences in the Co1 gene are all point mutations that just change a single nucleotide sequence of a gene, not the amino acid sequence it codes for. All mutations that occur in the Co1 gene are Point mutations. Point mutations arise when damage to DNA is imperfectly repaired or errors in DNA replication are not fully corrected, resulting in a new permanent change to the base sequence such that the changed sequence will be included in any subsequent copies. The probability of a point mutation being passed to future generations is entirely due to reproductive availability, so its frequency in the population is determined only by the mutation rate and the effective population size. Take a rapidly mutating genome of accumulating point mutations and add it to a small population with a fast generation time and the frequency is increased. Give that same point mutation rate to an already large and growing population and its frequency becomes low. This is why some populations have more and others less diversity. Take humans of the same family and culture with identical rates of point mutations and place half in a large population and isolate the other half. After a few short generations, the rates will have changed, as point mutations will reach fixation much faster in the smaller isolated population, especially since inbreeding will occur. This is what determines what gives the appearance of a younger or older, more diverse or less diverse people group after many decades. This is an example of one of the many factors one must consider when not only looking at mutation rates but also at the different diversity we find in nature and within even related populations, not just between species.
Overall in all life, the rate of new mutations arising is faster than predicted by evolutionary standards and this is one way we know that a bottleneck must have occurred. Especially since all life tested still has extremely low levels of mutational change, yet rates are fast throughout all animal mitochondria as you will soon discover.
As stated, the Co1 region has shown to be highly conserved and mutations that occur there are always synonymous. Meaning that all mutations that arise in this region are never altered by selection, which can theoretically affect other regions of the mitochondria, altering their true clock overtime. This is extremely important since these types of mutations are neutral single synonymous substitutions, meaning selection cannot see them and their rate of evolutionary change will be equal to the true mutation rate. This means that the minimal amount of variation we see in all life when looking at the Co1 gene, all occurred from "neutral" mutations that arose after a bottleneck. In other words, these mutations are all new and they are irrelevant in terms of the natural and sexual drivers of change. How similar or not these "neutral" mutations are to each other is like tree rings, they reveal the approximate age of a species. Since all Co1 differences within and among closely related animal species are always and always will be synonymous, the region becomes the ultimate testing grounds for finding a true mutation rate. Again this means that all the observed changes are non-selectable and neutral compared to non-synonymous substitutions (Kocher TD et al 1989; Kerr KCR 2011). This makes the mutations that accumulate within the region perfect for also making predictions based on, unlike other regions of the mitochondria where there is a chance that selection and drift can have an effect. If it is validated that this region ticks fast, as opposed to the slow evolutionary assumption rate based on the fossil record. Then it is a 100% falsification of deep time evolution and confirmation of the YEC timeline.
A uniformly low variation in bird populations from a few thousand in number up to several hundred million has shown us that just like humans, whose population is in the billions. That genetic diversity within their species remains extremely low. How can this be if humans have a similar mutation rate to primates, yet they do not have low variation within their populations? This data tells us that the faster a particular species grows in population size and expands across the world, the fewer mutations get passed between the population and the more rare substitutions are able to reach fixation. This causes less diversity within the species to be visible even though the species are the same age.
The best way to explain it would be comparing chimpanzees to humans who have similar mutation rates, yet the amount of total nucleotide substitutions within the chimps Co1 gene ranges from around 65 base pair differences on average. However, humans only have 10 point mutation differences maximum, since we have expanded and grown so fast as a population from this last bottleneck. On average, chimpanzee sequences contained 28.8 non-synonymous differences when compared with 8.91 observed in humans (Anne C. Stone et al 2010). Substitutions only were able to rise to fixation only early on in humans, during the three bottlenecks in the recent past (Creation, Flood, Babel), and each time the population exploded afterward. This makes new mutations much harder to reach fixation in today’s population in the billions, but still relatively easy in primates whose populations are always in the thousands. In regards to other primates, fixation kept occurring constantly and faster since they do not migrate nor expand in population size as humans do. Their population numbers always remain small, allowing for more diversity within the species as fixation is reached much quicker. Evolutionists Interpret these higher amounts of differences as evidence of deep time because they start with their conclusion and work backward. It’s the paradigm driving the Interpretation and conclusion.
I hypothesize that all species are adapting rapidly, continuously, and at fast but slightly different rates from one another for different variables. This is why obtaining an empirical Co1 mutation rate in different creatures even within the same family is so important. We still observe diversity continuing to rise today, thus synonymous point mutations in the Co1 region are still occurring. Meaning that saturation in this region has not yet occurred and has not been equilibrium reached.
Another way to know that mutation saturation has not yet occurred is by comparing this gene in the mtDNA to the entire mitochondria itself. Given that the total mtDNA is 16,569 base pairs in total. Dr. Jeanson regarding this mutation accumulation in his own study states: “If the individuals in this study had mutated to saturation such that every DNA position had been mutated, then the DNA identity between them should have been no different than a random alignment of DNA sequences. Since every position in a DNA sequence has four possibilities due to the four bases—A, T, G, C—in the DNA code, a random alignment matches 25% of the time by chance and mismatches 75% of the time. None of the comparisons in this study even came close to 25% identity. The lowest match was 86%—far in excess of 25%.”
In other words, if the mtDNA genome was mutationally saturated, then all-new mutations would be invisible as they would simply affect already mutated regions. If deep time were true, that is what we would expect to find and we would be unable to see newly arising mutations outside of the already currently mutated regions. Since this is not the case, we can be certain that equilibrium has not yet been reached and we are looking at a young genome and inevitably a recent bottleneck. A comparison of human and chimpanzee entire mtDNA reveals the two mtDNA genomes are far from mutational saturation – the 1,483 differences represent just 9% of the total human mtDNA genome length.
So if 12,000 mutations are what it takes to reach equilibrium, spread evenly over the entire mitochondria. Then this means a 12,000 mutation saturation point out of 16,569 equals 72.72% of the region allowing mutations to accumulate before they simply start to turn over already mutated regions, establishing equilibrium in the mtDNA. The sequence simply won’t become more or less similar after this point. Extrapolating this 72% in the Co1 region of just 658 base pairs means that 473.76 changes would have to occur before equilibrium is also reached. Nothing in nature is nowhere near this, just as there is nothing in nature near 12,000 in the entire mitochondria length. The entire Canis genus (Wolf, Jackal) combined not a single species has been found to have about 123 mutations Nothing above that, in the entire canid kind. Similarly, all Felidae also have a low amount of mutations accumulated. 118 nucleotide differences is the maximum found in any cat species. This means there is still room for another possible 355 mutations in this region before equilibrium is reached. Since selection is not playing a factor in the Co1 gene and removing possible mutations, then this is even stronger evidence of a young genome than even the entire mitochondria.
Since selection is not altering mutations in this region, powerful predictions on mutation rates can be made. And with them, we can also explain the pattern of diversity we see in nature today from a YEC perspective. Yes, unique patterns can still periodically arise, but this has only resulted from either interbreeding or when hybrid species cross with older more stable species. These unusual patterns in no way undermine the strength of DNA barcoding in any way. Barcoding will continue to deliver species-level resolution in 95% to 97% of all cases (Janzen et al 2005; Hebert et al 2004; Ward et al2005). This makes it extremely accurate and in my opinion, the overall best region of the mitochondria for testing and making predictions.
A universally selection-driven mtDNA clock tells us that based on the evolutionary theory that all organisms are mutating at about the same rate, this is the popular “Neutral theory”. The neutral theory posits that sequence differences within and among species are selectively neutral, so they are invisible to both adaptive and purifying selection based on generation time alone “generation-time effect”. However, the new data looking at the Co1 gene has been shown to contradict the key predictions of neutral theory, specifically, universal limited intraspecific variation and a universally similar molecular clock in all life. What we actually see is that some species with slow generation times can have more diversity than species with fast generation times. Take for instance the sea snail Echinolittorina. With a generation time of just 2 years on average, they have less diversity than a gorilla who has a generation time of 19 years, and supposedly evolved much earlier. Another example is that of different aquatic life forms. When comparing the generation times of invertebrates ranging from 8 days in the small hydrozoa freshwater animal species Hydra magnipapillata to the generation time of Sea snails species M. neritoides at 1,250 days. Evolution would predict that the M. neritoides mtDNA mutation rate would be on the lower side with less diversity. Yet, M. neritoides has more diversity and higher mtDNA mutation rates that do not fall within the range of mutation rates of other invertebrates with longer generation times than M. neritoides, i.e., from the boulder star coral species Montastraea annularis and the purple sea star Pisaster ochraceus. Since invertebrates with shorter generation times are always supposed to have higher mtDNA mutation rates since their mitochondrial genomes are copied more frequently (Thomas et al 2010). This makes no sense evolutionary and is contradictory to the neutral theory. Clearly, a universal generation time-based clock fails to explain this and many other patterns we find throughout nature. This is why predictions must be made regarding mutation rates, and observable pedigree studies are without a doubt the most optimal for this. As of now, the Co1 gene is only used to identify related species to one another. An empirical mutation rate is not paramount, so no one is testing this region for a mutation rate.
We will be investigating the effects of multiple theories that alter the molecular clock and determine which one if any, some or all play a role. With the metabolic rate hypothesis, we expect faster-reproducing organisms with higher metabolic rates, such as mice, compared to larger-bodied mammals like humans and whales, to have similarly higher mutation rates. This holds true for most cases, but not all. If a fast metabolism alone promotes faster mutation rates, then endotherms are predicted to have more rapid mutation rates than ectotherms. Such patterns are frequently reported, adding credence to the theory (Bowen, Nelson & Avise 1993; Thomas & Beckenbach 1989; Adachi, Cao & Hasegawa 1993; Avise et al 1992; Martin & Palumbi 1993). Where this hypothesis breaks down are birds, as avian metabolic rates are higher than those of mammals, but they have slower rates of molecular change (Prager et al 1974). There is also the problem with humans and great apes as well when using only the metabolic rate hypothesis. Humans have a much higher metabolic rate than any primate, yet our mutation rate is slower (Herman Pontzer et al 2016). This is best explained in how long we humans as a species live and the larger a generation time we have. Then there are also environmental conditions to account for, especially temperature. For example in recent years bird numbers and diversity declined dramatically. Until now, researchers have often assumed climate changes challenge mammals and birds in similar ways, because both need to maintain their body temperature. The energetic costs of cooling in birds were more than three times higher than in mammals.(Eric Riddell et al 2019). It was found that mammals do far better in warmer climate conditions and diversity increases more in these conditions. Also explain why Africans also have more mutation differences. So while I expect diversity to increase in all life, I expect birds to show the least amount of change because of current global temperatures. So clearly to make predictions on mutation rates within a wide variety of different species in different environments. Other factors besides mere generation time are valuable factors of consideration in obtaining an accurate mutation rate. The discrepancies in evolutionary Neutral theory are remedied by combining the Created Heterozygosity Model with the metabolic rate hypothesis with the generation time hypothesis for optimal results. Though other factors contribute, the main focus is that of predictions and results from historical ages that flow from these.
I should point out that just because intraspecific Co1 barcode variation is uniformly low regardless of census population size no matter where we look (Thaler 2018). This does not mean that all life is mutating at exactly the same rate, it simply means that the bottleneck was much more recent in history than we have assumed and mutation rates are also much faster than predicted by evolutionary standards. It also does not preclude the many alternative hypotheses to explain the pattern of diversity we see. Sequence differences remain neutral within “related animal kinds” even after new species are formed. This allows us to know what is more related to one species over another. It also shows us that a fairly constant mutation rate within the individual species is similar as well. This makes predictions possible, with high accuracy. Of course there will always be random outliers from things such as isolation and inbreeding. But an overall rate can still be obtained and variables accounted for. The discovery of universally low intraspecific variation contradicts a central prediction of neutral theory and is not readily accounted for by commonly proposed explanatory modifications.
Now we get into Hominidae Co1 gene mutation rate predictions.
The average generation age for humans in tribal societies was 29 years old in over 500 different societies tested.
Once I obtained the average (29) I then took the upper and lower generation limit - 22 and upper 35 years as my minimum and maximum range to make predictions.
Humans are not like animals in regards to the flood. It tells us that Noah brought his three sons and their wives. This is 3 different mitochondrial lines, so I will be making my human mutate rate prediction going back to creation. As for animals, it tells us they were bottle-necked down to a single pair (Genesis 6:19-20)–“And of every living thing of all flesh, you shall bring two of every kind into the ark, to keep them alive with you; they shall be male and female.”
Therefore using the date of creation 7,576 years ago. I predict humans will mutate at a rate of 0.0095 average (95%CI low 0.0014, High 0.0194) mutations per year in the Co1 gene.
Humans today have an Average Pairwise Difference (APD) of just 0.2%, between 0.1% - 0.3%. The majority of people share just a few nucleotide sequence differences. Since humans have explosive birth rates and rise in populations fast, few mutations become fixed and few point mutations get shared between all people groups. This is why we find so few within humans, yet far more in primates who have similar but not identical mutation rates.
There are greater differences among populations of modern chimpanzees, gorillas and orangutans than among modern humans. This is why even with a fast mutation rate, few differences are found as human population growth is rapid and it also explains why smaller populations of people in Africa have more differences than the rest of the world.
This low genetic similarity between all humans refrects three things; 1:), We all went through a recent bottleneck in the past. 2:) We exploded in population growth after this worldwide bottleneck which kept differences between humans low. 3:) Animals were reduced to a single pair during the flood bottleneck which was a mitochondria restart for all life at that time except humans, which we can see was Noah and his 3 sons and daughter in law. We see their 3 separate haplogroups today, validating this hypothesis. Since humans only go back a few thousand years till creation and all animals went through this recent bottleneck it explains why all life has low APD’s.
Using evolutionary phylogenetic assumption, it is believed that 50,000 years ago is the origin for non-African people groups diverged out of Africa (Bowler et al. 2003; Henn et al 2012, Poznik et al. 2013, Mellars et al. 2013; Higham et al. 2014; Lippold et al. 2014, Karmin 2015, Posth et al 2016). This means if humans really had remained in Africa in small groups for over 150,000 years, they would have far more fixed substitutions than just the 24 we see and the 8-10 mutations in the C01 gene at the highest end. Clearly all the genetic evidence tells us humanity is young and so is all animal life.
Remember evolution predicted and tells us that genetic variation is supposed to increase within a species as a whole due to selection for particular alleles in certain environments and/or from reproductive isolation. In either case, the prediction is a relative increase in variance within the modern human species compared to other animal species and a multimodal distribution of that variation in modern humans. While more fixed substitutions were found in Neanderthal and Denisovan who were both isolated and inbred, we expect this.. Yet modern day people that kept spreading out and growing in population size explains the low diversity we now see in humans but not in any primates .
So since genetic differences are supposed to go up within a species group as a whole due to selection for specific alleles in a particular environment. “Different geographic populations, subspecies, or races imply that the amount of variation in the species would be relatively large or that total variation would have discontinuous features (Templeton 2013).” Yet humans do not follow this rule because we live in the most diverse environments on Earth having many different selective pressures and also have large varying generational age gaps, including vastly different social structures while constantly growing in population size and migrating. This is why we have the lowest genetic diversity compared to primates. They admit that “it is peculiar that human genetic variation is so unique and is also controversial” (Fuentes 2012; Shiao et al. 2012; Templeton 2013; Fujimura et al. 2014; Yudell et al. 2016).
Mitochondrial inheritance is uni-parental and the entire mitochondrial genome forms a single “take it or leave it” linkage group (Neher 2013). This means that Noah’s flood that only lasted for a single generation and had only two pairs on the ark reset mitochondria diversity. Because genetic drift acts more quickly to reduce genetic variation in populations, undergoing a bottleneck can reduce a population's genetic variation by a lot, even if the bottleneck doesn't last for very many generations. The humans on the ark however had 3 separate mtDNA lines, therefore we can track back further to Eve, whereas there was only a single Y chromosome line on the Ark (Noah’s). This is why we can track the Y chromosome to Noah and not Adam.
Now for another important question. How do all primates have 60-105bp differences over this short time frame? Well gorillas and chimps not only remain isolated and often inbreed but also do not migrate over the globe like humans. They also have lower generational times and much shorter lifespans. All of these factors make diversity go up faster. They even begrudgingly admit that this makes sense.
Here is the big question evolutionists need to ask themselves. If they acknowledge that higher diversity is consistent with reproductive isolated groups. Then why do they deny that Neanderthal and Denisovan who were both isolated and inbreed would not have higher diversity because of those reasons? Clearly they would, as they have literally just admitted, and that is exactly what we see and what our model says happened.
Clearly the mutation rate in this region is faster than expected in the evolutionary model. The reason there is more diversity with them and not us is because of their faster mutation rate driven by generation time, isolation, inbreeding, warmer climate location, lack of migration and they also speciate.
Some are starting to notice mutational hyperdiversity is a lot more common than previously thought....
Chimpanzee (pan troglodytes).
First, what is the generation time for wild chimpanzees (pan troglodytes)? I found two good studies on wild primates. They both have close agreement, so I used both.
The average pairwise difference WITHIN each species is the 0% to 0.5% with an average APD of 0.2%. The most available data is for modern humans, who have an APD of 0.012% between all humans.. All chimpanzee species are closely related but very diverse with a APD range of 0.06%-0.2% differences between them all.
While the nucleotide differences between us and chimpanzee’s is about 60-65. This makes us extremely different from any primate in relation. From an evolutionary perspective this is just a variance dependent on deep time. Yet they can not make any predictions regarding this, so they have little confidence in the theory. I predict that the Co1 gene mutation rate will confirm the global flood occured about 5,320 years ago.
For the wild chimpanzee I predict a mutation rate per generation of 0.2937 (95%CI lower 0.2935, upper 0.2939). This prediction is based on the chimpanzee being a species that was on the Ark.
This is a 0.0084 nucleotide substitutions per year average with a maximum rate of 0.0127.
With my mutation rate, we could see an increase in maximum diversity as often as 68 years within the pan troglodytes species with an average increase as a whole every 116 years. Now if evolution was true, remember it takes 1 million years to get 40 nucleotide changes per 1,000 base pair. So in the Co1 gene fragment which is 648 base pairs in size, the math is done by taking 1,000,000 yrs and the changes would be 648/1000 x 40 = 25.9. This is how many changes would occur over 1,000,000 million years according to the evolutionary model.
Therefore the average single nucleotide chance would be every 39,000 years. This is 5.13 nucleotide changes every 200,000 years. The two models regarding mutation rates are off by an order of magnitude. Using my mutation rate and placing it on the evolutionary bottleneck 200,000 years ago the results show the contrast between models.
If the evolutionary timeline were true, chimps would have at minimum 975 nucleotide substitutions over time based on my mutation rate. We see nowhere near this, but rather mutation rates consistent with YEC.
Gorilla
I again found two separate studies that gave generation times of wild Western gorillas. They resulted in a close match, so I combined them. I used the low and high average of one study (18.2 years and 20.4 years) and the middle average of the other (19.28 years) since they were both so close. Also keep in mind female mountain gorillas give birth to one baby every 4 years.
My prediction on the Gorilla mutations rate per generation; 0.261 (95% CI Low 0.26, high 0.2615).
Pongo Abelii
Next we have the Bornean Orangutan. This primate begins to reach sexual maturity as early as 9 years of age, but does not have their offspring till 15-16 years of age. They wait 3-4 years between offspring and usually just have 1, sometimes 2.
I predict the Abelii Orangutan mutations rate per generation; 0.272 (95% CI Low 0.261, high 0.2834).
Pongo Pygmaeus
Next we have the Sumatran Orangutan. This primate has an even faster generation time as they can reach sexual maturity by 6 years of age and usually have their first offspring at 11.1 years of age.
I predict the Abelii Orangutan mutations rate per generation; 0.272 (95% CI Low 0.261, high 0.2834).
As you can see I predicted this species to arise later from Pongo Abelii. There are 50 differences between the 2 species, and this mutation rate and time-frame answers that.
You may have noticed species have differences in mutation rates per generation. As I explained earlier, evolutionists believe that differences represent deep time. To them more differences mean the farther back a species goes in time, the older it is. The reality is that mutation rates go right back to the same time just thousands of years ago and differences are based on many factors depending on the organism.
Canis Lupus
A wild wolf generation study was done in Superior National Forest (SNF) and Minnesota (MN) discovered a range from 4.3-4.7 years. (L. David Mech et al 2016). In the SNF, proportions of currently breeding females (those breeding in the year sampled) ranged from 19% at age 2 to 80% at age 5. In (MN) wolves range from 33% at age 2 to 100% at age 7. Sometimes social interactions delay many from reproducing until 5-6 years. Wolves have a lifespan of up to around 8 years in the wild. There are a total of 38 subspecies of gray wolf worldwide, a number of them have gone extinct. We will use the mean average of both wild wolves tested in SNF and MN for a 4.5 average generation time. Basal metabolic rate (BMR) also matters, and a species size can dictate metabolism (Brown et al 2004) including some other factors. The BMR was measured in 12 gray wolves (Canis lupus) (x̄ body wt = 33.0 kg) in winter. The BMR averaged 8.08 liters O2/hour; resting metabolic rate after feeding was about 45% higher (H. Okarma et al). On the basis of BMR and daily food consumption (DFC), it was calculated that an average wolf (35 kg) needs 13,421 calories daily, which corresponds to 1·74 kg of prey biomass. Calculations based on field metabolism rate yielded a 60% higher value, i.e. 2·77 kg of meat per day (Zbigniew Głowaciński et al 1997). Since changing of temperature affects body size and metabolic rate and different environments affect wolves worldwide, we have to use a baseline average. Therefore with a lifespan of 8 years, with an average size of 58.6 lbs. With a Typical body temperature of 38.3ºC or 100.9ºF and an average speciation event every 140 years. We see a correlation between metabolic rate and generation time. Therefore I predict the Canis Lupus Mutation rate per generation to be 0.0655 (95% CI Low 0.04, High 0.091).
Of course, some wolves in the arctic may be larger to help with cold and have a slower metabolic rate, while wolves near the equator tend to be smaller with faster metabolisms. But the mutation rate should equal out as an average. With the current predicted mutation rate, we expect to see additional nucleotide substitutions occur every 60 years within the Canis Lupus species on average. Diversity will continue to rise within the wolf kind with a high-end rate of diversity in wolves increasing every 47.5 years. As of now, the maximum number of mutations discovered within the species is 112. This is the maximum diversity found and this number will continue to climb every 5 decades based on the YEC model.
Using this fast mutation rate and placing it on an evolutionary bottleneck 200,000 years ago, the results show the striking contrast between models.
If the evolutionary timeline were true, wolves would have at minimum of 1,702 nucleotide substitutions over time based on my mutation rate. We see nowhere near this.
Next, we have the Sechuran fox aka Peruvian desert fox (Lycalopex sechurae). Other than the fact that the young are born in October, nothing is known about their social life or breeding habits. There are also no recognized subspecies either. Their gestation period, size of litter, age at sexual maturity, and longevity are all unknown. Their lifespan is very short, probably because they are the smallest of the genus (8.8lbs). One captive animal was documented to live 9.9 years (Richard Weigl 2005). The Sechuran fox is nocturnal, and they can live on seed pods, fruit and are capable of surviving on an entirely herbivorous diet when necessary. They live in a warm climate year-round ranging 62°F to 82°F in southwestern Ecuador and western Peru, at elevations from sea level to at least 1,000 meters. These many unknown variables make a prediction harder. Considering their short life, and the fact that Argentine gray fox “Lycalopex griseus” a South American gray fox species closely related to the Peruvian desert fox has a generation time of 1 year. I will assume theirs is close to that. I suspect the arrival of this species was also much later after the bottleneck since migration had already brought the parent species to South America then speciation occurred. So I will also place this date around 4,500 years ago based on the post-flood ice age migration diversity. I predict a basal metabolic rate of around 5.5000W / body mass 2744.2 g / 0.002004 W/g. We see correlation with generation time, and metabolic rate again. Therefore I predict the mutation rate per generation at 0.0202 (95%CI low 0.020, high 0.0204)
This means that this species has a fast mutation rate of an average overall increase of one new mutation within the species every 50.5 years. I expect diversity to increase within the species as mutations continue to arise and we will see the average go up from its current 105.44 nucleotide mutations (2020). On the high end, I predict maximum diversity to increase as often as every 45 years. This means the most diverse of the Peruvian desert foxes today will increase from 118 nucleotide differences to 119, then 120, etc… every 45 years, considering this lineage with the highest diversity continues living and passing on their mutations.
The Tibetan Corsac Fox (Vulpes ferrilata). This fox lives up to 13 years and reaches sexual maturity within 9-10 months (ADW) but reproduction does not start till the second year of life. The mating season starts in January and ends in March (Ovsyanikov, N. 2004). They weigh 2,700 g or 5.95 lbs. With only three subspecies, these foxes inhabit open grassy steppes and semi-deserts, while avoiding dense vegetation, mountainous regions, deserts with drifting sands and snowfields more than about 15 cm (6 in) deep. This makes the species more metabolically stable with a predicted metabolic rate of around 5.000 W / 2698.8 g / 0.001852 W/g. Again we see correlation with generation time, and metabolic rate again and since they do not speciate often if at all. It is much easier for predictions as speciation enhances rates. Therefore I predict the mutation rate per generation is 0.027 (95%CI low 0.024, high 0.030).
The maned wolf is a large canine of South America. It is the only species in the genus Chrysocyon (meaning "golden dog"). The life span of maned wolves in the wild is unknown. They weigh around 47 lbs and the max life expectancy is 15 years. The average age at reproductive maturity is 2 years according to https://animaldiversity.org/. With these numbers to go off and its location and lifespan, I predict an average mutation rate of 0.0189 per generation (95% CI low 0.0178, high 0.020). This means an average diversity increase via substitution every 53.2 years.
Another logical conclusion and conundrum for evolution would be differences between current domesticated dog breeds who have had little time to amass many differences within the species and between species. Yet between wolves and domestic dogs, there are 28.83 nucleotide differences. So if wolves obtain an average of 1 nucleotide difference in 60 years. Then for the Tibetan Mastiff which is 29 differences away from the wolf and assuming the mutation rate is near the same as the wolf. We are looking at around 1,740 years to obtain the average differences we observe today separating the two species. This easily explains the diversity we see between the two species Tibetan mastiff and the wild wolf.
This breed has been documented going back to the Qing dynasty, the last imperial dynasty of China. Which was established in 1636 and ruled China proper from 1644 to 1912.
Now let’s look at the cat "kind."
Neofelis
Regarding the mutation rate of wild cats, there is a wide range of diversity within the species but overall very low like all animal life. All cats descended from a single cat “kind” that was on board the Ark. Based on the Biblical timeline and no way to know what cat species was on the Ark. I will be choosing the closest one I can, the Sunda clouded leopard “Neofelis diardi”. With a weight between 28-43 lbs, max lifespan of 19.8 years, generation time of 2 -3 years of age and have anywhere between 1 to 5 cubs, with an average of 2 cubs per litter and a 12 to 15 years lifespan. No information on metabolism is available so I will assume it on cats of similar weight, body type, lifespan and environment (Metabolic rate per body mass 30.0000 W, 0.001423 W/g.) This cat is separated from the panthera leo by 82 base pairs (bp) differences, from the Panthera tigris by 84 bp and from the panthera onca by 79 bp.
These cats are poached very heavily and their habitat is dwindling. They have been listed as Vulnerable on the IUCN Red List since 2015, as the total effective population probably consists of fewer than 10,000 mature individuals, with a decreasing population trend. Obviously diversity will be much harder to predict as they are in decline, therefore I predict for both the Neofelis diardi and Neofelis nebulosa species an average mutation per year 0.032 (95%CI low 0.022, high 0.042)
Panthera tigris
Panthera tigris is one of the many that species branched off with others during speciation after the ark had already landed and animals began migration.
Panthera tigris was not on the Ark but formed later. With a typical body mass of 264 lbs (137900.0 g) and a body temperature of 37.5ºC or 99.5ºF with average basal metabolic rate of 133.8590 W, you get a metabolic rate per body mass 0.000971 W/g. Lifespan up to 26 years. Tigers have the slowest metabolic rate out of all cat’s, twice as slow as a cheetah. Stacked with their high generation time, this causes them to have the slowest mutation rate of all cat species. All tigers fall within an ADP of 0.47% between all tigers.
With an average generation times of 1,268 days in females and 1,415 days in males with an average generation time in days being 1,341.5 days, or years converted to days equalling 3.67305. I predict the mutation rate per generation will be 0.065 (95%CI low 0.064, high 0.066).
I predict the average substitution change will raise diversity within the species every 56 years and at the high end every 50.6 years we could see the peak diversity rise.
Lion (Panthera leo)
There have been contrasting estimates of generation time for lions (Bauer, H., Packer, C., Funston, P.F., Henschel, P. & Nowell, K. 2016). A common theme of 4 -5 years is the most consistent with other previous demographic estimates in the wild 20105.
With a typical body mass of 386 lbs (175,000 g) and a temperature of 37.9ºC or 100.2ºF with a basal metabolic rate of 94.5800 W, you get a metabolic rate per body mass 0.000965 W/g and a Lifespan up to 27 years. With an APD of 0.71%, these factors give me the power I need to make predictions on mutation rates compared to related cats.
I predict a mutation rate per generation of 0.0564 (95% low 0.0552, high 00.0566)
I predict that within the lion species, a substitution change will arise once every 65 years on average with a high rate of one new mutation every 53 years .We will see diversity continue to go up.
So with my mutation rate prediction, I will show how all things line up, giving us an overview of time, how new species arose and the differences obtained over time within and between them. For example with my mutation rate we see 73 nucleotide differences between the tiger and the jaguar yet only 58 between the lion and the tiger since they separated closer to one another. We can see the clear trajectory, and even base predictions off of this as well. For example the next nucleotide change we will see between the lion and tiger will be every 87 years, whereas every 63 years between the tiger and jaguar.
Now the question regarding Ancient Egypt and felines. When did cat domestication begin? What wild cats were involved and when did this happen? If this was recent, does this prove that nucleotide changes happen faster than evolution assumed? So many questions, let’s answer them and make some predictions.
Two wild cat species existed at this time to manipulate breeding for domestication.
Felis chaus is the first cat we will look at. We find small-bodied mammal species tend to have faster rates of molecular clocks than their larger relatives (Martin & Palumbi 1993). A generation time of 11-18 months with a possible 15-year lifespan in the wild for these cats.
I predict the mutation rate will be an average per generation mutation rate of 0.0189 (95%CI low 0.0187, high 0.019). This is an average mutation rate of 0.0158 nucleotide substitutions per year.
I predict the average substitution change will occur within the species every 63 years on average and at the high end every 48 years. Observable diversity will continue to rise.
The African wildcat (F. silvestris).
Their age at sexual or reproductive maturity male and female 9 to 12 months and give birth to 1 to 8 young. They live up to 16 years in the wild. I predict the mutation rate will be an average per generation of 0.0141 (95%CI low 0.0139, high 0.0143). This is an average mutation rate of 0.0171 nucleotide substitutions per year.
The average nucleotide change within the species will continue to raise diversity within the species every 71 years. With a high-end rate of change of 52.7 years.
These two cats were crossed and created the early breeds of Egyptian domesticated cats used for pest control named Egyptian Maus (Felis silvestris lybica). “Mau” is the Egyptian word for cat. The Egyptian Mau is the only naturally spotted domestic cat. They live for about 15 years and have a generation time of 8 to 10 months of age.
It was the two cats I mentioned above, the Felis catus and wild cat Felis Silvestris lybica that were crossed to breed into existence the first domestic cat, “the Manu” during the Middle Kingdom.
With a Typical body temp of 38.1ºC or 100.6ºF and a predicted Basal metabolic rate of 5.0000 W and a body weight of 3,900 g or 8.6 lbs. I predict a Metabolic rate per body mass 0.00050 W/g. Making these small cats have a faster metabolism than most all other cat species. And a rate of mutation higher than lions and tigers and bears oh my!
I predict diversity within domesticated cats “Felis catus” to continue to rise beyond its highest current maximum diversity of 101 mutations every 39 years. With an average rate of diversity increase within the Felis catus every 49 years. This is a rate of change of 0.0162 mutations per year average. This rate of rapid mutation explains why lions are 82 base pairs separated from felis catus. All cats range within just an APD of just 0.002% - 0.18%. Felis catus makes a good cat species for predictions because their numbers are more stable. As where cheetahs are inbred and dying out, so an accurate mutation rate would be hard to pin down since they may not even exist in 50 years.
As we now know, a global bottleneck was required to reset all animal mitochondria. I propose that this was a much more recent global event that reduced the genetic diversity in all living creatures’ mtDNA. Meaning these numbers we are looking at in terms of mutation diversity, all arose after this time and rapidly. If true, evolution has a contradiction on its hands and now has to account for the diverse patterns we see including the low genetic diversity we now see without ad hoc evolutionary presuppositions.
Evolutionists invoke slow mutation accumulation over hundreds of thousands of years to account for the genetic diversity we see. While on the alternative side, we can easily explain the diversity of the canis, vulpes, sea snails, and feline species within a short timeframe. Ponder this… According to Animal Planet, “The cat fancy as we know it today began in 1871 when the first modern-day type of cat show was held in London's Crystal Palace. At that show, 170 cats were exhibited. More than half of the breeds recognized by our cat associations have existed for less than 50 years.” So if we can generate over 85 cat breeds in under 50 years and observe genetic diversity increase via mutation in this short timeframe. What makes YEC proponents believe that it takes hundreds of thousands of years for these mutations to build up, yet we can see diversity increasing still today in modern-day domesticated animal breeds that are new arrivals. Also, when arguing against fast speciation rates, why do they imply that it is impossible for only a few wild cat species to arise via speciation over just a couple of thousands of years’ time? Especially since we can observe how fast it occurs today in real-time through breeding including observable studies on wild species? In both cases it’s not, that is your answer. An empty world for animals to migrate freely and speciate as needed only accelerated this process post flood.
Clearly, it doesn't take millions of years to form a few cat species, just like it has been discovered that it doesn't take 3,000 years for Darwin's finches to species but rather only 3 years (Fan Han et al 2018). Completely contradictory to what Darwin predicted based on evolutionary assumptions. So if speciation occurs quickly, mutation rates are fast, a recent bottleneck occurred, predictions can be made based on YEC that can both explain the pattern of diversity we see and mutation accumulation only goes back a few thousand years. Then we are looking at the clear evidence that falsifies evolution in multiple ways.
Here is the confirmation regarding these mutation differences being fast in my eyes. They admit cat domestication is no older than 4,000 years and is attributed to the Egyptians. Since the Egyptians documented everything and in great detail. We find only a handful of textual mentions regarding cats of any kind during the old kingdom period (2,663-2,195 BC). Then in the middle Kingdom (2,066-1,650BC), domestic cats became common in text and images including contexts that are clearly indicative of domestication (for example Neferronpet Kenro of 1,250 BC tomb.) The first-ever indication of a mummified cat dated 1,350 BC, assumed to be Prince Thutmose’s pet (Ikram et al 2002).
So with documented sources of cat domestication of Felis catus going back only 4,000 years maximum. This evidence from a YEC perspective is the only way to explain why modern house cats have more mutation differences than lions and tigers over such a short period of time. If evolution were true and big cats that have supposedly existed for millions of years (Brian David et al 2010), and it is believed by scientists currency that big cat and small cat lineages diverged from a common ancestor about 11.5 million years ago, with the big cat lineage splitting off first (6.5–15.3) MYA into the genera Panthera (lion, tiger, jaguar, and leopard). Followed by small cats (5.1–13.5) MYA into the genera Lynx (lynx, bobcat), Felis; including domestic cat, Geoffroy’s cat and Andean mountain cat (Donald W. Duszynski et al 2018). Is used as evidence of why so few mutations exist and why so few mutations are different between small and large cats based on neutral theory. The only problem with that is some large cats have more mutations than smaller cats like servals, ocelot’s, and all species of Prionailurus, a small wild cat. While other small cat species have more mutations like lynx, puma, mountain lion, and felis cactus. These clear contradictions show us that neutral theory fails in its explanatory . These types of discrepancies are remedied by the CHM and recent bottleneck with predictions made in this study, we can easily explain the diversity without contradiction.
The fact that this mitochondria region was reset during a recent worldwide bottleneck explains the pattern we see today, but only if the mutation rate is fast which all indicators seem to validate. These factors are the basis of my predictions and I can extrapolate that the region I have chosen to make my predictions on is indeed also fast since every region of the mitochondria tested thus far has been found to be fast. So it is not a stretch of the imagination to make the leap that this region as well ticks fast in all species alive as well.
Confirming
1:) All life is young, right out of a Global bottleneck and the evidence is undeniable (Thaler 2018). If big cats with longer generation times have near the same differences as small cats, it proves they cannot be separated by much time at all.
2:) Nucleotide changes are occurring fast in mitochondria and diversity is still increasing.
3:) With nothing over an average pairwise difference of over 0.5%, this is clear evidence that tells us a recent demise besets all life on Earth.
4:) Speciation happens fast, not slow as evolution theory has assumed and that Darwin predicted and is still claimed today. When paleontologist Steven M. Stanley (1998) examined fossil dynamics among different species; he suggested that it takes on average 1–2 million years to make new species, at least among mammals and vertebrates.
5:) Mutation rates are effected also by recombination rate's (Ingrid Berg et al 2011). Since this has shown us that recombination occures faster in Africans than Europen's, this explains why Africans look older genetically when in reality they are the same age.
The evidence is clear, evolution is a lie.
The waiting time to speciation will depend on many interacting factors, including the rate of supply of genetic variation, the level of gene flow between isolated populations, the nature of the genetic changes underlying reproductive isolation, population size, and nature of selective pressures. Many variables are to be considered, the neutral theory of mear generation time to explain everything fails.
Why is it important to use and consider observable mutation rates?
1:) We want to consider the divergence of an arbitrary number of species, not just a single pair of species;
2:) The substitution rate can vary between lineages;
3:) The fossil record is scarce, divergence times are unknown;
4:) We do not want to calibrate a clock with unknown speculative events in history to obtain a mutation rate. Far too many assumptions go into this. An accurate mutation rate takes away assumptions;
5:) Use of incorrect calibration point; and noise introduced from stochastic process of substitution (Wikstrom et al 2001).
6:) Fix incorrect tree branches. Also not to make use of, or correcting incorrect phylogenetic branches.
7:) Rate variations can invalidate the assumption of neutral theory method and resolve contradictory patterns;
8:) Recombination also invalidates the assumption of neutral theory method and resolve contradictory patterns;
9:) Saturation has yet to obscure the signal, so these rates especially in the Co1 gene are;
10:) Exclude combining nuclear DNA with mtDNA rates, as patterns of diversity contradict one another.
11:) Predictions can be made using an observable clock. If the observed fast rate is not accurate then predictions will fail and the empirical rate will be invalidated.
12:) Observed mutations can tell us that if mtDNA regions become saturated or reach equilibrium, then we can tell how old an organism is based on the mutation rate and total mutations that have occurred.
13:) We can use the observed mutation rate to determine what hypothesis accounts for the rate, whether it be metabolism, lifespan, generationtime, speciation, etc…
14:) Resolving incomplete lineage sorting discrepancies.
15:) Observed mutation rates determine the relatedness of people and who did or did not commit a crime.
16:) Obtaining accuracy of a bottleneck will help us determine how fast speciation is in all animal groups.
Until evolutionists can make future accurate predictions on speciation events, genetic diversity, and mutation rates. Their theory will remain unscientific and they will just continue to invoke that evolution can do anything and therefore is unpredictable and predictions cannot be me.
Dr. Natheniel Jeanson obtained a mutation rate Ding et al 2015 to obtain a mutation rate of 0.168 mutations per generation. His mutation rate is not far off from other pedigree studies. As shown below in table 1.
Since this is a stark difference from the evolutionary prediction, one must consider the alternative.
Consider what Lundstrom et al stated in 1992. The divergence predicted by Lundstrom was that 14 of every 1 million children will differ from their mother at a particular base pair within hypervariable region 1 (HVR1) in the coding region (D-loop). Since the sequence had a total span of 360 base pairs, it was predicted that 1/200 children will differ from their mother in that region.
Kocher and Wilson (1991) observed that 63% of all mutations in their sample of D-loop sequences occurred within a space of 400 base pairs that included the HVR1, Therefore Howell in 1997 estimated that 1/125 children should differ from their mother at some site within the entire D-loop. In other words, one mtDNA D-loop mutation should arise every 125 generations if the divergence rate predicted by Lundstrom et al is accurate.
In contrast to this was the evolutionary phylogenetic assumption, that predicted the ratio to drop to 1 child/400-1,200. Meaning they expected 1 mutation to arise every 800 generations on average, and up to 1 mutation every 1,200 years.
By analyzing a single deep lineage of related mtDNA sequences where they “know” the most recent common ancestor (MCRA). They can be certain that all new mutations that have arisen in that line are “new”. This brings us back to the discoveries of finding 1 mutation every 30-44 generations in many pedigree studies. Clearly incompatible with evolutionary timelines.
Conclusion
Regarding mutation rates and patterns it is clear that in hominidae, generation time plays the largest role in determining the mutation rate and population influx influences the mutation accumulation found within the species. This explains why humans who have the slowest mutation rate compared to primates have so few mutations in the population, while chimpanzees have so many mutations within their smaller more isolated populations within africa.
Within chimps, gorilla and pongo, lifespan also plays a factor. The correlation between how long the species lives also dictates how fast its mutation rate is. We find the faster mutation rate in the longest living primates ticks faster. Wild species of primates; Borean orangutan pongo have the fastest mutation rate and they also live the longest 35-45 years. Followed by the gorilla at 30-35 years and finally the chimpanzee at 15-30 (Christophe Boesch et al 2001). This is what makes humans very different as well as we have the longest lifespan of all and have the slowest mutation rate in comparison.
Felidae range between 98.6ºF - 102.2ºF body temperature. The marbled cat Pardofelis marmorata has the fastest mutation rate within the family. They live high in the Himalayas at around 8,200 feet. We know that cold increases metabolic rate and these cats live in very cold regions at high elevations. They have a moderate generation time with the range of reproductive maturity just 21-22 months. The next fastest mutation rate cat species is the bobcat “Lynx rufus” that lives in North America and ranges from Southern Canada to Oaxaca in Mexico. They are more active during the day in cold weather but mostly are active during twilight. They have a Basal metabolic rate of 23.4460 W with a body mass of 9400.0 g. This totals a Metabolic rate per body mass of 0.002494 W/g. With a much faster average reproductive maturity at 1 year for females and 2 years for males we see that a combination of metabolic rate trumps generation time. Let’s line up felids and see the trajectory.
Tigers have a Metabolic rate per body mass of 0.000971 W/g . Lions have a Metabolic rate per body mass of 0.000965 W/g. Jaguar have a Metabolic rate per body mass of 0.001238 W/g. Bobcat have a Metabolic rate per body mass of 0.002494 W/g. Ocelots have a Metabolic rate per body mass of 0.001654 W/g. Puma have a Metabolic rate per body mass of 0.001154 W/g. Cheetah have a Metabolic rate per body mass of 0.001607 W/g. Domestic modern typical cats have a metabolic rate per body mass of 0.00050 W/g. The trajectory is clear. Metastatic rates are the clear influencer of mutation rates in felidae. The correlation is too strong to be ignored. The metabolic factor is more of an influence than generation time alone when it comes to felidae. Generation time hypothesis alone cannot explain the pattern of diversity we see in Felidae nor the mutation rate. We see a clear trajectory; highest metabolisms -faster mutation rate - higher diversity.
Within canidae it is speciation, and geographical location and migration that influences the mutation accumulation rate more than anything else. Mutation rates however are driven by a combination of the metabolic rate hypothesis and generation time. For example the Crab eating Fox “cerdocyon thous” has a weight of 14 lbs and a body temperature of 100.8ºF with a basal metabolic rate of 21.5330 W. With a body mass of 7720.0 g. This equals a metabolic rate per body mass of 0.002789 W/g. With a generation time of 274 days or 9 months. Making it have the slowest mutation rate within Vulpes. The swift fox Vulpes velox has the fastest mutation rate and has Basal metabolic rate of 4.9480 W. With a body mass of 1769.0 g. This equals a Metabolic rate per body mass of 0.002797 W/g. With a generation time of 365 days or 12 months. This causes the Crab eating fox to have a slower mutation rate than the Swift fox. We notice this trend not just in foxes, but in Canis Lupus as well. Canis latrans aka Coyote has a weight of 29 lbs and a body temperature of 98.6ºF. With a basal metabolic rate of 19.4230 W. With a body mass of 10148.9 g. This equals a metabolic rate per body mass of 0.001914 W/g. With a generation time of 9-10 months, making its mutation rate slower than the Black-backed jackal which has a body temperature of 100.4ºF. A basal metabolic rate of 21.5330 W. With a body mass of 7720.0 g. This equals a metabolic rate per body mass of 0.002789 W/g. With a generation time of 8.2-10 months. The correlation between the metabolic rate hypothesis and generation time hypotheses best explain the correlation with the pattern of diversity we see within all canidae.
This means with just investigating three different animal families, we can see that the generation time hypothesis plays a major role and influences one family (hominoidea) with the longevity hypothesis affecting primates but not homosapiens, while the metabolic rate hypothesis controls and dictates the mutation rate in the other family (Felidae) while a combination of both dominates the outcome in another family (canidae). These results show us that multiple perspectives need to be taken into consideration when trying to figure out why different animal groups have different mutation rates and why different mutation rates even within the same species exist.
There is no doubt that mitochondrial DNA is the most popular marker of molecular diversity in animals, primarily because of its elevated mutation rate. Yet mtDNA hypermutability is still an unresolved issue and many theories have tried to resolve the contradictions found in Neutral theory to no avail. The problem is, that no one single thing is to blame for the discrepancies and the CHM has the most explanatory nature.
The neutral theory has always and still to this day predicts a wide range of variation in all life, with higher levels of variation in organisms that reproduce more rapidly, as the rate of diversity recovery after a genetic bottleneck is proportional to generation time (time to equilibrium variation is N generations; Hartl DL, Clark AG 2007; Bedford T, Cobey S, Pascual M 2011.) In contrast to this prediction, the widespread effectiveness of DNA barcoding reflects similarly low levels of intraspecific variation across the diversity of all animal life, including insects and vertebrates that differ 100-fold in generation time ( Hajibabaei M et al2006; Ward RD et al 2005).
The argument made by evolutionists for not finding geological evidence of a genetic bottleneck is using an argument that - since genes on the mitochondrial genome are strongly linked, an advantageous variant in one gene could potentially sweep to fixation through positive selection, bringing all variation on its particular genome with it (Maynard-Smith and Haigh 1974). This was originally proposed as a possible mechanism to reconcile peculiar patterns of diversity in the early 70s and lack of physical evidence for a bottleneck which still to this day remains a problem. Basically, it is just another way of saying, “well we discovered low genetic diversity exists in all life and we have no evidence for a bottleneck in our imagined geologic column, and this is the only other alternative explanation we can give for it, even though it has no evidence to back it up.” The main problem with this ad hoc rescue device hypothesis is that this “sweep” would have to occur in all animals both aquatic and land life worldwide at the same time. If they want to use hypothetical world wide selective sweep and selection as an explanation, then they need an example to show us, not just explain a hypothetical scenario. Since they have none, nor are able to make any predictions based on species for which diversity is unknown. Then the line of reasoning does not matter, since these are just so stories without evidence and without predictions. Nothing more than an excuse for the contradiction they find in nature.
Then there is the hurdle of natural selection to overcome rapid recombination that also speeds up point mutations. Since recombination is mutagenic even regarding point mutations, then this also reduces the effect of selection at any linked loci. Making not only mutation rates even faster, but making selection even less effective at removing mutations. This has been tested and observed in both humans and Drosophila (D. J. Begun et al 1992., M. W. Nachman et al 1998).
Even if selection theoretically could target and remove these neutral synonymous mutations. The power of selection to reduce the mutation rate is still limited by population size, by what is known as the drift-barrier (Lynch M 2011). So regardless of a random genetic drift, synergistic epistasis, or selection as alternative solutions that could possibly make an impact on mutation rates. There still remains a paradox related to the molecular clock that has not been resolved. In neutral theory, the molecular clock is proposed to be powered by drift and the clock rate equals µ (mutation rate per generation) (Kimura M 1968, Lanfear R, Kokko H, Eyre-Walker A 2014). Neutral theory predicts a chronologic clock rate proportional to generation time. However, multiple separate published studies have shown the mitochondrial molecular clock ticks at roughly the same rate in diverse animals with very different generation times (Weir JT, Schluter D 2008, Papadopoulou A, Anastasiou I, Vogler AP 2010). Even among mammals, mitochondrial evolutionary rates range from one substitution per 1-2 million years to one substitution per more than 100 million years. A difference of 2 orders of magnitude (Nabholz et al 2008). These clear contradictions are better resolved by uniting the metabolic rate hypothesis with the generation time hypothesis and Created Heterozygosity Model which considers a recent global bottleneck with fast mutation rates, causing rapid speciation and founder effect divergence. Taking animals from a heterozygous state to a more homozygous state over time.
So even if selection somehow overcomes this drift-barrier hurdle to actually affect mutation rates in the mitochondria. Selection would still have no impact on the conserved Co1 region since it has shown us we are only dealing with synonymous “neutral” single point mutations in the C0I gene. Also consider that Somatic mutations are not reduced to point mutations. Then we know we are not accidentally looking at somatic mutations in this region.
Considering we know that the species with the highest diversity today have lived to inherit the mutation difference we are now observing. There is no question regarding whether these mutations made it into the population, we know they did. They exist. Therefore The question is, how fast was this process? Does it really take 40 million years to make a single point mutation change in the Co1 gene of a 1,000 bp region like evolution predicts? Or is this mutation rate actually fast as predicted by YEC? Since ancestral polymorphisms still exist, mutation saturation has not yet reached (diversity is still increasing), patterns do not match evolutionary predictions, and large linkage blocks in the genome are still found. We can be very confident that we are looking at a young genome and recent bottleneck that reset mitochondrial diversity worldwide in all life.
We should not be surprised that mutation rates are highly responsive to environmental pressures. The metabolic rate hypothesis predicts that species with higher metabolic rates have increased mutation rates are due to mutagenic elements resulting from mitochondrial respiration. It is predicted that higher metabolic rates lead to more frequent mutations due to the increased production of free oxygen radicals generated during respiration escape in the mitochondrial electron transport chain that produces energy for the cell. (Andrew P. Martin 1993; Galtier et al 2009). Metabolic rates vary with activity level and environmental-climate conditions. More active animals have a higher metabolic rate than less active animals. Some animals enter a state of torpor in which their metabolism can slow down. Hibernation in the winter and estivation in the summer are forms of torpor. All of these factors play into different species mutation rates even within the same family. For example, in bears, we see more mutations in Pandas. Therefore it is concluded by evolution that they are the oldest bear species. Considering this bear species has the shortest generation time of all bear species, has the highest metabolic rate, does not hibernate, has a lower life expectancy than all other bears, and has moderately high levels of inbreeding. These factors have a huge impact on the higher diversity we see with this species. It is not that this bear species is older, they simply have more mutations from the above factors.
Overall mutation rates in different animal kinds are ultimately affected by a number of different biological aspects of the creature in question. The largest impacting factors within a species is that of generation time, body size, metabolism, maximum life expectancy, environment, geographic range, and inbreeding. Followed by population size and growth/dispersal rate in regards to fixation of these new arising mutations coming into the genome. Sometimes other external influences such as radiation or chemicals in our modern world known as mutagens can affect the rate as well. But overall, mutation rates, in general, would not be affected by these random rare outliers. They are exceptions to the rule, not the rule.
Therefore the Created Heterozygosity Model, incorporating the metabolic rate hypothesis and generation time hypothesis, while also taking into consideration where and how long the organism lives. All help us obtain an individual mutation rate in different creatures throughout the world and help us explain the observed patterns of diversity we see a lot better than the “neutral theory” hypothesis alone. No one hypothesis alone can explain the different mutation rates observed in different life forms nor the patterns we see. This is why evolution had to incorporate many contradictory theories like; gradualism (A slow gradual evolutionary process), stasis (where evolution doesn't move), saltationism (Sudden rapid evolutionary development), de-evolution (evolution in reverse), followed by punctuated equilibrium created by Eldridge and Gould which is idea that perhaps evolution is not a gradual process after all, but rather a process with distinct bursts of phenotypic and morphological change happen. (Eldredge and Gould 1972). All of these are falsification of the other and just ad hoc explanations for finding complete contradictions throughout the evolutionary made up idea. My framework outlined here explains why such a hypothesis had to be invented to save the theory because everywhere we look we see fast mutation rates and rapid speciation events.
Eight very well documented phenomena exist which contradict the evolutionary molecular clock-neutral theory. Namely, high metabolic rates (Gillooly et al 2005; Martin & Palumbi 1993), DNA repair mechanisms (Li et al. 1996), maximum lifespan expectancy, known as the longevity hypothesis (Samuels 2004) which was found to be stronger than that of either body mass or generation time (Welch et al 2008). Universal limited intraspecific variation within and between species using DNA barcoding (Thaller 2018), including a constant fast ticking universal molecular clock in all life. The created heterozygosity hypothesis predicts that genetic diversity for mitochondria originated recently and different rates of mutation are caused by rapid speciation rates and divergence as well. These rapid speciation events are also observed and well documented in everything from birds, plants, fish, and reptiles (Fan Han et al 2018; Joanna M. Buswell et al., 2010; Y. E. Stuart et al 2014; Fang Zhu et al 2013; Claire Brandenburger et al 2019; Hudson CM et al 2020), contrary to Darwinian evolution known as gradualism. Rather, the new observable data confirm predictions of the created heterozygosity model of creation. CHM states that genetic drift and recombination rates play a larger factor and this is exactly what we see when we study birds, as recombination rates in them correlate closely with chromosome size in avian genomes (Hillier, L. et al 2004). All of these published discoveries contradict key predictions of neutral theory. My predictions add credence to this evolutionary falsification by showing that the assumed calibrated Co1 rate of 1%/million years that is calibrated from fossils or older vicariant events (Crandall et al2012) is a presupposition. It is nothing more than an ad hoc explanation with the paradigm driving the conclusion.
The fact is, studies regarding molecular evolutionary rates have resulted in a wide range of different rates for diverse genes and taxa. More recent studies based on pedigree studies and population-level data have all produced unexpectedly high results of mutation rates, which strongly disagree with rates inferred in phylogenetic studies. This is why in 2005 Simon Ho et al concluded that it is invalid to extrapolate molecular rates of change across different evolutionary timescales. Moritz et al in 1987 was clear that the evolutionary phylogenetic mutation rate was not necessarily general to other lineages and neutral theory should not be inferred. This went ignored as evolution theory does what it always does and runs with something till it cannot then just ignore all falsification while at the same time begrudgingly admitting it was wrong.
These incorrect assumptions about evolutionary mutation rates are now easily falsified when you line up side by side comparisons of nucleotide divergences for Co1 sequences in primates. This shows us an average of 0.30% for conspecific comparisons and 5.88% for congeneric comparisons. Which are comparable with what is found among the barcode sequences of fish at 0.39% and 9.93% (Ward et al 2005) and birds at 0.43% and 7.93% (Hebert et al 2004). Concluding that a much more recent bottleneck of all life occurred, and the resetting mitochondrial diversity allows us to conclude that all the nucleotide differences we find in this region are new and have occurred after this bottleneck. Since different life forms have different levels of diversity even within the same related species, this is an invalidation of the evolutionary neutral theory hypothesis and evidence for the created heterozygosity model.
Brown et al in 1979 first made the mitochondrial molecular clock in primates based on fossil data. Their famous 2% per million-year rate was considered the best reference to use even in absence of fossil data regarding other mammals and vertebrates. However, since mtDNA variability is minimum across taxa and new discoveries show us that mutation rates are high. The conclusion is that our perception of deep evolutionary time was and still is incorrect and based on a misinterpretation of the data. If one were to take away the presupposition of evolution being true you are left with only the evidence that points right to a recent bottleneck with animal families having clear genetic boundaries (Thaller 2018).
The evidence could not be more clear, fast mutation rates with minimal diversity and low average pairwise difference between all life on Earth tells us unequivocally that all life went through a very recent bottleneck and a universal molecular clock described in neutral theory is wrong. The patterns we see are best explained from a recent bottleneck with fast mutation rates explaining the diversity we now see.
In conclusion, we now have the first-ever predictions based on fast mutation rates in a highly conserved gene that does not undergo selection. in multiple diverse species and a recent bottleneck. We see diversity still increasing today and can better explain the patterns of diversity with the Created Heterozygosity model combined with the metabolic rate hypothesis, generation time hypothesis along with considering how long an organism lives. With secondary considerations of factors such as migration, dispersal rate, geographic range size, population growth rate, inbreeding, and environmental conditions (temperature). We are able to not only delineate between different created kinds by observing ancestral pleomorphism and large linkage blocks that should not be there if deep time is true. I am also confident that the Co1 gene is a fast mutating region since every other region of the mitochondria tested thus far has been. Including all 37 genes, hypervariable regions, individual gene fragments, including the D-loop aka control region. Stack this with the fact that mutation saturation has not been reached and we have a trifecta of evidence that potentially confirms Young Earth Creation via the Created Heterozygosity model.
Discussion
The universally shared molecular clock idea is dying out. The neutral theory proposes that specifically in mammals, neutral evolutionary rates depend only on generation time, while non-synonymous rates depend solely on population size (Nikolaev et al 2007). What DNA barcoding sequences have shown us, however, is that mammals show a much higher mean of intraspecific divergence values compared to that of all other animal groups. Validating that generation time is only part of the factor playing into the mutation rate of species in question. Life expectancy can also play a major role rather than generation time alone. When we look at different Co1 values, they ranged from 0.60% to 1.1% in mammals (Lorenz et al2005, Hajibabaei et al 2006, Clare et al 2007; Borisenko et al 2008; Cai et al 2011) and less than half in other animal groups; 0.17% to 0.46% (Ward et al 2005; Kerr et al 2007; Hajibabaei et al 2006; Maturana et al 2011). These overall low differences, with high rates of change, do tell us a recent bottleneck occurred and the patterns cannot be explained with traditional neutral theory.
Since higher nuclear DNA diversity observed in marine vs. non-marine species, in invertebrates vs. vertebrates, and in small vs. large organisms, is not in line with patterns of mtDNA diversity (Leffler et al 2012; Bazin, Glémin & Galtier, 2006). Then the best way to explain the patterns is by the Created Heterozygosity Model (CHM). This means looking at the nuclear DNA as originally created with already diversity built-in so that the first created kinds of all life would have been able to create diverse offspring without complication. “The nuclear DNA clocks are not the product of mutation, and this interpretation is in error. Unlike mitochondrial DNA, nuclear DNA comes in two copies and is inherited from both parents, which means that DNA differences in offspring are the result of DNA mutation and of pre-existing DNA variation in the parents. For example, under the creation model, some of this pre-existing variation in humans traces back ultimately to the two parents, Adam and Eve, whom God created with pre-existing DNA differences. When this fact is accounted for, nuclear-genetic clocks point to recent creation, not millions of years.” And looking at mtDNA has each having their own brand new mitochondria without any mutations at all. After “the fall” mutations started building up and reduced during the Global flood bottleneck and started accumulating mutations all over again after that point. So we have two events in the past, creation where the most diversity would be seen, then the Global flood bottleneck which would have reduced all the animal species into just one species, limiting genetic diversity and restarting mtDNA within the creatures.
According to the CHM if we want to see what is more related, then we want to look at nuclear DNA followed by functional differences. If we want to test how old the species is, we focus on the mtDNA, not nuclear DNA. Yes, nuclear DNA does mutate at a rate of 78 base pairs per generation in both humans and chimpanzees, so a clock and predictions can be made. Dr Jeanson has compared these two in “Replacing Darwin”, but we will stay focused on the contradictory differences between mtDNA and nuclear DNA comparisons. Comparing nuclear DNA we can see that the sloth bear is closest to the sun bear for example. Yet mitochondrial DNA analyses and morphological studies placed sloth bears outside of all other ursine bears (Kutschera, V. E. et al 2014., Bidon, T. et al 2014., Pagès, M., et al 2009). Yet nuclear gene analyses favor a position close to sun bears ( Krause, J.et al 2008., Abella, J. et al 2012, Kutschera, V. E. et al 2014). This paradox is resolved only through the CHM. In the CHM, if we want to see what is related we want to trace nuclear DNA patterns of relatedness and see if the species closest to it carries similar DNA functions, orphan genes and can be in vitro fertilized, if so they are related. These other steps are often required because nuclear DNA is difficult to compare across species and since nested hierarchical patterns contradict when comparing anatomical, mtDNA, nuclear DNA, and non-protein coding nuclear DNA. Then we have to look to functional DNA differences as to what determines relatedness. This is what discriminates between the CHM and evolutionary models. These contrasting predictions by the evolutionary model and CHM allow for a head to head comparison regarding the nuclear genes and mtDNA mutation rates.
~ Robert W. Carter 2014 noted that we should be viewing mtDNA as starting off new and void of all mutations with no differences within related animal kinds at creation. This allows us to observe the fast rates of mutation in the mitochondria and take that back to a point of no mutations and make predictions based on what we would expect to see if life was far more recent. Unlike the genes in nuclear DNA, which can differ greatly from species to species, all animals have the same set of mitochondrial DNA, providing a common basis for comparison. Especially since mtDNA evolves fast enough to provide sufficient variation for the estimation of mutation rate (μ) over a two-decade period (Drummond et al 2003). This way we do not bother trying to reconcile the discrepancies between nuclear and mitochondrial rate differences, as they have no bearing on one another.
The Worldwide pattern of limited variation within species, with slightly larger differences between species, makes not only identification of separate Biblical “kinds” possible. But it also leads to future testable predictions that are the gold standard of science and any good theory. The easiest part about identifying an original kind with DNA barcoding is that even new species born today still retain ancestral polymorphisms (variants that arose by mutation prior to the speciation event that generated the species in which they segregate). Confirming multiple important things.
1:) All life is still very young and identifiable within and between species.
2:) Identification of created kinds is made much easier now as variants that arose by mutation prior to the speciation event were generated by the species in which they segregate from and can be traced back in time to their inevitable origin.
3:) Their presence complicates the evolutionary interpretation of molecular data and leads to incorrect phylogenetic inferences because taxonomic boundaries are crossed in the evolutionary paradigm. These ancestral polymorphisms point right to the species founder, the basal kind of each lineage. This is why evolutionists invoke incomplete lineage sorting and convergent evolution to try and deal with this problem.
4:) Large linkage blocks in the genome are still visible, something that if a lot of time had passed would not be the case.
5:) Genetic boundaries exist, we can see these limits within DNA barcoding.
6:) Mitochondria uniformity among all life tells us a recent worldwide bottleneck occurred and molecular clocks point to a MRCA for each different animal family just thousands of years ago.
The only odd diversity we ever get from barcoding comes down to two factors; hybridization or gene flow. However, since shared polymorphisms are otherwise uncommon in unrelated species, we can delineate what is related and what is not very easy now. We can clearly see that Neanderthal, Denisovan were never predecessors to modern-day people and were never hybrids at all. Rather all are clearly human, as DNA Barcoding shows us that three retain common ancestral polymorphisms from the root ancestor at this last bottleneck.
Since the Co1 gene is highly conserved, this explains why normal modern people have so few differences while at the same time explaining why Neanderthal and Denisovan had so many mutations. As highly conserved regions are also susceptible to faster rates of change but only from the worst scenarios like inbreeding. Their smaller populations would rapidly obtain more point mutations. Since selection has no effect on this region, it adds credence to why they had double what we have today over such a short time while the rest of humanity was growing in population size and migrating and expanding. Now if Denisovan and Neanderthal were hypermuting from isolation, inbreeding, iridium exposure in the northern atmosphere from worldwide volcanism, living in harsh freezing conditions. Including non-synonymous, synonymous and somatic mutations were building up even rapidly during their extended lifespans. Then we would expect to find these extra mutations in the mtDNA. Due to random extinction of lineages such as neanderthal, different branches of a reconstructed phylogeny will differ in how often they experienced such short episodes of accelerated substitution rates. This results in differences that may appear to be long branches of a lineage when in reality they are short lived hypermutated lineages.
Since DNA hyperdiversity is not uncommon in eukaryotes. Evolution must account for why mitochondrial (mtDNA) data retrieved by James et al 2016 shows us that in over 505 diverse animal species tested, all portrayed hyperdiversity when none was expected. Including many other studies where rapid speciation rates were observed in everything from birds, fish, plants, fruit flies, reptiles, and Nematoda (Fan Han et al 2018; Joanna M. Buswell et al., 2010; Y. E. Stuart et al 2014; Fang Zhu et al 2013; Claire Brandenburger et al 2019; Hudson CM et al 2020). It is clear that fast mutation rates and speciation is occurring much more rapidly than predicted by evolution and we can see this in multiple separate phyla (Chordata, Arthropoda, Plantae). Even a fast mutation rate beyond the error threshold has been reported as causing the extinction of yeast lines (Herr et al 2011).
This is why I believe we must investigate the observable data via pedigree studies on mtDNA regions such as the Co1 gene to obtain a true rate of change. Since selection does not remove mutations arising in this region of the mitochondria, and the small population tribes that Neanderthal lived in, explains why we find the Co1 diversity in neanderthal between 8-18. Yet in modern-day people today who have between 0-10. In the entire mitochondria, modern-day people have a maximum of 24 fixed substitutions. As where Neanderthal ranged from 20 -36 fixed substitutions. Clearly, they fall within the range of humans, but their inbreeding topped with small population size and living in the North during the post-flood harsh ice age. All these factors built up point mutations rapidly without selection able to remove them, that they are considered to be an outgroup of humanity, subhuman.
They made a retrodiction before all the evidence was in, then they had to alter the evidence after they discovered all humans share at least some Neanderthal DNA. Another thing evolution did not predict and ended up causing them to alter their preconceived notion. They were never a population that existed prior to us nor gave rise to us but were just an offshoot group of small populations that were diseases and inbred who seldom crossed paths with other people groups and intermingled.
It is simple. Neanderthals and Denisovan having more mutations than modern-day people are what deemed them older than humanity by scientists. Since as you know, evolutionists believe mutation rates have either remained constant and slow throughout evolutionary deep time or have only recently sped up. This explains their rationalization regarding Neanderthal having had more mutations, therefore, they must be older. Is flawed, just as it is with panda bears. Another explanation easily explains why they have more mutations, but to evolutionists, these extra mutations with higher diversity are why they are considered either subhuman predecessors, or a subspecies today. Including a few morphological features that they advocate are primitive features like their enlarged longer skull case, protruding brow ridge, and the receding angle of their chin. The reality is, their morphological features are better explained by inbreeding, and their skull shape/features are governed by genetic influences found in genes expressed in the human brain. So far a single locus, the LD block on chromosome 10 in the GPR26 gene which encodes a G-protein coupled receptor, showed the association with the skull structure of neanderthal discovered by Michael D. Gregory et al 2017. Though they stated in the study that it's likely that other genetic loci are also involved, they were yet to identify any and would need a larger sample size to prove it. So we have clear evidence that the morphological differences we see in neanderthal were nothing more than genetic abnormalities. We also know that as time went on Neanderthal just became more isolated and more inbred, before eventually dying out. This is why we should not use mitochondria as a marker regarding Neanderthal and Denisovan since it is well known that isolation by distance makes it unsuitable for reliability (Peter R. Teske et al 2018). Including the fact that Ohta, 1992 stated; “slightly deleterious changes (s < 0) will be nearly neutral and are more likely to go to fixation by chance in a smaller population”. Also, Eyre-Walker and Keightley in 2007 concluded; “The substitution of deleterious mutations will be faster in small populations and the effect is greater in a declining population. Given that advantageous mutations are relatively rare compared to deleterious mutations”. The rate of acquisition of reproductive isolation increases quadratically with genetic differences between populations is called the snowball effect (Orr, 1995). Multiple empirical studies have given some support for the snowball effect (Matute et al 2010; Moyle and Nakazato, 2010; Wang et al 2015). Clearly, the observation that they would have had more point mutations because of these facts points to a conclusion that they were not an older population. Rather, they were suffering as many isolated, inbred species suffer today. However unlike animals, without the ability to speciate and diverge.
We as human beings alive today still retain large linkage blocks in our genome that have not been recombined in all of human history. This makes sense only from a young-Earth Creation perspective. But not evolutionary, since recombination would have altered every single linkage block there is and no evidence of them would be found. Picture a chain-linked together that slowly loses a link from the ends every decade. The chains wouldn’t exist after hundreds of thousands of years at the rate the links are breaking today. Yet we still find these long connected chains linked together in our genome throughout all of humanity.
So even when studying humanity’s age, mitochondria has been an invaluable tool. The fact that Africans have much higher rates of recombination than other people groups (Ingrid L. Berg et al 2011) is even more evidence that gives the appearance of age to Africans when in reality humanity is all the same age. Including the rates of rapid mutations occurring in the mitochondria, yet minimal overall change confirms that humanity cannot be old. Carter RW 2007 using a data set of 827 carefully selected sequences, was used to create a worldwide human mitochondrial consensus sequence to explain the origins of modern humans. It is shown that modern humans contain extremely low levels of divergence from the mtDNA consensus sequence, differing by a mere 21.6 nucleotide sites on average. A comparison of this consensus sequence to several ancestral sequences derived from phylogenetic studies reveals a great deal of similarity. Meaning that finding many ancestral sequences in modern-day people, is only possible if not a lot of time has passed. Since Adam and Eve were created with nuclear DNA differences, meaning that their genomes were the first haplotype blocks in all of human history. Their “haplotype blocks” were, essentially, the length of entire chromosomes. Since then, every recombination and gene conversion event has been fragmenting these initially long blocks into smaller haplotype blocks. The fact that we still find these blocks at all is contradictory to deep time evolution.
By multiplying the observed published rate of recombination (Wang et al 2012) and several estimates of the frequency of gene conversion (Wang et al 2012; Palamara et al 2015; Williams et al 2015) dr Jeanson combined into a total rate of haplotype block division per generation. This was used by Dr. Jeanson to predict how many blocks would have arisen in each individual after 6,000 years. The combined gene conversion and recombination rate was divided by a range of generation time estimates for humans to determine the rate of haplotype block divisions per year. Dr. Jeanson 2016 multiplying this converted rate by 6,000 years estimated the number of haplotype blocks that would have resulted from 6,000 years of recombination and gene conversion in each generation in a single lineage. The results showed us that the observable rates clearly point to a recent arrival of humanity. Clearly, the discrepancy between an ancient bottleneck and a recent bottleneck is at odds with one another and only one can be true. It's not a matter of if a worldwide bottleneck happened, it's when did it happen that is the question. It was stated by Thaler in 2018 regarding genetic data results; Namely that the extant population, no matter what its current size or similarity to fossils of any age, has expanded from mitochondrial uniformity and this is one of the clearest, most data-rich, and general facts in all of evolution. Clearly undeniable at this point, and this covers everything from bacteria, yeast, humans, fish, and land animals. Nothing was immune to Noah’s flood and now the genetic evidence confirms it.
What predictions are evolutionists making regarding the Co1 gene or its mutation rate? None. Thus far they only use the assumption that the fossil record is an accurate representation of time and all models are based on that. The only thing that has happened recently is that demographic models of expansion have shown how their evolutionary assumptions have failed. All 3 marine invertebrates tested in the Sunda Shelf were found to have extremely elevated rates of mutation in the Co1 gene compared to the previous phylogenetic rate (Eric Crandall et a2011). Much higher than the typical rate of 1%/million years that is calibrated from fossils. Considering those are still biased as well since they also incorporate evolutionary assumptions, the next logical conclusion will be that the entire phylogenetic model of history will be exposed when they test this region for the empirical rate.
As of yet, no pedigree studies have been done regarding the Co1 gene mutation rate that my predictions are focused on. So these novel future predictions, for now, remain to be validated. However, what makes my predictions more unique than others is that there is another way to test the validity of them, it is through mere waiting. If my predictions are correct, then merely waiting alone will result in newly visible mutations arising within decades from one another within and between species. Contrary to the current predicted value of the Co1 phylogenetic mutation rate of 1% per million years or 40 changes per 1,000 base pairs over 1 million years which is calibrated from the fossils or older vicariant events (Crandall et al. 2012).
Since neutral theory fails to accurately capture the pattern of diversity in different animal life and fails to explain the discrepancies of mutation rates of different life forms. It, therefore, invalidates evolutionary phylogenetic trees created that are based upon the assumed universal molecular clock proposed by neutral theory. Since it also fails to answer both important aspects of the evolutionary model that hangs upon neutral theory being true, then an alternative is greatly needed in the field of biological evolution.
Contradictions abound with neutral theory and diversity is better explained by the predictive power of the created heterozygosity model that accounts for factors outside a universally driven generation-time effect molecular clock ticking the same rate in all life. Including the fact that mutation saturation has yet to be achieved in the mitochondria and likely the Co1 region as well. Then we have not only evidence of a recent bottleneck, but a model that is just as explanatory as the evolutionary model regarding diversity we see if not more valid since we are the only ones making future testable predictions based on our model regarding future diversity. Evolution is not, because the theory is a post hoc model based on retrodictions after the evidence is already in. DNA barcoding is the most accurate measurement to date and it invalidates the Neutral theory of evolution. Kuhn TS (1996) suggests a new paradigm is needed regarding neutral theory and since that time no other theory has been allowed in science since evolutionism is protected by law.
Only time will tell as answers to my predictions begin to manifest. Even without future pedigree studies performed on the Co1 gene, mere time alone will reveal to us that diversity is still increasing and nucleotide substitutions are still occurring today within the Co1 gene and this alone will reveal the fast mutation rate predictions presented in this study. Since pedigree studies are currently lacking in Co1 research, I believe future results testing the Co1 gene using the pedigree method will also confirm the predictions made here. Together these different facets will bring to fruition the truth about our history, and conclusions will indicate that deep time evolution is incorrect and that a recent global catastrophe of Biblical proportions is true.
The “young” Earth view is a deduction from a number of biblical evidences and teachings, not a starting point. It follows from the biblical big picture that God created a perfect creation that fell because of sin. Without this “bad news”, the good news of the Gospel with the redemption from sin lacks any foundation.
References;
Pairwise differences were obtained from Bold Systems Barcode of Life Data System http://www.boldsystems.org/index.php
Pairwise alignment was done using EZ bio-cloud https://www.ezbiocloud.net/tools/pairAlign
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1:) I.P. said it is possible that (IN THE BEGINNING) should not even be at the start of Genesis 1.1.
Reply; Thats fine, lets say for argument sake you are 100% correct and ill even give you that. I can answer this with a question - What does Jesus say about ADAM AND EVE? He said "
Matthew 19:4 "Have ye not read, that he which made them AT THE BEGINNING made them male and female?" Clearly we can see that even if it was removed in Genesis 1 it still applies regardless. More on this later...
2:) IP says that there are places in scripture where "bara" doesn't mean creation out of nothing. Therefore we cannot take with face value that bara in genesis directly means Creation - He uses the example of how psalm 51:10 the author asks God to create in him a new heart. But clearly he isn't given a new physically created heart.
Reply: IP is trying to make the argument that IF Earth was already existing and then God came along and created it to function properly, then it really doesn't mean that the world was Created at that moment. Now, again lets give this to him ok? Let's say Gods spirit was traveling over his prior Creation He made and He saw Earth and decided to make it functional and separated dry land from water. This still doesn't change the argument about WHEN did this happen. If he tries to argue that these "days" are massive undisclosed amounts of time then it undermines the Sabbath itself, since it is clearly a single day we are supposed to rest and set aside. Not an undisclosed period of time, or 1,000 year period like a lot of people grasp at (When Peter says that for God one day is as a thousand years and a thousand years as a day, he's talking about the timeless attribute of God, not that whenever day is mentioned in the Bible, it can mean 1000 years). Again I believe IP is trying to reconcile deep time evolution into scripture when there is no reason too. Literally the entire order of Creation is the exact opposite of evolution anyway (Water before dry land, plants before sun, Earth before sun, etc..). So just tossing an Old Earth in doesn't actually solve the problem as a theistic evolutionist. Just learn the science and you will see that it only comes down to interpretation of the data.
Lets focus on "Bara", it is used a total of 54 times in scripture. 42 times it directly means to "create", 3 times it means "creator", 1 time it means "done or complete" - referring to something created, and only in 8 other places does it mean something outside of that, and none of these appear anywhere near Genesis it seems.
Let's look at Genesis and see how often Bara is used and then ask ourselves if we should believe bara meaning something other than Originally Created - Of course we see it in Genesis 1:1 "In the beginning God created the heavens and the earth." Again IP says this is not a creation event but rather taking a previously created thing and making it function properly. Then we find it in Genesis 1:21 "So God created (bara) the great creatures of the sea and every living thing with which the water teems and that moves about in it, according to their kinds, and every winged bird according to its kind. And God saw that it was good." Now, were these Creatures already here and existing? Did God just make them function properly now? Let's look at more and see if bara should be used in Genesis for functionality or creation = Genesis 1:21 "So God created (bara) mankind in his own image, in the image of God he created them; male and female He created (bara) them." It seems like we have another Creation event out of nothing. We can see this throughout scripture when referring to mankind, "Deut; 4:32 "Ask now from one end of the heavens to the other about the days that long preceded you, from the day that God created (bara) man on earth:" Or how about in Genesis 5:2 where is specifically says "In the DAY when they were created (bara). So we have man who was not existing, just like animals and just like the Heavens and the Earth, then all of a sudden, in a single day all different things being created (bara) in Genesis 1. We see this in Psalms 89:47 "You have created (bara) all".
Now if there was an Old pre-existing Earth, then why would the text say "Bəreshit" at all in literally every known existent Biblical text on Earth? Bəreshit (בְּרֵאשִׁית, literally meaning = "In the beginning"). If the Earth was already existing then there would be zero reason for the text to say "In the Begining" and since this is mentioned throughout scripture even by Jesus himself who said "God created them both male and female in the Beginning". Then it seems clear, Genesis 1 was "The Beginning" of Creation of Earth and the Heavens and not a later rehashing of a function of a prior creation. Then it could no longer be consider "Beginning". This is cleared up in Genesis 2, so you do not have to just trust if Genesis 1:1 if it had Bəreshit, because we can see in Gen 2:4 "These are the generations of the Heavens and the Earth, when they were created (bara) in THE DAY that YHWH God made the Earth and the heavens". The text in other places in scripture really does seem to imply that Genesis 1:1 is referring to a single day Creation of the heavens and the Earth. Romans 1:20 Paul tells us directly that people are without excuse, seeing Gods power and glory in his creation FROM THE BEGINNING". it says directly "For ever since the world was created, people have seen the earth and sky." Clearly mankind was created and have existed since the beginning of this creation. This verse would not be true if the Earth were billions of years old, since man would not have existed since the beginning to see the Earth and sky.
3;) Genesis 1:28 IP says that Eden was Blissful and perfect, yet this verse tells us man has dominion over animals and subdue which is harsh and not perfect.
Reply; First of all God gave us dominion and control over Earth and the creatures that live in it. We are above them, and they were created for us. How is this at odds with a perfect Creation? I guess its a subjective argument because if you feel that riding a horse, using an ox to plow land, birds to carry messages, sheep for their wool. Then yes it is harsh to use them for this but it hardly would make Paradise a harsh world because of it don't you think?
Were Biblical slaves abused? They were never supposed to be mistreated, yet the word in scripture in regards to a slave would be to subdue. Well subdue in the dictionary has a few meanings, yes it means to conquer and bring into subjection but there was no nation or people to conquer. But it also means to "Bring land under cultivation" https://www.merriam-webster.com/dictionary/subdue What was Adam doing in Eden? Well he was cultivating. So clearly the text goes along with that definition of the word because no text anywhere refers to Adam having an altercation with anyone else at any time, even with animals. How about animals? Yes, we can use an ox to till the land and use a horse to ride, because we have dominion over them and we can subdue them. Is this evil? Not at all. This does not take away from God calling things "good" after he made them nor that Eden was a paradise. Man was not killing them to eat either, the first death we even see is after the fall of Adam, while they were naked hid from God and thus because of sin something must atone for it. Thus death was required for life and we see the first death of an animal used to cloth man. We clearly see all life was vegetarian and we see no mention of death ever anywhere in scripture. The matter of fact Isiah mentions that the next life will be akin to how it was in the pre-fall world where "The wolf will live with the lamb, the leopard will lie down with the goat, the calf and the lion and the yearling together; and a little child will lead them." Isaiah 11:6.
God wants us to be good to animals and kind. He that killeth an Ox is the same that killeth a man." Isaiah 66:3. We also see in Proverbs 12:10 "The righteous care for the needs of their animals, but the kindest acts of the wicked are cruel."
Man was never even permitted to Eat animals till after the flood. Clearly if God told Adam to subdue animals then Adam started abusing and killing them he would be doing something wrong. The text is pretty clear, but sadly vague. This is why IP is able to play semantics because stories are brief and vague to some extent. Clearly IP interoperation comes from his view of evolution and how evil it is in a world of killing that can only evolve through death and suffering and survival of the fittest. This midset is what is at odds with scripture, that is why he is trying to reconcile what he believes these words mean in the context.
4:) IP says how can there be a day and night in Genesis 1; 14-19 Days and night can only exist with a sun and earth. Yet the sun did not exist.
Reply; Think about it like this. The Bible tells us in the next life there is still a Sabbath right? It is FOREVER. And the Sabbath is the 7th (day). Yet how can their be days with no sun? Clearly the Bible says God melts away the sun and he is the light of the world. So we will no longer have a solar illusionary.
2 Peter 3:10 "But the day of the Lord will come as a thief in the night; in the which the heavens shall pass away with a great noise, and the elements shall melt with fervent."
2 Peter 3: 12-13 "At that time the heavens will be destroyed by fire. And the sun and moon and stars will melt away with much heat. We are looking for what God has promised, which are new heavens and a new earth."
So it seems to me that "days" exist with or without a rotation of the Earth nor the suns existence. God Created time regardless of our subjective opinion of how fast it ticks based on where we are on this planet or on another planet. God created a day to be 24 hours from the beginning here on Earth and days are made for us just like seasons are so we can know and understand seasons and sabbath. God was on this Earth during this time and God is light, so it was his presence that was supplying the light we read about, just like it will be again his light in the next life, sun or no sun, night or no night.
5:) IP mentions JER 4:23-26 where God took a disorder cosmos and made it function properly. We talked about this earlier. Ok fine, as I said we can argue over semantics and ill even award you with this. The next logical question then is when was this? You will find the answer again falls on YEC, timeline. So I do not understand how the argument helps IP because Creation of life and everything else is still pointing to YEC and all within days of each other. Even IF Earth and the Heavens were existing long before the other events of creation.
6:) IP says Genesis 2:4 is 1 of 2 creation stories. He even goes as far as to say that Adam and Eve were not the first two people.
Reply; No idea what humans existed before Adam and Eve unless you read Jewish lore and read about Lilith (Adams first wife). Eve is called Eve because she is the mother of all living. Kinda odd for her not to be first, don't you think? But lets focus on the 2 creation stories in Genesis 1 and then Genesis 2. He is correct there are two creation stories, one Eve was made with man, the other she was made from his rib. Chapter 1 is an overview, a laid out plan in regards to the Creation of Man, It's a story about WHY God created mankind.
Whereas Chapter 2 is God actually focusing on the creation specifics of man, and gives the details of the process. It is not focused on Why He created everything, nor the specifics of other things like the planets, or animals, because God created all of it - for mankind, and mankind is the focal point of this story. Remember, God created the Earth for mankind and we are the important part of this story and God wants us to know that.
So the reader of Genesis 1 is of a distant observer listening to God explain to his children in a very simple way the overall creation of the universe, Earth, and life regarding WHY He created mankind - (purpose)
As where Genesis 2 zooms in for a close-up on the “man” God created everything for, including some details of the process. We can see that Eve was taken directly from Adam's side - making females equal to men right from the start. God could have easily taken a hair from Adam to make Eve but this would have been interpreted that women are above men. Or he could have taken a small bone from the foot of man, but this would have placed women beneath men. So God wanted us to know that we are all equal and scripture cannot be twisted and interpreted wrong regarding this subject. You will also notice that God chose a rib, the only bone in the body that regrows after it is damaged or removed.
God is named 32 times in 31 verses in Genesis 1, and every time He’s the subject of the sentence; acting, intentionally building something “good.” Notice Chapter 1 describes “why” God is going to Create all things “for” man - “Fruit is for man’s food and good pleasure”. The animals were created so man will know his special status—and place, that he’s made for more and created above the beast of the field and to have dominion over them. Man did not evolve from them in scripture, they are brought to him and he names them and rules over them. So Chapter 2 is about the actual event occurring without the “WHY” involved.
Trying to say that God breathed into Adam and gave him a soul and this is what elected him as something special like some christians believe. Well this fails when you discover that soul is just the body. It say's God Breathed the breath of life into the first man (Adam) and he BECAME a living soul. This is a creation event of man, not a special election of Adam being different from other humans alive at this time.
7:) Genesis 4... The Tree of life obviously granted some form of life extension powers, why else even call it the tree of LIFE? Man was created perfect, but had to be removed from this tree after the fall as if he had kept consuming its fruit he would have remained youthful. This is why an angel was sent to guard any man from going near it, as to try to obtain longer life. It was probably most likely possible Adam could die falling off a cliff, but he was biologically unable to age and die being made "perfect". How does this argument go against YEC though? We clearly see Earth was Created for man, and we are the focal point of creation in scripture and God gave us a perfect world to live in disease free and it was only sin that brought death into the world. Maybe I am wrong here but I believe IP wants to tell us that death and discord was normal because that is what evolution teaches and he is a theistic evolutionist. I do not believe the two theories are really compatible, it has to be either 1 or the other. But I do not like the division it causes between theists. I think Creation is what separates Christians from non-christians. Remove creation and now the only difference is you go somewhere when you die. Remember without the "bad news" of the fall of man, then there is no "good news" of redemption. "For through one man, sin entered into the world and death by sin". If Genesis fall of Adam was not literal then nothing about Salvation even makes sense. How can there have been death before Adam then? Seems clear cut in my opinion.
8:) IP says YEC all believe the entire Bible literal (Kinda ridiculous claim). The fact that the Bible even has a single parable means it cannot be 100% literal. Not to mention there are psalms-poetry, allegories, proverbs, metaphors etc.. the entire thing doesn't have to be literal to determine if some parts are or are not. That is where the science and statistical probability come into play.
9:) Genesis 8:4-5 IP says the tops of mountains see. Yet Genesis 8:9 says waters upon face of whole Earth. Which is it? First of all, why is this a YEC problem? Or is this a Global flood argument ? Either way let's lay out the story so you can see... Here is IP argument, showing that they contradict.
First we see...
Genesis 8:4-5 "on the seventeenth day of the seventh month the ark came to rest on the mountains of Ararat. The waters continued to recede until the tenth month, and on the first day of the tenth month the tops of the mountains became visible."
But then later we see...
Genesis 8:9 "But the dove could find nowhere to perch because there was water over all the surface of the earth; so it returned to Noah in the ark. He reached out his hand and took the dove and brought it back to himself in the ark."
Ok, perhaps this can be answered by there being two different authors. A priestly source and perhaps a scribe of Noah... https://www.livius.org/articles/misc/great-flood/flood1-t-bible_2/
Regardless, here is the timeline;
The time the ark grounded on a mountain side on the 17th day of the 7th month, until the tops of the mountains were seen on the 1st day of the 10th month and until the dove was released the second time and bought back the olive leaf was approximately 4 months (the 11th month 11th day.) It was only after that, God told Noah he could leave the ark because the ground was dry enough. But from a botanical perspective it also means, that any grass, seeds or plant fragments that had survived the months of flooding, have now had several months to germinate or sprout on a warm moist earth, thus producing a lush, albeit short in height, coverage of planet earth, making for plenty of food to eat for the animals, without having time to produce thick jungles to impede rapid migration around the planet.
Look, we do not have to bicker over if scripture is trying to tell us if there was a global flood or not, we know there was. Worldwide low genetic diversity in all life has proven it = https://phys.org/news/2018-05-gene-survey-reveals-facets-evolution.html They were unable to find anything in their made up geologic column, so they had to retrofit the data after the fact. The fact is mtDNA mutates fast and all observable pedigree mutation rate studies validate this. Considering the study was focused on the Co1 gene in the mitochondria then we can be certain that it also ticks fast and this evidence points to a recent global bottleneck in ALL life (Fish, birds, animals and humans). Everything tested has low genetic diversity, contrary to evolutionary expectations.
10:) IP says Abraham and Sarah Didn't have kids over 100, including his father nor anyone that Abraham had ever know. Also the Masoretic text shows us that Abraham would have known old people. How can we reconcile this?
Reply; Easy. The Masoretic text alone cannot answer this, that is why. We must look at the difference between the Masoretic text and the Septuagint and every other ancient text regarding the post flood genealogies =
Since Jesus himself read from the Septuagint I think he would have noticed if the dates were wrong. Since he did not, then we have to assume that its the Masoretic text that is wrong since it is the only 1 that doesn't align whatsoever.
This means Abraham would not have known Shem or any of the patriarchs that were living to their 400s, and the verse now makes sense. The matter of fact Abraham himself was born to Terah when he was 130.
Not this -
Below is from the Greek Septuagint. Names are a little different, as they have not been translated yet like in the Masoretic. Shem = Sem, Salah = Sala, Eber = Heber, Reu = Ragau, Serug = Seruch, Nahor = Nachor and Tarah = Tharrha
https://youtu.be/ZQCezXiXmTI
First, it should be remembered that Abraham did not think it impossible to sire a child by Hagar at age 100 (Genesis 16). In fact, by insisting that Abraham engage in conjugal relations with her maid, Sarah exhibited confidence in his ability to raise up an heir. Remember Abraham had his first son at 86, we read that well after entering the land of Canaan at the age of 75 Abraham was “childless” with “no offspring” (Genesis 15:2-3). He had 6 other kids later (Genesis 25:1-6; 1 Chronicles 1:32)! Zimran, Joktan, Medan, Midian, Ishback, and Shuah were born sometime after Abraham was 86. Even though Inspiring philosophy believes that Abraham did not have kids after the age of 86 but rather they were all born before Isaac because Isaac would’ve gotten the inheritance which he didn’t. But I am going to go by scripture rather than assumption based on something else. So clearly in scripture we having Abrahams first kid being born when he was 86 and more kids later at over 100 years so age. So clearly this is NOT why would he be laughing at the prospect of him having another kid at 100. This would just be just a years after he just had a kid anyway, literally just 14 years earlier. Clearly it was Sarah's barrenness and inability to have kids and the joy it brought him to hear the good news that made him laugh at the idea. This is solidified in the fact that he continued to have many more kids after she died with other women (Genesis 24, 25:1-2). Abraham was more than 140 when Keturah bore him six sons.
Ellicott's Commentary Regarding Abraham laughing at God—The Jewish interpreters regard Abraham’s laugh as one of joy, and Sarah’s (Genesis 18:12) as one of unbelief. We may, however, well doubt whether there really was this difference between them; but our Lord confirms the View that joy was uppermost in Abraham’s heart (John 8:56).
Benson Commentary - When Abraham fell on his face, and laughed — It was a laughter of delight, not of distrust. Now it was that Abraham rejoiced to see Christ’s day; now he saw it and was glad; (John 8:56;) for as he saw heaven in the promise of Canaan, so he saw Christ in the promise of Isaac, and said, Shall a child be born to him that is a hundred years old? — He doth not here speak of it as at all doubtful, for we are sure he staggered not at the promise, (Romans 4:20,) but as wonderful, and that which could not be affected but by the almighty power of God.
Adam Clarke Commentary - Abraham fell on his face, ויצחק vaiyitschak, and he laughed; and to the joy which he felt on this occasion our Lord evidently alludes, John 8:56; : Your father Abraham Rejoiced to see my day; and he saw it, and was Glad. And to commemorate this joy he called his son's name Isaac.
Matthew Poole’s commentary regarding Abrahams “laugh”, was through admiration and holy rejoicing at so great a blessing, not through unbelief, as Sarah did, Genesis 18:12,13, as appears from Romans 4:19, 20. And though the outward act was the same in both, yet God discerned their differing dispositions and intentions therein.
Now, a couple of things to mention here, first of all, Abraham responds to God's promise with laughter. Now in chapter 18, we're going to discover that when Sarah hears this promise from God, she will also laugh. God will actually confront her for her laughter. He will rebuke her for her unbelief. But since there is no such rebuke here towards Abraham, it shows us clearly that Abraham's laughter was of good intentions and not of shock because of age. But because his wife who was barren was now able to conceive and explains why Sarah who was barren laughed out of unbelief. Because they both laughed, God tells Abraham that when Sarah has a son, he should name his son, Isaac. Isaac's name literally means laughter. Also consider Abraham was able to beget sons long after that as well (25:1-6). Clearly his age was not a problem but Sarah and her barren body since His own father was 130 when he bore him.
If you are still not convinced of a joyful laugh then consider there are several factors that may come into play as to why the text may be portraying Abraham as was somewhat baffled at the idea of having a child at the age of 100. It is theoretically possible that Abraham simply was failing in health at this time. This would not be surprising, considering his son experienced a serious failing in health about 44 years before he (Isaac) died (Genesis 27:1). Probably a similar genetic health problem his father passed on could have been what made Abraham unable to father any more kids at 100. But this is just a hypothesis because as I said, it seems clear that he had a kid literally just 14 years before that and considering that his father begat him at 130, and that even his own grandson sired a child at 100, Abraham’s statement about him being 100 years of age when Isaac was promised likely could easily be interpreted in light of a physical condition at the time rather than his actual age.
The main reason Sarah was so perplexed and laughed while Abraham was laughing with Joy at the promise of a son (Genesis 17:17) defiantly had to do with his wife’s physical condition. Genesis 18:11 states: “It had ceased to be with Sarah after the manner of women''. Luepold, 1942 state; Sarah’s “periods had ceased with the so-called change of life and with them the capacity to conceive…. Capacity for procreation and conception was extinct.” Abraham knew it would take a miracle for her to conceive a child (Hebrews 11:11).
The truth of matter is that Terah was 130 when Abraham was born. This fact is known because of the inspiration by which Stephen spoke and Luke wrote (Acts 7:4). So someone of old age was completely compatible with the times of Abraham for a man of his age to have a kid.
All of this information leads me to believe that Abraham’s amazement at the pronouncement of Isaac at age 100 was due to some other factor than just his being 100 years of age and most likely to the fact his wife was barren and he knew it and the laugh was of joy.
Where these Patriarchs real people? Well considering Egypt itself is named after Noah's Grandson, and Jesus himself referred to Adam and Eve as real people and Noah is considered a historical figure today. Then Yes, there is new scientific evidence to validate their old ages... Watch https://youtu.be/tidITbzkK6E
Geneticists even today like Dr. Aubrey De Gray who is a secular evolutionist admits that the human genetic potential in us all is 1,000 years. Now why is that? Why does it align so well with scripture? How come all this new evidence keeps landing perfectly on YEC timelines ? it didn't have too, yet it did in multiple different fields of science and independent research.
The “young” earth view is a deduction from a number of biblical teachings, not a starting point. It follows from the Biblical big picture that God created a perfect creation that fell because of sin. Without this “bad news”, the good news of the Gospel with the redemption from sin lacks any foundation. This alone makes Genesis a historical event.
I believe they were literal days based on how often yom is used in references too literal 24 hr days and also according to Exodus 20:9–11, God used the six literal 24 hr creation days of Genesis as a model for man’s workweek: work six days, rest one. Apparently, He had us in mind even before He made us (on the 6th day) and wanted to provide an example for us to follow. Certainly God is not a God of confusion 1 Corinthians 14:33, so why would day 1 and 2 be millions or billions of years and every day following that literal 24 hr days and no mention of these first 2 days being so vastly different than the rest? Obviously in Daniel 8:26, when yom was not being used in reference to a 24 hr day, the text made very sure we “the reader” knew it.
The Hebrew day begins in the EVENING thus Genesis 1 teaches the days had an "evening and morning"
So yes this word can be used for (a time), (age) or (season), BUT that is ONLY when this word is in the plural form, which is ימים (yamim), and should simply be translated as "day"! Not time, age or season, as this can lead to incorrect interpretations of the text.
The word היום (hayom) is the word יום (yom) with the prefix ה (ha) added and it literally means "the day," but we would translate it as "today."
Also, the Bible is very clear when it says “In 6 days God created the heavens and the Earth.”
We also see in Exodus 31:17 “It is a sign forever between me and the people of Israel that in six days the Lord made heaven and earth, and on the seventh day he rested and was refreshed.’ So we again see literal 6 days, why? For a sign on when to work and when to rest.
We also track genealogies to prove YEC in scripture and also consider what those who wrote it believed and today their very calendars say the year is 5780. All signs via scripture point to a literal 6 day creation.
I also ask you to consider this. Isaiah 45:18 “For thus says the LORD--He who created the heavens; He is God; He formed the earth and fashioned it; He established it; He did not create it to be empty, but formed it to be inhabited--"I am the LORD, and there is no other.
So if God created the Earth to be inhabited, then what is the point of God creating Earth to sit uninhabited for eons??
Anyway, using just Hebrew text, a case can be made on both sides, thus why the argument still exists to this day.
Those that argue against the literal day, use the fact that there was no sun yet, thus how could a 24 day exist?
This is Answered by me saying, in the next life there will be no more sun either. Remember scripture says, God will melt away even the sun in 2 Peter 3:10 / Revelation 22:5 & Revelation 21:23. Does this mean literal days are over and there is no more sabbath then? Of course not, The Sabbath is eternal Exodus 31:16 / Isa 66:23
In the new earth, 'all flesh' will come to worship God on the Sabbath.
Even God himself is bound to His own law and also keeps the Sabbath. (Genesis 2:2, Exodus 20:11, Exodus 31:17, Acts 18:4, Hebrews 4:4, Matthew 27:59; 28:1) and yes even the Angels still do a "lawful" work (Matthew 12:11, 12 & Psalm 103:20) on the Sabbath of ministering to fallen man and protecting them from evil. So even in the next life when there is no Sun, yet there are still literal days and sabbath!!
We can objectively determine how “yom” should be interpreted in Genesis 1:5–2:2 by comparing that context to the word’s usage elsewhere in Scripture. The Hebrew “yom” is used a total of 2,301 times in the Old Testament. Outside of Genesis 1, yom plus a number, is used 410 times, almost always indicates an ordinary biblical 24-hour day. There are only a few instances where “yom” and a number do not imply a literal, 24-hour day. So why believe the exception over the norm? It makes no sense that in a single paragraph where yom is used 5 times as a literal 24 day to just assume the 2 other versus do not mean the same. This is not a logical conclusion to come to or deduce from the text, and why I do not believe their argument is sound.
The words evening and morning together (38 times) most often indicate an ordinary day. The exact construction of evening, then morning, along with yom is only seen outside of Genesis 1 in one verse. This is Daniel 8:26, which clearly implies a long period of time. So it makes it clear that even though yom is the word, it needed to make the distinction that it is not an ordinary 24 hr day. Or else way go out of the way to explain that it isn't!?
All in all, the context in which the word yom is used in Genesis 1:5–2:2, describing each day as “the evening and the morning,” seems to suggest that the author of Genesis meant 24-hour periods. This was the standard interpretation of the days of Genesis 1:5–2:2 for most of Christian and jewish history. The real division came from early church fathers, such as Augustine, who noted that the vague nature of the “days” of Genesis could well suggest a non-literal interpretation. Thus all of Genesis 1 is allegorical and not to be taken literal and why today the Catholic church so readily accepts evolution over Creation.
If you want more details on why the Masoretic text was change read below;
The Samaritan Pentateuch, Liber Antiquitatum Biblicarum, the Greek Septuagint (XXL-A and XX-B), the Dead Sea Scrolls, the Vulgate, including apocryphal books like Enoch, all concur with one another that Genesis 11:10–26 has years that the Masoretic does not include. The fact that Terah and Shem’s age match in every single one of the ancient biblical texts solidifies the debate.
If that is not enough, even historical non-Biblical works by Demetrius (Greek, third century BC), Eupolemus (Hebrew/Greek, second century BC), Flavius Josephus (Hebrew-based, first century AD). Theophilus of Antioch (wrote Apology to Autolycus), Theophilus, Africanus, and Eusebius. All agree the ages of the post-flood generations had an extra 100 years added on starting after Shem and going to Nahor (who was 79, not 29). This tells us that when we look for corruption in a body of work, the odd one out is always the corrupted version. The Masoretic stands alone in this category. Therefore there should be an additional 780 years added onto the Masoretic timeline of Genesis 11:10–26 genealogies.
Eusebius in the early fourth century AD cited the Masoretic’s numbers but rejected them as having been deliberately changed by the rabbis. He was the first to notice this and make it public. Jerome (late fourth century AD) appears to be the first ancient author outside of rabbinic circles to even accept the MT’s shorter primeval chronology as valid.
The Masoretic texts (MT’s) complete altered chronology is first found in the Seder Olam Rabbah (ca. AD 150), Scholars agree that it was Seder Olam who reduced post-exilic history and I will explain that story next. When Ussher came along and did his chronological calculations, he only used the Masoretic texts which had the altered reduced ages, therefore this is how we got the date of a 6,000-year-old Earth today.
Since it can be shown that all other biblical texts including the Septuagint and Masoretic’s remaining years of Shem and Terah all matched in Genesis 11, this serves as a double witness to the original figures that the only alteration made of the birth ages of the first child is in the MT between Shem and Terah. The reconstruction was on purpose and deceitful to make Shem out to be Melchizedek. Let me explain…
The Apostle Paul connected Jesus to Melchizedek who was a priest of the Most High God! Abraham the patriarch reverenced Melchizedek by paying a tenth of the spoils of the slaughter of Chedorlaomer to him! This single point infuriated the Jews both in the first century and still even today!
So by deceitfully changing the chronology, it allows Shem to pass on the priesthood of Melchizedek to Abraham and not Jesus! Therefore making Paul a lair and taking the position of High Priesthood away from Jesus and giving it to Shem! So to force Shem to become Melchizedek they had to remove the 100 extra years from the descendants of Shem to Nahor and then wala, now they created their own historical narrative. Even though not a single scripture in the Bible anywhere says that Shem was Melchizedek or even alludes to that idea.
It all breaks down like this. Up until the end of the second Jewish war in 135 AD, actually changing the numbers in the Bible text was an academic concept and no one had dared to alter the sacred Hebrew scriptures. However in the city of Zippori(In the past it was called Diocaesarea, it was at the heart of the Galilee province). By 150 AD the Jews began corrupting their synagogue scripture genealogies dates.
However by 160 AD The book “Seder Olam Rabbah” was written by Rabbi Yose ben Halafta, and he had different views of a messiah. You see, the city of Zippori became the intellectual and scholastic center of Judaism in Canaan after Hadrian defeated the Jews in 135 AD. Since Rabbi Yose ben Halafta had such an influence and believed the messiah was not Jesus but rather had his hopes on “Simon Christ” (who was widely believed to be the messiah at this time). Rabbi Halafta’s work and beliefs were shared broadly. His work had most believing “Simon Christ” would usher in the “days of the Messiah”, and conquer the Romans and refute the sect of the Nazarenes who wrongly thought Jesus was.
At Zippori, only a very small number of Hebrew manuscripts existed and this is why when the texts were altered, all future replications brought the alteration with it. “The 2d century saw the rise of the rabbis at Sepphoris/Zippori. These sages perpetuated and participated in the reconstruction of Pharisaic attitudes and ideals.
Then came Rabbi Halaphta who was a leather-worker and leading Tannaʾ of the third generation, active from around [after] 120 C.E., and teacher of Judah I. He is the chief authority for the accepted Jewish chronology as fixed in the work of Seder Olam Rabbah ("The Great Order of the World") chronology detailing the dates of biblical events from the Creation to Alexander the Great's conquest of Persia. So of course these altered ages were accepted by the people. By 160-180 AD: The few existing Hebrew manuscripts were corrupted by Rabbi Yose ben Halafta and other leading Jews
“The traditional Hebrew text, called the Masoretic Text, achieved its standard form early in the second century AD.” (Tyndale Bible Dictionary, Masoretes, 2000 AD)
So again in closing. To determine what ages work, I use the principle of witnesses (statistical probability or p-value). Meaning, if you have two models and none agree with one and the majority agree with the other, then those that agree most likely are the most accurate and true version. I also considered that the oldest would be more valid than the more current. Therefore I feel the strongest evidence we have that the KJV bible has an error in the timeline from the Masoretic translation is that all the other Biblical texts agree with one another in the total ages of the patriarchs in Genesis 11. From Shem all the way to Abram on when they died. Also in the years of Shem and Terah agree, proving that something happened to the middle patriarchs in the Masoretic text. The only difference in any of these texts are in the Masoretic and it’s concerning the age of the birth of their first child.
Regarding other evidence, we have a direct series of events showing us that from Yose ben Halafta who authored “Seder Olam Rabbah” at the city of Zippori to the corrupting of the Hebrew Masoretic Bible at Zippori to the Mishnah (Series of interpretations passed down in oral form) which was finally out in print in 200 AD. Then this was passed to the Tiberian Masoretes 250-900 AD who preserved the corruption in print down to the present day KJV. This is why the vast majority of current Bibles have the missing ages since the majority are all translated from the Masoretic text. Yet the older manuscripts do not contain the errors.
So when you see what IP says "why would the Bible say that Abraham is full of years? When others are 400 when he is still alive" Now it all makes sense, the Masoretic is wrong and that is the confusion IP is having.
I just found a blog post and in it are more arguments. I notice that IP really believes there were other people before Adam, referring to the Fallen ones. This is resolved by looking at genealogies specifically in Genesis 5.
Only “Noah was a just man, perfect in his generations”, (Genesis 6:9). The word “generations” is the Hebrew word, toledoth. Its primary meaning is “descent” or “family lineage”.
Noah was free of sinful angelic heritage. His family line was perfect. Thus only he, his sons and their wives were exempt from extermination of the world wide flood, Unless the masses repented. Which none chose to do.
HERE IS A LIST OF THE PURE SETHIC FIRSTBORN
ADAM and Eve =====> ABEL (murdered by Cain)
\\
``===> SETH + Sister
ENOS + Sethic wife
CAINAN + Sethic wife
MAHALALEEL + Sethic wife
JARED + Sethic wife
ENOCH + Sethic wife
METHUSELAH + Sethic wife
LAMECH + Sethic wife
Last =======> NOAH + Cainite wife !
of the \\
Pure Sethic =====> 3 sons -- mixed seeds -- HYBRIDS -- Japheth, Ham, Shem
Firstborn
"These are the three sons of Noah: and of them, was the whole earth overspread" (Gen.9:19)
Since all the Adam’s first born were mentioned all the way up to Noah, we can be very sure that, except for Noah, their wives were of their own bloodline (Seth's). Many of the other sons and daughters of each firstborn had become fallen sons and daughters of God. For anyone to simply say that Enoch (or anyone for that matter except Noah) was the last of the pure seed, I can only say the person is only presuming, he has no Scriptural evidence. First of all, a genealogical record, is similar to a family tree. It will show its offshoot as long as it is genetically feeding on the same sap of life, that is, a direct descendant of Seth who bore the image and likeness of Adam (Gen.5:3). As long as Seth's descendants of a firstborn marry within the Sethic race, the next firstborn (offshoot) will have his name in the family tree. But if this firstborn marries outside the family race, his firstborn will never be listed in the family tree as the sap of life is no longer the same kind.
Notice what Moses wrote in (Gen.5:32).: "And Noah was five hundred years old: and Noah begat Shem, Ham, and Japheth". Why did Moses write it that way, unlike what he wrote of all those others before Noah? Also, why was the name of Noah's first born mentioned last and not first? It cannot be so difficult for us to see that there was a change in the "sap of life" for God had Moses wrote: "These are the three sons of Noah: and of them was the whole earth overspread" (Gen.9:19). And later in the Book of Acts were written this that God "...hath MADE OF ONE BLOOD (that is, the one bloodline [kinship, descent] from Noah and his wife) ALL NATIONS OF MEN FOR TO DWELL ON ALL THE FACE OF THE EARTH..." (Acts 17:26).
So, up to Noah himself, his lineage was all free of sinful angelic seed. His family line was perfect. However, because Hybridization of mixed marriages causes genetic disturbances and abnormalities. Noah descendants were soon to take a hit. Notice that every firstborn Seth-ite from Adam to Lamech gave birth to sons and daughters. That shows that all of them married a pure seed (Seth-ic) woman. But it was not so with Noah. He had only sons. This proves that his wife was not of pure seed (Seth-ic) woman.
Hybridization causes genetic disturbances/abnormalities. Notice that every firstborn Sethite from Adam to Lamech gave birth to sons and daughters. That shows that all of them married a pure seed (Sethic) woman. But it was not so with Noah. He had only sons. This proves that his wife was not a pure seed (Sethic) woman.
Gen.6:9 tells us "Noah was a just man and perfect in his generations, and Noah walked with God" . This verse tells us the kind of person that Noah was. No wonder "Noah found grace in the eyes of the Yahuuah" (Gen.6:8). Not only was he a just (righteous) man, but he was also perfect, and He walked with God. The word "perfect" used in this verse is translated from the Hebrew word "tamim" which means "without blemish" in terms of breed or pedigree. Hence, the Scriptures clearly show us that Noah was a "pure breed" Sethites, and not a hybrid.
I have been asked this question: "If Noah was a pure seed, and he, knowing the will of God concerning mixed marriages), why did he not marry a pure seed like the rest of the other sons of God?" The one who asked me this question believed that Enoch was the last of the pure seed. But he himself was unable to answer his own question as to why Enoch did not marry a pure seed either. Such a question we do not know the answer for, perhaps they were really hot. If Noah did take a pure seed and all his descendants had the same revelation to also take pure seed to wife (throughout all generations), then we would have a race of pure Sethic people on the earth today as all the Serpent/nephilim hybrid seeds were destroyed in the Flood. And with only Sethic people on earth, there would not have been wickedness, evil, etc. manifesting on the earth today. But it did not happen that way.
As sin had already entered the human race in the garden of Eden, pure seeds or not, mankind did continue to commit sins or make wrong choices. We see "that the sons of God saw the daughters of men that they were fair; and they took them wives of all which they chose" (Gen.6:). These were pure seeds. They knew the will of God concerning mixed marriages. Yet, they mixed married. So the question, "Why did they mix/Marry?" is irrelevant and silly. Just as the Fall of mankind did not catch God by surprise, the same is also true in Noah taking a seed not of his own race (Rom.8:20).
Since antediluvians are our first parents, they were all “men of great renown” with great intellectual power. So the Hebrew word "nephilim" does not just mean great “physical stature” but also deviant character as well. In fact a concordance tells us the word "nephil" comes from the root "naphal" which means "to lie" or “to overthrow”. The Hebrew word nephilim (plural) literally means“giants” or “tyrants, a bully.” Hence nephilim means not only “great stature” but also “wicked men.” I believe that the "sons of men" and the "sons of God," were two “classes” of humans who lived during the antediluvian (before the flood) era: "the sons of God" were the righteous descendants of Adam, through Seth which included Enoch, Methuselah, Lamech and Noah (Gen. 5:4-32). In fact Adam was the first human "son of God" (Luke 4:38) and Jesus says that righteous people are “sons of God” (Matthew 5:9), hence, biblically, the expression “the sons of God” refer to righteous people. In contrast, “the sons of men” or “the daughters of men” were the opposite, they were the apostate and wicked descendants of Cain (Gen. 4:16-24). Hence, Genesis 6:1-2 depicts the intermarrying of the righteous descendants of Seth and the wicked descendants of Cain resulting in the rapid moral decline of the human race (Gen. 6:5) so that if God did not intervene, humans would have destroyed themselves by their Giant strong, violent, tyrant and super intelligent wickedness. I believe these are a group of people that IP may be thinking lived before Adam and or during the same time. I could be wrong, I need to find a video where he talks about this subject because this blog was vague.
I believe Inspiring philosophy can only remain a theistic evolutionist because he does not know the new scientific data supporting YEC. Dr. Jeanson's Replacing Darwin Made Easy is where everyone should start. Once you learn the model, there is little doubt YEC is the way to go. It is easy to reconcile main stream thought and just go with the flow because its easy and that is what OEC seems to do. Is this bad? No, who wants to be the minority and hated? Thats illogical. Also, who wants to learn subjects that do not interest them such as genetics and biology if they have no desire? This is why most remain in the evolutionary camp, its easy to say sure, evolution is true and so is Biblical Creation. End of debate. I should try that next time I debate actually and just see the look on the opponents face. :)
I believe IP would easily take up YEC if he saw the science side of the topic. I hope he watches the two videos I listed earlier and gives feedback on why he thinks they are wrong.
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The highest number of pairwise mtDNA differences on record comes from a comparison of 7,098 mtDNA genomes (Kim and Schuster 2013) who reported a maximum mtDNA difference of ~123. The average was prair wise difference was ~77 Ingman et al. 2000
Dr. Jeanson used a rate of mtDNA mutations from European and Asian populations while assuming that African populations also had the same rate of mutation. Using even an average generation time of 22 years, the evolutionary model would expect 1,439 to find nucleotides of diversity in humans today. This number is not even close to what we observe, at just 123. Even using a lower rate of mutation and a generation time of 30 years, evolutionists would expect a minimum of 954 nucleotides of diversity. Yet again the maximum that we actually observe is just 123.
Now, here comes the issue with Dr. Jeansons original study and how I easily resolved it in my own. You see, Jeanson had to reduce the generation time to 15 years to make the numbers fit his model and make work. Meaning, using maximum divergence rate and a required unending chain of 291 generations in a subset of African lineage in which the mother in each generation must have been born when her mother was 15 years old had to occur. This is very low, and the critics of YEC have a huge problem with this.
Therefore they will be pleased to know that I am not bound to AIG, as Dr. Jeanson is. Meaning, I am not bound to only using the King James Version of the Bible to use as my only standard for Biblical dates and ages. I use the Greek Septuigent, which predates the Masoretic text by hundreds of years and it corroborates the dates of Creation and the flood with other ancient Biblical sources. Not to mention that when they discovered the Dead Sea scrolls they also agreed with the Septuigent, not the Masoretic. Also it was the Septuigent that the Apostles read from and even Jesus himself. So I believe, if the dates were wrong, I would think they would have noticed. Therefore I feel that the dates in the Septuigent are the correct ones based on their parsimony with all other Biblical and non-Biblical historical texts. Even though I believe the KJV is more valid overall, regarding the dates, they are not.
Dr. Jeanson used the empirical mutation rate using the whole genome mtDNA mutation rates that were calculated from the raw data in the published literature from Ding et al (2015). That study was used to calculate a mtDNA mutation rate. Amazingly when the resultant rate was finalized, it was virtually identical to the calculated mutation rate for the D-loop.
Since the D-loop region is much smaller, calculations are much easier. Therefore rather than work with the entire mitochondria 16,569 base pairs, we will use the small 1,124 base pair D-loop (control Region).
Taken directly from the Ding et al study, Dr Jeansons mutation rate calculation conclusion was 9.55×10^−6 or 0.0063 per site per year.
An anti-creation critic named Evograd complained in a blog he made trying to say that “Jeanson claims that Stoneking’s 2016 article supports his mutation rate is directly based on the data from Soares et al (2009), which is mutation rate data that explicitly disagrees with Jeanson’s mutation rate. Soares et al. estimated the mtDNA mutation rate to be about 35-70x slower than the figure Jeanson is using.”
First off, Soares et al was not even cited in the study even once. But now I want you to notice the wording that the critic uses? “Estimates”, he says. The Soares study was a phylogeny based study trying to prove evolution. So of course they estimated a pedigree rate because they didn't even perform one.
Stoneking’s 2016 was a pedigree study! They directly looked at 246 families representing 228 trios, Completely different!!! and Stoneking did NOT get his data directly from Soares.
Remember when Jeanson said Stoneking’s study agreed with his?
Remember Jeanson’s rate?
That's right, it was 9.55 x 10_6, now what was this study?
Basically Identical. That of the D-loop was 1.5 × 10_6 mutations per site per generation. Exactly what Jeanson said.
If you look at the same table from the Ding study, not the Soares phylogenetic study like Evograd is accusing Jeanson of. So to say that this argument invalidates Jeansons rate results doesn't stand up to scrutiny. In fact, sticking to just homoplasmic mutations is the most scientifically conservative approach to this question, and these are the rates we use in making predictions that take mtDNA Eve back to 6,000 years.
This study result using Jeansons mutation rate validates that his mutation rate obtained from Ding et al (which assumed that many of the somatic mutations were actually germline) vindicates with high probability that he was accurate in this assessment. There is also congruency between multiple studies now that tell us clearly the mutation rate is fast and the D-loop matches the entire mitochondrial mutation rate.
Even the critic Evograd begrudgingly admitted that this rate matches both the empirical mutation rate of both mtDNA and the D-Loop...
And yes...
My mutation rate chart using the Septuagint dates
As you can see in my study, a 20 year generation time clearly fits the data well without having to reduce to a continual 15 year generation time like Dr. Jeanson did using the Masoretic text.
Also notice Using a variety of generation times, a 9–22 nucleotide difference could easily have been produced in the ~2,256 years from Creation to the Flood. A 20 year generation time which easily encompasses the 2–8 nucleotide pre-Flood branch length.
The matter of fact, even using the average mutation rate with a generation time of 18 brings the results close to what is required.
Yet with mine, you can see 79 was easily reached, even when looking at the lower limit of mutation rate averages with a generation time of 20 years, it almost captures it. So clearly the evidence is more compatible with the Septuigent. I confirm this with my other study looking at De Novo mutation rates and comparing it to the Septuigent generation times.
By contrast, the evolutionary model puts the origin of African ethnic groups first, and dates this event at ~200,000 years ago (Gomez, Hirbo, and Tishkoff 2014). This is a significant problem for evolutionists because of their 200,000-year timescale. mtDNA sequences from even more individuals from a variety of ethnic groups to identify the maximum pairwise DNA difference. The highest divergence (117 nucleotides) resulted from a comparison, not between two Africans, but between an African San individual and an Asian Taiwanese Aborigine.
Math was done by using a divergence calculation (differences=mutation rate*time*2) rather than a coalescence calculation (differences=mutation rate*time) to predict the maximum possible DNA differences arising in the time elapsed since the Flood. Multiplying 5,319 years by the upper end of the 95% confidence interval of the mtDNA mutation rate (e.g., 0.197 mutations per generation), and then converting the mutation rate to mutations per year, demonstrated that 105 nucleotide differences could have easily arisen since the Flood, assuming a generation time of 20 years, not 15 like Dr. Jeanson.
Below is Jeansons chart, you can see...
Remember the Max 123 mtDNA difference was found in a San’s individual. My model shows there was an abundant margin to account for these differences (even using a much higher generation time) unlike Jeansons chart above. The Septuigent dates are more in conjunction with the average generational times we see today.
Comparing the evolutionary prediction to YEC predictions as well as to the maximum number of reported mtDNA differences (Kim and Schuster 2013) demonstrated that YEC conclusions still held true regardless of which ethnic groups were compared (Table. 2). The YEC predictions were successful under both short and long generation times. In short, the evolutionary model predicted a minimum number of differences nearly six times higher than the maximum number of mtDNA differences present today. By contrast, the YEC model exactly captured the full spectrum of mtDNA differences observable today (Table. 2). These results demonstrated the scientific robustness of the YEC model and intensified the explanatory challenge for the evolutionary timescale. By Multiplying a long generation time (30 years) by the slowest end of the 95% confidence interval for the mtDNA mutation rate (i.e., this represented a coalescence calculation, the calculation most generous to the evolutionary model) yielded the minimum number of mtDNA mutations that would have accumulated on the evolutionary timescale.
For the evolutionary model to be anywhere close to true, their minimum nucleotide differences using the fast mutation rate should give results around ours at 213 differences. Instead the minimum they can obtain is that of just 954. Let alone the average differences which places then at 1,439 in humans, given a generation time of 22 years.
Furthermore, the statistical averages for the mutation rate (e.g., 0.158 mutations per generation) and generation times (a generation time of 25 years) using the Septuigent dates easily captured the average genome-wide diversity in mtDNA (~77 nucleotides; average from Ingman et al. 2000).
Dr. Jeanson didn't just have a problem with maximum diversity in the African San’s people, but he also had a problem with even accounting for the average DNA difference of ~77 nucleotides. Since Dr. Jeanson holds to the Masoretic texts, placing the flood at 4,356 years ago, he is committed to this generation time. For him to reach the difference of 79 nucleotides, an unbroken chain of generation times of 15 years over 290 generations had to be used just to obtain the average African diversity
This is theoretically possible since we still see this practice today in many parts of Africa. The matter of fact if you think I am trying to falsify Jeanson you would be wrong, I actually help confirm his predictions in a video here = https://youtu.be/Gp8eGnkT5RE
I however feel that my model using Septuigent dates is superior, as it doesn't have to invoke such a low birthrate age. However, it is not hard to defend Jeansons work when we literally see this taking place today.
Next, Let’s take a look at mtDNA diversity from Creation in (Year 7,574 years ago in Septuigent) v.s. mtDNA diversity of the evolutionary model of 50,000 years.
First, another YEC prediction.
Now, Evolution diversity over 50,000 years (Note; Should expect somewhere around 123 diversity)
As you can see, using the lowest end of the mutation rate is still not in favor of evolution. A minimum of 477 nucleotide differences could be obtained which is 354 over the maximum diversity we see in the world today. Not looking too good for evolution is it?
CONCLUSION
Most important of all is when we look at the evolutionary model requirements with these mtDNA pedigree studies. Nothing even remotely close to the reality we see. This is why they deny the observable empirical mutation rate and hold to the evolutionary assumption phylogeny method.
At a minimum, this data should force the evolutionists to acknowledge that their conclusions about the relative timing of the various people groups stand only under the assumptions of equivalent generation times across ethnic groups. The evolutionary model still predicts human mtDNA differences far in excess of the actual number (Table. 2). Since the archaeological and paleontological basis for the evolutionary model relies on the assumption of constant rates of change in geological and geophysical processes (e.g., carbon-14 dating), and since these genetic predictions also assumed constant rates of change, the evolutionary model faces a serious scientific conundrum.
In my past study I also confirm that the Septuigent aligns more with the scientific evidence with my “Rate of De Novo Mutations on Antediluvian Patriarchs” study (see below).
Also, with the statistical averages for the mutation rate (e.g., 0.158 mutations per generation) and generation times (e.g., a generation time of 25 years) predicted and confirmed the average genome-wide diversity in mtDNA of (e.g., ~77 Ingman et al. 2000). Calculations were done by Multiple 5,318 years by average confidence interval mutation rate (0.158 mu per generation), and then converting the mutation rate to mutations per year.
As you can see, my model was able to obtain both the average and maximum diversity easily, without resorting to the upper 95% confidence interval mutation rate nor lowering the age of a generation time whatsoever.
Critics also do not like Dr Jeansons mutation rate, yet it corroborates closely with other secular peer reviewed mutation rates including the mutation rate of the control religion aka D-loop . The critics just point to the fact that Jeanson said this...
Meaning, until pedigree trials are done for the Ding study, we will not know be certain if these mutations were somatic (Not passed on) or germline (inherited). However, Howell and Parsons both made it clear that newly arising mutations that appeared to be somatic, were actually passed on through the germline. Contrary to what was expected and what critics say Jeanson should not have counted!
It seems clear that Jeanson was correct in his assumption. Also, if it was not correct then what are the odds that the evidence lines up so well with our model and predictions made to test its validity? Yet these results are so far off from what evolution requires that there is no good rescue device to save them.
Even if one were to use the slowest empirical pedigree mutation rate, they would get no where near what is required for the evolutionary model to be true. Mutation rates are evolution's death blow. This is why they fight against them so hard and invented the phylogenetic method to begin with.
Conclusion
Differential generation time data and a constant rate of mtDNA mutation are sufficient to explain human mtDNA diversity on the YEC timescale across all ethnic groups. These results potentially unify the YEC model of human genetic origins, and they intensify the explanatory challenge for the evolutionary model.
Now ask yourself “Why is it that when testing the entire mitochondrial DNA, or any of the 37 individual genes in the mtDNA, or the individual sections of the mtDNA like the D-loop region or CO1 fragment, or when testing Somatic mutations, or microsatellite mutations... No matter if the study is a diad or triad, or even when counting substitution rates. No matter where you look or what you test, all of them give similar results and confirm each other”.
Here were 8 reasons why Jeanson did not include other mutation rate studies in greater detail in his book...
1:) There is already agreement between two mtDNA mutation rate sets that exist.
The first set only looks at the D-loop (coding region) which is germine. This gave a mutation rate of 1X10-5 (per generation). The second set looks at the entire mitochondrial genome and Jeanson took at that data and it came out the same as the D-loop results.
2:) Jeanson also took into consideration Mark Stoneking’s lab’s 2016 mutation rate which looked at the human mitochondrial germline transmission bottleneck, which can be used as an indirect measure of mutation rates, and even still he found a similar overall mutation rate as the others. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4817766/
3:) He used this mutation rate to predict the transatlantic slave trade, because our model says that man is not of African Origins. So if they mutate faster then that will disprove L1 root while at the same time vindicate Biblical Creation.
4:) Since Jeanson has gone through multiple other species mutation rates and the answer is always the same, across multiple independent datasets rates are all the same. So he is safe to assume we are looking at the germline.
5:) Diad v.s. Triad results have already been performed for autosomal mutation rates as well and there's very little difference in results between the two. https://www.ncbi.nlm.nih.gov/pubmed/31549960
6:) If you have a problem with Jeansons section in the book, you actually have a problem with the world's leading science journals which still publish results from dyad studies confirming Jeansons mutation rate.
7:) Why do mitochondrial DNA clocks point towards a young-earth and reject a millions-of-years timescale for every other species in which the mitochondrial DNA mutation rate has been measured? Please note: In the fruit fly, roundworm, water flea, and yeast mitochondrial mutation rate studies, the rates were measured in mutation accumulation lines--in other words, over several generations of genealogically-related individuals. Almost by definition, these studies measure germline mutations--not somatic ones. Why do all of these studies agree so strongly?
8:) Jeanson made a specific future novel prediction in his book. This was that “the most diverse African groups will be found to mutate their mtDNA at a rate ~2-fold faster than reported here (e.g., at 0.2 to 0.3 mutations per genome per generation rather than 0.16 mutations per genome per generation).”That was taken directly from his work. Now if this is true, let’s run the number’s for him to show what this would look like.
This chart captures the max diversity in the African population using an average generation time of 25 years. As you can see, the numbers fit much better with a modern day generation time of between 22-33 years of age.
9:) Jeanson said “If the rate he cited from Ding's data is invalid, why does it agree with the 7+ studies that have been published previously? Why is there such strong scientific consistency across multiple independent scientific studies?”
I believe these 7 studies below are what Jeanson is referring too...
Lorena Madrigal et al 2012 who observed a minimum estimate of the observed mutation rate of 2/220 = 0.0091 mutations per site per generation. Accordingly, the divergence rate became = 1.78 × 10−6 per year. Our divergence rate is then = 5.02 × 10−6 substitutions per site per year. Our maximum estimate, 2.51 × 10−6 is very close to the value of Parsons et al., 1997. 25.3 × 10−6 substitutions per site per generation, and 0.89 × 10−6 substitutions per year. Accordingly, the divergence rate became = 1.78 × 10−6 per year. Mutation rate in the Costa Rican population of Atenas has 95% probability to fall between 0.27 and 3.17 × 10−6 substitutions per site per year. Even our minimum estimate is a still high 0.92 per site per million years.
Mumm et al obtained 1.51 Divergence Rate this is 0.0066 mutations per year. Using a 22.5 year generation time, this equals 0.0075 mutations per year (95% CI upper 11.71, lower 0.0033)
Narasimhan et al 2017 obtained a single-nucleotide mutation rate of 1.45 × 10−8 per bp per generation. a non-crossover gene conversion rate of 8.75 ± 0.05 × 10−6 per bp per generation.
Evelyne Heyer’s pedigree mutation rate gave 4 substitutions in 508 meiosis. The per-site mutation-rate estimates calculated separately for HVI and HVII segments have the same value. For the HVI sequences, we obtained 220 generations or 6,600 years, and for the HVII sequences 275 generations or 8,250 years given a generation age of 30 years old. Considering these pedigree’s were European and have an average to slow mutation rate, this is just more conclusive evidence of YEC and fast mutation rate’s clocks that falsify evolutionism. "This result additionally validates our estimate of ∼250 generations as an average time depth since expansion in our sample of the European HVI and HVII sequences analyzed separately above (see table 3). Our approach therefore appears to be valuable in dating past human expansions."
Bendall et al obtained 4 mutations after 360 generations or 1 every 90 (same as Howell 2003)."we calculated that the rate of mutation and fixation in the first hypervariable segment of the human mtDNA control region is between 1.2 x 10(-6) and 2.7 x 10(-5) per site per generation. This range is in good agreement with published estimates calculated by other methods." This works out to be 1.95 per site per generation or 0.0078 (25 year generation) with sampling error of 0.0056.
Parsons et al obtained 0.028 per segment per year, identical to Elena Jazin et al at 0.028. And nearly identical to Howell et al at 0.025 and Madrigal et al 0.026.
For those that do like Parsons nor his findings and wish to refute him, please read his response to us first.
Clearly this many similarities from different studies show that the mutation rate is fast and they clearly falsify evolution. But here is the thing, can testable predictions be made? Yes, clearly they can and the critic really should ask themselves “why do rates portray a YEC timeline?”. Why is it that we always find the MRCA of all humans just a few hundred generations ago if evolution is true? The answer should be obvious.
For those critics who say Selection is the answer to these differences...
For those who use heterogeneity as a rescue device...
But if this is not bad enough, linguistics, mathematics, writing systems, population growth curve, genealogies, and overall civilization points to having arisen in the last 5,000 years, all confirm the YEC model.
As I said above briefly, we also have genealogical records that if we follow back a single family line of royal blood going back to the oldest in history, what do we find? Well below is the British Kings list which shows an unbroken royalty lineage going all the way back to Adam himself.
Remember, blood lines are very important and always have been. Today we can prove relation through genetics, but before that, it was all in the details written down. This list goes through the ancestors of Queen Elizabeth II of England and goes back through the kings of Wessex to one Sceaf, “a son of Noah born in the Ark,” and then to father Adam. The original text is on display in the British museum of History and dated as authentic. So evidence in genealogy also validates these mutation rates and YEC.
But this is not the only genealogical discovery, others have been found as well. One of these traces through Irish royalty back to one Tamar Tephi, a daughter of King Zedekiah, who was king of Judah when Lehi left Jerusalem in 600 B.C. Another traces back through one Anna, a daughter of Joseph of Arimathea, who was a kinsman of Christ and the one who provided the Savior’s burial place. There are also others.
Evolutionists discovered ERV’s and immediately tossed them in the Junk bin, calling them 100% worthless and regarded them as “deleterious genomic parasites”. They predicted that ERVs would never be found to have function as they are just leftover fossil footprint remnants of long dead viruses. They even said that “If ERVs are found to have function, they would be highly unlikely to have come from retroviruses.” BAD NEWS EVOLUTION = Many ERVs (complete and also fragmented) are functional DNA elements! Without ERVs located at the 2 cell level, embryogenesis can't even occur!
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6387303/
Also; “We report the existence of 51,197 ERV-derived promoter sequences that initiate transcription within the human genome, including 1,743 cases whereopii transcription is initiated from ERV sequences that are located in gene proximal promoter or 5’ untranslated regions (UTRs).” https://www.ncbi.nlm.nih.gov/pubmed/18535086 It’s Codon redundancy that plays multiple functional roles. Abstract Endogenous retroviruses (ERVs), which are regarded as “deleterious genomic parasites”, were previously considered to be “junk DNA”. However, it is now known that ERVs, with limited conservatism across species, mediate conserved developmental processes (e.g., ZGA). Transcriptional activation of ERVs occurs during the transition from maternal control to zygotic genome control, signifying ZGA. ERVs are versatile participants in rewiring gene expression networks during epigenetic reprogramming. Particularly, a subtle balance exists between ERV activation and ERV repression in host–virus interplay, which leads to stage-specific ERV expression during pre-implantation embryo development. A large portion of somatic cell nuclear transfer (SCNT) embryos display developmental arrest and ZGA failure during pre-implantation embryo development. Furthermore, because of the close relationship between ERV activation and ZGA, exploring the regulatory mechanism underlying ERV activation may also shed more light on the enigma of SCNT embryo development in modern animals” https://www.mdpi.com/1422-0067/20/3/790 Learn even more here; genetic-degeneracy-goes-way-junk-dna/
https://www.ncbi.nlm.nih.gov/pubmed/18535086
https://academic.oup.com/bioinformatics/article/24/14/1563/182042
https://www.sciencedaily.com/releases/2014/12/141218141057.htm
That's right everyone! These supposed ancient dead junk viral proteins actually affect gene expression in the developing embryo by protecting the cells from infection by other viruses. Some ERVs found in humans are full-length and called (HERVKs) they are still functional as you have seen in embryogenesis. They also increase IFITM1 levels (a Protein Coding gene) on the cell surface and inhibit viral infection. While the smaller bits and pieces of ERVs (supposedly broken ERVs) also have crucial functions as well. Such as helping regulate genes, transcription, they play an important role in pluripotent stem cells and even determine cell types. So for them claiming they are all “co-opted” is nothing but pure assumption.
In 1999 Barbulescu, et al. showed that, of ten HERV-K proviruses cloned, eight were unique to humans, while only one was shared with chimpanzees and bonobos.
Another study here; “Our analysis revealed that retroviral sequences in the human genome encode tens-of-thousands of active promoters; transcribed ERV sequences correspond to 1.16% of the human genome sequence … and PET tags that capture transcripts initiated from ERVs cover 22.4% of the genome.” http://bit.ly/3bccb5F
ERV’s and most viruses are supposedly hundreds of millions of years old if not older. This is pure speculation as no one has ever seen an ERV do this and because what we see in the world today is how fast viruses change. That’s why people get a new flu shot every year. Viruses mutate so fast, that after only a few hundred years, basically nothing of the original genome may be left. See the contrast between reality and Darwinian theory?
ERV’s are actually vital to the placenta as well. ERVs also aid transcription in one-fifth of the human genome. Then they found that ERV’s are vital for the gene p53 “The ancient retroviruses … helped a gene called p53 become an important “master gene regulator” p53 was crowned “guardian of the genome,” as biologists now call it. Its job is to coordinate the surveillance system that monitors the well-being of cells. Indeed, p53 is so important that when it fails, cancer often results. About half of all human tumors contain a mutated or defective p53 gene.” Another study revealed they activate in gene dense regions to control gene expression. They are not spread randomly throughout the genome as previously thought. So DNA isn't full of parasites at all, but rather many sophisticated ways to control gene expression. An Evolutionists might ask why the positioning of human ERVs are so similar to the positioning of chimp ERVs if viruses didn’t put them in the common ancestor? There are many Similar ERVs in Unrelated Organisms; This study = talks about the brushtail possum http://jvi.asm.org/cgi/content/full/75/5/249 This study shows cat genus, Felis has the baboon RD114 virus http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1617120 How could it be that unrelated ERVs in different species created essentially the same gene? “ERVWE1/Syncytin-1 and ERVFRDE1/Syncytin-2 are specific to primates and thus do not exist in other placenta. However, this apparent endogenous retrovirus hijacking for placentation use is not restricted to the primates. Indeed two unique endogenous envelope genes of retroviral origin have been found in the mouse, i.e. Syncytin-A and –B …” http://AtlasGeneticsOncology.org/Genes/ERVWE1ID40497ch7q21.html The rescue device for this? You guessed it “Convergent evolution” LOL. One may try to argue that convergent evolution is the answer they want or need, One may try and argue that convergent evolution is the answer, as the author of the quote did, but this explanation has no real scientific basis. Convergent evolution is only ever used to explain similarities between organisms that are otherwise unrelated. It’s a rescue device you see all the time used by evolutionists.
Are ERVs dormant viruses today? That’s the real question… No. They tell us these (supposed) viral invaders populating our genome have mutated to the point that they no longer lead to active infections. So why think they ever were? Besides the obvious visible gag, pol & env we see looking at them. However, When they mutate today they lead to disease! You see, scientists assume that if a sequence of a viral DNA is found in two different animal species then they probably are related and must have had a common ancestor. We know this is wrong because circoviruses, for example, are a group of viruses that are known to cause stomach problems in dogs. But upon closer investigation, these viruses have been found in the genomes of dogs, cats and panda bears. Since we now know none of these had a common ancestor then that lends more credence to the fact ERV placement sequences in common species have no validity. https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1001191
The matter of fact there are multiple theories and models for where these viruses came from and they’re still debated today. One is the virus-first model, another is the Escape hypothesis, and even another is called Giant (mimivirus) viruses theory. https://www.nature.com/news/giant-viruses-open-pandora-s-box-1.13410 / The Regressive model combats these as well especially the mimivirus theory.
It is interesting to note that ERVs are different from the retroviral genomes from which they are supposed to have originated from. Evolutionists usually explain this away by claiming that the ERV sequences have evolved to the point where they are quite different from their ancestral genomes. If this is so, then there is consequently very little to lead us to the conclusion that ERVs are derived from retroviruses.
If ERVs really are a product of retroviruses, how could they have been inserted into reproductive cells thousands of times, without fatal damage to the host then turn out to not only be beneficial but essential in our survival? Having healthy and strong reproductive cells is mandatory to produce a viable zygote, so why would viral-infected reproductive cells be considered more fit than ones without ERVs? Furthermore, how could they survive for hundreds of thousands of years in two different species? Now imagine every species on Earth/
Changes to the reproductive cells are rare and often harm the animal. So why should we believe that ERVs were inserted many thousands of times and no real problems arose back then but do now? It’s not logical.“In short, the notion that molecules of germ cells … are in states of perpetual change is not, in our present understanding of cell biology, tenable. This doesn’t mean that “molecular change does not occur; only that mechanisms provoking such change in germ cells are likely instantaneous and stochastic and probably often lethal (Maresca and Schwartz 2006) — which will preclude their persistence into future generations.” http://www.mitpressjournals.org/doi/abs/10.1162/biot.2006.1.4.357
ERV’s play an important role in pluripotent stem cells. Which may help explain how these cells maintain a state of pluripotency and are able to differentiate into many types of cells, could have profound implications for therapies that would use pluripotent stem cells to treat a range of human diseases. https://www.sciencedaily.com/releases/2013/01/130123133930.htm Do evolutionists really think an old dead virus can just mutate and then play such a crucial role as the ability of a cell to develop into the three primary germ cell layers of the early embryo then mutate again into all cells of the adult body? That without ERVs life could not even exist because there could be no offspring!!! They are illogical. These cells basically assign cell types to cells. Stem cells are vital for life.
The word ‘virus’ means toxic or poison, and that is how most evolutionists perceive them. However, if 50% of our DNA is made up of viral elements, wouldn’t that indicate that they might be essential genetic elements and that these viral elements just might be another regulatory network in organisms? This is just another case why evolutionary-based science is a menace to scientific research, discovery, and progress.
1.Retrovirus HERV-H was highly associated with epigenetic markers
https://retrovirology.biomedcentral.com/articles/10.1186/1742-4690-9-111
So here we have VIRUSES or what you would call them. That normally would ravish its host, especially at that frequency! But instead its inducing pluripotency. It evolved in factors that bind to transcription binding sites (something viruses never do). And it is involved in chromatin and epigenetic markers.
You see, scientists assume that if a sequence of a viral DNA is found in two different animal species then they probably are related and must have had a common ancestor. We know this is wrong because circoviruses, for example, are a group of viruses that are known to cause stomach problems in dogs. But upon closer investigation, these viruses have been found in the genomes of dogs, cats and panda bears. Since we now know none of these had a common ancestor then that leads more credence to the fact ERV placement sequences in common species have no validity. https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1001191
The matter of fact there are multiple theories and models for where these viruses came from and they’re still debated today. One is the virus-first model, another is the Escape hypothesis, and even another is called Giant (mimivirus) viruses theory. https://www.nature.com/news/giant-viruses-open-pandora-s-box-1.13410 / The Regressive model combats these as well, especially the mimivirus theory. We found ERVs that contradict the animal phylogeny. Experts in the field claim this with their evidence: https://link.springer.com/chapter/10.1007%2F978-94-007-4899-6_3
Here we see ERV’s do not help them either
ERVs are required by the body and do not do the same thing in apes as they do in humans, so that's destroyed real easy.
When evolutionists actually compare the gene sequences of RNA viruses that exist today and make their typical assumptions about mutation rates and evolutionary dynamics, they come to the conclusion that the RNA viruses we see today originated, at most, 50,000 years ago according to the evolutionist's timescale. Why is this a paradox? Well, remember that retroviruses are RNA viruses, and they are supposed to have been infecting primates long before humans evolved. Thus, in evolutionary terms, they need to be much older than 50,000 years old.
"Yet a very different picture of RNA virus origins is painted if their gene sequences are compared; by using the best estimates for rates of evolutionary change (nucleotide substitution) and assuming an approximate molecular clock (21, 33), it can be inferred that the families of RNA viruses circulating today could only have appeared very recently, probably not more than about 50,000 years ago. Hence, if evolutionary rates are accurate and relatively constant, present-day RNA viruses may have originated more recently than our own species." - Molecular Clocks and the Puzzle of RNA Virus Origins, Edward C. Holmes, American Society for Microbiology Journal of Virology https://jvi.asm.org/content/77/7/3893.full
So, in humans, ERVs are necessary for many things; we have almost 98,000 bits and pieces of ERVs. What they are: are Broken DNA elements left over from our pristine state of creation Most are solo LTRs (retroviral promoters) initiate transcription. But today only a handful (50-60 HERVKs--youngest family of ERVs) are recognizably complete ERVs.
So humans have 50-60 complete HERVKs to compare. But, chimpanzees only have ~20 of the same family. 13 of these are not orthologous with humans at all, so they just tell the public that these were inserted after the human/chimp split. Just another rescue device for evidence that counters their story. ONLY a few complete ERVs are found in the same location!!
Overall it doest matter if ERVs are in the same place or not because it comes down to function. So any alignment is just pointless for proving evolutionary relation.
It's all about function, if ERV’s “are” or “were'' functional, then the entire argument falls apart and creation is vindicated. Lets recap on specific ERV’s and their function… Do these shared ERVs have function? YES THEY DO!
Regarding the HERV-E Family; “While both LTRs were shown to promote transcription in vivo and in vitro, their respective activity and tissue specificity appeared to differ even though they shared a high degree of sequence identity … The results from this study illustrate how slight variations in transcriptional regulatory sequences can have a profound effect on promoter activity and demonstrate the complex regulatory effects of human endogenous retrovirus elements on human gene expression.” Study Think about that for just a second, the same ERV in the same location in a primate does something totally different. And also consider “no infectious counterparts of human endogenous retroviruses (HERVs) are known to exist today” Study
Below is a picture of KAP1, a master gene regulator. You will notice an ERV attached to it! So without ERV’s no regulation of the KAP1 gene. This is utter proof of design, not evolution. The matter of fact, the ERV had to be present from the beginning and this is proof. So this alone destroys an insertion at a later time.
If ERV Elements Deteriorate Rapidly, Why Did Only One ERV Remain Active and Continue to Infect All Placental Mammals Over a 70 Million Year Period?
Evolutionists point to “lack of selection pressure” to explain why ERVs deteriorate rapidly, but then point to “bursts” of copy numbers when they need ERVs to be conserved: “Southern blot analysis of a large series of mammalian genomic DNAs shows that HERV-L-related elements—so-called ERV-L—are present among all placental mammals, suggesting that ERV-L elements were already present at least 70 million years ago. … Phylogenetic analyses allowed the establishment of a plausible evolutionary scheme for ERV-L elements, which accounts for the high level of sequence conservation and the widespread dispersion among mammals … One rather striking feature of our results is the observation of a high level of sequence conservation among ERV-L elements. It is generally admitted that such sequence conservation is a common feature of functional genes, whereas noncoding sequences as well as pseudogenes diverge more rapidly, due to the lack of any selection pressure …
Rather, a scheme in which sequence conservation is the unnecessary consequence of the transpositional activity of the transposable element itself (which requires both transcription activity and coding capacity), independent of any possible selective pressure imposed by the host, appears more plausible and would account for the data. According to this scheme, a functional sequence present in an ancestor of mammalian species would survive only if active, simply by generating a sufficiently high number of copies, so that despite the fact that such elements are submitted to genetic drift, as any pseudogene-like sequence, and also to elimination through transposon excision, there still remain functional copies of the founder element. Evidence for the transpositional activity of ERV-L elements is provided by the occurrence of bursts in both the primate and mouse branches, which resulted in large increases in ERV-L copy numbers.” http://jvi.asm.org/cgi/content/full/73/4/3301
“endogenous retroviruses in neural progenitor cells. Another intriguing finding in human brain cells and mouse models was that endogenous retrovirus HERV-K’s (complete ERVs) appears to be protective against neurotoxins.” This study even states that because they believe these are nothing but evolutionary leftovers and Despite their prevalence, the function of human endogenous retroviruses (HERVs) in humans is largely unknown. https://pubmed.ncbi.nlm.nih.gov/26818265/
Remember Members of the HERV-K family are typically found in areas near genes [which code for proteins]. The regulatory role of HERVs has been demonstrated in the liver, placenta, colon, and other locations. Source: Norbert Bannert and Reinhard Kurth, “Retroelements and the human genome: New perspectives on an old relation” [PDF], Proceedings of the National Academy of Sciences, 101:14572–14579, 2004.
HERV-K(HML-2), termed HK2, codes for all viral proteins and produce virus-like particles, it is not known if these virus particles package and transmit HK2-related sequences.”
HERV-H is a class of primate-specific endogenous retrotransposons. It is transcriptionally active in both human preimplantation embryos and PSCs, and plays a critical role in pluripotency, stem cell maintenance and somatic cell reprogramming. HERV-H is also epigenetically regulated and is associated with binding sites.
HERV-W The cytotrophoblast cells produced by HERV-W proliferate and invade maternal endometrium, which is key to implantation and placental development.
HERV-R aka (ERV3) is expressed in syncytiotrophoblasts not only in the placenta but also in hydatidiform moles and choriocarcinomas. It seems to be related to cell fusion. ERV3 env is expressed in certain embryonic tissues such as the adrenal gland and nervous tissues. Perhaps this will help explain the Nervous system, as of now. No such luck for evolutionists and we know they are not looking at ERVs for function,
“There is no evolutionary record of nervous systems...”
https://phys.org/news/2012-01-breakthrough-reveals-evolution-ancient-nervous.html
HERV-F HERV-F(XA34) Analyses of expressed sequence tags (ESTs) have identified the expression of HERV-F(XA34) sequences in placental tissue, fetal liver/spleen, and olfactory tissue.
HERV-Fb The analyses indicate that the 5'-LTR of HERV-Fb functions as an alternative poly A site of a Krüppel related zinc finger gene (ZNF195).
HERV-p53 shapes and controls the p53 or TP53 gene that codes for a protein that regulates the cell cycle. crowned “guardian of the genome,” Its job is to coordinate the surveillance system that monitors the well-being of cells as well as being a human tumor suppressor. Indeed, p53 is so important that when it fails, cancer results. About half of all human tumors contain a mutated or defective p53 gene.”
Erv-9 controls the ERV9-1 gene (Endogenous Retrovirus Group 9 Member 1) an Uncategorized gene in the database system. So who knows what it does for now.
Overall the HERV-E, HERV-F, and HERV-W families, were found to be active in all tissues with the exception of the rectum and ovary; and the HERV-FRD family, which is inactive only in PBMCs, stomach, and prostate.
ERV3 high expression was found in the following locations: Adrenal glands, Rathke's pouch and (probably) the pituitary gland, nerve roots, primitive glomeruli, peripheral ganglia and structures of the primitive skin. Study
“The majority of HERV elements are riddled with deleterious mutations, large deletions, and insertions of other repetitive elements https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1456821/ the accumulate of random mutations destroy a once complete HERVK making it eventually an inactive fossilized proviruses remnant. Because of this the vast majority of endogenous retroviruses are inactive. All ERVs have lethal mutations. They believe that HERVs play a multifactorial role based purely as a consequence of their abundance in the genome.
Molecular analysis (PCR and Southern hybridization) of CERV 2 elements demonstrates that this family is present in chimpanzees, bonobo, gorilla and old-world monkeys but absent in humans, the matter of fact they still cannot even find correlation between disease and ERVs. “Despite major interest in the link between HERV-W expression and human pathogenesis, no conclusive correlation has been demonstrated so far.”
So, according to them, after monkeys surfed to America from Africa, which all evolutionists believe happened. They are assumed to have brought ERVs with them according to the theory. When they started to split off these supposedly dead junk functionless ERVs got passed on because they are no longer viral invaders that caused harm. So if they have any function then they are not from a virus. Guess what? They do, end of story. The ERV argument is as dead as evolutionism.
“The HERV-W env gene product has also been shown to block infection by an exogenous retrovirus, suggesting that the expressed HERV-W env gene could have a beneficial function to the host (Ponferrada et al., 2003Down).” http://vir.sgmjournals.org/cgi/content/full/85/5/1203
“Thus, HERV-W Env confers host cell resistance to infection by SNV. This is the first report of a human endogenous retrovirus gene product blocking infection by any exogenous retrovirus.”http://www.ncbi.nlm.nih.gov/pubmed/12664292 So wait, a virus produced a gene to block viral infection! There is more evidence, “some avian and murine ERVs can block infection of related exogenous retroviruses at entry by receptor interference; mouse Fv-1 blocks infection at a preintegration step, also can be viewed as an ERV.” http://www.pnas.org/cgi/content/full/101/30/11117
And “in the case of both Fv4 and Rmcf, the mode of defense is by the domesticated env gene blocking the receptor required for retrovirus entry.” Study It gets even more crazy ! “These results suggest that the loss of ERV3 mRNA expression is associated with susceptibility to choriocarcinoma.”
What does evolution have to say about this? Well they had to say “We propose a model in which Iris has “switched sides,” having been recruited by host genomes to combate baculoviruses and retroviruses, which employ homologous envelope genes to mediate infection.” study That's right everyone, ERV’s infected us, then switched sides and turned on their own virus kind. LOL
Evolutionists might ask why the positioning of human ERVs are so similar to the positioning of chimp ERVs if viruses didn’t put them in the common ancestor? This becomes a pointless question when they realize that there are many Similar ERVs in Unrelated Organisms; “… and two closely related ERV genomes are found in a carnivore (fox) and a ruminant (sheep).”
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1617120
This study = talks about the brushtail possum http://jvi.asm.org/cgi/content/full/75/5/249
This study shows cat genus, Felis has the baboon RD114 virus http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1617120
“For instance gamma-retrovirus was isolated from trophoblastic cells of the baboon placenta. This virus was found to be very closely related antigenically and by sequence homology to the endogenous RD114 virus in cats (which is itself unrelated to endogenous FeLV). http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1617120
How could it be that unrelated ERVs in different species created essentially the exact same gene? “ERVWE1/Syncytin-1 and ERVFRDE1/Syncytin-2 are specific to primates and thus do not exist in other placentae. However, this apparent endogenous retrovirus hijacking for placentation use is not restricted to the primates. Indeed two unique endogenous envelope genes of retroviral origin have been found in the mouse, i.e. Syncytin-A and –B ….” http://AtlasGeneticsOncology.org/Genes/ERVWE1ID40497ch7q21.html
The rescue device for this? You guessed it “Convergent evolution” LOL.
Now look at this….
“Now it appears that another level of evolution occurs that is not driven by point mutations. Instead, retroviruses insert DNA sequences and rearrange the genome, which leads to changes in gene regulation and expression. If such a change in gene regulation is beneficial, it is passed onto future generations.” http://www.physorg.com/news114266805.html
Wait a minute... Did you see what they just said! LOL
That quote is very telling. There are tens of thousands of ERVs in human and chimp genomes. Yet they tell us they mostly are NOT beneficial, yet this article tells us the exact opposite and they will ONLY be passed on IF THEY ARE Beneficial!
So what if ERV’s are in the same spot. It's all about function! “Taken together, our findings suggest that HERVs behave like normal cellular genes and are a permanent component of the transcriptome of a cell.” http://jvi.asm.org/cgi/content/full/79/1/341
They admit they do not know anything here = “The question arises as to whether HERV elements can continue to change our genomic landscape through active retrotransposition or recombination events. While no direct evidence indicates that such events are ongoing in the human genome, members of the HERV-K family appear to be the most likely candidates for playing such a role.” [http://www.genetics.org/cgi/content/full/171/3/1183
Considering Viruses are tested to be young, it's over for them, ERV’s are not old either….
This study is awesome as well and shows viruses are young = https://jvi.asm.org/content/77/7/3893 “While the RNA viruses we see today may not date back quite this far, the evidence that some DNA viruses have evolved with their vertebrate hosts over many millions of years (24) makes an equally ancient history for RNA viruses a natural expectation. Yet a very different picture of RNA virus origins is painted if their gene sequences are compared; by using the best estimates for rates of evolutionary change (nucleotide substitution) and assuming an approximate molecular clock (21, 33), it can be inferred that the families of RNA viruses circulating today could only have appeared very recently, probably not more than about 50,000 years ago.” Hence, if evolutionary rates are accurate and relatively constant, present-day RNA viruses may have originated more recently than our own species.
Before discussing the solutions to this apparent paradox, it is important to determine exactly why the molecular clock estimates of RNA virus origins are so recent.
The data even shows viruses are young. But of course, the writers have to explain this phenomenon by creating Ad Hoc excuses as to why this clock is so young. Remember if a paper isn't worded correctly. It's a great possibility that it won't be published. Grant funding will be stopped and maybe your job will be lost if they are not going along with the paradigm.
It's simple people, ERV's are only about 500 to 600 bases in length. The genome is multilayered. You can just dump vital information into the genome and expect it to function . You can just co-opt hostile RNA sequences from viruses and expect them to play a large role in regulating a genome . Viruses were one functional element of the genome. Now they are corrupt. They have similar features but ERV's perform vital functions and viruses destroy the genome.
ERV’s cannot be from viruses. It's one assumption after another which disregards a plethora of data. The fact that these transposable elements code for regulatory factors that are critical for the regulation of gene expression that produces various organs verifies this. It's nonsense to believe the DNA of a virus could possess the information to regulate genes to produce organs in vastly more complex organisms, especially if one believes the nonsensical idea that they became co-opted for this function since the organ already existed prior to the imagined introduction of the viral DNA!
Humans and chimps were created separately. The matter of fact there are multiple theories and models for where these viruses came from and they’re still debated today. One is the virus-first model, another is the Escape hypothesis, and even another is called Giant (mimivirus) viruses theory. https://www.nature.com/news/giant-viruses-open-pandora-s-box-1.13410 / The Regressive model combats these as well, especially the mimivirus theory. We have also found ERVs that contradict the animal’s phylogeny. Experts in the field claim this with their evidence: https://link.springer.com/chapter/10.1007%2F978-94-007-4899-6_3 If ERVs are from viruses then the probability of this occurring is 0. Therefore, ERVs are not from viruses. Also, ERVs have the exact same mutations in completely separate organisms making it even more unlikely that ERVs are from viruses. There is no proof whatsoever in any study, laboratory or observation that these sequences are from viruses, just hypothetical theories of ERV insertions that supposedly took place millions of years ago because all their prior theories are dying. These sequences of nucleotide bases are part of the original genome.
Also consider this, in order for you to be immune to a virus you would have to be lacking the portion of DNA that the virus is going to affect. There are whole segments that are shared by multiple animals in common with humans and they have solely selected the segments from certain apes and assumed that because they are affected by the virus DNA wise, that we somehow have to be descended instead of realising that this is the same across any animal that has common segments of DNA. Either way, this just points out that the virus just distorts the DNA portion it is designed too and this is as far as it can go. Segments that are similar do not prove ancestry. They prove commonality in segments of DNA based on created functions. The whole point breaks down when you realize how viruses work and that the ERVs are present in all common DNA segments if function is required, revealing a created hierarchical pattern of design. It makes clearly no sense to assume when you realize the sheer number of mutations that would have been required for the vast differences between humans and apes.
If you are really into the technical papers on ERV’s I placed it here; https://docs.google.com/document/d/19K0QmvbtkTikp0uRq3ZzKKcLyO2Qtdfg5DZZNIvb1tc/edit?usp=sharing
As to not bore my readers to death with the details.
When secular science decides to be open minded and look specifically at all ERV’s for function, they will quickly realize the full role they served and still do serve and we will have even more evidence to vindicate creation. Until that time we just have to wait. The question that remains that most important is, were these created elements or later additions to the genome. Given their absolute necessity for life, it seems obvious. Until it's observed and proven that foregn viral invaders can assimilate the genome and turn from disease causing viruses into beneficial DNA elements, the secular camp will be nothing but pure storytelling regarding ERVs.
]]>Featured in: SPECIAL CREATION (Upcoming book Dec 2020)
We have covered endogenous retroviruses in great deal throughout all of our books and videos. There are still some very militant critics who refuse to admit that ERV’s are not evidence for universal common ancestry. One of these critics is named Barry Desborough and this is his blog that we will be debunking in this article:
https://barryhisblog.blogspot.com/p/in-science-we-apply-principle-of.html
Mr. Desborough has also attempted to assert ERV’s are evidence for universal common ancestry by looking to the “Phoenix Virus” Experiment. This can be found at his blog titled “ERV FAQ: What’s all this about the Phoenix Virus? Sounds like a Michael Crichton science fiction story! This experiment proves that ERVs originated as retroviruses.”
This critic completely misunderstands the point of dispute. The question is not whether ERV-like sequences can form viruses (in fact, one creationist hypothesis for the origin of viruses post-Fall is that they arose from ERV-like sequences in our genome--For example: instead of coming into our genome from the outside, they may have originated from within our genomes--More on this in the video). The more important question is: are ERV-like sequences functional units of DNA? The "Phoenix virus" experiment does not answer this question. The data strongly supports the VIGE model (Variation Inducing Genetic Elements). Dr. Peer Terborg points out why mainstream scientists are backwards in their thinking when it comes to these functional DNA elements all throughout the genomes of living organisms:
“The findings of the new biology demonstrate that mainstream scientists are wrong regarding the idea that transposable elements are the selfish remnants of ancient invasions by RNA viruses. Instead, RNA viruses originate from transposable elements that were designed as variation inducing genetic elements (VIGEs). Created kinds were deliberately frontloaded with several types of controlled and regulated transposable elements to allow them to rapidly invade and adapt to all corners and crevices of the earth. Due to the redundant character of VIGEs, their controlled regulation may have readily deteriorated and some of them may now merely cause havoc. The VIGE hypothesis provides elegant explanations for several biological observations that may otherwise be difficult to interpret within the creationist framework, including the origin of diseases (RNA viruses) and chromosome rearrangements. The VIGE hypothesis may be a framework for extended creationist research programs.” Source: Terborg, P., The design of life: part 4—variation inducing genetic elements and their function, Journal of Creation 23(1):107–114, 2009.
Are these DNA elements really evidence for universal common ancestry? Or are they evidence for God’s amazing design. The created heterozygosity and front-loading of DNA elements model best explains the data. Dr. Peer Terborg continues in the next sentence answering a number of important questions as to why these variety of DNA elements are created units of DNA function:
“Some intriguing questions can already be raised. 1. Were VIGEs intentionally designed to cause diseases? No, they were not. It is conceivable that the transposition and integration of VIGEs is not entirely random. The transposition of VIGEs may have been originally present in the baranome as controlled and regulated elements and activated upon intrinsic or external triggers. To induce variation in offspring, triggers for the transposition of VIGEs could be released during meiosis, when the reproductive cells are being produced. The emergence of RNA viruses from VIGEs may be a result of the Fall, when we were cut off from the regenerating healing power of the Creator.
2. Why are some VIGEs located in the exact same position in primates and humans? Each original baranome must have had a limited number of VIGEs, some of which we still find on the same location in distinct species. In distinct baranomes, VIGEs may have been located on the exact same positions (the T-zero location), which then explains why some VIGEs such as ERVs, can be found in the same location in, for instance, primates and humans. In addition, sequence-dependent integration of VIGEs may also contribute to this observation.
3. How could Bdelloid rotifers, a group of strictly asexually reproducing aquatic invertebrates, rapidly form novel species? Asexual production of progeny, as observed in Bdelloids, is found in over one half of all eukaryotic phyla and is likely to contribute to adaptive changes, as suggested by recent evidence from both animals and plants. The Bdelloids may have been derived from pluripotent baranomes containing numerous DNA transposons and retro elements, including active LTR retrotransposons containing gag, pol, and env-like open reading frames. These elements are able to reshuffle the genomes and facilitate instant variation and speciation.
4. Do we also observe remnants of DNA viruses in the mammalian genomes? If not, this advocates my idea that RNA viruses emerged from VIGEs, and implies DNA viruses have a different origin; probably, as with the Mimi-virus40, they originated from degenerated bacteria. 5. Why was a class of VIGEs designed with information for protein capsids? The capsid may have been acquired from the host’s genome or it may have been designed to prevent the RNA molecules from attaching themselves to, or finding, integration sites. A very speculative idea may be that these VIGEs were designed to shuttle information from the soma to the germ-line. One thing is clear, however: creation researchers have loads of work to do.”
In my book “The First Couple-Independent Origins”, I reference Dr. Jeffrey Tomkins who has examined the function of these front-loaded DNA elements in great detail.
“When it comes Transposable Elements (TEs), Dr. Jeffrey Tomkins in his review of Dr. Jonathan Well’s book The Myth of Junk DNA, points out that in every identified class of Transposable Elements, function has been identified:
“One class of DNA that has also been the target of evolutionary propagandists is the diverse group of DNA features called transposable elements (TEs), sometimes referred to as “jumping genes”. Many scientists have stated that all of the subclasses in this diverse group were merely genomic baggage conferred by ancient ancestral viruses that infested our DNA and have served no other purpose than to bloat and expand the genome with meaningless DNA fragments. However, the past several decades of research now show that every identified class of TEs (LINEs, SINEs, ERVs and DNA-transposons) all have important roles in the function of the genome during development, growth, and day-to-day physiological activity. Wells discusses the history of these discoveries along with detailed information about each sub-class of TE and its currently known functional characteristics. Interestingly, all of these TEs are now known to have multiple functions depending on the type of cell and its activity. Rather than cryptic viral genome contaminants, it is now clear that TEs are absolutely critical to genome function and survival. TEs apparently also play important roles in cell stress responses and other protective measures. The Myth of Junk DNA clearly shows how the various classes of TEs present in the genome are not useless trash, but indispensable functional factors.” Please see: Tomkins, J., The junk DNA myth takes a well-deserved hit, Journal of Creation 25(3):23-27, 2011. Also see: The Myth of Junk DNA by Jonathan Wells.”
In the next paragraph of my book cited above, I debunk the claim that these incredibly important functional roles could have been co-opted through evolutionary processes.
“Critics of biblical creation have attempted to say that the various functional roles discovered in Transposable Elements were co-opted. They have invented a fancy story to explain away the data that is contradictory to their evolutionary story. They have also attempted to downplay the evidence for function by asserting these functions are rare and only few. Is this really the case? I address these objections in my book “Why Human Evolution Is False: The Scientific Case For Independent Origins”.
“The evidence is irrefutable. The data is unquestionable. We can see a multitude of peer reviewed technical papers validating the remarkable functionality of these Endogenous Retroviruses. And not only the ERVs, but incredible functions for the other various classes of retrotransposons. Guardians of evolution will habitually downplay the function and say it's only a few trivial functional roles discovered in these retrotransposons.
Evolutionists once again are hopeless in their struggle to hold onto what they once claimed was the absolute best evidence for human evolution. These ERVs and other classes of retrotransposons are not just “kind of '' functional, they are extraordinarily functional to the point that they are critical to the health of living organisms. Then the evolutionist will try to say these functions were co-opted, when in fact, there is absolutely no evidence for this so-called co-option.
Anytime a proponent of evolution tries to say these functions, such as regulating genes and determining cell types, or even important in development, were co-opted, just know that it is a clear confession that they have no genuine empirical answer. This answer to the function of retrotransposons is a rescue device employed to desperately hang on to this last piece of evidence for human evolution. Declaring they were co-opted is nothing but fancy storytelling void of any real empirical data and real scientific substance. It is time for the evolutionists to tap out and accept the truth of Biblical creation and independent origins.” (pages 76-77)
In the same article, Dr. Jeffrey Tomkins explains why ENCODE has been so important in overturning the junk DNA paradigm:
“During the course of explaining these concepts, the publicly-funded ENCODE project (Encyclopedia of DNA Elements) is mentioned. ENCODE was a critical public research effort that discovered how much of the genome, even the parts that do not directly code for protein, is regulatory in some way. In fact, the regulation of gene expression by the wide variety of RNAs produced from non–protein-coding DNA sequence are now being perceived as more important targets of study than the actual protein-coding sections of the genome. The wide diversity of noncoding RNAs (ncRNAs) in a cell affects virtually all aspects of growth, development and physiology. The protein-coding sections of the human genome, comprising less than 3% of the whole, are somewhat analogous to the raw materials (bricks, boards, wire, etc.) one would use in a building construction project. It is the intelligent oversight, implementation and usage of these raw materials that makes the building take shape and function, and that seems to be what ncRNAs are used for.”
The evidence for genome-wide functionality is overwhelming.” Source: Standing For Truth. The First Couple: Adam and Eve – Independent Origins.
In his article titled “Large scale function for ‘endogenous retroviruses’”, Shaun Doyle points out that it is not just 1 or 2 functional roles found in these ERV’s as the proponents of ape-to-man evolution like to assert as a counter argument to the data:
“Moreover, researchers have recently identified an important function for a large proportion of the human genome that has been labelled as ERVs. They act as promoters, starting transcription at alternative starting points, which enables different RNA transcripts to be formed from the same DNA sequence.
‘We report the existence of 51,197 ERV-derived promoter sequences that initiate transcription within the human genome, including 1,743 cases where transcription is initiated from ERV sequences that are located in gene proximal promoter or 5’ untranslated regions (UTRs).’
And,
‘Our analysis revealed that retroviral sequences in the human genome encode tens-of-thousands of active promoters; transcribed ERV sequences correspond to 1.16% of the human genome sequence and PET tags that capture transcripts initiated from ERVs cover 22.4% of the genome.’
So we’re not just talking about a small scale phenomenon. These ERVs aid transcription in over one fifth of the human genome! ‘These data illustrate the potential of retroviral sequences to regulate human transcription on a large scale consistent with a substantial effect of ERVs on the function and evolution of the human genome.’3 This again debunks the idea that 98% of the human genome is junk, and it makes the inserted evolutionary spin look like a tacked-on nod to the evolutionary establishment. These results support the conclusions of the ENCODE project, which found that at least 93% of DNA was transcribed into RNA.” Source: Doyle, Shaun., Large scale function for “endogenous retroviruses’, Journal of Creation 22(3):3, 16, December, 2008. https://creation.com/large-scale-function-for-endogenous-retroviruses
The empirical data is exactly what a biblical creationist would expect—Why would God design life that is composed of mostly junk, evolutionary leftovers, ancient viral infections, and genomic fossils? Based on the design hypothesis, we would expect genomes of function and functional DNA elements.
Also—Please read these technical articles on this important topic (if the critics think they have any rebuttal at all—they have a lot of work to do):
Luskin, C., ‘Large Scale’ function for endogenous retroviruses: Intelligent Design prediction fulfilled while another Darwinist argument bites the dust, Discovery Institute, 21 August 2008,
Evidence for the design of life: part 1—genetic redundancy
Evidence for the design of life: part 2— Baranomes - Terborg, P., The design of life: Part 2—Baranomes, J. Creation 22(3):68–76, 2008.
The design of life: part 3—an introduction to variation-inducing genetic elements - Terborg, P., The design of life: Part 3—an introduction to variation-inducing genetic elements, J. Creation 23(1): 99–106, 2009.
The design of life: part 4—variation-inducing genetic elements and their function - . Terborg, P., The design of life: Part 4—variation inducing genetic elements and their function, J. Creation 23(1):107–114, 2009.
The ‘VIGE-first hypothesis’—how easy it is to swap cause and effect
(Search www.creation.com for these 5 must-read articles for further understanding on this topic)
Also—Please see: https://creation.com/koalavirus
PART TWO:
Answering Barry Desborough’s specific questions in his blog cited at the beginning of this article:
1:) What is reverse Transcriptase designed to do? Viral Genome Size Distribution Does not Correlate with the Antiquity of the Host Lineages; “Our results also suggest that since retroviruses appear to be restricted to plants and vertebrates, they could NOT have played a role in the evolutionary transition from primitive cellular RNA genomes to the extant DNA-based genetic systems of extant cells, nor the viral reverse transcriptase can be considered an evolutionary vestige of the polymerase that played a role in this transition.” The results presented here demonstrate that viral genome sizes are not randomly distributed, but do not appear to be correlated with the antiquity of their hosts. Therefore, viruses may be ancient, but not primitive. Link
2:) “What is integrase designed to do?” It was designed to be a multidomain enzyme. Here is another thing. “Most ERV copies suffer mutations over evolutionary time that prevent the normal assembly of viral particles, preventing horizontal transmission of infections between individuals.” Link
3:) Why are ERVs designed with a viral codon bias?” Because Taxonomic boundaries do exist and these originally designed ERV’s were not meant to be crossed. This is why Viruses from a bat cause things like Covid in humans but bat’s remain unaffected.
4:) “What is the design purpose of re-transcribable promoters?” Well if these are functional DNA elements with important factors then they need to be read like other promoters. Just because viral genes are robustly transcribed during the stage of infection when host transcription is reduced doesn't mean that this was their design purpose originally.
5:) “What were the HERVs that produced the consensus sequence that generated Phoenix designed for?” Since what I know about “the Phoenix virus”, is that French researchers resurrected a retrovirus that became trapped in the human genome. When they exposed Phoenix to cultured human and mammalian cells, they observed spiky virus particles pinching off from the cells and floating in between them. The genomes of the cells also contained new HERV-K sequences, indicating the viruses had infected them. Since this Phoenix virus belongs to the human endogenous retrovirus line only (K-type). Then it was probably an original functionally created ERV that worked in placental development like other HERV-Ks were discovered to do. This could be a reason that there’s so many fetal developmental problems today. I would imagine this died out from mutation, like most ERV’s are dying from today. Every known ERV has lethal mutations in them. What is funny is that “they” evolutionary secular sciensints, believe that this is one of the oldest ERV’s to infect humanity going back 5 million years ago. Yet, when it began to function and form particles capable of infecting mammalian cells in culture. They quickly stated that this happened because the (HML2) family is an evolutionarily "young" family of retroviral elements. The mutations in the resurrected Phoenix virus were still active even though the Phoenix virus is nearly dead. The resurrected Phoenix produced some 'genomic offspring' that may be responsible for the synthesis of the retroviral particles that can be observed in some human cancers such as germline tumors and melanomas.
Another thing, 5 million years is just an arbitrary number they pulled out of thin air. I could write an article on the Phoenix virus and say, no its 4.5 million years old and it would have just as much credibility because no one knows. But, use a date of just thousands of years ago and now all of a sudden this doesn't agree with Evolution and you are stirring the pot too much. When you see numbers tossed around like 5 million years old, you can take that with a grain of salt because they have no evidence, no proof, nothing. To show that this is true. Pure assumption, mixed in as truth, and sold to the public as fact. The story they wield is just retrofitted to fit the evolutionary model. They didn't predict that any ERV would have any function, let alone so many of them with vital functions! Their ad hoc rescue device about them gaining function has no evidence whatsoever. They just needed to say something about it because it was devastating to the theory.
6:) What is the design purpose of BOTH Exogenous and Endogenous KoRV? Weird question, ERVs do not constitute a separate taxonomic division from exogenous retroviruses. Here we find this comment “(This refers to ERVs as a whole; any individual ERV locus or family may still represent a novel (and possibly extinct) retroviral genus). Link So I will just say for example that their functions work in conjunction with one another, they have discovered “many ERVs is interrupted by termination codons, deletions or frameshift mutations, some ERVs are transcriptionally active and recent studies reveal protein expression or particle formation by human ERVs.”
7:) “If Chimp and humans have commonly located ERVs, what is the design purpose of giving these common ERVs common disabling mutations?” For the same reason similar genes break in unrelated species and related species. Some genes are just weaker than others. The more important, the more conserved. It must be noted that evolutionists believe that for each virus there are many thousands of sites at which it could insert. Thus the odds that they became inserted in the same region in primates and humans is proof of ancient common ancestor relation, but here is the thing. This is not true, that is an assumption. How can I say that? Easy! Observable evidence tells us this. Different types of regions literally show us that specific viruses favor insertion into a particular spot in the genome. For example, HIV (human immunodeficiency virus) tended to insert in gene-rich regions only. MLV (murine leukemia virus ) favored integration near transcription starts, while ASLV (avian sarcoma-leukosis virus) showed only a weak preference for active genes. So clearly when some viruses enter into the system they are attracted to similar places. So this is even more evidence that if these were not all created elements at the start, that their location inside similar species is not evidence of a common ancestor but similar reaction by the virus to bind at similar spots.
Over 100 LTRs have been demonstrated to help control transcription of human genes Link and several thousand other LTRs could potentially have that function as well. ERVs and other transposable elements are known to play roles in the three-dimensional organization of the genome by functioning as ‘anchors’ that serve to isolate regions of active transcription and by modifying the structure of chromatin. Link
8:) “What is the design purpose of giving some people certain HERV’s and others not?” Well you have to remember that humans originally did and that over time mutations and Polymorphism occurred in them and they are no longer shared in all people or they are missing all together because of it. For example, when it comes to HERV’s specifically “there are at least 8, and perhaps 11, of these elements are insertionally polymorphic, meaning, some human individuals have the insertion while other individuals have the empty, pre-insertion site. This shows that this virus family has been transcriptionally active within the age span of the human race.” Link
9:) What is the design purpose of creating different syncytins in different placental lineages? Well the ERVW-1 gene is EXTREMELY VITAL since it is required during placenta morphogenesis. The fact that there are different created syncytins in different placental lineages is just more proof that it was designed and created because what are the odds that different placental lineages all obtained an ERV that just happened to all “retain its original fusogenic properties and participates in trophoblast fusion and the formation of a syncytium during placenta morphogenesis.” Let that sink in. Link
Think about this everyone. Are bacteria important? Are they good for you? You bet they are. You couldn't even live without them. So of course they were created within us. The same applies with ERV’s. Are they important? Are they good for you? You bet they are. Life could not exist without them. Now, does this mean that some are not harmful to us in today's world? Of course not. But Genetic Entropy explains this.
]]>We can detect the Babel event in our genetics. Dr. Robert Carter makes an incredible observation in his article from The Journal of Creation 25 (2) titled “Can mutations create new information?” (References can also be found at the end of the book)
“I do not believe all current human genetic differences are due to mutation. We have to make a distinction between mutation and ‘designed variation’. There are a huge number of single letter differences between people, and these are mostly shared among all people groups.2 This indicates that much of the diversity found among people was designed: Adam and Eve carried a significant amount of diversity; this diversity was well-represented on the Ark and in the Babel population immediately after the Flood, and the post-Babel people groups were large enough to carry away most of the variation present at Babel. Most deletions (~90%), however, are not shared among the various human subpopulations.3. This indicates that a significant number of deletions have occurred in the human genome, but after Babel. Deletions are apparently not designed variation and are an example of rapid genomic decay. The same can be said of DNA insertions, but they are about 1/3 as common as the same-size deletion. The ubiquity of large, unique deletions in the various human subpopulations worldwide is evidence for rapid erosion or corruption of genetic information, through mutation.”
Another common objection made by critics who misunderstand the biblical model of ancestry has to do with alleles. Critics have put forth the argument that the highly variable positions found within the genome is a contradiction to the created heterozygosity hypothesis. Dr. Robert Carter addresses this objection in his article titled “Adam, Eve, and Noah vs Modern Genetics”:
“Most variable places in the genome come in two versions and these versions are spread out across the world. There are some highly variable places that seem to contradict this, but most of these are due to mutations that occurred in the different subpopulations after Babel.
There are indications, however, that Eve may not have been a clone. The ABO blood group is a textbook example of a gene with more than two versions.3 There are three main versions of the blood type gene (A, B, and O). However, many, but not all, people with type O blood carry something that looks very much like a mutant A (the mutation prevents the manufacturing of the type A trait on the outside of cells). So here is a gene with more than two versions, but one of the main versions is clearly a mutation. This is true for many other genes, although, as usual, there are exceptions. The important take home point is that essentially all of the genetic variation among people today could have been carried within two people, if you discount mutations that occurred after our dispersion across the globe. This is a surprise to many.”
Source: Robert W. Carter , “Adam, Eve and Noah vs Modern Genetics,” Creation Ministries (May 11, 2010), www.creation.com/noah-and-genetics.
As we can see, mutations can clearly occur after the flood and after Babel. These mutations would create additional versions of the original created alleles. There is no contradiction to the hypothesis that suggests God would have encoded Adam and Eve with front-loaded DNA diversity. What we see in terms of allele frequencies is exactly what one would expect if the biblical model of ancestry were true. This is all a reflection of the Babel dispersal.
In the same article (Adam, Eve and Noah vs Modern Genetics), Dr. Robert Carter points to some fascinating observations regarding X chromosomes as well as the Y chromosome.
“How many X chromosome lineages were on the Ark? That depends. If you count it all up, you get eight. If, by chance, Noah’s wife passed on the same X chromosome to each of her three sons (25% probability), then there were seven. If Noah had a daughter after the Flood (not expected, but possible), there could be as many as nine X chromosome lineages. Either way, this is a considerable amount of genetic material. And since X chromosomes recombine (in females), we are potentially looking at a huge amount of genetic diversity within the X chromosomes of the world.
Does this fit the evidence? Absolutely! It turns out that Y chromosomes are similar worldwide. According to the evolutionists, no “ancient” (i.e., highly mutated or highly divergent) Y chromosomes have been found.5 This serves as a bit of a puzzle to the evolutionist, and they have had to resort to calling for a higher “reproductive variance” among men than women, high rates of “gene conversion” in the Y chromosome, or perhaps a “selective sweep” that wiped out the other male lines.6 For the biblical model, it is a beautiful correlation and we can take it as is.”
Not only do the critics attack the biblical model of ancestry by misrepresenting it, they’ve also attacked it using non-scientific arguments that reflect a very poor understanding of basic genetics. Many critics that I have personally engaged with have challenged my arguments by asserting there is no possible way for Adam and Eve to carry as much genetic diversity that would be necessary to explain the genetic diversity we see in humans today. I have already addressed the fact that genetic diversity does not need to arise through millions of years of mutation accumulation since genetic diversity could be built in at creation. Once again, Dr. Robert Carter gives a phenomenal and very technical answer to this apparent problem and challenge to biblical creation and the model of independent origins. Dr. Carter presents this argument in his article titled “The Non-Mythical Adam and Eve! Refuting errors by Francis Collins and Biologos”. Please read this entire article for an amazing refutation of Francis Collins and Biologos. Here is the specific excerpt on created diversity and allele frequencies:
“Is it possible for a single person to carry this much diversity? I ran an analysis of the HapMap data to measure the amount of heterozygosity within the HapMap individuals. Population-level differences were slight, with a global average of 4.33 ± 0.234 × 105 (±SD) heterozygous alleles per person. Thus, approximately 30% of all HapMap alleles are heterozygous within each person. If there are 10 million common variants, a single individual would be expected to carry upwards of three or four million heterozygous alleles! Because most people are phenotypically normal, there is no reduction in fitness associated with these high levels of heterozygosity. Why should there be if most of this variation was created by God and engineered into the original genome? I expect Adam had about 10 million or more heterozygous loci and that each of his children had half that much.
Some alleles, however, have been added to the population through mutation. How much genetic diversity is due to mutation? Given the 10 million common variations in the human genome, there are many more ‘private’ and very rare variants that occur in one or a few individuals in specific populations. These should be mutations that have occurred since the Flood and Babel. With an average (modern) generation time of 30 years, there have only been about 150, perhaps as many 200, generations in all of human history. Assuming a conservative modern estimate of 100 new mutations per person per generation, that gives us between 15 and 20 thousand mutations per person. This is a huge number when added up across the world population, and most of these should be unique (perhaps even totaling more than the amount initially created). Yet, on the individual level, it might be expected that only a small fraction (less than 0.01%) of heterozygosity is due to mutation.”
Source: Robert W. Carter, “The Non-Mythical Adam and Eve! Refuting errors by Francis Collins and BioLogos,” August 20, 2011, www. creation.com/historical-adam-biologos.
Dr. Robert Carter has spent considerable time analyzing the HapMaP data and has come to some intriguing conclusions. In his article “Does Genetics Point to a Single Primal Couple? A response to claims to the contrary from BioLogos”, we find these intriguing conclusions. Does the data fit the biblical model of origins? Have a look for yourself:
“The HapMap Project3 was designed to catalog a significant fraction of human genetic diversity. They analyzed millions of variants in thousands of people from around the world and made the data freely available. One might wonder, if the HapMap is so unfriendly to the creation model, why do I have much of that data stored on my hard drive? In fact, I am quite happy with what we learned from the project (I am even happier with the 1000 genomes project, which is a step above HapMap, but which is not yet complete). What have we learned?
Source: Robert W. Carter, ““Does Genetics Point to a Single Primal Couple? A response to claims to the contrary from BioLogos” August 20, 2011, https://creation.com/historical-adam-biologos
As we know from scripture, there are a few events that would be considered bottlenecks. This would be the creation event, the flood, and Babel. I have personally engaged in well over 50 live debates and an incredibly common objection to the biblical model of ancestry has to do with these bottlenecks. They have made the argument that the flood bottleneck would have reduced levels of heterozygosity to a point that speciation and adaptation post-flood and post-Babel would have been implausible. This is an argument that I have dealt with in my previous books. If you have read these books, or seen my debates, you would know that the bottleneck at the flood was only one generation and it was followed up by rapid and exponential population growth. Extraordinarily little of the original created heterozygosity would have been lost based on these facts. Dr. Robert Carter has also addressed this argument in the same article that was previously cited (“Does Genetics Point to a Single Primal Couple? A response to claims to the contrary from BioLogos”).
“Another part of their error comes from the fact that the authors substitute an evolutionary bottleneck for the biblical one. In evolutionary mathematics and theory, one rarely considers a single-generation bottleneck. Rather, a “bottleneck” is defined as a restriction in the population size that lasts long enough to have an effect. A single-generation event (e.g., Noah’s Flood), with a rapid expansion of the population afterward (prior to and after Babel), will lead to a negligible loss of diversity.”
We can see here why there would have been minimal loss of heterozygosity. In the same article, Dr. Robert Carter states:
“The three founding Ark couples could have carried a huge percentage of the pre-Flood genetic variation (Adam and Eve’s diversity + pre-Flood mutations), with the exception of the Y chromosome (total loss of all but one line) and mtDNA (restricted to three lines). Hence, the biblical model fits the available data nicely and the data do not serve as an easy refutation of Adam and Eve.”
If you have engaged the proponents of evolution as much as I have, you will be familiar with their arguments against the so-called “races”. Before I answer this question, I want to point out that modern scientific data has demonstrated beyond a shadow of a doubt that there is one race, the human race! Let us get to the arguments made by the critics. Where did all the races come from and how do we account for them in just a few thousand years? The answer to this can be found in our genetics. This all goes back to Gregor Mendel. Mendel lived at the same time as Charles Darwin. Looking at basic genetics and basic genetic principles, we can look at it in terms of capital and lower-case letters (Big A, little a, big B, little b). These letters represent unique features and traits. For example, if you have a capital A for dark skin and a lower-case a for light skin, and if you have a couple such as Adam and Eve, we can then ask the question: what were Adam and Eve according to their skin tone? Let us figure this out together. If Adam and Eve were Capital A, capital A, capital B, capital B, then both have dark skin. This means all they can produce is dark skin. The same thing would be true if they were all lower-case letters, which would mean they can only produce light skin people. Since we look to the idea of front-loaded genetic diversity (created heterozygosity), we know that Adam and Eve would have had pre-existing DNA differences. It would make no sense scientifically, and theologically, for God to create Adam and Eve homogeneous. It is doubtful that God would have wanted Adam and Eve to produce clones. God did say to be fruitful and multiply. Would this command really have made any sense if God intended Adam and Eve to produce offspring exactly like themselves? Of course not. Pre-existing DNA differences is what makes sense. This model even leads to testable and falsifiable predictions. A few of these predictions involve speciation rates, mutation rates, and DNA function. We will touch on more of this later. And so, if Adam and Eve are a mix of capital and lowercase letters, capital A, lower case a, capital B, lower case b, and were a middle brown skin tone, they would have the potential to produce every shade of skin that exists on this planet. And this is all simply basic genetics! Adam and Eve would have had within their DNA the genetic potential to produce every shade of skin that exists on this planet or known to man. Essentially, there are no races. There is one race: the human race. The “races” all come from the genetic potential that exists within Adam and Eve. The reason why these genetic differences were sorted out and these groups were isolated goes back ultimately to Babel. This is where they would have been one language and mixed features. The spreading out from Babel explains the particular set of genetic features seen around the globe and these sets of genes are unique markers of their past lineages. We have literal traces of Babel in our genetics! This all comes back to the origin of genetic diversity. Critics of biblical creation have often pointed to the levels of genetic diversity in humans today as an objection to a literal Adam and Eve. I touched on this earlier in the chapter. But since this is such a common objection, I want to demolish it to the point where the critics may finally stop using arguments that have been addressed so thoroughly. It should make the creationist wonder if the critics are even paying attention. Are they truly looking for an answer? Well, I have also addressed this in my first book “Universal or Separate Ancestry? The Biblical Model of Origins Made Easy” on pages 53 and 54:
“Skeptics of the biblical creation model will often point to current human genetic diversity as an objection to a literal Adam and Eve. What they will say is that there is no feasible way scientifically for only two people to have the potential to generate all the genetic diversity and DNA differences we see in the world today. This argument reflects both a limited understanding of theology and a limited understanding of science.
God commanded Adam and Eve to be fruitful and multiply. Would it have made any sense for God to have created the first people genetically homogenous with absolutely no DNA diversity? God did not say be fruitful and clone yourselves. He said be fruitful and multiply. What makes the most sense biblically and scientifically is that God created Adam and Eve with front-loaded DNA differences. This is the concept of created heterozygosity (a state of DNA diversity or DNA differences). This hypothesis also makes testable predictions. The funny thing is that geneticists have attacked Adam and Eve using this unfounded argument. What does basic genetics tell us?
A man and a woman today could have thousands, even millions of children and no two children would be 100 percent identical. This is because they are heterozygous (a state of being genetically different). There exists built in diversity in millions of sites within the genome of the average person.
We propose that God created Adam and Eve to be heterozygous (millions of DNA differences in chromosome pairs), and this would in fact be optimal design. With this as a basic starting point, you could have as much human diversity and more than we have today in their first family. Time is not required for the diversity today, because diversity can be designed and built into Adam and Eve.”
Another objection thrown at biblical creation and independent origins is the claim that there is no way we could account for all the species we see today in just a few thousand years. Once again this comes down to the basic misunderstanding of the biblical creation model. Do biblical creationists propose mutations are the source for all genetic diversity? As you have seen, the answer to this question is no. Biblical creationists invoke created genetic diversity and front-loaded DNA differences. I also address this overused objection on pages 66-67 in “Universal or Separate Ancestry? The Biblical Model of Origins Made Easy”:
“These basic assumptions preclude the evolutionist from even considering the possibility that there was front-loaded genetic variety and created functional DNA differences from the start. They have overlooked this remarkable explanation for how millions of species and incredible variety could have come about in just a few thousand years. With front-loaded genetic diversity that applies not only to Adam and Eve, but also to the created biblical kinds, generating thousands of species after the flood is easy. All it would take is genetic processes such as recombination, gene conversion to create new chromosomal combinations and genetic variety in even a single generation. This is because the differences are already built in and we do not need millions of years to generate all the DNA differences by mutation. Other speciation related processes such as population breakaways, inbreeding, isolation, and shifts from heterozygosity to homozygosity would be all that is necessary to produce new species.”
If the differences are built in from the start, generating new species is easy. As a matter of fact, the numbers of species on the planet today are far better explained by the young earth creation model.
Before we conclude this chapter, I want to note that many critics of the front-loaded DNA diversity model have used an argument that reflects a poor understanding on how to best define allele. Dr. Nathaniel Jeanson has had an extensive written debate with Dr. Stefan Frello that can be found on the Answers In Genesis website in the Answers Research Journal section. Dr. Stefan Frello has also chosen to utilize this poor argument against the created heterozygosity hypothesis. Dr. Nathaniel Jeanson addresses the argument by first pointing to where Dr. Frello has accurately represented his model:
“Let’s start by identifying where Frello’s claims and representations of Replacing Darwin are correct. In these paragraphs, he clearly and unambiguously states the genetic compartment to which he refers—the nucleus (“15 nuclear genes”). He also correctly identified my explanation for the origin of the DNA differences in this nuclear DNA compartment as, “the majority of genetic variation within families is due to original created variation.”
But then Frello’s argument commits a common genetic mistake. In his endnote, he (correctly) defines an allele as “One of two or more versions of a particular DNA position” (emphasis mine). But then he contradicts himself in the paragraph above: “a maximum of four alleles1 of each gene could be present in this original pair” (emphasis mine). By definition, genes consist of more than one DNA position. So which is it? Is an allele a version of a particular DNA position? Or a version of a gene that contains hundreds to thousands of DNA positions? Frello can’t have it both ways.” (Most italics in this book have been added by this author)
Next, Dr. Nathaniel Jeanson points out that this argument that Dr. Stefan Frello has employed has been addressed in a prior published paper. This again goes to show that these militant critics of biblical creation fail to read the relevant literature before making an argument.
“In fact, his argument rests on his (erroneous) adoption of the second definition—that alleles are different versions of genes. Under this definition, he misrepresents my explanation for nuclear DNA differences. In fact, in one of my published papers (Jeanson and Lisle 2016) that I refer to at least 15 times in Replacing Darwin, I explicitly addressed Frello’s error:
If an allele is defined in terms of a gene unit, then generating “allelic” diversity by mutating just one gene per mutational event produces little diversity. Instead, if an allele is defined as a single genomic position, independent of its relationship to a gene, then enormous allelic diversity can be generated by mutation . . . As an aside, allelic diversity need not arise via mutation. Again, if we use the genomic position definition of an allele rather than the gene unit definition, other mechanisms besides mutation can generate allelic diversity. For example, a single gene typically spans thousands of nucleotides, and SNVs [SNVs = Single Nucleotide Variants] might be distributed throughout the gene—for example, at 90 of the nucleotides within the gene. If we allow for the genomic position definition of alleles, every single one of these 90 SNVs may have existed in a heterozygous state in each of the individuals of the pairs brought on board the Ark.
Expanding this single gene example across the entire genome reveals a tremendous potential for allelic diversity on the Ark. In just two diploid individuals, four genome copies exist. Since only four DNA base-pairs exist, virtually every possible genomic position allele (i.e., far more than 4–28 gene unit alleles) could have been present at the time of the Flood, if the individuals were heterozygous. (Jeanson and Lisle 2016, 99) [emphases in original paper]
In other words, every single one of the nuclear DNA differences in Frello’s graph could have existed in a heterozygous state in the felid ancestor on board the Ark—because my model defines alleles in terms of DNA position, not individual genes. Thus, Frello’s (apparent) claim—that a maximum of four versions of each gene could be present in this original pair—is incorrect.
Conversely, my model has no need for the mutation rates that Frello claims; in fact, in theory, it has no need for mutations in this example at all. Frello has made a common genetic error, which nullifies his conclusion.” Source: Jeanson, Nathaniel T. 2018. “Response to ‘No Replacement of Darwin: A Review of Replacing Darwin—The New Origin of Species’.” Answers Research Journal 11: 63–83.
I encourage the reader to analyze both sides of the written exchange between Dr. Stefan Frello and Dr. Nathaniel Jeanson. I genuinely believe it is a prime example as to why the evolutionary community is only capable of grasping at straws. As I have stated before, the critics of biblical creation have nothing left to offer.
Written exchanges found here:
Jeanson, Nathaniel T. 2017a. “Response to ‘On the Creationist View on mtDNA’.” Answers Research Journal 10: 183–186.
Jeanson, Nathaniel T. 2017b. Response to “Reply to ‘Response to ‘On the Creationist View on mtDNA’.” Answers Research Journal 10: 239–240.
Replacing Darwin book found here - Jeanson, Nathaniel T. 2017c. Replacing Darwin: The New Origin of Species. Green Forest, Arkansas: Master Books.
Jeanson, Nathaniel T. 2018. “Response to ‘No Replacement of Darwin: A Review of Replacing Darwin—The New Origin of Species’.” Answers Research Journal 11: 63–83.
Frello, Stefan. 2018a. “No Replacement of Darwin: A Review of Replacing Darwin—The New Origin of Species.” Answers Research Journal 11: 57–62.
Frello, Stefan. 2018b. “Still No Replacement of Darwin: A Reply to Nathaniel Jeanson’s Response to my Review of Replacing Darwin—The New Origin of Species.” Answers Research Journal 11: 275–284.
Response to “Still No Replacement of Darwin: A Reply to Nathaniel Jeanson’s Response to My Review of Replacing Darwin—The New Origin of Species” - https://answersingenesis.org/theory-of-evolution/still-no-replacement-darwin-response/
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