Statins a 3 Page Critical Review 12/23/15 http://healthfully.org/rc/id6.html It is essential for you to understand how pharma (pharmaceutical industry) distorts, and controls medical information, and guidelines, thus the practice of medicine--see Market Science and Misinformation side effects. Marketing pitch for the statins is based on high Total Cholesterol (TC) and LDL causing heart attacks, strokes and, CardioVascular Disease (CVD); but CVD is caused by bacterial and viruses within the artery wall (tunica media) and the immune system’s response, thus lowering cholesterol doesn’t work--see Cholesterol Myth. LDL has 2 functions, one is to as needed actively transport to cells cholesterol and triglycerides (fat), the other is its immune-system function: it neutralizes (binds) toxins produced by pathogens—see. LDL in the artery walls is a sign of pathogens causing inflammation. Thus the presences of LDL, cholesterol, and triglycerides in the plaque of artery walls is because of LDL’s immune function. LDL is like a fireman at a fire, a response. Lowering LDL promotes damage by toxins. Yes statins lower LDL and cholesterol, but that doesn’t benefit the patient. The doggy clinical trials ran by pharma for marketing purposes fail to show significant reduction in deaths, so pharma markets statins based on lowering cholesterol and rigs the clinical guidelines. Marketing and influence trumps medical science. The best-selling drug of all times is atorvastatin, marketed as Lipitor by Pfizer (US sales $12.4 billion in 2008, and world-wide total sales of $131 billion by 2007). With 50% of the men and 36% of the women age 65 to 74 taking statins (CDC/NCHS, Health, US, 2010); their human costs is incredible; made worse because better alternatives are shown harmful by pharma’s tobacco science. The cholesterol myth and effective prevention get little space in the corp. media.—watch YouTube documentaries. Statins discovery and approval casts doubts. In the early 1970s an extract from a fungus was shown reduce serum cholesterol, but the Japanese research stopped because of animal toxicity & cancer. Using a similar extract Merck in 1978 developed Mevacor (lavostatin). This “’Statin produced significant toxicity at high doses in a variety of animal species” (ibid 520). Animal studies showed it caused cancer (given the 20-year latency in humans, still a grave concern). Merck tested low-dose Mevacor for homozygous familial hypercholesterolemia. The FDA gave approval for this rare condition. Once approved--as is the norm--the population base was expanded based on “marketing science”. Because statins lower TC 30%, they were pushed as the only effective treatment for CVD. But weak epidemiological association of elevated TC with CVD doesn’t demonstrate cause. With in-house studies Merck and the manufacturers of the 9 me-too statins sold the world on “safe-and-effective”. In Braunwald, Heart Disease, 8th Ed. P 2286: “safe, effective, and well-tolerated pharmacologic agents that have greatly expanded the therapeutic armamentarium available to the physician to treat disorders of lipid metabolism.” But in Braunwald, p 1085 table, 3 of 4 listed studies didn’t support effective. Merck’s JUPITER Study, 2008, is used to push primary prevention, but has major internal inconsistency: the cooked results “do not support primary prevent of CVD”. Moreover, “statin therapy and top athletics seem to be almost incompatible,”73% dropped out. Statins don’t extend life and their side effects are grossly under-reported. Because statins don’t treat the causes of CVD, they are ineffective; thus there is a chorus of marginalized critics. 19 NEGATIVE EFFECTS: One, ED, it lowers testosterone , and nitrous oxide thus causes ED; a similar effect upon women for the steroids are synthesized from cholesterol. Two, COX-2 inhibitor, just like Vioxx, which increased heart attacks (MIs) over 300% . The American Heart Association warns: “accumulated evidence that non-steroidal, anti-inflammatory drugs [COX inhibitors], with the exception of aspirin, increase risk for heart attack and stroke”--promote atherogenesis. Three, blocks production of Q10, which enters LDL and inhibits oxidative damage that causes atherogenesis, and. Four, Plaque instability: “Vulnerability of plaques to rup¬ture and thrombosis is of greater clinical relevance than the degree of stenosis they cause” (Corti et al., 2003). “Statins affect plaque stability in a variety of ways. The meta-loproteinases degrade extra-cellular matrix components and thus “weaken the fibrous cap and destabilize the lesions” -- Goodman and Gilman pharmacology, 11th Ed, p 950. Rupture of plaque causes over 80% of MIs. Statins inhibit secretion MMP-1, 3, & 9 from SMC, and microphages make plaque less stable. Five, reduction in ATP: Q10 is needed for the conversion of APD to ATP (adenosine-5-triphosphate), the source of energy for muscles contraction. “ATP is often called the ‘molecular unit of currency’ of intracellular energy transfer including muscle contraction and for chemical reactions. ATP transports chemical energy within cells for metabolism”--Wikipedia. A reduction of 40% in CoQ10 is accepted. Six, The heart muscle under stress needs more ATP, not less. This is why pharma excludes the elderly and those with coronary heart failure (CHF) from trials. Thus, “the mean age of ME/CFS patients dying from CHF are 2.5 years younger than the control group.” CHF death rate has tripled since 1989. In a review of statins on depletion of Q10 concludes: “As the potency of statin drugs increases and as the target LDL cholesterol level decreases, the severity of Q10 depletion increases and heart-muscle function declines. This tragic scenario may very well be prevented by using supplemental Q10 with all HMG CoA reductase inhibitors [statins]” and, and. Thus “Lower cholesterol, poorer outcome in CHF patients.” Pharma ignores Q10 side effect. Seven, All Statins inhibit the rate controlling enzyme HMGCR of the mevalonate pathway. “This pathway generates a range of other products in addition to cholesterol, including coenzyme Q10, heme-A, [dolichol], the production of dimethylallyl prophosphate (DMAP), & isopentenyl pyrophosphate (IPP), which serve as the basis for the biosynthesis of molecules used in processes as diverse as terpenoid synthesis, protein prenylation and isoprenylated proteins which have pivotal roles in cell biology and human physiology and potential relevance to benefits as well as risks of statins. Drugs, such as the statins, stop the production of mevalonate by inhibiting HMG-CoA reductase” Wiki. “The Mevalonate pathway is important for, cell membrane maintenance, hormones, protein anchoring, and N-glycosylation. It is also a part of steroid biosynthesis” Wiki. “Dolichols are isoprenoids synthesized from mevalonate. They are vital to the process of Glycoprotein formation in the endoplasmic reticulum of cells. In this capacity it is critical to the formation of the Glycoproteins involved in neuro-peptides, cell identification, cell messaging and Immune defense. Reduced bioavailability of dolichols can affect every cellular process in the body” Wiki. And this is only a partial list. Eight, Cholesterol is essential for life. “It is the precursor for the biosynthesis of steroid hormones, bile acids, vitamin D, and is an essential component of cell membranes for proper permeability. Effects include pancreatic and hepatic dysfunction, ED, diabetes , muscle weakness and myopathy (muscle disease). The myelin is a cholesterol base coating around nerve cells ” (Wiki). Nine, Cognitive, the reduction Q10 & cholesterol for the myelin sheath causes cognitive decline--especially in the elderly where it often leads to an incorrect diagnosis of Alzheimer’s disease and of neuropathy. Ten, Causes Parkinson’s and Alzheimer’s diseases. These conditions are associated with low level of cholesterol—at Uffe p 56. Eleven Causes cancer a confirmation of earlier animal studies—summary of cancers, and. Twelve Stimulates atherosclerosis and heart disease by blocking the vital CoQ10, heme A, vitamin K2 (the cofactor for matrix Gla-protein activation) and biosynthesis of selenium containing proteins, one of which is vital glutathione peroxidase—at 2015. This article states that “statins stimulate atherosclerosis and heart failure”, and then provides the mechanisms. Thirteen Causes Interstitial lung disease is similar to emphysema in that it is a progressive condition that affects alveolar epithelium and other tissues. Of FDA reported side effects, it is 1/40th. Fourteen, Causes cancer in animal studies, and thus in humans, at. Fifteen, Polyneuropathy, damage affecting peripheral nerves, features weakness, numbness, pain, etc. is 26 times more common after 2 years on statins compared to general matched population—at. Sixteen Side effects account for the poor compliance in the elderly (75% stop within 2 years). Poor compliance also occurs with elite athletes (see 1st pg). Seventeen treats the wrong cause, cholesterol doesn’t cause ischemic events or atherosclerosis but rather infective agents (and) living in the tunica intima; thus statins are ineffective. Three out of 4 major studies of secondary prevention (ALL-HAT, ASCOT, & PROSPER) failed to find life extension from statins (Table 42-78, Braunwald’s Supra, p 1085). This table stands in opposition to the “safe & effective” claim (p 2286), which is pharma’s mantra, a mantra supported by their marketing studies and guidelines. Junk science is the norm (p 3) on TNT trial. Eighteen, Primary prevention of high risk no benefit huge meta-study found, in JAMA. Nineteen, drug interaction with serious side effects are common, considering that over half of senior in their 6th decade have taken statins, and seniors average age 72 average 6 drugs according to a hospital emergency admission study (polypharmacy). THREE POSITIVE EFFECTS: 1) Anti-inflammatory effect: but because of effect upon prostaglandins statins like the NSAIDs doesn’t inhibit atherogenesis inflammatory process—see Vioxx, and. 2) Statin reduces the risk for thrombosis by affecting clotting, just like aspirin. But rather than promote the sales of over-the-counter NSAID, pharma pitches lower TC. 3) For the rare familial hyperlipidemia extends life modestly at best—Prof. Ravnskov, Ignore the Awkward, chap. 3. On statins: Since “cholesterol synthesis occurs mostly at night” (Wiki), TC should be treated at night with short half-life & low dose: Zocor 2 hr. Mevacor 1.4 hr. Pravachol 1.75 hr. and niacin 35 min--avoid Lipitor 14 hr., Crestor 19 hr. Sorting it out, RECOMMENDATIONS: Atherogenesis is caused pathogens within the artery walls. This initiates an inflammatory immune response by macrophages. LDL which has an immune response is actively transported into the artery walls where it contents cholesterol from part of the resultant plaque. Because of this transport process, lowering LDL doesn’t affect the formation of plaque, thus statins don’t stop plaque formation or remove it from within artery walls (see illustration). The 32% drop in deaths from heart attacks and strokes (1960 to 1992) occurred prior to statins. With statins’ wide use, mortality rate has remained constant. Mevacor was approved in 1987 with only 60,000 taking it by 1990. Reduced death rate was from less cigarettes and better treatment. Statins reduce quality of life for the elderly: a large Canadian study had 75% dropout by 2 years, and 80% in a NJ study. Very common and under reported side effects are: fatigue, muscle weakness & cramps, mental confusion, pancreatic and liver dysfunction, diabetes, indigestion, cognitive decline, ED, & lower libido, especially for the elderly. Lowering TC with statins doesn’t affect the young unstable plaque that cause 85% MIs because pathogens are the cause of the plaque formation. . What to do: Don’t take a statin because they do not reduce mortality; they aren’t worth their side effects & expense. Lifestyle changes of low carbohydrate-sugar diet lowers damage to endothelial cells on the artery walls. Damage is caused mainly by glycation by fructose (7.5 times the rate of glucose). Avoid carbon monoxide (cigarettes main source) which exacerbates the damage. Endothelial cells block the migration of pathogens. Saturated and monounsaturated fats are the best source of energy. Everyone should take the antioxidants ascorbic acid and Q10, prevent oxidative damage. Take 325 mg aspirin with meals for its anti-inflammatory effect that prevents CVD; and aspirin prevents blood clots thus lowering ischemic events, etc5. Low dose aspirin is ineffective because of tolerance after 1 year. Take the natural estrogen (estradiol) & progesterone at menopause. Estrogen lowers risk of CVD 50%, osteoporosis and much more. For elderly men testosterone lowers risk & increases survival from an MI. Pharma attacks hormones & aspirin because they work. Read Marking Science, be skeptical of medical “wisdom.” If you still want to lower TC then take 250 mg slow release niacin or inositol hexanicotinate at night, when it is effective. Insulin produced following meals blocks the lipid lowering effect of niacin inositol & statins. High dose during the day is a pharma ploy to reduce the use of niacin. JK has exercised vigorously since 1975; 325 mg twice daily aspirin since 1992; testosterone high dose 2003; low-sugar low carb diet 2014, 300 mg CoQ10 2012, and vitamin C 1000 mg (as calcium ascorbate) 2014. Results: JK is in 7th decade, excellent muscle tone and strength, no joint pain, blood pressure averages 125/75, BMI 23, and total cholesterol 165. Pharma has turned hypertension, and cholesterol into medical conditions, and watch documentaries on YouTube.