Saturday, June 11, 2016

BioLogos and Vitellogenin Genes

This Problem Does Not Easily Go Away

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 explained 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.

[Ed: The opossum section has been retracted. The evolutionary explanation is more reasonable than was implied and this topic deserves its own post]

Tuesday, June 7, 2016

A New Theory Explains How Consciousness Evolved

Consciousness Arose as a Solution

Michael Graziano’s piece on how consciousness evolved in today’s Atlantic has a strange beginning:

Ever since Charles Darwin published On the Origin of Species in 1859, evolution has been the grand unifying theory of biology. Yet one of our most important biological traits, consciousness, is rarely studied in the context of evolution

Perhaps it’s just me, but how can evolution be the grand unifying theory of biology if it doesn’t explain one of the most important biological traits?

Perhaps this doesn’t bother Graziano because he is about to announce that this particular shortcoming is coming to an end:

The Attention Schema Theory (AST), developed over the past five years, may be able to answer those questions. The theory suggests that consciousness arises as a solution to one of the most fundamental problems facing any nervous system: Too much information constantly flows in to be fully processed. The brain evolved increasingly sophisticated mechanisms for deeply processing a few select signals at the expense of others, and in the AST, consciousness is the ultimate result of that evolutionary sequence.

So maybe evolution wasn’t so grand, but that is now changing. A new sub hypothesis, the Attention Schema Theory (AST), might just explain how consciousness arose. Of course by “explain” evolutionists mean something along the lines of “and then a miracle occurred.”

For example, Graziano explains that a special neuron action called selective signal enhancement “probably evolved sometime between hydras and arthropods—between about 700 and 600 million years ago.” And how do evolutionists know that? Well because arthropods had it and hydras didn’t. So it must have evolved between them. After all, selective signal enhancement had to have evolved at some point. Didn’t it?

That is often what passes for an explanation in evolutionary theory.

Then there is the part of the brain called the tectum which “probably evolved around then [520 million years ago], during the so-called Cambrian Explosion.” Because, well, why not?

One reason explanations come so easily to evolutionists is that, though the theory technically is restricted to aimless mechanisms, in fact the thinking is teleological. Look at the explanation above for example. Consciousness, the professor explains, arose “as a solution” to the problem of too much information.

As a solution for a problem? That is teleological thinking.

Somewhere Aristotle is smiling.

And again, the brain evolved increasingly sophisticated mechanisms “for deeply processing” a few select signals.

For deeply processing? That, in this strange language we call English, is another version of the infinitive form. And as we have seen many times, when it comes to origins, the infinitive form is the essence of teleological language.

Religion drives science, and it matters.

Monday, June 6, 2016

Larry Klayman: Federal Judges Are Human

Kangaroo Court

Our federal legal system has become the focus of the latest political battle and Larry Klayman has now weighed in, explaining that the federal judiciary is “politicized, frequently intellectually dishonest and in some quarters even totally corrupt.” Klayman adds that federal judges “frequently take the bench after confirmation without any training in how to be a judge.” What Klayman could have added is that such problems are not confined to the backwaters of the judiciary.

Consider Judge John Jones—exalted as one of Time magazine’s 100 Most Influential People of the Year—who unbelievably revealed that he wanted to see the movie Inherit the Wind a second time in preparation for the famous 2005 Dover case, over which he presided, because, after all, the film puts the origins debate into its proper “historical context.”

That is shocking.

Jones had been so indoctrinated by the Warfare Thesis that he actually believed the evolutionary propaganda to be historically accurate. What an incredible misconception.

Jones later reminisced about the trial, explaining that “I understood the general theme. I’d seen Inherit the Wind.”

If ever there was an example of judicial bias and a predetermined verdict, this is it.

BioLogos, Broken Genes, and Urate Oxidase

The Bigger They Come, The Harder They Fall

Arguments for evolution, the theory that the biological world arose strictly by chance and natural law, are at a high level. The details of how microbes, fish, amphibians, reptiles, birds and the rest actually were created by random mutations are hard to come by. But, evolutionists explain, the species look like they evolved. Don’t the comparisons of their anatomy, geographical locations, and so forth, make evolution the obvious explanation for their origin? One of the strongest such evidences, according to evolutionists such as Dennis Venema, are the so-called shared-errors. Meaningless or, better yet, harmful mutations found in allied species seem to be obvious signs of a common ancestor. For we would never expect such harmful mutations to have arisen independently. They must derive from a common ancestor. This argument has many problems and seems to be another example of how the stronger that an argument is for evolution, the more deeply it is flawed.

One of the problems with this argument is that it contains two suspicious, unspoken, assumptions.

First, the argument assumes that these mutations are meaningless or harmful. That assumption may well be true but, as any historian of evolutionary thought knows, it is a dangerous. The history of evolutionary thought is full of claims of bad, inefficient, useless designs which, upon further research were found to be, in fact, quite useful.

Second, the argument assumes that these mutations are random. In other words, it assumes there cannot be any common mechanisms, properly operating or otherwise, which could tend toward certain designs and mutations.

In fact convergence is ubiquitous and rampant in biology. Repeated designs appear in species so distant that, according to evolutionary theory, their common ancestor could not have had that design. So even evolutionists must agree that common designs must have arisen independently. And this must have occurred many times over, at both the morphological and molecular levels.

In other instances, such “convergence” must have occurred even in allied species. In fact this is true even for the so-called harmful mutations. For instance, evolutionists believe the urate oxidase enzyme, which catalyzes the oxidation of uric acid, was inactivated in humans and the great apes by harmful random mutations. But the different versions of the gene, in the different species, do not easily align with the expected evolutionary pattern. In fact, even evolutionists have to agree that several of the various inferred mutations, in these similar species, could not have arisen from a common ancestor. Instead, they must have arisen independently:

One exceptional change is a duplicated segment of GGGATGCC in intron 4 which is shared by the gorilla and the orangutan. However, because this change is phylogenetically incompatible with any of the three possible sister-relationships among the closely related trio of the human, the chimpanzee, and the gorilla, it might result from two independent duplications. Alternatively, though less likely, a single duplication occurred in the ancestral species of the great apes and had been polymorphic for a sufficiently long time to permit fixation of the duplicated form in the orangutan and the gorilla on one hand and loss in the human and the chimpanzee on the other hand.

The nonsense mutation (TGA) at codon 107 is, however, more complicated than others. It occurs in the gorilla, the orangutan, and the gibbon, and therefore requires multiple origins of this nonsense mutation.

In contrast, the exon 3 mutation is not shared by H. syndactylus but by the gorilla and the orangutan. The origin of this mutation is therefore multiple and relatively recent in the gibbon lineage.

In other words, when common mutations found in different species cannot easily be explained by common descent, evolutionists do not hesitate to explain them as a consequent of multiple, independent events. This means that, even according evolutionists, similar mutations in allied species do not imply or require common descent. This contradicts the shared-error argument that is supposed to be one of the most powerful evidences for evolution. Unfortunately evolutionists do not include this information in their presentations of the shared-error argument.

The stronger that an argument is for evolution, the more deeply it is flawed.

h/t: DC

Saturday, June 4, 2016

ASCB Addresses Problem of False Science

The Most Important Recommendation of All

The American Society for Cell Biology (ASCB) task force on reproducibility in life science research has issued an undated white paper on scientific rigor. The problem is, as we discussed here and here, life science research has been found to lack reproducibility. John Ioannidis is a bit more blunt as he explains that “most published research findings are false,” and that “claimed research findings may often be simply accurate measures of the prevailing bias.” The ASCB white paper is no doubt a step in the right direction. It offers 13 recommendations to encourage more rigor in training, publishing, and standards. But the most important recommendation of all continues to be ignored.

Daniel Sarewitz has noted not only the problem of bias in scientific research but also the causes. Note his final thought in this quote:

All involved benefit from positive results, and from the appearance of progress. Scientists are rewarded both intellectually and professionally, science administrators are empowered and the public desire for a better world is answered. The lack of incentives to report negative results, replicate experiments or recognize inconsistencies, ambiguities and uncertainties is widely appreciated — but the necessary cultural change is incredibly difficult to achieve.

And so it is that science’s much touted self-correcting, feedback loop which ensures science converges on the truth (after all, that’s what Mr. Wells told us in seventh grade science class) is sometimes a little slow to act.

And if the ASCB is still needing to remind scientists to clean their beakers and use checklists, imagine the difficulty in achieving more fundamental change?

This brings us to the recommendation that ASCB did not make—the most important of all. And that is for science to free itself of the excessive metaphysics. Unfortunately, progress on that front is glacial. As Sarewitz notes, one reason bias persists, and is so harmful, is that in the moment it is not perceived as bias. Asking an evolutionist to stop with the metaphysics goes nowhere because it isn’t recognized as metaphysics. Deep philosophy is a part of their “science” as much as red meat is a part of hamburgers.

Even if the ASCB task force members wanted to address this fundamental problem, they wouldn’t for the backlash would be overwhelming and their professional reputations would be ruined.

So while the pipettes will be sterilized and results double checked to the third decimal point, ASCB will continue to publish junk science driven by the Epicurean mandate that the world must have arisen spontaneously. Unfortunately, the ASCB task force has missed the most important recommendation of all.