Methylmercury

Seafood doesn't have to be a source of toxicity, but the unfortunate fact is that it usually does contain significant toxins. Methylmercury, an organic form of mercury that is vastly more toxic clinically than inorganic mercury or elemental mercury, is selectively concentrated in most fish and shellfish. This is why methylmercury is the contaminant of primary concern in seafood. However, throughout the nation seafood from both fresh and salt waters is significantly contaminated not only with methylmercury, but also with other highly toxic substances, including polychlorinated biphenyls (PCBs), dioxins, and chlorinated pesticides. In fact, if your seafood comes from a heavily industrialized area, methylmercury can actually be the minor contaminant.

The toxicity of ingested methylmercury has been very well documented. The original epidemiological treatment of methylmercury poisoning occurred in Minamata, Japan, between 1953 and I960, after a chemical company had been dumping tons of mercury into Minamata Bay for about three decades. Six hundred and twenty-eight people were studied, with seventy-eight deaths attributed directly to the poisoning. In addition, thousands of people living

McGraw-Hill's Tenns of Use around the bay sustained some degree of poisoning from eating the highly contaminated fish. The most common clinical manifestations of the poisoning were tingling sensations, tremors, muscle weakness, slurred speech, tunnel vision, hearing loss, unsteady walking, and other sensory disturbances. Autopsy studies revealed striking brain degeneration, with losses of almost 50 percent of the normal volume and weight of the brain tissue noted. Perhaps the most disturbing of the effects of this toxicity occurred in the womb. In all instances reviewed, congenital exposure resulted in a substantially higher incidence of symptoms than resulted when a comparable level of exposure occurred in an adult. In addition to the disturbances already listed, such exposure during fetal development would often substantially delay or even block multiple developmental milestones after birth.

Methylmercury poisoning returned to the spotlight in 1971, when an unknown but large number of Iraqi people ate tainted bread. Methylmercury-treated seed grain had been used in the making of this homemade bread. Bakir et al. were but one of the groups who published their study of this population.1 All of the symptoms noted in Minamata were again seen in the adults consuming large amounts of this bread. However, those exposed in the womb again showed the greatest sensitivity. Some congenitally exposed infants were afflicted with cerebral palsy, altered muscle tone, and delayed onset of the ability to walk.

It is important to emphasize at this point that a couple of the best ways to deal with an acute methylmercury exposure are vitamin C, N-acetylcysteine (NAC), and bioavailable forms of selenium. Vitamin C can be given both orally to bowel tolerance (onset of loose diarrhea or abdominal cramping) and intravenously in a dose of 50 to 60 grams over several hours. This dose can be repeated as needed, and it can reach a cumulative dose of up to 200 grams daily for a few days if the toxic exposure is severe enough. NAC can also be given along with the vitamin C.

Ballatori et al. have published data showing that mice drinking water with NAC will excrete roughly 50 percent of an administered load of methylmercury over a forty-eight-hour period, while the control animals without NAC would only excrete only 5 to 10 percent of that load.2 NAC can be taken regularly in doses of 600 to 1,200 milligrams daily, and several grams a day for a few days can be taken when the methylmercury exposure is known to be high. NAC is also believed to exert a protective effect against methylmercury for the growing fetus. Ornaghi et al. found that the effect of NAC was highly effective in blocking the ability of methylmercury in mice to either reduce fetus weight or cause fetal death.3

Selenium is known to bind to methylmercury. However, unlike NAC, it does not promote mercury excretion. In fact, selenium supplements do not lower the mercury levels in animals given methylmercury, and when appropriate amounts of selenium are given, even higher levels of mercury can accumulate without obvious signs of clinical toxicity. It appears, then, that selenium is a neu-tralizer of mercury toxicity, but it does not promote mercury's elimination from the body. However, do not jump to the conclusion that more selenium is always better. As discussed in greater detail in chapter 8, nearly all supplements can have their own toxicity. Too much needs to be avoided as diligently as too little.

The role that selenium plays in the neutralization of methylmercury might help to explain the variable clinical toxicity of fish and other seafood. Hagmar et al. showed that fishermen who had the highest fish intake also had the highest blood levels of selenium.4 It seems likely that the methylmercury content in some seafood will be less well "matched" with selenium in its edible flesh than other seafood. Although the amount of unneutralized mercury may not yet have poisoned the fish that ingested it, this fraction can be expected to be much more toxic to the human who eats the fish, since fish appear to be far less sensitive to consumed mercury than are humans. Conversely, some fish that are consumed might deliver its mercury in a more neutralized condition, with little apparent clinical toxicity in the consuming human. Furthermore, the actual content of mercury in fish and other forms of seafood can be highly variable, and larger ingested amounts of mercury, whether bound to selenium or not, can be expected to be more harmful and toxic in the long run.

The sensitivity of the person eating the seafood must also be considered. When your immune system has been sensitized to "protect" you from additional ingested mercury, secondary immune reactions can make you very ill when you eat seafood that contains even a small amount of this toxin. And when the immune system is just very weak from long-term toxic abuse and poor nutrition and unable to deal even with minor amounts of new toxins, fish and seafood can prove to be highly toxic meals. It must also be remembered that since selenium does not promote mercury excretion, body levels of mercury will continue to accumulate over time. Even if selenium is bound to the stored mercury, a point will be reached when that storage capacity will eventually be overwhelmed. At that point, toxic symptoms will appear.

Perhaps one of the most significant considerations is that greater amounts of stored mercury will result in greater amounts of released mercury when detoxification mechanisms are later stimulated. Many people do not even concern themselves with toxins and detoxification until they get a little older and begin to realize that they won't live forever. For this reason, the reemergence of the stored mercury as the body detoxifies will be even more toxic clinically in these people, because their immune systems will typically have been stressed and traumatized for a longer time, and immune protection against toxins will be lessened.

It is especially important for pregnant women to entirely eliminate their fish and seafood consumption. Although untainted seafood may have substantial nutritive value, it is difficult to have enough nutritive value to counterbalance the effects of any needless fetal exposure to additional methylmercury. Drexler and Schaller found that mercury levels in breast milk were directly and positively associated with fish consumption.5 Furthermore, they found that the mother's consumption of fish appeared to be a larger contributor of mercury to the breast milk than the presence of her mercury amalgam fillings.

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