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Cholesterol Lowering Drugs & Your Good Cholesterol–Bad News

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aspirin to protect your heart
Sergey Yarochkin/Dollar Photo Club

Despite all the less-than-stellar research on cholesterol lowering drugs, the powers-that-be want us to take even more of it.

The latest “cholesterol guidelines” released late in 2013 have drastically increased the number of patients who would potentially be given a statin.  They have finally dropped the fallacy that total cholesterol has any value (you know–total cholesterol–that lab value that you were taught to pay attention to so doctors would know when to put you on a cholesterol lowering medication..) and basically state that you should be given a statin if your doctor THINKS you might be at risk for a heart attack.

I have certainly been a vocal opponent of the statin class of drugs because the numbers just don’t make any sense.  Treat 1,000 people for 5 years to prevent 11 heart attacks (instead of 22 people who would’ve had heart attackes without the drugs), while at the same time causing diabetes in 8 more.  A net gain of 3.  Out of a thousand.  In 5 years.

That just sucks in my book.

And “they” think we should use it more on more patients.  None of this takes into account the very long list of side effects from this class of drugs (other then the already mentioned increased risk of diabetes).

And, as we treat more and more patients with cholesterol lowering drugs, the amount of people experiencing side effects is just going to skyrocket.  But at least they are not going to have a heart attack because of the statin drugs.

Right?

I guess that all depends.

This particular study looks at one of those little-known secrets about drugs to lower cholesterol.  While they all lower cholesterol levels (for whatever that is worth), in some individuals the drugs also lower HDL (the “good”) cholesterol.  This is generally not a good thing.  Specifically, researchers looked at 724 patients who had just started treatment with statins after having a heart attack and followed for 6 to 9 months.

Eighty-six percent (620) of these patients had his or her HDL-C level increase during the course of the study, while 14% (104) of patients had his or her HDL cholesterol go down.  Here’s what the researchers found when they looked closer at the group that had HDL levels drop:

  • Both groups had their LDL cholesterol levels drop below 100 mg/dl.
  • Adverse cardiovascular events (including death from all causes, heart attacks and stroke) happened more frequently in the decreased HDL group.
  • To be precise, this lower HDL group had these events at over TWICE the rate (15.4% vs 7.1%).
  • Overall, those who had lowered HDL as a result of the statin drugs (to protect the heart, I might add) were 95% more likely to have a cardiac event.

Let’s get this straight.  A drug given to lower cholesterol levels actually lowered good cholesterol levels in 14% of those patients taking them.  In this 14%, they were 95% MORE likely to have a cardiac event??

THIS is the wonder drug that seemingly all of medicine is hanging their hats on to save the world from heart disease?  I‘ll take lifestyle changes, thank you.

 

CRP–Mediated Low Density Lipoprotein Uptake by Macrophages – (03-22-01)

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CRP–Mediated Low Density Lipoprotein Uptake by Macrophages

I may need to clarify what this article is talking about. First, it is current theory that macrophages become foam cells once they take up LDL cholesterol from the bloodstream. These foam cells are what lead to the buildup of plaque on the arteries. This article is suggesting that CRP (a marker of chronic inflammation) increases the attraction (“opsonizes”) between the LDL and the macrophages. Low level chronic inflammation can come from so many different sources; and can in turn lead to a multitude of chronic diseases.

Circulation — Abstracts: Zwaka et al. 103 (9): 1194

Read entire article here

Effective and Safe Modification of Multiple Atherosclerotic Risk Factors – (02-12-01)

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Effective and Safe Modification of Multiple Atherosclerotic Risk Factors

This article looks at the lowering of multiple risk factor for atherosclerosis simultaneously. As far as I’m concerned, this is the ONLY way to address this problem. Of interesting note in this study was the use of niacin, 500mg twice daily (a very reasonable dose) to raise HDL levels 30%. Add some exercise and avoidance of saturated fat and your LDL/HDL ratios will be looking pretty good!!

Am Heart J 140(5):792-803, 2000 Patients with peripheral arterial disease (PAD) are at an increased risk of cardiovascular mortality and morbidity and thus are an excellent group in whom to evaluate the feasibility and the effect of an aggressive multifactorial intervention on atherosclerotic vascular disease risk factors. The Arterial Disease Multiple Intervention Trial (ADMIT) was designed to determine the efficacy, safety, and compliance of an multifactorial therapy on selected atherosclerotic disease risk factors in patients with PAD. Niacin increased HDL cholesterol levels by 30%, with the majority of effect achieved at a dosage of 500 mg twice daily. Warfarin had an anticoagulant effect. The antioxidant vitamins resulted in a significant increase in vitamin E, C, and beta-carotene plasma levels. Overall, compliance was high and few adverse effects were reported. ADMIT demonstrates that it is both feasible and safe to modify multiple atherosclerotic disease risk factors effectively with intensive combination therapy in patients with PAD.

Flavonoids in grape juice protect the LDL from becoming oxidized – (12-05-02)

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Comparison of antioxidant effects of Concord grape juice flavonoids & alpha-tocopherol on markers of oxidative stress

While the findings that flavonoids in grape juice have potent antioxidant properties should not drop anyone’s jaw, this is a good time to remind everyone that, while we throw on our blinders and look only at cholesterol as the “bad guy” in CVD, the reality is that LDL cholesterol does not do any damage until the LDL itself gets damaged. The flavonoids in grape juice protect the LDL from becoming oxidized.

AJCN — Abstracts: O’Byrne et al. 76 (6): 1367

Read entire article here

MAINTENANCE OF HIGH LDL CHOLESTEROL – (01-09-06)

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Maintenance of the LDL Cholesterol: HDL Cholesterol Ratio in an Elderly Population Given a Dietary Cholesterol Challenge

While Dr. Ornish may disagree (and actually-his program was much, much more than just a low-cholesterol diet), I’ve never been all that concerned with dietary cholesterol. It’s not as simple as more dietary cholesterol = higher blood cholesterol. In many cases, it’s endogenous production driving by high insulin levels that’s more imp’t. But physicians still demonize high cholesterol foods that are good for us. Avocados. Eggs (especially the high omega-3 type).

This study supports the fact that dietary cholesterol is not as closely tied to cardiovascular risk as many would think.

Read entire article here

NIACIN USED TO PREDICT HEART DISEASE RISK – (12-27-06)

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Effects of Extended-Release Niacin on Lipoprotein Particle Size, Distribution, and Inflammatory Markers in Patients With Coronary Artery Disease

While niacin has been known for a long time to be one of the few compounds used in a pharmacologic manner (soy, flax and exercise does as well–but these aren’t use in a pharmacologic approach), the beneficial subclass changes in the specific lipids in this study were quite surprising.  Recall that we have further delved into the HDL and LDL molecules and found that these particles can be furthered subdivided, and that these subclasses can have even more dramatic abilities to predict heart disease risk.

Niacin in this study was found to raise the “best of the best” as large particle HDL by 32% and reduced the small particle LDL by 12% while also raising the large particle LDL by 82%.  Taken together, these changes would suggest that niacin has a much greater ability to lower CVD risk than many other molecules available.

Read entire article here

DAMAGE TO LDL CHOLESTEROL RISKS HUMAN LIFE – (09-06-05)

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Plasma Oxidized Low-Density Lipoprotein, a Strong Predictor for Acute Coronary Heart Disease Events in Apparently Healthy, Middle-Aged Men

I frequently have patients come in with cholesterol that is just slightly elevated–maybe 210 or 220.  There have been times that these patients have been doing everything else right and their cholesterol is just a little elevated.  We need to remember that cholesterol does not do its damage until it gets damaged itself.  This damage to LDL cholesterol creates a compound called an oxysterol and THIS is what does the damage.

High intakes of fruits and veggies with lots of antioxidants can protect this cholesterol from becoming oxidized.  We can see from this current study that these oxidized cholesterols really do increase risk greatly (up to 4x the risk).

Read entire article here

KNOW THE VARIOUS FACTORS OF CARDIOVASCULAR DISEASE – (07-18-05)

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Oxidized Phospholipids, Lp(a) Lipoprotein, and Coronary Artery Disease

A quick review of biochemistry before we go on.  LDL is generally considered the “bad” cholesterol but this view is archaic.  The large, less dense LDL particles (called Type A) are much less damaging.  It is believed that the lipids on this particle are easily removed in the liver, leaving mainly protein.  On the other side of the coin is the small, dense LDL particles (called Pattern B).  The main protein component of this small, dense LDL is apo B100.  These show high correlations w/ CVD risk.  Lipoprotein a or lp(a), is a known risk factor for cardiovascular disease.

So, the researchers looked at the contribution of oxidized LDL (remember-cholesterol does not do damage to us until it gets damaged and becomes oxidized) and lp(a) together on the risk of CAD.  The highest levels of either oxidized LDL or lp(a) in a patient with high cholesterol produced a staggering odds ratio of 16.8 and 14.2 respectively.  That means your risk is 16 TIMES AS HIGH.  And, given that CVD is a top killer, this translates into some serious risk.  The problem?  Most clinicians probably are unaware of how to spell lp(a), let alone use it to assess risk.

Read entire article here