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Part 2: CVD Myths: Fats, sugars, cholesterol, and Statins id2.html

Part 1:  CVD Myths:  Fats, Sugars Cholesterol, and Statins  8/3/14 

The differences between fats and cholesterol:  For saturated fats to cause CVD they must pay a role causal role in oxidation of LDL or the inflammation response, but they don’t.  The same is true of cholesterol; both are bystanders found in plaque along with calcium, cell debris, muscle cells, fibrous connective tissue, and macrophage.  Moreover, diet has only a modest effect upon their serum levels (the complex role of diet in CVD is developed in Part 3 & Part 4.   A number of population studies confirm this.[1]  Guidelines on diets recommend low fat and low cholesterol.  Part 3 will show why low-fat diet promotes CVD.  Fats fit in with pharma’s “bad cholesterol” model, but cholesterol is a sterol (a modified steroid) not a fat—not structurally similar, nor converts to fats.  For cholesterol “Synthesis within the body starts with one molecule of acetyl CoA and one molecule of acetoacetyl-CoA, which are hydrated to form 3-hydroxy-3-methylglutaryl CoA (HMG-CoA)” Wiki.   “Fats are  triglycerides:   triesters of glycerol and any of several fatty acids,  Although the words "oils", "fats", and "lipids" are all used to refer to fats, technically “fat” is a subset of lipidWiki.  Triglycerides are three fatty acids bonded at each COOH (organic acid group) to each of OH (alcohol) group on glycerol with the loss of H2O— in below stick structure of a triglyceride, the red, blue, & green are fatty acids, and black is the glycerol to which they are bonded.  The black quite different structure below is cholesterol.


[1] The Women’s Health Initiative (WHI) diet wing, a major NIH study found no benefit for the low fat cohort, though the intervention was designed to reduce total fat intake to 20% of calories, and at year 6 resulted in “Low-density lipoprotein cholesterol levels, diastolic blood pressure, and factor VIIc levels were significantly reduced by 3.55 mg/dL, 0.31 mm Hg, and 4.29%, respectively…. Over a mean of 8.1 years, a dietary intervention that reduced total fat intake and increased intakes of vegetables, fruits, and grains did not significantly reduce the risk of CHD, stroke, or CVD in postmenopausal women and achieved only modest effects on CVD risk factors, suggesting that more focused diet and lifestyle interventions may be needed to improve risk factors and reduce CVD risk.”  Note bull shit finder:  the modest effect on CVD was 2% (CVD (HR, 0.98; 95% CI, 0.92-1.05”), clearly insignificant.   BS in the conclusion section is common in Pharma influenced studies.  Thought leaders use the conclusion to support their points, and doctors seldom read the article, but rather the conclusion.  That JAMA, Journal of the American Medical Association, allows this distortion is one more proof of who runs the show.

 

  

 

Cholesterol molecule (above)

 



AS         Atherosclerosis

 

N6         Omega 6 fatty acids   

CVD      Cardiovascular disease

 

MeS      Metabolic syndrome[1]

IR          Insulin resistance

 

NALFD  Non-alcoholic fatty liver disease

KOL      Key opinion leader

 

T2D       Type 2 Diabetes

N3       Omega 3 fatty acids   

 

TC          Total Cholesterol


 


Dietary cholesterol does not cause CVD:  Most dietary cholesterol is esterified, and esterified cholesterol is poorly absorbed. Moreover nearly all of the cholesterol is synthesized in the body.[2]  “The body also compensates for any absorption of additional cholesterol by reducing cholesterol synthesis[9]  Cholesterol synthesis can also be turned off when cholesterol levels are high. HMG-CoA reductase [what statins block] contains both a cytosolic domain (responsible for its catalytic function) and a membrane domain.” Wiki.  Thus dietary cholesterol does not affect blood cholesterol level.  Production is regulated through a homeostatic mechanism involving the SREBP protein which is activated when the cholesterol level is low and turned off when high.   “SREBP pathway regulates expression of many genes that control lipid formation and metabolism and body fuel allocation” Wiki.   Despite the common belief that high cholesterol is a significant risk factor for coronary artery disease, several independent population studies in healthy adults have shown that low total cholesterol is associated with cardiovascular and non-cardiac mortality, indicating that high total cholesterol is not a risk factor in a healthy populationBMJ 10//22/13.   Pharma misses the causes (prevention is not in their business plan) and treats high TC with statins, and other drugs for the consequences of metabolic syndrome.  The official push for low saturated fats & low cholesterol diet is based on a wrong assumption, an assumption that promotes consumption of sugar, starches, and unhealthy fats, whose main source are processed (manufactured) foods (see part 3 and Part 4).  Follow the dollars. 


 


Natural dietary fat does not cause high TC or CVD:  “According to the [started in the 50s] Farmingham Heart Study, people who consumed the most cholesterol in their diet did not have any higher blood cholesterol levels than those who consumed the least amount…. For most people—though not all—the effect of dietary cholesterol on serum cholesterol is insignificant” (Bowden & Sinatra 31).[3]  So why are the high fat & high cholesterol diets touted as a major risk factor for CVD?  One reason is that plaque (atheroma) in part contains cholesterol and looks like fat.[4]  Another reason is that in the 65 to 70 age group 72% of those who have a MI have elevated cholesterol; but by the age of 65, 70% of men & 39% of women have elevated cholesterol.  Moreover most of those with elevated cholesterol have other important risk factor such as HT, AS, and high sucrose diet.   Another reason is in the 1950s rabbits fed a cholesterol-rich diet developed AS.  But these results were not repeated in animals such as rats and baboon that are not herbivores.  Prof. Ancel Keys’ notice low rate of CVD in Mediterranean countries and did a study of their diet.  In his Seven-Country Study (1951) he concluded that high TC caused CVD.  The results received wide press & used to support the new dietary recommendation of lowering fats from 42% of calories to less than 30%.  Based on his study, Keys promoted the Mediterranean diet. “Critics pointed out that Keys had data for 22 countries, but selected data from just 6. (As an example, Keys excluded France, a country with a high fat diet and low rates of heart disease.)  Keys cheated;” at Diet Heart Publishing.  However, years later Keys reversed his position and stated in 1997:  “There’s no connection whatsoever between cholesterol in food and cholesterol in blood.  And we’ve known that all along.  Cholesterol in the diet doesn’t matter at all unless you happen to be a chicken or a rabbit” Bower supra 33.  This was confirmed in the diet component of the Women’s Health Initiative (WHI) diet section, fats:  there was no significant reduction in the risk of coronary heart disease, stroke, or cardiovascular disease,” Wiki.  Following the pattern of marketing studies, researchers were selected to run clinical trials that had proved their usefulness to pharma in the past.   And the panel for clinical guidelines “were selected to include experts who would predictable say that … all level of blood cholesterol in the United States are too high and should be lowered” Bowden 41 quoting Dr. Michael Oliver on the new guidelines of the National Institute of Health Consensus Development Conference Statement, December 10-12, 1984.  This guidelines state:  “The evidence justifies… the reduction of calories from fat… to 30 percent, calories from saturated fat to 10 percent or less, and dietary cholesterol to no more than 250 or 300 mg daily.”  But in Lipids 2010 in a thorough review article on dietary intervention: “Diets [weight loss] appear to have beneficial lipoprotein effects in individuals with atherogenic dyslipidemia, compared to high-carbohydrate diets; whereas the content of total fat or saturated fat in the diet appears to have little effect…. Over the years, data revealed that dietary saturated fatty acids (SFAs) are not associated with CAD and other adverse health effects.” A meta-analysis of 21 studies considered the effects of saturated fat intake and found that intake of saturated fat was not associated with an increased risk of CHD (coronary heart disease), stroke, or CVD (cardiovascular disease)” Wiki. Low-fat, low-cholesterol (thus high carbs) is not heart healthy but unhealthy because of fructose, starches, and unnatural fats-see Part 3 & 4).




[1] Pharma has added hypertension and high cholesterol-triglycerides.  This is more of pharma’s marketing, and is irrelevant as explained in Cholesterol Myth and its sequel.  Hypertension is a sign of atherosclerosis; it can only be healed by body and diet. 

[2]   About 20–25% of total daily cholesterol production occurs in the liver; other sites of higher synthesis rates include the intestines, adrenal glands, and reproductive organs Wiki.  Studies done to show a relationship between dietary cholesterol and AS use rabbits, a vegetarian, and thus are flawed by design.   For exampleIn contrast with the rabbit, man responds with only minimal changes of serum cholesterol concentration to changes of the cholesterol content of the diet.”

[3] Jonny Bowden PhD  & Stephen  Sinatra, MD, The Great Cholesterol Myth:  Why Lowering Your Cholesterol Won’t Prevent Heart Disease—and the Statin-Free Plan That Will, Fair Winds Press, Nov.  2012; a national bestseller, has 23 experts who praised the book and are quoted on the cover & first page, and at Amazon has a 4.8 star rating from 220 reviewers.   Getting a fair review of book is iffy because of heated nature of the topic and many the subscribers to pharma’s spin.  JK finds the book well supported in the critical portions on cholesterol’s role; but in spots questionable as to the alternative approaches to prevention of CVD.  A couple of years before reading this book, JK had arrived at those same conclusion as to risk of CVD and on some of their fixes. 

[4]  Atheroma is an accumulation and swelling in artery walls made up of (mostly) macrophage cells, or debris, and containing  lipids  (cholesterol and fatty acids), calcium and a variable amount of fibrous connective tissue… in the early stage an accumulation of mostly macrophages, that have taken up oxidized LKLWiki.



Natural dietary fat does not cause high TC or CVD:  “According to the [started in the 50s] Farmingham Heart Study, people who consumed the most cholesterol in their diet did not have any higher blood cholesterol levels than those who consumed the least amount…. For most people—though not all—the effect of dietary cholesterol on serum cholesterol is insignificant” (Bowden & Sinatra 31).[1]  So why are the high fat & high cholesterol diets touted as a major risk factor for CVD?  One reason is that plaque (atheroma) in part contains cholesterol and looks like fat.[2]  Another reason is that in the 65 to 70 age group 72% of those who have a MI have elevated cholesterol; but by the age of 65, 70% of men & 39% of women have elevated cholesterol.  Moreover most of those with elevated cholesterol have other important risk factor such as HT, AS, and high sucrose diet.   Another reason is in the 1950s rabbits fed a cholesterol-rich diet developed AS.  But these results were not repeated in animals such as rats and baboon that are not herbivores.  Prof. Ancel Keys’ notice low rate of CVD in Mediterranean countries and did a study of their diet.  In his Seven-Country Study (1951) he concluded that high TC caused CVD.  The results received wide press & used to support the new dietary recommendation of lowering fats from 42% of calories to less than 30%.  Based on his study, Keys promoted the Mediterranean diet. “Critics pointed out that Keys had data for 22 countries, but selected data from just 6. (As an example, Keys excluded France, a country with a high fat diet and low rates of heart disease.)  Keys cheated;” at Diet Heart Publishing.  However, years later Keys reversed his position and stated in 1997:  “There’s no connection whatsoever between cholesterol in food and cholesterol in blood.  And we’ve known that all along.  Cholesterol in the diet doesn’t matter at all unless you happen to be a chicken or a rabbit” Bower supra 33.  This was confirmed in the diet component of the Women’s Health Initiative (WHI) diet section, fats:  there was no significant reduction in the risk of coronary heart disease, stroke, or cardiovascular disease,” Wiki.  Following the pattern of marketing studies, researchers were selected to run clinical trials that had proved their usefulness to pharma in the past.   And the panel for clinical guidelines “were selected to include experts who would predictable say that … all level of blood cholesterol in the United States are too high and should be lowered” Bowden 41 quoting Dr. Michael Oliver on the new guidelines of the National Institute of Health Consensus Development Conference Statement, December 10-12, 1984.  This guidelines state:  “The evidence justifies… the reduction of calories from fat… to 30 percent, calories from saturated fat to 10 percent or less, and dietary cholesterol to no more than 250 or 300 mg daily.”  But in Lipids 2010 in a thorough review article on dietary intervention: “Diets [weight loss] appear to have beneficial lipoprotein effects in individuals with atherogenic dyslipidemia, compared to high-carbohydrate diets; whereas the content of total fat or saturated fat in the diet appears to have little effect…. Over the years, data revealed that dietary saturated fatty acids (SFAs) are not associated with CAD and other adverse health effects.” A meta-analysis of 21 studies considered the effects of saturated fat intake and found that intake of saturated fat was not associated with an increased risk of CHD (coronary heart disease), stroke, or CVD (cardiovascular disease)” Wiki. Low-fat, low-cholesterol (thus high carbs) is not heart healthy but unhealthy because of fructose, starches, and unnatural fats-see Part 3 & 4).

 

Unnatural and transfats are a risk factor for CVD: again we have an example of money trumping science.  Cheap fats mean high profits, and unsaturated fats are cheap.  Fields of corn, canola, and soybean yield vegetable oil and the waste product is sold as animal feed.  The problems arise in that these oils are high in polyunsaturated fats.  The unsaturated refers to a double bond on the carbon chain of the fat.  This double bond is the long energy point for which reactive chemical bond thereto.  Fructose and glucose in a reaction called glycation are common reactants. The product of this reaction results in a modification of the shape of the unsaturated fat which inhibit its metabolism, and thus proper utilization.  Like transfats, these modified fat molecules contribute to CVD, and other health problems.    For a discussion of rancidification read appropriate section in Part 4.  Again basic research lies dormant because of broken information system. 

 

High levels of cholesterol, LDL, and natural fats[3] do not cause AS, “Though few doctors know this, 20 studies have shown that elderly people with a high cholesterol level in their blood live longer than those with a low level” Donald Miller professor of surgery, lecture.  Thought cholesterol and fats are found in LDL--being present doesn’t entail causing.  Because LDL particles appear harmless until they are within the blood vessel walls and oxidized by free radicals it is postulated that ingesting antioxidants and minimizing free radical exposure may reduce LDL's contribution to atherosclerosis” Wiki.  This again is a partial truth, one uncovered by reading research nearly a century old on CVD and by reading the literature on the role of pathogens living in the artery walls.  Most of the damage to LDL found in the artery walls comes from its function as a receptor for toxic chemical produced by pathogens.  The role of pathogens in the artery walls and the immune function of LDL are demonstrated in the journal literature.  Thus the presence of LDL within the muscular portion of the artery walls and there active transport there are explained by their role in the immune system, and the oxidative damage referred to above and promoted by pharma as causal, is in fact mainly a result of toxins produced by pathogens.  It also explains why atherosclerosis is considered the results of an inflammatory process.  For a review of this evidence go to and also articles.   Pharma should be developing treatments to prevent atherosclerosis, but instead for reasons stated in Part 1, they lower cholesterol.  Cholesterol is manufactured in a 19 step process from acetyl-CoA  and acetoacetyl-CoA in the malev, neither of which resemble fatty acids in structure.  Cholesterol, LDL, and natural triglycerides are bystanders because in the degradation of oxidized LDL which houses them, they are released by the foam cells (swollen macrophages).   Pharma follows its pattern of selling the disease (high LDL, high TC and triglycerides), they then selling the treatments.  Thus the reasonable conclusion is that lowering TC and LDL won’t reduce CVD, and because of the essential functions of cholesterol, lowering it will have many and varied side effects.    The 800 pound gorilla sits upon the side effect, than utters “safe and effective.”  

Cholesterol lipoprotein basics:  looking at the many roles of cholesterol (below), clearly dramatically lowering its level below the norm will have major side effects.   Cholesterol is essential for health, so too is its transport system that takes cholesterol produced in the liver to cells throughout the body for vital functions.  Since cholesterol isn’t blood/water soluble, it is rapped in low density lipoproteins for transport, to cells, and returns to the liver when in excess as HDL.  ”About 15% of blood cholesterol comes from the diet; the other 85% is made from acetyl CoA by the liver and to a lesser extent by other body cells.[4]  Cholesterol is so essential that nearly every cell in the body can make cholesterol.  Lipoproteins vary considerable in their relative fat-protein compositions, but they all contain triglycerides, phospholipids, and cholesterol in addition to protein.  In general, the higher the percentage of lipid (fats) in the lipoprotein, the lower its density; and the greater the proportion of protein, the higher its density” Marieb, p 856-7. On the basis of centrifugal separation there are HDL, LDL, and VDL.[5]   VLD, LDL, and HDL are produced in the liver. VLD contain excess triacylglycerol and cholesterol that are not required by the liver for synthesis of bile acids.  LDL is the major blood carrier of cholesterol (approximately 1,500 molecules, 20% by weight).  LDL receptors on cells transported into cells where a vesicle then forms in which the cholesterol is hydrolyzed to form cholesterol esters.  Now within the cell, the cholesterol can be used for membrane biosynthesis or stored in its esterified form.  HDL functions to transport cholesterol back to the liver for subsequent transport or biosynthesis. Note it is the LDL rapping that is subjected to glycation and oxidation, not the cholesterol that causes the formation of plaque—thus cholesterol is a bystander in the process.  Because nature does nothing in vain, the lowering LDL and cholesterol is a bad idea. 

Principle functions of cholesterol:

Converted to bile in the liver and stored in the gallbladder.  The bile dissolves fats in the digestive track for intestinal absorption along with vitamins A, D, E, and K.  Up to 1 gm of cholesterol is used in this process. 

Absorption from the intestinal track of fats

Absorption from the intestinal track of vitamins A, D, E, and K

Precursor molecule in the synthesis of vitamin D

Precursor molecule in the synthesis of androgen steroids including the hormones testosterone, estradiol, progesterone

Precursor molecule in the synthesis of adrenal gland hormone cortisol and aldosterone:

Cortisol (hydrocortisone) produced by the adrenal gland is the main glucocorticoid under normal conditions and its actions include mobilization of fats, proteins, and carbohydrates and enhances the activity of other hormones including glucagone, catecholamines, activates anti-stress and anti-inflammatory pathways, plays an important role in the conversion of glycogen to glucose. During human pregnancy plays important roles in fetal development.  Cortisol reduces bone formation, calcium absorption in the intestines, and transports potassium out of cells and the exchange for sodium ions.  Cortisol counter acts insulin, raises free amino acids in the serum, acts as antidiuretic hormone, stimulates many copper enzymes, affects reproductive system, stimulates hepatic detoxification.

Aldosterone effects are on the distal convoluted tubule and collecting duct of the kidney where it causes increased reabsorption of sodium and increased excretion of both potassium (by principal cells) and hydrogen ions (by intercalated cells of the collecting duct)--Wiki.

Myelin sheath usually around only the axon of a neuron. It is essential for the proper functioning of the nervous system. Cholesterol is an essential constituent of myelin.  Demyelination results in diverse symptoms determined by the functions of the affected neurons.  is the loss of the myelin sheath insulating the nerves, and is the hallmark of someneurodegenerative autoimmune diseases, including multiple sclerosis.  Dysmyelination has been implicated in a number of human diseases including schizophrenia.

 

Statins lower TC but don’t prevent MI. Statins lower TC about 30%, but have no significant effect on ischemic events.   This is the conclusion I drew from Braunwald textbook[6]  section on statin.  An article in Therapeutics letter came to the same conclusion doing a meta-analysis using some of the same major clinical trials:  This cardiovascular benefit is not reflected in 2 measures of overall health impact, total mortality and total serious adverse events.  Therefore, statins have not been shown to provide an overall health benefit in primary prevention trials.”  And repeated in JAMA in a meta-analysis of 11 studies that included the clearly cooked Jupiter and xTNT Studies[7].   Assuming for good reason there is major positive bias, which is the industry norm; the statins are significantly negative.  However, those in the top 5% risk group for MI slightly reduce their risk.  If they followed lifestyle changes, they would benefit much more than from a statin.  Statins have a significant negative effect upon quality of life, especially among those above the age of 65, and it is counter-indicated for those above 75 because of increased death due to decreased Q10 and ATP—yet still frequently prescribed.  Side effect fall into two groups those apparent to patients, and those on a cellular level.  Inhibition of the mevalonate pathway causes the varied side effects.  In my article on statins fourteen are listed:

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%[8].  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 rup­ture 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.[9]  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 reductaseWiki.  “The Mevalonate pathway is important for, cell membrane maintenance,  hormonesprotein anchoring, and N-glycosylation.  It is also a part of steroid biosynthesisWiki.  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 bodyWiki.  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 and fluidity.  Effects include pancreatic and hepatic dysfunction, ED, diabetes[10], muscle weakness and myopathy (muscle disease). The myelin is a cholesterol base coating around nerve cells[11] (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 peroxidaseat 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.  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). 

Statins have serious side effects most of which come on gradually and there are drug interactions; both are often assumed to be part of the illness.  There is no incentive or requirement for a physician to report a suspected side effect, which is sent to the manufacturer, who then sits on the information sent by the doctor.  Eventually the manufacturer makes comments on reported side effect and sends them in to the FDA, often denying that their statin was the cause.    Knowing this, seldom does a doctor consume his time to send a report of a suspected side effect.   And patients knowing the faith their doctor has in statins and the limited time for an office visit, he often doesn’t give the negative news about side effects.  Seldom does the FDA act upon side effects.  This system is broken!

 

The results for statins are dismal:  A meta-analysis of predominantly industry sponsored data reported that in a low risk group of people aged 60-70 years taking statins the number needed to treat (NNT) to prevent one cardiovascular event in one year was 345.In this group [patients who had suffered an MI] the NNT is 415 for mortality over one year.  This doesn’t mean that each patient benefits a little, but rather that 414 will receive no prognostic benefit [only side effects].”  And it gets worse, because pharma would have selected in their pool those not suffering from congestive heart failure, for they would have fared much worse on statins, which increase significantly the mortality rate from a heart attack.  And there are many other doggy ways in which their study is biased such as wash out period, giving the drug to a selection population not on other heart medications such as for hypertension,  and what other way will produce favorable results.  Moreover, those studies with negative results are not published.  So, why do doctors have faith in statins?  As stated in part 1, the 800 pound gorilla has replaced evidence based medicine with expert based medicine, and the gorilla owns the clinical trials and provides the thought leaders.  These thought leaders repeat the mantra “safe and effective” which is also repeated in cardiology textbooks and guidelines. Secondly the thought leaders teach that plaque formation is strongly correlated with the TC, LDL blood levels, and the 30% average reduction in TC is entails a corresponding reduction in ischemic events, which is confirmed by their marketing studies, which minimalizes side effects, of course.  All this is fed to physicians in continuing education classes given to promote drugs.  Peer-pressure, clinic administrators, and the need to follow guidelines market statins and promoting the cholesterol myth.  Corporations have taken over the health-care system.   

Why does the FDA allow this:  As stated on page 2, the FDA functions as an extension of pharma?  This failure to supervise in the public’s interest is not covered in corporate media; but it is published elsewhere.  See for example the article Consumer Report article FDA:  From Watchdog to Lapdog?  Prof Marcia Angell in her book The Truth About the Drug Companies, chapter 12, gives a detailed history of Congress passing pharma-friendly legislation and its affects upon the FDA.  Allowing off label prescribing of drugs opens the doors wide, which averages over 50% of sales.  Merck tested Mevacor (the first statin) on a very select population of those with familial hypercholesterolemia (FH, about 1 in 1,500).  They have a genetic defect which causes their cholesterol to be several times above the norm.[12]  The surrogate end point lowering TC was used for FDA approval.  Moreover, “there are no interventional studies that directly show mortality benefit of cholesterol lowering in familial hypercholesterolemia patients” Wiki,   That is why Merck for Mevicor’s used the surrogate endpoint lower TC.  Once approved, their marketing department went to work.  All this is permitted by a very dysfunctional FDA—see Consumer Report article.

 

New Guidelines for cholesterol:  the future will bring more of the same, ever-lowering standards for treatment guideline, dismal results, more me-too-drugs (patented knock-offs), and FDA approval.  Now pharma, based on AstraZeneca’s Jupiter Study, has lowered the guideline bar:   US recommendations for low density lipoprotein cholesterol concentrations could put most of the Western world's adult population on statins.  This is the message from the American National Cholesterol Education Program published last year.1  Recently, Getz et al calculated that in Norway, one of the healthiest nations in the world, about 85% of men and more than 20% of the women over age 40 would be classified as high risk using this criterion.”2  The BMJ article then listed the known side effects of statins, quite different than the safe sales mantra.  But our physicians won’t hear of side effects in pharma’s continuing education classes, nor will the public from our corporate media.  “The government’s obsession with levels of total cholesterol, which has led to the overmedication of hundreds of millions of people with statins, has diverted our attention from the more egregious risk factor of atherogenic dyslipidaemia” BMJ. However, pharma has made such a mess of the causal process for CVD that bystanders are accused of being causes, this is the case with dyslipidaemia.  High serum fat level (dyslipidaemia) is a result of a high sugar diet—see last section.  The Western diet is the cause of the rise in CVD and obesity.  It is a result of the high combination of high fructose and high glucose.    

 

New cholesterol drugs:  Several block-buster statins have gone off patent—Lipitor costs now a $1 a day.  Thus pharma has been working on new molecular entities to lower cholesterol.  Several of them are in in phase III trials (trials used for FDA approval).   New major class of drugs, instead of blocking synthesis, act upon the cholesterol regulatory mechanism.  Alirocumab is a human monoclonal antibody designed for the treatment of  hypercholesterolemia.  This therapeutic is also known by the codes REGN727 and SAR236553.  It was discovered by Regeneron Pharmaceuticals and is being co-developed by Regeneron and Sanofi Wiki. Another is  PCSK9 has medical significance because it acts in cholesterol  homeostasis.  Drugs that block PCSK9 can lower low-density lipoprotein cholesterol (LDL-C)” Wiki.PCSK­9 inhibitors, in late-stage testing at Pfizer, Amgen Inc, and a partnership of Sanofi SA and Regeneron Pharmaceuticals Inc. PCSK9 are antibodies designed to block a protein whose natural function is to maintain the presence of LDL in the bloodstream” Reuters. Another is “Juxtapid from Aegerion Pharmaceuticals'; and Kynamro from Sanofi and Isis Pharmaceuticals.  Aegerion's Juxtapid[13] has been the early standout despite an annual treatment price tag that is more than $119,000 higher than KynamroMotley Fool.  Given the size of this trial and duration (16,000 patients with CHD, lasting 3.7 years) and thus cost, pharma knew that the FDA would accept the surrogate endpoint of lower cholesterol.  Otherwise pharma would have had a trial of under a 1,000 patients and ran it short-term.  Obviously AstraZeneca expected a positive outcome, and phase III trial, for the raw data must be submitted to the FDA.  With the revolving door and those working for the FDA can moonlight for pharma, the only risk pharma faced was deadly side effects in great numbers. Having passed that hurdle, these new drugs failed to save lives in clinical trials.  So the FDA notified pharma that these drugs must only pass the surrogate endpoint of lowering cholesterol:  “everyone knows that better endpoints come from lowering cholesterol.”  “Members of an experimental class of cholesterol-lowering drugs could get U.S. regulatory approval based on their ability to lower "bad" cholesterol, and may not need to show that they reduce the risk of heart attack and stroke, the Food and Drug Administration said on Thursday. The statement eased industry concerns that the agency would require more onerous "outcome" studies before approving the drugs, known as PCSK9 inhibitors.” Reuters.  This is another example of tag-team drug oversight.  Only a fool would take a drug that lowers cholesterol but doesn’t prolong life and prevent heart attacks.  That person (or society) would be paying for a drug that only offers serious side effects.  And it gets worse, as pointed out prior, positive spin is the norm for journal publish articles generated from phase III trial.  A major study of neuroleptic drugs found that Positive bias averaged 32% (range 11 to 69%) in a total of 74 journal articles.  Yes, statins and these new molecular entities work, just read the tobacco science in the journals.  A series of articles are hitting the press and the studies they are based on are being taught by pharma’s KOLs—for more.

 

So what is the cause of CVD?  The pharma generated literature holds that  CVD consists of atherosclerosis in the coronary arteries and other arteries, and that leaking young plaque from within the artery walls cause myocardial factions  (MI).  They also hold that atherosclerosis is an inflammatory process; however pharma and their key opinion leader ignore the role of pathogens.  The role of pathogens in the artery walls and the immune function of LDL are demonstrated in the journal literature.  Thus the presence of LDL within the muscular portion of the artery walls and there active transport there are explained by their role in the immune system.  They are actively transported by the endothelia cells to absorb the toxins generated by pathogen.  These pathogens also explains why a high number of white blood cells are within the artery walls.  These processes explain the entire process leading to the formation of plaque within the artery walls, in the same way that explains the formation of a boil in response to pathogens.  In fact the young, unstable atheroma within the artery wall resembles a boil.  For a review of this evidence go to and also articles.  There are a number of contributing factors for this process.  The two main ones are those which causes metabolic syndrome, namely a high sucrose (fructose) diet compound by high glucose mostly from starches (carbohydrates).  This combination cause fat storage in the liver which when accumulates in the liver adversely affects its metabolic controls.  Uncorrected over several year this will result in insulin resistance[14]  which often progresses to endothelial dysfunction in the arteries, and the conditions grouped by pharma as metabolic syndrome, which includes atherosclerosis, CVD, hypertension, obesity, and for some high Total Cholesterol (TC).[15]  Other major contributors to cardiovascular disease include rancidification of polyunsaturated fats, transfats, reactive products of metabolism including glycation by glucose and fructose.

 

Why the rise in CVD?  The cause is obvious, just look at the numbers, it is the Western diet.  And it is not the fast foods, sedentary lifestyle, but the one two punch of fructose and glucose.  Fructose mucks up the liver by being converted to fat in the liver the place where it is metabolized.  The high carb (glucose) Western diet results in high insulin which is secreted to lower the glucose.  Insulin sends a message to cells for to store fat and burn glucose; this causes an excess accumulation of fat in the liver, and this overtime mucks up the liver’s metabolic regulatory functions.  Fatty liver, typically a 40% or greater accumulation of fat in the liver, is now estimated at 30% of the US population as of 1999 by the NHANES study, and is labeled Non-Alcoholic Liver Disease (NAFLD).  The excess fat is stored in hepatocytes (liver cells), and thus affects their performance.   One result of this is that the body becomes less responsive to insulin, and from that there is a clear causal relationship to obesity, CVD, diabetes and other chronic conditions.   Yes it takes both fructose and glucose.  The Japanese eat a high carb diet consisting of white rice and noodles, which accounts for up to 85% of calories, yet they consume only 14 grams of sugar, and they have a very low rate of CVD.  Click on link for a detailed discussion of this topic.  This is not new science, just that food manufacturers and pharma wants us to chase the wrong causes.  

What is be done:   To ask pharma and their doctors is to ask for drugs.  It takes both high fructose and high glucose to bring on NAFLD and insulin resistance which Thus the obvious life-style change is that of diet:   avoid sugar (like the Japanese), lower carbs, and eat more saturated fats and green-leafy vegetables.  Depending on current health there are a number of paths.  The best choices have been described in concise form at and a longer form at.  In the following:  Part 3, a review of the evidence concerning carbohydrates; in Part 4, a review of fats.  The final section, Part 5, is on life-style changes, supplements, and drugs that reduce the risk of CVD and AS.  Part 6 is a listing of key points, a glossary of terms, and a guide to the first 4 Parts by subject headings and listing which page they are on, with a link to an easy-to-print posting of the first 5 Parts.   Part 7 is a guide on healthful videos and books.  Part 8 is on obesity and its health consequence; it looks at why we get fat.  Part 9 is a dictionary of terms, Part 10 is on the New Atkins diet, and Part 11 on Alternate Day Fasting.  Finally there is a summation article on healthful supplement for seniors--enjoy the documentary-lectures page, please.   



[1] Jonny Bowden PhD  & Stephen  Sinatra, MD, The Great Cholesterol Myth:  Why Lowering Your Cholesterol Won’t Prevent Heart Disease—and the Statin-Free Plan That Will, Fair Winds Press, Nov.  2012; a national bestseller, has 23 experts who praised the book and are quoted on the cover & first page, and at Amazon has a 4.8 star rating from 220 reviewers.   Getting a fair review of book is iffy because of heated nature of the topic and many the subscribers to pharma’s spin.  JK finds the book well supported in the critical portions on cholesterol’s role; but in spots questionable as to the alternative approaches to prevention of CVD.  A couple of years before reading this book, JK had arrived at those same conclusion as to risk of CVD and on some of their fixes. 

[2]  Atheroma is an accumulation and swelling in artery walls made up of (mostly) macrophage cells, or debris, and containing  lipids  (cholesterol and fatty acids), calcium and a variable amount of fibrous connective tissue… in the early stage an accumulation of mostly macrophages, that have taken up oxidized LKLWiki.

[3] The deviation from natural fats will be developed in part 3.  There you will find out the recent deviations from natural (high ratio of omega 6:  omega 3 fatty acids and the production of trans-fats through hydrogenation of vegetable oils) cause an assortment of conditions including CDV.  Thus the low fat diet replaces one unhealthful part of diet (unnatural fats) with a worse item sugars. 

[4] While cholesterol is also produced by the adrenal gland, intestines, and gonads, they do so for conversion to hormones and other molecules.  Over 80% of blood borne cholesterol is produced in the liver, some of which is recycled and returned to the liver via HDL. 

[5] VDL consists of approximately 13% phospholipids, 60% triglycerides, 18% cholesterol, and 7% proteins; LDL is 45% phospholipids, 10% triglycerides, 20% cholesterol, and 25% protein, and HDL 20% phospholipids, 5% triglycerides, 30% cholesterol, and 47% protein (Human Anatomy and Physiology 2nd Ed. Elaine Marieb, 1992, p 856).

[6]  Braunwald, Heart Disease, 8th Ed. P 1085 table.  There of the 4 major clinical trials, 3 of them the placebo cohort had as many major ischemic events as those treated with statins.  This book published by Bayer ignored the data to conclude the opposite. 

[7] For a detailed account of Pfizer’s TNT Study on how the evidence was worked to lower guidelines for statins (Lipitor).  The Jupiter study “a major discrepancy between significant reduction of nonfatal stroke and myocardial infarction, but no effect on mortality from stroke and myocardial infarction… raises troubling questions concerning the role of commercial sponsors “….  NIH, & Wiki.

[8] A reasonable assessment of total early deaths from the selective COX-2 inhibitors in the US would be over 200,000; and a much greater number for the non-selective COX inhibitors, the NSAIDs—but for aspirin.  Celebrex is still on the market, and though warnings about all COX inhibitors warning that they promote CVD, the oft-heard sales message prevails. 

[9] After 3 months treatment of healthy patients with a poor TC using pravastatin or simvastatin, the total cholesterol and CoQ10 (Q10) were lowered 40%, when compared to the placebo group.  “A diminution of Q10 availability may be the cause of membrane alteration with consequent cellular damage”Journal of clinical Pharmacology.  This finding is supported in other studies and widely accepted—summary article.  

[10] 9% increase in risk of developing diabetes over 4 years, meta study Lancet 2010 based on pharma trials--undoubtedly under-reported. 

[11]  The 2nd cause for neuropathy, the first low Q10.  The two are additive.

[12] At that abnormal level the rate of oxidative damage to LDL out-paces the cleanup process, and typically their first MI occurs in the 4 decades.  But this doesn’t prove that without other risk factors those with a TC near 350 are at significantly greater risk. 

[13] Juxtapid is a once-daily capsule taken in the evening well after a last meal; it works in conjunction with proper diet and exercise to remove LDL cholesterol from a patient's blood. While it did reduce LDL cholesterol levels by approximately half during the first 26 weeks of study in its phase 3 trial, it also comes with a boxed warning regarding liver toxicity: Juxtapid  can cause the accumulation of fat in the liver, as well as liver enzyme abnormalities. The FDA's approval was given on the condition [request] that Aegerion run three post-marketing studies regarding the safety of long-term use of the drug” Fool .  Rarely are requested trial completed timely, and penalties are non-existent.

[14] Insulin resistance is a condition in which the cells throughout the body became tolerant to the NORMAL high serum level of insulin which occurs in response to elevated blood glucose following a meal or a snack.  The pancreas as a consequence secrets even more insulin to bring the serum glucose level down to the normal range. 

[15]   There are other causes, nothing is simple:  Reactive chemical both produced by metabolism and environmental sources also are causal for CVD, MI, and related conditions.  Also contributory are unnatural fats, mainly trans and oxidized polyunsaturated fats.  High cholesterol (hyperlipidemia) given the cholesterol myth lacks a medical reason for inclusion in metabolic syndrome.   

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