so what i have been reading from bros some of u recomend running a estrogen inhibitor like arimidex or aromasin cause the big nasty cyst like pimple that occur during cycle are from excess estrogen in the body? i ask this cause i have had these problems all the time with cycles iam fine for first half cycle then they set in like a jumbo mesquito has been feedn on my back for days!!!!!!!! i never have ran arimidex or aromasin on cycle cause i do not have problems with gyno so is this remedy worth a try??? aromasin or arimidex while on cycle to keep bad acne away????
Yes. Absolutely. Acne is a perfect example of things going on unseen and "not affecting you" (aromatization happening), then bam, there it is.
AI's, used in Moderation, are one of the best additions I've made to cycles, ever. They are not just for Gyno. They also can help prevent prostate issues, which are largely due to Estrogen, not DHT as was thought in the past. HPTA shut-down: Estrogen. Try keeping gains, and restarting the HPTA with high estrogen. It wont happen.
Aromasin is better all around. But IME, Arimidex is stronger on cycle, and it's cheaper.
So either use Aromasin if you can, or Adex on cycle, and toward the end of cycle last couple weeks, and into PCT, switch to Aromasin. Aromasin is irreversible, better on lipid profiles and wont lead to rebound. Adex will "wear off" and lead to nasty rebound. Been there.
BTW: Here's an article showing the medical community's view on what causes HTPA suppression: ESTROGEN! Article is about clomid, but the first line is relevant. For clomid users...look at the effective doses. LOW. 150mg of Clomid is not necessary for more than 7 days. Other articles have even lower doses and same results.
"Department of Endocrinology, Royal Victoria Infirmary and University of Newcastle-upon-Tyne, Newcastle-upon-Tyne, United Kingdom.
OBJECTIVE:
Inhibition of pituitary gonadotropin secretion in men by T is principally mediated by aromatization to estrogen (E), which inhibits hypothalamic secretion of GnRH. We hypothesized that adult-onset isolated hypogonadotropic hypogonadism (IHH) might result from an altered central set-point for E-mediated negative feedback. DESIGN AND SETTING: Longitudinal clinical investigation unit-based evaluation of the clinical and biochemical response to E-receptor blockade. PATIENT(S): A 31-year-old man presenting with an 18-month history of sexual dysfunction resulting from severe adult-onset IHH (LH 1.7 U/L, FSH 2.0 U/L, T 3.5 nmol/L). INTERVENTION(S): Initial therapy with
50 mg of clomiphene citrate (CC) three times a day for 7 days, with overnight LH pulse profiling and 9 am T levels evaluated at baseline and on completion.
A 2-month washout period, followed by
low-dose maintenance therapy (25-50 mg/d) for 4 months. MAIN OUTCOME MEASURE(S): Baseline and stimulated T levels and LH pulsatility; effect on sexual function. RESULT(S): Clomiphene therapy resulted in complete normalization of pulsatile gonadotropin secretion, serum T level, and sexual function. CONCLUSION(S): Isolated hypogonadotropic hypogonadism may result from an acquired defect of enhanced hypothalamic sensitivity to E-mediated negative feedback. Whereas direct T replacement therapy can further suppress endogenous gonadotropin secretion, treating IHH men with gonadotropins can stimulate endogenous T secretion and enhance fertility potential. On theoretical grounds, reversal of gonadotropin deficiency with CC might be expected to have a similar biological effect.
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