Academic Brown Shirts

Phillip E. Johnson authored an essay entitled 'Ya Gotta Believe!.' It originally appeared in Touchstone: A journal of Mere Christianity and was republished at Access Research Network. Two paragraphs from the essay are quoted below and my comments follow. The entire essay can be read at the linked site.

"Biology professor Michael Dini of Texas Tech University made himself a media celebrity by publishing on his web page his criteria for recommending students to medical school. Dini requires that a student seeking a recommendation be earning an A in his class and be well known by him. So far so good, but he also demands that the student affirm “truthfully and forthrightly” a scientific answer to the question, “How do you think the human species originated?” Dini’s words appear to mean that a student seeking a recommendation must not only demonstrate an understanding of evolution but also affirm a personal belief that the human species originated purely by natural causes and not by divine creation."

Michael Dini not only wants students to deny any beliefs they hold about creation being of divine origin, he requires that they embrace his own religious views in exchange for a recommendation. If a student were to provide a truthful and forthright scientific answer, he would respond by indicating that science is unable to document life's origin by purely natural causes. Speculation abounds but speculation is not a scientific answer to how the human species originated. An honest response however, is not consistent with naturalism. A belief in naturalism should not be confused with natural explanations based on solid empirical evidence. It is a belief in the former that students are required to embrace- or else.

"I have wondered why no journalist perceived that the dispute, however offbeat, raised a significant issue of principle that ought to have appealed to liberals. That educators should require only knowledge and not belief is an important tenet of Enlightenment rationalism, often invoked in liberal circles to distinguish secular from religious education, to the disadvantage of the latter. It is commonplace in law schools to say that compulsory affirmation of belief is a defining feature of totalitarian regimes, because coerced endorsement is more intrusive than prohibition of dissent. That is why religious dissenters may not be compelled to salute the flag, even in wartime."

Good point Phillip Johnson. The fact that Dini did what he did to the applause of academics and jounalists alike is a chilling reminder of how tenuous our freedoms are.

Questioning the Assumption of Neutrality

A research paper by Professor Laurence Hurst and colleagues contains information that could impact both treatment of disease and thinking about evolution. A University of Bath news item refers to the paper. From the cited source:

The paper showed that the assumption that synonymous mutations (those that change DNA of a gene but not the resulting protein) occurring in the genomes of mammals were neutrally evolving – i.e. that chance alone determined their fate – was no longer valid.

This rolls back the front line of the debate concerning the role of selection and chance in molecular evolution, and is important because the assumption of neutrality of synonymous mutations has been a keystone of estimates for how often mutation occurs.

“Importantly it also showed how the selection acts and how this has implications for understanding human disease,” said Professor Hurst.

“It was often assumed that synonymous mutations could not be candidates for human disease.

“The paper shows that this isn’t true, and that many diseases are in fact owing to such changes.”

Self-Replicating RNA

In his usually brilliant style David Berlinski disposes of another Darwinian myth with scientific truth. Here is a part of his essay entitled 'On the Origins of Life.' My comments appear in bold print.


"In the grand progression by which life arose from inorganic matter, Miller Time has been concluded. It is now 3.8 billion years ago. The chemical precursors to life have been formed. A limpid pool of nucleotides is somewhere in existence. A new era is about to commence.

The historical task assigned to this era is a double one: forming chains of nucleic acids from nucleotides, and discovering among them those capable of reproducing themselves. Without the first, there is no RNA; and without the second, there is no life.

In living systems, polymerization or chain-formation proceeds by means of the cell’s invaluable enzymes. But in the grim inhospitable pre-biotic, no enzymes were available. And so chemists have assigned their task to various inorganic catalysts. J.P. Ferris and G. Ertem, for instance, have reported that activated nucleotides bond covalently when embedded on the surface of montmorillonite, a kind of clay. This example, combining technical complexity with general inconclusiveness, may stand for many others.

In any event, polymerization having been concluded—by whatever means—the result was (in the words of Gerald Joyce and Leslie Orgel) “a random ensemble of polynucleotide sequences”: long molecules emerging from short ones, like fronds on the surface of a pond. Among these fronds, nature is said to have discovered a self-replicating molecule. But how?"

Berlinski notes the need for a chemical catalyst of nucleotide polymers. He also alludes to the belief that nature generated a self-replicating polymer that initiated a series of reactions culminating in a self-replicating cell.

"Darwinian evolution is plainly unavailing in this exercise or that era, since Darwinian evolution begins with self-replication, and self-replication is precisely what needs to be explained. But if Darwinian evolution is unavailing, so, too, is chemistry. The fronds comprise “a random ensemble of polynucleotide sequences” (emphasis added); but no principle of organic chemistry suggests that aimless encounters among nucleic acids must lead to a chain capable of self-replication."

Berlinski exposes a slight of hand in pointing out that while Darwinian explanations begin with a self-replicating molecule, the self-replicating molecule itself needs explaining.

"If chemistry is unavailing and Darwin indisposed, what is left as a mechanism? The evolutionary biologist’s finest friend: sheer dumb luck.

Was nature lucky? It depends on the payoff and the odds. The payoff is clear: an ancestral form of RNA capable of replication. Without that payoff, there is no life, and obviously, at some point, the payoff paid off. The question is the odds."

So what is the explanation for the self-replicating molecule? Prebiotic conditions that made a self-replicating molecule virtually inevitable? Natural selection? It appears to be nothing short of good fortune; the stuff of OOL legends.

"For the moment, no one knows how precisely to compute those odds, if only because within the laboratory, no one has conducted an experiment leading to a self-replicating ribozyme. But the minimum length or “sequence” that is needed for a contemporary ribozyme to undertake what the distinguished geochemist Gustaf Arrhenius calls “demonstrated ligase activity” is known. It is roughly 100 nucleotides."

This is a key point that is applicable to many OOL experiments. Self-replicating ribozymes are not generated from simulated prebiotic soups. When the need for nucleic acids arises there are ready suppliers in the form of reliable biotechnology companies. The original source of biochemicals is of course a cell.

"Whereupon, just as one might expect, things blow up very quickly. As Arrhenius notes, there are 4100 or roughly 1060 nucleotide sequences that are 100 nucleotides in length. This is an unfathomably large number. It exceeds the number of atoms contained in the universe, as well as the age of the universe in seconds. If the odds in favor of self-replication are 1 in 1060, no betting man would take them, no matter how attractive the payoff, and neither presumably would nature.

“Solace from the tyranny of nucleotide combinatorials,” Arrhenius remarks in discussing this very point, “is sought in the feeling that strict sequence specificity may not be required through all the domains of a functional oligmer, thus making a large number of library items eligible for participation in the construction of the ultimate functional entity.” Allow me to translate: why assume that self-replicating sequences are apt to be rare just because they are long? They might have been quite common.

They might well have been. And yet all experience is against it. Why should self-replicating RNA molecules have been common 3.6 billion years ago when they are impossible to discern under laboratory conditions today? No one, for that matter, has ever seen a ribozyme capable of any form of catalytic action that is not very specific in its sequence and thus unlike even closely related sequences. No one has ever seen a ribozyme able to undertake chemical action without a suite of enzymes in attendance. No one has ever seen anything like it."

In other words why should we believe in a story linked to self-replicating molecules when their generation from conditions resembling a prebiotic starting point is not observed.

"The odds, then, are daunting; and when considered realistically, they are even worse than this already alarming account might suggest. The discovery of a single molecule with the power to initiate replication would hardly be sufficient to establish replication. What template would it replicate against? We need, in other words, at least two, causing the odds of their joint discovery to increase from 1 in 1060 to 1 in 10120. Those two sequences would have been needed in roughly the same place. And at the same time. And organized in such a way as to favor base pairing. And somehow held in place. And buffered against competing reactions. And productive enough so that their duplicates would not at once vanish in the soundless sea."

This is a dose of reality you will not get from OOL propagandists. Note the problematic conditions glossed over by RNA world advocates.

"In contemplating the discovery by chance of two RNA sequences a mere 40 nucleotides in length, Joyce and Orgel concluded that the requisite “library” would require 1048 possible sequences. Given the weight of RNA, they observed gloomily, the relevant sample space would exceed the mass of the earth. And this is the same Leslie Orgel, it will be remembered, who observed that “it was almost certain that there once was an RNA world.”

Initial enthusiam is tempered by sobering assessments.

"To the accumulating agenda of assumptions, then, let us add two more: that without enzymes, nucleotides were somehow formed into chains, and that by means we cannot duplicate in the laboratory, a pre-biotic molecule discovered how to reproduce itself."

Which puts OOLers back to square one and their faith based assumptions.

Mutations

I came across the following argument today.

1. Harmful mutations are usually eliminated.
2. Beneficial mutations are preserved.
3. Beneficial mutations quickly accumulate.

It is a fairly common one with many variations in wording. Mutations fatal to an organism tend to be eliminated for obvious reasons. Those that are slightly deleterious can accumulate. A beneficial mutation might be preserved but the larger question is would it become predominant throughout a population. The third point is poorly defined. How quick is quickly?

I wish to focus more on #2. The issue being not so much whether a beneficial mutation would be preserved but rather what would an actual pathway to an accumulation of such mutations look like?

Let's look at a specific system. Histone acetylation and deacetylation is associated with nucleosomes and gene regulation. A specific example of transcription inhibition occurs when histones are deacetylated by a complex of proteins known as N-CoR, Sin3 and RPD3.

What value does the above argument have in explaining how the proteins, involved in the above mentioned deacetylation function, came about? How did it occur sequentially? What value do the distinct proteins have when considered apart from the deacetylation protein complex? Anyone with sufficient imagination and a knowledge of homologous proteins can construct an explanatory story. Would it be testable though?

Proteins interact with other proteins. Protein complexes associated with specific functions are common. Changes occasioned by beneficial mutations rarely refer to such complexes when used in an educational context or a debating context for that matter.

Gene Regulation and E.coli

A news release from the University of Wisconsin-Madison entitled BASIC WORK ON E. COLI IDENTIFIES TWO NEW KEYS TO REGULATION OF BACTERIAL GENE EXPRESSION reveals an important functional relationship between DNA promotor regions and RNA polymerase discovered through research involving the bacterium E.coli. Some italicized paragraphs from the linked article follow along with my comments in block print.


MADISON - The cellular process of transcription, in which the enzyme RNA polymerase constructs chains of RNA from information contained in DNA, depends upon previously underappreciated sections of both the DNA promoter region and RNA polymerase, according to work done with the bacterium E. coli and published today (June 16) in the journal Cell by a team of bacteriologists from the University of Wisconsin-Madison.

This fundamental research about a key step in RNA synthesis has important implications for the study of gene expression in other organisms, and adds to the wealth of knowledge about E. coli contributed by scientists from the UW-Madison.

The article cites more detailed information about a known process involving the enzyme RNA polymerase and a region of DNA known as the promotor.


In his most recent study, Gourse investigated the interaction between RNA polymerase and promoters from the E. coli chromosome. RNA polymerase reads the information in DNA and transcribes it into chains of RNA, which are later translated into proteins. Promoter regions are specific sequences within the DNA chain that tell RNA polymerase when and where to begin transcription, and how much product to make from specific genes.

Gourse's group found that there is a specific region within DNA promoters that makes contact with a highly conserved but previously underappreciated segment of the sigma subunit of RNA polymerase. While the contact with sigma is very strong at promoters for most genes, it is particularly weak at promoters that make ribosomal RNA, which means that other factors like nutritional and environmental signals ultimately regulate the expression of those genes.

The sigma subunit of E.coli RNA polymerase is encoded by a particular gene known as rpoD.

There are five different polypeptide chains in E.coli RNA polymerase suggesting questions as to how the four core polypeptide subunits (alpha (a), beta (b), beta' (b'), and omega (w)) and another subunit known as sigma formed incrementally. The sigma subunit has a transient relationship to the holoenzyme and its function involves identifying the starting point for transcription initiation.

Uracil and A Repair Pathway

An EMBO report entitled 'Abrogation of the CLK-2 checkpoint leads to tolerance to base-excision repair intermediates' focuses attention on another DNA damage response pathway. Misincorporated uracil leads to the necessity of a repair mechanism. The variety and extent of errors and damage causing malfunction in the absence of repair mechanisms highlights the need for repair mechanisms at a very early point in the history of life. From the EMBO report:


Incorporation of uracil during DNA synthesis is among the most common types of endogenously generated DNA damage. Depletion of Caenorhabditis elegans dUTPase by RNA interference allowed us to study the role of DNA damage response (DDR) pathways when responding to high levels of uracil in DNA. dUTPase depletion compromised development, caused embryonic lethality and led to activation of cell-cycle arrest and apoptosis. These phenotypes manifested as a result of processing misincorporated uracil by the uracil-DNA glycosylase UNG-1. Strikingly, abrogation of the clk-2 checkpoint gene rescued lethality and developmental defects, and eliminated cell-cycle arrest and apoptosis after dUTPase depletion. These data show a genetic interaction between UNG-1 and activation of the CLK-2 DDR pathway after uracil incorporation into DNA. Our results indicate that persistent repair intermediates and/or single-stranded DNA formed during repair of misincorporated uracil are tolerated in the absence of the CLK-2 checkpoint in C. elegans.

Research Funded by the Discovery Institute

This press release description came courtesy of Yahoo news. It is noteworthy in that the Discovery Institute has been criticized for not supporting research. From the news report:


"Discovery Institute Has Put Over $4 Million Towards Scientific and Academic Research into Evolution and Intelligent Design in the Past Decade
Thursday October 5, 9:00 am ET


SEATTLE, Oct. 5 /PRNewswire/ -- Discovery Institute launched the Center for Science and Culture in 1996, recognizing the need for an institutional home for the emerging scientific theory of intelligent design. Even though the nascent theory of intelligent design was already being discussed by individual scientists around the world, it was not until the Center for Science and Culture was established that scientists were given the resources to research what has become the most exciting scientific story since the Big Bang.

The Center provides funding and support for scientists and scholars whose research challenges various aspects of neo-Darwinian theory and develops the scientific theory known as intelligent design. Saturday, October 21st, the Institute will host a ten year anniversary dinner to honor the achievements of the Center for Science & Culture, along with its Fellows and staff.

"In 1996, it was almost impossible to receive funding to do scientific research related to intelligent design," says Bruce Chapman, President of Discovery Institute. "And, in addition to a lack of funding and resources, it was clear that scientists working on intelligent design were facing more and more persecution and harassment, making it difficult for them to conduct research."

"So we started the Center, and now, just ten years later, we've put over $4 million directly into scientific and scholarly research on intelligent design and evolution."


In the last ten years the CSC has:

-- Supported research and writing by more than 50 scientists and scholars
in the sciences, social sciences and humanities.
-- Supported scientists and philosophers of science working on specific
journal articles, monographs, and books in such areas as biology,
biochemistry, cosmology, physics, probability theory, philosophy of
mind, and philosophy of science.
-- Financially supported a number of scientific and academic conferences,
including the International Symposium on the Origins of Animal Body
Plans in Chengjiang, China, the Nature of Nature conference at Baylor
University, and intelligent design conference at Yale University."

An Inquisitive Student

A biology student named Amanda recently posted a message within a Yahoo group asking some intelligent questions. Her post follows. My comments are in bold print.

"Are there any professional geneticists, embryologists, Morphologists, etc. in the forum? If so, maybe you can help me. I'm a Junior studying biology, seeking to go on to graduate school and go into either genetics or some type of cell or molecular research. I love this type of biology, I love organic chemistry, biochemistry, and research in general, and I also love the Word of God, and am a Christian. I completely comprehend the idea of Natural Selection as proposed by Darwin and find it to be completely logical and reasonable, but I cannot reconcile it with my knowledge of genetics, how the cell works, how genes are expressed, and so on.

I feel that Natural Selection makes sense when discussed simply in terms of an
entire organism, but I've never seen it tied with the way DNA actually works (even though I am continuously told that NS takes place genotypically, not phenotypically, otherwise LaMarch would have been right)."

Natural selection was a logical construct when first introduced and is still a concept that, for the most part, is unsupported by direct evidence. An article by David Berlinski entitled 'The Strength of Natural Selection in the Wild' is one of very few that refer to actual studies related to natural selection.

In order for NS to even start, there would have had to be an unimaginable number of random genetic mutations, and I think that is defended usually with the idea of an incredibly old earth-I guess people can accept that there is a chance that many mutations could take place over billions of years, and there's probably some type of equation for that (although personally i think the age of the earth has repeatedly been determined though circular reasoning.) But I simply can't accept that an enormous series of random mutations brought about the exact sequences of nucleotides necessary for the complex functions that even the simpliest cell must carry out in
order to survive.

Your skepticism is not without reason. Here is an interesting reference to work done by Dr. Ralph Seelke.

"Tryptophan Synthase A, a protein which enables E. coli to synthesize tryptophan, an amino acid necessary for life, is the target for this study. He was able to locate the trpA gene and “knock out” 1, 2, 3 or 4 sites which prevents this protein from being made. The E. coli were placed in a tryptophan poor environment in which they could live, but not do well. In so doing, Seelke replicated an environmental stress such as those theorized by Darwinians which drive evolution. If mutations occurred which enabled some bacteria to sythesize tryptophan, this would convey a selective advantage, and those bacteria would dominate.

The Results: Those E. coli who only had one site to overcome essentially evolved overnight. This one error was corrected and the adapted E. coli dominated. HOWEVER, if two independent events (two mutations) are needed, it appears nothing happens. After 1,000’s of generations, not one bacteria has overcome the barrier presented by the requirement of just 2 independent mutations. It appears, at this time, evolution cannot even produce two independent events needed to become fitter. This makes the idea that the 40 or so proteins required for the bacterial flagellum to all be produced in the right place at the right time sound downright ludicrous."

"This includes coding for the transciption factors necessary to even transcribe the DNA itself and manufacture proteins. Which is strange because Transcription factors are proteins-so how were the first proteins made? It takes a large number of complex reactions and comfirmational changes for a cell to make a protein, it's hardly a spontaneous reaction. There are so many intricate systems in life that would not work should one tiny thing change. I can't wrap my brain around how random genetic mutations could result in the amazingly complex, yet smallest unit of life-the cell."

Amanda has put her finger on the Achilles heel of Darwinism namely, the inability to formulate a coherent theory of descent from a prebiotic starting point. As indicated the synthesis of proteins not only requires a great deal of nucleotide specificity, it also entails proteins that bind to promotor regions, an enzyme- RNA polymerase- required to transcribe genes, a complex of tRNAs and tRNA aminoacyl synthetases required to correctly match codons with 20 different amino acids, ribosomes involved in peptide elongation and more. Amazingly the proteins needed to enable protein synthesis are themselves coded for by the same DNA whose transcription and translation they make possible.

"I find it especially difficult to comprehend since the frequency of mutations seen today is so small, and most mutations are harmful-the cell even has defenses against mutations, and mechanisms to check and correct them."

Another good point. Genomes come equiped with mechanisms designed to detect and correct errors leading to mutations and damage to DNA caused by environmental factors like ultraviolet light and chemical reactions. This blog has recently featured a series of posts on just this issue. The pervasiveness of DNA repair mechanisms among biological organisms leads to the question of how cellular life would have been possible without them at any point in time.

"Maybe I haven't completely grasped the whole evolutionary theory yet, maybe I'm missing something-but I feel like I'm stepping into a different world when I leave my genetics/development class and step into my vertabrate diversity class. There are theories of origen, and explanations for what we see phenotypically today, but nothing in between. Is there anyone who can provide some explanation?"

Amanda, I think you have a good grasp of evolutionary theory. In fact your grasp of it is better than that of most defenders of the theory. Your independent thinking is to be admired. I hope your intentions of a graduate degree in a biological field of study are realized. We could use some good young thinkers.

General Intelligent Design (GID)

Dr. Robert A. Herrmann, a retired professor of mathematics, is a proponent of an intelligent design theory he has called General Intelligent Design (GID). Not surprisingly his idea is argued mathematically. This alone probably accounts for the relative obscurity of his beliefs. For those unfamiliar with him and his positions here is a link to an article of his. A paragraph from the article follows:


"Once a natural law is accepted and is used for any scientific theory, then the laboratory results that verify the natural law can also be represented by a logic-system. Indeed, the generalization to all applicable entities also fits a logic-system. The natural law itself when applied to applicable physical entities can be considered a part of the "cause" that yields the correlation between observations. However, the acceptance of a statement as a natural law does not negate the possibility that this natural law can be deductively derived from other hypotheses that might be considered as more fundamental in character. It is an important exercise within physical science to "derive" rationally an expression for observed regularities from a more fundamental hypothesis. Logic-systems are more fundamental than the generated consequence operators since they give the details of how natural laws affect a natural-system's behavior. When a logic-system is fully presented, the intelligence being displayed is the intelligence required to translate the information the system contains into the actual effects the natural laws have upon a specific natural-system's behavior. What this all means for the GID interpretation is that it is rational to assume that the natural laws are intelligently designed in such a manner that corresponding laboratory-obtained (i.e. empirical) data are also intelligently designed since the data satisfy the GID logic-system characteristics."

The Logic of Viral Pathways to Life

Finding plausible pathways to life has been an effort plauged by dead ends and a shortage of useful supporting data. Frustration spawns unsound theoretical approaches. An example is the belief that since viruses are less complex than cellular organisms they would have been cellular precursors.

Viruses do have much smaller genomes than cellular organisms and are less complex yet they also contain nucleic acids with encoding capacities and have the capability to hijack the cellular machinery of a suitable host in order to replicate. Viruses utilize cellular transcriptional mechanisms to effect their replication. Although relatively small, viral genomes contain a good deal of sequence specificity. The specificity is related to the replication function and is clearly adapted to the mechanisms of their cellular hosts. Enzymes like integrase and reverse transcriptase illustrate the fit between viruses and cells. To put it in Darwinian terms the selective value of viral genes is host dependent.

That should give pause to thinking evolutionists intent on believing that simpler equates to an evolutionary precursor. If natural selection is invoked as an explanatory device then it would favor viral genomes most efficiently adapted to their parasitic functions and the specific host organisms serving the parastic role.

Of course an alternative viral theory of origins exists. Rather than having been precursors to cells, their origin could owe itself to a degenerative process that involved cells as the initial source of what later became viruses. However whether degenerative or precursor, the logical link between cells and viruses is clear. The functions of viral genomes are explained by their interactions with specific cellular hosts. Clear too is the selective value of viral genomes; that is there is clarity for those whose view is not determined by a precommitment to an origins paradigm devoid of purpose and intelligent direction.

The Notorious p53

The website for St. Jude Children’s Research Hospital features an article about p53 levels. P53 is associated with responses to damaged DNA occasioned by radiation and chemicals. More than any other gene, the gene that codes for the p53 protein is found mutated in cancer patients.

As the article entitled 'Mechanism controlling DNA damage response has potential novel medical applications' indicates, p53 is associated with cellular responses to stress. Research connected with it is linked to efforts to improve cancer therapies. A cause of cancer is believed to be damage to DNA brought about through radiation and chemical reactions.

An impact of the St. Jude study was a finding thatDNA damage led to an increase in p53 protein synthesis. This finding ran counter to a previously held notion that enhanced p53 levels resulted from a decrease in the rate in which the protein is broken down. A practical benefit to the discovery is apparant namely, a potential to manipulate the synthesis rate to occasion positive results following damage to DNA.

Following damage to DNA p53 can either prevent cellular division or trigger apoptosis or cellular suicide. In so doing p53 inhibits the proliferation of damaged cells which in turn can inhibit cancer.

The specifics of the mechanism controling the rate of p53 synthesis involve an untranslated region of mRNA coding for p53. This UTR acts as a control switch. A protein known as nucleolin suppresses synthesis of p53 by binding to the UTR of p53 mRNA. When DNA damage occurs however, another protein known as RPL26 binds the UTR and causes accelerated translation of the mRNA resulting in more p53.

Researchers were able to document the link between the regulating proteins and synthesis levels by inhibiting RPL26 production which short circuits an increase in p53 following damage to DNA. The p53 functions of halting cellular proliferation or apoptosis were correspondingly compromised. Likewise reduced nucleolin levels increase p53 production in response to DNA damage.

The article goes on to indicate a general approach to the phenomenon of protein synthesis shutdown which can result from damaged DNA or other factors like hypoxia- too little oxygen. By utilizing specific regulatory binding proteins a bypass strategy might be realized.

In an origins of life or evolutionary context nucleotide sequences with selective value would not only have to become predominant through a differential survival process, they would also have to survive environmental destructive factors. How this would have occured is unclear given the propensity for developmental mechanisms to preceed corrective functions.

Materialistic Assumptions

A post at 'The Constructive Curmudgeon' blog contains an argument responding to an argument grounded in materialism. Here it is:

1. If animal evolution is true (antecedent), then there can be no nonphysical properties in human beings (consequent).
2. Animal evolution is conceived as entirely physical.
3. Further, from the physical alone, the nonphysical cannot come. Causal principle.
4. The mind is not identical to matter. See Descartes’ and others’ arguments to that effect. These arguments appeal to the law of identity (A=A) and other logical principles.
5. Therefore (a), there are nonphysical properties in human beings (denying the consequent of (1).)
6. Therefore (b), materialism is false.
7. Therefore (c), animal evolution is not true.

Evolutionists have argued that the intellect is an emergent property of matter. It flows more from an attachment to metaphysical values than empirical results. Yes, there is data documenting causal links between physical phenomenon and thinking. There is also data indicating that our thought influences biochemical processes.

Douglas Groothuis is the thoughtful writer at 'The Constructive Curmudgeon.'