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EVIDENCE FOR HUMAN-CHIMP COMMON ANCESTRY (By Request)

TB2

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I was asked to explain some of the evidence that shows beyond a reasonable doubt that humans and chimpanzees share a common ancestor. There is quite a bit, but I will limit this to just two examples. In presenting this evidence, one should know I grew up YEC and rejected human-chimp ancestry for over thirty years. But the evidence kept accumulating to the point it became undeniable (or, at least it can't be reasonably denied). I still believe in the Bible's divine inspiration, and still believe the Fall was a real event, and Adam and Eve were real historical people. How this can be reconciled with Genesis is a matter of ongoing debate among believers. Some say it can't be reconciled. Others like John H. Walton in The Lost World of Adam & Eve, and William Lane Craig's recent book on the historical Adam have make attempts to reconcile science with the biblical account. Although, not everyone will find their 'answers' satisfying, we should still seek reconcilliation. Rejecting the Bible is not an option. But we also no longer have reasonable grounds to reject science. So, reconciliation attempts should be sought. My own 'answer' is perhaps less an 'answer' and more a refocus on what's important: I don't see how reconciliation (one way or the other) matters for the message. Reconciled, not reconciled. It still doesn't change the message. I know this is less than satisfying, but maybe that's part of the problem. We are trying to impose our own modern day questions and concerns on the Bible and trying to get the Bible to answer, when the Bible doesn't seem interested in doing so. And that might be the 'answer' we seek (or at least need to hear) that we need to focus more on what seems to be Scripture's priorities.

Example 1: Evidence for Human-Chimp Common Ancestry from Endogenous Retroviruses (ERVs)

Summary of Facts:


1. Endogenous Retroviruses (ERVs) are the remnants of viral genetic material that get randomly inserted into our DNA as a result of viral infections, and subsequently get inherited (passed down to offspring). All vertebrates have ERVs in their genomes. [Analogy: Imagine you purchased an ebook from Amazon and downloaded it to your phone. Also, imagine that there are millions of different 'computer viruses' (different ERVs) floating around in cyberspace that can 'infect' your ebook by inserting a different word in a random location in your ebook.]

2. In humans, there are >100,000 such places in our genome where genetic material from these ERVs has been randomly inserted. [Analogy: Imagine that your ebook has been 'infected' by >100,000 different words that have been randomly inserted in >100,000 different random places in your ebook.]

3. Over 99.9% of these >100,000 ERVs are also found in the chimpanzee genome in the same, corresponding locations. [Analogy: Imagine that a friend of yours has a copy of the same ebook. You expect your friend's ebook to be 'infected' too, but with different viruses (remember, there are millions of different viruses floating around in cyberspace). But when you compare ebooks, you are shocked to discover that your friend's ebook has not only been infected with the exact same >100,000 different words, but they are also in the same >100,000 different places as they are in your own copy of the ebook].

4. The chance that any ONE same ERV would just so happen to coincidentally be inserted in the same location of the genome in both humans and chimps is ~1 chance in 10,000. The chance that this would happen twice is 10,000 x 10,000 = 1 chance in 100 million. The chance that it would happen 100,000 times by luck is 1 chance in 10,000^100,000 (the number 10,000 raised to the 100,000th power) which is such an astronomically improbable number that it would be a miraculous occurrence on par with a functional RNA self-replicator spontaneously forming by chance abiogenesis. (If we reject the latter on the basis of probability, then to not reject the former is special pleading).

Which is the more likely (more reasonable) explanation?: (1) that your ebook and your friend's ebook just so happened all by luck to independetly acquire all the exact same >100,000 different words in the same >100,000 different places (INDEPENDENT ANCESTRY); OR, (2) that your friend got his/her ebook from Amazon, too, just like you did, and the original ebook from Amazon that you both downloaded already had these >100,000 different words in the >100,000 different places (COMMON ANCESTRY)?

Possible Objection: But couldn't God independently create them separately "according to a common design"?
Not in this case, because this is not original genetic material. These ERVs are viral genetic material from secondary viral infections that infected genomes after the fact (after creation).

It's Worse Than This: In fact, the evidence goes beyond this. ERVs are found in the genomes of all vertebrates, and as with humans and chimps can similarly be used to demonstrate common ancestry and shared evolutionary history for not just humans and chimps, but other primates, and vertebrates as well.


Here is a website that explains this in greater detail with helpful diagrams: https://letterstocreationists.wordpress.com/2015/11/
 
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Example 2: Evidence for Human-Chimp Common Ancestry from Primate Placenta Development

Primate placenta development: We observe that both humans and chimpanzees (and other primates) have the same protein syncytin-1 that is an essential protein in the development of the placenta. The blastocyst of a developing embryo has a layer of cells called the trophoblast, a good portion of which will become the placenta.

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Specifically, syncytin-1 is a cell-cell fusion protein that causes trophoblast cells to fuse together to form a single, multinucleated cell called the syncytiotrophoblast. See how the light blue (syncytiotrophoblast) is a single interconnected cell.

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This forms a barrier between fetal and maternal blood. Macrophages (white blood cells) from the mother can squeeze between cells and would then recognize and attack the fetus as an 'invader,' but the syncytiotrophoblast prevents this because the entire thing is a single cell barrier, so there are no multiple cells plural that the white blood cells can squeeze between. Thus, this cell-cell fusion caused by the syncytin-1 protein is essential and we (and other primates) would die without it. We share this protein (and the gene that codes it) in common with other primates, and it is on the same chromosome and same position in the genome as other primates like chimpanzees.

But that's not even the most significant part about all this. The most significant part is that we further observe the gene is an endogenous retrovirus (ERV), specifically, the gene ERVW-1-- a "fossil" remnant in our genome secondarily acquired by a viral infection in a common ancestor of primates.

Not only that, but this viral gene has the same function in viruses as it does in primates: it codes for a protein that causes the virus to fuse with surrounding cells and in the process escape detection by white blood cell macrophages.

It is too improbable for it to be independently acquired. It is too improbable an occurrence for the same virus to just so happen by luck to infect all primates and by luck just so happen to insert itself in the same part of the genome. And it can't be the case that God separately created the gene in all primates according to a common design, because it is not part of an original creation, but the result of a secondary viral infection.


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Conclusion: The most straightforward explanation for the observation that primates share a viral gene in the same location of the genome that codes for an essential protein in the development of the placenta, without which we would die, is that primates share a common ancestor that had acquired this gene. The fact that human placenta development is mediated by a viral gene that codes for an essential protein---that fact alone is indisputable evidence that the human genome has an evolutionary history (an evolutionary history shared with other primates), because it shows that this essential gene was not the result of an original creation, but the result of genomic evolution caused by a viral gene acquired during a secondary viral infection.
 
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3. Over 99.9% of these >100,000 ERVs are also found in the chimpanzee genome in the same, corresponding locations. [Analogy: Imagine that a friend of yours has a copy of the same ebook. You expect your friend's ebook to be 'infected' too, but with different viruses (remember, there are millions of different viruses floating around in cyberspace). But when you compare ebooks, you are shocked to discover that your friend's ebook has not only been infected with the exact same >100,000 different words, but they are also in the same >100,000 different places as they are in your own copy of the ebook].
I believe your conclusion to be incorrect.

If my friend visited the same site's I did and our internet usage and exposure were the same, it would be very likely that the infections would occur in the same areas in the book.

The same with the environmental conditions and the infection rates between humans and chimpanzees.

I would like to know how it was determined that these additions were due to remnants of ERV genomes placed into the human genome, and when these remnants ceased to be comparable.
 
But that's not even the most significant part about all this. The most significant part is that we further observe the gene is an endogenous retrovirus (ERV), specifically, the gene ERVW-1-- a "fossil" remnant in our genome secondarily acquired by a viral infection in a common ancestor of primates.
How was this established?

secondarily acquired by a viral infection in a common ancestor of primates
How do you know it was secondarily acquired by a common ancestor? Or that it is even an endogenous retrovirus. or a remnant of one?
 
I was asked to explain some of the evidence that shows beyond a reasonable doubt that humans and chimpanzees share a common ancestor
My reasonable doubt is the claim that remnants of viral genetic material get randomly inserted into our DNA as a result of viral infections is even remnants of viral genetic material. How do you know these remnants are indeed from a viral infection?
 
I believe your conclusion to be incorrect.

If my friend visited the same site's I did and our internet usage and exposure were the same, it would be very likely that the infections would occur in the same areas in the book.
That is incorrect. While ERVs cannot insert into DNA anywhere and everywhere, they do not insert at single locus specific sites. In the OP, I posted a link to a helpful website that explains all this in greater detail with helpful diagrams. I will repost it again here: https://letterstocreationists.wordpress.com/2015/11/
How was this established?


How do you know it was secondarily acquired by a common ancestor? Or that it is even an endogenous retrovirus. or a remnant of one?
Meaning it is not original to genome but foreign due to the fact that it is viral genetic material. https://letterstocreationists.wordpress.com/2015/11/
My reasonable doubt is the claim that remnants of viral genetic material get randomly inserted into our DNA as a result of viral infections is even remnants of viral genetic material. How do you know these remnants are indeed from a viral infection?
Again, see the following helpful website, which goes into great detail about what ERVs are, how we recognize them and know they are viral, and their effectively random insertion (again, ERVs cannot insert into DNA anywhere and everywhere, but they also do not insert at single locus specific sites; a good estimate is 1 in 10,000 possible random insertion sites to 'choose' from; which is the source of my figures: https://letterstocreationists.wordpress.com/2015/11/
 
4. The chance that any ONE same ERV would just so happen to coincidentally be inserted in the same location of the genome in both humans and chimps is ~1 chance in 10,000. The chance that this would happen twice is 10,000 x 10,000 = 1 chance in 100 million. The chance that it would happen 100,000 times by luck is 1 chance in 10,000^100,000 (the number 10,000 raised to the 100,000th power) which is such an astronomically improbable number that it would be a miraculous occurrence on par with a functional RNA self-replicator spontaneously forming by chance abiogenesis. (If we reject the latter on the basis of probability, then to not reject the former is special pleading).
Evolutionism runs into the same problem when a mutation supposedly responsible for a particular trait has to enhance a so-called previous mutation to the point a new trait is realized. This "process" must be repeated many, many times to produce the differences and advantages that a human has over a chimp.

For exmple how many so-called beneficial mutations are required to happen in the right place at the right time to allow a human predecesor to develope speech? Your odds presented above say that would be impossible...and we have only mentioned speech and not the other differences seen between humans and chimpanzees.
 
For exmple how many so-called beneficial mutations are required to happen in the right place at the right time to allow a human predecesor to develope speech? Your odds presented above say that would be impossible...and we have only mentioned speech and not the other differences seen between humans and chimpanzees.
Roll a 10-sided die 100 times and record the result each time. What are the odds that you came up with that particular combination? Hint: the odds are really, really bad. There's no way you could have rolled that combination. But you did. You only have to worry about odds when you're trying to get a desired outcome. If you want to get that particular combination of dice rolls, you can forget about it.

If you're starting with an early form of ancestor to humans and want to get speech, the odds are going to be pretty bad. But evolution doesn't care what the outcome is. Given enough generations, something is going to turn up. Might be speech, might be something else. Either the dice rolled for speech, or God tweaked things to ensure speech. Either way, the odds are irrelevant.
 
Evolutionism runs into the same problem when a mutation supposedly responsible for a particular trait has to enhance a so-called previous mutation to the point a new trait is realized. This "process" must be repeated many, many times to produce the differences and advantages that a human has over a chimp.

For exmple how many so-called beneficial mutations are required to happen in the right place at the right time to allow a human predecesor to develope speech? Your odds presented above say that would be impossible...and we have only mentioned speech and not the other differences seen between humans and chimpanzees.
You raise a separate question.

(1) Do we have evidence that humans-primate share a common ancestor?
(2) What is the mechanism to explain this? That caused this? [natural selection & mutation? God/an Intelligent Designer?]

You are questioning #2. It does not change the evidence for #1.

Although, you should know that the evidence we now have from comparative genomics shows that the vast majority of mutations/changes in genomes are neutral to slightly negative in fitness (i.e., most mutations have little to no effect on the organism)
 
Meaning it is not original to genome but foreign due to the fact that it is viral genetic material.
This is my point:
How do you know it is not original to the genome. It cannot be known.
Why is it a fact that it is a remnant of anything. And if it can be established with certainty that it is indeed a remnant why of a retrovirus!

Is it established that ONLY remnants of retroviruses attach to a genome?

I will look at the articles when I have more time.
 
This is my point:
How do you know it is not original to the genome. It cannot be known.
Why is it a fact that it is a remnant of anything. And if it can be established with certainty that it is indeed a remnant why of a retrovirus!

Is it established that ONLY remnants of retroviruses attach to a genome?

I will look at the articles when I have more time.
From link: https://letterstocreationists.wordpress.com/2015/11/

"The genetic signature of a retrovirus in the genome is very distinctive. ERVs have common features such as the genes that code for the viral coat protein and for the reverse transcriptase that copies the viral RNA genome into DNA. The ERV DNA codes for three groups of proteins, known as “gag” (matrix, capsid, nucleoproteins), “pol“ (protease, reverse transcriptase, RNaseH, dUTPase, integrase) and “env” (subunit and transmembrane). This genetic core is flanked by long terminal repeats (LTR) sections. Finally, when the retrovirus tears open the host genome for insertion, some of the torn original host DNA is recopied on either side of the viral insert.

Here is what all this looks like for the insertion of a particular retrovirus from the CERV 30 family into the chimpanzee genome:

Insertion of a member of the CERV 30 (HERVK10) family in chimps. The insertion occurred in the LINE element present in chromosome 10 of the chimpanzee genome. The orthologous LINE element is present in chromosome 12 in humans. In chimpanzees target site duplications (ATTAT) are identified. A single copy of TSD (ATTAT, the pre-integration site) is found inside the LINE element in humans. The LTRs of the element are 99.4% identical. Source: Nalini Polavarapu, Nathan J Bowen, and John F McDonald, Identification, characterization and comparative genomics of chimpanzee endogenous retroviruses, Genome Biol. 2006; 7(6): R51 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1779541/
Insertion of a member of the CERV 30 (HERVK10) family in chimps. The insertion occurred in the LINE element present in chromosome 10 of the chimpanzee genome. The orthologous LINE element is present in chromosome 12 in humans. In chimpanzees target site duplications (ATTAT) are identified. A single copy of TSD (ATTAT, the pre-integration site) is found inside the LINE element in humans. The LTRs of the element are 99.4% identical.

Source: Nalini Polavarapu, Nathan J Bowen, and John F McDonald, Identification, characterization and comparative genomics of chimpanzee endogenous retroviruses, Genome Biol. 2006; 7(6): R51"

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1779541/
 
You raise a separate question.

(1) Do we have evidence that humans-primate share a common ancestor?
(2) What is the mechanism to explain this? That caused this? [natural selection & mutation? God/an Intelligent Designer?]

You are questioning #2. It does not change the evidence for #1.

Although, you should know that the evidence we now have from comparative genomics shows that the vast majority of mutations/changes in genomes are neutral to slightly negative in fitness (i.e., most mutations have little to no effect on the organism)
What they consider as a mutation than enhances the fitness of an organism is very, very rare. With so many places for a mutation to occur that through a random process to think a repeated series of mutations will occur to a previous mutation in an animals progeny is very, very unlikely.

One must conclude that human life was designed by an intelligent being. I call Him the God of the bible.
 
What they consider as a mutation than enhances the fitness of an organism is very, very rare. With so many places for a mutation to occur that through a random process to think a repeated series of mutations will occur to a previous mutation in an animals progeny is very, very unlikely.

One must conclude that human life was designed by an intelligent being. I call Him the God of the bible.
Endogenous Retroviruses (ERVs) are not mutations like that. Any time you get a viral infection the virus inserts its genetic material into the DNA of your cells and then uses your cell's machinery to make more copies of the virus. Your body fights it off and inactivates so it's not harmful to you, but the viral insert in your DNA remains, so these provide genetic markers that can then be compared.
 
Endogenous Retroviruses (ERVs) are not mutations like that. Any time you get a viral infection the virus inserts its genetic material into the DNA of your cells and then uses your cell's machinery to make more copies of the virus. Your body fights it off and inactivates so it's not harmful to you, but the viral insert in your DNA remains, so these provide genetic markers that can then be compared.
If you like I could post this article....or you could go read it for yourself.
 
If you like I could post this article....or you could go read it for yourself.
You need to cite published peer reviewed scientific research. AiG is not an accredited research journal. The article you posted is filled with misinformation
 
You need to cite published peer reviewed scientific research. AiG is not an accredited research journal. The article you posted is filled with misinformation
Here we go again...this is what evos say when they hit bottom..."You need to cite published peer reviewed scientific research"

Then when I do you'll say...it's only YEC's that peered review your data.
 
Here we go again...this is what evos say when they hit bottom..."You need to cite published peer reviewed scientific research"

Then when I do you'll say...it's only YEC's that peered review your data.
It's the same professional peer review process for everyone and there are plenty of other YEC scientists I know who publish legitimate research work. If you want to establish a scientific claim that is the process one must go through to do so and validate their work.
 
It's the same professional peer review process for everyone and there are plenty of other YEC scientists I know who publish legitimate research work. If you want to establish a scientific claim that is the process one must go through to do so and validate their work.
You could get a subscription to the Creation Research Society Quarterly.
 
You could get a subscription to the Creation Research Society Quarterly.
That is not a recognized scientific journal. It must be in an accredited scientific journal. I can rattle off half a dozen YEC scientists I know who do legitimate research and publish in reputable journals. That's the process. Kurt Wise, Ken Coulson, Leonard Brand, Paul Buccheim, Tom Goodwin, Robert Cushman....
 
That is not a recognized scientific journal.
If you say so. I've noticed your questions were answered....and you've switched your attack against recognized scientific journals. Well done.
 
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