Barts-MS rose-tinted-odometer: ★★★★★
I am always being asked about what is the ideal diet for someone with MS. The simple answer is there is no ideal MS diet. What you eat is about personal choices and has to be compatible with your cultural background and your social circumstances. There is so much more to eating food than what you actually eat. I have written a piece on Medium called ‘Diet as a Philosophy’, which provides some context to this statement.
In short, my diet philosophy recommends that anyone with MS should eat socially, i.e try not to eat alone and make your meals a social occasion. To eat real food, i.e. avoid processed and ultra-processed food. To try and eat locally-produced food that is seasonal; I am aware that this easier said than done, particularly for economic reasons. Finally, it would help if you eat mindfully, in other words, think about what you are eating, why you are eating it and what impact it is having on the world.
The question about diet being an actual treatment for MS is a different question. Here I would support a ketogenic diet and intermittent fasting and I have written extensively on the science behind these diets and why I think these two diets may be disease-modifying for people with MS. At present, the evidence base for these diets working in MS remains weak and exploratory, but the good news is there are ongoing studies looking at these diets in pwMS. Despite this, the basic science on these diets from animal studies is so compelling that if I had MS I would be ketotic and fasting intermittently (5:2 or 16:8 diet).
Please note ketogenic diets and intermittent fasting are not incongruent with my diet philosophy.
I also don’t support one diet over another. The reason I don’t support a specific diet is simple; the evidence-base for anyone diet being better than another is weak and a lot of diets are not based on science. Yes, science. As scientists, we should be following the science. For example, the study below is interesting in that they flipped the question and looked at the metabolic responses to food and its influence on cardiometabolic disease. You may say what has this got to do with the central nervous system, but I believe in the aphorism ‘that what is good for the heart is good for the brain’.
What this study showed is that person-specific factors, such as gut microbiome, had a greater influence than the diet in relation to metabolism and that genetic variation only had a modest impact on the metabolic responses to food linked to cardiometabolic disease. The only metabolic output that was influenced by diet was blood glucose or sugar levels, which is dictated by carbohydrate intake and the type or quality of carbohydrates we consume.
In summary, apart from carbohydrate metabolism, it is horses for courses and personal factors (gut microbiome and genetics) which dominate how your diet impacts on your metabolism.
The good news is you can manipulate your carbohydrate metabolism; it is relatively simple. Both ketogenic diets and intermittent fasting reduce your sugar intake and blunt or flatten your blood glucose levels and the subsequent downstream insulin response, which is clearly the bad guy in driving cardiovascular risk.
Based on the above I hope you have enough information at hand for you to make an informed decision about your diet without having to ask me next time 😉
Berry et al. Human postprandial responses to food and potential for precision nutrition. Nat Med 2020 Jun;26(6):964-973. doi: 10.1038/s41591-020-0934-0. Epub 2020 Jun 11.
Metabolic responses to food influence risk of cardiometabolic disease, but large-scale high-resolution studies are lacking. We recruited n = 1,002 twins and unrelated healthy adults in the United Kingdom to the PREDICT 1 study and assessed postprandial metabolic responses in a clinical setting and at home. We observed large inter-individual variability (as measured by the population coefficient of variation (s.d./mean, %)) in postprandial responses of blood triglyceride (103%), glucose (68%) and insulin (59%) following identical meals. Person-specific factors, such as gut microbiome, had a greater influence (7.1% of variance) than did meal macronutrients (3.6%) for postprandial lipemia, but not for postprandial glycemia (6.0% and 15.4%, respectively); genetic variants had a modest impact on predictions (9.5% for glucose, 0.8% for triglyceride, 0.2% for C-peptide). Findings were independently validated in a US cohort (n = 100 people). We developed a machine-learning model that predicted both triglyceride (r = 0.47) and glycemic (r = 0.77) responses to food intake. These findings may be informative for developing personalized diet strategies. The ClinicalTrials.gov registration identifier is NCT03479866.