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Created on Saturday, 27 June 2020 17:58

Medicine is such a dogmatic institution, and its dogma permeates all over the world. For decades now, they have preached that the amount of cholesterol in the blood determines whether arterial plaquing takes place.  They say that if serum cholesterol is high, it causes atheromatous plaquing, and if serum cholesterol is low, it prevents it.  High is now defined as 200 or above. But, if your cholesterol is 150, you’re considered OK.

But, how could a 25% reduction in serum cholesterol have any effect on starting or stopping a pathological process? Cholesterol is a normal constituent, and it is vital. Every cell in your body depends on cholesterol to maintain its intracellular environment.  Without cholesterol in your cell membrane, your cells would dissolve! In other words, they couldn’t exist. Cholesterol is also a building block of steroid hormones, including testosterone and estrogen, and it provides vital cholic acid for digestion, which is synthesized from cholesterol. 

If the atheromatous process is driven by the amount of cholesterol in the blood, where a level of 200 milligrams per decaliter of blood drives it, then why shouldn’t 150 also drive it? Why should that little difference be the determining factor in whether plaque forms or not? It’s insane.  

It’s true that when people are on good health programs, where they are eating well, a diet consisting mostly, if not wholly, of: fruits, vegetables, nuts, beans, etc. that they are going to have lower cholesterol. And if they eat bad diets, consisting of burgers, shakes, cookies, etc., they are going to have higher cholesterol. So, the level of cholesterol in the blood may be a marker for the kind of diet they eat.  But, it doesn’t mean that the concentration of cholesterol in the blood is the determining factor in whether plaque is formed. 

There is one caveat, and that is that oxidized cholesterol, from frying meats and whatnot, has been shown to be irritating, and anything that irritates the endothelium can cause plaquing.  Tobacco smoke has no cholesterol, but it is very irritating, i.e. poisonous, and it is a powerful progenitor of arterial plaque.  

There are special tests that can determine how much of your blood cholesterol is oxidized, and that has significance. But, that aside, the idea that the amount of cholesterol in the blood is what determines whether your have open or clogged arteries is crazy.

But, what about the fact that when they give people statin drugs, that their cholesterol goes down, and it may go down a lot,  and their risk of heart attack and heart disease goes down with it? The truth is that the risk isn’t lowered that much from taking statin drugs. Maybe one heart attack gets prevented when 100 people take statins for a year. It’s something like that.  The demonstrable benefit from taking statin drugs is actually very small.

And that tiny risk reduction may be due to other things than cholesterol reduction. We know that statin drugs are anti-inflammatory, and we know that inflammation is directly involved in atherosclerosis.  It’s very telling that the slight reduction in heart attack risk has not been shown to be dose-dependent.  

Meanwhile, the demonstrable harms from taking statin drugs are much less obscure, including: an increased risk of diabetes, dementia, and even cancer.

Furthermore, statins are often prescribed in the absence of any clinical signs of heart disease; based solely on the cholesterol number. In other words: it’s a knee-jerk reaction to a blood test. 

“Mr. Jones, we see that your cholesterol is a little high, so we’ll be starting you on a statin drug. You’ll be taking it indefinitely- for the rest of your life. Have a nice day.”

That is the state of Modern Medicine today.  For all the money, and it’s about $20 trillion spent in the U.S. every year, for all the exalted research and science, and regardless of whether you, yourself, are a rich bastard or a dirt-poor pauper, that is what you get. That is what 21st century Medicine delivers and calls health care.