Neoliberal societies often put the onus of blame on the individual. It’s the individual’s fault they have diabetes, cardiovascular disease, obesity, and hypertension. Their diets are too high in the “bad fats”, they contain too much sugar, and too much grease. It’s their fault they’re obese and diabetic and have heart problems, right?

Well, in short – no.   A group of articles I’ve recently read emphasized the role of structural inequities in the prevalence of metabolic syndromes and chronic diseases (i.e. cardiovascular disease and diabetes) among marginalized populations and populations affected by imperialism (Kuzawa and Quinn 2009; Wells 2010). They demonstrated that structural inequities have profoundly impacted the health statuses of racialized groups through several generations, casting these groups in the “metabolic ghetto” (Wells 2010). Moreover, they all studied how one’s fetal environment could predict the health outcome of the resulting adult, arguing that an infant’s birth weight, as a proxy of the fetal environment, alongside a mother’s nutritional health could provide insight into whether the infant will experience a myriad of adult chronic diseases. However, while these racialized and marginalized groups fancy an exit from a lifetime of chronic disease and the management that comes with it, they are warned that too rapid an exit from the metabolic ghetto could lead to further health problems. So, where does that leave them? Are there missing pieces to the puzzle? Are birth weight and the mother’s nutritional status and overall maternal capital the only variables pertinent to predicting an infant’s susceptibility to adult chronic diseases?

Matthew Gillman, a physician and Professor and Director of the Obesity Prevention Program in the Department of Population Medicine at Harvard’s Pilgrim Health Care Institute, argues that there are several epidemiological challenges in studying the fetal origins of adult chronic disease. He maintains that while fetal life is an important “bottleneck” of development, it’s certainly not the only pertinent one in determining the susceptibility to adult chronic disease (Gillman 2002:294). Alternatively, he suggests that studies would benefit from having multiple measures of height and weight through the individual’s lifecourse, to distinguish prenatal influences from influences occurring at various points in infancy, childhood, and later (Gillman 2002:295). Gillman also argues that fetal growth and size at birth are not synonymous, as fetal size at birth is only a snapshot of the trajectory of fetal growth throughout gestation (2002:296). He maintains, “To what extent gestational age predicts adult outcomes is an unresolved question, but an important one. In general, determinants of preterm birth and fetal growth are not the same” (Gillman 2002:296). Finally, Gillman maintains that, “to make policy recommendations now regarding fetal programming is dangerous” (2002:298). He argues that as developing countries undergoing epidemiological transition from infectious disease to chronic disease, successive generations of individuals are likely to have even larger proportions of cardiovascular disease, type 2 diabetes, obesity, and hypertension. Moreover, this is heightened through the ‘nutrition’ transition from an active, low-calorie lifestyle to a sedentary, high-calorie lifestyle; thus, Gillman argues that it is premature to make policy recommendations regarding fetal programming, since birth weight is only a  marker for underlying aetiological or causal pathways, the true aetiological factors are still unknown (2002:298). Until they are identified, it is impossible to calculate the attributable risks or design interventions to modify them (Gillman 2002:298).

So, while Wells suggests that public health initiatives should target “multiple interventions through the transducing medium of maternal capital” (2010:13), Gillman maintains that these initiatives should “hold off” until the link between fetal origins and adult chronic diseases is more clearly understood – understandably so. Meanwhile, the biomedical paradigm of prevention is well underway, telling individuals to be #motivated, by encouraging them to #eatclean, #traindirty, #pushthepace, and #dominate. Unfortunately, not everyone necessarily has the means to do this – specifically, those marginalized populations. For those individuals in today’s neoliberal society looking to manage their diabetes, control their weight, or control their cholesterol to be a “good” and “healthy” citizen, eating “clean” and healthy comes with a price, whereas McDonald’s adds new items to their value meals and mails out coupons once a month. Moreover, these individuals are told that their lifestyles contributed to their chronic diseases; which, may be true. However, larger structural inequalities causing intergenerational health inequities may be the real aetiological pathways of adult chronic disease. It’s a classic case of what Arthur Kleinman calls, “social suffering” – if we find a treatment for society, we find a treatment for inequalities.