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Friday, March 1, 2024

The State of Glutathione Research

Dr. Debby Hamilton, MD, MPH
Introduction
Glutathione is the primary antioxidant in the body and therefore has a significant role in controlling oxidative stress in the body. It is formed primarily within cells from three amino acids including cysteine, glycine, and glutamic acid.1 Because it is an antioxidant, it is available in a reduced active form of glutathione (GSH) that neutralizes free radicals and transforms into the oxidized glutathione disulfide form (GSSH). The oxidized form GSSH is then recycled back to the reduced form GSH. 
Benefits of Glutathione
While glutathione plays a key role in managing oxidative stress in the body it also serves multiple other functions. It helps recycle other antioxidants such as vitamin C and vitamin E. Oxidative stress can contribute to damage of tissues and cells down to the level of the mitochondria.  Mitochondria are critical for energy production in the body.  Glutathione is essential for protecting the mitochondria and therefore protecting energy formation.2
Detoxification is another critical function served by glutathione including both environmental toxins and endogenous metabolic toxins.3 With its critical role in detoxification, high levels of glutathione are found in the liver and other detoxification organs such as the kidney and lungs.4,5 Levels of glutathione can be depleted with ongoing exposure to toxins.
Glutathione serves a key role in immune function.  It is involved in increasing natural killer cells and enhancing T cell function.6-8 By increasing multiple types of immune cells, it supports both the innate and adaptive immune systems.  Research studies have shown increases in natural killer cell function with the supplementation of liposomal glutathione.7,9 
Conditions with Increased Glutathione Needs
As the major antioxidant in the body, glutathione is essential for human health. With chronic disease, there is an increase in inflammation and oxidative stress leading to an increased need for glutathione. Aging is associated with lower levels of glutathione and increasing levels of oxidative stress.10 Multiple types of infections have been associated with low levels of glutathione including viral infections such as COVID-19, influenza, and HIV.11-13   Chronic infections such as Borrelia infections which impact an increasing number of people are associated with low levels of glutathione.14
Neuroinflammation is involved in neurodegenerative diseases in adults such as dementia but also in children with autism spectrum disorder. Chronic neuroinflammation leads to depletion of glutathione.15,16 Chronic cardiovascular, lung and liver diseases have been shown to have low levels of glutathione which impact severity of disease.17-19
Issues with Glutathione Supplementation
Because glutathione is a critical antioxidant in the body, the question becomes how to best supplement. Glutathione can shift rapidly between the reduced and the oxidized state so when taken in a direct form orally it gets oxidized in the stomach, so the active form is not absorbed. The human gastrointestinal tract contains significant amounts of the enzyme GGT, which recycles GSH precursors. This may decrease GSH absorption significantly from oral glutathione supplementation.20 To protect glutathione, liposomes which are lipids surrounding the glutathione, have been developed. Intravenous (IV) glutathione is used by many practitioners in their practice but because of cost and time is difficult to do frequently long term. Transdermal, intranasal, and nebulized glutathione are other forms of supplementation but have less research and less availability.  Practitioners also use precursors for glutathione such as N-Acetylcysteine (NAC). Research on glutathione absorption and clinical outcomes are reviewed below to evaluate efficacy of different glutathione supplementation methods. In vivo studies will be the focus to show practitioners how to best support their patients with glutathione supplementation.
Research on Oral Glutathione
Initial research on supplementing oral glutathione was done with the reduced GSH form without any change in the molecule or added lipids in the form of a liposome. In 1992, researchers gave a single dose of 3 grams of GSH to seven people and did not observe an increase in blood GSH levels.21  A randomized double-blind placebo-controlled trial was done in 2011 that had 40 participants given 500 mg twice a day for four weeks.20  Oxidative stress markers were not reduced and there was no increase in total reduced, GSH, oxidized GSSH, or change in ratio of GSH/GSSH.20 Since there were no changes in glutathione or oxidative stress markers, oral glutathione in its unmodified form was not thought to be an option for glutathione supplementation. From these results, companies developed patented liposomal glutathione preparations. Several of these have been studied for absorption and/or clinical symptom improvement. One patented form of liposomal glutathione was researched for 6 months in a randomized controlled trial where half of the participants received a low dose 250 mg/day and half received a high dose of 1000 mg/day.9   Both doses showed increases in glutathione levels with the higher dose showing greater improvements. The high dose of 1000 mg after 6 months showed an increase in GSH (reduced active form) of 30-35% in red blood cells, plasma, and lymphocytes (P<0.05).9   For immune function, natural killer cytotoxicity was measured with a > two fold increase in the high dose group after 3 months (P < 0.05).9   For oxidative stress evaluation a decrease in oxidized to reduced glutathione ratios in whole blood were seen at the end of the study.
A different patented liposomal glutathione was investigated for absorption and immune function. Participants who had glutathione levels at the low end of normal received either 500 mg or 1000 mg daily for one month.7 There were no differences observed between dose groups at the end of the study. The maximum increases in glutathione levels were found after 2 weeks with 500 mg daily of 40% in whole blood, 25% in erythrocytes, 28% in plasma and 100% in PBMCs occurring after 2 weeks(P<0.05).7 Oxidative stress markers decreased significantly and correlated with the increase in glutathione levels. Immune markers showed improvement also with an increase in natural killer cell cytotoxicity up by 400% in two weeks and an increase in lymphocyte proliferation of 60% in two weeks where both reached statistical significance. (P<0.05).7
Research on Topical/Transdermal Glutathione
Topical or transdermal glutathione is an easy way to supplement glutathione, but the initial research did not support the efficacy of it. Research compared oral liposomal glutathione versus transdermal glutathione in children with autism spectrum disorder who had low baseline levels of glutathione.15  The study was conducted over 8 weeks and the doses of both the transdermal and the oral liposomal glutathione began at ¼ recommended dose and increased weekly until the full dose per weight was given at 4 weeks and that dose was maintained throughout the study.15 The children taking the oral glutathione had significant increases in plasma reduced glutathione along with elevated levels of sulfate, cysteine, and taurine.15(Kern).  In the transdermal glutathione group, there were also significant increases in plasma sulfate, cysteine, and taurine levels but not in plasma glutathione levels.15 The results lead to the concern whether transdermal glutathione was sufficient for raising plasma glutathione levels.
In a comparable manner to altering oral glutathione to increase absorption, a modified version of topical glutathione was developed called glutathione–cyclodextrin nanoparticle complex (GSH-CD) The research studied both absorption levels of the topical GSH-CD along with immune markers for three days when participants were exposed to Mycobacterium avium.22
Topical GSH-CD after three days showed elevated GSH levels in blood mononuclear cells and red blood cells along with decreased levels of the oxidative stress marker malandialdehyde.22   Immune elevations in cytokines and an increase in clearance of the Mycobacterium avium infection were associated with the topical GSH-CD.22  The study showed that a modified form of transdermal or topical glutathione could increase blood cell levels of glutathione which were not found with previous unmodified topical glutathione.
Research on Intravenous Glutathione
Initial research on intravenous (IV) glutathione showed that after an infusion of 2 gms. of glutathione the concentration of both total glutathione and cysteine in the plasma increased significantly.23 Excretion of glutathione in the 90 minutes following infusion increased 300 fold for glutathione and was at a constant rate with a half-life corresponding to 14.1 +/- 9.2 min.23 Subsequent research on intravenous glutathione has focused more on improvement in clinical symptoms than in vivo absorption studies.  Two studies done on Parkinson’s patients have shown clinical improvements with IV glutathione given daily for a month, but these clinical improvements returned to baseline after approximately two months without glutathione in both studies.24,25  Clinical studies have compared IV glutathione to oral N-acetylcysteine (NAC) for preventing oxidative stress after coronary angiography which induces oxidative stress damage.26 IV glutathione prevented the increase in oxidative stress markers as predicted but oral NAC had no effect on the oxidative stress markers.26  Based on the research, although limited, it appears that IV glutathione is effectively getting into the blood stream.  The concern is how long this effect lasts based on the short half-life.
Research on Nebulized and Intranasal Glutathione
Both intranasal and nebulized forms of glutathione are available and used primarily for sinus and lung conditions. Absorption studies are minimal. A safety study on intranasal glutathione  found it to be helpful for symptoms in 62% of patients with 12% reporting side effects.27 Intranasal glutathione is also being researched for neurodegenerative diseases with its close proximity to the nervous system. A study showed high dose intranasal glutathione to improve Parkinsons’s symptoms, but the results were not statistically significant.28
Efficacy of N-acetylcysteine (NAC) for Glutathione Support
N-acetylcysteine (NAC) is often used as a supplement to increase glutathione levels. Cysteine is the rate limiting step in glutathione synthesis so the thought is it would lead to an increased production of glutathione. One concern with this is the body’s ability to synthesize glutathione from cysteine and other amino acids decreases with age and with certain chronic diseases especially if they involve liver dysfunction.29 Genetic SNIPS’s including glutathione building and glutathione recycling enzymes can also influence the rate of glutathione production from precursors. Studies of NAC have been inconsistent with showing levels of increased glutathione.29-33   Since the benefits of glutathione include improving immune function and decreasing oxidative stress, NAC has been studied for both functions.  Research has shown in specific studies that NAC does not influence immune function.33 or antioxidant function.31 Overall, the research on NAC appears to be limited in terms of being a good method for improving glutathione and supporting multiple glutathione functions.
Summary
Glutathione as our primary antioxidant is critical for health. With the toxins in our environment along with high rates of chronic disease and stress, many people are low in this critical nutrient. Because of this, practitioners have searched for ways to elevate glutathione. There is research that shows improvement with targeted forms of oral glutathione in the liposomal form and modified topical glutathione (GSH-CD). Improvements in clinical function have been found with the liposomal oral form. Intravenous glutathione according to research is absorbed and can improve clinical symptoms but the concern is the short half-life and the return of symptoms once the IV glutathione has been stopped. Because of cost and needing to be in a clinical setting, IV glutathione is not practical for daily use. Intranasal glutathione and nebulized glutathione as methods for targeted disease states could be helpful but are not adequately researched at this time. Overall, more research needs to be done to understand how to maximize the supplementation of glutathione to benefit patients.
References
  1. Zhang H, Forman HJ. Glutathione synthesis and its role in redox signaling. Semin Cell Dev Biol. 23:722–728.
  2. Forman HJ. et al. Glutathione: overview of its protective roles, measurement, and biosynthesis. Mol Aspects Med. 2009;30(1-2):1-12.
  3. Pastore A. et al. Analysis of glutathione: implication in redox and detoxification. Clin Chim Acta. 2003 Jul 1;333(1):19-39.
  4. Yuan L. et al. Glutathione in liver disease and hepatotoxicity. Aspects of Med. 2009. 29-41.
  5. Cantin A et al. Glutathione and Inflammatory Disorders of the lungs. 1991. 169:123-138.
  6. Guerra C. et al. Glutathione and adaptive immune responses against mycobacterium tuberculosis infection in healthy and HIV infected individuals.  PLOS One. 2011.
  7. Sinha R. et al. Oral supplementation with liposomal glutathione elevates body stores of glutathione and markers of immune function. Eur J Clin Nutr. 2018 Jan;72(1):105-111.
  8. Morris G. et al. Redox regulation of the immune response. Cell Mol Immunol. 2022 Oct;19(10):1079-1101.
  9. Richie JP Jr. et al. Randomized controlled trial of oral glutathione supplementation on body stores of glutathione. Eur J Nutr. 2015 Mar;54(2):251-63.
  10. Maher P. et al. The effects of stress and aging on glutathione metabolism. Ageing Research Reviews. Vol 4(2).
  11. Nencioni L. et al. Influenza A virus replication is dependent on an antioxidant pathway that involves GSH and Bcl-2. 2003;17:758–760.
  12. Polonikov A. Endogenous deficiency of glutathione as the most likely cause of serious manifestations and death in patients with the novel coronavirus infection (COVID-19): A hypothesis based on literature data and own observations. ACS Infect. Dis. 2020;6:1558–156.
  13. Ly J. et al. Liposomal Glutathione Supplementation Restores TH1 Cytokine Response to Mycobacterium Tuberculosis Infection in HIV-Infected Individuals.  Interferon. Cytokine Res. 2015;35:875–887.
  14. Peacock BN. et al. New insights into Lyme disease. Redox Biology. 2015;5:66-70.
  15. Kern JK. et al. A clinical trial of glutathione supplementation in autism spectrum disorders. Med Sci Monit. 2011;17(12):CR677-CR682.
  16. Hauser RA. Et al. Randomized, double-blind, pilot evaluation of intravenous glutathione in Parkinson’s disease. Mov Disord. 2009 May 15;24(7):979-83.
  17. Tan M. et al. Glutathione system enhancement for cardiac protection: pharmacological options against oxidative stress and ferroptosis. Cell Death Dis. 2023 Feb 16;14(2):131.
  18. Ghezzi P. et al. Role of glutathione in immunity and inflammation in the lung. Int J Gen Med. 2011;4:105–113.
  19. Bianchi G. et al.  Glutathione kinetics in normal man and in patients with liver cirrhosis.  Hepatol. 1997;26:606–613.
  20. Allen J, Bradley RD. Effects of oral glutathione supplementation on systemic oxidative stress biomarkers in human volunteers. J Altern Complement Med. 2011;17(9):827-833.
  21. Witschi A. et al. The systemic availability of oral glutathione. Eur J Clin Pharmacol. 1992;43:667–669. 
  22. Sasaninia K. et al. Topical Absorption of Glutathione-Cyclodextrin Nanoparticle Complex in Healthy Human Subjects Improves Immune Response against Mycobacterium avium Antioxidants (Basel). 2023 Jul 2;12(7):1375.
  23. Aebi S. et al. High-dose intravenous glutathione in man. Pharmacokinetics and effects on cyst(e)ine in plasma and urine. Eur J Clin Invest. 1991 Feb;21(1):103-10.
  24. Hauser RA. Randomized, double-blind, pilot evaluation of intravenous glutathione in Parkinson’s disease. Mov Disord. 2009 May 15;24(7):979-83.
  25. Sechi G. Reduced intravenous glutathione in the treatment of early Parkinson’s disease. Prog Neuropsychopharmacol Biol Psychiatry. 1996 Oct;20(7):1159-70.
  26. Saitoh T. et al. Intravenous glutathione prevents renal oxidative stress after coronary angiography more effectively than oral N-acetylcysteine. Heart Vessels. 2011 Sep;26(5):465-72.
  27. Mischley LK. et al. Safety survey of intransal glutathione.  The J Alt and Comp Medicine. 2013 19:5, 459-463.
  28. Mischley LK. et al. Phase IIb Study of Intranasal Glutathione in Parkinson’s Disease. J Parkinsons Dis. 2017;7(2):289-299.
  29. Schmitt B. et al. Effects of N-acetylcysteine, oral glutathione (GSH) and a novel sublingual form of GSH on oxidative stress markers: A comparative crossover study. Redox Biology6 (2015): 198-205.
  30. Treitinger A. et al. Effect of N-acetyl-L-cysteine on lymphocyte apoptosis, lymphocyte viability, TNF-alpha and IL-8 in HIV-infected patients undergoing anti-retroviral treatment. Braz J Infect Dis. 2004 Oct;8(5):363-71.
  31. Rushworth GF, Megson IL. Existing and potential therapeutic uses for N-acetylcysteine: the need for conversion to intracellular glutathione for antioxidant benefits. Pharmacol Ther. 2014 Feb;141(2):150-9. doi: 10.1016/j.pharmthera.2013.09.006. Epub 2013 Sep 28. PMID: 24080471.
  32. Paschalis V, Theodorou AA, Margaritelis NV, Kyparos A, Nikolaidis MG. N-acetylcysteine supplementation increases exercise performance and reduces oxidative stress only in individuals with low levels of glutathione. Free Radic Biol Med. 2018 Feb 1;115:288-297. doi: 10.1016/j.freeradbiomed.2017.12.007. Epub 2017 Dec 9. PMID: 29233792.
  33. Hamzeh N, Li L, Barkes B, Huang J, Canono B, Gillespie M, Maier L, Day B. The effect of an oral anti-oxidant, N-Acetyl-cysteine, on inflammatory and oxidative markers in pulmonary sarcoidosis. Respir Med. 2016 Mar;112:106-11. doi: 10.1016/j.rmed.2016.01.011. Epub 2016 Jan 22. PMID: 26831541.  

Monday, February 26, 2024

Quercetin Benefits Chronic Fatigue

 Quercetin Phytosome Benefits Chronic Fatigue

 

Chronic fatigue syndrome is a complex series of symptoms with uncertain etiologies. Quercetin has shown numerous mechanisms of action that might make it a candidate for consideration in cases of chronic fatigue syndrome – antioxidant, anti-inflammatory, immune-modulating, improved exercise endurance, and increased mitochondrial biogenesis and function. Therefore, a well-absorbed form of quercetin was tested for efficacy in individuals suffering from chronic fatigue.

 

In this study, 78 participants (average age 56; female=42; male=36) complaining of various aspects of chronic fatigue were randomized to receive 250 mg quercetin phytosome or placebo twice daily for two months. Potential participants with an identifiable cause of fatigue like hypothyroidism or anemia were excluded. The primary endpoint was a change from baseline in scores on the Fatigue Impact Scale (FIS-40). Secondary endpoints included sleep quality (measured by the Pittsburgh Sleep Quality Index), quality of life scores, and physical performance and endurance via several physical tests.

 

At the end of the study, changes in scores on the various tests were compared between the supplement and placebo groups. The quercetin group had significantly greater improvement compared to placebo on the primary endpoint using the FIS-40 score to assess aspects of fatigue. The supplement group also had comparatively and significantly greater improvement in sleep quality and physical performance/endurance. The specific areas of physical performance improvement included number of steps (measured by an armband sensor), gait speed, chair-stand test, and time-up-and-go (the time it takes to stand from an armchair, walk three meters, walk back, and sit down).


Reference

Rondanelli M, Riva A, Petrangolini G, et al. Two-month period of 500 mg lecithin-based delivery form of quercetin daily dietary supplementation counterbalances chronic fatigue symptoms: A double-blind placebo controlled clinical trial. Biomed Pharmacother 2023 Nov;167:115453. doi: 10.1016/j.biopha.2023.115453.

Sunday, November 12, 2023

Statins are NOT “Wonder Drugs” they are Metabolic Poisons that Kill One Cell at a Time

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/