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OVER 70 MEDICAL CONDITIONS CURED, HELPED OR PREVENTED BY LOW-CARB, HIGH-FAT DIET
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Multiple Sclerosis (MS) dietary information

Introduction

There are many conditions in Western industrialised societies today that were unheard of, or at least very rare, just a century ago. The same conditions are still unheard of in primitive peoples who do not have the 'benefits' of our knowledge. There is a very good reason for this: They eat what Nature intended; we don't. The diseases caused by our incorrect and unnatural diets are those featured on these pages.


Dietary causes of MS:

High-carb, 'healthy' diet?

Part 1: Multiple Sclerosis

I never again saw any increase of spasticity in patients with
multiple sclerosis that I put on the diet. Thereafter, results
were consistent and, time after time, confirmed the real value
of treating multiple sclerosis by carbohydrate restriction.

DR WOLFGANG LUTZ


Soon after my book, Eat Fat, Get Thin!, was published in 2000, I received a letter from E. K., a woman in her early thirties with multiple sclerosis (MS). In the letter she thanked me for my book because she felt so much better, and her symptoms had got better since adopting the low-carb, high-fat diet I recommended.

Up until then, I had given little thought to MS in the context of nutrition. Now I started to consider it more. I soon learned that MS first appeared about 175 years ago, and its prevalence has steadily increased from that time. In other words, MS is a modern disease. So could it be caused as a result of incorrect diet? As E. K.'s symptoms were apparently helped by her change of diet, it seemed possible that this was so.

What is MS?

MS is a disease of the nervous system which affects young and middle-aged adults. Think of the body's nerves as electrical cables carrying signals around the body. Just as the electrical wiring in your house has to be insulated to stop the wires shorting across, nerves are insulated with a fatty wrap called the myelin sheath in a similar way.

There is compelling evidence that MS is an autoimmune disease. MS is characterised by chronic inflammation and damage to myelin sheath tissues in the central nervous system (CNS).[1] This means it is the result of your own immune system attacking specific tissues in your body. In this respect it is similar to many other diseases such as coeliac disease and rheumatoid arthritis. Damage to the myelin sheath allows improper interaction between the nerves in the brain and spinal cord which, in turn, affects the functions of these nerves. As the condition can affect any nerves, all of which perform different functions, the disease has a wide and scattered range of symptoms. Typical of these are:

  • Unsteady gait and shaky movements of the limbs
  • Rapid involuntary movement of the eyes
  • Defects in speech pronunciation
  • Spastic weakness

The disease is characterised by recurrent relapses and remissions so that any treatment which seems to be of benefit in the short-term could be merely the result of an unrelated remission. For this reason the testing of potentially successful treatments can be a long drawn-out process.

Causes of MS

There have been suggestions that MS is caused by all manner of things from a genetic defect to something in our environment. None has proved particularly satisfactory but they do provide clues

Is MS a genetic disorder?

To answer this question, pairs of identical twins were studied in Europe and North America, both of which are high risk areas for MS. This research indicated that, if one identical twin had MS the other usually did not: only between twenty and thirty percent of such twins both had MS.[2] But this is still higher than among non-identical twins where only two percent of affected twins would both have both MS. As women are fifty percent more likely to get MS than men, this might also reflect a genetic dimension. However, the twin data also convincingly show that, in high prevalence areas, only just over half of individuals who are genetically capable of getting MS actually contract the disease. Thus almost half the people in high prevalence areas who have the genes for MS don't get it.

These facts support a case for there being genetically susceptible individuals. But it appears that rather than there being one dominant gene which determines genetic susceptibility, many genes may be involved, each having a small influence.[3]

Environmental cause for MS

The geographic distribution of MS suggests that it is a disease of civilisation. It occurs mainly in USA, Canada, Western Europe, New Zealand and Australia. In these areas the prevalence of MS is between fifty and one hundred cases per 100,000 population. In low risk areas, such as the West Indies, the prevalence is an order of magnitude less.[4] It has been suggested that this distribution is in part due to a genetic factor because all the high-risk areas are dominantly populated by individuals of European origin.[5] But this seems unlikely as, within these peoples, there is a noticeable north/south gradient with MS being more prevalent in higher latitudes; and there are also significant differences in MS prevalence and incidence within individual countries which are not related to differences in ethnic origin.


That the primary cause of MS is something in the environment rather than a genetic trait has been suggested by several observations:

  • There was a sudden increase in prevalence of MS in the Faroe Islands following World War II occupation by British troops.[6]
  • Residency in Hawaii increases the risk of MS for those of Japanese descent while simultaneously decreasing the risk for Caucasians.[7]
  • Immigrants to London from areas of low risk such as south-east Asia, Africa and the West Indies, have a low prevalence of MS but their British-born children have the same high prevalence as the indigenous British.[8]

Summary of evidence

Taking all the evidence together, it appears that certain people have a genetic makeup that makes them more susceptible to succumbing to MS but for them to get the disease, they have to be subjected to at least one dominant environmental factor. As MS is found all over the world, this factor must be common to most of the world, but it must also be much more prevalent in 'western' industrialised areas of the world. Thus there are a number of potential causes – industrial pollutants, pesticides, chemical food additives, individual foods, and more. These can be divided into two main areas:

  • Indigenous factors such as climate, sunlight, altitude. I think that all of these can be ruled out simply by the Faroe Islands experience. Nothing changed there other than the people coming to the islands. It has been suggested that the dramatic increase following World War II could have been caused by a virus brought in by the troops. But there is no evidence that MS is transmitted by any infectious agent: despite a very concerted effort to find a specific MS virus or bacterium in the central nervous system of people with MS, no physical evidence of one ever been found.[9]
  • Transportable factors: heavy metals, pollution, sanitation, diet. The first three of these can, I think, also be rejected. The most convincing reason for this conclusion is the greatly increased prevalence of MS for Japanese living in Hawaii versus Japan whereas these factors are much more common in Japan than in Hawaii. The Faroe Islands data, as well as the much higher prevalence of MS on the Canadian Prairies than in the highly industrialized area of southern Ontario, also are not compatible with these factors.

That really only leaves new foods. Part Two discusses these.

References

1. van Oosten BW, Truyen L, Barkhof F, et al. Multiple sclerosis therapy, a practical guide. Drugs 1995; 49: 200-212.
2. a. Ebers G, Bulman D, Sadovnick A, et al. A population-based study of MS twins. N Engl J Med 1986; 315: 1638-1642.
b. Mumford C, Wood N, Kellar-Wood H, et al. The British Isles Survey of multiple sclerosis in twins. Neurology 1994; 44: 11-15.
3. Ebers GC. Genetic epidemiology of multiple sclerosis. Curr Opin Neurol. 1996; 9: 155-8.
4. Kurtzke JF. Epidemiologic contributions to multiple sclerosis: an overview. Neurology 1980; 30: 61-79.
5. Poser CM. The epidemiology of multiple sclerosis: a general overview. Ann Neurol 1994; 36: S181-S193.
6. a. Kurtzke JF. Multiple sclerosis from an epidemiological point of view. in Field EJ (Ed), Multiple Sclerosis: A critical conspectus. MTP Press Inc, Lancaster, 1977, 83-142.
b. — Epidemiologic contributions to multiple sclerosis: an overview. Neurology 1980; 30: 61-79.
c. — MS epidemiology worldwide. One view of current status. Acta Neurol Scand 1995; Suppl 161: p. 23-33.
7. Alter M, Okihiro M, Rowley W, Morris T. Multiple sclerosis among Orientals and Caucasians in Hawaii. Neurology 1971; 21: 122-130.
8. Elian M, Nightingale S, Dean G. Multiple sclerosis among the United Kingdom-born children of immigrants from the Indian subcontinent, Africa, and the West Indies. J Neurol Neurosurg Psychiatry 1990; 53: 906-911.
9. Poser C. The pathogenesis of multiple sclerosis: Additional considerations. J Neuro Sci 1993; 115 (suppl): S3-S15.

Part 1: Multiple Sclerosis | Part 2: Foods and MS | Part 3: Diet for MS
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