So Let's Debate Conflicting Info About...

[DreDay187]

actualy all hormone comming from a derivate of sterol = steroids have influence on prolactin.

it not linked directly but, more androgenic the hormone is, and more the production of prolactine will increase. trenbolone is 300% more androgen than testosterone, in tehory even 500% more.

but we may concider than the ester used could have a ction to. more time the stroid is running inside the body, and more the body can produce prolaction by convertion.

SERM, A.I, inhibitor prolactin like cabergoline are used to prevent or reduce the prolactin formation, with succes.

we have to admit than some steroids act on descrease prolatine level, amazing but true, like stanozolol.

From my reading it's not all androgens that elevate prolactin, only aromatizable ones as estradiol has a direct influence on PRL secretion. I may be wrong but that's how I'm reading it at the moment.

 

[2rude4u]

From my reading it's not all androgens that elevate prolactin, only aromatizable ones as estradiol has a direct influence on PRL secretion. I may be wrong but that's how I'm reading it at the moment.

This is my understanding as well.

For example: Increased test = increased estro = increased prolactin.

So I guess now we need to address why the standard belief is that test, which aromatizes, does not increase prolactin and tren which does not aromatize, increases prolactin?

 

[DreDay187]

This is my understanding as well.

For example: Increased test = increased estro = increased prolactin.

So I guess now we need to address why the standard belief is that test, which aromatizes, does not increase prolactin and tren which does not aromatize, increases prolactin?

It was either you and I who had this discussion already or HeavyIron and I but the same conclusion was reached why it's always assumed the tren is causing PRL issues when many don't have blood work to support that. Anyway this is from Austinite:

19-Nortestosterone steroid such as nandrolone and Trenbolone can cause prolactin levels to become elevated MAINLY with the presence of excess estrogen. They are NOT a direct cause of high prolactin. While using prolactin inhibiting drugs will resolve issues, your first line of defense is controlling estrogen, as elevated estrogen can boost the effect of prolactin increase. It's not uncommon to prevent prolactin increase with the use of an Aromatase inhibitor (AI). But the doses of 19-Nor steroids today, may prove that is somewhat ineffective. Leading to the necessity of having a secondary (and direct) compound to combat the effects.

The way it works is entirely complicated and I couldn't even think of a way to put it in laymans terms. But in short, 19-Nor interaction with the estrogen receptors will boost prolactin secretion. This is why it's important to control estrogen first, and prolactin second. Also why I recommend that you have a secondary combat drug "on hand" and in some cases, used on cycle. You might wonder why I say "on hand", since I earlier said that low prolactin is not harmful. Well, these drugs have some fairly heavy side effects and if not used properly can really affect your progress on cycle. So it's OK to wait until needed for the sake of sanity. But I want to emphasize this again... if you have high prolactin and/or lactating, it's a near 100% confirmation that you failed to control your estrogen levels.

How To Control Prolactin

To control prolactin, or elevated prolactin, we use drugs that activate dopamine. Dopamine is a chemical launched by cells in the brain with the purpose of signaling nerve cells. So these drugs we're looking at are dopamine agonists. There are several things that affect prolactin but dopamine is the dominant one that makes the overall difference.

Dopamine works with the pituitary. They're friends, you see. But sometimes the pituitary gets a little excited and out of control, so Dopamine pays a visit to the pituitary and binds to the Dopamine receptors and slows prolactin production down to a reasonable level. This is all done with internal communication. What a nice friend to have. Make sense, folks? What a spectacular system we have. Even more reason to respect your body.

Now that we know how prolactin elevates and how to fix the problem, let's have a look at common drugs used for prolactin control. I'm getting kind of bored with this article so I'll keep this short since I still have to cover progesterone.

 

[2rude4u]

It was either you and I who had this discussion already or HeavyIron and I but the same conclusion was reached why it's always assumed the tren is causing PRL issues when many don't have blood work to support that. Anyway this is from Austinite:

This one is a little more difficult to interprete, but I believe it says the same thing.

The way I understand this is that Tren does not cause the increase in estro or prolactin, but possibly another compound increases the estro, which increases the prolactin.

From what I have read recently, I gather that PURE TREN will not aromitize or increases prolactin. However, most Tren is not Pure Tren which is where the issues arise.

 

[halfwit]

Sorry I'm late to the party, but I have yet to find a direct correlation between specific 19-nortestosterone derivatives and serum prolactin levels. The best I could do in my 15 minutes of playing on google was a study indicating the increase of PRL via progestin (which 19-nortestosterone derivatives are).

CONCLUSION:

This study demonstrated that PRL-R mRNA is expressed in both types of endometrial cells and that PRL-R mRNA and its protein are up-regulated by progestin, estrogen, and IGF-I during decidualization of endometrial stromal cells.

Source

We found a significant increase in the PRL levels on the 4th day after treatment with 100 mg of the two preparations. Moreover, we found that PRL basal values were significantly higher in those subjects whose T basal values were low.

Source
Which obviously agrees that testosterone can increase PRL values, but of course they neglect to mention why PRL is increased; which as the studies above note is a correlated effort between estrogen and prolactin via aromatization.

 

[ozzyozzy21]

Reps for all you bastards. Good stuff!

 

[Frank White]

You bastards starting fun threads while i'm at work and can't answer?! Wait...i'm too dumb to answer. Sorry guys. Interesting reading none the less...

 

[Frank White]

Double post. Original ones arent showing up until next day.

 

[2rude4u]

So taking this a step further and acknowledging that steroids increase prolactin by aromitazation into estro, it would explain excessive fat gain during cycle and difficulty dropping fat during a cut. Assuming of course that estro levels are not controlled or insufficient/no Aromatase inhibitor (AI) is utilized.


Increased body weight associated with prolactin secreting pituitary adenomas: weight loss with normalization of prolactin levels.

Greenman Y, Tordjman K, Stern N.


Source: Institute of Endocrinology, Tel Aviv-Elias Sourasky Medical Center, Israel.

OBJECTIVE:

Hyperprolactinaemia in humans may be associated with a high prevalence of obesity but the nature of this link is poorly defined. The aim of this study was to establish the relationship between hyperprolactinaemia and body weight in patients with prolactin-secreting pituitary tumours.

DESIGN:

We conducted a retrospective study of prolactinoma patients treated at the Endocrine Institute of the Tel Aviv Medical Center, Israel, during the period 1989-1996. Patients with clinically non-functioning pituitary macroadenomas (NFA) served as the control group. Data on demographic parameters, body weight before and during treatment, clinical presentation including history of weight fluctuations, tumour size as measured by computed tomography or magnetic resonance imaging, modalities and response to treatment, and pituitary function before and during treatment were recorded from medical files.

PATIENTS:

Forty-two patients with prolactinomas (PR) and 36 patients with clinically non-functioning macroadenomas (NFA) comprised the study population.

RESULTS:

Mean weight was 93 +/- 3.4 kg and 78 +/- 2.7 kg in male patients with PR and NFA respectively (P = 0.0007). Recent weight gain (8 to 22 kg) was a presenting symptom in 13 PR patients, whereas only one NFA patient had this clinical presentation (P = 0.001). Seventeen PR patients lost weight (mean change -8.3 +/- 1.5 kg, range -2-28 kg), during prolactin lowering therapy, 11 of whom had entirely normalized prolactin levels. Fourteen of the 18 patients who did not lose weight still had elevated prolactin levels (P = 0.01). Weight loss in patients with PR could not be attributed to altered pituitary function nor to compression of the third ventricle. In contrast to PR, no significant weight loss was observed in NFA patients.

CONCLUSION:

Weight gain and elevated body weight are frequently associated with prolactinomas regardless of a mass effect on the hypothalamus or pituitary function. In this series, weight loss was recorded in 70% of prolactinomas patients and in 90% of male patients who normalized their prolactin levels. We propose the inclusion of hyperprolactinaemia in the differential diagnosis of endocrine obesity and weight gain.

 

[DreDay187]

Yes estrogen being elevated can help promote fat gain or make fat loss difficult but there are many other pathways and interactions so it's not solely the result of elevated estrogen. Here's a quote from mike Arnold regarding fat loss and estrogen in context of high test on tren cycle:

Sorry, but I did not have time to read your counterpoint. However, I will provide my take on the original claim that estrogen increases fat storage. In short, the answer is yes, estrogen can indeed lead to an increased rate of fat gain, BUT (and this is an important "but") it is inaccurate to suggest that any elevation of estrogen will lead to fat gain. That is a blanket statment and no different than saying "Increasing your testosterone level will build muscle". Obviously, this is not always the case. Whenever T levels rise, the "potential" for growth may increase, but this does not mean growth will occur, as there are many possible counter-regulatory signals (either endogenous or exogenous) the human body can recieve which might override estrogen's fat storage promoting effects.

Therefore, stating that high test and tren will lead to a greater rate of fat storage over low test and tren is an assumption, as it assumes that any elevation of estrogen is sufficient for over-riding all counter-regulatory mechanisms which oppose fat storage. I can tell you right now with 100% certainty that many of these counter-regulatory mechanisms are capable of over-riding estrogen's fat storage promoting effect. In fact, they are even able to cause fat loss in the face of a ski high estrogen level. This fact is easily witnessed by watching a BB'r use a bunch of aromatizable drugs during a cutting phase. Such a BB'r may indeed have a very high systematic estrogen level, yet lose an enormous amount of bodyfat by doing nothing other than cutting calories...and this is just one of many mechanisms by which lipolysis & oxidation can be induced.

Now, it will be easier to lose bodyfat when one's estrogen level is properly managed, as it will be one less factor contributing to potential fat gain, but we certainly cannot state that elevated estrogen level result in fat gain.

 

[2rude4u]

Yes estrogen being elevated can help promote fat gain or make fat loss difficult but there are many other pathways and interactions so it's not solely the result of elevated estrogen. Here's a quote from mike Arnold regarding fat loss and estrogen in context of high test on tren cycle:

Sorry, but I did not have time to read your counterpoint. However, I will provide my take on the original claim that estrogen increases fat storage. In short, the answer is yes, estrogen can indeed lead to an increased rate of fat gain, BUT (and this is an important "but") it is inaccurate to suggest that any elevation of estrogen will lead to fat gain. That is a blanket statment and no different than saying "Increasing your testosterone level will build muscle". Obviously, this is not always the case. Whenever T levels rise, the "potential" for growth may increase, but this does not mean growth will occur, as there are many possible counter-regulatory signals (either endogenous or exogenous) the human body can recieve which might override estrogen's fat storage promoting effects.

Therefore, stating that high test and tren will lead to a greater rate of fat storage over low test and tren is an assumption, as it assumes that any elevation of estrogen is sufficient for over-riding all counter-regulatory mechanisms which oppose fat storage. I can tell you right now with 100% certainty that many of these counter-regulatory mechanisms are capable of over-riding estrogen's fat storage promoting effect. In fact, they are even able to cause fat loss in the face of a ski high estrogen level. This fact is easily witnessed by watching a BB'r use a bunch of aromatizable drugs during a cutting phase. Such a BB'r may indeed have a very high systematic estrogen level, yet lose an enormous amount of bodyfat by doing nothing other than cutting calories...and this is just one of many mechanisms by which lipolysis & oxidation can be induced.

Now, it will be easier to lose bodyfat when one's estrogen level is properly managed, as it will be one less factor contributing to potential fat gain, but we certainly cannot state that elevated estrogen level result in fat gain.

I agree with most of his statements, but I think it is difficult to make a blanket assumption, not knowing what each and every BB'r is using. We know that we are each different. Estro may not affect a small percentage of guys the way it does the majority. We also don't know what their prolactin levels might be or what they may be using to control it.

The study I posted above makes a strong arguement for keeping prolactin low. When you normalize prolaction in the study subjects and 90% lose fat, that's a very strong arguement for controlling it and estro imo.

 

[DreDay187]

I agree with most of his statements, but I think it is difficult to make a blanket assumption, not knowing what each and every BB'r is using. We know that we are each different. Estro may not affect a small percentage of guys the way it does the majority. We also don't know what their prolactin levels might be or what they may be using to control it.

The study I posted above makes a strong arguement for keeping prolactin low. When you normalize prolaction in the study subjects and 90% lose fat, that's a very strong arguement for controlling it and estro imo.

I agree with you to some degree but I only quickly glanced through your study. I didn't see any mention of diet or training control parameters which obviously would impact weight loss.

This is also one study and needs to be replicated to ensure the conclusions reached are correct but it's definitely interesting to say the least. Very nice find!

One final note is that they studied those with prolactinomas and people with PRL levels outside normal physiological ranges. We can't jump to the conclusion that lowering PRL in 'healthy' people with normal PRL levels will induce the same results or same amount of weight loss. The significance of these findings may only be applicable to those with chronically high PRL levels.

 

[DreDay187]

Do you have a link to the full study 2Rude? You made a great find and I'd love to read the entire thing before going much further.

 

[2rude4u]

I agree with you to some degree but I only quickly glanced through your study. I didn't see any mention of diet or training control parameters which obviously would impact weight loss.

This is also one study and needs to be replicated to ensure the conclusions reached are correct but it's definitely interesting to say the least. Very nice find!

One final note is that they studied those with prolactinomas and people with PRL levels outside normal physiological ranges. We can't jump to the conclusion that lowering PRL in 'healthy' people with normal PRL levels will induce the same results or same amount of weight loss. The significance of these findings may only be applicable to those with chronically high PRL levels.

My understanding of the study is they only lowered prolactin levels. I do not see mention of diet or training what-so-ever.

And yes, the study was performed utilizing subjects with elevated prolactin levels. I do not believe that those with normal levels would see any benefit by lowering it further. However, the topic of this converstaion is to address elevated levels of prolactin, not those in the normal range.

I believe now that we know even test increases prolactin it would be beneficial to many if they include prolactin in their labs.

 

[2rude4u]

Do you have a link to the full study 2Rude? You made a great find and I'd love to read the entire thing before going much further.

This was all I came with in regards to this study. I can dig a little further and see what I find.

UPDATE: Unforunatly it appears that a paid subscription is required to access the full study. However, there are many more studies I came across that specifically address increased fat and obesity in individuals with elevated prolactin, both male and female.

 

[DreDay187]

My understanding of the study is they only lowered prolactin levels. I do not see mention of diet or training what-so-ever.

My point...did they control diet or left it as a variable?

And yes, the study was performed utilizing subjects with elevated prolactin levels. I do not believe that those with normal levels would see any benefit by lowering it further. However, the topic of this converstaion is to address elevated levels of prolactin, not those in the normal range.

True and it'd be interesting to see how many of us actually have elevated PRL levels since not many get tested for it, even those on tren/deca rarely get tested and the common belief is only those compounds raise PRL.

I believe now that we know even test increases prolactin it would be beneficial to many if they include prolactin in their labs.

I will definitely be checking PRL next time I hop on the merry-go-round that's for sure

 

[2rude4u]

My point...did they control diet or left it as a variable?



True and it'd be interesting to see how many of us actually have elevated PRL levels since not many get tested for it, even those on tren/deca rarely get tested and the common belief is only those compounds raise PRL.



I will definitely be checking PRL next time I hop on the merry-go-round that's for sure

I cannot speak to the diet. All I can say is I did not read a reference to diet. I'm under the impression that they only lowered prolactin, but without the entire study I don't know for sure.

And I think checking your PRL is a good idea, since I'm willing to bet that less than 10% of this board (if that) have any clue what their levels are.

 

[DreDay187]

Another thing which should be quite obvious is to take a careful look at what, if any, prescription or OTC meds one is taking. Anything that inhibits the production or release of dopamine could artificially elevate prolactin levels. For example many anti-psychotic drugs will act as antagonists to the dopamine receptors which will adversely affect PRL levels.

 

[DreDay187]

J Neuroendocrinol. 2006 Dec;18(12):938-48.
Ovarian steroids but not the locus coeruleus regulate stress-induced prolactin secretion in female rats.
Poletini MO, Szawka RE, Franci CR, Anselmo-Franci JA.
Source
Departamento de Fisiologia, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, SP, Brazil.
Abstract
Stress has been proposed to stimulate prolactin release if its prestress levels are low, or to inhibit it if they are elevated, but the role of ovarian-steroid fluctuations in the prolactin stress response is not yet clearly understood. Because the noradrenergic nucleus locus coeruleus has been implicated in stress responses and generation of prolactin surges in female rats, the present study aimed to evaluate stress-induced prolactin secretion under different hormonal conditions, determining the effect of locus coeruleus lesion on each response. Blood samples were withdrawn from a jugular vein catheter 5 and 2 min before and 2, 5, 10, 15 and 30 min after ether stress in male rats, female rats during the oestrous cycle and ovariectomised rats treated with oil (OVX), oestradiol (OVE) or oestradiol plus progesterone (OVEP). Increased Fos immunoreactivity demonstrated locus coeruleus activation following ether stress. Ether stress increased both low (at 16.00 h in males, in OVX and on dioestrous and at 11.00 h on pro-oestrous and oestrous) and high plasma prolactin (at 16.00 h on oestrous and in OVE), but it decreased elevated prolactin levels during the afternoon on pro-oestrous and in OVEP. Locus coeruleus lesion prevented prolactin surges during the afternoon on pro-oestrous, oestrous, OVE and OVEP but did not modify either pattern (i.e. increase or decrease) or degree of prolactin stress response under any condition studied. The present data therefore suggest that oestradiol and progesterone modulate stress-induced prolactin secretion, regardless of its prestress levels. Moreover, the locus coeruleus is probably not involved in prolactin response to stress and most likely has a specific role in prolactin surges induced by ovarian steroids.
PMID: 17076769 [PubMed - indexed for MEDLINE]

Ovarian steroids but not the locus coerule... [J Neuroendocrinol. 2006] - PubMed - NCBI

 

[DreDay187]

Oh no, sex may increase PRL secretion

Psychoneuroendocrinology. 1998 May;23(4):401-11.
Neuroendocrine and cardiovascular response to sexual arousal and orgasm in men.
Krüger T, Exton MS, Pawlak C, von zur Mühlen A, Hartmann U, Schedlowski M.
Source
Division of Clinical Psychiatry, Hannover Medical School, Federal Republic of Germany.
Abstract
Data regarding the neuroendocrine response pattern to sexual arousal and orgasm in man are inconsistent. In this study, ten healthy male volunteers were continuously monitored for their cardiovascular and neuroendocrine response to sexual arousal and orgasm. Blood was continuously drawn before, during and after masturbation-induced orgasm and analyzed for plasma concentrations of adrenaline, noradrenaline, cortisol, luteinizing hormone (LH), follicle stimulating hormone (FSH), prolactin, growth hormone (GH), beta-endorphin and testosterone. Orgasm induced transient increases in heart rate, blood pressure and noradrenaline plasma levels. Prolactin plasma levels increased during orgasm and remained elevated 30 min after orgasm. In contrast, none of the other endocrine variables were significantly affected by sexual arousal and orgasm.
PMID: 9695139 [PubMed - indexed for MEDLINE]