BTTT
Good post!
BUMP!
I thought taking niacin with statins was a no-no?
If you value your brain (assuming you have one of course), stay off statins !
I wonder if I could take niacin. My gastro dr says to stay away from vit B because of the hep C & my liver. Maybe I should look into it.
Since when is a vitamin a drug?!
bttt
The disturbing thing is the notion that a vitamin is a drug.
bookmark
Plant sterols (block the dietary uptake of cholesterol?)
Niacin
Policasonal
Vitamin C, Lysine, Proline,
Fish oil
These are all natural solutions. As such, they can not be patented. A patent is a temporary monopoly granted and enforced by the Government. A monopoly can charge high, sometimes very high, prices. Natural products cannot be patented and are subject to fierce competition that drives the price way down.
Artificial, man-made products can be patented. As monopoly products, they can charge the high prices that is needed to pay for expensive testing and FDA review process.
Although natural products may more effective and have fewer (or no) side-effects, they cannot generate the revenue stream of patent drugs. The revenue stream of the patent drug makers pay for testing, jumping through FDA hoops, greasing the skids in Congress, advertising, a constant stream of customer sales representatives in Doctors’ offices, etc.
Although natural solutions are probably better/cheaper, they are marginalized and are just one step away from being declared quackery.
BS! Over-the-counter niacin is as good or better than the prescription Niaspan. And, of course, cheaper.
PIng
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
How Crystals Get Their Groove Back
FReepmail me if you want on or off my health and science ping list.
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.
ping
An Apple A Day Could Keep High Cholesterol Levels Away
http://cholesterol.about.com/b/2005/02/26/an-apple-a-day-could-keep-high-cholesterol-levels-away.htm
If I remember correctly I think that it reduces the level 5 - 10 % mainly due to the pectin in the apple that removes the bile acid from the intestines
what about regular niacin? How much should one take per day? I understand that sustained-released niacin may cause liver damage.