Getting off TRT by Using Enclomiphene

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sh1973

Well-Known Member
Has anyone tried this for coming off trt? I’d like to hear from anyone that’s tried enclomiphene and what your experiences are regarding side effects and positives. I’m assuming Taylor made pharmacy is the only place in the US to acquire it.
 
Defy Medical TRT clinic doctor
Has anyone tried this for coming off trt? I’d like to hear from anyone that’s tried enclomiphene and what your experiences are regarding side effects and positives. I’m assuming Taylor made pharmacy is the only place in the US to acquire it.

Still chasing the restart, I see. I don’t blame you. I don’t have any personal experience with enclomiphene, but I am also curious. I imagine that it would be like any restart. It would soften the landing, but the minute you stop the medication you would experience all the symptoms of low t. After being on testosterone for several years, I think my chance of recovery is zero. Supplementing with testosterone for several years makes hypogonadism permanent and more acute. At least, that has been my experience. I have a restart a solid year, and the best I could do is 109. Practically a eunuch at that point. Unless they come up with a cure that is certain, I’ll stay on test. Being extremely hypogonadal for a year was no joke. It took a toll on my physical and mental health. If you decide to jump on enclomiphene, I hope you keep a journal for us.
 
I’ve only tried Clomid for a restart before I went on full blown TRT. It was horrible - I started with too high a dose and had anxiety for a month next round did 25 mg EOD and ended up with a 900 Ng/DL Total Test but it quickly came back down to my previous shitty levels.

my point being - you don’t need bodybuilding PCT doses of these products to get the job done. BUT - depending on your age and how long you’ve been on TRT, there may not be any going back.
Why would you want to come off? Are you having issues?
 
[QUOTE = "Paco1973, publicación: 181628, miembro: 18744"]
Todavía persiguiendo el reinicio, ya veo. No te culpo No tengo ninguna experiencia personal con enclomifeno, pero también tengo curiosidad. Me imagino que sería como cualquier reinicio. Suavizaría el aterrizaje, pero en el momento en que suspendas el medicamento experimentarás todos los síntomas de baja t. Después de tomar testosterona durante varios años, creo que mi probabilidad de recuperación es cero. Complementar con testosterona durante varios años hace que el hipogonadismo sea permanente y más agudo. Al menos esa ha sido mi experiencia. Tengo un reinicio un año sólido, y lo mejor que puedo hacer es 109. Prácticamente un eunuco en ese punto. A menos que encuentren una cura segura, me quedaré en la prueba. Ser extremadamente hipogonadal durante un año no fue broma. Afectó mi salud física y mental. Si decides saltar al enclomifeno, espero que nos guardes un diario.
[/CITAR]

Cuantos años tienes
eres primaria o secundaria
 
I was more curious about its use in conjunction with test. Really curious if it would stimulate lh. I’ve accepted that I’m on for life at this point but was curious if endogenous production of lh could improve libido but I’d imagine not.
 
Should have worded the post differently I’m more curious if it carries the same side effects as clomid because the side effects from that are atrocious
 
Clomid was really harsh for me also. It would be cool to dump HCG for enclomiphene if it worked and the sides were less. You talk to your doc about it? I think Defy offers it. It’s on their medication portal.
 
Im going to ask them about it to see what they think. I really think that’s the missing piece for some men feeling normal just keeping some endogenous hormones going
 
What dose were you on? Is it dose dependent?
I started at 12.5 mg daily and went up from there. I had no LH/FSH response. As far as the OPs original concern I didn't experience any sides but then again I didn't really notice any sides when on clomid so perhaps I'm not a good data point.
 
I was more curious about [enclomiphene's] use in conjunction with test. Really curious if it would stimulate lh. I’ve accepted that I’m on for life at this point but was curious if endogenous production of lh could improve libido but I’d imagine not.
Generally this is a no-go because testosterone has a direct suppressive effect at the hypothalamus; enclomiphene stops suppression by estrogens only.

...I’m more curious if it carries the same side effects as clomid because the side effects from that are atrocious
Clomid should be viewed as enclomiphene plus estrogen. Naturally it's more likely to cause side effects than enclomiphene alone.

... I really think that’s the missing piece for some men feeling normal just keeping some endogenous hormones going
As you know, my experimentation supports this proposition. Although we're unlikely to see clinical trials anytime soon, if ever, I'm hopeful that there will be additional anecdotal evidence in the near future.
 
First of all I want to thank you for taking the time to discuss all of this. I find all of it fascinating and if we can encourage a few people to tackle this protocol in a scientific and stepwise manner we can really make a change in people's lives.

So let's go about building the protocol. Ideally we would wait until testosterone levels reach equilibrium on whatever delivery method we choose and then change variables one at a time. I especially want to add GNRH and kisspeptin separately just to see if I can discern the merits of each individually. I discontinued test cyp injections on Sunday and have switched to Natesto in order to get the long lasting ester out of my system. After a couple of weeks I can either continue natesto thrice daily or switch to your prop/enan blend.

After that we need to figure out how best to add:
Enclomiphene 12.5 mg thrice weekly
Progesterone - dose TBD (I get labs drawn tomorrow on that)
GNRH - 20,20,20,20,20,10
Kisspeptin

If you had to start all over again in order to determine the relative merits of each how would you have built this protocol so as to change one variable at a time?
 
... I discontinued test cyp injections on Sunday and have switched to Natesto in order to get the long lasting ester out of my system. After a couple of weeks I can either continue natesto thrice daily or switch to your prop/enan blend.
An alternative is to continue the Natesto while injecting small amounts of cypionate or enanthate a couple times a week. The Natesto is taking the place of the propionate, providing the necessary peak testosterone levels. The concern is that you may end up too low between doses. Some cypionate or enanthate would provide a support level—ideally at least 2-300 ng/dL.

...
Enclomiphene 12.5 mg thrice weekly
...

I should mention that the quantitative results from last year were acquired with an enclomiphene dose of 12.5 mg daily. The switch to EOD dosing was made about 90 days ago. While the subjective results are at least as good, I don't know yet if the gonadotropin levels have been fully maintained. It's possible that the higher dose leads to a faster restart, but there's enough uncertainty that I can't make a strong recommendation.

...
GNRH - 20,20,20,20,20,10
...
I had to knock the pre-bedtime dose down to 5 mcg. Anything more interferes with sleep. YMMV.

...
If you had to start all over again in order to determine the relative merits of each how would you have built this protocol so as to change one variable at a time?
• TRT
• HCG (optional)
• Progesterone
• GnRH + enclomiphene
• Kisspeptin

This isn't too different from what I did, except I didn't finalize the TRT ester blend until after the progesterone. If hCG is used then it can be phased out when LH hits low-normal.
 
An alternative is to continue the Natesto while injecting small amounts of cypionate or enanthate a couple times a week. The Natesto is taking the place of the propionate, providing the necessary peak testosterone levels. The concern is that you may end up too low between doses. Some cypionate or enanthate would provide a support level—ideally at least 2-300 ng/dL.



I should mention that the quantitative results from last year were acquired with an enclomiphene dose of 12.5 mg daily. The switch to EOD dosing was made about 90 days ago. While the subjective results are at least as good, I don't know yet if the gonadotropin levels have been fully maintained. It's possible that the higher dose leads to a faster restart, but there's enough uncertainty that I can't make a strong recommendation.


I had to knock the pre-bedtime dose down to 5 mcg. Anything more interferes with sleep. YMMV.


• TRT
• HCG (optional)
• Progesterone
• GnRH + enclomiphene
• Kisspeptin

This isn't too different from what I did, except I didn't finalize the TRT ester blend until after the progesterone. If hCG is used then it can be phased out when LH hits low-normal.
On my trial run of Natesto I was running a trough TT level of 500 first thing in the morning 12 hours after my last application. Would that suffice? Also based on your experience would you advocate for 25 mg or 12.5 on the enclomiphene to start?
 
On my trial run of Natesto I was running a trough TT level of 500 first thing in the morning 12 hours after my last application. Would that suffice? Also based on your experience would you advocate for 25 mg or 12.5 on the enclomiphene to start?
It seems like your response to Natesto more than suffices. I'm surprised that you have such a good level after 12 hours if this is without any endogenous production.

On the enclomiphene dose I guess I'd lean towards 12.5 mg daily for starters, since it worked for me. In the clinical trials there was an even better response to 25 mg, so this should be kept as an option. For long-term use, after a successful pituitary restart, I think one should be willing to consider experimenting with lower and/or EOD dosing. I have lingering concerns about blocking some useful estrogen receptors along with the ones causing HPTA suppression. This is pure speculation: Perhaps with enclomiphene's relatively short half-life it's beneficial to let it somewhat clear out with EOD dosing. I'm wondering now if EOD dosing is overrepresented among those rare individuals doing well with Clomid monotherapy.
 

MP76-07​

COMPARISON OF THE EFFECTS OF ORAL ENCLOMIPHENE CITRATE AND TOPICAL TESTOSTERONE GELS TREATMENT ON SERUM HORMONES, ERYTHROCYTOSIS, LIPIDS, AND PROSTATE SPECIFIC ANTIGEN

Alexander W. Pastuszak*, Houston, TX; Ronald D. Wiehle, Gregory Fontenot, Joseph Podolski, The Woodlands, TX; Larry I. Lipshultz, Houston, TX

INTRODUCTION AND OBJECTIVES: Testosterone therapy (TTh) is often the mainstay for hypogonadism treatment. Adverse ef- fects of TTh include lipid abnormalities, erythrocytosis, and increases in prostate specific antigen (PSA). Enclomiphene citrate (En) can raise T levels, but its effects on lipids, erythrocytosis, and PSA are unknown relative to TTh. Here, we compare effects of topical T gels and oral En in hypogonadal men on serum hormones, lipids, erythrocytosis, and PSA.

METHODS: Data from 11 prospective, randomized, blinded Phase 2/3 trials of oral En, placebo, and T gels were analyzed. Men with secondary hypogonadism based on two morning serum evaluations for total T (TT) <300 ng/dL and low-to-normal LH were enrolled; 130 men on T gels, 290 on placebo, and 953 on En completed the study protocols. TT, dihydrotestosterone (DHT), estradiol (E), hemoglobin (Hgb), hematocrit (Hct), PSA, total cholesterol (Tchol), triglycerides (TG), LDL- Chol, and HDL-Chol were evaluated at baseline (BL) and during regular follow-up for up to 1 year, and compared using a mixed model linear regression for repeated measures.

RESULTS: Both T gels and En raised serum TT, DHT and E levels, with a more significant increase in TT and E levels in men on En (En TT: 216 64 vs. 450 182 mg/dL at BL and 12 months; T gels



TT: 231 74 vs. 379 187 ng/dL at BL and 12 months), and a slower return to baseline after treatment was discontinued. In contrast, Hgb and Hct were higher in men on T gels (Hct 49.3% at 12 months) than En (46.9% at 12 months), although only one patient discontinued T gel due to erythrocytosis (Hct >54%); no erythrocytosis occurred in men taking En. Small, clinically insignificant increases in mean PSA were



observed with En (0.8 vs. 1.2 ng/mL at BL and 12 months) that were not observed in men on T gels (0.9 vs. 0.8 ng/mL at BL and 12 months). Decreases in TChol (En: 190 vs. 178 mg/dL; T gel 193 vs. 190 mg/dL at BL and 12 months), HDL-Chol (En: 49 vs. 41 mg/dL; T gel 42 vs. 42 mg/dL at BL and 12 months) and LDL-Chol (En: 106 vs. 101 mg/dL; T gel 115 vs. 117 mg/dL at BL and 12 months) were observed with both En and T gels, with more significant changes with En. Effects on triglycerides were variable and inconsistent for both En and T gels.

CONCLUSIONS: En therapy results in more significant and sustained increases in TT and E, as well as more significant and sus- tained decreases in TChol, HDL-Chol and LDL-Chol, than T gel therapy. Clinically insignificant effects on PSA, Hgb, and Hct are observed. En may represent an effective, low-risk treatment option for androgen deficient men with few adverse effects.

Source of Funding: AWP is a National Institutes of Health (NIH) K12 Scholar supported by a Male Reproductive Health Research Career (MRHR) Development Physician-Scientist Award (HD073917-01) from the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) Program (to Dolores J. Lamb).



MP76-08​

SERUM LEVELS OF ENCLOMIPHENE AND ZUCLOMIPHENE IN HYPOGONADAL MEN ON LONG-TERM CLOMIPHENE CITRATE TREATMENT

Sevann Helo*, Joseph Mahon, Albany, NY; Joseph Ellen, Richmond, VA; Greg Fontenot, Kuang Hsu, Ronald Wiehle, The Woodlands, TX; Paul Feustel, Charles Welliver, Andrew McCullough, Albany, NY

INTRODUCTION AND OBJECTIVES: Clomiphene citrate (CC) is a non-steroidal selective estrogen receptor modulator (SERM) that increases testosterone (T) production by blocking negative feedback inhibition of estradiol on the hypothalamic pituitary axis. It is used off label to treat hypogonadal men (HM) and exists as a 60/40 % racemic mixture of the stereoisomers enclomiphene (EN) and zuclomiphene (ZU), respectively. EN is a potent estrogen receptor antagonist reaching peak plasma concentration (Tmax) in 4 hours (hrs), with a half-life (T1/2) of 8 hrs. ZU is an estrogen receptor agonist that reaches a Tmax in 7 hrs, with T1/2 greater than 40 hrs. A study evaluating the relative concen- trations of EN and ZU in HM on long-term CC therapy has never been performed. Our aim was to evaluate the serum concentrations of each isomer in HM on long-term CC treatment.

METHODS: With institutional review board approval we recruited HM currently on CC treatment to have serum EN and ZU concentration levels drawn. All patients were on generic CC 25 mg daily for a minimum of 6 weeks. Patient characteristics, hormone levels, and duration of treatment were reviewed. EN and ZU serum concentration levels were obtained for each patient using liquid chromatography-mass spectrometry with a Kinetex XB-C18 reverse phase column.

RESULTS: A total of 15 men were enrolled from June 2015 to August 2015. Mean patient age was 42, mean BMI 31.8, and mean duration of treatment 31.5 months; 12 men were treatment naive. Mean T increase was 31.2% from baseline. Although CC was administered as a 3:2 EN:ZU racemic mixture, prolonged treatment resulted in a 1:27 EN:ZU ratio of serum concentration. Patient age, BMI, duration of treatment and serum T levels were not predictive of EN or ZU concentrations.

CONCLUSIONS: After prolonged treatment with CC in HM, ZU is the predominant isomer present in serum. Given the vastly different biochemical properties of EN and ZU, this study supports the need for development of a pure SERM for the treatment of HM.
 
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