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For those interested in using Prmaipexole in the place of Cabergoline...

MR. BMJ

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For those interested in using Pramipexole in the place of Cabergoline...

I think this was posted on one of the links by RS, but just in case it wasn't, the following info is great to read before using Pramipexole. It was written by Macrophage69alpha, who is kind of smart....lol, okay one of the smartest guys i've come across on the boards:)

Both Prami and Cabergoline are awesome compounds to use. Cabergoline has come under the spot light for it's possible threatening effects to I believe it was the heart valves, but keep in mind that the dosages used in these studies were WELL above the doses used by most on the boards for prolactin inhibition, and most only use Cabergoline for short periods at that. So imo, it gives us more than one way to skin a bird. Another thing to think about is that depending on your geographical location, it may be easier to obtain one over the other, and like Big A states, be sure to know your state/country's laws before ordering;)

Keep in mind that if questions are asked, I am not an expert, just relaying some information on the compound in case anybody is interested or has had success with using Cabergoline in the past and wants to use another option for a run. Also keep in mind that if you direct your questions towards RS, they may or may not be able to answer those questions depending on legality purposes, as is the case with most sponsors I believe.

But at any rate here is Macro's info on Prami:

First, it's important to note that high end dosing is NOT for prolactin suppression. High end dosing (over 1mg) also requires a lot of patience and adaptation as well as generally a VERY slow progression in dose. Have noticed many people trying high end dosing when they DO NOT NEED it for the purposes they are using it for.


--------------------------------------------------------------------------------------
Prolactin suppression using Pramipexole


For Prevention: when you are taking something that can cause prolactin issues or when you just want to lower prolactin, for the benefits of lowering prolactin.

0.125 (1/8) to 0.5mg (1/2) per day should generally be sufficient for most users. With prevention slow escalation should not be an

For Treatment: When you have ongoing prolactin issues, Gynecomastia flare, or are attempting to regress gynecomastia tissues (ductal, lobular and central gland mass).

0.375 up (3/8) to 1mg should generally be sufficient for most users. Most people will not need over 0.5mg. If you do, then SLOWLY escalate the dose. You still should start at 0.25mg and slowly work up.

Doses should be taken in the evening, 2-4 hours prior to bed. For the very low doses, an hour is probably fine. if it keeps you up, take it earlier. If it makes you sleepy "too soon" then take closer to bed. a good number of people will notice niether. taking with last meal of the day may be ideal for a lot of people.



Now for you people that want high end dosing benefits, which are not prolactin suppression. This is a lot more complex, and generally requires a VERY slow progression in dosing to acheive. Clinicals increased the dose by 0.125 every 3-5 days. there will typicallly be side effects for people at various point along the progression. IT IS EXTREMELY IMPORTANT THAT YOU BE AWARE OF THESE BEFORE YOU LAUNCH INTO HIGH END DOSING.
 
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I've had itchy puffy nips since starting gh and ghrp-6 six months ago (even while on letro, aromasin and nolvadex - not at the same time). I've read that this can be due to an increase in prolactin from the gh. I just ordered some of the pramipexole. What do you think would be a good dose to combat this. I'm 5'7" ~215lbs. Thanks.
 
From the user's i've seen report on it, definately go with low-end dosing 0.125 to 0.25mg per day. This will help against any nausea that some may experience the first week or two. What nausea that has been reported is gone after the first week or two. Some may be able to go higher, but i'd start out low and work your way up on it to be honost. The recommendations above in Macro's quoted summary are pretty much in line to what most report in regards to dosing.

Also, prolactin spikes seem to be more nocturnal, at night time for most while sleeping, and will have large spikes, thus peaks and valleys and inconsistent levels which may give rise to more sides (ie puffy nipples). I'd take at night starting out, then when you get up to 0.5mg per day, i'd take half in the morning and half at night sometime before going to bed. Some users have reported better experiences with bi-daily dosing.

High end dosing of 1mg or higher, is mainly used by people for sexual pleasure, etc.

BMJ
 
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I've had itchy puffy nips since starting gh and ghrp-6 six months ago (even while on letro, aromasin and nolvadex - not at the same time). I've read that this can be due to an increase in prolactin from the gh. I just ordered some of the pramipexole. What do you think would be a good dose to combat this. I'm 5'7" ~215lbs. Thanks.

Mucuna pruriens, 40% L-Dopa at 250mg EOD

Drugs are not needed.
 
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I'll give you a bump BMJ, sounds interesting, going to have to look into Prami.
 
Mucuna pruriens, 40% L-Dopa at 250mcg EOD

Drugs are not needed.

L-dopa can cause peripheral dopamine to raise and have serious long term side effects. Also it does not work for many (like myself). L-dopa is sold in most other countris as a drig. Make no mistake it is just as mucha drug as anything else and as with many other things like Ephedrine and Yohimbine, often the herbal version has worse side effects.
 
L-dopa can cause peripheral dopamine to raise and have serious long term side effects. Also it does not work for many (like myself). L-dopa is sold in most other countris as a drig. Make no mistake it is just as mucha drug as anything else and as with many other things like Ephedrine and Yohimbine, often the herbal version has worse side effects.

generally agree, particularly with respect to the effectiveness of l-dopa.

have found that most of the people that "rave" about b-6 and l-dopa, just did not have issues or even more common never actually used either or the combo with progestins.


just because you dont have issues does not mean that something worked. If taking something abrogates your symptoms, then you are in a position to make that claim. Not because you never got symptoms in the first place, some people are not prone (and in many cases its after repeated exposure and with age that these issues become more prevalant.


find it disturbing that people say with certainty things like "you dont need an AI with that dosage", because usually its based on personal experience that they did not "need" an AI with that dosage. Given that there is a very wide variance in aromatase levels as well as differing starting points such statements without more information are never a good idea.

ie JoedontneednoAI has only the minimalist of breast budding, where gynokid already has significant ductal and tissue development as well as one of the aromatase polymorphisms (yielding 7-11 times the amount of aromatase produced). JoedontneednoAI runs 600mg of test without even much bloating, he also happens to be in his early twenties and under 9% bodyfat. Gynokid is 35, has 17% percent bodyfat. He is not in the same position as JoedontneednoAI. But JoedontneednoAI tells him, with assuredness, that he has run 600mg and its rediculous to use an AI with that dosage. Not accounting for the vast gulf that separates their individual hormonal mileus.


now down the road, after many cycles, JoedontneednoAI finds that at the same doses he now is getting gyno, he adds an AI, still getting gyno because even the moderation of estrogen (which he exposed himself to over the years as well as a number of progestins) does not quell the effects of the prolactin which (even not using a progestin) is now elevated because of the impacts of earlier activities. He gets shut down like nobodies business and he cant figure out why. the reason is that, even though he was not getting gyno from those doses and exposures, he was laying the groundwork for this later fall from grace. Even just moderate steps taken prior to this would have limited, and in many cases abrogated the situations that now arise.

just some things to think about.
 
L-dopa can cause peripheral dopamine to raise and have serious long term side effects. Also it does not work for many (like myself). L-dopa is sold in most other countris as a drig. Make no mistake it is just as mucha drug as anything else and as with many other things like Ephedrine and Yohimbine, often the herbal version has worse side effects.

There is a difference between L-Dopa & Mucuna pruriens that contain 40% L-Dopa. The other constituents are important...it appears they prevent problems in peripheral tissue.

For instance:

"The therapeutic effect of Mucuna pruriens has been attributed to a combination of unidentified substances and levodopa and is found to be 2–3 times more effective than compatible doses of levodopa in the animal model of Parkinson’s disease (Hussain and Manyam, 1997). Unlike levodopa, Mucuna pruriens has shown not to induce dyskinesia in the monkey model of Parkinson’s disease (Subramanian et al., 2002) or in patients with Parkinson’s disease (Katzenschlager et al., 2004)."

And:

"Mucuna pruriens cotyledon powder (MPCP) has shown anti-parkinson and neuroprotective effects in animal models of Parkinson’s disease that is superior to synthetic levodopa. In the present study two different doses of MPCP protected both plasmid DNA and genomic DNA against levodopa and divalent copper-induced DNA strand scission and damage. It exhibited chelation of divalent copper ions in a dose-dependent manner. The copper chelating property may be one of the mechanisms by which MPCP exerts its protective effects on DNA."

And:

blah, blah, blah,
 
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mucuna does have impact, however it can also increase PRL. That is one of the caveats of using dopamine precursors. The real issue with most of the mucuna research is that it was done in india, which calls into question its validity. Not just from a clinical standpoint but also because asians response to hormonal modulation, particularly progestins and prolactin appears to be highly variant from at least europeans.

eg. test + nandrolone= 99+% effective contraceptive for asian males (thai, india, and chinese) 85-90% effective in european males.
 
Macro said:
mucuna does have impact, however it can also increase PRL.

Many things are biphasic (meaning having two phases). Gaba for instance.

It is not my job to reign in the "more is better" mentality...

The real issue with most of the mucuna research is that it was done in india, which calls into question its validity. Not just from a clinical standpoint but also because asians response to hormonal modulation, particularly progestins and prolactin appears to be highly variant from at least europeans.

I don't agree with the highlighted statement. In some cases such as Policosanol research your argument would be spot on as most of the positive research comes from Cuba where there is a financial interest in making use of byproducts of sugar cane AND where results have not been duplicated outside of Cuba (and in fact have been refuted in JAMA).

This is not the case w/ Mucuna. The quotes from my earlier post came from a study called, Anti-Parkinson Botanical Mucuna pruriens Prevents Levodopa Induced Plasmid and Genomic DNA Damage, published in the journal Phytotherapy Research in 2007.

The three authors were from:

- Department of Neurology, Scott & White Clinic, Temple, Texas, USA

- Department of Pharmacal Sciences, Harrison School of Pharmacy, Auburn University, Alabama, USA

- Texas A & M University System Health Science Center College of Medicine, Temple, Texas, USA​

I understand that this study doesn't specifically focus on prolactin. However the point is that this is not some "off the wall", bullshit herb (or snake oil masquerading as vitamin tonic :) )

Many of the authors of studies in this area are from India. But that does not invalidate research.

Macro said:
eg. test + nandrolone= 99+% effective contraceptive for asian males (thai, india, and chinese) 85-90% effective in european males.

This argument seems to focus on the differences between races as clinical subjects.

Looking at clinical studies is never instructive unless you have examined the molecular studies of the compound, examined in vitro data, examined data & studies in vivo which were meant to illicit "mode of actions".

If you undertake that type of analytical approach, for example, you can come to an understanding of how omega3 oil supplementation will increase cellular metabolism which will lead to increased energy expenditure and you do not care about clinical studies (which are usually not constructed to my liking) that demonstrate no fatloss from Omega3 supplementation in obese people.

In fact in some cases you can even then pick apart those clinical studies and find data that supports the opposite of what is concluded.

The approach you have chosen Macro is to read a clinical study and pick apart the pieces to discover variability among clinical subjects. That is outstanding and I am happy that you posses both the patience and intelligence to do that. Most people either take stuff at face value or question everything but in the end have not the ability to think for themselves.

But where you fall short is in failing to examine those footnotes & references that go backwards into studies to read for yourself "how do they know that", "what is the basis for that statement", "on what molecular level...on what in vitro studies...on what in vivo animal models is that understanding arrived at..."
 
But where you fall short is in failing to examine those footnotes & references that go backwards into studies to read for yourself "how do they know that", "what is the basis for that statement", "on what molecular level...on what in vitro studies...on what in vivo animal models is that understanding arrived at..."

understand where you are coming from but analysis did not fall short, just chose not to go into it.

Obviously, within different populations there are to some extent differing genetic polymorphic traits which are more or less common with population subsets. And while wishing to take credit for such a laborious effort, the differing response, as listed above, to these hormones has been explored in several studies and reviews.

certainly when it comes to hormone response, to progestins in particular, there is a fairly wide difference between europeans and asians. One can look at the guggulsterone studies, (taking them at face value on the indian side), and see how different the response is. Lowering cholesterol in asians, while actually raising cholesterol (ldl-c fraction at least) in europeans. Most likely due to receptor isoform differences, though certainly other associated genes may be at play. (see progins, ESr1 and Esr2 among others)
 
I understand that this study doesn't specifically focus on prolactin. However the point is that this is not some "off the wall", bullshit herb (or snake oil masquerading as vitamin tonic :) )

dont disagree, just feel its usefulness is limited and may produce the opposite of desired effect (likely both individual and dose dependant, while not ignoring the impacts of plasma peaks and troughs (as well as secondary metabolism).
 
Many of the authors of studies in this area are from India. But that does not invalidate research.


true, BUT it does call it into question both from its applicability across population subsets as well as the quality of both peer review and the impact of financial interests.

many supplement companies farm out thier studies to, or "fund" studies in, india, vietnam and eastern europe because its cheap, but also because "money talks" a little more loudly (a lot more really).
 
true, BUT it does call it into question both from its applicability across population subsets as well as the quality of both peer review and the impact of financial interests.

many supplement companies farm out thier studies to, or "fund" studies in, india, vietnam and eastern europe because its cheap, but also because "money talks" a little more loudly (a lot more really).

Macro I understand what you are saying.

But it is kind of a lazy approach to taint research solely by looking to the region where the research was conducted.

There is often very poor research published from U.S. sources as well particularly when it is a meta-analysis.

The primary reason I mentioned looking at studies in areas both tangential & on point to a study in question is that it gives you the opportunity to establish benchmarks against which you can measure what is purported to be "new ground".
 
not really "lazy", just different, and those are just elements of the analysis.... ie.. they are things that SHOULD be considered.

Agree, where its published is also important. there are lots of low end and pay to play journals.
 
What is the best way you have found to take Prami ?



varies considerably. IMHO the 1-2mg range is best for benefits, without the potential compulsion type sides that can manifest at higher doses.

split dose AM/PM seems to work well for most.
 

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