So, I was planning a long series of posts about human nature and the significance of genetic and hormonal influences in many areas. I will get to that, but I felt compelled to respond to a particular claim. Megan McArdle, a blogger at The Atlantic online, responded affirmatively to a story by Tara Parker Pope in The New York Times Magazine. I think she relied heavily on Gina Kolata’s recent book Rethinking Thin, which I have not read. McArdle asserted that no evidence showed exercise makes one thinner.
In my series, I will go into how some researchers argue that some members of the media and lay public misunderstand the meaning of genetic influence on human attributes and behavior. Exercise and diet are not the panacea that some might think growing up in the West. Still, is there truly no evidence that exercise does not make one thinner?
Several genetically informed studies have found that exercise attenuates a genetic propensity towards obesity. Other studies of twins have found that physically active twins are leaner than their more sedentary counterparts in discordant pairs.
In a 1998 study in Obesity Research (now Obesity), Rose et. al studied a sample of female twins. Here is the abstract of their findings on waist circumference.
This study examines genetic and behavioral determinants of waist-hip ratio (WHR) and waist circumference among women twins.
RESEARCH METHODS AND PROCEDURES:
Six hundred eighty participants from the second examination of the Kaiser-Permanente Women Twins Study (1989 to 1990) were included. Women ranged in age from 31 to 90 years, and included 59% monozygotic and 41% dizygotic twins. Heritabilities of WHR and waist circumference were estimated (range=0 to 1) using three different statistical methods. Linear regression models that adjusted for the lack of independence within twin pairs were used to assess associations between behavioral variables, WHR, and waist circumference.
Age and body mass index-adjusted heritability estimates ranged from 0.36 to 0.61 for WHR and 0.72 to 0.82 for waist circumference. When considered individually, after adjusting for age and body mass index, all behavioral characteristics, except calorie-adjusted fat intake, were significantly (p<0. 10) associated with waist circumference and WHR. Greater central adiposity was associated with lower education, higher alcohol consumption, lower physical activity, current cigarette smoking, higher parity, and postmenopausal status without hormone replacement therapy. In multivariate models, these associations persisted, except neither educational attainment nor alcohol intake was significantly associated with waist circumference. In longitudinal analyses, both measures were positively associated with current or recent-past smoking; infrequent or inconsistent physical activity; and long-term, daily consumption of alcohol.
These cross-sectional and longitudinal associations are consistent with genetic and behavioral predictors of waist circumference and WHR. Whereas the evidence for genetic influences is stronger for waist circumference, both body fat measures may be similarly influenced by the behavioral factors considered.
McCaffery et. al (2009) found effects of exercise on body mass index in a sample of Vietnam War-era male twins. Fortunately, this paper is open-access.
A recent meta-analysis compared sedentary and active individuals with an allele known to increase the risk of obesity. Its authors found that “All studies identified to have data on the FTO rs9939609 variant (or any proxy [r2>0.8]) and PA were invited to participate, regardless of ethnicity or age of the participants. PA was standardized by categorizing it into a dichotomous variable (physically inactive versus active) in each study. Overall, 25% of adults and 13% of children were categorized as inactive. Interaction analyses were performed within each study by including the FTO×PA interaction term in an additive model, adjusting for age and sex. Subsequently, random effects meta-analysis was used to pool the interaction terms. In adults, the minor (A−) allele of rs9939609 increased the odds of obesity by 1.23-fold/allele (95% CI 1.20–1.26), but PA attenuated this effect (pinteraction = 0.001). More specifically, the minor allele of rs9939609 increased the odds of obesity less in the physically active group (odds ratio = 1.22/allele, 95% CI 1.19–1.25) than in the inactive group (odds ratio = 1.30/allele, 95% CI 1.24–1.36). No such interaction was found in children and adolescents.
Some might argue that they’d like to see evidence such as trials, not just associations. I’ll discuss that in a later post.