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Niacin & Other Natural Cholesterol lowering drugs

Athersclerosis, a slice of an artery; with yellow
paque encapsulated in middle of wall

There are hundreds of journal articles demonstrating that infective agents play the key role in atherosclerosis and thus CHD (coronary heart disease).  There is strong evidence that besides transport of cholesterol and triglycerides by HDL and LDL, they play important immune functions.  This is why LDL and HDL are present in atheroma; there they among other things bond to, and thus disable endotoxins produce by the pathogens in the artery walls.  The infective agents also produce a response an immune response by white blood cells, thus their presence in the inflamed atheroma.  The strong experimental evidence thus accounts for the presence of both white bloods cells and the lipoproteins.  This is contrary to thestandard LDL theory where oxidized LDL (no mention of the bacterial and virus vectors or the immune role of HDL and LDL) produces an immune response by macrophages.  Since pharma and its opinion leaders can’t refute the infection cause, they simply ignore the issue.  Pharma’s oxidation theory makes atherosclerosis an auto-immune disease.  A much better explanation based upon experimental evidence is given by Prof. Uffe Ravnskov in his book and journal article of these events and the role of infective agents.  In the articles below bacterial living within the middle layer of the artery wall trigger the immune response by T-cells which are further aided by macrophages.  The damage caused in this process damage the arteriole (vasa vasorum) which supply blood to the muscle cells in the artery walls. A large body of clinical evidence (see for examples Ignore the Awkward! by Prof. Uffe Ravnskov—notes on this book), and also the notes on Anthony Calpo chapter 21 The Infection Connection, from The great Cholesterol Con, an excellent scholarly source. --jk. 

Other contributing factors to atherosclerosis are oxidative and glycation to endothelial cells which line the artery wall.  Thus diabetes with its high level of blood glucose and for other reasons not clearly describe adversely affects arteries.  Smoking because of the reactive carbon monoxide damages endothelial cells in blood vessels.  COX-2 inhibitors found in NSAIDs adversely affect endothelial cells in ways which promote the leakage of the immature plaque contained in atheromas, and thereby with long-term usage increase the risk of myocardial infarctions by 50 to 400%--the one exception is aspirin whose affects the production of COX-2 in a different way.  All this is confirmed in articles pasted in this website--jk.

Some articles on the above topic are at:  Cholesterol Myth   http://healthfully.org/rl/id5.html     Cholesterol Myth, source History   http://healthfully.org/rl/id10.html      Infection in Artery Walls the Major Cause of Atherosclerosis    http://healthfully.org/rl/id8.html    infection in artery wall causes Cardiovascular disease    http://healthfully.org/rl/id9.html

Niacin family and Other Natural Cholesterol Lowering Drugs -- (6/23/14) http://healthfully.org/rc/id4.html   

You ought to read as background the 2-page summation on the corporatization of medicine, Side Effects, and Statins. The pharmaceutical industry (hereafter referred to as pharma) controls the research, its publication, the continuing education of doctors, guidelines, etc. The perception in the press is the opposite of the truth, a truth which was succinctly stated by Harvard Prof. Marcia Angell:  “If we had set out to design the worst system that we could imagine, we couldn’t have imagined on as bad as we have.”   Adjustments in this paper have been made for Pharma’s marketing science and their junk article.  Pharma educates physicians and the public.  Based on over 500 hours reviewing the studies of statins, JK has concluded--along with a small chorus of researchers--that statins are not safe or effective. 

Though statins lower cholesterol, major studies have shown mixed endpoint (reducing MI & death) results.  Results depended on the degree of marketing manipulation (an example).  The first statin Mevacor by Merck was approved in 1987 by the FDA for familial hypercholesterolemia caused by genetic defects (a special rare situation where it is more effective than a placebo).  But once approved, the FDA permits expansion of usage without their review.  For basics on cardiovascular disease (CVD) Statins a Critical Review which explains why though they dramatically lower Total Cholesterol (TC), they fail to prevent death & MI.  The reliance on statins is based on marketing science; its usage has become an article of faith.  This paper is about niacin & other alternatives; unlike statins, they prevent death & MI.

Niacin (Nicotinic Acid, NA, vitamin B3):   In 1955 was shown to have a lipid lowering property, and thus improved total cholesterol (TC).   For the next 3 decades niacin was the first and only effective treatment for hyperlipidemia.  It raised HDL 33% and lowered the rate of heart attacks. Long before the first statin pharma mounted a campaign against niacin to promote their patented drugs.  Niacin family now accounts for 3% of the TC-treatment market, less in Europe.    

Parma marginalized niacin was by setting up a treatment protocol that has very low compliance:  a daytime dose of 1500-3000 mg.  This causes vascular dilation in skin which produces a very uncomfortable flushing.  Few will follow this program long-term.  With extended release niacin, the frequency of flushing is only moderately reduced--in the once patented Niaspan (25%, 12%).  Though liver toxicity is rare, reversible (it causes the visible jaundice), physicians perform regular blood work (another way of discouraging the use of niacin & Niaspan). 

Niacin reduces TC by lowering “plasma triglycerides [fats] mobilization from adipose tissue, and inhibiting hepatocyte diacylglycerol acyltransferace synthesis of triglyceride thereby lowering cholesterol and thus inhibits the synthesis of apo-lipoproteins and the influx of free fatty acids (FFA) into the liver, which is the precursor of triglycerides.”  “A single dose of niacin 200 mg given in the fasting state [at bedtime] provides a prompt and marked fall in serum FFA level, with a rebound after some hours.  A comparable fall in plasma FFA occurs normally following a carbohydrate-containing meal, when adipose tissue lipolysis [making lipoproteins] is inhibited by insulin, and re-esterification of FA in adipose tissue cells is increased by glucose. Therefore, the FFA level is usually low during the day, when carbohydrates are the predominant source of calories [thus preventing a niacin caused reduction in FFA].  Lipolysis becomes active in the post-absorptive state at night, when the FFA-level is approximately double the daily mean level.”  “Oral administration of niacin … during the day does not appreciably alter this pattern.  This is why blood cholesterol blood work requires fasting, and why niacin and IHN should be taken at night, when the insulin level is low. Thus a low dose at night-- 200 to 500 mg--is sufficient.  Plasma peak is for niacin 30 minutes, half life under 1 hour.  This entails rapid absorption and excretion during daytime is ineffective because FFA level is low.  Thus preferred is slow release Niacin such as IHN, Niacin works in 3 ways to lower MI risk: antioxidant, anti-inflammatory, and lowers lipid/FFA level.  It is also anti-microbial. 

 Pharma’s recommends a mega dose of niacin (ignores IHN) to create very low compliance due to severe flushing, & it is taken during the day; but works at night when the insulin level is low.  Pharma by this ploy promotes sales of statins. 

In the 1970s it was proven that cholesterol and lipids do not cause CVD, but rather it is chemical damage to protein portion of LDL.  Lowering cholesterol does not prevent CVD, but pharma makes billions treating the wrong problem, and related illnesses (all supported by tobacco science). Cholesterol produced in the liver is packaged in LDL for blood transport to cells to fill essential needs, thus lowering it is a bad idea.  A number of critics have gone public with little effect.  For detailed explanation with dispositive evidence read CVD, atherogenesis, diet, statins, and watch the videos. 

“The Coronary Drug Project [only published long-term endpoint niacin study uses 1.5-3 gm] was conducted between 1966 and 1975 to assess the long-term efficacy and safety of five lipid lowering drugs in 8,341 men with electrocardiogram-documented previous myocardial infraction…. With a mean follow-up of nearly 9 years after termination of the trial, mortality from all causes in each of the drug groups, except for niacin, was similar to that in the placebo group. Mortality in the niacin group was 11% lower than in the placebo grouplong.   Niacin has been shown to produce regression of atherosclerosis [AS] plaques and is the only drug that has demonstrated reduction of overall mortality in currently completed clinical trials… The versatile action of niacin on lipoprotein metabolism, as well as its low cost and long-term safety record, should make it the drug of choice in many patients with hyperlipidemia or coronary artery disease,” AJM 1991.  Other effects include “anti-thrombotic and vascular inflammation, improving endothelial function and plaque stability;” also noted.  These later effects improve endpoint results and thus give the illusion that lowering TC saves lives--for cholesterol myth, for healthful choices.      

Nicotinyl alcohol (pyridylcarbinol) is a niacin derivative used as a hypolipidemic agent and as a vasodilator.  Literature contains only 3 clinical trials (2 published in German).  These were quite favorable.     

Extended-release niacin (Niaspan etc.)  All studies are done according to pharma’s protocol of high dose during day. 

Xantinol {xanthinol} nicotinate, only one study on CVD: high dose caused flushing, and 25 of 33 patients were helped significantly.  It has an antiplatelet action and dilates most blood vessels. 

Nicotinamide also known as niacinamide and nicotinic acid amide (vitamin B3) (what niacin is converted to for its function as a vitamin).  It doesn’t cause flushing; however as the amide of niacin it does not lower cholesterol—see also the 1959 study, and the CP--different non-vitamin action.  But it is effective in the treatment of acne and some cancers. 

Inositol hexanicotinate (IHN):  The literature is thin.  IHN releases niacin at too low a rate to affect the same bio-pathway as niacin (IHN peak 8 hours).  (A criticism by Pharma, shown false in a quality studies using blood samples drawn at night).  INH affects Free Fatty Acids (FFA), rather than lipolysis as does niacin and statins.  FFA is a precursor of plasma triglycerides.  Lipolysis becomes active in the post-absorptive state at night, when the FFA-level is approximately double the daily mean level….  The Xanintol esters and IHN were superior at lowering FFA,” at Eur. J. Clin. Pharmacol. 16, 11-15 1979.  In another study “At 6 weeks of usage [1650 mg IHN] found a nearly 20% improvement in cholesterol profile.   Given a bio-pathway not effecting Q10, on thin evidence jk recommends INH over niacin.

Phenolic substances in red wine shown to inhibit oxidation in LDL.  Lack of quality studies leaves benefits speculative.  At higher than 8 ounces daily, the negative health consequences from ethanol’s metabolites become significant.

Hormone replacement therapy (HRT) estradiol & progesterone are cardiovascular protective; testosterone moderately.  Once eliminating pharma’s marketing-science attack, the evidence in support of HRT is overwhelmingly positive.

Aspirin: 325 with each meal for its anti-inflammatory effect which prevents oxidative damage to LDL thus CVD, and as an anticoagulant prevents MI and stroke, and by stimulating necrosis factor prevents cancer and increases survival.  Because of tolerance, the recommended low dose after one year won’t for most prevent clotting and thus MI and stroke.

Fish oil (omega-3 fatty acids, EPA & DHA):  recommended dose 1 gm/ day. Promote immune function reduces CVD risk .   

CoQ10 (Q10): reduced oxidation of low-density lipoprotein[43][44]; essential for muscle contraction including the heart.

Nutritional Yeast and red yeast extract:  lowers cholesterol in rats by effecting organoleptic properties (LDL and VLDL). 

RECOMMENDATIONS FOR HEALTH:  Remember the cholesterol myth and effects of too much sugar and carbohydrates will cause chemical damage to LDL.  Low-carb diet and exercise are the best defense.  If you feel that you must lower cholesterol and are under 75 years, then IHN 200-500 mgs before retiring to reduce free fatty acids.  A second choice would be niacin sustained release 200-500 mgs.  Both could be taken together, or on alternating days.  To counter niacin’s possible effect upon ATP production, take 300 mgs of Q10.  Because Q10 lowers blood pressure and as an effective anti-oxidant found in LDL, it inhibits atherogenesis, and it protects the mitochondria.  Q10 should be taken by everyone including children (atherogenesis early).  Aspirin 325 with each meal prevents atherogenesis, by inhibiting inflammation; and prevents cancer by over 40%, heart attacks by 50%. Testosterone lowers risk of MI, heart failure, and metabolic syndrome.  Estradiol is why women don’t develop cardiovascular disease until after menopause.  Watch the documentaries and lectures on bad pharma, diet, and GMOs.  .Read Marking Science, and be skeptical of medical (marketing) “wisdom”.  JK has since 1991 taken 325 mgs aspirin or more, high dose of testosterone since 2003, 300 mg Q10 since 2012,  and exercise daily  since 1974—cholesterol 155, blood pressure 125 over 75, and he is in his 7th decade. 

^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^  Non-technical summation

Niacin family and other natural cholesterol lowering drugs and cardiovascular disease (CVD):  Pharma recommends 1,500 to 3000 mgs of niacin (nicotinic acid) taken with meal; however insulin blocks its cholesterol lowering affect.  High dose causes the unpleasant flushing and thus low compliance.  The only long-term study (niacin usage 6 years and effects followed an additional 9 years) was of high dose niacin.  It produced a reduction in deaths from cardiovascular disease by only 11%.   However, a study based on blood work showed that 200 mgs of either niacin or its inositol formulation taken at bedtime was just as effective at lowering cholesterol, and without flushing.  In the same experiment similar results were obtained with inositol hexanicotinate, a source of niacin.  Niacin also possesses anti-inflammatory and antioxidant benefits, and thus inhibits atherogenesis.  Phenolic substances found in red wine are of value, as is nutritional yeast, red yeast extract, and omega-3 fatty acids (found in fish and fish oil supplement) all reduce risk of CVD.  For lowering cholesterol use 200 to 500 mgs at bedtime of either niacin or inositol hexanicotinate.  The reason niacin only makes a modest reduction in adverse events, and statin even less (once the bias of marketing science has been removed) is because high cholesterol is not the cause of CVD.  But rather it is reactive chemicals that damage LDL and the subsequent immune response.  This has been known for 4 decades and is widely acknowledge in journal and Wikipedia articles.  LDL, cholesterol, and triglycerides are essential for life; and saturated fats are health-wise the best source for energy.  Numerous scientists have exposed the myth about cholesterol and triglycerides that pharma spreads.  Pharma makes billions selling drugs that treat the symptoms of atherosclerosis.   Treating them this way is as effective as treating the fever accompanying the flu with a drug that lowers fever.  They make billions more treating the damage caused by a heart attack.  However, as explained in “Heart Issues”, the most important factor for CVD is the inflammatory response to damaged LDL, for which aspirin and CoQ10, and estradiol for postmenopausal women are truly protective.  Testosterone past the age of 70 lowers risk of MI, heart failure, and metabolic syndrome.  Changes in lifestyle are very effective; especially regular strenuous exercise and eating a low carb low sugar diet.  If you must lower cholesterol, then take 200-500 mg of sustained released niacin or inositol hexanicotinate at bedtime.


PhARMA has created an overly simplified and fundamentally incorrect picture of cardiovascular disease, which of course promotes sales of their most profitable family of drugs of all times, statins.  Understanding the process will help you understand in-part why statins fail to prevent CVD better than a placebo, and why the only long term study of niacin (6-years) lowered mortality by only 11%.  Using a surrogate marker of cholesterol level is misleading; the reasons are contained in the two explanations below. 

Important points:  It isn’t cholesterol that causes cardiovascular disease (CDV), but rather oxidative damage to low-density lipoproteins (LDL).  LDL is the blood transport system for cholesterol, which isn’t blood soluble.  Cholesterol is vital for all cells.  LDL is water (blood) soluble complexes, and house approximately 1,500 cholesterol molecules.  When damage by a reactive chemical, LDL elicits a response from a particular type of white-blood cell that start the process of forming plaque.  Over a lifetime the plaque accumulates and develops into cardiovascular disease (CDV).  Once developed, the most one can do is try to slow its progression and allow the body to slowly harden plaque into a stable form.  Soft plaque that leaks causes most of the strokes and heart attacks.  Thus cholesterol and LDL levels are moderately associated with CDV.  The more LDL and the more reactive chemicals (such as carbon monoxide from cigarettes) over a lifetime, the great is the extent of CDV.  PhARMA wants doctors and patients to believe that statin family of drugs because they lower cholesterol that they can make a big different—that’s B.S.   For well illustrated and easily   understood explanation of the atherogenesis process, go to http://healthfully.org/heart/id5.html.   JK.

Similar statement from a journal article:  Atherosclerosis develops over the course of 50 years, beginning in the early teenage years. The causes of this process appear to be lipid retention, oxidation, and modification, which provoke chronic inflammation at susceptible sites in the walls of all major conduit arteries. Initial fatty streaks evolve into fibrous plaques, some of which develop into forms that are vulnerable to rupture, causing thrombosis or stenosis. Erosion of the surfaces of some plaques and rupture of a plaque’s calcific nodule into the artery lumen also may trigger thrombosis. The process of plaque development is the same regardless of race/ethnicity, sex, or geographic location, apparently worldwide. However, the rate of development is faster in patients with risk factors such as hypertension, tobacco smoking, diabetes mellitus, obesity, and genetic predisposition.  At,%20Plaque%20development%20and%20plaque%20responses%20to%20medical%20treatment%20(Insull,%20Am%20J%20Med).pdf


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Disclaimer:  The information, facts, and opinions provided here is not a substitute for professional advice.  It only indicates what JK believes, does, or would do.  Always consult your primary care physician for medical advice, diagnosis, and treatment.