STATIN DRUG INFORMATION THAT MAY SAVE YOUR LIFE.

[Preciouslife1]

Lipitor No Better Than Other Cholesterol Drugs


According to a German study, Lipitor, Pfizer's cholesterol-lowering statin drug and the best-selling drug in the world, is no more effective than similar cholesterol drugs, and in some cases may have worse side effects.
Controversy Follows New Price Guidelines
The study demonstrating this stems from a controversy in Germany regarding the pricing of Lipitor and other statin drugs.
Health insurers in Germany introduced a fixed price for Lipitor at the end of 2004. Pfizer asked its patients to pay the difference between the price of Lipitor and the sum that would be paid by health insurers, then started an advertising campaign in newspapers arguing that Lipitor is better than other statins. Most other pharmaceutical companies lowered the price of their drugs after the fixed price was introduced.
Lipitor No Better and Often Worse
The study, which involved a survey of previous studies from around the world, found that:

• Lipitor did not prolong the life of people with chronic coronary heart disease
• For acute diseases, Lipitor, Zocor, and Pravastin provided similar results
• Lipitor did not prolong life in people with diabetes mellitus
• Some studies on Lipitor had to be stopped because it had more side effects compared with Zocor

The San Francisco Chronicle September 4, 2005

Dr. Mercola's Comment:


Lipitor is one of the best drugs on the market -- from the drug company's perspective, that is. It is designed to be taken for life, and you will pay thousands of dollars a year to the drug company until you die prematurely from the side effects produced by the drug.
A "cure" for a symptom having nothing to do with addressing the cause of your underlying illness, all it does is cost you money, put you at risk of serious and sometimes life-threatening side effects, and provide an excuse not to take actual steps that will help your heart and health, such as proper diet and exercise.
Other statin drugs, though, are frankly no better. Lipitor is simply the one with the best marketing program. If you want to know the real truth about statins and their dangers, read my past article The Truth About Cholesterol-Lowering Drugs.
In the case of an elevated cholesterol level, normalizing it without drugs is one of the easiest tricks in the book. All you need to do is radically reduce grains that are easily converted to sugar and sugars, which raise your insulin levels and cause your liver to make more cholesterol. Then add enough exercise to improve your HDL/cholesterol ratio.
Fine tuning would involve eating properly for your *me.tabolic type and following the other recommendations from the Total Health Program.

[Preciouslife1]

Lipitor May Suppress Immune System -- There Are Far Better Options


Lipitor, Mevacor and Pravachol have been found to suppress certain immune system cells known as helper T-cells, according to new research from Switzerland.
The researchers and subsequent media reports have focused on the fact that the drugs may be useful for treating transplant patients. However, how this immune suppression could affect the vast majority of patients taking the drugs is not discussed.
"This unexpected effect provides a scientific rationale for using statins as immunosuppressors, not only in organ transplantation, but in numerous other pathologies as well," the researchers conclude.
Researchers found that in laboratory-grown cells, the statin drugs suppressed the activation of helper T-cells. T cells, of which there are 4 types, are a group of lymphocytes produced in the thymus gland. The four types are:

• Helper T cells

• Killer T cells

• Suppressor T cells

• T4 cells
  

Helper T cells, the type suppressed by the statin drugs, act by recognizing foreign pathogens and then activating the production of the proper T cells and B cells in response.
The statin drugs used in the study included the following:

• Lipitor™ (atorvastatin)

• Mevacor™ (lovastatin)

• Pravachol™ (pravastatin)

Nature Medicine

[Preciouslife1]

'Experts' Recommend Higher Doses of Cholesterol Drugs

Experts reported that using higher doses of drugs to reduce cholesterol decreases the risk of heart attack, bypass surgery and chest pains. The finding could place new pressure on doctors to treat their patients more aggressively by using higher doses of statin drugs to reduce cholesterol levels in people with heart disease.
In the study it was found that people who took a double dose of the drug atorvastatin, sold under the brand name Lipitor, had their LDL levels drop to 62 milligrams per deciliter of blood compared to the patients whose LDL level dropped to 95 milligrams per deciliter after taking a standard dose of Pravachol.
The study showed that the patients treated with Lipitor lowered their risk of dangerous chest pain, heart attack and bypass surgery by 16 percent compared to those patients that took Pravachol.
This advice could mean a huge increase in health care costs because in the United States, only 11 million of the 36 million people who experts say should be taking cholesterol medication are actually taking them.
To get an idea of costs, a starting dose for Lipitor costs $900 per year and an 80-milligram dose that the new study is proposing would cost $1,400 annually.
The participants of the study included 4,162 volunteers at 349 medical centers in eight countries who had all been hospitalized for unstable chest pains or a heart attack. Benefits from the treatment became apparent within 30 days.
New England Journal of Medicine March 8, 2004
Dr. Mercola's Comment: An estimated 25 million people world wide are taking drugs known as statins to lower their cholesterol levels and according to ‘experts’ 200 million could use them. Now, researchers are claiming that doubling the doses that is currently used reduces the risk of heart attack, bypass surgery and chest pains more than ‘gentler’ doses.
This advice will most likely put pressure on doctors to use even more aggressive and expensive doses of statin drugs. The United States already spends $12.5 billion more on statins than any other medicine. When you consider that a starting dose for Lipitor will run you $900 per year, while the 80-milligram dose used in the new study costs approximately $1,400 annually, you get a good idea of how much more expensive this will be.
While there are likely to be some people who benefit from taking statins, it is probably far less than five percent of the people who currently take them. But even worse than the additional expense, and what these experts do not realize, is that statins can kill people, many people, and they can do great harm to many, many more. I strongly encourage you to read and get the truth about cholesterol-lowering drugs.

[Preciouslife1]

Low Cholesterol Linked to Stroke Risk

High cholesterol is a well-known risk factor for stroke. But new research suggests that low levels of cholesterol in the blood may also increase stroke risk. The study linking low cholesterol to increased stroke risk was presented recently at the 24th American Heart Association Conference on Stroke and Cerebral Circulation which was discussed in last week’s newsletter. About 80% of all strokes are ischemic, and 20% are hemorrhagic.
The researchers compared the cholesterol levels of the stroke patients to 3,700 other people in the Group Health Cooperative of Puget Sound who had not had a stroke. They found that as an individual's cholesterol level rose above 230 milligrams per deciliter of blood (mg/dL), their risk of ischemic stroke increased. For example, a person with a cholesterol level of 280 mg/dL had twice the risk of ischemic stroke as a person with 230 mg/dL.
But the researchers also found that as cholesterol dropped, the risk of -hemorrhagic stroke increased significantly. A person with a cholesterol level below 180 mg/dL had twice the risk of that type of stroke compared with someone at 230 mg/dL.
About 10% of the population have cholesterol levels below 180 mg/dL. It is not clear if the cholesterol is indeed the cause of the stroke, or related to some other cardiovascular factor that is responsible. High cholesterol levels probably increase blockages.
The theory with low cholesterol is that it is necessary to maintain integrity of the vessel wall. Low levels of cholesterol might lead to "leaky vessels." The Japanese have typically low cholesterol levels and a higher than average rate of hemorrhagic stroke.
Dr. Mercola's Comment:
It is encouraging to find some evidence (although not yet published) that shows that low cholesterol is a problem. I believe the optimum cholesterol is about 200. Levels below 180 appear to be a problem. Levels under 150 are a major dilemma. I am an expert in low cholesterol as my levels have been as low as 85.
I was trained in the "low fat" craze and I am sure I did some serious damage to my body trying to stay healthy. However, for the last seven years I had tried to raise it and was unable to get it above 135.Two weeks ago I was able to get it up to 175! For the last two months I have been using a supplement by Biotics that called Beta TCP that has whole beet concentrate and Taurine.
These items are very effective at thinning the bile in the gallbladder. Once the bile is thinned it can flow out and not remain in the gallbladder as sludge so it can emulsify the fat so we can absorb it. Trying to absorb fat without bile is like trying to wash greasy dishes without soap. It does not work very well at all. I am fairly convinced that most people with low cholesterol levels are due to a dysfunctional gallbladder.
Folks it took me SEVEN years to find someone who could teach me that piece of information. It is one of the best things I learned last year. Traditional medicine has no clue about how to treat this problem. There solution is to remove ONE MILLION gallbladders a year. I believe this is criminal malpractice. If a person is treated early enough, this operation is RARELY needed.
To add insult to injury, the surgeon does not even suggest that these patients take bile salts to help them digest their fats. If you know anyone who has had their gallbladder removed, you could greatly benefit them by telling them they need bile salts with EVERY meal for the rest of their life.

[Preciouslife1]

Statins Kill Your Brain


A Review of Statin Drugs Side Effects and the Misguided War on Cholesterol by Dr. Duane Graveline, M.D.


Self-Published, April 2005
Review Published September 13, 2005
"But statin drugs don't do that."
This was the answer Dr. Duane Graveline, MD, former NASA astronaut, heard repeatedly from doctors and pharmacists as he began to question whether Lipitor -- a drug he now titles "Thief of Memory" -- was the underlying cause of the transient global amnesia he experienced while taking the drug.
Although Dr. Graveline, now the author of Statin Drugs Side Effects and the Misguided War on Cholesterol, had been a flight surgeon for the U.S. Air Force, conducted space medicine research, been a NASA astronaut, practiced as a family physician for 20 years, and had written eight books during his retirement, he remembered none of these experiences during his second bout with Lipitor-induced amnesia.
Dr. Graveline's consciousness regressed to his teens, having precise recall of his high school classmates. Yet he remembered neither his wife nor his four children.
But statin drugs don't do that, he was told.
This was not the first time Dr. Graveline experienced transient global amnesia (TGA), a disease that involves a lapse in the ability to form memory for a period of minutes or hours, sometimes but not always involving the forgetting of past memories, from Lipitor. Nor was Dr. Graveline the only person to experience TGA as a side effect of the newest class of cholesterol-lowering drugs called "statins."
Lipitor -- Thief of Memory


Statin Drugs Side Effects and the Misguided War on Cholesterol tells the story about how Dr. Duane Graveline discovered that his experience with TGA was attributable to the statin drug Lipitor -- the only drug he was taking at the time -- and how he brought this side effect of statin drugs into the public consciousness with the publication of a letter, which generated hundreds more letters from patients who had similar experiences with statin drugs.
In Dr. Graveline's first experience with amnesia, he had been taking Lipitor for six weeks, prescribed by the physician overseeing his astronaut physical at the Johnson Space Center.
He'd gone for his usual morning walk in the woods, but when he returned, he circled about aimlessly through his driveway and yard. Although he failed to recognize his wife, he reluctantly accepted the milk and cookies she offered. Yet he refused to enter their home, and only consented -- hesitantly -- to be driven to the hospital after much coaxing by an old physician friend that his wife called on the phone.
The neurologist had no explanation for the condition, and Dr. Graveline had returned to normal-- though remembering nothing of what happened -- before he left the hospital. Dr. Graveline was given the diagnosis of "transient global amnesia, cause unknown." He considered various possible causes, and, after eliminating each of them, considered the possibility that Lipitor, a new drug for him, and the only one he was taking, might be the root cause of his problem.
"But statins don't do that," was the response he heard from each physician and pharmacist to whom he spoke. Nevertheless, Dr. Graveline terminated his Lipitor, and had no subsequent experience with amnesia.
The following year, he was once again prescribed Lipitor at his Johnson Space Center annual physical, at which point he began taking the drug again. Sure enough, six weeks later he experienced another bout of TGA. This time, he experienced a significant retrograde component to his memory loss, his consciousness regressing to that of his teen years.
Again, he was diagnosed with "transient global amnesia, cause unknown." Again, the doctors insisted Lipitor was not involved. Again, Dr. Graveline heard nothing from his colleagues except the refrain, "But statin drugs don't do that." After all, as his wife had hinted, "the aging process alone does terrible things to the body."
Statin Drugs Side Effects -- Kiss Your Memory Goodbye


That year, in 2000, Dr. Graveline initiated the first in-pouring of patient testimonies of statin-induced memory loss when the syndicated column "People's Pharmacy" published a letter he had sent to them about his experience. Since then, they have received hundreds of similar testimonies.
Yet there are millions of people taking statins, an industry that brought in $26 billion in 2004. Do "hundreds" of cases of TGA indicate a major side effect?
As Dr. Graveline points out throughout Statin Drugs Side Effects, we should expect TGA and other memory problems to be severely underreported.
Since memory loss is considered a natural part of the aging process, most people will simply chalk up any symptoms to the supposed effects of that process. Many will be embarrassed, and many more involved in operating machinery, aircraft, or other vehicles, might fear losing their job for reporting such problems. Even five years after the initial exposure, the average doctor still has no idea that statins have cognitive side effects, and any memory loss that is reported is highly unlikely to be considered as a possible effect of a statin drug by the supervising physician.
Dr. Graveline also points out that for every episode of TGA, there are likely to be thousands of less severe cases of forgetfulness, confusion, difficulty concentrating, or other cognitive symptoms that are simply chalked up to the gradual erosion of the body and mind by the aging process, when they are in fact attributable to cholesterol-lowering statin drugs.
In Statin Drugs Side Effects, Dr. Graveline cites a study by Muldoon, et al., that found "100% of patients placed on statins showed measurable decrease in cognitive function after six months, whereas 100% of placebo treated control patients showed measurable increase in cognitive function during the same time period."

In Issue #003 of our free newsletter a study was cited finding that the roughly 30% of patients who stop taking statins within 1-3 years of beginning them have an 88% increased risk of all-cause dementia and a 154% increased risk of Alzheimer's disease, compared to those who have never taken statins.

[Preciouslife1]

Part #2
Statin Drugs Side Effects -- It Doesn't Stop at Your Brain


Although a large focus of Statin Drugs Side Effects is transient global amnesia, Dr. Graveline discusses a variety of other side effects of statin drugs. Polyneuropathy, rhabdomyolysis -- a fatal condition involving the destruction of muscle tissue that was responsible for the recall of the lethal statin Baycol -- congestive heart failure, coenzyme Q10 (CoQ10) and carnitine deficiency, inflammation and rupture of tendons and ligaments, and interference with the production of endorphins are among the side effects that Dr. Graveline attributes to statins. He also discusses the possibility that CoQ10 depletion-induced mitochondrial mutations will present a cumulative effect over time increasing the risk of various diseases.
Perhaps the most interesting discussion of the effects of statin drugs that tends to be left out elsewhere is their inhibition of nuclear factor kappa B (NF-kB).
NF-kB inhibition is the mechanism by which statins inhibit inflammation, which is probably responsible for the mild decrease in heart disease mortality that relatively short-term studies have found for statins, rather than cholesterol-lowering, which is also achieved by a variety of drugs that fail to reduce mortality, including fibrates, which increase mortality. (Dr. Graveline cites a 10-year follow-up review of statin trials finding an increased risk of death attributable to statins, and other reviews have found that trial length is associated with a diminished finding of mortality protection.)
Yet in most discussions of statins' anti-inflammatory effects, an in-depth discussion of nuclear factor kappa B is usually absent. Even in reviews that are critical of the cholesterol hypothesis and statin treatment usually refer to their anti-inflammatory effects as uneq.uivocally a positive effect.
Yet Dr. Graveline applies a closer critical eye to statin-induced NF-kB inhibition. NF-kB is actually an important mechanism of the human body's immune system, which is regulated delicately in a complex system into which statins enter as a large, blunt and indiscriminating weapon.
Different infectious organisms modify NF-kB in different ways. E. coli and Salmonella, for example, are both organisms that are able to infect the body by, like statins, inhibiting human NF-kB. Chlamydia, on the other hand, exerts its dominance in the urogenital system by enhancing NF-kB.
The Epstein-Barr virus suppresses T cells in the blood, enhancing its ability to infect the blood tissue causing mononucleosis, by, like statins, inhibiting NF-kB. Yet when the same virus later triggers nasopharyngeal carcinoma and Burkitt's lymphoma, it does so through sustained NF-kB activation.
What is the ultimate long-term result of suppressing NF-kB through statin use? We simply don't know yet. Since NF-kB regulation is a complex system, its elevation being neither strictly "good" nor strictly "bad," it is likely that NF-kB reduction will have varying results, some good, some bad, in different people with different conditions.
As pointed out in Issue #005 of our free newsletter omega-3 fatty acids are almost twice as effective as statins at reducing mortality through their own anti-inflammatory mechanism. They are also much cheaper to supplement with, and even available in the right foods.
Yet omega-3 fatty acids do not inhibit NF-kB or any other important component of the body's immune and inflammatory system. Instead, they simply supply the body with a hormone precursor called "EPA" that is stored inside of cell membranes until the body decides to use it, releasing it enzymatically. Thus, the risk of side effects are much lower with omega-3 fatty acids, because they simply enable the body to utilize its own tightly regulated systems, rather than interfering with the body's tightly regulated systems like statins do.
Dr. Graveline Exonerates Cholesterol


Statin Drugs Side Effects not only details some of the wretched and even humanity-stripping side effects of statin drugs (like the loss of memory of your life experience, wife, and children), but Dr. Graveline is also one of a growing number of physicians and researchers who lead the way in overturning the decades-long triumph of junk science over reason that has led us to blame cholesterol as the cause of heart disease.
Dr. Graveline discusses the work of Dr. Uffe Ravnskov, author of The Cholesterol Myths, Dr. Paul Rosch, Sally Fallon and Dr. Mary Enig of the Weston A. Price Foundation, and others. He devotes particular attention to the work of Dr. Kilmer McCully, who questioned the attribution of heart disease to elevated cholesterol levels from the beginning, and began discovering the link between homocysteine and heart disease in the 1960s.

The importance of Dr. McCully's research shows that not only does the cholesterol hypothesis indentify the wrong culprit, but its paradigm is fundamentally backward. While the cholesterol hypothesis falsely identifies heart disease as a disease of excess, McCully's more thoughtful and evidence-based research shows heart disease to be a disease of deficiency-- a deficiency of certain B vitamins, lost in modern processing and modern food preferences, that are used to me.tabolize the abrasive and toxic homocysteine into a harmless byproduct.

Contrary to the cholesterol hypothesis of heart disease, Dr. Graveline uses Statin Drugs Side Effects to show that cholesterol is one of the most important and valuable molecules in the body, responsible for the production of steroid hormones, bile acids, and the formation of synapses. This is a message that this website strives to hit home, but one that has been lost on most people in the mire of anti-cholesterol hysteria.

[Preciouslife1]

Who Should Read Statin Drugs Side Effects


Anyone who has suffered the ravages of statin-induced memory loss will identify with this book. But more importantly, if you have a friend or family member on statins, or who is considering using statins, this may be the most important book you could use to convince them to consider other options.
If your doctor is not aware of the cognitive side effects of statins, you must alert her or him to the existence of this book. Unfortunately, most doctors even in 2005 are not aware that statin drugs have serious cognitive side effects. Your doctor needs to be aware of this even if she or he has no intention of prescribing alternative treatments to her or his patients. It is imperative that when physicians are encountered with a case of amnesia or other type of memory dysfunction that they consider the statin drugs the patient is on as a probable contributor to this problem.
If they do not, serious damage to the patient, the patient's family, or even the public could be a result. If a pilot suddenly has an attack of TGA while flying a plane, or a driver while driving a truck or car, and this involves a serious retrograde component where memory is lost through the period during which the operator received her or his training, will the operator be able to drive the truck, car, or fly the plane? We do not yet know the answer to this question.
While transient global amnesia is generally rare, its incidence has exploded since the advent of the strong statin drugs such as Lipitor. For the sake of both public and patient safety, every physician needs to know that TGA is a side effect of statin drug use.
Drawbacks of Statin Drugs Side Effects


If there is a fault to Statin Drugs Side Effects, it is its organization. For example, after three chapters on TGA, case reports of TGA again appear in half of the "How the Statin Drugs Work" chapter, and there is a general tendency to muddle the distinction between chapters and topics.
A secondary effect of this tendency is the tendency to duplicate information. Topics that appear in multiple chapters sometimes have almost identical paragraphs explaining a concept, rather than a simple reference to the previous explanation in a previous chapter.
While the separation of the book into the main body meant for all readers and a very lengthy addendum for more scientifically oriented individuals is meant to benefit the reader, its primary effect is to introduce another layer of unnecessary duplication.
Dr. Graveline tends to use moderately flowery language, which the more scientifically oriented individuals might be disappointed to find reduces the information density of the book somewhat-- an effect that, on the other hand, will probably make the book more easy to read for the typical reader.
Add Statin Drugs Side Effects to Your Library


Drawbacks aside, Statin Drugs Side Effects, though geared towards the lay reader, is not only essential for physicians to read, but is a valuable contribution to the scientific inquirer's library. In particular, Dr. Graveline's discussion of the inhibition of nuclear factor kappa B is a unique contribution that is generally overlooked in most discussions of statins.
It is reassuring to see more and more doctors and researchers joining the ranks of those skeptical of the cholesterol hypothesis and aware that just because America's favorite drug habits are legal does not mean they are safe.

Statin Drugs Side Effects is a welcome addition to our collective pool of knowledge, and Dr. Graveline must be commended for his brave and persistent resistance of the common denial to uncover the truth about the side effects of statins.

[Preciouslife1]

New Study To Test Statin-Parkinson's Link




Researchers are sufficiently worried by new study results that they are planning clinical trials involving thousands of people to examine the possible link between Parkinson's disease and statins, the world's biggest selling drugs, reports Patrick Walter in Chemistry & Industry, the magazine of the SCI.

Suggestions of a statin link are not new, but the results of a recent study linking low LDL cholesterol to Parkinson's provide the strongest evidence to date that it could be real, because statins work by reducing LDL cholesterol. The study by researchers at University of North Carolina showed that patients with low levels of LDL cholesterol are more than three and a half times more likely to develop Parkinson's disease than those with higher LDL levels.

When asked whether she was concerned by the new results, study leader Xuemei Huang said: 'Yes I am very concerned, which is why I am planning a 16000-patient prospective study to examine the possible role of statins.' Huang was quick to point out, however, that a causal link with statins had not yet been proven. And Yoav Ben-Shlomo, a professor of clinical epidemiology at University of Bristol said that it is also a possibility that LDL cholesterol is a consequence rather than a cause of Parkinson's.

But according to Huang, the well-established link between Parkinson's and apoE2, a gene associated with lower LDL cholesterol, supports her theory that low LDL is the culprit in many cases of Parkinson's.

Huang says that if there is a link with statins, we could see big surges in the number of Parkinson's diagnoses in the next five years, because at that stage, statins will have been in common usage for more than a decade.

Huang's new study will examine the statin link. A total of 16000 patients for whom 20 years of baseline fasting cholesterol measurements are available will be involved. Another large-scale trial investigating a cholesterol link with Parkinson's risk is underway at Harvard. This study differs in that there are no baseline data available for the study group.

Pfizer's statin Lipitor is the world's biggest selling drug with $12.2bn in sales in 2005. Parkinson's has previously been linked with pesticides. Pfizer were unavailable for comment. ......UH, HUH, I'm sure they weren't available for comment as usual as their cash cow will be coming off patent and their other high profile billion dollar drug that failed in FDA testing to raise your HDL is causing some pricky heat rash on the Pfizer execs tushies me thinks...

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[Preciouslife1]

DNAPrint Genomics, Inc. (OTC BB:DNAG.OB - News), today announced that the Company's research staff has discovered a genetic marker for statin-induced myalgia (chronic muscle pain), that a patent has been filed to protect the discovery and that the research on which the discovery is based will be published in an upcoming issue of The Journal of Pharmacogenetics and Genomics (JPG).


The marker was the primary discovery from the Company's Statnome project initiated in 2000 and the manuscript to be published in JPG describes the validation of this finding in different patient samples.

"Myalgia or chronic muscle pain is a common side effect reported by patients who take statins for cholesterol control, and it is likely to be part of a disease continuum that includes myositis and rhabdomyolysis, which is a breakdown of muscle fibers that frequently results in kidney damage and is a potentially fatal side-effect," according to DNAPrint Chief Science Officer Tony Frudakis, Ph.D. "Deaths associated with statin-induced rhabdoymyolysis lead Bayer to withdraw Cerivistatin in 2001. We are satisfied to have brought one of our first pharmacogenetics programs full circle from discovery through validation and we consider the R&D phase for this project complete. With the filing of a patent to protect this discovery, the Company will be able to develop a proprietary test for this gene variant and thereby reduce the likelihood of illness or death in those patients who are taking statins. This study also criticizes the original clinical trials for statins, which did not fully or adequately explore the relationship between statins and myalgia or even rhabdomyolysis."

"This is the culmination of a project that was begun when the company was founded," stated DNAPrint President and Chief Executive Officer Richard Gabriel. "It has taken until now to validate the original findings, but validated they are. The Company has filed a patent to protect this process. We plan to bring to market a definitive test product to identify this genetic variant and to potentially prevent painful -- and in some cases, fatal -- side effects in thousands of patients who are taking a very common prescription drug." DNAPrint's study of 750 patients who had taken either atorvastatin (Lipitor®) or simvastatin (Zocor®) showed that patients carrying one specific genetic marker were approximately 2.5 times more likely to experience mild to severe muscle pain (myalgia). The effect was most pronounced for atorvastatin and the study showed that approximately one half of the patients who were removed from atorvastatin therapy due to muscle symptoms possess this genetic marker, whereas in the general population (with and without cardiovascular disease) only approximately 15%-25% of people carry the marker. DNAPrint applied its technology for measuring population structure (e.g., ancestry) in order to prove that the finding in both the discovery and validation samples was genuine, and in so doing received praise from JPG reviewers. This observation indicates that the genetic marker may be related not only to response to statins but also to a possible relationship with higher cholesterol levels, according to the study.

[Preciouslife1]

CoQ10 helps relieve statin induced muscle pain


Roman Bystrianyk, "CoQ10 helps relieve statin induced muscle pain", Health Sentinel, July 12, 2007,

Statins are a class of drug that are used to lower cholesterol levels. Lipitor, Mevacor, Crestor, Zocor, and Vytorin are some of the more well known brand names that belong to this class of drug. These drugs are extremely profitable generating billions of dollars in sales. According to CNN Money, Lipitor is the top-selling drug of all time with nearly $13 billion in 2006 sales.

Despite a large analysis presented in a study in the April 2005 issue of Archives of Internal Medicine showing that omega-3 fatty acids decreased the risk ratio for death by 23% and that statins only decreased the risk of death by 13%, statins are still used as the primary way to treat people with high cholesterol. Lipitor alone has been prescribed to over 18 million Americans to help them treat their cholesterol levels.

Muscle symptoms commonly occur with statin drugs. In some cases myopathy, or damage to the muscle tissue, can actually occur. Very rarely, if myopathy occurs and statin therapy is not stopped a very dangerous condition called rhabdomyolysis can occur which can sometimes be fatal.

According to an article in USA Today, Public Citizen, a consumer watchdog group, “linked 72 fatal and 772 non-fatal cases of muscle breakdown, known as rhabdomyolysis, to all six of the statins sold between October 1997 and December 2000. The study found 29 earlier deaths.”

Statins decrease cholesterol production by inhibiting an enzyme in the body called HMG-CoA, which is short of 3-hydroxy-3-methylglutaryl. The same biosynthesis pathway that is blocked in order to reduce cholesterol also reduces the production of a key nutrient in the body called coenzyme Q10 or CoQ10 for short. Studies have shown that blood levels of CoQ10 drop by 25% to 50% after statin treatment.

CoQ10 is a key component in energy production that takes place in the mitochondria. Mitochondria are known as the powerhouses of the cell and are key to life. CoQ10 deficiency resulting from statin treatment may impair muscle energy production and contribute to the muscle symptoms and more serious conditions in patients using statins.

A study in the May issue of The American Journal of Cardiology examined the use of CoQ10 supplements to improve muscle symptoms in patients being treated with statins. The controlled, double-blind study provided half of 32 patients 100 milligrams (mgs) of CoQ10 a day for a month and the other half 400 IU of vitamin E.

At the end of the month the patients who were reporting statin related muscle pain that received the CoQ10 showed “decreased muscle pain by 40% and improved the interference of pain with daily life activities by 38%”. In contrast, the vitamin E group showed no improvement in muscle pain.

The authors note that, “these findings suggest the coenzyme Q10 may be beneficial for patients using statins by ameliorating myopathic [related to muscle disease] symptoms and improving subjects’ well-being and functioning in daily life activities.” This positive study showed the benefits of CoQ10 in offsetting some of the negative effects in people that are receiving statins. The fact remains however that statins interfering with CoQ10 synthesis resulting in negative consequences for patients have been known for quite some time.

In a previous article I asked Dr. Barry S. Kendler Professor of Nutrition at the University of Bridgeport Human Nutrition Institute about CoQ10 and statins and he said, “the pharmaceutical industry has not been helpful in this context, although they had full knowledge of the effects of statins on CoQ10 and the possible consequences of this, even before statins were marketed. In fact, one of the companies has a patent on including CoQ10 with the statin, but chose not to market the combination, possibly for financial reasons.”

In addition, an October 2004 newsletter by Dr. Sinatra, a medical doctor, board certified in internal medicine and cardiology, and a fellow of the American College of Cardiology indicated that Merck Pharmaceuticals has had a patent combining their popular statin drug Lovastatin [brand name Mevacor] and CoQ10 for years.

“Merck Pharmaceuticals has been sitting on a patent for combining Lovastatin and CoQ10 in the same capsule for 15 years, and I can't understand why they don't launch this product. I hope that as more studies show that higher dose statins, used over extended periods, are associated with greater side effects that include carcinogenicity [ability of a substance to cause cancer] and cardiomyopathy [weakening of the heart muscle], Merck will feel political pressure to act on these patents and create a product combining CoQ10 and Lovastatin at last.”

SOURCE: The American Journal of Cardiology, May 15, 2007, Vol. 99, No. 10, pp. 1409-1412

Posted by samlion on the IHUB.com DNAG board. .>)

[Preciouslife1]

What Happens When Your Cholesterol Goes Too Low?

POSTED BYDr. Mercola
July 26 2007
People who take statin drugs to lower their cholesterol as much as possible may have a higher risk of cancer, according to a me.ta analysis of over 41,000 patient records from 23 statin drug trials.

The analysis raises concerns about how low cholesterol levels should actually go. Researchers found one extra case of cancer per 1,000 patients with the lowest levels of LDL (low-density lipoprotein) cholesterol, the so-called “bad” cholesterol, compared to patients with higher LDL levels.

Past studies have found an increased risk of Parkinson’s disease among people with extra-low cholesterol. Meanwhile, statin drugs may cause damage to the liver and muscles.

The analysis included records from patients taking statins such as Lipitor and Zocor, but did not include newer statins such as Crestor and Vytorin.

Statins, the world’s top-selling drugs, are thought to have a beneficial effect on inflammation in the body, and lowering the risk of heart attack and stroke. They may also decrease the risk of death from influenza, pneumonia and smoking.

Journal of the American College of Cardiology July 31, 2007; 50:409-418
Reuters July 24, 2007





This is a topic near and dear to my heart, as my cholesterol has been as low as 75 when I was a naive young doctor and felt that your cholesterol could not be too low.
While many people worry that their cholesterol is too high, few give a thought to the damage that can result if your cholesterol is too low. When it comes to cholesterol, lower is not always better.

I speak from personal experience on this, because, as many of you know, I have struggled with low cholesterol for much of my life. Cholesterol is not the villain it has been made out to be. Quite to the contrary, cholesterol:

• Acts as your body’s repair substance
• Helps you to digest fats
• Is the precursor to vitamin D
• Is necessary for hormone production
• Functions as a powerful antioxidant

If your cholesterol dips too low, you will increase your risk of depression, stroke, violent behavior, and suicide.

Despite this, in 2004 the U.S. government's National Cholesterol Education Program panel advised those at risk for heart disease to attempt to reduce their LDL cholesterol to specific, very low, levels.

Prior to this, a 130-milligram LDL cholesterol level was considered healthy. The updated guidelines, however, recommended levels of less than 100, or even less than 70, for patients at very high risk.

Their recommendations for obtaining these incredibly low LDL levels? Taking cholesterol-lowering statin drugs … sometimes up to two or three varieties.

There is no evidence to support that such low cholesterol levels are beneficial, and increasing numbers of studies like the one above are pointing to the risks.

Meanwhile, even if you DID want to lower your cholesterol, taking statin drugs is the last option you should consider. Cholesterol-lowering drugs have been linked to everything from nerve damage to memory loss, and, because they deplete the body of beneficial Coenzyme Q10 (CoQ10), may actually INCREASE the risk of heart disease.

There’s no need to risk dangerous statin side effects to keep your cholesterol levels where they should be. All you need to do is follow these steps:

• Exercise regularly
• Normalize your insulin levels by eliminating grains and sugars from your diet
• Take a high-quality source of omega-3 fats, like krill oil

Additionally, if you are a man, or if you are a woman in menopause, you should get your iron level checked. Elevated iron levels can raise cholesterol and cause serious damage to your heart and other organs.

[Preciouslife1]

Cholesterol is Needed to Help Your Brain Cells Communicate

Cholesterol in your brain is key to the cell connections needed for memory and learning.
Past research has suggested that brain "support cells" known as glial cells produce a substance that allows the brain's nerve cells, or neurons, to communicate.
Cholesterol levels in the blood do not determine the brain's supply, as blood cholesterol molecules are too large to cross the blood-brain barrier. The blood-brain barrier is a mechanism that strictly controls the type of molecule allowed to enter into the brain from blood vessels.
Instead, glial cells appear to churn out their own cholesterol supply. The researchers zeroed in on cholesterol through experiments with cells in which the lipid triggered the formation of synapses -- the connections through which nerve cells communicate.

Thus the availability of cholesterol appears to limit synapse development.
In addition, the investigators found that, when cultured alone, neurons produced some cholesterol. But only when glial cells were present was there a cholesterol supply abundant enough for "massive" synapse formation.
According to the researchers, these findings suggest that any "genetic or age-related defects" in the brain's cholesterol use may impair the circuitry behind mental functioning

[Preciouslife1]

No Evidence That Widely Prescribed Statins Protect Against Prostate Cancer

Science Daily — A large community-based study refutes previous findings that statins -- a top-selling drug class, worldwide -- might cut one's risk of developing prostate cancer by reducing production of the male hormones that fuel cancer growth.

Researchers from the New England Research Institutes found that while men using statins did indeed have lower blood levels of androgens such as testosterone, it was more likely attributable to poor health rather than the use of statins.
"The public health significance is that our study provides evidence that statins may not have a clinically meaningful impact on testosterone in the blood, although further studies should be done," said study author, Susan A. Hall, Ph.D., a research scientist at the New England Research Institutes. "That doesn't mean that statins may be lowering prostate cancer risk through one or more alternative pathways, but it doesn't appear to be working through reduction of male hormones,
Statins lower cholesterol and are commonly prescribed to treat and prevent heart disease. Since cholesterol is required for the production of male hormones researchers have theorized that statins may reduce production of these hormones. A large, recent study found that men using statin drugs were at lowered risk of developing ********************static or fatal prostate cancer, especially if the drugs were used over a long period of time. But other studies on statin use and prostate cancer risk have had mixed results, according to Hall.
To study a narrow question-- whether statin use reduces androgen concentrations in the blood -- the researchers examined data from the Boston Area Community Health (BACH) survey, a population-based, NIH-sponsored, epidemiologic study. Data were collected between 2002 and 2005 on thousands of men and women with equal representation of African American, Caucasian and Hispanic populations.
The value of the BACH study, according to Hall, is that "we capture real world use of medications in the community, which might be a more realistic representation of their impact on the body, compared to outcomes seen in a clinical trial."
Hall's team studied the medical histories of 1,812 men, including 237 statin users, and analyzed their blood for "free" or unbound testosterone, for total testosterone, and for other associated compounds.
The researchers found no relationship between statin use and free testosterone and most of the other associated compounds. There was a significant association between statin use and level of total testosterone in the blood, but that association vanished when researchers considered the patients' age, body weight, and history of cardiovascular disease and diabetes. "We know that men with higher body mass index, diabetes and cardiovascular disease tend to have lower testosterone levels, and this largely accounted for the drop in testosterone in statin users," Hall said.
"In this study, statin use was just a marker for presence of other illnesses," she said. "This study may inform that debate, however, by suggesting that any protective pathway offered by statins, if it exists, is not through androgen suppression."
Findings are published in the August issue of Cancer Epidemiology, Biomarkers & Prevention, a journal of the American Association for Cancer Research.
The BACH Survey was supported by the National Institute of Diabetes and Digestive and Kidney Diseases.

[Preciouslife1]

No Evidence That Widely Prescribed Statins Protect Against Prostate Cancer

Science Daily — A large community-based study refutes previous findings that statins -- a top-selling drug class, worldwide -- might cut one's risk of developing prostate cancer by reducing production of the male hormones that fuel cancer growth.

Researchers from the New England Research Institutes found that while men using statins did indeed have lower blood levels of androgens such as testosterone, it was more likely attributable to poor health rather than the use of statins.
"The public health significance is that our study provides evidence that statins may not have a clinically meaningful impact on testosterone in the blood, although further studies should be done," said study author, Susan A. Hall, Ph.D., a research scientist at the New England Research Institutes. "That doesn't mean that statins may be lowering prostate cancer risk through one or more alternative pathways, but it doesn't appear to be working through reduction of male hormones,
Statins lower cholesterol and are commonly prescribed to treat and prevent heart disease. Since cholesterol is required for the production of male hormones researchers have theorized that statins may reduce production of these hormones. A large, recent study found that men using statin drugs were at lowered risk of developing ********************static or fatal prostate cancer, especially if the drugs were used over a long period of time. But other studies on statin use and prostate cancer risk have had mixed results, according to Hall.
To study a narrow question-- whether statin use reduces androgen concentrations in the blood -- the researchers examined data from the Boston Area Community Health (BACH) survey, a population-based, NIH-sponsored, epidemiologic study. Data were collected between 2002 and 2005 on thousands of men and women with equal representation of African American, Caucasian and Hispanic populations.
The value of the BACH study, according to Hall, is that "we capture real world use of medications in the community, which might be a more realistic representation of their impact on the body, compared to outcomes seen in a clinical trial."
Hall's team studied the medical histories of 1,812 men, including 237 statin users, and analyzed their blood for "free" or unbound testosterone, for total testosterone, and for other associated compounds.
The researchers found no relationship between statin use and free testosterone and most of the other associated compounds. There was a significant association between statin use and level of total testosterone in the blood, but that association vanished when researchers considered the patients' age, body weight, and history of cardiovascular disease and diabetes. "We know that men with higher body mass index, diabetes and cardiovascular disease tend to have lower testosterone levels, and this largely accounted for the drop in testosterone in statin users," Hall said.
"In this study, statin use was just a marker for presence of other illnesses," she said. "This study may inform that debate, however, by suggesting that any protective pathway offered by statins, if it exists, is not through androgen suppression."
Findings are published in the August issue of Cancer Epidemiology, Biomarkers & Prevention, a journal of the American Association for Cancer Research.
The BACH Survey was supported by the National Institute of Diabetes and Digestive and Kidney Diseases.

[Preciouslife1]

Scientists Identify Gene Responsible For Statin-induced Muscle Pain

Main Category: Statins
Also Included In: Pain / Anesthetics; Genetics

Statins, the popular class of drugs used to lower cholesterol, are among the most commonly prescribed medications in developed countries. But for some patients, accompanying side effects of muscle weakness and pain become chronic problems and, in rare cases, can escalate to debilitating and even life-threatening damage.

Now a study led by investigators at Beth Israel Deaconess Medical Center (BIDMC), helps explain the source of these problems. Published in the December 2007 issue of The Journal of Clinical Investigation, the findings offer the first evidence that a gene known as atrogin-1 plays a key role in statin-related muscle toxicity.

"Although it is not known exactly how many of the 500 million individuals who take statins experience muscle pain and weakness, muscle symptoms are generally considered the most common side effects of these medications," explains co-senior author Vikas P. Sukhatme, MD, PhD, Vice Chair of Medicine for Interdepartmental and Translational Programs, Chief of the Division of Nephrology, and Chief of the Division of Interdisciplinary Medicine and Biotechnology at BIDMC.

"Statin users describe a wide spectrum of symptoms - at the most extreme end is a severe breakdown of skeletal muscle known as rhabdomyolysis," says Sukhatme, who is also the Victor J. Aresty Professor of Medicine at Harvard Medical School (HMS). "At the other end is 'grumbling muscles,' milder, more diffuse muscle soreness and cramps. This kind of symptomatic muscle weakness and pain is quite frequent, but often difficult to quantitate."

Known by such trade names as Lipitor, Zocor, Pavacol and Mevacor, statins lower cholesterol by inhibiting HMG-CoA reductase, a key enzyme in cholesterol synthesis.

Approximately five years ago, the study's co-senior author Stewart Lecker, MD, PhD, and colleagues in the HMS laboratory of Alfred Goldberg, MD, first discovered the atrogin-1 gene, so named for its role in muscle atrophy.

"We learned that atrogin-1 is rapidly turned on in wasting muscle," explains Lecker, who is an investigator in the Division of Nephrology at BIDMC and Assistant Professor of Medicine at HMS. Muscle wasting occurs in a large number of disease states, including cancer, AIDS, and kidney disease and can also occur when muscles are underused due to injury or lack of exercise. "In the absence of atrogin-1 activation," he adds, "muscle atrophy is diminished."

Since this initial discovery, atrogin-1 has been found in every existing model of muscle wasting, prompting Lecker and Sukhatme to investigate whether cholesterol-lowering statins might also be "turning on" this gene.

"We reasoned that since atrogin-1 plays a key role in the development of wasting in skeletal muscle, it might also mediate part of [patients'] sensitivity to statins," the authors write.

They proceeded to conduct three separate experiments to test this hypothesis. They first examined the expression of the atrogin-1 gene in biopsies of 19 human quadricep muscles from five control patients, six patients with muscle pain who were not being treated with statins and eight patients with muscle pain/damage who were using statins. Their results showed that atrogin-1 expression was significantly higher among the statin users.

Next, the scientists studied statins' effects on cultured muscle cells treated with various concentrations of lovastatin. Compared with control samples, the lovastatin-treated cells became progressively thinner and more damaged. But remarkably, say the authors, the cells lacking the atrogin-1 gene were resistant to statins' deleterious effects.

Finally, the authors tested the drug in zebrafish. And, they showed that just as in mammalian muscle cell culture, lovastatin led to muscle damage, even at low concentrations; as the concentration was increased, so too was the damage. And, once again, they observed that fish lacking the atrogin-1 gene were resistant to statin-induced damage.

"These three complementary experiments demonstrate that atrogin-1 has a fundamental role in statin-induced toxicity," notes Lecker. "Future experiments will be aimed at understanding how statins turn on the atrogin-1 response in muscle, and in ascertaining what transpires in muscle following atrogin-1 activation that leads to muscle damage and atrophy. The hope is that eventually patients will be able to glean statins' positive benefits to cholesterol ********************bolism and reduction of cardiovascular events while being spared accompanying muscle toxicities."