im lost

[DEMONSathleet]

hey guys sry if im being stupid or whatever, but im searching but i cant find the answers, what all do you need for pct? and how long do you take it? what meds do what and everything, if yall would just help me out man ill be rollin

[Jantzen4k]

hey guys sry if im being stupid or whatever, but im searching but i cant find the answers, what all do you need for pct? and how long do you take it? what meds do what and everything, if yall would just help me out man ill be rollin

not to flame but there are hundreds of articles on pct, if you search


Steroid Usage Basics For Beginers. 101

[DEMONSathleet]

dude thanks alot! man i havent seen this one, this answers all my questions, dude your awesome

[BDTR]

All the info you really need for a good PCT is are in the sticky threads about this. Check out pheednos pct plan.

[Swole33]

use
1mg arimidex daily
500 iu hcg
.5 cabergoline once weekly
50-100 clomid daily

This gets me back on track fast!

[BDTR]

HCG should not be used post cycle alongside clomid an an effort to restore natural HPTA function.

use
1mg arimidex daily
500 iu hcg
.5 cabergoline once weekly
50-100 clomid daily

This gets me back on track fast!

[BDTR]

Also thats too much Ari.

[Swole33]

opinions vary as to the most effective protocol with HCG and Clomid and unfortunately we have little if any science to fall back on. After using Clomid and HCG primarily as post cycle ancillaries, I’m now still using Clomid in the traditional way after a cycle, but employing weekly injections of HCG throughout the cycle to (hopefully) reduce testicular atrophy. As most readers know, HCG acts like LH, stimulating the testicular Leydig cells. Probably more than anything else, testicular atrophy is what prolongs recovery. Studies have shown that post cycle, the pituitary recovers much more quickly than do the testes. In fact, after the pituitary has recovered several weeks post cycle, pituitary LH secretion becomes supraphysiological, presumably as the body tries to stimulate the still atrophied testes (Am J Sports Med 1987 Jul-Aug;15(4):357-61 Androgenic -anabolic steroid effects on serum thyroid, pituitary and steroid hormones in athletes. Alen M, Rahkila P, Reinila M, Vihko R. )
. If we can reduce the atrophy by keeping the testes “primed” with HCG recovery should be quicker.

[Swole33]

I say use 1mg arimidex because it increases testosterone 58%, and ill take any increase during PCT. HEres a journal that states just that....


Arimidex Boosts Testosterone
Estrogen suppression in males: metabolic effects.
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 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 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 and FSH 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.

J Clin Endocrinol Metab 2000 Jul;85(7):2370-7 (ISSN: 0021-972X)
Mauras N; O'Brien KO; Klein KO; Hayes V.

[DEMONSathleet]

thanks swole for all the information