im just confused to exactly what he means by the no legal study's post.
I think he is confused as well!! Perhaps he should explain.
Not gonna say anything more than i cover this particular topic in my sticky.
You can google HCG and read about the increase. I like this one:
"As a result, his free testosterone doubled from 86 to 157."
http://www.physioage.com/faq/SuccessStories.php
As for Adex studies they are out there also:
http://www.************.com/forum/an...ne-134791.html
Study Shows That Arimidex Boosts Testosterone
Estrogen suppression in males: metabolic effects.
J Clin Endocrinol Metab 2000 Jul;85(7):2370-7 (ISSN: 0021-972X)
Mauras N; O'Brien KO; Klein KO; Hayes V [email protected].
We have shown that testosterone (T) deficiency per se is associated with
marked catabolic effects on protein, calcium metabolism, and body
composition in men independent of changes in gh - growth hormone (somatropin) - or insulin-like growth
factor I production. It is not clear,,however, whether estrogens have a
major role in whole body anabolism in males. We investigated the metabolic
effects of selective estrogen suppression in the male using a potent
aromatase inhibitor, Arimidex (Anastrozole). First, a dose-response study of
12 males (mean age, 16.1 +/- 0.3 yr) was conducted, and blood withdrawn at
baseline and after 10 days of oral Arimidex given as two different doses
(either 0.5 or 1 mg) in random order with a 14-day washout in between. A
sensitive estradiol (E2) assay showed an approximately 50% decrease in E2
concentrations with either of the two doses; hence, a 1-mg dose was selected
for other studies. Subsequently, eight males (aged 15-22 yr; four adults and
four late pubertal) had isotopic infusions of [(13)C]leucine and
(42)Ca/(44)Ca, indirect calorimetry, dual energy x-ray absorptiometry,
isokinetic dynamometry, and growth factors measurements performed
before and after 10 weeks of daily doses of Arimidex. Contrary to the effects of T
withdrawal, there were no significant changes in body composition (body mass
index, fat mass, and fat-free mass) after estrogen suppression or in rates
of protein synthesis or degradation; carbohydrate, lipid, or protein
oxidation; muscle strength; calcium kinetics; or bone growth factors
concentrations. However, E2 concentrations decreased 48% (P = 0.006), with
no significant change in mean and peak gh - growth hormone (somatropin) - concentrations, but with an 18%
decrease in plasma insulin-like growth factor I concentrations. There was a
58% increase in serum T (P = 0.0001), sex hormone-binding globulin did not
change, whereas lh - leutenizing hormone - and FSH - follicle stimulating hormone - concentrations increased (P < 0.02, both). Serum
bone markers, osteocalcin and bone alkaline phosphatase concentrations, and
rates of bone calcium deposition and resorption did not change. In
conclusion, these data suggest that in the male 1) estrogens do not
contribute significantly to the changes in body composition and protein
synthesis observed with changing androgen levels; 2) estrogen is a main
regulator of the gonadal-pituitary feedback for the gonadotropin axis; and
3) this level of aromatase inhibition does not negatively impact either
kinetically measured rates of bone calcium turnover or indirect markers of
bone calcium turnover, at least in the short term. Further studies will
provide valuable information on whether timed aromatase inhibition can be
useful in increasing the height potential of pubertal boys with profound
growth retardation without the confounding negative effects of gonadal
androgen suppression.
hGH:
I would go pull the studies but there is no point it public knowledge...
nolv.... public knowledge it is needed for hcg estro sides...
I didnt include IGF-1 or slin to the HRT mix but the advanced user can do that.
<<<<<
Note that all the studies in the prior post are not on our sub group.
Like I stated before there are studies on other sub groups, on hypogonatics, sure there are studies on older males, and there are studies on HIV/AIDES patients.
I've used Proviron successfully at 25-50mg/ED during PCT.
It boosts labido and reduces circulating SHBG.
As for Dbol bridging, never done it. But can 10mg thats active for 4-5 hours only, really aid in keeping ones gains post cycle? Whilst also compromising endogenous T production somewhat? Doesnt seem worth it on paper IMHO. But then, I'll probably give it a go anyway...
Correct me if i'm wrong but don't we have a PCT SECTION???
The only good thing that has come of this thread is the realization or acknowledgment (by some) that no theory in recreational AAS usage is 100% certifiable. It's not like some university has an entire section devoted to studies on the juicing athlete.. 99% of info we have garnered are abstracted and derived from studies with a whole set of different objectives and an entirely different set of test subjects.
back to proviron. I have used it successfully for so many PCTs and cant imagine a PCT without it. Those of you who say "mesterolone is steroid and should be avoided cuz all steroids shut you down" are just making blanket statements based on oversimplification IMHO Unless you guyz can actually say/prove that proviron was the actual cause you did not recover from a cycle, then your point is moot.
no comment on the dbol, never tried it so i wouldn't know
cheers
There are currently 1 users browsing this thread. (0 members and 1 guests)