What Ethic Group is This?

 

map

23 and Me map of genetic relatives, rounded. 

An ethnic group is a set of people with a common ancestry, culture, and language. The Han Chinese, at a 1.3 billion strong, are an ethnic group; the Samaritans, of whom there are fewer than a thousand, are also an ethnic group. Ishi was, before his death, an ethnic group of one: the last surviving member of the Yahi people of California. 

We sit within nested sets of genetic relatives:

Family<clan<tribe<ethnic group<race<species<genus

(You are most likely part Homo neanderthalensis, because different species within the Homo genus have interbred multiple times.)

Interestingly, Wikipedia lists African American as an ethnicity on its list of ethnic groups page (as they should, because it is). 

Four or five hundred relatives, from parents and children to fifth cousins, are enough to begin to describe an ethnic group. It certainly looks, based on the map, like I hail from an ethnic group–yet neither Wikipedia nor 23 and Me recognize this group.

According to Wikipedia

Larger ethnic groups may be subdivided into smaller sub-groups known variously as tribes or clans, which over time may become separate ethnic groups themselves due to endogamy or physical isolation from the parent group. Conversely, formerly separate ethnicities can merge to form a pan-ethnicity, and may eventually merge into one single ethnicity. Whether through division or amalgamation, the formation of a separate ethnic identity is referred to as ethnogenesis.

Of course, no one wants to submit their DNA to 23 and Me and get the result “You’re a white person from America.” (Nor “You’re a black person from America.”) We know that. People take these tests to look at their deeper history. 

But focusing only on the past makes it easy to lose sight of the present. You aren’t your ancestors. The world didn’t halt in 1492. I’m no more “British” or “European” than I am “Yamnaya” or “Anatolian farmer.” 

History moves on. New ethnic groups form. The past tells us something about where we’ve been–but not where we’re headed. 

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What does “Heritable” mean? 

“Heritable” (or “heritability”) has a specific and unfortunately non-obvious definition in genetics.

The word sounds like a synonym for “inheritable,” rather like your grandmother’s collection of musical clocks. Musical clocks are inheritable; fruit, since it rots, is not very inheritable.

This is not what “heritable” means.

“Heritability,” in genetics, is a measure of the percent of phenotypic variation within a population that can be attributed to genetics.

Let me clarify that in normal speak. “Phenotype” is something you can actually see about an organism, like how tall it is or the nest it builds. “Phenotypic variation” means things like “variation in height” or “variation in nest size.”

Let’s suppose we have two varieties of corn: a giant strain and a dwarf strain. If we plant them in a 100% even field with the same nutrients, water, sunlight, etc at every point in the field, then close to 100% of the variation in the resulting corn plants is genetic (some is just random chance, of course.)

In this population, then, height is nearly 100% heritable.

Let’s repeat the experiment, but this time, we sow our corn in an irregular field. Some patches have good soil; some have bad. Some spots are too dry or too wet. Some are sunny; others shaded. Etc.

Here it gets interesting, because aside from a bit of random chance in the distribution of seeds and environmental response, in most areas of the irregular field, our “tall” corn is still taller than the “short” corn. In the shady areas, both varieties don’t get enough sun, but the tall corn still grows taller. In the nutrient-poor areas, both varieties don’t get enough nutrients, but the tall still grows taller. But when we compare all of the corn all over the field, dwarf corn grown in the best areas grows taller than giant corn grown in the worst areas.

Our analysis of the irregular field leads us to conclude that water, sunlight, nutrients, and genes are all important in determining how tall corn gets.

Height in the irregular field is still heritable–genes are still important–but it is not 100% heritable, because other stuff is important, too.

What does it mean to be 10, 40, or 80% heritable?

If height is 10% heritable, then most of the variety in height you see is due to non-genetic factors, like nutrition. Genes still have an effect–people with tall genes will still, on average, be taller–but environmental effects really dominate–perhaps some people who should have been tall are severely malnourished.

In modern, first world countries, height is about 80% heritable–that is, since most people in first world countries get plenty of food and don’t catch infections that stunt their growth, most of the variation we see is genetic. In some third world countries, however, the heritability of height drops to 65%. These are places where many people do not get the nutrients they need to achieve their full genetic potential.

How do you achieve 0% heritability?

A trait is 0% heritable not if you can’t inherit it, but if genetics explains none of the variation in the sample. Suppose we seeded an irregular field entirely with identical, cloned corn. The height of the resulting corn would would vary from area to area depending on nutrients, sunlight, water, etc. Since the original seeds were 100% genetically identical, all of the variation is environmental. Genes are, of course, important to height–if the relevant genes disappeared from the corn, it would stop growing–but they explain none of the variation in this population.

The heritability of a trait decreases, therefore, as genetic uniformity increases or the environment becomes more unequal. Heritability increases as genetics become more varied or the environment becomes more equal. 

Note that the genes involved do not need to code directly for the trait being measured. The taller people in a population, for example, might have lactase persistence genes, which let them extract more calories from the milk they drink than their neighbors. Or they might be thieves who steal food from their neighbors.

I remember a case where investigators were trying to discover why most of the boys at an orphanage had developed pellagra, then a mystery disease, but some hadn’t. It turns out that the boys who hadn’t developed it were sneaking into the kitchen at night and stealing food.

Pellagra is a nutritional deficiency caused by lack of niacin, aka B3. Poor Southerners used to come down with it from eating diets composed solely of (un-nixtamalized) corn for months on end.

The ultimate cause of pellagra is environmental–lack of niacin–but who comes down with pellagra is at least partially determined by genes, because genes influence your likelihood of eating nothing but corn for 6 months straight. Sociopaths who steal the occasional ham, for example, won’t get pellagra, but sociopaths who get caught and sent to badly run prisons, however, increase their odds of getting it. In general, smart people who work hard and earn lots of money significantly decrease their chance of getting it, but smart black people enslaved against their will are more likely to get it. So pellagra is heritable–even though it is ultimately a nutritional deficiency.

What’s the point of heritability?

If you’re breeding corn (or cattle,) it helps to know whether, given good conditions, you can hope to change a trait. Traits with low heritability even under good conditions simply can’t be affected very much by breeding, while traits with high heritability can.

In humans, heritability helps us seek out the ultimate causes of diseases. On a social level, it can help measure how fair a society is, or whether the things we are doing to try to make society better are actually working.

For example, people would love to find a way to make children smarter. From Baby Einstein to HeadStart, people have tried all sorts of things to raise IQ. But beyond making sure that everyone has enough to eat, no nutrient deficiencies, and some kind of education, few of these interventions seem to make much difference.

Here people usually throw in a clarification about the difference between “shared” and “non-shared” environment. Shared environment is stuff you share with other members of your population, like the house your family lives in or the school you and your classmates attend. Non-shared is basically “random stuff,” like the time you caught meningitis but your twin didn’t.

Like anything controversial, people of course argue about the methodology and mathematics of these studies. They also argue about proximate and ultimate causes, and get caught up matters of cultural variation. For example, is wearing glasses heritable? Some would say that it can’t be, because how can you inherit a gene that somehow codes for possessing a newly invented (on the scale of human evolutionary history) object?

But this is basically a fallacy that stems from mixing up proximate and ultimate causes. Obviously there is no gene that makes a pair of glasses grow out of your head, nor one that makes you feel compelled to go and buy them. It is also obvious that not all human populations throughout history have had glasses. But within a population that does have glasses, the chances of you wearing glasses is strongly predicted by whether or not you are nearsighted, and nearsightedness is a remarkable 91% heritable. 

Of course, some nearsighted people opt to wear contact lenses, which lowers the heritability estimate for glasses, but the signal is still pretty darn strong, since almost no one who doesn’t have vision difficulties wears glasses.

If we expand our sample population to include people who lived before the invention of eyeglasses, or who live in countries where most people are too poor to afford glasses, then our heritability estimate will drop quite a bit. You can’t buy glasses if they don’t exist, after all, no matter how bad your eyesight it. But the fact that glasses themselves are a recent artifact of particular human cultures does not change the fact that, within those populations, wearing glasses is heritable.

“Heritability” does not depend on whether there is (or we know of ) any direct mechanism for a gene to code for the thing under study. It is only a statistical measure of genetic variation that correlates with the visible variation we’re looking at in a population.

I hope this helps.

Links Post: Evolution and More

road-to-bigger-brains
From State of the Science: Finding Human Ancestors in New Places

The Puerto Rican rainforest is beautiful and temporarily low on bugs. (Bugs, I suspect, evolve quickly and so can bounce back from these sorts of collapses–but they are collapses.)

More evidence for an extra Neanderthal or Denisovan interbreeding event in East Asians and Melanesian genomes:

 In addition to the reported Neanderthal and Denisovan introgressions, our results support a third introgression in all Asian and Oceanian populations from an archaic population. This population is either related to the Neanderthal-Denisova clade or diverged early from the Denisova lineage.

(Congratulations to the authors, Mondal, Bertranpetit, and Lao.)

Really interesting study on gene-culture co-evolution in Northeast Asia:

Here we report an analysis comparing cultural and genetic data from 13 populations from in and around Northeast Asia spanning 10 different language families/isolates. We construct distance matrices for language (grammar, phonology, lexicon), music (song structure, performance style), and genomes (genome-wide SNPs) and test for correlations among them. … robust correlations emerge between genetic and grammatical distances. Our results suggest that grammatical structure might be one of the strongest cultural indicators of human population history, while also demonstrating differences among cultural and genetic relationships that highlight the complex nature of human cultural and genetic evolution.

I feel like there’s a joke about grammar Nazis in here.

Why do we sleep? No one knows.

While humans average seven hours, other primates range from just under nine hours (blue-eyed black lemurs) to 17 (owl monkeys). Chimps, our closest living evolutionary relatives, average about nine and a half hours. And although humans doze for less time, a greater proportion is rapid eye movement sleep (REM), the deepest phase, when vivid dreams unfold.

Sleep is pretty much universal in the animal kingdom, but different species vary greatly in their habits. Elephants sleep about two hours out of 24; sloths more than 15. Individual humans vary in their sleep needs, but interestingly, different cultures vary greatly in the timing of their sleep, eg, the Spanish siesta. Our modern notion that people “should” sleep in a solid, 7-9 hour chunk (going so far as to “train” children to do it,) is more a result of electricity and industrial work schedules than anything inherent or healthy about human sleep. So if you find yourself stressed out because you keep taking a nap in the afternoon instead of sleeping through the night, take heart: you may be completely normal. (Unless you’re tired because of some illness, of course.)

Interestingly:

Within any culture, people also prefer to rest and rise at different times: In most populations, individuals range from night owls to morning larks in a near bell curve distribution. Where someone falls along this continuum often depends on sex (women tend to rise earlier) and age (young adults tend to be night owls, while children and older adults typically go to bed before the wee hours).

Genes matter, too. Recent studies have identified about a dozen genetic variations that predict sleep habits, some of which are located in genes known to influence circadian rhythms.

While this variation can cause conflict today … it may be the vestige of a crucial adaptation. According to the sentinel hypothesis, staggered sleep evolved to ensure that there was always some portion of a group awake and able to detect threats.

So they gave sleep trackers to some Hadza, who must by now think Westerners are very strange, and found that at any particular period of the night, about 40% of people were awake; over 20 nights, there were “only 18 one-minute periods” when everyone was asleep. That doesn’t prove anything, but it does suggest that it’s perfectly normal for some people to be up in the middle of the night–and maybe even useful.

Important dates in the evolution of human brain genes found:

In May, a pair of papers published by separate teams in the journal Cell focused on the NOTCH family of genes, found in all animals and critical to an embryo’s development: They produce the proteins that tell stem cells what to turn into, such as neurons in the brain. The researchers looked at relatives of the NOTCH2 gene that are present today only in humans.

In a distant ancestor 8 million to 14 million years ago, they found, a copying error resulted in an “extra hunk of DNA,” says David Haussler of the University of California, Santa Cruz, a senior author of one of the new studies.

This non-functioning extra piece of NOTCH2 code is still present in chimps and gorillas, but not in orangutans, which went off on their own evolutionary path 14 million years ago.

About 3 million to 4 million years ago, a few million years after our own lineage split from other apes, a second mutation activated the once non-functional code. This human-specific gene, called NOTCH2NL, began producing proteins involved in turning neural stem cells into cortical neurons. NOTCH2NL pumped up the number of neurons in the neocortex, the seat of advanced cognitive function. Over time, this led to bigger, more powerful brains. …

The researchers also found NOTCH2NL in the ancient genomes of our closest evolutionary kin: the Denisovans and the Neanderthals, who had brain volumes similar to our own.

And finally, Differences in Genes’ Geographic Origins Influence Mitochondrial Function:

“Genomes that evolve in different geographic locations without intermixing can end up being different from each other,” said Kateryna Makova, Pentz Professor of Biology at Penn State and an author of the paper. “… This variation has a lot of advantages; for example, increased variation in immune genes can provide enhanced protection from diseases. However, variation in geographic origin within the genome could also potentially lead to communication issues between genes, for example between mitochondrial and nuclear genes that work together to regulate mitochondrial function.”

Researchers looked at recently (by evolutionary standards) mixed populations like Puerto Ricans and African Americans, comparing the parts of their DNA that interact with mitochondria to the parts that don’t. Since mitochondria hail from your mother, and these populations have different ethnic DNA contributions along maternal and paternal lines. If all of the DNA were equally compatible with their mitochondria, then we’d expect to see equal contributions to the specifically mitochondria-interacting genes. If some ethnic origins interact better with the mitochondria, then we expect to see more of this DNA in these specific places.

The latter is, in fact, what we find. Puerto Ricans hail more from the Taino Indians along their mtDNA, and have relatively more Taino DNA in the genes that affect their mitochondria–indicating that over the years, individuals with more balanced contributions were selected against in Puerto Rico. (“Selection” is such a sanitized way of saying they died/had fewer children.)

This indicates that a recently admixed population may have more health issues than its parents, but the issues will work themselves out over time.

Review: The Blank Slate, by Steven Pinker 5/5 Stars

Steven Pinker’s The Blank Slate was one of my top reads of 2018. Simultaneously  impassioned, philosophic, and rational, Pinker covers everything from art to parenting, morality to language. What makes us us? Where does human nature–and individual personality–come from? And what are the moral implications if blank slateist views of human nature are false?

Yes, Pinker writes from a liberal perspective, for a liberal audience–Pinker hails from a liberal culture and addresses the members of his own culture, just as a French writer addresses a French audience. But this is about as far as conventions like “left” and “right” can take you in this book, for it is clear that Pinker thinks breaking down political ideology and morality based on the seating patterns of an eighteenth-century French legislature is not terribly meaningful. 

Is the blank slate–the idea that humans are born essentially similar in personality, temperament, abilities, and potential, and that environmental plays a substantial role in determining whether we turn out to be Nobel Prize winners or drag queens, Jeff Bezos or homeless, criminals or lion tamers–moral? 

Its adherents claim that it is–indeed, some react to any suggestion that humans have any innate or biological nature with a vehemence normally reserved for rapists and murderers. 

Pinker responds that the denial of human nature causes unimaginable suffering. Humans cannot cast aside their natures simply because an ideology (or religion) tells them to. To attempt to remake man is to destroy him. 

Further, it is blatantly untrue, and the promotion of obvious lies in pursuit of ideological outcomes is bound to backfire–turning people away from the academics and fields that promote such lies. (Pinker may be overly optimistic on this point.) 

Chapter 1 is a bit slow if you are already familiar with the history of psychology and the blank slate in philosophy, but after that it picks up nicely. 

There is an unstated conclusion we may draw here that psychology as a discipline has been hampered by the kinds of people who go into the psychology. Perhaps this is my own theory I am imposing onto Pinker’s work, but it seems like people with a good, intuitive grasp of how people work don’t go into psychology–they go into sales. The folks in psychology (and psychiatry, perhaps) seem drawn to the field because they find people mysterious and fascinating and want to understand them better. 

But without an intuitive understanding of how people work, there are often big areas they miss. 

Since I listened to this in audio book format, quoting is tricky, but I have tried to transcribe this bit:

Until recently, psychology ignored the content of beliefs and emotions, and the possibility that the mind had evolved to treat biologically important categories in different ways. … Theories about memory and reasoning didn’t distinguish between thoughts about people and thoughts about rocks or houses. Theories of emotion didn’t distinguish fear from anger, jealousy, or love. Theories of social relation didn’t distinguish between family, friends, enemies, and strangers.

Indeed, the topics in psychology that most interest lay people–love, hate, work, play, food, sex, status, dominance, jealousy, friendship, religion, art–are almost completely absent from psychology textbooks.

It’s hard to see what you can’t see.

The field was also historically rather short on women, especially women with normal lives. Many of these blank slateist quotes from psychologists and philosophers about human nature and instincts seem like the kinds of ideas that raising a few children would quickly disabuse you of.  

Next he discusses Durkheim’s observation that people behave differently in groups than they do singly or would behave had they not been part of a group. From this I think Durkheim derives his idea that “human nature” and “human behavior” are not innate or instinctive, but culturally induced. 

Some years ago, I realized there is probably an important key to human behavior that is rarely explicitly discussed because if you have it, it is so obvious that you don’t even notice it, and if you don’t have it, it’s so non-obvious that you can’t figure it out: an imitation instinct.

People desire to be like the people around them, and for probably evolutionarily sound reasons. 

If everyone else in your tribe says, “Don’t drink that water, it’s bad,” you’re better off avoiding the water than taking your chances by doing an independent test on the water. If your tribe has a longstanding tradition of “don’t eat the red berries, no I don’t know why, grandpa just told me to never ever eat them,” it’s probably best to go along. As Chesterton says, don’t tear down a fence if you don’t know why it’s there. 

I think a compulsion to fit in, imitate, and go along with others is very deep. It’s probbly not something people are explicitly aware of most of the time. This results in people using arguments like “That’s weird,” to mean, “That’s bad,” without explaining why “weird” is bad. They just intuitively know, and expect that you understand and agree with the speaker’s intuition that weird and different are inherently bad things. 

This leads to 1. self-policing–people feel very out of place when they aren’t going along with the group and this can make them deeply unhappy; and 2. other-policing–people feel unhappy just looking at someone else who is out of place, and this makes them respond with anger, hostility, and sometimes even violence toward the other person. (Even when what that other person is doing is really quite inconsequential and harmless.)

Anyway, I think Durkheim has missed that step–that connection between group activity and individual activity.

Obviously people are shaped by their groups, since most hunter-gatherer babies grow up to be hunter-gatherers and most people in our society grow up and figure out how to use cell phones and computers and cars. But I think he has missed the importance of–and critically, the usefulness of–the underlying mental trait that lets us learn from our cultures.

So people don’t behave differently in groups than when they’re alone because they lack some inherent human nature, but because part of our nature compels us to act in concordance with our group. (Most of us, anyway.) 

(This is about where I stopped taking notes, so I’m working from memory.)

Pinker then discusses the neurology of learning–how do we learn language? How does the brain know that language is something we are supposed to learn? How do we figure out that the family pet is not named “No no bad dog, get off the sofa”? 

There are some interesting experiments done on mice and kittens where experimenters have done things like reverse the parts of the brain auditory or visual inputs go to, or raise the kittens in environments without vertical lines and then introduce them to vertical lines, etc. The brain shows a remarkable plasticity under very strange conditions–but as Pinker points out, these aren’t conditions humans normally encounter. 

Sure, you can teach people to be afraid of flowers or like snakes, but it is much, much easier to teach people to like flowers and be afraid of snakes. 

Pinker points to the ease with which we learn to fear some objects but not others; the ease with which we learn to talk (except for those of us with certain neurological disorders, like brain damage or autism) verses the difficulty we have learning other things, like calculus; the rapidity with which some behaviors emerge in infancy or childhood (like aggression) verses the time it takes to instill other behaviors (like sharing) in children. 

In short, we appear to come into this world equipped to learn certain things, to respond to certain stimuli, and behave in particular ways. Without this basic wiring, we would not have any instinct for imitation–and thus babies would not coo in response to their mothers, would not start babbling in imitation of the adults around them, and would not learn to talk. We would not stand up and begin to walk–and it would be just as easy to train people to enjoy being victims of violence as to train people not to commit violence. 

Throughout the book, Pinker discusses the response of the more extreme left–people whom we today call SJWs or antifa–to the work and theories put out by academics who are undoubtedly also culturally liberal, like Napoleon Chagnon, the famous anthropologist who studied the Yanomamo tribesmen in the Amazon. For his meticulous work documenting Yanomamo family trees and showing that the Yanomamo men who killed more people wound up wound up with more children than the men who killed fewer people, he was accused by his fellow academics of all sorts of outlandish crimes.

In one absurd case, he was accused of intentionally infecting the Yanomamo with measles in order to test a theory that Yanomamo men had more “dominant genes,” which would give them a survival advantage over the measles. This is a serious accusation because exposure to Western diseases tends to kill off the majority of people in isolated, indigenous tribes, and absurd because “dominant genes” don’t confer any more or less immunity to disease. The accuser in this case has completely misunderstood the meaning of a term over in genetics. (It is rather like someone thinking the word “straight” implies that heterosexuals are supposed to have straighter bones than homosexuals, and then accusing scientists of going around measuring people’s bones to determine if they are gay or not.)

The term “dominant” does not mean that a gene gives a person any form of “dominance” in the real world. It just means that in a pair of genes, a “dominant” one gets expressed. The classic example is blue verses brown eyes. If you have one gene for blue eyes from one parent, and one for brown eyes from your other parent, anyone looking at you will just see brown eyes because only that gene gets used. However, you might still pass on that blue eye gene to your children, and if they receive another blue gene from your spouse, they could have blue eyes. Since blue eyes only show up if both of a person’s eye color genes are blue, we call blue eyes “recessive.” 

But having a “dominant” gene for eye color doesn’t make someone any more “dominant” in real life. It doesn’t make you better at beating people up or surviving the flu–and nothing about the Yanomamo lifestyle suggests that they would have more “dominant genes” than anyone else in the world. 

Side note: this strange misconception of how genes work made it into Metal Gear Solid: 

“I got all of the recessive genes! You took everything from me before I was even born!”

The fact that the far left often engages in outright lies to justify real violence against the people they dislike–people who aren’t even conservatives on the American scale–makes one wonder why Pinker identifies at all with the left’s goals, but I suppose one can’t help being a part of one’s own culture. If a Frenchman objects to something happening in France, that doesn’t turn him into a German; a Christian doesn’t stop believing in Jesus just because he objects to Fred Phelps. 

The book came out in 2002, before “antifa” became a household term. I think Pinker expected the evils of communism to become more widely known–not less. 

There is an interesting discussion of E. O. Wilson’s Sociobiology and how a better understanding of human family dynamics (especially whether they become controlling and harmful) could improve women’s lives, not harm them. (Wilson’s work I would like to explore in more depth.) 

Pinker proceeds to a moving chapter parenting (I teared up at the end, though that might have just been the effects of several days of inadequate sleep.) How much effect do parents have on how their children turn out? At least within the normal range of parenting, not much–kids seem to turn out as they will, despite our best efforts. Sure, there’s plenty of evidence that you can damage kids by shaking them, dropping them on their heads, or locking them in the closet for years–but this is not normal parenting. Meanwhile, there’s very little evidence in favor of any interventions that can raise a child’s IQ (or any other trait) above what it would have been otherwise. It’s much easier to break a complicated system than enhance it. 

People often respond along the lines of “If I cannot shape my children like clay, determining how they turn out as adults, what’s the point of parenting at all?” 

It’s a terrible response, as Pinker points out. Children are human and deserve to be valued for the people they are (and will be,) not because you can change them. You are not kind to your spouse because you expect to change them, after all, but because you like them and value them. Likewise, be kind to your children because you love and value them, not because you can program them like tiny computers. 

In search of the reasons people turn out the way they do, Pinker (and other writers) turns to the random effects of “the environment”–things like “the friends you had in highschool.” Certainly environment explains a good deal, like what language you speak or what job options exist in your society, but I think he neglects an alternative possibility for some traits: random chance. There are aspects of us that are just “who we are” and aren’t obviously determined by anything external. One child loves dogs, another horses. One person enjoys swimming, another biking, a third Candy Crush. 

Here a religious person might posit a “soul” or some other inner essence. 

The difficulty with the theory that children take after their peers–they do what it takes to fit in with their friends–is it neglects the question of why a child becomes friends with a particular group of other children in the first place. I don’t know about you, but my friends aren’t chosen randomly from the people around me, but tend to be people I have something in common with or enjoy being around in the first place. 

At any rate, it is certainly possible for well-meaning parents to isolate a child from peers and friends in an attempt to alter personalty traits that are actually innate, or at least not caused by those other children.

The meat of the book wraps up with a discussion of “modern art” and why it is terrible. 

Overall, it was an excellent book that remains fresh despite its age. 

Book Club: The 10,000 Year Explosion pt 7: Finale

 

Niels Bohr
Niels Bohr: 50% Jewish, 100% Quantum Physics

Chapter 7 of The 10,000 Year Explosion is about the evolution of high Ashkenazi IQ; chapter 8 is the Conclusion, which is just a quick summary of the whole book. (If you’re wondering if you would enjoy the book, try reading the conclusion and see if you want to know more.)

This has been an enjoyable book. As works on human evolution go, it’s light–not too long and no complicated math. Pinker’s The Blank Slate gets into much more philosophy and ethics. But it also covers a lot of interesting ground, especially if you’re new to the subject.

I have seen at least 2 people mention recently that they had plans to respond to/address Cochran and Harpending’s timeline of Jewish history/evolution in chapter 7. I don’t know enough to question the story, so I hope you’ll jump in with anything enlightening.

The basic thesis of Chapter 7 is that Ashkenazi massive over-representation in science, math, billionaires, and ideas generally is due to their massive brains, which is due in turn to selective pressure over the past thousand years or so in Germany and nearby countries to be good at jobs that require intellect. The authors quote the historian B. D. Weinryb:

More children survived to adulthood in affluent families than in less affluent ones. A number of genealogies of business leaders, prominent rabbis, community leaders, and the like–generally belonging to the more affluent classes–show that such people often had four, six, sometimes even eight or nice children who reached adulthood…

800px-Niels_Bohr_Albert_Einstein_by_Ehrenfest
Einstein and Bohr, 1925

Weinryb cites a census of the town of Brody, 1764: homeowner household had 1.2 children per adult; tenant households had only 0.6.

As evidence for this recent evolution, the authors point to the many genetic diseases that disproportionately affect Ashkenazim:

Tay-Sachs disease, Gaucher’s disease, familial dysautonomia, and two different forms of hereditary breast cancer (BRCA1 and BRCA2), and these diseases are up to 100 times more common in Ashkenazi Jews than in other European populations. …

In principle, absent some special cause, genetic diseases like these should be rare. New mutations, some of which have bad effects, appear in every generation, but those that cause death or reduced fertility should be disappearing with every generation. … one in every twenty-five Ashkenazi Jews carries a copy of the Tay-Sachs mutation, which kills homozygotes in early childhood. This is an alarming rate.

What’s so special about these diseases, and why do the Ashkenazim have so darn many of them?

Some of them look like IQ boosters, considering their effects on the development of the central nervous system. The sphingolipid mutations, in particular, have effects that could plausibly boost intelligence. In each, there is a buildup of some particular sphingolipid, a class of modified fat molecules that play a role in signal transmission and are especially common in neural tissues. Researchers have determined that elevated levels of those sphingolipids cause the growth of more connections among neurons..

There is a similar effect in Tay-Sachs disease: increased levels of a characteristic storage compound… which causes a marked increase in the growth of dendrites, the fine branches that connect neurons. …

We looked at the occupations of patients in Israel with Gaucher’s disease… These patients are much more likely to be engineers or scientists than the average Israeli Ashkenazi Jew–about eleven times more likely, in fact.

Einstein_oppenheimer
Einstein and Oppenheimer, Father of the Atomic Bomb, c. 1950

Basically, the idea is that similar to sickle cell anemia, being heterozygous for one of these traits may make you smarter–and being homozygous might make your life considerably shorter. In an environment where being a heterozygous carrier is rewarded strongly enough, the diseases will propagate–even if they incur a significant cost.

It’s a persuasive argument.

I’d like to go on a quick tangent to Von Neumann’s Wikipedia page:

Von Neumann was a child prodigy. When he was 6 years old, he could divide two 8-digit numbers in his head [14][15] and could converse in Ancient Greek. When the 6-year-old von Neumann caught his mother staring aimlessly, he asked her, “What are you calculating?”[16]

Children did not begin formal schooling in Hungary until they were ten years of age; governesses taught von Neumann, his brothers and his cousins. Max believed that knowledge of languages in addition to Hungarian was essential, so the children were tutored in English, French, German and Italian.[17] By the age of 8, von Neumann was familiar with differential and integral calculus,[18] but he was particularly interested in history. He read his way through Wilhelm Oncken‘s 46-volume Allgemeine Geschichte in Einzeldarstellungen.[19] A copy was contained in a private library Max purchased. One of the rooms in the apartment was converted into a library and reading room, with bookshelves from ceiling to floor.[20]

JohnvonNeumann-LosAlamos
Von Neumann

Von Neumann entered the Lutheran Fasori Evangélikus Gimnázium in 1911. Wigner was a year ahead of von Neumann at the Lutheran School and soon became his friend.[21] This was one of the best schools in Budapest and was part of a brilliant education system designed for the elite. Under the Hungarian system, children received all their education at the one gymnasium. Despite being run by the Lutheran Church, the school was predominately Jewish in its student body [22] The school system produced a generation noted for intellectual achievement, which included Theodore von Kármán (b. 1881), George de Hevesy (b. 1885), Leó Szilárd (b. 1898), Dennis Gabor (b. 1900), Eugene Wigner (b. 1902), Edward Teller (b. 1908), and Paul Erdős (b. 1913).[23] Collectively, they were sometimes known as “The Martians“.[24] 

One final thing in The 10,000 Year Explosion jumped out at me:

There are also reports of individuals with higher-than-average intelligence who have nonclassic congenital adrenal hyperplasia (CAH)… CAH, which causes increased exposure of the developing fetus to androgens (male sex hormones), is relatively mild compared to diseases like Tay-Sachs. At least seven studies show high IQ in CAH patients, parents, and siblings, ranging from 107 to 113. The gene frequency of CAH among the Ashkenazim is almost 20 percent.

Holy HBD, Batman, that’ll give you a feminist movement.

If you haven’t been keeping obsessive track of who’s who in the feminist movement, many of the early pioneers were Jewish women, as discussed in a recent article by the Jewish Telegraph Agency, “A History of the Radical Jewish Feminists and the one Subject they Never Talked About“:

Heather Booth, Amy Kesselman, Vivian Rothstein and Naomi Weisstein. The names of these bold and influential radical feminists may have faded in recent years, but they remain icons to students of the women’s liberation movement …

The Gang of Four, as they dubbed themselves, were among the founders of Chicago’s Women’s Liberation Union. …

Over weeks, months and years, no subject went unturned, from the political to the sexual to the personal. They were “ready to turn the world upside down,” recalled Weisstein, an influential psychologist, neuroscientist and academic who died in 2015.

But one subject never came up: the Jewish backgrounds of the majority of the group.

“We never talked about it,” Weisstein said.

Betty Friedan was Jewish; Gloria Steinem is half Jewish. There are a lot of Jewish feminists.

Of course, Jews are over-represented in pretty much every intellectual circle. Ayn Rand, Karl Marx, and Noam Chomsky are all Jewish. Einstein and Freud were Jewish. I haven’t seen anything suggesting that Jews are more over-represented in feminism than in any other intellectual circle they’re over-represented in. Perhaps they just like ideas. Someone should come up with some numbers.

Here’s a page on Congenital Adrenal Hyperplasia. The “classic” variety is often deadly, but the non-classic (the sort we are discussing here) doesn’t kill you.

Paul_Erdos_with_Terence_Tao
Paul Erdős with Terrence Tao, 1984 (Tao isn’t Jewish, of course.)

I’ve long suspected that I know so many trans people because some intersex conditions result in smarter brains (in this case, women who are better than average at math.) It looks like I may be on the right track.

Well, that’s the end of the book. I hope you enjoyed it. What did you think? And what should we read next? (I’m thinking of doing Pinker’s Blank Slate.)

Book Club: The 10,000 Year Explosion pt. 6: Expansion

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Welcome back to the Book Club. Today we’re discussing chapter 6 of Cochran and Harpending’s The 10,000 Year Explosion: Expansions

The general assumption is that the winning advantage is cultural–that is to say, learned. Weapons, tactics, political organization, methods of agriculture: all is learned. The expansion of modern humans is the exception to the rule–most observers suspect that biological difference were the root cause of their advantage. … 

the assumption that more recent expansions are all driven by cultural factors is based on the notion that modern humans everywhere have essentially the same abilities. that’s a logical consequence of human evolutionary stasis” If humans have not undergone a significant amount of biological change since the expansion out of Africa, then people everywhere would have essentially the same potentials, and no group would have a biological advantage over its neighbors. But as we never tire of pointing out, there has been significant biological change during that period.

I remember a paper I wrote years ago (long before this blog) on South Korea’s meteoric economic rise. In those days you had to actually go to the library to do research, not just futz around on Wikipedia. My memory says the stacks were dimly lit, though that is probably just some romanticizing. 

I poured through volumes on 5 year economic plans, trying to figure out why South Korea’s were more successful than other nations’. Nothing stood out to me. Why this plan and not this plan? Did 5 or 10 years matter? 

I don’t remember what I eventually concluded, but it was probably something along the lines of “South Korea made good plans that worked.” 

People around these parts often criticize Jared Diamond for invoking environmental explanations while ignoring or directly counter-signaling their evolutionary implications, but Diamond was basically the first author I read who said anything that even remotely began to explain why some countries succeeded and others failed. 

Environment matters. Resources matter. Some peoples have long histories of civilization, others don’t. Korea has a decently long history. 

Diamond was one of many authors who broke me out of the habit of only looking at explicit things done by explicitly recognized governments, and at wider patterns of culture, history, and environment. It was while reading Peter Frost’s blog that I first encountered the phrase “gene-culture co-evolution,” which supplies the missing link. 

800px-National_IQ_per_country_-_estimates_by_Lynn_and_Vanhanen_2006
IQ by country

South Korea does well because 1. It’s not communist and 2. South Koreans are some of the smartest people in the world. 

I knew #1, but I could have saved myself a lot of time in the stacks if someone had just told me #2 instead of acting like SK’s economic success was a big mystery. 

The fact that every country was relatively poor before industrialization, and South Korea was particularly poor after a couple decades of warfare back and forth across the peninsula, obscures the nation’s historically high development. 

For example, the South Korean Examination system, Gwageo, was instituted in 788 (though it apparently didn’t become important until 958). Korea has had agriculture and literacy for a long time, with accompanying political and social organization. This probably has more to do with South Korea having a relatively easy time adopting the modern industrial economy than anything in particular in the governments’ plans. 

Cochran has an interesting post on his blog on Jared Diamond and Domestication: 

In fact, in my mind the real question is not why various peoples didn’t domesticate animals that we know were domesticable, but rather how anyone ever managed to domesticate the aurochs. At least twice. Imagine a longhorn on roids: they were big and aggressive, favorites in the Roman arena. … 

The idea is that at least some individual aurochs were not as hostile and fearful of humans as they ought to have been, because they were being manipulated by some parasite. … This would have made domestication a hell of a lot easier. …

The beef tape worm may not have made it through Beringia.  More generally, there were probably no parasites in the Americas that had some large mammal as intermediate host and Amerindians as the traditional definite host. 

They never mentioned parasites in gov class. 

Back to the book–I thought this was pretty interesting:

One sign of this reduced disease pressure is the unusual distribution of HLA alleles among Amerindians. the HLA system … is a group of genes that encode proteins expressed on the outer surfaces of cells. the immune system uses them to distinguish the self from non-self… their most important role is in infections disease. … 

HLA genes are among the most variable of all genes. … Because these genes are so variable, any two humans (other than identical twins) are almost certain to have a different set of them. … Natural selection therefore favors diversification of the HLA genes, and some alleles, though rare, have been persevered for a long time. In fact, some are 30 million years old, considerably older than Homo sapiens. …

But Amerindians didn’t have that diversity. Many tribes have a single HLA allele with a frequency of over 50 percent. … A careful analysis of global HLA diversity confirms continuing diversifying selection on HLA in most human populations but finds no evidence of any selection at all favoring diversity in HLA among Amerindians.

The results, of course, went very badly for the Indians–and allowed minuscule groups of Spaniards to conquer entire empires. 

The threat of European (and Asian and African) diseases wiping out native peoples continues, especially for “uncontacted” tribes. As the authors note, the Surui of Brazil numbered 800 when contacted in 1980, but only 200 in 1986, after tuberculosis had killed most of them. 

…in 1827, smallpox spared only 125 out of 1,600 Mandan Indians in what later became North Dakota.

The past is horrific. 

I find the history ancient exploration rather fascinating. Here is the frieze in Persepolis with the okapi and three Pygmies, from about 500 BC.

The authors quote Joao de Barros, a 16th century Portuguese historian: 

But it seems that for our sins, or for some inscrutable judgment of God, in all the entrances of this great Ethiopia we navigate along… He has placed a striking angel with a flaming sword of deadly fevers, who prevents us from penetrating into the interior to the springs of this garden, whence proceed these rivers of gold that flow to the sea in so many parts of our conquest.

Barros had a way with words. 

It wasn’t until quinine became widely available that Europeans had any meaningful success at conquering Africa–and even still, despite massive technological advantages, Europeans haven’t held the continent, nor have they made any significant, long-term demographic impact. 

EX-lactoseintolerance
Source: National Geographic

The book then segues into a discussion of the Indo-European expansion, which the authors suggest might have been due to the evolution of a lactase persistence gene. 

(Even though we usually refer to people as “lactose intolerance” and don’t regularly refer to people as “lactose tolerant,” it’s really tolerance that’s the oddity–most of the world’s population can’t digest lactose after childhood.

Lactase is the enzyme that breaks down lactose.)

Since the book was published, the Indo-European expansion has been traced genetically to the Yamnaya (not to be confused with the Yanomamo) people, located originally in the steppes north of the Caucasus mountains. (The Yamnaya and Kurgan cultures were, I believe, the same.) 

An interesting linguistic note: 

Uralic languages (the language family containing Finnish and Hungarian) appear to have had extensive contact with early Indo-European, and they may share a common ancestry. 

I hope these linguistic mysteries continue to be decoded. 

The authors claim that the Indo-Europeans didn’t make a huge genetic impact on Europe, practicing primarily elite dominance–but on the other hand, A Handful of Bronze-Age Men Could Have Fathered 2/3s of Europeans:

In a new study, we have added a piece to the puzzle: the Y chromosomes of the majority of European men can be traced back to just three individuals living between 3,500 and 7,300 years ago. How their lineages came to dominate Europe makes for interesting speculation. One possibility could be that their DNA rode across Europe on a wave of new culture brought by nomadic people from the Steppe known as the Yamnaya.

That’s all for now; see you next week.

A theory of male and female Sociopathy, pt 2

Note: this is just a theory, developed in reaction to recent conversations. 

As we were discussing Friday, one form of female sociopathy (at least relevant to this conversation) likely involves manipulating or coercing others into providing resources for her children.

There are a couple of obvious tropes:

  1. The evil stepmother, who shunts resources away from a man’s first child, toward his later children. 
  2. The cuckoldress, who tricks or convinces a man to care for another man’s children (this is not always seen as evil, since the male drive to provide for children is triggered at least partly by their proximity, since men cannot give birth, and thus men feel genuine affection for children who happen to be around them,)
  3. The crazy ex, who sues a man for all he is worth, doing her best to prevent him from being able to provide for any future children. 

How crazy are women? 

NSDUH_AMI-_2012_GRAPH_148270_2

22%–slightly more than 1 in 5–women have been diagnosed with a mental illness, at least according to all of the data I’ve seen. Since mental illness peaks during the childbearing ages and falls off quickly after menopause, we can also assume that this rate is closer to 1 in 4 during these years. 

(The dramatic problems our Native American communities are facing is a separate matter, deserving of its own post.)

The odd thing about this data is that mental illness rates are higher for women than men, despite the fact that mental retardation and mental disability rates are higher for men than women. Men are more likely than women to have serious conditions like non-verbal autism and schizophrenia, more likely to be homeless or commit suicide. When things go terribly wrong, the sufferers are disproportionately male (an unfortunate side effect of the Y chromosome causing greater male variability than female variability on a variety of traits.) 

So why on earth do more women than men suffer from mental illness? 

Perhaps some forms of mental illness confer some unexpected benefits on women. 

Many (perhaps most) “mental illnesses” correlate with a single personality trait–neuroticism

“Previously we thought that mental illnesses such as depression, schizophrenia, bipolar disorder, and substance abuse, were completely separate diseases,” Ystrøm says.

But research has now shown that these illnesses are often linked. If you suffer from one mental illness, you are more likely to develop another. And if someone in your immediate family has a psychiatric illness, your risk increases not only for this disorder, but for all other disorders.

These findings have led researchers to suspect that there could be a common underlying factor that increases an idividual’s risk of mental illness, overall. … 

Ystrøm and colleagues have used new statistical methods to look for patterns in personality, mental disorders, genes, and environmental factors, among the twins in the Twin Register. 

And the answer to the question the researchers asked is: yes, neuroticism seems to be the personality trait that best describes the risk of all mental disorders. …

“This one trait doesn’t explain everything. Anyone can develop a mental illness…”

And in women, neuroticism correlates with… more surviving offspring (in at least one study)

Taking an evolutionary approach, we use data from a contemporary polygynous high-fertility human population living in rural Senegal to investigate whether personality dimensions are associated with key life-history traits in humans, i.e., quantity and quality of offspring. We show that personality dimensions predict reproductive success differently in men and women in such societies and, in women, are associated with a trade-off between offspring quantity and quality. In women, neuroticism positively predicts the number of children, both between and within polygynous families. Furthermore, within the low social class, offspring quality (i.e., child nutritional status) decreases with a woman’s neuroticism, indicating a reproductive trade-off between offspring quantity and quality. 

What is neuroticism, in the Big 5 Personality Traits* sense? 

*Note: I am not endorsing or denying all five traits one way or another.

It’s worrying. Mothers who worry more about their offspring have more offspring–though it’s quite easy to imagine that the causality points in the opposite direction as the study’s authors conclude–poor women with lots of skinny babies have more reason to worry about their children than women with a few fat babies. 

When are women most likely to experience mental illness?

Immediately after the birth of a child. It’s called post-partum depression, and it can be very bad–one woman in my moms’ group ended up in the mental hospital after developing post-partum psychosis. Andrea Yates famously drowned her five children during a bout of post-partum depression/psychosis.

Why on earth would women develop a debilitating mental illness at the most vulnerable time in their offspring’s life? Wouldn’t natural selection select rather quickly against anything that makes women worse at taking care of their offspring? 

Let’s turn to everyone’s favorite genetic disease, sickle cell anemia. SCA is famous for being a relatively simple genetic mutation of the sort where if you have one copy of the sickle cell gene, you are less likely to get malaria, and if you have two copies, you tend to die. In areas where malaria is common, the cost of having a quarter of your children die from SCA is lower than the cost of loosing them to malaria. 

Personality traits, including neuroticism, generally exist on a continuum. People may become more neurotic when life warrants it, and less neurotic when they don’t need to worry. A mother with a new baby is in a very vulnerable state–she has just lost a good deal of blood, may not be able to walk, and has an infant to care for every other hour, day and night. It is not a normal state by any measure. It is a time when being extra attentive and extra aware of threats and predators is in a woman’s interest.

It is also a time when women are most in need of help from their mates, relatives, or other friends. Increased neuroticism may also prompt others to attend more closely to the new mother, helping her out. . Increased neuroticism may be so helpful during this time period that a few women getting way too much neuroticism and becoming extremely depressed or even killing their children is a cost outweighed by the increased survival of babies whose mothers had moderate levels of neuroticism. 

Let us note that nature doesn’t care about your feelings. Male praying mantises who allow themselves be eaten by their mates have more offspring than the ones who don’t, but that doesn’t mean male praying mantises enjoy getting eaten. Children who die of sickle

cell anemia don’t much appreciate that their siblings were protected from malaria, either.

An increase in neuroticism immediately after the birth of a baby may prompt a mother to take better care of it, but that doesn’t mean she enjoys the neuroticism. Neither does it mean that post-partum depression is healthy, any more than sickle cell anemia is healthy just because it’s a side effect of a trait that helps people avoid malaria. 

But wait, I have more studies!

Reproductive Fitness and Genetic Risk of Psychiatric Disorders in the General Population

The persistence of common, heritable psychiatric disorders that reduce reproductive fitness is an evolutionary paradox. Here, we investigate the selection pressures on sequence variants that predispose to schizophrenia, autism, bipolar disorder, major depression and attention deficit hyperactivity disorder (ADHD) using genomic data from 150,656 Icelanders, excluding those diagnosed with these psychiatric diseases. … Higher polygenic risk of autism is associated with fewer children and older age at first child whereas higher polygenic risk of ADHD is associated with having more children. We find no evidence for a selective advantage of a high polygenic risk of schizophrenia or bipolar disorder. Rare copy-number variants conferring moderate to high risk of psychiatric illness are associated with having fewer children and are under stronger negative selection pressure than common sequence variants. …

In summary, our results show that common sequence variants conferring risk of autism and ADHD are currently under weak selection in the general population of Iceland. However, rare CNVs that also impact cognition are under stronger selection pressure, consistent with mutation-selection balance. The hypothesis that a selective advantage accounts for the prevalence of sequence variants conferring risk of schizophrenia and bipolar disorder is unproven, but rather this empirical evidence suggests that common sequence variants largely escape selection as their individual effect sizes are weak.

Unfortunately, this study mostly looks at the data in aggregate, instead of breaking it down by males and females. (And I don’t know why they would bother excluding people who actually have the conditions they are trying to study, but perhaps it doesn’t make much difference.) 

Thankfully, they did break down the data by male/female in the tables–Table 1 and Table 2. These tables are confusing, but the takeaway is that mental illness has a bigger effect on male fertility than female fertility. 

Also: Fecundity of Patients with Schizophrenia, Autism, Bipolar Disorder, Depression, Anorexia Nervosa, or Substance Abuse vs. their Unffected Siblings

Results Except for women with depression, affected patients had significantly fewer children (FR range for those with psychiatric disorder, 0.23-0.93; P < 10−10). This reduction was consistently greater among men than women, suggesting that male fitness was particularly sensitive. Although sisters of patients with schizophrenia and bipolar disorder had increased fecundity (FR range, 1.02-1.03; P < .01), this was too small on its own to counterbalance the reduced fitness of affected patients. Brothers of patients with schizophrenia and autism showed reduced fecundity (FR range, 0.94-0.97; P < .001). Siblings of patients with depression and substance abuse had significantly increased fecundity (FR range, 1.01-1.05; P < 10−10). In the case of depression, this more than compensated for the lower fecundity of affected individuals.

Conclusions Our results suggest that strong selection exists against schizophrenia, autism, and anorexia nervosa and that these variants may be maintained by new mutations or an as-yet unknown mechanism. Bipolar disorder did not seem to be under strong negative selection. Vulnerability to depression, and perhaps substance abuse, may be preserved by balancing selection, suggesting the involvement of common genetic variants in ways that depend on other genes and on environment.

Now, this study gets interesting in its graphs: 

m_yoa120017f1
From Fecundity of Patients with Schizophrenia, Autism, Bipolar Disorder, Depression, Anorexia Nervosa, or Substance Abuse vs their Unaffected Siblings

In every case, mental illness has a bigger effect on male fertility than female–and in the case of depression, it has no effect on female fertility. 

But wait: 

m_yoa120017f2
Same source.

This graph is confusingly labeled, but it is breaking down the correlation on the brothers and sisters of people with mental disorders. So the first dot represents the brothers of people with schizophrenia; the second dot represents the sisters of people with schizophrenia. 

None of these effects are huge, and some of them changed when “comorbidities were included in the analysis,” though it’s not clear exactly what that means–the word comorbidity in this context refers to people with more than one diagnosis. 

For the objectives of this study, we first analyzed each disorder separately without accounting for comorbidities. A secondary analysis was then performed that corrected for comorbidities by analyzing all disorders simultaneously.

So when you analyze all of the disorders together, sisters of schizophrenics had no increased fertility, and neither did the siblings of people with bipolar. Depressed men had average fertility, while depressed women actually had slightly above average fertility. The results for anorexia, substance abuse, and autism didn’t change. 

And from Spain: Seven Dimensions of Personality Pathology are Under Sexual Selection in Modern Spain

Personality variation is increasingly thought to have an adaptive function. This is less clear for personality disorders (PDs)—extreme variants of personality that cause harm in most aspects of life. However, the possibility that PDs may be maintained in the population because of their advantages for fitness has been not convincingly tested. In a sample of 959 outpatients, we examined whether, and how, sexual selection acts on the seven main dimensions of personality pathology, taking into account mating success, reproductive success, and the mediating role of status. We find that, to varying extents, all personality dimensions are under sexual selection. Far from being predominantly purifying, selective forces push traits in diverging, often pathological, directions. These pressures differ moderately between the sexes. Sexual selection largely acts in males through the acquisition of wealth, and through the duration (rather than the number) of mates. This gives a reproductive advantage to males high in persistence–compulsivity. Conversely, because of the decoupling between the number of mates and offspring, the promiscuous strategy of psychopaths is not so successful. Negative emotionality, the most clinically detrimental trait, is slightly deleterious in males but is positively selected in females, which can help to preserve variation. 

It’s interesting that the invention of birth control may have inadvertently selected against promiscuous psychopaths–rather similar to the theory that abortion is responsible for the decrease in crime since the early 90s. 

“Negative emotionality” is likely equivalent to “neuroticism.”

There are two obvious reasons why mental illness might have more of an effect on males than females–one is that mental illness might simply be mores severe for males than females, on average. The second is that mental illness interferes more with holding down a job than with being a housewife, so women with mental illnesses have more options than men. 

Less obvious, though, is that some of these traits might actually be beneficial–in small quantities–for women.

That’s enough for now; let’s continue this discussion on Friday. (Wednesday is book club.) 

Book Club: The 10,000 Year Explosion: pt 5: Gene Flow

Genghis Khan, spreader of genes

Welcome back to the book club. Today we’re discussing Chapter 5 of The 10,000 Year Explosion, Gene Flow. In this chapter, Greg and Henry discuss some of the many ways genes can (and sometimes can’t) get around.

You know, sometimes it is difficult to think of something really interesting to say in reaction to something I’ve read. Sometimes I just think it is very interesting, and hope others find it so, too. This is one of those chapters.

So today I decided to read the papers cited in the chapter, plus a few more related papers on the subject.

High-Resolution SNPs and Microsatellite Haplotypes point to a single, Recent Entry of Native American Y Chromosomes into the Americas

Single-nucleotide polymorphism (SNP) analysis indicated that three major haplogroups, denoted as C, Q, and R, accounted for nearly 96% of Native American Y chromosomes. Haplogroups C and Q were deemed to represent early Native American founding Y chromosome lineages; however, most haplogroup R lineages present in Native Americans most likely came from recent admixture with Europeans. Although different phylogeographic and STR diversity patterns for the two major founding haplogroups previously led to the inference that they were carried from Asia to the Americas separately, the hypothesis of a single migration of a polymorphic founding population better fits our expanded database. Phylogenetic analyses of STR variation within haplogroups C and Q traced both lineages to a probable ancestral homeland in the vicinity of the Altai Mountains in Southwest Siberia. Divergence dates between the Altai plus North Asians versus the Native American population system ranged from 10,100 to 17,200 years for all lineages, precluding a very early entry into the Americas.

However, Asymmetric Male and Female Genetic Histories among Native Americans from Eastern North America

We found that sociocultural factors have played a more important role than language or geography in shaping the patterns of Y chromosome variation in eastern North America. Comparisons with previous mtDNA studies of the same samples demonstrate that male and female demographic histories differ substantially in this region. Postmarital residence patterns have strongly influenced genetic structure, with patrilocal and matrilocal populations showing different patterns of male and female gene flow. European contact also had a significant but sex-specific impact due to a high level of male-mediated European admixture. Finally, this study addresses long-standing questions about the history of Iroquoian populations by suggesting that the ancestral Iroquoian population lived in southeastern North America.

And in Mexico, your different racial mix has something to do with your risk of Type 2 Diabetes, but you know, race is a social construct or something:

Type 2 diabetes (T2D) is at least twice as prevalent in Native American populations as in populations of European ancestry, so admixture mapping is well suited to study the genetic basis of this complex disease. We have characterized the admixture proportions in a sample of 286 unrelated T2D patients and 275 controls from Mexico City and we discuss the implications of the results for admixture mapping studies. … The average proportions of Native American, European and, West African admixture were estimated as 65, 30, and 5%, respectively. The contributions of Native American ancestors to maternal and paternal lineages were estimated as 90 and 40%, respectively. In a logistic model with higher educational status as dependent variable, the odds ratio for higher educational status associated with an increase from 0 to 1 in European admixture proportions was 9.4 (95%, credible interval 3.8-22.6). This association of socioeconomic status with individual admixture proportion shows that genetic stratification in this population is paralleled, and possibly maintained, by socioeconomic stratification. The effective number of generations back to unadmixed ancestors was 6.7 (95% CI 5.7-8.0)…

In other words, Conquistador men had children with a lot of the local ladies. 

Oh hey, while we’re at it: 

The Genomic Landscape of Western South America: 

Studies of Native South American genetic diversity have helped to shed light on the peopling and differentiation of the continent, but available data are sparse for the major ecogeographic domains. These include the Pacific Coast, a potential early migration route; the Andes, home to the most expansive complex societies and to one of the most spoken indigenous language families of the continent (Quechua); and Amazonia, with its understudied population structure and rich cultural diversity. Here we explore the genetic structure of 177 individuals from these three domains, genotyped with the Affymetrix Human Origins array. We infer multiple sources of ancestry within the Native American ancestry component; one with clear predominance on the Coast and in the Andes, and at least two distinct substrates in neighboring Amazonia, with a previously undetected ancestry characteristic of northern Ecuador and Colombia. Amazonian populations are also involved in recent gene-flow with each other and across ecogeographic domains, which does not accord with the traditional view of small, isolated groups. Long distance genetic connections between speakers of the same language family suggest that languages had spread not by cultural contact alone. Finally, Native American populations admixed with post-Columbian European and African sources at different times, with few cases of prolonged isolation. 

In other news: 

Strong Selective Sweep Before 45,000 BP Displaced Archaic Admixture Across the X Chromosome

The X chromosome in non-African populations has less diversity and less Neanderthal introgression than expected. We analyzed X chromosome diversity across the globe and discovered seventeen chromosomal regions, where haplotypes of several hundred kilobases have recently reached high frequencies in non-African populations only. The selective sweeps must have occurred more than 45,000 years ago because the ancient Ust’-Ishim male also carries its expected proportion of these haplotypes. Surprisingly, the swept haplotypes are entirely devoid of Neanderthal introgression, which implies that a population without Neanderthal admixture contributed the swept haplotypes. It also implies that the sweeps must have happened after the main interbreeding event with Neanderthals about 55,000 BP. These swept haplotypes may thus be the only genetic remnants of an earlier out-of-Africa event.

Why not a later out-of-Africa event? Or a simultaneous event that just happened not to mate with Neanderthals? Or sweeps on the X chromosome that happened to remove Neanderthal DNA due to Neanderthal and X being really incompatible? I don’t know. 

The Neolithic Invasion of Europe:

Who are Europeans? Both prehistoric archaeology and, subsequently, classical population genetics have attempted to trace the ancestry of modern Europeans back to the first appearance of agriculture in the continent; however, the question has remained controversial. Classical population geneticists attributed the major pattern in the European gene pool to the demographic impact of Neolithic farmers dispersing from the Near East, but archaeological research has failed to uncover substantial evidence for the population growth that is supposed to have driven this process. … Both mitochondrial DNA and Y-chromosome analyses have indicated a contribution of Neolithic Near Eastern lineages to the gene pool of modern Europeans of around a quarter or less. This suggests that dispersals bringing the Neolithic to Europe may have been demographically minor and that contact and assimilation had an important role.

I wouldn’t call a quarter “minor.” But it is true that the Anatolian farming people who invaded Europe didn’t kill off all of the locals, and then later Europe was invaded by the non-Anatolian, Indo-European people. 

Revealing the prehistoric settling of Australia by Y chromosome and mtDNA analysis

(i) All Australian lineages are confirmed to fall within the mitochondrial founder branches M and N and the Y chromosomal founders C and F, which are associated with the exodus of modern humans from Africa ≈50–70,000 years ago. The analysis reveals no evidence for any archaic maternal or paternal lineages in Australians, despite some suggestively robust features in the Australian fossil record, thus weakening the argument for continuity with any earlier Homo erectus populations in Southeast Asia. (ii) The tree of complete mtDNA sequences shows that Aboriginal Australians are most closely related to the autochthonous populations of New Guinea/Melanesia, indicating that prehistoric Australia and New Guinea were occupied initially by one and the same Palaeolithic colonization event ≈50,000 years ago, … (iii) The deep mtDNA and Y chromosomal branching patterns between Australia and most other populations around the Indian Ocean point to a considerable isolation after the initial arrival. (iv) We detect only minor secondary gene flow into Australia, and this could have taken place before the land bridge between Australia and New Guinea was submerged ≈8,000 years ago…

Aboriginal Australian mitochondrial genome variation

Aboriginal Australians represent one of the oldest continuous cultures outside Africa, with evidence indicating that their ancestors arrived in the ancient landmass of Sahul (present-day New Guinea and Australia) ~55 thousand years ago. … We have further resolved known Aboriginal Australian mitochondrial haplogroups and discovered novel indigenous lineages by sequencing the mitogenomes of 127 contemporary Aboriginal Australians. In particular, the more common haplogroups observed in our dataset included M42a, M42c, S, P5 and P12, followed by rarer haplogroups M15, M16, N13, O, P3, P6 and P8. We propose some major phylogenetic rearrangements, such as in haplogroup P where we delinked P4a and P4b and redefined them as P4 (New Guinean) and P11 (Australian), respectively. Haplogroup P2b was identified as a novel clade potentially restricted to Torres Strait Islanders. Nearly all Aboriginal Australian mitochondrial haplogroups detected appear to be ancient, with no evidence of later introgression during the Holocene.

Meanwhile, in Indonesia

We find that recent population history within Indonesia is complex, and that populations from the Philippines made important genetic contributions in the early phases of the Austronesian expansion. Different, but interrelated processes, acted in the east and west. The Austronesian migration took several centuries to spread across the eastern part of the archipelago, where genetic admixture postdates the archeological signal. As with the Neolithic expansion further east in Oceania and in Europe, genetic mixing with local inhabitants in eastern Indonesia lagged behind the arrival of farming populations. In contrast, western Indonesia has a more complicated admixture history shaped by interactions with mainland Asian and Austronesian newcomers, which for some populations occurred more than once. Another layer of complexity in the west was introduced by genetic contact with South Asia and strong demographic events in isolated local groups.

I liked the quote from Jared Diamond (say what you will about him, I like Diamond. He at least tries hard to tackle difficult questions):  

“When I was living among Elopi tribespeople in west New Guinea and wanted to cross the territory of the neighboring Fayu tribe in order to reach a nearby mountain, the Elopis explained tome matter-of-factly that the Fayus would kill me if I tried. From a New Guinea perspective, it seemed so perfectly natural and self-explanatory. Of course the Fayus will kill any trespasser…”

This is why people often claim that we moderns are the WEIRDOs. 

Evidence that Alexander the Great got around (the world)–Y-Chromosomal Evidence for a Limited Greek Contribution to the Pathan population of Pakistan

Three Pakistani populations residing in northern Pakistan, the Burusho, Kalash and Pathan claim descent from Greek soldiers associated with Alexander’s invasion of southwest Asia. … In pairwise comparisons between the Greeks and the three Pakistani populations using genetic distance measures sensitive to recent events, the lowest distances were observed between the Greeks and the Pathans. Clade E3b1 lineages, which were frequent in the Greeks but not in Pakistan, were nevertheless observed in two Pathan individuals, one of whom shared a 16 Y-STR haplotype with the Greeks. The worldwide distribution of a shortened (9 Y-STR) version of this haplotype, determined from database information, was concentrated in Macedonia and Greece, suggesting an origin there. Although based on only a few unrelated descendants this provides strong evidence for a European origin for a small proportion of the Pathan Y chromosomes.

Of course, who can discuss genetic spread without mentioning that lord of men, Genghis Khan? 

We have identified a Y-chromosomal lineage with several unusual features. It was found in 16 populations throughout a large region of Asia, stretching from the Pacific to the Caspian Sea, and was present at high frequency: ∼8% of the men in this region carry it, and it thus makes up ∼0.5% of the world total. The pattern of variation within the lineage suggested that it originated in Mongolia ∼1,000 years ago. Such a rapid spread cannot have occurred by chance; it must have been a result of selection. The lineage is carried by likely male-line descendants of Genghis Khan, and we therefore propose that it has spread by a novel form of social selection resulting from their behavior.

“Novel” lol. 

And finally, Blue Eyes

Several studies have shown that the OCA2 locus is the major contributor to the human eye color variation. By linkage analysis of a large Danish family, we finemapped the blue eye color locus to a 166 Kbp region within the HERC2 gene. … The brown eye color allele of rs12913832 is highly conserved throughout a number of species. … 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. Hence, our data suggest a common founder mutation in an OCA2 inhibiting regulatory element as the cause of blue eye color in humans. In addition, an LOD score of Z = 4.21 between hair color and D14S72 was obtained in the large family, indicating that RABGGTA is a candidate gene for hair color.

What about you? What did you think of this chapter?

Two Denisovan Admixture Events?

Recent genetic analysis suggests that humans mated with the mysterious Denisovans not once, but twice

Asian genomes carry introgressed DNA from Denisovans and Neanderthals

East Asians show evidence of introgression from two distinct Denisovan populations

South Asians and Oceanians carry introgression from one Denisovan population

I can’t read the whole paper, because it’s paywalled, but if correct, this is quite the change. Previously, only small amounts of Denisovan were detected in East Asians, while large amounts (2-6%) were detected in Oceanians (ie, Melanesians, Papuans, and Australian Aborigines.) 

According to Wikipedia:

Statistical analysis of genomic DNA sequences from different Asian populations indicates that at least two distinct populations of Denisovans existed,[50][51] and that a second introgression event from Denisovans into humans occurred. A study of Han ChineseJapanese and Dai genomes revealed that modern East Asian populations include two Denisovan DNA components: one similar to the Denisovan DNA found in Papuan genomes, and a second that is closer to the Denisovan genome from the Altai cave. These components were interpreted as representing separate introgression events involving two divergent Denisovan populations. South Asians were found to have levels of Denisovan admixture similar to that seen in East Asians, but this DNA only came from the same single Denisovan introgression seen in Papuans.[52]  …

The Denisovans, in case you’re new here, are a human species similar to the Neanderthals who lived… well, we’re not sure exactly where they lived, other than the Altai Cave, Siberia. We also don’t know what they looked like, because we have only found a few of their bones–a finger bone and some teeth–but they might have looked a bit like the Red Deer Cave People. Remarkably, though, these were in good enough condition (Siberia preserves things very well,) to allow scientists to extract sufficient DNA to determine that they are indeed a human species, but one that split from the ancestors of Homo sapiens about 600,000-750,000 years ago, and from the Neanderthals about 200,000 years later. 

Just as Homo sapiens mated with Neanderthals, so Denisovans mated with Neanderthals and Homo sapiens–the human family tree is growing increasingly complex. 

We don’t know exactly where these interbreeding events happened, since we know so little about the Denisovans (at least one of the Neanderthal interbreeding events probably happened in the Middle East, given that all non-Africans [and some Africans] have Neanderthal DNA,) but a clue lies in the DNA of the Negrito peoples. 

The Negritoes are a variety of peoples who live in south east Asia and, like the Pygmies of Africa, are rather short. Some of them, like the Aeta of the Philippines, have almost Papuan levels of Denisovan admixture, while others, like the Onge of India, have almost none. Assuming the Negritos are related to each other and not just isolated examples of island dwarfism, this suggests that the interbreeding event really did take places somewhere east of the major Indonesian islands of Sumatra and Borneo (which probably weren’t islands at the time, but connected to the mainland). The Denisovans may have been clever enough to build boats and cross the Wallace Line, surviving in the more isolated islands of Indonesia and the Philippines. 

On a related note, the article I just linked to from John Hawks, “This is where Scientists Might Find the Next Hobbits,” is truly excellent: 

In May, an international team of scientists led by Thomas Ingicco revealed new archaeological findings from Kalinga, in the northernmost part of Luzon, Philippines. Until now, scientists have mostly assumed that the Philippines were first inhabited by modern humans, only after 100,000 years ago. But the artifacts unearthed by Ingicco and coworkers were much older, more than 700,000 years old. …

Luzon was never connected to the Asian mainland, even when sea level was at its lowest during the Ice Ages. To get there, ancient hominins had to float. Who were they, and how did they get there?

Timeline of ancient Indonesian and Filipino hominin findings, from John Hawks’s article

I recommend you read the whole thing.

What’s all of this Denisovan DNA good for, anyway? Quoting Wikipedia again:

The immune system’s HLA alleles have drawn particular attention in the attempt to identify genes that may derive from archaic human populations. Although not present in the sequenced Denisova genome, the distribution pattern and divergence of HLA-B*73 from other HLA alleles has led to the suggestion that it introgressed from Denisovans into humans in west Asia. As of 2011, half of the HLA alleles of modern Eurasians represent archaic HLA haplotypes, and have been inferred to be of Denisovan or Neanderthal origin.[54] The apparent over-representation of these alleles suggests a positive selective pressure for their retention in the human population. A higher-quality Denisovan genome published in 2012 reveals variants of genes in humans that are associated with dark skin, brown hair, and brown eyes – consistent with features found with Melanesians today.[16] A study involving 40 Han Chinese and 40 people of ethnic Tibetan background identified a region of DNA around the EPAS1 gene that assists with adaptation to low oxygen levels at high altitude found in Tibetans is also found in the Denisovan genome.[55][56] In Papuans, introgressed Neanderthal alleles have highest frequency in genes expressed in the brain, whereas Denisovan alleles have highest frequency in genes expressed in bones and other tissues.[57]

It is a great era in genetics. 

Book Club: The 10,000 Year Explosion: pt 4 Agriculture

Welcome back to EvX’s Book Club. Today we’re discussing Chapter 4 of The 10,000 Year Explosion: Consequences of Agriculture.

A big one, of course, was plague–on a related note, Evidence for the Plague in Neolithic Farmers’ Teeth:

When they compared the DNA of the strain recovered from this cemetery to all published Y. pestis genomes, they found that it was the oldest (most basal) strain of the bacterium ever recovered. Using the molecular clock, they were able to estimate a timeline for the divergence and radiation of Y. pestis strains and tie these events together to make a new, testable model for the emergence and spread of this deadly human pathogen.

These analyses indicate that plague was not first spread across Europe by the massive migrations by the Yamnaya peoples from the central Eurasian steppe (around 4800 years ago)… Rascovan et al. calculated the date of the divergence of Y. pestis strains at between 6,000 and 5,000 years ago. This date implicates the mega-settlements of the Trypillia Culture as a possible origin point of Y. pestis. These mega-settlements, home to an estimated 10,000-20,000 people, were dense concentrations of people during that time period in Europe, with conditions ideal for the development of a pandemic.

The Cucuteni-Trypilia Culture flourished between the Carpathian Mountains and the Black Sea from 4800-3000 BC. It was a neolithic–that is, stone age–farming society with many large cities. Wikipedia gives a confused account of its demise:

According to some proponents of the Kurgan hypothesis of the origin of Proto-Indo-Europeans … the Cucuteni–Trypillia culture was destroyed by force. Arguing from archaeological and linguistic evidence, Gimbutas concluded that the people of the Kurgan culture (a term grouping the Yamnaya culture and its predecessors) … effectively destroyed the Cucuteni–Trypillia culture in a series of invasions undertaken during their expansion to the west. Based on this archaeological evidence Gimbutas saw distinct cultural differences between the patriarchal, warlike Kurgan culture and the more peaceful egalitarian Cucuteni–Trypillia culture, … which finally met extinction in a process visible in the progressing appearance of fortified settlements, hillforts and the graves of warrior-chieftains, as well as in the religious transformation from the matriarchy to patriarchy, in a correlated east–west movement.[26] In this, “the process of Indo-Europeanization was a cultural, not a physical, transformation and must be understood as a military victory in terms of successfully imposing a new administrative system, language, and religion upon the indigenous groups.[27]

How does it follow that the process was a cultural, not physical transformation? They got conquered.

In his 1989 book In Search of the Indo-Europeans, Irish-American archaeologist J. P. Mallory, summarising the three existing theories concerning the end of the Cucuteni–Trypillia culture, mentions that archaeological findings in the region indicate Kurgan (i.e. Yamnaya culture) settlements in the eastern part of the Cucuteni–Trypillia area, co-existing for some time with those of the Cucuteni–Trypillia.[4]Artifacts from both cultures found within each of their respective archaeological settlement sites attest to an open trade in goods for a period,[4] though he points out that the archaeological evidence clearly points to what he termed “a dark age,” its population seeking refuge in every direction except east. He cites evidence of the refugees having used caves, islands and hilltops (abandoning in the process 600–700 settlements) to argue for the possibility of a gradual transformation rather than an armed onslaught bringing about cultural extinction.[4]

How is “refugees hiding in caves” a “gradual transformation?” That sounds more like “people fleeing an invading army.”

The obvious issue with that theory is the limited common historical life-time between the Cucuteni–Trypillia (4800–3000 BC) and the Yamnaya culture (3300–2600 BC); given that the earliest archaeological findings of the Yamnaya culture are located in the VolgaDonbasin, not in the Dniester and Dnieper area where the cultures came in touch, while the Yamnaya culture came to its full extension in the Pontic steppe at the earliest around 3000 BC, the time the Cucuteni–Trypillia culture ended, thus indicating an extremely short survival after coming in contact with the Yamnaya culture.

How is that an issue? How long does Wikipedia think it takes to slaughter a city? It takes a few days. 300 years of contact is plenty for both trade and conquering.

Another contradicting indication is that the kurgans that replaced the traditional horizontal graves in the area now contain human remains of a fairly diversified skeletal type approximately ten centimetres taller on average than the previous population.[4]

What are we even contradicting? Sounds like they got conquered, slaughtered, and replaced.

Then Wikipedia suggests that maybe it was all just caused by the weather (which isn’t a terrible idea.) Drought weakened the agriculturalists and prompted the pastoralists to look for new grasslands for their herds. They invaded the agriculturalists’ areas because they were lush and good for growing grain, which the pastoralists’ cattle love eating. The already weakened agriculturalists couldn’t fight back.

ANYWAY. Lets get on with Greg and Henry’s account, The 10,000 Year Explosion:

The population expansion associated with farming increased crowding, while farming itself made people sedentary. Mountains of garbage and water supplies contaminated with human waste favored the spread of infectious disease. …

Most infectious diseases have a critical community size, a  number and concentration of people below which they cannot persist. The classic example is measles, which typically infects children and remains infectious for about ten days, after which the patient has lifelong immunity. In order for measles to survive, the virus that causes it, the paramyxovirus, must continually find unexposed victims–more children. Measles can only persist in a large, dense population: Populations that are too small or too spread out (under half a million in close proximity) fail to produce unexposed children fast enough, so the virus dies out.

Measles, bubonic plague, smallpox: all results of agriculture.

Chickenpox: not so much.

I wonder if people in the old Cucuteni–Trypillia area are particularly immune to bubonic plague, or if the successive waves of invading steppe nomads have done too much genetic replacement (slaughtering) for adaptations to stick around?

Harpending and Cochran then discuss malaria, which has had a big impact on human genomes (eg, sickle cell,) in the areas where malaria is common.

In general, the authors play it safe in the book–pointing to obvious cases of wide-scale genetic changes like sickle cell that are both undoubtable and have no obvious effect on personality or intelligence. It’s only in the chapter on Ashkenazi IQ that they touch on more controversial subjects, and then in a positive manner–it’s pleasant to think, “Why was Einstein so smart?” and less pleasant to think, “Why am I so dumb?”

However:

It’s time to address the old chestnut that biological differences among human populations are “superficial,” only skin-deep. It’s not true: We’re seeing genetically caused differences in all kinds of functions, and every such differences was important enough to cause a significant increase in fitness (number of offspring)–otherwise it wouldn’t have reached high frequency in just a few millennia.

As for skin color, Cochran and Harpending lean on the side of high-latitude lightening having been caused by agriculture, rather than mere sunlight levels:

Interestingly, the sets of changes driving light skin color in China are almost entirely different from those performing a similar function in Europe. …

Many of these changes seem to be quite recent. The mutation that appears to have the greatest effect on skin color among Europeans and neighboring peoples, a variant of SLC24A5, has spread with astonishing speed. Linkage disequilibrium… suggests that it came into existence about 5,800 years ago, but it has a frequency of 99 percent throughout Europe and is found at significant levels in North Africa, East Africa, and as far east as India and Ceylon. If it is indeed that recent, it must have had a huge selective advantage, perhaps as high as 20 percent. It would have spread so rapidly that, over a long lifetime a farmer could have noticed the change in appearance in his village.

Wow.

In humans, OAC2 … is a gene involved in the melanin pathway… Species of fish trapped in caves… lose their eyesight and become albinos over many generations. … Since we see changes in OCA2 in each [fish] case, however, there must have been some advantage in knocking out OCA2, at least in that underground environment. The advantage cannot like in increased UV absorption, since there’s no sunlight in those caves.

There are hints that knocking out OCA2, or at least reducing its activity, may he advantageous… in humans who can get away with it. We see a pattern that suggests that having one inactive copy of OCA2 is somehow favored even in some quite sunny regions. In southern Africa, a knocked-out version of OCA2 is fairly common: The gene frequency is over 1 percent.

And that’s an area with strong selection for dark skin.

A form of OCA2 albinism is common among the Navajo and other neighboring tribes, with gene frequencies as high as 4.5 percent. The same pattern appears in southern Mexico, eastern Panama, and southern Brazil. All of which suggests that heterozygotes…may ave some advantage.

Here is an article on the possibility of sexual selection for albinism among the Hopi.

So why do Europeans have such variety in eye and hair color?

Skeletons

The skeletal record clearly supports the idea that there has been rapid evolutionary change in humans over the past 10,000 years. The human skeleton has become more gracile–more lightly built–though more so in some populations than others. Our jaws have shrunk, our long bones have become lighter, and brow ridges have disappeared in most populations (with the notable exception of Australian Aborigines, who have also changed, but not as much; they still have brow ridges, and their skulls are about twice as thick as those of other peoples.)

This could be related to the high rates of interpersonal violence common in Australia until recently (thicker skulls are harder to break) or a result of interbreeding with Neanderthals and Denisovans. We don’t know what Denisovans looked like, but Neanderthals certainly are noted for their robust skulls.

Skull volume has decreased, apparently in all populations: In Europeans, volume is down about 10 percent from the high point about 20,000 years ago.

This seems like a bad thing. Except for mothers.

Some changes can be seen even over the past 1,000 years. English researchers recently compared skulls from people who died in the Black Death ([approximately] 650 years ago), from the crew of the Mary Rose,a  ship that sank in Tudor times ([approximately] 450 years ago) and from our contemporaries. The shape of the skull changed noticeably over that brief period–which is particularly interesting because we know there has been no massive population replacement in England over the past 700 years.

Hasn’t there been a general replacement of the lower classes by the upper classes? I think there was also a massive out-migration of English to other continents in the past five hundred years.

The height of the cranial vault of our contemporaries was about 15 percent larger than that of the earlier populations, and the part of the skull containing the frontal lobes was thus larger.

This is awkwardly phrased–I think the authors want the present tense–“the cranial vault of our contemporaries is…” Nevertheless, it’s an interesting study. (The frontal lobes control things like planning, language, and math.) 

We then proceed to the rather depressing Malthus section and the similar “elites massively out-breeding commoners due to war or taxation” section. You’re probably familiar with Genghis Khan by now. 

We’ve said that the top dogs usually had higher-than-average fertility, which is true, but there have been important exceptions… The most common mistake must have been living in cities, which have almost always been population sinks, mostly because of infectious disease. 

They’re still population sinks. Just look at Singapore. Or Tokyo. Or London. 

The case of silphium, a natural contraceptive and abortifacient eaten to extinction during the Classical era, bears an interesting parallel to our own society’s falling fertility rates. 

And of course, states domesticate their people: 

Farmers don’t benefit from competition between their domesticated animals or plants… Since the elites were in a very real sense raising peasants, just as peasants raised cows, there must have been a tendency for them to cull individuals who were more aggressive than average, which over time would have changed the frequencies of those alleles that induced such aggressiveness.

On the one hand, this is a very logical argument. On the other hand, it seems like people can turn on or off aggression to a certain degree–uber peaceful Japan was rampaging through China only 75 years ago, after all. 

Have humans been domesticated? 

(Note: the Indians captured by the Puritans during the Pequot War may have refused to endure the yoke, but they did practice agriculture–they raised corn, squash and beans, in typical style. Still, they probably had not endured under organized states for as long as the Puritans.)

There is then a fascinating discussion of the origins of the scientific revolution–an event I am rather fond of. 

Although we do not as yet fully understand the true causes of the scientific and industrial revolution, we must now consider the possibility that continuing human evolution contributed to that process. It could explain some of the odd historical patterns that we see.

Well, that’s enough for today. Let’s continue with Chapter 5 next week.

How about you? What are your thoughts on the book?