Cialis: The amazing drug and all its benefits - For On or Off cycle use.

theblitzkrieg said:
I have some generic version with a break like. I'll be giving it another go at 10mg / day. Even though everything is great downstairs since I'm on 600mg test, I'll be taking it for NO, prostate health and blood pressure. I've always had highish BP.

I wonder if the change in vascularity and pumps will be visible.
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If it works like niacin (and the flushing) you can start with small doses and work your way up. Just have to build up some tolewrance slowly.
 
wheres that post cycle therapy (pct) and how to keep gains on cycling austinite?....again...If possible....
 
Megatron28 said:
Why is deca known for increasing prolactin levels given it is less likely to aromatize than testosterone is? How does deca raise prolactin levels?
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There is no evidence that they do raise prolactin. It sucks because it leaves a wide range of possibilities. Partly why I didn't dive into the subject in my prolactin/progest thread. But I've never experienced, or heard of anyone else's experience where either progesterone and/or prolactin were elevated while Estrogen was low. It goes E2 --> Progesterone --> Prolactin.

So E2 management is the first line of defense. There are studies that show that Nandrolone is a mixed PR agonist/antagonist. Others say that's not the case. What I do know is that progestins like Nandrolone and Trenbolone really don't boost/elevate prolactin. Not directly. They do however, upregulate prolactin receptors everywhere except the breast. But again, this doesn't happen unless in the presence of higher E2 levels. Even a slight increase in E2 could amplify the effects. We could technically use anti-progesterone drugs, but you're looking at heavy side effects, worse than caber/prami. This happens in the presence of excess estrogen. I've never experienced or seen a case of elevated prolactin on a 19-nor cycle while estrogen was low.

The idea is that you do not have to have an E2 level of 150 pg/mL. This could occur with as little as 45 pg/mL. This topic is far too deep with very little available evidence. But there are some facts that are not deniable and they clearly say that 19-Nors do not directly cause prolactin secretion.
 
Austinite said:
There is no evidence that they do raise prolactin. It sucks because it leaves a wide range of possibilities. Partly why I didn't dive into the subject in my prolactin/progest thread. But I've never experienced, or heard of anyone else's experience where either progesterone and/or prolactin were elevated while Estrogen was low. It goes E2 --> Progesterone --> Prolactin.

So E2 management is the first line of defense. There are studies that show that Nandrolone is a mixed PR agonist/antagonist. Others say that's not the case. What I do know is that progestins like Nandrolone and Trenbolone really don't boost/elevate prolactin. Not directly. They do however, upregulate prolactin receptors everywhere except the breast. But again, this doesn't happen unless in the presence of higher E2 levels. Even a slight increase in E2 could amplify the effects. We could technically use anti-progesterone drugs, but you're looking at heavy side effects, worse than caber/prami. This happens in the presence of excess estrogen. I've never experienced or seen a case of elevated prolactin on a 19-nor cycle while estrogen was low.

The idea is that you do not have to have an E2 level of 150 pg/mL. This could occur with as little as 45 pg/mL. This topic is far too deep with very little available evidence. But there are some facts that are not deniable and they clearly say that 19-Nors do not directly cause prolactin secretion.
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An abstract only but posted by Heavyiron back in June.

Growth hormone, insulin, prolactin and total thyroxine in the plasma of sheep implanted with the anabolic steroid trenbolone acetate alone or with oestradiol.

AuthorsDonaldson IA, et al. Show all Journal
Res Vet Sci. 1981 Jan;30(1):7-13.
Affiliation
Abstract
The mode of action of the anabolic steroid trenbolone acetate (19-norandrost-4,9,11-trien-3-one-17-acetate) was studied through the endogenous hormonal response of castrated male sheep to subcutaneous implantation of 140 mg of trenbolone acetate and 20 mg of oestradiol both separately and in combination. Radioimmunoassay of delta-4,9,11-trienic steroids and oestradiol-17 beta in plasma confirmed that simultaneous administration of trenbolone acetate with oestradiol led to a significantly greater persistence of oestradiol-17 beta residues in plasma (P less than 0.05) than with implantation of oestradiol alone. Oestradiol treatment increased concentrations of growth hormone and insulin (P less than 0.05; P less than 0.001 respectively) in plasma samples collected weekly. Trenbolone acetate by itself had no significant effect and the oestrogenic response was blocked on the simultaneous implantation of trenbolone acetate and oestradiol (despite higher plasma levels of oestradiol-17 beta with this treatment). Plasma total thyroxine was markedly depressed to 45 per cent of its basal level by trenbolone acetate, alone or with oestradiol (P less than 0.001) and depressed to 80 per cent of basal by oestradiol treatment alone (P less than 0.001). Plasma prolactin was unaltered by the above treatments.

PMID 7017853 [PubMed - indexed for MEDLINE]
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Last edited:
Austinite said:
^^ Thanks. Last sentence there: Plasma prolactin was unaltered by the above treatments.
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The only thing I'd say is we don't have the full study, at least I don't have access to it, and it was done on sheep but tren studies on humans aren't exactly bursting at the seams lol
 
So takeaways are:

- Aromatase inhibitor (AI) is first line defense. Keeping E2 down keeps prolactin down.
- Prami/Caber are second line defense should E2 become elevated.
- High E2 normally doesn't have a big effect on prolactin, but in the presence of a 19-nor it does due to upregulated prolactin receptors from the 19-nor.

Did I get the takeaways correct?

Thanks for the education on this guys!
 
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