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300 + Reasons To Avoid Statin Drugs and Ignore Your Cholesterol Level
ABSTRACT
The statin drug class has now been marketed very effectively for management of high cholesterol levels for over 30 years. Statins have been the most successful pharmaceutical class of medication in history with millions of people from all over the world and all ages placed on them. By lowering cholesterol levels, statins are supposed to protect us from heart disease. However, the health benefits of statins and lower cholesterol levels have come under scrutiny since 2005. What if the epidemic of heart disease and diabetes is from the way we were taught to eat? This article is a review with references of what we have been taught about food over the last century with an emphasis on the last 40 years when we were told to switch to a higher carbohydrate and lower fat diet. The article explores the lack of scientific evidence for USDA food recommendations and reviews the basis for statin recommendations that were developed from dishonest and flawed clinical trials. A list of suppressed side effects from statin use is provided and why their action of lowering cholesterol levels may not be good for your health. The link between insulin resistance and statin use, leading to FDA labeling requirements, is explored. The epidemic of insulin resistance leading to chronic inflammation is discussed. Finally, the article discusses how this information can be used to create healthier choices for avoiding or reversing chronic disease.
Cholesterol has gotten a bad rap over the years. When I was in medical school, we were taught about cholesterol in Biochemistry. It seemed like an important compound. That’s because it is. Without cholesterol, we would not function and we would die. However, fat was considered to be a bad part of our national diet. We kept hearing about eating low fat food and how that would help reduce our chances of having heart attacks and heart disease.
We were urged to eat sugar for quick energy and increase the amount of carbohydrates in our diet. We were told to switch to margarine to avoid the coronary artery clogging fats of real butter. All of this came soon after publication of Dr. Robert Atkins “Diet Revolution” book in 1972. He recommended a low carbohydrate/high fat diet for optimal health. He quickly became a “quack” in the eyes of those in the know about what causes heart disease. Yet, it turns out that Dr. Atkins was on the right track. Despite many people thinking he had a heart attack, he died from a traumatic brain injury after a fall on an icy sidewalk at age 72.
After listening for years to low fat diet experts touting claims of lower heart disease rates, it turns out they were wrong as we find new research showing that lowering cholesterol rates has minimal impact on the development of heart disease. The recommended goals for optimal levels of cholesterol have been lowering since I was in medical school in the 1980s. Now, ideal total cholesterol should be under 200mg/dL with LDL levels less than 100mg/dL, down from 150 just a few years ago.
So now what?
History of Government Food Recommendations
Let’s look at the history of food recommendations. The first nutritive guide to food was published in 1902 by Wilbur Olin Atwater PhD. who founded what is today known as the USDA. He focused his research on the caloric value of different types of food and the energy they produced.
How to Select Foods, the first USDA recommendations for food, was published in 1917. The emphasis of this publication was 5 groups of food: sugars, fats, cereals, milk and meats, vegetables and fruit. This guide also discussed the discovery of vitamins and minerals which could be obtained from food.
The Recommended Daily Allowance from the USDA came during World War II when food was categorized into 7 groups: dairy products, meat-poultry-fish-eggs-beans-peas-nuts, bread-flour-cereals, green and yellow vegetables, potatoes, citrus-tomato-cabbage-salad greens, and butter-fortified margarine.
Then, as now, there were confusing and contradictory diet recommendations. Serving sizes were added to new recommendations when they were published in 1956. These recommendations dropped from 7 to 4 food groups: Milk, Meat, Fruits & Vegetables and Grain products.
In 1958, an American physiologist named Ancel Keys began what came to be known as the Seven Countries Study. He hypothesized that diets high in saturated fats were the cause of cardiovascular disease based on his research showing that countries where fat consumption was highest had the most heart disease. Sounds reasonable right?
Unfortunately, he managed to manipulate his data by intentionally leaving out countries where people eat a high fat diet and have little heart disease, as well as countries where dietary fat is low but heart disease rates are high. If it doesn’t fit, you must quit and Mr. Keys didn’t do that. His hypothesis was invalid.
During this time, Senator George McGovern, who ran for president in 1972, was involved in a government committee to eradicate malnutrition in the United States. That committee believed they had achieved their goal by 1969. They began looking for further funding in the realm of nutrition and its effects on health.
Ancel Keys research had given him influence with the American Heart Association. The AHA began recommending lower cholesterol and fat consumption for better cardiovascular health, despite having no scientific study proving a link between the two. Based on this faulty logic, the development of the USDA Food Pyramid began under the direction of Senator McGovern’s committee. In 1977, this committee published the first Dietary Goals for the United States, the goal being to reduce the heart disease epidemic in this country.
The basic recommendation was for Americans to reduce consumption of fat, saturated fat and cholesterol. Americans were told to increase their carbohydrate consumption to 55-60% of total calories and avoid less refined processed sugar. The USDA agreed and the era of low fat-high carbohydrate diet was in place.
The recommendations were revised in late 1977 after the cattle, egg and dairy industries became incensed by the government telling citizens that animal products were unhealthy and promoted heart disease. Even with revisions, Americans were eating less meat, eggs and dairy products and those industries continued to suffer from these declines.
The Department of Health & Human Services teamed with the USDA to issue the first Dietary Guidelines for Americans which eventually led to development of the USDA Food Pyramid in 1992. Throughout the 1980s and early 1990s, the prevailing force behind dietary recommendations was the low fat-high carbohydrate concept of “good” nutrition guidelines.
Interestingly, the food pyramid graphic itself was obtained by the USDA from copying Sweden’s food pyramid. Sweden’s heart disease death rate is higher than in the U.S. Nevertheless, copping the graphic seemed like a good idea to someone in the scientific realm of the USDA.
Research studies continue to provide evidence of the health benefits of a lower carbohydrate, natural and whole food diet including natural fat intake. Yet the crusaders of higher carb, lower fat intake prevail, even in revisions to the USDA food pyramid in 2010 and 2016. Scientists at the USDA ignore this research and continue to tout the benefits of their non-research based recommendations.
Evidence based research is the gold standard when it comes to clinical recommendations. Basically, if you can’t prove it, don’t do it. Here are 27 health and nutrition tips that are evidence based: https://www.healthline.com/nutrition/27-health-and-nutrition-tips Read them and weep because you won’t hear them from the USDA or the FDA.
Debunking the Cholesterol Scare
So what does this all really mean for cholesterol? If the food pyramid is based on faulty science, is the science on cholesterol faulty as well? It turns out that it is. Watching a documentary on Netflix called “Prescription Thugs” got me to thinking about cholesterol lowering statins. In the film, a former pharmaceutical representative is very transparent about her involvement with Pfizer, the maker of Lipitor.
In the documentary, she states that there were never any studies that showed a lowering of heart disease in patients taking Lipitor (atorvastatin) and that side effect data was suppressed. Potential side effects were not to be discussed with doctors during sales calls. Research papers presented on Lipitor included manipulating statistics favoring the drug. This is reminiscent of Mark Twain’s quote: “There are three kinds of lies; lies, damned lies and statistics.”
Lipitor came on the market in 1996 becoming the most prescribed medication in history with over 29 million patients given the drug in the United States alone. Total sales were $125 billion over 14 years before the patent expired. Lipitor was not the first statin. Mevacor (simvastatin) was on the market over ten years before Lipitor was FDA approved.
Lipitor was touted to lower LDL cholesterol levels (which it does) as well as to treat and prevent heart attacks (both of which it does not).
In light of the USDA recommendations for more carbohydrates and less fat (cholesterol), Lipitor sales took off and the generic version is still recommended by physicians all over the U.S. My current physician told me my cholesterol level “sucked” at a level of 246 and that I needed a statin. I politely refused and could have taken the opportunity to engage in an intellectual debate about why I wouldn’t take a statin of any kind, but I passed.
Before we get into the reasons why you should not take a statin, let’s talk about cholesterol and what it does.
What does cholesterol do?
First of all, if you had no cholesterol in your body, you would die. Close to 80% of cholesterol production occurs in the liver. If your dietary cholesterol intake is only 200mg, your body will make 800mg of circulating cholesterol because it is needed for health and well being. What you eat is only 1/5 of the cholesterol circulating. To a lesser extent, cholesterol is also produced in the adrenal glands, intestines and reproductive organs. Synthesis of cholesterol begins with two molecules which are dehydrated to form a molecule called HMG-CoA. This molecule is reduced to mevalonate by an enzyme called HMG-CoA reductase. This irreversible step is blocked by statins leading to lower cholesterol levels.
Cholesterol is a needed precursor for your body to produce steroid hormones (cortisol, aldosterone and DHEA), sex hormones (estrogens, testosterone and progesterone) and Vitamin D. Your body produces about 800mg of cholesterol daily and total body content is about 35 grams. A typical intake of cholesterol from food is about 200 mg daily and the body responds to this intake by decreasing synthesis. The liver is also involved in excreting cholesterol using bile in the digestive tract. Around half of the cholesterol excreted is reabsorbed further along the small intestine for reuse.
The functions of cholesterol in human physiology are myriad and important. Cholesterol is intimately involved in cell membrane physiology including synthesis of cell walls. Cholesterol prevents passage of positively charged ions through the cell membrane for maintaining proper acid-base balance and pH.
Molecules of cholesterol serve as signalers and transporters involved in cell membrane physiology as well. Cholesterol is involved in conduction along nerves and engulfment of foreign molecules by immune cell endocytosis.
What are the different types of cholesterol?
Cholesterol is a fat and therefore not water soluble. It needs a transport mechanism in order to travel through the body and this is accomplished by packaging cholesterol with carriers called lipoproteins. Some of the controversy about cholesterol regards these particles and what risk they pose. The names of these little cholesterol taxis are chylomicrons, very-low-density lipoproteins, intermediate-density lipoproteins, low-density lipoproteins and high-density lipoproteins.
Chylomicrons transport triglycerides from the food you eat. Your level of triglyceride is reflective of how much fatty acid you’ve recently eaten. These large molecule vehicles are made in the digestive tract.
Very-Low-Density Lipoproteins (VLDL cholesterol) are made in the liver and also transport triglycerides. They are transformed into intermediate sized lipoproteins as the body uses the triglycerides being transported.
Intermediate-Density Lipoproteins form as triglyceride is removed from VLDL. These lipoproteins are cleared by the liver.
Low-Density Lipoproteins (LDL cholesterol) are the transport particles that get lots of attention. They are called “bad” cholesterol since they are involved in arterial plaque formation. LDL delivers a purer cholesterol (less triglycerides since they’ve already been extracted) to the body tissues. Elevation of LDL above 100mg/dL has been associated with an increased risk of heart attack and stroke.
High-Density Lipoprotein (HDL cholesterol) is the transport vehicle removing cholesterol from the blood and delivering it to the liver for excretion. It also removes cholesterol from the arterial wall. HDL is considered protective at levels above 60 mg/dL and reduce the risk for heart attack and stroke.
When you get a fasting lipid panel blood test, the result will give you the volumes these four types of cholesterol. Usually, the measured volumes are total cholesterol, triglycerides, LDL and HDL cholesterol. Some panels include VLDL cholesterol. The total cholesterol level is the sum of the other types of cholesterol.
A frequent concern is total cholesterol level. Consider a patient with a total cholesterol level of 221, the goal being less than 200. It is more important to know the breakdown of that number. An LDL cholesterol level of 100 with a VLDL cholesterol level of 35 (normal 5-40) combined with a HDL cholesterol level of 86 gives a total cholesterol level of 221. What elevates the total cholesterol level over 200 is the excellent level of HDL cholesterol in this example. What am I saying? You need to figure out the mixture of cholesterols which make up the total cholesterol level. This is one of the reasons that measuring only total cholesterol levels is meaningless. That number really doesn’t tell you all you need to know.
The Cholesterol Controversy
If a person is only consuming 20% of their total body cholesterol and the body is producing 80% of circulating cholesterol, restricting dietary cholesterol intake should not make that much difference. If you consume more cholesterol, your body’s production lowers in response. So how would dietary cholesterol be related to heart disease, heart attack and stroke? What is debatable is the role blood cholesterol levels play in these diseases and whether or not cholesterol lowering statins actually reduce heart disease rates and increase life expectancy.
In medical school, I was taught information from the Framingham Heart Study which began in 1948. This study included three generations of over 14,000 people finding high blood pressure and high cholesterol to be major risk factors for cardiovascular disease. This study led physicians to check patients for high blood pressure, high cholesterol, a history of smoking, unhealthy eating patterns, physical inactivity and unhealthy weight.
In a review, the World Journal of Cardiology found that blood cholesterol distributions were similar in the original Framingham Study wether or not participants had coronary heart disease. The only statistical difference between the two groups was if cholesterol was higher than 380 or lower than 150. In other words, the association of cholesterol with heart disease did not necessarily imply causation. In fact, an analysis of 72 dietary studies published in 2014 concluded that reduction of dietary saturated fat had no effect on death from heart disease.
There are many drugs that will lower cholesterol levels but none of them have shown a reduction in cardiac deaths. The American Heart Association guidelines conclude that none of these drugs will lower the mortality from heart disease. Drugs that lower cholesterol levels include Niacin, fibrates (fenofibrate), bile acid sequestrants (Questran) and the statins.
Statin Studies
Early clinical trials of statin drugs reportedly show a reduction in mortality from heart disease which led to the idea that they provide primary prevention from developing heart disease. They were considered so safe and effective that a UK physician suggested they be put in the water supply like fluoride (which is a whole other article). Statins have been prescribed to men, women, children, the elderly and to those with or without heart disease based on these early studies and the reported safety profile.
The first commercial statin with FDA approval was lovastatin in 1987. Simvastatin was next and then several others including semi-synthetic and synthetic statins all of which were reported to lower cholesterol levels and prevent deaths from heart attacks and stroke.
This all sounds wonderful but are the studies accurate and true? Are the safety profiles believable?
In actuality, none of these studies are accurate. First, many were funded by pharmaceutical companies who also provided oversight. The pharmaceutical industry has profited significantly from the outcome of these studies. Other concerns include biased results, patients who were lost to follow up, under-reported adverse effects of the study drug and early termination of trials. The Lancet published a major study in September 2016 looking at 30 years of statin evidence. That paper stated that statins were safe, prevent 80,000 heart attacks a year, and reports of side effects had “inappropriately dissuaded” people from taking them.
The Lancet author concluded that the number of people on statins should double which would lead to 1 in 3 adults worldwide taking statins. Two months later a group led by a cardiologist criticized the Lancet study indicating that some of the data behind the trials was unpublished and that statin use impact was based on forecasts rather than real numbers. Only the drug companies and those involved in the trials have access to the raw data of these studies, making independent analysis impossible. The lead author stated: “Decades of misinformation on cholesterol and the gross exaggeration of statin benefits with downplaying of side effects has likely led to the overmedication of millions of people across the world.” That statement was supported by a Harvard statin expert, a former president of the Royal College of Physicians and the president of the International Society for Vascular Surgery.
It is clear that you can select results that support your hypothesis while ignoring results that refute your hypothesis. That is called academic dishonesty. The doctor that published a study implicating vaccines in autism faked his data. He lost his medical license over it. Scientific conclusions without evidence and suppressed data is how we got the food pyramid. If we add statistical deception on top of the non transparent results data and the potential money that has been made in proceeding this way, it is obvious how statins became so lucrative. A critical assessment of the research on cholesterol level lowering by statins leading to reduction in heart disease reveals these studies have failed to improve cardiovascular outcomes. A recent article describes the deceptive approach used in early statin studies. Using a statistical tool called Relative Risk Reduction created the appearance that lower cholesterol levels lead to improved cardiovascular outcomes. This statistic is used to show impressive results to a rather trivial improvement achieved by statin use. The authors also accused the trial directors of minimizing the adverse events associated with these drugs.
Analysis of trial after trial fails to show a benefit in reducing cholesterol levels to reduce mortality from heart disease. Cholesterol Treatment Trialists analyzed 27 trials and concluded that statin treatment reduced cardiovascular events. However, when looking at mortality, these same 27 trials failed to show any benefit in reducing death from heart disease. Looking at statin therapy for primary prevention in patients at high risk for heart disease also fails to show a reduction in mortality.
Further manipulation of data have been used to show that conditions other than death from heart disease are improved with statin treatment. But isn’t death the clinical endpoint most of us worry about? There are those who argue that LDL levels are directly correlated to Coronary Heart Disease events. However, each study defines a Coronary Heart Disease event differently. If you lump them together into one definition with different meanings, how accurate are your studies? What IS known is that lower LDL levels do not correlate with reduced death from heart disease.
Statin Side Effects
Side effect information about statin drugs has been hidden and underreported. The largest survey ever undertaken on statin users was reported by the National Lipid Association. They found that muscle aches occurred in 30% of people on statins and 57% stopped them due to side effects. When used in the elderly population for primary prevention of heart disease, 75% of patients stopped their statin due to side effects. The FDA now requires that statin manufacturers disclose the possible association of statins and dementia. My generation (Baby Boomers) doesn’t mind getting older, but we certainly don’t want to get dementia. There are lots Boomers who have been on statins for years. Degenerative brain disease and dementia are increasing all across the United States.
I promised you 300+ reasons to avoid statins. Those reasons are related to clinical trials and studies (there are 3000 of them related to statins) in which over 300 adverse effects were covered up or underreported. Here is a list that enumerates over 300 adverse health effects of statins from over 216 studies.
Muscle damage including rhabdomyolysis is the most frequent: https://www.greenmedinfo.health/toxic-ingredient/statin-drugs?ed=44387
Nervous system damage including peripheral neuropathy, psychiatric effects and possible cognitive impairment:
https://www.greenmedinfo.health/toxic-ingredient/statin-drugs?ed=35335
Liver damage including chronic hepatitis and liver failure:
https://www.greenmedinfo.health/toxic-ingredient/statin-drugs?ed=35669
Endocrine disorders including lower testosterone, decreased growth hormone and decreased sperm counts:
https://www.greenmedinfo.health/toxic-ingredient/statin-drugs?ed=35562
Cancer risk including breast, prostate, colorectal and thyroid cancers:
https://www.greenmedinfo.health/toxic-ingredient/statin-drugs?ed=1137
Increased diabetes risk:
https://www.greenmedinfo.health/toxic-ingredient/statin-drugs?ed=37045
Cardiovascular damage from reduction in CoEnzyme Q10 levels (which already decrease with age):
https://www.greenmedinfo.health/toxic-ingredient/statin-drugs?ed=35779
Birth defects including brain toxicity, limb abnormalities and heart malformation:
https://www.greenmedinfo.health/toxic-ingredient/statin-drugs?ed=35663
In 2015, the FDA approved labeling changes on statins to warn the public about side effects. These included warnings involving memory loss, confusion, elevations in blood sugar and Hemoglobin A1C levels, as well as increased risk of muscle damage when statins were used with fibrates (for lowering cholesterol), niacin (for lowering cholesterol), colchicine (for gout) and Ranexa (for chest pain).
CoEnzyme Q10 is involved in improving cardiac muscle function and reducing oxidative stress so lower levels from statin use actually makes these drugs toxic to the heart, the very organ they are purported to keep healthy! In addition to lowering CoEnzyme Q10 levels, statins reduce selenium levels. Selenium is a trace mineral involved in cognition and fertility. Selenium may help prevent cardiovascular disease, cancer formation and cognitive decline.
In 2015, the American College of Cardiology published an article entitled “Statin Intolerance: Not A Myth”. In their expert analysis it was clear that excluding all but statin associated muscle symptoms might underestimate the number of patients who discontinue statins due to adverse side effects.
The European Atherosclerosis Society recommended doctors avoid the term “statin intolerance” since that might create a negative impression of these drugs. A position paper published in 2015 attempted to define the term statin intolerance based on the most common side effects of the drugs. Here are the conditions with increased risk for those on statins:
Respiratory system: interstitial lung disease, upper respiratory infection, pharyngitis, rhinitis, sinusitis, bronchitis and cough
Neurologic and Psychiatric: suicide, aggression, headache, asthenia, dizziness, fatigue, depression in stroke patients, hemorrhagic stroke, severe irritability, insomnia, somnolence, agitation, confusion, hallucination and nightmares
Endocrine: new onset diabetes for moderate statin doses increasing another 12% with higher statin doses
Gastrointestinal tract: constipation, diarrhea, heartburn, flatulence, dyspepsia, nausea and vomiting
Liver: elevated liver enzyme activity and liver toxicity in coronary artery disease patients
Skin: alopecia, lichenoid eruption, dermographism, chronic urticaria, toxic epidermal necrolysis and rash
Eye: cataracts (27% higher risk), double vision, eyelid droop and ophthalmoplegia
Renal: proteinuria, renal failure
Reproductive: erectile dysfunction, decreased libido, gynecomastia, decreased testosterone levels
Blood: thrombotic thrombocytopenia purpura
Bones and Joints: tendinitis, arthralgia, arthritis, lupus, polymalgia rheumatic
At the end of their expert analysis paper, The American College of Cardiology recommends strategies for doctors to use in order to keep patients affected by these side effects on their statin drugs. The goal is to avoid lowering the dose of the statin by employing a step by step approach to keep patients on the drug. Lowering statin dose is itself considered a statin intolerance implying that a physician is failing in protecting the patients health by doing so. Don’t even think about stopping the drug. I guess that would be considered heresy. I think most of us would not continue a statin if we developed liver failure or rhabdomyolysis after starting. This list of horrors illuminates the toxicity of these drugs, yet most physicians have been taught that side effects are merely the “cost” of practicing good medicine. Look up the ones you don’t know about and see if you would like to have any of them.
Alternate Reasons for Plaque Formation and Heart Disease
Other theories regarding atherosclerosis (hardening of the arteries) and the development of heart disease have nothing to do with cholesterol. The main culprit of heart disease seems to be chronic inflammation. You can modify chronic inflammation. The other risk factor is family history and you can’t alter or modify your genes (yet).
Examination of the inner lining of coronary arteries reveals inflammatory damage to the walls of these vessels. A cardiovascular surgeon describes these arteries looking like someone took a wire brush to their inner walls. The cracks and inflammation lining arterial walls lead to immune cell activation to fight off these changes. It appears these changes to the arterial lining allow plaque formation and buildup whereas arteries with little to no inflammatory change allow cholesterol to pass right through with no attachment to the vessel walls.
A 2013 article in the Expert Review of Clinical Pharmacology journal reported the results of 17 international physicians reviewing the clinical data on 1.3 million patients and concluded that there is no evidence that high cholesterol levels cause heart disease. Their review showed that high LDL cholesterol (the “bad” one) was unrelated to heart disease both in the general population and even in individuals with a family history of high LDL cholesterol levels. The data from statin trials for primary prevention of heart disease were deemed questionable.
Interestingly, the data from this paper showed that patients who experienced a heart attack had lower than normal LDL cholesterol levels and healthy people with low LDL levels had an increased risk of cancer and infections. There was no association with high cholesterol levels and hardening of the arteries.
The “strongest finding” was that patients over 60 years of age with LDL cholesterol levels over 200 lived the longest.
This finding is supported by a 2019 study. In this one, 12,815,006 people had health screens between 2001-2004 and were followed until 2013. The study population included men and women from age 18-99. During the study period, there were 694,423 deaths and these were analyzed for mortality based on total cholesterol levels. The total cholesterol level with the lowest mortality was 210-249 except in men aged 18-34 years and women from age 18-44. These data indicate that the recommendations to keep total cholesterol under 200 are the exact opposite from what will keep you alive longer, especially as you get older. In addition, health risks and mortality rose significantly when total cholesterol was lower than 150 in all age groups except 18-34.
In this prospectively studied group, it was not until total cholesterol levels approached 300 before a significant rise in mortality occurred. The death rate from stroke was not improved in people with cholesterol levels less than 200. Lower total cholesterol levels have been associated with increased risk of the following: hemorrhagic stroke, respiratory disease including Chronic Obstructive Pulmonary Disease, liver disease, digestive disease and several cancers. As far back as 2001, a Lancet study showed that people with lower total cholesterol levels maintained over 20 years had the worst all cause mortality when followed over those same 20 years.
Recommended ideal cholesterol levels are based on the statin studies, of course, and it is clear they are flawed when looked at from these points of view. In fact, most of the statin trials included people who already had heart disease, especially men who already had a 50% risk of dying from a heart attack. If there is any group in whom statins may be beneficial, it is people who have already experienced a heart attack. In that group, statins reduce the death rate from further heart attacks.
Statins show minimal if any benefit for primary prevention of heart disease and studies on large populations actually reveal a higher risk of death with cholesterol levels less than 200. In fact, total cholesterol levels are probably not good markers for improved health when you consider the higher risks of other diseases. In the study cited which looked at almost 13 million people, only 10% of study participants were on a statin so you could surmise that lowering cholesterol rates even further would make the number of people who died during the study even higher.
It is probably time to have recommendations for desired cholesterol levels based on all cause mortality, not just on heart disease risk. That is likely the prime concern for most of us. You can reverse many diseases but you can’t reverse death. These large populations studies indicate that the lower your cholesterol, the higher chance you will die or get a disease that may not be reversible such as liver failure, cancer or hemorrhagic stroke.
Now let’s get to the crux of the disease that IS elevating heart disease risk. It is reversible but rampant in the United States.
Statins and Diabetes
Sugar intolerance. Weight gain. Insulin resistance. Metabolic syndrome. Type 2 Diabetes. If you don’t know what these are, it would behoove you to learn about them if you want to stay healthy and live a long life. We are in the midst of an epidemic from all of them. The common denominator? Sugar. It is addictive, as dangerous as heroin and lethal. Too much of it may eventually lead to Type 2 Diabetes. When in medical school, I was taught that Type 2 Diabetes was inevitable if you lived long enough. It was a chronic disease that required drugs and medical management but a patient would never be cured of diabetes. Well, they were wrong. I have gotten a lot of patients off their diabetic medications over the years, including those on insulin. Type 1 diabetes is a different story since it is irreversible. Type 2 diabetes is not only preventable; it is also reversible.
Diabetes is comparable to coronary artery disease for risk of death. Heart disease is the leading cause of death in the U.S. with complications of diabetes (one of which is heart disease) coming in 7th. A diagnosis of diabetes dramatically increases the risk of cardiovascular problems including coronary artery disease, peripheral vascular disease, heart attack and stroke. Yet, diabetics typically do not have elevated cholesterol levels.
As an example, I recently consulted with a woman concerned about her 307# body weight. In her mid thirties, she is not diabetic but has insulin resistance and metabolic syndrome. Her total cholesterol is 187 with normal triglyceride levels and LDL cholesterol measuring 117. You would think that with an 110 pound weight gain over the past two years, she would have a horrible lipid panel. But hers is in the recommended guidelines. Her “kryptonite” is ice cream.
Clearly there is something other than cholesterol at work causing diabetics to have much higher risks of cardiovascular diseases. Other studies indicate that those who drink “sugary” drinks have a much higher risk of coronary heart disease. How about dietary interventions that recommend a low fat diet to reduce LDL cholesterol levels? The ACCELERATE study, based on the hypothesis that lowering cholesterol levels prevents heart disease, was a 30 month prospective study involving 12,092 participants randomized to placebo or a drug to inhibit cholesterol transfer and cholesterol levels. The inclusion criteria included acute coronary syndrome (chest pain) within 30-365 days, diabetes with coronary artery disease, peripheral vascular disease, cerebrovascular disease and statin use for at least 30 days. In other words, these were people with a high risk for vessel disease and heart attacks. The result? The trial was terminated due to futility. Despite a 130% increase in HDL cholesterol and a 37% decrease in LDL cholesterol, there was no difference in heart disease rates between those that received the drug and those that took a placebo.
How about the hypothesis that obesity and eating too many calories is the contributor to heart disease? Over 2 billion people in the world are considered overweight and 600 million of them meet the criteria for obesity. In the United States, 30 million people have diabetes and 100 million have insulin resistance. While obesity and diabetes are correlative, one does not always exist with the other. There are countries like Iceland, Mongolia and Micronesia with significant obesity populations without diabetes. Other countries have less obesity and higher diabetes rates including India, Pakistan and China. It is apparent that eating too much and weighing too much is not the culprit.
The Metabolic Syndrome defines a subgroup of people who are at high risk for developing heart disease and Type 2 Diabetes. The four central features of metabolic syndrome are insulin resistance, visceral obesity, plaque forming lipids and dysfunction of arterial blood vessel walls. The diagnosis of metabolic syndrome is the presence of any three of the following: waist circumference >40 inches in men and >35 inches in women, fasting glucose >100mg/dL or a requirement for glucose control medications, triglyceride levels >150mg/dL or a requirement for lipid lowering medications, HDL cholesterol levels <40mg/dL in men or <50mg/dL in women and blood pressure >130/85 or a requirement for blood pressure controlling medications.
The most important criteria of the 5 listed is insulin resistance. Without it, there is no metabolic syndrome. Why? Because insulin resistance leads to the other criteria. Here’s how. Eating a meal increases blood glucose and the pancreas responds by producing and releasing insulin. Insulin leads to increased uptake of glucose from the blood and reduces glycogen (stored glucose) release from the liver with a net effect of reducing circulating glucose levels. This leads to increasing glucose conversion to its storage form: glycogen and fat. Insulin resistance causes the fat cells, liver and skeletal muscle to stop responding appropriately, resulting in higher circulating glucose levels. High blood glucose levels cause chronic inflammation, the basis of most chronic disease.
Chronic inflammation causes oxidative stress to the body. Insulin resistance and visceral obesity lead to plaque forming lipids and cholesterol elevation. Inflammatory changes are related to dysfunction of the lining cells of arteries. The lining cells (endothelium) are protective and biologically active, responding to changes in normal and abnormal processes occurring in the body. Disruption of their normal function leads to arterial wall damage and this damage allows plaque build up to “stick” to the vessel walls. The pathophysiology is detailed but the basics include reduced availability of Nitric Oxide which is produced in the endothelium. Nitric Oxide is a potent blood vessel relaxation compound and is needed for increased circulation and managing blood pressure. It protects against vessel damage that can occur due to reduced blood flow through arterial vessels.
Dr. Jason Fung, a Canadian kidney specialist, has described diabetes as “rotting from the inside out”. He has spent years studying sugar and its effects on the body. His article “Type 2 Diabetes Reversal-The Quick Start Guide” explains the dangers of sugar better than anything I’ve read. You can read it here: https://medium.com/@drjasonfung/type-2-diabetes-reversal-the-quick-start-guide-6187210f14ce. Diabetes leads to heart disease, kidney disease, peripheral vascular disease, blindness, amputations and early death.
Earlier, we discussed the fact that statins increase blood sugar and HgbA1C levels. Therefore, statin use has insulin resistance as a side effect. That potential side effect is now required for labeling on statin drugs. The mechanism that causes this effect was uncovered by researchers at McMaster University who found that statins alter insulin action through the immune system and increase pro-inflammatory cytokine levels. This biochemistry team continues to study the inflammation risks diabetes.
So shouldn’t watching your caloric intake and losing weight reduce your heart disease risk? It turns out that it does not. About 80% of obese people have components of metabolic syndrome but 20% of even the morbidly obese do not. They are healthy and have normal life spans. Up to 40% of normal weight individuals have metabolic syndrome with high blood pressure, fatty liver disease, elevated lipids and cardiovascular disease.
There is also a syndrome called lipodystrophy from which people have too little body fat rather than too much. This can be genetically acquired or can occur with autoimmune disorders, panniculitis (inflamed subcutaneous fat) or HIV infection. These people have the highest rates of cardiovascular disease and Type 2 Diabetes. They aren’t getting these diseases from eating too much or being obese.
It turns out that it’s not the number of calories you eat that reduces insulin resistance. It is what type of calories you eat that reduces insulin resistance and heart disease. Simply put: Eat real food, don’t eat or drink sugar, quit counting calories and move more. In addition, incorporate intermittent fasting into your lifestyle to experience improved energy and less fatigue while you watch the pounds drop off.
The focus needs to change from the amount of calories eaten to the sources of those calories. The conventional wisdom of the past 40 years incorporates the idea that calories high in natural fat are bad. That turns out to be erroneous thinking. As discussed, lowering LDL cholesterol by reducing calories and low fat food actually worsens rates of death from heart disease. Insulin resistance promotes the development of metabolic syndrome which can develop by eating low fat high carbohydrate calories.
Even the ratio of fats we have been eating has changed over the years. In society today, we are eating a lot of Omega-6 fatty acids. In years past, we ate more Omega-3 fatty acids. Both are polyunsaturated fats and both are essential to our health. They are termed “essential fatty acids” since your body cannot make them. You have to get them from what you eat. They are both structurally involved in cell membranes but they also serve important biologic functions such as regulating gene expression, vision, nervous system health, inflammation and blood clotting. In the preindustrial era, the consumption of these fatty acids approximated Omega 6:Omega 3 ratios from 4:1 to 1:4 and traditionally close to 1:1.
In a typical Western diet, the consumption has climbed to Omega 6:Omega 3 ratios from 16:1 to 20:1. Soybean oil is the largest source of Omega 6 in the processed foods we eat. The problem is that Omega 6 fatty acids promote chronic inflammation, the basis of chronic disease that is now epidemic. Body fat storage of Omega 6 has increased 200% over half a century. Increased amounts of Omega 6 in cell membranes has been associated with development of heart disease.
There are no studies that show the effects of Omega 6 on heart disease but there are plenty of studies showing that Omega 3 is beneficial to heart function and mental health disorders like depression and bipolar disorder. Many of the vegetable oils that are used for processing and cooking food have significant amounts of Omega 6 in them.
Good sources of Omega 3 fatty acid involve animal food and consumption of animal food has dropped dramatically. Even in carnivores, the meat from grain feeding is high in Omega 6. The reason you see meat that states ”From grass-fed animals” is that this meat is rich in Omega 3 due to a grass fed (Omega 3) versus grain fed (Omega 6) diet.
Oils that are low in Omega 6 and rich in Omega 3 include olive, coconut, butter, lard and palm. Sunflower, corn, soybean and cottonseed oils contain the most Omega 6. An easy way to get good ratios of Omega 6:Omega 3 is by eating fatty fish like salmon twice weekly or taking an Omega 3 supplement daily. These are basic recommendations I make to all health coaching clients. The health benefits of the Mediterranean diet are due to the high Omega 3 content in foods such as nuts, vegetables, olive oil and fatty fish. It is an anti-inflammatory way of eating.
Who Should Take Statins?
With the information above installed in your mind, is there anyone that could benefit from statins? First let’s review people for whom statins do not help. Again, we are looking at reduction in mortality from heart disease. Statins do lower cholesterol levels but that effect may actually increase your mortality.
The evidence shows that statins DO NOT:
-increase survival in the elderly although the PROSPER trial showed a decreased heart disease mortality in this age group. However, that was mitigated by the increased risk of death from cancer. Overall, mortality was not improved.
-increase survival in women. Heart disease mortality only decreases in women who already have heart disease, not in healthy women as primary prevention. However, there is an increased risk of death from other causes in women taking statins. Therefore, overall mortality is unchanged in women with heart disease. There may be a reduction in cardiovascular events in women with heart disease but there was insufficient evidence to make that conclusion.
-increase survival in healthy people. No study has ever shown statins to be beneficial in healthy people whose only “risk” factor for heart disease is an elevated total cholesterol. The heart attack rate is modestly reduced in this population but there is no mortality reduction.
The evidence shows that statins DO:
-appear to be beneficial in those young and middle aged men who already have heart disease or those who are at high risk for heart disease. However, the results are variable and not uniform with some studies showing no benefit at all. Those individuals are also at risk for some fairly horrid side effects while using statins.
-appear to reduce the risk of stroke in patients with high blood pressure and multiple risk factors for cardiovascular disease. They also appear to reduce the risk of further stroke in patients who have already had a stroke, especially if they have heart disease. Note that this refers to an ischemic (lack of blood flow) stroke. Statins do not prevent hemorrhagic (bleeding) strokes.
How to Stay Healthy Without Statins
Going back to the question from the beginning of this article: So now what? How can a person reduce their risks of heart disease, heart attack, stroke and insulin resistance? Here are some guidelines.
Don’t smoke. Probably the single most important thing you can do.
Drink moderate amounts of alcohol. It is a dangerous drug but in moderation has some heart protective benefits.
Avoid sugar. The second most important thing you can do. If you don’t get insulin resistance, you may not get heart disease. And switching from sugary drinks to diet ones actually makes things worse. To ruin all of your soft drink fun, a study published in September 2019 showed higher all cause mortality for people consuming just two sweetened soft drinks per day. The study looked at 451,000 people from 10 European countries followed for 16 years. Compared to individuals consuming one sweetened soft drink per month, there was an increased risk of death from colon cancer, Parkinson’s disease, digestive diseases and heart disease. Sorry.
Eat natural foods that consist of high fats, moderate proteins and low carbohydrates. Aim for less than 20 grams of carbohydrates per day which will necessitate you reading labels. It is amazing how many foods can push your carbohydrate intake upwards. Try to make sure any carbohydrates you eat are complex (beans, nuts, fruit with skin, vegetables, sweet potatoes, squash, brown rice) and not simple sugars (dairy, white bread, desserts, anything with corn or high fructose corn syrup, breakfast cereal, sweetened soft drinks).
Eat healthy fats and don’t count calories. The following are some healthy choices. Eat one avocado a day. Consume full fat natural cheeses but not the individually wrapped American “cheese” because that’s not cheese. Dark chocolate is healthy fat and also improves brain function. Whole eggs. They contain omega 3 fatty acids and the yolks have all the nutrients. Fatty fish like salmon, mackerel, trout, sardines and herring. If you can’t stomach sea food take a good Omega 3 or cod liver oil supplement. Nuts reduce your risk of obesity, diabetes and heart disease. Chia seeds are not only good for you, they reduce inflammation. Extra Virgin Olive Oil is almost universally considered to be the healthiest fat in any diet.
Here is a link to a good Omega 3 supplement from Krill Oil (naturally low in contaminants and has a potent antioxidant) for a company I am an affiliate for:
http://www.anrdoezrs.net/links/9120933/type/dlg/https://www.lifeextension.com/vitamins-supplements/item01988/super-omega-3-plus-epa-dha-fish-oil-sesame-lignans-olive-extract-krill-astaxanthin
Here is a link to a good cod liver oil:
http://www.anrdoezrs.net/links/9120933/type/dlg/https://www.lifeextension.com/vitamins-supplements/item21532/arctic-cod-liver-oil
Incorporate intermittent fasting into your way of life. This is the means to rest your gut similar to how your brain needs rest while you are sleeping. Aim for one meal a day to avoid triggering an insulin response during the rest of the day. This is easiest if you eat your one meal in the evening at least three hours before bedtime. Follow the guideline above when you feast during your one meal a day and don’t restrict your calories or even pay attention to them. Take at least twenty minutes to eat (in other words, slow down), eat until you are full and then stop. If you get hungry during the day, drink water with Himalayan salt in it. In the morning, put heavy whipping cream if you drink coffee but avoid sweeteners if you can. Following this pattern will increase your energy, decrease your fatigue and you will begin to lose weight if you are overweight. It’s not as hard as it sounds and I’ve done it. Twice to lose weight and then continuing on to maintain my weight. You can also do your fasting for 18 hours and eat during the intervening six hours. If weight loss is a goal, this will just take longer.
Get up and move around. Even small amounts of exercise can make a difference in your health. I’m not talking about running marathons and bench pressing huge amounts of weight. I’m talking about brisk walking for 30 minutes three times a week. Even light biceps curls have major benefits in elderly people. Movement of your body will help reverse insulin resistance and extend your life.
If you feel you must take a pill, make it a baby aspirin. A British Medical Journal, looking at cost effectiveness for treatments to reduce coronary artery disease, found that an 81 mg aspirin (baby aspirin) was as effective as simvastatin and 20 times more cost effective. Also cost effective was initial treatment of high blood pressure with a diuretic and beta blocker, and more intensive high blood pressure treatment adding a calcium channel blocker. The least cost effective treatments were Simvastatin and Plavix.
My Success Story
Most of this article may seem counterintuitive to all you’ve ever heard about health, chronic disease and food. The research is there and cited for you below to check out for yourself. I have almost been reeled into the traditional thinking on cholesterol and statins. My doctor prescribed Lipitor for me in 2010. My total cholesterol was 286, my LDL cholesterol was 199, my HDL cholesterol was 37, I had high blood pressure and I was at least 35 pounds overweight. My response to those issues was to lose 41 pound in 30 days with the HCG diet. I then went on a maintenance phase to keep from gaining the weight back which is basically a ketogenic Atkins type way of eating. My morning meal was three fried eggs (in butter) and six strips of bacon. I had no carbohydrates and ate raw vegetables, a good protein, nuts, peanut butter. You know, good and fun stuff.
Seven weeks after my doctor put me on high blood pressure medication and a statin (I took the blood pressure medicine but not the statin), I redid my labs. My total cholesterol was 141. My LDL cholesterol was 130 (which was high normal at that time) and my HDL cholesterol had risen to 44. My weight had dropped from 205 to 163 pounds. She thought I had sent her the wrong labs until she saw me and could see the 40# weight loss. I maintained that weight loss for about 8 years by avoiding carbohydrates. I had some personal stressors for a couple of years that led to emotional eating and a weight gain of 20 pounds placing me at 187#. Facing another doctor who wanted me on a statin (total cholesterol 234), I lost 20 pounds in 7 weeks by intermittent fasting and low carbohydrate high fat meals. I had one meal a day from 6-7 pm and fasted the rest of each 24 hour period. Just in that short period of time, I came back down to 165 pounds and have maintained that by avoiding carbohydrates.
I have been teaching this way of health and way of life for a number of years. If you want individualized help, get in touch with me through my web site at www.healthwithoutrisk.com and I’ll design a program to help you achieve your health goals and avoid the nasty side effects of potentially toxic medications.
Feedback on my articles is always appreciated. If you disagree with me, I enjoy a good debate. I’ll win, of course, but good debates are fun.
In addition, here is a guide to diet plans for you to consider as you think about all of the information in this article:
https://www.consumersadvocate.org/diet-plans
References
https://www.health.harvard.edu/heart-health/how-its-made-cholesterol-production-in-your-body
https://www.healthline.com/health/high-cholesterol/why-is-cholesterol-needed#goals
https://www.healthline.com/nutrition/27-health-and-nutrition-tips
https://www.healthline.com/nutrition/modern-nutrition-policy-lies-bad-science
https://www.ketogenic-diet-resource.com/usda-food-pyramid.html
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4513492/
Kannel WB, Castelli WP, Gordon T. Cholesterol in the prediction of atherosclerotic disease. New perspectives based on the Framingham study. Ann Intern Med. 1979;90:85–91.
Stone NJ, Robinson JG, Lichtenstein AH, Bairey Merz CN, Blum CB, Eckel RH, Goldberg AC, Gordon D, Levy D, Lloyd-Jones DM, et al. 2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2014;63:2889–2934.
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https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(16)31357-5/fulltext
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https://kellybroganmd.com/cracking-cholesterol-myth-statins-harm-body-mind/?fbclid=IwAR3GXbE1mtl2maQDSFbHlRFSsc52lAvUGeVLDhqDrikAFg5dyT0Nl7oMxew
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6367420/
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https://www.acc.org/latest-in-cardiology/articles/2015/08/11/09/16/statin-intolerance-not-a-myth
https://www.acc.org/latest-in-cardiology/clinical-trials/2016/03/29/22/34/accelerate
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https://www.healthline.com/nutrition/optimize-omega-6-omega-3-ratio
https://www.pharmaceutical-journal.com/opinion/insight/the-cholesterol-and-calorie-hypotheses-are-both-dead-it-is-time-to-focus-on-the-real-culprit-insulin-resistance/20203046.article?firstPass=false
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0072642
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