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Aminoglutethimide

madmitch

New member
Does anyone know when Aminoglutethimide aka (Cytadren or Orimeten) was first synthesised?

And when was it first used by bodybuilders?
 
madmitch said:
Does anyone know when Aminoglutethimide aka (Cytadren or Orimeten) was first synthesised?

And when was it first used by bodybuilders?

Any info on this drug? Who has used it? It is supposedly a cortisol blocker. Anybody use this in conjunction w/Deca?

Price check? Availability in TJ?

FHG
 
It is used as an anti-E and as a cortisol blocker. it is not a very effective anti-E. And as far as being a cortisol blocker - well that can be a good thing and bad thing. It was said that this is what Ronnie put on extra lbs. with but they say alot of things. It is something I would do alot of research on before considering use and would only use during a high androgen cycle.

Nautica
 
Andrea's Munzer was the first person I heard of using it, but then he was rumoured to be using up to 2 grams of the stuff per day.

The recomended dose for bodybuilders is 250 mg per day (1 Tablet) 2 days on 2 days off.

The reason it is dangerous in high amounts is that it shuts down your Cortisol production completely. Therefore your body is unable to deal with stress and injuries.

Even Paul Borreson advised a maximum of 2 tablets per day (500mg), 2 days on 2 days off.

It's main use is for lowering cortisol levels after a steroid cycle.
 
I used it. It is very good aromatise inhibitor, and even MAY BE better then Arimidex, for the only reason, that unlike Arimidex, Cytadren doesn't lower IGF-1 level, but, actually increases it.
It's not a good idea to try to use it as desmolase inhibitor (stopping production of cortisol) because it will require higher doses, about 1g a day and higher. After about 3 weeks feedback mechanism will kick in, and your body will start overproducing cortisol, despite presence of Cytadren.
As anti-estrogen, you don't need to use more then 500mg/day, in most cases 250mg/day is enough (I used 250mg/day with a gram of Testosteron and had very little bloat) With such a low doses, there's almost no desmolase inhibition, so cortisol left alone, it's just anti-estrogen.
Very effective, I liked it a lot.
I went as high as 500mg/day and had no problems or side effects of any kind.
It is definately, the most cost effective aromatise inhibitor.
Using off cycle is not recomended, because it inhibit androgen production as well.
 
Hi Panerai

Borreson and WAR both said to use it at the end of a cycle to help lower cortisol.

An Endocrinologist told me the reason why Bodybuilders Testosterone levels drop of the face of the earth is due to the high levels of cortisol accumulated during a cycle.

So does that mean that Cortisol is what creates the negative feed back to the Hypothalamus ordering it to stop Natural Testosterone production?

It is a known fact that when extra Testosterone is introduced into a body, Cortisol levels also increase.

Could this be one explaination for why steroids work well for so many weeks then the effects start to wear off. i.e the bodies (catabolic) cortisol production catches up with the (Anabolic/Anticatabolic) injected Testosterone?
 
Use of AAS doesn't effect cortisol level. Cortisol has nothing to do with natural testosteron production.
There's no need to lower cortisol level at the end of the cycle, the goal is not to get it greatly increased after the cycle.
Anyway, you can't use Cytadren for inhibition of cortisol production, and you should not.
If you use Cytadren during cycle, you have to stop 72 hours before starting Clomid therapy, that's how long your body need to recover its ability to start producing androgens, after use of Cytadren.
 
Cortisol
Cortisol is a catabolic hormone which induces the breakdown of cellular proteins. Cortisol increases as intense exercise is prolonged (Di Pasquale, 1992c). Submaximal exercise at lower intensities (i.e. 63% maximum oxygen consumption) stimulates lower cortisol response than higher intensities (i.e. 86% maximum oxygen consumption) (Farrell, Garthwaite, & Gustafson, 1983; Naveri, 1985). In men, significant elevations in cortisol seem to reduce endongenous testosterone by acting directly upon the testis to impair the biosynthesis of testosterone (Di Pasquale, 1992c).
 
It has nothing to do with AAS users. If you want to talk about natural athletes, then it's different story.
But, then it's a wrong forum.
 
Anti-Catabolic Effects Of Anabolic Steroids

Many athletes have said that anabolic steroids help them train harder and recover faster. They also said that they had difficulty making progress (or even holding onto the gains) when they were off the drugs. Anabolic steroids may have an anti-catabolic effect. This means that the drugs may prevent muscle catabolism that often accompanies intense exercise training. Presently, this hypothesis has not been fully proven.

Anabolic steroids may block the effects of hormones such as cortisol involved in tissue breakdown during and after exercise. Anabolic steroids may prevent tissue from breaking down following of an intense work-out. This would speed recovery. Cortisol and related hormones, secreted by the adrenal cortex, also has receptor sites within skeletal muscle cells. Cortisol causes protein breakdown and is secreted during exercise to enhance the use of proteins for fuel and to suppress inflammation that accompanies tissue injury.

Anabolic steroids may block the binding of cortisol to its receptor sites, which would prevent muscle breakdown and enhances recovery. While this is beneficial while the athlete is taking the drug, the effect backfires when he stops taking it. Hormonal adaptations occur in response to the abnormal amount of male hormone present in the athlete's body. Cortisol receptor sites and cortisol secretion from the adrenal cortex increase.

Anabolic steroid use decreases testosterone secretion. People who stop taking steroids are also hampered with less male hormone than usual during the "off" periods. The catabolic effects of cortisol are enhanced when the athlete stops taking the drugs and strength and muscle size are lost at a rapid rate.

The rebound effect of cortisol and its receptors presents people who use anabolic steroids with several serious problems: (1) psychological addiction is more probable because they become dependent on the drugs. This is because they tend to lose strength and size rapidly when off steroids. To stave off deconditioning, athletes may want to take the drugs for long periods of time to prevent falling behind. (2) Long-term administration increases the chance of serious side-effects. (3) Cortisol suppresses the immune system. This makes steroid users more prone to diseases, such as cold and flu, during the period immediately following steroid administration.
 
panerai said:
Use of AAS doesn't effect cortisol level. Cortisol has nothing to do with natural testosteron production.
There's no need to lower cortisol level at the end of the cycle, the goal is not to get it greatly increased after the cycle.
Anyway, you can't use Cytadren for inhibition of cortisol production, and you should not.
If you use Cytadren during cycle, you have to stop 72 hours before starting Clomid therapy, that's how long your body need to recover its ability to start producing androgens, after use of Cytadren.

i agree w/ panerai totally on this one...
 
Madmitch, tell me, what part of my advice how to use Cytadren, you are desagree with? That was original question, wasn't it?

If you want to change the subject to cortisol and AAS use, that's fine, let's talk about it.
Yes, streroids, probably do have some kind of anti-catabolic effect, most likely so. Still, your Di Pasquale reference was about natural athlete. Because, there're number of studies, which show that administration of AAS to athletes doesn't effect cortisol level.
Meaning, that without use of AAS, cortisol level will be elevated.
So, obvioulsy, while one is on cycle, cortisol level shouldn't be of any concern, because AAS will take care of it.
Exersises=higher level of cortisol
Exersises+AAS=no effect on cortisol level
AAS by itself, will very effectively supress natural testosteron production, so uneffected already cortisol has and will have nothing to do with zero amount of your own testosteron.
After the cycle: no AAS, so you become "natural", at least temporary. Yes, cortisol is the problem at this point, it's going to "waste" your muscles away. But, not because of some kind of "rebound", simply because you are "natural", so cortisol level will increase.
What you can do? Get your natural testosteron production back to normal ASAP, and try to minimise cortisol production.
Obviously, Cytadren is useless, in this situation.
Drugs, like HCG, Clomid, Arimidex, Bromocriptin, nootropics, vitamins, minerals might help you in first part.
Eating well, may be, short break from gym, and then short and heavy exersise, avoid any kind of stress, look for positive emotions, etc, may help you with second.
One more time: there's no cortisol rebound and use of AAS doens't increase cortisol level.
 
That is not what an Endocrinologist told me and they are supposed to be experts in the field of hormone therapy.

So many bodybuilders think the pot belly and the bloated face side effects of roid use are due to estrogen causing an increase in water retention and fat.

The Endocrinoligist told me it's cortisol that causes these side effects in Bodybuilders using Steroids. They are the same symtoms that people with Cushing's syndrome get. i.e. people suffering from Cushing's syndrome have high levels of Cortisol. What drug is used to treat Cushing's syndrome? >>>>> Cytadren.

Oh and one other thing, ALL Cushings syndrome sufferers have low Natural Testostrone levels. Surely if Cortisol had no effect on Natural Testosterone they should have normal Testosterone levels.

The original question was when did bodybuilders first start using Cytadren?

Just interested in knowing is this a drug that has been know about in bodybuilding for a long time. Eg if it was used back in the 60's, 70's it would explain why the guy's back then, like Arnold etc. didn't get Gyno.
 
Physiological responses to resistance-exercise in athletes self-administering anabolic steroids.
J Sports Med Phys Fitness 1990 Dec;30(4):354-60 (ISSN: 0022-4707)
Rozenek R; Rahe CH; Kohl HH; Marple DN; Wilson GD; Stone MH [Find other articles with these Authors]
Department of Physical Education, California State University Long Beach.
Endocrine and metabolic responses to resistance exercise were compared in 5 athletes self-administering (SL) anabolic steroids and 8 athletes (L) not using these compounds. Exercise consisted of 5 sets of 10 repetitions in the squat and quarter squat. Blood samples were collected before (pre) and immediately after (post) exercise, and following 30 minutes of recovery (post-30). Except for significantly lower lactate concentrations in SL (p less than 0.015) at post-30, the responses to exercise and recovery were similar in both groups. Significantly higher hematocrits (p less than 0.0001), total androgen concentrations (p less than 0.0001), and androgen/cortisol ratios (p less than 0.0001) were observed in the SL group across all time periods. Plasma androgen concentrations increased about 22% in SL following exercise, even though plasma LH concentrations were significantly lower (p less than 0.0001) than in L. Plasma ACTH and cortisol concentrations were not significantly affected. Both groups displayed similar endocrine and metabolic responses to an acute bout of resistance exercise. The higher androgen/cortisol ratios and lower plasma lactate concentrations during recovery are two potential factors which may help explain the lower subjective level of fatigue following training sessions often reported by individuals who use anabolic steroids.
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Response of serum hormones to androgen administration in power athletes.
Med Sci Sports Exerc 1985 Jun;17(3):354-9 (ISSN: 0195-9131)
Alen M; Reinila M; Vihko R [Find other articles with these Authors]
Endocrine effects of self-administration of high doses of anabolic steroids and testosterone were investigated in five power athletes during 26 wk of training, and for the following 12-16 wk after drug withdrawal. After 26 wk of anabolic steroid and testosterone administration, serum testosterone concentrations had increased 2.3-fold. This was associated with increased concentrations of serum estradiol, which rose 7-fold to values (0.48 nmol X 1(-1) typical for females. There was a major decrease in serum FSH and LH concentrations, but they returned to control levels following drug withdrawal. However, serum testosterone concentrations stayed at low levels (9 nmol X 1(-1) ) during this follow-up period, indicating long-lasting impairment of testicular endocrine function. Serum ACTH concentrations were also decreased during steroid administration, possibly due to a corticoid-like effect of some of the anabolic steroids taken in high doses. However, no changes were seen in serum cortisol. The only consistent change in the control group was an increase in serum LH concentrations during the most intensive training, suggesting that a decreasing tendency of serum testosterone was compensated for by augmented LH secretion.
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Resistance exercise effects on plasma cortisol, testosterone and creatine kinase activity in anabolic-androgenic steroid users.
Int J Sports Med 1990 Aug;11(4):293-7 (ISSN: 0172-4622)
Boone JB; Lambert CP; Flynn MG; Michaud TJ; Rodriguez-Zayas JA; Andres FF [Find other articles with these Authors]
University of Toledo, Exercise Physiology Lab, OH 43606.
Anabolic-androgenic steroids (AS) users have been reported to have an improved ability to withstand exhaustive resistance workouts and to recover more rapidly. The purpose of this investigation was to study the effects of AS usage on the cortisol (C), testosterone (T) and creatine kinase (CK) response to a resistance training session. Eleven trained body builders and power lifters (5.0 +/- 1.6 training years, mean +/- SD), 5 AS users (SU) and 6 nonusers (NU), completed a standardized resistance training session consisting of 10 sets of back squats at preset percentages of the subject's 1 RM max. Blood samples were obtained at rest, immediately post exercise and 24 hours after the exercise session. SU had significantly lower T at rest. Neither group exhibited a significant change in T at 1 min or at 24 h post exercise. Both the NU and SU exhibited a significant increase in CK at 1 min post exercise (129 +/- 23.3 U.l-1, 81 +/- 15.3 U.l-1, respectively), with the NU response significantly greater than the SU. After 24 h, CK for NU was significantly elevated (171.9 +/- 54.5 U.l-1) above resting level. In contrast, CK for SU had returned to resting level NU had a significant increase in cortisol (C) (p less than 0.05) at 1 min post exercise (156.8 +/- 10.9 nmol.l-1), while the SU cortisol was not significantly changed. By 24 h C for the NU returned to resting level. The results of this investigation support the concept that AS users have a diminished CK response and an altered stress response to a single bout of resistance exercise.
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Endocrine, seminal and peripheral effects of depot medroxyprogesterone acetate and testosterone enanthate in men.
Int J Androl 1988 Aug;11(4):265-76 (ISSN: 0105-6263)
Hedman M; Gottlieb C; Svanborg K; Bygdeman M; de la Torre B [Find other articles with these Authors]
Reproductive Endocrinology Research Unit, Karolinska Sjukhuset, Stockholm, Sweden.
Depot medroxyprogesterone acetate (D-MPA, 250 mg) and testosterone enanthate (TE, 200 mg) were administered twice with a 4-week interval to nine healthy men, and the levels in blood of steroids, gonadotrophins, lipoproteins, sex hormone binding globulin (SHBG) and prostaglandins (PGs) were measured, as well as steroid levels in semen and the sperm count and motility. The hormones analysed were: MPA, testosterone, androstenedione (A), dihydrotestosterone (DHT), oestradiol (E2), cortisol (C), luteinizing hormone (LH), follicle stimulating hormone (FSH) and the sulphoconjugated forms (-S) of testosterone, DHT, pregnenolone (5-P) and dehydroepiandrosterone (DHEA). Peak values of MPA (10.2 +/- 4.6 nmol/l) and testosterone (28.0 +/- 10.0) were found in the first blood samples 2 days after each injection. Thereafter the levels of MPA decreased gradually and reached the limit of detection 18-20 weeks after the second injection. Blood levels of testosterone fell sharply from the peak values and were grossly subnormal 2 weeks after each injection; levels did not return to pretreatment values during 24 weeks of follow-up. The pattern of change of DHT, A, E2 and sulphonated androgens was similar to that of testosterone. These data suggest that D-MPA and TE are absorbed at similar rates, and that the TE is metabolized rapidly. The subsequent reduction in the levels of A, testosterone-S and DHT-S was less marked and reached pretreatment values earlier than did the testosterone levels. No obvious changes were found in the levels of C, 5-P-S and DHEA-S or in the seminal plasma levels of the various steroids studied. The blood levels of LH and FSH fell precipitously 2 days after the first injection, then started to increase 4 weeks after the second injection to reach pretreatment values 12 weeks later. Of the lipoproteins studied only the levels of HDL-cholesterol and SHBG were found suppressed after treatment. Severe oligozoospermia and the complete absence of progressively motile sperm, in at least one semen sample, was observed in all subjects at 3-7 and at 5-16 weeks, respectively, after the last injection, suggesting that the men were infertile for at least 1 month after treatment. A spurious increase in the PG content of semen was also observed. In spite of the low blood testosterone levels, no subject reported changes in sexual behaviour or other signs of anabolic imbalance during or after the study. However, the increase in levels of E2 in some individuals should be kept in mind as a possible cause of side-effects.(ABSTRACT TRUNCATED AT 400 WORDS).
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Cytadren....have you tried it yourseld, Madmitch, or know anyone, besides me, of course, hehe.. who did..? :)
 
The never ending Cortisol debate... I do not think anybody really knows. Stress Hormones have different effects on different people. That is why some people can handle stress better than others. What may be good for one person may not be good for another. I do not think anyone will be able to come up with a definitive answer to this one.
 
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