T Nation

Clomid During Cycle

Has anyone used clomid DURING AND AFTER your cycle? I want some thoughts on the usefulness of this technique. In theory, it should keep from supressing normal test production during the cycle, lessen estrogenic effects, and quicken the recovery (everything it does after the cycle).

Since it is binding to the estrogen receptor, it shouldn’t be competeing with androgen binding hormones, right? So why not use it during a cycle? I have done this before … seems safer, right? Am I missing anything? Why isn’t everyone doing this? Clomid is pretty cheap.

[quote]lattimus wrote:
Has anyone used clomid DURING AND AFTER your cycle? I want some thoughts on the usefulness of this technique. In theory, it should keep from supressing normal test production during the cycle, lessen estrogenic effects, and quicken the recovery (everything it does after the cycle).

Since it is binding to the estrogen receptor, it shouldn’t be competeing with androgen binding hormones, right? So why not use it during a cycle? I have done this before … seems safer, right? Am I missing anything? Why isn’t everyone doing this? Clomid is pretty cheap.[/quote]

This is simply not true…First off, while on cycle your body is receiving a supraphysiological amount of androgens, which depending on a number of factors, such as the AAS’s affinity for the androgen receptor, will cause the hpta to become suppressed.
Now post cycle, when the amount of androgens present is nil or close to it, clomid will aid in regenerating the hpta.
If suppression is a major concern for you, keep the duration of the cycle short to moderate and run an aggressive pct. Just my 2 cents.


So, mikekatz. Are you trying to tell me that the hypothalmus will stop the pituitary from producing LH while in the supraphysiologic state? And that using clomid during cycle will only help in estrogen blocking, since it will still bind to estrogen receptors? And that only after cycle can clomid stimulate the hypothalmus, which acts on the pituitary to produce LH, and cause any anti-supressive effects? I am not trying to be an ass, just trying to be clear.

You mentioned the hpta (hypothalmus-pituitary-testes-axis) which is good, so I hope you understand what I am saying. But do you feel that clomid can still stimulate the hypothalmus during the cycle, competitively (I know that the hypothalmus receives neural signals and there is not really competetive receptor binding going on), or give mixed signals to the hypothalmus?

Bro, you are answering your own questions…Yes, suppression will occur even if clomid were used in conjunction with AAS…If it were this easy to avoid suppression, bbers wouldn’t be concerned about coming off aas to keep the hpta “healthy”

Clomid and Nolvadex can both be classified as SERMS…however, I have found nolvadex to be far superior in warding off gyno, and reserve clomid for it’s regenerating effects on the hpta post cycle. Hope this helps.


i only run clomid when i’m on if i have met some chick i wanna blow a huge load all over…in all seriousness, its a waste during your cycle. nolva is a superior SERM for protecting against gyno as MK said, and AI’s are far better.

to answer your question…i copied a part of a post originally submitted by LuvMuhRoids from another board.

Selective Estrogen Receptor Modulator (SERM) Compounds that bind with estrogen receptors and exhibit estrogen action in some tissues and anti-estrogen action in other tissues. The ideal SERM would deliver all the benefits of estrogen without the adverse effects. ex: Clomiphene Citrate (Marketed as Clomid or Serophene). Tamoxifen (Marketed as Nolvadex).

Aromatise Inhibitor (AI) Aromatase inhibitors exhibit a very different mechanism of action than SERM?s. Aromatase inhibitors prevent the conversion of androgens into estrogen in fat, muscle, breast, and brain. ex: Anastrazole (brand name Arimidex). FEMARA (letrozole tablets).

NOTE: Clomid and Nolvadex are both anti-estrogens belonging to the same group of triphenylethylene compounds. They are structurally related and specifically classified as selective estrogen receptor modulators (SERMs) with mixed agonistic and antagonistic properties. This means that in certain tissues they can block the effects of estrogen, by altering the binding capacity of the receptor, while in others they can act as actual estrogens, activating the receptor. In men, both of these drugs act as anti-estrogens in their capacity to oppose the negative feedback of estrogens on the hypothalamus and stimulate the heightened release of GnRH (Gonadotropin Releasing Hormone). LH output by the pituitary will be increased as a result, which in turn can increase the level of testosterone by the testes.

Although these two are related anti-estrogens, they appear to act very differently at different sites of action. Nolvadex seems to be strongly anti-estrogenic at both the hypothalamus and pituitary, which is in contrast to Clomid, which although a strong anti-estrogen at the hypothalamus, seems to exhibit weak estrogenic activity at the pituitary.

by William Llewellyn

Clomid, 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.

Nolvadex, is very comparable to Clomid, behaves in the same manner in
all tissues, and is a mixed estrogen agonist/antagonist of the same
type as Clomid. The two molecules are also very similar in structure.
It is not correct that Nolvadex reduces levels of estrogen: rather, it
blocks estrogen from estrogen receptors and, in those tissues where it
is an antagonist, causes the receptor to do nothing.

Cyclofenil, similar to HCG and Clomid in action. This drug is most
commonly used to increase endogenous testosterone levels after a cycle
in an attempt to avoid a hard crash while waiting for your hormone
levels to naturally balance. Similar to HCG and Clomid, cyclofenil
seems to quickly and effectively raise natural levels. Cyclofenil is
an estrogen that works as an anti-estrogen as well as a testosterone

Femara, (letrozole tablets) for oral administration contain 2.5 mg of
letrozole, a nonsteroidal aromatase inhibitor (inhibitor of estrogen
synthesis). Letrozole is a nonsteroidal competitive inhibitor of the
aromatase enzyme system; it inhibits the conversion of androgens to

Cytadren, (aminoglutethimide) at moderate doses, is a fairly effective inhibitor of aromatase and a weak inhibitor of desmolase (an enzyme needed for the
production of all steroids), and at higher doses becomes an effective
inhibitor of desmolase. It is therefore useful when using aromatizable
steroids, though it is not the drug of choice for this purpose.

Aromasin, tablets for oral administration contain 25 mg of exemestane,
an irreversible, steroidal aromatase inactivator. Exemestane is
chemically described as 6-methylenandrosta-1,4-diene-3,17 -dione.

Anastrozole,(Arimidex) is the aromatase inhibitor of choice. The drug
is appropriately used when using substantial amounts of aromatizing
steroids, or when one is prone to gynecomastia and using moderate
amounts of such steroids. It is manufactured by Zenica Pharmaceuticals
and was approved for use in the United States at the end of Dec 1995.

Proviron, is also an estrogen antagonist which prevents the
aromatization of steroids. Unlike the antiestrogen Nolvadex which only
blocks the estrogen receptors (see Nolvadex) Proviron already prevents
the aromatizing of steroids. Therefore gynecomastia and increased water
retention are successfully blocked. Since Proviron strongly suppresses
the forming of estrogens no re-bound effect occurs.

Teslac,is unique in its effectiveness as an antiestrogen. Like
Proviron, it prevents the aromatizing process of the steroids from the
basis. Thus, Teslac prevents almost completely the introduction of more
estrogens into the blood and subsequent bonding with the estrogen

6-OXO, contains a naturally occurring aromatase inhibitor that is devoid of any direct hormonal or prohormonal activity (androgenic or estrogenic). It is what science refers to as a “suicide inhibitor” of aromatase.

L-Dex, same as arimidex or anastrozole; known as an AI and popular on chemical supply sites. This is the name given on chemical supply sites instead of it’s original name. L-Dex meaning “Liquidex”.

There are a number of chemical research sites that sell liquid products similar to the above mentioned items. These products are the same but in liquid form such as liquid clomid, liquid nolva, liquid femera, and liquid arimidex.

Dosage’s are usually adminstered by droppers but dosage amounts per ml differ from site to site.

Just some notes you guys may be interested in.
I and many others hate clomid cause it makes me a bitch. A-dex is often too strong 0.5mg eod is usually enough. It can kill sex drive and people will blame their cycle. Nolvadex is my favorite anti-e and works against gyno from test and dbol…Remember a-dex/clomid/nov will not prevent gyno from tren, drol and other progesterone/prolactin gyno. Only estrogen related gyno.

To keep the boys going I’ve used two opposing methods and both worked well. One is Cy’s plan of using androgel OR injecting 100mg Test E. during the first few off weeks. The other is using 500IU (NOT 5000) 1-2 days/week of HCG while on ONLY…to keep the balls from atrophying (is that a word?)

Hi Again,
I wanted to point out Cy is against HCG as he?s got data showing it desensitizes the testicles to LH. More and more I favor his plan listed (and defended) below. It comes from his Steroids for Health 2003 article and a QA article.

[quote]End of Cycle Concerns
When it comes to maintaining gains, what you do at the end of your cycle is most crucial. First, we have to find a way to restore endogenous Testosterone production while fighting the catabolic effects of being in a hypogonadal state (which is the end result of sudden cessation of steroids).

It’s been demonstrated in normal, healthy young men that suppression of endogenous Testosterone production leads to a marked decrease in muscle mass and an increase in fat mass, and this is the reason why we experience the “loss of gains” after cessation of use in addition to the “shitty” feeling in general. It has nothing to do with the body having a mind of its own and dictating exactly how much muscle mass it will and will not allow you to have. (18)

So, what do we do? Simple, we must first get T levels up to normal, while at the same time not suppressing endogenous Testosterone production. How can this be accomplished? Well, the best choice is Androgel since its pharmacokinetic properties allow for an increase in Testosterone yet no suppression of LH and endogenous Testosterone production.

The next best thing would be to use around 100 mg of Testosterone enanthate weekly as the peak seen is still very close to remaining within the physiological range. (19) In addition to this, you should be taking 50 to 100 mg/day of clomiphene so that you can restore endogenous Testosterone production quickly and thus wean yourself off of the Androgel.

While that will take care of steroid-induced low endogenous Testosterone levels, you’ll still lose some muscle. After all, you weren’t simply in normal physiological state while using androgens. We’ve lost the great nutrient-partitioning effects of androgens and thus need to make some quick adjustments.

Here’s one way to think about it: If you were to be ranked on a 1-10 scale in terms of lipolysis and protein synthesis, 5 would be your average physiological state, 3 would be when you’re hypogonadal (post cycle), and anything in the 6-10 range would be where you’re at when using supraphysiological doses of Testosterone or other androgens. So, using Androgel and clomiphene will ensure that we at least get back to a 5 and thus minimize loss of gains, but the next step is necessary in order to keep us at a higher range and thus further minimize loss of gains.

We need to pick some compounds which also have nutrient partitioning effects yet don’t affect hormonal levels. Biotest’s Methoxy-7 and a beta-2 agonist like ephedrine are the perfect combination. Both compounds will allow for an increase in nitrogen retention, as well as an increase in lipolysis and/or inhibition of lipogenesis.

When these two compounds are added in, we’re much closer to the range in which our gains were made and thus, we greatly minimize or completely prevent any loss of gains and prevent any fat gain. Similarly, you could also use forksolin along with Methoxy-7 and leave the ephedrine out. (20-23)

Androgel, Maintaining Gains and Message Board “Gurus”
Q: Concerning your ideas about maintaining gains from your Steroids for Health article, you said Androgel will work provided that an estrogen antagonist or aromatase inhibitor is used concurrently. But Androgel is nearly impossible for me to get, so what about the next best alternative you wrote about: 100 mg/week of Testosterone enanthate? Would propionate work as well? Also, where?s the data to shut those people up who insist it can?t be done?

A: Your alternative will still work well when you consider the peak concentration of Testosterone in the bloodstream. We have data supporting that suppression of LH can be prevented when elevating Testosterone up to a peak concentration of 2,044 ng/dl, provided that an estrogen antagonist or aromatase inhibitor is used.

When I recommended the 100 mg dose of Testosterone enanthate, I was basing that on the pharmacokinetic data which demonstrated that a 200 mg dose in seven eugonadal men resulted in a mean peak concentration of 1,965 ng/dl and 100 mg of enanthate given to seven eugonadal men resulted in a mean peak concentration of 1,181 ng/dl.

Oh, and before some genius decides to say “you can?t use that data because the person is in a hypogonadal state after a cycle and those people were eugonadal,” I want to point out that the peak concentrations when administered to hypogonadal men would be even less, as common sense would tell you, so it makes an even better case for my 100 mg/week of enanthate.

If common sense isn?t enough, research has shown the mean peak Testosterone concentration following the administration of 200 mg of Testosterone enanthate to seven hypogonadal men was 1,233 ng/dl. As you can see, the peak concentration is nowhere near 2,044 ng/dl. So, you could technically use 200 mg/week with my post cycle protocol and still be fine, but I?m going to stick to my original recommendation of 100 mg/week.

As for using the propionate ester, I suppose you could but I don’t have exact data on it. With what I do have, I’d say 25 mg every three days or so would be okay.

Lastly, as I’ve been saying to people for the past few years, I only recommend that you use Testosterone when employing such a protocol as it’s the only androgen where we have data demonstrating that at a certain blood level (? 2,044 ng/dl), LH isn’t suppressed provided that an estrogen antagonist or an aromatase inhibitor is used concurrently. From this, we can then apply our pharmacokinetic data we have with administration of various forms of Testosterone and figure out a protocol.

These two key pieces of information aren’t something that’ll be easily located with other androgens. Fluoxymesterone (10 mg every six hours) may be an exception as we have data on that, but again, to make things less complicated, I suggest you only use Testosterone.

Oh, and administration of even 10 grams of Androgel won?t get total Testosterone past 1,100 ng/dl so considering that, I recommend only 5 grams. There?s no way that suppression is an issue provided an estrogen antagonist or aromatase inhibitor is used. I also go more in depth about the studies listed in the upcoming print issue, explaining why it was shown to work, as well as explaining the involvement of the AR (Androgen Receptor) and ER (Estrogen Receptor), so be sure to check it out.

The data I?ve presented here as well as that in the upcoming print issue of Testosterone will shut those people up once and for all. That and the fact that every person who?s used my protocol (and reported back to me) has retained or even made gains while recovering endogenous Testosterone production. I?ve presented both “real world” and scientific evidence so there?s no doubt in my mind it works. (19-24)

When I make recommendations, I?m not simply pulling things out of thin air; I?m basing them on some pretty solid data. Unfortunately, not everyone will simply take your word for it and that?s fine. To those who don?t believe me, look up the referenced studies in their full text yourself and then maybe we can drop the idea that our HPTA works via magical mechanisms, where it literally “senses” things and “can?t be tricked” as if it thinks or has cognitive abilities to begin with.

Of course, there will be those uneducated message board imbeciles (oops, I mean “gurus”) who’ll try to dissuade you from thinking this can be done despite the evidence demonstrating it can be done and the complete lack of evidence supporting the idea it can?t. To them, data is just a bunch of words on a piece of paper they don?t understand. They?d rather believe in magic or Jo-Jo the local gym clown instead of the principle matters and research involved with molecular biology and endocrinology.
So there.

How, a lot of good research (secondary sources,of course), and some good experience opinions. Thanks to all. I asked specifically about clomid becuause I couldn’t really find a lot of research on its use in men. Nolvadex has been studied extensively as an anti-estrogen in breast cancer cases, so there is a lot of info available on it. Good stuff.

I’m having a slow reaction from my doctor for prescribing a good AI during my 100mg/week Cyp cycle (2.5 wks into my first treatment) because I’m currently not showing any adverse side effects. I have a script of clomid he prescribed if I start showing any symptoms of Gyno to be specific (His recommendation)

So my question is, will taking 25mg ED-or 50mg EOD of clomid While on my first HRT cycle (doc and I felt HRT was worth a trial period to see if it improved my labs/wellbeing, will revisit the topic of perminent HRT once my body has had time to feel the hopefully positive effects) Midigate the chances of me getting Gyno?. From a lot of reading on other threads (not HRT specific) most guys seem to be stacking an AI with their T to prevent a lot of the side effects of too much E2 and saving the clomid(SERMs) for PCT.

Is my Doc out to lunch with his prescribed method for minimizing E2 sides while at the early stages of my therapy? Should I try pressing him harder for an AI script before I get any further into my treatment. Any feedback/opinions are much appreciated.