Role of environmental vs. metabolic factors in the etiology of obesity: time to focus on the environment.

In the obesity research literature and in the mass media,a reduced metabolic rate is probably one of the most fre-quently cited causes of obesity. In the current issue ofObesity Research (pp. 351–359), Luke et al. (1) describe theresults of a fascinating study that examined this hypothesis.Specifically, they examined whether genetically relatedpeople of West African origin, living in vastly differentenvironments with large differences in the prevalence ofobesity (4% to 5% in Nigeria, 35% to 50% in the UnitedStates) had any difference in resting metabolic rate. Lowmetabolic rate has been observed in many cross-sectionalstudies that have examined subgroups of the population athigh risk of obesity, including African Americans living inthe U.S. (2–5), Pima Indians living in southwestern Arizona(6), and children (7) and infants (8) of overweight parents.It has even been postulated that the lower resting metabolicrate in women (9,10) may explain the higher adiposity inwomen compared to men. However, other more detailedstudies, which have compared groups at low and high risk ofobesity, have failed to find evidence to support a role forresting metabolic rate (11,12). For example, Pima Indiansliving in Mexico who are much thinner than their geneticrelatives in Arizona have a very similar metabolic physiol-ogy, despite large differences in adiposity (13).The comparison of African American with white peo-ple has been of recent interest because of the much higherprevalence of obesity and obesity-related health risk inthe African American population. Several cross-sectionalstudies in children (2,4), adolescents (5), and adults (14–16) have shown that African Americans have a lowerresting metabolic rate, although this observation is notconsistent across all studies (17). Several papers in theliterature have extrapolated from this finding to implythat the reduced metabolic rate is the cause of the obesity.Why would this be so? Is there any reason to believe thatthe homeostatic regulation that finely matches energyintake to energy expenditure is less likely to performaccurately at a low level of resting metabolic rate? Itseems unlikely, given that resting metabolic rate onlyexplains about 50% of the variance in total energy ex-penditure (18), and in growing children, neither high orlow resting energy expenditure or total energy expendi-ture can predict which children will gain excessive bodyfat during subsequent growth (12).In terms of the lower resting metabolic rate in AfricanAmericans, the more fundamental questions may be, 1) doestheir lower metabolic rate influence subsequent develop-ment of obesity, and 2) what is the mechanism underlyingtheir lower metabolic rate? Regarding question #1, suffi-cient data now exist to indicate that a relatively low restingmetabolic rate represents an inherent, probably geneticallydetermined, characteristic of persons of African origin thatmay be more of a function of body composition. However,this characteristic probably does not explain their greaterlikelihood of weight gain in African Americans. Our recent,still unpublished follow-up data on 52 normal-weightwomen (mix of weight-reduced and never-obese AfricanAmericans and whites) indicated that the African Americanwomen gained over 60% more weight after just 1 year.Greater weight gain in the women, however, was not pre-dicted by inherent metabolic characteristics such as lowerrates of sleeping or resting metabolic rate, fat oxidation, orinsulin sensitivity. Rather, greater weight gain was pre-dicted by potentially modifiable factors, including lessphysical strength, less daily free-living physical activity,and lower total daily (but not resting) energy expenditure.Of particular interest are other recent data suggesting thatAfrican Americans are not only more energy efficient thanwhites at rest but also during physical activity, resulting in