This is the third of 6 guest posts on infectious causes of chronic disease.

By Whitney Baker

While working out at the gym last night, I was perusing the latest SHAPE magazine to help pass the time. In it, I read a small article about researchers finding an association between Adenovirus-36 and human obesity. Since I am in the infectious disease field, I was already aware of this proposed link- an infectious cause (or contributor) for obesity. But for the millions of health-conscious readers hearing of this for the first time, what would they make of it? Would they have visions of medicines or vaccines that make them skinny? Would they think that diet and exercise no longer matter? Luckily mainstream media hasn’t started a commotion over this. But it did get me to wondering, that if there really is a link, what accountability is then transferred to the media? Reports of a looming “skinny shot” could have a detrimental affect by spawning false impressions of health and fitness, especially for those most vulnerable to obesity.

(More after the jump…)

Quite a few peer-reviewed articles have addressed the issue of infectious obesity. Experts say that the obesity epidemic has an etiology epidemiologically analogous to an infectious origin because of its rapid spread worldwide. Obesity has increased significantly since the early 80s, and not just in the US, but in both developed and developing countries. And, to my surprise, not just Adenovirus-36 has been implicated as a culprit to America’s bulging waistline. A 2007 review paper by Richard Atkinson discussed 5 animal viruses (canine distemper virus, Rous-associated virus type 7, Borna disease virus, scrapie agent, and an avian adenovirus, SMAM-1) and 3 human viruses (adenovirus (Ad) 36, Ad-37, and Ad-5). Another 2007 review by Vasilakopoulou and Roux delineated these same pathogens in their review as well. All 8 of these viruses could be linked to the obesity epidemic. A 2007 seroepidemiological study by Thjodleifsson et al. studied individuals in Iceland, Sweden, and Estonia for IgG antibodies against Helicobacter pylori’s cagA protein, hepatitis A virus, Toxoplasma gondii, herpes simplex virus 1, Chlamydia pneumonia, Epstein-Barr virus, and cytomegalovirus. The researchers found a significant association between being overweight and being infected with H. pylori or C. pneumoniae, and a combined seropositivity of these two had a synergistic effect. Adenovirus-36 (which was not a target in the aforementioned seroprevalence study), was recently shown to play a role in adipocyte (fat cell) differentiation. Ad-36 can take adult stem cells and transfer them into fat cells (adipogenesis), thus contributing to the world’s expanding waistline.

So with that said, I suppose SHAPE magazine wasn’t too far out there in reporting on the story. Evidence seems to support an infectious component to obesity. But what about the weight-loss industry being such big hitters and people looking for the “quick fix” and falling for the latest fad diets or the miracle pill? The FDA estimates Americans spend an estimated $30 billion dollars on diet programs and products each year, and 50 million Americans will go on a diet this year. They’ll invest in anything that has a promise of a brighter– and skinnier– future. With so many gullible Americans out there, what are the consequences of informing people that they may be fat because of an infectious disease? I can see it now- late night infomercials selling medicine to cure the “disease”. You know, Kevin Trudeau, the infomercial guy who first came on the scene for something like real estate or making money fast, then all of a sudden lost a lot of weight and became an expert on natural cures for disease and even wrote several books. I can see him now… trying to tell Americans what the government doesn’t want them to know. Obesity is an infectious disease! And with this pill, it’s curable! Oh my…

But perhaps infomercials are at the far end of the spectrum and probably don’t even count as a media outlet. So imagine Fox News or CNN getting a hold of this story on a slow news day, and making consumers wonder when they can get vaccinated against the obesity bug. We all know the media is not known for providing ALL the facts; they go for the dramatic, captivating headlines. They’re not going to say there “may” be a link and an infectious agent “may” be a contributory factor to gaining weight. They’re not going to highlight that there is still a strong behavioral component to obesity, and most likely diet and exercise are the best ways to be healthy and to slim down. No, they’ll go for the attention grabber. And in return, a number of people (those who donate to the weight-loss industry in particular) might have visions of “cure me” rather than taking personal responsibility for where they are at and how they got there.

With the available data, it seems like an infectious agent does contribute to obesity. It is an attractive concept, as many chronic diseases have squashed long-standing opinions and are now recognized to have infectious etiologies (e.g. H. pylori and peptic ulcers, the human papillomavirus and cervical cancer, and the hepatitis B virus and liver cancer). More and more, pathogens are being implicated, so it doesn’t seem like a stretch to make a link to obesity. But for as long as the culprit remains unidentified and the model of pathogenesis a mystery, the theory of an infectious cause to the obesity epidemic should remain in the scientific field. Consumers are too eager, too desperate, and too amateur. The media should take care to not flaunt the idea of a “skinny shot”. Because even if you get rid of the fat cell-generating Ad-36, being a couch potato and having a Big Mac, large fries, and a shake every day is going to do way more damage to your health (and to your waistline) in the long run.

Whitney has been interested in infectious diseases since the 8th grade. She has a Bachelor’s in microbiology and a Master’s in Public Health in epidemiology. Two years after landing a university job in infectious disease epidemiology research, she began working toward a PhD in epi. Whitney’s focus area is emerging zoonotic diseases- in particular, the epi of cross-species pathogen transmission from animals to humans- but she has no idea what she’ll do when she’s no longer in school.

Works cited

Atkinson RL. Viruses as an etiology of obesity. Mayo Clinic proceedings 2007;82(10):1192-8. PubMed link.

Vasilakopoulou A, le Roux CW. Could a virus contribute to weight gain? Int J Obes (Lond) 2007;31(9):1350-6. Link.

Thjodleifsson B, Olafsson I, Gislason D, Gislason T, Jogi R, Janson C. Infections and obesity: A multinational epidemiological study. Scand J Infect Dis 2007:1-6. Link.

Pasarica M, Mashtalir N, McAllister EJ, et al. Adipogenic Human Adenovirus Ad-36 Induces Commitment, Differentiation and Lipid Accumulation in Human Adipose-derived Stem Cells. Stem Cells. 2008. Link.

Rogers PM, Fusinski KA, Rathod MA, et al. Human adenovirus Ad-36 induces adipogenesis via its E4 orf-1 gene. Int J Obes (Lond) 2007. Link.

Image from http://metabolism.com/images/dreamstime_1868442obese.jpg

Comments

  1. #1 Jacoby
    February 26, 2008

    Huh. So is it known how the other microbes besides adenovirus might cause or influence weight gain?

  2. #2 Brian
    February 26, 2008

    I really think that in this day and age of “super obese” people are still looking for any possible excuse they can for their weight other than placing the blame on themselves. News media knows this and they cash in on it by sensationalizing headlines and results. Although research like this is needed, it begs to questions the motivations of the researchers involved. Are they too trying to cash in on the epidemic by placing importance and grant money on a causative mechanism that is an insignificant fraction of the greater reason for obesity?

  3. #3 Lodger
    February 26, 2008

    Are they too trying to cash in on the epidemic by placing importance and grant money on a causative mechanism that is an insignificant fraction of the greater reason for obesity?

    But do we know it’s insignificant? Diet and exercise aren’t everything, and it’s beyond hard to get people to change their lifestyle. If there was a “skinny shot” that could at least contribute to lessening the obesity epidemic, wouldn’t that be worth the research money?

  4. #4 Brian
    February 26, 2008

    I challenge you to find someone who counts calories (for real) and exercises for 30 minutes 5 days a week that is even marginally obese. The simple fact is that to become fat you bring in more than you burn off. A viral protein may tip the balance against you slightly, but I can’t believe it’s a major or significant causative agent for the obesity epidemic.

    I think the money could be better spent in education courses that both inform people on the dangers of overeating, and physically show them how to reverse those effects. Don’t give people yet another excuse to sit on the couch and wait for scientists to produce a quick fix for their laziness and lack of will power.

  5. #5 Lodger
    February 26, 2008

    I challenge you to find someone who counts calories (for real) and exercises for 30 minutes 5 days a week that is even marginally obese. The simple fact is that to become fat you bring in more than you burn off. A viral protein may tip the balance against you slightly, but I can’t believe it’s a major or significant causative agent for the obesity epidemic.

    “For real”–no true scotsman? My wife counts calories “for real.” She’s been on every diet known to man (now she’s not any special diet, just tries to eat healthy and in moderation), swims regularly, and still is considered “obese” by physicians’ standards. She’s not alone either. Many overweight people count calories and exercise regularly–it’s not only “calories out > calories in,” but also about efficiently your body uses those calories. Conceivably, this is where things like viruses come in.

    I think the money could be better spent in education courses that both inform people on the dangers of overeating, and physically show them how to reverse those effects. Don’t give people yet another excuse to sit on the couch and wait for scientists to produce a quick fix for their laziness and lack of will power.

    The problem is that many people are well aware of these dangers and how to reverse them–yet either they don’t care (which you’re not going to change with all the education in the world), or they’ve done what they can and they’re still overweight. You’re simplifying a problem (and a solution; who’s suggesting anyone just “sit on the couch?”) that I think is much more multifactorial than just “eat less, move more.”

  6. #6 wright
    February 26, 2008

    Very interesting, Whitney. You have a very clear, engaging style of writing; I encourage you to pursue that skill. Perhaps a career as a science writer and popularizer? We literally cannot have too many like you…

  7. #7 Whitney Baker
    February 26, 2008

    Dear Jacoby:

    In looking at the Atkinson review, out of the 5 animal viruses, only one has been linked to human obesity.

    The first 4 have only shown to influence obesity in animal models. Canine distemper virus, Rous-associated virus type 7, BDV, and scrapie agent attack the central nervous system and damage the hypothalamus, which is believed to cause obesity (see articles C Baylis et al. Hypertension, 1996 and AF Debons et al. Endocrinology, 1982, or this report by Dr Jonathan Pinkney of the Bristol Royal Infirmary (http://www.pituitary.org.uk/content/view/166/122/), suggesting that “the urge to eat is so powerful it is difficult to resist, and can be greatly increased in the presence of pituitary and hypothalamic disease”). Canine distemper virus damaged the CNS in mice; Rous-associated virus type 7 damaged the CNS in chickens and produced hypothyroidism; and BVD in rats showed to damage the CNS. Scrapies was a little less believable, but one researcher did show a link to obesity for one the ME-7 strain ME-7 in mice.

    As for the one animal virus (SMAM-1) studied in humans, unlike the aforementioned CNS-damaging pathgens, SMAM-1 plays more of a role in adipogenesis. It was shown to increase body fat in chickens- but not affect lean body mass- “suggesting that fat was preferentially stored, even at the expense of lean body mass”. (Atkinson)

    SMAM-1 in humans: Straight from Dhurandhar NV et al.’s Obes Res, 1997 abstract… The researchers “screened the serum of 52 humans with obesity in Bombay, India, for antibodies against SMAM-1 virus using the agar gel precipitation test (AGPT) method. Bodyweights and serum cholesterol and triglyceride levels were compared in SMAM-1-positive (P-AGPT) and SMAM-1-negative (N-AGPT) groups. Ten subjects were positive for antibodies to SMAM-1, and 42 subjects did not have antibodies. The P-AGPT group had a significantly higher bodyweight (p < 0.02) and body mass index (p < 0.001) compared with the N-AGPT group. Also, the P-AGPT group had significantly lower serum cholesterol (p < 0.02) and triglyceride (p < 0.001) values compared with the N-AGPT group.” These researchers therefore deduced that “the presence of increased obesity, antibodies to SMAM-1, reduced levels of blood lipids, and viremia that produces a typical infection in chicken embryos suggests that SMAM-1, or a serologically similar human virus, may be involved in the cause of obesity in some humans.”

    The human adenoviruses seem to affect adipogenesis, similar to the avian adenovirus. So it goes to show that many theories are out there. Time and research will only tell which, if any, are true.

  8. #8 MEC
    February 26, 2008

    I guess a good question to start with is what were all these obesity viruses doing before 1980?

  9. #9 Brian
    February 26, 2008

    “For real”–no true scotsman? My wife counts calories “for real.” She’s been on every diet known to man (now she’s not any special diet, just tries to eat healthy and in moderation), swims regularly, and still is considered “obese” by physicians’ standards. She’s not alone either. Many overweight people count calories and exercise regularly–it’s not only “calories out > calories in,” but also about efficiently your body uses those calories. Conceivably, this is where things like viruses come in.

    Not to step on any toes, but I think in a lot of cases perception and reality aren’t the same thing. I come from a family “afflicted” with obesity. I say afflicted because the only thing afflicting my family was a lack of will power, secret eating and constant snacking.

    Now, I’m not saying your case is the same Jacoby, but I don’t believe that viruses or genes (aside from having a thyroid imbalance or Prader-Willi…) PREVENT you from losing weight, they will just make things a little more inefficient which means you have to work harder. The solution IS as simple as cutting calories and exercising. The complicated part is getting past all of the emotional garbage that stands in the way of that. One of which is “I don’t care,” which really just means, “I’m in denial” and its easier to say that than actually do something about it.

    Seriously, just watch a season of Biggest Loser and tell me that hard work an eating right gets you nowhere.

  10. #10 Dunbar
    February 26, 2008

    I find the solution to obesity, namely controlling diet and exercise, to be often delivered in a sanctimonious and repugnant way. It is true, however, that people do have to take responsibility at some level for whatever medical condition, be it obesity or say taking ARV drugs for AIDS. On the other hand, it is overly reductionist to tell an obese person to stop “eating burgers and drinking milkshakes.” Obesity, like many other medical diseases, is multi-factorial in etiology. Some people, like native Hawaiians, have genetic predispositions to obesity in context of a Western diet. Some people do not have the social networks to help them treat their obesity. Some people are genuinely addicted to food, and it’s odd to treat it differently from any other addition. As someone else pointed out, many do not have the education on obesity to begin to approach it. There are countless factors. One should not have such a smarmy attitude to obesity, any more than to poverty, or other stuff I’m too irritated to think of right now.

  11. #11 Fleming
    February 26, 2008

    Man, I thought I’ve seen it all. Newsflash — if you are fat, I suggest 2 things: Stop eating more than your fair share of food and start walking a few miles a day.

    It may not solve the problem, but it will damn well help.

  12. #12 Dunbar
    February 27, 2008

    I’m not saying controlling one’s diet or exercise is ineffective; rather, I agree that they are the main mechanisms to treat obesity. I’m railing against attitudes which treat obesity, or many other medical conditions for that matter, as a problem with a facile solution without other considerations. Obesity is a disease, not just a personal problem like a break-up. While this blog post cautions against over-expectations for a miracle cure for obesity, it somehow didn’t caution the same for the sanctimonious solutions I described.

    As a final thought, no one would counsel a homeless person to stop being lazy and get a job to get off the streets, no?

  13. #13 Stagyar zil Doggo
    March 2, 2008

    Whitney,
    Thank you for an interesting post. I would appreciate clarification on a couple of points though.

    1. You say

    A 2007 review paper by Richard Atkinson discussed 5 animal viruses (…, scrapie agent …

    My understanding is that Scrapie is a disease in sheep and is caused by an infectious Prion Protein, not a virus. It is also currently not considered transmissible to humans. Could you please clarify? Also if you’re looking at the prospect of Spongiform Encephalopathy, you’re probably not going to worry too much about a little adiposity. :)

    2. Regarding the idea that infectious agents cause (or at least contribute to) obesity, an alternative explanation could be that obesity/hyperlipidemia/etc. cause immune deficiencies which increase the likelihood of secondary infections. How far along are we towards meeting Koch’s postulates in establishing this infectious hypothesis? Are there any animal RCTs supporting this proposed aetiology, for example?

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