Most people may a problem understanding that Heart Failure, Coronary Artery Disease and Elevated Cholesterol are three completely independent disease states. Therefore, a person with heart failure may also show evidence of coronary artery disease or elevated cholesterol. Similarly, evidence of coronary artery disease and subsequent myocardial infarction may occur in a person without elevated cholesterol. Meanwhile, up to half of the individuals having heart attacks may have normal cholesterol. The following material will look at the cause of each one of these diseases and the natural means by which the severity of the problem can be minimized and possibly normal status restored.
Historical Overview: Understand Coronary Artery Disease
Long before there were prescription medications for cholesterol and as early as the turn of the 20th century, there was no discernible coronary artery disease. People died from infections whether it was the pandemic flu of 1919 or pneumonia. The first report of deaths from coronary artery disease were considered an oddity except by a few.1 Instead, by the end of the 21st century, coronary artery disease would become the number one cause of death in western civilizations.
Coronary Artery disease-CAD is the partial obstruction of the major arteries that bring blood, oxygen and nutrients to the heart muscle. It is postulated that deposits of cholesterol form plaques that attach to the arteries. When these plaques break or fall off, they may cause complete obstruction of some part of the coronary artery. The obstruction of blood to the muscle of the heart can cause the myocardial infarction, i.e. heart muscle death. If enough of the heart or the electrical system is affected, then the heart is unable to pump blood and the patient dies.
Heart failure is different in that there are many different disease processes that can weaken the heart enough to cause ‘failure’. Coronary Artery Disease may progressively destroy more and more heart muscle or infection, or a genetic condition or a metabolic condition may occur that leaves the heart muscle just too weak to pump blood. While coronary heart disease is seen primarily in the 40 to 70 year old men, congestive heart failure occurs in the majority of those living into their 80’s.
Cholesterol is the pre-cursor to many of the bio-identical hormones. It is essential for human survival. Since the 1920’s, biochemists have used natural and plant based cholesterol to synthesize estrogen, testosterone, DHEA, pregnenolone and progesterone. Even Vitamin D needs cholesterol to function properly. There are a number of inherited or genetic diseases that result in very high levels of cholesterol related lipids: They are defined by high levels of various cholesterols, high levels of triglycerides and abnormal distributions of large and small chylomicrons that hold the fat. As some of these rare lipid diseases are associated with increased cardiac mortality, it was logical to expect researchers to associate abnormal levels of cholesterol with the rapid increase in coronary artery disease.
After World War II, Ancel Keys2, a physiologist performed an epidemiologic study of dietary habits and heart disease in countries around the world. He concluded that the cause of heart disease was directly related to the intake of animal fat. However, his study was flawed in that he selected out only 6 of the 22 countries to ‘stratify’ his study. And as every good mathematician knows, you can prove anything with ‘stratified’ data.
But the doctors and the pharmaceutical companies, in their desire to treat and prevent heart disease, adopted and promoted Ancel Keys’ work. Medication after medication has been proposed to block fat and treat/cure coronary artery and heart disease, only to be removed, drug after drug from the F.D.A. approved list. Over the last 25 years, various medications have been suggested as ‘cure alls’ only to be abandomed from use because of unforeseen complications. The lists includes:
Atromid-S: Approved in 1975 for the treatment of extremely rare medical conditions where the serum triglycerides normal 100-200 go over 2000. a large study of 5000 men for 5 years of active drug and one year of follow up showed, under the World Health Organization supervision, a 44% increase in mortality, half from cancer.3
Statins: Statins were approved in 1987 to treat abnormal lipids-dyslipidemia. Every one of the statins is reported to have complications of rhadbdomyolysis, a sometime fatal breakdown of muscle tissue. More than 800 cases were reported to the FDA with a watch group asking for the removal of Crestor®. Bayer Pharmaceutical voluntarily removed Baycol® in 1991.4-6
Rezulin®: Rezulin® was the first troglitazone used to lower insulin resistance in adults with diabetes mellitus. The complications of this medication included liver toxicity. It was removed within 2-3 years of launch and after sales reached almost one billion dollars per year.7
Yet today, with these and their closely related pharmaceutical products still on the market and accounting for billions of dollars of health costs, the people of the United States and Europe still suffer with one of the highest rates of coronary artery deaths in the world.
Could it be that cholesterol was never the cause of heart disease and that these cholesterol lowering medications are just one more liver poison? Could statins only artificially suppress lipid profiles while the real culprit continues to make these cardiac health matters worse?
Cholesterol is a necessary part of human existence. From cholesterol in the diet and cholesterol manufactured in the liver originates many of the major hormones that fuel the human endocrine system. Cholesterol begets Pregnenolone, Progesterone, Cortisol, DHEA, Testosterone, Estrone, Estradiol and during pregnancy, Estriol. Understand that cholesterol is necessary for human life.
If the body is stressed and the adrenals are not working properly from under nutrition or physical exhaustion, the cholesterol levels will physiologically increase to attempt to manufacture more DHEA and cortisol. If the thyroid is under performing, then the cholesterol levels increase to produce more of the other hormones. If a woman has polycystic ovaries with an imbalance of testosterone over estrogen, the cholesterol increases. And if the man is low in testosterone or becomes diabetic, his cholesterol increases.
The point is that hypercholesterolemia is a sign that the body’s hormones are not in balance. To treat the symptom, the alleged high cholesterol in the blood, by poisoning the HMG-CoA system, is absolutely ludicrous. Why not understand the cause of the problem, whether it is diet, nutrition or hormones and address that directly?
Total cholesterol levels up to 300 mg/ml were not considered important until there were pharmaceutical drugs available to lower the levels. Dr. Lichten does not prescribe cholesterol-lowering medications except to rare individuals with true defined classes of hyperlipidemia. Rather, he will first and foremost treat the cause of the cholesterol as a problem of nutrition and a problem of hormone imbalance.
Understanding Cholesterol’s Role as a Bio-Identical Hormone
Cholesterol is necessary for normal human function. Without cholesterol, the following functions do not occur properly:8
- Bile salts, which are necessary for absorption of essential fats and minerals including Vitamin A, D, E and K are derived from cholesterol.
- Cholesterol is necessary for vitamin D production.
- Cholesterol is incorporated into the inner layers of every cell wall.
- Cholesterol is incorporated into the myelin sheath that insulates every large peripheral nerve cell.
- Cholesterol is necessary for normal action of circulating T-cells, lymphocytes and Helper B-cells part of the immune system.
In the liver, energy components from the Kreb’s cycle, Acetyl-CoA is metabolized to HMG-CoA and onto cholesterol, which makes Ubiquinone. Ubiquinone is commonly called Co-enzyme Q10. Co-Q10 is the very important carrier molecule in the oxidation-phosphorylation cycle within the cell that produces energy that powers the cell. Poisoning the HMG-CoA system can bring down the energy system for the entire body. One of the complications noted with statins is the loss of adequate levels of Co-enzyme Q10.
When one of the pharmaceutical companies sought to add Coenzyme Q10 to their statin, it was our governing bodies that stopped this single attempt to correct a wrong. Maybe it was an attempt to not give one company an advantage. Meanwhile, there is no logic in taking a statin drug without massive amounts of Co-Q 10. More about this will be addressed later.
So, why the Hype over “Know your cholesterol level?”
In 1985, the National Cholesterol Education Program (NCEP)9 was created by the National Heart, Lung and Blood Pressure Institute of the Federal Government. The purpose of the NCEP was to raise public cholesterol awareness including cooperative efforts with the American Heart Association. While everyone now knows their blood cholesterol level, the medical science has yet to prove that “lowering your cholesterol will significantly lower your risk of coronary artery or heart disease”.9
The reason for this false dicotomy or fuzzy logic is that the pharmaceutical companies and the university and hospital based physicians have forgotten the basic rule of science. Established more than 150 years ago, the only proof of a theorem relies on the completion of (4) steps. These steps represent the principles of the Scientific Method10 upon which science is based. The principles are clear:
- Make an observation
- Collect data
- Establish a hypothesis to explain the observations
- Accept all challenges to your hypothesis, if it withstands all challenges, then the theory is accepted. Results must be reproducible.
But in the last 20 years, a bastard theory called Evidence Based Medicine has become the teaching point for physicians and the public. Evidence based medicine makes no proofs, one only has to perform steps 1, 2 and 3. Evidence based medicine is nothing more than dogma: “my drug is better than your drug,” or more often “my drug is better than nothing.” While the true scientist could look at these studies and retort, “neither of your drugs are necessary.” The failure to consider that the doctor would first measure the appropriate hormone laboratory values to determine what was the cause of the underlying disease is the thorn in the ‘fuzzy logic’ studies. Replacing the inherently deficient thyroid or testosterone hormones, for example, corrects the patient’s underlying medical condition and negates statin intervention.
And that is the point. Just because cholesterol levels are elevated in coronary artery disease or heart failure does not mean that high cholesterol was in any manner, the cause of the malady.
But, before rejecting the pharmaceutical proof that cholesterol-lowering drugs are beneficial, let us review their Evidence Based Data.
- Heart Protection Study11 in 2002 of 20,536 adults in the England aged 40-80 with high risk for heart disease. Randomized to simvasatin (Zocor®) 40mg daily. Difference in survival at 6 years was 87.1% for Zocor® versus 85.4% for placebo. But the complications of statins include cognitive impairment, depression and suppression of the immune system and liver dysfunction and muscle changes were not factored into continuation of the drug..
- Prosper study12 2002 of 5804 patients on Pravechol® versus placebo. Mortality difference of 0.2% not statistically significant.
- ALLHAT13 2003 study of 10,355 on Pravachol® versus placebo. Mortality difference 0.4%. Not statistically significant.
- ASCOT-LLA14 study of 19,342 hypertensive patients on Lipitor®. The study showed a decrease in cardiac mortality but an increase in other mortalities. The statistical difference between groups again was 0.465%. Not significant..
- PROVE-IT15 2004 study of 4,162 patients who had a heart attack or angina randomized to Lipitor® or Pravachol. ® Both groups had small reduction in calculated death rates 2.2% Lipitor® and 3.2% Pravachol® but without a control group.
The point is, there is no great and overwhelming proof that $12 billion dollars in cholesterol lowering drugs are doing anything to improve the health of the American public. In this chapter is listed peer reviewed and published medical studies that address bio-identical hormone deficiencies as the cause of heart failure and coronary artery disease. First, Dr. Lichten states, “Treat the cause”. And, then from a scientific and logical standpoint, the pharmaceutical companies are asked to explain how a statin which lowering cholesterol levels by poisoning the liver really can make mankind live longer and better. It just does not make sense.
The Truth About Heart Disease
Before there were cholesterol-lowering drugs there was heart disease. As physicians we need only look back 100 years to see that there was a major problem with heart disease in the form of congestive heart failure causing untold deaths. The term used was dropsy. The cause of death was hypothyroidism.
In the paper presented at the 1997 meeting of the American Thyroid Association, R, Arem showed what every doctor learned in medical school: that there exists a strong link between abnormal thyroid function, elevated cholesterol, elevated triglyceride levels and heart disease. But what physicians knew in the 1890’s; that replacement of thyroid medication could prevent and treat ‘dropsy;’ has been lost on the physicians in practice today. Dropsy is the end stage of hypothyroid induced congestive heart failure. There is fluid retention that is seen in the lower legs as edema, in the abdominal cavity as ascites, in the lungs as pulmonary edema, and in and around heart as a pericardial effusion. Low thyroid function can also increases the risk of hypertension, increases vascular resistance, and contributes to other complications of heart disease. Treatment then and now with appropriate ‘natural’ thyroid replacement that has the active thyroid molecules, will reduce not only 1) the heart failure and 2) lower the cholesterol and strikingly 3) triglyceride levels, sometimes to normal. Arem16 said so at the American Thyroid Association meeting and said so in his book: The Thyroid Solution by Ballantine books. 1999.
The history of thyroid disease and medical treatment unfortunately took a wrong turn in 1939. As Broda Barnes,17 M.D., the leading clinician and researcher in thyroid disease revealed in his book entitled Hypothyroidism, he was approached by the pharmaceutical manufacturers to promote synthetic thyroid, Synthroid®. He allegedly first explained that Synthroid® was an incomplete thyroid containing only T4, whereas Armour thyroid®, also a prescription medication had both thyroxine-T4 and tri-iodothyronine-T3 from the thyroid glands of pigs or beef cattle. By marketing an incomplete thyroid, Barnes predicted that Synthetic thyroid would wreak havoc on the endocrine system. The pharmaceutical company took no heed and proceeded to make synthetic thyroid the drug of choice. Doctors today are taught to be adamant that synthetic is better because they have heard this nonsense hundreds of times. The marketing falsehoods spread about natural or Armour thyroid have obviously been important in the shifting of the vast majority of prescription thyroid to Synthroid 15:1 and away from Armour thyroid. Yet the medical literature is now replete with the unique functions for T3 in heart disease.
To summarize what Barnes and others have stated about normal thyroid function 70 years ago and appropriate scientifically today:
- Normal thyroid function is necessary for health, life and normal fertility.
- Appropriate replacement of thyroid necessitates both T4 and T3 in a balance that reestablishes normal body temperature.
- Laboratory tests are guidelines, not absolutes, in treating the patients with thyroid disease.
Conclusion #1: Check for Hypothyroidism as a Cause of Elevated Cholesterol
Thyroid disease is definitely one of the causes of high cholesterol. It goes unrecognized and under-diagnosed in individuals with heart disease. Why worry about lowering cholesterol with some statin when there is an FDA approved thyroid and appropriate laboratory tests to prove there exists a thyroid deficiency concurrently in the first place? Bio-identical, Armour thyroid might not only lower cholesterol and lower blood pressure but there is a 100-year history of it being used to prevent and treat congestive heart failure. Replacing natural thyroid will not only treat those cold hands and feet, increase mental focus and fix the brittle nails, hair loss and thinning eyebrows, but it by nature of cause-and-effect, might lower cholesterol. Bio-identical thyroid has scientifically proven to be so much more important in the cholesterol-CAD-heart disease continuum than a statin because thyroid replacement treats the cause Why then not treat hypothyroidism first, recheck the cholesterol and lipid levels and follow up with a diet high in omega-3 fatty acids, appropriate nutraceuticals and instruction to the patient in a change of lifestyle, before deciding to add statins or recheck other parameters?
Is the physician’s concern only the allegedly cholesterol laden plaque in the coronary arteries of 50 and 60 year-old heart attack victims or the epidemic of heart failure seen in both men and women today?
The incidence of congestive heart failure-CHF in the United States is increasing with more than 500,000 new cases per year. While heart failure occurs in 1% of people at age 50, 5% of people at age 75, it occurs in 25% of people aged 85 and older. Congestive heart failure is the most frequent reason for admission to the hospital under Medicare.18 Could the cause of this increase in admissions be due to misdiagnosed hypothyroidism or the precarious policy of prescribing statins to everyone whose total cholesterol is now only over 200 mg/ml?
Statins may be compounding the problem. A study of 20 patients on Lipitor® showed a 66% occurrence of abnormalities of the diastole or filling stage of the heart. This is a major component of congestive heart failure.19 Could statins do more than block production of necessary Co-enzyme Q-10? A search of the literature finds a double-blind study that established clearly that statins do no good for individuals with CHF.20 There were no demonstrable changes in heart function for those individuals with heart failure placed on high dose statins. Stephen Sinatra, M.D.21 says in his book, The Sinatra Solution, that to treat and prevent heart disease one needs to consider bio-identical nutrient replacement: Co-enzyme Q-10, N-acetyl choline and D-ribose. After organizing Continuing Medical Educational Courses with Dr. Lichten, Dr. Sinatra admits to prescribing more bio-identical hormones for his cardiac patients, specifically, testosterone to men.
Testosterone and Heart Failure
Another missed cause of heart failure is the absence of testosterone. As men age, there is both a natural drop in testosterone levels and an increase in SHBG that bind up more testosterone. To this double whammy is added the increased estrogen poisoning in our food and the xeno-estrogens of plastics and DDT. Men, at an alarming rate, are experiencing heart failure at a rate not seen before. And modern medication with statins and medical diagnostic equipment tests are missing the connection between low testosterone and heart failure and low testosterone and coronary artery disease.
The answer to heart failure is right there in every heart cell. The heart is a muscle that must beat billions of times in a lifetime. It never stops to rest. So these heart cells are the most finely tuned energy machines in the entire human body. They are irreplaceable. And they are in tune to testosterone. The heart has more testosterone receptors than any other muscle in the body. 22 Actually, the heart has more dihydrotestosterone receptors.23 Why would it be so sensitive to testosterones if it weren’t the most important connection the heart has to the total body’s function? Being strong, healthy and virile is the only way that nature can assure reproduction of the human race.
Now, we know that it is a fact that testosterone allows a man or woman to run faster. Ben Johnson was a top-notch athlete who became the Olympic gold metal sprinter with supplementary testosterone. Women runs like Florence Griffith Joiner won races at speeds never achieved previously only to die of heart problems from allegedly using performance-enhancing steroids. In the cases of athletes and normal people alike, testosterone for men offers improved cardiac function in all measurable cardiac parameters. Testosterone improves heart muscle pumping capacity and requires less energy to do so. Testosterone should be of primary importance in treating older men with heart failure.24 And as the following will show, starting testosterone early may prevent the development of other heart problems.
Testosterone is an anabolic steroid. It can make new and bigger muscles as to what bodybuilders can attest. The same applies to those weak and flabby heart muscles. But to make new muscles, the body needs protein, minerals, vitamins and essential fats. These are called nutraceuticals. In Chapter 14 is listed the necessary supplements and how much Dr. Lichten prefers to prescribe.
Note that a number of Dr. Lichten’s testosterone deficient patients both with and without diabetes have recorded a 100 point drop in total cholesterol that persists month after month while on testosterone replacement.
Coronary Artery Disease
Coronary Artery Disease refers to plaque narrowing of the major vessels to the heart. These narrowed channels impair blood flow. When there is a period of stress, the body is supposed to release Nitric Oxide-NO into the coronary circulation. This assures that the vessels will dilate in a fight-or-flight stress mode. The problem with coronary artery disease is that there may be a paroxysmal constriction instead of dilatation in the region with the plague. This spasm can cause the drop in blood flow that may lead to a myocardial infarction.
While cardiologist and pharmaceutical companies have focused on the cholesterol-laden plaque, other researchers have found a way to keep the arteries from contracting. That drug is called testosterone and its lack in seen in men with coronary artery disease.25
Coronary Artery Disease
The testing for coronary artery disease began in 1903. At that time, Einthoven in Holland invented the Electro-Kardiac Graph-EKG. Recording the normal electrical conduction of the heart, he was able to delineate changes that were consistent with myocardial infarction-MI, enlargement of the heart chambers, heart failure and changes predictive of old or new cardiac wall damage. A brilliant piece of medical discovery, no doubt; it is relatively cheap and available in almost every doctor’s office. And when coupled to the treadmill test, doctors feel that they have a good screening test for heart disease. And to some extent they do, but putting all medical faith in the 100 year-old test leads to too many false assumptions. For up to half of the individuals admitted to the hospital with a diagnosis of myocardial infarction have a normal or nonspecific EKG.26
The hospitals of the last 50 years have become home to expensive equipment that serve relatively little purpose in the diagnosis of heart disease. The Thallium stress test is still available at a cost of nearly $5000, yet it shows almost nothing of value to most heart patients. The reason is that these nuclear scans show only large areas of tissue destruction, and in the heart patient, this information should be discernible clinically. Neither should be, in our opinion, the only line of diagnosis or treatment. Let us tell you what we believe would be a better way
For more than 20 years, the rapid Electronic Beam Tomography (EBT) has been able to pick up calcium scarring in the coronary arteries. This is a test that takes multiple slices of the heart in 30 seconds and recreates the 3-dimensional images in the computer and its image speed is 200 to 400 times faster than the traditional CT scan and 10 times faster than a helical CT scan.27 The EBT gives a calcium score. The calcium score correlates to arterial wall damage. Young people score well under 100; those at risk score over 100, and those with need for immediate intervention may score 400 or more. In a study of men screened for chest pain and awaiting hospital admission the EBT was able to exclude emergency admission in 74%.28
So, whether you are 35 or 85, the test will tell you to a significant degree whether you are at risk for having coronary artery disease.29 If you have a low calcium score, why take the statins because you are not at risk; if you have high calcium scores, your cardiologist will put you on statins after placing the surgical stents. In the latter, you would take medication for a definite purpose, not just to ‘lower cholesterol.’
The newest EBT equipment has the ability to take hundreds of cross-sectional pictures of the coronary arteries. Coupled with a radio-opaque dye, EBT-A will give a computer rendition of the 3-dimensional appearance of the coronary arteries. Performed as an outpatient procedure for approximately $800 dollars, EBT-A gives pictures almost as clear as they would appear at time of cardiac catheterization. But, again the health insurance carriers refuse to pay for this EBT-A test but will pay for the $50,000 heart catheterization and thallium tests.
What to Do First for Heart Disease
In a comprehensive review of published medical articles, by cross-referencing the six sets of the key bio-identical hormones listed in Chapter 6 against coronary heart disease and heart failure, we find many proofs of the interaction of hormone dysfunction and cardiac disease. Scientifically, Vitamin D, human growth hormone, thyroxine and tri-iodothyronine, DHEA, and testosterone in men and estradiol in women have strong cardio-protective or therapeutic applications
To make the case in point, it is good medicine to treat the cause of heart disease. Dr. Lichten suggests supplementing the bio-identical hormones to mid-normal physiologic levels first, then add the proper nutritional supplements in order to maximize repair of cardiac and coronary disease. Supplements can incidentally assist in normalizing cholesterol levels.
The Case Against Statins for Cholesterol and Heart Disease
Statins like all foreign chemicals will have adverse effects on the human body. Those listed on the package insert appear in italics:
- Muscle pain and weakness and add joint stiffness to symptoms typical on statins. This is because it blocks the production of Co-enzyme Q10, which is necessary for optimal muscle function. If the muscle pain progresses, it may be a sign of rhabdomyolysis, which can lead to a fatal disease of muscle destruction. Physicians need to monitor not only liver but also the muscle enzyme creatine kinase (CK) for this condition.
- Co-enzyme Q 10 deficiency: Concern has been raised that a worsening heart status could occur because of Co-enzyme Q10 depletion.
- Brain fog can be a major complaint of patients on statins. This may be due to ultra low cholesterol levels.
- Cancer. The cholesterol drugs formerly and presently on the market, are associated with increased rates of cancer.30 Breast cancer rates on women with statins is 1500% increased over controls.31
It has been Dr. Lichten’s position that treating the laboratory test for cholesterol is fraught with danger for the patient. First, it gives both the patient and physician a false sense of having done something, while in truth, the disease process associated with high cholesterol goes untreated. Secondly, using a liver poison to change laboratory values is not only illogical but also dangerous.
Many physicians are unsure about what statins are supposed to do, anyway. Dr. Lichten reports seeing elderly women with total cholesterols of 220 and HDL-cholesterols of 80 being prescribed this drug. Patients with normal total cholesterol/ HDL ratios are not statin candidates. And one the studies listed above showed no benefit to prescribing cholesterol-lowering drugs to those over the age of 70.
Dr. Lichten suggests that the appropriate laboratory tests listed in Appendix-LABTESTS be ordered before beginning any course of lipid lowering drug; that the patient and physician have a face-to-face discussion about the information described about hormones; and that a program of high fiber, vitamins, mineral and omega-3 supplements be taken for a full 2-3 months before repeating the laboratory lipid profile. Then, if the diet and supplement program is successful, no statin need be prescribed. Not taking a statin drug is always preferred.
Replacement of Bio-Identical Hormones to improve Cardiac Function
The material appearing below appears in referenced medical peer reviewed publications. These are scientific publications and are included here to reinforce the concept that physicians treat the cause of symptoms, which is often a hormonal deficiency, before treating a symptom, i.e., cholesterol level.
Vitamin D, references in Chapter 1, is necessary for the absorption of minerals from the gastro-intestinal tract and parathyroid function that regulates calcium metabolism. As salt balance is integral to the energy of the cell, Vitamin D deficiencies may directly and indirectly affect heart disease. The genetic marking of alleles finds that the Vitamin D allele is proximal located to genetic markers for both coronary artery disease and diabetes.
- Vitamin D concentrations are low in patients with congestive heart failure.32 Vitamin D3 is found to increase the speed to peak relaxation portion of the heart cycle.32 Heart failure is noted by a prolonged filling stage, therefore, a shorter filling stage is healthier.
- Zitterman33 present results indicating that an insufficient vitamin D status may contribute to the etiology/pathogenesis of CHF. Data include a vitamin D-mediated reduction of elevated blood pressure as well as a vitamin D-mediated prevention of enhanced parathyroid hormone levels, a patho-physiological state that contributes to cardiovascular disease. Based on population-attributable risks, hypertension and cardiovascular disease have a high impact, accounting for the majority of CHF events.
- One of the complications of CHF is development of aldosteronism and secondary hyperparathyroidism because of the loss of calcium in the urine. This affects the energy flow of calcium-magnesium in the energy of the cell. Animal studies show that the addition of vitamin D and micro-minerals of calcium and magnesium were able to reverse both aldosteronism and secondary hyperparathyroidism.34
- Genetic typing now shows that the allele for vitamin D is associated with development of both coronary artery disease and diabetes.35
Human Growth Hormone deficiency is associated with premature heart disease and death in those so afflicted. Not only is growth hormone and low levels of IGF-1 associated with unfavorable risk factors, Fazio36 used hGH to treat the worst cases of cardiomyopathy, as did Lichten in Chapter 11.
- Our meta-analysis suggests that GH treatment improves several relevant cardiovascular parameters in patients with CHF.37
- In those men and women born with growth hormone deficiency-GHD, there is an increased risk of heart disease and most die a premature death. These data suggest that abnormal lipid and glucose metabolism, and atherosclerotic changes occur frequently in adult patients with Growth Hormone Deficiency38
- In cross sectional studies, low IGF-I levels have been associated with unfavorable CVD risk factors profile, such as atherosclerosis, abnormal lipoprotein levels and hypertension, while in prospective studies, lower IGF-I levels predict future development of ischemic heart disease.39
- Recombinant human growth hormone administered for three months to patients with idiopathic dilated cardiomyopathy increased myocardial mass and reduced the size of the left ventricular chamber, resulting in improvement in hemodynamics, myocardial energy metabolism, and clinical status.36
Thyroid Hormone has been a recognized cause of heart failure for more than 100 years. With the environmental influx of minerals that displace iodine, they’re in an ongoing increase in thyroid disease as noted in Chapter 3. Recent research from Europe is demonstrating that the use of thyroid supplements must contain T3 to be effective.
- Thyroid hormone metabolic disarray has been identified as a risk factor for the progression of heart disease and the development of heart failure (HF). Both hyper- and hypothyroidism have been associated with a failing myocardium. Poor cardiac contractility and low cardiac output due to hyperthyroidism is a rare occurrence and is mostly seen in patients with preexisting heart disease. Referred to as a “rate related” phenomenon, hyperthyroid-induced sustained sinus tachycardia or atrial fibrillation may further reduce ventricular contractility. Increasingly, the hypothyroid state, and in particular a low triiodothyronine level, has been associated with a reduced cardiac performance and poor prognosis in HF, even in the presence of normal thyroid-stimulating hormone levels. Low thyroid hormone levels alter cardiac gene expression and increase systemic vascular resistance, both resulting in a reduction of cardiac contractility and cardiac output. This review summarizes current data on thyroid dysfunction and HF as well as the emerging implications of the “low triiodothyronine state.”40
- These findings suggest that symptoms of depression in patients with CAD are associated with changes in thyroid axis function [T3/ T3r] and with cardiac impairment, especially in men.41
- Sub-clinical hypothyroidism may be an independent risk factor for coronary heart disease.42
The Adrenal Hormones, specifically the anabolic hormone, Dehydroepiandosterone-DHEA, along with T3, testosterone and IGF-1 are ‘spark plugs’ that trigger energy production. It is logical and scientifically evident that men with congestive heart failure live longest with the highest levels of these anabolic hormones. Not only is DHEA produced in the adrenal glands, but recent discoveries show that DHEA is produced normally in the heart itself. Low levels of DHEA may be associated with coronary artery disease as well.
- Men with CHF and normal levels of all anabolic hormones had the best 3-year survival rate (83%, 95% CI 67% to 98%) compared with those with deficiencies in 1 (74% survival rate, 95% CI 65% to 84%), 2 (55% survival rate, 95% CI 45% to 66%), or all 3 (27% survival rate, 95% CI 5% to 49%) anabolic endocrine axes (P<0.0001). CONCLUSIONS: In male CHF patients, anabolic hormone depletion is common, and a deficiency of each anabolic hormone is an independent marker of poor prognosis. Deficiency of >1 anabolic hormone identifies groups with a higher mortality.43
- CYP17 gene expression and production of DHEA were demonstrated in human control heart. Also, we found that cardiac production of DHEA was suppressed in failing heart. We postulated that DHEA and/or its metabolites exert a cardio-protective action through anti-hypertrophic effects.44
- CONCLUSIONS: The present findings suggest that, in men, low serum levels of DHEAS may be associated with coronary heart disease.45
INSULIN resistance and DIABETES are TESTOSTERONE DEFICIENCY interrelated diseases. As elucidated in Chapter 5, diabetes in men is a disease associated with low levels of bio-identical testosterone. The number one cause of death in diabetics is coronary heart disease. To be diagnosed as diabetic raises one’s risk of a heart attack to the same status as one who has already had an MI. Insulin resistance is an important characteristic of those with heart failure.
- CHF is a complex metabolic disorder. Metabolic abnormalities include insulin resistance and lack of anabolic hormone activity46
TESTOSTERONE has so many cardiac protective properties that space precludes listing them all. Testosterone is a vasodilator that keeps the coronary arteries open; an energy amplifier that strengthens the heart muscle’s ability to pump blood, and it has anti-diabetic properties.
- Testosterone reduced [a measure of insulin resistance]HOMA-IR (-1.9+/-0.8, p=0.03) indicating improved fasting insulin sensitivity, a marker of CHF.47
- In clinical trials testosterone confers symptomatic benefits in patients with coronary heart disease and heart failure, acting as a vasodilator. These observations lend support to the notion that testosterone could be a potential treatment for patients with PAH as vasodilator therapy remains the mainstay of treatment.48
- Beyond sexual function regulation, male steroids are operative in several physiologic homeostatic systems including the cardiovascular system. By ways of specific androgen receptors, testosterone can mediate cardiomyocyte trophicity, in physiologic states as in diseases involving cardiac hypertrophy. Androgenic hormones also regulate pathologic levels of inflammatory cytokines as 11-6 or TNF, in advanced heart failure. They also mediate vascular resistance with, in vitro and in vivo, proved coronary vasodilatation. Reduced free testosterone serum levels (age-mediated or in premature coronary artery disease patients (CAD) promote a pro-atherogenic lipid profile expressed as HDL-cholesterol decrease and up-regulation of triglycerides levels). The latter observation has relevant clinical significance for evaluation and treatment of CAD disease. As most of normal and diseased cardiovascular system functions are influenced by androgens, we can foresee an increasing interest for further evaluation of their physiologic implications as well as for large and rigorous studies of their therapeutic potential in two leading disabling pathologies, CAD and heart failure.49
- CONCLUSIONS: Short-term intra-coronary administration of testosterone, at physiological concentrations, induces coronary artery dilatation and increases coronary blood flow in men with established coronary artery disease.50
ESTRADIOL and heart disease in women is the subject of Chapter 9. The W.H.I. statements must be considered limited to oral Prempro® since scientific and physiologic studies show estradiol dilates coronary arteries; a very positive effect.
- CONCLUSIONS: Physiological levels of 17beta-estradiol acutely and selectively potentiate endothelium-dependent vasodilatation in both large coronary conductance arteries and coronary microvascular resistance arteries of postmenopausal women. This effect may contribute to the reduction in cardiovascular events observed with estrogen replacement therapy.51
Within this chapter, the material presented has shown a direct correlation between the bio-identical hormone levels and symptoms of cardiac disease. The author has also suggested that each patient have baseline laboratoryt measurements:
- Vitamin D
- Thyroxine (T4); Tri-iodothyronine (T3)
- DHEA-sulfate, morning cortisol
- Fasting insulin, Hemoglobin A1c
- Total Testosterone, total Estradiol and Sex Hormone Binding Globulin
- Complete blood count
- Metabolic panel
- Lipid panel: fasting
- Prostate Specific Antigen
A form to order these tests appear in the Appendix-LABTESTS
The final point to be made about cholesterol is that it cannot form plaques until it is oxidized. Oxidization is what rust is to metal; oxidation leaves the cholesterol foam cell, rough and sticky. Another term for these oxidative changes is an inflammatory response. Inflammatory responses occur because of excess insulin, smoking, drinking, drugs and bad food that damage the cells. Therefore, the treatment for all anti-inflammatory processes is to use anti-oxidant supplements and for all men, testosterone. Be aware that testosterone is overwhelmingly the most potent anti-oxidant for men and can offer a profoundly positive improvement in his cardiac, coronary and lipid parameters.52
Relative Cost of Cholesterol Lowering Drugs
1 month supply
|Naispan®||slo-niacin||500 mg||1-3 daily||$ 193.00||100/$14.39|
|Omacor®||omega-3||1000 mg||3-6 daily||$ 125.36||100/$ 5.80|
|Mevacor®||lovastatin||20 mg||1 daily||$ 68.99||30/$ 22.99|
|Lipitor®||atorvastatin||20 mg||1 daily||$ 109.19||30/$|
|Zocor®||simvastatin||20 mg||1 daily||$ 139.99||30/$ 27.99|
|Prevachol®||prevastatin||20 mg||1 daily||$ 93.99||30/$ 17.99|
|Crestor®||rosuvastitin||20 mg||1 daily||$ 96.61||30/$|
|Lescol®||fluvastatin||20 mg||1 daily||$ 74.72|
|Zetia®||ezetimibe||10 mg||1 daily||$ 87.99||30/$|
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