General advice for TRT and Anabolic Steroid use
  1. If my joints are hurting I will add Nandrolone. If I want some horsepower I will add more Testosterone. If I add an oral it will be D-bol. If I want body recomping I will add Tren.

    Deca @ 3 mg/kg a week(about 270 mg/wk for a 200 lb male) will increase procollagen III levels by 270% by week 2. Procollagen III is a primary indicator used to determine the rate of collagen syn. As you can see, deca is a very good drug at giving you everything you want -- an increase in collagen synthesis, an increase in skeletal muscle, and increases in bone mass and density. The one thing it does not give you is wood!  Usual dosage for joint and ligament protection 100-200 mgs IM weekly. To plan a cycle where the goal is to increase skeletal muscle mass/strength while at the same time increase joint/tendon/ligament strength, enough to keep up with the dramatic increase in skeletal muscle, you must choose drugs like Eq, Deca, Anavar, or Primo as the base of your cycle. Testosterone and its esters can be added to your cycle to keep levels within a 'normal' physiological range (ie, 100-200 mg/wk) but must not go above this. Since drugs like eq, deca, anavar and primo will reduce endogenous, natural levels of test, these levels may be maintained with exogenous test in the 100-200 mg/wk range. Test at this dose will not inhibit collagen syn, but paradoxically, will help increase it. It is when exogenous testosterone is used > 200 mg/wk that collagen syn is inhibited.

  2. I never go lower than 250mg weekly on T but I prefer 300mg. I have used high strength test creams but I would rather pin. I would never recommend using less than 200mg T weekly for TRT.

  3. I always run HCG with my T and I like AI's to control estro. I only use SERM's like Nolva for emergency gyno treatment or Clomid for PCT. I sometimes use T3 and rarely HGH.

  4. Testosterone, HCG, Aromasin and an occasional Cialis. For older guys there is nothing like T and dialed in ancillaries. My favorite stacks are always sex drive friendly.
Ideal Hormone and Testosterone Levels to Shoot For:

- Total Testosterone 800 - 1,000 ng/dl

- Free Testosterone 250 - 300 pg/ml (for most men over age 40 is to be in the upper one-third tes-tosterone range of the 21- to 29-year-old group. Based on the following reference range chart from LabCorp, this means that optimal free testosterone levels should be between 21-26.5 nanogram/dL in aging men).

- Estradiol(E2) 20 - 30 pg/ml

- SHBG 10 - 30 nmol/l

- DHT 60 - 70 ng/dl

- Prolactin 2 - 3 ng/ml

- DHEA-S ~ 300 ug/dl

- PSA Under 2.6 ng/mL
- (optimal range)
Standard reference range is up to 4, but if your level is persistently 2.6 or above, have a blood test to measure the percentage of free vs. bound PSA and a digital rectal exam to help rule out prostate cancer.

My New TRT Protocol Paper

The pictures above of Sylvester Stallone are self explanatory for a man of over 60years young!

This paper is about to be published in The American Academy of Anti-Aging Medicine 2004 Clinical Updates:


By John Crisler, DO

In my paper “My Current Best Thoughts on How to Administer TRT for Men”, published in A4M’s 2004/5 Anti-Aging Clinical Protocols, I introduced a new protocol where small doses of Human Chorionic Gonadotrophin (HCG) are regularly added to traditional TRT (either weekly IM testosterone cypionate or daily cream/gel). The reasons and benefits of this protocol are as follows, along with a new improvement I wish to share:

Any physician who administers TRT will, within the first few months of doing so, field complaints from their patients because they are now experiencing troubling testicular atrophy. Irrespective of the numerous and abundant benefits of TRT, men never enjoy seeing their genitals shrinking! Testicular atrophy occurs because the depressed LH level, secondary to the HPTA suppression TRT induces, no longer supports them. It is well known that HCG—a Luteinizing Hormone (LH) analog—will effectively, and dramatically, restore the testicles to previous form and function. It accomplishes this due to shared moiety between the alpha subunits of both hormones.

So, that satisfies an aesthetic consideration which should not be ignored. Now let’s delve into the pharmacodynamics of the TRT medications. For those employing injectable
testosterone cypionate, the cypionate ester provides a 5-8 day half-life, depending upon the specific metabolism, activity level, and overall health of the patient. It is now well-established that appropriate TRT using IM injections must be dosed at weekly intervals, in order to avoid seating the patient on a hormonal, and emotional, roller coaster. Adding in some HCG toward the end of the weekly “cycle” compensates for the drop in serum androgen levels by the half-life of the cypionate ester. Certainly the body thrives on regularity, and supplementing the TRT with endogenous testosterone production at just the right time—without inappropriately raising androgen OR estrogen (more on that later)—approximates the excellent performance stability of transdermal testosterone delivery systems for those who, for whatever reason or reasons, prefer test cyp.

But there’s another metabolic reason to employ this protocol. The P450 Side Chain Cleavage enzyme, which converts CHOL into pregnenolone at the initiation of all three metabolic pathways CHOL serves as precursor (the sex hormones, glucocorticoids and mineralcorticoids), is actively stimulated, or depressed, by LH concentrations. It is intuitively consistent that during conditions of lowered testosterone levels, commensurate increases in LH production would serve to stimulate this conversion from CHOL into these pathways, thereby feeding more raw material for increased hormone production. And vice versa. Thus the addition of HCG (which also stimulates the P450scc enzyme) helps restore a more natural balance of the hormones within this pathway in patients who are entirely, or even partially, HPTA-suppressed.

It is important that no more than 500IU of HCG be administered on any given day. There is only just so much stimulation possible, and exceeding that not only is wasteful, doing so has important negative consequences. Higher doses overly stimulate testicular aromatase, which inappropriately raises estrogen levels, and brings on the detrimental effects of same. It also causes Leydig cell desentization to LH, and we are therefore inducing primary hypogonadism while perhaps treating secondary hypogonadism. 250IU QD is an effective, and safe, dose. After all, we are merely replacing that which is lost to inhibition.

In my previous report I recommended 250IU of HCG twice per week for all TRT patients, taken the day of, along with the day before, the weekly test cyp injection. After looking at countless lab printouts, listening to subjective reports from patients, and learning more about HCG, I am now shifting that regimen forward one day. In other words, my test cyp TRT patients now take their HCG at 250IU two days before, as well as the day immediately previous to, their IM shot. All administer their HCG subcutaneously, and dosage may be adjusted as necessary (I have yet to see more than 350IU per dose required).

I made this change after realizing that the previous HCG protocol was boosting serum testosterone levels too much, as the test cyp serum concentrations rise, approaching its peak at roughly the 72 hour mark. The original goal of supporting serum androgen levels with HCG had overshot its mark.

Those TRT patients who prefer a transdermal testosterone, or even testosterone pellets (although I am not in favor of same), take their HCG every third day. They needn’t concern themselves with diminishing serum androgen levels from their testosterone delivery system. These patients will, of course, notice an increase in serum androgen levels above baseline.

While HCG, as sole TRT, is still considered treatment of choice for hypogonadotrophic hypogonadism by many , my experience is that it just does not bring the same subjective benefits as pure testosterone delivery systems do—even when similar serum androgen levels are produced from comparable baseline values. However, supplementing the more “traditional” TRT of transdermal, or injected, testosterone with HCG stabilizes serum levels, prevents testicular atrophy, helps rebalance expression of other hormones, and brings reports of greatly increased sense of well-being and libido. My patients absolutely love it. As time goes on, we are coming to appreciate HCG as a much more powerful--and wonderful--hormone than previously given credit.

Copyright John Crisler, DO 2004. This article may, in its entirety or in part, be reprinted and republished without permission, provided that credit is given to its author, with copyright notice and 2. clearly displayed as source. Written permission from Dr. Crisler is required for all other uses.

Proviron...All you need to know.....!!!

Big Cats profile on Proviron.

Mesterolone is an orally active, 1-methylated DHT. Like Masteron, but then actually delivered in an oral fashion. DHT is the conversion product of testosterone at the 5-alpha-reductase enzyme, the result being a hormone that is 3 to 4 times as androgenic and is structurally incapable of forming estrogen. One would imagine then that mesterolone would be a perfect drug to enhance strength and add small but completely lean gains to the frame. Unfortunately there is a control mechanism for DHT in the human body. When levels get too high, the 3alpha hydroxysteroid dehydrogenase enzyme converts it to a mostly inactive compound known as 3-alpha (5-alpha-androstan-3alpha,17beta-diol), a prohormone if you will. It can equally convert back to DHT by way of the same enzyme when low levels of DHT are detected. But it means that unless one uses ridiculously high amounts, most of what is administered is quite useless at the height of the androgen receptor in muscle tissue and thus mesterolone is not particularly suited, if at all, to promote muscle hypertrophy.

Proviron has four distinct uses in the world of bodybuilding. The first being the result of its structure. It is 5-alpha reduced and not capable of forming estrogen, yet it nonetheless has a much higher affinity for the aromatase enzyme (which converts testosterone to estrogen) than testosterone does. That means in administering it with testosterone or another aromatizable compound, it prevents estrogen build-up because it binds to the aromatase enzyme very strongly, thereby preventing these steroids from interacting with it and forming estrogen. So Mesterolone use has the extreme benefit of reducing estrogenic side-effects and water retention noted with other steroids, and as such still help to provide mostly lean gains. Its also been suggested that it may actually downgrade the actual estrogen receptor making it doubly effective at reducing circulating estrogen levels.

The second use is in enhancing the potency of testosterone. Testosterone in the body at normal physiological levels is mostly inactive. As much as 97 or 98 percent of testosterone in that amount is bound to sex hormone binding globulin (SHBG) and albumin, two proteins. In such a form testosterone is mostly inactive. But as with the aromatase enzyme, DHT has a higher affinity for these proteins than testosterone does, so when administered simultaneously the mesterolone will attach to the SHBG and albumin, leaving larger amounts of free testosterone to mediate anabolic activities such as protein synthesis. Another way in which it helps to increase gains. Its also another part of the equation that makes it ineffective on its own, as binding to these proteins too, would render it a non-issue at the androgen receptor.

Thirdly, mesterolone is added in pre-contest phases to increase a distinct hardness and muscle density. Probably due to its reduction in circulating estrogen, perhaps due to the downregulating of the estrogen receptor in muscle tissue, it decreases the total water build-up of the body giving its user a much leaner look, and a visual effect of possessing "harder" muscles with more cuts and striations. Proviron is often used as a last-minute secret by a lot of bodybuilders and both actors and models have used it time and again to deliver top shape day in day out, when needed. Like the other methylated DHT compound, drostanolone, mesterolone is particularly potent in achieving this feat.

Lastly Proviron is used during a cycle of certain hormones such as nandrolone, with a distinct lack of androgenic nature, or perhaps 5-alpha reduced hormones that don't have the same affinities as DHT does. Such compounds, thinking of trenbolone, nandrolone and such in particular, have been known to decrease libido. Limiting the athlete to perform sexually being the logical result. DHT plays a key role in this process and is therefore administered in conjunction with such steroids to ease or relieve this annoying side-effect. Proviron is also commonly prescribed by doctors to people with low levels of testosterone, or patients with chronic impotence. Its not perceived as a powerful anabolic, but it gets the job done equally well if not better than other anabolic steroids making it a favorite in medical practices due to its lower chance of abuse.

Mesterolone is generally well liked nonetheless as it delivers very few side-effects in men. In high doses it can cause some virilization symptoms in women. But because of the high level of deactivation and pre-destination in the system (albumin, SHBG, 3bHSD, aromatase) quite a lot of it, if not all simply never reaches the androgen receptor where it would cause anabolic effects, but also side-effects. So its relatively safe. Doses between 25 and 250 mg per day are used with no adverse effects. 50 mg per day is usually sufficient to be effective in each of the four cases we mentioned up above, so going higher really isn't necessary. Unlike what some suggest or believe,

I will post an abstract to refute these next statements at the bottom of the page

Its not advised that Proviron be used when not used in conjunction with another steroid, as it too is quite suppressive of natural testosterone, leading to all sorts of future complications upon discontinuation. Ranging from loss of libido or erectile dysfunction all the way up to infertility. One would not be aware of such dangers because Proviron fulfills most of the functions of normal levels of testosterone.

Stacking and Use:

Mesterolone is an oral alkylated steroid. If used primarily as an anti-aromatase drug, using it throughout a longer cycle (10-12 weeks) of injectables may elevate liver values a little bit, though much, much less than one would expect with a 17-alpha-alkylated steroid. Eventhough instead of inhibiting gains, mesterolone may actually contribute to gains. So that's a bit of a shame. Its not quite as toxic since its not alkylated in the same fashion, but at the 1 position, which reduces hepatic breakdown, but not like 17-alpha alkylation. The reason for the change of position I assume, is because alkylating at the 17-alpha position has been shown to reduce affinity for sex hormone binding proteins. This would in turn decrease its ability to free testosterone. Nonetheless the delivery rate is quite good. Its taken daily in 50-100 mg doses.

The best thing to stack it with is testosterone of course. Its most easily bound to SHBG and albumin, and deactivated for up to 98%. Since the DHT can compete for these structures with higher affinity it would naturally lead to a higher yield of whatever testosterone product you stacked it with. Since DHT levels are notably higher now there is also more stimulation of the androgen receptor causing more strength gains, and because of its affinity for aromatase the overall estrogen level decreases as well. This has as a result that gains are leaner, and once again the overall testosterone yield is increased as less I converted at the aromatase enzyme.

It's of course used in other stacks with products such as methandrostenolone, boldenone and nandrolone to reduce estrogenic activity and increase muscle hardness. The addition of proviron makes boldenone a dead lock for a cutting stack and for some may even make it possible to use nandrolone while cutting, although the use of Winstrol or a receptor antagonist in conjunction is wishful as well. The benefit of adding it to a nandrolone stack is that it may also help you reduce the decrease in libido suffered from nandrolone, since the latter is mostly deactivated by 5-alpha reductase, an enzyme that makes other hormones more androgenic.

Proviron is an anti-aromatase, so obviously anti-estrogens would be futile and redundant. Blood pressure medication for those prone to hypertension may be wise, as this DHT can increase the blood pressure.

Abstract refuting that Proviron is not highly suppressive

Here is the study I was referring to. Only 85 men out of 250 showed any suppression. Proviron did not shut down the HPTA in any of the subjects and that was at 150mg for 1 year. I would say its pretty safe and has very little effect on one's HPTA

This study shows no effect on normal LH and FSH with 100-150mg/ d mesterolone, and decrease of FSH/LH that were elevated.
Proviron doesn't substitute Clomid as hpta therapy, but doesn't get in the way, either.
The effect of mesterolone on sperm count, on serum follicle stimulating hormone, luteinizing hormone, plasma testosterone and outcome in idiopathic oligospermic men.

Varma TR, Patel RH.

Department of Obstetrics & Gynaecology, St. George's Hospital Medical School London, U.K.

Two hundred fifty subfertile men with idiopathic oligospermia (count less than 20 million/ml) were treated with mesterolone (100-150 mg/day) for 12 months. Seminal analysis were assayed 3 times and serum follicle stimulating hormone (FSH) luteinizing hormone (LH) and plasma testosterone were assayed once before treatment and repeated at 3, 6, 9 and 12 months after the initiation of treatment. One hundred ten patients (44%) had normal serum FSH, LH and plasma testosterone, 85 patients (34%) had low serum FSH, LH and low plasma testosterone. One hundred seventy-five patients (70%) had moderate oligospermia (count 5 to less than 20 million/ml) and 75 patients (30%) had severe oligospermia (count less than 5 million/ml). Seventy-five moderately oligospermic patients showed significant improvement in the sperm density, total sperm count and motility following mesterolone therapy whereas only 12% showed improvement in the severe oligospermic group. Mesterolone had no depressing effect on low or normal serum FSH and LH levels but had depressing effect on 25% if the levels were elevated. There was no significant adverse effect on testosterone levels or on liver function. One hundred fifteen (46%) pregnancies resulted following the treatment, 9 of 115 (7.8%) aborted and 2 (1.7%) had ectopic pregnancy. Mesterolone was found to be more useful in patients with a sperm count ranging between 5 and 20 million/ml. Those with severe oligospermia (count less than 5 million) do not seem to benefit from this therapy.

PMID: 2892728 [PubMed - indexed for MEDLINE]

One more...
Effect of non aromatizable androgens on LHRH and TRH responses in primary testicular failure.

Spitz IM, Margalioth EJ, Yeger Y, Livshin Y, Zylber-Haran E, Shilo S.

We have assessed the gonadotropin, TSH and PRL responses to the non aromatizable androgens, mesterolone and fluoxymestrone, in 27 patients with primary testicular failure. All patients were given a bolus of LHRH (100 micrograms) and TRH (200 micrograms) at zero time. Nine subjects received a further bolus of TRH at 30 mins. The latter were then given mesterolone 150 mg daily for 6 weeks. The remaining subjects received fluoxymesterone 5 mg daily for 4 weeks and 10 mg daily for 2 weeks. On the last day of the androgen administration, the subjects were re-challenged with LHRH and TRH according to the identical protocol. When compared to controls, the patients had normal circulating levels of testosterone, estradiol, PRL and thyroid hormones. However, basal LH, FSH and TSH levels, as well as gonadotropin responses to LHRH and TSH and PRL responses to TRH, were increased.

Mesterolone administration produced no changes in steroids, thyroid hormones, gonadotropins nor PRL.

There was, however, a reduction in the integrated and incremental TSH secretion after TRH.
Fluoxymesterone administration was accompanied by a reduction in thyroid binding globulin (with associated decreases in T3 and increases in T3 resin uptake). The free T4 index was unaltered, which implies that thyroid function was unchanged.

In addition, during fluoxymesterone administration, there was a reduction in testosterone, gonadotropins and LH response to LHRH.

Basal TSH did not vary, but there was a reduction in the peak and integrated TSH response to TRH. PRL levels were unaltered during fluoxymesterone treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Proviron has four distinct uses in the world of bodybuilding. The first being the result of its structure. It is 5-alpha reduced and not capable of forming estrogen, yet it nonetheless has a much higher affinity for the aromatase enzyme (which converts testosterone to estrogen) than testosterone does. That means in administering it with testosterone or another aromatizable compound, it prevents estrogen build-up because it binds to the aromatase enzyme very strongly, thereby preventing these steroids from interacting with it and forming estrogen. So Mesterolone use has the extreme benefit of reducing estrogenic side-effects and water retention noted with other steroids, and as such still help to provide mostly lean gains. Its also been suggested that it may actually downgrade the actual estrogen receptor making it doubly effective at reducing circulating estrogen levels.

The second use is in enhancing the potency of testosterone. Testosterone in the body at normal physiological levels is mostly inactive. As much as 97 or 98 percent of testosterone in that amount is bound to sex hormone binding globulin (SHBG) and albumin, two proteins. In such a form testosterone is mostly inactive. But as with the aromatase enzyme, DHT has a higher affinity for these proteins than testosterone does, so when administered simultaneously the mesterolone will attach to the SHBG and albumin, leaving larger amounts of free testosterone to mediate anabolic activities such as protein synthesis. Another way in which it helps to increase gains. Its also another part of the equation that makes it ineffective on its own, as binding to these proteins too, would render it a non-issue at the androgen receptor.

Thirdly, mesterolone is added in pre-contest phases to increase a distinct hardness and muscle density. Probably due to its reduction in circulating estrogen, perhaps due to the downregulating of the estrogen receptor in muscle tissue, it decreases the total water build-up of the body giving its user a much leaner look, and a visual effect of possessing "harder" muscles with more cuts and striations. Proviron is often used as a last-minute secret by a lot of bodybuilders and both actors and models have used it time and again to deliver top shape day in day out, when needed. Like the other methylated DHT compound, drostanolone, mesterolone is particularly potent in achieving this feat.

Lastly Proviron is used during a cycle of certain hormones such as nandrolone, with a distinct lack of androgenic nature, or perhaps 5-alpha reduced hormones that don't have the same affinities as DHT does. Such compounds, thinking of trenbolone, nandrolone and such in particular, have been known to decrease libido. Limiting the athlete to perform sexually being the logical result. DHT plays a key role in this process and is therefore administered in conjunction with such steroids to ease or relieve this annoying side-effect. Proviron is also commonly prescribed by doctors to people with low levels of testosterone, or patients with chronic impotence. Its not perceived as a powerful anabolic, but it gets the job done equally well if not better than other anabolic steroids making it a favorite in medical practices due to its lower chance of abuse.

Anti- Estrogens In Bodybuilding:

Among athletes Proviron is primarily used as an anti-estrogen. It is believed to act as an anti-aromatase in the body, preventing or slowing the conversion of steroids into estrogen. The result is somewhat comparable to Arimidex (though less profound), the drug acting to prevent the buildup of estrogen in the body. This is in direct contrast to Nolvadex, which only blocks the ability of estrogen to bind and activate receptors in certain tissues. The anti-aromatization effect is preferred, as it is a more direct and efficient means of dealing with the problem of estrogenic side effects. One can say that proviron cures the problem of aromatization at its root while Nolvadex simply cures the symptoms. For this reason male athletes should prefer Proviron to Nolvadex. With Proviron the athlete obtains more muscle hardness since the androgen level is increased and the estrogen concentration remains low. This, in particular, is noted positively during the preparation for a competition when used in combination with a diet.

The anti-estrogenic properties of Proviron are not unique to this compound. A number of steroids have in fact demonstrated similar activity. Dihydrotestosterone and Masteron (2methyl-dihydrotestosterone) for example have been successfully used as therapies for gynecomastia and breast cancer due to their strong anti-estrogenic effect. It has been suggested that nandrolone may even lower aromatase activity in peripheral tissues where it is more resistant to estrogen conversion (the most active site of nandrolone aromatization seems to be the liver). The anti-estrogenic effect of all of these compounds is presumably caused by their ability to compete with other substrates for binding to the aromatase enzyme. With the aromatase enzyme bound to the steroid, yet being unable to alter it, and inhibiting effect is achieved as it is temporarily blocked from interacting with other hormones.

Sustanon 250mgs:

Sustanon 250 mg, under the name, Dura-Testin and Sostenon. Sustanon 250 contains 188 mg of free based testosterone per 250 mg solution.This drug is a blend of four testosterone components that have been found to react very positively together. This drug is fast acting and has a long life in the blood. It is becoming very popular lately in the U.S where it is still rather new to the market. Sustanon 250has been sold in Europe for many years and has been the most popular testosterone used by European athletes for a long time. The injection has most probably got its name from the word “sustained”. It is also called depot injection. It has shown to be very effective with many things going for it. To start with it is more effective at lower dosages. For most users of domestics like Cypionate and Enanthate, the drugs tend to require increased dosage each time they are used to provide the user with good results. Eventually many find themselves using 1200 mg per week or more to get results. Sustanon’s primary advantage is that it has been effective in continued use or return use at a reasonable dosage. A dose of 250 mg per week or 500 mg every 10 days is about all one needs of the Sustanon 250to get good results. Because of the blend of testosterones in Sustanon 250 it seems to be recognised by the steroid receptors for longer periods of time than the previously mentioned domestics, Because a person can use less Sustanon 250 and still get results, he will see less side effects. Users report less aromatisation, less water retention, less liver stress, and less endocrine system disturbances, but still they have quality gains from the Sustanon. We did say LESS, not NO side effects. Users report the usual irretability and aggressiveness with Sustanon. There is almost a synergistic action to sustanon 250, meaning that the combination of the various testosterones in it work better together than the sum of their parts.  In this example, 1+1+1+1=5! However, you can ward off many of the side effects associated with the increased level of estrogen using an antiestrogen such as Nolvadex (tamoxifen citrate) or Proviron (mesterolone).
 The most popular way to use Sustanon 250 is on a weight gaining cycle in a stack with an oral anabolic like Anavar or Winstrol. Sustanon 250 lasts up to four weeks in the system while still remaining active, so shots can be taken as little as every two weeks.
Stacking Info
Very powerful drug which stacks with other steroids very well in a bulking cycle.  Sostanon 250 is commonly taken along with anadrol 50, dianabol, deca durabolin if they are looking to "mass up".  You can take with parabolan, winstol, or primobolan if you are looking for more quality muscle gains that would also tend to stay with you longer.  It is not typically taken precontest as there is still some water retention associated with taking this drug. Sustanon 250 is available in a redi-ject syringe from Mexico under the name Sostenon, or from Europe in 1-cc ampoules under the names Dura-Testin or Sostanon. The ampoules cost about $10 per vial. This steroid can be found quite easily on the black market.

Each sustanon 250 preload contains the following:

Testosterone propionate      30 mg

Testosterone phenylpropionate      60 mg

Testosterone isocaproate        60 mg

Testosterone decanoate        100 mg

250 mgs. / 1 cc. vials or preloads.  Sustanon 250 is one of the most popular steroids and for good reason.  It is precisely set up to give you results for up to a month after injection because each of the testosterones that make up sustanon 250 stay active in the body for differing time periods.  It gives you almost instant results that you can feel since it will hit you about 3 hours after your first injection.  The reason for this is the fast acting properties of the testosterone propionate that is in it.  The Testosterone phenylpropionate and testosterone isocaproate will typically stay active for about 2-3 weeks each and the testosterone decanoate stays active in the body for up to a month.  This combination is what gives sustanon 250 its quick onset which continues to hit you for about 4 weeks after the last injection.  This drug also degrades and tapers nicely for the same reasons.  Some people will argue that sostanon is good because since it is made up of multiple types of testosterone, that it "will hit multiple androgen receptors."  This could not be further from the truth.  You only have one type of androgen receptor.   All steroids hit the same androgen receptor regardless of what you are taking.  

Sustanon 250 is highly anabolic as well as highly androgenic.  This makes it a favorite of those trying to bulk up.  It is a steroid that gives you what you are looking for; that 20-25 lbs during a 6 week cycle for most steroid novices.  You gain mass rapidly and get a nice kick in stength as well while taking this drug.  There is almost a synergistic action to sustanon 250, meaning that the combination of the various testosterones in it work better together than the sum of their parts.  In this example, 1+1+1+1=5!

Another nice aspect of sostanon 250 is that it aromatizes less and gives you less water retention than other testosterones.  This translates  to a lower risk of gyno and will tend to not give you as much of a "puffy look" as say testosterone cypionate or enanthate would.   For these reasons alone, you can see why Sustanon 250 would be preferred to other steroids.  It is also fairly easy to obtain on the black market and a cinch to buy in Mexico as just about every pharmacy stocks the bodybuilders friend, Sustanon 250!

Side Effects

The side effects tend to resemble other types of testosterones but it tends to not be as harsh.  The typical side effects can include the following:  nausea, leukopenia, symptoms resembling a peptic ulcer, acne, edema (water retention), excitation or increased aggressiveness (commonly referred to as roid rage), sleeplessness, chills, vomiting, diarrhea, hypertension, prolonged blood clotting time, increase in libido.  Females had reported:  menstrul irregularities, post-menopausal bleeding, swelling of the breasts, hoarseness or deepening of the voice, enlargement of the clitoris, and water retention.  Men had reported:  cases of impotence, chronic priapism, epididymitis, inhibition of testicular function, oligospermia, and bladder irritability.  Some people that take sostanon 250 have reported "flu like" symptoms as well.  These symptoms include a higher than normal fever, stomach aches, being tired, etc.  These side effects tend to go away after a few days and should not deter you from your goals of gaining muscle mass!

Effective Dose

250 - 1000 mg / weekly.  Sustanon 250 is designed to be a time released steroid though and could theoretically be taken as little as once a month since it stays active in your body for that time period, but for bodybuilding purposes, this is not practical.  More commonly, bodybuilders will take between 500 - 750 mg per week for the desired effects.  I have heard, and I am saying heard of people taking obscene amounts of Sustanon 250 though.  I am talking about 3000 mg a week for some of these people.  This is of course both stupid and wasteful, but I thought I would fill you in on the extremes.

1. Depot steroids Drug Active half-life

Deca-durabolin (Nandrolone decanate) 14 days
Equipoise 14 days
Finaject (trenbolone acetate) 3 days
Primobolan (methenolone enanthate) 10.5 days
Sustanon or Omnadren 15 to 18 days
Testosterone Cypionate 12 days
Testosterone Enanthate 10.5 days
Testosterone Propionate 4.5 days
Testosterone Suspension 1 day
Winstrol (stanozolol) 1 day

Steroid esters Drug Active half-life

Drug Active half-life
Suspension within 1 hour
Acetate 1 day
Propionate 1 day
Phenylpropionate 1-2 days
Butyrate 2-3 days
Valerate 3 days
Hexanoate 3 days
Caproate 4-5 days
Isocaproate 4-5 days
Heptanoate 5-6 days
Enanthate 5-6 days
Octanoate 6-7 days
Cypionate 6-7 days
Nonanoate 7 days
Decanoate 7-8 days
Undeclenate 8-9 days
Undecanoate Approx 20 days

2. Testosteron Ester- actual mg/100mg dose

test no ester 100
test prop 83
test enanth 72
test cyp 70
test undecan 63


Milligrams below are the estimated amount of active hormone per 100mg of hormone and ester.

Boldenone base: 100mg
Boldenone acetate: 83mg
Boldenone Propionate: 80mg
Boldenone Cypionate: 69mg
Boldenone Undecylenate: 61mg

Clostebol Base: 100mg

Clostebol Acetate: 84mg
Clostebol Enanthate: 72mg

Drostanolone Base: 100mg
Drostanolone Propionate: 80mg
Drostanolone Enanthate: 71mg

Methenolone Base: 100mg
Methenolone Acetate: 82mg
Methenolone Enanthate: 71mg

Nandrolone Base: 100mg
Nandrolone Cypionate: 69mg
Nandrolone Phenylpropionate: 63mg
Nandrolone Decanoate: 62mg
Nandrolone Undecylenate: 60mg
Nandrolone Laurate: 56mg

Stenbolone Base: 100mg
Stenbolone Acetate: 84mg

Testosterone Base: 100mg

Testosterone Acetate: 83mg
Testosterone Propionate: 80mg
Testosterone Isocaproate: 72mg
Testosterone Enanthate: 70mg
Testosterone Cypionate: 69mg
Testosterone Phenylpropionate: 66mg
Testosterone Decanoate: 62mg
Testosterone Undecanoate: 61mg

Trenbolone Base: 100mg
Trenbolone Acetate: 83mg
Trenbolone Enanthate: 68mg
Trenbolone Hexahydrobenzyl Carbonate: 65mg*
Trenbolone cyclohexylmethylcarbonate: 65mg*

Detection times for AAS

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


Active half-life


3 days


1.5 days


5 days


6 hours


6 hours


10 hours

Proviron® (mesterolone)
Active Life: 8-12 hours (effects last about 24 hours)

The plasma half-lives of anastrozole (1 mg once daily), letrozole (2.5 mg once daily), and exemestane (25 mg once daily) are 41-48 h, 2-4 days, and 27 h, respectively.
Time to steady-state plasma levels is 7 days for both anastrozole and exemestane and 60 days for letrozole.

Test Injection Frequency Graphs

Testosterone Propionate

Note: Cycle is based off 500mg/week total for comparison.

Dose: 71.42mg
Half-life: 2 days
Dose Frequency: Every 1 days
Cycle Length: 49 days

Note: The blood levels are not quite as stable as they appear on this graph
Dose: 142.85mg
Half-life: 2 days
Dose Frequency: Every 2 days
Cycle Length: 49 days

Last edited by SmittyTheOX; 08-09-2008 at 11:00 PM. Reason: fix graphs

Testosterone Phenylpropionate

Note: Cycle is based off 500mg/week total for comparison.

Dose: 142.85mg
Half-life: 3 days
Dose Frequency: Every 2 days
Cycle Length: 49 days

Dose: 214.3mg
Half-life: 3 days
Dose Frequency: Every 3 days
Cycle Length: 49 days

Testosterone Cypionate

Note: Cycle is based off 500mg/week total for comparison.

Dose: 214.3mg
Half-life: 7 days
Dose Frequency: Every 3 days
Cycle Length: 49 days

Dose: 500mg
Half-life: 7 days
Dose Frequency: Every 7 days
Cycle Length: 49 days

Testosterone Enanthate

Note: Cycle is based off 500mg/week total for comparison.

Dose: 214.3mg
Half-life: 7 days
Dose Frequency: Every 3 days
Cycle Length: 49 days

Dose: 500mg
Half-life: 7 days
Dose Frequency: Every 7 days
Cycle Length: 49 days


Sustanon 250

Note: Cycle is based off 500mg/week total for comparison.

Drug: Testosterone Propionate
Dose: 25.716mg
Half-life: 2 days

Drug: Testosterone Phenylpropionate
Dose: 51.432mg
Half-life: 3 days

Drug: Testosterone Isocaproate
Dose: 51.432mg
Half-life: 5 days

Drug: Testosterone Decanoate
(Initial) Dose: 85.72mg
Half-life: 9.5 days

Dose Frequency: Every 3 days
Cycle Length: 49 days

Deca-Durabolin (Nandrolone Decanoate)

An athlete attempting to use Deca only for these two effects alone (increasing bone mineral content and collagen synthesis) should be using 100mgs of deca every week- even though half of this value was used in different series on Menopausal women and HIV positive patients, which showed definite inbcrease in collagen synthesis and bone matrix mineralisation synthesis and anabolic reaction and increase of muscular mass in HIV underweight patients..Deca also has a very long active life. We can see from the chart below that a 100mg shot Deca (represented by the circles) produced relatively active and stable plasma nandrolone levels until day almost 10, hence once a week shots are all that´s necessary for stable levels of nandrolond decanoate (as a side note, the nandrolone phenylpropionate used in this study was active, and only experienced a severe drop off around day 5, shooting NPP every 4th day is the way to go). You´ll also note that higher blood plasma levels of Nandrolone are found with Gluteal injections as opposed to Deltoid injections (this is true for all oil-based steroids, I suspect).

PLEASE NOTE GRAPH BELOW: Nandrolone (Deca) its effects explored used in this study was active, and only experienced a severe drop off around day 5, also note that higher blood plasma levels of Nandrolone are found with Gluteal injections as opposed to Deltoid injections (this is true for all oil-based steroids, I suspect)

In another study of HIV+ men (6) we can see that deca ( 200mgs on week 1, 400 on week 2 and 600mgs for weeks 3-12) caused NO negative side effects in total or LDL cholesterol, triglycerides, or insulin sensitivity and there was a reduction of HDL cholesterol(8-10 points) in both groups. Also, in most studies with HIV+ subjects, deca also improved immune function.

Deca Information:

Nandrolone Base + Decanoate Ester)
    Molecular Weight(base):274.4022
    Molecular Weight (ester):172.2668
    Formula (base): C18 H26 O2
    Formula (ester):C10 H20 O2
    Melting Point (base): 122-124°C
    Melting Point (ester):31 - 32 C
    Manufacturer: Organon
    Release Date (in USA): 1962
    Effective Dose (Men): 200-600mgs/week (2mg/lb of Bodyweight)
    Effective Dose (Women): 50-100mgs/week
    Active life: 15 days
    Detection Time: Up to 18 months
    Anabolic/Androgenic ratio: 125:37a

Much debate has arisen over the effects of Nandrolone.
I am providing multiple scientific studies on those effects to help us understand this popular compound.

Collagen synthesis in postmenopausal women during therapy with anabolic steroid or female sex hormones.

Hassager C, Jensen LT, Pødenphant J, Riis BJ, Christiansen C.

Department of Clinical Chemistry, Glostrup Hospital, University of Copenhagen, Denmark.

The effect of anabolic steroid therapy and estrogen-progestogen substitution therapy on serum concentration of procollagen type III aminoterminal peptide (PIIINP), a measure of collagen synthesis, in postmenopausal women was studied in two double-blind studies: (1) 39 women allocated to treatment with either 50 mg nandrolone decanoate as an intramuscular depot or placebo injections every third week for 1 year, and (2) 40 women allocated to receive either 2 mg 17 beta-estradiol plus 1 mg norethisterone acetate daily or placebo tablets for 1 year. Serum PIIINP was measured every 3 months during the study. Anabolic steroid therapy resulted in a more than 50% increase (P less than .001) in serum PIIINP at 3 months, which thereafter decayed but remained significantly increased throughout the study period. Serum PIIINP showed the same pattern during estrogen-progestogen therapy, but to a lesser degree. We conclude that anabolic steroids stimulate type III collagen synthesis in postmenopausal women, while estrogen-progestogen therapy may have such an effect, but only to a lesser degree.

Here is an interesting one on bone mass;

Nandrolone decanoate for men with osteoporosis.

Hamdy RC, Moore SW, Whalen KE, Landy C.
James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN USA.
To compare the efficacy and safety of nandrolone decanoate and calcium (NDC) with those of calcium alone (CAL) in men with idiopathic osteoporosis, a 12-month, randomized, prospective, controlled study, was performed in an outpatient clinic. Twenty-one men with idiopathic osteoporosis (as determined by radiological and dual energy x-ray absorptiometry findings) were randomly allocated to either 50 mg nandrolone decanoate intramuscularly (im) weekly and 1,000 mg oral calcium carbonate daily (NDC group) or to 1,000 mg oral calcium carbonate daily (CAL group). Bone densitometry (total body, left femur, and lumbar spine), serum, and urine biochemical parameters were measured at 3-month intervals. In the NDC group, bone mineral density initially increased, reached a plateau, and then decreased to near baseline levels at 12 months. Increases in lean muscle mass mirrored these changes. Free and total testosterone significantly decreased. Hemoglobin increased in all patients in this group. Patients in the CAL group exhibited no significant change in either total body or bone mineral density or biochemical parameters. Thus, nandrolone decanoate, 50 mg im weekly, transiently increases the bone mass of men with idiopathic osteoporosis in this preliminary study. Careful monitoring is necessary.
PMID: 10099043 [PubMed - indexed for MEDLINE]

Our own MD advocates low dose Nandrolone!

This one is interesting since this is exactly my experience with my rotator cuff.

Nandrolone Decanoate and Load Increase Remodeling and Strength in Human Supraspinatus Bioartificial Tendons

Ioannis K. Triantafillopoulos, MD*,, Albert J. Banes, PhD,,, Karl F. Bowman, Jr||, Melissa Maloney, MS¶, William E. Garrett, Jr, MD, PhD# and Spero G. Karas, MD*,,**

From * the Shoulder and Elbow Service, University of North Carolina, Chapel Hill, North Carolina, Department of Orthopaedics, University of North Carolina, Chapel Hill, North Carolina, Flexcell International Corporation, Hillsborough, North Carolina, the Department of Biomedical Engineering, the || School of Medicine, University of North Carolina, Chapel Hill, North Carolina, Flexcell International Corporation, Hillsborough, North Carolina, and the # Department of Orthopaedics, Duke University, Durham, North Carolina

** Address correspondence to Spero G. Karas, MD, Chief, Shoulder and Elbow Service, University of North Carolina, Department of Orthopaedics, CB#7055, Chapel Hill, NC 27599-7055

Background: To date, no studies document the effect of anabolic steroids on rotator cuff tendons.

Study Design: Controlled laboratory study.

Hypothesis: Anabolic steroids enhance remodeling and improve the biomechanical properties of bioartificially engineered human supraspinatus tendons.

Methods: Bioartificial tendons were treated with either nandrolone decanoate (nonload, steroid, n = 18), loading (load, nonsteroid, n = 18), or both (load, steroid, n = 18). A control group received no treatment (nonload, nonsteroid [NLNS], n = 18). Bioartificial tendons’ remodeling was assessed by daily scanning, cytoskeletal organization by staining, matrix metalloproteinase–3 levels by ELISA assay, and biomechanical properties by load-to-failure testing.

Results: The load, steroid group showed the greatest remodeling and the best organized actin cytoskeleton. Matrix metallo-proteinase–3 levels in the load, steroid group were greater than those of the nonload, nonsteroid group (P < .05). Ultimate stress and ultimate strain in the load, steroid group were greater than those of the nonload, nonsteroid and nonload, steroid groups (P < .05). The strain energy density in the load, steroid group was greater when compared to other groups (P < .05).

Conclusions: Nandrolone decanoate and load acted synergistically to increase matrix remodeling and biomechanical properties of bioartificial tendons. Clinical Relevance: Data suggest anabolic steroids may enhance production of bioartificial tendons and rotator cuff tendon healing in vitro. More research is necessary before such clinical use is recommended.

The benefits of SubQ test injections are as follows:

Blood tests were unquestionably consistent. For exactly 100% of patients enrolled, testosterone levels remained in the physiological (normal) range for the entire duration of the study, including both peak and trough levels

Injections were extremely well tolerated. Each patient took over 50 injections and not one single adverse reaction was noticed at the injection site.

The investigation concluded that not only was subcutaneous testosterone enanthate a viable option as far as drug release, but it was safe, cheap and far more comfortable for their patients compared to intramuscular injections.

When you speak of "absorption", are you referring to the rate or amount of absorption? My research indicates the amount of absorption is consistent over time, yet the rate or speed of absorption may be slightly slower. Testing confirms both. Everything I have read (or been told by physicians) indicates the amount absorbed is quite good. I have not found anything to contradict this. Therefore, the total amount of medicine delivered is the same, whether IM or SubQ; the difference is SubQ has a more consistent release (less peaks and valleys).s necessary for stable.

The best treatment for boils is as follows (anabolic steroid use may increase the probability of furuncolisis):

    • Heat compress or pads soaked in hot water are used to cure boils. Applying them several times in a day helps in the ripening of the boil.
    • If the boil is large and painful, then it has to be lanced or drained by a doctor. The area around the boil is numbed initially. Then an incision is made on the skin and the pus removed.
    • Antibiotics need to be taken in conjunction with the lancing because it is an effective remedy to curb the infection and thus, prevent it from spreading to the nearby areas.
    • The best treatment for boils also includes some natural and home remedies. Placing tomato slices over the boils helps in getting rid of them as the citric juice present in the tomatoes is helpful as a cure.
    • Tea bags which have been soaked in warm water are placed over the boils for a quick recovery.
    • Hygiene plays an important role in treating as well as preventing them. Use of anti- bacterial soaps, creams etc help in keeping the bacteria in control.
    • A paste made from cumin seeds mixed and water is applied on the boils. It kills the bacteria and drains the pus quickly.
    • Turmeric is an age old and effective cure for boils and is considered as one of the best treatment for boils. It hasantiseptic properties and helps in quick ripening of the boil too.
    • If the boils are blood filled ones, the juice of bitter gourd is an ideal cure for them. A mixture of bitter gourd juice with a little lime juice is consumed on an empty stomach for a few days for quick recovery.
    • Betel leaf is warmed slightly and coated with castor oil. It is used to cover the boil. This process hastens the ripening of the boil, hence the recovery.
    • Margosa leaf poultice or decoction made by boiling it in water is a good remedy for boils.
    • Epsom salt is mixed in the bath tub for a hot bath. This treatment when repeated a few time a week, helps in curing boils.

12 Simple Home Concoctions for Treating Acne Scars

Looking for a cheap yet effective way of how to treat acne scar? Here are some things that you can concoct in the comfort of your own home:

1. Squeeze the juice out of fresh lemons or limes. Apply the juice directly on your acne scars using a cotton ball. Let your skin soak up the lemon juice for a while before washing it off with water. Lemon juice improves the appearance of dark acne scars and blemishes by lightening them.

2. Mix sandalwood with a few drops of rosewater to make a paste. The sandalwood and rosewater paste can be used as a facial mask and can be directly applied on the scarred area. Leave the paste on for more than an hour. Wear it overnight if you can. Wash off completely with water. This is an effective method of how to treat acne scar because of sandalwood’s soothing and cooling effect on the skin.

3. Slice up a tomato and place it over your face. Tomatoes are rich in vitamin A that hinders overproduction of sebum that causes acne. Vitamin A also has antioxidant qualities that refreshes and renews scarred and damaged skin.

4. Olive oil does not only improve the taste of food, but can also improve the appearance of acne scars. Massage olive oil on the scarred skin. Olive oil has a moisturizing quality that softens the skin’s texture and reduces visibility of acne scars.

5. Honey is another natural moisturizer that can help in treating acne scars. You can use honey as a mask or orally take a specially formulated honey acne scar treatment.

6. To treat acne scars, use this mixture as a face mask: 1 tablespoon of sour cream, 1 tablespoon of yogurt, 1 tablespoon of oatmeal, and a few drops of lemon juice. Pat the mixture onto acne scars, leave on for 10 minutes, and rinse off.

7. A popular way of how to treat acne scar is to use a face mask made out of tomatoes and cucumbers. These two combined can greatly reduce the visibility of acne scars. Using a tomato and cucumber face mask also tightens the pores of the skin giving it a nice, even texture.

8. To get a quick relief from acne scars, rub some ice cubes in a pack on the affected area. This soothes the irritated skin and also shrinks the size of pores.

9. Fenugreek is an effective solution to how to treat acne scar. You can make a paste out of fenugreek leaves and use it as a face mask. You can also boil Fenugreek seeds in water and use the solution on acne scars after it cools down.

10. Saturate a cotton ball with a few drops of acne-fighting essential oil such as lavender oil. Apply it on acne scars at least two times a day.

11. Use cucumber juice or fresh cucumber paste as a face mask. Cucumber soothes inflammation, refreshes the skin, and heals acne scars.

12. Egg whites are a cheap yet effective way of how to treat acne scar. Dab some egg whites onto acne scars using a cotton ball and leave on overnight to prevent acne and treat acne scars.

I like the anti-biotic Minocycline 100mg caps clear it right up in a few days.
I was prescribed 200mg a day but found 100mg EOD keeps the acne away.


Vitamin b 5 acne treatment is a very safe and effective treatment. For some people Vitamin b 5 (d-Calcium Pantothenate) works better than any other acne treatment.
Vitamin B-5, PANTETHINE is a biologically active (coenzyme) form of B5, and precursor of Coenzyme A. Studies have shown strong antiinflammatory properties and lowered LDL cholesterol levels. 10 grams a day to load, with a maintenence dose of 3-5 grams per there after. Take the 10 grams untill the acne subsides.

Does vitamin B 5 acne treatment work?

The vitamin b 5 acne treatment is based on a clinical study by Dr. Lit-Hung Leung. According to his study, acne is caused by a deficiency in vitamin b 5 (d-Calcium Pantothenate).
Taking high doses of vitamin b 5 creates high amounts of something called coenzyme-A. It is also believed that people with acne have a decreased ability to metabolize fats due to the low levels of coenzyme-A in the body. As a result, the fats do not break down and they get deposited in oil glands when secreted as sebum. Bacteria like P. acne feed off the sebum and cause the oil gland to become inflamed. This is known as acne.

With the extra coenzyme-A produced through high doses of vitamin b5, the fats can be broken down thus decreasing the potential for oily skin.

Is vitamin B 5 acne treatment safe?

Vitamin B5 is a water-soluble vitamin and is very safe to take in high quantities. In rare cases, side effects do occur. The only occasional side effects of vitamin b 5 we have seen is mild diarrhea. Besides the minor diarrhea, no adverse reactions have ever been reported to us. Numerous studies have confirmed its safety.

ketoconazole (nizoral) shampoo on my face and shoulders to treat AAS induced acne with fantastic success.

I'm only taking TRT (250mg/week) but it's enough to give me acne that I otherwise would not have. I'm fairly sure it would work on acne induced by higher doses as well.

The only downside is a bit of soreness and dryness, mostly on my nose and cheekbones. I've been using it twice per day, and it may be possible to prevent the acne with less frequent usage while avoiding this minor discomfort.

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.

In depth Arimidex (Anastrozole) Profile:

“Arimidex is a must for anyone using Test over 250mgs a week. You grow and keep water retention down to a minimum”.


Arimidex seems to have somewhat become the holy grail of anti-estrogens. Due to its limited availability, high price and extreme effectiveness, its become a much desired product on the black market. The compound anastrozole is indeed a revolution in the treatment of breast cancers. It's a new generation of aromatase blocker. It also has the additional, unique advantage of increasing “Free” testosterone.  Up until recently the main product for this purpose was the androgenic steroid Mesterolone (Proviron). But the problem here was that Proviron was not particularly strong and in the required doses of 50 to 100 mg per day, androgenic side-effects were not uncommon. Proviron is after all a DHT derivative. It could also never be used longer than the cycle lasted, because to some extent (despite readily being deactivated) it was suppressive of natural testosterone production. Anastrozole seems to do the job more. In clinical trials a single tab daily proved to have a profound effect. In steroid circles, mostly due to the high cost, experimentation with half and quarter tabs proved it to be almost unbelievably strong. So much, that really half a tab per day suffices for most users. Arimidex not only lowers circulating estrogen but it also increases LH and FSH concentrations in addition to increasing testosterone by about 58% in men. Arimidex decreases Estradiol by about 50% while raising Testosterone by about 58% in males. Anastrozole, even at low doses, increases serum LH and testosterone levels robustly while decreasing serum estrogen levels in a more modest fashion. Arimidex also works well as an adjunct to Hormone Replacement Therapy. It keeps estrogen low thus preventing possible prostate enlargement while it helps to maintain some natural testosterone production even while taking an exogenous source of testosterone as well.  Overall,not a bad deal. In studies that have been done, Arimidex has been shown to reduce estrogen in the body by roughly 50%. This is a good balance for bodybuilders, because some estrogen is needed in order for the full anabolic benefits of the steroids being taken to be achieved. These results are typically the same with a dosage of .5 mg a day as they are with a dosage of 1 mg a day, meaning that in most cases, a half tablet a day will be sufficient for estrogen control throughout a cycle. Typically, bodybuilders using Anastrozole will begin taking it the day they start their cycle, and will run it throughout the duration of steroid administration. It is also important to point out Arimidex’s ability to increase testosterone in the body. Some studies have shown that natural testosterone levels have increases as much as 60% after the use of this substance for 7 days. Because of this, bodybuilders find this drug extremely effective during PCT. Additionally, the use of anastrozole may decrease fat mass, which can also be tied to estrogen levels. The result can be a harder and much more defined look to the muscles and physique, which makes this agent of interest for dieting and cutting purposes as well.

Anastrozole operates by blocking the aromatase enzyme, the primary enzyme for the conversion of testosterone to estrogen. A steroid that is altered by this enzyme is referred to as an aromatizing steroid, and such steroids can cause estrogen build-up. This has several potential side-effects such as water retention, fat gain and lets not forget gynocomastia (the growth of breast tissue in men). To prevent such effects anti-aromatase products can be used. Often times during a cycle most will want to allow for some estrogen, since it heavily promotes strength and gains as well (increases GH, upgrades the androgen receptor, improves glucose utilization). These people will generally opt for an estrogen receptor antagonist such as Nolvadex (tamoxifen) or Clomid (Clomiphene). These products do not stop the formation of estrogen, but stop the estrogen from exerting its effects by competitively taking up the receptors for this hormone. This allows them to stop any problems dead in their tracks, acting very fast, but upon discontinuation allowing for immediate influx of estrogen again as well. This has the benefit that they can be used as soon as problems arise, and discontinued when they subside, thereby only reducing estrogen-mediated gains for the time-span of the occurring problem (mostly gyno). Aromatase blockers like arimidex and proviron on the other hand are more useful for those seeking to eliminate estrogen from a cycle of aromatizable steroids all together. People who are willing to settle for slower gains, in an attempt to stay lean throughout, or for those who are truly sensitive to estrogen and do not want to take the risk of problems occurring. And arimidex is the clear weapon of choice here, at least to those who can afford it.

Things one needs to note while using arimidex is that the benefits of estrogen become non-existent as well. First of all that means gains can be drastically reduced. They will be leaner and more qualitative, but they will nonetheless be seriously reduced. A second problem is that estrogen seems to have a positive effect on cholesterol levels. Since estrogen is reduced, the use of arimidex may have a profound impact on HDL to LDL ratio's in your cholesterol profile. In this aspect the use of Nolvadex is more user-friendly, because despite its anti-estrogenic effects in most tissues, it seems to exert positive estrogenic effects in the liver and promote a better cholesterol profile.

Lastly, the major problem with arimidex is the cost. I've seen people who were willing to fork over 250 dollars for a 28 tablet box of legit arimidex. That's the price of fame. Of course these prices are rididculous, but most people don't really know where to look. I've found the generic anastrozole tabs for as low as 2.2 dollars per tab, which is less than half the average street price. So it all comes down to shopping around a bit. Its not that anastrozole is that expensive to make, just that its patented. Which means that besides legit arimidex, all versions in existence are generics. This also means they could be slightly off on content or impure, if trustworthy at all. So be sure to check this with someone who has tried them or had them tested before buying a generic. The liquidex sells legit for not that much more, Around 3 to 4 bucks per gram and is generally a good buy as well, although content may be off. Since few will be investing in this to mess around with low doses and will generally opt to take 1 mg a day (1/4 cc), this shouldn't be a problem. The anastrozole powder is a real buy at merely 2-3 dollars per mg, but obviously no one will ship that for less than 100 mg orders.

Stacking and Use:

As mentioned, arimidex is an ancillary that is supposed to be stacked with aromatizing steroids in order to stop all formation of estrogen. Its seemingly very potent, so doses of 0.5 to 1 mg are enough. Some claim that 0.25 mg is enough, but for anyone doing any sort of serious cycle, I would not advise less than 0.5. These steroids are, without exception testosterone, nandrolone, norethandrolone, boldenone and methandrostenolone. And all of their derivatives as well. The drug oxymetholone (anadrol) has estrogenic effects as well, but they seem to be the result of oxymetholone's acidic A-ring activating the estrogen receptor by itself, rather than by conversion to estrogen. So Nolvadex would be more advisable in that case. To understand the whole story, I refer you to my profile on Anadrol.

Although it does block gains, aromatase blockers are generally used for the extent or a certain duration on a cycle, whereas receptor antagonists are used mostly to solve problems. Because it takes some time for an aromatase blocker to take effect (even when aromatase is blocked, there is still a level of circulating estrogen) and again some time to bring estrogen back upon discontinuation (new estrogen needs to be made again), acute problems are best solved with Nolvadex or clomid. When an aromatase blocker is used, Arimidex is the best choice by far. Proviron may be more apt when using with testosterone, due to its other characteristics and positive benefits on testosterone, but for all other intents and purpose arimidex should be preferred in these instances. Results vary but ¼ of a tab  (1/4 mg) either every other day or even every 3 days  is usually sufficient for most cycles where testosterone is less than 750 mgs a week. When checking estrogen levels with a blood test, the optimum level for both health and appearance should be between 10-20 ngs.

Arimidex is pretty mild on blood lipids and does not seem to impact libido the way other anti aromatases can.  In fact,  many men report a libido boost while using it.


Gyno Protect.

LH/Test (Up)

Estrogen (Down)

Cost Per Effective Unit




































*These drugs prevent estrogen from binding but do not actually reduce the amount of estrogen production.

**I realize that with this and every other drug on this list, the pharmacy and "street" prices will vary significantly.
Knowing that clomiphene is so cheap on the black market, I had to give it a great cost rating.
I’d also like to note that Arimidex isn’t that expensive when you consider how little you need for it to work.

The Effects of Injected Testosterone Dose and Age on the Conversion of Testosterone
to Estradiol and Dihydrotestosterone in Young and Older Men.

Lakshman KM, Kaplan B, Travison TG, Basaria S, Knapp PE, Singh AB, Lavalley MP, Mazer NA, Bhasin S.

Division of Endocrinology, Diabetes, and Nutrition, and Boston Claude D. Pepper Older Americans Independence Center for Function Promoting Therapies (K.M.L., T.G.T., S.Ba., P.E.K., S.Bh.), Boston University School of Medicine, Boston Medical Center, Boston, Massachusetts 02118; Lahey Clinic Medical Center (B.K.), Burlington, Massachusetts 01805; Charles Drew University (A.B.S.), Los Angeles, California 90059; Department of Biostatistics (T.G.T., M.P.L.), Boston University School of Public Health, Boston, Massachusetts 02118; and Hoffman LaRoche (N.A.M.), CH-4070 Basel, Switzerland.


Background: During testosterone (T) therapy, T is partly converted to 17beta-estradiol (E2) and 5alpha-dihydrotestosterone (DHT). Effects of age, testosterone dose, and body composition on total and free E2 and DHT levels are unknown. Objective: We evaluated age and dose-related differences in E2 and DHT levels in response to graded doses of testosterone enanthate in young and older men.

Methods: Fifty-one young (aged 19-35 yr) and 52 older (aged 59-75 yr) men completed treatment with monthly injections of a GnRH agonist plus randomly assigned weekly doses of testosterone enanthate (25, 50, 125, 300, or 600 mg) for 5 months.

Results: During testosterone administration, total and free E2 levels increased dose-dependently (dose effect, P < 0.001) in both young and older men. Total and free E2 levels and E2:T ratios during T administration were higher in older than young men, but age-related differences in free E2 and free E2:T ratios were not significant after adjusting for testosterone levels, percentage fat mass, and SHBG. DHT levels and DHT:T ratios were dose-related but did not differ between young and older men. Mechanistic modeling of free hormone data revealed that the conversions of T to E2 and DHT were both consistent with saturable Michaelis-Menten kinetics. The in vivo Km values were estimated to be 1.83 nM for aromatase and 3.35 nM for 5alpha-reductase, independent of age. The Vmax parameter for E2 was 40% higher in older men than younger men, but Vmax for DHT was not significantly different between age groups.

Conclusions: During im testosterone administration, E2 and DHT levels exhibit saturable increases with dose. The rate of whole body aromatization is higher in older men, partly related to their higher percentage fat mass, SHBG, and testosterone levels.

(J Clin Endocrinol Metab 95: 0000

Cabergoline- the latest in libido enhancement

Dostinex-Cabergoline is also recognized as Dostinex-Cabaser.Cabergoline increases the levels of dopamine through its action of stimulating D2 receptor sites, Dostinex-Cabergoline has also been utilized effectively for numerous other purposes such as restoring testosterone levels and increasing libido (sex drive).  Dostinex-Cabergoline is also effective within the treatment of Parkinson’s disease, & it is successfully used to treat Restless Legs Syndrom (RLS). Dostinex -Cabergoline blocks up unnecessary lactation. It meliorates energy reduction & fatigue as well as best in the treatment of Acromegaly.

However, cabergoline (brand name Dostinex has been described as being able to do everything that Viagra can’t! This is because rather than induce an erection (as Viagra can); cabergoline has been shown to improve libido, orgasm and ejaculation (which Viagra has not).


Cabergoline is from the dopaminergic family of drugs that increase the level of dopamine and also decreases the levels of the hormone prolactin. Dostinex-Cabergoline raises dopamine, a brain chemical, that is connected with the emotions of joy as well as happiness. The increase in dopamine levels often brings about a unique increase in sexual need, improvement in mood, vigilance, learning ability as well as inventiveness. Off-label uses linked with Dostinex-Cabergoline include sex drive enhancement and elevated ejaculation volume, mood elevation, urge for food suppression & extra fat loss. Jocks and musclemen also used Dostinex-Cabergoline to depress prolactin ranges resulting from drug and steroids use.
Prolactin is the hormone secreted in women after giving birth and to enhance their lactation for breast feeding. However, prolactin has recently been shown to be an inhibitor to a healthy libido, this may help explain why many women have a low sex drive after giving birth- whilst they are breast feeding. But men can also suffer from prolactinoma (high levels of prolactin) leading to a lack of sex drive- as well as developing breasts, particularly as prolactin levels tend to increase for most men with age.

Recently it has been discovered that prolactin is released immediately after an ejaculation and may be part of the reason men like to go sleep after sex with no will for further love making.

Cabergoline has been proven to significantly decrease prolactin and in so doing increase the sex drive (libido) substantially. There have been reports of enhanced and multiple orgasms as well as stronger ejaculations. Dostinex will shorten the time you need to recover and gain an erection between orgasms, and can significantly enhance all parameters of sexual drive and function (6). In other words, if you’re not worried about sexual issues and you take Dostinex anyway…it’ll still help you out in bed. And from what I have heard, it’s well worth the money for that effect.  To date, bromocriptine has been the main drug of choice to reduce prolactin levels, however clinical studies have confirmed that cabergoline is much more effective in this regard. For example in 450 tested subjects over 8-weeks 77% of the subjects had their prolactin levels returned to normal using 0.5mg of cabergoline twice a week, compared to 59% of subjects using bromocriptine at 2.5mg twice a day. Furthermore, side effects were far fewer in the cabergoline group, recorded at 2% of incidences compared with 60% of those taking bromocriptine.

One fascinating trial on 60 healthy males, between the ages of 22 and 31 discovered that they needed a break of 19 minutes between love making. However, after taking cabergoline, they were able to have several orgasms within a few minutes!
You see Dopamine is what’s called a monoamine, which is naturally produced in the body by modifying an amino acid.


And it’s this structure which makes it very interesting to us. Dostinex as you already know is what’s known as a dopamine “agonist”- or substance that triggers a response in a specific body tissue or group of cells by binding to specific receptor on or inside the cells, as if it were actually the bodily substance that usually binds to that receptor. Probably the one that most people are familiar with, with regards to agonists is ephedrine, which is an andrenergic agonist. This is why ephedrine makes you feel “wired”…it “feels” like adrenaline to your body. Cabergoline is a dopamine agonist…which makes it “feel” like dopamine to your body.

So what does that mean? Well, in the brain, dopamine helps control the flow of information from other areas of the brain. So a dopamine agonist will help you process information more quickly, and possibly improve your memory also. Some athletes use Dostinex because it helps them learn new motor skills more quickly and thus they can learn new techniques or plays at a faster rate than their competition; needless to say this gives the athletes using Dostinex a huge advantage over their competition. This ability to work on your bodies information pathways and nervous system are doubtless why it’s been successfully been used to fight Parkinsons disease (7)(8).
But does this actually work in real athletes? Well, actually, that’s why I started reading about Dostinex. See, I have the fortune of being able to basically call some of the most famous strength coaches in the world whenever I want. And, recently the last time I spoke to one about training and anabolic steroids, I asked him about different training programs for a person on steroids- and his answer said that it depends on whether that person was taking a nootropics or not. And as you may remember, Dostinex is a nootropic. It was that conversation that made me really take a closer look at Dostinex. And of course, that strength coach told me that his athletes have used nootropics with great success. The down side of knowing internationally renowned strength coaches is that their sense of humor is usually a little off, and if you have the fortune of being able to pick their brains on training, you also invariably have the misfortune of ending up on their group e-mail list which gets you a whole host of bizarre forwarded e-mails…
In fact, when you don’t have enough dopamine, you may even have difficulty concentrating…low dopamine levels have also been cited as a possible underlying cause for Attention deficit disorder (ADD) and Attention deficit/ Hyperactivity disorder (ADHD). In fact, many several medications used to treat ADD and ADHD will also serve to stimulate dopaminergic, and this could be one of their possible mechanisms of action.
Dopamine is also what’s called a “pleasure chemical”…it’s usually released by your body when you experience a rewarding experience such as eating your favorite food, having sex, winning the lottery….whatever. Interestingly, since this “happy” effect is felt when you are satiated from food, it’s highly possible that Dopamine agonists will cause you to feel “full” more often and decrease desire for food without the discomfort that dieting usually brings. Dopamine is released when you eat a nice big meal…so…a dopamine agonist like Dostinex may make you not want to eat as much, and help you feel full even if you don’t eat enough. Dostinex, therefore, may be of great interest to precontest bodybuilders and other dieters, who want to avoid some of the discomfort and anxiety that calorie restriction can bring.
Certain recreational drugs also have a lot to do with their effects on dopamine. Cocaine is what is known as a dopamine transporter blocker; what this means is that it competitively inhibits dopamine uptake to increase the amount of time released dopamine is active in your body. This makes you feel good, while the dopamine is floating around your body.  Methamphetamine is another illicit (illegal) recreational drug that acts on dopamine as well. It actually serves to competitively inhibit dopamine uptake as well as increasing dopamine flow through a dopamine transporter pathway. That’s how those drugs make you “feel good.” Dostinex is, of course, neither physically nor mentally addictive, but since it is a dopamine agonist, its users often experience an enhanced positive sense of well being. So besides helping with all of the things discussed earlier, Cabergoline will also just make you feel damn good.

Dr. Manfred Schedlowski, who was involved in this trial in Germany, said; “Cabergoline raised the libido to enable the male to orgasm again more quickly. We saw that prolactin rises after orgasm and then thought that maybe prolactin is a negative feedback system. Our subjects who took cabergoline had decreased prolactin levels and reported their orgasm was better and there was a shorter refractory period.”

Dr. Schedlowski went on to say; "We interviewed the subjects and found they were able to have multiple orgasms in very rapid succession. This is sitting very nicely with our hypothesis that orgasms and sexual drive are steered by prolactin and dopamine in the brain."

Furthermore, cabergoline had no side effects on men during the tests; this was reported in an article for the International Journal of Impotence Research. The researchers now plan to carry out trials to investigate whether cabergoline will have the same effect on women.

Another medical study by the Federico University, in Naples, Italy published in the European Journal of Endocrinology showed cabergoline to be very potent in increasing libido and sexual potency. The study examined cabergoline vs. bromocriptine and proved that cabergoline was superior in all respects to bromocriptine.

17 males with prolactinoma were treated with cabergoline or bromocriptine for 6 months. All patients initially suffered from libido impairment, with 10 suffering from reduced sexual potency and 6 were infertile. Before treatment all patients suffered from low number of erections and had a low sperm count. After 1 month of treatment prolactin levels were significantly reduced in both groups of patients. A notable increase in the number of erections during the first 3 months was recorded and continued throughout the 6 months of treatment. However the improvements in seminal fluid parameters and sexual function were more evident and rapid in patients treated with cabergoline. A significant increase in the serum levels of testosterone and dihydrotestosterone were also recorded. At the beginning of treatment, mild side-effects were recorded in 2 patients using cabergoline compared to 5 in the bromocriptine patients.

Conclusion It is now recognised that the stimulation of dopamine can enhance sexual arousal and this has been shown to occur with drugs such as bromocriptine, deprenyl and Sinemet. Now that prolactin is being recognised as an inhibitor of sexual function and desire, a drug such as cabergoline that enhances dopamine levels and reduces prolactin levels is being heralded as a significant libido enhancer- despite the fact that it has not yet been approved for this purpose. Dostinex really is the libido wonder drug. And mind you: cabergoline doesn't just work for men. It has the same sexualizing effect on women. This is the case because it acts not on those sexual organs that differentiate men and women, but on mankind's primary sexual organ, which is not located in a person's groin but on top of his neck: the brain. While Viagra is useful primary for men, and while for testosterone (or tongkat ali extract), starkly different dosages are proper for men and women, cabergoline can be used for and by women just in the same manner, in the same dose, and with the same effect as it is used for men. Actually, because male sexual problems are often just erection-related, while those of women usually are libido-related, the potential that Dostinex has in the treatment of female sexual dysfunction exceeds its potential as a libido enhancer for men.

(Dostinex restored testosterone levels and increases libido (sex drive)!

“Six months of treatment with cabergoline normalized testosterone levels in most cases, thus restoring and maintaining during treatment the capability of normal sexual activity in hyperprolactinemic males”

De Rosa M, Zarrilli S, Vitale G, Di Somma C, Orio F, Tauchmanova' L, Lombardi G, Colao A.
Department of Molecular and Clinical Endocrinology and Oncology, Federico II University of Naples, 80131 Naples, Italy. Feb 2004


Elimination—63 to 69 hours

Time to peak concentration:

Within 3 hours

Peak serum concentration:

30 to 70 picograms/mL (66.4 to 155 picomoles/L), reported in healthy volunteers taking single doses of 0.5 to 1.5 mg cabergoline. The steady-state serum concentration in patients using multiple weekly doses is expected to be 2 to 3 times higher than that reported for single doses.

Time to peak effect:

48 hours (single 0.6-mg dose of cabergoline in hyperprolactinemic patients)

Duration of action:

Up to 14 days (single 0.6-mg dose of cabergoline in hyperprolactinemic patients)

Packaging and storage:
Store below 40 ºC (104 ºF), preferably between 15 and 30 ºC (59 and 86 ºF), unless otherwise specified by manufacturer.

Take 0.25mg or 0.5mg no more than twice per week,( the lowest effective dose is 0.25 mg twice a week) unless treating a serious medical disorder whereupon the dosage may differ according to your physician's guidance, usually built up slowly to no more than 1mg twice weekly, at intervals of every four weeks. From the reading I’ve done, you only need about half a milligram (1/2mg) a week to experience all of the anti-prolactin, prosexual, antidepressant, and cognitive effects of Dostinex, but that’s on the very low end of the effectiveness scale. This stuff has an extremely long active life in the body, so once a week dosing is fine…but if it were me, and I were taking this stuff, I’d probably be using about .25mgs-.5mgs twice a week.
It should be taken before bed-time, because it may actually help you sleep a bit better, (9), Can be taken with or without food and not alter the pharmacokinetics (how it functions in your body) (10), and (incidentally) according to the literature is a much more efficient drug than Bromocriptine (11).

Side effects:
The side effects linked with Dostinex-Cabergoline are nausea, giddiness, drowsiness, stuffy nose, vivid dreams, numbness, constipation, hallucinations, confusion, severe, progressive head pain; vision troubles; ringing within the ears; or tiring effortlessly. If any of these side effects happen, inform your physician  instantly.

Cabergoline can contraindicate with psychoactive and hypotensive drugs such as phenothiazines, butyrophenones, thioxanthenes and metoclopramides. Furthermore caution must be advised if taken concurrently with other dopamine (D2) enhancing drugs, such as bromocriptine, deprenyl and Sinemet. Although often dependant on the dosages used, these should only be administered concurrently under a physician's guidance. Cabergoline’s effects can also be exaggerated when combined with other ergots, including hydergine and nicergoline, particularly those who may be sensitive to them. Cabergoline must not be used by pregnant or lactating women.

Effects of acute prolactin manipulation on sexual drive and function in males

TH Kruger, P Haake, J Haverkamp, M Kramer, MS Exton, B Saller, N Leygraf, U Hartmann, and M Schedlowski

The neuroendocrine response to sexual activity in humans is characterized by a pronounced orgasm-dependent increase of plasma levels of prolactin. In contrast to the well-known inhibitory effects of chronic hyperprolactinemia on sexual drive and function, the impact of acute prolactin alterations on human sexual physiology is unknown. Therefore, this study was designed to investigate the effects of acute manipulation of plasma prolactin on sexual behavior.Ten healthy males participated in a single-blind, placebo-controlled, balanced cross-over design. Prolactin levels were pharmacologically increased to high levels (protirelin, 50 micro g i.v.) or reduced to low physiological concentrations (cabergoline, 0.5 mg p.o.). Sexual arousal and orgasm were then induced by an erotic film and masturbation. In addition to continuous neuroendocrine and cardiovascular recordings, the quality and intensity of the acute sexual drive, arousal, orgasm and refractory period were assessed by extensive psychometric measures.Administration of cabergoline decreased prolactin levels and significantly enhanced all parameters of sexual drive (P<0.05), function (P<0.01) and positive perception of the refractory period (P<0.01). Administration of protirelin increased prolactin concentrations and produced small, but not significant reductions of sexual parameters. The sexual effects observed from cabergoline were completely abrogated by coadministration of protirelin. Although different pharmacological sites of action of prolactin-altering drugs have to be considered, these data demonstrate that acute changes in prolactin plasma levels may be one factor modulating sexual drive and function. Therefore, besides a neuroendocrine reproductive reflex, a post-orgasmic prolactin increase may represent one factor modulating central nervous system centers controlling sexual drive and behavior. In a series of studies we have consistently demonstrated that prolactin plasma concentrations are substantially increased for over 1 h following orgasm in men and women, but unchanged following sexual arousal without orgasm.  Cabergoline induced hypoprolactinemia significantly enhanced all parameters of sexual drive and function.These findings may offer a new pharmacological approach for the treatment of sexual disorders.

Dostinex - The Sex Drug FAQ

What is Dostinex?

Dostinex (Also known as Cabergoline / Cabaser) is a relatively new drug Dostinex was primarily invented for the purpose of lowering prolactin in patients with a pituitary tumors and other prolactin related conditions. However it seems the potential of Dostinex goes far beyond the treatment of tumours. Dostinex can make sex better, much better for almost anyone, that’s the reason some refers to it as ‘The pleasure drug’ or the ‘Miracle drug’.

How much Dostinex is needed for sex enhancement?

Usually people report that half a tab every 4 days is enough to cause the desired increase in sex drive and libido. However, some prefer a full tab every 4 days. Keep in mind that Dostinex is not approved as a sexual enhancement tool, most medical studies about Dostinex were for treating patients with hyperprolactinemia.

How long will one bottle of Dostinex last me?

One bottle of Dostinex contains 8 tabs. If you take 1 tab every 4 days, it will last you about a month. If you decide to use just half a tab each time, it will last about two months.
Dostinex is the pleasure drug of choice that can work for everybody and not just for people with sexual dysfunction. Dostinex may have the same sexualizing effect on women. This is due to the fact that Dostinex works on the primary sexual order: The brain! While Viagra may be useful for making an erection, Dostinex is useful for actually wanting the erection and enjoying it.

SELEGILINE: deprenyl (Selegiline, Jumex).- the anti-ageing aphrodisiac



Selegiline retards the metabolism not just of dopamine but also of phenylethylamine, a trace amine also found in chocolate and released when we're in love.Selegiline hydrochloride is a levorotatory acetylenic derivative of phenethylamine. It is commonly referred to in the clinical and pharmacological literature as l-deprenyl. The chemical name is: (R)-(-)-N,2-dimethyl-N-2-propynylphenethylamine hydrochloride. It is a white to near white crystalline powder, freely soluble in water, chloroform, and methanol, and has a molecular weight of 223.75. The molecular formula is C13H17•HCl.
The structural formula is as follows:\
Each tablet, for oral administration, contains 5 mg selegiline hydrochloride. Inactiveingredients are citric acid, anhydrous lactose, magnesium stearate, and microcrystalline

Beginning at about age 45, the destruction of dopamine in the brain by MAO-B begins increasing.  The amount of dopamine in the typical about human brain begins decreasing by 13 percent every decade. Sonsalla and Golbe discuss reasons for believing that deprenyl may be a useful preventive therapy for Parkinson's Disease (PD), warning that in autopsies of elderly persons who had no Parkinson's symptoms during life, eight to 10 percent show pathological indications of Parkinson's Disease. The mechanisms accounting for selegiline's beneficial adjunctive action in the treatment of Parkinson's disease are not fully understood. Inhibition of monoamine oxidase, type B,activity is generally considered to be of primary importance; in addition, there is evidencethat selegiline may act through other mechanisms to increase dopaminergic activity.
Selegiline is best known as an irreversible inhibitor of monoamine oxidase (MAO), an intracellular enzyme associated with the outer membrane of mitochondria. Selegiline
inhibits MAO by acting as a 'suicide' substrate for the enzyme; that is, it is converted by MAO to an active moiety which combines irreversibly with the active site and/or the
enzyme's essential FAD cofactor. Because selegiline has greater affinity for type Brather than for type A active sites, it can serve as a selective inhibitor of MAO type B if it
is administered at the recommended dose.MAOs are widely distributed throughout the body; their concentration is especially high in liver, kidney, stomach, intestinal wall, and brain. MAOs are currently subclassified into two types, A and B, which differ in their substrate specificity and tissue distribution. In humans, intestinal MAO is predominantly type A, while most of that in brain is type B. In CNS neurons, MAO plays an important role in the catabolism of catecholamines (dopamine, norepinephrine and epinephrine) and serotonin. MAOs are also important in the catabolism of various exogenous amines found in a variety of foods and drugs. MAO in the GI tract and liver (primarily type A), for example, is thought to provide vital
protection from exogenous amines (e.g., tyramine) that have the capacity, if absorbed intact, to cause a 'hypertensive crisis,' the so-called 'cheese reaction.' (If large amounts
of certain exogenous amines gain access to the systemic circulation - e.g., from fermented cheese, red wine, herring, over-the-counter cough/cold medications, etc. -
they are taken up by adrenergic neurons and displace norepinephrine from storage sites within membrane bound vesicles. Subsequent release of the displaced norepinephrine
causes the rise in systemic blood pressure, etc.)

In theory, since MAO A of the gut is not inhibited, patients treated with selegiline at a dose of 10 mg a day should be able to take medications containing pharmacologically
active amines and consume tyramine-containing foods without risk of uncontrolled hypertension. Although rare, a few reports of hypertensive reactions have occurred in
patients receiving selegiline at the recommended dose, with tyramine-containing foods. In addition, one case of hypertensive crisis has been reported in a patient taking the
recommended dose of selegiline and a sympathomimetic medication, ephedrine. The pathophysiology of the 'cheese reaction' is complicated and, in addition to its ability to
inhibit MAO B selectively, selegiline's relative freedom from this reaction has been attributed to an ability to prevent tyramine and other indirect acting sympathomimetics
from displacing norepinephrine from adrenergic neurons. However, until the pathophysiology of the 'cheese reaction' is more completely understood, it seems prudent to assume that selegiline can ordinarily only be used safely without dietary restrictions at doses where it presumably selectively inhibits MAO B (e.g., 10 mg/day).
In short, attention to the dose dependent nature of selegiline's selectivity is critical if it is to be used without elaborate restrictions being placed on diet and concomitant drug use although, as noted above, a few cases of hypertensive reactions have been reported at the recommended dose. (See WARNINGS and PRECAUTIONS.)
It is important to be aware that selegiline may have pharmacological effects unrelated to MAO B inhibition. As noted above, there is some evidence that it may increase
dopaminergic activity by other mechanisms, including interfering with dopamine reuptake at the synapse. Effects resulting from selegiline administration may also be
mediated through its metabolites. Two of its three principal metabolites, amphetamine and methamphetamine, have pharmacological actions of their own; they interfere with
neuronal uptake and enhance release of several neurotransmitters (e.g., norepinephrine, dopamine, serotonin). However, the extent to which these metabolites contribute to the effects of selegiline are unknown.

Effects on Age-Associated Mental Impairment

Dr. Knoll points to the normal decrease in dopamine in the aging brain as an indication of how deprenyl works to increase life span.  He said that it is no coincidence that even the healthiest humans die at about the time the dopamine content of their brain drops below the critical 30 percent level.  According to our present knowledge, the neurons (brain cells) that use dopamine are the most rapidly aging neurons in the human brain.

AGE in yrs




















Low-dose deprenyl (selegiline) is thought to protect the brain from aging by specifically inhibiting monoamine oxidase B (MAO B) in the brain. Deprenyl was approved for use in Parkinson's disease in the 1980s and was often combined with L-dopa (levodopa). However, one study raised concerns about combining high doses of deprenyl (10 mg per day) with L-dopa due to an apparent increase in mortality in the deprenyl group (Lees 1995). The results of that paper were hotly debated and several flaws were found in the study design. Later studies showed clinical benefit with deprenyl without a decrease in mortality and no toxic effects, particularly when lower doses were used (5 mg a per day or every other day) (LeWitt 1991; Shoulson 1992, 1998).

Deprenyl has long been recommended in very low doses (10 mg a week) as part of an overall anti-aging program because it has been shown to extend lifespan in animal studies. Deprenyl has also been shown to stimulate the efflux of norepinephrine, dopamine, and serotonin in vitro by a direct action on the hypothalamus. Professor Knoll, who developed Selegiline is convinced of its anti-aging effect and recommends for this a dose 5 mg per week (in two doses of 2.5 mg each). Some researchers are proposing that deprenyl may be considered as an alternative to levodopa for starting treatment in Parkinson's disease patients (Caracenia et al. 2001; Mohan Kumar et al. 2001).

Deprenyl has also been shown to induce rapid increases in nitric oxide (NO) production in brain tissue and cerebral blood vessels and also to protect the vascular endothelium from the toxic effects of amyloid-beta peptide (Thomas 2000). Another study showed that deprenyl protected cells from apoptosis induced by a neurotoxin, N-methyl(R)-salsolinol, and reactive oxygen species, nitric oxide and peroxynitrite (Naoi et al. 2000). Additionally, Zhu et al. (2000) showed that deprenyl significantly improved the cognitive function of rats after traumatic brain injury.

A study of 17 patients with Alzheimer's disease found that the Mini-Mental State Examination scores were significantly higher in those patients receiving selegiline (deprenyl) than in those receiving placebo (Alafuzoff et al. 2000). In India, another study of 32 patients with Parkinson's disease found a significant improvement in memory in patients treated with 10 mg a day of deprenyl as compared to placebo (Dixit et al. 1999).

Scientists who conducted lifespan studies using deprenyl have estimated the ideal dose to slow brain aging in humans to be about 1.5 mg daily. Because deprenyl is usually sold in 5-mg tablets and has a long-acting effect on the brain, most Life Extension members take a low dose of 5 mg of deprenyl twice a week.

However, Hydergine seems to be more effective when higher doses are used. European physicians often prescribe 4.5-20 mg daily of Hydergine without concern for toxicity. Persons seeking protection from neurological aging and wanting to boost cognitive function have used high-dose Hydergine and low-dose deprenyl together for more than 16 years. No adverse effects have been reported when using these two medications together.

Care should be taken when administering dopamine to patients who have been using deprenyl (selegiline). One journal article noted a drastic increase in systolic blood pressure after a critically ill man using selegiline was given an infusion of dopamine (Rose et al. 2000).

Rationale for the Use of a Selective Monoamine Oxidase Type B Inhibitor in Parkinson's Disease Many of the prominent symptoms of Parkinson's disease are due to a deficiency of
striatal dopamine that is the consequence of a progressive degeneration and loss of a population of dopaminergic neurons which originate in the substantia nigra of the
midbrain and project to the basal ganglia or striatum. Early in the course of Parkinson's Disease, the deficit in the capacity of these neurons to synthesize dopamine can be
overcome by administration of exogenous levodopa, usually given in combination with a peripheral decarboxylase inhibitor (carbidopa). With the passage of time, due to the progression of the disease and/or the effect of sustained treatment, the efficacy and quality of the therapeutic response to levodopa diminishes. Thus, after several years of levodopa treatment, the response, for a given dose of levodopa, is shorter, has less predictable onset and offset (i.e., there is 'wearing off'), and is often accompanied by side effects (e.g., dyskinesia, akinesias, on-off phenomena, freezing, etc.).
This deteriorating response is currently interpreted as a manifestation of the inability of the ever decreasing population of intact nigrostriatal neurons to synthesize and release
adequate amounts of dopamine. MAO B inhibition may be useful in this setting because, by blocking the catabolism of dopamine, it would increase the net amount of dopamine available (i.e., it would increase the pool of dopamine). Whether or not this mechanism or an alternative one actually accounts for the observed beneficial effects of adjunctive selegiline is unknown. Selegiline's benefit in Parkinson's disease has only been documented as an adjunct to levodopa/carbidopa. Whether or not it might be effective as a sole treatment is unknown, but past attempts to treat Parkinson's disease with nonselective MAOI monotherapy are reported to have been unsuccessful. It is important to note that attempts to treat
Parkinsonian patients with combinations of levodopa and currently marketed nonselective MAO inhibitors were abandoned because of multiple side effects including
hypertension, increase in involuntary movement and toxic delirium. Pharmacokinetic Information (Absorption, Distribution, Metabolism and Elimination - ADME)
The absolute bioavailability of selegiline following oral dosing is not known; however, selegiline undergoes extensive metabolism (presumably attributable to presystemic
clearance in gut and liver). The major plasma metabolites are N-desmethylselegiline, Lamphetamine and L-methamphetamine. Only N-desmethylselegiline has MAO-B
inhibiting activity. The peak plasma levels of these metabolites following a single oral dose of 10 mg are from 4 to almost 20 times greater than that of the maximum plasma
concentration of selegiline (1 ng/mL). The maximum concentrations of amphetamine and methamphetamine, however, are far below those ordinarily expected to produce
clinically important effects. Single oral dose studies do not predict multiple dose kinetics, however, at steady state the peak plasma level of selegiline is 4 fold that obtained following a single dose. Metabolite concentrations increase to a lesser extent, averaging 2 fold that seen after a single dose.
The bioavailability of selegiline is increased 3 to 4 fold when it is taken with food. The extent of systemic exposure to selegiline at a given dose varies considerably among
individuals. Estimates of systemic clearance of selegiline are not available. Following a single oral dose, the mean elimination half-life of selegiline is two hours. Under steady
state conditions the elimination half-life increases to ten hours. Because selegiline's inhibition of MAO-B is irreversible, it is impossible to predict the extent of MAO-B inhibition from steady state plasma levels. For the same reason, it is not possible to predict the rate of recovery of MAO-B activity as a function of plasma levels. The recovery of MAO-B activity is a function of de novo protein synthesis; however, information about the rate of de novo protein synthesis is not yet available. Although platelet MAO-B activity returns to the normal range within 5 to 7 days of selegiline discontinuation, the linkage between platelet and brain MAO-B inhibition is not fully understood nor is the relationship of MAO-B inhibition to the clinical effect established (see CLINICAL PHARMACOLOGY).

Special Populations
Renal Impairment
No pharmacokinetic information is available on selegiline or its metabolites in renallyimpaired subjects.
Hepatic Impairment
No pharmacokinetic information is available on selegiline or its metabolites in hepaticallyimpaired subjects.

Although a general conclusion about the effects of age on the pharmacokinetics ofselegiline is not warranted because of the size of the sample evaluated (12 subjects
greater than 60 years of age, 12 subjects between the ages of 18 to 30), systemicexposure was about twice as great in older as compared to a younger population given a
single oral dose of 10 mg.


No information is available on the effects of gender on the pharmacokinetics ofselegiline.


Selegiline Hydrochloride Tablets USP are indicated as an adjunct in the management ofParkinsonian patients being treated with levodopa/carbidopa who exhibit deterioration in
the quality of their response to this therapy. There is no evidence from controlled studies that selegiline has any beneficial effect in the absence of concurrent levodopa therapy.
Evidence supporting this claim was obtained in randomized controlled clinicalinvestigations that compared the effects of added selegiline or placebo in patients
receiving levodopa/carbidopa. Selegiline was significantly superior to placebo on allthree principal outcome measures employed: change from baseline in daily
levodopa/carbidopa dose, the amount of 'off' time, and patient self-rating of treatment success. Beneficial effects were also observed on other measures of treatment success
(e.g., measures of reduced end of dose akinesia, decreased tremor and sialorrhea,improved speech and dressing ability and improved overall disability as assessed by
walking and comparison to previous state).


According to Dr. Knoll, deprenyl has "proved to be a safe drug in man.  Neither hypertensive reactions nor the need for special dietary care were ever encountered during long-term (2-8 years) daily administration of the drug."  Knoll said that the lethal dose of the drug is more than 1000 times its effective daily dose.  Knoll called this safety margin "remarkable."Selegiline hydrochloride is contraindicated in patients with a known hypersensitivity tothis drug.
Selegiline is contraindicated for use with meperidine. This contraindication is oftenextended to other opioids. (See Drug Interactions.)


Selegiline should not be used at daily doses exceeding those recommended (10mg/day) because of the risks associated with non-selective inhibition of MAO.

The selectivity of selegiline for MAO B may not be absolute even at the recommended daily dose of 10 mg a day. Rare cases of hypertensive reactions associated with
ingestion of tyramine-containing foods have been reported in patients taking therecommended daily dose of selegiline. The selectivity is further diminished with
increasing daily doses. The precise dose at which selegiline becomes a non-selective inhibitor of all MAO is unknown, but may be in the range of 30 to 40 mg a day.
Severe CNS toxicity associated with hyperpyrexia and death have been reported withthe combination of tricyclic antidepressants and non-selective MAOIs (Phenelzine,
Tranylcypromine). A similar reaction has been reported for a patient on amitriptyline and selegiline. Another patient receiving protriptyline and selegiline developed tremors,
agitation, and restlessness followed by unresponsiveness and death two weeks afterselegiline was added. Related adverse events including hypertension, syncope,
asystole, diaphoresis, seizures, changes in behavioral and mental status, and muscularrigidity have also been reported in some patients receiving selegiline and various tricyclicantidepressants. Serious, sometimes fatal, reactions with signs and symptoms that may includehyperthermia, rigidity, myoclonus, autonomic instability with rapid fluctuations of the vitalsigns, and mental status changes that include extreme agitation progressing to deliriumand coma have been reported with patients receiving a combination of fluoxetinehydrochloride and non-selective MAOIs. Similar signs have been reported in somepatients on the combination of selegiline (10 mg a day) and selective serotonin reuptakeinhibitors including fluoxetine, sertraline and paroxetine.Since the mechanisms of these reactions are not fully understood, it seems prudent, in
general, to avoid this combination of selegiline and tricyclic antidepressants as well as selegiline and selective serotonin reuptake inhibitors. At least 14 days should elapse
between discontinuation of selegiline and initiation of treatment with a tricyclicantidepressant or selective serotonin reuptake inhibitors. Because of the long half lives
of fluoxetine and its active metabolite, at least five weeks (perhaps longer, especially iffluoxetine has been prescribed chronically and/or at higher doses) should elapse
between discontinuation of fluoxetine and initiation of treatment with selegiline.


Some patients given selegiline may experience an exacerbation of levodopa associatedside effects, presumably due to the increased amounts of dopamine reaction with super
sensitive, post-synaptic receptors. These effects may often be mitigated by reducing the dose of levodopa/carbidopa by approximately 10 to 30%.
The decision to prescribe selegiline should take into consideration that the MAO systemof enzymes is complex and incompletely understood and there is only a limited amount
of carefully documented clinical experience with selegiline. Consequently, the fullspectrum of possible responses to selegiline may not have been observed in premarketing
evaluation of the drug. It is advisable, therefore, to observe patients closely foratypical responses.


Epidemiological studies have shown that patients with Parkinson's disease have ahigher risk (2-to approximately 6-fold higher) of developing melanoma than the general
population. Whether the increased risk observed was due to Parkinson's disease or other factors, such as drugs used to treat Parkinson's disease, is unclear. For the
reasons stated above, patients and providers are advised to monitor for melanomasfrequently and on a regular basis when using selegiline for any indication. Ideally,
periodic skin examinations should be performed by appropriately qualified individuals (e.g., dermatologists).

Information for Patients

Patients should be advised of the possible need to reduce levodopa dosage after theinitiation of selegiline therapy.
Patients (or their families if the patient is incompetent) should be advised not to exceed the daily recommended dose of 10 mg. The risk of using higher daily doses of selegiline
should be explained, and a brief description of the 'cheese reaction' provided. Rarehypertensive reactions with selegiline at recommended doses associated with dietary
influences have been reported.Consequently, it may be useful to inform patients (or their families) about the signs andsymptoms associated with MAOI induced hypertensive reactions. In particular, patientsshould be urged to report, immediately, any severe headache or other atypical orunusual symptoms not previously experienced.
There have been reports of patients experiencing intense urges to gamble, increasedsexual urges, and other intense urges and the inability to control these urges while
taking one or more of the medications that increase central dopaminergic tone, that aregenerally used for the treatment of Parkinson’s disease, including selegiline. Although it
is not proven that the medications caused these events, these urges were reported tohave stopped in some cases when the dose was reduced or the medication was
stopped. Prescribers should ask patients about the development of new or increasedgambling urges, sexual urges or other urges while being treated with selegiline. Patients
should inform their physician if they experience new or increased gambling urges,increased sexual urges or other intense urges while taking selegiline. Physicians should
consider dose reduction or stopping the medication if a patient develops such urgeswhile taking selegiline.

Laboratory Tests
No specific laboratory tests are deemed essential for the management of patients onselegiline. Periodic routine evaluation of all patients, however, is appropriate.

Drug Interactions

The occurrence of stupor, muscular rigidity, severe agitation, and elevated temperaturehas been reported in some patients receiving the combination of selegiline and
meperidine. Symptoms usually resolve over days when the combination is discontinued. This is typical of the interaction of meperidine and MAOIs. Other serious reactions
(including severe agitation, hallucinations, and death) have been reported in patientsreceiving this combination (see CONTRAINDICATIONS). Severe toxicity has also been
reported in patients receiving the combination of tricyclic antidepressants and selegilineand selective serotonin reuptake inhibitors and selegiline. (See WARNINGS for details.)
One case of hypertensive crisis has been reported in a patient taking the recommendeddoses of selegiline and a sympathomimetic medication (ephedrine).

Carcinogenesis, Mutagenesis, and Impairment of Fertility

Assessment of the carcinogenic potential of selegiline in mice and rats is ongoing for alldosage forms. Selegiline did not induce mutations or chromosomal damage when tested
in the bacterial mutation assay in Salmonella typhimurium and in an in vivochromosomal aberration assay. While these studies provide some reassurance that selegiline is not mutagenic or clastogenic, they are not definitive because ofmethodological limitations. No definitive in vitro chromosomal aberration or in vitro mammalian gene mutation assays have been performed.The effect of selegiline on fertility has not been adequately assessed.


Pregnancy Category C
No teratogenic effects were observed in a study of embryo-fetal development inSprague-Dawley rats at oral doses of 4, 12, and 36 mg/kg or 4, 12 and 35 times the human therapeutic dose on a mg/m2 basis. No teratogenic effects were observed in astudy of embryo-fetal development in New Zealand White rabbits at oral doses of 5, 25,
and 50 mg/kg or 10, 48, and 95 times the human therapeutic dose on a mg/m2 basis;however, in this study, the number of litters produced at the two higher doses was less
than recommended for assessing teratogenic potential. In the rat study, there was adecrease in fetal body weight at the highest dose tested. In the rabbit study, increases in
total resorptions and % post-implantation loss, and a decrease in the number of livefetuses per dam occurred at the highest dose tested. In a peri- and postnatal
development study in Sprague-Dawley rats (oral doses of 4, 16, and 64 mg/kg or 4, 15,and 62 times the human therapeutic dose on a mg/m2 basis), an increase in the number
of stillbirths and decreases in the number of pups per dam, pup survival, and pup bodyweight (at birth and throughout the lactation period) were observed at the two highest
doses. At the highest dose tested, no pups born alive survived to Day 4 postpartum.Postnatal development at the highest dose tested in dams could not be evaluated
because of the lack of surviving pups. The reproductive performance of the untreatedoffspring was not assessed.There are no adequate and well-controlled studies in pregnant women. Selegiline shouldbe used during pregnancy only if the potential benefit justifies the potential risk to thefetus.

Nursing Mothers

It is not known whether selegiline hydrochloride is excreted in human milk. Because many drugs are excreted in human milk, consideration should be given to discontinuing
the use of all but absolutely essential drug treatments in nursing women.

Pediatric Use

The effects of selegiline hydrochloride in children have not been evaluated.

The number of patients who received selegiline in prospectively monitored pre-marketingstudies is limited. While other sources of information about the use of selegiline are
available (e.g., literature reports, foreign post-marketing reports, etc.) they do not providethe kind of information necessary to estimate the incidence of adverse events. Thus,
overall incidence figures for adverse reactions associated with the use of selegilinecannot be provided. Many of the adverse reactions seen have also been reported as
symptoms of dopamine excess.Moreover, the importance and severity of various reactions reported often cannot beascertained. One index of relative importance, however, is whether or not a reactioncaused treatment discontinuation. In prospective pre-marketing studies, the followingevents led, in decreasing order of frequency, to discontinuation of treatment withselegiline: nausea, hallucinations, confusion, depression, loss of balance, insomnia,orthostatic hypotension, increased akinetic involuntary movements, agitation,
arrhythmia, bradykinesia, chorea, delusions, hypertension, new or increased anginapectoris and syncope. Events reported only once as a cause of discontinuation are ankle
edema, anxiety, burning lips/mouth, constipation, drowsiness/lethargy, dystonia, excessperspiration, increased freezing, gastrointestinal bleeding, hair loss, increased tremor,
nervousness, weakness and weight loss.Experience with selegiline obtained in parallel, placebo controlled, randomized studiesprovides only a limited basis for estimates of adverse reaction rates. The followingreactions that occurred with greater frequency among the 49 patients assigned toselegiline as compared to the 50 patients assigned to placebo in the only parallel,placebo controlled trial performed in patients with Parkinson's disease are shown in thefollowing Table. None of these adverse reactions led to a discontinuation of treatment.

Adverse Event Number of Patients Reporting Events
selegiline placebo
N=49 N=50
Nausea 10 3
Dizziness/Lightheaded/ Fainting 7 1
Abdominal Pain 4 2
Confusion 3 0
Hallucinations 3 1
Dry mouth 3 1
Vivid Dreams 2 0
Dyskinesias 2 5
Headache 2 1
The following events were reported once in either or both groups:
Ache, generalized 1 0
Anxiety/Tension 1 1
Anemia 0 1
Diarrhea 1 0
Hair Loss 0 1
Insomnia 1 1
Lethargy 1 0
Leg pain 1 0
Low back pain 1 0
Malaise 0 1
Palpitations 1 0
Urinary Retention 1 0
Weight Loss 1 0

In all prospectively monitored clinical investigations, enrolling approximately 920 patients, thefollowing adverse events, classified by body system, were reported.

Central Nervous System
increased tremor, chorea, loss of balance, restlessness, blepharospasm, increasedbradykinesia, facial grimace, falling down, heavy leg, muscle twitch*, myoclonic jerks*,
stiff neck, tardive dyskinesia, dystonic symptoms, dyskinesia, involuntary movements, freezing, festination, increased apraxia, muscle cramps.

Mental Status/Behavioral/Psychiatric
hallucinations, dizziness, confusion, anxiety,depression, drowsiness, behavior/mood change, dreams/nightmares, tiredness,
delusions, disorientation, lightheadedness, impaired memory*, increased energy*,transient high*, hollow feeling, lethargy/malaise, apathy, overstimulation, vertigo,
personality change, sleep disturbance, restlessness, weakness, transient irritability.

Pain/Altered Sensation
headache, back pain, leg pain, tinnitus, migraine, supraorbital pain, throat burning,generalized ache, chills, numbness of toes/fingers, taste disturbance.

Autonomic Nervous System
dry mouth, blurred vision, sexual dysfunction.

orthostatic hypotension, hypertension, arrhythmia, palpitations, new or increased anginapectoris, hypotension, tachycardia, peripheral edema, sinus bradycardia, syncope.

nausea/vomiting, constipation, weight loss, anorexia, poor appetite, dysphagia, diarrhea,heartburn, rectal bleeding, bruxism*, gastrointestinal bleeding (exacerbation of preexisting ulcer disease).

slow urination, transient anorgasmia*, nocturia, prostatic hypertrophy, urinary hesitancy, urinary retention, decreased penile sensation*, urinary frequency. *Indicates events reported only at doses greater than 10 mg/day.

Skin and Appendages
increased sweating, diaphoresis, facial hair, hair loss, hematoma, rash, photosensitivity.

asthma, diplopia, shortness of breath, speech affected.

Postmarketing Reports
The following experiences were described in spontaneous post-marketing reports.
These reports do not provide sufficient information to establish a clear causalrelationship with the use of selegiline hydrochloride.


Seizure in dialyzed chronic renal failure patient on concomitant medications.


No specific information is available about clinically significant overdoses with selegiline hydrochloride. However, experience gained during selegiline's development reveals that
some individuals exposed to doses of 600 mg of d,l-selegiline suffered severe hypotension and psychomotor agitation. Since the selective inhibition of MAO B by selegiline hydrochloride is achieved only at doses in the range recommended for the treatment of Parkinson's disease (e.g., 10 mg/day), overdoses are likely to cause significant inhibition of both MAO A and MAO B. Consequently, the signs and symptoms of overdose may resemble those observed with marketed non-selective MAO inhibitors (e.g., tranylcypromine, isocarboxazide, and phenelzine).

Overdose with Non-Selective MAO Inhibition
NOTE: This section is provided for reference; it does not describe events that have actually been observed with selegiline in overdose.
Characteristically, signs and symptoms of non-selective MAOI overdose may not appear immediately. Delays of up to 12 hours between ingestion of drug and the appearance of
signs may occur. Importantly, the peak intensity of the syndrome may not be reached for upwards of a day following the overdose. Death has been reported following
overdosage. Therefore, immediate hospitalization, with continuous patient observation and monitoring for a period of at least two days following the ingestion of such drugs in
overdose, is strongly recommended. The clinical picture of MAOI overdose varies considerably; its severity may be a function of the amount of drug consumed. The central nervous and cardiovascular systems are prominently involved.
Signs and symptoms of overdosage may include, alone or in combination, any of the following: drowsiness, dizziness, faintness, irritability, hyperactivity, agitation, severe
headache, hallucinations, trismus, opisthotonus, convulsions, and coma; rapid and irregular pulse, hypertension, hypotension and vascular collapse; precordial pain,
respiratory depression and failure, hyperpyrexia, diaphoresis, and cool, clammy skin.

Treatment Suggestions for Overdose
NOTE: Because there is no recorded experience with selegiline overdose, the following suggestions are offered based upon the assumption that selegiline
overdose may be modeled by non-selective MAOI poisoning. In any case, up-todate information about the treatment of overdose can often be obtained from a
certified Regional Poison Control Center. Telephone numbers of certified Poison Control Centers are listed in the Physicians' Desk Reference (PDR).
Treatment of overdose with non-selective MAOIs is symptomatic and supportive. Induction of emesis or gastric lavage with instillation of charcoal slurry may be helpful in
early poisoning, provided the airway has been protected against aspiration. Signs and symptoms of central nervous system stimulation, including convulsions, should be
treated with diazepam, given slowly intravenously. Phenothiazine derivatives and central nervous system stimulants should be avoided. Hypotension and vascular collapse
should be treated with intravenous fluids and, if necessary, blood pressure titration with an intravenous infusion of a dilute pressor agent. It should be noted that adrenergic
agents may produce a markedly increased pressor response. Respiration should be supported by appropriate measures, including management of the
airway, use of supplemental oxygen, and mechanical ventilatory assistance, as required. Body temperature should be monitored closely. Intensive management of hyperpyrexia
may be required. Maintenance of fluid and electrolyte balance is essential.

Selegiline hydrochloride tablets USP are intended for administration to Parkinsonian patients receiving levodopa/carbidopa therapy who demonstrate a deteriorating
response to this treatment. The recommended regimen for the administration of Selegiline Hydrochloride Tablets USP is 10 mg per day administered as divided doses of
5 mg each taken at breakfast and lunch. There is no evidence that additional benefit will be obtained from the administration of higher doses. Moreover, higher doses should
ordinarily be avoided because of the increased risk of side effects. After two to three days of selegiline treatment, an attempt may be made to reduce the
dose of levodopa/carbidopa. A reduction of 10 to 30% was achieved with the typical participant in the domestic placebo controlled trials who was assigned to selegiline
treatment. Further reductions of levodopa/carbidopa may be possible during continued selegiline therapy.

For life extension purposes:
Since selegiline binds to MAO-B irreversibly, a single 5 mg dose can cause 90% reduction in dopamine for 5 days and does not return to baseline for 2 weeks. However, past the age of 45 there is a dramatic increase in the levels of MAO-B synthesized by glial cells, so optimal MAO-B inhibition may require higher doses of selegiline. I would say that 5 mg per day is not unreasonably high for a person in their 40s. When taking 5 mg a day of deprenyl over an extended period of time, it is important to make sure there is no problem with increasing or decreasing blood pressure. If anti-depressant drugs are being used, deprenyl (especially in higher doses) is contraindicated. That is why The Foundation continues to recommend a conservative dose of 5 mg of deprenyl to be taken twice a week. Some of the Foundation's advisors, however, recommend that people over age 45 take 5 mg a day of deprenyl based on the large body of evidence showing that this drug prote cts against brain aging in many unique ways and may extend life span.
 In a report in the August 1992 Journal of the American Geriatric Society, Dr. Knoll concluded his report on deprenyl by saying, "We propose that the healthy population be maintained on 10-15 mg deprenyl weekly starting at age 45 to combat the age-related decline of the nigrostriatal dopaminergic neurons.  Prophylactic deprenyl medication seems to offer a reasonable prospect of improving the quality of life in the later decades, delaying the time of natural death and decreasing the susceptibility of age-related neurological diseases."
 It is probably unwise for anyone to use deprenyl without rather large doses of supplementary antioxidant vitamins, especially vitamins C and E.

Selegiline Hydrochloride Tablets USP 5 mg are available for oral administration as white
or slightly mottled, round, unscored tablets imprinted with on one side and “3438” on
the other side. They are supplied as bottles of 60 (NDC 60505-3438-3) and bottles of
500 (NDC 60505-3438-8).

Store at 20° to 25°C (68° to 77°F) [see USP Controlled Room Temperature].
Dispense in a tight, light-resistant container [see USP] with a child-resistant closure as
5 mg
Manufactured by: Manufactured for:
Apotex Inc. Apotex Corp.
Toronto, Ontario Weston, Florida
Canada M9L 1T9 3332