I went to see my urologist last night. His recommendation is clomid. I asked him to prescribe FSH in addition to boosting my HCG dose and he said it was out of his expertise but would defer to another urologist he works with who is better versed in fertility. While I was there I got bloodwork done. Now I know why my libido is shot... fucking deca still doing its dirty deeds SEVEN weeks later. My prolactin is out of range on the high end and my SHBG is in the absolute gutter. My dick works fine and my morning wood has come back raging this week but I still have no arousal. It's like a loaded gun without wanting to shoot. I also have a small amount of gyno in my right nipple that seems to go crazy even at 100mg of deca... I must be very very sensitive to it.
This was done about 20 hours before my absolute trough. I'm on 80mgs of test cyp Actavis 2x per week and I had just bumped my HCG to 1000iu on the previous inject (same day as my test inject)
My DHEA is fine and the pregnenlone vial lost its top on the way to the lab... I'm guessing it's ok if my DHEA is as well... which means my 250iu 2X/weekly HCG was probably helping my upstream hormones. I think the deca boosted my prolactin too high (if its still out of range 7 weeks later it must have been way higher weeks ago)... and crushed absolutely crushed my SHBG.
Testosterone | 1026 H | 249-836 (ng/dL) |
SEX HORMONE BINDING GLOBULIN | 12.7 L | 19.3-76.4 (nmol/L) |
FREE TESTOSTERONE (Calculated) | 352.0 H | 48.0-250.0 (pg/mL) |
F | RBC | 5.21 | 4.40-6.10 (MILL/CMM) |
F | HEMOGLOBIN | 16.1 | 13.0-18.0 (G/DL) |
F | HEMATOCRIT | 49.3 | 39-52 (%) |
DHEA SULFATE | 290.0 | 88.9-427 (ug/dL) |
F | PSA (Roche Cobas e) | 2.080 | 0-4.00 (ng/mL) |
F | Free PSA (Roche Cobas e) | 0.549 | (ng/mL) |
F | PSA, % Free | 26 | >25% (%) |
F | PROLACTIN | 23.2 H | 2.0-21.0 (ng/mL) |
Will my prolactin come back into range given enough time? I don't have any caber but have heard B6 works. It's strange bc I still have the ability to orgasm and ejaculate multiple times in a day (I did it 4 times in 2 hours to last week just to test things/I did not want to) I just have no desire. I have been here before and it just feels blocked in my brain. I can tell when it goes away it is just taking longer than I thought.
How can I raise SHBG quickly?
Also it was my uro's opinion that I had zero testicular atrophy and the palpability was normal. So my HCG protocol seemed to be working for testicular size.
There is a strong chance that your weekly hCG dose was too low.
As you should very well know exogenous T will have a strong impact on the shut down of the HPG axis.
All AAS including nandrolone will also have a strong impact on the suppression of the endogenous T/shut down HPG axis.
Regarding serum levels, nandrolone would have cleared your system before the 6-week mark after your last injection as serum levels will decline over the following weeks due to the half-life of the decanoate ester although urinary metabolites have been detected up to 6-8 months later and in some cases longer than 1 year.
Nandrolone can definitely have a negative impact on fertility but this could most likely be overcome with the use of hCG + FSH especially when using a therapeutic dose of nandrolone (50-100 mg ND/week)!
Excess (very high) levels of prolactin can have a negative impact on libido.
Prolactin <425 µg/L (20 ng/mL) in most cases would not be a cause for concern.
Comes down to the individual and although yours is slightly elevated it is far from being considered absurdly high.
Not sure where your SHBG sat pre-trt but it is horribly low now.
Testosterone /AAS especially when using high enough doses can hammer down SHBG.
Even when using a therapeutic dose of T some men may notice a larger drop in SHBG whereas others may only see a small drop or in many cases it will barely budge.
Keep in mind that even though your trough TT 1000s is far from what would be considered absurdly high your trough FT will be very high with an absurdly low SHBG 12.7 nmol/L.
Peak TT/FT/estradiol level will be higher.
Your FT was tested using the outdated linear law-of-mass action cFTV (Vermeulen method) and as you can see your trough levels are high.
The only way to know where your FT level truly sits is to have it tested using the most accurate assays ED or UF.
Put $$$ on it that if you had your FT tested using the most accurate assays such as the gold standard Equilibrium Dialysis or Ultrafiltration (next best).....with a TT 1000s and low SHBG 12.7 nmol/L your FT would be very high as in almost 40 ng/dL.
The main reasons to use hCG along with exogenous T would be for those looking to preserve/maintain fertility and prevent/minimized testicular atrophy.
When it comes to preserving/maintaining fertility while on TTh or when coming off some men may do better with hCG + FSH.
Exogenous testosterone’s deleterious effects on male reproduction stem from its disruption of the above-described male HPG axis and the resulting decreases in both serum FSH and LH [23]. Without appropriate stimulation from FSH, Sertoli cells become incapable of supporting spermatogenesis while sub-par levels of LH leads to decreased production of endogenous testosterone from Leydig cells. Although serum testosterone levels are maintained with exogenous administration, appropriate intra-testicular levels of testosterone can only be achieved by endogenous production and are essential for normal spermatogenesis [16]. Consequently, exogenous testosterone almost universally leads to low intra-testicular testosterone with resulting atrophy of the germinal epithelium and subsequent azoospermia in upwards of 40% of men [24]. Although most men will eventually experience a return of sperm to the ejaculate following cessation of testosterone use, complete restoration of prior fertility is uncertain [25,26]. Even with adjunctive therapy, up to 30% of previously azoospermic men may fail to achieve total motile counts greater than 5 million [25].
RECOVERY OF FERTILITY AFTER PREVIOUS ANDROGENIC ANABOLIC STEROID USE
Consequently, there has been increasing interest in the use of HCG to help speed these patients’ recoveries. Wenker et al [69] first reported on the use of combination HCG and SERM therapy to hasten the return of sperm to the ejaculate for men with a history of TTh and AAS use in 2015. Forty-seven out of 49 men with azoospermia or severe oligospermia experienced a return of sperm to the ejaculate or significant improvement in SA parameters. Since that initial investigation, the author’s proposed treatment algorithm has been refined and streamlined [18]
As a rule, all men who are actively trying for pregnancy should immediately stop taking testosterone or AAS. This may include men taking non-prescribed AAS or men receiving TTh for an established history of hypogonadism. These men should instead start a regimen consisting of 3,000 IU HCG intramuscular or subcutaneous every other day [18]. CC 25 to 50 mg PO (per os, by mouth) daily should also be incorporated to help promote FSH production and pituitary function [69]. During this time, repeat SA’s should be obtained every 2 to 3 months along with serum labs [70]. A detailed treatment algorithm is provided in Fig. 1. Men with oligospermia should be offered cryopreservation when appropriate while men with persistent azoospermia despite treatment and no prior history of fertility or sperm on SA should have genetic studies performed to rule out an easily diagnosable pre-existing etiology. If pregnancy is achieved with neither FSH levels nor SA parameters showing improvement, clomiphene should be discontinued and recombinant FSH 75 to 150 IU every other day should be added [18]. If this fails, testicular sperm retrieval with possible microdissection should be offered in conjunction with in-vitro fertilization as a final chance for biologic paternity. Once pregnancy has been achieved, a discussion regarding the reinitiation of TTh can be had with special consideration to future fertility goals.
MAINTENANCE OF FERTILITY WITH CONCURRENT TESTOSTERONE USE
Preserving testicular function and reproductive ability remains an ongoing challenge to practitioners prescribing TTh. Exogenous testosterone is known to decrease intratesticular testosterone and thus impair spermatogenesis. Indeed, in 1996 the World Health Organization investigated weekly injections of 200 mg of testosterone enanthate (TE) as a form of contraception. The task force demonstrated that TE caused azoospermia in approximately 75% of men after only 6 months of use [71]. Both the American Urological Association and the Endocrine Society published guidelines in 2018 which recommend against TTh in men wishing to preserve fertility [2, 72].
Current evidence suggests, however, that adjuvant medications can be prescribed in an effort to maintain testicular health and fertility while receiving TTh.
Coadministration of HCG with TTh has been shown to help preserve spermatogenesis in men by maintaining physiologic intratesticular testosterone levels throughout treatment. In 2005, Coviello et al [58] demonstrated that TTh caused intratesticular testosterone levels to drop by 94% in otherwise healthy, reproductive-aged men. However, adding subcutaneous 250 IU HCG every other day to their TTh regimen prevented this precipitous fall with intratesticular testosterone levels only dropping 7% from baseline. Furthermore, men who received TTh and 500 IU of HCG every other day actually experienced an increase in their intratesticular testosterone by 26% [58]. This study showed that intratesticular testosterone could be reliably maintained while on TTh. Future studies would prove that spermatogenesis itself, and thus the male's fertility, could likewise be persevered throughout therapy.
A retrospective study published by Hsieh et al [73] in 2013 found that out of 26 men treated with TRT and intramuscular 500 IU HCG every other day, no patient became azoospermic. Nineteen of the 26 patients received injectable testosterone while seven were treated with transdermal testosterone gels. Mean serum hormone levels before vs during treatment were: testosterone 207.2 vs. 1,055.5 ng/dL (p<0.0001), free testosterone 8.1 vs. 20.4 pg/mL (p=0.02). No differences in SA parameters were observed during greater than 1 year of follow-up. During the study's follow-up, nine men established a pregnancy with their partner [73]. This study continues to serve as the foundation of ‘fertility-preserving TTh regimens currently utilized today.
Sensibly, all men wishing to preserve fertility while on TTh should obtain a baseline SA. During the initial consultation, it is also important to identify the patient's goals with regard to the timing of pregnancy (Table 1). If the patient desires pregnancy within the next 6 months and has not yet started, they should abstain from initiating TTh until pregnancy has been achieved. If they desire pregnancy within 6 months and are already receiving TTh, it is recommended that they stop all TTh and follow a recovery regimen identical to what was detailed in the previous section.
Table 1. Summary of recommendations for maintenance of spermatogenesis with TTh or AAS use
If a planned pregnancy is desired within the 6 to 12 months time frame, the authors suggest continuing TTh with adjuvant 500 IU HCG every other day [18]. CC at a dose of 25 mg per day should be considered an optional addition throughout this time. When planning for pregnancy over a year away, TTh with adjuvant 500 IU HCG may be continued but patients should be cycled off every six months given the increased risk of impaired fertility with prolonged, uninterrupted TTh [25]. Each off-cycle involves a four-week cycle of 3,000 IU of HCG every other day and CC 25 mg daily. During any of these above regimens, anastrozole may be added and titrated in dose to address any elevations in estradiol. Patients who cannot tolerate CC should substitute tamoxifen 10 mg twice daily.
Many men receiving TTh may not be interested in fertility but still, wish to maintain normal testicular size. It is recommended that these individuals take 1,500 IU HCG weekly while on TTh. This dose is thought to be enough to maintain adequate levels of intratesticular testosterone in order to minimize testicular volume loss. Some men feel that periodically cycling off of TTh is symptomatically beneficial but this is an anecdotal observation and primarily a matter of patient preference.
