posted Mon, 01/14/2013 - 06:45
1882
Gyno??!!**
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Okay here we go.. Im 32 180pounds,very lean.. Been off the test c for near a month was doing 500mg for 14 weeks.POst cycled 40 mg novaldex for two weeks 20 for a week an a half now. also started at the end of the test cylce ghrp6 and cjc no dac. 100mcg twice a day.. Well woke up this morning itchy sore nips..Bummer! I also take remeron, which has been shown to lower prolaction levels.. Anyone wanna chime in? Any ideas would be a great help..
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miloif i knew how to post graphs id post them..Remeron lowers ur prolactin and cortisol..i dont care what the sero or the nore does.. I wouldnt care if it did back flips, bottom line is it drops lactin, so does Wellbutrin..because there dopamine agonist... I ordered my prami and I posted to figure out a game plan.. I dont need to argue about..
Yea I been taking wellbutrin for 4 years and it wasn't enough to lower prolactin.
I also used prami and its been great!!
to avoid sides with prami, start very low. Dose it at 0.1mg 1 hour before bed. Do this for 2 days then bump up to 0.2/0.25. You can slowly work your way up to 0.5 if 0.25 isn't cutting it. Though 0.25 should knock it out.
miloIn the present study the effects of acute PO-administration of 15 mg mirtazapine on the growth hormone (GH), prolactin (PRL), and cortisol (COR) secretion were examined in eight physically and mentally healthy male subjects, compared to placebo. Mirtazapine is a new antidepressant agent which does not inhibit the reuptake of norepinephrine or serotonin but is an antagonist of presynaptic and, presumably, postsynaptic alpha 2-receptors as well as an antagonist of postsynaptic 5-HT2 and 5-HT3-receptors. After insertion of an i.v. catheter, blood samples were drawn 1 h prior to the administration of mirtazapine or placebo, at time of application, and during the time of 4 h after application in periods of 30 min. Plasma concentrations of GH, PRL, and COR were determined in each blood sample by double antibody RIA methods. The area under the curve (AUC) value was used as parameter for the GH, PRL, and COR response. With respect to GH and PRL secretion, mirtazapine did not show any effects in comparison with placebo. However, in all subjects, the COR concentrations were remarkably lower after mirtazapine compared to placebo, the difference being obvious in the mean value graphs 60 min after the application up to the end of the measurement period. The t-test for paired samples revealed a highly significant difference (P < 0.01) in COR-AUC-values between the mirtazapine group (mean COR-AUC: 1558.07 micrograms/100 ml x 240 min) and the placebo group (mean COR-AUC: 2698.86 micrograms/100 ml x 240 min). Further studies have to elucidate the question whether the demonstrated inhibition of COR secretion after application of 15 mg mirtazapine is caused by central or peripheral effects of this substance.
"Mirtazapine is a new antidepressant agent which does not inhibit the reuptake of norepinephrine or serotonin but is an antagonist of presynaptic and, presumably, postsynaptic alpha 2-receptors as well as an antagonist of postsynaptic 5-HT2 and 5-HT3-receptors."
Bro read this.
IT DOES NOT INHIBIT the reuptake of norepinephrine or serotonin. (REMEMBER reuptake means regulating and lowering.) so if it does not inhibit the reuptake then it does not lower norepinephrine & sero. levels.
It is an antagonist of alpha2 autoreceptors. Alpha2 autoreceptor is part of the feedback loop in signal transduction. Basically alpha2 recycles neurotransmitters. Since remeron is an antagonist it reduces the amount recycled resulting in high sero and norad levels.
miloIts opposite..google it
"It is a noradrenergic and specific serotonergic antidepressant (NaSSA) that acts by antagonizing the adrenergic alpha2-autoreceptors and alpha2-heteroreceptors as well as by blocking 5-HT2 and 5-HT3 receptors. It enhances, therefore, the release of norepinephrine and 5-HT1A-mediated serotonergic transmission."
http://www.ncbi.nlm.nih.gov/pubmed/11607047
The 5-HT receptors are associated with serotonin.
The alpha2 autoreceptor lowers norepinephrine levels, and Remeron antagonizes the autoreceptor. Resulting in higher adrenaline levels.
remeron is actually an anti depressant that specifically targets serotonin and norepinephrine. High levels of serotonin = high prolactin levels.
Working amazing. Nips no longer puffy, libido is good, and zero sides. There were a little sides first week but none now.
less sides than caber for me. Caber made me tired all day and sick to the stomach and headaches.
miloyes it is a dopamine agonist.. i ordered some prami.. but in the meantime im pounding the b6.
GHRP can significantly increase prolactin in people sensitive. Remeron is not enough to control prolactin.
if prolactin is the issue and you dont have access to caber/prami start dosing b6 2x day at 300mg
IronCladdthe gyno is comingfrom the peptides. I came off last cycle and started ghrp6 and cjc no dac as a bridge. after my month long pct everything was fine, istopped ai's and continued the peptides. A month later puffy sore ass nip, took caber for a few days as advised and it went away. I do believe prolactin to be an issue when using peptides, from my personal experience. g/l
miloIronclad, thats what I was thinking to, possible prolactin issuse.. But the remeron I take is also a dopamine agonist..I beleive... This sucks..
miloUsed Arimidex .50 when needed..No clomid..Just novaldex 40mg 2wk,
20mg 1 1/2wk..Im still on the 20mg novla
I expect the peptides to help me aid in sticking my gains from the test,maybe lean me out a little more..(so far the peps work well) Just dont understand where the gyno is coming from..
What AI's did you run during the cycle and at what dosage?
Did you use clomid for your PCT?
What results did you expect to get from the GHRP-6 and CJC w/out DAC?