The myth that lowering cholesterol with statins prevents heart attacks and strokes is still widespread in modern medicine. This is in spite of the fact that there has never been a consistent relationship between lowering LDL (so called “bad” cholesterol), heart attack, stroke, and death. The “lower the better” mantra often parroted by the “experts” is just not tenable or evidence based.
by Simon Lee, Science Officer, Anew UK
The Gravy Train.
“Statins lower LDL, but they do not change outcomes in any significant fashion.” Dr. Jack Wolfson (cardiologist)
The statin industry generates 20 billion a year and has caused life-threatening nutrient deficiency in millions of otherwise healthy people. There has been active discouragement to publish any negative studies on the effects of statins by those aboard the lucrative statin gravy train.
In the U.S. alone, 40 million adults take statins, despite the questionable effectiveness and safety they are still being recommended for many people. The use of lucrative statins doubled among U.S. adults from 2000 to 2011 in the false belief that they reduce heart disease risk.
Cholesterol is still largely vilified, and statin use is still heavily promoted. In spite of “target” cholesterol levels having been achieved, a systemic review by DuBroff et al published in BMJ Evidence-Based Medicine stated:
“The negative results of numerous cholesterols lowering randomized controlled trials call into question the validity of using low density lipoprotein cholesterol as a surrogate target for the prevention of cardiovascular disease.”
Another systematic review and meta-analysis reached similar conclusions. According to one of the authors, Dr Maryanne Demasi:
“The study found no consistent relationship between lowering LDL-C with statins and death, heart attack or stroke. Statins are very effective at lowering LDL-C, but in some trials, which did not necessarily translate into a meaningful benefit for the patient. This contradicts the prevailing view…that there is a strong “linear” relationship between lowering LDL-C and cardiovascular outcomes from statin therapy.”
A Cochrane systemic review by Taylor et al found evidence of selective reporting of outcomes and failure to report adverse events.
In reality, high cholesterol levels have been shown to be protective in the elderly and heart failure patients. Low cholesterol patients had a higher incidence of intra-cerebral bleeds, depression, and cancer.
Statins have done nothing to slow the trend of rising heart disease but have increased the risk of many health problems linked to their use including diabetes, dementia, cancer, cataracts, musculoskeletal disorders (myalgia, muscle weakness, muscle cramps, rhabdomyolysis and autoimmune muscle disease), depression, erectile dysfunction, plus an increased risk of several infectious diseases.
All of these effects are dose dependant, persist during treatment and sometimes even after treatment has stopped.
The Gateway Drug.
The negative effects of statins on human health are often described as “adverse reactions” or “side effects” of the drugs. These terms imply an unintended and unpredictable effect of a drug due to an unknown mechanism. The mechanism by which statins damage human health is known, it is entirely predictable, and it was entirely intentional.
Very little disease is ever attributed to statins because doctors refuse to acknowledge the harms that these widely prescribed drugs do and because the harms usually develop slowly in a group that often accepts the symptoms as an inevitable part of aging.
Because statins block the rejuvenating cell cycle, they accelerate the aging and dying process. If statins are taken for long enough, they can cause premature aging, hair loss, and blindness, because the skin, hair and eye lens are cholesterol rich.
In the skin and hair, cholesterol creates a watertight barrier. In the lens of the eye, cholesterol helps to create a cementing lubricating matrix that aligns the molecules in the lens. When cholesterol and lipid bound proteins are reduced in the eye lens cataracts can form.
Physicians usually specialise by organs, making it difficult for them to spot multiple organ failures, caused by common cellular injury, which can manifest as multiple problems in many different tissues and organs.
Statins kill people slowly. People are given 1/100th the dose that kills lab animals in weeks or months, so it takes years or decades for the same injuries to kill people.
Statins are therefore a highly profitable gateway drug to other expensive drugs and medical procedures used to treat the effects of the statins.
No Pain no Gain?
Fatigue and muscle pain are very common effects of statin use. A study of over 350 people taking statins found that 93% reported muscle pain and fatigue, and 85% reported weakness. This is not surprising because statins are known to deplete Coenzyme Q-10 (CoQ10), which is crucial for mitochondrial function. Mitochondria are like cellular batteries that generate energy for the entire body at the cellular level.
Many doctors are familiar with patients reporting muscle-related problems while taking statins but misinterpret study evidence, and presume the symptoms are unrelated, “telling patients that the symptoms are merely psychological, due to age, stress, or other factors.”
General myopathy (muscle pain and weakness) can sometimes develop into the more serious condition, rhabdomyolysis, in which the muscle cells break down and block the kidneys. This can result in permanent kidney damage and death from kidney failure.
The severity of muscle damage is not correlated with duration of statin use and in some cases the muscle damage does not resolve even when statins are discontinued.
When muscle cells are damaged, they release the enzyme creatine kinase (CK) into the blood which can be detected in lab tests. The pharmaceutical company Merck set the standard for this test at ten times above the upper limit of normal. This had the effect of reducing the reported incidence of statin induced myopathy from the clinically observed rate of 10-15% to just 0.5%.
Muscle biopsies are the gold standard for assessing muscle damage. When the Merck determined CK test levels were compared to biopsies, it was found that 57% of patients with an abnormal biopsy had a “normal” CK enzyme level.
This situation went unchallenged for 22 years until 2009. This is an egregious example of medical gaslighting because it convinced many people that their genuine statin induced muscle damage was “all in their head”.
“In contrast to the current belief that cholesterol reduction with statins decreases atherosclerosis, we present a perspective that statins may be causative in coronary artery calcification and can function as mitochondrial toxins that impair muscle function in the heart and blood vessels…Thus, the epidemic of heart failure and atherosclerosis that plagues the modern world may paradoxically be aggravated by the pervasive use of statin drugs. We propose that current statin treatment guidelines be critically re-evaluated.” Dr Harumi Okuyama et al (Expert Review of Clinical Pharmacology)
More than fifty-five trials on statin use have been done with some trials spanning 12 years, in several countries, over the course of four decades. These trials have shown little or no impact on the risk of coronary heart disease (CHD) mortality or morbidity.
Statins were approved for use on the basis of lowering blood LDL cholesterol levels. There was never any requirement to demonstrate a lowered Cardio-vascular disease (CVD) risk, all that was required was an effect on this surrogate marker.
We now have a similar situation with the Covid-19 “vaccines” where the manufacturers point to induction of antibodies as proof of efficacy without having to demonstrate any real beneficial effect at all.
Ironically, for a drug which has been marketed to lower the risk of CVD, a strong association of statin use to the progression of coronary artery plaque has been identified.
Statins have also been correlated with a greater incidence of severe coronary artery stenosis, as well as an increase in the number of coronary vessels developing obstructive coronary artery disease. Furthermore, statins have been linked to an increase in the prevalence and extent of mixed calcific arterial plaque.
Five prospective studies have shown that statins do not induce any coronary calcium regression and evolution of coronary calcium continues regardless of statin treatment. The Veteran Affairs Diabetes Trial showed that statins accelerated progression of Coronary Artery Calcification (CAC) in people with Type 2 diabetes without previous coronary artery disease, despite the fact that statin users had significantly lower and nearly “optimal” LDL-cholesterol levels.
Statins increase arterial calcification of vascular smooth muscle cells and mesenchymal cells and lower the lipid-rich core of atherosclerotic plaques, enhancing the density of cal- cification. This leads to accelerated progression of calcified atherosclerosis. Statins are associated with triple the risk of coronary artery and aortic calcification.
Statins activate the Atrogen-1 Gene which results in muscle atrophy, wasting, and damage and they cause CoQ10 deficiency resulting in cardiomyopathy. Lowering LDL with statins by 50%also lowers CoQ10 by 50% which increases the risk of heart muscle failure.
Statins inhibit the production of vitamin K2, which can be damaging to the heart, and they reduce ketone production. Ketones are essential nutrients for mitochondria and are important regulators of metabolic health and longevity.
It is clear that statins have been a colossal failure and a public health disaster. In 1900, CVD accounted for just 10% of all deaths worldwide. By 2005, this had risen to 29% and the numbers are still rising. By 2015, CVD accounted for 30% of all deaths worldwide. CVD became the leading cause of death in all developing countries with modernised public water supplies in 2010.
The Brain Drain.
Almost a quarter of the total amount of cholesterol in the body can be found in the central nervous system (brain and spinal cord). Cholesterol is an essential component of neurons and is essential for developing and maintaining neuronal function and plasticity. Cholesterol is critical for synapse formation, the connections between neurons, which enable thinking, learning, and forming memories.
Cholesterol plays an important role in the synthesis, transportation and metabolism of steroid hormones as well as lipid-soluble vitamins, both of which have an impact on synaptic integrity and neurotransmission.
Half of the brain matter consists of cholesterol and each neuron is wrapped in a protective myelin sheath which is mostly cholesterol.
Animal studies have shown that blocking cholesterol metabolism can cause the usually compact myelin sheath to unravel into an abnormally loose arrangement.
Defective myelination of the optic nerve can lead to blindness, whereas damage to other nerves can cause difficulties with hearing, touch, temperature control, and balance.
It is estimated that by 2030 75 million people will have dementia. Low levels of Low-Density Lipoprotein (LDL) ( “bad” cholesterol) have been linked to a higher risk of dementia, according to a study of nearly 4,000 people aged 50 and over.
High levels of LDL cholesterol were found to be inversely associated with dementia, even after controlling for other factors that might increase risk, including demographic characteristics, health behaviour, mood assessment and medical history. This association was so strong that the researchers concluded a high level of LDL cholesterol may be considered as a “potential protective factor against cognition decline”.
Cholesterol levels in the “high-normal” range are associated with better cognitive performance in people aged 65 years and over. Lower cholesterol levels are associated with cerebral atrophy which is “a typical anatomic syndrome of dementia.”
In one study, researchers tested the cognitive function of older adults with Alzheimer’s disease who were also taking statins. The patients stopped statins for six weeks, and their cognitive function significantly improved. When they resumed taking the statins, their cognition deteriorated to its original state.
A separate study found that among patients with early mild cognitive impairment, statin use was associated with more than twofold risk of progressing to dementia and “with highly significant decline in metabolism of posterior cingulate cortex” ( the region of the brain known to decline most significantly in the earliest stages of Alzheimer’s disease).
A strong association between lower cholesterol and Parkinson disease risk has been reported, such that each mmol/L increase in total cholesterol was accompanied by a 23% decrease in the risk of developing Parkinson disease.
Statins have also been linked to the neuromuscular degenerative disease Amyotrophic Lateral Sclerosis (ALS), also known as Lou Gehrig’s disease.
People taking statins are more likely to develop peripheral neuropathy which is characterised by weakness, tingling and pains in the hands and feet, and walking difficulties.
Diabetes and Cancer
A systematic review that included almost 47 million people found a link between statins and reduced insulin sensitivity, as well as insulin resistance. These are both major factors in the development of Type 2 diabetes. Statins were also found to reduce glycaemic control and raise fasting glucose levels.
“High” cholesterol is indicative of good overall nutritional status and health, whereas “low” cholesterol is linked to a higher risk of mortality and is associated with malnutrition and chronic diseases, including cancer.
Vinogradova et al have shown that long term statin use is associated with an increased risk of colorectal cancer, bladder cancer and lung cancer. Women with “high” cholesterol had a 28% lower mortality risk than women with low cholesterol.
Blocking Mevalonate-the Pathway of Life
“We are now in a position to witness the unfolding of the greatest medical tragedy of all time. Never before in history has the medical establishment knowingly created a life-threatening nutrient deficiency in millions of otherwise healthy people.” Dr Peter H Langsjoen MD
Statins are inhibitors of the HMG-CoA reductase enzyme. This enzyme activates the mevalonate pathway in order to produce mevalonate which sustains cells. Mevalonate is cellular food, and it can be made from any food type. Mevalonate is used to make cholesterol and isoprenoids which are ubiquitous five-carbon molecules. This is the mevalonate pathway, and it is essential for cell renewal and life.
Both cholesterol and isoprenoids, stimulate the cell cycle whereby the cells grow, replicate their DNA, and divide into two cells. When a cell cycles it must grow (G1 phase), before replicating its DNA (S phase for DNA synthesis), then growing some more (G2 phase), and finally dividing into two new cells (M phase for mitosis). Without the cholesterol and isoprenoids provided by mevalonate none of this can happen. Without the cell cycle, cells age and die.
Isoprenoids are the largest and most diverse of over 25,000 molecules made by animals and plants. Some examples of isoprenoids include vitamin A which is crucial for good eyesight, vitamin E which is a powerful antioxidant with anti-cancer and heart protective properties, and CoQ10 which is crucial for providing cellular energy.
Blocking CoQ10 production hinders aerobic metabolism and is as potentially deadly as arsenic, cyanide, and carbon monoxide that likewise block aerobic metabolism in cells.
Cholesterol is also a major part of the cell cycle because it builds cell membranes and before a cell divides into two the membrane must grow. Without the mevalonate to make cholesterol and isoprenoids cells die.
Statins are potent HMG-CoA reductase poisons because the reductase has a 10,000 times greater affinity for a statin than it does for HMG-CoA which the statin mimics.
Human cells that are exposed to statins cultured in a lab stop growing, stop replicating, lose their normal appearance and die without producing progeny. Cells with the fastest turnover rates are affect the most ( intestinal cells, skin cells, red blood cells, liver cells ).
The effects of six FDA approved statins ( Pravastatin, Lovastatin, Simvastatin, Atorvastatin, Fluvastatin, Cerivastatin) on four common types of human cells ( smooth muscle cells, fibroblasts, endothelial cells, myoblasts) were studied. All of these cell types stopped replicating in the presence of all of these approved statins.
Cerivastatin, the Bayer produced “superstatin” called Baycol, had to be recalled and removed from the market in 2001 following a series of rapid fatalities.
Dr Marvin D Siperstein did much of the pioneering work in this field. He discovered that mevalonate was crucial for DNA synthesis, cell growth and replication. He also discovered that cancer cells have a defective mevalonate pathway. His work remains largely ignored while less deserving people have been rewarded with Nobel prizes for their contribution to statin sales.
Statins are Deadly Mycotoxins.
Statins are derived from mycotoxins which are toxins produced by fungi in nature. Fungi produce these toxic secondary metabolites to kill off competing microbial life. Statins are “anti-life” or “anti-bios”, in other words they are non-selective antibiotics that indiscriminately kill any cell, including human cells.
Cholesterol synthesis and cellular LDL cholesterol receptor synthesis are co-regulated. When statins inhibit cellular cholesterol synthesis the cell produces more LDL receptors to grab cholesterol from the blood thereby lowering blood LDL levels.
By pulling LDL cholesterol out of the bloodstream, statins cause elevated cellular cholesterol levels, which can be toxic and cause apoptosis, which is a type of programmed cell death.
Many mycotoxins can suppress the immune system, and many are carcinogenic by virtue of the molecule having a lactone ring. Statins have a lactone ring.
Conclusion: They Know What They Are Doing
“What became clear is that there was and is a plan. It has been a systematically executed endeavour to take over national health care by hiring and corrupting scientists and infiltrating every public health care agency in the country for profit. It is beyond malevolent.” James B Yoseph, Dr Hannah Yoseph M.D.
Merck scientists and the other statin developers clearly understood the risks of using a pathogenic fungal mycotoxin to lower what they called “bad” cholesterol.
One of these scientists was the Japanese scientist Dr Akira Endo. When Dr Endo was asked why he didn’t take a statin for his own high cholesterol he replied with the Japanese proverb “The indigo dyer wears white trousers.” Indigo dye is very toxic to humans, so the smart indigo dyer doesn’t wear the trousers that he sells to others.
A couple of 1990 Merck patents for adding CoQ10 to statins demonstrates that they had foreknowledge of the harms that statins would cause, but they did not use or disclose the CoQ10 antidote to statin poisoning.
Merck and other statin manufacturers successfully avoid public scrutiny by settling damage claims out of court.
It is clear that statins have been a colossal failure and a public health disaster. Calling the effects of statins “side effects” when they are really predictable primary effects is fraudulent and deceptive.
“Our medical system is now like two snakes wrapped around a pole sitting on top of a pile of dung and hissing at us, daring us to require it to change. We need to snatch its twin tails, break its backs and return it to the dung heap.” James B Yoseph, Dr Hannah Yoseph M.D.
1) Hit or miss: the new cholesterol targets. Robert DuBroff, Aseem Malhotra, Michel de Lorgeril BMJ Evid Based Med. 2021 Dec;26(6):271-278. https://pubmed.ncbi.nlm.nih.gov/32747335/
2) Evaluating the Association Between Low-Density Lipoprotein Cholesterol Reduction and Relative and Absolute Effects of Statin Treatment: A Systematic Review and Meta-analysis Paula Byrne et al JAMA Intern Med. 2022 May 1;182(5):474-481 https://pubmed.ncbi.nlm.nih.gov/35285850/
3) Just Say No to Statins HEALTH VIEWPOINTS Dr Joseph Mercola
4) Statins: The Lesser-Known Dangers, and a Good Alternative FEATURED DRUGS & TREATMENTS Vance Voetberg
5) Statins: Most Prescribed Drug with Hyped Benefits and Downplayed Side Effects by Vance Voetberg
6) Statins stimulate atherosclerosis and heart failure: pharmacological mechanisms. Harumi Okuyama et al (2015) Expert Review of Clinical Pharmacology, 8:2, 189-199 https://doi.org/10.1586/17512433.2015.1011125
7) Statin Use Linked to Dementia. Dr. Joseph Mercola
8) How statin drugs really lower cholesterol and kill you one cell at a time. James B Yoseph. Hannah Yoseph M.D.
9) The Ugly Side of Statins. Systemic Appraisal of the Contemporary Un-Known Unknowns. Sherif Sultan, Niamh Hynes (2013) Open Journal of Endocrine and Metabolic Diseases http://dx.doi.org/10.4236/ojemd.2013.33025
by Simon Lee, Science Officer, Anew UK
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