I have been critiquing Dr. John Sanford’s “genetic entropy” hypothesis for some time, leveling a number of specific, and often technical criticisms against the idea.
See here for a list of links to those critiques: Reddit - Dive into anything
I’ve also debated this topic with Sal Cordova on two occasions, and further explained my critiques in video, all of which can be found here: https://studio.youtube.com/channel/UCZmhEtG-QIrmyWoW0M6TIgQ
Paul Price and Drs. Rob Carter and John Sanford of CMI have seen fit to respond to a number of specific critiques of the genetic entropy hypothesis, including several that I have made, in a recent piece “Responding to supposed refutations of genetic entropy from the ‘experts’, which can be found here: https://creation.com/genetic-entropy-defense
In this piece, they describe and respond to six specific criticisms of genetic entropy. I am specifically referenced in three of them, so I will respond to those three items below.
Comments on Style and Tone
Before getting into the specifics, I want to comment on the style and tone of this piece. Dr. Sanford, I believe, would like for genetic entropy to be taken seriously as a scientific idea. For that to happen, proponents of that idea need to meaningfully engage with critics in good faith, take the arguments seriously, and respond specifically to them.
What we see throughout this piece instead is what I read as basically that the authors are affronted that anyone would have the nerve to dispute such obviously correct ideas, along with a number of slights at critics, everything from the scare quotes in the title (‘experts’), to Dr. Sanford’s repeated accusations that the critics have not actually thought through what they are saying.
And speaking personally, I want to note that it’s pretty rich for a non-scientist (Price), a marine biologist (Carter), and a plant geneticist (Sanford) to say:
The ‘experts’ mentioned below are very well-credentialed scientists. Yet, they are not experts on the specific topic at hand. They have not spent the last twenty years studying the problem of mutation accumulation.
Mutation accumulation and fitness was one of the subjects of my Ph.D. thesis; part of my work involved a novel approach to inducing error catastrophe in populations of bacteriophages. So I am an expert in this very specific topic, thanks for asking. (That’s to say nothing of the absurdity saying Dr. Joseph Felsenstein is not an expert in population genetics, which is ultimately what “genetic entropy” comes down to.)
So let’s get into the specific responses.
1. Mutations & Equilibrium
Price, Carter, and Sanford (PCS going forward) first respond to the argument that, if we accept Sanford’s premise that all mutations have a constant fitness value (which is wrong but we’re granting it for the sake of argument), as deleterious mutations accumulate, the frequency of future deleterious mutations declines and the frequency of future beneficial mutations increases.
An analogy illustrating this dynamic might involve 10 lights that could be either red or green that change colors randomly one at a time with equal probability. If all the lights start out as red, the frequency of a change from green to red is zero. But after two lights have turned green, that frequency is now 0.2, and the frequency of red-to-green changes has declined to 0.8. Once five lights are green, the system is at equilibrium and there will be no directional trend towards either color on net. So too must be the case with deleterious and beneficial mutations, if we accept Sanford’s premises.
PCS respond to this by…responding to a different argument:
Mutation-drift equilibrium is a standard part of many evolutionary models. Given many millions of years, one would expect genomes to become saturated with mutations, reaching an equilibrium where the number of new mutations is balanced by the number of mutations lost through random genetic drift and purifying selection. (emphasis mine)
I’m not talking about drift and selection here. I’m just talking about the set of possible future mutations and how that set changes as mutations occur. They seem to acknowledge that such and equilibrium would exist mathematically (which is good, because…it has to), but then make a completely unrelated point by arguing that extinction would occur before that point.
That’s immaterial to the question. If the equilibrium exists (it does!), then Sanford’s model is wrong, because that model requires the accumulation of deleterious mutations at an approximately constant rate. So PCS can do all the hand-waving they want here, but the nature of the equilibrium is immaterial the the criticism I have leveled. If we acknowledge the equilibrium exists, then Sanford’s model is flawed.
Sanford, in his specific comments on this, does not seem to understand the critique:
Obviously, rapidly accumulating deleterious mutations do not lead to more and more beneficial mutations.
It is not the case that deleterious mutations cause more beneficial mutations. The problem (for Sanford) is that if you take his assumption of fixed fitness values for each specific mutation at face value, then as deleterious mutations occur, the universe of possible future mutations necessarily shifts in favor of a higher frequency of beneficial mutations, and this necessarily reaches an equilibrium point at which the rates of beneficial and deleterious mutations are equal. At that point, deleterious mutations no longer accumulate.
So, on this first point, PCS don’t really address the critique, but obliquely acknowledge that it is valid (i.e. that such an equilibrium exists) before moving to the nature of that equilibrium, which is immaterial to the critique.
2. Natural selection equilibrium
The next critique they address is that, as deleterious mutations accumulate, fitness will be affected, which means those mutations can be selected against. Which means the population will not experience infinite and terminal deleterious mutation accumulation without selection operating.
PCS say that “This is essentially the ‘mutation count’ hypothesis.”
No it is not. It’s not a question of the number of mutations. It’s a question of the cumulative fitness effects of those mutations. The only way for selection to not operate on a population in which deleterious mutations are occurring would be for the relative fitness of every individual to be the same (i.e. for population-wide relative fitness to be 1). That is simply unrealistic; mutations and their fitness effects are probabilistic; it is not reasonable to posit that the accumulation of unique sets of mutations within individuals in a population will have exactly the same effects on absolute fitness in every individual. But that is what is required for selection to be unable to operate. Which means that is what is required for genetic entropy to be correct.
Sanford goes on to invoke interference between mutations making selection for or against any one mutations all but impossible, but he ignores that individual mutations are not selected; genomes, i.e. combinations of mutations, are selected for or against. The only requirement for selection to operate is that some genomes are more fit than others, meaning there are differences in relative fitness. If that is the case, then by definition selection is operating. For this to fail to occur, Sanford’s model requires completely unrealistic uniformity of mutation fitness effects.
On points 3-5
I was not specifically referenced in responses 3, 4, or 5, so I’m not going to respond to each at length. I do want to note, though, that part 5 references junk DNA, and Dr. Sanford seems to be of the opinion that there is little if any junk DNA in the human genome, which is simply not a serious position to take. Even ENCODE’s follow-up work to their well-publicized 2012 paper has shown that the human genome is largely non-functional (see, for example, their 2014 follow-up). But that’s neither here nor there, so onward to part 6.
6. Allegations regarding the research into the H1N1 virus by Sanford and Carter
The problems with C&S’s 2012 H1N1 paper (A new look at an old virus: patterns of mutation accumulation in the human H1N1 influenza virus since 1918 - PubMed) are myriad. They claimed fitness declined, but didn’t measure fitness directly. The two proxies they used, virulence and codon bias, are completely inappropriate as measures of viral fitness. They ignored pandemic dynamics and the different selection pressures imposed by intrahost and interhost competition. They asserted with no evidence that the mutations they documented were responsible for the changes in virulence, and further asserted with no evidence that these mutations “attenuated” the virus in some way (i.e. disrupted its replication mechanisms in such a way that hampered its ability to reproduce). Oh, and for good measure, the virus they claim went extinct continues to circulate.
But putting all of that aside, here we’re talking about a different problem: That for the purposes of documenting mutation accumulation in the 1918-2009 H1N1 lineage, C&S used as a reference strain a 2009pdm H1N1 genome. “pdm” here stands for “pandemic”, as in the 2009 H1N1 pandemic.
The problem is that the 2009 pandemic H1N1 lineage was unrelated to the 1918 H1N1 lineage. They do not share common ancestry as H1N1 in humans. The 2009 strain was the result of reassortment between several swine and avian influenza strains and human H3N2. So the differences between the 2009 strain and the 1918 lineage are due to recombination, not point mutations. So you can’t just count all the differences and say “relative mutation count” – a huge chunk of those differences were from a different process, and in any event, you can’t just treat two different lineages as though they are a single lineage.
PCS show part of an alignment to defend their conduct, but actually illustrate the problem:
Here is a screen shot of one of the worst sections in the alignment. This is part of the hemagglutinin (HA) gene. Strains from 1918 through 1936 are shown. The human and swine H1N1 reference genomes are also there. We see one three-letter deletion (keeping the downstream codons in-frame) and many single-nucleotide changes. There is no evidence for large-scale rearrangements, either within or among the eight segments of the H1N1 genome.
Yes, because 1918 to 1936 reflects a single lineage, and nobody has said otherwise. The problem is the 2009 pandemic clade, which is distinct from the 1918 lineage. I’m not sure why PCS thought the above quoted paragraph would address that problem.
When you do this correctly, you actually have to detect and remove recombinant and reassorted sections from your genome alignments, so the recombination doesn’t mess with your mutation calculations. There are lots of ways to do that, but despite PCS saying everyone involved was well aware that reassortment occurred, they didn’t do anything about it! Just treated those differences like any other mutations, which…no! You can’t just do that.
So the mutation counts, a foundation of that paper, are wrong.
Comments on Sanford and Carter’s Concluding Remarks
Let’s finish by looking at their concluding remarks, which I will quote in full:
In reviewing the many attempted rebuttals from these various evolutionist experts, a few general observations can be noted. First, it often takes a lot of ‘doing’ to get any straight or direct answers as to why they reject Genetic Entropy. Second, we rarely see any evidence that these detractors have actually read Dr. Sanford’s book (as many of their objections are dealt with in the book itself) or any of the papers that have come via Mendel’s Accountant. Third, it is clear they oppose any challenge to Darwinism in principle. They take it as their ‘Primary Axiom’ and consider it unassailable. Finally, it is impossible to miss the fact that, even among the experts, there is no consensus as to why Genetic Entropy is supposed to be wrong. If you ask ten experts why they reject it, you’ll likely get ten different answers, often that contradict one another. This really is a huge ‘Achilles’ heel’ for evolutionary theory! Real science disproves Darwinian speculations. Attempts to show God’s design is not needed to explain the diversity of life on our planet all fall short.
The two words for this paragraph are “gratuitous” and “unprofessional”. Accusations that critics are deliberately unclear, accusations that we haven’t read Dr. Sanford’s book, accusations that the objections are just knee-jerk defenses of “Darwinism” (Aside: “Darwinism”? What year is it?). And wow different people raise different objections? Yes. That’s because there is so much wrong with genetic entropy, different people will point out different problems, any one of which fatally undermines the idea.
Conclusion
The takeaway here is that this does not read like a serious attempt to engage with the specific, technical critiques of the genetic entropy hypothesis. If PCS were interested in this idea gaining widespread acceptance within the scientific community, the way to do that would be to engage with critics, and make a concerted effort to address their concerns. You can convince me I’m wrong by showing that my math is wrong, not by saying I haven’t thought this through and probably haven’t even read the book I’m critiquing.
But I suspect PCS are not interested in such conversations. I reached out to CMI to invite Mr. Price, Dr. Carter, and/or Dr. Sanford for a conversation about this response. I think face-to-face conversations are the most productive for things like this because we can clarify points of misunderstanding in the moment. None of the authors were interested in such a conversation, despite Mr. Price publicly debating this very topic on YouTube recently. I don’t know what to make of that accept that while PCS seem happy to promote their ideas to nonscientific audiences there seems to be a reluctance to engage with actual scientists in the relevant fields (or perhaps I should have invited the authors for a debate, instead). Of course, nobody is under any obligation to engage with anyone in any specific way, but if PCS ultimately want this idea taken seriously by scientists, they are making odd choices in terms of how they are going about it.