Glutathione for the Treatment of MTHFR Genetic Polymorphisms, Parkinson’s Disease, Migraines, Chronic Fatigue and other Diseases of Impaired Detoxification
Glutathione has become the focus of much interest in the treatment of many degenerative disorders such as Parkinson’s and Alzheimer’s as well as MTHFR genetic polymorphisms, migraines, traumatic brain injury and chronic fatigue. It is a substance that your body naturally produces and it is critical to the detoxification processes. When its production is low, it can lead to dysfunction and degenerative disease.
We learned at an early age that breathing and oxygen is a necessity for life, but we don’t often talk about why that is on a cellular level. If you think back to school, you may have a distant (and perhaps not overly fond!) memory of aerobic respiration, or the combination of carbohydrates, fats and protein with the oxygen that we breathe to form energy for our bodies to function. This energy production occurs within each one of our cells. During this critical production of energy, free radicals or reactive oxidative species (ROS) are formed. ROS scavenge the body looking for electrons and will take them from whatever they can find: proteins, cells, tissues and DNA. ROS are thought to be responsible for cellular damage, damage to DNA and the processes of aging. Any situation where there is a chronic overconsumption of oxygen can lead to increased production of ROS and oxidative damage. We see this in disease processes such as cancer, Parkinson’s disease and Alzheimer’s disease.
A chemical that neutralizes a ROS is known as an “antioxidant” and one of the most powerful antioxidants in the body is glutathione. Glutathione works by donating electrons to these ROS scavengers. There is great interest in the research and medical community about this “super antioxidant” as several studies have demonstrated that it is a critical factor in protecting organisms against toxicity and disease8,11,12. Many degenerative diseases have been associated with oxidative damage and decreased production of glutathione. One in particular, Parkinson’s disease, is caused by the progressive destruction of the substantia nigra of the brain; the area that produces dopamine. When the substantia nigra of people with Parkinson’s was analyzed, they found low glutathione levels. And when those with early, untreated Parkinson’s were given glutathione intravenously, there was an improvement in symptoms and possibly a slowing of the progression of the disease13. In addition, people with the MTHFR genetic polymorphism5, those with chronic migraines2,7, children with autism10 and people with asthma have been shown to produce less glutathione.
Glutathione is also a big player in the role that the liver plays in the detoxification and removal of drugs, environmental toxins and metabolic waste from your body. In fact, when people overdose on acetaminophen (Tylenol), they are given N-acetylcysteine; an amino acid that helps people make more glutathione. After traumatic brain injury (i.e. concussion), glutathione has been shown to significantly improve outcomes6. It has a couple of different delivery systems including intravenous, oral liposomal and transdermal (through the skin).
What conditions could benefit from glutathione?
Coronary artery disease4
Peripheral vascular disease1
Chronic fatigue and fibromyalgia3
Autism spectrum disorders10
HIV and AIDS14
Traumatic brain injury6
Liver disease and alcoholism14
And the list keeps growing…
In B.C., naturopathic physicians are licenced to administer IV glutathione. It is important that you speak to your naturopathic physician about glutathione as it may not be indicated for you or interact with your medications/supplements. We welcome you to call and book a free 15 minute consultation with a licenced ND to see if glutathione could be right for you.
- Arosio, E., De Marchi, S., Zannoni, M., Prior, M. and Lechi, A. (2002). Effect of glutathione infusion on leg arterial circulation, cutaneous microcirculation, and pain-free walking distance in patients with peripheral obstructive arterial disease: a randomized, double-blind, placebo-controlled trial. Mayo Clin Proc. 77(8):754-9.
- Bolayir, E., Celik, K., Kugu, N., Yilmaz, A., Topaktas, S. and Bakir, S. (2004). Intraerythrocyte antioxidant enzyme activities in migraine and tension-type headaches. J Chin Med Assoc. 67(6):263-7.
- Bounous, G. and Molson, J. (1999). Competition for glutathione precursors between the immune system and the skeletal muscle: pathogenesis of chronic fatigue syndrome. Med Hypotheses. 53(4):347-9.
- De Chiara, B., Mafrici, A., Campolo, J., Famoso, G., Sedda, V., Parolini, M., Cighetti, G., Lualdi A, Fiorentini C, Parodi O. (2007). Low plasma glutathione levels after reperfused acute myocardial infarction are associated with late cardiac events. Coron Artery Dis. 18(2):77-82.
- Đorđević, V., Nikolić A., Ljujić M., Nestorović, A., Ristanović M., Tulić, C. and Radojković, D. (2010). Combined effect of GSTM1 gene deletion, GSTT1 gene deletion and MTHFR C677T mutation in male infertility. Archives of Biological Sciences 62(3): 525-530.
- Eakin, K., Baratz-Goldstein, R., Pick, C.G. et al. (2014). Efficacy of N-Acetyl Cysteine in Traumatic Brain Injury. Borlongan CV, ed.PLoS ONE. 9(4).
- Erol, I., Alehan, F., Aldemir, D. and Ogus, E. (2010). Increased vulnerability to oxidative stress in pediatric migraine patients. Pediatr Neurol. (1):21-4.
- Kerksick C, Willoughby D. The Antioxidant Role of Glutathione and N-Acetyl-Cysteine Supplements and Exercise-Induced Oxidative Stress.(2005). Journal of the International Society of Sports Nutrition. 2005;2(2):38-44.
- Kusumi, M., Ishizaki, K., Kowa, H., Adachi, Y., Takeshima, T., Sakai, F. and Nakashima, K. (2003). Glutathione S-transferase polymorphisms: susceptibility to migraine without aura. Eur Neurol. 49(4):218-22.
- Main, P.A., Angley, M.T., O’Doherty, C.E., Thomas, P. and Fenech, M. (2012). The potential role of the antioxidant and detoxification properties of glutathione in autism spectrum disorders: a systematic review and meta-analysis. Nutr Metab (Lond). 9(35).
- Marí, M., Morales, A., Colell, A., García-Ruiz, C. and Fernández-Checa, J.C. (2009). Mitochondrial glutathione, a key survival antioxidant. Antioxid Redox Signal. 11(11).
- Pastore, A., Federici, G., Bertini, E. and Piemonte, F. (2003). Analysis of glutathione: implication in redox and detoxification. Clin Chim Acta. 333(1):19-39.
- Sechi G, Deledda MG, Bua G, Satta WM, Deiana GA, Pes GM, Rosati G. (1996). Reduced intravenous glutathione in the treatment of early Parkinson’s disease. Prog Neuropsychopharmacol Biol Psychiatry. 20(7):1159-70.
- Zeevalk GD, Razmpour R, Bernard LP. (2008). Glutathione and Parkinson’s disease: is this the elephant in the room? Biomed Pharmacother. 62(4):236-49.