We all know that obesity endangers health. But now researchers at HSPH have given us one more reason to put on our gym clothes and shun that bacon cheeseburger—preferably starting in our teens.
Multiple sclerosis (MS) is an as-of-yet incurable disease in which the immune system attacks the central nervous system. New findings link obesity, particularly in late adolescence, with an increased risk of developing MS later in life.
A study led by Kassandra Munger, research associate in the group of professor of epidemiology and nutrition Alberto Ascherio, examined the association between body size and risk of MS in two large cohorts of women for whom health data over a period of decades was readily available, the Nurses’ Health Study I and II. It was the first longitudinal investigation to examine this potential link.
“Women who were obese at age 18 had a greater than twofold increased risk of MS as compared to women who were normal weight at age 18,” said Munger. Obesity in childhood, early adolescence, or later adulthood did not appear to be as important as obesity at this age in predicting MS risk.
Munger and colleagues studied obesity because they had previously found that vitamin D protects against MS, and obese individuals are believed to have lower circulating blood levels of vitamin D. The observed importance of body size during late adolescence aligns with previous data from Ascherio’s team suggesting that high levels of vitamin D during late adolescence protect more strongly against MS than high levels during adulthood.
The current study, however, does not establish whether diminished vitamin D levels contribute to the obesity–MS link. Another biological factor to consider is that fat tissue has inflammatory properties that can affect immune function. So the immune system may behave differently when excess fat tissue is present in the body.
Further analyses must be conducted to confirm the apparent link between obesity and MS and establish whether it can be generalized to race, gender and geographical populations different from the one in the current study. “This is so far the only study looking at this association in this way, and it’s important for these findings to be replicated in other populations,” Munger explained.
“Replication is really key to establishing risk factors.” These findings are reported in the Nov. 10 issue of Neurology.
Students may contact Kassandra Munger at kgorham@hsph.harvard.edu for more information.
Conflict Disclosure: The authors declare no conflicts.
Funding Sources: The National Institutes of Health; the authors are solely responsible for the content of this work.
