6OXO in conjunction to Nolva post cycle

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    6OXO in conjunction to Nolva post cycle


    I posted this over at bb.com but so far have not received a lot of feedback.

    If anyone has any information please post.


    According to Patrick Arnold....

    "taking ERAs like nolvadex will cause your estrogen levels to go up quite high (like 300%). As a result, after discontinuation you may have a period of high estrogen without receptor protection

    AIs do not have this problem as they stop estrogen production itself.

    If you do take nolva it probably is wise to either taper down slowly, or better yet switch to an AI at the end of the cycle."



    Seth Roberts explains....

    "The best course of action might be to use TACL (Nolva or Clomid) and AI's (6oxo). TACL will stimulate LH secretion and testosterone production and an AI will prevent the rise in estrogen levels that occur with TACL therapy. Also the partial agonist nature of TACL will allow for some estrogenic stimulation."

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    with my last couple PCT, i've been tapering nolva with transdermal 6-OXO and extending the 6-OXO for a week or two after stopping nolva. Can't really tell if it's better in combo or by itself, but i can say that my last post cycle was really tough after 2 M1T cycles. It took 4 weeks for me to get my libido back which is the longest yet. Wasn't sure if i was ever gonna feel like a man again, but thank God!
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    Thanks for the feedback Lancelot
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    Ive been following the thread over there myself. Personally, im going to give it a go after my next cycle. Ive already got some fl7 so im going to throw in a few grams of 6-oxo and use it after my nolva is over. This might not be for a while since im still in the planning stage of it all. But ill be sure to post feedback.
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    This is where Pat and SWALE disagree. I happen to agree with SWALE since he has the blood tests of hundreds of clients to show for it. He never likes using AI's post cycle because believes lowering estrogen to such a point where its unhealthy causes problems with lipid profiles and also estrogen rebound once use is discontinued. Through most of his tests it show that when testosterone is suppressed it actually returns to a higher level upon completion of PCT then returns to normal (you can find this in studies too). He believes this can also happen when you suppress estrogen to very low levels as an AI will do. Now according to Pats study estrogen isn't even lowered that much so using 6-OXO with Nolva might be ok but I don't really see any benefit. Your only going to respond to an anti-e so fast. Doubling or tripling up on anti-e won't make the testes respons any faster to LH than when only using one. Bacially all your doing is cresating an imbalance. Once thats achieved thats all you need to start prodcuing LH. The only thing that can speed this process up is HCG.

    So many people have used Nolvadex during PCT and have never had problems with estrogen so I don't understand his worries.


    Your best bet is to post this over at CEM in the anabolic section and let SWALE and Nandi take a look. They are the biggest supporters of Nolva and I happen to agree with them.
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    Plus estrogen is good for your libido....
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    In terms of AI's lowering estrogen to unhealthy levels post cycle, i think it was using formestane causing this problem not 6-OXO.
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    Quote Originally Posted by Bobo
    This is where Pat and SWALE disagree. I happen to agree with SWALE since he has the blood tests of hundreds of clients to show for it. He never likes using AI's post cycle because believes lowering estrogen to such a point where its unhealthy causes problems with lipid profiles and also estrogen rebound once use is discontinued. Through most of his tests it show that when testosterone is suppressed it actually returns to a higher level upon completion of PCT then returns to normal (you can find this in studies too). He believes this can also happen when you suppress estrogen to very low levels as an AI will do. Now according to Pats study estrogen isn't even lowered that much so using 6-OXO with Nolva might be ok but I don't really see any benefit. Your only going to respond to an anti-e so fast. Doubling or tripling up on anti-e won't make the testes respons any faster to LH than when only using one. Bacially all your doing is cresating an imbalance. Once thats achieved thats all you need to start prodcuing LH. The only thing that can speed this process up is HCG.

    So many people have used Nolvadex during PCT and have never had problems with estrogen so I don't understand his worries.


    Your best bet is to post this over at CEM in the anabolic section and let SWALE and Nandi take a look. They are the biggest supporters of Nolva and I happen to agree with them.
    Thank you for the feedback Bobo. Could you please give me the web address for CEM as I am not a member or familiar with the site. Thank you.
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    Quote Originally Posted by lancelot
    In terms of AI's lowering estrogen to unhealthy levels post cycle, i think it was using formestane causing this problem not 6-OXO.
    I used Nolva (4 weeks) followed with Aromazap (2 weeks) after my M 1-T cycle and FWIW my blood tests came back normal. Incidentally, I am still waiting for results of the less common tests like DHEA and LH, which had to go to a special lab.
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    There is a lot of disscussion going on right now as to weather or not AI's are really needed during an AAS cycle. Big Cat posted a new study that he's working on regarding this subject which I agree with 100%. A higher then normal amount of estrogen being present can actualy increase the gains one sees while on cycle and pose no threat to side effects. This has not been backed by any studies, but it is no doubt that it is not good to totaly eliminate all estrogen.

    Points to consider
    1.Estrogenic problems are not as frequent as you think they are. In fact, they are quite rare in cycles of 750 mg of test or less. If you are using no other estrogenic drugs, risk will be minimal, even with other estrogenic drugs risk is not that great. Many people will commence on anti-estrogens immediately, not even knowing what effect the drugs being taken would have had on them in the first place. For newbies its often of a bigger concern to discuss anti-e strategies than the things that really matter, like post-cycle therapy. Something you should really consider.

    2.The reason that made me raise this point to begin with was when i noticed increased incidences of gyno after use of anti-e's. Some people after a cycle, and post-cycle, started to get gyno. I dismissed this initially as an imbalance of estrogen to androgen. Then I started noticing people got gyno in milder cycles, where they got none in heavier cycles they did prior to starting anti-e's. At this point androgen levels are considerably higher. So what gives ?

    3.Well, the first thing that came to mind is that estrogen is not linear. Its not because you have a certain estrogen level at 500 mg of test per week, that using 750 mg per week will automatically give you 50% more estrogen. Estrogen seems to downregulate the aromatase enzyme (1). that means with every increase in dose of an aromatizing hormone, the concommitant estrogen increase will be smaller each time. Making it unlikely that such increases yield a much greater risk. Conclusion ? You probably don't need an anti-estrogen if gyno is what you are concerned about.

    4.The second thing that came to mind is that estrogen seems to downregulate its receptor as well in most tissues. This means in very low levels of estrogen (like those that will occur with aromatase blockers) we will actually see an upregulation (2) of the estrogen receptor. When You then stop taking your AI, the estrogen level that was previously there is acting on a greater density of receptors and will be more prone to cause problems.

    5.The points made above suggest that a lot of you who are overly stressed about gyno may be using expensive drugs that you do not need, only to result in the fact that after using them once, you may need them infinitely to avoid problems that you might otherwise not have had, resulting in more cost (and if you subscribe to my theory, less gains as well).

    Now, a lot to consider. But we are ignoring two obvious things :

    A.What if problems do arise ? Well, for starters wait it out and see if problems do arise. Learn the difference between an itchy nipple and onsetting gyno. If gyno does appear to be setting on, it is best to treat it with SERMS (Nolva and Clomid). Because they act as partial agonists and do not reduce circulating estrogen levels, they will not have as great an impact as AI regarding points 3 and 4. Thes edrugs are after all inevitable since they are essential for post-cycle therapy, and the problems described above do not seem to occur regurlarly with these products. So if estrogen control is needed, then preferably use SERMs over AI's.

    B.What if you want to take this risk, what if you ARE willing to pay more for peace of mind, since you don't believe estrogen is helping and you happen to believe the excess estrogen is a risk you are not willing to take ? Then what is stopping you from using AI's ? Absolutely nothing at all. But do consider a few things : supressing estrogen too much, will result in less health and less gains. This means if you want to keep estrogen right where you want it, you will need to get weekly or bi-weekly blood tests to make sure estrogen is neither too high, nor too low. If this seems feasible to you (after all I don't recommend using any prescription drugs, not even steroids themselves without being under the care of a licensed medical professional) then I can do nothing but applaud you efforts. You may or may not be sacrificing gains, by keeping estrogen normal you may be avoiding longer term health problems. But that only works if you actually make the effort to do the tests and keep estrogen in the proper range.

    Taken from Big Cat's Article

    (1) Nakamura J, Lu Q, Aberdeen G, Albrecht E, Brodie A.
    The effect of estrogen on aromatase and vascular endothelial growth factor messenger ribonucleic acid in the normal nonhuman primate mammary gland.
    J Clin Endocrinol Metab. 1999 Apr;84(4):1432-7.

    (2) Agarwal VR, Sinton CM, Liang C, Fisher C, German DC, Simpson ER.
    Upregulation of estrogen receptors in the forebrain of aromatase knockout (ArKO) mice.
    Mol Cell Endocrinol. 2000 Apr 25;162(1-2):9-16
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    Quote Originally Posted by lancelot
    In terms of AI's lowering estrogen to unhealthy levels post cycle, i think it was using formestane causing this problem not 6-OXO.
    I am referring to ALL AI's along with SI's.


    Plus formestane's anti-estrogenic effects start to diminsh after 1 week.
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    Quote Originally Posted by NO MERCY
    Thank you for the feedback Bobo. Could you please give me the web address for CEM as I am not a member or familiar with the site. Thank you.

    www.cuttingedgemuscle.com


    Post it in the anabolic pharmacology section.
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    Quote Originally Posted by Bobo
    www.cuttingedgemuscle.com


    Post it in the anabolic pharmacology section.
    Got cha thanks
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    It's apparent that nobody has checked out the PDF file on www.ergopharm.com about the 6-OXO study. Those of you saying that it completely knocks out estrogen and therefore is no good, might want to do your homework first. The body strives for homeostasis; just because we introduce an AI into the system, it doesn't mean estrogen is just going to disappear.
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    Well first off the health drawbacks from some A.I.'s such as the non-steroidal anastrozole and letrozole are probably not an issue with the steroidals like 6-OXO and exemestane (I would not use exemestane post-cycle though because it is slightly androgenic). I say this because in the breast cancer literature the steroidal inhibitors do not seem to negatively alter lipid parameters or bone health. I'm not sure yet why this is the case, but some of the researchers seem to think it might be that the A.I. itself may be 'filling in' for the missing estrogens because of the similarities between androstenedione and many of the steroidal A.I.'s.

    PA's study actually showed an improvement in the lipid profile from 6-OXO. Now, I know what some may be thinking: "yeah but that can be explained by 6-OXO not lowering estrogens (despite the increase in T)". Well yes, 6-OXO did not lower plasma estrogens in that study but that doesn't mean its not preventing/impairing estrogen action in the tissues (such as the liver and the brain). The clear evidence that the plasma levels are pretty irrelevant is the fact that 6-OXO is raising T so much (more than doubled in one of the studies I believe) in the first place. Think about it. How do A.I.'s increase T production? -- by decreasing estrogen action in the hypo and pituitary (negative feedback). Thus, if the normal plasma levels of estrogens are present along with doubled normal T there is really no other explanation other than the A.I. decreasing estrogen action in the tissues (regardless of normal plasma levels).

    So then the question becomes (regarding the 6-OXO study): "well okay then, lets say that the normal plasma estrogen levels do not translate into lipid/bone health but that is okay because 6-OXO itself is somehow providing the good effects of estrogen, and that estrogen action is being significantly impaired in the tissues, but this doesn't explain why the plasma estrogen levels are still normal".

    And the answer to this is increased substrate for aromatase. Possibly, the doses of 6-OXO used resulted in a dramatic decrease in estrogen negative feedback, which brought T really high, but the increased T was high enough to result in enough aromatization (despite decreased aromatase) to bring the plasma levels back up to normal. If this is the case, then mega-dosing (as in 1 gram+ maybe) would result in enough aromatase inhibition that the rate limiter would become AR-negative feedback at the hypo (from the very high levels of natural T) and you would get more of what you would expect from a blood test while on an A.I. (low E and high T).

    On top of all of this, lets just pretend that (even though they don't IMO) 6-OXO/steroidal A.I.'s DO cause the health problems (lipid values, etc..) that people associate with the non-steroidals ... If someone were to not use 6-OXO for recovery from an M1T cycle based solely on this -- that doesn't make much sense because what do they think they are doing to their lipid profile while on the actual cycle (assuming M1T is being run alone)?

    Regarding the potential "estrogen rebound" from A.I. use. Once again, this is something that the non-steroidals have more of a potential for... the steroidals on the other hand do not upregulate aromatase protein/mRNA unlike the non-steroidals. In fact, I think the "estrogen rebound" risk is more likely to result from SERM use than 6-OXO.

    As discussed on the avant board, the only real argument against A.I. use (in my mind at least) that seems to hold water is the SHBG/Total T issue raised by Nandi (maybe Swale too). I don't agree with it really but its still a good argument.

    I'm no expert, I just think that there are factors involved that people are overlooking.
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    candle, you do raise an good point in your post about A.I. use on-cycle. namely, that estrogen itself plays a role in ER regulation and thus decreasing estrogen action could upregulate the ER. that makes sense, but SERMs will do the same thing anyway...

    but I do have to disagree with some things.. dare we enter into the never-ending "do SERM's/A.I.'s limit gains" debate. yes, estrogens are beneficial to growth via many mechanisms and their action is certainly needed for libido, sperm maturation/transport, and many other physiological roles -- but they also have some downsides regarding growth... one such downside has recently been discussed on the CEM board, and that is that estrogens have negative effects on muscle recovery after resistance training/exercise.

    its really such a mixed bag (as with most things/issues/drugs)...

    and lastly, there are alot more things involved in gyno than just estrogen... I don't think it would be smart to run a 750mg/week test cyp cycle if one was prone to gyno, despite the homeostatic/regulatory interactions between estrogen and aromatase... there are so many other things involved.
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    Quote Originally Posted by Onslaught
    It's apparent that nobody has checked out the PDF file on www.ergopharm.com about the 6-OXO study. Those of you saying that it completely knocks out estrogen and therefore is no good, might want to do your homework first. The body strives for homeostasis; just because we introduce an AI into the system, it doesn't mean estrogen is just going to disappear.

    Umm....mayde you didn't read my post before you made your generalization.

    "Now according to Pats study estrogen isn't even lowered that much so using 6-OXO with Nolva might be ok "

    And those patients do NOT represent someone coming of a cycle in a hypogonadal state. Those patients ARE producing a significant of testesterone already, hence higher amounts of estrogen. Those studies simply state that it raises testosterone. Even Pat said he didn't know why estrone levels were high. And also 6-OXO does not react like Letrozole and Arimidex in which they DO suppress estrogen levels dramatically.

    So please, do YOUR homework.
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    Quote Originally Posted by nightop

    - but they also have some downsides regarding growth... one such downside has recently been discussed on the CEM board, and that is that estrogens have negative effects on muscle recovery after resistance training/exercise.

    .

    Yeah but thats very questionable and even then the effects are proably non existant in terms of real world results. Hell there are a million things that decrease mucle recovery but it just doesn't equate to noticable effects. Caffeine is one of them. I think eliminating estrogen has much more negative effects than postive for overall health. You can easily control it instead of eliminating it.
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    At what point did i mention Letrozole and Arimidex?

    And I didn't direct my post at you; notice I said "those of you saying..."

    A bit defensive?
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    Quote Originally Posted by nightop
    Well first off the health drawbacks from some A.I.'s such as the non-steroidal anastrozole and letrozole are probably not an issue with the steroidals like 6-OXO and exemestane (I would not use exemestane post-cycle though because it is slightly androgenic). I say this because in the breast cancer literature the steroidal inhibitors do not seem to negatively alter lipid parameters or bone health. I'm not sure yet why this is the case, but some of the researchers seem to think it might be that the A.I. itself may be 'filling in' for the missing estrogens because of the similarities between androstenedione and many of the steroidal A.I.'s.

    PA's study actually showed an improvement in the lipid profile from 6-OXO. Now, I know what some may be thinking: "yeah but that can be explained by 6-OXO not lowering estrogens (despite the increase in T)". Well yes, 6-OXO did not lower plasma estrogens in that study but that doesn't mean its not preventing/impairing estrogen action in the tissues (such as the liver and the brain). The clear evidence that the plasma levels are pretty irrelevant is the fact that 6-OXO is raising T so much (more than doubled in one of the studies I believe) in the first place. Think about it. How do A.I.'s increase T production? -- by decreasing estrogen action in the hypo and pituitary (negative feedback). Thus, if the normal plasma levels of estrogens are present along with doubled normal T there is really no other explanation other than the A.I. decreasing estrogen action in the tissues (regardless of normal plasma levels).

    So then the question becomes (regarding the 6-OXO study): "well okay then, lets say that the normal plasma estrogen levels do not translate into lipid/bone health but that is okay because 6-OXO itself is somehow providing the good effects of estrogen, and that estrogen action is being significantly impaired in the tissues, but this doesn't explain why the plasma estrogen levels are still normal".

    And the answer to this is increased substrate for aromatase. Possibly, the doses of 6-OXO used resulted in a dramatic decrease in estrogen negative feedback, which brought T really high, but the increased T was high enough to result in enough aromatization (despite decreased aromatase) to bring the plasma levels back up to normal. If this is the case, then mega-dosing (as in 1 gram+ maybe) would result in enough aromatase inhibition that the rate limiter would become AR-negative feedback at the hypo (from the very high levels of natural T) and you would get more of what you would expect from a blood test while on an A.I. (low E and high T).

    On top of all of this, lets just pretend that (even though they don't IMO) 6-OXO/steroidal A.I.'s DO cause the health problems (lipid values, etc..) that people associate with the non-steroidals ... If someone were to not use 6-OXO for recovery from an M1T cycle based solely on this -- that doesn't make much sense because what do they think they are doing to their lipid profile while on the actual cycle (assuming M1T is being run alone)?

    Regarding the potential "estrogen rebound" from A.I. use. Once again, this is something that the non-steroidals have more of a potential for... the steroidals on the other hand do not upregulate aromatase protein/mRNA unlike the non-steroidals. In fact, I think the "estrogen rebound" risk is more likely to result from SERM use than 6-OXO.

    As discussed on the avant board, the only real argument against A.I. use (in my mind at least) that seems to hold water is the SHBG/Total T issue raised by Nandi (maybe Swale too). I don't agree with it really but its still a good argument.

    I'm no expert, I just think that there are factors involved that people are overlooking.
    1. I tihnk exemestane is worse than all of them. Also you can't compare lipid profiles of 6-OXO to other AI's because the study was done on normal men for only 3 weeks. Hardly conclusive in anything other than it raises testosterone. These are not the effects that would be seen in hypogonadal state (mainly estrogen levels)

    2.If it impaired action in the other tissues such as the brain, there would be a decrease in libido most likely and that hasn't been reported in most cases.

    3. Plasma levels could remaine somewhat normal because these drugs do not block ALL aromatiziation not to mention circulating estrogen levels that were present before the study started. This is why it would have been better if it was on hypogonadal men and many conclusion on 6-OXO are just specualtion. THe only real thing the study proved was that it raised test in normal men.

    4. Estrogen rebound has nothing to do with upregulating recpetors IMO, it has everything to do with the amount and length of being suppressed. The analogy is that of test production usually rises to a higher than normal levels post cycle (documented in a number of cases) before returning to normal because of the strong suppression. If you do this to estrogen (suppress it strongly) you could have a much nastier rebound and levels could rise above natural levels before returning to normal. I think the whole arguemenet that SERMS are more likley to do that is complete bunk or you would have a number of cases of people developing gyno after using Nolva for extened peroids of time and they just don't exist in any significant numbers.


    As for Nandi and Swales theory, Pat wouldn't respond when I asked him about it on bb.com. Its not that I don't think he could at all its just the majority of stuff is just unknown and nobody know WHY certain things happen. Even Clomid isn't fully understood and they have studies clinically proving to reverse andropause from steroid abuse.
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    Quote Originally Posted by Onslaught
    At what point did i mention Letrozole and Arimidex?

    And I didn't direct my post at you; notice I said "those of you saying..."

    A bit defensive?
    You said AI's. Letrozole and Arimidex are Aromatase Inhibitors.

    You said "Its apparent nobody has read the study....


    I did cover his study in my post. You seem to conclude raising test in normal men equates to raising test in hypogonadal men. Its FAR from it.
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    Have anything to back up your "far from it" comment? I agree that they are very different situations, but is there any evidence to support that 6-OXO wouldn't have the same effect?

    My bad, I shouldn't have said "an AI". You got me there.
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    Yes. Instead of me doing it for you, go look at studies dealing with reversing andropause in patients that abused steroids. Also its just basic understanding of a functionong HPTA (normal), and one that is not (hypogonadal). In one case the testes are responsive to LH pulses. In the other, they are not. You could take Nolva, 6-OXO, Clomid, Letro, Exemestane and whatever else you could find all together and if the testes are not responding to LH, it won't make difference how low your estrogen is. It the delay to LH that needs to be as fast as possible and the ONLY thing that hleps that is HCG. SERMS are the only other thing that has been proven medically to help the condition. AI's probably will also but then you have the prlblems of too much suppression and lipid profiles. Its bascically overkill IMO and SWALES blood tests of numerous patients shows the same. So I would take his word since his practice is based on this sort of thing.

    Here's a good one for start.

    Use of clomiphene citrate to reverse premature andropause secondary to steroid abuse

    Robert S. Tan M.D., , a and Deepa Vasudevan M.D.a

    a Programs in Geriatrics and Andrology, Department of Family and Community Medicine, University of Texas Health Sciences Center, Houston, Texas, USA

    Received 19 February 2002; accepted 15 May 2002. ; Available online 7 January 2003.
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    Quote Originally Posted by Onslaught
    Have anything to back up your "far from it" comment? I agree that they are very different situations, but is there any evidence to support that 6-OXO wouldn't have the same effect?

    This one too.

    Pituitary testicular responsiveness in male hypogonadotropic hypogonadism
    Weinstein R.L.; Reitz R.E.

    Clin. Investigat. Cent., Nav. Hosp., Oakland, Calif., US
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    Quote Originally Posted by Bobo
    Yeah but thats very questionable and even then the effects are proably non existant in terms of real world results. Hell there are a million things that decrease mucle recovery but it just doesn't equate to noticable effects. Caffeine is one of them. I think eliminating estrogen has much more negative effects than postive for overall health. You can easily control it instead of eliminating it.
    Yeah, I can agree with that regarding the recovery effects.
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    Quote Originally Posted by Bobo
    1. I tihnk exemestane is worse than all of them. Also you can't compare lipid profiles of 6-OXO to other AI's because the study was done on normal men for only 3 weeks. Hardly conclusive in anything other than it raises testosterone. These are not the effects that would be seen in hypogonadal state (mainly estrogen levels)
    I agree that exemestane is a poor choice, but only because of its minor androgenic effect.

    Maybe I wasn't clear in my previous post, or you didn't understand what I tried to explain. That because 6-OXO is raising T so much despite normal plasma E levels, and because it showed no ill effects regarding the lipid profile, and because the research on steroidal A.I.'s (like 6-OXO is) have shown no ill effects on the lipid profile of subjects despite significantly lowered plasma E values, it is quite reasonable to conclude that 6-OXO does not have the potential health problems regarding the lipid profile -- that are surely found with non-steroidal A.I.'s.

    In other words, 6-OXO should not be condemned as unhealthy because people are improperly associating it with non-steroidal A.I.s (which is what Swale uses). And as I said before, one explanation for the ability for steroidal A.I.'s to not cause lipid profile problems despite decreased estrogen levels/action is that they are somehow filling the protective role of estrogen, either directly or though unknown metabolites. So yes, while plasma E levels will be quite low post cycle when using 6-OXO (most likely), that does not at all mean you are going to experience lipid profile problems.

    And as said before, on top of all of this -- even if I'm wrong, i just find it strange that people use the lipid profile risks as a reason to use Nolva, after using things like M1T alone (where their lipid profile is getting wrecked).

    2.If it impaired action in the other tissues such as the brain, there would be a decrease in libido most likely and that hasn't been reported in most cases.
    Not necessarily, but yes I do find it strange that there are not more reports of libido problems with 6-OXO... might be due to increased DHT action. Good point to raise though.

    3. Plasma levels could remaine somewhat normal because these drugs do not block ALL aromatiziation not to mention circulating estrogen levels that were present before the study started. This is why it would have been better if it was on hypogonadal men and many conclusion on 6-OXO are just specualtion. THe only real thing the study proved was that it raised test in normal men.
    Yes, but if they used a higher dose, as stated, I would guess that the plasma levels would drop... because the T would peak from direct AR mediated negative feedback and the aromatase levels would be so low that there is not enough substrate to bring the levels back up (like there is with the normal doses, as seen in the study).

    And yes, ideally the study would be on hypogonadal men, but that doesn't mean its not useful for supporting reasoned conclusions indirectly, in conjunction with other knowledge/studies on steroidal A.I.s.

    4. Estrogen rebound has nothing to do with upregulating recpetors IMO, it has everything to do with the amount and length of being suppressed. The analogy is that of test production usually rises to a higher than normal levels post cycle (documented in a number of cases) before returning to normal because of the strong suppression. If you do this to estrogen (suppress it strongly) you could have a much nastier rebound and levels could rise above natural levels before returning to normal. I think the whole arguemenet that SERMS are more likley to do that is complete bunk or you would have a number of cases of people developing gyno after using Nolva for extened peroids of time and they just don't exist in any significant numbers.
    Well "estrogen rebound" is sort of used as a misnomer. More technically ppl should say "estrogen action rebound"... its all about whats happening in the tissues. Yes, the ER upregulation is probably not that big a factor in the big picture, I agree with that.

    The reason that I feel SERMs have more potential for this effect is that upon cessation plasma T/E ratio will be low. With A.I.'s, the ratio will normalize as the drug's effect will slowly decrease after the last dose -- so despite a very high amount of substrate, plasma E levels won't rebound above normal because it takes time to produce aromatase protein because suicidal A.I.'s when bound remove the enzyme completely. Thus you get a sort of automatic tapering effect. I do think there is rebound potential with the non-steroidals though, as they upregulate aromatase and only competitively inhibit (not destroy).

    As for Nandi and Swales theory, Pat wouldn't respond when I asked him about it on bb.com. Its not that I don't think he could at all its just the majority of stuff is just unknown and nobody know WHY certain things happen. Even Clomid isn't fully understood and they have studies clinically proving to reverse andropause from steroid abuse.
    Yes, the SHBG/Total-T theory is interesting.. I don't really agree with it, but I'm not ready to argue against it at this point.

    We know that SERMs work, I'm not contesting that. I just think that 6-OXO is at least equally effective (and safe), based on the on-paper mechanisms, and could also have some minor advantages over the SERMs...
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    Quote Originally Posted by nightop
    I agree that exemestane is a poor choice, but only because of its minor androgenic effect.

    Maybe I wasn't clear in my previous post, or you didn't understand what I tried to explain. That because 6-OXO is raising T so much despite normal plasma E levels, and because it showed no ill effects regarding the lipid profile, and because the research on steroidal A.I.'s (like 6-OXO is) have shown no ill effects on the lipid profile of subjects despite significantly lowered plasma E values, it is quite reasonable to conclude that 6-OXO does not have the potential health problems regarding the lipid profile -- that are surely found with non-steroidal A.I.'s.

    In other words, 6-OXO should not be condemned as unhealthy because people are improperly associating it with non-steroidal A.I.s (which is what Swale uses). And as I said before, one explanation for the ability for steroidal A.I.'s to not cause lipid profile problems despite decreased estrogen levels/action is that they are somehow filling the protective role of estrogen, either directly or though unknown metabolites. So yes, while plasma E levels will be quite low post cycle when using 6-OXO (most likely), that does not at all mean you are going to experience lipid profile problems.

    And as said before, on top of all of this -- even if I'm wrong, i just find it strange that people use the lipid profile risks as a reason to use Nolva, after using things like M1T alone (where their lipid profile is getting wrecked).



    Not necessarily, but yes I do find it strange that there are not more reports of libido problems with 6-OXO... might be due to increased DHT action. Good point to raise though.



    Yes, but if they used a higher dose, as stated, I would guess that the plasma levels would drop... because the T would peak from direct AR mediated negative feedback and the aromatase levels would be so low that there is not enough substrate to bring the levels back up (like there is with the normal doses, as seen in the study).

    And yes, ideally the study would be on hypogonadal men, but that doesn't mean its not useful for supporting reasoned conclusions indirectly, in conjunction with other knowledge/studies on steroidal A.I.s.



    Well "estrogen rebound" is sort of used as a misnomer. More technically ppl should say "estrogen action rebound"... its all about whats happening in the tissues. Yes, the ER upregulation is probably not that big a factor in the big picture, I agree with that.

    The reason that I feel SERMs have more potential for this effect is that upon cessation plasma T/E ratio will be low. With A.I.'s, the ratio will normalize as the drug's effect will slowly decrease after the last dose -- so despite a very high amount of substrate, plasma E levels won't rebound above normal because it takes time to produce aromatase protein because suicidal A.I.'s when bound remove the enzyme completely. Thus you get a sort of automatic tapering effect. I do think there is rebound potential with the non-steroidals though, as they upregulate aromatase and only competitively inhibit (not destroy).



    Yes, the SHBG/Total-T theory is interesting.. I don't really agree with it, but I'm not ready to argue against it at this point.

    We know that SERMs work, I'm not contesting that. I just think that 6-OXO is at least equally effective (and safe), based on the on-paper mechanisms, and could also have some minor advantages over the SERMs...
    1. I undertand what your saying but there really is no evidence to make conclusions about lipid profiles from one 3 weeks study. Even when Letro and Arimidex are used, some studies indicate only a 50% reduction in plasma estrogen levels but still a negtaive effect on lipid profiles so it sill up in the air. It really is unknown what causes it and is only one of the possible problems with 6-OXO. I have never condemned 6-OXO, in fact I said it probably is fine for weaker type hormones that don't bind as strongly to the AR and/or cause a significant amount of suppression. I have used it myself and from my own findings it does work, just not as well as Nolva. But that is pure opinion as I don't have blood tests to prove anything so people can take that with a gain of salt if they wish. It has no scientific credibility. The evidence is just not there for 6-OXO as far as recovery from a hypogonadal state and until it is this is all speculation.


    2. Even if there is increased DHT its usually estrogen that play a more singifanct role in libido. But even there questions are still unanswered...We're dealing with the "unknown" here.

    3. The problem with making conclusions like your stating is you need to have some sort of evidence that it could possibly reverse a hypogonadal state. We know it raises testosterone in normal men but so do a lot of things. That doesn't mean it will react the same in hypogonadal men. But you don't need me to tell you this. Its just a completely different situation. I agree since it does seem to work through estrogen suppression it should probably work but how effective, nobody knows. On the hand, SERMS are proven to work in reversing a hypogonadal state directly causes by the abuse of steroids. There is documented and scientific proof in that area.

    4. Your point on rebound could be possible but we simply do not know what the effects of prolonged suppression of estrogen will do in hypogonadal men. SERMS are usually tapered so the chance of a sudden rise in estrogen is very remote and even in the majority of studies is just isn't present. Only recently have I heard of this possible problem with SERMS but IMO it simply doens't hold water based on numerous accounts and the look at different studies on various subjects. Even the theory that estrogen could bounce back to above normal levels is speculation but since testosterone shows a tendecy to do this post cycle, it is viable theory. Its funny how these things tend to act the same but who knows...To me using both is unecessary when we know one has been proven to work. Like I said earlier you can drive estrogen to the subphysiological levels but it won't speed up the response of the testes to LH in the long run. Only HCG can accomplish this. All you need is to create a deficit, theoretically. I dont' see a need a drive estrogen levels extremely low and most AI's will do this in a hypogonadal state. With 6-OXO we don't know but considering its mechanism of action I suspect it does. LH rises quickly regardless of an anti-e.


    Well we can agree to disagree on the subject. I don't see any evidence to make the conclusion that 6-OXO is equal to SERMS on any level just because there is a lack of scientific evidence but everyone is entitled to their opinion. That doesn't mean it won't be proven as effective in time but right now I would rather recommend to people something that has been proven to work. Everything I have seen on 6-OXO is based on speculation that comes from one study done on normal men that lasted only 3 weeks. In terms of real recovery that is a very short peroid of time. The long term effects are still unknown.

    What we need is people to do some blood tests and maybe we can see a difference.
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