All of our fish are free of hazardous levels of mercury, for the reasons explained on our website's Purity Story page.
So we have no dog in the ongoing fight over seafood safety, and are not members of any seafood trade associations engaged in the debate, which typically sheds more heat than light.
But we are dismayed that so few people know about solid, mainstream research that explains the virtual absence of any seafood-related mercury harm in societies where people eat far more ocean fish than most Americans consume … such as Japan, Iceland, and the Seychelles Islands.
The mercury-selenium connection, explained quickly and clearly
More than 40 years ago, evidence began accumulating that health risks from the tiny traces of mercury in ocean fish are negated by their much higher levels of selenium.
The brain-toxicity of mercury is entirely due to its very strong tendency to bind to selenium in the body, thereby robbing it of critical antioxidant enzymes that depend on the mineral.
In two video interviews, researcher Nick Ralston, Ph.D., explains why groups of people who eat far more ocean fish than Americans show no signs of harm ... click here to view Dr. Ralston Part 1 and Dr. Ralston Part 2.
Professor Ralston leads research into human and environmental health at the University of North Dakota's Energy & Environmental Research Center. Most of his funding comes from the U.S. Environmental Protection Agency (EPA).
Our quick review of the facts
Unlike frequent consumption of any shellfish or almost any commercial fish, it can be detrimental to commonly consume marine mammals (whale, porpoise).
It's also unwise to frequently eat the few ocean fish that are extremely high in mercury, with insufficient offsetting selenium … namely shark, swordfish, tilefish, king mackerel (not our small chub mackerel, which are very low in mercury).
We should note that the team behind one of the major studies on mercury risks to children in fish-loving populations found no relationship between selenium-mercury ratios and cognitive test scores (Choi AL et al. 2007).
But virtually every other piece of epidemiological and lab evidence – including all other population studies – supports the idea, based on undisputed metabolic facts, that fish with a high selenium-mercury ratio are safe (i.e., all ocean fish except shark, swordfish, tilefish, king mackerel, and grouper).
In fact, it appears that eating ocean fish – including tuna – actually offsets the ill effects of mercury consumed from sources that are relatively high-mercury/low-selenium, such as shark and whale meat.
Here's how Dr. Ralston and a colleague explain the basics in a review paper published last year (Ralston NV, Raymond LJ 2010). We've broken out the key points in this bulleted list:
Dietary selenium (Se) status is inversely related to vulnerability to methylmercury (MeHg) toxicity.
Mercury exposures that are uniformly neurotoxic and lethal among animals fed low dietary Se are far less serious among those with normal Se intakes and are without observable consequences in those fed Se-enriched diets.
Although these effects have been known since 1967, they have only lately become well understood. Recent studies have shown that Se-enriched diets not only prevent MeHg toxicity, but can also rapidly reverse some of its most severe symptoms.
It is now understood that MeHg is a highly specific, irreversible inhibitor of Se-dependent enzymes (selenoenzymes). Selenoenzymes are required to prevent and reverse oxidative damage throughout the body, particularly in the brain and neuroendocrine tissues.
Inhibition of selenoenzyme activities in these vulnerable tissues appears to be the proximal cause of the pathological effects known to accompany MeHg toxicity.
Because Hg's binding affinities for Se are up to a million times higher than for sulfur, its second-best binding partner, MeHg inexorably sequesters Se, directly impairing selenoenzyme activities and their synthesis.
This may explain why studies of maternal populations exposed to foods that contain Hg in molar excess of Se, such as shark or pilot whale meats, have found adverse child outcomes, but studies of populations exposed to MeHg by eating Se-rich ocean fish observe improved child IQs instead of harm.
However, since the Se contents of freshwater fish are dependent on local soil Se status, fish with high MeHg from regions with poor Se availability may be cause for concern.
Their paper's introduction ends with this plea: “Further studies of these relationships are needed to assist regulatory agencies in protecting and improving child health.”
You can say that again.
By the way, elsewhere in this issue we cover a new study affirming importance of selenium to disease prevention and anti-aging, and the likely inadequacy of the U.S. RDA ... see “Selenium Seen as Key to Anti-Aging”.
Berry MJ, Ralston NV. Mercury toxicity and the mitigating role of selenium. Ecohealth. 2008 Dec;5(4):456-9. Epub 2009 Feb 6.
Choi AL, Budtz-Jørgensen E, Jørgensen PJ, Steuerwald U, Debes F, Weihe P, Grandjean P. Selenium as a potential protective factor against mercury developmental neurotoxicity. Environ Res. 2008 May;107(1):45-52. Epub 2007 Sep 12.
Ralston NV, Blackwell JL 3rd, Raymond LJ. Importance of molar ratios in selenium-dependent protection against methylmercury toxicity. Biol Trace Elem Res. 2007 Dec;119(3):255-68.
Ralston NV, Ralston CR, Blackwell JL 3rd, Raymond LJ. Dietary and tissue selenium in relation to methylmercury toxicity. Neurotoxicology. 2008 Sep;29(5):802-11. Epub 2008 Aug 9.
Ralston NV, Raymond LJ. Dietary selenium's protective effects against methylmercury toxicity. Toxicology. 2010 Nov 28;278(1):112-23. Epub 2010 Jun 16. Review.
Ralston NV. Selenium health benefit values as seafood safety criteria. Ecohealth. 2008 Dec;5(4):442-55. Epub 2009 Apr 14.