You mentioned in the "nobody is born gay" post that you don't think Cochran is right about the pathogen hypothesis for homosexuality - why do you think that?

Most of our best minds cannot afford to think in certain ways, even if it makes sense: homosexuality impairs one’s ability to survive and reproduce; it’s a costly reduction in fitness; it’s a hugely impractical evolutionary strategy. I was simply lamenting this unfortunate fact.

In fact, i think Cochran’s theory regarding male homosexuality is damn plausible (female homosexuality may be a whole different kind of crazy — transsexuality certainly is).

You should have good reason to expect this the case because of:

low heritability of male same-sex attraction and low identical twin concordance

relative absence of homosexuality in isolated hunter-gatherer populations (Bushmen, some hunter-gatherer groups in Indonesia and the Philippines, pre-contact Polynesians) who have no word for it

the relatively high frequency of homosexuality (~4%? in the U.S.)

the lack of any sort of plausible evolutionary explanation - clearly, male disinterest in sex with females is always evolutionary maladaptive. (Again, such a reduction in fitness should be rare, but it’s not)

it shows no signs of selection; sexually antagonistic selection was ruled out; the gay uncle theory was ridiculous — it doesn’t even happen, and it doesn’t work if you divide by two, which E.O. Wilson didn’t do.

I’ve read all other asks, will get to them in time.

That large GWAS study (of over 23,000 individual genomes) ruled out any sort of sexually antagonistic selection (the phenomenon of a reproductive advantage aiding one sex while disadvantaging the other) for homosexuality:

Our GWAS results did not identify any genetic loci reaching genome- wide significance at p < 5 x 10 -8 among men or women. Among men, the peak (non-significant) hit was in chromosome 8q12.3 (chr8:63532921 in NKAIN3 , p= 7.1 x 10 -8 ). We did not find evidence of an association between sexual identity and SNPs on the X chromosome in men, women or the samples combined at genome-wide significance. We calculated that the study had 80% power to detect a genome-wide significant association with an odds ratio over 1.7 in women and over 1.3 in men for a minor allele frequency of 0.3.

The other explanations (that posit homosexuality was positively selected for) in the social science literature just don't work, e.g., E.O. Wilson’s ridiculous "gay uncle" hypothesis says that homosexuality evolved as a way to help siblings produce extra nieces and nephews, because providing for a cousin would still incur a gene survival advantage. Not only does this not even happen, it’s also impossible. Do some simple adding up and the relationship coefficients don’t work: Nephews and nieces are only half as closely related as your own kids, so you’d need four extra to break even, rather than two, as with your own kids. It also goes nowhere in explaining why homophobia is so highly heritable, as mentioned.

It’s what you’re exposed to that can sway the heart to evil. Check out this study done in identical twins (identical twins share the same genetics)

http://www.hollanddavis.com/?p=3647

"Identical twins have the same genes or DNA….

Those twin studies show a high (80%) discordance rate, and the few heritability studies estimate homosexuality to be about about 20% genetic (that's maxima, but higher for women). They also find, as they always do, that the shared-environmental influence (from upbringing, parents, what you were taught, and so forth) is very weak, even close to zero. So that rules out the spiel about liberal brainwashing turning people gay. Although in twin studies we know that, expectedly, homophobic attitudes, like all traits, are also heritable — ironically much more than homosexuality itself — about ~50% genetic, and the shared-environment for this trait vanishes when you correct for assortative mating (i.e., assortative mating is strong for social attitudes, and this tends to inflate the environmental estimate at the expense of the genetic one). So, naturally, that rules out the spiel about conservative propaganda turning people into homophobes.

So, we do have some answers, but the real question seems to be how does homosexuality originate, or rather, perpetrate itself? Testing this -- and producing the wrong answer -- is a quick way to ensure no grant money for the rest of your career, so no one bothers. Gregory Cochran surmises that homosexuality has a biological substrate, one that’s caused by an infectious agent, likely a virus. It's the wrong thought to have, but he has a few models.

Natural selection should eliminate homosexuality, it should be uncommon—like most genetic conditions that impair one’s ability to survive and reproduce, but it's not -- reasonable estimates say about ~4% of the US population is homosexual? Or thereabouts. So that schizophrenia point is interesting. High discordance among twins does not say there is no genetic component to homosexuality; the predisposition seems to be interacting with something in the environment. On a related note: tuberculosis shows higher twin concordances than homosexuality does, but the cause of TB is mycobacterium tuberculosis, and you won’t get TB if you’re not exposed to the bug. Perhaps there’s some kind of infectious agent that selectively alters certain parts of the brain while leaving the rest intact. This happens, of course, see; Human parvovirus (Fifth disease).

There’s nothing to say this behaviour modification (homosexuality) helps spread the disease itself though, but having your fingers fall off doesn’t help spread leprosy - yet it goes ahead and does that anyway, eventually.

You're not meant to think like this, but disinterest in sex with the opposite sex is a damn poor evolutionary strategy; such a reduction in fitness is the prime indicator of a Darwinian disease state. You can't dress it up.

Physicist Gregory Cochran, in an exchange with a critic:

Critic: Is it not likely that human sexuality is in fact a bell curve, with “strict homosexual” on one end and “strict heterosexual” on the other end, and the majority of the people falling somewhere in between? (With the caveat that sexual preference and sexual practice are not necessarily the same thing). Cochran: No, it is not likely. Sheesh. That would make exactly as much sense as a bell curve of food preferences ranging from steak at the left to granite at the right, in which people in the middle liked steak and rocks equally well. Is an even split between a behavior that works and one that never does what you expect from biology? Do you expect half the geese to fly north for the winter?

No one is born gay.

It’s what you’re exposed to that can sway the heart to evil. Check out this study done in identical twins (identical twins share the same genetics)

http://www.hollanddavis.com/?p=3647

"Identical twins have the same genes or DNA. They are nurtured in equal prenatal conditions. If homosexuality is caused by genetics or prenatal conditions and one twin is gay, the co-twin should also be gay."

"Numbers of people who have changed towards exclusive heterosexuality are greater than current numbers of bisexuals and homosexuals combined. In other words, ex-gays outnumber actual gays."

-Ivy Wolf

Genes for IQ Differ Among Racial Groups

Table 1a. (above):  Frequencies of alleles that had a positive association with educational attainment. Shaded columns, L-R: Racial Group; Average IQ; Average Allele Frequency.

The phenotype known as intelligence, as measured by IQ and IQ-like tests such as the SAT, admission tests, and so forth, is a highly heritable and polygenic trait, that is, no single gene is known to a have large effect — instead there are many genes involved, each with a very small effect.

Genome-Wide Association Studies (GWASs) are able to detect variants at genomic loci that are associated with complex traits in a population and, in particular, at detecting associations between common single-nucleotide polymorphisms (SNPs) and common diseases such as heart disease, diabetes, auto-immune diseases, and psychiatric disorders. GWASs have also been used to detect common variants for height and body mass index, not least intelligence.

More recent GWASs have identified several SNPs whose different alleles are associated with differences in performance on PISA or IQ tests, moreover, significant genetic correlations are found between the general (g) factor of cognitive ability and language, mathematics, and reading. A massive GWAS of over 100,000 individual genomes identified ten SNPs associated with educational attainment that reached suggestive genome-wide significance:

GWAS of 126,559 Individuals Identifies Genetic Variants Associated with Educational Attainment

The results support the findings from SNP-based heritability studies that a significant fraction of total genetic variance is due to common variants. Three of the genome-wide significant and replicable SNPs that influence educational performance were rs9320913, rs11584700 and rs4851266. Several other SNPs are associated with differences in performance on PISA or IQ tests, two of which include:

Rs236330, as tested in two separate studies:

Genome-wide association studies establish that human intelligence is highly heritable and polygenic Childhood intelligence is heritable, highly polygenic and associated with FNBP1L

Rs324650, as replicated in four association studies:

Role of the cholinergic muscarinic 2 receptor (CHRM2) gene in cognition Association of CHRM2 with IQ: converging evidence for a gene influencing intelligence Association between the CHRM2 gene and intelligence in a sample of 304 Dutch families Exploring the functional role of the CHRM2 gene in human cognition: results from a dense genotyping and brain expression study

Since intellectual capacity has risen through small incremental changes at very many genes, have these changes been the same in all human racial groups?

To test this, another study used seven SNPs (including rs9320913, rs11584700, rs4851266, rs236330, and rs324650) that are associated with differences in performance on PISA or IQ tests. The study then looked up the prevalence of each allele that seems to increase performance for a total of fifty human populations, and then calculated the average prevalence of these alleles at seven genes:

Factor Analysis of Population Allele Frequencies as a Simple, Novel Method of Detecting Signals of Recent Polygenic Selection: The Example of Educational Attainment and IQ:

The results are similar across the HapMap and 1000 Genomes data sets: East Asian populations (Japanese, Chinese) have the highest average frequency of “beneficial” alleles (39%), followed by Europeans (35.5%) and sub-Saharan Africans (16.4%). [...] Factor analysis showed that they are strongly statistically associated at the population level, and the resulting factor score was highly related to average population IQ (r=0.90). Moreover, allele frequencies were positively correlated with aggregate measures of educational attainment in the population, average IQ, and with two intelligence increasing alleles that had been identified in different studies. [...] The polygenic score of educational attainment alleles was a good predictor of PISA scores (r=0.84, p<.05).

Table 1a (above this post): Frequencies of alleles that had a positive association with educational attainment in the combined dataset in the large GWAS study of genetic variants associated with educational attainment. In the table:

AFR: African; AMR: American; ASN: Asian; EUR: European; ASW: African ancestry in SW USA; LWK: Luhya, Kenya; YRI: Yoruba, Nigeria; CLM: Colombian; MXL: Mexican ancestry from LA, California; PUR: Puerto Ricans from Puerto Rica; CHB: Han Chinese in Bejing, China; CHS: Southern Han Chinese; JPT: Japanese in Tokyo, Japan; CEU: Utah Residents with Northern and Western European Ancestry; FIN: Finnish in Finland; GBR: British in England and Scotland; IBS: Iberian population in Spain; TSI: Toscani in Italy.

Table 1c (below): Frequencies for the 50 populations, along with their factor score and estimated racial IQ: 

As seen here, the average allele frequency for the selected SNPs is lowest among the San Bushmen and Mbuti Pygmies of sub-Saharan Africa.

Additionally, in early GWASs there was found to be no genome-wide significant variants determining height (also a polygenic trait whose allele frequencies differ among populations, not least between closely-related European populations) despite decades worth of studies finding height to be a highly heritable trait. It was only when larger sample sizes were used (>15,000 individuals) did GWASs start to find “GWAS hits” (SNP associations) affecting height -- lots, in fact:

Source: Five Years of GWAS Discovery

The prior cognitive enhancing-SNPs associated represent only a handful of total genome-wide variation, but much like with height, geneticists expect a steady accumulation of SNP 'hits' associated with intelligence once they pass the statistical power threshold. Since intelligence is a polygenic trait, a single SNP produces meager results, on the other hand, an accumulation of several more cognitive enhancing-SNPs than the average person produces notable differences — and the incidence of the current crop of such SNP variants differ among racial groups. Finally, all but one of the ten alleles in the study were specific to humans and not shared with ancestral primates. Evidently, these are recent variants that arose independently during a time of recent and divergent human evolution and which show varying differences (on selection pressures) among human groups:

[Piffer, 2013] Nine of the 10 alleles associated with educational attainment were derived, thus unique to humans and not shared with non-human primates. This result was significant (p=0.01) and is predicted on the basis of the assumption that humans have evolved by natural selection to become more intelligent than their primate cousins. The results show that this evolutionary process, which was already far advanced at the time when modern humans spread across the globe approximately 65,000 years before present, has continued in modern human populations after that time. It invalidates theories that assume, explicitly or implicitly, that human cognitive evolution has ended with the first appearance of physically modern Homo sapiens (e.g., Tooby and Cosmides, 1992).

Related Post:

Ongoing Adaptive Evolution in Human Brain Size - Varying differences among human racial groups on gene variants that confer brain growth.

If "cankrist" wants numbers on blacks in South Africa, he can consult (no doubt among others) Richard Herrnstein and Charles Murray's *The Bell Curve*, where he'll find documented the fact that their avg IQ is 70. Amusingly, the initial result was 71; when complaints surfaced that the questions were culturally biased, the test was adjusted and the avg. dropped a point.

I glanced at his blog, nothing warranted even acknowledging him. He is the exemplar future liberal arts scholar that the quote (by a Physicist turned geneticist, no less) was lamenting.

Of course, there's lots of data on human achievement, as he requests - and the results are the same for racial groups, wherever they exist, as the quote pointed out (minus some Indian castes and Chinese that tend to do better in the West). Plainly, people whose ancestors originate from sub-Saharan Africa produce very few scientific papers – on average – no matter where they live. This is also the case (to a lesser extent) for mestizos from central and South America, for Filipinos and Malays, and most of the Indian castes.

For instance, this map below shows countries resized according to the number of scientific papers they produce [Source]:Evidently, population size plays a role, but average productivity matters more. Singapore, with a population of 5 million, looks bigger than Indonesia, with 240 million people. Equally, scientific productivity does not depend on science funding, rather than regional differences in talent. It depends more on the distribution of talent. Generally this pattern is about what you would expect from the world distribution of IQ, coupled with the fact that science is generated by people out in the tail of the intelligence distribution.

Some may suspect that the pattern would change if only more extreme and important examples of scientific creativity were looked at, rather than counting every paper. But in this scenario, in terms of Nobel prizes in the sciences, or Fields medals, the differences become starker. Whole nations disappear. Single individuals outdo whole civilizations. It's worse from the egalitarian point-of-view.

Everyone can and does observe the various differences we see in the attributes of people and societies in different places and times, but it's considered polite not to notice. I've said it before: you’d think you’d find one place on Earth where a Chinatown looks closer to Haiti than it does to Shenzhen, but you don’t. Culture matters, but invoking it to explain all the commonness you see around you simply defies the imagination. The world looks a certain way - maybe it is?

One of the fun parts about these gormless discussions about race consists of people who talk as if we don’t really know anything about the phenotypes under discussion. Like, who really knows what intelligence is, and who really knows if groups vary in average intelligence, blah blah blah. The funny thing is that a lot of those discussing these issues really don’t know. At this point, the average graduate student in physical anthropology doesn’t know that different populations have significant differences in average brain volume – so why would you expect Jerry Coyne to? Does he know that there’s a fair-sized correlation between brain volume and measured intelligence? Even if he doesn’t, he would immediately understand why that was highly likely. Is he moderately familiar with modern psychometrics? Probably not. Does he know that there is a one-std difference in IQ between blacks and whites, and that it shows up before kindergarten? I doubt it. James Heckman knows. There is of course lots of other evidence that clearly shows that schools are not the cause of that difference, not least the observation that blacks do poorly in the same prosperous, integrated, liberal schools (Shaker Heights!) where whites and northeast Asians do just fine. How many know that the observed rank-orderings of groups are apparently the same everywhere? Bring in Japanese as farm workers, and they’re in the upper middle class in four or five generations. Bring the Chinese into Malaysia as illiterate tin miners, and they end up owning and running all the industry in the country (and the Communist party too, back in the day). How many of those talking about clines and races know that black 12th graders in the US score lower than white 8th graders on reading and math? How many know that blacks are hugely underrepresented in the upper tails of the achievement distribution? How many remember the tens of times that we’ve been told that some new intervention is going to erase these gaps, and then seen the story dribble away to nothing? While we’re at it, why do these interventions always consist of a bunch of liberal arts graduates talking with great sincerity – isn’t there anything else to try? Something new, something with at least a Chinaman’s chance of success? Modafinil? Trancranial magnetic stimulation? Caning? Tarts for nerds? Parenthetically, none of these practical questions have anything to do with typological questions: a population that originated from the other end of a cline can be very different, and it’s the differences that matter, not whether there’s a natural seam between populations (like the Sahara, or the Himalayas). This is obvious to anyone who’s ever thought seriously about the matter. Both of us! Since it is obvious that ‘clines vs races’ argument has no relevance to the real question – the enduring achievement gaps between different populations in the US and other countries – why do people keep bringing it up? I used to think that such people were blowing smoke, deliberately lying to make a point, but I am increasingly willing to consider the possibility that they’re just stupid. Mixed explanations are also possible: such nonsense has worked in the past, and the current practitioners are following a beaten path, rather than rationally planning a deception campaign. Of course, when someone says that “Genes matter, but they are only a small part of the whole evolutionary picture”, you figure that he’s just an idiot.

Physicist Gregory Cochran

Intelligence and Longevity

In a meta-analysis [image above] comprising 16 studies of over one million participants, there was found a strong a relationship between IQ and mortality: a 1 standard deviation increase in cognitive ability in childhood was associated with 24% lower risk of mortality -- higher IQ individuals live longer, on average, than lower IQ individuals do:

Intelligence in youth and all-cause-mortality: systematic review with meta-analysis [image above]

These were longitudinal studies, they followed the subjects from a minimum of 17 years in some studies to a maximum of 69 years in others. Evidently, IQ measured in childhood and early adulthood is a pretty good prediction of mortality. Adjusting for alcohol use, blood pressure, blood glucose, body mass index, socioeconomic status, and so forth did not significantly weaken the association.

Adult socioeconomic status and educational attainment have only modest effects, whilst IQ (as measured by simple reaction time -- well correlated with IQ) stood as the predictor of mortality:

Reaction Time Explains IQ’s Association With Death:

After AH4 scores and each of the reaction time measures were adjusted for sex, smoking status, social class, and years of education, all effects remained significant, and the hazard ratios were only slightly attenuated (Table 1). Thus, the relation between IQ and mortality in this sample was not substantially mediated by social class, education, or smoking. Nor was the relation between reaction times and mortality substantially mediated by these variables.

IQ in late adolescence/early adulthood, risk factors in middle age and later all-cause mortality in men: the Vietnam Experience Study:

[...] we adjusted for a range of physiological, behavioural, psychological and social risk factors that can be considered as mediating variables in the IQ–mortality relation. The influence of controlling for these factors can be broadly divided into three strata. In the first, despite being associated with both IQ and mortality, adjusting individually for marital status, alcohol consumption, systolic and diastolic blood pressure, pulse rate, blood glucose, body mass index and psychiatric and somatic illness at medical examination had very little, if any, impact on the age-adjusted IQ–death relation (<10% attenuation in risk)

This study followed the outcomes of 4316 Vietnam War veterans, which had access to their Armed Forces test scores upon entry into the military, as well as a medical exam in 1986 which measured the subjects’ BMI, among other things. IQ again stood as by far the strongest predictor of death. Most of the typical predictors of good health, as detailed above, had a negligible "<10% attenuation in risk”.

Reaction Time and Mortality from the Major Causes of Death: The NHANES-III Study:

In fully adjusted models which also adjusted for educational attainment, occupational grade, poverty/income ratio, health behaviors and CVD risk factors, the association was attenuated but remained statistically significant for all-cause mortality (HR = 1.15, 95% CI 1.02,1.29; 37% attenuation), and CVD mortality (HR = 1.22, 95% CI 1.15,1.29; 36% attenuation).

IQ, or simply genes, are a better indicator of longevity. Moreover, despite the conventional wisdom, in longitudinal controlled clinical trials, weight and other 'common markers of health' (e.g., nonsmoker, body-mass index <25 kg/m2, physical activity, diet consistent with recommendations, untreated cholesterol <200 mg/dL, and so forth) have only a small effect on mortality rates:

Every Study Finds Variable Response to Exercise

Variation in health outcomes and longevity cannot be explained by behavioural variation. In the developed world at least, this fraction is in fact quite limited.

Wasn't there some research this past year that said that European hunter-gatherers were dark skinned and blue-eyed until the adoption of farming caused them to become light skinned due to a lack of vitamin D? How does this fit in with the theory that light hair, skin and eyes were sexually selected for?

Diverse European hair and eye colour came about through a selection pressure that acted on different genes (SLC45A2, SLC24A5, and TYRP1 for skin; MC1R for hair; HERC2-OCA2 for eyes).

Those hunter-gatherers they tested, from Luxembourg and Spain were later hunters (8,000 and 7,000 years ago respectively), i.e., they may have had admixture from the early European farmers from the Levantine. Nevertheless, new research also finds that European skin turned ‘white’ a lot longer ago than expected: 11,000 and 19,000 years ago according to this study (2013) or between 7,600 and 19,200 years (testing only SLC24A5) according to this study (2014).

Peter Frost thinks that although different genes are responsible for eye, hair, and skin colour, there was probably a single selection pressure that seems to have acted primarily on early European women [The Puzzle of European Hair, Eye, and Skin Color]. Moreover, that this sexual pressure took place in the harsh continental steppe tundra of Northern and Eastern Europe during the last ice age: harsh climates with no year-round agriculture and where the only food is dispersed and mobile animals, so females require males for provision of them and their children, many males end up dying hunting, thus a large number of women end up competing for a small number of men, who have control of sexual selection, and so forth.

The Luxembourg guy lacked the variants at all three genes involved in the whitening of European skin. You don’t find genotypes like that in unadmixed Europeans today. The guy from Spain had one of the variants at TYRP1, the other two were ancestral. [http://www.nature.com/nature/journal/vaop/ncurrent/full/nature12960.html]. Seems outside of the steppe-tundra, brown-skinned Europeans lived long after the time period when European skin turned white elsewhere, and it seems lighter eyes came first outside of the steppe-tundra.

Also, the hunter-gatherers still had the ancestral variant for KITLG. KITLG is involved in the first stage of skin lightening that affected the common ancestors of Europeans and East Asians about 30,000 years ago [http://mbe.oxfordjournals.org/content/30/1/24.short]. Seems then, that in both cases, both lightening processes (30,000 years ago, and 10,000 years ago) affected Europeans, but only within parts of Europe.

Lastly, (in the study I think you’re referencing) they find that strong selection for white skin, non-brown eyes, and non-black hair continued to occur in the historical period, some 5,000 years ago [http://www.pnas.org/content/111/13/4832.full.pdf]. They do posit that the shift from hunting and gathering to farming led to a decrease in dietary vitamin D, the main problem is that farming came late to many parts of Europe: only about 2,000 to 3,000 years ago for East Baltic peoples and less than 3,000 years ago for Finnish peoples (and it didn’t reach all of them) - these are pretty light-skinned populations today and that timeframe is not long for a rapid loss of pigmentation. Generally, to resolve all of this there needs to be more ancient DNA from these populations, which will likely happen over the next few years anyway, don’t be surprised if we find some milky-white, blue-eyed, blondes living >10,000 ago during the last ice age.

Human Eye Hue Variation - Continued

Table Above: HERC2 rs12913832 variant and pigmentation

Although eye colour is polygenic (i.e., controlled by several genes), variants at two SNPs (rs12913832 and rs1129038) account for most cases of blue eyes:

Blue eye color in humans may be caused by a perfectly associated founder mutation in a regulatory element located within the HERC2 gene inhibiting OCA2 expression

So, for blue eyes, a single variant of the OCA2 gene explains much of its appearance since the colour first appeared <10,000 years ago. Blue eyes are caused by a change in a DNA sequence that regulates the expression of OCA2, a sequence that is embedded in HERC2, the gene next to OCA2. A part of the HERC2 gene contains a switch which regulates OCA2 expression:

“One single haplotype, represented by six polymorphic SNPs covering half of the 3' end of the HERC2 gene, was found in 155 blue - eyed individuals from Denmark, and in 5 and 2 blue - eyed individuals from Turkey and Jordan, respectively”. [http://www.ncbi.nlm.nih.gov/pubmed/18172690]

Evidently, the mutation that causes blue eyes is a “founder mutation” i.e., it is shared by both North European individuals and subjects from Turkey and Jordan. All blue - eyed individuals carry the same mutation which seems to have appeared about 10,000 years ago. Moreover, light eyes are found in Berbers from the Atlas Mountains of Morocco, and even in Tuaregs living in the Sahara. Light eyes are fairly common in Kurds living in the Zagros Mountains along the border between Iraq and Iran, and people with light eyes live as far away as Afghanistan, over 3,000 miles from Vilnius, Lithuania, the small village in which blue are believed to have originated some 10,000 years ago.

[Expanding on the table above]: In a Polish sample, 89% of the blue-eyed individuals had both copies of the ‘C’ variant at rs12913832 and no copies of the alternate ‘T’ variant:

Interactions Between HERC2, OCA2 and MC1R May Influence Human Pigmentation Phenotype

As can be seen among the CT heterozygotes (two variants for two different colours; either which can be expressed), although the C variant is relatively recessive for expression of blue eyes, it shows strong heterozygote effects for expression of green or hazel eyes [see table above post]:

Blue or grey-eyed individuals: 89% had both copies, 10% one copy, 1% no copies

Green-eyed individuals: 67% had both copies, 30% one copy, 2% no copies

Hazel-eyed individuals: 9% had both copies, 80% one copy, 11% no copies

Brown-eyed individuals: 0% had both copies, 84% one copy, 16% no copies 

In short, the C variant is less dominant, but not truly recessive. Even in the heterozygous state, it usually produces hues that visibly diverge from the human norm of brown eyes. Truly recessive traits are usually lost in the next generation, as a rare variant fails to occur twice in the same person, before selection can even start its work.

The evolutionary selection for pigmentation traits include UV radiations causing skin cancer and vitamin D synthesis from precursors in diet food requiring UV radiations reaching the deep layers of derma, but this cannot explain the strong sexual pressures on variants that resulted in high frequencies of light skin, hair, and eyes in the Baltic and Scandinavian regions, as this appears to in fact be a result of intense male sexual selection of females (rare in mammals):

The Evolution of Light Skin

Sexual Selection and Hair/Eye Hue Variation (previous post)

Race & Academic Censorship: The Liberal Suppression of Dissent - Continued

Source of figure: Cavalli-Sforza’s 1966 paper Population Structure and Human Evolution: one of the first papers showing that when DNA is aggregated, more genetic variation exists between populations than within them. It demonstrated that human racial groups genetically cluster into readily identifiable groups.

In the postwar period, geneticists were all too aware of the cloud of suspicion over the concept of human races. Cultural anthropologists were mostly the ones who talked about race, but they downplayed its importance. This silence was broken in the late 1960s by two academics: physicist, William Shockley, and psychologist, Arthur Jensen. In 1969, Jensen argued in the Harvard Educational Review that African-American children had lower IQs for genetic reasons and that efforts to close the IQ gap were doomed to failure [full article], a premise he later expanded on in his work The g Factor: The Science of Mental Ability.

Later, Joshua Lederberg, wrote a letter (that was later published in the Scientific American) to the NYtimes attacking attempts to link race to IQ. One of its signatories was Walter Bodmer, who wanted to refute this new racism in a high-profile journal, with a view to shutting down research on race and IQ.

The early 1970s saw the beginning of efforts to purge academia of ‘racist’ professors. For instance, after Jensen’s 1969 article, students and faculty staged large protests outside his U.C. Berkeley office. He was denied reprints by his publisher and not permitted to reply to letters of criticism. Similar harassment was directed at other academics.

In 1968-69, Cavalli-Sforza, one of the foremost population geneticists,  started his trial year at Stanford, becoming friends with both Bodmer and Lederberg.

In 1970, Bodmer, who had no credibility in the field of human genetics, asked Cavalli-Sforza to co-author a manuscript on race and IQ to be published in Scientific American. Cavalli-Sforza had never written on the subject before, but it was difficult for him to refuse Bodmer’s request. He had no tenure at Stanford and his only close colleagues there were Bodmer and Lederberg. The latter, in particular, helped Cavalli-Sforza rebuild his career during the difficult postwar years and had been instrumental in getting him a position at Stanford. In return for past favours, Cavalli-Sforza lent credibility to an article that might otherwise have attracted less attention or, perhaps, never have been published.

Despite saying nothing at all about it in his autobiography, by co-authoring this particular article in 1970, Cavalli-Sforza helped initiate a process with long-lasting consequences. As an expert on human genetics, Cavalli-Sforza gave support at a key time to the soft totalitarianism that would overrun much of academia. The following decades would see increasing control of the marketplace of ideas.

Richard Lewontin went even further: arguing that human races do not exist. At all. No races, no race differences. He concluded:

Human racial classification is of no social value and is positively destructive of social and human relations. Since such racial classification is now seen to be of virtually no genetic or taxonomic significance either, no justification can be offered for its continuance. [The Appointment of Human Diversity, Lewontin, 1972]

He analysed the way various genes vary among human populations, specifically genes whose variants produce different blood groups, serum proteins, or red blood cell enzymes, and found that only 15% of variation existed between human groups. However, this same kind of genetic overlap exists between many sibling species that are nonetheless distinct in anatomy and behaviour [not least between dog breeds]. Population differences are more sharply defined if several gene loci are compared simultaneously:

Lewton's Fallacy

This fallacy has the status of Holy Writ in every anthropology textbook you can find, but it is simply never the case that an African will be genetically closer to a European than to another African.

What did renowned population geneticist, Cavalli-Sforza, have to say about this? Two decades of silence. Anthony Edwards, a former colleague of Cavalli-Sforza, noted:

When in the 1960s I started working on the problem of reconstructing the course of human evolution from data on the frequencies of blood-group genes my colleague Luca Cavalli-Sforza and I sometimes unconsciously used the word ‘race’ interchangeably with ‘population’ in our publications. In one popular account, I wrote naturally of ‘the present races of man’. Quite recently I quoted the passage in an Italian publication, so it needed translating. Sensitive to the modern misgivings over the use of the word ‘race’, Cavalli-Sforza suggested I change it to ‘population’. At first I was reluctant to do so on the grounds that quotations should be accurate and not altered to meet contemporary sensibilities. But he pointed out that, as the original author, I was the only person who could possibly object. [Race: a social destruction of a biological concept - pg. 147]

Cavalli-Sforza was not the only silent geneticist, as Lewtontin's dishonest research received little criticism. Not surprising, considering the wave of attacks on 'racist' professors during the early 1970s.

In 1988, Harvard researcher Mark Snyderman published the book The IQ Controversy, the Media and Public Policy -- which by surveying hundreds of North American psychologists, sociologists and educationalists, analysing the reporting on intelligence testing by the press and television in the US for the period 1969–1983, and conducting an opinion poll of 207 journalists and 86 science editors about IQ testing -- demonstrated that from the late 1960s to the early 1980s there was majority support for every single one of the main contentions put forward regarding genetics, race, and intelligence, clarifying that there was never any real debate about the matter among the relevant scientists.

In 1991, Cavalli-Sforza announced the Human Genome Diversity Project (HGDP), along with a collaboration of scientists in what would be the crowning achievement of his career. The program was to collect and analyse DNA from all human populations, providing valuable information on human genetic diseases. 

Cavalli-Sforza had been involved in this kind of research for the past twenty-five years, doing and saying (or not saying) all the right things (especially about genetics and human behaviour). The project even had support from Bodmer. It's crime, however, was that it could draw attention to the existence of human populations and could therefore frame questions about the ways people differ from each other -- and this couldn't be allowed. Unfortunately, funding dried up and the HGDP remains uncompleted to this day, in its originally intended form, that is.

Previous post:

Decline in the Acceptance of Race

My prof of Phys. Anthropology once asserted (with a wicked smile) that the Chinese govt. had in its possession a skull predating the "Out-of-Africa" migration time that was found on Chinese soil, and that it had shovel-shaped incisors. He predicted they would announce the find in our generation's lifetime. Anyway, do you give any credence to the idea that possibly humans could have evolved in more than one place, or is it a certainty that Africa is our common homeland?

All of the data in genetics, archaeology and palaeoanthropology point to the African landmass for the origin of modern humans as well as the deepest lines of the genus homo. It’s also where 4 out of 5 great ape species are found (chimps, bonobos, gorillas, and humans).

Just about everything sees that the original Out-of-Africa and multiregional theories are now incorrect. The original Out-of-Africa theory posited zero admixture with archaic populations (because apparently they couldn’t) and a single-founder population. Of course, the vast majority of human ancestry outside of Africa derives from a population that lived in Africa on the order of 100,000 years ago, i.e., the multiregional theory just doesn’t seem to work based on ancestry.

Homo sapiens originated in East Africa and then migrated across Africa as well as out of Africa, where they encountered archaic humans. All present-day humans can be traced to this population. Moreover, early modern humans were already divided into different populations in Pleistocene Africa, after which there followed a complex migration pattern.As I understand it, about half a million years ago all of Africa was inhabited by an archaic population similar to the Neanderthals in Europe and the Denisovans in Asia. Over time, these archaics differentiated into two populations: (a) an evolutionarily conservative one in western and southern Africa; and (b) a more evolving one in eastern Africa.Around 120,000 years ago, these eastern humans expanded north into the Levant (the Skhul-Qafzeh skulls). They were now almost like modern humans in anatomy, albeit with some archaic features. Around 80,000 years ago, a sub-population of the eastern humans underwent a series of expansions. Then, around 60,000 years ago, a final expansion eclipsed the preceding ones and gave rise to true modern humans: Basal Eurasians and all that, e.g., Aboriginal Australians are descendants of an early human dispersal into eastern Asia, separate from the one that gave rise to modern Asians.

Upon expansion out of Africa, admixture with archaics added quite a bit of new adaptive variation: modern humans diverged. ‘Basal Eurasians’ picked up archaic admixture as they spread out of Africa and into Eurasia. Modern Eurasians have 1-4% Neanderthal admixture, and Melanesians have an additional 4-6% from the Denisovans.Within Africa, the new modern humans initially expanded into territory inhabited by ‘almost moderns,’ like the Skhul-Qafzeh people of the Levant. Archaic admixture thus entered the gene pool of modern sub-Saharan Africans and today represents about 13% of the total. As modern humans pushed farther into western and southern Africa, they encountered much more archaic humans, more different than Neanderthals, having diverged something like a million years ago, so it seems about 2% of the African gene pool comes from a now-extinct member of the Homo genus that broke away from the modern human lineage a million years ago.

There seems to be this common tendency (I see it all the time) to think of modern humans as having evolved from today’s Black sub-saharan African populations, I suppose this is the way in which the original Out-of-Africa theory has been presented. Of course, ‘Asselar Man’ (6,500 BP) seems to be the oldest skeleton that approximates the physical characteristics of present-day black Africans: they didn’t exist until long after modern humans had migrated out of Africa. This concept of a modern African race, unchanged from times immemorial (minus some physical adaptations to a lack of UV light and all that) persists, although it has to, the fact that human evolution still somehow continued (and accelerated) once modern humans first appeared has kept a century worth of liberal academics (Gould, Boas) busy.

Characteristics of East Asians

Image source: Population locations and allele frequencies. Pie charts present the allele frequencies of EDARV370A , with 370V in white and 370A in black.

A single gene known as EDAR, or more specifically, a single SNP in the EDAR gene, 370A, produces the characteristics typical of East Asians: thicker/straighter hair, shovel-shaped incisors, greater number of eccrine sweat glands, and smaller breasts.

When you insert the variant into mice they too develop phenotypes characteristic of East Asian populations: thicker hair shafts, extra sweat glands, and less breast tissue. The variant itself shows strong signs of selection, i.e., only throughout the evolution of East Asian peoples was this variant (whatever its true evolutionary advantage) strongly selected for, meaning differential selection acted on a trait among different human populations.

In the past people who played a prominent role in promulgating falsehoods about race (Richard Lewontin, Stephen Jay Gould, Franz Boas), mainly that there are no significant interpopulation differences. Lewontin, for instance, tried to argue away the significance of phenotypic (physical) differences between different human populations using genetic statistics [see here]. Remarkably, Lewontin was able to show that overall genetic variation in humans most is within-group, rather than between groups, of course this same kind of genetic overlap exists between dog breeds, in fact it exists between many sibling species that vary wildly in size, appearance, lifespan, anatomy and behaviour.

In summary, one SNP of the EDAR genes accounts for an infinitesimal fraction of overall human genetic variation between races, and yet it causes big phenotypic differences. Can any such fraction of genetic change invoke behavioural differences? The existence of such differences [between human races] seems obvious enough, and there’s nothing theoretically difficult about them – natural selection naturally takes a different course in different circumstances, nor does it take very long to generate differences of the kind and magnitude we see around us.

According to Lewontin's logic, and seemingly every graduate in anthropology, dog breeds, who show the same kind of genetic overlap as humans, are all really the same, even though they may seem to vary wildly in size, appearance, lifespan, and behaviour. Apparently, human evolution wouldn't work the same way it does in the animal kingdom: producing only phenotypic, never behavioural, differences.

Is there enough evidence to make strong statements about the origin of specific group differences? Probably, but most importantly it’s not all that sensible to think that no genetically grounded group differences in behaviour exist.

Well, you’d think you’d find one place on Earth where a Chinatown looks closer to Haiti than it does to Shenzhen, but you don’t. Culture matters, but invoking it to explain all the commonness you see around you simply defies the imagination. The world looks a certain way - maybe it is?

To what extent, if any, do you see Lewontin's manipulation of genetic science as a reaction to (his perceptions of) anti-Semitism? Is it possible that his polemics toward a generic "Everyman," genetically speaking, is intended as a kind of shield for his own ethnic group? After all, if you can't identify specific populations, then you can't criticize them.

From what I gather, about the only between-population difference in intelligence that is mentionable in society is that between Ashkenazi Jews and general Europeans. This is different, of course, partly because you’re saying that smart population A is on average smarter (ignoring spatial abilities, I guess) than smart population B – which is entirely different from saying that population B is on average dumber than population A – but also because it flatters an influential group that is more averse to noticing or mentioning such differences than any other.

In 1969, Joshua Lederberg wrote a letter (that was later published in the Scientific American) to the NYtimes attacking attempts to link race to IQ. One of its signatories was Walter Bodmer, who had experienced anti-Semitism (he lived in Germany during the 30s) as a child and was intent on ‘refuting’ this new racist research in a high-profile journal, with a view to shutting down research on race and IQ.

The only reason that letter garnered any credibility was because renowned geneticist Cavalli-Sforza gave his backing to a later manuscript by Bodmer on race and IQ (in exchange for a place at Stanford and a chance to rebuild his career, no less).

In general the early 1970s saw the beginning of efforts to purge academia of ‘racist’ professors, Jensen in particular.

In short, yes I agree, and to a large extent. Those who have played a prominent role in promulgating falsehoods about race, mainly that there are no significant interpopulation differences: Franz Boas [see here], Jared Diamond, Stephen Jay Gould [here], Ashley Montagu, Lewontin [here] - they do all have a few things in common.

I'm wondering if you have read Nicholas Wade's book (A Troublesome Inheritance) and what you thoughts are on it. It seems that the main criticism leveled against Wade is that as race is clinal, we can't know how many races there are and therefore that race is a social construct. The geneticist Jennifer Raff has taken this line. A lot of others claim this line is obfuscation. What do you think of this?

In this climate of suspicion and control over marketplace ideas, he criticises those who have played a prominent role promoting falsehoods about race, particularly interpopulation difference, anyone who attacks Boas, Lewontin, Gould, and so forth is deserving of praise.

The group letter attacking Wade’s book features some prominent geneticists, so it’s probably worth considering. One signatory of the letter, Neil Risch, a prominent geneticist in his own right, doesn’t believe in selection acting on humans, in fact he doesn’t believe that lactose tolerance was selected and has doubts about sickle cell. What’s the story with the others? Jerry Coyne, for instance: my guess is they’re watching their backs. Better to sign a letter condemning the racist book than do nothing at all: or worse yet come out in support. The criticism levied at Wade, who is not a geneticist, is mostly about speculating without firm evidence, which he explicitly admitted to anyway.

Is there enough evidence to make strong statements about the origin of specific group differences? Just about, but most importantly it’s not at all sensible to think that no genetically grounded group differences in behaviour exist.

The existence of such differences is obvious enough, and there’s nothing theoretically difficult about them – natural selection naturally takes a different course in different circumstances, nor does it take very long to generate differences of the kind and magnitude we see around us. A good clear example, as always, is the Domesticated Silver Fox Experiment: all you’re doing with ‘artificial’ selection is gradually increasing the frequency the gene variants you favour, this is the same evolutionary change for natural selection.

Population differences are a reflection of histories of gene flow and genetic drift. The idea of group differences being products of natural selection is abhorrent to many, so in human genetics, selection hasn’t garnered much interest. Selective pressures operate a lot faster than anyone wants to believe, and such pressures are different within Europe, within England, not just on opposite sides of a continental divide. Interpopulation differences are the regional differences in genomic patterns: race-specific genes are why mankind genetically clusters the way it does.

The danger is that if you look for population differences, you will find them, but that’s too bad.

As for interpopulation, or rather, intrapopulation differences, I actually think Gregory Clark’s work, that demonstrate a pattern of slow long-term social mobility, that posits a Darwinian natural selection breeding humans more adapted to stable societies, patience, aversion to violence, and general middle class values — generally everything that spawned the industrial revolution and rapid advance in human knowledge (far greater than other period in human history) — was much more inflammatory, yet he has somehow attracted little-no condemnation from the usual suspects.

There’s a few prior posts about his work below:

Human Accomplishment & The Industrial Revolution

Social Mobility is Predictable from Lineage

Accelerated Evolution and Social Darwinism

For the first time since starting this blog, I've amassed a series of thought-provoking asks -- you know, ones worth replying to and publishing. I'm currently not active enough to reply, but will in due course.

Would you agree that since the mechanism of the five sense and emotions are totally explained by biochemistry, it essentially refutes that free will exists if one accepts the premise that chemical reactions does not have will.

Of course. There’s an idea that there’s some sort of struggle between genes and will, as if biology represents basal urges and people’s thinking and deliberation is something else. What’s missing here is that meta-thoughts and behaviours (thinking about thoughts) are themselves heritable too.The human brain responds to input, and produces output in response to such input. These are a result of your intricate neural ‘machinery’. When eating out at a restaurant you can stuff yourself until your full, until the point where that one last unseasoned baked potato is too just much. Yet, you’re more than ready for a large bowl of ice cream — apparently a result of a conscious deliberation in deciding how to act. The driving force that stimulates your ice cream-craving tastesbuds are based in your biological details. Individual subjective experience ('I'm just treating myself to a bowl of ice cream') has people thinking otherwise, after all, evaluating free will requires some nuance beyond our immediate intuitions.I prefer having this discussion with libertarians who are dead serious that the social patterns they favour actually work. You know the types: if we let ordinary Joe to his own devices, ensuring individual personal responsibility in making his own decisions, like choosing whether to wear a seat belt, he’d pick the right answer – the answer that worked in practice, tended to keep him alive. On any question. I prefer the real true-blue libertarians though, who would say that whatever ordinary Joe chose would be the right answer by definition, even if it decapitated his head from his neck, but these guys are rarer. Either way, they’ll most likely spend a lot of effort arguing that there must be good reasons for this.

There are a few ways of busting gaps between two populations for which there exist documented and intractable differences in academic performance. For one, you can assess group performance through exams that are so facile that just about everybody performs better across the spectrum. The psychologist Joseph Fagan, as you cite, amazingly demonstrated just that. Apparently, when you administer verbal IQ tests to black and white children along with handy algorithms that provide the answer to nearly all the difficult problems (which of course, is supposed to control for “cultural bias” — really?), the IQ gap among black and white children magically diminishes to zero. Who knew? But to who is phenomenon supposed to be revelatory to exactly? How convenient that test scores no longer matter once you destroy the predictive value of test scores. You point to a source which states: "Since Spearman's theory of g is about as refuted as a statistical hypothesis gets." At first I didn't realise it's Cosma Shalizi's much loved (in certain quarters) g, a Statistical Myth. Anyone who actually understands the relevant subject matter does not endorse this article. Here's a refutation.

There are group differences in g, as esatablished in this meta-analysis - Ethnic group differences in cognitive ability in employment and educational settings: a meta-analysis

This fact that cognitive abilities reliably have positive correlation is highly nontrivial. Again, for American blacks, the variance in IQ and IQ-like tests is significantly smaller than it is in whites – 65-80% as big, or again -- 1 standard deviation lower.

'g' is well correlated with learning abilities. Look, if none of the eigenvectors of the covariance matrix had particularly large eigenvalues – if there was nothing like ‘g’, one population could still score higher than another on most or all of independent factors. It would not matter whether blacks suffered from a score deficit on one or ten or one hundred factors.

Let's assume that the brain actually has some evolutionary purpose other than cooling the blood, from that you’d think that its development would be fairly robust, i.e., not easily derailed by moderate environmental differences, as you suggest. In other words, the factors that in practice don’t have much effect should never have been expected to, and for adult outcomes they simply don't.

People like you do not like anything that draws attention to the existence of human populations, for it could therefore frame questions about the ways people differ from each other. You end with the typical knee jerk reaction we're all too familiar with. The human sciences, so called, consistently react in this manner. There is this soft totalitarianism that has overran much of academia.

Imagine if a biochemist discovered a new mechanism of oncogenesis, and the only reaction his colleagues gave was one of shock -- how would this make cancer patients feel? Such research is deemed socially damaging and therefore must be suppressed. We can’t imagine such a response from scientists yet in the human social sciences this is common order.

IQ

Noticing the psychometric evidence, or even mentioning the well-established differences in cognitive ability between different populations, can drastically alter your chances of employability in certain disciplines. But that is how things are. For instance, in American blacks, the variance in IQ tests (and similar) is significantly smaller than it is in whites, or about 1 standard deviation lower: Smaller for IQ, SAT, MCAT, etc:

Figure 11.1 (above): When IQ is scaled to a mean of 100 and a standard deviation (SD) of 15 in the white population, large representative samples of the black population of the whole United States (rather than a local subgroup) show a mean close to 85. For most samples and tests, the range is 80 to 90. The black SD of IQ is approximately 12, ranging in most samples from 11 to 14. The g Factor: The Science of Mental Ability

Such tests predict performance on complex tasks moderately well. You do not see people with sub-average scores doing well in, or even passing, difficult subjects like engineering, mathematics, or the natural sciences. This predictive value is about the same for blacks and whites (and other groups). If these tests didn’t predict performance—if people with low scores excelled, the tests would be worthless. But this isn’t the case.

Figure 11.1: As can be seen even a moderate difference in means between two populations makes a big difference in the fraction that exceeds a high threshold: that’s just a consequence of the shape of the distribution, which falls off more and more rapidly as you get farther from the mean. So the difference in the mean between two groups has many implications. For one thing, it implies that between-population differences become much larger at the highest levels of ability.

Thus, since blacks in the US score about one standard deviation lower in IQ than whites, you would expect to see differences in representation that varied according to the intelligence threshold requires for the particular job or field – and there are such thresholds. And that’s what you see.

This raises implications for the theory that people possess “different “types of intelligence.” Populations with low average IQ produce very few individuals that are good at innovation. Very few. If there were one or a few kinds of intelligence that were not measured well by IQ tests, but allowed people with low IQs to accomplish remarkable things – you’d think we would notice. We know that they don’t invent railroads or transistors or penicillin: what comparably important and useful things have they done? The answer is invariably dependant upon their IQ.

Furthermore, intelligence as measured by IQ is simply a quantitative trait which is normally distributed within populations. People of every race can be theoretically be found at every level of the IQ distribution. It’s just a question of probability, and differences are always more pronounced at the edge of the distribution, just like any other quantitative trait. 

You’ll see the same between-group differences of this magnitude everywhere you look. (e.g., the Chinese in Malaysia who arrived as illiterate tin miners and now run all the industry). Most people think that they must be environmental group differences – but no one has succeeded in substantially changing them. In the US and the West at large there is a legal mandate to eliminate such gaps – but nobody knows how to do it. Moreover, racism is not more pronounced in the more difficult fields of study, in fact when cognitive ability is accounted for, the racial (black-white) income gap does not exist in the U.S. Equally, the same holds true for the racial economic mobility gap. Nor is wealth or income driving IQ differences – it’s simply not the case. They’ve looked.