I have been sounding the alarm about these dangerous drugs for years and came across this excellent article.
If you are taking a statin drug or know of someone
that is, please read this and/or pass this on.
If you are worried about your cholesterol or other lipids, the best way
to really determine if you have a problem is to ask your doctor for one of
these tests.
Cholesterol
particle size tests that can shed light on your particular cholesterol subtype
situation:
Lipoprotein
Particle Profile (LPP) Test, developed by SpectraCell
NMR
LipoProfile Test, developed by LabCorp
Cardio
IQ Report, offered through Quest Diagnostics
Any of these tests are good options for getting a more detailed look at the various types of cholesterol particles in your blood, and a more accurate picture of your cardiovascular risk.
Statins
are NOT “Wonder Drugs” they are Metabolic Poisons that Kill One Cell at a Time.
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.
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 dependent, 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 specialize 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”.
Broken Hearts
“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 calcification. 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 modernized 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
behavior, 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 characterized 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 glycemic 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 endeavor 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.
REFERENCES
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. Hit or miss: the new cholesterol targets - PubMed
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 Evaluating the Association Between Low-Density
Lipoprotein Cholesterol Reduction and Relative and Absolute Effects of Statin
Treatment: A Systematic Review and Meta-analysis - PubMed
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
https://expose-news.com/2023/11/10/statins-are-not-wonder-drugs-they-are-metabolic-poisons-that-kill-one-cell-at-a-time/
The main ways the body rids itself of old, faulty, or diseased cells is through something called programmed cell death, or apoptosis. 
Control cell-signaling pathways
Cheon's team also tested the nanoparticles in combination with magnets, with astounding success. In a series of lab experiments, the team placed nanoparticle-treated bowel cancer cells between two