Amyotrophic lateral sclerosis (ALS) is a degenerative disease of the nervous system. It damages the motor nerves which are necessary for movement of muscles. Several varieties of ALS occur in humans and in some animals, the most common human variation being sporadic Charcot ALS (SC-ALS). In SC-ALS the early symptoms are bulbar (brain stem) at the onset, with weak speech, problems breathing and swallowing, and later involvement of the arms and legs. Symptoms include asymmetrical muscle weakness and muscle atrophy.
In several forms of animal ALS molybdenum (Mo) deficiency is a predisposing factor. Therefore, there is concern that Mo deficiency* might play a part in human SC-ALS as well. Mo deficiency endangers the nervous system from toxic overload due to inactivation of two important cellular enzymes: (1) xanthine oxidase (XO) which protects the nervous system from purine overload** and (2) sulfite oxidase which protects from sulfite overload***.
With XO deficiency, purine loading has been shown to cause astrocyte cell degeneration around nerve cells. Loss of normal transmission of electricity results in nerves when there is Mo deficiency in sheep. Ingestion of breakdown products of purines in the diet in Mo deficient sheep can produce syndromes similar to SC-ALS.
Sulfite loading in Mo deficiency blocks the conversion of amino acid methionine to cysteine, which results in an increase of homocysteine and reduced cysteine levels. Both high homocysteine and low cysteine levels favor neurodegeneration. Also, cysteine deficiency results in glutathione deficiency and impaired immunity.
The author proposes that the low uric acid levels often seen in SC-ALS patients are further evidence for the association of Mo deficiency with ALS. That deficiency results in reduced XO activity, causing low uric acid levels.
There is research evidence that there are genetic factors related to the occurrence of SC-ALS. It may be that these factors work in conjunction with Mo deficiency to cause the disease.
CONCLUSION: People who have genetic susceptibility for developing ALS may have the symptoms triggered by molybdenum deficiency. This could result from the inactivity of important enzymes which metabolize natural neurotoxins.
NOTES: *Hair analysis is a useful way to reliably diagnose Mo deficiency. Another helpful test is red blood cell Mo levels.
**Purines are found in animal products, especially wild animals. People with gout are sensitive to purines and develop high uric acid levels, causing crystals of uric acid to deposit in joints. Gout can be treated with xanthine oxidase inhibitors and low purine diets. Purine loading is caused by the following digestive products of purine-containing food: xanthine, inosine, adenosine, guanosine, xanthosine, hypoxanthine, adenine, and guanine.
***Sulfites occur in food, especially wine and the broccoli family. Sensitivity to sulfites can result in symptoms of asthma, dermatitis, and vomiting after drinking wine.