Read Daniel Engber’s “Science” article about the true cost of obesity.
“Nature tops nurture in childhood obesity,” a wire story announced last week. The article’s first sentence reported that according to a new study, “Diet and lifestyle play a far smaller role than genetic factors in determining whether a child becomes overweight.”
I’ve read and written a lot about obesity lately, and one thing I’ve learned, especially from my mistakes, is that genetics and “lifestyle” are rarely that simple. In this case, their relationship is particularly complicated. Obesity is indeed genetic. And diet and lifestyle are crucial to controlling it.
Genetic propensity to gain weight is hardly a new idea. Previous studies have suggested that adult body-mass index (BMI) is 55 percent to 85 percent heritable. But those studies left two questions unanswered. One was whether the kind of household in which a person grew up might affect that person’s weight as a child, even if such effects were washed out later in life. The other question was whether today’s kids—unlike today’s adults, who grew up decades ago—might be differently affected by today’s “obesogenic environment.”
To answer these questions, the new study, published in the American Journal of Clinical Nutrition, examined 5,000 pairs of British twins aged 8 to 11. By comparing similarities of outcome between identical twins (who share all their genes) and fraternal twins (who share half), the authors calculate that BMI in the sample was 77 percent heritable. That is, 77 percent of the variation between thinner and fatter kids could be attributed to genetic differences. Of the remainder, “shared environment” (growing up in the same household) accounted for 10 percent, and “non-shared environment” (for example, being the eldest kid instead of the youngest) accounted for 13 percent.
The authors conclude that parents shouldn’t be blamed for child obesity. After all, they note, the data show that “siblings’ experience of being served similar food, being given the same options for television viewing and active outdoor play, seeing the same behaviors modeled by parents, and going to the same school does not make siblings more similar,” in terms of BMI or waist circumference, “than would be expected from their genetic similarity.” Consequently, “Excessive weight gain in a child is unlikely to be the fault of the parents and is more likely to be due to the child’s genetic susceptibility to the obesogenic features of the modern environment.”
How do we know the modern environment is a factor? Because the obesity rate has soared in less than a generation. As the authors point out, “The dramatic rise in childhood obesity in the past 15 years is clearly due to changes in the environment, because genes have not altered.” But this implies a paradox: “Obesity is both predominantly environmental … and predominantly genetic.”
How can this be? Because genetic and environmental influences are measured differently. What’s genetic is the weight variation within a population, such as the kids in your neighborhood. What’s environmental is the weight variation between populations: kids in your neighborhood today, compared with kids in your neighborhood 15 years ago.
The superficial media spin—that “diet and lifestyle play a far smaller role than genetic factors”—is misleading in several ways. First, even if genes and behavior were utterly distinct, shared environmental factors accounted for 10 percent of total BMI variation and 40 percent of environmental BMI variation in the studied population. As the authors note, that much correlation, in the case of heart disease, is regarded by doctors as more than enough to justify behavioral recommendations.
Second, heritability by itself can’t prove the limits of what environmental changes might produce. An editorial on the study, published in the same journal, explains:
[T]he shared-environment effect is the result of the degree of variability of environments that were observed in the sample, and, therefore, it cannot be used to infer the possible effects of altering the environment in which we all live and that may vary only modestly among families. If all homes, for example, had the same poor dietary and exercise practices, the shared-environment effect would be estimated as zero, and yet it would be entirely appropriate to attribute much of the obesity to parental behaviors.
In other words, environmental changes can significantly raise or lower average weight—as, in fact, they have—even if genes largely determine your weight relative to your peers.
Third, not all environmental factors fit into the categories evaluated in heritability studies. Non-shared environment is specific to you. Shared environment is specific to your household or some other setting. But any environmental factor that affects the whole study population is too big to show up in the analysis. I’m not talking about things each family could do. I’m talking about things that affect nearly all families simultaneously: urbanization, pollution, the arrival of television, and the proliferation of fast food.
Fourth, just because something is genetically caused doesn’t mean it can’t be behaviorally controlled. As an example, the authors cite phenylketonuria, a genetic disease whose symptoms are commonly averted by altering the patient’s diet.
Fifth, diet and lifestyle can themselves be genetic pathways. In the case of hereditary overweight, the authors observe, “Part of the genetic effect may well be due to variations inappetite and satiety.” Fidgeting has been shown to burn lots of calories; it’s highly plausible that fidgeting is genetically influenced and that it drives people to exercise. To the extent that genetics overlaps with fattening behavior, old dichotomies have to be chucked. You can’t just blame fat people for eating too much. Nor can you assume that because fat is hereditary, there’s nothing they or society can do about it.
Accordingly, the authors propose a “behavioral, genetic model” of overweight. They embrace the liberal idea of “creating healthier external environments,” along with the conservative idea of “teaching vulnerable persons to adopt life-long prudent habits.” Note the latter formulation. Not everyone needs good habits. Only “vulnerable persons” do.
That’s my personal takeaway from the study: Those of us who don’t get fat should stifle our piety. Our relative thinness is 77 percent hereditary. I should know: I eat like a horse and can’t gain weight. We need to think of obesity the way we think of alcoholism or allergies: as an unevenly distributed biological predisposition to seek or suffer harm from common environmental factors. Yes, we should struggle against it. But it’s more of a struggle for some than for others.