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Thread: Prolactin sides possible from Test Prop/Masteron??

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    against_grain is offline Junior Member
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    Prolactin sides possible from Test Prop/Masteron??

    Title sums it up, been running Test Prop and masteron each at 100mgEOD. Had some clear fluid discharge from each nipple when applying pressure/squeeze- a very small amount like basically a bead of clear fluid. No lumps, no other signs of gyno.

    I had previously been running adex at 0.5mg EOD, adex from a Legit ancillaries source. So I increased Adex to 1mg ED, ran that for several weeks and still the fluid persists!

    I ordered Caber and Letro, planning to switch to these two ancillaries. Letro to follow the gyno reversal/estrogen protocols, and Caber in the event this is a prolactin issue.


    SO my question is: Can we get prolactin issues from Test/masteron? my research says not normally.

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    Docd187123 is offline Banned
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    Yes, you can get PRL increases from test

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    Test increases dopamine. Dopamine suppressed prolactin. Decreased testosterone can lead to elevated prolactin and vice versa, imho.
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    I will tell you Patrick Arnold has an interesting theory on aas and lactation and why people not even taking progestins can experience lactation. He believes it is possibly from oxytocin. I have been looking into this for some time. Its an interesting theory with some merit.

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    Testosterone replacement -induced hyperprolactinaemia: case report and review of the literature.

    Authors
    Sodi R1, Fikri R, Diver M, Ranganath L, Vora J.
    Author information
    Journal
    Ann Clin Biochem. 2005 Mar;42(Pt 2):153-9.
    Affiliation
    Abstract
    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.

    PMID 15829128 [PubMed - indexed for MEDLINE]
    Testosterone replacement-induced hyperp... - PubMed Mobile - NCBI

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    Some interesting stuff here guys:

    Pharmacological causes of hyperprolactinemia

    Def interested in what DD has to say about this.
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    Ha, that was fast!
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    Another use study:

    CLINICAL CASE SEMINAR
    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
    MARY P. GILLAM, STEWART MIDDLER, DANIEL J. FREED, AND MARK E. MOLITCH
    Division of Endocrinology, Metabolism, and Molecular Medicine (M.P.G., M.E.M.), Northwestern University, The Feinberg Medical School, Chicago, Illinois 60611; and Cedars-Sinai Medical Center (S.M.), University of California at Los Angeles School of Medicine, Los Angeles, California 90048


    Despite the effectiveness of dopamine agonists in attenu- ating hyperprolactinemia and inducing tumor shrinkage, hy- pogonadism persists in up to 50% of cases of males with macroprolactinomas, even in individuals in whom PRL lev- els are normalized (5, 8, 9). Consequently, androgen replace- ment is required in many of these patients. In general, tes- tosterone replacement is straightforward; however, testosterone replacement in this case was associated with secondary elevations in PRL levels. Evidence for the causal relationship between testosterone replacement and a rise in PRL was suggested by the observation that PRL levels de- clined when testosterone was temporarily discontinued and rose again with its readministration. We postulate that the rise in PRL was a result of the aromatization of testosterone to estradiol, which in turn stimulated PRL synthesis and release. An accumulating body of evidence suggests that estrogen plays an integral role in the pathogenesis and pro- gression of lactotroph tumors (14). Specifically, estrogen ex- erts a stimulatory effect upon PRL secretion by disrupting the inhibitory influence of dopamine; chronic exposure to es- trogen functionally uncouples the anterior pituitary D2 re- ceptor from its G protein-coupled receptor (15). Estradiol in vitro stimulates PRL gene transcription and prevents the ability of dopamine agonists to inhibit PRL synthesis and secretion (16***8211;20). In vivo, large doses of estrogens have in- duced prolactinomas in rats and may induce them in humans as well (21***8211;23).
    The frequency of testosterone-associated increases in PRL levels is unknown, because it has not been formally ad- dressed by any of the major trials evaluating dopamine ag- onist therapy in the treatment of males with macroprolacti- nomas who subsequently receive androgen replacement. In the only other report in the literature that describes this phenomenon, Prior et al. (24) reported a patient with a 6-cm invasive macroprolactinoma (initial PRL, 13,969 ***56319;***56320;g/liter) who responded to bromocriptine with a 63% reduction in PRL levels and the disappearance of his visual field defect. Testosterone replacement was followed by visual field de- terioration, increased tumor size, and return of PRL levels to baseline values. Indeed, this dramatic response is highly unusual. Testosterone replacement in the patient reported
    here led to a more modest PRL rise. Nevertheless, the re- sponse was clinically significant because it required the in- troduction of a second agent (anastrazole) to ultimately at- tenuate this effect. A study that specifically analyzes PRL responses after testosterone replacement in hypogondal males with prolactinomas would be necessary to determine whether this response is a unique behavioral characteristic of rare prolactinomas or is one that is observed more commonly.
    In the present case, the use of an aromatase inhibitor in conjunction with cabergoline facilitated testosterone replace- ment, because it prevented the secondary rise in PRL and, ultimately, the potential for tumor enlargement. The aro- matase inhibitor was specific for this effect, because discon- tinuation of anastrozole again led to rises in PRL levels. Interestingly, PRL levels reached their nadir during the pe- riod of aromatase inhibitor therapy. These levels were lower than at any other time point, including the period during which the patient was taking his maximum dose of caber- goline (21 mg/wk) without receiving testosterone. This sug- gests that further lowering of even relatively low levels of estradiol appears to have been beneficial. Consequently, the coadministration of very high doses of cabergoline with anastrozole may have permitted PRL levels to remain low for a duration sufficient to restore the normal pulsatility of GnRH. This in turn led to recovery of the endogenous go- nadal axis.
    An alternative explanation for the recovery of endogenous testosterone production in this patient may relate to the powerful effect of estradiol deficiency on stimulation of GnRH neurons. Several recent studies have confirmed the observation that lack of estradiol serves as a more potent stimulator of gonadotropin secretion than testosterone de- ficiency on a molar basis, at both the hypothalamic and pituitary level (25***8211;29).
    Short-term administration of aromatase inhibitors has not been associated with adverse effects upon protein or inter- mediary metabolism or a negative impact on body compo- sition, muscle strength, or measures of bone turnover in healthy eugonadal men (30). However, the long-term effects of aromatase inhibitors are uncertain. As observed in men afflicted with mutations in cytochrome p450 aromatase en- zyme or in the estrogen receptor ***56319;***56321; gene, chronic estrogen deficiency may have important clinical implications (31). In these individuals, estrogen deficiency has been associated with abnormal carbohydrate/lipid metabolism, abnormal skeletal development, disordered gonadotropin secretion, and infertility. Whether these effects would similarly de- velop in postpubertal males is not known.
    In summary, this case illustrates several intriguing aspects of the management of a giant prolactinoma demonstrating relative dopamine agonist resistance, including 1) the step- wise reduction in PRL levels afforded by stepwise increases in cabergoline to very high doses; 2) the disproportionate degree of pituitary tumor shrinkage despite a dramatic low- ering of PRL levels; 3) the facilitation of testosterone replace- ment by an aromatase inhibitor; and 4) eventual recovery of endogenous gonadal function. Extraordinary pharmacolog- ical maneuvers may permit successful medical treatment of some patients with invasive macroprolactinomas.

    The Journal of Clinical Endocrinology & Metabolism 87(10):4447***8211;4451 Printed in U.S.A. Copyright 2002 by The Endocrine Society doi: 10.1210/jc.2002-020426
    https://thinksteroids.com/community/...inar-pdf.7314/

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    Interesting! Especially as I have one of those f'n tumors. That said, it seems to be more related to the adenoma in this case?
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    Docd187123 is offline Banned
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    Quote Originally Posted by Michael Scally, MD
    The answers to your questions are fairly obvious. If the compound aromatizes, interacts with the estradiol receptor, then there will be an effect on prolactin secretion. The same effects would be expected in a "healthy" person taking AAS. The abstracts above address the questions directly. The estradiol produced from testosterone in testosterone replacement therapy (TRT) will "overpower" the negative dopamine agonist effect of cabergoline, therefore the use of an aromatization inhibitor.

    An overview of the regulation of prolactin secretion. Prolactin secretion is paced by a light-entrained circadian rhythm, which is modified by environmental input, with the internal milieu and reproductive stimuli affecting the inhibitory or stimulatory elements of the hypothalamic regulatory circuit. The final common pathways of the central stimulatory and inhibitory control of prolactin secretion are the neuroendocrine neurons producing prolactin inhibiting factors (PIF), such as dopamine (DA), somatostatin (SST), and gamma-aminobutyric acid (GABA), or prolactin releasing factors (PRF), such as thyrotropin releasing hormone (TRH), oxytocin (OT), and neurotensin (NT).

    PIF and PRF from the neuroendocrine neurons can be released either at the median eminence into the long portal veins or at the neurointermediate lobe, which is connected to the anterior lobe of the pituitary gland by the short portal vessels. Thus lactotrophs are regulated by blood-borne agents of central nervous system or pituitary origin (alpha-melanocyte stimulating hormone) delivered to the anterior lobe by the long or short portal veins. Lactotrophs are also influenced by PRF and PIF released from neighboring cells (paracrine regulation) or from the lactotrophs themselves (autocrine regulation).



    Direct effects of neurotransmitters, neuromodulators, and peripheral hormones on the activity of tuberoinfundibular dopaminergic system (TIDA). The inhibitory agents (left) will promote an increase of prolactin secretion as a result of diminishing TIDA activity. On the other hand, the stimulatory neurotransmitters and progesterone (right) will tend to decrease prolactin secretion as a result of increasing output of TIDA neurons.

    It should be noted, however, that many of these agents have multiple levels of action, often with opposing biological effect. Therefore, in some cases (*), effects on PRF and/or directly at the lactotrophs will prevail over the influence on TIDA activity.

    Key: 5-HT, serotonin; NE, norepinephrine; HA, histamine; EOP, endogenous opioid peptides (endorphin, enkephalin, dynorphin, nociceptin/orphanin); GAL, galanin; SST, somatostatin; CCK8, cholecystokinin-8; GABA, gamma-aminobutyric acid; NO, nitric oxide; ACh, acetylcholine; TRH, thyrotropin releasing hormone; OT, oxytocin; VP, vasopressin; VIP, vasoactive intestinal polypeptide; PACAP, pituitary adenylate cyclase-activating peptide; ANG II, angiotensin II; NT, neurotensin; NPY, neuropeptide Y; CT, calcitonin; BOM, bombesin-like peptides (gastrin-releasing peptide, neuromedin B, neuromedin C); ANP, atrial natriuretic peptides.
    Quote from Dr. Scally ^^^

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    Docd187123 is offline Banned
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    Quote Originally Posted by kelkel View Post
    Interesting! Especially as I have one of those f'n tumors. That said, it seems to be more related to the adenoma in this case?
    In the first one I posted it talks about testosterone -induced prolactinomas but I agree most of these cases have some underlying issues as well.

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    So that falls back to controlling estrogen. Interesting stuff from Scally.
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    So Scally is saying that the ai is the key if I understand him correctly. Which isnt always easy.

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    Done on rats not humans

    Horm Metab Res. 1996 Apr;28(4):171-6.
    Effects of tamoxifen on serum prolactin levels, pituitary immunoreactive prolactin cells and uterine growth in estradiol-treated ovariectomized rats. Effects of tamoxifen on serum prolactin level... [Horm Metab Res. 1996] - PubMed - NCBI
    Spritzer PM, Ribeiro MF, Oliveira MC, Barbosa-Coutinho LM, Silva IS, Dahlem N, Cericatto R, Pavanato MA.

    Abstract

    Pituitary effects of the antiestrogen tamoxifen are not well established, although estrogen is known to have a stimulatory role in prolactin secretion. Effects of tamoxifen on serum prolactin levels, pituitary wet weight and number of prolactin cells were studied. Ovariectomized female Wistar rats were injected, subcutaneously, with estradiol valerate, 50 or 300 micrograms/rat per week for 2 or 10 weeks. Tamoxifen was injected during the last days of estrogen treatment. Data were compared with two other groups, treated with estradiol valerate alone or estradiol valerate plus the dopamine agonist bromocriptine. Serum prolactin levels were increased by estrogen treatment with all doses used. Furthermore, rats treated with 300 micrograms of estradiol valerate, for 2 and 10 weeks, showed a clear increase in pituitary weight and number of prolactin cells (p < 0.05). Bromocriptine decreased prolactin levels, pituitary weight and the number of prolactin cells (p < 0.05). Tamoxifen associated to subacute period of estrogen administration resulted in a significant reduction of serum prolactin levels and pituitary weight (p < 0.05). No effects on prolactin levels or number of prolatin cells were observed with tamoxifen associated to chronic estrogen treatment. Tamoxifen also presented a dose-related inhibitory effect upon estrogen-stimulated rises in uterine weight and DNA content. In conclusion, the results of the present paper showed that tamoxifen reduced estrogen-stimulated prolactin levels in some, but not in other hormonal conditions and that these effects were not mediated by an inhibition of lactotroph cell growth. Further studies are needed to define the exact role of antiestrogens at molecular level in hyperprolactinemic states and their eventual connection with dopamine and its agonists.

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    Quote Originally Posted by Docd187123 View Post
    In the first one I posted it talks about testosterone-induced prolactinomas but I agree most of these cases have some underlying issues as well.
    My tumor's just one of my many underlying issues. Good stuff here.
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    Quote Originally Posted by kelkel View Post
    My tumor's just one of my many underlying issues. Good stuff here.
    I'm just copying and pasting them from a similar topic/discussion I had with someone on another board. We both scoured pubmed for anything prolactin related lol. I figured I'd post it up here to get your guys' opinions on it as well.

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    against_grain is offline Junior Member
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    thanks for the info! See for me the fact that I ran 1mg/day of known legit adex for several weeks indicated it is likely a prolactin issue!

    My prior research had only found prolactin issues in the 19-nor compounds (tren -deca ) So good to know prolactin issues can happen with just test!

    you guys support jumping on caber?

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    Quote Originally Posted by against_grain View Post
    thanks for the info! See for me the fact that I ran 1mg/day of known legit adex for several weeks indicated it is likely a prolactin issue!

    My prior research had only found prolactin issues in the 19-nor compounds (tren -deca ) So good to know prolactin issues can happen with just test!

    you guys support jumping on caber?
    I say yes

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    Curious if you've gotten any BW?
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    Quote Originally Posted by kelkel View Post
    Curious if you've gotten any BW?
    crossed my mind as well....

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    against_grain is offline Junior Member
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    Bloods yeah, pending.

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    against_grain is offline Junior Member
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    Here was the other thing that crossed my mind, was the possibility that my masteron was not in fact masteron. Say it was some other 19-nor compound, or a blend of mast and another compound and just mislabeled.

    I considered this, but more or less ruled it out for a few reasons

    1. I have great results from the mast, and results that IMO match with masteron's profile. (not huge gain in size but big gains in density and hardness)

    2. I believe my source to be excellent, very good reputation, and I've had many excellent products from them in the past. So it would seem a bit off for them to have mislabeled mast.

    3. I have no sexual dysfunction, in fact the opposite. My libido is pretty much as high as possible. (So no "deca -dick)

    Therefore I really do believe I have been doing legit masteron and test prop. Which says from my experience prolactin sides are def. possible with these two.

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    I think you had Mast based on what you said. I want to see bloods. I have some thoughts but I would like to see bloods before I go throwing them out there. The thing is this, if you are lactating I would start caber or prami.

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    I think you should just stop squeezing your nipples if you have no other symptoms.

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    Quote Originally Posted by Bonaparte View Post
    I think you should just stop squeezing your nipples if you have no other symptoms.
    Agreed. Only makes things much worse. Good point.

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    This is off-topic, and I hope that's OK because it looks like the question has been answered but- the OP is authenticating his Masteron by "big gains in hardness and density". How the hell can Masteron make muscles harder or more dense compared to other steroids ? What's the science?

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    Because it's a DHT, promotes fat burning and has anti-E properties. Works well if lean or prepping for a contest.
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    Quote Originally Posted by kelkel View Post
    Because it's a DHT, promotes fat burning and has anti-E properties. Works well if lean or prepping for a contest.
    That's what I was thinking too, it must be the anti-E properties. It dries you out, that's why it only shines with low body-fat. So, really, it gives a perceived hardness and density- the muscles are not actually harder or denser. Well, maybe denser if there's less water in the muscle- if that's even possible. Thanks.

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    against_grain is offline Junior Member
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    Quote Originally Posted by jimmyinkedup View Post
    Agreed. Only makes things much worse. Good point.
    I will stop this. To be honest the only reason I even noticed this was after I had shaved my chest there was essentially a blocked pore/acne/ingrown hair right at the edge of the nipple.

    So that only reason I had to squeeze that area in the first place, I wasn't just in the habit of doing that.

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    BW Posted below: The blood was taken a few days after I started Caber and Letro, So hopefully I didn't render them worthless as an assessment tool.



    ALT 32 (10-60) IU/L
    AST 27 (10-42) IU/L

    Urea 8.6 (2.5-6.6) mmol/L

    Gluc 4.6 (3.9-6.1) mmol/L

    RBC: 4.92
    WBC 7.01 (3.7-10)
    Hb 181 (130-170) g/l

    Estradiol 23 (0.0-56.0) 

    Prolactin 273 (57-281) MIU/L

    Total Test 3171 ng/dl (241-827)

    Free test 78.3 ng/dl (6.1-27/1) nmol/L

    LH 3.0 (1.24-8.62)
    FSH 4.2 (1.27-19.26)

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    Couple things:

    Estradiol is the wrong test. Need a Sensitive E2 Assay. Estradiol tends to run higher than E2 and you are already low there. Letro will crush you here so be careful.
    Prolactin is at the top, damn! Caber will turn it around for you.
    If you're on cycle how on earth can you have a viable LH & FSH reading?
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    Thanks Kelkel. -already on Caber from a legit source, any tips on dose? Ive read 0.5mg 2Xweek, that seems low?

    I just went over the form again and I misinterpreted/misread the LH and FSH readings- they were crossed out and hand written in the margin (it looked like they may have been double checked or confirmed)

    both LH and FSH were written in as <0.1 (and highlighted *facepalm*)


    So is this an extremely abnormal case? Would you define this as gyno? I've read lots and generally only found people recommending caber with 17-nor compounds.

    You agree with my plan to switch to Letro and Caber, for how long?

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    Your estrogen is fine, and your prolactin isn't that bad. Again, you can use a bit of caber, but I think you should just leave it alone.

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    Quote Originally Posted by against_grain View Post
    Thanks Kelkel. -already on Caber from a legit source, any tips on dose? Ive read 0.5mg 2Xweek, that seems low?

    I just went over the form again and I misinterpreted/misread the LH and FSH readings- they were crossed out and hand written in the margin (it looked like they may have been double checked or confirmed)

    both LH and FSH were written in as <0.1 (and highlighted *facepalm*)


    So is this an extremely abnormal case? Would you define this as gyno? I've read lots and generally only found people recommending caber with 17-nor compounds.

    You agree with my plan to switch to Letro and Caber, for how long?
    .5 caber is overkill, imho. .25 x 2 if you choose to run it.
    Much better on the LH/FSH readings....
    Not abnormal and not gyno. It's 19-Nor compounds, progestins.
    I do not agree with letro unless you follow it up with BW. Don't care for it.
    You could also heed the words of Bonaparte. Stop squeezing them and ride things out.
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    Quote Originally Posted by kelkel View Post
    .5 caber is overkill, imho. .25 x 2 if you choose to run it.
    Much better on the LH/FSH readings....
    Not abnormal and not gyno. It's 19-Nor compounds, progestins.
    I do not agree with letro unless you follow it up with BW. Don't care for it.
    You could also heed the words of Bonaparte. Stop squeezing them and ride things out.
    How are you supposed to milk it without squeezing it

    And to not hijack the thread I would agree with both Bonaparte and Kel

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    Thanks for the info/answers, I am pretty much clear on everything except where you said "its 19-Nor Compounds"
    my understanding was that masteron is defined as a DHT compound, and not in fact a 19-nor?

    I agree the letro was more of a panic reflex, I was already running lots of AI and this issue seems to be more prolactin related so the letro I don't think is necessary.




    Quote Originally Posted by kelkel View Post
    .5 caber is overkill, imho. .25 x 2 if you choose to run it.
    Much better on the LH/FSH readings....
    Not abnormal and not gyno. It's 19-Nor compounds, progestins.
    I do not agree with letro unless you follow it up with BW. Don't care for it.
    You could also heed the words of Bonaparte. Stop squeezing them and ride things out.

  37. #37
    DrewZ's Avatar
    DrewZ is offline Productive Member
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    Just read this, interesting read - thought I would chime in on my recent experience on the matter.

    Had this happen as well while on Test Cyp 250mg x2 a week + adex 0.25mg EoD.

    I did pre and mid cycle bloods - my E2 went from 25 to 42 on the sensitive test which wasn't bad but my libido wasn't as strong as it had been.

    I didn't notice that I had this problem until I gave them a squeeze around week 7.
    Note: no signs of gyno either - no tenderness, no lumps nothing, everything going smoothly.

    I upped my adex to 0.5mg EoD and upped my Zinc from 25mg to 75mg daily. Problem went away in less than 48 hours and never returned, libido got stronger too.

  38. #38
    kelkel's Avatar
    kelkel is offline HRT Specialist ~ AR-Platinum Elite-Hall of Famer ~ No Source Checks
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    Quote Originally Posted by against_grain View Post
    Thanks for the info/answers, I am pretty much clear on everything except where you said "its 19-Nor Compounds"
    my understanding was that masteron is defined as a DHT compound, and not in fact a 19-nor?
    Correct. Mast = DHT. 19 nors are tren /deca ...
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  39. #39
    Swolabetic is offline New Member
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    Bumping an old thread. I thought Materone itself had "anti prolactin" traits itself?

  40. #40
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    Octaneforce is offline Senior Member
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    Quote Originally Posted by Swolabetic View Post
    Bumping an old thread. I thought Materone itself had "anti prolactin" traits itself?
    Well i think mast just stops the symptoms of estro and prolactin, not necessarily lowering the amount found on bloodwork. I could be wrong.
    Swolabetic likes this.

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