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Courtesy Razib Khan’s Pinboard Feed:
ScienceDaily (July 15, 2012) — Your genes determine much about you, but environment can have a strong influence on your genes even before birth, with consequences that can last a lifetime. In a study published online in Genome Research, researchers have for the first time shown that the environment experienced in the womb defines the newborn epigenetic profile, the chemical modifications to DNA we are born with, that could have implications for disease risk later in life.
Epigenetic tagging of genes by a chemical modification called DNA methylation is known to affect gene activity, playing a role in normal development, aging, and also in diseases such as diabetes, heart disease, and cancer. Studies conducted in animals have shown that the environment shapes the epigenetic profile across the genome, called the epigenome, particularly in the womb. An understanding of how the intrauterine environment molds the human epigenome could provide critical information about disease risk to help manage health throughout life.
Twin pairs, both monozygotic (identical) and dizygotic (fraternal), are ideal for epigenetic study because they share the same mother but have their own umbilical cord and amniotic sac, and in the case of identical twins, also share the same genetic make-up. Previous studies have shown that methylation can vary significantly at a single gene across multiple tissues of identical twins, but it is important to know what the DNA methylation landscape looks like across the genome.
In this report, an international team of researchers has for the first time analyzed genome-scale DNA methylation profiles of umbilical cord tissue, cord blood, and placenta of newborn identical and fraternal twin pairs to estimate how genes, the shared environment that their mother provides and the potentially different intrauterine environments experienced by each twin contribute to the epigenome. The group found that even in identical twins, there are widespread differences in the epigenetic profile of twins at birth.
“This must be due to events that happened to one twin and not the other,” said Dr. Jeffrey Craig of the Murdoch Childrens Research Institute (MCRI) in Australia and a senior author of the report. Craig added that although twins share a womb, the influence of specific tissues like the placenta and umbilical cord can be different for each fetus, and likely affects the epigenetic profile.
Interestingly, the team found that methylated genes closely associated with birth weight in their cohort are genes known to play roles in growth, metabolism, and cardiovascular disease, lending further support to a known link between low birth weight and risk for diseases such as diabetes and heart disease. The authors explained that their findings suggest the unique environmental experiences in the womb may have a more profound effect on epigenetic factors that influence health throughout life than previously thought.
Furthermore, an understanding of the epigenetic profile at birth could be a particularly powerful tool for managing future health. “This has potential to identify and track disease risk early in life, said Dr. Richard Saffery of the MCRI and a co-senior author of the study, “or even to modify risk through specific environmental or dietary interventions.”
What these researchers have done is discover one of the mechanisms behind developmental noise; that is, the force that causes a degree of “error” in how genes are expressed. The most poignant example of developmental noise is the fact that identical twins (who share virtually 100% of their genes) have different fingerprints, and often have other subtle physiological differences between them. This is highly significant, because psychologically, identical twins are far from identical, and indeed, the heritability of most behavioral traits hover in the 0.4-0.6 range, far from 100%, and often a lot less.
The existence of developmental noise means that traits that are not 100% heritable (few are—one such example is one’s sex), but rather have a considerable “unexplained variance”, as measured from most behavioral genetic tests, can still be wholly “biological” in nature. That is, they are “inborn”—usually unchangeable—and not necessarily affected by the post-natal environment (i.e., experience).
This can be true even if the measured heritability estimate is pretty low. One such example is the heavily discussed issue of sexual orientation. Here, heritability estimates can be as low 0.22. The low heritability, it has been suggested, may point to a non-genetic, perhaps pathogenic source, and perhaps that’s the case. But it is also possible that the source stems from the effect of certain genes which can give rise to same-sex attraction if their effects are sidetracked by semi-random events in-utero, such as exposure to opposite-sex hormones. These events may be fairly rare, and may require a genome that is sensitive to such events to develop into homosexuality. Given the apparent low heritability of same-sex attraction in men (~0.22), and given the prevalence of homosexuality in the male population (~4%) the percentage of men who are genetically potential gays could be as high as 20%! Of course (for those who were alarmed), if same-sex attraction is solely caused by forces that occur in-utero, most won’t and can’t develop this trait.
Developmental noise has important implications for other psychological traits, including IQ and personality. In the Western world, the heritability of IQ is >80%, near the limit of test reliability. It is possible—indeed likely—that some, or perhaps even all, of the remainder is due to developmental noise. This could further dash the hopes of those that seek to fix the problem of “failing schools” through intervention, and this leads me to my next post.
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Regarding your comment on the difficulty of fixing schools by intervention: depends on what you mean by “intervention.” Clearly current methods of education “reform” aren’t working (in NYC, a recent Daily News article suggests an “improvement” rate of just 30%)…however, as we discussed extensively on SC, we can start by making standardized exams more psychometric in nature. This has two advantages – one, this makes it much more difficult to cheat on the tests (still a major problem with test-based curricula and lowered standards); second, we’ll get a real measure of a student’s current level of understanding and an assessment of their ability to tackle future material.
The exams should also ramp up in difficulty (similar to how the Raven’s Progressive Matrices get harder as one proceeds), culminating in a fully-(g)-loaded SAT (and for prospective grad students, GRE, etc.)
Next, diversify curricula and raise the standards. Though not everyone is necessarily “fit” for college-level work, for example, if primary and secondary school curricula feature enough classes and extracurricular activities (say, in the arts), cats may have avenues through which they can prosper, even if they have middling or slightly-below-average IQs. (I say this, because the research is somewhat at odds – some papers state that IQ and creativity are positively correlated, while others imply the opposite.)
Wonder what your “next” post on this matter will feature…
Unfortunately, I’ve seen a lot of heredity-denialists bring up epigenetics as if it were the sudden vindication of Lamarck and Lysenko, elevating it from an interesting and possibly illuminating explanation for non-heritable factors affecting certain traits, to somehow disproving the existence of heritable differences between individuals and populations, and thus propagandizing it. I’m agnostic on the causes of the White-Black IQ gap myself. Chuck the Occidentalist cited a lot of evidence that at least throws it into more doubt than the Lynn et al narrative suggests.
Interestingly, your other post on dopamine index-affecting genes could suggest a genetic origin of the gap that does not directly affect intelligence, but that may affect it indirectly via the sort of environments people create for themselves (Higher-DI people being less likely to create environments that promote intellectual development, for example).
Yup, people discover some variability in gene expression (some of which is necessary to explain how one’s cells—all with the same DNA—differentiate into different types) and act as if it tosses all of genetic inheritance out the window. Nice try, I have to say.
What, exactly, of his are you referring to? The last word that I have found of his on this subject is this:
Part of heritability of most traits do not stem from direct genetic effects, but from indirect effects, such as gene-environment correlations as you describe. Part of the reason that low-IQ individuals tend to be poorer performers is because low-IQ individuals tend to be less motivated to stick out tough tasks. Of course, this doesn’t affect the utility of IQ tests, because the real-world performance of lower-IQ individuals is impacted both by their poorer intellectual ability and their poorer task-commitment, as Steve Sailer explains.
Additionally, a little known fact is that many cognitive tests overpredict Black performance, that is, they perform worse than their test scores would indicate. A share of that stems from statistical phenomena (high scores from low-mean groups are more likely to be erroneous), but part of that may be from that motivational aspect, as with the dopamine index. Smarter Blacks may be less inclined to work as hard as similarly intelligent Whites, hence, poorer performance.
I should probably have been more specific. I remember Chuck posting data that suggested that the African-European gap may be mostly environmental internationally. The crux of it seemed to hinge on the performance of Africans in the UK and the Netherlands on standardized tests. At the time, he also said that the gap in the US may differ from the gap in other countries because of selective pressures (maybe more intelligent blacks immigrate to Europe?). I’ve held out a lot of hope that, if the Black-White gap is the result of a relatively small genetic difference compounded by gene-environment interactions, that the environmental side could be positively influenced through positive intervention.
This post here was the one I was thinking of:
http://occidentalascent.wordpress.com/2012/04/05/a-gaping-hole-in-the-masters-evolutionary-theory/
Obviously, since it’s from early April, he may have found something that changed his mind since then. Like I said, I’ve been out of the loop for a while. I did see the post you’re referring to. I’ll go back and investigate further. Come to think of it, I probably should have done that before I posted. I suppose it happens to the best of us when we know something probably is so, but really wish it weren’t.
Enjoyed the post. Recently discovered your blog, but may I suggest a different background. I have great reading vision, but this white on black is really, really tough, enough to keep me from reading all but the shortest posts.
Regarding the heritability of personality traits in twins, one should keep in mind that twins will usually contest for dominance in the womb. If winning or losing that battle does not affect epigenetics you can color me amazed.