#DietSpeak: is there an ideal MS diet?

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.

CoI: multiple

Twitter: @gavinGiovannoni         Medium: @gavin_24211

#T4TD: biohacking

Did you know two lifestyle options, i.e. exercise and diet, are probably the most effective add-on neuroprotective therapies for treating MS? 

Exercise induces long-lasting changes in the brain, which includes upregulation of growth factors and release of endorphins, that are almost certainly neuroprotective. Similarly, diets (caloric restriction, intermittent fasting and low-carbohydrate ketogenic) stimulate metabolic pathways that are both anti-inflammatory and neuroprotective. Why would someone with MS not want to hack their metabolism to derive these benefits? 

CoI: none in relation to this post

#T4TD = Thought for the Day

P.S. Please note that if you are overweight you need to lose weight first to exercise properly. Exercise, without a change in your diet, is not an effective weight-loss strategy.

Marmite on toast: the social crisis and MS

Recently one of my patients chastised me for telling her off for her poor diet, which consisted mainly of bread. She lives alone, which may explain why she eats so poorly. She has marmite or jam on toast for breakfast, a sandwich for lunch and if she feels hungry another piece of toast for dinner.

Interestingly, my mother used to refer to her elderly stepmother as a tea-and-toast lady and I never knew why until I became a doctor. My step-grandmother, we used to call her Aunty Betty, didn’t do marmite but stuck to marmalade. She prefered lime to orange marmalade suggesting she had at least preserved her senses of taste and smell. She lived into her late 80’s and died of frailty. For those of you who don’t know the tea-and-toast syndrome is well described. The following excerpt is from Wikipedia:

“Tea and toast syndrome is a form of malnutrition commonly experienced by elderly people who are unable to prepare meals and tend to themselves. Their diets often dwindle to tea and toast resulting in a deficiency of vitamins and other nutrients. The syndrome often manifests itself as hyponatremia, a low concentration of the electrolyte sodium in the bloodstream, due to the lack of salt in the diet.

The syndrome often occurs once children have moved away, and a partner has died or is dying. An elderly person with nobody left to cook for, or without the skills to cook, will revert to a diet of simple foods such as bread, cheese and crackers, and canned foods. According to the New York Times, as many as 60% of seniors living at home are either malnourished or at risk of becoming malnourished. In addition to the problems lack of nutrients will cause, this state also means that the complications of other illnesses, even the common cold, can be much more severe.

Factors that lead to the syndrome include social isolation, psychological issues such as depression, illness, and physical limitations. Though less of a factor than psychological issues, the increased number of medications often taken by elderly people can also affect eating habits. These medications may suppress appetite, make food taste different, or affect how nutrients are absorbed, making it even less likely seniors will get the required nutrients. Typical laboratory findings for tea and toast syndrome include a low serum osmolality (hypotonicity) with a normal urine osmolality since antidiuretic hormone levels are normal.”

Maybe I should update the Wikipedia entry to include multiple sclerosis and other socially-isolating chronic conditions as a cause of this syndrome?  Interestingly, my patient is not underweight, which implies she is getting enough calories. She wants to eat other food, but simply can’t afford more nutritious meals, nor does she have the physical energy to cook because of her MS. Her story is not unique. Three years ago when we did a dietary audit of a group of our Barts-MS patients I was horrified at how poor their diets were in general. Most of our patients eat large quantities of cheap processed foods. The main reason is cost and convenience. I suspect with increasing austerity over the last few years things could have only gotten worse and may get even worse if food prices rise, as predicted, if and when Brexit goes ahead.

An editorial in last week’s British Medical Journal, by Michael Marmot, does not pull any punches. It explains why the social crisis is leading to a health crisis with knock-on effects. Marmot in his final paragraph states: ‘A stalling or reversal of long term improvements in health and increases in health inequalities are of great concern to anyone who cares about health’.  This applies to me as a neurologist working in the NHS. I see the impact of austerity and the social crisis is having on my patients week after week and it is getting worse. The question is what can we do about it? Yes, we. This is not something that can be tackled by one person it is something society has to address.

Our second variance meeting in relation to MS services, called ‘Raising the Bar’, in Birmingham next month (8th & 9th July) has a workstream dedicated to the social determinants of health. At the end of year 3, we want all participating centres to be working differently and managing MS holistically. This will include programmes to screen and manage comorbidities and promote lifestyle interventions. To make sure it is not only MSers in the top echelons who benefit most from changes in service provision we want all HCPs to adopt a ‘no patient left behind’ philosophy as part of this holistic management and embed this philosophy in all MS services.

How we make this happen with fewer resources is going to require ingenuity and a different way of working. We are going to have to create disruptive new systems to make sure that all people with MS, who are covered by a particular service, have access to that service.  We don’t want vulnerable, less educated, ethnic minorities or less well off patients to be disadvantaged by the service.

This is why we are reaching out to all HCPs and people with MS and their families to help us change the current and outdated ‘Victorian’ model of healthcare, which is configured around the HCP and to make the person with the disease the person who controls their care. I anticipate the changes happening gradually and incrementally; one brick at a time. By linking the changes to a national audit and the MS Academy, a platform to share best practice and resources, we will hopefully create an environment that will transform the way people with MS are managed in the NHS.

What concerns me, however, is how do we tackle the social crisis? Our patients not having enough money to buy food or access transport to attend group therapy to tackle social isolation? Surely we need more resources for the NHS and social care? Marmot politicises his Editorial by linking the social crisis to changes in government: ‘In the UK, the fact that the break in the long term rise in life expectancy began in 2011 and has been accompanied by an increase in health inequalities must lead to serious questions about whether the government elected in 2010, with its flagship austerity policies, made a difference for the worse’. This makes you worry that under the current government there will simply be no new resources for implementing our ideas. This raises many challenges and will make the task harder. We may have to mobilise a volunteer army of helpers or we are going to have to show senior NHS managers that the changes we are proposing will save the NHS money.

In a parallel editorial to Marmot’s, Rajan and Mckee remind HCPs that we have a duty to speak out. The following are a few excerpts:

…. Nothing Left in the Cupboards, by Human Rights Watch, describes a country in which tens of thousands of families lack enough food to live on. The second report, by Philip Alston, the UN special rapporteur on extreme poverty and human rights, also examines food poverty but goes much broader, covering the many ways in which successive British governments have been “dismantling the social safety net.” Neither report makes comfortable reading for the British government. The Human Rights Watch report talks of “a grim picture of the grinding reality that teachers are dealing with,” with children arriving at school hungry, without warm clothes or dry shoes. Alston describes a situation that is not just “a disgrace, but a social calamity and an economic disaster rolled into one.”…..

…… In 2002, Derek Wanless published a landmark report commissioned by Gordon Brown, then chancellor of the exchequer. It concluded that sustainable NHS funding into the future required a “fully engaged” scenario, with investment in action on the determinants of health allowing people to live longer in better health. Yet, since 2010, mortality has been stagnating and, for some groups, increasing……

……Yet the British government is currently in a state of near paralysis as it struggles with the Brexit process. And as Alston notes, “If Brexit proceeds, it is likely to have a major adverse impact on the most vulnerable.” When added to the damage that any Brexit will do to the NHS, the outlook is extremely concerning…..

…… Over 150 years ago Rudolf Virchow said that doctors are “natural advocates of the poor.” When, as Alston argues, “the government has remained determinedly in a state of denial,” it is time for all health professionals to stand up for those who are falling through the increasingly large holes in our social safety nets. We must do so not only for the individuals concerned but for the future of the NHS, which, as Wanless pointed out, cannot continue to pick up the pieces following failures by others…….

If the issues in this blog post affect you, or someone close to you, please do not hesitate to reach out to us or your local MS team. We are committed to improving the care we provide all of our patients with MS and that includes helping you with your social issues.  

Michael Marmot. A health crisis is a social crisis. BMJ 2019;365:l2278.

Rajan & McKee. NHS is picking up the pieces as social safety nets fail. BMJ 2019;365:l2360.

The new black death is ageing

I say to many of patients one of the most powerful predictors of progressive, or more correctly worsening, MS is ageing. Age also predicts recovery of function; the younger you are the better you do. This study shows that ageing restricts the ability of stem cells to make oligodendrocytes to promote remyelination.

As you are aware age also predicts response, or lack or response, to DMTs. The older you are the less effective DMTs are. The list linked to ageing and poor prognosis goes on ….

I have always said ‘life is a sexually transmitted neurodegenerative disease with a 100% mortality’. This usually gets a mutated laugh until people start pondering the joke and its implications and then gradually realise that I am being serious.

Evolution never designed, and selected, the human brain and nervous system to function much past the age of 35. It is only relatively recently that life expectancy has increased dramatically with the requirement of our brains to function into ‘old age’. It is clear that when we measure cognitive function, and brain volume, it is all downhill from about 35 years of age.

Those of us who are older than 35 notice the subtle cognitive impairments that increase with age and the gradual malfunction and deterioration in our nervous systems. When last have you tried tight-rope walking? Your failing balance system is simply a reflection of the global rot that is also shredding your cognition. Fortunately, we have enough reserve to adapt and cope with the slow decline in our mental faculties. However, if we live long enough we are all likely to become demented. Dementia in this setting is simply the reduction of cognition to a point when you can’t manage socially and occupationally. To prevent the inevitable consequence of ageing is there anything we can do to optimise our brain health so our ‘brains outlive’ our ‘bodies’?

There is a lot we can do to improve brain health. However, some of the interventions may require the administration of medications in the future. For the anti-ageing revolution to happen, and be adopted by society, we need to make ageing a disease.

By defining ageing as a disease it changes everything. Firstly, it creates incentives for the pharmaceutical industry to invest in the necessary R&D to get drugs to market. If ageing is a disease healthcare providers will pay for interventions. The corollary is that if ageing is not defined as a disease, any interventions to delay or modify ageing, will be limited to lifestyle interventions. By defining ageing as a disease it will allow us to develop tools for population screening to identify people who are either healthy or in the presymptomatic phase of known neurodegenerative disease. This will then allow us to test preventive strategies to delay the onset of symptomatic disease.

If on the other hand, you have MS we already know you have a neurodegenerative disease that shreds reserve capacity and brings forward ageing mechanisms, which is why we need to manage MS as early and as effectively as possible and holistically. This is why the new treatment target is ‘to maximise brain health for the lifetime of the person with MS’.

Please be aware that ageing is a biological process and hence we can target the biology with both lifestyle interventions and drugs. For example, recent evidence suggests metformin, a diabetes drug, may reverse some of the ageing programmes. Dimethyl fumarate (DMF), a licensed MS DMT, seems to activate antiageing pathways that overlap with pathways linked to specific dietary interventions, i.e. calorie-restricted, intermittent fasting and ketogenic diets. Should all MSers be on metformin and/or DMF and/or one of these diets? We need trials to test these hypotheses. But at least there are investigators exploring the questions.

Please let me know if you find the anti-ageing hypothesis of MS compelling; it overlaps with diet, sleep, exercise and many other things that I can discuss in future blog posts.

Rivera et al. Aging restricts the ability of mesenchymal stem cells to promote the generation of oligodendrocytes during remyelination. Glia. 2019 Apr 30. doi: 10.1002/glia.23624.

Multiple sclerosis (MS) is a demyelinating disease of the central nervous system (CNS) that leads to severe neurological deficits. Due to their immunomodulatory and neuroprotective activities and their ability to promote the generation of oligodendrocytes, mesenchymal stem cells (MSCs) are currently being developed for autologous cell therapy in MS. As aging reduces the regenerative capacity of all tissues, it is of relevance to investigate whether MSCs retain their pro-oligodendrogenic activity with increasing age. We demonstrate that MSCs derived from aged rats have a reduced capacity to induce oligodendrocyte differentiation of adult CNS stem/progenitor cells. Aging also abolished the ability of MSCs to enhance the generation of myelin-like sheaths in demyelinated cerebellar slice cultures. Finally, in a rat model for CNS demyelination, aging suppressed the capability of systemically transplanted MSCs to boost oligodendrocyte progenitor cell (OPC) differentiation during remyelination. Thus, aging restricts the ability of MSCs to support the generation of oligodendrocytes and consequently inhibits their capacity to enhance the generation of myelin-like sheaths. These findings may impact on the design of therapies using autologous MSCs in older MS patients.

CoI: multiple

Food coma: does it affect you?

This post explains why eating may exacerbate MS-related fatigue and what you can do to counteract it.

Do you suffer from food coma or excessive sleepiness and fatigue after eating a meal?

For ‘normal people’, we call this phenomenon postprandial somnolence or the siesta syndrome. Others refer to it as the ‘food coma’. It is my anecdotal experience that people with MS, in particular, people with more advanced MS, are particularly sensitive to postprandial sleepiness and fatigue. Why?

Postprandial somnolence (PPS) is a normal state of drowsiness or lassitude following a meal. PPS is a real phenomenon and has two components: (1) a state of perceived low energy related to activation of the parasympathetic nervous system in response to expansion of the stomach and duodenum from a meal. In general, the parasympathetic system slows everything down.  (2) A specific state of sleepiness, which is triggered by the hormone cholecystokinin (CCK) that is released in response to eating and changes in the firing and activation of specific brain regions. The reflexes responsible for PPS are referred to as neurohormonal modulation of sleep through the coupling of digestion and the brain. The signals from the gut to the brain travel via the vagus nerve.

My index patient is so affected by PPS that she now only eats one meal a day; her evening meal. She does this quite late so that she can crash and sleep about an hour after eating. She is a professional and needs to be functional during the day and finds if she eats anything substantial in the day she simply can’t work because of her overwhelming desire to sleep. We have tried caffeine, modafinil and amantadine to counteract PPS, but they only had a small effect in counteracting her PPS and allowing her to work productivel. Other patients reporting this have noticed some benefit from stimulants. Interestingly, my index patient, like a few others, finds carbohydrate-rich foods particularly potent at inducing ‘food coma’

Physiologists think that not all foodstuffs are made equal when it comes to causing PPS and it appears that glucose, or sugar, induced insulin is one of the drivers of this behavioural response. I suspect this why people who fast or eat very low carbohydrate or ketogenic diets describe heightened alertness and an ability to concentrate for much longer periods of time.

The reason for doing this post is to find out how common PPS is in the MS population and to give you some simple advice to counteract it. If you suffer from PPS can I suggest you review your diet and see if you identify ways to modify your eating habits and/or diets to coounteract PPS?

  1. You could adopt the above extreme solution and only eat one meal per day. Clearly, this not for everyone and is very difficult to implement. I say this, but many of my Muslim patients report feeling so much better during Ramadan when they essentially practice this type of eating pattern.
  2. You could reduce your meal size and cut out any carbohydrates from your daytime meals. You may find this difficult because it takes time for your metabolism to become optimised for ketosis. If any of you are interested in the science of ketosis I have written a Medium post on ketogenic and low-carbohydrate diets.
  3. Some of my patients find micro-meals helpful, i.e. instead of large meals you eat multiple small snacks during the day.
  4. The judicious use of stimulants. I tend to recommend caffeine, followed by modafinil and them amantadine. Please note you should probably not take stimulants later than about 3-4 pm as they have a long half-life and can cause insomnia.
  5. Some of my patients have also reported that exercise has helped them deal with PPS. I am not sure how exercise works except by possibly lowering glucose and insulin levels and improving insulin sensitivity. The latter will reduce hyperinsulinaemia that will not only cause PPS, but is an impotant driver and component of the metabolic syndrome.

Please note that PPS will be worse if you suffer from a sleep disorder and suffer from daytime sleepiness. Most pwMS have a sleep disorder so there is little point in focusing on PPS and ignoring the elephant in the room.

If you have a few minutes to spare can you please complete this survey and let us know if you come across any other effective treatments to manage your PPS.