L-Dopa and Prolactin control question about a stack.

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    L-Dopa and Prolactin control question about a stack.


    So as of recent I have seen a lot of discussion on using l-dopa for prolactin control. The biggest contenders being Dopadex vs Inhibit-p. After seeing plenty of people saying any form of b6 will cause l-dopa to convert before the bbb, and the only people saying the synergistic effect of inhibit-p controls prolactin not just the l-dopa were the SNS reps.

    I was looking at Dopadex, but then realized I was also out of ZMA for my sleeping, and then realized ZMA is loaded with B6. So I ended up on 2 bottle's of I-Force Lights out for sleeping/l-dopa my 8 week run of AI DAA, EP and ABE.

    Since Lights out has not yet been discussed much just want your input if you think I made the right choice.

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    The B6 in Inhibit-P is not a deterrant to the product's overall function of prolactin control. I can't stress this enough. The Vitex extract is the main contender here. Ensuring that someone with high prolactin is not in such a state due to central B6 deficiencies (P5P) or dopamine production deficiencies (L-dopa from mucuna) is the function of the other two ingredients. They could have been spaced apart, but since we wanted to create an all-in-one product to address the issue of deficiencies, and since the mucuna extract is at 50% l-dopa and no peripheral issues were found in testing, the product was designed as it was. The Vitex will act strongly centrally, and actually has synergistic interactions with the non-L-dopa constituents of Mucuna.
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    Any other opinions?
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    Ldopa/p5p/B6/pyridoxine
    or a combo of the two.

    Combining the two is a terrible idea. P5p/B6 causes ldopa to be metabolized into dopamine OUTSIDE the brain.
    Dopamine cannot pass the blood brain barrier so taking B6/P5p with ldopa makes them both worthless to reduce prolactin levels.

    Instead, Ldopa must be run concurrently with a decarboxylase inhibitor and ideally also a COMT inhibitor in order to prevent metabolism and allow the ldopa to pass the Blood brain barrier and convert into dopamine within the brain.

    Prolactrone does this.
    Other products currently being offered....combine B6 and Ldopa meaning your paying for expensive urine and elevated prolactin levels. Can link studies as well.

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    I just run l-dopa for my prolactin control, if you have trouble falling asleep I think Lights out was a good choice.
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    Quote Originally Posted by Lhns2 View Post
    Ldopa/p5p/B6/pyridoxine
    or a combo of the two.

    Combining the two is a terrible idea. P5p/B6 causes ldopa to be metabolized into dopamine OUTSIDE the brain.
    Dopamine cannot pass the blood brain barrier so taking B6/P5p with ldopa makes them both worthless to reduce prolactin levels.

    Instead, Ldopa must be run concurrently with a decarboxylase inhibitor and ideally also a COMT inhibitor in order to prevent metabolism and allow the ldopa to pass the Blood brain barrier and convert into dopamine within the brain.

    Prolactrone does this.
    Other products currently being offered....combine B6 and Ldopa meaning your paying for expensive urine and elevated prolactin levels. Can link studies as well.

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    Well being that I already have the lights out on order on a killer deal 35 bucks bogo, it has 500mg mucuna at 50% l-dopa so basically 250mg l-dopa per pill I planned on taking 2 a night for a total of 500mg l-dopa. Reading around on decarboxylase inhibitors and COMT inhibitors there isn't a ton of info quick but EGCG did pop up pretty quickly i actually have some now EGCG 400mg caps at 50% EGCG, would it be beneficial to dose those with the lights out? and if so how much?

    Secondly if I am going to be dosing the Orange Triad 3/3 should I be wary of the b6 in that effecting the l-dopa, if so how far apart should I space the dosages?
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    Quote Originally Posted by 00S4Boy

    Well being that I already have the lights out on order on a killer deal 35 bucks bogo, it has 500mg mucuna at 50% l-dopa so basically 250mg l-dopa per pill I planned on taking 2 a night for a total of 500mg l-dopa. Reading around on decarboxylase inhibitors and COMT inhibitors there isn't a ton of info quick but EGCG did pop up pretty quickly i actually have some now EGCG 400mg caps at 50% EGCG, would it be beneficial to dose those with the lights out? and if so how much?

    Secondly if I am going to be dosing the Orange Triad 3/3 should I be wary of the b6 in that effecting the l-dopa, if so how far apart should I space the dosages?
    I think that dose would be just fine (egcg). As to b6, studies show it peaks in half hour-three hours depending on dosages. Fasting periods come at 3-5 hour mark. Highest dosage was at 10mg. Highest urinary extraction rate is at 3 hours. So... maybe a 3-5 hour window. I could be wrong someone might correct me on this.

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    Quote Originally Posted by Lhns2 View Post
    I think that dose would be just fine (egcg). As to b6, studies show it peaks in half hour-three hours depending on dosages. Fasting periods come at 3-5 hour mark. Highest dosage was at 10mg. Highest urinary extraction rate is at 3 hours. So... maybe a 3-5 hour window. I could be wrong someone might correct me on this.

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    So for my dosing of 500mg of l-dopa(from 100mg of Mucuna) 200mg of EGCG(from 400mg of Green Tea Extract) if sufficient, and if I plan on sleeping around 11pm dosing of Orange triad should be no later then 7-8pm?

    Also in regard's to the lights out, switching from a ZMA + Melatonin mix, with the 50mg's of 5-HTP I'm guessing I should drop the melatonin? or should I continue with 3mg melatonin?
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    Would b6 by itself be effective at reducing prolactin? I know it not good to combine with l dopa but i'm just wondering if it reduces prolactin by itself.
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    Lhns, you have many incorrect remarks in your posts..
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    Quote Originally Posted by mr.cooper69 View Post
    Lhns, you have many incorrect remarks in your posts..
    He is correct about B6 and L-dopa.

    Unfortunately, the dose of EGCG required to mildly inhibit COMT is around 5 grams. If piperine is added, the dose goes down marginally.
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    Quote Originally Posted by lronFist View Post
    He is correct about B6 and L-dopa.

    Unfortunately, the dose of EGCG required to mildly inhibit COMT is around 5 grams. If piperine is added, the dose goes down marginally.
    The dose of EGCG is actually exactly what I was referring to. I consulted with someone named IronFist to come to that conclusion.
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    You able to elaborate more on it? And what about toxicity dosages? I definitely don't mean to argue I just want to understand where you're coming from

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    L-Dopa as a standalone. Also toss in some I3C and magnesium, as dopamine tends to be a magnesium dependent neurotransmitter. (Magnesium Glycinate showed the most potent delivery if I recall)

    IIRC the dosage for Vitex to have any effect on PRL was in the 1200mg range.


    B6 is also advised, in the clinical profession, to not be administered with L-Dopa as it can reduce its effectiveness.

    Levodopa (L-dopa)-- Vitamin B6 reduces the effectiveness of levodopa, a medication used to treat Parkinson's disease. However, your doctor may be able to determine a dose of B6 that can help reduce side effects of levodopa without interfering with the drug's action. Taking vitamin B6 along with levodopa should be done only under the strict guidance of a physician.
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    Lights out is a great product,I just finished a bottle myself.And at that deal you can't beat it.
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    Quote Originally Posted by Lhns2 View Post
    You able to elaborate more on it? And what about toxicity dosages? I definitely don't mean to argue I just want to understand where you're coming from

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    [www]plosone [dot] org/article/info:doi/10.1371/journal.pone.0011951?imageURI= info:doi/10.1371/journal.pone.0011951.g005#pone-0011951-g005

    This study was done on rats. Extrapolating for HED & BSA, the amount of EGCG which caused statistically significant inhibition of COMT turns out to be 4.54 grams.

    For reference:
    400mg/kg rat dose x [6 km rat/37 km human] x 70 kg human
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    So the inhibit-p I just bought was a waste?
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    No. The primary active is vitex.
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    Quote Originally Posted by beastybean View Post
    So the inhibit-p I just bought was a waste?
    Hardly. I'd put Inhibit-P up against any other prolactin control product.
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    Quote Originally Posted by Rhadam View Post
    Hardly. I'd put Inhibit-P up against any other prolactin control product.
    How long would it take to notice any results from use of Inhibit-P?
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    Oh woo, awesome. I will be running daa and other natty boosters and want all chances of gyno sides gone since I'm gyno prone.
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    Quote Originally Posted by beastybean View Post
    So the inhibit-p I just bought was a waste?
    Not necessarily, but it wouldn't be my first choice.

    Dopadex (Or Even "Lights Out" from iForce)+I3C+Magnesium for PRL control

    Zinc would also be beneficial, it tends to be absorbed best with the least side effects if in glycinate/arginate, amino acid, or gluconate bound forms
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    Dopamine agonists, like vitex, negatively regulate adrenal androgen production (1), while promoting LH/FSH secretion from the pituitary in the presence of hyperprolactinemia. In the absence of the latter, DA agonists produce negligable effects in raising serum testosterone, although if prolactin is lowered too much, testosterone will actually decrease (2).

    In this (3) en vivo study, Vitex was given to male mice with normal serum prolactin levels. Vitex treatment resulted in a statistically significant decrease in both testosterone and LH. The take-home message is that dopamine agonism should be used only in the presence of hyperprolactinemia. The exact quantity of prolactin required to necessitate dopamine agonism is up for speculation, but human studies have clearly shown only mild (or none) elevations in testosterone, or other testosterone-induced end-points in those with mild hyperprolactinemia (4).

    (1) [www] ncbi [dot] nlm [dot] nih [dot] gov/pubmed/11499189
    Our data suggest a modulation by PRL of adrenal androgen production. DA treatment reduces PRL and serum androgens. It results in a significant clinical improvement in acne and hirsutism.
    (2) [www]ncbi . nlm . nih.gov/pubmed/10624504
    hypoprolactinemia produces a decrease of basal testosterone levels without any alteration of the response of this steroid to hCG.
    (3) [www] ncbi . nlm . nih.gov/pubmed/19070148
    Vitex agnus castus (Vac.) extract decreased significantly the LH and testosterone levels. The coadministration of Vac. extract and bromocriptine decreased LH and testosterone.
    \
    (4) [www] ncbi. nlm. nih. gov/pubmed/10624504
    No relationship between the PRL and other hormone concentrations was found. No changes were noted in the LH, FSH, testosterone, or estradiol concentrations, or in the sperm density and motility after treatment. ... In infertile men who are mildly hyperprolactinemic, bromocriptine administration does not improve semen analysis, although it does normalize the PRL.
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    Quote Originally Posted by DJBeanPole View Post
    How long would it take to notice any results from use of Inhibit-P?
    Depends per user. I noticed reduced acne and pec changes within the first week. And that was using the recommended 2 cap per day dosage.

    Quote Originally Posted by beastybean View Post
    Oh woo, awesome. I will be running daa and other natty boosters and want all chances of gyno sides gone since I'm gyno prone.
    Endogenous testosterone supplementation should not create "gyno sides."
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