Monday, February 01, 2010

Half Sigma's flawed post on DTNBP1   posted by ben g @ 2/01/2010 10:33:00 AM

A while back, Mark and I were working on a comprehensive post which would try to tally the results of the various IQ-gene studies to see what they said about racial differences. We began this quest bright-eyed and hopeful that we would help contribute to ending a calamitous debate that has gone on for way too long. However, as we learned more about genetics, and these studies in particular, we came to realize that it's too early to take IQ-genes seriously.

We began with an approach similar to what Half Sigma did 2 years ago with the DTNBP1 gene. However, we soon learned that this approach was incredibly flawed and misleading. I wasn't going to write this post, but recently Half Sigma's DTBP1 post was linked from Reddit and tens of thousands of people are viewing it. When I saw that, I frustratedly criticized HS. He responded that I should give a more diplomatic and reasoned response, so here it is:

  1. You cannot simply add up SNPs from the same gene or chromosome. Half Sigma simply adds the observed effects of the SNPs to one another, ignoring that the alleles are highly correlated with one another, and not independently inherited, which is referred to as linkage disequilibrium (LD). The study that Half Sigma used provides the following table of LD for its SNPs:


    As can be seen in this table, pairwise LD goes as high as 1.0, meaning that two of the alleles are always inherited together. Adding these SNP's together is therefore like counting them twice.

  2. Group comparisons require replication in both groups. Because different populations have systematic genetic and environmental differences, an effect in one group may not occur in another. The study that Half Sigma uses relies primarily on a (small) sample of Dutch people. It is unclear whether these effects would exist in a population of African ancestry, let alone another European one.

  3. Candidate-gene association studies are not reliable. This is the most important point. Candidate gene association studies have largely failed to replicate. In fact, there have been no common IQ polymorphisms which have been replicated. Genome-wide association studies, which don't suffer as severely the various biases of candidate-gene association studies like publication bias or the winner's curse have not shown common SNP-associations with IQ.

    IQ is highly heritable, so the problem is the current methods, not the search for genes. With the development of sequencing technology and huge cohorts, we will be able to see the genes that are really behind normal IQ variation. With replication in multiple ethnicities and races, we will also see to what extent various genes and environments are responsible for group differences. There's no need to make proclamations of victory for hereditarianism or environmentalism in the mean time.

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Tuesday, December 08, 2009

Does the family matter for adult IQ?   posted by ben g @ 12/08/2009 05:57:00 AM

A frequent claim in the IQ debates is that which family you are raised in has no lasting impact on your IQ. Jensen argues in The g Factor that the only causes of IQ similarities between adult identical twins are genetic. Many researchers go so far as to argue that by 12 years of age, the shared environment has no impact.

Based on my limited knowledge of the behavior genetic research, I used to hold this position as well. But thanks to some recent in depth reading, I have come to the conclusion that which family you are raised in matters significantly for your IQ as an adult, especially so for people of lower socioeconomic status. I'll detail the behavior genetic evidence here, and argue that it points to significant shared environmental influences on adult IQ scores.

Twin Studies

The most recent and comprehensive survey of twin studies on IQ comes from Haworth et al (2009). Using pooled twin data from around the world, they modeled genetic and environmental influences as a function of age. Here is what they found regarding the effects of the shared environment:
[S]hared environment shows a decrease from childhood (33%) to adolescence (18%) but remained at that modest level in young adulthood (16%).
In an email exchange with Dr. McGue (one of the co-authors of the paper) he told me that while the latest data may not fit with earlier estimates, it's actually more reliable due to the unprecedented sample size (11,000 pairs of twins).

One failing of this study, though, is that it doesn't go far enough into adulthood. The young adult group ranges from 14 to 34 years of age, with an average age of 17. In contrast, McGue (1993) looked seperately at data on adults over 20 years of age. He found that the shared environment diminished to zero impact at that point. Here's his chart:
Looking at that chart, you might quickly conclude that shared environmental influence evaporates by age 20. However, this conclusion is premature. Twin studies make a great number of assumptions, some of which increase and others of which decrease estimates of the shared environment. A straightforward way of bypassing these assumptions is to compare monozygotic twins reared apart (MZAs) to monozygotic twins reared together (MZTs). The following data comes from a comparison of MZTs and MZAs, of average age 41, in Bouchard (1990):

MeasureMZA correlationMZT correlation
WAIS IQ-Full Scale0.690.88
WAIS IQ-Verbal0.640.88
WAIS IQ-Performance0.710.79

Differences between MZA's and MZT's on Raven's Progressive Matrices follow the same pattern but are even more extreme. Bouchard (1981) reported a median correlation of only 0.58 for adult MZA's on the Raven's. Curiously, though, MZA's are equally if not more correlated than MZT's on the Mill-Hill vocabulary test. Apparently, the pattern is that more g-loaded tests tend to show stronger evidence of lasting shared environmental impact.

It's worth noting that MZT vs. MZA comparisons are actually biased towards an underestimation of shared environmental impact. Bouchard's study of twins reared apart found an environmental correlation of .22 for MZAs on various environmental measures, with some having a small but significant correlation with IQ scores. Also MZA's share the womb. To summarize: when the assumptions of the twin method are effectively controlled for, lasting shared environmental impacts are revealed.

Adoption Studies

To date, most adoption studies of IQ have concluded that being adopted by a new and typically well-off family has no effect on adult IQ scores. Here is a chart of adoption studies from Bouchard (2009):As you can see by clicking it, the IQ correlation between unrelated individuals in the same family decreases (on average) from .26 in childhood to .04 in adulthood (which begins at age 17 for the purposes of this graph).

However, as with the previous chart, the quick conclusion that shared environmental influences don't matter in adulthood shouldn't be so quickly accepted. To begin with, we can see that the adoption data underestimates the shared environment relative to the twin literature. This most likely occurs because of the assumptions that go into adoption studies.

Stoolmiller (1999), for example, highlighted the issue of range restriction-- the idea that the limited range of adoptee and adoptive family environments will lower estimates of the shared environment. This idea is supported by studies which make the extra effort to include individuals of lower SES. The French adoption studies that made such an effort buck the trendline seen above, in finding that nurture matters almost as much as nature for the IQ of 14 year olds. Scarr (1993) is the outlier in the adoption graph above, finding a .19 correlation between unrelated adolescent siblings. Perhaps her results differed from others because her sample was multi-racial and therefore less range restricted. Lastly, there are other lines of evidence supporting the idea of range restriction, such as Turkheimer's work on SES and cognitive ability.

It's worth noting, however, that McGue (2007) looked for evidence of range restriction effects within the "broad middle class" and did not find any. He used statistical methods that are over my head to estimate the effects of range restriction based on a range restricted sample and state census data. Unfortunately there are no studies which have critiqued his as of yet. Any commenters who are familiar with the statistics involved are invited to comment. Even if McGue is right about restriction of range, my point stands that assumptions inherent in the adoption studies deflate c^2 estimates.

Future Directions

Future work will help sort out the still unanswered question of shared environmental influences on adult IQ scores. There are large longitudinal adoption studies currently under way, and I believe that Haworth's twin study will be followed-up on and include data on older twins. There are also interesting (albeit less methodologically agreed upon) studies coming out like this one, which find significant shared effects on IQ in adulthood.

My reading of the available evidence is that there is a significant shared environmental input to adult IQ, and that it is associated with socioeconomic status. To what extent it's the neighborhood or the parents themselves that matters is unclear. Just as the most g-loaded tests show the most shared environmental effects in the MZA-MZT comparison, so too does the Flynn effect occur on the most g-loaded tests, suggesting that whatever is loading onto the "shared environment" within generations is also responsible for differences between them.

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Wednesday, October 28, 2009

Germs, collectivism and serotonin   posted by Razib @ 10/28/2009 01:38:00 PM

Culture-gene coevolution of individualism-collectivism and the serotonin transporter gene:
Culture-gene coevolutionary theory posits that cultural values have evolved, are adaptive and influence the social and physical environments under which genetic selection operates. Here, we examined the association between cultural values of individualism-collectivism and allelic frequency of the serotonin transporter functional polymorphism (5-HTTLPR) as well as the role this culture-gene association may play in explaining global variability in prevalence of pathogens and affective disorders. We found evidence that collectivistic cultures were significantly more likely to comprise individuals carrying the short (S) allele of the 5-HTTLPR across 29 nations. Results further show that historical pathogen prevalence predicts cultural variability in individualism–collectivism owing to genetic selection of the S allele. Additionally, cultural values and frequency of S allele carriers negatively predict global prevalence of anxiety and mood disorder. Finally, mediation analyses further indicate that increased frequency of S allele carriers predicted decreased anxiety and mood disorder prevalence owing to increased collectivistic cultural values. Taken together, our findings suggest culture-gene coevolution between allelic frequency of 5-HTTLPR and cultural values of individualism-collectivism and support the notion that cultural values buffer genetically susceptible populations from increased prevalence of affective disorders. Implications of the current findings for understanding culture-gene coevolution of human brain and behaviour as well as how this coevolutionary process may contribute to global variation in pathogen prevalence and epidemiology of affective disorders, such as anxiety and depression, are discussed.

Here's what I see going on:

High pre-modern pathogen load → collectivist values → S allele & dampening of psychological responses associated with S allele in populations where it is extant at lower frequencies.

It's Open Access so you can look at their regressions yourself. The association with pre-modern levels of pathogens is a strong point for me, these sorts of biological factors would result in a consistent "push" over long periods of times which culture itself might not have. The agricultural civilizations of Asia were always going to be rich ecologies for infectious diseases. So it would be interesting to look at the frequencies of the S & L alleles on a finer scale; for example, in the islands of Japan. Though that case I suspect that lower-density areas would have had so much migration that selection wouldn't have time to maintain different allele frequencies.


Wednesday, September 30, 2009

High Anxiety   posted by Razib @ 9/30/2009 08:45:00 PM

Understanding the Anxious Mind. Jerome Kagan, Robert Plomin and Steven Pinker all make appearances. From personality psychology to fMRI.


Monday, September 28, 2009

Creativity & psychosis   posted by Razib @ 9/28/2009 12:49:00 PM

Possible confirmation of folk wisdom? Genes for Psychosis and Creativity: A Promoter Polymorphism of the Neuregulin 1 Gene Is Related to Creativity in People With High Intellectual Achievement:
Why are genetic polymorphisms related to severe mental disorders retained in the gene pool of a population? A possible answer is that these genetic variations may have a positive impact on psychological functions. Here, I show that a biologically relevant polymorphism of the promoter region of the neuregulin 1 gene (SNP8NRG243177/rs6994992) is associated with creativity in people with high intellectual and academic performance. Intriguingly, the highest creative achievements and creative-thinking scores were found in people who carried the T/T genotype, which was previously shown to be related to psychosis risk and altered prefrontal activation.

Also see ScienceDaily


Tuesday, September 22, 2009

People who spank are aggressive   posted by Razib @ 9/22/2009 11:11:00 PM

A follow up to the previous post. I keep seeing the research from this paper in the press, Spanking detrimental to children, study says:
Berlin and colleagues found that children who were spanked as 1-year-olds tended to behave more aggressively at age 2, and did not perform as well as other children on a test measuring thinking skills at age 3. The study is published in the journal Child Development.

The idea is that spanking has negative consequences, making children less intelligent and more aggressive. But what do you think? My thought was that there are two other reasons of possible interest:

1) The kids being spanked are more incorrigible in general, which results in more frustration on the part of the parents.

2) The parents themselves are less intelligent, lack impulse control and are aggressive.

The above two traits of course could exhibit heritability betwen parent and child. Yes, there are plenty of confounds; acceptability of spanking varies from culture to culture. But I think the hypothesis that this is just a correlation between heritable traits and the behavior in question explains the why the "effects were somewhat small."

This sort of thought process kicks into action with a lot of the developmental psychology I see being reported in the press. But a headline such as "Aggressive impulsive parents more likely to beat their children" is probably less palatable....

Note: I'm against spanking personally in regards to how I'd raise my children. But I assume that my children wouldn't be totally incorrigible because I was not (those who know me personally might consider this a mischaracterization, but I am not including outlier behavior!).


Behavior is heritable you know....   posted by Razib @ 9/22/2009 08:58:00 PM

Genes May Explain Why Children Who Live Without Dads Have Earlier Sex:
Mendle and her colleagues looked at more than 1,000 cousins ages 14 and older from the National Longitudinal Survey of Youth. The study design tested for genetic influences as well as factors such as poverty, educational opportunities, and religion. It compared children who were related in different ways to each other, and who differed in whether they'd lived with their fathers. The more genes the children shared, the more similar their ages of first intercourse-regardless of whether or not the children personally had an absent father. This finding, the researchers say, suggests that environmental theories don't fully explain the puzzle. Instead, genetic influence can help us understand the tie between fathers' absence and early sex.

"While there's clearly no such thing as a 'father absence gene,' there are genetic contributions to traits in both moms and dads that increase the likelihood of earlier sexual behavior in their children," notes Mendle. "These include impulsivity, substance use and abuse, argumentativeness, and sensation seeking."These traits get passed down from parents to children, resulting in a situation known as 'passive gene-environment correlation,' because the same genetic factors that influence when children first have intercourse also affect the likelihood of their growing up in a home without a dad."

This issue is known to anyone who has read Judith Rich Harris' The Nurture Assumption. Nevertheless a lot of the psychological and social research published today routinely ignores the possibility of passive gene-environment correlation from what I can tell. Of course heritable propensities express themselves in an environmental context, so for example the rank order of average age of first intercourse among a set of unrelated families may remain the same in a Mormon "treatment" as opposed to a Wicca treatment (this is a thought experiment obviously), but the average age for the two cases would probably differ somewhat.


Saturday, September 12, 2009

Sex hormones & genes   posted by Razib @ 9/12/2009 01:16:00 PM

Quantitative trait loci predicting circulating sex steroid hormones in men from the NCI-Breast and Prostate Cancer Cohort Consortium (BPC3):
Twin studies suggest a heritable component to circulating sex steroid hormones and sex hormone-binding globulin (SHBG). In the NCI-Breast and Prostate Cancer Cohort Consortium, 874 SNPs in 37 candidate genes in the sex steroid hormone pathway were examined in relation to circulating levels of SHBG (N = 4720), testosterone (N = 4678), 3-androstanediol-glucuronide (N = 4767) and 17β-estradiol (N = 2014) in Caucasian men. rs1799941 in SHBG is highly significantly associated with circulating levels of SHBG (P = 4.52 x 10–21), consistent with previous studies, and testosterone (P = 7.54 x 10–15), with mean difference of 26.9 and 14.3%, respectively, comparing wild-type to homozygous variant carriers. Further noteworthy novel findings were observed between SNPs in ESR1 with testosterone levels (rs722208, mean difference = 8.8%, P = 7.37 x 10–6) and SRD5A2 with 3-androstanediol-glucuronide (rs2208532, mean difference = 11.8%, P = 1.82 x 10–6). Genetic variation in genes in the sex steroid hormone pathway is associated with differences in circulating SHBG and sex steroid hormones.


Wednesday, September 09, 2009

What's "natural" is heterogenous   posted by Razib @ 9/09/2009 09:43:00 PM

Seems to be the "take away" message from Bryan Caplan's post, Monogamy and Heterogeneity. Interestingly, I've run into nature-based arguments in regards to human behavior and norms (e.g., "it's the natural way" or "it's against nature") mostly from two sets, back-to-nature-hippies and social conservatives. As Caplan suggests there is a tendency in these cases for the two groups to generalize from their own likely innate preferences, though the defections and deviations from both groups over time suggest that there's a lot of heterogeneity within them and some people are just conforming to the ideologies and leaders of their packs. Humans are supposed to have good Theory of Mind, but I think even that is a little outmatched by the enormous sample space of possible choices available in a post-industrial consumer society living well above the margins of subsistence. Minor innate behavioral dispositions which might have been marginal or buffered in a small-scale society may snowball due to the unending positive feedback loops which can be generated by the diversity of choices we can make today.

The pre-modern polyamorist was likely constrained in the number of individuals they might have sexual relations with because the number of people in their social world was small. Similarly, there wasn't nearly as much temptation and opportunity (or perceived opportunity cost) for the pre-modern monogamist. The realized distribution of behavior may be much more stretched out in modern society than in the past. After all, how nerdy would most of the readers of this weblog be if they'd been peasants? How many ways are there to plant a seed? (I'm sure I'm going to get answers to that rhetorical question)

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Tuesday, September 01, 2009

No one believes genes affect personality   posted by Razib @ 9/01/2009 06:47:00 PM

I looked in the GSS, post at Secular Right. There isn't that much deviation from the mean of ~25% who believe genes play a major role in personality. Interestingly, women are more accepting of the idea of genes effecting personality than men. Not surprisingly, the old are also more open to the idea of genes effecting personality than the young.


Friday, August 21, 2009

Friends & fat   posted by Razib @ 8/21/2009 12:05:00 AM

In the McArdle vs. Frum diavlog I alluded to earlier there was a dispute centered around two seemingly contradictory results. First, the fact that heritability of obesity is rather high, in twins-separated-at-birth studies the correlation between monozygotic twins raised apart is on the order of ~0.75. And yet people tend to track the weight of their peer group. The causality here has to be teased apart of course, but consider this study, The presence of friends increases food intake in youth:
Design: Twenty-three overweight and 42 nonoverweight youths had the opportunity to play and eat with a friend (n = 26) or with an unfamiliar peer (n = 39). The dependent variables of interest were the amount of nutrient-dense and energy-dense foods children consumed and their total energy intake.

Results: Participants eating with a friend ate substantially more than did participants eating with an unfamiliar peer. Furthermore, overweight youth, but not nonoverweight youth, who ate with an overweight partner (friend or unfamiliar peer) consumed more food than did overweight participants who ate with a nonoverweight eating partner. Matching of intake was greater between friends than between unfamiliar peers.

Naturally twins raised apart were not placed into a "design" whereby they were forced to eat with strangers. Rather, they selected their peer groups. Heritability of many traits increases with age because individuals seek out particular environments which eventually dampen the "noise" which reduces the correlation between those with similar genetic propensities. Assortative friendship by weight then might result in amplifiers of mean deviation from phenotypic norms; that is, thin peer groups might model specific behaviors and apply certain pressures which differ greatly from overweight peer groups. Gene-environment correlation. So naturally in the interests of public health we need integration across weight classes....

Also see ScienceDaily.

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Friday, July 31, 2009

Red hair and rotten teeth   posted by Razib @ 7/31/2009 08:38:00 PM

Genetic Variations Associated With Red Hair Color and Fear of Dental Pain, Anxiety Regarding Dental Care and Avoidance of Dental Care:
Background. Red hair color is caused by variants of the melanocortin-1 receptor (MC1R) gene. People with naturally red hair are resistant to subcutaneous local anesthetics and, therefore, may experience increased anxiety regarding dental care. The authors tested the hypothesis that having natural red hair color, a MC1R gene variant or both could predict a patient's experiencing dental care-related anxiety and dental care avoidance.

Methods. The authors enrolled 144 participants (67 natural red-haired and 77 dark-haired) aged 18 to 41 years in a cross-sectional observational study. Participants completed validated survey instruments designed to measure general and dental care-specific anxiety, fear of dental pain and previous dental care avoidance. The authors genotyped participants' blood samples to detect variants associated with natural red hair color.

Results. Eighty-five participants had MC1R gene variants (65 of the 67 red-haired participants and 20 of the 77 dark-haired participants) (P < .001). Participants with MC1R gene variants reported significantly more dental care-related anxiety and fear of dental pain than did participants with no MC1R gene variants. They were more than twice as likely to avoid dental care as were the participants with no MC1R gene variants, even after the authors controlled for general trait anxiety and sex.


Friday, July 17, 2009

Achievement Beyond IQ: A Genetic Story   posted by Herrick @ 7/17/2009 11:45:00 AM

It's nice to see a bad idea demolished. And that's what Greven, et al. do in "More than just IQ." Their subtitle tells most of the story:
School achievement is predicted by self-perceived abilities (SPAs)--but for genetic rather than environmental reasons.

So asking kids "Are you good at math and English?" is indeed a good way to find out who is good at math and English; and basic twin-study methods show that the answers to those questions are in fact genetically-driven, with heritability of 51% and family environment explaining 2%.

Another family environment channel shot down. The authors drive that fact home:

Despite the fact that not a single twin or adoption study has investigated the genetic and environmental etiologies of SPAs, researchers have cited environmental factors as a leading causal explanation for constructs related to SPAs, such as self-efficacy...and self-concept..... Moreover, one of the most established theories of SPAs assumes that the development of individual differences in SPAs is shaped primarily by parents' beliefs, expectations, attitudes, and behaviors...

Of course, the bulk of the academic literature will surely go right on assuming that self-construct is driven by shared environment: "Surely, you don't mean to imply that an entire field of research was a waste of time, do you?" And in the policy and non-profit worlds these results won't stop those "Book in Every Home" campaigns. Alas....

More results:

The genetic component of self-perceived abilities (SPA) is a good predictor of achivement, after you control for IQ.

Even after you control for IQ and self-perceived ability, there's still a big genetic residual--about as big as IQ's genetic channel: So there are big genetic drivers of school achievement that don't fit into the two simple boxes of IQ and SPA. Sounds like an opportunity for some productive data-mining....

The big genetic residual fits in with the fact that a person's income is vastly more heritable than can be explained by the IQ channel alone. There are more things in gene expression, Horatio, than are dreamt of in your WAIS-R.

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Sunday, July 12, 2009

Homo sapiens, not economicus   posted by Razib @ 7/12/2009 03:43:00 PM

Robert Frank is promoting his idea that Charles Darwin will become more important than Adam Smith as an intellectual forebear of future economics in The New York Times. That is fine as it goes but I suspect that the bigger issue in the sciences of humanity is that there will be problems with relying on only one disciplinary framework and one general model. For example Frank points out that evolutionary fitness is generally conceived of in a relative sense (population mean fitness being the baseline), but the same dynamic crops up in neuroscience due to biophysical computational efficiencies from relative heuristics as opposed to a laundry list of absolute fixed preferences. R. A. Fisher famously wished to lay the seedbed for a thermodynamics of evolution in The Genetical Theory of Natural Selection. Whether one can envisage this in evolutionary genetics, it seems even less likely in the human sciences, at least to the extent of making a generalization which is not trivial. The rut which orthodox evolutionary psychology has found itself in is probably due to this assumption that our species is at some biobehavioral equilibrium due to an exceedingly unrealistic model of evolutionary dynamics.

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Monday, July 06, 2009

Politics & personality   posted by Razib @ 7/06/2009 12:52:00 PM

Econlog has been having a running debate between Bryan Caplan and Arnold Kling on the relationship between politics and personality.


Wednesday, May 20, 2009

OXTR & prosociality   posted by Razib @ 5/20/2009 11:19:00 PM

The Oxytocin Receptor (OXTR) Contributes to Prosocial Fund Allocations in the Dictator Game and the Social Value Orientations Task:
The demonstration that genetic polymorphisms for the OXTR are associated with human prosocial decision making converges with a large body of animal research showing that oxytocin is an important social hormone across vertebrates including Homo sapiens. Individual differences in prosocial behavior have been shown by twin studies to have a substantial genetic basis and the current investigation demonstrates that common variants in the oxytocin receptor gene, an important element of mammalian social circuitry, underlie such individual differences.

Here's a figure from the paper:

And the SNPs from the HGDP (G = C & A = T for the first SNP, or at least the paper and PubMed agree on this):

Related: It's hard out here for a vole. Heritability of the Ultimatum Game. Altruism and Risk-Taking: Kinda Heritable. Can someone put the psychic unity of makind out of its misery? DRD4, politics & friendship.

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Thursday, April 09, 2009

Parents don't matter as much as you think....   posted by Razib @ 4/09/2009 04:49:00 PM

Jonah Lehrer interviews Judith Rich Harris on the topic of The Nurture Assumption. Related but coincidently I pointed to new research on the investment and returns which adoptive parents get, and how the results are not surprising in a behavior genetic context.


Tuesday, March 10, 2009

COMT & Fear   posted by Razib @ 3/10/2009 07:17:00 PM

Genetic Gating of Human Fear Learning and Extinction: Possible Implications for Gene-Environment Interaction in Anxiety Disorder:
Pavlovian fear conditioning is a widely used model of the acquisition and extinction of fear. Neural findings suggest that the amygdala is the core structure for fear acquisition, whereas prefrontal cortical areas are given pivotal roles in fear extinction. Forty-eight volunteers participated in a fear-conditioning experiment, which used fear potentiation of the startle reflex as the primary measure to investigate the effect of two genetic polymorphisms (5-HTTLPR and COMTval158met) on conditioning and extinction of fear. The 5-HTTLPR polymorphism, located in the serotonin transporter gene, is associated with amygdala reactivity and neuroticism, whereas the COMTval158met polymorphism, which is located in the gene coding for catechol-O-methyltransferase (COMT), a dopamine-degrading enzyme, affects prefrontal executive functions. Our results show that only carriers of the 5-HTTLPR s allele exhibited conditioned startle potentiation, whereas carriers of the COMT met/met genotype failed to extinguish conditioned fear. These results may have interesting implications for understanding gene-environment interactions in the development and treatment of anxiety disorders.

Also see ScienceDaily. Here's the COMT SNP in SNPedia. Also, here it is in the HGDP browser. A/A is low activity variant.

Related: Other posts on COMT.

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Sunday, March 01, 2009

Education & money   posted by Razib @ 3/01/2009 03:28:00 PM

About His Deposit...:
Caroline Hall was supposed to sign the contract a month ago guaranteeing a kindergarten spot for her son at an Upper East Side private school. He had already spent two happy years attending its early-childhood program.

But Ms. Hall, a corporate counsel, began ducking the school's calls. Where was her deposit toward the $22,000 tuition? The school had an eager waiting list.

Related, Privileged children excel, even at low-performing comprehensives:
Middle-class parents obsessed with getting their children into the best schools may be wasting their time and money, academics say today.

They found that children from privileged backgrounds excelled when they were deliberately sent to inner-city comprehensives by parents opposed to private schooling.

Most of the children "performed brilliantly" at GCSE and A level and 15 per cent of those who went on to university took places at Oxford or Cambridge.

See The Nurture Assumption: Why Children Turn Out the Way They Do. Also this Bryan Caplan post:
The bottom line for parents, as usual, is: Chill out. Your kid will probably do fine whatever you do. And even if he does badly, your parenting is unlikely to help.

Reminder: these are behavior genetic insights. Parents presumably have more information about their individual child; i.e, how susceptible your offspring might be to retarded peer pressure. I had many friends with whom I played b-ball as a teenager who would laugh at the fact that I read books for fun and talked shit about it, but that has pretty much zero impact on me. The esteem of my fellow man has always been rather low on the pecking order of my values (this somewhat autistic tendency explains my youthful flirtation is hardcore libertarianism).


Friday, February 20, 2009

A test for the pathogenic theory of homosexuality?   posted by ben g @ 2/20/2009 11:04:00 AM

Compare monochorionic to dichorionic twins. If there's a teratogen causing homosexuality then it should show up as a statistical difference in concordance for homosexuality.

Of course this would only tell us whether there is a prenatal pathogen. It wouldn't rule out the possibility that there is a pathogen that only strikes later on.


Monday, February 09, 2009

"Smoking related" anti-sociality heritable, not environment?   posted by Razib @ 2/09/2009 09:55:00 PM

Disentangling prenatal and inherited influences in humans with an experimental design:
Exposure to adversity in utero at a sensitive period of development can bring about physiological, structural, and metabolic changes in the fetus that affect later development and behavior. However, the link between prenatal environment and offspring outcomes could also arise and confound because of the relation between maternal and offspring genomes. As human studies cannot randomly assign offspring to prenatal conditions, it is difficult to test whether in utero events have true causal effects on offspring outcomes. We used an unusual approach to overcome this difficulty whereby pregnant mothers are either biologically unrelated or related to their child as a result of in vitro fertilization (IVF). In this sample, prenatal smoking reduces offspring birth weight in both unrelated and related offspring, consistent with effects arising through prenatal mechanisms independent of the relation between the maternal and offspring genomes. In contrast, the association between prenatal smoking and offspring antisocial behavior depended on inherited factors because association was only present in related mothers and offspring. The results demonstrate that this unusual prenatal cross-fostering design is feasible and informative for disentangling inherited and prenatal effects on human health and behavior. Disentangling these different effects is invaluable for pinpointing markers of prenatal adversity that have a causal effect on offspring outcomes....

I guess that's what economists would call a "natural experiment." In any case, these results are in light with the sort of arguments Judith Rich Harris lays out in her books. Much of the correlation we see behaviorally between parents and children actually being genetic, even though we have prior assumptions as to the importance of socialization in the behaviors in question. Here's the primary figure:


From the results:
These results therefore point to the importance of inherited factors in the association between prenatal smoking and offspring antisocial behavior and suggest that gene-environment correlation is important in explaining this association

The data show that mothers who smoked in the sample tended to have anti-social offspring. There was a correlation. But when broken down by relatedness the data showed that the effect existed among related mothers and offspring, but not unrelated. The inference then is that the smoking-anti-sociality likely had more to do with personality traits in women who would smoke while pregnant, and who would pass those personality traits to their offspring.

Addendum: What kind of maniac would go through in vitro and then smoke! Just sayin'.


Tuesday, February 03, 2009

Genes and Social Networks   posted by Piccolino @ 2/03/2009 04:13:00 PM

Heritability estimates are slippery animals, but this recent PNAS paper is a great illustration of how they can be used to discipline theories of social network formation. The authors start by showing that three building blocks of social networks are heritable, namely the number of friends you have, the number of people who name you as a friend, and the likelihood that two of your friends are also friends. They then ask if existing theories of social network formation are consistent with empirical fact that a large share of individual variation in these buildling blocks is explained by individual characteristics. Perhaps not too surprisingly to readers of this blog, a model which allows individuals to differ ex ante does considerably better than models which make a blank slate assumption. The paper also fits in nicely in the tradition of behavior genetic work which emphasizes how people based on their inherited traits self-select into particular environments. Razib pointed out the other day that we can taxonomize traits into those whose genetic architecture we understand pretty well (skin coloration) and those that are still a puzzla (IQ). I am curious to see where the social network building blocks fit in. I have no doubt we will have the answer to this question very soon.


Sunday, February 01, 2009

Behavior genetics + economics = ?   posted by Razib @ 2/01/2009 12:03:00 AM

A week ago I posted MAOA, aggression and behavioral economics. In a related vein, I thought I would point again to Genetic Variation in Preferences for Giving and Risk-Taking (see Herricks' post on this last fall). From the conclusion:
In this paper, we have presented an empirical investigation into the relative contributions of individual differences in genes an environment to observed variation in economic preferences for risk and giving...While our results do not allow us to be as assertive as Sir Francis Galton, they do suggest that humans are endowed with genetic variation in their proclivity to donate money to charity and to take risks. By now there is a plethora of studies exploring th sources of individual variation in economic experiments and games, yet up until recently considerations of genetic influences have remained relativel absent. Here we have argued that this failure to consider genes obscures an important source of preference heterogeneity. Ultimately, we hope that a better understanding of the underlying individual genetic economic preferences, and the adaptive pressures under which these preferences evolved will lead to a more comprehensive economic science that can bridge some of the unexplained gaps between empirical data and economic theory....

You can read the whole paper at the link provided. The paper mentions the AVRP1a gene's association with variation in the dictator game. Of course, variation on this locus has many correlates, so I'm sure that the dopamine receptor related genes will also pop-up in the behavior economic literature soon enough. Get a big enough alphabet soup of genes, and perhaps we can go from talking about behavioral genetics & economics, to behavioral & economic genomics. I'm betting this game will resemble the genetic architecture of skin color more than IQ or height. Note how some of these loci show up over & over again in the literature, in different disciplinary contexts & behavioral phenotypes.


Friday, January 23, 2009

MAOA, aggression and behavioral economics   posted by Razib @ 1/23/2009 07:18:00 PM

Monoamine oxidase A gene (MAOA) predicts behavioral aggression following provocation:
Monoamine oxidase A gene (MAOA) has earned the nickname "warrior gene" because it has been linked to aggression in observational and survey-based studies. However, no controlled experimental studies have tested whether the warrior gene actually drives behavioral manifestations of these tendencies. We report an experiment, synthesizing work in psychology and behavioral economics, which demonstrates that aggression occurs with greater intensity and frequency as provocation is experimentally manipulated upwards, especially among low activity MAOA (MAOA-L) subjects. In this study, subjects paid to punish those they believed had taken money from them by administering varying amounts of unpleasantly hot (spicy) sauce to their opponent. There is some evidence of a main effect for genotype and some evidence for a gene by environment interaction, such that MAOA is less associated with the occurrence of aggression in a low provocation condition, but significantly predicts such behavior in a high provocation situation. This new evidence for genetic influences on aggression and punishment behavior complicates characterizations of humans as "altruistic" punishers and supports theories of cooperation that propose mixed strategies in the population. It also suggests important implications for the role of individual variance in genetic factors contributing to everyday behaviors and decisions.

Regularly readers know we've talked about MAOA in the past, it's one of those big-effect genes which keeps popping up in behavior genetic studies. It definitely increases my confidence in the reality of past associations to see it produce results in experimental situations which match our predictions. Along with the dopamine receptor loci this is likely a keeper. The issue of mixed strategies is something I've been mentioning periodically, the idea of evolutionary game theory has been around for nearly two generations, and frequency dependent selection is over a century old. But I think far too often people who are interested in the intersection between biology and behavior start conversations which assume that these are minor or trivial dynamics. At a certain point if "transient" states are more common than periods when there is an ESS, you need to reorient your frame. Human environments (that is, cultures) change a lot. Sometimes that change is exogenous (consider shifting climate), but in many cases instability in the background parameters upon which an ESS is conditional might result in periodic shifts in state.* Peter Turchin's work to some extent describes this on the macro-level, while Martin Nowak has developed models on a smaller scale. The main unfortunate byproduct of accepting this relatively more complex explanatory framework is that it makes glib assertions about natural selection on behavioral traits more difficult.

Here's the ScienceDaily summary.

* Basically, if you figure out an "unbeatable" strategy at winning a game, you are screwed when the rules change.


Wednesday, October 29, 2008

Evolution and trustworthiness   posted by Razib @ 10/29/2008 11:20:00 PM

Evolution of trust and trustworthiness: social awareness favours personality differences (Open Access):
Interest in the evolution and maintenance of personality is burgeoning. Individuals of diverse animal species differ in their aggressiveness, fearfulness, sociability and activity. Strong trade-offs, mutation-selection balance, spatio-temporal fluctuations in selection, frequency dependence and good-genes mate choice are invoked to explain heritable personality variation, yet for continuous behavioural traits, it remains unclear which selective force is likely to maintain distinct polymorphisms. Using a model of trust and cooperation, we show how allowing individuals to monitor each other's cooperative tendencies, at a cost, can select for heritable polymorphisms in trustworthiness. This variation, in turn, favours costly 'social awareness' in some individuals. Feedback of this sort can explain the individual differences in trust and trustworthiness so often documented by economists in experimental public goods games across a range of cultures. Our work adds to growing evidence that evolutionary game theorists can no longer afford to ignore the importance of real world inter-individual variation in their models.

The fact that evolutionary psychology traditionally focuses on universal traits which are genetically fixed while behavior genetics is preconditioned on heritable variation of similar traitshas been a distinction which has been brought to light by skeptics of any biological component to human behavior. In The Undiscovered Mind John Horgan attempted to throw cold water on the rise of neuro and cognitive sciences precisely using this sort of tactic. Though I think many critics of evolutionary psychology argue in bad faith, at the end of the day some of their criticisms land on target because of the huge sample space of laugh-out-loud "theorizing" by scholars fixated on an outmoded paradigm.

Humans are not the same. We vary. And we vary in part because of heritable biological factors. Some evolutionary psychologists, Satoshi Kanazawa comes to mind, work under an old model where deviations from their expectation of human modal behavior is treated simply as trivial holdovers along the transient from the ancestral to the derived phenotype, or noise introduced by environmental factors. Because of he elegant simplicity of their model evolutionary psychologists of this school are expert verbal showmen.

Certainly there are plenty of human universals. But there are plenty of non-universals. We are familiar with the Red Queen hypothesis in relation to our immune systems. This model arose in large part because of the necessity for constant evolution in the forever war with parasites. If humans are a cultural animal par excellence for whom the flexibility of their behavioral toolkit is essential, should it surprise us if frequency dependent evolutionary dynamics result in a large number of morphs constantly cycling? Perhaps H. sapiens is the environment of evolutionary adaptedness of H. sapiens?

Related: Heritability of the Ultimatum Game, Altruism and Risk-Taking: Kinda Heritable and Variation as the ultimate.

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Thursday, September 25, 2008

Altruism and Risk-Taking: Kinda Heritable   posted by Herrick @ 9/25/2008 03:08:00 PM

Economists are getting into the twin-study game more often. The latest entry is forthcoming in the Harvard-MIT run Quarterly Journal of Economics. They ran tests on a bunch of Swedish twins, tests that involved real money. The goal: See how altruistic they were (how much money did they share with a pro-homeless charity?) and see how risk-tolerant they were (how big does the reward have to be before they'd take a risky gamble?).

Key quote:
[W]e have used standard behavior genetic techniques to decompose variation in preferences for giving and risk-taking into environmental and genetic components. We document a significant genetic effect on risk taking and giving, with genes explaining approximately 20% of phenotypic variation in the best fitting models. The estimated effect of common environment, by contrast, is smaller.

So E>A>C, a common result. Since economists have spent a fair amount of time arguing for the social construction of preferences, it's good to have some evidence that shared family environment--presumably one important kind of "social construction"--apparently has only a modest association with routine economic preferences.

Note: This is the same group of researchers that found that 40% of "responder" behavior in an ultimatum game was heritable.

Conclusions: 1. The Swedish Twin Registry is a treasure. 2. Responder behavior (basically, willingness to punish even when it's expensive to punish) seems about twice as heritable as risk-taking and altruism. We're only going on two studies here, but that's an interesting result: Perhaps "Desire for justice/revenge" is more heritable than "Fear of loss" and "Kindness."


Friday, July 18, 2008

The Inheritance of Inequality: Big Insight, Small Error   posted by Herrick @ 7/18/2008 03:58:00 PM

Gintis and Bowles have done great work cleaning up a lot of the discussion about cooperation, evolution, and economic outcomes. A Google Scholaring of their names turns up 14 items with over 100 citations, most of which would be well worth reading for GNXP regulars.

But that said, in their 2002 Journal of Economic Perspectives piece "The Inheritance of Inequality," they appear to make a small error. It's an error that's all-too-easy for even good folks to make: They apparently squared the h-squared.

Their big insight and their small error are all part of answering a simple question: How much of the correlation of income between parent and child can be explained by the heritability of IQ? You might think it's straightforward: IQ is highly heritable, so if there's some channel linking IQ to income, then it's all over but the shouting.

But numbers matter. And Gintis/Bowles work out the numbers, finding that there's a weak link in that causal chain: The low correlation (0.27 according to Gintis and Bowles) between IQ and wages. The causal chain goes like this:

1. Parental earnings have a 0.27 correlation with parent's IQ.
2. Heritability of IQ between parent and child is a bit more than 1/2 of h-squared (why a bit more? assortive mating). They take an h-squared of 0.5 for IQ.
3. Child's earnings have a 0.27 correlation with child's IQ.

So the net result is 0.27*0.3*0.27 = 0.022 (page 10). A very small number, especially since the raw parent-child income correlation in U.S. data is about 0.4. So yes, knowing a parent's income helps you predict their adult (especially male) child's income. But only 5% (or 0.022/0.4) of the total correlation can be explained by IQ's impact on wages. Small potatoes.

(Oh, but where's the small error? It's where Gintis and Bowles report that the net result is 0.01 instead of 0.022--a difference that I can most easily attribute to a mistaken squaring of the h-squared.)

If I really wanted to get that net result up from a measly 5%--if I knew in my heart that IQ really was a driving force in intergenerational income inequality--then how would I do it? Well, I might use a higher heritability of IQ, I might assume more assortive mating, or I might assume a bigger correlation between wages and IQ.

Hard to do much to budge that IQ/wage link: Zax and Rees's paper only has a 0.3 correlation between teenage IQ and middle-aged wages, and when Cawley, Heckman et al. regress NLSY wages on the first 10 principal components of the AFQT, they get a similar result.

So you think maybe a higher heritability of IQ will save you? Well, let's just go all the way to perfect heritability of IQ and perfect assortive mating on IQ. In other words, let's see if "IQ clones" will be have enough similarity in wages to match the 0.4 intergenerational correlation of income.

Will the IQ clones have similar incomes? Not so much. (0.3^2)*1 still equals something small: 0.09. Less than 1/4 of the intergeneration correlation in income. Medium-sized potatoes, but we had to make a ton of ridiculous assumptions to get there.

It's that doggone low correlation between IQ and wages, a correlation that has to be squared because we're comparing parent to child. So a high heritability of IQ doesn't imply a high heritability of IQ-caused-income. Another reminder that lots of things impact your wages: Not just how smart you are.

Gintis and Bowles work through some finger exercises to argue for big environmental effects, and that's all well and good. But to my mind, the interesting fact is that income is still highly heritable!

G/B report that MZT (identical twin) earnings correlation is 0.56, and DZT (fraternal twin) earnings correlation is 0.36, so using the crudest of approximations, the heritability of earnings is still (0.56-0.36)*2=0.4. So income apparently has a modestly high heritability, but most of it can't be explained by the IQ-wage channel. Looks like the genetic heritability of income is being driven mostly by non-IQ channels.

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Friday, June 27, 2008

Heritability of voting   posted by Razib @ 6/27/2008 01:44:00 PM

Genetic Variation in Political Participation:
The decision to vote has puzzled scholars for decades...The results show that a significant proportion of the variation in voting turnout can be accounted for by genes. We also replicate these results with data from the National Longitudinal Study of Adolescent Health and show that they extend to a broad class of acts of political participation. These are the first findings to suggest that humans exhibit genetic variation in their tendency to participate in political activities.

Additive genetic variance ~ 0.50. You can read the whole paper, though I've blogged it elsewhere.


Sunday, June 22, 2008

Expel the 7R?   posted by Razib @ 6/22/2008 12:25:00 PM

Dan at Genetic Future, a great guy, has another DRD4 post up. He has reproduced a chart from an article in The Economist which shows a trend where a higher frequency of the 7R (ADHD correlated variant) is found in groups which have migrated a greater distance. He asks whether "the "novelty-seeking" behavior associated with ADD may have extended into a desire to explore new territories." My first thought was this: perhaps people with the 7R variant were more likely to be kicked out of the tribe or village because they couldn't/wouldn't conform. Certainly the chart seems to imply that stable populations hovering around the Malthusian limit probably aren't too congenial for nonconformists. This is the argument at the heart of books such as The Moral Consequences of Economic Growth and Age of Abundance, though obviously there wasn't a genetic perspective there.

In any case, I think there's going to be some interesting stuff coming out of this area correlating lifestyle with personality profiles. You might recall that in Farewell to Alms Greg Clark repeated the old truism that farmers tended not to be more affluent than hunter-gatherers, and in fact the balance of the data implies most hunter-gatherer and nomadic groups have a median physiological fitness that is greater than that among farmers as measured by size and nutrition as evidenced by enamel growth. The genius of farming is that it obviously increased the productivity per unit area in terms of calories and so supported larger populations (physiological fitness obviously does not translate into reproductive fitness always), but it seems to me that the less violent and risky nature of this lifestyle (famines notwithstanding) meant that there was also less room for the nonconformists on the margins. I've argued in the past in some ways theat modern individualistic Westerners have more in common with hunter-gatherers than with peasants in "traditional" societies in regards to their mores. I wonder if the need and necessity for straight-jacket social control in village life induced a powerful bout of purifying selection against 7R across much of Eurasia, a pressure that is only now being relaxed.

Addendum: The expulsion of male misfits is one of the accounts given of the founding of Greek colonies. Of course, it could simply be that the annalists used the argument that these men were misfits to get rid of them and they were actually economical marginals who were a burden upon the citizenry.

Update: I want to be clear here to note that I don't expect that all H & G societies would favor 7R more than farmers. Just that I think that the constraints of an agrarian lifestyle around the Malthusian limit would result in less tolerance of variance of behavior on the margins. The marginal slack for H & G groups I assume would be due to more frequent tribe-level extinctions, war and interpersonal violence, as well as localized ecological parameters which have a more direct impact on H & G peoples.

Related: DRD4 posts.


Friday, June 20, 2008

The benefits of the bad: they "hit it" (males at least)   posted by Razib @ 6/20/2008 01:08:00 AM

Bad guys really do get the most girls:
But being just slightly evil could have an upside: a prolific sex life, says Peter Jonason at New Mexico State University in Las Cruces. "We have some evidence that the three traits are really the same thing and may represent a successful evolutionary strategy."
This observation seems to hold across cultures. David Schmitt of Bradley University in Peoria, Illinois, presented preliminary results at the same meeting from a survey of more than 35,000 people in 57 countries. He found a similar link between the dark triad and reproductive success in men. "It is universal across cultures for high dark triad scorers to be more active in short-term mating," Schmitt says. "They are more likely to try and poach other people's partners for a brief affair."
"They still have to explain why it hasn't spread to everyone," says Matthew Keller of the University of Colorado in Boulder. "There must be some cost of the traits." One possibility, both Keller and Jonason suggest, is that the strategy is most successful when dark triad personalities are rare. Otherwise, others would become more wary and guarded.

Frequency dependence. Control for environment and one might assume that personality morphs will hit an equilibrium in terms of relative proportion; but of course one assumes that any normal environment will be subject to exogenous shocks which jar the equilibrium on a regular basis. I wish popular science articles would bring up Hawk vs. Dove dynamics more often to introduce the general concept of variant strategies in populations. The relevance of this sort of result to recent posts should be pretty obvious, and is also one reason many people were always less than enthusiastic about Evolutionary Psychology's monomaniacal focus on human universals.


Thursday, June 19, 2008

Dogs, behavior & genomics   posted by Razib @ 6/19/2008 12:30:00 PM

A reader pointed me to this paper, Single-Nucleotide-Polymorphism-Based Association Mapping of Dog Stereotypes:
...Analysis of other morphological stereotypes, also under extreme selection, identified many additional significant loci. Less well-documented data for behavioral stereotypes tentatively identified loci for herding, pointing, boldness, and trainability. Four significant loci were identified for longevity, a breed characteristic not under direct selection, but inversely correlated with breed size. The strengths and limitations of the approach are discussed as well as its potential to identify loci regulating the within-breed incidence of specific polygenic diseases.

I've placed an important table below the fold.


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Sunday, June 15, 2008

More DRD4   posted by Razib @ 6/15/2008 04:58:00 PM

Since I've been posting on DRD4 a bit, a reader asked that I post this link: A gene X gene interaction between DRD2 and DRD4 is associated with conduct disorder and antisocial behavior in males. It's Open Access, so you can read the whole thing. Also, you might be interested p-ter's critique of the MAOA research program before you go whole-hog on a behavior genetic kick.


Wednesday, June 11, 2008

DRD4, politics & friendship   posted by Razib @ 6/11/2008 12:56:00 PM

Dan points me to this working paper, Friendships Moderate an Association Between the DRD4 Gene and Political Ideology:
Studies of identical and fraternal twins suggest that political ideology has a heritable component...but no specific gene associated with...political ideology has so far been identified. Using data from the National Longitudinal Study of Adolescent Health, we investigate the moderating influence of friendships on the contribution of the 7R allele of the DRD4 gene to liberal political ideology. The number of self-nominated friendships in adolescence moderates the influence of the gene on political ideology; the more friends nominated, the stronger the liberal ideological identification of the respondent in early adulthood. This is the first study to elaborate a specific gene-environment interaction that contributes to ideological self-identification.


Related: Optimal personality and way of life. Heritability of the Ultimatum Game.


Monday, June 09, 2008

Optimal personality and way of life   posted by Razib @ 6/09/2008 06:21:00 PM

Update: Here's the paper, Dopamine receptor genetic polymorphisms and body composition in undernourished pastoralists: An exploration of nutrition indices among nomadic and recently settled Ariaal men of northern Kenya. I've put the most relevant figure below the fold.

Is ADHD An Advantage For Nomadic Tribesmen?:
While those with the DRD4/7R allele were better nourished in the nomadic population, they were less well-nourished in the settled population. Although the effects of different versions of dopamine genes have already been studied in industrialized countries, very little research has been carried out in non-industrial, subsistence environments like the areas where the Ariaal live, despite the fact that such environments may be more similar to the environments where much of human genetic evolution took place.

6 years ago, In our genes:
Our hypothesis suggests that the absence of 7R in East Asia is recent, consequent to the establishment of powerful polities that allowed population growth and forced agricultural intensification. It is of interest in this context that 2R alleles in China are probably derived from 7R alleles by recombination, suggesting that the loss of 7R is indeed recent.

Besides lowland South America, another well known region with local anarchy and female farming is highland New Guinea. Our model of the dynamics of 7R predict that the frequency is very high in those populations. Because they have been there for tens of thousands of years and they have not moved, the Chen et al. (2) model predicts a low frequency of 7R there. This is a natural test to distinguish the two hypotheses. A 7R frequency of 0.25 was reported (2) for a sample from New Guinea, but it is not reported even in the original source of the data whether it was from a highland or coastal population.

In some societies 7R allele may lower fitness even when rare, as is probably the case in East Asia and among the !Kung Bushmen. In such populations it would stay rare even in the presence of gene flow from neighboring populations, even from neighbors with a social system that favors 7R alleles. Neutral genes would show no sharp boundary between the two populations, whereas alleles affecting behavior should show a sharp spatial gradient. This is likely to be the case with the 7R allele because some adjacent populations have very different 7R frequencies.

Here's a map which shows some geographic variation for the 7R repeat.

Related: Genetic Future has more.


Tuesday, January 29, 2008

Plagues & molecules?   posted by Razib @ 1/29/2008 08:14:00 PM

Two interesting articles out in the PNAS early release feed.

Molecular insights into human daily behavior:
Human beings exhibit wide variation in their timing of daily behavior. We and others have suggested previously that such differences might arise because of alterations in the period length of the endogenous human circadian oscillator. Using dermal fibroblast cells from skin biopsies of 28 subjects of early and late chronotype (11 "larks" and 17 "owls"), we have studied the circadian period lengths of these two groups, as well as their ability to phase-shift and entrain to environmental and chemical signals. We find not only period length differences between the two classes, but also significant changes in the amplitude and phase-shifting properties of the circadian oscillator among individuals with identical "normal" period lengths. Mathematical modeling shows that these alterations could also account for the extreme behavioral phenotypes of these subjects. We conclude that human chronotype may be influenced not only by the period length of the circadian oscillator, but also by cellular components that affect its amplitude and phase. In many instances, these changes can be studied at the molecular level in primary dermal cells.

Weird. ScienceNow notes some implications:
...raises the possibility of an inexpensive and objective test of a person's "owlness" or "larkness." Such a test would be no small matter, given the prevalence of sleep disorders and the fact that many drugs, including cholesterol medications and chemotherapy, work more effectively if administered at certain points in a person's sleep/wake cycle. Pinpointing individual clock cycles could pave the way for personalized sleep and drug therapies, says Achim Kramer, a Free University chronobiologist who helped design the study.

Selectivity of Black Death mortality with respect to preexisting health:
Was the mortality associated with the deadliest known epidemic in human history, the Black Death of 1347-1351, selective with respect to preexisting health conditions ("frailty")? Many researchers have assumed that the Black Death was so virulent, and the European population so immunologically naive, that the epidemic killed indiscriminately, irrespective of age, sex, or frailty. If this were true, Black Death cemeteries would provide unbiased cross-sections of demographic and epidemiological conditions in 14th-century Europe. Using skeletal remains from medieval England and Denmark, new methods of paleodemographic age estimation, and a recent multistate model of selective mortality, we test the assumption that the mid-14th-century Black Death killed indiscriminately. Skeletons from the East Smithfield Black Death cemetery in London are compared with normal, nonepidemic cemetery samples from two medieval Danish towns (Viborg and Odense). The results suggest that the Black Death did not kill indiscriminately-that it was, in fact, selective with respect to frailty, although probably not as strongly selective as normal mortality.

We've all read Farewell to Alms, so we know the argument that quick die offs can be good for standards of living by relieving some of the Malthusian pressure. Though if you ever took a normal medieval history course you'd probably be told about the premium on labor which emerged after the Black Death due to shortages and its affect on the collapse of the old manorial system (I was). But this data is interesting because it confirms that the most economically productive proportion a society where muscle power might was of essence have increased as a proportion of the population after these sorts of epidemics swept through. Perhaps these are the sorts of shocks that social systems need to shift toward another equilibrium? (I know, morbid)

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Tuesday, January 15, 2008

Life is not random, there are patterns in numbers....   posted by Razib @ 1/15/2008 11:56:00 PM

Jonathan Rauch has an amusing piece in Reason, The Coming American Matriarchy. To some extent it is not noteworthy, it's the sort of thing you see in the mainstream press when journalists skim over data sets for some superficial insights. I know some D.C. libertarians do read this weblog, so they should point out the silliness of the column to Rauch. Consider:

The number 1.5 is, in this case, a ratio. According to projections by the National Center for Education Statistics, in 2017 half again as many women as men will earn bachelor's degrees. In the early 1990s, six women graduated from college for every five men who did so; today, the ratio is about 4-to-3. A decade from now, it will be
3-to-2-and rising, on current trends.
A college degree used to be a rarity: a mark of privileged or professional status. As recently as 1950, fewer than half of Americans even finished high school, let alone went on to college.
In other words, today's young people already live in a world where, among their peers, women are better educated than men. As the grandparents die off, every year the country's college-educated population will become more feminized. In a couple of decades, America's educational elite will be as disproportionately female as it once was male.

Here's the problem here: having a college degree once meant that you were part of the educational elite because a college degree was rare. Rauch admits that it is no longer rare, and likely at some point in the future the majority of young adults will be expected to have a college degree of some sort as a minimal qualification for a non-manual job. If the majority have a particular credential, it is no longer a good elite signaler. Additionally, it is a relatively well known fact across many domains of achievement males are disproportionately found at the higher ranks even if there is numerical parity. About the same number of medical school graduates are now male or female, but the latter tend to go into "low status" tracks relative to the former (e.g.,
surgery vs. family practice). Here is Helena Cronin:
Similarly, consider the most intellectually gifted of the USA population, an elite 1%. The difference between their bottom and top quartiles is so wide that it encompasses one-third of the entire ability range in the American population, from IQs above 137 to IQs beyond 200. And who's overwhelmingly in the top quartile? Males. Look, for instance, at the boy:girl ratios among adolescents for scores in mathematical-reasoning tests: scores of at least 500, 2:1; scores of at least 600, 4:1; scores of at least 700, 13.1.

These patterns are banal and well known to regular readers of this weblog, to the point where I don't post on these topics much. But Jonathan Rauch seems like a smart enough fellow, and Reason is heterodox enough to publish someone like Ron Bailey. There are real issues here of possible interest. For example, as the proportion of female lawyers increases I wonder if firm culture may change enough so that the billable hour system becomes a thing of the past. Such a transformation might have have the outcome of diminishing the handicap that women face in making partner (because women are, on average, burdened with more expectations in family life than men). I also don't think that intelligence or its distribution are the only characteristics to consider; personality seems to be a major area of difference between the sexes that might shape their life outcomes. Finally, there are studies which suggest women tend to be much more critical of female co-workers, a powerful united sisterhood might not be a good model for the shape of future XX dominated professions. Numbers like this can stimulate some interesting projections...but imagining a 'matriarchy' really is a waste of column space.

Addendum: Terms like 'patriarchy' or 'matriarchy' make it seems like men or women in the plural dominate the other sex. This of course elides over intrasexual dynamics. For example, extreme patriarchies such as the Saudi kingdom, do not benefit all men at the expense of all women. Rather, usually these extremely sex differentiated systems as a matter of course crystallize and reinforce the dominance of a particular oligarchic clique (e.g., the House of Saud and their clients). Marginalized males may also be quite oppressed by the patriarchy. My own opinion is that the relative weakness of sisterhoods as opposed to brotherhoods is the main reason that patriarchy has become so common over the last 10,000 years.


Wednesday, December 19, 2007

Cheaters beware   posted by Razib @ 12/19/2007 12:37:00 PM

More 'altruistic' punishment in larger societies:
...Second-party punishment is when you punish someone who defected on you; third-party punishment is when you punish someone who defected on someone else. Third-party punishment is an effective way to enforce the norms of strong reciprocity and promote cooperation. Here we present new results that expand on a previous report from a large cross-cultural project. This project has already shown that there is considerable cross-cultural variation in punishment and cooperation. Here we test the hypothesis that population size (and complexity) predicts the level of third-party punishment. Our results show that people in larger, more complex societies engage in significantly more third-party punishment than people in small-scale societies.


Monday, November 05, 2007

Breastfeeding & IQ & norm of reaction   posted by Razib @ 11/05/2007 06:07:00 PM

Read it here.

Update: Eye on DNA has much more.

Jason M. adds: In the comments HapMap Jockey Marc again applies the wisdom from p-ter's HapMap How-2 to the latest IQ genes:
In the study itself, there were two cohorts: a British cohort and a New Zealand cohort. In both cohorts, presence of the C allele (as either CC or CG) was associated with a hike in IQ by 6.4 and 7.0 points (from around 99-100 to around 106) in the two samples. But those without the C allele (GG) had mean IQs of 99.5 in Britain and 100.3 in New Zealand.

Incidentally, I plugged rs174575 into the ol' Hapmap, and it seems that the C allele has a frequency rate of 72% among Utah whites, 73% among Yorubans, 89% among the Chinese, and 90% among the Japanese.

Assuming these numbers are representative, universal breastfeeding alone would lead to a gap of 1.12 to 1.225 in IQs between East Asians and whites, favoring East Asians.

On the other hand, since whites and blacks have nearly the same C allele frequency (assuming, again that these numbers are representative of white and black populations), but whites breastfeed their babies at higher rates than blacks (60% vs. 30%, according to Steve), this is pretty solid evidence that increasing the percentage of black women who breastfeed their children will have a diminishing effect on the black white IQ gap.

Since I'm already blowing off work (damn you, Gene Expression!) I might as well do the calculations. Let's see... The 30% difference in breastfeeding is responsible for between 1.4 and 1.53 points in the black-white IQ gap! (I got these figures by multiplying the frequency rate of the C allele in Yorubans with the percentage difference in breastfeeding between blacks and whites with the effects of breastfeeding on the IQs of C allele carriers.)

Steve Sailer is vindicated!

Additional props to Rob in the comments at FuturePundit.

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Monday, October 15, 2007

Martin Nowak profile   posted by Razib @ 10/15/2007 10:27:00 AM

Another profile of Martin Nowak, Cooperation counts for math professor.


Tuesday, October 02, 2007

Heritability of the Ultimatum Game   posted by Razib @ 10/02/2007 11:12:00 AM

Finally, behavioral economics & human variation! Heritability of ultimatum game responder behavior:
Experimental evidence suggests that many people are willing to deviate from materially maximizing strategies to punish unfair behavior. Even though little is known about the origins of such fairness preferences, it has been suggested that they have deep evolutionary roots and that they are crucial for maintaining and understanding cooperation among non-kin. Here we report the results of an ultimatum game, played for real monetary stakes, using twins recruited from the population-based Swedish Twin Registry as our subject pool. Employing standard structural equation modeling techniques, we estimate that > 40% of the variation in subjects' rejection behavior is explained by additive genetic effects. Our estimates also suggest a very modest role for common environment as a source of phenotypic variation. Based on these findings, we argue that any attempt to explain observed ultimatum bargaining game behavior that ignores this genetic influence is incomplete.

That means that 40% of the variation in response to the Ultimatum Game is due to variation in genes. Yes, I know the Ultimatum Game is pretty bizarre. And I know there might be all sorts of complexities. But it's a start!

(and it's Open Access)


Wednesday, August 22, 2007

Demon rum   posted by Razib @ 8/22/2007 09:05:00 PM

Baltic neighbours face alcohol crisis:
The Estonian government plans to raise taxes on alcohol by 30% next year as the small Baltic nation of 1.3 million is struggling with a drink problem....

Finland has traditionally had very strict controls on alcohol. Strong drinks can only be bought in the state-controlled Alko shops - rather uninviting buildings which have few signs outside advertising their wares.

In related news, Evidence of positive selection on a class I ADH locus:

...Products of the three class I ADH genes that share 95% sequence identity are believed to play the major role in the first step of ethanol metabolism...we used genomic data to test the hypothesis...Both the F(st) statistic and the long-range haplotype (LRH) test provided positive evidence of selection in several East Asian populations...Interestingly, this haplotype is present at a high frequency in only some East Asian populations, whereas the specific allele also exists in other East Asian populations and in the Near East and Europe but does not show evidence of selection with use of the LRH test. Although the ADH1B*47His allele conveys a well-confirmed protection against alcoholism, that modern phenotypic manifestation does not easily translate into a positive selective force, and the nature of that selective force, in the past and/or currently, remains speculative.

What's going on here? As a great man once said, maybe it's agriculture?

Though seriously, I doubt that protection against alcoholism here is a major issue. So why is it being selected? Who knows. It seems likely that ADH1B is somehow involved in metabolization of various biochemicals which might have fitness implications. What are these populations consuming? And what aren't the other populations consuming? Or, perhaps they're consuming similar things (at least biochemically), but other (e.g., Near Eastern) populations have different selected alleles or functionally relevant loci which result in no great selection on the ADH1B allele in question.

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Tuesday, August 07, 2007

ADHD & DRD4   posted by Razib @ 8/07/2007 10:45:00 AM

Polymorphisms of the Dopamine D4 Receptor, Clinical Outcome, and Cortical Structure in Attention-Deficit/Hyperactivity Disorder:
Possession of the DRD4 7-repeat allele was associated with a thinner right orbitofrontal/inferior prefrontal and posterior parietal cortex. This overlapped with regions that were generally thinner in subjects with ADHD compared with controls. Participants with ADHD carrying the DRD4 7-repeat allele had a better clinical outcome and a distinct trajectory of cortical development. This group showed normalization of the right parietal cortical region, a pattern that we have previously linked with better clinical outcome. By contrast, there were no significant effects of the DRD1 or DAT1 polymorphisms on clinical outcome or cortical development.

A correlation between the 7-repeat allele, which exhibits variation in frequency between populations, and ADHD is interesting and important. But it is nice to get some more functional specificity to clarify the chain of causation responsible for the correlation we see.

Related: In Our Genes.