Low testosterone / hypogonadism - OTC/Peptide Restart

[Guineapig]

Hello everyone,

I am starting this thread to present a problem I am facing in the hopes that someone can provide some useful insight.

I am 28 year old male, used to be very active with rockclimbing, mountainclimbing and weightlifting. Up until three years ago I had all the signs of healthy levels of testosterone . Strength, libido, mood. Libido was in fact through the roof and I suffered from little to none refractory period. I would get multiple erections a day and could "perform" several times in a row without somuch as a hint of fatigue. I was a happy young man.

Then something changed. I started experiencing mood swings and the signs of fluctuating test levels such as intermittent ED, acne outbreaks (never had them before). At this time I was referred to several psychiatrists as I thought the problem could be stress. I was placed on SSRI which aside from enhancing the problem served no poblem. The problems persisted. I never used AAS but please continue reading as the following details and protocol could be helpful regardless of this fact.

I then did several tests in the next years the results of which are here listed (I do not have access to the entire documentation as I am abroad right now except for one blood panel)

April 2014 - testosterone : 9,56 ng/ml [956 ng/dl if you covert the measurement units] (1,75-7,81) LH: 14,56 mIU/ml (1,24-8,62);
Estradiol 43 pg/ml (20-75)

August 2014 - testosterone: 6,70 ng/ml (1,75-7,81) LH: 13,56 mIU/ml (1,24-8,62);
Estradiol N/A

February 2015 - testosterone 2,58 ng/ml (1,75-7,81) LH: 3 mIU/ml (1,24-8,62);
Estradiol N/A

April 2015 (after a week of abstinence from sexual activity and exercise)
Testosterone: 16,30 nmol/L (8-42) = 461 ng/dl
FSH 4,19 (1.37-13.58)
LH 2,20 (1,8-8.16)
Estradiol 19 pg/ml (10-50)
SHBG 25 nmol/L (10-50)
PRL 251 (50-400)
Albumin 4,5g/dl (3.5-5)

At this point testicular volume was 15ml each.

Then I moved abroad at the situation worsened.

1 April 2016
Testosterone: 273ng/dl
LH 4.3
Prolactin 255
No ranges given (UK NHS)

All the symptoms worsened with testicular volume diminishing. Rough calculations put me at 10ml bilateral.

* * *

I tried to contact endos and doctors and all have declined to help me on the counts that the stupid test done without sex or exercise put me above the lower threshold.

My diagnosis is some form of primary hypogonadism which I tried to compensate for with increased LH but eventually the levels settled at an all time low (desensitizing of leydig cells/pituitary?)

I have not tried to perform a PCT for two reasons. The first is that the use of HCG which could counteract the testicular atrophy would disrupt an already injured HPTA. I fear it would hinder any form of restoration. I will suggest a low course of nolvadex or clomid to the next endocrinologist I see but I fear that the idea will be rejected.

My attempts so far:

***
- I have been running two months of the following combination of peptides in the hopes of offsetting the decline in physical condition and restore LH signalling:

4x day CJC-1295 no DAC + GHRP 2 100mcg/100mcg
1x day DSIP 300mcg as it has been showed that it can activate an increase in LH signalling by interacting with the neurocircuitry of the HPTA.

OTC supplements:

2x/day triazole (total 2 caps)
1x/day vitamin D 10,000iu
2x/day DAA 3g total
1x/day multivitamin
1x/day ZMA (total 2 caps at night. Brand ON)
1xday B6 long lasting 500mg
3x day huperzine-A
12mg daily Boron
1 capsule ECGC

For ED

L-citrulline 6g/day
L-Arginine 2g/day

The peptides have done their magic and I experienced a fantastic weight drop and a general body recomposition which has been going on until now. My mood has increased and my muscle tone has improved. I look like a healthy muscular guy while I have the testosterone of a 90 year old....

I have also 100mcg of tripoterelin to try.

***

The goal:

I would like to avoid TRT although I might have no options.
My peptide run was designed to help me avoid the aesthetics of having low testosterone but there is one added goal in my mind.

Peptides work by stimulating endogenous stimulation of GH and IGF-1. The ECGC and Huperzine A I take are designed to reduce somatostatin in order to greatly enhance the effects of the peptides pulsation. I have seen the effects of this cycle and can vouch for its efficacy. Abs started showing by the end of month 1 and the process is still ongoing.

The DSIP is also a proven somatostatin inhibitor and ever since introducing it to the stack I have seen an improvement in body composition.

However, as far as I know the endogenous GH does not only affect muscle tissue but all tissues in the body. Logic would suggest that all tissues in the HPTA should be affected including the leydig cells in the testicles. If this is the case my thinking is that if I manage to keep my LH elevated for as long as possible I could stimulate the body to make use of the elevated GH/IGF-1 to restore my axis. I know it sounds desperate and stupid but I am desperate. Using ED medication at 28 is something I don't hope for anyone.

Anyways, I am currently at day 10 of my 2nd month of peptides and started the OTC regime in full (as described) since the beginning of the second month. DSIP was added 10 days ago. My next blood test will be on the 15th of April and the next in May.

Any suggestions, ideas and opinions would be greatly appreciated.

I know it is not steroid related but please consider these reasons behind me posting:

- you guys have a combined understanding of HPTA workings than most endos and knowledge of many non-standard techniques to raise testosterone levels ;

- my primary hypogonadism could be something steroid users would be looking at after long cycles without HCG and consequent testicular atrophy. If it helps please consider me as an ex bodybuilder who after years of AAS use has primary hypogonadism and hopes to restart without going on TRT.

I would greatly appreciate any response.

Thanks

P.S. It would also be helpful to see what kind of LH levels are normal in my age group in the morning on an empty stomach. I could provide me with a baseline. The ranges are too wide to help in understanding my values.

[Guineapig]

No idea anyone? I should get my results today from the latest bood draw.

[kelkel]

So your LH tracked at an elevated rate in effort to stimulate testicular production. Over time this subsided. This is what has me curious. Why did it diminish on it's own. It's as if it just gave up!

Have you ever suffered any testicular trauma or been checked for varicoceles?
Have you considered an HCG Stimulation Test to see exactly what happens (re-T production)?
Not really a fan of Triptorelin. Scary stuff!

Interested in seeing the new results.

[Guineapig]

Results are back....

381ng/dl and unknown LH (UK NHS policy not to disclose results until appointment).

I figure my OTC regimen has worked a little to increase testosterone but it is obviously insufficient.

My feeling is that I might have suffered a form of mumps or other viral/bacterial trauma. I tried to compensate with increase GNRH and LH/FSH but eventually my pituitary grew insensitive and now is a low responder hence my failing values.

It is to some extent the same situation which arises from continued tripoterlin use. The increased activity in GHRH receptor sites leads to a flare and then a reduction in hormonal output.

I will try and get a GNRH test (to see if the pituitary is responding). If it is downregulated then I basically self castrated myself in an effort to compensate for some for of permanent or transient primary hypogonadism.

I was checked and had no varicoceles but was operated for fixing of mobile testicles.

[Guineapig]

Not really a fan of Triptorelin. Scary stuff!

If I have downregulated receptor sites in my pituitary, triptorelin is the last thing I want to use!

However, I do not have enough info at the moment.

Actually if I am right this means that overextended PCTs using SERMS could be detrimental to recovery!

[kelkel]

Actually if I am right this means that overextended PCTs using SERMS could be detrimental to recovery!

If you mean down-regulation after cessation of use or de-sensitization I'm not ready to buy into that. Key is, serms will either prove to work for you in a very short time frame and the results will be verifiable and if they don't, then you know for sure the issue is downstream.

That's why I said Trip is scary stuff. Too much in one shot or continued use can result in a chemical castration, as you well noted.

Really sorry to hear all this GP. For some it's just the hand they're dealt. At least the options are available if and when you choose to take them.

[Guineapig]

Yes, indeed I made a bold statement which should have been more hypothetical.

However, this a theory I have (free to call "BS" on it)

The HP axis is capable of a limited amount of GnRH and LH/FS output in any given time. In males using SERMS, the latter bind to the estrogen receptors fooling the pituitary/hypothalamus into thinking that the level of serum estrogens is low. Since the main source of estrogen is conversion of testosterone frome aromatase, the pituitary/hypothalamus will work synergistically to increase signally of LH and FSH, thus testosterone production and thus increasing the presence of the substrate for conversion.

I assume that - under SERM use - both GnRH and LH/FSH increase (if not in parallel, at least both above baseline).

Triptorelin works by over activating the GnRH receptors in the pituitary which results over a prolongued period of time into reduced serum levels of LH/FSH.

So if under SERMS, GnRH is artifically pushed above baseline (hence the LH increase 3-4x fold under SERM use as per blood work of several AAS users) and GnRH agonists such as Triptorelin produce the equivalent effect of overstimulation of GnRH receptor site, how does the risk of castration differ? In both cases we have hyperstimulation of the GnRH receptor sites in the pituitary (albeit from different mechanisms).

The only consideration I can think of is that Tritorelin far exceeds any level of stimulation that the hypothalamus can produce on the pituitary at any given time.

Or, in other words, GnRH downregulation of the pituitary is not possible endogenously at any given level of GnRH production by the hypothalamus simply because the hypothalamus is simply not capable of outputing enough GnRH to overstimulate the receptors while Triptorelin is potent enough and long acting enough to achieve that result (hence its clinical use in suppressing androgen production in men).

I hope this makes sense. It's the only thing I can think of.

I really need to see what is happening at the hypothalamic level.

[kelkel]

Very well said. To sum it up simply, SERMS are basically a slow controlled stimulation working on both volume and amplitude. Triptorelin it like using a defibrillator, imho. I would like to know the answer as to whether over-stimulation is possible as well.

Continue to update this please.

[Proximal]

Isn't prolactin at 255 high? Maybe I read through this too quickly and missed something that mentioned this, if so very sorry.

[Guineapig]

No worries, thanks for posting. I believe the unit is mIU/L. The top threshold for men I believe is 400 mIU/L so I would appear to be in range.

On a side note I have been reading info on Triptorelin and I believe I could experiment with a low does protocol once every month... 50mcg as opposed to the 100mcg used in the restart thread. This guy https://thinksteroids.com/community/...4333375/page-3 would appear to have used triptorelin successfully injecting monthly or periodically.

There are several reasons which push me towards this experiment:

TRT is not something I look forward to given the risk of infertility, the continuous pinning (longers esters can be used but HCG would still have to be injected twice a week).

Low doses of SERMS are unproven in the very long run and people can develop vision and emotional sides (hopefully enclomiphene - androxal - wil come out in a few months).

Very low dose of triptorelin bursts would keep both LH and FSH elevated and - if the hyperstimulation holds for at least 30 days - it could be repeated monthly. I am not willing to try anything more than 50-100mcg once a month to avoid castration (although, to be honest, I am just a few steps away).

To Kelkel: maybe turning the triptorelin dose down just enough can make it so that a defibrillator becomes a pacemaker.

[Guineapig]

Attachment 163027

7 months of pharma grade monthly triptorelin doses (100mcg each). Apparently 100mcg monthly is part of a fertility protocol for women. Seems promising. I am sure no pharma company or doctor will allow women to damage their own fertility by means of a fertility drug. Possibly this protocol was the source of the idea for the restart described in the (in)famous Italin study on the male bodybuilder.

[kelkel]

There are several reasons which push me towards this experiment:

TRT is not something I look forward to given the risk of infertility, the continuous pinning (longers esters can be used but HCG would still have to be injected twice a week).


To Kelkel: maybe turning the triptorelin dose down just enough can make it so that a defibrillator becomes a pacemaker.

No doubt you want to do all that is possible to avoid TRT, but there will come a point of no return. Even with low dose trip the results, both positive and negative are unknown for you. Long esters such as Aveed have been quite successful and when coupled with HCG you can maintain relatively normal parameters of intra-testicular T & E as well as sperm.

Preserving fertility in the hypogonadal patient: an update

[Guineapig]

Very true!

Another theory has been suggested elsewhere that it may be varicocele which would explain the extremely high variability in testosterone levels .

Can someone confirm that going from 279 ng/dl to 480 ng/dl (fasting morning draws) is abnormal?

I have a slight feeling of something being swollen in my right testicle. Maybe I've been barking up the wrong tree all along.

[kelkel]

Remember I mentioned varicoceles in post #3. An ultrasound or palpation from a knowledgeable doc can probably rule this in or out.
BW is just a snapshot in time and even a few hours difference can change results. The younger you are the more of a swing you can have in T levels when times are off a bit. How much is a crap shoot.

[Guineapig]

oh S***** Sorry Kelkel, my bad!!

I salute your intuition then!

So 100% each morning is possible and normal? That would basically put me under or above the threshold of normality at any given time.... I don't feel that would be normal for a human being. You confirm that going from 270ng/dl to 480 ng/dl is entirely possible?

[kelkel]

Possible, yes. Likely, can't really answer that. But instincts say it's too much of a swing.
So many factors can play into what your levels are on any given day.

[Guineapig]

GP referred me to an endo.

UK NHS tested for testosterone but not for LH so can't really say if the 100 point increase was due to increased pituitary activity.

At this point I will do more tests but I will certainly run triptorelin.

On a side note.....

One of the arguments I get from doctors is that I hold too much mass to be deficient in testosterone. I think this is stupid because I lost plenty and currently I am 1.73m 79/80 kg at 15% which to me seems rather standard for someone who has spent most of his life doing tough sports. Maybe I even have a little bloat from the peptides but my stats seem pretty normal..

Should I necessarily be fatter or hold less mass at 278-300 ng/dl?

[kelkel]

Should I necessarily be fatter or hold less mass at 278-300 ng/dl?

Not necessarily. Genetic predisposition and lifestyle impact this greatly. From personal experience I was functioning at a 59 total T level for a while before discovering a pituitary tumor. Lost a little weight but not an extraordinary or alarming number. Zero fat gain.

[Guineapig]

Thank you as always for your reply. I am sorry to hear about the tumor. I hope you solved the problem!

If you don't mind me asking, what were your hormone values before confirming the tumor? I imagine high prolactin perhaps?