Medication-Induced Mitochondrial Damage
Damage to mitochondria is understood to play a role in the development of a wide range of seemingly unrelated disorders such as schizophrenia, Alzheimer's, cardiovascular disease, diabetes, and others. Mitochondrial damage is also a hallmark of ME/CFS and Fibromyalgia.
Common causes of mitochondrial dysfunction in ME/CFS and Fibromyalgia are numerous. They include:
Dysbiosis
Chronic viral infections
Metabolic dysfunction (poor insulin control, nutrient depletion)
Toxin exposure (metals, mold, other environmental factors)
Another cause of mitochondrial dysfunction that is less frequently mentioned is medication usage. Mitochondrial toxicity testing is NOT required by the FDA before a drug is approved. Medications can hinder mitochondria through direct or indirect mechanisms.
Certain medications interact with mitochondrial DNA and inhibit the creation of protein complexes necessary for ATP production. Other medications block metabolic pathways that interfere with the way fats and carbohydrates are utilized. By indirect means, some medications promote oxidative stress, which damages mitochondria and depletes antioxidants like glutathione. It is believed that many side effects from medications are due to mitochondrial insult.
Some classes of medications are known as mitochondrial poisons and are often prescribed for various reasons to ME/CFS and Fibromyalgia patients. Unbeknownst to your doctor (who is not aware of your illness or doesn't understand it as a mitochondrial disease) he or she may be contributing to a major setback in your recovery.
If medication is required, attempting to counteract the deleterious effects with mitochondrial support is warranted!
The Culprits
All classes of psychotropic drugs have documented toxic mitochondrial effects. Many of which block key enzymes in the electron transport chain of the mitochondria. Statin drugs completely block the enzyme HMG-CoA reductase, which severely inhibits CoQ10 production—a necessary nutrient for mitochondrial function. As another example, acetaminophen is known to be hepatotoxic due to the inability to clear its metabolite during liver detoxification. This is believed to be due to glutathione depletion--an indirect cpnsequence of mitochondrial dysfunction. It is not surprising then, that the antidote for acetaminophen poisoning is N-acetylcysteine (NAC), which increases glutathione.
A specific list of mitochondrial disrupters may look like this:
Antidepressants: Amitriptyline, Celexa, Prozac
Pain Relievers: Acetaminophen, Voltaren, Naproxen, Aspirin
Blood Pressure Medications: Propranolol
Cholesterol Medications: Lipitor, Crestor, Zocor
Diabetes Medications: Metformin
Antibiotics: Erythromycin, Tetracycline
Anti-Anxiety Medications: Xanax, Valium
Benzodiazepines: Klonopin, Ativan
Dose-Dependent?
Everyone is acutely aware of the side effects of all medications. Acute episodes may be rare, but do still occur. The chronic, insidious side effects are what should be of concern to patients on any of the above medications.
Long-term mitochondrial damage from medications can only worsen the ME/CFS or Fibromyalgia state through the creation of excessive oxidative stress and interrelated factors. (In the past I was prescribed tetracycline for over 1 year! Sorry mitochondria. Sorry microbiome.) This ultimately leads to the destruction of the mitochondria and the release of mediators that culminate in the destruction of the entire cell.
Have you been prescribed one of these medications? Consider sharing this article and the accompanying research citations with your doctor to determine if continuation is necessary.
References
1 Neustadt J, Pieczenik SR. (2008) Medication-induced mitochondrial damage and disease. Mol Nutr Food Res. 52(7):780-8. http://www.ncbi.nlm.nih.gov/pubmed/18626887
2 Amacher DE. (2005) Drug-associated mitochondrial toxicity and its detection. Curr Med Chem. 12(16):1829-39. http://www.ncbi.nlm.nih.gov/pubmed/16101504
3 Parikh S, et al (2009) A modern approach to the treatment of mitochondrial disease. Curr Treat Options Neurol. 11(6):414-30. http://www.ncbi.nlm.nih.gov/pubmed/19891905
4 Kovacic P, et al (2005) Mechanism of mitochondrial uncouplers, inhibitors, and toxins: focus on electron transfer, free radicals, and structure-activity relationships. Curr Med Chem. 12(22):2601-23. http://www.ncbi.nlm.nih.gov/pubmed/16248817
