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Old 01-15-2008, 08:43 AM
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Default Zinc for Cardiac Disease


Zinc reduces intimal hyperplasia in the rat carotid injury model

Michael Bergera, Esthie Rubinrauta, Iris Barshackb, Arie Rotha, Gad Kerena and Jacob George, , a
a The Cardiovascular Research Laboratory, The Department of Cardiology, Elias Sourasky, Tel Aviv Medical Center, Tel Aviv University Sackler Faculty of Medicine, 6 Weizmann St., Tel Aviv, Israel
b The Institute of Pathology, Sheba Medical Center, Tel Hashomer, Tel Aviv, Israel
Received 17 February 2003; Revised 13 February 2004; accepted 17 March 2004. Available online 19 June 2004.


Background: The response to arterial injury following balloon dilatation is known to involve proliferative and inflammatory processes. The current widespread use of stents to maintain arterial patency not only does not eliminate but possibly exaggerates the proliferative and inflammatory phenotype and although drug-eluting stents are available, their long-term safety is yet to be determined.

Zinc is a trace element that serves as a cofactor of many enzymes. Interestingly, it has been shown to have anti-inflammatory and anti-proliferative properties. We thus sought to investigate its effect on smooth muscle cell proliferation and intimal thickening in the rat carotid artery injury model. Methods and results: Smooth muscle cells (SMC) were cultured from carotid arteries of rats and proliferation was assessed by thymidine incorporation after exposure to different concentrations of zinc. Next, carotid artery injury was induced in rats by balloon dilatation and they were either treated with I.P injections of zinc or PBS for 2 weeks until sacrifice for assessment of neointimal formation and lumen area.

Zinc inhibited in vitro SMC proliferation in a dose-dependent manner. In vivo, zinc treatment resulted in a 50% reduction in neointimal area and a significant decrease in neointimal/media ratio with no significant change in lumen area. Conclusion: Thus, zinc appears to reduce neointimal growth and should be tested by local delivery systems including stent coatings.

Author Keywords: Intimal thickening; Zinc; Smooth muscle cell; Proliferation

Corresponding author. Fax: +972 3 5469832.

Volume 175, Issue 2, August 2004, Pages 229-234
"Everything we hear is an opinion, not a fact. Everything we see is a perspective, not the truth." Marcus Aurelius
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Old 01-15-2008, 08:46 AM
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Default Further info On Zinc & Cardiac Disease Dr Eby part 1


by George Eby

revision date: December 21, 2006

Medical Hypotheses. 2005 Aug 3; (Pubmed Abstract with link to original journal article)
PDF of original journal article and
HTML of original journal article (with links to difficult-to-find orginal articles / references).
New: Journal article: Zinc supplementation inhibits lipid peroxidation and the development of atherosclerosis in rabbits fed a high cholesterol diet

What is Angina Pectoris?

According to the American Heart Association, angina pectoris is the medical term for chest pain or discomfort due to coronary heart disease. Angina is a symptom of a condition called myocardial ischemia. It occurs when the heart muscle (myocardium) doesn't get as much blood (hence as much oxygen) as it needs. This usually happens because one or more of the heart's arteries (blood vessels that supply blood to the heart muscle) is narrowed or blocked. Insufficient blood supply is called ischemia. Angina also can occur in people with valvular heart disease, hypertrophic cardiomyopathy (this is an enlarged heart due to disease) or uncontrolled high blood pressure. These cases are rare, though. Typical angina is uncomfortable pressure, fullness, squeezing or pain in the center of the chest. The discomfort also may be felt in the neck, jaw, shoulder, back or arm. Many types of chest discomfort aren't related to angina. Acid reflux (heartburn) and lung infection or inflammation are examples.

One needs to go to the Center for Disease Control page to learn that: "Blockages in the arteries in our body is caused by arteriosclerosis (hardening of the arteries) brought on, and/or aggravated, by several health risk factors. The main culprit ingredient is cholesterol, which mostly come from saturated fats that we eat, like red meats (pork, beef, etc.), eggs, butter, lard, dairy products, etc. Ingestion of these foods leads to high level of the bad cholesterol, which thickens the blood consistency, which leads to thick cholesterol "paint" deposits on the inside walls of the tiny coronary arteries, which are only 1 to 3 millimeters in diameter, like the size of a round toothpick. This situation is like using thick paint applied layers after layers, every second, day after day, year after year, onto the inner walls of these tiny pipes. Just like the sewer or drain pipes in our homes, this cholesterol "junk" could clog up our coronary arteries, as small as they are."

Experimental Evidence for Efficacy of Zinc in the Treatment and Prevention of Angina Pectoris.

In 1981 while Dr. William W. Halcomb DO, (currently of Mesa, Arizona) and myself were running our clinical trial of zinc gluconate throat lozenges and common colds, a man in his 60s entered the trial and received zinc gluconate. His cold did not respond to zinc and he used the 23 mg zinc lozenges each 2 hours for seven days. Even though our questionnaire was designed to detect and remove people from the trial who had any disorder other than a cold, he had sneaked in. That man had been on a railroad disability for angina pectoris for 15 years and was only moderately comfortable using nitroglycerin like candy all day long - but only if he did not exert himself physically. His pain was sufficiently intense that he had not worked for 15 years and he was essentially house bound.

The man returned a few days after the trial was over and told us that he wanted to know whether or not he received zinc or placebo, and if it was placebo (as he suspected) what was the placebo. We looked up the record, and told him he had received zinc gluconate. He then told us that after about 5 days on zinc, his angina pectoris pain disappeared for the first time in 15 years. After his zinc, he went snow skiing for the first time in over 15 years and had no trouble. This man obtained a new job and felt fine working hard all day - as long as he took his zinc!

Nearly immediately after that experience in 1981, a 70 year old father of a friend of mine tried zinc tablets, not as lozenges, but as dietary supplements to treat his excruciatingly painful 24/7 angina pectoris. He had no ability to exert himself due to angina pectoris pain. He was heavy, about 300+ pounds (150 kg) and 180 mg of zinc did not help him, but 300 mg of zinc (from zinc gluconate) after 30 days of treatment cured his angina pectoris - so he said. After about a year of freedom from angina pectoris and resumption of an active lifestyle, this man's cardiologist, while remarking his great pleasure with his progress, told my friend's father to discontinue the zinc because zinc would significantly decrease serum high-density lipoprotein concentration but would slightly increase low-density lipoprotein (the harmful type). Although such is true in healthy adults, less is known about changes in cholesterol in aging and/or unhealthy adults due to dietary supplements of zinc. Furthermore, I hypothesize that transient increases in low density serum cholesterol could easily have resulted from release of tissue bound cholesterol. In other words, would a serum increase in low density cholesterol result if zinc removed cholesterol from arteries??? I think such is possible, and offer some evidence. Also, excesses of zinc can lower copper and iron serum levels. Reductions in iron may be beneficial in several ways important in cardiology. Regardless, my friend's father died of congestive heart failure (possibly due to a taurine deficiency) about one month after stopping zinc. See this page for the role of taurine in cardiology.

In 1981, Dr. Halcomb nearly immediately incorporated these observations into his daily clinical practice. Since 1981 he found that control of angina pectoris with as little as 60-mg zinc tablets 3 times a day along with dietary changes and smoking cessation occurred in most of patients in clinical practice allowing either termination or substantial reduction in nitroglycerin intake. He said that more patients might respond to higher oral dosages, as long as zinc serum concentrations remain in the high part of the normal zinc serum range (about 140 micrograms zinc per deciliter).

How Can Zinc Cure Angina Pectoris?

How can zinc cure angina pectoris? Possibilities include: Zinc stabilizes cell membranes of the cardiovascular system. Zinc depletes excess stores of iron and cadmium (cadmium greatly worsens cardiovascular disease). Zinc competes with iron for gut absorption sites and blood transport proteins. Zinc prevents arterial scarring from viral infections of the arteries. Zinc ion is also anti inflammatory. Clearly, variations in normal zinc status (un-supplemented) as determined using zinc content of fingernails is not correlated with incidence of acute myocardial infarction.

I asked this same question to Dr. Ananda S. Prasad, M.D., PhD, of Wayne State University. Dr. Prasad is the foremost authority on zinc biochemistry on Earth and a distinguished professor of medicine. Dr. Prasad discovered zinc to be an essential human nutrient many years ago and has published extensively for more than 50 years on the role of zinc in biochemistry. Here are most of his papers, and here is a Google search for Dr. Ananda S. Prasad. Dr. Prasad's answer was very interesting. He said:

"Dear George,

Many thanks for your letter. I am indeed very excited about the Cardio-vascular events and zinc. The present day concept is that elderly subjects produce increased amounts of cytotoxic cytokines such as TNF-alpha , IL-beta and IL-8 and these cytokines affect the vascular endothelium and they generate activated endothelial cell molecules such as ICAM, VCAM and E- Selectin etc. These molecules trap platelets, red cells, neutrophil, monocytes etc. and plug up the blood vessels (thus angina and Sickle Cell Pain Crisis). Furthermore the monocytes-macrophages get activated and produce free radicals and reactive oxygen species (ROS) which lead to DNA oxidation and lipid peroxidation. Lipid peroxidation and LDL oxidation is believed to be critical for arteriosclerosis, and DNA- oxidation may be a pathogenetic factor for development of cancer.

I am sending you a paper which I published last year, defining basic roles of Zinc on inflammatory cytokines and oxidative stress. I am trying to get a NIH grant to do more work in the elderly.

Also you should see a paper published in Archives of Ophthalmology, May 2004 which reports that subjects who received zinc for prevention of blindness in age related macular degeneration, showed decreased mortality. All theses observations are very exciting for the role of zinc. I think that zinc may have decreased incidence of infections, decreased oxidative stress, or decreased mortality due to cardiovascular events or even cancer. All these need to be studied and documented.

So I am at it! Life goes on and it is becoming more difficult to get funds. Many, many thanks for your previous support.

Your sincerely,
Ananda Prasad
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Going a step further, Dr. Prasad's abstract of his article Zinc modulates mRNA levels of cytokines. reads: "Zinc plays an important role in cell-mediated immune function. Altered cellular immune response resulting from zinc deficiency leads to frequent microbial infections, thymic atrophy, decreased natural killer activity, decreased thymic hormone activity, and altered cytokine production. In this study, we examined the effect of zinc deficiency on IL-2 and IFN-gamma in HUT-78 (Th0) and D1.1 (Th1) cell lines and TNF-alpha, IL-1 beta, and IL-8 in the HL-60 (monocyte-macrophage) cell line. The results demonstrate that zinc deficiency decreased the levels of IL-2 and IFN-gamma cytokines and mRNAs in HUT-78 after 6 h of PMA/p-phytohemagglutinin (PHA) stimulation and in D1.1 cells after 6 h of PHA/ionomycin stimulation compared with the zinc-sufficient cells. However, zinc deficiency increased the levels of TNF-alpha, IL-1 beta, and IL-8 cytokines and mRNAs in HL-60 cells after 6 h of PMA stimulation compared with zinc-sufficient cells. Actinomycin D study suggests that the changes in the levels of these cytokine mRNAs were not the result of the stability affected by zinc but might be the result of altered expression of these cytokine genes. These data demonstrate that zinc mediates positively the gene expression of IL-2 and IFN-gamma in the Th1 cell line and negatively TNF-alpha, IL-1 beta, and IL-8 in the monocyte-macrophage cell line. Our study shows that the effect of zinc on gene expression and production of cytokines is cell lineage specific."

Role of Nuts in Preventing Cardiovascular Disease

The battle against cardiovascular disease has a ready ally in nuts high in zinc. Nuts are a rich source of many minerals such as zinc and other nutrients required to prevent cardiovascular disease in general. Nuts? You have been told to avoid them due to their fat content? That is some of the worst health advice ever given. Before I go on about nuts, read this wonderful article about nuts and their ability to reduce cardiovascular disease by over 50%. Initial evidence for the benefit of nut consumption came from population studies which looked at the diets of large numbers of people over long periods of time. In four US studies, the Adventist Health Study, the Iowa Women's Health Study, the Nurses' Health Study and the Physicians' Health Study, a total of over 160 000 men and women were followed for between 6 and 14 years. These studies showed very consistent indications for the health benefits of nuts. When compared with never eating nuts, the effect of eating small quantities of nuts (30 g) four to five times per week or more was a reduction in CVD risk of between 18 and 51%.

Variant Angina (Prinzmetal's angina)

In the case of "variant angina" (Prinzmetal's angina), I am personally convinced that the cause of the spasms occurring in variant angina or Prinzmetal's angina is magnesium deficiency, and at least 500 milligrams of magnesium should be taken every day in 125 mg doses at mealtimes and bedtime to maintain health generally and to prevent Prinzmetal's angina. I had a single episode of variant angina or Prinzmetal's angina (without any detectable arteriosclerotic plaque buildup) in 1998 (after ingesting much zinc since 1980), and the attending physician gave me an intravenous drip of magnesium sulfate (Epsom Salts). This, my only bout with variant angina or Prinzmetal's angina, was over in a few hours. I was instructed to increase my magnesium intake and variant angina has never returned. Magnesium deficiency is an extremely common nutrient deficiency in the West and some believe magnesium deficiency is the cause of much morbidity and mortality. Magnesium deficiency will cause much mental and cardiac problems. Note: Magnesium oxide is not biologically available.

My physician was right about magnesium, and this exact very rapid response was first reported by Czech doctors in 1973, later in 1986, and most recently by Israeli doctors in 1987. The Israeli doctors abstract showed that:

"The antithrombogenic effect of magnesium sulfate in vivo is shown at the site of endothelial damage induced by partial coronary and carotid artery constriction. The left anterior descending coronary artery of dogs and the right common carotid artery of rabbits were subjected to partial constriction with suture thread (40-60% reduction in transluminal diameter). Distal blood flow, as measured by electromagnetic flow probe, was not reduced. Scanning electron-microscopic examination of vessels fixed by glutaraledhyde perfusion and dried by the critical-point technique showed endothelial damage at the site of partial constriction ranging from crater- and balloon-like vesicular defects to cellular desquamation. Marked platelet deposition on exposed subendothelium and microthrombi could be seen with the maximum degree of luminal protrusion reaching 30% of the luminal diameter. Animals pretreated with magnesium sulfate (50 mg/kg, i.v.) showed platelet deposition restricted to a maximum of 1 or 2 discontinuous layers of platelets with most vessels showing only isolated platelets on exposed subendothelium. Microthrombi were not seen in any of the magnesium-treated animals. It is suggested that the therapeutic implications of magnesium in ischemic heart disease might be extended from its use in certain tachyarrhythmias and in arterial spasm associated with Prinzmetal's angina to the more classic episodes of ischemic heart disease where thrombus formation plays an unequivocally major role. Clearly magnesium sulfate is the treatment of choice for variant angina (Prinzmetal's angina). We will investigate further the effects of zinc in angina pectoris.

In 1996, Bernhard Hennig, et. al. wrote an article titled "Antiatherogenic Properties of Zinc: Implications in Endothelial Cell Metabolism". They pointed out that: Zinc is an essential component of biomembranes and is necessary for maintenance of membrane structure and function. There is evidence that zinc can provide antiatherogenic properties by preventing metabolic physiologic derangements of the vascular endothelium. Because of its antioxidant and membrane-stabilizing properties, zinc appears to be crucial for the protection against cell-destabilizing agents such as polyunsaturated lipids and inflammatory cytokines. Zinc also may be antiatherogenic by interfering with signaling pathways involved in apoptosis. Most importantly, we have evidence that zinc can protect against inflammatory cytokine-mediated activation of oxidative stress-responsive transcription factors, such as nuclear factor KB and AP- 1. It is very likely that certain lipids and zinc deficiency may potentiate the cytokine-mediated inflammatory response and endothelial cell dysfunction in atherosclerosis. Thus, the antiatherogenic role of zinc appears to be in its ability to inhibit oxidative stress-responsive factors involved in disruption of endothelial integrity and atherosclerosis. We discuss antiatherogenic properties of zinc with a focus on endothelial cell metabolism. Nutrition 1996; 12:71 l-717.

Later in 2000, Hennig, et al. wrote: "Little is known about the requirements and function of zinc in maintaining endothelial cell integrity, especially during stressful conditions, such as the inflammatory response in cardiovascular disease. There is evidence that (my emphasis) zinc requirements of the vascular endothelium are increased during inflammatory conditions such as atherosclerosis, where apoptotic cell death is also prevalent. Apoptosis is a morphologically distinct mechanism of programmed cell death which involves the activation of a cell-intrinsic suicide program, and there is evidence that factors such as inflammatory cytokines (e.g., tumor necrosis factor [TNF]) and pure or oxidized lipids are necessary to induce the cell death pathway. Because of its constant exposure to blood components, including prooxidants, diet-derived fats, and their derivatives, the endothelium is very susceptible to oxidative stress and to apoptotic injury mediated by blood lipid components, prooxidants, and cytokines. Thus, it is likely that the cellular lipid environment, primarily polyunsaturated fatty acids, can potentiate the overall endothelial cell injury by increasing cellular oxidative stress and cytokine release in proximity to the endothelium, which then could further induce apoptosis and disrupt endothelial barrier function. Our data suggest that zinc deficiency exacerbates the detrimental effects of specific fatty acids (e.g., linoleic acid) and inflammatory cytokines, such as TNF, on vascular endothelial functions. We propose that a major mechanism of zinc protection against disruption of endothelial cell integrity during inflammatory conditions, is by the ability of zinc to inhibit the pathways of signal transduction leading to apoptosis and especially mechanisms that lead to upregulation of caspase genes."

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Role of Taurine in Zinc for Angina Pectoris

One related aspect of zinc metabolism in aging involves taurine, a conditional amino acid made in the liver in non-infants. Taurine levels have been shown to decline in aging, resulting in cardiac and mental injury and reduced energy levels. Taurine appears to play a role in lipid metabolism, and it may inhibit atherosclerosis by regulating the bloods levels of zinc, copper and calcium. Perhaps, since atherosclerosis occurs primarily in older people, taurine must be supplemented to allow zinc, copper and calcium to have their natural, youthful cardioprotective effects. Recently scientists found that taurine treatment accelerates the regression of cholesterol-induced atherosclerotic lesions in rabbits without having any effect on the plasma and aorta lipid and lipid peroxide levels. Indeed, 2 grams of taurine 4 or 5 times a day is the only consistent treatment that prevents one hundred percent pre atrial contraction (PACs) cardiac arrhythmias in my 64-year old heart. Would you drive a 64 year old car in need of preventative maintenance? Doesn't that thought put things into perspective? Supplemental taurine is vital in aging for many different reasons and you may want to visit this link for much more information. Also, you may want to consider the multiple roles of taurine. In Timothy C. Birdsall, ND's article: "Therapeutic Applications of Taurine", he writes in his abstract: "Taurine is a conditionally-essential amino acid which is not utilized in protein synthesis, but rather is found free or in simple peptides. Taurine has been shown to be essential in certain aspects of mammalian development, and in vitro studies in various species have demonstrated that low levels of taurine are associated with various pathological lesions, including cardiomyopathy, retinal degeneration, and growth retardation, especially if deficiency occurs during development. Metabolic actions of taurine include: bile acid conjugation, detoxification, membrane stabilization, osmoregulation, and modulation of cellular calcium levels. Clinically, taurine has been used with varying degrees of success in the treatment of a wide variety of conditions, including: cardiovascular diseases, hypercholesterolemia, epilepsy and other seizure disorders, macular degeneration, Alzheimer's disease, hepatic disorders, alcoholism, and cystic fibrosis. See full article here: Alt Med Rev 1998;3(2):128-136. All of these disorders are "diseases of aging". One way in which the liver fails in aging is by loosing its ability to produce taurine, thus precipitating, and/or worsening these disorders. Interestingly, and profoundly important if this works in people, taurine augments (improves) the proliferative responses of T cell lymphocytes from both young and old mice. Taurine at 12 grams per day completely eliminates many cardiac arrhythmias and has a broad role in cardiology. In fact, there is no other nutrient that has such a beneficial effect on cardiology as taurine, perhaps because taurine production declines and can cease in aging, producing a large number of cardiovascular problems including death. See this article for much more information. Taurine is found in meat and especially in conch but is not found in the vegetarian diet, making supplementation vital to many in aging.

Why do we have such an epidemic of angina pectoris and cardiovascular disease? I vote for depletion of nutrients from the wheat refining process. Take out the zinc, magnesium vitamin B-6 and other nutrients, and presto, an instant boon to pharmaceutical industry!

Patenting Zinc for Angina Pectoris

Thinking we had discovered something new, Dr. Halcomb and myself filed U.S. Patent Application Serial Number 935,951 (11/28/86) for a patent titled METHOD FOR ALLEVIATING ANGINA PECTORIS ATTACKS. The patent was rejected because the role of zinc in preventing and treating angina pectoris was "well known in the art" and therefore not patentable. There was an article written in Polish that preceded our work, and this article is so important that it is republished in English as follows.

L. Giec, A. Wnuk-Wojnar, M. Trusz-Gluza, A. Szulc, and W. Kargul*:

Epidemiological evaluation of the coronary risk in physical laborers in nonferrous metallurgy. Part II: Coronary disease. [Epidemiologiczna ocena zagrozenia choroba wiencowa u pracownikow fizycznych przemyslta hutniczego metali niezelaznych. Czesc II: Choroba wiencowa.** Przegl Lek 1980;37(6):507-10.

*First Cardiology Clinic of the Cardiology Institute of the Silesian Academy of Medicine in Katowice. Director Prof. Dr. Hab. Med. L. Giec. Authors' address: I Klinika Kardiologii SI. AM, ul. Ziolowa 4, 40-634 Katowice. [First Cardiology Clinic of the Cardiology Institute of the Silesian Academy of Medicine in Katowice, 4 Ziolowa St., 40-634 Katowice, Poland]

*Accepted December 19, 1979.

Translated from Polish by the Ralph McElroy Co., Custom Division P.O. Box 4828, Austin, Texas 78765 USA


Analysis was performed in 1000 physical workers (900 males, 100 females) aged 21-60 years with the professional exposure to zinc, lead or cadmium. Angina of effort according to Rose was present in 14.1% of studied population. True and probable features of coronary heart disease were found respectively in 0.5 and 3.4% of resting electrocardiograms. The sub maximal exercise test revealed probable ischemia response in 10.1% of studied persons. It has been shown that coronary pain is more frequent in workers exposed to cadmium. However, either angina in history or positive exercise test were less frequent in the persons exposed to zinc.

ADDITIONAL KEY WORDS: angina of effort - electrocardiogram at rest - exercise test - zinc - lead - cadmium


The results of clinical, epidemiological, and experimental animal studies indicate a correlation between an excess or deficiency of certain trace elements and the onset and development of coronary disease [2, 15, 19]. Most of these correlations have not been unambiguously explained or even proved.

We decided to evaluate the incidence of coronary disease in a population occupationally exposed to zinc, lead, and cadmium, looking for any correlation between the disease and exposure to these elements.

Materials and methods

A description of the observed population of 1000 physical laborers (900 men and 100 women), aged 21-60, in nonferrous metallurgy, and an outline of the plan of study were given in Part I [17]. The subjects were interviewed concerning the working environment and given a modified and expanded Rose questionnaire [13]. All the subjects were given a 12-lead resting electrocardiogram (EGG) with a three-channel Multicard apparatus. Subsequently, if there were no contraindications from the resting EGG recording or a medical examination, they were exercised on a cycloergometer with submaximal exercise (75-85%). Electrocardiograms were recorded during, immediately after, and 2.5 and 5 minutes after exercise. They were evaluated using a modified [13] Minnesota code.

An epidemiological diagnosis of definite, probable, or questionable coronary disease was made on the basis of criteria given by Askanas and Rywik [1].

In addition, all the workers were tested for serum concentrations of lead and zinc, and the lead, zinc, and cadmium concentrations in the air of their workplaces were measured [4, 11, 17]. The data were statistically processed using the chi square test on an Odra 1305 computer.


A detailed analysis of the measurements of zinc, lead, and cadmium in the air of the workplace and in the serum was given in the previous article [17]. Concentrations above the maximum permitted [threshold limit] concentration for the air of the workplace were found in 74.3% of the workers for lead, 57.9% for zinc, and 7% for cadmium. It also turned out that the degree of exposure did not differ significantly in different age ranges.

There was a positive interview for first and second degree angina of effort in 14.1% of the patients, while in another 9.8% there was pain in the chest cavity which did not meet Rose's criteria [13]. Pain reminiscent of myocardial infarction was reported by 3.6% of the patients. The frequency of subjective symptoms of angina of effort rose with age in 19.3% of men in their fifties and 32.2% of women in their forties. Only 1.2% of the workers were found to have had a previous medical diagnosis of coronary heart disease, while 0.2% had been treated for myocardial infarction.
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Default Part 4 Copper and Zinc for Angina, Aneurysm, Hemorrhoids

I have edited some paragraphs out of this section. Go to the website for a complete read.

Does Zinc Prevent and Cure Angina Pectoris?

From Dr. Prasad's comments, research (finding decreased mortality with extra zinc), Bernhard's work, the Polish report, Henzel's book article and our direct observations of the effects of more than 200 milligrams of zinc per day zinc in terminating angina pectoris, zinc seems to me to be important in preventing and perhaps curing arteriosclerosis and angina pectoris. Zinc in the treatment and prevention of arteriosclerosis and angina pectoris merits much more research. We do know that in aging, people either reduce their consumption of zinc, or loose their ability to absorb zinc from their food (or both), perhaps contributing to, or causing, arteriosclerosis and, therefore, angina pectoris and premature death. However, direct evidence of zinc treatment to benefit angina pectoris and arteriosclerosis is anecdotal, and much more evidence is needed. Clearly, zinc deficiency is found in elderly hospitalized patients, and higher proportions of respiratory infections, cardiac failure, and depression were observed among zinc deficient patients as compared with the group of patients with normal zinc status. One thing that I have noticed from the literature. There are a number of articles reporting that up to 100 milligrams of zinc had no effect on cholesterol. Remember that each of the reports that used zinc beneficially to terminate angina pectoris or prevent angina pectoris used much larger doses. For example our doses were over 200 milligrams a day and dosages of 300 mg per day were clearly associate with INCREASED serum concentrations of low density cholesterol.

I now interpret the observation of higher serum concentrations of low density cholesterol from 300 mg of zinc per day to mean that zinc removed low density cholesterol from cardiovascular surfaces such as arteries and veins, thus decreasing arteriosclerosis and increasing circulation thus terminating angina pectoris and restoring youthful cardiac function.

These are the some of the best food sources of zinc, and you will probably realize that you rarely eat them. Another excellent source of zinc is East coast oysters. If you, the reader with concerns about angina pectoris (and arteriosclerosis), decide to take large amounts of zinc, there are some side effects that must be prevented. First, over 300 mg of zinc per day was strongly immunosuppressive after 30 day in healthy adults in at least one study. The immunosuppression reversed upon cessation of zinc treatment. Consequently, large amounts of zinc should never be taken for long without medical supervision to test for immune system problems. Second, if blood levels of copper are already low, 300 mg of zinc per day could easily lower copper serum levels with perhaps lethal results. You do not want "artery aneurysm formation with rupture and high mortality" as found in copper-deficient chicks and pigs by O'Dell and other scientists!

Copper deficiency has clearly been linked to aneurysms and even the very common rectal hemorrhoids. If you have had aneurysms or rectal hemorrhoids in the past or now, you are very likely to be copper deficient, and supplementation of large amounts of zinc without also supplementing copper first for several weeks might be very harmful or kill you. Study some of these Scholar.Google search articles for "copper" and "aneurysms", and this google search for "copper" and "hemorrhoids" as described by my friend Charles Weber.

On the other hand copper is being depleted to treat lymphomas and other cancers. The concept of treating cancer by restricting the blood supply to malignant tumors has recently gathered intense interest in the medical community and the press. In January 2000, University of Michigan researchers published a preliminary report of a human trial showing that reducing body copper levels can be a minimally toxic means to inhibit the growth of small blood vessels feeding solid tumors, thus being a means of slowing or stopping the development of some cancers. See this article. Consequently, one can see that there is much to be learned about manipulating metals to treat diseases, and no one knows all of the answers yet.

People with white hair have lower copper content than those with colored hair, consequently caution is strongly advised for white haired people. If you decide to supplement with copper, I suggest that the best plan would be to supplement with 4 to 6 milligrams of copper for 14 days prior to starting high dose zinc, and to limit high dose zinc to no more than 14 days of treatment.

Copper solution chemistry is a bit different than other metals in that ligands (the thing that the copper is attached to) that are common in dietary supplements often bind copper so tightly that copper is not biologically available and will not be helpful.

These copper compounds are biologically available from solution chemistry data: copper malate, copper sulfate, copper lactate, copper chloride, copper succinate, and copper tartrate. These copper compounds will be dissociated by stomach acid into ionic copper and the ligand.

Common dietary supplement forms that are not biologically available from solution chemistry data include: copper oxide, copper gluconate, copper aspartate, copper citrate, copper cysteinate, copper EDTA, copper glutamate, copper glycinate and copper histidinate. These copper compounds will NOT be dissociated by stomach acid into ionic copper and the ligand.

Eat a high copper died for two weeks prior to starting high dose zinc. Would you like oysters and liver, twice or three times a day?

According to Ripa and Ripa, the relationship between zinc and atherosclerosis is shown. Administration of strong doses of the mineral can turn out atherogenic through three mechanisms: (1). Through the alterations of the lipidic arrangement: decrease of HDL, increase of total cholesterol and LDL cholesterol (action promoted by the induced hypocupremia). (2). Through the alterations of the vasal wall, in consequence of the biochemical modifications of the basic substance (again, through secondary hypocupremia) [this is strong reason to give copper]. (3). Through the increased platelet aggregation which seems to be produced by strong doses of zinc. In addition to these harmful actions, the antioxidative action, typical of zinc, must be stressed, which prevents oxidation of LDL and consequently stops the main mechanism of atherogenesis. Besides, the mineral restricts and nullifies the loss of metallothionein in zinc, produced by free radicals and subsequent functional alterations. Moreover, the calcium antagonist action of zinc (like that of magnesium) must be considered: it blocks calcium and its several favorable actions on atherogenesis.

In consideration of these last aspects, the rule of zinc, in suitable doses, could be considered as basic in the context of a strategy of prophylaxis and therapy of the atherosclerosis process. BASIC? BASIC? BASIC? Yet, no physician that I know, except Dr. William W. Halcomb, DO, of Mesa Arizona, uses zinc to treat angina pectoris.

Regardless, do not use "zinc oxide", rather use highly biologically available "zinc gluconate" or "zinc sulfate", because zinc oxide is not very biologically available. In other words, zinc oxide will not work. Be aware that zinc, magnesium, taurine and copper deficiencies are relatively common in the West, particularly in the elderly who have reduced their caloric intake and their meat intake due to fears of "cholesterol". Unfortunately, this reduction also reduces intake of zinc, magnesium, taurine and other vital nutrients since meat is the main source of these nutrients in the Western diet. Good sources of many trace minerals necessary for cardiac and muscle function are cashew nuts as shown here, and all whole grains, nuts and seeds.

Understand that zinc for angina pectoris (and arteriosclerosis) remains experimental and the results if obtained by others (such as yourself) are of immense importance. Upon request, I will post your results on this page, either good bad or indifferent. I suspect that 1.25 milligram of zinc per pound of body weight would be equivalent to the dosages used in Dr. Halcomb's patients and should provide equivalent beneficial results. I also think that dosages should be limited to 60 mg per meal with some more - if needed - at bedtime, and that 4 mg of copper (as suggested in this link) should be supplemented daily also to prevent potentially lethal aneurysms. However, please remember that copper was not added in the studies that were effective in raising low density cholesterol or in eliminating angina pectoris symptoms. Additive copper may defeat the beneficial function of large doses of zinc in treating angina pectoris, but I do not know. A very cautious approach seems advised to me. One final comment. Doses of zinc gluconate in excess of 30 to 40 mg zinc often produce nausea. On the other hand, some people do not become nauseated at these doses or even much higher doses. I do not know what these symptoms means other than the obvious.

I very strongly suspect your physician will advise you against experimentation with zinc for arteriosclerosis and angina pectoris, due to their general concern about patients "experimenting" with "unproven" treatments. They are absolutely correct, and I do not "recommend" that you take large amounts of zinc, because zinc for treatment of cardiac issues needs to be studied in controlled, clinical trials under the most careful of circumstances. Unfortunately, Big Pharma has control of research funds for nearly all drugs, and since zinc is very cheap and is not patentable, zinc will likely never find a commercial use in the treatment of angina pectoris. What is a person to do? Beats me, it's your life and your wallet!
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