The Merriam-Webster Dictionary defines a hoax this way: act intended to trick or deceive

And when it comes to linking cholesterol to heart disease in a causative manner, that’s just what has been happening in the last 30 years. You, and I, have been duped.Mainstream medicine, and the pharmaceutical industry, would have us believe that high cholesterol causes heart disease. But that is far from a true and accurate statement. While high cholesterol may been seen in many individuals with heart disease, the link is far from direct and certainly not one of causality. Meaning, while we often see the two occurring together in one individual (concurrence), the relationship between the two is not one of causality.

This was proven definitively in the largest medical study to date focused on heart disease, The Framingham Study, which showed that only half of those with high cholesterol ever get heart disease, and half of those with heart disease have normal cholesterol, even when they are not on cholesterol lowering medications (statins). If there was direct causation, where high cholesterol actually caused heart disease, then almost everyone with high cholesterol would have heart disease, and all you would have to do is look at someone’s numbers and know exactly what is goin got happen.  And that is simply not the case.

In fact, it might surprise you to learn that total cholesterol, “bad” LDL-cholesterol, and Triglyceride levels are very poor performers at predicting heart disease. You simply can’t look at someone’s “lipid panel” and know who will, and will not, have a heart attack or stroke. Medical research suggests that if you take 100 people with high cholesterol and follow them over time, that 3 of them will have a heart attack or stroke (remembering that risk factors predispose to, but don’t guarantee something). Putting all of these 100 people on a statin drug that reduces cholesterol, reduces the number of people who will have a heart attack to 2 people instead of 3. Now, for that 1 person who avoided the heart attack – that’s fantastic and significant. But that means that the other 2 people will have a heart attack regardless of the medication, and that the other 97 people are on a drug, usually for a lifetime, that is doing nothing for them, and has some potential side effects.

Let’s add one more item to this rapidly deteriorating picture.  Back in the 1960s, well before the first statin drug was invented around the 1980s, well before the explosion of heart disease (again int he 80s) and well before the average person had even heard of the word cholesterol, the upper limit of cholesterol as published in medical textbooks was about 285.

In the early 1990’s this number was revised downward to about 240. In the late 1990’s it was revised farther downward to 220, and now sits right at 200 (with some advocates pushing to get the acceptable number even lower still).

So where did all the hype about cholesterol causing heart disease start? For that answer we have to go all the way back to the early 1900s to some faulty research.

Just before the Roaring Twenties, the earliest cholesterol research involved injecting a cholesterol “solution” into rabbits, who then went on to develop arterial plaques and exhibit the signs and symptoms of heart disease. Autopsy confirmed the build up of a waxy substance on the inside of blood vessels…which was identified as cholesterol. The logical conclusion, or so it seemed, was that high cholesterol builds up in blood vessels, blocking blood flow to the heart, causing heart disease. But hold on there, not so quick.

What was discovered several decades later, after the cholesterol craze had already taken hold, was that the cholesterol solution used in the initial research was not pure cholesterol, but included a synthetic preservative, which turns out to be pro-inflammatory. Later studies (since the 1980s) have shown that injecting pure cholesterol, without the pro-inflammatory preservative, does NOT cause plaque build up. But interestingly, injecting the preservative by itself does.

This new understanding shifted the direction of heart disease research into an inflammatory model, meaning that if something causes damage to, and inflammation of, your blood vessels, that this is the cause of heart disease. As of right now we know that there are several things that can cause damage and inflammation in blood vessels

  • Stress
  • Blood sugar handling problems (like diabetes and pre-diabetes)
  • Environmental chemicals
  • Infections (Bacterial and viral)
  • Autoimmunity against proteins in the heart and/or blood vessels
  • And others..

 

In the last few years, other organizations have added to the growing understanding of heart disease, and continue to help shift the focus away from the cholesterol model. The MESA study has been ongoing since 2000, with over 6,800 participants from multiple ethnicities. As of the writing of this blog article there have been over 1,000 scientific papers written with data from this study alone, and along with other information streams has greatly enhanced our understanding of the true nature of heart disease.

Not only do we now understand arterial disease to be the result of any mechanism that can inflict injury to the lining of your blood vessels, we ar enow starting to understand that “plugged” vessels are more a dysfunction of blood clotting, which takes us very far away from high cholesterol indeed.

Turns out that you can have a cholesterol plaque that reduces the size of your blood vessel 90% or more, but still get enough blood flow to not have an incident. Thanks to the researchers in the Framingham and MESA studies (and others) we now understand that when new plaque if formed, it is consider “unstable”, meaning it is susceptible to cracks and fissues. This unstable plaque can rupture, causing to things to happen.

The first is that a plaque fragment may break off and get stuck further downstream as the blood vessels get smaller, an event called thrombosis.

The second is that when a new plague cracks, it causes localized bleeding, which turns on the clotting process. Now this part can get very technical very quickly, but here is the quick summary. There are many factors that determine how large a clot will form, whether or not our natural defenses can break down the clot, or if the clot will continue to grow.

The bottom line is this – most heart attacks occur not because of cholesterol buildup, but because something has inflamed the blood vessels, causing unstable plaque to form, which then either cracks and fractures, potentially sending fragments to plug up smaller vessels, or (and this is the most common problem) triggering a local bleed, that then clots, enlarging to block the vessel and impeded blood flow enough to create an event.

Needless to say, if high cholesterol is not the cause of heart disease, one must question the wisdom of measuring only the “lipid panel” and why the conventional medical community (with some exceptions) continues to promote the cholesterol hoax.

I say “only” the lipid panel because in the last 10 years we have seen a new generation of lab tests that focus on the real issues, like inflammation, and markers relating to unstable plaque, which is where the true risk comes from. It might surprise you to know that the ability to