Heritability: I do not think it means what you think it means.
There’s been a spate of posts about obesity, started by a post by Megan McArdle. In these posts, a high heritability for obesity is bandied about (0.9!!! ZOMG!! TEH GENEZ R MAKIN U FAT!). But this demonstrates a lack of understanding of what heritability estimates mean–and, more importantly, what they do not mean.
A couple of years ago, the Three-Toed Sloth wrote a wonderful post about heritability, and I’ll quote liberally from it here (instead of rephrasing it inelegantly) and add some additional commentary. I should note that most people familiar with quantitative genetics will not see anything new here–as Three-Toed Sloth notes, this was covered over thirty years ago. Moving right along….
First, Herr Doktor Three-Toed Sloth gives a very succinct definition of what heritability does and does not tell us (italics original; boldface mine):
Heritability is a technical measure of how much of the variance in a quantitative trait (such as IQ) is associated with genetic differences, in a population with a certain distribution of genotypes and environments. Under some very strong simplifying assumptions, quantitative geneticists use it to calculate the changes to be expected from artificial or natural selection in a statistically steady environment. It says nothing about how much the over-all level of the trait is under genetic control, and it says nothing about how much the trait can change under environmental interventions.
One of the mistakes that is commonly made regarding heritability is that a high heritability (heritability ranges from zero to 1.0) means that most of the absolute value of a trait, such as BMI, is genetic. Not exactly (italics original; boldface mine):
Saying a trait is highly heritable is saying that, in a given distribution of genotypes and environments, most of the variance in that trait is associated with genetic differences. Maybe the most important point I’ll make here is that this is not the same most of the value of the trait being genetically controlled. The textbook example is that (essentially) all of the variance in the number of eyes, hearts, hands, kidneys, heads, etc. people have is environmental. (There are very, very few mutations which alter how many eyes people have, because those are strongly selected against, but people do lose eyes to environmental causes, such as accident, disease, torture, etc.) The heritability of these numbers is about as close to zero as possible, but the genetic control of them is about as absolute as possible.
There’s a flip side to this–heritability estimates are made within the context of the environments in which the estimates are made:
Similarly, heritability says nothing about malleability, about how much or how easily the trait changes in response to environmental manipulations: heritability is defined with respect to a given distribution of environments, and does not predict the response to environmental changes….
What heritability does predict is the response to selection, in a constant distribution of environments. This is why quantitative geneticists developed and retained the concept. If a population is subjected to directional selection on a trait, whether the selection is natural or artificial, and the trait follows the classical decomposition into additive, uncorrelated components, the degree to which the genetic component of the trait changes will depend on the intensity of selection, the variance in the trait, and its heritability. The response to selection, the phenotypic change in the next generation, will be large if the selection pressure, the trait’s variance, and the trait’s heritability are all high, assuming that the distribution of environments is held fixed and uncorrelated with genotype.
But the crux of the matter is can not environmental changes alter phenotypes, even if those phenotypes are highly heritable? Well, yes:
It’s banging on an often-sounded drum, but it’s worth doing because it makes the point clearly: height is heritable, and estimates for the population of developed countries put the heritability around 0.8. Moreover, tall people tend to be at something of a reproductive advantage. Applying the standard formulas for response to selection, we straightforwardly predict that average height should increase. If we select a population without a lot of immigration or emigration to mess this up, say 20th century Norway, we find that that’s true: the average height of Norwegian men increased by about 10 centimeters over the century. But that’s much more than selection can account for. Doing things by discrete generations, rather than in continuous time, height grew by 2.5 centimeters per generation. (The conclusion is not substantially altered by going to continuous time.) If the heritability of height is 0.8, for this change to be due entirely to selection, the average Norwegian parent must have been 3 centimeters taller than the average Norwegian [today]. This, needless to say, was not how it happened; the change was almost entirely environmental. The moral is that highly heritable traits with an indubitable genetic basis can be highly responsive to changes in environment (such as nutrition, disease, environmental influences on hormone levels, etc.).
Conversely, the very low heritability of eye number does not tell us that it is easy to increase how many eyes someone has by exercise, education and training, manipulating diet, manipulating ambient light, trepanation, etc.
So when McArdle claims:
Twin studies and adoptive studies show that the overwhelming determinant of your weight is not your willpower; it’s your genes. The heritability of weight is between .75 and .85. The heritability of height is between .9 and .95. And the older you are, the more heritable weight is.
…that’s irrelevant. Phenotypes can be very environmentally malleable even though they are very heritable (see the aforementioned Norwegians). That is, diet can make a difference (if not necessarily in adulthood).
I would add that an additional complication is that the irreversibility of a trait is often confused with its genetic basis. In other words, if childhood (or young adult) behaviors and environments ‘lock in’ (or often do so) obesity in adulthood, that does not imply that obesity is ‘genetic’, in the same way that food deprivation as a child which stunts growth is also not ‘genetic.’
What upsets me the most about all of this is that we know obesity is correlated with adult-onset diabetes. More importantly, we know that adult-onset diabetes, while having a genetic component, can be controlled with diet, yet this kind of obesity genetics-as-destiny fatalism gives cover to a lot of people with unhealthy habits.