Cancer And The Cholesterol Myth

The basic premise we're going to lay out in this article is that the prevailing mainstream view on cholesterol and saturated fat, which has been going on for over 60 years, has been proven false decades ago. As a result of this outdated science, nearly every single dietary guideline from each of the major health institutions around the world continue to be based on this false premise. As it turns out, following these guidelines are actually furthering the incidence of CVD disease, all-cause mortality, and cancer as the data clearly shows 40+ years into this nutritional experiment.

The mainstream view is based on the Lipid Hypothesis, which states that high blood cholesterol is the cause of atherosclerosis, which is responsible for cardiovascular disease. It assumes that anything that causes a rise in blood cholesterol (particularly the “bad” LDL) will be disease causing, and anything that lowers it would be protective against CVD. It also states that dietary intake of saturated fat and cholesterol (primarily from animal fats) contributes to increases in blood cholesterol and therefore CVD.

So we have our # 1 enemy scapegoat to blame for our problems: cholesterol and saturated fat. “LDL” bad. “HDL” good. Simple right? The question is.. is cholesterol really the root cause of CVD? Does it even have anything to do with it at all? The short answer is no. Most doctors on the ground unfortunately don’t know any better, because this is how they’ve been trained. So as with anything, if you want the truth, you have to do a little digging yourself rather than blindly trust the conclusions of our experts. We will do a little digging together here in this article, but keep in mind all of the information presented here is really only scratching the surface of the issue.

What is Cholesterol?

Cholesterol is an essential lipid that your body produces. It is required for the phospholipid membrane health of every single cell in your body. It is essential to the makeup of all your steroid hormones (estrogen, testosterone, cortisol, etc), Vitamin D production, and your stomach bile. Without adequate cholesterol, you will have severe abnormalities (including death), as is seen with those with Smith–Lemli–Opitz Syndrome (SLOS), and even those taking statin drugs to chemically suppress their cholesterol levels.

It’s also important to note that when we talk about blood tests for cholesterol, we are dealing with the lipoproteins LDL (low-density-lipoproteins) and HDL (high-density-lipoproteins), not cholesterol itself. These are special protein molecules that transport lipids through our water-soluble blood. The actual makeup of cholesterol in HDL and LDL molecules is identical. The reason they’ve labeled LDL bad is because it contains a higher concentration of cholesterol compared to other components: proteins, phospholipids, and triglycerides. The reason LDL has more cholesterol is because it is the lipoprotein that transports cholesterol throughout the body to all the cells that require it. HDL on the other hand has lower levels of cholesterol and is used to transport cholesterol from cells back to the liver for recycling. Your liver is what makes cholesterol, along with other cells in your body, and will actually attempt to make more or less in response to your dietary intake of saturated fat.

CVD History

Cardiovascular disease (CVD) is the #1 chronic disease and #1 cause of death worldwide amongst industrialized countries. It includes all conditions affecting the vasculature and heart: heart attack, stroke, coronary artery disease, angina, atherosclerosis, hypertension, peripheral artery disease, congestive heart failure, and others. Being that CVD is the leading cause of death worldwide, as you can imagine for over 60 years there has been significant government spending involved, along with a long history of controversial political interference in the science, as well as the public health recommendations; all of which have completely failed to reduce the continual growth of CVD and heart disease.

Along with the dietary recommendations surrounding CVD, we have the #1 selling drug category of all time: statins; which equate to a trillion dollar industry. This drug has become the medical standard of care for millions of healthy individuals with what we’ve deemed to be a “bad” LDL blood marker. So you can certainly see what’s at stake behind maintaining the lie. And there is a long, messy, and well documented history behind it, much of which we won’t get into here.

It all started with a number of studies in the 50’s, 60’s and 70’s, aiming to determine the root cause of the America's rising CVD death rate. Some of the main studies include “The Lipid Hypothesis”, “Seven Countries Study”, and “Coronary Primary Prevention Trial”. Others include “LA Veterans Trial”, “Finnish Mental Hospital Trial”, “Oslo Study”, “The Anti-Coronary Club”. An American psychologist named Ancel Keys was at the center of this research in the 50’s and 60’s and was famously on the cover of Time magazine promoting a low-fat diet. This marked the beginning of a series of strong guidelines and recommendations that sparked the low-fat food industry in the 80’s. Ironically 53 years later, Time magazine put out this cover in 2014, completely reversing the narrative. The long story short is while nearly all studies were able to reduce serum cholesterol by replacing saturated fat with PUFA oils substitutes, none of them showed any statistically significant outcomes in reducing death by CVD; and in many cases actually showed an increased risk and incidence of cancer. To this day, no study is able to validate the Lipid Hypothesis.

So we have a situation of mostly well-meaning scientists and researchers scrambling to find the cause of a rising heart disease problem around the end of WW2. They based it on an old hypothesis that started in 1913 with a rabbit study that attempted to link cholesterol to atherosclerosis. The correlation was loose, humans are not rabbits, and all the future attempts to validate the hypothesis since then have been unsuccessful.

The Study of Studies

It’s important to know the mechanisms behind how well meaning researchers and scientists can use statistics to create just about any conclusive narrative they desire.

“There are three kinds of lies: lies, damned lies and statistics.” – Mark Twain

One small but significant example is the use of relative vs. absolute figures. Say you have a new statin drug being studied, and the drug reduces heart attack incidence from 2 per 1000 to 1 per 1000 compared to the placebo. In the world of actual science and statistics, such a small degree of change is considered meaningless; it’s just noise in the data. But with those numbers, the headline can read “New statin drug reduces heart attack incidence by 50%.” Big difference there.

Another is the omission of data that doesn’t support the desired conclusion (and then blocking access to the raw data behind the study). The lesson here is you should never rely solely on headlines, study abstracts or conclusions. You have to know how to dive into the details yourself, or listen to experts who themselves have looked into the details with a critical eye.

Shortcomings of the Lipid Hypothesis

To restate, the Lipid Hypothesis states that the cause of cardiovascular disease is high blood serum cholesterol (LDL). If this is the case, you would need to have a way of tying all of the causal factors of CVD to this hypothesis, and this cannot be done. How can causal factors like smoking and sickle cell anemia produce the exact same atherosclerosis as an obese person, where you get exactly the same plaque buildup blocking the arteries?

The truth is, high LDL is only loosely correlated with only some of those who get CVD. In fact, up to 75% of people who have a heart event have cholesterol levels in the healthy range. And 50% have a cholesterol level in the optimal range.

Another shortcoming of the Hypothesis is the fact that arterial plaques actually form behind the endothelial wall. It’s not like we’ve imagined that we have all this LDL floating in our blood stream gunking up the passage of blood. The plaques form behind the blood vessel wall, before endothelial progenitor cells come in to create a new layer of wall, creating a narrower and narrower passage for the blood as this process is repeated. So how does LDL get deposited behind this endothelial wall that is specifically designed with tight junctions making particles like lipoproteins impossible to get through on their own? The answer is there has to first be some sort of damage to this wall, also known as a vascular lesion. LDL does not create these lesions. So we're essentially looking at our immune system’s response to tissue damage and blaming that for being the problem. In reality, the initial damage to the endothelium of our blood vessels is the root cause of CVD. All we had to do to get the hypothesis correct is ask “what creates endothelial damage?”.

Before we continue, keep in mind this has been the basis of federal and institutional dietary recommendations for over 50 years. It’s the reason we have carbs at the base of our food pyramid and why “low-fat” food products is still thought of to be healthy. It's the reason why we replaced all our saturated fat sources with inflammatory poly-unsaturated fats, such as the use of seed oils like margarine and vegetable oil. Meanwhile our incidence of obesity, diabetes, mental illness, cancer, and yes even heart disease has only gone up. They have all accelerated since the introduction of these dietary guidelines, not slowed down. If these guidelines were correct, the heart disease rates of countries like France, who eat copious amounts of saturated fat, should have even more heart disease, but the exact opposite is true.

So What Really Causes CVD?

The root cause of all forms of cardiovascular disease is endothelial dysfunction/damage. There are a number of known causal factors for this dysfunction:

Smoking, high stress, gut dysbiosis, nutrient deficiencies, sickle-cell anemia, diabetes/hyperglycemia, PTSD, use of steroids, etc.

None of these causal factors have anything to do with high LDL cholesterol. What they (and all other causes of CVD) have in common is they cause damage to the endothelial lining of your blood vessels. When this layer becomes damaged, your body in all its infinite intelligence, goes to repair that damage via a thrombosis, or blood clot. If your body did not respond in this way, these micro lesions would eventually cause you to bleed out internally and die. When you have repeated damage to your endothelium, you get blood clot on top of blood clot, and this forms the plaque that actually sits behind the repaired endothelium, making the lumen (the opening) of your blood vessels narrower and narrower. This is what is known as atherosclerosis.

This plaque is made of many different components commonly found in blood clots, only one of which is cholesterol. This is not even the “bad” LDL cholesterol we talk about, but a completely different form known as cholesterol crystals. The real source of the cholesterol found in atherosclerotic plaques are the red blood cells themselves, which are comprised of 40% fat. Regardless, it is only one of many necessary components needed to form the clot.

It's only when a piece of a forming blood clot breaks off, circulates in your bloodstream, and flows back through a previously narrowed section of your coronary arteries and gets lodged, that you get a myocardial infarction (aka heart attack).

It’s also worth noting that you will rarely see atherosclerosis in the veins, despite there being just as much LDL cholesterol as in arteries. Why is that? Because arteries (especially those closest to the heart) are where the greatest blood pressure is. When you have constituents in the blood that do damage to the endothelial lining, the damage is going to be greatest where there is the highest blood pressure. That is why young people with sickle cell anemia have a 50,000% increased risk of CVD. In this situation, the actual sickle shape of the blood cells itself is what is creating this mechanical abrasive damage to the endothelium.

In truth, CVD is a multi-causal problem. It is a symptom of metabolic syndrome, in which you have multiple critical systems of the body not functioning properly due to a variety of factors which are typically lifestyle and diet related. Instead of cholesterol, here are the actual known causes of CVD under this alternative theory:

Actual causes of CVD: smoking (includes air pollution, wood fires, car exhaust, etc), insulin resistance/diabetes, hypertension (high blood pressure), chronic stress, genetic disorders (sickle cell anemia, familial hypercholesterolemia), chronic inflammation, oxidative stress/low antioxidant status, vitamin C deficiency, metabolic endotoxemia (due to leaky gut), dysbiosis, bacterial/viral infections, elevated homocysteine, nutrient deficiencies, nutrient toxicities, some pharmaceutical medications and more.

CVD Testing

Should you worry if you have a high LDL level? Not from that information alone, no. There are many factors that cause the blood serum LDL to go up, including dietary intake of saturated fat, systemic inflammation, LDL resistance, oxidative stress and hypothyroidism/Hashimoto’s.

Here are better markers to assess your risk:

Triglyceride levels: measures TG levels in VLDL. Optimal range 75-100mg/dL

TG/HDL-C ratio: above 2 indicates metabolic syndrome risk; identifies insulin resistance, advanced atherosclerosis, and extensive CVD.

C-reactive protein (CRP): need a high sensitivity CRP test; Low risk: hs-CRP <1 mg/dL; Moderate risk: hs-CRP between 1-3 mg/dL; High risk: hs-CRP > 3 mg/dL

Coronary artery calcium (CAC) / Coronary calcium index (CCI): 1-10 CVD risk is low, 11-100 mild heart disease risk and moderate heart attack risk, 101-400 certain heart disease and plaque; chance of getting heart attack moderate to high, 400+ 90% chance plaque is blocking the arteries; high chance of heart attack. Not much to do to reverse it, but let’s you know the level of past damage indicating current risk.

LP(a) levels: genetic test; diet/drugs do not change levels; however if your levels are high, your CVD risk goes up.

NMR LipidProfile: tests LDL particle number, may indicate high endotoxin load; ideal below 1000nm/L.

OxLDL: ideal is <60U/L; testing may not be accurate.

Conclusion

So this is the brief overview landscape of what’s really going on with all situations of CVD. As you can see, it has nothing to do with too much “bad” LDL clogging your arteries like a plumbing system. What causes CVD is endothelial dysfunction/damage, and there are many different causal factors to this. If you want to reduce your risk of CVD, you must figure out which of the causal factors you potentially have going on, and make the appropriate diet/lifestyle changes.

We hope this information has helped give you a more nuanced perspective on not only cholesterol, but mainstream science and medicine as a whole. If you have any additional questions or would like to work with ICCA, please get in touch with us.

References

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