In my medical anthropology class, we’ve been reading Gina Kolata’s Rethinking Thin: The New Science of Weight Loss and the Myths and Realities of Dieting.  Kolata argues for a biological approach to obesity, that weight is largely under genetic control and that there is no ideal diet which is going to help all people lose weight.  In other words, Kolata is taking up the “nature” side of the nature/nurture debate, with a direct critique of the idea that if overweight people could simply use their willpower and follow the age-old recommendation of eat less and exercise more, they would be ideally thin like the beautiful people we see on television—the Brad Pitts and Angelina Jolies of the world. 

Kolata sums up these points in a very amusing interview on The Colbert Report.  As Fat Fu summarizes about Kolata, “you can actually learn something about the state of the science. And which don’t conclude with exhortations to diet or insinuations that fat people are lazy and ignorant. In fact she doesn’t think diets work.” 

I like Kolata’s book, which is why I assigned it in my class.  And I certainly see the weight of the evidence as supporting many of her main points: heritability and biological regulation of body weight, as well as the absurdity of an “ideal diet” that will simply work for everyone (that’s called ideology, folks).  But Kolata gives us an approach that recreates the mind/body and culture/biology dichotomies, and resorts to a genetic determinism that both obscures the genetics and doesn’t leave much room for anthropology.  For example, she uses one study, a classic one by Stunkard et al. in 1990, to tell us that “70 percent of the variation in people’s weight’s may be accounted for by inheritance,” which is greater heritability than with “mental illness, breast cancer or heart disease.” 

I’ll admit, I am not the biggest fan of twin studies.  They are generally done in western populations without much variance in environment or development and with relatively homogenous populations.  In public, these researchers generally claim the higher range of heritability estimates.  And perhaps most bothersome, these studies seem to provide us with a “why” that is not really there—“genetic” becomes tantamount to cause. 

I have to lecture on the human biology of weight and obesity on Tuesday, so I’ve decided to put together something like my “lecture notes” here on the blog.  I am planning to cover four areas on Tuesday—genetics, weight set points, hunger and appetite, and “will power”—and will hopefully cover most of those by Tuesday.  This time it will be genetics. 

In a recent review (open access pdf available), Farooqi and O’Rahilly (2007) confirm that “heritable factors are likely to be responsible for 45-75% of the inter-individual variation in body mass index.”  Maes et al. in a 1997 review found that “genetic factors explained 50 to 90% of the variance in BMI.”  Thus, variation in the data is greater than implied by Kolata.  And if we’re cautious scientists, we could take the lower estimates as the ones supported by all the science, so we’re talking about roughly 50% heritability. 

And what accounts for this relatively high heritability?  Is it some “obese” gene?  What I do find striking in these discussions is one simply fact that is generally left out.  We know height is one of the most heritable traits we have, in the range of 60-80% heritability (see this Scientific American article) with some estimates going into the 80-90% range in Western populations.  Since BMI is calculated by an individual’s weight divided by the square of their height, one might reasonably assume that height drives a lot of the heritability in body mass index. 

That said, more direct measures of adiposity have indicated high heritabilities for both total and regional fat in two studies that I saw (Malis et al. 2005; Carey et al. 1996).  So the weight side of the BMI equation also appears to be shaped genetically.  But my basic point holds—there is greater variation in the heritability estimates than often presented by genetic researchers and science writers who have a stake in making an argument to the public. 

Moreover, lifetime variation in BMI matters, and matters a lot, both in terms of the health impact and in terms of how environment can impact body weight.  For example, here’s an underappreciated fact about twins.  Pietiläinen et al. (2002) found that “[e]ven in monozygotic twins who share their genetic background, the initially larger twin tended to remain larger, demonstrating the long-lasting effects of fetal environment on final body size.”  As Kuzawa et al. (2007) argue (pdf), fetal programming and uterine environment play a significant role in the development of obesity.  It’s not simply genetics, end of story. 

Indeed, I found it interesting that heritability estimates for BMI went down over the lifespan in one study.  Height stays relatively stable, but both weight and BMI drop in “heritability” as a person ages.  As the researchers write, “nonshared environmental variance increased with age.”  So, in terms of what is driving changes in BMI over the lifespan, one could use the fetal programming and the drop-off in heritability to argue that development and environment are the determinative factors, rather than genetics. 

I’m not actually saying that.  Here’s what I would say: Partitioning the world into genes and environment is a pretty crude strategy, and misses out on how things actually work.  Heritability estimates are not absolute figures but a rough guide to what sorts of traits are more heritable than others.  Height, for example, appears more heritable than weight. 

Also, saying something is genetic doesn’t mean you are analyzing the “difference that makes a difference.”  For example, language ability is surely largely genetic—after all, other species don’t speak full-blown languages, only humans.  However, what really matters in today’s world is what language you speak—English versus Spanish versus Mandarin versus Arabic versus Persian. 

So is obesity a problem of species differences, that humans are relatively fat compared to other species and now live in an “obesogenic” environment?  Or is obesity a problem of cultural variations, of patterns of development and of eating, of historical environments that push sugar and other profit-oriented products?  Myself, I’d take the Super Size Me version—that it is the everyday dimensions of obesity, and not solely the genetic dimensions of obesity, that play a more determinative role in who has a problem or not. 

Do those everyday dimensions play out against significant biological variation?  Most definitely yes.  Can we use our understanding of that variation to understand that “will power” or the “perfect” diet won’t be as effective for most people on the “wrong” side of that variation?  Here I’ll offer a more qualified yes, because this question, unlike the first one, frames the problem as nature versus nurture.  And obesity involves both nature and nurture and their significant interactions. 

Molecular genetic and biological mechanism research actually point to significant variation in “obesity” that is important.  A small percentage of obese individuals have “genetic obesity syndromes” (Farooqi & O’Rahilly 2007), for example, congenital leptin deficiency.  So it’s certainly not a one-size fits all approach.  However, this is precisely what the measurement of BMI does, give a number to a person irrespective of age, gender, muscle-building activities, or any number of other things found to shape BMI scores.

In reviewing the genetic research, what I did find striking is the conclusion that in most cases, obesity appears to be driven more by regulation of appetite and energy intake (Farooqi & O’Rahilly 2007).  As these authors write, “The genetic defects found to date all impair satiety, affecting the function of appetite control centres in the brain rather than being due to a ‘slow metabolism.’  This indicates that we must think of human food intake not as an entirely voluntarily controllable phenomenon but one driven by powerful biological signals from relatively primitive brain areas.  When these basic signaling mechanisms are severely disrupted, it is very difficult to overcome the drive to eat (38).”

Kolata’s book is filled with stories of people who successfully lose weight and then gain it back, driven by hunger.  Even though from the outside it might appear that they are not hungry—how could they be, all that extra weight?—their bodies respond as if they are hungry, as if they don’t have enough energy or even that they are starving.  It is one of the most convincing parts of her book, how she brings together the research evidence showing how heavier subjects react to weight loss like thin people put on starvation diets and the descriptions of struggles with weight loss and the powerful urges to eat described by the people in her book.