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.

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