SAM-e: Difference between revisions
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SAM-e is an [[endogenous]] molecule that has numerous roles including methyl donation in neurotransmitter synthesis, antioxidative effects (radical scavenging, glutathione precursor), anti-inflammatory effects, and neuroprotective effects.<ref name="Mischoulon">{{cite journal | vauthors=((Mischoulon, D.)), ((Fava, M.)) | journal=The American Journal of Clinical Nutrition | title=Role of S-adenosyl-L-methionine in the treatment of depression: a review of the evidence | volume=76 | issue=5 | pages=1158S–61S | date= November 2002 | issn=0002-9165 | doi=10.1093/ajcn/76/5.1158S}}</ref> | SAM-e is an [[endogenous]] molecule that has numerous roles including methyl donation in neurotransmitter synthesis, antioxidative effects (radical scavenging, glutathione precursor), anti-inflammatory effects, and neuroprotective effects.<ref name="Mischoulon">{{cite journal | vauthors=((Mischoulon, D.)), ((Fava, M.)) | journal=The American Journal of Clinical Nutrition | title=Role of S-adenosyl-L-methionine in the treatment of depression: a review of the evidence | volume=76 | issue=5 | pages=1158S–61S | date= November 2002 | issn=0002-9165 | doi=10.1093/ajcn/76/5.1158S}}</ref> | ||
SAM-e, in addition to providing ATP to the cell, also can convert nicotinamine into N-methyl-nicotinamide (NMNA) via nicotinamide N-methyltransferase, NMNA which can prevent choline efflux from the brain and neuron, a process which may account for some of SAM-e's[[nootropic]] effects.<ref>{{cite journal | vauthors=((Williams, A. C.)), ((Ramsden, D. B.)) | journal=Medical Hypotheses | title=Nicotinamide homeostasis: a xenobiotic pathway that is key to development and degenerative diseases | volume=65 | issue=2 | pages=353–362 | date= 2005 | issn=0306-9877 | doi=10.1016/j.mehy.2005.01.042}}</ref> The involvement of SAM-e in the process of synthesizing serotonin, creatine and dopamine likely play a role in nootropic effects as well. | SAM-e, in addition to providing ATP to the cell, also can convert nicotinamine into N-methyl-nicotinamide (NMNA) via nicotinamide N-methyltransferase, NMNA which can prevent choline efflux from the brain and neuron, a process which may account for some of SAM-e's [[nootropic]] effects.<ref>{{cite journal | vauthors=((Williams, A. C.)), ((Ramsden, D. B.)) | journal=Medical Hypotheses | title=Nicotinamide homeostasis: a xenobiotic pathway that is key to development and degenerative diseases | volume=65 | issue=2 | pages=353–362 | date= 2005 | issn=0306-9877 | doi=10.1016/j.mehy.2005.01.042}}</ref> The involvement of SAM-e in the process of synthesizing serotonin, creatine and dopamine likely play a role in nootropic effects as well. | ||
==Subjective effects== | ==Subjective effects== |