Some additional thoughts on the post cycle

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  1. 1. Wrong. It pulses thorughouth the day and is maximized during the first REM cycle.

    2. You can't slip anything under the radar.

    3. 17 methyl E2 (a metabolite of Dbol) has a half life up to 72 hours and is more suppressive than Dbol itself so its 4.5 hour half-life means nothing.

    4. The theory doens't even take into account receptor binding times.


    IOW, its pure bs.
    My point was exactly this, that "bridging" with any aas simply isnt going to work. Perhaps stepping down to something less supresive like anavar for the final two weeks before starting your pct may help, but I havent tried it, and I wont speculate on it.

    As for natty test being maximized durring the first REM cycle, that is the first time i've heard that. But if that is so, it does not mean that your test levels dont spike (as I've read more then a few times) upon waking.


  2. Ok, having gone and done some reasearch I think I'm going to minorly revise my previous statement of intention. Not being familiar enough with all the pharmacokinetc properties of hcg and its efficacy in supressing LH release, I'm going to advise continued administration until exogenous testosterone levels have retrned to the physiologically "normal" range.

    First, I advise everyone who hasn't read this article to go read it now: http://www.avantlabs.com/magmain.php...D=30&page****77

    This article indicates to me that LH production begins to recover as soon as t levels fall within normal range, regardless of whether or not there are exogenous hormones in the body. The mind&muscle article also seems to indicate that LH recovery happens at a fairly constant rate regardless of testosterone levels (as long as they are sufficient to induce LH recovery) In addition to the data from the article, I unearthed a good studiy that show that low dose androgen administration does not completely supress LH and FSH production.

    Thus, I propose that complete recovery may be attained with little or no post cycle crash by having a cruising period at the end of the cycle, which lasts ~10 weeks from the time exogenous testoserone levels have decreased to a physiologically "normal" level, with tapered weekly doses from 50-100 mg (depending on lbm) down to ~20mg. During this cruising period, a combiniation of ATD and a SERM would be used to aid in recovery (though the dosage would not have to be very high) with the continuation of ATD/SERM use for 1-2 weeks past the cessation of injections. This actually makes a lot of sense to me on many levels, as downward dosage titration is a very common medical practice in many instances. One might even take this a step further using a less supressive compound such as anavar, though the control of dosage would be more difficult and there is no clinical data surrounding its efficacy in this role.

    Effects of chronic testosterone administration in normal men: safety and efficacy of high dosage testosterone and parallel dose-dependent suppression of luteinizing hormone, follicle-stimulating hormone, and sperm production.

    Matsumoto AM.

    Geriatric Research, Education, and Clinical Center, Veterans Administration Medical Center, Seattle, Washington 98108.

    In normal men, chronic testosterone (T) administration results in negative feedback suppression of gonadotropin and sperm production. However, azoospermia is achieved in only 50-70% of men treated with high dosages of T. Furthermore, the relative sensitivity of LH and FSH secretion to chronic administration of more physiological dosages of T is unclear. We determined whether a T dosage higher than those previously given would be more or less effective in suppressing spermatogenesis and whether, within the physiological range, T would exert a more selective effect on LH than on FSH secretion. After a 4- to 6-month control period, 51 normal men were randomly assigned to treatment groups (n = 9-12/group) receiving either sesame oil (1 mL) or T enanthate (25, 50, 100, or 300 mg, im) weekly for 6 months. Monthly LH and FSH levels by RIA and twice monthly sperm counts were determined. During treatment, T levels were measured daily between two weekly injections. Chronic T administration in physiological to moderately supraphysiological dosages resulted in parallel dose-dependent suppression of LH, FSH, and sperm production. T enanthate (50 mg/week) suppressed LH and FSH levels and sperm counts to 50% of those in placebo-treated men (ED50). T enanthate (300 mg/week), was no more effective than 100 mg/week in suppressing LH, FSH, and sperm production. Serum T levels in men who received 100 and 300 mg/week T enanthate were 1.5- and 3-fold higher than those in placebo-treated men, respectively. Except for mild truncal acne, weight gain, and increases in hematocrit, we detected no significant adverse health effects of chronic high dosage T administration. We conclude that 1) LH and FSH secretion are equally sensitive to the long term negative feedback effects of T administration; 2) sperm production is suppressed in parallel with the LH and FSH reductions induced by chronic T administration; and 3) even at the clearly supraphysiological dosage of 300 mg/week, T enanthate does not reliably induce azoospermia in normal men. However, there was also no evidence of a stimulatory effect of this T dosage on spermatogenesis. Furthermore, we found no evidence of major adverse health effects of T administered chronically even at the highest dosage.

    PIP: In Seattle, Washington, health workers randomly assigned 51 healthy men (mean age, 29 years) to a group that was to receive either 1 ml sesame oil or testosterone enanthate (T enanthate) at various doses once a week for 6 months so an investigator could determine the safety and efficacy of long-term administration of T enanthate in suppressing spermatogenesis and whether it would bring about a more selective feedback effect on luteinizing hormone (LH) than on follicle stimulating hormone (FSH) secretion. 4-6 months prior to treatment, observations and measurements were performed with no administration of hormones. T enanthate effected a significant dose-dependent suppression of both serum LH and FSH levels. At 50 mg of T enanthate per week, the LH level was 65% and the FSH level was 62% of control values; at 100 mg/week, the levels were at 32% and 34% of control values, respectively. T enanthate also contributed to a significant dose-dependent suppression of both sperm counts and concentrations. At 50 mg/week, the sperm count was 36% of control values; at 100 mg/week, it was 0.8% of control values. T enanthate at a dose of 300 mg/week was no more effective than 100 mg/week. The dose-dependent suppression curves were parallel for the hormones, sperm counts, and sperm concentrations. Men who received 100 mg and 300 mg T enanthate per week had higher T levels than the men treated with sesame oil. These levels were at and above the upper limits of the normal range. The men suffered from no significant adverse health effects. There were cases of mild truncal acne, weight gain, and increases in hematocrit. These findings show that LH and FSH secretion are sensitive to long-term negative feedback effects of T administration as well as is spermatogenesis. T enanthate may prove to be a useful male contraceptive agent.
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  3. Quote Originally Posted by exnihilo
    I'm looking for a way to avoid feeling like crap for 3 weeks and "blah" for an additional two weeks post cycle.
    Reduce your cycle length.

  4. Quote Originally Posted by exnihilo
    .
    Yes, LH can and will start to recover even when using exogenous androgens as long as it's within the body's own normal to high normal levels...noones' disputing that. But we're talking about natty T production, not LH. Natty T cannot recover when there is exogeneous androgens present...even if it's in the range of normal T production. It's not LH we're worried about, it's raising natty T. So using something mild like var is still not gonna work.

    But again, if it makes you feel better and you think it helps you, then fantastic...but until some kind of new compound that comes out that somehow bypasses the feedback loops, then there is just no way this is going to happen. Not trying to be a dick, this is just common endocrinology.

  5. Quote Originally Posted by lifted
    Yes, LH can and will start to recover even when using exogenous androgens as long as it's within the body's own normal to high normal levels...noones' disputing that. But we're talking about natty T production, not LH. Natty T cannot recover when there is exogeneous androgens present...even if it's in the range of normal T production. It's not LH we're worried about, it's raising natty T. So using something mild like var is still not gonna work.

    But again, if it makes you feel better and you think it helps you, then fantastic...but until some kind of new compound that comes out that somehow bypasses the feedback loops, then there is just no way this is going to happen. Not trying to be a dick, this is just common endocrinology.
    Would you be so kind as to explain the to me why increased levels of LH do not stimulate production of testosterone when the quantity of exogenous hormone is at near or sub-physiological levels? That is what would happen normally, does exogenous testosterone have some special property that is completely supressive of testosterone production regardless of quantity, unlike our naturally produced testosterone? Seems like a molecule is a molecule to me (not counting things like optical isomers or molecules with chiral atoms).

    The point I am making is that from what I have read it appears to me that testosterone production should increase in proportion to the increases in LH production, barring testicular atrophy. If you look at graph Bill made for the the mind and muscle article I posted, it appears that once testosterone falls to within the physiological range, LH levels begin to increase, and increase at a fairly contsant rate regardless of how low testosterone levels actually fall, until complete recovery at week 10. The reason I made the suggestions I did is that I believe that if testicular atrophy has been avoided by using HCG throughout the entire cycle, then LH is the primary indicator of recovery, as it directly stimulates testosterone production in the leydig cells of the testes. Wouldn't you prefer to let testosterone levels fall to just low enough for LH levels to recover, gradually reducing the amount of exogenous testosterone in your body as your LH levels recover and thus your body is capable of producing more testosterone on its own, rather than crash completely? By using a SERM you could even theoretically use slightly higher amounts of testosterone while still making a full recovery. And what if you could even use a non-aromatizing compound that was also a mild androgen but also showed powerful anabolic properties (i.e. at least as anabolic and less supressive than testosterone mg/mg) such as anavar? If ATD pans out (I hope it does) that might allow you to use additional hormones while still recovering fairly completely. Finishing off a cycle with 10-15mg of anavar a day and feeling TOTALLY fine when you come off? Seems like a distinct possibility to me, and I am willing to be the guinea pig if need be (though I hope other people are willing to try it out as well, n=1 studies aren't very useful).

    Of course, if I have overlooked something, please be patient and explain it to me so that I can learn. Thank you.
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  6. Quote Originally Posted by exnihilo
    Would you be so kind as to explain the to me why increased levels of LH do not stimulate production of testosterone when the quantity of exogenous hormone is at near or sub-physiological levels? That is what would happen normally, does exogenous testosterone have some special property that is completely supressive of testosterone production regardless of quantity, unlike our naturally produced testosterone? Seems like a molecule is a molecule to me (not counting things like optical isomers or molecules with chiral atoms).

    The point I am making is that from what I have read it appears to me that testosterone production should increase in proportion to the increases in LH production, barring testicular atrophy. If you look at graph Bill made for the the mind and muscle article I posted, it appears that once testosterone falls to within the physiological range, LH levels begin to increase, and increase at a fairly contsant rate regardless of how low testosterone levels actually fall, until complete recovery at week 10. The reason I made the suggestions I did is that I believe that if testicular atrophy has been avoided by using HCG throughout the entire cycle, then LH is the primary indicator of recovery, as it directly stimulates testosterone production in the leydig cells of the testes. Wouldn't you prefer to let testosterone levels fall to just low enough for LH levels to recover, gradually reducing the amount of exogenous testosterone in your body as your LH levels recover and thus your body is capable of producing more testosterone on its own, rather than crash completely? By using a SERM you could even theoretically use slightly higher amounts of testosterone while still making a full recovery. And what if you could even use a non-aromatizing compound that was also a mild androgen but also showed powerful anabolic properties (i.e. at least as anabolic and less supressive than testosterone mg/mg) such as anavar? If ATD pans out (I hope it does) that might allow you to use additional hormones while still recovering fairly completely. Finishing off a cycle with 10-15mg of anavar a day and feeling TOTALLY fine when you come off? Seems like a distinct possibility to me, and I am willing to be the guinea pig if need be (though I hope other people are willing to try it out as well, n=1 studies aren't very useful).

    Of course, if I have overlooked something, please be patient and explain it to me so that I can learn. Thank you.
    I totally see what you're talking about here, and if it did work that way, then yes, it would be a great way to do things. But you can still have LH output, and ultra low test levels.

    Let me try to explain myself another way....>>>
    Take for example a 50 yr. old that has ULTRA low T levels, even for his age. We'll say he produces naturally 50ng/ml of natty test tops. Well, he is still producing LH of course, but is not producing anywhere near the amount of natty T in order to build or maintane massive amounts of muscle. See what I mean? ehh, maybe that was a bad example...lol.

    Basically, just because LH is rebounding, that doesn't mean that natty T will start to recover as long as you're using exo-T. HCG is only mimicking LH anyways, so as soon as you come off, LH will soon drop again, then it will restart, so it's only going to prolong your recovery. I don't know how to explain it any simpler.

    And like I said, just because (IMO) it will prolong recovery, that doesn't mean that your points aren't valid. I think that even though it does prolong recovery, you "could" still benefit from it since you'd slowly be weening yourself off androgens and then slowly weening yourself back to full recovery. So I do agree that it is def worth the trials since it is a slower weening compared to BAM! crash, and then trying like hell to bring T back up. I would also be very intrigued if you were to do this and test the waters vs. conventional PCT methods. If you do, try to get some bloodwork done so we can further disect this. I would even be game to try it w/ you, but I'm having a hard time with libido and acne from my last cycle...so I gotta lay off the sauce for awhile longer.

  7. Quote Originally Posted by exnihilo
    Would you be so kind as to explain the to me why increased levels of LH do not stimulate production of testosterone when the quantity of exogenous hormone is at near or sub-physiological levels?
    This is because when you come off of HCG, LH is just gonna drop off again. Then the whole recovery process (LH/FSH>>natty T recovery) has to start over.

  8. Quote Originally Posted by exnihilo
    I remember hanging out on a forum (or perhaps it was a newsgroup) a while ago where several doctors were discussing hCG for hypogonadal males; I don't remember the exact dosages (though I seem to remember 500iu being thrown about for something) that were being discussed I do remember several doctors lamenting the fact that the dosage had to be increased over time in order to achieve the same effect, so yes I think in the real world some desensitization occurs even with low doses.

    I am aware that the LH response rebounds quickly, the reason I suggested HCG during pct is that it is effective at increasing testosterone levels (though not to such a degree as to be any kind of truly effective anabolic) while being only SLIGHTLY supressive, if at all (again, my source for this was several forum conversations between medical doctors, though I admit as it has been a long time so I may not recall everything properly).

    As for your statement that multiple compounds would be complete overkill, in my personal experience 55mg of nolvadex daily (the only cap size my source had) was not enough to prevent me from feeling like **** for three solid weeks (weeks ~6-9 after the final shot) so I'm interested in re-arranging my pct practices (hcg for two weeks after the final shot, nolvadex 55mg/day weeks 2-10) in order to avoid this in the future.


    All you have to do is check the reaseach. The dose causes desentization, not the length of treatment. You can simply ask Dr. Crisler who is an authority in the area and he will tell you the same. In fact Tamoxifen even helps with the desensitization from high doses.

    "The problem with high doses of HCG is that it, like its analog LH, stimulates aromatase activity. My understanding is that aromatase is toxic to Leydig cells. Therefore taking too much HCG induces primary hypogonadism (which is permanent) while attempting to treat acquired secondary hypogonadism (which USUALLY is temporary).

    In Endocrinology, we are always trying to strike a balance between risk and benefit (the closet philosophers out there will likely apply this concept to all of life). Some HCG is very, very good. Too much is bad. Where is the breakpoint? IMPO, something less than 500IU at a time."

    Most of the sutides are done on HH men and there is a marked difference in acute and chronic administration. Desentization was seen after 23 months at 1500 IU's 3x per week although test levels still remained normal.

    J Clin Endocrinol Metab 1982 Jul;55(1):76-80


    Testicular responsiveness to chronic human chorionic gonadotropin administration in hypogonadotropic hypogonadism.

    D'Agata R, Vicari E, Aliffi A, Maugeri G, Mongioi A, Gulizia S.



    4 Compunds is completely overkill. If you want to limit the crash then use HCG during a cyucle to keep leydig cell response normal then use a SERM during PCT. Using 4 drugs in which 2 can handle IS overkill.
    For answers to board issues, read the Suggestion and News forum at the bottom of the main page.

  9. Quote Originally Posted by hrdgain81
    My point was exactly this, that "bridging" with any aas simply isnt going to work. Perhaps stepping down to something less supresive like anavar for the final two weeks before starting your pct may help, but I havent tried it, and I wont speculate on it.

    As for natty test being maximized durring the first REM cycle, that is the first time i've heard that. But if that is so, it does not mean that your test levels dont spike (as I've read more then a few times) upon waking.
    No, Anavar won't work either because at little at 2.5mg of Anavar suppresses the HTPA.

    It is so, check Pubmed. Its also the time GH pulses are at its highest as well. In fact, it drop when you wake up.

    Relationship between rapid eye movement sleep and testosterone secretion in normal men.

    Lubo****zky R, Herer P, Levi M, Shen-Orr Z, Lavie P.

    Endocrine Institute, Haemek Medical Center, Afula, Israel.

    The relation between the pituitary-gonadal hormones' rhythm and sleep physiology in men is not fully elucidated. To examine whether the reproductive hormones are correlated with sleep architecture, we determined the nocturnal serum levels of testosterone, luteinizing hormone (LH), and follicle-stimulating hormone (FSH) in six healthy young men. Serum hormone levels were obtained every 15 minutes from 1900 to 0700 hours with simultaneous polysomnographic sleep recordings. Hourly testosterone levels were lowest when subjects were awake (1900-2200 hours) than during sleep (2300-0700 hours). Testosterone nocturnal rise antedated the first REM by about 90 minutes. The rise in testosterone levels was slower when REM latency was longer. Mean nocturnal testosterone levels did not correlate with the number of rapid eye movement (REM) episodes. Also, pre-non-REM (NREM) testosterone levels were higher as compared with the pre-REM periods and lower during the first NREM period as compared with other nocturnal NREM periods. Serum LH levels disclosed a nocturnal rise that preceeded a similar rise in testosterone by about an hour. We conclude that in young adult men, testosterone levels begin to rise on falling asleep, peak at about the time of first REM, and remain at the same levels until awakening.

    .

    It doens't matter if they spike or not (which it doens't), its the same physiological response you will get in the middle of the day and you can't "pigg-back" anything.


    Effect of low dose oxandrolone and testosterone treatment on the pituitary-testicular and GH axes in boys with constitutional delay of growth and puberty.

    Crowne EC, Wallace WH, Moore C, Mitchell R, Robertson WH, Holly JM, Shalet SM.

    Department of Endocrinology, Christie Hospital Trust, Manchester, UK.

    OBJECTIVE: To investigate the effect of low dose oxandrolone and testosterone on the pituitary-testicular and GH-IGF-I axes. DESIGN: Prospective double-blind placebo-controlled trial. PATIENTS: Sixteen boys with constitutional delay of growth and puberty (CDGP) with testicular volumes 4-6 ml were randomized to 3 months treatment: Group 1 (n = 5), daily placebo: Group 2 (n = 5), 2.5 mg oxandrolone daily or Group 3 (n = 6), 50 mg testosterone monthly intramuscular injections with assessment (growth, pubertal development and overnight hormone profiles) at 0, 3, 6 and 12 months. MAIN OUTCOME MEASURES: LH and GH profiles (15-minute samples) were analysed by peak detection (Pulsar), Fourier transformation and autocorrelation. Testosterone levels were measured hourly and insulin, SHBG, IGF-I, and IGFBP-3 levels at 0800 h. Statistical analysis was by multivariate analysis of variance for repeated measures. RESULTS: LH and testosterone parameters increased significantly with time in all 16 (LH AUC, P < 0.001; peak amplitude, P = 0.02; number of peaks, P = 0.02; testosterone AUC, P = 0.02; morning testosterone, P = 0.002). In Group 2, however, LH and testosterone parameters decreased at 3 months followed by a rebound increase at 6 and 12 months. SHBG levels were markedly reduced at 3 months (P = 0.006) and a wider range of dominant GH frequencies was present although GH AUC was not increased until 6 months, with an increase in GH pulse frequency but not amplitude. IGF-I levels were increased at both 3 and 12 months. In Group 3, pituitary-testicular suppression was not apparent, but GH levels increased with an increase in GH amplitude at 3 and 12 months. CONCLUSION: Oxandrolone transiently suppressed the pituitary-testicular axis and altered GH pulsatility. Testosterone increased GH via amplitude modulation.
    For answers to board issues, read the Suggestion and News forum at the bottom of the main page.

  10. Quote Originally Posted by lifted
    The fact that many are forgetting here is that recovery simply takes time. As Bobo said, LH rebounds quickly, so the only thing that is left to worry about is simply bringing T levels back up to normal. And the only thing that is gonna do this best is time. Sure, several products will help you "feel" better but that does not mean that it is helping restore natty test any sooner. HCG during PCT will only delay the inevitable.
    This is exactly right. The only thing that will speed recovery time is for you to use a drug that will increase Leydig cell sensitivity and that is HCG. Using HCG during PCT makes no sense because you are just going to delay the inevitable. Using HCG DURING a cyle makes perfect sense because when you come off Leydig cell sensitivity is still within a normal range (because of HCG) which will the decrease the time that Leydig cells responds to natural LH.

    Using this and that to help you "feel" good has absolute zilch to do with true recovery. Libido has more to do with DHT and estrogen anyway so its not a good indiciator of recovery.
    For answers to board issues, read the Suggestion and News forum at the bottom of the main page.

  11. Quote Originally Posted by Bobo
    All you have to do is check the reaseach. The dose causes desentization, not the length of treatment. You can simply ask Dr. Crisler who is an authority in the area and he will tell you the same. In fact Tamoxifen even helps with the desensitization from high doses.

    "The problem with high doses of HCG is that it, like its analog LH, stimulates aromatase activity. My understanding is that aromatase is toxic to Leydig cells. Therefore taking too much HCG induces primary hypogonadism (which is permanent) while attempting to treat acquired secondary hypogonadism (which USUALLY is temporary).

    In Endocrinology, we are always trying to strike a balance between risk and benefit (the closet philosophers out there will likely apply this concept to all of life). Some HCG is very, very good. Too much is bad. Where is the breakpoint? IMPO, something less than 500IU at a time."

    Most of the sutides are done on HH men and there is a marked difference in acute and chronic administration. Desentization was seen after 23 months at 1500 IU's 3x per week although test levels still remained normal.

    J Clin Endocrinol Metab 1982 Jul;55(1):76-80


    Testicular responsiveness to chronic human chorionic gonadotropin administration in hypogonadotropic hypogonadism.

    D'Agata R, Vicari E, Aliffi A, Maugeri G, Mongioi A, Gulizia S.



    4 Compunds is completely overkill. If you want to limit the crash then use HCG during a cyucle to keep leydig cell response normal then use a SERM during PCT. Using 4 drugs in which 2 can handle IS overkill.
    I asked this in another thread, but in light of the HCG>aromatase thing, would using HCG and ATD during cycle make sense?

  12. The 3 wisest words:


    I don't know.

    For answers to board issues, read the Suggestion and News forum at the bottom of the main page.

  13. Quote Originally Posted by lifted
    And like I said, just because (IMO) it will prolong recovery, that doesn't mean that your points aren't valid. I think that even though it does prolong recovery, you "could" still benefit from it since you'd slowly be weening yourself off androgens and then slowly weening yourself back to full recovery. So I do agree that it is def worth the trials since it is a slower weening compared to BAM! crash, and then trying like hell to bring T back up. I would also be very intrigued if you were to do this and test the waters vs. conventional PCT methods. If you do, try to get some bloodwork done so we can further disect this. I would even be game to try it w/ you, but I'm having a hard time with libido and acne from my last cycle...so I gotta lay off the sauce for awhile longer.
    Yeah, at this point I don't think there's that much more I can get from armchair science, I think I just need to test the bitch and have bloodwork done in order to see how it works. The main limitation for me right now is money - I need a new computer badly, my teeth need $1000 worth of work out of pocket, and my ride needs some work pretty badly. The juice is on the back burner if you get my drift Though I suppose if I skipped the tren this run I could afford to do a decent cycle for under $200.

  14. Quote Originally Posted by Bobo
    The 3 wisest words:


    I don't know.

    hmmm.....
    if Bobo doesn't know...........

    I think I'll kick the ATD back in at 25mg/day while using HCG and see how things go.

  15. Quote Originally Posted by exnihilo
    Yeah, at this point I don't think there's that much more I can get from armchair science, I think I just need to test the bitch and have bloodwork done in order to see how it works. The main limitation for me right now is money - I need a new computer badly, my teeth need $1000 worth of work out of pocket, and my ride needs some work pretty badly. The juice is on the back burner if you get my drift Though I suppose if I skipped the tren this run I could afford to do a decent cycle for under $200.
    I hear ya on that...I just had to drop $238 on a bonding for one of my front teeth yesterday since I have no dental coverage....health can be very pricey that's for sure.
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