Postgraduate Medicine

ISSN: 0032-5481 (Print) 1941-9260 (Online) Journal homepage:

Diet and multiple sclerosis William H. Olson To cite this article: William H. Olson (1976) Diet and multiple sclerosis, Postgraduate Medicine, 59:5, 219-221, DOI: 10.1080/00325481.1976.11714369 To link to this article:

Published online: 07 Jul 2016.

Submit your article to this journal

View related articles

Full Terms & Conditions of access and use can be found at Download by: [Australian Catholic University]

Date: 21 August 2017, At: 19:30

dietand health

Downloaded by [Australian Catholic University] at 19:30 21 August 2017

special series

• Multiple sclerosis (MS) is a disease of the central nervous system which primarily affects the white matter. It is characterized by a localized inflammatory response which results in or is caused by destruction of myelin. During the inflammatory phase, a neurologie deficit related to the site of the lesion is present. Recovery of sorne but not ali of the lost function during remissions is usual. The lesions may occur in any part of the white matter, but sites of predilection are the periventricular areas, optic nerves, and white matter relating to the cerebellum. The diagnosis of MS is primarily clinical. A patient usually but not always may be found to have mild pleocytosis, slight elevation of prote in in the cerebrospinal fluid, and, on electrophoresis, an increase in gamma globulin. 1 The course of MS is highly unpredictable. Sorne patients suffer repeated attacks in rapid succession and become severely crippled or die within a short time while others show slow progression of the disease over decades. Steroid therapy may shorten the disability from an attack, but it has been established that chronic steroid therapy does not significantly alter the outcome of the disease. 2 It is presumed that sorne patients with unilateral retrobulbar neuritis have MS, even though vision returns almost to normal and a second attack does not occur. There is clear evidence that the incidence of MS is higher in sorne geographie areas than in others. The disease is more common in the high latitudes, and childhood locale tends to determine adult experience with the disease among persans who move to more southerly regions. There are many theories about the cause, with a majority of observers favoring an autoimmune or a viral hypothesis. Sorne consider it possible that MS has multiple causes. The striking geographie distribution has prompted several investigations of the possible role of diet as a cause.

diet and multiple sclerosis William H. Oison, MD University of North Dakota Fargo

The question of the role of diet in multiple sclerosis is far from settled, but sorne interesting theories have been advanced. The most promising one is inhibition of lymphocytic responsiveness by dietary linoleic acid. Manipulations of the diets of patients with this disease are not yet justified.

How Diet Might Influence Development of MS

ldentifying the dietary cause of a disease is difficult. Examples of dietary deficiencies that may result in damage to the central nervous system are thiamine deficiency (related to One of a special series of pa pers on diet and health coordinated by Dr. George V. Mann. Vanderbilt University School of Medicine, Nashville. Tennessee.

Vol. 59 • No. 5 • May 1976 • POSTGRADUATE MEDICINE


Ail these questions may not be answerable, but careful readers should at !east consider them. Review of Relevant Reports William H. Oison

Downloaded by [Australian Catholic University] at 19:30 21 August 2017

Dr. Oison is professor of neurology and chairman, division of neurology, department of neuroscience, University of North Dakota, Fargo.

Wernicke-Korsakoff syndrome) and vitamin B 12 deficiency (combined system disease, or subacute combined degeneration of the spinal cord). In Wernicke-Korsakoff syndrome, the basic defect probably is a combination of dietary deficiency and inhibition of absorption of thiamine by ethanol. In combined system disease, the basic defect in most cases is a Jack of intrinsic factor rather than a dietary deficiency of vitam in B 12 . Min amata disease is related to ingestion of seafood containing an excess of alkyl mercury compounds. It is conceivable that diet could influence the development of MS by aggravating a preexisting metabolic disorder (inherited or acquired), by opening the door for attack by an unrelated agent (virus), or by introducing into the body an unidentified taxie substance. How to Judge Claims Made for Diet in MS

Keeping in mind the unpredictability of MS and the difficulties in studying the disease, and considering the complexity of the hypothesis that diet is somehow related to its development, how can one judge therapeutic daims relative to diet and MS? In a ward, carefully. One should keep in mind the foiiowing questions when reading reports of studies on diet and MS: 1. What hypothesis is being tested? 2. How carefully does the investigator define MS? 3. How is the study controiied? (An uncontroiied study is at best anecdotal.) 4. What are the criteria for success or failure of the therapy? 5. Has the work been independently reproduced by another, equaiiy careful study? 6. Does a return to a "normal" diet result in reactivation of the disease?


Miiiar and associates 3 in 1973 reported the results of a double-blind study of diet and MS comparing the therapeutic efficacy of vegetable oil mixtures containing predominantly Iinoleic acid or oleic acid. As a rationale for the study, these investigators cited earlier writings suggesting (1) th at there are changes in the relative proportions of saturated and unsaturated fatty acids in the brain Iipids of patients with MS, (2) th at the amount of Iinoleic acid in the serum is reduced in MS, 4 • 5 and (3) that geographie distribution of the disease may be related to a dietary deficiency of polyunsaturated fatty acids. 6 In addition, Millar and associates had access to data on uncontroiied therapeutic trials in which replacement of saturated fatty acids in the diets of patients with MS with unsaturated dietary fats 7 gave promising results. The study conducted by Millar and associates3 was unusuaiiy weil designed and yielded the conclusion that patients with MS who received Iinoleic acid (unsaturated) fared better clinically than those receiving oleic acid (mono-unsaturated). Total duration of the study was two years. The leve! of serum fatty acids was monitored. Subsequent! y, polyunsaturated ac ids were reported to inhibit the responsiveness of lymphocytes, with Iinoleic acid effecting a greater degree of inhibition in patients with MS th an in COntrol SUbjeCtS. H If it iS aSSUmed th at Iymphocytic responsiveness is directly reIated to the development of the lesion of MS, this observation seems promising. At present, sorne controversy surrounds technical aspects of the inhibition of Iymphocytic responsiveness by Iinoleic acid. 9 • 10 Sorne studies have indicated that the amount of Iinoleic acid in the serum of patients with MS may not be reduced. 11 Field and Shenton 12 expressed the opinion that the value of diets rich in lino leie ac id as a treatment for MS needs confirmation by further study. Agranoff and Goldberg 13 have suggested that the relative predisposition to MS among persans residing in certain geographie areas



May 1976


Vol. 59


No. 5

Downloaded by [Australian Catholic University] at 19:30 21 August 2017

may be related to milk production or consumption, basing this observation on an analysis of milk consumption per capita and incidence of deaths from MS in several geographie regions. For the areas surveyed, the results are statistieally signifieant, but crities have pointed out that in certain areas of Africa the milk consumption per capita is very high and the incidence of MS is Iow. 14 Speculations by Agranoff and Goldberg 13 on how their observation might correlate biologically with MS ranged from a disturbance in lipid metabolism to a slow-virus infection transmitted through milk. They pointed out the possibility that any correlation could be spurious and stressed the need for additional epidemiologie study relative to the possible role of milk in the development of MS. Epidemiologie studies are extremely valuable when they suggest possible etiologie factors in the development of disease, but certainly much more work needs to be done before we proscribe milk consumption by patients with MS. Shatin15 set forth a different hypothesis, suggesting a relationship between the geographie distribution of MS and the cultivation of wheat. According to this hypothesis, the disease bas a high incidence in wheat- and rye-growing areas, bas a low incidence in corn-growing regions, and is virtually absent

in are as where cassava, millet, and riee are the staple foods. The hypothesis is expanded to suggest that gluten intolerance increases susceptibility to MS. Data to support the hypothesis are not supplied. Gluten-free diets have been tried in MS. Sorne individual accounts of such trials are favorable, 16 but larger studies conducted for longer periods seem to indieate that gluten-free diet bas no effect on the diseaseY Like the milk hypothesis, the wheat hypothesis needs more careful testing before wheat ingestion is proscribed. Conclusion

Many patients facing the reality ofhaving a chronie disabling disease will submit to almost any therapy, proved or not. Given the complexity of dietary influences on health and the unpredietability of multiple sclerosis, we will need to give our best scientifie efforts to study of this disease if its etiology is to be established. The most promising development bas been the linoleic acid hypothesis, but determining the validity of this and other relevant concepts may weil take years. At present, there is not sufficient evidence to justify dietary manipulations either as a preventive measure or as part of management of MS. • Address reprint requests to William H. Oison, MD, Neuropsychiatrie Institute, 700 First Ave S, Fargo, ND 58102.

References 1. Cosgrove JB, Agius P: Studies in multiple sclerosis. Il. Cornparison of the beta-garnrna globulin ratio, gamma globulin elevation, and first-zone colloidal gold curve in the cerebrospinal fluid. Neurology 16:197-204, 1966 2. Cooperative Study in the Evaluation ofTherapy in Multiple Sclerosis: ACTH vs. placebo: Final report. Neurology 20:1-59, 1970 3. Millar JH, Zilkha KJ, Langrnan MJ, et al: Double-blind trial of linoleate supplernentation of the diet in multiple sclerosis. Br Med J 1:765-768, 1973 4. Baker RW, Thompson RH, Zilkha KJ: Serum fatty acids in multiple sclerosis. J Neurol Neurosurg Psychiatry 27:408-414, 1964 5. Tichy J, Vyrnazal J, Michale CC: Serum lipoproteins, cholesterol esters and phospholipids in multiple sclerosis. Acta Neurol Scand 45:32, 1969 6. Allison RS: Sorne neurological aspects of medical geography. Proc Roy Soc Med 57:71-76, 1963. 7. Swank RL: Multiple sclerosis-twenty years on low fat diet. Arch Neurol 23:460-474, 1970 8. Mertin J, Shenton BR, Field EJ: Unsaturated fatty acids in

Vol. 59 • No. 5 • May 1976 • POSTGRADUATE MEDICINE

multiple sclerosis. Br Med J 1:777-778, 1973 9. Offner H, Clausen J: Inhibition of lymphocyte response to stimulants induced by unsaturated fatty acids and prostaglandins. (Letter) Lancet 2:400-401, 1974 10. Mertin J, Hughes D, Caspary EA, et al: Non-specificity of laboratory tests for diagnosis of multiple sclerosis. Br Med J 4:567-569, 1974 11. Wolfgrarn F, Myers L, Ellison G, et al: Serum linoleic acid in multiple sclerosis. Neurology 25:786-788, 1975 12. Field EJ, Shenton BK: Linoleic acid in multiple sclerosis. Br Med J 1:456, 1975 13. Agranoff BW, Goldberg D: Diet and the geographical distribution of multiple sclerosis. Lancet 2:1061-1066, 1974 14. Tworney J: Diet and multiple sclerosis. Lancet 2:1204, 1974 15. Shatin R: Multiple sclerosis and geography. Neurology 14:338-344, 1964 16. Hunt BS: Diet and multiple sclerosis. Lancet 2:1204, 1975 17. Jellinek EH: Multiple sclerosis and diet. Lancet 2:1006, 1974


Diet and multiple sclerosis.

Postgraduate Medicine ISSN: 0032-5481 (Print) 1941-9260 (Online) Journal homepage: Diet and multiple sclerosis...
629KB Sizes 0 Downloads 0 Views