jmorgan7845
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what do you guys think of this as a cycle? run it for 8 weeks then 4 off then 8 weeks again?
Yup!!Add in some Now Dopa Macuna or, if money is not an issue, Inhibit-p or Endosurge to block any possible prolactin issues and you're set.
OK, but that doesn't explain why mucuna is being pushed for use with DAA then. In those cases, it is exactly DAA-induced elevations that we are all talking about. Mucuna has its place for dealing with prolactin, but not in use with DAA.Subbed for comment. Cliffs for now:
Study 1- l-dopa will still lower systemic prolactin. When discussing prolactin, total prolactin, not DAA-induced elevations in prolactin, is the cause for potential side effects.
Study 2- En vitro studies of NMDAR agonism are really never relevant given the sheer depth of regulatory mechanisms that exist en vivo.
1- Again, prolactin-induced side effects are a function of total prolactin levels. It doesn't matter which source you control, you are still lowering total prolactin.2- Did I write it off? I haven't read it yet! Hence the brief "cliffs" on my stance.OK, but that doesn't explain why mucuna is being pushed for use with DAA then. In those cases, it is exactly DAA-induced elevations that we are all talking about. Mucuna has its place for dealing with prolactin, but not in use with DAA.Re: #2, you can't write off a study because it is in vitro!!! Are you serious?
How does dopamine lower total prolactin? It functions at the source and if that is negated by DAA, then it does not work. Estrogen is the bigger concern for the larger population.1- Again, prolactin-induced side effects are a function of total prolactin levels. It doesn't matter which source you control, you are still lowering total prolactin.2- Did I write it off? I haven't read it yet! Hence the brief "cliffs" on my stance.
No, dopamine regulation of prolactin release, as with many other (but not all!) anterior pituitary functions, does not occur at the site. It rather occurs at the hypothalamus (DA release) which then makes its way to the anterior pituitary. So this theory is all well and good, but the hypothalamus is not the primary culprit of DAA-induced prolactin release, suggesting a different MOA than the one stated above: The role of D-aspartic acid and N-methyl-D-asp... [Endocrinology. 2000] - PubMed - NCBI (also note that the anterior pituitary was the primary tissue of ip daa localization, again showing that the hypothalamus takes a "backseat" as the mediator of prolactin release).How does dopamine lower total prolactin? It functions at the source and if that is negated by DAA, then it does not work. Estrogen is the bigger concern for the larger population.
I mention estrogen because that should be the number one concern with users of DAA. The paper you posted does not mention dopamine one single time. I never said that the pituitary was the source as I'm well aware of my biology thanks, but you and others keep pushing mucuna as something that is needed for DAA use and I'm saying that it is not needed and doesn't work when used alongside DAA.No, dopamine regulation of prolactin release, as with many other (but not all!) anterior pituitary functions, does not occur at the site. It rather occurs at the hypothalamus (DA release) which then makes its way to the anterior pituitary. So this theory is all well and good, but the hypothalamus is not the primary culprit of DAA-induced prolactin release, suggesting a different MOA than the one stated above: The role of D-aspartic acid and N-methyl-D-asp... [Endocrinology. 2000] - PubMed - NCBI (also note that the anterior pituitary was the primary tissue of ip daa localization, again showing that the hypothalamus takes a "backseat" as the mediator of prolactin release).
The discussion noted that: "However, it is also reported that in some particular physiological conditions, NMDA can induce an inhibitory effect on PRL release and secretion, i.e. in female rats during lactation (54), in prepubertal female rats (55), in hypoprolactinaemic female rats (56), and in oestrogenized male rats (57)."
Citation #56 is the citation you listed above, which is an extenuating circumstance that contradicts the primary modality of NMDA.
Lastly, their concluding statements:
"In conclusion, the results obtained in this work provide evidence that D-Asp and NMDA are present in rat neuroendocrine tissues as endogenous compounds. D-Asp constitutes the natural precursor for the biosynthesis of NMDA and both D-Asp and NMDA play a role in the regulation of PRL release. D-Asp acts directly on the adenohypophysis, whereas NMDA on the hypothalamus promoting the release of some hypothalamic factor/s, which in turn reinforce/s the PRL release from the adenohypophysis."
Not sure what estrogen has to do with any of this.
My first stack I ever ran and logged was endosurge / erase / bulk DAA... I loved it.Add in some Now Dopa Macuna or, if money is not an issue, Inhibit-p or Endosurge to block any possible prolactin issues and you're set.
personally id take more time off but thats finewhat do you guys think of this as a cycle? run it for 8 weeks then 4 off then 8 weeks again?
Yeah, 8 and 4 is the minimum that I would ever recommend, but I've been doing 8 and 8 a lot and just running different types of things with different goals.personally id take more time off but thats fine
Please don't misquote me; it's one of my pet peeves. If you can find a single time where I said prolactin is a major concern with DAA, I will give you a cookie (I actually am the guy who comes in and says that DAA alone is fine and that prolactin control is not necessary unless predisposed to gyno, FYI). What you have read me say is that I'm a big fan of mucuna pruriens as an overall ingredient, which I am.I mention estrogen because that should be the number one concern with users of DAA. The paper you posted does not mention dopamine one single time. I never said that the pituitary was the source as I'm well aware of my biology thanks, but you and others keep pushing mucuna as something that is needed for DAA use and I'm saying that it is not needed and doesn't work when used alongside DAA.
LOL PMs clear but no apology necessary dude. My favorite discussions on this board are with you, simply because we agree on so little but at least use an evidence-based approach in ironing out our "issues."Hey Mr. Popular!!! Clear out your inbox so I can apologize there too!!!
That's what I was trying to say... Only you're smarter than meBig difference in modulating estrogen and prolactin while on testosterone boosters, like DAA, with the biggest difference being that only anti-estrogens (AIs like Erase in particular) have a chance to be synergistic in effect. Blocking the conversion of T to E will result in a greater total T level....which is the goal here.
Antiestrogens make test boosters better...