Mitochondrial “Collateral Damage” Thanks to Big Pharma – Iatrogenic Drug and Vaccine-induced Mitochondrial Disorders
“All classes of psychotropic drugs have been documented to damage mitochondria, as have statin medications, analgesics such as acetaminophen, and many others.” – John Neustadt, MD and Steven Pieczenik, MD
The conference centered entirely upon the rare congenital/inherited forms of mitochondrial disorders that are first diagnosed in infancy and which comprise about 10 – 15 % of cases of known mitochondrial disorders.
Nothing was said by the presenters about the 85 – 90 % of acquired forms of mitochondrial disorders, which could, of course, be preventable if knowledge of the root causes were transmitted to us physicians and patients.
Ever since that suspicious episode I have maintained an interest in mitochondrial disorders, and since then I have discovered many articles in the basic science literature that have dealt with drug and vaccine-induced mitochondrial disorders, none of which ever gets published in the mainstream medical journals, at least those that take advertising money from pharmaceutical companies.
So this Duty to Warn column is about the multitude of common iatrogenic (drug- or doctor-caused) diseases that can be caused by the commonly prescribed drugs and/or commonly injected vaccine ingredients that are making many of us highly drugged, malnourished, environmentally-toxic and also thoroughly vaccinated. We Americans (infants, children, adolescents and adults) are among the sickest, most chronically-ill people in the developed world.
I include excerpts from just three examples from a multitude of peer-reviewed medical journal articles that have been trying to tell us clinicians (and our most aware patients) that there are many common, preventable disorders that the powers-that-be want us to believe are either the fault of the patient-victim (“shame-on-you”) or are simply inherited from our guilty parents (and thus neither preventable nor curable).
Many of these disorders (see list below) are actually caused by prescription drugs, vaccines and/or other toxic chemicals that are poisoning the mitochondria in our brains, nerves, muscles and other organs. Thus we are being afflicted by preventable, iatrogenic- or industry-caused diseases. Both realities are taboo subjects in the current era of mind-control by America’s powerful, profit-motivated, multinational corporations in BigPharma, BigChemical, BigMedicine, BigMedia, BigFood and BigAgribusiness industries. That pervasive group prefers our ignorance, and each of them spends unlimited amounts of money to ensure it.
The avarice of these industries for larger market-share, higher share price, bigger profits, lower wages and more aggressive wealth extraction knows no bounds, and their brain-disabling products makes their goals ever easier to attain.
The first excerpt below is about the injectable, toxic aluminum adjuvants that have been added to virtually all infant and adult vaccines for the past 70+ years There is no safe dose of aluminum or mercury, and neither have any nutritional value. (Aluminum is poorly absorbed when swallowed [0.5% absorption] but is 100% absorbed into the blood stream when injected.) The CDC/AAP (American Academy of Pediatrics)-mandated immunization schedule ensures that a total of nearly 5,000 micrograms of the mitochondrial toxin aluminum will be injected into the average American baby by the time he or she reaches 18 months (before which, by the way, is when many of the alleged “inherited” mitochondrial diseases become manifest)!
The second excerpt talks about how poisonous mercury is to the mitochondria that are in human brain, nerve, muscle and body cells. Over the last 20 years there have been at least a hundred peer-reviewed medical journal articles that have been warning physicians about the neurotoxicity of mercury, the second-most toxic metal known to man (plutonium is first).
Mercury, in the form of Eli Lilly & Company’s Thimerosal, has been in most infant and adult vaccines for several generations and was only removed from a number – but not all – of them when the AAP pleaded with the vaccine manufacturers to remove it from all vaccines because many concerned pediatricians were rightfully convinced that the rapidly escalating autism epidemic was at least partially caused by the rapidly escalating dosing of vaccines: and they were correct. But the neurotoxic aluminum, often given in multiple inoculations simultaneously, remained in the over-vaccination schedule, and the epidemic of chronic, autoimmune disorders among fully vaccinated children continued.
Nevertheless, the pharmaceutical companies, the CDC and the AAP continue to recommend annual (aluminum and mercury-containing) flu shots for immature, immune-vulnerable, brain-undeveloped babies as young as 6 months of age, and for their pregnant mothers! What could possibly go wrong? One must ask: who are the benefactors and who are the victims?
The third article below consist of extracts from a literature review of the subject of mitochondrial damage and the role of medications, chemicals, pesticides, metals, drugs, vaccine ingredients and other mitochondrial poisons that put every cell in our bodies at increased risk of permanent damage. It is titled “Medication-induced Mitochondrial Damage and Disease”. Alarmingly, no mitochondrial patient advocacy website that I could find has links to this or any of the scores of articles that discuss acquired or iatrogenic mitochondrial disorders. Go figure.
1) Aluminum-induced Defective Mitochondrial Metabolism Perturbs Cytoskeletal Dynamics in Human Astrocytoma Cells
By  J. Lemire, R. Mailloux, S. Puiseux-Dao, and V. D. Appanna
Posted at: http://onlinelibrary.wiley.com/doi/10.1002/jnr.21965/abstract
Although aluminum (Al), a known environmental toxin, has been implicated in a variety of neurological disorders, the molecular mechanism responsible for these conditions is not fully understood. In this report, we demonstrate the ability of Al to trigger mitochondrial dysfunction and ineffective adenosine triphosphate (ATP) production. This situation severely affected cytoskeletal dynamics. Whereas the control cells had well-defined structures, the Al-exposed astrocytoma cells appeared as globular structures. Creatine kinase (CK) and proﬁlin-2, two critical modulators of cellular morphology, were markedly diminished in the astrocytoma cells treated with Al. Antioxidants such as a-ketoglutarate and N-acetylcysteine (NAC) mitigated the occurrence of the globular-shaped cells promoted by Al toxicity. Taken together, these data reveal an intricate link between ATP metabolism and astrocytic dysfunction and provide molecular insights into the pathogenesis of Al-induced neurological diseases.
2) Thimerosal-Derived Ethylmercury Is a Mitochondrial Toxin in Human Astrocytes
By M. A. Sharpe , A. D. Livingston , and D. S. Baskin – Published online 6/28/2012 in the Journal of Toxicology , (posted at: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3395253/ )
Thimerosal generates ethylmercury in aqueous solution and is widely used as a (bactericidal) preservative. We have investigated the toxicology of Thimerosal in normal human astrocytes, paying particular attention to mitochondrial function and the generation of specific oxidants. We find that ethylmercury not only inhibits mitochondrial respiration leading to a drop in the steady state membrane potential, but also concurrent with these phenomena increases the formation of superoxide, hydrogen peroxide, and Fenton/Haber-Weiss generated hydroxyl radical. These oxidants increase the levels of cellular aldehyde/ketones. Additionally, we find a five-fold increase in the levels of oxidant damaged mitochondrial DNA bases and increases in the levels of mtDNA nicks and blunt-ended breaks. Highly damaged mitochondria are characterized by having very low membrane potentials, increased superoxide/hydrogen peroxide production, and extensively damaged mtDNA and proteins. These mitochondria appear to have undergone a permeability transition, an observation supported by the five-fold increase in Caspase-3 activity observed after Thimerosal treatment.
Thimerosal is a preservative that is widely used in medical products, including as a preservative in vaccines, immunoglobulin preparations, skin test antigens, antivenins, ophthalmic and nasal products, and tattoo inks, and is composed of 49.6 percent ethylmercury by weight. The widespread use of Thimerosal exposes many to its potential toxic effects, especially in utero and in neonates. We report the results of a series of experiments using cultured normal human astrocytes (NHA) exposed to Thimerosal to study the compound’s effect on astrocyte mitochondria.
The brain utilizes 20% of the oxygen consumed by the body but constitutes only 2% of the body’s mass. <<snip>>
3) Medication-induced Mitochondrial Damage and Disease
By John Neustadt and Steve R. Pieczeni
Mitochondria Structure and Function
Cellular energy requirements control how many mitochondria are in each cell. A single somatic cell can contain from 200 to 2000 mitochondria, while human germ cells such as spermatozoa contain a fixed number of 16 mitochondria and oocytes have up to 100 000. The largest number of mitochondria are found in the most metabolically active cells, such as skeletal and cardiac muscle and the liver and brain. Mitochondria are found in every human cell except mature erythrocytes (red blood cells).
Acquired Conditions in which Mitochondrial Dysfunction has been Implicated (as of 2007)
Cancer including hepatitis-C virus-associated hepatocarcinogenesis
Nonalcoholic steatohepatitis (NASH – late stage of nonalcoholic fatty infiltration of the liver)
Cardiovascular disease, including atherosclerosis
Sarcopenia (muscle-wasting disease, mainly of the elderly)
Fatigue, including chronic fatigue syndrome, fibromyalgia, and myofascial pain
Medications Documented to Induce Mitochondrial Damage (as of 2007)
Alcoholism medications Ex: Antabuse
Alzheimer’s dementia drugs Ex: Tacrine (Cognex), Galantamine
Analgesics (for pain) and anti-inflammatory drugs, Ex: Aspirin, acetaminophen (Tylenol), indomethacin, Naproxen
Anesthetics Ex: lidocaine, propofol (also general anesthetics likehalothane. isoflurane, sevoflurane)
Angina medications Ex: amiodarone
Antiarrhythmic (regulates heartbeat) Ex: amiodarone (also beta blockers)
Antibiotics Ex: tetracycline (also chloramphenicol, Cipro)
Antidepressants Ex: amitriptyline, citalopram (Celexa), fluoxetine (Prozac, Symbyax, Sarafem)
Antipsychotics Ex: chlorpromazine, fluphenazine, haloperidol, risperidone, quetiapine, clozapine, olanzapine
Anxiety medications Ex: (Every benzodiazepine), including alprazolam (Xanax), diazepam (valium)
Barbiturates Ex: amobarbital, phenobarbital, pentobarbital, , propofol, secobarbital
Cholesterol-lowering medications Ex: All statins – atorvastatin, fluvastatin, lovastatin, pravastatin, rosuvastatin (Crestor), simvastatin, cholestyramine, clofibrate (Atromid-S)
Cancer (chemotherapy) medications Ex: Mitomycin C, profiromycin, adriamycin
Diabetes medications Ex: metformin, Glucophage, troglitazone, rosiglitazone, buformin
HIV/AIDS medications Ex: (AZT, zidovudine)
Epilepsy/Seizure medications Ex: valproic acid (Depakene, depakote, divalproex sodium)
Parkinson’s disease medications
Vaccine Ingredients Ex: Mercury, aluminum, ethylene glycol
Mechanisms of Mitochondria-induced Injury
Damage to mitochondria is caused primarily by reactive oxygen species (ROS) generated by the mitochondria themselves. <<snip>>
As a medical concern, hyperglycemia induces mitochondrial superoxide production by endothelial cells, which is an important mediator of diabetic complications such as cardiovascular disease. Endothelial superoxide production also contributes to atherosclerosis, hypertension, heart failure, aging, sepsis, ischemia-reperfusion injury, and hypercholesterolemia. Inflammatory mediators such as tumor necrosis factor alpha (TNF-a) have been associated in vitro with mitochondrial dysfunction and increased ROS generation. <<snip>>
Vitamins, minerals, and other metabolites act as necessary cofactors for the synthesis and function of mitochondrial enzymes and other compounds that support mitochondrial function, and diets deficient in micronutrients can accelerate mitochondrial decay and contribute to neurodegeneration. For example, enzymes in the pathway for hemoglobin synthesis require adequate amounts of pyridoxine, iron, copper, zinc, and riboflavin. Deficiencies of any component of the TCA cycle or ETC can lead to increased production of free radicals and mtDNA damage. For example, low iron status decreases mitochondrial activity by causing a loss of complex IV and increasing oxidative stress.
Medication-induced Mitochondrial Damage
Mitochondrial dysfunction is increasingly implicated in the etiology of drug-induced toxicities, but mitochondrial toxicity testing is still not required by the US FDA for drug approval. Mitochondria can be damaged both directly and indirectly by medications.
Reversing Mitochondrial Damage with N-acetylcysteine (NAC)
Recently it has become known that iatrogenic mitochondrial damage explains many adverse reactions from medications. Mitochondrial toxicity testing as part of the preapproval process for medications may help protect the public by identifying the most toxic medications before they are allowed to reach the market. By understanding the mechanisms underlying drug-induced mitochondrial damage, it may be possible to develop nutritional strategies to decrease the potentially toxic effects of medications.
While targeted nutrient therapies using antioxidants or their precursors (e. g., N-acetylcysteine [NAC]) holds promise for improving mitochondrial function, there are large gaps in our knowledge. The most rational approach is to understand the mechanisms underlying mitochondrial damage for specific medications, and attempt to counteract their deleterious effects with nutritional therapies. While randomized, controlled trials are lacking in this regard, they hopefully will be designed and conducted in coming years so that clinicians will have a clearer understanding of how to best protect and treat their patients.
N-Acetyl Cysteine (NAC) has many medical and holistic uses, but most importantly, and fundamentally, it promotes optimal health. NAC is a metabolite of the sulfur-containing amino acid, Cysteine. While Cysteine is found in high protein foods, NAC is not; but, under healthy circumstances NAC is produced within the human body. Cysteine plays a role in the sulfation cycle, acting as a sulfur donor in phase II detoxification and as a methyl donor in the conversion of homocysteine to methionine. Cysteine also helps synthesize glutathione, one of the body’s most important natural antioxidants and detoxifiers. NAC is the acetylated form of L-Cysteine.
NAC Increases Glutathione Levels and Aids Detoxification
NAC is rapidly metabolized to intracellular glutathione—the super antioxidant, blood booster and cell detoxifer. NAC also protects the body from acetaminophen toxicity and is used in hospitals for patients with acetaminophen poisoning. It has also been shown to be effective at treating liver failure from other causes as well.
NAC Supports a Healthy Immune System
Glutathione, metabolized from NAC, is known to aid in the transport of nutrients to lymphocytes and phagocytes, two major classes of immune cells. In addition it is known to protect cell membranes. While purified glutathione is available as a dietary supplement, absorption is low, and NAC is thought to be a better method of boosting cellular glutathione levels.
Evidence suggests that NAC may reduce the propagation of certain cells in the colon, thus reducing the likelihood of colon and rectal cancer in people with recurring colon polyps; though this evidence is not yet conclusive. However, NAC is generally regarded as a powerful antioxidant which should make it effective in protecting against many types of cancer.
NAC is believed to detoxify and remove heavy metals like mercury and lead from the body.
NAC and Other Possible Benefits
There is evidence that NAC can have beneficial effects on pancreatic b-cell function in diabetes. A 1999 study concluded that a sufficient supply of antioxidants (NAC, vitamin C plus vitamin E, or both) may prevent or delay b-cell dysfunction in diabetes by providing protection against glucose toxicity.
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