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    daa and erase


    what do you guys think of this as a cycle? run it for 8 weeks then 4 off then 8 weeks again?

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    Very standard should like alot.
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    Yes, Erase makes the most sense to run with DAA. 8 weeks on, 4 off, repeat and rejoice!
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    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.
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    Quote Originally Posted by leprechaun1
    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.
    Yup!!

    Id actually choose Endosurge over inhibit p and mucuna..due to the fact it also has Div 3,4

    Also to the OP,i would add some Creapure Creatine Monohydrate to the stack,for even better results.
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    Effects of N-methyl-D-aspartic acid and kainic acid on prolactin secretion in hyper- and hypoprolactinaemic conditions.

    Eur J Endocrinol. 1998 Apr;138(4):460-6

    Pinilla L, Tena-Sempere M, Aguilar R, Aguilar E.
    Source

    Department of Physiology, Faculty of Medicine, University of Córdoba, Spain.

    Abstract

    OBJECTIVE:

    The stimulatory and inhibitory effects of N-methyl-D-aspartic acid (NMDA) and kainic acid on prolactin (PRL) secretion have been correlated with the serum prolactin concentrations before drug administration. In the present experiments, we analysed the role of NMDA and kainic acid in PRL secretion in females with different serum concentrations of PRL.
    METHODS:

    Hypoprolactinaemic females were obtained by ovariectomy or after administration of diethyldithiocarbamate (an inhibitor of dopamine-beta-hydroxylase). Chronic hyperprolactinaemia was induced by neonatal administration of testosterone or oestradiol and acute hyperprolactinaemia was induced either by administration of alpha-methyl-p-tyrosine (an inhibitor of tyrosine hydroxylase) or by ether exposure. To analyse the role of dopamine in the effects of NMDA, we measured pituitary concentrations of dopamine after NMDA treatment and the effects of pretreatment with domperidone.
    RESULTS:

    (1) NMDA, but not kainic acid, stimulated PRL release in cyclic females. This effect was independent of serum PRL concentrations and was not accompanied by a decrease in pituitary concentrations of dopamine. (2) NMDA did not change PRL secretion in neonatally androgenized females, whereas NMDA and kainic acid inhibited PRL release in neonatally oestrogenized females. The inhibitory effects of NMDA and kainic acid were blocked by domperidone. (3) Kainic acid inhibited PRL secretion in prepubertal hyper- and hypoprolactinaemic rats. (4) Hyperprolactinaemia induced by ether stress was counteracted by administration of NMDA and kainic acid.
    CONCLUSIONS:

    (a) NMDA has a dual effect on prolactin secretion that is independent of prior prolactin concentrations and of dopamine activity, but kainic acid is only inhibitory. (b) The stimulatory or inhibitory effects of NMDA and kainic acid on PRL secretion were not strictly related to basal PRL concentrations and necessarily involved a change in the secretion of prolactin releasing factors, as no correlations were observed between changes in pituitary concentrations of dopamine and serum PRL concentrations. (c) Females rendered hyperprolactinaemic by neonatal administration of testosterone or oestradiol responded differently after NMDA administration. (d) NMDA and kainic acid blocked the mechanisms involved in stress-induced PRL secretion.




    Neuroreport. 2002 Dec 3;13(17):2341-4.
    The effect of D-aspartate on luteinizing hormone-releasing hormone, alpha-melanocyte-stimulating hormone, GABA and dopamine release.

    Pampillo M, Scimonelli T, Bottino MC, Duvilanski BH, Rettori V, Seilicovich A, Lasaga M.
    Source

    Centro de Investigaciones en Reproducción, Facultad de Medicina, Piso 10, Universidad de Buenos Aires (C1121ABG), Buenos Aires, Argentina.

    Abstract

    Since D-aspartate stimulates prolactin and LH release, our objective was to determine whether D-aspartate modifies the release of hypothalamic and posterior pituitary factors involved in the control of their secretion and whether its effects on these tissues are exerted through NMDA receptors and mediated by nitric oxide. In the hypothalamus, D-aspartate stimulated luteinizing hormone-releasing hormone (LHRH), alpha-melanocyte-stimulating hormone (alpha-MSH) and GABA release and inhibited dopamine release through interaction with NMDA receptors. It increased nitric oxide synthase (NOS) activity, and its effects on LHRH and hypothalamic GABA release were blunted when NOS was inhibited. In the posterior pituitary gland, D-aspartate inhibited GABA release but had no effect on dopamine or alpha-MSH release. We report that D-aspartate differentially affects the release of hypothalamic and posterior pituitary factors involved in the regulation of pituitary hormone secretion.





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    I'm still not convinced that mucuna will do anything for prolactin when taking it with DAA. In fact, DAA seems to inhibit dopamine release. If anybody would like to cite differently, please do so. Until then I will keep saying that Erase is the single best option when taking DAA.
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    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. Also, the latter study came to those conclusions in the hypothalamus, whereas analysis of the pituitary yielded quite different results. Since DAA is distributed with a high propensity towards pituitary and testicular tissue in vivo, it's tough to draw any conclusions at all from this.
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    Quote Originally Posted by mr.cooper69 View Post
    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.
    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?
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    Quote Originally Posted by Aleksandar37 View Post
    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?
    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.
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    Quote Originally Posted by mr.cooper69 View Post
    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.
    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.
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    Quote Originally Posted by Aleksandar37 View Post
    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.
    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.
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    Quote Originally Posted by mr.cooper69 View Post
    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.
    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.
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    Quote Originally Posted by leprechaun1
    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.
    My first stack I ever ran and logged was endosurge / erase / bulk DAA... I loved it.

    Good advice!
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    Quote Originally Posted by jmorgan7845 View Post
    what do you guys think of this as a cycle? run it for 8 weeks then 4 off then 8 weeks again?
    personally id take more time off but thats fine
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    Quote Originally Posted by R1balla View Post
    personally id take more time off but thats fine
    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.
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    Quote Originally Posted by Aleksandar37 View Post
    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.
    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.

    The paper I posted details the site of activity of DAA wrt prolactin release: which is primarily at the anterior pituitary with a mechanism different from the in vitro hypothalamus study you posted above.

    I still don't get where estrogen comes into any of this. I was linked to this thread because someone thought I may find your post interesting and stimulate discussion. Now I'm getting the sense that you're viewing this as Erase vs. Inhibit-P, or along those lines. If that's the case, you should know me better. I came to have a discussion; you know I love mucuna, but I certainly never say that prolactin or estrogen control is necessary with DAA, only that Erase or Mucuna can increase the quality of a DAA run, which they can.

    I know you're well-educated but I don't know your precise background with respect to neurobiology, and my intention was not to undermine your intelligence. Anyway, good day sir!
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    Dude! You know I have nothing but respect for you. I apologize if I thought you were here to defend using mucuna with DAA as that seems to be the knee jerk reaction lately when somebody mentions using Erase. I was simply going with the theme of the thread which is DAA and Erase. I like mucuna and like controlling prolactin...nothing against either one. Carry on everybody...nothing to see here!
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    Hey Mr. Popular!!! Clear out your inbox so I can apologize there too!!!
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    Quote Originally Posted by Aleksandar37 View Post
    Hey Mr. Popular!!! Clear out your inbox so I can apologize there too!!!
    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."
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    Big 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...
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    Quote Originally Posted by nattydisaster
    Big 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...
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