The Study Of Nature

by Steven Gussman

        In the field of biology, what is commonly taken as, “environmental causation,” is more-or-less mythical.ⁱ All explanations of life terminate in genetic evolution with the, “environment,” playing a different role than almost anyone means by their mention of it. "Biology" is the scientific study of life; "genetics" is the scientific study of the unit of hereditary information which encodes the blueprint of life (and also plays the role of the unit of selection in evolutionary theory). "Determinism" is the philosophical idea that the world is explicable through tight chains of cause and effect with no room for fundamental noise (though ample room for practical noise). Post-Darwin, it's perverse that, "adaptationists," have sometimes been considered something of a disputed school of thought within evolutionary biology (though like, “biological/genetic determinism,” this is mostly achieved through a straw-man that doesn't fit the term).ⁱⁱ Like, “originalists,” in constitutional law, the term ought to be synonymous with the discipline, and automatic. (Perhaps surprisingly, the opposition in both cases often comes from the same political persuasion). Given the history of the major discoveries in the field of biology, isn't it strange that, "biological determinism," and, "genetic determinism," are such dirty terms? When Richard Dawkins argues that the causal properties of individual genes are only statistically determinant,ⁱⁱⁱ this is true in practice. In principle, whatever the totally deterministic mechanism at play is, it is thoroughly genetic. As every biologist appears forced to write: there is no one alive who thinks that genes somehow stand up and enact their designs in some direct, supernatural way; therefore, this bad definition of "biological/genetic determinism" is a straw-man.^iv But on the other hand, a great many academics actually do believe in a magical, arbitrary, limitless kind of, "environmental," causation.^v If genes don't largely determine an organism, what exactly do they do? They hold the info that determines their traits (and were thereby selected among by the environment).^vi Of course this is the case, otherwise, what are we even talking about? We don't have this same argument about information in other contexts. It is well understood that the bits in this text file are the most important determinant in making my piece what it is.^vii Of course you also need a computer with a screen (or a printer) to finally produce it in readable form, yet we still speak of the predetermined nature of the article itself (and in fact, legally, we emphasize the intellectual property above the ownership of any copy). We designed computer networks such that these files will find themselves in the right environment. But gene machines work similarly: the internal environment of the organism is itself the developmental endpoint of other genes!^viii E. O. Wilson even speaks of pheromones evolving, in the sense that an organism is naturally selected for its ability to create, secrete, and interpret the presence of these chemicals in its environment.^ix

        The importance of genes can be seen from both directions. On the one hand, it is true that there is nothing metaphysically separate about a gene. It is made of the same stuff as the, "environment" (it's a real object described by physical chemistry). On the other hand, it's admitted that the, "environment," is typically defined as everything but the organism in question's genes!^x So what makes the gene so special as to be singled out in this way? Could it be that it plays the central determinant role in biology?

        Even staunch defenders of biology, such as John Alcock, can be placed on the defensive to such a degree as to be made to play into the double-standards applied against the relevant fields. In The Triumph Of Sociobiology, Alcock writes, “... all biologists know that every visible attribute of every organism is the product of a marvelously complex and all-pervasive interaction between genes and environment."^xi In his biography of E. O. Wilson, Richard Rhodes relays that Wilson's early estimate for the heritability of behavioral traits was a meager 10%.^xii In Consilience, E. O. Wilson wrote, “... a gene 'causing' a particular behavior... would make no more sense than its converse, the idea of behavior arising from culture without the intervention of brain activity.”^xiii In The Blank Slate: The Modern Denial Of Human Nature, Steven Pinker writes, “'all traits are heritable' is a bit of an exaggeration, but but not by much.”^xiv Richard Dawkins recently said of The Selfish Gene, “... there's nothing to do with humans, I didn't write about humans at all... I was using the language of selfishness in a special way... The book is actually largely about altruism... the selfish gene programs the individual organism to be altruistic—that's the point... The selfish gene is precisely not about the selfish individual, it's about the altruistic individual.”^xv And then there's the fact that everyone knows you're supposed to say, 'why are we still talking about nature versus nurture? All enlightened people know that it is a mix of both (but mostly my favored side).'^xvi There is even a palpable moral dimension to people's over-willingness to emphasize the importance of, “environmental,” causation. I'm picking on these thinkers because they are our staunchest defenders of genetic evolution. All of the conservative estimation, careful couching, and even appeasement leave one wondering if a reader with absolutely no knowledge of genetics could possibly put together what a gene is or does, by reading such statements. Likewise, I suspect these statements generally do not reflect what the great biologists understood themselves to be discovering along the way.^xvii It is often impressed that, 'there are no genes for behavioral traits, only for kicking off pathways which are partially environmental, thereby leading to certain traits in certain environments.'^xviii The layers of this nitpick are onion-esque, and this kind of compounding-couching can obscure our understanding of biology. Of course, no one complains that there are genes for brute morphological phenotype (that was Gregor Mendel's entire point about heredity and central to Charles Darwin's point about selection).^xix Here, too, it is the case that genes kick off developmental pathways leading (one might even say, “determining,”) distally, to traits.^xx Dawkins makes this argument the other way around in The Extended Phenotype. His hypothesis of the extended phenotype is that an organism's genes can be expressed as the phenotype of another organism (or its environment).^xxi As one major example, Dawkins cites a snail whose shell-thickness turns out to be determined by an evolutionarily stable tug-of-war between its own most-fit softness, and an infectious parasite's preferred hardness.^xxii For another, he cites caddis larvae which, rather than growing a shell, are naturally selected to behaviorally select a certain (fit) kind of stone off of the floor of a stream, to use on its back similar to how we use our own clothing-tools.^xxiii For an example in which the phenotype is expressed in the environment, Dawkins relays William D. Hamilton's hypothesis that aeroplankton may well be naturally selected for an ability to induce the cloud formation so useful to them—in this sense, cloud formation itself would be in part the adaptive phenotype of the aeroplanktins' genome (would this be all that different than a mother's genome producing the womb-environment her fetus finds itself in?).^xxiv In defense of the seemingly indirect nature of the causation between a gene in one organism, and the phenotype expressed in another (or in the environment), Dawkins points out that this is hardly less-so the case in normal behavioral (and even morphological) traits.^xxv The gene encodes a contribution to a protein, kicking off a mechanism terminating in the phenotype available to selection by the environment.^xxvi Arguably, then, genes for behaviors are the median case in terms of causal complexity, sandwiched between the, "very," complex pathway from a gene to a morphological trait, and the, "extremely," complex pathway from a gene in one organism to a trait in some other organism.^xxvii Distally, all phenotype may be expressed as a fitness value (all phenotype either reduce or increase the tendency of an organism to successfully reproduce). This phenotype, central to evolutionary theory and the construction of adaptation, is the most distal a trait could possibly be. Therefore, we should not worry about the distance of any other phenotype (such as culture) from its genotype.^xxviii Further, much of the complex developmental chain from protein synthesis to trait will act as an, "environmental," effect on other genes', "expression."

        All of the squeamishness with biological mechanics places us in perverse territory. The ancients, and surely prehistoric peoples, have always noticed the rather obvious experiential fact of heredity—both that children often look and behave similarly to their parents (and that this is causally due to children being of their parents). Along the same lines, our ancestors also knew to selectively breed work-animals for desirable traits (such artificial selection would be the first empirically confirmed prediction of Darwin's theory of evolution by natural selection).^xxix

        Mendel's pea plant experiments suggested that there exist units of heredity, and described how their cross-bred combinations give rise to (evidently, encoded) traits. Darwin's and Alfred Russel Wallace's theory of natural selection argues that selection pressures in the environment (the natural tendency for organisms which inherited a better ability to reproduce to pass on that heritable ability to reproduce and therefore show up more in the future than alternatives) can, over the generations, produce tremendously complex adaptations.^xxx Erwin Schrödinger and the first biophysicists, made predictions, on the basis of physical chemistry, of what the physical units of heredity might be like.^xxxi Francis Crick and James Watson deduced the physical structure (the double helix) of the DNA which holds an organism's genome.^xxxii Ever since, the neo-Darwinnian synthesis has woven this interconnected knowledge together into a kind of standard model of modern biology. Stones don't have anything that we would call, “phenotype,” including, “environmentally caused phenotype—” because they have no genes! This is what makes something alive—it is genes which give rise to the adaptive traits which organize matter (as in an, “organism”). Only those things categorized as, “alive,” have any of the traits we are interested in—and only these things have genes (all objects have an environment, yet none respond to it without genes for doing so).^xxxiii How could the ubiquitous complex adaptations which require the selection of cumulative mutations over millennia possibly evolve if the gene-phenotype link wasn't particularly causally strong, regardless of environmental influence on, “expression?”^xxxiv For all of their careful wording, when the environment changes, evolutionary biologists do not immediately think of, “expression,” changing to pick up the slack—they think of a mismatch in which that same trait is no longer fit in this new environment and so its genetic complement decreases in frequency in favor of other alleles (which give rise to traits which are fit in this environment). Naturally selected genes lead to, “intentional,” low-entropic adaptations; purely environmental causation in development is more likely to be an entropic deviation therefrom—to damage and cause malfunction rather than new or different function (as we see with mutations in the first place).^xxxv E. O. Wilson even writes that the, “[decommissioning of] natural selection,” will come, not from, “environmental,” interventions, but from directly editing human genomes!^xxxvi

        I take no issue in principle with the thoroughness of the full “interactionist” answer, as long as the emphasis remains in the right place, but I do not believe special care has been taken to make sure that readers recognize the central causal role of genes in biology (including in every case of, "environmental," causation).^xxxvii In fact, many social scientists deny even this very carefully couched version of the role of genes, with all of the details. Hell, even the, "radical," biologists like Richard Lewontin and Stephen Jay Gould were capable of specializing in these areas one moment, and denying them outright the next (in the service of preserving their political ideologies).^xxxviii

        Though we speak as though it is obvious what is meant by, “environment,” there are roughly two kinds.^xxxix The common sense environment is that of the macroscopic world (and includes everything from the average temperature to other nearby life—that is, other nearby gene machines).^xl The other portion of the environment is the microscopic: the biochemical substrate involved, largely internally, in carrying out developmental processes kicked off and regulated by genes.^xli Of course both are strictly operative in our full understanding of the phenotypical outcome of a given set of genes, as we can illustrate in the extreme.^xlii If one is developing in a 400 °F oven, or one's body is internally awash in bleach, then a gene for, say, one additional IQ point,^xliii is unlikely to be able to, “express,” that phenotype (in either of these extreme environmental conditions, the organism will quickly perish, no longer exhibiting many recognizable traits at all). Indeed, per statistical mechanics, it is understood that most mutations of genes (which complex organisms' internal machinery actually attempt to correct for, itself a genetic adaptation for thereby reducing the mutation rate to stability) will break the delicate balance of an organism, and lead to a reduction in fitness (or even death), and thereon be rapidly selected out.^xliv The biology of individuals is all about the conservation of stable organisms as encoded in their genetic blueprint (a minority of “in-play” variation is used to get there).^xlv In this Darwinnian sense, most of the ways, "genes interact with environments," causes no good phenotype at all, but utter failure or death.^xlvi Mutations are dangerous things. If changes in the environment are more likely to select other alleles than cause the currently dominant allele to, "express differently," (except insofar as it distally leads to fitness or not), but most mutations (single genetic changes) prove fatal, this too asserts the greater magnitude of genetic causation. Meanwhile, even in situations where genes express differently in different environments, one can expect natural selection to choose those alleles which increase fitness across such environments.^xlvii

        Our three major genetic theories applied to humans are behavioral genetics, kin selection, and reciprocal altruism. The latter two quite reasonably define the, "relatedness," as the shared proportion of the genetic variance. This is reasonable because when it comes to the balance of competition and cooperation between organisms of the same species, the variance, however small in an absolute sense, is everything. Behavioral geneticists' definition of, "heritability," is moreso imposed by circumstance: the reality of the most available methods of measurement is that they may only account for the variance (even though in principle, behavioral geneticists would love to know the role of genes in all behaviors, including shared behaviors).^xlviii To the untrained eye, one can easily be confused by these reduced versions of "relatedness" and "heritability" and falsely conclude that genes play a far smaller role in organisms' traits than they do. Further, heritability estimates are inherently flawed because in samples with high environmental variance, the heritability measure is lowered and vice versa.^xlix Because the, “environmentalist,” tide has been so strong for decades, writers seem happy to simply use these “50/50” heritability-of-variation estimates to impress that genetics play a significant role at all.^l

        So how touchy is a gene's expression to the environment, really? It's tough to say, and surely varies by the trait (this has been called the norm of reaction).^li The fact is, all homo sapiens (for example) are born on Earth, within certain conditions (which must be quite narrow with respect to the rest of the cosmos; it simply only gets so hot or cold, for example, on this planet).^lii Nearly every human being that survives childbirth has an automatically beating heart and automatically breathing lungs.^liii The vast majority, too, have ten fingers and toes.^liv For these traits, and the genes that give rise to them, the norm of reaction is evidently zero.^lv The supreme complexity of this feat cannot be discounted. We take these stable traits for granted, but it certainly cannot be ignored that the vast majority of the human genome is stable and encoding for human universals, explaining how strangers are instantly recognizable as the same species.^lvi That we share some 98.8% of our genome with chimpanzees explains our species' rather obvious likeness to theirs (believe it or not, this is indeed because chimpanzees and humans share genes for those eyes, mouths, digits and so forth; and so it must be with many of our behavioral homologies).^lvii There is no example of shared environmental causation which supports this kind of homology (unless you count the thoroughly genetic process of convergent evolution, in which similar environments select for genes which give rise to similar traits).^lviii In fact, genetic determinism is such that convergent evolution sometimes converges not just on the same solution, but the same gene uses to get there (as with lactose-tolerance's LCT gene across humanity and the eye's Pax-6 gene across species).^lix Keep in mind that the relatedness variable in Hamilton's theory of kin selection (R = ½ for siblings, and so on) does not represent the proportion of the entire genome shared (which is of course something like 99.6% between total strangers), but the shared proportion of the minority of the genome that currently encodes the variance in phenotype between individuals (including the rather obvious differences that allow you to discriminate your brother from a stranger).^lx Because most of the genome is stable, we take for granted the vast majority of our genetic inheritance. In fact, pleiotropy has it that even genes currently under variation and selection will be merely contributing to traits which are also contributed to by established parts of the genome—a genetic contribution to likely every trait which will not show up in the heirtability estimates from experiments such as twin studies (as these measure the heritability of variance in traits).^lxi Polygenic scoring will not be any better at solving this problem, because one cannot in principle correlate shared genes with shared traits—explicitly causal pathways from gene to behavior will need to be directly discovered for the vast majority of cases.^lxii Difficult experiments in varying the shared genome by force of gene editing, and observing human development thereafter, would be scientifically ideal, but deeply unethical.^lxiii Even then, the sheer number of possible human genomes is staggeringly intractable to test, experimentally. One could probably learn something by meticulously measuring the genome of every person born to catch every (likely maladaptive) mutation in the stable genome, but this would require an intractable length of time.

        Genotype-phenotype stability (or low norm of reaction) is what allows doctors to work on patients based on learning about the human species in general: medical professionals never receive a cardiac arrest patient only to find that his, "heart," is green, triangular, pumps Kool-aide, and resides in his left leg. This despite all of the variance in both the microscopic and macroscopic environments in which the genes for a functioning heart have had to carry out their designs in the tens-of-billions of humans ever born (to say nothing of our expectation for those yet to be born).^lxiv The same is of course true for the vast majority of our traits, which are shared so tightly that taxonomists may call homo sapiens a single species to which we are each a member. Why then should we be so quick to exaggerate the role of the, “environment,” in, “gene expression,” for our variable traits? Remember: all shared traits began as a quirky mutation in what was then the variable portion of the genome, and which only rose to prominent frequency over time because it increased the number of viable offspring its gene-machines left to future generations.^lxv Though evolution can be used to explain differences between populations, it is most often used to explain the shared traits of the species—the adaptations built by genes so frequent in the gene pool that they are shared by the entire (and in fact define the) species.^lxvi Again: because these traits, morphological and behavioral, are shared, they of course don't show up in the heritability estimates for variant traits, causing us to take them for granted, and leave them out of our nature v. nurture scoreboard. Given that the shared region of the genome is 249× larger than the variable portion,^lxvii we are significantly under-estimating the proportion of our behavioral traits explicable through genetics. And while they are not literally identical, identical twins reared apart are difficult to tell apart! In this case, it likely is true that many of their differences are due to the different experiential training of their neural networks, not so much because their genes, “expressed,” differently due to environmental conditions (but even this is confounded by differences in the experience of the womb, and the potential for the extended phenotypic effects of other organisms).

        The environment shared between family members accounts for roughly none of the variance in traits.^lxviii In the context of shared traits, it would be really strange for the un-shared environment or the un-shared genetic variance to be playing a significant role.^lxix We know humans share 99.6% of our genome, though it is more difficult to estimate how much of our traits are shared (let alone our environment).^lxx In terms of traits, despite the fact that the bias of social scientists has tended to be to exaggerate diversity (both by literally being wrong about the societies they study, and by emphasizing the small differences in details riding atop of highly similar phenomena), we still end up concluding that from morphology, to behavior, and even up through, “culture,” human societies are majorly similar (think, “wears head-accessories at all,” not, “wears turbans versus baseball caps”).^lxxi From a cosmic perspective, 100% of humans live on Earth, under the same gravitational force, and in a relatively narrow band of temperatures, humidities, and within the same chemical atmosphere).^lxxii But from the human point of view, human societies run a gamut of environmental diversity: from deserts, to the tropics, to temperate climes, and even the arctic. It is perhaps difficult to believe that these locales are 99.6% similar. They were different enough that races which were only partially isolated for about 2,500 generations have very clearly genetically adapted to these locales (a genetic difference that of course falls into the 0.4% of the unshared genome).^lxxiii From the point of view of behavioral genetics, it seems overwhelmingly likely that the shared traits of humanity (the majority of traits) are genetic in origin, and how else could it be? Bottom line, if you could remove (or maximally change) the environment, you would still recognize the resulting beings as human. If you removed the genome? You would not be looking at an organism at all.^lxxiv If you stipulated that all of the same chemical atoms be about, you would have nothing but a mess!^lxxv Given the environment shared between siblings is evidently inert, and that some ill-understood non-shared environment is responsible for half of humanity's differences, it seems quite unlikely that either kind of environment would play much of a role in determining our shared (special) traits.

        From the field of behavioral genetics, it is well-known that, on average, about half of the variance of psychological and behavioral traits are heritable.^lxxvi What is perhaps less-well-known is that about zero of this is contributed by the environment shared between siblings (and half of it is from the so-called, “un-shared,” environment).^lxxvii Much (and perhaps most) of the so-called, "un-shared environment," may be caused by counter-intuitive versions of the, “environment” (or even of genes).^lxxviii As mentioned before, there is our majority-shared genome to worry about in tallying points for nature v. nurture. In addition, neuro-scientist Kevin Mitchell has emphasized the role of the prenatal womb (in-utero) in environmentally causing innate traits.^lxxix Comparisons between identical twins, fraternal twins, siblings, as well as observations of surrogacies should be able to estimate the effects of this environment in particular. Being that the uterine environment is moreso shared by twins than by siblings, and not shared at all in surrogacy, it is likely that some amount of the uterine environment has been showing up in both categories: heritable and environmental. Finally, there are extended phenotype of other organism's genes.^lxxx This might sound far-fetched, yet we already take it for granted in our mother-donated mitochondria, which have their own genome separate from humanity's.^lxxxi One might suspect that the thousand-or-so genes encoding a trait^lxxxii are interacting non-linearly, that the different pair-wise interactions of genes matter. This predicts that the heritability correlation between identical twins' traits should be exponentially more similar than those between normal siblings (rather than only twice as similar). Not so with intelligence: identical twins' IQ correlates at almost exactly 2× fraternal twins':^lxxxiii there is evidently no interaction between genes here, only the genes' linear combination.

        The consequential prenatal, "environment," of one's mother's womb (far from the, "environment," of Sigmund Freud, to say nothing of the postmodernists) is itself majorly influenced by the mother's genome of which this complex system is the expression.^lxxxiv A genome, I might add, that is 99.8% replicated in the rapidly developing fetus it houses and nurtures (or should I say, "natures"). The point is that a much better label for all of the stuff we place under, “environmental,” would be, “not yet accounted for.”^lxxxv When people say, “environment,” they speak of a kind of common-sense view: one's traits being forever changed, as in stories, by fateful events (often social) in one's life.^lxxxvi But we cannot simply assume we know the ways in which such causation actually works (if at all).

        Though the following differences do show up as, “heritable,” in the heritability estimates, many people will confuse them for, “environmental.”^lxxxvii Siblings' genetic differences can ultimately cause them to demand differential care from their parents; likewise, the parents' genes can ultimately cause them to respond to such demands in the ways that they do (does a parent do what a child asks, or something else?).^lxxxviii Here the, "environmental," interaction of a mom reading more to her daughter because she asks her to do so more often; and watching TV more with her son because he asks her to do so more often, is transformed into a complex structure of genetically encoded phenotype. Even, "common sense environmentalism," is more complicated (and has much more to do with genes) than is usually admitted.^lxxxix Take human weight.^xc If I experimentally force one identical twin to eat 3,000 calories a day of Oreos, and the other to eat 1,500 calories a day of chicken, we can expect the former to be fatter than the latter over time (and in addition, the attendant health and social consequences that obesity leads to). But the world does not play out under experimental conditions. Is the presence of Oreos versus chicken the, “environment?” Or do we genetically inherit mental traits such as taste preferences and levels of self control? And how about heritable traits of a much less visible kind: in what ways does our body use and store what we put into it?^xci Does one have a fast or slow metabolism?^xcii Dose one have a proclivity towards calorie-burning activities or not? Further, in direct contradiction to naive environmentalism, behavioral traits tends to become more heritable with age—the more time you've had to be shaped by your environment, the more your behaviors instead correlate with your biological parents', in direct contradiction to the prediction of almost anyone's idea of, “environmental causation.”^xciii

        It is helpful to review the world-view that modern biology gives us. The original heritable phenotypical trait is replication (as this was needed to get the evolution of life started). It is inferred that the physical chemistry on Earth some five billion years ago must have given rise to some kind of simple molecule which, in chemical reaction with its environment, replicated itself (the ancestor of all metabolism); this is the ancestor of DNA, and thereby of all life on Earth.^xciv It was random mutations in this molecule which caused some branches of its descendants to better-replicate, which kicked off evolution by natural selection, eventually leading to all of the biodiversity of life we see, today.^xcv There was nothing anything like life before this occurred, and there has been nothing similar since produced by any other mechanism (except, perhaps, for some cases of human engineering). In this light, it is perverse to assume that traits should be thought of as arising significantly from, “environmental,” factors in real-time (environments have always existed, but rocks are rocks, regardless of their environments, whereas life—complex gene machines generated by evolution by natural selection—only interacts with its environment because its genes allow—indeed, direct—this process).^xcvi Likewise, once it has been properly and unapologetically admitted that genes' whole and sole purpose is to give rise to traits (ultimately deriving trait-replicative-fitness), and that such, “traits,” simply do not exist outside of living things (gene machines), we can recognize that this is the, “new,” (now centuries old) null hypothesis.^xcvii There is little room for the, “environmental,” causation of a trait in the miasmatic sense people take comfort in—this, “environment,” has never given rise to morphological complexity, certainly not behavior, and by no means, culture.^xcviii “Environment,” alone, gives us things like rocks, not rabbits.^xcix As it is usually meant (and probably even moreso received), the, “environment,” is a myth in much the way that, “free will,” is.^c Modern biology (proximal genetics and ultimate evolution) is what guides Ariadne's thread from the abstractions of the life sciences down to the hard science of physical chemistry (the, “environment,” has not, and cannot provide this consilience).^ci Capitulation to those who place biologists on defensive footing succeeds in eliciting from biologists what the, “environmentalists,” want: an exaggeration of the, “causal environment,” (an organism's interaction with which must always be integrally genetic);^cii and a de-valuing of what is known of genetics (including that these stably cause phenotype). There is something strange keeping us from fully accepting the modern science of life. It strikes me as just one example of a postmodern tendency to downplay the majority, norm, or first approximation in favor of exaggerating the minority, special case, or Nth-approximate details.^ciii To emphasize some ill-specified, “environment,” pitted against, “biology,” perverts one's entire understanding of the natural world, turning it inside out.^civ Routinely, even among defenders of unpopular scientific facts, scientists will couch and appease their understanding, and leave lay-readers with room to preserve the opposite impression of what the writers actually believe the evidence to support. Alcock doesn't spend a lot of time worrying about the, “environmental,” side of, “gene-expression,” nor the vagaries of the pathways used to get from gene to phenotype (and in fact, he explicitly notes that, “sociobiologists,” do not fret over such things on the whole).^cv He sees a complex trait, assumes it is adaptive (meaning it is the result of genes for it, and that this trait increases fitness), forms an adaptive hypothesis, discovers predictions of this hypothesis, and empirically checks them.^cvi How is this not, “genetic determinism,” and what is wrong with that? Why are biologists apologizing for the incredible discovery that genes encode for traits, and that natural selection of said genes explains all of biodiversity?^cvii

Footnotes:

i. See “Behavior = Genes + Environment” by Steven Pinker (Harper Perennial / Edge) (2014) (https://www.edge.org/response-detail/25337)

ii. See The Extended Phenotype: The Long Reach Of The Gene by Richard Dawkins (Oxford University Press) (1982 / 2016) (pp. 45-83) and The Triumph Of Sociobiology by John Alcock (Oxford University Press) (2001) (pp. 57-68).

iii. See The Extended Phenotype (pp. 32).

iv. See The Triumph Of Sociobiology (pp. 41-44), The Blank Slate: The Modern Denial Of Human Nature by Steven Pinker (Penguin Books) (2003 / 2016) (pp. 112-113), The Ape That Understood The Universe: How The Mind And Culture Evolved by Steve Stewart-Wiliams (Cambridge University Press) (2018) (pp. 286-287), The Selfish Gene by Richard Dawkins (Oxford University Press) (1976 / 2016) (pp. 359-360), The Extended Phenotype (pp. 14-21), and Consilience: The Unity Of Knowledge by Edward O. Wilson (Vintage) (1998) (pp. 205). While I do not believe that my views on the determinants of organisms' traits are very different from these authors', they spend a lot of time dressing up that view to de-emphasize the central role of genes, only in sections dedicated to addressing their (dishonest) critics.

v. See The Blank Slate (pp. 1-194), The Triumph Of Sociobiology (pp. 129-147), and Consilience (pp. 206).

vi. See Consilience (pp. 149), The Extended Phenotype (pp. 53-54), and my January 13^th, 2020 tweet: https://twitter.com/schwinn3/status/1216932021953540096?t=lAHY95xAcEfUTyrHLtlqVA&s=19.

vii. See “Behavior = Genes + Environment”.

viii. See The Extended Phenotype (pp. 242, 247, 269, 297, 310, 339, 343, 345, 350, 384), Consilience (pp. 149, 152-153), The Selfish Gene (pp. 53), and The Blank Slate (pp. 60, 69).

ix. See Scientist: E. O. Wilson: A Life In Nature by Richard Rhodes (Doubleday) (2021) (85-87, 91).

x. See The Triumph Of Sociobiology (pp. 43).

xi. See The Triumph Of Sociobiology (pp. 44).

xii. See Scientist (pp. 165).

xiii. See Consilience (pp. 149).

xiv. See The Blank Slate (pp. 375).

xv. See “A Moral Philosopher And An Evolutionary Biologist In Conversation” with Richard Dawkins and Peter Singer (The Poetry Of Reality) (2023) (8:56-11:52) (https://youtu.be/VTLMEIBUic8?t=535). Of course the genetic and evolutionary ideas in Dawkins' book generally do apply to humans, ecology being held equal. It is rather obvious that basic, “selfishness—” the tendency to put oneself and one's interests ahead of those of others, then of family (nepotism), then of trade-partners including friends—is a universal trait of organisms, including humans. Why mince words and be embarrassed by the fact that the selfish gene (evolution by natural selection of replicating genes) explains why that is the case, and how behaviors we don't think of as, “selfish,” nevertheless develop?

xvi. See “Michael Shermer With Dr. Debra Lieberman — Objection: Disgust, Morality And The Law” by Michael Shermer and Debra Lieberman (Skeptic) (2018) (https://www.youtube.com/watch?v=tyBksb89d70) and The Blank Slate (pp. xiii, xiv).

xvii. See The Blank Slate (pp. 395-396). Co-discoverer of the double-helix structure of DNA, James Watson, appears to be something of a genetic determinist, see “James Watson: To Question Genetic Intelligence Is Not Racism” by James Watson (Independent) (2007) (https://www.independent.co.uk/voices/commentators/james-watson-to-question-genetic-intelligence-is-not-racism-5328720.html). His son, Rufus, defended his father from the charge of racism, saying James takes a, “rather narrow interpretation of genetic destiny,” see “James Watson: Scientist Loses Titles After Claims Over Race” (BBC) (2019) (https://web.archive.org/web/20190113184300/https://www.bbc.com/news/world-us-canada-46856779).

xviii. See The Selfish Gene (pp. 53, 56, 78-80, 364-365, 375-376), The Extended Phenotype (pp. 33-44, 41-43, 142-143, 233, 299, 406), and The Triumph Of Sociobiology (pp. 52-57).

xix. See The Extended Phenotype (pp. 7, 30-31, 35, 127, 300, 303), The Blank Slate (pp. 146), and Gad Saad's June 27^th, 2013 tweet: https://x.com/GadSaad/status/350298812243382272?s=20.

xx. See The Extended Phenotype (pp. 48-49, 52, 299) and The Triumph Of Sociobiology (pp. 43, 46).

xxi. See The Extended Phenotype and The Selfish Gene (pp. 302-344).

xxii. See The Extended Phenotype by (pp. 316-346).

xxiii. See The Extended Phenotype (pp. 301-302, 323-324) and communications between Gabi N. Waite and Katie Gussman.

xxiv. See Flights Of Fancy: Defying Gravity By Design And Evolution by Richard Dawkins (Apollo) (2022) (pp. 208-209).

xxv. See The Extended Phenotype (pp. 34-35, 298-299, 348-350) and The Blank Slate (pp. 377).

xxvi. See The Extended Phenotype (pp. 21, 53-54, 268-269, 297,441), The Triumph Of Sociobiology (pp. 71), and Consilience (pp. 149).

xxvii. See The Extended Phenotype (pp. 298-299).

xxviii. See The Extended Phenotype (pp. 242, 298-299, 343-344, 348-350, 354) and Consilience (pp. 181).

xxix. See The Triumph Of Sociobiology (pp. 18, 49).

xxx. See The Extended Phenotype (pp. 401).

xxxi. See In Search of Schrödinger's Cat: Quantum Physics and Reality by John Gribbin (Bantam) (1984) (pp 149).

xxxii. See “Speed read: Deciphering Life’s Enigma Code” by Joachim Pietzsch (Nobel Prize Outreach) (https://www.nobelprize.org/prizes/medicine/1962/speedread/).

xxxiii. See Consilience (pp. 181-2, 204-5).

xxxiv. See The Extended Phenotype (pp. 401).

xxxv. See “Behavior = Genes + Environment”, The Selfish Gene (pp. 39), The Extended Phenotype (pp. 208, 401), The Red Queen: Sex And The Evolution Of Human Nature by Matt Ridley (Harper Perennial) (1993) (pp. 45), and Cosmos (pp. 28).

xxxvi. See Consilience (pp, 302-303).

xxxvii. See The Triumph Of Sociobiology (pp. 31, 46), The Extended Phenotype (pp. 18, 34-35, 350), and “Behavior = Genes + Environment”.

xxxviii. See The Blank Slate (pp. 109-114, 122-128, 132-133, 378, 149-150, 162-163) and Scientist: E. O. Wilson: A Life In Nature by Richard Rhodes (Doubleday) (2021) (pp. 157-158, 161-164, 179-181).

xxxix. See Consilience (pp. 151).

xl. See The Selfish Gene (pp. 59-85) and The Extended Phenotype (pp. 339).

xli. See The Extended Phenotype (pp. 48, 242, 247, 269, 297-299, 310, 316, 343-345, 350, 384), The Triumph Of Sociobiology (pp. 43), Consilience (pp. 149, 151-153), The Selfish Gene (pp. 53), and The Blank Slate (pp. 60, 69).

xlii. See The Triumph Of Sociobiology (pp. 43, 46), The Extended Phenotype (pp. 34-35, 52), and “Behavior = Genes + Environment”.

xliii. See "Best Evidence Yet That A Single Gene Can Affect IQ" by Andy Coghlan (New Scientist) (2012) (https://www.newscientist.com/article/dn21705-best-evidence-yet-that-a-single-gene-can-affect-iq/).

xliv. See “Behavior = Genes + Environment”, The Selfish Gene (pp. 39), The Extended Phenotype (pp. 31, 40, 208, 241-242, 401-402), The Red Queen: Sex And The Evolution Of Human Nature (pp. 45), and Cosmos (pp. 28).

xlv. The Extended Phenotype (pp. 31, 40, 138, 141-142) and The Blank Slate (pp. 142-143).

xlvi. See “Behavior = Genes + Environment”, The Selfish Gene (pp. 39), The Extended Phenotype (pp. 31, 40, 208, 241-242, 401-402), The Red Queen (pp. 45), and Cosmos (pp. 28).

xlvii. See The Extended Phenotype (pp. 41-43), Consilience (pp. 149), and The Red Queen (pp. 186-193).

xlviii. See The Blank Slate (pp. 373-374).

xlix. See The Blank Slate (pp. 374-5).

l. See The Blank Slate (pp. xiii-xiv, 372).

li. See Consilience (pp. 149).

lii. See Consilience (pp, 150-151, 181) and The Blank Slate (pp. 90).

liii. See Consilience (pp, 150-151, 181) and The Blank Slate (pp. 90).

liv. See Consilience (pp, 150-151, 181) and The Blank Slate (pp. 90).

lv. See Consilience (pp, 150-151, 181) and The Blank Slate (pp. 90).

lvi. See The Blank Slate (pp. 101), Cosmos (pp. 28), and The Extended Phenotype (pp. 31).

lvii. See “DNA: Comparing Humans And Chimps” (American Museum Of Natural History) (https://www.amnh.org/exhibitions/permanent/human-origins/understanding-our-past/dna-comparing-humans-and-chimps#:~:text=Humans%20and%20chimps%20share%20a,%2D%2Dand%20yet%20so%20different%3F).

lviii. See The Triumph Of Sociobiology (pp. 72-73), Consilience (pp. 149), The Extended Phenotype (pp. 53-54), and “Evolutionary Convergence” by Simon Conway Morris (CellPress Current Biology) (1998) (https://www.cell.com/current-biology/pdf/S0960-9822(06)02143-9.pdf).

lix. See The Ape That Understood The Universe (pp. 270) and “Evolutionary Convergence”.

lx. See "Genetics By The Numbers" by Chelsea Toledo and Kirstie Saltsman (2012) (National Institute of General Medical Sciences) (https://www.nigms.nih.gov/education/Inside-Life-Science/Pages/Genetics-by-the-Numbers.aspx#:~:text=99.6,also%20contributes%20to%20our%20individuality), The Blank Slate (pp. 374-375), and Consilience (pp, 150).

lxi. See The Extended Phenotype (pp. 31, 138, 141-142, 208-209, 299, 350), The Blank Slate (pp. 49-50, 142, 373-374, 377), and Consilience (pp. 152-3).

lxii. See Consilience (pp. 151, 154).

lxiii. See Consilience (pp. 151).

lxiv. See “How Many People Have Ever Lived On Earth?” by Toshiko Kaneda and Carl Haub (PRB) (1995 / 2022) (https://www.prb.org/articles/how-many-people-have-ever-lived-on-earth/#:~:text=No%20demographic%20data%20exist%20for,ever%20been%20born%20on%20Earth), The Blank Slate (pp. 90).

lxv. See The Extended Phenotype (pp. 31-32, 34-35, 39-40, 138, 141-142).

lxvi. See “The Consuming Instinct | Dr. Gad Saad | Talks At Google” by Gad Saad (Talks At Google) (2017) (https://youtu.be/_qHYmx7qPes?t=1621) (27:01-28:51), The Blank Slate (pp. 49-50, 142-143, 260, 344, 374, 377), and The Extended Phenotype (pp. 31, 39-40, 138, 141-142).

lxvii. See "Genetics By The Numbers".

lxviii. See The Blank Slate (pp. 378-381).

lxix. See The Blank Slate (pp. 373, 378-381).

lxx. See "Genetics By The Numbers".

lxxi. See The Triumph Of Sociobiology (pp. 129-147) and The Blank Slate (pp. 455-459) which both cite the work of Donald Brown on compiling human universals,

lxxii. See Consilience (pp. 150-151, 181).

lxxiii. See Who We Are And How We Got Here: Ancient DNA And The New Science Of The Human Past by David Reich (Vintage) (2018) (pp. 49, 52).

lxxiv. See “Carl Sagan Cosmos - The Stuff of Life” uploaded by YouTube user WeAreStarStuff51 from Cosmos: A Personal Voyage (Episode 2: “One Voice In The Cosmic Fugue”) (https://www.youtube.com/watch?v=_2xly_5Ei3U) and “Carl Sagan On Chemical Components” uploaded by YouTube user espivalis from Cosmos (https://www.youtube.com/watch?v=FRTF4UMhTDc).

lxxv. See “Carl Sagan On Chemical Components”.

lxxvi. See The Blank Slate (pp. 373-380).

lxxvii. See The Blank Slate (pp. 380-381).

lxxviii. See my January 7^th, 2022 Tweet; https://twitter.com/schwinn3/status/1479475712813940736?t=bvbfJeOVWBIzzQwC4owW9g&s=19.

lxxix. See my January 7^th, 2022 Tweet: https://x.com/schwinn3/status/1479475715468845057?s=20.

lxxx. See previous footnote.

lxxxi. See The Extended Phenotype (pp. 271, 339).

lxxxii. See “The Human Genome” from The Cell: A Molecular Approach 2nd Edition by Geoffrey M. Cooper (Sinauer Associates) (2000) (https://www.ncbi.nlm.nih.gov/books/NBK9907/#:~:text=The%20human%20genome%20is%20distributed,as%20a%20metaphase%20chromosome%20band), “What is noncoding DNA?” (MedlinePlus) (accessed January 2024) (https://medlineplus.gov/genetics/understanding/basics/noncodingdna/#:~:text=Only%20about%201%20percent%20of,%2C%E2%80%9D%20with%20no%20known%20purpose), and The Extended Phenotype (pp. 141-142).

lxxxiii. See The Triumph Of Sociobiology by Alcock (pp. 50).

lxxxiv. See my January 7^th, 2022 Tweet: https://twitter.com/schwinn3/status/1479475712813940736?t=bvbfJeOVWBIzzQwC4owW9g&s=19.

lxxxv. See “Behavior = Genes + Environment” and The Blank Slate (pp. 378-379).

lxxxvi. See “Behavior = Genes + Environment”.

lxxxvii. See The Blank Slate (pp. 387-9).

lxxxviii. See The Blank Slate (pp. 387-9).

lxxxix. See The Triumph Of Sociobiology (pp. 46), Consilience (pp. 152-153, 181-182), The Blank Slate (pp. 60, 69, 74-75, 328), The Ape That Understood The Universe (pp. 241), and "Behavior = Genes + Environment".

xc. See Consilience (pp. 150) and The Extended Phenotype (pp. 268-269).

xci. See The Extended Phenotype (pp. 269).

xcii. See The Extended Phenotype (pp. 269).

xciii. See The Blank Slate (pp. 375).

xciv. See The Selfish Gene (pp. 15-25) and Cosmos (pp. 27).

xcv. See The Selfish Gene (pp. 15-25).

xcvi. See The Triumph Of Sociobiology (pp. 46), Consilience (pp. 152-153, 181-182), The Blank Slate (pp. 60, 69, 74-75, 328), The Ape That Understood The Universe (pp. 241), and "Behavior = Genes + Environment".

xcvii. See The Selfish Gene (pp. 28), The Extended Phenotype (pp. 28-29), and Science In The Soul: Selected Writings Of A Passionate Rationalist by Richard Dawkins (Bantam Press) (2017) (pp. 145).

xcviii. See "Behavior = Genes + Environment", See The Selfish Gene (pp. 28), The Extended Phenotype (pp. 28-29), and Science In The Soul (pp. 145).

xcix. See The Selfish Gene (pp. 28), The Extended Phenotype (pp. 18, 21, 28-29, 34-35, 127, 138, 141-142, 299), Consilience (pp. 181-182), The Blank Slate (pp. 69, 74-75, 90, 386-387), Cosmos (pp. 28), Science In The Soul (pp. 145), The Triumph Of Sociobiology (pp. 31), and the “Computation” chapter in The Philosophy Of Science. (https://footnotephysicist.blogspot.com/2022/09/chapter-v-computation-philosophy-of.html).

c. See “Behavior = Genes + Environment”, Free Will, The Extended Phenotype (pp. 26-27), and “The Consciousness Conundrum”.

ci. See Consilience (pp. 72-104), The Blank Slate (pp. 30), The Selfish Gene (pp. 28), The Extended Phenotype (pp. 28-29), and Science In The Soul (pp. 145).

cii. See The Triumph Of Sociobiology (pp. 46), Consilience (pp. 152-153, 181-182), The Blank Slate (pp. 60, 69, 74-75, 328), The Ape That Understood The Universe (pp. 241), and "Behavior = Genes + Environment".

ciii. See The Triumph Of Sociobiology (pp. 135).

civ. See The Triumph Of Sociobiology (pp. 134).

cv. See The Triumph Of Sociobiology (pp. 24, 27-28, 32, 48-49, 57-58, 63, 71-72).

cvi. See The Triumph Of Sociobiology (pp. 58-59, 61, 65, 67-71), The Extended Phenotype (pp. 28-29, 31-32, 40, 44), Consilience (pp. 154), The Blank Slate (pp. 377), The Selfish Gene (pp. 28), and Science In The Soul (pp. 145).

cvii. See How To Create A Mind: The Secret Of Human Thought Revealed by Ray Kurzweil (Viking) (2012) (pp. 14-16), The Blank Slate (pp. 30), The Selfish Gene (pp. 15-17), Parallel Worlds: A Journey Through Creation, Higher Dimensions, And The Future Of The Cosmos by Michio Kaku (Doubleday / Anchor) (2004) (187), Cosmos (pp. 271-2), and The Life Of The Cosmos by Lee Smolin (Oxford University Press) (1997) (pp. 45).