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Clinical Use of Anabolics and Hormones
Clinical Use of Anabolics and Hormones
Does anyone use Nandrolone (Deca Durabolin) ?
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<blockquote data-quote="Wilson7" data-source="post: 161569" data-attributes="member: 39729"><p>New to this board, excellent source of real life info on TRT and nandrolone. After reading through this thread some thoughts. The age mgmt docs I know do not use AI unless there are Sx of E2 excess. I've tried them with my current HRT (100 mg/TC sc every 4 days and 500 IU HCG every 4 days). They tanked my E2 < 20. Without them I run in the 60 - 80 range, no issues with E2 excess. Only when I was younger and had a T < 200 ng/dl did I have gyno issues. I also ran deca 200 mg/2 weeks and 350 IU HCG 2x/wk for 10 years 1995 to 2005 because of the gyno. Primary issue was erythrocytosis. I have mild concentric hypertrophy but not different than in the early 90's, some fibrosis (cardiac MRI) but they are seeing it in older guys that lift or run more now regardless. Little change in cardiac function (echo or dimensions) since the 90's. I've been through the animal lit on nandrolone, also have talked to docs that have seen some systolic/diastolic dysfunction in high dose nandrolone uses, note high dose probably along with other AAS and stimulants so it is very hard to tease out whether nandrolone is the problem or dosing and other confounding variables are making it a problem. In rabbits only the 10 mg/kg dose caused cardiac issues, the 4 mg/kg did not. Remember the high dose animal studies are there to dissuade AAS abuse, it doesn't help us sort out any potential problems with clinical dosing. We need human data, speculation is useless. If you are concerned about the effects of nandrolone, get a baseline echo and then compare in a year. At the very least track BNP (brain natriuretic peptide) along with you labs. If your value is under 35 pg/ml and stable, it is a good indication that there are no pressure changes occurring in the heart relating to function. If there is an issue and you catch it early, it can likely be reversed in the case of AAS. Nelson, did you ever have an echo done to confirm or refute any changes in cardiac function related to the nandrolone? I think the only way we get to an answer on this is to have men/women using nandrolone have baseline and follow up echos. Collect enough data on dosing/duration and family history and we can at least get some direction on the topic. To date though, I have not seen case reports with clinical dosing leading to cardiac dysfunction in the absence of other risk factors. Lastly, decreased HDL risks are overstated. There is a difference between endogenously low HDL or a dysfunctional HDL transport system with normal or elevated HDL and pharmacologic manipulation. It is clear now that efforts to increase circulating HDL pharmacologically have not lead to meaningful decrease in CAD risk, men on ADT have increased HDL but also increased CAD risk, there are populations with high HDL and increased risk of CAD. Androgens increase hepatic lipase activity and scavenger receptor b1 that increase turnover of HDL, that is very different than a situation where someone has an intrinsically low and cardiovascular disease. Obviously suppressing HDL to < 10 with high doses of oral androgens may be another story, taking it into the 30's probably isn't. I've always been 35 - 40. CT angiogram score this year at age 61 was zero. That's 35 yrs on HRT, 10 of those on deca. Prior to HRT I was in the 60's, LDL was always less than 100, now around 65. As you get older you become more sensitive to erythrocytosis, regular phlebos or blood donation (assuming you're not on proscar or avodart) is the simple solution. I get one every 10 weeks and keep HCT < 52%, again androgen induced erythrocytosis is not the same as that of polycythemia vera. Guys in Denver on HRT have HCTs of 60 and are not stroking out. Not that it should be taken lightly but it is easily managed.</p></blockquote><p></p>
[QUOTE="Wilson7, post: 161569, member: 39729"] New to this board, excellent source of real life info on TRT and nandrolone. After reading through this thread some thoughts. The age mgmt docs I know do not use AI unless there are Sx of E2 excess. I've tried them with my current HRT (100 mg/TC sc every 4 days and 500 IU HCG every 4 days). They tanked my E2 < 20. Without them I run in the 60 - 80 range, no issues with E2 excess. Only when I was younger and had a T < 200 ng/dl did I have gyno issues. I also ran deca 200 mg/2 weeks and 350 IU HCG 2x/wk for 10 years 1995 to 2005 because of the gyno. Primary issue was erythrocytosis. I have mild concentric hypertrophy but not different than in the early 90's, some fibrosis (cardiac MRI) but they are seeing it in older guys that lift or run more now regardless. Little change in cardiac function (echo or dimensions) since the 90's. I've been through the animal lit on nandrolone, also have talked to docs that have seen some systolic/diastolic dysfunction in high dose nandrolone uses, note high dose probably along with other AAS and stimulants so it is very hard to tease out whether nandrolone is the problem or dosing and other confounding variables are making it a problem. In rabbits only the 10 mg/kg dose caused cardiac issues, the 4 mg/kg did not. Remember the high dose animal studies are there to dissuade AAS abuse, it doesn't help us sort out any potential problems with clinical dosing. We need human data, speculation is useless. If you are concerned about the effects of nandrolone, get a baseline echo and then compare in a year. At the very least track BNP (brain natriuretic peptide) along with you labs. If your value is under 35 pg/ml and stable, it is a good indication that there are no pressure changes occurring in the heart relating to function. If there is an issue and you catch it early, it can likely be reversed in the case of AAS. Nelson, did you ever have an echo done to confirm or refute any changes in cardiac function related to the nandrolone? I think the only way we get to an answer on this is to have men/women using nandrolone have baseline and follow up echos. Collect enough data on dosing/duration and family history and we can at least get some direction on the topic. To date though, I have not seen case reports with clinical dosing leading to cardiac dysfunction in the absence of other risk factors. Lastly, decreased HDL risks are overstated. There is a difference between endogenously low HDL or a dysfunctional HDL transport system with normal or elevated HDL and pharmacologic manipulation. It is clear now that efforts to increase circulating HDL pharmacologically have not lead to meaningful decrease in CAD risk, men on ADT have increased HDL but also increased CAD risk, there are populations with high HDL and increased risk of CAD. Androgens increase hepatic lipase activity and scavenger receptor b1 that increase turnover of HDL, that is very different than a situation where someone has an intrinsically low and cardiovascular disease. Obviously suppressing HDL to < 10 with high doses of oral androgens may be another story, taking it into the 30's probably isn't. I've always been 35 - 40. CT angiogram score this year at age 61 was zero. That's 35 yrs on HRT, 10 of those on deca. Prior to HRT I was in the 60's, LDL was always less than 100, now around 65. As you get older you become more sensitive to erythrocytosis, regular phlebos or blood donation (assuming you're not on proscar or avodart) is the simple solution. I get one every 10 weeks and keep HCT < 52%, again androgen induced erythrocytosis is not the same as that of polycythemia vera. Guys in Denver on HRT have HCTs of 60 and are not stroking out. Not that it should be taken lightly but it is easily managed. [/QUOTE]
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Clinical Use of Anabolics and Hormones
Clinical Use of Anabolics and Hormones
Does anyone use Nandrolone (Deca Durabolin) ?
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