This finding was observed among women who did not take hormone therapy after menopause.

Obesity is known to be a risk factor for developing breast cancer after menopause, according to background information in the article. Estrogens may accumulate in fat tissue, potentially initiating or promoting the growth of cancerous cells in the breast.

Jiyoung Ahn, Ph.D., of the National Cancer Institute, Bethesda, Md., and colleagues analyzed data from 99,039 postmenopausal women who were part of the National Institutes of Health “AARP Diet and Health Study. In 1996, the women reported their current body measurements and weight, plus their weight at ages 18, 35 and 50. Body mass index (BMI) was used to classify the women as underweight, normal weight, overweight or obese.

Through 2000, 2,111 of the women developed breast cancer. In women who did not take menopausal hormone therapy, gaining weight in the early reproductive years (age 18 to 35), late reproductive years (age 35 to 50), perimenopausal and postmenopausal years (age 50 to the current age) and throughout adulthood (age 18 to the current age) were each associated with an increased risk of developing breast cancer compared with maintaining a stable weight during those periods.

Women who were not obese or overweight at age 18 but were at ages 35 and 50 had 1.4 times the risk of developing breast cancer compared with women who maintained a normal weight. Women who lost weight had the same breast cancer risk as those whose weight remained stable.

Because weight gain during adulthood mainly reflects the deposition of fat mass rather than lean body mass, weight gain potentially represents age-related metabolic change that may be important in breast cancer development, the authors write. These findings may reinforce public health recommendations for the maintenance of a healthy weight throughout adulthood as a means of breast cancer prevention.

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In the mid-1970s, a virus called SMAM-1 was believed responsible for an increased death rate among commercially raised chickens in India. SMAM-1 is associated with decreased immune function and an increased accumulation of body fat in infected chickens. Dr. Atkinson reports that one study tested 52 obese humans for antibodies to SMAM-1. About 20 percent had SMAM-1 antibodies, indicating exposure to this virus. The study participants who had these antibodies were heavier and had a higher body mass index compared with the antibody-negative group.

Dr. Atkinson's article also explores what current research has to say about the possible mechanisms underlying virus-induced obesity. Some research suggests that viral infections have a direct effect on adipocytes, cells that manufacture and store fat, turning on the enzymes of fat accumulation and recruitment of new adipocytes.

What's the next step for this research? According to Dr. Atkinson, the body of evidence linking adenoviruses to obesity in humans is now sufficient to think about the next step. Ideally, we could prevent infection and virus-induced obesity with a vaccine for the obesity viruses. Development of a human vaccine will take several years.

A peer-review journal, Mayo Clinic Proceedings publishes original articles, reviews and editorials dealing with clinical and laboratory medicine, clinical research, basic science research and clinical epidemiology. Mayo Clinic Proceedings is published monthly by Mayo Foundation for Medical Education and Research as part of its commitment to the medical education of physicians. The journal has been published for more than 80 years and has a circulation of 130,000 nationally and internationally. Articles are available online at mayoclinicproceedings.

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