HDL-Cholesterol: the Scene is Changing

Atherosclerotic blood vessel
Cholesterol-filled atherosclerotic coronary artery
Credit: Courtesy: University of Pennsylvania School of Medicine

  by Hans Diehl, DrHSc, MPH  

Ever since my heady clinical days at the residential Pritikin Longevity Center, I advised participants following its very low-fat, fiber-rich, plant-food centered diet not to worry about the common lack of improved HDL-cholesterol levels. This was in contrast to the clinical practice, which has not changed over the last 35 years, where clinicians advise their patients to try to increase their cardio-protective HDL numbers (their "good" cholesterol) by enhancing their daily exercise, losing excess weight, and by using some wine. And yet, in this residential, well-controlled lifestyle environment, HDL numbers more often than not did not go up over a period of 4 weeks in spite of a rigorous daily exercise program accompanied by loss of excessive weight.

A Paradox
This obviously led to some concern in the scientific community because people with naturally higher HDL-cholesterol levels living in Western society by and large have fewer heart problems in spite of their high LDL numbers (their atherogenic, bad and dangerous cholesterol). But while the good cholesterol numbers often did not increase in the Pritikin program, the LDL numbers usually went down quite stunningly 20 to 35% within the four week lifestyle intervention program, and that in the absence of any cholesterol-lowering drugs. And the narrowing of the coronary arteries began to decrease. The plaques began to melt down. The atherosclerotic disease process began to regress!

LDL/HDL Ratios
These observed trends led many researchers to take a look at the LDL/HDL ratio. Any lowering of this ratio would signal a reduced coronary risk. For instance: if participants with initial LDL levels of 120 mg% and HDL levels of 40 mg% and thus a ratio of 3.0 would lower their LDL to 80 mg% with an accompanying decrease in HDL to 35 mg%, their new LDL/HDL ratio of 2.29 would have demonstrated reduced coronary risk in spite of the lowering of the HDL value going from 40 to 35 points.

Increasing HDL: the Pharma fiasco
While this new understanding seemed to be reasonable, clinicians and the pharma-industry stood by their old maxim: let's get the good cholesterol up to protect people from the danger of their high LDL.

And they tried. And here are the results:
#1 The National Institutes of Health recently announced the results of a major Clinical Trial involving 3,414 heart disease patients that raising HDL pharmaceutically did not protect against heart attacks. In this study, the participants were given either Zocor (to lower LDL) plus a placebo, or Zocor plus a high dose niacin drug called Niaspan, which raises HDL. The trial was intended to last for 32 months. But it was cut short after only 18 months. While Zocor had lowered the LDL, and Niaspan had increased the good cholesterol, the patients taking the Niaspan experienced no clinical benefit in protection against heart attacks over Zocor therapy alone. If anything, they had a slightly higher stroke risk.

#2 The disappointing results were similar to a 2006 study when Pfizer, the world's largest drug company, pulled the plug on a 15,000-patient trial of their drug Torcetrapib that was forecast as the next best seller. While their drug was quite successful in raising HDL levels, the drug was also found to increase the risk of death by more than 60%. Since then, Pfizer has abandoned any further development of this drug.

#3 And a 2010 study using a fibric acid drug known to increase HDL in combination with a statin drug to reduce LDL applied to more than 10,000 American diabetic adults found that the addition of the HDL-raising fibric acid drug did not provide any benefit over using the statin drug alone in reducing the risk of heart attacks and stokes.

The Bottom Line
Raising cardio-protective HDL numbers pharmacologically does not translate into fewer cardiovascular events. It may paradoxically actually increase the cardiovascular risk and death.

Dr. Jay Kenney from the Pritikin Longevity Center summarized it: "Those who make the simplistic argument that low-fat, fiber-rich, plant-food centered diets are bad because they lower HDL are being naive and scientifically uninformed."

The Morphing of HDL
We should have taken heed to the findings that there are many long living cultures in the world that have very low heart disease rates, yet their HDL numbers may be in their 20s. In the meanwhile, all too often, many clinicians are still very eager to see the HDL numbers in the 50 and 60 ranges. But it may not be the absolute numbers that determine the outcome as much as how the HDL functions, because most recent studies have suggested that HDL can be functioning both as a good protective (anti-inflammatory) substance or as a bad erosive (pro-inflammatory) substance. Much of this may appear to be related to the amount of saturated fat in the diet.

Diet: Defeating LDL, the Little Devils
And then, there is still the powerful atherogenic cholesterol particle LDL. The higher the number, the greater the coronary risk. But fortunately, those LDL levels come down consistently within a few weeks in response to a very low fat, fiber-rich, plant-food centered diet, both in residential treatment centers and in our community and corporate-wide CHIP programs. Every 1% drop in LDL translates into a 3% drop in coronary risk. With a 20% drop in LDL within four weeks, you can slash your coronary risk in half!


This article is reprinted with permission from the CHIP Health Newsletter. To subscribe to the CHIP Health Newsletter, click here.