AlexPowell
Well-known member
****!
1 month after Trestolone/test PCT and toremifene failed
- Thread starter wormwood
- Start date
****!
bobi593
Active member
as i said before take something strong before workout , many years ago i run also quite suppressive stack deca/winstrol and low dosage of test prop . The recovery time was difficult too, to combat low motivation to train i used ephedra
sanguine
New member
For what its worth, the study says the supression was fully reversed after cessation of the treatment.
wormwood
Member
uggghhhh.... this is agonizing.. I am considering going on TRT just so I don't feel so ****ty... I just don't want to cause any further damage to my HPTA... I'm figuring I still have somewhere around 300mg of active compound in me.. it could be a year before I get all this **** out of me...
CATdiesel76
Well-known member
Cruise on TRT test for a few months while it clears your system and try again. That's the best I can think of
CATdiesel76
Well-known member
Probably not a bad idea
wormwood
Member
Does anyone know if 7-alpha-methyl-estradiol will show up as E2 (estradiol) in a blood test? I am finding it hard to believe that I am within normal range on my estrogen level. Something just feels off but It may very well be the clomid doing this...
I remember reading that methyl estrogen is more potent than regular estradiol... can anyone with more expertise than me chime in on this? the doc wouldn't put me on an AI bc my E2 levels are within normal range - I have some arimidex and a little exemestane on hand - I have been off it for a month and my E2 level is at 27. I've read that Ideal E2 level is at 20 but the clinic says I just need to be under 39.
My thoughts - If the methyl estrogen is significantly more potent than estradiol then the "normal" E2 level in my bloodwork may not be a correct indicator for the estrogenic activity that I'm experiencing. If I still have somewhere around 300mg of trestolone (based on the dose I was taking and 15 day half life) in me - some of it may be converting to this methyl estrogen and wreaking havoc on my psyche... :/
Should I go over my Docs head to combat this potential problem? He seemed to not be very familiar with trestolone when I was discussing it with him. Didn't go as in depth as I would have liked to on the chemistry behind what's going on... Thoughts?
I remember reading that methyl estrogen is more potent than regular estradiol... can anyone with more expertise than me chime in on this? the doc wouldn't put me on an AI bc my E2 levels are within normal range - I have some arimidex and a little exemestane on hand - I have been off it for a month and my E2 level is at 27. I've read that Ideal E2 level is at 20 but the clinic says I just need to be under 39.
My thoughts - If the methyl estrogen is significantly more potent than estradiol then the "normal" E2 level in my bloodwork may not be a correct indicator for the estrogenic activity that I'm experiencing. If I still have somewhere around 300mg of trestolone (based on the dose I was taking and 15 day half life) in me - some of it may be converting to this methyl estrogen and wreaking havoc on my psyche... :/
Should I go over my Docs head to combat this potential problem? He seemed to not be very familiar with trestolone when I was discussing it with him. Didn't go as in depth as I would have liked to on the chemistry behind what's going on... Thoughts?
wormwood
Member
further research has led me to come across this on ************* forums:
7-Alpha-Methyl-Estrogen Conversion
Trestolone should be run with an aromatase inhibitor due to its ability to convert to potent estrogens (2). Trestolone also has a unique property which testosterone does not have: it can aromatize directly in the liver. Testosterone conversion to estrogen depends on Cytochrome P450 aromatase which removes the 19-methyl on testosterone through a series of oxidation reactions before it can introduce the double bonds into the A ring and natural enolization of the 3-keto to produce estrogen (2). There is no Cytochrome P450 aromatase in the liver to remove the 19-methyl and thus, estrogen is not produced in the liver from testosterone. Trestolone on the other hand is already missing the 19-methyl so there is no need to interact with cytochrome P450 aromatase (2). There are other hepatic cytochrome P450 enzymes in the liver which can introduce double bonds into the A ring of trestolone converting it to an estrogen. This is seen this with 19-nortestosterone derivatives like norethisterone, norethynodrel, or tibolone. In addition, 7-alpha methyl estrogens have a stronger affinity for the estrogen receptors and are incapable of binding to SHBG making them very potent estrogens (3). The high metabolic clearance rate of trestolone could in part be due to a high degree of aromatization.
From what I gather - the conversion to estrogen speeds the process by which trestolone is metabolized - something I want to happen as I want this compound out of my body ASAP.
Now the question is - is the 7alpha-methyl-estradiol competing with clomid for binding to estrogen receptors???
Would I be better off taking some type of AI to prevent this conversion? Would it be wiser to take Arimidex or Aromasin for this purpose? I know that these two AIs are fundamentally different in how they operate - would this slow down the metabolization of the trestolone - causing it to stay in my body for longer?
Is this estrogen conversion something I should just suffer through? OR
would I be better off taking an AI to prevent this conversion - potentially allowing the clomid to work it's magic on estrogen receptors to stimulate LH production?
Would the one of these AIs hinder Clomid's ability to work?? anyone?? bump??
It would be nice if someone with a biochemistry or endocrinological research background could chime in on this. Separating fact and science from the "bro-science" that permeates steroid message boards is nauseating and making my head spin.
7-Alpha-Methyl-Estrogen Conversion
Trestolone should be run with an aromatase inhibitor due to its ability to convert to potent estrogens (2). Trestolone also has a unique property which testosterone does not have: it can aromatize directly in the liver. Testosterone conversion to estrogen depends on Cytochrome P450 aromatase which removes the 19-methyl on testosterone through a series of oxidation reactions before it can introduce the double bonds into the A ring and natural enolization of the 3-keto to produce estrogen (2). There is no Cytochrome P450 aromatase in the liver to remove the 19-methyl and thus, estrogen is not produced in the liver from testosterone. Trestolone on the other hand is already missing the 19-methyl so there is no need to interact with cytochrome P450 aromatase (2). There are other hepatic cytochrome P450 enzymes in the liver which can introduce double bonds into the A ring of trestolone converting it to an estrogen. This is seen this with 19-nortestosterone derivatives like norethisterone, norethynodrel, or tibolone. In addition, 7-alpha methyl estrogens have a stronger affinity for the estrogen receptors and are incapable of binding to SHBG making them very potent estrogens (3). The high metabolic clearance rate of trestolone could in part be due to a high degree of aromatization.
From what I gather - the conversion to estrogen speeds the process by which trestolone is metabolized - something I want to happen as I want this compound out of my body ASAP.
Now the question is - is the 7alpha-methyl-estradiol competing with clomid for binding to estrogen receptors???
Would I be better off taking some type of AI to prevent this conversion? Would it be wiser to take Arimidex or Aromasin for this purpose? I know that these two AIs are fundamentally different in how they operate - would this slow down the metabolization of the trestolone - causing it to stay in my body for longer?
Is this estrogen conversion something I should just suffer through? OR
would I be better off taking an AI to prevent this conversion - potentially allowing the clomid to work it's magic on estrogen receptors to stimulate LH production?
Would the one of these AIs hinder Clomid's ability to work?? anyone?? bump??
It would be nice if someone with a biochemistry or endocrinological research background could chime in on this. Separating fact and science from the "bro-science" that permeates steroid message boards is nauseating and making my head spin.
jbryand101b
Banned
Letrozole, problem solved.
00S4Boy
Active member
I much prefer exemestane for estrogen regulation, arimadex and letro are to aggressive and their competitive not suicidal nature makes rebound a very risky situation.
But yes if on trestolone some form of AI should be implemented to prevent conversion, will this extend the half life of trest in vivo, probably not.
As for ER competition, i don't believe 7a methylation increases binding, but it increases agonization.
But like i said ealier, with the intensively supressive nature of trestolone(and secondly through 7a methyl estrogen) because yes, androgens and estrogens cause supression in men. Because mens estrogens come from androgens, and if your body sees an excess of estrogen, it greatly supresses androgen production to try to counteract that. Hence why a SERM like clomid works, it binds to the ER in the brain but doesn't agonize it making the brain think it has very little to no estrogen so it ramps up androgen production to try and get estrogen to normal levels.
But yes if on trestolone some form of AI should be implemented to prevent conversion, will this extend the half life of trest in vivo, probably not.
As for ER competition, i don't believe 7a methylation increases binding, but it increases agonization.
But like i said ealier, with the intensively supressive nature of trestolone(and secondly through 7a methyl estrogen) because yes, androgens and estrogens cause supression in men. Because mens estrogens come from androgens, and if your body sees an excess of estrogen, it greatly supresses androgen production to try to counteract that. Hence why a SERM like clomid works, it binds to the ER in the brain but doesn't agonize it making the brain think it has very little to no estrogen so it ramps up androgen production to try and get estrogen to normal levels.
wormwood
Member
I know that my doctor favors the use of arimidex... I am thinking I may have to order some exemestane if I want to go this route. Unless there is some body of evidence I could show him that would indicate that exemestane is more favorable for my situation - even still - I don't know if he would do it or what the availability of pharmaceutical grade aromasin is.
Aromasin is a suicide inhibitor.. does that mean that it will negatively affect the ability for clomid to mediate the estrogen receptor to signal LH production??
OR
is the 7a-methyl-estrogen binding so strongly to the estrogen receptors that the clomid isn't even working... and may also be the reason why the toremifene failed as well. Although in my most recent bloodwork my testosterone levels did increase after taking clomid and hcg for a month - they are still only at 91 - I would consider hcg and clomid to be failing in this case.
agghhhhhhh this is so frustrating.
Aromasin is a suicide inhibitor.. does that mean that it will negatively affect the ability for clomid to mediate the estrogen receptor to signal LH production??
OR
is the 7a-methyl-estrogen binding so strongly to the estrogen receptors that the clomid isn't even working... and may also be the reason why the toremifene failed as well. Although in my most recent bloodwork my testosterone levels did increase after taking clomid and hcg for a month - they are still only at 91 - I would consider hcg and clomid to be failing in this case.
agghhhhhhh this is so frustrating.
wormwood
Member
also - where and how does intra-testicular E2 play a role in this equation for HPTA recovery?
I am thinking I may have to search for the email of a researcher who has had experience handling these compounds and ask them what is going on. Why would a TRT doctor not be more familiar with aromasin and be so headstrong about arimidex?
I am thinking I may have to search for the email of a researcher who has had experience handling these compounds and ask them what is going on. Why would a TRT doctor not be more familiar with aromasin and be so headstrong about arimidex?
00S4Boy
Active member
It's highly unlikely that you will sway a doctor for medication for treatment in a case like this. Just order some RC exemestane and call it a day.
Suicidal inhibitors just mean once it binds to aromatase it binds until it is metabolized inert, not for a period of time then released to aromatase is active again. Binding to an enzyme shouldn't have any effect of the ER.
It probably just is a combo of trest because your using it in decanoate ester and it is extremely supressive even at tiny amounts and 7a methyl estrogen furthering supression.
Suppression stems from the brain not intratesticular anything. Brain reads androgens and estrogens and outputs LH and FSH accordingly.
TRT is still relatively new, and doctors are pretentious so as much as the situation sucks, sometimes it just takes trial and error on your own to get things right.
jbryand101b
Banned
Rebound?
I would of thought someone who spends considerable time at phf would of put aside the bro science of suicide an non suicide rebound issues.
wormwood
Member
I went to a TRT clinic because I knew they would be more accomodating than a PCP or general practitioner and speaking frankly about 10 years of steroid use to a doctor in a lab coat is not an easy thing to do. I do get the feeling that they are more interested in having me put on testosterone replacement therapy when it may not be in my best interests..
for TRT purposes - i'm sure arimidex is quite fine. for my situation i guess aromasin is better.
either way I want to make sure I am forthright in discussing this with him - I don't want to present a combative situation and don't want to take anything with contraindications to the hcg and clomid that I am being prescribed. I may just need to knuckle up and order some RC exemestane - it would probably cost about the same as getting it as a prescription anyway. I am just reluctant to order exemestane from the same people that I bought this trestolone crap from..
I wish I had never taken trestolone - I am never going to take any form of steroid ever again If I recover from this. I really hope I don't have to spend the rest of my life on testosterone - I really don't want to have to deal with being a pin cushion for the rest of my life.
for TRT purposes - i'm sure arimidex is quite fine. for my situation i guess aromasin is better.
either way I want to make sure I am forthright in discussing this with him - I don't want to present a combative situation and don't want to take anything with contraindications to the hcg and clomid that I am being prescribed. I may just need to knuckle up and order some RC exemestane - it would probably cost about the same as getting it as a prescription anyway. I am just reluctant to order exemestane from the same people that I bought this trestolone crap from..
I wish I had never taken trestolone - I am never going to take any form of steroid ever again If I recover from this. I really hope I don't have to spend the rest of my life on testosterone - I really don't want to have to deal with being a pin cushion for the rest of my life.
00S4Boy
Active member
There is no bro science in this competative inhibition versus suicidal inhibition. With competitive inhibition be it Arimadex or Letrozole, will bind and release the enzyme unlike a steroidal suicide inhibitor. So if you drastically reduce aromatase activity with competitive inhibition without an appropriate taper off so slowly let androgens aromatise and render aromatase eventually inert you will end up with a spike of aromtase and, inturn a spike of estrogen.
jbryand101b
Banned
This isn't any different with suicidal or non suicidal.
You won't find any data supporting non suicidal ai's have any more chance of causing rebound than suicidal ones. (hence the bro lore of rebound scares)
And using the same bro logic, drastically reducing aromatase will cause a imbalance the body will attempt to fix by producing more aromatase. This will cause a rebound effect.
But it's all irrelevant.
The end result is the same, you should taper off your ai regardless of the type.
wormwood
Member
I have roughly 8mg of arimidex and 125mg of aromasin on hand.. should I take a combination of both or should I take arimidex and then switch to aromasin? I figure I might as well use them both up since I already have them on hand - even if one or both of these compounds aren't ideal.
wormwood
Member
Isn't aromasin better about sparing igf-1 production in the liver? that alone would make it a better choice right?
- I do agree that either one should be tapered as I come off regardless. I feel like I need to be on this long term as it may very well take another 3 months to for the remaining trestolone to clear my system. If aromasin is better on lipids or liver than arimidex - that would be a more attractive option.
- I do agree that either one should be tapered as I come off regardless. I feel like I need to be on this long term as it may very well take another 3 months to for the remaining trestolone to clear my system. If aromasin is better on lipids or liver than arimidex - that would be a more attractive option.
00S4Boy
Active member
It doesn't have to be specific data for aromatase inhibitors.
It's simply how Suicidal Inhibition works vs Competitive inhibition.
jbryand101b
Banned
Nvm, don't know why I bother.
End point for those with sense.
Use what ai works best with you.
Taper the dosage when stopping it.
Rebound is a risk with both ai's, and non aromatizing steroids.
wormwood
Member
took 1mg of arimidex yesterday and today.. Joints already aching... ugh.. makes working out a bitch. I think i'm going to lower my dose to .5mg
If this methyl estrogen doesn't bind to shbg - is there anything I can take to combat it? I feel like that has to be the culprit. I'm sure there's a lot of it built up. I want that **** gone.
If this methyl estrogen doesn't bind to shbg - is there anything I can take to combat it? I feel like that has to be the culprit. I'm sure there's a lot of it built up. I want that **** gone.
wormwood
Member
so I came across this post on patrick arnold's blog that indicated that 100mg/kg oral dose of Taurine was able to offset 10mg/kg IM dose of nandrolone decanoate's adverse effects on testicular function.
"Results of the present study showed that taurine reversed nandrolone decanoate-induced perturbations in sperm characteristics, normalized serum testosterone level, and restored the activities of the key steroidogenic enzymes; 3β-HSD, and 17β-HSD. Moreover, taurine prevented nandrolone decanoate-induced testicular toxicity and DNA damage by virtue of its antioxidant, anti-inflammatory, and anti-apoptotic effects."
study abstract:
Invalid Link Removed
Given the fact that nandrolone and trestolone are both 19-nor compounds - Do you guys think that taking taurine would help my situation?
100mg /kg dose would translate into roughly a 10gram daily dose for me - definitely doable and not too expensive.
Maybe this dose of taurine should be reviewed as standard protocol for a cycle of any anabolic steroid?
"Results of the present study showed that taurine reversed nandrolone decanoate-induced perturbations in sperm characteristics, normalized serum testosterone level, and restored the activities of the key steroidogenic enzymes; 3β-HSD, and 17β-HSD. Moreover, taurine prevented nandrolone decanoate-induced testicular toxicity and DNA damage by virtue of its antioxidant, anti-inflammatory, and anti-apoptotic effects."
study abstract:
Invalid Link Removed
Given the fact that nandrolone and trestolone are both 19-nor compounds - Do you guys think that taking taurine would help my situation?
100mg /kg dose would translate into roughly a 10gram daily dose for me - definitely doable and not too expensive.
Maybe this dose of taurine should be reviewed as standard protocol for a cycle of any anabolic steroid?
wormwood
Member
wellll I have purchased some Taurine. I figured either way it can't hurt. I'm going to be adding 10g/day taurine to my current regimen of:
500 IU hcg 3x weekly (mon/wed/fri)
25mg of Clomid taken at night
.5mg arimidex taken in AM - until I run out - then I will switch to aromasin
12-18g/day Norwegian Salmon OIl - with meals throughout day
325 mg (5GR) Ferrous Sulfate taken in AM
Since trestolone is lipophillic - I am going to gradually increase my level of cardio in addition to weightlifting to hopefully clear this out of my system a little quicker
Anyone see a problem with this? any suggestions?
500 IU hcg 3x weekly (mon/wed/fri)
25mg of Clomid taken at night
.5mg arimidex taken in AM - until I run out - then I will switch to aromasin
12-18g/day Norwegian Salmon OIl - with meals throughout day
325 mg (5GR) Ferrous Sulfate taken in AM
Since trestolone is lipophillic - I am going to gradually increase my level of cardio in addition to weightlifting to hopefully clear this out of my system a little quicker
Anyone see a problem with this? any suggestions?
AlexPowell
Well-known member
I agree Letro is the best course of action here
1.25mg EOD should do it.
I also use raloxifene, it's a SERM that doesn't ****ing suck. 30mg a day is enough. It will crush gyno to the point where only the breast tissue remains
1.25mg EOD should do it.
I also use raloxifene, it's a SERM that doesn't ****ing suck. 30mg a day is enough. It will crush gyno to the point where only the breast tissue remains
AlexPowell
Well-known member
Yeah the trest won't be out your system for ages and you're desensitising you leydig cells to gonadotropins only to continue being shut down lol
Come off EVERYTHING
Take some letro, don't go ****ing nuts with it either
Take a serm, whatever you have on hand. Order some raloxifene then switch to that
Take "natural" test boosters like trib so you can actually get it up and feel good lol (won't boost your test)
Ride it out
Hope that your test levels return to ~400
If so, you're good
Any more is a blessing
400 is enough anyway, not like test within the physiological ranges makes a difference anyway
wormwood
Member
I have had gynecomastia surgery before several (10) years ago - no chance of that coming back anyway
SquatsAndOats
Active member
Uhh what else would there be besides breast tissue in his gyno? Gyno IS breast tissue...
wormwood
Member
I don't have gyno anyway.. Please keep any suggestions you have to those supported by current research.. I understand that leydig cell burnout can occur - my doctor has told me that the dose I am taking should avoid that and retain normal testicular function and sperm count while the clomid restores hpta.
Hopefully the Taurine will help this - it seems to have a promising effect against leydig cell apoptosis brought on by nandrolone in the study I linked above.
I wonder if these effects of Taurine can apply to other anabolics besides nandrolone - that is the question.
Hopefully the Taurine will help this - it seems to have a promising effect against leydig cell apoptosis brought on by nandrolone in the study I linked above.
I wonder if these effects of Taurine can apply to other anabolics besides nandrolone - that is the question.
AlexPowell
Well-known member
Lots of the time it is just inflammation. The gyno can be inflammed and get very large. When the swelling goes down you may not even be able to feel it
It's still there
wormwood
Member
I've decided to get on TRT.. I can't handle feeling miserable like this anymore.. had bloodwork done again today and am having more labs done tomorrow for insurance purposes - my insurance will cover 90% of the treatment - awesome.
clomid and hcg were so ineffective I had to start taking lexapro to manage the major depression and anxiety i'm experiencing - been taking that for 2 weeks now. My plan is to be on TRT for a year or so while the MENT clears my system and then I will attempt another restart with clomid. I am under the impression that I will probably be given a dose of somewhere around 200mg/week and I'm considering doing blasts of test propionate in betweeen bloodwork (every quarter) to kick my efforts in the gym back in high gear.
I may run ostarine and igf-1 DES or MGF - haven't run these compounds before. I've used Igf-1 lr3 and quite enjoyed it. I figure I might as well take advantage of hyperplasia while my test levels are high. I will continue to use Taurine (10g/day) with the hopes that I can at least somewhat ameliorate the effects of shut down.
This new TRT doc I found seems to really know his stuff. Wants to establish a dose of test to get my levels between 900-1200ng/dl and wants to keep estrogen below 25 (as opposed to the other doc that was ok with levels as high as 39. he said he will continue the hcg regiment I was on from the previous doc as well.
libido is in the tank since starting lexapro... been unable to ejaculate- frustrating as all hell..
Will report back tomorrow and let you guys know what my labs look like. Hopefully they'll be able to start me on TRT tomorrow and I can get back to feeling normal as quick as possible.
clomid and hcg were so ineffective I had to start taking lexapro to manage the major depression and anxiety i'm experiencing - been taking that for 2 weeks now. My plan is to be on TRT for a year or so while the MENT clears my system and then I will attempt another restart with clomid. I am under the impression that I will probably be given a dose of somewhere around 200mg/week and I'm considering doing blasts of test propionate in betweeen bloodwork (every quarter) to kick my efforts in the gym back in high gear.
I may run ostarine and igf-1 DES or MGF - haven't run these compounds before. I've used Igf-1 lr3 and quite enjoyed it. I figure I might as well take advantage of hyperplasia while my test levels are high. I will continue to use Taurine (10g/day) with the hopes that I can at least somewhat ameliorate the effects of shut down.
This new TRT doc I found seems to really know his stuff. Wants to establish a dose of test to get my levels between 900-1200ng/dl and wants to keep estrogen below 25 (as opposed to the other doc that was ok with levels as high as 39. he said he will continue the hcg regiment I was on from the previous doc as well.
libido is in the tank since starting lexapro... been unable to ejaculate- frustrating as all hell..
Will report back tomorrow and let you guys know what my labs look like. Hopefully they'll be able to start me on TRT tomorrow and I can get back to feeling normal as quick as possible.
wormwood
Member
He didn't have labs ready today. Did another blood draw for insurance purposes and gave me a shot of 125mg of Test Cypionate, 500iu of HCG, and 1mg of anastrozole.
Says he will have labs ready for me next week when I come in for my next shot. I am continuing to take taurine - I'm considering bumping my dose up to 15 grams/day from the current 10g per day.
I still have some hcg on hand - I will likely use this if I feel any shut down between shots. I have a feeling I may.
Considering picking up some formestane?
I came across this and the effects of formestane being able to ameliorate hpta suppression are really interesting to me. I wonder if this has anything to do with it's ability to increase igf-1?
Invalid Link Removed
he says he compiled this data from logs and research. It would be nice to separate quality research from broscience and online anecdotes.
also see this as well:
Invalid Link Removed
Anyone have thoughts about these articles? Do you think Formestane would show increased test levels on my labs due to its metabolites? I know it is a prohormone of sorts and a steroidal AI as well. The doc I am seeing isn't comfortable using anything other than anastrozole. I am just worried this won't be enough to counter the effects of the 7a-methylethinyl-estradiol that is still circulating my blood.
Has anyone here used a formestane product? I am really uncomfortable with using transdermals. I would much prefer an injectable form - I remember it being available at one point but I'm not sure if that is still available.
I am thinking I may throw in some IGF-1 as well. Do you think LR3 or DES would be more beneficial for my situation? - as in my goal is to minimize suppression from TRT - might as well get the benefits of hyperplasia if I am on TRT.
Thanks in advance guys.
Says he will have labs ready for me next week when I come in for my next shot. I am continuing to take taurine - I'm considering bumping my dose up to 15 grams/day from the current 10g per day.
I still have some hcg on hand - I will likely use this if I feel any shut down between shots. I have a feeling I may.
Considering picking up some formestane?
I came across this and the effects of formestane being able to ameliorate hpta suppression are really interesting to me. I wonder if this has anything to do with it's ability to increase igf-1?
Invalid Link Removed
he says he compiled this data from logs and research. It would be nice to separate quality research from broscience and online anecdotes.
also see this as well:
Invalid Link Removed
Anyone have thoughts about these articles? Do you think Formestane would show increased test levels on my labs due to its metabolites? I know it is a prohormone of sorts and a steroidal AI as well. The doc I am seeing isn't comfortable using anything other than anastrozole. I am just worried this won't be enough to counter the effects of the 7a-methylethinyl-estradiol that is still circulating my blood.
Has anyone here used a formestane product? I am really uncomfortable with using transdermals. I would much prefer an injectable form - I remember it being available at one point but I'm not sure if that is still available.
I am thinking I may throw in some IGF-1 as well. Do you think LR3 or DES would be more beneficial for my situation? - as in my goal is to minimize suppression from TRT - might as well get the benefits of hyperplasia if I am on TRT.
Thanks in advance guys.
CATdiesel76
Well-known member
Man I know you want to get over this fast so you can get back to normal but I would say you are overthinking things. I have ready of many people it took 6 months + to recover from deca. Ride out this TRT for a bit and try to restart things again. Run an oral or something if you want and Maybe save the peps for when you come off to aid holding gains
mixedup
Well-known member
I hope you got some short esthers
CATdiesel76
Well-known member
Hell run the Trest deconate. Do some mega dosing and it will be in your system almost the whole time. Anything else and you will hit rock bottom 2-3 weeks in there. Not the ideal time to turn into an emotional wreck
wormwood
Member
maybe i should see if I can get some test undecanoate? I read somewhere that the half life for that is 50 some odd days?
I'm never touching trest again - I think it's conversion to 7a-methylethinyl-estradiol is what made me an emotional wreck a few weeks ago. I still have 4 vials of that garbage left that I don't know what to do with. I don't seem to have much luck with any compound that has progestogenic activity. I'm just gonna stick to test and DHT derived compounds from here on out. I'm sure some guys can handle it just fine but I'd rather not **** with it.
I'm never touching trest again - I think it's conversion to 7a-methylethinyl-estradiol is what made me an emotional wreck a few weeks ago. I still have 4 vials of that garbage left that I don't know what to do with. I don't seem to have much luck with any compound that has progestogenic activity. I'm just gonna stick to test and DHT derived compounds from here on out. I'm sure some guys can handle it just fine but I'd rather not **** with it.
rtmilburn
Well-known member
Probably good idea. Just run it at high doses because the mix ester there is only a limited amount of the long esters. Then start pct when you get back. Which should be long enough to let the esters clear
mixedup
Well-known member
Can you get anadrol or dbol it won't last but first impressions are big I'd run that and test cyp
wormwood
Member
Alright, well it's been several months since I've visited these forums but I thought I would give a more positive update to this awful anecdote.
I have been on TRT for the greater part of 6 months now and am doing exponentially better. My jail sentence ended up being work release jail so I was only locked up between the hours of 10pm and 4am every night and was free to go out and work, workout, and whatnot during the day.
In June I got in touch with a doctor that is an expert in the field of anabolic steroids, TRT, Anti-aging, etc. We decided that trying to test for serum levels of the super estrogen metabolite of trestolone (7a-methyl-estradiol) would be of little value as it doesn't require binding to SHBG and thus wouldn't be an accurate count of it's presence in peripheral tissues - namely fat (which accumulated substantially throughout my attempted hpta restart).
Given this and the trest decanoate ester's outrageously long half-life combined with the retarded dosages I was using, we figured it may very well take me 2-3 years to flush out these substance before I could reasonably expect to recover. We decided that I might as well take advantage of the situation by maximizing my opportunity to use TRT to offset some of the negative effects of the excess estrogens and reduce body fat (up to 18% caliper at it's worst)
From June until now, He had me on a dose of 500mg/week test cyp with 1mg/day anastrozole. 4weeks on, one week off on the test injections. We are keeping an eye on my e2 levels to make sure they do not go above 15pg/dl. Also was prescribed 1000iu/week of HCG (for testicular size). Test levels are to be kept at no more than 2,000ng/dl with the 4 on/1 off protocol.
During this time I have been promoted at work (25% pay increase), lost 4% bodyfat, re-enrolled at University to continue my biochem degree (1 year left!) and completed a full semester with a 3.5 gpa full time while working 50hrs/week. Strength is up, wallet is fatter, much more productive and proactive. Overall, I feel pretty good. although in the last month I do notice that hcg isn't working as well as it did in the first 3-4months.
I just had blood drawn a few days ago to see where my levels are at and given a new round of 6-month scripts. Test dose to be increased to 600mg/week (2 injections) with same 4 on 1 off protocol. hcg to 1500iu/week (3 injections). Continue anastrozole at 1mg/day and also adding exemestane 25mg twice per week (i will take this the same day as i do my test injections). also got hooked up with oxandrolone at 40mg/day split dose 20mg in am and pm.
As far as supplementation goes I am currently taking 5g/day krill oil, and 10000iu vit d3 every 2 days in addition to a balanced diet high in protein.
I am looking into adding zinc orotate (leaning towards this form over other forms of zinc but i am still researching this), boron, magnesium, osthole/cnidium monnieri, tongkat ali, forskolin, and mucuna pruriens. I am taking advantage of my unlimited access through my university to the full text of any published study involving these minerals and herbs to determine wether or not i'll use them. So far Z and Mg look to be very promising and I like what I see on osthole so far.
I am considering adding in some form of peptide to work synergistically with the test and anavar for hyperplasia. I might throw in some melanotan II just for fun since spring break isn't far away and I think I may head to a beach.
On the subject of reduced response to hcg - I considered adding HMG (Human Menopausal Gonadotropin) as an adjunct with hcg and brought it up to the doc but we decided to try to up the dose for right now and I think that it's possible that I may just be short on Zinc from the high-stress I've been under at school and work. Not ruling that out right now though.
I have been on TRT for the greater part of 6 months now and am doing exponentially better. My jail sentence ended up being work release jail so I was only locked up between the hours of 10pm and 4am every night and was free to go out and work, workout, and whatnot during the day.
In June I got in touch with a doctor that is an expert in the field of anabolic steroids, TRT, Anti-aging, etc. We decided that trying to test for serum levels of the super estrogen metabolite of trestolone (7a-methyl-estradiol) would be of little value as it doesn't require binding to SHBG and thus wouldn't be an accurate count of it's presence in peripheral tissues - namely fat (which accumulated substantially throughout my attempted hpta restart).
Given this and the trest decanoate ester's outrageously long half-life combined with the retarded dosages I was using, we figured it may very well take me 2-3 years to flush out these substance before I could reasonably expect to recover. We decided that I might as well take advantage of the situation by maximizing my opportunity to use TRT to offset some of the negative effects of the excess estrogens and reduce body fat (up to 18% caliper at it's worst)
From June until now, He had me on a dose of 500mg/week test cyp with 1mg/day anastrozole. 4weeks on, one week off on the test injections. We are keeping an eye on my e2 levels to make sure they do not go above 15pg/dl. Also was prescribed 1000iu/week of HCG (for testicular size). Test levels are to be kept at no more than 2,000ng/dl with the 4 on/1 off protocol.
During this time I have been promoted at work (25% pay increase), lost 4% bodyfat, re-enrolled at University to continue my biochem degree (1 year left!) and completed a full semester with a 3.5 gpa full time while working 50hrs/week. Strength is up, wallet is fatter, much more productive and proactive. Overall, I feel pretty good. although in the last month I do notice that hcg isn't working as well as it did in the first 3-4months.
I just had blood drawn a few days ago to see where my levels are at and given a new round of 6-month scripts. Test dose to be increased to 600mg/week (2 injections) with same 4 on 1 off protocol. hcg to 1500iu/week (3 injections). Continue anastrozole at 1mg/day and also adding exemestane 25mg twice per week (i will take this the same day as i do my test injections). also got hooked up with oxandrolone at 40mg/day split dose 20mg in am and pm.
As far as supplementation goes I am currently taking 5g/day krill oil, and 10000iu vit d3 every 2 days in addition to a balanced diet high in protein.
I am looking into adding zinc orotate (leaning towards this form over other forms of zinc but i am still researching this), boron, magnesium, osthole/cnidium monnieri, tongkat ali, forskolin, and mucuna pruriens. I am taking advantage of my unlimited access through my university to the full text of any published study involving these minerals and herbs to determine wether or not i'll use them. So far Z and Mg look to be very promising and I like what I see on osthole so far.
I am considering adding in some form of peptide to work synergistically with the test and anavar for hyperplasia. I might throw in some melanotan II just for fun since spring break isn't far away and I think I may head to a beach.
On the subject of reduced response to hcg - I considered adding HMG (Human Menopausal Gonadotropin) as an adjunct with hcg and brought it up to the doc but we decided to try to up the dose for right now and I think that it's possible that I may just be short on Zinc from the high-stress I've been under at school and work. Not ruling that out right now though.
wormwood
Member
So... Does anyone have a recommendation for the best form of zinc? I've read a lot of people say positive things about orotate, but I haven't found any studies that reflect this supposed better bioavailability. I found one document that seems to indicate that citrate is the preferable form, and seen a study done in the 80s that wasn't a positive review of orotate. There seems to be a lot of conflicting information on this...
bananagains
Banned
Just another reason I'll never fuk with 19-Nor compounds