Severe Eczema Drug Is Approved by F.D.A.; Price Tag Is $37,000 a Year

The Food and Drug Administration on Tuesday approved a drug to treat people with a serious form of eczema, a potential breakthrough for people who have suffered for years without relief. But it will not come cheap.

The drug, to be called Dupixent, will carry a list price of $37,000 a year, a hefty price tag for patients who are increasingly being asked to pay a larger share of the drugs they take. Still, its price is a bit lower than many other commonly used biologic drugs, such as Humira and Enbrel, that treat other skin diseases.

In an effort to head off another public battle over the soaring cost of some prescriptions, the drug makers Regeneron Pharmaceuticals and Sanofi took the unusual step of directly negotiating with insurers over the price and other details ahead of time. What consumers pay for drugs has come under heightened scrutiny in the last few years, most recently by President Trump, who has promised several times to take drug companies to task over their costly products.

“Things have really deteriorated in our industry,” said Dr. Leonard S. Schleifer, the chief executive of Regeneron. “There’s so much concern over drug pricing that there’s an enormous amount of finger-pointing that is going on that’s counterproductive. It isn’t necessarily incentivizing the right behavior.”
The best-selling products Humira and Enbrel, which treat the skin disease psoriasis and other conditions, carry annual list prices of about $50,000.

Although many patients with insurance will not be asked to pay the full $37,000, consumers have been more exposed to rising prices in recent years because insurers often require them to pay a percentage of a drug’s list price — sometimes up to half — or pay the full price until their deductible is met.

They also often must demonstrate that other, cheaper drugs did not work before an insurer will cover more expensive drugs. Regeneron has said it also negotiated a more streamlined approval process, although patients will still have to try other drugs first. It also said it had a patient assistance program to help people who have troubling paying.

Regeneron and Sanofi held much of the bargaining power in negotiating Dupixent’s price because it has been shown to work well and has no real competition, said Dr. Steve Miller, the chief medical officer at Express Scripts, the nation’s largest pharmacy benefit manager, which often negotiates with drug makers on behalf of clients like insurers and large employers.

With breakthrough treatments, “companies can really go to the high end of that demand for reimbursement,” Dr. Miller said, “and all we have is the bully pulpit to complain about it.”

In trying to reach an agreement before approval, Dr. Miller said, “this is how the system is supposed to work.”

Christine Cramer, a spokeswoman for CVS Health, another leading pharmacy benefit manager, said, “While we believe our advocacy on behalf of our clients did ultimately influence Regeneron’s initial pricing strategy, the drug will be expensive.”
But Peter Maybarduk, director of the Access to Medicines program at Public Citizen, a consumer group, noted that negotiations still took place out of the public eye and within the context of a system that is inherently unfair. “It’s the arrangement that corporations found beneficial in a system that provides monopolies and rewards secrecy, and we should ask for considerably more as the standard,” he said.

Dupixent treats severe to moderate atopic dermatitis, a common form of eczema that goes beyond the occasional bouts of itchy, dry skin that many people get. For people with serious forms of the disease, other treatments often do little to calm their skin, leading to sleeplessness, depression and social anxiety. Regeneron said Tuesday that an estimated 300,000 people in the United States could qualify for its drug.

“I always say that atopic dermatitis doesn’t kill you, it just ruins your life,” said Dr. Elaine Siegfried, a professor of pediatrics and dermatology at the St. Louis University School of Medicine. She was not involved in the clinical trials that led to approval, but she said she was likely to enroll patients in pediatric studies that are getting underway. Dupixent, she said, appears to work well, with few serious side effects. “It is groundbreaking,” she said.
Debbie Byrnes, a sixth-grade teacher from San Antonio who participated in the clinical trial, had suffered for years with severe eczema that often covered her face. “That was the really difficult thing for me — I could never hide it,” she said. “I would have days when I went into school, and the kids would look at me and say, ‘What happened to you?’ ”

Ms. Byrnes said she began noticing a difference about five days after her first dose and has now been using the drug for two years. Her skin is now almost completely clear, and occasional flare-ups are quickly brought under control. “If you saw me,” she said, “you wouldn’t know that I ever had atopic dermatitis.”

Before a drug is approved, pharmaceutical companies usually keep the price a secret and do not directly negotiate with insurers until the product is approved by the F.D.A., in part because of concerns that doing so could violate agency rules. But in January, the agency said that drug companies were allowed to discuss price and other issues with insurers in advance.

Even if Dupixent’s $37,000 list price is below those of established drugs like Humira, Regeneron and Sanofi will very likely get to keep more than AbbVie, which makes Humira. That is because the net price of Dupixent, Dr. Schleifer said, will still be over $30,000. Although the rebates that drug makers negotiate with insurers are not public, Richard T. Evans, an analyst for SSR Health, a stock analysis company, has estimated that AbbVie would get to keep less than that, or about $27,500 a year for each patient who uses Humira.

He said a similar drug, nemolizumab, is also being tested for people with moderate to severe eczema and could hit the market in a few years. “Right now they have the benefit of being alone,” Mr. Evans said. “But going forward, I think there will be a lot of price competition.”

In reaching tentative agreements ahead of time, Regeneron and Sanofi appear to have been trying to avoid the pushback they encountered in 2015, when their expensive drug to treat high cholesterol, Praluent, was approved. Although Praluent and a similar drug, known as PCSK9 inhibitors, have been found to be beneficial to patients who don’t respond to other treatments, insurers have limited access and sales have not lived up to expectations.

“We all got that wrong,” Dr. Schleifer said. “But if we can make all of it work so that everybody’s feeling good, then we’ve really changed the paradigm.”

What Is LDL-P and Apolipoprotein B (apoB) ?

LDL-C is usually calculated using the Friedewald equation. However, this measure can underestimate LDL-C level as triglycerides increase. Direct LDL-C measurements are also available and better reveal individual issues, but are less often promoted or done due to slightly higher costs.

LDL-C reflects the total content or concentration of cholesterol within LDL-C particles in mg/ml or mmol/L. Since the amount of cholesterol in each particle may vary, measuring LDL-C does not necessarily reflect the actual number of particles.

LDL-P (LDL particle number) measures the actual number of LDL particles (particle concentration, nmol/L). It appears that LDL-P may be a stronger predictor of cardiovascular events than LDL-C.

Low LDL-P is a much stronger predictor of low risk than low LDL-C. In fact, about 30 – 40% of those with low LDL-C may have elevated LDL-P. Therefore you can have low LDL-C but still be at risk for CVD, particularly if your LDL-P is elevated. Discordance is when LDL-C differs from LDL-P.

Lipoproteins play an essential role for the initiation and progression of atherosclerosis. Therefore it is very important for us to understand what regulates the production and clearance of atherogenic lipoprotein particles and how these mechanisms may be influenced.

LDL-C is only a measure of the cholesterol mass within LDL-particles. Thus, LDL-C only indirectly reflects the atherogenic potential of LDL particles. Apolipoprotein B (apoB) and LDL-P on the other hand reflect the number of atherogenic particles, with no mention of cholesterol mass. Therefore apoB and LDL-P are believed to be better risk predictors than LDL-C.
Reference Range for LDL-P

LDL-P is measured by a so-called NMR lipid profile test. A value of less than 1.000 is considered ideal. Above 2.000 is considered very high.

Apolipoprotein B (apoB)

Apolipoprotein B (ApoB) is an important component of many lipoproteins that are involved in atherosclerosis and cardiovascular disease.

Lipoproteins are the particles that transport cholesterol and triglycerides in the blood stream.

Lipoproteins are comprised of proteins (apolipoproteins), phospholipids, triglycerides and cholesterol. The lipoproteins vary in the major lipoprotein present, and the relative contents of the different lipid components. ApoB is an important component of many of the most atherogenic lipoprotein particles.

ApoB occurs in 2 main forms, apoB 48 and apoB 100. ApoB 48 is synthesized mainly by the small intestine. ApoB 100 is the apolipoprotein found in lipoproteins synthesized by the liver. Therefore, from the viewpoint of atherosclerosis and cardiovascular risk, apoB100 is the important one. ApoB 48 is primarily found in chylomicrons.

ApoB 100 is found in chylomicrons, VLDL, IDL, LDL and LP(a) particles. All these particles are atherogenic. Each of these particles contains a single apoB molecule. Therefore, measurements of apoB represent the total burden of the main lipoprotein particles involved in the atherosclerotic process.

Usually, 85-90 percent of apoB represent LDL particles. Thus, apoB reflects particle concentration, similar to LDL-P. Although measurements of apoB are not widely available, the assay has been standardized and does not require a fasting sample.

Apo B containing lipoproteins are the ones that are most likely to enter the wall of the arteries. They are capable of trafficking cholesterol into the artery wall, and if present in increased numbers they may be the main initiating factor in atherosclerosis. Retention of ApoB containing lipoprotein particles within the arterial wall is an essential part of the process.
The normal range for apoB is 40-125 mg/dL.

Usually less than 100 mg/dL is considered desirable in low or intermediate risk individuals.

Less than 80 mg/dL is desirable in high risk individuals, such as those with cardiovascular disease or diabetes.

Statins Impair Immune System Function

The statin drug Zocor (simvastatin) has been shown to directly compromise the immune response¹ to an opportunistic infection.  This is not good news for any person taking any statin, as the type of impairment involved seriously compromises basic immune system function.

The production of cholesterol is much like an automobile assembly line, except with multiple branches that build other things at the same time (a novel system of efficiency).  The various molecules produced are vital to your survival.  Indeed, cholesterol synthesis is the backbone of survival.  The primary cholesterol production line is called the HMG-CoA reductase pathway.  Important branches include the production of selenoproteins that run your antioxidants and thyroid, as well as the production of coenzyme Q10 and vitamin D.  One of these branches involves the production of novel compounds called isoprenoids (geranylgeranyl pyrophosphate and farnesyl pyrophosphate).  Isoprenoids also occur in nature in fat-soluble nutrients like carotenes.  In fact, the power of tocotrienol vitamin E compared to regular vitamin E is due primarily to the fact that tocotrienols have a side chain molecule that is an isoprenoid.  These isoprenoids play a vital role in attaching fatty substances to proteins, a process called protein prenylation.  Proper protein prenylation is required for the healthy function of many cells in your body, including the prevention of cancer.  Taking any statin reduces the protein prenylation activities in your body via suppressing the production of the isporenoids needed to carry out this activity.  This is a highly undesirable side effect of statins.

The new research looked into the function of macrophages, important members of your front line immune troops.  Some macrophages were treated with Zocor at a relevant physiologic dose and others were not.  They were then exposed to a common bacterial infection.  The Zocor-treated macrophages experienced a double-negative whammy.  Their ability to engulf the bacteria was crippled.  Next, the macrophages generated excessive inappropriate inflammatory signals.  The researchers traced the molecular malfunction to the fact that the statin blocked proper protein prenylation within the macrophage, crippling its function.

While I have tried to make this rather complex issue as simple as possible to understand, the bottom line is that this is a highly adverse effect on human immunity that will cause more severe infections in humans or allow low-grade infections to gain a hold within the human body and wreak havoc to health.  In turn, these infections will increase the overall inflammatory burden that is now known to be a primary contributing factor to poor health and all “diseases of aging.”  On this point alone the use of statins should be banned for 95% of the people currently taking them as there is no way the benefits could possibly outweigh the risks.  The medical profession prescribing these drugs invariably ignores or doesn’t understand this type of study and hopes the general public doesn’t understand health well enough to be concerned.

The Statin Scam Marches On

Considering that tens of millions of Americans now take statins to lower cholesterol, the following headline was conspicuously absent from the major media this month:  “Statins Found to Turn On Gene that Causes Muscle Damage.”  It’s now a fact of science; a new study shows that taking statins destroys your muscle to a greater or lesser degree.  And let’s not forget that the heart is a muscle. 

Place this study juxtaposed to another rather interesting recent finding:  the more fit you are the longer you will live – and the two just don’t add up.  How can you destroy muscle and be more fit?  You can’t.  Sure you can drug your cholesterol number lower, but will you be healthier, fit, and live longer?

In the new study researchers found that statins activate a gene signal in muscles called atrogen-1.  When this gene activates it targets key muscle proteins for destruction.  The activation of this gene drives the process of muscle atrophy and muscle wasting.  It is induced in cardiac muscle in failing hearts.  Why on earth would any person want this gene activated by a drug? 

The researchers tested statin-taking humans who were complaining of severe muscle pain.  Muscle biopsy found that the atrogen-1 gene was activated, compared to people with severe muscle pain not on statins and controls.  They went on to show through various experiments that statins activate the gene.  This is extremely bad news for any person taking a statin.

Right now doctors ignore the majority of muscle aches and pains caused by statins, and in their mind only consider the problem serious when it is debilitating (rhabdomyolysis), which apparently happens less than 1% of the time.  However, at least 5% - 7% of statin users experience significant muscle problems.  The number is greater than 10% if a person is taking the now commonly prescribed higher doses.  And if a person is trying to be fit and exercise the number jumps to 25%.  These numbers are clearly on the low end as it has now been shown that doctors are ignoring their patients, not reporting the side effects of statins to the FDA, and telling them the side effects they are experiencing are not from the drug! 

This new science shows that as soon as the atrogen-1 gene is activated by statins it starts destroying muscle.  This means that even mild aches or pains while taking a statin is a sign that muscle is being destroyed, an entirely new and sobering perspective on the side effects of statins.  Statins directly work against being physically fit, as is evidenced by the difficulty statin users have exercising without troubling symptoms.

Cardiomyopathy (serious weakening of the heart muscle) is a known adverse and often not reported side effect of statin therapy, previously thought to be the result of a statin-induced coenzyme Q10 deficiency.  It is likely that the combination of Q10 deficiency with atrogen-1 activation is behind this problem.

Statins – Perversion of Science for Profit

The statin industry is a 20-billion-a-year propaganda machine, producing more yearly revenues from one class of drug than all professional U.S. sports combined.  Just like any hot-selling drug on the market, negative studies are discouraged to say the least.  They are either thrown in the trash can when they don’t work out or critical researchers are often blackmailed, meaning if they publish something negative they will never again get research money from the industry.  These well known tactics discourage basic research on drug-related toxicity problems.

When statistics are honestly looked at in the case of using statins for many years to prevent a first heart attack, for every life that is saved (1% over 10 years use) statins cause an equal number of adverse deaths due to accidents, infection, suicide, and cancer (1% over 10 years use).  This means that as a general public health measure, which is now the lion’s share of current statin use, they are an ineffectual waste of money.  It has now been proven that middle-age men would be better off taking an aspirin a day for a tiny fraction of the cost (of course there are many supplement options).  Statin-taking for a number of years does not reduce mortality rate.  None of these facts faze the statin industry, which keeps churning out positive spin and moving right along regardless of the damage being doing and the money wasted.

The fraud of statins inside one’s body centers on the regulation of an enzyme known as HMG CoA reductase.  Statins work by reducing the function of this enzyme, the higher the dose the more the enzyme is reduced, and the less cholesterol is made.  It is well known that individuals with naturally lower cholesterol (LDL at 130, total less than 200) in their 40s and 50s have fewer cardiovascular problems as they grow older.  However, taking a statin to reduce cholesterol to these levels or even lower is not the same thing as natural healthy function. 

In healthy individuals with lower cholesterol the HMG CoA reductase enzyme is active at a high level as part of health.  It is part of a complex communication system within the body that regulates energy, immunity, fat metabolism, leptin, cellular thyroid hormone activity, liver-related synthesis, stress tolerance, adrenal function, sex hormone synthesis, and brain function.  This system is core to survival!  The high activity of this enzyme is a type of metabolic fitness, similar to the idea of muscle fitness.  The enzyme is very active in a healthy state for a variety of important and vital needs.

Drugging this enzyme is similar to making a person get around in a wheelchair, whether they need one or not.  If you put a person’s metabolism in a statin-induced straightjacket, then maybe Humpty Dumpty won’t fall off the wall so easily.  That may be a useful concept for someone in brittle cardiovascular health, but it has little to do with the average person concerned about general cardiovascular well being and maintaining a healthy level of fitness and vitality. 

Doctors don’t use statins to try and reduce HMG CoA activity a little bit, with the idea of approximating some type of healthy function of the enzyme (the lowest and least toxic dose possible to provide improvement).  Doctors actually could care less what healthy function of the enzyme actually is.  Rather, the new “gold standard of medical care” is to batter the enzyme into a state of submission so that cholesterol levels are abnormally low.  Any apparent benefits of a statin, many of which are falsely touted, is accomplished by poisoning some aspect of health.  How long can such a charade be allowed to continue on millions of unsuspecting Americans?  Why won’t the FDA demand drug companies include a correct risk profile as part of the labeling?  As normal, the FDA continues to sleep on duty.

Double the Dose – Rake in the Billions

In 2004 the government-funded National Cholesterol Education Program selected a panel of nine “experts” to review statin drug use and make recommendations as to guidelines doctors should follow to reduce cardiovascular disease.  They recommended that individuals at high cardiovascular disease risk attain LDL levels < 100 mg/dL and individuals at very high cardiovascular risk attain LDL levels < 70 mg/dL (levels that are abnormal, levels which are seldom ever this low in healthy people with no cardiovascular disease). Their advice was published in the marketing journal of the American Heart Association, Circulation.  This “scientific journal” failed to disclose that six of the nine authors had direct financial ties to the makers of statin drugs.

Today, in doctor’s offices around the country, these abnormal cholesterol levels are being pushed on anyone over the age of 40, requiring a double or triple dose of statins or combination with some other toxic drug (like fibrates) to achieve these completely unnatural and unhealthy levels of cholesterol.  In hindsight we can see that these recommendations boosted yearly statin sales by seven billion dollars.  A class-action lawsuit has already been filed against Pfizer for illegal Lipitor promotion.  Many others are sure to follow as this fraud becomes better understood by those who are injured and those footing the bill.

Further highlighting this fraud is a study appearing in the October 3, 2006, issue of the Annals of Internal Medicine.  Researchers reviewed all studies relating to cholesterol-lowering benefits by statin drugs, with a focus on the new abnormally low cholesterol levels promoted by the American Heart Association. Their conclusion, “current clinical evidence does not demonstrate that titrating lipid therapy to achieve proposed low LDL cholesterol levels is beneficial or safe.”  That is a rather shocking conclusion coming more than two years after the fact.  The finding did not faze the statin marketing machine or the prescribing habits of any physician.

Make Vitamin E a Scapegoat

During the time in 2004 that Big Pharma was plotting its statin bonanza it needed to fire cannonballs at its most widely recognized competition, Vitamin E and other antioxidants. No problem. First, in August 2004, the American Heart Association used its marketing magazine to print a bogus article contradicting hundreds of nutritional studies, stating that antioxidants A, C, and E are not effective for cardiovascular disease risk reduction. Then, in November of 2004, with trumpets blaring at their yearly AHA meeting, they make the brazenly fraudulent claim that vitamin E increases the risk of death by 6%!!!

Outside the marketing meeting masquerading as a scientific conference, the chairman, Dr. Raymond Gibbons of the Mayo Clinic in Rochester, Minnesota, was holding a dog and pony show press conference. “I spend all my time trying to tell patients why they should not take vitamin E. Too often in terms of the supplements there’s very scant science. In this area, we have the science. Vitamin E doesn’t work.” He implored his captive audience of reporters to help him convince patients to stop taking Vitamin E and take the “proven” drugs. The next day, all major media ran the story telling consumers vitamin E was dangerous. Program effective. Damage done.

Within weeks the American Heart Association had brainwashed doctors and the American public to actually think vitamin E was dangerous, clearing out the primary competition to statins for the prevention and treatment of cardiovascular disease. Doctors were telling all their patients to stop taking vitamin E. The anti-vitamin rhetoric spread like wild fire through doctor’s offices around the nation and continues to this day.

Within a week the bogus vitamin E information coming from the American Heart Association meeting was debunked. Physician and nutritional expert, Alan Gaby, pointed out all the flaws as well as the safe and effective track record of vitamin E. By April of 2005 the leading antioxidant scientists in the worldhad published a comprehensive review showing the safety of vitamin E up to doses of 1600 IU per day, again debunking the false vitamin E story and explaining the high degree of safety of antioxidant nutrients. The media was nowhere to be found; the public never heard vitamin E was truly safe and vital for immune function, prevention of cognitive decline, and a wonderful nutrient for cardiovascular support.

In July of 2005, the Journal of the American Medical Association published the results of an amazing vitamin E and heart disease study. After tracking 40,000 women for eight years it was proven that vitamin E lowered the risk of cardiovascular death by 24%! However, JAMA authors, going along with the vitamin E smear campaign, concluded that vitamin E was not worth recommending! Any drug with that kind of statistical evidence would be a billion dollar blockbuster. The media failed to look at the study and reported everywhere that vitamin E was not needed, denying women the true information about a wonderful cardiovascular support nutrient.

Likewise, an August 2007 randomized, double-blind, placebo-controlled cardiovascular study published in the Archives of Internal Medicine found that natural vitamin E reduced cardiovascular death or serious cardiovascular disease by a statistically significant 13%, the primary end point of the study.  Natural vitamin E also showed improvement in secondary end points, including a 22% reduction in heart attacks, a 27% reduction in strokes (31% when combined with vitamin C), and a 9% reduction in cardiovascular death.  Once again the study results were hidden deep in the paper, downplayed by the authors, and not correctly reported in the media. And in November the American Journal of Clinical Nutrition reported the results of another randomized, double-blind, placebo-controlled vitamin E study showing that vitamin E was completely safe at doses of 1200 IU per day in patients with existing cardiovascular disease.  Once again the media was nowhere to be found.

It is hard to calculate how many elderly people have been injured and killed by the proclamation not to take vitamin E and to take statins in super-high doses.  Vitamin E is absolutely vital for heart function and healthy immunity in older Americans.  When a statin-taking senior dies the physician never notes the deterioration of health that often begins with taking a statin or increasing the statin dose.  Rather, the physician simply blames the health of the patient for the death – isn’t that convenient.  Thus, statin-induced deaths are hidden and grossly under-reported.

A New Statin Fraud Emerges

The statin golden pot at the end of the rainbow has recently been threatened due to the fact that several best-selling statin drugs have lost patent protection and are now open to generic competition for pennies on the dollar ((Lipitor sales are off 25%).  Newer cholesterol drugs in the pipeline have turned out to be a total bust.  In order to get insurers to keep coughing up unnecessary money Big Pharma had to be creative – and dishonest (no surprise there).

Merck and Schering-Plough have joined forces to market Zetia (which works in the digestive tract differently than a statin) and Vytorin (which is a combination of Zetia and a statin).  By combining a statin in this way generic competition can be avoided.  Either Zetia or Vytorin sell for $3 a day, compared to $0.25 for a generic statin.  By adding Zetia to any other statin or by taking the combination pill cholesterol can be lowered an additional 15%.  This has created a $5 billion dollar share of the statin market for these two drugs.

Is lowering cholesterol an extra 15% worth it?  That is the billion dollar question.  Forbes was the first to blow the lid on what is obviously a rip-off.  The Wall Street Journal is also covering the story.  Vytorin has never been proven to prevent heart attacks, strokes or deaths any better than a plain generic statin.  In 2002 Merck/Schering Plow undertook a study to prove that the combination prevented plaque build up in the arteries better than a statin alone.  The study was completed in April of 2006.  The drug companies are sitting on the results, and now have announced they are changing the primary outcome of the study after it is done – a scientific farce.

It is obvious that the top executives in these companies know the results are not good.  They can’t throw the data away as their marketing campaign was built on the expectation of a favorable outcome of these studies.  Even doctors are complaining about the stalling tactic.  The longer they can stall the longer they can collect their $5 billion in yearly sales, swindling Americans of hard earned money.  This is, unfortunately, an example of typical drug company behavior.  The FDA is of course snoozing on the job – they should be warning consumers of the dangers of lowering cholesterol excessively.

Take Health into Your Own Hands

The medical profession has lost almost all credibility.  There is no short cut to being healthy.  The majority of drugs are best used for a short duration, which is not in the best interest of Big Pharma profits.  Some people in poor health need to be managed with drugs.  Drugs as a tool for general health and prevention are a travesty.  The statin industry is a scam gone wild.  Space in this article has only allowed me to define a few of the primary statin side effects.  There are many more that are seldom explained, including weakened immunity and cognitive decline.  Statins are a slow and insidious poison wherein the side effects gradually get worse the longer a person takes them.  This means that people often don’t realize their decline in health is from the statin, until someone points this issue out to them and they look at how their health in general has deteriorated since being on a statin.  No, it’s not that the person is simply getting older – it’s the statin!  You may read about all the statin side effects for free in my book, Fight for Your Health:  Exposing the FDA’s Betrayal of America (chapters 19-21).

If we want a renaissance in cardiovascular fitness and quality of life in the over 50 crowd then most of the meds need to go in the trash and be replaced with consistent exercise programs, a fresh and organic diet, stress management programs, improved quality of sleep, and appropriate dietary supplements that support fitness and healthy cardiovascular function. Seniors need to have a rightful and respected place in our culture.

Statin Drugs Cause Atherosclerosis and Heart Failure

“Statin Drugs stimulate atherosclerosis and heart failure” is the title of a research study published this past week. It has not made mainstream news at the time of this article writing, but it is of utmost importance to the health of the tens of millions taking statin drugs for cholesterol. The evidence continues to pile up and prove that statin drugs are hazardous to your heart and health.

The study, published in Expert Review of Clinical Pharmacology February 6, 2015, discusses the process of how statin drugs cause the demise of heart health, worsen atherosclerosis and induce heart failure. The study’s authors are located in Japan at the Nagoya City University. If and when this news reaches the American public, the tens of millions of patients on statin drugs with worsening heart disease and heart failure should be flooding their physician’s office and the drug companies’ door with phone calls demanding explanations and reprimand. So far that has not happened.

Vitamin K2

The study presented insightful information describing the physiological mechanisms on how statin drugs cause coronary artery calcification or stiffening of blood vessels perpetuating the atherosclerosis. The plaque build-up occurs because statin drugs inhibit vitamin K2 function in the body. Vitamin K2 protects arteries from calcification. Without proper levels and function of vitamin K2, plaque levels worsen because of negative interaction with the Gla-protein and the inhibition of vitamin K2. This was previously described in a large study in 2012 with the same conclusion – statin use causes increased presence of coronary plaques. They did not identify the link with vitamin K2. The tool that cardiologists use to prevent atherosclerosis actually worsens it.

Mitochondria Damage

The second finding of the study is of little surprise. It shows that statin drugs are toxic to the mitochondria, or the energy producers in cells. Mitochondrial damage in the heart is a downward slope to cardiomyopathy or heart failure. This is a dangerous, although often subtle, effect. Statins impair the heart muscle mitochondria function, severely disrupt ATP production, and alter intracellular signaling proteins. This impairment leads to muscle cell dysfunction and eventually apoptosis or muscle cell death. This is like pouring concrete into the cellular engines of energy production and heart muscle contraction. Statins are notorious for depleting coenzyme Q10 out of the heart muscle and the body. This profoundly interferes with mitochondria function. Statins also interfere with the protein called heme A. Heme A is a component of hemoglobin that helps bind onto oxygen and carry iron to the muscle cells in the heart. Without the ability to transport iron and oxygen to the heart cells, energy production is further compromised. Iron deficits in the heart myoglobin may occur and possibly contribute further to heart failure.

Coenzyme Q10

Statin drugs interfere with coenzyme Q10. This has been documented repeatedly in medical literature with strong evidence. In fact, a black box warning for statin drugs or HMG CoQ reductase inhibitors was proposed to the FDA. The proposed black box warning was:

“HMG CoA reductase inhibitors block the endogenous biosynthesis of an essential co- factor, coenzyme Ql0, required for energy production. A deficiency of coenzyme Q10 is associated with impairment of myocardial function, with liver dysfunction and with myopathies (including cardiomyopathy and congestive heart failure). All patients taking HMG CoA reductase inhibitors should therefore be advised to take 100 to 200 mg per day of supplemental coenzyme Q10.” 

The FDA blocked the attempt of putting a black box warning on statin drugs in 2014. How egregious is that?

Selenium

Another factor discussed in the initial study was the interference of the production of selenium containing proteins. Statin drugs inhibit the biosynthesis of these selenoproteins. One of the most important selenoproteins in the body is a compound called glutathione peroxidase. Its job is to protect the organism, especially muscle tissue, from oxidative damage coming from hydrogen and lipid peroxides. Lack of the glutathione peroxidase enzyme promotes high levels of free radical activity and tissue damage. Blocking the selenoprotein enzyme glutathione peroxidase is akin to pouring gasoline on the fire of inflammation and free radicals, which damages muscle tissue. In fact, the scientists described this blocking of the selenoproteins reminiscent of selenium deficiency induced heart failure, known as Keshan’s disease first identified in the 1930s. Scientists have strongly recommended that individuals suffering from non-ischemic heart failure have their selenium levels tested. This is a blood test that is readily available. Get an RBC selenium level checked at your next appointment. Certainly our selenium depleted foods and soils are not helping this situation when combined with drug-nutrient induced deficits.

Other Side Effects

Expand this picture further. We have skeletal muscle, cardiac muscle, and smooth muscle. The side effects of statin drugs are often discussed as skeletal muscle weakness and pain and in recent years the increased development of heart failure (cardiac muscle failure). This is most often in the context of high dose statins. There are, however, other side effects that may be linked with statin drugs and how they affect mitochondria. Common side effects with the drug simvastatin include headaches and constipation. One doesn’t normally think of headaches and constipation concerns linked with mitochondria, but they can be. Both the nervous system and smooth muscles have high levels of mitochondria. Bowel motility is dependent upon smooth muscle function and nervous system activity. When there is a disruption in the health of mitochondria in the body, one of the symptoms may be constipation.

This is the same with migraines. Some types of headaches, i.e. some subtypes of migraines are related with mitochondria dysfunction. Joint pain and tendon problems may also be related. Don’t forget the brain and side effects of being forgetful or depressed. Our brain desperately needs healthy mitochondria to function effectively. It is common to dismiss these symptoms, attributing them to poor diet, stress, or aging. Yet, how many statin users have the common symptoms of constipation, headaches, joint pain, and feel a little less energetic, forgetful, and weaker than they did a few years ago and chalk it up to aging. Often they go to their physician and because they do not have outright symptoms of rhabdomyolysis and liver failure from the statin drug, it is chalked up to stress and getting older. The traditional medical and research communities are heavily debating these side effects and are not owning up to the real damage caused by statins. Many are looking for more ways to prescribe statins other than for cholesterol problems.

The question remains:  how many people are going to suffer further heart disease with sky-rocketing rates of heart failure and subsequent loss of function and life linked with statin induced side effects? How many burgeoning statin drug class action law suits will it take to stop the pharmaceutical industry from this massive debacle and cover-up resulting in human tragedy? One is too many. It is time for the medical and pharmaceutical industry to acknowledge the truth and look at real solutions for heart disease.

Proactive Steps

If you are on statin drugs for any reason, make sure that you are taking at least 200 mg of coenzyme Q10 per day. Higher amounts, up to 600 - 800 mg, may be used for serious fatigue, mitochondrial injury, and cardiomyopathy disorders. The form of coenzyme Q10 plays a substantial role in how well coenzyme Q10 is absorbed, gets into the blood stream, and where it is used in the cell. Wellness Resources recommends the use of water and fat soluble coenzyme Q10 in either ubiquinone or ubiquinol forms.

Supporting selenium levels is also of primary concern. Brazil nuts, some seafood, mushrooms, asparagus, poultry and beef may provide good dietary sources of selenium or consider nutritional supplementation for standardized activated forms of selenium, like seleno-methionine.

Vitamin K2 must be present in adequate amounts to offset the drug-nutrient interaction. It is found in fermented foods and limited quantities in animal products. It is also produced by healthy gut bacteria and available in supplemental form.

Protecting the mitochondria from further oxidative damage should also be a priority. This is irrespective of statin drug use. Antioxidant rich, deep colored fruits and vegetables help protect the mitochondria from oxidative stress. Nutrients described above and others such as resveratrol, carnitine, bacopa monniera, curcumin, all B vitamins, vitamin C, vitamin E, K1, NAC, and lipoic acid are just some of the nutrients essential for protecting the heart from ischemic/heart attack damage, heart failure, and mitochondria injury.

Interestingly, in the last ten years melatonin has been found to protect the heart after heart attack injury in animal studies. Melatonin stopped heart cells from dying and protected the structural integrity of the mitochondria in heart cells and avoided marked worsening of heart damage. This too can be added to the arsenal of support for protecting the heart.

The link of melatonin and its ability to protect the heart and mitochondria leads into another tangent – the thought of sleep deprivation, sleep hygiene, and light exposure in the body and its effect on the body. With heart disease, heart failure and mitochondrial disorders at epidemic levels, it makes one question the age of electricity, sleep deprivation, and compromised melatonin production as causing a fundamental shift in the health of our heart and mitochondria. If scientists ever tackle this issue, it will be an astronomical feat for any conclusion to occur but it is an interesting thought. Until then, find ways to improve your melatonin status and improve sleep to see how you and your heart feel.

The researchers from the headline study said “Thus, the epidemic of heart failure and atherosclerosis that plagues the modern world may paradoxically be aggravated by the pervasive use of statin drugs. We propose that current statin treatment guidelines be critically reevaluated.” They were polite in their request and recommendations, but what about you? Are you going to follow the mainstream herd mentality, or are you going to look at the physiology and stand up for your health? Talk to your cardiologists and see if they understand these principles of physiology. If they did, they should be the first to stop prescribing these dangerous meds. Take charge of your health today!

Statins & Type 2 Diabetes: The Straw that Breaks the Camel’s Back

Two recent studies have shown that high-dose statin therapy can induce the onset of type 2 diabetes, worsening the health of those who are already in poor health.  These studies lend further credence to the FDA’s recent warning for patients across the country to get off high-dose statin therapy due to concerns of muscle damage. Let’s not forget that the heart is a muscle.

The new study takes into account all statins that are commonly used, and was published today in the Journal of the American Medical Association¹.  It found that high-dose statin therapy increased the risk of type 2 diabetes by 12% compared to low-dose statin therapy. Of course, these studies never compare the risk of a drug to someone actually becoming more fit and healthy through natural means, as the increased risk would be so dramatic the drug would have to be pulled from the market. In this case the researchers are comparing a high dose of poison to a lower dose of poison. The new study is extremely embarrassing to the statin industry, as it was picked up by news outlets around the world and ran as a headline. 

Performing statistical mumbo-jumbo the researchers concluded that the benefits still outweigh the risks, as they implied that more cardiovascular deaths were prevented than diabetes caused. It is always fascinating to watch a Big Pharma calculator in action – no matter what data is put in a positive spin on taking the drug is always the answer. 

A second study published in April in the Journal of the American College of Cardiology² found similar results, while focusing only on the statin Lipitor. However, this study analyzed more details of the health status of those before they went on high-dose statin therapy.  It found that those in the worst metabolic condition (higher fasting glucose, more overweight, higher blood pressure, and higher triglycerides) were the most likely to develop new onset type 2 diabetes. This means that high-dose statin therapy was more likely to push a person into type 2 diabetes if they were already knocking at the door.  And in direct conflict with the risk/benefit conclusion of the above study, this study found that those with new onset type 2 diabetes had a higher risk for major cardiovascular events.

These studies highlight the extreme difficulty physicians have in titrating poisons to be “appropriate” for any person, especially as their health worsens.  Unfortunately, the majority of statin-prescribing physicians don’t think about actual risks of what they are doing.  To the contrary, the worse off the metabolic health of the patient, the greater the number of toxic substances are prescribed, typically in the highest amount possible.

The most valuable asset you have is your health. Protect it and preserve it. If you get off track make a diligent effort to fix your issues. The failure to do so on your part will land you in front of a pill-pushing Big Pharma advocate, a supposed health professional who will now titrate poisons on your behalf, a person who typically has no clue how those poisons will actually behave in your body. It is a shame that the subject of medicine has been reduced to such a barbaric approach to managing the health of millions. It is little wonder that our health care costs skyrocket while the life expectancy of Americans dramatically lags behind other developed nations and is actually headed in the wrong direction.

Statins CAN cause heart disease - Shock research warns drug risks hardened arteries

CONTROVERSIAL drug statins can actually increase the risk of heart disease, shock new research has shown.
People taking the drugs are more likely to suffer from hardening of the arteries, a leading cause of heart problems.

In addition, researchers found the drugs block a process that protects the heart.

This can “cause, or worsen, heart failure”, according to a study.

The lead author says: “I cannot find any evidence to support people taking statins.”
The findings, published in Expert Review of Clinical Pharmacology, will add to the debate surrounding the drugs, which are routinely given to up to 12 million patients in the UK, or around one in four adults.

Supporters say they save lives by lowering cholesterol and UK health regulators say they are safe.

Oxford professor Sir Rory Collins has warned that overstating concerns about statins could “cause very large numbers of unnecessary deaths from heart attacks and stroke”.

Opponents have pointed to the side effects, such as skeletal weakness and muscle pain, and say the risks outweigh the benefits.
Now Professor Harumi Okuyama, whose team studied a series of more than 20 major research papers on the drugs, says they could cause heart disease.

Dr Okuyama, of Nagoya City University, Japan, said: “We have collected a wealth of information on cholesterol and statins from many published papers and find overwhelming evidence that these drugs accelerate hardening of the arteries and can cause, or worsen, heart failure. I cannot find any evidence to support people taking statins and patients who are on them should stop.”

The researchers say the hypothesis that statins protect the heart by lowering cholesterol is flawed and that high cholesterol is not necessarily linked to heart disease.

They also found statins have a negative effect on vital body processes linked to heart health.

They discovered patients taking the drugs were more likely to have calcium deposits in their arteries, a phenomenon directly linked to heart attacks.

This is because statins block a molecule needed for the body to produce a vital K vitamin, which prevents calcification of the arteries.

Dr Okuyama and his team say many earlier industry-sponsored studies, which show the benefits of statins, are unreliable.
They claim this is because they were carried out before new European regulations were introduced in 2004 which insisted on all trial findings, both negative and positive, being declared.

The study states that before these new rules came into effect “unfair and unethical problems were associated with clinical trials reported by industry-supported scientists”.

Dr Okuyama’s team looked at studies before and after 2004.

They found: “The epidemic of heart failure and atherosclerosis (hardening of the arteries) that plagues the modern world may paradoxically be aggravated by the pervasive use of statin drugs. We propose that current statin treatment guidelines be critically re-evaluated.”
Dr Malcolm Kendrick, who has studied heart health and statins, said: “This study demolishes the argument that these drugs should be prescribed to anyone, as the harms clearly outweigh any previously suggested benefits.”

Dr Peter Langsjoen, a heart specialist based in Texas who is co-author of the study, said: “Statins are being used so aggressively and in such large numbers of people that the adverse effects are now becoming obvious. These drugs should never have been approved for use. The long-term effects are devastating.”

A spokesman for the MHRA, the Government drug regulator, said: “The benefits of statins are well established and are considered to outweigh the risk of side effects in the majority of patients. "Any new significant information on the efficacy of statins will be carefully reviewed and action be taken if required"