A Critique of the NEJM Amalgam Studies

0 Flares Twitter 0 Facebook 0 Google+ 0 LinkedIn 0 0 Flares ×

Current Exposures and Clinical Manifestations

The 2003 Clarkson, Magos, Myers mercury article in NEJM is very poorly done with a lot of inaccuracies, misstatements, and poor research. The following provides documentation for some examples of such affecting important issues. Summary fact sheets citing peer-reviewed studies and clinical results were analyzed along with peer-reviewed study references because listing all the references would make this review extremely long. There are over 1000 peer-reviewed studies referenced, supporting the premise of the fact sheets, which are contrary to the statements in the authors’ paper. The authors write: “Fish are the main if not the only source of methylmercury” (p. 1731) and that “among humans, the sole source of exposure to methylmercury is the consumption of fish and sea mammals” (p. 1733). This is wrong and contrary to published research and clinical experience. People with no exposure to fish or sea mammals can easily be found by test to have significant levels of methylmercury in blood, saliva, and brain from exposure to other forms of mercury. Dental amalgam is documented to be the largest source of mercury in most people who have several amalgam fillings, and other forms of mercury are methylated in the body by bacteria, yeast, and other methyl donors, making amalgam the largest source of methyl mercury in many.

Under mercury vapor they don’t point out that dental amalgam is the largest source of mercury vapor in most and that the studies that they show aren’t relevant to this exposure. There is a huge amount of documentation in the medical literature regarding the common adverse health effects from exposure due to dental amalgam that is disregarded by the authors, including over 60,000 clinical cases of recovery from over 30 chronic conditions after amalgam replacement. The authors don’t mention that thimerosal/ethyl mercury are documented to be a major factor in autism, ADHD, eczema, etc.

The authors state that chelation is not effective for methylmercury and ethyl mercury poisoning, which is contrary to evidence and experience. The fact that some people with acute exposures are irreparably harmed doesn’t warrant blanket statements that chelation isn’t effective in general. Thousands are treated with positive results by doctors throughout the country each year by many variations of what would be called chelation or detoxification. Since mercury forms vapor and inorganic and organic are being converted back and forth continuously in the body, one cannot neatly split exposure. Treatment results cannot be altered for the different forms of mercury exposure, although there are known differences in general effects and mechanisms.

Regarding mercury exposure from amalgam, the authors state wrongly: “it was realized that the actual inhaled dose was small, due to the small volume of the oral cavity” (p. 1732). This statement is strange since the authors go on to say dental amalgam is the chief source of exposure to mercury vapor for most. How, the fact is that the exposure isn’t small but rather very large, and more than the federal health guideline level is well documented in the medical literature from the many studies of mercury excretion in those with amalgam. Perhaps the problem is that these researchers do not have experience diagnosing and treating mercury toxicity and are not aware of what it means to talk of a small exposure in something as toxic as mercury.

The fact that all sewers and sewer sludge have high (and dangerous levels of mercury) with the largest source being from dental amalgam (dental offices and excretion of those with amalgam into sewers) is also disregarded. There is a typo in the reference the authors quote on level of exposure to mercury from amalgam (p. 1732) The number should be 5 rather than 8. The authors write: “Today’s occupational exposures, such as in the dental office are lower and may lead to mild, reversible effect on the kidney or mild cognitive changes and memory loss” (p. 1733). They site only one fairly old reference that didn’t focus on this issue, even though there are hundreds of studies and clinical investigations that document significant neurological, reproductive, cognitive, and immune effects of dental office exposures. There is substantive documentation that those with dental office exposures have exposures and body burdens much higher than the general population and higher than those patients with amalgam fillings on average. Additionally, the authors fail to mention that long-term adverse effects are common.

The authors state that “current evidence shows no connection” for a link between chronic mercury exposure and chronic neurological or autoimmune conditions such as Alzheimer’s, multiple sclerosis, Parkinson’s, etc.” (p. 1733). In fact, substantive documentation in the literature demonstrates that their statement is not true; again, the authors do not fully review the literature and clinical experience, which is extensive, and cite only three studies which they say agree with their position. The main study they cite, the Nun study, is known to have serious methodological flaws that meant the study would not be published by a scientifically peer-reviewed journal, including no valid control population or measurements of body burden. Another study used serum blood mercury levels to judge body burden, which is well documented to not be reliable for this purpose. None of the studies used reliable measures of body burden, nor did they bother to measure any of the known susceptibility factors, such as ability to excrete mercury or immune reactivity, which are documented in the literature to be the major factors in those who are adversely affected by mercury exposure.

The authors did not review the many hundreds of studies which document the mechanisms by which mercury causes the conditions seen in Alzheimer’s, Parkinson’s, multiple sclerosis, chronic fatigue, fibromyalgia, lupus, Lou Gehrig’s Disease, etc. or the thousands of cases of recovery or significant improvement from these conditions after treatment for mercury toxicity:

  • Alzheimer’s;
  • ALS;
  • Parkinson’s;
  • CFS;
  • FM;
  • lupus; and
  • other conditions.

Regarding the authors statements discouraging replacement of amalgam fillings (p. 1733), they do not point out that when amalgam fillings are replaced the increased exposure is temporary and limited where properly done. Nor do they discuss that daily exposure levels are reduced 60 to 90% in the long run (as documented in the literature) which has obvious benefits.

The peer reviewed studies and clinical studies document that thousands have recovered or had significant improvement from serious chronic conditions after amalgam filling replacement. The authors’ statement that “there is no clear evidence supporting the removal of amalgams” is obviously wrong and irresponsible because large numbers of reviewed studies have documented conditions where most who have amalgams replaced recover, and thousands are documented to have recovered from over 30 chronic conditions. The authors in dealing with prenatal exposure focus attention and limit discussion to methylmercury (p. 1735). However, it is well documented in the literature that adverse developmental effects are more common and occur at lower levels for mercury vapor exposure (as from dental amalgam) than for methylmercury. For example, it is well documented that prenatal exposure to thimerosal (rhogam shots) and amalgam from mothers are major factors in causation of autism and other children’s neurological developmental conditions.

The authors state that “it is reassuring that the only clinical reports of mercury poisoning from fish consumption are those from Japan in the 1950s and 1960s” (p. 1735) and “the risk posed by exposure to mercury is currently speculative” (p. 1735). The authors appear to either not be very knowledgeable about the medical literature regarding health effects from mercury or choose for unknown reasons to ignore the overwhelming evidence since there are extensive and well publicized studies and reports as well as government panel conclusions of adverse effects all over the world from mercury exposure through eating fish and marine mammals that eat fish.

Then, the authors quote the Seychelles study as an example of study that found no adverse effects from eating seafood (p. 1735). However, they don’t point out that it is well documented that the main assumptions in that study were faulty and incorrect. The study did not control for other significant mercury and neurotoxic exposures and excluded from the study those who experienced conditions, like epilepsy, that are known to be often be caused by mercury toxicity and did not control for or take into account known susceptibility factors. The main measure of mercury toxicity or exposure was hair level, which is known for those who are affected most by mercury exposure/toxicity to be inversely proportional to body burden and health effects—the opposite from the authors’ assumptions.

Another study found that prenatal mercury exposures and susceptibility factors such as ability to excrete mercury appear to be major factors in those with chronic neurological conditions like autism. Infants whose mothers received prenatal Rho D immunoglobulin injections containing mercury thimerosal or whose mothers’ had high levels of amalgam fillings had a much higher incidence of autism. While the hair test levels of mercury of infants without chronic health conditions, like autism, were positively correlated with the number of the mother’s amalgam fillings, vaccination thimerosal exposure, and mercury from fish, the hair test levels of those with chronic neurological conditions were much lower than the levels of controls and those with the most severe effects had the lowest hair test levels, even though they had high body mercury levels. This is consistent with past experience of those treating children with autism and other chronic neurological conditions. Very low levels of exposure have been found to seriously affect relatively large groups of individuals who are immune sensitive to toxic metals or have an inability to detoxify metals due to such as deficient sulfoxidation or metallothionein function or other inhibited enzymatic processes related to detoxification or excretion of metals. Those with the genetic allele ApoE4 protein in the blood have been found to detox metals poorly and to be much more susceptible to chronic neurological conditions than those with types ApoE2 or E3.

Note: While hair test mercury level is not a reliable indicator of mercury body burden or mercury toxicity effects in those susceptible to mercury toxicity effects, the hair test results are useful in indicating those with mercury toxicity. Since mercury toxicity affects cell membrane permeability, essential mineral absorption, and cellular balance, a pattern of essential mineral imbalances in those with normal diets is an indicator of mercury toxicity.

The authors state again that “methyl mercury is more potent” than other forms, which is not supported by scientific evidence, as previously seen. All of the forms are extremely toxic and are converted to other forms in the body and no categorical statement can be supported of this nature. Studies on thimerosal/vaccine effects document that ethyl mercury has toxicity effects of similar magnitude as methylmercury, and mercury vapor exposure has developmental effects at lower levels of exposure than methylmercury. The authors state that since the half-life of ethyl mercury in the blood is less than that of methylmercury. However, there is no scientific evidence supporting this conclusion and no plausible explanation of why the researchers would think so. Besides the fact that the conclusion of shorter half-life in the blood does not imply that body burden is less or decreased. Having a shorter half-life in the blood has no proven significance in the degree of developmental damage by a highly toxic neurologic substance. Mercury vapor, which has a far shorter half-life in the blood than the other two forms, has the most developmental effects at lower levels of exposure.

Additional data shows:

  1. Dental amalgam is the main source of human total mercury body burden because individuals with amalgam have 2-12 times more mercury in their body tissues compared to individuals without amalgam;
  2. There is not necessarily a correlation between mercury levels in blood, urine, or hair and in body tissues, and none of the parameters correlate with severity of symptoms; the half-life of mercury deposits in brain and bone tissues could last from several years to decades, and thus mercury accumulates over time of exposure;
  3. Mercury, in particular mercury vapor, is known to be the most toxic nonradioactive element, and is toxic even in very low doses; and
  4. Some studies which conclude that amalgam fillings are safe for human beings have important mythological flaws.


  1. Leistevuo J, et al. Dental amalgam fillings and the amount of organic mercury in human saliva. Caries Res. 2001; 35(3): 163-6.
  2. Sellars WA, Sellars R. Methyl mercury in dental amalgams in the human mouth. Journal of Nutritional & Environmental Medicine. 1996; 6(1): 33-37.
  3. Bjorkman L, et al. Mercury in saliva and feces after removal of amalgam fillings. Toxic App Pharm. 1997; 144(1): 156-62.
  4. Sandborgh-Englund G, et al. Mercury in biological fluids after amalgam removal. J Dental Res. 1998; 77(4): 615-24.
  5. Holmes AS, Blaxill MF, Haley BE. Reduced levels of mercury in first baby haircuts of autistic children. International Journal of Toxicology. 2003.
  6. Salonen JT, et al. Intake of mercury from fish and the risk of myocardial infarction and cardiovascular disease in eastern Finnish men. Circulation. 1995; 91(3): 645-55.
  7. Wisconsin Bureau of Public Health. Imported seabass as a source of mercury exposure: A Wisconsin case study. Environ Health Perspect. 1995; 103(6): 604-6.
  8. Watanabe KH, Desimone FW, Thiyagarajah A, Hartley WR, Hindrichs AE. Fish tissue quality in the lower Mississippi River and health risks from fish consumption. Total Environ. 2003; 302(1-3): 109-26.
  9. Oskarsson A, et al. Mercury levels in hair from people eating large quantities of Swedish freshwater fish. Food Addit Contam. 1990; 7(4): 555-62.
  10. Dickman MD, Leung KM. Hong Kong subfertility links to mercury in human hair and fish.
  11. Sci Total Environ. 1998, 214: 165-74.
  12. Kinjo Y, et al. Cancer mortality in patients exposed to methyl mercury through fish diet. J Epidemiol.1996; 6(3): 134-8.
  13. Choy C, et al. Seafood consumption linked to infertility. BJOG. 2002; 109: 1121-5.
  14. Grether J, Croen L, Theis C, Blaxill M, Haley B, Holmes A. Baby hair, mercury toxicity and autism. Int J Toxicol. 2004; 23(4): 275-6.
  15. Clarkson TW. Research on genetic aspects of nutrition and toxicology supported in part by the Heinz Institute of Nutritional Sciences and CanTox. J. Amer. Coll. Nutr. 2001; 20: 119-28.
Print Friendly