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  1. hello, what would be a good pct after 10 weeks of winstrol and test prop cycle (both injectibles)? What do you suggest?
  2. G_nome76

    Injury break: TRT or PCT

    Going in to the VA Tomorrow to see if anything is broken don't think it is but just to be sure better safe than sorry now if I do have broken things and can't training should I PCT then when my test crash go in for blood work from my doc and try to get a script for pct? Thoughts, opinions, experiences... I'm 36 6'3" 280lbs and around 15-18% BF. Been lifting most my life been using gear off and on for around 5 years now. Sent from my iPhone using Tapatalk
  3. LittleTom

    Letrozole (Femera)

    Letrozole (Femara) belongs to a category and class of drugs known as aromatase inhibitors (AIs). Aromatase inhibitors belong to an even broader class of drugs known as anti-estrogens. The other subcategory of drug under the anti-estrogens category is known as selective estrogen receptor modulators (SERMs), such as Nolvadex and Clomid. AIs and SERMs make up anti-estrogens. Aromatase inhibitors differ greatly from SERMs in their action and how they deal with the issues of estrogen control. The misunderstanding that SERMs, such as Nolvadex and Clomid, serve to lower estrogen levels must first be addressed before delving into any further details. This is a persistent rumor among the anabolic steroid using community that has begun to erode as of late, but the rumor still persists. SERMs serve to block the action of Estrogen at the receptor sites in breast tissue by occupying the receptor sites in place of Estrogen so that Estrogen itself cannot exert its effects there through receptor site binding. Conversely, SERMs will also act as Estrogens at receptor sites at other cells in other areas of the body (the liver, for example in Nolvadex’s case). SERMs do not lower circulating levels of Estrogen in blood plasma. Aromatase inhibitors serve to do this by eliminating the production of Estrogen through binding to and disabling the aromatase enzyme, which is the enzyme responsible for the conversion (or aromatization) of androgens into Estrogen. Letrozole is a non-steroidal and non-suicidal aromatase inhibitor, and belongs to the third generation line of aromatase inhibitors. Letrozole is very identical to Arimidex and is one of the three major aromatase inhibitors available (Arimidex, Aromasin, and Letrozole). The difference between Letrozole and the other two major aromatase inhibitors is the fact that although it is utilized for the treatment of post-menopausal female breast cancer patients, it is actually specifically utilized for what is known as Estrogen receptor unknown breast cancer. This is a breast cancer condition in which the diagnosis indicates that it is unknown as to whether or not Estrogen is the culprit, or whether or not the breast cancer is aggravated by Estrogen. As with all other aromatase inhibitors, Letrozole is normally utilized after first-line treatments (such as Nolvadex) has failed, but various conditions may require Letrozole to be used as a first-line treatment, though this is rare. Letrozole was developed after Arimidex but before Aromasin, and it is the strongest and most potent of the three aromatase inhibitors by far. Novartis had manufactured the drug after it was approved for sale on the American prescription drug market in 1997, and was sold as the brand name Femara as well as a separate brand name Femar in certain other select countries across the world (mostly in a few countries in Europe). As with other aromatase inhibitors, it has become extremely widespread and common not only in North America, but also in international regions, countries, and markets where it is believed to be that well over 70 countries carry Letrozole, with the brand name Femara being the most popular and most widely used. In addition to the primary brand names, Letrozole can also be found as countless other generic brands. Letrozole (Femara) has caught on naturally with anabolic steroid using athletes, bodybuilders, and invidiuals, as is common with all aromatase inhibitors. This is because of the Estrogen controlling and reducing capability of Letrozole, which is favored in anabolic steroid users that are engaging in the use of aromatizable anabolic steroids (such as Testosterone,Dianabol, Equipoise, etc.) and that it can be effectively utilized to control issues resultant of excess Estrogen (bloating, blood pressure, gynecomastia, etc.). [h=3]Chemical Characteristics of Letrozole[/h] Letrozole (Femara) is a non-steroidal aromatase inhibitor. This is to say that it does not possess the characteristic four ring cycloalkane ring carbon structure common of all types of steroids, unlike the steroidal aromatase inhibitor Aromasin (Exemestane). [h=3]Properties of Letrozole[/h] Letrozole’s effects on serum Estrogen level control are perhaps the strongest and most effective of the three major aromatase inhibitors as noted in studies[1]. Even the informational pamphlets included with the pharmaceutical product have stated that at its standard tablet dose of 2.5mg is effective enough to reduce circulating Estrogen levels by an average of 78%. However, actual real clinical data has demonstrated far more effective reductions (remember that 78% is a determined average). Letrozole in studies has exhibited at least 98% reduction or more of serum Estrogen levels[2]. Letrozole can be so effective at inhibiting the aromatase enzyme and thereby reducing Estrogen levels that this compound is typically only administered to post-menopausal females, and/or utilized when other first-line treatments for breast cancer has failed. This is actually a common usage aspect of all three major aromatase inhibitors, as they are all very effective compounds for the purpose of Estrogen reduction, with Letrozole by far being the most effective. Arimidex and Letrozole are both classified as non-steroidal and non-suicidal aromatase inhibitors that compete with the substrate for binding to the enzyme active site. This is very different from Aromasin (Exemestane), which is a steroidal and suicidal aromatase inhibitor that acts as a mechanism-based steroidal inhibitor that mimics the substrate, is converted by the enzyme to a reactive intermediate, and results in the inactivation of the aromatase enzyme[3]. For ease of understanding, what this means to the layman is that Aromasin’s chemical structure resembles the traditional ‘targets’ that aromatase binds to (Testosterone, for example) and that it essentially ‘fools’ the aromatase enzyme into binding with it, only to become inhibited/deactivated. Because the binding strength is so great, this inhibition becomes permanent for the aromatase enzyme that Aromasin has become bound to. Arimidex and Letrozole, being non-suicidal aromatase inhibitors, both compete with the enzyme’s traditional ‘targets’ rather than being assured a permanent spot (which is the advantage that Aromasin has over the other two). Letrozole, as is common with all aromatase inhibitors has also demonstrated the ability to increase the endogenous production of LH (Luteinizing Hormone), FSH (Follicle Stimulating Hormone), and consequently, Testosterone levels in men, but this will be further covered in greater detail under the Letrozole doses section of the profile. Bodybuilders and athletes utilizing anabolic steroids will usually favor aromatase inhibitors such as Letrozole for its ability to eliminate risingEstrogen levels at its root cause: aromatase. By disabling the aromatase enzyme, supraphysiological levels of aromatizable androgens (such as Testosterone, Dianabol, Deca-Durabolin, etc.) cannot convert into Estrogen, thereby eliminating any possible risk of Estrogen-related side effects.
  4. Chief Swole

    PCT question

    I have a buddy on deca and test.. what would be a basic cheap pct?
  5. LittleTom

    HCG

    Chorionic gonadotropin is a hormone found in the female body during the early months of pregnancy (it is produced in the placenta). It is in fact the pregnancy indicator looked at by the over the counter pregnancy test kits, as due to its origin it is not found in the body at any other time. Blood levels of this hormone will become noticeable as early as seven days after ovulation. The level will rise evenly, reaching a peak at approximately two to three months into gestation. After this point, the hormone level will drop gradually until the point of birth. As a prescription drug, HCG offers us some interesting benefits. In the United States, we have the two popular brands, Pregnyl, made by Organon, and Profasi, made by Serono. These are FDA approved for the treatment of undescended testicles in young boys, hypogonadism (underproduction of testosterone) and as a fertility drug used to aid in inducing ovulation in women. When prepared as a medical item, this hormone comes from a human origin. Although there is often a fear of biological origin products, there is little research to be found regarding pathogen or sterility problems with HCG. The problems seen with human origin growth hormone are certainly not to be repeated with HCG, as this compound is obtained in a much different way. While HCG offers the female no performance enhancing ability, it does prove very useful to the male steroid user. The obvious use of course being to stimulate the production of endogenous testosterone. The activity of HCG in the male body is due to its ability to mimic LH (luteinizing hormone), a pituitary hormone that stimulates the Leydig's cells in the testes to manufacture testosterone. Restoring endogenous testosterone production is a special concern at the end of each steroid cycle, a time when a subnormal androgen level (due to steroid induced suppression) could be very costly. The main concern is the action of cortisol, which in many ways is balanced out by the effect of androgens. Cortisol sends the opposite message to the muscles than testosterone, or to breakdown protein in the cell. Left unchecked (by an extremely low testosterone level) in the body, cortisol can quickly strip much of your new muscle mass away. The main focus with HCG is to restore the normal ability of the testes to respond to endogenous luteinizing hormone. After a long period of inactivity, this ability may have been seriously reduced. In such a state testosterone levels may not reach a normal point, even though the release of endogenous LH has been resumed. Many who have suffered severe testicular shrinkage may be able to relate, as it is often some time before normal testicle size and feelings of virility are restored if ancillary drugs had not been used. The excessive stimulation brought forth by administration of HCG can likewise cause the testicles to rapidly return to their normal size and level of activity. We are not simply looking for it to fix the problem however, as the resulting high testosterone level can itself trigger negative feedback inhibition at the hypothalamus. Estrogen production is also heightened with the use of HCG, due to its ability to increase aromatase activity in the Leydig's cells'9. This is due to the main action of HCG, namely the increase of cycIicAMP (a secondary messenger that regulates cellular activity). When stimulated by HCG, the ability of the testes to aromatize androgens could potentially be heightened several times greater than normal. This also may inhibit testosterone production, so we therefore use HCG only as a quick shock to the testes. The usual protocol is to inject 1500-3000 I.U. every 4'" or 5t" day, for a duration usually no longer than 2 or 3 weeks. If used for too long or at too high a dose, the drug may actually function to desensitize the Leydig's cells to luteinizing hormone, further hindering a return to homeostasis. Timing the initial dose is also very crucial. If your were coming off a cycle ofSustanon for example, testosterone levels in your blood will likely stay elevated for at least 3 to 4 weeks after your last injection. Taking HCG on the day of your last shot would therefore be useless. Instead one would want to calculate the last week in which androgen levels are likely to be above normal, and begin ancillary drug therapy at this point. In this case HCG would be started around the third or fourth week. Likewise, after ending a cycle of Dianabol (an oral) your blood levels will be sub normal after the third day. Here you may want to begin HCG therapy a few days before your last intake of tablets, giving it a few days to take effect. One would also want to give some thought to the level of suppression that the cycle might have brought about. After an 8 week cycle of Equipoise® for example, 1500-2500 I.U. would likely be a sufficient initial dosage. The lower amount of hormonal suppression one associates with this drug would probably not require much more. On the other hand, 750-1000mg of Sustanonper week might incline the user to inject a much larger HCG dose, perhaps as much as 5000 I.U. for the opening application. It may thereafter also be a good idea to reduce the dosage on subsequent shots, so as to step down the intake of HCG during the two or three weeks of intake. As discussed above, HCG acts only to mimic the action of LH. It is likewise not the perfect hormone to combat testosterone suppression, and for this reason it is used most often in conjunction with estrogen antagonists such as Clomid®, Nolvadex® or cyclofenil. These drugs have a different effect on the regulating system, namely inhibiting estrogen-induced suppression at the hypothalamus. This of course also helps to restore the release of testosterone, although through a much different mechanism than HCG. A combination of both drugs appears to be very synergistic, HCG providing an immediate effect on the testes (shocking them out of inactivity) while the antiestrogen helps later to block inhibition on the hypothalamus and resume the normal release of gonadotropins from the pituitary. The typical procedure involves giving the Clomid®, Nolvadex® dose from the start with HCG, but continuing it alone for a few weeks once HCG has been discontinued. This practice should effectively raise testosterone levels, which will hopefully remain stable once Clomid®,Nolvadex® have been discontinued. While unfortunately there is no way to retain all of the muscle gains produced by anabolic steroids, using ancillaries to restore a balanced hormonal state is the best way to minimize the loss felt with ending a cycle.
  6. Guest

    Caber sides

    Anyone else have major leg/body trembling or shaking while on caber ? Especially when asleep, to the point where someone else might think you're possibly having a minor seizure. The only thing that has changed in my test subjects regimen, is from prami to caber. That's when it all seemed to have started. My test subject hasn't noticed it. But the case workers noticed it on the first night of administration. @.25 mg. then 2nights later a dose of .5 was given, again @ bedtime. The case worker on duty noted a abnormal sleep pattern was noticed, almost as if the test subject was having major restless leg syndrome. Again the worker noted that the subject was unaware of these involuntary movements and uncontrollable spasms.
  7. LittleTom

    Arimidex

    Arimidex is a very new drug developed for the treatment of advanced breast cancer in women. Its manufactured by Zenica Pharmaceuticals and was approved for use in the United States at the end of December 1995. Arimidex acts by blocking the enzyme aromatize, subsequently blocking the production of estrogen, since most breast cancer is stimulated by estrogen levels. This product is used during very high androgenic steroids such as Dianabol and testosterone where estrogen levels need to be watched because of gynecomastia and water retention purposes. Arimidex is a very new drug developed for the treatment of advanced breast cancer in women. Its manufactured by Zenica Pharmaceuticals and was approved for use in the United States at the end of December 1995;. Arimidex acts by blocking the enzyme aromatize, subsequently blocking the production of estrogen, since most breast cancer is stimulated by estrogen levels. This product is used during very high androgenic steroids such as Dianabol and testosterone where estrogen levels need to be watched because of gynecomastia and water retention purposes. Drug Dosage: Arimidex dosage of 1-2 tablets per day can produce estrogen suppression by 80% of some patients. Drug Side Effects: This drug is relatively mild, but when estrogen levels are decreased the risk of HDL levels can dramatically drop causing cholesterol problems.
  8. LittleTom

    Good Article on Blood Work

    If you want to use AAS safely, blood tests are essential. A pre-course check will warn of any reason not to use AAS at that time, and will give a baseline for comparison later on. It is also wise to check mid-cycle, when things should be at their worst from a health point of view. Finally, a test after PCT to ensure things have returned to normal. [h=2]Where to get private / anonymous blood work[/h] There are many services through out the world that provide individuals the capability to get anonymous and private paid blood work. These services are invaluable to AAS users to monitor our health and safety. [h=3]In the USA[/h] There are several providers in the USA to choose from. [h=4]Private Med Labs[/h] Private Medical Labs -- A good and trusted lab with many locations. Not available in some states due to state laws. Female Hormone Testing is recommended. Hormone Panel with F&T Testosterone LC/MS-MS is similar to the Female Hormone Panel but uses LC/MS for testosterone. This will provide an actual value rather than "> 1500". Anything with Test 070195 will show the actual value for testosterone, rather than "> 1500". Thyroid TSH, T4 and T3 Panel Liver Panel for you Oral users This is included in the Hormone Panel for Females. You do not need to order it separately. Lipid Test to check Cholesterol levels Anything with Test 303756 contains a lipid panel. The Hormone Panel Unisex panel includes thyroid, lipids, estrogen and F&T Testosterone LC/MS-MS. [h=4]LabsMD[/h] Hormone Panel for Females will provide the actual number for testosterone rather than "> 1500". The assay used for testing estradiol will not give a false reading when using tren. [h=4]Walgreens[/h] Cholesterol tests are available at most locations. Hormone testing is available at some Walgreens locations. [h=3]In the UK[/h] [h=4]Medichecks[/h] Medichecks [h=4]Blue Horzon[/h] Blue Horizon Medical [h=3]In Canada[/h] Related Post Unconfirmed: Go to a walk in clinic. When the doc comes in say you are taking a test booster and you feel moody and your nipples are sensitive. S/he will send you for a blood test. Make sure you say your nipples are sensitive or s/he wont check the e2 boxes on the form The forms are good for a year, so once you have them, just give blood when you want. [h=2]Blood Work Considerations[/h] [h=3]Tren[/h] When testing estrogen while running tren, make sure to get the LCMS estrogen reading. Most estrogen tests are ECLIA or RIA, which will count tren as estrogen. This will give you a false estrogen reading if you are trying to dial your AI in. [h=3]Other[/h] Of importance to look at is: LFT's or Liver Function Tests; fractionated cholesterol (HDL/LDL), and the relevant hormones. Below is a full list of recommended tests. Haematology: Measures haemoglobin, red blood cell numbers and size, as well as distribution of white blood cell types. Electrolytes and LFT's: gives information on liver and kidney function. Fractionated cholesterol: HDL/LDL ratio and triglycerides. Iron studies: Total serum iron, transferrin levels (the carrier protein) and ferritin (the tissue storage protein). Thyroid Function Tests: Include free T3 and T4 as well as Thyroid Stimulating Hormone (TSH). Cortisol Insulin and Glucose LH/FSH: The gonadotrophins that stimulate the testes to produce testosterone. Testosterone and SHBG: Free testosterone should be measured not calculated. Estradiol IGF-I (if available): Especially useful for those using hGH or hGH releasing peptides to measure effectiveness. A moderate rise will be seen with AAS use alone. Redditors in North America can access on-line blood tests at http://www.privatemdlabs.com/ and in Australasia at http://www.bloodworks.com.au/ Regardless of whether you get your bloods done by your local doctor or by an online service, you can get expert interpretation of blood tests either re-cycle, mid-cycle, or after PCT at http://www.bloodworks.com.au/ (Please mention Reddit to receive this service for AUD$80). hGH/IGF-1 hGH stands for human Growth Hormone a 171 amino acid polypeptide hormone released from the Anterior Pituitary gland in the brain. Its release is controlled by at least two hormones from the Hypothalamus...GH Releasing Factor and Somatostatin. GHRF stimulates GH in a pulsitile manner, while Somatostatin inhibits it's release. IGF-I, which is released from the liver into the circulation in response to GH release, is also thought to inhibit GH release in a negative feedback loop. IGF-I is thought to mediate many of the effects of hGH... and in response to hGH, muscle and many other tissues, can make their own IGF-I inside the cells. The resultant IGF-I synthesis effects both neighboring cells, and the cell itself via the Akt pathway (autocrine/paracrine secretion). Some of those neighboring cells in muscle are satellite cells, which are stem cells present inside the muscle sarcolemma, but outside of the actual muscle cells. IGF-I has the effect of increasing their number, and to differentiate (change them) into muscle cells. The satellite cell changes into a myoblast (primitive muscle cell) which then fuses into an existing fibre (particularly an inured one) and donates its nucleus. When a muscle has to grow or repair, it requires more DNA which is donated by the satellite cells. This is to keep the protein/DNA ratio constant as a cell grows. Skeletal muscle is unusual in that it is a multi-nucleated cell. This is thought necessary as skeletal muscle cells are so relatively large that one nucleus could not adequately serve the whole cell. The effects of IGF-I administration for BB purposes are controversial in terms of efficacy of low (microgram) dosages. In clinical trials it has been used in the range of 8-10 milligrams per day. There seems to be a great disparity here between anecdotal reports and published studies. While the effectiveness of direct IGF-I administration is debated, the use of synthetic recombinant hGH is clear. It has been shown that doses upwards of 4 iu/day confer significant anabolic effects in muscle. Does this increase in muscle size relate to an increase in strength? Research says yes, but not as much of an increase in strength as seen with AAS. That is the strength per cross sectional area will increase in response to androgens, while remaining fairly constant for hGH administration. This has been put down to the synthesis of non-contractile elements, such as collagen. GHRP's GHRP's are peptide hormones (short chain of amino acids) that stimulate either directly or indirectly hGH release in humans. GRP6 or GHRP2 are relatively short acting, while CJC1295 is longer acting. GHRP6 stimulates Gherelin release, resulting in hunger. GHRP2 does not have the same effect on Gherelin, but like GHRP6, it elevates cortisol. Ipamorelin stimulates GH release without the increases in Gherelin and cortisol seen with the others. Myostatin Inhibitors: Myostatin is a protein hormone that stops muscle growing too big. It is thought that most organs, including skeltal muscle, have a specific growth regulating protein. In Skeletal muscle, that is myostatin or GDF8, Growth and Development Factor 8. So if myostatin stops muscles from growing too big, why not suppress or inhibit it? There is much research to try and accomplish this in humans without side effects. There are three viable methods for myostatin inhibition. Firstly, there is the antibody approach. This entails injecting a monoclonal (very specific) antibody into a subject, which will bind to, and tie up circulating myostatin levels. (see MYO-029:http://en.wikipedia.org/wiki/Stamulumab) Secondly, there is the "small molecule approach" that use inhibitors of the myostain receptor, such as SB 431 542 and GW 788 388. These receptor inhibitors act in a similar manner to Nolvadex as a blocker of the estrogen receptor. It won't reduce the amount of myostatin, but it will block its effects at the receptor level. Thirdly, there is the use of a soluble portion of the receptor (ActIIb receptor), which mops up myostatin in the blood and acts essentially as a binding protein for myostatin. Analogous to SHBG, which we are all familiar with, which mops up (binds) testosterone and its analogues in the blood. ActIIb receptor binds too and deactivates myostatin. The Activin receptor and the myostatin receptor are essentially the same thing. http://www.reddit.com/r/steroids/comments/1vysry/so_you_got_your_blood_work_but_what_does_it_all/
  9. LittleTom

    Clomid

    Clomid (Clomiphene Citrate) belongs to a category and class of drugs known as selective Estrogen receptor modulators (SERMs). Selective Estrogen receptor modulators belong to an even broader class of drugs known as anti-estrogens. The other subcategory of drug under the anti-estrogens category is known as aromatase inhibitors (AIs), such as Aromasin (Exemestane) and Arimidex (Anastrozole). AIs and SERMs make up anti-estrogens. Aromatase inhibitors differ greatly from SERMs in their action and how they deal with the issues of estrogen control. The misunderstanding that SERMs, such as Nolvadex and Clomid, serve to lower estrogen levels must first be addressed before delving into any further details. This is a persistent rumor among the anabolic steroid using community that has begun to erode as of late, but the rumor still persists. SERMs serve to block the action of Estrogen at the receptor sites in breast tissue by occupying the receptor sites in place of Estrogen so that Estrogen itself cannot exert its effects there through receptor site binding. Conversely, SERMs will also act as Estrogens at receptor sites at other cells in other areas of the body (the liver, for example in Nolvadex’s case). SERMs do not lower circulating levels of Estrogen in blood plasma. Aromatase inhibitors serve to do this by eliminating the production of Estrogen through binding to and disabling the aromatase enzyme, which is the enzyme responsible for the conversion (or aromatization) of androgens into Estrogen. Clomid was developed and approved for use in the early 1970s for the treatment of female infertility (and later on subsequently expanded to treating male infertility as well). Not too long after its release in the United States, its popularity and use spread internationally where, like Nolvadex, its popularity and rate of use is so massive that it is widely and freely available in the majority of countries and regions across the world under an almost infinite number of brand names as well as generic products. Its popularity and cheap cost make it a very easily attainable compound for both medical use as well as off-label use for the anabolic steroid using community. Clomid, although it is classified as an anti-Estrogen, is actually utilized for the treatment of female infertility resulting from ovulation failure (anovulatory infertility). Although Clomid is a very close relative to Nolvadex with both belonging to the SERM category of drugs, Clomid in reality operates at a much poorer efficiency compared to Nolvadex in regards to its Estrogen antagonistic activity in breast tissue. This is to say that it is a weaker Estrogen blocker in breast tissue, where Nolvadex is much better suited for this task. Instead, Clomid’s prime application in medicine is that of a non-steroidal ovulatory stimulant for women. Because Clomid is a SERM, like Nolvadex, it exhibits mixed Estrogen agonist and antagonist effects in various tissues of the body. Like Nolvadex, Clomid acts as an Estrogen antagonist in the hypothalamus, pituitary gland, ovaries, endometrium, vagina, and cervix. This is to say that in these tissues and areas of the body, Clomid serves to mitigate (inhibit or block) the action of Estrogen. In males as well as females, its Estrogen antagonistic effect on the hypothalamus will trigger a release of LH (Luteinizing Hormone) and FSH (Follicle Stimulating Hormone). These two hormones in men are the signal hormones that signal the testes to begin or increase its production of Testosterone, and this total process is known as the HPTA (Hypothalamic Pituitary Testicular Axis). In females, this same action occurs, except LH and FSH will trigger the release of eggs from from the ovaries (known as follicular rupture), which would lead to increased chances of contraception. This total process in females is known as the HPOA (Hypothalamic Pituitary Ovarian Axis). Much like Nolvadex, Clomid is what would be considered an Estrogen that acts as a ‘fake’ Estrogen in areas of the body, such as breast tissue (so as to block the effects of ‘real’ Estrogen, while it also works as an actual Estrogen in other areas of the body. This is another manner of describing the agonistic/antagonistic nature of Clomid in regards to Estrogen. For anabolic steroid using athletes and bodybuilders that are for the most part males, Clomid can serve as an effective anti-Estrogen for the purpose of mitigating one particular unwanted side effect of Estrogen as a result of the use of aromatizable anabolic steroids (such as Testosterone, Dianabol, Boldenone, etc.). This particular unwanted side effect is that of gynecomastia, which refers to the development of breast tissue resulting from excess Estrogen levels in body. Because of Clomid’s Estrogen antagonistic effects on the hypothalamus resulting in the increased production of gonadotropins LH and FSH, Clomid can effectively be utilized to increase endogenous Testosterone production in males. This is especially important for anabolic steroid using individuals that wish to restore proper hormonal function during the weeks following the conclusion of an anabolic steroid cycle, a period known as PCT (Post Cycle Therpay). The traditional protocol for such a use is that of a combination of Nolvadex, Clomid, and HCG (Human Chorionic Gonadotropin) for the duration of several weeks, and although much better more modern protocols have been developed, this long-standing traditional PCT protocol is still effective. The use of Clomid for this purpose will be covered in further detail under the Clomid doses section of this profile. All of the tripohenylethylene compounds under the SERM family (Nolvadex, Clomid, and Toremifene) also exhibit Estrogen agonistic effects in the liver, meaning the liver is one such area of the body where SERMs such as Clomid (Clomiphene Citrate) will act as an Estrogen rather than block Estrogenic activity there. In studies, this has shown to be a beneficial aspect of SERMs, as Estrogens as well as Estrogen agonists (such as Clomid and Nolvadex) impart a positive effect on cholesterol values through actions in the liver. This is the reason as to why the reduction of Estrogen levels through the use of an aromatase inhibitor (AI) is not always the best decision, as the reduction in Estrogen often results in negatively impacted cholesterol profiles as demonstrated anecdotally as well as in clinical studies. [h=3]Chemical Characteristics of Clomid[/h] Clomid (Clomiphene Citrate) is a non-steroidal selective Estrogen receptor modulator (SERM) that possesses both mixed agonistic as well as antagonistic properties in relation to Estrogen in different areas of the body. Clomid belongs to a family of compounds known as triphenylethylene compounds, of which Nolvadex (Tamoxifen Citrate) is also a member of, and a very closely related compound to Clomid. [h=3]Properties of Clomid[/h] Clomid’s primary use within the medical field is that of a fertility drug in females but also among males as well. It has already been established that Clomid, being a SERM, does not reduce circulating Estrogen levels in the body, but instead serves to occupy the receptor sites in breast tissue so that Estrogen itself cannot bind to these receptors due to Clomid’s stronger binding strength to it. In layman’s terms, Clomid essentially acts as a ‘fake’ Estrogen that acts as a placeholder at the receptor sites in breast tissue. As a result, Estrogen cannot activate gene transcription in the cells there in order to formulate gynecomastia, and any existing Estrogen that has already bound to receptor sites will essentially be ‘forced’ out of the receptor sites by Clomid which then occupies the receptor site instead. However, it must be noted that Clomid’s action in this area is far weaker and less efficient than its close relative compound Nolvadex, which serves as a better choice for this purpose. Although Clomid could indeed be utilized by anabolic steroid using individuals that wish to prevent or eliminate and reverse formulatinggynecomastia in its early stages, its more effective and promising role is that of an endogenous Testosterone production stimulating compound. This is the primary purpose and function of Clomid among anabolic steroid using athletes and bodybuilders, and is the primary desired effect in this sense. It must be noted, however, that research has also demonstrated various advantages that Nolvadex does possess over Clomid in this sense as well, which will be further covered in the next section of this profile. As a SERM, Clomid will not serve to block or reduce any other Estrogenic side effects, however, as it serves only to block Estrogenic activity at the breast tissue area (when major Estrogenic side effects are concerned). Clomid does not (nor do any SERMs) serve to reduce bloating,water retention, rising blood pressure (as a result of water retention), or acne formation – these are all side effects resultant from increasing blood plasma Estrogen levels.
  10. LittleTom

    Clomid

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