I n 1997, researchers presented a claim at the Experimental Biology meeting in New Orleans (a city known for food) that obesity could be caused in part by an infectious agent, adenovirus-36 (Ad-36). Nikhil Dhurandhar (then at Wayne State University, Detroit, Mich. and now at the Pennington Biomedical Research Center at Louisiana State University in Baton Rouge) and Richard Atkinson (Obetech, Richmond, Virg.) undertook to show that "this increase [in obesity] is the type of pattern that might occur with a new infectious disease, as has been seen with the AIDS virus" (Anon. "Virus May Be Linked to Obesity" 1997). Both were engaged in obesity research. Indeed, Atkinson was a founder of the American Obesity Association and an editor of the association's flagship journal. They speculated that Ad-36 makes animals fat by stimulating the growth and reproduction of adi-pocytes (fat cells), as well as by causing immature adi-pocytes to mature more quickly. Thus, they claimed that animals infected with Ad-36 may have as much as three times more fat cells than uninfected animals, as well as vastly decreased metabolisms.
In a subsequent paper, Dhurandhar noted that this may well solve the mystery of the rapid spread of obesity [which] has been called the number one public health problem in America. The etiology of obesity is considered to be multifactorial . . . While genetic and behavioral components of obesity have been the focus of intense study, an infection as an etiological factor has received little attention. Although "infectobesity," a new term to describe obesity of infectious origin, appears to be a new concept, over the past 20 years six different pathogens have been reported to cause obesity in animal models. The relative contribution of these pathogens to human obesity is unknown.
(Dhurandhar 2001: 2794S)
But, of course, no greater "magic bullet" can be imagined for human obesity than an antiviral agent that would simply "cure" obesity or even a vaccine that could prevent it. "In 10 years," Dhurandhar stated, people may be able to walk into a clinic and be told that their obesity is due to X cause, such as genes, the endocrine system, or pathogens. That may have a more productive outcome than a blanket treatment right now, [which] is not very successful. And because viruses are hard or impossible to treat, prevention through vaccines will be key.
These claims were based on decades of research. As early as the 1970s, Dhurandhar had observed that a chicken adenovirus, isolated in Bombay, caused chickens to accumulate as much as 50 percent more fat than healthy birds. The virus also lowered the animals' cholesterol and triglyceride levels before it killed them. "Normally, obesity in any species is associated with high levels of cholesterol and triglycerides," Dhurandhar noted (Neporent 2005). What interested him at that time though was the odd fact that infected chickens ate no more than uninfected ones. As a result, Dhurandhar and his colleagues identified the infectious agents as Ad-36. This agent was first isolated in humans in 1978 in the fecal matter of a seven-year-old diabetic girl.
Based upon the discovery of Ad-36, Dhurandhar began to theorize that it might be a contributing factor to the skyrocketing obesity epidemic in humans. He next looked for evidence of infection with the chicken virus in a group of fifty-two obese people. Ten showed signs of infection; therefore, it was an avian-spread virus that was postulated as the cause, a "bird-flu" model that might spread to human beings. This work led Steven Heyms-field of the Columbia University College of Physicians and Surgeons in New York City to observe, "Their work on obesity-related viruses has a strong experimental base in animal models and their descriptive epi-demiological data appears sound. Whether or not their hypothesis holds up in appropriately designed prospective human studies remains to be answered as far as I know" (Powledge 2004).
Commentators also responded immediately to the "possibility that obesity is a viral disease." Some argued that Ad-36 had serious social consequences as "it may give people ammunition to fight for insurance coverage for weight-loss treatment because they could argue: 'I've got a reason. I'm not just a fat slob' " (Marchione 1997). The moral claim that obesity was simply a public sign of the lack of will, one of the most powerful notions driving the moral panic about obesity, could be stilled by the very notion that its cause was beyond the individual (even beyond the individual's genetic makeup) and was to be found in the ever more dangerous world of infectious diseases. "The implications are enormous," said John Foreyt, a behavioral psychologist at Baylor College of Medicine. He called the research "startling" and "potentially a real breakthrough" in explaining the swift rise of the obesity epidemic (Marchione 1997). Twenty-six percent of American adults were obese in 1980, and more than 35 percent or more are now. It also could help explain the odd demographics of the "obesity epidemic" as it moved from the coasts and then toward the mid-section of the U.S.A. "People are still struggling with why this enormous increase in obesity" since "diet, sedentary lifestyles, genetic predispositions and metabolism problems don't explain the whole trend," Foreyt noted (Mar-chione 1997). If confirmed, these commentators argued, infectobesity would answer multiple problems and a drug that could combat it would be a worldwide blockbuster (Dobson 2004).
While clearly important, Dhurandhar's research was not the first attempt to define obesity as the symptom of an infectious disease. The noted Rockefeller University geneticist, Jules Hirsch, attempted to do so very early in his career. In a 1982 paper, he and his colleagues found "An obesity syndrome . . . in a number of mice infected as young adults with canine distemper virus, a morbillivirus antigenically related to measles" (Lyons et al. 1982: 82). These mice, according to Hirsch, had more and larger fat cells than their noninfected littermates. The researchers thought that the infections might well have altered brain pathways to encourage cell alteration and growth. No "natural" (genetic) process here but rather a response to a pathological agent (Lyons et al. 1982). This trajectory, however, was quickly abandoned for a "genetically" determined hypothesis for the existence of obesity.
Here is the perfect model to imagine how the fear that lies behind the very notion of infectious diseases can be used to focus and define a moral panic that may well have only a tangential relationship to the very notion of infection itself. What is remarkable about the notion of infectious diseases in the age of AIDS is that it couples the idea of the origin of disease in a distant foreign place with the fear of an uncontrolled spread answered almost simultaneously with the announcement of a cure, a quick fix or magic bullet. E.B.R. Desapriya warned "A 1% increase in the prevalence of obesity in such countries as India and China leads to 20 million additional cases" (Desapriya 2004). Imagine each of these cases being a potential source of infection for the West!
It is no accident that the assumption of global, evidence-based medicine is that such plagues—specific-ally those that deal with the transmission of disease from animals to human beings—originate in the East. "Bird 'flu" in the twentieth-first century has not crossed the "species barrier" any more than bubonic plague did, but bubonic plague had animals (rats and lice) as its vector. The relatively small number of cases of bird flu today seems to be the result of direct exposure to infected animals. Bird flu is being treated much like bubonic plague in that intimacy with animals is seen to be its cause (and more importantly) seen to pose a risk that the disease will cross the species barrier so that human beings could infect other humans without an animal vector.
The fascination with a viral cause for obesity also comes in the context of the SARS (severe acute respiratory syndrome) as well as other, more recent Asian avian influenzas of the past decade (McLean et al. 2005). The view that these diseases invade healthy spaces through an infectious process seems to be a commonplace. All of these claims about disease reflect the potential for mass death associated with an earlier disruption of the food chain: BSE (Bovine Spongiform Encephalopathy, "mad cow disease") which haunted Europe (and North America) when it entered the public's awareness in 1990 with the publication in European newspapers of the association between BSE and neurological diseases such as vCJD (Variant Creutzfeldt-Jakob disease) in human beings (Pennington 2003).
While the origin of BSE was originally not seen as the exotic reaches of the Orient or Africa, it quickly became the English disease on the continent or the Canadian disease in the U.S.A. BSE, caused evidently by the use of technology that ground animal offal (by-products) into animal feed, became the model for the notion that food kills—but only food that infiltrates from beyond our borders. Recently, the argument has been made that BSE originated in the consumption of animal feed made from bones and organic scraps imported for animal feed from Bangladesh, India, and Pakistan in the 1960s and 1970s. Rather than being an "indigenous" disease, having its source in the viral disease Scrapie among sheep in Europe, it spread from ingestion of diseased organic matter from the bodies of infected "Orientals" (Colchester and Colchester 2005). Or, as the authors of the recent study stated, that the route of infection was oral, through animal feed containing imported mammalian raw materials contaminated with human remains; and that the origin was the Indian subcontinent, from which large amounts of mammalian material were imported during the relevant time period. Human remains are known to be incorporated into meal made locally, and may still be entering exported material.
(Colchester and Colchester 2005: 856)
Cannibalism is always a significant charge in drawing the line between acceptable and unacceptable levels of civilization and health.
Does the anxiety about barriers to disease not lie at the heart of our desire that obesity, too, can be quickly fixed, once it is recognized as "merely" an infectious disease, rather than a reflex of national or personal character? The quick fix here is not to repair the food chain or end fast food, but to change the world so that such depression is eliminated. No quick fix is promised; why not hope for a vaccine against modernity, hopelessness, and fat? Simply because such quick fixes never truly eliminate the moral panic associated with this newest epidemic.
See also Aboulia; Genetics; Obesity Epidemic; Metabolism
References and Further Reading
Anon. "Virus May Be Linked to Obesity," University of Wisconsin-Madison News Service. Available online at <http://www.news.wisc.edu/4754> (accessed June 23, 2007).
Colchester, A.C. and Colchester, N.T. (2005) "The Origin of Bovine Spongiform Encephalopathy: The Human Prion Disease Hypothesis," The Lancet 366 (9488): 856-61. Desapriya, E.B.R. (2004) "Letter: Obesity Epidemic," Lancet 364 (9444): 1488.
Dobson, Roger (2004) " 'Fat War' Scramble to Develop Wonder Pill to Fight Obesity," Independent on Sunday (London), May 2.
Dhurandhar, Nikhil V. (2001) "Infectobesity: Obesity of Infectious Origin," Journal of Nutrition 131: 2794S-2797S.
Jones, Deborah (2005) "Vaccine May Target Obesity in the Future," Agence France Presse—English, October 18.
Kolata, Gina (2007) Rethinking Thin: The New Science of Weight Loss—and the Myths and Realities of Dieting, New York: Farrar, Straus and Giroux.
Lyons, M., Faust, J.I.M., Hemmes, R.B., Buskirk, D.R., Hirsch, J., and Zabriskie, J.B. (1982) "A Virally Induced Obesity Syndrome in Mice," Science 216 (454l): 82-5.
Marchione, Marilynn (1997) "Virus Is Linked to Weight Problems in Humans," Seattle Post-Intelligencer, April 8.
McLean, Angela, May, Robert M., Pattison, John, and Weiss, Robert A. (eds) (2005) SARS: A Case Study in Emerging Infections, Oxford: Oxford University Press.
Neporent, Liz (2005) "Can a Virus Make You Fat?" New York Daily News, November 2.
Pennington, T. Hugh (2003) When Food Kills: BSE, E. Coli, and Disaster Science, Oxford, New York: Oxford University Press.
Powledge, Tabitha M. (2004) "Is Obesity an Infectious Disease?" The Lancet Infectious Diseases 4 (10): 599.
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