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Section 8: Cardiac Arrest

If, as Guallar et al. suggest, mercury increases the risk of myocardial infarction by more than 100 percent when the hair mercury level reaches 2 ppm, how can one explain the absence of effects at doses greater than 100 ppm?
- Plante and Babo (2003)

Eating lots of ocean fish isn’t much of a hazard compared to missing out on the benefits from not eating fish. A slew of scientific reports have shown that eating fish helps protect against cardiovascular disease and enhances brain development before and after birth. Overstating the almost negligible risk of mercury could adversely affect millions of people who face the risk of heart disease.
-Dr. Tom Clarkson, University of Rochester Seychelles researcher

Chicago Tribune:

Other studies suggest the heart benefits of eating fish might be offset by mercury. Though the American Heart Association recommends eating fish twice a week to "benefit heart health," two major European studies found that mercury exposure can increase the risk of fatal heart attacks in men. (CT - December 11, 2005)

Response:

Study Problems

The results of the European studies referred to have been found, upon subsequent review, to be weak and to perhaps have not accounted sufficiently for cross-cultural differences and other confounders. An easily accessible reference is CSPP’s paper, “Fish, Mercury and Cardiac Health” , in which specifically examined is the question, “Does the trace amount of mercury in fish overwhelm the nutritional benefits for heart health?” A brief summary follows.

First, a description of the two European studies claiming negative cardiac health associated with fish consumption.

(1) The Finnish Study published in Salonen et al. (1995, 2000) + update in Virtanen et al. (2002) + latest update in Virtanen et al. (2005) .

This study of 2005 men from Kuopio, eastern Finland found that men in the highest quarter (> 2.5 ppm) of Hg exposure had a 1.6-fold risk of CVD death and 1.7-fold risk of CHD death when compared to men in the lowest three quarters after adjusting for numerous risk factors including age, LDL (bad) cholesterol + triglyceride, intake of saturated animal fatty acids, etc.

(2) The European/Israeli Study by Guallar et al. (2002) .

This is a case-control study of 684 men with 724 controls that reported increasing toe nail mercury levels from 0.11 to 0.66 ppm (about 0.34 to 2 ppm in equivalent hair mercury levels) is associated with a doubling of the risk of myocardial infarction after adjusting for numerous risk factors like age, family history of heart attack, smoking status, alcohol intake, diabetes, history of hypertension, selenium intake and etc.

Numerous risk factors other than MeHg in fish more likely explain most of the findings in both Salonen et al. (1995, 2000) and Guallar et al. (2002).

Specific criticisms on Salonen et al. (1995, 2000) include the following:

(1) Salonen et al. (1995)’s own admission: “Theoretically, our findings could be specific only for men in Eastern Finland, who traditionally have a high intake of meat, fish, and saturated animal fat and a low intake of selenium and vitamin C and, most likely, other vegetable-derived antioxidants.”

Image

(2) The Kuopio population has one of the highest recorded rates of CHD and high consumption of animal fat with high measured levels of LDL (bad) cholesterol. (See Fig. 8-A)

(3) Stern (2005) pointed out that even in the first report of Kuopio study by Salonen et al. (1995) as long as 9 years already elapsed between the collection of hair + urine samples and the recording of a CVD + CHD + death event. An updated report of KIHD Hg-related results in Virtanen et al. (2002) extends the elapse time to as long as 16 years and hence contributes to a serious potential misclassification of causes and effects. The latest updates in Virtanen et al. (2005) covered deaths through 2002 and thus extends the elapse time another 2 years.

(4) Clarkson (2002) noted that highest recorded hair level is 15.7 ppm, more than 6 standard deviations from the mean and only a small % of the population has high hair Hg. Yet high-value points may play a major role in this type of study, “it would have been of interest to see if these correlations persisted when the very high mercury levels were excluded.”

(5) No clear accounting for stress—which is believed to be a major risk factor.

It is relevant that in an earlier experimental study of 62 healthy students from the same region (Kuopio, Finland), Agren et al. (1988) had instead found:

“A moderate intake of fish-containing meals has some beneficial effects on plasma lipid and prostanoid metabolism, when coronary heart disease risk factors are considered.”

Also relevant, the selected Kuopio students ate fish an average of 3.7 times per week, for 15 weeks. These meals consisted of 87% locally caught freshwater fish (vendace, pike, perch and rainbow trout) and 13% Baltic herring from brackish water. The largest decrease in CHD risk was found for those 21 students which consumed freshwater fish and restricted their lipid intake, compared to two other groups. In other words, health benefits were reported for the University of Kuopio students who both restricted intake of saturated fatty acids, and consumed freshwater fish.

Criticisms of Guallar et al. (2002) include the following:

(1) It is contradicted by results from Yoshizawa et al. (2002), a 5-year follow-up study of 33,737 U.S. male health professionals. The Yoshizawa study examines a wider range of toenail mercury levels, from 0 to 14.6 ppm (or about 45 ppm in equivalent hair), and that these levels were not significantly associated with risk for CHD.

(2) Why is LDL cholesterol not measured and identified as a risk factor (while HDL and total cholesterol were measured)?

(3) Guallar has been seriously challenged by Plante and Babo (2003) : “Patients with Minamata disease and hair mercury levels above 100 ppm did not have a higher rate of death from heart disease than controls, nor did they have a higher degree of arteriosclerosis. In the Minamata region of Japan, a population of approximately 50,000 with an average hair mercury level of 50 ppm did not have a higher rate of death from heart disease than a reference population of 800,000 with an average level of 9 ppm. ... Cree Indians with an average hair mercury concentration of 10 ppm have a lower risk of death from circulatory disease than the rest of the population in Quebec, in which the average hair mercury level is 0.5 ppm. If, as Guallar et al. suggest, mercury increases the risk of myocardial infarction by more than 100 percent when the hair mercury level reaches 2 ppm, how can one explain the absence of effects at doses greater than 100 ppm?” [Emphasis added]

Cardioprotective benefits

In sharp contrast to the suspect European studies relied upon by CT, there exists indubitable evidence that consumption of fish and omega-3 fatty acids provides numerous cardioprotective benefits.

Notably, clinical evidence demonstrates that fish consumption lowers risk for “sudden death”:

“The n-3 fatty acids found in fish are strongly associated with a reduced risk of sudden death among men without evidence of prior cardiovascular disease. As compared with men with levels of long-chain n-3 fatty acids in the lowest quartile, those with levels in the highest quartile had an 81 percent lower risk of sudden death.” (Albert et al., 2002)

“[W]e have summarized the growing clinical evidence that these n-3 fatty acids are antiarrhythmic and can prevent sudden cardiac death in humans. These n-3 fatty acids have been part of the human diet for some 2 to 4 million years ... They are safe and have been listed on the GRAS (‘generally regarded as safe”) list according to the Food and Drug Administration in amounts up to 3.5 g of fish oil per day.” (Leaf et al. 2003)

“Alexander Leaf and colleagues ... suggest a hypothesized cellular mechanism through which n-3
polyunsaturated fatty acid (PUFAs) affection channels to reduce the risk of arrhythmia. The messages ... are clear. For clinicians, it is time to implement the current American Heart Association dietary guidelines that recommend the dietary intake of 1 to 2 fish meals, particularly fatty fish, each week. For policymakers, there is a need to consider new indication for treatment with low-dose n-3 PUFAs supplements ...” (Siscovick et al., 2003) [Emphasis added]

Speaking on cardiac risk concerns, Professor Tom Clarkson, Distinguished Professor of Environmental Medicine at the University of Rochester commented:

“Eating lots of ocean fish isn’t much of a hazard compared to missing out on the benefits from not eating fish. A slew of scientific reports have shown that eating fish helps protect against cardiovascular disease and enhances brain development before and after birth. Fish is a rich source of low-fat protein and is full of fatty acids known to lower cholesterol. Overstating the almost negligible risk of mercury could adversely affect millions of people who face the risk of heart disease.”

Dr. Eric Rimm, Professor of Epidemiology and Nutrition at Harvard School of Public Health agreed:

“The message of fish being good has been lost and people are learning more about the hypothetical scare of a contaminant than they are of the well-documented benefits of coronary disease reduction. The danger of the tuna fish is not well documented compared to the potential dangers for a 50-year-old male or female who are at a much higher risk of coronary health.”

ImageAlso, there are the findings in “Fish Intake and Risk of Incident Atrial Fibrillation,” published in the American Heart Association’s journal, Circulation. In a 12-year follow-up for a cohort of 4,815 men and women over age 65 (in 4 U.S. communities), Mozaffarian et al. (2004) reported that adults consuming tuna or other broiled or baked fish 1 to 4 times per week had 28% lower risk of developing atrial fibrillation when compared to those who ate fish less than once per month. Those eating fish five times or more per week showed a 31% lower risk. Mozaffarian et al. (2004) concluded that “fish intake may influence risk of this common cardiac arrthymia” that affects more than 2 million individuals in the United States.

Finally, in a recent study by Calo et al. (2005) , researchers report that the use of the omega-3 PUFAs was significant for reducing the incidence of postoperative atrial fibrillation (AF) in patients undergoing coronary artery bypass graft surgery. Risk reductions were 18% absolute and about 54% relative (See Fig. 8-B).

The use of omega-3 fatty acids was also associated with a shorter hospital stay. Calo et al. (2005) explained:

“The main hypothesis of our study was that antiarrhythimic properties of PUFAs could also extend to the atrial myocardium, thereby protecting against the occurrence of AF. [O]ur findings represent the first direct evidence that PUFA supplementation may, indeed, be effective in preventing AF. Furthermore, our findings are in keeping with a recent study in which the consumption of tuna, and other broiled or baked fish, was associated with a 30% lower incidence of AF in a 12-year follow-up [i.e., the study of Mozaffarian et al. (2004) discussed above].”

Conclusion

Uncritical repetition of worrisome claims, such as examined above, exposes a demographically aging, at-risk society to unnecessary harm, and maybe preventable “sudden death.”
 
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