There are opinions that are required in most of academia (and government, press, etc), if you want to keep your job (or ever be invited to parties). Naturally, most of them are false or silly: what would be the point of requiring people to avow things that were obviously true?  That would be like an initiation rite that consisted of eating an ice-cream cone.  Of course, they can only require public support, not real private belief: as yet there is no “sincerometer”.

In a  previous post, a correspondent mentioned famous environmentalists that privately buy into our hypothesis on Ashkenazi IQ – I know one of those myself.  That’s the sort of thing I’m wondering about – there are of course others.  I don’t necessarily think that such people are incredibly common – really, I don’t know – but I would be interested in hearing of other examples.  Famous is good, but really funny is perhaps even better. Mainly I’m curious.

If details would tend to incriminate you, feel free to send an email to gcochran9@comcast.net.


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The Fluidity of Race

Emily Nix and Nancy Qian just put out a paper – The Fluidity of Race – that has gotten some attention. They claim (based on their analysis of US Census records from 1880-1940) that at least 19% of black males ‘passed’ for white during this period, with about 10% switching back.  And this wasn’t a one-time thing: it kept happening for at least several generations, so there was a continuing net black-to-white flow, about 20% of each generation! They don’t talk about women, since their surnames change, but presumably there would be at least some race-switching among black women as well.

So let’s say that 17% of black males permanently passed over into the white category. During the time in question,  the black percentage of the US population was around 11%;  1 13.1% in 1880, 11.6% in 1900,  with a low in 1930 of 9.7% due to lots of recent immigration from Europe.

I think we can assume that half of the black population was male, at least until someone publishes claims of long-secret, industrial-scale parthenogenesis.

The period in questions covers about two generations.  So:

the fraction of the population called white should have absorbed  about

2 generations x 17% of the black male population x 0.5 (male fraction) x 11% (black fraction of the population) = 1.87% .  The white population during this period was about 89% of the population.    So you’d expect that whites in this country, on average would have about 2% black ancestry.  Or maybe less, since blacks average about 75% African ancestry: more like 1.5% African ancestry.

But they don’t : the average amount of African ancestry among self-labeled whites is , according to a recent, massive 23andme study,  0.19%.  The majority don’t have any African ancestry at all. 0.19% is way less, at least ten times less, than suggested by  the Nix-Qian paper.  Considerably less than you’d see in one generation, if they were right, and remember that they thought this was an ongoing process over many decades.  Moreover, for most of those whites that have any detectable African ancestry at all, the amount is small, a percent or two – which suggests the admixture event happened quite a while ago.

In the South, the amount of African admixture is larger among whites: about 5% of self-labelled whites in South Carolina have at least 2% African ancestry.  About 12% have over 1% African ancestry. But that amounts to an average African ancestry well under 1% among whites in South Carolina, a state in which blacks used to be the majority. That strongly suggests that the fraction of blacks that ever successfully passed into the white zone,  over the entire history of the US,  is more like 1 in 100, rather than 20% per generation.

So: what can we conclude about this paper? It’s a classic case of economic imperialism, informed by what ‘intellectuals’ [ those that have never been introduced to Punnet squares, Old Blue Light, the Dirac equation, or  Melungeons] would like to hear.

It is wrong, not close to right.


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Mitochondrial male sterility

Most plants are hermaphrodites, producing both pollen and seeds, but there are many species in which some individuals are morphodites and others are purely female.  Often this femaleness (male sterility) is caused by a mitochondrial mutation.

I once heard Bob Trivers explain this: it’s simple and interesting.  Hermaphroditic individuals often self-fertilize, which is a gift and a curse. It’s a gift because seeds from self-fertilization have two copies of the plant’s genome, rather than one: fitness is increased, all else equal.  It’s a curse because of inbreeding depression: lots of homozygosity makes one weak.  From the plant’s point of view, having two sexes and selfing is a good thing as long as the extent of inbreeding depression is less than one-half.  But mitochondria are only transmitted maternally, and  so have nothing to gain from inbreeding- no extra copies get transmitted. While they suffer from being inside inbred, gap-toothed seeds.  So,  any mitochondrial mutation that prevents selfing (by eliminating pollen production) increases mitochondrial fitness, while generally reducing nuclear gene fitness.

Also, energy spent on pollen production is now available for making more seeds, but that’s a secondary effect, usually.


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The central notion of evidence-based medicine is that our understanding of human biology is imperfect.  Some of the idea we come up with for  treating and preventing disease are effective, but most are not, worse than useless. So we need careful, rigorous statistical studies before implementing those ideas on a wide scale. A good example of doing this the wrong way was when when doctors started recommending having babies sleep prone,  which roughly doubled the incidence of sudden infant death syndrome for the next several decades.

It seems to me that our understanding of psychology, sociology, economics, political science, and education is at least as imperfect as our understanding of biomedicine.

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Lewontin wins the Crafoord Prize


The Crafoord Prize for 2015 was awarded to Richard Lewontin and Tomoko Ohta,  for their discovery that there was very much more genetic variation that had been expected.  Lewontin discovered this using protein gel electrophoresis to study a number of loci in Drosophila.  It’s an important result.  The problem is, virtually everything he’s said and done since that time has been a pile of steaming ideological crap.  He has argued that the distribution of genetic variation in humans (more within-population variation than between-population variation) means that populations can’t really be very different.  Except for skin color ( just a few alleles), height (Pygmies exist and really are short), brain volume,  etc etc.  The argument is crap: you need to look at allele frequencies weighted by their phenotypic effects.  One funny allele like EDAR370a  contributes an infinitesimal amount to interpopulation genetic variation, but it sure makes a difference.  Mild differences in the frequency of a few hundred alleles can cause big differences in highly polygenic traits.  I’ve talked about this, here and here.

Lewontin has criticized adaptationism, but as far as I  can see, that was all crap too – not least The Spandrels of San Marco ( a big paper by Lewontin and  Stephen J. Gould, yet another graduate of Commie Martyrs High School) .  I am of course not  joking in calling Lewontin a Marxist – he says so himself – and it matters, because Marxism makes you stupid. Not just a fanboy of mass murderers – it fucks you up.  Lysenko was a feature, not a bug.

Which is why he does silly things, like oppose hybrid seed corn as a creation of the bloated lackeys of the imperialist toy-mongers.

Why he does he deny the results of behavioral genetics, particularly the high heritability of IQ?  The same reason that Marc Feldman does – because he doesn’t like those results, what else?  There’s nothing like bringing up an argument that could be true in some other world, but just happens not to be in this one.  Couldn’t populations that do poorly in one environment have superior performance in another?  Sure – but there’s no existing environment where that reversal actually happens. The rank-ordering on IQ is the same everywhere.

For a long time, Richard Lewontin has done his level best to increase the sum total of misinformation in the world, not without success.  That’s what I used to think, anyhow – but there may be another explanation.

This complicates the question of  suitability for the prize. Generally, being some kind of asshole is not considered relevant in considering this kind of prize.  That seems fair:  it’s the work that matters, not your bad breath or devotion to the Lost Cause.  But what is the right course when the same person who did the excellent work spend most of his career trying to corrupt that same field?

Others have faced a similar question:  what’s the right way to acknowledge Benedict Arnold’s  early contributions to the American Revolution, before his treason?


This statute commemorates Arnold’s service and wounding at the battle of Saratoga – without mentioning his name.


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Son of Edar

The EDAR V370A variant, almost fixed in northeast Asia, is known to cause coarser hair,  smaller breasts with increased branch density,  shovel-shaped incisors,  more eccrine sweat glands, and changes in the shape of the earlobe. The changes in eccrine sweat glands and the hangey-down part of the ear have only been noticed recently.

It’s a gain-of-function mutation: you’re getting more of the effect that EDAR normally has.

Some people have loss-of-function mutations in EDAR: hypohydrotic extodermal dysplasia, HED.  This was first identified by Charles Darwin. In The Variation of Animals and Plants under Domestication, he noted a family in India that produced ten men in four generations, all suffering from missing teeth, very little hair, inability to sweat, etc.

HED patients also have messed-up fingernails and have problems with the lacrimal glands (tear glands), the sebaceous glands, the Meibomian glands, and salivary glands. Presumably you would see the opposite effects in people with a gain-of-function mutation like EDAR V370A.

So – somebody should look for characteristic racial differences in tears, sebaceous glands, Meobomian glands, and salivary glands. And possibly fingernails. They may well exist,  be driven by this EDAR mutation, and some might play a role in its selective advantage.

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Stockpile Stewardship

A lot of our nuclear weapons are old, and it’s not clear that they still work. If we still did underground tests, we’d know for sure (and could fix any problems) – but we don’t do that.  We have a program called stockpile stewardship, that uses simulation programs and the data from laser-fusion experiments in an attempt to predict weapon efficacy.

I talked to some old friends who know as much about the nuclear stockpile as anyone: neither believes that that stockpile stewardship will do the job.  There are systems that you can simulate with essentially perfect accuracy and confidence, Newtonian gravitational mechanics for example: this isn’t one of them.

You had two approaches to a problem that was vital to the security of the United States:  option A was absolutely sure to work, option B might possibly work.

The Feds picked B.



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