Prolactin: why "control your E2 and everything will be fine" is both dangerous & wrong

[automatondan]

Reference? Unless it's animal data in which case don't worry about it.
The part in bold doesn't contradict your original thought because of the 2nd part in bold. Nandrolone increasing Dopamine makes no sense whatsoever. The MOA isn't there. It definetly inhibits it - the question is whether that level of inhibition is more/less than other forms of AAS.

Regarding amphetamine use, we don't need more serotonin in the system - AAS gives us plenty of that as it is. Considering the availability of Caber, I fail to see any reason to go with a more general form of medication to a very specific problem.

I have three references, but they all used rats... I can still post the studies if you like, but you said you didn't want to see them above...

I was not suggesting that ND increased DA, just that there was an observed increase in up-regulation of DA transporters, thus increasing DA activity. Not suggesting it increases DA, just that any DA related activity was increased.

 

[hulksmash]

I found the reference. It's rats. My stance on animal data is well known.
Regardless, the part in bold doesn't contradict your original thought because of the 2nd part in bold. Nandrolone increasing Dopamine makes no sense whatsoever. The MOA isn't there. It definetly inhibits it - the question is whether that level of inhibition is more/less than other forms of AAS.

Regarding amphetamine use, we don't need more serotonin in the system - AAS gives us plenty of that as it is. Considering the availability of Caber, I fail to see any reason to go with a more general form of medication to a very specific problem.

Buddy, AAS is neuroactive. It's well known to mess with dopamime, serotonin, etc; especially Test.

I know its a shock that I'm not posting in the thread; I just ran outta time for a minute

 

[MrRippedZilla]

Buddy, AAS is neuroactive. It's well known to mess with dopamime, serotonin, etc; especially Test.
I know its a shock that I'm not posting in the thread; I just ran outta time for a minute

It is well known to inhibit dopamine and increase serotonin, yes. Something I've already stated however many times on the audio and in the cliffs.

 

[automatondan]

It is well known to inhibit dopamine and increase serotonin, yes. Something I've already stated however many times on the audio and in the cliffs.

Zilla, did you see my response to you in post #21?

I was curious about the increase in DA transporters because I happen to be perscribed a low dose of Adderall for ADD, and was curious if this was potentially increasing/inhibiting prolactin...

 

[hulksmash]

It is well known to inhibit dopamine and increase serotonin, yes. Something I've already stated however many times on the audio and in the cliffs.

No, this was with dopamime being released by test. I'd have to find the research.

 

[MrRippedZilla]

Zilla, did you see my response to you in post #21?
I was curious about the increase in DA transporters because I happen to be perscribed a low dose of Adderall for ADD, and was curious if this was potentially increasing/inhibiting prolactin...

Does Adderall have any direct D2 agonism going on? If so, the stronger the binding affinity, the more it will help with lowering Prolactin. If no, then it wouldn't help at all. If it antagonizes D2, which many stimulants do, then it would actually increase Prolactin further.

I dug up the reference plus one of the rat papers they cited by the way.
They didn't measure Dopamine directly and yet claim that the increase in dopamine transporter density could reflect increased Dopamine activity. Uh Huh. They then claim this is through D2 based on previous rat data. Despite not looking at D2 themselves. Uh Huh. They then mention that previous work shows AAS to inhibit Dopamine. No explanation as to why Nandrolone would be different in this regard. Uh Huh. I think this paper sucks. I don't buy that Nandrolone is really special and does the exact opposite of other forms of AAS when it comes to Dopamine, D2 and therefore Prolactin.

You owe me rep points for making me look at rat data. Just saying.

 

[hulksmash]

Does Adderall have any direct D2 agonism going on? If so, the stronger the binding affinity, the more it will help with lowering Prolactin. If no, then it wouldn't help at all. If it antagonizes D2, which many stimulants do, then it would actually increase Prolactin further.

I dug up the reference plus one of the rat papers they cited by the way.
They didn't measure Dopamine directly and yet claim that the increase in dopamine transporter density could reflect increased Dopamine activity. Uh Huh. They then claim this is through D2 based on previous rat data. Despite not looking at D2 themselves. Uh Huh. They then mention that previous work shows AAS to inhibit Dopamine. No explanation as to why Nandrolone would be different in this regard. Uh Huh. I think this paper sucks. I don't buy that Nandrolone is really special and does the exact opposite of other forms of AAS when it comes to Dopamine, D2 and therefore Prolactin.

You owe me rep points for making me look at rat data. Just saying.

You can't just look at D2; just like my research on beating fatigue by finding agonists for wakefulness. DAT can play a role; acting like a DRI can play a role, etc.

The truth of prolactin with what I came to via research-by the way, I respect you for your work; I thought I was alone as far as spending so many hours researching shit-is that we don't know.

I gave up, believe AAS affects dopamine in an agonist manner (look into sexual function, libido, etc), will affect prolactin at a high enough dose, and closed my case.

ALL amphetamines are norepinephrine-dopamine-releasing agents, or NDRA's.

Ya'll need to think about every mechanism that happens a dopamime released cascade, not just DAT and D2

 

[hulksmash]

How about orexin and its relation to dopamine? AAS obviously affects orexin, so dopamine will be affected, too.

How does nandrolone affect orexin, then? Histamine-3 receptors? There are hundreds of connections to dopamine.

You may come to a point where there isn't any data. That's okay, too.

 

[automatondan]

Does Adderall have any direct D2 agonism going on? If so, the stronger the binding affinity, the more it will help with lowering Prolactin. If no, then it wouldn't help at all. If it antagonizes D2, which many stimulants do, then it would actually increase Prolactin further.

I dug up the reference plus one of the rat papers they cited by the way.
They didn't measure Dopamine directly and yet claim that the increase in dopamine transporter density could reflect increased Dopamine activity. Uh Huh. They then claim this is through D2 based on previous rat data. Despite not looking at D2 themselves. Uh Huh. They then mention that previous work shows AAS to inhibit Dopamine. No explanation as to why Nandrolone would be different in this regard. Uh Huh. I think this paper sucks. I don't buy that Nandrolone is really special and does the exact opposite of other forms of AAS when it comes to Dopamine, D2 and therefore Prolactin.

You owe me rep points for making me look at rat data. Just saying.

Thanks for the feedback. Yes, Amphetamines act presynaptically (to increase DA release), and post, to increase binding for all D receptor types. So in theory, it could help reduce prolactin it seems....

 

[hulksmash]

Thanks for the feedback. Yes, Amphetamines act presynaptically (to increase DA release), and post, to increase binding for all D receptor types. So in theory, it could help reduce prolactin it seems....

In theory, BUT..

Amphetamines don't cause dopamine release from the terminals of tuberoinfundibular neurons like they do in other dopamine pathways

So, no tuberoinfundibular action=prolactin ain't gonna be affected much, if at all

 

[automatondan]

In theory, BUT..

Amphetamines don't cause dopamine release from the terminals of tuberoinfundibular neurons like they do in other dopamine pathways

So, no tuberoinfundibular action=prolactin ain't gonna be affected much, if at all

I don't know much about tuberoinfundibular action (or don't remember), so I will have to look into that, thanks.

 

[MrRippedZilla]

You can't just look at D2; just like my research on beating fatigue by finding agonists for wakefulness. DAT can play a role; acting like a DRI can play a role, etc.
The truth of prolactin with what I came to via research-by the way, I respect you for your work; I thought I was alone as far as spending so many hours researching shit-is that we don't know.
I gave up, believe AAS affects dopamine in an agonist manner (look into sexual function, libido, etc), will affect prolactin at a high enough dose, and closed my case.

ALL amphetamines are norepinephrine-dopamine-releasing agents, or NDRA's.

Ya'll need to think about every mechanism that happens a dopamime released cascade, not just DAT and D2

I combined your posts to keep this thread relatively "clean".

When it comes to practical relevance, yes actually, you can just look at D2 for Prolactin. That is why the gold standard form of treatment for hyperprolactemia is Caber - a strong D2 agonist. If you agonize D2, you solve your Prolactin problems. The rest of the system is irrelevant.

I know amphetamines are NDRIs. I also know that they have different levels of binding affinity to the Dopamine receptors. You have 5 receptors, we only give a shit about D2. That is why I asked about how strong the affinity is - important if you want to know how effective Adderall will be for Prolactin control for example.

 

[hulksmash]

I combined your posts to keep this thread relatively "clean".

When it comes to practical relevance, yes actually, you can just look at D2 for Prolactin. That is why the gold standard form of treatment for hyperprolactemia is Caber - a strong D2 agonist. If you agonize D2, you solve your Prolactin problems. The rest of the system is irrelevant.

I know amphetamines are NDRIs. I also know that they have different levels of binding affinity to the Dopamine receptors. You have 5 receptors, we only give a shit about D2. That is why I asked about how strong the affinity is - important if you want to know how effective Adderall will be for Prolactin control for example.

They aren't irrelevant because we're messing with hormones.

You'll probably push me aside, but please think of how genetic research is now showing researchers how 1 or 2 mechanisms aren't the only things to control a phenomena-

Like fat loss last year: "holy shit we're wrong; natriuretic peptides control fat loss, too!"

D2 isn't where your time should be spent with exogenous hormone manipulation and prolactin; research is there already.

I'm just saying you won't find an answer because the answer is still hidden in other mechanisms for being the cause of prolactin increases.

 

[HollyWoodCole]

Much of this kind of makes sense to me although I am admittedly far less educated than most of you in these areas it seems.

I've always noticed that it seems like my sex drive drops after being on for awhile even when I'm only on test and my E2 is in check. Never understood it but a higher prolactin level would explain it. Time for some bloodwork and caber to confirm the assertions made here.

 

[hulksmash]

Much of this kind of makes sense to me although I am admittedly far less educated than most of you in these areas it seems.

I've always noticed that it seems like my sex drive drops after being on for awhile even when I'm only on test and my E2 is in check. Never understood it but a higher prolactin level would explain it. Time for some bloodwork and caber to confirm the assertions made here.

That's not just prolactin to look at-

The biggest mistake on every AAS forum is people focus on 1 or 2 variables as causes for effects, like "you should check estrogen or prolactin for lowered libido"

The right way to do it is research the problem (lower libido) and what CREATES libido in the first place, and then research what factors can lower the things that create libido, like serotonin.

Lowered sex drive? Okay, whay creates libido? List every single variable. Now what is an antagonist to every single variable? Then find out how to remove antagonists.You gotta go through every single variable, crossing off what doesn't apply.

HWC, your dropped libido? Serotonin could be why. Aromataze issues could be the answer. Dopamine itself could be the culprit. What about norepinephrine levels being high-goodbye libido.

I hope ya'll get my point.

 

[MrRippedZilla]

That's not just prolactin to look at-
The biggest mistake on every AAS forum is people focus on 1 or 2 variables as causes for effects, like "you should check estrogen or prolactin for lowered libido"
The right way to do it is research the problem (lower libido) and what CREATES libido in the first place, and then research what factors can lower the things that create libido, like serotonin.
Lowered sex drive? Okay, whay creates libido? List every single variable. Now what is an antagonist to every single variable? Then find out how to remove antagonists.You gotta go through every single variable, crossing off what doesn't apply.
HWC, your dropped libido? Serotonin could be why. Aromataze issues could be the answer. Dopamine itself could be the culprit. What about norepinephrine levels being high-goodbye libido.
I hope ya'll get my point.

Or he can just focus on E2 and Prolactin since those are the usual culprits, can be checked easily, and can be dealt with easily. That is what a medical professional would do too. Instead of engaging in a massive mental masturbation session from the get go, which is essentially what you are asking for.

Focusing on Serotonin, for example, is pure mental masturbation and I think you know it. Serotonin is complex, difficult to measure and impossible to isolate. Making treatment at best a shot in the dark, at worst ****ing stupid.

 

[hulksmash]

Or he can just focus on E2 and Prolactin since those are the usual culprits, can be checked easily, and can be dealt with easily. That is what a medical professional would do too. Instead of engaging in a massive mental masturbation session from the get go, which is essentially what you are asking for.

Focusing on Serotonin, for example, is pure mental masturbation and I think you know it. Serotonin is complex, difficult to measure and impossible to isolate. Making treatment at best a shot in the dark, at worst ****ing stupid.

Common sense is to focus on prolactin and E2 first. If you think my point was to not do the common sense things first, then you aren't comprehending.

Our AAS usage is complex, difficult to measure, and impossible to isolate.

That point is what you're not getting. This whole thread is "mental masturbation" if you tryin to keep it real-

You dissin a method of doing a check-off of every variable is what's stupid. If you got a problem, and only look at 2 variables and stop, then you're being an idiot

Guess what-you ain't gonna find shit on prolactin; its already a dead-end several posts back.

There ain't shit out there on using AAS like we do. That's why I say to check all the variables, not just 2. You find the answer that way. But who cares, go masturbate mentally on D2 receptors without ever getting the answer you want.

 

[PillarofBalance]

That's not just prolactin to look at-

The biggest mistake on every AAS forum is people focus on 1 or 2 variables as causes for effects, like "you should check estrogen or prolactin for lowered libido"

The right way to do it is research the problem (lower libido) and what CREATES libido in the first place, and then research what factors can lower the things that create libido, like serotonin.

Lowered sex drive? Okay, whay creates libido? List every single variable. Now what is an antagonist to every single variable? Then find out how to remove antagonists.You gotta go through every single variable, crossing off what doesn't apply.

HWC, your dropped libido? Serotonin could be why. Aromataze issues could be the answer. Dopamine itself could be the culprit. What about norepinephrine levels being high-goodbye libido.

I hope ya'll get my point.

I hear ya and I don't necessarily disagree, but to focus on the most likely things makes sense. Prioritize essentially. That can be tough for someone newer to jewcing and a short history of blood work to reference.

 

[MrRippedZilla]

This whole thread is "mental masturbation" if you tryin to keep it real-
Guess what-you ain't gonna find shit on prolactin; its already a dead-end several posts back.
But who cares, go masturbate mentally on D2 receptors without ever getting the answer you want.

Those 3 lines tell me that you couldn't be bothered listening to the audio and couldn't comprehend the cliff notes.

This thread was made as a direct response to members on this board suffering from hyerprolactinemia related sides including lactation. The focus on controlling E2 made things worse and so, this thread should help folks know what to do next time they have a Prolactin problem. It's about as far removed from "mental masturbation" as you're going to get.
I found plenty on Prolactin. To the point where I was able to give practical advice on how to deal with it without focusing solely on E2. "Dead end" it never was.
That practical advice involves taking a drug that agonizes D2 and solves the Prolactin problem. That means focusing on D2 was not "mental masturbation" but was actually the answer everyone should've been seeking. Prolactin problems can occur even with normal E2 and are dealt with using a DA - that might sound obvious to you but it wasn't to the majority.

I can tell that this discussion with you is a gigantic waste of time on my behalf so this will be my final post on the matter as I place you on the ignore list. Nothing personal & certainly no disrespect intended

 

[hulksmash]

Those 3 lines tell me that you couldn't be bothered listening to the audio and couldn't comprehend the cliff notes.

This thread was made as a direct response to members on this board suffering from hyerprolactinemia related sides including lactation. The focus on controlling E2 made things worse and so, this thread should help folks know what to do next time they have a Prolactin problem. It's about as far removed from "mental masturbation" as you're going to get.
I found plenty on Prolactin. To the point where I was able to give practical advice on how to deal with it without focusing solely on E2. "Dead end" it never was.
That practical advice involves taking a drug that agonizes D2 and solves the Prolactin problem. That means focusing on D2 was not "mental masturbation" but was actually the answer everyone should've been seeking. Prolactin problems can occur even with normal E2 and are dealt with using a DA - that might sound obvious to you but it wasn't to the majority.

I can tell that this discussion with you is a gigantic waste of time on my behalf so this will be my final post on the matter as I place you on the ignore list. Nothing personal & certainly no disrespect intended

I told everyone about D2 and prolactin already through the years. Your advice was given by me A MONTH AGO but no one reads my shit. I even brought up hyperprolactinemia.

Dead end=you only know prolactin's relation with D2

Your posts say what I've said many times, and helps people. I'm thankful for that, even with me being ignored

You still missed my point: non-D2 prolactin research is what's needed.