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I am planning a 20-20-20 3-week LMG cycle followed by a 20-20-20 3-week nolva PCT.
Is that ALL I need for PCT? If nolva just takes up estrogen receptors so that estrogen cannot... why doesn't the estrogen still F you up right after you stop nolva? I want to get started soon, but I don't wanna mess around. I want to know EVERYTHING before I start... not worth the rest of my life for 6 weeks. Reassure me a little and give me some info?
Thanks
Hmm.. been reading alot more. What about 20mg ED 3 weeks Nolva and .25mg ED Arimidex 3 weeks for PCT? How do you know if you are getting rid of TOO much estrogen... or using enough AI to hurt your lipids alot more?
20-20-20 of LMG will basically do nothing for you at all.
Hmm... what's the mildest noticeable cycle you can recommend. I just wanna play it relatively safe atm.
I recommend you just keep reading and wait to do any sort of Prohormone or AAS. You seem to know very little on the matter. Not flaming you, everyone starts out somewhere. But keep reading and planning and later in the year do something according to the knowledge you have. Don't just do something because people tell you it works. A lot of people get fvcked up doing that.
Stay Safe
USAMM
You dont need to worry about bitch tits on egromax lmg. If its a short cycle like 30 days at 10 or 20 mg dont worry about shutdown
I think I am just gonna keep researching and do a small cycle maybe next fall or winter.
On a sidenote.. does anyone ever speed up gains by running JUST an AI like LDex for 3-4 weeks at a low dose? Would this increase protein synthesis in the body?
You need to do far more research before embarking on any cycle of AS/ProHormone IMHO.
I'd say it doesnt:Quote:
Originally Posted by speakerman
Estrogen suppression in males: metabolic effects.
Mauras N, O'Brien KO, Klein KO, Hayes V.
Nemours Research Programs at the Nemours Children's Clinic, Jacksonville, Florida 32207, USA. [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 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 alk****e 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.