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There seems to be a lot of cotroversy on a lot of boards right now about Clomid vs. Nolvadex for PCT in the BB community. Myself I am worried about the sides from Clomid. I never did PCT before, I just cyckled and ate like a horse. So whats the valid points for each?
Posted by LMR @ freakymuscle
Clomid (Clomiphene Citrate), stimulates the hypophysis to release more gonadotropin so that a faster and higher release of follicle stimulating hormone aud luteinizing hormone occurs. This results in an increase of the body's own testosterone production. Clomid is a synthetic estrogen, however it does also work as an anti-estrogen. How does it work? Because it is a weak synthetic estrogen, it will bind to the estrogen receptor (ER) and not cause any problems. At the same time the increase in estrogen
from steroids are blocked from attaching to the ER.
Clomid therapy usually is administered in dosages of a 300/100/50 split. Administration is done orally at 300mg day1, 100mg 10days, 50mg 10days. Other methods have shown recovery but this seems to be the preferred method.
It is in my opinion, clomid is a weak anti-estrogen blocker and is a selective SERM. Clomid is selective towards hypothalamus & pituitary(also the ovary, endometrium, vagina, and cervix), which also accounts for the de-sensitization to GnRH. As opposed to nolvadex.
Clomid and Nolvadex are both anti-estrogens belonging to the same group of triphenylethylene compounds but they act very differently at different sites of action. In my opinion this is one reason why both should be used in conjuction to stimulate LH levels and restore HPTA.
It is suggestable to administer clomid therapy post cycle in different times after last injection. Reason is, androgen levels must be low enough so not to render clomid useless or inhibit its actions to stimulate LH levels. Also, If the androgen receptors are still active it sends signals through the HPTA so shut test down. Thus clomid is in a useless battle and only purpose is to serve as an anit-estrogen blocker.
Clomid stimulates the LH levels back to normal for proper restoration of the HPTA. Nolvadex along with clomid being two serms are individualy seletive to certain tissue. So it is ideal to run both. When you cease steroid administration a certain estrogen backlash will happen. This is because you have no testosterone in your system as well as the non-production of your own test. At this point estrogen floods the receptors and you will experience a crash and become subceptable to gyno symptoms or inflamation of the mammory glands.
Clomid is has anti-estrogen abilities but not nearly as strong as nolvadex thus you need them both. Important note: Clomid does not stimulate the release of natural testosterone, but rather works at reducing the oestrogenic inhibition caused by the steroid cycle.
Below is a reference chart to resort to for clomid therapy. It is suggested to run 20mg of nolvadex in conjuction with clomid therapy. This combo is ideal. Higher dosages of course are needed if gyno symptoms or inflamation of the glands appear at about 60-80mg's through out until symptoms subside.
Anadrol50/Anapolan50 8 - 12 hours 3 weeks
Deca durabolan 3 weeks 4 weeks
Dianabol 4 - 8 hours 3 weeks
Equipoise 17 - 21 days 3 weeks
Finajet/Trenbolone 3 days 3 weeks
Primabolan depot 10 - 14 days 2 weeks
Sustanon 3 weeks 3 weeks
Cypionate 2 weeks 3 weeks
Enanthate 2 weeks 3 weeks
Propionate 3 days 3 weeks
Suspension 4 - 8 hours 2-3 weeks
Winstrol 8 - 12 hours 2-3 weeks
LMR
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got this from LawnSaver on 1morerep.
Good Article on Understanding HPTA Inhibition and Recovery from AS
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.
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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.
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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:
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.
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.
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.
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Drugs of Use With Regard to Inhibition
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.
I'll be nonest and say I've never ran a thing for pct before,and experienced little to no muscle loss.But that doesn't mean I recovered properly.My sex drive was ok after cycle,but I have no idea what my blood test might have shown.
After reading that I think I will do the Clomid and Nolvadex together. The thing that makes me want to stay away from L-Dex is it may cancel out the HDL benefits of olvadex.
Reread Pheedno's pct and explanations many times over. All of the arguments for nolva over clomid are based on misinformation. The ONLY potential argument is the sides some experience with clomid. IMO, this is a minor trade off for proper pct. Clomid, nolva and Ldex....I'm still waiting for a valid argument against this.
That is exactly correct. Arguments of nolva over clomid are based on misinformation. I keep coming across an article or two on several writers that, in my opinion, did not do proper research before they wrote an article. So now these articles are floating around the net and causing confusion. One article in particular is biased and clearly shows no research but a personal opinion against clomid.
In my research, I have read, studied, and deciphered articles of testings of clomiphene citrate and tamoxiphen citrate. The studies cleary show the selectiveness to certain tissue's. The studies cleary showed what nolvadex does and what clomid does during administration. In some of my pins or articles on many boards I have these links to prove it. Im sure if you read Pheedno's articles he will have them too.
Bottom line is, for proper PCT and restoration both SERMS are necessary. I am just learning that now for proper restoration and the control of Sex Hormone Binding Globulin that an AI is necessary during PCT as well.Quote:
Originally Posted by einstein1905
Hey lozgod i was worried about clomids sides to, im a moody person and i did not need a month of deppresion.Anyway i used clomid,nolva tribulus and b-12 injections(I thought the b-12 would help with deppresion because i feel so awsome on that stuff)I didnt experiance any deppresion or unwanted side effects.
i am on a month long clomid depression, b 12 helps, but it is a rollercoaster ride with emotions, for me at least, 1 more week, but i have kept amost all my gains, lost a little weight, went from 195 to 185 but i kept my size, i use 100 mgs clomid 20 mgs nolva ed and 6 g's trib ed, even though depression sucks, i would use both clomid and nolva again, also i am going to run 20 mgs nolva ed and l dex 25 mgs ed after clomid therapy for 1 week, but b 12 is awesomeQuote:
Originally Posted by sniper320
The first time period is how long the half life is and the second is how long after the last taking of the drug before starting pct, correct?Quote:
Originally Posted by Da Bull
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Originally Posted by dirtdawg
I did a nolva/Trib only PCT and lost 5 lbs...I was waiting for more time to pass before posting what I was able to keep but enough time has passed at this point that I feel confident that it is all I will lose. I ran my PCT a little longer than the average (5 weeks). I did lose some of the strength gains though...Bench went down from 515 to 475 and other body parts dropped about the same percentage.After my next cycle (starts July 1 ends Oct 1) I will try both the clomid/nolva and trib to see if that affects the gains any differently.
i was actually considering clomid for 4 weeks instead of 3, i used 300 mgs clomid day 1 and 100 mgs ed from then on, i really want to stop taking clomid as soon as possible though, i lost a lot of strength as well, but hey i look good though, boys are back to full size, i think, and i am still a horny little bastard :banana:Quote:
Originally Posted by Benches505
bumpQuote:
Originally Posted by Mu'min