New Ways of Marketing Statins: Cholesterol Lowering Drugs for the Flu?

 

New Ways of Marketing Statins: Cholesterol Lowering Drugs for the Flu?

by Dr. Mercola
A new study has led to what is perhaps the most ludicrous recommendation for flu treatment ever — statin drugs!
The researchers reported that statin use may reduce death risk in people hospitalized with the flu, and the media is reporting sensational headlines like “Statins reduce flu death risk by half.”
This is particularly outrageous, because the study was seriously flawed and designed to make statin drugs useful for another condition while they do nothing to address the underlying cause.
To validly determine if statin drugs are effective for flu they need to compare it to placebo, not a poison.
So what did they do?
They compared statin drugs to other toxic drugs, this time antiviral medications. So what the study actually found was that, more than likely, antiviral drugs were killing people twice as quickly as the statins!

What did the Study Really Show?

In the observational study published in The Journal of Infectious Disease, researchers examined data from 3,000 patients hospitalized with the flu, 33 percent of whom were given statins while the rest received antiviral drugs. The results showed that people who did not receive statins were twice as likely to die.
Another way of saying this, of course, is that people who received antiviral drugs were twice as likely to die as those given statins. And what this really means is that the antiviral medications were exceptionally harmful, not that statins were beneficial.
Still, it is not surprising that the drug’s manufacturer and the media are reporting favorable results for statin drugs, even though the researchers themselves pointed out the many limitations to their study, noting, for example:
” … it was difficult to ascertain the underlying functional health status of these patients, which may potentially confound the relationship between statins and severity of influenza.”
Further, one of the study’s authors has been a consultant to numerous drug companies, including Sanofi Pasteur, Novartis, Pfizer, Dynavax, and GlaxoSmithKline, whereas the study itself was funded by the Emerging Infections Program Cooperative Agreement of the U.S. Centers for Disease Control and Prevention (CDC), which also has worrisome ties to the drug industry.

Statins are Not Wonder Drugs

The drug companies started pushing their statin drugs, which are ordinarily prescribed to lower cholesterol levels, for the flu back in 2009 during the swine flu scare, and they are working hard to get the accepted as “wonder drugs” for the treatment of everything from pneumonia to Alzheimer’s disease.
However, as Dr. Stephanie Seneff, a senior scientist at MIT, explains, statins are dangerous because they suppress the synthesis of a true biological wonder drug, namely cholesterol. And she believes it is actually cholesterol (in high amounts prior to patients’ starting statin therapy) that is responsible for many of the statins’ alleged benefits:
“Statin drugs are particularly problematic because they suppress the synthesis of a biological wonder drug, namely cholesterol. Repeatedly, retrospective studies have shown an alleged benefit for statins, which is actually a benefit derived from the many years of high cholesterol that preceded statin treatment. This game has been played out for sepsis, pneumonia, multiple sclerosis, diabetes, and Alzheimer’s, and these are just the ones I’m aware of. When the proper placebo-controlled study is done, the effect reverses — statins make the situation worse. But these negative results are kept well concealed from the public’s eyes. This is how the myth has been kept alive that statins, instead of cholesterol, are the wonder drug.”
There are, in fact, 304 adverse health effects that may be associated with statin drugs, and this may only be the tip of the iceberg.

The Truth About Antiviral Flu Drugs

Anti-viral flu drugs like Tamiflu and Relenza are conventional medicine’s go-to option for treating the flu, but you should know that they carry serious side effects — and may only shorten the time you are sick by one to two days. These drugs are part of a group of anti-influenza drugs called neuraminidase inhibitors, which work by blocking a viral enzyme that helps the influenza virus to invade cells in your respiratory tract.
The problem is that your nervous system also contains neuraminidase enzymes essential for proper brain functioning, and when blocked with these dangerous drugs, severe neurotoxicity may ensue (especially in the infants and children whose blood-brain barrier has not yet developed sufficiently).
Serious side effects include convulsions, delirium or delusions, suicidal behavior and 14 deaths in children and teens have been reported as a result of neuropsychiatric problems and brain infections. Japan actually banned Tamiflu for children in 2007 because of the steep risks.
It was also around this time that the U.S. Food and Drug Administration (FDA) began reviewing reports of abnormal behavior and other brain effects in more than 1,800 children who had taken Tamiflu. Further, the drug commonly causes a myriad of side effects that, ironically, resemble the flu symptoms the drug claims to treat. You can decide for yourself whether these risks are worth a measly one- or two-day reduction in your flu symptoms:

Nausea	Vomiting
Diarrhea	Headache
Dizziness	Fatigue
Cough	Behavioral side effects (such as reports of children jumping off roofs shortly after taking the drug)

Statin Study Highlights Flu Shot Ineffectiveness

Whenever I address the topic of influenza, I like to mention flu shots, simply because the propaganda supporting them is so widespread — and the truth deserves to be heard. Not only is there a shocking lack of evidence supporting the use of the flu vaccine, but a number of studies have actually confirmed the danger and ineffectiveness of the shots.
One major study determined that the best the flu vaccine could do during a season where, in the rare case, the vaccine actually matched the wild-type strains in circulation, was to reduce the risk of influenza infection by a paltry 1 percent relative to unvaccinated controls. This means that despite receiving the shot – riddled, as it is, with side effects such as the debilitating and potentially deadly nerve disease Guillain-Barre Syndrome — there is still an overwhelming likelihood that you will not be protected from the flu as a result of receiving the vaccine.
The reason for this has to do with how flu strains work. Along with the faulty science behind the creation of the vaccine, the act of determining which flu strains will affect your area is pretty much a guessing game. Mainstream medical officials urge you to receive the shot, but health officials are fully aware that it is truly impossible to know for sure which strain to vaccinate against.
With such a wide selection of strains (hundreds, if not thousands), it is very rare for officials to actually pick the correct strains – the best case scenario is that an appropriate match will occur 10 percent of the time, according to the study. Interestingly, as it was not the researchers’ intent, the statin-flu study also highlighted the striking lack of effectiveness of the flu vaccine in preventing flu deaths:
“Our finding that vaccine was not effective in preventing mortality from influenza is likely explained by the timing of our study. We evaluated the impact of statins on influenza mortality in 2007–2008, a year in which the vaccine was not well matched to the circulating viruses … In addition, vaccination status may not impact mortality in the event of vaccine failure regardless of match to circulating strains; 50% of our patients were over the age of 70, an age group in which influenza vaccine is known to be less effective.”

Why Doesn’t the CDC Fund a Study on Vitamin D for Flu Treatment?

Apparently the CDC would rather throw money at a potential cash cow for the drug makers than promote the real natural alternatives that can stop the flu in its tracks without any side effects. Where is the CDC-sponsored study on vitamin D and the flu, for instance? According to the findings from a 2010 study that didn’t get any widespread attention, vitamin D is a highly effective way to avoid influenza. In fact, children taking low doses of vitamin D3 were shown to be 42 percent less likely to come down with the flu.
Dr. John Cannell, founder of the Vitamin D Council, was one of the first to introduce the idea that vitamin D deficiency may actually be an underlying cause of influenza, which would help explain its apparent benefits as a flu-fighter. His hypothesis was published in the journal Epidemiology and Infection in 2006, which was followed up with another study published in the Virology Journal in 2008.
Dr. Cannell’s hypothesis received further support and confirmation when, in the following year, the largest and most nationally representative study of its kind to date discovered that people with the lowest blood vitamin D levels reported having significantly more recent colds or cases of the flu. You can find my full recommendations for how to optimize your vitamin D levels in this past article.

There are Effective Natural Options for Beating the Flu

I have not caught the flu in over two decades, and you can avoid it too, without using drugs or getting vaccinated. Following these guidelines will help to keep your immune system in optimal working order so that you’re far less likely to acquire the infection to begin with — and if you do, these strategies will help you to get better, faster.

• Optimize your vitamin D levels. As I’ve previously reported, optimizing your vitamin D levels is one of the absolute best strategies for avoiding infections of ALL kinds, and vitamin D deficiency is likely the TRUE culprit behind the seasonality of the flu — not the flu virus itself. This is probably the single most important and least expensive action you can take.If you are coming down with flu-like symptoms and have not optimized your levels, you can take doses of 50,000 units a day a vitamin D3 for three days to treat the acute infection.
• Avoid sugar and processed foods. Sugar decreases the function of your immune system almost immediately, and as you likely know, a strong immune system is key to fighting off viruses and other illness. Be aware that sugar is present in foods you may not suspect, like ketchup and fruit juice.In fact, the first thing you want to do when you feel yourself coming down with a cold or flu is to avoid ALL sugars, artificial sweeteners, and processed foods.
• Get enough rest. Just like it becomes harder for you to get your daily tasks done if you’re tired, if your body is overly fatigued it will be harder for it to fight the flu. Be sure to check out my article Guide to a Good Night’s Sleep for some great tips to help you get quality rest.
• Implement effective tools to address your stress. We all face some stress every day, but if stress becomes overwhelming then your body will be less able to fight off the flu and other illness.If you feel that stress is taking a toll on your health, consider using an effective energy psychology tool such as the Emotional Freedom Technique, which is remarkably effective in relieving stress associated with all kinds of events, from work to family to trauma.
• Exercise. When you exercise, you increase your circulation and your blood flow throughout your body. The components of your immune system are also better circulated, which means your immune system has a better chance of finding an illness before it spreads. You can review my exercise guidelines for some great tips on how to get started.
• Take a good source of animal-based omega-3 fats like krill oil. Increase your intake of healthy and essential fats like the omega-3 found in krill oil, which is crucial for maintaining health. It is also vitally important to avoid damaged omega-6 oils like trans fats found in most processed foods, as it will seriously damage your immune response.
• Wash your hands. Washing your hands will decrease your likelihood of spreading a virus to your nose, mouth or other people. Be sure you don’t use antibacterial soap for this — antibacterial soaps are completely unnecessary, and they cause far more harm than good. Instead, identify a simple chemical-free soap that you can switch your family to.
• Eat garlic regularly. Garlic works like a broad-spectrum antibiotic against bacteria, virus, and protozoa in your body. And unlike with antibiotics, no resistance can be built up so it is an absolutely safe product to use. However, if you are allergic or don’t enjoy garlic it would be best to avoid as it will likely cause more harm than good.
• Avoid hospitals whenever possible. I’d recommend you stay away from hospitals unless you have an emergency, as hospitals are prime breeding grounds for infections of all kinds, and could be one of the likeliest places you could be exposed to flu bugs.

For even more details on specific immune-boosting foods and supplements that can help boost your immune function to help you kick your cold or flu faster, without drugs, please see my article The First Thing to do When a Cold or Flu Strikes.
Read the Full Article Here: http://articles.mercola.com/sites/articles/archive/2012/01/12/statin-drugs-for-flu-treatment.aspx


http://healthimpactnews.com/2012/new-ways-of-marketing-statins-cholesterol-lowering-drugs-for-the-flu/

Wisdom from The British Medical Journal blogger

BMJ's Ten Commandments for the Ideal Physician

The British Medical Journal's great blogger Richard Lehman has published the following Ten Commandments for excellent clinical practice. These are great rules of thumb for any savvy health care practitioner--but they do require that wee bit of extra work to truly understand the statistics behind the medical literature.

 

The New Therapeutics: Ten Commandments

• Thou shalt treat according to level of risk rather than level of risk factor.
• Thou shalt exercise caution when adding drugs to existing polypharmacy.
• Thou shalt consider benefits of drugs as proven only by hard endpoint studies.
• Thou shalt not bow down to surrogate endpoints, for these are but graven images.
• Thou shalt not worship Treatment Targets, for these are but the creations of Committees.
• Thou shalt apply a pinch of salt to Relative Risk Reductions, regardless of P values, for the population of their provenance may bear little relationship to thy daily clientele.
• Thou shalt honour the Numbers Needed to Treat, for therein rest the clues to patient-relevant information and to treatment costs.
• Thou shalt not see detailmen, nor covet an Educational Symposium in a luxury setting.
• Thou shalt share decisions on treatment options with the patient in the light of estimates of the individual’s likely risks and benefits.
• Honour the elderly patient, for although this is where the greatest levels of risk reside, so do the greatest hazards of many treatments.

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http://carlatpsychiatry.blogspot.com/2012/01/bmjs-ten-commandments-for-ideal.html

Why Doesn’t My Doctor Know All of This?

The following is not specifically about heart disease or cholesterol as is most of this blog content. But it does apply. Thyroid dysfunction can be tied in with heart disease if in no other way than making certain lipid abnormalities difficult or nearly impossible to normalize in the quest to reduce plaque growth. In short, I believe this is a valuable discussion of an important issue applicable to CAD.

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Why Doesn’t My Endocrinologist Know All of This?

A question often raised by patients is: “Why doesn’t my physician know about the inaccuracies and limitations of standard thyroid tests?” The reason is that the overwhelming majority of physicians (endocrinologists, internists, family practitioners, rheumatologists, etc.) do not read medical journals. When asked, most doctors will claim that they routinely read medical journals, but this has been shown not to be the case. Many reasons exist, but it comes down to the fact that doctors do not have the time — they are too busy running their practices. The overwhelming majority of physicians rely on what they have learned in medical school and on consensus statements by medical societies, such as the Endocrine Society, the American Association of Clinical Endocrinologists or the American Thyroid Association, to direct treatment decisions.

Historically, relying on a consensus statement to treat or not to treat a particular patient has been shown to result in poor care and, as such, society consensus statements and practice guidelines are considered to be worst level of evidence in support of a particular therapy or treatment. A number of organizations, including the World Health Organization and others, have ranked the strength and accuracy of various types of evidence used in the medical decision process. In all scoring systems, the highest strength of evidence is randomized control trials and meta-analyses, with lower scores for other types of evidence. All grading systems place consensus statements and expert opinion by respected authorities (societies) as the poorest level of evidence, because historically they have failed to adopt new concepts and treatments based on new knowledge or new-found understanding demonstrated in the medical literature (1-6).

For instance, a recent study published in the 2009 Journal of American Medical Association studied the evidence supporting the practice guidelines and consensus statements published by the American College of Cardiology and the American Heart Association. It was found that only 11% of the recommendations, practice guidelines and consensus statements were based on quality evidence and over half were based on poor quality evidence that was little more than the panel’s opinion. The review also found that even the strongest (Class 1) recommendations, which are considered medical dogma, cited as a legal standards and often go unquestioned as medical fact, were only supported by high quality evidence 19% of the time and not revised based on new evidence (6).

Similarly, the Endocrine Society, the American Association of Clinical Endocrinologists and the American Thyroid Association also have a long history of guidelines and recommendations that are not supported by the medical literature and fail to adjust or abandon recommendations when new understanding and knowledge contradicts their recommendations. A case in point is the recommendation by these societies that a normal TSH adequately rules out thyroid dysfunction, despite massive amounts of literature that demonstrate this not to be the case (see Diagnosis of Hypothyroidism) or that T4 only replacement is adequate for most patients. A doctor who simply follows outdated society treatment guidelines that relies on a simple laboratory test and ignores the clinical aspects of a patient is not practicing evidence-based medicine. (1-7). Such doctors may be adequate as lab technicians, but as doctors and clinicians they fall short (1-7). This method of practice is consistently rebuked as improper and poor medicine, but has become the standard used by a large percentage of endocrinologists and physicians who feel medicine can be related to simply reading “normal” or “abnormal” in a laboratory column.

Discussing the lack of scientific basis of most medical society’s consensus statements and treatment guidelines in Internal Medicine News, Dr. Diana Petritti, states, “Expert opinion and consensus statements can be quite misleading when used as the basis for a practice. Expert opinions imply that there is something that the experts know that clinician doesn’t know. I don’t think it’s always appreciated that it’s only opinion. There is a tendency to make guidelines and recommendations seem authoritative. I believe that physicians think that there is a great deal more behind authoritative recommendations than there might be when you lift the lid of the box and see what’s underneath(8).”

There has been significant concern by health care organizations and medical experts that physicians are placing too much reliance on consensus statements and failing to learn of new information presented in medical journals. Thus, they lack the ability to translate this new information into treatments for their patients. The concern is that doctors fail to practice evidence-based medicine, erroneously relying on what they have previously been taught and on “expert” societies instead of changing treatment philosophies based on new information as it becomes available. This is especially true for endocrinological conditions, where physicians are very resistant to changing old concepts of diagnosis and treatment — despite overwhelming evidence to the contrary — because it is not what they were taught in medical school and endocrinology residency.

This concern is particularly clear in an article published in the New England Journal of Medicine entitled “Clinical Research to Clinical Practice: Lost in Translation” (9). The article was written by Claude Lenfant, M.D., Director of National Heart, Lung and Blood Institute, and it is well supported. He states that there is great concern that doctors continue to rely on what they learned 20 years before and are uninformed about scientific findings. According to Dr. Lenfant, medical researchers, along with public officials and political leaders, are increasingly concerned about physicians’ inability to translate research findings in their medical practice to benefit their patients. He says that very few physicians learn about new discoveries from reading medical journals or by attending scientific conferences; thus, they lack the ability to translate new knowledge in the field into enhanced treatments for their patients. He states that a review of past medical discoveries reveals how excruciatingly slow the medical establishment is to adopt novel concepts, noting that even simple methods to improve medical quality are often met with fierce resistance. “Given the ever-growing sophistication of our scientific knowledge and the additional new discoveries that are likely in the future, many of us harbor an uneasy, but quite realistic suspicion that this gap between what we know about disease and what we do to prevent and treat them will become even wider. And it is not just recent research results that are not finding their way into clinical practice; there is plenty of evidence that ‘old’ research outcome have been lost in translation as well (1).”

Dr. Lenfant discusses the fact that the proper practice of medicine involves the combination of medical knowledge, intuition and judgment and that physicians’ knowledge is lacking because they don’t keep up with the medical literature. He states that there is often a difference of opinion among physicians and reviewing entities, but that judgment and knowledge of the research pertaining to the patient’s condition is central to the responsible practice of medicine. “Enormous amounts of new knowledge are barreling down the information highway, but they are not arriving at the doorsteps of our patients. (9).”

These thoughts are echoed by physicians who have researched this issue as well, such as William Shankle, M.D., Professor, University of California, Irvine. He states, “Most doctors are practicing 10 to 20 years behind the available medical literature and continue to practice what they learned in medical school….There is a breakdown in the transfer of information from the research to the overwhelming majority of practicing physicians. Doctors do not seek to implement new treatments that are supported in the literature or change treatments that are not (10).”

This view is echoed by the Dean of Stanford University School of Medicine who states that in the absence of translational medicine the delivery of medical care would remain stagnant and uninformed by the tremendous progress taking place in science and medicine (11).

This concern has also received significant publicity in the mainstream media. An example is an article by Sidney Smith, M.D., former president of the American Heart Association, published in 2003 in the Wall Street Journal entitled Too Many Patients Never Reap the Benefits of Great Research. Dr. Smith is very critical of physicians for not seeking out available information and applying that information to their patients, arguing that doctors feel the best medicine is what they’ve been doing and thinking for years. They discount new research, Dr. Smith says, because it is not what they have been taught or practiced, and they refuse to admit that what they have been doing or thinking for many years is not the best medicine. He states, “A large part of the problem is the real resistance of physicians…; many of these independent-minded souls don’t like being told that science knows best, and the way they’ve always done things is second-rate (12).” The National Center for Policy Analysis also expresses concern for the lack of ability of physicians to translate medical therapies into practice (13).

A review published in The Annals of Internal Medicine found that there is clearly a problem of physicians not seeking to advance their knowledge by reviewing the current literature, believing proper care is what they learned in medical school or residency and not basing their treatments on the most current research. The review found that the longer a physician is in practice, the more inappropriate and substandard the care (14). Thus, it is not a surprise that the scientific evidence as expressed in the literature is often opposite to what is continually repeated as dogma by most physicians and those considered to be “experts.”

Another example is a study published in the Journal of the American Medical Informatics Association (15). In reviewing the study, the National Institute of Medicine reports that there is an unacceptable lag between the discovery of new treatment modalities and their acceptance into routine care: “The lag between the discovery of more effective forms of treatment and their incorporation into routine patient care averages 17 years.” (16) In response to this unacceptable lag, the Business and Professions Code passed an amendment relating to the healing arts. This amendment — CA Assembly Bill 592; An Act to Amend Section 2234.1 of the Business and Professions Code — states: Since the National Institute of Medicine has reported that it can take up to 17 years for a new best practice to reach the average physician and surgeon, it is prudent to give attention to new developments not only in general medical care but in the actual treatment of specific diseases, particularly those that are not yet broadly recognized [such as the concept of tissue hypothyroidism, chronic fatigue syndrome and fibromyalgia] (17).

The Principals of Medical Ethics adopted by the American Medical Association in 1980 states that a physician shall continue to study, apply, and advance scientific knowledge, make relevant information available to patients, colleagues, and the public (18). This has, unfortunately, been replaced with a goal of providing merely “adequate” care. The current insurance reimbursement system in the United States fosters this thinking, as the worst physicians are financially rewarded by insurance companies. While it is true that the best physicians are continually fighting to provide cutting edge treatments and superior care that the insurance companies deem not medically necessary, even these physicians eventually get worn down and are forced to capitulate to the current system that promotes substandard care.

This was clearly demonstrated in a study published in the March 2006 edition of The New England Journal of Medicine entitled “Who is at Greater Risk for Receiving Poor-Quality Health Care.” The study found that the majority of individuals received substandard, poor-quality care, and that there was no significant difference among different income levels or whether or not the individual was covered by insurance. It used to be the case that only those in low socioeconomic classes without insurance received poor-quality care. But insurance company restrictions on treatments and diagnostic procedures have made the same poor care afforded to those of low socioeconomic status the new standard-of-care for society at large (19). An example of this is a physician’s failing to spend the time to adequately assess a potential hypothyroid patient and instead simply does a TSH test.

Most physicians will satisfy their required amount of continuing medical education (CME) by going to a conference a year, usually at a highly desirable location that has skiing, golf, boating, etc. Physicians are rarely monitored as to whether or not they actually showed up for the lectures or went skiing instead. One must also understand that the majority of conferences organized by medical societies are in fact sponsored by pharmaceutical companies. These payments by pharmaceutical companies are called unrestricted grants, so that the society has free reign to do what they want with the money and thus can claim there is no influence of lecture content by the companies. The problem, however, is that if the society wants to continue getting these “unrestricted” grants, they must think twice about providing content that the sponsoring pharmaceutical company might disapprove of. Consequently, ground breaking research that goes against the status quo and does not support the drug industry receives little attention.

Evidence-based medicine involves the synthesis of all available data when comparing therapeutic options for patients. Evidence-based medicine does not mean that data should be ignored until a randomized control trial of a particular size and duration is completed. A physician who tries to avoid the need of being a physician and is fine with just being a technician or health care provider will adamantly defend the “one-size fits all” method of diagnosis and treatment. But the best doctors who truly practice evidence-based medicine and not merely the perception of such will not rely on consensus statements to best provide their patients. Instead of relying on old dogma, the best physicians will seek out and translate both basic science results and clinical outcomes to decide on the safest, most efficacious treatment for their patients. Further, the best physicians will continually assess the current available data to decide which therapies are likely to carry the greatest benefits for patients and involve the lowest risks.

http://nahypothyroidism.org/why-doesn%E2%80%99t-my-doctor-know-all-of-this/

From: Oxford University Press Quarterly Journal of Medicine.
http://qjmed.oxfordjournals.org/content/early/2010/11/29/qjmed.hcq230.full

Statin-induced diabetes: perhaps, it’s the tip of the iceberg

The meta-analysis by Mills et al.¹ involving 170 255 patients randomized in 76 trials reported on the efficacy and safety of statin therapy for the prevention of cardiovascular disease (CVD) and found a relative 9% increased risk in the development of incident diabetes (P = 0.001) among subjects randomized to statins compared with placebo in the 17 trials reporting on diabetes development. It is noteworthy that the average age of the subjects in the meta-analysis was 59.6 years, average follow-up was 2.7 years and more than half of the subjects were randomized for the primary prevention of CVD. We feel that the implications of statin-induced diabetes are not trivial, but of major concern, particularly in the primary prevention of CVD when statin therapy might be used for decades in individuals at relatively low risk²; many questions need answering before statin therapy can be safely recommended across broad populations.

Interestingly, a recently published meta-analysis involving 91 140 patients randomized in 13 trials³ specifically looking at the risk of incident diabetes from statin therapy also revealed a significant 9% increased relative risk of the development of diabetes over a mean overall trial period of 4 years. Disturbingly, 2 of the 13 trials demonstrated very high incidence of the development of diabetes among the statin-treated subjects. The Justification for the Use of Statins in Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER),⁴ a primary prevention trial of 1.9-year duration in subjects with a mean age of 66 years, demonstrated a significant relative increase in diabetes incidence of 26% among subjects randomized to rosuvastatin; the absolute rate of incident diabetes expressed in events per 1000 patient-years was 13 and 16 among the placebo and rosuvastatin subjects, respectively. Low-density lipoprotein (LDL) cholesterol was decreased robustly by 50% in the rosuvastatin subjects and the median LDL cholesterol at the end of follow-up was 55 mg/dl. The PROspective Study of Pravastatin in the Elderly at Risk (PROSPER),⁵ a combined primary and secondary prevention trial of 3.2-year duration in subjects with a mean age of 76 years, demonstrated a significant relative increase in diabetes incidence of 32% among subjects randomized to pravastatin; the absolute rate of incident diabetes expressed in events per 1000 patient-years was 16 and 21 among the placebo and pravastatin subjects, respectively. LDL cholesterol was decreased by 31% in the pravastatin subjects. Therefore, it appears that the risk of statin-induced diabetes is more prominent with aggressive LDL cholesterol lowering and among the elderly subjects. It is of concern that thought leaders in the cardiovascular arena strongly suggest that statin use should be increased from 16 to 100 million people in the USA and LDL cholesterol should be aggressively lowered.⁶ This issue takes even more relevance given that the prevalence of diabetes is rapidly increasing in the USA⁷ and worldwide⁸; alarmingly, three-quarters of the elderly in the USA have diabetes or pre-diabetes.⁷

In vivo studies have demonstrated that despite lowering LDL cholesterol levels, some^9–11 but not all statins¹¹ significantly increase fasting plasma insulin levels and significantly decrease insulin sensitivity in hypercholesterolemic patients in a dose-dependent manner. Statins can significantly increase fasting plasma insulin levels and glycated hemoglobin levels in the absence of significant changes in fasting glucose.^9–11 Additionally, some statins have been shown to significantly decrease plasma adiponectin levels.^10,11

In vitro and animal studies^12,13 have shown that statins can significantly decrease the expression of the insulin-responsive glucose transporter 4 (GLUT4) in adipocytes. GLUT4 is distributed in the intracellular compartment in the basal state and relocates to the cell membrane in response to insulin signaling. Moreover, statins increase the expression of GLUT1¹² in adipocytes; GLUT1 is localized in the cell membrane. It is unclear how statins change the expression of GLUT1 and GLUT4; perhaps, it is related to an inhibition of isoprenoid biosynthesis by statins¹² or cholesterol lowering, leading to a change in membrane lipid raft structure resulting in decreased insulin signaling.¹⁴ Since GLUT4 concentrations are not reduced in skeletal muscle in obese subjects and subjects with diabetes, and skeletal muscle is the primary source of insulin-stimulated glucose disposal, it has been argued that whole-body insulin sensitivity cannot be explained by a decrease in the production of GLUT4¹⁵; however, it has been shown that the downregulation of GLUT4 and resulting glucose transport in adipose tissue can cause insulin resistance.¹⁶ It is notable that GLUT4 concentrations are decreased in skeletal muscle in elderly compared with younger subjects,¹⁵ which might explain why the elderly are more sensitive to the diabetes promoting effects of statin therapy. Furthermore, dysregulation of cellular cholesterol may attenuate pancreatic β-cell function, since cholesterol maintains normal function of voltage gated calcium channels and is vital in the mobilization and fusion of insulin granules with the cell membrane.¹⁷ In summation, there are many ways by which statin therapy might lead to hyperinsulinemia, insulin resistance, prediabetes and diabetes.

In addition to the classic complications of diabetes such as CVD, renal failure, blindness and neuropathy, epidemiological studies demonstrate that diabetes is related to the increased risk of many cancers.¹⁸ These include liver, pancreas, kidney, endometrial, colorectal, bladder and breast cancer and non-Hodgkin’s lymphoma. A large European population study with a median follow-up of 15.8 years has shown that compared with individuals with normal glucose tolerance, men and women with prediabetes or diabetes had a significant increase in cancer mortality, irrespective of the body mass index.¹⁹ There is epidemiological evidence that insulin resistance is associated with cancer in Eastern populations.²⁰ Interestingly visceral fat mass, assessed by computed tomography, but not subcutaneous fat mass, correlates positively with cancer²¹; indeed, visceral fat is a strong determinant of insulin resistance and hyperinsulinemia.

There are many ways by which hyperinsulinemia can promote cancer.^18,22 Hyperinsulinemia results in an increase in the biologically active free circulating insulin-like growth factor-1 (IGF-1) by increasing hepatic IGF-1 production²² and decreasing IGF-1 binding proteins.¹⁸ Tumor cells are replete with IGF-1 receptors and two isoforms of insulin receptors (IR-A and IR-B).²³ IGF-1 primarily signals through the IGF-1 receptor resulting in mitogenic effects and, not surprisingly, higher IGF-1 blood levels have been associated with an increased risk of several cancers.^24,25 Insulin signaling through the IR-A and IR-B results in mitogenic and metabolic effects, respectively.²² Hyperinsulinemia can persist for decades in prediabetic states and it is certainly conceivable that this prolonged mitogenic stimulus increases cancer promotion as has been seen in epidemiological studies.

Statin therapy might affect tumor metabolism by insulin independent means. As previously mentioned, some statins decrease adiponectin levels.^10,11 This is potentially problematic over the long-term since adiponectin is anti-proliferative and anti-angiogenic and has other oncostatic properties.²⁶ Furthermore, obesity is associated with lower circulating adiponectin levels and this might partially explain the association of obesity and various cancers. Additionally, the fact that statin therapy might increase GLUT1 expression¹² is of concern since GLUT1 is already overexpressed and is the main glucose transporter in cancer cells.²⁷ Glucose uptake by cancer cells is extremely avid and up to 30 times that of normal cells and utilized by glycolysis for energy and supplying important metabolites for rapid cellular proliferation.²⁸ Indeed, in human studies, increased expression of GLUT1 in cancer cells has been associated with poor prognosis of many cancers.^27,29

The Western diet is permissive to the diabetogenic effects of statin therapy. The prevalence of obesity has been steadily increasing in the USA and more than two-thirds of adults are overweight or obese.³⁰ As mentioned, the prevalence of diabetes has been increasing in the USA and a majority of the elderly subjects in the USA now have pre-diabetes or diabetes.⁷ Interestingly, total cholesterol and LDL cholesterol have been decreasing in the USA likely due to cholesterol awareness and the increased use of lipid-lowering medication, and more than half of the elderly subjects in the USA have reported using lipid-lowering medications.³¹ However, blood triglyceride levels have been steadily increasing despite the increasing use of lipid-lowering therapy.³¹ Intriguingly, it is now believed that abnormalities in fatty acid metabolism are at the root of diabetes, and ectopic lipid accumulation in muscle, liver and pancreatic β-cells leads to the development of insulin resistance by interfering with insulin signaling.^32,33 The increase in blood triglyceride levels is driven by a high carbohydrate diet and partially fueled by the increase in dietary sweetener consumption.³⁴ Unfortunately, fructose consumption, largely from sweetened beverages, has escalated drastically in North America over the past three decades³⁵ and excessive fructose intake leads to increased hepatic de novo lipogenesis resulting in hepatic steatosis, visceral fat accumulation and ectopic lipid deposition in skeletal muscle, thereby all leading to insulin resistance.

We are living in times when there seems to be a much stronger emphasis on the use of drugs over lifestyle change to prevent disease. The food industry has been uncooperative and blames personal responsibility as a cause of the obesity problem.³⁶ There is a belief among many patients that they can eat whatever they want as long as they are on statin therapy.³⁷ This has been amplified by a proposal to offer powdered statin in packets to be sprinkled on hamburgers at fast-food restaurants in order to neutralize the detrimental effect of the food choice.³⁸ Plant-based diets have been shown to decrease both CVD and cancer risk and even result in a rapid change in gene expression in neoplastic tissue, and they are not diabetogenic.^39–41 Moreover, a Mediterranean diet has been shown to counter the insulin raising effects of simvastatin therapy.⁴² It is extremely troubling that a goal has been proposed for decreasing the LDL cholesterol levels of all subjects worldwide to below 100 mg/dl and ideally below 60 mg/dl by statin therapy.⁴³

In conclusion, many important questions need answering before expanding the use of statin therapy, particularly for the primary prevention of CVD. In what proportion of subjects do statins increase plasma insulin levels, even if there is no progression to diabetes? Are some statins more likely than others to cause hyperinsulinemia because of physiochemical differences? Will prolonged statin therapy result in chronic hyperinsulinemia and potentially increase prediabetes, diabetes and/or cancer? Will this risk outweigh any perceived benefits, particularly in the elderly or in aggressively treated patients? Will the Western diet and lifestyle encourage the use of more statin therapy and provide a metabolic substrate to further perpetuate hyperinsulinemia and its subsequent complications? Is the increase in diabetes prevalence in the elderly subjects fueled partially by the increasing use of statins in this age group? What statins decrease blood adiponectin levels, and is it continuous, and, if so, what are the long-term clinical implications? How should physicians monitor patients for the adverse metabolic effects of statin therapy? Should subjects have a plasma insulin level measured prior to initiating and during statin therapy? What diet or diets will mitigate the hyperinsulinemic effects of statin therapy? Will statin therapy used by subjects with a history of cancer increase the chance of hyperinsulinemia increasing the promotion of occult micrometastatic disease? Finally, physicians should realize that statin-induced diabetes, as seen in the relatively short-term clinical trials, might be just the tip of the iceberg, and properly designed clinical trials must be done to determine what else lurks beneath the water in order to ensure the safety of patients on long-term treatment with these drugs.

• © The Author 2010. Published by Oxford University Press on behalf of the Association of Physicians. All rights reserved. For Permissions, please email: journals.permissions@oup.com

Busted! Scientists leave out data to produce bogus findings

Clinical trials of drugs and other medical therapies are carefully carried out and are the very gold standard of scientific proof, right? According to an in-depth review of this question just published in the British Medical Journal (BMJ,) the answer is no. In fact, the BMJ is sounding the alarm that data reported by scientists is too often not the truth -- because the researchers leave out inconvenient evidence. The result of facts-gone-missing could well be harming patients, spiking up healthcare costs by the selling of medical treatments based on bogus findings, and threatening the very integrity of medicine.

These warnings come from multiple papers released by the BMJ. The whistle-blowing authors of these articles examined the extent, causes, consequences of hidden facts, figures, and other data scientists discover as they do human trials. It turns out this is no "once in a while" kind of problem, either. The BMJ claims a "large proportion of evidence from human trials is unreported, and much of what is reported is done so inadequately."

In an editorial, Dr. Richard Lehman from the University of Oxford and BMJ Clinical Epidemiology Editor, Dr. Elizabeth Loder, nail the current state of medical research as a "culture of haphazard publication and incomplete data disclosure." They call for full access to raw trial data to allow better understanding of the benefits and harms of many treatments.

Bottom line: when data is left out, the missing facts distort the scientific record and published results of a study. This then leads doctors to make potentially dangerous clinical decisions about what drugs or procedures patients need because the docs are relying on skewed and even bogus "evidence."

Conveniently missing facts left out of drug trials and more

Papers in the current issue of BMJ include a study by Dr. Beth Hart and colleagues, which document how unpublished data is "conveniently missing" from many published meta-analyses of drug trials. That's right. Big Pharma's pills and potions are often pushed based on studies that simply ignore and leave out major data about what was really discovered about a medication lacking of benefits, potential dangers, side effects and more. Dr. Hart's team argues that access to full trial data is necessary to allow drugs to be independently assessed.

Two additional studies show the requirements for mandatory trial registration and timely sharing of results are poorly followed, if at all. For example, it turns out that less than half of US National Institutes of Health funded trials are published in a peer reviewed journal within 30 months of completion and only 22 percent of trials that are supposed to be subject to mandatory reporting had results available within one year of completion.

"When the word mandatory turns out to mandate so little, the need for stronger mechanisms of enforcement becomes very clear," the researchers report.

And what happens when ethical, dedicated scientists try to assess true harms vs benefits of Big Pharma drugs and other interventions? It's not a pretty picture for their careers, apparently. Additional studies published in the special BMJ issue highlight the many difficulties these researchers face when they try to buck the system.

Dr. Lehman and Dr. Loder, however, are bravely speaking out and directly saying that a concealment of data in clinical trials is anything but unusual. They label this "a serious ethical breach" and demand that clinical researchers who fail to disclose data "should be subject to disciplinary action by professional organizations. These changes have long been called for, and delay has already caused harm. The evidence we publish shows that the current situation is a disservice to research participants, patients, health systems, and the whole endeavor of clinical medicine."

For more information:

http://www.bmj.com/

http://www.naturalnews.com/medical_errors.html

Learn more: http://www.naturalnews.com/034577_quack_science_clinical_trials_BMJ.html#ixzz1iaunAKmd

300+ Health Problems Linked To Statin Drugs

Consumer Alert: 300+ Health Problems Linked To Statin Drugs

Post date:

Mon, January 2nd 2012 at 7:15 pm by Sayer Ji

A growing body of clinical research now indicates that the cholesterol-lowering class of drugs known as statins, are associated with over 300 adverse health effects -- research boldly flying in the face of national health policy, medical insurance premium guidelines, statin drug manufacturer advertising claims, and the general sentiment of the public, with approximately 1 in every 4 adult Americans over 45 currently using these drugs to "prevent heart disease."
The Cholesterol Myth
For well over 40 years, statin drugs have successfully concretized a century old myth about the primary cause of heart disease: namely, that cholesterol "causes" plaque build up in the arteries, ultimately leading to obstruction of blood flow, and subsequent morbidity and mortality.
Indeed, the medical establishment and drug companies have been singing the praises of this "cholesterol myth," to the tune of 25 billion dollars in statin drug sales, annually.
While it is true that oxidized low-density lipoprotein is found within the atheromatous plaque that is found in damaged arteries, it is less likely a cause than an effect of heart disease. The underlying damage to the lining of the artery, which could be infectious, chemical, stress and/or nutritionally-related, comes before the immune response that results in plaque buildup there. Blaming LDL cholesterol for causing heart disease, is like blaming the scab for the injury that caused it to form, or, like blaming the band-aid for the scab it is covering -- this is, after all, the inborn and fatal flaw of allopathic medicine which focuses only on symptoms of disease, which it then -- fool-heartedly -- attempts to suppress by any chemical means necessary.

Death By Statins?

No one can deny that statins do exactly what they are designed to do: suppress cholesterol production and reduce measurable blood serum levels. The question is, rather, at what price do they accomplish this feat, and for what ultimate purpose?
With the National Cholesterol Education Program Guidelines, having been designed by "experts" on the payroll of statin drug manufacturers, requiring ultra-low levels to obtain a strictly theoretical and numerical definition of "health," statin drugs are guaranteed to receive first-line treatment status in the goal of the preventing and treating heart disease through lipid suppression.
What is at question here, is whether the unintended, adverse effects of this chemical class of drugs are less, the same or worse than the purported "cardiovascular" benefits they provide?
Fundamentally, statin drugs damage the muscles and nerves in the body -- so much so that a dose as low as 5 mg a day can kill a human. There are well over 100 studies demonstrating the myotoxic, or muscle-harming effects of these drugs, and over 80 demonstrating the nerve-damaging effects, as well. When you consider that a vast proportion of our body is comprised of muscles and coordinating nerve systems, this drug has the potential to cause damage to the entire body, and undoubtedly does so universally, differing only in the matter of degree -- the damage occurring acutely in those at the tip of the iceberg, asymptomatically in the majority of others at the base.
Moreover, statin myotoxicity is not exclusive to skeletal muscle. If you consider that the heart is also a muscle, in fact, is our most tireless muscle, an obvious red flag should go up. It is a remarkable fact that it took over 40 years before the biomedical research and publishing fields were able to produce a human study, like the one published in the Journal of Clinical Cardiology in Dec. 2009, showing that statin drugs, despite billions of advertising/marketing dollars to the contrary, actually weaken the heart muscle.
These results, while disturbing, are to be expected given the well-known problem associated with statin drug use, namely, the inhibition of the mevalonate pathway necessary to produce the heart-essential nutrient coenzyme Q10. Coenzyme Q10 deficiency itself may be a major contributing cause to heart disease. There is also research that statin drugs deplete the body of the cardioprotective minerals (and associated mineral-protein complexes) zinc and selenium. This finding may also explain why rates of heart failure may be increasing in the general population given these drugs.
While the discovery that statin drugs, instead of preventing heart disease, likely contribute to it, is surprising and counterintuitive, it should not distract from the more disturbing discovery that they contribute to over 300 disease and/or adverse health effects.
Millions of statin drugs users around the globe are risking their lives on a bad bet that taking a magic chemical pill will reduce their risk of dying of a disease that is not caused by a lack of the drug. What is more likely to happen, however, is that the quality and duration of their lives will be reduced, profoundly, along with billions of dollars of squandered cash that could have been spent on authentically medicinal and cardioprotective foods, nutrients, minerals and vitamins.
In light of these findings, a very serious question is raised: are those who are party to the manufacture, promotion, administration and/or prescribing of this chemical class of drugs, in violation of the medical ethical principle of informed consent? And is this ethical violation, insofar as it results in injury to those who have been mislead and/or coerced to take these drugs, also a legal/criminal one?

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http://www.greenmedinfo.com/blog/consumer-alert-300-health-problems-linked-statin-drugs

Niacin and Cholesterol - AIM-HIGH study analysis by Jon Barron

Heart Disease Prevention | Heart Health Newsletter

Date: 11/28/2011 Written by: Jon Barron © 1999-2011 The Baseline of Health Foundation

Niacin and Cholesterol

I recently commented that I could easily spend my entire life doing nothing but responding to silly studies "disproving" natural remedies. And in fact, the last three newsletters have done just that. Unfortunately, we now have to make it four in a row, as we turn to a study on niacin and cholesterol. But this one has a curious difference. Unlike virtually every other study that concludes that natural remedies are useless, this one went virtually unreported by the mainstream media. And yes, I'm sure conspiracy theorists will see some nefarious plot to damage alternative medicine in this non-reporting, but in fact, non-reporting, in this case, runs counter to that agenda. That argument would make sense if the study concluded that niacin actually prevented heart disease -- and the establishment was trying to suppress that information. But, in fact, it came to the exact opposite conclusion, that niacin did not reduce heart attacks and strokes -- so why wasn't that trumpeted from the rafters?
In truth, I think the answer is far more banal than conspiracy. I think the news services didn't pick it up because they found it boring. Just like a story about Tiger Woods would make headlines around the world, but a story about Andy Matthews (number 999 in the Official World Golf Rankings1) would not; stories about the ineffectiveness of vitamin E and A and C make the news, whereas one on niacin does not. As far as the media is concerned, when it comes to stories about vitamins, niacin is on the D-List.
But in this case, the mainstream missed a huge story. Yes, the conclusion that niacin doesn't help prevent heart attacks and strokes is correct, but that's not the real story. In truth, if you actually understand what the study is really proving, it rips the facade off one of the biggest medical rackets in the world -- one that bilks gullible consumers out of billions and billions of dollars each and every year, for almost no benefit. And yes, we're talking about statin drugs. Now that's a headline worth running!
With that in mind, let's take a look at the actual study. Then we can peak behind the curtain and see what the researchers missed.

Niacin, Cholesterol, and Heart Disease

As the study itself says, more than 18 million North Americans have coronary heart disease, and despite the use of drugs and surgical intervention, both the levels of heart disease and death remain high.2 Despite all the talk of cancer, heart disease is still a big deal -- still the leading cause of death in the US, North America, and the world. And according to the medical community, elevated levels of LDL cholesterol are a primary predictor of coronary heart disease. And also, according to the researchers, a number of trials have shown a significant reduction of 25 to 35% in the risk of cardiovascular "events" when statin therapy is used. As we will discuss a bit later, this doesn't necessarily mean what everyone thinks it means, but we'll discuss that in detail a bit later. In any event, the reason for the study was to find out if adding extended-release niacin to a statin drug regimen that was already controlling cholesterol and triglyceride levels could provide an incremental benefit. As such, this study did not include a test of the ability of niacin alone to help in this regard, but merely whether or not using niacin in combination with an already implemented statin drug routine provided any additional benefit.
The trial, known as AIM-HIGH, followed more than 3,414 patients with cardiovascular disease who had used statin drugs to lower their LDL cholesterol. They then received either a high dose (1,500-2,000 mg) of extended-release niacin (Niaspan) along with their statin drug, or a placebo along with their statin drug for 32 months, at which point the trial was stopped. While the niacin-statin combination therapy increased HDL ("good") cholesterol and lowered the amount of fat in the blood better than the use of a statin-only regimen, it didn't reduce the number of heart attacks, strokes, or hospitalizations for certain other heart problems. And, in fact, according to the study, it actually slightly increased the risk of stroke. In other words, although the addition of niacin further reduced over cholesterol levels, reduced triglycerides, and improved the HDL to LDL ratio in the subjects' blood, that didn't translate into any perceivable health benefit. Interesting, yes?
As a result, the National Institutes of Health's National Heart, Lung, and Blood Institute (NHLBI), which funded the research, stopped the study more than a year early. In an accompanying NEJM editorial, Dr. Robert Giugliano of Brigham and Women's Hospital in Boston, suggested that, based on the results, it might be time to "retire" niacin, used as a cholesterol reducer since 19553 -- even making the suggestion part of the article's title, "Niacin at 56 Years of Age -- Time for an Early Retirement?"

"Given the lack of efficacy in this trial … and the unresolved question of an increased risk of ischemic stroke, one can hardly justify the continued expenditure of $800 million per year in the United States for branded extended-release niacin."

In any event, this conclusion seems a bit premature since prior research has shown significant niacin-associated declines in the rates of death, heart attacks and strokes -- but when used differently. All this study shows is that although niacin still demonstrates an ability to improve cholesterol numbers when used as a statin adjuvant, that improvement doesn't translate into improved outcomes. But it doesn't nullify the use of niacin without statins. Nor does it make clear whether the problem lies with the niacin, the statin drugs, or the cholesterol theory of heart disease itself. We'll return to this concept a bit later.

Medical comment on the study

On the positive side, after two years of using the niacin, HDL and triglyceride levels improved markedly in the niacin group, with a 25 percent increase in good cholesterol, a 29 percent drop in triglycerides and a further decrease (beyond what the statin drugs had achieved on their own) in bad cholesterol of approximately 12 percent. By contrast, in the placebo group, there was minimal change, with a 10 percent increase in good cholesterol and an 8 percent drop in triglycerides. Based on all assumptions the medical community makes based on the cholesterol theory of heart disease, this should have produced improved outcomes in patients with heart disease. The question Dr. Giugliano should have been asking is not whether or not niacin should be retired but whether or not the cholesterol theory of heart disease should be retired. As the theory goes, the lower your overall cholesterol level, the better your HDL to LDL ratio, and the lower your triglyceride levels, the better your heart outcomes should be. Unfortunately, the theory was not supported by the results. Instead, the trial found, contrary to theory, that the further lowering of "numbers" produced by niacin did not further reduce the risk of cardiovascular events, including heart attacks and stroke… at all. And in fact, this lack of benefit led the National Heart, Lung and Blood Institute, upon the recommendation of its Data Safety Monitoring Committee, to decide to stop the trial 18 months before its planned completion.
The bottom line is that niacin did exactly what it was supposed to. The theory, however, did not. Instead of questioning the theory itself, the researchers instead opted to throw out the supplement that exposed its deficiencies.
Of course, some doctors did point out that this study actually only applies to a limited number of patients. If you are among the majority of patients seen in routine clinical settings, where more than 80 percent are unable to lower their cholesterol levels through statin drugs alone as seen in the study, then niacin might still play a role in your treatment. In other words, the AIM-HIGH only applies to a narrowly defined patient population.
In the end, Dr. William Boden, lead researcher for the study, made a profound leap of faith, and pronounced that the most relevant observation that could be made from the study is that "in this modern era of statin therapy, we've made profound progress in controlling LDL."
Well hooray for statin drugs and bad on natural substances such as niacin.

Deconstructing the myth -- Part 1, HDL/LDL

The medical literature says that LDL cholesterol is bad and that HDL is good. In fact, the relationship is not quite that simple. The basis for understanding low density lipoprotein (LDL) cholesterol came from Nobel Prize winning research conducted in the 1970's and 80's. It clarified the genetic basis behind the inability of some people to remove LDL from their blood. Subsequently, research began to note that effects of LDL cholesterol were somewhat balanced out by levels of high density lipoprotein (HDL) cholesterol in the body. Studies indicated that high HDL correlates with low heart attack numbers. In fact, the primary study that pointed to the benefits of high HDL was the Coronary Drug Project of 1965-1974,4 which examined the effects of niacin on cholesterol levels. It probably should be noted that over a quarter century later, niacin is still the most effective FDA approved means of raising HDL-cholesterol. Then again, niacin also lowers LDL-cholesterol and triglycerides, which meant that it was unclear whether niacin's benefits come from its ability to raise HDL or lower LDL.
In any event, the AIM-HIGH study was designed to make that determination -- sort of. Because of its design, it couldn't determine whether or not niacin alone was beneficial. Nor could it determine whether niacin and statin drugs together were more beneficial than statin drugs alone in people who were "newly" diagnosed with high cholesterol. Its design only allowed it to determine whether or not "adding" niacin to a statin regimen that was already lowering LDL cholesterol provided any benefit. And within those tightly defined parameters, the study was able to conclude that although adding niacin to an already effective regimen of statin drugs improved cholesterol "numbers", it did not seem to provide any actual added health benefit. But is that a knock on niacin, since it did indeed improve the blood serum profile as promised, or a knock on the cholesterol theory of heart disease, since the theory did not perform as expected given the significantly improved cholesterol and triglyceride numbers?

Deconstructing the myth -- Part 2, statin drugs save lives

Statin drugs are considered one of the great achievements of modern medicine -- credited with saving millions of lives. And, encouraged by the pharmaceutical industry, the FDA has regularly lowered the numbers for acceptable cholesterol levels, thus continually expanding the market for these drugs -- not to mention recommendations from pediatric community to lower the age of prospective users to as young as eight.5 It has been joked by some in the medical community that we should just add statin drugs to the water supply and be done with it. (And on a different note, that is already happening to some degree.)
But do statin drugs deserve such adulation?
In truth, studies have indeed confirmed that the use of statin drugs reduces coronary heart disease "incidents" such as heart attack and stroke in populations that use them; and you would think that might settle the issue. But it doesn't! It turns out that medical researchers may have been asking the wrong question.
What is the right question?
Quite simply: do statin drugs help you live longer; do they increase your life expectancy; does the reduced incidence of coronary heart disease "events" add even one single day of life to those who use the drugs? And surprisingly, the answer to this question appears to be a resounding "no"!
Yes, the drugs do in fact lower LDL cholesterol levels. Unfortunately, research shows that lowering cholesterol usually doesn't necessarily lower heart-attack risk. According to a number of studies, patients on statin drugs reap no measurable extension of life unless they had a previous heart attack before taking the drugs.6,7,8,9 And in fact, this is the big news in today's study. Not that niacin doesn't work, because it did. It did exactly what it was supposed to do. It improved cholesterol and triglyceride numbers. The problem is that once again, the cholesterol theory of heart disease failed to perform as advertised. This is the story the mainstream media missed in not reporting the study.
In fact, the claims of success touted in ads for statin drugs are downright misleading -- even the ones that merely talk about reduced incidents. One printed advertisement reads, "Lipitor reduces the risk of heart attack by 36%...in patients with multiple risk factors for heart disease." An asterisk at the bottom includes tiny print that notes that "....in a large clinical study, 3% of patients taking a sugar pill or placebo had a heart attack compared to 2% of patients taking Lipitor." This means that for every 100 people, three who don't take Lipitor will have heart attacks; while two who do take it will have heart attacks anyway. In other words, Lipitor prevents only one heart attack per 100 users.
And yet, the FDA and the medical community keep finding ways to lower the bar and shuttle more and more patients into statin prescriptions, tripling the numbers of users since 2001.

Deconstructing the myth -- Part 3, the entire cholesterol theory of heart disease

I have addressed the cholesterol myth in other newsletters and don't need to repeat the arguments here, other than to summarize the key points.

• The evidence that connects cholesterol to heart disease is contradictory at best.
• Cholesterol is present in both arteries and veins, and yet veins don't harden and clog up -- only arteries. If cholesterol is the problem, why not?
• Statin drugs do lower cholesterol levels, but they don't add one single day to your life unless you've had a previous heart attack. Again, if cholesterol is the problem, why not? As it stands, this runs totally counter to the theory of cholesterol induced heart disease.
• Niacin too lowers LDL cholesterol and raises HDL cholesterol, but it also does not seem to extend your life by one single day -- again running counter to the theory of cholesterol induced heart disease.

Keep in mind, the cholesterol theory of heart disease is called into question, not just by me, but by many in the medical community. There is no evidence that forcing cholesterol levels down using drugs adds one single day to your life…unless you've had a previous heart attack. Statin drugs have serious side effects -- including liver damage. And keep in mind, the liver is the organ in your body that actually regulates cholesterol levels in your body. How smart can it be to take a drug to regulates cholesterol by further damaging the organ responsible for regulating cholesterol in the first place?
So, what do we make of this? What connects all the pieces together -- that explains why statin drugs "work" but don't "help"?
In fact, it appears inflammation is the thread that ties everything together. Inflammation damages the walls of the arteries -- but not the veins -- forcing the body to "repair" the damage using cholesterol-based, cement-like plaque to patch over the problem areas. Over time, with continued inflammation and continued repairs, the patches start thickening, hardening, and narrowing the arteries. Statin drugs work, then, not because they lower cholesterol, but because they reduce arterial inflammation. As it turns out, statin drugs suppress T-cell activation and inhibit the release of inflammatory cytokines that are critical mediators of the inflammation response.10,11,12 Statin drugs also help lower C-reactive protein levels -- a known inflammation marker and independent risk factor in the development of ischemic stroke -- again, entirely separate from their effect on serum cholesterol.13,14,15
In the end, cholesterol is blamed, not because it actually harms you, but because, as a key component of arterial plaque, it is found at the scene of the crime.

Conclusion

Which brings us to the final question of the day. Why would you want to use pharmaceutical drugs (statins), whose primary effect (lowering cholesterol), looks to be of virtually no benefit in preventing death from heart disease, merely to cash in on its secondary benefit (coronary inflammation reduction), when other options for reducing inflammation exist that are far more effective…and far safer? Specifically, I'm speaking of proteolytic enzymes.
For further information, I suggest you read:

• Understanding the Liver and Cholesterol
• The Cholesterol Myth
• A Proteolytic Enzyme Formula

• 1. Official World Golf Ranking. (Accessed 19 Nov 2011)
• 2. The AIM-HIGH Investigators. "Niacin in Patients with Low HDL Cholesterol Levels Receiving Intensive Statin Therapy." NEJM. 15 Nov 2011.
• 3. Robert P. Giugliano, M.D., S.M. "Niacin at 56 Years of Age -- Time for an Early Retirement?" NEJM 15 Nov 2011. (Accessed 21 Nov 2011).
• 4. The Coronary Drug Project Research Group. "Clofibrate and Niacin in Coronary Heart Disease." JAMA. 1975;231(4):360-381.
• 5. Stephen R. Daniels, MD, PhD, Frank R. Greer, MD, and the Committee on Nutrition. "Lipid Screening and Cardiovascular Health in Childhood." PEDIATRICS Vol. 122 No. 1 July 1, 2008 pp. 198 -208.
• 6. Thavendiranathan, P., A. Bagai, et al. "Primary prevention of cardiovascular diseases with statin therapy: A meta-analysis of randomized controlled trials." Archives of Internal Medicine 166: 2307-2313.
• 7. Vrecer, M., S. Turk, et al. "Use of statins in primary and secondary prevention of coronary heart disease and ischemic stroke. Meta-analysis of randomized trials." International Journal of Clinical Pharmacology and Therapeutics 41(12): 567-577.
• 8. Hayward, R.A., T.P. Hofer, et al. "Narrative review: Lack of evidence for recommended low-density lipoprotein treatment targets: A solvable problem." Annals of Internal Medicine 145(7): 520-530.
• 9. University of British Columbia. "Do statins have a role in primary prevention? A review by the Therapeutics Initiative of the Department of Pharmacology & Therapeutics of the University of British Columbia." Therapeutics Letter March-April 2010.
• 10. Di Napoli P, Taccardi AA, Oliver M, et al. "Statins and stroke: evidence for cholesterol-independent effects." Eur Heart J. 2002;23:1908-1921.
• 11. Vaughan CJ. "Prevention of stroke and dementia with statins: effects beyond lipid lowering." Am J Cardiol. 2003;91:23B-29B.
• 12. Vaughan CJ, Gotto AM Jr, Basson CT. "The evolving role of statins in the management of atherosclerosis." J Am Coll Cardiol. 2000;35:1-10.
• 13. Ridker PM, Rifai N, Rose L, et al. "Comparison of C-reactive protein and low-density lipoprotein cholesterol levels in the prediction of first cardiovascular events." I. 2002;347:1557-1565.
• 14. Curb JD, Abbott RD, Rodriguez BL, et al. "C-reactive protein and the future risk of thromboembolic stroke in healthy men." Circulation. 2003;107:2016-2020.
• 15. Ridker PM, Rifai N, Clearfield M, et al., for the Air Force/Texas Coronary Atherosclerosis Prevention Study Investigators. "Measurement of C-reactive protein for the targeting of statin therapy in the primary prevention of acute coronary events." N Engl J Med. 2001;344:1959-1965. http://www.ncbi.nlm.nih.gov/pubmed?term=11430324

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Location of original post HERE. Emphasis added by bd.