Written by: Kevin Cann
The Environmental Protection Agency (EPA) on July 5, 2006 launched the EPA’s Roadmap for Mercury. This is an 87 page document that outlines the dangers of human consumption of mercury. This document can be viewed on the EPA’s website here, http://www.epa.gov/hg/roadmap.htm . In a nutshell it explains the dangers associated with mercury consumption. The primary form of mercury that humans are exposed to is methyl-mercury and fish consumption is the primary means in which people are exposed.
This government program is going to cost roughly $9.6 billion. With the national deficit rising is this the best way for the government to be spending their people’s money? The EPA cites research that shows methyl-mercury in humans can lead to liver, kidney, and immune system problems (http://www.cdc.gov/exposurereport/pdf/FourthReport.pdf ). About 95% of methyl-mercury is absorbed by the gastrointestinal tract and then deposited in various tissues throughout the body. The mercury then may reside in the tissues for up to 50 days.
A major fear of the EPA is the levels of methyl-mercury that may come into contact with a fetus and a newborn baby. The fear is that high levels of mercury may have effects on fetal development such as limb deformations and mental retardation. The EPA’s Fourth Report cites studies that show in animals there is a greater amount of mercury in the cord blood when compared to the mother’s blood. There are also low concentrations of mercury found in breast milk with the transfer being greatest with the inorganic forms. The report goes on to show research that shows the high levels of prenatal exposure to mercury lead to mental retardation and limb deformities with lower levels leading to a decline in cognitive testing in children.
The human studies are epidemiological. This means they show a possible correlation, but not necessarily causation. Also, the methods used to test for blood mercury levels (blood, urine, and hair) do not correlate well with serum levels (http://www.hindawi.com/journals/jeph/2012/460508/ ). Does this mean that we should not be concerned about mercury? The answer to that question is that we should be concerned.
Autopsies of humans with Alzheimer’s disease have shown increased levels of mercury in the brain, and in vitro the pathology of mercury exposure showed similarities to that seen in Alzheimer’s disease (http://www.ncbi.nlm.nih.gov/pubmed/20847438?dopt=AbstractPlus ). The potential risks of mercury exposure are definitely something to be concerned about. The problem with this research is it is short sighted and only looking at one thing: mercury exposure equals disease. Could there have been other factors associated with the Alzheimer’s patients having higher levels of mercury in the brain? The answer is yes.
Adequate levels of selenium actually protect us from the problems associated with mercury. In a study performed on rats the groups that had the high mercury and low selenium diets had the highest rates of growth impairments. These impairments were predictable based on mercury to selenium ratios (http://www.ncbi.nlm.nih.gov/pubmed/18761370 ). Rats and humans do differ dramatically in some ways so how would this correlate to human metabolism?
Selenium’s protective effects against mercury happen in two ways. First, a selenol group can actually bind to the mercury, and also selenium’s role in the body as an antioxidant actually protects us from the oxidative damage that mercury causes (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1367848/ ). The studies done on humans in this context have the same downfalls as the previous ones. They are epidemiological and use testing methods that may not be ideal. However, in this case the tests looked at the relationship between selenium and mercury.
In that previous study they looked at 72 subjects. The mercury miners that showed higher levels of mercury exposure also showed higher concentrations of glutathione peroxidase and selenoprotein P. The latter bound more mercury at higher mercury levels found in testing. Glutathione is one of our body’s strongest antioxidants. I wrote about glutathione in a previous article that can be read here, http://robbwolf.com/2013/03/13/understanding-combating-oxidative-stress-huntingtons-disease/ .
There are actually five selenium containing glutathione peroxidases. They help protect us from oxidative damage. Selenoprotein P (that the previous study mentions) is a transport protein for selenium, as well as an antioxidant. A selenium deficiency actually leads to a decrease in glutathione peroxidases (http://lpi.oregonstate.edu/infocenter/minerals/selenium/ ). This tells us a couple of things, for one mercury does lead to oxidative stress. This is seen from the increase in glutathione and selenoproteins. It also shows that we have a protection from the dangers of mercury. Other studies have shown that selenium actually bonds to mercury as well (http://www.ncbi.nlm.nih.gov/pubmed/698281 ).
What these studies tell us is that we need more selenium then mercury to protect us from the damages associated with mercury. This is for adequate glutathione production to protect us from oxidative damage, as well as enough selenium to bond with the mercury. What are our best natural sources of selenium? Brazil nuts, and ironically fish. In fact the only fish shown to have more mercury then selenium is the Mako shark (http://www.naturalnews.com/026729_selenium_mercury_fish.html ). That means your tuna and salmon have more selenium then mercury, rendering the mercury harmless. This is good because consuming fish 1-2 times per week showed a 36% decrease in cardiovascular disease and a 17% decrease in overall mortality (http://www.ncbi.nlm.nih.gov/pubmed/17047219 ).
Mercury does lower our total selenium, and fish is not the only source of exposure. The air we breathe, water we drink, and even dental fillings are all places we may be exposed to mercury. Replacing dental fillings that contain mercury with safer ones, drinking filtered water, and using air purifiers in your home are all ways to limit mercury exposure. Also, stick to eating fish that contain higher levels of selenium then mercury. There is a list known as the Selenium Health Benefit Value where you can look up the types of fish (http://www.ncbi.nlm.nih.gov/pubmed/19365692 ).
Also, maintaining adequate levels of selenium. The daily intake of selenium should be 200mcg. An ounce of Brazil nuts contains 544mcg of selenium and a serving of tuna contains about 90mcg. A couple Brazil nuts per day will allow for adequate selenium levels. The mercury in vaccines is another big topic in media outlets and this information may even help you weigh the risk versus reward for those as well.
In conclusion, the government spending $9.6 billion to lower the mercury levels in fish is unnecessary. Maintaining adequate levels of selenium can protect us from mercury toxicity by binding to mercury as well as protecting us from oxidative damage. On top of that, the fish consumed by humans (except for the Mako shark and possibly some species of whales) contain more selenium than mercury. This makes it safe to get all the positive health aspects associated from eating fish 1-2 times per week.
Thanks for the information. I will try to get some Brazil nuts and eat a few every day.
One thing to note, may want to fix this.
You say “On top of that, the fish consumed by humans (except for the Mako shark and possibly some species of whales) contain more selenium than mercury.” – Whales are mammals, not fish.
Great article, sorry I have to be picky!
Great article! I used to eat tinned tuna like there was no tomorrow. Soon cut that out when I started reading the research journals out there on mercury.
Glad I’ve always been big on brazil nuts too, probably balanced out the issue.
Thanks for this!
Ian
The fact that Selenium confers some protection against Methyl-Mercury exposure does not mean that EPA should not spend money to clean up Methyl-Mercury. That is a non sequitur. That’s like saying wearing shoes prevents broken glass from puncturing your feet, so it’s unnecessary to clean up broken glass on the sidewalk.
Mike-
did you miss the terrible ROI on this?
Great to see another myth about real food busted. i first head about this in a peice by researchers at (of all places) North Dakota U! Here’s their wee doco. Spread the word! http://www.undeerc.org/fish/documentary.aspx
Having adequate amounts of bifido bacteria in the intestinal tract also helps people avoid mercury toxicity. It essentially eats up the mercury and then “flushes” it from the body.
Mercaptovores! fascinating.
Fascinating is right! Here is a brief abstract. Not much out there on it, but doesn’t come as much of a surprise. http://onlinelibrary.wiley.com/doi/10.1002/jobm.3620260811/abstract;jsessionid=FC10445BEA12EE610D89AFEADAACCD8A.d03t01?deniedAccessCustomisedMessage=&userIsAuthenticated=false
Here is an article that mentions it too:
http://www.dockidd.com/html/articals/autism.htm
You mention weighing risk versus reward on vaccinations. Any mercury contained in vaccines is ethyl mercury purposely added during the manufacture process as opposed to methyl mercury which has been shown to be neurotoxic at above normal levels.
The body has been shown to rapidly clear ethyl mercury before it can accumulate in tissues. Ethyl mercury is used as a preservative with the intention of preventing microbes from establishing residence in vaccine vials, but as of 2001 ethyl mercury has not been added to vaccines administered during childhood as a precaution against possible developmental defects, largely due to public outcry. Ethyl mercury is still added to some vaccines administered to adults.
There are many subtle distinctions to make when dealing with biochemistry and this is one can be important when making health decisions.
Robb, I had a conversation with a guy on YouTube about mercury exposure. His response to my saying that it wasn’t an issue was this…
“Actually, the mercury in fish is still not completely harmless, regardless of selenium levels. That myth has been debunked, and there are respected studies to prove it. In one study, it only took eight weeks of mercury exposure from just fish for mice to start developing serious complications. Look it up for yourself. If it makes you feel better, ignore it, but the fact remains that consumption of fish is still by far the most significant source of ingestion-related mercury exposure in humans.”
Can you offer a rebuttal?
further to this I found this article. I’d really like an answer regarding this subject. Is fish on or off the menu? http://suppversity.blogspot.co.uk/2012/08/mercury-in-fish-not-harmless-regardless.html
Hi Robb,
personally, I am not convinced that the high levels of mercury in fish such as tuna and swordfish are safe if they exist in the presence of equimolar or higher concentrations of selenium.
The definitive study on this issue is Chang’s, in which16 kittens were fed a diet of tuna containing 0.3 to 0.5 ppm mercury, plus supplementary nutrients and vitamins. After a period of seven months, two of the cats had mild ataxia and one had severe ataxia. The cats were sacrificed at 11 months and autopsy revealed extensive liver damage including damage to the mitochondria. In this case the selenium in the fish was not protective.
In his review on Mercury: selenium interactions and health implications Dr Ralston, a supporter of the protective effect of selenium, says that “the ‘protective effect’ of selenium against mercury exposure may actually be backwards. Mercury’s propensity for selenium sequestration in the brain and endocrine tissues may inhibit formation of essential Se-dependent proteins (selenoproteins). Hence selenium’s ‘protective effect’ against mercury toxicity may simply reflect the importance of maintaining sufficient free selenium to support normal selenium-dependent enzyme synthesis and activity.” But even that may not be enough to completely nullify mercury’s toxic effects.
In the same review he mentions the study by Friedman into the protective effects of dried swordfish on methylmercury toxicity in rats. He states that rats fed a diet of swordfish and methylmercury showed no signs of neurotoxic effects, while rats fed a control diet spiked with methylmercury without swordfish did. Dr Ralston attributes this to the protective effects of selenium. However, the protective effect is not that impressive.
In spite of the proposed protective effect of selenium, both the control group and the experimental groups died, at 4.6 and 5.3 weeks respectively. If the rats had lived longer, there would have been more chance for any neurological effects to manifest. It should also be noted that the control diet included 15% casein which has been shown to reduce mercury excretion in rats, and thus may have exacerbated the effects of mercury toxicity in the control rats.
These studies do not take into account the long-term effects of mercury exposure. The lower the dose of mercury, the greater the delay in the manifestation of symptoms. Deborah Rice fed monkeys a diet of 50 micrograms of methylmercury for 7 years. After cessation, blood levels quickly dropped to normal levels. When the monkeys were tested at 13 years of age they displayed clumsiness and loss of fine motor skills as well as decreased sensitivity to touch. Humans are exposed to mercury for decades and have longer to develop overt signs of mercury toxicity.
One of the problems with the studies from the Seychelles and the Faroe Islands on the effect of methylmercury on neurodevelopment is that they rely on hair testing of mercury levels. This is often accurate, but does not take into account the fact that mercury disrupts cellular transport due to its affinity for sulfhydryl molecules. These molecules often form the active site in cellular transport proteins. Mercury binds to these active sites, altering mineral transport. This can result in hair readings for mercury and other toxic elements that are artificially low. Thus children with high exposure may actually be classed as having low exposure. Hair analysis actually provides a measure of how much mercury is being excreted. The most important factor is how much mercury is being retained in the body but that is difficult to measure.
Amy Holmes found that autistic children, even though they had higher exposures to mercury through their mothers’ dental amalgams and Rhogam injections, had lower levels of mercury in their hair, implying a reduced ability to excrete mercury. The following hair test illustrates the ability of mercury to disrupt mineral transport – http://www.livingnetwork.co.za/files/hairtest_564.pdf
This is clearly an abnormal distribution of elements (all except one of the essential elements are below the 50th percentile) associated with a low reading for mercury.
It may be safe for some individuals with optimal antioxidant and metallothionein status to consume tuna and other high mercury fish, but I think for many it would be safer to stick to fish such as sardines and salmon, which also have high levels of omega 3s, but much lower levels of mercury.
David Hammond
author – Mercury Poisoning: The Undiagnosed Epidemic.
References
Chang, L. W., & Yamaguchi, S. (1974). Ultrastructural changes in the liver after long-term diet of mercury-contaminated tuna. Environmental Research, 7(2), 133-148.
Raymond, L. J., & Ralston, N. V. (2004). Mercury: selenium interactions and health implications. Seychelles Medical and Dental Journal, 7(1), 72-77.
Rowland, I. R., Robinson, R. D., & Doherty, R. A. (1984). Effects of diet on mercury metabolism and excretion in mice given methylmercury: role of gut flora. Archives of Environmental Health: An International Journal, 39(6), 401-408.
Rice DC. Delayed neurotoxicity in monkeys exposed developmentally to methylmercury. Neurotoxicology. 1989 Winter; 10(4):6450-50.
Holmes, A. S., Blaxill, M. F., & Haley, B. E. (2003). Reduced levels of mercury in first baby haircuts of autistic children. International journal of toxicology , 22 (4), 277-285.