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  1. #1
    rage22 is offline New Member
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    clomid during cycle?? I know many post on this exist

    My question is, I bought 60 chlomid to take post cycle.(only comes in box of 30) now from reading and what i have seen everyone post, 300 first day, 100 for next ten and 50 for ten after that which comes out to 36 pills. Im coming on my conclusion of my cycle and so far I have had no side effects or gyno. Can I or should I, run any of the extra clomid during my cycle??

  2. #2
    big N's Avatar
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    during ??no it deafeats the purpose bro ,ur trying to stimulate test production with ingestion of clomid while at the same time ur killing it with the gear .

  3. #3
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    no, don't run it during...save it for your next cycle. it's not effective as an anti-e...it would be a waste and might hurt your gains.

  4. #4
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    I have been useing clomid my whole cycle. 50mg EOD for the past 16 weeks. It helps estrogen from converting, and also keep natural test going....Which keeps the boys hanging low. I know of other mods and vets who use this method as well.

  5. #5
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    that's interesting...so clomid during your a test/deca cycle would keep your nuts from taking a vacation? Why haven't I heard that before?...tell me more...

    moto

  6. #6
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    This always makes for a good discussion! IMO, the majority concensus is right. Let me just say that what I present applies more to longer heavy androgenic cycles. Once you are inhibited, you are staying inhibited until hormone levels fall enough for the HP to begin signaling again. Clomid will do nothing during a heavy cycle as far as preventing/reversing inhibition. Clomid may decrease estrogen levels, and may bind and inhibit estrogen receptors on the hypothalamus and pituitary, but IMO cannot prevent inhibition because you still have high levels of other inhibitory hormones, ie. DHT, androgens and androgen related hormones, progestins and progesterone related hormones (there are many others, and upregulation/downregulation of different receptors also come into play). On paper, it sounds good. But in practicality I don't see how it can work out. Your hypothalamus and subsequently your pituitary cannot begin normal function/signaling until all hormones are in check (low enough to do so). These two delicate glands do not care for which type of hormone is elevated and thereby causing inhibition. They just sense excess hormone production and act accordingly. This is why clomid appears to be effective after cycle when androgen levels have begun to decline. At this point, the HP wont be as susceptible to inhibition by high androgen levels. This leaves the high estrogen levels to worry about, and these drugs take care of this. As far as preventing/reversing testicular atrophy, again I don't see how clomid used during heavy cycle would benefit. It is not capable of stimulating the HP axis to produce LH, and like I said above, while you are on high dose androgens it is impossible to maintain proper LH function in any case. This is why we use hCG . All hCG does is act as LH in the body. It does nothing for preventing inhibition in the hypo/pit. It just functions as synthetic LH and signals the testes to produce test, just as if LH were never missing in the first place.
    But if we were to talk about shorter cycles using shorter acting drugs and possibly drugs that appear less inhibitory than test, this may be a different story. The HP axis seems to go through phases in regards to inhibition. At first, there may be upregulation of GnRH receptors on the hpothalamus, but as time goes on, it seems that inhibition gets deeper. So this is when we begin to talk about shorter cycles, shorter acting AAS, and AAS that don't appear to be as inhibitory. Like I said, this always makes for good debate. So chime in people!
    As far as the answer to rages question, I would say it depends on your cycle length, AAS used etc. IMO it would be a waste of clomid in trying to prevent inhibition while on cycle. Unless you use it for gyno protection, favorable lipid profile etc.

  7. #7
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    I don't have an opinion, I've just always been curious as to how a female fertility drug kickstarts testosterone production post-cycle.

  8. #8
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    I have just theoretical knowledge about chlomid but I agree with ichabodcrane!

  9. #9
    ichabodcrane's Avatar
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    Originally posted by Fif the Great
    I don't have an opinion, I've just always been curious as to how a female fertility drug kickstarts testosterone production post-cycle.
    Here, let me give you one
    First off when it comes to the hypothalamus and pituitary glands in men and women, we are not that different. So the mechanism of how these drugs work in women also work the same in men, at the hypothalamus/pituitary axis anyways (but since women have a uterus and men don't this is where things tend to differ, in other ways as well). In short, these drugs are both estrogenic and antiestrogenic depending on the specific tissue they bind. But to keep it short, they act as antiestrogens in the hypothalamus and pituitary glands when bound to these tissue receptors. These "fertility"drugs produce a positive feedback mechanism (one which increases the gonadotropic hormones LH/FSH), we want this. They bind estrogen receptors in the afformentioned glands and produce no effect or block the receptors(antagonist). Normally, plain old estrogen binds these same receptors producing an agonistic or stimulating effect, and cause a decrease in LH/FSH production. So you see this is why estrogen is inhibitory. So nolva/clom basically occupy the estrogen receptor and do nothing but prevent normal estrogen from binding the receptors in the hypo/pit and help prevent inhibition that would normally occur if estrogen itself were to bind these receptors. The effects of nolva/clomid are differnet in other tissues, but we are not concerned with that yet. When the hypo/pit. senses increased levels of estrogen in the blood stream, it is basically receiving commands to stop production of LH and FSH(we don't want this). LH and FSH in men stimulate the testes to produce testosterone and spermatogenesis. So by stopping this process (which is what happens when estrogen levels are high-or androgens levels as well) we get what is called inhibition. So you see that by having high levels of estrogens, this produces inhibitory effects on the hypothalamus and pituitary and prevents the release of LH/FSH, so our nuts can't get the proper signal needed to begin natural test production. When we come off cycle, our androgen levels gradually decline, leaving the catabolic hormones to run amuck. We don't want this. We need to get our natural test production back as fast as possible to avoid the negative catabolic effects. So by using clomid/nolva, we are basically "tricking" the hypo/pit glands into producing LH and FSH again, which normally would (without these compounds) take much longer to accomplish. So that's pretty much it in a nutshell. It can be more complicated than what I stated, and so many other factors/hormones also regulate hypothlalmus/pituitary gonadotropin secretion. Like I said in other threads, high androgens, progestins, estrogens, DHT also are inhibitory. In regards to the progestins (progesterone), this is why clomid doesn't work well in helping restore inhibition. Drugs like Deca and Anadrol (possibly Fina) are known to have progestagenic effects and if you are shut down by high levels of progestins or progestin related drugs, than you need things other than clomid/nolva to combat inhibition such as bromocryptine which acts as a dopamine agonist. It can get complicated, and in fact it is. But that is why we are here.......to learn

  10. #10
    motoxxxguy's Avatar
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    damn ichabod...I guess the lesson here is "ask and you shall receive!"

    seriously though, that's how I beleived clomid worked but how about what bigtraps said about "keeping the boys hanging low?" It doesn't seem like clomid could do that on its own. Maybe with the help of HCG ...

    Just trying to milk a little more knowledge from the bros...

    "I am a sponge of learning; wet me with your knowledge"
    -Unknown

    moto

  11. #11
    G-S Guest
    Ichabod-

    Your assumption is that Clomid only works in one way. It doesn't it has two pathways, one being a direct effect on the testicles. It mimics LH, and thus functions as LH bypassing the HPTA much like HCG . If your theory is correct, you would have no testicul.ar stimulation via Clomid during a cycle; however there is and that is something your theory leaves out. And, the anti-estrogenic effect of Clo is not what causes it. ON that account, the HPTA would have to clear to produce LH, but your androgen levels would still be too high for it to function properly.

    As well, degreed inhibition is something that needs to be proven, not merely stated. I want a study on that before I believe anything close to it. That body is usually binary, it either works or it shuts down. At some level the androgen level suppresses it, there is no gradation.

    So, while I think your thoughts are well reasoned, they are based on the faulty assumption of Clomiphene ONLY working through LH stimulation and not on the second function of Clo as well.

  12. #12
    ichabodcrane's Avatar
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    Originally posted by G-S
    Ichabod-

    Your assumption is that Clomid only works in one way. It doesn't it has two pathways, one being a direct effect on the testicles. It mimics LH, and thus functions as LH bypassing the HPTA much like HCG . If your theory is correct, you would have no testicul.ar stimulation via Clomid during a cycle; however there is and that is something your theory leaves out. And, the anti-estrogenic effect of Clo is not what causes it. ON that account, the HPTA would have to clear to produce LH, but your androgen levels would still be too high for it to function properly.

    As well, degreed inhibition is something that needs to be proven, not merely stated. I want a study on that before I believe anything close to it. That body is usually binary, it either works or it shuts down. At some level the androgen level suppresses it, there is no gradation.

    So, while I think your thoughts are well reasoned, they are based on the faulty assumption of Clomiphene ONLY working through LH stimulation and not on the second function of Clo as well.
    I told you this would make for a good debate! Anyways, all I have is to say is that you are lucky my computer took a dump on me earlier, cuz I had the perfect reply for ya. Now I will have to make it short and sweet. Anyways, clomid in no way relates to LH chemically. So it cant "mimick" LH. It does not have a direct effect on the testes because it does not bind LH receptors in the leydig cells of the testes. (A good note is that there is estrogen receptors in the testes, but to what effect clomid has on these is unclear). Clomiphene cant bypass the hypophysis because it acts on the hypophysis. It was designed to act on estrogen receptors (and depending on the tissue specific receptor, either produces an effect or it does not. In the hypothalamus/pituitary, clomid binds to and antagonizes the receptor thereby preventing any effect. It merely occupies the receptor so estrogen cannot bind. The hypothalamus senses this decrease in estrogen and signals the anterior pituitary to begin producing LH, which travels via bloodstream to the testes to signal them to begin producing test. Yes, if you were to have only high levels of estrogen and low levels of androgen clomid works to block the inhibitory effects of estrogen. But when on a heavy androgen cycle, you are inhibited not only by increased estrogens but by increased androgens as well. Clomid does nothing in regard to preventing inhibition at this level. If you have proof of clomid working another way, please lead me to it! Otherwise take a look at the mecahnism of action and the pharmacology of clomid.
    Now for you saying the body is usually binary, I am not sure what you mean by this. But the body does not work by a simple "on/off" mechanism. Otherwise, how do you explain up/down regulation, tolerance etc, inhibition, disinhibition etc. There are many effects that take place when a hormone (lets say d-bol) binds to its receptor. It does not just merely turn on that receptor, it involves an entire cascade of events affecting not only that receptor, but many other cells, receptors and mechanisms as well. It is a complicated event, with some things manifesting quickly (CNS effects), and others taking more time (protein synthesis). Look at what happens in a womans body when they go through menses or when a woman is pregnant! There are many changes in their levels of hormones. When a woman goes through menses, GnRH in the hypothalamus triggers release of LH/FSH from the anterior pituitary ,subsequently stimulating estrogen/progesterone levels, which in turn come back and turn off GnRH production and LH/FSH production. It is a delicate balance. Their bodies are going through phases of inhibition and disinhibition by both positive and negative feedback mechanisms involving more than just an on/off type of mechanism. It is obvious if I were to do a short cycle with short acting AAS, I would recover quicker than if I were to do a full blown 12-15 week cycle. Your nuts don't just disappear overnight, they gradually begin to atrophy and the extent depends on the depth of inhibition(as well as length of cycle, AAS used, doses etc). Just like your nuts don't just magically reappear after a long cycle. I wish it worked like that, but it doesn't. How can you say this is not "gradation"? Just like I said, your nuts just dont "turn off, or turn on". It is a process, and a very complicated one at that.

  13. #13
    Ozzy's Avatar
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    I can see it now.....G.S. and ichabodcrane as our next new Mod's Good debate bro's........I would like to see more concrete evidence also. Thanks for that

  14. #14
    ichabodcrane's Avatar
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    Originally posted by Ozzy
    I can see it now.....G.S. and ichabodcrane as our next new Mod's Good debate bro's........I would like to see more concrete evidence also. Thanks for that
    I tell you what ozz! You rip out crazy train for me, and I will give you all the "concrete" evidence you want. But really, if you think about it,it is just basic science (which can still be complicated). Go anywhere and look up the MOA of clomid, do a search on Pubmed/Ovid/Medline etc for the MOA of SERM's. You will find plenty of data on how they act as estrogens/antiestrogens in the various tissues. Clomid is a triphenylethylene derivative, it does not "look" or "act" like LH. It merely brings about LH production from the pituitary gland. Like I said above, it in no way resembles LH and does not act like LH. LH is a glycoprotein and hCG is structurally similar to LH.

    As far as inhibition, well we all know everyone is different. Everyone has a "set point" or level where their body maintains homeostasis in regards to hormone levels. It is an anomaly to state the body only functions as an on/off switch. Look at hormone up/down regulation, positive/negative feedback, inhibition/disinhibition in any physiology or pharmacology book and you will see it is not this simple. Like I said, there are a complexity of events that happen when a hormone binds a receptor. Look at the fact that a biphasic phenomenon occurs during continuous administration of LHRH (GnRH) analogues. Initially there is a rise in LH and testosterone as these agents stimulate release of pituitary gonadotropins (LH/FSH). But, after 3-4 weeks repeated dosing there is a fall in LH and testosterone levels which reach castration levels. If we were to graph this and you were to pick a point somewhere around 1 week, do you think the levels would be the same as they would be around 3.5 weeks? No they wouldn't. It doesn't go from 0 to 100 and back to 0 again. There are all the little numbers inbetween that matter too.

  15. #15
    G-S Guest
    Once again, it does. If you really want me to do the pharmacodynamics talk I will. Clo does not have to have the same chemical composition to mimic LH. Does HCG have the same chemical structure as LH? Fuck no it doesn't and it stimulates the testes just fine by MIMICING LH.

    I have a link to a diagram at the Univeristy of Utah's med school. I will post it. Notice the pathways in that diagram. One is a direct effect on the ovaries and the other is through the HPTA. TWO paths, not just one.

    As well, I suggest you go to Animal's board and read the LLewellyn thread where he takes your little theory apart piece by piece.

    You've also missed my whole point. I NEVER said using Clo would help you recover your HPTA while on. Go back and read what I wrote to you. Your HPTA is shut down but since Clo mimics LH, you get virtually the same effect from Clomid as you would HCG but without the bad side effects of an estrogen bump.

    Honestly, I am not sure what you are trying to prove here anymore. My posit is simple. Using Clo during a cycle will help keep testicular atrophy to a minimum by mimicing LH and stimulating the testicles. When you go off, your recovery will be quicker due to the mass retained in the testicle.

    You on the other hand have turned this into a debate about inhibition--and that's not the point. Your inhibited at that point, I grant you that...and I never argued differently.

    Good day.

  16. #16
    G-S Guest
    Here is the link. Sorry for the ommission.

    http://medlib.med.utah.edu/kw/human_...rinfert_14.gif

  17. #17
    ichabodcrane's Avatar
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    You know, I am glad you want to talk about pharmacodynamics/pharmacokinetics because this is my major. If you look at that dynamic diagram again, it shows clomid binding to ESTROGEN RECEPTORS IN THE OVARIES!!!! How can you relate this to men? You don't need to get upset bro, this is merely a healthy debate. I have read lots of Bill L's theories and they seem to differ from what he first stated. Although he does seem pretty knowledgeable! But I will go through them again. Like I said, clomid binds estrogen receptors, it does not bind leydigs cell receptors.
    HCG is a polypeptide hormone produced by the human placenta. It is composed of an alpha and a beta sub-unit. The alpha sub-unit is ESSENTIALLY IDENTICAL to the alpha sub-units of the human pituitary gonadotropins, luteinizing hormone (LH) and follicle-stimulating hormone (FSH), as well as to the alpha sub-unit of human thyroid-stimulating hormone (TSH). The beta sub-units of these hormones differ in amino acid sequence. So come again! If these alpha sub-units are virtually identical to each other, how can they be so different in structure?
    Sorry I have to go, but believe I will have more to say when I come back. Meantime, I suggest you do a search on the mechanism of action of clomid.

  18. #18
    ichabodcrane's Avatar
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    "Once again, it does. If you really want me to do the pharmacodynamics talk I will. Clo does not have to have the same chemical composition to mimic LH. Does HCG have the same chemical structure as LH? Fuck no it doesn't and it stimulates the testes just fine by MIMICING LH."

    Like I already stated, hCG infact does posess simular chemical structures relating to LH/FSH. This is how it is able to "mimick" LH.
    Clomid in no way structurally resembles LH, therefore does not "mimick" LH.

    "I have a link to a diagram at the Univeristy of Utah's med school. I will post it. Notice the pathways in that diagram. One is a direct effect on the ovaries and the other is through the HPTA. TWO paths, not just one."

    Ok, I went and found that particular site you were referencing to. Note they merely state what I already stated:
    'The predominant site of action of clomiphene citrate is the hypothalamus. Clomiphene possesses both estrogen agonist and antagonist properties and binds to hypothalamic estrogen receptors. The hypothalamus in turns perceives a hypoestrogenic state, which results in the accentuation of discharge of gonadatropin-releasing hormone. GnRH then affects the anterior pituitary gland to produce and secrete follicle-stimulating hormone and luteinizing hormone. Clomiphene may also directly affect the ovary and other estrogen-dependent tissues, as well. Patients who initiate clomiphene therapy will notice hot flushes while taking the drug.'

    Note: they say clomid may directly affect the OVARY and other ESTROGEN-DEPENDENT tissues. This is because clomid was designed to bind estrogen receptors. Nowhere do they say it mimicks LH, or bypasses the hypothalamus/pituitary to posess a direct effect. Clomid functions indirectly, via hypothalamus estrogen receptor binding, to signal production of gonadotropins LH/FSH.

    "As well, I suggest you go to Animal's board and read the LLewellyn thread where he takes your little theory apart piece by piece."

    Here is the link for anybody interested.
    animalkits.be
    click on forum> 9th link down (Ana, clo, nol, let, Anti-EE's HCG, gyno), when in this post it will be the 7th link down (Llewellyn article on post cycle recovery)

    What in here do you find to be so controversial to what I stated?

    "You've also missed my whole point. I NEVER said using Clo would help you recover your HPTA while on. Go back and read what I wrote to you. Your HPTA is shut down but since Clo mimics LH, you get virtually the same effect from Clomid as you would HCG but without the bad side effects of an estrogen bump."

    Again, clomid does not "mimick" LH and you do not get the same effect you would as using hCG. I already covered this in my first post reply. This is why you use hCG to help prevent/reverse testicular atrophy.

    "Honestly, I am not sure what you are trying to prove here anymore. My posit is simple. Using Clo during a cycle will help keep testicular atrophy to a minimum by mimicing LH and stimulating the testicles. When you go off, your recovery will be quicker due to the mass retained in the testicle."

    I will agree with you here, only in the regard I do tend to ramble on. But, I am not trying to "prove" anything. I am merely trying to show you how clomid works/does not work, and show you that the body is not binary and does not function as such. There is degreed inhibition, and I think anyone who has been cycling long enough will agree. Running a heavy 4 week cycle proves less inhibitory than running the same drugs/doses for 12-15 weeks. Again, clomid does not mimick LH. Yes if you were to prevent testicular atrophy (using hCG), recovery will be easier, because the testes will be more receptable to LH due to the fact that they will act as this gonadotropin was never missing in the first place. You keep them stimulated, when normally without LH they are not stimulated. When you take proper signal (LH) away from the testes, in time they will atrophy. They aren't receiving LH during cycle, so they see no need to function.

    "You on the other hand have turned this into a debate about inhibition--and that's not the point. Your inhibited at that point, I grant you that...and I never argued differently."

    Sorry if I turned this into a debate about inhibition, but I think inhibition is very relevant in this regard. It's easy to just respond with a yes/no type answer, but getting back to the problem and processes related is important, sometimes, in providing a proper answer.

  19. #19
    ichabodcrane's Avatar
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  20. #20
    G-S Guest
    You've studied. So have I. End of story.

  21. #21
    ichabodcrane's Avatar
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    Originally posted by G-S
    You've studied. So have I. End of story.
    Because You seem so determined to prove me wrong, I am curious to know the extent of your studies/schooling. I told you I have nothing to prove, but it seems that most of your theories came from animals board and from what he himself stated. You are the one who chimed in and said said I was wrong. I gave you perfectly logical reasoning to my theory, and I can give you much more, as much as you want. I don't want this to turn into a stupid argument, but when you come on here and try to disprove my logical theories based from what I can tell seemes solely from what animal stated in his thread, than you need to realize there is more to it than just that. I have been in school for 7 years. I don't know everything, nor have I ever claimed to. But I will tell you that when it comes to drugs and how they work in the body, well like I said before, this is my major. I just want you to realize that how you think you understand clomid works by "bypassing" the HP, "mimicking LH" and having a "direct" effect on the testes is wrong. I told you that it does possess direct effects in the ovaries, but that is only because it binds estrogen receptors in them and has nothing to do with our discussion, and you have to admit it does not work like that. I want you to also realise the body is not, how you say, binary. There is much more to it than that. The same goes with how you said hCG does not chemically relate to LH. I am interested to know where you got this from. Did you even bother to look up anything about hCG and how it does in fact relate to LH structurally? Please don't ever base your theories just from what another person states (yes I am referring to animals respone to that thread). It just seems like your reasoning came from what he stated. I encourage you to further investigate this. Just because someone seems knowledgeable and may have their own board, or be a mod, or even a doctor, does not mean their theory is the only right one, or their theory is infact correct. I know many medical professionals who are clueless when it comes to our lifestyle, and they often try and give ME false info based on god knows what. Animal never gave ample studies to back up his theory. I think he saw the same site you did at the U of U, and drew his conclusion from there that clomid must, in some how bypass the HP to act directly upon the testes. I told you if you were to read what they said on their site, they never stated anything about how clomid "mimicks" LH in the testes. So it is your turn to give me feedback. We can work together on this or not. It is up to you. I never once tried to put you down, nor would I. This board is for us to learn and share experiences. I want to know if you still believe that clomid works by how you stated in your other reply? Have you really done any research on this compound, other than just looking at animals board and his reply? Did you really find anything that Bill L. stated to be so conflicting to what I stated? I think it is your turn to dig in and give me a solid reply!!!!!!!!! I told you I don't want to turn this into a pissing match, but you started taking it in that direction.

  22. #22
    G-S Guest
    Okay. Thanks for the info. I've learned some, and you should have too. The debate can only degenerate from here.

    But, my theories have worked, for me and others - they've been tested. That's how I know they work.

    Good day.

  23. #23
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    Cool! So no hard feelings bro! I agree, if it works for you, than by all means do it!

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