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How Statin Drugs Really Lower Cholesterol: And Kill You One Cell at a Time Paperback – March 12, 2012
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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.)
By 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.
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.
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?