Toxins Cause Heart Failure and Cardiomyopathy – Dr. Joseph Mercola

According to research¹ published in 1999, people with severe heart failure have 12,000-fold more antimony in their myocytes (the heart muscle cells responsible for contraction) than healthy controls. They also have 22,000-fold more mercury.

Mercury is a highly toxic metal that causes oxidative stress, weakening of the antioxidant defense system, enzyme inactivation and increased oxidative damage, all of which contribute to the deterioration of heart function.² Long-term exposure to antimony has also been linked to cardiovascular problems. Antimony also has estrogenic activity, which drives many chronic diseases, including cancer.

The oxidative stress caused by heavy metals is one of the primary ways in which they destroy your mitochondrial function. Some heavy metals, including mercury, cadmium and copper, also interfere directly with the mitochondrial electron transport chain,³ leading to reduced ATP production, which is crucial for cellular energy.

Mercury’s interaction with mitochondrial enzymes and membranes further amplifies oxidative damage, impairs cellular respiration, and can trigger cell death.

High Concentrations of Heavy Metals Are Nearly Always Present in Failing Hearts

In a November 2023 article,⁴ Dr. Thomas Levy, contributing editor for the Orthomolecular Medicine News Service, pointed out that the heart is “the preferred collection site” for most heavy metals, and as such, heavy metal toxicity is a common contributor to, and sometimes direct cause of, heart failure.

Various toxins, especially heavy metals like lead, copper, iron, mercury, aluminum, cadmium and others, can accumulate in heart tissue, contributing significantly to heart failure by directly damaging heart muscle cells and affecting their function. As reported by Levy:⁵

“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:

Levy cites studies showing how each of these toxic agents damage your heart and deteriorate cardiac function. Lead, for example, is linked to acute heart failure and myocarditis; copper toxicity to hypertrophic cardiomyopathy; iron to congestive heart failure; and mercury to idiopathic dilated cardiomyopathy (IDCM).

Recognizing and treating heavy metal toxicity can dramatically improve heart function, Levy notes, adding that chelation therapy has shown promise in reversing toxicity-related heart damage.

The Safest Way to Lower Your Iron

While Levy reviews the use of an iron chelator (deferoxamine) for severe iron overload, routine phlebotomy (blood donation) is another, likely safer, option. Side effects of deferoxamine include but are not limited to allergic reactions, respiratory issues, vision disturbances, hearing loss, muscle spasms and bone pain.⁶

For those with elevated iron levels, I recommend donating blood two to four times a year. If losing 10% of your blood in one sitting is too problematic, you can remove blood in smaller amounts once a month on the schedule listed below. If you have congestive heart failure or severe COPD, you should discuss this with your doctor, but otherwise this is a fairly appropriate recommendation for most.

Men	Postmenopausal Women	Premenopausal Women
150 ml	100 ml	50 ml

As reported by Levy:⁷

“[A] case report described a 27-year-old woman with ‘severe heart failure’ completely normalizing on an iron removal regimen. 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. Iron overload cardiomyopathy occurs most commonly in patients with hereditary hemochromatosis or secondary hemochromatosis (as with β-thalassemia and sickle cell anemia).

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.

Excess iron in the heart is also a predisposing factor to developing atrial fibrillation, an arrhythmia that contributes its own increased morbidity and mortality.

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.

Of note, resveratrol supplementation has been shown to dramatically improve heart function in animal models of iron overload cardiomyopathy. In another animal study,⁸ either deferiprone or N-acetylcysteine was effective in decreasing cardiac iron concentration.”