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Hightower and Moore investigated the relationship between methyl mercury exposure, fish consumption, and the U.S. EPA's RfD -- not the relationship between methyl mercury and health effects.Chicago Tribune: Hightower is one of the few American physicians who have diagnosed and treated people with elevated mercury levels. After discovering that some of her patients had complaints suggesting mercury poisoning, such as headaches, fatigue and loss of concentration, she tested 123 children and adults who had symptoms or who reported eating fish. In a peer-reviewed study published in 2003, Hightower reported that 89 percent of the patients showed high mercury levels in their blood. (CT - December 11, 2005) Response: Personal opinions are not science
CT implies that Dr. Jane Hightower is successfully fighting an epidemic of fish mercury poisoning in the higher than average fish-consuming population of San Francisco; that nearly nine of every ten patients suffer some level of poisoning; that the successful treatment consists simply of reducing or removing fish from their diets. CT further attempts to add scientific authority to the Hightower paper with the qualifier “peer reviewed.” Fact-checking again exposes these claims as problematic. First, it is highly doubtful that Dr. Jane Hightower has ever actually seen anyone with true mercury poisoning. She has apparently been treating a laboratory value and assuming it is mercury poisoning. Her comment (2003) that hair loss first alerted her to heavy metal toxicity is revealing; it is not a symptom that has been reported in mercury poisoning according to expert knowledge. Secondly, San Franciscans eat seafood. Not finding ultra-trace mercury in their bodies would be surprising. Nearly everyone consulting a physician presents complaints, many of them variations on the symptoms listed by Hightower and reported by CT. The key issue is not a correlation between mercury presence and complaints. After all, flu outbreaks and winter holiday seasons are highly correlated, but one cannot militate against the flu by banning celebration of Thanksgiving, Christmas, Hanukkah and lunar calendar’s New Year. The real question is whether Hightower demonstrated that mercury has caused poisoning episodes, as CT clearly implies. The answer is no because Hightower never even investigated this relationship! Dr. Hightower did not try to establish causality. Experts point out that she merely developed a hypothesis based on a study of her patients (high-end fish consumers) and expressed her personal opinion about causality. An actual study of causality would have required a longitudinal scientific investigation with blinding to exposure. For example, in a post-publication commentary on Hightower and Moore (2003) , Schoen (2004) states: “Hightower and Moore investigated the relationship between methyl mercury exposure, fish consumption, and the U.S. EPA's RfD -- not the relationship between methyl mercury and health effects. Not all readers of EHP [Environmental Health Perspectives, the journal that printed Hightower and Moore, 2003] will appreciate the difference between documenting exposure levels and providing evidence for health effects, and not every reader will have followed the ongoing international controversy over the health effects of methyl mercury for fish consumers.” Another way of stating Schoen is that Hightower performed a descriptive (cross sectional) study of fish consumption and blood mercury levels, which, by definition, cannot be used to infer causality. Even so, people do it all the time; it just isn’t good science. Cross sectional studies can be used to develop a hypothesis, but then a proper study is required to prove it. Schoen’s elucidation is actually verified by Hightower herself: “Cause and effect regarding symptoms was not fully addressed in this study for the following reasons. A chart of symptomatology on all patients presenting to the office in the 1-year period of the study was not done. Therefore, a comparative analysis for the purpose of control is not available. Many patients who present to their doctor have symptoms that may be caused by other conditions. It is difficult to determine whether mercury is causing or exacerbating these symptoms, especially in the case of autoimmune phenomena, chronic fatigue syndrome, fibromyalagia, depression, sinusitis, coronary artery disease, and menopause, to name but a few [to say nothing of controlling for diet or health-damaging behaviors such as smoking or drug and alcohol abuse] where there is either a possible link to or an overlap of symptoms with mercury exposure. Second, the subjective nature of symptoms makes standardization difficult. Last, because only mercury was tested in these individuals, other contaminants [or non-contaminants such as diabetes, depression, thyroid malfunction, etc.] responsible for symptoms cannot be ruled out. Often the clinician recommends elimination of diets [or more likely, further tests] to establish whether the patient is affected by an exposure. It is important to demonstrate the normalization of blood mercury levels for clinicians who may want to try this as a diagnostic approach for certain individuals.” [Emphasis and comments added] The critical point is that Hg may have no relationship to Hightower’s findings whether there is or is not an association. Hightower is saying – albeit in a somewhat obfuscatory way – that she did not study cause and effect. That is, she cannot be sure the relationship between mercury and the symptoms is real. In addition, she doesn't know if mercury even contributes to the symptoms. She then goes on to imply that trying an elimination diet will help the physician sort out the issue. In sum, she is simply presenting her opinion with no evidence to back up a causal relationship. An elimination diet is not proof. To repeat, proving a relationship would be quite complicated and require blinding of exposure and the return of symptoms when exposed again. Additionally, by leaving out “a chart of symptomatology on all patients” Hightower and Moore were able to claim improvement with treatment without the burden of showing what was actually improved. Dropping someone’s blood mercury level – or any other measurable parameter – is not a cure; it is simply changing a measurement result. Dr. Hightower also fails to mention that average exposures in other countries (Japanese at 2 ppm, Faroese at 4 ppm, Seychellois at 6 ppm) occur without the reported symptoms seen in her patients (see Sec.6). “Treating” Sophie
Remember, Hightower was Sophie Chabon’s treating physician. There is no scientific validity for persisting in the popular claim that Sophie was “poisoned” by eating tuna. Not even Hightower herself makes such claims. Contradictions
It is also highly relevant that Hightower and Moore (2003) revealed some contradictory findings. They reported a reasonable scenario correlating higher consumption of swordfish with elevated blood mercury levels. There is nothing astonishing or alarming about this – not even for 550-year old mummified remains of native, marine-eating Alaskans with mercury levels twice those of living Alaskans. However, they also reported the puzzling and highly inconsistent scenario that the more red snapper and sole their patients ate, the lower their blood mercury levels! In the face of such contradiction, Hightower and Moore (2003) loosely offered their caution that "cause and effect regarding symptoms is not addressed in this article." Also, CT’s noting that 89 percent of Hightower’s patients recorded “high” mercury levels is, by implication, another unfortunate misuse of EPA’s RfD for methylmercury. An RfD is defined as a “safe” dose to consume daily over a lifetime . ( see Sec. 1) Reinterpreting the RfD
Of serious concern is reinterpreting the meaning of the RfD; to emotively insinuate that anything above the RfD presents risk of “permanent brain damage” in fetuses or young children. Rarely clarified is that EPA built in a safety factor of 10 (1/10 of what EPA considered risky – 58 ppb in blood, a number itself open to question). It is misleading to assert that anything exceeding the RfD is risky. Even the Faroes studies from which the RfD is derived don’t say the children examined had a disability [the finger tapping difference between controls and exposure was one finger tap ]. Further, results from the extensive Seychelles studies have consistently found no adverse effects from prenatal exposure to MeHg in fish among a population consuming on average about 10 times the daily intake of Americans. Another unreported numerical confusion in Hightower and Moore (2003) is the apparent unjustified lowering by them of EPA's RfD equivalent for mercury in hair to 5.0 ppb from 5.8 ppb. This problem extended to the next one: while the abstract of the Hightower and Moore (2003) paper claimed that 89% of their 89-subject sample exceeded the RfD, the discussion on the subsequent page suggests that 82 subjects and hence 82/89 = 92% of their sample had blood mercury above 5 ppb. The often quoted value of 89% apparently was derived from a larger sample of 103 patients with levels above 5.0 ppb, itself from an initial sample of 116 patients. One can understand how this confusion spilled over to a congressional "Dear Colleague" letter by Representative Mark Kirk of Illinois (see Sec. 17). Conclusion
The terminal problem with the Hightower report is that there is nothing to link exposure with symptoms. She did a cross sectional descriptive study that is useful for developing hypotheses. However, such studies tell us nothing about causation. If she believes there is a causal relation she should find and report it. |
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