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Post updated, 9/14/14 6/5/14. See below!

In my earlier post on Gregory Clark’s work, The Son Becomes The Father, I laid bare the case for the known high heritability of human behavioral traits (including values and attitudes) and life outcomes. As well, equally important, I illustrated the complete absence of shared environment influences on these – that is, the effect common environmental forces that children growing up together share. This includes parents and upbringing, making it abundantly clear that parents don’t leave a lasting impact on who we grow up to be. These are towards what I’m calling the “75-0-25 or something” rule, which echos Satoshi Kanazawa’s “50-0-50 rule” summarizing behavioral genetic research, only more accurately so. This “75-0-25 or something” rule means the following:

For the variance in behavioral traits and life outcomes, each factor accounts for the following fractions:

  • Heredity: 75% (though the variance is typically anywhere from 65% to almost 100%)
  • Shared environment: 0%
  • Unknown (classified as the “unique environment” or the “unshared environment”): 25%

(See also behavioral genetics in a nutshell | hbd* chick)

About that third component, the unexplained variance, or the “unique environment,” we have thus far failed to reliably find anything that can account for it. It is deemed “environmental” in the sense that it is not heritable and presumably not genetic in origin (although that is not likely entirely accurate), but we have no idea what factors comprise it.

It’s important to note these values only represent the estimates within a generation. It doesn’t necessarily hold between generations (or between other contexts), where gross environmental changes can and do have large effects on the manifestation of human traits. See my post Why HBD. (Anyone who fails to absorb this gets an automatic F grade.)

However, the large heritability estimates and the failure to find any reliable environmental modulates of within-cohort differences casts doubt on most any environmental theory. Quite likely, as with the case with diet and lifestyle (see Tweet of the Week), most of the ones you’ve heard are bunk. It seems likely that the human genome draws up a design for a certain organism (that is more or less faithfully executed) that is designed to function to process and negotiate its environment in a certain set of ways, and precise behavior depends on the circumstances of the day and the specifics of the situation (see my post Environmental Hereditarianism). This may be as good of an explanation as any, but I am looking for evidence of reliable environmental modulation. One apparent environmental modulation is that some individuals with certain sensitive temperaments may be permanent modified by certain environmental exposure. Post-traumatic stress disorder (PTSD), for example, appears to be highly heritable. As well, it seems only certain individuals are susceptible, even after experiencing traumatic events. This illustrates that the susceptibility and extent of environmental modification of human traits is bounded by genetic prescription.

The high heritability of behavioral traits and the general lack of environmental effect on human behavioral traits (along with knowledge of the past and evolutionary theory) also leads one to understand that differences between human groups, be those groups be races, nationalities, ethnic groups, regional populations, even clans/families (as with Gregory Clark’s work), must also have some (rather large) genetic basis. “Culture” then is to be understood as the collective manifestation of those differences – the product of each individual’s innate propensity acting on each other’s and the circumstances of the day. Hence, genetic factors underlie these divisions:

Europe Corruption 2013upinarms-mapgenmap3

For the above reasons, this should be a given, but, we see how that is received in this day and age.

Even for those who accept heritable human differences, there is some discomfort at their full implications. My earlier post More Twitter Wisdom featured discussion of the unease many people have with this notion. Ironically, this itself is due to heritable factors (and yes, for those who can’t connect the dots, the ease that I have with this idea is in part the product of my genetic inheritance). Some people fight this notion tooth and nail, often eschewing logic in the process. Useful information can come out of these discussions, however, and this post will be an example. A recent troll commenter took that track, and here I will answer his claims.

Heritability, as established by behavioral genetics, comes from multiple lines of evidence, spanning completely different study methods. Most poignant today are Genome-wide Complex Trait Analyses (GCTA), which look at the correlation between resemblance in phenotype to directly measured resemblance in genotype. These have confirmed the (additive, anyway) heritable contribution to traits like IQ, BMI, and alcoholism, etc. However, even before these direct analyses came on the scene, the older methods firmly established the high heritability of behavioral and cognitive traits.

The bulk of behavioral genetic studies compare identical twins (monozygotic, MZ) raised together with fraternal (dizygotic, DZ) twins raised together. This is a particularly powerful method, because you control for a vast array of confounds, down to shared uterine environment. The difference in similarity between MZ twins and DZ twins estimates heritability. However, this method has weaknesses. It truly can’t rule out shared environmental influences as being behind the twin correlation. And further still, even to the extent that it produces a shared environment measure, it can’t separate the effect of assortative mating from this (which inflates the DZ twin correlation). You need confirmation from other methods. And such other methods exist.

The most “pure,” in terms of assessing heritability, are studies looking at twins raised apart (MZA and DZA, as opposed to MZT and DZT). Indeed MZA studies give you direct measurements of the heritability estimate. Additionally, there are adoption studies, which – when looking at adopted siblings – give you a direct measurement of the shared environment. Other pedigree studies (full siblings vs half-sibs, sibs vs. adoptees) buttress these. And finally, the extended twin design, which look at not just twins, but parents, spouses, cousins, etc. can allow you to separate a variety of influences.

One study gives a chart neatly summarizing the results of all of these for IQ:

IQ Heritability Age This is from The Wilson Effect: The Increase in Heritability of IQ With Age (2013). The heritability of IQ in adulthood from large samples of twins reliably returns in the 0.8 range. As we see here, a few studies, including a reasonably sized (n ~ 500) from Sweden that was a MZT-MZA-DZT-DZA study found a heritability of IQ of 0.91 at age 65. One study (a biological sibling-adoption study, small sample though) found a heritability pushing 100%!

As seen here, adoption studies confirm the high heritability of adult IQ.

MZA studies, which are few and small, also confirm this. An apparent gap between the heritability found in MZA studies and the others is seen here. However, the combined sample size of MZA studies is only 187! The average heritability estimate from these of 0.74 is not horrendously off when one considers the small sample sizes.

The high early shared environment influence shows that in youth, environmental factors can make a difference. These influences diminish and disappear with time, dashing hopes of lasting parental influence. Some voices – including preeminent behavioral geneticist Robert Plomin himself – often try to claim that the increasing heritability of IQ and other behavioral traits can be boiled down to “gene-environment correlations” (rGE). The idea being that people seek out environments to suit their genetic proclivities (which they do), and the influence of that environment leads to the final trait. This is a nice rosy idea, because it appears to leave the door open to environmental manipulation, if we could intervene in the “proper” ways. However, it is fantasy. We clearly saw in my earlier post that the “gene-environment co-variance” was often negative! One’s environment seemed to be “making” one the opposite of what one would expect. Our experiences don’t shape our political attitudes like we think they do. So is the case with IQ.

Indeed, a meta-analysis of longitudinal twin and adoption studies attempted to test this idea. It sought to determine whether the increasing heritability of IQ could be explained by on-going environmental influence or genetic “amplification”; that is, the compounding of genetic effects over time. This is likely because the effect of each additional gene becomes more and more relevant as children grow up. Indeed, amplification is what they found:

Amplification IQ

Edit, 9/14/2014: [See also the work of John Feurst on the matter:

Genetic amplification versus G-E correlations | Occidentalist
Jensen and genetic amplification | Occidentalist
IQ and Genetic Amplification | Occidentalist

From the first link:

Initially, the rGE explanation seems reasonable; when it comes to individuals differences, it doesn’t seem outlandish to suppose that naturally born intellectuals might increase their verbal IQ through bookish behavior. On the subpopulation level, likewise, it’s doesn’t seem implausible that a propensity for studiousness might lead to cognitive enhancement. Yet, there are a few bumps which preclude a simple rGE model. For one, it’s not merely this or that measure of intelligence that increases but, rather, the central factor and its numerous correlates[6]. In effect, rGE theorists are forced to maintain that g is created from the outside in. (See theoretical diagram below). Since g is structurally the same across individuals, cultures, sexes, and subpopulations, not only would the patterns of one’s environment have to construct g, the patterns of everyone’s environment would have to construct the same g.

Additionally, IQ g has numerous endophenotypic correlates, such as the volume of white and grey matter, the mass of the prefrontal lobe, and total brain size [1, 11, 13] and the overlap between IQ (g) and many of these endophenotypes is entirely due to genetic influences [1, 13]. To explain this genetic covariation, rGE theorists must maintain that genetics sets the parameters for environmental selection, which leads to the development of different cognitive phenotypes, which, in turn, molds the endophenotypic differences, thus creating the three way correlation. Since the Phenotypic/endophenotypic correlations have been found to be a function of differential rates of change during the development process[9] (see figure 2), rGE theorists must maintain that this environmentally induced endophenotypic molding occurs primarily during the developmental process and starts early on. If we kept in mind what we said above, that the genes that lead to slight genetic IQ differences in infancy are the same genes that lead to large genetic based differences in adulthood, and note that the heritability of many dispositions also increases with age[4], we can readily identify the problem with this conception. Somehow, dispositional differences, which are under heavy environmental influence early on, must set the phenotypic/endophenotypic molding (environmental) parameters in a way that happens to correspond to the genetic driven phenotype that the individual will later express.

Also, from the third link above:

All of this should now be a moot point since Davies et al. (2011) has established the high narrow heritability (i.e., breeding value) of IQ. (If the high heritability or increasing heritability found in conventional twin studies was a function of (passive/evocative/active) GE correlations, as was argued, Davies et al. (2011) would have found a much lower narrow heritability in their study.)

***End Edit***]

Another criticism of the heritability of IQ is that it is modulated by socioeconomic status (SES) – that IQ is less heritable in poor families. A large and extensive study co-authored by Robert Plomin reviewed the literature on the gene-SES interaction and conducted their own analysis of this phenomenon (with a sample of 8,716 twin pairs) and found no such effect. The heritability was constant across SES, but the shared environment vs. unique environment varied (this was done on children).

As well, for the record, though the overwhelming bulk of data for behavioral genetic studies comes from Northwestern European countries and their derivatives, behavioral genetic results have been gathered outside the Western world. The same results for the genetic and environmental influences on IQ has been found in Japan, for example (additive heritable influence, A ~ 0.8; shared environment, C = 0). This is in line with other behavioral genetic results generated there and in South Korea, as mentioned in my earlier post. Many behavioral genetic studies are underway outside the West, and we should have these results soon.

But on that point, another criticism leveled at behavioral genetic studies is that, in the United States at least, IQ is less heritable for racial minorities such as Blacks and Hispanics. However, this too is false. Over at Human Varieties, analyses by bloggers Chuck and Dalliard (also here) found no modulation of the heritability of IQ by race.

Proponents of the efficacy of nurture – especially parenting – often repeat a few erroneous arguments. Here I will address them. One of them is the idea that parenting, while ineffective for most, may make a difference for individuals with certain temperaments. For example, perhaps the low IQ/shiftless/delinquent/criminal or otherwise poorly dispositioned might benefit from more authoritative parenting, say. It’s a nice idea to think about, but it doesn’t happen. This is essentially “Stolen Generations” wisdom. As we’ve seen in my earlier post, a massive review of twin and adoption studies found no significant shared environment effect on criminality in adults (well, modeling found a shared environment contribution of 0.09, which can generally regard to be non-significant given the enormous measurement error expected). Even an effect that operated on some children but not others would contribute to the overall average shared environment, which was negligible.

Edit, 6/5/14: [I wanted to expand on the above mentioned review of criminality (by Rhee & Waldman, R&W), particularly the appearance of a small but nonzero (though non-significant) shared environment finding. As we saw, the age the subjects are assessed seems to make a difference. As well, as discussed in my analysis on adolescent psychopathology below, the particular measure used – such who is doing the ratings – affect the values found. For example, self-ratings or ratings by parents tend to attenuate the heritability estimate, and both appear to inflate the shared environment estimate, at least in youth. The Rhee & Waldman meta-analysis is no exception. Here are the ADCE (A, or a2 = additive genetic variance; D, or d2 = non-additive genetic variance; C, or c2 = shared environment; E, or e2 = remaining variance) components as computed based on information given by different raters:

Rating method a2 d2 c2 e2 Total no. of pairs in category
Self-report 0.39 - 0.06 0.55 13,329
Other report (usually parents) 0.53 - 0.22 0.25 6,851
Criminal records 0.33 0.42 - 0.25 34,122

The total, or broad-sense heritability, H2 , is the sum of the additive (the narrow-sense heritability) and the non-additive genetic components. As we can see, when actual criminal records (a semi-objective metric) are used, as we've seen, the heritability shoots up to the usual range, at 0.75, and the shared environment estimate vanishes. The criminal record analysis also captures the largest number of subjects, bolstering its reliability. Parent reports, as seen below, inflate the shared environment measure. The self-report gives a negligible shared environment estimate, but reports a lower heritability estimate – which is not surprising, given that we can expect self-reported criminal behavior to be poorly reliable. It is unfortunate that R&W don't separate out parents from peers and other non-relative raters in "other report." Additionally, the adoption studies found a negligible shared environment impact of 0.05 between adoptive parents and adoptees. It is also too bad that R&W don't cross tabulate the results by rating and age. But, as discussed below, adolescent shared environment effects maybe an artifact of unreliable raters anyway.

(For the record, the countries spanned by the studies in the meta-analysis include the U.S., Canada, the U.K., Australia, Denmark, and Sweden.)

The bottom line, it's clear that when it comes to anti-social behavior, the 75-0-25 rule holds perfectly firm. Parents and parenting do nothing to create upstanding citizens, and heredity is considerably important. ***End Edit***]

Indeed, also supporting this is another massive meta-analysis of behavioral genetic influences on adolescent psychopathology (personality disorders). These captures various types of child misbehavior and dysfunction, including convenient diagnoses such as “oppositional-defiant disorder.” A look and the breakdown of their results is far more interesting than their main reported results. Typically, shared environment effects are seen in children (<18 years old). The main study reported this, but fortunately, they decomposed the type of measurements used. In addition to self-report and parental report, they also had teacher report, peer reports, and clinical diagnoses. The self and parental reports showed lower heritabilities (0.3-0.5) and significant (though small) shared environment components. However, when teacher or peer reports were used, they found much higher heritabilities, in the 0.65-0.8 range. As well, the shared environment impact vanished. Using clinical diagnosis also produced a zero shared environment impact. Considering the sheer size of this review, it’s clear that parental behavior dosen’t contribute to this malaise, even at these ages.

The problem of somewhat unreliable measurements (noise), especially coming from self-report, was illustrated in my earlier posts. Averaged peer ratings serve to adjust for this problem to an extent both by providing more proper social context by which to make accurate comparative ratings and by cancelling out fluke readings. Indeed, one behavioral genetic study, which attempted to investigate the idea of a “general factor of personality” (GFP), akin to g for cognitive ability, found that when using the combined scores of self and peer ratings, the heritabilities of the Big Five personality traits shot through the roof, with the additive heritable component being:

  • Extraversion: 0.86
  • Openness: 0.92
  • Neuroticism: 0.59
  • Agreeableness: 0.85
  • Conscientiousness: 0.81

This demonstrates that more accurate measurements consistently push up the heritability estimate (even pushing them towards 100%), giving us the basis of the 75-0-25 or something rule.

As for the sixth dimension of personality, “honesty-humility”, the H component of the six factor HEXACO, evidence of its high heritability is also established, as we saw previously. Indeed, a recent post by Peter Frost (Evo and Proud: Compliance with moral norms: a partly heritable trait?) discussed a twin study from Sweden that looked at various forms of dishonesty, such as fraudulently claiming sick benefits or evading taxes. And sure enough, these particular behaviors showed considerable heritability. There is a desperate need for cross cultural behavioral genetic analyses. Many dimensions of personality systems like the HEXACO (as imperfect as they are) are likely to systematically vary from culture to culture.

The usefulness of behavioral genetics – indeed, the single most powerful and solid area of all social science – is highly evident. But behavioral genetic methods can be used to address several long-standing questions. Here we see it’s clear that parents don’t leave much of an impact on our behavioral traits. But what about people who aren’t parents? Here I will look at two sets of important people, spouses and peers.

It is no secret that spouses correlate on behavioral traits. This, assortative mating, is a powerful force, as we’ve seen previously. There are two aspects where spouses are highly correlated – the things you don’t talk about in a bar: politics and religion. Some have assumed that a good bit of this is because spouses grow more similar with time. But is this the case?

This is where the “extended twin” design comes in handy. One large study (N > 20,000) in particular looked at precisely that. By including twins, their spouses, and parents, etc, they were able to directly measure assortative mating. What did they find? Spouses were correlated for several traits. But the traits they were most correlated in were political orientation and religiosity. Social “homogamy” (having the same background as your spouse) couldn’t explain this, as the correlation between MZ twins and their co-twin’s spouse were consistently higher than that of DZ twins, and so on. As well, spouses weren’t influencing each other, as the correlation between spouses was not affected by length of the marriage (even when only couples married <2 years were examined).

The study was also able to lay to rest another persistent myth. We’ve heard that we choose spouses like our opposite sex parent (like our mothers for men and like our fathers for women). Anyone who’s remotely genetically informed should be able to see that this could just be due to choosing mates like ourselves. And so is the case. As the authors put it:

there was no evidence for the sexual imprinting hypothesis. Twins’ partners were not significantly more similar in any trait to the twin’s opposite-sex parent than to the twin’s same-sex parent or a DZ co-twin of either sex, nor was there even a trend in this direction

These results were also consistent with the Peter Hatemi et al extended twin study on political attitudes featured previously.

The similarity between spouses has nothing to do with mutual influence, but assortment. At least this bit is common sense. I suspect few long married individuals will believe that they changed their spouse.

On that note, a key theory put forward by the woman who first elucidated the non effect of parents, Judith Rich Harris, was that the unique environment “influence” might be boiled down to peer influence. Staffan did a nice recap of Harris’s theory (see The Nurture Enigma – How Does the Environment Influence Human Nature? | Staffan’s Personality Blog). We all have heard of peer pressure. And indeed, peers seem to be an important force when it comes to language and behaviors like smoking initiation. But do peers really have this great influence, as Harris posits? Well, as I posted over at the Lion of the Blogosphere:

Most research into peer effects is confounded by the same thing that standard parenting studies are: inability to control for the effect of heredity.

And:

A behavioral genetic study (on the Add Health data) that looked specifically at GPA and found that 72% of the similarity between U.S. high school students and their peers could be explained by genetic factors. In other words, school performance and the apparent peer “influence” is really just kids choosing to associate with kids of similar intelligence and motivation:

A behavior genetic analysis of the tendency for youth to associate according to GPA

Peers seem like a fine avenue to get excited about, because it seemed like a vehicle through which parents could assert some influence. But, when you really consider it, peers can’t really be all that important in the long run, because if there were systematic effects of peers on adult outcomes, it’d turn up in the shared environment, which it doesn’t. One could posit that the effect of peers is completely random, but if that were true (aside from the major violation of Occam’s Razor that presents), why worry about it?

The “75-0-25 or something” rule is robust and reliable. This instructs that should we find some major deviation from this, it can be taken to be a sign something is seriously amiss. We saw that with male homosexuality (see Greg Cochran’s “Gay Germ” Hypothesis – An Exercise in the Power of Germs). Now I will discuss two curious exceptions to this pattern.

One rather astonishing example was the heritability of social trust. A behavioral genetic study out of the Netherlands found that the heritability of trust in others, as measured by:

The trust-in-others and trust-in-self scales were designed to include three items that were central in existing scales … thereby capturing items with positive valence (“I completely trust most other people”) and negative valence (“When push comes to shove, I do not trust most other people”), both of which explicitly used the word “trust”, and an item that captured the broad behavioral implication of the trust: the intention to accept vulnerability, as explicated in one of the most widely-accepted definitions of trust … (“I dare to put my fate in the hands of most other people”)

…found no significant heritable influence on these. The extent that people trusted, at least as captured by these measures, was virtually entirely a function of the unique environment.

This was a puzzling result. The clear pattern of the high heritability of all behavioral traits was established, as I’ve discussed. So how could a propensity to trust not also be influenced by genetic factors? One explanation touted around was that trust is contingent on experience; if we found people trustworthy, we would trust. If we didn’t, we would not. While that might sound convincing, the trouble is that the same could be said for many other behavioral traits. Is general trust less socially contingent than say bigoted feelings against some groups, like homophobia (which is at least 54% heritable)? That seems rather unreasonable.

One key question: how do they assess “trust”? Just how good was their measurement? Measurements in social science need to meet three basic criteria: they need to be reliable (that is multiple testing instances of the same individual should give roughly the same results), they need to be “valid” (that is, be predictive of some real-world outcome), and they should be heritable. This trust measure clearly fails on the third criterion. However, the study authors claim the test-retest correlation was good, so it is reliable. But what about the second? Does this trust measure actually predict anything?

To find out, I looked at a study that sought to answer that very question. This study, done in Germany, looked in detail at the reliability and the validity of their measurement of trust, a measurement very similar to the Dutch study. The noted a key point, one HBD Chick will appreciate. That is, trust is multi-faceted. There is trust in institutions, which is distinct from trust in known others, which is distinct from trust in strangers (I’d imagine HBD Chick would break it down one more, and separate “known others” into family and non-family). But more importantly, to question of validity, they assessed this by the correlation between trust in strangers and trusting behavior in the “dictator game.” They found a correlation, but only with trust in strangers.

But their correlation was very small (Spearman’s rho = 0.17) – and this is with a game which itself has questionable relation to trust behavior in the real world. I suspect that their instrument is not predictive of any trusting behavior in the real world. It’s worth mentioning another (fairly small) study of the heritability of trust from Australia found a non-insignificant heritability, though a smallish one (0.14-0.31).

The situation with trust is unclear. But this brings me to another example of a feature for which the heritability estimate appears to be trivial. That is the female G-spot. A study on about 1,800 female twins from Britain found that the heritability of the reported presence of a G-spot wasn’t significant. The result was virtually entirely unshared environment. Debate has raged on as to whether or not the female G spot exists at all, but that is to be expected, since research into human sexual behavior is among the most difficult to conduct properly. But, the result from this study indicating that the G spot isn’t heritable is puzzling. If the G spot was a real anatomical feature, and one that wasn’t universal, then one would expect a rather significant heritable impact. The finding that it’s not heritable points to one of two conclusions. One, perhaps the G-spot is in fact universal, but only some women have “discovered” it. That seems rather implausible, given the rather significant variation in heritable morphological features of sex organs in women. The second possibility is that the G-spot in fact doesn’t exist at all, and women who claim to have one are mistaken. That seems more likely, but I wouldn’t want to completely dismiss the claims of women who state they have such a feature. The mystery remains.

The findings of behavioral genetics, particularly the highly significant impact of heredity and the absence of shared environment effects, in addition to the complete failure to find reliable environmental sources that contribute to the “unique environment” component of the variance, calls into question virtually every pet environmental theory that has been put forward. It guides one to be suspicious of most “environmental” explanations of behavior. Now, let me be clear, I am not saying that these environmental influences don’t exist. I am not saying that if they do exist, we won’t be able to ever find them. I am also not saying that development doesn’t require a complex interplay between genes and environment. Try going without food, water, air, or speaking to another person if you don’t believe me. I am also not saying that the secular changes in human traits that are brought about by gross environmental changes don’t happen. The increase in average height over the past century disproves that. But what I am saying is that you should be doubtful of most pet theories of how the environment influences us, especially those that promise we can control, or sometimes even predict it. For as we see, that’s far from an easy task.

(Republished from JayMan's Blog by permission of author or representative)
 
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  1. Luke Lea says: • Website

    You have gradually and quite completely won me over to your “extreme” position on the issues you discuss. Still, it seems to me their is room for misunderstanding (or maybe I am misunderstanding?) in terms of the take-away that a lot of people will have to your position. For instance, a generation or two back African Americans were famous for their good manners, no doubt because of the way they were taught be their parents in combination with the fact that white society would not tolerate the kind of bad manners (ghetto manners) which are so common today. Maybe you cover this when you emphasize that your position does not hold when different generations are being discussed?

    Or take the issue of child sexual abuse: obviously different children are affected in different ways by such abuse (I know a woman for whom it seems to have triggered a borderline personality disorder) and let us stipulate for the purposes of argument that you are absolutely correct (and I believe you are) when you say these different reactions are mediated by genetic differences. Still, it would be a shame if people came away with the idea that child sexual abuse didn’t matter. Somehow you need to emphasize this side of your argument more effectively if you want it to be more widely accepted. I think.

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    • Replies: @JayMan
    @Luke Lea:

    You have gradually and quite completely won me over to your “extreme” position on the issues you discuss.
     
    I've corrupted another poor soul...

    For instance, a generation or two back African Americans were famous for their good manners,
     
    Were they actually all that different though?

    no doubt because of the way they were taught be their parents in combination with the fact that white society would not tolerate the kind of bad manners (ghetto manners) which are so common today
     
    I think a general way of looking at what parents teach us is that if it fits with our own temperaments, it will be retained. Wide social forces also modulate behavior, part of the gross environment that imposes itself on us.

    Maybe you cover this when you emphasize that your position does not hold when different generations are being discussed?
     
    Did you see this post?

    Still, it would be a shame if people came away with the idea that child sexual abuse didn’t matter.
     
    People are stupid. I can't help that. ;) My wife is the marketing person, I can only speak the truth. Yes, I would say you shouldn't do bad things to children because they are bad. I mean, is that not reason enough?
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  2. ckp says:

    >One key question: how do they assess “trust”? Just how good was their measurement? Measurements in social science need to meet three basic criteria: they need to be reliable (that is multiple testing instances of the same individual should give roughly the same results), they need to be “valid” (that is, be predictive of some real-world outcome), and they should be heritable.

    Doesn’t the third criterion make the “all behavioral traits are heritable” a tautology?

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    • Replies: @JayMan
    @ckp:

    It would if there were a slew of traits that showed no significant heritability. But since that doesn't happen – these are the rare exceptions right here – it's not a problem.

  3. JayMan says: • Website
    @ckp
    >One key question: how do they assess “trust”? Just how good was their measurement? Measurements in social science need to meet three basic criteria: they need to be reliable (that is multiple testing instances of the same individual should give roughly the same results), they need to be “valid” (that is, be predictive of some real-world outcome), and they should be heritable.

    Doesn't the third criterion make the "all behavioral traits are heritable" a tautology?

    It would if there were a slew of traits that showed no significant heritability. But since that doesn’t happen – these are the rare exceptions right here – it’s not a problem.

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  4. Anonymous says: • Disclaimer

    I feel that everything has a genetic component, and part of that is the susceptibility to a triggering event or the possibility that a therapeutic intervention can make a difference or not. Personally, I’d rather see the strong evidence for heritability and work around that for exceptions and modifications than deal with the “Environmental Causation” folks who don’t narrow down the factors they’re looking at because they are so insightful that they “look at the big picture.”

    Even in the strongest arguments for the genetic heritability of behaviors and disorders, I don’t see such a degree of absolute determinism that modification to environment or behavior is completely dismissed out of hand.

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  5. As you know, although Handscombe’s study failed to find an SES-heritability interaction there are a number of papers other than Turkheimer’s 2003 paper that have found this effect. Given that at least some of these studies have reasonable sample sizes and utilize the normal MZA-DZA model. Why do you think some studies find an interaction affect and others don’t ?

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    • Replies: @JayMan
    @Test Subject:

    That's enough for a whole post of its own. ;)

  6. JayMan says: • Website
    @Luke Lea
    You have gradually and quite completely won me over to your "extreme" position on the issues you discuss. Still, it seems to me their is room for misunderstanding (or maybe I am misunderstanding?) in terms of the take-away that a lot of people will have to your position. For instance, a generation or two back African Americans were famous for their good manners, no doubt because of the way they were taught be their parents in combination with the fact that white society would not tolerate the kind of bad manners (ghetto manners) which are so common today. Maybe you cover this when you emphasize that your position does not hold when different generations are being discussed?

    Or take the issue of child sexual abuse: obviously different children are affected in different ways by such abuse (I know a woman for whom it seems to have triggered a borderline personality disorder) and let us stipulate for the purposes of argument that you are absolutely correct (and I believe you are) when you say these different reactions are mediated by genetic differences. Still, it would be a shame if people came away with the idea that child sexual abuse didn't matter. Somehow you need to emphasize this side of your argument more effectively if you want it to be more widely accepted. I think.

    You have gradually and quite completely won me over to your “extreme” position on the issues you discuss.

    I’ve corrupted another poor soul…

    For instance, a generation or two back African Americans were famous for their good manners,

    Were they actually all that different though?

    no doubt because of the way they were taught be their parents in combination with the fact that white society would not tolerate the kind of bad manners (ghetto manners) which are so common today

    I think a general way of looking at what parents teach us is that if it fits with our own temperaments, it will be retained. Wide social forces also modulate behavior, part of the gross environment that imposes itself on us.

    Maybe you cover this when you emphasize that your position does not hold when different generations are being discussed?

    Did you see this post?

    Still, it would be a shame if people came away with the idea that child sexual abuse didn’t matter.

    People are stupid. I can’t help that. ;) My wife is the marketing person, I can only speak the truth. Yes, I would say you shouldn’t do bad things to children because they are bad. I mean, is that not reason enough?

    Read More
  7. JayMan says: • Website
    @Anonymous
    I feel that everything has a genetic component, and part of that is the susceptibility to a triggering event or the possibility that a therapeutic intervention can make a difference or not. Personally, I'd rather see the strong evidence for heritability and work around that for exceptions and modifications than deal with the "Environmental Causation" folks who don't narrow down the factors they're looking at because they are so insightful that they "look at the big picture."

    Even in the strongest arguments for the genetic heritability of behaviors and disorders, I don't see such a degree of absolute determinism that modification to environment or behavior is completely dismissed out of hand.

    @AlisonM:

    That’s pretty much it.

    Read More
  8. JayMan says: • Website
    @Test Subject
    As you know, although Handscombe's study failed to find an SES-heritability interaction there are a number of papers other than Turkheimer's 2003 paper that have found this effect. Given that at least some of these studies have reasonable sample sizes and utilize the normal MZA-DZA model. Why do you think some studies find an interaction affect and others don't ?

    That’s enough for a whole post of its own. ;)

    Read More
  9. “There are two aspects where spouses are highly correlated – the things you don’t talk about in a bar: politics and religion”

    But what is your theory to explain the high correlation on religiosity and political trends between spouses? it seems you are suggesting a homotypic preference.

    First we should bear in mind that within-pair matching for a feature may arise even if people pay no attention to this feature in prospective partners. So marry each other depends partly on the structure of the marriage market and social stratification, the effect propinquity / nearness has on our pool of potential mates, and also involves cultural norms of endogamy, or the choice to marry within a group.

    Owing to physical proximity and ease to contact, people in a romantic pair tend to come from the same rather than different social groups. This is why partners are usually similar in characteristics associated with a social group, such as age (due to attending to schools), education and social status, etc.

    On the other hand, I doubt that there is a mate preference for these kind of personality traits (i.e. religiosity, politics) determined by a genetic locus.

    Furthermore, from an overall genetic framework, we should not forget such mechanisms as inbreeding depression and heterozygous advantage, so I’d assume that same-type matings are less fertile than different-type mating. If all individuals have a disassortative mating preference a viability-reducing trait may be maintained even without the fertility cost of same-type matings; a disassortative mating preference can be established even if it is initially rare, when there is a fertility cost of same-type matings.

    Moreover, an assortative mating preference is less likely to evolve than a disassortative mating preference. This may be applicable to the evolution of MHC-disassortative mating preferences documented in animals and humans.

    Read More
    • Replies: @JayMan
    @Tyrion Lannister:

    First we should bear in mind that within-pair matching for a feature may arise even if people pay no attention to this feature in prospective partners. So marry each other depends partly on the structure of the marriage market and social stratification, the effect propinquity / nearness has on our pool of potential mates, and also involves cultural norms of endogamy, or the choice to marry within a group
     
    All of this was covered in the post and in the papers I've linked to. As I said:

    Spouses were correlated for several traits. But the traits they were most correlated in were political orientation and religiosity. Social “homogamy” (having the same background as your spouse) couldn’t explain this, as the correlation between MZ twins and their co-twin’s spouse were consistently higher than that of DZ twins, and so on.
     
    ---

    On the other hand, I doubt that there is a mate preference for these kind of personality traits (i.e. religiosity, politics) determined by a genetic locus.
     
    That is what they found. It's not that people seek out specific traits, they just end up with people like themselves. Some of the genetic preferences is attenuated because marriage is a two-way enterprise. The choosee must also choose the chooser.

    Furthermore, from an overall genetic framework, we should not forget such mechanisms as inbreeding depression and heterozygous advantage, so I’d assume that same-type matings are less fertile than different-type mating.
     
    The best evidence we have on that comes out of Iceland. Eventual fitness (number of grandkids) is maximized in 3rd and 4th cousins, and falls off going both ways. Of course, we don't know how well this generalizes to the rest of the world.
  10. JayMan says: • Website
    @Tyrion Lannister
    “There are two aspects where spouses are highly correlated – the things you don’t talk about in a bar: politics and religion”

    But what is your theory to explain the high correlation on religiosity and political trends between spouses? it seems you are suggesting a homotypic preference.

    First we should bear in mind that within-pair matching for a feature may arise even if people pay no attention to this feature in prospective partners. So marry each other depends partly on the structure of the marriage market and social stratification, the effect propinquity / nearness has on our pool of potential mates, and also involves cultural norms of endogamy, or the choice to marry within a group.

    Owing to physical proximity and ease to contact, people in a romantic pair tend to come from the same rather than different social groups. This is why partners are usually similar in characteristics associated with a social group, such as age (due to attending to schools), education and social status, etc.

    On the other hand, I doubt that there is a mate preference for these kind of personality traits (i.e. religiosity, politics) determined by a genetic locus.

    Furthermore, from an overall genetic framework, we should not forget such mechanisms as inbreeding depression and heterozygous advantage, so I'd assume that same-type matings are less fertile than different-type mating. If all individuals have a disassortative mating preference a viability-reducing trait may be maintained even without the fertility cost of same-type matings; a disassortative mating preference can be established even if it is initially rare, when there is a fertility cost of same-type matings.

    Moreover, an assortative mating preference is less likely to evolve than a disassortative mating preference. This may be applicable to the evolution of MHC-disassortative mating preferences documented in animals and humans.

    First we should bear in mind that within-pair matching for a feature may arise even if people pay no attention to this feature in prospective partners. So marry each other depends partly on the structure of the marriage market and social stratification, the effect propinquity / nearness has on our pool of potential mates, and also involves cultural norms of endogamy, or the choice to marry within a group

    All of this was covered in the post and in the papers I’ve linked to. As I said:

    Spouses were correlated for several traits. But the traits they were most correlated in were political orientation and religiosity. Social “homogamy” (having the same background as your spouse) couldn’t explain this, as the correlation between MZ twins and their co-twin’s spouse were consistently higher than that of DZ twins, and so on.

    On the other hand, I doubt that there is a mate preference for these kind of personality traits (i.e. religiosity, politics) determined by a genetic locus.

    That is what they found. It’s not that people seek out specific traits, they just end up with people like themselves. Some of the genetic preferences is attenuated because marriage is a two-way enterprise. The choosee must also choose the chooser.

    Furthermore, from an overall genetic framework, we should not forget such mechanisms as inbreeding depression and heterozygous advantage, so I’d assume that same-type matings are less fertile than different-type mating.

    The best evidence we have on that comes out of Iceland. Eventual fitness (number of grandkids) is maximized in 3rd and 4th cousins, and falls off going both ways. Of course, we don’t know how well this generalizes to the rest of the world.

    Read More
  11. As you mentioned before labelling the “25% or something” of human traits as unique enverionment is misleading, since this might not be environmental at all. Possibilities include among others:

    - alterations in somatic genome (Mosaicism, Chimerism, X-inactivation for women etc.)
    - “noise” from small auto-immune reactions based at random (receptor rearrangement) events during T and B cell maturation
    - microbiome (pathogenes alter somatic genome as well)

    What do you think are the most likely sources of this 25% non-inherited variability? What percentages would you assign to each possible source?

    With the advent of surrogacy the effect of uterine environment could actually be deduced. It is tricky, because they cannot be seperated from effects directly caused by the artificial surrogacy (implementation, in vitro fertilisation). Do you know any studies looking at uterine environmental effects?

    Read More
  12. […] culture isn’t something they have within themselves? Something that affects behavior while being highly heritable and stable over the lifespan? And why are there so many Asian Americans holding on to face culture […]

    Read More
  13. Staffan says: • Website

    Great post,

    I should say that Harris’ theory talks of peer pressure to differentiate rather than to conform so it’s hard to see how this could turn up as shared environment. While the company is shared the treatment will be differential and it’s the treatment that is the social environment. I suppose the evidence would be found in correlations between peers as adults, if they stabilize as more (inversely) correlated than control groups. That said, these increasing heritability estimates are making the mystery of unique environment a shrinking one.

    Read More
    • Replies: @JayMan
    Thanks!

    All the "concrete" evidence we have for peer effects seems to indicate assimilation, not differentiation. Differentiation within peer groups sounds as spectacular as parent-child interactions, which Harris herself criticized. But Harris admitted this is in her second book, but the theory she proposes there, while very interesting, is also just as speculative.

  14. JayMan says: • Website
    @Staffan
    Great post,

    I should say that Harris' theory talks of peer pressure to differentiate rather than to conform so it's hard to see how this could turn up as shared environment. While the company is shared the treatment will be differential and it's the treatment that is the social environment. I suppose the evidence would be found in correlations between peers as adults, if they stabilize as more (inversely) correlated than control groups. That said, these increasing heritability estimates are making the mystery of unique environment a shrinking one.

    Thanks!

    All the “concrete” evidence we have for peer effects seems to indicate assimilation, not differentiation. Differentiation within peer groups sounds as spectacular as parent-child interactions, which Harris herself criticized. But Harris admitted this is in her second book, but the theory she proposes there, while very interesting, is also just as speculative.

    Read More
  15. There are dramatic difference in average outcomes between *groups* proportional to how sealed off those *groups* are from the dominant culture in the post-60s West and how much those *groups* promote different behaviors (Mormons, Muslims, Amish etc).

    One explanation is boiling off over generations.

    Another possibility is that as humans are a social animal then as well as hereditability of individual behaviors there may also be heritability of group conforming behaviors. This might not alter the frequency of inherited individual behaviors but it would alter the level of display of those behaviors.

    The change in the dominant culture since the 60s and the change in average behavior among groups not sealed off from the dominant culture – mostly media driven – has been so sudden and dramatic that boiling off is not an option imo so we have a very clear experiment showing that the average difference in behavior between *groups* in the same dominant culture is proportional to how much their group rejected the post 60s culture *and* critically how much their group was also able to seal themselves off from the dominant culture into a sub-cultural bubble.

    The post 60s cultural experiment shows that both are required: rejection of the dominant culture and relative isolation from it.

    So individual hereditability of behaviors yes, individual parental powerlessness against the dominant culture yes but also the hereditability of group conformity behavior means *groups* who isolate themselves into a sub-cultural bubble can resist the dominant culture.

    Read More
  16. Meng Hu says: • Website

    When you say rGE is often negative, it depends on which one you are thinking. Passive ? Reactive ? Active ? For the last one, it’s impossible, because it means that people tend to seek environments contra their own genetic propensities. It’s extremely difficult to conceive that. But I can easily conceive that parents and teachers prefer to invest more on low IQ children, thus, in that case you have your passive/reactive negative rGE. Such outcome seems very likely in most of the modern (western) societies where the dominant political orientation is the supra-egalitarianism (just look at how the new book of the french economist Thomas Piketty encounters its success). Now that is said, I want to precise that it seems unlikely that behavioral researchers think about passive/reactive rGE when they use that argument for the explanation of the increase in h2 with age. No, they think about active rGE. It’s obvious when you think that shared environment (c2) don’t have much impact in adulthood, and that rGE shifts from passive to active from childhood to adolescence/adulthood. Nonetheless, you can have a rather strong critic of active rGE from Brant (2013) “The Nature and Nurture of High IQ: An Extended Sensitive Period for Intellectual Development”.

    The most prominent theory of developmental increases in the heritability of IQ posits that across development, individuals gain more scope to shape their own environments on the basis of their genetic propensities (active gene-environment correlation), which causes an increase in genetic influence over time (Haworth et al., 2010; Plomin, DeFries, & Loehlin, 1977). Our results challenge this explanation, as they show a later increase in heritability for individuals of higher IQ. To explain our results in the context of active gene-environment correlations, one would need to posit, counterintuitively, that higher-IQ individuals seek out environments concordant with their genetic propensities later in development than do lower-IQ individuals.

    The reason for developmental increases in the heritability of IQ thus remains unclear. Other possibilities include amplification of existing genetic influence by increasing population variance in cognitive ability and the simultaneous limiting of environmental influences and introduction of new genetic influences as a result of synaptic pruning processes and myelination at the end of the sensitive period (Plomin, 1986; Plomin et al., 1977; Tau & Peterson, 2010).

    Like I used to say, it’s interesting that they dismiss rGE when at the same time they have opened another possibility. The genetic amplification. To be sure, it’s John Fuerst who suggested me this idea, first. Look here.

    http://occidentalascent.wordpress.com/2011/01/30/genetic-amplification/

    Now, just some ideas, when I was reading your article :

    Lot of people expect heritability (h2) to be upwardly biased. In the case of twins, it’s always MZ correlation that is suspected to be biased upwardly. One reason is rGE effects. Suppose that’s true. In that case, I expect rMZ to be much higher than the double of full sibling correlation, because the double is just what an additive model surely expects to find. Because rMZ seems to be just the double of full sibling correlation, that makes me believe there is a high genetic additive component in the IQ. But another, better way to disentangle that difficult question is to look at the h2 of the trait in question in different countries, preferably in very different social environments. For example, you can expect h2 in poor countries such as Africa and India for IQ to be lower. A failure to find difference in h2 would surely dismiss any rGE hypotheses. That’s the best test of the “locality” of h2.

    I mention IQ but evidently it goes the same for all behavior traits. It’s just that I did not find the data for them. But if h2 is similar for, say, happiness, trust, agression, openness, and some other things like those, among different countries, with different political regimes, cultures, and different regions, e.g., rural versus urban, then if the h2 are quite comparable under diverse condition, it would seem that neither rGE or GE interaction is likely to produce most of the h2. When researchers attempt to use model-fitting for choosing which hypothesis needs to be retained, it’s no sufficient enough. They must always be accompanied with experiments. Even if your data tells you that you model looks very likely, has the “best fit to the data” that’s meaningless if experiments lead you to reject your model anyway. It’s the same kind of guys who believed they can model financial behaviors, coming to the conclusion that the crisis won’t happen. Well, we see it’s not true. The subprimes reveal quite a lot of bad investments.

    Concerning h2 interaction with SES, I don’t think we should be surprised by a possible lower h2 at lower SES. h2 may be expected to move closer to 100% when environments become stable and/or better because in this particular case you don’t have much environmental variation, but on the other hand, the high-risk environments will just add more environmental variation and thus will act to reduce h2. That seems to be common sense. For instance :

    One comprehensive review of class and health surveyed mortality rates in Britain from 1921 to 1971 (Black, 1980; Townsend & Davidson, 1982). Everyone was living longer, but the professional classes gained more years than semiskilled and unskilled workers. In 1930, people in the lowest social class had a 23% higher chance of dying at every age than people in the highest social class. By 1970, this excess risk had grown to 61%. A decade later, it had jumped to 150%. In Britain, a National Health Service has long existed to minimize inequalities in access to medical care. The increasing correlation of health and social class makes sense when one realizes that removing environmental impediments makes individual-difference variables more dependent on innate characteristics. (Placing intelligence into an evolutionary framework or how g fits into the r–K matrix of life-history traits including longevity, Rushton 2004)

    This aside, the topic is highly controversial, and the topic is fulled of dishonest claims. Researchers always cite Turkheimer, but rarely the studies contra such conclusions. That said, I just wanted to point out this document.

    Genotype by Environment Interactions in Cognitive Ability: A Survey of 14 Studies from Four Countries Covering Four Age Groups (Molenaar 2013)

    It’s a very important article. They say explicitly that lack of representativeness can distort the direction and magnitude of the GxE interaction. At some extremes, maybe the interaction disappears, or magnifies. IQ measurement is also a possible cause of the inconsistency. Sometimes, it’s verbal IQ that is measured, sometimes, full IQ, sometimes nonverbal IQ. Another problem, less known, is the error measurement in the IQ. In ACE model-fitting, the E component also includes measurement error, and the portion of E that is tied to error variance can give rise to spurious GxE effects. Thus you must use multiple IQ measurements (see how many subtests in your battery, how many items per subtests, etc.) and try to reduce error variance as much as possible. But, interestingly, age can make a difference. Indeed, Molenaar and his team found that in childhood, there is negative GxE, which means lower E at higher level of G. In adolescents, no effect at all. And in adulthood, E was stronger (not smaller) for higher level of G. That runs contra Turkheimer/Rowe/Sluis/Tucker-Drob. Unfortunately, the final result is not easily interpretable because you have lot of differences between the studies and the countries (look their figure 2). In other words, it’s not sure that aggregation makes sense at all. The Molenaar paper is infinitely more important than the Hanscombe. I don’t understand why no one else cited it. Because it’s by far the best one available on that topic. And everyone should read it.

    There is also another feature worth noting in Molenaar paper. The authors explicitly stated that the unmodeled GxE interaction might be one reason for the “missing” heritability in GWAS estimates. Another factor of under-estimated GWAS h2 may be population stratification, as mentioned by :

    A genome-wide association study for reading and language abilities in two population cohorts (Luciano 2013)

    Among the last paragraphs they wrote that when they exclude non-white people in the analysis, the correlation was significant whereas it didn’t when non-whites were included. Stats stuff is really, really, highly complex.

    Read More
    • Replies: @JayMan
    @Meng Hu:

    Great exposition! Thanks for sharing your insights. I think the next phase in behavioral genetics is definitely moving into the non-Western world (and, at least, non-Whites/non-Asians in the West). Then we will see how well the findings (which have held up incredibly well for the Western world) carry over to these differing environments.

    , @Meng Hu
    Hm... concerning Molenaar (2013) you should take my earlier comment with pinch of salt. They said that GxE interaction could have diminished GWAS heritability. I thought I could believe them, but after reading the references they cite, it says the opposite. It's curious they mis-understood it, or maybe their sentence was poorly phrased. After all, GWAS heritability is supposed to get only the additive portion, and GxE can't be additive, by definition.

    Honestly, GWAs seem more important than what the skeptics tend to believe. Since GCTA/GWAS sample only the nonrelated individuals, thus no genetic similarity (unlike twins) the necessary consequence is to remove (almost) entirely GE correlations of all types. This argument does not work anymore. It's finished. And who is attempting to use that argument again is either a complete ignorant of GWAS or he is still locked up in his ideology.

  17. […] the dad despite the clear folly of this as per my earlier posts The Son Becomes The Father and More Behavioral Genetic Facts), who has his own 8-factor causal proclamation. It doesn’t occur to many of these people that […]

    Read More
  18. […] have recently updated two key posts, my post More Behavioral Genetic Facts and More Maps of the American […]

    Read More
  19. JayMan says: • Website
    @Meng Hu
    When you say rGE is often negative, it depends on which one you are thinking. Passive ? Reactive ? Active ? For the last one, it's impossible, because it means that people tend to seek environments contra their own genetic propensities. It's extremely difficult to conceive that. But I can easily conceive that parents and teachers prefer to invest more on low IQ children, thus, in that case you have your passive/reactive negative rGE. Such outcome seems very likely in most of the modern (western) societies where the dominant political orientation is the supra-egalitarianism (just look at how the new book of the french economist Thomas Piketty encounters its success). Now that is said, I want to precise that it seems unlikely that behavioral researchers think about passive/reactive rGE when they use that argument for the explanation of the increase in h2 with age. No, they think about active rGE. It's obvious when you think that shared environment (c2) don't have much impact in adulthood, and that rGE shifts from passive to active from childhood to adolescence/adulthood. Nonetheless, you can have a rather strong critic of active rGE from Brant (2013) "The Nature and Nurture of High IQ: An Extended Sensitive Period for Intellectual Development".

    The most prominent theory of developmental increases in the heritability of IQ posits that across development, individuals gain more scope to shape their own environments on the basis of their genetic propensities (active gene-environment correlation), which causes an increase in genetic influence over time (Haworth et al., 2010; Plomin, DeFries, & Loehlin, 1977). Our results challenge this explanation, as they show a later increase in heritability for individuals of higher IQ. To explain our results in the context of active gene-environment correlations, one would need to posit, counterintuitively, that higher-IQ individuals seek out environments concordant with their genetic propensities later in development than do lower-IQ individuals.

    The reason for developmental increases in the heritability of IQ thus remains unclear. Other possibilities include amplification of existing genetic influence by increasing population variance in cognitive ability and the simultaneous limiting of environmental influences and introduction of new genetic influences as a result of synaptic pruning processes and myelination at the end of the sensitive period (Plomin, 1986; Plomin et al., 1977; Tau & Peterson, 2010).
     

    Like I used to say, it's interesting that they dismiss rGE when at the same time they have opened another possibility. The genetic amplification. To be sure, it's John Fuerst who suggested me this idea, first. Look here.
    http://occidentalascent.wordpress.com/2011/01/30/genetic-amplification/

    Now, just some ideas, when I was reading your article :

    Lot of people expect heritability (h2) to be upwardly biased. In the case of twins, it's always MZ correlation that is suspected to be biased upwardly. One reason is rGE effects. Suppose that's true. In that case, I expect rMZ to be much higher than the double of full sibling correlation, because the double is just what an additive model surely expects to find. Because rMZ seems to be just the double of full sibling correlation, that makes me believe there is a high genetic additive component in the IQ. But another, better way to disentangle that difficult question is to look at the h2 of the trait in question in different countries, preferably in very different social environments. For example, you can expect h2 in poor countries such as Africa and India for IQ to be lower. A failure to find difference in h2 would surely dismiss any rGE hypotheses. That's the best test of the "locality" of h2.

    I mention IQ but evidently it goes the same for all behavior traits. It's just that I did not find the data for them. But if h2 is similar for, say, happiness, trust, agression, openness, and some other things like those, among different countries, with different political regimes, cultures, and different regions, e.g., rural versus urban, then if the h2 are quite comparable under diverse condition, it would seem that neither rGE or GE interaction is likely to produce most of the h2. When researchers attempt to use model-fitting for choosing which hypothesis needs to be retained, it's no sufficient enough. They must always be accompanied with experiments. Even if your data tells you that you model looks very likely, has the "best fit to the data" that's meaningless if experiments lead you to reject your model anyway. It's the same kind of guys who believed they can model financial behaviors, coming to the conclusion that the crisis won't happen. Well, we see it's not true. The subprimes reveal quite a lot of bad investments.

    Concerning h2 interaction with SES, I don't think we should be surprised by a possible lower h2 at lower SES. h2 may be expected to move closer to 100% when environments become stable and/or better because in this particular case you don't have much environmental variation, but on the other hand, the high-risk environments will just add more environmental variation and thus will act to reduce h2. That seems to be common sense. For instance :


    One comprehensive review of class and health surveyed mortality rates in Britain from 1921 to 1971 (Black, 1980; Townsend & Davidson, 1982). Everyone was living longer, but the professional classes gained more years than semiskilled and unskilled workers. In 1930, people in the lowest social class had a 23% higher chance of dying at every age than people in the highest social class. By 1970, this excess risk had grown to 61%. A decade later, it had jumped to 150%. In Britain, a National Health Service has long existed to minimize inequalities in access to medical care. The increasing correlation of health and social class makes sense when one realizes that removing environmental impediments makes individual-difference variables more dependent on innate characteristics. (Placing intelligence into an evolutionary framework or how g fits into the r–K matrix of life-history traits including longevity, Rushton 2004)
     
    This aside, the topic is highly controversial, and the topic is fulled of dishonest claims. Researchers always cite Turkheimer, but rarely the studies contra such conclusions. That said, I just wanted to point out this document.

    Genotype by Environment Interactions in Cognitive Ability: A Survey of 14 Studies from Four Countries Covering Four Age Groups (Molenaar 2013)

    It's a very important article. They say explicitly that lack of representativeness can distort the direction and magnitude of the GxE interaction. At some extremes, maybe the interaction disappears, or magnifies. IQ measurement is also a possible cause of the inconsistency. Sometimes, it's verbal IQ that is measured, sometimes, full IQ, sometimes nonverbal IQ. Another problem, less known, is the error measurement in the IQ. In ACE model-fitting, the E component also includes measurement error, and the portion of E that is tied to error variance can give rise to spurious GxE effects. Thus you must use multiple IQ measurements (see how many subtests in your battery, how many items per subtests, etc.) and try to reduce error variance as much as possible. But, interestingly, age can make a difference. Indeed, Molenaar and his team found that in childhood, there is negative GxE, which means lower E at higher level of G. In adolescents, no effect at all. And in adulthood, E was stronger (not smaller) for higher level of G. That runs contra Turkheimer/Rowe/Sluis/Tucker-Drob. Unfortunately, the final result is not easily interpretable because you have lot of differences between the studies and the countries (look their figure 2). In other words, it's not sure that aggregation makes sense at all. The Molenaar paper is infinitely more important than the Hanscombe. I don't understand why no one else cited it. Because it's by far the best one available on that topic. And everyone should read it.

    There is also another feature worth noting in Molenaar paper. The authors explicitly stated that the unmodeled GxE interaction might be one reason for the "missing" heritability in GWAS estimates. Another factor of under-estimated GWAS h2 may be population stratification, as mentioned by :

    A genome-wide association study for reading and language abilities in two population cohorts (Luciano 2013)

    Among the last paragraphs they wrote that when they exclude non-white people in the analysis, the correlation was significant whereas it didn't when non-whites were included. Stats stuff is really, really, highly complex.

    Great exposition! Thanks for sharing your insights. I think the next phase in behavioral genetics is definitely moving into the non-Western world (and, at least, non-Whites/non-Asians in the West). Then we will see how well the findings (which have held up incredibly well for the Western world) carry over to these differing environments.

    Read More
  20. Meng Hu says: • Website
    @Meng Hu
    When you say rGE is often negative, it depends on which one you are thinking. Passive ? Reactive ? Active ? For the last one, it's impossible, because it means that people tend to seek environments contra their own genetic propensities. It's extremely difficult to conceive that. But I can easily conceive that parents and teachers prefer to invest more on low IQ children, thus, in that case you have your passive/reactive negative rGE. Such outcome seems very likely in most of the modern (western) societies where the dominant political orientation is the supra-egalitarianism (just look at how the new book of the french economist Thomas Piketty encounters its success). Now that is said, I want to precise that it seems unlikely that behavioral researchers think about passive/reactive rGE when they use that argument for the explanation of the increase in h2 with age. No, they think about active rGE. It's obvious when you think that shared environment (c2) don't have much impact in adulthood, and that rGE shifts from passive to active from childhood to adolescence/adulthood. Nonetheless, you can have a rather strong critic of active rGE from Brant (2013) "The Nature and Nurture of High IQ: An Extended Sensitive Period for Intellectual Development".

    The most prominent theory of developmental increases in the heritability of IQ posits that across development, individuals gain more scope to shape their own environments on the basis of their genetic propensities (active gene-environment correlation), which causes an increase in genetic influence over time (Haworth et al., 2010; Plomin, DeFries, & Loehlin, 1977). Our results challenge this explanation, as they show a later increase in heritability for individuals of higher IQ. To explain our results in the context of active gene-environment correlations, one would need to posit, counterintuitively, that higher-IQ individuals seek out environments concordant with their genetic propensities later in development than do lower-IQ individuals.

    The reason for developmental increases in the heritability of IQ thus remains unclear. Other possibilities include amplification of existing genetic influence by increasing population variance in cognitive ability and the simultaneous limiting of environmental influences and introduction of new genetic influences as a result of synaptic pruning processes and myelination at the end of the sensitive period (Plomin, 1986; Plomin et al., 1977; Tau & Peterson, 2010).
     

    Like I used to say, it's interesting that they dismiss rGE when at the same time they have opened another possibility. The genetic amplification. To be sure, it's John Fuerst who suggested me this idea, first. Look here.
    http://occidentalascent.wordpress.com/2011/01/30/genetic-amplification/

    Now, just some ideas, when I was reading your article :

    Lot of people expect heritability (h2) to be upwardly biased. In the case of twins, it's always MZ correlation that is suspected to be biased upwardly. One reason is rGE effects. Suppose that's true. In that case, I expect rMZ to be much higher than the double of full sibling correlation, because the double is just what an additive model surely expects to find. Because rMZ seems to be just the double of full sibling correlation, that makes me believe there is a high genetic additive component in the IQ. But another, better way to disentangle that difficult question is to look at the h2 of the trait in question in different countries, preferably in very different social environments. For example, you can expect h2 in poor countries such as Africa and India for IQ to be lower. A failure to find difference in h2 would surely dismiss any rGE hypotheses. That's the best test of the "locality" of h2.

    I mention IQ but evidently it goes the same for all behavior traits. It's just that I did not find the data for them. But if h2 is similar for, say, happiness, trust, agression, openness, and some other things like those, among different countries, with different political regimes, cultures, and different regions, e.g., rural versus urban, then if the h2 are quite comparable under diverse condition, it would seem that neither rGE or GE interaction is likely to produce most of the h2. When researchers attempt to use model-fitting for choosing which hypothesis needs to be retained, it's no sufficient enough. They must always be accompanied with experiments. Even if your data tells you that you model looks very likely, has the "best fit to the data" that's meaningless if experiments lead you to reject your model anyway. It's the same kind of guys who believed they can model financial behaviors, coming to the conclusion that the crisis won't happen. Well, we see it's not true. The subprimes reveal quite a lot of bad investments.

    Concerning h2 interaction with SES, I don't think we should be surprised by a possible lower h2 at lower SES. h2 may be expected to move closer to 100% when environments become stable and/or better because in this particular case you don't have much environmental variation, but on the other hand, the high-risk environments will just add more environmental variation and thus will act to reduce h2. That seems to be common sense. For instance :


    One comprehensive review of class and health surveyed mortality rates in Britain from 1921 to 1971 (Black, 1980; Townsend & Davidson, 1982). Everyone was living longer, but the professional classes gained more years than semiskilled and unskilled workers. In 1930, people in the lowest social class had a 23% higher chance of dying at every age than people in the highest social class. By 1970, this excess risk had grown to 61%. A decade later, it had jumped to 150%. In Britain, a National Health Service has long existed to minimize inequalities in access to medical care. The increasing correlation of health and social class makes sense when one realizes that removing environmental impediments makes individual-difference variables more dependent on innate characteristics. (Placing intelligence into an evolutionary framework or how g fits into the r–K matrix of life-history traits including longevity, Rushton 2004)
     
    This aside, the topic is highly controversial, and the topic is fulled of dishonest claims. Researchers always cite Turkheimer, but rarely the studies contra such conclusions. That said, I just wanted to point out this document.

    Genotype by Environment Interactions in Cognitive Ability: A Survey of 14 Studies from Four Countries Covering Four Age Groups (Molenaar 2013)

    It's a very important article. They say explicitly that lack of representativeness can distort the direction and magnitude of the GxE interaction. At some extremes, maybe the interaction disappears, or magnifies. IQ measurement is also a possible cause of the inconsistency. Sometimes, it's verbal IQ that is measured, sometimes, full IQ, sometimes nonverbal IQ. Another problem, less known, is the error measurement in the IQ. In ACE model-fitting, the E component also includes measurement error, and the portion of E that is tied to error variance can give rise to spurious GxE effects. Thus you must use multiple IQ measurements (see how many subtests in your battery, how many items per subtests, etc.) and try to reduce error variance as much as possible. But, interestingly, age can make a difference. Indeed, Molenaar and his team found that in childhood, there is negative GxE, which means lower E at higher level of G. In adolescents, no effect at all. And in adulthood, E was stronger (not smaller) for higher level of G. That runs contra Turkheimer/Rowe/Sluis/Tucker-Drob. Unfortunately, the final result is not easily interpretable because you have lot of differences between the studies and the countries (look their figure 2). In other words, it's not sure that aggregation makes sense at all. The Molenaar paper is infinitely more important than the Hanscombe. I don't understand why no one else cited it. Because it's by far the best one available on that topic. And everyone should read it.

    There is also another feature worth noting in Molenaar paper. The authors explicitly stated that the unmodeled GxE interaction might be one reason for the "missing" heritability in GWAS estimates. Another factor of under-estimated GWAS h2 may be population stratification, as mentioned by :

    A genome-wide association study for reading and language abilities in two population cohorts (Luciano 2013)

    Among the last paragraphs they wrote that when they exclude non-white people in the analysis, the correlation was significant whereas it didn't when non-whites were included. Stats stuff is really, really, highly complex.

    Hm… concerning Molenaar (2013) you should take my earlier comment with pinch of salt. They said that GxE interaction could have diminished GWAS heritability. I thought I could believe them, but after reading the references they cite, it says the opposite. It’s curious they mis-understood it, or maybe their sentence was poorly phrased. After all, GWAS heritability is supposed to get only the additive portion, and GxE can’t be additive, by definition.

    Honestly, GWAs seem more important than what the skeptics tend to believe. Since GCTA/GWAS sample only the nonrelated individuals, thus no genetic similarity (unlike twins) the necessary consequence is to remove (almost) entirely GE correlations of all types. This argument does not work anymore. It’s finished. And who is attempting to use that argument again is either a complete ignorant of GWAS or he is still locked up in his ideology.

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    • Replies: @JayMan
    @Meng Hu:

    Indeed, GCTA make it impossible to argue that some peculiarity about twins or adoptees is driving the behavioral genetic results we see (a criticism which itself was silly given the consistency between results from the two sets).


    And who is attempting to use that argument again is either a complete ignorant of GWAS or he is still locked up in his ideology.
     
    Well, it might be surprising how much of that is still going on. Probably not to you, though.
  21. JayMan says: • Website
    @Meng Hu
    Hm... concerning Molenaar (2013) you should take my earlier comment with pinch of salt. They said that GxE interaction could have diminished GWAS heritability. I thought I could believe them, but after reading the references they cite, it says the opposite. It's curious they mis-understood it, or maybe their sentence was poorly phrased. After all, GWAS heritability is supposed to get only the additive portion, and GxE can't be additive, by definition.

    Honestly, GWAs seem more important than what the skeptics tend to believe. Since GCTA/GWAS sample only the nonrelated individuals, thus no genetic similarity (unlike twins) the necessary consequence is to remove (almost) entirely GE correlations of all types. This argument does not work anymore. It's finished. And who is attempting to use that argument again is either a complete ignorant of GWAS or he is still locked up in his ideology.

    Indeed, GCTA make it impossible to argue that some peculiarity about twins or adoptees is driving the behavioral genetic results we see (a criticism which itself was silly given the consistency between results from the two sets).

    And who is attempting to use that argument again is either a complete ignorant of GWAS or he is still locked up in his ideology.

    Well, it might be surprising how much of that is still going on. Probably not to you, though.

    Read More
  22. […] More Behavioral Genetic Facts – The sequel to the previous post, I continue to tie up additional dangling points and affirm the high heritability and lack of “shared environment” impact on traits such as IQ, criminality, emotional/mental problems. I talk about the extended twin design and how it can clear up some dangling questions, like who do we choose our mates? Do spouses influence each other? I mention the key findings of behavioral genetics, namely: […]

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  23. Meng Hu says: • Website

    Concerning your update “Edit, 6/5/14″ it is interesting to see that self-report measures have higher shared-environmental effect compared to criminal report. I’m not surprised by this result. These measures surely reflect some shared familial experience. If you want studies on the heritability of income, see here. Try to do an CTRL+F and enter “Hyytinen”. One other thing I have noticed is that EEA may be violated for income. Try to enter “EEA appears to be violated”.

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    • Replies: @JayMan
    @Meng Hu:

    Thanks! I'm going to have to spend quite a while digging into that.

  24. JayMan says: • Website
    @Meng Hu
    Concerning your update "Edit, 6/5/14" it is interesting to see that self-report measures have higher shared-environmental effect compared to criminal report. I'm not surprised by this result. These measures surely reflect some shared familial experience. If you want studies on the heritability of income, see here. Try to do an CTRL+F and enter "Hyytinen". One other thing I have noticed is that EEA may be violated for income. Try to enter "EEA appears to be violated".

    Thanks! I’m going to have to spend quite a while digging into that.

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  25. […] Environmental Hereditarianism The Son Becomes The Father More Behavioral Genetic Facts […]

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