I am in a state of confusion right now, I belong to another board and people tell me I need to run an anti-prolactin with Tren, though I have read elsewhere that this is a myth. My other question is would Dextroamphetamine have an anti-prolactin effect since it raises dopamine levels (this would be convenient since I have it and not an anti-prolactin). Also I am running Test and Tren, 3 weeks on and 3 off, would an anti-prolactin even be warranted with such a short cycle, if it is even necessary at all.
The first problem is you're getting information from other boards. Why would you do that?
Second, without a legitimate medical need for d-amphetamine, its use is pointless because you're trying to treat something that doesn't exist, i.e., trenbolone induced hyperprolactinemia.
Regardless, here are a couple of papers looking at the effect of d-amphetamine on PRL.
Horm Metab Res. 1983 Sep;15(9):439-43.
Prolactin lowering effect of amphetamine in normoprolactinemic subjects and in physiological and pathological hyperprolactinemia. Prolactin lowering effect of amphetamine in n... [Horm Metab Res. 1983] - PubMed - NCBI
DeLeo V, Cella SG, Camanni F, Genazzani AR, Müller EE.
Abstract
The effect on plasma prolactin (PRL) of d-amphetamine (Amph) was studied in normo- and hyperprolactinemic subjects. In normoprolactinemic women Amph failed to lower plasma PRL levels when infused intravenously over 1 h at the dose of 7.5 mg, but induced at the dose of 15.0 mg a modest inhibition of plasma PRL (maximum PRL inhibition 20 +/- 4.5% at 45 min). Likewise, in puerperal women Amph at the dose of 7.5 mg did not decrease significantly plasma PRL levels but it was active in this respect (maximum inhibition 37 +/- 10% at 120 min) at the dose of 15.0 mg. In subjects with presumptive evidence of a PRL-secreting adenoma, Amph at either the 7.5 mg or the 15.0 mg dose failed to alter baseline PRL levels.
These results indicate that Amph is a poor PRL suppressor in either normo- or hyperprolactinemic subjects. It is proposed that this may be due to the drug's ability to effect release of dopamine mainly from a non-granular pool of the amine.
Gynecol Obstet Invest. 1987;23(2):103-9.
Prolactin changes after administration of agonist and antagonist dopaminergic drugs in puerperal women. Prolactin changes after administration... [Gynecol Obstet Invest. 1987] - PubMed - NCBI
Petraglia F, De Leo V, Sardelli S, Mazzullo G, Gioffrè WR, Genazzani AR, D'Antona N.
Abstract
Prolactin (PRL) is an anterior pituitary hormone which plays a large part in the reproductive function of mammals. Its only well-documented effect in humans is that of initiating and maintaining lactation. Among hypothalamic neurotransmitters regulating the anterior pituitary function, dopamine (DA) is currently considered to correspond to the PRL-inhibiting factor. The central control mechanisms which induce high PRL levels in puerperal women are not well understood. To study DA tonus in puerperium we tested plasma PRL levels in different groups of puerperal subjects (6 per group) after acute administration of direct or indirect DA agonists or placebo: DA, L-dopa (a DA precursor), L-dopa plus carbidopa (a peripheral dopa-decarboxylase inhibitor), nomifensine (a DA-releasing and blocking or reuptake agent) and amphetamine (a DA releaser). The same tests with the same drug doses were performed on groups of healthy volunteers. A consistent reduction in plasma PRL levels after both direct and indirect DA agonist drugs compared to placebo was evident in puerperal and in control women. A different trend was only observed with the use of DA and amphetamine in puerperal subjects, who, unlike controls, failed to show a rebound in plasma PRL levels after the termination of drug infusion. These findings support the view that the inhibitory control of tuberoinfundibular neurons over PRL secretion is maintained in puerperium and changes in the affinity of DA receptors are related to the endocrine milieu which occurs during gestation.