Mitochondrial “Collateral Damage” Thanks to Big Pharma
Iatrogenic Drug and Vaccine-induced Mitochondrial Disorders
“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
“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
Several
years ago I attended a conference that was sponsored by the United
Mitochondrial Disease Foundation (UMDF), an organization which seems to
be a combination patient advocacy group and a funding organization for
mitochondrial researchers.
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.
During
the Q & A, a mitochondrial research scientist in the audience got
up and talked 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. The author had not been able to get her paper published, and I
have found no evidence that it was ever published. No comments were
forthcoming from the UMDF expert that was leading the conference, and
the discussion went back to the rare hereditary forms of the disease.
Being naturally suspicious
of “experts” who may have professional or financial conflicts of
interest, my curiosity was aroused; so I talked to the researcher who
raised the obviously unwelcome question. He gave me his email address,
but my several attempts to contact him by email failed to get any
response. I later discovered that the researcher had at one time
received research grants from Pfizer.
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.
Interestingly, UMDF has a
convenient privacy policy that keeps it from revealing who are their
donors, although five pharmaceutical or genetic testing companies
(Reata, Transgenomic, Courtagen,
Raptor and Stealth BioTherapeutics) have their logos displayed, but no
discussion about acquired or iatrogenic mitochondrial disorders could be
found on its website. I could find only one statement (on www.Mitoaction.org’s
website) about non-inherited mitochondrial disorders. It said that
“Medicines or other toxic substances can trigger mitochondrial disease.” No elaboration or links to more information were provided. I smelled a rat, and so should we all.
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
Published in the Journal of Neuroscience Research 87:1474–1483 (2009)
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 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.
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