Nearly 20 years ago, Nikhil Dhurandhar was chatting at the home of S M Ajinkya, a family friend who happened to be a pathologist working at the Bombay Veterinary College, about a new virus the researcher had found.
In 1983, Dr Ajinkya and his associate Dr A N Mulbagal had discovered SMAM-1 (named after both of them), a virus that infected chickens. But they were intrigued that the infected animals, instead of being emaciated as most sick animals are expected to be, had gained weight.
Dr Ajinkya told Dr Dhurandhar the chickens had big livers and pale kidneys with fat around them while other organs such as the thymus were shriveled.
Dr Ajinkya has spoken to just the right person. For Nikhil Dhurandhar, who was finding his way into research, was the son of Dr Vinod Dhurandhar, the father of obesity treatment in India [ Images ] and the founder-president of the Indian Obesity Association.
Dr Nikhil Dhurandhar, now an associate professor at the Pennington Biomedical Research Centre, Baton Rouge, Louisiana, US, had grown up hearing about fat deposition, weight loss, and how the first could be slowed and the latter speeded up.
"It was a critical point in my life," he says. "He (Dr Ajinkya) could have said, I don't think so. Instead, he said, 'I don't know. You are doing a PhD. Why don't you find out?'"
After facing much opposition when he suggested that viruses could cause obesity, Dhurandhar took it up and began checking out what SMAM-1 did to chicken fat.
He found that fat deposition indeed increased in infected chickens and, oddly enough, cholesterol and fat levels in the blood were lower than in uninfected chickens.
And when humans were tested, 20 percent of the obese people had antibodies to the virus, suggesting they had been infected at some point.
Nikhil Dhurandhar finally won a young scientist award from the National Institute of Nutrition in India for his research on the prevalence of obesity in Mumbai [ Images ].
He decided he ought to take his research further and, once he was done with his PhD, decided he ought to do post-doctoral research on viruses that promote fat storage. But no one in the United States was interested in the idea and a post-doctoral fellow who did his own research instead of the mentor's.
But he convinced one researcher, Richard Atkinson, and so moved with him to the University of Wisconsin in 1994. Finally ready to go, Dhurandar tried to import SMAM-1 viruses from India, but his request for the same was rejected by the US Department of Agriculture.
Disheartened but not discouraged, he decided to see if there were viruses in the US that were associated with obesity.
Serendipity led him to adenovirus-36 (AD-36), one of the 50 viruses associated with cold-like symptoms. He found that, like many viruses, AD-36 encouraged the cell it was in to divide.
But he found that this virus also targeted fat cells, unlike other viruses that give them a wide berth.
The viruses then infect stem cells which are not differentiated into specialised cells yet and convert those into fat cells.
And he has seen the effect when the virus was included in cultured tissue and, indirectly, when people became fat.
Dr Dhurandhar says there could have been an evolutionary advantage in it for the virus and for early humans because storing fat ensured survival in a time when food is hard to find. This would ensure both the virus and its host survive.
But this is no longer true in modern times where fat is not in shortage. And AD-36 antibodies was associated with 30 percent of the obese people but only 11 percent of lean people.
But even those 11 percent were significantly heavier than 89 percent of non-obese, he says.
Now studies have shown that children in Korea and the US tend to be fatter if they have antibodies for the virus. And canine distemper virus, Rous associated virus 7, and Borna disease virus, among others, have been shown to be associated with obesity.
Dr Dhurandhar cautions that there are many causes for obesity but only two solutions: Eat less and move around more.
"We know a lot about obesity, but don't have an adequate treatment on a community level. We can say a cousin lost weight, etc. But we don't have a cause-effective treatment," he says, adding, "Unlike in the case of diabetes, people often ignore natural factors."
But if infection was a factor, a vaccine developed to treat the AD-35 infection would clean up the problem in about 30 percent of the cases. The infection could be eradicated the way smallpox has been, he says.
Suggestions for Indians:
- Don't go by the American Body Mass Index, which is not right for Indians. Complications of obesity, medical complications and mortality increases after a BMI of 25. Beyond 30, things get worse rapidly.
- If you take people with the same BMI in Caucasian Americans and Indian Americans, Indians have more body fat, less muscle mass.
- If you look at the risk posed by a given BMI, Indians face a higher risk at the same BMI level.
- For Indians, the cut-off for BMI should be 23, according to a paper published last year.
- Obesity is more prevalent among vegetarians.
- Drugs can either reduce appetite or block the absorption of fat. Every drug has some side effect but there is a particular bias against taking obesity drugs. But they are not to be used indiscriminately.
- Obesity cannot be reduced to a character flaw. The same is true of surgery. Morbidly fat people get excellent results form surgery.
Image: Dr Nikhil Dhurandhar