Statin – what dat mean Wikipedia?

So, THEY want to put me on statins…I want to understand:

1. what it is?
2. why am I being herded on to it?
3. when should I be herded on to it?
4. how can herding me help me? how can herding me hurt me?
5. where do I get unprejudiced, non-herding advice on the subject?
6. who is the best person to inform me going forward without herding?
7. which, if I’m convinced to take statins should I be herded on to?

When I write THEY, I mean every medical professional I encounter from a diddle-eyed-joe to a damned if I know. There are clinical studies which tout the benefits of statins as great and the side effects as rare. There are observational studies which find that benefits are brought into question and the risk of side effects is significantly higher than the “clinic” counter. Then there are the real life encounters with real herd people (Vern Den Herder) on “the statin”. Their experience with benefit is nil (so far) but their experience with side effects is TOTAL! That being said, I refuse to be SOLD on statins. I prefer, greatly, to be convinced.

Statins are effective in lowering LDL cholesterol. Statins reduce illness and mortality in those who are at high risk of cardiovascular disease. They are used for primary prevention in people at high risk of cardiovascular disease, as well as in secondary prevention for those who have developed cardiovascular disease. Side effects include muscle pain, risk of diabetes and abnormal blood levels of liver enzymes. Also, rare but severe adverse effects, particularly muscle damage. There are various forms of statins. The W.H.O. lists statins as an essential medicine.

In people over the age of 70, statins decrease the risk of cardiovascular disease but ONLY in those with a history of heavy cholesterol blockage in their arteries. Treatment without history of CD reduces events but provides no mortality benefit. Studies overestimate the risk and recommend statins for patients who will not benefit.

Secondary prevention is defined as those having a prior heart attack, stroke, stable or unstable angina, aortic aneurysm, or other arterial ischemic disease, in the presence of atherosclerosis. Patients with vascular diseases reported that simvastatin and pravastatin did not impact cognition. Simvastatin and pravastatin appear to have a reduced incidence of side-effects.

Only a small fraction of side effects reported by people on statins are actually attributable to the statin according to review. Evidence does not support an association between statin use and cognitive decline. The FDA includes a warning about the potential for non-serious and reversible cognitive side effects with the medication (memory loss, confusion).

In observational studies 10–15% of people who take statins experience muscle problems (pain), much higher than those seen in randomized clinical trials. CoQ10 supplements are sometimes used to treat statin-associated myopathy. Myopathy risk was over 10-fold greater if cerivastatin was used, or if the standard statins were combined with a fibrate. Lovastatin promotes muscle fiber damage.

Oh, yeah, here’s one for you: Studies have found that the use of statins may protect against getting osteoporosis and fractures OR may lead to getting osteoporosis and fractures. Dosage, THEY say, is the key.

Natural statins are produced by fungi. Most circulating cholesterol comes from internal manufacture rather than the diet. Liver cells sense the reduced levels of liver cholesterol and seek to compensate by synthesizing LDL receptors to draw cholesterol out of the circulation. Oh, I forgot to mention, this is a known fact but in reference to rabbits.

Inhibiting of lipids binding to protein molecules results in a number of unwanted side effects associated with statins. The multiple effects of statins remain controversial. Statins are divided into two groups which are fermentation derived and synthetic. Natural statins occur in foods such as oyster mushrooms and red yeast rice. The first statin agent was mevastatin produced by penicillium. As of 2016 misleading claims exaggerating the adverse effects of statins had received widespread media coverage, with a consequent negative impact to public health

So, how did I do? Did I get answers to all of my questions…let’s see:

1. what it is? Statins are effective in lowering LDL cholesterol.
2. why am I being herded on to it? Secondary prevention for…aortic aneurysm.
3. when should I be herded on to it? AAA
4. how can herding me help me? how can herding me hurt me?

Help=if prevents rupture.

Hurt=muscle pain or damage, diabetes, abnormal blood levels, memory loss

1. where do I get unprejudiced, non-herding advice on the subject?

Critical studies not pharmaceutical company related

1. who is the best person to inform me going forward without herding?

Non-involved doctor or scientist, non-cardiologist

1. which, if I’m convinced to take statins should I be herded on to? Simvastatin and pravastatin

“How statin drugs really lower cholesterol & kill you one cell at a time” is a book review by Dr. Zoe Harcombe, PH.D. found on http://www.zoeharcombe.com.  This is a review of a book written by James & Hannah Yoseph entitled by the same name.  My interest is in content and also technique.

Ms. Harcombe starts her introduction by stating three things: the importance of cholesterol to the body, the admonition to read this book BEFORE prescribing or taking statins, not after, and the three key contributions of this book (to be looked at later).  The main headings in this review are:

1) How statin drugs really lower cholesterol

     Familial Hypercholesterolemia (FH)

2) What was known by whom and when as statins were pushed through to approval?

3) The conflicts of interest:

Conclusion

The Executive Summary:

Okay, now for the content and technique.  Zoe divided the review into three parts which makes easy to approach.  The titles of each part do not intimidate and do draw you in.  A conclusion and an Executive Summary give the reader some context or vitals as needed by each individual interested.

Back to the three key contributions of this book (as written by Ms Harcombe, italics mine):

1) She explains how statins work in the human body (and in animals where they have been used for drug testing).  Important here…how statins work in humans, how statins are tested in animals.

2) She documents medical journal articles detailing the precise mechanism statins work, proving  proponents knew the fallacy of statins.  How statins work has not been a mystery, how they harm should neither be a mystery.

3) She details the conflict of interest endemic in the pharmaceutical industry and approval processes, which deteriorated the human race. The book takes one drug company, Merck, and the American Food & Drug Administration (FDA) and a number of other related bodies (e.g. the National Cholesterol Education Program NCEP) and a handful of individuals and traces in incredible detail the role that each played in this scandal. And statins constitute a scandal.  The scandal of statins links back directly to conflict of interest.

Now in detail…the article:

1) How statin drugs really lower cholesterol

The Yosephs (authors of the book by the same title as this review) describe how cells work in simple language.  My summary is “Without …cholesterol…cells age and die.  When statins disrupt the pathway to cell replication – the cell cycle ends”.  A flow chart provides details and labels all the scientific names.  The next portion of this section describes how statins kill us one cell at a time.

Statins kill us one cell at a time.  Cells get the cholesterol they need by making it or taking it from the blood stream.  Statins inhibit cells from making cholesterol, so the cells take it from the blood stream, lowering the cholesterol in the blood stream.  Statin fed cells are dying but try to live by searching out vital cholesterol in the blood.  The protein LDL in the blood that carries cholesterol to and from the cells.  By the cell’s consumption of the LDL, it is lowered, and the dying cell attempts to save our life.

Familial Hypercholesterolemia (FH)

The genetic condition FH renders the body unable to remove LDL from the bloodstream resulting in high LDL.  The condition results from cell LDL receptors not working well.  An FH sufferer can therefore have heart problems – because of too little LDL reaches the heart cells – not because of too much LDL!  Doctors call high LDL “bad” because people with heart disease have this characteristic, but the body’s inability to absorb LDL deserves to be labeled “bad”.  HDL carries lipids and cholesterol back to the liver.  Statins give nothing to carry back to the liver and makes HDL low (because LDL is not being consumed).  A medication for FH suffers to stimulate cholesterol production solves the problem – but none exists.

2) What was known by whom and when as statins were pushed through to approval?

In 1982, researchers knew statins caused cells to die.  Despite this, in 1984 the FDA approved lovastatin  in record time.  In 1985, the Nobel Committee awarded Brown and Goldstein the Nobel Prize! (these guys wrote the cells die paper in 1982).  B&G also wrote that statins both inhibited and stimulated the substance that poisoned cells in 1980.  In 1982, the FDA allowed Merck to give Lovastatin to humans in the first human trial even though, researchers knew statins were toxins.  They blocked the cell replication pathway, and that when statins block the pathway, it caused cell death.  Nothing could be added back to the body to prevent cell death and the toxic effect of statins.  Where is the disconnect?  How do we “know” these things?  Who are the “good” guys?  Who are the “bad” guys?

In 1982 Brown and Goldstein wrote…: “If reducatase cannot increase sufficiently to overcome the inhibition by compactin, the cells die.”  Good Guys.  Prior to that, in 1980, Sankyo (Japanese pharmaceutical)  cancelled clinical trials of their statin on humans after half their laboratory dogs died of cancer.  Good Guys.  In 1980, Endo (Japanese researcher) co-authored a paper, writing…nothing we could add back to the cell, to compensate for the damage we had done, could prevent the toxic effect (of statins).  Good Guy.

Also in 1980,  Brown and Goldstein co-authored papers…stating: statins convert the cells into …auxotrophs….an auxotroph loses the ability to synthesize certain substances needed for its growth and metabolism; statins block mevalonate formation… and cultured cells die.

In 1980, Brown and Goldstein wrote the following in The Journal of Lipid Research (we’ll see who’s behind this journal later): “When the regulator of reductase is identified, it may be possible to administer this compound to animals and perhaps to patients, preventing the compensatory rise in reductase…” Hence Brown and Goldstein knew by 1980 that statins both inhibited and stimulated reductase. Medicine must prevent the “compensatory rise in reductase”.

In 1980, Brown and Goldstein co-authored a paper in The Journal of Biological Chemistry stating: “CoA reductase is inhibited by compactin, mevalonate formation is blocked and cultured cells die.” (p14)

In 1980, Brown and Goldstein co-authored a paper in The Journal of Lipid Research stating: “Incubation of cultured cells with compactin blocks mevalonate production and converts the cells into mevalonate auxotrophs.” (p172) An auxotroph is something that has lost the ability to synthesize certain substances needed for its growth and metabolism.

3) The conflicts of interest:

Daniel Steinberg wrote the book Cholesterol Wars.  He founded and chaired journals and committees, including American Heart Association council.  A Merck scientific advisor and an FDA advisory speaker, he influenced AMA and FDA policy and approvals.  With scientific support, he stated abnormal cells are not cancer, compactin not toxic, and LDL cholesterol causes Coronary Vascular Disease (CVD).  Steinberg recommended that a National Cholesterol Education Program (NCEP) be adopted.

The NCEP lowers cholesterol targets and set the recommended age for cholesterol use at nine.  All guideline participants received payments or grant funds from drug companies.  Twenty drug companies contributed funds to guideline doctors. Doctors averaged 8 drug company contributors each among 8 doctors and the 20 drub companies.

		Doctor Names Receiving funds or grants
#	Pharmaceutical	Scott Grundy	Bairey	Brewer	Clark	Hunninghake	Pasternak	Smith	Stone	Total
1	Abbott	1			1				1	3
2	Astra Zeneca	1	1	1	1	1	1		1	7
3	Bayer	1	1							2
4	BMS-Sanofi						1			1
5	Bristol-Myers Squibb	1	1		1	1			1	5
6	Esperion			1						1
7	Fournier			1						1
8	Glaxo SmithKline	1								1
9	Johnson & Johnson						1			1
10	Kos	1	1			1	1		1	5
11	Lipid Sciences			1						1
12	Merck	1	1	1	1	1	1	1	1	8
13	Novartis		1	1		1	1		1	5
14	Pfizer	1	1	1	1	1	1		1	7
15	Procter & Gamble		1							1
16	Reliant								1	1
17	Sankyo	1		1					1	3
18	Takeda						1			1
19	Tularik			1						1
20	Wyeth		1							1
	Doctor Totals	9	9	9	5	6	8	1	9	56

In 1987, when the FDA reviewed Merck’s lovastatin, Merck participants outnumbered FDA advisors 13-10.  A Merck toxicologist revealed short comings of the drug which went unquestioned. When put to meter it sounds like this:

Rabbits died a rapid death; Statins failed hamsters; It damaged dog liver cells; Cause cataracts? did not answer. Dr Richard Cenedella DID state that all of the hyper-lipidemic drugs induce cataracts in mice. Jonathan Tobert was Merck’s Clinical Director for all trials.  He contradicted himself by stating: no cataracts seen in humans taking lovastatin and co-authored a paper documenting an increase in lens opacities (i.e. cataracts) in 101 lovastatin consumers.

Conclusion

The Yoseph book describes how statins lower cholesterol and shows that statin dangers were known all along the approval process.  A few key players work with Merck and infiltrate the FDA, influence NIH establish the NCEP comprised of drug company funded representatives.  The statin scandal made billions by demonizing cholesterol and discovering and promoting a poison that causes disease and death in humans.  Rats adapt to statins rapid.  Rabbits die quick.  If humans died as quickly as rabbits, statins would be off the market.  Because of slow death, statins will be slow to be taken off the market.

The Executive Summary:

Cholesterol gives life to body cells.  The body must manufacture cholesterol because dietary cholesterol does not suffice.  If statins stopped 100% of cholesterol production there would be a 100% death rate.  Statins block the mevalonate pathway.  Cells cannot replicate or repair.  Blocking the mevalonate pathway means that every cell in the body dies…eventually.  Nothing can compensate for blocking the mevalonate pathway. This lowers blood cholesterol levels and ignorant doctors are happy.  There is a second way in which the body tries to save itself – it tries to increase the production of reductase, hoping that this may unblock the mevalonate pathway. It can’t. Hence reductase is both stimulated and inhibited at the same time.  LDL receptor activity and reductase activity increase in parallel.

The inventors of statins patented adding CoQ10 to their statins but then never bothered to add it.  Statins were only originally intended for the 1 in 500 people with Familial Hypercholesterolemia.  Ironically, the most serious form of Familial Hypercholesterolemia would receive no benefit from statins anyway.