Infectobesity Adenovirus 36 and Childhood Obesity

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Virus in Chicken Could Be Linked to Obesity

Recently, there has been research examining the connection between poultry consumption and weight gain. One study out of the Netherlands examining about 4,000 people, correlated chicken consumption with weight gain. Another study followed 89,000 people in four other countries and found that animal protein intake was associated with long-term weight gain, and poultry was the worst, with 40 percent more weight gain than red meat or processed meat.

What makes poultry so bad? Yes, chickens are fatty these days because of the way we’ve genetically manipulated them—up to ten times more fat and calories than they used to have—but one bizarre theory postulated that it might be due to an obesity-causing chicken virus. In one study, one in five obese humans tested positive to the chicken virus SMAM-1, with those exposed to the chicken virus averaging 33 pounds heavier than those testing negative.

SMAM-1 was the first chicken virus to be associated with human obesity, but not the last. The original obesity-causing chicken virus SMAM-1 was able to effectively transmit obesity from one chicken to another when caged together, similar to a human adenovirus Ad-36, a human obesity-associated virus first associated with obesity in chickens and mice. Ad-36 spreads quickly from one chicken to another via nasal, oral or fecal excretion and contamination, causing obesity in each chicken. This, of course, raises serious concerns about Ad-36-induced adiposity in humans.

The easiest way to test this hypothesis is to experimentally infect humans with the virus. However, ethical reasons preclude experimental infection of humans, and so, the evidence will have to remain indirect. In the absence of direct experimental data, we must rely on population studies, similar to how researchers nailed smoking and lung cancer. About 15 percent of Americans are already infected with Ad-36; so, we can follow them and see what happens. That’s exactly what a research team out of Taiwan did (highlighted in my video Infectobesity: Adenovirus 36 and Childhood Obesity). They followed 1,400 Hispanic men and women for a decade and found that not only were those exposed to the virus fatter than those who were not, but also over the ten years, those with a history of infection had a greater percentage of body fat over time.

Most studies done to date on adults have found a connection between exposure to Ad-36 and obesity, and all studies done so far on childhood obesity show an increase in prevalence of infection in obese children compared to non-obese children. We’re now up to more than a thousand children studied with similar findings. Obese children who tested positive for the virus weighed 35 pounds more than children who tested negative.

The virus appears to both increase the number of fat cells by mobilizing precursor stem cells and increase the accumulation of fat within the cells. If we take liposuction samples of fat from people, the fat cell precursors turn into fat cells at about five times the rate in people who came to the liposuction clinic already infected. Fat taken from non-infected people that was then exposed to the virus start sucking up fat at a faster rate, potentially inducing obesity without increasing food intake.

Just as Ad-36 can be transmitted horizontally from one infected chicken to another in the same cage, subsequently causing obesity in each chicken, this same virus is also easily transmitted among humans, raising the question as to whether at least some cases of childhood obesity can be considered an infectious disease. Researchers publishing in the International Journal of Pediatric Obesity speculate that this animal adenovirus may have mutated to become a human adenovirus capable of infecting humans and causing obesity.

In health,
Michael Greger, M.D.

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Michael Greger M.D., FACLM

Michael Greger, M.D. FACLM, is a physician, New York Times bestselling author, and internationally recognized professional speaker on a number of important public health issues. Dr. Greger has lectured at the Conference on World Affairs, the National Institutes of Health, and the International Bird Flu Summit, testified before Congress, appeared on The Dr. Oz Show and The Colbert Report, and was invited as an expert witness in defense of Oprah Winfrey at the infamous "meat defamation" trial.

31 responses to “Virus in Chicken Could Be Linked to Obesity

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  1. This is depressing, given that there doesn’t seem to be a whole lot that any of us can do about this. I assume the viral infection persists even after chicken consumption ends? And if it’s communicable, then even dietary changes may be futile.

    1. From reading one of the papers Dr G links to in the article (, it is unclear if the virus actually persists or rather acts in a “hit and run” fashion, but either way the effects seem to persist. Yes I agree it’s a bit disconcerting, but even if the virus is a factor in obesity, it’s of course not the sole determinant. After all, there are plenty of people who eat chicken (or in my case, used to eat chicken) who are at a healthy body weight due to other lifestyle choices.

      1. If the virus “increases the number of fat cells”, then I assume you’re stuck with them for life (unless you have liposuction)

  2. Um, last I knew, we are born with a specific number of fat cells in our body. They do not increase or decrease over a lifetime. It’s a preset number. The only thing that changes is how much or how little they store, hence, how FAT you are. Science, it’s a marvelous thing.

    1. Now that they know more about stem cells, it seems to be more complex than that. Stem cells can turn into whatever kind of cell is wanted or needed. If this virus is demanding fat cells, the stem cells seem to be turning them out.

    2. Not true. One does increase their number of fat cells if they overeat, especially prior to adulthood. And once cell number increases it doesn’t reduce, and this makes it easier throughout the rest of one’s life to gain fat. Hence, childhood obesity is a serious problem. BTW, 10% of all fat cells are turned over every year. So theoretically one has no fat cells older than 10 years.

    3. This has been studied by numerous medical and research facilities over decades. Your fat cells count never changes over your lifetime. The size of those cells can change. Research it.

  3. Is this virus really spread by chicken consumption or is that what is insinuated in this article? I’m not doubting that the AD36 virus could increase fat deposition in adipose tissue, but is there any evidence that consuming chicken spreads this virus? When I search adenovirus transmission I found that it is spread like the cold virus – by coughing and sneezing. I wonder if cooking chicken would kill these viruses?

  4. I know that I shouldn’t ask this question but I cannot stop myself from doing it …..

    Is this the reason why we see so many fat chicks these days?

  5. The basic question, I would like answered is: how does poultry consumption correlate with obesity and/or the other health issues referred to here. Moreover, is there any data distinguishing between poultry raised without antibiotics; poultry raised without animal meal or organic/ free-range poultry.

  6. So, what are the chances of contracting chicken born viruses from shopping in a common grocery store that sells, cuts, processes, and package raw chickens?

  7. Two thoughts:
    I understood that few if any virus’ would persist in slaughtered meat; even less a possibility in cooked product?
    I would wonder that the effects of this virus should be more apparent in farm workers in contact with live chickens exposure rates near 100% in infected poultry operations, I’d guess). I haven’t heard any folkloric tales such.

  8. OMG Dr. Greger, is there anything that people who want to eat meat and live on a tight budget do to avoid getting sick or dying?

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