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A Tale of Three Creationists, Part 3

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February 7, 2011 Tags: Genetics
A Tale of Three Creationists, Part 3

Today's entry was written by Dennis Venema. You can read more about what we believe here.

Reasons to Believe, Scurvy, and a (Guinea) Pig in a Poke

After the recent exchanges between Fazale Rana of Reasons to Believe (RTB) and myself, I had intended to move on to other important issues. However, Rana’s final response to my critique is so inaccurate - and so badly misleads his audience - that to not reply would be irresponsible. There is no room for a “pig-in-a-poke” in science or the church.

If you have been following this series, you will know that one of the strongest pieces of evidence in favor of common ancestry between humans and chimpanzees (and other organisms) is a large number of “broken” genes, otherwise known as pseudogenes. When they are damaged in exactly the same way and exactly the same spot in closely related organisms, by far the simplest explanation is that they are copies of a single gene that was damaged in a common ancestor.

One way of illustrating this is to think of a 25 page manuscript: pretend that there is a mistake of one letter out of the 75,000 letters. Let’s say that a “g” had been inadvertently removed from the word “missing”, so that it now reads “missin.” Now let’s say that you collect 10 copies of this manuscript from various people and five of them have exactly the same mistake—the word “missing” on page 22, line 15, word 7, is spelled “missin” instead of missing. Every one of the other 74,999 letters in the 25 pages is perfect. Would you not conclude that the five identically mistaken manuscripts are derived from a single source? Would you not have to strain very hard to come up with an alternative explanation?

Rana is similarly desperate. The RTB model—based as it is on their specific interpretation of scripture— requires that they find an alternative to the common descent model overwhelmingly accepted by biologists. Rana feels a need to respond to pseudogene evidence since it so powerfully supports the creation of humans through an evolutionary process. The fact that different mammalian species, including humans, have many pseudogenes with multiple identical abnormalities (mutations) shared between them is a problem for any sort of non-evolutionary, special independent creation model. The fact that shared mutations are present in patterns that match other independent lines of evidence such as sequence identity (see here and here) and shared synteny (see here) only makes matters worse. The data from these different areas are congruent and I am not aware of any paper in the peer-reviewed scientific literature that attempts to argue for a non-evolutionary interpretation of these data.*

The topic of Rana’s rebuttal is a single portion (termed the tenth exon) of a single pseudogene, the GLO pseudogene, which, when not broken, makes an enzyme required for vitamin C biosynthesis. In “dry-nosed” primates (a group which includes humans,) this gene is “broken.” It is because of this that we get scurvy if we do not ingest enough vitamin C in our diet. Many of the mutations in the GLO pseudogene are shared between humans and other primates, indicating that these mutations have been inherited from a common ancestor. The only other possible explanation is that a large number of identical mutations occurred independently in many species – something so improbable as to be not worth considering. Yet this is exactly the strained interpretation that Rana chooses to argue for:

Comparison of the rat’s exon X (10th exon) DNA sequence with those in humans, chimpanzees, and orangutans reveals a number of the same mutations in the same locations for the primate sequences. Of particular significance is position 97 in which it appears as if a deletion took place in the primate sequences. Evolutionary biologists argue that this deletion and the other shared mutations are clear evidence for common ancestry, with these changes having occurred before apes diverged from Old World monkeys.

The RTB genomics model offers a different explanation for the similarities in the primate DNA sequences. The shared features are interpreted as the outworking of nonrandom, reproducible changes that happened independently in humans, chimpanzees, and orangutans.

Rana then goes on to claim that there is empirical evidence for the RTB view. The GLO gene is also a pseudogene in guinea pigs, but this species lost GLO function independently of the primate common ancestor. Not surprisingly, the mutations in the guinea pig pseudogene are different from those in the primate pseudogene, but Rana claims that there are a few shared mutations between primates and guinea pigs in exon X:

Support for this interpretation comes from comparisons of the primate exon X sequences with the corresponding region of the guinea pig GLO pseudogene. The structure of the guinea pig GLO pseudogene is dramatically different than that of the human pseudogene. Presumably, guinea pigs and primates lost this gene independently. If mutations were random, then few if any of the changes in the primate and guinea pig exon X sequences would be the same. Yet, as biologist Peter Borger points out, fifty percent of the mutations in the primate and guinea pig exon X sequence are identical. In addition, the guinea pig exon X region shows a mutation at position 97, the location in the primate genomes where a deletion took place. These shared features could not have resulted because guinea pigs and primates shared a common ancestor. Instead, they must reflect nonrandom, reproducible changes.

In other words, the RTB genomics model can reasonably account for the shared features of the GLO pseudogene in primates without resorting to common ancestry as the explanation.

There are several problems with this argument, but none would be apparent to a non-specialist. On the face of it, it seems like a strong case. If indeed there are shared mutations in two independent gene-to-pseudogene conversion events, it would lend (some) credence to Rana’s assertion that all shared mutations are the result of non-random events. The GLO pseudogene sequences in question are as follows. At six sites (in yellow) the human and guinea pig sequences match each other but differ from the rat (purple). The anti-evolutionary source Rana cites (PDF) claims that these sites are the result of independent mutation to the same nucleotide. (Position 97, which has a single-nucleotide deletion in humans and other primates, is shown in blue.)

Despite Rana’s insistence that there is only one possible explanation for this pattern, there are two possibilities. The possibility that Rana does not discuss is this: the human and guinea pig sequences match because they are not mutations, but rather the original ancestral sequence of the functional GLO gene that was present in the last human – guinea pig common ancestor. This would make the rat sequence at these six positions the mutations, not the human / guinea pig sequences. There is a simple way to test this hypothesis, of course: examine the GLO sequence of other mammalian species in this region. If many other species match the human and guinea pig sequences, then we know this sequence is the ancestral sequence. If many other species match the rat sequence, the rat sequence is ancestral and the evidence supports multiple independent mutations in the primate and guinea pig lineages. Unfortunately for RTB, even a cursory examination of other species in this region demonstrates that the human / guinea pig sequence is ancestral. At each of the six positions, the consensus sequence matches the human / guinea pig sequence. The so-called “shared mutations” are not mutations at all:

The RTB model thus has no support for the proposal that shared mutations observed between species are the result of non-random, parallel mutation events. As such, Rana’s assertion that the RTB model adequately accounts for shared mutations in pseudogenes is incorrect. Unitary pseudogenes with shared mutations remain an insurmountable problem for RTB.

Beyond the scientific flaws in this argument, what I found troubling about Rana’s response is that this analysis I have presented here is nothing new – it has been known for years (see for example here and here). Rana should have known about this. But even if he didn’t the fact remains that it would have been easy for Rana to test the claims himself. For example, I assembled the alignments in this post using public databases and search tools freely available on the web. (It would have been possible simply to use figures presented elsewhere, but I wanted to (a) confirm the data myself, and (b) ensure that the relevant sequences have not been updated with corrections in the last few years). If I can do this, Rana should be able to do so as well, especially before presenting flawed arguments to non-specialists (such as RTB supporters or public in general) who will take him at his word.

As the young earth creationist, Todd Wood, pointed out in the conclusion to his recent series on RTB, the reasons behind this unfortunate pattern in RTB scholarship are somewhat irrelevant. What matters is that believers know that until RTB makes amends, their model is untrustworthy. Indeed, if RTB had developed a scientifically credible model to explain shared pseudogenes from an anti-common descent perspective, Todd Wood would be very interested (since he, being a young earth creationist, does not believe in common descent). Todd’s view of the RTB model, however, agrees with mine - and he too has called on RTB to correct their errors:

Venema and I have documented a sad but consistent and ongoing pattern of erroneous summaries of published works on the part of RTB (Rana and Ross, but mostly Rana).There's really no way to deny these mistakes have been made or to explain them away, so what are you going to do about them? I recommend apologizing for the mistakes, correcting them if you can, and instituting some kind of serious fact-checking filter on everything you publish…

As far as I'm concerned, RTB's credibility is completely shot. I would recommend that no one accept any of RTB's arguments without fact-checking their claims first. I do not know whether these problems are due to lazy scholarship, ignorance, intentional deception, or ideological blinders. What I do know is that you cannot trust Reasons to Believe.

Hopefully in the coming days RTB will follow Todd’s advice. Please, Dr. Rana, for the sake of RTB’s followers (and the church as a whole), let your audience know that you have made a mistake. Let them know that the RTB model is flawed. Admit that it misrepresents well-established science. Then start the work of making it right. This, after all is how real science works. We admit when old ideas don’t work anymore and we move on.

I would also suggest that you surround yourself with people who have expertise in this area of biology. Please have your ideas thoroughly vetted by those who know the field. As your brother in Christ, I would be happy to work with you in arranging that. While I cannot speak for Todd personally, I have every confidence that he too would be willing to help with an honest overhaul of the RTB model. Without that (significant) overhaul, however, the RTB model is a (guinea) pig in a poke. Caveat emptor.

* - “I previously stated in this post that I was convinced that no geneticist at a secular, research university would see this data differently. I have now received what I consider reliable information that this is not the case, but rather that there are at least a few biologists at secular institutions who privately hold to a young earth creationist view. As such, they do see the data differently, though for religious reasons. I should have been more clear: I am convinced that there is no biologist at a secular institution who objects to a common ancestry interpretation of these data for scientific reasons. Certainly, if there is such an individual, they have not made their case in the scientific literature, the proper place for contesting current scientific consensus.”

Dennis Venema is professor of biology at Trinity Western University in Langley, British Columbia. He holds a B.Sc. (with Honors) from the University of British Columbia (1996), and received his Ph.D. from the University of British Columbia in 2003. His research is focused on the genetics of pattern formation and signaling using the common fruit fly Drosophila melanogaster as a model organism. Dennis is a gifted thinker and writer on matters of science and faith, but also an award-winning biology teacher—he won the 2008 College Biology Teaching Award from the National Association of Biology Teachers. He and his family enjoy numerous outdoor activities that the Canadian Pacific coast region has to offer. Dennis writes regularly for the BioLogos Forum about the biological evidence for evolution.

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Argon - #50352

February 7th 2011

The vocabulary skill-building word for today is: “apomorphy”

Gordon - #50358

February 7th 2011

The problem I have with all this (as a non believer) is that this argument between science and pseudo science is actually a false war. The existence of God and the Christian claims about Jesus are primarily theological arguments. I don’t think science can add or detract from these discussions.

In fact, I wrote an article recently called “Atheism before Darwin” which shows that in spite of scientific advances the real questions asked by real people about issues of faith have not changed:


In other words:

Christians should not rely on pseudo science to prove that the gospel is true.
Scientists should not rely on science to prove that God does not exist.

Daniel Maldonado - #51121

February 14th 2011

That all depends on your presuppositions before interpreting the evidence.  For example, by inference to the best explanation, the facts surrounding the events after the burial of Jesus (a well established historical fact, at least to the majority of scholars) point to the fact that Jesus actually resurrected from the dead.

If you have presuppositions that exclude including a possible supernatural event in history, then you will obviously fail to use “God rose Jesus from the dead” as an explanation, regardless of how ridiculous some of the alternative explanations postulated by critics (i.e., Jesus’ followers were taking drugs and hallucinating, Jesus had a twin brother)

Berend de Boer - #50362

February 7th 2011

Peter Borger visits the whole argument in this paper: http://aufiles.creation.com/images/pdfs/tj/j21_3/j21_3_118-127.pdf

Dennis Venema - #50363

February 7th 2011

Hi Berend,

Thanks for that link to that paper. I find it interesting that Borger has shown that his previous conclusions were incorrect, published a paper discussing them, and yet we see Rana using his original paper as if it were correct.

A quick skim of the new paper shows that Borger is still reaching for a non-evolutionary explanation. His proposals don’t work, unfortunately - they’re pretty stained and ad hoc, as far as I can see from a quick skim - and there are several statements in the paper that make me wonder if he truly understands evolutionary theory at all.

I’d also like to thank Darrel for quite a bit of editing work on this piece. It’s listed as authored by me only, but Darrel had a significant hand in shaping parts of this. Divining what is Darrel and what is me is left as an exercise to the reader.

Berend de Boer - #50368

February 7th 2011

Thanks for the quick response Dennis. I find Peter’s argument pretty convincing I must say.

Let me address your “stained and ad hoc” by quoting you on something I actually know something about: “Every one of the other 74,999 letters in the 25 pages is perfect. Would you not conclude that the five identically mistaken manuscripts are derived from a single source? Would you not have to strain very hard to come up with an alternative explanation?”

Perhaps in precisely this case, but certainly not if there are more shared mistakes. I’m currently engaged in doing exactly this kind of thing: determining the shared history (if any) of a single electronic text. Doing what you do, assuming that an identical difference is due to shared ancestry doesn’t work. The same input methods, scanners for example, tend to produce the same kind of errors. People using the same word processor or spell-checker also generate the same errors, and with other techniques you can show there is no common ancestry, and sometimes you simply know the ancestry.

So if your technique doesn’t work for the case you highlight as THE example, does it work in biology?

Dennis Venema - #50373

February 7th 2011

Berend, are you familiar with textual criticism? It’s basically the same issue for comparative genomics.

As two texts share more and more errors in common, it is less and less likely that those shared errors were independently introduced to the text. It becomes harder and harder to argue that the two texts are not related by some form of copying (one from the other, or both from a common source).

In biology, there is no evidence that the types of nested patterns that we see in nature can be explained by non-random events that lead to the same mutations occurring over and over again in unrelated organisms. (If there was such evidence, you can be certain that Todd Wood would be very interested in it!)

Even if there WAS evidence for something along these lines, you’d have to explain why this supposed non-random mechanism only produces mutations in a nested hierarchy that every other line of evidence we have also matches. Anti-evolutionary creationists need to explain the pattern of evidence we have - a congruent and compelling pattern.

Common ancestry is a very simple and compelling explanation for the pattern that easily makes testable predictions (that continue to be supported by new genomics evidence).

pluribara - #50885

February 12th 2011

It has always been tacitly assumed that mutations are randomly introduced in a DNA sequence. Most likely they are not. They might be introduced in DNA sequences as a function of that sequence. Of course, this extraordinary claim requires extraordinary evidence…

The incidence of molecular homoplasy is much higher than expected from theoretical considerations and this already hints at a non-random accumulation of point mutations.

In addition, in environments with natural high radiation most of the mutations fall at known hot spots.

That is rather extraordinary. 

If we see an organism as a whole, and not merely reduce it to a “bag of genes”, we start to realize that the unique genes found in organism falsify universal common descent. Hence, the alignment of mutations often observed in intraspecies comparisons can only be explainded as homoplasies: non-randomly accumulated point mutations.

GUToB holds: We cannot discern between alignments caused by common descent and those caused by common mechanisms.


Jarrod - #50400

February 7th 2011

Interesting article Dennis. I appreciate your passion and desire for scientific and intellectual integrity.

You lost me with your interpretation of the evidence at one part (or rather, I’m assuming that you are familiar with data that non-specialists would not be). Here’s this part:

“If many other species match the human and guinea pig sequences, then we know this sequence is the ancestral sequence. If many other species match the rat sequence, the rat sequence is ancestral and the evidence supports multiple independent mutations in the primate and guinea pig lineages.

I am having difficulty seeing how RTB’s model and the standard evolutionary model cannot end up being empirically equivalent in this instance. You seem to be saying that, if it is a non-random mutation, then the mutation should be absent from SOME mammals sharing common ancestors with humans/guinea pigs. While this would falsify the common ancestry interpretation, the lack of this variability seems irrelevant to RTB’s interpretation. Indeed, the variation in this mutation should depend on whatever non-random factors purportedly fix it. Am I missing something? Thanks for your time.

Marshall - #50415

February 8th 2011

I think the issue is that Dr. Rana’s interpretation is that those particular mutations happened twice, once in the guinea pig lineage and again in the primate lineage. Since the mutations are identical, this would falsify the nested hierarchy.

What Dr. Venema pointed out is that they are easily explained as happening once in the rat lineage since its divergence from guinea pigs. Then, at these locations, primates and guinea pigs should also match most other organisms that have this gene, regardless of whether it is functional. The data presented show that this is the case.

RTB’s model obscures this obvious solution by implying the rat gene is the pristine original without any mutations since it is functional. However, rats would accumulate mutations in this gene as well, but they would be mutations that are either silent (a change in “spelling” without changing the amino acid coded for) or generally neutral. A further test would be to see if this pattern holds for these particular mutations. If the mutations happened twice in genes that were already nonfunctional, there would be no such constraint. (Maybe someone who, unlike me, has biology education beyond the high school level could look into that!)

Jarrod - #50405

February 7th 2011

I apologize if I have multiple posts; my comment is not showing up.

I’ve been re-reading the article, and I’m going to try to better articulate my question.

Psuedogenes provide a defeater for a model like RTB’s. To counter or undercut a defeater, one must simply offer a logically possible way out, which Rana seemed to do. Based on your response to Berend, it seems that you are saying that, given the number of psuedogenes and the lack of an identified mechanism for these non-random mutations, belief that non-random variations account for psuedogenes such as these is unwarranted. Thus, although the deductive argument has been undercut, the inductive argument against RTB’s model still stands strong. Is that accurate? Thanks again for your time.

Argon - #50407

February 7th 2011

pg 124 of the Truman & Borger paper:
We would prefer to make predictions based on a thorough knowledge of design factors and not simply on visible morphologies, but we are unfortunately still far from being able to understand cell complexity at a sufficient level to allow us to do this. A creation scientist is not strictly forced to expect similar genetic features in chickens and ducks, for example.

That pretty much sums up the problems inherent in creation models: No reason to expect nested hierarchies.

Dennis Venema - #50417

February 8th 2011

Hi Jarrod,

I’m not sure I fully understand what you’re asking, but here’s a stab at a reply:

Shared mutations in pseudogenes are very easily explained by common ancestry - that these multiple shared errors were copied from a common source (the common ancestor of the two species). The fact that mutations are present in “nested hierarchies” (google it, the wikipedia article may help) fits with common ancestry.

Rana / RTB recognize that this is powerful evidence for common ancestry, including for humans.

RTB would thus very much like to find a plausible alternative explanation for shared mutations (as would any antievolutionary creationist). So far, no plausible explanation has been put forward. This attempt by Rana is especially poor, since what he claims are “shared mutations” are in fact the starting sequence in the human/GP common ancestor. So, not only has RTB not refuted the evidence, they’ve provided (even more) evidence that they are not competent in this area of biology (and I say that merely as the plain facts, not with animosity).



Gregory - #50420

February 8th 2011

“Borger is still reaching for a non-evolutionary explanation” - Dennis Venema

Is that a problem in some academic fields, if not in others? I’ve been ‘reaching for non-evolutionary explanations’ for a decade now. The fruits of this in the fields of my scholarly work are abundant & undeniable. I applaud scholars who are looking for unconventional answers to scientific questions & do not accept that ‘evolution’ is an ‘end-in-itself’, outside of which no knowledge is possible.

T. Dobzhansky’s confusions & errors about agency, culture & language seem to be willingly perpetuated in Venema’s evolutionary creationism.

It is interesting that Venema is now using the term ‘antievolutionary creationist.’ This would supposedly be in order to counter-position himself as an ‘evolutionary creationist,’ which is the point of this series.

I still have not heard anything about Venema introducing his ‘creationism’ into biology, i.e. not just at a private Christian university, but into the greater & wider global Academy. Perhaps that is reserved for later posts in the series.

Gregory - #50421

February 8th 2011

“Bubbles are evolutionary” - Wall Street 2: Money Never Sleeps

pluribara - #50427

February 8th 2011

The joke is: molecular phylogeneticists are analyzing hot spot mutations!

As long as nobody is able to address the genetic novelties (miRNA genes for meta-regulation) in the human genome, the non-random mutation-explanation I proposed in the J Creation (2010) is superior.

The Darwinians never excluded the possibility that, in actuality, they could be studying mutations that are generated due to a similar mechanims, which then gives an illusion of common descent. They study homoplasies (!) instead of common descent.

Worse still,

E = Common Descent + Modification cannot be falsified.

How can we falsify a hypothesis that proposes all common traits of organisms are due to common descent (CD), whereas all traits that are not due to CD are modifications (M)?

And Natural Selection (NS) = flogiston (it kan have all possible values, ranging from negative via neutral to positive).

E(NS) = CD + M = non-science.

Darwin invented the greatest pseudoscience ever. There is no scientific reason whatsoever to believe in the prophet and his beard. 

Have a nice day,

Peter Borger

pluribara - #50428

February 8th 2011

And of course I solved the

....a well kept Darwinist’s secret.



will historically be remembered as the science stoppers of the 20th century.

Endogenous Retroviruses are nothing but

and degenerate remnants thereof, which easily transform in RNA viruses (read my series of articles in the science journal J Creation 2009). Together, this explains diseases as secondary, recent genetic events.


Peter Borger

pluribara - #50429

February 8th 2011

. The fact that different mammalian species, including humans, have many pseudogenes with multiple identical abnormalities (mutations) shared between them is a problem for any sort of non-evolutionary, special independent creation model.

The error in thinking stems from the creed that the major part of mutations occurs at ranodm in a DNA sequence. We know now that this is scientifically untenable. There are hot-spots, super-hot-spots, cold-spots and super-cold-spots. Where do we get an alignment of mutations when species are compared? Exactly here!

They line up and create an illusion of common descent!

Our paper was one of the first in depth analyses of the GULO gene. We pointed out both creationists and evo-illusionists were wrong. We argued for a non-random mechanism of mutation-generation. That was the message of our paper. Wasn’t that clear?

In 2010, I published a paper in JoC that provided more arguments to back up our earlier claim.


pluribara - #50434

February 8th 2011

The problem of the followers of Darwin is that they are completely fooled by similarities.

If we want to make a compelling decision about common descent, however, why would we look at similarities or homologies at all?

I prefer to look at the differences, and what we find in the human genome relative to chimps is compelling evidence against common descent.

First, the quantitative difference is huge (up to 15% if we are to include the whole genome sequence). Second, there is an qualitative and specific difference in the recently discovered regulatory miRNA (and other) genes.

If followers of Darwin are able to address the origin of these genes, they would have a point. If they don’t, the most parsimonous explanations for an alignment is a common mechanism, not common descent.

Anaway, a holistic view on biology systems obliterates Darwins hypotheses. That’s how it is. I cannot change that.


pluribara - #50438

February 8th 2011

What most redunctionists don’t realize is that biology is built of systems that operate as 3-dimensional systems, called hierchical networks. These networks make up an even greater network of thousands of nodes working togehther. The effect is redunancy and back up systems that easily substitute for each other.

Individual nodes are not required to let the biological system work as a whole.

Natural selection is NOT acting to preserve individual nodes…it cannot even do that! it is only capable of preserving networks as a whole.

The discoveries of systemsbiology makes Darwian evolutonary biology driven by natural selection absolutely falsified. There is no doubt about that. Creation is the only remaining possibility. In my dutch book (Terug naar de Oorsprong; Darwins Revisited), I propose a novel theory that explains biology as it is.

An english version of my book is available. All it requires is a publisher.



Argon - #50456

February 8th 2011

Peter Borger (pluribara - #50427): The joke is: molecular phylogeneticists are analyzing hot spot mutations!

This seems to be a theme in the creation literature: Mutations aren’t random, they’re ‘pre-programmed’.

Every mutation can’t be at a hot spot. And even hot spots don’t necessarily obliterate all historical signals. Good researchers analyzing molecular phylogenies are well aware of potential problems with variable mutation rates and do take pains to identify and evaluate these effects on their analyses. Consider engaging the results and misunderstandings you perceive in those same journals.

Argon - #50457

February 8th 2011

Peter Borger (#50427): How can we falsify a hypothesis that proposes all common traits of organisms are due to common descent (CD), whereas all traits that are not due to CD are modifications (M)?

That’s not the hypothesis, it’s the assumption of the hypothesis. The hypothesis is that organisms are linked by common descent. There is abundant positive evidence supporting the hypothesis (as your YEC colleague Todd Wood notes). If nested heirarchies weren’t observed or if the fossil record was more jumbled or non-existent, or if the world was thousands of years old, or if variation was never inherited , it’s possible a ‘true-believer’ might still support common descent, but it wouldn’t fly with most people. I know this is possible because we still find scientists who think the world is <10K years old. But not everyone holds doctrinally inflexible mindsets.

At one time common descent could have been considered more ‘iffy’. If Earth’s geology or life’s patterns been different it would still. Instead, as we’ve learned more it’s become one of the stronger hypotheses. My suggestion: Give up searching for ‘magic bullets’ to kill evolution and work on a positive, strong theory of creation instead.

Argon - #50462

February 8th 2011

Peter Borger: “An english version of my book is available. All it requires is a publisher.”

Paper and eBooks.

See also:

Dennis Venema - #50466

February 8th 2011

Hi Peter,

I’ll echo what Argon has said - if you want to propose a non-random mechanism that mimics the pattern predicted by common ancestry, you have to explain why it only produces these mutations in a nested hierarchy. Shared mutations come in a pattern - and this pattern was predicted by common ancestry. Finding numerous shared mutations that don’t fit the nested hierarchy would be good reason to start proposing models other than common ancestry - yet we don’t see them. What he see supports common ancestry, and very strongly so. 

Also, your work hasn’t even convinced other young-earth creationists (for example, Todd Wood, who has the expertise to evaluate it). If Todd thought your work had merit I’d be more interested in looking it over in detail.



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