Posted on 11/21/2009 9:06:11 PM PST by neverdem
The findings led to an early halt of a small study comparing Niaspan and Zetia, two compounds commonly used along with statins to reduce heart attack risk
ORLANDO, Fla. — Adding a pharmaceutical form of the B vitamin niacin — but not the drug ezetimibe — to a cholesterol-lowering statin drug appears to reduce artery plaque buildup in patients with coronary artery disease, according to much-anticipated results announced at a press conference November 15.
The results were from a study that was relatively small — only 208 patients — but provided a head-to-head comparison of niacin and ezetimibe, known by the brand name Zetia. Despite studies last year that questioned its effectiveness, Zetia remains a blockbuster drug for Merck & Co. Inc. The form of niacin used in the study is an extended-release, prescription-only formulation of niacin called Niaspan, made by Abbott, which funded the new trial.
The new findings were simultaneously published online by the New England Journal of Medicine and presented during the American Heart Association’s Scientific Sessions 2009. Niacin has been shown to raise levels of HDL, the type of cholesterol that protects against heart disease. Zetia is designed to work differently, by lowering levels of LDL, the cholesterol that contributes to heart disease. Niacin also lowers LDL, but is better known for raising HDL. Zetia’s performance fell flat in two recent trials, leading many doctors to question its usefulness.
For the new study, researchers enrolled 363 patients from Walter Reed Army Medical Center in Washington, D.C., and Washington Adventist Hospital in Takoma Park, Md. The patients were randomly assigned to take their prescribed statin drug with the addition of either Niaspan or Zetia. The drugs’ effects were gauged by measuring plaque buildup in each participant’s carotid arteries.
Investigators stopped the study in June when it became...
(Excerpt) Read more at sciencenews.org ...
"Carotid Intima–Media Thickness" refers to the thickening of the "wall" of the carotid artery, presumably by atherosclerosis. That thickening of the "wall" decreases the inside diameter, the lumen, causing what's called a stenosis, a narrowing of the inside diameter. It's not blocked completely, but the flow is abnormal.
that would be nitrates not niacin
That’s a shame...unfortunately women have a much higher hypersensitvity to Statins...especially the big ones...
I take 80mg Pravachol daily with zip bad side effects or liver panels.
My lipids are like a 12 year old.
as luck would have it I was born with a badly formed LAD and have a compromised but functioning heart and am lucky to be alive...so I ain’t whining but my cardiologist now at Vandy believes in Statins if you can handle them
on Zetia, I take it too and it helps improve lipids but apparently the hoped for atherosclerotic reversals ain’t happening..
one thing though....a big thing....after two open hearts in 13 months in 04-05 to correct aforementioned issue, I have constricted pulmonary to some degree...i quit taking my daily 100mg COENZMQ10 and after 3 months noticed a pretty fast decline in heart strength and breathing...got back on them quick....big believer in CEQ10...no doubt.
(they gave me Advair but damn...that stuff is way high...300 bucks a month)
Go to Life Extension to find out. www.lef.org
Niacin’s role in cholesterol and plaque reduction has been known since the fifties.
You will find the abstracts and protocol suggestions.
In addition, Life Extension Foundation, if you join, will allow you to chat with health care specialists, including doctors, regarding YOUR situation. I can’t recommend them enough.
It's the dosage spike in blood level causing flushing with the non-time release Niacin that is the big difference between the two. With a huge surge of temporary niacin, the flushing side effect is so bad, you cannot get people to stay on it.
Niaspan has been the only effective medication for me. I got into serious trouble with statins.
That is a well founded concern. There is the possibility of liver damage from Niacin. The solution: have a periodic blood test that will show up any liver problems. That is what I do.
Also it is worth pointing out that there are other adverse effects from Niacin. Flushing is the primary one that people worry about. Using a time release (over-the-counter) version and taking a baby aspirin just before the Niacin pretty much takes care of that problem.
A more important issue, and one that seems to be less well understood is the effect of too much Niacin. Typical dosages are in 500 mg tablets (I'm talking over-the-counter here, not prescription versions). I take two a day at the same time and have no problem. At the urging of a former cardiologist I did at one time take 2000 mg (4 tablets). The result: 24/7 nagging stomach and extreme lethargy. This went on for several months until I did a self diagnosis, guessed that it was the Niacin, and quit abruptly. All symptoms were gone in less than 24 hours.
The bottoms line: take it easy and find out your tolerance for the Niacin. Make sure you get your liver tested periodically - probably every 6 months at first and then maybe once a year or so. Ask your doctor and do what he says.
Absolutely true. I wouldn't even consider using Niaspan. Buy your Niacin in time-release form at Walgreens.
Yes, it’s dosage dependent.
I forgot. There's also a difference between a a physiologic dose, such as in a multivitamin(MVI), and a pharmacologic dose. My MVI has 20 milligrams of niacin as its niacinamide analog. This study used doses up to 100 times that amount of niacin, IIRC.
Ezetimibe was licensed by the Food and Drug Administration in 2002 exclusively on the basis of its ability to reduce the LDL cholesterol level while having an acceptable short-term side-effect profile. An understanding of ezetimibe's mechanism of action has subsequently evolved and appears to be increasingly more complex than the purported simple inhibition of cholesterol absorption at the enterocyte and than can be inferred from murine and other animal models.28 The drug, systemically absorbed and enterohepatically recirculated in a potent glucuronidated form,29 inhibits multiple, key cholesterol-transport proteins including the primarily intracellular lipid cholesterol transport receptor, Niemann–Pick C1-L1.30 In addition, ezetimibe has been reported to have diverse actions including mild inhibition of acyl-coenzyme A:cholesterol acyltransferase,30 a mechanism of action shown to potentially worsen atherosclerosis and clinical cardiovascular events.31,32,33 Ezetimibe can inhibit scavenger receptor B1, the high-affinity HDL receptor that may be responsible for up to 50% of HDL binding.20 This effect, which includes inhibition of the in vitro uptake of cholesterol by means of scavenger receptor B134,35 and transcriptional down-regulation of this and other key cholesterol-transport proteins,36 may disrupt the process of HDL-mediated, reverse transport of cholesterol. Thus, we hypothesize that the seemingly paradoxical association of greater ezetimibe-induced reduction of LDL cholesterol level with a greater increase in carotid intima–media thickness is biologically plausible if it is associated with the unintended disruption of reverse cholesterol transport.If viewed properly, this hypothesis-generating finding is not an indictment of the overall importance of reducing LDL cholesterol for the purpose of preventing cardiovascular events, as illustrated by therapies based on statins or nonstatins (e.g., bile acid sequestrants).37 Rather, this adverse relationship may be attributable to the net effect of ezetimibe, a drug with diverse actions, not all of which are measured through its effects on intestinal cholesterol absorption and LDL cholesterol level. Taken together with a preexisting concern regarding the clinical effectiveness of ezetimibe,38,39,40 our findings challenge the usefulness of LDL cholesterol reduction as a guaranteed surrogate of clinical efficacy, particularly reduction achieved through the use of novel clinical compounds. For ezetimibe, our results indicate a disconnect between reductions in the LDL cholesterol level and increases in the carotid intima–media thickness in patients with dyslipidemia who are receiving statin therapy. Thus, we believe that prudent clinical practice currently favors the avoidance of ezetimibe, with consideration of further restriction on its use in lieu of clinically validated regimens, until its net effect on clinical outcomes can be fully ascertained.
A limitation of this comparative-effectiveness study is that it used carotid intima–media thickness as a surrogate for clinical end points. The finding of a clinical benefit in cardiovascular outcome with niacin, although based on a small number of events, provides additional support for the validity of this imaging end point and is consistent with outcome effects seen in other trials.6,7,8 Further clinical certainty regarding ezetimibe and niacin will require data from ongoing clinical trials. The trial could not be conducted in a completely blinded manner because of the use of drugs acquired by the sponsor from a commercial source and their disparate side-effect profiles; therefore, the trial was designed to include the blinded evaluation of end points and automated border-detection methods for quantitation of the carotid intima–media thickness. The reproducibility of measurements of the carotid intima–media thickness in the ARBITER 6–HALTS study is among the highest ever achieved in a clinical trial.
The ARBITER 6–HALTS trial shows regression of carotid intima–media thickness when extended-release niacin was combined with statin therapy in patients with coronary heart disease, or a coronary heart disease risk equivalent, and an LDL cholesterol level of less than 100 mg per deciliter and an HDL cholesterol level of less than 50 or 55 mg per deciliter. This approach was more efficacious for both carotid intima–media thickness and clinical cardiovascular events than was the combination of ezetimibe and statin therapy. The use of ezetimibe led to a paradoxical increase in the degree of atherosclerosis in association with greater reduction in LDL cholesterol, an effect we hypothesize may stem from unintended biologic effects of this agent.
Phys Ed: Why Exercise Makes You Less Anxious
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Everything on there looks good, except the plant sterols.
Um, Red yeast rice also has statins in it. Just because it’s natural doesn’t make it any better than statins.
One thing to beware is I heard the other night that if you take large quantities of niacin, you should also take folic acid, because niacin for some reason raises the homocysteine levels.
No Statins, be they be chemical or natural, be taken without Co-Q-10.As all statins deplete Co-Q-10 in the body.
Niacin has been around for thirty years for this type of high cholesterol.
The problem is that the doses needed cause severe flushing. (Think hot flashes of menopause but worse).
Most of my patients just couldn’t manage to slowly increase the dosage to get on a high enough dose because of this. Most of them just stopped taking it.
Niacin in these doses can also cause liver problems.
In other words, yes it is a normal vitamin, and good for you.
But when taken in huge doses it is a lousy drug.
Antioxidant ping. Worth buying. If you want more info, FReepmail me.
I’ve read that statins reduce the production of CoQ10, weakening muscles, including the heart muscle. My wife took statins and acquired muscle pains. She stopped, but it took a while before the pain went away.
Interesting, educational post/thread. Thanks to all posters.
Health/life BTTT!
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