The Unz Review - Mobile
A Collection of Interesting, Important, and Controversial Perspectives Largely Excluded from the American Mainstream Media
Email This Page to Someone

 Remember My Information

 TeasersiSteve Blog

Bookmark Toggle AllToCAdd to LibraryRemove from Library • BShow CommentNext New CommentNext New Reply
🔊 Listen RSS
Over at West Hunter, Greg Cochran has been introducing a a fairly new and potentially important theory of the genetic origins of race differences in IQ.  It’s less a theory of evolution than of devolution. The mechanism causing effective differences, he argues, is less selection for higher IQ due to differences in the environment (e.g., winter versus tropics selecting for forethought); instead, a large driver is differential rates in random mutation leading to differences in average level of deleterious genetic load, which tend to correlate with climate warmth.


What would happen if people moved somewhere where the mutation rate was far lower? 

Their genetic load would decrease with time, assuming that they were still subject to much selection. Today, everybody has hundreds of nicked or broken genes:  selection keeps eliminating them, while mutation keeps creating them.  The suspicion is that their effect is quite large.  This hypothetical population would have fewer and fewer.  In a few thousand years, they would lose most of the variants that decrease fitness by 1% or more.

Cochran’s next post looks at some data on the rates at which random mutations creep into the reproduction process.

Too Darn Hot? 

Posted on July 14, 2012 by gcochran9 

Several recent papers  give me the impression that there is regional variation in mutational load.   One can slice this a number of ways. Dan MacArthur and company looked for mutations that knocked out genes – loss-of-function or LOF mutations.  Mutational load is the sum of all deleterious mutations – LOF mutations are a clear-cut subset of total mutational load. 

Some of the LOF mutations they are found are common, and are presumably neutral, maybe even beneficial, but most are rare and likely deleterious.  The kicker is that they found significantly more LOF mutations in their African population sample than in their European and East Asian samples – 25% higher.  That was unexpected. 

Population history (and mutation rate) determine the variation you expect to find in neutral genes, but significantly deleterious mutations should be in mutation-selection balance.  A neutral variant might easily be a million years old, but a deleterious variant will  last, on average, 1/s generations, when s is the decrease in fitness caused by that variant.  A mutation that decreases fitness by 1% should disappear in  100 generations or so, about 2500 years.  Ancient bottlenecks should not influence the frequency of such noticeably deleterious mutations. 

Another related paper, by Jacob Tenessen et al,  looked at a large set of coding genes, sequencing many times (average depth of 111x)  for high accuracy. As in in MacArthur’s paper they found that the average person carries many probably-deleterious mutations, mutations which are individually rare.  Each person carried, on average, mutations expected to change function (almost always for the worse, although usually only a little for the worse)  in 313 genes (out of the 15,585 they studied. 

They looked at African-Americans and Americans of European descent, about a thousand of each.  They saw what MacArthur’s group did: there were significantly more probably-deleterious mutations in the 80%-African population.  When they used a loose definition of functional variation, about 20% more : with a more conservative definition,  which should have a higher fraction of truly deleterious genes, about 29% more. 

…    The only simple explanation (that I can think of)  is a higher mutation rate.

One possibility is that heat tends to cause a higher mutation rate.

Henry Harpending then summed up:

Pre-term Births 

Posted on July 16, 2012 by harpend= 

The model that Greg is dancing around suggests (1) that there is variation in mutation rate dependent on temperature or something correlated with temperature, (2) higher mutation rates cause a higher genetic burden in human populations, (3) leading to IQ reduction and other minor dings

Here’s my model of this theory (which is probably pretty woozy):

Imagine, say, a factory that builds a complex product, such as a car, according to a complicated set of instructions. But, the instructions on how to build the next car are passed on via the Game of Telephone, with mistakes inevitably creeping in. Sometimes, big mistakes are made, and the resulting car is such a disaster that it can’t function at all and has to be scrapped. But, most of the individual mistakes are minor and just mean, say, that instead of delivering 268 horsepower, the engine generates 267. Over time, the Telephone Game build up mistakes until a car is completely unusable and has to be scrapped. At that point the workers go find a better car and get the instructions for that car relayed to them. So, on average, most cars don’t come off the assembly line performing at spec, but they perform well enough to make it through a test drive. 

Now imagine two factories making the same car from roughly the same overall design. One is in Nagoya and the other in Lagos. It’s so hot and humid alla the time in Nigeria, unfortunately, that the workers get distracted during their Game of Telephone and have a higher rate of errors when transmitting plans from one generation to the next. 

In the comments, commenter extraordinaire Jason Malloy writes:

See these posts from February and April for the conceptual background. 

While not fully or explicitly articulated, this is the first New Big Theory of race differences in quite a while, and an interesting alternative to the reigning sociobiological models available since the 1980s. In the latter models intelligence and reproductive differences are seen as consequences of natural selection in divergent latitudes, but this new model replaces natural selection with accumulated mutational burdens. The differences at lower latitudes are not selectively advantageous, but dysfunctional. 

Dr. C
ochran notes that complex adaptive systems, involving the functioning of many genes, should be the most vulnerable to genetic load, so this would obviously be the brain and probably reproductive physiology. So in addition to higher general mortality, dysfunctions associated with mutational burdens might include: 

- Lower intelligence
- Higher retardation
- Higher mental illness 

- Lower birthweight
- Higher premature births
- Higher infertility
- Higher reproductive deformities
- Higher miscarriage (and general obstetric complications)
- Lower sperm quality 

Of course there is a difference between establishing population differences in genetic load, and proving that this is related to population differences in socially valued traits. I’m not sold on this as a replacement for sociobiological models, although there are aspects that make it useful and attractive in different ways. For example, I recently found that ethnic differences in rate of homosexuality are inversely correlated with latitude. Since theories of selectively advantageous homosexuality fall flat, this theory seemed like a better fit.

In the comments to Henry’s post, I offer a couple of tentative criticisms, which you can read there.

🔊 Listen RSS
From the New York Times:

Earliest Americans Arrived in Waves, DNA Study Finds 


North and South America were first populated by three waves of migrants from Siberia rather than just a single migration, say researchers who have studied the whole genomes of Native Americans in South America and Canada. 

Some scientists assert that the Americas were peopled in one large migration from Siberia that happened about 15,000 years ago, but the new genetic research shows that this central episode was followed by at least two smaller migrations from Siberia, one by people who became the ancestors of today’s Eskimos and Aleutians and another by people speaking Na-Dene, whose descendants are confined to North America. The research was published online Wednesday in the journal Nature. 

The Na-Dene speakers include the Navajo and Apache of the American Southwest, although no U.S. tribes were included in the study because of political opposition to genetic research. It’s my vague impression that Na-Dene speaking Indians tend to look more Siberian than other American Indians, which wouldn’t be surprising since they had ancestors in Siberia more recently.

The finding vindicates a proposal first made on linguistic grounds by Joseph Greenberg, the great classifier of the world’s languages. He asserted in 1987 that most languages spoken in North and South America were derived from the single mother tongue of the first settlers from Siberia, which he called Amerind. Two later waves, he surmised, brought speakers of Eskimo-Aleut and of Na-Dene, the language family spoken by the Apache and Navajo. 

But many linguists who specialize in American languages derided Dr. Greenberg’s proposal, saying they saw no evidence for any single ancestral language like Amerind. “American linguists made up their minds 25 year ago that they wouldn’t support Greenberg, and they haven’t changed their mind one whit,” said Merritt Ruhlen, a colleague of Dr. Greenberg, who died in 2001.

Reductionism is popular in physics, but not in the social sciences since the 1960s, or maybe not since the stock market crash of 1929. Anthropologist Robin Fox jokes that his field suffers from “ethnographic dazzle” or stamp collectoritis.

The new DNA study is based on gene chips that sample the entire genome and presents a fuller picture than earlier studies, which were based on small regions of the genome like the Y chromosome or mitochondrial DNA. Several of the mitochondrial DNA studies had pointed to a single migration. 

A team headed by David Reich of the Harvard Medical School and Dr. Andres Ruiz-Linares of University College London report that there was a main migration that populated the entire Americas. They cannot date the migration from their genomic data but accept the estimate by others that the migration occurred around 15,000 years ago. This was in the window of time that occurred after the melting of great glaciers that blocked passage from Siberia to Alaska, and before the rising waters at the end of the last ice age submerged Beringia, the land bridge between them. 

They also find evidence for two further waves of migration, one among Na-Dene speakers and the other among Eskimo-Aleut, again as Dr. Greenberg predicted. But whereas Dr. Greenberg’s proposal suggested that three discrete groups of people were packed into the Americas, the new genome study finds that the second and third waves mixed in with the first. Eskimos inherit about half of their DNA from the people of the first migration and half from a second migration. The Chipewyans of Canada, who speak a Na-Dene language, have 90 percent of their genes from the first migration and some 10 percent from a third. 

It is not clear why the Chipewyans and others speak a Na-Dene language if most of their DNA is from Amerind speakers. Dr. Ruiz-Linares said a minority language can often dominate others in the case of conquest; an example of this is the ubiquity of Spanish in Latin America.

• Tags: Genetics, Race 
🔊 Listen RSS
At West Hunter, Gregory Cochran writes about the distinction between extremely deleterious genetic mutations that frequently kill people before they pass on their bad gene (e.g., Huntington’s Disease) and mildly detrimental mutations that reduce Darwinian fitness in the range of 1 percent. Not surprisingly, the latter are more common because they can build up over the generations before they keep an individual from reproduciing.

… So… most  genetic load in humans is made up of many, many  mutations that each have fairly small effects.  A smaller fraction of the genetic load consists of mutations with big effects on fitness. 

… One important point is that a single highly deleterious mutation has a good chance of pushing the whole organism in some odd direction in phenotype space.  In other words, the same mutation that drops your IQ, or damages your heart, may also make you look funny.  At lower IQs, more and more kids are considered to suffer from ‘organic’ retardation.  On the other hand, a higher-than-average number of small-effect mutations should also interfere with really complex systems such as the brain (and reduce IQ), but because of the law of large numbers, wouldn’t tend to have any particular direction in phenotype space.  As far as I can tell, an extra-large dose of small-effect mutations, which we will henceforth call genetic noise, would not make you funny-looking.

Would the converse be true? Would good-looking but not very bright people also tend to have more genetic noise, as well, just in different places

Individuals can vary in the amount of genetic noise they carry, and populations can as well, depending on the relative intensity of selection and on the mutation rate, which might also differ.  For example, although having an unusually old father does not much affect the amount of genetic  noise an individual carries, a culture in which fathers were typically 55 would undoubtedly accumulate an unusually high amount of genetic noise, over a couple of millennia. 

If a kid’s parents have a higher-than-average amount of genetic noise, on average the kid will as well. This sure looks like what we usually call non-organic or familial retardation. 

Most of the within-population variation in IQ looks to be familial rather than organic.  If I’m right, this means that most IQ variation – what we might call the normal range – is caused by differences in the number of slightly deleterious mutations.  None of them would show up in a QTL search, because all are rare. And that is where we stand thus far:  no  intelligence QTLs have been found – although you never know what you’ll see in the next population.  On the other hand, shared chromosomal segments would mostly contain the same slightly deleterious mutations,  and so IQ should correlate with genetic similarity, which is what Visscher has found.

So, think of models for the genetics of IQ like horsepower in cars. In one model, a lot of people get the engine designed for 200 horsepower, some get the engine designed for 400 horsepower,  and some get the engine designed for 100 horsepower. Occasionally, something very bad happens in the manufacturing process or the maintenance process (e.g., Down’s Syndrome) and people get an engine that only delivers 50 horsepower. 

Cochran’s new model is at the other end of the spectrum: Most people get engines designed for 300 horsepower, but there are a whole lot of minor glitches in the manufacturing process (some because the blueprints have had accumulating errors creep into them in copying until they get thrown out, some de novo). So, most people get a mental engine somewhere in the 100 to 300 horsepower range, typically falling out in a bell curve. 

But what about the 400 horsepower people known to history?

Many great scientists and mathematicians have likely had relatively low levels of genetic noise combined with some fairly deleterious de novo mutations; with the net effect of a powerful mental engine strangely focused on some particular topic not directly related to fitness.  Low noise, high weirdness.   Math, not sheilas. One might look for advanced paternal age in such cases.

Read the whole thing there. There’s one phrase in it that hints at the next stage of his theory, but I’ll leave it at that.

🔊 Listen RSS
Gina Kolata writes in the NYT:

Study Says DNA’s Power to Predict Illness Is Limited 

“The punch line is that this sort of personalized medicine will not in any way be the most important determinant of patient care,” said Dr. Bert Vogelstein of Johns Hopkins, who, with his colleagues and his son Joshua, analyzed the power of sequencing all of a person’s DNA to determine an individual’s risk of disease. The study, published online Monday in the journal Science Translational Medicine, involved data from 53,666 identical twins in registries from the United States, Sweden, Finland, Denmark and Norway. The registries included data on 24 diseases, telling how often one twin, both or neither got a disease. 

Since identical twins share all of their genes, the investigators could ask to what extent genes predict an increased chance of getting a disease. Using a mathematical model, they reached an answer: not much. Most people will be at average risk for most of the 24 diseases.

• Tags: Genetics 
🔊 Listen RSS
Today’s conventional wisdom that Science has proved that race does not exist (and all the more or less comic variants on that) seems to my recollection to have reached a crescendo in the single year, 2000, when there was a vast amount of hype over the Human Genome Project. For leaders of the vastly well-funded undertaking, as well as their political overseers such as Bill Clinton, it was seen as essential to put the right racial spin on DNA research.

For example, below are excerpts from a big New York Times article by Natalie Angier from 2000, “Do Races Differ? Not Really, DNA Shows.”

That was hardly the worst Race Does Not Exist article from 2000, but, still, this is pretty embarrassing to read a dozen years later in an era when Henry Louis Gates is ready to roll with his 3rd reality series on PBS later this month, in which he has celebrities get their DNA tested and then springs on them the results of what their racial admixture is.

The irony, of course, is the that the rapid development of the gene sequencing technology celebrated in 2000′s orgy of Race Does Not Exist pronouncements, immediately began undermining the dogma in its moment of greatest triumph.

Still, very few people notice the contradiction between this dogma about what Science Says that they absorbed in 2000 and have held ever since versus all the scientific discoveries of the last 12 year. For example, reporter Nicholas Wade of the New York Times published dozens of the articles over the next decade systematically dismantling Angier’s article, but almost nobody noticed. A lie gets halfway around the world before the truth gets its boots on, especially when the lie ties into the status system. 

August 22, 2000 

Do Races Differ? Not Really, DNA Shows 


Scientists say that while it may be easy to tell at a glance whether a person is Asian, African or Caucasian, the differences dissolve when one looks beyond surface features and scans the human genome for DNA hallmarks of “race.” 

The Science of Differences
If racial labels have “little or no biological meaning,” what is the best way to address racial differences, politically or scientifically? 

In these glossy, lightweight days of an election year, it seems, they can’t build metaphorical tents big or fast enough for every politician who wants to pitch one up and invite the multicultural folds to “Come on under!” The feel-good message that both parties seek to convey is: regardless of race or creed, we really ARE all kin beneath the skin. 

Yet whatever the calculated quality of this new politics of inclusion, its sentiment accords firmly with scientists’ growing knowledge of the profound genetic fraternity that binds together human beings of the most seemingly disparate origins. 

Scientists have long suspected that the racial categories recognized by society are not reflected on the genetic level. 

But the more closely that researchers examine the human genome — the complement of genetic material encased in the heart of almost every cell of the body — the more most of them are convinced that the standard labels used to distinguish people by “race” have little or no biological meaning. 

They say that while it may seem easy to tell at a glance whether a person is Caucasian, African or Asian, the ease dissolves when one probes beneath surface characteristics and scans the genome for DNA hallmarks of “race.” 

As it turns out, scientists say, the human species is so evolutionarily young, and its migratory patterns so wide, restless and rococo, that it has simply not had a chance to divide itself into separate biological groups or “races” in any but the most superficial ways. 

“Race is a social concept, not a scientific one,” said Dr. J. Craig Venter, head of the Celera Genomics Corporation in Rockville, Md. “We all evolved in the last 100,000 years from the same small number of tribes that migrated out of Africa and colonized the world.” 

Dr. Venter and scientists at the National Institutes of Health recently announced that they had put together a draft of the entire sequence of the human genome, and the researchers had unanimously declared, there is only one race — the human race. 

Dr. Venter and other researchers say that those traits most commonly used to distinguish one race from another, like skin and eye color, or the width of the nose, are traits controlled by a relatively few number of genes, and thus have been able to change rapidly in response to extreme environmental pressures during the short course of Homo sapiens history. 

And so equatorial populations evolved dark skin, presumably to protect against ultraviolet radiation, while people in northern latitudes evolved pale skin, the better to produce vitamin D from pale sunlight. 

“If you ask what percentage of your genes is reflected in your external appearance, the basis by which we talk about race, the answer seems to be in the range of .01 percent,” said Dr.
Harold P. Freeman, the chief executive, president and director of surgery at North General Hospital in Manhattan, who has studied the issue of biology and race. “This is a very, very minimal reflection of your genetic makeup.” … 

By contrast with the tiny number of genes that make some people dark-skinned and doe-eyed, and others as pale as napkins, scientists say that traits like intelligence, artistic talent and social skills are likely to be shaped by thousands, if not tens of thousands, of the 80,000 or so genes in the human genome, all working in complex combinatorial fashion.
The possibility of such gene networks shifting their interrelationships wholesale in the course of humanity’s brief foray across the globe, and being skewed in significant ways according to “race” is “a bogus idea,” said Dr. Aravinda Chakravarti, a geneticist at Case Western University in Cleveland. 

… Dr. Eric S. Lander, a genome expert at the Whitehead Institute in Cambridge, Mass., admits that, because research on the human genome has just begun, he cannot deliver a definitive, knockout punch to those who would argue that significant racial differences must be reflected somewhere in human DNA and will be found once researchers get serious about looking for them. But as Dr. Lander sees it, the proponents of such racial divides are the ones with the tough case to defend. 

“There’s no scientific evidence to support substantial differences between groups,” he said, “and the tremendous burden of proof goes to anyone who wants to assert those differences.”
Although research into the structure and sequence of the human genome is in its infancy, geneticists have pieced together a rough outline of human genomic history, variously called the “Out of Africa” or “Evolutionary Eve” hypothesis. 

By this theory, modern Homo sapiens originated in Africa 200,000 to 100,000 years ago, at which point a relatively small nu
mber of them, maybe 10,000 or so, began migrating into the Middle East, Europe, Asia and across the Bering land mass into the Americas. As they traveled, they seem to have completely or largely displaced archaic humans already living in the various continents, either through calculated acts of genocide, or simply outreproducing them into extinction. 

Since the African emigrations began, a mere 7,000 generations have passed.

A mere 7,000 generations?

And because the founding population of émigrés was small, it could only take so much genetic variation with it. 

As a result of that combination — a limited founder population and a short time since dispersal — humans are strikingly homogeneous, differing from one another only once in a thousand subunits of the genome. 

“We are a small population grown large in the blink of an eye,” Dr. Lander said.

🔊 Listen RSS
I have to say that I’ve never quite gotten the excitement over epigenetics as a revolutionizing nature-nurture debates. This is not to say that the study of epigenetics isn’t valuable in and of itself, it just seems to have less implication for the kind of arguments that people really care about than its publicists assume. 
If I say, “Twin studies, adoption studies, and so forth suggest that for a lot of traits, there’s roughly a 50-50 breakdown between the effects of heredity and environment, over the last few years,” I constantly get told that: “Oh, no, that’s so 20th Century. You see, some of the genes are also being affected by the environment.”
Me: “Okay, but that still leaves us with the results of twin and adoption studies. So, what it sounds like you are saying is that genes aren’t just 50% of the importance, they’re something like 75%, but maybe 1/3rd of the genes are influenced by the environment, so we’re right back to 50-50, right?. I mean, we have to get back to what the studies report.”
For example, here’s Helen Fisher, a biological anthropologist at Rutgers, writing in literary agent John Brockman’s annual January question confab at his

To me, epigenetics is the most monumental explanation to emerge in the social and biological sciences since Darwin proposed his theories of Natural Selection and Sexual Selection. Over 2,500 articles, many scientific meetings, the formation of the San Diego Epigenome Center as well as other institutes, a five-year Epigenomics Program launched in 2008 by the National Institutes of Health, and many other institutions, academic forums and people are now devoted to this new field. Although epigenetics has been defined in several ways, all are based in the central concept that environmental forces can affect gene behavior, either turning genes on or off. … 

The consequences of epigenetic mechanisms are likely to be phenomenal. Scientists now hypothesize that epigenetic factors play a role in the etiology of many diseases, conditions and human variations—from cancers, to clinical depression and mental illnesses, to human behavioral and cultural variations. 

Take the Moroccan Amazighs or Berbers, people with highly similar genetic profiles who now reside in three different environments: some roam the deserts as nomads; some farm the mountain slopes; some live in the towns and cities along the Moroccan coast. And depending on where they live, up to one-third of their genes are differentially expressed, reports researcher Youssef Idaghdour. 

For example, among the urbanites, some genes in the respiratory system are switched on—perhaps, Idaghdour suggests, to counteract their new vulnerability to asthma and bronchitis in these smoggy surroundings. Idaghdour and his colleague Greg Gibson, propose that epigenetic mechanisms have altered the expression of many genes in these three Berber populations, producing their population differences.

Genes hold the instructions; epigenetic factors direct how those instructions are carried out. And as we age, scientists report, these epigenetic processes continue to modify and build who we are. Fifty-year-old twins, for example, show three times more epigenetic modifications than do three-year-old twins; and twins reared apart show more epigenetic alterations than those who grow up together. Epigenetic investigations are proving that genes are not destiny; but neither is the environment—even in people. 

Okay, but we already knew that genes are not destiny, but neither is the environment. 

I am hardly the first to hail this new field of biology as revolutionary—the fundamental process by which nature and nurture interact. But to me as an anthropologist long trying to take a middle road in a scientific discipline intractably immersed in nature-versus-nurture warfare, epigenetics is the missing link.

I’m not saying that it isn’t valuable to know that one way the environment affects traits is through sending a message to the genes to turn themselves on or off, but that that doesn’t tell us anything terribly significantly new about what people get hot under the collar about: the limits of environmental influence. 

• Tags: Genetics 
🔊 Listen RSS
For the last couple of decades, there has been a popular theological concept that every living human being was 100% descended from modern humans who came Out of Africa about 50,000 years ago, so therefore there hasn’t been enough time for evolution to cause any changes among people, so, therefore, Science Proves the complete genetic equality of all human racial groups.
So, what happened to the not-so-modern humans who were around back then, like the Neanderthals? Well, to Prove Racism Wrong, they had to have been utterly exterminated, the victims of a 100% genocide with no living descendants whatsoever. You see, old theories that some of the old non-African humans weren’t completely obliterated were racist, because that would imply that living humans aren’t all identical by descent, so they had to be utterly wrong. So, the old humans had to die. You can’t make anti-racist omelet without exterminating a few lineages.
In reality, it’s not actually a good idea to get too worked up over some theory you hold about the distant past. It’s especially not a good idea to create political/moral/religious dogmas dependent upon some assumption you make about the far past. You never know what somebody might dig up. 
It’s a better idea to keep an open mind about the present. If, say, men of West African descent keep making the Olympic 100m finals, well, that’s pretty interesting. There are a variety of ways that that could have come about, and there’s a variety of evidence for assessing those theories. In contrast, the conventional wisdom that anybody who notices these patterns must be evil because Science Proves that these patterns shouldn’t exist is just setting yourself up for a fall.  
Not long ago, it turned out that, sure enough, non-Africans tended to be a few percent Neanderthal by descent. Then, it turned out that some people (but not others) were related to an archaic group christened Denisovans. 
A new paper that came out today finds evidence of Denisovan ancestry in various islands off the southeast coast of Asia, such as the Mamanwa negritos of the Philippines and Australian Aborigines. Dienekes has some follow-up on it.
Meanwhile, a second big paper that came out today (see below) says that Australian Aborigines didn’t intermarry with anybody after they got to Australia 44,000 years ago. 
You’ll notice that there seem to be at least superficially contradictory lessons here about human nature: the ancestors of Australian Aborigines mated with a different quasi-species somewhere in the past, then maintained splendid isolation genetically for many tens of thousands of years in Australia, with no subsequent intruders mating with them until the 18th Century. So, maybe the general rule to draw from this is that You Can’t Tell about human history. You’ve got to go look it up.

🔊 Listen RSS
Nicholas Wade writes in the NYT:

A lock of hair, collected by a British anthropologist a century ago, has yielded the first genome of an Australian Aborigine, along with insights into the earliest migration from the ancestral human homeland somewhere in northeast Africa. 

The Aboriginal genome bolsters earlier genetic evidence showing that once the Aborigines’ ancestors arrived in Australia, some 50,000 years ago, they somehow kept the whole continent to themselves without admitting any outsiders. 

The Aborigines are thus direct descendants of the first modern humans to leave Africa, without any genetic mixture from other races so far as can be seen at present. Their dark skin reflects an African origin and a migration and residence in latitudes near the equator, unlike Europeans and Asians whose ancestors gained the paler skin necessary for living in northern latitudes. 

“Aboriginal Australians likely have one of the oldest continuous population histories outside sub-Saharan Africa today,” say the researchers who analyzed the hair, a group led by Eske Willerslev of the Natural History Museum of Denmark. 

Dr. Willerslev is an expert at working with ancient DNA, which is usually highly fragmented. Use of the ancient hair reduced the possibility of mixture with European genes and sidestepped the political difficulties of obtaining DNA from living Aborigines.

The “political difficulties” boil down to the fear that current Australian Aborigines aren’t closely related to the people who left archaeological traces in Australia, as long as 44,000 years ago, but are instead related to dingo dog-owning Asians or Polynesians who would have shown up a few thousand years ago. I’m not exactly sure why that would be politically bad for Aborigines, but Australian history is highly emotional, kind of like academic politics, perhaps because so little happened in the history of Australia. (A few years ago, a friend sent me an excellent history of Australia, but when I got done reading it, the only name I could remember is Sir Don Brad fordman, the great cricket player.) 
But ironically, this end run around Aboriginal sensitivities appears to have confirmed their fondest hopes about their vastly ancient pedigree. (I very seldom take an independent stand on specific questions of what happened tens of thousands of years in the past, because, well, what do I know?) 
The rest of the article is quite interesting, too, because it lays out all the reasons for why these results seem unexpected.

One thing worth noting is that despite evidently being separated for thousands of generations, Aborigines and Europeans are not only interfertile, but tend to come out looking overall European in just a few generations. The 1/8th Aborigine boy above looks like the young Bing Crosby, which is not uncommon. This is relevant to the question of how Neanderthals, Denisovans, and modern humans could successfully mate after a long separation.

By way of comparison, here are pictures, also from Ahnenkult, of the Greenland Eskimo descendants of Matthew Henson, the black sharecropper who was the right hand man of polar explorer Robert Peary. The half black / half Eskimo son looks like a comedian on BET, while the 1/4 black grandson doesn’t look all that black but the 1/8th black great-grandson does. He looks like the actor in a 1990ss episode of Arliss who played a part-black part-Eskimo tennis prodigy.

• Tags: Genetics 
🔊 Listen RSS
Keep an eye out on Tuesday for a new study of IQ genetics from Ian Deary and others.

• Tags: Genetics, IQ 
🔊 Listen RSS
This Washington Post article illustrates that the widespread conceptual confusion over what race is can be bad for health care:

Race reemerges in debate over ‘personalized medicine’ 

By Rob Stein 

Federal examiners have rejected patents for genetic screening tests because the applicants did not explore their effectiveness for different races, adding to the debate about whether race has scientific validity in modern DNA-based medicine. 

Presumably, Patent Office staffers got a memo encouraging them to make sure that genetic tests work on minorities and aren’t just being optimized for whites. But this upsets the Race Does Not Exist crowd.

Some geneticists, sociologists and bioethicists argue that “black,” “white,” “Asian” and “Hispanic” are antiquated categories that threaten to revive prejudices. Others, however, say that meaningful DNA variations can track racial lines and that ignoring them could deny many benefits of “personalized medicine,” which aims to develop tests and treatments tailored to a person’s genetic makeup. …

Jonathan Kahn, a law professor at Hamline University in St. Paul, Minn., discovered the patent rejections when he began sifting through applications, prompted by a 2008 patent office presentation that raised the race issue. 

“Constructions of race as genetic are not only scientifically flawed, they are socially dangerous, opening the door to new forms of discrimination or the misallocation of scarce resources needed to address real health disparities,” Kahn wrote in a report in the journal Nature Biotechnology in May. …

Similarly, in 2009, an examiner rejected a patent for a test for a propensity for prostate cancer because it did not specify the risk the variation posed among different races, Kahn found.
And in 2010, an examiner denied a patent for a test for a genetic marker for asthma and eczema because it was vetted only in whites and Asians. 

The prostate cancer and asthma rulings were reversed on appeal. But the colorectal cancer applicant narrowed the application to win approval. 

“There’s no telling how many people will just give in and use race in a way that the scientists clearly do not think is an appropriate way to use race,” Kahn said. 

Just the fact that patent applications are including such information is disturbing, he and other critics say. 

“This gives almost scientific legitimacy to the false categories of race — that somehow being white or being European is a strong category you can use in research,” said Troy Duster, who studies the racial implications of scientific research at New York University. 

For decades, demagogues — and even some scientists — argued that racial groups were genetically distinct and, in some ways, biologically inferior or superior, justifying laws barring interracial marriage and other discriminatory practices. 

Genetic predispositions — such as for sickle cell anemia, which occurs more frequently among African Americans, and Tay-Sachs disease, which is found more often in descendants of Ashkenazi Jews — clearly can pass down through generations. But as scientists developed modern tools of molecular biology, they produced ever more convincing evidence that genes vary as much among people who identify themselves as the same race as among groups segregated along traditional racial lines.

Except that they don’t. Statistically, genes vary a lot within races, just as they vary a fair amount among siblings within a nuclear family, but they vary even more among individuals across races.

“What we are learning is that ancestry is really the key here,” said Charles N. Rotimi, director of the center for research on genomics and global health at the National Human Genome Research Institute.

Because ancestry and race don’t have much to do with each other, I guess.

“The labels for race, at least as we currently use them, distort some of the things we want to understand in terms of ancestry.” 

Then perhaps we need for doctors to use more accurate terms. For example, Professor Kahn is up in arms about a Patent staffer who supposedly treated “Hispanic” as a racial group. This suggests that the medical profession ought to revive more genetically useful terms such as “mestizo” and “mulatto.” Doctors use technical terms for lots of things that are considered inappropriate to mention in polite society, so why shouldn’t they use “mestizo” and “mulatto?” It’s their job, after all.

For example, although sickle cell anemia is more common among African Americans, the blood disorder is also rare in some parts of Africa and common in some predominantly Caucasian populations.

This is the kind of race-does-not-exist talking point that’s more likely to confuse nonspecialist doctors than to help them make more accurate diagnoses. For the purposes of figuring out which tests to run on sick African American children, it doesn’t particularly matter that sickle cell anemia “is rare in some parts of Africa” because traditional African-Americans (i.e., the descendants of American slaves) are a blended population with no ability to accurately tell a doctor something like, “My baby can’t have sickle cell anemia because all 512 of my great-great-great-great-great-great-great-grandparents were from parts of Africa where sickle cell anemia is rare.” The point is that if your baby is African-American, sickle cell anemia should be a concern for your pediatrician. Now, if you and your spouse just got off the plane from, say, the highlands of Ethiopia, well, maybe not, but you are the exception.

Likewise, it would be good for doctors to know that if your baby is, say, 100% Sicilian, then there’s a small chance of sickle cell anemia because there was some falciparum malaria in Sicily.

The ultimate goal of genetic-based personalized medicine is to match care to each patient’s genetic makeup, Rotimi and others say. 

“You are truly going to be looking at that individual, whether black, white or Asian. It’s the individual’s genome that becomes important to their disease risk as opposed to their socially identified race or ethnicity,” said Vence L. Bonham Jr., an associate investigator at the institute, which is part of the National Institutes of Health.

But in the mean time … Look, this individualized medical genomics thing hasn’t working out as fast as people thought it would. What is progressing fast is racial genomics. Scientists are getting very good at figuring out people’s racial backgrounds from their DNA.

Injecting race back into the mix carries myriad dangers, critics say. On a practical level, it may result in doctors using tests or treatments on one ethnic group and not another, denying people care based on the color of their skin.

Because less information is better when making diagnoses.

… On a more disturbing level, it could fuel racism. 

“It has the social consequence of making it seem that differences among groups are fundamentally biological,” said Barbara A. Koenig, a medical ethicist and anthropologist at the Mayo Clinic in Minnesota. “Inevitably, in our history, that leads back to the idea that one race is better than another.” 

But others say that although race is far from perf
ect, some genetic variations with meaningful implications for health can be much more common among certain groups. 

For example, the anti-seizure drug Tegretol produces a life-threatening skin rash more frequently among certain Asians than others; the best dose of the common blood thinner Warfarin varies by race and African Americans appear to be at an increased risk for kidney failure because they more often carry certain mutations. 

“I don’t think race/ethnicity and personalized medicine are mutually exclusive,” said Neil Risch, a professor of human genetics and epidemiology at the University of California at San Francisco. “You can call it sociological, cultural — whatever. It’s all of the above. That doesn’t mean it’s devoid of genetic meaning.”

In other words, racial medicine doesn’t work in theory, but it does work with human beings. That suggests that we need a better theory.

In fact, recent analyses have indicated that many common diseases probably are caused by genetic variations in different populations, making it crucial to assemble diverse databases, researchers said in an article published online July 13 by the journal Nature. 

Two large genetic analyses published July 20 by the journals Nature and Nature Genetics found hundreds of genetic discrepancies between people of African American and European descent. And two papers published online Sunday by Nature Genetics found four unique genetic variations associated with asthma in people in Japan and people of African ancestry. Until scientists learn more about individual genetic predisposition, race provides a useful proxy, some say. 

“I think there’s a healthy debate right now about the role of race in medicine,” said Noah A. Rosenberg, a professor of biology at Stanford University.

One of the reasons that this debate has dragged on in a confused fashion for so many years, probably killing a few patients along the way, is that doctors aren’t given a solid concept of race. Doctors are busy, practical people. They need the conceptual heavy lifting to be done by intellectuals, but the intellectual class has overwhelmingly failed when it comes to understanding what race is.
The problem is that because it’s easy to poke holes in the crudest forms of old-fashioned American racial concepts, such as the one-drop rule, that means you can jump all the way to Race Does Not Exist, which is even cruder and stupider. What we need instead is a more sophisticated way for doctors to think about race. Fortunately, I invented* that way back in the 1990s: a racial group can most profitably be thought of as an extended family that is partly inbred. This is very close to being tautological, and, not surprisingly, lots of recent genetic data supports this insight.
The good news is that doctors shouldn’t have too much trouble grasping my concept because it fits nicely as an extension of a concept they use all the time: the family medical history. The Surgeon GeneralAMA  and the Mayo Clinic advocate that patients draw up a family medical history for themselves.
Race fits into the notion of a family medical history by allowing your family medical history to be extended beyond relatives whose medical histories you happen to know. Thinking of race as a partly inbred extended family means implies that statistical tendencies should also be garnered from large numbers of members of your more extended families.
The bad news is that almost nobody is explaining this concept to doctors. Thus, we see confused and confusing articles like this one.
* I’m sure lots of other people invented it before me.
🔊 Listen RSS
hbd chic k has made an interesting response to my review in The American Conservative of Francis Fukuyama’s The Origins of Political Order. First, another excerpt from my review:

William D. Hamilton’s math was popularized by Edward O. Wilson’s 1975 bombshell Sociobiology and by Richard Dawkins’s 1976 bestseller The Selfish Gene. (A more accurate title would have been The Dynastic Gene.) According to Fukuyama, however, political science has scandalously ignored the implications of these famous books. That’s true in general, although I have on my bookshelves academic works pointing out the fascinating political implications of kin selection by Pierre L. van den Berghe, Frank Salter, Tatu Vanhanen, and J.P. Rushton, none of whom Fukuyama cites. 

… Fukuyama is worried enough by this unpublicized but powerful line of logic that he tries to brush off the entire concept of ethnic nepotism: 

“Since virtually all human societies organized themselves tribally at one point, many people are tempted to believe that this is somehow a natural state of affairs or biologically driven. It is not obvious, however, why you should want to cooperate with a cousin four times removed rather than a familiar nonrelative just because you share one sixty-fourth of your genes with your cousin.”

Indeed, it is “not obvious,” but Fukuyama’s challenge is hardly unanswerable. In arranged-marriage cultures, clans, tribes, and castes can perpetuate themselves indefinitely, making states typically either ineffective or tyrannical. For example, as I’m writing, Colonel Gaddafi has so far survived NATO aerial bombardment by rallying many Bedouin tribes to his banner. Even though most Libyan nomads have settled down, they’ve maintained tribalism as what anthropologist Stanley Kurtz calls their “social structure in reserve” precisely for violent times like these when you can only trust blood relations. 

In the West, in contrast, over the generations familiar nonrelatives—i.e., neighbors—tend to turn into relatives, or at least potential in-laws, because European cultures frequently permitted love marriages with the girl next door. Moreover, as Fukuyama notes, the Catholic Church discouraged even fourth-cousin marriages. The resulting broad but shallow regional blood ties help explain why Western cultures were able to organize politically on a territorial basis without always being looted by self-interested clans.

hbd chick expands my rebuttal to Fukuyama into a General Theory of the West:

No, being tribal is not necessarily the natural state of affairs, but it IS biologically driven. as is being non-tribal. 

Europeans used to be tribal, but that’s because they used to marry their cousins, too, just like the afghanis or iraqis or saudis or libyans of today. the church put an end to all that and then some — it also put an end to all sorts of endogamous practices like polygamy and marrying your dead brother’s wife. first- and second-cousin marriage was banned in 506 a.d., and by the 11th century the church had banned marriage up to SIXTH cousins. 

This forced exogamy resulted in, as steve describes it, “broad but shallow regional blood ties.” almost all of european (and western) history hinges on these loose genetic ties. the whole evolution of european societies from tribes to city-states (think of the venices and the hamburgs of europe) to the nationalistic movements — this was made possible because extended family ties were continually loosened over centuries of european history (from the fall of rome onwards). the broadening of political structures (tribe, city-state, national-state) mirrors the underlying broadening of the genetic ties.

🔊 Listen RSS
Race can’t exist because the boundaries are too vague. The existence of species, however, is assumed in the name of the Endangered Species Act. Yet, when we stop and think about dogs, wolves, and coyotes, it’s not immediately obvious whether these familiar beasts should be classified as three species or three races within one species.
A press release has some genetic relevant to this old conundrum:

ALBANY, NY.- A State Museum scientist has co-authored a new research article, representing the most detailed genomic study of its kind, which shows that wolves and coyotes in the eastern United States are hybrids between gray wolves, coyotes and domestic dogs.  

Dr. Roland Kays, the Museum’s curator of mammals, was one of 15 other national and international scientists who collaborated on the study that used unprecedented genetic technology, developed from the dog genome, to survey the global genetic diversity in dogs, wolves and coyotes. The study used over 48,000 genetic markers, making it the most detailed genomic study of any wild vertebrate species.  

The research results are especially relevant to wolves and coyotes in the Northeast. The study shows a gradient of hybridization in wolves, with pure wolves in western states and increasing hybridization as you move east. Wolves in the western Great Lakes area averaged a genetic makeup of 85 percent wolf and 15 percent coyote, 

My wife saw one of these wolf-coyote hybrids in Racine, Wisconsin a dozen years ago: it looked big, assertive, and scary like a wolf, but was fairly solitary, like a coyote. In Southern California, in contrast, there are no wolves, and coyotes furtively skulk around by themselves.

while wolves in Algonquin Park in eastern Ontario averaged 58 percent wolf, and the ‘red wolf’ in North Carolina was only 24 percent wolf and 76 percent coyote. Populations of eastern coyotes, which only colonized the region in the last 60 years, were also minor hybrids, with some introgression of genetic material from wolves and domestic dogs. For example, Northeastern coyotes, including those in New York State, had genetic material primarily from coyotes (82 percent), with a minor contribution from dogs (9 percent) and wolves (9 percent).  …

Kays said “In most cases this breeding across species lines seems to have happened at times when humans were hunting eastern wolves to extinction, and the few remaining animals could find no proper mates, so took the best option they could get.” Kays continues, “The exceptions were an older hybridization between coyotes and wolves in the western Great Lakes dating from 600-900 years ago, and a coyote-dog hybridization in the eastern U.S. about 50 years ago, when coyote were first colonizing eastern forests.”  

This study also provides fresh data on the controversy over the species status of the Red Wolf in North Carolina, and the Eastern Canadian Wolf in Ontario. Both are medium-sized wolves that some have argued represent unique species. However, this new detailed genetic data shows both are the result of hybridizations between coyotes and wolves over the last few hundred years, and do not share a common origin in a unique eastern wolf species.  

This research is also relevant to a recent U.S. Fish and Wildlife proposal to remove the western Great Lakes wolves from the Endangered Species Act by showing that those wolves are only marginally hybridized with coyotes, should be considered a subspecies of the Gray Wolf, and have no genetic ties to a more endangered form of eastern wolf. 

As with modern humans and Neanderthals, introgression allows rapid evolution to adapt to new environments:

This study follows another research paper co-authored by Kays last year in the journal Biology Letters, which used museum specimens and genetic samples to show that eastern coyotes hybridized with wolves to rapidly evolve into a larger form over the last 90 years, dramatically expanding their geographic range and becoming the top predator in the Northeast. This hybridization contributed to the evolution of coyotes from mousers of western grasslands to deer hunters of eastern forests. The resulting coy-wolf hybrids are larger, with wider skulls that are better adapted for hunting deer. 

Are Neanderthals and modern humans different species? I dunno.
• Tags: Dogs, Genetics, Race 
🔊 Listen RSS

From FOXNews:

Scientist: All Blue-Eyed People Are Related  

“If you’ve got blue eyes, shake the hand of the nearest person who shares your azure irises: He or she may be a distant cousin. 

Danish researchers have concluded that all blue-eyed people share a common ancestor, presumably someone who lived 6,000 to 10,000 years ago. 

‘Originally, we all had brown eyes,’ Professor Hans Eiberg of the University of Copenhagen said in a press release. ‘But a genetic mutation affecting the OCA2 gene in our chromosomes resulted in the creation of a ‘switch,’ which literally ‘turned off’ the ability to produce brown eyes.’”

Me, Peter Brimelow, Norman Podhoretz, Mrs. Paul Krugman, and Jorge Ramos of Univision should schedule a family reunion!

• Tags: Genetics 
🔊 Listen RSS
Here’s that big new science story I teased a couple of days ago. By Carl Zimmer in the New York Times:
An international team of scientists has identified a previously shadowy human group known as the Denisovans as cousins to Neanderthals who lived in Asia from roughly 400,000 to 50,000 years ago and interbred with the ancestors of today’s inhabitants of New Guinea. 
All the Denisovans have left behind are a broken finger bone and a wisdom tooth in a Siberian cave. But the scientists have succeeded in extracting the entire genome of the Denisovans from these scant remains. An analysis of this ancient DNA, published on Wednesday in Nature, reveals that the genomes of people from New Guinea contain 4.8 percent Denisovan DNA. 
An earlier, incomplete analysis of Denisovan DNA had placed the group as more distant from both Neanderthals and humans. On the basis of the new findings, the scientists propose that the ancestors of Neanderthals and Denisovans emerged from Africa half a million years ago. The Neanderthals spread westward, settling in the Near East and Europe. The Denisovans headed east. Some 50,000 years ago, they interbred with humans expanding from Africa along the coast of South Asia, bequeathing some of their DNA to them.  …

Next, the researchers looked for evidence of interbreeding. Nick Patterson, a Broad Institute geneticist, compared the Denisovan genome to the complete genomes of five people, from South Africa, Nigeria, China, France and Papua New Guinea. To his astonishment, a sizable chunk of the Denisova genome resembled parts of the New Guinea DNA.

“The correct reaction when you get a surprising result is, ‘What am I doing wrong?’ ” said Dr. Patterson. To see if the result was an error, he and his colleagues sequenced the genomes of seven more people, including another individual from New Guinea and one from the neighboring island of Bougainville. But even in the new analysis, the Denisovan DNA still turned up in the New Guinea and Bougainville genomes. …

Dr. Bustamante also thinks that other cases of interbreeding are yet to be discovered. “There’s a lot of possibility out there,” he said. “But the only way to get at them is to sequence more of these ancient genomes.”  

If the genomes of New Guineans come almost 5% from non-modern humans, then the obvious next step is to test the genomes of Australian Aborigines, who are last in line in the original Southern, Indian Ocean shoreline route Out of Africa. However, there are a lot of regulatory barriers against testing Aborigines, perhaps out of fear that scientists will find something like this. After all, Aborigines look a little archaic, so it wouldn’t be terribly surprising if their genes turn out to be a little archaic.

It was lucky that the first findings of non-modern human ancestry involved Europeans, or it would have been hard to get up the political courage to publish this.

So, the Out of Africa model of evolution of the current human race turns out to be mostly, but not wholly, correct. Greg Cochran calls the new model “Out of Africa, with Benefits:” modern humans picked up useful genes from older human types, and not all of those inheritances spread equally to the entire current human race, probably in part because they aren’t equally useful in all environments.

Here’s an FAQ by John Hawks. And here are comments by Dienekes.

By the way, here’s an interesting 2006 article on Nick Patterson, one of the scientists involved. He’s had successful three careers, first as British and American government cryptologist, then as a quant for James H. Simons’ hedge fund Renaissance Technologies, and now as a genome researcher.

🔊 Listen RSS

For quite a number of decades, it has been apparent that agriculture was first invented in the “Fertile Crescent” of the Middle East, then spread into Europe. But that raised the question of how agriculture spread: did Middle Easterners colonize Europe or did existing European hunter-gatherers pick up Middle Eastern techniques? A couple of decades or so ago, geneticists entered this debate. L.L. Cavalli-Sforza argued that most Europeans today are descended from Middle Eastern farmers. Bryan Sykes responded that most Europeans are descended from indigenous hunter-gatherers who switched to farming.

The latest view is that Cavalli-Sforza was even more right than he claimed. Matthias Schultz writes in Der Spiegel in “How Middle Eastern Milk Drinkers Conquered Europe:

At around 5300 BC, everyone in Central Europe was suddenly farming and raising livestock. The members of the Linear Pottery culture kept cows in wooden pens, used rubbing stones and harvested grain. Within less than 300 years, the sedentary lifestyle had spread to the Paris basin.

The reasons behind the rapid shift have long been a mystery. Was it an idea that spread through Central Europe at the time, or an entire people?

Peaceful Cooperation or Invasion?

Many academics felt that the latter was inconceivable. Agriculture was invented in the Middle East, but many researchers found it hard to believe that people from that part of the world would have embarked on an endless march across the Bosporus and into the north.

Jens Lüning, a German archaeologist who specializes in the prehistoric period, was influential in establishing the conventional wisdom on the developments, namely that a small group of immigrants inducted the established inhabitants of Central Europe into sowing and milking with “missionary zeal.” The new knowledge was then quickly passed on to others. This process continued at a swift pace, in a spirit of “peaceful cooperation,” according to Lüning.

But now doubts are being raised on that explanation. New excavations in Turkey, as well as genetic analyses of domestic animals and Stone Age skeletons, paint a completely different picture:

  • At around 7000 BC, a mass migration of farmers began from the Middle East to Europe.
  • These ancient farmers brought along domesticated cattle and pigs.
  • There was no interbreeding between the intruders and the original population.

Mutated for Milk

The new settlers also had something of a miracle food at their disposal. They produced fresh milk, which, as a result of a genetic mutation, they were soon able to drink in large quantities. The result was that the population of farmers grew and grew.

These striking insights come from biologists and chemists. In a barrage of articles in professional journals like Nature and BMC Evolutionary Biology, they have turned many of the prevailing views upside down over the course of the last three years. …

In a bid to solve the mystery, molecular biologists have sawed into and analyzed countless Neolithic bones. The breakthrough came last year, when scientists discovered that the first milk drinkers lived in the territory of present-day Austria, Hungary and Slovakia.

But that was also where the nucleus of the Linear Pottery culture was located. “The trait of lactose tolerance quickly became established in the population,” explains Joachim Burger, an anthropologist from the University of Mainz in southwestern Germany who is a member of the Leche team.

There’s a good accompanying graphical map here.

Of course, all this raises even more questions, such as in regard to the recently surmised Neanderthal introgression

Having seen opinion shift several times on this topic over the last decade and a half, I look forward to future developments.

This lactose tolerant-centric view of the pre-history of Europe may provide some posthumous vindication to Raymond D. Crotty, an Irish dairy farmer turned economist, who emphasized the importance of the mutation to facilitate dairy farming as crucial to the dense populating of Northern Europe.

P.S. John Hawks comments here. Razib comments here.

P.P.S. Greg Cochran comments in the Comments.

• Tags: Genealogy, Genetics 
🔊 Listen RSS
Robert Plomin of King’s College London has been plugging away at the genetics of IQ for decades. It’s been frustrating, but now he thinks he’s getting somewhere. The London Sunday Times reports:
Scientists have identified more than 200 genes potentially associated with academic performance in schoolchildren.

Those schoolchildren possessing the “right” combinations achieved significantly better results in numeracy, literacy and science.

The finding emerged from a study of more than 4000 British children to pinpoint the genes and genetic combinations that influence reasoning skills and general intelligence.

One of its main conclusions is that intelligence is controlled by a network of thousands of genes with each making just a small contribution to overall intelligence, rather than the handful of powerful genes that scientists once predicted.

… There are potentially many millions of these variations, but the team restricted their search to looking at the million or so of the most common, to find out which gene variants were most frequently found in children with either a high or low level of academic achievement.

“Out of the gene variants we looked at, a couple of hundred are emerging which seem to have a small but significant relationship with ability in maths and English,” said Professor Plomin.

… Research into height, for example, has picked out 300 genes that affect how tall people will grow, but even these genes can only explain 15 per cent of the total variations in human height. It implies that hundreds more genes must also play a part.

John Hawks points out a recent Nicholas Wade article in the NYT making a similar point the lessons of an experiment on fruit flies to breed for earlier hatching:
One well-known path to change is a heavily favorable mutation in a single gene. But it may be well known only because it is easy to study. Another path is exploitation of mildly favorable differences that already exist in many genes. 

The question has considerable practical importance because if complex traits, including susceptibility to disease, are influenced by just a few genes, then it should be easy to develop treatments that target the few genes’ products. But if tens or hundreds of genes are involved in each trait, the task may be close to impossible….

The conventional view is that evolutionary change is generally mediated by a favorable mutation in a gene that then washes through the whole population, a process called a hard sweep because all other versions of the gene are brushed away. The alternative, called a soft sweep, is that many genes influence a trait, in this case the rate of maturation, and that the growth-accelerating versions of each of these genes become just a little more common. Each fly has a greater chance of inheriting these growth-promoting versions and so will mature faster.

In sequencing their subjects’ genomes, the researchers found that a soft sweep was indeed responsible for the earlier hatching. No single gene had swept through the population to effect the change; rather, the alternative versions of a large number of genes had become slightly more common.

The debate about whether evolution proceeds by altering one or many genes started 90 years ago among the three founders of population genetics, Ronald Fisher, Sewall Wright and J. B. S. Haldane. Haldane favored the single mutation mechanism, but Fisher and Wright backed multiple gene change. The fruit fly experiment “is a total vindication of Wright and Fisher and a major defeat for Haldane and a lot of conventional geneticists who have sided with him,” Dr. Rose said.

The demise of the Haldane view “is very bad news for the pharmaceutical industry in general,” Dr. Rose said. If disease and other traits are controlled by many genes, it will be hard to find effective drugs; a single target would have been much simpler.

So, it’s not surprising that intelligence is dependent upon a lot of genes. That’s generally true for a lot of complicated traits.
• Tags: Genetics 
🔊 Listen RSS

From the NYT:

Scientists Square Off on Evolutionary Value of Helping Relatives

Why are worker ants sterile? Why do birds sometimes help their parents raise more chicks, instead of having chicks of their own? Why do bacteria explode with toxins to kill rival colonies? In 1964, the British biologist William Hamilton published a landmark paper to answer these kinds of questions. Sometimes, he argued, helping your relatives can spread your genes faster than having children of your own.

For the past 46 years, biologists have used Dr. Hamilton’s theory to make sense of how animal societies evolve. They’ve even applied it to the evolution of our own species. But in the latest issue of the journal Nature, a team of prominent evolutionary biologists at Harvard try to demolish the theory.

The scientists argue that studies on animals since Dr. Hamilton’s day have failed to support it. The scientists write that a close look at the underlying math reveals that Dr. Hamilton’s theory is superfluous. “It’s precisely like an ancient epicycle in the solar system,” said Martin Nowak, a co-author of the paper with Edward O. Wilson and Corina Tarnita. “The world is much simpler without it.”

Other biologists are sharply divided about the paper. Some praise it for challenging a concept that has outlived its usefulness. But others dismiss it as fundamentally wrong.

“Things are just bouncing around right now like a box full of Ping-Pong balls,” said James Hunt, a biologist at North Carolina State University.

Dr. Hamilton, who died in 2000, saw his theory as following logically from what biologists already knew about natural selection. Some individuals have more offspring than others, thanks to the particular versions of genes they carry. But Dr. Hamilton argued that in order to judge the reproductive success of an individual, scientists had to look at the genes it shared with its relatives.

We inherit half of our genetic material from each parent, which means that siblings have, on average, 50 percent [1/2] of the same versions of genes. We share a lower percentage with first cousins [1/8], second cousins [1/32] and so on. If we give enough help to relatives so they can survive and have children, then they can pass on more copies of our own genes. Dr. Hamilton called this new way of tallying reproductive success inclusive fitness.

Each organism faces a trade-off between putting effort into raising its own offspring or helping its relatives. If the benefits of helping a relative outweigh the costs, Dr. Hamilton argued, altruism can evolve.

The idea wasn’t exactly wholly new. J.B.S. Haldane liked to joke in the 1950s when he was asked if he’d give up his life for his brother: No, but maybe for 2 brothers or 8 first cousins.
Dr. Hamilton believed that one of the things his theory could explain was the presence of sterile females among ants, wasps, and some other social insects. These species have peculiar genetics that cause females to be more closely related to their sisters than to their brothers, or even to their own offspring. In these situations, a female ant may be able to spread more genes by helping to raise her queen mother’s eggs than trying to lay eggs of her own.
Wilson didn’t like Hamilton’s theory the first time he heard of it either. In his delightful autobiography Naturalist, Wilson described how he wrestled with Hamilton’s epochal papers during an 18-hour train ride in 1965:

“Impossible, I thought, this can’t be right. Too simple… By dinnertime, as the train rumbled on into Virginia, I was growing frustrated and angry… And because I modestly thought of myself as the world authority on social insects, I also thought it unlikely that anyone else could explain their origin, certainly not in one clean stroke… By the time we reached Miami, in the early afternoon, I gave up. I was a convert and put myself in Hamilton’s hands. I had undergone what historians of science call a paradigm shift.”

Zimmer continues:
But as the years passed, Dr. Wilson’s enthusiasm for the theory waned. “It was getting tattered,” he said. Many species with sterile females, for example, do not have the strange genetics of ants and wasps. And many species with the right genetics have not produced sterile females. …
A number of scientists strongly disagree, though. “This paper, far from showing shortcomings in inclusive fitness theory, shows the shortcomings of the authors,” said Frances Ratnieks of the University of Sussex.

Dr. Ratnieks argues that the Harvard researchers cannot rule out kinship as a driving force in social evolution because their model is flawed. It does not include how closely related animals are.

That would seem to be a big factor. 
Read the rest of the article here

To see some of the more interesting implications of Hamilton’s theory, see my 2004 article.

🔊 Listen RSS
Some of the most prevalent Dumb Ideas about Race that crystallized as conventional wisdom around the time of Bill Clinton’s celebration ceremony for the Human Genome Project revolve around the idea that genetic differences couldn’t possibly cause differing behavioral tendencies among the races because we’re all 99.999% (insert as many “9s” as you feel necessary to make the point) the same!
From the New York Times:
Wide Variety of Breeds Born of Few Genes

Spaniels have notably floppy ears, basset hounds have extremely short legs, and St. Bernards are large and big boned. Not to mention Chihuahuas.

Humans have bred dogs to produce tremendous variety. But a new study reports that the physical variance among dog breeds is determined by differences in only about seven genetic regions.

These seven locations in the dog genome explain about 80 percent of the differences in height and weight among breeds, said Carlos Bustamante, a geneticist at Stanford University and one of the study’s authors. The findings, published in Public Library of Science-Biology, are a result of what is the largest genotyping of dogs to date, involving more than 1,000 dogs and 80 breeds.

So, in the big picture, Labrador retrievers and pit bulls don’t actually differ very much genetically. They do differ genetically on a very small number of genes. But some of those few genes that differ are related to biting. Labs tend to retract their teeth and gum whatever they’re handling with their mouths, while pit bulls tend to bite down and, more unusually, not let go while they whip their heads back and forth. So, that tiny, tiny fraction of the dog genome is important when deciding which breed of dog to buy depending on your needs — e.g., pet for your toddlers or guard dog for your crack stash.

By the way, here’s Malcolm Gladwell in 2006 arguing that opposition to pit bulls is racial profiling and therefore immoral and ineffective, just like racial profiling of humans must, therefore, be.

The great thing about Malcolm is that he lacks the Uh-Oh-Let’s-Not-Go-There gene that makes most spouters of the conventional wisdom prudently change the subject when they find that the logic of their argument has carried them to the edge of reductio ad absurdum.

• Tags: Dogs, Genetics 
🔊 Listen RSS
Sometimes I get discouraged when I realize that I’ve been debunking dumb ideas for many years now, yet dumb ideas remains wildly popular. 
But think how Nicholas Wade, the genetics correspondent of the New York Times, must feel. He has the top soapbox in the world for educating the public, the New York Times, and he covers for the NYT the trendiest topic in science, genetics. He has spent the last decade (here are VDARE articles I wrote praising Wade’s NYT work in 2003 and 2006) diligently debunking the reigning dumb ideas of our age, such as “Race doesn’t exist,” “Race is just skin deep,” and “Racial differences couldn’t have evolved because there hasn’t been enough time.” For nine or ten years, he has used dozens of New York Times articles to aim a firehose of the latest scientific findings at these dogmas … and, as far as I can tell, nobody ever notices
They don’t Watson him. I’ve never noticed anybody objecting to Wade. They just don’t ever get what he’s saying. It doesn’t register. The conventional wisdom is so comforting and so status-raising that relentless reporting in the New York Times can’t dent it, or even make most NYT readers notice that their favorite beliefs are being subverted. Wade has been engaging in Popperian falsification of the age’s dominant theories, and nobody notices.
Perhaps the average NYT subscriber reads each Wade article on the latest findings of genetic differences among racial groups, nods complacently, and then says to himself, “Yes, those Red State racist Republicans are just too stupid to realize that Darwin proves that race does not exist, whereas I live in New York and subscribe to the Times which keeps me up to date on … on … well, on whatever this article was about, but whatever it was about, I know, because I subscribe to the Times, that it proves that science shows that race is only skin deep, because there wasn’t enough time for differences to evolve like those stupid Jesus fish people believe who don’t believe in evolution, sometimes they just make me so angry because they come from a long line of hereditary idiots,” and then he moves on to closely peruse an article about how to get his kid into a Park Slope school district with really good schools.
From the NYT:
by Nicholas Wade

Ten thousand years ago, people in southern China began to cultivate rice and quickly made an all-too-tempting discovery — the cereal could be fermented into alcoholic liquors. Carousing and drunkenness must have started to pose a serious threat to survival because a variant gene that protects against alcohol became almost universal among southern Chinese and spread throughout the rest of China in the wake of rice cultivation.

The variant gene rapidly degrades alcohol to a chemical that is not intoxicating but makes people flush, leaving many people of Asian descent a legacy of turning red in the face when they drink alcohol. 

I imagine American Indians left too early to didn’t get this gene?

Here’s a question I’ve wondered about. There are two scandalous scenes of drunkenness in the Book of Genesis, Noah and Lot, but how many are there in the rest off the Bible? The Wedding at Cana, for example, is non-scandalous.

The spread of the new gene, described in January by Bing Su of the Chinese Academy of Sciences, is just one instance of recent human evolution and in particular of a specific population’s changing genetically in response to local conditions.

… Many have assumed that humans ceased to evolve in the distant past, perhaps when people first learned to protect themselves against cold, famine and other harsh agents of natural selection. But in the last few years, biologists peering into the human genome sequences now available from around the world have found increasing evidence of natural selection at work in the last few thousand years, leading many to assume that human evolution is still in progress….

So much natural selection has occurred in the recent past that geneticists have started to look for new ways in which evolution could occur very rapidly. Much of the new evidence for recent evolution has come from methods that allow the force of natural selection to be assessed across the whole human genome. This has been made possible by DNA data derived mostly from the Hap Map, a government project to help uncover the genetic roots of complex disease. The Hap Map contains samples from 11 populations around the world and consists of readings of the DNA at specific sites along the genome where variations are common.

One of the signatures of natural selection is that it disturbs the undergrowth of mutations that are always accumulating along the genome. As a favored version of a gene becomes more common in a population, genomes will look increasingly alike in and around the gene. Because variation is brushed away, the favored gene’s rise in popularity is called a sweep. Geneticists have developed several statistical methods for detecting sweeps, and hence of natural selection in action.

About 21 genome-wide scans for natural selection had been completed by last year, providing evidence that 4,243 genes — 23 percent of the human total — were under natural selection. This is a surprisingly high proportion, since the scans often miss various genes that are known for other reasons to be under selection. Also, the scans can see only recent episodes of selection — probably just those that occurred within the last 5,000 to 25,000 years or so. The reason is that after a favored version of a gene has swept through the population, mutations start building up in its DNA, eroding the uniformity that is evidence of a sweep.

Unfortunately, as Joshua M. Akey of the University of Washington in Seattle, pointed out last year in the journal Genome Research, most of the regions identified as under selection were found in only one scan and ignored by the 20 others. The lack of agreement is “sobering,” as Dr. Akey put it, not least because most of the scans are based on the same Hap Map data.

From this drunken riot of claims, however, Dr. Akey believes that it is reasonable to assume that any region identified in two or more scans is probably under natural selection. By this criterion, 2,465 genes, or 13 percent, have been actively shaped by recent evolution. The genes are involved in many different biological processes, like diet, skin color and the sense of smell.

A new approach to identifying selected genes has been developed by Anna Di Rienzo at the University of Chicago. Instead of looking at the genome and seeing what turns up, Dr. Di Rienzo and colleagues have started with genes that would be likely to change as people adopted different environments, modes of subsistence and diets, and then checked to see if different populations have responded accordingly.

She found particularly strong signals of selection in populations that live in polar regions, in people who live by foraging, and in people whose diets are rich in roots and tubers. In Eskimo populations, there are signals of selection in genes that help people adapt to cold.

Among primitive farming tribes, big eaters of tubers, which contain little folic acid, selection has shaped the genes involved in synthesizing folic acid in the body, Dr. Di Rienzo and colleagues reported in May in the Proceedings of the National Academy of Sciences.

The fewest signals of selection were seen among people who live in the humid tropics, the ecoregion where the ancestral human population evolved. “One could argue that we are adapted to that and that most signals are seen when people adapt to new environments,” Dr. Di Rienzo said in an interview.

… Several of the 25 skin genes bear strong signatures of natural selection, but natural selection has taken different paths to lighten people’s skin in Europe and in Asia. A special version of the golden gene, so called because it turns zebrafish a rich yellow color, is found in more than 98 percent of Europeans but is very rare in East Asians. In them, a variant version of a gene called DCT may contribute to light skin. Presumably, different mutations were available in each population for natural selection to work on. The fact that the two populations took independent paths toward developing lighter skin suggests that there was not much gene flow between them. …

That’s interesting because you can walk from, say, Normandy to Korea. The physical anthropologists of Carleton Coon’s mid-century generation believed from looking at bones that the biggest division in mankind was caused by the Himalayas and other mountains dividing West Afro-Eurasia from East Asia, although subsequent genetics studies suggested the biggest division was between sub-Saharan Africa and the rest of the world. But, the old bone guys must have been a little bit right about this Europe-Asia divide.

Most variation in the human genome is neutral, meaning that it arose not by natural selection but by processes like harmless mutations and the random shuffling of the genome between generations. The amount of this genetic diversity is highest in African populations. 

By the way, this is the source of the widely held dogma/ urban legend for the quasi-educated that black Africans are the most genetically diverse people on Earth, or, in increasingly crazier variants, that two white Americans might less related to each other than to a black African, or that you and your brother are less similar to each other genetically than you are to an African. This is true for neutral (“junk”) genes that aren’t selected not for functional genes. (I debunked this ten years ago in Seven Dumb Ideas about Race.)

Diversity decreases steadily the further a population has migrated from the African homeland, since each group that moved onward carried away only some of the diversity of its parent population. This steady decline in diversity shows no discontinuity between one population and the next, and has offered no clear explanation as to why one population should differ much from another. But selected genes show a different pattern: Evidence from the new genome-wide tests for selection show that most selective pressures are focused on specific populations.

One aspect of this pattern is that there seem to be more genes under recent selection in East Asians and Europeans than in Africans, possibly because the people who left Africa were then forced to adapt to different environments. “It’s a reasonable inference that non-Africans were becoming exposed to a wide variety of novel climates,” says Dr. Stoneking of the Max Planck Institute. …

But the new evidence that humans have adapted rapidly and extensively suggests that natural selection must have other options for changing a trait besides waiting for the right mutation to show up. In an article in Current Biology in February, Dr. Pritchard suggested that a lot of natural selection may take place through what he called soft sweeps.

Soft sweeps work on traits affected by many genes, like height. Suppose there are a hundred genes that affect height (about 50 are known already, and many more remain to be found). Each gene exists in a version that enhances height and a version that does not. The average person might inherit the height-enhancing version of 50 of these genes, say, and be of average height as a result.

Suppose this population migrates to a region, like the Upper Nile, where it is an advantage to be very tall. Natural selection need only make the height-enhancing versions of these 100 genes just a little more common in the population, and now the average person will be likely to inherit 55 of them, say, instead of 50, and be taller as a result. Since the height-enhancing versions of the genes already exist, natural selection can go to work right away and the population can adapt quickly to its new home. 

A lot of human biodiversity at the phenome level is relative rather than absolute, quantitative rather than qualitative.

🔊 Listen RSS
From the Washington Post last week:

China pushing the envelope on science, and sometimes ethics
By John Pomfret

SHENZHEN, CHINA — Last year, Zhao Bowen was part of a team that cracked the genetic code of the cucumber. These days, he’s probing the genetic basis for human IQ.

Zhao is 17.

Centuries after it led the world in technological prowess — think gunpowder, irrigation and the printed word — China has barged back into the ranks of the great powers in science. With the brashness of a teenager, in some cases literally, China’s scientists and inventors are driving a resurgence in potentially world-changing research.

Unburdened by social and legal constraints common in the West, China’s trailblazing scientists are also pushing the limits of ethics and principle as they create a new — and to many, worrisome — Wild West in the Far East.

A decade ago, no one considered China a scientific competitor. Its best and brightest agreed and fled China in a massive brain drain to university research labs at Harvard, Stanford and MIT.

But over the past five years, Western-educated scientists and gutsy entrepreneurs have conducted a rearguard action, battling China’s hidebound bureaucracy to establish research institutes and companies. Those have lured home scores [i..e., at least 40] of Western-trained Chinese researchers dedicated to transforming the People’s Republic of China into a scientific superpower.

“They have grown so fast and so suddenly that people are still skeptical,” said Rasmus Nielsen, a geneticist at the University of California at Berkeley who collaborates with Chinese counterparts. “But we should get used to it. There is competition from China now, and it’s really quite drastic how things have changed.”

… China has jumped to second place — up from 14th in 1995 — behind the United States in the number of research articles published in scientific and technical journals worldwide.

Backed by the Bill and Melinda Gates Foundation, Chinese medical researchers, partnering with a firm in the United States, beat out an Indian team last year to develop a new test for cervical cancer that costs less than $5. The goal is to test 10 million Chinese women within three years. …

Meanwhile, Chinese military researchers appear to be on the cusp of a significant breakthrough: a land-based anti-ship ballistic missile that is causing concern within the U.S. Navy.

In 2007, Chinese geneticists discovered vast differences in the genetic makeup of Africans, Asians and Caucasians. They will soon report a breakthrough showing why some people — such as Tibetans — can live effortlessly at high altitudes while others can’t.

There are challenges. China is still considered weak at innovation, and Chinese bureaucrats routinely mandate discoveries — fantasy-world marching orders that Western scientists view as absurd.

In 2008, the Ministry of Science and Technology gave researchers two years to come up with 30 medicines ready for clinical trials and only five days to apply for grants to fund the work. That’s despite the fact that since the communist revolution in 1949, China has developed only one internationally recognized drug — Artemisinin — to fight malaria.

Chinese science and technology is also awash in scams and sometimes-troubling practices. More than 200 institutions in China practice controversial stem cell therapies for people suffering from injuries, diseases or birth defects. Although the government moved last year to regulate the industry, none of the techniques has been subjected to rigorous clinical trials.

China is also the leading source of what are known as “junk” patents — ridiculous claims of “inventions” that are little more than snake-oil scams.

“This discovery is going to shake the world!” bellowed Liu Jian, chief executive of Hualong Fertilizer Technique Co. Liu says he has developed a method to reduce fertilizer use by half through the use of nanotechnology, although officials at the Agriculture Ministry mock the claim. “Will you help us raise some capital?” Liu asked in an interview.

Finally, plagiarism and doctored results seem to be as common as chopsticks. A study by Wuhan University uncovered an entire industry of bogus report and thesis writers who raked in $145 million last year, a fivefold increase since 2007.

The emergence of China as a nascent scientific superpower raises questions about the U.S. relationship with Beijing. Ever since the United States opened the door to Chinese students in the 1970s, hundreds of thousands have flocked to America. Most have studied science or engineering and have been welcomed in research institutions across the land. But with China becoming a competitor, U.S. experts have begun to question that practice.

FBI officials allege that there is a large-scale operation in the United States to pilfer American industrial, scientific, technological and military secrets. In the past few years, dozens of Chinese have been convicted of stealing American technology and shipping it to China.

“The science and technology relationship with China has always stood up against all kinds of political pressures,” said Richard P. Suttmeier, who has researched China’s rise for the National Science Foundation. “Now that you have competition going on, finding the basis for cooperation in the absence of trust is an issue. It goes to questions of espionage and a hunger for technology.”

That hunger is evident in the halls of BGI, home to Zhao Bowen and more than 1,500 other Chinese scientists and technicians. Located in an industrial zone in the southern Chinese megalopolis of Shenzhen, BGI has grown into one of the world’s leading genomics institutes devoted to deciphering the genetic blueprint of organisms.

Over the past few years, scientists at BGI sequenced the genes of a chicken, a silkworm, a panda, a strain of rice and 4,000-year-old human remains from Greenland.

In January, BGI made the biggest purchase of genome sequencing equipment ever, buying 128 ultra-high-tech machines from California-based Illumina. With that one acquisition, BGI could very well surpass the entire gene-sequencing output of the United States.

Inside the 11-story facility, the vibe is pure Silicon Valley start-up: shorts, flip-flops, ankle bracelets, designer eyewear and a random tattoo. Zhao came to BGI on a summer internship last year to work on cucumbers. Now a full-time employee while continuing his studies, Zhao is turning his attention to a topic Western researchers have shied away from because of ethical worries: Zhao plans to study the genes of 1,000 of his best-performing classmates at a top high school in Beijing and compare them, he said, “with 1,000 normal kids.”

• Tags: Genetics, IQ 
Steve Sailer
About Steve Sailer

Steve Sailer is a journalist, movie critic for Taki's Magazine, columnist, and founder of the Human Biodiversity discussion group for top scientists and public intellectuals.

The “war hero” candidate buried information about POWs left behind in Vietnam.
The evidence is clear — but often ignored
The unspoken statistical reality of urban crime over the last quarter century.
The major media overlooked Communist spies and Madoff’s fraud. What are they missing today?
What Was John McCain's True Wartime Record in Vietnam?