Saturday, 3 June 2023
On confirmation bias re: genetic evidence for Darwinism
BioLogos and Vitellogenin Genes
Recently I have been responding to several articles by evolutionist Dennis Venema. Venema has made various arguments about how genetic evidences strongly support evolution and I have provided rebuttals to those claims. For instance, I explained Here that while Venema discusses evidences that are consistent with evolutionary expectations, he does not list or mention the substantial body of scientific findings that are inconsistent with evolution. This is a problem with the evolution literature: the scientific evidence is too often selectively presented. In fact, I have often seen evolutionists claim that there are no contrary evidences, and that the science fully backs evolution. This sort of confirmation bias presents a roadblock to meaningful discourse on the topic of origins.
Next Venema focused his claim on the specific case of human evolution, and the similarity between the human and chimpanzee genomes. Again, Venema made high claims about the evidence. He concluded: “These observations strongly support the hypothesis that our species arose through an evolutionary process.”
But, in fact, as I explainqed Here, there are several significant problems with this claim. For example, the chimpanzee and human genomes have differing patterns that do not fit evolutionary expectations. There is also a big difference between viruses in the genomes of humans and the other primates. Again, these differences do not fit the expected evolutionary pattern. Furthermore, the chimp-human genome beneficial differences are few and appeals to alternate splicing differences (another big difference between the genomes of humans and the other primates) to evolve humans lead to astronomically improbable pathways.
As always, I explained that the point is not that evolutionary explanations are not possible. Speculative explanations are always possible. Perhaps evolution did this, perhaps it did that. But that does not change the fact that the primate genomes do not “strongly support the hypothesis that our species arose through an evolutionary process,” as Venema and the evolutionists claim.
Next Venema focused even more narrowly on a particular genetic detail: human chromosome two, which he presented as a powerful example of an evolutionary confirmation. And yet as I explained here, not only did Venema not mention several scientific problems with his claim but the claim, even if true, would not demonstrate evolution as evolutionists claim. There is no evolutionary relationship revealed. Even if evolution were true, these data would give us no evidence for it. What was disturbing about this example was Venema’s recounting of a deceptive lecturing strategy he uses in presenting this topic in his class.
Next Venema presented pseudogenes which Venema argued are powerful and compelling evidences for common descent. It is, explained Venema, “one of the strongest pieces of evidence in favor of common ancestry between humans and chimpanzees (and other organisms).” And again, I explained, here and here, that there are several, fundamental, problems with this evolutionary claim.
In this case, however, Venema discussed his underlying religious belief that this evidence is a problem for creationism type theories. Venema was highlighting one of the important beliefs at the foundation of evolutionary thought. This belief, if true, does indeed require evolution to be true. But of course it is not falsifiable.
Vitellogenin genes
Now we move on to Venema’s next Topic , the vitellogenins. Vitellogenin genes are found in a wide range of species and, like most genes, perform multiple functions including helping to provide the nutrients in egg yolks. Also like most genes, the pattern they form amongst the species does not always correspond very well to the expected evolutionary pattern. Of course there are always explanations, and evolutionists draw upon a variety of mechanisms, including lineage-specific events, to explain the vitellogenin genes.
For example, this paper focuses on mosquito vitellogenin genes. It concludes that the genes arose by a series of duplication events, and that the pattern of duplication was different in each mosquito genus. The Paper also uses purifying selection, gene conversion, unequal crossover, and concerted evolution to explain the observed pattern of the mosquito vitellogenin genes, and concludes that these mechanisms must have also worked, independently, in other invertebrate species, and vertebrate organisms as well.
Similarly, this Paper examines the evolution of vertebrate vitellogenins and also draws upon a variety of events and lineage-specific mechanisms. As I have discussed many times, while the basic idea of evolution is that the species share common designs as a consequence of common ancestry, in fact biology is loaded with unique, one-off designs for which evolutionists need to appeal to “lineage-specific” evolution. Consequently evolution can explain a wide variety of observations and patterns, and this applies equally well to the vitellogenins.
Clearly evolutionary theory is fine with a range of patterns when it comes to the vitellogenins. Of course this is true for molecular, and morphological, designs in general, as we have seen many times. Designs can fall into an evolutionary common descent pattern, or not.
The advantage of this flexibility is that evolutionary theory can explain a wide range of observables. The disadvantages, however, are many. The theory becomes less parsimonious. It becomes more resistant to falsification. And it loses its evidential arguments. If a theory can explain A, and B, and C, … and so forth, then the finding of A is hardly compelling evidence for the theory.
Yet this is what Venema argues. The vitellogenin genes in chickens share a weak similarity with corresponding genetic segments in humans. Evolutionists view the human segments as pseudogenes—broken versions of vitellogenin genes inherited from their egg-laying ancestors. Given this vitellogenin similarity between humans and chickens, for example, evolutionists such as Venema incredibly conclude that, therefore, humans and chickens evolved by random mutations from a common ancestor. Not only does that not follow, but it takes Venema to the unlikely solution of random mutations creating humans and chickens, and of course all the other species.
Venema also argues that the similarity of the vitellogenin genes between humans and chickens extends to, and is all the more confirmed by, their positioning within their respective genomes. But this argument from synteny is no different from what we saw above. When there is a loss of synteny evolution is not harmed, and the theory has another set of explanatory mechanisms available for just about any outcome. If the vitellogenin genes had been in a different order, evolution could have explained it just fine.
Affirming the consequent
In spite of these problems with his argument, Venema is enthusiastic about this evidence. In fact his enthusiasm leads to the fallacy of affirming the consequent, as he equates shared synteny (genes with similar positioning in the genomes of different species) with common descent
This evidence increases our confidence that we are indeed looking at regions with shared synteny: in other words, a region in two present-day species that was once a region in the genome of their common ancestral population.
That is a fallacy. Ignoring the problems discussed above for the moment, even if evolution did make a hard prediction of shared synteny, and even if it was universally observed, that would not prove evolution. In that case, you would have a confirmed prediction. That is good, but it is not equivalent to a finding of evolution. Venema violates this scientific fundamental when he defines shared synteny as “a region in two present-day species that was once a region in the genome of their common ancestral population.” Unfortunately, affirming the consequent is not uncommon in the evolution literature.
Primeval tech continues to troll Darwinism.
Engineering and Evolution in the Microbial World
This year’s Conference on Engineering in Living Systems (CELS) is going on right now, exploring design principles at work in living things. In case you couldn’t be there, we pulled this classic ID the Future episode from the archive. Host Jonathan Witt gives us a behind-the-scenes interview with Dustin Van Hofwegen, a biology professor at Azusa Pacific University in California. The occasion was a previous Conference on Engineering in Living Systems. The two discuss the event, which brought together biologists and engineers to study how engineering principles and a design perspective can and are being applied to biology — to plants and animals but also to Van Hofwegen’s area of focus, the realm of microbial biology. The two move into a conversation about Van Hofwegen’s article in the Journal of Bacteriology, co-authored with Carolyn Hovde and Scott Minnich, based on research they did at the University of Idaho.
As Van Hofwegen explains, the research focused on one of the most ballyhooed evolutionary changes to come out of Richard Lenski’s long-term evolution experiment, a decades-long study of many thousands of generations of E. coli bacteria. Perhaps the biggest evolutionary development in the course of the experiment involved some bacteria beginning to feed on citric acid. Interesting, to be sure, but as Van Hofwegen explains, E. coli already has this capacity; it’s just a matter of switching it on. Van Hofwegen, Hovde, and Minnich demonstrated this through do-or-die experiments with E. coli, which led to the bacteria developing the capacity not in years or decades, as in the Lenski experiment, but in 14 days, that is, in as little as 100 generations. Van Hofwegen explains why this is an embarrassing result for neo-Darwinism. The pair conclude with a discussion of another study on antibiotic resistance with a similar result, that the resistance observed came not by evolving anything new but by tweaking something already present. Download the podcast or listen to it Here
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