June 14, 2018 | News |

Obesity linked to multiple sclerosis

A number of studies have now reported that obese children and teens have a higher risk of developing multiple sclerosis then their normal-weight peers (Ascherio and colleagues. Semin Neurol 2016;36:103-114). So what’s behind this apparent MS-obesity link?

A number of explanations have been proposed – which may provide a clue to the foods that may help or hurt MS.

First of all, what is the evidence that obesity may contribute to the development of MS? One study found that the risk of developing MS was twice as high among people with a higher body-mass index (BMI) at age 20 compared to people who were normal weight (Hedstrom and colleagues. Mult Scler 2012;18:1334-1336). (BMI is calculated according to a person’s height and weight, and there are many BMI calculators available online. A BMI of 27 to 30 is considered ‘overweight’; a BMI above 30 is considered ‘obese’.) A similar risk was seen for children with obesity (Munger and cslleagues. Mult Scler 2013;19:1323-1329), although one study found that MS risk was higher only in girls (Langer-Gould and colleagues. Neurology 2013;80:548-552). A separate study found that among women with MS, those with a higher body weight developed MS symptoms at an earlier age (Kavak and colleagues. Mult Scler 2015;21:858-865).

While these studies suggest a link between obesity and MS, they can’t show a true cause and effect. In part this is because obesity is somewhat arbitrarily defined, and is a complex state that is the result of genetic, environmental, physical and lifestyle factors – very much like MS itself.

But obesity can provide some clues about the nature of MS. A recent article suggested that two obesity-related factors may contribute to the development of MS (Huitema and colleagues. Curr Neurol Neurosci Rep 2018;18:18).

The first factor is the microorganism community that lives in our gastrointestinal tract. These organisms – bacteria, viruses, fungi and archeota – form a complex ecosystem in our gut, called the microbiome. In fact, the billions of organisms outnumber the number of cells in our body. These organisms aren’t there to cause disease; rather, they digest our food, process nutrients and interact with our immune system (most immune tissue is found in the gut). Immune interactions in the gut can then influence immune function throughout the body.

Several studies have now shown that the microbiome is different in people with MS compared to those without MS (Jangi and colleagues. Nat Commun 2015;7:12015. Miyake and colleagues. PLoS One 2015;10:e0137429. Chen and colleagues. Sci Rep 2016;6:28484). The relative proportion of different types of bacteria differs. There is some dispute about which types of bacteria are important, and arguably finding the bad actors among the countless species of organisms is unlikely. What is probably more important are the shifting relationships of dozens of organisms, and science will have a hard time unravelling these interactions.

It is known that some bacteria promote inflammation, while others have the opposite effect. And changing your diet is known to change the microbiome, which has led some researchers to recommend certain dietary modifications. For example, a recent pilot study reported that people with MS who consumed a high vegetable/low protein diet for at least a year had fewer relapses and less progression of disability compared to people who stuck to the Western diet (Saresella and colleagues. Front Immunol 2017;8:1391). Other researchers have advocated the Mediterranean diet as the one that makes most sense (Mische and colleagues. Curr Treat Options Neurol 2018;20:8). Other studies are now looking at whether probiotic supplements are helpful.

Obesity, because of food choices, will have an impact on the microbiome, but this relationship is more complicated than one might think. The microbiome can also cause obesity. This was shown in fecal microbiota transfer experiments which, as you might expect, transplant feces from one subject to another (a procedure now used to successfully treat some human diseases). In one experiment, fecal transfer from obese humans to non-obese mice caused the mice to become obese (Zhang and colleagues. ISME J 2017;11:676-690), suggesting that the types of organisms present in the gut can promote weight gain.

A second factor to consider is that fat tissue produces hormones, and one such hormone (called leptin) is known to have effects on the immune system. One study found that leptin levels were higher in people with MS compared to healthy individuals, and high leptin levels were associated with a more overactive immune response (Kraszula and colleagues. Neurol Neurochir Pol 2012;46:22-28). This difference was seen independently of obesity, but it suggests that fat tissue behaves somewhat differently in people with MS. The inflammation and immune reactivity that leptin promotes may be just enough to initiate a process that culminates in the development of MS.

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