Testosterone+ HCG Preserves Healthy Sperm in Men on Testosterone Replacement Therapy (Injections and gels)

Tung-Chin  Hsieh, Alexander  W. Pastuszak, Kathleen Hwang and Larry I. Lipshultz*,†

From the Division of Urology, University of California-San Diego (TCH), San Diego, California, Scott Department of Urology, Baylor College of

Medicine (AWP, LIL), Houston, Texas, and Department of Urology (KH), Brown University School of Medicine, Providence, Rhode Island

Purpose: Testosterone replacement therapy results in decreased serum gonadotropins (hormones produced by the pituitary gland- LH and FSH- that jump start testicular function) and  intratesticular testosterone (inside the testicles), and  impairs spermatogenesis (sperm production), leading to azoospermia (no viable sperm) in  40%  of patients. However, intratesticular  testosterone can  be maintained during testosterone replacement therapy with co-administration of low dose human chorionic gonadotropin, which  may  support continued spermatogenesis in patients on testosterone replacement therapy.

Materials and Methods: We retrospectively reviewed the  records of hypogonadal men  treated with testosterone replacement therapy and  concomitant low dose  human chorionic gonadotropin (HCG). Testosterone replacement consisted of daily  topical gel or weekly intramuscular injection with intramuscular human chorionic gonadotropin (500 IU) every  other day.  Serum and  free testosterone, estradiol, semen parameters and  pregnancy rates were  evaluated before  and  during therapy.

Results: A total of 26 men  with a mean age  of 35.9  years were  included in  the study. Mean followup  was 6.2 months. Of the men  19 were  treated with injectable testosterone and   7  were  treated with transdermal gel.  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) and  estradiol 2.2 vs 3.7 pg/ml  (p = 0.11).  Pretreatment semen parameters were  volume 2.9 ml,  density 35.2 million per ml, motility 49.0% and  forward progression 2.3. No differences in semen parameters  were  observed during greater than 1  year of followup. No impact on semen parameters was  observed as  a function of testosterone formulation. No patient became azoospermic during concomitant testosterone replacement and  human chorionic gonadotropin therapy. Nine  of 26 men  contributed to pregnancy with the  partner during followup.

Conclusions: Low dose  human chorionic gonadotropin appears to maintain semen  parameters in hypogonadal men  on testosterone replacement therapy. Concurrent testosterone replacement and  human  chorionic gonadotropin use  may preserve fertility in hypogonadal males who desire fertility preservation while  on testosterone replacement therapy.


***********************

 Low-Dose Human Chorionic Gonadotropin Maintains Intratesticular Testosterone in Normal Men with Testosterone-Induced Gonadotropin Suppression

This study shows that HCG can keep intratesticular (inside the testes) testosterone - ITT normal even when they are exposed to testosterone injections. An HCG dose of 500 IU every other day increased ITT to levels higher than baseline. All other doses failed to achieve normalization of baseline ITT. ITT is crucial for Leydig cells to work properly so that they do not atrophy (lose volume due to inactivity)

http://www.ncbi.nlm.nih.gov/m/pubmed/15713727/


*************************

More information on HCG+TRT

Which Medications Can Cause Man Boobs?

Drug-Induced Gynecomastia

Deepinder F, Braunstein GD. Drug-induced gynecomastia: an evidence-based review. Expert Opin Drug Saf.http://informahealthcare.com/doi/abs/10.1517/14740338.2012.712109 

Drugs are estimated to cause about 10 - 25% of all cases of gynecomastia. Over the course of several decades, multiple medications have been implicated in the development of gynecomastia mostly in the form of case reports and case series. However, these reports suffer from a multitude of deficiencies, including poor quality of evidence. Areas covered: Studies were selected for this review by performing an extensive electronic and hand-search using BIOSIS, EMBASE and Medline, from 1940 to present, for all reported drug associations of gynecomastia and their possible pathophysiology. Quality of evidence was assessed on a three-point scale: good, fair and poor, and each of the drugs reported to cause gynecomastia was assigned a level of strength.

The pathophysiology of gynecomastia is also discussed in detail for each of the drugs found to have a good or fair evidence of association with gynecomastia. Expert opinion: Most of the reported drug-gynecomastia associations were based on poor quality evidence.

The drugs definitely associated with the onset of gynecomastia are spironolactone, cimetidine, ketoconazole, hGH, estrogens, hCG, anti-androgens, GnRH analogs and 5-alpha reductase inhibitors. Medications probably associated with gynecomastia include risperidone, verapamil, nifedipine, omeprazole, alkylating agents, HIV medications (efavirenz), anabolic steroids, alcohol and opioids.

More information

Free Testosterone Booklet- Boost Your Physical, Mental and Sexual Vitality

Use this link to download a free 14 page chapter of the book "Testosterone: A Man's Guide" with an interview with expert physician Dr Michael Scally who provides details that every man should know

Testosterone Benefits and Potential Side Effects-

 The book can be bought (in paperback and Kindle) at:
Click here

You can also watch a free lecture on testosterone here:
Nelson Vergel Provides Details on Testosterone

How to Stop Testosterone Safely and Possibly Reset Your Hormonal Axis

From the book: Testosterone: A Man's Guide (click here)

Some men need to stop using testosterone or other androgens because side effects are a problem (e.g. low sperm count interferes with their goal to have children). Most physicians advise the patient to just stop testosterone without thinking about the possible consequences of the hypogonadal state after treatment cessation.  Will the patient be worse off than when he started? 

Testosterone  replacement therapy and anabolic steroids can lead to  HPTA (Hypothalamic-Pituitary-Testicular Axis- shown in figure below) dysfunction.  Supplemental testosterone can inhibit the release of the body’s own testosterone production through negative feedback inhibition on LH levels. This feedback inhibition also results in suppression of FSH levels, leading to suppression of sperm production (spermatogenesis).

Not all studies show a shutdown of the HPTA in patients after testosterone cessation. In a study previously mentioned in the Moodiness section, Dr. Rabkin compiled data for 42 patients who were treated with testosterone for 12 weeks and then randomized (double blind) to receive placebo injections for six weeks. At week 13 (one week after their first placebo injection and three weeks since the last active injection), mean testosterone level was 286 ng/dL. At week 15 (after 2 placebo injections), mean testosterone level was 301, and after week 17 (after 3 placebo injections), mean serum level was 324 ng/dL. None of these values was statistically different from the mean baseline testosterone level of 308 ng/dL. These data suggest that for men who were already hypogonadal there was no further decline in the body’s production of testosterone once testosterone therapy was discontinued after 12 weeks of use. It is not known if longer term testosterone use would have the same results.

When high-dose testosterone use (as in bodybuilding) is discontinued the HPTA dysfunction that occurs when it is stopped may be a lot more pronounced.  Stopping treatment may cause the patient to suffer all the symptoms of hypogonadism for weeks or months.  Many lose a lot of the muscle mass they gained through their cycle of anabolics plus testosterone. In some cases a specific medical protocol is required for HPTA normalization. If you go to bodybuilding sites, you will see Clomid and HCG mentioned a lot for this purpose.

There is no controlled data from studies using any protocols to accelerate the normalization of normal testosterone production in men who have used either supplemented physiologic (normal) or supraphysiologic (above normal) doses of testosterone for long periods.

For men who had normal testosterone before starting testosterone or anabolic steroids (athletes, bodybuilders or certain people with wasting syndrome) and who want or need to stop those compounds, some physicians have attempted to jump-start testicular testosterone production using a combination of products that have different effects on the HPTA and estrogen receptors. One such physician is Dr. Michael Scally from Houston (read the interview with him: Click here ) who presented a poster at the Lipodystrophy and Adverse Reactions in HIV conference in San Diego in 2002 that reported the use of a protocol to normalize testosterone production in HIV-positive patients after prolonged anabolic steroid and testosterone use for their wasting syndrome.

The protocol consisted of the use of HCG, clomiphene citrate, and tamoxifen (read about each of these products in their respective sections). Treatment takes place over two discrete intervals. The first treatment interval is to initiate the restoration of gonadal function. The second interval is to restore the hormonal pathways among the hypothalamus, the pituitary and the gonads. The medications are initiated simultaneously after cessation of androgens when it is expected that the body would try to start to slowly make its own testosterone. If the testosterone ester (cypionate, enanthate, undecanoate, Sustanon) that the patient used is known (the most common one in the United States is depo testosterone or testosterone cypionate), its half-life in the body can be estimated so that the date to begin the medical protocol can be predicted with some accuracy to assess a time when no pharmaceutical testosterone remains in the body.

The protocol for HPTA normalization contains: 

       First 15 days:

  HCG 2,500 IU (subcutaneous) once every other day; 

Clomiphene citrate 50 mg orally twice a day; and

Tamoxifen 20 mg orally once a day.

A satisfactory testosterone level on day 15, typically 350 ng/mL or greater, is followed by the oral medications (no HCG) for an additional

15 days.

This protocol has not been tested in many patients but has shown good results in restoring HPTA in a month. I know that this sounds like a long time but without treatment the body’s restoration process would take about the same length of time that somebody was using androgens.  In some, HPGA function and testosterone production never returns to normal. Hopefully we will see data on approaches like this one used in patients who need to stop testosterone or anabolics after long term use. However, no such studies are listed in clinicaltrials.gov.

Most doctors will refuse to prescribe the protocol above since they are not familiar with it. But remember that this protocol will likely not help most men who had low testosterone before starting TRT anyway.  It is more likely to be helpful to those who used testosterone and anabolics for muscle building purposes and who were not hypogonadal before starting their muscle building cycles.

More information