It is important to understand the role that stigma plays in producing disease amongst overweight and obese persons for many reasons. Foremost, the assumptions surrounding the pathophysiology of overweight and obesity could be partially incorrect. Second, if stigma-induced stress plays a role in the pathophysiology of obesity, it suggests that social constructs of idealized body image can have harmful health effects. If so, it raises pragmatic questions surrounding the net health benefits of public health communications campaigns, which often promote thinness. Finally, overweight and obesity are associated with over 7 million QALYs annually in the U.S., potentially making it one of the major causes of death.[2
Nonetheless, the evidence I appraise here is far from conclusive. First, there is evidence that fatty tissue does have metabolic function. This is true not only of steroid production and function,[47
] but may also be true of cytokine production. [4
] Further work in this area will help clarify the relationship between immune tissue and fatty tissue in the production of pro-inflammatory and pro-thrombotic mediators.
Complementary hypotheses also exist. For instance, there is strong evidence that stress increases the risk of central obesity.[49
] Thus, there is not only room for confounding in some of the data I discuss, but the findings are partially explained by reverse causality. As discussed above, reverse causality can only play a limited role, since dieting can reverse the metabolic effects of obesity.[17
] However, neither hypothesis explains why a discrepancy between one's perceived ideal weight and his or her actual weight is a stronger predictor of morbidity than BMI.[38
] Nor do they explain why differences in body image norms among different racial and ethnic groups appear to be strong predictors of obesity-related mortality.
There are other reasons why the obesity-induced stigma hypothesis cannot explain all of the association between obesity and morbidity. For instance, there is evidence that adiposity is independently linked to some obesity-related illnesses.[67
] In particular, there is a link between internal obesity, which is less visible, and the metabolic syndrome in Asians.[68
] This suggests that genes, developmental environment, or reverse causality play a role in this group. Moreover, genetic makeup in general might simultaneously affect one's propensity to gain weight as well as his or her physiologic response to being overweight.[69
] Nevertheless, the obesity-related stigma hypothesis is logical and complements, rather than refutes, the adiposity hypothesis.
There are certainly conditions and illnesses that can be clearly attributed to obesity. One of these is sleep apnea, which has also been linked to metabolic disruptions.[70
] Sleep deprivation has also been linked to excess stress mediator production in high stress populations, such as persons of low socioeconomic status. This highlights the many psychophysiological pathways at work in producing obesity-associated morbidity.
One final concern is that a wide array of other complex psychosocial factors contributes to obesity-associated morbidity and mortality, and it is difficult to tease them apart. For instance, stress can reduce cognitive function via damage to the hippocampus (a region of the brain important in memory), potentially contributing to heavy persons' lower educational attainment.[71
] Lower educational attainment, in turn, may explain some of the health and longevity effects of obesity. Likewise, stress can play a role in obese persons' higher incidence of smoking. Like stress, smoking is associated with dyslipidemia, atherosclerosis, and elevated CRP levels.
In developing nations where food is scarce, obesity might be seen as a proxy measure for affluence (and thus dominance in social hierarchies). As nations industrialize, however, cheap, calorie-dense food becomes plentiful and leisure time becomes scarce. Thus, thinness replaces plumpness as a proxy measure for affluence. By looking at case studies such as Mauritania, which still values plumpness, we should be able to observe an increase in obesity-associated pathophysiology that is coincident with shifts in depictions of beauty in the media.
If shifts in depictions of beauty in the media are partially to blame for the health effects of obesity, public health officials may have unwittingly exacerbated the problem by promoting thinness. This paper's hypothesis thus speaks to larger examinations of public health policy, and health communications campaigns. If the obesity epidemic is partially attributable to social constructs surrounding ideal body types, there is a need for new research and policy paradigms that emphasize fitness and healthy eating habits[73
] alongside social acceptance of heavier members of society.