Human biodiversity in adiposity

First, the study: Racial differences in abdominal depot-specific adiposity in white and African American adults

Katzmarzyk PT, Bray GA, Greenway FL, Johnson WD, Newton RL Jr, Ravussin E, Ryan DH, Smith SR, Bouchard C.

Pennington Biomedical Research Center, Louisiana State University System, Baton Rouge, LA 70808-4124, USA.

There is increasing interest in understanding racial differences in adiposity in specific body depots as a way to explain differential health risks associated with obesity.

Our aim was to examine the differences in abdominal visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) between white and African American adults.

The sample included 1967 adults aged 18-84 y, including 790 white women, 435 African American women, 606 white men, and 136 African American men. Total body fat was measured by using dual-energy X-ray absorptiometry, whereas abdominal VAT and SAT cross-sectional areas (L4-L5 level) were measured by using computed tomography. Sex-specific differences in SAT and VAT between racial groups were analyzed by the use of general linear models, which controlled for age and total body fat. Additional models tested for racial differences in VAT and SAT and controlled for age, total body fat, smoking, and menopausal status. Statistical significance was accepted at P < 0.05. RESULTS: Abdominal VAT was significantly higher in white than in African American men and women, even after adjustment for covariates. White women had significantly lower SAT than did African American women, both before and after adjustment for covariates. White men had significantly higher SAT than did African American men, but after adjustment for covariates, their SAT was lower than that of African American men. CONCLUSIONS:

Abdominal visceral adiposity is significantly greater in white men and women. After adjustment for covariates, white men and women had significantly lower SAT than did African American men and women. The results of this study highlight the heterogeneity of human body fat distribution across racial groups.This trial was registered at as NCT00959270.

The American Journal of Clinical Nutrition published a companion piece on this: Causes and consequences of human variation in visceral adiposity. In it, the author speculates on the causes of racial differences in adiposity:

Circulating concentrations of the antiinflammatory hormone adiponectin are lower and insulin concentrations are higher in African Americans than in whites, which may explain their paradoxically high diabetes risk, despite lower visceral adiposity. Similarly, Asian populations have higher diabetes risk at a lower waist circumference and body mass index (BMI) than do European populations, and lower screening cutoffs for consideration of treatment in Asian populations have been suggested and used (eg, reference 3). Following on the results presented by Katzmarzyk et al (2) and others, are different BMI and waist circumference cutoffs necessary for African Americans? Meta-analysis of abdominal imaging and disease incidence data from existing population-based epidemiologic cohorts of subjects of African ancestry, as was previously conducted for waist circumference (4), is a key next step to discern appropriate screening cutoffs and to evaluate their clinical utility.

Obesity has been hypothesized to have reached epidemic proportions due to the higher inclusive reproductive success of individuals who carry gene variants that predispose to the ability to rapidly store lipids in adipose tissue, which could reasonably buffer these individuals from starvation and loss of fecundity during periods of famine but which exceed needs in periods of plenty(5). The natural selection of varied adipose tissue deposition patterns in humans is more difficult to imagine, because it must invoke a population-variable benefit of allocating excess dietary energy to ectopic fat depots. An interesting hypothesis is that ethnic variation in adipose tissue patterning stems from adaptations to geographic variation in dominant endemic infectious diseases. The functional relation here is in the cross-talk between particular adipose tissue depots and the lymphatic system and specifically the local stimulation of adipocyte lipolysis to support lymphocyte proliferation near the site of infection, which varies by disease and by geographic region (6). Preferential ectopic adipose tissue growth and systemic inflammation may thus be the deleterious vestige of immunologic defense strategies shaped to particular disease landscapes.

Regardless of how the genetic control of visceral adiposity may have been shaped over evolutionary history, there is certainly evidence that such genes will be found, and that they may vary across populations. First, adipose tissue patterning is significantly heritable; additive genetic effects explain ≈40–60% of the variance in visceral and subcutaneous adipose tissue mass (7). Second, European genetic admixture in African American subjects is positively associated with BMI-adjusted waist circumference (8). Third, recent genome-wide association studies (thus far restricted to studies of anthropometric proxies such as waist circumference) in European or European American cohorts have identified a small set of genes that are preferentially associated with central adiposity (9, 10). These include TFAP2B, MSRA, and LYPLAL1, which are expressed in adipocytes and regulate glucose transport, and lipolysis, and NRXN3, which is expressed in the central nervous system. Studies are currently underway to determine whether allelic variations at these and/or other genetic loci have similar association with central adiposity in African Americans and whether or not they occur at similar frequencies. Significant work remains to identify the functional variant or variants at each locus (which may be easier in populations that exhibit lower average linkage disequilibrium, as in individuals with African ancestry) and to characterize how they may interact with sex, age, and behavioral factors. It is expected that common variants that predispose to elevated visceral adiposity will explain only a small proportion of the phenotypic variance, as observed for other common disease traits. Epigenetic modification of identified genes via dietary or other exposures that differ by race may result in differential gene expression levels that will explain additional variation in adipose tissue patterning.

Understanding why African American adults have lower visceral adiposity, on average, despite carrying a higher burden of risk factors that generally increase adiposity, is a fruitful avenue for transdisciplinary genetic and environmental research. Elucidation of the molecular origins of sex and age variation in ectopic fat deposition, which are equally unclear and of even greater magnitude, may reveal additional targets for diabetes and cardiovascular disease prevention.

Conclusion: the manner in which fat is deposited in the body, e.g. viscerally vs. subcutaneously, as well as the amount of fat deposited, is substantially heritable, varies between races, and that variation may be due to differences in infectious disease risk over time periods long enough for natural selection to act.


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