Fat Virus | Medical-Weight-Loss-Guide.com

The idea that there is a fat virus may seem absurd at first. However, there are some studies that support the theory that a virus causes fat to accumulate in humans. There is other research on obesity viruses that infect animals. Of the fat viruses that have an effect on humans, only two have positive scientific evidence. They are SMAM-1 and Adenovirus 36 (Ad-36). The term infectobesity refers to the theory that infections cause people to be overweight.

SMAM-1 is actually a bird adenovirus that can infect people. In chickens, it causes an accumulation of body fat and increased levels of triglycerides in their livers. This was noted even though the chickens ate the same amount of food as those not infected. SMAM-1 was the first obesity virus discovered.

In a study on humans, people who had antibodies toward SMAM-1 were about 30 lbs heavier with a BMI of 35.3 vs. 30.7 compared to those who did not have these antibodies in their blood. The presence of antibodies indicated that these people had been exposed to SMAM-1 at some point. It was also noted that people with the antibodies had better cholesterol levels.

Adenoviruses in general cause common colds, respiratory infections, conjunctivitis (pink eye), and other infectious diseases. Human Adenovirus 36 (Ad-36) was the first human adenovirus to be tested for an association with obesity, and there is more research on this fat virus than SMAM-1. Chickens, mice, and rats infected with Ad-36 gain weight.

In human studies, people who are antibody positive for Ad-36 weigh more that those who do not have the antibodies. There are several types of antibodies. Some are present during early and active infections. Others are produced by our bodies when we no longer have that particular type of infection, helping to make us immune. In studies, the long term type of antibodies for Ad-36 were detected. This means that even a remote expose to the fat virus leaves its obesity effects in place for several years.

Just like in SMAM-1, people and animals who had been exposed to Ad-36 had better cholesterol levels.

Further studies on the mechanisms of how Ad-36 may cause obesity have shown that the virus likely acts in two ways: 1.) It causes certain genes to be expressed which trigger a form of stem cells to develop into fat cells, and 2.) It triggers certain cellular signaling pathways that alter how cells behave.

This means, the fat viruses can cause our bodies to produce more fat cells. There is also research that shows the Ad-36 virus can tell cells to become more sensitive to insulin. Further understanding of these facts along with the alteration in cholesterol will have a profound effect on our knowledge and treatment of diabetes and metabolic syndrome.

It does seem a little strange that a fat virus would cause a person to have better cholesterol. There are a few ways this might happen. Ad-36 seems to activate some specific cell signals that are also activated by diabetes medicines like metformin. These signals include PPARg2 (PPAR-gamma 2) and others. Simulating the effects of diabetes medicines can improve cholesterol.

Also, by producing more fat cells, the cholesterol and triglycerides in your blood and liver now have a place to go. These new fat cells could sequester cholesterol and keep it out of your blood. This would cause lab tests on your blood to show lower cholesterol levels.

Additionally, infection with Ad-36 seems to decrease MCP-1, a marker of inflammation. Inflammation, high cholesterol, and insulin resistance place people at greater risk for heart disease and strokes. Even though there is an association with increased obesity, Ad-36 may have some beneficial effects.

As mentioned above, these obesity viruses can directly affect cells' behaviors and how they develop. These viruses can activate cellular signals that cause fat to accumulate in our bodies. Activating these signaling pathways can also cause changes in our cholesterol levels.

Another theory is that certain infections have an effect on the brain. An area of the brain called the hypothalamus regulates hunger and several other body functions. By altering its function, people may tend to eat more and their metabolisms could change.

In addition to viruses, there is some research that suggests prion infections and the make-up of intestinal bacteria may be related to obesity. There is very little research on prion associated obesity. The work done on intestinal bacteria seems to suggests there is a pattern to the types of bacteria living in the gastrointestinal tracts of overweight people. However, it may just be that this bacterial pattern is present because those people eat less healthy foods.

It is important you discuss any weight loss or exercise plan with your doctor. Only you and your physician can decide what is best for you. Some people have certain conditions that prevent them from doing all exercises, and goal body weights may be different for different people. You need to discuss all these things with your physician before starting any weight loss or exercise program.