By Jacqui Cotton
The obesity epidemic has been framed and reframed by clinicians, policymakers, and the public: a disease of individual poor eating habits, a consequence of upbringing and family lifestyle, an addiction to food, a medicalized health condition. However, these perspectives ignore the salient impact of that which is external to the individual—the food environment. I believe the obesogenic food environment, is the most compelling reason for the massive increase in the rates of obesity in adults and particularly children in the past 30 years. A publication from the Harvard School of Public Health describes the food environment as lurking silently, and often unnoticed, in the background—“it plays a major role in the food choices people make, even for the most independent-minded consumer.”
I argue that the food environment can be conceptualized as a fundamental cause. It is part of the “social condition that provides access to resources” and it can prevent or promote negative health consequences. The USDA sites the following factors that interact and create the food environment: store/restaurant proximity, food prices, food and nutrition assistance programs, and community characteristics. These factors contribute to an individual’s or a community’s external social condition, access to resources, and subsequently health. The idea has been promoted in other literature, notably in Kelly D. Brownell’s book Food Fight: The Inside Story of the Food Industry, in which the term “toxic food environment” was coined. Brownell, too, believes that the root of obesity lies in the environment, specifically the social and cultural influences that contribute to over-eating and an over-abundance of food.
The food environment also meets the theoretical criteria of a fundamental cause as promoted by Link & Phelan. First, it can influence multiple disease outcomes, for example cardiovascular disease and diabetes, and potentially psychological conditions. Second, the environment affects disease outcomes through multiple risk factors, for example consumption of high-fat, high-sugar foods and beverages, lack of access to fruits and vegetables, and landscape non-conducive to physical activity. Third, the food environment inherently involves access to resources which may help mitigate consequences of disease, or in the case of the toxic food environment, promote the disease condition. Lastly, the link between the food environment and obesity is reproduced over time despite numerous interventions such as personal diets, exercise regimens, prevention and education programs, and point-of-sale calorie counts, to name a few. Despite modifications to the causal pathway, this fundamental relationship between the food environment and obesity persists.
Although their position focuses on the link between SES and health, Fresse & Lutfey discuss several other metamechanisms that can contribute to what they refer to as an enduring narrative of the roots of health patterns, regardless of time and space. First, they discuss the notion of habitus, as described by Bourdieu, and synthesized by Cockerham as “a cognitive map or set of perceptions that routinely guides and evaluates a person’s choices and options.” In fact, eating has been categorized as an “automatic behavior” by Cohen & Farley, and it falls squarely within the habitus framework: it is quite routine, our choices are usually habitual, and our options are relatively standard within our typical environments. It is very easy—even mindless—
to over-eat or to make poor dietary choices, but the process of resisting food or consciously making healthier decisions is indeed very challenging and a more difficult behavior to maintain. Accordingly, the idea of habitus follows that while it is possible to modify one’s patterns, it is often a difficult and very deliberate process requiring purposive action in spite of external forces. Cockerham further conceptualizes habitus as the interplay between one’s agency and structure, and in this case, a diet that causes obesity is at the intersection of individual food choices which are both limited and reinforced by an obesogenic food environment. Thus, while an individual’s dietary autonomy clearly plays a role as a proximate cause of obesity, I would argue that the fundamental cause, upstream of one’s agency, is the toxic food environment.
Another metamechanism discussed is spillover within social networks, which connect individuals and have the power to impact their health in attitudinal or actionable ways. In the case of the food environment, this mechanism is extremely apt, because individuals in close social proximity to each other are likely to interact with and navigate their environment in similar ways. Families and neighbors are embedded in the same food environments and thus spillover effects (whether positive or negative) are likely to occur. For example, if the food environment includes access to a local farmers’ market, and most neighbors on the block frequent it, this behavior is likely to confer, or spill over, to other families and individuals in the area.
The last metamechanism described is institutional agency, and how the dynamic actions of institutions can play a role in health pathways. In relation to the food environment, I see the food industry as a major institutional player in individual health outcomes. Food advertising and marketing, packaging and labeling, and geographic distribution of food vendors play a crucial role is shaping food environments and thus affect how individuals can and do eat, which ultimately impacts their waistlines and health. There are boundless criticisms of the pervasive, highly influential nature of the food industry and how it strategically impacts individual’s purchasing, consumption, and health patterns. These mechanisms combine to propagate the toxic food environment which fundamentally leads to obesity.