What about people who say ‘There is no evidence for diet in MS’?

What about people who say ‘There is no evidence for diet in MS’?

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 people entering the study 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 my book ‘Overcoming Multiple Sclerosis’.

Many people fall into the trap of asserting that there is no evidence base for this approach. As one of the key figures in the development of evidence- based medicine stated: “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 real 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. I prefer to have hope that I will be like others before me 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 progressing; disease progression in MS is far from inevitable.

Some interpret my strong support of diet (and other lifestyle approaches) in MS management as being somehow in conflict with drug therapy. I do not see any 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 analysed, were mostly due to the disease worsening. This failure to perform intention-to-treat analyses seriously weakens the studies. And the studies were drug company sponsored; we know that drug company sponsored studies are more likely to be favourable to a company’s product than independently conducted research3; authors of company-sponsored research are more than five times as likely to recommend the company drug as independent authors, regardless of results4; and researchers with industry connections are far more likely to favour 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 be covered 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 four weeks’ supplementation with fish oils.6 IL-1beta, IL-2, IFN-gamma and TNF-alpha were significantly decreased. The decreases were more pronounced after three and then six 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 system 9,10, 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 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