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Originally posted by PB&J How do you buy clomid? I heard you don't need a prescription. Where would you get it? |
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Originally posted by Mudge You can buy it online, its not a controlled substance but its not "legal" to buy without a scrip. www.liquidresearch.com would be one such company. |
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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. |
works though
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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. |
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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 |
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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. |
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There seems to be increasing evidence that progesterone may be valuable in restoring or maintaining HPTA functioning. One study examined the effects of testosterone and estrogen on NPY receptors. Progesterone administration showed and increase in serum LH levels. The study demonstrated that Progesterone was an antagonist of the Y2 NPY receptor, which may account for a greater stimulation of the Y1 receptor, known to increase gnRH output. Parker SL, Carroll BL, Kalra SP, St-Pierre S, Fournier A, Crowley WR. Neuropeptide Y Y2 receptors in hypothalamic neuroendocrine areas are up-regulated by estradiol and decreased by progesterone cotreatment in the ovariectomized rat. Endocrinology. 1996 Jul;137(7):2896-900 This would suggest that at least short-term controlled administration of progesterone may have an effect on HPTA restoration. |
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In females estrogen does exert a positive feedback effect on LH secretion immediately before ovulation. The LH surge is thought to actually induce ovulation. When progesterone synthesis is blocked with enzyme inhibitors, the LH surge is absent. So progesterone is clearly important for the preovulatory LH surge (1). Males of any species, unlike females, are not supposed to exhibit any positive feedback effect of estrogen on LH production, or so the dogma goes. But your post got me searching medline to see if I could find any evidence of a positive effect of estrogen on LH in males when progesterone was administered. Remarkably, it seems to happen, at least in rats (2). I found that astonishing. (1) Neuroendocrinology. 2003 Jul;78(1):29-35. The luteinizing hormone surge is preceded by an estrogen-induced increase of hypothalamic progesterone in ovariectomized and adrenalectomized rats. Micevych P, Sinchak K, Mills RH, Tao L, LaPolt P, Lu JK. (2) Biol Reprod. 1982 Dec;27(5):1222-9. Induction of luteinizing hormone, follicle-stimulating hormone surge in the estrogen-primed castrated male rat by progesterone. McPherson JC 3rd, Mahesh VB. |
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1: Clin Endocrinol (Oxf). 2003 Apr;58(4):506-12. Demonstration of progesterone receptor-mediated gonadotrophin suppression in the human male. Brady BM, Anderson RA, Kinniburgh D, Baird DT. Contraceptive Development Network and MRC Human Reproductive Science Unit, Centre for Reproductive Biology, University of Edinburgh, Edinburgh, UK. OBJECTIVE: Synthetic gestogens in combination with testosterone have potential as a male hormonal contraceptive, predominantly acting by augmenting suppression of gonadotrophin secretion. Little is known, however, of the effects of gestogens in the male. Gestogens have affinity for both androgen and progesterone receptors but the relative contribution of action at these two receptors in gonadotrophin suppression remains unclear. In this study the effects of progesterone, with no significant androgen-receptor affinity are compared to desogestrel, a synthetic gestogen with relatively low affinity for the androgen receptor, on gonadotrophin secretion in normal men. DESIGN: Subjects received either 50 mg progesterone intramuscularly (i.m.) or 300 micro g desogestrel orally daily for 7 days. Frequent blood sampling over 12 h was undertaken before and after drug administration. GnRH [100 micro g intravenously (i.v.)] was administered 2 h before the end of the frequent sampling period. SUBJECTS: Twenty healthy men were randomly allocated to the two treatment groups. RESULTS: Both progesterone and desogestrel administration resulted in decreases in the concentration of both LH and FSH secretion, as well as testosterone. Analysis of the pulsatile nature of LH secretion indicated that both treatments reduced LH pulse amplitude, and that progesterone reduced LH pulse frequency. Progesterone, but not desogestrel, treatment also reduced the increase in LH secretion in response to GnRH. CONCLUSIONS: The effects of progesterone were at least as marked as those of a maximally effective dose of desogestrel. As progesterone has negligible affinity for the androgen receptor, these results are compatible with the suppressive effects of synthetic 19-norgestogens on gonadotrophin secretion in the male being mediated via the progesterone receptor, with its androgenicity contributing minimally to gonadotrophin suppression. Publication Types: Clinical Trial Randomized Controlled Trial PMID: 12641635 [PubMed - indexed for MEDLINE] |
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Effect of test on LH/FSH: Testosterone suppression of the HPT axis. MacIndoe JH, Perry PJ, Yates WR, Holman TL, Ellingrod VL, Scott SD. Department of Psychiatry, College of Medicine, University of Iowa, Iowa City, USA. BACKGROUND: Although studies have demonstrated the suppression of normal gonadal function in the experimental setting, the specific mechanisms by which androgenic-anabolic steroids impact male gonadal function remain ill defined. Following 2 consecutive weekly injections of an identically appearing testosterone cypionate (TC) placebo, subjects were randomized to a TC dose of 100 mg/wk, 250 mg/wk, or 500 mg/wk. Following the last weekly injection of active agent the subjects received 12 consecutive weeks of TC placebo injections. RESULTS: Spermatogenesis was impaired by each of the doses of TC employed in this study, but the observed decreases in, sperm count were neither strictly dose dependent nor consistent between individuals treated with the same dose. Basal leuteinizing hormone (LH) and follicle stimulating hormone (FSH) became undetectable 2 weeks after the start of 250 and 500 mg/wk TC injections and were lost within 5 to 6 weeks of starting 100 mg doses. Pituitary gonadotropin responses to leutinizing hormone releasing hormone (LHRH) disappeared more slowly with FSH responses being lost 1 to 3 weeks after the loss of basal FSH activity. Leuteinizing hormone responses to LHRH appeared to be suppressed last, disappearing 4 to 6 weeks after FSH responses to LHRH. CONCLUSIONS: Exogenous testosterone-mediated inhibitory influences on the hypothalamic-pituitary-testicular axis were reversed following the cessation of drug treatment. ----------------------------------- Evidence that follicle-stimulating hormone is necessary for the maintenance of quantitatively normal spermatogenesis in man: J Clin Endocrinol Metab 1986 Jun;62(6):1184-92 Related Articles, Links Chronic human chorionic gonadotropin administration in normal men: evidence that follicle-stimulating hormone is necessary for the maintenance of quantitatively normal spermatogenesis in man. Matsumoto AM, Karpas AE, Bremner WJ. The role of FSH in the maintenance of spermatogenesis in man is poorly understood. To determine whether normal serum levels of FSH are necessary for the maintenance of quantitatively normal spermatogenesis, we first studied the effect on sperm production of selective FSH deficiency induced by chronic administration of hCG in normal men. Then, we determined the effect of FSH replacement in some of these men. After a 3-month control period, eight normal men (aged 30-39 yr) received 5000 IU hCG, im, twice weekly for 7 months. Then while continuing the same dosage of hCG, subjects simultaneously received 200 mg testosterone enanthate (T), im, weekly for an additional 6 months. hCG administration alone resulted in partial suppression of the mean sperm concentration from 88 +/- 24 (+/-SEM) million/ml during the control period to 22 +/- 7 million/ml during the last 4 months of hCG treatment (P less than 0.001 compared to control values). With the addition of T to hCG, sperm counts remained suppressed to the same degree. Except for one man who became azoospermic while receiving hCG plus T, sperm motilities and morphologies remained normal in all subjects throughout the entire study. During both the hCG alone and hCG plus T periods, serum FSH levels were undetectable (less than 25 ng/ml), and urinary FSH levels were comparable to those in prepubertal children and hypogonadotropic hypogonadal adults. We replaced FSH activity in four of the eight men in whom prolonged selective FSH deficiency and partial suppression of sperm production were induced by hCG administration. Immediately after the period of hCG plus T administration, T was stopped in four men who continued to receive hCG alone (5000 IU, im, twice weekly) for 3 months. Then, while continuing the same dosage of hCG, these men received 100 IU human FSH, sc, daily (n = 2) or 75 IU human menopausal gonadotropin, sc, daily (n = 2) for 5-8 months. During the second period of hCG administration alone, serum FSH levels were undetectable (less than 25 ng/ml), and sperm concentrations were suppressed (34 +/- 13 million/ml) compared to the control values for these four men (125 +/- 39 million/ml; P less than 0.001). With the addition of FSH to hCG, FSH levels increased (213 +/- 72 ng/ml) and sperm concentrations rose significantly, reaching a mean of 103 +/- 30 million/ml (P less than 0.03 compared to hCG alone... --------------------------- Eur J Endocrinol 2002 Nov;147(5):617-24 Related Articles, Links Maintenance of spermatogenesis in hypogonadotropic hypogonadal men with human chorionic gonadotropin alone. Depenbusch M, von Eckardstein S, Simoni M, Nieschlag E. Institute of Reproductive Medicine of the University, Domagkstr. 11, Munster D-48149, Germany. OBJECTIVE: It is generally accepted that both gonadotropins LH and FSH are necessary for initiation and maintenance of spermatogenesis. We investigated the relative importance of FSH for the maintenance of spermatogenesis in hypogonadotropic men. SUBJECTS AND METHODS: 13 patients with gonadotropin deficiency due to idiopathic hypogonadotropic hypogonadism (IHH), Kallmann syndrome or pituitary insufficiency were analyzed retrospectively. They had been treated with gonadotropin-releasing hormone (GnRH) (n=1) or human chorionic gonadotropin/human menopausal gonadotropin (hCG/hMG) (n=12) for induction of spermatogenesis. After successful induction of spermatogenesis they were treated with hCG alone for maintenance of secondary sex characteristics and in order to check whether sperm production could be maintained by hCG alone. Serum LH, FSH and testosterone levels, semen parameters and testicular Volume were determined every three to six Months. RESULTS: After spermatogenesis had been successfully induced by treatment with GnRH or hCG/hMG, hCG treatment alone continued for 3-24 Months. After 12 Months under hCG alone, sperm counts decreased gradually but remained present in all patients except one who became azoospermic. Testicular Volume decreased only slightly and reached 87% of the Volume achieved with hCG/hMG. During treatment with hCG alone, FSH and LH levels were suppressed to below the detection limit of the assay. CONCLUSION: Once spermatogenesis is induced in patients with secondary hypogonadism by GnRH or hCG/hMG treatment, it can be maintained in most of the patients qualitatively by hCG alone, in the absence of FSH, for extended periods. However, the decreasing sperm counts indicate that FSH is essential for maintenance of quantitatively normal spermatogenesis. |
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HCG - info and faq Upon researching hcg and post cycle therapy i came across what i allready knew.........thus conflicting arguments on usage . certain gurus say at the start and during , while the opposite side of the spectrum some say post cycle....... the following is relative info in which i came across: HCG: This does nothing with regard to inhibition of the hypothalamus and pituitary. Rather it acts like LH, and causes the testicles to produce testosterone just as if LH were present. It is useful then for avoiding testicular atrophy during the cycle. The best dosing method is to use small amounts frequently: 500 IU per day is sufficient, and 1000 IU may optionally be used. The amount may be given as a single daily dose or divided into two doses. Administration may be intramuscular or subcutaneous. More is not better: too much HCG can result in downregulation of the LH receptors in the testes, and is therefore counterproductive. Overdosing of HCG can also result in gynecomastia. |
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Steroids: The New Rules - Bringing The Science of steroid use into the 21st century....by Brock Strasser I have some news for you that should change the way you look at and subsequently use and cycle anabolic steroids. For the longest time, we’ve developed and based our cycling theories on the limited pharmacodynamic and pharmacokinetic data that we’ve extrapolated from primarily murine (mice) and rat models. I don’t have to tell you that the effects a steroid has on a rodent probably aren’t homologous to the effects that a steroid will have on a human. Sure, they run around their cages flexing in the mirror all the time and tend to be more popular with all the lady mice, but despite this similarity with humans, there are differences. After all, in rodents, steroids like Primobolan (methenolone esters) are better mass builders than Testosterone. Try telling any bodybuilder he should give up his DepoTest for Primobolan and at the very least, you’ll get laughed at. The rest of the "data" we’ve used comes from anecdotal reports overheard in the gym and on internet message boards. This isn’t exactly the most reliable data either, considering some people have hidden agendas (e.g. they’re selling a particular steroid) or they aren’t entirely forthcoming regarding what they used, when they used, and how much. And I haven’t even mentioned the "fudge factor" and imaginary gains claimed by some so they won’t appear to be slackers in the gym. Because of this, perhaps more so than in any other therapeutic area in medicine, we don’t know a whole lot about steroids and how they interact with the human body. I’m going to change all that. I’ve located a mind-expanding study conducted on humans using two anabolic steroids, nandrolone phenylpropionate and nandrolone decanoate. My article here, based entirely on this study, is going to shatter some misconceptions regarding anabolic steroids. Sit back and prepare to be educated. HPTA Suppression Is Imminent Anyone who’s used anabolic steroids for any length of time will easily observe that when they discontinue using, they invariably "crash." That is to say, their body is producing next to zero endogenous androgens. This can lead to significant loss of muscle gain, loss of strength gains, lethargy, depression and a whole host of other disorders. Of course, drugs like HCG, HMG, clomiphene and similar gonadotrophics can help to ameliorate such symptoms, but these aren’t 100% cure-alls. The success or failure of such secondary drug use varies considerably between individuals. In a quest to minimize HPTA insult, my friend and Biotest developmental team partner, Bill Roberts, came up with an innovative speculation: If you limit your use of anabolic steroids to short-acting compounds and don’t exceed two weeks of continual usage without a four week period of no usage, you might not depress endogenous androgen levels too much, if at all. This is the now famous "two on/four off" protocol. I have the utmost respect for Bill and he possesses more knowledge about drugs than I ever will, but on this one topic, I don’t agree with him. The study I just reviewed utilized ten healthy male volunteers who were randomized to receive either the phenylpropionate or decanoate ester of nandrolone via intramuscular, oily depo injection. A single injection of only 100 mg of nandrolone phenylpropionate caused almost complete suppression of endogenous Testosterone by day three and lasted until around day eight. Endogenous levels of Testosterone didn’t return to baseline levels for almost fifteen days, while the same type of injection with nandrolone decanoate caused almost complete inhibition of endogenous by day four. Endogenous levels of Testosterone didn’t return to baseline levels for greater than twenty days! All this from a single, 100-mg injection of nandrolone! This tells me that no matter what you do, whether it’s a short lasting ester or a long lasting ester, you’ll end up totally shutting down your body’s ability to make androgens for at least two to three weeks. Since nobody (well, at least nobody male) uses only 100 mg of nandrolone per week, it’s reasonable to conclude that the suppression caused by 500mg of an esterified anabolic per week (an average dose) would be much greater than two to three weeks. This study didn’t deal with fast acting orals like stanozolol and oxandrolone, but there’s no reason to think that these won’t cause HPTA insult as well. So what does this mean? To me, it means that HPTA insult is inevitable and should be planned for accordingly in your cycle. That is to say, you should plan on crashing for a few weeks post-cycle no matter what. Because of this, you’re going to want to extend and "beef up" your cycle so that you overshoot your final goal. Remember, you’re going to crash and lose some of your gains. So if you want to gain "X" pounds of muscle, shoot for "X+Y" pounds of muscle and accept that within two to six weeks after the cycle, you’ll end up losing most of the "Y" portion. Volume and Concentration Steroids come in all shapes and sizes. In other words, you can find nandrolone (or Testosterone or boldenone) esters in 25 mg/ml, 50 mg/ml, 100 mg/ml, 200 mg/ml and so forth. Is a 400 mg injection using two milliliters of a 200 mg/ml oily solution the same as using four milliliters of a 100 mg/ml solution? After all, the net amount is still 400 mg, right? Unfortunately, this isn’t the case. Steroid concentration in the solution greatly affects the dynamics and kinetics. In this study, some of the men received a 100 mg/ml injection of nandrolone decanoate and other men received a 100 mg injection using a 25 mg/ml solution (which means they received four milliliters, of course). Those that received the 100 mg/ml injection reached significantly higher (between 30% and 50%) plasma levels of nandrolone than those who got 100 mg via the 25 mg/ml solution. To top it off, the 100 mg/ml group’s plasma nandrolone level stayed elevated for a little bit longer; however, the length of suppression of endogenous Testosterone was almost identical. What does this tell us? It tells us that if we want to maximize plasma levels of hormone (and thereby, maximize gains in lean muscle) we want to opt for the most concentrated version of whatever steroid(s) we decide we’re going to use. If we’re using Testosterone, we surely want to use a 200mg/ml enanthate over something like 100mg enanthate. If we’re using nandrolone, we want to use Ttokkyo’s 300mg/ml stuff over 50mg/ml or 100mg/ml nandrolone decanoate made by others. Injections Sites Another thing that superficially seems trivial but makes a huge difference in plasma steroid concentrations is where you inject. That’s right, this seems utterly trivial but this study concluded that gluteal injections yielded far superior plasma levels as opposed to injections in the deltoid. Of all the locations that nandrolone injections were given in this study (100 mg/ml x 1 ml in the glutes, 25 mg/ml x 4 ml in the glutes and 100 mg/ml x 1 ml in the deltoid), the deltoid injections yielded the lowest plasma levels of nandrolone by a huge factor, with peak concentrations being 50% lower than the 100 mg/ml gluteal injection and around 10% lower than the 100 mg/ml x 4ml gluteal injection. Lesson learned here: Only inject in the glutes for maximal steroidal efficacy. Short Esters Are Better Esters Perhaps the most important thing I learned in reviewing this study is that short-chain esters (steroids of shorter half life) yield a much higher plasma concentration of steroid than steroids of longer side chain esters. In this study, a single 100 mg/ml x 1 ml intragluteal injection of nandrolone phenylpropionate caused a peak plasma concentration of almost double that of the 100 mg/ml x 1 ml intragluteal injection of nandrolone decanoate. This level remained increased for almost seven days, too. By fourteen days, even though the nandrolone decanoate ester demonstrated a much higher plasma level than the nandrolone phenylpropionate level, the net amount of both was so low as to be ineffective. This tells me that the effects I can see from using 500 mg of Testosterone enanthate per week probably won’t be the same as using 500 mg of Testosterone propionate or even Testosterone suspension per week. I’m going to see better results with the propionate and even better results with the suspension. Sure, I may need to inject the propionate and suspension more often, but in the long run it’ll pay off for me. (Not that I’d use steroids, of course. No sir, not me. They’re illegal!) Conclusions To recap everything mentioned here in this article, remember the following: 1) HPTA suppression is virtually inevitable. Even a single 100mg injection of nandrolone will cause full suppression for almost a week and you won’t return to a normal HPTA for at least two weeks. Plan your cycle accordingly and overshoot your goals knowing you’ll lose something. 2) Injection volume and concentration are important. When available, opt for the highest concentration on a mg/ml basis. 3) Injection site is important. The best place for maximal plasma levels seems to be the glutes. 4) Side chain ester length is probably the single most important factor in influencing plasma levels. The shorter the ester (and the half life) the better. You may have to inject more often, but in the long run it’ll be worth it. There you go, the new "rules" of steroid use. Put them to use wisely! Reference The Journal of Pharmacology And Experimental Therapeutics, Vol 281, No. 1; 93-102, 1997. |
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Worst side of AAS use and how to counter Why is it that users don't realize that the worst side of steroid use is a VERY shitty lipid profile. Well I think it's because one cannot SEE a shitty lipid profile and you don't feel bad with it. I would venture to say that it is universal with men that are taking even half decent doses of gear. Total cholesterol usually doesn't go up that much with roids, although it can climb, and triglycerides sometimes go down but usually stay about the same. What makes steroid use so scarry is the TERRIBLE affect it have on hdl. Hdl(good cholesterol) really takes a dive. Hdl to total cholesterol ratio's are OFTEN as bad as 15 or 20 to 1 and that is very significant indeed. The last time I had my lipid profile checked my doc had a COW!! I don't know if I will ever do test and tren again for a long eight week cycle. People with a low hdl have a significantly higher risk for heart disease. There is plenty of evidence to suggest that heart disease doesn't happen in a few years in old or middle age. It is most often though to be the result of a slow build up of aterial plaque over many many years and perhaps starting in childhood! So with all this in mind it makes sence to limit androgen use as much as possible and to take plenty of time off between cycles. SUGGESTIONS Bill Llewellyn suggests moderate doses of non 17aa mild aromatizing androgens like EQ and perhaps a liitle nandrolone. Low doses of test are not that bad either. Seems that a little estrogen may be helpful here. Nothing hammers my hdl more than tren and we know it is the most powerful androgen and doesn't aromatize. Bill also suggests the use of an estrogen blocker throughout the cycle , such as clomid or nolva. He reports that Nolva has helped his hdl. There are a couple studies that suggest that nolva can be helpful for men with heart disease but these men are not on AAS. Nolva has not helped me BTW but perhaps it's worth a try. Short two week cycles may be an option for some as even if the lipid profile is hammered the short time would reduce risks associated with this change. I have posted a good deal on two weekers over at Elite. They can work IF done properly. Huge gains cannot be expected of course but decent gains can be made. DRUG THERAPY. Niacin increases hdl more than any drug. Lipidor and the like are better at reducing ldl. Niacin needs to be taken in high dose in order to be effective. 1500mg to 3000 mg per day. Do NOT use the old time released niacins as they are very hard on the liver. Even regular niacin can have some impact so be sure to be followed by your doc. I take non fluch niacin at about 1800mg per day and it does seem to help. BEWARE..the flush from regular niacin is UNREAL but some poeple actually grow to enjoy it he he he . Start slow and build up. FOODS Omega 3 and 6 oils help so get some flax seed and grind it up in a coffee grinder and throw it into your protein drinks...a few table spoons is good. Flax is a great source of Omega three's. You can also buy flax oil or combo oils like Udo's select oil. Salmon Tuna Macheral and Sarines are pretty good sources of Omegas three, especially sardines..so start making your Grampa's sardines sandwiches. Avoid saturated fat like the plague(land animal fat and egg yolks) Okay some is okay but be careful as a high saturated fat diet WILL mess with your lipid profile. Limit cholesterol a little, although saturated fat is FAR WORSE...just don't be eating a half dozen egg yolks per day. Avoid trans fats. Trans fatty acids are man made fats and are found in large doses in PARTIALLY hydrogenated oils(margerine). Another way of saying partially hydrogenated is "Vegetable oil shortening." Avoid all store bought oils except extra virgin olive oil. All oils, except for cold pressed olive oil, have been super heated to over 400 degree's and as a result their chemical composition changes and they become toxic as hell and really mess with your lipid profile! Butter is a neutral fat and is far better than margerine or corn oil etc, even though its saturated. NEVER fry with any oil above 250 degree's ..get an electric frying pan. The safest oils to fry with are olive oil and butter. NEVER EVER fry with oils high in Omega 3 or 6 as they become very unstable. Buy the book "Fats that Heal Fats that Kill" by Udo Erasmus. EXTREMELY EXCELLENT BOOK! CARDIO Do 30 minutes of cardio at a decent intensity three time per week as this help increase hdl. |
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"An Uncontrolled Clinical Trial for Treatment of Androgen Induced Hypogonadism" by Michael C. Scally, M.D. And Andrew L. Hodge, M.S. : "It was discovered that although both clomiphene citrate and tamoxifen met with some success, when combined together they achieved a more significant increase in gonadotropin production." |
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Originally posted by DrJMW 1. Use a superior antiestrogen and/or a superior antiprolactin/antiprogestronic DURING the cycle. Aromasin is the superior antiestrogen and Dostinex is the superior antiprolactin med. dostinex is useful when using DECA, Tren/FINA, etc. 2. Keep your AAS cycles eight weeks or so long. 3. Keep your dosing moderate. This advise applies to those with average genetics (the majority). There are a small number of you who can successfully exceed or ignore these guidelines (the true mesomorphs). 4. Begin your recovery cycle the same week or the next week after the AAS cycle. Weeks one thru three of recovery: 2,000U of HCG, IM, Mon, Wed, Fri 20mg Nolvadex daily. Weeks four thru six: 20mg Nolvadex daily. Clomid 50mg daily should be added, paralleling Nolvadex, if you are coming off a prolonged, heavy cycle. This cycle may need to be repeated once or even twice. If you do not recover, then you need to see an endocrinologist for exam to check for other physiological problems and possible lifelong HRT. Most young, healthy people recover, assuming they have something to recover. How do you know if you have something to recover? Baseline Testos blood levels. After reading the boards for over four years, I am still amazed at the number of people not using ancillaries, not doing a recovery cycle, not doing blood testing, and not doing adequate recovery cycles. |
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Clomid Pharmaceutical Name: Clomiphene (as citrate) Molecular weight of base: 405.9663 Molecular weight of ester: 192.125 (citric acid, 6 carbons) Effective dose: 100-150 mg/day orally ______________ Nolvadex Pharmaceutical Name: Tamoxifen (as citrate) Molecular weight of base: 371.5212 Molecular weight of ester: 192.125 (citric acid, 6 carbons) Effective dose: 20-40 mg / day orally Info: While practically similar compounds in structure, few people ever really consider Clomid and Nolva to be similar. Its not just a common myth in steroid circles, but even in the medical community. This misconception originates from their completely different uses. Nolvadex is most commonly used for the treatment of breast cancer in women, while clomid is generally considered a fertility aid. In bodybuilding circles, from day one, clomid has generally been used as post-cycle therapy and Nolvadex as an anti-estrogen. But as I intend to demonstrate this is in essence the same. I believe the myth to have originated because Nolva is clearly a more powerful anti-estrogen, and the people selling clomid needed another angle to sell the stuff, so it was mostly used as a post-cycle aid. But few users really understand how clomid (and also Nolvadex, logically) works to bring back natural testosterone in the body after the conclusion of a cycle of androgenic anabolic steroids. After a cycle is over, the level of androgens in the body drop drastically. The body compensates with an overproduction of estrogen to keep steroid levels up. Estrogen as well inhibits the production of natural testosterone, and in the period between the return of natural testosterone and the end of a cycle, a lot of mass is lost. So its in everybody's best interest to bring back natural test as soon as humanly possible. Clomid and Nolvadex will reduce the post-cycle estrogen, so that a steroid deficiency is constated and the hypothalamus is stimulated to regenerate natural testosterone production in the body. That's basically how the mechanism works, nothing more, nothing less. Both compounds are structurally alike, classified as triphenylethylenes. Nolvadex is clearly the stronger component of the two as it can achieve better results in decreasing overall estrogen with 20-40 mg a day, than clomid can in doses of 100-150 mg a day. A noteworthy difference. Triphenylethylenes are very mild estrogens that do not exert a lot, if any activity at the estrogen receptor, but are still highly attracted to it. As such they will occupy the receptor and keep it from binding estrogens. This means they do not actively work to reduce estrogen in the body like Proviron, Viratase or arimidex would (by competing for the aromatase enzyme), but that it blocks the receptor so that any estrogen in the body is basically inert, because it has no receptor to bind to. This has advantages and disadvantages. The disadvantage is that when use is discontinued, the estrogen level is still the same and new problems will develop much sooner. The advantage is that it works much faster and has results sooner than with an aromatase blocker like Proviron or arimidex. Therefor, when problems such as gynocomastia occur during a cycle of steroids one will usually start 20 mg/day of Nolva or 100 mg/day of clomid straight away, in conjunction with some Proviron or arimidex. The proviron or arimidex will actively reduce estrogen while the clomid or Nolvadex will solve your ongoing problem straight away. This way, when use is discontinued there is no immediate rebound. So which one should you use? Well personally, I'd have to say Nolvadex. Both as an on-cycle anti-estrogen and a post-cycle therapy. As an anti-estrogen its simply much stronger, demonstrated by the fact that better results are obtained with 20-40 mg than with 100-150 mg of clomid. For post-cycle, this plays a key role as well. It deactivates rebound estrogen much faster and more effective. But most importantly, Nolvadex has a direct influence on bringing back natural testosterone, where as clomid may actually have a slight negative influence. The reason being that Tamoxifen (as in Nolvadex) seems to increase the responsiveness of LH (luteinizing hormone) to GnRH (gonadtropin releasing hormone), whereas clomid seems to decrease the responsiveness a bit1. Another noteworthy fact about Nolvadex is that it acts more potently as an estrogen in the liver. As you remember, I mentioned that clomiphene and tamoxifen are basically weak estrogens. Well, tamoxifen is apparently still quite potent in the liver. This offers us the positive benefits of this hormone in the liver, while avoiding its negative effects elsewhere in the body. As such Nolvadex can have a very positive impact on negative cholesterol levels2 in the body, and therefore too should be considered a better choice than clomid. It will not solve the problem of bad cholesterol levels during Steroid use, but will help to contain the problem to a larger degree. Another reason why I promote the use of Nolvadex over Clomid post-cycle (as if being 3-4 times stronger and having more of a direct effect on restoring natural test wasn't enough) is because it's a lot safer. Not just because it improves lipid profiles, but also because it simply doesn't have the intrinsic side-effects that Clomid has. Clomid causes more acne for sure, but that's mainly because you need to use a 3-4 times higher dose. But Clomid seems to also affect the eyesight. Long-term clomid therapy causes irreversible changes in eyesight3 in users. Irreversible. For me that alone is reason enough to prefer Nolvadex. Lastly, one should be aware that use of these compounds can reduce the gains made on steroids. Nolvadex more so than clomid, simply because it is stronger. Estrogen is responsible for a number of anabolic factors such as increasing growth hormone output, upgrading the androgen receptor and improving glucose utilization. This is why aromatizing steroids like testosterone are still best suited for maximum muscle gain. When reducing the estrogen levels, we therefore reduce the potential gains being made. For this reason one may opt to try clomid during a cycle instead of Nolvadex. Although I would imagine that the problem that needed solved would be of more concern, in which case Nolva remains the weapon of choice. It's a plain fact that there is a high correlation between gains and side-effects. Either you go for maximum gains and tolerate the side-effects, or you reduce the side-effects, and with it the gains. That's life, nothing is free. Stacking and Use: If problems of Gynocomastia or other estrogen related symptoms tend to pop up during a cycle the use of 20-30 mg of Nolvadex or 100 mg of Clomid daily should easily contain the problem, and be used until a few days after the problem subsides. For best results and the least amount of problems upon cessation it is best stacked with Proviron (50 mg) or arimidex (0.5 mg) for this duration as well. Its not advised that these products be ran concomitantly with the steroid for the entire duration of the stack, as this will reduce your gains. Instead cease the usage of anti-estrogens once the problem is contained, and should the problem resurface, simply recommence the use of the products in the same manner as described above. Once a cycle of steroids is concluded one should always initiate a post-cycle therapy to help bring back natural testosterone as soon as possible. This will help you to retain the mass you gained. How this is done depends highly on the type of steroid used. If only orals were used, therapy should start immediately, even the last day of the stack. If short-acting esters or water-based injectables were used, therapy should commence within 4-7 days after last injection, and if long-acting esters were used then it should commence 1.5 to 2 weeks after the last injection was given. The length of the therapy will vary as well, from 3-5 weeks. The longer acting the product was, the longer therapy should be continued to make sure all suppressive factors are cleared before use of Clomid/Nolvadex is discontinued. For best results, it is best stacked with HCG (Human Chorionic gonadotrophin), which functions as an LH analog and can help bring testicle size back up. HCG use starts the last week of a cycle, and on from there every 5-6 days (usually 1500-3000 IU) and discontinued 1.5 to weeks prior to the cessation of Nolvadex/clomid. The reason being that HCG itself is also suppressive of natural testosterone and should be out of the body before therapy is over, or it will inhibit natural testicle function. But I can not stress enough that HCG possibly plays a more important role in post-cycle therapy than clomid/Nolvadex. For Clomid and Nolvadex, doses are usually tapered down. Its best to start with 40-50 mg of Nolvadex or 150 mg of Clomid for the first week or the first two weeks, and then finish the program with 20-25 mg of Nolvadex or 100 mg of Clomid for an additional two weeks. ************************************* -BigCat |
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Clomid and HCG By Nick and Bigfella - MuscleTalk.co.uk moderators Nick can be contacted through the Muscletalk forum for any questions or comments. One of the most frequently asked questions on MuscleTalk is how to use Clomid and HCG correctly. (A note to Americans - when I say 'oestrogen' I mean 'estrogen' - we spell it correctly in the UK!) Why Bodybuilders Use Clomid Clomid is a generic name for Clomiphene Citrate and is a synthetic oestrogen. It is prescribed medically to aid ovulation in low fertility females. Another generic name is Serophene. Most anabolic steroids, especially the androgens, cause inhibition of the body's own testosterone production. When a bodybuilder comes off a steroid cycle, natural testosterone production is zero and the levels of the steroids taken in the blood are diminishing. This leaves the ratios of catabolic : anabolic hormones in the blood high, hence the body is in a state of catabolism, and, as a result, much of the muscle tissue that was gained on the cycle is now going to be lost. Clomid stimulates the hypothalamus to, in turn stimulant the anterior pituitary gland (aka hypophysis) to release gonadotrophic hormones. The gonadotrophic hormones are follicle stimulating hormone (FSH) and luteinizing hormone (LH - aka interstitial cell stimulating hormone (ICSH)). FSH stimulates the testes to produce more testosterone, and LH stimulates them to secrete more testosterone. This feedback mechanism is known as the hypothalamic-pituitary-testes axis (HPTA), and results in an increase of the body's own testosterone production and blood levels rise, to, in part, compensate for the diminishing levels of exogenous steroids. This is vital to minimise post cycle muscle losses. Not all steroids do cause shut down of the feedback mechanism. Everyone is different and you must also take into account how long you have been using a certain steroid and at what dose in order to determine if you need Clomid or not. Clomid also works as an anti-oestrogen. As it's a weak synthetic oestrogen, it binds to oestrogen receptors on cells blocking them to oestrogen in the blood. This minimises the negative effects like gynecomastia and water retention that may be a result of oestrogen that has aromatised from testosterone. It's effect as an anti-oestrogen are quite weak though, and it should not be relied upon if you are going to be using androgenic steroids that aromatise at a rapid rate, or if you are pre-disposed to gynecomastia. Arimidex and Nolvadex (Tamoxifen) are far more effective anti-oestrogens. Important note: Clomid does not, as is often thought, stimulate the release of natural testosterone, but rather works at reducing the oestrogenic inhibition caused by the steroid cycle. It does this in a similar manner to the way it and Nolvadex block oestrogen receptors in nipples to combat gyno development, i.e. by blocking the oestrogen receptors in the hypothalamus and pituitary thus reducing the inhibition from the elevated oestrogen. This allows LH levels to return to normal, or even above normal levels, and in turn, natural testosterone levels to also normalise. Inhibition of the HPTA is caused by either elevated androgen, oestrogen or progesterone levels. On cessation of the steroid cycle, androgen levels begin to fall and Clomid dosing is normally commenced according to the half-life of the longest acting drug in the system (see below). This may also explain the reason individuals often find post-deca recovery more difficult, as the progesterone presence is untouched by the Clomid. We know that Clomid and Nolvadex (being very similar chemically) are both ineffective with regard to reducing progesterone related gyno, so it is reasonable to assume that Clomid has little effect against progesterone levels. Clomid During A Cycle When we use anabolic steroids, the level of androgens in the body rises causing the androgen receptors to become more highly activated, and through the HPTA, a signal tells our testes to stop producing testosterone. During a cycle the body has far higher than normal levels of androgens and, as long as this level is high enough, Clomid will not help to keep natural testosterone production up. It will be almost all but completely shut off, in theory. Some heavy androgen users, however, do advocate a small burst of Clomid mid-cycle, though it must be hard for them to say if it really of any benefit, due to the amount of gear they are using. Therefore, the only purpose of Clomid during a cycle is as an anti-estrogen. When To Start Clomid The correct time to commence Clomid depends on the type and cycle of steroids you have been using. Different steroids have different half-lifes (indicates the time a substance diminishes in blood), and Clomid administration should be taken accordingly. As we have seen above, Clomid taken when androgen levels in our blood are still high will be a waste. It is crucial to wait for androgen levels to fall before implementing our Clomid therapy. However, if taken too late we could possibly lose gains. The list below determines when you should start Clomid. Select from the list any steroids you've used in your cycle and whichever one has the latest starting point is the time to commence Clomid. For example, if Dianabol, Sustanon and Winstrol were cycled, the time for administering Clomid should be 3 weeks post cycle, as Sustanon remains active in the body for the longest period of time. Steroid Time after last administration Length of Clomid Cycle Anadrol50/Anapolan50: 8 - 12 hours 3 weeks Deca durabolan: 3 weeks 4 weeks Dianabol: 4 - 8 hours 3 weeks Equipoise: 17 - 21 days 3 weeks Finajet/Trenbolone: 3 days 3 weeks Primabolan depot: 10 - 14 days 2 weeks Sustanon: 3 weeks 3 weeks Testosterone Cypionate: 2 weeks 3 weeks Testosterone Enanthate/Testaviron: 2 weeks 3 weeks Testosterone Propionate: 3 days 3 weeks Testosterone Suspension: 4 - 8 hours 2-3 weeks Winstrol 8 - 12 hours 2-3 weeks How To Take Clomid Clomid has a long half-life (possibly 5 days), so there is no need to split up doses throughout the day. If Sustanon has been used and Clomid is commenced 3 weeks after the last injection, I would estimate that androgen levels are low enough to start sending the correct signals. If androgen levels are still a little high, we need to start at a high enough amount that will work or help, even if androgen levels are still a little high. Try 300mg on day 1; then use 100mg for the next 10 days; followed by 50mg for 10 days. Using HCG It is our opinion that HCG is probably one of the most misunderstood and misused compounds in bodybuilding. Hopefully this information will go some way towards rectifying that for the members of MuscleTalk. HCG stands for Human Chorionic Gonadotrophin and is not a steroid, but a natural peptide hormone which develops in the placenta of pregnant women during pregnancy to controls the mother's hormones. (Incidentally, this is the reason you may hear of people testing for growth hormone (HGH) with a pregnancy testing kit - If their HGH shows 'pregnant', they've been ripped-off with cheaper HCG - but we digress slightly). Its action in the male body is like that of LH, stimulating the Leydig cells in the testes to produce testosterone even in the absence of endogenous LH. HCG is therefore used during longer or heavier steroid cycles to maintain testicular size and condition, or to bring atrophied (shrunken) testicles back up to their original condition in preparation for post-cycle Clomid therapy. This process is necessary because atrophied testicles produce reduced levels of natural testosterone, this situation should be rectified prior to post-cycle Clomid therapy. HCG administration post-cycle is common practice among bodybuilders in the belief that it will aid the natural testosterone recovery, but this theory is unfounded and also counterproductive. The rapid rise in both testosterone, and thus oestrogen due to aromatisation, from the administration of HCG causes further inhibition of the HPTA (Hypothalamic/Pituitary/Testicular Axis - feedback loop discussed above); this actually worsens the recovery situation. HCG does not restore the natural testosterone production. The typically observed dosing of 2000 to 5000IU every 4 to 5 days causes such an increase in oestrogen levels via aromatisation of the natural testosterone that this has been responsible for many cases of gynecomastia. From the above discussion it is clear that HCG is best used during a cycle, either to: 1) Avoid testicular atrophy, or 2) Rectify the problem of an existing testicular atrophy. 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. |
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Originally posted by DrJMW I just finished reading ALR's book, Building the Perfect Beast. I highly recommend your reading this book. There was a line in this book that got me thinking about Nolvadex vs. Clomid. I still believe that HCG use--either throughout the cycle or during a distinct PCT cycle--is required. It is imperative to rapidly increase testicular mass. Now, previously, I was touting Nolvadex as the antiestrogen of choice to use along with the HCG. Nolvadex acts as an antiestrogen here to block new estrogen formation as a result of recovery and it stimulates the pituitary to begin releasing LH again. The only pitfall with using Nolvadex is that it does, in fact, reduce IGF-1 levels. This is important--we do not want to reduce IGF-1 levels..EVER. So, let's substitute Clomid in place of Nolvadex. I believe that, despite the debate of Clomid vs Nolvadex (effectiveness, sides, etc), lowering IGF-1 levels is taboo. Clomid does everything that Nolvadex does. Clomid has not been proven to lower IGF-1 levels, as far as I know. Thanks to ALR and his great book, Building the Perfect Beast. |
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Originally Posted by rhouser30
got a question alittle off topic but is most of this stuff gotten from overseas that is what i have seen, how legit is it?
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