Multiple Sclerosis

Dietary Fat and MS

Besides hormone therapy, a number of dietary factors may also play a role in decreasing the risk of developing MS or reducing the severity of symptoms. The most striking of these appears to be dietary fat.

In 1991, the results of a 34-year study conducted on patients with MS were published. Between 1949 and 1984, 150 patients were directed to consume low-fat diets. Their intake of proteins, fats, and oils was documented, and subsequent disabilities and deaths were noted. The research team found that people who consumed a low-fat diet had less disease progression and increased survival than their counterparts who ate a higher-fat diet (Swank RL 1991).

The link between MS and the types and amount of dietary fats consumed has also been established through epidemiological analysis. A high or increased intake of saturated fats, animal fats, and dairy products (another source of saturated fats, except in the case of low-fat dairy products) is associated with an increased risk of developing MS (Agranoff BWA et al 1974; Lauer K 1997; Schwarz S et al 2005; van Meeteren ME et al 2005).

Conversely, evidence shows that a higher consumption of polyunsaturated fatty acids, including omega-6 and especially omega-3 fatty acids, is associated with a decreased risk of MS and slower disease progression in people who have milder forms of the disease (Agnello E et al 2004; Bates D 1990; Swank RL et al 1990; Swank RL 1991; Zhang SM et al 2000). In fact, increased consumption of specific polyunsaturated fatty acids, such as long-chain omega-3 fatty acids, may moderate the course of the established disease. Omega-3 fatty acids, such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are found in relatively high amounts in cold water fish and dietary supplements (Agnello E et al 2004; Ferrucci L et al 2005; Nordvik I et al 2000; Shapiro H 2003).

Recently, researchers discovered that omega-3 fatty acids serve as precursors for newly described anti-inflammatory compounds, called docosatrienes and neuroprotectins, while simultaneously reducing the autoimmune response found in MS (Bannenberg GL et al 2005; Harbige LS et al 2001; Serhan CN 2005a,b; Serhan CN 2004).

A small, randomized, double-blind study investigated the effects of dietary fat consumption on the course of disease in patients who have relapsing-remitting MS. Researchers found that a low-fat diet supplemented with omega-3 fatty acids had moderate benefits in terms of physical components of health status and quality of life. Patients also experienced lower relapse rates while on the supplemented diet than they did in the preceding year (Weinstock-Guttman B et al 2005).

Nutritional Approaches to MS

In addition to adequate vitamin D intake and maintaining a proper balance between omega-3 and omega-6 fatty acids, a number of other nutrients have been studied in the context of MS. These include:

Linoleic and gamma-linolenic acids. Linoleic acid is an essential omega-6 fatty acid. At least one research team has reported that some patients who have MS have abnormally low levels of this nutrient (Homa ST et al 1981). The results of several double-blind, placebo-controlled clinical trials of linolenic acid supplementation for the treatment of MS were evaluated by meta-analysis. The conditions of 87 patients with MS and 85 normal control subjects were assessed for neurological changes over 2.5 years. Patients with low levels of disability at the beginning of the study had a smaller increase in disability over the study period than did the control subjects. In addition, linoleic acid was found to reduce the severity and duration of MS episodes in patients at all levels of the disease (Dworkin RH et al 1984).

In the body, linoleic acid is converted to gamma-linolenic acid (GLA), another omega-6 fatty acid. But this conversion is occasionally interrupted or inhibited, especially in inflammatory disease states such as diabetes and atopic dermatitis (Horrobin DF 1997, 2000; Jamal GA 1994; Kidd PM 2001). Defects in conversion may have a genetic basis, which is thought to predispose some people to inflammatory conditions (Horrobin DF 2000). GLA quells inflammation by competing with pro-inflammatory arachidonic acid. In animals with MS, GLA-fed animals fared significantly better than did control animals (Harbige LS et al 2000).

Antioxidants. Patients who have MS tend to have abnormally low levels of certain key antioxidants, such as glutathione peroxidase (Mai J et al 1990; Mazzella GL et al 1983; van Meeteren ME et al 2005). Supplemental antioxidants support cellular antioxidant defenses by scavenging free radicals; reducing inflammatory cell responses by interfering with gene transcription, protein expression, and enzyme activity; and by chelation of metals. Antioxidant therapy in animals with MS have yielded decreases in clinical signs of the disease (van Meeteren ME et al 2005).

In Denmark, researchers conducted a small study in which patients with MS were given an antioxidant mixture containing 6 mg of sodium selenite (equivalent to 2740 micrograms of elemental selenium), 2 grams of vitamin C, and 480 mg of vitamin E, once a day for 5 weeks. Although glutathione peroxidase levels were initially lower in patients with MS than in normal control subjects, after 5 weeks of antioxidant therapy, levels of this antioxidant increased 5-fold; side effects were minimal (Mai J et al 1990). This is an important demonstration of the ways in which supplements can help boost the body's own antioxidant mechanisms.

Although glutathione is available in supplement form, it is poorly absorbed. A better strategy for increasing the body's supply of glutathione is taking the oral supplement N-acetylcysteine (NAC), a potent antioxidant that serves as a precursor to glutathione (Arfsten D et al 2004; Kidd PM 2001). NAC has been shown to increase depleted levels of glutathione. While its specific use in the treatment of MS has not been investigated, its theoretical usefulness in the treatment of the disease has been noted by some researchers (Kidd PM 2001; Singh I et al 1998). In animals with MS or related diseases, NAC has been shown to reduce nitric oxide production in brain-supporting tissues and reduce clinical symptoms and microscopic evidence of brain cell injury and inflammation (de Bustos F et al 2000; Gilgun-Sherki Y et al 2005; Syburra C et al 1999).

Coenzyme Q10 (CoQ10) is another antioxidant of potential usefulness in treating MS and, while there is some debate, its levels may be low in patients with MS (Syburra C et al 1999). Although CoQ10 has not been investigated specifically for the treatment of MS, it is generally recognized as safe, well tolerated, and potentially useful in the treatment of neurodegenerative disorders. CoQ10 is a naturally occurring, lipid-soluble antioxidant that serves as a co-factor in the mitochondrial respiratory chain. Mitochondria are subcellular organelles present in all cells; they are responsible for the production of cellular energy. As an added bonus, CoQ10 is capable of regenerating the antioxidant capacity of spent vitamin E in the body. Decreased levels of CoQ10 are associated with many disease states, including heart disease, cancer, and neurodegenerative diseases (Bonakdar RA 2005; Siemieniuk E et al 2005).

Lipoic acid. Lipoic acid has been studied specifically in MS. Known to cross the blood-brain barrier and to penetrate cellular mitochondria, lipoic acid decreases the activity of intercellular adhesion molecule-1 (ICAM-1). ICAM-1 is a small molecule that plays a role in the genesis of MS. It is believed that ICAM-1 and other adhesion molecules are responsible for allowing certain pro-inflammatory immune system cells, namely T-lymphocytes, to cross the blood-brain barrier, paving the way for induction or exacerbation of damage to neurons (Biernacki K et al 2004; Cournu-Rebeix I et al 2003; Dedrick RL et al 2003).

In experiments on rodents with MS, lipoic acid produced significant reduction of demyelination and reduced the infiltration of inflammatory T-cells across the blood-brain barrier (Marracci GH et al 2002, 2004; Morini M et al 2004).

Other teams have followed up on these studies. A research team recently published the results of a small clinical trial of lipoic acid in the treatment of patients with MS. Thirty-seven patients with MS were randomly assigned to receive various doses of lipoic acid (up to 2400 mg/day) or placebo. After just 2 weeks, patients were assessed for levels of ICAM-1, and tolerability of high-dose lipoic acid was also evaluated. Lipoic acid was generally well tolerated and reduced ICAM-1 levels, as well as interfered with T-cell migration into the central nervous system (Yadav V et al 2005).

Vitamin B12. Vitamin B12 plays a key role in the generation of myelin. Studies have shown that patients with MS often have abnormally low levels of vitamin B12 in their cerebrospinal fluid and/or blood serum (Reynolds EH 1992). In fact, clinical vitamin B12 deficiency and MS share remarkably similar characteristics, occasionally rendering correct diagnosis difficult (Miller A et al 2005). For more than three decades, many physicians have prescribed vitamin B12 injections for patients who have MS. Patients who have received vitamin B12 supplements have reportedly experienced consistent clinical improvements in their symptoms (Kidd PM 2001).

In the United Kingdom , researchers investigated the effects of 6 months of vitamin B12 injections (1 mg/week) on 138 patients with MS, in a double-blind, placebo-controlled, randomized study. Patients were assessed using a standardized evaluation of neurological disability. Although the treatment regimen also included the eventual addition of two other compounds, the researchers concluded that the conditions of patients with MS improved after starting vitamin B12 injections (Wade DT et al 2002).

Additional Considerations: Excessive Heat

Many patients with MS report that their condition is exacerbated by overheating. This is unfortunate, as exposure to sunlight increases vitamin D naturally, and vitamin D may be helpful in the context of MS. It is ironic that many patients with MS deliberately avoid exposure to sunlight because they associate the warming rays of the sun with aggravated symptoms. Evidence suggests that patients with MS do not regulate body temperature normally (Smith KJ et al 1999). As a result, sunbathing or immersion in hot tubs may elevate core body temperature while triggering symptoms. In extreme cases, this has led to the deaths of patients who experienced muscle weakness and died when they were unable to escape the source of the heat (Henke AF et al 2000; Kohlmeier RE et al 2000). Clearly, patients with MS should not use hot tubs or elevate their body temperature excessively.