Limitations Of Biological Determinism: Ideas In Our Reenchantment & Rectification

The Big Toe

Science has known for some time now that bodies exist only to perpetuate big toes. Big toes, or similar appendages on other creatures, including those nascent toe-like organelles found inside the cells of unicellular beasties and plants, are essential to life.

For instance, big toes provide the balance predators need to make sharp turns while pursuing prey, increasing their chances of survival, and thus passing on their big toes to the next generation. They also equip prey to “spring” into action faster, which also increases their chances of survival. Big toes allow people to reach objects that would otherwise be out of reach (“tippy toes”), increasing the chance our ancestors could gather more foodstuffs, which in turn increased their chance of survival so that they could pass on big toes to their progeny. Namely us.

Big toes only exist to perpetuate big toes. Big toes are selfish. We are their mere containers; though perhaps helper apparatuses is a better term. The only purpose of big toes is to ensure bodies make copies of big toes, passing big toes on to future generations. The big toes that, on average, aide in survival of their carriers, such as by becoming flatter in wet environments, or growing thicker shaper nails in predators, are more likely passed on than less useful big toes. Your big toe will allow you to trip and fall to save two or more siblings, because their big toes closely resembles yours.

Because of all this, it can be said that our behavior is caused by the need for big toes to survive and pass on copies of themselves. Just think of the incredible pain you suffer when you stub your big toe. This is the toe sending a signal that it is crucial to all life, especially yours.

Nice Genes, Baby

Well. It is clear you can go on like this for some time. And it works for whatever you care to use as your exemplar. Kidneys, gall bladders, navels, and even genes.

Genes are more fun because they are hidden, at least to most creatures most of the time. You can therefore get away with ascribing more behaviors to them, at least because the accusations are harder to check. You can say they are selfish, metaphorically, or you can say they long to pass on copies of themselves. That this is their goal. That their only purpose is to produce copies. Genes have will.

The case for genes is made stronger because of DNA, which hosts genes, and genes help produce the chemicals which are necessary (but not sufficient) to life—just as, say, oxygen and gravity are.

It is here the Big Split happens, a branch in the Road of Causality. One path is Determinism, which says all life is nothing but collections of mindless blind (yet selfish!) chemical interactions. The other path is Essence, which says genes, big toes and the like, exist like oxygen does in water, which is to say not by themselves as independent entities, but as assimilated parts of a whole. The whole is greater than the sum of parts. The organism as a whole is key in Essence, its constituent parts are what counts in Determinism.

Determinism is simple to explain. Chemicals interact, and the bodies in which the chemicals are housed respond strictly according to the “laws” of chemistry and physics. And it must be “laws”, because these are all that exists. The forces and interactions are inevitable, and subject only to predictive uncertainty because of occasional quantum behavior, which is anyway uncontrollable. Organisms move, think, and act in ways determined, ultimately, by these “laws.” It remains only to describe which chemical and physical interactions produce this or that behavior, thought, or action.

If it is genes which drive the majority of the chemical interactions, then we can, in principle anyway, discover which gene or genes are responsible, i.e. cause, which behavior. Genes lack perfect determinism only because of “chance” due to varying conditions of the environment, which may or may not allow a gene to express, occasional quantum indeterminism, and the like. Because of all this, to discover which gene is “associated with” or “linked to” (i.e. causes) which behavior we need statistics to sort through all that “chance”.

The man most responsible for the popularizing Determinism is Richard Dawkins, who scored with his 1976 The Selfish Gene. About Dawkins’s thesis, here is David Stove in his sadly neglected (1995) Darwinian Fairytales. Stove said that however true genetic determinism is for the birds and beasts, this “genetic Calvinism” is obviously not true for man. (Note: I can only quote a small portion of this chapter, which contains only a fraction of Stove’s argument: read the book.)

I do not believe that humans are the helpless puppets of their genes, and cannot even take that proposition seriously. Why? Because I have heard far too many stories like that one before, and because it is obvious what is wrong with all of them.

‘Our stars rule us,’ says the astrologer. ‘Man is what he eats? said Feuerbach. ‘We are what our infantile sexual experiences made us,’ says the Freudian. ‘The individual counts for nothing, his class situation for everything,’ says the Marxist. ‘We are what our socioeconomic circumstances make us,’ says the social worker. ‘We are what Almighty God created us,’ says the Christian theologian. There is simply no end of this kind of stuff.

What is wrong with all such theories is this: that they deny, at least by implication, that human intentions, decisions, and efforts are among the causal agencies which are at work in the world.

This denial is so obviously false that no rational person, who paused to consider it coolly and in itself, would ever entertain it for one minute. No one ever doubts, at least while he has or remembers having a big fish on his line, that the intentions and efforts of even a fish can make a difference to the outcome of a situation; especially if the fish gets away after all. And if even fish efforts sometimes have causal efficacy, then human efforts can hardly be altogether without it.

The falsity of all these theories of human helplessness is so very obvious, in fact, that the puppetry theorists themselves cannot help admitting it, and thus are never able to adhere consistently to their puppetry theories. Feuerbach, though he said that man is what he eats, was also obliged to admit that meals do not eat meals. The Calvinistic theologian, after saying that the omnipotent Creator is everything and his creatures nothing, will often then go on to reproach himself and other creatures with disobeying this Creator. The Freudian therapist believes in the overpowering influence of infantile sexual experiences, but he makes an excellent living by encouraging his patients to believe that, with his help, this overpowering influence can be itself overpowered. And so on…

Here is another specimen of Dawkins contradicting his own theory. He says, ‘let us try to teach generosity and altruism’, is but also says that ‘altruism [is] something that has no place in nature, something that has never existed before in the whole history of the world’. Well, I wonder where we are, if not ‘in nature’? And (as Midgley pertinently asked), who are Dawkins’ ‘us’: the ones that are to teach altruism?…

The determinist answers these criticism by saying that intension, intention, pain, joy and so forth are mere chemical reactions, and that any notion these indicate a real presence (such as you, dear reader) which has will and intellect is an illusion. Yet they never say how a chemical reaction can reason it is having an illusion. Because there has to be an entity “above” the illusion to recognize that it is having an illusion, and what is that?

Never mind, they say, ignoring the unanswerable, for here is a mathematical formula indicating “inclusive fitness.” This math says that this or that behavior is veered towards things like selfish altruism, where selfish altruism is defined as supporting copies of the genes an organism has, but which are encapsulated in other bodies. Genes, being wily, induce behaviors that ensure copies of themselves perpetuate, even if those copies are not in the hosts that carry them. How the genes you carry, for instance, know of copies of genes in others is, of course, a mystery. Genetic telepathy? Yet whatever signals genes use to communicate must, at times, be blocked, such as in North America from 1861 to 1865 (“Father against son, son against brother”). Are we to look forward to the paper “On the effects of cannon smoke and increased heritability”?

In any case, you will, says the math, gladly sacrifice yourself for some modest number of first cousins, or a slightly larger group of second cousins, and so on, because there will be in those cousins lots of copies of the genes you have. Genes somehow force this cooperation and self-sacrifice by those chemical interactions.

Alas, places like hospitals, adoption agencies, abortion chambers, churches and so forth negate this math. Never mind those, say the theorists, for these are evolutionary dead ends. But how do these facilities and acts arise and persist? Hospitals, at least in days of yore before the DIE, were the opposite of dead ends. They would pass on genes of others at the expense of the doctors and nurses working there, a medico being a dangerous occupation compared to, say, writing. But perhaps the math can be modified to have some individuals in a species be hyper-altruistic. Yet that would be tough, and similar to the case of genes “for” homosexuality.

Both doctors (or soldiers: ask Englishmen in 1915) and sodomy enjoyers pass on their genes at rates below and far below those not as altruistic (for medicos) or selfish (for sodomy enjoyers; Stove has a list of determinist-unexplainable behaviors in the last chapter of his book; like adoption, abortion, contraception, etc.). How then could these behaviors persisted? The genes “for” these behaviors, since they cause non-reproductive behaviors, should have died out by now. This has led some to suppose the genes “for” homosexual behavior increase “group cohesion” or “group selection” and so forth. One wonders if these theorists have never seen a “Pride parade.” Anyway, nobody has explained how genes can cooperate in groups. Except by pointing back to the math, which becomes the Deadly Sin of Reification.

And just what gene is “for” the human behavior of, say, restocking sturgeon in Swedish rivers? It’s one thing to say one man will sacrifice himself for another because the other has copies of the first’s genes. But sacrifice oneself, by expending energy necessary for the continuation and propagation of one’s genes, for sturgeon? Or perhaps newts or darter snails, which man does not even eat. Man shares few genes with sturgeon and newts. And it’s exceedingly unlikely these fishies and creepy crawlies will ever repay the favor, so tit-for-tat gene-generated altruism is out. Of course, it’s always possible to tell the tale of how expending energy agitating for newts in the end, through complex paths, boosts reproductive value. But telling the tale is not proof of the tale. And many of these tales would make Paul Bunyan blush.

Mary Midgley, in her famous review, called Dawkins’s book “Gene juggling“, bringing up these and other points about altruism that cannot be explained by genetic determinism, and I encourage you to read it all. Dawkins opens his book saying “We are survival machines—robot vehicles blindly programmed to preserve the selfish molecules known as genes.” Midgley says “Not a word of caution about metaphors follows.” And, on the rare disavowals of literalness later in Dawkins’s book, “like the paternosters of Mafia agents, they have no force against his practice of habitually relying on the literal sense.” Dawkins can never make clear exactly what his model is:

…Dawkins’s crude, cheap, blurred genetics is not just an expository device. It is the kingpin of his crude, cheap, blurred psychology. For selection to work as he suggests by direct competition between individual genes, the whole of behaviour would have to be divisible into units of action inherited separately and each governed by a single gene…One gene must govern each ‘strategy’ if their ‘interests’ are supposed to be always in competition…[But] genes are essentially co-operative; they are linked together in the most complex and hierarchical ways and affect each other’s working to an incalculable extent. The idea of a one-one correlation is not genetics at all.

This has been recognized since Dawkins’s book, and greater than one-one correlations have been sought. We’ll come to one way of handling that, such as with polygenic scores, in a moment.

There is evolution to consider. That is too large a subject, so we will explore it separately another day. Except to say Determinism’s premise is that genes are the “unit” of evolution. Yet why not big toes? Big toes can’t make themselves. All right, that’s silly. But why not those chemicals that make up genes, i.e. nucleotides? Why isn’t evolution a strategy for nucleotides to perpetuate themselves? Or maybe it’s really proteins, which are from amnio acids which genes use. Which means it might really amino acids that seek to selfishly make copies of themselves. Or the hydrogen that goes into amino acids. Hydrogen atoms are the real single-minded behind-the-scenes actors, which fool amino acids, which drive proteins, which bend genes, and eventually us, to their wills.

My Genes Made Me Do It

Let’s use genes, because everybody else does. Genes, we will say, must at least influence, if not cause, some or all behaviors.

Let us suppose that genetic Calvinism is so. Genes (up to “chance”) determine our behavior and thoughts, which include propensities toward certain acts and thoughts. How have we been doing with tying this or that gene or genes with that and this behavior?

There have been many early successes in gene-behavior discoveries. There are, for instance, males and females, and these act and think in many different ways because of their natures, natures which rely on their biology. Males and females have distinct chromosomes. But which came first? The gene or the nature? Hilariously (though not with Dawkins, who has here remained sane), many of the same people who hyperventilate over “denying” evolution, and the influence of genes, will support with equal vehemence ideas like “being trapped in the wrong body.” But we are not here interested in such gross absurdities.

It’s true that our biologies make us hungry, and, being hungry, we seek food. Though I haven’t heard (likely due to my limited reading) of a gene or genes for (i.e. to cause) seeking food. Nor for many other common behaviors. Like wearing clothes. And not jumping from high places and attempting to fly. We also seek out sexual intercourse, the urges coming and going with known biological changes. Yet certain experiences can overwhelm genes here, as those Pride parades prove.

Even Scrooge knew we are, at least sometimes, slaves to our biology. He rightly says of his own impressions of a ghost, “You may be an undigested bit of beef, a blot of mustard, a crumb of cheese, a fragment of underdone potato. There’s more of gravy than of grave about you, whatever you are!” Maybe that’s not a good example, because biology lost that round.

At any rate, our biology determines at least some of our behavior, or at least the limits of it (no flying), and, say determinists, genes cause all of it. All right. How much has been proven of our behavior being determined by genes?

Proud Of My Wee P

Almost nothing, says Steve Pittelli in his “The Question That Must Be Asked: Is Behavioral Genetics a Null Field?“. You must read this paper in its entirety.

Behavioral genetics has not been successful, says Pittelli. Many successes have been claimed, and trumpeted, especially in the “media”, only to fade away under closer scrutiny. The field has its own replication crisis, which plagues all subjects that rely on classical statistics (hypothesis testing, p-values, Bayes factors, parameter estimates). I won’t here go into all that, as regular readers will already know and the material can be found with ease in my other writings, except to say that no result that relies on these methods can be trusted only because of those methods. Proof has to arrive in other forms, such as in predictive clinical relevance, as Pittelli argues (he appears to accept classical statistics, though).

Determinist scientists are ever hopeful: “there is a never-ending sense, in the moment, that the latest study is more evidence for a genetic basis for one trait or another, despite the fact that so many studies in the past were accepted as true findings, then faded from consciousness when they could not be consistently replicated.”

His critique “is not a denial of the importance of genetics in human biology. Certainly, pathological genetic/chromosomal disorders, such as Down Syndrome, Fragile X Syndrome, Huntington’s chorea or other genetic disorders can lead to significant intellectual, behavioral or neurological difficulties or deficiencies.” Pittelli accepts monogenic behavioral (mainly disease-causing) findings.

Here is the tricky point, a distinction hard to keep in mind in our age of computer metaphors and materialism. There is a difference between the presence or absence of genes that through complex chains of causation might lead to the performance or avoidance of certain behaviors, and that of genes causing behaviors. Pittelli does not dispute the first interpretation. He does not believe the second has been proved.

For instance, some east Asians, Pittelli reminds us, have a mutation that can lead to easy drunkenness and an allergic-like reaction to alcohol. Since that is not pleasurable, behaviors to avoid drinking can develop, even across an entire culture. That behavior can be taught by parents to children, but this behavior (the teaching) isn’t “genetic heritability”. That’s the first interpretation. Determinists go further and say the mutation can cause one to become a drunk. The gene will lead the body to the well, and the gene will make that body drink well drinks.

Some have genes that cause greater muscle mass or height and the like, which can lead to developing, or avoiding, certain athletic behaviors. These genes change the limit of behaviors. Black Africans can seek out the sun, and swamps, more than their Northern European cousins. But not so much milk. These kinds of genetic “determinism” are no different than seeking out food or clothing, or even air. Nobody holds that our biology is not limiting in this sense. We cannot live on the surface of the sun, and don’t try to.

Genetic modifications of organisms aims at the first idea. By changing the limitations or ranges of possible behaviors. For instance, ensuring this or that mutation increases yield of some crop. Or (it is hoped) by inserting a “good” gene in place of a “bad” one and curing a monogenic disease.

Pittelli rejects genes causing behaviors because all evidence in favor of that interpretation has the bad habit of crumbling under critical examination. The “canonical premise of behavioral genetics [is] the assumption that a quantitative summation of common genetic variants in individuals, or shared within groups, influence human character, intelligence or the risk of developing a mental disorder.” Intelligence is another large and difficult subject, and I differ from Pittelli in thinking this may be, up to a point, more like muscle mass. Different capabilities exist and propagate. I base this on the innumerable experiments and programs conducted in myriad different circumstances funded by tsunamis of money that fail to show differences in some aspects of intelligence can be eliminated. But we can let that pass here.

There isn’t space to discuss twin studies, except to say that these, too, have been largely a disappointment. Among many criticisms, Pittelli notes “monozygotic twins are not treated the same as dizygotic twins, are perceived more as a pair by others and themselves, and often model their behavior accordingly.” Even studies with excellent data may be confounded by external causes like these. For instance, there was found a 14.8% concordance rate in the Danish Twin study of schizophrenia for monozygotic twins, and 4% for dizygotic twins.

It is also worth noting that psychiatrists are taught to favor the diagnosis of schizophrenia if a monozygotic twin has that diagnosis, so even this 14.8% figure might be inflated for that reason, alone. Moreover, regardless of diagnosis, monozygotic twins are three times more likely to live together than dizygotic twins, so they are more likely to share the same mental health treatment, which could also inflate the concordance rate for monozygotic twins…

The fact of the matter is that twin and adoption studies are blunt scientific instruments that, while giving some early justification for the field of behavioral genetics, have little to offer in the modern era, where we can look at the actual genetics of individuals to see whether the heritability claims of twin and adoption studies hold up. In truth, they have not. On the contrary, the difference between heritability claims from twin and adoption studies and genetic studies are profound, leading researchers to search for this missing heritability, without ever considering whether the heritability was ever there. Twin and adoption studies had their purpose, but at this point in time, they seem like little more than quaint exercises for graduate psychology students interested in an archaic vestige of their field.

Finally to genes! Pittelli reminds us that “Hundreds of candidate [single] gene studies were performed, mostly in the 1990’s and early 2000’s that claimed correlations between specific genetic variants and psychiatric disorders, personality traits and human intelligence.” But “None of them consistently replicated.”

See if this sounds familiar to you:

…we already have an example of this field producing false positive results for years, with near unanimous acceptance of the results by researchers, who then publicized these results in mainstream media outlets, creating a consensus in the public eye that our differences are genetic in nature. These studies were blithely waved in the face of skeptics, characterizing them as unscientific and even questioning the mental health of those critical of such studies. They were also used as a rationale for a more biological approach to psychiatry, transforming the psychiatric profession to the delight of pharmaceutical companies and health care insurers. Despite this, all of these studies were abandoned with little self-reflection or public correction. Instead, there was a pivot in the field to a new type of genetic research, seemingly without concern that they might be repeating the entire debacle once again.

That pivot was to genome-wide association studies (GWAS).

Any trait that could be gleaned from a questionnaire could then be evaluated for genetic correlations by this method. The trait could be a traditional behavioral genetic trait, such as psychiatric diagnoses, personality traits or intelligence, but also more dubious traits like “church attendance,” “ice cream flavor preference,” or “walking at a brisk pace.”…

Previously, it was assumed that there would be fewer genes with larger effects affecting behavioral traits. GWAS are meant to detect genetic variants with much smaller effects. It is worth noting that this shift was not due to discoveries in the field, but instead due to a lack of discoveries [in candidate gene studies].

It’s here we at last meet the mighty magical wee P. And, unsurprisingly, the concomitant failure to replicate. From what else but a wee P could you make science out of correlating groups of alleles with “walking at a brisk pace” as judged by a questionnarie?

There were attempts at forms of verification, but these were not independent, predictive tests. Pittelli has details, which I’ll save for more technical criticisms on the statistical methodology. These were not independent replications. Plus, a reminder that correlation (which statistics gives you) is not causation:

Generally, researchers performing GWAS attempt to remove population stratification, which will give spurious genetic correlations due to varying frequencies of minor alleles in genetically distant ancestries. A classic example would be chopstick use. Clearly, a GWAS would find many spurious correlations for chopstick use that are simply ancestral markers for people of Asian descent from countries that favor chopstick use. That is a clearer example, but when doing GWAS and looking for tiny correlations, there is a potential for more subtle population stratification due to geography from genetic drift, as well as cultural identity, socioeconomic status, religious affiliation, etc., due to assortative mating. Clearly, there will be genetic correlations that have no causal connection to the phenotype.

Worse, the correlations “discovered” are usually small. “For example, the most recent Schizophrenia ‘meta-analysis’ had 2.6% of the variance explained via the statistically significant correlations”. And that is the parametric correlation, which is necessarily higher than the predictive, i.e. the real-life one.

Enter polygenic risk scores. I earlier criticized technical details of these, which can be summed up as drawing lines through blobs of data, forgetting the data, and touting the lines. Polygenic risk scores are, more or less, linear sums of large numbers of genes, smoothed out in one way or another, and then “correlated” to something, like a disease or quantified answers on a questionnaire. These sums are then used to give a “risk score” for the disease or trait. Pittelli: “If a person has a high PRS for a trait, then this suggests that they would be more likely to have the trait in question.”

One issue, though, is that two people with identical risk scores might not both have the trait. Moreover, someone might have a high PRS and not have the trait and someone with a low PRS might still have the trait. Again, we are left with the question of what is in the ether?

Another issue with PRS scores is that variants that did not reach clinical significance in the GWAS are often used to develop the score…

Moreover, different PRS’s for different ethnicities might also suggest that the PRS is picking up a large amount of population stratification. One could easily create a “chopstick” PRS with some predictability. So, to call a PRS “causal” without being able to specify what any of the SNP’s involved have to do with a phenotype is, charitably, premature.

These scores must be checked predictively, which is the only way. Here’s one instance in which this was done:

[A polygenic risk score] developed for schizophrenia was used in a sample of individuals from the Netherlands to test how well it could predict whether someone had a diagnosis of schizophrenia. This gave a dismal performance, with a 0.5% prediction success. To put that in perspective, if one predicted that someone had the diagnosis of schizophrenia based solely on the fact that he was a a young male, that would be twice as good a predictor.

In technical terms, we say the polygenic model has no skill with respect to the naive “young male” model (and it is a model). We therefore should not use the polygenic risk score.

Pittelli recognizes the danger of bad models becoming self-fulfilling prophecies:

Another issue with PRS’s is that, whether they are valid, they have the potential to create a fait accompli if someone is told at an early age that they don’t have the genes for, say, musical ability, or mathematical aptitude or “educational attainment.” If you started to encourage individuals with a high musical aptitude PRS into pursuing music, you will begin to “validate” the PRS. If you begin developing academic curriculum around a PRS for mathematical aptitude, you are reinforcing the PRS, even if it is invalid.

In this way, genetic determinism can seem to real when it is not.

His criticisms are not directed at things like “heritability”. Obviously, parents pass genes on to their children: genes are inherited. Heritability numbers are not direct statements of how much a behavior is influenced/caused by genes, and instead give statistical, model-based numbers of how close variability in measurable behavior are in groups of parents and their kids. These calculations invariably (good pun!) overstate how heritable behaviors are, at least because parents usually live with their kids, and even adopted children are often living in similar circumstance to adoptive adults, so separating out environmental conditions from biological cause is difficult. We’ll save an investigation of these matters for another day.

Top Down

Accepting all these criticisms means we still do not have final proof that genes cannot influence or cause behaviors. It is only that looking at individual genes or those in gross linear combination has not proven it. The first approximation to functions is linear, so additive effects were natural to check. But there is nothing guaranteeing that genes work together additively. So it remains that non-linear, or non-linear plus environmental conditions, might prove out.

Yet there is a stronger consideration.

Mechanistic reductive philosophy says we are machines. Complex, of course. Blind gears, driven by exterior forces and operating by “laws”. That is the philosophy driving much (all?) research into genetic determinism. It it because this philosophy—scarcely named—is believed that research is unflagging, even in the face of serial failure. If the philosophy is true, then it must be that genes, or proteins, or something like that, is causing (and not merely constraining) behavior. It only remains to discover what exactly that something is. Giving up is thus not an option.

Unless—and I hope you saw this coming—that philosophy is false.

It could be that genes don’t exist—independently. They are like hydrogen and oxygen in water: once together, each can be said to only exist virtually. Only water remains; only water really exists. In biology, only the organism really exists. Its parts are not separate. They form part of the whole, which is greater. Each part affects each other part necessarily, because the whole is supreme. This is some non-linearity! It may not be possible, therefore, to separate out genes from all behaviors, especially complex behaviors. Genes are not alive: we are. We are not slaves to genes, but genes are slaves to us, or to all organisms.

This is Essence. It says, among the least things it says, that Determinists have it backwards. Cause works the other way around, from the organism to its parts, not its parts to the organism. Organisms have an end, or various ends, to which their behavior is directed. And in the case of man, reason and intention, which drive at least some behaviors. This drive or cause is teleological. Materialists have unsuccessfully been trying to purge teleology from science, for at least the fear that final cause (its other name) reopens a door they believe they had nailed shut.

Stove (who claimed to be an atheist, you recall) recognized the failed attempts at removing Essence (in the same book as above):

Darwin, for example, published in 1862 a book entitled The Various Contrivances by which Orchids are Fertilised by Insects. He knew, and all his readers knew, that he did not really mean the word ‘contrivances’. Everyone understood perfectly well, (a) that you cannot call something a contrivance without implying that it was intended, and (b) that Darwin did not mean that these ‘contrivances’ of orchids were ever intended by anything.

He therefore owed his readers an explanation of what he did mean by ‘contrivances’: a translation of that word into language free from the implication of intendedness. [Which he did not provide.]

…Darwinians cannot reasonably expect, any more than anyone else can, to be allowed to have things both ways. They cannot, on the one hand, describe adaptations as contrivances for this or as designed for that, while denying that they mean that these adaptations were ever intended; and on the other hand, decline to explain what they do mean by expressions like ‘designed for’ and ‘contrivance for’.

“Darwinians,” Stove goes on to say, “have never paid, or even acknowledged, the debt they have all along owed the public: a reconciliation of their teleological explanations of particular adaptations, with their non-teleological explanation of adaptation in general. And not only have they never paid this debt: they have in fact become progressively less conscious, with time, of the fact that they owe this debt.”

They will never be able to pay that debt, for it is not possible to speak of the “goals” of anything, like genes let alone whole organisms, while simultaneously decrying teleology. Teleology always sneaks through the cracks in the door. No matter how much Determinists try to eliminate, because those efforts themselves (as is easy to see) are themselves telelogical.

This isn’t yet the worst case scenario for determinists. This next, and last, argument is.

Don’t Mind Me

Man, as is obvious to many, but not Determinists, is unlike any other beast. Man has the ability to think rationality. Your reading and understanding this sentence, and your pet orangutan’s inability, is proof of it. Of course, having the ability does not mean exercising the ability, nor does it mean that all can exercise it equally, but let these points pass.

Supposing it is true, as all evidence suggests, that man is not only different in degree, but in kind, from all other organisms, and is different because of ability for rational thought. Determinists are bound to reject this evidence, and do so by issuing another promissory note that such proof of man’s non-uniqueness will be forthcoming. They then assume the note has been paid because it has been issued in good faith. I call this, and other similar efforts, The Great Bluff. You wouldn’t think it would fool anybody, but it does, because of the desire the note will in fact be repaid.

In any case, what follows from our being rational (homo sapiens was chosen for good reason), is that our intellects cannot be material. And if our intellects are not material, then they cannot be caused by genes, which are material. Given that our rational thought informs our wills, and that we subsequently carry out certain behaviors in accord with our wills, biological determinism must be false. At least in those activities guided, at last, by our intellects. This does not remove biological limitations in other areas. We still cannot unaided fly, and must eat, even though we might “rationally” convince ourselves that we can.

There is no space here to discuss the arguments in favor of intellectual immaterialism. They are nicely laid out, e.g., in Feser’s “Kripke, Ross, and the Immaterial Aspects of Thought“, a dense work which you must read and which carefully carries out the argument, and answers the objections you might have; and then even more you might have are answered here. One objection might be that rational thought is not, in fact, different than other kinds of thoughts. My favorite refutation of that (from the second link, and which is in, other places, CS Lewis’s Miracles):

…you have unambiguously to grasp what it is to add or to apply modus ponens in the very act of denying that we ever unambiguously grasp what it is to add or apply modus ponens.  You have unambiguously to apply formal rules of inference in the very act of giving an argument for the conclusion that we never unambiguously apply any formal rules of inference.

You have to use rationality to deny you have it. You have to reason, as Lewis shows us, that biology does not equip us to reason to truths, but only to survive, which you reason is true. And, hilariously, you have to implicitly argue that you alone have ascended beyond the limitations of biology to prove that we cannot ascend beyond the limits of biology.

And So?

Biological determinism, however true it might be in lower beasts, is not true in man. What is true are biological limitations. We cannot breathe beer (alas), a man, unless initiated into strange practices, will look approvingly on a woman, we must rely absolutely absolutely on others for the first years of our lives, if we have short legs we cannot play basketball against professionals, if we are limited intellectually the best we can do is listen to NPR. And so on.

None of this, as convincing as it is, answers queries like, Given are intellects are immaterial, how does in form part of our bodies? How does the whole function? Strange questions! But no stranger than (as we recently saw: blog, Substack) asking how two entangled particles can communicate at impossible speeds, or in asking how a wave function can “collapse”. Those events invoke non-material causes, too, and might even be the same causes involved in our thinking. Nobody knows. Some are trying to know. Why don’t you try and find out.

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