How Much Do We Know About “Good” Cholesterol?

When it comes tocholesterol, we’ve viewed things in black and white.  Total cholesterol is bad.  LDL is bad.  HDL is good.

When drugs to lower total cholesterol and LDL cholesterol failed miserably (yes—the statins), the drug companies tried to make a drug that raised HDL cholesterol.  Ironically enough, the money for research and development likely came from the money from sales of the near-worthless statin, atorvastatin (Lipitor).

Torcetrapib, the first drug of its time made by Pfizer, indeed did raise HDL cholesterol but ended up killing patients 60% faster in phase III clinical trials so the drug was scrapped.

So what happened?

For some reason, the drug companies still don’t get it.  They don’t seem to understand that it’s not about the NUMBER, it’s about what the number represents.  Any number on your blood work, whether it’s total cholesterol, HDL, fasting glucose, HbA1c or liver enzymes, are merely the snapshot of the entire picture.  You see water leaking from 10 different locations in your house; do you plug all the individual leaks and throw down towels?  Or do you figure out what the problem is (like maybe the roof…) and fix it??

While this seems so obvious with home repair, it seems to have escaped the realm of common sense in medicine.  We find some type of lab value and latch onto it like a toddler with a new toy (or rather, a toddler with the box from the new toy…).  Then we put all of our focus into that lab value and build an entire approach to a disease based on this single lab value.

Back to the HDL issue.  HDL is not a single molecule.  Rather, as this particular study points out, it is actually made up of at least 85 different subtypes of proteins.  85.  So which ones are the best of the best and which ones are irrelevant as far as your risk of heart disease?  Many prescription drugs are designed to target a very specific pathway.  In the example above given for Torcetrapib, it is highly likely that the drug only affected a very small number of the 85+ types of HDL molecules.  Given that we don’t even understand how each of these types of HDL molecules work in concert, messing with only one could potentially lead to disaster, which is what happened.

Contrast this with lifestyle.  Lifestyle changes do not affect a single pathway.  It is likely that the right lifestyle changes geared towards lowering your risk of heart attack and moving you away from diabetes will lead to alterations in a large number of these HDL protein molecules.  Some will shift lower, some will shift higher, all moving in the direction they are supposed to go to protect you from chronic diseases.  Picture the most elaborate concert you have ever heard; each instrument orchestrating beautifully among one another to produce the perfect outcome.  THAT is what lifestyle does.

Pharmaceutical drugs, on the other hand, would be like throwing 2 or 3 toddlers with bats into the percussion section of a philharmonic orchestra.  Not pretty.

This same reason is why, despite the near universal salivation by the drug companies to create a drug that raises HDL cholesterol levels and magically lowers the risk of dying from a heart attack (while at the same time miraculously boosting profits), it will never happen.  Too many variables at play.  Stick with GMO-free soy, exercise and nuts to raise your cholesterol levels instead.

For more than a decade, Dr. Bogash has stayed current with the medical literature as it relates to physiology, disease prevention and disease management. He uses his knowledge to educate patients, the community and cyberspace on the best way to avoid and / or manage chronic diseases using lifestyle and targeted supplementation.







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