As we have previously discussed (Not the Next Tobacco: Defense to Obesity Claims), a major obstacle for obesity plaintiffs is causation. One reason causation will often be hard to prove is that genetic factors play a substantial role in obesity. A recent article provides new support for that conclusion. Wardle, J., Carnell, S., Haworth, C.M.A., and Plomin, R., “Evidence for a strong genetic influence on childhood adiposity despite the force of the obesogenic environment,” 87 Am. J. Clin. Nutr. 398-404 (2008) was an effort to quantify genetic and environmental influences on BMI and central obesity in children growing up after the onset of the so-called “obesity epidemic.” Theirs is reportedly the first study to assess the heritability of waist circumference in children. The authors performed twin analyses of BMI and waist circumference (“WC”) in a British sample of 5,092 twin pairs aged 8-11. They found substantial heritability for both BMI and WC (77% for both). The authors discovered that although the genetic influence on WC was largely common to BMI (60%), it is also a significant independent genetic effect (46%). The authors suspect that weight variation is attributable to large numbers of genes, each exerting small effects.
While the authors concede that genes have not changed dramatically in recent years, they also observe that not all children are obese. The investigators note that, contrary to widespread assumptions about the influence of the family environment, living in the same home in childhood seems to confer little similarity in adult BMI beyond that expected from the degree of genetic resemblance. That is, the “shared-environment effect” is relatively meager. The “shared-environment effect” means the extent to which the family environment makes family members more similar than would be expected from their genetic relatedness. Siblings from the same family were only slightly more similar in severity of overweight than would be expected from a genetic similarity. The shared environment effect was estimated as just over 10%. They authors write: “Although contemporary environments have made today’s children fatter than were children 20 years ago, the primary explanation for variations within the population, then and now, is genetic differences between individual children…The fact 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 is a challenge for etiologic models that highlight the home environment as the root cause of obesity.”
Plaintiffs bringing claims against food companies, and the experts they hire, will probably have to confront this problem, and may well find it difficult to overcome.