More evidence links a virus to obesity, this time in children


New evidence indicates that children who are exposed to a virus called adenovirus-36 are more likely to be obese than those who are not exposed to it, and to be heavier than other obese kids who were not exposed to it, researchers said this week. The virus, known informally as Ad-36, is one of about 55 adenoviruses that are known to cause colds and is the only member of the family to be linked to obesity. But it is one of 10 bacteria and viruses that have been associated with a propensity for putting on plural poundage.

Animal species have been shown to gain weight after being infected with Ad-36. Previous studies have shown that about 30% of obese adults have antibodies to Ad-36, compared with only 11% of those who are not obese. A study in South Korea found antibodies to the virus in 30% of children attending an obesity clinic, but not did examine healthy children.

In a study published online Monday in the journal Pediatrics, Dr. Jeffrey B. Schwimmer of UC San Diego and his colleagues studied 124 children, ages 8 to 18. Sixty-seven of the children were in the 95th percentile or higher for body mass index and the rest were not obese. The researchers found antibodies to Ad-36 in 15 of the obese children and four of the nonobese children. Children with antibodies, on average, weighed 50 pounds more than those without the antibodies. Within the obese group, those with the antibodies weighed an average of 35 pounds more than those without them.

Researchers are not yet sure how the virus can make people fat. But in a study three years ago, researchers from Louisiana State University found that infecting human fat extracted during liposuction with the virus caused stem cells in the fat to become fat cells, which then grew and accumulated and stored fat. After fat cells are formed in the body, they never go away. They may shrink during dieting, but always remain there ready to begin storing fat again if the person consumes too many calories.

-- Thomas H. Maugh II / Los Angeles Times