I thought it was fascinating, since my mother and one of her sisters were slim, but the third sister was obese. Of course, after reading the entire article, I discovered that the only recommendations they came up with for people who are obese AND have the antibodies for a fat virus were: Eat less and exercise more. Haaaaaaaaa.
. . .The idea of infectobesity dates to 1988, when Nikhil Dhurandhar was a young physician studying for his doctorate in biochemistry at the University of Bombay. He was having tea with his father, also a physician and the head of an obesity clinic, and an old family friend, S. M. Ajinkya, a pathologist at Bombay Veterinary College. Ajinkya was describing a plague that was killing thousands of chickens throughout India, caused by a new poultry virus that he had discovered and named with his own and a colleague’s initials, SMAM-1. On autopsy, the vet said, chickens infected with SMAM-1 revealed pale and enlarged livers and kidneys, an atrophied thymus and excess fat in the abdomen.
The finding of abdominal fat intrigued Dhurandhar. “If a chicken died of infection, having wasted away, it should be less fat, not more,” he remembered thinking at the time. He asked permission to conduct a small experiment at the vet school.
Working with about 20 chickens, Dhurandhar, then 28, infected half of them with SMAM-1. He fed them all the same amount of food, but only the infected chickens became obese. Strangely, despite their excess fat, the infected obese chickens had low levels of cholesterol and triglycerides in their blood — just the opposite of what was thought to happen in humans, whose cholesterol and triglyceride levels generally increase as their weight increases. After his pilot study in 1988, Dhurandhar conducted a larger one with 100 chickens. It confirmed his finding that SMAM-1 caused obesity in chickens.
But what about humans? With a built-in patient population from his clinic, Dhurandhar collected blood samples from 52 overweight patients. Ten of them, nearly 20 percent, showed antibody evidence of prior exposure to the SMAM-1 virus, which was a chicken virus not previously thought to have infected humans. Moreover, the once-infected patients weighed an average of 33 pounds more than those who were never infected and, most surprisingly, had lower cholesterol and triglyceride levels — the same paradoxical finding as in the chickens.
The findings violated three pieces of conventional wisdom,
Dhurandhar said recently: “The first is that viruses don’t cause
obesity. The second is that obesity leads to high cholesterol and
triglycerides. The third is that avian viruses don’t infect humans.”
Needless to say, there is a lot of controversy surrounding a microbe theory for fatness. It should be pointed out that eating too much used to be considered the only reason for fatness. So fat people were assumed to be weak willed and somehow morally inadequate. This was followed by the discovery that along with eating too much, genetics can play a part. Think Pima Indians.
Now there's a third
option. Which is being met with great skepticism, needless to
say. Because the status quo has been upset.
The writer of the
article pointed out that the Australian researchers, who discovered that almost all
ulcers are caused by a microbial infection, had to wait a long time for their proof to receive
acceptance, too, despite all the evidence.