Five years ago (2009) Wainwright et al Wrote:
Current guidelines encourage ambitious long term cholesterol lowering with statins, in order to decrease cardiovascular disease events. However, by regulating the biosynthesis of cholesterol we potentially change the form and function of every cell membrane from the head to the toe. As research into cell morphology and membrane function realises more dependencies upon cholesterol rich lipid membranes, our clinical understanding of long term inhibition of cholesterol biosynthesis is also changing.
I suspect most people are aware that new drugs go through many stages of ‘testing’ before the drug is approved for use by members of the public…. this is no big secret. What may be a little more secretive is the fact that after the behind the scenes laboratory testing has been done, and there has been sufficient favourable / positive (more positive than negative) results brought to light and the drug gets the Green Light from the necessary National Agency – a new – more vigorous and far more population based trial then begins.
This is known as Phase Four (stage 4) Post Marketing Surveillance. LINK
Even the FDA admits all possible adverse reactions cannot be found during the initial pre drug release testing period:
………active post marketing surveillance of drug adverse effects is also essential. Because all possible side effects of a drug can’t be anticipated based on preapproval studies involving only several hundred to several thousand patients, FDA maintains a system of post marketing surveillance and risk assessment programs to identify adverse events that did not appear during the drug approval process. FDA monitors adverse events such as adverse reactions and poisonings. The Agency uses this information to update drug labelling, and, on rare occasions, to re-evaluate the approval or marketing decision. LINK
There are a number of points about this that many people have failed to consider in my opinion. Firstly when a doctor prescribes a patient a drug, I cannot think of many who were advised ‘you are now taking part in stage four drugs trials and all side effects and strange symptoms will be reported to the FDA by me‘…….. In fact you are now a part of an ongoing phase four drugs trial – albeit unknowingly.
I have to ask exactly how many Adverse Reactions to say Statin Drugs, have been reported to the relevant authority by prescribing doctors after the patient makes them known…… I know paperwork is darn time consuming, however the patients need should be met and the reporting done. Is it any wonder (if this reporting did not take place as required) that drug companies could and did continually down play the side effects of their drugs.
Stephanie Seneff pointed me towards the Wainwright et al published paper, and she adds: …………… statin drugs are never worth the risk of their side effects. Cholesterol is a vital nutrient, without which mammalian cells cannot survive, and it is inconceivable to me that crippling the body’s ability to synthesize cholesterol can ever be a good idea. In an excellent and highly informative review article published in 2009, Wainwright et al.  developed a strong argument that statin drugs, by depleting cholesterol, lead to a destabilization of cell membranes “from head to toe.” This problem, in turn, increases risk to a long list of serious health conditions and diseases, including diabetes, multiple sclerosis, cognitive problems, hemorrhagic stroke, cancer, and even ALS (amyotrophic lateral sclerosis, also known commonly as Lou Gehrig’s disease). Their arguments are backed up by references to 85 peer-reviewed journal publications.
She also believes (when discussing how many doctors ignore complaints by patients relating to statin drugs as ‘just getting old’…… ): statin side effects can best be interpreted as an acceleration of the aging process.
Many of us know already that Statin Drugs have done to us – what is considered irreparable damage – that is, even after the drugs are discontinued, the agony, cramps, pains, inability to use parts of our body in a normal way, as we used to prior to Statins being prescribed – has gone. For many of us our lives as we knew them will never revert to normalcy. The most commonly reported side effects to statin therapy are muscle pain and weakness. If left unchecked, these symptoms can progress to rhabdomyolysis (severe muscle damage) and kidney failure. Muscle weakness in the lungs can lead to breathing difficulties; in the heart it leads to heart failure. Statin users are reassured by their doctors that they can halt statin therapy if their liver and muscle enzymes rise too high. In practice, however, it’s possible to suffer irreversible muscle damage (the problem does not go away after the statin therapy is stopped), and this can happen even when the enzyme levels are not above the normal range. LINK (January 2010)
I find it rather amazing that doctors do not know or even consider when a patient complains of muscle pain, even after all blood tests for markers of this type have come back in the so called ‘normal range’, that damage can and often has occurred – can be happening without an elevation of these markers. It is as if they have not bothered to read the literature which shows, without a doubt patients can and do(in some cases) suffer muscle damage from Statin drugs without any elevation in markers being visible.
But the new study suggests the test for elevated levels of an enzyme associated with muscle injury, known as creatine phosphokinase or CPK, may be less accurate than widely believed.
“The patients in our study were unusual in that they had experienced weeks to months of persistent muscle problems,” Richard H. Karas, MD, PhD, tells WebMD. “We found that these patients can have evidence of microscopic damage to their muscles even with a normal CPK.”
……. many patients with evidence of muscle injury had CPK levels in the normal range.
The finding that CPK testing can confirm, but not rule out, statin-related muscle injury comes as no surprise to cardiologist Sidney C. Smith, Jr., MD, who is a past president of the American Heart Association. He tells WebMD that several smaller studies have shown the same thing.
Smith is a professor of medicine at the University of North Carolina at Chapel Hill.
“This is not a new, but it is important research,” he says…. LINK July 6th, 2009
(In a written statement, a spokesperson for Lipitor manufacturer Pfizer Inc. tells WebMD that patients taking a statin should always report any unexplained muscle pain, tenderness, or weakness to their doctor.
“The incidence of muscle injury in the absence of elevated CPK levels in patients treated with Lipitor has not been determined,” writes Sally Beatty of Pfizer.)
The paper (2009) out of Canada – Association between statin-associated myopathy and skeletal muscle damage LINK found:
Although muscle symptoms typically improve rapidly after stopping statin therapy, our findings suggest that some patients are more susceptible to statin-associated myotoxicity and persistent structural injury. These findings have several important clinical implications.
Back in 2002 scientists were noting muscle damage (statin induced) that might or might not be associated with increases in CK levels, one must ask why it took so long to filter through to both mainstream medical reporting and practising doctors in general (?do they actually read medical/scientific articles).
The mechanism of statin-induced skeletal injury is not well understood. Animal models show that type II white muscle fibers are mainly affected. Oxidation injury may be a central issue. Coenzyme-Q-biosynthesis is decreased (12) and at least in some patients increased levels of isoprostanes (IP; 13) have been found. The percentage of patients with elevated IP is higher in the presence of CK elevation, but can also be seen in the absence of elevated CK. The extent of IP elevation showed no correlation to CK and/or symptoms. An increase in IP has been reported in myopathy (14) and rhabdomyolysis (15,16). If IP appeared to be increased, there was a comparable elevation in serum, plasma and urine. Although vitamin E in single cases may cause alleviation of the symptoms (17), its general use does not result in clinical benefit. LINK
What is most interesting is the comment:
Apparently there are at least two types of muscle pains. These are either ache- or cramp-like with a ratio of about 3:1. In rare cases we saw both types in a particular patient at the same time (45). Interestingly, they may show different times of onset after start of statin therapy ranging from days to weeks. Starting regular physical exercise may manifest these symptoms even after years. Recently, we separated a third type of “flue-like” symptoms including myalgia, weakness, exhaustion, paining joints elevated acute phase response markers and sometimes subfebrile temperature (46). This type of side effects might be dose-dependent. Concerning appearance or type of muscle pains we are not aware of different responses to the various statins. A certain type of muscle weakness seen mainly in older patients (> 70 a) after statin therapy of >1 year is not yet definitely attributed to the treatment.
Here we have scientists showing that muscle damage not only can and does happen in a high percentage of people on Statin Drugs, but that some will continue to have these serious problems even after (months? years?) the drugs have been stopped. And not only that, but scientists have published on the possible mechanisms or causality – in reference to autoimmune causation of serious permanent myopathy.
In addition to inducing a self-limited myopathy, statin use is associated with an immunemediated necrotizing myopathy (IMNM), with autoantibodies that recognize _200-kd and _100-kd autoantigens. The purpose of this study was to identify these molecules to help clarify the disease mechanism and facilitate diagnosis.
(ARTHRITIS & RHEUMATISM Vol. 63, No. 3, March 2011, pp 713–721) (Andrew L. Mammen, Tae Chung, Lisa Christopher-Stine, Paul Rosen, Antony Rosen, Kimberly R. Doering, and Livia A. Casciola-Rosen)
It appears to be well known in the science/medical world that some patients are more susceptible (more likely) to get statin associated myotoxicity and PERSISTENT structural injury. Again one must ask the question is my doctor reporting my muscle pain and possible structural damage to the relevant authority? Has my doctor, your doctor ordered a muscle biopsy to determine what damage has occurred?
Anyone who reads by blogs will know how anti Statin Drugs I am. I believe we are interfering with an absolutely essential biological pathway and causing untold stress / damage to every cell in the human body. I am not a subscriber to the Cholesterol Theory of Heart Disease, and I believe what the pharmaceutical companies have done – with this ‘Cash Cow’ of theirs (statin drugs) is in fact bordering on the criminal – these drugs kill people at the worst, and at the very least they make cripples out of once healthy people.
While collecting information for this paper, I did contact a couple of well known and highly respected scientists, looking for dates and scientific publication data. Professor Uffe Ravnskov very kindly pointed me to a couple of scientific articles which I have used and referenced above. Stephanie Seneff (MIT) agreed with me that these drugs do serious harm to those prescribed them and that merely stopping them does not fix problems/side effects for some. She has a theory about why this may be so.
I am well aware though that some people stop their statin and don’t get better. I think it’s a consequence of an autoantibody that develops against the enzyme that statins suppress. The body gets confused and thinks the enzyme itself is foreign, because it is attached to the statin drug, which looks foreign to the body (this is just a hypothesis I have). I don’t know why patients are so forgiving of their doctors. I am very frustrated with the medical establishment right now, and I think they are the ones who are in a position to notice that this drug is harming their patients. They need to stop trusting the pharmaceutical companies so much! (Stephanie Seneff . Senior Research Scientist. MIT Computer Science and Artificial Intelligence Laboratory)
I do hope some of the above information will be useful to you in your arsenal – your weaponry against these drugs, the prescribers of these drugs and the manufacturers of these drugs. Why should we be Mr & Mrs Guinea Pig and suffer the consequences, while those who make the money deny responsibility?
Some further links/references
Mitochondrial myopathy developing on treatment with the HMG CoA reductase inhibitors — simvastatin and pravastatin . Article first published online: 25 MAR 2008 DOI: 10.1111/j.1445-5994.1995.tb01912.x
- J. D. F. ENGLAND1,*, J. C. WALSH2, P. STEWART3, I. BOYD4,
- A. ROHAN5, G. M. HALMAGYI6
Spacedoc (Doc Graveline) on damage and muscle biopsy
Drug Related Myopathies of which the clinician should be aware LINK
A growing body of literature suggests that statins, in addition to being direct myotoxic agents, may also promote, unmask, or potentiate an underlying autoimmune myopathy, including a newly recognized autoimmune-necrotizing myopathy [28•, 29•], dermatomyositis, and polymyositis, in which these diagnoses are supported by histologic findings, often in combination with specific associated autoantibodies. Increasing evidence also indicates that apoptosis is involved in autoimmunity, possibly because of impaired clearance of apoptotic cells, which may in turn incite an autoimmune response. Statins, particularly simvastatin, have been shown to induce apoptosis in many types of cells, including B lymphocytes, cardiac myocytes, hepatocytes, vascular smooth cells, and human skeletal muscle cells . How statins exert this proapoptotic effect is unknown, but the mechanism may involve protein prenylation, an effect reversible by mevalonate .