November 28, 2012
Beyond Counting Calories
Taking the Obesity Fight to Environmental Toxins, Stress, and Capitalism
The prevailing obesity discourse has obscured alternative explanations, from environmental toxins to chronic stress, and failed to address the broader influence of capitalism, which has deeply shaped our neighborhoods, habits, and health.
In many respects, the problem of obesity has been defined in relation to socially acceptable solutions, particularly in efforts to get people to eat more fresh fruits and vegetables, whether through health education, snack taxes, or the creation of farmers’ markets in so-called food deserts. The food movement thus found in the “obesity epidemic” a problem to which it could be a solution. This is not to disparage fresh fruits and vegetables; it is to note that the solution in some sense wags the dog of the problem statement, for it assumes that obesity is caused by a lack of fruit and vegetable consumption.
In this sense, Helen Lee has laid out a set of arguments in “The Making of the Obesity Epidemic” that are very close to my own. Yet existing assumptions about obesity’s causes and consequences have not only enabled a certain kind of activism. They have also foreclosed other ways of thinking about obesity as a problem. This is evident in the current emphasis on stopping and reversing the upward trend in obesity rates rather than investigating the ways in which bigger bodies affect biological functionality. The possibility that fat is not necessarily pathological and may even be adaptive, for example, is entirely absent from the public conversation. As a result, the prevailing discourse has obscured other possible causes for obesity, from environmental toxins to chronic stress, and failed to address the broader influence of capitalism, which has deeply shaped our neighborhoods, habits, and health.
Lee is right to criticize the food desert, or “obesogenic environment,” thesis. As I detail in Weighing In: Obesity, Food Justice, and the Limits of Capitalism, studies that attempt to show relationships between neighborhood environments and obesity have been inconclusive, inconsistent, and presumptuous about the causes of obesity. They have also tended to ignore the salient roles of race and class in creating food deserts, such that many of the frowned-upon neighborhoods are so because residents lack income or “social capital” to draw high-end supermarkets to the neighborhood.
Of course, so-called food deserts exist also because of past rounds of racist redlining and disinvestment. Even more suburban obesogenic environments, loaded with strip malls and short of high end “market halls,” reflect the buying power of those who inhabit them. Here I would add that the very concept of the obesogenic environment reveals unstated preferences for places with the amenities often associated with urbane, privileged environments, including university towns, artsy enclaves, gentrified urban cores, and even older well-heeled suburbs. Evidently, thin real estate is expensive.
My critique of the obesity conversation is even more fundamental. I call into question the commonly held belief that obesity results from an excess of calories taken in relative to those expended. Aside from a growing body of research that questions the calorie as an indicator of food’s weight-producing qualities — the calorie, after all, is a measure derived from literally burning food and does not exist as a constituent molecule of any food — a significant array of emerging research on the biological etiology of obesity at least complicates this energy balance model and potentially topples it as the primary factor determining weight status.
For instance, disruption in sleep patterns is associated with increased body fat and altered metabolism.1 Within nutrition science, there is increased recognition that the timing and pattern of food intake affects weight gain and loss, with earlier diurnal eating leading to faster metabolism.2 Researchers also posit that chronic stress plays a role in obesity through constant release of the hormone cortisol.3 Work in epigenetics — a relatively new field that considers the role of psychosocial and nutritional stress on gene expression — has shown transgenerational effects on phenotype, including weight status.4-6 Some in this field have thus theorized that long term exposures to stress and past nutritional deprivations could help explain the relationship between low socioeconomic status and obesity prevalence that many assume is a consequence of the current day dietary habits of the relatively poor.7
Perhaps most significant is research that points to the role of environmental toxins in contributing to the rise in obesity. Crucially, this research points to biological pathways to obesity that are almost entirely independent of calories (as opposed to pathways that affect mechanisms of internal regulation and thus interact with caloric metabolism).8,9 The most paradigm-shifting research is about the role of endocrine-disrupting chemicals. Both animal and lab experiments have found that maternal exposure to a range of chemicals can alter genetic pathways for fetuses in ways that generate adult obesity.
For instance, both low and high doses of synthetic estrogens given to mice during gestation and immediately following birth have resulted in significantly higher body weight at adulthood than that of genetically identical control groups fed the same diet. Demonstrating an epigenetic effect, this research has found that the genes that direct fat distribution are permanently altered by the exposure such that the tendency toward high fat tissue would be passed onto offspring were the mice to reproduce.10 Other studies have found that certain chemicals stimulate the growth of already existing fat cells as well as the development of fat cells from stem cells — those with undefined destination.11,12
The epidemiological data, while thus far inconclusive, has provided some empirical support for how these mechanisms might affect humans.13 Scientists in North Carolina found that children exposed to higher levels of PCBs and DDE before birth had higher body mass indexes than those exposed to lower levels.14 The thus far unexplained surge in obesity rates since 1980 to which Lee refers may well owe to the massive exposures to environmental toxins in the 1950s and 60s that in light of these epigenetic qualities did not manifest visibly until the 1980s.
While research on environmental toxins, epigenetics and obesity is still relatively new, as put by two leading scientists in this research, “the existence of chemical obesogens in and of themselves suggests that the prevailing paradigm, which holds that diet and decreased physical activity alone are the causative triggers for the burgeoning epidemic of obesity, should be reassessed."11 There are, in other words, other possible explanations for the rise of obesity and for variations in obesity as related to socioeconomic status that in the rush to point fingers at fast food diets have been overlooked.
Then there is the question of the role of neoliberal capitalism in all of this — a question that Lee does not broach. And yet it is one that deserves consideration. Many of the features associated with the obesogenic built environment can be traced back to policies that aimed to reduce the role of government under the auspices of encouraging investment and restoring profitablity. Tax rollbacks certainly helped build much of what is associated with the foodscapes of fast food/national chain strips, box store malls, and even food deserts. Specifically, localities starved for tax revenue encouraged such retail development to generate sales tax revenue, with California’s Proposition 13 that rolled back property taxes to 1976 assessments being the example par excellence.15 What Lee rightfully calls “money deserts’’ (rather than food deserts) is largely attributable to the reduction or curtailment of job training, welfare, and other poverty alleviation programs since 1980.
The continued use of obesogenic environmental toxins can also be traced to these neoliberal policies. Beginning with President Reagan, a key objective of the Republican Party and, sadly, some of the Democratic Party, was to remove or disable regulations seen as unfriendly to business. Accordingly, the Environmental Protection Agency slowed down and in some cases stopped review of potentially toxic chemicals (not to mention endocrine disrupters). Agency mandates turned to nonenforcement of existing prohibitions. The Food and Drug Administration became an utter patsy in preventing food substances of questionable safety and necessity from being put on the market. It is not at all clear that such policies delivered on the promise of jobs, either.
As much as fast food and big box chain stores have been growth industries in American capitalism — both of which have putatively gotten people to eat more — let us not forget that the rhetoric of obesity, and its tendency to dignify obsessions that equate thinness and beauty, is also hugely profitable. It has proved a boom for a $100 billion dollar per year weight-loss industry (by some estimates) that distributes specialized products and services, alongside the money made on bariatric and cosmetic surgery. Jenny Craig and Weight Watcher’s frozen dinners, the thousands of diet books, and pay-as-you-go group weight-loss therapy all demonstrate that diets can be sold and bought, and that weight loss itself is a commodity.16-18 For that matter, the pharmaceutical industry has much to gain by hyping up an obesity epidemic, and, in fact, the research-oriented International Obesity Task Force receives much of its funding from the pharmaceutical industry which pins its hopes on finding a magic bullet to “cure” obesity.19
What we have, in effect, is a political economy of bulimia. Unfettered capitalism has generated many of the food qualities, built environments, and chemical exposures associated with obesogenesis. At the same time, it has made available for investment and marketing many, but by no means all manner of solutions to problems it has generated. As such, the body has become a site where capitalism’s inherent growth problems are literally embodied — at a significant cost to our psyches as much as our health.
Julie Guthman is Professor of Social Sciences at the University of California, Santa Cruz, and author of Weighing In: Obesity, Food Justice, and the Limits of Capitalism.
Photo Credit: Mother Nature Network (right); Callie Richmond/Pegasus News (left)
1. Bray MS, Young ME. Circadian rhythms in the development of obesity: potential role for the circadian clock within the adipocyte. Obesity Reviews. 2007;8(2):169-181.
2. Arble DM, Bass J, Laposky AD, Vitaterna MH, Turek FW. Circadian Timing of Food Intake Contributes to Weight Gain. Obesity. 2009;17(11):2100-2102.
3. Björntorp P. Do stress reactions cause abdominal obesity and comorbidities? Obesity Reviews. 2001;2(2):73-86.
4. Dolinoy DC, Jirtle RL. Environmental epigenomics in human health and disease. Environmental and Molecular Mutagenesis. 2008;49(1):4-8.
5. Faulk C, Dolinoy DC. Timing is everything: the when and how of environmentally induced changes in the epigenome of animals. Epigenetics. 2011;6(7):791-797.
6. Kuzawa CW, Sweet E. Epigenetics and the embodiment of race: Developmental origins of US racial disparities in cardiovascular health. American Journal of Human Biology. 2009;21(1):2-15.
7. Thayer Z, Kuzawa C. Biological memories of past environments: epigenetic pathways to health disparities. Epigenetics. 2011;6(7):798-803.
8. Baillie-Hamilton P. Chemical Toxins: A Hypothesis to Explain the Global Obesity Epidemic. Journal of Alternative and Complementary Medicine. 2002;8(2):185-192.
9. Grun F, Blumberg B. Minireview: The Case for Obesogens. Molecular Endocrinology. August 1, 2009 2009;23(8):1127-1134.
10. Newbold RR, Elizabeth P-B, Wendy NJ, Jerrold JH. Effects of endocrine disruptors on obesity. International Journal of Andrology. 2008;31(2):201-208.
11. Grun F, Blumberg B. Environmental Obesogens: Organotins and Endocrine Disruption via Nuclear Receptor Signaling. Endocrinology. June 1, 2006 2006;147(6):s50-55.
12. Masuno H, Kidani T, Sekiya K, et al. Bisphenol A in combination with insulin can accelerate the conversion of 3T3-L1 fibroblasts to adipocytes. Journal of Lipid Research. May 1, 2002 2002;43(5):676-684.
13. Hatch EE, Nelson JW, Stahlhut RW, Webster TF. Association of endocrine disruptors and obesity: perspectives from epidemiological studies. International Journal of Andrology. 2010;33(2):324-332.
14. Gladen BC, Bagan NB, Rogan WJ. Pubertal growth and development and prenatal and lactational exposure to polychlorinated biphenyls and dichlorodiphenyl dichloroethene. The Journal of Pediatrics. 2000;136(4):490-496.
15. Schrag P. Paradise Lost: California's Experience, America's Future. Berkeley: University of California Press; 1998.
16. Austin SB. Commodity Knowledge in Consumer Culture: the Role of Nutritional Health Promotion in the Making of the Diet Industry. In: Sobal J, Maurer D, eds. Weighty Issues: Fatness and Thinness as Social Problems. New York: Aldine De Gruyer; 1999:159-181.
17. Fraser L. Losing It: False Hopes and Fat Profits in the Diet Industry. New York: Penguin; 1998.
18. Fine B. The Political Economy of Diet, Health and Food Policy. London: Routledge; 1998.
19. Oliver JE. Fat Politics: The Real Story Behind America's Obesity Epidemic. New York: Oxford University; 2006.