The Truth about Cholesterol

This month I’d like to do something a little different and share this special report on the truth about cholesterol by Dr. Guy Schenker and Dr. Ronald Grisanti that I find incredibly valuable.  Many of my patients are on statins or other cholesterol lowering drugs when they begin care, and many don’t understand why or what side effects may occur from such use.  The fact is, what is considered “high cholesterol” has dropped significantly over the past few decades as the business of cholesterol lowering drugs has taken off.  Adequate cholesterol is integral to many physiological processes and is protective in nature. Cholesterol lowering drugs are not without side effects, either, many producing musculoskeletal and energy complaints that bring people into my office.

Please read below to understand more.

The Cholesterol Farce

Guy Schenker D.C. and Ronald Grisanti D.C., D.A.B.C.O., M.S.

Are you interested in knowing the truth behind cholesterol?

CHOLESTEROL IS NOT A PRIMARY RISK FACTOR FOR CARDIOVASCULAR DISEASE.

• Elevated serum cholesterol is not a cause of heart attacks and strokes.
• Eating foods high in cholesterol is not a cause of elevated serum cholesterol.
• Eating high cholesterol foods is not a cause of heart attacks and strokes, and in fact …
• It is the foods high in cholesterol and saturated fat (such as eggs, meat, fish, and poultry) that will actually keep serum cholesterol down to normal levels. What!?” you ask. “Half the people in the world have been marching with the cholesterol crusade for decades. Virtually all us have been victimized by the anti-cholesterol propaganda campaign. The idea that …
• CHOLESTEROL IS AN ESSENTIAL SUBSTANCE … and not at all the deadly demon of popular mythology, will come as a shock to you, but it is my obligation to help you know the truth. Do understand, however, that I am not saying high serum cholesterol is good, or even that it is clinically unimportant. Quite the contrary, high serum cholesterol definitely indicates the presence of a metabolic imbalance.
• High cholesterol has no specific relation to the risk of cardiovascular disease (CVD). If the presence of cholesterol in the serum has absolutely nothing to do with the risk for heart attacks and strokes, just what is the pathological process involved in cardiovascular disease?

DOES CHOLESTEROL HAVE A PURPOSE?

Cholesterol makes hormones. It also lines the nervous system and allows electrical flows. Cholesterol heals damaged tissues. It feeds the eyes, particularly the lens of the eye, which has no direct blood supply, so it can only grow via cholesterol-rich cells. Because of this, anything that interferes with cholesterol metabolism (e.g., anti-cholesterol drugs) has the potential to cause cataracts.

Other side effects of cholesterol-lowering drugs include the following:

• 700 percent increase in colon cancers
• 12-fold increase in breast cancer
• 45 percent increase in gallstones
• 145 percent increase in gastritis
• An increase, rather than the expected decrease, in heart- and circulation-related deaths and twice as many heart attacks.
• Internal bleeding and severe constipation
• Liver disease and ulcers of the stomach and intestines.
• Anemia, taste and smell disturbances, and visual difficulties
• Dizziness and a lowered white blood cell count
• Angina (heart pain), heart rhythm abnormalities, phlebitis
• Cancer
• Increased death rate (in a 5,000-patient study, there was a 36 percent increase in deaths as compared to those taking a placebo)
• Increased incidences of impulsive homicidal and suicidal behavior
• 175 percent increase in appendicitis

THE HISTORY OF CHOLESTEROL

•   Back in the 1960’s when only a few mavericks in the medical profession and some people in the fledgling natural health foods movement were claiming that cholesterol was a problem. The average medical doctor totally ignored cholesterolemia unless it exceeded 300. Before long, the anti-cholesterol uproar became impossible to ignore, and so the establishment condescended to acknowledge the problem of high cholesterol.
• Now, anything above 250 was considered a problem, and it was generally recommended that people should avoid eating too many eggs or too much meat because of the risk of heart disease from cholesterol intake. Interestingly, it wasn’t the medical profession that was spearheading this anti-cholesterol movement; it was the processed food industry, lead in particular by the seed oil industry. Archer Daniels Midland wanted to sell an ocean of soybean oil, and thus lead the charge against cholesterol in particular and saturated fat in general. Coconut and palm oils were banned from importation, and everyone “knew” that margarine was going to save our nation from what was sure to have been an epidemic of cardiovascular disease from eating dreaded saturated fat.
• The billions of dollars worth of propaganda from the processed food industry was enough to sway the minds and change the lifestyles of millions of Americans, but the medicalpharmaceutical establishment continued to largely ignore the perceived cholesterol threat. Then what happened? The Statin drugs were invented, (predictably) accompanied by a paradigm shift in the establishment. Now, cholesterol was the demon of the century, and our doctors and pharmacists were going to exorcise the evil that lurked within us all from our ill-advised intake of meat and eggs. The all-out war against cholesterol has been waged for over 25 years. The intensity of that war has not waned in the least despite the fact that for at least 5 years now it has been known that cholesterol is not (never has been, and never will be) a primary risk factor for cardiovascular disease. That brings me to a critical point of information..

THE DANGERS OF CHOLESTEROL LOWERING DRUGS

• There are two critical reasons why these drugs are unacceptably dangerous. The first danger is liver damage. Statin drugs work by blocking the enzyme HMG CoA reductase so that the liver can no longer synthesize its own cholesterol. Sounds quite simple and perfectly harmless until you realize that the drug does not act locally on one single enzyme in one particular metabolic pathway. Rather, the drug puts a tremendous load on overall liver function. That is why it is generally recommended that once beginning Statin drugs, the patient should have his liver enzymes checked every six months. This idea of the liver producing a “deadly demon” like cholesterol may come as a shock to you. The truth is, your liver produces 2000 milligrams of cholesterol every day. Is your liver trying to destroy you with cardiovascular disease? Of course not, cholesterol (contrary to the case fabricated against it, first by Archer Daniels Midland, then by the pharmaceutical industry) is an absolutely essential substance, with many critical functions in the body. So — the Statin drugs interfere with normal liver metabolism, inhibit the liver’s production of many substances essential for health, and damage the liver in the process. Liver damage is quite a high price to pay for the illusion of exorcising a mythological demon. And though the cholesterolemia to cardiovascular disease connection is a myth, high serum cholesterol does indicate a metabolic problem — yet the cause of that problem is never addressed by the Statin drug.
• The second danger from taking Statin drugs is musculoskeletal pain that can be severe, and is very frequently misdiagnosed. Since most doctors are not aware that myalgia is a common side effect of the Statins, people that suffer this side effect are often given diagnoses of tendinitis, tendinosis, tenosynovitis, tendinopothy, bursitis, rotator cuff syndrome, and so forth. There are many cases reported in the literature of patients undergoing surgery for musculoskeletal pathologies that did not really exist. The myopathy caused by Statin drugs involves elevated serum creatininephosphokinase (CPK), indicative of muscle breakdown. In severe cases, muscular necrosis will occur, which can overload the kidney with CPK, and with myoglobin (with its associated toxic iron) and other products of necrosis, leading to kidney failure and even death.
• A number of these patients have experienced kidney failure and even death; others have had such severe muscular pain and weakness that they are eventually unable to stand or breath on their own. In my chiropractic practice I have seen many patients whose musculoskeletal pain was completely unresponsive to chiropractic correction, yet cleared when the patient was taken off Statin drugs. Unfortunately, for those that have been on these drugs for a long time the myalgia can persist for two months following discontinuation of the drug.

ARE YOU STILL CONVINCED THAT CHOLESTEROL IS BAD?

• If you are convinced that high serum cholesterol is bad and low serum cholesterol is somehow healthy, I want to enlighten you with the fact that … PEOPLE WITH LOW SERUM CHOLESTEROL (LESS THAN 180) HAVE THREE TIMES THE INCIDENCE OF STROKES AS THE GENEREAL POPULATION. Even William Castelli, M.D., a former director of the Framingham Heart Study (the one that originally supposedly implicated cholesterol as a problem in cardiovascular disease (CVD)) notes that …
• PEOPLE WITH LOW CHOLESTEROL (LOWER THAN 200) SUFFER NEARLY 40% OF ALL HEART ATTACKS. People with low cholesterol (lower than 200) suffer nearly 40% of all heart attacks –William Castelli, M.D., a former director of the Framingham Heart Study Think of those two facts — low serum cholesterol means that you have three times the chance of having a stroke, and, high cholesterol has been shown not to be significantly correlated with heart attacks since 40% of the people who have heart attacks have cholesterol that is lower than average. The evidence against any relation of cholesterol to CVD has been pouring out from everywhere over the last 7 or 8 years. A study done by Gilman, et al and published in the December 24, 1997 Journal of the American Medical Association found that …
•  THE MORE SATURATED FAT YOU EAT, THE LESS LIKELY YOU ARE TO SUFFER A STROKE. This study found that polyunsaturated fats (the ones that the propagandists will have us believe are good for us) have no protective effect. Best of all, this study actually was able to quantify the protective effect of saturated fats: Y
• OUR RISK OF STROKE DECREASES BY 15% FOR EVERY 3% INCREASE IN YOUR SATURATED FAT INTAKE. Here is another interesting study done by Leddy, et al and published in 1997 in Medicine and Science in Sports and Exercise, Volume 29. The subjects of this study were elite male and female endurance athletes, who were placed alternately on a high fat diet and then a low fat diet. On a high saturated fat diet the patients maintained low body fat, normal weight, normal blood pressure, normal resting heart rate, normal triglycerides and normal serum cholesterol levels. All their fitness and training parameters were maintained at the elite level. When put on the low fat (high complex carbohydrate) diet, however, it was found that the low fat diet negated many of the beneficial effects that exercise is expected to produce. The athletes experienced a measurable decline in athletic performance. Most interesting, however, was the fact that the subjects on the low fat diet actually suffered a significant drop in HDL cholesterol (the “good” cholesterol), along with higher triglycerides (both of which are significant CVD risk factors. — In fact, the ratio of triglycerides to HDL cholesterol is probably the number one risk factor for CVD. In other words, you want high cholesterol of the HDL type, and low triglycerides.) I realize this information may hard to accept. Remember, you have been exposed to millions of dollars worth of anti-fat, anticholesterol propaganda over a period of decades. So — you see how difficult sharing the truth.
•  Here is another study: Research published in the Journal of the American Medical Association, 1999; 281(15):1387-94) showed that there was absolutely no connection between eating eggs and the risk of heart disease or stroke in either men or women. The Lies of the Seed Oil Industry Margarine, mayonnaise, cooking oil, salad dressings, and anything made with corn oil, soy oil, safflower oil, canola oil, peanut oil, or any of the rest of the vegetable oils (except olive, coconut oil, or palm oil) will accelerate the aging process in general, create catabolic damage throughout the body, and will specifically cause the oxidative damage in the blood vessel walls and in the heart that precipitates a cardiovascular crisis. Research shows that there is absolutely no connection between eating eggs and the risk of heart disease or stroke in either men or women –American Medical Association, 1999; 281(15):1387-94
• A study in The Journal of Lipid Research, 2000;41(5):834-39), showed that eating vegetable oils in the form of either soy bean oil or margarine raised LDL (bad cholesterol) and lowered HDL (good cholesterol). Meanwhile, eating butter (one of those “forbidden foods” saturated with cholesterol) actually lowered LDL cholesterol and raised HDL cholesterol.
• It may surprise you to learn that cholesterol is not a terrible demon at all. In fact, cholesterol is an absolutely vital substance; you would become very weak and die without cholesterol, it is that important. DID YOU KNOW THAT… ™ Your brain is made of cholesterol; 5% of the dry weight of your brain is made of cholesterol. ™ Your nerves are made of cholesterol. ™ Your body uses cholesterol to make all your important sex hormones and adrenal hormones. ™ Without cholesterol to help your digestion, you couldn’t absorb any of your fat soluble vitamins like vitamin A and vitamin E? ™ Every single cell in your body is surrounded by a membrane containing cholesterol, and that without that cholesterol membrane no cell in your body could function? ™ Cholesterol is so important that your liver produces 2000 milligrams of cholesterol every day. ™ When following a low cholesterol diet, your liver makes up the difference by producing more cholesterol just to be sure you have enough. ™
• High cholesterol in the blood doesn’t come from eating foods high in cholesterol; it comes from a metabolism that is not efficient at handling the cholesterol you 7 need. What is one of the primary causes of heart attacks and strokes? It is triglycerides (the other blood fat), that is the primary risk factor increasing your chance of having a heart attack or stroke. Many people are surprised to learn that even though triglycerides are a fat, the unhealthy diet that raises triglycerides has nothing to do with fat intake; triglycerides (and cholesterol as well) are elevated by eating sugar. The other dietary factor that in some cases will raise cholesterol is polyunsaturated oils (the ones that the propaganda says will help prevent cardiovascular disease). Neither triglycerides nor cholesterol are elevated by eating saturated fat in general or high cholesterol foods in particular. Remember, while cholesterol is not a primary risk factor for CVD, triglycerides are, and are probably the most significant.
• A study published in Circulation (October 21, 1997, shows the result of Harvard research indicating that … THE 25% OF THE POPULATION WITH THE HIGHEST TRIGLYCERIDE TO HDL RATIO HAS 16 TIMES MORE HEART RELATED EVENTS THAN THE 25% WHOSE RATIOS WERE THE LOWEST. The 25% of the population with the highest triglyceride to HDL ratio has 16 times more heart related events than the 25% whose ratios were the lowest –Circulation (October 21, 1997

SO WHAT ARE THE REAL CAUSES OF HEART ATTACKS AND STROKES?

•   High triglycerides ‰ Low HDL cholesterol ‰ Dietary deficiency of saturated fats and cholesterol. Yes, you read it right. Low intake of saturated fat is a factor in increasing your risk of heart disease. The following facts on saturated fats are from Mary G. Enig, PhD president of the PricePottenger Nutrition Foundation
•  ƒ Saturated fatty acids raise HDL, the so-called good cholesterol, whereas the trans fatty acids lower HDL cholesterol. ƒ Saturated fatty acids lower the blood levels of the atherogenic lipoprotein (a), whereas trans fatty acids raise the blood levels of Lp(a) ƒ Saturated fatty acids conserve the good omega-3 fatty acids whereas trans fatty acids cause the tissues to lose the good omega-3 fatty acids. ƒ Saturated fatty acids do not inhibit insulin binding whereas trans fatty acids do inhibit insulin binding. ƒ Saturated fatty acids are the normal fatty acids made by the body and they do not interfere with enzyme functions such as the delta-6-desaturase, whereas trans fatty acids are not made by the body and they interfere with many enzyme functions such as delta-6-desaturase. ƒ Some saturated fatty acids are used by the body to fight viruses, bacteria and protozoa and they support the immune system whereas trans fatty acids interfere with the function of the immune system. ƒ Stearic acid, a naturally saturated fatty acid, is the preferred food for the heart whereas trans fatty acids replace these saturated fatty acids in the cell membrane, thus depriving the heart of its optimum energy source. ƒ Saturated fatty acids are needed for proper modeling of calcium in the bones whereas trans fatty acids cause softening of the bones. ƒ Saturated fatty acids from animal sources are carriers for vital fat-soluble vitamins whereas factory-produced trans fatty acids are devoid of these important nutrients. ‰
• Excess dietary polyunsaturated fats. Polyunsaturated fat is found in vegetable oils like soyabean, corn, sunflower and safflower. Excess polyunsaturates have been shown to contribute to heart disease, cancer, weight gain and many other health problems. ‰ Excess Dietary carbohydrates (particularly fructose sugar) ‰ Thyroid insufficiency ‰ Excess estrogen ‰ Testosterone insufficiency ‰ Excess Catecholamines (epinephrine, norepinephrine and dopamine) Studies have found that the increased secretion of stress hormones when someone is angry (epinephrine, norepinephrine and dopamine) can damage the endothelium, a layer of thin, flattened cells that line the arteries and can accelerate the development of atherosclerosis. The damage of artery walls and plaque build-up in atherosclerosis is what is ultimately responsible for most heart attacks. Excess amounts of epinephrine, norepinephrine and dopamine, collectively known as catecholamines, also can disrupt the electrical rhythm of the heart. Catecholamines are also associated with platelet adhesion. Platelets assist in normal, healthy blood clotting, but they also can adhere to sites of endothelium damage, which can lead to blockages in veins and arteries. This sort of plaque buildup can lead to a complete blockage. ‰

• ‰ Excess insulin (Syndrome X) Increased insulin levels have been found to be responsible for atherosclerotic lesions. Controlling insulin levels should be an important objective towards averting heart attack. Excess insulin has also been responsible for vasoconstriction and blood clotting, two more factors that contribute to arterial blockages. ‰ Oxidative stress to the heart and arteries Apples turn brown. Butter turns rancid. Iron rusts. All are everyday signs of oxidative stress -destruction caused by free radical molecules. But none of these nuisances compare to what these unstable molecules can do inside the body, especially to cells of the brain and the vessels of the heart. 10 A single free radical can set off a chain reaction that can destroy an enzyme, a strand of DNA, or even an entire cell. Ongoing free radical damage leads to destruction of organ tissues and artery walls, and may be a contributing factor in the production of cancer cells. ‰ Excess and rapid growth of cells lining the arteries causing narrowing ‰ Platelet aggragation When there is a vascular injury, platelets rush to the site of the injury and form a plug (blood clot) commonly called a platelet plug. However, when there is an abnormal increase in platelet formation unwanted blood clots could develop causing them to lodge in an artery going to the brain leading to a stroke. If one finds itself in a coronary artery it can stop blood flow to the heart muscle and cause a heart attack. ‰
• Excess prostaglandins Prostaglandins, it seems, can cause platelets in the blood to stick together, which can eventually lead to blocked blood vessels and prevent delivery of oxygen-rich blood to the tissues. ‰ Excess vasoconstriction Vasoconstriction increases the risk of blockage simply by reducing the diameter of the vessel. Hypertension, or high blood pressure, is a good indicator of vasoconstriction. ‰ Magnesium Deficiency ‰ Excess calcium (pushing out magnesium) in the heart, blood vessels and vasomotor nerves ‰ Trace mineral deficiencies Quite an exhaustive list, isn’t it? (Note that elevated serum cholesterol is not on the list, and neither is excess dietary intake of cholesterol — which is the point I have been making.

CLINICAL INDICATORS OF CARDIOVASCULAR DISEASE RISK

Here is a list of clinical indicators of CVD risk. In other words, this is a list of factors indicating the likelihood that one or more of the above listed causes of CVD are at work in your body setting you up for a heart attack or stroke.

• Cardiac arrhythmia
• Elevated triglycerides (particularly elevated triglycerides to HDL cholesterol ratio) Elevated blood levels of triglycerides, but not cholesterol, have been associated with an impaired fibrinolytic system. Studies have implicated triglycerides in the progression of both coronary atherosclerosis.
• Elevated homocysteine: Homocysteine acts as a molecular abrasive by scraping the inner layer of blood vessels. Thus high levels of homocysteine have been correlated with damaged endothelium and the formation of atherosclerotic lesions. One study found that men with extremely high homocysteine levels were three times more likely to have an associated myocardial infarction.
• Elevated insulin: Hyperinsulinemia with normal blood glucose is a factor associated with the etiology of hyperlipidemias and is an independent risk factor for heart disease.
• Elevated cortisol levels: High levels of cortisol are associated with hypertension, and, interestingly, it has been found that simply having a family history of hypertension predisposes an individual to exaggerated cortisol excretion in response to stress. Patients with heart diseases exhibit higher cortisol levels than do controls.
• Elevated estrogen in respect to progesterone
• Low testosterone (in men) Higher levels of testosterone has been found to offer men greater than five-fold protection against atherosclerotic coronary artery disease. Chronically low testosterone levels, may actually precede coronary artery disease and thrombosis in men. Low testosterone is linked to higher levels of fibrinogen and plasminogen activator inhibitor which play a crucial role in blood viscosity, plaque formation, and platelet aggregation. Experimental studies also show testosterone capable of triggering vasodilation of the arteries—a relaxant effect believed to have a beneficial impact on angina and other cardiovascular impairments. A normal physiological level of testosterone may protect against the development of hyperlipidaemia, hyperinsulinism, hypertension echoed British cardiologists in the Quarterly Journal of Medicine. 12
• High testosterone (in women): though testosterone may produces strong beneficial effects on an amazingly wide array of CVD risk factors in men, high levels of testosterone exert a detrimental influence on cardiovascular health in women.
• Lipid Perixoide: Lipid peroxides are the products of chemical damage done by oxygen free radicals to the lipid components of cell membranes. This test is an assay of total thiobarbituric acidreactive substances (TBARS) in serum that measures total serum lipid peroxidation, an indicator of whole body free radical activity. High levels of lipid peroxides are associated with cancer, heart disease, stroke, and aging. A normal physiological level of testosterone may protect against the development of hyperlipidaemia, hyperinsulinism, –Quarterly Journal of Medicine.
• Elevated C-reactive protein: Inflammation may be a crucial factor in the pathogenesis of atherothrombosis. C-reactive protein is a marker associated with production of inflammatory cytokines. These cytokines appear to encourage coagulation and damage to the vascular endothelium, increasing the potential threat to cardiovascular health. A recent study published in the New England Journal of Medicine found that plasma Creactive protein (CRP), a marker for systemic inflammation, is a strong predictor of myocardial infarction and stroke. Men with CRP values in the highest quartile had three times the incidence of myocardial infarction and two times the incidence of ischemic stroke. Significantly, these relationships remained steady over long periods, and were independent of other lipid and non-lipid factors, including smoking.
• Mineral deficiencies
• Fatty acid imbalance

References: Filipovsky J, Ducimetaere P, Eschwaege E, Richard JL, Rosselin G, Claude JR. The relationship of blood pressure with glucose, insulin, heart rate, free fatty acids and plasma cortisol levels according to degree of obesity in middle-aged men. J Hypertens 1996;14(2):229-35. Fredrickson M, Tuomisto M, Bergman-Losman B. Neuroendocrine and cardiovascular stress reactivity in middle-aged normotensive adults with parental history of cardiovascular disease. Psychophysiol 1991;28(6):656-64. Stahl F, Schnorr D, Pilz C, Dörner G. Dehydroepiandrosterone (DHEA) levels in patients with prostatic cancer, heart diseases and under surgery stress. Exp Clin Endocrin 1992;99:68-70. English KM, Steeds R, TH Jones, Channer KS. Testosterone and coronary heart disease: is there a link? QJM 1997;90:787-791. Phillips GB, Pinkernell BH, Tian-Yi J. The association of hypotesteronemia with coronary artery disease in men. Arterioscler Thromb 1994;14(5):701-706. Chute CG, Baron JA, Plymate SR, Kiel DP, Pavia AT, et. al. Sex hormones and coronary artery disease. Am J Med 1987;853-859. Sewdarsen M, Vythilingum S, Jialil I, Desai RK, Becker P. Abnormalities in sex hormones are a risk factor for premature manifestation of coronary artery disease in South African Indian men. Atherosclerosis 83:111-117. Alexandersen P, Haarbo J, Christiansne C. The relationship of natural androgens to coronary heart disease in males: a review. Athersclerosis 1996;125(1-13). Stampfer MJ, Malinow MR, Willet WC, Newcomer LM, Upson B, Ullmann D, et al. A prospective study of plasma homocyst(e)ine and risk of myocardial infarction in US physicians. JAMA 1992;268(7):877-881. Miller AL, Kelly GS. Homocysteine Metabolism: Nutritional modulation and impact on health and disease. Alt Med Rev 1997;2(4):234-254. Hiraga T, Shimada M, Tsukada T, Murase T. Hypertriglyceridemia, but not hypercholesterolemia, is associated with the alterations of fibrinolytic system. Horm Metab Res 1996; 28(11):603-6. 15 16 Davignon J, Cohn JS. Triglycerides: a risk factor for coronary heart disease. Atherosclerosis 1996;124:S57-64. Frohlich JJ. Lipoproteins and homocysteine as risk factors for atherosclerosis: assessment and treatment. Can J Cardiol 1995:11(Suppl C): 18C-23C. Grau AJ, Buggle F, Beeher H,etal. The association of leukocyte count, fibrinogen, and c-reactive protein with vascular risk factors and ischemic vascular diseases. Thromb Res 1996; 82(3):245- 255. Ridker PM, Cushman M, Stampher MJ, Tracy RP, Hennekens CH. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. N Engl J Med 1997; 336(14):973-9. Assman G, Schulte H. Triglycerides and atherosclerosis: results from the prospective cardiovascular Münster study. Atheroscler Rev 1991; 22:51-63. National Institutes of Health:Conference Statement: Triglyceride High Sensity Lipoprotein and Coronary Heart Disease. JAMA 1993;269:505-510. Chiropractic Mentors