The role of diet in MS
Those of you who read our blog regularly will have surely heard it mentioned before, but there still remains a rather loud and large proportion of healthcare professionals who when asked about the role of diet in MS will respond “there is no evidence for any of that”.
To be clear, this is wrong. There has been high-class evidence for the role of diet in MS since Prof. Roy Swank’s landmark study was published in “The Lancet” in 1990, and in fact for a very long time before that in smaller studies. Since then, the evidence base has grown rapidly and consistently demonstrates the vital role of diet and lifestyle in modifying one’s risk of developing this condition, and on its long-term trajectory.
The difficulty in studying lifestyle interventions
That being said, the constant thorn in the side of our argument is the difficulty in studying lifestyle interventions in a manner that produces results that doctors and scientists will readily accept. To many, it is simply a randomised control trial (RCT) or nothing. That is, of course, not the fundamental premise of evidence-based medicine, but rather we should aim to attain the highest possible level of evidence in a given area. In the field of lifestyle modification, it is very difficult to perform an RCT, you cannot easily feed someone “fake steak” or mimic meditation.
Another issue with observational cohort studies (one of the main formats for lifestyle research) is that it can be very difficult to separate cause from effect. So the concept of “reverse causality” is often thrown back at promising results, showing that people with MS living healthy lifestyles have fewer relapses and disabilities. The dietary nihilists would say that because a person has fewer symptoms and disability, they are therefore more able to eat better and exercise more, rather than deriving any benefit from a particular intervention. Whilst we can use statistical modelling to try and control for these confounding factors, nevertheless, it can limit the wider acceptability of some very important results.
Fortunately, as with most things, nature knows best. There is a phenomenon known as “Mendelian randomisation” which in simple terms is nature’s version of a randomised control trial. It uses the transmission of gene variations with known functions from parents to offspring to establish whether or not the modifiable factor (in this case body fat) is a cause or an effect of a disease.
In a ground-breaking piece of research published in “Multiple Sclerosis Journal”, researchers from University College London used Mendelian randomisation to examine whether body fat content had an influence on a person’s risk of developing MS, and whether it increased their risk of higher disability levels over time once they had MS. Importantly, they specifically looked at body fat, rather than body mass index (BMI), which can be an unreliable method of determining the risk of disease. For example, an elite athlete may be technically obese using BMI, yet have an extremely low body fat percentage and high lean muscle mass, significantly reducing their risk of illness compared to someone with the same BMI but markedly increased body fat levels.
The results of the study
The results firstly confirmed that a higher BMI leads to a greater risk of developing MS, but found no evidence that MS risk has any influence on BMI or other measures of body fat. This supports previous studies that found an association between raised BMI and increased risk of developing MS.
In addition, the team examined the effects of fat stored in different compartments of the body, and also non-fat tissues. Their findings suggest that people with greater fat stored in the whole body, legs, arms and trunk are at high risk of developing MS, whereas height and non-fat mass are unlikely to contribute to MS risk.
With regards to body fat levels and MS severity, again the results were clear. Obesity was a significant contributor to disability progression, and higher BMI, with fat accumulation in the whole body, arms, legs and trunk were significantly associated with greater disability in people with MS. Again, there was no correlation between height and non-fat mass and disease severity. So here we have Class 1 evidence showing body fat directly influences MS, not the other way round.
As with most studies, there were some limitations. For example, the differences in body composition between women and men, and the effects of ageing on fat accumulation could potentially have influenced the results. There were other complex and technical areas of the analyses that may provoke discussion and debate, but regardless, this study clearly demonstrates that carrying excess body fat significantly increases the risk of MS and its severity over time.
Whilst the researchers didn’t specifically study any one dietary pattern; a whole food, plant-based diet such as the one recommended in the OMS program is well-known to facilitate weight loss and the maintenance of a healthy weight. Given that this also reduces a person’s chances of developing many other common diseases such as heart disease, diabetes and some cancers, following such a diet in my own view really is a very clear and simple choice to make.
No one is saying that weight loss is easy, especially if MS symptoms and disability make healthy eating and exercise more difficult, but OMS is here to support you in that choice and to provide lots of useful resources to make it easier for you.
The authors concluded, “Our findings provide evidence from human genetics that a range of features linked to obesity is an important contributor to MS development and MS severity, but height and non-fat mass are not. Importantly, these findings also identify a potentially modifiable factor that may reduce the accumulation of further disability and ameliorate MS severity”.
Let’s see them try and ignore that one.
Almramhi MM, Storm CS, Kia DA, Coneys R, Chhatwal BK, Wood NW. The role of body fat in multiple sclerosis susceptibility and severity: A Mendelian randomisation study. Multiple Sclerosis Journal. May 2022. doi:10.1177/13524585221092644