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The Natural Doctor’s Casebook

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WDDTY addresses your most pressing health issues with promising alternative treatments and those proven to work.

Motor neuron disease:

Q
I’ve noticed motor neuron disease in the news a lot recently, thanks to the ice-bucket challenge. Have you done any investigation into the condition and whether there are any promising
alternative treatments? I’d be interested to know if there are any nutritional deficiencies associated with motor neuron disease. D.B., via email A Motor neuron disease (MND) is an all-embracing term used to describe a number of progressive neurological disorders that destroy motor neurons, the nerve cells that control muscle movements. In the US, the term ‘amyotrophic 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 (brain) and lower (spinal cord) motor neurons. 1 Symptoms of MND include 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 medication that prolongs MND survival: the benzothiazole antiglutamate drug riluzole. This only extends lifespan by two or three months, though, and comes with unpleasant side- effects like nausea, fatigue and, ironically, weakness and spasticity. 2 Non-invasive ventilation, where the patient is given a mask ventilator system to wear, usually overnight, is another treatment being used with some benefit. One study found it can improve quality of life and prolong survival, but only by about six weeks.

It also only works for the subgroups of patients with milder disease. 3 Nutritional deficiencies There is evidence – as you suspect – that nutritional deficiencies may play a role in MND. Patients with the disease are often malnourished, and it is now recognized that nutrition and appropriate dietary supplements are important factors in managing symptoms and improving survival. 4 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 deposits of calcium and aluminium in neurons. 5 More recently, scientists at the Linus Pauling Institute in Oregon reported that zinc deficiency may be involved in MND. Based on studies in mice, they speculated that an increased intake of zinc may help to prevent the disease in some cases. 6 Dietary copper could be important too. In two copper-deficient patients given a presumptive diagnosis of MND, copper supplementation led to stabilization or improvement of their muscle weakness. 7 MND sufferers also appear to metabolize certain amino acids abnormally. Patients who supplemented with 12 g of l-leucine, 8 g of l-isoleucine and 6.4 g of l-valine daily for one year maintained muscle strength and the ability to walk longer than those taking a placebo. 8 Environmental pollutants Heavy-metal toxicity, pesticides and other chemicals also seem to have an influence on MND.

Researchers have hypothesized that an impaired ability to break down these toxins because of differences in vital detoxification genes could underlie some cases. 9 In one recent Australian
study, heavy metals in neurons were found in significantly more MND patients than in controls. Mercury, in particular, is linked to MND. There’s even a reported case of a Swedish woman who
recovered from ALS after having her amalgam fillings removed. 10 These findings suggest a role for detoxification techniques and amalgam filling removal in MND (see Dr Sarah Myhill’s detox protocol on pages 62-7). Alternative treatments Although much of the research has so far only been done in animals (so it might not apply to humans), a variety of natural treatments are showing promise for MND. Vitamin E. Oxidative stress is thought to play a part in MND, so major antioxidant vitamin E has been the subject of lots of studies. Animal studies have
shown benefit with vitamin E supplements (delaying disease onset and slowing its progression), but human trials have not been as definitive as was hoped. 11 Still, vitamin E did appear to delay the progression of mild MND to a more severe form when taken in conjunction with riluzole. 12 Other evidence suggests that vitamin E supplements have a protective effect against MND, reducing the risk of developing the disease in the first place. 11 In one study, people with high intakes of vitamin E and polyunsaturated fatty acids (PUFAs) were 50 to 60 per cent less likely to have the condition. 13 Also, foods high in carotenoids – specifically, lutein and beta-carotene – have been associated with a reduced risk of MND. 14 Ketogenic diet. Often prescribed for children with epilepsy, this high-fat, adequate-protein, low- carbohydrate diet has been found to slow the progression of MND, at least in a mouse model of ALS. 15 Methylcobalamin.

Ultra-high doses (25 mg/day) of this vitamin B12 analogue have been shown to slow muscle wasting and increase survival time in preliminary human studies. 16 Ginkgo biloba. A study in mice suggests that a standardized extract of this herb might have gender-specific (favouring men) neuroprotective effects in patients with MND. 17 Red wine. Rich in antioxidants, red wine is being studied for its effects on MND. In one mouse study, the animals given freeze-dried red wine in their drinking water lived significantly longer than the ones not drinking the wine. 18 Exercise. Moderate-intensity endurance exercise involving the limbs and trunk, done or 15 minutes twice a day, can improve spasticity, and resistance exercise may also be helpful. 19 Magnet therapy. Preliminary evidence suggests that repetitive transcranial magnetic stimulation (rTMS) – non-invasive brain stimulation using magnets – may improve motor function and quality of life in MND patients, and perhaps even slow their rate of decline. 20

References
1 N Engl J Med, 2001; 344:
1688-700
2 Evid Based Complement
Alternat Med, 2013; 2013:
613596; N Engl J Med, 1994;
330: 585-91
3 Cochrane Database Syst Rev,
2013; 3: CD004427
4 Curr Opin Clin Nutr Metab
Care, 2002; 5: 631-43
5 Neurology, 1985; 35: 193-8
6 Neurosci Lett, 2005; 379:
42-6
7 Muscle Nerve, 2006; 34:
789-93
8 Lancet, 1988; 1: 1015-8
9 Am J Med Genet B
Neuropsychiatr Genet, 2007;
144B: 885-90
10 Acta Neuropathol Commun,
2013; 1: 81; J Occup Med
Toxicol, 2011; 6: 2
11 Amyotroph Lateral Scler
Frontotemporal Degener,
2013; 14: 246-51
12 Amyotroph Lateral Scler Other
Motor Neuron Disord, 2001;
2: 9-18
13 J Neurol Neurosurg Psychiatry,
2007; 78: 367-71
14 Ann Neurol, 2013; 73: 236-45
15 BMC Neurosci, 2006; 7: 29
16 Muscle Nerve, 1998; 21:
1775-8; Brain Nerve, 2007;
59: 1141-7
17 J Mol Neurosci, 2001; 17:
89-96
18 Phys Med Rehabil Clin N Am,
2008; 19: 573-89
19 Cochrane Database Syst
Rev, 2012; 2: CD004156;
Neurology, 2007; 68:
2003-7
20 J Neurol Sci, 2008; 270:
18-22; Neurosci Lett, 2006;
408: 135-40

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