It's about heritability….

By Razib Khan | March 27, 2011 2:25 pm

I’m going to promote a comment:

…would knowing the root biological cause for differences which are already apparent to us change anything?

It’s obvious to you that there’s a contradiction here, but to the average educated person this makes total sense.

The proximal reason seems to be that in thinking about “genetic” and “environmental” factors, the average educated person still fundamentally views “genetics” as equivalent to genetic determinism and “environmental” factors as equivalent to social norms or parenting tactics. In this black-and-white view of human development, quantitative distinctions and complex causal models have no place. Genetic causes are irremediable and ever-lasting, whereas environmental causes are a generation-away from disappearing with the right appropriations to social programs. That’s why an environmental cause for phenotypic differences doesn’t “count” but a genetic one is game changing.

It seems as if the nature-nurture world view painted in the 1970s by the anti-heredity crowd has remained largely intact with only minor modifications in the mind of the average educated person. Since the 1970s, they now know to respond to questions about nature-vs-nurture by saying “both”, but their understanding goes no deeper than that. As best as I can tell, “both” to them just means genetic-determinism in some cases and environmental effects in other cases. When pressed, they also seem to believe that the environment ultimately determines which matters when — “genetics” matters only because we are nurturing enough.

With this in mind, imagine their confusion and horror at being told about non-zero heritability. It’s as if a person who believes the world is flat is told that someone can sail westward from Europe to Asia. Because they can’t imagine a round world, they have to instead imagine that there’s a portal on the edge of the world that takes you from one side to the other. Granted that’s a limited analogy, but I think that’s what you’re seeing here — total confusion. Importantly, this is basically what everyone believes.

Alas, I’m not a good communicator. At least not to my satisfaction. Long time readers still speak about “nature” and “nurture” in a colloquial manner which makes it clear that they haven’t internalized what heritability implies about the irrelevance of the structure of their argument. Almost all of the discourse about genetics, and quantitative traits, whether it be behavioral or physical (e.g., obesity in the latter case), in the public domain is basically in a “not-even-wrong” category of incoherence. But we must muddle on. What else can we do? I wish David Dobbs the best of luck with his new enterprise.

CATEGORIZED UNDER: Behavior Genetics, Genetics, Genomics
  • biologist

    Here’s an example of why heritability matters.

    Lehtovirta M, Pietiläinen KH, Levälahti E, Heikkilä K, Groop L, Silventoinen K, Koskenvuo M, Kaprio J. Evidence that BMI and type 2 diabetes share only a minor fraction of genetic variance: a follow-up study of 23,585 monozygotic and dizygotic twins from the Finnish Twin Cohort Study. Diabetologia. 2010 Jul;53(7):1314-21. Epub 2010 Apr 17.


    AIMS/HYPOTHESIS: We investigated whether BMI predicts type 2 diabetes in twins and to what extent that is explained by common genetic factors.

    METHODS: This was a population-based twin cohort study. Monozygotic (n = 4,076) and dizygotic (n = 9,109) non-diabetic twin pairs born before 1958 answered a questionnaire in 1975, from which BMI was obtained. Information on incident cases of diabetes was obtained by linkage to nationwide registers until 2005.

    RESULTS: Altogether, 1,332 twins (6.3% of men, 5.1% of women) developed type 2 diabetes. The HR for type 2 diabetes increased monotonically with a mean of 1.22 (95% CI 1.20-1.24) per BMI unit and of 1.97 (95% CI 1.87-2.08) per SD of BMI. The HRs for lean, overweight, obese and morbidly obese participants were 0.59, 2.96, 6.80 and 13.64 as compared with normal weight participants. Model heritability estimates for bivariate variance due to an additive genetic component and non-shared environmental component were 75% (men) and 71% (women) for BMI, and 73% and 64%, respectively for type 2 diabetes. The correlations between genetic variance components (r (g)) indicated that one fifth of the covariance of BMI and type 2 diabetes was due to shared genetic influences. Although the mean monozygotic concordance for type 2 diabetes was approximately twice the dizygotic one, age of onset of diabetes within twin pair members varied greatly, irrespective of zygosity.

    CONCLUSIONS/INTERPRETATION: A 28-year follow-up of adult Finnish twins showed that despite high trait heritability estimates, only a fraction of covariation in BMI and incident type 2 diabetes was of genetic origin.

  • biologist

    Here’s another:

    Clifton Bogardus. “Missing Heritability and GWAS Utility” Obesity (2009) 17 2, 209–210. doi:10.1038/oby.2008.613

    The environment is largely responsible for differences in BMI between populations; genetics is largely responsible for differences in BMI within populations. Evidences in support of the environmental effect are many. The prevalence of obesity differs greatly between countries, even among developed countries (1). On a smaller scale, differences in the “built environment” within a city are associated with differences in BMI. In New York City a greater density of bus and subway stops and greater variety in uses of land within a neighborhood are associated with lower BMIs (2). Closely genetically related populations living in different environments differ considerably in average BMI (3). The environment clearly can be more or less obesegenic.

    But there is strong evidence that within a population the variance in BMI is largely genetically determined. The weight of adoptees correlates better with the BMI of their biologic parents than with that of their adoptive parents (4). Twin studies indicate that about two-thirds of the variance in BMI is attributable to additive genetic factors (5). The most convincing study of the heritability of BMI in twins was that of Stunkard and colleagues, who studied 93 adult pairs of monozygotic twins who had been separated as young children and reared apart (6). These authors similarly estimated that about two-thirds of the variance in BMI was due to genetic factors.

  • dan

    i think you may even be giving baby boomers too much credit, Razib. i get the impression that when they hear “50% genetic” they definitely think a trait is “50% genetic and 50% environment” in the same person….whatever that means. i think a simple double sliding scale graphic would clear this up pretty easily and it’d give them a start. ultimately, though, they really really don’t care. they simply refuse to believe in the limits of genetic potential and i don’t think anything will change their mind. the “eating more won’t make you taller” gives them pause but then they just try forget about it as soon as they can.

  • Chris T

    biologist – Would it be correct to say:
    From a practical perspective, the question should be what minimum environment is required to maximize heritability? (Which cannot be 100%, since there a lot of influences that are simply random [biological and non-biological].)

    It would seem the best way to tease this out is to use heritability estimates between several genetically similar populations and compare them. A high estimate would indicate that there is something shared between the two populations’ environments and a low estimate would indicate the absence of such.

    This would seem to be the only real way forward for figuring out effective interventions (rather than the scatter shot method we employ now; which has gotten us no where).

  • biologist

    Chris T, I don’t know if anyone has tried that approach. Seems like it might work, but getting a large enough study cohort to detect differences in heritability might be hard.

  • German Dziebel

    Nicely put, biologist! But…

    “That’s why an environmental cause for phenotypic differences doesn’t “count” but a genetic one is game changing.”

    Sure, when we’re lucky enough to get at a causal mechanism we can dismiss everything else as irrelevant.

    “but getting a large enough study cohort to detect differences in heritability might be hard.”

    Well, it’s really not about heritability then but about the process of ascertaining what’s heritable and what’s not. If we all could get to the roots of the issues we’re dealing with, we all would’ve turned into “above-average-educated-people.” We got lucky with finally figuring out that the earth ain’t flat but it took us a while to get there. I wish we could invent a program of sorts – it doesn’t need to be heritable – to speed up the process of sorting out genes vs. environment components and then celebrating the former.

  • biologist

    “That’s why an environmental cause for phenotypic differences doesn’t “count” but a genetic one is game changing.”

    To clarify, that was my summary of the (common) mistaken view.

    On that precise issue, I couldn’t say with certainty that a genetic cause is always as (un-)remediable as an environmental one, but certainly they both “count” in producing phenotypic variance.

    More importantly, it’s the causal networks that matter ultimately, and multivariant genetic models like the paper I linked to help to sort them out much better than comparable non-genetically informed (correlation) studies. Thus, heritability studies should be a part of the usual toolkit of those in the human (social) sciences and the average educated person should be generally conversant with their implications.

  • E. Manhattan

    And now, of course, we’re finally beginning to learn about the possible effects of our personal bacterial / archaerial / viral / floral / faunal bionomes on our behavior, weight and general health. There are plenty of surprises in the pipeline there, and plenty of possible revisions to existing heritability studies.

    Should the bacteria and archaea, mites and other tiny things which evolved with us and only live on humans count in heritability studies? How much of family trait heritability involves familial microorganisms handed down during birth and childhood? How many of our health problems have been caused by messing up our symbionts via learned behavior? Will parents feel guilty about damaging their children’s microorganisms in mistaken attempts to nurture them? Will the word “bionome” continue to be misused to sell face cream?

  • Shecky R.

    in 30 yrs. we may look upon today’s understanding of genetics the same way you’re now looking upon genetic determinism or “nature vs. nurture”… in 30 yrs. we may be discussing something akin to epi-epi-epi-epigenetics, that today we can’t even foresee. I concur with Manhattan, “There are plenty of surprises in the pipeline there, and plenty of possible revisions to existing heritability studies.”

  • miko

    biologist said: On that precise issue, I couldn’t say with certainty that a genetic cause is always as (un-)remediable as an environmental one, but certainly they both “count” in producing phenotypic variance.

    I think it’s a common misperception (not yours) that environmental factors are a) better understood, and b) easier to modify. It might be true that in principal the environment is easier to modify than the genome, but we at least have a robust scientific model for how genes might affect behavioral traits. Yes, we don’t know any specifics, but we can presume that at some point genomics, development, neuroscience and the fields that don’t exist yet that will define modern human ecology and how it effects these processes are going to meet.

    But currently we have no idea what or how environmental factors might affect most traits. E. Manhattan raises our personal microbiomes–almost completely unexplored territory, but certainly a major player in our evolution, metabolism, and probably behavior. In the mean time, it has become acceptable in human studies to list 5 or 6 easily measurable “environment” variables (usually borrowed from the social sciences) and declare equivalence, or at least claim you’ve controlled for something or other.

    Anyway, point being, ease of remediation is at this stage (and for a long time to come) independent of being “genetic” or “environmental” (see, even for those of us who get it we semantically get drawn back into discussing them as and/or). Take PKU: a 100% genetic disorder that is 100% “curable” with simple environmental changes (low Phe diet). Genetic factors that cause unwanted phenotypes do not necessarily require “genetic” solutions. We can find broken/variant genes (sometimes)–this does not tell us what to do about a disease state at the physiological/organismal level. This is why the “finding drug targets” paradigm of the pharmaceutical industry for the last two decades has been such a flop, and cancer is still treated with broad spectrum cellular toxins from the 70s.

  • German Dziebel

    “Thus, heritability studies should be a part of the usual toolkit of those in the human (social) sciences and the average educated person should be generally conversant with their implications.”

    I absolutely agree. Thanks for the clarification.

  • miko

    And as we bemoan the terrible public understanding of heritability, take a minute to pity us poor neuroscientists (though we will get the last laugh when we replace the judicial system with fMRI and are able to program voters with campaign leaflet color schemes). David Brooks is trying to do to neuroscience what Nicholas Wade does to genetics with his dumb book and LOLzy talks like this upcoming one at the Kennedy School: “Politics, the Brain and Human Nature.” Apparently, someone told him about neurotransmitters and he’s really run with it!

  • E. Manhattan

    And Miko was quite kind in reminding me that it’s biome, not bionome – the latter will undoubtedly continue to be used to sell face cream.

  • Mark

    As an undergraduate, I was an English Major. I am now in Law School. Draw whatever inferences about my intelligence and degree of scientific literacy from these facts as you find appropriate.

    Anyway, I’m struggling to understand the whole heritability/genes-environment distinction. I think I grasp that heritability “is the fraction of the variance in a population’s phenotype that can be attributed to genetic variation among individuals.” (Wiki) That seems pretty straightforward. My question is, am I correct in thinking that since heritability refers to populations, it is still appropriate, when talking about individuals, to talk about what portion of a particular phenotype can be chalked up to “nature” (genes, and I suppose other biological factors) what portion involves “nurture” (i.e. environmental inputs), and what portion is due to some complex interaction between biological/genetic factors and environmental inputs? Or is there a better way to think about the influences on an individual’s phenotype?

  • Sergy

    Do you know something about genetics of Olmecs? I tried to find something, after reading (just out of curiosity) article in Wikipedia about Olmecs, but I find no reliable information (except some “out of Africa” crap; or may be not crap – I’m confused). So, I decide to ask you about it – it seems that you are interested in things like that, may be you know something.

    I already tried Google Scholar and gbooks – and it didn’t help much (possibly because of my poor English). Was there any research with DNA from Olmecs remains or something? Do you know anything about this?

  • miko

    Mark, the Wikipedia article on gene-environment interaction is a good place to start, but as an exercise for think about contributions to complex traits, ponder trying to assign percent contributions of barley, hops, water and yeast to the deliciousness (or other traits) of beer.

  • David Dobbs


    Thanks for the good wishes for my own foray into closing the loop — or erasing the distinction — between nature and nurture. It’s my hope/fantasy — O, the goals we indulge in — to show how they are a circle rather than a spectrum. The muddyness of which phrase emphasizes my challenge.

    Ironically, I think sometimes precision — such as XX% genetic — can fog things, since it implies a sort of measuring out of distinct influences: Put in 62% genetic, 38% environmental, you get Z. It sounds like we’re adding distinct entities rather than describing a sort of conversation. The need for precision in quantitative understanding can block a qualitative understanding.

    Which is why English majors like me think we can crack this thing with metaphors.

    GIve me some time here, I’m working on it.

  • biologist

    Mark, consider the underlying source of the data. These studies typically ask, how similar are various categories of siblings? So they do allow us to make counterfactual statements about what “we” would have been like if we rewound the clock and tried again (under the same or different conditions). They can tell us how different we might be under different circumstances. However, the coefficients do not indicate the degree of importance to your current phenotype — both your environment and your genotype were essential to producing your phenotype.

    Consider monozygotic twins raised together. They have essentially the same genomes and are raised by the same parents. Any differences between them in a phenotype demonstrate the extent to which that phenotype is *determined* by neither genetics nor parents.

    Adopted siblings, dizygotic siblings raised together, dizygotic siblings raised apart, and monozygotic siblings raised apart each parcel out a different aspect of the question.

  • ohwilleke

    “would knowing the root biological cause for differences which are already apparent to us change anything?”

    Yes. For better or for worse, we seem to be as a people, more comfortable with having society take responsibility for deficiencies caused either by genetic causes, or by causes that seem “random” (e.g. date of birth during the calendar year), while we as a people tend to impose individual moral responsibility where something has an environmental cause that is not random, on the theory that one could have secured a different results by living/parenting differently and that better parenting/living should have appropriate rewards.

  • ohwilleke

    “The need for precision in quantitative understanding can block a qualitative understanding.”

    A key point, I think, is to use limiting language rather than global language when talking about heritability, especially with precision. The notion that heritability of IQ is lower at low SES than at high SES, and that both might differ from the average from the population as a whole is one of the most helpful examples. Another really helpful example is the gene that governs resiliency in the face of abuse – it is easy to see an environment x gene relationship there.

  • Chris T

    Any differences between them in a phenotype demonstrate the extent to which that phenotype is *determined* by neither genetics nor parents.

    It is important to note that this does not necessarily mean influences under human control.


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About Razib Khan

I have degrees in biology and biochemistry, a passion for genetics, history, and philosophy, and shrimp is my favorite food. In relation to nationality I'm a American Northwesterner, in politics I'm a reactionary, and as for religion I have none (I'm an atheist). If you want to know more, see the links at


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