B6 as an Alternative to Caber/Bromo/Prami?

[vtje6wu9]

With the recent crackdown on the chem. companies I'm finding myself wishing I ordered cabergoline in advance, as my local source is useless for ancillaries. I've utilized B6 in the past for recovery, but does anyone have experience using it solely as their prolaction inhibitor? Also, what's a suggested dose? I'm guessing we'd be looking at near 1g per day.

[Swifto]

1g/ED! Are you kidding?

How did you get to that figure?

100-150mg is what I suggest because any higher and you risk damaging the CNS.

[Swifto]

I've said this a million times, but becuase on how prolactin is regulated (by estrogen) if you control estrogen, you will control prolactin. Its called the Long Feedback Mechanism.

Here is some data supporting my theory:



Clin Endocrinol (Oxf) 1982 Nov;17(5):495-9 Related Articles, Links


Hydrotestolactone lowers serum oestradiol and PRL levels in normal men: evidence of a role of oestradiol in prl secretion.

D'Agata R, Aliffi A, Maugeri G, Mongioi A, Vicari E, Gulizia S, Polosa P.

The effect on serum PRL levels of lowering serum oestradiol (E2) concentration by short-term administration of an aromatase activity inhibitor, hydrotestolactone (HT), was studied in six healthy male subjects. After HT administration serum E2 levels decreased from 68 +/- 5.8 to 26 +/- 2.5 pmol/l (mean +/- SE, P less than 0.05). These E2 changes were accompanied by a significant decrease in mean 2-h PRL levels from 11.2 +/- 2.1 to 6.5 +/- 1.6 ng/ml mean +/- SE, P less than 0.05) . The evaluation of individual percentage change from basal concentrations showed a varying decrease in all subjects. These findings suggest that under physiological conditions E2 may be one of the factors which control blood PRL concentrations in men.

---------------------------------------

Acta Endocrinol (Copenh) 1984 Feb;105(2):167-72

Testosterone-induced hyperprolactinaemia in a patient with a disturbance of hypothalamo-pituitary regulation.

Nicoletti I, Filipponi P, Fedeli L, Ambrosi F, Gregorini G, Santeusanio F.

A case of a patient with hypopituitarism due to a disturbance of hypothalamo-pituitary regulation is presented, who developed high-grade hyperprolactinaemia after the initiation of substitutive therapy with testosterone esthers.The increase in serum Prl was strictly related to testosterone aromatization to oestradiol, since anti-oestrogen compounds were effective in reducing (clomiphene) or abolishing (tamoxifen) the enhanced Prl secretion. The oestrogen effect in raising Prl release was not attributable to a reduction in the dopamine inhibition of Prl-secreting cells, as the dopamine-antagonist domperidone failed to increase Prl serum levels in the same patient. This suggests that, in man, the oestrogen effect in enhancing Prl release is mainly enacted directly on the pituitary lactotrophs rather than exerted through a reduction in the hypothalamic dopamine activity

-------------------------------------

Effect of androgenic anabolic steroids on sperm quality and serum hormone levels in adult male bodybuilders.

Torres-Calleja J, Gonzalez-Unzaga M, DeCelis-Carrillo R, Calzada-Sanchez L, Pedron N.

Unidad de Investigacion Medica en Biologia de la Reproduccion, Instituto Mexicano del Seguro Social, Mexico, DF.

The purpose of this study was to assess the influence of the administration of high doses of androgenic anabolic steroids (AAS) on endocrine and semen parameters. Thirty volunteering bodybuilders were studied (ages ranging between 26.6 +/- 4.1 years). A history of anabolic steroid administration was recorded for fifteen subjects, and results of semen analysis and endocrine parameters were compared with data from fifteen bodybuilders not using steroids. In those subjects using AAS, eight had sperm counts under the lower normal limit (20 x 10(6) sperm/ml), three had azoospermia, two polyzoospermia, and two had normal sperm counts. The percentage of morphologically normal sperm was significantly reduced, only 17.7% had normal spermatozoa. In the control group, only one subject had oligozoospermia.The hormonal parameters revealed reduced FSH (1.5 +/- 3.2 vs 5.0 +/- 1.6, p < 0.001) and PRL (5.1 +/- 4.9 vs 9.2 +/- 4.4, p < 0.01) levels. LH, T, E2 and DHEA levels did not vary.

[vtje6wu9]

If I recall correctly, the studies I read suggested that 300mg-500mg admistered intraveniously would equate to the same benefit offered by the typical dosages of bromocriptine with minimal-to-no side effects. Given the fact my administration would be oral, I assumed approx. 2-2.5 times the dosage would be required.

Seeing your response is somewhat frightening as I've never been a believer in controlling estrogen to control prolactin (as the most efficient method that is), but of course I'm aware of your knowledge, and am really in no position to debate what you have to say. I'm going to give your data a read, and see if I can dig around and find the studies I had previously encountered to hear further elaboration from yourself. Thanks for the help Swifto, always appreciated. Any other elaboration on the matter you can provide would be a great asset.

[vtje6wu9]

I'd also like to note through my experiences I've been obnoxiously sensative to 19-nors. Running as little as 125mg of deca per week has caused me erectile issues and nipple sensativity (without any ancillaries), compared to running as much as 1.5g of test per week having caused no issues (without any ancillaries).

[Swifto]

You asked for it, you got it:



Sodi R, Fikri R, Diver M, Ranganath L, Vora J.

Testosterone replacement-induced hyperprolactinaemia: case report and review of the literature. Ann Clin Biochem 2005;42(Pt 2):153-9.

Half of all men with prolactin (PRL)-producing macroadenomas present with hypogonadism, decreased libido and impotence, and therefore require testosterone replacement. However, very little is known about the effect of testosterone on prolactinomas. We report a case of an 18-year-old obese man who presented with hypogonadism and hyperprolactinaemia and underwent a transphenoidal hypophysectomy after a computer tomography scan showed the presence of a suprasellar macroadenoma. On separate occasions, we documented a rise in PRL when testosterone replacement was started and a fall in PRL when testosterone replacement was stopped (r = 0.6090, P = 0.0095). Furthermore, imaging studies suggested the possibility of tumour re-growth after testosterone therapy. We hypothesize that the exogenous testosterone was aromatized to oestradiol, which stimulated the release of PRL by the anterior pituitary. This was supported by the increase in oestradiol levels after testosterone replacement, although statistical significance was not achieved due to the availability of only a few data points. This case highlights the need to be aware of testosterone-replacement-induced hyperprolactinaemia, an under-recognized complication of androgen replacement in this setting. The use of aromatase inhibitors together with testosterone-replacement therapy or the use of non-aromatizable androgens might be indicated in such patients. Taken together, this report and previous studies show that dopamine agonists apparently do not suppress the hyperprolactinaemia induced by testosterone replacement.


Gill-Sharma MK. Prolactin and male fertility: the long and short feedback regulation.

Int J Endocrinol 2009;2009:687259.

In the last 20 years, a pituitary-hypothalamus tissue culture system with intact neural and portal connections has been developed in our lab and used to understand the feedback mechanisms that regulate the secretions of adenohypophyseal hormones and fertility of male rats. In the last decade, several in vivo rat models have also been developed in our lab with a view to substantiate the in vitro findings, in order to delineate the role of pituitary hormones in the regulation of fertility of male rats. These studies have relied on both surgical and pharmacological interventions to modulate the secretions of gonadotropins and testosterone. The interrelationship between the circadian release of reproductive hormones has also been ascertained in normal men. Our studies suggest that testosterone regulates the secretion of prolactin through a long feedback mechanism, which appears to have been conserved from rats to humans. These studies have filled in a major lacuna pertaining to the role of prolactin in male reproductive physiology by demonstrating the interdependence between testosterone and prolactin. Systemic levels of prolactin play a deterministic role in the mechanism of chromatin condensation during spermiogenesis.


Gillam MP, Middler S, Freed DJ, Molitch ME.

The novel use of very high doses of cabergoline and a combination of testosterone and an aromatase inhibitor in the treatment of a giant prolactinoma

J Clin Endocrinol Metab 2002;87(10):4447-51.

Most prolactinomas respond rapidly to low doses of dopamine agonists. Occasionally, stepwise increases in doses of these agents are needed to achieve gradual prolactin (PRL) reductions. Approximately 50% of treated men remain hypogonadal, yet testosterone replacement may stimulate hyperprolactinemia. A 34-yr-old male with a pituitary macroadenoma was found to have a PRL level of 10,362 micro g/liter and testosterone level of 3.5 nmol/liter. Eleven months of dopamine agonist therapy at standard doses lowered PRL levels to 299 micro g/liter. Subsequent stepwise increases in cabergoline (3 mg daily) further lowered PRL levels to 71 micro g/liter, but hypogonadism persisted. Initiation of testosterone replacement resulted in a rise and discontinuation in a fall of PRL levels. Aromatization of exogenous testosterone to estradiol and subsequent estrogen-stimulated PRL release was suspected. Concomitant use of cabergoline with the aromatase inhibitor anastrozole after resuming testosterone replacement resulted in the maintenance of testosterone levels and restoration of normal sexual function, without increasing PRL. Ultimately, further reduction in PRL on this therapy permitted endogenous testosterone production. Thus, novel pharmacological maneuvers may permit successful medical treatment of some patients with invasive macroprolactinomas.


Prior JC, Cox TA, Fairholm D, Kostashuk E, Nugent R.

Testosterone-related exacerbation of a prolactin-producing macroadenoma: possible role for estrogen.

J Clin Endocrinol Metab 1987;64(2):391-4.

Men with PRL-producing macroadenomas often present with hypogonadism and impotence. This report documents exacerbation of a PRL-secreting tumor after two separate 200-mg testosterone enanthate (T) injections despite continued bromocriptine (BRC) therapy. A 37-yr-old man with a 60-mm invasive tumor and a serum PRL level of 13,969 +/- 332 ng/ml (mean +/- SD) responded to BRC therapy with rapid disappearance of visual field defect, headache, and facial pain as well as decrease in serum PRL to 5,103 +/- 1,446 ng/ml. T injection was followed by severe headache, facial pain, and increase in PRL to 13,471 ng/ml. Visual field deterioration and increased tumor size (height, 40-43 mm) by computed tomography were documented. A relationship between T injection and exacerbation of the prolactinoma was not recognized until after a second T injection 3 months later. After that therapy, baseline PRL increased from 6,900 to 12,995 ng/ml. The hypothesis that T was aromatized to estradiol, directly stimulating lactotrophs, was supported by an increase in serum estradiol from 24 to 51 pg/ml after the second T injection. Although T treatment is accepted as appropriate therapy for hypogonadism in men with prolactinomas, it may not only interfere with the response of the tumor to BRC therapy, but even stimulate tumor growth and secretion.


I have two PDF's as well, which I cannot upload and make for VERY good ready. If you PM me your email addy, I will forward them too you.

In fact, post your email as you cannot PM and I will remove it.

[vtje6wu9]

My username at safe-mail.net.

Thanks again! More data to read the better. So, in your advice, running exemestane at a managable dosage would be optimal?

[Ashop]

With the recent crackdown on the chem. companies I'm finding myself wishing I ordered cabergoline in advance, as my local source is useless for ancillaries. I've utilized B6 in the past for recovery, but does anyone have experience using it solely as their prolaction inhibitor? Also, what's a suggested dose? I'm guessing we'd be looking at near 1g per day.

You could try the B6 and report back to us what you experience.

[Swifto]

My username at safe-mail.net.

Thanks again! More data to read the better. So, in your advice, running exemestane at a managable dosage would be optimal?

Email sent. Let me know what you think here.

Run an AI, Aromasin 10mg/ED and keep a D2-agonist on hand if you need it run it.

Same with Tamoxifen, kept on hand.

If you're getting those sort of sides from 19-Nor's, it may be prolactin causing your issues.

[Swifto]

You could try the B6 and report back to us what you experience.

AI + B6 on cycle.

D2-agonist + Tamox on hand.

Good call A lin.

[vtje6wu9]

Email sent. Let me know what you think here.

Run an AI, Aromasin 10mg/ED and keep a D2-agonist on hand if you need it run it.

Same with Tamoxifen, kept on hand.

If you're getting those sort of sides from 19-Nor's, it may be prolactin causing your issues.

Always have a bottle of tamox and clomid laying around, just in case. As for having the D2-agonist, that was my primary reason for pursuing B6: I no longer have a source without AR-R, RUI, or Great White - since my local supplier is useless. So I'm really looking for OTC options.

I also hinted at the arimidex in hope you'd give the nod. Personally, I much prefer the properties of aromasin, but my local supplier only has adex. Do you feel adex in conjunction with B6 would be sufficient, knowing I have no other course of action to take against the prolactin? I have recently spoke with a local business owner whom has suggested a variety of supplements for the cause, however I haven't had the time to research them (one of which I believe was Vitex).

I suppose outlining my current cycle may be of benefit as well: generally I am running between 500mg-750mg of test per week for 13 weeks (frontloading with a short esther and tapering off into a long esther). In addition I am running 250mg (or less) of deca through 11 weeks. And for orals I've got four weeks of dbol at the beginning and four weeks of winny towards the end.

Another quick question (you're probably dreading responding to this thread :P): do you believe I have a genetic inclination to suffer prolactin related issues, or could this be associated with my diet/lifestyle? I'm having a tough time putting my finger on it. Perhaps some bloodwork could be of assistance.

[vtje6wu9]

Also, thanks for the e-mail Swifto, will check it out after work tonight.

[mastablasta7]

Use Aromasin from the beginning of your cycle and you wont have problems. If you start to feel some gyno then use b-6 at 400mg/d for a couple days then lower to 100mg/d.
Also torem will help stop tren gyno, i remember reading a study that showed it lowered prolactin.

[dec11]

I've said this a million times, but becuase on how prolactin is regulated (by estrogen) if you control estrogen, you will control prolactin. Its called the Long Feedback Mechanism.

Here is some data supporting my theory:



Clin Endocrinol (Oxf) 1982 Nov;17(5):495-9 Related Articles, Links


Hydrotestolactone lowers serum oestradiol and PRL levels in normal men: evidence of a role of oestradiol in prl secretion.

D'Agata R, Aliffi A, Maugeri G, Mongioi A, Vicari E, Gulizia S, Polosa P.

The effect on serum PRL levels of lowering serum oestradiol (E2) concentration by short-term administration of an aromatase activity inhibitor, hydrotestolactone (HT), was studied in six healthy male subjects. After HT administration serum E2 levels decreased from 68 +/- 5.8 to 26 +/- 2.5 pmol/l (mean +/- SE, P less than 0.05). These E2 changes were accompanied by a significant decrease in mean 2-h PRL levels from 11.2 +/- 2.1 to 6.5 +/- 1.6 ng/ml mean +/- SE, P less than 0.05) . The evaluation of individual percentage change from basal concentrations showed a varying decrease in all subjects. These findings suggest that under physiological conditions E2 may be one of the factors which control blood PRL concentrations in men.

---------------------------------------

Acta Endocrinol (Copenh) 1984 Feb;105(2):167-72

Testosterone-induced hyperprolactinaemia in a patient with a disturbance of hypothalamo-pituitary regulation.

Nicoletti I, Filipponi P, Fedeli L, Ambrosi F, Gregorini G, Santeusanio F.

A case of a patient with hypopituitarism due to a disturbance of hypothalamo-pituitary regulation is presented, who developed high-grade hyperprolactinaemia after the initiation of substitutive therapy with testosterone esthers.The increase in serum Prl was strictly related to testosterone aromatization to oestradiol, since anti-oestrogen compounds were effective in reducing (clomiphene) or abolishing (tamoxifen) the enhanced Prl secretion. The oestrogen effect in raising Prl release was not attributable to a reduction in the dopamine inhibition of Prl-secreting cells, as the dopamine-antagonist domperidone failed to increase Prl serum levels in the same patient. This suggests that, in man, the oestrogen effect in enhancing Prl release is mainly enacted directly on the pituitary lactotrophs rather than exerted through a reduction in the hypothalamic dopamine activity

-------------------------------------

Effect of androgenic anabolic steroids on sperm quality and serum hormone levels in adult male bodybuilders.

Torres-Calleja J, Gonzalez-Unzaga M, DeCelis-Carrillo R, Calzada-Sanchez L, Pedron N.

Unidad de Investigacion Medica en Biologia de la Reproduccion, Instituto Mexicano del Seguro Social, Mexico, DF.

The purpose of this study was to assess the influence of the administration of high doses of androgenic anabolic steroids (AAS) on endocrine and semen parameters. Thirty volunteering bodybuilders were studied (ages ranging between 26.6 +/- 4.1 years). A history of anabolic steroid administration was recorded for fifteen subjects, and results of semen analysis and endocrine parameters were compared with data from fifteen bodybuilders not using steroids. In those subjects using AAS, eight had sperm counts under the lower normal limit (20 x 10(6) sperm/ml), three had azoospermia, two polyzoospermia, and two had normal sperm counts. The percentage of morphologically normal sperm was significantly reduced, only 17.7% had normal spermatozoa. In the control group, only one subject had oligozoospermia.The hormonal parameters revealed reduced FSH (1.5 +/- 3.2 vs 5.0 +/- 1.6, p < 0.001) and PRL (5.1 +/- 4.9 vs 9.2 +/- 4.4, p < 0.01) levels. LH, T, E2 and DHEA levels did not vary.

i can also back this up with the fact that adex hammered my tren related gyno during a summer cycle

[dec11]

1g/ED! Are you kidding?

How did you get to that figure?

100-150mg is what I suggest because any higher and you risk damaging the CNS.

would b6 actually even do anything for this?

[Swifto]

Always have a bottle of tamox and clomid laying around, just in case. As for having the D2-agonist, that was my primary reason for pursuing B6: I no longer have a source without AR-R, RUI, or Great White - since my local supplier is useless. So I'm really looking for OTC options.

I also hinted at the arimidex in hope you'd give the nod. Personally, I much prefer the properties of aromasin, but my local supplier only has adex. Do you feel adex in conjunction with B6 would be sufficient, knowing I have no other course of action to take against the prolactin? I have recently spoke with a local business owner whom has suggested a variety of supplements for the cause, however I haven't had the time to research them (one of which I believe was Vitex).

Arimidex is fine, as long as you control estrogen. I prefer Aromasin though.

Vitex is fine as well.

I suppose outlining my current cycle may be of benefit as well: generally I am running between 500mg-750mg of test per week for 13 weeks (frontloading with a short esther and tapering off into a long esther). In addition I am running 250mg (or less) of deca through 11 weeks. And for orals I've got four weeks of dbol at the beginning and four weeks of winny towards the end.

Age, stats?

HCG 250ius 2x week in addition.

Another quick question (you're probably dreading responding to this thread :P): do you believe I have a genetic inclination to suffer prolactin related issues, or could this be associated with my diet/lifestyle? I'm having a tough time putting my finger on it. Perhaps some bloodwork could be of assistance.

Have you actually had PRL tested on cycle? As if you havent, although, your sides seem like its PRL related, I cant comment.

bolds

Use Aromasin from the beginning of your cycle and you wont have problems. If you start to feel some gyno then use b-6 at 400mg/d for a couple days then lower to 100mg/d.
Also torem will help stop tren gyno, i remember reading a study that showed it lowered prolactin.

I'd go with 200-300mg/ED, then down to 100mg/Ed perosnally. I dont like the sound of high doses of B6.

That study on Tore was also done on women and I have not read the full paper. If you have access to it? Please email it to me or PM me.

I have no idea how a SERM can lower PRL, there is no clear MOA at all. I'd be wary of it.

[Swifto]

would b6 actually even do anything for this?

Yes.

[Swifto]

vtje6wu9

I deleted your other post for obvious reasons. We cant discuss that sort of thing here.

I know you were vague, but it would be enough to raise eye brows if your a newbie.

[Pac Man]

I tried b6 but it doesn't hold a candle to Caber.

[Swifto]

I tried b6 but it doesn't hold a candle to Caber.

Also came up short against Bromocriptine.

I think we have to remember vitamins and herbs are not going to compete against drugs.

[BG]

Now would it be a good idea to add injectible b-6 if your using prami say and its just not quite cutting it? Sounds like it could be benifitial in afew ways.