T Nation

Treat Symptons Not NUMBERS!!!! Need Help?


I went to the endo a couple of weeks ago. Finally got a letter in the mail today. I have been trying to resolve the low Test prolems for a couple of months now. Thought I had it.

Total Test- 242 (250-100)
Free - 1.56 (1.5-2.20)

Said everything else was in the normal range. Im having the results faxed to me tomorrow. Now he prescribed me 25mg of CLOMID a day, and wants to see me back in a month to six weeks. Why the hell is it so damn hard to do this shit the easy way. I'll stick myself with a needle all day long rather than take pills every day. Easy, convenient and cheap.

Anybody have any experience with Clomid only? Should I take an AI with it?


Also what are some of the side effects of Clomid. I've read "vision, mood swings, light depression.


Bah clomid for testosterone boosting ???

It will work, but its a stupid way to solve this.

I would buy some reserach chem letro for about 60 bucks and go on long term low dose self medication.

It will lower your E2, raise your T, and generally improve your quality of life.

It will also cost MAYBE 50 cents a day.

If your still unhappy with that, I recommend trying to get HRT.

If you get desperate you can always tank your testosterone levels by using fast acting orals to shutdown your HPTA and then coming off with no SERM

Your E2 will spike, your T will plummet and you SHOULD get an AI and test, or "androgel" atleast.

Again intentionally crashing the hell out of your endocrine system is a "last resort" or all "last resorts" move, but it is an option after the huge list of other ones are exhausted.


Side effects wise from clomid you will not see many at 25mg/day.

Long term usage may be an issue, and many users react differently.

No one I know has ever used clomid at 25mg/day, most users will dose at at least 50mg for PCT purposes.

The vision problems generally occur at higher doses, closer to 100mg/day. But if you see alot of "floaties" or flashes of light in your peripheral, or trouble focusing, fuzziness, then youll need to drop the clomid.

The mood swings and depression are the famous "clomid blues" and are again, from taking higher doses, closer to 100mg/day.

Clomid is actually an estrogen, but it binds only to certain receptor sites.

The estrogenic effects are what throw your body out of whack, your more "chick like" for lack of a better explanation. Higher estrogenic compound levels can cause emotional imbalances.

But the effects are exaggerated because the male body is much more sensitive to estrogen level changes.

For example, when I used to use clomid for PCT's at 75-100mg/day I would cry about shit sometimes.
If I saw something really sad on TV, or an inspirational story, I would tear up a bit.

This was VERY disturbing at first as I had not cried since I was a child.


Just filled it. Not covered by insurance, so the endo is getting a call tomorrow. This is the Endo's way to trying to get around HRT. I've even tried to play dumb while at the doctors to try and get on HRT. When you know more than they do, and I know very little it tends to go the wrong way.

I'll treat myself for the price I just paid.


I have cited this article before:[i]

Complete reversal of adult-onset isolated hypogonadotropic hypogonadism with clomiphene citrate.

Ioannidou-Kadis S, Wright PJ, Neely RD, Quinton R.
Department of Endocrinology, Royal Victoria Infirmary and University of Newcastle-upon-Tyne, Newcastle-upon-Tyne, United Kingdom.
OBJECTIVE: Inhibition of pituitary gonadotropin secretion in men by T is principally mediated by aromatization to estrogen (E), which inhibits hypothalamic secretion of GnRH. We hypothesized that adult-onset isolated hypogonadotropic hypogonadism (IHH) might result from an altered central set-point for E-mediated negative feedback. DESIGN AND SETTING: Longitudinal clinical investigation unit-based evaluation of the clinical and biochemical response to E-receptor blockade. PATIENT(S): A 31-year-old man presenting with an 18-month history of sexual dysfunction resulting from severe adult-onset IHH (LH 1.7 U/L, FSH 2.0 U/L, T 3.5 nmol/L). INTERVENTION(S): Initial therapy with 50 mg of clomiphene citrate (CC) three times a day for 7 days, with overnight LH pulse profiling and 9 am T levels evaluated at baseline and on completion. A 2-month washout period, followed by low-dose maintenance therapy (25-50 mg/d) for 4 months. MAIN OUTCOME MEASURE(S): Baseline and stimulated T levels and LH pulsatility; effect on sexual function. RESULT(S): Clomiphene therapy resulted in complete normalization of pulsatile gonadotropin secretion, serum T level, and sexual function. CONCLUSION(S): Isolated hypogonadotropic hypogonadism may result from an acquired defect of enhanced hypothalamic sensitivity to E-mediated negative feedback. Whereas direct T replacement therapy can further suppress endogenous gonadotropin secretion, treating IHH men with gonadotropins can stimulate endogenous T secretion and enhance fertility potential. On theoretical grounds, reversal of gonadotropin deficiency with CC might be expected to have a similar biological effect.


Your doc is not a fool. Personally, I would have measured at least an LH as well to establish whether you have IHH.
The clomid protocol is used to achieve normality; not just a normal mid-range T, but pulsatile excretion from your own nuts.
It can achieve this in 5 days of use, and after 4 months, some men are restored to normal--needle-free, pill-free and normal.

(Westclock, regarding clomid, is not entirely correct. To answer the other question, taking a low dose of an AI can boost T to higher ranges of normal in intact men.)


I was on clomid and T and my mood was excellent while on it. When I came off it was different story. Sometimes clomid is given by itself to kick start the testes and see if that works. It's funny while I was on the clomid and T I was as happier than hell, couldn't really get mad over crap but I had low energy. They took me off it and gave me a higher dose of t, mood went down energy went up.


I do not believe that clomid therapy should be used long term. Even many commonly prescribed AI's such as Adex should not be used long term.

My experience isn't with Over 35 Lifters, Ive really only seen situations where the problem was an improperly run PCT or other mistakes using AAS in men with otherwise healthy systems.

In these situations we generally recommended two options...simply continuing dosing nolva at 20mg/day, extending the PCT a few more weeks, can correct most imbalances caused by such situations, and a comparable dose of clomid or other comparable SERM would no doubt do the same.

Dosing an AI such as letro or adex will also generally correct these issues quickly post cycle, if the standard PCT fails to provide full recovery.

But that is assuming his system is actually capable of functioning at a "normal" output and was merely unbalanced.

I have had to extend my PCT almost 3 weeks before before my blood work was more acceptable.

If he needs constant usage to boost his test into acceptable ranges, then clomid seems a poor choice from a cost and safety standpoint. I would prefer letro, or fullblown HRT in such case.

If I am wrong on any of this, please feel free to correct me, my experience in this matter is limited to attempting to fix "broken", fellow, 20-something juice heads. And may not be completely relevant to his situation.


In the note he dictated me, he said that the LH and prolactin #'s were normal. I'm getting the results today to have the numbers in front of me.

If your estrogen level is low, would the Clomid be less effective? Also the not covered by insurance is a deal breaker. $51.00 a month for 15 pills.


Seeing the complete bloodwork would help alot.

If the E2 is low-normal (which is what we shoot for, around 20), then letro isn't going to help as much.

The clomid may be more effective in this case.


And it is a sterling service which you perform, sir!

I was just commenting in passing that it may be reasonbable to think of clomiphene, as tamoxifen, as a weakily estrogenic mixed anatagonist. It serves as an E antagonist at hypothatlamus and at pituitary, and the OP's physician is using it in this way.

To answer the OP, yes, AIs work well, but despite my efforts to start a trial, the medical literature is not as well developed as it is with clomid. By my very small (and unpublished) experience, AIs and clomid will stimulate GnRH (and T) production, even if E is low.


Either they were closed today or everytime I called, nobody answered. So no full test results. As far as "broken", I am broken just not in the self inflicted way. No drop in T because of a cycle. It's just disheartening to know that what's wrong with me can be fixed in a multitude of ways, but finding the right doctor that trust you enough to not abuse the medication. I just want my energy back.

Thanks for the info and first hand exp. I'll keep posting on this issue.


Dr.Skpx-- what journal/pub is this abstract from?


Yes, clomid can do that for some and the article demonstrates some mechanics -cause and effect. It does not address side effects, long term effects or other therapeutic issues. One has to be careful when extrapolating from narrow studies like this.

The effect has been widely known and understood. What is demonstrated is that the known increase in gonadotrophins is pulsatile. In retrospect, it would be totally unexpected to be otherwise.

With the effect demonstrated, one needs to assume that this effect exists for other SERMs and choose an SERM that has less side effects or better suitability for men such at toremifene.

Interesting thing about pulsatile stimulation of the pituitary. This may help maintain the general functioning of all pituitary functions as there are cross activation effects... the most common and understood of these is high TSH levels increasing gonadotrophins as seen in PCOS.

I have wondered if HPTA shutdown limits GH release... no basis in fact for this thought.


Here ya go, Bud; #2 is the article for which I pasted the abstract.

Complete reversal of adult-onset isolated hypogonadotropic hypogonadism with clomiphene citrate.
Ioannidou-Kadis S, Wright PJ, Neely RD, Quinton R.
Fertil Steril. 2006 Nov;86(5):1513.e5-9.
PMID: 17070201 [PubMed - indexed for MEDLINE]
Related Articles
Select patients with hypogonadotropic hypogonadism may respond to treatment with clomiphene citrate.
Whitten SJ, Nangia AK, Kolettis PN.
Fertil Steril. 2006 Dec;86(6):1664-8. Epub 2006 Sep 27.
PMID: 17007848 [PubMed - indexed for MEDLINE]
Related Articles
Clomiphene citrate effects on testosterone/estrogen ratio in male hypogonadism.
Shabsigh A, Kang Y, Shabsign R, Gonzalez M, Liberson G, Fisch H, Goluboff E.
J Sex Med. 2005 Sep;2(5):716-21.
PMID: 16422830 [PubMed - indexed for MEDLINE]
Related Articles
Clomiphene increases free testosterone levels in men with both secondary hypogonadism and erectile dysfunction: who does and does not benefit?
Guay AT, Jacobson J, Perez JB, Hodge MB, Velasquez E.
Int J Impot Res. 2003 Jun;15(3):156-65.
PMID: 12904801 [PubMed - indexed for MEDLINE]
Related Articles
Use of clomiphene citrate to reverse premature andropause secondary to steroid abuse.
Tan RS, Vasudevan D.
Fertil Steril. 2003 Jan;79(1):203-5.
PMID: 12524089 [PubMed - indexed for MEDLINE]
Related Articles


The others are to show that this is not a "narrow" band of interest.

Whether other SERMs are interchangeable is arguable and testable but not proven equivalent. Yes, AIs and tamoxifen can cause a rise in T, but I do not know if the same is true for toremifene and raloxifene. KSman infers that pulsatile GnRH production would be obvious, and a effect common to the other SERMs, but there is no proof there. (i.e. enclomiphene may have very different CNS kinetics than entamoxifen and nortamoxifen.)

The prinicpal trials use only 4 months of clomiphene at a variety of doses. It is hard to think that there are important lasting side effects, and none were reported among the hundreds of men in these trials.


We know that young men on GEAR, aka more normal than hypogonadics, report a lot of side effects from clomid, mostly in the context of short duration. It is not hard to extrapolate from these reports from short term use to the implications of life long TRT use. Many have stated that clomid is not suitable for long term use when looking at the QOL envelope.

It is reasonable to assume that all SERMs will involve pulsatile stimulation of the pituitary LH release until someone gets grant money to do some research that shows otherwise.

We know that a constant elevated level of Gonadotropin-releasing hormone (GnRH) actually shuts down LH release.

This is worth reading:


"""Agonists do not quickly dissociate from the GnRH receptor. As a result initially there is an increase in FSH and LH secretion (so-called "flare effect").

However after about ten days a profound hypogonadal effect (i.e. decrease in FSH and LH) is achieved through receptor downregulation by internalization of receptors. Generally this induced and reversible hypogonadism is the therapeutic goal."""

SERMs elevate GnRH levels. If the GnRH levels were constant [not pulsatile] then the GnRH receptors would down regulate and shut down LH and FSH release.

With these facts at hand, I stand firmly by my prior statements.


My report is I felt very very good on clomid. Like all meds it's situational about side effects. Guys are put on it for fertility all the time and report no side effects. Guys shooting T for a cycle are way and above normal ranges and even if they didn't take clomid I'm sure they might be having some of the same effects as if they didn't take it but to a larger degree. Hell I was on T and clomid and actually got depressed shortly after discontinuing the clomid and depression was never one of my symptoms for low t.


When you stopped the clomid, your LH and FSH shutdown and your testes stopped producing T and pregnenolone. You may have felt the pregnenolone loss. Note that when HPTA shutdown guys start hCG they very often report an improvement in mood - again often attributed too pregnenolone. The T increase when hCG in introduced is often not major compared to the TRT established baseline.

hCG does what SERMs do in terms of getting the testes functional as far as LH equivalency goes. That is done without the sides of SERMs.

Note that TRT induced HPTA shutdown can accurately be described as a therapeutically induced hormone deficiency [LH and pregenenolone] and the atrophy of the testes can create physical changes that can be described as therapeutically induced organ failure.


Now I see what you meant.
I was emphasizing that the clomid info was developed to demonstrate this restoration of pulsatile GnRH, and that the same had not been proven for other SERMs. They may work equally well. There are two minor points to be made: first, estrogen antagonism (or deprivation) has different effects on the hypothalamus and the pituitary. The active metabolites of each parent compound may act differently in those 2 places. Second, in women, the end-organ effects of tamoxifen, clomiphene and raloxifene are different; these differences may be mediated in part by different effe cts on the HPTA.


If you are under age of 25 and if you pass the clomid challege test then 6 weeks on clomid is given at specify dosage at every 3 days then blood is drawn on 3 weeks in to see where levels are at. After 6 weeks it is stopped and 3 weeks blood is drawn and tested. If it holds great and retest in 8 weeks again. If it does not hold then HCG is given while proper nutrients are given to help produce hormones increases their chances of being successful. While this is going on thyroid and adrenals should be addressed as well because these are essential in proper hormone production.

Age dependent then TRT may be commenced as well as supporting other hormones at same time.