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20150322_150101abEditor’s Note: Modern Medical Education, Research and Industries have abandoned morally imbued erudition and methods for the sake of profits and vanity. This is largely the result of Material Reductionism:

Below is evidence on the matter from Dr. Khols and others on the very real matter of iatrogenic illness which is affecting nealy everyone, especially as a result of careless approaches to immunizations. I suggest that readers abandon doctors who practice only allopathic medicine unless absolutely necessary. Most are dangerous practioners wandering in a valley of profound ignorance and excessive bias. – oz

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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.

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)

http://psychrights.org/research/Digest/NLPs/DrugsCauseMitochondrialDamage.PDF

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)

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.

Dr Kohls is a retired physician who practiced holistic mental health care for the last decade of his career. Virtually all of his patients exhibited iatrogenic (prescription drug-related) syndromes such as are mentioned in the article above. In retrospect, those patients were actually manifesting iatrogenic mitochondrial diseases. His practice mainly consisted of helping his patients, through brain nutrient therapy, psycho-educational psychotherapy and the gradual reduction or elimination of the psychotropic medications that were sickening them. He now writes a weekly column for the Reader Weekly, an alternative newsweekly published in Duluth, Minnesota, USA. Many of Dr Kohls’ columns are archived at http://duluthreader.com/articles/categories/200_Duty_to_Warn.