New data on diet and MS
AAN 2015 – Part 2
American Academy of Neurology 67th annual meeting
Washington, DC, April 18-25, 2015
Recent studies have indicated that obesity in childhood and adolescence is a risk factor for developing MS (Wesnes and colleagues. Mult Scler 2014; epublished September 2, 2014; Kavak and colleagues. Mult Scler 2014; epublished November 12, 2014). The current thinking is that obesity promotes inflammation, which reinforces the inflammatory processes that are present in MS.
This obesity-related inflammation might be expected to make things worse once MS develops, and a new study suggests that this is the case (Ben-Zacharia A. AAN 2015; abstract P2.212). Patient records were examined over a five-year period. The mean age was 45 years; mean body-mass index (BMI) was 27 (e.g. a woman, height 5 feet 4 inches weighing 158 pounds [71.8 kg] or a man, height 6 feet weighing 200 pounds [90.9 kg]). BMI uses height and weight to calculate overweight (25-30) and obesity (above 30). People who were overweight or obese had more inflammatory activity as assessed by magnetic resonance imaging (MRI). In addition, the odds of having a relapse over a five-year period was four-fold higher in obese people compared to people with normal weight.
Obesity may also affect MS fatigue. A small study in Italy looked at fatigue symptoms before and after people began a weight-loss regimen (Rocco Totaro and colleagues. AAN 2015; abstract P2.211). The diet was low in saturated fats and high in antioxidant foods (e.g. tomatoes, broccoli, green tea). After six weeks, the percent body fat was reduced, and people reported that their MS fatigue was significantly improved. Weight loss also boosted physical, mental and social functioning.
Diet can influence inflammation, not least because most of the body’s immune tissues are found in the gastrointestinal tract. A study in animals reported that the composition of dietary fats may matter (Haghikia and colleagues. AAN 2015; abstract P2.210). Short-chain fatty acids (such as plant-based omega-3) enhanced the production of regulatory immune cells (called Tregs), which quieten the autoimmune response. In contrast, medium- and long-chain fatty acids (such as animal-based omega-3 and omega-6) promoted inflammatory immune cells (Th1 and Th17).
A separate study looked at this same issue from a different perspective by analysing stool samples from people with MS (Tankou and colleagues. AAN 2015; abstract P2.206). Among those with higher vitamin D levels, there was an abundance of a type of gut bacteria (called ruminococcaceae) – which are known to break down short-chain fatty acids. What you eat influences the various populations of bacteria in the gut, which in turn influences inflammatory processes throughout the body. However, it’s too early to base any dietary recommendations on these intriguing but preliminary findings.
Low vitamin D levels are often cited as a factor contributing to more severe MS, but the mechanisms behind this are poorly understood. A further complication is ethnicity. A U.S. study examined vitamin D levels in African-Americans and Hispanics newly diagnosed with MS (Langer-Gould and colleagues. AA 2015; abstract P2.207). Higher vitamin D levels didn’t appear to lower the risk of MS in Hispanics; in African-Americans, higher vitamin D appeared to be detrimental. So the recommendation to take vitamin D supplements may only apply to Caucasians with MS.
A year ago, MSology reported that consumption of red wine may actually lower the risk of developing MS-related disability (see Lifestyle choices: the good and bad news, MSology, December 12, 2013). Similar results have now been reported in a new U.S. study (Diaz-Cruz and colleagues. AAN 2015; abstract P2.213). It found that alcohol intake was associated with less disability and less severe MS symptoms. The same was shown for red wine, but to a somewhat lesser degree. It remains to be seen if alcohol has an actual impact on the MS disease process or whether the finding is simply serendipity.
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