Diet

This is a complex subject. The protein butyrophilin is a component of the membrane of the fat globules in cow’s milk. Closely related proteins are found in the fat globule membranes of the milk of many other species (goat, sheep, etc.). It is one of the proteins that has been implicated in molecular mimicry in MS causation, along with BSA (bovine serum albumin). BSA is also found in the muscle of cows (beef), along with proteins similar in structure to butyrophilin. It is not clear whether butyrophilin in the milk of other species or butyrophilin-like proteins from muscle are potentially involved in MS causation, as only butyrophilin from cow’s milk has been studied in laboratory research. However, on balance it seems wise to avoid the milk of animals other than humans. The principal reason to avoid meat in MS is because the saturated fat content of meat, although not specifically studied to date, contains proteins like BSA and butyrophilin-like proteins, which may also be an issue.

We hope that helps make sense of a complex issue.

This is actually not an exact science and is quite complex. Our recommendations come from a synthesis of many sources. Omega-3s are helpful in MS in two ways:

  • In a structural way, in forming part of the body’s cell membranes and making them more pliable and soft (due to their low melting points)
  • In an immune way, as they are the precursors of the cytokines and eicosanoids that the immune system Th2 cells secrete to dampen down inflammation

If one is eating an ultra-low saturated fat diet, as with the OMS program, it doesn’t take much omega-3 to get a structural benefit; i.e., an improvement in the pliability and resilience of cell membranes. It takes quite a bit more to get the optimal immune benefit. That is why the standard dose (often recommended by specialists) of 3g a day of fish oil is inadequate; it doesn’t really provide the immune system benefit.

In studies where they have measured the dose of omega-3s to get the optimal immune benefit, they have used standard-strength fish oil. This has 120mg DHA and 180mg EPA in each 1,000mg (1g, or 1ml) capsule (i.e., a total of 300mg DHA/EPA combined). The studies suggest that a dose of around 20g (20mls or 20 capsules) of this standard-strength fish oil gives you the optimal immune benefit. You can of course get refined fish oil where these constituents (the actual total omega-3s DHA and EPA) are concentrated, and so this dose needs to be adjusted accordingly. If for instance a super-strength fish oil had 240mg DHA and 360mg EPA in each capsule, you would need to take only 10 caps. The calculation for flaxseed oil is much more complicated, as it contains ALA, which is converted in the body to DHA and EPA, but the percentage conversion varies from person to person (see pages 288-290 in the OMS book). To simplify matters, we recommend the same dose (20mls) once you have been on the diet and taken fish oil supplements for a while and already have high tissue levels of DHA and EPA.

One of the issues with all oil supplements is that they contain saturated fat; fish oil contains around 30% and flaxseed oil around 9%. The figure of 20mls (20g, 20 capsules) of standard fish or flaxseed oil we recommend is a minimum to achieve the immune benefits, but more can be taken, particularly if oil intake from other sources is very limited. The body really does need some oil, and people can get dry skin and hair and lose energy if there is too little fat in the diet.

If you feel you need more oil, then increase your flaxseed oil dose, because it contains the least saturated fat. Many people prefer to stop counting, and they just use flaxseed oil regularly on their pasta, baked potatoes, salads, etc. (after cooking of course). It is quite delicious used in this way once you are used to it. In reality, people probably get more like 30-40mls/day using flaxseed oil in this way, and that is still in accordance with the OMS program, and may well result in more energy as well as a potent structural and anti-inflammatory effect.

Legumes, including soy, are extremely healthy foods and are full of protein, which is useful for people not eating animal products. They have been used for centuries by many societies, and there is no clear documentation of any health problems associated with their use. Some have suggested that people with immune-based diseases should avoid them, but there appears to be no strong basis for this suggestion. Soy in particular would appear to have many advantages over dairy products, and most studies suggest better health outcomes for those consuming soy products regularly.

Gelatin is not a problem in relation to MS. While it is an animal product, it contains no saturated fat. However, some people are either allergic to the capsules or have ethical concerns, so they may try to source non-gelatin products, which tend to be more expensive and less widely available.

There is sufficient iron in this diet to keep most people from getting anaemic, although women with heavy periods may find they get iron-deficient. Iron is found in a variety of vegetables. It is possible to get tested at the local doctor for iron deficiency if it is suspected. If you have low iron, a natural herbal iron replacement like Floradix is recommended.

There is abundant calcium in the OMS diet. The real problem with calcium in Western societies is lack of sunlight. Sunlight results in vitamin D being produced in the body, and vitamin D’s main job is to absorb calcium from the diet. A whole calcium supplementation industry has grown in Western countries as a result of sun avoidance. Foods such as dairy are heavily promoted as being healthy because they contain calcium, ignoring the real health problems they may cause. With adequate vitamin D from sun or supplements, there is no problem with inadequate calcium. Osteoporosis is also unlikely for people who get enough vitamin D.

It is incorrect to say there is no evidence for diet in MS. Swank’s 34-year study of a low saturated fat diet supplemented with polyunsaturated fatty acids was a landmark study in MS.1 Naturally, given that the study began in 1949, it was not a randomized controlled trial, as these had not yet been devised. It was, however, a prospective clinical intervention study supported by grants from the MS Society of Canada, the Montreal Neurological Institute, the Department of Health and Welfare of Canada, the MS Society of Portland and other sources. Data collection on diet was meticulous over 34 years. Only 6 of 150 subjects dropped out, and the differences in outcomes between those who adhered to the diet and those who did not were astounding. People on the diet essentially did not deteriorate significantly over 34 years. No other treatment has come close to the magnitude of this effect.

But Swank is only part of the diet story. We have strongly supportive data from laboratory and animal research, epidemiological research, case-control studies, observational cohort studies and a randomized controlled trial to support the view that this diet profoundly modifies MS progression. Indeed, I can find no literature that is in conflict with these data. The evidence base behind these and other lifestyle approaches to MS is covered in much more detail in the book “Overcoming Multiple Sclerosis.”

Many people fall into the trap of asserting that there is no evidence base for this approach. As noted in one of the key studies in the development of evidence-based medicine: “Evidence-based medicine is not restricted to randomized trials and meta-analyses. It involves tracking down the best external evidence with which to answer our clinical questions… If no randomized trial has been carried out for our patient’s predicament, we follow the trail to the next best external evidence and work from there.”2 The literature supporting diet in MS is wide-ranging, congruent and highly persuasive.

It is disappointing to see people occasionally saying that a dietary approach to MS just gives people false hope. There is no such thing as false hope. If one person can be diagnosed with MS and live a long, healthy life without further problems, then that is all that is needed for anybody else to have genuine hope that they too can be like that person. The real problem is that often MS societies and doctors give us “false no hope” — that is, they make us believe that all of us will be disabled eventually. We prefer to have hope that we will be like others before us who have remained well, many of them in Swank’s study. It is entirely reasonable to have the real hope that diet and other therapies may stop the disease from progressing. Disease progression in MS is far from inevitable.

Some interpret our strong support of diet (and other lifestyle approaches) in MS management as being somehow in conflict with drug therapy. We see no conflict. Why would people not do everything possible to stop the progression of this serious illness? To imply that drug therapies are proven, effective therapies, and diet is not, is to ignore the serious methodological problems with the drug trials, particularly the interferon studies. Because of easily detected side effects, these studies were essentially unblinded studies, and they did not account for drop-outs, which — when analyzed — were mostly due to the disease worsening. This failure to perform intention-to-treat analyses seriously weakens the studies. And the studies were sponsored by drug companies. We know that:

  • Drug company-sponsored studies are more likely to be favorable to a company’s product than independently conducted research3
  • Authors of company-sponsored research are more than 5 times as likely to recommend the company drug than independent authors are, regardless of results4
  • Researchers with industry connections are far more likely to favor company products.5

Importantly, the trials have not been at all convincing in showing any effect on disease progression.

It has been said that there is no plausible biological mechanism by which diet works in MS. There is too large an evidence base on the anti-inflammatory effects of vegan diets and the neuroprotective effects of PUFA supplementation to cover here. In short, the effect of essential fatty acid intake on eicosanoids has been studied in great detail in people with MS. Gallai and co-workers showed that there was a marked decrease in pro-inflammatory chemicals after only 4 weeks’ supplementation with fish oils.6 IL-1beta, IL-2, IFN-gamma and TNF-alpha were significantly decreased. The decreases were more pronounced after 3 and then 6 months. The pro-inflammatory eicosanoids PGE2 and LTB4 were also decreased. These eicosanoids have been shown to be involved in causing relapses in MS patients.7,8 McCarty proposes a number of theories why vegan diets plus fish oil and vitamin D may be of wide-ranging benefit to people’s health, largely through their effects on the immune system9,10, and UK scientists have added new experimental evidence for the benefits of fish oil in regulating inflammation.11 Das has also published extensively on the anti-inflammatory effects of fish-based Mediterranean-type diets.12-14

It is quite reasonable for people with MS to use diet in their quest for health, and to enthusiastically embrace the potential of staying well through their own efforts, with real hope and confidence in their futures.

References:

  1. Swank RL, Dugan BB. Effect of low saturated fat diet in early and late cases of multiple sclerosis. Lancet 1990; 336:37-39
  2. Sackett DL, Rosenberg WM, Gray JA, et al. Evidence based medicine: what it is and what it isn’t. BMJ 1996; 312:71-72
  3. Bodenheimer T. Uneasy alliance–clinical investigators and the pharmaceutical industry. N Engl J Med 2000; 342:1539-1544
  4. Als-Nielsen B, Chen W, Gluud C, et al. Association of funding and conclusions in randomized drug trials: a reflection of treatment effect or adverse events? JAMA 2003; 290:921-928
  5. Stelfox HT, Chua G, O’Rourke K, et al. Conflict of interest in the debate over calcium-channel antagonists. N Engl J Med 1998; 338:101-106
  6. Gallai V, Sarchielli P, Trequattrini A, et al. Cytokine secretion and eicosanoid production in the peripheral blood mononuclear cells of MS patients undergoing dietary supplementation with n-3 polyunsaturated fatty acids. J Neuroimmunol 1995; 56:143-153
  7. Calabrese V, Bella R, Testa D, et al. Increased cerebrospinal fluid and plasma levels of ultraweak chemiluminescence are associated with changes in the thiol pool and lipid-soluble fluorescence in multiple sclerosis: the pathogenic role of oxidative stress. Drugs Exp Clin Res 1998; 24:125-131
  8. Toshniwal PK, Zarling EJ. Evidence for increased lipid peroxidation in multiple sclerosis. Neurochem Res 1992; 17:205-207
  9. McCarty MF. Upregulation of lymphocyte apoptosis as a strategy for preventing and treating autoimmune disorders: a role for whole-food vegan diets, fish oil and dopamine agonists. Med Hypotheses 2001; 57:258-275
  10. McCarty MF. A moderately low phosphate intake may provide health benefits analogous to those conferred by UV light – a further advantage of vegan diets. Med Hypotheses 2003; 61:543-560
  11. Flower RJ, Perretti M. Controlling inflammation: a fat chance? J Exp Med 2005; 201:671-674
  12. Das UN, Ramos EJ, Meguid MM. Metabolic alterations during inflammation and its modulation by central actions of omega-3 fatty acids. Curr Opin Clin Nutr Metab Care 2003; 6:413-419
  13. Chrysohoou C, Panagiotakos DB, Pitsavos C, et al. Adherence to the Mediterranean diet attenuates inflammation and coagulation process in healthy adults: The ATTICA Study. J Am Coll Cardiol 2004; 44:152-158
  14. Zampelas A, Panagiotakos DB, Pitsavos C, et al. Fish consumption among healthy adults is associated with decreased levels of inflammatory markers related to cardiovascular disease: the ATTICA study. J Am Coll Cardiol 2005; 46:120-124

There is a lot of discussion about whether flaxseed oil is “as good” as fish oil. Given that our oceans are gradually becoming more polluted, particularly with heavy metals like mercury, and that heavy metals are known to cause neurological problems, it would be good if a plant-based oil like flaxseed oil could provide all our omega-3 needs.

The problem is that the fatty acid in flaxseed oil, alpha linolenic acid (ALA), needs to be converted in the body to the fish oil fatty acids, eicosapentaenoic acid (EPA) and then docosahexaenoic acid (DHA). I have seen various figures put on this conversion, mostly up to 10% of it being converted, dependent on general health, saturated fat consumption, alcohol consumption, and a number of other variables. Udo Erasmus in his excellent book “Fats That Heal, Fats That Kill” does the best calculation I have seen on this. Erasmus quotes a figure of 2.7% per day of the ALA being converted to EPA. He says that this figure is likely to be higher for people getting all the essential nutrients from diet and supplements. As most people’s fat deposits contain about 2% ALA (quite a bit higher for those following the diet and supplements here), this is about 200g of ALA, which could make about 5,400mg of EPA (as there is 180mg EPA in a 1,000mg capsule of fish oil, this is equivalent to about 30 of the 1,000mg capsules of fish oil).

If there is no ALA in your fat deposits at all (if you had been taking no omega-3s in your diet whatsoever), then just taking two tablespoons of flaxseed oil would supply enough ALA to make about 378mg of EPA, equivalent to what is in two 1,000mg fish oil capsules. But as can be seen from the above calculation of body stores, most people have enough stored, if they are supplementing every day, to make quite adequate amounts of EPA and DHA.

The advantage of doing it this way, rather than taking it as fish oil, is related not only to chemical toxins like mercury in fish oil (and to questions about the sustainability of our fish stocks), but also to the fact that EPA made this way is fresher, in the body every day. Another bonus: there is minimal saturated fat intake this way, as fish oil contains quite a bit of saturated fat. I prefer to take two dessert spoons of flaxseed oil a day (20mls) on the days when I don’t eat oily fish.

My suggestion would always be to use therapies that have been shown in trials to be helpful in MS, or that have shown equivalence with such therapies in well-designed clinical trials. For the New Zealand green-lipped mussel extract (Lyprinol), it is too early to tell, as most studies are in experimental models rather than patients, but the effect is likely to be small.

We have had success with SLE (lupus), Sjogren’s syndrome and rheumatoid arthritis. The diet and supplements, sunlight, meditation and stress management are very anti-inflammatory and so are helpful for most immune-based conditions. They are also anti-degenerative, and you would expect to get some benefit in degenerative conditions like Parkinson’s disease, dementia, macular degeneration and so on.

Sounds like you are doing fantastically well. You are not getting anything wrong. Your issue is clearly your family history of hypercholesterolemia. That means that you have a genetic predisposition to making more cholesterol in your own body. The good news is that all the things you are doing are preventing it from being higher. The only slight change that might help bring it down would be to increase omega-3 supplements. You are only taking 4,000mg at this stage (i.e., 4 caps). I recommend 20. But I would add them as pure liquid flaxseed oil, spooned over dinner (pasta, salad, baked potatoes, etc.). I would increase that to perhaps 30mls a day. That should make a difference. But remember, the aim is to stay well, and you are! These are just numbers.

They all appear to contain the offending protein, butyrophilin, as per this old piece of research:

Lipid globule membranes were isolated from human and bovine milk and from the milk of sheep, goat, pig, rat and guinea pig, and their polypeptide compositions were analyzed. The major polypeptides with molecular weights similar to that of bovine butyrophilin were separated by gel electrophoresis, isolated and characterized with respect to isoelectric point, molecular weight, immunological cross-reactivity and peptide composition after proteolytic cleavage. We show that in all species examined, these proteins are similar to bovine butyrophilin in (i) their relative insolubility in buffers of low and high ionic strength and in non-denaturing detergents, (ii) the occurrence of several isoelectric variants, and (iii) patterns of peptides obtained by protease digestion. It is concluded that closely related proteins are major constituents of the cytoplasmic coat structures associated with milk lipid globule membranes of many species, and we propose the name butyrophilins for this group of proteins. Bovine and human butyrophilins are glycosylated with relatively large amounts of glucosamine, mannose, glucose and galactose but little fucose, sialic acids or galactosamine. Most if not all of the sugar residues are associated with an acetone-soluble peptide fragment of Mr 12,000-16,000 focusing at about pH 4.0. We suggest that this fragment contains a membrane-spanning peptide sequence and is involved in the attachment of the cytoplasmic coat to the membrane of the milk lipid globule.

Reference:
Heid HW, Winter S, Bruder G, Keenan TW, Jarasch ED. Butyrophilin, an apical plasma membrane-associated glycoprotein characteristic of lactating mammary glands of diverse species. Biochim Biophys Acta 1983;728:228-38

There is a lot of controversy about the oils in coconut and their effect on health. While some reputable authorities like Udo Erasmus argue that the short chain fatty acids in coconut may be quite healthy, Swank was very clear in eliminating coconut from the diets of those in his landmark study. We know that most of the fats in coconut are saturated fats. One of the key issues with saturated fats is their melting point. If the melting point of a fat is above body temperature, then that fat will essentially behave in body cell membranes like a solid fat at body temperature, making the cell membranes rigid, inflexible and sticky, thereby encouraging degeneration and inflammation. It is worth noting that the melting points of the common fats in coconut are as follows:

  • Lauric acid (12:0 carbon chain) 44.2C
  • Myristic acid (14:0 carbon chain) 53.9C
  • Palmitic acid (16:0 carbon chain) 63.1C.

These fats are solid at body temperature and are likely to significantly worsen MS. We do not recommend them in any quantity.

Because, knowing that saturated fat is a real problem for people with MS, why take any in at all if you can avoid it. After a while, most people don’t miss meat at all.

These fats are cooked and ideally, it is best not to eat cooked and therefore altered fats. I think they should be avoided. Nuts (preferably uncooked) make a good snack.

No. The problem with chocolate is the cocoa butter, which is very high in saturated fat. Worse, there is an allowable limit of 15% altered fats in cocoa butter. Chocolate is just cocoa (which is a good, healthy product) that’s been turned into junk food.

A number of researchers contend that, in an evolutionary sense, legumes, and gluten in cereals, are relatively recent additions to the human diet. These protein-rich foods may be implicated in a host of autoimmune diseases, including MS. The most severe form of gluten intolerance is celiac disease. Here, people develop serious digestive system disorders due to an immune response to the gluten in wheat. One might expect, if gluten were a key ingredient to avoid in MS, that people with MS might have a higher incidence of celiac disease. Or vice-versa: that people with celiac disease might have a higher incidence of MS. A major population study published in mid-2007 examined 14,000 people in Sweden with celiac disease and compared them with 70,000 other people without the disease, who acted as controls.1 One would have expected a higher rate of MS (or other CNS degenerative disease) in those people with celiac disease than in the controls if gluten were involved in causing these diseases. But the researchers found no statistically significant association between celiac disease and subsequent MS, Parkinson’s disease, Alzheimer’s disease, hereditary ataxia, the symptom ataxia, Huntington’s disease, myasthenia gravis or spinal muscular atrophy. This is very strong evidence that there is no link with gluten.

If there were indeed a link, one would at least expect to find in people with MS antibodies to gluten, which would indicate intolerance. In fact, Italian researchers looking at 95 patients with MS found not a single patient with elevated antibody levels.2 UK researchers tested 49 patients with MS for their antibody levels and found 12% had raised levels. But this compared with 13% of unselected blood donors, so it was unlikely that people with MS had any special sensitivity to gluten.3 Iranian researchers tested 166 people with MS for antibodies and compared them to people without MS.4 They found no difference in antibody levels.

Italian researchers used an alternative approach to investigate this problem. They fed a gluten-free diet to animals with the experimental form of MS, EAE. The animals on the gluten-free diet initially had a more severe disease course.5 Later, they seemed to be doing better than those animals eating gluten. The study in my view provided an indeterminate result.

The molecular mimicry theory of MS causation is perfectly valid, and it probably explains why cow’s milk protein, for example, sets off the chain of events that leads to myelin attack by the immune system. We now have good evidence from the laboratory that a segment of cow’s milk protein is identical to a segment of myelin oligodendrocyte glycoprotein. The immune system, in setting up defenses against this foreign protein, is “tricked” into also attacking this part of myelin. Whenever something like this is proposed as an explanation for the immune attack on myelin, it is important to validate it against what we actually see in human populations.

For cow’s milk, this is easy. The world map of MS distribution is almost exactly the same as the world map of cow’s milk consumption. That is, there is almost a direct correlation epidemiologically between cow’s milk consumption and MS incidence. This is a kind of cross-check that the theory is correct. As a result, we strongly advise people to avoid cow’s milk.

For gluten, for example (or tomato for that matter), there are several major problems with the theory. First, there is no clear biochemical similarity between part of the gluten compound and myelin, as far as we are aware. Second, when we run the epidemiological cross-check, populations that consume wheat do not appear to have a higher incidence of MS than other populations do. A further cross-check is to see whether people who do develop autoimmunity to wheat (those with celiac disease) also get autoimmunity to myelin. The data show that there is not a higher incidence of celiac disease in those with MS or vice-versa. And finally, the animal data don’t support a link either.

So we advise people that gluten should be relatively safe. It is important to try to base these recommendations on evidence, not just theory, and we feel comfortable that the evidence does not sufficiently support a link with gluten to recommend avoiding it. Overall, the evidence of any effect of gluten in MS is not convincing enough to warrant changing our diet to exclude wheat products.

References:

  1. Ludvigsson JF, Olsson T, Ekbom A, et al. A population-based study of coeliac disease, neurodegenerative and neuroinflammatory diseases. Aliment Pharmacol Ther 2007; 25:1317-1327
  2. Salvatore S, Finazzi S, Ghezzi A, et al. Multiple sclerosis and celiac disease: is there an increased risk? Mult Scler 2004; 10:711-712
  3. Pengiran Tengah CD, Lock RJ, Unsworth DJ, et al. Multiple sclerosis and occult gluten sensitivity. Neurology 2004; 62:2326-2327
  4. Borhani Haghighi A, Ansari N, Mokhtari M, et al. Multiple sclerosis and gluten sensitivity. Clin Neurol Neurosurg 2007
  5. Di Marco R, Mangano K, Quattrocchi C, et al. Exacerbation of protracted-relapsing experimental allergic encephalomyelitis in DA rats by gluten- free diet. Apmis 2004; 112:651-655

Most people actually find that they feel better, but the real effect is on reducing the rate of relapses. This only becomes clear with time. It took people in Swank’s study 3 to 5 years to stabilize on the diet, that is, to get their relapse rates down to a minimum, although there was a big difference by about 9 to 12 months.

For optimal health, it is important to have both omega-3 and omega-6. These are essential fatty acids; health cannot be sustained without them. The right omega-6 to omega-3 balance ranges from about 2:1 to 4:1. This is much lower than the current ratio in our society of about 16:1 up to 25:1. It is the higher ratio that promotes inflammation.

Yes. All types of alcohol are OK in moderation. Moderation means not more than 2 standard drinks a day, with at least 2 alcohol-free days a week. Alcohol in excess is harmful to health. Moderation is required for reasons other than MS.

There is a general problem with pollution in our oceans, as in our land. The oceans are increasingly polluted, particularly with heavy metals like mercury. Mercury is concentrated in the flesh of bigger fish that eat smaller fish. So the higher up the food chain the fish is, the more mercury it will contain, in general. In some parts of the world, eating shark is banned because of the very high levels of mercury it contains. In smaller fish like sardines, there is much less of a problem. Some people may feel it is safer to get their omega-3s from flaxseed oil. That is quite reasonable after about 9 months of eating fish and/or taking fish oil, so as to get good tissue levels of the important fatty acids EHA and DPA.

Yes. Fish, scallops, lobster, prawns, crab, calamari, mussels, oysters, clams, crayfish – they’re all OK.