Pulse question for Dr. D or any other gurus

ThisGuy02

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Question about pulsing, and you guys feel free to say it’s not a good idea. That’s why I’m asking, I don’t know myself if it’s a good idea or worth the trouble/money. I’m only theorizing this possible cycle, and am not yet planning to run it, but could I run a 4 week pulse cycle into a standard 4 week? I had the idea for a cutter, because I’ve been extremely interested in trying both Epi and pulsing, but have decided on the part you’ll see listed as the second leg. Let me know what you guys think:

Weeks 1 – 4:
Epi 40mg (M, W, F)

Weeks 5 – 8:
WinZtrol 150mg ed
Propadrol 60mg ed
Cytomel ramped up to 50 or 75 mcg (depending on sides), then back down

Weeks 9 – 12 (PCT):
Novla (40/40/20/20)
Clomid (100/100/50/50)
Trione (600/600/300/300)
L-Tyrosine
 
DR.D

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... Weeks 9 – 12 (post cycle therapy):
Novla (40/40/20/20)
Clomid (100/100/50/50)
Trione (600/600/300/300)
L-Tyrosine
It looks good but the post cycle therapy needs some changes:

Clomid (100/100/0/0)
Novla (0/0/40/20)
Trione (100/200/300/300)

You don't need the overlapping SERMs and the trione is too high. 600mg of 6-oxo lowers LH levels, 300mg raises them. You also want to invert it with the SERM so that the AI increases as test levels increase. The pulse sounds good though.
 
Eric Potratz

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6-oxo is a steroidal compound. I wouldn’t use this for PCT, as it would not increase LH unless it managed to somehow reduce estrogen and remove some the ER inhibition on the hypothalamus. The study I have on 6-oxo didn’t measure LH and it actually showed an increase in overall estrogen. Everything points to the fact that trione probably converts directly to testosterone, or the blood test mistakes trione for testosterone itself. Eitherway, it has no practical use for PCT. I can send the study to anyone who is interested in seeing it.

Im not familiar with the WinZtrol or Propadrol. Do you know the active compounds of these pro-hormone sounding sups?

Also, that is way more SERM than you need for PCT. The most nolva you will ever want for PCT is 10mg day and the most clomid you would ever want is 25mg day (unless you are battling a gyno emergency) The amount of SERM you plan on using would no-doubtingly reduce your libido and erectile function.

-Pp
 
ThisGuy02

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Thanks to both!

PP, I’ve run about 5 pcts this way in the past year and a half and had complete bounce back, perfect libido, and no setbacks. AI is a solid addition to PCT in my opinion.

Dr. D, I’m not questioning your judgment, and in fact, your AI comment makes perfect sense to me. But just for my own knowledge, what’s the advantage of using Clomid at 100 for two weeks and then Nolva for 2 at 40/20? This isn’t too sudden a dropoff? As I said, I’ve always used the pct listed with great success. Is it just overkill in your opinion?

Also, about the pulse, do you think it would be an effective addition to the cut? I'm actually now thinking if I'm going to do this, I may want to front load my T3 on the last week of epi pulse, so I'm beginning the 50mg doses the same day I start the Ztrol/Props. What do you think?
 
Eric Potratz

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Thisguy,

That is good for you and your PCT. Not everyone bounces back so easily. I suppose the clomid/novlva PCT problems became more apparent to me after several years of cycling. I no longer use either of these drugs.

-Pp
 
ThisGuy02

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Thisguy,

That is good for you and your post cycle therapy. Not everyone bounces back so easily. I suppose the clomid/novlva PCT problems became more apparent to me after several years of cycling. I no longer use either of these drugs.

-Pp
no need to get testy, dude. I'm sorry those don't work for you anymore, and I'm not arguing what does. I'm just saying they always have for me.
 
Eric Potratz

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no need to get testy, dude. I'm sorry those don't work for you anymore, and I'm not arguing what does. I'm just saying they always have for me.
Wasn’t trying to come off rude at all bro… just giving my experience.

-Pp
 
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6-oxo is a steroidal compound. I wouldn’t use this for post cycle therapy, as it would not increase LH unless it managed to somehow reduce estrogen and remove some the ER inhibition on the hypothalamus. The study I have on 6-oxo didn’t measure LH and it actually showed an increase in overall estrogen. Everything points to the fact that trione probably converts directly to testosterone, or the blood test mistakes trione for testosterone itself. Eitherway, it has no practical use for PCT. I can send the study to anyone who is interested in seeing it.

Im not familiar with the WinZtrol or Propadrol. Do you know the active compounds of these pro-hormone sounding sups?

Also, that is way more SERM than you need for PCT. The most nolva you will ever want for PCT is 10mg day and the most clomid you would ever want is 25mg day (unless you are battling a gyno emergency) The amount of SERM you plan on using would no-doubtingly reduce your libido and erectile function.

-Pp
Can I get a link to a copy of that study? or a copy by some other means... Also, what do you use for PCT now that you dont use either clomid or nolva?
 
ThisGuy02

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Wasn’t trying to come off rude at all bro… just giving my experience.

-Pp
No worries, man, and I appreciate your taking the time to provide input. Everyone's experience is different, and that's exactly why this board is so useful.
 
Eric Potratz

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Can I get a link to a copy of that study? or a copy by some other means... Also, what do you use for post cycle therapy now that you dont use either clomid or nolva?
Please email me - [email protected] and I will send you a copy of the study.

I use our Dermacrine Sustain product, sometimes in combination with hCG. However, I believe hCG should always be used on cycle so PCT is less of challenge.

-Pp
 
Patrick Arnold

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6-oxo is a steroidal compound. I wouldn’t use this for post cycle therapy, as it would not increase LH unless it managed to somehow reduce estrogen and remove some the ER inhibition on the hypothalamus. The study I have on 6-oxo didn’t measure LH and it actually showed an increase in overall estrogen. Everything points to the fact that trione probably converts directly to testosterone, or the blood test mistakes trione for testosterone itself. Eitherway, it has no practical use for PCT. I can send the study to anyone who is interested in seeing it.

Im not familiar with the WinZtrol or Propadrol. Do you know the active compounds of these pro-hormone sounding sups?

Also, that is way more SERM than you need for PCT. The most nolva you will ever want for PCT is 10mg day and the most clomid you would ever want is 25mg day (unless you are battling a gyno emergency) The amount of SERM you plan on using would no-doubtingly reduce your libido and erectile function.

-Pp

both 6-oxo studies measured LH. and LH went up in both. there is no conceivable way it can convert to testosterone either.

sorry but your information is very faulty
 
Eric Potratz

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Pat,

Glad to get your attention.

In the Thomas Incledon Study funded by LPJ research, I see that LH was not measured, and that total estrogen increased (E1/E2) Can you explain these results?

I would attach the study but for some reason the attach function will not let me do it. Ill also take a look at the study you linked.

Thanks.

-Pp
 
Eric Potratz

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the long term study is here. you can clearly see that LH is measured and it does increase

https://beardocs.baylor.edu/bitstream/2104/3014/1/daniel_rohle_masters.pdf
In the study you linked, LH went down in the 300mg/day group and slightly increased in the 600mg/day group.

I see that total estrogen also increased significantly in both groups. That doesn’t sound like an aromatase inhibitor to me… and it certainly is a different result from what I’ve seen with other steroidal AI studies which reduce total estrogen.

-Pp
 
Patrick Arnold

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Pat,

Glad to get your attention.

In the Thomas Incledon Study funded by LPJ research, I see that LH was not measured, and that total estrogen increased (E1/E2) Can you explain these results?

I would attach the study but for some reason the attach function will not let me do it. Ill also take a look at the study you linked.

Thanks.

-Pp

i am almost positive that LH and FSH were both measured in the Incledon study. the results aren't shown in his abstract however.

as you can see in the baylor study though they were measured and increased

estrone went up and that could be because of a cross reactivity with 6-oxo estrone (which is formed as a by product)

now you may argue that testosterone cross reacts with 6-oxo testosterone but notice that DHT went up proportionally with testosterone (which is expected).

SHBG also dropped in both studies which is indicative of lower hepatic exposure to estrogens

the results are pretty solid. i have debated these things time and time again and considered the facts time and time again as well
 
jomi822

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PA id really like to see you chime in on my ATD thread....
 
Patrick Arnold

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In the study you linked, LH went down in the 300mg/day group and slightly increased in the 600mg/day group.

I see that total estrogen also increased significantly in both groups. That doesn’t sound like an aromatase inhibitor to me… and it certainly is a different result from what I’ve seen with other steroidal AI studies which reduce total estrogen.

-Pp
please do a literature search on pubmed if you do not believe 6-oxo is an aromatase inhibitor. androst-4-ene-3,6,17-trione is the key word

are all these studies faulty as well?

It is apparent to me that estrogen is being blocked, at least at the hypothalamus. Enough so that LH rises and testosterone is increased. Yes, this is most readily apparent in the 600mg group and not so much in the 300mg group
 
DR.D

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Thanks to both!

PP, I’ve run about 5 pcts this way in the past year and a half and had complete bounce back, perfect libido, and no setbacks. AI is a solid addition to post cycle therapy in my opinion.

Dr. D, I’m not questioning your judgment, and in fact, your AI comment makes perfect sense to me. But just for my own knowledge, what’s the advantage of using Clomid at 100 for two weeks and then Nolva for 2 at 40/20? This isn’t too sudden a dropoff? As I said, I’ve always used the post cycle therapy listed with great success. Is it just overkill in your opinion?

Also, about the pulse, do you think it would be an effective addition to the cut? I'm actually now thinking if I'm going to do this, I may want to front load my T3 on the last week of epi pulse, so I'm beginning the 50mg doses the same day I start the Ztrol/Props. What do you think?
Then by all means, go with what has worked for you in the past because results always speak louder than theory! Estrogenic metabolites of Clomid start to become significant after a few weeks though, that's why I'd replace it with the Nolva. I hate Nolva too. Toremifene all the way is better @ 90,60,60-30,30 w/ a 120mg front load the first 3 nights only.

I would not front load T3! Always ramp it up slow, 12.5-25mcg increments every 2-3 days.
 
jomi822

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6-oxo is a steroidal compound. I wouldn’t use this for post cycle therapy, as it would not increase LH unless it managed to somehow reduce estrogen and remove some the ER inhibition on the hypothalamus. The study I have on 6-oxo didn’t measure LH and it actually showed an increase in overall estrogen. Everything points to the fact that trione probably converts directly to testosterone, or the blood test mistakes trione for testosterone itself. Eitherway, it has no practical use for PCT. I can send the study to anyone who is interested in seeing it.

Im not familiar with the WinZtrol or Propadrol. Do you know the active compounds of these pro-hormone sounding sups?

Also, that is way more SERM than you need for PCT. The most nolva you will ever want for PCT is 10mg day and the most clomid you would ever want is 25mg day (unless you are battling a gyno emergency) The amount of SERM you plan on using would no-doubtingly reduce your libido and erectile function.

-Pp
can you post up the entire study? This would be the first time i have heard mention of 6-oxo containing a steroidal compound. that would be quite the fact...since it is advertised as a non-steroidal inhibitor.

What type of estrogen was it measuring? e2? estrone? some other metabolite?

However, LH output would probably be a better indication of 6-oxo's ability to speed recovery in post cycle therapy. I have seen plenty of studies showing tamoxifen/chlomiphene raise estrogens as well.
 
jomi822

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I would not front load T3! Always ramp it up slow, 12.5-25mcg increments every 2-3 days.
agreed....t3 is not a compound to joke with, and there is no need for a "frontload" of a completely unestrified compound...
 
DR.D

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... SHBG also dropped in both studies which is indicative of lower hepatic exposure to estrogens ...
So why do you suppose Tt dropped in the 600mg group compared to the 300?

Kinda strange if DHT is proportional too.
 
Patrick Arnold

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can you post up the entire study? This would be the first time i have heard mention of 6-oxo containing a steroidal compound. that would be quite the fact...since it is advertised as a non-steroidal inhibitor.

What type of estrogen was it measuring? e2? estrone? some other metabolite?

However, LH output would probably be a better indication of 6-oxo's ability to speed recovery in post cycle therapy. I have seen plenty of studies showing tamoxifen/chlomiphene raise estrogens as well.

6-oxo is 6-oxo androstenedione. yes its a steroid. it is non androgenic and non anabolic however.

we never said it was non steroidal
 
Patrick Arnold

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So why do you suppose Tt dropped in the 600mg group compared to the 300?

Kinda strange if DHT is proportional too.

look more carefully D. the 300 group had about a 20% higher starting baseline than the 600. there was no drop

it is absolutely expected that DHT would rise in proportion. why on earth would it not unless 6-oxo had some sort of 5alpha-reductase blocking action?
 
Patrick Arnold

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why do i have only one crown?

and wtf is a crown anyway?
 
jomi822

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6-oxo is 6-oxo androstenedione. yes its a steroid. it is non androgenic and non anabolic however.

we never said it was non steroidal
does it bind to the AR....

It has no anabolic or androgenic properties whatsoever?
 
bigschmidt821

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6-oxo is 6-oxo androstenedione. yes its a steroid. it is non androgenic and non anabolic however.

we never said it was non steroidal
if it is steroid how can u produce it? i thought after BALCO you couldnt produce anything of that nature. but then again if it isnt anabolic or androgenic then its ok which brings me to 11 oxo, you market it as cortisol blocking but it doese have anabolic and androgenic properties, how are you able to produce that if you are not allowed to produce anything of that nature after "conspiring to sell steroids"
btw we get a crown after every 1000000 rep points.
 
Eric Potratz

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i am almost positive that LH and FSH were both measured in the Incledon study. the results aren't shown in his abstract however.

as you can see in the baylor study though they were measured and increased

estrone went up and that could be because of a cross reactivity with 6-oxo estrone (which is formed as a by product)

now you may argue that testosterone cross reacts with 6-oxo testosterone but notice that DHT went up proportionally with testosterone (which is expected).

SHBG also dropped in both studies which is indicative of lower hepatic exposure to estrogens

the results are pretty solid. i have debated these things time and time again and considered the facts time and time again as well
Pat,

LH was not measured in the Incledon study unless they left it out of the full text.

I’ve never seen any convincing research that androst-4-ene-3,6,17-trione is an aromatase inhibitor in humans. Now that Ive seen the in-vivo research, I’m definitely not convinced. I guess if there is cross–reactivity happening the results would be hard to interpret either way. I suppose 6-oxo DHT could have cross reacted as well? IMO, an effective oral aromatase inhibitor would give results similar to the study seen below.

My original point is that 6-oxo would not be conducive to PCT. The effects on LH/FSH are certainly not positive enough to consider 6-oxo as a “natural” test booster, and whether or not 6-oxo is an aromatase inhibitor is probably a mute point anyway, especially if it converts to its own estrogenic metabolites. (which appear to negatively effect LH in the lower dosed group and FSH in the higher dosed group)

Im sure 6-oxo can be an effective product in and of itself as a performance enhancer, but I don’t believe it’s a good choice for PCT.

-Pp

Reversal of the hypogonadotropic hypogonadism of obese men by administration of the aromatase inhibitor testolactone.
Zumoff B, Miller LK, Strain GW.
Metabolism. 2003 Sep;52(9):1126-8.

Studies from this laboratory have shown that obese men have elevated serum estrogen levels and diminished levels of follicle-stimulating hormone (FSH - follicle stimulating hormone - ) and free and total testosterone, all in proportion to their degree of obesity. The decreases in testosterone and FSH constitute a state of hypogonadotropic hypogonadism (HHG), and we have hypothesized that it results from feedback suppression of the pituitary by the elevated estrogen levels. We tested this hypothesis by lowering the serum estrogens of 6 health obese men (body mass index [BMI], 38 to 73) by administering the aromatase inhibitor testolactone (1 g daily for 6 weeks). Twenty-four-hour mean serum testosterone rose in every subject, from a mean of 290 +/- 165 ng/dL to a mean of 403 +/- 170 (P <.0003); 24-hour mean serum estradiol decreased in every subject, from a mean of 40 +/- 10.8 pg/mL to a mean of 29 +/- 6.7 (P <.004); and 24-hour mean serum luteinizing hormone (lh - leutenizing hormone - ) increased in every subject, from a mean of 14.3 +/- 4.1 mIU/mL to a mean of 19.3 +/- 5.1 (P <.004). The rise in mean LH was due to an increase in the amplitude of the individual secretory pulses, especially at night. Twenty-four-hour mean serum estrone decreased nonsignificantly, from 48 +/- 14 pg/mL to 39 +/- 6.4, and 24-hour mean serum FSH - follicle stimulating hormone - increased nonsignificantly, from 13.5 +/- 5.3 mIU/mL to 15.0 +/- 5.4. The results are in accordance with the hypothesis, in that inhibition of estrogen biosynthesis (through administration of the aromatase inhibitor testolactone) results in alleviation of the HHG of our obese male subjects.
 
Eric Potratz

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can you post up the entire study? This would be the first time i have heard mention of 6-oxo containing a steroidal compound. that would be quite the fact...since it is advertised as a non-steroidal inhibitor.

What type of estrogen was it measuring? e2? estrone? some other metabolite?

However, LH output would probably be a better indication of 6-oxo's ability to speed recovery in post cycle therapy. I have seen plenty of studies showing tamoxifen/chlomiphene raise estrogens as well.

I cant post the study. For some reason my attach feature wont work. I can email it to you if you like.

E1 and E2 were both measured in the study. E1 went way up and E2 went down a little. According to Pat this is cross-reactivity from the 6-oxo estrone…?

Neither of the 6-oxo studies show a positive effect on LH or FSH.

-Pp
 
Eric Potratz

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if it is steroid how can u produce it? i thought after BALCO you couldnt produce anything of that nature. but then again if it isnt anabolic or androgenic then its ok which brings me to 11 oxo, you market it as cortisol blocking but it doese have anabolic and androgenic properties, how are you able to produce that if you are not allowed to produce anything of that nature after "conspiring to sell steroids"
btw we get a crown after every 1000000 rep points.
Yes, 6-oxo is a steroid… even progesterone sold and Wall mart is a steroid.

Your not supposed to sell hormones with androgenic or anabolic nature. That is why DHEA and pregnenolone are still legal to sell… because there androgenic/anabolic nature is debatable.

-Pp
 
DR.D

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look more carefully D. the 300 group had about a 20% higher starting baseline than the 600. there was no drop

it is absolutely expected that DHT would rise in proportion. why on earth would it not unless 6-oxo had some sort of 5alpha-reductase blocking action?
I just reread that section and still don't understand why Tt was lower in the 600 group (especially if ELISA cross reactivity was suspected!) because it said all baselines were subtracted out?
 
bigschmidt821

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I cant post the study. For some reason my attach feature wont work. I can email it to you if you like.

E1 and E2 were both measured in the study. E1 went way up and E2 went down a little. According to Pat this is cross-reactivity from the 6-oxo estrone…?

Neither of the 6-oxo studies show a positive effect on LH or FSH.

-Pp
yes but i am now reffering to 11 oxo and that Patrick Arnold has been deemed, to my knowledge, not allowed to produce or sell anything of anabolic nature
 
DR.D

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does it bind to the AR....

It has no anabolic or androgenic properties whatsoever?
The author of the study concluded there was no increase in muscle mass or positive body composition associated with the use of 6-oxo at any dose, in spite of increased test levels. He therefore suggests that 6-oxo probably does bind to ARs as a competitive substrate to nullify the effect of testosterone. Kinda like how we were talking ATD does centrally in that other thread.
 
jomi822

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The author of the study concluded there was no increase in muscle mass or positive body composition associated with the use of 6-oxo at any dose, in spite of increased test levels. He therefore suggests that 6-oxo probably does bind to ARs as a competitive substrate to nullify the effect of testosterone. Kinda like how we were talking ATD does centrally in that other thread.
effin fantastic...

however i am much more comfortable seeing studies with LH actually rising in response to 6-oxo use...as opposed to the ATD studies in which only total T levels were assayed....which ATD shows up as anyway.

alright this stuff is too cloak and dagger for me. it seems these substances have too many little secrets for my liking.
 
Patrick Arnold

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does it bind to the AR....

It has no anabolic or androgenic properties whatsoever?
i don't know whether it binds to the AR

but we have had a hershberger done at U of I chicago. that uses castrated rats. it showed no ana or and activity
 
Patrick Arnold

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if it is steroid how can u produce it? i thought after BALCO you couldnt produce anything of that nature. but then again if it isnt anabolic or androgenic then its ok which brings me to 11 oxo, you market it as cortisol blocking but it doese have anabolic and androgenic properties, how are you able to produce that if you are not allowed to produce anything of that nature after "conspiring to sell steroids"
btw we get a crown after every 1000000 rep points.
that stipulation was only during pre-trial

god you must really follow have followed my case closely
 
Patrick Arnold

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Pat,

LH was not measured in the Incledon study unless they left it out of the full text.

I’ve never seen any convincing research that androst-4-ene-3,6,17-trione is an aromatase inhibitor in humans. Now that Ive seen the in-vivo research, I’m definitely not convinced. I guess if there is cross–reactivity happening the results would be hard to interpret either way. I suppose 6-oxo DHT could have cross reacted as well? IMO, an effective oral aromatase inhibitor would give results similar to the study seen below.

My original point is that 6-oxo would not be conducive to post cycle therapy. The effects on LH/FSH are certainly not positive enough to consider 6-oxo as a “natural” test booster, and whether or not 6-oxo is an aromatase inhibitor is probably a mute point anyway, especially if it converts to its own estrogenic metabolites. (which appear to negatively effect LH in the lower dosed group and FSH in the higher dosed group)

Im sure 6-oxo can be an effective product in and of itself as a performance enhancer, but I don’t believe it’s a good choice for PCT.

-Pp

Reversal of the hypogonadotropic hypogonadism of obese men by administration of the aromatase inhibitor testolactone.
Zumoff B, Miller LK, Strain GW.
Metabolism. 2003 Sep;52(9):1126-8.

Studies from this laboratory have shown that obese men have elevated serum estrogen levels and diminished levels of follicle-stimulating hormone (FSH - follicle stimulating hormone - ) and free and total testosterone, all in proportion to their degree of obesity. The decreases in testosterone and FSH constitute a state of hypogonadotropic hypogonadism (HHG), and we have hypothesized that it results from feedback suppression of the pituitary by the elevated estrogen levels. We tested this hypothesis by lowering the serum estrogens of 6 health obese men (body mass index [BMI], 38 to 73) by administering the aromatase inhibitor testolactone (1 g daily for 6 weeks). Twenty-four-hour mean serum testosterone rose in every subject, from a mean of 290 +/- 165 ng/dL to a mean of 403 +/- 170 (P <.0003); 24-hour mean serum estradiol decreased in every subject, from a mean of 40 +/- 10.8 pg/mL to a mean of 29 +/- 6.7 (P <.004); and 24-hour mean serum luteinizing hormone (lh - leutenizing hormone - ) increased in every subject, from a mean of 14.3 +/- 4.1 mIU/mL to a mean of 19.3 +/- 5.1 (P <.004). The rise in mean LH was due to an increase in the amplitude of the individual secretory pulses, especially at night. Twenty-four-hour mean serum estrone decreased nonsignificantly, from 48 +/- 14 pg/mL to 39 +/- 6.4, and 24-hour mean serum FSH - follicle stimulating hormone - increased nonsignificantly, from 13.5 +/- 5.3 mIU/mL to 15.0 +/- 5.4. The results are in accordance with the hypothesis, in that inhibition of estrogen biosynthesis (through administration of the aromatase inhibitor testolactone) results in alleviation of the HHG of our obese male subjects.

both studies showed decreases of SHBG, which is an expected result of aromatase inhibition in the liver. the best possible explanation for what is going on with 6-oxo is aromatase inhibition if you put everything together. yes there are anomalies in the data, but to say that its all due to coincendtal cross reactivity that is exactly the same for test and dht is a little too much to believe
 
Patrick Arnold

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Pat,

LH was not measured in the Incledon study unless they left it out of the full text.

I’ve never seen any convincing research that androst-4-ene-3,6,17-trione is an aromatase inhibitor in humans. Now that Ive seen the in-vivo research, I’m definitely not convinced. I guess if there is cross–reactivity happening the results would be hard to interpret either way. I suppose 6-oxo DHT could have cross reacted as well? IMO, an effective oral aromatase inhibitor would give results similar to the study seen below.
.
\

it is not uncommon for an AI to raise testosterone and leave estrogens unaffected. this is due to the escape phenomenon. when AI dosages get high enough to overcome the bodies ability to keep up testosterone production (estrogen substrate production) you then see estrogens drop

6-oxo is likely within the escape phenomenon range
 
Patrick Arnold

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I just reread that section and still don't understand why Tt was lower in the 600 group (especially if ELISA cross reactivity was suspected!) because it said all baselines were subtracted out?
are you trying to tell me that the numbers in table 8 for Tt are lower for 600mg

they are not. read again.

and no, cross reactivity is not suspected for testosterone.

one thing that might confuse you guys is that in table 8, the number 1 is the first week on. it is not baseline
 
Patrick Arnold

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The author of the study concluded there was no increase in muscle mass or positive body composition associated with the use of 6-oxo at any dose, in spite of increased test levels. He therefore suggests that 6-oxo probably does bind to ARs as a competitive substrate to nullify the effect of testosterone. Kinda like how we were talking ATD does centrally in that other thread.
if it were both an AR agonist and an AI antagonist you would have seen a different endocrinological profile in the subjects. For starters, LH FSH and testosterone would probably have been markedly higher.
 
Patrick Arnold

Patrick Arnold

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effin fantastic...

however i am much more comfortable seeing studies with LH actually rising in response to 6-oxo use...as opposed to the ATD studies in which only total T levels were assayed....which ATD shows up as anyway.

alright this stuff is too cloak and dagger for me. it seems these substances have too many little secrets for my liking.
you are going to let one misguided comment (he was purely offering a hypothetical explanation) by the author of the study convince you that 6-oxo is garbage?

cloak and dagger? i am trying to discuss all of this openly here and offer explanations. if i were cloak and dagger i would be much more evasive don't you think?
 
ThisGuy02

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Then by all means, go with what has worked for you in the past because results always speak louder than theory! Estrogenic metabolites of Clomid start to become significant after a few weeks though, that's why I'd replace it with the Nolva. I hate Nolva too. Toremifene all the way is better @ 90,60,60-30,30 w/ a 120mg front load the first 3 nights only.

I would not front load T3! Always ramp it up slow, 12.5-25mcg increments every 2-3 days.
"Front load" wasn't really the right word. I meant I'd start 9 days out from my regular cycle (supported by the last 9 of the pulse w/ epi) so I'm at 12.5 the first 3 days of T3, 25 the next 3, 37.5 the next 3, and 50mcg from day 1 of the daily cycle (prop/zol), going most of the 4 weeks but ramping down beginning 9 days from the last day by the same increments in reverse. Id still be pulsing the epi in high doses, so I figured that paired w/ sufficient protein intake and below 50mcg, I'd avoid the potentially catabolic effects. You're saying this isn't a good idea?

By the way, I re-read your thread on pulsing. By the examples you gave I could safely go as high as 60mg on my 3 weekly pulse days, right? Maybe 30/40/50 to ease in my first week and 60 from there out?
 
DR.D

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if it were both an AR agonist and an AI antagonist you would have seen a different endocrinological profile in the subjects. For starters, LH FSH and testosterone would probably have been markedly higher.
I think the author who conducted the study is pretty clear in his opinion. He is not suggesting that it behaves as an AR agonist. If it were, then it would have to be far weaker than testosterone since it eliminates and nullifies the benefit of testosterone on muscle growth. What he is saying is that it's probably an androgen (defined by it's receptor affinity) but possesses only weak or maybe slightly inverse expression as such.

It's funny how you start a big stink about 6-Br with related speculation but the author of your own study actually concludes this same flaw about 6-Oxo based on 11 wks of bloodwork on multiple participants! At least with 6-Br you get results. It's not even a substrate for AR much less an agonist or you would not see higher test levels, combined with positive strength and mass gains.

It will be a good day when I see the hypocrisy die. Chemists should not try to be businessmen too, it betrays the science and will backfire in time.
 
DR.D

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... By the way, I re-read your thread on pulsing. By the examples you gave I could safely go as high as 60mg on my 3 weekly pulse days, right? Maybe 30/40/50 to ease in my first week and 60 from there out?
Sorry, I misunderstood, that sounds good with the slow, linear T3 ramp. And yes, the plan with Epi looks solid. I can't suggest over 60 because that's the highest I've gone personally, but I have seen guys pulse up to 90 with no adversity.
 
Patrick Arnold

Patrick Arnold

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I think the author who conducted the study is pretty clear in his opinion. He is not suggesting that it behaves as an AR agonist. If it were, then it would have to be far weaker than testosterone since it eliminates and nullifies the benefit of testosterone on muscle growth. What he is saying is that it's probably an androgen (defined by it's receptor affinity) but possesses only weak or maybe slightly inverse expression as such.

It's funny how you start a big stink about 6-Br with related speculation but the author of your own study actually concludes this same flaw about 6-Oxo based on 11 wks of bloodwork on multiple participants! At least with 6-Br you get results. It's not even a substrate for AR much less an agonist or you would not see higher test levels, combined with positive strength and mass gains.

It will be a good day when I see the hypocrisy die. Chemists should not try to be businessmen too, it betrays the science and will backfire in time.
I meant to say antagonist, not agonist. It assuredly is not an agonist since i have data showing it has no anabolic androgenic activity. i can post it if you like, i just have to shrink the jpgs

thought we were having a decent discussion but it appears you had to act like a jerk and ruin it

and please point me to your 6-bromo study. if you want to compare data then have some actual verifiable data to back it up
 

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