Marijuana and the active compound inside it, THC, are both known to shrink tumor size and inhibit cancer cell growth, which has been publicized by the federal government in recent publications (Scott). The mechanisms of how this actually occurs are somewhat less clear. The answer appears to be, interestingly enough, in the dopamine receptors. While addictive activities and substances are measured by their effect on DA1 receptors, which constitute the majority of dopamine receptors in the brain, there are actually 5 such subsets of receptors: DA1-5. These smaller groupings or clusters of dopamine receptors are well known to have various physical effects on the body by regulation of hormones and other physical mechanisms
The effect of marijuana on DA1 activation is less than a good meal, sex, alcohol, or a wide range of chemicals as shown in a PBS broadcast and that the effect of marijuana does not impact the widespread DA1 receptors, which are causally and correlatively shown to cause addiction (French), which explains the non-addictive nature of the plant. Understanding the hormonal and physical effects, however, requires further investigation. Activation of DA2 receptors has been shown to reduce prolactin levels, a hormone virtually non-existent in males, but present in females and very high in pregnant females (Poste). This phenomenon is relatively recent, but reduction of prolactin levels as a result of THC administration has been known since the early 1980's at least (Steger, et al.).
Elevated prolactin levels have been shown to cause a re-activation of tumor growth since the 1960's at least, and it can be assumed that as a DA2 agonist, marijuana suppresses such re-activation or tumor growth (Pearson, et al.). This is confirmed by a cannabinoid breakdown activation levels on various parts of the brain, classified as cannabinoid receptors which include some DA1 receptors, but also D2 receptors (Consroe). These parts of the brain also contain DA3 receptors, as shown more recently (Stanwood), agonism of which can inhibit Parkinson and tremors (such as epilepsy). Use of dopamine agonists has been shown more recently to encourage new blood vessel growth and inhibit growth of tumors (Goth, et al.), however many available agonists do not act selectively on specific dopamine receptors, but also activate the clusters which constitute the D1 areas of the brain (basal ganglia and other interior parts of the brain). Due to marijuana's, or THC's, low activation of D1 receptors (less than a good meal, as mentioned before), this appears to be a non-addictive and safe way to prevent cancer and obesity, which are the two leading killers in the USA after Alzheimer's related diseases.
Works Cited:
Consroe, Paul. "Brain cannabinoid systems as targets for the therapy of neurological disorders." Neurobiology of disease 5.6 (1998): 534-551.
French, Edward D. "Δ 9-Tetrahydrocannabinol excites rat VTA dopamine neurons through activation of cannabinoid CB1 but not opioid receptors." Neuroscience letters 226.3 (1997): 159-162.
Góth, M. I., Hubina, E., Raptis, S., Nagy, G. M. and Tóth, B. E. (2003), Physiological and pathological angiogenesis in the endocrine system. Microsc. Res. Tech., 60: 98–106. doi: 10.1002/jemt.10248
Pearson, Olof H., et al. "Prolactin-dependent rat mammary cancer: a model for man?." Transactions of the Association of American Physicians 82 (1969): 225-38.
Poste, George, and Stanley T. Crooke. Dopamine receptor agonists. Springer Science & Business Media, 2013.
The effect of marijuana on DA1 activation is less than a good meal, sex, alcohol, or a wide range of chemicals as shown in a PBS broadcast and that the effect of marijuana does not impact the widespread DA1 receptors, which are causally and correlatively shown to cause addiction (French), which explains the non-addictive nature of the plant. Understanding the hormonal and physical effects, however, requires further investigation. Activation of DA2 receptors has been shown to reduce prolactin levels, a hormone virtually non-existent in males, but present in females and very high in pregnant females (Poste). This phenomenon is relatively recent, but reduction of prolactin levels as a result of THC administration has been known since the early 1980's at least (Steger, et al.).
Elevated prolactin levels have been shown to cause a re-activation of tumor growth since the 1960's at least, and it can be assumed that as a DA2 agonist, marijuana suppresses such re-activation or tumor growth (Pearson, et al.). This is confirmed by a cannabinoid breakdown activation levels on various parts of the brain, classified as cannabinoid receptors which include some DA1 receptors, but also D2 receptors (Consroe). These parts of the brain also contain DA3 receptors, as shown more recently (Stanwood), agonism of which can inhibit Parkinson and tremors (such as epilepsy). Use of dopamine agonists has been shown more recently to encourage new blood vessel growth and inhibit growth of tumors (Goth, et al.), however many available agonists do not act selectively on specific dopamine receptors, but also activate the clusters which constitute the D1 areas of the brain (basal ganglia and other interior parts of the brain). Due to marijuana's, or THC's, low activation of D1 receptors (less than a good meal, as mentioned before), this appears to be a non-addictive and safe way to prevent cancer and obesity, which are the two leading killers in the USA after Alzheimer's related diseases.
Works Cited:
Consroe, Paul. "Brain cannabinoid systems as targets for the therapy of neurological disorders." Neurobiology of disease 5.6 (1998): 534-551.
French, Edward D. "Δ 9-Tetrahydrocannabinol excites rat VTA dopamine neurons through activation of cannabinoid CB1 but not opioid receptors." Neuroscience letters 226.3 (1997): 159-162.
Góth, M. I., Hubina, E., Raptis, S., Nagy, G. M. and Tóth, B. E. (2003), Physiological and pathological angiogenesis in the endocrine system. Microsc. Res. Tech., 60: 98–106. doi: 10.1002/jemt.10248
Pearson, Olof H., et al. "Prolactin-dependent rat mammary cancer: a model for man?." Transactions of the Association of American Physicians 82 (1969): 225-38.
Poste, George, and Stanley T. Crooke. Dopamine receptor agonists. Springer Science & Business Media, 2013.
Scott KA, Dalgleish AG, Liu WM. The combination of cannabidiol and Δ9-tetrahydrocannabinol enhances the
anticancer effects of radiation in an orthotopic murine glioma model. Mol Cancer Ther. 2014;13(12):2955-67.
Stanwood, Gregg D., Irwin Lucki, and Paul McGonigle. "Differential regulation of dopamine D2 and D3 receptors by chronic drug treatments." Journal of Pharmacology and Experimental Therapeutics 295.3 (2000): 1232-1240.
Steger, R. W., et al. "Interactions of Δ9-tetrahydrocannabinol (THC) with hypothalamic neurotransmitters controlling luteinizing hormone and prolactin release." Neuroendocrinology 37.5 (1983): 361-370.
Stanwood, Gregg D., Irwin Lucki, and Paul McGonigle. "Differential regulation of dopamine D2 and D3 receptors by chronic drug treatments." Journal of Pharmacology and Experimental Therapeutics 295.3 (2000): 1232-1240.
Steger, R. W., et al. "Interactions of Δ9-tetrahydrocannabinol (THC) with hypothalamic neurotransmitters controlling luteinizing hormone and prolactin release." Neuroendocrinology 37.5 (1983): 361-370.
No comments:
Post a Comment