Women’s Birth Control vs TRT as Contraceptives and Potential Infertility

[JRos895]

There is generally no fear of women permanently losing their fertility when they start birth control, even though birth control (generally a mix of estradiol and progesterone) is intended to shut down a woman’s HPG axis, leads to the lack of ovarian stimulation, and leads to ovarian shrinkage.

Why is there such a fear then among doctors about given men testesterone? Are the testicles less durable than the ovaries? Is there something about women’s birth control that I am not properly understanding?

 

[Nelson Vergel]

Testosterone is a schedule 3 compound.

Contraceptives are not.

That is the main reason.

US Federal and State Regulations on Testosterone and HCG

Table of Contents Testosterone is a controlled substance in the US, specifically a Schedule-III controlled substance (in all but one State), and this includes any form of testosterone including injectable, transdermal, patches, pellets, and any compound or product containing testosterone as...

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[Guided_by_Voices]

Also, women have all their eggs early in life and their bodies gradually release them in a process which can start and stop. Men have to produce sperm on an ongoing basis and if the ability to create sperm is lost, that is a big problem. That said, there are lots of other issues involved as Nelson points out, some of which are valid and some of which aren't regarding "reluctance".

 

[Gladiator]

Testosterone isn’t a contraception. Many of men have made babies on trt. Even on high steroid cycles.

 

[Wilson7]

The studies done on 200 mg/wk of T for male contraception yielded mixed results, very high genetic variability, some men were shut down, others were not. Running HCG concurrently can prevent infertility, but I wouldn't bet the farm on it. If you're going to use HRT or run a cycle for cosmetic reasons, esp if nandrolone is involved and having kids is something you think is in your future, donate sperm and bank it. One less issue to have on your mind.

 

[madman]

The use of testosterone as a male contraceptive (1998)
JOHN K. AMORY MD
WILLIAM J. BREMNER MD, Ph.D.


Testosterone functions as a contraceptive by suppressing the secretion of the pituitary gonadotropins luteinizing hormone and follicle-stimulating hormone. Low levels of these hormones decrease endogenous testosterone secretion from the testis and deprive developing sperm of the signals required for normal maturation. Interference with sperm maturation causes a decline in sperm production and can lead to reversible infertility in men, raising the possibility that testosterone could be utilized in a commercially available contraceptive. To this end, testosterone has been studied alone and in combination with either gonadotropin-releasing hormone analogs or progestins in efforts to improve its contraceptive efficacy. In this chapter, we will review efforts to use testosterone to create a safe, convenient, efficacious contraceptive method for men.



Since the introduction of the progestin-estrogen oral contraceptive for women in the early 1960s, there has been interest in developing a similarly safe and effective means of contraception for men. Given the success of the endocrine approach in the creation of the women's pill, researchers have attempted to use hormones to provide contraception for men. Testosterone and its derivatives are the most widely tested hormones. Testosterone can be used alone or in combination with a second agent to impair spermatogenesis and thereby function as a contraceptive.

In women, the progestin-estrogen oral contraceptive prevents ovulation by limiting the production of the pituitary gonadotropins follicle-stimulating hormone (FSH) and luteinizing hormone (LH). Similarly, in men, exogenous testosterone impairs spermatogenesis by an inhibition of LH and FSH production by negative feedback at the level of the pituitary. Normally, LH stimulates the production of testosterone by Leydig cells in the testis, while FSH acts on Sertoli cells in the seminiferous tubules of the testis to facilitate sperm maturation. In men, a blockade of LH production shuts down the testicular production of testosterone. A complete absence of testosterone, however, is impractical in the long term as testosterone is necessary to prevent the signs and symptoms of hypogonadism and maintain the normal male phenotype. In addition to its importance in sexual behavior and libido, testosterone plays a role in the maintenance of muscle mass, mineral and bone metabolism, kidney function, and hemopoiesis. The absence of FSH, or a blockade of the FSH receptor, has a deleterious effect on sperm counts as well, but mature sperm capable of fertilization persist (Matsumoto and Bremner, 1989).

Many substances, including estrogen, progestins, gonadotropin analogs, and, of course, testosterone can provide the negative feedback necessary to depress pituitary gonadotropin production, but only testosterone can maintain the male phenotype. Testosterone, however, possesses some limited ability to maintain spermatogenesis, even in the absence of FSH and LH. This fact has bedeviled researchers in this area for decades; testosterone, necessary to prevent hypogonadism, stimulates spermatogenesis.

Attempts at a solution to this dilemma are the subject of this review. In the broadest terms, researchers have approached this problem by attempting to either:

I. provide just enough testosterone to decrease LH and FSH production and prevent hypogonadism, but not so much as to stimulate spermatogenesis;

2. use a second agent such as progestin or gonadotropin-releasing hormone (GnRH) analog intended to decrease the production of LH and FSH while also administering sufficient testosterone to prevent hypogonadism.


In this chapter, we will first discuss the nomenclature and preparations of testosterone commonly used, as well as the side-effects and drawbacks of such preparations when used as potential male contraceptives. Then, in the following three sections, we will follow this research as it progressed through three phases: the first in which testosterone was used alone; a second phase in which (GnRH) agonists and antagonists were given in combination with testosterone to further decrease the production of LH and FSH; and the third and current phase of research, which involves the combination of testosterone with a progestin.




TESTOSTERONE CONTRACEPTIVE TRIALS: GENERAL CONSIDERATIONS

In assessing the efficacy of a potential male contraceptive, it is important to determine what level of sperm inhibition is necessary to achieve infertility; however, this is not precisely known. The range of normal sperm counts can vary widely, from 20 to 200 million sperm per ml of ejaculate. The absence of sperm in the ejaculate, a condition termed azoospermia, renders fertilization impossible and is, therefore, the ultimate goal of male contraception. Unfortunately, azoospermia has not been achieved reliably in all normal men using existing hormonal techniques. To date, all studies report some subjects who sustain a severe but incomplete reduction of their sperm counts, a condition called oligospermia. There is good evidence that sperm counts below 3 million sperm per ml ejaculate are associated with decreased rates of pregnancy (World Health Organisation, 1996). This 'severe oligospermia' considerably decreases the chances of conception and is considered to be an intermediate goal for male contraceptive research.

Additional factors important in the design of a contraceptive include time until onset of action and method of administration. Hormonal contraceptives do not incapacitate existing sperm: they block sperm production. Since sperm takes an average of 72 days to reach maturity, it is probable that any contraceptive based on manipulation of the hormonal axis will be associated with some delay in the onset of full contraceptive potency. The lack of safe, orally active testosterone means that existing regimens rely on frequent injections, but injections are problematic for many men. The need for injections is a significant drawback to current efforts to find a widely appealing method, and the need for sterile needles and syringes may limit its applicability in less developed countries, where contraception is most needed. Last, it is important to consider ethnic differences in interpreting the results of contraceptive trials. For unknown reasons, volunteers in Asia were more susceptible to the steroid suppression of spermatogenesis than were men studied in Europe, North America, and Australia (Handelsman et al, 1995). This difference is not solely a function of body mass and may point to either increased sensitivity to lowered FSH and LH levels, or to a decreased conversion of testosterone to DHT in the testis by differing isoforms of 5~-reductase (Anderson et al, 1996). While the mechanism remains to be elucidated, these differences are important in interpreting the results of various clinical trials and make extrapolation of the data to different populations difficult.




CONTRACEPTIVE TRIALS

Testosterone alone

Testosterone given at slightly supraphysiological levels can suppress both FSH and LH production and simultaneously replace the androgen deficit caused by decreased LH levels. Low levels of LH also lead to decreases in intratesticular testosterone as the Leydig cell production of testosterone falls. This decrease in intratesticular testosterone is of crucial importance as normal local concentrations of testosterone and DHT are necessary for spermatogenesis (Morse et al, 1973).

As early as the 1930s, the administration of testosterone was shown to suppress sperm counts (Heckel, 1939); however, the first systematic studies of testosterone as a contraceptive date from the 1970s. Several small studies were reported in 1977 (Steinberger and Smith, 1977a,b; Swerdloff et al, 1979) using TE alone given by intramuscular injection. In these trials of Caucasian men, more than half of the subjects were rendered azoospermic, and most of the others became severely oligospermic. As expected, the onset of azoospermia was at around 72 days, and the recovery of normal sperm counts occurred 3-4 months after testosterone was discontinued.

Based on these initial encouraging results, two large, multicentre trials of TE were conducted by the World Health Organization (WHO) (1990, 1996). The first study enrolled 271 subjects who were given weekly doses of 200 mg TE intramuscularly for a 6-month induction phase. Sixty-five percent of these men achieved azoospermia, and an additional 30% were rendered severely oligospermic. The fertility of the azoospermic men was then tested in a 12-month efficacy phase. Of the 119 couples who became azoospermic, continued the injections, and used no other form of birth control, only one pregnancy occurred. This pregnancy rate of 0.8 pregnancies per 100 person-years demonstrates that, in men rendered azoospermic, TE is an effective contraceptive. Patients discontinued involvement with the study mainly because of regimen failure and dislike of the injection schedule.

The second WHO study examined the fertility of both the men who became azoospermic and the men who achieved severe oligospermia on the TE regimen (World Health Organization, 1996). A total of 399 men were enrolled in this study. Of these, all but eight (2%) became severely oligospermic or azoospermic. In terms of fertility, there were no pregnancies fathered by the men who became azoospermic; in men whose sperm counts were suppressed to below 3 million per ml, fertility was reduced to 8.1 pregnancies per 100-person years. The combined fertility rate for oligospermic and azoospermic men was 1.4 per 100-person years. Therefore, the overall failure rate (including the men who failed to suppress to oligospermia) was 3.4%, for an overall contraceptive efficacy of 96.6%.

This research demonstrated that testosterone is safe, fully reversible, and effective as a contraceptive in the majority of men. Drawbacks to testosterone-alone methods are, however, apparent. While effective in those who achieve azoospermia, some men fall to suppress below 3 million sperm per ml and therefore presumably remain fertile. In addition, the necessity of weekly intramuscular injections is a deterrent. Twenty-five percent of patients in the second WHO study discontinued involvement for personal or medical reasons, or because of a dislike of the injection schedule. Last, high-dose testosterone has been shown to decrease serum high-density lipoprotein (HDL) cholesterol, which could contribute to accelerating atherosclerosis (Bagatell et al, 1994; Meriggiola et al, 1995). These failings have led to two additional avenues of research: (a) the addition of a second agent, either a GnRH analog or a progestin; and (b) attempts to improve the characteristics of testosterone administration.




CONCLUSION

Testosterone is useful as a contraceptive in human males; however, a regimen with 100% effectiveness has remained elusive. Combinations with GnRH antagonists improve the efficacy of testosterone but are presently impractical for widespread use. Testosterone combinations with progestins appear promising. Ongoing trials with testosterone plus LNG and CPA may offer a usable option for men, but difficulties in testosterone delivery may hinder their use. Recent insights into the molecular regulation of transcription by estrogen receptors may point to the existence of similar complexity in the androgen receptor and may provide new avenues for the generation of a male hormonally derived contraceptive. A better understanding of the molecular regulation of spermatogenesis will clearly increase the chances of successfully manipulating these systems to create an easily usable, long-term contraceptive for men, and something, finally, to complement the success of the estrogen-progestin pill for women.

Testosterone Is a Contraceptive. Should It Not Be Used in Men Who Desire Fertility?

Testosterone has a variety of functions and is commonly used in older men to treat symptoms of hypogonadism, such as decreased libido, decreased mood and erectile dysfunction. Despite its positive effects on sexual function, it has a negative effect on fertility. Exogenous testosterone therapy...

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Testosterone Is a Contraceptive and Should Not Be Used in Men Who Desire Fertility (2018)
Amir Shahreza Patel, Joon Yau Leong, Libert Ramos, Ranjith Ramasamy


Testosterone has a variety of functions and is commonly used in older men to treat symptoms of hypogonadism, such as decreased libido, decreased mood, and erectile dysfunction. Despite its positive effects on sexual function, it has a negative effect on fertility. Exogenous testosterone therapy can negatively affect the hypothalamic-pituitary-gonadal axis and inhibit the production of follicle-stimulating hormone and luteinizing hormone. The purpose of this review is to discuss the contraceptive properties of testosterone therapy and to discuss strategies to increase testosterone in men with the desire to preserve fertility.




INTRODUCTION

Testosterone is a pleiotropic hormone that plays various physiological roles in the development of male genitalia in utero and during puberty. Classically, testosterone is a hormone associated with masculinity. Testosterone is used as a treatment for males with late-onset hypogonadism, a condition in men who experience symptoms caused by a decrease in serum testosterone. Symptoms associated with low testosterone can include decreased libido, decreased muscle mass, depressed mood, and/or erectile dysfunction. The use of testosterone replacement therapy (TRT) among men over the age of 40 years has increased more than 3-fold over the last decade [1].

Exogenous testosterone comes in various preparations and each form carries various risks. Along with an increase in hematocrit, a major adverse effect of TRT is diminished sperm production because of the decreased intra-testicular concentration of testosterone and suppression of the hypothalamic-pituitary-gonadal (HPG) axis [2-4]. Suppression of follicle-stimulating hormone (FSH) release from the pituitary gland impairs sperm production and suppression of luteinizing hormone (LH) release inhibits intra-testicular testosterone production

The purpose of this review is to evaluate the contraceptive effect of testosterone, discuss how the use of exogenous testosterone can negatively impact a man’s fecundity, and identify the importance of family planning in men who are planning to receive TRT.




The exogenous administration of testosterone suppresses the release of gonadotropins (FSH and LH) to levels below that required for spermatogenesis. Spermatogenesis is largely dependent on the action of FSH on Sertoli cells coupled with high intra-testicular testosterone concentrations. Within the seminiferous tubules, only Sertoli cells possess receptors for both FSH and testosterone. Numerous signaling pathways are activated when FSH binds to FSH receptors on these cells. It acts synergistically with testosterone to increase fertility and the efficiency of spermatogenesis [6]. The inhibition of LH release by exogenous testosterone leads to the suppression of endogenous testosterone production by the Leydig cells. The decreased intra-testicular testosterone combined with the suppression of FSH leads to decreased germ cell survival and maturation (Fig. 1).

Intra-testicular testosterone is required in spermatogenesis for the formation of the blood-testis barrier (BTB). The BTB is a series of tight and adherens junctions between the Sertoli cells that separates postmeiotic germ cells in the adluminal compartment of the seminiferous tubules from the basal compartment containing the blood supply. During spermatogenesis, the BTB is disrupted and reformed as preleptotene spermatocytes pass through this barrier. In the absence of testosterone stimulation, spermatogenesis can only proceed as far as the prophase 1-leptotene stage of meiosis [7].

Testosterone is also required in maintaining connections between Sertoli cells and the haploid spermatid germ cells. Round spermatids are initially connected to Sertoli cells via desmosomes. As the spermatids mature and elongate, the desmosomes are replaced with stronger, specialized adherens junctions called ectoplasmic specializations, which are maintained until the release of mature sperm. Testosterone aids in this process and increases the efficiency of germ cell attachment to Sertoli cells. Testosterone is also essential for the release of mature spermatozoa from Sertoli cells. It has been shown that in the absence of testosterone stimulation, sperm are not released but are instead phagocytized by Sertoli cells [7].

Ultimately, the low intra-testicular testosterone results in decreased proliferation of spermatogonia, defects in spermiation of mature spermatozoa by Sertoli cells, and accelerated apoptosis of spermatozoa [8- 11]. Since 80% of testicular volume consists of germinal epithelium and seminiferous tubules, a reduction in these cells is usually manifested by testicular atrophy and this reflects the loss of both spermatogenesis and Leydig cell function [12,13].





Testosterone as a contraceptive can suppress spermatogenesis and lead to azoospermia in 65% of normospermic men within 4 months of use [14]. Cessation of exogenous testosterone will lead to the reversal of hormonally-induced azoospermia in 64% to 84% of men with a median time of about 110 days [13-15]. All men in these studies recovered to baseline levels after cessation of therapy; however, it took up to 2 years for some men to recover. These studies were performed in a controlled setting for a clinical trial, with a limited duration of testosterone use. In actual practice, recovery may not be as pronounced. Kohn et al [16] studied spermatogenesis recovery with human chorionic gonadotropin (hCG) and selective estrogen receptor modulators (SERM) in men with infertility associated with testosterone use. Thirty percent of the 66 men were not able to achieve a total motile sperm count of more than 5 million after 12 months in the study. They found that the failure of recovery is associated with older patients and longer TRT duration.

If fertility is affected because of TRT, couples may require the use of in vitro fertilization or intra-cytoplasmic sperm injection for future conception. These assistive reproductive technologies are expensive and are not always successful [17,18].

In summary, despite the androgenic effects of testosterone on sexual function, libido and mood; its effect on gonadotropins leads to the inhibition of sperm production [13]. This effect may diminish with the cessation of testosterone intake, but the extent of recovery is not clear for chronic users [16,19].




TESTOSTERONE AS A MALE CONTRACEPTIVE

Compared to the long list of contraceptive options available to women, men are limited to vasectomy and condoms. The former is challenging to reverse and the latter has failure rates as high as 18% because of noncompliance. Partners who correctly and consistently use condoms have failure rates of 2% [20,21]. As it is a user-dependent method, many couples seek easier-to-use options like female oral contraceptive pills or intrauterine devices [22]. However, there is a demand for alternatives. A survey of over 9,000 men from different populations in 2005 found that 29% to 71% of men are interested in using a form of hormonal male contraception [22,23]

In 1978, a newly available oral testosterone preparation known as testosterone undecanoate (TU) was investigated as a possible form of male contraception. The study found that regular testosterone use for 10 to 12 weeks causes suppression of sperm production, and even azoospermia, albeit inconsistently [24]. Ever since that study, testosterone has undergone extensive clinical trials as a hormonal method of male contraception and many have found testosterone to be efficacious, reversible, and safe with minimal short-term side effects [23]

Unfortunately, the contraceptive effect of testosterone is not reliable. This has been proven in multiple studies, including two by the World Health Organization (WHO) Task Force on Methods for the Regulation of Male Fertility [14,15,25]. These two studies found an azoospermia rate of 64% to 75% in 6 months with testosterone enanthate [6,7]. A sperm concentration of 3 million/mL was used as a threshold for effective suppression of spermatogenesis in this study [14,15]. In a Chinese study of a monthly intramuscular TU injection, an azoospermia rate of 93% to 98% was achieved after 6 months with 1 million/mL as the criteria for effective suppression [25,26]. The different rates of azoospermia can be explained by the variable criteria and by ethnic differences in testosterone response [26,27]. These studies confirm the effectiveness of testosterone as a contraceptive and provide evidence that men who desire fertility should not be prescribed TRT.

Even with this evidence, testosterone has not been approved by the USA Food and Drug Administration (FDA) for use as a contraceptive. In 2011, a phase II study for a combined TU/norethisterone enanthate formulation ended prematurely because of higher than anticipated adverse effects including mood changes (such as depression), increased libido, acne, and weight gain [27,28].

More recent advancements were shown in the 2018 Endocrine Society meeting, with dimethandrolone undecanoate shown to effectively decrease sperm counts without adverse effects in a double-blind study in 2 academic sites. More extensive research on the safety of testosterone as a contraceptive needs to be done before testosterone can be used as a safe and reliable contraceptive [29].




FORMULATIONS OF TESTOSTERONE REPLACEMENT THERAPY

In terms of the contraceptive effect of the different formulations of testosterone, most research has shown that transdermal and intramuscular testosterone seems to be the strongest contraceptive formulations. The WHO and Chinese studies used testosterone enanthate and TU, respectively. The topical formulations of testosterone have variable contraceptive effects. The testosterone patch was shown to be an ineffective contraceptive [41] while the gel had mixed results [42,43].

However, the sample size for most of these studies is not large enough to truly assess the extent to which fecundity is affected. More research needs to be done to evaluate the contraceptive effect of the various formulations of testosterone.




USING TESTOSTERONE IN THE TREATMENT OF HYPOGONADISM IN MEN WHO DESIRE FERTILITY

Considering that there is abundant evidence demonstrating that TRT significantly decreases sperm production, it is important that clinicians consider the evidenced risks of male infertility before starting patients on TRT. It can be surprising to patients that testosterone can suppress fertility, contrary to its stimulatory effects on libido and erectile function. The patient’s desire for fertility must be discussed in-depth and established prior to initiating testosterone. The discussion must also include future thoughts on fertility. This will allow the physician to manage the timing of hypogonadism treatment, essentially balancing the alleviation of hypogonadal symptoms with the patient’s desire for fertility. This could also open discussion about cryopreservation of sperm as an option for the patient to preserve fertility further down the line

Physicians should also educate men already on TRT. There has been an increase in TRT use among men aged 18 to 45 years and more than 20% of these men did not get a baseline testosterone level prior to initiation of TRT [49]. Some of these men may not know about its effects on fertility and may not have discussed it with their prescribing physician. The study also showed that less than 2% of men on TRT obtained a baseline semen analysis [49]. In addition to the routine serum total testosterone, LH, and hematocrit prior to starting TRT, every man of reproductive age should have a baseline semen analysis [3]. The baseline semen analysis will identify men with a decreased baseline sperm count, as a reference value for future semen analyses after TRT use.

If a patient currently desires fertility, TRT should be avoided or discontinued immediately. A semen analyses should be performed if the patient has discontinued TRT. Azoospermia or severe oligospermia may be seen in these patients, but most men should return to baseline semen analyses in 6 to 9 months after cessation of TRT [13-15]. A 2006 integrated analysis showed that 90% of patients were expected to return to baseline sperm concentration values 12 months after cessation of treatment and 100% after 24 months [50]. Furthermore, evidence in a 2015 study of 49 men showed that 3,000 units of hCG subcutaneously every other day is effective in supporting the recovery of spermatogenesis without significant adverse effects [11].

Regardless, the recovery of spermatogenesis is unclear for patients on chronic TRT. Physicians should take caution when treating hypogonadism in men who desire future fertility, but also acknowledge the reversible azoospermia seen in controlled studies [51]. Adjunctive hCG and clomiphene can be used with TRT to maintain testicular size and intra-testicular testosterone concentrations [52]. Referral to a reproductive urologist should be considered in a male with low testosterone interested in fertility.





ALTERNATIVES TO TESTOSTERONE THERAPY IN PATIENTS WHO WISH TO PRESERVE FERTILITY

Clomiphene and enclomiphene citrate provide an alternative treatment option for hypogonadal men that desire fertility as it does not affect sperm production. Clomiphene is a non-steroidal SERM. It selectively binds to estrogen receptors in the hypothalamus, antagonistically inhibiting negative feedback, increasing the levels of gonadotropins, and stimulating the testicular production of testosterone in men [53].

Even though enclomiphene citrate is not currently FDA approved, it has been shown to increase serum testosterone by raising the serum LH and FSH levels without negatively affecting semen parameters [54]. Kaminetsky et al [55] conducted a proof-of-principle, randomized, open-label, fixed-dose, controlled, two-center phase IIB study that compared 25 mg of enclomiphene citrate daily to topical testosterone in hypogonadal men. The results showed higher testosterone levels and sperm counts in men receiving enclomiphene citrate. This corroborates with other studies which show improved semen parameters with the use of clomiphene citrate, with some studies describing it as a treatment for male infertility [56,57].

hCG has also been used (often with clomiphene citrate, tamoxifen, or anastrozole) because it stimulates the production of endogenous testosterone without compromising spermatogenesis. Although the exact mechanism of action and production site in males are not fully understood, it is known that hCG mimics the effects of LH and stimulates the Leydig cells in the testicles to produce endogenous testosterone [3,58-60]. Additionally, studies have shown that low-dose hCG can be used with TRT to maintain high levels of intratesticular testosterone while men are being treated for hypogonadism [52,61]. While hCG is effective in increasing testosterone, various studies have shown that it is also efficacious in inducing spermatogenesis [62,63]. It is even effective in helping with the recovery of spermatogenesis in men who were on TRT [11]. Clinicians generally agree on using 2,000 IU of hCG administered subcutaneously 3 times per week as defined by the 2002 American Association of Clinical Endocrinologists guidelines [64]




CONCLUSIONS

Testosterone therapy is a contraceptive, albeit a poor one. Men of reproductive age with low testosterone should be counseled on the adverse effects of TRT on fertility. Obtaining a semen analysis and possible cryopreservation of sperm should be offered if TRT is prescribed to men interested in preserving fertility. Options such as clomiphene citrate and hCG along with a referral to a reproductive urologist should be considered to naturally increase testosterone levels in those men with low testosterone who want to avoid TRT.

 

[madman]

Testosterone Is a Contraceptive. Should It Not Be Used in Men Who Desire Fertility?

Testosterone has a variety of functions and is commonly used in older men to treat symptoms of hypogonadism, such as decreased libido, decreased mood and erectile dysfunction. Despite its positive effects on sexual function, it has a negative effect on fertility. Exogenous testosterone therapy...

www.excelmale.com

Testosterone Is a Contraceptive and Should Not Be Used in Men Who Desire Fertility (2018)
Amir Shahreza Patel, Joon Yau Leong, Libert Ramos, Ranjith Ramasamy


*The study also showed that less than 2% of men on TRT obtained a baseline semen analysis [49]. In addition to the routine serum total testosterone, LH, and hematocrit prior to starting TRT, every man of reproductive age should have a baseline semen analysis [3]. The baseline semen analysis will identify men with a decreased baseline sperm count, as a reference value for future semen analyses after TRT use

Do I need to come off TRT to use HCG for fertility?

Good Morning everyone, I current receive TRT treatment and then do HCG sub Q 500iu twice weekly I’m addition to testosterone and anastrozole and cabergoline. If I wanted to get my wife pregnant, would I have to come off of TRT or does the HCG keep me fertile while being on TRT? Thanks for the help.

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Low-dose hCG can prevent sterility in men prescribed testosterone

Strategy for clinicians

To maintain fertility in men with hypogonadism prescribed testosterone, Lipshultz said, clinicians should first insist on a semen analysis before beginning testosterone treatment.

“Patients need to realize that 2% of all men are sterile,” Lipshultz said. “We need to know where the individual is before we introduce testosterone because our endpoint may not be able to be any better than pre-treatment level.”

If the man desires a future pregnancy, the clinician should prescribe hCG concurrent with testosterone therapy, typically at 500 U subcutaneous three times per week or 1,500 U once weekly if the patient wishes only to prevent testicular atrophy. The patient should cycle off of testosterone twice yearly, at a rate of 3,000 U three times per week for 4 weeks, adding 25 mg daily clomiphene therapy during that period, Lipshultz said. However, for men desiring a pregnancy, 3,000 U hCG three times per week should be prescribed in addition to clomiphene therapy. Clinicians should check the patient’s follicle-stimulating hormone (FSH) level and conduct a semen analysis after 4 months for men desiring pregnancy; if the FSH level is not sufficiently elevated, the clinician should discontinue clomiphene and instead introduce FSH concurrent with the hCG, he said.

“To date, we have not had any patients who did not return to baseline,” Lipshultz said, referring to the regimen. – by Regina Schaffer

 

[madman]

Sperm Maturation and Fertilization

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