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



## MrRippedZilla (Mar 11, 2019)

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

45 mins of Prolactin talk, which is why I've added cliff notes for those not able to tolerate that level of British-ness:*
*https://vocaroo.com/i/s0Y4qiZ0rX9L
*

Cliff notes
*
- We have multiple anecdotal examples of members, on this board, suffering with hyperprolactinemia despite normal E2 levels. These examples requires reassessing the commonly given advice of "control E2 and Prolactin will be fine". 

- Prolactin is under the inhibitory control of Dopamine. To increase Prolactin, you need to inhibit Dopamine. To decrease Prolactin, you need to increase Dopamine. D2 is the key receptor of interest here. 

- Pituitary Prolactin secretion is reflected by serum levels and is our main concern. Prolactin is produced locally in different tissues too but at lower levels that stay in the same vicinity and are not reflected by serum levels. 

- Bf% is irrelevant for serum, pituitary secreted, Prolactin levels. 

- Hyperprolactinemia causes multiple side effects including loss of libido, premature ejaculation, erectile dysfunction (very common), insulin resistance and galactorrhea (milk production). It is common to associate these negative sexual side effects with high E2 but without bloodwork, you don't really know if it's an E2 or Prolactin problem. 

- Several causes for hyperprolactinemia: lack of sleep, stress, intense exercise, opiod use, antipsychotic medication, *serotonin*, *GH*, *TRH* (Thyrotropin-releasing hormone) *chronically elevated E2*, etc. All of these work primarily through dopamine depletion. Those in bold are the most relevant to us. 

- Testosterone alone causes serotonin to increase, which is why it is seen as an effective anti-depressive for some folks. Insufficient data to suggest how different forms of AAS impact serotonin. Practically, an irrelevant source of Prolactin increase. 

- GH has the ability to bind to the Prolactin receptor and mimic some of the actions of Prolactin. It might cause problems if GH or it's analogues are used at high doses. Bloodwork is recommended to keep an eye on it. 

- The relationship between TRH, Dopamine and Prolactin is complex (though I did a ****ing great job explaining it 13mins in). Essentially, TRH in the hypothalamus is responsible for telling TSH, in the pituitary, to work harder to produce more T3/T4 if it senses a lack of T3/T4 in circulation. Dopamine normally inhibits TSH, which makes TSH's job kind of difficult so TRH inhibits Dopamine in order to allow TSH to do it's thing. Once T3/T4 numbers are good, TRH goes down, Dopamine goes back up, TSH goes down - back to homeostasis. 
TRH, by inhibiting dopamine, increases Prolactin. This is seen in 1/3 of primary hypohyroid patents. Problem is fixed with T3/T4 supplementation. 
It might be a good idea to add a replacement dose of T3 to your cycle depending on the anabolics being used (data is lacking to show which ones cause the biggest negative, transient, impact on thyroid numbers).   

- E2 inhibits dopamine = high Prolactin. E2 is necessary to stimulate Prolactin *but,* at high levels, it prevents actual lactation. *This means that bumping up the AI dose to deal with Prolactin can actually cause lactation, not prevent it. *E2 does not need to be high for Prolactin to be high. 

- Progesterone can inhibit dopamine but the impact seems to insignificant since pituitary Prolactin levels (what matters when it comes to serum Prolactin levels & the side effects we deal with) are unchanged. The data doesn't support the idea that 19-nors, which also work through progesterone activation, have a bigger impact on Prolactin levels. Anecdotal data (based on bloodwork) is mixed on the subject. 

- You can deal with with high Prolactin levels in 2 ways: do nothing or take a DA (Caber being the preferred choice). Doing nothing is a valid option if you are asymptomatic. Otherwise, Caber at 0.25mg 2xweek is the way to go. 

- Caber's common side effects include nausea, dizziness, headaches, constipation and sexual awesomeness. 

- The risk of negative *psychological *side effects (lack of impulse control, psychosis, "hypersexuality", etc) is below 5% at the doses we use (below 2.5mg per week). This risk is commonly exaggerated by folks extrapolating data from Parkinson patients and other groups using much higher doses (3-11mg per week). The exception to this low risk involves patients with current mental health disorders (psychosis, depression, schizophrenia) - these individuals should avoid DAs altogether. 

- The risk of cardiovascular problems (vascular/pulmonary fibrosis, heart regurgitation, etc) are non-existent for this community (dosing below 2.5mg/week, use is limited to less than 2 years straight, etc, etc).  

- All side effects can be minimized by titrating down the dose of Caber. All side effects subside when Caber is discontinued. Tolerance is seen as a relative non-issue within the data.  

- _Skip to 39mins for answers to the questions asked in a previous thread that isn't covered above._ 

*Summary: 
*- You do not need high E2 to have high Prolactin.
- Crashing your E2 levels to solve hyperprolactinemia is really stupid and causes more problems than it solves in a lot of cases. 
- If you have Prolactin related side effects, get bloodwork to confirm before treating it with Caber. 
- You have the option of taking Caber from the start vs waiting for sides/bloodwork. This is up to you - same story with AIs. 
- If you're asymptomatic, you have the option of not doing anything.   
- Data is lacking to suggest what anabolics have more/less of an impact on Prolactin. 


*References

*Impact of prolactin receptor isoforms on reproduction
Diagnosis and treatment of hyperprolactinemia: an Endocrine Society clinical practice guideline - highly recommended practical guide
60 years of neuroendocrinology: the hypothalamo-prolactin axis
Prolactin (PRL) in adipose tissue: regulations and functions - focuses more on locally produced prolactin but the author, Nira Ben-Jonathan, is the best Prolactin researcher on the planet. 
Prolactin and its role in human reproduction - 2019 review on the topic, highly recommended
http://www.druglib.com/druginfo/cabergoline/side-effects_adverse-reactions/


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## Spongy (Mar 11, 2019)

dude.  just.  dude.  

I just read the cliff notes at this time. But can't wait to listen to the whole thing.  Great stuff.


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## Rhino99 (Mar 11, 2019)

Zilla,
This is just awesome.
I also will read more in depth tonight but I have 1 question pertaining to this statement:
The exception to this low risk involves patients with current mental health disorders (psychosis, depression, schizophrenia) - these individuals should avoid DAs altogether.

So if you're prone to depression, anxiety, etc, and you shouldnt take a DA, how would you treat high prolactin?


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## IHI (Mar 11, 2019)

Gunna have to read all this later, really appreciate the time you vest into these things!


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## MrRippedZilla (Mar 11, 2019)

Rhino99 said:


> Zilla,
> This is just awesome.
> I also will read more in depth tonight but I have 1 question pertaining to this statement:
> The exception to this low risk involves patients with current mental health disorders (psychosis, depression, schizophrenia) - these individuals should avoid DAs altogether.
> So if you're prone to depression, anxiety, etc, and you shouldnt take a DA, how would you treat high prolactin?


Honestly dude, if you suffer from mental health issues then you have no business cycling in the first place. 

Using patients on anti-psychotics who have hyperprolactinemia as an extreme example, here is what the data says is the correct approach to treatment:
1) Stop taking the medication that is causing the hyperprolactinemia. Unlike us, these folks may not be able to stop taking their medication for obvious reasons so...
2) Substitute something else in place of the medication causing the hyperprolactinemia. It is difficult for us to do that since we don't know how exactly different forms of AAS impact Prolactin but we could go with more mild forms in general (Anavar, Primo , etc). Most anti-psychotics deplete dopamine and increase prolactin so this may not be an option for these patients either so...
3) Take a DA anyway and monitor closely. This is controversial and is seen as a last resort for these patients. We have the option of stopping the cycle and using other, milder, forms of anabolics so it should never get to this step.


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## gymrat827 (Mar 11, 2019)

very nice info

bet this will stir some AI discussions


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## ToolSteel (Mar 12, 2019)

MrRippedZilla said:


> Honestly dude, if you suffer from mental health issues then you have no business cycling in the first place.
> 
> Using patients on anti-psychotics who have hyperprolactinemia as an extreme example, here is what the data says is the correct approach to treatment:
> 1) Stop taking the medication that is causing the hyperprolactinemia. Unlike us, these folks may not be able to stop taking their medication for obvious reasons so...
> ...


Are you aware of any data detailing the effectiveness of B6?


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## MrRippedZilla (Mar 12, 2019)

ToolSteel said:


> Are you aware of any data detailing the effectiveness of B6?


I'm aware of a couple of 24hr papers showing it to reduce prolactin but nothing more than that. It was a form of treatment many decades ago before DAs were a thing. DAs, Bromocriptine to begin with, were much better at the job and so B6 fell out of favor. It isn't mentioned once in any of the literature I referenced nor in my textbook. It also isn't used as an official form of treatment for any patients (mental health disorder or not) suffering from hyperprolactemia. Read into that what you will. 

It also doesn't really get around the fact that you have to mess around with the Dopamine system in order to get Prolactin back in range - something folks with mental health disorders probably shouldn't be doing. B6 works by increasing the activity of the PLP enzyme, which converts L-DOPA into Dopamine. It's a shittier way of messing with the system but it's still messing with the system. Not something I would personally recommend over DAs under any circumstances.


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## hulksmash (Mar 12, 2019)

I've said all this about prolactin in posts through the years..

Well, at least people will finally read what'd been said


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## Straight30weight (Mar 12, 2019)

Zilla is one of those guys that when they speak, you should listen. I read the cliff notes, will listen tonight.


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## PillarofBalance (Mar 12, 2019)

Ok this is starting to make better sense now... Appreciate the post Zilla. 

Also sounds like prolactin should absolutely be on the blood work list no matter the cycle. Any clues as to where the notion that 19 nor was responsible for this?


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## Jin (Mar 12, 2019)

Straight30weight said:


> Zilla is one of those guys that when they speak, you should listen. I read the cliff notes, will listen tonight.



I jerk off to his accent even though it’s fake. 

He’s such an imposter he told me British don’t use the term “guv’” or “govenor”.


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## DieYoungStrong (Mar 12, 2019)

PillarofBalance said:


> Ok this is starting to make better sense now... Appreciate the post Zilla.
> 
> Also sounds like prolactin should absolutely be on the blood work list no matter the cycle. Any clues as to where the notion that 19 nor was responsible for this?



If I had to guess after reading this, I’d say they don’t armomatize traditionally but still can cause prolactin to spike, therefore 19-nors spike prolactin in bro science.


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## MrRippedZilla (Mar 12, 2019)

PillarofBalance said:


> Any clues as to where the notion that 19 nor was responsible for this?


The bro-sumption of "well, they interact with the progesterone receptor so that must mean they are responsible for the prolactin increase". Or misinterpretation of in-vitro data. One of those two. 

For the record, we have zero quality data on the impact of 19-nors on Prolactin, which is why I cannot say conclusively that they don't have a bigger impact on Prolactin either. What I can say conclusively is that Test alone is capable of increasing Prolactin even with normal/controlled E2. Therefore, as you said, bloodwork including Prolactin for all cycles (apart from maybe really mild stuff) with Caber on hand just in case is the way to go.


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## Bro Bundy (Mar 12, 2019)

does body fat have anything to do with it? Thanks for taking time to write a good piece bro..I deff notice when my body fat is high i get more E sides


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## motown1002 (Mar 12, 2019)

Great stuff Zilla!  Thanks for posting.


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## MrRippedZilla (Mar 12, 2019)

Bro Bundy said:


> does body fat have anything to do with it? Thanks for taking time to write a good piece bro..I deff notice when my body fat is high i get more E sides


Locally, you will produce more Prolactin the fatter you are since the adipose (fat) tissue itself secretes it. But, local levels tend to stay in the same area and therefore don't play a big role in causing the bad sides (ED, lactation, etc). Local levels also don't show up on bloodwork by the way.

When it comes to Prolactin coming from the pituitary, which is the real problem since it comes in much larger amounts than what you store locally, bf% doesn't play a role.


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## automatondan (Mar 12, 2019)

Thanks for posting Zilla. 

I have been chewing on all this all morning and then started looking at certain compounds effects (whether inhibitory or increasing) dopamine in the body. 

I found something interesting in regards to nandrolone. Increased up-regulation of DA transporters in the caudatum/putemen has been observed following administration of nandrolones (even months later), (suggesting) a reflected enhancement of DA activity. So, contrary to my original thought/theory that maybe deca/npp somehow inhibited DA activity and thus increased prolactin seems to be false. This would be a good thing in regards to our usage of ND correct? But then as I think about it more, would the positive effects of increased up-regulation only be present if there were not somehow a decrease in DA...? 

It also made me wonder if amphetamine usage (ADHD meds) at low doses (especially in conjunction with ND) could help mitigate increases in prolactin due to it's increase of DA and serotonin.  

Anyways, it's been many years since I studied Neuro so I am quite foggy. These were just some ideas I had....


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## automatondan (Mar 12, 2019)

PillarofBalance said:


> Any clues as to where the notion that 19 nor was responsible for this?



See post #18, I was surprised at what I found as well...


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## MrRippedZilla (Mar 12, 2019)

automatondan said:


> Thanks for posting Zilla.
> I found something interesting in regards to nandrolone. *Increased up-regulation of DA transporters in the caudatum/putemen has been observed following administration of nandrolones (even months later), (suggesting) a reflected enhancement of DA activity. *So, contrary to my original thought/theory that maybe deca/npp somehow inhibited DA activity and thus increased prolactin seems to be false. This would be a good thing in regards to our usage of ND correct? But then as I think about it more, *would the positive effects of increased up-regulation only be present if there were not somehow a decrease in DA...? *
> 
> It also made me wonder if amphetamine usage (ADHD meds) at low doses (especially in conjunction with ND) could help mitigate increases in prolactin due to it's increase of DA and serotonin.
> ...


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.


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## automatondan (Mar 12, 2019)

MrRippedZilla said:


> 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.


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## hulksmash (Mar 12, 2019)

MrRippedZilla said:


> 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


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## MrRippedZilla (Mar 12, 2019)

hulksmash said:


> 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.


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## automatondan (Mar 12, 2019)

MrRippedZilla said:


> 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...


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## hulksmash (Mar 12, 2019)

MrRippedZilla said:


> 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.


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## MrRippedZilla (Mar 12, 2019)

automatondan said:


> 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.


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## hulksmash (Mar 12, 2019)

MrRippedZilla said:


> 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 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


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## hulksmash (Mar 12, 2019)

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.


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## automatondan (Mar 12, 2019)

MrRippedZilla said:


> 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.
> ...



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....


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## hulksmash (Mar 12, 2019)

automatondan said:


> 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


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## automatondan (Mar 12, 2019)

hulksmash said:


> 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.


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## MrRippedZilla (Mar 12, 2019)

hulksmash said:


> *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.
> 
> ...


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.


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## hulksmash (Mar 12, 2019)

MrRippedZilla said:


> 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.


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## HollyWoodCole (Mar 12, 2019)

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.


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## hulksmash (Mar 12, 2019)

HollyWoodCole said:


> 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.


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## MrRippedZilla (Mar 12, 2019)

hulksmash said:


> 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.
> ...


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.


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## hulksmash (Mar 12, 2019)

MrRippedZilla said:


> 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.


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## PillarofBalance (Mar 12, 2019)

hulksmash said:


> 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"
> 
> ...



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.


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## MrRippedZilla (Mar 13, 2019)

hulksmash said:


> 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


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## hulksmash (Mar 13, 2019)

MrRippedZilla said:


> 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.
> ...



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.


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## hulksmash (Mar 13, 2019)

PillarofBalance said:


> 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.



Yea, I was hoping my post inferred the use of common sense and check things like E2 first.

I'm trying to write with less trust in "oh, people will know to use commom sense" lol


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## Bro Bundy (Mar 13, 2019)

If u got shit to add to help people that mayb zilla missed make your own thread


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## Jin (Mar 13, 2019)

Bro Bundy said:


> If u got shit to add to help people that mayb zilla missed make your own thread



Agreed. Let’s keep on track here.  Please respect the leader of this forum and the works he has put in.


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## Straight30weight (Mar 13, 2019)

MrRippedZilla said:


> I place you on the ignore list. Nothing personal & certainly no disrespect intended


Is there really an ignore list?? I need to find that


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## HollyWoodCole (Mar 13, 2019)

Definitely wasn't trying to cause a pissing contest.  

I'm very thankful that we have educated members here that can help chase down issues and eradicate broscience with real science. Ordering up a test in the next day or so to show results for E2 and prolactin both, my guess is that prolactin will be elevated.


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## hulksmash (Mar 13, 2019)

Bro Bundy said:


> If u got shit to add to help people that mayb zilla missed make your own thread



-prolactin could be messed with by things beside d2 mechanisms
That was it, my only point

*I will apologize for being confrontational.*
I got insulted so I wanna split the dude's wig as a reflex
That reflex wasn't controlled (doesn't matter why), so I'm sorry.

I want to be a gentleman and keep it cordial, really.



Jin said:


> Agreed. Let’s keep on track here. Please respect the leader of this forum and the works he has put in.


Agreed and apologized.

I also blame Zilla's posts being read and appreciated, while mine saying the exact same things were always ignored. "Hulksmash" means keep scrolling around here. Zilla, sorry for getting jealous.


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## Straight30weight (Mar 13, 2019)

hulksmash said:


> Agreed and apologized.
> 
> I also blame Zilla's posts being read and appreciated, while mine saying the exact same things were always ignored. "Hulksmash" means keep scrolling around here.
> 
> Zilla, sorry for getting jealous.


Can I shed a little light on why that may be? You come off as completely reckless. Seriously man, you do things that are so far out that how can people take you seriously? You have a huge knowledge base, you know some shit, yet you become paralyzed and act like it’s not a big deal. People don’t just lose the function of their legs for periods of time! Slow down man, people will listen to you but not if you’re on here talking about all the shit you take (which isn’t normal) and then you’re paralyzed yet you never had any trauma. People relate that shit. 

Dont take offense to that that cause I don’t mean it offensively. All I’m saying is theres a reason people scroll past.


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## PillarofBalance (Mar 13, 2019)

This is a section for scientific stuff. If you all want to explore feelings, a section that Zilla mods is gonna be the wrong place for that. 

Take it to pm?


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## HollyWoodCole (Mar 13, 2019)

Looking through PrivateMD for the right blood test is a little confusing.  From what I've seen there is a test that includes Prolactin for a total of $102 but hormone levels will only be shown as >1500.

To get a full view of any hormone levels in excess of 1500 you have to get a different type of test done and it doesn't appear as though prolactin is bundled into any of those.  Below is what I think is the way to go, can someone confirm this?

Hormone Panel with Testosterone LC/MS-MS  $88.99
*Prolactin  $50.49

*Total: $139.48*


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## HollyWoodCole (Mar 13, 2019)

Hormone Panel with Testosterone LC/MS-MS  

Includes: 
Complete Blood Count (CBC) w/ Differential: Hematocrit; hemoglobin; mean corpuscular volume (MCV); mean corpuscular hemoglobin (MCH); mean corpuscular hemoglobin concentration (MCHC); red cell distribution width (RDW); percentage and absolute differential counts; platelet count; red cell count; white blood cell count; immature granulocytes 
Comprehensive Metabolic Profile ( includes eGFR ): A:G ratio; albumin, serum; alkaline phosphatase, serum; ALT (SGPT); AST (SGOT); bilirubin, total; BUN; BUN:creatinine ratio; calcium, serum; carbon dioxide, total; chloride, serum; creatinine, serum; globulin, total; glucose, serum; potassium, serum; protein, total, serum; sodium, serum; eGFR 
Estradiol 
Follicle-Stimulating Hormone (FSH) 
Luteinizing Hormone (LH) 
Testosterone, Total - Women, Children, and Hypogonadal Males, LC/MS-MS

Note: Actual Total Testosterone levels will be provided with this test if levels exceed 1500. 

Patient Instructions: Patient should fast for 12 hours preceding collection of specimen. If using a testosterone cream please be sure you have not rubbed any into the antecubital area of your arm for the last 24 hours as it can give elevated results. 

Estimated turnaround for results is 7 business days.  If confirmation testing is required, the estimated time may be extended.


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## MrRippedZilla (Mar 13, 2019)

HollyWoodCole said:


> Looking through PrivateMD for the right blood test is a little confusing.  From what I've seen there is a test that includes Prolactin for a total of $102 but hormone levels will only be shown as >1500.
> To get a full view of any hormone levels in excess of 1500 you have to get a different type of test done and it doesn't appear as though prolactin is bundled into any of those.  Below is what I think is the way to go, can someone confirm this?
> Hormone Panel with Testosterone LC/MS-MS  $88.99
> *Prolactin  $50.49
> *Total: $139.48*


This one, for $122.99, gives you Prolactin, sensitive E2 and LC/MS for testosterone (so you'll see your real levels even if they are above 1500): https://www.privatemdlabs.com/lab_t...s&show=3090&category=14&search=prolactin#3090

Unless I'm missing something obvious, it would seem to be the most cost effective option to go with.


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## HollyWoodCole (Mar 13, 2019)

MrRippedZilla said:


> This one, for $122.99, gives you Prolactin, sensitive E2 and LC/MS for testosterone (so you'll see your real levels even if they are above 1500): https://www.privatemdlabs.com/lab_t...s&show=3090&category=14&search=prolactin#3090
> 
> Unless I'm missing something obvious, it would seem to be the most cost effective option to go with.


Very much appreciated Zilla, not sure why I couldn't find that myself.  I'll get it ordered up and see when I can get in for testing.


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## hulksmash (Mar 13, 2019)

PillarofBalance said:


> This is a section for scientific stuff. If you all want to explore feelings, a section that Zilla mods is gonna be the wrong place for that.
> 
> Take it to pm?



10-4, I got ya loud and clear


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## dk8594 (Mar 13, 2019)

MrRippedZilla said:


> This one, for $122.99, gives you Prolactin, sensitive E2 and LC/MS for testosterone (so you'll see your real levels even if they are above 1500): https://www.privatemdlabs.com/lab_t...s&show=3090&category=14&search=prolactin#3090
> 
> Unless I'm missing something obvious, it would seem to be the most cost effective option to go with.



This is the one I use.  I have tried different combinations and this one always ended up being the cheapest.


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## HollyWoodCole (Mar 14, 2019)

I'll be going in shortly for the blood draw and it says it will take 10-14 days for results to post.

I'm honestly hoping I do see elevated prolactin as that seems like it would be a pretty easy fix.


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## Texan69 (Mar 15, 2019)

You mentioned two ways of dealing with high prolactin and one was doing nothing about it if you are asymptotic, I’m assuming this means high prolactin levels will go back down on its own after what causes the elevation is out of you system? Is this correct? 
Thank you for the awesome post as well!! Very helpful and you made it very easy to follow along with and understand 
you’re a true asset to this board Zilla!!!


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## MrRippedZilla (Mar 15, 2019)

Texan69 said:


> You mentioned two ways of dealing with high prolactin and one was doing nothing about it if you are asymptotic, I’m assuming this means high prolactin levels will go back down on its own after what causes the elevation is out of you system? Is this correct?
> Thank you for the awesome post as well!! Very helpful and you made it very easy to follow along with and understand
> you’re a true asset to this board Zilla!!!


Prolactin levels will return to normal once your cycle is over, yes


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## hulksmash (Mar 15, 2019)

MrRippedZilla said:


> Prolactin levels will return to normal once your cycle is over, yes



Has this been proven?

Common sense says that should be true.

However, messing with hormones can have permanent effects, like increased satellite cell count.

Some people may keep ****ed prolactin levels after cycling off and never know. Then they cycle again. The ****ed hormone levels, like prolactin, would continue to **** them forever.

A curious hypothesis of mine, that's all.


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## ToolSteel (Apr 29, 2019)

Finally took the time to listen to the whole thing. 

HIGHLY RECOMMEND IT 

Thanks again for doing this zilla.


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## Mythos (Apr 30, 2019)

I listened to the whole thing.. Very interesting. The one thing I wonder is what are the consequences if you really let prolactin get away from you.. Is it anything beyond sort of annoying side effects or can you have any major issues.?


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## MrRippedZilla (Apr 30, 2019)

Mythos said:


> I listened to the whole thing.. Very interesting. The one thing I wonder is what are the consequences if you really let prolactin get away from you.. Is it anything beyond sort of annoying side effects or can you have any major issues.?


I noted the main side effects in the OP. The worst being galaactorrhea and the sexual stuff (premature ejaculation, ed, etc). I would certainly classify galaactorrhea as a major issue and much more than simply "annoying". In fact, pretty sure the folks who develop that side would be tempted to shoot you for dismissing it's severity like that 

Hyperprolactinemia won't kill you. It'll just reduce the quality of life fairly drastically. I'm a quality over quantity kind of guy so, for me, that's worse.


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## Mythos (Apr 30, 2019)

I don't know how bad it can get but guess I picture galactorrhea as being a little occasional seepage but I imagine even a little has to be embarrassing and scary as shite. 
I guess the bottom line is that we're not taking the cardiovascular risks of using AAS just to be shite in bed and seeping man milk.


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## Crom (May 12, 2021)

Just read over the notes. Not sure if this is true or not. I heard B6 can help with prolactin. Is this true? Healthy prolactin levels would improve ones refractory times correct?


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## MrRippedZilla (May 12, 2021)

Crom said:


> Just read over the notes. Not sure if this is true or not. I heard B6 can help with prolactin. Is this true? Healthy prolactin levels would improve ones refractory times correct?


B6 does a good job, yes. No idea about how to use it because the scientific community gave up on it long ago once we got better drugs (DAs) and...so did I. I'll let others chime in with dosing, etc. 

On paper lowering your prolactin levels should help with refractory times. I personally noticed little difference. Probably because I never had a problem to begin with (#humblebrag).


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## CJ (May 12, 2021)

These 2 studies convinced me to preemptively use B6 during my cycles with Tren and NPP, although I had Caber on hand, just in case. 

There's a link in this link to download the full paper... 
"(PDF) The Role of Vitamin B6 in Reducing Serum Prolactin in Comparison to Cabergoline" https://www.researchgate.net/public..._Serum_Prolactin_in_Comparison_to_Cabergoline


"Effects of pyridoxine hydrochloride (vitamin B6) on chlorpromazine-induced serum prolactin rise in male rats - PubMed" https://pubmed.ncbi.nlm.nih.gov/501547/

My prolactin levels tested in range using B6, but there's no way to tell if that would've been the case regardless. I considered it an insurance policy.

I've heard a couple of people say it has to be used preemptively for it to work though, you can't just take it if you run into an issue. No idea if that's true or not though.


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## MrRippedZilla (Sep 22, 2021)

CJ275 said:


> I've heard a couple of people say it has to be used preemptively for it to work though, you can't just take it if you run into an issue. No idea if that's true or not though.


Not ideal. You don't really want to bring in problem solvers unless you have a problem. Some level of pyridoxine neuropathy might also be an issue with high doses + long periods of use - again, someone who's looked into it more would have to comment. 

My overall thoughts on B6 can be found here. I have nothing against people opting for it - cheaper for sure - but not for me personally. Caber is the gold standard for prolactinomas, it's side effects are greatly exaggerated at the doses we're dealing with, and B6 is never mentioned in any of the references I cited in the OP. The latter point in particular kills it as an option. JMO, my 2c, etc.


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