atrollappears
Bluelighter
So I came across these studies while deciding whether or not to use SAMe:
"Depletion of nigrostriatal and forebrain tyrosine hydroxylase by S-adenosylmethionine: a model that may explain the occurrence of depression in Parkinson's disease." Charlton CG.
http://www.ncbi.nlm.nih.gov/pubmed/9247319
"Striatal dopamine depletion, tremors, and hypokinesia following the intracranial injection of S-adenosylmethionine: a possible role of hypermethylation in parkinsonism." Charlton CG, Crowell B Jr.
http://www.ncbi.nlm.nih.gov/pubmed/8748929
These studies are essentially saying that SAMe can damage the reward/movement system of the brain. But, I'm guessing that the doses used in these studies correspond to doses higher than those used by humans, because acute hypokinesis is seen in rats, while SAMe in doses used by humans displays antidepressant effects. My question is this: do normal human doses of SAMe have the potential to cause nigrostriatal degeneration over time? Why hasn't this question come up, as far as I can tell through google?
"Depletion of nigrostriatal and forebrain tyrosine hydroxylase by S-adenosylmethionine: a model that may explain the occurrence of depression in Parkinson's disease." Charlton CG.
http://www.ncbi.nlm.nih.gov/pubmed/9247319
"Striatal dopamine depletion, tremors, and hypokinesia following the intracranial injection of S-adenosylmethionine: a possible role of hypermethylation in parkinsonism." Charlton CG, Crowell B Jr.
http://www.ncbi.nlm.nih.gov/pubmed/8748929
These studies are essentially saying that SAMe can damage the reward/movement system of the brain. But, I'm guessing that the doses used in these studies correspond to doses higher than those used by humans, because acute hypokinesis is seen in rats, while SAMe in doses used by humans displays antidepressant effects. My question is this: do normal human doses of SAMe have the potential to cause nigrostriatal degeneration over time? Why hasn't this question come up, as far as I can tell through google?
