posted May 16, 2000 07:39 AM            

If I must take the proviron, when should I start taking it, hal way through ?
And how much>?
before a meal?
after?
On an empty stomac?
there is some stuff who
have these restriction for better absorption.
Please help!

posted May 16, 2000 07:48 AM            

cause i assume by 250 you mean some kind of test so you should take clomid 50mg EOD
then 100mg ED at end of cycle for 2to3 weeks

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Check out my HardCore Pic sitehttp://www.dell.homestead.com/conan/index.html "When I give the signal, unleash HELL!" -Maximus

posted May 16, 2000 08:42 AM            

it was real good and it basically shows that
proviron is not as efffective

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Check out my HardCore Pic sitehttp://www.dell.homestead.com/conan/index.html "When I give the signal, unleash HELL!" -Maximus

posted May 16, 2000 08:47 AM            

As can be surmised by the commonly used term anti-estrogen, the primary goal of therapy with an estrogen maintenance drug is to block the side effects associated with this hormone from becoming apparent during ******* use (though often they are also used at the conclusion of a cycle to help restore the release of endogenous testosterone). For the purpose of combating estrogen a number of substances have been used successfully over the years, and more have recently become available due to advances in the field of breast cancer research (treatment of breast cancer is the primary clinical use for most of these agents). Likewise the athlete now has several pharmaceutical options to select from when shopping, which can make the choice of what drug may be best for any particular case a confusing one. Since a number of issues including cost, availability, potential side effects and efficacy may factor into this decision, I thought a closer look at both the old and newer agents might be in order.
Aromatization is the technical term for it. It is a natural process in which an androgen (male sex hormone) such as testosterone can be converted to an estrogen (female sex hormone) in the human body. In normal situations of course the male body will produce estrogens only in very small amounts, though they still do play an important role metabolically (including visceral/organ fat disposition, bone growth/maturity and blood lipid regulation). Athletes however may find that estrogen can become an extremely dramatic problem with the administration of anabolic/androgenic *******s. With the natural process of aromatization in place, and extremely heightened androgen level can result in a troubling buildup of estrogens. This may cause the onset of estrogen related side effects such as noticeable fat and water retention, as well as the buildup of female breast tissue (gynecomastia). Gynecomastia is a particularly upsetting occurrence for the *******-using male athlete, as the characteristic unsightly buildup of tissue mass is usually permanent. Although many synthetic anabolic agents are resistant or not open to the process of aromatization at all, our standard bulking drugs such as testosterone and Dianabol are still readily aromatized. This has prompted the athletic community to seek the benefit of estrogen maintenance drugs when taking such *******s, a class of medications that are now considered standard remedies in the athletes' drug arsenal.

Nolvadex and Clomid (estrogen receptor antagonists)

Estrogen receptor antagonists, more simply referred to as anti-estrogens (though this term is often loosely applied to all estrogen maintenance drugs), are drugs that block estrogens from exerting activity in the body. This is actualized by the ability of a particular substance to bind to a segment of the estrogen receptor, yet not activate it. This in turn prevents other estrogens from binding and activating the same receptor site. In a clinical setting an estrogen antagonist, most prominently the drug tamoxifen citrate (sold under the brand name Nolvadex) is typically used as the first line of defense during advanced breast cancer therapy. Its use can efficiently deprive estrogen responsive cancer cells of necessary hormone, allowing a high rate of response in patients with such forms of cancer. Stronger agents such as aromatase inhibitors (discussed below) are usually a second choice, substituted when conventional antiestrogen therapy fails to elicit the desired response.

A drug like tamoxifen is preferred over other agents as the first course of breast cancer treatment for a number of reasons, most due to the fact that that it is both extremely effective yet does not inhibit the actual formation of estrogen in the body. Among other things, this may allow Nolvadex therapy to be somewhat more comfortable for the patient. Although many women (particularly pre-menopausal) seem to suffer menopausal-like side effects with virtually all estrogen maintenance drugs, estrogen antagonists are often somewhat more tolerable than agents that block the synthesis of estrogen. In fact the activity of tamoxifen is itself variable, such that in certain target tissues it may actually act as an agonist (activator) of the estrogen receptor. It therefore does not completely diminish the biological activity of estrogens, though it does considerably reduce it nonetheless.

It is also well understood in medicine today that estrogens play a supportive role in the cardiovascular system. For example, studies show that a rise in the estrogen level (as in post-menopausal estrogen replacement therapy) is typically linked with a reduction in LDL (bad) cholesterol, and a rise in HDL (good) cholesterol. The ability of tamoxifen to act as an estrogen agonist in the liver likewise gives it what may be its most welcome property, namely that it exhibits an estrogenic, rather than antiestrogenic, effect on blood lipid (cholesterol) values. As a 1998 study by the Department of Clinical Oncology in the Netherlands Cancer Institute shows, during long-term treatment with tamoxifen (6 months) a lowered LDL cholesterol level, and significantly elevated HDL cholesterol level and HDL-C/total-cholesterol ratio may result. This trend should reduce an important risk factor for heart disease, obviously a welcome effect during treatment. For the *******-using athlete already faced with negative alterations in lipid profiles, such an effect could obviously an important consideration.

Clomid (clomiphene citrate) is very similar in structure to Nolvadex, both drugs being classified as triphenylethylene compounds and used clinically for similar purposes (breast cancer as well as female infertility treatment). As well as we see with Nolvadex, Clomid is a partial agonist/antagonist of the estrogen receptor depending on the target tissue in question. Although athletes most commonly think of Clomid as a testosterone-stimulating drug only (another effect of antiestrogenic compounds), to be used at the conclusion of ******* treatment, its activity in the human body is not at all dissimilar to Nolvadex. It should likewise be thought of not as a drug with its own niche of use, but instead as another efficient remedy for gynecomastia similar to Nolvadex (with the related ability to support the release of testosterone). It could clearly replace Nolvadex as a preventative measure against gynecomastia during cycles with aromatizable *******s without noticeably altering the level of effect received, just as Nolvadex can be used effectively to increase the synthesis of testosterone in the body at the conclusion of ******* use (though admittedly Nolvadex may be slightly more potent in both regards)

Aromatase Inhibitors

Aromatase inhibitors are another, perhaps more direct, way of dealing with estrogen in the body. Instead of blocking estrogen at its receptor, these agents have the more direct task of targeting the enzyme responsible (aromatase) for the biosynthesis of estrogen. By inhibiting this enzyme, circulating levels of estrogen can be efficiently and significantly reduced. This class of drugs seems to be the current area of focus for many in the medical community, as a dependable inhibitor of aromatase can potentially offer more to patients with related forms of cancer than antiestrogenic agents. Athletes will likewise find that the more recently developed aromatase inhibitors are the most potent remedies available for the prevention of related side effects.

Before detailing the various inhibitors of aromatase it is important to discuss further the potential drawbacks to this type of therapy. The most prominent being a negative impact on cholesterol profiles. Although ******* use is of course expected to negatively effect cholesterol levels, we find that when aromatization is inhibited this harmful tendency is greatly enhanced. A study published in 1990 shows this possibility very clearly. During this 12-week investigation the effects of testosterone enanthate (280 mg weekly) were compared to the effects of the same dose combined with an aromatase inhibitor (testolactone 250mg 4 times daily). The group taking testosterone only displayed no significant decrease in HDL cholesterol values during the course of treatment, whereas the group combining the dose with testolactone already noted a marked reduction (25%) by the fourth week of therapy. Clearly those concerned about the possibility of heart disease (especially those with poor lipid values to begin with) might want to think twice before simply using an aromatase inhibitor during ******* cycles.

Alternately choosing an antiestrogen such as Nolvadex however does not offer us a 100% guarantee that lipid values will not worsen over using no estrogen maintenance drug at all. In studies combining tamoxifen with estrogen replacement therapy for instance, it was shown that this compound could interfere with the beneficial effects of estrogen-based drugs on lipid values, though not completely diminish them. Since the effects of Nolvadex during treatment with a ******* such as testosterone have not been fully investigated (admittedly it is a small and not legitimately supported corner of use for tamoxifen), it remains to be seen whether or not it is truly beneficial in terms of lipid values when given with an aromatizable *******. For now however, should an estrogen maintenance drug be indicated, we can still consider it to be a safer alternative to any of the following aromatase inhibitors.

Teslac (testolactone)

Testolactone is a *******al aromatase inhibitor, structurally similar to testosterone. It was first made available in the 1960's, at a time when conventional breast cancer therapies included androgenic *******s. It was developed in an effort to produce an effective agent for breast cancer that was devoid of virilizing activity, and to that end testolactone fits well; it is completely devoid of androgenic activity (at high doses its activity is in fact antiandrogenic). It is quite interesting to note that it was not discovered to act by inhibiting aromatase until 1975. By this time testolactone had already fallen out of favor with the medical community, due in part to its low rate or response, as well as the utilization of stronger agents such as aminoglutethimide.

Although testolactone may still be available, it is a poor choice for the athlete. There are just too many drawbacks to its use. It is expensive, and studies show that 4 tablets (1000mg) are typically needed each day for a sufficient level of estrogen suppression. It may also be an antagonist of the androgen receptor to some extent, certainly an unwanted effect for the ******* user. Being a testosterone derivative it is additionally a controlled substance in the Unites States. Though it does admittedly work as a weak aromatase inhibitor, the hassle of obtaining it combined with the obvious greater effectiveness of other agents such as tamoxifen make it a rare find these days.

Cytadren (aminoglutethimide)

Aminoglutethimide is another of the earliest to be developed aromatase inhibitors, and was also the first drug to gain widespread acceptance for this purpose. Like testolactone, it was also made available as a prescription drug long before its mechanism of action was fully understood. In fact it has quite an interesting history. This compound, a derivative of the hypnotic glutethimide, was first sold in the United States as an anticonvulsant medication in 1960. By 1966 however, adrenal insufficiency was being reported in patients taking the drug and it was soon taken off of the market. Studies began looking at this compound in a new light not long after though, eventually warranting its return to the market. Aminoglutethimide ultimately came to be of the most prescribed and researched aromatase inhibitors available. Its effect on cortisol secretion also makes it an effective treatment for an illness such as Cushing's syndrome, where the body over produces cortisol.

Developing a proper dosage regimen for aminoglutethimide has also proven to be a confusing process. When first being applied to patients it was shown to be only transiently effective at lowering inhibiting adrenal ******* secretion (typically lasting for only for 3-7 days). Dubbed the adrenal escape phenomenon, it was shown that the body would notice the lowered output of cortisol, and triggers the heightened release of ACTH (adrenocorticotropic hormone) in response. This restores the normal release of adrenal *******s and nullifies the effect of aminoglutethimide. Clinically a small dose of hydrocortisone (40mg) is used to avoid this response, which for some time had also been the accepted practice for use in breast cancer treatment.

In later studies however, we find that the main mechanism in which this drug benefits breast cancer patients (inhibition of peripheral aromatase activity) is different from that which interferes with adrenal hormones. We also see that the dosage was important in triggering each particular response. It appears that aromatase inhibition is achieved at a much lower dose than is needed to block ******* production by the adrenal gland. While a daily dosage of 1000mg is typically needed to inhibit the demolase enzyme (the enzyme responsible for converting cholesterol to pregnenolone, and the target when reduced adrenal output is needed), maximum suppression of aromatase and estrogen levels is achieved at a dosage between 250 and 500mg (a point where adrenal ******* blockage should not be noted). There also seems to be no added benefit by adding cortisol in terms of survival/response rate among patients, and subsequently there is need to supplement cortisol when taking this drug for the purposes of inhibiting aromatase (nor for the athlete to implement a rotating dose schedule). Another suggested athletic use however remains to be that of an anti-catabolic, which is discussion in of itself.

In effectiveness this compound rates highly, with aromatase activity shown to decrease as much as 92% after administration of only 250mg. Patient response studies also show aminoglutethimide to be at least as effective as tamoxifen therapy in treating estrogen dependent cancer cells, more so under certain conditions. However, due to its discussed broad range of activity, including the potential inhibition of not only cortisol and estrogens but also aldosterone and androgens as well, it is not regarded as highly in terms of patient comfort. This is not to give the impression that complaints are very common though, as aminoglutethimide still has an extremely good safety record. Athletes can likewise consider it to be an extremely effective remedy for estrogenic side effects should it be available on the black market, at least as much so as Nolvadex.

Proviron (mesterolone)

Proviron is not technically classified as an anti-aromatase, but is an oral androgenic *******. Specifically it contains a derivative of the potent ******* dihydrotestosterone, differing only by the addition of 1 methylation (the same alteration used to increase the oral efficacy of Primobolan). Its use as an antiaromatase stems from studies showing a nonaromatizing androgen such as dihydrotestosterone may interfere with this enzyme reaction. It is believed to interfere with aromatase by competing with an aromatizable ******* such as testosterone for binding to the enzyme site. With dihydrotestosterone (or Proviron) interacting with this enzyme, yet producing no reaction, the enzyme is temporally prevented from altering other hormones, and an anti-estrogenic effect is achieved. Overall however, Proviron is much less reliable than any one of the mentioned antiestrogens or aromatase inhibitors. Though it may add some benefit when taken concurrently with a drug such as tamoxifen (though in such a case tamoxifen would be doing most of the work), I don't think that it is potent enough as an aromatase inhibitor to recommend using along during strong cycles. As with testolactone, Proviron also has the added drawback of being a controlled substance. Likewise it is often harder to obtain than many of the other agents.

Arimidex (anastrozole)

Anastrozole is a much more recently developed, selective, non-*******al aromatase inhibitor. It represents quite an advance in breast cancer treatments, as it can efficiently block aromatase activity without affecting enzymes involved in the biosynthesis of other adrenal *******s (hence the term selective). Its activity is therefore much more specific than aminoglutethimide, a trait that also makes it more tolerable for the patient. Numerous studies also support the superiority of this inhibitor over previously prescribed treatments, including many in which patients responded favorably to anastrozole (as a second-line therapy) after ceasing to respond to tamoxifen. In fact of all the aromatase inhibitors discussed in this article, Arimidex is shown to be the most effective and reliable.

The recommended dosage for anastrozole clinically is a single 1mg tablet daily. This is the lowest dose shown to produce maximum suppression of estrogen levels, and to spite expectations of greater results, doses of up to 10mg daily were not shown to appreciably increase the long-term response rate. In many cases the 1mg dose will produce estrogen suppression near 100%, so there seems to be little need for the athlete to venture higher. Price would probably prevent such experimentation in any event, as this new therapy is quite expensive. While tamoxifen will typically cost no more than $1-1.50 dollars per tablet, the price can be as high as $10 for anastrozole. This has prompted some to tinker with lower dosages (1/2 tablet daily) or alternating schedules (often in conjunction with tamoxifen) in order to stretch the money a little further.

Formestane (4-OH androstenedione)

Formestane is the first in a new line of selective, *******al-based aromatase inhibitors. It is currently available in a few European countries, and is expected to reach U.S. shelves before long. Formestane is structurally a derivative of androstenedione, most specifically 4-OH androstenedione. Androstenedione is a readily aromatized *******, so clearly this similarity welcomes interaction with the aromatase enzyme. Its activity in the body is in fact that of a suicide inhibitor, meaning that the compound will become inextricably bound to the aromatase enzyme upon contacting it. Its effect is therefore comparatively much more lasting than that seen with reversible, competitive inhibitors. This is no doubt the reason formestane was shown in studies to be as much as 60 times more potent than aminoglutethimide. As with Arimidex, this compound can help achieve near total suppression of aromatase.

Due to poor oral bioavailability, formestane is commercially prepared as an injectable product. The typical recommendation is an injection of 250mg (typically 1 ampule or injection) every two weeks. Though estrogen suppression can be marked with this dosing pattern, some studies do suggest that by the second week (near the time the dosage is to be repeated) estrogen levels may begin to recover. Although a more frequent schedule may provide more stable results, again cost is a prohibiting factor. I am looking at a current mail-order list in which a single 250mg ampule of formestane sells for $249. This would equate to a monthly expense of around $500, roughly twice the cost of the recommended anastrozole dose. It is of course also very doubtful that, with the high potency of this compound, an athlete would ever have trouble with the recommended schedule.

The BEST estrogen maintenance drug?

Clearly there is more to consider in choosing an estrogen maintenance drug than just which is the most effective. The discussed differences in cholesterol alterations between anti-estrogens and aromatase inhibitors for example are worth taking into account. In this regard an antiestrogen such as tamoxifen or clomiphene would be most preferred. Cost may also be important for many, as the newer selective aromatase inhibitors can cost between $250 and $500 per month. This is in great contrast to aminoglutethimide, Nolvadex or Clomid, which can cost $100 or less monthly. By measure of which is the most efficient remedy for estrogenic side effects, it would seem that Arimidex and formestane would technically be the most effective. Though more expensive, formestane was actually shown to be slightly less reliable than Arimidex in head to head studies, so its higher price should not automatically lead us into thinking it is the superior of the two. Ultimately however, it is doubtful that either of the new selective aromatase inhibitors (or other related agents slated to be released) will prove to be leagues ahead of the already tried and accepted estrogen maintenance drugs Nolvadex, Clomid and aminoglutethimide in the eyes of athletes. This is simply because the mentioned agents all deal with the action/buildup of estrogen quite effectively (in terms of clinical effectiveness of three agents compare closely to the new selective inhibitors), and outside of a medical setting the high cost of these newer agents will likely prohibit wide spread use.

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Check out my HardCore Pic sitehttp://www.dell.homestead.com/conan/index.html "When I give the signal, unleash HELL!" -Maximus

posted May 17, 2000 09:31 AM            

SO WHEN AND HOW SHOULD I TAKE IT??????

I originally bought it in cae of gyno..that's all, nothing else, buit now i found out i could make me harder and denser and make me loose water, so probably a good idea to take it at the end, or only stat if I feel pain or tingling in the tits as a sign of possible gyno coming.
I just don't wanna make my testo weaker, since i don't take that much(testoviron depot 250---500mg/week--i was told the half life will pyramid it for me)..then take HCG to start my testes off at the end

it's so contracdictory on the board sometimes--some people say proviron is bettr ,others say novaldex is(for anti gyno purposes)
it's very confusind to get mixed uop answers..how do I decide then>?????
...I don't want ot hear to get rid of it...good answer..

sorry,i'm grouchy a bit--just was at the dentist had a dead nerve in a tooth pulled and it's inflammed...so bare with me ok