how log does it take generally for natty production to kick back on?

[wasp]

well, last summer i was told i had "borderline " low free test..............my dr , who ive stopped going to cuz i dont think he has a clue about this stuff,told me my total was in the 300s, which to him was fine....................so he gave me androgel, this was just naturally, im 44, and never touched aas................

until i realised the androgel wasnt going to do much so i jumped on test enth myself, i did a 500mg 10 week run, then cruised on 125mg for about 2 months..........great gains and libido, however

my rbc and hct were high after cruising, hct 52, so i decided to get off for 3 or 4 months and let body readjust...............

im starting my 4th week on nolvadex tomm 20/20/10/10

my libido and morning wood are both non existent.............i have the androgel but am holding off to see if my body can come back on its own...............

at what point should i start to see morning wood etc or at what point should i just go back on the androgel and accept it.....................

and another thing my dr never mentioned, does androgel raise rbc and hct as well? or only im, can i do androgel while waiting for hct and rbc to come back down b4 i do another run? or will this slow down the process.....................to be honest, id jump back on the enth in a sec but at my age i dont wana push the issue with high hct, i dont have a 20 yr olds' heart, tho my heart is in good shape,so is chol etc


i know your going to say go get bloodwork, but ill be moving in a month and finding a new dr there, no sense trying to find one here for only a month and im not going back to my old dr, too many times ive left there wondering why the f he never mentioned something, and im sure it will show low test, i just wana know if im waiting for something that isnt going to happen

 

[tenny]

assuming your not using hcg or clomid

i would say 9 months to a year to get back to complete normal

this might not have been the answer you want

sorry

 

[Ness]

Yup, may take a few months to....well....never.

 

[wasp]

why clomid over nolva? reading i found :


I have received a lot of heat lately about my preference for Nolvadex over Clomid, which I hold for all purposes of use (in the bodybuilding world anyway); as an anti-estrogen, an HDL (good) cholesterol-supporting drug, and as a testosterone-stimulating compound. Most people use Nolvadex to combat gynecomastia over Clomid anyway, so that is an easy sell. And for cholesterol, well, most bodybuilders unfortunately pay little attention to this important issue, so by way of disinterest, another easy opinion to discuss. But when it comes to using Nolvadex for increasing endogenous testosterone release, bodybuilders just do not want to hear it. They only seem to want Clomid. I can only guess that this is based on a long rooted misunderstanding of the actions of the two drugs. In this article I would therefore like to discuss the specifics for these two agents, and explain clearly the usefulness of Nolvadex for the specific purpose of increasing testosterone production.

Clomid and Nolvadex
I am not sure how Clomid and Nolvadex became so separated in the minds of bodybuilders. They certainly should not be. Clomid and Nolvadex are both anti-estrogens belonging to the same group of triphenylethylene compounds. They are structurally related and specifically classified as selective estrogen receptor modulators (SERMs) with mixed agonistic and antagonistic properties. This means that in certain tissues they can block the effects of estrogen, by altering the binding capacity of the receptor, while in others they can act as actual estrogens, activating the receptor. In men, both of these drugs act as anti-estrogens in their capacity to oppose the negative feedback of estrogens on the hypothalamus and stimulate the heightened release of GnRH (Gonadotropin Releasing Hormone). LH output by the pituitary will be increased as a result, which in turn can increase the level of testosterone by the testes. Both drugs do this, but for some reason bodybuilders persist in thinking that Clomid is the only drug good at stimulating testosterone. What you will find with a little investigation however is that not only is Nolvadex useful for the same purpose, it should actually be the preferred agent of the two.

Pituitary Sensitivity to GnRH
Studies conducted in the late 1970's at the University of Ghent in Belgium make clear the advantages of using Nolvadex instead of Clomid for increasing testosterone levels (1). Here, researchers looked the effects of Nolvadex and Clomid on the endocrine profiles of normal men, as well as those suffering from low sperm counts (oligospermia). For our purposes, the results of these drugs on hormonally normal men are obviously the most relevant. What was found, just in the early parts of the study, was quite enlightening. Nolvadex, used for 10 days at a dosage of 20mg daily, increased serum testosterone levels to 142% of baseline, which was on par with the effect of 150mg of Clomid daily for the same duration (the testosterone increase was slightly, but not significantly, better for Clomid). We must remember though that this is the effect of three 50mg tablets of Clomid. With the price of both a 50mg Clomid and 20mg Nolvadex typically very similar, we are already seeing a cost vs. results discrepancy forming that strongly favors the Nolvadex side.

But something more interesting is happening. Researchers were also conducting GnRH stimulation tests before and after various points of treatment with Nolvadex and Clomid, and the two drugs had markedly different results. These tests involved infusing patients with 100mcg of GnRH and measuring the output of pituitary LH in response. The focus of this test is to see how sensitive the pituitary is to Gonadotropin Releasing Hormone. The more sensitive the pituitary, the more LH will be released. The tests showed that after ten days of treatment with Nolvadex, pituitary sensitivity to GnRH increased slightly compared to pre-treated values. This is contrast to 10 days of treatment with 150mg Clomid, which was shown to consistently DECREASE pituitary sensitivity to GnRH (more LH was released before treatment). As the study with Nolvadex progresses to 6 weeks, pituitary sensitivity to GnRH was significantly higher than pre-treated or 10-day levels. At this point the same 20mg dosage was also raising testosterone and LH levels to an average of 183% and 172% of base values, respectively, which again is measurably higher than what was noted 10 days into therapy. Within 10 days of treatment Clomid is already exerting an effect that is causing the pituitary to become slightly desensitized to GnRH, while prolonged use of Nolvadex serves only to increase pituitary sensitivity to this hormone. That is not to say Clomid won't increase testosterone if taken for the same 6 week time period. Quite the opposite is true. But we are, however, noticing an advantage in Nolvadex.

The Estrogen Clomid
The above discrepancies are likely explained by differences in the estrogenic nature of the two compounds. The researchers' clearly support this theory when commenting in their paper, "The difference in response might be attributable to the weak intrinsic estrogenic effect of Clomid, which in this study manifested itself by an increase in transcortin and testosterone/estradiol-binding globulin [SHBG] levels; this increase was not observed after tamoxifen treatment". In reviewing other theories later in the paper, such as interference by increased androgen or estrogen levels, they persist in noting that increases in these hormones were similar with both drug treatments, and state that," ***8230;a role of the intrinsic estrogenic activity of Clomid which is practically absent in Tamoxifen seems the most probable explanation".
Although these two are related anti-estrogens, they appear to act very differently at different sites of action. Nolvadex seems to be strongly anti-estrogenic at both the hypothalamus and pituitary, which is in contrast to Clomid, which although a strong anti-estrogen at the hypothalamus, seems to exhibit weak estrogenic activity at the pituitary. To find further support for this we can look at an in-vitro animal study published in the American Journal of Physiology in February 1981 (2). This paper looks at the effects of Clomid and Nolvadex on the GnRH stimulated release of LH from cultured rat pituitary cells. In this paper, it was noted that incubating cells with Clomid had a direct estrogenic effect on cultured pituitary cell sensitivity, exerting a weaker but still significant effect compared to estradiol. Nolvadex on the other hand did not have any significant effect on LH response. Furthermore it mildly blocked the effects of estrogen when both were incubated in the same culture.

Conclusion
To summarize the above research succinctly, Nolvadex is the more purely anti-estrogenic of the two drugs, at least where the HPTA (Hypothalamic-Pituitary-Testicular Axis) is concerned. This fact enables Nolvadex to offer the male bodybuilder certain advantages over Clomid. This is especially true at times when we are looking to restore a balanced HPTA, and would not want to desensitize the pituitary to GnRH. This could perhaps slow recovery to some extent, as the pituitary would require higher amounts of hypothalamic GnRH in the presence of Clomid in order to get the same level of LH stimulation.
Nolvadex also seems preferred from long-term use, for those who find anti-estrogens effective enough at raising testosterone levels to warrant using as anabolics. Here Nolvadex would seem to provide a better and more stable increase in testosterone levels, and likely will offer a similar or greater effect than Clomid for considerably less money. The potential rise in SHBG levels with Clomid, supported by other research (3), is also cause for concern, as this might work to allow for comparably less free active testosterone compared to Nolvadex as well. Ultimately both drugs are effective anti-estrogens for the prevention of gyno and elevation of endogenous testosterone, however the above research provides enough evidence for me to choose Nolvadex every time.






i used hcg for a few months while on but always thought on pct was not advised


9 months, wow, why is pct always time on = time off then?

i planned on getting back on end of june after rbc and hct was down, if i were to use the androgel while "off" , would my rbc and hct still come down by the end of june? again, i cant seem to find any reading on how androgel effects rbc and hct..............i mean , it is an outside source



im still baffled how guys stay on year round and dont have high rbc and hct

 

[Tendon Snapper]

i would say 9 months to a year to get back to complete normal

For me personally the above has proven to be the case.

 

[scrapper13]

from research i have read age is a big factor in this, the older you are the longer it can take

 

[wasp]

i see, what if i were to do ten week runs of 500-750 and then cruise on androgel for 3 months, after the andro, check my levels then repeat..................would my rbc and hct still come down on the androgel?...........................i think its safe to say, at my age, given what the dr has said, and what ive done, i think i may be waiting for a train thats never coming...............just wana make sure my rbc and hct stay somewhat normal................thats why i was cruising on 125mg/week instead of using the androgel and they still rose for some reason...........im thinking the androgel may not be as severe but yet would still give me some benefits of libido, mood etc................

 

[Stewie Griffon]

why clomid over nolva?

gotta agree, clomid is a complete waste. people that still recommend it are stuck in old school thinking

HCG is the best bet

AAS trigger the hypothalamus to shut down its production of GnRH from the hypothalamus. without GnRH, the pituitary gland stops releasing luteinizing hormone (LH). LH triggers the production and release of testosterone. without LH, the testes shut down testosterone production. HCG helps restore testosterone production by mimicking LH

 

[wasp]

but the majority of what i read says no hcg for pct,

 

[tenny]

but the majority of what i read says no hcg for pct,

if you start believing everything you read

then get read for the end of the world 12/2012

 

[shawnkarbabacz]

HCG is a peptide hormone manufactured by the embryo in the early stages of pregnancy and later by the placenta to help control a pregnant woman’s hormones (can anything really be said to control a pregnant woman’s hormones except ice-cream and chocolate?). Obviously, as you can guess from the name, it is a substance that stimulates the gonads (hence: gonadotropin). It does this by initiating gene transcription that is identical to that of Luetenizing Hormone, thereby causing the Leydig Cells to produce testosterone. Sounds great right? We can stimulate LH and FSH production with our Nolvadex, and then directly stimulate the Leydig Cells as well, to produce tons of testosterone by different routes! Well...it’s not all that simple.

Unfortunately, while HCG increases Testosterone, it increases estrogen as well(12). As you probably know, estrogen acts directly on the Leydig cells to effect changes in the activities of enzymes important for testosterone synthesis (13) and may actually be considered an important part of that negative feedback loop I mentioned earlier. In addition, an increase in circulating levels of LH have been shown to induce down-regulation of LH-receptors in both rodent studies (14), as well as in human studies (15); since HCG mimics LH, you can expect it to do the same. This LH downregulation can cause an increase in steroidogenic cholesterol (the cholesterol earmarked by your body for conversion into testosterone). (16). Thus, after the initial HCG induced surge in testosterone is over, if you have used enough to downregulate your LH-receptors and increase estrogen too much, then more steroidogenic cholesterol is available. This is telling me that less is being converted to testosterone. In fact, rodent models suggest that if you take a dose large enough to cause a sharp increase of plasma testosterone, you will actually desensitize your Leydig cells to your next shot, and will possibly not experience any rise in testosterone from the second dose at all, or may only experience a very slight one at best (17.). Since this is due to LH-Receptor downregulation, and that occurs in human models too, it is pretty fair to assume that if your first dose of HCG is too large, your second won’t be very effective. Unfortunately, this lack of an increase in testosterone doesn’t necessarily mean that the HCG may be unable to increase circulating levels of Estrogen (18) And remember that increase in Estrogen will (most likely) cause your body ultimately to produce less testosterone. Low LH post-cycle is not the primary cause of slow recovery, because LH generally rises to levels above baseline after a cycle much sooner than testosterone production does. This is probably because the pituitary is working very hard to get your atrophied Leydig cells to start producing testosterone again. HCG should also bring back testicular volume; I feel the need to mention this because it’s important to me and I suspect most men as well. It would also appear that HCG works very well when it’s used on men who have low levels of LH to begin with (as you would be after a cycle), as many studies on pre-pubertal boys and Hypogonadotropic Hypogonadal men would suggest (19)

This suggests that a pre-exposure to normal LH levels or gonadatropins in general is necessary for HCG-induced Leydig Cell desensitization. This, of course is not a problem for us, as we’ll be using it when LH/Gonadatropin levels are very low anyway …we just need to stop using it before we regain normal function, or it will work against us eventually. (19) (20). Luckily, the temporary Anabolic steroid induced hypogonadism that is experienced after a cycle basically allows us to respond to HCG like anyone with low LH levels (21), and thus, as I told you, a lot of the possible inhibitory effect of HCG is not going to be relevant because there was no prior “priming” by circulating gonadotrophins. This is great news for us, because we are going to be using HCG during PCT, when we need to get back some HPTA function, and not when we have levels of gonadatropins high enough to cause HCG-induced desensitization.

But are we still risking some inhibition and possibly delaying our recovery by using HCG? Probably not…you see, some studies in humans have shown that HCG does not actually have a direct effect on inhibiting LH release in men (22)(23), but rather (probably) works to inhibit LH secretion indirectly, simply by stimulating the production of testosterone (thus activating the negative feedback loop). Another factor involved is the induction of testicular aromatase, which raises estrogen levels, again causing inhibition. Unfortunately, yet another process, the downregulation of the Leydig Cell LH receptor itself, seems to also play a role in high dose HCG testicular desensitization. This is also done by HCG actually blocking the conversion of 17 alpha-hydroxyprogesterone (17 OHP) to testosterone (24). Nolvadex actually stops this blocking-action of HCG from taking place (25). Most likely, because of Nolvadex’s direct antiestrogenic effect and LH-upregulating effect on the Pituitary, suppression of gonadotropins via HCG is (25) almost totally stopped with concurrent administration of Nolvadex! So if we Use Nolvadex and we are only using HCG when we are low in gonadatropins, we won’t be inhibited by it at all! Right?

Well…maybe…but there’s still the issue of estrogen caused by that HCG-stimulated surge in testosterone. Well…we can use low doses (300iu or so) to avoid some of that major spike in estrogen, and thus cause far less inhibition from the HCG (26). Of course, I’d want to use a bit more HCG per injection (500iu), if I could, to get my body functioning fully more quickly, and lose less of my gains. Maybe we can get away with taking some Vitamin E with our HCG, since it increases the responsiveness of plasma testosterone levels to HCG, making them significantly higher during vitamin E administration than without it (27). So we can get a better response with our HCG by taking Vitamin E (I recommend 1,000iu/day), but that doesn’t get rid of the problem that we have, which is the estrogen increase the HCG will cause.








Very informative article on PCT. (this just a cut and copy of the HCG part). I too have always thought hcg was no good for PCT until i did more digging around and got the help of more seasoned and read guys.

 

[Stewie Griffon]

if you start believing everything you read

then get read for the end of the world 12/2012

LMAO - great analogy!

also whatever happened to the world 'technology meltdown' that was supposed to have occurred in 2000? funny how for a year before there were endless tv shows and magazine articles explaining in detail the chaos that was about to come. i would LOVE to have seen all the fools who talked about that come out with a year full of tv shows saying how wrong and stupid they were

 

[wasp]

HCG is a peptide hormone manufactured by the embryo in the early stages of pregnancy and later by the placenta to help control a pregnant woman’s hormones (can anything really be said to control a pregnant woman’s hormones except ice-cream and chocolate?). Obviously, as you can guess from the name, it is a substance that stimulates the gonads (hence: gonadotropin). It does this by initiating gene transcription that is identical to that of Luetenizing Hormone, thereby causing the Leydig Cells to produce testosterone. Sounds great right? We can stimulate LH and FSH production with our Nolvadex, and then directly stimulate the Leydig Cells as well, to produce tons of testosterone by different routes! Well...it’s not all that simple.

Unfortunately, while HCG increases Testosterone, it increases estrogen as well(12). As you probably know, estrogen acts directly on the Leydig cells to effect changes in the activities of enzymes important for testosterone synthesis (13) and may actually be considered an important part of that negative feedback loop I mentioned earlier. In addition, an increase in circulating levels of LH have been shown to induce down-regulation of LH-receptors in both rodent studies (14), as well as in human studies (15); since HCG mimics LH, you can expect it to do the same. This LH downregulation can cause an increase in steroidogenic cholesterol (the cholesterol earmarked by your body for conversion into testosterone). (16). Thus, after the initial HCG induced surge in testosterone is over, if you have used enough to downregulate your LH-receptors and increase estrogen too much, then more steroidogenic cholesterol is available. This is telling me that less is being converted to testosterone. In fact, rodent models suggest that if you take a dose large enough to cause a sharp increase of plasma testosterone, you will actually desensitize your Leydig cells to your next shot, and will possibly not experience any rise in testosterone from the second dose at all, or may only experience a very slight one at best (17.). Since this is due to LH-Receptor downregulation, and that occurs in human models too, it is pretty fair to assume that if your first dose of HCG is too large, your second won’t be very effective. Unfortunately, this lack of an increase in testosterone doesn’t necessarily mean that the HCG may be unable to increase circulating levels of Estrogen (18) And remember that increase in Estrogen will (most likely) cause your body ultimately to produce less testosterone. Low LH post-cycle is not the primary cause of slow recovery, because LH generally rises to levels above baseline after a cycle much sooner than testosterone production does. This is probably because the pituitary is working very hard to get your atrophied Leydig cells to start producing testosterone again. HCG should also bring back testicular volume; I feel the need to mention this because it’s important to me and I suspect most men as well. It would also appear that HCG works very well when it’s used on men who have low levels of LH to begin with (as you would be after a cycle), as many studies on pre-pubertal boys and Hypogonadotropic Hypogonadal men would suggest (19)

This suggests that a pre-exposure to normal LH levels or gonadatropins in general is necessary for HCG-induced Leydig Cell desensitization. This, of course is not a problem for us, as we’ll be using it when LH/Gonadatropin levels are very low anyway …we just need to stop using it before we regain normal function, or it will work against us eventually. (19) (20). Luckily, the temporary Anabolic steroid induced hypogonadism that is experienced after a cycle basically allows us to respond to HCG like anyone with low LH levels (21), and thus, as I told you, a lot of the possible inhibitory effect of HCG is not going to be relevant because there was no prior “priming” by circulating gonadotrophins. This is great news for us, because we are going to be using HCG during PCT, when we need to get back some HPTA function, and not when we have levels of gonadatropins high enough to cause HCG-induced desensitization.

But are we still risking some inhibition and possibly delaying our recovery by using HCG? Probably not…you see, some studies in humans have shown that HCG does not actually have a direct effect on inhibiting LH release in men (22)(23), but rather (probably) works to inhibit LH secretion indirectly, simply by stimulating the production of testosterone (thus activating the negative feedback loop). Another factor involved is the induction of testicular aromatase, which raises estrogen levels, again causing inhibition. Unfortunately, yet another process, the downregulation of the Leydig Cell LH receptor itself, seems to also play a role in high dose HCG testicular desensitization. This is also done by HCG actually blocking the conversion of 17 alpha-hydroxyprogesterone (17 OHP) to testosterone (24). Nolvadex actually stops this blocking-action of HCG from taking place (25). Most likely, because of Nolvadex’s direct antiestrogenic effect and LH-upregulating effect on the Pituitary, suppression of gonadotropins via HCG is (25) almost totally stopped with concurrent administration of Nolvadex! So if we Use Nolvadex and we are only using HCG when we are low in gonadatropins, we won’t be inhibited by it at all! Right?

Well…maybe…but there’s still the issue of estrogen caused by that HCG-stimulated surge in testosterone. Well…we can use low doses (300iu or so) to avoid some of that major spike in estrogen, and thus cause far less inhibition from the HCG (26). Of course, I’d want to use a bit more HCG per injection (500iu), if I could, to get my body functioning fully more quickly, and lose less of my gains. Maybe we can get away with taking some Vitamin E with our HCG, since it increases the responsiveness of plasma testosterone levels to HCG, making them significantly higher during vitamin E administration than without it (27). So we can get a better response with our HCG by taking Vitamin E (I recommend 1,000iu/day), but that doesn’t get rid of the problem that we have, which is the estrogen increase the HCG will cause.








Very informative article on PCT. (this just a cut and copy of the HCG part). I too have always thought hcg was no good for PCT until i did more digging around and got the help of more seasoned and read guys.

this is an anthony roberts article,unless its just worded similar, from what ive read,to be taken lightly

 

[maldorf]

gotta agree, clomid is a complete waste. people that still recommend it are stuck in old school thinking

HCG is the best bet

AAS trigger the hypothalamus to shut down its production of GnRH from the hypothalamus. without GnRH, the pituitary gland stops releasing luteinizing hormone (LH). LH triggers the production and release of testosterone. without LH, the testes shut down testosterone production. HCG helps restore testosterone production by mimicking LH

If you use HCG though, that is going to suppress your own LH output that much longer. All you are doing really is prolonging your natural production from coming back. You sure do feel well though while on the HCG. Once you come off the HCG though you will crash again.

 

[Stewie Griffon]

If you use HCG though, that is going to suppress your own LH output that much longer. All you are doing really is prolonging your natural production from coming back. You sure do feel well though while on the HCG. Once you come off the HCG though you will crash again.

true, but using small amounts for a short period will help somewhat. using just enough to stimulate test a bit before heavy suppression of LH - some kind of a midway point. not full recovery but not enough to completely throw LH off. (by small amounts i mean 250iu every other day)

also i have read that HMG stimulates LH, other places i have read that HMG contains some LH as well as FSH, maybe this would help if included.

 

[jalsmiley]

true, but using small amounts for a short period will help somewhat. using just enough to stimulate test a bit before heavy suppression of LH - some kind of a midway point. not full recovery but not enough to completely throw LH off. (by small amounts i mean 250iu every other day)

also i have read that HMG stimulates LH, other places i have read that HMG contains some LH as well as FSH, maybe this would help if included.

in theory you are both correct...and to actually help counteract hcg's suppression of lh you can add a little nolv...supposedly the force behind lh suppression is estrogen release...so a little bit of hcg and some nolv to block the est that hcg converts to may be a good start...all just theory...i personally like test taper with little hcg...adding nolv next time too see if works...

also feel as if the crash off hcg may not be as bad as a crash from just dropping the test...so recovery may be one step away instead of two steps away

 

[rubiconman500]

This isnt anything my doc said or ive done but, but I normally read posts relating to low test levels as im 23 and have low test.

I found another guy on a different board who was in the same boat as me but was seeing different docs about his situation, and he stated that the best hrt supplement that was administered and worked for him was hcg. But once cycling off of the hcg he said libido would almost be completely gone...

 

[jalsmiley]

This isnt anything my doc said or ive done but, but I normally read posts relating to low test levels as im 23 and have low test.

I found another guy on a different board who was in the same boat as me but was seeing different docs about his situation, and he stated that the best hrt supplement that was administered and worked for him was hcg. But once cycling off of the hcg he said libido would almost be completely gone...

yes there is a big push in the medical community to utilize natural means of producing testosterone(i listen to dr radio nyu langone medical school broadcast daily which has great programming for those interested in medicine, it also has great men's health shows which talk a lot about test...sirius/xm channel 114)...which they say using hcg to trigger you balls to produce is preferred method...this will ensure that if needed to produce a child you can do so...utilizing str8 test inj will shut down balls....i see there rationale but what one must also remember is the removing the hcg will produce a crash also...as stated above it will shut down LH which in turn iinhibits t production...thus back to the old school thinking of no pct as any way you look at it there is a crash...it is just finding the lesser of the evils i guess...

 

[rubiconman500]

using hcg to trigger you balls to produce is preferred method...this will ensure that if needed to produce a child you can do so...

I never knew hcg was used for this...
But again I havent read much about medical uses of hcg

 

[maldorf]

in theory you are both correct...and to actually help counteract hcg's suppression of lh you can add a little nolv...supposedly the force behind lh suppression is estrogen release...so a little bit of hcg and some nolv to block the est that hcg converts to may be a good start...all just theory...i personally like test taper with little hcg...adding nolv next time too see if works...

also feel as if the crash off hcg may not be as bad as a crash from just dropping the test...so recovery may be one step away instead of two steps away

I do know that yeah, the crash coming off the hcg is not nearly as bad as the crash of going cold turkey. I used to taper down my AAS dose at the end of cycles too, and that seemed to have about the same crash as coming off of HCG. Taper down over about 2-3 weeks worked decent for me, as well as using the HCG at least.