jhotsauce7
TID Board Of Directors
- Jan 18, 2011
- 2,805
- 684
Saw this elsewhere and thought it was interesting enough to repost. Doesn’t address all the aspects of SHbg lowering on 19nors.
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Nandrolones (tren, deca) raise prolactin. Every bro knows this. That’s why we run caber or B6 to reduce prolactin, and definitely not for the reduction in refractory period to engage in unlimited amounts of debauchery. In an earlier article on tren I state that reliable data on tren and its relationship with progesterone receptors is lacking however we do know it binds to the progesterone receptor with about 22% the affinity of progesterone and an effective increase in one changes the other.
Yet something bothered me about this section - why couldn’t I find any bovine studies (where nandrolone is commonly used, specifically tren) that showed an increase in prolactin in cattle? Any tissue growth is notable, and the concern of hormones making it through to human consumption is well researched. So let’s dig into it, and test our long held assumption.
Our primary piece of evidence comes from a human trial for treatment of anemia. After baselines were established, Group A received 200mg of nandrolone, while Group B received 400mg of testosterone weekly, for 6 months. The groups were then switched, so that Group A received testosterone, and Group B received nandrolone. Nandrolone treatment resulted in a reduction of prolactin from a baseline of 71ng/ml to 42ng/ml, while testosterone slightly increased prolactin to 78ng/ml.
Nandrolone almost halved prolactin compared to baseline. Testosterone increased it marginally over baseline. This completely flies in the face of what I’ve been told by broscience. Granted, testosterone was administered a 2x the quantity of nandrolone. But the obvious question is why does prolactin seem to increase on our nandrolone cycles? I’m going to wager that it doesn’t:
Our observation that only aromatizable androgens can stimulate prolactin secretion clearly indicates that prior conversion to estrogens in vivo may be required for androgens to enhance prolactin release
Aromatizable androgens being the key word. DHT has no such effect:
DHT consistently failed to stimulate prolactin secretion... DHT actually suppressed PRL release. These findings do not support generalizations, based entirely on findings with testosterone, that both “androgens” and estrogens exert stimulatory actions on prolactin secretion.
So we’re left with aromatization of testosterone to estrogens as a potential culprit. Perhaps there is an synergistic increase in prolactin caused by a combination of testosterone and nandrolone compounds (perhaps by the role e2 plays in increasing the binding effect of androgens to androgen receptors) - that’s to be investigated another time.
Conclusion
Nandrolone (deca, tren) does not increase prolactin like conventional broscience tells us. Instead, such increases are coming from testosterone and specifically estrogen.
Key takeaways:
——-
Nandrolones (tren, deca) raise prolactin. Every bro knows this. That’s why we run caber or B6 to reduce prolactin, and definitely not for the reduction in refractory period to engage in unlimited amounts of debauchery. In an earlier article on tren I state that reliable data on tren and its relationship with progesterone receptors is lacking however we do know it binds to the progesterone receptor with about 22% the affinity of progesterone and an effective increase in one changes the other.
Yet something bothered me about this section - why couldn’t I find any bovine studies (where nandrolone is commonly used, specifically tren) that showed an increase in prolactin in cattle? Any tissue growth is notable, and the concern of hormones making it through to human consumption is well researched. So let’s dig into it, and test our long held assumption.
Our primary piece of evidence comes from a human trial for treatment of anemia. After baselines were established, Group A received 200mg of nandrolone, while Group B received 400mg of testosterone weekly, for 6 months. The groups were then switched, so that Group A received testosterone, and Group B received nandrolone. Nandrolone treatment resulted in a reduction of prolactin from a baseline of 71ng/ml to 42ng/ml, while testosterone slightly increased prolactin to 78ng/ml.
Nandrolone almost halved prolactin compared to baseline. Testosterone increased it marginally over baseline. This completely flies in the face of what I’ve been told by broscience. Granted, testosterone was administered a 2x the quantity of nandrolone. But the obvious question is why does prolactin seem to increase on our nandrolone cycles? I’m going to wager that it doesn’t:
Our observation that only aromatizable androgens can stimulate prolactin secretion clearly indicates that prior conversion to estrogens in vivo may be required for androgens to enhance prolactin release
Aromatizable androgens being the key word. DHT has no such effect:
DHT consistently failed to stimulate prolactin secretion... DHT actually suppressed PRL release. These findings do not support generalizations, based entirely on findings with testosterone, that both “androgens” and estrogens exert stimulatory actions on prolactin secretion.
So we’re left with aromatization of testosterone to estrogens as a potential culprit. Perhaps there is an synergistic increase in prolactin caused by a combination of testosterone and nandrolone compounds (perhaps by the role e2 plays in increasing the binding effect of androgens to androgen receptors) - that’s to be investigated another time.
Conclusion
Nandrolone (deca, tren) does not increase prolactin like conventional broscience tells us. Instead, such increases are coming from testosterone and specifically estrogen.
Key takeaways:
- Blood tests are key on-cycle when using nandrolone + test
- Use data to dial in your e2 control
- Use data to dial in your prolactin control
- Can prolactin be controlled purely by controlling aromatization? I.e. aromatase inhibitors
- Does e2 and nandrolone react synergistically to increase prolactin / progesterone?
- Should testosterone only cycles control for prolactin?