Genetic Analysis Of Social Class Mobility

pnas |  Our analysis suggests three take-home messages. The first take-home message is that genetics research should incorporate information about social origins. For genetics, our findings suggest that estimates of genetic associations with socioeconomic achievement reflect direct genetic effects as well as the effects of social inheritance correlated with genetics. Future genetic studies of social attainment can refine inferences about direct genetic effects by including measures of social origins in their study designs. The same is true for genetic studies of other phenotypes, because childhood socioeconomic circumstances are implicated in the etiology of many different traits and health conditions (54⇓–56). Such analysis will help clarify interpretation of studies that analyzed GWAS data and found evidence of genetic overlap between educational attainment and several biomedical phenotypes (57, 58). The advent of national biobanks and other large genetic datasets is increasing the power of GWAS to map genetic risks. Research to investigate how much of the genetic risk measured from GWAS discoveries arises within a single generation and how much accrues from social inheritance correlated with genetics across successive generations is needed.

The second take-home message is that social science research should incorporate information about genetic inheritance. For the social sciences, our findings provide molecular evidence across birth cohorts and countries of genetic influence on social attainment and social mobility. This evidence supports theory in the social sciences that frames genetics as one mechanism among several through which social position is transmitted across generations (9, 20, 21, 59). These theories imply that genetic factors can confound estimates of social environmental effects. However, because genetics have been difficult to measure, studies addressing these theories have had to estimate genetic contributions to attainment indirectly, while other social science research has simply ignored the problem. Now, genetically informed theories of social attainment and mobility can be revisited, tested, and elaborated using molecular genetic data available in an ever-growing array of genetically informed social surveys and longitudinal cohort studies.

Beyond theory, integration of measured genetic inheritance into research on social mobility can add value in at least three ways. First, genetic controls can improve the precision of estimates of environmental effects (11, 14), e.g., of how features of parents’ social circumstances shape children’s development. Second, genetic measurements can provide a starting point for developmental investigations of pathways to social mobility (16, 60), e.g., to identify skills and behaviors that can serve as targets for environmental interventions to lift children out of poverty. Third, genetic measurements can be used to study gene–environment interplay; e.g., how policies and programs may strengthen or weaken genetic and nongenetic mechanisms of intergenerational transmission (61). In our analysis, modeling effects of social origins attenuated genetic-effect sizes by 10–50%, depending on the outcome and cohort. This variation is consistent with evidence that genetic influences on individual differences may vary across cultures and cohorts and across stages of the life course (62, 63). Research is needed to understand how molecular genetic effects on socioeconomic attainment may operate differently across environmental, historical, or economic contexts and the extent to which they may wax or wane across adult development.

The third take-home message is that genetic analysis of social mobility can inform programs and policies that change children’s environments as a way to promote positive development. The genetics we studied are related to socioeconomic attainment and mobility partly through channels that are policy-malleable. Personal characteristics linked with the attainment-related genetics we studied involve early-emerging cognitive and noncognitive skills, including learning to talk and read, act planfully, delay gratification, and get along with others (10, 16). These skills represent intervention targets in their own right, for example by policies and programs that safeguard perinatal development and provide enriching, stable family and educational environments (64). A significant contribution of our study is that the nongenetic social and material resources children inherit from their parents represent a further mechanism linking genetics and attainment over the life course. Policies and programs cannot change children’s genes, but they can help give them more of the resources that children who inherit more education-linked genetics tend to grow up with. Our findings suggest that such interventions could help close the gap. The next step is to find out precisely what those resources are.

Conclusion

A long-term goal of our sociogenomic research is to use genetics to reveal novel environmental intervention approaches to mitigating socioeconomic disadvantage. The analysis reported here takes one step toward enabling a study design to accomplish this. We found that measured genetics related to patterns of social attainment and mobility, partly through direct influences on individuals and partly through predicting the environments in which they grew up. Specifically, parents’ genetics influence the environments that give children their start in life, while children’s own genetics influence their social mobility across adult life. As we learn more about how genetics discovered in GWAS of education influence processes of human development that generate and maintain wealth and poverty, we can identify specific environments that shape those processes. Ultimately, this research approach can suggest interventions that change children’s environments to promote positive development across the life-course.

behavioral genetics is pseudo-science

ScientificAmerican | Last spring, I kicked up a kerfuffle by proposing that research on race and intelligence, given its potential for exacerbating discrimination, should be banned. Now Nature has expanded this debate with “Taboo Genetics.” The article “looks at four controversial areas of behavioral genetics”—intelligence, race, violence and sexuality—”to find out why each field has been a flashpoint, and whether there are sound scientific reasons for pursuing such studies.”

The essay provides a solid overview, including input from both defenders of behavioral genetics and critics. The author, Erika Check Hayden, quotes me saying that research on race and intelligence too often bolsters “racist ideas about the inferiority of certain groups, which plays into racist policies.”

I only wish that Hayden had repeated my broader complaint against behavioral genetics, which attempts to explain human behavior in genetic terms. The field, which I’ve been following since the late 1980s, has a horrendous track record. My concerns about the potential for abuse of behavioral genetics are directly related to its history of widely publicized, erroneous claims.

I like to call behavioral genetics “gene whiz science,” because “advances” so often conform to the same pattern. Researchers, or gene-whizzers, announce: There’s a gene that makes you gay! That makes you super-smart! That makes you believe in God! That makes you vote for Barney Frank! The media and the public collectively exclaim, “Gee whiz!”

Follow-up studies that fail to corroborate the initial claim receive little or no attention, leaving the public with the mistaken impression that the initial report was accurate—and, more broadly, that genes determine who we are.

Over the past 25 years or so, gene-whizzers have discovered “genes for” high IQ, gambling, attention-deficit disorder, obsessive-compulsive disorder, bipolar disorder, schizophrenia, autism, dyslexia, alcoholism, heroin addiction, extroversion, introversion, anxiety, anorexia nervosa, seasonal affective disorder, violent aggression—and so on. So far, not one of these claims has been consistently confirmed by follow-up studies.

These failures should not be surprising, because all these complex traits and disorders are almost certainly caused by many different genes interacting with many different environmental factors. Moreover, the methodology of behavioral geneticists is highly susceptible to false positives. Researchers select a group of people who share a trait and then start searching for a gene that occurs not universally and exclusively but simply more often in this group than in a control group. If you look at enough genes, you will almost inevitably find one that meets these criteria simply through chance. Those who insist that these random correlations are significant have succumbed to the Texas Sharpshooter Fallacy.

To get a sense of just how shoddy behavioral genetics is, check out my posts on the “liberal gene,” “gay gene” and God gene” (the latter two “discovered” by Dean Hamer, whose record as a gene-whizzer is especially abysmal); and on the MAOA-L gene, also known as the “warrior gene.” Also see this post, where I challenge defenders of behavioral genetics to cite a single example of a solid, replicated finding.

Ever since I first hammered behavioral genetics in my 1993 Scientific American article “Eugenics Revisited,” critics have faulted me for treating the field so harshly. But over the last 20 years, the field has performed even more poorly than I expected. At this point, I don’t know why anyone takes gene-whiz science seriously.

behavioral genetics - bad science and worse just-so storytelling...,

scientificamerican |  Last spring, I kicked up a kerfuffle by proposing that research on race and intelligence, given its potential for exacerbating discrimination, should be banned. Now Nature has expanded this debate with "Taboo Genetics." The article "looks at four controversial areas of behavioral genetics"—intelligence, race, violence and sexuality—"to find out why each field has been a flashpoint, and whether there are sound scientific reasons for pursuing such studies."

The essay provides a solid overview, including input from both defenders of behavioral genetics and critics. The author, Erika Check Hayden, quotes me saying that research on race and intelligence too often bolsters "racist ideas about the inferiority of certain groups, which plays into racist policies."

I only wish that Hayden had repeated my broader complaint against behavioral genetics, which attempts to explain human behavior in genetic terms. The field, which I've been following since the late 1980s, has a horrendous track record. My concerns about the potential for abuse of behavioral genetics are directly related to its history of widely publicized, erroneous claims.

I like to call behavioral genetics "gene whiz science," because "advances" so often conform to the same pattern. Researchers, or gene-whizzers, announce: There’s a gene that makes you gay! That makes you super-smart! That makes you believe in God! That makes you vote for Barney Frank! The media and the public collectively exclaim, "Gee whiz!"

Follow-up studies that fail to corroborate the initial claim receive little or no attention, leaving the public with the mistaken impression that the initial report was accurate—and, more broadly, that genes determine who we are.

Over the past 25 years or so, gene-whizzers have discovered "genes for" high IQ, gambling, attention-deficit disorder, obsessive-compulsive disorder, bipolar disorder, schizophrenia, autism, dyslexia, alcoholism, heroin addiction, extroversion, introversion, anxiety, anorexia nervosa, seasonal affective disorder, violent aggression—and so on. So far, not one of these claims has been consistently confirmed by follow-up studies.

These failures should not be surprising, because all these complex traits and disorders are almost certainly caused by many different genes interacting with many different environmental factors. Moreover, the methodology of behavioral geneticists is highly susceptible to false positives. Researchers select a group of people who share a trait and then start searching for a gene that occurs not universally and exclusively but simply more often in this group than in a control group. If you look at enough genes, you will almost inevitably find one that meets these criteria simply through chance. Those who insist that these random correlations are significant have succumbed to the Texas Sharpshooter Fallacy.

To get a sense of just how shoddy behavioral genetics is, check out my posts on the "liberal gene," "gay gene" and God gene" (the latter two "discovered" by Dean Hamer, whose record as a gene-whizzer is especially abysmal); and on the MAOA-L gene, also known as the "warrior gene." Also see this post, where I challenge defenders of behavioral genetics to cite a single example of a solid, replicated finding.

Genetics in the Madhouse: The Unknown History of Human Heredity

nature  |  Who founded genetics? The line-up usually numbers four. William Bateson and Wilhelm Johannsen coined the terms genetics and gene, respectively, at the turn of the twentieth century. In 1910, Thomas Hunt Morgan began showing genetics at work in fruit flies (see E. Callaway Nature 516, 169; 2014). The runaway favourite is generally Gregor Mendel, who, in the mid-nineteenth century, crossbred pea plants to discover the basic rules of heredity.

Bosh, says historian Theodore Porter. These works are not the fount of genetics, but a rill distracting us from a much darker source: the statistical study of heredity in asylums for people with mental illnesses in late-eighteenth- and early-nineteenth-century Britain, wider Europe and the United States. There, “amid the moans, stench, and unruly despair of mostly hidden places where data were recorded, combined, and grouped into tables and graphs”, the first systematic theory of mental illness as hereditary emerged.

For more than 200 years, Porter argues in Genetics in the Madhouse, we have failed to recognize this wellspring of genetics — and thus to fully understand this discipline, which still dominates many individual and societal responses to mental illness and diversity.

The study of heredity emerged, Porter argues, not as a science drawn to statistics, but as an international endeavour to mine data for associations to explain mental illness. Few recall most of the discipline’s early leaders, such as French psychiatrist, or ‘alienist’, Étienne Esquirol; and physician John Thurnam, who made the York Retreat in England a “model of statistical recording”. Better-known figures, such as statistician Karl Pearson and zoologist Charles Davenport — both ardent eugenicists — come later.

Inevitably, study methods changed over time. The early handwritten correlation tables and pedigrees of patients gave way to more elaborate statistical tools, genetic theory and today’s massive gene-association studies. Yet the imperatives and assumptions of that scattered early network of alienists remain intact in the big-data genomics of precision medicine, asserts Porter. And whether applied in 1820 or 2018, this approach too readily elevates biology over culture and statistics over context — and opens the door to eugenics.

In 2018 Saletan Watched Watson Die On The Race And IQ Hill And Chose The Better Part Of Valor

Slate |  The race-and-IQ debate is back. The latest round started a few weeks ago when Harvard geneticist David Reich wrote a New York Times op-ed in defense of race as a biological fact. The piece resurfaced Sam Harris’ year-old Waking Up podcast interview with Charles Murray, co-author of The Bell Curve, and launched a Twitter debate between Harris and Vox’s Ezra Klein. Klein then responded to Harris and Reich in Vox, Harris fired back, and Andrew Sullivan went after Klein. Two weeks ago, Klein and Harris released a two-hour podcast in which they fruitlessly continued their dispute.

I’ve watched this debate for more than a decade. It’s the same wreck, over and over. A person with a taste for puncturing taboos learns about racial gaps in IQ scores and the idea that they might be genetic. He writes or speaks about it, credulously or unreflectively. Every part of his argument is attacked: the validity of IQ, the claim that it’s substantially heritable, and the idea that races can be biologically distinguished. The offender is denounced as racist when he thinks he’s just defending science against political correctness.

I know what it’s like to be this person because, 11 years ago, I was that person. I saw a comment from Nobel laureate James Watson about the black-white IQ gap, read some journal articles about it, and bought in. That was a mistake. Having made that mistake, I’m in no position to throw stones at Sullivan, Harris, or anyone else. But I am in a position to speak to these people as someone who understands where they’re coming from. I believe I can change their thinking, because I’ve changed mine, and I’m here to make that case to them. And I hope those of you who find this whole subject vile will bear with me as I do.

Here’s my advice: You can talk about the genetics of race. You can talk about the genetics of intelligence. But stop implying they’re the same thing. Connecting intelligence to race adds nothing useful. It overextends the science you’re defending, and it engulfs the whole debate in moral flames.

I’m not asking anyone to deny science. What I’m asking for is clarity. The genetics of race and the genetics of intelligence are two different fields of research. In his piece in the Times, Reich wrote about prostate cancer risk, a context in which there’s clear evidence of a genetic pattern related to ancestry. (Black men with African ancestry in a specific DNA region have a higher prostate cancer risk than do black men with European ancestry in that region.) Reich steered around intelligence where, despite racial and ethnic gaps in test scores, no such pattern has been established.

It’s also fine to discuss the genetics of IQ—there’s a serious line of scientific inquiry around that subject—and whether intelligence, in any population, is an inherited social advantage. We tend to worry that talk of heritability will lead to eugenics. But it’s also worth noting that, to the extent that IQ, like wealth, is inherited and concentrated through assortative mating, it can stratify society and undermine cohesion. That’s what much of The Bell Curve was about.

The trouble starts when people who write or talk about the heritability of intelligence extend this idea to comparisons between racial and ethnic groups. Some people do this maliciously; others don’t. You can call the latter group naïve, credulous, or obtuse to prejudice. But they might be open to persuasion, and that’s my aim here. For them, the chain of thought might go something like this: Intelligence is partly genetic, and race is partly genetic. So maybe racial differences on intelligence tests can be explained, in part, by genetics.

taboo "genetics"

Nature | Growing up in the college town of Ames, Iowa, during the 1970s, Stephen Hsu was surrounded by the precocious sons and daughters of professors. Around 2010, after years of work as a theoretical physicist at the University of Oregon in Eugene, Hsu thought that DNA-sequencing technology might finally have advanced enough to help to explain what made those kids so smart. He was hardly the first to consider the genetics of intelligence, but with the help of the Chinese sequencing powerhouse BGI in Shenzhen, he planned one of the largest studies of its kind, aiming to sequence DNA from 2,000 people, most of whom had IQs of more than 150.

He hadn't really considered how negative the public reaction might be until one of the study's participants, New York University psychologist Geoffrey Miller, made some inflammatory remarks to the press. Miller predicted that once the project turned up intelligence genes, the Chinese might begin testing embryos to find the most desirable ones. One article painted the venture as a state-endorsed experiment, selecting for genius kids, and Hsu and his colleagues soon found that their project, which had barely begun, was the target of fierce criticism.

There were scientific qualms over the value of Hsu's work (see Nature 497, 297–299; 2013). As with other controversial fields of behavioural genetics, the influence of heredity on intelligence probably acts through myriad genes that each exert only a tiny effect, and these are difficult to find in small studies. But that was only part of the reason for the outrage. For decades, scientists have trodden carefully in certain areas of genetic study for social or political reasons.

At the root of this caution is the widespread but antiquated idea that genetics is destiny — that someone's genes can accurately predict complex behaviours and traits regardless of their environment. The public and many scientists have continued to misinterpret modern findings on the basis of this — fearing that the work will lead to a new age of eugenics, preemptive imprisonment and discrimination against already marginalized groups.

“People can take science and assume it is far more determinative than it is — and, by making that assumption, make choices that we will come to regret as a society,” says Nita Farahany, a philosopher and lawyer at Duke University School of Law in Durham, North Carolina.

But trying to forestall such poor choices by drawing red lines around certain areas subverts science, says Christopher Chabris of Union College in Schenectady, New York. Funding for research in some areas dries up and researchers are dissuaded from entering promising fields. “Any time there's a taboo or norm against studying something for anything other than good scientific reasons, it distorts researchers' priorities and can harm the understanding of related topics,” he says. “It's not just that we've ripped this page out of the book of science; it causes mistakes and distortions to appear in other areas as well.”

Here, Nature looks at four controversial areas of behavioural genetics to find out why each field has been a flashpoint, and whether there are sound scientific reasons for pursuing such studies.

The Burden of Proof Sits on the Party Making the Affirmative Statement

theatlantic |  Jedidiah Carlson was googling a genetics research paper when he stumbled upon the white nationalist forum Stormfront. Carlson is graduate student at the University of Michigan, and he is—to be clear—absolutely not a white nationalist. But one link lead to another and he ended up reading page after page of Stormfront discussions on the reliability of 23andMe ancestry results and whether Neanderthal interbreeding is the reason for the genetic superiority of whites. Obsession with racial purity is easily channeled, apparently, into an obsession with genetics.

Stormfront has been around since the 90s, which means it’s been around for the entirety of the genomic revolution. The major milestones in human genetics—sequencing of the first human genome, genetic confirmation that humans came out of Africa, the first mail-in DNA ancestry tests—they’re all there, refracted through the lens of white nationalism. Sure, the commentators sometimes disagreed with scientific findings or mischaracterized them, but they could also be serious about understanding genetics. “The threads would turn into an informal tutoring session and journal club,” observes Carlson. “Some of the posters have a really profound understanding of everyday concepts in population genetics.”

We Won't Engineer Superhumans Any Time Soon...,

aeon |  A paper published in Nature Genetics in 2017 reported that, after analysing tens of thousands of genomes, scientists had tied 52 genes to human intelligence, though no single variant contributed more than a tiny fraction of a single percentage point to intelligence. As the senior author of the study Danielle Posthuma, a statistical geneticist at the Vrije Universiteit (VU) Amsterdam and VU University Medical Center Amsterdam, told The New York Times, ‘there’s a long way to go’ before scientists can actually predict intelligence using genetics. Even so, it is easy to imagine social impacts that are unsettling: students stapling their genome sequencing results to their college applications; potential employers mining genetic data for candidates; in-vitro fertilisation clinics promising IQ boosts using powerful new tools such as the genome-editing system CRISPR-Cas9.

Some people are already signing on for this new world. Philosophers such as John Harris of the University of Manchester and Julian Savulescu of the University of Oxford have argued that we will have a duty to manipulate the genetic code of our future children, a concept Savulescu termed ‘procreative beneficence’. The field has extended the term ‘parental neglect’ to ‘genetic neglect’, suggesting that if we don’t use genetic engineering or cognitive enhancement to improve our children when we can, it’s a form of abuse. Others, like David Correia, who teaches American Studies at the University of New Mexico, envisions dystopian outcomes, where the wealthy use genetic engineering to translate power from the social sphere into the enduring code of the genome itself.

Such concerns are longstanding; the public has been on guard about altering the genetics of intelligence at least since scientists invented recombinant DNA. As long ago as the 1970s, David Baltimore, who won a Nobel Prize, questioned whether his pioneering work might show that ‘the differences between people are genetic differences, not environmental differences’.

I say, dream on. As it turns out, genes contribute to intelligence, but only broadly, and with subtle effect. Genes interact in complex relationships to create neural systems that might be impossible to reverse-engineer. In fact, computational scientists who want to understand how genes interact to create optimal networks have come up against the kind of hard limits suggested by the so-called travelling salesperson problem. In the words of the theoretical biologist Stuart Kauffman in The Origins of Order (1993): ‘The task is to begin at one of N cities, travel in turn to each city, and return to the initial city by the shortest total route. This problem, so remarkably simple to state, is extremely difficult.’ Evolution locks in, early on, some models of what works, and hammers out refining solutions over millennia, but the best computer junkies can do to draw up an optimal biological network, given some input, is to use heuristics, which are shorthand solutions. The complexity rises to a new level, especially since proteins and cells interact at higher dimensions. Importantly, genetics research is not about to diagnose, treat or eradicate mental disorders, or be used to explain the complex interactions that give rise to intelligence. We won’t engineer superhumans any time soon.

about that practice making perfect....,

sciencedaily |  Mom or dad may have driven you to cello rehearsal all those years, but you can also thank your genes for pushing you to practice, according to new research led by a Michigan State University professor. 

Genetics and environment work together to help people become accomplished musicians, finds the study of 850 sets of twins. It's another arrow in the quiver of the argument that both nature and nurture play a role in developing expertise.

"The nature vs. nurture debate has raged since the beginning of psychology," said Zach Hambrick, MSU professor of psychology. "This makes it very clear that it's both. Not only in the sense that both nature and nurture contribute, but that they interact with each other."

The study breaks new ground in ascertaining the specific roles of genes. Essentially, it found:

• Accomplished musicians practiced much more than those who weren't accomplished.
• That propensity to practice was fueled partly by genetics, which the researchers were able to establish by comparing identical twins, who share 100 percent of their genes, with fraternal twins, who share 50 percent of their genes. The finding suggests genetics influence the sorts of activities we pursue.
• When it came to music accomplishment, genes had a bigger influence on those who practiced than those who didn't.

Writers such as Malcolm Gladwell argue that experts are almost entirely "made" and that a lack of innate ability can be overcome with enough training. The way to master that cello, in other words, is to practice for at least 10,000 hours, as past research has suggested.

But the new study challenges that theory by showing genes had a major contribution on the musicians who practiced and became successful. For those who didn't practice, there was essentially no genetic contribution.

"Contrary to the view that genetic effects go away as you practice more and more," Hambrick said, "we found that genes become more important in accounting for differences across people in music performance as they practice."

essence has no rights absolute capitalism is bound to acknowledge?

Quadrant |  Despite warnings by moral conservatives, advances in genetics and reproductive technology have created the conditions for a consumer-driven mass eugenics industry. Like it or not, science has is about to pose a slather of moral, ethical and societal dilemmas

 A legal, social and biological revolution is taking place worldwide without much serious thinking of the consequences. Consider this: in Britain the House of Commons recently approved the use of “three-parent IVF” to remove defective mitochondrial DNA from babies.[1]

 

Each year in Britain about 100 children are born with mutated mitochondrial DNA, resulting in about ten cases of fatal disease to the liver, nerves or heart. A new in vitro fertilisation (IVF) technique developed at the University of Newcastle allows doctors to replace a mother’s defective mitochondrial DNA with that of a healthy donor, presumably using pre-implantation sequencing and microscopic operation on the zygote. Mitochondrial DNA does not affect appearance, personality or intelligence, and it reduces kinship—genetic similarity—by only about 1 per cent. Still, the resulting child, though its nuclear DNA would come from its main parents, would have three parents.

Critics warned that this would set society off down a slippery slope to eugenics and “designer babies”. A government official, the “British Fertility Regulator”, replied to this warning with the observation that most people support the therapy. This was intended to assuage the concerns expressed. In fact it would seem to confirm them, since widespread support for a product or service indicates a readiness to adopt it. Sure enough, though there had been little public discussion in advance of the Commons debate, the new techniques were nonetheless approved by a large parliamentary majority. Australian scientists have since called for the British policy to be emulated.[2]

Despite half a century of warnings by moral conservatives, advances in genetics and reproductive technology have created the conditions for a consumer-driven mass eugenics industry. Here is the Oxford dictionary definition of “Eugenics”: “the science of improving a population by controlled breeding to increase the occurrence of desirable heritable characteristics”. It has a bad historical reputation because authoritarian governments have denied civil liberties in the name of eugenics. But as we shall see, both the definition and the reputation of eugenics have been overtaken by advances in science, medicine and marketing. Eugenics has since reappeared in many countries in the form of voluntary genetics counselling—a medical service provided to help parents avoid genetic disorders in their children[3]; and IVF has become a sizeable industry that offers parents the genetic screening of embryos and other eugenic choices.

Genetic improvement is becoming a market phenomenon—a situation discernible as long ago as the 1980s when Daniel Kevles, the leading historian of eugenics in the USA, quoted a biotechnology expert thus: “‘Human improvement’ is a fact of life, not because of the state … but because of consumer demand.”[4]

ruining genetics

TechnologyReview | In 2009, a group of researchers based in the Netherlands published a stunning study on the genetics of human height—stunning because it failed to find much of a genetic component in one of the most obvious of inherited human traits. The group analyzed 54 recently identified genetic locations that statistical analysis suggested were the main contributors to height and discovered that all of them together accounted for only 4 to 6 percent of the height variance in thousands of subjects.

The "missing heritability" in the height study typifies many recent research reports in which large-scale genetic screens, known as genome-wide association studies, have identified a multitude of genes (or at least genetic neighborhoods) that are statistically associated with a biological trait like height or a disease like obesity, yet account for mystifyingly little of its propensity to run in families. What is interesting about Nadeau's findings is that even though they diminish the significance of single genes and the DNA sequences of individuals, the research preserves—and in some ways increases—the significance of family history, since even the genetic variants that parents and grandparents don't pass down through DNA seem to influence the traits of their children or grandchildren.

Nadeau, who is silver-haired and cheerful, has been investigating what he sometimes calls "funky" genetic results ever since sophisticated sequencing technologies became available about 10 years ago. Some of those results have been hinted at by traditional epigenetics, which has begun to trace changes that are transmitted from one generation to the next in animals even though the basic DNA sequence remains the same. (For example, researchers have found that rats whose cognitive performance was improved through environmental factors can pass those improvements down to offspring.) But where that field has typically focused on chemical modifications of DNA, Nadeau's work expands the notion of epigenetics to include genetic effects that may be transmitted by different molecular players: ribonucleic acids (or RNAs), which exert powerful regulatory effects on DNA.

Key evidence for Nadeau's general views on unconventional modes of inheritance grew out of a dissertation project that one of his students began around 2001. In the long tradition of misguided doctoral advice, everyone told Man-Yee Lam that her project was boring, derivative, and hardly worth doing; for five or six years, nothing in her results suggested otherwise. The focus of the project was testicular germ-cell tumors. It didn't become clear until much later that the experiment represented the first rigorous demonstration of a transgenerational effect, showing that genetic variations in a parent—even though they were not passed along to offspring—could dramatically change disease risks in those offspring.

Lam set out to see if she could identify interactions between several "modifier" genes—interactions that would increase susceptibility to testicular cancer in mice. She found lots of these interactions (some quite strong), completed her thesis, and graduated. Then, when the group started to write up the results for publication, they noticed something very peculiar: the effects had also occurred in some of the control animals bred from the same original population. In other words, males that had been bred so as not to inherit the disease mutations still had a statistically significant increase in their risk for testicular cancer, simply because the parents possessed a particular genetic variant. The results suggested that there could be patches of DNA in parents that affected the traits of children, even if the children did not inherit this bit of parental DNA.

Even before publication in 2007, Nadeau began describing the findings—to decidedly mixed reviews. He says, "If they were geneticists, there were all sorts of technical [objections] or 'It's not fair to talk about this in public. This is just too complicating, too—it's too everything!' One even said, 'Are you trying to ruin genetics?' "

your "ism" is not my heredity

Video - Pokemon Black or White Black Nerd Rant.

Scientific American | Nothing about the field of IQ studies is free of political influence. It's naive to believe that any kind of research on a purported measure of individual merit could be politics-free in a self-proclaimed meritocracy with wide inequalities. Binet's original work was meant to determine which children should have access to additional educational resources. IQ scores are used occasionally to sort out "inappropriate" candidates for various jobs, including those whose IQs are too high for a role. IQ as a proxy for merit is used to argue that a group does or does not face discrimination in educational or career opportunities. This is all terribly political.

The question isn't whether there are politics surrounding this issue or where. They're everywhere. The question is where does the politics get in the way of the science? Again, the answers don't favor Pinker's view of a fatwa against genetic explanations of individual differences.

No one is pretending BGI Hong Kong doesn't exist or that it isn't looking for genes associated with variability in IQ scores. No one is issuing fatwas to stop them or even protesting their work. Some people are questioning IQ as a proxy for intelligence, but no one is saying the work shouldn't go forward until a better proxy is found. Similarly, no one is pretending that Paul Thompson isn't doing some fascinating work in brain imaging and variability in brain structure.

What is in dispute is the likelihood that genes will be found that account for any significant fraction of the variability found in human intelligence and whether the current literature on the topic is sufficient to predict that. Here is where disagreement with Thompson comes into play. He has published a number of papers with "genetics" in the title ("Genetic influences on brain structure," "Genetics of brain structure and intelligence," "Genetics of brain fiber architecture and intellectual performance") that involve no genetic testing whatsoever.

Instead, these studies rely on degree of relatedness (usually between identical and fraternal twins) as a measure of shared genes. This sounds reasonable, and to a degree it is. However, unless researchers can measure or control for the way genes unrelated to intelligence interact with the environment, these studies can't tell us how much variation in brain structure is due to shared genes that code for intelligence and shared genes that code for something else, such as illness that limits time in school. Until these studies are designed to look for genetic influences in addition to environmental influences, these studies are useless for their intended purpose. Fist tap Arnach.

as we harvest ever more genomes, one fact remains unshakeable...,

guardian |  Genetics has a blighted past with regards to race. Even today, important figures from its history – notably James Watson, co-discoverer of the double helix – express unsupportable racist views. The irony is that while Galton spawned a field with the intention of revealing essential racial differences between the peoples of the Earth, his legacy – human genetics – has shown he was wrong. Most modern geneticists are much less like Galton and more like Darwin. A dreadful book published last year by former New York Times science writer Nicholas Wade espoused views about racial differences seemingly backed by genetics. As with Watson, the reaction from geneticists was uniformly dismissive, that he had failed to understand the field, and misrepresented their work.

We now know that the way we talk about race has no scientific validity. There is no genetic basis that corresponds with any particular group of people, no essentialist DNA for black people or white people or anyone. This is not a hippy ideal, it’s a fact. There are genetic characteristics that associate with certain populations, but none of these is exclusive, nor correspond uniquely with any one group that might fit a racial epithet. Regional adaptations are real, but these tend to express difference within so-called races, not between them. Sickle-cell anaemia affects people of all skin colours because it has evolved where malaria is common. Tibetans are genetically adapted to high altitude, rendering Chinese residents of Beijing more similar to Europeans than their superficially similar neighbours. Tay-Sachs disease, once thought to be a “Jewish disease”, is as common in French Canadians and Cajuns. And so it goes on.

We harvest thousands of human genomes every week. Last month, the UK launched the 100,000 Genomes project to identify genetic bases for many diseases, but within that booty we will also find more of the secret history of our species, our DNA mixed and remixed through endless sex and continuous migration. We are too horny and mobile to have stuck to our own kind for very long.

Race doesn’t exist, racism does. But we can now confine it to opinions and not pretend that there might be any scientific validity in bigotry.

The Selfish Gene Is Actually A Crippling, Zero-Sum Theory Of Evolution

aeon  |  In late summer of 1976, two colleagues at Oxford University Press, Michael Rodgers and Richard Charkin, were discussing a book on evolution soon to be published. It was by a first-time author, a junior zoology don in town, and had been given an initial print run of 5,000 copies. As the two publishers debated the book’s fate, Charkin confided that he doubted it would sell more than 2,000 copies. In response, Rodgers, who was the editor who had acquired the manuscript, suggested a bet whereby he would pay Charkin £1 for every 1,000 copies under 5,000, and Charkin was to buy Rodgers a pint of beer for every 1,000 copies over 5,000. By now, the book is one of OUP’s most successful titles, and it has sold more than a million copies in dozens of languages, spread across four editions. That book was Richard Dawkins’s The Selfish Gene, and Charkin is ‘holding back payment in the interests of [Rodgers’s] health and wellbeing’.

In the decades following that bet, The Selfish Gene has come to play a unique role in evolutionary biology, simultaneously influential and contentious. At the heart of the disagreements lay the book’s advocacy of what has become known as the gene’s-eye view of evolution. To its supporters, the gene’s-eye view presents an unrivalled introduction to the logic of natural selection. To its critics, ‘selfish genes’ is a dated metaphor that paints a simplistic picture of evolution while failing to incorporate recent empirical findings. To me, it is one of biology’s most powerful thinking tools. However, as with all tools, in order to make the most of it, you must understand what it was designed to do.

When Charles Darwin first introduced his theory of evolution by natural selection in 1859, he had in mind a theory about individual organisms. In Darwin’s telling, individuals differ in how long they live and how good they are at attracting mates; if the traits that enhance these strengths are heritable, they will become more abundant over time. The gene’s-eye view discussed by Dawkins introduces a shift in perspective that might seem subtle at first, but which comes with rather radical implications.

The idea emerged from the tenets of population genetics in the 1920s and ’30s. Here, scientists said that you could mathematically describe evolution through changes in the frequency of certain genetic variants, known as alleles, over time. Population genetics was an integral part of the modern synthesis of evolution and married Darwin’s idea of gradual evolutionary change with a functioning theory of inheritance, based on Gregor Mendel’s discovery that genes were transmitted as discrete entities. Under the framework of population genetics, evolution is captured by mathematically describing the increase and decrease of alleles in a population over time.

The gene’s-eye view took this a step further, to argue that biologists are always better off thinking about evolution and natural selection in terms of genes rather than organisms. This is because organisms lack the evolutionary longevity required to be the central unit in evolutionary explanations. They are too temporary on an evolutionary timescale, a unique combination of genes and environment – here in this generation but gone in the next. Genes, in contrast, pass on their structure intact from one generation to the next, ignoring mutation and recombination. Therefore, only they possess the required evolutionary longevity. Traits that you can see, the argument goes, such as the particular fur of a polar bear or the flower of an orchid (known as a phenotype), are not for the good of the organism, but of the genes. The genes, and not the organism, are the ultimate beneficiaries of natural selection.

This approach has also been called selfish-gene thinking, because natural selection is conceptualised as a struggle between genes, typically through how they affect the fitness of the organism in which they reside, for transmission to the next generation. At an after-dinner speech at a conference banquet, Dawkins once summarised the key argument in limerick form:

An itinerant selfish gene
Said: ‘Bodies a-plenty I’ve seen.
You think you’re so clever,
But I’ll live for ever.
You’re just a survival machine.’

In this telling, evolution is the process by which immortal selfish genes housed in transient organisms struggle for representation in future generations. Moving beyond the poetry and making the point more formally, Dawkins argued that evolution involves two entities: replicators and vehicles, playing complementary roles. Replicators are those entities that copies are made of and that are transmitted faithfully from one generation to the next; in practice, this usually means genes. The second entity, vehicles, are where replicators are bundled together: this is the entity that actually comes into contact with the external environment and interacts with it. The most common kind of vehicle is the organism, such as an animal or a plant, though it can also be a cell, as in the case of cancer.

the invention of the jewish people

counterpunch | Perhaps the most persuasive source cited by Sand on the proselyte origins of Ashkenazi Jewry is Tel Aviv University linguist Paul Wexler, author of The Ashkenazic Jews: A Slavo-Turkic People in Search of a Jewish Identity  (and of The Non-Jewish Origins of the Sephardic Jews). Wexler argues that “the language known as Yiddish…developed in the bilingual Germano-Slavic lands in the 9th century as a Judaized form of Sorbian.” Sorbian is a Slavic language spoken today by about 50,000 people in southeast Brandenburg. “Yiddish is not a ‘form of German.’” The “tiny Jewish communities in the monolingual western German lands” cannot have been the basis of the millions of east European Jews. “Judeo-Sorbian underwent ‘re-lexification’…beginning with the 9th-10th centuries, but at the latest by the early 13th century.” “The result was…the grafting of [eastern] High German vocabulary…onto a Judeo-Sorbian syntax, phonology, phonotactics, and to some extent, morphotactics. Thus, despite its ‘German look,’ Yiddish remains a west Slavic language.” Modern Hebrew is also a Slavic language, not a “rebirth” of Old Semitic Hebrew, which is “impossible…because there are no native speakers to provide a native norm.” “Modern Hebrew simply embodies the syntax and sound system of the Eastern Yiddish language spoken by the first Modern Hebrew language planners in Ottoman Palestine, while its lexicon…was systematically replaced by Biblical and Mishnaic Hebrew vocabulary.”

Wexler argues from linguistic and other evidence “that the Ashkenazic Jews must have consisted of a mix of Greek, Balkan Romance and Balkan Slavic, Germano-Slavic and Turkic (Khazar, Avar) converts to Judaism and their descendants and only a minority of ethnic Jews—many of whom in all probability came from other parts of Europe rather than Palestine itself.” Wexler rejects the Khazar mass migration hypothesis on linguistic grounds, arguing that there was more conversion in place than migration. “Hence, contemporary Judaism is best defined not as the continuation of the Judaism which served as an antecedent of Christianity and Islam, but as a newly Judaized variant of European (mainly Slavic) paganism and Christianity…most of the features of Old Palestinian Judaism and Semitic Hebrew to be found in Ashkenazic ‘Judaism’ and Medieval Ashkenazic/Modern Israeli ‘Hebrew’ were latter borrowings rather than original inheritance [original emphasis].” This thesis has been obscured by philo-German and anti-Slavic chauvinism among scholars, Jewish and non-, of Ashkenazi Jewry, by disciplinary blinders, and by inertia.

Sand also considers Zionist racialism, from proto-Zionist Moses Hess, who “needed a good deal of racial theory to dream up the Jewish people,” to kibbutz godfather Arthur Ruppin’s “ideas about the Darwinist struggle of the ‘Jewish race’,” including consultations with “experts” in Nazi Germany, to the discreet attempt of Israeli genetics after 1948 “to discover a biological homogeneity among the Jews in the world” while investigating Jewish diseases, which revealed east European carriers of Tay-Sachs, but also Yemeni and Iraqi carriers of favism.  “Israel’s rule since 1967 over a growing non-Jewish population,” and concomitant need to “find an enclosing ethnobiological boundary” which highlights “the basic genetic similarities…and the small proportion of ‘alien’ genes in the genetic stock characteristic of Jews” led to “new findings” which “corroborated the literature about the dispersal and wanderings of the Jews from ancient times to the present. At last, biology confirmed history,” in the current pseudo-science of “Jewish genetics.”

Israel “became a world leader in the ‘investigation of the origins of populations’” even as “Israeli researchers…regularly blended historical mythologies and sociological assumptions with dubious and scanty genetic findings.” These included mitochondrial DNA purportedly showing that “40 per cent of all Ashkenazis in the world descend from four matriarchs (as in the Bible),” and a haplotype carried by 50 per cent of men named Cohen, which “proved” that “the Jewish priesthood was was indeed founded by a common ancestor thirty-three centuries ago.” This dreck appeared in publications such as Nature and the American Journal of Human Genetics, and was respectfully reported in Haaretz and elsewhere, but rarely skepticism or contrary findings. “Yet so far, no research had found unique and unifying characteristics of Jewish heredity based on a random sampling of genetic material whose ethnic origin is not known in advance…after all the costly ‘scientific’ endeavors, a Jewish individual cannot be defined by any biological criteria whatsoever.”

Sand’s account of Judaism, from exclusive Israelite genealogy, to Hellenic proselytizing, to proselytizing and conversion on the margins of Christianity, in Arabia, North Africa, Spain, and among the Khazars and the Slavs, to defensive introversion amidst the final triumph of Christianity, is the interesting and compelling story of a religious minority subject to normal historical forces.

The contrary view of the unitary Jewish people expelled from its homeland, and wandering aloof in exile for two thousand years, until beginning its return in the late 19th c., is a reactionary myth which Zionism has deployed to conquer Palestine and compel support for it. The myth prevails unchecked today not only in Israel but worldwide. Nothing “has challenged the fundamental concepts that were formed in the late nineteenth and early twentieth centuries.” Advances in the study of nations and nationalism have not “affected the departments of the ‘History of the People of Israel’ (aka Jewish history) in Israeli universities.

if violence is in your genes, ta loco...,

theverge | In 2009, an Italian court reduced a murderer's sentence by one year because doctors had identified a gene in the defendant's DNA, called MAOA, that had been linked to violent behavior. The ruling was controversial and some scientists objected to the sentence reduction. "MAOA findings have been generally used in murder trials, sometimes to suggest diminished capacity of the defendant to premeditate his criminal behavior," but most often to reduce a sentence, writes Paul Appelbaum, a psychiatrist at Columbia University, in an essay published today in Neuron. In the essay, Appelbaum explains that genetic evidence demonstrating a defendant's predisposition for antisocial behavior or mental illness is showing up in courtrooms at an ever-quickening pace. And that pace, he warns, might be outrunning the legal system's ability to interpret it.

"Premature introduction of genetic evidence in court carries a number of risks," said Appelbaum in an email to The Verge. "The most obvious is that the purported associations [between genetics and behavior] are not real and will be disproved over time." But even the most replicated and widely accepted findings, he said, can be misinterpreted by judges and jurors.

In the case of the Italian court, the gene that was used has indeed been associated with impulsiveness and criminal behavior among men in a number of studies. Moreover, childhood maltreatment has been linked to lower MAOA activity — providing a great example of how a genetic predisposition can be triggered by environmental factors. Most experts agree, however, that even evidence as strong as that surrounding MAOA shouldn't be used to absolve someone of responsibility for their actions. "The major mistake the people make is to think that if you've identified a cause, it must mean that people are excused or mitigated," says Stephen Morse, a professor of law at the University of Pennsylvania who has written on the subject. But that isn't how the law works. Only a limited number of impairments — such as failing to appreciate the wrongfulness of one's acts — are considered exculpatory. So "if someone is a rational agent," Morse says, "I don't care if they have bad genetics."

Jorim Tielbeek, a neuroscientist and criminologist at VU Medical Center Amsterdam who has studied the effects of genetics on antisocial behavior, agrees with Morse, stating in an email to The Verge that a "higher genetic liability towards committing a crime doesn't necessarily mean a lessened responsibility." Although scientists have made links between certain genes and antisocial behavior, Tielbeek says, there is "no clear predictive relationship between a single gene and a criminal act — especially since hundreds of genes are involved in criminal behavior, and that each have a very small effect."

The Basques May Not Be Who We Think They Are

discover |  In terms of historical genetics these assumptions result in the Basque population be used as a “reference” for the indigenous component of the European ancestry which reaches back to the Last Glacial Maximum, and expanded from the Iberian refugium after the ice retreated. One of reasons for the assumption of Basque antiquity & purity are genetic peculiarities of the Basques. Foremost among them is that the Basque seem to have the highest frequency of Rh- in the world, primarily because of the high frequency of the null allele within the population (it is a recessively expressed trait). Rh- is very rare outside of Europe, but its frequency exhibits a west-east gradient even within the continent. It has been suggested that the mixing of Rh- and Rh+ blood groups reflects the mixing of hunter-gatherers and farmers in after the Ice Age. The map above the illustrates the frequencies of this trait, and you can see how the Basque region is cordoned off. It’s an old map because blood group were widely collected in the early 20th century. Because of the early knowledge of this heritable trait you have a lot of weird anthropological theories which hinge around blood group genetics having emerged in the early 20th century. But even as late as the mid-90s L. L. Cavalli-Sforza reported in The History and Geography of Human Genes using classical markers that the Basques exhibited some distinctiveness. Over the years with the rise of Y and mtDNA phylogenetics this distinctiveness has taken a hit. I think the data have a tendency of confirming expectations, or it is often interpreted as such. But the recent story of the R1b haplogroup strongly implied that the Basques are no different from other west Europeans, and are likely the descendants of Neolithic farmers themselves! A new paper in Human Genetics supports the contention that the Basque are just like other Europeans, A genome-wide survey does not show the genetic distinctiveness of Basques:

Basques are a cultural isolate, and, according to mainly allele frequencies of classical polymorphisms, also a genetic isolate. We investigated the differentiation of Spanish Basques from the rest of Iberian populations by means of a dense, genome-wide SNP array. We found that F ST distances between Spanish Basques and other populations were similar to those between pairs of non-Basque populations. The same result is found in a PCA of individuals, showing a general distinction between Iberians and other South Europeans independently of being Basques. Pathogen-mediated natural selection may be responsible for the high differentiation previously reported for Basques at very specific genes such as ABO, RH, and HLA. Thus, Basques cannot be considered a genetic outlier under a general genome scope and interpretations on their origin may have to be revised. 

huff whoops wade like he stole something..., MUCH more impressed with this chick than I am with myself!

violentmetaphors |  To begin with, Wade can’t provide a clear definition of “race.” He tries to rely instead on loose associations rather than definitive characteristics, which forces him to conclude both that physical traits define race but that the traits can vary from person to person: “races are identified by clusters of traits, and to belong to a certain race, it’s not necessary to possess all of the identifying traits” (p. 121).

With such a shifty, casual footing, it’s no surprise that Wade’s conclusions are unsound. He can’t keep the number of races straight:

Wade can’t settle on a definite number of races because he can’t come up with a consistent, rigorous definition of what “race” means. He uses terms like “major race”, “race”, “subrace”, “group”, or “population,” but doesn’t provide any serious, objective ways to distinguish between these terms for arbitrary groupings of people arbitrary groups.

Rather than just announcing his subjective opinions about race, Wade wants to ground them in science. He tries to use genetics: “Such an arrangement, of portioning human variation into five continental races, is to some extent arbitrary. But it makes practical sense. The three major races are easy to recognize. The five-way division matches the known events of human population history. And, most significant of all, the division by continent is supported by genetics.” (p. 94)

To support his claim, Wade relies heavily on a 2002 paper (by Rosenberg et al.) that used a program called structure to group people based on similarities in markers distributed across the genome. He notes that the program identified five major clusters in this 2002 study, which corresponded to the major geographic regions (Africa, Eurasia, East Asia, Oceania, and America) of the world. Therefore, Wade argues, these results clearly show that humans are divided up into racial categories that match continents.

Charles Murray, author of The Bell Curve, who recently reviewed Wade’s book in the Wall Street Journal, agrees:

A computer given a random sampling of bits of DNA that are known to vary among humans—from among the millions of them—will cluster them into groups that correspond to the self-identified race or ethnicity of the subjects. This is not because the software assigns the computer that objective but because those are the clusters that provide the best statistical fit.

But Wade and Murray are both wrong. Structure didn’t simply identify five clusters. It also identified two, three, four, six, and seven clusters. (Rosenberg et al. 2002 actually identified up to 20 divisions, but 1-7 are the primary ones they discussed. They also divided their worldwide sample up into regions, and then ran structure within those regions, to look at more fine-scale population structure.)

Why? Researchers using structure have to define the number (K) of clusters in advance, because that’s what the program requires. The program was designed to partition individuals into whatever pre-specified number of clusters the researcher requests, regardless of whether that number of divisions really exists in nature. In other words, if the researcher tells structure to divide the sampled individuals into 4 clusters, structure will identify 4 groups no matter what–even if there is really only 1 group, or even if there are really 14 groups.

So, when Rosenberg et al. (2002) told structure to use K=6? They got six clusters, with the sixth corresponding to a northwestern Pakistani group, the Kalash. Does this make the Kalash a separate race? Wade doesn’t think so. When they told structure to use K=3? They got three clusters back, corresponding to Africa, Europe/Middle East/South Asia, and East Asia/Oceania/Americas. So are Native Americans and Australians not separate races? Rosenberg et al. never published any statistical evidence that justifies picking 5 races instead of 7, or 4, or 2 (although such methods do exist–see Bolnick et al. 2008). Wade seems to like K=5 simply because it matches his pre-conceived notions of what race should be:

“It might be reasonable to elevate the Indian and Middle Eastern groups to the level of major races, making seven in all. But then many more subpopulations could be declared races, so to keep things simple, the five-race, continent-based scheme seems the most practical for most purposes.” (p. 100)

Practical. Simple. Wade wants us to cut up human diversity into five races not because that’s what the statistical analyses show, but because thinking about it as a gradient is hard.

Wade isn’t even using the tools of genetics competently. The authors of the paper he relied on, as well as subsequent studies, showed that different runs of the program with the same data can even produce different results (Bolnick, 2008). Structure’s results are extremely sensitive to many different factors, including models, the type and number of genetic variants studied, and the number of populations included in the analysis (Rosenberg et al. 2005). When Rosenberg et al. (2005) expanded the 2002 dataset to include more genetic markers for the same population samples, they identified a somewhat different set of genetic clusters when K=6 (Native Americans were divided into two clusters and the Kalash of Central/South Asia did not form a separate cluster). In fact, Rosenberg et al. (2005) explicitly said:

“Our evidence for clustering should not be taken as evidence of our support of any particular concept of ‘biological race.’”

Finally, the creators of structure themselves caution that it will produce rather arbitrary clusters when sampled populations have been influenced by gene flow that is restricted by geographic distance (i.e. where more mating occurs between members of nearby populations than between populations that are located farther apart, a pattern we geneticists refer to as isolation by distance). As this pattern applies to the majority of human populations, it makes the results of structure problematic and difficult to interpret in many cases. These limitations are acknowledged by anthropological geneticists and population biologists, who interpret the results of structure cautiously. It’s very telling that Wade, a science reporter, chose to ignore the interpretations of the experts in favor of his own.

I - Why Has David Mills Internalized Racist Pseudo-Science?

This past week, I asked the journalist and screenwriter David Mills the following question;

“The main question I’d like answered is how precisely did you get hoodwinked and bamboozled to serve as a host and conduit of racist thought David? What was the intrinsic appeal of IQ heritability pseudo-science that made you buy into it hook, line, and sinker?”

I gather from the response posted at his blog, that the origin of his belief in the genetic determination of IQ consists of three parts ;

1. An episode of Good Times
2. Murray and Herrnstein's The Bell Curve
3. Tryon's (1940) selective breeding for maze "Bright" and "Dull" mice - which was the basis for Cooper and Zubek's 1958 demonstration of genetic interactionism. (the link is to a recent analysis of the complexity involved with a genetic interpretation of "selective breeding")
   

Additional influences may pertain - and I encourage David to state these - however, these are the three he cited. In addition to the above, he managed to ask one factually distorted question of me;

So, at least in Gould’s case, we’ve narrowed down the area of interest: figuring out just how major or minor is the acknowledged influence of genetics on intelligence. Craig Nulan won’t grant even that much. (I wonder why?)

- to which I'll respond very simply - I'm an interactionist. The interactionist consensus prevails in science today rather than the popularly held dualism of nature/nurture and their effect on physiological or behavioral phenotypes.

Neither the exclusive or the additive models make any biological sense whatsoever. No genetic factor can properly be studied independent of, or just in addition to, the environment. The same is true for the environment. The concept of the environment includes a wide variety of very different causes and factors, from the genomic environment of a gene, over its chromatin packaging and cellular context, up to ecological, social and cultural influences over the whole organism. In addition to the complex facts pertaining to genetic science, I reject the genetic determinism of IQ because;

1. I know exactly what the history and politics of IQ measurement in America
2. I know what IQ measures and doesn't measure
3. I know that science has had no part whatsoever in the construction of this uniquely value-laden psychometric enterprise
   

The politically motivated dualisms which ascribe aspects of behavior or the underlying cognitive mechanisms to either innate/genetic or acquired/environmental causes - drastically confuses the issue and leads to objective error by introducing he following error sources;

1. Political bias
2. Lack of basic biological knowledge in political science and psychology.
3. Misunderstanding of what counts as an explanation

Explanations may be in terms of;

causal mechanisms

developmental processes

function and fitness values

evolutionary origin of the behavior in question

The interactionist scientific examination of genetics will continue, hopefully with a minimum of politically motivated distortion from the popular political controversy over nature versus nurture.

A little background housekeeping is in order before I proceed with my analysis of the question du jour - why has David Mills internalized racist pseudo-science?

First - I was in the interdisciplinary AI program at MIT and I studied neurophysiology and computer science and was awarded the Thomas Marill scholarship for AI my senior year.

Second - Stephen J. Gould was not an influence on my thinking in this area - at all. My primary influence was Dr. Stephan Chorover. Unlike Gould an anthropologist, Murray an alleged political scientist, or others involved in the popular political discourse - Chorover is a neuropsychologist who served for many years on the board of directors of the National Institutes of Mental Health (NIMH). He wrote the book From Genesis to Genocide (1979) in part to expose experimentation and activities funded by the NIMH that he felt violated fundamental human rights.