So as far as I've been able to gather, Andy asserts that inorganic mercury, (Hg++) cannot be methylated within the body.
The only source of methylmercury is minor amounts methylated by gut bacteria, seafood, and inhalation.
He also makes it clear that if we were able to methylate mercury, it wouldnt be an issue in the first place, as we would excrete it.
He also warns against NAC, as it will mobilize mercury around the body but never excrete it due to a weak bond.
Just curious what you guys think of the following study.
On NAC and methylmercury elimination.
"Methylmercury is a ubiquitous environmental pollutant and potent neurotoxin. Treatment of methylmercury poisoning relies almost exclusively on the use of chelating agents to accelerate excretion of the metal. The present study demonstrates that oral administration of N-acetylcysteine (NAC), a widely available and largely nontoxic amino acid derivative, produces a profound acceleration of urinary methylmercury excretion in mice. Mice that received NAC in the drinking water (10 mg/ml) starting at 48 hr after methylmercury administration excreted from 47 to 54% of the 203Hg in urine over the subsequent 48 hr, as compared to 4-10% excretion in control animals. When NAC-containing water was given from the time of methylmercury administration, it was even more effective at enhancing urinary methylmercury excretion and at lowering tissue mercury levels. In contrast, excretion of inorganic mercury was not affected by oral NAC administration. The ability of NAC to enhance methylmercury excretion when given orally, its relatively low toxicity, and is wide availability in the clinical setting indicate that it may be an ideal therapeutic agent for use in methylmercury poisoning."
And concerning the methylation of inorganic mercury to methylmercury we have only methylcobalamin in nature. As seen countless times in vivo and vitro that Hg2++ is methylated non enzymatically by methylcobalamin, hence the immediacy of methylation.
Looking at just the chemistry we have a guarantee in vitro that methylcobalamin with react with inorganic mercury.
In biology we see the buildup of methylated mercury, and CNS myelin damage in animals coexposed to methylcobalamin and inorganic mercury.
So given the fact that methylcobalamin methylates mercury, and NAC efficiently removes methylmercury in accute exposure. Would methylb12 supplementation followed shortly after by NAC not be a much quicker and safer method of chelation than ALA in the presence of other heavy metals? Or at the very least in conjunction with the mobilization of inorganic mercury out of cells?