so i think the connection between inbreeding (or outbreeding) and the evolution of the “innate social aptitudes of man” [pdf] works something like this:

inbreeding in and of itself does not change the frequency of genes (alleles) in a population [pg. 65], but it does move them around, concentrating them in certain family lines.

if, then, some sort of genetic mutation arises in one family line which, let’s say for the sake of argument, results in the carriers somehow behaving more altruistically towards their fellow family members than strangers, and this results in them being able to increase their inclusive fitness, then that genetic mutation will be selected for.

it will really be selected for (i.e. the selection rate will be accelerated) because of the inbreeding because: 1) since the inbred family will have greater than average numbers of this “altruism gene” because it is inbreeding, its members will likely execute a greater total number of altruistic behaviors towards one another and, so, they will really benefit fitness-wise from this new gene. also, 2) perhaps — perhaps — all else being equal, the inbred family members will feel even more strongly altruistic towards their fellow family members than an outbred family would since they are so much more genetically similar to their family members. to be honest with you, i’m not so sure about that second proposition, so i’m just going to skip it for now and focus on the first one.

wrt the first proposition, that the rate of selection of “genes for altruism” is faster in an inbreeding population is exactly what wade and breden found when they ran some models — the more inbreeding, the more rapid the selection of the altruism genes:

you can imagine why.

if you have a bunch of different families in a population, and one of those families possesses some sort of “familial altruism” gene which means that its members help each other out (or whatever) more than the members of the other families do, and this increases the fitness of a majority of this special family’s members, then they are simply going to be more successful than the other families. they’ll leave more descendants behind and, thus, more of those genes behind. IN ADDITION, if this successful family ALSO inbreeds, each of its members is much more likely to have at least one, or even two, copies of this familial altruism gene, so more members of this successful family will be even more altruistic to each other and voilà! — they’ll increase their fitness and success even more than they would have done without the inbreeding.

these familial altruism genes — genes that lead to behaviors in which individuals somehow favor their own family members over non-family members — and by family members i mean extended-family members — are only going to arise, of course, in a population in which there is more than one family. if you’ve got some tiny band somewhere that has absolutely no contact with any other group (doubt that’s ever existed), then my evolutionary scenario simply won’t happen. it’s the competition between the individuals from the different families that is driving this.

naturally, genes in any population — even an inbreeding one — won’t remain restricted to any one family for very long. no family anywhere inbreeds 100% exclusively, so if some successful familial altruism genes do arise in some inbreeding family somewhere, they will quickly spread to the other families in that population. thus, there is probably an ongoing familial altruism genetic arms race in inbreeding populations.

also, i think fewer familial altruism genes — or not such strong ones, perhaps — are going to arise in a comparatively outbreeding population. the accelerated selection due to the inbreeding won’t be there, nor will this arms race to keep one step ahead of the joneses when it comes to familial altruism. additionally, i think that in an outbreeding population, there’ll be greater selection pressures than in an inbreeding population for “reciprocal altruism” genes — i.e. genes which lead people to be willing to cooperate more with non-family members — since more of those sorts of behaviors will likely be required to be successful in life.

so what do these “familial altruism” genes look like?

i dunno.

maybe there are differences in oxytocin-related genes? — the luuuuv hormone that “turns out to be the hormone of the clan.”

or — ya’ll know that i’m kinda fascinated by interclan fighting which is the flip-side of being nice to your family (i.e. be extra un-nice to your non-family) — so maybe one familial altruism gene is the “warrior gene” (MAO-A gene)? dunno.

one that i speculated about before is CYP21A2, the gene connected to congenital adrenal hyperplasia (CAH), a recessive genetic condition which affects the production cortisol which, in turn, affects the production of androgens (like testosterone) — notably, in the most common form of CAH, androgen levels are increased. the condition is a recessive one, so you need to have two copies of the deleterious allele to have the condition, but as i mentioned in my previous post on CAH, carriers with one copy of the allele have been found to have excess androgens — and androgens have been connected to aggression. (also, children with CAH have been found to have smaller amygdalae, so … they’re less fearful? don’t know if this also holds true for adults with CAH.)

increased aggression? fighting at the drop of a hat? interclan fighting? see where i’m going with this?

the interesting thing is — at least i think it’s interesting — is that there are different frequencies of CAH found in different populations. what we’d really want to know, of course, are the gene frequencies for CAH for different populations, but in lieu of those … here are some incidence rates of classical CAH in different populations [numbers acquired from or via here and here]:

1:282 – Yupik Eskimos, Alaska
1:2,141 – La Reunion
1:4,081 – Western Australia Aborigines
1:5,000 – GLOBAL
1:5,000-7,000 – Moroccan Jews
1:5,041 – Zurich, Switzerland
1:7,000 – Kuwait
1:10,866 – France (Whites)
1:10,866 – Italy (Whites)
1:11,500 – Sweden
1:11,764 – Netherlands
1:14,300 – Hungary
1:14,403 – Croatia
1:14,500-23,344 – New Zealand
1:14,869 – Western Australia
1:15,518 – Emilia-Romagna, Italy (Whites)
1:15,800-18,000 – Japan
1:17,098 – Scotland
1:19,939 – Minas Gerais, Brazil
1:20,000 – Norway

i dunno, but i see — maybe — the more inbred clannish fighters (yupik eskimos, moroccan jews, kuwaitis) having more cases of CAH than the more outbred peaceniks (new zealanders, norwegians, even northern italians). also…

- “The Texas data indicate a lower disease frequency in African-Americans when compared with Caucasians, and international data indicate higher frequencies in native Yupik Eskimos, Brazilians, residents of La Reunion, and Filipinos.” [source]

- “The prevalence of the disease [non-classical CAH] in Ashkenazi Jews was 3.7%; in Hispanics, 1.9%; in Yugoslavs, 1.6%; in Italians, 0.3%; and in the diverse Caucasian population, 0.1%.” [source] (non-classical CAH refers to a less severe form of CAH which might not get noticed until adulthood when it expresses itself in features like a woman having, perhaps, a bit too much facial hair.)

again, what we’d really want to know are the gene frequencies for CAH in different populations. then the über-human savants that we call population geneticists could do their math wizardry to see if these genes were under positive selection or not (zey hav vays av mayking ze data talk). (another interesting thing, btw, is that there are many different mutations in this gene which cause a range of CAH conditions from mild to severe — and different mutations are more common in different populations — see here and here and here for instance.)

of course, maybe these mutations in CYP21A2 aren’t being selected for for increased aggression/upside-down familial altruism. maybe it’s something else. witchel, et al., found that heterozygotes for mutated CYP21A2 alleles (i.e. individuals with just one copy of the cr*ppy gene) had increased cortisol levels and cortisol is, apparently, important for the immune system, so maybe these mutants simply survive infections better. others have found a possible connection between higher iq and CAH (masculinization = higher iq?) — see here and here and here — so maybe that’s it.

or maybe these genes are not being selected for at all. however, fertility rates of people (women) with CAH are low, so it seems like a strange bunch of genes to have around if they don’t have some sort of benefit.

previously: inbreeding and the evolution of altruistic behavior and looking for altruism genes and visions of altruism genes

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