The Fascinating Relationship of Cholesterol and Statin Drugs

Cholesterol is a term that gets thrown around all the time, and almost always in a negative light.  It is this bad reputation of cholesterol that has led to the rise of popular cholesterol lowering statin drugs such as Lipitor and Crestor.  But what is cholesterol?  Is it a bad thing?  Are statin drugs necessary?  How do they work?

Let’s start with cholesterol.  It is a lipid (aka fat) produced in the liver that is vital to life and serves as the precursor for various hormones (cortisol, testosterone, estrogen, progesterone, etc.) and vitamin D.  It is also what makes up the outer membrane of virtually every cell in our bodies.  Anytime a cell is damaged by way of direct trauma or inflammation, more cholesterol is required to rebuild and repair.

The correct level of cholesterol varies from person to person.  A total cholesterol level of over 240 may be perfectly healthy for some, but an indicator of a potential risk factor for others.  As a matter of fact the acceptable total level of CHL used to be well over 250, but has been lowered and lowered. Why?  Well, some speculate that by continuously lowering the normative value, you extend that umbrella wider and wider for statin drug customers.

Statin drugs came about after a study by Ancel Keys (The Seven Countries Study) directly attributed cardiovascular disease to high cholesterol.  The powers that be (including the American Heart Association) took this finding and ran with it as the country became obsessed with lowering CHL.  Only problem is the study had gaping holes in it and has since been disproven by numerous scientists and nutritionists around the globe.

The correct thing to do here would be to recant, admit the mistake, and take proactive steps going forward.  For some reason this doesn’t happen as CHL continues to be bashed and statins continue to rake in the dollars.

The story gets worse when we actually break down how statins do their work.  Trust me on this one, this is actually quite fascinating.

First we have a rise of inflammation in the body due to too many grains, dairy, soy, corn, sugar…pick your poison.  This inflammation causes internal damage and as we discussed, CHL is required to assist in the repairing.

The liver then sends out LDL (low density lipoproteins aka “bad” cholesterol).  So as we can see, it is the consumption of too many carbs or inflammatory foods (not fats) that can indirectly raise “bad” CHL.   I say indirectly because in actuality only a small percentage of our total CHL is derived directly from CHL containing foods, such as eggs.  But back to the story.

So CHL is sent out from the liver as LDL to assist in the rebuild due to inflammation.   However, when this inflammation persists, damage is done to the receptors on the cells that receive the LDL.  So now the cells that are in need of CHL, aren’t getting it and request for the liver to send more.  The liver, being the people pleaser it is, obliges and sends out more CHL in the form of LDL.

At this point, due to inflammation, we have internal destruction going on.  At the same time, bad CHL levels (LDLs) are also up due to the inflammation, but not the direct cause of the destruction correlated with things like cardiovascular disease.

Hang in there, here comes the good stuff.

Due to the perception that high CHL is the reason for CVD, a drug was created to combat it.  Statin drugs work by actually damaging the part of the liver that makes CHL.  So we see a drop in total CHL.  It gets even more diabolical in that the liver, now requiring materials to rebuild, needs additional CHL.  The CHL that persisted in the periphery as “bad” CHL now is transported back to the liver as HDL or “good” cholesterol.  The numbers have been manipulated from dangerous to healthy, all while destroying the liver and allowing the causative systemic inflammation to persist.

Cherry on top here is that one of the key markers of inflammation is something called C-reactive protein (CRP). Where do you think this is made? You guessed it, the liver.  Liver destruction leads to less CRP, and we lose one of our methods to accurately detect systemic inflammation.

I guess this is why the ads for statin drugs flat out state that they have not been shown to prevent heart attacks, heart disease, or strokes.  Oh, they lower CHL in the manners we discussed, but not the risk they were originally intended to decrease.  Yet they are still heavily utilized.  I don’t know about you, but I found this simultaneously fascinating, frustrating and ingenious all in one.

This article isn’t intended to instruct anyone to stop taking any medications.  Always consult with your trusted doctor before stopping or starting any aspect of treatment, especially medications.  However, it is designed to provoke thought and questions.  And as we can see, when it comes to cholesterol and statins, there certainly are a lot to be answered.

 

REFERENCES

http://www.nlm.nih.gov/medlineplus/ency/article/003502.htm

http://www.ncbi.nlm.nih.gov/pubmed/23959724

http://www.ncbi.nlm.nih.gov/pubmed/23782756

http://www.mayoclinic.com/health/statin-side-effects/MY00205

http://www.npr.org/blogs/health/2013/04/03/176145911/side-effects-prompt-patients-to-stop-statins-cholesterol

 

 

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One response to “The Fascinating Relationship of Cholesterol and Statin Drugs

  1. Pingback: “High” Cholesterol? Statin Time? | Clarke Chiropractic and Wellness

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