We
are seeing the gradual dismantling of the Big Pharma propaganda
regarding vaccine safety, childhood vaccine schedule and the incentive
payments for physicians. That is huge progress in reversing the
unscientific politicization and influencing patient physician
relationships through money - called pay for performance.
Doctors Will No Longer Receive Financial Rewards for Vaccinating Kids
Another
big area factoring into physician pay for performance bonuses is the
prescription of cholesterol lowering statin drugs. About 40 Million
Americans currently take statins. Many bonus incentive programs of
health care providers are based on Center of Medicare pay for
performance metrics that were implemented two decades ago and now have
evolved to affect every area of medical care given.
MEDICARE “PAY FOR PERFORMANCE (P4P)” INITIATIVES
The
integration of medical records systems have provided for continuity of
care purposes transferable and accessible records within large health
care systems about these metrics tied to physician reimbursement. These
are “standards of care”, and anybodies cholesterol that is above a set
very low goal number is automatically alerted to the provider for the
initiation of statin drug prescription. This is reinforced by Insurance
companies who send letters to clinicians who are not meeting “standards
of care”.
The
idea that high cholesterol causes atherosclerosis has been
fundamentally debunked by great cardiologist Dr. Thomas Levy decades
ago. His books explaining that Vitamin C deficiency is the primary
driver of atherosclerosis have provided important paradigm shifting
information and insights, ignored by the Big Pharma aligned health care
system. Additionally, it is known that toxic heavy metals cause
artherosclerosis as well. While published in reputable medical journals,
these causes are ignored by conventional medical doctors and
cardiologists:
Low-Level Environmental Exposure to Lead Unmasked as Silent Killer
Menke et al7
analyzed the database of the Third National Health and Nutrition
Examination Survey (NHANES III) to investigate the relation between
total and cause-specific mortality and blood lead in a representative
sample of the US population. All 13 946 participants (≥17 years of age)
included in the analysis had a blood lead concentration <0.48 μmol/L
(10 μg/dL). (To convert micromoles per liter of lead into micrograms per
deciliter, multiply by 20.712.) Follow-up lasted until December 31,
2000. With adjustments applied for confounders, subjects in the highest
third of the blood lead distribution (≥0.17 μmol/L), as compared with
those in the lowest third (<0.09 μmol/L), experienced a significantly
higher risk of death. Estimates of the excess risk amounted to 25% and
55% for total and cardiovascular mortality, respectively, and 89% and
151% for myocardial infarction and stroke.
Just
like I have in my office for years reversed Atherosclerosis verifiably
with EDTA Chelation, Vitamin C and Nitric Oxide supplementation, Dr Levy
also has advocated for these methods and explained their medical
validity from the viewpoint of orthomolecular medicine. Since statins
are known mitochondrial toxins, he also advocated for decades against
them.
You can see our important interview here:
Dr
Levy also alerted me that Antimony and other toxic metals directly are
correlated with congestive heart failure in published studies, and since
these metals are ubiquitous in vaccinations and sprayed on us via
geoengineering operations, hence also affecting our food and water
supply - this is another ignored correlation of direct environmental
risk contributing to cardiac disease.
The Possible Role Of Toxic Metals In C19 Shots In Development Of Heart Damage - Another Reason For Preventative EDTA Chelation
One
of my all time favorite medical books is Stop America’s #1 Killer -
Proof that the origin of all Coronary Heart Disease is clearly
reversible Arterial Scurvy ( Vitamin C deficiency). I highly recommend
it to my readers.
One
of the first tests I do when patients come to my office is a Urine
Vitamin C level. Over 80% of people who have not already been listening
to my interviews on Vitamin C have scurvy. I follow Linus Paulings
recommendation of up to 10000mg ( ten thousand) Vitamin C daily
according to bowel tolerance, great for reversing a lot of chronic
diseases. These are some of Dr Levy’s books.
Dr
Levy’s findings were supported by another great cardiologist, who
bravely published papers regarding the evidence that statins in fact
increase atherosclerosis and congestive heart failure, hence making
people worse. This is the article showing that statins increase
congestive heart failure and atherosclerosis.
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 through the depletion of coenzyme Q10 and 'heme A', and thereby
ATP generation. Statins inhibit the synthesis of vitamin K2, the
cofactor for matrix Gla-protein activation, which in turn protects
arteries from calcification. Statins inhibit the biosynthesis of
selenium containing proteins, one of which is glutathione peroxidase
serving to suppress peroxidative stress. An impairment of selenoprotein
biosynthesis may be a factor in congestive heart failure, reminiscent of
the dilated cardiomyopathies seen with selenium deficiency. Thus, the
epidemic of heart failure and atherosclerosis that plagues the modern
world may paradoxically be aggravated by the pervasive use of statin
drugs. We propose that current statin treatment guidelines be critically
reevaluated.
Of
course doctors like us who have gone against the mainstream narrative
have been persecuted and marginalized. I remember a cardiologist telling
one of my patients that I should loose my license for not prescribing
statins. Interestingly, I reversed that patients atherosclerosis,
subsequent ischemia and congestive heart failure with my methods,
leaving these colleagues uncomfortably silent. Often the discharge
summaries will say, patient opts for chelation therapy instead of triple
bypass.
Recent
studies have confirmed reversal of heavy atherosclerosis with EDTA -
nanoparticles are unnecessary, regular EDTA has been used for this
purpose for a century:
Site-specific
chelation therapy with EDTA-loaded albumin nanoparticles reverses
arterial calcification in a rat model of chronic kidney disease
Reversal
of heavy arterial calcification in a rat model of chronic kidney
disease using targeted ethylene diamine tetraacetic acid-loaded albumin
nanoparticles
Conclusions: This
is the first study showing the removal of calcium from heavily
calcified arteries by using intravenous targeted EDTA therapy. Such
therapy also reversed vascular smooth muscle cell osteoblastic
transition and apoptosis in the arterial tissue, thereby potentially
creating an environment for suitable tissue repair.
Targeted
chelation therapy decreases NLRP3 expression by vascular cells and acts
as senomorphic in chronic kidney disorder induced vascular
calcification.
Arora
S, Halsey G, Zohora FT, Swiss A, Vyavahare N.Int J Immunopathol
Pharmacol. 2025 Jan-Dec;39:3946320251391142. doi:
10.1177/03946320251391142. Epub 2025 Dec 15.PMID: 41399092Free PMC
article.
Site-specific
chelation therapy with EDTA-loaded albumin nanoparticles reverses
arterial calcification in a rat model of chronic kidney disease.
Karamched
SR, Nosoudi N, Moreland HE, Chowdhury A, Vyavahare NR.Sci Rep. 2019 Feb
22;9(1):2629. doi: 10.1038/s41598-019-39639-8.PMID: 30796300Free PMC
article.
Targeted
chelation therapy with EDTA-loaded albumin nanoparticles regresses
arterial calcification without causing systemic side effects.
Lei
Y, Nosoudi N, Vyavahare N.J Control Release. 2014 Dec 28;196:79-86.
doi: 10.1016/j.jconrel.2014.09.029. Epub 2014 Oct 5.PMID: 25285609Free
PMC article.
Fulgenzi
A, De Giuseppe R, Bamonti F, Vietti D, Ferrero ME. Efficacy of
chelation therapy to remove aluminium intoxication. J Inorg Biochem.
2015 Nov;152:214-8. doi: 10.1016/j.jinorgbio.2015.09.007. Epub 2015 Sep
24. PMID: 26404567.
Of
course historical humans studies have shown beneficial effects for
years, but there are many people spreading disinformation and the FDA
historically has waged war against EDTA:
Efrain Olszewer MD, James Carter MD EDTA Chelation Therapy: A Retrospective Study of 2870 Patients. J Adv Med 1989;2:197-211
Retrospective
study EDTA chelation in 470 patients with peripheral vascular disease.
Improvement 80-91%. Of 92 patients referred for surgical intervention
only 10 required ultimate surgery saving an estimated 3 Million Dollars
of insurance money. No adverse effects over 6 years.
Here are more systemic studies showing remarkable improvements:
Maybe
the new evidence coming forward will change clinicians mind regarding
their practices. However, that will never happen if the financial
incentives do not change.
This
new article now shows how statins injure muscles. Our heart is a muscle
and is not excluded from this injury. The authors from Columbia
University call for a reevaluation of statin therapy. I think this issue
should be high on the MAHA agenda, since 40 Million Americans are
having their mitochondria, the powerhouse of the cells, injured by
statin drugs. Mitochondrial dysfunction can contribute to all diseases
of aging.
Even Web MD talks about the substantial side effects -
The most common statin side effects include:
Headache
A hard time sleeping
Flushing of the skin
Muscle aches (myalgia), tenderness, or weakness
Drowsiness
Dizziness
Nausea or vomiting
Belly cramping or pain
Bloating or gas
Diarrhea
Constipation
Rash
Low levels of blood platelets
Less common side effects you may have with statins are:
Nausea
Hair loss
Pins and needles sensations, such as pricking, numbness, or tingling on your skin
Liver inflammation, which can make you feel like you have the flu
Pancreas inflammation, which can cause stomach pain
Skin problems such as rashes or acne
Sexual problems, such as erectile dysfunction or a low sex drive
Statins
also carry warnings that memory loss, mental confusion, neuropathy,
high blood sugar, and type 2 diabetes are possible side effects. It’s
important to remember that statins may also interact with other
medications you take.
Adequate
Vitamin C levels can help lower cholesterol, studies referenced can be
found in Dr. Levy’s book. I use Citrus Bergamot, a polyphenol, in my
patients with statin intolerance
Clinical application of bergamot (Citrus bergamia) for reducing high cholesterol and cardiovascular disease markers
Here is the article:
Summary:
A
new discovery may explain why so many people abandon
cholesterol-lowering statins because of muscle pain and weakness.
Researchers found that certain statins can latch onto a key muscle
protein and trigger a tiny but harmful calcium leak inside muscle cells.
That leak may weaken muscles directly or activate processes that slowly
break them down, offering a long-sought explanation for statin-related
aches.
__________________________________________________________________________
Many
people who are prescribed statins to lower cholesterol end up stopping
the medication because of muscle pain, weakness, or ongoing fatigue.
These symptoms are among the most common reasons patients abandon the
drugs.
New research from Columbia University suggests a possible explanation for why this happens in some individuals. The
study indicates that certain statins can attach to a protein inside
muscle cells, triggering a leak of calcium ions that disrupts normal
muscle function.
“It
is unlikely that this explanation applies to everyone who experiences
muscular side effects with statins, but even if it explains a small
subset, that’s a lot of people we could help if we can resolve the
issue,” says Andrew Marks, chair of the Department of Physiology and
Cellular Biophysics at the Vagelos College of Physicians and Surgeons.
Statins
are widely used in the United States. Roughly 40 million adults take
them to control cholesterol levels, and about 10 percent develop muscle
related side effects.
“I’ve
had patients who’ve been prescribed statins, and they refused to take
them because of the side effects. It’s the most common reason patients
quit statins, and it’s a very real problem that needs a solution,” Marks
says.
A Longstanding Puzzle Around Statin Muscle Pain
Scientists
have been trying to understand statin related muscle problems since the
drugs first became available in the late 1980s. Statins work by binding
to an enzyme involved in cholesterol production, but they can also
attach to other unintended targets in the body.
Earlier
research hinted that muscle side effects might occur when statins
interact with a specific protein in muscle tissue. Until now, the
details of that interaction were unclear.
Using
cryo-electron microscopy, a powerful imaging method that allows
researchers to see structures down to individual atoms, the Columbia
team was able to directly observe how a statin interacts with muscle
cells.
Calcium Leaks Inside Muscle Cells
The
images showed that a commonly prescribed statin, simvastatin, binds to
two specific sites on a muscle protein known as the ryanodine receptor.
This binding opens a channel in the protein, allowing calcium to leak
into areas of the cell where it does not normally flow.
According to Marks, this calcium leak may explain muscle pain and weakness linked to statins. The excess calcium can weaken muscle fibers directly or activate enzymes that gradually break down muscle tissue.
Toward Safer Cholesterol Drugs
The
findings point to new possibilities for reducing statin side effects.
One approach would be to redesign statins so they continue to lower
cholesterol but no longer bind to the ryanodine receptor in muscle
cells.
Marks is currently working with chemists to develop statins that avoid this unwanted interaction.
Another
potential strategy focuses on stopping the calcium leak itself. The
researchers showed that in mice, statin related calcium leaks can be
closed using an experimental drug created in the Marks laboratory for
other disorders involving abnormal calcium flow.
“These
drugs are currently being tested in people with rare muscle diseases.
If it shows efficacy in those patients, we can test it in statin-induced
myopathies,” Marks says
Study Details and Disclosures
Andrew
Marks is also the Clyde and Helen Wu Professor of Medicine at Columbia
University Vagelos College of Physicians and Surgeons, a professor of
biomedical engineering, and director of the Wu Center for Molecular
Cardiology.
The
study was published Dec. 15 in “Structural basis for
simvastatin-induced skeletal muscle weakness associated with RyR1 T4709M
mutation,” in the Journal of Clinical Investigation.
Gunnar
Weninger, Haikel Dridi, Steven Reiken, Qi Yuan, Nan Zhao, Linda Groom,
Jennifer Leigh, Yang Liu, Carl Tchagou, Jiayi Kang, Alexander Chang,
Estefania Luna-Figueroa, Marco C. Miotto, Anetta Wronska, Robert T.
Dirksen, Andrew R. Marks. Structural basis for simvastatin-induced skeletal muscle weakness associated with type 1 ryanodine receptor T4709M mutation. Journal of Clinical Investigation, 2025; 135 (24) DOI: 10.1172/JCI194490
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