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Half Lives - PCT etc etc etc

Half Lives - List of Sides

Oral steroids Drug Active half-life
Anadrol / Anapolan50 (oxymetholone) 8 to 9 hours
Anavar (oxandrolone) 9 hours
Dianabol (methandrostenolone, methandienone) 4.5 to 6 hours
Methyltestosterone 4 days
Winstrol (stanozolol)
(tablets or depot taken orally) 9 hours



Depot steroids Drug Active half-life
Deca-durabolin (Nandrolone decanate) 15 days
Equipoise 14 days
Finaject (trenbolone acetate) 3 days
Primobolan (methenolone enanthate) 10.5 days
Sustanon or Omnadren 15 to 18 days
(I have now seen data from a lab tech 'proving' that EOD is neccessary for good blood levels with sust)
Testosterone Cypionate 12 days
Testosterone Enanthate 10.5 days
Testosterone Propionate 4.5 days
Testosterone Suspension 1 day
* Winstrol (stanozolol) 1 day


*Winstrol depot does not actually possess a classical half-life because it is un-esterified. Instead, the microcrystals dissolve slowly. Once they have all dissolved levels of the drug fall very rapidly. It is still an important consideration, and we have included it with a half-life of one day.


Steroid esters Drug Active half-life
Formate 1.5 days
Acetate 3 days
Propionate 4.5 days
Phenylpropionate 4.5 days (dont believe this is correct)
Butyrate 6 days
Valerate 7.5 days
Hexanoate 9 days
Caproate 9 days
Isocaproate 9 days
Heptanoate 10.5 days
Enanthate 10.5 days
Octanoate 12 days
Cypionate 12 days
Nonanoate 13.5 days
Decanoate 15 days
Undecanoate 16.5 days



Ancillaries Drug Active half-life
Arimidex 3 days
Clenbuterol 1.5 days
Clomid 5 days
Cytadren 6 hours
Ephedrine 6 hours
T3 10 hours


A practical example is if one was to inject 100mg of testosterone propionate and allow blood levels to peak. In 4.5 days time (half-life duration from the above tables) and providing no other injections had taken place, the level would be reduced to 50mg. Again, a further 4.5 days down the line and levels would have dropped to 25mg, and the value keeps halving every 4.5 days.

http://www.muscletalk.co.uk/article-steroid-half-life.asp

Detection times for AAS

Boldenone Undecyclenate 4-5 months
Clen 4-5 Days
Ephedrin 6-10 Days
Halo 2 months
Proviron 5 weeks
D-Bol 5 weeks
Methamphetamin 6-10 Days
Primo Depot 4-5 weeks
Deca 18 months
Nandrolon Phenylprop 12 months
Anavar 3 weeks
Anadrol 2 months
Winny oral 3 weeks
Winny inj 2 months
Test cyp 3 months
Test enat 3 months
Sustanon 3 months
Test Prop 2-3 weeks
Andriol 1 week
Tremolon Acet 4-5 weeks
Test supspenison No metabolites. t/e should
be back to normal in days.

Factors which influence the detection times


Metabolism
Fluid intake
Tolerance to the drug
Frequency of intake
Duration of intake
Body fat
Potency of drug
Dosage

Ester actual mg/100mg dose
test no ester 100
tren acetate 87
test prop 83
test enanth 72
test cyp 70
test undecan 63
 
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More gr8 info bud....keep it coming...I'm sure it's well appreciated:thumb:
 
How do you buy clomid? I heard you don't need a prescription.

Where would you get it?
 
Look in my sig line!
 
Originally posted by PB&J
How do you buy clomid? I heard you don't need a prescription.

Where would you get it?
Click to expand...

You can buy it online, its not a controlled substance but its not "legal" to buy without a scrip.

DG, I could only find Liquid Nolva but no Clomid at AvantLabs?

www.liquidresearch.com would be one such company.
 
Muscle Gelz Transdermals
IronMag Labs Prohormones
That's one, but universalkits.com has it also!
 
Injectible Esters - weight of total substance

1. Ester Size: Acetate. No. Carbons: 2, Frequency of Inj.: 2-3 days, Percentage of weight: 13%

2. Ester Size: Propionate. No. Carbons: 3, Frequency of Inj.: 3 days, Percentage of Weight: 17%

3. Ester Size: Enanthate. No. Carbons: 7, Frequency of Inj.: 1 week, Percentage of Weight: 28%

4. Ester Size: Cypionate. No, Carbons: 8, Frequency of Inj.: 1 week, Percentage of Weight: 30%

5. Ester Size: Phenylpropionate. No. Carbons: 9, Frequency of Inj.: 4-5 days, Percentage of Weight: 33%

6. Ester Size: Decanoate. No. Carbons: 10, Frequency of Inj.: 10-12 days, Percentage of Weight: 36%

-Credits, Muscular Development magazine 2003
 
More from T-Mag

Recharging the Boys

Q: Should a steroid user "load" Clomid? I've heard mixed opinions. What about other anti-estrogen drugs?

A: It really depends on the situation. If you're experiencing symptoms of gynecomastia and need to achieve a high blood concentration of the drug quickly, then yes, you should use large dosages over a short period of time. If you simply wish to restore yourself to a eugonadal state, I don't think it's as important to "load." However, I'd really like people to use the following protocol based on what little info we have concerning the restoration of the HPTA.

Essentially, you need to use 100 mg/day of clomiphene (50 mg, twice daily) for at least 2 months. This protocol is based on both anecdotal evidence as well as a few case reports.

One recent case report involved the reversal of a hypogonadal state in a man who'd previously used nandrolone decanoate, stanozolol, and methenolone for several months. The man complained of common hypogonadal symptoms (i.e., loss of libido, fatigue, depression, etc.) and upon investigation his total and free Testosterone levels were 71 ng/dl and 29 pg/ml respectively. (The reference ranges were 260-1000 ng/dl and 34-194 pg/ml, by the way.)

He was then given 100 mg of clomiphene for 5 days and reevaluated 2 weeks later. He reported an improvement in mood, energy, and libido and his total Testosterone was 828 ng/dl. However, after a follow up 2 months later, his symptoms had returned and his total Testosterone concentration was 301 ng/dl. In other words, he suffered a relapse.

They then gave the man 100 mg per day for 2 months and then reevaluated his blood work. They found his total Testosterone was 705 ng/dl and no relapse occurred in subsequent blood work. A similar case reported restoration of the HPTA using the same dosage of clomiphene over a 5 month period.

Anecdotally, I receive many letters from people explaining that they were feeling great when using clomiphene the first 2-4 weeks after their cycle, but seemed to suffer dramatic drops in terms of body composition, mood, energy levels, etc, thereafter.

My guess is that we've been underestimating the amount of time it takes to recover, even when using compounds like clomiphene. Granted, this probably can't be applied across the board as we have to take in many individual factors including what particular androgens the person was using, dosages, length of time, etc., but extended use of the drug seems to be the way to go. (1-2)

------------------
Can T levels be restored in former anabolic steroid users?

The Study: Two hypogonadal former anabolic steroid users were studied. Normal levels of LH are >3.6 IU/L and Testosterone are 300???1000 ng/dl. Former anabolic steroid users often have suppressed levels of both.

The Results: Subject #1 is a 6', 206lb former user of 500???2000+ grams per week of anabolics. His baseline numbers were: LH<1IU/L, Test=191ng/dl. This suject underwent a 32 day treatment of 2500 IU of HCG every 4 days, 50 mg of clomid 2 times per day, and 10 mg nolvadex per day. 15 days after treatment his numbers were: LH=5.2IU/L, Test=1072 ng/dl.

Subject #2 is a 5'10", 184lb male who used 400 mg per week of nandrolone. His baseline numbers were: LH<1IU/L, Test=45ng/dl. This subject's 32 day treatment consisted of 2500 IU of HCG every 4 days, 50 mg of clomid 2 times per day, and 10 mg nolvadex per day. There was no change. He underwent another treatment consisting of 60 days of 5000 IU of HCG every 4 days for 4 injections, then 2500 IU every 4 days for 4 injections, 50 mg of clomid 2 times per day, and 10 mg nolvadex per day. Still, no change. For the next 32 days, this subject received 5000 IU of HCG every other day for 6 injections, then 2500 IU every other day for 6 injections given with 150 IU of menotropins, 50 mg of clomid 2 times per day, and 10 mg nolvadex 2 times per day. 15 days after treatment his numbers were: LH=9.8IU/L, Test=507 ng/dl.(20)

Comments: The authors of this paper have presented some very interesting data that the medical community needs to learn from. When dealing with former androgen users, there may be better ways to increase Testosterone than the standard patch treatment (which will only prolong the problem of decreased T production.) Hypogonadal former androgen users need a treatment, not a band-aid. If you need to jump start your Testosterone after an androgen cycle, this combination of HCG, Clomid, and Nolvadex may be just what the doctor ordered. Now, trying to get him to order it is another story!

--------------------

Bodybuilders and Breeding

I've got a question which has probably crossed the minds of many guys who've used steroids at one time or another. Will the use of steroids, say, two or three eight-week cycles a year, destroy a man's ability to father children?

Depends on exactly where you're injecting, studboy. Okay, honestly, this is a common question with no really easy answer. The best response that I can give is "yes and no." It would depend on a lot of things, such as how much "drug" you were taking, whether you used Clomid or other anti-aromatics, and how many years you were doing this. In general (and this is very vague), the longer you do this and the bigger the doses you use, the more likely you are to decrease your chance of spawning little tricycle engines.

Additionally, many guys experience "transitional infertility" post-cycle. In other words, it may take 4-16 weeks to become normopotent after a cycle. If you're infertile secondary to AAS use, discuss this with your physician and see if he'll prescribe some Clomid or HCG to increase your sperm count. There's quite a bit of data in peer-reviewed journals to support the use of these drugs in this situation.
Click to expand...
 
Sorry, there is no source posting or requesting. Things of that nature put this board or any board with such activity in jeapordy, more than one board has been shut down from open source posts.

Thanks
 
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watch out for that research liquid stuff.. i got some liquidex from pnp... holy hell it tastes bad :barf: works though
 
Understanding Post Cycle ???T??? Recovery
By William Llewellyn




O.K. You have been on an awesome 4-month cycle of Sustanon and Dianabol. You???ve gained a massive 20 lbs, and are extremely pleased with your results. You can???t stop looking in the mirror. But there is a problem now starting to eat away at you. You are going to run out of steroids very soon (you know you need a break anyway), and your testicles are the size of raisins. Your body is producing less testosterone than a 9-year-old girl, and you are scrambling to figure out what to do to avoid a nasty post-cycle crash that could potentially strip away some of your hard-earned muscle. The opinions on how to restore endogenous testosterone production post-cycle seem to be different everywhere you look. What option is best? Without an understanding of exactly what is going on in your body, and why certain compounds help to correct the situation, choosing the right post-cycle program can be quite confusing. In this article I would therefore like to discuss the role of anti-estrogens and HCG during this delicate window of time, while detailing an effective strategy for their use.



The Axis



The Hypothalamic-Pituitary-Testicular Axis, or HPTA for short, is the thermostat for your body???s natural production of testosterone. Too much testosterone and the furnace will shut off. Not enough, and the heat is turned up, to put it very simply. For the purposes of our discussion here we can look at this regulating process as having three levels. At the top is the hypothalamic region of the brain, which releases the hormone GnRH (Gonadotropin-Releasing Hormone) when it senses a need for more testosterone. GnRH sends a signal to the second level of the axis, the pituitary, which releases Luteinizing Hormone in response. LH for short, this hormone stimulates the testes (level three) to secrete testosterone. The same sex steroids (testosterone, estrogen) that are produced serve to counter-balance things, by providing negative feedback signals (primarily to the hypothalamus and pituitary) to lower the secretion of testosterone when too much of this hormone is sensed. Synthetic steroids, of course, suppress testosterone the same way. This quick background of the testosterone-regulating axis is necessary to furthering our discussion, as we need to first look at the underlying mechanisms involved before we can understand why natural recovery of the HPTA post-cycle is a slow process. Only then can we implement an ancillary drug program to effectively deal with it.



Testicular Desensitization


Although steroids suppress testosterone production primarily by lowering the level of gonadotropic hormones discussed above, the big roadblock to a restored HPTA after we come off the drugs is surprisingly not the level of LH itself. This problem is made clearly evident in a study published in Acta Endocrinologica back in 1975(1). Here blood parameters, including testosterone and LH levels, were monitored in male subjects whom were given testosterone enanthate injections of 250mg weekly for 21 weeks. Subjects remained under investigation for an additional 18 weeks after the drug was discontinued. At the start of the study, LH levels became suppressed in direct relation to the rise in testosterone, which is to be expected. Things looked very different, however, once the steroids had been withdrawn (see Figure I). LH levels went on the rise quickly (by the 3rd week), while testosterone barely budged for quite some time. In fact, on average it was more than 10 weeks before any noticeable movement started. This lack of correlation makes clear that the problem in getting androgen levels restored is not the level of LH, but in fact testicular atrophy and desensitization to this hormone. After a period of inactivation the testes have apparently lost mass (atrophied), making them unable to perform the workload required by heightened levels of LH.


Post-Cycle LH Levels


Post Cycle Testosterone Levels



Figure I. LH and Testosterone measurements starting 1 week after the last injection of 250mg of testosterone enanthate (pretreated measures were 5 mU/ml and 4.5 ng/ml respectively). Note that between weeks 1 and 5, as testosterone levels are declining due to the cessation of exogenous androgen administration, LH levels are already rebounding. From weeks 5 to 10 testosterone levels are at or very near baseline, to spite the substantial LH levels by this point. No significant increase in testosterone is noted until after the 10-week mark.



The Role of Anti-estrogens


It is important to understand that anti-estrogens alone do not do much to restore endogenous testosterone release after a cycle. Normally they only foster LH by blocking the negative feedback of estrogens, and we now see that LH rebounds quickly without help anyway. Plus, post cycle there is not an elevated level of estrogen for anti-estrogens to block, as testosterone (now suppressed) is a major substrate used for the synthesis of estrogens in men. Serum estrogen levels will actually be lower here as a result, not higher. Any estrogen rebound that occurs post-cycle likewise happens concurrently with a rebound in testosterone levels, not prior to it (note there is an imbalance in the ratio post cycle, but this is another topic altogether). We are seeing no mechanism in which anti-estrogenic drugs can really help here. We can see why this fact would not be difficult to overlook, however. The medical literature is filled with references showing anti-estrogenic drugs like Clomid and Nolvadex to increase LH and testosterone levels, and in normal situations these drugs do indeed increase endogenous androgen production by blocking the negative feedback of estrogens. Combine this with the fact that just as many studies can be found to show that steroid use lowers LH levels when suppressing testosterone, and we can see how easy it would be to jump to the conclusion that post-cycle we need to focus on restoring LH. We would miss the true problem of testicular desensitization unless we were really looking into the actual recovery rates of the hormones involved. When we do, we immediately see little value in using anti-estrogenic drugs.



HCG


So we now see, contrary to the dominating opinion of the times, that anti-estrogens alone will do little to raise testosterone levels in the early weeks of the post-cycle window. This leaves us to focus on a very different level of the HPTA in order to hasten recovery: the testes. For this we will need the injectable drug HCG. If you are not familiar with it, HCG, or Human Chorionic Gonadotropin, is a prescription fertility agent that mimics the bodies own natural LH. Although the testes are equally desensitized to this drug as LH (they both work through the same mechanism), we are administering it as a measured drug and are therefore not constrained by the limits of our own LH production. We similarly can use HCG to provide a bolus dose of LH (of our choosing), which works only to augment the recovering LH levels we already have in the body. In essence we are looking to shock them with an overwhelmingly high level of LH activity, coming from both endogenous and exogenous sources. We want it to reach a level far above what our body, even when supported by anti-estrogens, could possibly do on its own. The result can be a rapid restoration of original testicular mass and functioning, which would allow normal levels of testosterone to be output much sooner than without such an ancillary program. What we are looking at now is HCG actually being the pivotal post-cycle drug, while anti-estrogens are relegated to a supportive role at best.



Finalizing the Program


An ideal post-cycle recovery program will focus on two things really. The first is hitting the testes hard with HCG. It is important, however, not to overuse this drug. Taken for too long, or at too high a dosage, the LH receptor will actually become desensitized to LH(2) , which may further exacerbate our post-cycle problem instead of helping it (this is why I am not in favor of regular HCG use on-cycle). My experience with HCG has led me to feel comfortable using it for a course of three weeks, at a dosage of maybe 5000-7500IU weekly. Often the last week I limit the dose to 2,500IU, unless the cycle has been particularly long or potent. This is timed so at least half of the total administered drug dosage will be given when there is still exogenous steroid in the body. On our graph above this would be at about the 3-week mark after the last injection of testosterone. This will give the testes some time to get back into shape before the baseline is actually hit with T levels. Secondly, Anti-estrogens are used to play a supportive role at the same time, so 20mg of Nolvadex or 50-100mg of Clomid would typically be added ( my last article for Mind and Muscle discusses the comparative differences with these two agents). This is to combat the suppressive effects of estrogen as testosterone levels start to go back up, as well as potential side effects (HCG has been shown to increase testicular aromatase activity as well (3)). Although in the first couple of weeks the anti-estrogen does little, it may indeed be helpful when testosterone levels actually start to get back up near normal. To further stimulate the HPTA, and support continuingly high LH levels, the anti-estrogen remains to be used for 2 to 3 weeks after the HCG therapy has been stopped. A sample program, as it would be instituted in our sample post-cycle window, is provided below.



Sample Post-cycle Plan:


Week 3: 5000IU HCG total + 20mg Nolvadex daily
Week 4: 5000IU HCG total + 20mg Nolvadex daily
Week 5: 2500IU HCG total + 20mg Nolvadex daily
Week 6: 20mg Nolvadex daily
Week 7: 20mg Nolvadex daily
Week 8: 20mg Nolvadex daily



In Closing


I hope this article provided a well-needed new look at the mechanisms involved in post-cycle testosterone recovery. Indeed I believe it should debunk a commonly held belief these days, as we seen now that those advocating the sole use of Clomid post cycle are sorely missing the mark. The problem goes much deeper than just getting LH levels back. In fact, we see that LH doesn???t even need much help kicking back into gear, and a drug like Clomid will do very little to help this anyway in the absence of significant estrogen levels anyway. HCG is a drug with undeniable usefulness during the post-cycle window, and many bodybuilders have been much too quick to abandon it. It is truly fundamental to an effective recovery program, and would not consider any dose or combination of anti-estrogens or aromatase inhibitors capable of doing the job without it.


References:

1. Effect of long-term testosterone oenanthate administration on male reproductive function: Clinical evaluation, serum FSH, LH, Testosterone and seminal fluid analysis in normal men. J. Mauss, G. Borsch et al. Acta Endocrinol 78 (1975) 373-84

2. Desensitization to gonadotropins in cultured Leydig tumor cells involves loss of gonadotropin receptors and decreased capacity for steroidogenesis. Freeman DA, Ascoli M Proc Natl Acad Sci U S A 1981 Oct;78(10):6309-13

3. Acute stimulation of aromatization in Leydig Cells by Human Chorionic Gonadotropin In-vitro. Proc Natl Acad Sci USA 76:4460-3,1079
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By William Llwellyn

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," ???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.
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Clomiphene Citrate

Clomiphene citrate (brand name Clomid, Serophene) is used to induce ovulation. It revolutionized the field of infertility in the late 1950s.

Description

Clomiphene citrate is an orally administered medication. The initial dosage is 50 mg per day for five days, from day three to seven of the woman's cycle. The dose may be increased in subsequent cycles if the minimum dose does not result in ovulation.

Clomiphene citrate appears to act on the hypothalamus and is useful for women who do not ovulate because of hypothalamic or pituitary problems. Given early in the menstrual cycle (day three to seven), it suppresses the amount of naturally circulating estrogen. This "tricks" the pituitary into producing more follicular stimulating hormone (FSH) and luteinizing hormone (LH). These hormones then stimulate the ovary to ripen a follicle and release an egg. Of patients who are properly screened for use of this drug, about 70 percent will ovulate, and 40 percent of those will become pregnant. If a patient ovulates but does not become pregnant, the physician should check cervical factors. The anti-estrogenic effect of clomiphene citrate can create a "hostile" environment for conception.

Use

We usually start with the lowest dosage to minimize adverse reactions. We then increase the dose in a subsequent cycle if ovulation does not occur. The patient should begin testing urine for an LH surge daily with an ovulation test kit, beginning on day 11 or 12 of the cycle. Call the office when an LH surge occurs.

In most cases, we will examine you with transvaginal ultrasound to see whether the follicles are ready for ovulation and check the size of the ovaries. If they are excessively enlarged, we will stop treatment until the ovaries are back to the pre-treatment size. If the follicles are ready to ovulate, we will proceed with your treatment, which may include scheduling an intrauterine insemination, or advising you when to have natural intercourse.

Risks

Women with liver disease should not use clomiphene citrate. Patients with abnormal or irregular uterine bleeding should be examined for endometrial or cervical abnormalities before treatment. This medicine should not be given to patients with ovarian cysts, since they may grow larger. It should not be taken by a patient who may be pregnant, although there is no proof of fetal damage. If a patient has not had a menstrual period for a significant length of time, there may a benefit from inducing menstruation with progesterone before using clomiphene citrate therapy.

Some patients who use clomiphene citrate get blurred vision or other visual symptoms. In these cases, driving and operating machinery may be dangerous, especially in conditions of variable lighting. If eye symptoms persist, therapy should be stopped, and the patient should have a complete eye examination. Common side effects include ovarian cysts and ovarian enlargement. Some women feel "throbbing" in the ovaries before ovulation, and others report occasional "hot flashes," insomnia, or irritability. About six percent of clomiphene citrate-induced pregnancies are multiple pregnancies, which is more common than for spontaneous ovulation. Most of the multiple pregnancies are twins
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How Does Clomiphene work?
Clomiphene acts by blocking the ability of cells in the hypothalamus (a specialized gland in the brain which orchestrates the body's hormonal changes) to detect the amount of estrogen (a hormone produced by the ovarian follicle(s) present in the blood. When the hypothalamus senses a deficiency of estrogen, it responds by releasing messages to the pituitary gland (a small structure suspended by a stalk from the base of the brain, located above the roof of the mouth). The pituitary gland in turn releases high amounts of Follicle Stimulating Hormone (FSH). The function of FSH is to initiate the growth of ovarian follicles which as mentioned, contain eggs and produce estrogen. Estrogen prepares the uterine lining to receive the embryo(s) about six days after ovulation. As soon as estrogen levels rise sufficiently, either in response to clomiphene or in natural cycles, there should be a rapid release of luteinizing hormone (LH) from the pituitary gland. It is LH that triggers the ovulation process and maturation of the eggs.
When clomiphene is administered, a spontaneous LH surge will usually take place; however, in order to ensure that ovulation actually occurs, the administration of human Chorionic Gonadotropin (hCG) is sometimes recommended. hCG is a hormone produced during pregnancy that is similar to LH in structure and effect. It is given when the follicle(s) have attained optimal growth, as indicated by ultrasound examination and the measurement of plasma estradiol concentrations. In patients who receive clomiphene from cycle day 2 through 6, this peak response can be anticipated around day 12 of the treatment cycle. It is for this reason that ultrasound examinations and plasma estradiol measurements are performed at this time. The administration of hCG on the 12th day of an optimally stimulated clomiphene cycle is an insurance aimed at making certain that ovulation occurs even if the pituitary gland does not initiate its own LH surge.

How is Clomiphene Taken?
Clomiphene is administered for five days during the early menstrual cycle. Some clinicians prescribe the drug from the 5th through the 9th day of the cycle while others recommend that the drug be taken from cycle day 3 through 7 because some physicians believe that the earlier clomiphene is administered, the more likely it is to promote the development of the optimal number of follicles (fluid-filled spaces in the ovary(ies) that harbor the maturing egg(s) and produce the hormone estrogen).

How is Clomiphene Monitored?
Since clomiphene is used to induce ovulation, your doctor should ensure that ovulation has indeed taken place. There are several ways to do this. You may be asked to do basal body temperature monitoring or urinary LH monitoring at home with an ovulation predictor kit.. Other tests to document ovulation include transvaginal ultrasound monitoring of follicle development and the mid-luteal progesterone test. The transvaginal ultrasound is an easy test done in the office that enables the doctor to see the size and maturity of growing follicles (see tests: ultrasound scans). Ovulation can be closely predicted and confirmed using this type of monitoring. An alternative is the mid-luteal progesterone test, which is a blood test usually done on CD 21 (of a 28 day cycle). If your cycle is not 28 days, it is done 7 days prior to the anticipated date of the next period. The progesterone test can confirm that you ovulated and can be useful to adjust the dosage of clomiphene.

If any of the above tests indicate that you have not ovulated, it is likely that your doctor will increase your dosage by 50mg until ovulation is confirmed. Typically, the maximum dose of clomiphene is 150-200 mg per day.

What Are The Side Effects of Clomiphene?
Clomiphene citrate is rarely associated with life-endangering complications. The most common side effects are hot flashes, minor visual disturbances, headaches, irritability and anxiety. In some cases, your period may be lighter or heavier than usual, and your cycles may be longer or shorter than usual. The side effects are temporary and subside once clomiphene is stopped. In some cases, ovarian cysts may develop and remain for 4-6 weeks following discontinuation of clomiphene. These cysts are usually harmless. Very rarely, a large number of cysts will develop in association with very high levels of estrogen, resulting in accumulation of free fluid in the abdominal area and symptoms such as vomiting, diarrhea, and abdominal distention. This is referred to as the Hyperstimulation Syndrome and is very rare in association with clomiphene. It occurs more commonly (although still fortunately quite rare) in association with HMG/FSH therapy. If you experience any of these symptoms, call your doctor immediately.

How Common Are Multiple Births with Clomiphene?
There is a higher multiple birth rate in women who conceive following clomiphene citrate therapy (5%-10%) than in the rest of the population. The incidence is far less than that which has been reported in association with hMG and/or FSH therapy (25%-30%). In most cases, the multiple pregnancies are twins. The risk of having twins in women who do not take any fertility drugs is about 1.2%

Does Clomiphene Cause Birth Defects?
Clomiphene has never been incriminated in causing the development of birth defects in humans.

Although clomiphene is administered for only five days, its effect is maximal in the period following discontinuation. This means, that by the time you ovulate, little of the drug remains in your system and is therefore unlikely to have any significant effect on the developing egg, the resulting embryo, or the implanting conceptus.

How Effective is Clomiphene?
The reported pregnancy rate following the appropriate use of clomiphene is between 15% and 30% per cycle of treatment, provided that there is no associated pelvic disease, that the husband is fertile, and the primary problem relates to irregular or abnormal ovulation.
Click to expand...
 
Now that is extremely interesting.....
 
Its looking like HCG is important for anyone that notices shrinkage of the jewels, for a quicker recoup. Otherwise cycle breaks should be longer IMO from the above reading.
 
How to mix HCG

HCG is unlike the steroid injections in that it requires two ampoules in combination to make one treatment.
Thus two ampoules brought into place for one injection.
One amp contains a white powdery freeze dried substance and the other contains a solution of isotonic sodium chloride.
The solution should be pumped into the dried powder ampoule with a syringe and the two substances mixed.
When the solvent contacts with the white powder the powder instantly appears to vanish leaving a crystal clear substance.
The injection is extremely easy and leaves no after pain.

How to inject HCG

When you have mixed the solution draw into the insulin needle.
Simply pinch the flesh on the stomach and insert the needle.

Dosage

Take 1/3 of a mixed amp 3 times a day. This is the way to fully absorb the compound.

Doses of HCG

Smaller doses, more frequently during a cycle will give best overall results with least unwanted side effects. Somewhere between 500iu and 1000iu per day would be best over about a two-week period. These doses are sufficient to avoid/rectify testicular atrophy without increasing oestrogen levels too dramatically and risking gynecomastia. This dosing schedule also avoids the risk of permanently down-regulating the LH receptors in the testes.

Presentation and Administration of HCG

Synthetic HCG is often known as Pregnyl (generic name) and is available in 2500iu and 5000iu (not ideal for the above doses!). Administration of the compound is either by intra-muscular or subcutaneous injection. It comes as a powder which needs to be mixed with the sterile water. The powder is temperature-sensitive prior to mixing and should not be exposed to direct heat. After mixing, it should be kept refrigerated and used within a few weeks - though there are sterility issues which need to be considered after mixing
Click to expand...
 
HCG/ Nolvadex rationale:

Tamoxifen does not suppress LH and T ! Keep looking and you will find human studies clearly showing this, and in fact its superiority over Clomid in stimulating both. I'm thinking of putting together a comprehensive article on this, so you guys understand how Clomid and Nolvadex work, and their differences, a little better. Plus if any SERM has estrogenic effects in the AP it is Clomid, not Nolvadex, which is why I prefer tamoxifen( it is a technical advantage, not a big one in the real world though)

And I say again, fostering a little extra LH post cycle with Clomid, Nolvadex, or Arimedex does'nt do a whole hell of alot. The brain increases LH rapidly post-cycle anyway, the testes just dont respond to it well because they have lost mass. This is why we need Bolus LH (HCG) plus an anti-estrogen.

*****#2

I have tried Clomid alone a few times years ago, but typically used Nolvadex and HCG. I have always found it to work very well for me. As for Arimedex, no , I have not tried to use this in a post cycle recovery program. Years ago I had a scare with extremely messed up cholestorol ( all LDL almost no HDL), and since have stayed away from aromatase inhibitors altogether. Consider this though:
Both Clomid, which mind you I have always contended works a s a T stimulating drug, just not like Nolvadex ( just technically not as good)
and Arimedex counter HPTA suppression by blocking the negative feedback caused by estrogens. They support LH release obviously.
Now post cycle it has clearly been shown that LH levels rebound quickly, while T levels are much slower to return to normal, why? The reason is that the testes, after a period of inactivity, have lost mass and are not able to respond as well to LH in terms of T output. If your recovery program only focuses on LH support it is missing the more important problem, testicular mass. HCG as you know can provide an additional bolus dose of LH. It can essentially help shock them back into shape, whereas it will take many weeks relying on heightened endogeous LH alone....................END

**************************************************
******
I thought this was interesting. But as Stonecold posted the other day this is one of the most controvesial topics going. Take what you need and leave the rest............... I for one hate Clomid. hate being cranky, hate feeling like a woman emotionally, and hate having zits. Although I understand everyone is different.

Again this article is credited to DRJMW it is not composed by myself.
Click to expand...
 
HMG

Humegon
Pergonal
In Canada-

Humegon
Pergonal

Other commonly used names are human menopausal gonadotropins (hMG) , human gonadotropins , and menotrophin .



--------------------------------------------------------------------------------
Category

Gonadotropin
Infertility therapy adjunct

--------------------------------------------------------------------------------
Description

Menotropins (men-oh-TROE-pins) are a mixture of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) that are naturally produced by the pituitary gland.

-

Use in females-FSH is primarily responsible for stimulating growth of the ovarian follicle, which includes the developing egg, the cells surrounding the egg that produce the hormones needed to support a pregnancy, and the fluid around the egg. As the follicle grows, an increasing amount of the hormone estrogen is produced by the cells in the follicle and released into the bloodstream. Estrogen causes the endometrium (lining of the uterus) to thicken before ovulation occurs. The higher blood levels of estrogen will also tell the hypothalamus and pituitary gland to slow the production and release of FSH.

LH also helps to increase the amount of estrogen produced by the follicle cells. However, its main function is to cause ovulation. The sharp rise in the blood level of LH that triggers ovulation is called the LH surge. After ovulation, the group of hormone-producing follicle cells become the corpus luteum, which will produce estrogen and large amounts of another hormone, progesterone. Progesterone causes the endometrium to mature so that it can support implantation of the fertilized egg or embryo. If implantation of a fertilized egg does not occur, the levels of estrogen and progesterone decrease, the endometrium sloughs off, and menstruation occurs.

Menotropins are usually given in combination with human chorionic gonadotropin (hCG). The actions of hCG are almost the same as those of LH. It is given to simulate the natural LH surge. This results in ovulation at an expected time.

Many women choosing treatment with menotropins have already tried clomiphene (e.g., Serophene) and have not been able to conceive yet. Menotropins may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or fertilization (IVF).

-

Use in males-Menotropins are used to stimulate the production of sperm in some forms of male infertility.

Menotropins are to be given only by or under the supervision of your doctor. It is available in the following dosage form:

Parenteral
Injection (U.S. and Canada)
 
Try medsmex.com

They have both.

Order took about 14 days to get for me. I had to sign for it, but then they are not eligle either, so no big deal.
 
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