Heart Failure or Therapy Failure? Toxins Cause Cardiomyopathy
Thomas E. Levy, MD, JD, Contributing Editor Orthomolecular Medicine News Service, November 3, 2023 OMNS (November 3, 2023) Cardiomyopathy simply means heart muscle disease. [1] It can occur as a primary affliction of the heart muscle, from a secondary condition negatively impacting heart function, or from a combination of both these clinical conditions. [2,3] Relatively recent changes in the definition of cardiomyopathy have been put forward that differ somewhat with these long-standing categorizations of heart disease. However, for the practicing clinician, the most important considerations in approaching the cardiomyopathy patient with clinical heart failure are:- Is the heart muscle itself diseased?
- Is the heart muscle normal but being forced into failure by non-cardiac factors?
- Is the clinical presentation a combination of both these conditions?
- Is the treatment protocol aimed only at relieving symptoms or also at resolving the underlying pathology resulting in the clinical heart failure?
Heart Failure Pathophysiology
When the function of the heart is impaired sufficiently to decrease the amount of blood that should be pumped with every heartbeat (cardiac output), a clinical picture of heart failure will eventually emerge. As the body can clinically compensate reasonably well for early heart failure, it is only when the decreased function is severe enough and chronic enough that heart failure symptoms become clear-cut. Because of this, even seemingly mild heart failure symptoms should be taken very seriously, with a complete diagnosis (especially in the ongoing pandemic setting), and the application of scientifically-based treatments for supporting and improving heart function. Common symptoms of heart failure include the following, due basically to the abnormal accumulation of fluid in the lungs and the rest of the body from inadequate heart pumping ability: [7,8]- Shortness of breath at rest or too quickly with exertion
- Shortness of breath when lying flat
- Waking up suddenly short of breath
- Fatigue
- Swelling in feet, ankles, and eventually legs and/or abdomen
- Accelerated heart rate, palpitations
Toxins and the Heart
While toxin accumulation in the heart muscle can be the singular cause of advanced heart failure, it will much more often be one of several factors contributing to decreased heart contractility. Also, the chronicity of the heart failure, regardless of cause, will play a large role in determining its reversibility, as more and more inflamed heart cells will eventually die and not just remain in a chronically inflamed state. Such inflammation is consistently seen on the microscopic study of heart biopsies in toxin- and infection-related cardiomyopathy. [14,15] 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
- Facilitating COVID pathogen entry into cells (ACE2 receptor binding). [89-91]
- Overstimulation of the immune response by being chronically present, evolving into an autoimmune disease. [92-94]
- Attacking not only tissue and organ cells directly, but also the walls of the blood vessels and the platelets circulating in them, resulting in the increased formation of blood clots. [95,96]
- Intrinsic toxicityof both the complete spike protein as well as fragments of it. [97-99]
- The ability to enter the genome of the cell where it currently cannot reliably be eradicated, along with the seeming ability to be replicated indefinitely. [100]
ATP Physiology and Cardiomyopathy
No cell, whether in the heart or elsewhere, is healthy when mitochondrial function and ATP production are chronically suppressed. Such suppression will reliably occur when the reduction-oxidation balance inside the cells is sufficiently shifted toward excess oxidation. All diseased cells have too little antioxidant presence, and this is reflected in higher cellular levels of calcium and lower cellular levels of magnesium, vitamin C, and glutathione. When these levels remain abnormal, mitochondrial ATP production will always be depressed as well. These cellular abnormalities are always present in diseased tissues or organs. [110,111] When cardiac ATP production can be restored to optimal levels with a normal increase capability for exercise, a healthy heart will result, unless irreversible damage has already taken place. [112] Of note, mitochondria are especially abundant in heart tissue, and more than 90% of the energy of the heart is generated by these mitochondria. As the heart completely renews its ATP content every 20 seconds or so, it can demonstrate clear mitochondrial insufficiency (heart failure) when other organs appear to be less affected or completely unaffected. [113,114] No organ consumes more energy per gram of tissue than the heart. [115] As the mitochondria are the intracellular sites of ATP (energy) production, significant research has been directed at finding ways to reverse or lessen “mitochondrial dysfunction.” [116] Most cases of mitochondrial dysfunction are due to the increased oxidative stress resulting from chronic infection and toxin accumulation, although rare genetic defects in mitochondrial function can result in the same clinical pictures of decreased energy production. [117] Much of this mitochondrial research has focused on defects in the electron transport chain (ETC) embedded in the membranes of the mitochondria. The ETC directly fuels the ATP synthase enzyme vital to the production of ATP at the end of that chain. The ETC has four main complexes, or steps, that work to optimally shuttle electrons to the terminal ATP-producing enzyme. [118,119] These complexes and their significant characteristics can be summarized and simplified as follows:- Complex I: NAD (nicotinamide adenine dinucleotide) in its reduced form, NADH, starts the electron donation sequence.
- Complex II: FAD (flavin adenine dinucleotide) in its reduced form, FADH2, continues the electron relay to ubiquinone (oxidized coenzyme Q10 [CoQ10]).
- Complex III: Ubiquinol (reduced CoQ10) relays the electrons to cytochrome c.
- Complex IV: Cytochrome c oxidase then receives the electrons where molecular oxygen is bound and reduced to water.
- ATP synthase (also known as complex V) is then activated to complete the ETC electron shuttling with the subsequent production of ATP.
- Brain disorders, including Parkinson’s disease and Alzheimer’s disease, stroke, and depression [149-152]
- Autism [153]
- ADHD (Attention Deficit Hyperactivity Disorder) [154]
- Hypertension (high blood pressure) [155-158]
- Coronary artery disease (atherosclerosis) and acute myocardial infarction [159-162]
- Improved clinical outcome post-coronary bypass and post-coronary angioplasty [163,164]
- Atrial fibrillation [165]
- Asthma [166,167]
- Obesity [168]
- Fibromyalgia [169]
- Diabetes (improved glucose and lipid profile) [170]
- Multiorgan failure when genetically deficient [171]
- Improvement in chronic kidney disease [172]
- Chronic lung disease [173]
- Fatty liver disease [174]
- Chronically increased oxidative stress [175]
- Vertigo [176]
- Sepsis and any critical illness [177-179]
- Statin cardiomyopathy [180]
- Statin myopathy (skeletal) [181]
- Eye disease [182]
Cardiomyopathy Treatment
The proper treatment of any form of cardiomyopathy, but especially advanced congestive heart failure due to an enlarged and poorly contracting heart, needs to be directed primarily at:- Toxin elimination
- Restoring normal cellular energy production
Until definitively established otherwise, an enlarged and poorly-contracting heart (advanced congestive cardiomyopathy) must be assumed to be secondary to mercury and antimony accumulation in the heart muscle.
As discussed at length above, the evidence indicates that cardiomyopathies can been assumed to have significant heavy metal accumulation and/or ongoing low-grade chronic inflammation. Also, toxin presence in the form of spike protein accumulation will be encountered with increasing frequency in this continuing COVID pandemic. Regardless of any test results, all cardiomyopathy patients should be taking one or more chelating, or toxin-mobilizing, agents. Furthermore, follow-up blood, urine, and/or hair testing should be done to establish that toxins are being mobilized because of the chelator administration. When testing clearly indicates high levels of one or more heavy metals in the heart, potent prescription chelation administration is often advisable, especially when heart failure is advanced. Such agents include, but are not limited to, the following: [236]- EDTA (orally, intravenously; calcium disodium EDTA best choice)
- DMSA (orally; especially good for mercury and antimony) [237,238]
- DMPS (intravenously-very potent, can cause substantial detox symptoms)
- Dimercaprol (British anti-Lewisite [BAL]) [239]
- Penicillamine
- Deferoxamine
- Trientine (especially copper)
- Organic acids, including alpha lipoic acid, citric acid, and ascorbic acid [240-243]
- NAC (N-acetylcysteine)
- Glycine
- IP6 (inositol hexaphosphate)
- Carnitine [244]
- As much of a wide variety of antioxidants as is feasible, including bioflavonoids, amino acids, and any supplement or food with a high organosulfur content. [245]Most chelators, including the prescription agents, are synthetic amino acid derivatives . [246]
- Vitamin C as ascorbic acid or sodium ascorbate, three to nine grams daily
- Magnesium, any of multiple forms, one to three grams daily
- Vitamin D3, 3,000 to 10,000 units daily, with a blood level target of 50 to 100 ng/cc
- Niacinamide, one to three grams daily (or NAD supplementation)
- Riboflavin, 200 to 400 mg daily
- Coenzyme Q10 (ubiquinone or ubiquinol), 300 to 900 mg daily
- Methylene blue, 10 to 25 mg daily
- Tyrosine (a CoQ10 precursor)
- Selenium (often depleted in cardiomyopathy)
- Succinate [253]
- 5-aminolevulinic acid (supports cytochrome c oxidase function) [254]
- Glycine (helps produce 5-aminolevulinic acid) [255]
- Ribose (rate-limiting precursor for adenine nucleotide synthesis and ATP production) [256]
- Carnitine (increases ATP; its deficiency also induces cardiomyopathy) [257,258]
Recap
The heart muscle in all cardiomyopathies is depleted in ATP, the most important energy-producing molecule in the body. The worse the cardiomyopathy, the more severe the depletion. Nearly all the time, this ATP-depleted state is precipitated and maintained by heavy metal accumulations, often accelerated by earlier pathogen-provoked myocardial inflammation (myocarditis). Such myocarditis is typically undetectable on routine chemistries, and only more invasive testing can clearly document it. When a patient presents with an enlarged, poorly contracting heart, it must be assumed that significant heavy metal accumulations are present and the treatment protocol must include chelation/toxin mobilization therapy. Depending on the patient history and laboratory findings, the clinician needs to decide whether chronic COVID with low-grade spike protein-mediated inflammation is a major (or entire) part of the pathology involved. If this is confirmed, or if clinical suspicions are high, measures to eradicate the spike protein should be vigorously pursued. [80-83] In addition to the heavy metal/toxin removal measures, targeted supplementation designed to directly support and heal the failing ability of the cardiac mitochondria to produce normal levels of ATP is essential for an optimal cardiac and clinical response. Even if there is refusal to acknowledge the likely presence of heavy metals in the failing heart muscle, which will continue to be the rule rather than the exception among traditional cardiologists, non-prescription nutrient chelators and ATP production promoters can still be taken as desired, and substantial benefit will result most of the time. Thomas E. Levy, MD, JD is a former Assistant Professor of Medicine at Tulane Medical School and a past Fellow of the American College of Cardiology. He is also a bar-certified attorney. He can be reached at televymd@yahoo.com. All his articles for the Orthomolecular Medicine News Service can be accessed at https://www.tomlevymd.com/health_ebytes.php. Note: To access any of the references below, type in the PMID number following the citation in the search box at this link: https://pubmed.ncbi.nlm.nih.gov/. References- Brieler J, Breeden M, Tucker J (2017) Cardiomyopathy: an overview. American Family Physician 96:640-646. PMID: https://pubmed.ncbi.nlm.nih.gov/29431384
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