Overview of Mitochondrial disease

Mitochondrial disease is when mitochondria, which are specialized compartments in the blood stream that are responsible for processing oxygen and converting substances from the food we eat into energy, fail. When they do fail, the body is limited on the amount of energy it can generate within a cell and the cell becomes injured or dies. If this process continues, whole systems throughout the body can fail and can threaten one’s life. The disease is most commonly present in children, but it can develop in adults.

Most susceptible to damage caused by mitochondrial disease, according to the United Mitochondrial Disease Foundation, are the brain, heart, liver, skeletal muscles, kidney, and the endocrine and respiratory systems. Cells are not able to make RNA or DNA in order to grow and function without functioning mitochondria.

The development of mitochondrial disease is caused by either inherited or spontaneous mutations in genes, which lead to altered functions of the proteins or RNA molecules that normally reside in mitochondria.

Common symptoms associated with mitochondrial disease are loss of motor control, muscle weakness, muscle pain, gastro-intestinal disorders, cardiac disease, liver disease, diabetes, developmental delays and poor growth, respiratory complications, seizures, visual and hearing problems and infection susceptibility.

There is no cure for mitochondria disease, so treatment focus is on reducing symptoms and delaying or preventing the disease’s progression with vitamins, supplements, diet therapy and anti-oxidant treatments.

Findings: Effects of Cannabis on Mitochondrial disease

Most of the research on cannabis’ effect on mitochondrial disease focuses on the symptomatic relief it offers by improving seizure control and reducing pain. Scientific reviews analyzing previously-published research on cannabis’ effect on epilepsy conclude that a major cannabinoid found in cannabis, cannabidiol (CBD) is a well-tolerated and promising therapeutic treatment that has demonstrated the ability to reduce or even eliminate seizures (Blair, Deshpande & DeLorenzo, 2015). Cannabis has also demonstrated the ability to significantly lower pain that has proven refractory to other treatments (Boychuck, Goddard, Mauro & Orellana, 2015).

Research does suggest, however, that the function of mitochondria is modulated by the endocannabinoid system—a system that regulates a variety of cellular and physiological processes through the activation of receptors (Lipina, Irving & Hundal, 2014). The cannabinoid receptors (CB1 and CB2) are activated by the major cannabinoids found in cannabis. The activation of cannabinoid receptors has shown to have a number of positive effects on the integrity of mitochondria, including oxidative phosphorylation and energy production (Lipina, Irving, & Hundal, 2014).

In support of the endocannabinoid system’s role in mitochondrial health is one particular study, which found that cannabis improved the mitochondrial function in rodents. The researcher suggested that cannabis triggers the release of antioxidants, which serve as a cleaning mechanism to remove damaged cells and ultimately improve the efficiency of mitochondria (Bilkei-Gorzo, 2012). Cannabis has also been shown to have the capability to restore all mitochondrial parameters to normal after they had been deliberately aberrated, and to improve mitochondrial membrane potential (Lu & Anderson, 2015). Cannabis treatments have also been shown effective at increasing mitochondrial activity (Silvestri, et al., 2015).

References

  1. Bilkei-Gorzo, A. (2012, October 29). The endocannabinoid system in normal and pathological brain ageing. Philosophical Transactions of the Royal Society, B, 367(1607). Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3481530/.

  2. Blair, R.E., Deshpande, L.S., and  DeLorenzo, R.J. (2015, September). Cannabinoids: is there a potential treatment role in epilepsy? Expert Opinion on Pharmacology, 16(13), 1911-4. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4845642/.

  3. Boychuck, D.G., Goddard, G., Mauro, G., and Orellana, M.F. (2015 Winter). The effectiveness of cannabinoids in the management of chronic nonmalignant neuropathic pain: a systematic review. Journal of Oral & Facial Pain and Headache, 29(1), 7-14. Retrieved from https://goo.gl/R28LWD.

  4. Hao, E., Mukhopadhyay, P., Cao, Z., Erdélyi, K., Holovac, E., Liaudet, L., Lee, W.S., Hasko, G., Mechoulam, R., and Pacher, P. (2015). Cannabidiol Protects against Doxorubicin-Induced Cardiomyopathy by Modulating Mitochondrial Function and Biogenesis. Molecular Medicine, 21(1), 38–45. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4461586/.

  5. Lipina, C., Irving, A.J., and Hundal, H.S. (2014, July 1). Mitochondria: a possible nexus for the regulation of energy homeostasis by the endocannabinoid system? American Journal of Physiology. Endocrinology and Metabolism, 307(1). Retrieved from http://ajpendo.physiology.org/content/307/1/E1.long.

  6. Lu, Y., and Anderson, H.D. (2015, June). 6B.09: Effect of Cannabinoid Receptor Activation on Aberrant Mitochondrial Bioenergetics in Hypertrophied Cardiac Myocytes. Journal of Hypertension. 33. Retrieved from https://goo.gl/2YhsGl.

  7. Ryan, D., Drysdale, A.J., Lafourcade, C., Pertwee, R.G., and Platt, B. (2009, February 18). Cannabidiol Targets Mitochondria to Regulate Intracellular Ca2 Levels. Journal of Neuroscience, 29(7), 2053-63. Retrieved from http://www.jneurosci.org/content/29/7/2053.long.

  8. Silvestri, C., Paris, D., Martella, A., Melck, D., Guadagnino, I., Cawthorne, M., Motta, A., and Di Marzo, V. (2015, June). Two non-psychoactive cannabinoids reduce intracellular lipid levels and inhibit hepatosteatosis. Journal of Hepatology, 62(6), 1382-90. Retrieved from http://www.journal-of-hepatology.eu/article/S0168-8278(15)00003-3/abstract.

  9. What is Mitochondrial Disease? (n.d.). United Mitochondrial Disease Foundation. Retrieved from http://www.umdf.org/site/c.8qKOJ0MvF7LUG/b.7934627/k.3711/What_is_Mitochondrial_Disease.htm.

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