Heart Attack
The Human Cardiovascular System Is Under Attack by Lab-produced SARS-CoV-2 and by COVID “Vaccines”—Can Natural Therapies Be of Assistance?
Those of us who subscribe to a number of the independent physicians and scientists on Substack and elsewhere are aware that both lab-created SARS-Cov-2 and the COVID injections can damage the cardiovascular system. Before this last year, probably very few people knew what the terms “myocarditis” and “pericarditis” even meant; now, however, they are much more often understood.
While both COVID-19 and the COVID jabs (“vaccines”) can induce myocarditis and pericarditis (the latter etiology—the jabs—even acknowledged by our Pharma-captured FDA and CDC and evidenced in detail in numerous published studies in scientific journals), some insightful practicing cardiologists (e.g., Dr. Peter McCullough) have observed that the myocarditis induced by the “vaccines” seems to be more serious than that ensuing from the infection itself. (https://performance.wordpay.dev/2021/11/myocarditis-covid-vaccines/) The grim reality is that myocarditis of whatever origin can lead to blood clots, arrhythmias, stroke, heart attack, or even heart failure. Scar tissue (fibrosis) can occur in the myocardium, further increasing the risk for long-term complications such as those just enumerated. It is a sad fact that non-fulminant active myocarditis has a mortality rate of 25% to 56% within 3 to 10 years, owing to the progressed conditions mentioned above.—Kühl and Schultheiss. 2012. Dtsch Arztebl Int. 109(20):361-68.
Endothelial damage is another potential consequence of both COVID-19 and the COVID injections (Gundry. 2021. Circulation 144:Suppl_1; https://odysee.com/@OracleFilms:1/Dr.-Sucharit-Bhakdi-Oracle-Films-Message-HD:1), with the spike protein being the most likely initiating factor.—Lei et al. 2021. Circulation Research.128:1323–1326
Therefore, the question looms: Can we do anything to protect and to heal our wonderfully designed cardiovascular system? I believe that we can. And that is by implementing time-tested botanical medicines, nutrients, and nutraceuticals. I will outline some of these below. Note here, however, that such material should be understood to be only one sliver in a possible overall approach to long-haul COVID and COVID “vaccine” injuries that must also include immune, microbiome, mitochondrial, anti-inflammatory, and antioxidant support. Such a comprehensive (and tested) plan will be the subject of a forthcoming newsletter.
The most important nutrients for heart health are magnesium and potassium (both often found together in certain foods, especially many fruits and vegetables), vitamin E and selenium (these also tend to occur together in certain foods, such as seeds and nuts), vitamin D and omega-3 fatty acids (these two nutrients also occur together in certain foods, such as fish), and several of the B vitamins. As to some foods particularly friendly to the cardiovascular system, pomegranate (a personal favorite of mine) has been shown to powerfully protect the endothelium (Delgado et al. 2020. Curr Pharm Des. 26[30]:3684-3699) and cranberries have been shown to support endothelial function as well. (Heiss et al. 2022. Food Funct. 13[7]:3812-24) (Note that both pomegranate extracts and cranberry extracts are available on the supplement market for those who do not wish to regularly ingest these fruits.) As is well known, too, the antioxidant and anti-inflammatory effects of a large variety of berries and spices are also demonstrable factors in maintaining cardiovascular health.
Nutraceuticals for cardiovascular health have especially attracted the attention of investigators over the last 30 to 40 years. I will provide a brief summary of three of the major ones below.
L-Carnitine
Carnitine is an amino-acid-like compound and conditionally essential nutrient that is synthesized in the human liver from the amino acids lysine and methionine, but dependant upon sufficient levels of vitamin C, iron, and vitamin B6. Thereafter, it is taken up by the bloodstream, from which skeletal and cardiac muscle store and utilize most of that supply. It is also widely distributed in animal foods (the word “carnitine” being derived from the Latin word for “flesh,” carnis), but not in vegetative sources. Carnitine exists as one of two stereoisomers: L-carnitine (the “L” being an abbreviation for “levo”) and D-carnitine. The form present in the body is L-carnitine, which is also the form present in food. Altogether, the body makes about 25% of its needs, with the diet ideally supplying the remaining 75%.
Supplemental Sources of Carnitine
Supplemental sources of carnitine are widely available on the supplement market—primarily as capsules, but also in liquid form. A drawback assessed by some users is the fishy odor that is emitted. In some persons, this fishy odor can be emitted from the skin, but usually only if higher doses (several grams) of carnitine supplements are consumed. Carnitine should be taken on an empty stomach in order to achieve the best effectiveness. Unwanted side effects are rare; when they do occur, they tend to take the form of digestive discomfort and/or loose stools.
Functions of Carnitine
Carnitine is concentrated in tissues like skeletal and cardiac muscle that metabolize fatty acids as an energy source. This is because carnitine is crucial for fat metabolism in the body: it ensures the transport of long-chain fatty acids into the inner mitochondrial compartment where they undergo oxidation and serve to provide energy. It also facilitates the elimination of various metabolic wastes—which, if not eliminated, could damage cell membranes.
Benefits of Carnitine Supplementation
One of the most easily discernible benefits of carnitine supplementation is an improvement in energy and a consequent reduction in fatigue. This is not only easily observable clinically, but is widely acknowledged in the scientific literature. For example, in one study patients with cardiovascular disease were able to exercise more when taking carnitine supplements.—Thomsen et al. 1975. Amer J Cardiol 43[2]:300-06
Clinical Applications of Carnitine Supplements
Cardiomyopathy and Congestive heart failure
If the heart muscle (myocardium) distorts or enlarges or otherwise degenerates, this is referred to as cardiomyopathy. There are, however, several forms. Dilated cardiomyopathy, one of the more common forms, is where the myocardium is dilated—pulled and thinned. However, when the myocardium’s contractile strength begins to falter, so that cardiac output is reduced, this is referred to as heart failure. If either or both of the ventricles fail, congestion in the body will result, so that congestive heart failure (CHF) is experienced. The seriousness of the condition is reflected by the heart’s ejection fraction, which progressively falls as the condition worsens, and by a laboratory marker, brain natriuretic peptide (BNP), that rises with progression of the disease. Patients are classified into four stages, designated New York Heart Association (NYHA) 1-IV, with the higher the number, the worse the diseased state.
In a double-blinded, randomized, controlled clinical trial, 60 patients with CHF (ejection fraction < 50%, NYHA class II or III) received either propionyl-L-carnitine (a form of carnitine used in Europe, but less available and little appreciated in the USA) at a dose of 50 mg, t.i.d., or a placebo for 180 days. During the study, digoxin and diuretics were allowed. Significant improvements in maximum exercise times and ejection fractions were reported (ejection fraction actually improved from 41% to 47%). (Mancini et al. 1992. Arzneimittelforschung 42:1101-1104) In another clinical trial published in the same year, oral administration of L-carnitine for 12 weeks significantly improved the exercise tolerance of patients with angina. Notably, in nine patients with chronic congestive heart failure, 5 of them (55%) moved to a lower NYHA class and the overall condition was improved in 6 patients (66%) after the treatment with L-carnitine. —Kobayashi et al. 1992. Jpn Circ J 56[1]:86-94
In 2017, a meta-analysis of seventeen randomized clinical trials utilizing L-carnitine or propionyl-L-carnitine for 1625 patients with congestive heart failure was published online. It found that the carnitine treatment was associated with considerable improvement in overall efficacy, left-ventricular ejection fraction, strike volume, and cardiac output and in decreasing elevated laboratory markers of dysfunction (BNP and NT-proBNP).—Song et al. 2017.Biomed Res Int 2017:6274854.
A meta-analysis of 23 clinical trials that was published in January of 2021 looked at the supplementation of L-carnitine for dilated cardiomyopathy in 1,455 patients. It found that the treatment was associated with a considerable improvement in the overall efficacy, left-ventricular ejection fraction, and cardiac output as compared to the control groups. It was also determined that the L-carnitine therapy significantly decreased the elevated laboratory markers of dysfunction.—Weng et al. 2021. Biomed Res Int 12:9491615.
Ischemic Disease/Angina/Myocardial infarction/Arrhythmia
When blood and oxygen cannot get to vital parts of the body as a result of blockage, those areas are said to be ischemic. If the choked supply is to the heart, this is referred to as myocardial ischemia. A sharp chest pain, referred to as angina pectoris, is often a signal that ischemia is occurring in this region. Occlusion of the coronary arteries is most often the mechanism responsible. Plaque is often the occluding agent here, but a spasm (which can be caused by low magnesium levels, among other instigators) can also be responsible. Regardless of what is causing the occlusion, however, the eventual result is usually a “heart attack,” typically manifested by a prolonged, squeezing pain behind the sternum and some referred pain to other areas (shoulders, back, arms, fourth and fifth fingers, etc.) of the body. This situation entails a killing of part of the heart muscle, i.e. a myocardial infarction.
L-carnitine can have profound benefits in ischemia, in angina, and in post myocardial infarction, as several excellent clinical trials have demonstrated. As one example, in a double-blinded, placebo-controlled, randomized, crossover trial, 44 men with chronic stable angina received either L-carnitine (1 g/b.i.d.) or placebo for four weeks. The carnitine group achieved significant improvements in mean exercise workload, watts to onset of angina, and ST segment depression. Moreover, 22.7% of the patients became free of angina with L-carnitine, whereas only 9.1% did so with placebo.—Cherchi et al. 1985. International Journal of Clinical Pharmacology , Therapy, and Toxicol 23(10):569-72
A larger trial randomized 200 patients with exercise-induced stable angina to L-carnitine (2 g/day) for six months. Improved exercise tolerance, as measured during cycle ergometric testing, was one notable result, as well as a reduction in the number of premature ventricular contractions (PVC) at rest. This was accompanied by improvement in cardiac function and resultant performance that even eventuated in a reduction in the consumption of their cardioactive drugs. Furthermore, laboratory analysis showed an improvement in plasma lipid levels.—Cacciatore et al. 1991.Drugs Exp Clin Res 17:225-235
In yet another study, published in 2000, forty-seven patients with chronic, stable angina were randomized to receive L-carnitine (as a dose of 2 g/day) or placebo for three months. In the L-carnitine group, there was a statistically significant improvement in the exercise duration and in the time needed for the ST changes to revert to baseline. The authors concluded that L-carnitine improves the duration of exercise and the time to recovery of ST changes.—Iyer et al. 2000. J Assoc Physicians India 48(11):1050-2
L-carnitine has also been studied in post-infarction patients. In a controlled study, 160 post-infarction patients were followed for one year, with the study group taking L-carnitine at 2 g/b.i.d.. A pronounced decrease in mortality was seen with the carnitine group (only 1.2% died) compared to the control group (12% died).—Davini et al. 1992. Drugs Exp Clin Res 18:355-365
A multicenter, double-blinded, placebo-controlled, randomized clinical treated 472 subjects within 24 hours after a first anterior myocardial infarction with either L-carnitine (9 g IV daily for five days, then 6 g/d orally) or placebo for 12 months. Carnitine significantly attenuated left-ventricular dilation in the first year of treatment. The increases in end-systolic and end-diastolic volumes were markedly lessened by carnitine. The combined incidence of death and congestive heart failure after discharge was 14 (6%) in the L-carnitine treatment group versus 23 (9.6%) in the placebo group.—Iliceto et al. 1995. J Am Coll Cardiol 26:380-387
A review of clinical trials published in 2004 favorably summarized carnitine’s anti-ischemic and anti-anginal effects that were rather consistently demonstrated in the trials. (Ferrari et al. 2004. Ann N Y Acad Sci 1033:79-81) Then, too, a review and meta-analysis of thirteen controlled trials published in Mayo Clinic Proceedings in 2013 concluded: “Compared with placebo or control, l-carnitine is associated with a 27% reduction in all-cause mortality, a 65% reduction in VAs [ventricular arrhythmias], and a 40% reduction in anginal symptoms in patients experiencing an acute myocardial infarction.”—DiNicolantonio 2012. Mayo Clin Proc 88[6]:544-51
Coenzyme Q10 (CoQ10)
Coenzyme Q10 (CoQ10) is a lipid-soluble, vitamin-like compound that occurs naturally in the body and is most highly concentrated in the kidneys, pancreas, liver, and especially the heart. It serves as an outstanding antioxidant in cell membranes. As such, it protects cell structures against oxidative damage and even recycles vitamin E back to its active, antioxidant form after that vitamin has neutralized free radicals.
CoQ10 is a cofactor in the mitochondrial electron transport chain and has been shown to improve mitochondrial oxidative phosphorylation in humans. More precisely, it is one of a number of factors utilized in mitochondrial respiration to generate energy via adenosine triphosphate (ATP) because its enzymatic processes facilitate electron transfer.
It especially supports cardiovascular health. How so? For one thing, it continually supports the cellular energy production (ATP) by this never resting organ. Secondly, it increases the utilization of oxygen by the myocardium (heart muscle). It has also been shown to decrease the oxidation of LDL cholesterol—important because oxidized LDL cholesterol is implicated in cardiovascular disease. CoQ10 also supports a healthy endothelium. Finally, it helps to maintain an optimal blood pressure.
Natural Sources of CoQ10
Coenzyme Q10 is found in very small amounts in certain foods (especially animals foods—meat and fish), but the human liver makes the lion’s share of what our bodies require for optimal health. This occurs via a multi-step process that requires vitamin C and a number of the B vitamins, trace elements, and the amino acid tyrosine.
Supplemental Sources of CoQ10
As is well known, CoQ10 is widely available on the supplement market—in two forms: (1) ubiquinone (the oxidized form, which has been on the market for quite a few years) and (2) ubiquinol (the non-oxidized, or “reduced,” form that is newer on the market). (Both of these forms also occur in the body, with ubiquinone converting to ubiquinol in the mitochondria, as needed.)
Benefits of CoQ10 Supplements
CoQ10 as a supplement can provide many benefits to users, most of which relate to its antioxidant and energy-producing effects. Increased exercise tolerance and capacity are among its most appreciated benefits. For example: In a study of 41 subjects divided into a treatment group receiving 200 mg of CoQ10 and another group receiving a placebo, the treatment group experienced a greater resistance to exercise-related exhaustion as against the placebo group. —Cooke et al. 2008. J Int Soc Sports Nutr 5:8
Anti-fatigue effects for CoQ10 (at a dose of 300mg) were demonstrated in a controlled study of 17 persons using bicycle ergometers, with the study group showing better results in maximum velocity achieved and in experiencing less fatigue than subjects in the control group. —Mizuno 2008. Nutrition 24(4):293-99
In a placebo-controlled study of 100 healthy and well-trained exercise enthusiasts over a period of 2 weeks, 200mg/day of ubiquinol before exercise decreased oxidative stress and increased plasma nitric oxide (NO) in the study group as against the control group, leading to improved endothelial function, energetic substrate supply, and muscle recovery after strenuous exercise.—Sarmiento et al 2016. Biofactors. 42(6):612-22.
When CoQ10 Levels Are Not Optimal
Advanced age (esp. over the age of 69) is connected with lower coenzyme Q10 production, although there is a noticeable decrease after age 40. The liver similarly reduces production when the vascular system is stressed.
A number of pharmaceuticals also deplete bodily levels: statins, beta-blockers, phenothiazines, and tricyclic antidepressants being major players here. (Depletion with statins occurs because the production of both cholesterol and CoQ10 stems from the same biochemical pathway—the Mevalonate Pathway—which statins interrupt quite early in its flow.)
Hyperglycemia, obesity, inflammation, cholesterol oxidation, and left-ventricular dysfunction can occur when coenzyme Q10 levels are less than optimal. As to the latter, a study published in the American Journal of Cardiology found that when fourteen persons with elevated cholesterol took atorvastatin at a dosage of 20 mg/day (the standard dosage), ten of them were found to develop left-ventricular dysfunction. The administration of coenzyme Q10 (100 mg, three times a day) to nine of these subjects found this cardiac dysfunction improved or even rectified in eight of them, and that within a period of only three months.—Silver et al 2004. Am J Cardiol 94(10):1306-10.
Clinical Applications of CoQ10
Acute Viral Myocarditis
In a blinded, randomized clinical trial published in 2016, coenzyme Q10 was administered to 42 patients suffering from acute viral myocarditis, while 39 patients received trimetazidine and 43 patients received a combination of the two agents. Both coenzyme Q10 and trimetazidine individually decreased inflammatory and oxidative stress biomarker levels compared with baseline measurements, but the combination of the two achieved a more powerful effect than either agent alone.—Shao et al. 2016. J Cardiovasc Pharmacol. 68(2):150-54
Congestive heart failure
In 1992, cardiac specialists K. Folkers and P. and P. H. Langsjoen noted in a paper for a medical journal: “Twenty years of international open and seven double blind trials established the efficacy and safety of coenzyme Q10 (CoQ10) to treat patients in heart failure.” In the same paper, they reported on the administration of CoQ10 to 11 persons with heart failure awaiting heart transplants. The authors noted that all of these patients improved, with nine of them even moving from late stages of heart failure to earlier stages, with some no longer even requiring medication.—Folkers et al. 1992. Biochem Biophys Res Commun 182(1):247-53
When 2664 heart-failure patients in New York Heart Association (NYHA) classes II and III were enrolled in an open, non-comparative, three-month study in 173 Italian centers and given CoQ10 to the tune of 50-150mg/day (78% received 100mg/day), marked improvement was achieved in serious symptoms (edema, palpitations, vertigo, insomnia, dyspnea, sweating, vertigo, and others) by day 90 for the vast majority of the subjects—Baggio et al. 1994. Mol Aspects Med 15(Suppls):287-94
A double-blind, placebo-controlled, crossover trial was published in 2005 involving 21 heart-failure patients in NYHA class II and III who were divided into a treatment group that received coenzyme Q10 at 100 mg, 3 times a day, and a control group. The four-week-long trial resulted in the treatment group experiencing significantly improved left-ventricular ejection fraction that resulted in enhanced functional capacity.—Belardinelli et al. 2005. Biofactors 25(1-4):137-45.; cf. a trial published a year later by some of the same authors: Belardinelli et al. 2006. Eur Heart J 27(22):2675-81; cf., also, re: improvement in ejection fraction and survival: Langsjoen and Langsjoen. 2008. Clin Pharmacol Drug Dev 3(1):13-17
In a 2008 paper entitled “Coenzyme Q10, an Independent Predictor of Mortality in Chronic Heart Failure,” researchers found that the plasma concentration of CoQ10 was “an independent predictor of mortality” for 236 patients admitted to the hospital with CHF.—Molyneux et al 2008. J Am Coll Cardiol 52(18):1435-41
With the year 2014 came the results of the now-famous, two-year-long Q-SYMBIO trial, in which moderate to severe heart failure patients (420 altogether) were given either 100mg of CoQ10 three times a day or a placebo, in addition to standard drug therapy. The exciting results revealed pronounced improvement in the coenzyme Q10 group for cardiovascular mortality (9% vs. 16%, p = 0.026), all-cause mortality (10% vs. 18%, p = 0.018), and incidence of hospital stays for heart failure. In addition, a significant improvement of NYHA class was found in the CoQ10 group at the 2-year terminus of the study.—Mortensen et al. 2014. JACC Heart Fail 2(6):641-49
Finally, a recent meta-analysis of 14 randomized clinical trials involving 2149 heart-failure patients found that the CoQ10-treated patients experienced a lower mortality and a higher exercise capacity improvement than did those given a placebo.—Li and Yan. 2017. BMC Cardiovasc Disord Jul 24;17(1):196.
D-Ribose
D-ribose (also known as D-furanose) is a pentose sugar (a 5-carbon monosaccharide) in the cells of our body—and particularly in their mitochondria—that is involved in the production of energy intermediates such as adenosine triphosphate (ATP), NADH, and FADH, enabled through its binding to various nucelic acids.
Supplemental Sources of D-ribose
D-ribose is available on the supplement market, both in a powdered form and as capsules. The powder is sweet tasting and, in the opinion of many (myself included), delicious! It is typically dosed between 5 and 30 grams a day, depending on the reason for its supplementation.
D-Ribose Functions and Benefits
Supplemental D-ribose has been shown to improve cellular processes when there is mitochondrial dysfunction. It assists in the production of ATP through the pentose phosphate pathway (PPP), an alternative to the primary pathway fueled by glucose. It thereby increases phosphoribosyl pyrophosphate (PRPP), the precursor for de novo ATP synthesis and leads to an enhanced production of myocardial adenine nucleotide biosynthesis.
Theoretically, increasing adenine nucleotide availability could enhance high intensity exercise capacity. To test this supposition, a number of clinical trials have been conducted. While those trials involving healthy subjects have typically not yielded markedly significant benefits for D-ribose supplementation over placebo, results have been quite different when trial participants had existing cardiovascular issues, such as detailed below…
Clinical Applications of D-Ribose
Myocardial Ischemia / Coronary Artery Disease
With myocardial ischemia, a depression in myocardial tissue levels of high-energy compounds (preeminently ATP) occurs and the heart’s ability to distribute blood is reduced. This state can precipitate a heart attack or even a serious abnormal heart rhythm.
It is known, however, that myocardial adenine nucleotide precursor availability is an important limiting factor in the recovery of myocardial ATP post-ischemia. Not surprisingly, then, human and animal studies have demonstrated that D-ribose can help replenish deficient cellular energy levels following myocardial ischemia, as well as improve depressed cardiac function overall. In a 1992 study, W. Pliml and colleagues investigated the effects of oral D-ribose in 20 persons with coronary artery disease: First, the participants underwent treadmill tests. Then, each patient was given 60 g of either D-ribose or placebo, in four divided doses, for 3 days. On day 5, the treadmill test was repeated. The result was that the D-ribose group demonstrated increased treadmill exercise time before the onset of angina and/or the development of ischemic electrocardiographic changes during the exercise.—Pliml et al. 1992. Lancet. 340:507–510.
In a 2007 study, 143 persons with coronary artery disease—66 of whom had presented with myocardial infarction—underwent revascularization with off-pump cardiopulmonary bypass surgery. Cardiac indices were determined before and after revascularization and all of the patients received oral doses of D-ribose. Quite significantly, 43% of these patients showed an increase in their cardiac indices, which compared favorably to a historic increase of only 13% in such a situation. (Perkowski et al. 2007. J Card Surg. 22[4]:370-71) Then, in a randomized, double-blind, crossover clinical trial comparing the effects of infused D-ribose and placebo on regional wall motion, D-ribose improved contractile responses to dobutamine in viable myocardium with resting dysfunction in patients with ischemic cardiomyopathy.—Sawada et al. 2009. Cardiovasc Ultrasound. 7:5
Congestive Heart Failure
In that research has shown that there is a direct relationship between inadequate myocardial ATP levels and the development of congestive heart failure (CHF) in its ventricular diastolic form, several studies have been performed to determine if supplementary D-ribose could be of benefit in CHF.
One of the earliest of these was a prospective, randomized, double-blind study published in 2003 in which 15 patients with NYHA class II and III CHF and coronary-artery disease were given either D-ribose or a placebo—each at a dose of 5 g, t.i.d., on a daily basis for three weeks. After a hiatus of one week, the patients switched what they had been taking to the alternate type of supplementation (i.e., ribose to placebo and placebo to ribose) for an additional three weeks. The outcome was that in the treatment group only there was a significant improvement in quality of life as well as improvement in certain cardiac parameters—particularly, a shortened E-wave deceleration, an improvement in the atrial contribution to left ventricular filling, and a smaller atrial chamber size.—Omran et al. 2003. Eur J Heart Fail. 5(5):615-19
The year 2005 saw two published clinical trials demonstrating the benefits of D-ribose in CHF patients. In the first of these, supplementation of D-ribose in 14 NYHA Class II-III CHF patients with left ventricular dysfunction significantly maintained their maximal volume of oxygen (VO2max), concordant with a maintenance in maximal exercise capacity, as well as improved their ventilatory efficiency—powerful predictors of survival. The subjects also experienced improvement in their quality of life measurements (Carter, O. et al. 2005. J Am Coll Cardiol. 45:185 abstr). In the second of these, D-ribose was studied in a trial of NYHA Class II-IV CHF patients. In this trial, significant improvements in ventilatory efficiency were observed in the Class III-IV patients only, while the Class II patients achieved improved ventilatory efficiency that was not determined to be statistically significant.—Vijay et al. 2005. J Card Fail. 95 abstr.
An interesting study was published in 2008 wherein 16 patients with NYHA class III-IV heart failure took 5 g of D-ribose, t.i.d., for eight weeks and were assessed for VO(2), tidal volume/VCO(2), and heart rate/tidal volume. The welcome result was that every one of these participants manifested a significant improvement in ventilatory exercise status! (MacCarter et al. 2008. Int J Cardiol. 137[1]:79-80) Next, chronologically, was a study by Ohio State University researchers wherein 11 patients with NYHA Class II-IV heart failure and clinical symptoms but with normal left ventricular systolic function and diastolic dysfunction were given only 5 g of D-ribose daily for six weeks. Sixty-four per cent of these patients achieved improvements in cardiac function (tissue Doppler velocity [E']), which were still present three weeks after the end of the trial. Five patients also showed an improvement in their early diastolic filling velocity (E) to early annulus relaxation velocity (E’), while four manifested improvement in their maximum predicted VO2 values.—Bayram et al. 2015. Ther Adv Cardiovasc Dis. 9:56–65
The general conclusion from these clinical trials is that D-ribose helps to replenish deficient ATP levels in subjects with CHF. More precisely, its supplementation enables the cells to bypass a key metabolic enzyme needed for the production of ATP and to assist the failing heart to produce energy and thus to reduce diastolic dysfunction. —Krueger et al. 2021. Ann Transl Med. 9(19):1504
Botanical Medicine
This is yet another therapy that can favorably influence cardiovascular issues. Below, then, I will review some of the chief botanicals that have good supportive evidence. I will discuss these as they relate to specific cardiovascular conditions. In so doing, I will sometimes cite the professional experience of the Eclectic physicians who practiced in America from the mid-1800s until the mid-1900s. These physicians—who were trained not only in orthodox medicine but in botanical medicine, homeopathy, and other alternative therapies—actually encompassed one-sixth of the physicians practicing during those years and made an enormous positive impact upon the health of their patients—most noticeably observed during the time of the Spanish Influenza, when the botanical remedies prescribed by them (esp. boneset, Eupatorium perfoliatum) were observed to save many lives from that viral contagion.
First, let’s discuss the big topic of the day:
Myocarditis and Pericarditis
Botanical medicine for these two conditions has been utilized in America since the 1800s, and most prominently so by the Eclectic physicians. As a point aside, though, I’ve found it of interest that the alkaloid colchicine, derived from the autumn crocus (Colchicum autumnale) plant, has been used for pericarditis in modern orthodox medicine, with published research showing benefits from this plant-derived drug for this condition. (Imazio et al. 2014. Lancet. 383(9936):2232-37) Colchicine has also been used by orthodox clinicians as one form of therapy in myocarditis ensuing from the COVID “vaccines,” with one analysis of 238 such patients over a year’s time finding that 21.1% of them were treated with colchicine. (Ilonze and Guglin. 2022. Heart Fail Rev. 22:1–11) Fascinatingly, the autumn crocus plant has been utilized as an anti-inflammatory agent since 1500 B.C.E.
Bugleweed (Lycopus virginicus) herb
This is a mint that tends to grow next to water or in damp soil and is widely distributed throughout the central and eastern U.S., with related species occurring in Europe. Several of these species are available on the U.S. herb market—primarily in tincture form.
This botanical was highly esteemed by the Eclectics for heart health. The Eclectic physician Harvey Wickes Felter and the Eclectic pharmacist John Uri Lloyd observed: “Cardiac diseases, both organic and functional, have been markedly impressed by lycopus. Administered to patients suffering from endocarditis [inflammation of the inner lining of heart valves] and pericarditis it quickly subdues the inflammation.” (Felter, H. W. and Lloyd, J. U. 1906. King’s American Dispensatory) Similarly, the Eclectic physician Finley Ellingwood noted: “In pericarditis and endocarditis its sedative actions lessen the frequency of the pulse, irritability, and its attendant inflammation, in a manner equaled by no other remedy.”—Ellingwood, Finley. 1915. American Materia Medica, Therapeutics, and Pharmacognosy.
Cactus [Night-blooming Cereus] fresh stem (Selenicereus grandiflorus)
This cactus species, available on the U.S. herb market primarily in tincture form, was greatly praised by the Eclectics for cardiac health, but used only under specific indications (e.g., shortness of breath on exertion, feeble or irregular pulse, a feeling of constriction around the chest, angina, and weakness due to cardiac inadequacy), as it was understood that it had a potential for harm if used incorrectly (e.g., with forceful pulse, systolic hypertension, or mitral stenosis) or in too high a dose. In chronic pericarditis, Eclectic physician Rolla Thomas observed: “Cactus, especially, will be a good remedy to continue indefinitely, three or four doses per day.” He also indicated it for chronic myocarditis. —Thomas, Rollah. 1907. The Eclectic Practice of Medicine,
Echinacea (Echinacea angustifolia) root &/or Wild indigo (Baptisia tinctoria) root
The Echinacea species mentioned here is not the well-known species typically available on the market (Echinacea purpurea, the purple coneflower), but a species (known as narrow-leaved coneflower) growing in the Great Plains that is less commonly available, but still obtainable—as a capsule, a tincture, in tea bags, or in bulk form. Wild indigo [Baptisia], a plant of dry meadows and open woodlands, is, on the other hand, typically only available as a tincture.
One, or both, of these powerful anti-infective herbs was especially thought to be indicated in pericarditis with effusion of fluid. Here, Rolla Thomas noted: “If the effused fluid be of a purulent character, echinacea, baptisia,… would be used according to special conditions as expressed by the tongue.” He also prescribed these herbs for endocarditis of an ulcerative nature.—Thomas, 1907, Ibid.
Hawthorn (Crataegus oxyacantha) fruit/flower/leaf
Hawthorn is a shrub or small tree in the rose family comprising a large variety of species that grows in temperate areas of North America, Europe, and Asia. The flower and the leaf are most widely utilized in Europe and are the most scientifically studied parts, although the fruit has been the most popular form used in North America. Some of the available preparations—in the form of capsules, tablets, tea bags, tinctures, or the bulk herb—use all three parts of the shrub/tree.
The Eclectic physician H. W. Felter highlighted this botanical’s fine reputation among some of his colleagues in helping to manage chronic endocarditis, myocarditis, and pericarditis, and personally observed: “There can be no question as to its value as a tonic to the heart-muscle.” (Felter, H. W. 1922. The Eclectic Materia Medica, Pharmacology, and Therapeutics) Eli Jones, an Eclectic physician in practice for forty years, noted that hawthorn was the medicine of choice in myocarditis when “there is great difficulty of breathing, palpitation, rush of the blood to the head.” He advised a dose of ten drops of the tincture, given every three hours. —Jones, Eli. 1911. Definite Medication, Containing Therapeutic Facts Gleaned from Forty Years Practice
In the present day, a lengthy article on “Changes in Diffuse Myocardium” by family physician Alexey Portnov and reviewed by cardiologist Bella Koifman, recommends that myocarditis patients drink an infusion of equal amounts of dried hawthorn flowers and fruit, rose hips, nettle leaves, lemon balm herb, lovage roots, and valerian root, three to four times a day. — https://m.iliveok.com/health/changes-diffuse-myocardium_128866i15949.html
In a 2008 study, a powerful anti-inflammatory effect was observed in the carrageenan-induced rat-paw edema test using an ethanolic extract (tincture) of the fruit. —Tadić et al. 2008. J Agric Food Chem. 56(17):7700-9
Cardiomyopathy and Congestive Heart Failure
Arjuna (Terminalia arjuna) bark
This botanical, the bark of an Asian tree that grows about 60-80 ft tall, is the most important herb in Ayurvedic medicine for cardiovascular support. It is available on the Western market as a capsule, tablet, tincture, or in bulk form. It contains cardioactive glycosides (Yadav & Rathore. 2001. Fitoterapia 72[4]:459-61) and is being utilized to support cardiovascular function in dilated cardiomyopathy and congestive heart failure, based upon a number of scientific studies showing that it was able to regress signs of both, reducing dyspnea and fatigue. —Bharani et al. 1995. Int J Cardiol, 49:191-199; Verma and Bordia. 1988. J Res Educ Indian Med, 7:31-36; Antani, et al. 1991. J Assoc Physicians India, 39:801; Reichert. 1996. Quarterly Review of Natural Medicine, Fall, 177-178
Hawthorn (Crataegus oxyacantha) leaf, flower, and fruit
The German physician-phytotherapist Rudolf Weiss highlighted a threefold effect of this botanical upon the cardiovascular system, confirmed by studies and clinical experience: (1) Improvement of functional heart activity through an affectation of metabolism in the myocardium; (2) enhancement of coronary blood flow, partly through dilation of the coronary arteries; and (3) anti-arrhythmic action. (Weiss, Rudolf F. 1988. Herbal Medicine) Weiss and a co-author reported that they found hawthorn to be an effective therapeutic option in their own respective practice for cardiomyopathy. (Weiss, Rudolf F.. and Volker Fintelmann. 2000. Herbal Medicine, 2d ed. rev) The herb's flavonoids have been scientifically investigated and found to be strongly contributory to the increase in coronary blood flow that has been observed.—Schussler et al. 1995. Arzneimmitelforschung 45(8):842-45
. In harmony with these demonstrated and observed physiological effects, clinical trials have shown a positive effect upon early-stage congestive heart failure (NYHA Class II) and moderate-to-advanced congestive heart failure (NYHA Class III), both as measured by exercise capacity. In the most important of these, which enlisted over 200 subjects who received this botanical or a placebo for sixteen weeks, hawthorn was demonstrated to markedly improve exercise tolerance and to reduce heart-failure symptoms as against the placebo. (Tauchert. 2002. Amer Heart Jour 143:910-15) Likewise, in 2001, a randomized, placebo-controlled, double-blind clinical study on the clinical efficacy of Crataegus extract in 40 female and male outpatients suffering from congestive heart failure NYHA class II was performed which found the treatment group improving in exercise tolerance while the placebo group nosedived. Moreover, the heart rate x systolic blood pressure decreased by 26.8% in the treatment group, but only by 2.7% in the placebo group (Zapfe . 2001. Phytomedicine. 8[4]:262-66.) A 2003 meta-analysis of randomized, double-blind, and placebo controlled studies using hawthorn extract monopreparations in chronic heart failure found them to provide a “significant benefit” as adjunctive treatment; dyspnea and tiredness after exertion were especially observed to improve.—Pittler et al. 2003. Am J Med. 114:665–74
Stone root (Collinsonia canadensis) leaf, flower, & rhizome
This is a perennial mint native to the Eastern U.S. and Canada. It is available on the herb market as a tincture and as capsules. The Eclectic physician Herbert Webster praised this botanical as “a heart tonic of direct and permanent influence,” explaining that “continued use induces steady, permanent and highly satisfactory improvement in the strength and character of the organ, and a correspondingly improved general circulation.” (Webster, Herbert. 1893. Dynamical Therapeutics: A Work Devoted to the Theory and Practice of Specific Medication) Likewise, Felter and Lloyd highlighted J. M. Scudder’s clinical observations as to “its superior influence in quieting irritation, giving increased strength and regularity to the heart’s action, and increasing the strength of the patient,” and then added their own observation: “Collinsonia acts upon the tissues and valves of the heart, relieving irritation, increasing its power to act, and regulating its contractions.... Mitral regurgitation and the distressing cough of heart disease are greatly benefited by its administration.”—Felter and Lloyd. 1898. Ibid
Ischemia, Angina, Heart Attack, Stroke, Endothelial Damage
Arjuna (Terminalia arjuna) bark
Numerous studies have shown an anti-ischemic effect from this botanical, resulting in an improvement in exercise tolerance and a reduction in the frequency of anginal attacks in stable angina patients. (Dwivedi et al. 1989. Altern Med 3:115-122; Jain et al. 1992. Indian Med Gaz,36:56-59; Dwivedi and Agarwal. 1994. J Assoc Physicians India 42:287-289; Dwivedi and Jauhari. 1997. Indian Heart J 49:507-510; Bharani et al. 2002. Indian Heart J 54:170-175; Bhawania et al. 2013. J Pharm Res 6:493-498) A controlled study revealed that arjuna was even able to reverse the impairment of endothelial function that existed in chronic smokers.—Bharani et al. 2004. Indian Heart J 56 123-128
Garlic (Allium sativum) bulb (Warming, Drying)
Powdered, aged-garlic preparations have been shown to scavenge free radicals (exhibit antioxidant activity) and to protect endothelial cells and lipoprotein from oxidant injury, (Ide and Lau. 1997. J Pharm Pharmacol 49[9]:908-11; Imai, et al. 1994. Planta Med 60:417-20; Yamasaki and Lau. 1997. Nippon Yakurigaku Zasshi 110 Suppl 1:138P-141P) enhance endothelial integrity and production of nitric oxide, (Williams et al 2005. Phytother Res 19[4]:314-19; Weiss et al. 2006. J Nutr 136[3 Suppl]:750S-754S; Sun & Ku 2006. Am J Physiol Heart Circ Physiol. 291[5]:H2431-8; Morihara et al. 2002. Life Sci 71[5]:509-17) inhibit platelet aggregation, (Allison et al. 2006 J Nutr 136[3 Suppl]:782S-788S) and reduce coronary calcification. (Budoff et al. 2004. Prev Med 39[5]:985-91) When healthy adults took 300 mg/day of "standardized garlic powder" for two years or more, it was found to attenuate the typical, age-related increase in aortic stiffness, thus manifesting a protective effect on aortic elasticity.—Breithaupt-Grogler et al 1997. Prev Med 39(5):985-91
Hawthorn (Crataegus oxyacantha) fruit/flower/leaf
Although this botanical is primarily used in Western herbalism as a cardiotonic (see above) and antihypertensive, it has demonstrated anti-ischemic and endothelial protective effects as well: In animal studies, pretreatment with hawthorn reduced damage from experimentally induced myocardial infarction, (Veveris et al. 2004. Life Sci 74[15]:1945-55) prevented or reduced oxidative damage and pathological changes, (Jayalakshmi and Niranjali Devaraj. 2004. J Pharm Pharmacol 56[7]:921-26; Jayalakshmi et al. 2006. Mol Cell Biochem 292[1-2]:59-67) and stymied ischemic damage to both the brain and the heart. (Al Makdessi et al. 1996. Arzneimmittelforschung 46:25-27; Nasa et al. 1993. Arzneimittelforschung 43[9]:945-49; Zhang et al. 2004. Naunyn Schmiedebergs Arch Pharmacol 369[2]:232-38) Another study showed that hawthorn leaf flavonoids protected human umbilical endothelial cells from hypoxia through a regulating effect on nitric oxide and calcium ions. —Lan et al. 2005. Space Med Med Eng (Beijing) 18(3):157-60
Kudzu (Pueraria lobata) flower & dried root (Cooling)
This perennial vine, a transplant from Asia, is known as “The Vine that Ate the South” because it has proliferated as a weedy growth in this region of the U.S. It has, however, pronounced medicinal benefits: Sticking just with the cardiovascular system, scientific research has shown that this botanical accelerates the flow of blood in coronary arteries. (Lai and Tang. 1989. Zhongguo Zhong Yao Za Zhi 14[5]:308-11) In a clinical trial of arteriosclerotic subjects, it reduced cardiac ischemia and oxygen consumption, as well as improved cerebral blood flow. (Qicheng. 1980. J Ethnopharmacol 2[1]:57-63) A number of studies have revealed the positive effects that both this botanical and its active agent, puerarin, have had on inflammation, myocardial ischemia, oxidative stress, endothelial injury migration, cardiac hypertrophy, and myocardial fibrosis.—Jiang et al. 2022. Biomed Pharmacother. 147:112655.
Padma 28
This is a Tibetan herbal formula, available on the North-American market in a very slightly altered form (as Padma Basic) that I learned about in the mid-1990s from Dr. Terry Willard, one of my early teachers. It is a magnificent circulation-enhancing and anti-inflammatory formula. In one study, an aqueous extract of the formula “strongly decreased” the production of the proinflammatory cytokines TNF-alpha, IL-1beta, Il-6, and IL-8. (Barak et al. 2004. Eur Cytokine Netw 15[3]:203-09) A 2006 study found this formula capable of reducing the C-reactive-protein (CRP)-induced expression of the proflammatory cell-adhesion molecule E-selectin, while upregulating heme oxygenase-1(HO-1), a protective enzyme in human aortic endothelial cells. (Exner et al. 2006. Forsch Komplementarmed 13 Suppl 1:13-17) Padma 28 has even been shown in studies to support angiogenesis (the creation of new blood vessels) in healthy tissue, but not in cancer-ridden tissue, thus evidencing a modulatory effect upon angiogenesis (i.e., an angioregulatory effect).—Radomska-Leśniewska et al. 2017. Cent Eur J Immunol. 42(4):370-76; Radomska-Leśniewska et al. 2015. Cent Eur J Immunol. 40(2):249-62.
Tribulus (Tribulus terrestris) fruit
This is a widely distributed annual herb that was introduced into the U.S. and thrives as a weed in the southern and western portions of the country and as far north in the west as British Columbia. Its fruit is available on the herb market as a capsule, tincture, and bulk herb.
Tribulus has been widely used in China for cerebral arteriosclerosis, thrombosis, coronary artery disease, and myocardial infarction. (Chui et al. 1992. New Drugs Clinic Remed. 11: 202–04; Lu et al. 1994. Acta Univ. Med. Second. Shanghai 14[1]:78–79 ) In a Chinese clinical trial, saponins from the botanical were shown to be 82.3% effective in remitting angina pectoris, which seems to have occurred owing to a vasodilatory effect upon the coronary arteries and a circulation-enhancing effect in the whole of the coronary system. (Wang et al. 1990. Zhong Xi Yi Jie He Za Zhi 10[2]:85-87, 68.) The saponins perform these functions, at least in part, by increasing the discharge of nitric oxide from the endothelium and nitrergic nerve endings. (Adaikan et al. 2000. Ann. Acad. Med. Singap. 29[1], 22–26) In a rat study, the botanical showed anti-ischemic cardioprotection by means of a MAPK-mediated anti-apoptotic pathway. (Reshma et al. 2019. Biomed Pharmacother. 111:1342-52) Tribulus has also been shown to ameliorate mitochondrial dysfunction during ischemia.—Reshma et al. 2016. Life Sci. 152:220-30.
Conclusion
I hope you’ve enjoyed this initial newsletter article of mine and found the information to be of interest or value. I realize that it is pretty heady stuff and I want to thank you for taking the time to read it. If you feel inclined to leave feedback, please do so.
I’d like to conclude by pointing out that the above time-tested and scientifically demonstrated natural therapies have, sadly, been all but ignored during the current COVID crisis. This could well be to the great detriment of the many sufferers of the cardiovascular ills that have ensued from either COVID or the COVID injections. The fact, moreover, that these therapies are non-prescription and that they produce little or no side effects when utilized correctly should logically beckon clinical investigation for such ills. If, then, this newsletter article stimulates clinical interest in these remedies relative to the Corona Crisis, I will be most pleased.
Finally truth and compassion! I'll spread the word far and wide! There's more than a few doctors and media outlets that could learn a thing or two here. We are fortunate for your work and talent. May the universe protect you.
EXCELLENT, Matthew! You not only wrote with your 'pen' but with your heart. Always ready to share your knowledge and passion for the betterment of mankind! Thank you!!