How Statins Really Work Explains Why They Don't Really Work.

by Stephanie Seneff

1. Introduction

The statin industry has enjoyed a thirty year run of steadily increasing profits, as they find ever more ways to justify expanding the definition of the segment of the population that qualify for statin therapy. Large, placebo-controlled studies have provided evidence that statins can substantially reduce the incidence of heart attack. High serum cholesterol is indeed correlated with heart disease, and statins, by interfering with the body's ability to synthesize cholesterol, are extremely effective in lowering the numbers. Heart disease is the number one cause of death in the U.S. and, increasingly, worldwide. What's not to like about statin drugs?

I predict that the statin drug run is about to end, and it will be a hard landing. The thalidomide disaster of the 1950's and the hormone replacement therapy fiasco of the 1990's will pale by comparison to the dramatic rise and fall of the statin industry. I can see the tide slowly turning, and I believe it will eventually crescendo into a tidal wave, but misinformation is remarkably persistent, so it may take years.

I have spent much of my time in the last few years combing the research literature on metabolism, diabetes, heart disease, Alzheimer's, and statin drugs. Thus far, in addition to posting essays on the web, I have, together with collaborators, published two journal articles related to metabolism, diabetes, and heart disease (Seneff1 et al., 2011), and Alzheimer's disease (Seneff2 et al., 2011). Two more articles, concerning a crucial role for cholesterol sulfate in metabolism, are currently under review (Seneff3 et al., Seneff4 et al.). I have been driven by the need to understand how a drug that interferes with the synthesis of cholesterol, a nutrient that is essential to human life, could possibly have a positive impact on health. I have finally been rewarded with an explanation for an apparent positive benefit of statins that I can believe, but one that soundly refutes the idea that statins are protective. I will, in fact, make the bold claim that nobody qualifies for statin therapy, and that statin drugs can best be described as toxins.

2. Cholesterol and Statins

I would like to start by reexamining the claim that statins cut heart attack incidence by a third. What exactly does this mean? A meta study reviewing seven drug trials, involving in total 42,848 patients, ranging over a three to five year period, showed a 29% decreased risk of a major cardiac event (Thavendiranathan et al., 2006). But because heart attacks were rare among this group, what this translates to in absolute terms is that 60 patients would need to be treated for an average of 4.3 years to protect one of them from a single heart attack. However, essentially all of them will experience increased frailty and mental decline, a subject to which I will return in depth later on in this essay.

The impact of the damage due to the statin anti-cholesterol mythology extends far beyond those who actually consume the statin pills. Cholesterol has been demonized by the statin industry, and as a consequence Americans have become conditioned to avoid all foods containing cholesterol. This is a grave mistake, as it places a much bigger burden on the body to synthesize sufficient cholesterol to support the body's needs, and it deprives us of several essential nutrients. I am pained to watch someone crack open an egg and toss out the yolk because it contains "too much" cholesterol. Eggs are a very healthy food, but the yolk contains all the important nutrients. After all, the yolk is what allows the chick embryo to mature into a chicken. Americans are currently experiencing widespread deficiencies in several crucial nutrients that are abundant in foods that contain cholesterol, such as choline, zinc, niacin, vitamin A and vitamin D.

Cholesterol is a remarkable substance, without which all of us would die. There are three distinguishing factors which give animals an advantage over plants: a nervous system, mobility, and cholesterol. Cholesterol, absent from plants, is the key molecule that allows animals to have mobility and a nervous system. Cholesterol has unique chemical properties that are exploited in the lipid bilayers that surround all animal cells: as cholesterol concentrations are increased, membrane fluidity is decreased, up to a certain critical concentration, after which cholesterol starts toincrease fluidity (Haines, 2001). Animal cells exploit this property to great advantage in orchestrating ion transport, which is essential for both mobility and nerve signal transport. Animal cell membranes are populated with a large number of specialized island regions appropriately called lipid rafts. Cholesterol gathers in high concentrations in lipid rafts, allowing ions to flow freely through these confined regions. Cholesterol serves a crucial role in the non-lipid raft regions as well, by preventing small charged ions, predominantly sodium (Na+) and potassium (K+), from leaking across cell membranes. In the absence of cholesterol, cells would have to expend a great deal more energy pulling these leaked ions back across the membrane against a concentration gradient.

In addition to this essential role in ion transport, cholesterol is the precursor to vitamin D3, the sex hormones, estrogen, progesterone, and testosterone, and the steroid hormones such as cortisol. Cholesterol is absolutely essential to the cell membranes of all of our cells, where it protects the cell not only from ion leaks but also from oxidation damage to membrane fats. While the brain contains only 2% of the body's weight, it houses 25% of the body's cholesterol. Cholesterol is vital to the brain for nerve signal transport at synapses and through the long axons that communicate from one side of the brain to the other. Cholesterol sulfate plays an important role in the metabolism of fats via bile acids, as well as in immune defenses against invasion by pathogenic organisms.

Statin drugs inhibit the action of an enzyme, HMG coenzyme A reductase, that catalyses an early step in the 25-step process that produces cholesterol. This step is also an early step in the synthesis of a number of other powerful biological substances that are involved in cellular regulation processes and antioxidant effects. One of these is coenzyme Q10, present in the greatest concentration in the heart, which plays an important role in mitochondrial energy production and acts as a potent antioxidant (Gottlieb et al., 2000). Statins also interfere with cell-signaling mechanisms mediated by so-called G-proteins, which orchestrate complex metabolic responses to stressed conditions. Another crucial substance whose synthesis is blocked is dolichol, which plays a crucial role in the endoplasmic reticulum. We can't begin to imagine what diverse effects all of this disruption, due to interference with HMG coenzyme A reductase, might have on the cell's ability to function.

3. LDL, HDL, and Fructose

We have been trained by our physicians to worry about elevated serum levels of low density lipoprotein (LDL), with respect to heart disease. LDL is not a type of cholesterol, but rather can be viewed as a container that transports fats, cholesterol, vitamin D, and fat-soluble anti-oxidants to all the tissues of the body. Because they are not water-soluble, these nutrients must be packaged up and transported inside LDL particles in the blood stream. If you interfere with the production of LDL, you will reduce the bioavailability of all these nutrients to your body's cells.

The outer shell of an LDL particle is made up mainly of lipoproteins and cholesterol. The lipoproteins contain proteins on the outside of the shell and lipids (fats) in the interior layer. If the outer shell is deficient in cholesterol, the fats in the lipoproteins become more vulnerable to attack by oxygen, ever-present in the blood stream. LDL particles also contain a special protein called "apoB" which enables LDL to deliver its goods to cells in need. ApoB is vulnerable to attack by glucose and other blood sugars, especially fructose. Diabetes results in an increased concentration of sugar in the blood, which further compromises the LDL particles, by gumming up apoB. Oxidized and glycated LDL particles become less efficient in delivering their contents to the cells. Thus, they stick around longer in the bloodstream, and the measured serum LDL level goes up.

Worse than that, once LDL particles have finally delivered their contents, they become "small dense LDL particles," remnants that would ordinarily be returned to the liver to be broken down and recycled. But the attached sugars interfere with this process as well, so the task of breaking them down is assumed instead by macrophages in the artery wall and elsewhere in the body, through a unique scavenger operation. The macrophages are especially skilled to extract cholesterol from damaged LDL particles and insert it into HDL particles. Small dense LDL particles become trapped in the artery wall so that the macrophages can salvage and recycle their contents, and this is the basic source of atherosclerosis. HDL particles are the so-called "good cholesterol," and the amount of cholesterol in HDL particles is the lipid metric with the strongest correlation with heart disease, where less cholesterol is associated with increased risk. So the macrophages in the plaque are actually performing a very useful role in increasing the amount of HDL cholesterol and reducing the amount of small dense LDL.

The LDL particles are produced by the liver, which synthesizes cholesterol to insert into their shells, as well as into their contents. The liver is also responsible for breaking down fructose and converting it into fat (Collison et al., 2009). Fructose is ten times more active than glucose at glycating proteins, and is therefore very dangerous in the blood serum (Seneff1 et al., 2011). When you eat a lot of fructose (such as the high fructose corn syrup present in lots of processed foods and carbonated beverages), the liver is burdened with getting the fructose out of the blood and converting it to fat, and it therefore can not keep up with cholesterol supply. As I said before, the fats can not be safely transported if there is not enough cholesterol. The liver has to ship out all that fat produced from the fructose, so it produces low quality LDL particles, containing insufficient protective cholesterol. So you end up with a really bad situation where the LDL particles are especially vulnerable to attack, and attacking sugars are readily available to do their damage.

4. How Statins Destroy Muscles

Europe, especially the U.K., has become much enamored of statins in recent years. The U.K. now has the dubious distinction of being the only country where statins can be purchased over-the-counter, and the amount of statin consumption there has increased more than 120% in recent years (Walley et al, 2005). Increasingly, orthopedic clinics are seeing patients whose problems turn out to be solvable by simply terminating statin therapy, as evidenced by a recent report of three cases within a single year in one clinic, all of whom had normal creatine kinase levels, the usual indicator of muscle damage monitored with statin usage, and all of whom were "cured" by simply stopping statin therapy (Shyam Kumar et al., 2008). In fact, creatine kinase monitoring is not sufficient to assure that statins are not damaging your muscles (Phillips et al., 2002).

Since the liver synthesizes much of the cholesterol supply to the cells, statin therapy greatly impacts the liver, resulting in a sharp reduction in the amount of cholesterol it can synthesize. A direct consequence is that the liver is severely impaired in its ability to convert fructose to fat, because it has no way to safely package up the fat for transport without cholesterol (Vila et al., 2011). Fructose builds up in the blood stream, causing lots of damage to serum proteins.

The skeletal muscle cells are severely affected by statin therapy. Four complications they now face are: (1) their mitochondria are inefficient due to insufficient coenzyme Q10, (2) their cell walls are more vulnerable to oxidation and glycation damage due to increased fructose concentrations in the blood, reduced choleserol in their membranes, and reduced antioxidant supply, (3) there's a reduced supply of fats as fuel because of the reduction in LDL particles, and (4) crucial ions like sodium and potassium are leaking across their membranes, reducing their charge gradient. Furthermore, glucose entry, mediated by insulin, is constrained to take place at those lipid rafts that are concentrated in cholesterol. Because of the depleted cholesterol supply, there are fewer lipid rafts, and this interferes with glucose uptake. Glucose and fats are the main sources of energy for muscles, and both are compromised.

As I mentioned earlier, statins interfere with the synthesis of coenzyme Q10 (Langsjoen and Langsjoen, 2003), which is highly concentrated in the heart as well as the skeletal muscles, and, in fact, in all cells that have a high metabolic rate. It plays an essential role in the citric acid cycle in mitochondria, responsible for the supply of much of the cell's energy needs. Carbohydrates and fats are broken down in the presence of oxygen to produce water and carbon dioxide as by-products. The energy currency produced is adenosine triphosphate (ATP), and it becomes severely depleted in the muscle cells as a consequence of the reduced supply of coenzyme Q10.

The muscle cells have a potential way out, using an alternative fuel source, which doesn't involve the mitochondria, doesn't require oxygen, and doesn't require insulin. What it requires is an abundance of fructose in the blood, and fortunately (or unfortunately, depending on your point of view) the liver's statin-induced impairment results in an abundance of serum fructose. Through an anaerobic process taking place in the cytoplasm, specialized muscle fibers skim off just a bit of the energy available from fructose, and produce lactate as a product, releasing it back into the blood stream. They have to process a huge amount of fructose to produce enough energy for their own use. Indeed, statin therapy has been shown to increase the production of lactate by skeletal muscles (Pinieux et al, 1996).

Converting one fructose molecule to lactate yields only two ATP's, whereas processing a sugar molecule all the way to carbon dioxide and water in the mitochondria yields 38 ATP's. In other words, you need 19 times as much substrate to obtain an equivalent amount of energy. The lactate that builds up in the blood stream is a boon to both the heart and the liver, because they can use it as a substitute fuel source, a much safer option than glucose or fructose. Lactate is actually an extremely healthy fuel, water-soluble like a sugar but not a glycating agent.

So the burden of processing excess fructose is shifted from the liver to the muscle cells, and the heart is supplied with plenty of lactate, a high-quality fuel that does not lead to destructive glycation damage. LDL levels fall, because the liver can't keep up with fructose removal, but the supply of lactate, a fuel that can travel freely in the blood (does not have to be packaged up inside LDL particles) saves the day for the heart, which would otherwise feast off of the fats provided by the LDL particles. I think this is the crucial effect of statin therapy that leads to a reduction in heart attack risk: the heart is well supplied with a healthy alternative fuel.

This is all well and good, except that the muscle cells get wrecked in the process. Their cell walls are depleted in cholesterol because cholesterol is in such short supply, and their delicate fats are therefore vulnerable to oxidation damage. This problem is further compounded by the reduction in coenzyme Q10, a potent antioxidant. The muscle cells are energy starved, due to dysfunctional mitochondria, and they try to compensate by processing an excessive amount of both fructose and glucose anaerobically, which causes extensive glycation damage to their crucial proteins. Their membranes are leaking ions, which interferes with their ability to contract, hindering movement. They are essentially heroic sacrificial lambs, willing to die in order to safeguard the heart.

Muscle pain and weakness are widely acknowledged, even by the statin industry, as potential side effects of statin drugs. Together with a couple of MIT students, I have been conducting a study which shows just how devastating statins can be to muscles and the nerves that supply them (Liu et al, 2011). We gathered over 8400 on-line drug reviews prepared by patients on statin therapy, and compared them to an equivalent number of reviews for a broad spectrum of other drugs. The reviews for comparison were selected such that the age distribution of the reviewers was matched against that for the statin reviews. We used a measure which computes how likely it would be for the words/phrases that show up in the two sets of reviews to be distributed in the way they are observed to be distributed, if both sets came from the same probability model. For example, if a given side effect showed up a hundred times in one data set and only once in the other, this would be compelling evidence that this side effect was representative of that data set. Table 1 shows several conditions associated with muscle problems that were highly skewed towards the statin reviews.

I believe that the real reason why statins protect the heart from a heart attack is that muscle cells are willing to make an incredible sacrifice for the sake of the larger good. It is well acknowledged that exercise is good for the heart, although people with a heart condition have to watch out for overdoing it, walking a careful line between working out the muscles and overtaxing their weakened heart. I believe, in fact, that the reason exercise is good is exactly the same as the reason statins are good: it supplies the heart with lactate, a very healthy fuel that does not glycate cell proteins.

5. Membrane Cholesterol Depletion and Ion Transport

As I alluded to earlier, statin drugs interfere with the ability of muscles to contract through the depletion of membrane cholesterol. (Haines, 2001) has argued that the most important role of cholesterol in cell membranes is the inhibition of leaks of small ions, most notably sodium (Na+) and potassium (K+). These two ions are essential for movements, and indeed, cholesterol, which is absent in plants, is the key molecule that permits mobility in animals, through its strong control over ion leakage of these molecules across cell walls. By protecting the cell from ion leaks, cholesterol greatly reduces the amount of energy the cell needs to invest in keeping the ions on the right side of the membrane.

There is a widespread misconception that "lactic acidosis," a condition that can arise when muscles are worked to exahustion, is due to lactic acid synthesis. The actual story is the exact opposite: the acid build-up is due to excess breakdown of ATP to ADP to produce energy to support muscle contraction. When the mitochondria can't keep up with energy consumption by renewing the ATP, the production of lactate becomes absolutely necessary to preventacidosis (Robergs et al., 2004). In the case of statin therapy, excessive leaks due to insufficient membrane cholesterol require more energy to correct, and all the while the mitochondria are producing less energy.

In in vitro studies of phospholipid membranes, it has been shown that the removal of cholesterol from the membrane leads to a nineteen fold increase in the rate of potassium leaks through the membrane (Haines, 2001). Sodium is affected to a lesser degree, but still by a factor of three. Through ATP-gated potassium and sodium channels, cells maintain a strong disequilibrium across their cell wall for these two ions, with sodium being kept out and potassium being held inside. This ion gradient is what energizes muscle movement. When the membrane is depleted in cholesterol, the cell has to burn up substantially more ATP to fight against the steady leakage of both ions. With cholesterol depletion due to statins, this is energy it doesn't have, because the mitochondria are impaired in energy generation due to coenzyme-Q10 depletion.

Muscle contraction itself causes potassium loss, which further compounds the leak problem introduced by the statins, and the potassium loss due to contraction contributes significantly to muscle fatigue. Of course, muscles with insufficient cholesterol in their membranes lose potassium even faster. Statins make the muscles much more vulnerable to acidosis, both because their mitochondria are dysfunctional and because of an increase in ion leaks across their membranes. This is likely why athletes are more susceptible to muscle damage from statins (Meador and Huey, 2010, Sinzinger and O'Grady, 2004): their muscles are doubly challenged by both the statin drug and the exercise.

An experiment with rat soleus muscles in vitro showed that lactate added to the medium was able to almost fully recover the force lost due to potassium loss (Nielsen et al, 2001). Thus, production and release of lactate becomes essential when potassium is lost to the medium. The loss of strength in muscles supporting joints can lead to sudden uncoordinated movements, overstressing the joints and causing arthritis (Brandt et al., 2009). In fact, our studies on statin side effects revealed a very strong correlation with arthritis, as shown in the table.

While I am unaware of a study involving muscle cell ion leaks and statins, a study on red blood cells and plateletshas shown that there is a substantial increase in the Na+-K+-pump activity after just a month on a modest 10 mg/dl statin dosage, with a concurrent decrease in the amount of cholesterol in the membranes of these cells (Lohn et al., 2000). This increased pump activity (necessitated by membrane leaks) would require additional ATP and thus consume extra energy.

Muscle fibers are characterized along a spectrum by the degree to which they utilize aerobic vs anaerobic metabolism. The muscle fibers that are most strongly damaged by statins are the ones that specialize in anaerobic metabolism (Westwood et al., 2005). These fibers (Type IIb) have very few mitochondria, as contrasted with the abundant supply of mitochondria in the fully aerobic Type 1A fibers. I suspect their vulnerability is due to the fact that they carry a much larger burden of generating ATP to fuel the muscle contraction and to produce an abundance of lactate, a product of anaerobic metabolism. They are tasked with both energizing not only themselves but also the defective aerobic fibers (due to mitochondrial dysfunction) and producing enough lactate to offset the acidosis developing as a consequence of widespread ATP shortages.

6. Long-term Statin Therapy Leads to Damage Everywhere

Statins, then, slowly erode the muscle cells over time. After several years have passed, the muscles reach a point where they can no longer keep up with essentially running a marathon day in and day out. The muscles start literally falling apart, and the debris ends up in the kidney, where it can lead to the rare disorder, rhabdomyolysis, which is often fatal. In fact, 31 of our statin reviews contained references to "rhabdomyolysis" as opposed to none in the comparison set. Kidney failure, a frequent consequence of rhabdomyolysis, showed up 26 times among the statin reviews, as opposed to only four times in the control set.

The dying muscles ultimately expose the nerves that innervate them to toxic substances, which then leads to nerve damage such as neuropathy, and, ultimately Amyloid Lateral Sclerosis (ALS), also known as Lou Gehrig's disease, a very rare, debilitating, and ultimately fatal disease which is now on the rise due (I believe) to statin drugs. People diagnosed with ALS rarely live beyond five years. Seventy-seven of our statin reviews contained references to ALS, as against only 7 in the comparison set.

As ion leaks become untenable, cells will begin to replace the potassium/sodium system with a calcium/magnesium based system. These two ions are in the same rows of the periodic table as sodium/potassium, but advanced by one column, which means that they are substantially larger, and therefore it's much harder for them to accidentally leak out. But this results in extensive calcification of artery walls, heart valves, and the heart muscle itself. Calcified heart valves can no longer function properly to prevent backflow, and diastolic heart failure results from increased left ventricular stiffness. Research has shown that statin therapy leads to increased risk to diastolic heart failure (Silver et al., 2004, Weant and Smith, 2005). Heart failure shows up 36 times in our statin drug data as against only 8 times in the comparison group.

Once the muscles can no longer keep up with lactate supply, the liver and heart will be further imperilled. They're now worse off than they were before statins, because the lactate is no longer available, and the LDL, which would have provided fats as a fuel source, is greatly reduced. So they're stuck processing sugar as fuel, something that is now much more perilous than it used to be, because they are depleted in membrane cholesterol. Glucose entry into muscle cells, including the heart muscle, mediated by insulin, is orchestrated to occur at lipid rafts, where cholesterol is highly concentrated. Less membrane cholesterol results in fewer lipid rafts, and this leads to impaired glucose uptake. Indeed, it has been proposed that statins increase the risk to diabetes (Goldstein and Mascitelli, 2010, Hagedorn and Arora, 2010). Our data bear out this notion, with the probability of the observed distributions of diabetes references happening by chance being only 0.006.

7. Statins, Caveolin, and Muscular Dystrophy

Lipid rafts are crucial centers for transport of substances (both nutrients and ions) across cell membranes and as a cell signaling domain in essentially all mammalian cells. Caveolae ("little caves") are microdomains within lipid rafts, which are enriched in a substance called caveolin (Gratton et al., 2004). Caveolin has received increasing attention of late due to the widespread role it plays in cell signaling mechanisms and the transport of materials between the cell and the environment (Smart et al., 1999).

Statins are known to interfere with caveolin production, both in endothelial cells (Feron et al., 2001) and in heart muscle cells, where they've been shown to reduce the density of caveolae by 30% (Calaghan, 2010). People who have a defective form of caveolin-3, the version of caveolin that is present in heart and skeletal muscle cells, develop muscular dystrophy as a consequence (Minetti et al., 1998). Mice engineered to have defective caveolin-3 that stayed in the cytoplasm instead of binding to the cell wall at lipid rafts exhibited stunted growth and paralysis of their legs (Sunada et al., 2001). Caveolin is crucial to cardiac ion channel function, which, in turn, is essential in regulating the heart beat and protecting the heart from arrhythmias and cardiac arrest (Maguy et al, 2006). In arterial smooth muscle cells, caveolin is essential to the generation of calcium sparks and waves, which, in turn, are essential for arterial contraction and expansion, to pump blood through the body (Taggart et al, 2010).

In experiments involving constricting the arterial blood supply to rats' hearts, researchers demonstrated a 34% increase in the amount of caveolin-3 produced by the rat's hearts, along with a 27% increase in the weight of the left ventricle, indicating ventricular hypertrophy. What this implies is that the heart needs additional caveolin to cope with blocked vessels, whereas statins interfere with the ability to produce extra caveolin (Kikuchi et al., 2005).

8. Statins and the Brain

While the brain is not the focus of this essay, I cannot resist mentioning the importance of cholesterol to the brain and the evidence of mental impairment available from our data sets. Statins would be expected to have a negative impact on the brain, because, while the brain makes up only 2% of the body's weight, it houses 25% of the body's cholesterol. Cholesterol is highly concentrated in the myelin sheath, which encloses axons which transport messages long distances (Saher et al., 2005). Cholesterol also plays a crucial role in the transmission of neurotransmitters across the synapse (Tong et al, 2009). We found highly skewed distribution of word frequencies for dementia, Parkinson's disease, and short term memory loss, with all of these occurring much more frequently in the statin reviews than in the comparison reviews.

A recent evidence-based article (Cable, 2009) found that statin drug users had a high incidence of neurological disorders, especially neuropathy, parasthesia and neuralgia, and appeared to be at higher risk to the debilitating neurological diseases, ALS and Parkinson's disease. The evidence was based on careful manual labeling of a set of self-reported accounts from 351 patients. A mechanism for such damage could involve interference with the ability of oligodendrocytes, specialized glial cells in the nervous system, to supply sufficient cholesterol to the myelin sheath surrounding nerve axons. Genetically-engineered mice with defective oligodendrocytes exhibit visible pathologies in the myelin sheath which manifest as muscle twitches and tremors (Saher et al, 2005). Cognitive impairment, memory loss, mental confusion, and depression were also significantly present in Cable’s patient population. Thus, his analysis of 351 adverse drug reports was largely consistent with our analysis of 8400 reports.

9. Cholesterol's Benefits to Longevity

The broad spectrum of severe disabilities with increased prevalence in statin side effect reviews all point toward a general trend of increased frailty and mental decline with long-term statin therapy, things that are usually associated with old age. I would in fact best characterize statin therapy as a mechanism to allow you to grow old faster. A highly enlightening study involved a population of elderly people who were monitored over a 17 year period, beginning in 1990 (Tilvis et al., 2011). The investigators looked at an association between three different measures of cholesterol and manifestations of decline. They measured indicators associated with physical frailty and mental decline, and also looked at overall longevity. In addition to serum cholesterol, a biometric associated with the ability to synthesize cholesterol (lathosterol) and a biometric associated with the ability to absorb cholesterol through the gut (sitosterol) were measured.

Low values of all three measures of cholesterol were associated with a poorer prognosis for frailty, mental decline and early death. A reduced ability to synthesize cholesterol showed the strongest correlation with poor outcome. Individuals with high measures of all three biometrics enjoyed a 4.3 year extension in life span, compared to those for whom all measures were low. Since statins specifically interfere with the ability to synthesize cholesterol, it is logical that they would also lead to increased frailty, accelerated mental decline, and early death.

For both ALS and heart failure, survival benefit is associated with elevated cholesterol levels. A statistically significant inverse correlation was found in a study on mortality in heart failure. For 181 patients with heart disease and heart failure, half of those whose serum cholesterol was below 200 mg/dl were dead three years after diagnosis, whereas only 28% of the patients whose serum cholesterol was above 200 mg/dl had died. In another study on a group of 488 patients diagnosed with ALS, serum levels of triglycerides and fasting cholesterol were measured at the time of diagnosis (Dorstand et al., 2010). High values for both lipids were associated with improved survival, with a p-value < 0.05.

10. What to do Instead to Avoid Heart Disease

If statins don't work in the long run, then what can you do to protect your heart from atherosclerosis? My personal opinion is that you need to focus on natural ways to reduce the number of small dense LDL particles, which feed the plaque, and alternative ways to supply the product that the plaque produces (more about that in a moment). Obviously, you need to cut way back on fructose intake, and this means mainly eating whole foods instead of processed foods. With less fructose, the liver won't have to produce as many LDL particles from the supply side. From the demand side, you can reduce your body's dependency on both glucose and fat as fuel by simply eating foods that are good sources of lactate. Sour cream and yogurt contain lots of lactate, and milk products in general contain the precursor lactose, which gut bacteria will convert to lactate, assuming you don't have lactose intolerance. Strenuous physical exercise, such as a tread machine workout, will help to get rid of any excess fructose and glucose in the blood, with the skeletal muscles converting them to the much coveted lactate.

Finally, I have a set of perhaps surprising recommendations that are based on research I have done leading to the two papers that are currently under review (Seneff3 et al, Seneff4 et al.). My research has uncovered compelling evidence that the nutrient that is most crucially needed to protect the heart from atherosclerosis is cholesterol sulfate. The extensive literature review my colleagues and I have conducted to produce these two papers shows compellingly that the fatty deposits that build-up in the artery walls leading to the heart exist mainly for the purpose of extracting cholesterol from glycated small dense LDL particles and synthesizing cholesterol sulfate from it, providing the cholesterol sulfate directly to the heart muscle. The reason the plaque build-up occurs preferentially in the arteries leading to the heart is so that the heart muscle can be assured an adequate supply of cholesterol sulfate. In our papers, we develop the argument that the cholesterol sulfate plays an essential role in the caveolae in the lipid rafts, in mediating oxygen and glucose transport.

The skin produces cholesterol sulfate in large quantities when it is exposed to sunlight. Our theory suggests that the skin actually synthesizes sulfate from sulfide, capturing energy from sunlight in the form of the sulfate molecule, thus acting as a solar-powered battery. The sulfate is then shipped to all the cells of the body, carried on the back of the cholesterol molecule.

Evidence of the benefits of sun exposure to the heart is compelling, as evidenced by a study conducted to investigate the relationship between geography and cardiovascular disease (Grimes et al., 1996). Through population statistics, the study showed a consistent and striking inverse linear relationship between cardiovascular deaths and estimated sunlight exposure, taking into account percentage of sunny days as well as latitude and altitude effects. For instance, the cardiovascular-related death rate for men between the ages of 55 and 64 was 761 in Belfast, Ireland but only 175 in Toulouse, France.

Cholesterol sulfate is very versatile. It is water soluble so it can travel freely in the blood stream, and it enters cell membranes ten times as readily as cholesterol, so it can easily resupply cholesterol to cells. The skeletal and heart muscle cells make good use of the sulfate as well, converting it back to sulfide, and synthesizing ATP in the process, thus recovering the energy from sunlight. This decreases the burden on the mitochondria to produce energy. The oxygen released from the sulfate molecule is a safe source of oxygen for the citric oxide cycle in the mitochondria.

So, in my view, the best way to avoid heart disease is to assure an abundance of an alternative supply of cholesterol sulfate. First of all, this means eating foods that are rich in both cholesterol and sulfur. Eggs are an optimal food, as they are well supplied with both of these nutrients. But secondly, this means making sure you get plenty of sun exposure to the skin. This idea flies in the face of the advice from medical experts in the United States to avoid the sun for fear of skin cancer. I believe that the excessive use of sunscreen has contributed significantly, along with excess fructose consumption, to the current epidemic in heart disease. And the natural tan that develops upon sun exposure offers far better protection from skin cancer than the chemicals in sunscreens.

11. Concluding Remarks

Every individual gets at most only one chance to grow old. When you experience your body falling apart, it is easy to imagine that this is just due to the fact that you are advancing in age. I think the best way to characterize statin therapy is that it makes you grow older faster. Mobility is a great miracle that cholesterol has enabled in all animals. By suppressing cholesterol synthesis, statin drugs can destroy that mobility. No study has shown that statins improve all-cause mortality statistics. But there can be no doubt that statins will make your remaining days on earth a lot less pleasant than they would otherwise be.

To optimize the quality of your life, increase your life expectancy, and avoid heart disease, my advice is simple: spend significant time outdoors; eat healthy, cholesterol-enriched, animal-based foods like eggs, liver, and oysters; eat fermented foods like yogurt and sour cream; eat foods rich in sulfur like onions and garlic. And finally, say "no, thank-you" to your doctor when he recommends statin therapy.

References

Improve Your Digestion Naturally

Fermented foods boost digestive function

Suspicions have been confirmed for those wary of vaccinating their children. A recent large study corroborates other independent study surveys comparing unvaccinated children to vaccinated children.

They all show that vaccinated children have two to five times more childhood diseases, illnesses, and allergies than unvaccinated children.

Originally, the recent still ongoing study compared unvaccinated children against a German national health survey conducted by KiGGS involving over 17,000 children up to age 19. This currently ongoing survey study was initiated by classical homoeopathist Andreas Bachmair.

However, the American connection for Bachmair’s study can be found at VaccineInjury.info website that has added a link for parents of vaccinated children to participate in the study. So far this ongoing survey has well over 11,000 respondents, mostly from the U.S.A. Other studies have surveyed smaller groups of families.

Nevertheless, the results were similar. Of course, none of these studies were picked up by the MSM (mainstream media). None were funded by the Centers for Disease Control and Prevention (CDC) or the World Health Organization (WHO) or any national or international health agency or medical profession group (http://healthimpactnews.com).

Dramatic, debilitating, or lethal vaccine injuries were not the focus since so few, five percent or less, actually get reported to VAERS (Vaccine Adverse Injury Reporting System) in the U.S.A. for various reasons including:

Consequently, even the most terrible adverse reactions are minimally acknowledged, while long term negative health issues resulting from vaccines are not even considered relevant.

Different surveys summarized

The childhood diseases usually posed to respondents by the independent surveys involved asthma, reoccurring tonsillitis, chronic bronchitis, sinusitis, allergies, eczema, ear infections, diabetes, sleep disorders, bedwetting, dyslexia, migraines, hyperactivity, ADD, epilepsy, depression, and slower development of speech or motor skills.

In 1992, a New Zealand group called the Immunization Awareness Society (IAS) surveyed 245 families with a total of 495 children. The children were divided with 226 vaccinated and 269 unvaccinated. Eighty-one families had both vaccinated and unvaccinated children.

The differences were dramatic, with unvaccinated children showing far less incidence of common childhood ailments than vaccinated children (http://www.vaccineinjury.info/images/stories/ias1992study.pdf).

From a different survey in the South Island New Zealand city of Christchurch, among children born during or after 1977, none of the unvaccinated children had asthma events where nearly 25% of the vaccinated children were treated for asthma by age 10 (http://www.vaccineinjury.info/images/stories/ias1992study.pdf).

Many of the comments from non-vaccinating parents to VaccineInjury.info for the ongoing Bachmair survey mentioned vaccination danger and developing true immunity naturally were concerns (http://www.vaccineinjury.info).

A PhD immunologist who wrote the book Vaccine Illusion, Dr. Tetyana Obukhanych, has gone against the dogma of her medical training and background. She asserts that true immunity to any disease is not conferred by vaccines. Exposure to the disease, whether contracted or not, does (http://www.vaccinationcouncil.org).

Perhaps the most informal grass-roots survey going on now is by Tim O’Shea, DC, author of Vaccination is Not Immunization. He simply has non-vaccinating parents email him with comparisons of their children’s health to friends and families they know with vaccinated children. That and more is available on his site (http://www.thedoctorwithin.com).

Sources for this article include:

http://healthimpactnews.com

http://www.vaccineinjury.info/images/stories/ias1992study.pdf

Link to participate in Bachmair survey here: http://www.vaccineinjury.info

http://www.vaccinationcouncil.org

http://www.thedoctorwithin.com

Source : http://www.naturalnews.com/036220_vaccinated_children_disease_allergies.html#ixzz1yHhh899a

Infographic: High Intensity Interval Training (HIIT)

Oxygen Debt | The Excess Post-Exercise Oxygen Consumption Effect

 

Brad Taylor
NaturalSociety
May 13, 2012

Everyone knows that exercise leads to a healthy body, strong muscles, reduced stress, and weight loss. But what many people don’t consider is what happens on an internal level after exercise is complete. The number of techniques or strategies which could be implemented into your workout for greater achievement is endless. Some people think that steady, long, low-intensity workouts provide the best results, but this isn’t true. Jogging is a healthy activity, and walking may even be better, but rigorous exercise has a more profound impact on an effect that occurs in your body following exercise known as excess post-exercise oxygen consumption in order to take care of what’s referred to as oxygen debt.

Excess Post-Exercise Oxygen Consumption

EPOC refers to the rate of oxygen consumed in order to return to a homeostasis state and ‘fix’ the body’s oxygen debt. Although a light worker does trigger EPOC, the effect is bound to be more powerful and continue for a longer period of time after a vigorous workout. After performing a low-intensity workout, the body’s demand for oxygen simply isn’t as pertinent.

To attain a higher demand for oxygen and use more oxygen in the process of a workout, a high-intensity, anaerobic exercise should be performed. For every liter of oxygen consumed, approximately 5 calories are burned, making high intensity workouts trigger a greater oxygen debt, EPOC response. Exercising hard enough to cause heavy breathing is the level to aim for.

Oxygen Debt and the Effect of EPOC

In addition to returning to a homeostasis state, the body releases energy at a higher rate. During this time period, the body begins to restore itself.

• Replenishing it’s Energy Resources – Your body needs to replenish it’s energy, especially immediate sources of energy. To do this, your body taps into what’s known as the phosphagen system and restores the creatine phosphate and ATP.  In addition, lactic acid is being reconverted to glucose, and muscle glycogen levels are being restored during this process.

• Re-oxygenating the Blood & Renewing Circulatory Hormones - Energy is expended in order to re-oxygenate the blood for excess oxygen use. In addition, circulatory hormones which become elevated after exercise return to normal levels.

• Decrease in Temperature – Energy is expended in an attempt to go back to normal body temperature.

• Rebound to Normal Heart Rate – In an attempt to return to a normal heart and breathing rate, the body expends energy at an increased level.

When is oxygen debt mostly experienced?

Research suggests that maximal EPOC response is generated through the following list with 1 being the most effective method and 3 being the least effective method. In terms of EPOC response, the amount of elevation of oxygen consumption and the lasting effects are based on the length and intensity of the workout. Here are ways to ignite higher EPOC response.

1. Highly intense resistance workouts
2. Highly intense cardiovascular workouts
3. Highly intense cardiovascular workouts revolving around interval training

High-intensity interval training, or HIIT, is one  intense interval training workout proven to stimulate greater EPOC response.

There are certain aerobic exercises such as cycling that may bring forth a lesser magnitude (amount of increased oxygen consumption) and duration (length of increased oxygen consumption) of EPOC than heavy weight training based on research conducted.

FOODS TO Limit or AVOID

Avoiding Foods That Cause Problems

Don't Just Remove. Replace!

There's no need to go hungry on The Hallelujah Diet. There's a healthy alternative for almost everything you crave.

Click here to download our handy replacement guide.

Watch out for these!

What most people do not realize is that almost every physical problem they experience, other than accidents, has a diet related cause.

Because our physical body is designed by God to be nourished with living (raw) foods, it is imperative that the greatest percentage of our daily food intake be composed of raw foods—and that we avoid the foods that are causing the problems in the first place.

Here are a list of foods that are excluded from The Hallelujah Diet. Although this list is far from comprehensive, using it as a guide will help you determine whether or not other foods are beneficial.

Beverages

• Alcohol
• Coffee (grain coffees like Pero and Roma are fine)
• Teas containing caffeine (caffeine-free herb teas are fine)
• Carbonated beverages and soft drinks
• All artificial and sugar containing drinks, sport drinks, and all juices containing preservatives, refined salt, sugar, and artificial sweeteners

Refined sugar suppresses the immune system and prevents its ability to protect us from germs, viruses, and bad bacteria. One 12 oz soft drink contains approximately 11 teaspoons of sugar and if consumed daily for one year, adds 15 pounds of weight.

Dairy

• All milk, cheese, ice cream, whipped toppings, and non-dairy creamers

Cow milk and cheese are some of the most dangerous foods we can place into our body. Read Dr. T. Colin Campbell’s book, The China Study for documentation (it will change your life).

Soy Milk and other Soy Products

• Most soy products should be avoided

Soy is high in estrogen. The estrogen in soy formulas has been known to cause baby girls to develop breast buds as young as two years of age, and the age of puberty, which should be past the age of 15 years, is now as early as 8, 9, and 10 years.

The growth hormones in animal flesh and dairy are also contributing to this problem. Estrogen can be a contributing factor in all female cancers, and the high protein content of soy can actually feed cancers.

Processed Fruits

• Canned and sweetened fruits
• Non-organic and sulfured dried fruits

Refined Grains

• Refined, bleached flour products, most cold breakfast cereals, and white rice

Refined grains are devoid of fiber and thus one of the leading causes of constipation. Animal-source foods are also totally devoid of fiber.

All Meats and Eggs

• Beef, pork, fish, chicken, eggs, turkey, hamburgers, hot dogs, bacon, sausage, bologna, etc.

All animal-source foods are harmful to the body and are the cause of up to 90% of all physical problems. Eliminating animal source foods can practically eliminate the fear of having a heart attack, stroke, cardiovascular problems, cancer, diabetes, osteoporosis, heartburn, gout, acid stomach, and the list goes on and on.

Certain Nuts and Seeds

• All roasted and/or salted seeds and nuts

Peanuts in particular are not a nut but a legume, and very difficult to digest.

Certain Oils

• All lard, margarine, shortenings, and anything containing hydrogenated oils or trans fats

Certain Seasonings

• Refined table salt and any seasonings containing it

Unlike mineral-rich unrefined salt, which is beneficial, refined table salt is devoid of such minerals, containing 97% to 99% sodium chloride. It is a leading cause of high blood pressure. Celtic or Eden Sea Salt, a natural, unrefined salt from the sea, is a good choice.

Certain Soups

• Any canned, packaged, or creamed soups containing salt or dairy products

Certain Sweets

• All refined white or brown sugar (brown sugar is simply refined white sugar with some molasses added for color)
• Sugar syrups
• Chocolate (carob is a wonderful chocolate substitute)
• Candy, gum, cookies, donuts, cakes, pies, or other products containing refined sugars or artificial sweeteners

Acceptable sweeteners include raw unfiltered honey, stevia, agave nectar, and pure maple syrup (use any of these sparingly).

Processed Vegetables

• All canned vegetables with added salt or preservatives
• Vegetables fried in oil

All Drugs

Though these are not foods, most are addictive and very destructive within the body:

• Alcohol
• Nicotine
• Caffeine
• Marijuana, cocaine, heroin, etc.
• Many over the counter and doctor-prescribed drugs

NOTE: Do not discontinue doctor prescribed drugs without doctor’s permission.

Why Your Doctor’s Advice May Be Fatally Flawed

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by Dr. Mercola

Curious about the prevalence and extent of scientific misconduct, researchers at the University of Illinois at Chicago’s Center for Pharmacoeconomic Research investigated the reasons why research studies were retracted, and from whereⁱ.

The highest number of incidents of misconduct occurred in the drug literature, as compared to general biomedical literature. Nearly 75 percent of the retracted drug studies were attributed to scientific misconduct, which includes:

• Data falsification or fabrication
• Questionable veracity
• Unethical author conduct
• Plagiarism

This is a significant rise when compared to a 1998 review—cited in the featured NewsWise article—in which 37 percent of scientific retractions between 1966 and 1997 were due to scientific misconduct. Even more shocking: According to data from Thomson Reuters, the numbers of scientific retractions have climbed more than 15-fold since 2001ⁱⁱ!

The most unfortunate thing about this is that these are the types of studies many health care professionals rely on to make treatment recommendations. Large numbers of patients can be affected when false findings are published, as the average lag time between publication of the study and the issuing of a retraction is 39 months. And that’s if it’s ever caught at all.

Just How Scientific is “Science-Based Medicine” Really?

I am a big believer in the scientific method, provided it’s applied appropriately that is. And that’s the key issue here. In order to qualify in the first place, the research must be unbiased, unprejudiced and free from any significant conflicts of interest. Sadly, this is not the case with most of modern medicine—especially not when it comes to drug research, as evidenced by the featured findings.

It’s quite shocking that nearly three-quarters of all retracted drug studies are due to pure falsification of data. Especially when you consider that even well-researched drugs can still have significant side effects.

Just imagine the potential for tragedy when a drug is based largely on pure fantasy!

Vioxx is perhaps one of the better examples of what can happen when a drug is manufactured and sold under false pretenses. It killed more than 60,000 people in just a few years time, before it was removed from the market. In the case of Vioxx, there are lingering questions about the soundness of the research backing the drug in the first place. Back in 2008, Dr. Joseph S. Ross of New York’s Mount Sinai School of Medicine came across ghostwritten research studies for Vioxx while reviewing documents related to lawsuits filed against Merck.

According to an April 16, 2008 article on MedHeadlinesⁱⁱⁱ:

“In about 96 journal publications, Ross and his colleagues discovered internal Merck documents and e-mail messages pertaining to clinical study reports and review articles, some of which were developed by the company’s marketing department, not its scientific department. In others, there is little evidence that the authors recruited for the report made substantial contribution to the research itself. … Some of the authors listed in the Merck study reports of concern… question the true nature of ghostwriting. One neurologist originally listed as “External author?” and then listed as Dr. Leon J. Thal, of the University of California, San Diego in the final draft, died a year ago in an airplane crash.”

An editorial published in the Journal of the American Medical Association (JAMA)^iv that year by Drs. Psaty and Kronmal also questioned whether Merck might have deliberately manipulated dozens of academic documents published in the medical literature, in order to promote Vioxx under false pretenses.

Avandia is another potent example. This diabetes medication hit the market in 1999 and quickly became a blockbuster drug. By 2006 its annual revenue was $3.2 billion. A year later, a damning study published in the New England Journal of Medicine (NEJM) linked Avandia to a 43 percent increased risk of heart attack and a 64 percent higher risk of cardiovascular deaththan patients treated with other methods.

Between 1999 and 2007, Avandia is estimated to have caused over 80,000 unnecessary heart attacks^v, although the actual numbers of people harmed or killed by the drug is still largely unknown. The most recent analysis by the Cleveland Clinic in 2010^vi, which used data from 56 clinical Avandia trials, calculated that for every 37 to 52 patients who take Avandia for five years, one additional heart attack can be expected as a result of the drug. As a result, the authors of this meta-analysis estimate the number of deaths caused by Avandia to be around 48,000, between 1999 and 2009.

This is a steep price, to say the least, for a disease that does not require drugs to begin with. Avandia is a poster child for the lethal paradigm of faux science as GlaxoSmithKline, the manufacturer of Avandia, hid damaging information about the drug for over 10 years^vii, as it would adversely affect sales!

Again and again we are confronted with indisputable evidence that the drug paradigm is about money, not health, and certainly not dependable scientific inquiry.

Since that 2007 NEJM study, data from various trials, studies and meta-analyses have consistently confirmed the dangers of Avandia, and based on the evidence amassed over the past three years, the European Medicines Agency is now recommending the withdrawal of rosiglitazone-containing diabetic drugs due to the increased risk of ischaemic heart disease. NEJM also hit the nail on its head with the statement that,

“[T]he case of rosiglitazone underscores the need for a robust evidence base to demonstrate the safety of medicines administered long-term.”

Unfortunately, a committee of independent experts recommended that Avandia remain on the US market, despite its risks, and an FDA oversight board voted 8 to 7 to accept the advice.

It’s important to understand that our current medical system has been masterfully orchestrated by the drug companies to create a system that gives the perception of science when really it is a heavily manipulated process designed to manipulate and deceive you into using expensive and potentially toxic drugs that benefit the drug companies more than it benefits your health. Across the board, drugmakers do an excellent job of publicizing the findings they want you to know, while keeping very quiet about the rest.

It’s important to realize that all research is NOT published. And it should come as no surprise that drug studies funded by a pharmaceutical company that reaches a negative conclusion will rarely ever see the light of day… What this means is that even if you scour the medical literature to determine what the consensus is on any given medical topic, what you’ll find is an overwhelming preponderance of data in favor of the drug approach that in no way, shape or form reflects the reality of the scientific investigation that went into that specific drug.

How Drug Companies Manipulate Research Evidence to Fool You

The pharmaceutical industry as a whole has become the poster-child for fraud, deception, and manipulation of science for profit. Nearly 20 percent of the top 100 Corporate Criminals listed for the 1990s were in fact drug companies!

In an online series called Transparency and Medicine featured on the web site The Conversation^viii, Jon Jureidini discusses how science-based medicine is clouded by marketing departments that control and distort information in the medical literature. Jureidini is a professor of psychiatry at the University of Adelaide (Australia), who got an inside look at this murky mess while examining drug company internal documents as an expert witness in a case against a pharmaceutical company. The voluminous amounts of documents he was given access to showed “serious misrepresentation” of both the effectiveness and safety of certain drugs, with published articles making the research appear positive, while negative secondary outcomes were deleted.

When you consider that this is the type of research data that then ends up being used to make treatment decisions for years to come by many expert review panels, is it any wonder the United States has the most expensive health care in the world, while STILL experiencing a decline in life expectancy and other health indexes? The whole idea that modern medicine is science-based has become laughable, as the evidence tells a whole different story…

The Snowball Effect Caused by Fabricated Research

Last year, the Office of Research Integrity at the U.S. Department of Health found that a Boston University cancer scientist had fabricated two of his studies^ix. This case is a perfect example of how even a small number of fraudulent studies can wreak havoc with the science-based paradigm. The fabricated work of Sheng Wang, PhD, was published in two journals in 2009, and he’s been ordered to retract them^x.

But important studies by other scientists, like those at the Mayo Clinic, have in turn based their work on his flights-of-fantasy… As a result of the fall-out, 17 papers published in nine different research journals have been retracted, according to the Mayo Clinic.

Another example is that of Dr. Scott Reuben, a well-respected, prominent anesthesiologist, former chief of acute pain of the Baystate Medical Center, Springfield, Mass. and a former professor at Tufts University’s medical school, who in 2009 was found to have fabricated the data for 21 studies! Dr. Reuben succeeded in getting many of them published, and those studies were used to sway the prescribing habits of doctors. It was only due to a routine audit raising a few red flags that a larger investigation was later launched.

Consider the implications of this for a moment.

If one case involving just two falsified studies led to the retraction of 17 others, just imagine how many studies are affected or effectively invalidated by the 742 studies retracted between 2000 and 2010!^xi

Unfortunately, despite retractions, fabricated research may still inadvertently live on, as it has been cited by other studies, and once a finding is accepted in the medical community, it’s difficult to reverse it. What’s worse, according to a 2011 study in the Journal of Medical Ethics^xii, nearly 32 percent of retracted papers were not noted as having been retracted by the journal in question, leaving the readers completely in the dark about the inaccuracies in those studies!

Beyond Fabrication—Flawed Research and Unsupported Conclusions

Peer-reviewed research published in medical journals gets the golden star of approval in the media, yet many of the findings—even if they’re not outright fabrications—can, and frequently are, incredibly misleading. One of the best exposé’s on this topic came from Dr. Marcia Angell, the former editor-in-chief of the New England Journal of Medicine (NEJM) who wrote the book The Truth about Drug Companies: How They Deceive Us and What to Do About It. According to Angell:

“Trials can be rigged in a dozen ways, and it happens all the time.”

Also, back in 2005, Dr. John Ioannidis, an epidemiologist at Ioannina School of Medicine, Greece, showed that there is less than a 50 percent chance that the results of any randomly chosen scientific paper will be true!^xiii According to his study:

“Simulations show that for most study designs and settings, it is more likely for a research claim to be false than true.”

He noted problems with the experimental and statistical methods used, including factors such as small sample sizes, poor study design, researcher bias and selective reporting. In 2008, Dr. Ioannidis again showed that much of scientific research being published is highly questionable…

The system itself is in large part to blame, because journals tend to be more likely to publish studies that show dramatic results, positive results, or results from “hot” competitive fields. For instance, a Cochrane Collaboration review and analysis of publishedflu vaccine studies found that flu vaccine studies sponsored by industry are treated more favorably by medical journals even when the studies are of poor quality.

It Gets Worse… Nearly 90 Percent of Cancer Studies Cannot be Replicated

As if things couldn’t get any worse, disturbing news reported by Reuters^xiv earlier this year showed that the vast majority of the “landmark” studies on cancer are unreliable—and a high proportion of those unreliable studies come from respectable university labs. Former drug company researcher Glenn Begley looked at 53 papers in the world’s top journals, and found that he and a team of scientists could NOT replicate 47 of the 53 published studies—all of which were considered important and valuable for the future of cancer treatments! The allegations appeared in the March 28 issue of the prestigious journal Nature^xv.

“It was shocking,” Glenn Begley, now senior vice president of privately held biotechnology company TetraLogic, told Reuters. “These are the studies the pharmaceutical industry relies on to identify new targets for drug development. But if you’re going to place a $1 million or $2 million or $5 million bet on an observation, you need to be sure it’s true. As we tried to reproduce these papers we became convinced you can’t take anything at face value.”

Part of the problem, they said, is that scientists often ignore negative findings in their results that might raise a warning. Instead, they opt for cherry-picking conclusions in an effort to put their research in a favorable light. Begley’s experience echoes a report from scientists at Bayer AG last year. Neither group of researchers alleges fraud however; nor would they identify the research they had tried to replicate, Reuters said.

Clearly, if we are to ever move forward, we cannot continue basing treatments on fraudulent and/or inaccurate research… It’s important to realize that if a study cannot be successfully and reliably reproduced, it is, quite simply, wrong. In order to be truly science-based, our medical protocols and drug treatments must be based on findings that are replicable.

Sadly, much of today’s “science” is financially motivated. According to NBC News^xvi:

“As Begley and Ellis detail it, “To obtain funding, a job, promotion or tenure, researchers need a strong publication record…Journal editors, reviewers, and grant review committees… often look for a scientific finding that is simple, clear and complete—a ‘perfect’ story. It is therefore tempting for investigators to submit suspected data sets for publication, or even to massage data.” Whatever the motivation, the results are all too often wrong.

Begley and Ellis call for nothing less than a change in the culture of cancer research. They demand more willingness to admit to imperfections and an end to the practice of failing to publish negative results. “We in the field,” they say, “must remain focused on the purpose of cancer research: to improve the lives of patients.”

How to Get Solid Information in an Era of Confusion and Corruption

Ultimately, the take-home message here is that even if a drug or treatment is “backed by science,” this in no way guarantees it is safe or effective. Likewise, if an alternative treatment has not been published in a medical journal, it does not mean it is unsafe or ineffective.

You’ve got to use all the resources available to you, including your own sense of common sense and reason, true experts’ advice and other’s experiences, to determine what medical treatment or advice will be best for you in any given situation. I advise you to remain skeptical but open — even if it is something I’m saying, you need to realize that YOU are responsible for your and your family’s health, not me, and certainly not drug companies trying to sell their wares and convince you to take dangerous “symptom-cover-ups” disguised as science-based solutions.

Since it is very well established that most prescribed drugs do absolutely nothing to treat the cause of disease, it would be prudent to exercise the precautionary principle when evaluating ANY new drug claim, as it will more than likely be seriously flawed, biased, or worse…

If you’re facing a health challenge it is best to identify a qualified natural health consultant—someone who really understands health at a foundational level and has had extensive experience in helping others resolve their health care challenges. Just make sure to see a competent regular physician to make certain any serious disorders like cancer are ruled out as well.

References:

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Read the Full Article Here: http://articles.mercola.com/sites/articles/archive/2012/07/12/drug-companies-on-scientific-fraud.aspx