Infectobesity: Adenovirus 36 & Childhood Obesity

Infectobesity: Adenovirus 36 & Childhood Obesity
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Studies on more than a thousand children suggest that a viral infection may play a role in childhood obesity by increasing both the number and size of fat cells.

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This study, correlating chicken consumption with weight gain, was performed in just one country on about 4000 people. This study included 4 other countries, and included 89,000 people. Animal protein intake was associated with long term weight gain, and again poultry was the worst, associated with 40% more weight gain than red meat or processed meat. Why poultry? Yes they’re so fatty these days because of the way we’ve genetically manipulated them: up to 10 times more fat and calories than they used to have, but one bizarre theory was that it might be due to an obesity-causing chicken virus, to which 1 in 5 obese humans tested positive, and those with exposure to the chicken virus averaged 33 pounds heavier than those testing negative.

This chicken virus was the first to be associated with human obesity, but not the last. It’s similar to chicken embryo lethal orphan virus, which is common among poultry in the US. The original obesity-causing chicken virus was able to effectively transmit obesity from one chicken to another when caged together, similar to adenovirus #36, a human obesity-associated virus first reported to cause obesity in chickens and mice, spreading quickly from one chicken to another via nasal, oral and fecal excretion and contamination. This of course raises serious concerns about transmissibility in people.

The easiest way to test this is to just experimentally infect humans with the virus and see how fat they get. Alas, ethical reasons preclude experimental infection of humans, and so the evidence will have to remain indirect. In the absence of direct experimental data, we have to rely on population studies like how they nailed smoking and lung cancer. Can’t force people to smoke a pack a day, but there are people that smoke on their own and we can see if they get more lung cancer. Similarly, about 15% of Americans are already infected with this virus, so let’s just follow them out and see what happens. 1,400 Hispanic men and women were followed for a decade, and not only were those exposed to the virus fatter than those who were not, but over 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 this virus and obesity, and all of the studies done so far on childhood obesity show an increase in prevalence of infection in obese compared to non-obese children. Now we’re 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 increase the number of fat cells by mobilizing fat cell precursor stem cells, and then may increase the accumulation of fat within the cells. If you take liposuction samples of fat from people, the fat cell precursors turn into fat cells at about 5 time the rate in people who came to the liposuction clinic already infected. And fat taken from noninfected people exposed to the virus start sucking up fat at a faster rate, so may induce obesity without increasing food intake.

Just like adenovirus 36 infection can be transmitted horizontally from one infected chicken to another in the same cage, and then they subsequently became obese. This same virus is also easily transmitted among humans, this raises the question as to whether at least some cases of childhood obesity can be considered an infectious disease. They speculate that this animal adenovirus may have mutated to become a human adenovirus capable of infecting humans and causing obesity.

To see any graphs, charts, graphics, images, and quotes to which Dr. Greger may be referring, watch the above video. This is just an approximation of the audio contributed by Katie Schloer.

Please consider volunteering to help out on the site.

Images thanks to GrahamColm via Wikimedia Commons.

This study, correlating chicken consumption with weight gain, was performed in just one country on about 4000 people. This study included 4 other countries, and included 89,000 people. Animal protein intake was associated with long term weight gain, and again poultry was the worst, associated with 40% more weight gain than red meat or processed meat. Why poultry? Yes they’re so fatty these days because of the way we’ve genetically manipulated them: up to 10 times more fat and calories than they used to have, but one bizarre theory was that it might be due to an obesity-causing chicken virus, to which 1 in 5 obese humans tested positive, and those with exposure to the chicken virus averaged 33 pounds heavier than those testing negative.

This chicken virus was the first to be associated with human obesity, but not the last. It’s similar to chicken embryo lethal orphan virus, which is common among poultry in the US. The original obesity-causing chicken virus was able to effectively transmit obesity from one chicken to another when caged together, similar to adenovirus #36, a human obesity-associated virus first reported to cause obesity in chickens and mice, spreading quickly from one chicken to another via nasal, oral and fecal excretion and contamination. This of course raises serious concerns about transmissibility in people.

The easiest way to test this is to just experimentally infect humans with the virus and see how fat they get. Alas, ethical reasons preclude experimental infection of humans, and so the evidence will have to remain indirect. In the absence of direct experimental data, we have to rely on population studies like how they nailed smoking and lung cancer. Can’t force people to smoke a pack a day, but there are people that smoke on their own and we can see if they get more lung cancer. Similarly, about 15% of Americans are already infected with this virus, so let’s just follow them out and see what happens. 1,400 Hispanic men and women were followed for a decade, and not only were those exposed to the virus fatter than those who were not, but over 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 this virus and obesity, and all of the studies done so far on childhood obesity show an increase in prevalence of infection in obese compared to non-obese children. Now we’re 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 increase the number of fat cells by mobilizing fat cell precursor stem cells, and then may increase the accumulation of fat within the cells. If you take liposuction samples of fat from people, the fat cell precursors turn into fat cells at about 5 time the rate in people who came to the liposuction clinic already infected. And fat taken from noninfected people exposed to the virus start sucking up fat at a faster rate, so may induce obesity without increasing food intake.

Just like adenovirus 36 infection can be transmitted horizontally from one infected chicken to another in the same cage, and then they subsequently became obese. This same virus is also easily transmitted among humans, this raises the question as to whether at least some cases of childhood obesity can be considered an infectious disease. They speculate that this animal adenovirus may have mutated to become a human adenovirus capable of infecting humans and causing obesity.

To see any graphs, charts, graphics, images, and quotes to which Dr. Greger may be referring, watch the above video. This is just an approximation of the audio contributed by Katie Schloer.

Please consider volunteering to help out on the site.

Images thanks to GrahamColm via Wikimedia Commons.

24 responses to “Infectobesity: Adenovirus 36 & Childhood Obesity

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  1. Did they compare infected people who exercised with those who didn’t. If they ate the same amount of food as non-infected people, the fat had to come from somewhere, perhaps because less muscle was being made or sustained- and that, perhaps due to a lack of exercise. Or perhaps the virus slows down the rate of metabolism while leaving hunger at the same level. Exercise would likely return the metabolism to the correct rate. Even if more stem cells convert to fat cells, what’s filling these cells with fat if they eat no more than normal and especially if they exercise. I’d like to see a study done to test the effect of exercise of various kinds on infected people.




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      1. Yeah we shouldn’t be having this virus in the first place. It would be nice to know how exercise or an increase in plant intake would impact the effects of the virus though.




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        1. So, your plan is to eat chicken and “protect” yourself by throwing in some green veggies and doing pushups? That didn’t work for the polio virus.




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    1. Exercise doesn’t prevent other viruses from spreading. Regardless, it’s not likely avid exercisers were culled out of the study.
      Considering we are an obese population of epidemic proportion, how would we survive if the chicken fat virus could mutate and transfer from human to human.




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  2. Dr G – Is this the same adenovirus that is attacking kids here in Colorado, or is it a different strain? Viruses are some of the smallest living things, much smaller than a human cell. I wonder if adv36 has adapted to the point where it can control the fat mechanisms in the human body so it is able to hide there to avoid the immune system? It is clear that viruses can and do hide in the human body – as demonstrated by the ability of the chicken pox virus to hide for decades, then re-emerge as shingles decades later. No sign of the virus in between, and the adaptation of the immune system to destroy it in the first place does not work for the later shingles version. What does this say about ebola, which is also a virus?




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  3. Why poultry showed highter gains might also be due to meateaters eating more chicken nowadays in response to all the red meat scares. Either way, best to not eat meat at all.




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  4. Big pharma is coming! Antiviral therapy for obesity…NOT! Even better, blend antiviral drugs into ground meat together with a statin drug.




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  5. It may be that our immune systems are compromised due to issues with virus, bacteria and Protozoa (specifically FL1953) that live in and is protected by biofilm. Fat feeds this protozoa and makes it stronger. Until we can lower the fat not only in our diet but also on our bodies our immune systems can’t detect these pathogens that hide in this fat and biofilm. A good portion of our immune system lie in our guts. The one thing that ONLY WE have control over is our diet. But sadly it’s the one thing many sick people refuse to change. They are looking for a pill to “fix” things without making any lifestyle changes. Becoming a low fat, whole food, vegan is our key toward better health.

    Issie




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  6. Wow, the implications of this are staggering, even beyond the obesity factor. The whole virus thing in relation to factory farming alone is enough to scare one away from eating animal products, even if they had no ethical or previous health concerns! HINT HINT!




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    1. I’m sure it will be on the nightly news this evening so Americans are warned to stop eating chicken. Media has our backs. (snicker)




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  7. My question is — does the virus eventually die off, or is there anything that people who already have this virus can do to get rid of it? Does dietary change make any difference after the fact? Thank you!




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  8. Dr. G,

    Steve here, in San Diego. I moved your car once to prevent a ticket.

    Anyway, you’ve presented a problem that many of us may already have.

    How do we treat/cure this?




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