Amyotrophic lateral sclerosis (ALS), more commonly known as Lou Gehrig’s disease, is another “idiopathic” neurological disorder. ALS was first identified a few years after mercury/silver fillings came into common use. The clinical picture is quite interesting when considered in light of the documented neurotoxicity of mercury and the potential for neurotoxicity frommercury/silver fillings, often referred to as amalgam. Like MS, some people with ALS havefound that their condition improved dramatically upon the removal of their amalgam fillings.Others have not improved which may be the result of poor technique resulting in high exposure tomercury during the removal process or they may be genetically a non-excreter of mercury. The correlation to mercury exposure was first suggested by Brown in 1954.
A 1961 study of eleven cases of chronic mercurialism from consumption of bread treatedwith a mercury-containing fungicide presented neurological symptoms akin to ALS with somemore closely resembling progressive muscular atrophy. The paper concluded:
1. Since the same causative factor was operative in all these cases, it would appearthat amyotrophic lateral sclerosis and progressive muscular atrophy are probablynosologically identical.
2. Amyotrophic lateral sclerosis should not be considered a disease entity butrather a syndrome of variable etiology.
3. Chronic mercurialism is a possible etiologic factor in amyotrophic lateral sclerosis.” (emphasis added)” 
A 1978 report by Barber is also noteworthy. This involved two employees in a mercuryoxide manufacturing plant who developed previously non-existent neurological symptomsresembling that of ALS. An additional nineteen employees precipitously developed signsand symptoms which may be regarded as the early onset of a symptom complex of mercuryintoxication that would likely have progressed to the ALS-like syndrome if the progression hadnot been interrupted by removal of the individuals from exposure to mercury. All symptoms,signs, and laboratory findings returned completely to normal after approximately three months ina mercury free work environment.
In 1983 the Journal of the American Medical Association reported of a 54-year-oldman with symptoms resembling ALS after a brief but intense exposure to elemental mercurywhich resolved shortly thereafter, as his urinary mercury levels fell. This man who hadbreathed mercury vapor while “salvaging the liquid mercury from industrial-grade thermometers”developed symptoms so similar to that of ALS that his neurologists gave him a “presumptivediagnosis of ALS.” The man’s physicians confirmed his exposure to mercury with a urine test”several weeks” after his exposure, which registered 99 micrograms of mercury per liter of urine,an alarmingly high concentration. Two months later, the man had recovered nearly completely.His “neurological findings were completely normal.” His urine test indicated his mercury levelhad dropped to 29 micrograms, which is still much higher than the norm of 4 to 5 micrograms perliter. And “several weeks” later his mercury level had fallen to only 8 micrograms.
A 1989 a Japanese study was done on ALS victims in the vicinity of the biggest mercury mine in Japan. That study found mercury at higher levels in ALS victims than in controls. Theyfollowed this with a study in 1990 which compared the mercury and selenium content in the hairof thirteen (13) ALS cases using neutron activated analysis and concluded that mercury with a low content of selenium might be one of the environmental factors.
There are other studies indicating a connection between mercury and ALS, a casereport describing recoveries from ALS after the removal of mercury/silver fillings, andanother case report of ALS developing after the accidental injection of mercury. A 1990 study in the U.S. also involved neutron activated analysis of the brain, spinal cord, blood cells,serum, and nails of ALS victims compared to controls. Imbalances were detected in a numberof trace and minor abundance elements in the tissue of ALS patients and more widespreadchanges were noted in the concentrations of mercury. The authors cautioned that the variation inmercury concentrations need not necessarily indicate active toxicity, as it could merely representan enlarged pool of detoxified mercury or perhaps a labeling of a specific cellular ligand bymercury in ALS.
Unlike MS there are not many adverse reaction reports to the FDA involving ALS and the removal of mercury silver fillings and it is very important to note there are individuals who have ALS and have never had mercury/silver fillings. So while mercury may be one cause of ALS as the foregoing suggests, it certainly is not the only one.
Despite this considerable evidence linking ALS and mercury, the NIH has refused to fund further research into mercury as a possible cause of this tragic disease which disables and–usually within two to five years– kills five thousand Americans each year.