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Thread: Why is it important to run an AI when on cycle?

  1. #41
    mnt51 is offline New Member
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    Thanks, trying to plan first cycle. Question if using an AI on cycle and then you early gyno signs do you up AI dose or treat with nolvadex ?

  2. #42
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    Quote Originally Posted by Sgt. Hartman View Post
    You already know about this Swifto but I'll post it anyway for others to give a real life example.

    Running about 500mg test with 12.5mg exemestane ED I noticed my nipples were a little sensitive. I doubled the AI dose and nothing changed, didn't get any worse but still a little sensitive so I upped it again and still had no change. I suspected that my research chem exemestane was probably bunk and went and had blood work done. Estradiol was in the mid 300's, over 6 times the top end of my reference range. I didn't have any lumps or gyno, no acne at all, no excessive water retention or any other estrogen related sides, only slightly sensitive nipples. I'd imagine if my E would have been below 300 or so I probably wouldn't have had any sides at all, all the while not knowing that I had extremely dangerous estrogen levels.

    Two lessons learned: don't trust research chems, and don't ever assume your estrogen levels are in check just because you don't have estrogen related sides.
    Could you PM me? Was it a well known research chem

  3. #43
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    Hey swifto, which would you suggest while cruising Aromasin or anastrozole?

  4. #44
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    Quote Originally Posted by slimshady01 View Post
    Guys i cant say on here but please if you are nervous just do some searching or join a board that can talk open source...*********** companies are the Bomb...

    i go ugl for gear but for AI, HCG PCT etc please try to get pharma...
    C'mon man...........U kno better........

  5. #45
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    I know research chem talk is kind of "ify" around here, but I think if someone gets faked chems, the community should be notified, just like a scamming source.

  6. #46
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    Quote Originally Posted by Dante Diamond
    I know research chem talk is kind of "ify" around here, but I think if someone gets faked chems, the community should be notified, just like a scamming source.
    Good luck with that.

  7. #47
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    Quote Originally Posted by Dante Diamond View Post
    I know research chem talk is kind of "ify" around here, but I think if someone gets faked chems, the community should be notified, just like a scamming source.
    We haqve a board sponsor that sells research chems....if that doesnt point people in a solid direction i dont know what would.

    So anyway im pretty sure this thread is about the prudence of using an ai on cycle ...not where u get them. Might be wise to keep such a great ,informative thread on topic.

  8. #48
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    Quote Originally Posted by The Bear 79 View Post
    C'mon man...........U kno better........
    Sorry man i didnt realize anything was wrong... Was looking to delete but it looks like someone took care of that...

    This needs a solid bump anyway and also a good possible sticky.

  9. #49
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    Quote Originally Posted by slimshady01 View Post
    Sorry man i didnt realize anything was wrong... Was looking to delete but it looks like someone took care of that...

    This needs a solid bump anyway and also a good possible sticky.
    I did.

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    Swifto - what is your opinion about those who say that it's better to run a SERM for on-cycle ERSE prevention instead of an AI?

  11. #51
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    Quote Originally Posted by Sgt. Hartman View Post
    Swifto - what is your opinion about those who say that it's better to run a SERM for on-cycle ERSE prevention instead of an AI?
    swifto can correct me if im wrong but SERMS just block estrogen at the receptors but dont actually lower estrogen.

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    Yes that's true that SERMs don't lower serum E levels but there's been a lot of questions on here lately and foolish people who say that it's better to run tamox instead of an AI on cycle and I wanted Swifto to put the issue to rest.

  13. #53
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    Yeha i would like to see his views on that as well. I pretty much guide all my friends on gear because they are to lazy to do any research. Anytime they they get gyno symptoms I put them on an AI and Tamox. When the symptoms go away i tell them to drop the Nolva but keep the AI.

    Would love to hear if im going about that right. Its always worked but there could be better ways im sure

  14. #54
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    Here was something i was looking for and found it!

    Another reason why Aromasin is preferred for your AI.. It just much more then just lower Estrogen..


    ABSTRACT FROM JOURNAL OF CLINICAL ENDOCRONOLOGY AND METABOLISM

    Suppression of estrogen, via estrogen receptor or aromatase blockade, is being investigated in the treatment of different conditions. Exemestane (Aromasin) is a potent and selective irreversible aromatase inhibitor. To characterize its suppression of estrogen and its pharmacokinetic (PK) properties in males, healthy eugonadal subjects were recruited. In a cross-over study, 12 were randomly assigned to 25 and 50 mg exemestane daily, orally, for 10 d with a 14-d washout period. Blood was withdrawn before and 24 h after the last dose of each treatment period. A PK study was performed (n = 10) using a 25-mg dose.

    RESULTS :

    The 25- and 50-mg doses of daily exemestane had comparable effects in suppressing circulating estrogen concentrations, with 38 ± 24% (mean ± SD; P = 0.002 vs. baseline) and 32 ± 29% (P = 0.008) decreases in estradiol concentrations, 71 ± 12% (P < 0.0001) and 74 ± 12% (P < 0.0001) decreases in estrone concentrations, and 45 ± 27% (P = 0.004) and 51 ± 20% (P = 0.02)

    BUT THERE'S MORE

    There was an increase in circulating testosterone concentrations after both 25 mg (60 ± 58%; P = 0.001) and 50 mg (56 ± 48%; P = 0.003) exemestane. Androstenedione concentrations were increased as well after 25 mg (32 ± 36%; P = 0.004) and 50 mg (47 ± 59%; P = 0.052) exemestane, respectively (Fig. 1Go and Table 2Go).

    SHBG concentrations were decreased by 21 ± 7% (P = 0.0003) and 19 ± 39% (P = 0.18) at 25 and 50 mg exemestane, respectively.

    Free testosterone concentrations were increased by 117 ± 74% (P = 0.0001) and 154 ± 95% (P < 0.0001) at both doses, due to the decrease in SHBG and the increase in total testosterone.
    devil-1986 and Lee_1978 like this.

  15. #55
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    So, Swifto, I'm crusing at 125mg/wk test e and 250mg/wk deca . I've been on this regiment for about 3 month and plan on cruising with it longer term. I just ordered aromasin . Would you recommend 10mg/eod for me? I haven't felt issues with estro yet. For whatever dose you recommend, how long would you recommend I run this? Do you run AIs like this throughout the whole cycle (or trt duration) or do you only do it for a few weeks at a time, then stop for a couple months?
    Last edited by Charlie6; 01-14-2012 at 11:13 AM.

  16. #56
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    Quote Originally Posted by Dante Diamond View Post
    I know research chem talk is kind of "ify" around here, but I think if someone gets faked chems, the community should be notified, just like a scamming source.
    we don't discuss scammers on this board. But order them from the sponsor ar-r and you dont need to worry

  17. #57
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    Good Post.

    A few questions for ya.. .

    Do you think that an AI is needed even on the basic Test cycle and no sides are shown? Aromatization is a basic rate in the body and the amount of androgen doesnt bother with it (assuming test only). Could introducing an AI increase the issues due to Test and DHT by reducing the ratio of estrogen by inhibiting aromatiase, which increases test in the system which then would increase DHT?

    With regards to the Prostate issue, according to the bolded area of the study posted; it seems estrogen help in preventing the proliferation of prostate tissue, and since DHT is a primary compound in prostate issues, could inhibiting estrogen increase the probability of prostate growth?

    As for the prolactin issue, That is due to testosterone long feedback not necessarily estrogen. Estrogen makes the prolactin in the body more 'effecient' as what its feminizing function is due to the genomic changes at the chromatin level that estrogen does. But high levels of testosterone can increase prolactin levels seperately from estrogen (very supraphysiologic levels however, but that is what we are refering to in a cycle). So use of an AI is very wise on a stack, especially with 19-nors (tren definately due to the androgen binding strength), and very high levels of test. To keep the proactin 'efficiency' down in possible elevated levels due to high androgen levels.

    What about SHBG levels for after the cycle? Since its highly estrogen dependent on formation in the liver, and high androgen levels reduce the amount of SHBG, would it be wise to stop the AI in the last week or so to allow SHBG to elevate some to help keep the negative feed back loop a little longer from stabilization to keep the body producing more test? Or would you rather use Torem and due to its actions at the liver (acting like estrogen) to increase SHBG following the suppression on a cycle?
    *My logic behind this is that if SHBG gets to low on a cycle, once the cycle is over the androgen produced is alot more bioavailable which its uptake in the body would be much faster, and in a 'rebooting HPTA' setting where test production is at a low anyways what is being produced is being 'used' to fast then you introduce the symptoms of 'low test' which then would somewhat correlate with the circadian rhythm of LH pulses throughout the day. SO by increasing SHBG towards the end of the cycle, you would be able to hold on to the test you have a little bit longer but wouldnt have the drops throughout the day.

  18. #58
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    Quote Originally Posted by Sgt. Hartman View Post
    Swifto - what is your opinion about those who say that it's better to run a SERM for on-cycle ERSE prevention instead of an AI?
    SERMs dont lower circulating estrogen levels, so the CHD risks are still evident IMO.

    I mentioned the risk of prostate cancer from increased levels of estrogen and Tamoxifen (SERM) used as a treatment. I dont know if its been studies as a preventative measure. Even then, if you were to use Tamox for that reason, its toxic itself and its use should be limited. Tamoxifen also reduces IGF-1 in males, so it may impact gains. Its liver toxic, occular and geno-toxic. The same cannot be said for Aromasin .

    Put simply, I think Aromasin is much better and should be used as a preventative agent because of the reasons in post 1. Tamoxifen is a poor choice for "preventative agent" in my book. Its best used as a "treatmeant" and should be kept on hand because of that. I wont cycle without it on hand.

    Quote Originally Posted by slimshady01 View Post
    swifto can correct me if im wrong but SERMS just block estrogen at the receptors but dont actually lower estrogen.
    Correct.

    Quote Originally Posted by slimshady01 View Post
    Here was something i was looking for and found it!

    Another reason why Aromasin is preferred for your AI.. It just much more then just lower Estrogen..



    ABSTRACT FROM JOURNAL OF CLINICAL ENDOCRONOLOGY AND METABOLISM

    Suppression of estrogen, via estrogen receptor or aromatase blockade, is being investigated in the treatment of different conditions. Exemestane (Aromasin) is a potent and selective irreversible aromatase inhibitor. To characterize its suppression of estrogen and its pharmacokinetic (PK) properties in males, healthy eugonadal subjects were recruited. In a cross-over study, 12 were randomly assigned to 25 and 50 mg exemestane daily, orally, for 10 d with a 14-d washout period. Blood was withdrawn before and 24 h after the last dose of each treatment period. A PK study was performed (n = 10) using a 25-mg dose.

    RESULTS :

    The 25- and 50-mg doses of daily exemestane had comparable effects in suppressing circulating estrogen concentrations, with 38 ± 24% (mean ± SD; P = 0.002 vs. baseline) and 32 ± 29% (P = 0.008) decreases in estradiol concentrations, 71 ± 12% (P < 0.0001) and 74 ± 12% (P < 0.0001) decreases in estrone concentrations, and 45 ± 27% (P = 0.004) and 51 ± 20% (P = 0.02)

    BUT THERE'S MORE

    There was an increase in circulating testosterone concentrations after both 25 mg (60 ± 58%; P = 0.001) and 50 mg (56 ± 48%; P = 0.003) exemestane. Androstenedione concentrations were increased as well after 25 mg (32 ± 36%; P = 0.004) and 50 mg (47 ± 59%; P = 0.052) exemestane, respectively (Fig. 1Go and Table 2Go).

    SHBG concentrations were decreased by 21 ± 7% (P = 0.0003) and 19 ± 39% (P = 0.18) at 25 and 50 mg exemestane, respectively.

    Free testosterone concentrations were increased by 117 ± 74% (P = 0.0001) and 154 ± 95% (P < 0.0001) at both doses, due to the decrease in SHBG and the increase in total testosterone.
    Seen this, but thanks for the addition.

    Its very similar to the study I linked in post 1.

    Quote Originally Posted by Charlie6 View Post
    So, Swifto, I'm crusing at 125mg/wk test e and 250mg/wk deca. I've been on this regiment for about 3 month and plan on cruising with it longer term. I just ordered aromasin. Would you recommend 10mg/eod for me? I haven't felt issues with estro yet. For whatever dose you recommend, how long would you recommend I run this? Do you run AIs like this throughout the whole cycle (or trt duration) or do you only do it for a few weeks at a time, then stop for a couple months?
    Get BW done and go from there.

    You may not require an AI on an HRT dose.

  19. #59
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    Quote Originally Posted by Lemonada8 View Post
    Good Post.

    A few questions for ya.. .

    Do you think that an AI is needed even on the basic Test cycle and no sides are shown? Aromatization is a basic rate in the body and the amount of androgen doesnt bother with it (assuming test only). Could introducing an AI increase the issues due to Test and DHT by reducing the ratio of estrogen by inhibiting aromatiase, which increases test in the system which then would increase DHT?

    What do you mean by "basic rate"?

    When androgen levels increase, so does aromotase activity and estrogen?

    DHT provides the body with lots of benifits, one of which is that its a potent inhibitor of estrogen. It may increase the instances of acne. If acne is your worry, then estrogen, high testosterone and increased DHT levels all contribute.

    I think you're trying to complicate things and are over analyzing.


    With regards to the Prostate issue, according to the bolded area of the study posted; it seems estrogen help in preventing the proliferation of prostate tissue, and since DHT is a primary compound in prostate issues, could inhibiting estrogen increase the probability of prostate growth?

    I said that it may reduce the risk of further prostate issues. Which I think is a realistic claim.

    If you worried abour increased DHT and prostate issues arising from lowered estrogen, then you have SERMs like Tamoxifen.


    As for the prolactin issue, That is due to testosterone long feedback not necessarily estrogen. Estrogen makes the prolactin in the body more 'effecient' as what its feminizing function is due to the genomic changes at the chromatin level that estrogen does. But high levels of testosterone can increase prolactin levels seperately from estrogen (very supraphysiologic levels however, but that is what we are refering to in a cycle). So use of an AI is very wise on a stack, especially with 19-nors (tren definately due to the androgen binding strength), and very high levels of test. To keep the proactin 'efficiency' down in possible elevated levels due to high androgen levels.

    Prolactin does have a direct effect on prostate cell proliferation. If you want to know how its directly important?

    Inside the prostate, prolactin attaches to its receptor that belongs to the cytokine 1 receptor superfamily and is localized in chromosome 5. In addition the receptor
    has 2 domains that are separate in the resting state but that become homodimerized once they are joined to prolactin. In this manner intracellular signaling is produced by means of JAK-STAT kinases.

    Once prolactin is attached to its receptor that carries out tyrosine kinase activity, it phosphorylates JAK 2 and STAT-1, 3 and 5a and b. Later on STAT-5 a/b dimers are formed and they are translocated to the nucleus to act on DNA sequences which in turn activate promoter sequences for prostate cell proliferation, differentiation and survival, in normal as well as malignant cells.


    What about SHBG levels for after the cycle? Since its highly estrogen dependent on formation in the liver, and high androgen levels reduce the amount of SHBG, would it be wise to stop the AI in the last week or so to allow SHBG to elevate some to help keep the negative feed back loop a little longer from stabilization to keep the body producing more test? Or would you rather use Torem and due to its actions at the liver (acting like estrogen) to increase SHBG following the suppression on a cycle?
    *My logic behind this is that if SHBG gets to low on a cycle, once the cycle is over the androgen produced is alot more bioavailable which its uptake in the body would be much faster, and in a 'rebooting HPTA' setting where test production is at a low anyways what is being produced is being 'used' to fast then you introduce the symptoms of 'low test' which then would somewhat correlate with the circadian rhythm of LH pulses throughout the day. SO by increasing SHBG towards the end of the cycle, you would be able to hold on to the test you have a little bit longer but wouldnt have the drops throughout the day.

    Why would we want to increase SHBG levels and reduce Free T going into PCT? Isnt the point of PCT to increase TT and FT, Freet T. is proabbly more important.

    SHBG levels are of little importance on cycle because Free T is so high.

    As usualy your overanalyzing and trying your hardest to disagree with me or something I have suggested.

    bolds

  20. #60
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    Good thread. I've always wondered why there wasn't a thread about on-cycle supps. I'd like to know which drugs to take for each specific steroid , ie, what's best when on tren , what's best when on deca .

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    Quote Originally Posted by NewMuscle83 View Post
    Good thread. I've always wondered why there wasn't a thread about on-cycle supps. I'd like to know which drugs to take for each specific steroid, ie, what's best when on tren, what's best when on deca.
    Test + aromotasble compounds = Use an AI (Aromasin ) and Tamoxifen or Rolaxifene on hand. I also keep a D2-agonist on hand anyhow.

    Test + 19-Nor's = Use an AI + Tamoxifen or Rolaxifene on hand + D2-agonist (Caber/Prami) on hand.

    Test + DHT = Possible lower AI dose + Tamoxifen or Rolaxifene on hand.

  22. #62
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    Quote Originally Posted by Swifto View Post
    Test + aromotasble compounds = Use an AI (Aromasin ) and Tamoxifen or Rolaxifene on hand. I also keep a D2-agonist on hand anyhow.

    Test + 19-Nor's = Use an AI + Tamoxifen or Rolaxifene on hand + D2-agonist (Caber/Prami) on hand.

    Test + DHT = Possible lower AI dose + Tamoxifen or Rolaxifene on hand.
    Would test anavar = possible lower AI dose since var is technically a DHT?

  23. #63
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    Quote Originally Posted by Swifto View Post
    Test + aromotasble compounds = Use an AI (Aromasin ) and Tamoxifen or Rolaxifene on hand. I also keep a D2-agonist on hand anyhow.

    Test + 19-Nor's = Use an AI + Tamoxifen or Rolaxifene on hand + D2-agonist (Caber/Prami) on hand.

    Test + DHT = Possible lower AI dose + Tamoxifen or Rolaxifene on hand.
    Thanks for the info. How bout Gh? Anything needed while one. I'm probably gonna start on 4iu pretty soon.

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    Quote Originally Posted by slimshady01 View Post
    Would test anavar = possible lower AI dose since var is technically a DHT?
    Thats what I said, yes.

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    Quote Originally Posted by NewMuscle83 View Post
    Thanks for the info. How bout Gh? Anything needed while one. I'm probably gonna start on 4iu pretty soon.
    Watch prolactin.

    Get BW, as with all hormone changes.

  26. #66
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    Quote Originally Posted by Swifto View Post
    Thats what I said, yes.

    Thanks bro,

    I asked because Var for example does not showcase some of the other sides as other DHTs such as winnie, primo... IE hair loss shedding..

  27. #67
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    Quote Originally Posted by Swifto View Post
    What do you mean by "basic rate"?
    When androgen levels increase, so does aromotase activity and estrogen?
    DHT provides the body with lots of benifits, one of which is that its a potent inhibitor of estrogen. It may increase the instances of acne. If acne is your worry, then estrogen, high testosterone and increased DHT levels all contribute.
    I meant that the T/E ratio remains constant regardless of the amount of test in the body. And my question was if you lower the E part by inhibiting the enzyme, wouldnt that increase DHT? Because there is also a T/DHT ratio that is kept relatively constant also.

    Quote Originally Posted by Swifto View Post
    I said that it may reduce the risk of further prostate issues. Which I think is a realistic claim.
    If you worried abour increased DHT and prostate issues arising from lowered estrogen, then you have SERMs like Tamoxifen.
    In prostate cancer, ERbeta activation appears to limit cell proliferation directly or through ERalpha inhibition, and loss of ERbeta has been consistently associated with tumor progression
    this is the quote i was referring to, that ERbeta is activated by binding of estrogen; so back to my question is that assuming what i said above is true about elevating DHT with an AI; and DHT is a key component in prostate growth, wouldnt less estrogen in the system and elevated DHT increase the risk of prostate growth?
    Also with the increased androgens, there is a loss of ER's in the prostate, so with less ERbeta activation and loss of ERbeta receptors and increased DHT; wouldnt that increase risk of prostate growth?
    ERbeta is typically 'lost' in prostate cancer, along with the enzyme that modifies DHT in the prostate which help keep abnormal proliferation to a minimum.


    Quote Originally Posted by Swifto View Post
    Prolactin does have a direct effect on prostate cell proliferation. If you want to know how its directly important?
    I was agreeing with you on the bit about using an AI to help control the efficacy of prolactin due to the efficacy of prolactin is increased in elevated estrogen levels.

    Quote Originally Posted by Swifto View Post
    Why would we want to increase SHBG levels and reduce Free T going into PCT ? Isnt the point of PCT to increase TT and FT, Freet T. is proabbly more important.
    SHBG levels are of little importance on cycle because Free T is so high.
    Right, on cycle free T is skyrocketed. But what about after the cycle? Low free T is the cause for "low T" symptoms. With SHBG being decreased while on a cycle, then when you try to recover from the cycle, yes you want your test to increase; but total test is more important in the true sense of recovery than free test b/c the test will dissociate from SHBG when levels are too low. By stopping the inhibitory affect on SHBG in the end of the cycle would allow it to increase during the weeks of PCT where it holds onto the Test longer. The actual recovery would be longer due to less test is free and doing what it needs to do in the body, but since free T didnt get elevated to the same extent after PCT when SHBG is lower than normal, that it would allow a closer-to-normal recovery b/c SHBG would be back to normal and following leveling of the HPTA and test production would be sustained throughout the day.
    Say you produce 100units of test a day normally, and SHBG (before cycle) can hold onto 50% of that test and thats how you normally are naturally before a cycle.
    Then after the cycle, say you get back to the same production of test at 100units but now since SHBG was decreased on cycle it can only hold onto 35%, so the 'spending' of test elevated which would initially increase free test but it would also 'run out of currency' which would end up lowering free test totals because the body would use up the test to fast b/c the intial free test following the cycle's value of free test upregulated the AR would suck up the test much faster since the SHBG cant hold onto it as long.
    So by increasing SHBG towards the end of the cycle, the free T wouldnt be as high initially which wouldnt activate the feedback nearly as much, but the sense of 'low test' would take a little longer to get over but with an longer pct of nolva at the end increasing the effectiveness of LH would help the body produce the test back to an appropiate level.

    Quote Originally Posted by Swifto View Post
    As usualy your overanalyzing and trying your hardest to disagree with me or something I have suggested.
    nah not trying to automatically disagree with what you are saying, just asking some questions :-)
    and blowing off studying lolz.

    all in all, i do think its a wise idea to run an AI on a cycle, especially if there are ESRE...

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    I get sensitive nips all the time. You know...itchy and tingling.

    120 mg test cyp weekly with 1 mg AI split twice a week - NOT a cycle TRT.

    Worried I had elevated E2 with the "symptoms".

    BW showed E2 at 23 pg/ml.

    Only BW will tell the truth...not symptoms.

    High sustained levels of E2 are insidious and can causes everything from prostate cancer to hypothyroidism to cardiovascular disease.

    This is one of the best posts I've seen here yet.

    Posts like these take considerable amount of time to author so a big thank you swifto!
    Last edited by steroid.com 1; 01-14-2012 at 11:12 PM.

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    Quote Originally Posted by Lemonada8 View Post
    I meant that the T/E ratio remains constant regardless of the amount of test in the body. And my question was if you lower the E part by inhibiting the enzyme, wouldnt that increase DHT? Because there is also a T/DHT ratio that is kept relatively constant also.

    Theoretically, yes.

    More available test = more aromotase, but then you have to take into account DHT is also a potent inhibitor of estrogen. How?

    By decreasing estrogen-induced RNA transcription, aromotase inhibition and is an antagonist to the ER in tissues.

    Quote Originally Posted by Lemonada8 View Post
    this is the quote i was referring to, that ERbeta is activated by binding of estrogen; so back to my question is that assuming what i said above is true about elevating DHT with an AI; and DHT is a key component in prostate growth, wouldnt less estrogen in the system and elevated DHT increase the risk of prostate growth?
    Also with the increased androgens, there is a loss of ER's in the prostate, so with less ERbeta activation and loss of ERbeta receptors and increased DHT; wouldnt that increase risk of prostate growth?
    ERbeta is typically 'lost' in prostate cancer, along with the enzyme that modifies DHT in the prostate which help keep abnormal proliferation to a minimum.
    DHT's role is complicated in prostate growth and BPH. In early life, puberty and adulthood its role is positive and its needed for growth. But in later adulthood, it can become detrimental. This happens becuasue its the key regulater (as well as AR) in cell proliferation and apoptosis. Why does it become a problem? Probably becuase DHT levels dont really decrease with age, like testostrone levels do. That would indicate DHT is a large contributor to BPH and test/estrogen isnt, but recent reserch has also pointed the finger at estrogen.

    If DHT levels increase moreso than we had expected when using an AI, then we can emply the use of a 5-AR inhibitor. But I think this needs to be something that is determined by BW, age and risks of BPH (genetic).

    Are you stating that an AI should'nt be used because of this and estrogen should be allowed to get out of control on cycle? Because as usual, I don't know where your headed with your questions, neither do you I dont think.

    Read this by Patrick Arnold (specifically the last paragraph)...



    Quote Originally Posted by Lemonada8 View Post
    I was agreeing with you on the bit about using an AI to help control the efficacy of prolactin due to the efficacy of prolactin is increased in elevated estrogen levels.
    Ok.

    Quote Originally Posted by Lemonada8 View Post
    Right, on cycle free T is skyrocketed. But what about after the cycle? Low free T is the cause for "low T" symptoms. With SHBG being decreased while on a cycle, then when you try to recover from the cycle, yes you want your test to increase; but total test is more important in the true sense of recovery than free test b/c the test will dissociate from SHBG when levels are too low. By stopping the inhibitory affect on SHBG in the end of the cycle would allow it to increase during the weeks of PCT where it holds onto the Test longer. The actual recovery would be longer due to less test is free and doing what it needs to do in the body, but since free T didnt get elevated to the same extent after PCT when SHBG is lower than normal, that it would allow a closer-to-normal recovery b/c SHBG would be back to normal and following leveling of the HPTA and test production would be sustained throughout the day.
    Say you produce 100units of test a day normally, and SHBG (before cycle) can hold onto 50% of that test and thats how you normally are naturally before a cycle.
    Then after the cycle, say you get back to the same production of test at 100units but now since SHBG was decreased on cycle it can only hold onto 35%, so the 'spending' of test elevated which would initially increase free test but it would also 'run out of currency' which would end up lowering free test totals because the body would use up the test to fast b/c the intial free test following the cycle's value of free test upregulated the AR would suck up the test much faster since the SHBG cant hold onto it as long.
    So by increasing SHBG towards the end of the cycle, the free T wouldnt be as high initially which wouldnt activate the feedback nearly as much, but the sense of 'low test' would take a little longer to get over but with an longer pct of nolva at the end increasing the effectiveness of LH would help the body produce the test back to an appropiate level.
    Your saying we want to limit the effect of testosterone having on the negative feedback loop during PCT to further increase testosterone "in the long run" by not decreasing SHBG levels towards the end of the cycle?

    Quote Originally Posted by Lemonada8 View Post
    nah not trying to automatically disagree with what you are saying, just asking some questions :-)
    and blowing off studying lolz.
    Your not suggesting much in the way of laymens terms (compounds/doses) with the disagreements you've raised.

    Quote Originally Posted by Lemonada8 View Post
    all in all, i do think its a wise idea to run an AI on a cycle, especially if there are ESRE...
    Me too.

  30. #70
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    Quote Originally Posted by jimmyinkedup View Post
    We haqve a board sponsor that sells research chems....if that doesnt point people in a solid direction i dont know what would.

    So anyway im pretty sure this thread is about the prudence of using an ai on cycle ...not where u get them. Might be wise to keep such a great ,informative thread on topic.
    ........nevermind.
    Last edited by Black; 01-15-2012 at 05:45 PM.

  31. #71
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    Bump for others to see

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    bump

  33. #73
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    Can we sticky this? I know I will be searching for it again in the future.

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    Quote Originally Posted by Macon_Bacon View Post
    I thought I had read in a pct post that aromasin is a suicide inhibitor to estrogen (thus killing all of it in your system) while arimidex will just inhibit the estrogen from binding to receptors (decreasing estrogen effects by 80%, this is just from memory so might be wrong).
    On a side note, this is incorrect. Arimidex does not compete for the estrogen recepter, that is the role that SERM's play. Instead Arimidex works by blocking the aromatase enzyme responsible for the production of estrogen in the first place. This is the difference between Aromotase Inhibitors and Selective Estrogen Regulating Modulators.

  35. #75
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    Quote Originally Posted by JohnnyVegas
    Can we sticky this? I know I will be searching for it again in the future.
    x2

    I've linked/seen this linked a dozen + times in the last day

    Definitely stickie material

  36. #76
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    agreed

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    if it doesn't get stickied, just save the link in your "big list of important links" that you should have somewhere on your hard drive..

    http://forums.steroid.com/showthread...o#.TxhJRvkwJ8E

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    Just added Exemestane's effect on lipid profile, or lack of.

  39. #79
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    Swifto ive always had a a suspicion that high estrogen that I am known to be prone of keeps fat on my gut off and during cycles. In a wife beater i look 9% and dry everywhere else "avi" yet still have a fat covering my abs with an extremely clean diet.

    The only times i get my abs out are on Dave Palumbo style keto diet with test and var.

    This cycle i started without an AI but added upon seeing this post. It almost seems now that I am able to eat more carbs and total calories vs previous cycles without gaining fat.

    My sex drive over the last 4 months or so had also simmered "i do self trt". Even on 750 test it hasnt been anything special, but about 4 days after adding Aroma at 12.5 ED its coming back strong..

    So without any noticable sides with high E.. for someone like me could it be still wreaking havic on my fat metabolism, how i store fat or process carbs etc?

    I got 4 of my friends now going to run AI during all their cycles..

    Thanks again for the post.
    Last edited by slimshady01; 01-21-2012 at 08:06 PM.

  40. #80
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    Do you suggest using an ai all the way up to pct or just up till last pin?

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