Naturalistic Treatments (positive)
CHOLESTEROL fighters NIACIN & INOSITOL
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Aspirin--prevents cancer and heart attacks, etc.
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Natural Estrogen--far better than your doctor has been taught
CHOLESTEROL fighters NIACIN & INOSITOL
CoQ10--clearly the best anti-oxidant
Meta-analysis of niacin on cardiovascular events
Studies suggest that niacin is better than statins

Below is a study of about 200 hours including to 2 trips to the UCSD medical college library.  This is part of a very skeptical look at the use of statins, and thus a look at alternative treatments.  Read carefully if you are taking a statin or have concerns about your blood vessels.   
 

 Niacin family and Natural Cholesterol Profile Lowering -- (7/13/13) 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, their trade organization) controls the research, its publication, the continuing education of doctors, 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 influence upon the beliefs of physicians.  Based on over 300 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—depending on the degree of marketing manipulation of these studies (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; for Statins a Critical Review which explains why though they dramatically improve CP, they fail to improve endpoints (there are 6 negative reasons).  The reliance on statins is based on marketing science; its usage has become an article of faith.  This paper is about niacin & other alternatives; they improve the endpoints.

 

Niacin (Nicotinic Acid, NA, vitamin B3):   In 1955 it was discovered that niacin has a lipid lowering property, and thus improved the cholesterol profile (CP).  It is the first treatment and remained the first choice for hyperlipidemia for the next 3 decades because it very effectively improved CP, including dramatically raising HDL 33% and lowered the rate of heart attacks. Long before the first statin PhARMA mounted a campaign against niacin to promote their patented alternatives.  Currently niacin family accounts for 3% of the CP-treatment market, and less in Europe.    

One way that PhARMA marginalized niacin was by setting up a treatment protocol that has very low compliance.   In their recommended medicinal dose (1500-3000 mg) to improve CP, niacin causes vascular dilation in skin which produces a very uncomfortable flushing.  To limit this, PhARMA recommends starting at a low dose, and gradually increase it over 8 weeks—only marginally effective.  Few will follow this program long-term.  With extended release niacin, the frequency of flushing is only modestly reduced--in the once patented Niaspan (75%, 88%).  Though liver toxicity is rare, reversible, and causes a visible jaundice, physicians recommend regular blood work (another way of discouraging the use of niacin & Niaspan).  Moreover doctors believe that statins are far more effective, thus most patients are persuaded. 1) Does the evidence support the protocol?  2) How effective is niacin?

Niacin improves CP by lowering of plasma triglycerides 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 1 & INH at 8 hours.  PhARMA thus recommends mega dose of niacin (ignores INH) to create very low compliance due flushing, and during the day for minimal effectiveness.                                          

 

“The Coronary Drug Project [only published long-term endpoint niacin study] was conducted between 1966 and 1975 to assess the long-term efficacy and safety of five lipid influencing drugs in 8,341 men with electrocardiogram-documented previous myocardial infraction…. With a mean follow-up of 15 years, 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 group.”   “Niacin has been shown to produce regression of atherosclerosis plaques and is the only drug that has demonstrated reduction of overall mortality in currently completed clinical trials [2-4]… 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,”  September 1991, American Journal of Medicine V. 91, 239.  “Other effects include anti-thrombotic and vascular inflammation, improving endothelial function and plaque stability;” also noted.  These later effects are more important than its improvement in CP for reduction in risks.  Results for niacin are comparable to low dose statins for CP, but without the serious side effects, and superior endpoint results. 

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.   PhARMA seeks to maximize profits.   

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.  But it is effective in the treatment of acne and some cancers.  

Inositol hexanicotinate (IHN):  The literature is thin, since PhARMA members won’t research a flush-free, effective treatment for CP.  Though IHN releases niacin, it does at too low a rate to affect the same bio-pathway as niacin (peak for Niacin is 45 minutes, IHN 8 hours).  (A criticism by PhARMA, shown false in a quality study 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 CoQ10, 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.  For example it has been known for at least 70 years that alcoholics (not just winos) have lower incidents of atherosclerosis.  Estrogen levels (and presumable testosterone) which are higher with alcohol.  It could be a factor, since those in the highest quintile of these hormones have the lowest incidence of cardiovascular disease. 

Hormone replacement therapy (HRT) testosterone and especially estradiol are cardiovascular protective.  Once eliminating PhARMA’s marketing science, the evidence in support of HRT is overwhelmingly positive.

Aspirin: a 325 mg for not just preventing heart attacks but also cancer, cancer survival, Alzheimer’s disease, etc.

Fish oil (omega-3 fatty acids):  recommended dose by American Heart association 1 gm per day based on thin science. 

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). 

RECOMMENDATION:  For those with CVD or cholesterol above 300 below who are below 75 years: IHN 200-500 mgs before retiring is the sensible intervention because of its reasonable price, lack of side effects, and its effect upon free fatty acids.  A second choice would be niacin (instant release), also 200-500 mgs.  Both could be taken.  For cholesterol level under 300, the benefits are minor unless other risk factors are present for CVD.  To counter niacin’s effect upon ATP production, 300 mgs of CoQ10 should also be taken.  The research behind CoQ10 supports everyone taking it because it is an effective anti-oxidant in the in LDL thus reducing atherogenesis and protects the mitochondria.  Given Q10’s safety and those two benefits, I would give it to children (atherogenesis is present in all children).  The decline of endurance with age is a result of life-long oxidative damage to the mitochondria.  Nutritional yeast, a source of niacin, lowers CP.   Sorry, but definitive research has not been conducted.  Read Marking Science, and be skeptical of medical “wisdom”.   JK has since 1991 taken 325 mgs aspirin, testosterone since 2003, daily exercise since 1974, and 7 gm daily of nutritional yeast sprinkled on foods since 1981—his CP is 165 and blood pressure 125 over 75. 

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 ftp://82.239.144.183/bibli/-%20Revue%20Articles%20FB/Biblio%20090410/110.0901-Pathology%20of%20AthS,%20Plaque%20development%20and%20plaque%20responses%20to%20medical%20treatment%20(Insull,%20Am%20J%20Med).pdf

 

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