Emerging research is challenging the long-held belief that tissue damage following myocardial infarction is permanent and irreversible.
For decades, the conventional medical view has been that damaged myocardium cannot regenerate, owing to the fact that heart cells are not as readily replaced as are other cells in the body.
Several research teams around the world, including a group based at Baylor College of Medicine and Texas Heart Institute, are studying the mechanisms that put the brake on myocyte regeneration. This line of inquiry suggests that the myocardium might, in fact, have regenerative capacities, opening up a whole new world of treatment approaches.
That’s good news, given that CVD is the still the number one cause of death in North America. Every year, over 800,000 people in the US have heart attacks. Though 90%, at least initially, long-term sequelae can be debilitating.
CVD prevalence will continue to rise if present trends continue. In a recent report from the Bogalusa Heart Study, nearly one-third of young adults (32%) in their 20s and 30s already show arterial plaque formation (Razavi AC, et al. JAHA. 2021). Much of the blame for that lies with unhealthy diet and lifestyle.
A Common Problem
A review of the literature confirms that a vast majority of heart attack patients sustain considerable cellular damage during an MI.
COVID-19 can also cause myocardial damage. Many infected people suffer from rapidly-developing blood clots, endothelial inflammation, pericarditis, and myocarditis. Inflammation of the myocardium can lead to cardiomegaly, scarring, and death.
Emerging research is challenging the long-held belief that tissue damage following myocardial infarction is permanent and irreversible. This line of inquiry suggests that the myocardium might, in fact, have regenerative capacities, opening up a whole new world of treatment approaches.
There are also a small but significant number of myocarditis cases—usually transient—in people who have received the Pfizer or Moderna COVID vaccines. This seems to be most prevalent with 18-39 year-old males, and tends to occur after the second dose. According to a recent report by Steven Gundry, MD, in the journal Circulation, the vaccines can trigger a rise in inflammation markers like IL-16, soluble Fas, and hepatocyte growth factor (HGF) (Gundry S. Circulation. 2021).
COVID long-haul patients are also drawing renewed attention to the issue of myocardial damage, since so many experience chronic heart problems.
After treating long COVID sufferers for over fifteen months, it became clear to me that while most could achieve a general recovery from COVID via intensive nutrition and lifestyle-based protocols, roughly 50% need extra help resolving the cardiovascular problems.
As I dug deeper into the medical literature I discovered research about nutraceuticals that show promise for helping COVID long-haulers to recover faster and better. Many of these nutrients and herbs may also help regenerate myocardium and improve cardiovascular function in people with non-COVID myocardial damage.
Vitamin C: Vitamin C is crucial to the production of collagens, the most abundant proteins in the extracellular matrix (ECM), and therefore the most abundant proteins in the body. The ECM has a fibrillar structure that provides a framework for tissue/organ morphogenesis, as well as for regeneration after injury.
Vitamin C impacts ECM homeostasis by regulating collagen synthesis and maturation. It is also an antioxidant, able to prevent damage caused by free radicals. In the cardiovascular context, vitamin C’s antioxidant capacity may mitigate endothelial damage following a heart attack or a viral infection such as COVID-19.
Vitamin C is also influential as a co-factor in many enzymatic reactions that determine how stem cells differentiate during tissue repair. It therefore plays an important role in both the production of myocardial cells, and in cellular repair and replacement (D’Aniello C, et al. Stem Cells Intl. 2017).
Vitamin D3: The roles of vitamin D3 in bone health, genetic expression, antiviral protection, and cancer prevention/treatment are well known. Less well known is the impact it has on cellular repair, especially cells in the heart and circulatory system.
The endothelium is an active organ, not simply an inert lining which allowed water and electrolytes to pass through. One of its key functions is the maintenance of nitric oxide levels. Vitamin D3 plays a central role in that process, by increasing cytoprotective nitric oxide (NO) while reducing peroxynitrite—an unstable nitrate isomer that can cause considerable oxidative damage. This favorable rebalancing allows endothelial cells to be repaired more rapidly.
Experiments using human umbilical vein endothelial cell cultures showed that vitamin D3 could effectively restore healthy NO/peroxynitrite balance in tissue perturbed by angiotensin-II. The authors conclude that “vitamin D3-stimulated improvement of endothelial function may directly benefit the treatment of the dysfunction of the cardiovascular system.” (Khan A, et al. Intl J Nanomedicine. 2017).
Vitamin E: Vitamin E is particularly effective in protecting and repairing cell membranes due to its strong anti-oxidant properties. The benefits of vitamin E—and tocotrienols in particular–in the treatment of heart disease, vascular disease, brain disorders, and fatty liver disease are well-documented.
Vitamin E is also an efficient scavenger of reactive oxygen species (ROS), specifically targeting lipid oxidation. It can prevent oxidized fats from damaging DNA. Vitamin E also helps to extend the antioxidant neutralizing capacity of vitamin C, making these nutrients a powerful one-two punch .
Modified Citrus Pectin (MCP): Citrus pectin is a naturally-occurring soluble fiber in the cell walls of citrus fruit peels. It is rich in beneficial β-galactoside. However, pectin’s long-chain polysaccharides are too large to be digested and absorbed into the bloodstream. So, the benefits of ordinary citrus pectin are limited to the GI tract.
It is possible to shorten the pectin fibers enzymatically, and through controlled changes in pH and heat. This enhances absorption, hence the term “modified citrus pectin.” Another step called de-esterification decreases the cross-linkages and gelling effects seen with unmodified pectin. It also renders the fiber ends more available to bind and inhibit Galectin-3, an adhesive cell surface protein that is a strong predictive marker for CVD and other inflammatory conditions.
The Prevention of REnal and Vascular ENd-stage Disease (PREVEND) study showed that elevated serum Gal-3 correlated with a three-fold increase of all-cause mortality in a cohort of nearly 8,000 general population subjects followed for a median of 10 years (DeBoer RA, et al. J Intern Med. 2012). Data from nearly 3,000 patients in the Framingham Heart Study showed that elevated circulating Gal-3 correlates strongly with abdominal adiposity, dyslipidemia, hypertension, and other indicators of CVD (Nayor M, J Am Heart Assoc. 2016).
MCP has a specific and very high binding affinity for human Gal-3. Researchers at the Hebei University of Chinese Medicine, showed that MCP ameliorated cardiac dysfunction, decreased myocardial injury and reduced collagen deposition in a rodent model of myocardial fibrosis.
The MCP downregulated a host of pathogenic biomarkers related to inflammation and fibrosis. The data, though preclinical, do support the notion that Gal-3 is a therapeutic target in post-infarction myocardial fibrosis, and that MCP may help to reduce the damage (Xu GR, et al. Biomed & Pharmacotherapy. 2020).
CoEnzyme Q10: This valuable nutraceutical has a proven track record for the prevention and the treatment of hypertension, ischemic heart disease, MI, heart failure, viral myocarditis, cardiomyopathies, dyslipidemia, obesity, type 2 diabetes mellitus, and other cardiometabolic conditions.
CoQ10 can significantly improve cardiomyopathy related to genetic or acquired dysfunctions in the left ventricle or mitral valve. A daily dose of 200 mg ameliorated fatigue and dyspnea, reduced posterior wall thickness, and improved mitral valve function. In viral myocarditis, it is able to quell inflammation. It also exhibited strong anti-inflammatory properties during various heart surgery procedures, and during recovery, as measured by C-reactive protein levels.
CoQ10 reduces the negative side effects—especially myopathy—of statin drugs.
It helps to both prevent and treat heart failure by improving the heart’s contractile force and increasing cellular oxygen levels. It also improves myocardial cell survival during ischemic events, and limits post-infarction myocardial remodeling (Zozina V, et al. Current Cardiol Rev. 2018).
Magnesium: Severe magnesium deficiency can lead to heart attacks. Magnesium deficiency also sensitizes the myocardium to the toxic effects of various drugs, as well as to hypoxia. Long term magnesium deficiency may also lead to chronic electrical instability of the myocardium, by affecting the sodium and calcium flow into the cells.
Extracellular magnesium ions exert a profound beneficial influence on the flexibility and structure of the arteries, arterioles, and veins. Most importantly, it is the transport agent that delivers glucose and oxygen to cell membranes and to the mitochondria for energy production.
Several studies have shown that anywhere from 40% to 50% of all patients hospitalized for CVD-related events are magnesium deficient (DiNicvolantonio JJ, et al. OpenHeart. 2018). Supplementation has significant potential cardioprotective benefits. But one of the challenges is that while supplemental magnesium may cross cell membranes and enter into target cells, it does not always reach the mitochondria. The addition of berberine along with magnesium can help.
Berberine: Berberine is a natural compound found in plants such as European barberry (Berberis vulgaris), Oregon Grape (Mahonia aquifolium), and Goldenseal (Hydrastis canadensis). It enhances cellular energy production via interactions with the Glut-4 molecule to transport glucose and oxygen from the inside of the cellular membrane to the mitochondria. By increasing the efficiency of glucose delivery, it lowers the levels of circulating glucose that can cause oxidative damage to the cardiovascular system
Berberine possesses a variety of pharmacological and biological properties that can potentially enhance cardiovascular performance: it reduces myocardial apoptosis and necrosis; it is a potent antioxidant and anti-inflammatory agent that can mitigate myocardial ischemia/reperfusion injury; and also lowers serum cholesterol and LDL (Yu L, et al. Oxidative Med Cell Longevity. 2016)
Specialized Pro-Resolving Mediators (SPMs): The ultimate goal of cardiac repair is to regenerate functionally viable myocardium, to prevent cardiac death. SPMs have unique properties that can play a big role in the repair process.
SPMs are a subtype of Omega-3 fatty acids. The category includes lipoxins, resolvins, protectins, and maresins. Physiologically, SPMs signal the immune system to stop generating pro-inflammatory signals, and instead to accelerate the return to homeostasis. They play a unique role in helping the body to shut down the immune response, to minimize additional inflammation, to clear away damaged tissue, and to promote tissue remodeling.
The degree of post-MI inflammatory damage is a major determinant of both the subsequent healing process and the long-term prognosis. Cardiomyocyte death leads to wall thinning, ventricular dilatation, fibrosis, and ultimately to ventricular dysfunction and heart failure.
In the wake of an MI, neutrophils, macrophages and lymphocytes contribute to the clearance of dead cells, while activating reparative pathways. SPMs act on specific receptors to regulate the activity of these various leukocytes.
SPMs also blunt the release of inflammatory mediators, and downregulate endothelial cell activation and platelet aggregation. Supplementation with SPMs typically normalizes biomarkers of inflammation, including C-reactive protein (Leoni G, Soehnlei O. Front Pharmacol. 2018).
Astaxanthin: Astaxanthin is a red carotenoid pigment naturally produced by a type of microalgae called Haematococcus pluvialis and by some forms of yeast. It is well known for its ability to scavenge free radicals.
Astaxanthin is itself able to capture free radicals, and it also stimulates production of antioxidant enzymes such as catalase, superoxide dismutase, peroxidase, and glutathione-S-transferase. Physiologically it is anti-inflammatory, capable of downregulating numerous pro-inflammatory signals including IL-1β, IL-6, IL-8, and TNF-α. It also decreases apoptosis, and modulates autophagy.
In the context of CVD, there are several animal studies showing cardiac muscle preservation when astaxanthin is given either orally or intravenously prior to the induction of ischemia. The evidence is promising, though not yet confirmed in human studies (Fassett RG, Coombes JS. Molecules. 2012).
Several recent review articles propose a role for astaxanthin in mitigating the cardiovascular and respiratory damage caused by the COVID-19 cytokine storm. Given its myriad anti-oxidant and anti-inflammatory effects, this is a reasonable hypothesis though again, there are not yet any clinical trials to prove efficacy.
L-Taurine: Taurine is a unique sulfur-containing amino acid that influences many cellular functions including osmoregulation, antioxidation, ion movement modulation, and conjugation of bile acids. It is found in high concentrations in seaweed, shellfish, and fish, and to a lesser degree in beef, lamb, pork, and poultry.
Taurine is much more than simply a building block for proteins. It is anti-inflammatory, and there’s some evidence that it can benefit the cardiovascular system, possibly by inhibiting the renin-angiotensin system.
Following ischemia induced by coronary artery occlusion, taurine resulted in significantly smaller myocardial infarct size. It also elevated superoxide dismutase levels, and decreased interleukin and TNF-α. In patients with heart failure, taurine improved tolerance and recovery during increased exercise.
In a study of obese women, supplementation with 3 grams of taurine per day for eight weeks, resulted in meaningful weight loss and also significant drops in systemic inflammation (Rosa TC, et al. Eur J Nutr. 2014)
In another study, continued supplementation with taurine corrected cardiomyopathy by restoring mitochondrial function and improving cardiac energy metabolism (Qaradakhi T, et al. Nutrients 2020).
Arterosil: This innovative product is a supplemental form of rhamnan sulfate, a sulfated polysaccharide extracted from two types of sea algae (Monostroma Latissium and Monostroma Nitidum). Rhamnan sulfate is an antithrombin-dependent anticoagulant and also an anti-inflammatory agent (Okamoto T. J Natural Med. 2019).
Arterosil is particularly effective in repairing damage to the endothelial glycocalyx, the gel-like glycoprotein layer that coats the inner surfaces of blood vessels. The glycocalyx is, essentially, the first line of endothelial defense, preventing the penetration of harmful substances like oxidized LDL, cholesterol, fats, inflammatory compounds and clotting factors. Glycocalyx damage is one of the first steps in the pathogenesis of atherosclerosis, and it correlates strongly with many biochemical markers of CVD.
Arterosil has myriad cardiovascular benefits. A Baylor University study showed that within hours of ingestion, arterial elasticity increased by an average of 89.6%.
MRI studies of men and women with high-risk carotid artery plaques, showed average plaque regressions of 46.8% in men and 64% in women who took Arterosil for 3 months. There was also a 56% average reduction of the lipid core size in the carotid plaques, indicating a shift away from unstable plaques prone to rupture.
Arterosil markedly lowers diastolic blood pressure, with improvements beginning within the first month of supplementation (Patil N, et al. Front Cardiovasc Med. 2018).
In addition to the above list, the following nutraceuticals also deserve honorable mention in the context of preventing and treating CVD: Resveratrol, Quercetin, D-ribose, L-Carnitine, Nicotinamide Adenine Dinucleotide, Omega-3 fatty acids, Grapeseed extract, Folate, Inositol, L-Arginine, Garlic, Serrapeptase, Nattokinase, Lumbrokinase, and Hawthorn berry.
Charles K. Bens, PhD, is a nutritionist and educator based in Sarasota, FL. He is the founder of Healthy at Work, a corporate wellness program, and the author of 9 books, including Healthy at Work: Health in Your Pocket: Your Pocket Guide to Good Health. Reach Dr. Bens at: email@example.com