Prolactone vs Inhibit-P

Rostam

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In a thread about Prolactone (Black Lion Research) it was mentioned that Ldopa shoudn’t be taken at the sametime as P5P because combining ldopa and P5p causes ldopa to be metabolized into dopamine outside of the brain. Since dopamine cannot pass the blood brain barrier, taking P5P with ldopa makes them both worthless to reduce prolactin levels.

Now reading the ingeedient lsit of Inhibit-P I see that it includes 50 mg of P5P. If P5P make ldopa useless for prolactin reduction it is strange that a company like SNS is adding it to their formula. If it doesn’t interfere with ldopa’s action it is strange Black Lion Research says it does.

Any thought / idea to shed some light on this?
 
Quads_of_Stee

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p5p is often recommended for lower prolactin as well. I've never read that far into it but it seems Inhibit-P just wanted to hit everything
 
Woody

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There was an older thread with a huge debate about this. Let me see if I can find it.

I can't post links. So I'll PM you. It turns into a heavy weight slug fest
 
Rostam

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p5p is often recommended for lower prolactin as well. I've never read that far into it but it seems Inhibit-P just wanted to hit everything
The problem is that if P5P makes Ldopa useless then additing it to the formula will not /hit everything' but inhibit the positive effect inhibit-p may have.
 
Rostam

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There was an older thread with a huge debate about this. Let me see if I can find it.

I can't post links. So I'll PM you. It turns into a heavy weight slug fest
Thank you.

But as long as I can see the issue was mentioned in the thread you are referring to but we still don't know why inhibit-p has p5p in the ingredient list.
 
Woody

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The problem is that if P5P makes Ldopa useless then additing it to the formula will not /hit everything' but inhibit the positive effect inhibit-p may have.

IIRC, that was just BLR saying to attack Inhibit-P. Every thread I've read since the one I sent you regarding the two together has backed that thought up.
 
Woody

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Taken from other threads:

There is a study from the 70's that essentially shows L-Dopa w/out B6 is better for GH, while L-Dopa + B6 is optimal for prolactin (I think).

L-Dopa converts to dopamine and dopamine inhibits somatostatin secretion in the hypothalamus. When you have B6 in conjunction with L-Dopa, you enhance the rate L-Dopa converts to dopamine outside the brain instead of inside. Inside of the brain what you're looking for in regards to increasing GH.
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.
 
Rostam

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IIRC, that was just BLR saying to attack Inhibit-P. Every thread I've read since the one I sent you regarding the two together has backed that thought up.
That's what I thought but it's interesting that Copper or no one from SNS provided explanation or any data (as they usualy do) to show that what BLR is saying is wrong. in none of the threads. they were always focusing on ldopa topic and nothing about it's interaction with p5p of B6. So now I'm wondering who is right.
 
Rostam

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Taken from other threads:
So it mean that they are not 'using' the positive effect of ldopa on prolactin inhibition but rely only on other ingredients, I believe.
 
Woody

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I could be wrong, as I am not a scientist and won't even begin to say I understand half of how most supements work, but what I've taken from the threads I've looked at for you is that Inhibit-P is more of a preventative and control and uses Vitex as the main ingredient and as B6 and L-Dopa in case you have deficiency caused prolactin. Plus, Mucuna has other benefits besides L-Dopa

I'm using dopadex bc I'm poor and my student loans don't post for another three weeks lol. It was set to expire so I got it at a steal.
 
Woody

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So if I got it right we need ldopa to metabolized OUT of the brain for prolatine inhibition and IN the brain for GH increase?
Before I tell you something wrong,
Jiigzz mw1 Synapsin mr.cooper69
 
Jiigzz

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Before I tell you something wrong,
Jiigzz mw1 Synapsin mr.cooper69
Thanks for the mention :D we'll dig up some stuff and post here in a sec (just got to work).

This has been addressed in another thread but thanks OP for asking in this section so we have an opportunity to defend our product.
 

De__eB

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On its own, Pyridoxine can reduce prolactin.

L-Dopa + Pyridoxine = Greater decreases in prolactin, lower increases in GH

Additionally, just because you're increasing some metabolism outside the BBB does not mean you are eliminating all metabolism inside the brain, also, peripheral hormones while not passable through the primary BBB do have alternative routes to the hypothalamus, and to the arcuate nucleus specifically, where dopamine-regulated prolactin production occurs.

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Here's some information on the pituitary, Pyridoxine, and interaction between L-Dopa and Pyridoxine:

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The design of barriers in the hypothalamus allows the median eminence and the arcuate nucleus to enjoy private milieus: the former opens to the portal blood and the latter to the cerebrospinal fluid.

The blood-brain barrier (BBB) is a single uninterrupted barrier that in the brain capillaries is located at the endothelial cells and in the circumventricular organs, such as the choroid plexuses (CP) and median eminence (ME), is displaced to specialized ependymal cells. How do hypothalamic hormones reach the portal circulation without making the BBB leaky? The ME milieu is open to the portal vessels, while it is closed to the cerebrospinal fluid (CSF) and to the arcuate nucleus. The cell body and most of the axons of neurons projecting to the ME are localized in areas protected by the BBB, while the axon terminals are localized in the BBB-free area of the ME. This design implies a complex organization of the intercellular space of the median basal hypothalamus. The privacy of the ME milieu implies that those neurons projecting to this area would not be under the influence of compounds leaking from the portal capillaries, unless receptors for such compounds are located at the axon terminal. Amazingly, the arcuate nucleus also has its private milieu that is closed to all adjacent neural structures and open to the infundibular recess. The absence of multiciliated cells in this recess should result in a slow CSF flow at this level. This whole arrangement should facilitate the arrival of CSF signal to the arcuate nucleus. This review will show how peripheral hormones can reach hypothalamic targets without making the BBB leaky.
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Dissociation of growth hormone and prolactin response to levodopa during pyridoxine administration.

500 mg of levodopa was administered orally to 8 normal subjects and induced an increase of growth hormone (GH) and a decrease of prolactin (PRL) secretion. The levodopa-induced GH release was inhibited by an intravenous infusion of pyridoxine; on the contrary, the PRL response to levodopa was enhanced by pyridoxine infusion. This dissociation of GH and PRL responses to levodopa during pyridoxine infusion appears to be mediated by peripheral acceleration of the conversion of levodopa to dopamine. Since dopamine does not penetrate the blood-brain barrier, the enhanced PRL decrease observed during pyridoxine infusion might be explained only on the basis of a mechanism of action exerted by dopamine on extra blood-brain barrier sites.
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Pyridoxine (B6)-Induced Inhibition of Prolactin Release in the Female Rat

The present studies were carried out to determine whether pyridoxine (B6) inhibits PRL release in the rat and to define its site of action. Adult female rats were injected with 50 mg B6 of diluent (C) ip at 1200 h on proestrus. B6 prevented the increase in PRL secretion normally observed at 1300 h and this inhibition was prolonged until at least 1500 h by a second injection of B6 at 1400 h. All B6-treated and control animals had normal proestrous LH surges and ovulated the next day. To determine whether the inhibitory effect of B6 on PRL release was due to enhanced dopamine synthesis or to a direct effect on the pituitary, ovariectomized rats were treated with a potent inhibitor of dopamine synthesis, α-methyl-p-tyrosine (α-MPT). The administration of B6 either with or 4 h after α-MPT significantly decreased the PRL rise observed in animals treated with α-MPT alone. B6 also significantly suppressed the TRH-induced PRL rise in both α-MPTtreated and normal rats, but had no effect on the TRHinduced rise in plasma TSH concentration. These studies demonstrate that pharmacological doses of Be reduce the proestrous PRL surge and that this reduction may be at least partially due to a direct effect on the pituitary, inasmuch as B6 decreased the PRL rise after α-MPT and/or TRH administration. (Endocrinology 102: 362, 1978)
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Effect of pyridoxine on human hypophyseal trophic hormone release: a possible stimulation of hypothalamic dopaminergic pathway.

A single dose of pyridoxine (300 mg iv) produced significant rises in peak levels of immunoreactive growth hormone GH and significant decrease of plasma prolactin PRL in 8 hospitalized healthy subjects. Serum glucose, luteinizing hormone LH, follicle stimulating hormone FSH and thyrotropin TSH were not altered significantly. In addition, in 5 acromegalic patients who were studied with both L-dopa and pyridoxine, inhibition of GH secretion followed either agent in a similar pattern. These data suggest a hypothalamic dopaminergic effect of pyridoxine.
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Pyridoxal phosphate inhibits pituitary cell proliferation and hormone secretion.

Pyridoxal phosphate (PLP), a bioactive form of pyridoxine, dose-dependently (10-1000 microm) inhibited cell proliferation in rat pituitary MMQ and GH3 cells and in mouse AtT-20 cells. After 4 d, MMQ cell numbers were reduced by up to 81%, GH3 cell numbers were reduced by up to 64% (P < 0.05), and AtT-20 cell numbers were reduced by up to 90%. Cell proliferation rates recovered and dose-dependently reverted to control levels after PLP withdrawal. After 4 d, PLP (400 and 1000 microm) decreased [3H]thymidine incorporation by up to 71% (P < 0.05). PLP (400-1000 microm) reduced GH3 cell GH and prolactin secretion and AtT-20 cell ACTH secretion (adjusted for cell number) by approximately 70% after 2 d. The 100 microm PLP also inhibited prolactin secretion (65%, P < 0.05) in primary rat pituitary cells treated for 2 d. PLP decreased the percentage of AtT-20 and GH3 cells in S phase and increased those in G0-G1 phase. Furthermore, PLP induced AtT-20 and GH3 cell apoptosis (28 vs. 6, P < 0.05; 26 vs. 3, P < 0.05, respectively) and dose-dependently reduced content of the antiapoptosis gene Bcl-2. These results indicate that pharmacological doses of PLP inhibit pituitary cell proliferation and hormone secretion, in part mediated through PLP-induced cell-cycle arrest and apoptosis. Pyridoxine may therefore be appropriate for testing as a relatively safe drug for adjuvant treatment of hormone-secreting pituitary adenomas.
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mw1

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IIRC, that was just BLR saying to attack Inhibit-P. Every thread I've read since the one I sent you regarding the two together has backed that thought up.
Correct.
I think Coop schooled him on that a long time ago
 
Woody

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Correct.
I think Coop schooled him on that a long time ago
I don't think schooled him is the right word. Coop ate his soul for breakfast. Absolutely nasty lol. It was like Randy Couture vs James Toney.
 
baxtecal

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Great thread this is the stuff I was trying to figure out when I posted a thread about both products
 
GreekTheBrick

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Thanks for your time and knowledge De__eB
 
Rostam

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Great info De_eB.
All seems clear now.
Thanks.
 
kingjameskjf

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A little anecdotal experience from myself, I added Inhibit-P into my PCT's and it has worked great so far without any issues.
 
furion

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That's what I thought but it's interesting that Copper or no one from SNS provided explanation or any data (as they usualy do) to show that what BLR is saying is wrong. in none of the threads. they were always focusing on ldopa topic and nothing about it's interaction with p5p of B6. So now I'm wondering who is right.
The (hypothetical) research that suggests that co-administration of pyridoxine with L-Dopa reduces central distribution of the dopamine precursor was performed with L- Dopa and not a Mucuna extract. Inhibit-P contains Mucuna standardised to 60% L-Dopa.
Mucuna also contains several other constituents including tetrahydroisoquinolone alkaloids which are believed to have affinity for dopa decarboxylase.

Additionally the research suggesting the increase L-Dopa biotransformation was performed in Parkinson's disease (PD) patients testing outcomes measured by worsening of Parkinson's symptoms- henceforth it was hypothesised that it could have been pyridoxine increasing the peripheral conversion and reducing centrally available L-Dopa. Not only is this a terrible model to extrapolate a claims suggesting the combination would not provide benefit for prolactin control- it is actually almost contradicted in later research. The current, more convincing research into the actual pathology of PD has identified that PD patients have altered central catecholamine synthesis and metabolism whereby there is an accumulation of endogenous metabolites which act as false transmitters and reduce dopamine transmission in the cerebellum. It was identified that pyridoxine can increase the presence of these metabolites- hence would worsen Parkinson's symptoms- which provides a much more sound explanation and also reassures the effectiveness of the combination in Inhibit-P.
 
StatePlan1425

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Question for this distinguished panel: thoughts on taking Inhibit-P and MK-677 in parallel rather than in series?
 
furion

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Question for this distinguished panel: thoughts on taking Inhibit-P and MK-677 in parallel rather than in series?
Parallel would make more sense for both prolactin control and also potentiating the ghrelin stimulated GH secretion from MK 677.
The increase in prolactin observed with MK677 is similar to other ghrelin mimetics whereby the initial doses stimulated the greatest peaks- which alone should be enough reason to take Inhibit-P from the beginning. Additionally, L-Dopa stimulated GH secretion has been demonstrated to be mediated through GHRH release, albeit not as strong as GHRH- however in the absence of a coadministered GHRH analogue it would certainly seem plausible that it may amplify the pulse.
 
goodvibes

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Parallel would make more sense for both prolactin control and also potentiating the ghrelin stimulated GH secretion from MK 677.
The increase in prolactin observed with MK677 is similar to other ghrelin mimetics whereby the initial doses stimulated the greatest peaks- which alone should be enough reason to take Inhibit-P from the beginning. Additionally, L-Dopa stimulated GH secretion has been demonstrated to be mediated through GHRH release, albeit not as strong as GHRH- however in the absence of a coadministered GHRH analogue it would certainly seem plausible that it may amplify the pulse.
Been doing this since day 1 of mk677. I'm still on 10mg/day but Im reaping the benefits of these two combined. Sleep is so much deeper and recovery is definitely increased.
 

test112

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Apologies if this is slightly off-topic, but the write-up for BLR Letrone states that it potentiates ghrelin secretion.

Would this have any marked effect on prolactin? Did anyone who has gotten bloodwork done while using letrone see any changes in prolactin levels?
 
cumminslifter

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On its own, Pyridoxine can reduce prolactin.

L-Dopa + Pyridoxine = Greater decreases in prolactin, lower increases in GH
came to say this, left satisfied
 
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baxtecal

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Apologies if this is slightly off-topic, but the write-up for BLR Letrone states that it potentiates ghrelin secretion.

Would this have any marked effect on prolactin? Did anyone who has gotten bloodwork done while using letrone see any changes in prolactin levels?
Post in Letrone thread, youll get answered there
 

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