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 The Cholesterol Obsession Robert A. Erickson, M.D. 2008 I frequently see patients in my practice who have cholesterols above 200mg/dL and have either been advised by a physician to take a statin drug to lower their cholesterol, or they are concerned on their own that their cholesterol level may be too high. I will share information on controversies in cholesterol therapy and whether the current guidelines to lower cholesterol are evidence-based.
Our society’s obsession with cholesterol goes back to the famous Framingham Heart Study initiated in 1948, where a correlation between heart attacks and high cholesterol turned up when studying diets, lifestyles and environments of a large number of families. The high cholesterol correlation was found in men, but not women. In 1956, the American Heart Association drew on the conclusions of the Framingham study and Ancel Keys, a famous pubic health scientist of the time, stating that butter, lard, beef and eggs were the cause of coronary heart disease. Because lowering cholesterol did not reduce the risk of death from heart disease, the Cholesterol Consensus Conference in 1984 developed the guideline that a lower “acceptable” level of cholesterol (the magic 200mg/dL number) was needed. When lowering total cholesterol levels below 200 did not translate into saving lives from heart attacks, the focus was then turned to LDL cholesterol levels. The unfortunate patient who had an LDL cholesterol level of above 130 was now condemned to a lifetime of expensive drugs. In addition, when a person with a completely normal LDL cholesterol level suffered a heart attack, he would still be placed on a cholesterol-lowering drug. In 1977, Dr. Michael DeBakey, the internationally renowned heart surgeon, pointed out that only 30-40% of people with blocked arteries and heart disease had elevated blood cholesterol levels. He asked “how do you explain the other 60 – 70%?” Looking at non-US populations such as Crete or France, average cholesterol levels of their populations are well above 200 mg/dL with diets rich in butter, cheese, creamy sauces, and, of course, red wine. These populations have less heart disease than the US population. One famous French investigation, the Lyon Diet Heart Study, published in the late 1990s, showed heart attack survivors following a Mediterranean diet were far less likely to experience a second heart attack or heart failure that individuals on the typical low-fat diet endorsed by the American Heart Association. The Mediterranean diet, rich in anti-oxidant foods such as fresh vegetables and fruits, fish and fish oil clearly protected participants from heart disease. What was also found was that people with higher cholesterols had less deaths from cancer, respiratory failure, suicides, and automobile accidents. Why accidents and suicides? You need cholesterol to make brain cells and for memory! High Cholesterol, a “New Disease” Although high cholesterol is only a finding on a blood test, the medical establishment and pharmaceutical industry, backed by the government in the 20th century made it into an actual disease. Unlike most other diseases, the most common symptom of high cholesterol is feeling normal. According to most experts, the only treatment for this new disease is to use cholesterol-lowering drugs. In over 4 decades of use of these drugs heart disease and stroke still remain the number one cause of death in both men and women, where one out of two men and women will die of atherosclerosis related disease. What is Cholesterol? Cholesterol is a waxy substance that occurs naturally in all parts of the body and that your body needs to function normally. It is produced in your liver and also occurs in foods such as dietary fats and egg yolk. It is present in cell walls or membranes everywhere in the body, including the brain, nerves, muscle, skin, liver, intestines, and heart. Your body uses cholesterol to produce many hormones including estradiol, progesterone and testosterone. Your body also uses cholesterol to manufacture vitamin D and the bile acids that help to digest fat. Our bodies make about 800mg of cholesterol a day to cover those needs. Cholesterol and other fats can't dissolve in the blood. They have to be transported to and from the cells by special carriers called lipoproteins. There are several kinds, but the ones to focus on are low-density lipoprotein (LDL) and high-density lipoprotein (HDL). What are LDL and HDL cholesterol? Is LDL really bad? HDL cholesterol is responsible for clearing out the LDL cholesterol that sticks to the arterial walls. Exercise, anti-oxidant minerals and vitamins, and omega-3 fish oils increase the amount of HDL cholesterol. LDL cholesterol is not bad. As a matter of fact, it is critical to maintain life. LDL transports cholesterol and triglycerides from the liver to peripheral tissues. LDL also regulates cholesterol synthesis at these sites. It only becomes harmful when it is oxidized by free radicals. The oxidized form of LDL cholesterol sticks to the arterial walls and initiates the formation of plaque. This is a very important point for our readers to understand. For example, we know cigarette smoking increases the risk of many diseases such as heart disease, stroke and cancer. Smokers with normal levels of LDL cholesterol have a greatly increased risk of developing heart disease compared to non-smokers with the same LDL level. Of course the reason why a smoker with normal levels of LDL cholesterol is at greater risk is because his LDL cholesterol gets oxidized at an incredible rate. Homocystine levels are also increased by cigarette smoking which further oxidizes LDL cholesterol and the arterial lining itself. The degree of oxidation directly corresponds to the risk of developing heart disease, not the level of LDL cholesterol. But statin drugs do not address the true bad cholesterol, the oxidized LDL cholesterol. What is Atherosclerosis?Atherosclerosis (or ateriosclerosis) is damaged, hardened and possibly clogged arteries throughout the body due to plaque formation. Plaque can be of two types. Stable plaque, covered with fibrous tissue, slowly expands inward and shrinks the diameter of arteries. Unstable, vulnerable plaque is much more dangerous. It can rupture, spilling its contents into the arteries and shut off blood flow, causing a heart attack or stroke. When a stroke occurs, either there is a lack of blood to an area of the brain or the blood vessel has leaked, spilling blood into the brain. Interestingly enough, plaque is only about 5% cholesterol and 95% calcium. Although plaque can develop slowly, it can also develop within 6 months. Many cardiologists have seen this. Stress can speed things up. For a cardiac patient, emotional stress is deadly, and blood vessels can spasm and tighten up, further reducing blood flow. If plaque develops slowly, the body can form natural bypasses called collaterals. A patient may have a slowly closing coronary artery and not have a heart attack or require surgery or stents. Death by Inflammation, not High CholesterolIn 2000, doctors at Harvard University published the first of a series of landmark research studies showing heart disease was an inflammatory disease, just as we think of rheumatoid arthritis as an inflammatory disease. I was privileged to hear one of the Harvard cardiologists at a medical conference I was attending present this dramatic finding. He made a point that he could do a cardiac catheterization on a patient, not find significant blockage or hardening of the arteries, and within 6 months this same patient could return with plaque formation or a heart attack. This concerned him. What was going on? The Harvard researchers found that it was the vascular inflammation that caused the oxidized LDL cholesterol to stick in the arteries. They found C reactive protein to be a key biochemical substance that indicated the presence of vascular inflammation. Like a silent smoldering fire, low-grade inflammation leads to weakening and eventual rupture of arterial plaques that directly trigger heart attacks and strokes. This explains why more than half of heart attack and stroke victims have normal cholesterols. At the Center, all new adult patients have screening high sensitivity C reactive protein and homocystine (another inflammation causing substance) levels checked in addition to cholesterol levels. Let’s Look At Current RecommendationsThe National Cholesterol Education Program is part of the National Heart, Lung, and Blood Institute, meaning it is part of our federal government. In 2004 it selected a panel of nine “experts” to review statin drug use and make recommendations as to guidelines doctors should follow to reduce cardiovascular disease. Their findings were published in the journal Circulation in July 2004. It was recommended that individuals at high cardiovascular disease risk attain levels of LDL less than 100mg/dL and for individuals at very high risk, the LDL target was less than 70mg/dL. This is very difficult to do because these targets create an unnatural physiological condition. This requires very high doses of statin drugs, doubling or tripling the dose, oftentimes in combination with other drugs. What Circulation failed to do was disclose that six of the nine “experts” had direct financial ties to the makers of statin drugs. Even though this conflict of interest was disclosed in the media at the time, no action was taken to review the credibility of their conclusions by other less biased researchers. These guidelines immediately boosted the sales of statins from 15 billion dollars per year to over 22 billion dollars in 2005. Statins are the number one selling medication in the United States. On October 3, 2006, after extensive review of all studies relating to cholesterol-lowering statin drugs, scientists reported in the Annals of Internal Medicine that “current clinical evidence does not demonstrate that titrating lipid therapy to achieve proposed low LDL cholesterol levels is beneficial or safe.” This shocking review also exposed the deceitful manipulation of statistics. A Lack of EvidenceIn November 2007 I attended the ACAM conference in Phoenix, Arizona. One of the speakers was James Wright M.D., PhD, CRCP(C). He is a professor in the Departments of Anesthesiology, Pharmacology & Therapeutics and Medicine at the University of BC, Vancouver, Canada. He is also the Managing Director of the Therapeutics Initiative, a government funded organization with a mandate to provide evidence-based practical information about drugs and other therapies to health professionals in BC. He gave an eye-opening lecture on whether the lipid lowering guidelines are evidence based. Just because a major medical journal publishes a study doesn’t mean the data or statistical analysis is accurate, or the study design was the way it was supposed to be, or the conclusions of the authors factual. Due to space considerations, I am greatly condensing his lecture points, but Dr. Wright’s website www.ti.ubc.ca can be viewed and includes therapeutics letters and drug assessment reports. The first issue he addressed was that there are 7 different guidelines for treatment of high cholesterol, depending upon which country you live in, even though the guidelines are based on the identical evidence presented in published reports. The USA had the strictest guidelines. Dr. Wright pointed out that the guidelines make unproven assumptions and extrapolations. For example, in the MEGA trial published in the medical journal Lancet, Pravostatin (Pravachol) plus diet versus diet alone in a primary prevention population of 8214 randomized patients was looked at. However 382 patients were for some unknown reason excluded from the analysis. He asked what happened to these people. Did they die? No one knows, so the data and study conclusions cannot be accepted as accurate. When a doctor or drug company proposes a treatment the question “Do the benefits exceed the risks?” should be asked. In other words, all therapies have both benefits and harms, and patients should be made aware of them. This is called informed consent. The best measure of treatment risk is what is called a “serious adverse event” or SAE. This is any event that leads to death, hospitalization, prolongation of hospitalization, permanent disability, or is considered threatening by a physician. SAEs must be reported and documented in clinical trials. But they weren’t in most cases. Do the therapies proposed reduce SAEs? Again, what Dr.Wright found was a bias in reporting. He repeatedly requested in writing the data from all the primary prevention trial authors from all major statin drug trials. In some cases he received no response. In other cases he received pages of data. In nocase did he receive the SAE data requested!! Of course, the question that comes up is if these drugs are truly showing the benefits outweigh the risks of taking the drug, why aren’t the drug manufacturers or authors of the studies sending the SAE data? What are they hiding? What Dr. Wright did find reported was “total mortality,” not cardiovascular mortality. This gets a bit more complicated, but I’ll simplify his conclusions. Conclusions on Statin Drug TherapyDrug companies evaluated the use of their statin drugs in two different populations. The first population contained patients that had an event -- heart attack, stroke, leg amputation, TIA, or if a patient had documented peripheral vascular disease or heart disease. These are called secondary prevention populations. In the statin trials that had to do with secondary preventionpopulations, statins were found to reduce total mortality. But by how much? If 50 people were treated for 5 years, one death would be prevented. If 20 people were treated for 5 years one cardiovascular event would be prevented. In other words, taking a statin drug reduces the chance of heart attack or stroke by about 5% and death by about 2% over 5 years if you have documented atherosclerosis. So if you are reading this and have documented atherosclerosis and are taking a statin drug, you need to ask yourself if the benefits to you outweigh the risks and side effects of the treatment. The other group of patients he looked at was the primary prevention populations. This accounts for 80% of the patients taking statin drugs today. These are people who have risk factors such as diabetes or high cholesterol levels, but no documented heart or peripheral vascular disease. Statins did not reduce mortality in this population. His conclusion was that people with diabetes, hypertension, smokers, hypercholesterolemia, etc. but who have no proven occlusive vascular disease, should not be taking statin drugs because there was no evidence of a net health benefit in this population. And Dr. Wright is not alone in this opinion. Dr. Stephen Sinatra is one of a minority of cardiologists who incorporate nutritional therapies as the mainstay of treatment of heart disease. In his book Reverse Heart Disease Now, he points out that one third of the patients on statin drugs have side effects, and he doesn’t prescribe statins to lower cholesterol or in patients without evidence of cardiovascular disease. This class of medications has a long list of potentially serious side effects that are not clearly explained to the patients taking them or even to the doctors prescribing them. I agree with Dr. Wright and Dr. Sinatra and do not prescribe statins to lower cholesterol. I realize this opinion does not reflect what most cardiologists or primary care physicians believe or how they are prescribing statin drugs. This does not mean that risk factors shouldn’t be treated in some manner. A healthy diet and exercise is the foundation for any person’s health program, and for many this approach is adequate. Unfortunately, nutritional supplements that lower cholesterol and oxidative stress, and have virtually no side effects are considered by the FDA (Food and Drug Administration) to be an illegal health claim. Instead, the FDA expects Americans to use statin drugs to accomplish this goal. A Summary of the Cholesterol Obesession Elevated cholesterol levels are being treated obsessively by doctors with cholesterol-lowering statin drugs in both healthy and unhealthy people to bring down LDL levels to unnatural levels. In spite of this approach, one in six American men will sustain a fatal or nonfatal heart attack before age 65, and half of all men and women will suffer disability or death from atherosclerosis. Cholesterol is a substance needed throughout your body and especially your brain. It is a “relative” risk factor for heart disease, and it’s influenced by other factors. It is not an independent or absolute risk factor in the same way high blood pressure is. I discussed how LDL cholesterol is completely safe unless it interacts with molecular fragments called free radicals where the LDL becomes oxidized. It is the oxidized cholesterol that penetrates endothelial cells lining the arteries to become plaque. So the problem is really not cholesterol, but whether your body’s antioxidant system can effectively neutralize free radicals that damage your LDL molecules. This is why heart disease is an inflammatory disease much like arthritis. There is a highly dangerous subtype of LDL cholesterol called Lp(a) that can cause heart disease. It is a very small molecule that can easily slip between the cells lining the arteries to produce plaque. We are now able to measure this type of cholesterol and if it is elevated, offset it with nutrients such as niacin or vitamin C. No drug, including the statins, can reduce Lp(a). If fact, the statins can actually raise this type of cholesterol! Testosterone in men and estradiol in women may lower Lp(a). There are also other subtypes of LDL cholesterol, some of which are small particle sizes and some of which are larger particle sizes (and do not cause heart disease). Measuring the milligrams of LDL does not tell a patient or physician about the particle size. There are four labs in the USA presently that can measure particle size as a risk factor. We can now order a very comprehensive lipid study that includes LDL subtypes and particle sizes/counts through Spectracell labs. True Risk Factors For Heart DiseaseSo if cholesterol is a relative risk factor for heart disease, what are some of the true risk factors? Genetics. Heart disease can run in families and we are just learning specific information about genetic factors related to heart disease. Nutritional therapies can modify genetic expression and reduce risk. High Blood Pressure. Hypertension puts a greater stress and workload on the heart, and damages arterial walls and leads to atherosclerosis. Patients with poorly controlled blood pressures have a several fold higher risk of heart attack or stroke. Physical inactivity. People who are inactive, or "sedentary," are at a higher risk for heart disease. Regular, moderate-to-vigorous exercise is essential to prevent cardiac and vascular disease. The more vigorous the activity, the greater the benefits to your cardiovascular system. Exercise also helps control diabetes, obesity, reduce stress, and has been shown to lower blood pressure in some people. If you do not currently exercise, begin slowly. Even moderate exercise has benefits. If you haven't exercised in a long time, talk to your doctor first to ensure you are healthy enough to participate in regular exercise. Vigorous exercise isn't necessary to achieve good outcomes and reduce your risk of heart disease; even moderate activity such as walking (but doing so on a regular basis) 3 or more times weekly, will be of benefit to you. Hormones. Both estrogen and testosterone have heart protective benefits. As we age, our hormone levels decline and our risk of atherosclerosis and clots increases. Synthetic hormone replacement in women, especially with progestin drugs, puts women at higher risk for heart attacks and strokes. This risk, on the other hand, is reduced with natural human identical hormones such as natural progesterone and estradiol. Excessive insulin. Insulin is secreted by the pancreas and causes glucose to move from the blood into cells. When insulin levels are elevated (as is true in type II diabetes and in people who regularly consume large amounts of sugar or refined carbohydrates), a chain reaction of events occurs within the body that lead to arterial inflammation. Emotional stress. Chronic, uncontrolled stress causes the adrenal glands to secrete cortisol and adrenaline. These stress hormones promote arterial constriction and spasm, elevate blood pressure, increase heart rate, cause blood clotting, and lead to cholesterol oxidation. Severe stress can cause a heart attack or stroke. Oxidative stress. Oxidative stress from free radicals causes LDL cholesterol to stick in the arteries. Oxidative stress can be due to smoking, high sugar intake, excessive physical or emotional stress. Heavy metals such as lead, cadmium, and mercury cause oxidative stress. These toxins are in our environment and foods, and can poison enzyme systems and mitochondrial function, elevate blood pressure and damage arterial walls. Few cardiologists are aware of the relationship between toxic metals and heart disease. Some drugs can cause oxidation. Oxidative stress leads to age-related degenerative diseases and accelerates aging as well. Another source of oxidative stress are X-rays and other medical procedures that use radiation. Anti-oxidant supplements can be protective against radiation and may protect the sensitive lining of the arterial walls and other cells of the body. Micro-organisms. Bacterial and viral infections cause inflammation in the body. A leading cause of bacterial infection is periodontal gum disease. We can see heart disease in vegetarians who eat no meat and have low cholesterol levels, but whose dental hygiene is poor. Trans fatty acids. Most trans fats consumed today are industrially created by partially hydrogenating plant oils — a process developed in the early 1900s and first commercialized as Crisco in 1911. These unnatural fatty acids are used to prolong the shelf-life of processed foods. They raise Lp(a), promote cholesterol oxidation, and lower HDL. High heat necessary to fry foods also causes trans fat formation. Read labels on the foods you buy and avoid those that say “hydrogenated” or “partially hydrogenated” at all costs. Other factors. Homocystine is a chemical in the blood that causes inflammation when it becomes elevated. Homocystine levels should be below 10mg/dL and ideally in the 7-8 or lower range. Genetic factors and B vitamin deficiencies can cause homocystine elevation. Cardiac C reactive protein is a key indicator of inflammation and it, along with homocystine, are measured at the Center in our patients at the time of their initial comprehensive evaluations. Lp(a) increases as the result of diabetes, menopause, vitamin C deficiency and genetic factors. Excess ferritin or iron can contribute to cholesterol oxidation. Excessive fibrinogen, a protein that helps regulate the clotting process and is influenced by smoking, diabetes and insulin overload, can make blood too thick and lead to clotting. Protect Your MitochondriaAt the Spring 2008 ACAM (American College for Advancement in Medicine) meeting Dr. Stephen Sinatra, a board-certified nutritional cardiologist, author, and world-wide lecturer, presented one of the keynote lectures on plaque stabilization and reversal. He discussed the importance of mitochondrial function and the heart. Mitochondria are microscopic structures within the cells that create energy via ATP production. There are over 5000 mitochondria in each myocyte (heart cell), and mitochondria represent 35% of the weight of the heart itself. Certain nutrients are critical to mitochondrial function, including coenzyme Q10, D-ribose, magnesium and carnitine. Dr. Sinatra also pointed out “electoceuticals” enhance ATP production – red light laser, magnetic therapy, far infra red sauna therapy, and perhaps the most important, “alive” water (distilled water is “dead” water) that has trace minerals. Our bodies are 70% water, so this makes a lot of sense. Many drugs are mitochondrial toxins, including NSAIDs, Viagra, Aricept, antihypertensives, and others. Toxic metals (especially mercury) are mitochondrial toxins as well. In patients with a condition called IDCM (idiopathic dilated cardiomyopathy) where the heart muscle becomes weakened and the heart becomes enlarged, biopsies of heart muscle showed mercury concentrations 22,000 times those in normal hearts. This is one reason reduction of an increased body burden of toxic metals via chelation therapy is helpful in patients with heart disease. It is important to remember that ATP restores and repairs the heart muscle cells. I would suggest obtaining Dr. Sinatra’s book “Reverse Heart Disease Now” as the nutritional therapies he discusses are beyond the scope of this newsletter. Glutathione and Prevention of Atherosclerosis
A significant number of our patients with toxicities due to toxic metals or other sources have received intravenous glutathione therapy. This is a critical substance for both detoxification and improvement of immune system function. Oral glutathione up until now has not been very useful as it is poorly absorbed. What has not been described in the medical literature is how glutathione can prevent atherosclerosis. Dr. F.T. Guilford, a board certified ENT surgeon who became interested in heavy metal detoxification, was another one of the physician speakers at the ACAM conference. Dr. Guilford presented a study using a new form of glutathione called liposomal glutathione. Liposomal glutathione is much better absorbed by mouth that other oral forms of glutathione, and has anti-oxidant properties that significantly slow the oxidation of LDL and HDL cholesterol in humans. Glutathione has a unique role in humans in maintaining antioxidant function in the body and we need a continuous supply of glutathione to prevent oxidized LDL accumulation. What Dr. Guilford found was glutathione provides the substrate for the enzyme glutathione peroxidase, and along with the mineral selenium, protects both HDL and LDL cholesterol from oxidation and atherosclerosis formation. The Center now carries Essential GSH, which is a high quality liposomal glutathione. Actions to Take:
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