How Statin Drugs Really Lower Cholesterol: And Kill You One Cell at a Time

Hannah Yoseph and James B. Yoseph, How Statin Drugs Really Lower Cholesterol: and kill you one cell at a time.About Me (since this is anonymous).I have read this book and curtailed my statin intake, in my case simvastatin, for the time being because of certain concerns I have about its affects. I am a layman, not a scientist. I am a 78 year old diabetic male with an ancestry many of whom lived into their 90s, some beyond that, although my parents, both diabetics, died in their 80s. I think that I manage my sugars better than they were able to do. However, I noticed that I now need 30 units of Lantus rather than 25 units to maintain fasting blood glucose of between 80 and 90 since suspending statin intake. I am also on Byetta, 10 mcg., prior to the morning and evening meal, although I have trouble with always remembering the dose for the evening meal, and I take Glimipiride, 4mg. This combination seems to work well, delivering and A-1c of 6.5 or so, and most recently 6.1. This allows me to use less insulin, resulting in better maintenance of my weight. Morning, fasting blood sugar readings run about 90 as long as the day prior has not been a reckless “feast” day.Since stopping the statins, a fungus beneath the toenail of the great toe on the right foot cleared up, and I require fewer “Tums” to suppress esophagus irritation, and my memory has improved. On February 4, 2015 cholesterol was 195, without the aid of statins. This is my direct experience.I see that there are studies showing among patients using statin drugs increased development of cataracts as well as intestinal, liver, lung, and kidney injury. Other complications reported have included memory and cognition loss, mental illness, muscle injury, nerve injury, pancreatic injury ( In my case, diabetes preceded the use of statins), sexual dysfunction, skin injury, tendon and thyroid injury and others.I had a Rouen-y gastric bypass surgery several years ago at the Mayo Clinic in Rochester. At the time I had reached a weight level of 266 lbs., and I am only 5’6” tall. I lost 90 lbs, down to 176, but at this point I am at 191 in the buff. I “think” about exercise, but do it less than I think about it. Otherwise, I am active for a 78 year old, sort of. I had a heart scare a few months ago, resulting in no damage to the heart, according to an OSF cardiologist. There is a 100 percent blockage on one of the secondary arteries below the heart. I eat somewhat carefully, tilting towards Atkins, plus an occasional salad and frequent fruit. I consistently eat under 1700 calories a day. I drink port wine, trying to keep total intake of alcohol under 28 grams per day, but it usually runs closer to 33 grams. I am a non-smoker.I understand that since the body gets cholesterol from two sources, what it manufactures and what we eat, statins by blocking the mevalonate pathway interfere with the first of these two sources of cholesterol, and the body absorbs some of what is needed from the blood stream, yielding an impressive reduction in blood cholesterol level. But there are also negatives to this process. Statins may kill you "one cell at a time." (You may think that this over dramatizes the matter, but that is the question.)A CaveatBy the way, two points: I do not believe in any “conspiracy theory” on this subject, nor do I want to advance one, but I do understand something about scientific paradigms, and that sub-sets of a scientific community within a prevailing paradigm can have an agenda and seek profits, which to some degree, by reshaping the paradigm can diminish objective science. For any profession, it may be difficult to maintain professional objectivity when that objectivity encounters financial opportunity. The financial incentive affect is a two-edged sword. It inspires effort in behalf of an endeavor, and it does so whether it is for good or for ill.I understand the use of the term, “conspiracy,” to be the pejorative name given to any activity involving cooperation, especially when we don’t like it. “Conspiracy theory” is the pejorative name given to explanations that we don’t agree with.The concerns:Cell Replication (The cell cycle)Reductase activates the mevalonate pathway.Mevalonate makes cholesterol and Isoprenoids needed for DNA and cell replication.Statin drugs block the mevalonate pathway.Adding mevalonate rescues cells from statin toxicity. So for cell life, don't block the mevalonate pathway. This may mean one should not take statins.Blocking the mevalonate pathway interferes with the body’s production of Isoprenoids.Isoprenoids are five carbon molecules that stimulate cells to grow—vital for cell and DNA replication. Deprivation causes problems.Isoprenoids production curbed by statin drugs in the mevalonate pathway include: Co Q-10 for normal cell energy, Isopentenyladenine for normal cell cycles, Heme-A for cell energy and drug metabolism, Dolichol for membrane, nerve and fetal development, and Signaling proteins, for normal cell cycles.My first question: Why does blood stream as opposed to other cholesterol need to be low? It appears, by the way, that statin drugs achieve lower cholesterol levels indirectly through the “back door.” They do not attack blood cholesterol directly.Since this may be the case, my second question: is supplemental Co Q-10 and other isoprenoids advisable for statin users and does the body absorb co Q-10 when taken as a supplement? I am prompted to ask this because if true that the mevalonate pathway is blocked, creating a shortage of Co Q-10, a supplement would seem desirable. However I have heard that supplements such as vitamins in pills are not absorbed as well as from natural food sources. Also, for example, I was prescribed cyanocobalamin (vitamin B-12) to be administered once per month by injection and was told that the body does not absorb it very well when taken as vitamin B-12 tablets. So, does the body readily absorb isoprenoid supplements?Cholesterol is an unsaturated fat. According to the conventional wisdom this type of fat is less threatening than either saturated fat or trans fat.About LDL and HDL—LDL—Low-density lipoprotein is not cholesterol. HDL—High-density lipoprotein is also not cholesterol. My own inference from this claim is that LDL and HDL are “proteins” and not “fat” equivalents. However I have always understood “lipids” to denote fat. Therefore “lipoprotein” is both fat and protein. Accordingly, LDL and HDL are “markers” for cholesterol. I am not clear on the referent for “density” in HDL and LDL, but I understand it has to do with the size “density” of the molecule—the smaller the molecule, the denser it is.Third question: How can unsaturated fat “clog” arteries? Isn’t the fact that blood cholesterol (in suspension?) is found circulating in the blood stream a good thing? It seems that statins are attacking the wrong thing, and have not yet identified the correct target.Familial hypercholesterolemia is reportedly caused by a gene defect of chromosome 19. It is my understanding that statin drugs do not control this very well.The layman’s language source that I consulted, the Yosephs, contends that some heart problems are caused when too little LDL (not HDL) reaches heart cells. Fourth question: is it clearly established in scientific community that the stuff that clogs arteries is “oxidized cholesterol,” and do statins do anything with the oxidized cholesterol which “clogs” arteries?One part of the negative aspect of statin drugs is through a “lactones ring” in statin drugs, which conducts a “lethal fungal mimicry.” Statins act as the poisonous secondary metabolite, which “mimics” the primary metabolite, and is a deadly toxin for certain microbes. The explanation goes that this poisonous "secondary metabolite" (a euphemism for its toxic status) mimics the primary metabolite. Reductase is "tricked" in to bonding with the statin, and then dies. This deactivates the mevalonate pathway. In a flourish of exuberance, the report noted that it was like adding snake venom.Also---Statin drugs are called reductase inhibitors, but they are also said to be reductase stimulators, and that they can be genotoxic. They report that "statins can induce an increase in reductase, which can lead to an over production of ras proteins--leading to cancer.” For ras proteins to function, isoprenoids are added to them. Statins block prenylation for ras proteins. Blocking prenylation for ras `proteins can cause uncontrolled cell division--cancer. It sounds to me that if this is true, statins are performing dual duty. Fifth question: Is there some particular way that statins performing as reductase inhibitors is not offset by statins performing as reductase stimulators?Statins are mycotoxins, it is my understanding, not unlike aflatoxin, and citrinin, and my source contends that they are all cancer causing. You may recall a scare a few years ago from an increase in aflatoxin in grain being brought to elevators in the Midwest by farmers at harvest time, and the scare was due to the known cancer causing characteristics of aflatoxin.My sixth question: If I reduce my simvastatin dosage, but still take it, does the lower dose reduce some of the claimed negative affects?I read an article which cited data suggesting that for diabetics, statin therapy lowers mortality from cardiovascular disease and stroke by as much as thirty percent. Damned if you do and damned if you don’t!I understand that this behavior on my part is similar to that of a lawyer trying to be his own legal counsel and who has a fool for a client. Still ultimately, we have to be a little responsible for what we put in our mouth.PS. I am not a Dr.—at least not an M.D. But I may be able to give the impression that I know more than I understand. Can someone give an enlightened comment on the things that I have said?

"How Statin Drugs Really Lower Cholesterol and kill you one cell at a time, by James B. Yoseph and Hannah Yoseph, MD, has unequivocal proof that statins are deadly and that a major conspiracy promoted their use. The scientists who later received Nobel prizes for their work on statins, Akira Endo, Michael Brown and Joseph Goldstein, spent years trying unsuccessfully to resolve the toxicity problem before realizing that what makes statins lower serum cholesterol also makes them toxic.Statins do not lower serum cholesterol by "inhibiting endogenous cholesterol synthesis" as is widely believed. Statins lower cholesterol by disabling existing reductase, and enzyme in cells that makes mevalonate,the source of "cell foods" (isoprenoids), including cholesterol, that are vital to cell function. Cells respond to statin deactivation of their source of nutrients by producing more reductase, and hence more cholesterol, to meet cellular nutritional needs. Simultaneously, cells increase the number of LDL receptors to provide cells a second source of nutrients. The increased LDL receptors move cholesterol from the bloodstream to cells thereby lowering serum cholesterol while stuffing cells with more cholesterol than they can metabolize. When scientists looked inside statin-treated cells they found crystals of excess cholesterol.The FDA initially approved statin trials for patients with defective LDL receptors (FH) who have high serum cholesterol. Statins caused a 50% increase in serum LDL cholesterol in patients with 100% defective LDL receptors because the increased cholesterol synthesized by the liver could not be removed from the bloodstream by defective receptors. In patients with 50% defective receptors the increased number of LDL receptors triggered by the statin blockade of mevalonate lowered serum cholesterol. This was the first clue that statins lower serum cholesterol by increasing the number of LDL receptors.The statin blockade of mevalonate deprives cells of isoprenoids vital to normal cell functions, including isopentenyl adenine that is required for DNA replication, CoQ10 which is needed for cellular energy production and regeneration of anti-oxidants, and GGPP that is essential for prevention of neuro-degeneration and contractile dysfunction of skeletal muscles. Statins thereby cause many injuries including cognitive dysfunction, blindness, diabetes, muscle wasting, kidney failure, liver failure, heart failure and cancer.The Japanese Nobel prize winning scientist Akira Endo was known to occasionally tell the truth when a lie would have served him better. When Endo was asked why he did not take statins for his high cholesterol, he responded with a Japanese proverb: "The indigo dyer wears white trousers." Endo knows that indigo and statins are both toxic.Almost all recent clinical trials of statins have failed to show and benefit according to a cited study by French scientist Michel de Lorgeril. Prior to the 2004 withdrawal of Merck's Vioxx from the market there were more than a dozen major statin trials that reported beneficial effects of statins. In 2004, a controversy erupted within FDA which showed the cozy relationship between drug makers and the FDA. A drug safety reviewer, Dr. David Graham, was prevented by his superiors from publishing his findings that Merck's painkiller Vioxx had caused an estimated 28,000 premature heart attacks and strokes. Graham was threatened by fellow FDA employees for pursuing the matter and had to go outside the agency for help. It was revealed that Merck had withheld evidence regarding Vioxx safety. Merck abruptly withdrew the drug from the market. As a consequence of the Vioxx debacle, new clinical trial regulations came into force which required that investigators comply with demanding regulations or face criminal proceedings. After the new regulations were in place there have been more than a dozen trials that filed to show any significant beneficial effect of statins in the prevention of coronary heart disease. De Lorgeril concluded that the failure of recent cholesterol lowering trials has cast doubt on the validity of the lipid theory and suggests that statin treatment of CHD should be reappraised.The authors provide thorough documentation of the scientific data used in developing statin drugs. In contrast, their opinions regarding the causes of coronary heart disease, which constitute only a small part of the book, are limited in scope and depth and, with respect to omega-6 vegetable oils, are inconsistent with scientific findings. The authors erroneously state that increased intake of linoleic acid (LA), the main component of most vegetable oils, reduces risk of coronary heart disease because it reduces serum cholesterol. While excessive intake of LA does indeed reduce serum cholesterol, it increases risk of coronary heart disease because it increases oxidation of LDL cholesterol and stimulates an increase in oxidized LDL receptors (LOX-1) which reduces oxidized (and total) LDL in the bloodstream by moving it to the endothelium where it causes dysfunction and increases risk of CHD. In spite of these shortcomings the book is of great value due to the excellent information on statin toxicity which is not available elsewhere.

Trusting my family doctor, I decided to try statins (rosuvastatin 10mg). Just a few days after starting the treatment the following side effects appeared:Severe pain in the joints, especially in the legs.Night vision affected.My memory was seriously affected.The sexual desire was annihilated.And deep depression appeared quickly.I stopped the treatment 36 days after it started because I began to fear for my life.So I decided to buy this book, just to reaffirm the horrifying truth behind these poisons.

This book is very detailed. It gives a lot of information on the negative effects of statins. It explains how it came to be developed and how the FDA, NIH, drug companies and medical providers are pushing statins unnecessarily.

For anybody who has had a doctor try to force these drugs on them, this is certainly the book to read. Even if you have had adverse reactions to this drug, some doctors will try to persuade that another brand is safer. The Statinistas in the medical fraternity will blame the adverse reactions on anything other than Statins. When it is pointed out that among all the other serious side effects the FDA now warn that Statins can cause diabetes, these blind doctors ask if you saw that in the Daily Mail.This book is extremely well researched and will enable people to understand how drug companies are only interested in money, your health is of little importance to them.

I was excited to get this book but I was a little disappointed in the format and writing style. I got everything I needed to know in a matter of an hour or so. They go on and on at infinitum about demonizing big farma and the nefarious doctors. Being a chemist, it didn't take me long to absorb the dangers here. I know that they were trying to give indisputable evidence, but I think it could have been summarized better. Otherwise I would have given a higher rating

After i read this I decided that I would prefer to manage my cholesterol through diet. I'm lucky that I can. We need cholesterol for brain cell growth and damping down production might have undesirable effects. It's unclear to me that simply taking statins addresses the real problem of LDL pattern B cholesterol.

This book starts admirably by drawing attention to the limitations and misinterpretations of the Framlingham study, which is, as they say, very bad science. unfortunately they then go on to commit similar errors of at least potential misinterpretation of scientific data. For example they quote animal and human research with adverse effects with no reference to the dose, whether it is within or outside the potential therapeutic range. Yes statins are potentially lethal, but so is water if you drink too much of it! They do themselves no favours by not critically evaluating the data that they cite, and the whole thing ends up as a diatribe against the pharmaceutical industry - which may well be fully justified, but NOT by this book!

Excellent book. I love the way it details how statins work and hence demonstrates that the so called side effects are actually direct and ultimately inevitable effects of the drug.