10 Facts About Fluoride
Attorney Michael Connett summarizes 10 basic facts about fluoride that should be considered in any discussion about whether to fluoridate water. To download the flyer that accompanies this video, visit: http://www.fluoridealert.org/uploads/…. To watch Michael debate two advocates of fluoridation, see: http://www.wpsu.org/conversationslive….
Brazil looks to ban Monsanto’s Roundup, other toxicity risks
RT | March 27, 2014
Brazil’s public prosecutor wants to suspend use of glyphosate, the active ingredient in Monsanto’s pervasive herbicide Roundup. A recent study suggested glyphosate may be linked to a fatal kidney disease that has affected poor farming regions worldwide.
The Prosecutor General’s office is also pursuing bans on the herbicide 2,4-D and seven other active herbicide ingredients in addition to glyphosate: methyl parathion, lactofem, phorate, carbofuran, abamectin, tiram, and paraquat, GMWatch reported.
The Prosecutor General of Brazil “seeks to compel the National Health Surveillance Agency (ANVISA) to reevaluate the toxicity of eight active ingredients suspected of causing damage to human health and the environment,” according to the prosecutor’s website. “On another front, the agency questions the registration of pesticides containing 2,4-D herbicide, applied to combat broadleaf weeds.”
The two actions have already been filed with Brazil’s justice department.
The prosecutor is also seeking a preliminary injunction that would allow the Ministry of Agriculture, Livestock and Supply to suspend further registration of the eight ingredients until ANVISA can come to a conclusion.
The country’s National Biosafety Technical Commission has been asked to prohibit large-scale sale of genetically modified seeds resistant to the 2,4-D as ANVISA deliberates.
Last week, Brazil’s Federal Appeals Court ruled to cancel use of Bayer’s Liberty Link genetically-modified maize. Earlier this month, France banned the sale, use, and cultivation of Monsanto’s genetically-modified maize MON 810. New research found insects in the United States are developing a resistance to the genetically-engineered maize.
As for glyphosate, new research suggests it becomes highly toxic to the human kidney once mixed with “hard” water or metals like arsenic and cadmium that often exist naturally in the soil or are added via fertilizer. Hard water contains metals like calcium, magnesium, strontium, and iron, among others. On its own, glyphosate is toxic, but not detrimental enough to eradicate kidney tissue.
The glyphosate molecule was patented as a herbicide by Monsanto in the early 1970s. The company soon brought glyphosate to market under the name “Roundup,” which is now the most commonly used herbicide in the world.
Two weeks ago, Sri Lanka banned glyphosate given the links to an inexplicable kidney disease, Chronic Kidney Disease of Unknown etiology, known as CKDu, according to the Center for Public Integrity. CKDu has killed thousands of agricultural workers, many in Sri Lanka and El Salvador.
El Salvador’s legislature approved in September a ban on glyphosate and many other agrochemicals, yet the measure is not yet law.
Related article
How Statins Really Work Explains Why They Don’t Really Work
By Stephanie Seneff | March 11, 2011
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.
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 to increase 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.
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.
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.
Side Effect # Statin Reviews # Non-Statin Reviews Associated P-value Muscle Cramps 678 193 0.00005 General Weakness 687 210 0.00006 Muscle Weakness 302 45 0.00023 Difficulty Walking 419 128 0.00044 Loss of Muscle Mass 54 5 0.01323 Numbness 293 166 0.01552 Muscle Spasms 136 57 0.01849 Table 1: Counts of the number of reviews where phrases associated with various symptoms related to muscles appeared, for 8400 statin and 8400 non-statin drug reviews, along with the associated p-value, indicating the likelihood that this distribution could have occurred by chance.
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.
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 prevent acidosis (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 platelets has 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.
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 Amyotrophic 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.
Side Effect # Statin Reviews # Non-Statin Reviews Associated P-value Rhabdomyolysis 31 0 0.02177 Liver Damage 326 133 0.00285 Diabetes 185 62 0.00565 ALS 71 7 0.00819 Heart Failure 36 8 0.04473 Kidney Failure 26 4 0.05145 Arthritis 245 120 0.01117 Memory Problems 545 353 0.01118 Parkinson’s Disease 53 3 0.01135 Neuropathy 133 73 0.04333 Dementia 41 13 0.05598 Table 2: Counts of the number of reviews where phrases associated with various symptoms related to major health issues appeared, besides muscle problems, for 8400 statin and 8400 non-statin drug reviews, along with the associated p-value, indicating the likelihood that this distribution could have occurred by chance.
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).
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.
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.
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.
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
[1] K.D. Brandt, P. Dieppe, E. Radin, “Etiopathogenesis of osteoarthritis”. Med. Clin. North Am. 93 (1): 1–24, 2009.
[2] J. Cable, “Adverse Events of Statins – An Informal Internet-based Study,” JOIMR, 7(1), 2009. [3] S. Calaghan, “Caveolae as key regulators of cardiac myocyte beta2 adrenoceptor signalling: a novel target for statins” Research Symposium on Caveolae: Essential Signalosomes for the Cardiovascular System, Proc Physiol Soc 19, SA21, University of Manchester, 2010.
[4] K.S. Collison, S.M. Saleh, R.H. Bakheet, R.K. Al-Rabiah, A.L. Inglis, N.J. Makhoul, Z.M. Maqbool, M. Zia Zaidi, M.A. Al-Johi and F.A. Al-Mohanna, “Diabetes of the Liver: The Link Between Nonalcoholic Fatty Liver Disease and HFCS-55” Obesity, 17(11), 2003-2013, Nov. 2009.
[5] J. Dorstand, P. Ku ̈hnlein, C. Hendrich, J. Kassubek, A.D. Sperfeld, and A.C. Ludolph. “Patients with elevated triglyceride and cholesterol serum levels have a prolonged survival in amyotrophic lateral sclerosis,” J Neurol. in Press:Published online Dec. 3 2010.
[6] O. Feron, C. Dessy, J.-P. Desager, andJ.-L. Balligand, “Hydroxy-Metholglutaryl-Coenzyme A Reductase Inhibition Promotes Endothelial Nitric Oxide Synthase Activation Through a Decrease in Caveolin Abundance,” Circulation 103, 113-118, 2001.
[7] M.R. Goldstein and L. Mascitelli, “Statin-induced diabetes: perhaps, its the tip of the iceberg,” QJM, Published online, Nov 30, 2010.
[8] S.S. Gottlieb, M. Khatta, and M.L. Fisher. “Coenzyme Q10 and congestive heart failure.” Ann Intern Med, 133(9):745–6, 2000.
[9] J.-P. Gratton, P. Bernatchez, and W.C. Sessa, “Caveolae and Caveolins in the Cardiovascular System,” Circulation Research, 94:1408-1417, June 11, 2004.
[10] D.S. Grimes, E. Hindle and T. Dyer, “Sunlight, Cholesterol and Coronary Heart Disease,” Q. J. Med 89, 579-589, 1996; http://www.ncbi.nlm.nih.gov/pubmed/8935479
[11] J. Hagedorn and R. Arora, “Association of Statins and Diabetes Mellitus,” American Journal of Therapeutics, 17(2):e52, 2010.
[12] T.H. Haines, “Do Sterols Reduce Proton and Sodium Leaks through Lipid Bilayers?” Progress in Lipid Research, 40, 299-324., 2001; http://www.ncbi.nlm.nih.gov/pubmed/11412894
[13] T. Kikuchi, N. Oka, A. Koga, H. Miyazaki, H. Ohmura, and T. Imaizumi, “Behavior of Caveolae and Caveolin-3 During the Development of Myocyte Hypertrophy,” J Cardiovasc Pharmacol. 45:3, 204-210, March 2005.
[14] P.H. Langsjoen and A.M. Langsjoen, “The clinical use of HMG CoA-reductase inhibitors and the associated depletion of coenzyme Q10. A review of animal and human publications.” Biofactors, 18(1):101–111, 2003.
[15] J. Liu, A. Li and S. Seneff, “Automatic Drug Side Effect Discovery from Online Patient-Submitted Reviews: Focus on Statin Drugs.” Submitted to First International Conference on Advances in Information Mining and Management (IMMM) Jul 17-22, 2011, Bournemouth, UK.
[16] M. Löhn, M. Fürstenau, V. Sagach, M. Elger, W. Schulze, F.C. Luft, H. Haller, and M. Gollasch, “Ignition of Calcium Sparks in Arterial and Cardiac Muscle Through Caveolae,” Circ. Res. 2000;87;1034-1039
[17] A. Maguy, T.E. Hebert, and S. Nattel, “Involvement of Lipid rafts and Caveolae in cardiac ion channel function,” Cardiovascular Research, 69, 798-807, 2006.
[18] B.M. Meador and K.A. Huey, “Statin-Associated Myopathy and its Exacerbation with Exercise,” Muscle and Nerve, 469-79, Oct. 2010.
[19] C. Minetti, F. Sotgia, C. Bruno, et al., “Mutations in the caveolin-3 gene cause autosomal dominant limb-girdle muscular dystrophy,” Nat. Genet., 18, 365-368, 1998.
[20] O.B. Nielsen, F. de Paoli, and K. Overgaard, “Protective effects of lactic acid on force production in rat skeletal muscles.” J. Phhsiology 536(1), 161-166, 2001.
[21] P.S. Phillips, R.H. Haas, S. Bannykh, S. Hathaway, N.L. Gray, B.J. Kimura, G. D. Vladutiu, and J.D.F. England. “Statin-associated myopathy with normal creatine kinase levels,” Ann Intern Med, October 1, 2002;137:581–5.
[22] G. de Pinieux, P. Chariot, M. Ammi-Said, F. Louarn, J.L. LeJonc, A. Astier, B. Jacotot, and R. Gherardi, “Lipid-lowering drugs and mitochondrial function: effects of HMG-CoA reducase inhibitors on serum ubiquinone and blood lactate/pyruvate ratios.” Br. J. Clin. Pharmacol. 42: 333-337, 1996.
[23] R.A. Robergs, F. Ghiasvand, and D. Parker, “Biochemistry of exercise-induced metabolic acidosis.” Am J Physiol Regul Integr Comp Physiol 287: R502–R516, 2004.
[24] G. Saher, B. Brügger, C. Lappe-Siefke, et al. “High cholesterol level is essential for myelin membrane growth.” Nat Neurosci 8:468-75, 2005.
[25] S. Seneff, G. Wainwright, and L. Mascitelli, “Is the Metabolic Syndrome Caused by a High Fructose, and Relatively Low Fat, Low Cholesterol Diet?” Archives of Medical Science, 7(1), 8-20, 2011; DOI: 10.5114/aoms.2011.20598
[26] S. Seneff, G. Wainwright, and L. Mascitelli, “Nutrition and Alzheimer’s Disease: the Detrimental Role of a High Carbohydrate Diet,” In Press, European Journal of Internal Medicine, 2011.
[27] S. Seneff, G. Wainwright and B. Hammarskjold, “Cholesterol Sulfate Supports Glucose and Oxygen Transport into Erythrocytes and Myocytes: a Novel Evidence Based Theory,” submitted to Hypotheses in the Life Sciences.
[28] S. Seneff, G. Wainwright and B. Hammarskjold, “Atherosclerosis may Play a Pivotal Role in Protecting the Myocardium in a Vulnerable Situation,” submitted to Hypotheses in the Life Sciences.
[29] H. Sinzinger and J. O’Grady, “Professional athletes suffering from familial hypercholesterolaemia rarely tolerate statin treatment because of muscle problems.” Br J Clin Pharmacol 57,525-528, 2004.
[30] E.J. Smart, G.A. Graf, M.A. McNiven, W.C. Sessa, J.A. Engelman, P.E. Scherer, T. Okamoto, and M.P. Lisanti, “Caveolins, Liquid-Ordered Domains, and Signal Transduction,” Molecular and Cellular Biology, 19, 7289–7304, Nov. 1999.
[31] A.J. Shyam Kumar, S.K. Wong, and G. Andrew, “Statin-induced muscular symptoms : A report of 3 cases.” Acta Orthop. Belg. 74, 569-572, 2008.
[32] M.A. Silver, P.H. Langsjoen, S. Szabo, H. Patil, and A. Zelinger, “Effect of atorvastatin on left ventricular diastolic function and ability of coenzyme Q10 to reverse that dysfunction.” The American Journal of Cardiology, 94(10):1306–1310, 2004.
[33] Y. Sunada, H. Ohi, A. Hase, H. Ohi, T. Hosono, S. Arata, S. Higuchi, K. Matsumura, and T. Shimizu, “Transgenic mice expressing mutant caveolin-3 show severe myopathy associated with increased nNOS activity,” Human Molecular Genetics 10(3) 173-178, 2001. http://hmg.oxfordjournals.org/content/10/3/173.abstract
[34] M. J. Taggart, “The complexity of caveolae: a critical appraisal of their role in vascular function,” Research Symposium on Caveolae: Essential Signalosomes for the Cardiovascular System, Proc Physiol Soc 19, SA21, University of Manchester, 2010.
[35] P. Thavendiranathan, A.Bagai, M.A. Brookhart, and N.K. Choudhry, “Primary prevention of cardiovascular diseases with statin therapy: a meta-analysis of randomized controlled trials,” Arch Intern Med. 166(21), 2307-13., Nov 27, 2006.
[36] R.S. Tilvis, J.N. Valvanne, T.E. Strandberg and T.A. Miettinen “Prognostic significance of serum cholesterol, lathosterol, and sitosterol in old age; a 17-year population study,” Annals of Medicine, Early Online, 1–10, 2011.
[37] J. Tong, P.P. Borbat, J.H. Freed, and Y. Shin, “A scissors mechanism for stimulation of SNARE-mediated lipid mixing by cholesterol.” Proc Natl Acad Sci U S A 2009;106:5141-6.
[38] L. Vila, A. Rebollo, G.S. AÄ‘alsteisson, M. Alegret, M. Merlos, N. Roglans, and J.C. Laguna, “Reduction of liver fructokinase expression and improved hepatic inflammation and metabolism in liquid fructose-fed rats after atorvastatin treatment,” Toxicology and Applied Pharmacology 251, 32–40, 2011.
[39] Walley T., Folino-Gallo P., Stephens P et al, “Trends in prescribing and utilisation of statins and other lipid lowering drugs across Europe 1997-2003,” Br J Clin Pharmacol 60, 543-551, 2005.
[40] K.A. Weant and K.M. Smith, “The Role of Coenzyme Q10 in Heart Failure,” Ann Pharmacother, 39(9), 1522-6, Sep. 2005.
[41] F. R. Westwood, A. Bigley, K. Randall, A.M. Marsden, and R.C. Scott, “Statin-induced muscle necrosis in the rat: distribution, development, and fibre selectivity,” Toxicologic Pathology, 33:246-257, 2005.
Stephanie Seneff can be contacted by email at seneff@csail.mit.edu
Related articles
America’s most popular prescription sleep medication linked to mass shootings
RT | January 20, 2014
A new report describing the bizarre and dangerous side effects of the sleep aid Ambien has once again raised questions about one of the United States’ most popular prescription drugs.
In a story by the Fix, Allison McCabe chronicled the numerous cases in which Ambien has caused individuals to commit unsafe, and sometimes deadly acts.
In 2009, 45-year-old Robert Stewart was convicted on eight charges of second-degree murder after he killed eight people in a nursing home. He was originally charged with first-degree murder, but by claiming his tirade was Ambien-induced he was able to have the charges lessened and sentenced to 142-179 years in prison.
In a similar case, Thomas Chester Page of South Carolina was sentenced on five counts of attempted murder despite his claims that Ambien was the cause of a shootout with officers. He received 30 years of prison on each count, to be served concurrently.
Although the Food and Drug Administration approved Ambien in 1992, its warning labels have changed significantly over the last two decades as evidence mounted documenting the drug’s ability to induce dangerous behavior.
“After taking AMBIEN, you may get up out of bed while not being fully awake and do an activity that you do not know you are doing,” the label currently reads. “The next morning, you may not remember that you did anything during the night… Reported activities include: driving a car (“sleep-driving”), making and eating food, talking on the phone, having sex, sleep-walking.”
In the courtroom, cases related to Ambien use have ranged from shootings to child molestation charges to car accidents. In one such case, flight attendant Julie Ann Bronson from Texas ran over three people – including an 18-month old who suffered from brain damage as a result. When Bronson woke up in jail the next morning, she could barely comprehend what she had done.
“It was surreal. It was like a bad dream,” she said in May 2012. “I did the crime but I never intended to do it. I wouldn’t hurt a flea. And if I would have hit somebody, I would have stopped and helped. We’re trained in CPR.” Bronson pleaded guilty to the felony charges, but also received lesser charges by citing Ambien as the reason for her actions.
While some drug companies work on sleep aids that do not induce the kind of unpredictable and risky behavior Ambien does, the popularity of the medication raises concern over America’s prescription drug culture. The market for sleeping pills is a billion-dollar industry, yet dangerous side effects continue to be reported.
Last year, a report by the Department of Health and Human Services highlighted about 2,200 doctors for suspicious activities such as over-prescribing drugs. More than 700 Medicare doctors were also flagged for issuing what could be seen as “extreme” and potentially harmful prescriptions.
Although the report noted that some prescriptions could have been effective, it added, “prescribing high amounts on any of these measures may indicate that a physician is prescribing drugs which are not medically necessary or that he or she has an inappropriate incentive, such as a kickback, to order certain drugs.”
Soon after that report was issued, the Centers for Disease Control and Prevention found that roughly 18 women a day are dying in the United States due to prescription drug overdose, namely from painkillers like Vicodin and Oxycontin. With women making up 40 percent of all overdose deaths in 2010, these numbers marked a 400 percent increase compared to data from 1999.
The benefits of medication have also been placed under heavy scrutiny when it comes to other health issues, such as attention deficit hyperactivity disorder (ADHD). In December 2013, RT reported that the authors of the primary study promoting medication over behavioral therapy in order to treat ADHD now have serious concerns over their original results.
“I hope it didn’t do irreparable damage,” said one of the stud’s co-authors, Dr. Lilly Hechtman of Montreal’s McGill University. “The people who pay the price in the end is the kids. That’s the biggest tragedy in all of this.”
British MPs raise alarm over drug trials, say only half data published
RT | January 5, 2014
British MPs have voiced concern that doctors and researchers are being denied access to around half the results from all clinical trials. An influential parliamentary committee has condemned the selectiveness as damaging medicine as a whole.
This apparently standard practice of withholding critical medical test information impairs decision-making by professionals, worsens patients’ treatment and prevents independent assessment of medicines, the MPs wrote. And the practice, they say, dates back all the way to the 1980s.
In the report, the MPs write that they are “surprised and concerned to discover that information is routinely withheld from doctors and researchers about the methods and results of clinical trials on treatments currently prescribed in the United Kingdom. This problem has been noted for many years in the professional academic literature, with many promises given, but without adequate action being taken by government, industry or professional bodies.”
“This has ramifications for the whole of medicine. The ability of doctors, researchers and patients to make informed decisions about treatments is being undermined,” said Richard Bacon, a senior member on the committee that published the report.
The MPs argue that this is a great problem also because the issue of access to clinical trials from previous years is absent from all new proposals. And test results on humans provide researchers with key evidence to support or oppose the use of a given medicine. There are unprecedented dangers when this framework is not operating as intended, they said.
Compounding the problem further, MPs say, is that aside from the non-publication of all clinical trial tests, for some reason positive results started popping up twice as much as negative ones. This is bad when all trial results on all uses of all chemicals should be provided, the report argues.
As a result, the committee’s MPs have given strong recommendations to the government and the country’s health bodies – among them, firstly, that the full results of clinical trials from now on be disseminated to all doctors and researchers in the UK, with full audits carried out regularly to check for transgressions; and secondly, that the Department of Health and the Medicines and Healthcare products Regulatory Agency (MHRA) ensure that all past and future trial results and the methods used to achieve them be published in a unified register for further use.
Bacon expressed alarm that the absence of past results invariably impact doctors’ decisions on treatment. “Regulators and the industry have made proposals to open up access, but these do not cover the issue of access to the results of trials in the past which bear on the efficacy and safety of medicines in use today,” he said.
The worrying implication here is that so much medicine has been tested and approved over the past few decades, but only half of it we know the full truth about, it turns out.
One particular medicine that became a focus for alarm was Tamiflu – the popular flu medicine that gained popularity in 2009-10 during the great flu pandemic. Apparently, the UK Department of Health, without having access to exhaustive information on the medicine, had made a 424-million-pound decision to stockpile it between the years 2006-7 and 2012-13.
That kind of attitude, the MPs argue, is predicated on judgment, rather than real science. There is still no agreement on how the popular medicine works and disagreement on whether full information was provided to regulators by the MHRA during the licensing process. As it turns out from studies conducted by the non-profit NGO, Cochrane Collaboration, Tamiflu “did not reduce influenza-related lower respiratory tract complications.”
The organization is now in talks with Roche to receive the full details of Tamiflu’s testing, which will be included in a thorough upcoming review on its effectiveness. Both the government and the medical bodies will take part, as MPs share the think tank’s concern when it wrote that “we find it perplexing that the regulators continue to state that they had all the available evidence.”
Regarding Tamiflu and the wider practice as a whole, Bacon recommended that “before spending money in future to maintain the stockpile, the department needs to review what level of coverage is appropriate. It should look at the level of stockpiling in other countries, bearing in mind that the patent for the medicine runs out in 2016.”
UK food poverty a ‘public health emergency’, say leading experts
RT| December 4, 2013
A group of high-profile academics has written an open letter warning that food poverty has become an “emergency” in the UK. Use of food banks has tripled in the past year alone, but the government says this does not mean more people are starving.
“This has all the signs of a public health emergency that could go unrecognised until it is too late to take preventive action,” said the letter, co-signed by six leading public health experts, and addressed to the prestigious British Medical Journal (BMJ).
The authors, led by David Taylor-Robinson from the Medical Research Council, speculate that “the rising cost of living and increasingly austere welfare reforms” from the Conservative-Liberal government are at fault.
“The effects of these policies on nutritional status in the most vulnerable populations urgently need to be monitored… Access to an adequate food supply is the most basic of human needs and rights.”
Official statistics show that the number of those admitted to hospitals with malnutrition has risen from 3,161 in 2008/09 to 5,499 in 2012/13.
Even those who are not on the verge of starvation are suffering. The signatories cite a recent report by the Institute for Fiscal Studies that claimed that families are spending 8.5 percent less on food than before the recession, and there has been a “reduction in quality” of produce consumed during a “substitution towards processed sweet and savoury food and away from fruit and vegetables” particularly by poorer and single-parent families.
Leading food bank charity The Trussell Trust, which operates 400 outlets, says that three times more people have asked it for help than just a year ago. Nearly 350,000 people have received at least three days’ worth of meals from it in the 12 months leading to October.
British Red Cross has also started its first food aid collection drive since World War II.
The government has not only refused to take blame for increased food poverty, but has questioned that there has been an increase at all.
“The benefits system supports millions of people who are on low incomes or unemployed and there is no robust evidence that welfare reforms are linked to increased use of food banks,” said an official statement in response to the open letter.
“In fact, our welfare reforms will improve the lives of some of the poorest families in our communities with the universal credit making three million households better off – the majority of these from the bottom two fifths of the income scale.”
Government officials have said that the rise of food banks – which are made up from private donations – has actually been the result of greater generosity from private citizens, and charities opening new access points. Another issue is that of entitlement to receiving meals from the food banks. In order to be given a free meal, a needy individual has to be issued a voucher by a local official, policeman, or church minister. In recent months, employment office workers have begun to offer more food vouchers, whereas before, they might have handed out cash benefits.
But no definitive, non-ideological estimations of the scale of the food poverty problem are likely at least until the publication of an official Department for Environment Food and Rural Affairs (Defra) report on the issue commissioned last February, which has been completed but not released to the public.
The authors of the BMJ letter and The Trussel Trust have both hit out at the government for failing to publish the report – supposedly finished in July – implying that it is hiding the devastating effect of its welfare reforms, which include stricter criteria for receiving state aid and greater penalties for those who fail to comply with them.
In response Defra has said that it is simply conducting the “necessary review and quality assurance process” before publication.
Clean-up doubts: Many Fukushima evacuees may never return home
RT | November 13, 2013
Many of the people who were forced to evacuate after the 2011 triple meltdown at the Fukushima nuclear power plant may never return, Japanese lawmakers admitted, overturning initial optimistic government pledges.
A call to admit the grim reality and step back from the ambitious Fukushima decontamination goals came from Prime Minister Shinzo Abe’s coalition parties. Japan has so far spent $30 billion on the clean-up program, which has proven to be more difficult to carry out than initially expected.
The new plan would be for the government to fund relocation to new homes for those who used to live in the most contaminated areas.
“There will come a time when someone has to say, ‘You won’t be able to live here anymore, but we will make up for it’,” Shigeru Ishiba, the secretary General of Abe’s Liberal Democrat party said in a speech earlier this month.
On Tuesday, evacuees reacted with anger at the government’s admission.
“Politicians should have specified a long time ago the areas where evacuees will not be able to return, and presented plans to help them rebuild their lives elsewhere,” Toshitaka Kakinuma, a 71-year-old evacuee, told the Asahi Shimbun newspaper.
Some 160,000 people escaped the vicinity of Fukushima Daiichi, when a powerful earthquake and tsunami transformed the plant into the world’s worst nuclear disaster since Chernobyl. About a third of them are still living in temporary housing. They were promised that this would not last for longer than 3 years.
In August the death toll among the evacuees surpassed the threshold of 1,599 lives, which is how many people in the prefecture were killed by the disaster itself. The displaced residents are suffering from health problems, alcoholism and high rates of suicide.
The Ministry of Environment wanted to decontaminate 11 townships in the affected area, bringing the average annual radiation dose to 20 millisieverts, a level deemed safe by the International Centre for Radiological Protection. It further pledged to pursue a long-term goal reducing it to 1 millisievert per year.
The clean-up, however, has been marred by delays and reports that workers sometimes simply dumped contaminated waste rather than collect it for safe storage, causing the environment ministry push back the deadline. There are also calls on the government to abandon the more ambitious dose target, arguing that it is unrealistic.
Some evacuees said they wouldn’t return even after the first phase of the cleanup, saying the dose of 20 millisieverts per year still poses health risks.
“No matter how much they decontaminate I’m not going back because I have children and it is my responsibility to protect them,” Yumi Ide, a mother of two teenage boys, told Reuters.
The fear of radiation has soared in Japan in the wake of the Fukushima disaster, with rallies against the use of nuclear power scoring record attendance. The government shut down all 50 remaining Japanese reactors for safety checks, and there is strong pressure to keep them offline.
The Japanese government is reportedly seeking to borrow an extra $30 billion for the Fukushima cleanup and compensations, which would raise the total cost of the disaster response to $80 billion. The figure does not include the cost of decommissioning reactors to be carried out by the plant operator, Tepco. The company recently complained about the huge expense of the process, which may last at least 30 years.
Norway may ban non-medical circumcision of boys
RT | November 13, 2013
Norway’s Health Ministry is considering a proposal on regulating the circumcision of boys. Some political parties are calling on a complete ban of the practice on minors, a possibility that would affect Jewish and Muslim communities.
Two years ago, the ministry was tasked with reviewing circumcision and how it should be practiced in Norway. It is yet to finalize its stance, but intends to submit its legislative proposal before Easter next year, Health Minister Bent Hoie told Aftenposten, Norway’s largest newspaper.
The issue was brought to public attention after the recent call by Norway Children’s Ombudswoman Anne Lindboe to ban circumcision of boys before age 16, unless the procedure is warranted by medical needs.
“This is not due to any lack of understanding of minorities or religious traditions, but because the procedure is irreversible, painful and risky,” she argued.
Lindboe’s position is shared by some members of the Labor Party, which currently holds the largest share of 55 seats in Norway’s 169-strong legislative and is in opposition to the ruling Conservative-Progress coalition.
“As a modern society, we should work to eliminate practices that expose children and people to unnecessary suffering,” said Labor’s Ruth Mari Grung, who is a member of the parliamentary Committee on Health and Care Services.
A ban is also supported by the Center Party, which has 10 seats in the parliament.
Other parliamentary parties are yet to formulate their official position on the issue. Hoie, a Conservative member, who used to chair the Health Committee before getting his ministerial appointment, voiced concerns that a ban would force the groups practicing ritual circumcision underground, where the procedure would be performed by non-medics and pose greater health risks to the children.
The Norwegian lawmakers also disagree on whether circumcision should be covered by the budget under the national healthcare system. Some parties insist that ritual circumcision should be paid for by parents.
According to the newspaper, an average of about 2,000 Muslim and seven Jewish newborns are circumcised in Norway each year.
Regulation of ritual circumcision in Europe made the headlines in June, when a German court ruled that the procedure constitutes a minor bodily harm and outlawed performing it on minors. The decision sparked nationwide debate on the conflict between religious freedoms and protection of children.
The issue was further stressed in early October, when the Council of Europe branded the practice “a violation of the physical integrity of children” and called on EU members to protect children. The latter should include a ban on performing circumcision on those who cannot consent to it, the non-binding resolution said.
Sweden, Finland, Denmark, Iceland and Greenland are among the European countries where public debate on ritual circumcision of boys is hotly debated.
Related article
US makes first step toward banning trans fats
RT | November 7, 2013
The Food and Drug Administration announced on Thursday that it would require the food industry to phase out the use of artificial trans fats in its products.
The FDA said it has made a preliminary determination that the primary source of trans fat – partially hydrogenated oils – is no longer “generally recognized as safe,” and that it plans to ban their use in the market. Some trans fat is naturally generated in meat and dairy products, and the ban will only apply to trans fat added to foods.
According to FDA Commissioner Margaret Hamburg, the decision could potentially prevent 20,000 heart attacks a year and 7,000 deaths.
Over the last decade, American consumption of trans fat has declined significantly. In 2006, the average citizen was consuming 4.6 grams of trans fat a day, while the number decreased to roughly one gram a day in 2012. Still, Hamburg said they “remain an area of significant public health concern,” according to NBC News.
Many companies began eliminating the use of trans fat when the FDA required them to list the ingredient on nutritional labels in 2006, but it can still be found in common products like frozen pizza, microwave popcorn, margarine, coffee creamer, and various desserts.
“The artery is still half clogged,” Dr. Thomas Frieden, the director of the Centers for Disease Control and Prevention, said to the New York Times. “This is about preventing people from being exposed to a harmful chemical that most of the time they didn’t even know was there.”
“It’s quite important,” he added, referring to the FDA’s new proposal. “It’s going to save a huge amount in health care costs and will mean fewer heart attacks.”
Numerous studies have shown that there is virtually no health benefit to consuming trans fat. It lowers the level of “good” cholesterol and raises levels of “bad” cholesterol, clogging the arteries and increasing the risk of heart attacks.
The FDA did not lay out a timetable for the ban. It will open its proposal to public comment for 60 days while it formulates a schedule that gives food manufacturers enough time to cooperate with the new rule.
“We want to do it in a way that doesn’t unduly disrupt markets,” Michael Taylor, the FDA’s deputy commissioner for foods, said to the Associated Press. At the same time, he said the food “industry has demonstrated that it is by and large feasible to do.”
Public health groups have welcomed the FDA’s proposal, which the agency has been collecting data for since 2009.
Should the FDA move forward with its plan, the United States will join other nations such as Denmark, Iceland, and Switzerland, in banning the ingredient.
Still, there are numerous other ingredients that have been outlawed in various countries while still being sold in the U.S. An, article by BuzzFeed over the summer noted that brominated vegetable oil, which has been linked to birth defects and organ damage, continues to be used in sports drinks and the popular soda Mountain Dew. It’s been banned in more than 100 countries.
Meanwhile, synthetic hormones rGBH and rBST, linked to cancer and infertility, continue to be given to cows and show up in dairy products that aren’t labeled otherwise. They’ve been banned in Japan, Canada, New Zealand, Australia, and the European Union.
Earlier this month, the FDA banned three out of the four brands of arsenic-laced animal feed that was being given to chickens, turkeys, and pigs. The decision came four years after the Center for Food Safety called on the FDA to remove the feed, but one brand remains on the market.
Related article
‘Globesity’: US junk food industry tips global scales
By Robert Bridge | RT | September 07, 2013
From Mexico to Qatar, obesity rates are soaring to unprecedented levels. The alarming trend is damaging economic performance, as well as the health of millions of consumers worldwide.
Take our increasingly sedentary lifestyles, mix in a generous portion of American fast-food and dubious agricultural practices, add a dash of corporate duplicity and you have a recipe for high obesity rates across the planet.
The newly released United Nations report on global nutrition does not make for very appetizing reading: Amid an already floundering global economy, the reality of a fattening planet is dragging down world productivity rates while increasing health insurance costs to the tune of $3.5 trillion dollars per year – or 5 percent of global gross domestic product (GDP).
31.8 percent of US adults are now considered clinically obese. This is a remarkable figure, especially considering that it is approximately double the US obesity rate registered in 1995, according to data from the Center for Disease Control and Prevention.
An individual is considered obese when their body mass index (BMI), a measurement obtained by dividing a person’s weight in kilograms by the square of the person’s height in meters, exceeds 30 kg/m2, according to the World Health Organization.
Meanwhile, much of the international community is quickly catching up with the global consumption superpower. Mexico, for example, just surpassed US obesity rates with a whopping 32.8 percent of Mexican adults now considered to be clinically obese.
The unprecedented weight gains in Mexico, however, as well as many other countries, appear to be no accident.
Following the passage of the North American Free Trade Agreement (NAFTA), Mexico became the dumping ground for a slew of cheap fast food and carbonated drinks, according to a Foreign Policy report.
Thanks to NAFTA, there was a more than 1,200 percent increase in high-fructose corn syrup exports from the US to Mexico between 1996 and 2012, according to the US Agriculture Department. In an effort to place a cap on the high-calorie drinks, Mexican officials introduced a tax on beverages containing high-fructose corn syrup. American corn refiners, however, cried foul and the tax was voted down by the World Trade Organization.
Mexicans now consume 43 gallons of soda per capita annually, giving the country the world’s highest rate of soda consumption, according to estimates by Mexico’s national statistics agency.
Yet another disturbing casualty on the obesity trail is tiny Qatar, an oil-rich Arab nation of 250,000 people that is also rich in fast food diets.
“Like most people in the Arab Gulf, (Qataris) were traditionally desert-dwelling and therefore much more physically active,” according to a 2012 report by Policymic.com. “Now, cars have replaced camels and fast food and home deliveries take the place of home cooking. Even housework and child rearing is left to maids and nannies.”
Today, some 45 percent of Qatari adults are obese and up to 40 percent of school children are obese as well.
Last month, nutrition experts from around the world shared their views at an obesity and nutrition conference in Sydney. For many of the attendees, the primary culprit in the global obesity scourge is out-of-control corporate power, where the free market decides everything.
The rise of global fast food outlets has been a key change in our environment leading to fattier foods and fatter people, Bruce Neal, professor at the George Institute for Global Health in Sydney, told the Indo-Asian News Service.
“As fast as we get rid of all our traditional vectors of disease – infections, little microbes, bugs – we are replacing them with the new vectors of disease, which are massive transnational, national, multinational corporations selling vast amounts of salt, fat and sugar,” Neal said.
John Norris, writing in Foreign Policy, explained some of the global dynamics that contributed to the so-called “globesity” epidemic, including the soft drink industry’s move to use cheaper high-fructose corn syrup instead of sugar in many of their products.
“Suddenly, it was cheaper to put high-fructose corn syrup in everything from spaghetti sauce to soda. Coke and Pepsi swapped out sugar for high-fructose corn syrup in 1984, and most other US soda and snack companies followed suit,” Norris wrote. “US per capita consumption of high-fructose corn syrup spiked from less than half a pound a year in 1970 to a peak of almost 38 pounds a year in 1999.”
While some might be tempted to downplay the negative effects of such a harmless sounding additive, researchers from Canada’s University of Guelph, as pointed out by Norris, discovered that a high-fructose corn syrup diet in rats produced “addictive behavior similar to that from cocaine use.”
As obesity explodes, US fast food companies look abroad.
Americans, thanks in part to First Lady Michele Obama’s ‘Let’s Move’ program, have recently woken up to the unsustainability of their soda guzzling, fast food ways. Other politicians and activists have also weighed in on the debate, making the environment for the fast food industry not as comfortable as in the past.
In March, New York City Mayor Michael Bloomberg attracted the ire of the soft drink industry when he placed a ban on the sale of sodas in sizes larger than 16 ounces. Violators will be fined $200.
In his 2004 a documentary film, “Super Size Me,” Morgan Spurlock stunned audiences by tracking the physical effects on his body – none of them positive – after consuming nothing but McDonald’s food for 30 days. As a result of the experiment, Spurlock gained 24½ lbs. (11.1 kg), a 13 percent body mass increase, and a cholesterol level of 230, among other negative side-effects.
Perhaps the biggest wake-up call for the fast food industry came in 2002 when two teenagers accused McDonald’s of deceptively marketing its menu from 1985 to 2002, causing them, they alleged, to become obese. The judge dismissed the case in 2010, but the message to the industry was crystal clear.
As a result of these and other public awareness campaigns, the American fast food industry – although slower than some may like – has been gradually rewriting their menus and marketing campaigns, many of which are aimed at kids.
At the same time, the junk food industry – sensing the sea change of attitudes in the United States as the physical effects of junk food manifests itself – are investing increasingly in foreign markets where public awareness of the subject is not so developed.
Similar to the crackdown on the tobacco industry in the late 1990s, US fast food companies are busy setting up shop abroad for easy, unregulated markets to hawk their wares.
Already the size of their presence is breathtaking: “Coca-Cola and PepsiCo together control almost 40 percent of the world’s $532 billion soft drink market, according to the Economist. Soda sales, meanwhile, have more than doubled in the last 10 years, with much of that growth driven by developing markets. McDonald’s investors were disappointed that the company only turned $1.4 billion in profit during the second quarter of 2013, having become used to years of double-digit gains every three months,” according to the Foreign Policy report.
So while the United States is steadily finding ways to regulate its fast food, soft drink industry, and thus nip the obesity epidemic in the bud, it is, at the same time, legislating on behalf of unhealthy exports abroad.
Now the question is, will the rest of the world bite the hand that feeds?
Related articles
Featured Video
SANCTIONED: Col Jacques Baud Explains Being the EU’s TARGET
or go to
Aletho News Archives – Video-Images
From the Archives
9/11 and the Zionist Question: Is Noam Chomsky a Disinfo Agent for Israel? (Part 2)
The Kevin Barrett-Noam Chomsky Dispute in Historical Perspective
Prof. Tony Hall | American Herald Tribune | July 14, 2016
… Chomsky in discouraging skeptical investigation of 9/11 reveals himself to be a Trojan horse that has succeeded in subverting the Left from within. … Read full article
Blog Roll
Recent Comments
Gemma on Israel’s diamond industr… Bill Francis on Victoria Moves to Force Online… papasha408 on The Empire of Lies: How the BB… loongtip on US Weighs Port Restrictions on… Bill Francis on Chris Minns Defends NSW “Hate… Sheree Sheree on I was canceled by three newspa… Richard Ong on Czech–Slovak alignment signals… John Edward Kendrick on Colonel Jacques Baud & Nat… eddieb on Villains of Judea: Ronald Laud… rezjiekc on Substack Imposes Digital ID Ch… loongtip on US strikes three vessels in Ea… eddieb on An Avoidable Disaster
Aletho News- SANCTIONED: Col Jacques Baud Explains Being the EU’s TARGET
- Fuel rationing chaos looms in New York State
- Higher Mortality Rates Detected in Vaccinated 3-Month-Olds Compared With Unvaccinated Infants
- The Rebirth of ISIS, Israel and the Continuation of Syria’s Civil War
- Europe’s Panic Economy: Frozen Assets, Empty Arsenals, and the Quiet Admission of Defeat
- Israel’s diamond industry is going extinct. That’s a billion-dollar problem for the IDF.
- Iran says no basis for inspection of bombed nuclear sites
- How reporting facts can now land you in jail for 14 years as a terrorist
- Bill Gates, Pfizer CEO Albert Bourla Ordered to Testify in Dutch COVID Vaccine Injury Lawsuit
- The vindication (and brutal punishment) of Dr. Reiner Fuellmich
- If Americans Knew
- Palestinian Christians offer “Kairos,” an alternative Christmas Day sermon – Not a Ceasefire Day 76
- The Faces of AIPAC: the largest pro-Israel lobbying org in the US
- Gazan Christians mark 3rd Christmas under genocide – Not a Ceasefire Day 75
- Israeli scams children with cancer out of millions fundraised for their treatment, BBC finds
- Casey Kennedy Fired from AG Scientific Amid Zionist Troll Campaign Over Track AIPAC Work
- The Hasmoneans: The Jewish Dynasty That Gave Us Hanukkah Is a Symbol of Murder, Not Heroism and Hope
- Int’l NGOs may be blocked from Gaza starting Jan. 1 – Not a Ceasefire Day 74
- From Churches to ChatGPT: Israeli Contracts Worth Millions Aim to Influence U.S. Public Opinion
- Who is the Pro-Israel Clique behind TikTok’s US Takeover?
- Medical Crisis in UK Prisons – 800 Doctors Warn of ‘Imminent Deaths’ Among Palestine Action Strikers
- No Tricks Zone
- Meteorologist Dr. Ryan Maue Warns “Germany Won’t Make It” If Winter Turns Severe
- Merry Christmas Everybody!
- Two More New Studies Show The Southern Ocean And Antarctica Were Warmer In The 1970s
- Der Spiegel Caught Making Up Reports About Conservative America (Again)
- New Study: 8000 Years Ago Relative Sea Level Was 30 Meters Higher Than Today Across East Antarctica
- The Wind Energy Paradox: “Why More Wind Turbines Don’t Always Mean More Power”
- New Study Reopens Questions About Our Ability To Meaningfully Assess Global Mean Temperature
- Dialing Back The Panic: German Physics Prof Sees No Evidence Of Climate Tipping Points!
- Astrophysicist Dr. Willie Soon Challenges The Climate Consensus … It’s The Sun, Not CO2
- Regional Cooling Since The 1980s Has Driven Glacier Advance In The Karakoram Mountains
Aletho News 