Ozzie, got the okay to publish this.  Thank you Ozzie and Also professor Dingle.

MS - a Preventable Disease Lack of sunlight and poor diet causing increase in multiple sclerosis (MS) in Australia and high latitude countries

Associate Professor Peter Dingle
Environmental and Nutritional Toxicologist
School of Environmental Science
Murdoch University
Murdoch  WA 6150,  Australia

Just over a year ago, a student of mine motivated me to look into Multiple Sclerosis (MS). Bruce put up a slide quoting the official authorities saying there was no link between MS and nutrition. He then presented a slide with more than 40 peer reviewed scientific papers on the link between MS and nutrition.

Together with Bruce, I am continually confused as to why such supposed authorities continue to deny the existence of nutritional treatments and, even worse, the role of poor nutrition in causing disease.

Since that slide inspired me, I have now seen dozens of people suffering from MS begin a new life through really simple changes in nutrition - and one of the simplest changes follows on from one of my earlier articles on vitamin D. Many Australians just don't get enough sun anymore. But more on that later. What is even more important is that this information can help prevent the development of MS in the beginning.

There is now overwhelming evidence that the risk of developing MS is linked to a number of environmental factors such as excessive dietary intake of saturated fats and deficiencies in polyunsaturated fatty acids, vitamin D and antioxidants (1,2). As a result of these findings, good nutrition appears critical in limiting the development and ongoing effects of MS and enhancing the quality of life, while limiting the risk of secondary conditions (3).

Over the past 200 years, MS has significantly increased in incidence and prevalence. MS is a disease that affects an estimated 2.5 million people worldwide with over 18, 000 people in Australia with the disease; the incidence rate in Australia is increasing by 7% each year and financially costs approximately 2 billion dollars each year (4). It is twice as common in females as in males (females have lower vitamin D levels than males), and is the most frequently occurring neurodegenerative disease in young adults (5,1). Geographically, MS is common across northern Europe, Scandinavia and across the US and is much higher in incidence among whites then other racial groups (5). The disease is very rare in Japan, the Indian subcontinent and is unknown to black Africans. However, these groups are at significant risk of developing MS when they go to other places to live, which supports the concept that an environmental factor is responsible for the disease (5).

MS is a chronic, degenerative and autoimmune initiated inflammatory disease of the central nervous system, which may involve the brain, optic nerve or spinal cord and is characterised by demyelination (5). That is, the myelin that wraps around and insulates the nerve axons in the central nervous system suffers self destruction and degeneration (7). This means damaged myelin results in damaged nerve axons and causes the various disabilities of MS(7). It is worth noting here that myelin is around 80% lipids (fats), and cholesterol (which I have written on in past articles in NOVA) makes up an indispensable component of myelin membranes (8). The inflammatory reactions are poorly controlled and result in substantial damage to the myelin(7). As a result of demyelination, MS patients suffer functional impairments such as abnormal walking mechanics, poor balance, muscle weakness and fatigue, which result in reduced ability to perform daily activities(9).

The single most important factor linked to the development of MS is a reduced supply of vitamin D (7), which I have written on extensively in the past. Research has shown that the active hormonal form of vitamin D, 1,25-dihydroxyvitamin, is a natural immune system regulator with anti-inflammatory action (10). We receive vitamin D from two sources, diet and sunshine, but it is considered that diet provides insignificant amounts and so sensible exposure to sunlight is considered the most effective source (11). Even Scandinavian diets (rich in oily fish) scarcely exceed a few hundred IU/d of vitamin D (12).

Sunshine is thus the principal natural source of vitamin D, providing approximately 90% of requirements.

Sunbathing can provide 10,000-20,000 IU in 15 to 30 minutes, but this will only last a few weeks before it needs to be replenished (13,14). It is interesting to note that women generally have lower serum levels than men (15,16) and have significantly higher levels of MS.

There is a 41% decrease in MS risk for every 50 nanomoles per liter increase in vitamin D (1,25-hydroxyvitamin) in the blood. The prevalence of MS is highest where environmental supplies of vitamin D are lowest (18).

There is significant epidemiological data from Australia that shows a very strong correlation between vitamin D supply from ultraviolet (UV) radiation and MS prevalence (7). The correlation is indeed stronger than that of UV radiation exposure and melanoma development (7). Globally, countries of high latitudes with insufficient UV radiation for most of the year report a higher incidence of MS (19,20). One case control study has also shown that vitamin D status in individuals at the time of diagnosis of MS is significantly lower then healthy controls, indicating a further link (19).

It is theorised that vitamin D deficiencies may lead to an increase in T-helper cell autoimmune responses, thereby resulting in excessive damage to the myelin and MS symptoms (21).

Vitamin D supply through dietary intake also appears critical, as it has been reported that through vitamin D supplements there is an inverse relationship with MS (19). The role of vitamin D is supported by animal studies where mouse models have shown that vitamin D deficient mice succumb faster to MS, but once administered with vitamin D the symptoms diminish (22).

The idea that an increase in saturated fats in modern diets may result in increased risks for MS (and diabetes type 2) has been known since the early 1950s and reinforced on several occasions (23). Epidemiological studies in Norway have shown that inland farming communities with a high intake of animal products have higher MS incidence rates then coastal communities where fish consumption is high. Subsequent studies have also shown a negative correlation between MS and the consumption of fish, fruits and vegetables (23). Any wonder the rates of MS are increasing so fast in Australia knowing the poor diets of most kids. It has been shown that MS sufferers have deficiencies in essential polyunsaturated fatty acids (PUFA), primarily the omega 3 fats. This is demonstrated by alteration in the lipid and fatty acid composition in plaque tissue from the MS brain, compared to normal brain white matter (1).

It is believed that humans evolved on a diet with a ratio of omega 6 to omega 3 of approximately 1:1, whereas in Western diets the ratio varies between 15:1 and 20:1 (24). We just have too much vegetable oil (omega 6) in our diet. It is added liberally to all processed foods.

A large study conducted over a 35 year period showed a diet with low saturated fat and supplementation with cod liver oil provided MS patients with long term benefits relating to mortality, relapse severity and disability, particularly if initiated during the earliest stages of the disease (25). These results have shown that MS patients can expect to survive and be mobile and otherwise normal to an advanced age if they follow an extremely low fat diet and omega-3 supplementation (26).

The rarity of MS in the Japanese, whose diet consists of low levels of saturated fat and high levels of omega 3 fatty acids, is another indication of the role of omega 3 oils in MS (27). There is now significant evidence to show it is a contributing factor to the development of the disease in conjunction with other environmental factors (7).

The development of MS is also believed to be linked to oxidant stress in the body from a lack of antioxidants (28). Along with other possible environmental factors, the actual role of oxidative stress in patients with MS is poorly understood (29). The brain and nervous system are particularly susceptible to oxidative damage due to the low content of antioxidants in this area of the body as they have to be imported (30).

Studies have shown that oxidative stress causes pro-inflammatory chemical messengers called cytokines to be produced, contributing to the process of demyelination 31. Sufficient antioxidants thus ensures neuroprotection by suppressing inflammation; this limits the effects of MS (29,31,32).

Oligodendrocytes, a particular type of brain cell, that produces the extensive myelin sheaths are known to be particularly vulnerable to oxidative stress; this helps explain the lack of remyelination during remission stages (1). Oxidation (free radicals) literally stops the repair work on any damage to the myelin sheath.

In helping to prevent and restrict the development of MS, we can be guided by a number of recommendations determined through scientific studies:

  • Regular moderate sun exposure (15-30 min/day)
  • Reduced intake of saturated fat and omega-6 PUFA together with a higher consumption of omega-3 PUFA. We can achieve this through eating fish and taking supplements
  • A daily supplement of vitamin D to ensure the circulating level of vitamin D remains between 100 - 150 nanomoles per liter
  • Consume at least 5-7 serves of antioxidant rich fruits and vegetables each day and supplement.

Acknowledgements: Bruce Greatwitch

Dr Peter Dingle PhD is an environmental and nutritional toxicologist and Associate Professor
in Health and the Environment at Murdoch University, Western Australia.


1. Meeteren et. al. 2005
2. Liuzzi et. al. 2007
3. Timmerman, Stuifbergin 1999
4. MS research Australia 2008
5. Undurti 2003
6. Kanwar, 2005
7. Embry 2004
8. Saher et al 2005
9. White et. al. 2004
10. Van Amerongen 2004
11. Cantorna, Mahon 2004
12. Mark and Carson, 2006
13. Hollis, 2005
14. Vieth, 2007
15. Yetley, 2008
16. Zadshir et al 2005
17. Anonymous 2007
18. VanAmerongen et. al. 2004
19. Barnes et. al. 2007
20. Kampman et. al. 2007
21. Toohey 2004
22. Mandavilli 2007
23. Nordvik et. al. 2000
24. Simopoulos 2002
25. Swank cited in Weinstock-Guttman et. al. 2005
26. Swank, Goodwin 2003
27. Undurti 2003
28. Lutskii, Esaulenko 2007
29. Koch et. al. 2006
30. Syburra, Passi, 1999
31. Gonsette 2008
32. Gilgun-Sherki et. al. 2004

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