More tren, less test....anyone here do that?

[waynaferd]

I've been reading/searching/studying, and was wondering if anyone doses their tren higher than their test on a cycle.

This is the shoretest/easiest explanation of why since I'm sure someone will think I need a gram of test for a base, LOL....

-----------------------------------------
Testosterone and tren use the same receptor sites.

Tren binds faster and stronger to the receptor site than testosterone. So what will happen is that the tren will overtime saturate all the receptors it possibly can, testosterone will fill the rest.

Unfortunatly, all the testosterone that didn't get to bind to the receptor will do one of two things: it will convert to estrogen or it will convert to DHT.

The test that convers to DHT will start to beat out tren for it's receptors because of DHT's afinity to AR's.

---------------------------

Anyway, anyone have thoughts on this? I'm now considering tren A at 50 ED and prolly Test E around 300/week, maybe even lower, like 250, and bump up the tren a bit higher, maybe 60/day

 

[icon0561]

Im currently running test prop at 50mg ED and tren 75 ED. I usually run test at low doses just for libido and mood and let tren work its magic.

 

[Hazcat]

Tren is so androgenic test doesn't have much of a chance for getting on the receptor so I use very little test until I drop tren from the cycle. After I drop the tren I up the test dose at that point.

 

[RedwolfWV]

Very interesting explanation Waynaferd. I think I will give this a try next Tren cycle.

 

[Alphaanimal]

sounds good to me im doing 100mg prop daily and 130 tren ace daily and love this

 

[waynaferd]

Good to know you guys like doing this....it makes sense to me but I always read use a lot of test for cycles.

Can't wait to start!!

 

[ssbackwards]

well, if i were you and running iot that way,

MILD AI, and a MILD DHT blocker.

when i say mild DHT blocker i guess an OTC like formestane or something because when u block DHT it makes tren more potent, but you want more test to stay as test... get where im coming from. This way you can dose tren a lil lower with same effects due to increased potency.

I actually go gyno from running fini with my tren, so i was careful, with my AI, it since went away, but id look into form so it blocks both e2 and DHT

 

[DetroitHammer]

Can you explain how reducing DHT will make Tren more potent? I understand that DHT competes for the AR along with Tren, but only about 5% of testosterone undergoes 5α-reduction, so there are still plenty of AR's out there. And if you block DHT, you essentially block the benefits of test. And what do you mean when you say you want test to remain test? I just don't understand.

well, if i were you and running iot that way,

MILD AI, and a MILD DHT blocker.

when i say mild DHT blocker i guess an OTC like formestane or something because when u block DHT it makes tren more potent, but you want more test to stay as test... get where im coming from. This way you can dose tren a lil lower with same effects due to increased potency.

I actually go gyno from running fini with my tren, so i was careful, with my AI, it since went away, but id look into form so it blocks both e2 and DHT

 

[ssbackwards]

you want test to not aromatize.... in terms of how it makes it more potent, ill have to check seth roberts anabolic pharmacology for a scientific answer, bc i cant pretend i know it off hand.

 

[heckler7]

op thats what I hear too run tren higher

 

[Yaz]

well, if i were you and running iot that way,

MILD AI, and a MILD DHT blocker.

when i say mild DHT blocker i guess an OTC like formestane or something because when u block DHT it makes tren more potent, but you want more test to stay as test... get where im coming from. This way you can dose tren a lil lower with same effects due to increased potency.

I actually go gyno from running fini with my tren, so i was careful, with my AI, it since went away, but id look into form so it blocks both e2 and DHT

Can you explain how reducing DHT will make Tren more potent? I understand that DHT competes for the AR along with Tren, but only about 5% of testosterone undergoes 5α-reduction, so there are still plenty of AR's out there. And if you block DHT, you essentially block the benefits of test. And what do you mean when you say you want test to remain test? I just don't understand.

Second to that, i would like an explanation, because i don't seem to understand the logic behing this.

 

[waynaferd]

Now I'm confused fo sho!!

So would a drop of Nolva be the thing to have, instead of an AI?

 

[Yaz]

Now I'm confused fo sho!!

So would a drop of Nolva be the thing to have, instead of an AI?

AIs during cycle, SERMs only PCT.

 

[waynaferd]

I used inhibit-E last time, and that did the trick for test/deca.....then needed caber for "certain" side effects, LOL....lemme re-read whats above again

 

[ssbackwards]

Second to that, i would like an explanation, because i don't seem to understand the logic behing this.

i will bust out that book tomorrow.

i dont wanna write word for word, but i can kinda qoute main points.

 

[DetroitHammer]

AIs during cycle, SERMs only PCT.

Yaz, what about prostrate concerns? I follow your logic as it applies to gyno, but SERMs won't help the prostrate. After recovering from prostatitis, I would err on the side of caution and probably stick to an AI. But very few young guys probably have to worry about their prostrate so a SERM would be sufficient.

 

[Yaz]

Yaz, what about prostrate concerns? I follow your logic as it applies to gyno, but SERMs won't help the prostrate. After recovering from prostatitis, I would err on the side of caution and probably stick to an AI. But very few young guys probably have to worry about their prostrate so a SERM would be sufficient.

Supplements like Saw Palmetto [FONT=Verdana, Arial, Helvetica][SIZE=-1][FONT=Verdana, Arial, Helvetica][SIZE=-1]extract[/SIZE][/FONT][/SIZE][/FONT], Lycopene, [FONT=Verdana, Arial, Helvetica][SIZE=-1][FONT=Verdana, Arial, Helvetica][SIZE=-1]Pygeum Africanum [/SIZE][/FONT][/SIZE][/FONT][FONT=Verdana, Arial, Helvetica][SIZE=-1][FONT=Verdana, Arial, Helvetica][SIZE=-1]extract[/SIZE][/FONT][/SIZE][/FONT][FONT=Verdana, Arial, Helvetica][SIZE=-1][FONT=Verdana, Arial, Helvetica][SIZE=-1], Nettle Root extract[/SIZE][/FONT][/SIZE][/FONT][FONT=Verdana, Arial, Helvetica][SIZE=-1][FONT=Verdana, Arial, Helvetica][SIZE=-1] will [/SIZE][/FONT][/SIZE][/FONT] help.

 

[DetroitHammer]

Supplements like Saw Palmetto [SIZE=-1][SIZE=-1]extract[/SIZE][/SIZE], Lycopene, [SIZE=-1][SIZE=-1]Pygeum Africanum [/SIZE][/SIZE][SIZE=-1][SIZE=-1]extract[/SIZE][/SIZE][SIZE=-1][SIZE=-1], Nettle Root extract[/SIZE][/SIZE][SIZE=-1][SIZE=-1] will [/SIZE][/SIZE] help.

I posted a study about a month ago where they disproved SP having any benefit at all for the prostrate. I can't swear by the study, but it seemed more exhaustive than previous studies. (http://www.npr.org/templates/story/story.php?storyId=5198053) (http://www.cbsnews.com/8301-504763_162-20112695-10391704.html) I asked my doctor and he said there was no clinical study supporting SP as an effective treatment for an enlarged prostrate.

The only two things that can cause prostrate enlargement would be DHT or estrogen. Both of mine were high, but I suspect it was the estrogen that caused my prostatitis. Fact is, very little has been done as far as studying prostrate problems caused by estrogen, compared to studies on breast cancer for instance.

Like I said, I doubt most of the guys here have to worry about their prostrate just yet, so SERMs and root extracts may do the trick.

Thanks

 

[Yaz]

I posted a study about a month ago where they disproved SP having any benefit at all for the prostrate. I can't swear by the study, but it seemed more exhaustive than previous studies. (http://www.npr.org/templates/story/story.php?storyId=5198053) (http://www.cbsnews.com/8301-504763_162-20112695-10391704.html) I asked my doctor and he said there was no clinical study supporting SP as an effective treatment for an enlarged prostrate.

The only two things that can cause prostrate enlargement would be DHT or estrogen. Both of mine were high, but I suspect it was the estrogen that caused my prostatitis. Fact is, very little has been done as far as studying prostrate problems caused by estrogen, compared to studies on breast cancer for instance.

Like I said, I doubt most of the guys here have to worry about their prostrate just yet, so SERMs and root extracts may do the trick.

Thanks

- Indeed DHT and estrogen can damage prostate - for the first you should go with the herbs i wrote down( bunch o studies FYI) and for the 2nd AIs obviously.
- As far medical studies for Saw Palmetto there you go:
http://www.ncbi.nlm.nih.gov/pubmed/21109292 (in Combo with Lycopene + Selenium)
http://www.ncbi.nlm.nih.gov/pubmed/21855911 (in Combo with Lycopene + Selenium)
http://www.ncbi.nlm.nih.gov/pubmed/21969849 (Review)
http://www.ncbi.nlm.nih.gov/pubmed/21656602


I can keep going on Saw Palmetto (if you notice these studies are just VERY new).
- Didn't mention Selenium, i forgot because i usually don't recommend cause it's quite easy to intoxicate yourself if you aren't careful enough.
- I have to agree with you, being 57 you should by all means be crazy careful on prostate + lipis + kidneys. IMO all guys above 35 should use prostate support supp if the use strong androgens.

I thank you sir, because we always have great discussions.

 

[ssbackwards]

alright YAZ, heres from the book. sorry it took so long. i will qoute

"in most cases, 5alpha reduction results in a more potent androgen"

"in the case of nandrolone and nandrolone derivitives, 5-alpha reduction results in less potent derivitives" 103 (metabolism and receptor binding of nandrolone and testosterone under in vitro and in vivo conditions)

Goes on to say....
"in this case, nandrolone is converted to DHN. DHN has les affinity for the AR then Nandrolone. "

" an interesting side effect of 5-alpha reductase inhibition is an increase in testosterone due to a decrease in androgenic feedback at the hypothalamus. Also less testosterone is "broken down" to DHT; therefore, more remains in circulation" (effects of the 5 alpha-reductase inhibitor finisteride on serum levels of gonadal, adrenal, and hypophyseal hormones and its clinical significance; a perspective clinical study. steroids.)

all qouted from Seth Roberts Anabolic pharmocology.

 

[DetroitHammer]

I think the assumption is that if test doesn't convert to DHT, it undergoes more anabolic transcription. Testosterone will still bind to the AR, only not as strongly as DHT. So if there are more androgen receptors, then more test will bind to them. Also, more test will be aromatized, hence, more estrodial.

In regards to making Tren more potent, that connection hasn't been made. The only reason you could make assumptions along those lines would be thinking that if you free up ARs more Tren will bind to them and become more "potent." However, tren has an affinity five times stronger than test to bind to the AR while DHT has 3 times the affinity, so Tren's affinity should remain as strong with or without DHT competing for the AR. I don't know how competition for the AR works, but I believe that the 5% of test that converts to DHT, if blocked, would have little impact on the ultimate binding to the AR. Maybe Yaz can shed some light on this?

alright YAZ, heres from the book. sorry it took so long. i will qoute

"in most cases, 5alpha reduction results in a more potent androgen"

"in the case of nandrolone and nandrolone derivitives, 5-alpha reduction results in less potent derivitives" 103 (metabolism and receptor binding of nandrolone and testosterone under in vitro and in vivo conditions)

Goes on to say....
"in this case, nandrolone is converted to DHN. DHN has les affinity for the AR then Nandrolone. "

" an interesting side effect of 5-alpha reductase inhibition is an increase in testosterone due to a decrease in androgenic feedback at the hypothalamus. Also less testosterone is "broken down" to DHT; therefore, more remains in circulation" (effects of the 5 alpha-reductase inhibitor finisteride on serum levels of gonadal, adrenal, and hypophyseal hormones and its clinical significance; a perspective clinical study. steroids.)

all qouted from Seth Roberts Anabolic pharmocology.

 

[ssbackwards]

its simply to use a 5 alpha reductase inhibitor so you can lower the dose of the progestin to create the same effect .

 

[Yaz]

I think the assumption is that if test doesn't convert to DHT, it undergoes more anabolic transcription. Testosterone will still bind to the AR, only not as strongly as DHT. So if there are more androgen receptors, then more test will bind to them. Also, more test will be aromatized, hence, more estrodial.

In regards to making Tren more potent, that connection hasn't been made. The only reason you could make assumptions along those lines would be thinking that if you free up ARs more Tren will bind to them and become more "potent." However, tren has an affinity five times stronger than test to bind to the AR while DHT has 3 times the affinity, so Tren's affinity should remain as strong with or without DHT competing for the AR. I don't know how competition for the AR works, but I believe that the 5% of test that converts to DHT, if blocked, would have little impact on the ultimate binding to the AR. Maybe Yaz can shed some light on this?

First of all, ssbackwards written speech can be mistaken, i'm not offensive towards you just trying to get this conversation going.
Second, i have to agree with DH i don't understand how Tren can be more potent by blocking DHT. Anyway thanks for the info.


P.S. DH, man you did not respond at the comment i did for your question about Saw Palmettos efficancy - how'd you like 'em studies ?

 

[ssbackwards]

First of all, ssbackwards written speech can be mistaken, i'm not offensive towards you just trying to get this conversation going.
Second, i have to agree with DH i don't understand how Tren can be more potent by blocking DHT. Anyway thanks for the info.


P.S. DH, man you did not respond at the comment i did for your question about Saw Palmettos efficancy - how'd you like 'em studies ?

has to do with its metabolites being waeker when the hormones broken down by 5 alpha reductase enzyme.

hey man this kinda dialogue teaches a lot and forces growth man,. all good.

 

[ssbackwards]

I think the assumption is that if test doesn't convert to DHT, it undergoes more anabolic transcription. Testosterone will still bind to the AR, only not as strongly as DHT. So if there are more androgen receptors, then more test will bind to them. Also, more test will be aromatized, hence, more estrodial.

In regards to making Tren more potent, that connection hasn't been made. The only reason you could make assumptions along those lines would be thinking that if you free up ARs more Tren will bind to them and become more "potent." However, tren has an affinity five times stronger than test to bind to the AR while DHT has 3 times the affinity, so Tren's affinity should remain as strong with or without DHT competing for the AR. I don't know how competition for the AR works, but I believe that the 5% of test that converts to DHT, if blocked, would have little impact on the ultimate binding to the AR. Maybe Yaz can shed some light on this?

These assumptions can be made for not using proviron while on cycle bc it binds yet has no activity thus just taking up room on ARs.

i guess it can go both ways. but when i did the tren with fini, **** was strong!

 

[DetroitHammer]

P.S. DH, man you did not respond at the comment i did for your question about Saw Palmettos efficancy - how'd you like 'em studies ?

Sorry about that... From what I gather, and I'm just summarizing what I think I understand, the varies root extracts, including SP, have shown to inhibit the conversion to DHT, albeit mildly. They act almost like an AI would, only with much less conviction. I have Flomax, a drug, that acts like a SERM, in that it targets just the receptors in the prostrate and bladder. Sides, aside, Flomax is probably a better choice for anyone who is actually combating a case of prostatitis. I sort of concluded that the roots are a good organic source of reducing the likelihood of DHT related prostrate enlargement, but in my case, the effects are too mild. I need a specific modulator which Flomax is. Currently, I don't use anything because I'm basically in denial, but if I feel the need, I'll probably take Flomax until the swelling goes down. I do have some SP that I may start taking just because I have it and don't see any real harm in taking it.

Thanks for the references...

 

[Yaz]

Sorry about that... From what I gather, and I'm just summarizing what I think I understand, the varies root extracts, including SP, have shown to inhibit the conversion to DHT, albeit mildly. They act almost like an AI would, only with much less conviction. I have Flomax, a drug, that acts like a SERM, in that it targets just the receptors in the prostrate and bladder. Sides, aside, Flomax is probably a better choice for anyone who is actually combating a case of prostatitis. I sort of concluded that the roots are a good organic source of reducing the likelihood of DHT related prostrate enlargement, but in my case, the effects are too mild. I need a specific modulator which Flomax is. Currently, I don't use anything because I'm basically in denial, but if I feel the need, I'll probably take Flomax until the swelling goes down. I do have some SP that I may start taking just because I have it and don't see any real harm in taking it.

Thanks for the references...

Yeah those were more support type of supps, so i guess in this case you know better - glad you like 'em !