“An analysis of cholesterol values in 1,700 patients with atherosclerotic disease revealed no definite correlation between serum cholesterol levels and the nature and extent of atherosclerotic disease.”
– Michael DeBakey, M.D. (world-renowned cardiac surgeon)
It’s time to end the cholesterol/plaque/heart disease lie once and for all. This lie finds its roots in shaky ground, digging deep into poorly done studies with cherry-picked results.
The truth is that heart disease and cholesterol is no more difficult to understand than a clogged fuel line in a car that won’t start. Cause and effect – it’s in everything. If you can figure out the cause, then you can understand the effect and, more importantly, the solution.
How the Cholesterol Lie Got Started
The cholesterol/plaque/heart disease lie has been going on for almost 100 years, ever since a Russian researcher names Nikolai Anichkov first proposed the idea.
Anichkov fed cholesterol to rabbits, and upon their autopsy he found atherosclerotic plaque in their arteries (the plaque that causes heart disease). Over the next few years, based on this one poorly done experiment, the cholesterol/plaque/heart disease lie was born.
In an attempt to repeat the experiment, researchers found that if rabbits were fed minerals along with the cholesterol, the animals did not form arteriosclerosis, plaque, or heart disease. Anichkov’s theory has actually been disproven many times via many well-performed studies.
But the cholesterol/plaque/heart disease lie continued to build when in 1953 Dr. Ancel Keys published the “Seven Countries Study.” This study sought to establish a direct relationship between increased cholesterol consumption and heart disease, serving as the new basis for the cholesterol theory of heart disease. This study is still to this day taught to medical students.
The problem is that it was actually a 22-country study, and Dr. Keys cherry picked only the results that served his purpose. When all countries in the study are considered, there exists no correlations between animal fat consumption, serum cholesterol, arterial plaque and heart disease1.
Ignoring Evidence to the Contrary
Evidence against the cholesterol/plaque/heart disease lie has mounted over the years, and yet mainstream media and medicine continues to ignore it.
One of the largest studies of its kind, The Framingham Heart Study, began in 1948 and continues to this day, studying residents of Framingham, Massachusetts and following them through the generations (they’re currently on their third generation). They study has clearly demonstrated that total cholesterol is not a good indicator of heart disease.
This was again proven through a series of studies known as JUPITER, published in the New England Journal of Medicine in 2009. This randomized double-blind placebo-controlled study investigated 17,802 healthy people with no history of heart disease. They were put on ‘preventative’ cholesterol medication (available ubiquitously now as ‘statins’).
The results showed that for 1.9 years, one heart attack was prevented for every 244 people that took statins. That is a 0.0004% success rate (or 0.0002% per year). Meanwhile, all 244 people suffered from side effects ranging from skin rashes to heart palpitations to liver damage, and yes, even life-threatening situations. That is a 100% side effect rate.
Even with these obviously poor results, the panel of 14 author physicians still recommended that everyone with even slightly high cholesterol go on a statin drug. Not surprisingly, the study was sponsored by AstraZeneca, the makers of Crestor. Later examination found that 9 of the 14 physicians had financial ties to pharmaceutical companies.
There must be a special place in hell for people who purposely poison other people for financial gain.
The Role of Cholesterol in the Body
In my office I inform my patients that cholesterol is an essential nutrient. Cholesterol is necessary for a large number of biological functions and is produced by our liver and supplemented by the cholesterol we eat. The fact that animal meat has cholesterol is not a weird accident of nature. Animals need it, just like us. God didn’t screw this one up.
Cholesterol is necessary for a WIDE variety of functions:
- Converts the sun’s rays on our skin into vitamin D
- Maintains the integrity of our skin and our cells – every cell in our body is wrapped in a cholesterol membrane, which allows them to communicate with each other and to take up nutrients.
- Ensures healthy digestion and liver function
- Converts into cortisol and aldosterone (adrenal hormones) that allow us to respond to stress
- Enhances brain function and memory
- Enables healthy sexual function – I recently saw a bumper sticker that read “Cholesterol is for lovers.” Increased cholesterol consumption has been shown to improve one’s sex life
Blocking cholesterol is devastating to the body. In fact, 13,290 complaints of depression and 9,044 other complaints have been made to the FDA Adverse Event Reporting System (AERS) regarding cholesterol-lowering drugs.
Here are some of the most common:2
- Fatigue and Weakness
- Memory Loss and Reduced Mental Capacity
- Neuropathy and Slowed Reactions
- Muscle Wasting leading to Back Pain and Heart Failure
- Intestinal Disease
- Pancreatic Problems
- Reduced Libido
How Cholesterol Works in the Body and What the Numbers Mean
Breaking Down LDL
Think of cholesterol like the U.S. military of your body. If you were standing on the East Coast of the U.S. in 1942, you would have seen the military mobilizing for World War II. These departing soldiers are akin to LDL cholesterol.
LDL cholesterol is mobilized in the liver and sent out when called upon. Some people call this “bad” cholesterol. Again, it’s not a cosmic joke that we have cholesterol in our bodies, and the military soldiers are not inherently bad. They’re just responding to a problem somewhere in the body, and we would no more want to block them then we do our national defense.
Some of LDL’s duties include carrying fat soluble vitamins and CoQ10 around the body. Most importantly, studies show that lowering LDL with drugs does not decrease mortality rates at all.
The AFCAPS trial, a 5.2 year study of cholesterol drugs, showed the following when taking the drug Lovastatin:
- if LDL was less than 142, event rate was 4.9
- if LDL was 143-156, event rate was 4.8
- if LDL was above 157, event rate was 7.0
The “event” referred to in the above study is any cardiovascular event. The study showed you have a 2.2% greater risk of having an event as your “bad” cholesterol goes higher. However, there is NO difference in mortality between those that artificially lower LDL and those that do not.
Breaking Down Total Cholesterol
Total cholesterol levels are supposed to increase naturally with age – you need the extra cholesterol for brain function and hormone production.
Total cholesterol levels vary with stress, time of day, lab methods, etc. Research has shown that a total cholesterol level over 300 carries a slight risk. Under 300 there is no appreciable increased risk of heart disease3.
In women and the elderly, the reverse is actually true: higher cholesterol levels are associated with longer lifespan4.
Studies have also shown there is absolutely no correlation between healthy animal fat intake and degree of atherosclerosis or serum cholesterol5.
So why are we recommended drugs to lower LDL or Total cholesterol?
The answer should be obvious: $$$$.
“Lies, Damned Lies, and Statistics”
Mark Twain once said “Lies, Damed lies, and Statistics,” referring to the use of statistics to bolster weak arguments.
With the AFCAPS trial referenced above, the pharmaceutical companies divided the 4.8 into the 7, instead of by 100, and proudly stated that there was a 30% difference in events from lowering LDL cholesterol with drugs. What they should have done is divide by 100 (those not taking the drug) and documented a 2.2% difference with taking the toxic drug. Even with this 2.2%, mortality rates were not lowered.
However, drug companies hailed this as an unmitigated success and said: “Lovastatin reduces the risk for the first acute major coronary event in men and women with average …and suggest the need for reassessment of the National Cholesterol Education Program guidelines regarding pharmacological intervention.”6
Drug companies twist the numbers to sell the American people into a sham.
So please, dear reader, fret not about your LDL and total cholesterol numbers. Don’t even bother noticing them (as long as the total is under 300 for men). If your doctor tells you he or she wants to give you a drug to lower your cholesterol, walk out of their office immediately.
And slam the door on the way out.
Breaking Down HDL
If you were standing on the East Coast in 1945 and you saw all the ships coming back full of soldiers, you would know the war is over. This represents HDL cholesterol and is often called the “good” cholesterol: Its good because the war is over and we don’t need so many soldiers out in the body doing their work. HDL’s particles are the scavengers that pick up old cholesterol and bring them back to the liver.
The Total Cholesterol / HDL ratio is actually one of the best predictors of heart disease. You want your HDL to be 1/4 of the total. So if your total cholesterol is 240 and your HDL is 60, you’re all good. If your total cholesterol is 200 and your HDL is 20, you have a problem.
Breaking Down Triglycerides
High triglycerides are bad, simply put. When you eat too many carbohydrates, at a certain point your liver becomes unable to eliminate, store, and process those carbs. It then converts those excess carbohydrates into triglycerides.
Triglycerides are a fat in the blood which, in elevated levels, can cause hardening of the arteries, poor circulation, and ultimately heart disease.
To summarize, the only things we should look at to determine risk of heart disease are:
- Total cholesterol/HDL ratio
- Triglyceride levels
If the ratio is off, triglycerides are high, or total cholesterol is above 300 (in men) a change must be made.
How to [ACTUALLY] Lower Your Risk of Heart Disease
The first and most import thing we need to do is change our diet and perform what we call the DNA Reset.
In the DNA Reset, we have our patients eliminate sugar and carbohydrates from their diet for a period of no less than 21 days. We need to get the carbohydrates that convert into triglycerides out of our diet. This includes alcohol, cereal, rice, potatoes and all forms of sugar. We need to replace these high-carbohydrate foods with healthy meats and vegetables.
It’s also critical to eat more green vegetables like kale, broccoli, brussels sprouts, spinach, etc. A recent study showed that just .63 of a cup of kale daily over a three-month time period can significantly improve serum lipid profiles and reduce the risk of coronary artery disease7. Green vegetables provide necessary micronutrients and minerals like magnesium that the body desperately needs to heal.
Support Digestive Capacity
While undergoing these dietary modifications, it’s strongly encouraged to support your digestive capacity and ensure proper liver drainage. Excess cholesterol is removed by the digestive system and the liver, so if these systems aren’t functioning properly, you’ll never fully recuperate.
Supplementation, coupled with diet changes, is a surefire way to heal leaky gut and increase digestive capacity to ensure our bodies are absorbing all the vitamins and minerals in our diet.
Supplements like Stomach Juice, Digestive Enzymes, Liver/Gallbladder Drainage, and Pre and Probiotics are essential to help eliminate excess cholesterol from the liver and bowels, lower blood pressure and reduce overall inflammation in the body.
Diet modification and supplementation are the only way to give your body a chance to heal itself. Within two months, most people see dramatic improvement in their symptoms, improved blood chemistry numbers, lowered blood pressure and increased energy.
1 Lustig, Robert, M.D., M.S.L. (2012). Fat Chance: Beating the Odds Against Sugar, Processed Food, Obesity, and Disease, Plume (Penguin), ISBN 978-0-14-218043-3, pp. 110-111.
2 See: askapatient.com, search for Lipitor
3 American Heart Journal 1987, 114, 413.
5 Laboratory Investigations 1968 18:498
6 JAMA. 1998;279(20):1615-1622. doi:10.1001/jama.279.20.1615.