The adenovirus AD-36, which has long been known to cause respiratory and eye infections in humans, more recently was shown to cause obesity in various lab animals—chickens, monkeys, rats, and mice. Whether it also has this effect on humans is a controversial open question, with many studies pointing to both confirmation and refutation. A Mayo Clinic study found the virus in 30% of obese humans and only 11% of non-obese humans.
Another study, from the University of California at San Diego, was reported in Pediatrics in 2010. This one couched its findings in more alarming terms, concluding that children with the virus weighed on average 52 pounds more than their virus-free peers. Even among obese children there seems to be a difference, with virus-affected obese kids weighing 35 pounds more than children in whom no trace of AD-36 was found. On the bright side, so far it looks like this is the only human adenovirus linked with obesity.
Just a few months ago, the National Institutes of Health published on overview of everything that is currently known on the topic of AD-36 infection as a possible cofactor that abets the development of obesity. As always, the authors include the disclaimer that obesity is “a multifactorial disease caused by the interaction between genetics, metabolism, social, cultural and environmental factors” as well as disease processes.
The relationship appears to be a two-way street, because “excessive adipose tissue,” also known as fat, is itself a predisposing factor for many infections. Conversely, adenoviruses appear able to directly influence adipose tissue. The physiological changes include not only increased body weight, but also increased glucose absorption and a decrease in the secretion of leptin and cholesterol. This carries implications for, among other things, diabetes management. The authors say:
Studying the favorable effect of Adv36 on metabolic consequences of obesity may provide insight to novel treatments that improve glycemic control despite adiposity. Identifying the viral protein responsible for influencing glucose disposal may help in developing novel anti-diabetic therapeutic agents.
On another front, it seems that surviving childhood cancer is a mixed blessing, with a downside marked by a 14% increased likelihood of obesity as compared to children who never suffered from cancer.
St. Jude Children’s Research Hospital looked at the records of 1,996 childhood cancer survivors who had subsequently lived for 25 years without a recurrence. At the time of the study, their average age was 32. Obesity is not the only potential problem, says corresponding author Kirsten Ness, Ph.D., because “Childhood cancer survivors are known to be prone to developing chronic disease.”
As might be expected, kids who were already obese when cancer hit had even worse statistics. Those survivors turned out about five times as likely to be obese in adulthood. Brain irradiation, a treatment for acute lymphoblastic leukemia (ALL) and brain tumors, increased the risk dramatically, and this proclivity is suspected of originating in genetic variations.
47 percent of survivors who received brain irradiation as part of their treatment were obese, compared to 29.4 percent of survivors who received other therapies… In this study, 43 percent of the ALL survivors were obese, which is higher than the 19 to 32 percent reported in previous research.
St. Jude researchers see the importance of incorporating a weight management component into the overall pediatric oncology protocols. It seems that this particularly at-risk demographic could benefit from the features of the W8Loss2Go smartphone application.
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Source: “Children Exposed to Virus Weigh 52 pounds More, Obesity Researchers Find,” Bloomberg.com, 09/19/10
Source: “Adenovirus 36 and Obesity: An Overview,” NIH.gov, 07/08/15
Source: “Childhood Cancer Treatment and Age Influence Obesity Risk for Childhood Cancer Survivors,” Newswise.com, 05/11/15
Image by David Cesarino de Sousa
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