Masters of Health Magazine December 2023 | Page 26

Many different toxins, including many heavy metals, have been either linked to heart failure or clearly shown to be the direct cause. Furthermore, one or more of these toxins is nearly always present in high concentrations in the affected heart muscle. A partial list of such agents includes the following:

•         Lead

•         Copper

•         Iron

•         Mercury

•         Aluminum

•         Cobalt/Chromium

•         Cadmium

•         Gold/Silver

•         Chemotherapy

•         COVID Spike protein

 

Lead: In a 3-year-old girl with chronic lead poisoning, acute heart failure developed that was clinically reversed after four days of calcium EDTA chelation therapy. [16] Children who died from heart failure secondary to acute lead poisoning were documented to have the microscopic findings of myocarditis. [17] Lead has been shown in other studies to target the heart and the vascular system. [18-21] Animal studies have also shown that enough lead exposure will reliably cause myocarditis and vascular damage as is seen in humans. These studies show that lead exposure will cause atherosclerosis and high blood pressure as well. [22-24]

Copper: A transition metal necessary for normal cell function but easily pushed to excess and toxic levels in the body, copper is another culprit toxin commonly involved in cardiomyopathy patients. [25,26] Excess copper appears to be especially toxic to the heart, as the infusion of copper into the coronary circulation of rats results in impaired heart function in only minutes. [27] Hypertrophic cardiomyopathy has been strongly linked to the excess copper levels seen in Wilson's disease. Trientine, a selective chelator of copper, has been shown to improve cardiac function in hypertrophic cardiomyopathy patients. [28]

In a randomized, placebo-controlled trial on diabetic patients with left ventricular thickening (that can lead to hypertrophic cardiomyopathy), copper chelation significantly decreased the heart wall thickening. This study did not even screen for elevated copper levels. [29,30] Furthermore, trientine chelation in diabetic rats with advanced left ventricular failure over an eight-week period demonstrated significantly improved heart function. [31] Another heavy metal-removal study in diabetic rats with either trientine or citrate (citric acid) significantly protected heart function. [32] In a case report a patient with scleroderma and a congestive cardiomyopathy improved dramatically on penicillamine, an effective chelator of copper, lead, and mercury. No copper level testing was reported as part of the evaluation of this patient. [33] These studies further indicate that toxicity from copper and/or other heavy metals in the heart is often a significant contributing factor in patients with early heart wall thickening and then its later decompensation into decreased cardiac function and heart failure.

It appears that a clear diagnosis of copper excess does not need to be made before just treating patients presumptively as having too much copper in their heart, especially when heart wall thickening is present in a diabetic patient. [34] It has also been shown a copper-overload state is a primary factor in the pathogenesis of damage to any organ in the diabetic. [35] Copper removal has also been shown to decrease the inflammatory response to radiofrequency ablation treatment for liver cancer in rats. [36] These findings strongly suggest that:

The unsuspected presence of excess copper in tissues and organs can impair the resolution of ANY pathology being treated, indicating a positive role for copper removal for nearly all medical conditions.

Iron: Congestive heart failure secondary to severe iron overload in the body has been described. The daily administration of an iron chelator (deferoxamine) in a congestive cardiomyopathy patient over roughly a year dramatically improved heart function and cardiac output, with heart pumping ability more than doubling (ejection fraction from 20% to 48%). [37] Another case report described a 27-year-old woman with "severe heart failure" completely normalizing on an iron removal regimen. [38] Patients with severe iron overload cardiomyopathy have an average survival of only one year when therapeutic phlebotomy (blood donation) and iron chelation are not utilized. This form of cardiomyopathy begins with restricted filling of the heart (diastolic dysfunction), and then evolving into a congestive cardiomyopathy. [39]

Iron overload cardiomyopathy occurs most commonly in patients with hereditary hemochromatosis or secondary hemochromatosis (as with β-thalassemia and sickle cell anemia). [40] However, excess iron short of that seen in full-blown hemochromatosis can still be expected to inflict its own dose-dependent toxicity. Most adults already have excess levels of iron in their bodies, as reflected by elevated ferritin levels that erroneously remain regarded as normal in laboratory reference ranges. [25] Excess iron in the heart is also a predisposing factor to developing atrial fibrillation, an arrhythmia that contributes its own increased morbidity and mortality. [41]

In animal studies, excess cellular iron in heart cells has been shown to increase oxidative stress and impair the ability of the mitochondrial electron transport chain (ETC) to produce ATP. As ATP is the primary energy-providing molecule in the body, any decrease in its production always results in compromised cellular function and disease. [42,43] Of note, resveratrol supplementation has been shown to dramatically improve heart function in animal models of iron overload cardiomyopathy. [44-46] In another animal study, either deferiprone or N-acetylcysteine was effective in decreasing cardiac iron concentration. [47]

Mercury: As the most toxic non-radioactive element, mercury is a heavy metal that causes grave damage wherever it accumulates. A landmark study directly compared toxic heavy metal concentrations in biopsies of heart muscle against control muscle biopsies in patients with idiopathic dilated cardiomyopathy (IDCM), meaning advanced heart failure of unknown cause. The cardiomyopathy heart muscle had 22,000 times more mercury in it than in normal heart muscle. Versus normal specimens, the same diseased heart muscle had 12,000 times more antimony, 11 times more gold, 13 times more chromium and 4 times more cobalt. Of great significance, there was no primary screening to detect increased heavy metal exposure in the study group, meaning these accumulations likely represent the finding in most cases of IDCM. [48] Unless excess exposures to heavy metals are readily apparent, the widespread effects of such poisonings make it very unlikely that such a toxicity will be suspected and then correctly diagnosed. [49]

In another study, the heart muscle in cardiomyopathy patients examined at autopsy revealed significantly higher levels of lead, nickel, copper, and manganese, and significantly lower levels of zinc compared to the heart muscle in non-cardiomyopathy patients. Mercury and antimony levels were not reported and presumably had not been measured. [50] This study indicates that most patients with IDCM have not only astronomical levels of mercury and antimony, but also significant elevations of lead, nickel, and copper. If it was not a vital organ, the ability of the heart to selectively remove heavy metals out of the blood and the rest of the body could be considered a protective mechanism for the health of the body! This leads to the conclusion that:

Cardiac muscle in patients with advanced congestive cardiomyopathy is the preferred collection site for most of the heavy metals taken into the body.