All About Genes

by Steven Gussman

        Despite all of the posturing about, “interactionist,” models of phenotype (to say nothing of pure, “environmentalis,”) all of the theories of biology (and much of the controversial hypotheses still being argued over) are integrally genetic. You wouldn't know it from most discussions of behavioral genetics, but there are indeed reports of, “vacuum behaviors,” in the animal kingdom (let alone the obvious cases of vacuum morphology).ⁱ Richard Dawkins writes:

        The urge to feel 'grateful' in a vacuum, when there's nobody there to thank, is very strong. Animals sometimes perform complicated patterns of behavior in a vacuum – they are even called 'vacuum activities'. The most spectacular example I know is from a German film I once saw of a beaver... Beavers probably don't understand why they do it. They just do it without thinking, because they have a mechanism in the brain that goes off like clockwork. They are like little dam-building robots. The clockwork behavior patterns that form the components of dam-building routines are quite complicated and very different from the movements that any other animal does – because no other animal builds dams.

        Now the beaver in the German film was a captive beaver, which had never built a real dam in its life. It was filmed in a bare room, with a bare cement floor: no river to dam, and no wood to dam it with. But, amazingly, this poor lonely beaver went through all the motions of building a dam in a vacuum. It would pick up phantom pieces of wood in its jaws, and carry them to its phantom dam, shoving them in, tamping them down, generally behaving as though it 'thought' there was a real dam there, and real wood to tamp into it.

        I think this beaver felt an overwhelming urge to build a dam, because that is what it would do in nature. And it went ahead and 'built' a phantom dam in a vacuum.ⁱⁱ

This should perhaps not be so surprising: how could heredity (and the age-old practice of breeding—which is far less precise work than, say, editing individual genes) work if genes didn't encode stable phenotypical consequences (as Mendel demonstrated)?ⁱⁱⁱ Further, how could natural selection of said genes over the last four billion years of life on Earth have worked if genes did not have stable phenotypical consequences (and therefore relatively stable fitness consequences, as in Darwin)?^iv

        Sexually reproducing species serve to clarify the role of genes. Any adaptations which have been selected during the last two billion years of evolution since sexual reproduction evolved in our lineage^v did so under circumstances where offspring only received half of the genes of each parent (though the vast majority of these are shared between the parents, as-is).^vi In these circumstances, every child is impressively unique compared to, say, a cell which reproduces by splitting (mitosis), in which the only genetic variance introduced is rare mutation (not unique combination).^vii To put a finer point on this: the reason individuals in a sexually reproducing species are more unique is because each has a more unique genome (not because of environmental variance). Unlike with Mendel, the environment (everything outside of a singular gene held constant)^viii actually does factor into Darwin's successful theory of evolution by natural selection. It does so, to a first approximation, by acting as a selection pressure^ix (varying through time, as the environment changes) on relatively stable alleles (if these genes weren't for something, the changing environment could hardly select from them over the eons, let alone build complex, cumulative adaptations such as organs; in fact, the phenotype they encoded would be changing wildly with the environment).^x It is essential to evolutionary theory that gametes' genes express similarly to one's parents—this is what fitness is, the tendency to express phenotype which make one more likely to successfully reproduce; it cannot be a crap-shoot whether those genes reliably encode phenotype, or no adaptation could evolve, much less of the complex variety.^xi Contrary to general belief, it is the genes play the major role within lifetimes, while the environment plays the major role over generations.^xii When a gene changes, we call this a mutation, and sensibly expect a resulting change in phenotype. When the environment changes, we view it as a change in the selection pressure on the genes (this must have been moreso the case than that it merely changes the expression of genes, even though the latter mechanism itself can be selected for as conditional adaptation).^xiii Nobody thinks that life evolves because genomes remain constant and change their expression in response to the environment (an expression cannot really be selected for; as with any complex trait, multiple genes must be simultaneously or sequentially selected for an environmentally-responsive phenotype to evolve). Changing environments changes the curves of the adaptive landscape and potentially puts the, "stable," portion of the genome back into play (this doesn't generally change the likelihood of mutation in those regions, but changes the likelihood that a new mutation will increase the organism's fitness). The evolution of even the, “simplest,” organisms requires the stable genotype-phenotype relationship of thousands of alleles over many generations of selection.^xiv

        Even when we view the environment on Darwinnian terms, as a variant selection pressure, there are serious regularities at play (in the extreme, the laws of physical chemistry are of course shared everywhere in the cosmos, much less everywhere on Earth).^xv So much so is this the case that a recurrent phenomenon called convergent evolution occurs, wherein species share phenotype (say, a sensory organ like the eye) not because they share a common ancestor with that phenotype and thereby inherited it, but because it independently evolved in each of these species due to its objectively fit design (the eye evolved tens of known times, independently).^xvi So normal is this phenomenon that Alcock holds the falsifiable prediction of convergent evolution between species in similar environments to be the gold standard of testable sociobiology.^xvii One wonders how important the, “environment,” is to the expression of a gene, when in fact the natural selection of random mutations has so often reliably given rise to the same adaptation (even through different genes)! Such convergence suggests that many aspects of the environment are so uniform as to re-select the same same traits (sometimes through selection of the same genes).^xviii

        Mismatch hypotheses (the idea that our rapidly changing technological environment has rendered some of our slowly-evolved adaptations—like a limitless taste for sugary calories—as maladaptations) are predicated on the idea that the environment is a slow-rolling selection pressure,^xix and not something which determines an organism's traits in-situ.^xx The idea is that, for example, we have genes for eating as though we're in a prehistoric environment of caloric scarcity, and that the environment has changed too quickly for natural selection to have kept up; the genes still cause the same behavior, but the environmental context (near limitless, cheap food) leaves our fitness hurt instead of helped by this phenotype.^xxi The genes determine the actual traits, and their, “interaction with the environment,” simply determines the one-dimensional value of whether this trait is fit or not.

        Ironically, as the eusocial insects demonstrate, the surprisingly different developmental outcomes of genetic clones is only programmed to happen the way that it does because of these hive-mates' high degree of genetic relatedness.^xxii In the hive, not only is there little-to-no variation in genes (and therefore roughly only variation in environment), but there only exists the, "selflessness," required to become such a specialized tool for the queen because of the kin selection at play. As long as you serve as a tool for a genetic clone (rather than for a stranger), it doesn't matter if you're sterile (and serve only a special purpose); the queen's children are the workers' children, genetically speaking.^xxiii One sees the same thing with the cells of a single body (be it a the multi-cellular body of a single eusocial bee or that of a heterogeneous human), it's simply that we have a harder time seeing bees', “individual,” bodies as, "organs," of their queen (and likewise, we have a hard time seeing the single cells of our organs as organisms in themselves).^xxiv The original single-celled organism was a germ-line replicator in its division. Those in our body (which all have the same genome that we, the brain-and-body call, “ours”) instead replicate somatically for the purpose of growth, healing, and overall maintenance of the body (in service of the replication of the germline sperm or ovum).^xxv This is not selfless altruism on the part of the cell—somatic growth in a human body is small peanuts compared to the generations of man.^xxvi Like the eusocial insects, your cells share a common genome, and therefore a common goal with your overall body (or, “gene machine,”): sexual reproduction (getting half of your genome into the future, not just into the space next to you).^xxvii As the castes of an ant-hill or bee-hive demonstrate (all highly morphologically and behaviorally distinct), environmental cues allow one genome to support the development of many different kinds of cells, which ultimately makes up the different organs (pancreatic cells are trait-specialized very differently than the way skin cells or bladder cells are specialized).^xxviii Yet for all of this, notice that the different classes of a given species (say, a particular kind of bee) are still far and away more similar than not—genes explain why you can tell a bee from a frog, even if the environment plays a role (at the genes' discretion) in why you can tell a sterile worker from the queen. So much can be explained in terms of eusocial / somatic versus germline.^xxix Genetically heterogeneous individuals tend to be generalists (and therefore more similar) because they are in competition (here, competition between small variant alleles reigns). When it is every man for himself, he better be able to do everything himself. On the other hand, homogeneous cells can environmentally specialize so as to cooperate. What allows cooperation, and therefore specialization, are kin-selection (genetic homogeneity) and reciprocal altruism (mutually beneficial trade between unrelated individuals).^xxx It is well-accepted that once a human population graduates from a nomadic lifestyle to become sedentary agriculturalists, its members create a specialized economy of reciprocity, each member benefiting from others' specialties.^xxxi

        Genes can code for both environmental sensors (which could be as simple as a different chemical reaction occurring when in a bath of a different chemical, or as complex as the photo-sensors we call eyes detecting all manner of information then processed by our brains) and expression (ultimately, of a morphological or behavioral consequence) conditioned on the, "readings," of those sensors.^xxxii In other words, the same set of alleles could have been selected because they encode trait A in environment x, and trait B in environment y (indeed, all that is needed is that such a set of genes confers greater fitness than sets of genes which only encode trait A or B, regardless of environmental stimulus).^xxxiii A gene that finds itself in a male versus a female body (itself part of a gene's, “environment,”) might well have a very different expression (meaning that even the shared portion of the genome can account for innate differences which have nothing to do with the familial or cultural differences usually in the minds of those invoking, "environmental," causation).^xxxiv No one seems to realize that when they say, “the environment, A, causes trait, Y,” what they are ultimately saying is that, the organism contains genes for trait Y in environment A (or at most, genes for a brain which learns to respond with Y to environment A).^xxxv Though many examples have been discovered (from birds learning to fly, to humans learning who to avoid incestual sexual relations with), no one has systematically looked into how much of what we call learning can be modeled in the following way: we're pre-wired to learn certain things (and not others) from the (expected) environment (though E. O. Wilson claimed such biased learning is always found upon inspection).^xxxvi Some (including Dawkins!) may think this kind of explanation overly complicated, but the same can be said of the brain in the first place; and nevertheless, sometimes it will have been the mutational pathway that was taken, regardless of whether there's a more efficient, hard-wired possibility (in terms of morphology, Dawkins points out that the natural history of an artery in the giraffe explains its poor design).^xxxvii

        Innate developmental characteristics feature not only conditional adaptation (as with older siblings and younger siblings—often the same individual employing a different strategy under different circumstances—using different mechanisms to identify kin in the context of incest avoidance),^xxxviii but redundancy! So powerful are the genes that, if they, "want," (read: if it is significantly more fit to, "do so,") they can evolve multiple different developmental pathways to ensure the correct phenotype arises in different environments. This is clearly the case with sex-determination: when the normal chromosomal mechanism fails (which is rare), different mechanisms have evidently been selected to produce normal sex determination after-all (meaning at least both of these mechanisms need to fail for an intersex person to be born).^xxxix

        Genetic drift (the noise involved in a changing genome over time) and, "spandrels," (side-effect traits—a hypothesis I believe natural selection obviates)^xl also admit of, "genetic determinism," (rather than environmental causation). Genetic drift plays a role much more like mutation than selection, and therefore cannot be the terminus of an explanation for complex traits.^xli Spandrels are ripe for exaptation,^xlii and therefore are expected to be removed, kept, and/or modified in direct proportion to their serving of the organism's fitness (ordinary natural selection).

        Or take horizontal gene transfer (HGT), which is sometimes construed as a challenge to Darwinism.^xliii It turns out that some microscopic life-forms have the ability to meet up, and essentially edit each other's genes (by sending usable code over, “horizontally,” rather than, “vertically,” or by descent).^xliv Does this present a serious challenge to the neo-Darwinnian synthesis? HGT is certainly not Lamarckian, as the resulting traits are acquired through sharing static genes, not through striving in environments. Further, the ability to carry out HGT (both sending and receiving)—the organelles, behavior, and which genes are sent/received, and by whom—are all the parts of a complex apparatus, which only natural selection (and not HGT itself) can explain. It is therefore predicted that HGT, like any other form of altruism, will have been naturally selected to be utilized in contexts of kin selection (sharing resources with close relatives who share a good proportion of genes, already) and reciprocal altruism (in which unrelated organisms make trades whose individual benefits outweigh the individual costs).^xlv In principle, if one performs enough HGT with the same organism, it will become kin—though this may be precluded by the number of genes at play, HGT could close the gap between reciprocal altruism and genuine kin in such microorganisms. Far from a challenge, HGT is at most texture atop the neo-Darwinnian synthesis which gave rise to it.^xlvi And in any event, whether vertical or horizontal, genetic determinism is genetic determinism (only all the moreso if it turns out to be true that HGT can successfully occur between members of different species).^xlvii

        Nor does group-selection do anything to dethrone genetics (let alone biology). Even for hard-group selectionists, the raw traits of the individuals of a group must have been provided by the prior natural selection of genes.^xlviii It is actually admitted that group selection (which is largely not ascribed-to in mainstream evolutionary biology) is at best another way to frame the genetic selection of some traits.^xlix Here too, it is the selection of genetics, not of groups, that has explained biodiversity.^l These ancillary concepts often serve as a cynical, pseudo-scientific repertoire for anti-evolutionists to pull from (be they Christian fundamentalists or radical feminists).^li

        The nature v. nurture debate is ultimately bizarre on its face, from the perspective of the sciences: nature is what the scientist studies (indeed, modern science grew out of a tradition known as, “natural philosophy,” and naturalism remains absolutely integral to the scientific method)! “Nurture,” “culture,” and what have you—these are all part of the natural world—phenomena to be understood via ordinary philosophy of science (but they are almost always invoked in the exact opposite spirit, by academics and laypeople alike: as magical, random, or otherwise comforting refuge for people who want to believe they are not bound by any kind of limits).^lii Even if you prefer to call it the, “genes versus environment,” debate: the, “environment,” of which almost everyone actually means (either directly, or through sleight-of-hand—as if the amount of prenatal testosterone in a womb is indistinguishable from Marxist historical materialism, or from a Freudian model of parenting) cannot provide the kind of magic the critics of evolution and genetics (tellingly, only in the context of humans) demand.^liii Ultimately, life is the successful replication of genes which hold the blueprint for the organism and its developmental phenotype which must be caused by that genotype, or else Darwinnian evolution couldn't have happened, and we would be back to square one with explaining (and unifying) the biodiversity evident all around us.^liv This is what the neo-Darwinnian theory (evolution by natural selection of genes) provides for us; “environment,” explains nothing (and certainly not the four billion year natural history of life on Earth, adaptation, speciation, nor any of the other major topics in the life sciences).^lv

        Furthermore, it is moreso the case that the genes in living organisms affect their environment than the other way around. For example, it is understood that the metabolism of the prehistoric population of blue-green algae changed the atmosphere of the planet to a high proportion of oxygen, drastically changing the natural history of life on Earth).^lvi In fact, the (as far as we can tell) lifless alien worlds observed in our solar system are far less interesting than ours; this is not because they, “lack environments,” but genes. Bi-directional complexity is surely important to our continued discovery toward a final theory of what makes the natural world tick. But we should not lose sight of the explanatory power of even the most naive version of Darwinism, which views stable genes-for-traits as being selected by a variable-environment.^lvii It is this basic model which explains the regularity and form of the animal kingdom, and which serves as the linchpin of our understanding of life.^lviii By contrast, gene-expression-extremely-sensitive-to-the-environment could hardly cause phenotype stable enough to be selected for, generation over generation, to produce the familiar adaptations we see everywhere around us.^lix “Gene expression,” refers to the turning on and off of genes by repressor and promoter proteins.^lx Yet even repressor and promoter proteins are, you guessed it, ultimately regulated by the genes, which design a machine in which such proteins are present and function the way that they do in the first place. Such proteins are the heritable effects of genes, which affect the fitness of the organism, and are therefore subject to—in fact, originally created by—natural selection among genetic alleles (genes must have preceded that which came to, “regulate,” them). Therefore even the mechanism of, “gene-expression,” is ultimately caused by the information contained in genes (and not by some disconnected, “environment”). The closest concepts to non-genetic causation from the environment are the random effects of mutation, or otherwise the non-random, selective pressures acting on causal genetic alleles (in other words, not-so-non-geneitc). Often, we're expected to take deviations from classical Darwinism to be extremely important, when in reality, they're either isolated to some minority domain, or otherwise simply subsumed by the neo-Darwinnian synthesis (evolutionary genetics).^lxi

The view that there exists the, “environmental,” development, as a gap between the gene and the phenotype, is mythical; this developmental process is itself encoded in the genome (it is phenotype caused by genes for this process), and if it did not reliably lead to the more obvious phenotypic endpoint (the trait being developed), it would not have been selected into the gene pool.^lxii Far from an independent causal factor as-or-more powerful than genetics, developmental processes are the phenotype the relevant genes encode for.^lxiii

        Nearly all of the practice of medicine is the practice of implementing, “environmental,” interventions to prevent or cure disease. The machinery the genes ultimately built can be bathed in a certain drug (or not,) and thereby yield drastically different outcomes. Yet most would still not call this process an example of, “gene expression,” contingent on environmental variables. By contrast, there do exist therapeutics which make direct use of DNA and RNA, including the mRNA covid-vaccines. These vaccines work by taking the snippet from SARS-COV-2's genome which encodes for the spike protein, and delivering it to your molecular machinery which then reliably builds many copies of the spike protein (and not something else) for your immune system to more safely learn from.^lxiv A viruse such as SARS-COV-2 was naturally selected (that is, its genes encode for it to function in this way) to commandeer its hosts' bio-molecular machinery to produce copies of itself—this is what an infection is.^lxv Granted, the virus needs be inside of a viable host's body, but once there, though the road between RNA and replicants is complex, one can rely upon the stable relationship between that RNA (genome) and the copies of itself it ultimately gives rise to: SARS-COV-2 never accidentally, due to, “environmental,” interactions, causes your machinery to produce influenza virons, instead (though mutations may well fork some lineages on the gradual path to a new variant of SARS-COV-2). (Further, when I say that the, “environment,” that matters here is a, “viable host—” this is the bio-chemical micro-environment encoded in the host-organism's genome).^lxvi It is worth dwelling on this point: your body, never meant to build the magnificently complex SARS-COV-2 virus, can nevertheless reliably be expected to do so countless times over once exposed to the right genes for doing so (in fact, a human body from three-hundred-thousand years before this virus existed should be able to do so more successfully because less of an immune response can have developed; this is why smallpox was so harmful to Amerindians).^lxvii Outside of random mutations, the infected body simply replicates perfect copies of SARS-COV-2 (meanwhile the randomness of mutational accidents with respect to their phenotypic consequences too relies on the theory of genetic determination). Surely, you may think, the immune response itself is, "environmental." Not really. The immune system is certainly a complex adaptation given rise to by genes. Specific immunity to novel infections is actually a great example of, "biased learning—" the body makes note of the agent's phenotype as part of its memory of attack.^lxviii Even Skinnerean behaviorism (including Pavlovian conditioning) is integrally genetic—another example of biased learning. Something similar could be said of somatic maintainence—when you have a cut that needs healing, you better hope that its skin cells, as defined in the genome (and not something else, at the whims of the environment), which replaces your old skin. In fact, with technologies like CRISPR, we are increasingly finding ourselves with the ability to directly edit genomes, gene by gene. Tellingly, E. O. Wilson did not say that environmental interventions would, “decommission natural selection—” (and presumably thereby determine our traits), he said that the ability to edit our genes would do so.^lxix Astonishingly, the same gene can sometimes encode the same phenotype across species.^lxx So it is with the famous trick in which bio-phosphorescence is taken from jellyfish and planted in rabbits and bacterium.^lxxi More practically, so-called, “golden rice,” uses maize and soil bacteria genes to create rice which contains more beta carotene nutrients.^lxxii Such transgenes are a rather dramatic demonstration that genes are encoding for phenotype.

        In recent decades, there has also been an, “ancient DNA revolution,” in which we are learning much of what we know about our deep ancestry (and cousins) through DNA, alone.^lxxiii How would we get the sense that we can learn much about these people if genes weren't the primary determinant of organisms?

        Notice that the same moralizing and discomfort with genetic determinism doesn't plague research on gene-editing (which has to deal with its own critics in ethics departments), as it does with the natural selection of human nature. Perhaps this is because the debate isn't actually about the reality or un-reality of genetic determinism, but about being in control (as with gene editing), or not being in control (as with the prehistoric endowment of human nature).^lxxiv While a vocal minority (if not an outright majority of academics) can be heard doubting the existence of a heritable general intelligence, one rarely hears anyone doubting the eventual effectiveness of gene editing for exactly this (and other) purpose(s).^lxxv It would seem that this is because, in the, "right," hands, gene-editing offers a potential boon, not a challenge, for those who want to design the minds of others.

        The meta-truth about the field of biology is that, even spanning all controversies in biological theory, there is no controversy over genetic determinism, which is central to every single viable model in the life sciences.

Footnotes:

i. See Science In The Soul: Selected Writings Of A Passionate Rationalist by Richard Dawkins (Bantam Press) (2017) (pp. 244-5), The Blank Slate: The Modern Denial Of Human Nature by Steven Pinker (Penguin Books) (2003 / 2016) (pp. 90), and Consilience: The Unity Of Knowledge by E. O. Wilson (Vintage) (1998) (pp. 150-151, 181).

ii. See Science In The Soul (pp. 244-5).

iii. See The Triumph Of Sociobiology (pp. 18).

iv. See The Triumph Of Sociobiology (pp. 17-18) and Cosmos (pp. 27).

v. See “Sexual Reproduction And The Evolution Of Sex” by Sarah P. Otto (Nature Education) (2008) (https://www.nature.com/scitable/topicpage/sexual-reproduction-and-the-evolution-of-sex-824/#:~:text=The%20first%20eukaryotes%20to%20engage,neurons%20capable%20of%20assessing%20pleasure) and Cosmos by Carl Sagan (Ballantine Books) (1980 / 2013) (pp. 28).

vi. 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 Extended Phenotype (pp. 143-144), and The Selfish Gene (pp. 189).

vii. See The Red Queen: Sex And The Evolution Of Human Nature by Matt Ridley (Harper Perennial) (1993) (pp. 45-47) and The Selfish Gene by Richard Dawkins (Oxford University Press) (1976 / 2016) (pp. 31-33, 39).

viii. See The Triumph Of Sociobiology by John Alcock (Oxford University Press) (2001) (pp. 43).

ix. See Consilience (pp. 149) and The Extended Phenotype: The Long Reach Of The Gene by Richard Dawkins (Oxford University Press) (1982 / 2016) (pp. 143).

x. See The Extended Phenotype (pp. 40, 44, 127, 401), The Selfish Gene (pp. 28), and Science In The Soul (pp. 145).

xi. See The Extended Phenotype (pp. 40, 44, 127, 401), The Selfish Gene (pp. 28), and Science In The Soul (pp. 145).

xii. See The Triumph Of Sociobiology (pp. 15-16).

xiii. See Consilience (pp. 149) and The Extended Phenotype (pp. 143).

xiv. See The Triumph Of Sociobiology (pp. 16).

xv. See “Evolutionary Convergence” by Simon Conway Morris (Current Biology) (1998) (https://www.cell.com/current-biology/pdf/S0960-9822(06)02143-9.pdf), Consilience (pp. 150-151, 181), and The Blank Slate (pp. 90).

xvi. See “Mother Nature Can't Stop Evolving Eyes” by Troy Farah (Salon) (2023) (https://www.salon.com/2023/04/16/mother-nature-cant-stop-evolving-eyes/).

xvii. See The Triumph Of Sociobiology (pp. 72-3).

xviii. See “Evolutionary Convergence”, Consilience (pp. 150-151, 181), The Blank Slate (pp. 90), and The Ape That Understood The Universe: How The Mind And Culture Evolved by Steve Stewart-Wiliams (Cambridge University Press) (2018) (pp. 270).

xix. See The Blank Slate (pp. 219), The World Until Yesterday: What Can We Learn From Traditional Societies? by Jared Diamond (Viking) (2012) (pp. 414), and The Ape That Understood The Universe (pp. 45-47, 50-51, 56, 209, 290-291).

xx. See The Blank Slate (pp. 219), The Ape That Understood The Universe (pp, 45-56, 143, 209, 290-291), and The World Until Yesterday (pp. 276-279, 414).

xxi. See “The Consuming Instinct | Dr. Gad Saad | Talks at Google” by Gad Saad (Talks At Google) (2017) (https://youtu.be/_qHYmx7qPes?t=3271) (54:31-55:18).

xxii. See The Extended Phenotype (pp. 127-128, 130, 250-251) and The Triumph Of Sociobiology (pp. 98-100).

xxiii. See The Selfish Gene (pp. 226, 229-233, 420-421), The Extended Phenotype (pp. 115, 214), The Triumph Of Sociobiology (pp.96-103), The Ape That Understood The Universe (pp. 24-6, 138, 176, 185, 209, 212, 216, 288)?, and Scientist: E. O. Wilson: A Life In Nature by Richard Rhodes (Doubleday) (2021) (pp. 105-6).

xxiv. See The Extended Phenotype (pp. 7-8, 127-128) and “The False Allure Of Group Selection” by Steven Pinker (Edge) (2012) (https://zoo-web02.zoo.ox.ac.uk/group/west/PDF-media/Pinker_Edge_2012.pdf).

xxv. See The Extended Phenotype (pp. 7-8, 127-128, 130, 250-251) and “The False Allure Of Group Selection”.

xxvi. See The Extended Phenotype (pp. 7-8, 127-128, 204-205) and “The False Allure Of Group Selection”.

xxvii. See The Extended Phenotype (pp. 7-8, 127-128, 204-205) and “The False Allure Of Group Selection”.

xxviii. See The Extended Phenotype (pp. 127-128, 130, 250-251) and The Triumph Of Sociobiology (pp. 98-100).

xxix. See The Extended Phenotype (pp. 127-128).

xxx. See The Selfish Gene (pp. 114-40, 239-44, 261-301, 390-1), The Extended Phenotype (pp. 41-2, 219, 233-4, 236-7, 296), The Blank Slate (pp. 221, 243, 257-8, 260, 285, 438), and The Ape That Understood The Universe (pp. 25-6, 131, 134, 177-202, 197, 202, 204-9, 212, 288, 290).

xxxi. See The Blank Slate (pp. 167-8).

xxxii. See The Extended Phenotype (pp. 41-43, 52, 143, 343, 350, 384), Consilience by Wilson (pp. 52, 149, 152-153, 180-182), The Red Queen (pp. 186-193), The Triumph Of Sociobiology (43), and The Blank Slate (pp. 73-102, 315-316).

xxxiii. See The Extended Phenotype (pp. 41-42, 52, 143, 184-185, 343, 350, 384) and The Blank Slate (pp. 315-316).

xxxiv. See The Extended Phenotype (pp. 143-145, 205, 211-214).

xxxv. See The Extended Phenotype (pp. 41-43, 52, 143, 343, 350, 384), Consilience by Wilson (pp. 52, 149, 152-153, 180-182), The Red Queen (pp. 186-193), The Triumph Of Sociobiology (43), and The Blank Slate (pp. 73-102, 315-316), “Michael Shermer With Dr. Debra Lieberman — Objection: Disgust, Morality And The Law” (4:28-6:06, 27:24-30:03), and The Ape That Understood The Universe (pp. 222, 238, 315).

xxxvi. See “Michael Shermer With Dr. Debra Lieberman — Objection: Disgust, Morality And The Law” (4:28-6:06, 27:24-30:03), Consilience (pp. 181), and The Ape That Understood The Universe (pp. 222, 238, 315).

xxxvii. See “Richard Dawkins Demonstrates Laryngeal Nerve Of The Giraffe” from Inside Nature's Giants (Channel 4 / NatGeo) (2009) uploaded to YouTube by MysOxen (https://www.youtube.com/watch?v=cO1a1Ek-HD0) and The Extended Phenotype (pp. 41-42, 45-83).

xxxviii. See “Michael Shermer With Dr. Debra Lieberman”.

xxxix. See Emma Hilton's November 21^st, 2018 tweet: https://twitter.com/FondOfBeetles/status/1065234950914478080?t=GMAOne3Mxb6tmnJXT6Q3Ew&s=19; my November 14^th, 2019 tweet: https://twitter.com/schwinn3/status/1195068130927824898?t=HBjqGiMZ3zlCDkBobB8-Ow&s=19; my May 25^th, 2020 tweet: https://twitter.com/schwinn3/status/1264975410665840640?t=HjV2ViWw1lwL_7zZqSpeLQ&s=19; my January 5^th, 2021 tweet: https://twitter.com/schwinn3/status/1346552826789572611?t=vNWkfaTXKwP1OXm_PLP3gg&s=19; and my January 6^th, 2022 tweet: https://twitter.com/schwinn3/status/1533981061251796992?t=hvkQDY7iroH1ujxHL4TAVw&s=19.

xl. See my February 12^th, 2021 tweet: https://twitter.com/schwinn3/status/1360128261985095680?t=t7GQFanYbzA3kGEUtbNLOg&s=19; and “Jordan Peterson Is Back! - Bret Weinstein's DarkHorse Podcast” (DarkHorse Podcast) (2021) (https://youtu.be/O55mvoZbz4Y?list=PLjQ2gC-5yHEug8_VK8ve0oDSJLoIU4b93&t=5960) (1:39:19-1:44:35).

xli. See Science In The Soul (pp. 143-145), The Extended Phenotype (pp. 28-29), and The Selfish Gene (pp. 28).

xlii. See "Exaptation" by W. Tecumseh Fitch (Harper Perrenial / Edge) (2017) (https://www.edge.org/response-detail/27220); my February 12^th, 2021 tweet: https://twitter.com/schwinn3/status/1360128261985095680?t=t7GQFanYbzA3kGEUtbNLOg&s=19; and “Jordan Peterson Is Back! - Bret Weinstein's DarkHorse Podcast” (1:39:19-1:44:35).

xliii. See “My WaPo Review Of David Quammen’s New Book On Evolutionary Trees (And A Comparison With Other Reviews) by Jerry Coyne (Why Evolution Is True) (2018) (https://whyevolutionistrue.com/2018/08/24/my-wapo-review-of-david-quammens-new-book-on-evolutionary-trees/)”

xliv. See The Red Queen (pp. 30, 95-96), The Extended Phenotype (pp. 242-243, 246-247, 345), and Carl Sagan by William Poundstone (Henry Holt) (1999) (pp. 36, 63, 81).

xlv. See The Selfish Gene (pp. 114-40, 239-44, 261-301, 390-1), The Extended Phenotype (pp. 41-2, 219, 233-4, 236-7, 296), The Blank Slate (pp. 221, 243, 257-8, 260, 285, 438), and The Ape That Understood The Universe (pp. 25-6, 131, 134, 177-202, 197, 202, 204-9, 212, 288, 290).

xlvi. See “My WaPo Review Of David Quammen’s New Book On Evolutionary Trees (And A Comparison With Other Reviews)” and The Extended Phenotype by Dawkins (pp. 174, 252-3).

xlvii. See “My WaPo Review Of David Quammen’s New Book On Evolutionary Trees (And A Comparison With Other Reviews)” by Coyne.

xlviii. See Robert Trivers' thoughts on Stephen Jay Gould in “What Prominent Biologists Think Of Stephen Jay Gould” by Nathan Confas which excerpts Trivers' thoughts from “Vignettes Of Famous Evolutionary Biologists, Large And Small” by Robert Trivers (The Unz Review) (2015) (https://www.unz.com/article/vignettes-of-famous-evolutionary-biologists-large-and-small/) (though I have not yet read the rest of this piece); and “The False Allure Of Group Selection” by Steven Pinker (Edge) (2012) (https://www.edge.org/conversation/steven_pinker-the-false-allure-of-group-selection).

xlix. See “The False Allure Of Group Selection”, The Selfish Gene (pp. 10, 122), The Extended Phenotype (pp. 126, 174), The Blank Slate (pp. 258-259), The Triumph Of Sociobiology (pp. 32), and The Ape That Understood The Universe (pp. 211-12).

l. See “The False Allure Of Group Selection”.

li. See The Extended Phenotype (pp.153).

lii. See The Blank Slate (pp. 1-194), The Triumph Of Sociobiology (pp. 129-147), Consilience by Wilson (pp. 206), and “Jordan Peterson Is Back! - Bret Weinstein's DarkHorse Podcast” (1:39:19-1:44:35).

liii. “Behavior = Genes + Environment” by Steven Pinker (Harper Collins / Edge) (2014) (https://www.edge.org/response-detail/25337), The Triumph Of Sociobiology (pp. 129), and Gad Saad's June 27^th, 2013 tweet: https://x.com/GadSaad/status/350298812243382272?s=20.

liv. 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) (pp. 187), Cosmos (pp. 271-2), and The Life Of The Cosmos by Lee Smolin (Oxford University Press) (1997) (pp. 45).

lv. See The Triumph Of Sociobiology (pp. 17), Cosmos (pp. 27), Science In The Soul (pp. 143-145), The Extended Phenotype (pp. 28-29), and The Selfish Gene (pp. 28).

lvi. See “Blue-Green Algae Key To Unlocking Secrets Of Ancient Past” (University Of Bristol) (2021) (https://www.bristol.ac.uk/news/2021/august/blue-green-algae-unlocks-secrets-of-past-.html).

lvii. See Consilience (pp. 149) and The Extended Phenotype (pp. 143).

lviii. See The Selfish Gene (pp. 15-17, 28), The Extended Phenotype (pp. 28-29, 127), and Science In The Soul (pp. 143-145), How To Create A Mind (pp. 14-16), The Blank Slate (pp. 30), Parallel Worlds (pp. 187), Cosmos (pp. 271-2), and The Life Of The Cosmos (pp. 45).

lix. See The Extended Phenotype (pp. 40, 44, 127, 401).

lx. See "Repressor" by Paul P. Liu (NIH/NHGRI) (2023) (https://www.genome.gov/genetics-glossary/Repressor#:~:text=A%20repressor%2C%20as%20related%20to,of%20messenger%20RNA%20(mRNA)).

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

lxii. See The Extended Phenotype (pp. 297, 299, 310, 343, 348-350), Consilience (pp. 159), and The Blank Slate (pp. 377).

lxiii. See The Extended Phenotype (pp. 269, 297, 384) and Consilience (pp. 150-151, 181-182), The Blank Slate (pp. 69, 317, 328, 377).

lxiv. See The Extended Phenotype (pp. 242-243, 345).

lxv. See The Extended Phenotype (pp. 212, 242-243, 335, 247, 345).

lxvi. See The Extended Phenotype (pp. 48, 143-144, 242-243, 247, 269, 297-299, 310, 316, 339, 343-345, 350, 384), The Selfish Gene (pp. 53), Consilience (pp. 149, 151-153), The Triumph Of Sociobiology (pp. 43), and The Blank Slate (pp. 60, 69).

lxvii. See In The Hands Of The Great Spirit: The 20,000 Year History Of American Indians by Jake Page (Free Press) (2003) (pp. 101, 103, 105, 133).

lxviii. See The introduction and “10-21. Immunological Memory Is Long-Lived After Infection Or Vaccination” from Immunobiology: The Immune System in Health and Disease: 5^th Edition by Charles A. Janeway, Jr., Paul Travers, Mark Walport, and Mark J Shlomchik (Garland Science) (2001) (though I have only read this small section); “Michael Shermer With Dr. Debra Lieberman — Objection: Disgust, Morality And The Law” (4:28-6:06, 27:24-30:03); Consilience (pp. 181); and The Ape That Understood The Universe (pp. 222, 238, 315).

lxix. See Consilience (pp. 302-303).

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

lxxi. See “Scientists breed glow-in-the-dark rabbits” by Amanda Holpuch (The Guardian) (2013) (https://www.theguardian.com/world/2013/aug/13/glow-in-dark-rabbits-scientists).

lxxii. See “GM Crops Like Golden Rice Will Save The Lives Of Hundreds Of Thousands Of Children” by Matt Rdidley (Quillette) (2019) (https://quillette.com/2019/12/01/gm-crops-like-golden-rice-will-save-the-lives-of-hundreds-of-thousands-of-children/).

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).

lxxiv. See The Blank Slate (pp. 1-194), The Triumph Of Sociobiology (pp. 129-147), Consilience (pp. 206), and “Jordan Peterson Is Back! - Bret Weinstein's DarkHorse Podcast” (1:39:19-1:44:35).

lxxv. See Richard Dawkins' March 17^th, 2013 Tweet: https://x.com/RichardDawkins/status/313194413021085696?s=20 and his February 16^th, 2020: https://x.com/RichardDawkins/status/1228943686953664512?s=20 for an example of a situation where the far left really did deny the effectiveness of, in this case human breeding, for intelligence.