“My HDL is low. What does that mean?”

For years, people attending the Pritikin Longevity Center have said to our doctors and dietitians: “I love how the Pritikin Program has improved my health, especially my LDL bad cholesterol, but my HDL is low.  Shouldn’t my HDL good cholesterol be higher?”

And for years, our doctors and dietitians have replied, “Don’t focus on your HDL. What’s far more important is the healthy lifestyle you’ve learned at Pritikin because this lifestyle, more than anything else, will give you optimal protection against heart attacks, diabetes, hypertension, and strokes.”

Raising HDL via drugs does not seem to translate into fewer heart attacks and strokes.

The findings of an important recent 3,414-person trial* from the National Institutes of Health affirm that raising HDL should not be our focus.

In the trial, the participants, all of whom had heart disease, were given either Zocor (a statin to lower LDL) plus a placebo, or Zocor plus a high-dose niacin drug called Niaspan, which raises HDL.

Trial stopped

The participants were intended to be followed for 32 months. But the trial was halted after 18 months. While both drugs had done their lipid-improving jobs (Zocor lowered LDL and Niaspan raised HDL), the patients taking Niaspan saw no benefit in protection against heart attacks over statin therapy alone. They also had a slightly increased risk of stroke.

Bottom Line: Raising HDL via drugs does not seem to translate into fewer heart attacks and strokes.

It’s not the first study casting doubt over drug-induced raising of HDL. In 2006, the pharmaceutical giant Pfizer had a new drug that very effectively raised HDL, but there was one big problem: the drug was also found to increase the risk of death. Pfizer halted further development of the drug.

No lower risk of heart attacks and strokes

And a few years ago, the ACCORD study (Action to Control Cardiovascular Risk in Diabetes) had disappointing results. In this large clinical trial tracking more than 10,000 American adults with Type 2 diabetes, scientists had hoped that adding a fibric acid derivative (known to increase HDL) to statin therapy would further reduce the risk of cardiovascular-related events, like heart attacks and strokes, compared to statin therapy alone. It didn’t, despite the better-looking HDL numbers of those on the fibric-statin therapy. **

“These drug studies clearly show that supposedly favorable changes in HDL via pharmacology is not necessarily accompanied by reduced cardiovascular disease risk, and, in some cases, may paradoxically increase the risk of cardiovascular-related events and deaths,” states Dr. Jay Kenney, Nutrition Research Specialist and Educator at the Pritikin Longevity Center.

“The fact is, the way blood lipids function to deliver cholesterol to artery walls and remove excess cholesterol from artery walls is very complex. Moreover, those who make the simplistic argument that low-fat diets are bad because they lower HDL are being naïve.”

And scientifically uninformed.

Documented benefits of healthy lifestyle change

It is a low-fat, fiber-rich, Pritikin-style eating plan plus daily exercise (not HDL-raising drugs) that has been scientifically documented to relieve angina, regress atherosclerosis, and reduce cardiovascular events and total mortality. “We do not have comparable data for any drug or drug combination, or for higher ‘good fat’ diets like those recommended by the American Heart Association and National Cholesterol Education Program,” asserts Dr. Kenney

And it is a low-fat, fiber-rich, Pritikin-style eating plan that is followed by populations who enjoy the lowest incidences of heart disease in the world, such as the people of Okinawa and other rural regions of Japan. They also, by the way, tend to have very low levels of HDL, often in the 20s and even lower.

Quantity vs quality

For heart health, what may be far more important than quantity of HDL, research is now finding, is quality, or more precisely, how our HDL is functioning.

Artery injury

Let’s back up a bit and talk about atherosclerosis, the disease that injures our arteries and leads to heart attacks. Atherosclerosis is an inflammatory process. Just as our outside skin becomes inflamed when infection sets in, the inside skin of our arteries becomes inflamed, chronically so, if we eat too much saturated fat and cholesterol from a rich, fatty diet.

Inflammation

Here’s what happens. Excess LDL cholesterol seeps into the artery wall, where it becomes oxidized, or rancid, like food forgotten in the back of the fridge. The inflammatory process kicks in. White blood cells rush in, “eating” the oxidized cholesterol till these cells burst. The released cholesterol forms abscesses, or plaque. These abscesses also age and oxidize. So once again white blood cells rush in, create more inflammation – and more plaque. Plaques that burst can lead to heart attacks.

Anti-inflammatory HDL

When it’s functioning well, HDL has anti-inflammatory powers, which means it can decrease the amount of LDL that is going rancid, or oxidizing.

Pro-inflammatory HDL

But HDL can also turn pro-inflammatory, increasing LDL oxidation. Research has found that a saturated-fat-rich diet can mess up the ability of HDL to protect against damage to arteries, turning the HDL from “good” (anti-inflammatory) cholesterol into “bad” (pro-inflammatory) cholesterol.

In research published in 2006,*** scientists at UCLA obtained blood samples of 22 men, ages 46 to 77, attending a three-week program at the Pritikin Longevity Center. On entry, the men tended to have pro-inflammatory HDL, “suggesting their HDL, despite being quantitatively normal, was not protective against LDL oxidation,” wrote lead author Dr. Christian K. Roberts and colleagues.

Becoming “good” again

But after just three weeks of following the Pritikin Program of diet and exercise, exit blood tests showed that HDL had converted from pro- to anti-inflammatory – despite the fact that total levels of HDL had actually gone down a little.

“These data,” summarized the authors, “indicate that intensive lifestyle modification improves the function of HDL even in the face of reduced levels.”

“It is reasonable,” they concluded, to state that the function of HDL “may be more important than the steady-state plasma [blood] levels.”

Summing up…

“Don’t focus on HDL.  Focus instead on embracing a healthy Pritikin lifestyle,” counsels Dr. Ron Scheib, cardiologist and Medical Director at the Pritikin Longevity Center.

“Yes, it’s easier to pop a pill, but by changing your lifestyle, you’ll not only prevent atherosclerosis, you’ll greatly lessen your risk of many other woes, including diabetes, hypertension, obesity, cancer, arthritis, and impotence, because all these afflictions often share the same root cause – a lousy lifestyle.

“There’s more good news. A Pritikin lifestyle perks up everyday life. When guests leave us after two weeks here at Pritikin, they often say, ‘I didn’t know I could feel this good at my age.’ They’re physically fit, alert, and energized. They’re living better. That’s what matters most of all.”


* http://www.nhlbi.nih.gov/news/press-releases/2011/nih-stops-clinical-trial-on-combination-cholesterol-treatment.html

** http://www.nhlbi.nih.gov/health/prof/heart/other/accord/

*** Roberts, CK, et al. Effect of a short-term diet and exercise intervention on inflammatory/anti-inflammatory properties of HDL in overweight/obese men with cardiovascular risk factors. J Appl Physiol, 2006; 101: 1727-1732.



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