(Note from Erin: I was so pleased when I stumbled upon this story crafted by Dr. Kohls and published at the Canadian site, Global Research. After attending a conference sponsored by the United Mitochondrial Disease Foundation (UMDF), Kohls became interested in the topic of mitochondrial health (a topic my better half is also very passionate about). As you will no doubt be able to tell from reading, Dr. Kohls did an enormous amount of research. We are thankful for his time and effort and happy to provide you with the information below. Please make sure to share this story with all your loved ones.)

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While the conference Kohls attended focused entirely on the rare congenital/inherited forms of mitochondrial disorders, first diagnosed in infancy and comprising of around 10 – 15 % of known cases, nothing was said about the 85 – 90 % of acquired forms of mitochondrial disorders. And he wasn’t too concerned about that until a mitochondrial research scientist got up and spoke “about a colleague of his that had written an academic paper that identified 72 commonly-prescribed drugs that were mitochondrial poisons. He mentioned Pfizer’s Lipitor and Zoloft as two examples.”1 (The author had never been able to get the paper published and Kohls couldn’t find it.)

Upon further research, Kohls discovered that many articles that deal with drug and vaccine-induced mitochondrial disorders ever get published in mainstream medical journals, at least none that take money from Big Pharma.

And why do you suppose that is?

“Mitochondrial damage is now understood to play a role in a wide range of seemingly unrelated disorders such as schizophrenia, diabetes, Parkinson’s disease, chronic fatigue syndrome, and nonalcoholic steatohepatitis. Recently it has become known that iatrogenic (physician or treatment-caused) mitochondrial damage explains many adverse reactions from medications.” — John Neustadt, MD and Steven Pieczenik, MD 2 (Taken from their paper, http://psychrights.org/research/Digest/NLPs/DrugsCauseMitochondrialDamage.PDF)

Americans of all ages, and across all socio-economic groups, are some of the sickest, most chronically-ill people in the developing world. And it’s the drugs we’re taking that are keeping us there. 

“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 3(Taken from their paper, http://psychrights.org/research/Digest/NLPs/DrugsCauseMitochondrialDamage.PDF)

The three examples below were selected by Dr. Kohls, from peer-reviewed medical journals, in an attempt to enlighten clinicians to the fact 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),”4 when in fact many of the disorders are actually caused by prescription drugs, vaccines and/or other toxic chemicals.

These disastrous chemicals poison the mitochondria in our brains, nerves, muscles and other organs. In short, we are being “afflicted by preventable, iatrogenic- or industry-caused diseases.”5

“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)!”6

“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).

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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?”7

“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.”8

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

Published in the Journal of Neuroscience Research 87:1474–1483 (2009) 

Posted at: http://onlinelibrary.wiley.com/doi/10.1002/jnr.21965/abstract

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/)

Abstract

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.

Introduction

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.

Oxidative Stress and Brain

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

Published in Molecular Nutrition and Food Research. 2008, 52, pp 780 – 788

This article is posted in its entirety at: http://psychrights.org/research/Digest/NLPs/DrugsCauseMitochondrialDamage.PDF

Abstract

Since the first mitochondrial dysfunction was described in the 1960s, the medicine has advanced in its understanding the role mitochondria play in health and disease. Damage to mitochondria is now understood to play a role in the pathogenesis of a wide range of seemingly unrelated disorders such as schizophrenia, bipolar disease, dementia, Alzheimer’s disease, epilepsy, migraine headaches, strokes, neuropathic pain, Parkinson’s disease, ataxia, transient ischemic attack, cardiomyopathy, coronary artery disease, chronic fatigue syndrome, fibromyalgia, retinitis pigmentosa, diabetes, hepatitis C, and primary biliary cirrhosis.
Medications have now emerged as a major cause of mitochondrial damage, which may explain many adverse effects.
All classes of psychotropic drugs have been documented to damage mitochondria, as have statin medications, analgesics such as acetaminophen, and many others. While targeted nutrient therapies using antioxidants or their precursors (e. g., N-acetylcysteine [NAC]) hold 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. This article reviews our basic understanding of how mitochondria function and how medications damage mitochondria to create their occasionally fatal adverse effects.

Introduction

Mitochondria are the powerhouses of our cells. They are responsible for generating energy… <<snip>> …mitochondria are the only other subcellular structure aside from the nucleus to contain DNA. However, unlike nuclear DNA (nDNA), mitochondrial DNA (mtDNA) are not protected by histones. nDNA wraps around histones, which then physically shield the DNA from damaging free radicals and are also required to repair DNA breaks. Since mtDNA lacks the structural protection of histones and their repair mechanisms, they are quite susceptible to damage. <<snip>>

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)

  • Diabetes
  • Huntington’s disease
  • Cancer including hepatitis-C virus-associated hepatocarcinogenesis
  • Alzheimer disease
  • Parkinson’s disease
  • Bipolar disorder
  • Schizophrenia
  • Aging and senescence
  • Anxiety disorders
  • Nonalcoholic steatohepatitis (NASH – late stage of nonalcoholic fatty infiltration of the liver)
  • Cardiovascular disease, including atherosclerosis
  • Sarcopenia (muscle-wasting disease, mainly of the elderly)
  • Exercise intolerance
  • 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 like halothane, 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)
  • Mood stabilizers Ex: lithium
  • 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.

Conclusions

Since the first mitochondrial dysfunction was described in the 1960s, the central role mitochondria play in health and disease has been widely documented. Mitochondrial damage is now understood to play a role in a wide range of seemingly unrelated disorders such as schizophrenia, diabetes, Parkinson’s disease, chronic fatigue syndrome, and nonalcoholic steatohepatitis (late-stage fatty infiltration of the liver).

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.

Sources and References

  1. Global Research, May 6, 2015.
  2. Global Research, May 6, 2015.
  3. Global Research, May 6, 2015.
  4. Global Research, May 6, 2015.
  5. Global Research, May 6, 2015.
  6. Global Research, May 6, 2015.
  7. Global Research, May 6, 2015.
  8. Global Research, May 6, 2015.