What diet?

It is easy saying you are what you eat, but what happens when you can’t afford to eat healthily and/or depend on hand-outs?

The Trussel Trust food banks, which mission is to stop UK hunger, handed out 1,332,952 three-day emergency food supplies in the financial year 2017–2018. This is a 46% increase compared to 5 years ago. These figures are on a backdrop of the government claiming record unemployment rates and a growing economy. Employment and a growing economy for whom?

If you have a chronic disease such as multiple sclerosis you are more likely to be unemployed and more likely to be reliant on benefits. This is why I found it so upsetting when one of my patients told me a few weeks ago that they couldn’t afford to buy healthy foods and had to rely on cheap ready meals purchased from the corner shop. This is the reality of living with MS in the UK for some.

Last week Anna Taylor, the executive director of the Food Foundation, in a BMJ Opinion article stated ‘that in the poorest 20% of households, buying a healthy diet would use 42% of disposable income’. She went on to say ‘Food insecurity can create immense stress and anxiety in households, and it contributes to irregular eating patterns and a pressure to buy the cheapest calories to alleviate hunger….. If we can record the scale of the problem, it’ll be the first step towards changing it’.

With this backdrop, I find myself between a rock and a hard place. I want to give dietary advice based on science, but my advice would put my patients under increasing financial strain.

I am always being pressurised into giving dietary advice to my patients and to comment on ‘quack’ and ‘fad’ diets that have many loyal followers without the evidence to support their utility in managing MS. My default position has been to fall back on the British Heart Foundation’s dietary recommendations, but even these are not ‘evidence-based’ and are heavily criticised from some quarters.

Tackling the issue from a scientific approach and looking at experimental data from animal studies caloric restriction, intermittent fasting and ketogenic diets have all been shown to neuroprotective and trigger anti-ageing mechanisms. Are these diets feasible as an adjunct to treating MS?

Caloric restriction leads to hunger and loss of muscle mass, which may exacerbate MS-related weakness. Therefore, caloric restriction is not a good idea and simply does not work long term.

What about intermittent fasting? This is easier said than done and then which fasting protocol would you use? Some of my patients use the 5:2 diet, others do 3–5 days of fasting every one to three months and others use the so-called 16/8 diet.

What is the 5:2 diet? Eat what you want five days a week, eat next to nothing for two. The simplicity of the diet and the fact you can eat pretty much what you like five days a week, are the reason why it is so popular. Dieters are recommended to consume a ‘normal’ number of calories five days a week and then, for two, non-consecutive days, eat just 25% of their usual calorie total — 500 calories for women and 600 for men.

What is the 16/8 diet? 16/8 intermittent fasting involves limiting consumption of foods and calorie-containing beverages to a set window of eight hours per day and abstaining from food for the remaining 16 hours. This cycle is repeated from just once or twice per week to every day. In addition to enhancing weight loss, 16/8 intermittent fasting is claimed to improve blood sugar control.

Intermittent fasting is likely to work and improve MS symptoms, but until more data emerges on which protocol to promote I am reluctant to make a general recommendation to my patients about intermittent fasting. Despite this, I think it is a good idea.

The ketogenic diet or variants of this diet, such as low-carbohydrate high-fat (LCHF, Banting, Ducan, etc.) and/or high-protein diets (Atkin’s) are easier to do because they don’t require caloric restriction and/or fasting. Therefore they don’t cause hunger or loss of muscle mass.

At ECTRIMS last year a pilot study was presented which showed that a ketogenic diet is feasible for pwMS and it has the added advantage of improving fatigue & depression, weight loss and the overall metabolic profile (see below). Another advantage is that ketogenic diets deal with food coma or post-prandial hypersomnolence that is a recognised problem in people with multiple sclerosis.

I have previously written about the science behind ketosis and why a low-fat diet, the corollary of a ketogenic diet, is bad for you. Although the case for trying a ketogenic diet in MS is overwhelming we need more evidence to make the claims that it is neuroprotective. Like other aspects of science, we need to reproduce studies, so that we can be confident the findings are real.

In summary, the scientific evidence supports ketosis as a potential treatment for multiple sclerosis, but the problem I have is that a ketogenic diet is expensive. Swapping out processed carbohydrates for fats and protein costs money. We as a society have allowed the food landscape to change so much that we are finding it difficult to wind back the clock and eliminate sugars and processed carbohydrates from our diets.

So when pwMS are poor and are on the breadline how can you tell them to try a ketogenic diet? You can’t, therefore the best default position is to simply do what you have been doing for decades and to fall back on the British Heart Foundation’s dietary recommendations. However, the more I research the field the more I realise that this position is untenable. What should I do about it?

Brenton et al. Application of a modified ketogenic diet in relapsing-remitting multiple sclerosis: a pilot study. ECTRIMS Online Library. Brenton J. Oct 11, 2018; 228801

Introduction: Dietary intake influences an individual’s immune profile and response. The impact of diet in multiple sclerosis (MS) is clinically meaningful, with evidence supporting an association between diet and disability. Ketogenic diets (KDs) are high-fat, low-carbohydrate diets that attenuate pro-inflammatory pathways, reduce oxidative stress, and promote mitochondrial biogenesis. The tolerability of KDs in the MS population is unknown.

Objectives/aims: To provide evidence of tolerability of a KD in relapsing MS patients and elucidate effects of a KD on common MS co-morbidities.

Design/methods: Twenty patients with a diagnosis of relapsing-remitting multiple sclerosis that had been clinically- and radiographically-stable for at least 1 year were enrolled. Subjects were educated in-person by a trained dietitian on how to adhere to a modified KD (i.e. modified Atkins). Adherence to diet was objectively monitored by daily urine ketone testing. Patient-reported fatigue and depression outcome measures and fasting laboratory values for insulin resistance, liver function, electrolytes, and adipokines (leptin/adiponectin) were obtained at baseline (pre-diet) and after 6 months of treatment. Brain magnetic resonance imaging was obtained at baseline and 6 months.

Results: No subject experienced worsening clinical or radiographic disease while on diet. Improvements were noted in both fatigue (p=0.04) and depression scores (p=0.03), and reductions in body mass index (BMI) (p=0.003). Insulin resistance and serologic leptin levels were significantly reduced at 3 months, independent of BMI change (p=0.01). Longitudinal data collection is ongoing.

Conclusions: KDs in relapsing-remitting MS patients appears to be safe, feasible, and well-tolerated. A modified ketogenic diet improves common MS-comorbidities, such as fatigue and depression scores, while also serving to produce weight loss and reduce levels of serologic, pro-inflammatory adipokines.