HRT/always on crowd: What do you do with your balls?

[Anakin]

My only concern about HRT is that my nuts would dissapear from inactivity. How do you guys do it? You can't use hcg all the time because you will become desensitized to it. Do you just live with raisins or what?
This would especially be a concern for those that do this before the age of 40. Imagine if you start HRT at age 30. By age 40 I assume that hcg won't do the trick anymore.

 

[E23]

try one week of HCG every 3 months and constant use of clomid and aromasin.

 

[Stillgoing]

try one week of HCG every 3 months and constant use of clomid and aromasin.

Yeah, most use HCG periodically or once a week, low dose. Also, many have no issue with atrophy. I wouldn't use clomid just for that, I hate that shit. Aromasin does seem to help too.

 

[thx9000]

low dose HCG through out is a good idea, don't go over 500iu EW. I wouldn't run the clomid, not good for IGF-1.

 

[E23]

I thought only nolva reduced levels of IGF-1. I guess I'll need to look into that.

 

[thx9000]

I thought only nolva reduced levels of IGF-1. I guess I'll need to look into that.

Nolva, clomid, arimidex...

Link

Plasma concentrations of IGF-I decreased by 31.5% (434 +/- 84 versus 297 +/- 71 ng/ml; P: < 0.05) after 5 days of clomiphene therapy, whereas plasma concentrations of IGFBP-1 increased by approximately 28.1% (26.3 +/- 4 versus 36.6 +/- 7 ng/ml; P: < 0.05).

Link

In normal subjects, CC treatment led to a significant increase in estradiol (84 +/- 10 to 234 +/- 62 pmol/L, untreated and CC treated; P < 0.05) and estrone (125 +/- 14 to 257 +/- 29 pmol/L; P < 0.05) levels with a significant lowering of IGF-I levels (297 +/- 25 to 230 +/- 17 micrograms/L; P < 0.05). Similarly, in PCOS patients a significant increase in estradiol (110 +/- 11 to 245 +/- 58 pmol/L; P < 0.05) and estrone (301 +/- 32 to 401 +/- 90 pmol/L; P < 0.05) levels and a significant lowering of IGF-I levels (330 +/- 43 to 214 +/- 27 micrograms/L; P < 0.05) were observed after CC treatment.

(edited aromasin mistake)

 

[E23]

"CC treatment led to a significant increase in estradiol" in females that is, but I'm not touching that shit again.

E2, E2, E2 WTF have you been teaching me all this time!?!

 

[sh4dowf4lcon]

Nolva, clomid, arimidex, aromasin....

Link

Plasma concentrations of IGF-I decreased by 31.5% (434 +/- 84 versus 297 +/- 71 ng/ml; P: < 0.05) after 5 days of clomiphene therapy, whereas plasma concentrations of IGFBP-1 increased by approximately 28.1% (26.3 +/- 4 versus 36.6 +/- 7 ng/ml; P: < 0.05).

Link

In normal subjects, CC treatment led to a significant increase in estradiol (84 +/- 10 to 234 +/- 62 pmol/L, untreated and CC treated; P < 0.05) and estrone (125 +/- 14 to 257 +/- 29 pmol/L; P < 0.05) levels with a significant lowering of IGF-I levels (297 +/- 25 to 230 +/- 17 micrograms/L; P < 0.05). Similarly, in PCOS patients a significant increase in estradiol (110 +/- 11 to 245 +/- 58 pmol/L; P < 0.05) and estrone (301 +/- 32 to 401 +/- 90 pmol/L; P < 0.05) levels and a significant lowering of IGF-I levels (330 +/- 43 to 214 +/- 27 micrograms/L; P < 0.05) were observed after CC treatment.

I dont think Aromasin affects IGF-1. It has always been considered the one anti-e that works this way. Are you saying Aromasin actually hinders IGF-1?

 

[thx9000]

I dont think Aromasin affects IGF-1. It has always been considered the one anti-e that works this way. Are you saying Aromasin actually hinders IGF-1?

Whops, that was a mistake didn't mean to say that. Aromasin and Femera appear to be okay so far.

 

[sh4dowf4lcon]

http://www.ncbi.nlm.nih.gov/entrez/...ve&db=PubMed&list_uids=14671195&dopt=Abstract

Pharmacokinetics and dose finding of a potent aromatase inhibitor, aromasin (exemestane), in young males.

Mauras N, Lima J, Patel D, Rini A, di Salle E, Kwok A, Lippe B.

Nemours Children's Clinic and Research Programs, Jacksonville, Florida 32207, USA. [email protected]

Suppression of estrogen, via estrogen receptor or aromatase blockade, is being investigated in the treatment of different conditions. Exemestane (Aromasin) is a potent and selective irreversible aromatase inhibitor. To characterize its suppression of estrogen and its pharmacokinetic (PK) properties in males, healthy eugonadal subjects (14-26 yr of age) were recruited. In a cross-over study, 12 were randomly assigned to 25 and 50 mg exemestane daily, orally, for 10 d with a 14-d washout period. Blood was withdrawn before and 24 h after the last dose of each treatment period. A PK study was performed (n = 10) using a 25-mg dose. Exemestane suppressed plasma estradiol comparably with either dose [25 mg, 38% (P <or= 0.002); 50 mg, 32% (P <or= 0.008)], with a reciprocal increase in testosterone concentrations (60% and 56%; P <or= 0.003 for both). Plasma lipids and IGF-I concentrations were unaffected by treatment. The PK properties of the 25-mg dose showed the highest exemestane concentrations 1 h after administration, indicating rapid absorption. The terminal half-life was 8.9 h.Maximal estradiol suppression of 62 +/- 14% was observed at 12 h. The drug was well tolerated. In conclusion, exemestane is a potent aromatase inhibitor in men and an alternative to the choice of available inhibitors. Long-term efficacy and safety will need further study.

Publication Types:

* Clinical Trial
* Randomized Controlled Trial


PMID: 14671195 [PubMed - indexed for MEDLINE]