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Motor neuron disease

MagazineApril 2009 (Vol. 20 Issue 1)Motor neuron disease

Q) Have you done any investigation into motor neuron disease, and whether there are any nutritional deficiencies associated with the disease?-D

Q) Have you done any investigation into motor neuron disease, and whether there are any nutritional deficiencies associated with the disease?-D.B., via e-mail

A) Motor neuron disease (MND) is an all-embracing term to describe a number of progressive neurological disorders that destroy motor neurons, the nerve cells that control muscle movements. In the US, the term 'amyo-trophic lateral sclerosis' (ALS) is often used to describe these disorders, but ALS can also refer to a specific form of MND-the most common type-which affects both upper and lower motor neurons (N Engl J Med, 2001; 344: 1688-700).

Symptoms of MND include the progressive wasting of the muscles of the hands, forearms and legs, although it can spread to most of the body, making speaking, breathing and swallowing difficult. The common assumption in medicine is that the patient will be dead within one to five years, but some individuals-such as cosmologist Stephen Hawking-can long outlive this prognosis.

At this time, there is only one approved treatment that prolongs MND survival: the sodium-channel blocker riluzole. However, the effective-ness of the drug appears to be limited to early-stage disease and to specific subgroups of patients, such as the elderly (Eur J Neurol, 2007; 14: 262-8). It also comes with an unattractive listof side-effects including sleepiness, nausea, vomiting, dizziness, headache and, ironically, weakness and spasticity (Pharm J, 2001; 267: 714-7; N Engl J Med,

1994; 330: 585-91). It is not surprising, therefore, that many sufferers seek alternative approaches.

There is evidence-as you suspect-that nutritional deficiencies may playa role in MND. Patients with the disease are often malnourished, andit is now recognized that nutrition is an important factor in managing symptoms and improving survival (Curr Opin Clin Nutr Metab Care, 2002; 5: 631-43).

A number of observational studies link calcium deficiency to MND. Some researchers postulate that calcium and magnesium deficiencies can lead to abnormal mineral metabolism, and deposition of calcium and aluminium in the neurons (Neurology, 1985; 35: 193-8).

More recently, scientists at the Linus Pauling Institute in Oregon found a link with zinc deficiency. Although the research is preliminary, they speculate that an increasedintake of zinc may help to prevent the disease in some cases (Neurosci Lett, 2005; 379: 42-6).

Dietary copper may also be impor-tant. In two copper-deficient patients given a presumptive diagnosis of MND, copper supplementation resulted in stabilization and improved muscle weakness (Muscle Nerve, 2006; 34: 789-93), as did vitamin B12 given to patients with neurological complaints, includ-ing spasticity and muscle weakness (N Engl J Med, 1988; 318: 1720-8; Medicine [Baltimore], 1991; 70: 229-45).

MND sufferers also appear to metabolize certain amino acids abnormally. Patients who supplement-ed with 12 g of l-leucine, 8 g of l-isoleucine and 6.4 g of l-valine daily maintained muscle strength and the ability to walk longer than those taking a placebo (Lancet, 1988; 1: 1015-8).

Environmental factors, too, may have an influence on MND. Heavy-metal toxicity, pesticides and other chemicals appear to be risk factorsfor MND, and researchers have hypothesized that an impaired ability to break down these toxins, because of differences in detoxification genes, could underlie some cases of the disease (Am J Med Genet B Neuropsychiatr Genet, 2007; 144: 885-90).

For this reason, WDDTY panel member Dr Melvyn Werbach advises checking for heavy-metal toxicity (see WDDTY vol 19 no 2, Q&A) before trying anything else for MND.

Promising natural treatment

- Vitamin E. Animal studies show benefit, but human trials of vitamin E supplementation are disappointing (J Neural Transm, 2005; 112: 649-60; Neurol Neurochir Pol, 2001; 35 [1 suppl]: 101-6). Still, vitamin E did appear to delay the progression of mild MND to its more severe form (Amyotroph Lateral Scler Other Motor Neuron Disord, 2001; 2: 9-18). Also, antioxidants may be preventative: a high intake of vitamin E along with polyunsaturated fatty acids (PUFAs) led to a 50- to 60-per-cent reduced risk of MND in one

trial (J Neurol Neurosurg Psychiatry, 2007; 78: 367-71).

- Ketogenic diet. A 2006 mouse study (which may not apply to humans) found that diet, specifically a high-calorie ketogenic diet, slowed the progression of MND (BMC Neurosci, 2006; 7: 29).

- Methylcobalamin. Ultra-high (25 mg/day) doses of this B12 analogue can also slow muscle wasting and increase survival time in preliminary human studies (Muscle Nerve, 1998; 21: 1775-8; Brain Nerve, 2007; 59: 1141-7).

- Coenzyme Q10. Following neuroprotective effects seen with CoQ10 in rat studies, an eight-month trial in MND patients found that doses as high as 3000 mg/day were also safe and well tolerated (Neurology, 2005; 65: 1834-6).

- Ginkgo biloba. A study in mice suggests that a standardized extract of this herb might have a gender-specific (favouring men) neuroprotective effect in patients with MND (J Mol Neurosci, 2001; 17: 89-96).

- Exercise. Moderate-intensity endurance exercise involving the limbs

and trunk, performed for 15 minutes twice a day, can improve spasticity (Cochrane Database Syst Rev, 2004; 1: CD004156). Resistance exercise may also help (Neurology, 2007; 68: 2003-7).

- Magnetic therapy. Preliminary evidence suggests that repetitive transcranial magnetic stimulation (rTMS) may improve motor function and quality of life in MND patients, as well as slow their rate of decline

(J Neurol Sci, 2008; Feb 26; Epub ahead of print; Neurosci Lett, 2006; 408: 135-40).


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