Infectobesity is a theory that obesity and weight gain could have an infectious origin. It also refers to the growing field of research attempting to find links between infectious pathogens and weight gain. Medically, obesity does not just refer to cosmetic weight differences. It is a condition that increases the risk of diabetes, high blood pressure, and many other health issues. Experts hope that breakthroughs in infectobesity research will help combat the obesity epidemic.
The term "infectobesity" was coined by Dr.Nikhil Dhurandhar, chair of the department of nutrition at Texas Tech University. While studying adenoviruses, Dhurandhar published details about one type, which causes fat cell growth in animals, and its associations with human obesity. Over the years, researchers have found several other links between viruses or bacteria and obesity. Due to the rising rates of obesity in the world, medical professionals are searching for better approaches to preventing and managing obesity. This led to increased interest in the idea of infectobesity.
One of the main focuses of infectobesity research is the association between obesity and bacteria. Gut flora, the microorganisms that live inside the human digestive tract, differs greatly between lean and obese individuals. Currently, it is unclear if obesity is the cause or the result of this difference. A 2008 article suggests that gut bacteria play a role in energy processes and weight changes. Additional research is necessary to determine to what extent gut bacteria influence obesity. However, in the future, treatments to change a person's gut flora could help adjust their weight.
A possible explanation for gut bacteria's links to obesity involves short-chain fatty acids. We are unable to digest certain foods, so gut bacteria ferment them, creating short-chain fatty acids, which our bodies can use as an energy source. Research in rodents indicates that certain levels of short-chain fatty acids can influence gut hormones, which can affect appetite and hunger, glucose tolerance and insulin resistance, gut inflammation, and lipid metabolism. Essentially, short-chain fatty acid levels could play a critical role in weight gain and obesity-related type 2 diabetes.
Researchers have also studied several viruses associated with obesity in humans and some animal species. Currently, several animal viruses and many human adenoviruses have links to obesity. While some of these viruses do not affect humans, researching how different viral sources influence obesity in any mammal could help us better understand human weight gain from viral pathways.
The first virus discovered to cause obesity in mice is canine distemper virus, which is responsible for an extremely contagious disease that affects domestic and wild species of dogs. This virus impacts the gastrointestinal and respiratory tracts, as well as the brain and spinal cord. In tests on mice, researchers found that the canine distemper virus caused obesity by attacking the central nervous system and creating numerous large fat cells. While there is no record of this virus affecting humans, it is similar to the human measles virus.
One of the more interesting infectobesity viruses is Rous-associated virus type 7, which causes obesity in chickens. Despite having similar levels of food intake to healthy chickens, those with the virus developed obesity, as well as enlarged fatty livers, anemia, and immunosuppression. Researchers believe these viral effects stem from low thyroid hormone due to damage to the central nervous system. Because several animal viruses use this method to cause obesity, similar human viruses could do the same.
The Borna disease virus, which can affect many warm-blooded animals, may also cause obesity. In rodent studies, the virus caused obesity by attacking the central nervous system. Whether the virus affects humans is a point of debate among experts. Some studies suggest the virus may be associated with neuropsychiatric disorders such as depression, schizophrenia, and bipolar disorder.
In the 1970s, large numbers of chickens in India died due to an unknown disease. Virus experts discovered that an avian adenovirus, which they named SMAM-1, was responsible. This virus lowered immune function in chickens while causing an increase in body fat, regardless of food intake. Interestingly, the increase in body fat did not always accompany an increase in weight — the virus was causing the body to store fat at the expense of lean mass. SMAM-1 was the first virus that experts could link to human obesity in a study that demonstrated higher body weight and body mass index in study participants who had SMAM-1 antibodies versus those who did not. It is not clear, however, if the human subjects had developed the antibodies to the avian adenovirus SMAM-1, or to a similar adenovirus affecting humans.
Because SMAM-1 was an animal adenovirus that could cause obesity in humans, researchers suggested that human adenoviruses could do the same. There are 51 human adenoviruses. Of those, three have caused obesity in animals, and two have not. Adenovirus-36 is notable because it causes obesity in the largest number of animals and is the only virus that seems to do so in humans When testing twins, the sibling with the virus was heavier and had more fat than the sibling without the virus. The virus targets adipocytes to release enzymes that encourage fat accumulation and fat cell creation. Researchers note that the discovery of adenovirus-36 occurred just before the worldwide rise in obesity. Additionally, tests to diagnose adenovirus-36 seem to be somewhat inaccurate, meaning that infections may be more prevalent than statistics suggest.
Perhaps the biggest reason for researching infectobesity is finding ways to treat obesity by targeting responsible viruses. Currently, several ongoing trials aim to discover the best method of managing obesity-causing viruses and identify how treatments can affect fat accumulation and storage. In one study on mice, a vaccine against adenovirus-36 reduced the amount of inflammation, weight gain, and fat developed from the infection. This could act as the basis for a human vaccine to target infectobesity.
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