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Anabolic Steroids
Anabolic Steroid Induced Hypogonadism (ASIH) by Michael Scally, MD
- Thread starter Millard
- Start date
Reginald
New Member
Gh deficit from gh abuse
HI,I don't know if I write in right sito..( I'm italian boy so..I don't understand english...sorry for my own)..
I have a very little great problem...
I used a GH cycle (0.6 mg Genotropin for 16/20 days)without a exit post cycle after GH cycle..
I havn't done any sermorelin or GHRP cycles after GH cycles ...so I have a GH deficiency...
I diagnosis this in hospital with stimulus test GHRH+arginine....I have GH deficit....
I want to know if now with a 10 days sermorelin cyle 0.2mg can restore my GH own.
thanks
HI,I don't know if I write in right sito..( I'm italian boy so..I don't understand english...sorry for my own)..I have a very little great problem...
I used a GH cycle (0.6 mg Genotropin for 16/20 days)without a exit post cycle after GH cycle..
I havn't done any sermorelin or GHRP cycles after GH cycles ...so I have a GH deficiency...
I diagnosis this in hospital with stimulus test GHRH+arginine....I have GH deficit....
I want to know if now with a 10 days sermorelin cyle 0.2mg can restore my GH own.
thanks
Reginald
New Member
Re: Anabolic Steroid Induced Hypogonadism (ASIH) bichael Scally, MD
Ihave GH deficit because I havn't done a peptides post cycle after a GH cycle to restore or jump-stsrt my GH own
Ihave GH deficit because I havn't done a peptides post cycle after a GH cycle to restore or jump-stsrt my GH own
NeuroEndoDO
New Member
Hackskii,
How has your axis been recently?
Did you never experience any nipple tenderness or acne during those high (2500 IU) doses of hCG?
How has your axis been recently?
Did you never experience any nipple tenderness or acne during those high (2500 IU) doses of hCG?
no, because I use nolva @ 20mg Ed and also 100mg clomid ED, nipple tenderness is not an issue with those in the mix.
I get nipple tenderness anything over 500iu without the use of an AI or SERM.
My axis I really dont know but I feel fantastic.
I finished a PCT about a month ago, felt good, now I am taking proviron @ 50mg ED and doing some weight loss.
I really like that proviron in the mix, I am not sure if it is curbing estrogen, or what, but the nuts are really plumping up and I have been getting night time wood often.
I cant explain it but I feel very good and this is the first time I have ran proviron for any length of time.
I got a deal I could not pass up, so that is why I am taking it this go around.
I can only imagine a bump of lets say 2iu a day with growth hormone and I bet this dieting would really work out nice.
Hacksii
Do you know if HCG therapy is as necessary if you have a good LH response to SERM's?
I was on T enathanate 100mg weekly for 5 years for IHH. I started Arimidex, did HCG 250/day for about 2-3 weeks, and now am on a Clomid/Nolva combination (100 mg/20mg) for the past 6-7 weeks. Total T at the beginning was 145. Now it is 380-400, . I am hoping that my T levels keep rising, even slowly, as to be able to use either Clomid or Nolva as TRT. Should I restart/continue HCG? FYI, my last LH was 13 (1.3-7.2).
Thanks
Do you know if HCG therapy is as necessary if you have a good LH response to SERM's?
I was on T enathanate 100mg weekly for 5 years for IHH. I started Arimidex, did HCG 250/day for about 2-3 weeks, and now am on a Clomid/Nolva combination (100 mg/20mg) for the past 6-7 weeks. Total T at the beginning was 145. Now it is 380-400, . I am hoping that my T levels keep rising, even slowly, as to be able to use either Clomid or Nolva as TRT. Should I restart/continue HCG? FYI, my last LH was 13 (1.3-7.2).
Thanks
380 to 400 range is in the mid lower end of normal.
Perhaps you might want to check your estrgoen levels due to you responding so nicely on SERMS.
Many men with alot of belly fat will have more aromitization.
More aromitization will promote more estrogen.
More estrogen will lower T levels due to E is made from T.
The only way the body can keep estrogen in check is to lower testosterone.
Diet and lifestyle both play a rather large roll in estrogen production.
Perhaps you might want to check your estrgoen levels due to you responding so nicely on SERMS.
Many men with alot of belly fat will have more aromitization.
More aromitization will promote more estrogen.
More estrogen will lower T levels due to E is made from T.
The only way the body can keep estrogen in check is to lower testosterone.
Diet and lifestyle both play a rather large roll in estrogen production.
Body fat is not an issue. I am monitoring e2 levels, SHBG etc., so far so good, but they are rising too. I will use adex if necessary.
T, 380-400, but free T is 0.88 (0.95-4.30). I feel best when T is in the 600-650 range, I hope I can get it there without throwing too much out of whack.
Do you think HCG supp. would further prime the nuts, or do you think the LH response is good enough?
T, 380-400, but free T is 0.88 (0.95-4.30). I feel best when T is in the 600-650 range, I hope I can get it there without throwing too much out of whack.
Do you think HCG supp. would further prime the nuts, or do you think the LH response is good enough?
Clomid @ 100mg ED after 5 to 7 days doubles LH output and can elivate FSH by 20% to 50%.
I think that HCG at this point is like using a sledge hammer to swat a fly.
Everything will return.
I think that HCG at this point is like using a sledge hammer to swat a fly.
Everything will return.
Interactions between tamoxifen and antidepressants
Desmarais JE, Looper KJ. Interactions between tamoxifen and antidepressants via cytochrome P450 2D6. J Clin Psychiatry 2009;70(12):1688-97.
OBJECTIVE: Women taking tamoxifen for the treatment or prevention of recurrence of breast cancer are likely to take antidepressants either for a psychiatric disorder or for hot flashes. Recent evidence suggested that some antidepressants inhibit the metabolism of tamoxifen to its more active metabolites by the cytochrome P450 2D6 (CYP2D6) enzyme, thereby decreasing the anticancer effect. This article reviews the literature on the interactions between newer antidepressants and tamoxifen via CYP2D6 and offers treatment recommendations. DATA SOURCES: A literature search of clinical and nonclinical studies published prior to September 2008 was conducted on PubMed. We performed 3 different searches combining the terms tamoxifen and SSRIs; tamoxifen and CYP2D6 inhibitors; and antidepressant and breast cancer recurrence. A fourth search with CYP2D6 inhibition and the generic names of individual antidepressants was carried out. STUDY SELECTION: Seven clinical research articles were selected. Nonclinical research articles about antidepressants were included if they mentioned in vitro or in vivo inhibition of CYP2D6. DATA SYNTHESIS: There is consistent evidence that paroxetine and fluoxetine have a large effect on the metabolism of tamoxifen and should not be used. Indirect evidence indicates that bupropion may also have a large effect on the metabolism of tamoxifen. Venlafaxine has little or no effect on the metabolism of tamoxifen and may be considered the safest choice of antidepressants. Desvenlafaxine is not metabolized by the P450 system and may consequently be another option. Mirtazapine has not been extensively studied, but existing research suggests minimal effect on CYP2D6. The remaining commonly prescribed antidepressants have mild to moderate degrees of CYP2D6 inhibition. CONCLUSIONS: Clinicians treating patients with breast cancer should review the prescription profiles of their patients to evaluate the need for treatment modification. There are safe options for the treatment of depression and clinicians and patients should bear in mind the health risks of untreated depressive states.
Desmarais JE, Looper KJ. Interactions between tamoxifen and antidepressants via cytochrome P450 2D6. J Clin Psychiatry 2009;70(12):1688-97.
OBJECTIVE: Women taking tamoxifen for the treatment or prevention of recurrence of breast cancer are likely to take antidepressants either for a psychiatric disorder or for hot flashes. Recent evidence suggested that some antidepressants inhibit the metabolism of tamoxifen to its more active metabolites by the cytochrome P450 2D6 (CYP2D6) enzyme, thereby decreasing the anticancer effect. This article reviews the literature on the interactions between newer antidepressants and tamoxifen via CYP2D6 and offers treatment recommendations. DATA SOURCES: A literature search of clinical and nonclinical studies published prior to September 2008 was conducted on PubMed. We performed 3 different searches combining the terms tamoxifen and SSRIs; tamoxifen and CYP2D6 inhibitors; and antidepressant and breast cancer recurrence. A fourth search with CYP2D6 inhibition and the generic names of individual antidepressants was carried out. STUDY SELECTION: Seven clinical research articles were selected. Nonclinical research articles about antidepressants were included if they mentioned in vitro or in vivo inhibition of CYP2D6. DATA SYNTHESIS: There is consistent evidence that paroxetine and fluoxetine have a large effect on the metabolism of tamoxifen and should not be used. Indirect evidence indicates that bupropion may also have a large effect on the metabolism of tamoxifen. Venlafaxine has little or no effect on the metabolism of tamoxifen and may be considered the safest choice of antidepressants. Desvenlafaxine is not metabolized by the P450 system and may consequently be another option. Mirtazapine has not been extensively studied, but existing research suggests minimal effect on CYP2D6. The remaining commonly prescribed antidepressants have mild to moderate degrees of CYP2D6 inhibition. CONCLUSIONS: Clinicians treating patients with breast cancer should review the prescription profiles of their patients to evaluate the need for treatment modification. There are safe options for the treatment of depression and clinicians and patients should bear in mind the health risks of untreated depressive states.
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