The joy of Turkheimer

I've been a fan of psychologist Eric Turkheimer's work for some time.

In a previous post I discussed the following article, which shows that in the case of extreme poverty (by US standards) the genetic heritability of intelligence is drastically reduced. It is the first study I had heard of which really showed a clear case of nonlinear response to environment (excluding cases of severe malnutrition). See related discussion of heritability and regression here.

Turkheimer, E., Haley, A., D'Onofrio, B., Waldron, M & Gottesman, I. (2003). Socioeconomic status modifies heritability of IQ in young children. Psychological Science, 14, 623-628.

In this paper he discusses interactions between genes and environment, and why they make social science hard:

Turkheimer, E. (2004). Spinach and Ice Cream: Why Social Science Is So Difficult. In. L. DiLalla (Ed). Behavior genetics principles: Perspectives in development, personality, and psychopathology. (pp. 161-189). Washington, DC, US: American Psychological Association.

Recently, he gave the following talk at Stanford, emphasizing how the problems faced by state of the art genomic science (e.g., genome wide association or gwa studies) mirror those of social science. That is, outcomes depend nonlinearly on a large number of (possibly correlated) causes. This is the "Gloomy Prospect" first referred to by psychologist Robert Plomin. I highly recommend the audio version -- Turkheimer is a good speaker and the discussion at the end is interesting.

Gloomy Prospect Wins

slides (ppt) , iTunes audio

The contemporary era has seen a convergence of genomic technology and traditional social scientific concerns with complex human individual differences. Rather than finally turning social science into a replicable hard-scientific enterprise, genomics has gotten bogged down in the long-standing frustrations of social science. A recent report of an extensive genome wide association study of human height demonstrates the profound difficulties of explaining uncontrolled human variation at a genomic level. The statistical technologies that have been brought to bear on the problem of genomic association are simply modifications of similar methods that have been used by social scientists for decades, with little success. The motivation for the statistical methods in genomics is the same as it is in traditional social science: An attempt to discern linear causation in complex systems when experimental control is not possible.

In the talk Turkheimer gives the following definition of social science, which emphasizes why it is hard:

Social science is the attempt to explain the causes of complex human behavior when:

There are a large number of potential causes.

The potential causes are non-independent.

Randomized experimentation is not possible.

He proposes that genomics will also be hard for similar reasons. Final slide:

The question is not whether there are correlations to be found between individual genes and complex behavior— of course there are—but instead whether there are domains of genetic causation in which the gloomy prospect does not prevail, allowing the little bits of correlational evidence to cohere into replicable and cumulative genetic models of development. My own prediction is that such domains will prove rare indeed, and that the likelihood of discovering them will be inversely related to the complexity of the behavior under study.

Tiger mothers and behavior genetics

Everyone seems to want to know what I think about the WSJ excerpt Why Chinese Mothers Are Superior, from Amy Chua's new book Battle Hymn of the Tiger Mother. See here for some discussion on Quora.

When I first read the piece I thought Chua sounded like a nutcase -- more extreme than even the nuttiest mothers of the other Chinese kids I had grown up with. Later I realized that the excerpt is not from a parenting book, but rather a memoir, and that Chua is making fun of her younger self in the excerpted chapter. See this interview with Leonard Lopate for more nuanced comments from Chua, and this NYTimes article.

The WSJ excerpt has been widely discussed, but I have yet to see anyone point out what the real data says about parents' ability to shape their children (other than by passing on their genes). See here for a long post I wrote just over a year ago on the subject:

In what may have been the most influential article ever written in the field of developmental behavior genetics, Plomin and Daniels (1987) reviewed evidence that a substantial portion of the variability in behavioral outcomes could not be explained by the additive effects of genotype or the environmental influences of families. They suggested that this residual term, which they called the nonshared environment, had been neglected by environmentally oriented researchers who assumed that the most important mechanisms of environmental action involved familial variables, like socioeconomic status [SES] and parenting styles, that are shared by siblings raised in the same home and serve to make siblings more similar to each other. Indeed, Plomin and Daniels argued, once genetic relatedness has been taken into account, siblings seem to be hardly more similar than children chosen at random from the population.

In other words, despite a lifetime of proximity, your adopted child may bear no more similarity to you (in terms of, e.g., intelligence) than someone selected at random from the general population. The shared family environment that your children (biological or adopted) experience has little or no measurable effect on their cognitive development. While there are environmental effects on intelligence (the highest estimates of heritability for adult IQ are around .8, and some would argue for a lower value; see here for Turkheimer's work suggesting low heritability in the case of severe deprivation), they seem to be idiosyncratic factors that can't be characterized using observable parameters such as the parents' SES, parenting style, level of education, or IQ. It is as if each child experiences their own random micro-environment, independent of these parental or family characteristics.

... The naive and still widely held expectation is that, e.g., high SES causes a good learning environment, leading to positive outcomes for children raised in such environments. However, the data suggests that what is really being passed on to the children is the genes of the parent, which are mainly responsible for, e.g., above average IQ outcomes in high SES homes ...

The implications are quite shocking, especially for two groups: high investment parents (because the ability of parents to influence their child's development appears limited) and egalitarians (because the importance of genes and the difficulty in controlling environmental effects seem to support the Social Darwinist position widely held in the previous century).

I have no doubt that certain narrow skill sets (like piano playing, swimming, baseball) can be transmitted through parental effort. But the evidence seems to point the other way for intelligence, personality, religiosity and social attitudes. Are Chinese moms such outliers that they constitute a counterexample to the large-statistics studies cited above? It was shown by Turkheimer that in cases of extreme deprivation heritability can decrease significantly. Can Tiger Moms have the same effect at the positive end of the spectrum?

As a parent myself I am used to the very sloppy epistemology that is par for the course: we did X to the kids when they were younger, which is why they are so Y now, or: if you do X to your kids now, they are more likely to be Y later. In reality, as with any complex system, it is nearly impossible to relate cause and effect in a remotely rigorous way. Nevertheless, the world is full of (often contradictory) parenting advice, and most parents are absurdly overconfident in their opinions.


See figure below (click to enlarge) from Sources of human psychological differences: Minnesota study of twins reared apart, Bouchard et al. (p. 142). MZA = MonoZygotic twins raised Apart, MZT = MonoZygotic twins raised Together. On the personality inventories the MZA and MZT correlations are almost identical -- even more so than for g. Shared family environment did not make twins more similar in personality, and only slightly more similar in IQ.




I stole this figure from Razib. It's from Turkheimer's paper showing that heritability of IQ increases with SES. Thus, Tiger Moms are fighting against diminishing returns: once the child's environment is already pretty good (say, 80th percentile SES), most variation is due to genetics. Note Turkheimer's results show more shared environmental variance than Plomin and Daniels found, but everything is consistent within errors. One objection to Turkheimer's results is that his measurements are of young children, and in other studies it is found that heritability increases with age -- perhaps because children gain more control over their lives and their genetic proclivities become more manifest.

Scientific Consensus on Cognitive Ability?

From the web site of the International Society for Intelligence Research (ISIR): a summary of the recent debate involving Charles Murray, Sam Harris, Richard Nisbett, Eric Turkheimer, Paige Harden, Razib Khan, Bo and Ben Winegard, Brian Boutwell, Todd Shackelford, Richard Haier, and a cast of thousands! ISIR is the main scientific society for researchers of human intelligence, and is responsible for the Elsevier journal Intelligence.

If you click through to the original, there are links to resources in this debate ranging from podcasts (Harris and Murray), to essays at Vox, Quillette, etc.

I found the ISIR summary via a tweet by Timothy Bates, who sometimes comments here. I wonder what he has to say about all this, given that his work has been cited by both sides :-)

TALKING ABOUT COGNITIVE ABILITY IN 2017

[ Click through for links. ]

2017 has already seen more science-lead findings on cognitive ability, and public discussion about the origins, and social and moral implications of ability, than we have had in some time, which should be good news for those seeking to understand and grow cognitive ability. This post brings together some of these events linking talk about differences in reasoning that are so near to our sense of autonomy and identity.

Middlebury
Twenty years ago, when Dr Charles Murray co-authored a book with Harvard Psychologist Richard Herrnstein he opened up a conversation about the role of ability in the fabric of society, and in the process made him famous for several things (most of which that he didn‘t say), but for which he, and that book – The Bell Curve – came to act as lightning rods, for the cauldron of mental compression of complex ideas, multiple people, into simpler slogans. 20 years on, Middlebury campus showed this has made even speaking to a campus audience fraught with danger.

Waking Up
In the wake of this disrupted meeting, Sam Harris interviewed Dr Murray in a podcast listened (and viewed on youtube) by and audience of many thousands, creating a new audience and new interest in ideas about ability, its measurement and relevance to modern society.

Vox populi
The Harris podcast lead a response in turn, published in Vox in which IQ, genetics, and social psychology experts Professors Eric Turkheimer, Paige Harden, and Richard Nisbett responded critically to the ideas raised (and those not raised) which they argue are essential for informed debate on group differences.

Quillette
And that lead in turn lead to two more responses: First by criminologists and evolutionary psychologists Bo and Ben Winegard, Brian Boutwell, and Todd Shackelford in Quillette, and a second post at Quillette, also supportive of the Murray-Harris interaction, from past-president of ISIR and expert intelligence research Professor Rich Haier.

And that lead to a series of planned essays by Professor Harden (first of which is now published here) and Eric Turkheimer (here). Each of these posts contains a wealth of valuable information, links to original papers, and they are responsive to each other: Addressing points made in the other posts with citations, clarifications, and productive disagreement where that still exists. They’re worth reading.

The answer, in 2017, may be a cautious “Yes, – perhaps we can talk about differences in human cognitive ability”. And listen, reply, and perhaps even reach a scientific consensus.

[ Added: 6/15 Vox response from Turkheimer et al. that doesn't appear to be noted in the ISIR summary. ]

In a recent post, NYTimes: In ‘Enormous Success,’ Scientists Tie 52 Genes to Human Intelligence, I noted that scientific evidence overwhelmingly supports the following claims:

0. Intelligence is (at least crudely) measurable
1. Intelligence is highly heritable (much of the variance is determined by DNA)
2. Intelligence is highly polygenic (controlled by many genetic variants, each of small effect)
3. Intelligence is going to be deciphered at the molecular level, in the near future, by genomic studies with very large sample size

I believe that, perhaps modulo the word near in #3, every single listed participant in the above debate would agree with these claims.

(0-3) above take no position on the genetic basis of group differences in measured cognitive ability. That is the where most of the debate is focused. However, I think it's fair to say that points (0-3) form a consensus view among leading experts in 2017.

As far as what I think the future will bring, see Complex Trait Adaptation and the Branching History of Mankind.

Intelligence, nature and nurture

Some new data on genetic vs environmental influences on IQ in this recent Times magazine article. Until recently, twins studies could only examine the effect of environmental variation within a limited range -- from working to upper class -- because very poor families are generally not allowed to adopt babies. The effect of family background has been found to recede to almost nothing by late adulthood in these twins studies, but the possibility that severe deprivation might have a stronger effect has not been ruled out. Recent investigations, as detailed below, have focused on very poor families and found a significant effect. We might characterize this as discovering the non-linear region of gene--family environment interaction :-)

NYTimes: A century’s worth of quantitative-genetics literature concludes that a person’s I.Q. is remarkably stable and that about three-quarters of I.Q. differences between individuals are attributable to heredity. This is how I.Q. is widely understood — as being mainly “in the genes” — and that understanding has been used as a rationale for doing nothing about seemingly intractable social problems like the black-white school-achievement gap and the widening income disparity. If nature disposes, the argument goes, there is little to be gained by intervening. In their 1994 best seller, “The Bell Curve,” Richard Herrnstein and Charles Murray relied on this research to argue that the United States is a genetic meritocracy and to urge an end to affirmative action. Since there is no way to significantly boost I.Q., prominent geneticists like Arthur Jensen of Berkeley have contended, compensatory education is a bad bet.

...When quantitative geneticists estimate the heritability of I.Q., they are generally relying on studies of twins. Identical twins are in effect clones who share all their genes; fraternal twins are siblings born together — just half of their genes are identical. If heredity explains most of the difference in intelligence, the logic goes, the I.Q. scores of identical twins will be far more similar than the I.Q.’s of fraternal twins. And this is what the research has typically shown. Only when children have spent their earliest years in the most wretched of circumstances, as in the infamous case of the Romanian orphans, treated like animals during the misrule of Nicolae Ceausescu, has it been thought that the environment makes a notable difference. Otherwise, genes rule.

Then along came Eric Turkheimer to shake things up. Turkheimer, a psychology professor at the University of Virginia, is the kind of irreverent academic who gives his papers user-friendly titles like “Spinach and Ice Cream” and “Mobiles.” He also has a reputation as a methodologist’s methodologist. In combing through the research, he noticed that the twins being studied had middle-class backgrounds. The explanation was simple — poor people don’t volunteer for research projects — but he wondered whether this omission mattered.

Together with several colleagues, Turkheimer searched for data on twins from a wider range of families. He found what he needed in a sample from the 1970’s of more than 50,000 American infants, many from poor families, who had taken I.Q. tests at age 7. In a widely-discussed 2003 article, he found that, as anticipated, virtually all the variation in I.Q. scores for twins in the sample with wealthy parents can be attributed to genetics. The big surprise is among the poorest families. Contrary to what you might expect, for those children, the I.Q.’s of identical twins vary just as much as the I.Q.’s of fraternal twins. The impact of growing up impoverished overwhelms these children’s genetic capacities. In other words, home life is the critical factor for youngsters at the bottom of the economic barrel. “If you have a chaotic environment, kids’ genetic potential doesn’t have a chance to be expressed,” Turkheimer explains. “Well-off families can provide the mental stimulation needed for genes to build the brain circuitry for intelligence.”

The uses of gloom

Omri Tal writes on the history of The Gloomy Prospect. Apparently, the term originally referred to non-shared environmental effects (see Random microworlds), before Turkheimer applied it to genetic causation.

Personally, I'm an optimist -- I believe in Pessimism of the Intellect but Optimism of the Will  :-)

Hi Steve,

Just to point out with regard to your recent interesting post.

1. The Gloomy Prospect is a term originally by Plomin and Daniels (1987). As Turkheimer (2000) notes:

Plomin and Daniels (1987) almost identified the answer to this question, but dismissed it as too pessimistic:

"One gloomy prospect is that the salient environment might be unsystematic, idiosyncratic, or serendipitous events such as accidents, illnesses, or other traumas . . . Such capricious events, however, are likely to prove a dead end for research. More interesting heuristically are possible systematic sources of differences between families. (p. 8)"

The gloomy prospect is true. Nonshared environmental variability predominates not because of the systematic effects of environmental events that are not shared among siblings, but rather because of the unsystematic effects of all environmental events…
-- But indeed, it is Turkheimer's paper that has made the term famous.

2. The Gloomy Prospect is predominately about the unsystematic 'nonshared environment', rather than about missing heritability. In the section you quote, he extends this notion to include unknown genetic factors, but it's not the "classic" use ;)

Two interesting papers by Omri, at his web page:

Tal O, 2013. Two Complementary Perspectives on Inter-Individual Genetic Distance. BioSystems. Volume 111, Issue 1, Pages 18–36

Tal O, 2012. Towards an Information-Theoretic Approach to Population Structure. Proceedings of Turing-100: The Alan Turing Centenary. p353-369

Kathryn Paige Harden Profile in The New Yorker (Behavior Genetics)

This is a good profile of behavior geneticist Paige Harden (UT Austin professor of psychology, former student of Eric Turkheimer), with a balanced discussion of polygenic prediction of cognitive traits and the culture war context in which it (unfortunately) exists.

Can Progressives Be Convinced That Genetics Matters? 

The behavior geneticist Kathryn Paige Harden is waging a two-front campaign: on her left are those who assume that genes are irrelevant, on her right those who insist that they’re everything. 

Gideon Lewis-Kraus

Gideon Lewis-Kraus is a talented writer who also wrote a very nice article on the NYTimes / Slate Star Codex hysteria last summer.

Some references related to the New Yorker profile:

1. The paper Harden was attacked for sharing while a visiting scholar at the Russell Sage Foundation: Game Over: Genomic Prediction of Social Mobility 

2. Harden's paper on polygenic scores and mathematics progression in high school: Genomic prediction of student flow through high school math curriculum 

3. Vox article; Turkheimer and Harden drawn into debate including Charles Murray and Sam Harris: Scientific Consensus on Cognitive Ability?

A recent talk by Harden, based on her forthcoming book The Genetic Lottery: Why DNA Matters for Social Equality

Regarding polygenic prediction of complex traits 

I first met Eric Turkheimer in person (we had corresponded online prior to that) at the Behavior Genetics Association annual meeting in 2012, which was back to back with the International Conference on Quantitative Genetics, both held in Edinburgh that year (photos and slides [1] [2] [3]). I was completely new to the field but they allowed me to give a keynote presentation (if memory serves, together with Peter Visscher). Harden may have been at the meeting but I don't recall whether we met. 

At the time, people were still doing underpowered candidate gene studies (there were many talks on this at BGA although fewer at ICQG) and struggling to understand GCTA (Visscher group's work showing one can estimate heritability from modestly large GWAS datasets, results consistent with earlier twins and adoption work). Consequently a theoretical physicist talking about genomic prediction using AI/ML and a million genomes seemed like an alien time traveler from the future. Indeed, I was.

My talk is largely summarized here:

On the genetic architecture of intelligence and other quantitative traits 

https://arxiv.org/abs/1408.3421 

How do genes affect cognitive ability or other human quantitative traits such as height or disease risk? Progress on this challenging question is likely to be significant in the near future. I begin with a brief review of psychometric measurements of intelligence, introducing the idea of a "general factor" or g score. The main results concern the stability, validity (predictive power), and heritability of adult g. The largest component of genetic variance for both height and intelligence is additive (linear), leading to important simplifications in predictive modeling and statistical estimation. Due mainly to the rapidly decreasing cost of genotyping, it is possible that within the coming decade researchers will identify loci which account for a significant fraction of total g variation. In the case of height analogous efforts are well under way. I describe some unpublished results concerning the genetic architecture of height and cognitive ability, which suggest that roughly 10k moderately rare causal variants of mostly negative effect are responsible for normal population variation. Using results from Compressed Sensing (L1-penalized regression), I estimate the statistical power required to characterize both linear and nonlinear models for quantitative traits. The main unknown parameter s (sparsity) is the number of loci which account for the bulk of the genetic variation. The required sample size is of order 100s, or roughly a million in the case of cognitive ability.

The predictions in my 2012 BGA talk and in the 2014 review article above have mostly been validated. Research advances often pass through the following phases of reaction from the scientific community:

1. It's wrong ("genes don't affect intelligence! anyway too complex to figure out... we hope")

2. It's trivial ("ofc with lots of data you can do anything... knew it all along")

3. I did it first ("please cite my important paper on this")

Or, as sometimes attributed to Gandhi: "First they ignore you, then they laugh at you, then they fight you, then you win.”

See also To Predict the Future it is useful to understand the Past.

Technical note: 

In 2014 I estimated that ~1 million genotype | phenotype pairs would be enough to capture most of the common SNP heritability for height and cognitive ability. This was accomplished for height in 2017. However, the sample size of well-phenotyped individuals is much smaller for cognitive ability, even in 2021, than for height in 2017. For example, in UK Biobank the cognitive test is very brief (~5 minutes IIRC, a dozen or so questions), but it has not even been administered to the full cohort as yet. In the Educational Attainment studies the phenotype EA is only moderately correlated (~0.3 ?) or so with actual cognitive ability.

Hence, although the most recent EA4 results use 3 million individuals [1], and produce a predictor which correlates ~0.4 with actual EA, the statistical power available is still less than what I predicted would be required to train a really good cognitive ability predictor.

In our 2017 height paper, which also briefly discussed bone density and cognitive ability prediction, we built a cognitve ability predictor roughly as powerful as EA3 using only ~100k individuals with the noisy UKB test data. So I remain confident that  ~million individuals with good cognitive scores (e.g., SAT, AFQT, full IQ test) would deliver results far beyond what we currently have available. We also found that our predictor, built using actual (albeit noisy) cognitive scores exhibits less power reduction in within-family (sibling) analyses compared to EA. So there is evidence that (no surprise) EA is more influenced by environmental factors, including so-called genetic nurture effects, than is cognitive ability.

A predictor which captures most of the common SNP heritability for cognitive ability might correlate ~0.5 or 0.6 with actual ability. Applications of this predictor in, e.g., studies of social mobility or educational success or even longevity using existing datasets would be extremely dramatic.

Low SES does not decrease heritability of cognitive ability (N=300k)

These researchers, from Stanford, Northwestern, and the University of Florida, analyze a large population of twins and siblings (~24k twins and ~300k children in total, born 1994-2002 in Florida). They find no evidence of SES (Socio-Economic Status) moderation of genetic influence on test scores (i.e., cognitive ability). The figure above shows the usual pattern of lower pairwise correlations in test performance between non-identical twins and ordinary sibs, consistent with strong heritability. (In figure, ICC = Intraclass Correlation = ratio of between-pair variance to total variance; SS/OS = Same/Opposite Sex.) The researchers find, via further analysis (see below), that lower SES does not decrease heritability. No large GxE effect at low SES.

Earlier work by Turkheimer and collaborators (with much smaller sample size) suggested that low SES can drastically reduce the genetic heritability of intelligence. Their result has been widely publicized, but over time evidence is accumulating against it.

Note that Economics Nobelist James J. Heckman is the editor at PNAS who handled this paper. Heckman is an expert statistician and one of the most highly cited researchers in the area of childhood education and human capital. He was also a vocal critic of The Bell Curve, but seems (now) to accept the validity of general intelligence as a construct, its heritability, and the difficulty of increasing intelligence through environmental intervention. He tends to focus on other, more trainable, factors that influence life success, such as (my interpretation) Conscientiousness, Rule Following, Pro-Sociality, etc. ("non-cognitive skills").

Socioeconomic status and genetic influences on cognitive development
PNAS doi: 10.1073/pnas.1708491114

Significance
A prominent hypothesis in the study of intelligence is that genetic influences on cognitive abilities are larger for children raised in more advantaged environments. Evidence to date has been mixed, with some indication that the hypothesized pattern may hold in the United States but not elsewhere. We conducted the largest study to date using matched birth and school administrative records from the socioeconomically diverse state of Florida, and we did not find evidence for the hypothesis.

Abstract
Accurate understanding of environmental moderation of genetic influences is vital to advancing the science of cognitive development as well as for designing interventions. One widely reported idea is increasing genetic influence on cognition for children raised in higher socioeconomic status (SES) families, including recent proposals that the pattern is a particularly US phenomenon. We used matched birth and school records from Florida siblings and twins born in 1994–2002 to provide the largest, most population-diverse consideration of this hypothesis to date. We found no evidence of SES moderation of genetic influence on test scores, suggesting that articulating gene-environment interactions for cognition is more complex and elusive than previously supposed.

From the paper. Note SS/OS = Same/Opposite Sex, SES = Socio-Economic Status.

First, Turkheimer and Horn indicate that “the between-pair variance of MZ pairs decreases in poor environments” (ref. 21, p. 63). Contrary to this relationship, we found that the between-pair variance of SS twins is actually lowest in the highest SES families. Given that SS twins are a relatively equal combination of MZ and DZ twins, one possibility is that a pattern supporting the hypothesis among MZ SS twins is masked by an even stronger pattern in the opposite direction among DZ SS twins. However, Fig. 3 shows that corresponding results for OS twins (all of whom are DZ) give no indication of such a pattern. Between-pair variances in achievement test scores for high-school educated parents of OS twins are higher in all cases than it is for parents without a high school diploma.

Second, Turkheimer and Horn report that “the within-pair variance of MZ twin pairs increases at lower levels of SES: poverty appears to have the effect of making MZ twins more different from each other” (ref. 21, p. 61). We would therefore expect in our data that the within-pair variance for SS twins whose mother did not graduate from high school would be higher than the variance for SS twins whose mother has a high school diploma. However, this is not the case in any of the SS twin comparisons shown in Fig. 3.

Via SSC -- thanks, Scott!

Added remarks about context and broader implications: This paper does not exclude SES effects on intelligence. Rather, it excludes a hypothesis (big nonlinear effect at low SES; GxE!) that has been widely discussed: In good environments individuals can achieve their full genetic potential, and consequently measured heritability is high. However, in bad environments individuals don't achieve their full genetic potential, and (perhaps) do not even realize the full effect of beneficial genetic variants, so heritability is much reduced. This reasonable sounding hypothesis is not supported by the Florida data, suggesting that genetic influence is similarly strong in both high and low SES families.

Now, just how strong is this genetic influence? Many large studies have been conducted on populations of twins (raised together and apart), adoptees (who end up resembling their biological parents much more than the adoptive parents who raised them), and ordinary siblings. The results suggest very high heritability of adult intelligence -- broad sense heritability may be as high as ~0.8!

Wikipedia: Recent twin and adoption studies suggest that while the effect of the shared family environment is substantial in early childhood, it becomes quite small by late adolescence. These findings suggest that differences in the life styles of families whatever their importance may be for many aspects of children's lives make little long-term difference for the skills measured by intelligence tests.

Eric, why so gloomy?

Eric Turkheimer wrote a blog post reacting to my comments (On the verge) about some recent intelligence GWAS results.

I'm an admirer of Eric's work in behavior genetics, as you can tell from this 2008 post The joy of Turkheimer. Since then we've gotten to know each other via the internet and have even met at a conference.

Eric is famous for (among other things) his Gloomy Prospect:

The question is not whether there are correlations to be found between individual genes and complex behavior— of course there are — but instead whether there are domains of genetic causation in which the gloomy prospect does not prevail, allowing the little bits of correlational evidence to cohere into replicable and cumulative genetic models of development. My own prediction is that such domains will prove rare indeed, and that the likelihood of discovering them will be inversely related to the complexity of the behavior under study.

He is right to be cautious about whether discovery of individual gene-trait associations will cohere into a satisfactory explanatory or predictive framework. It is plausible to me that the workings of the DNA program that creates a human brain are incredibly complex and beyond our detailed understanding for some time to come.

However, I am optimistic about the prediction problem. There are good reasons to think that the linear term in the model described below gives the dominant contribution to variation in cognitive ability:

The evidence comes from estimates of additive (linear) variance in twin and adoption studies, as well as from evolutionary theory itself. Fisher's Fundamental Theorem of Natural Selection identifies additive variance as the main driver of evolutionary change in the limit where selection timescales are much longer than recombination (e.g., due to sexual reproduction) timescales. Thus it is reasonable to expect that most of the change in genus Homo intelligence over the last millions of years is encoded in a linear genetic architecture.

GWAS, which identify causal loci and their effect sizes, are in fact fitting the parameters of the linear model that appears in the slide above. (Most effect sizes x_i will be zero, with perhaps 10k non-zero entries distributed according to some kind of power law.) Once we have characterized loci accounting for most of the variance, we will be able to predict phenotypes based only on genotype information (i.e., without further information about the individual). This is the genomic prediction problem which has already been partially solved for inbred lines of domesticated plants and animals. My guess is that it will be solved for humans once of order millions of genotype-phenotype pairs are available for analysis. Understanding the nonlinear parts will probably take much more data, but these are likely to be subleading effects.

Pinker on personal genomics

Read the whole thing in the Times magazine. More on Eric Turkheimer's work here.

My Genome, My Self: ...To study something scientifically, you first have to measure it, and psychologists have developed tests for many mental traits. And contrary to popular opinion, the tests work pretty well: they give a similar measurement of a person every time they are administered, and they statistically predict life outcomes like school and job performance, psychiatric diagnoses and marital stability. Tests for intelligence might ask people to recite a string of digits backward, define a word like “predicament,” identify what an egg and a seed have in common or assemble four triangles into a square. Personality tests ask people to agree or disagree with statements like “Often I cross the street in order not to meet someone I know,” “I often was in trouble in school,” “Before I do something I try to consider how my friends will react to it” and “People say insulting and vulgar things about me.” People’s answers to a large set of these questions tend to vary in five major ways: openness to experience, conscientiousness, extraversion, agreeableness (as opposed to antagonism) and neuroticism. The scores can then be compared with those of relatives who vary in relatedness and family backgrounds.

The most prominent finding of behavioral genetics has been summarized by the psychologist Eric Turkheimer: “The nature-nurture debate is over. . . . All human behavioral traits are heritable.” By this he meant that a substantial fraction of the variation among individuals within a culture can be linked to variation in their genes. Whether you measure intelligence or personality, religiosity or political orientation, television watching or cigarette smoking, the outcome is the same. Identical twins (who share all their genes) are more similar than fraternal twins (who share half their genes that vary among people). Biological siblings (who share half those genes too) are more similar than adopted siblings (who share no more genes than do strangers). And identical twins separated at birth and raised in different adoptive homes (who share their genes but not their environments) are uncannily similar.

...Behavioral genetics has repeatedly found that the “shared environment” — everything that siblings growing up in the same home have in common, including their parents, their neighborhood, their home, their peer group and their school — has less of an influence on the way they turn out than their genes. In many studies, the shared environment has no measurable influence on the adult at all. Siblings reared together end up no more similar than siblings reared apart, and adoptive siblings reared in the same family end up not similar at all. A large chunk of the variation among people in intelligence and personality is not predictable from any obvious feature of the world of their childhood.

Think of a pair of identical twins you know. They are probably highly similar, but they are certainly not indistinguishable. They clearly have their own personalities, and in some cases one twin can be gay and the other straight, or one schizophrenic and the other not. But where could these differences have come from? Not from their genes, which are identical. And not from their parents or siblings or neighborhood or school either, which were also, in most cases, identical. Behavioral geneticists attribute this mysterious variation to the “nonshared” or “unique” environment, but that is just a fudge factor introduced to make the numbers add up to 100 percent.

No one knows what the nongenetic causes of individuality are. Perhaps people are shaped by modifications of genes that take place after conception, or by haphazard fluctuations in the chemical soup in the womb or the wiring up of the brain or the expression of the genes themselves. Even in the simplest organisms, genes are not turned on and off like clockwork but are subject to a lot of random noise, which is why genetically identical fruit flies bred in controlled laboratory conditions can end up with unpredictable differences in their anatomy. This genetic roulette must be even more significant in an organism as complex as a human, and it tells us that the two traditional shapers of a person, nature and nurture, must be augmented by a third one, brute chance.

The discoveries of behavioral genetics call for another adjustment to our traditional conception of a nature-nurture cocktail. A common finding is that the effects of being brought up in a given family are sometimes detectable in childhood, but that they tend to peter out by the time the child has grown up. That is, the reach of the genes appears to get stronger as we age, not weaker. Perhaps our genes affect our environments, which in turn affect ourselves. Young children are at the mercy of parents and have to adapt to a world that is not of their choosing. As they get older, however, they can gravitate to the microenvironments that best suit their natures. Some children naturally lose themselves in the library or the local woods or the nearest computer; others ingratiate themselves with the jocks or the goths or the church youth group. Whatever genetic quirks incline a youth toward one niche or another will be magnified over time as they develop the parts of themselves that allow them to flourish in their chosen worlds. Also magnified are the accidents of life (catching or dropping a ball, acing or flubbing a test), which, according to the psychologist Judith Rich Harris, may help explain the seemingly random component of personality variation. The environment, then, is not a stamping machine that pounds us into a shape but a cafeteria of options from which our genes and our histories incline us to choose.

Random microworlds: the mystery of nonshared environment

One of the most mysterious aspects of the nature-nurture question is the difficulty in characterizing the nurture component.

Turkheimer and Waldron: When genetic similarity is controlled, siblings often appear no more alike than individuals selected at random from the population. ... it has become widely accepted that the source of this dissimilarity is a variance component called nonshared environment.

... In what may have been the most influential article ever written in the field of developmental behavior genetics, Plomin and Daniels (1987) reviewed evidence that a substantial portion of the variability in behavioral outcomes could not be explained by the additive effects of genotype or the environmental influences of families. They suggested that this residual term, which they called the nonshared environment, had been neglected by environmentally oriented researchers who assumed that the most important mechanisms of environmental action involved familial variables, like socioeconomic status [SES] and parenting styles, that are shared by siblings raised in the same home and serve to make siblings more similar to each other. Indeed, Plomin and Daniels argued, once genetic relatedness has been taken into account, siblings seem to be hardly more similar than children chosen at random from the population.

In other words, despite a lifetime of proximity, your adopted child may bear no more similarity to you (in terms of, e.g., intelligence) than someone selected at random from the general population. The shared family environment that your children (biological or adopted) experience has little or no measurable effect on their cognitive development. While there are environmental effects on intelligence (the highest estimates of heritability for adult IQ are around .8, and some would argue for a lower value; see here for Turkheimer's work suggesting low heritability in the case of severe deprivation), they seem to be idiosyncratic factors that can't be characterized using observable parameters such as the parents' SES, parenting style, level of education, or IQ. It is as if each child experiences their own random micro-environment, independent of these parental or family characteristics.

The nonshared influences are by far the largest environmental (non-genetic) influences on intelligence -- in fact, they are the only detectable non-genetic influences. (Click figure for larger version; from a review by Plomin. More recent overview here.)



Identical twins, whether raised together or apart, turn out to be very similar, but one still finds differences in IQ and personality. The cause of those differences must be the different environments experienced by the twins, but can't be characterized by simple variables of the sort listed above: it is not the case that the twin raised by the higher SES family has, on average, a much higher IQ! In fact, twins raised in the same family are about as similar as those raised apart, so family shared environment does not produce a large measurable influence. See below for a plausible model that accounts for such outcomes.

By now these results are well understood and accepted by experts, but not by the general population or even policy makers. (See the work of Judith Rich Harris for popular exposition). The naive and still widely held expectation is that, e.g., high SES causes a good learning environment, leading to positive outcomes for children raised in such environments. However, the data suggests that what is really being passed on to the children is the genes of the parent, which are mainly responsible for, e.g., above average IQ outcomes in high SES homes (surprise! high SES parents actually have better genes, on average). Little or no positive effect can be traced to the SES variable for adopted children.

The implications are quite shocking, especially for two groups: high investment parents (because the ability of parents to influence their child's development appears limited) and egalitarians (because the importance of genes and the difficulty in controlling environmental effects seem to support the Social Darwinist position widely held in the previous century).

It is plausible to me that each child tends to create their own environment over time, by selectively seeking out or avoiding stimuli of various types. A bookish kid may end up at the library regardless of whether their father takes them there. An athletic kid may end up on the playground whether or not their mother takes them there. It has been argued that this effect is the reason that the heritability of IQ increases with age: over time, genetic influences assume greater importance as they cause the individual to create or seek out their preferred environment.

In a previous post I discussed individual cognitive profiles as described by an n-vector. Similarly, one could think of an individual's learning profile and learning environment as two more n-vectors. These n-vectors may or may not be well-matched, leading to outcomes with significant and hard to characterize variability. For example, one can imagine that both the environment (provided by parents, siblings, teachers and peers) and a particular child's reactions vary in each of the factors listed below.

Pressure and competition

Stimulation through stories and pretend play; flights of imagination

Ability to learn from repetition and drill / tendency to boredom

Isolated study vs group activities

Visual vs aural vs mechanical stimulation

Level of discipline or structure imposed

Close mentoring vs freedom of exploration

Abstraction vs experimentation

(One can think of many more.)

The factors listed are not intrinsically good or bad for learning -- what matters is whether the learning environment is matched to the nature of the individual child. Some react well to discipline or pressure or story telling, others do not. Further, none of the factors is obviously correlated with SES, parental education level or IQ. Even if they were, it's plausible that a child to some extent creates their learning environment outside the control of parents and teachers (e.g., through peer group or choice of play activities).

An individual whose learning vector (learning style) is well matched to their environment will thrive: the nonshared environmental component in their development will be large and positive. For others, the environment will have a smaller or even negative impact. Because both the learning vector and the environment vector vary in a many-dimensional space, and over time, prediction or control of the overall environmental effect on development is difficult.

Nonshared environmental contributions to development, which are the largest environmental contributions, are effectively random. They are not amenable to control, either by parents or policy makers. Note, this picture -- that each child creates their own environment, or experiences an effectively random one -- does not seem to support the hypothesis that observed group differences in cognitive ability are primarily of non-genetic origin. Nor does it suggest that any simple intervention (for example, equalizing average SES levels) will eliminate group differences. However, it's fair to say our understanding of these complex questions is limited.

Technical remark: if n is large, and factors uncorrelated, the observed environmental variation in a population will be suppressed as n^{-1/2} relative to the maximum environmental effect. That means that the best or worst case scenarios for environmental effect, although hard to achieve, could be surprisingly large. In other words, if the environment is perfectly suited to the child, there could be an anomalously large non-genetic effect, relative to the variance observed in the population as a whole. Of course, for large n these perfect conditions are also harder to arrange. (As a super-high investment parent I am actually involved in attempting to fine tune n-vectors ;-)

Environmental effects cause regression to the mean of a child relative to the parental midpoint. Parents who are well above average likely benefited from a good match between their environment and individual proclivities, as well as from good genes. This match is difficult to replicate for their children -- only genes are passed on with certainty.

Some recommended reading

Robert Wald reviews the 2010 book Many Worlds?: Everett, Quantum Theory, and Reality, based on meetings at Oxford and at the Perimeter Institute, commemorating the 50th anniversary of Everett's paper.

A central issue in the Everett interpretation is the status of the `Born rule', which asserts that, for state ψ, the probability of obtaining a particular outcome of a measurement is ||Pψ||2, where P is the projection operator onto the eigensubspace associated with the measurement outcome. In traditional interpretations, the Born rule is simply postulated as part of the collapse hypothesis. In the Everett interpretation, it is far from obvious that the Born rule even has any meaning—if all outcomes occur, how can one talk about the probability of a particular outcome? Given the importance of this issue, it is highly appropriate that four chapters of the book (by Saunders, Papineau, Wallace, and Greaves and Myrvold) are devoted to addressing probability and the Born rule from the Everett viewpoint, and three chapters (by Kent, Albert, and Price) are devoted to criticising these views.

... In any case, if the conclusion of a mathematically correct argument is that rational decision strategies require the Born rule, then there must be quite a bit lying in the assumptions. The articles by Kent, Albert, and Price do a good job of fleshing out these assumptions and pointing out the weaknesses and flaws in the probability and decision theory discussions within the Everett framework. ...

See here for my thoughts on this.

The origin of the Everettian heresy (see also Byrne's excellent biography of Everett).

... These efforts gave rise to a lively debate with the Copenhagen group, the existence and content of which have been only recently disclosed by the discovery of unpublished documents. The analysis of such documents opens a window on the conceptual background of Everett’s proposal, and illuminates at the same time some crucial aspects of the Copenhagen view of the measurement problem. Also, it provides an original insight into the interplay between philosophical and social factors which underlay the postwar controversies on the interpretation of quantum mechanics.

... Here is a tentative chronology of the thesis versions and of the related papers:

(1a) Objective vs Subjective probability, short manuscript (first half of 1955).
(1b) Quantitative Measure of Correlation, short manuscript (summer 1955).
(1c) Probability in Wave Mechanics, short manuscript (summer 1955).

(2) Wave Mechanics Without Probability, second version of the dissertation (the long thesis) (winter 1955–1956), published as The Theory of the Universal Wave Function (1973).

(3) On the Foundations of Quantum Mechanics, final dissertation (winter 1956–1957), published as ‘‘Relative State’’ Formulation of Quantum Mechanics (July 1957).

A Commentary on ‘Common SNPs Explain a Large Proportion of the Heritability for Human Height’ by Yang et al. (2010). (Ungated pdf.) Why do Visscher and company have to speak so slowly and enunciate so carefully in order to be understood?

During the refereeing process (the paper was rejected by two other journals before publication in Nature Genetics) and following the publication of Yang et al. (2010) it became clear to us that the methodology we applied, the interpretation of the results and the consequences of the findings on the genetic architecture of human height and that for other traits such as complex disease are not well understood or appreciated ...

Well before reading the Yang et al. paper, but after hearing much about "missing" heritability, I asked impatiently why GWAS researchers had not tried to make a global fit of total heritability, as opposed to searching for individual alleles. See also Heritability 2.0.

Turkheimer on heritability: Still Missing.

A century of familial studies of twins, siblings, parents and children, adoptees, and whole pedigrees has established beyond a shadow of a doubt that genes play a crucial role in the explanation of all human differences, from the medical to the normal, the biological to the behavioral ...

As a social scientist and twin researcher, I had to struggle with the biological and statistical genetics underlying the Yang et al. analyses, but the analysis of variance, the acausal “capturing” and “tracking” of one domain of variance with another came naturally to me. The situation was reversed for the geneticists who were the target audience of the paper: biologically based scientists, accustomed to genes that have an actual causal pathway to their outcomes. Over and above its technical brilliance, the real contribution of the Yang et al. article is to bring into focus this conceptual chasm between biological and quantitative genetics, and thus between the physical sciences and social science. Genomics is only now learning a hard lesson that social scientists had to learn a long time ago: sometimes prediction is just prediction. That is what the missing heritability problem is really about, and why it has not yet been solved

For more Turkheimer, see here. Note that although he emphasizes the difficulty of teasing out causality in a complex system, for some "engineering" applications (such as genetic engineering), prediction may be enough, as long as the correlations between genetic variant and phenotype are confirmed to be robust across a variety of environments. The specific causal mechanism is not as important as the ability to modify and control ;-)

The Fourth Law of Behavior Genetics?

I believe the law stated below almost follows from the observation that humans brains are complex machines: hence the DNA blueprint has many components, and variance is spread over these components  :^)

However, note the evidence for discrete genetic modules of large effect in other species: Discrete genetic modules can control complex behavior (burrowing behavior in cute mouse in picture at bottom), As flies to wanton boys are we to the gods (discrete genetic controls on drosophila behavior).

THE FOURTH LAW OF BEHAVIOR GENETICS

Christopher F. Chabris, Union College
James J. Lee, University of Minnesota Twin Cities
David Cesarini, New York University
Daniel J. Benjamin, Cornell University and University of Southern California
David I. Laibson, Harvard University

Abstract
Behavior genetics is the study of the relationship between genetic variation and psychological traits. Turkheimer (2000) proposed “Three Laws of Behavior Genetics” based on empirical regularities observed in studies of twins and other kinships. On the basis of molecular studies that have measured DNA variation directly, we propose a Fourth Law of Behavior Genetics: “A typical human behavioral trait is associated with very many genetic variants, each of which accounts for a very small percentage of the behavioral variability.” This law explains several consistent patterns in the results of gene discovery studies, including the failure of candidate gene studies to robustly replicate, the need for genome-wide association studies (and why such studies have a much stronger replication record), and the crucial importance of extremely large samples in these endeavors. We review the evidence in favor of the Fourth Law and discuss its implications for the design and interpretation of gene-behavior research.

Twitter Attacks, and a Defense of Scientific Inquiry

I have not responded to these nasty Twitter attacks, but unfortunately they have gotten enough traction that I feel I need to respond now. [ Note: I have been informed that some of the signatures on their petition are fake, including one purported to be from my colleague Corey Washington! See counter petition and support letters on my behalf. ]

The attacks attempt to depict me as a racist and sexist, using short video clips out of context, and also by misrepresenting the content of some of my blog posts. A cursory inspection reveals bad faith in their presentation.

The accusations are entirely false -- I am neither racist nor sexist.

The Twitter mobs want to suppress scientific work that they find objectionable. What is really at stake: academic freedom, open discussion of important ideas, scientific inquiry. All are imperiled and all must be defended.


One of the video clips is taken from an interview I did with YouTuber Stefan Molyneux in 2017. Molyneux was not a controversial figure in 2017, although he has since become one. Prominent scientists working on human intelligence who were interviewed on his show around the same time include James Flynn and Eric Turkheimer. (Noam Chomsky was also a guest some time after I was.) Here is what I said to Molyneux about genetic group differences in intelligence:



Here is a similar interview I did with Cambridge University PhD student Daphne Martschenko:



As you can see, contrary to the Twitter accusations (lies), I do not endorse claims of genetic group differences. In fact I urge great caution in this area.


The tweets also criticize two podcasts I recorded with my co-host Corey Washington: a discussion with a prominent MSU Psychology professor who studies police shootings (this discussion has elicited a strong response due to the tragic death of George Floyd), and with Claude Steele, a renowned African American researcher who discovered Stereotype Threat and has been Provost at Columbia and Berkeley. The conversation with Steele is a nuanced discussion of race, discrimination, and education in America.






The blog posts under attack, dating back over a decade, are almost all discussions of published scientific papers by leading scholars in Psychology, Neuroscience, Genomics, Machine Learning, and other fields. The papers are published in journals like Nature and the Proceedings of the National Academy of Sciences. However, a detailed reading is required to judge the research and related inferences. I maintain that all the work described is well-motivated and potentially important. Certainly worthy of a blog post. (I have written several thousand blog posts; apparently these are the most objectionable out of those thousands!)

In several of the blog posts I explicitly denounce racism and discrimination based on identity.


This paper, from 2008, discusses early capability to ascertain ancestry from gene sequence. The topic was highly controversial in 2008 (subject to political attack, because it suggested there could be a genetic basis for “race”), but the science is correct. It is now common for people to investigate their heritage using DNA samples (23andMe, Ancestry) using exactly these methods. This case provides a perfect example of science that faced suppression for political reasons, but has since been developed for many useful applications.

https://infoproc.blogspot.com/2008/01/no-scientific-basis-for-race.html


This 2016 paper is by the UCSD Pediatric Imaging, Neurocognition, and Genetics collaboration. They claim that fMRI features of brain morphology can be predicted by genetic ancestry via machine learning.

https://infoproc.blogspot.com/2016/03/genetic-ancestry-and-brain-morphology.html


These blog posts discuss the firing of software engineer James Damore by Google over a memo on diversity practices. The first post describes the legal situation and quotes a professor of labor law at Notre Dame. The second compares the claims made in Damore’s memo to an article in the Stanford Medical School magazine, which covers similar material and was (by coincidence) published around the same time.

https://infoproc.blogspot.com/2017/08/damore-vs-google-trial-of-century.html
https://infoproc.blogspot.com/2017/08/meanwhile-down-on-farm.html


These papers discuss evidence from large DNA datasets for recent natural selection in human evolution. This research has been attacked for political reasons, but should be defended since it addresses fundamental questions in deep human history and evolution.

https://infoproc.blogspot.com/2018/10/the-truth-shall-make-you-free.html


Regarding my work as Vice President for Research, the numbers speak for themselves. MSU went from roughly $500M in annual research expenditures to about $700M during my tenure. We have often been ranked #1 in the Big Ten for research growth. I participated in the recruitment of numerous prominent female and minority professors, in fields like Precision Medicine, Genomics, Chemistry, and many others. Until this Twitter attack there has been not even a single allegation (over 8 years) of bias or discrimination on my part in promotion and tenure or faculty recruitment. These are two activities at the heart of the modern research university, involving hundreds of individuals each year.

Academics and scientists must not submit to mob rule.


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Media coverage:

A Twitter Mob Takes Down an Administrator at Michigan State (Wall Street Journal June 25)

Scholar forced to resign over study that found police shootings not biased against blacks (The College Fix)

On Steve Hsu and the Campaign to Thwart Free Inquiry (Quillette)

Michigan State University VP of Research Ousted (Reason Magazine, Eugene Volokh, UCLA)

Research isn’t advocacy (NY Post Editorial Board)

Podcast interview on Tom Woods show (July 2)

College professor forced to resign for citing study that found police shootings not biased against blacks (Law Enforcement Today, July 5)

"Racist" College Researcher Ousted After Sharing Study Showing No Racial Bias In Police Shootings (ZeroHedge, July 6)

Twitter mob: College researcher forced to resign after study finding no racial bias in police shootings (Reclaim the Net, July 8)

Horowitz: Asian-American researcher fired from Michigan State administration for advancing facts about police shootings (The Blaze, July 8)

I Cited Their Study, So They Disavowed It: If scientists retract research that challenges reigning orthodoxies, politics will drive scholarship (Wall Street Journal July 8)

Conservative author cites research on police shootings and race. Researchers ask for its retraction in response (The College Fix, July 8)

Academics Seek to Retract Study Disproving Racist Police Shootings After Conservative Cites It (Hans Bader, CNSNews, July 9)

The Ideological Corruption of Science (theoretical physicist Lawrence Krauss in the Wall Street Journal, July 12)

Foundation for Individual Rights in Education: "chilling academic freedom" (Peter Bonilla, July 22)

As flies to wanton boys are we to the gods

An earlier post, Discrete genetic modules can control complex behavior, described genetic control of burrowing behavior in deer mice. A reader commented that the results were entirely unsurprising. I wasn't aware of similar results in mammals, but of course this sort of thing has long been known in drosophila, thanks to Seymour Benzer and collaborators.

WSJ: ... When the great California Institute of Technology geneticist Seymour Benzer set out in the mid-1960s to find mutations in fruit flies that affected behavior, rather than mere anatomy, he was ridiculed for challenging the consensus that all behavior must be learned.

Benzer told the geneticist Max Delbrück about the plan to find behavioral mutants; Delbrück said it was impossible. To which Benzer replied: "But, Max, we found the gene, we've already done it!" (Benzer's mother was more succinct: "From this, you can make a living?") He was soon able to identify mutations related to hyperexcitability, learning, homosexuality and unusual circadian rhythms, like his own: Benzer was almost wholly nocturnal.

Since then, thanks to studies of human twins and a rash of genetic investigations in animals, it has become routinely accepted that most things, including personality, sexual orientation and intelligence, are to some degree affected by genes. The University of Virginia's Eric Turkheimer has declared what he calls the "first law of behavior genetics": that all human behavioral traits are heritable.

Benzer started in solid state physics, migrated to molecular biology, and then to neuroscience.

Caltech Oral History:  ... I had my nose on the transistor. It’s like Max Delbrück [professor of biology at Caltech; d. 1981] failed to discover fission, and he had it under his nose. [Laughter] I failed to discover the transistor, because I had three electrodes in there, and I was measuring things—using one to measure what the other one was doing—but I never had the idea of trying to use that arrangement as an amplifier. Instead, I had a different idea; I had the idea of making a crystal amplifier, but it was too sophisticated. It was based on putting a metal layer on top of a semiconductor and using a tunnel effect to control the current that’s passing through, but I never got it to work. Instead, the Bell Labs guy did the most simpleminded thing, which was to have just these two wires next to each other and have one influence the other. It escaped me, and it was under my nose. Some time later, there was a big demonstration of it at Bell Labs. These guys grabbed me and said, “You should have done this.” [Laughter] And they were right. But, you know, maybe to some extent, because I was already into biology at that time, I wasn’t really focused on that problem. Of course, being a graduate student and not being all that able or having big resources [played a role]. But by the time I got my Ph.D. in 1947, I was already interested in biology.

Aspaturian: What had happened?

Benzer: I was always interested in biology. But two things happened. One of the guys in the lab — his name was Lou [Louis L.] Boyarsky—told me about mapping genes on chromosomes, the work that had been done here at Caltech by [Alfred H.] Sturtevant and [Thomas Hunt] Morgan and their group. I thought that was very exciting. And then I read this book by [Erwin] Schrödinger, written around 1944, called What Is Life?, which inspired a number of other people as well—Francis Crick, for one. Max Delbrück was in the book—he had been at Caltech in the thirties, switching from physics to biology—and there’s a chapter in there on Delbrück’s model of mutation. ...

Aspaturian: What brought you to Caltech, the first time you came?

Benzer: During the sixties, I was getting more and more interested in behavior. One reason was my two children. I have two daughters with very different personalities. If you have one daughter, you don’t notice anything, but if you have a second one, you begin to wonder, “Are we doing things differently, or is it genetic?” So I got interested in this general problem of personality and behavior—how much is genetics and how much is environment? And how do you study such a problem? I had actually begun to be interested even before that time. There was a meeting about ’63, I think, at Cold Spring Harbor, where I remember having a conversation with Marshall Nirenberg. We had this feeling that all the molecular biology problems were on the verge of being solved. It was a little bit like the physicists at the end of the nineteenth century saying, “All we have left to do is one more decimal place.” Little did we anticipate all the recombinant DNA technology. So that was another part of it, the fact that molecular biology was going so well, becoming rather crowded. When things get to that stage, you wonder why you should be doing something somebody else is already doing. It’s just redundant. ...

Aspaturian: Would you say that Drosophila is about the most complex organism with which you can get really rigorous results in this kind of research?

Benzer: Well, I don’t know. It depends on what you want to study. You can get rigorous results with humans now. Modern technology makes it almost as easy to work with humans as with flies, and that’s why I have the courage to get into the human business now.

Aspaturian: But there are so many more behaviors to look at in humans.

Benzer: Humans are wonderful. There’s a book on viewing disorders of man, containing 4,000 hereditary disorders in humans, one or two thousand of which have been actually mapped on the chromosome. Many of these have behavioral components, and hundreds affect the eye. There’s a similar book on Drosophila. And we’re finding that more and more of the genes correspond to one another.

See also this video interview of Benzer. Among other things, he discusses specific mutations that control sexual behavior in drosophila (e.g., length of copulation, courtship), learning ability, memory, etc. Of course, these are just flies  ;-)

For more on Max Delbruck, see For the historians and the ladies; for more on physicists and early molecular biology, see The Eighth Day of Creation.


King Lear, Act 4, Scene 1:

GLOUCESTER: "As flies to wanton boys are we to the gods. They kill us for their sport."

Childhood SES amplifies genetic effects on adult intelligence

Timothy Bates, a professor of psychology at the University of Edinburgh, and an occasional commenter on this blog, has a new paper out, which looks quite interesting. [See comments for references to additional literature and an overview from Tim!]

Childhood Socioeconomic Status Amplifies Genetic Effects on Adult Intelligence

Studies of intelligence in children reveal significantly higher heritability among groups with high socioeconomic status (SES) than among groups with low SES. These interaction effects, however, have not been examined in adults, when between-families environmental effects are reduced. Using 1,702 adult twins (aged 24–84) for whom intelligence assessment data were available, we tested for interactions between childhood SES and genetic effects, between-families environmental effects, and unique environmental effects. Higher SES was associated with higher mean intelligence scores. Moreover, the magnitude of genetic influences on intelligence was proportional to SES. By contrast, environmental influences were constant. These results suggest that rather than setting lower and upper bounds on intelligence, genes multiply environmental inputs that support intellectual growth. This mechanism implies that increasing SES may raise average intelligence but also magnifies individual differences in intelligence.

See also WSJ coverage by Alison Gopnik:

... When psychologists first started studying twins, they found identical twins much more likely to have similar IQs than fraternal ones. They concluded that IQ was highly "heritable"—that is, due to genetic differences. But those were all high SES twins. Erik Turkheimer of the University of Virginia and his colleagues discovered that the picture was very different for poor, low-SES twins. For these children, there was very little difference between identical and fraternal twins: IQ was hardly heritable at all. Differences in the environment, like whether you lucked out with a good teacher, seemed to be much more important.

In the new study, the Bates team found this was even true when those children grew up. IQ was much less heritable for people who had grown up poor. This might seem paradoxical: After all, your DNA stays the same no matter how you are raised. The explanation is that IQ is influenced by education. Historically, absolute IQ scores have risen substantially as we've changed our environment so that more people go to school longer.

Richer children have similarly good educational opportunities, so genetic differences among them become more apparent. And since richer children have more educational choice, they (or their parents) can choose environments that accentuate and amplify their particular skills. A child who has genetic abilities that make her just slightly better at math may be more likely to take a math class, so she becomes even better at math.

But for poor children, haphazard differences in educational opportunity swamp genetic differences. Ending up in a terrible school or one a bit better can make a big difference. And poor children have fewer opportunities to tailor their education to their particular strengths. ...