Phenotype Quotes

The point is this: if you cannot separate the phenotype of mental illness from creative impulses, then you cannot separate the genotype of mental illness and creative impulse.

But race is not biology; race is sociology. Race is not genotype; race is phenotype. Race matters because of racism. And racism is absurd because it’s about how you look. Not about the blood you have. It’s about the shade of your skin and the shape of your nose and the kink of your hair. Booker

With only a little imagination we can see the gene as sitting at the centre of a radiating web of extended phenotypic power.

In the world of the extended phenotype, ask not how an animal's behaviour benefits its genes; ask instead whose genes it is benefiting.

Putting these three things together we arrive at our own ‘central theorem’ of the extended phenotype: An animal’s behaviour tends to maximize the survival of the genes ‘for’ that behaviour, whether or not those genes happen to be in the body of the particular animal performing it.

There are species that retain their characteristics even in conditions that are relatively different from their natural ones; other species in similar circumstances instead become extinct; otherwise what takes place is racial mixing with other elements in which no assimilation or real evolution occurs. The result of this interbreeding closely resembles Mendel’s laws concerning heredity: once it disappears in the phenotype, the primitive element survives in the form of a separated, latent heredity that is capable of cropping up in sporadic apparitions, even though it is always endowed with a character of heterogeneity in regard to the superior type.

This 'web of discourses' as Robyn called it...is as much a biological product as any of the other constructions to be found in the animal world. (Clothes too, are part of the extended phenotype of Homo Sapiens almost every niche inhabited by that species.An illustrated encyclopedia of zoology should no more picture Homo Sapiens naked than it should picture Ursus arctus-the black bear- wearing a clown suit and riding a bicycle.

And analogies were mostly meaningless—a matter of phenotype rather than genotype (to use another analogy).

Genes affect proteins, and proteins affect X which affects Y which affects Z which . . . affects the phenotypic character of interest.

genotype + environment + triggers + chance = phenotype

Is Obama Anything but Black? So lots of folk—mostly non-black—say Obama’s not black, he’s biracial, multiracial, black-and-white, anything but just black. Because his mother was white. But race is not biology; race is sociology. Race is not genotype; race is phenotype. Race matters because of racism. And racism is absurd because it’s about how you look. Not about the blood you have. It’s about the shade of your skin and the shape of your nose and the kink of your hair. Booker T. Washington and Frederick Douglass had white fathers. Imagine them saying they were not black. Imagine Obama, skin the color of a toasted almond, hair kinky, saying to a census worker—I’m kind of white. Sure you are, she’ll say. Many American Blacks have a white person in their ancestry, because white slave owners liked to go a-raping in the slave quarters at night. But if you come out looking dark, that’s it. (So if you are that blond, blue-eyed woman who says “My grandfather was Native American and I get discrimination too” when black folk are talking about shit, please stop it already.) In America, you don’t get to decide what race you are. It is decided for you. Barack Obama, looking as he does, would have had to sit in the back of the bus fifty years ago. If a random black guy commits a crime today, Barack Obama could be stopped and questioned for fitting the profile. And what would that profile be? “Black Man.

...catching a glimpse of his rather hippyish form in a mirror, he wonders at this atavism of apparel, is it an inversion of foetal ontogeny, in which the phenotype passes through previous fashion stages? Soon there will be gaiters and gloves...I will probably die, he thinks, clad in animal skins.

How does one undermine the framework of racial reasoning? By dismantling each pillar slowly and systematically. The fundamental aim of this undermining and dismantling is to replace racial reasoning with moral reasoning, to understand the black freedom struggle not as an affair of skin pigmentation and racial phenotype but rather as a matter of ethical principles and wise politics, and to combat the black nationalist attempt to subordinate the issues and interests of black women by linking mature black self-love and self-respect to egalitarian relations within and outside black communities. The failure of nerve of black leadership is its refusal to undermine and dismantle the framework of racial reasoning.

The genes in one organism’s cells, then, can have extended phenotypic influence on the living body of another organism; in this case a parasite’s genes find phenotypic expression in the behaviour of its host.

A replicator may be said to ‘benefit’ from anything that increases the number of its descendant (‘germ-line’) copies.

phenotypic plasticity,

Finally, at the end of the chapter, we saw that genes ‘sharing’ a given extended phenotypic trait might come from different species, even different phyla and different kingdoms.

One is that phenotypes that extend outside the body do not have to be inanimate artefacts: they can themselves be built of living tissue.

The other idea is that wherever there are ‘shared’ genetic influences on an extended phenotype, the shared influences may be in conflict with each other rather than cooperative

The second point of this present chapter is that the genes that bear upon any given extended phenotypic trait may be in conflict rather than in concert with one another.

My instinct, of course, is to imagine us as one of many planets racing its evolution against its sun--merely one in the galactic Darwinian pursuit. But maybe we're not. Maybe all this talk of the inevitability of aliens is garbage and we're miraculously, beautifully alone in our biological success. What if we're winning? What if we're actually the most evolved intelligence in all this big bang chaos? What if other planets have bacteria and single-celled genotypes but nothing more? The precedent is all the more pressing. Humans alone could be winning the race against our giant gas time bomb and running with the universal Olympic torch. What an honor. What a responsibility. What a gift we have been given to be born in an atmosphere with oxygen and carbon dioxide and millions of years and phenotypes cheering us on with recycles of energy. The thing is, I think we can make it. I think we can shove ourselves into spaceships before things get too cold. I only hope we don't fuck things up before that. Because millions of years is a long time and I don't want to let the universe down.

Almost 48 percent of those who identified as Hispanic or Latina/o categorized themselves as white, even though many do not meet the dominant racial phenotypic notion of U.S. whiteness.

But no. That was analogy rather than homology. What in the humanities they would call a heroic simile, if he understood the term, or a metaphor, or some other kind of literary analogy. And analogies were mostly meaningless — a matter of phenotype rather than genotype (to use another analogy). Most, of poetry and literature, really all the humanities, not to mention the social sciences, were phenotypic as far as Sax could tell. They added up to a huge compendium of meaningless analogies, which did not help to explain things, but only distorted perception of them. A kind of continuous conceptual drunkenness, one might say. Sax himself much preferred exactitude and explanatory power, and why not? If it was 200 Kelvin outside why not say so, rather than talk about witches’ tits and the like, hauling the whole great baggage of the ignorant past along to obscure every encounter with sensory reality? It was absurd.

If two beavers working on the same dam have different genes for dam height, the resulting extended phenotype will reflect the interaction between the genes, in the same way as bodies reflect gene interactions.

Just as every gene is the centre of a radiating field of influence on the world, so every phenotypic character is the centre of converging influences from many genes, both within and outside the body of the individual organism.

If the phenotypic change in the artefact had an influence on the success of replication of the new gene, natural selection would act, positively or negatively, to change the probability of similar artefacts existing in the future.

Most of the replicators in the world have won their place in it by defeating all available alternative alleles. The weapons with which they won, and the weapons with which their rivals lost, are their respective phenotypic consequences

From the viewpoint of this book an animal artefact, like any other phenotypic product whose variation is influenced by a gene, can be regarded as a phenotypic tool by which that gene could potentially lever itself into the next generation.

It is these phenotypic effects that we see as adaptations to survival. When we ask whose survival they are adapted to ensure, the fundamental answer has to be not the group, nor the individual organism, but the relevant replicators themselves.

The gene’s extended phenotypic effect, say an increase in the height of the dam, affects its chances of survival in precisely the same sense as in the case of a gene with a normal phenotypic effect, such as an increase in the length of the tail.

McKusick's belief in this paradigm-the focus on disability rather than abnormalcy-was actualized in the treatment of patients in his clinic. Patients with dwarfism, for instance, were treated by an interdisciplinary team of genetic counselors, neurologists, orthopedic surgeons, nurses, and psychiatrists trained to focus on specific disabilities of persons with short stature. Surgical interventions were reserved to correct specific deformities as they arose. The goal was not to restore "normalcy"-but vitality, joy, and function. McKusic had rediscovered the founding principles of modern genetics in the realm of human pathology. In humans as in wild flies, genetic variations abounded. Here too genetic variants, environments, and gene-environment interactions ultimately collaborated to cause phenotypes-except in this case, the "phenotype" in question was disease. Here too some genes had partial penetrance and widely variable expressivity. One gene could cause many diseases, and one disease could be caused by many genes. And here too "fitness" could not be judged in absolutes. Rather the lack of fitness-illness [italicized, sic] in colloquial terms- was defined by the relative mismatch between an organism and environment.

In the United States both scholars and the general public have been conditioned to viewing human races as natural and separate divisions within the human species based on visible physical differences. With the vast expansion of scientific knowledge in this century, however, it has become clear that human populations are not unambiguous, clearly demarcated, biologically distinct groups. Evidence from the analysis of genetics (e.g. DNA) indicates that most physical variation, about 94%, lies within so-called racial groups. Conventional geographic "racial" groupings differ from one another only in about 6% of their genes. This means that there is greater variation within "racial" groups than between them. In neighboring populations there is much overlapping of genes and their phenotypic (physical) expressions. Throughout history whenever different groups have come into contact, they have interbred. The continued sharing of genetic materials has maintained all of humankind as a single species.

We have now also seen that, in precisely the same sense as it is ever possible to talk of a gene ‘for’ a behaviour pattern, it is possible to talk of a gene, in one organism, ‘for’ a behaviour pattern (or other phenotypic characteristic) in another organism.

An organism is the physical unit associated with one single life cycle. Replicators that gang up in multicellular organisms achieve a regularly recycling life history, and complex adaptations to aid their preservation, as they progress through evolutionary time.

If replicators exist that are active, variants of them with certain phenotypic effects tend to out-replicate those with other phenotypic effects. If they are also germ-line replicators, these changes in relative frequency can have long-term, evolutionary impact.

An extended phenotypic character is the product of the interaction of many genes whose influence impinges from both inside and outside the organism. The interaction is not necessarily harmonious—but then nor are gene interactions within bodies necessarily harmonious,

An active replicator is any replicator whose nature has some influence over its probability of being copied. For example a DNA molecule, via protein synthesis, exerts phenotypic effects which influence whether it is copied: this is what natural selection is all about.

Each gene works in a world of phenotypic consequences of other genes. Some of those other genes will be members of the same genome. Others will be members of the same gene-pool operating through other bodies. Yet others may be members of different gene-pools, different species, different phyla.

Of course genes are not directly visible to selection. Obviously they are selected by virtue of their phenotypic effects, and certainly they can only be said to have phenotypic effects in concert with hundreds of other genes. But it is the thesis of this book that we should not be trapped into assuming that those phenotypic effects are best regarded as being neatly wrapped up in discrete bodies (or other discrete vehicles). The doctrine of the extended phenotype is that the phenotypic effect of a gene (genetic replicator) is best seen as an effect upon the world at large, and only incidentally upon the individual organism—or any other vehicle—in which it happens to sit.

Two kinds of factor will affect this half-life. Firstly, replicators whose phenotypic effects render them successful at their business of propagating themselves will tend to have a long half-life. Replicators with longer half-lives than their alleles will come to predominate in the population, and this is the familiar process of natural selection.

Natural selection favours those genes that manipulate the world to ensure their own propagation. This leads to what I have called the central theorem of the extended phenotype: An animal’s behaviour tends to maximize the survival of the genes ‘for’ that behaviour, whether or not those genes happen to be in the body of the particular animal performing it.

Why are genetic determinants thought to be any more ineluctable, or blame-absolving, than ‘environmental’ ones?

The whole purpose of our search for a ‘unit of selection’ is to discover a suitable actor to play the leading role in our metaphors of purpose.

The controversy about group selection versus individual selection is a controversy about the rival claims of two suggested kinds of vehicle.

I define a replicator as anything in the universe of which copies are made.

Replicators may be classified in two ways. They may be ‘active’ or ‘passive’, and, cutting across this classification, they may be ‘germ-line’ or ‘dead-end’ replicators.

In principle, we may consider any portion of chromosome as a potential candidate for the title of replicator.

Germ-line replicators, then, are units that actually survive or fail to survive, the difference constituting natural selection.

Active replicators have some effect on the world, which influences their chances of surviving.

It is the effects on the world of successful active germ-line replicators that we see as adaptations.

Any effect that a meme has on the behaviour of a body bearing it may influence that meme’s chance of surviving.

A further important point is that Maynard Smith was seeking the ‘best’ strategy in only a special sense. In fact he was seeking an ‘evolutionarily stable strategy’ or ESS.

The ESS has been rigorously defined (Maynard Smith 1974), but it can be crudely encapsulated as a strategy that is successful when competing with copies of itself.

A passive replicator is a replicator whose nature has no influence over its probability of being copied.

But whether it succeeds in practice or not, any germ-line replicator is potentially immortal. It ‘aspires’ to immortality but in practice is in danger of failing.

As I said, the active/passive distinction cuts across the germ-line/dead-end distinction. All four combinations are conceivable.

Particular interest attaches to one of the four, the active germ-line replicator, for it is, I suggest, the ‘optimon’, the unit for whose benefit adaptations exist.

To the extent that active germ-line replicators benefit from the survival of bodies other than those in which they sit, we may expect to see ‘altruism’, parental care, etc.

The word replicator is purposely defined in a general way, so that it does not even have to refer to DNA.

I am, indeed, quite sympathetic towards the idea that human culture provides a new milieu in which an entirely different kind of replicator selection can go on.

One of the greatest problems for systems programmers (the people who write compilers, interpreters, assemblers, and other programs to be used by many people) is to figure out how to write error-detecting routines in such a way that the messages which they feed to the user whose program has a "bug" provide high-level, rather than low-level, descriptions of the problem. it is an interesting reversal that when something goes wrong in a genetic "program" (e.g., a mutation), the "bug" is manifest only to people on a high level - namely on the phenotype level, not the genotype level. Actually, modern biology uses mutations as one of its principal windows onto genetic processes, because of their multilevel traceability.

To the extent that active germ-line replicators benefit from the survival of the bodies in which they sit, we may expect to see adaptations that can be interpreted as for bodily survival.

The point about recurrent reproduction life cycles, and hence, by implication, the point about organisms, is that they allow repeated returns to the drawing board during evolutionary time.

What does complementariness mean for genes? Two genes may be said to be complementary if the survival of each, relative to its alleles, is enhanced when the other is abundant in the population.

Most of the DNA molecules in our bodies are dead-end replicators. They may be the ancestors of a few dozen generations of mitotic replication, but they will definitely not be long-term ancestors.

The controversy about gene selection versus individual (or group) selection is a controversy about whether, when we talk about a unit of selection, we ought to mean a vehicle at all, or a replicator.

the conclusion I wish to draw is not really disputable. If host behaviour or physiology is a parasite adaptation, there must be (have been) parasite genes ‘for’ modifying the host, and the host modifications are therefore part of the phenotypic expression of those parasite genes. The extended phenotype reaches out of the body in whose cells the genes lie, reaches out to the living tissues of other organisms.

The integrated multicellular organism is a phenomenon which has emerged as a result of natural selection on primitively independent selfish replicators. It has paid replicators to behave gregariously. The phenotypic power by which they ensure their survival is in principle extended and unbounded. In practice the organism has arisen as a partially bounded local concentration, a shared knot of replicator power.

Natural selection is the process whereby replicators out-propagate each other. They do this by exerting phenotypic effects on the world, and it is often convenient to see those phenotypic effects as grouped together in discrete ‘vehicles’ such as individual organisms. This gives substance to the orthodox doctrine that each individual body can be thought of as a unitary agent maximizing one quantity—‘fitness’,

the behaviour of an individual may not always be interpretable as designed to maximize its own genetic welfare: it may be maximizing somebody else’s genetic welfare, in this case that of a parasite inside it.

We are fundamentally interested in natural selection, therefore in the differential survival of replicating entities such as genes. Genes are favoured or disfavoured relative to their alleles as a consequence of their phenotypic effects upon the world. Some of these phenotypic effects may be incidental consequences of others, and have no bearing on the survival chances, one way or the other, of the genes concerned.

If the parasite’s means of genetic exit from the host’s body is the same as the host’s, namely the host’s gametes or spores, there will be relatively little conflict between the ‘interests’ of parasite and host genes.

Adoption and contraception, like reading, mathematics, and stress-induced illness, are products of an animal that is living in an environment radically different from the one in which its genes were naturally selected.

As evolutionary neurobiologists Leah Krubitzer and Jon Kaas put it, Although the phenotype generated is context-dependent, the ability to respond to the context has a genetic basis. . . . In essence, the Baldwin effect is the evolution of the ability to respond optimally to a particular environment. Thus, genes for plasticity evolve, rather than genes for a particular phenotypic characteristic, although selection acts upon the phenotype.

Phenotypic effects of genes, whether at the level of intracellular biochemistry, gross bodily morphology, or extended phenotype, are potentially devices by which genes lever themselves into the next generation, or barriers to their doing so. Incidental side-effects are not always effective as tools or barriers, and we do not bother to regard them as phenotypic expressions of genes, either at the conventional or the extended phenotype level.

To the extent that active germ-line replicators benefit from the survival of the group of individuals in which they sit, over and above the two effects just mentioned, we may expect to see adaptations for the preservation of the group.

It is fundamental to the idea of a replicator that when a mistake or ‘mutation’ does occur it is passed on to future copies: the mutation brings into existence a new kind of replicator which ‘breeds true’ until there is a further mutation

It is, of course, true that ‘Memes are utterly dependent upon genes, but genes can exist and change quite independently of memes’ (Bonner 1980). But this does not mean that the ultimate criterion for success in meme selection is gene survival.

Replicator selection is the process by which some replicators survive at the expense of other replicators. Vehicle selection is the process by which some vehicles are more successful than other vehicles in ensuring the survival of their replicators

A dead-end replicator (which also may be active or passive) is a replicator which may be copied a finite number of times, giving rise to a short chain of descendants, but which is definitely not the potential ancestor of an indefinitely long line of descendants.

Evolution is the external and visible manifestation of the differential survival of alternative replicators (Dawkins 1978a). Genes are replicators; organisms and groups of organisms are best not regarded as replicators; they are vehicles in which replicators travel about.

To recapitulate, the significance of the difference between growth and reproduction is that reproduction permits a new beginning, a new developmental cycle, and a new organism which may be an improvement, in terms of the fundamental organization of complex structure, over its predecessor.

These phenotypic consequences are conventionally thought of as being restricted to a small field around the replicator itself, its boundaries being defined by the body wall of the individual organism in whose cells the replicator sits. But the nature of the causal influence of gene on phenotype is such that it makes no sense to think of the field of influence as being limited in this arbitrary way, any more than it makes sense to think of it as limited to intracellular biochemistry. We must think of each replicator as the centre of a field of influence on the world at large.

It seems to follow from the thesis of this book that there is no important distinction between our ‘own’ genes and parasitic or symbiotic insertion sequences. Whether they conflict or cooperate will depend not on their historical origins but on the circumstances from which they stand to gain now.

A germ-line replicator (which may be active or passive) is a replicator that is potentially the ancestor of an indefinitely long line of descendant replicators. A gene in a gamete is a germ-line replicator. So is a gene in one of the germ-line cells of a body, a direct mitotic ancestor of a gamete.

I am suggesting here that organisms have a built-I capability of adapting to their environment. I am suggesting that to the extent that evolution occurs, it occurs at the level of the organism. This suggestion differs sharply from the thesis of the NDT, which holds that evolution occurs only at the level of the population. Organisms contain within themselves the information that enables them to develop a phenotype adaptive to a variety of environments. The adaptation can occur by a change in the genome through a genetic change triggered by the environment, or it can occur without any genetic change.

Returning, for clarification, to DNA as our archetypal replicator, its consequences on the world are of two important types. Firstly, it makes copies of itself, making use of the cellular apparatus of replicases, etc. Secondly, it has effects on the outside world, which influence the chances of its copies’ surviving.

When we talk of a program as ‘doing better’ or as being ‘successful’ we are notionally measuring success as capacity to propagate copies of the same program in the next generation: in reality this is likely to mean that a successful program is one which promotes the survival and reproduction of the animal adopting it.

Pattee explains there is a basic and extremely important distinction between laws and rules in nature.11 Laws are inexorable, meaning they are unchangeable, inescapable, and inevitable. We can never alter or evade laws of nature. The laws of nature dictate that a car will stay in motion either until an equal and opposite force stops it or it runs out of energy. That is not something we can change. Laws are incorporeal, meaning they do not need embodiments or structures to execute them: there is not a physics policeman enforcing the car’s halt when it runs out of energy. Laws are also universal: they hold at all times in all places. The laws of motion apply whether you are in Scotland or in Spain. On the other hand, rules are arbitrary and can be changed. In the British Isles, the driving rule is to drive on the left side of the road. Continental Europe’s driving rule is to drive on the right side of the road. Rules are dependent on some sort of structure or constraint to execute them. In this case that structure is a police force that fines those who break the rules by driving on the wrong side. Rules are local, meaning that they can exist only when and where there are physical structures to enforce them. If you live out in the middle of the Australian outback, you are in charge. Drive on either side. There is no structure in place to restrain you! Rules are local and changeable and breakable. A rule-governed symbol is selected from a range of competitors for doing a better job constraining the function of the system it belongs to, leading to the production of a more successful phenotype. Selection is flexible; Newton’s laws are not. In their informational role, symbols aren’t dependent on the physical laws that govern energy, time, and rates of change. They follow none of Newton’s laws. They are lawless rule-followers! What this is telling us is that symbols are not locked to their meanings.

It will be remembered that the ‘central theorem’ of the selfish organism claims that an animal’s behaviour tends to maximize its own (inclusive) fitness. We saw that to talk of an individual behaving so as to maximize its inclusive fitness is equivalent to talking of the gene or genes ‘for’ that behaviour pattern maximizing their survival.

Replicators need not last forever. They need only last long enough to produce additional replicators [fecundity] that retain their structure largely intact [fidelity]. The relevant longevity concerns the retention of structure through descent. Some entities, though structurally similar, are not copies because they are not related by descent.

A DNA molecule in the germ-line of an individual who happens to die young, or who otherwise fails to reproduce, should not be called a dead-end replicator. Such germ-lines are, as it turns out, terminal. They fail in what may metaphorically be called their aspiration to immortality. Differential failure of this kind is what we mean by natural selection.

The genotype may be a ‘physiological team’, but we do not have to believe that that team was necessarily selected as a harmonious unit in comparison with less harmonious rival units. Rather, each gene was selected because it prospered in its environment, and its environment necessarily included the other genes which were simultaneously prospering in the gene-pool. Genes with complementary ‘skills’ prosper in each others’ presence.

If a program or strategy is successful, this means that copies of it will tend to become more numerous in the population of programs and will ultimately become almost universal. It will therefore come to be surrounded by copies of itself. If it is to remain universal, therefore, it must be successful when competing against copies of itself, successful compared with rare different strategies that might arise by mutation or invasion.

A stick insect looks like a replicator, in that we may lay out a sequence consisting of daughter, granddaughter, great-granddaughter, etc., in which each appears to be a replica of the preceding one in the series. But suppose a flaw or blemish appears somewhere in the chain, say a stick insect is unfortunate enough to lose a leg. The blemish may last for the whole of her lifetime, but it is not passed on to the next link in the chain.

The facts are as follows. The total amount of DNA in different organisms is very variable, and the variation does not make obvious sense in terms of phylogeny. This is the so-called ‘C-value paradox’. ‘It seems totally implausible that the number of radically different genes needed in a salamander is 20 times that found in a man’ (Orgel & Crick 1980). It is equally implausible that salamanders on the West side of North America should need many times more DNA than congeneric salamanders on the East side.

My thesis has been that the slight further conceptual step outside the immediate body is a comparatively minor one. Nevertheless it is an unfamiliar one, and I tried to develop the idea in stages, working through inanimate artefacts to internal parasites controlling their hosts’ behaviour. From internal parasites we moved via cuckoos to action at a distance. In theory, genetic action at a distance could include almost all interactions between individuals of the same or different species. The living world can be seen as a network of interlocking fields of replicator power.

But there is nothing magic about Darwinian fitness in the genetic sense. There is no law giving it priority as the fundamental quantity that is maximized. Fitness is just a way of talking about the survival of replicators, in this case genetic replicators. If another kind of entity arises, which answers to the definition of an active germ-line replicator, variants of the new replicator that work for their own survival will tend to become more numerous. To be consistent, we could invent a new kind of ‘individual fitness’, which measured the success of an individual in propagating his memes.

In fact, the entire range of human variation for some genetic traits can be found on the African continent.77 A person from the Congo, a person from South Africa, and a person from Ethiopia are more genetically different from each other than from a person from France.78 This seems astonishing because we are so used to focusing on a tiny set of physical features, especially skin color, to assign people to racial categories. It turns out that the genes contributing to these phenotypic differences represent a minute and relatively insignificant fraction of our genotypes and do not reflect the total picture of genetic variation among groups.79 What’s more, these phenotypic differences do not even fall neatly into the categories known as races. Rather, the physical features are “discordant” among groups—they are assorted randomly and do not come assembled in racial packages. “Sub-Saharan Africa is home to both the tallest (Maasai) and the shortest (pygmies) people, and dark skin is found in all equatorial populations, not just in the ‘Black race’ as defined in the United States,” writes Richard S. Cooper, a physician epidemiologist at Loyola University.80 And most genetic variation is found within any human population.81

To the extent that active germ-line replicators benefit from the survival of the bodies in which they sit, we may expect to see adaptations that can be interpreted as for bodily survival. A large number of adaptations are of this type. To the extent that active germ-line replicators benefit from the survival of bodies other than those in which they sit, we may expect to see ‘altruism’, parental care, etc. To the extent that active germ-line replicators benefit from the survival of the group of individuals in which they sit, over and above the two effects just mentioned, we may expect to see adaptations for the preservation of the group.