Obesity is a complex problem with biological, social, and psychological causes. The control of food intake (how much you eat and how much it takes for you to feel full) and food metabolism (how you convert food to energy) appears to be regulated, at least in part, by a system of hormones produced by cells of the nervous system. The interaction between these “neurohormones” is currently the subject of intense study and compounds that affect these hormones are the focus of a billion dollar diet drug industry.
It might not surprise you that the actions of hormones produced in the brain contribute to obesity, but another link to obesity may surprise you, since the source isn’t human. It’s a virus called adenovirus-36 or “Ad-36.” Ad-36 is a member of a family of about 50 DNA viruses that are associated with some very familiar illnesses ranging from the common cold to pink eye.
As early as 1997, Dr. Nihil V. Dhurandhar reported that 10 of 52 obese subjects he screened while at the University of Bombay had antibodies against a type of bird adenovirus, SMAM-1. Dhurandhar and colleagues in the U.S. later investigated human adenovirus strains. They found that approximately 30% of the obese people in their study had been infected with the Ad-36 virus compared to 11% of non-obese people.
To see if the virus has a causal connection to obesity, researchers have taken the virus and experimentally infected monkeys with it. The result? The infected monkeys gained significant weight. Surprisingly, serum cholesterol was lowered in these animals.
While these studies suggest a link between the Ad-36 virus and obesity, questions remain – like how does the virus contribute to obesity? In a recent study, scientists at Louisiana State University took samples of tissue from individuals who had liposuction and removed adult stem cells from the samples. Stem cells are cells that have the potential to turn into more specialized cells. When infected by the Ad-36 virus, greater than 50% of the cells turned into fat cells, while only a small number of non-infected cells turned into fat cells. The virus-infected fat cells were also bigger than typical fat cells, seemingly capable of storing more fat.
Because the causes of obesity are complex, no one treatment method may be a cure-all. However, interesting avenues of research identified by the Louisiana State study include the possibility of creating vaccines or drugs that target particular genes of the adenoviruses linked to obesity. Understanding the reason why some people infected with Ad-36 aren’t obese and why Ad-36 infection is associated with lower cholesterol may be just as interesting.