07 June 2008

Is obesity transmitted by airborne droplets?

Alexander Borisov, "Pravda.<url>", based on the materials of the magazine "New Scientist".

Increasingly, doctors recognize representatives of the microcosm as the culprits of various diseases, as it was recently, for example, with peptic ulcer disease. But to think that in a subway car or on a bus you can get ... obesity, somehow for a long time it did not occur to anyone. But here it is! And the scientific world is seriously discussing the problem: is there an obesity virus and is it transmitted by airborne droplets?

In recent decades, the obesity epidemic has hit not only prosperous Western countries, but also those that cannot be attributed to them, like Samoa, where 50% of the population suffers from obesity. Such a sharp increase in the number of obese people, both in rich and poor countries, confuses specialists engaged in the study of this phenomenon. After all, it is quite obvious that during this time there has not been a commensurate aggravation of the factors traditionally associated with obesity – poor nutrition and lack of physical activity.

The specialists had a feeling that they were missing something very important in their analysis. "Indeed, the fat content in the diet is excessive, and there is obviously a decrease in physical activity, but, in our opinion, this is not enough to explain the problems with obesity observed today," says Arne Astrup from the University of Copenhagen.

And what if this problem is literally connected with the epidemic: is a pathogenic virus walking across countries and continents, leaving mountains of fat in its path? This possibility has always intrigued Richard Atkinson, an obesity researcher at the University of Madison, Wisconsin. Atkinson knew that there were three other viruses, including canine distemper and Bourne's disease, that cause obesity in animals by destroying the part of the brain that regulates appetite.

In his lectures, he often jokingly talked about the likelihood that obesity in humans can also be infectious. "I asked my listeners to imagine how, entering the elevator, they find themselves in the company of a fat man who, sneezing at the wrong time, infects them with obesity. Usually everyone laughed." But it never occurred to Atkinson to develop this idea seriously.

Bombay, India, 1988. Nikhila Durandhar was a doctor and, like his father before him, was engaged in the treatment of obese patients. He had a thriving practice, and within a year he saw a thousand patients. This lasted until the time when a phrase accidentally said changed his whole life.

A family friend, a veterinarian pathologist named Sharad Azhinskiya, once mentioned in a conversation that he was studying a viral epidemic that had engulfed chickens and was killing them by the hundreds of thousands. Azhinskiya was struck by one oddity: the presence of significant fat deposits in the dead bird. Durandhar was amazed: how can a bird that has died from a severe viral disease be overweight? "There should be no fat at all, the bird should be emaciated."

The doctors decided to join forces and injected several chickens with the SMAM-1 virus. After six weeks, infected chickens had 50% more body fat than healthy chickens. But at the same time, it turned out that fat chickens have less cholesterol and triglycerides in their blood, which would be more typical for thin and slender individuals, and not for "fatties".

Without hesitation, Durandhar tested the blood of 52 of his obese patients for the presence of antibodies to the SMAM-1 virus. The virus was found in 10 people, moreover, in those who had the greatest weight of the entire group. At the same time, their cholesterol levels were low. The "chicken" picture was repeated.

For further research, more advanced equipment and facilities were required. Durandhar began writing to the US research centers that study obesity. Nikhila soon realized that no one was going to take a chance by betting on an unnamed scientist from India with a strange hypothesis. Durandhar decided to go to the USA himself. He managed to get a job as a researcher at North Dakota State University in Fargo, but for two years he could not find anyone who would be willing to finance his work on the chicken virus. But at the moment when the researcher was ready to return to Bombay, one of his letters landed on Atkinson's desk. A few months later, Durandhar moved to Madison, starting work as a researcher at the new Atkinson Laboratory.

The first thing they had to face was a ban on the use of the SMAM–1 virus in research. No one wanted to face an epidemic among chickens if the virus broke free. Then the scientists decided to start experimenting with some other virus. Since the SMAM-1 virus belongs to the group of adenoviruses, they first looked at a list of about 50 human adenoviruses, samples of which can be purchased in the United States. These viruses cause colds, diarrhea and conjunctivitis.

They decided to start with the Ad-36 virus, mainly for the reason that it differs from other adenoviruses sufficiently that antibodies formed by the body to fight it could be detected without any problems. Scientists knew almost nothing about this virus, except that it was first isolated from a young German woman suffering from an intestinal disorder.

The choice was successful. After just three weeks, chickens infected with the Ad-36 virus had two-thirds more abdominal fat deposits than chickens that were not infected. At the same time, they were also characterized by an unusually low level of cholesterol in the blood. In other words, the new virus they selected from the catalog had exactly the same effect as the banned Indian virus. This could mean only one thing: at least several other viruses should have a similar effect.

When Ad-36 was administered to mice, the effect was identical: an increase in body fat by two-thirds compared to the control group and a reduced cholesterol content in the blood. As follows from the report presented by Durandhar and Atkinson, when the virus was injected into monkeys, three infected monkeys in six months of the experiment began to weigh three times more compared to uninfected ones.

According to Atkinson, experiments on monkeys should help convince skeptics that all this is most directly related to humans. You can ignore the results obtained in experiments on chickens, you can ignore the results obtained in experiments on mice, but it is much more difficult to ignore the results obtained in experiments on monkeys.

So, if you are unlucky and you have picked up this virus, then you are very likely to be obese. "It's scary to even think about it," says John Forate, a researcher at Baylor College of Medicine in Houston, Texas, who deals with obesity.

Or maybe the fact is that obese people are more likely to get this virus than thin people? After all, it is known that obesity often causes a weakening of the immune system. To test this hypothesis, Durandhar and Atkinson searched for antibodies to three other adenoviruses – Ad-2, Ad-31 and Ad-37. It turned out that they are found equally often in both thin people and obese people, while there is no connection between the presence of such antibodies and a characteristic decrease in cholesterol levels in the blood. But Durandhar and Atkinson's attempts to convince their colleagues to accept their theory face great difficulties.

"This is not surprising," says Frank Greenway, an obesity specialist at the Pennington Biomedical Research Center in Baton Rouge, Louisiana. – I think this is typical for the scientific community: people feel uncomfortable when it comes to a sharp change of orientation.

But none of the experts on obesity problems could dismiss the fact that some cases of obesity may be caused by a virus, although they were in a hurry to add that this idea has not yet been confirmed in experiments "on humans". Durandhar agrees with this: "Everyone wants me to say with confidence that this virus causes obesity in people. I'm not ready to do that yet."

Getting really convincing evidence of the impact of the virus on people is not so easy. To take a group of people, infect half of them with a virus and see what happens – it is quite obvious that it would not be very ethical. There remains another way: to study the mechanism of the virus. When scientists understand which molecular triggers are activated by the virus, forcing animals to get fat, they will be able to find out whether similar mechanisms work in humans.

Similarly, if scientists can figure out how the virus lowers cholesterol, they will be able to determine whether such a reduction is beneficial for the carrier of the virus. "Where does this cholesterol go? If it gets on the walls of blood vessels, then it's bad," says Durandhar. On the other hand, if the liver decomposes it and removes it from the body, or if the liver simply produces less of it, then scientists may be able to learn how to reduce elevated cholesterol levels using drugs that mimic the effect of this virus.

And what happens if the efforts of Durandhar and Atkinson ultimately prove that it is the Ad-36 virus that is responsible for the obesity of some of the people suffering from this disease today? Firstly, there is some evidence that people with antibodies to this virus in the body respond better to treatment with anti-obesity drugs. Therefore, it will be easier to treat them. The development of the disease in these people can be prevented with the help of an antiviral drug, ultimately with the help of a vaccine.

Durandhar also believes that the authorities should organize a check of blood donors for the presence of this virus. His research shows that the virus persists in the blood even with prolonged storage, that is, there is a risk of infection of the recipient during transfusion. The researchers hope that if it is possible to prove the infectious nature of obesity, it will help at least partially relieve overweight people from the stigma that they are forced to bear in our society.

But what should people do who are forced to be on public transport, at work and in the theater together with potential carriers of the virus? Should I be careful and avoid communicating with overweight people even more than I am now? Durandhar thinks he shouldn't. So far, he has found only antibodies to this virus in the body of obese people, but not the live virus itself.

"The main question is the following: does this virus persist in the human body for many years and are overweight people carriers of the virus more often than thin ones?" For example, in monkeys, the excretion of a live virus with feces stopped after 60 days. And if this is considered a characteristic case, then people suffering from obesity due to a viral infection have most likely passed the infectious stage of the disease for a long time, although traces of the previous disease in the form of antibodies have been preserved in their blood.

According to Atkinson, a fat person who has become obese due to the virus will not do anything bad to you. You need to be afraid of the thin one who sneezes and coughs in front of you.

Portal "Eternal youth" www.vechnayamolodost.ru07.06.2008

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