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i hear alot of things being said about how the number one reason why younger aged maes shouldnt do anabolics is because it shuts down your endocrine system..thus leading to messin up ur body...
can someone please explain this, how does un-natty and/or high test levels shut down your endocrine system...thank you for clearing this up, if you do.
Your body has a built in testosterone set point if you will. Once you introduce AAS the body detects the higher levels and in an attempt to return to it's "set point" it stops it's natural production.
yes but in turn how does that SHUT DOWN the endocrine system?
i guess im asking this because im not really sure wut the endocrine system is reasponsable for? im guessing now that it has to do with the bodys natty test production?....please explain more
search buddy, don't make us answer your newbie questiosn because your too lazy or maybe just not smart enough?
The entire endocrine system isn't adversely affected, mainly jsut the HPTA.
Bro eGGz, gave the simplest explanation one could give. Let me try, your body has a hormone regulator, when test is low it sends a signal and LH. Which signals the testes to produce test. If you already have elevated test, that regulator will not signal the testes to produce test and the testes will shrivel up. I'm sure I missed some of the mechanics, but you get the general idea.Quote:
Originally Posted by BDbuddy7
The problem with young guys is shutting it down, could cause it not to recover fully, when the hormonal system is in the development stage, that could cause problems.
JohnnyB
ya, dude don't get on the horn if you have yet to do your home work; don't post your question like you know what your talking about when you don't even know what your endocrine system does.
Ugh, I just had an exam in my molecular endocrinology class....
But anyways, one thing you should always keep in mind is that the body has a feedback mechanism for everything (well almost everything), and your testosterone levels are no exception. Adding exogenous hormone to your body while young (aka still developing) can throw off your development. This doesn't mean it WILL, but that it is a definite possibility, and that's why it is largely advised to not take anabolics while still young.
are you guys slow jus a lil bit...i asked a question about how the endocrine system works and why un natty test shuts it down...wut is wrong w/ u ppl? first of all UNOID..i asked why/how regaurding what the system does because i couldnt find it anywere...dont worry..i searched...second...jus shut up n dont comment...third...thank you johnny b, Eggz n edman for giving educated asnwers...you know...the ones i asked for in the title...
oo oo i know the answer. many enzymes and chemical systems in the body have "feedback" systems
thats in any biology book bro, most of these guys you are calling slow did their own goddamn homework. I have been doing mine since i was 17
whats your major dudeQuote:
Originally Posted by EdMan2
I'm a double major in Molecular Cell Biology (with and emphasis on biochemistry), and Math.Quote:
Originally Posted by IronReload04
thats cool, i am thinking about heading that way myself.
Yea if you're interested in the way all this stuff works it's definitely a good choice. Good luck on your choice.Quote:
Originally Posted by IronReload04
Yeah... and when the body notices the exogenous use - it inhibits it's endogenous production. The realization that it stays inhibited until all outside sources are discontinued lead to the fall of pyramiding down your doses. So, you don't taper anymore - just come off and begin PCT drugs to get the testes back to full production as soon as possible.Quote:
Originally Posted by EdMan2
A teenager's natural androgen levels are going crazy (I can't remember the exact numbers by age and sex) - major fluctuations occur all the time. Which leads to the increased body hair, lowering of the voice, musculature, increased size of the sex organs... even mood swings and aggression. It's like being on a cycle month after month. If you use exogenous hormones at this time, before you're finished maturing - you are essentially taking over your development and maturization - basically telling your body, and nature - I GOT CONTROL THIS TIME... which could lead to a lifetime predictatment... complications. This is not recommended until you have fully matured - normally the blanket age for maturity would be 21... but sh!t, some take less time - others can take more...
WOW LOOK AT THAT...THE KID ASNWERD THE QUESTION...UNLIKE U TARDS
thanks bro
another one who really knows how to make friends...Quote:
Originally Posted by BDbuddy7
Well said, ....however there is more to this than just production by the testies, this is 1/25th of the equation. I think your explanation in the 2nd paragraph is quite good. I would wait till 26-27 or more.Quote:
Originally Posted by Warrior
Btw I am in medicine and my knowledge with endocrine function is excellent. Wait till levels start till normalize or decline (around 27).
exactly, STILL in the development stage till 26-27 (filling out the width development). So don't do it in the development stage or you SCREW yourself basically. Not a good plan huh?Quote:
Originally Posted by JohnnyB
When you're younger your hormones are skyhigh and you don't need AAS anyway. You'll just shut down what you have naturally, kinda dumb idea.
i've been thinking of laying off AAS for a while after this cycle. i started when i was 19 and i am currently in my second course. this type of info really makes me think.
although, what's done is done, i don't know if i can change any damage i have induced. i'm gonna get blood work done after pCT so i can see where i'm at. sorry to hijack fellas
dragon69 - I see your point about waiting until levels level off or decline... that would be another great recommendation. But when I was 24 and busting my ass in the gym and looking into AAS for the first time - I doubt I could have been pursuaded to wait that long... although that recommendation is probably the safest. Do you know the age when androgen spikes from adolecents start to really level off, and stabilize to "normal" adult levels?
Thats a great field you are researching... I'll be looking into formal education in it, during another life :wg:
BDbuddy7 read on... from Bill Roberts:
Nothing in this article is intended to take the place of advice from a licensed health professional. Consult a physician before taking any medication.
One of the most significant side effects of anabolic/androgenic steroid (AAS) use is inhibition of natural testosterone production. There is no way to entirely avoid the problem, but there are ways to minimize the problem and recover natural testosterone levels reasonably quickly after a cycle. In this article, we will look at the problem of inhibition, its causes, and the best solutions currently known.
The Causes of Inhibition
Elevated hormone levels, in general, will cause inhibition of natural testosterone production. Many bodybuilders have come to believe that elevated estrogen levels alone are the sole cause of inhibition, and believe that by blocking estrogen, they can block inhibition.
This is not true. For example, consider the results seen in the second 2-on / 4-off cycle case study reported on Meso-Rx where Jim used 50 mg/day of trenbolone acetate, which does not aromatize, 50 mg/day of Dianabol, which does aromatize, with 250 mg/day of Cytadren as an aromatase inhibitor and 50 mg/day Clomid as an estrogen receptor blocker. His estrogen levels remained in the normal range, though elevated from baseline, since apparently the Cytadren was not sufficient to block aromatization completely. The Clomid should easily have been able to overcome normal estrogen levels, and so if the estrogen-only theory of inhibition were correct, Jim should have been suffering no inhibition. But the fact is, his testosterone levels dropped to only 1/10 his baseline value. Estrogen alone was not the cause of his inhibition. It could not have been the cause of any of it, given the normal levels and the Clomid use.
So much for the estrogen-only theory of inhibition that has been claimed by other writers. That isn’t to say, though, that estrogen is not also inhibitory: it is.
What then besides estrogen can cause inhibition? DHT, which does not aromatize, has been extensively shown to cause inhibition of testosterone production. Androgen alone, then, is sufficient to cause inhibition. In Jim’s case, androgen use was moderately heavy, and androgen alone would seem the cause of the inhibition.
Progesterone is another hormone that can cause inhibition, when used long-term. Paradoxically, in the short term it can be stimulatory. Other relevant factors include beta agonists, opiates, melatonin, prolactin, and probably other compounds. With the exception of beta agonists (e.g. ephedrine and Clenbuterol) and opiates (natural endorphins on the one hand being inhibitory, and Nubain blocking such inhibition) manipulation of these would not seem useful in bodybuilding.
The Hypothalamic/Pituitary/Testicular Axis (HPTA)
To understand inhibition of testosterone production, we need to know first how it is produced and how production is controlled. The broad general picture is that the hypothalamus receives a variety of inputs, for example, levels of various hormones, and decides whether or not more sex hormones should be produced. If the inputs are high, for example, high estrogen or high androgen or both, then it decides that little or no sex hormones should now be produced, but if all inputs are low, then it may decide that more sex hormones should be produced. It seems that the hypothalamus doesn’t respond only to current hormone levels, but also to the past history of hormone levels.
The hypothalamus itself cannot produce any sex hormones – instead it produces LHRH, or luteinizing hormone (LH) releasing hormone, also called GnRH (gonadotropin releasing hormone.) This then stimulates the pituitary gland.
The pituitary uses the amount of LHRH as one of its signals in deciding how much LH it should produce. Proper response depends on having sufficient receptors for LHRH. These receptors must be activated for LH to be produced. The pituitary also uses sex hormone levels, both current and the past history, in deciding how much LH to produce. Some aspects of the pituitary’s behavior are peculiar. For example, too much LHRH results in the pituitary downregulating LHRH receptors, with the result that very high LHRH production, which one would think should result in high testosterone production, actually lowers testosterone production. Another oddity is that while high estrogen levels inhibit the pituitary, still some estrogen is required to maintain a high number of LHRH receptors. So both very low and high levels of estrogen can inhibit LH production.
LH produced by the pituitary then stimulates the testicles to produce testosterone. Here, the amount of LH is the main factor, and high levels of sex hormones do not seem to cause inhibition at this level.
Inhibition From AAS Cycles
Because high androgen levels sustained around the clock will cause inhibition, traditional cycles simply cannot avoid inhibition of LH production while on cycle. There are three ways to avoid it:
Where AAS doses are sufficient for good gains, an interesting pattern is seen. For the first two weeks of the cycle, only the hypothalamus is inhibited, and it produces much less LHRH as a result of the high levels of sex hormones it senses. The pituitary is not inhibited at all: in fact, it is actually sensitized, and will respond to LHRH (if any is provided) even moreso than normally. After two weeks however, the pituitary also becomes inhibited, and even if LHRH is provided, the pituitary will produce little or no LH. This then is a deeper type of inhibition. After this point, there seems to be no definite further "switching point" where inhibition again becomes deeper and harder to reverse. As a general rule, I would say that there seems to be little difference between using AAS for 3 weeks vs. 8 weeks: recovery is about the same either way. Between 8 and 12 weeks, it becomes more and more likely that recovery will be difficult and slow, though even at 12 weeks it is common for recovery to not be too problematic, taking only a few weeks. Cycles past 12 weeks seem much more likely to cause substantial problems with recovery. In the hundreds of consultations I have done for people with recovery problems, very few (I can recall two) were for very short cycles such as 6 weeks, while most were for usages of 12 weeks straight or more.
- Avoid having high androgen levels around the clock. This can be done, for example, by using oral AAS only in the morning, with the last dose being approximately at noontime. Even 100 mg/day Dianabol can be used in this fashion with little inhibition. The problem with this approach is that gains are not very good compared to what is seen when high androgen levels are sustained around the clock.
- Use an amount and kind of AAS that is low enough to avoid much inhibition. Primobolan at 200-400 mg/week may achieve this effect. Again, gains will be compromised compared to a more substantial cycle. Testosterone esters and Deca are substantially inhibitory even at 100 mg/week so using a low dose of these drugs will simply result in both inhibition and poor gains.
- In principle, one could use an antiandrogen, but this would totally defeat the purpose of the cycle.
I do not know what changes take place in the hypothalamus and pituitary over a long period of time that result in this problem, but it certainly is true that long-term inhibition makes recovery more difficult on average. I suspect the problem may have to do with change in the "clock" that regulates the pulse rate of LHRH secretion, but I am not sure that that is so.
Drugs of Use With Regard to Inhibition
Cytadren: This drug can be used to reduce conversion of testosterone, Dianabol, and Equipoise (not an exclusive list of aromatizable AAS, but the main ones) to estrogen. Some feel that when estrogen levels are kept under control during the cycle, recovery is faster after the cycle is over, though that is not proven. It is a good idea though. And if testosterone esters were used prior to ending the cycle, some levels of these will remain for weeks, and continued use of Cytadren will help prevent conversion to estrogen, and thereby reduce inhibition. The best dosing pattern, in my opinion, is to take ½ tab (125 mg) on arising, and then ¼ tab at six and 12 hours later. Use of more Cytadren than this, or a different pattern, may lead to an adverse effect on cortisol production, with subsequent cortisol rebound after discontinuing the drug. Some individuals suffer some lethargy (feeling of tiredness and laziness, or sleepiness) from Cytadren, but that is uncommon at this dose.
Arimidex: This accomplishes the same purposes as Cytadren but without the possible side effects mentioned above. It is however far more expensive. A typical dose is 1 mg./day. The timing of the dosage does not matter, since the drug has a long half-life.
Clomid: After a cycle is over, Clomid at 50 mg/day is usually very effective in restoring natural testosterone production. It acts by blocking estrogen receptors at the hypothalamus and pituitary. If androgen levels are not elevated, this is enough to cause production of at least normal amounts of LH, or often more LH than normal. During the cycle Clomid cannot prevent inhibition, though some think using it during the cycle will allow a faster recovery afterwards. That is not proven though. If nothing else, though, it is useful as an antigyno/antibloating agent during the cycle.
Nolvadex: This works in the same manner as Clomid, but not nearly so well with regard to reversing inhibition. It is better to use this only as an anti-gyno/antibloating agent, if at all. If Clomid is used, there is no need for Nolvadex.
HCG: This does nothing with regard to inhibition of the hypothalamus and pituitary. Rather it acts like LH, and causes the testicles to produce testosterone just as if LH were present. It is useful then for avoiding testicular atrophy during the cycle. The best dosing method is to use small amounts frequently: 500 IU per day is sufficient, and 1000 IU may optionally be used. The amount may be given as a single daily dose or divided into two doses. Administration may be intramuscular or subcutaneous. More is not better: too much HCG can result in downregulation of the LH receptors in the testes, and is therefore counterproductive. Overdosing of HCG can also result in gynecomastia.
Ephedrine/clenbuterol: It is possible that the beta agonist activities of these drugs may assist in recovery. Personally, I do recommend the use of ephedrine post-cycle to those who can use it. Clenbuterol has the same effect but acts around the clock, having a longer half life, and allowing a higher effective dose (amount times potency) due to having less relative effect on beta receptors in the heart. I am not sure that clenbuterol has any better effect with regard to recovery though.
Oral AAS: These do not assist recovery of natural testosterone production, but if used only in the morning, can help sustain muscle mass while in the recovery phase, with little or no adverse effect on recovery.
Tribulus: If this is of benefit, I have not been able to observe it myself. I have only tried the Tribestan brand, but this is the brand that earned tribulus its reputation.
Melatonin: While disrupted sleep patterns definitely inhibit recovery, I have seen no evidence that taking melatonin at night speeds recovery. It is useful though for those who have allowed their sleep patterns to be disrupted and who wish to reset their natural clocks.
General Recommendations
Pharmaceutical drugs should of course not be self-prescribed: the following are simply recommendations of what works well, not of what to do without physician’s advice. Enough said.
The best cycle plans are either brief two week cycles with short acting drugs, which allow a very fast recovery (less than one week) or cycle of approximately 6-10 weeks, which usually allow reasonable recovery and allow quite a bit of time to make gains. Cycles in the 3-5 week range are less efficient because they combine the disadvantage of relatively little time gaining with the disadvantage of slower recovery.
If a cycle lasts 8 weeks or longer, I think it is best to use HCG during the cycle if possible, as described above. HCG should not be used during the recovery itself since it will increase androgen and estrogen levels, which will be inhibitory to the hypothalamus and pituitary.
Clomid use should begin, if it was not used during the cycle, as soon as androgen levels drop enough that recovery becomes possible. This would be about two weeks after the last injection of long acting steroid esters, assuming reasonable doses such as 500 mg/week. Clomid use should start with 300 mg on the first day (50 mg six times) to quickly get blood levels as high as needed, and then maintained with 50 mg/day. This is needed because of the half-life of the drug. It should be continued until one is sure that natural testosterone production is back and testicle size is returned to normal, with the exception that if use has been more than about 6 weeks, one might try dropping it for a few weeks to see what happens. If no further improvement occurs, then Clomid would be resumed. It has been studied medically for long-term use and found safe for periods of at least a year. However, a small percentage of users develop vision problems from Clomid, which are generally reversible upon discontinuing the drug. So if you have this problem, certainly the drug should be discontinued.
If aromatizable injectables were used, an antiaromatase would be useful for 3 weeks or so after the last injection, or 4 weeks if dosage was high (a gram per week or more.)
Lastly, ephedrine seems to be of some help. The same dose as used for dieting (e.g. 25 mg three times per day) seems quite sufficient.
Long term inhibition can potentially be a serious side-effect of AAS use, and this risk should be minimized by avoiding excessively long cycles. This really does not compromise gains greatly, since the body cannot grow rapidly week in, week out, 52 weeks per year anyway. And even moderate post-cycle inhibition is something we wish to minimize, since it is frustrating to lose much of one’s gains in the first few weeks after a cycle as a result of low natural testosterone and no AAS being used. The advice given above is generally successful in minimizing such losses, and I hope you will find it useful.
good info
Warrior, your info is decent, but just for everyones information here (we're here to learn after all), there is SOOOO much more to this. You see, most steroid information and research seems to revolve around test production and its circuit (GnRH, LH etc.).
However the reality here is that MANY, MANY hormones are affected other than these. Androgen levels from the adrenals will be compromised as will most of the hormones which are released from the pituitary. THIS right there (the panhypopituitaryism) is one mechanism which causes prolactin to rise, so it shows just how many pituitary hormones are affected.
So thyroid function will also be impaired somewhat as well, which I suspect is the reason that many long time users develop bone problems (since the then increased parathormone will cause release of minerals from bones). Again, prolactin will also be increased here, further proof that AAS use decreases thyroid function.
The list goes on and I really don't have the time to go through it all. But the point is that there is so much more to AAS induced endocrine dysfunction than just GnRH, LH and Test. This is a very good point and for this reason I think this should be made into a sticky for future reference.
The Hypothalamus/Pituitary axis is a delicate balancing act, as is the relationship between thyroid, adrenals, etc with Pituitary. Not something to screw with when you're young and have superman levels going already.
But I agree with you, youngsters ALSO don't have a fully developed MIND yet either and will do it anyway. But without educating people, there are those that will hurt themselves that would have listened too.
Mods: Make this a sticky please. Anyone else want this as a sticky?
Great info Warrior. I'm almost 3 weeks into my PCT and I've done most of the things you posted. I find the morning oral AAS during recovery very interesting, that makes sense. Do you do this?
I've only lost about 4lbs total and my strength is about the same. So far so good. I'm just about at the end but I have been doing: 70mgs clomid, 3000mgs tongkat, clenbuterol ed. I ran HCG at 500ius ed for the last 2 weeks of my 100mg ed prop cycle. I also had igf-1 for the last 4 weeks and I still had a week left into PCT.
Did you mention longer resting periods between muscle groups to avoid over training?
I'm 19, and i was planning on doing a cycle of M1T for 4 weeks, i'm guessing this is a bad idea?
The morning oral idea really only applies to bridgeing using something with a short half life, like Dianabol, on its own... or an esterless injectable steroid, like testosterone suspension. Since the half/active life is very short taking the whole dose in the morning keep endogenous levels from dropping since your body has a daily chance to redeem itself, so to speak - according to Roberts.Quote:
Originally Posted by Seattle Junk
I don't bridge... and no, I haven't guinea pigged this idea... :wg: If I did I would try testosterone suspension once a day for a few weeks. You'd have to keep the doses relatively low to keep from causing too much of a hormonal rollercoaster during the day... which can also lead to increases inhibition (from constant swings in blood androgen levels).
Yeah, I guess for bridging that makes sense. I just believe on being totally off for at least 60 days after a full cycle. It should be 90 days or the same amount of time of the preceeding AAS cycle. If your sex drive is normal and your balls keep their size, PCT was successful. I hate PCT cause you're going to lose a little size and the pump isn't the same as on AAS. You just have to understand that this is part of keeping your endocrine system healthy so you can have kids or a normal sex life in the future.Quote:
Originally Posted by Warrior
I chose muscle biology on a cellular and molecular level.Quote:
Originally Posted by EdMan2
Yeah - bridging should only be used when you have blown past what your natural androgen levels can support... completely unassisted and off cycles. And when getting even bigger yet is part of your lifestyle/profession - such as a bodybuilder. The average joe should never need to bridge - rather keep the risk:benefit ratio more in his favor.Quote:
Originally Posted by Seattle Junk
Getting big and strong while learning how to keep it naturally is the safest endeavor (time on=time off)... but if you really need to go past the "genetic potential" limit, then longer cycles with things like bridging can become necessary.