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Clinical Use of Anabolics and Hormones
Clinical Use of Anabolics and Hormones
Oxandrolone and Joints
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<blockquote data-quote="Wilson7" data-source="post: 192182" data-attributes="member: 39729"><p>15 mg of oxandrolone will cut total T by 35% in 5 days (Sheffield-Moore, et al. 1999). SHBG is also reduced significantly esp with C-17 orals. DHT and E2 would parallel those decreases, and with low SHBG clearance would increase. It would make no sense to take oxandrolone without a base of testosterone and/or HCG (to maintain endogenous and intratesticular T) along with E2 and DHT. On a side note because it is consistently raised as a concern, the decreased HDL and its relationship to increased risk of CAD is questionable. Yes, low endogenous HDL is associated with an increased risk of CAD, however raising HDL phamacologically has not resulted in a meaningful reduction in CAD risk. It is not as simple as high or low HDL = low or high CAD risk esp when the effect is influenced pharmacologically. Patients treated with stanazolol for HAE for periods of 20+ years have not shown an increased incidence of CAD. Sure their dosing is low, but sufficient to lower HDL. You'd think after 20 years there would be a measureable negative effect. On a personal note regarding E2, I've had levels with HRT ranging from 10 to 100 depending on HRT dose, inclusion of HCG and/or an AI. I have not noticed any difference regardless. Most of the docs I know in HRT don't worry about E2 unless something like gyno presents. The concern is too low E2, not too high and that AIs are over prescribed, unnecessary and potentially harmful.</p></blockquote><p></p>
[QUOTE="Wilson7, post: 192182, member: 39729"] 15 mg of oxandrolone will cut total T by 35% in 5 days (Sheffield-Moore, et al. 1999). SHBG is also reduced significantly esp with C-17 orals. DHT and E2 would parallel those decreases, and with low SHBG clearance would increase. It would make no sense to take oxandrolone without a base of testosterone and/or HCG (to maintain endogenous and intratesticular T) along with E2 and DHT. On a side note because it is consistently raised as a concern, the decreased HDL and its relationship to increased risk of CAD is questionable. Yes, low endogenous HDL is associated with an increased risk of CAD, however raising HDL phamacologically has not resulted in a meaningful reduction in CAD risk. It is not as simple as high or low HDL = low or high CAD risk esp when the effect is influenced pharmacologically. Patients treated with stanazolol for HAE for periods of 20+ years have not shown an increased incidence of CAD. Sure their dosing is low, but sufficient to lower HDL. You'd think after 20 years there would be a measureable negative effect. On a personal note regarding E2, I've had levels with HRT ranging from 10 to 100 depending on HRT dose, inclusion of HCG and/or an AI. I have not noticed any difference regardless. Most of the docs I know in HRT don't worry about E2 unless something like gyno presents. The concern is too low E2, not too high and that AIs are over prescribed, unnecessary and potentially harmful. [/QUOTE]
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Clinical Use of Anabolics and Hormones
Clinical Use of Anabolics and Hormones
Oxandrolone and Joints
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