Using Clomiphene or Tamoxifen to treat male subfertility
Please consult with your Dr about this first, I think your Dr will be receptive since less is more. Dr's I have consulted with has seen a huge increase in response for prolong usage with this approach in the past. IT does not cause LH down regulation, or put the person at high risk of e2 issues, or possible eye issues (yellow tint) due to higher amounts of clomid. Even though these are coming from a logical conclusion it is always best to touch base with your Dr before self adminstration. Many people are on this dosage or little or more less holding 7-1000 ng/dl TT for >6 months. Mind you they have also taking the proper steps to insuring other imbalances in body be addressed and hormonal pathways are back filled in order to increase their chances.
If one is focusing on testosterone specific while on clomid, LH, e2, SHBG (not accurate reading due to serm) TT, DHT. One should always have done blood work first for proper thyroid, adrenals and many other factors. Please refer to my LAb testing getting to the core thread for further testing with you and your DR.
I originally wrote a response with a lot of links for you, but it would not let me post it since I have under 50 posts, so this is a much smaller revision of it.
There are numerous studies on using anti-oestrogens on treating male subfertility.
Most studies show that using Clomiphene or Tamoxifen by itself have little to no effect.
Clomiphene or tamoxifen for idiopathic oligo/asthenospermia.
Abstract
BACKGROUND:
Oligo-astheno-teratospermia (sperm of low concentration, reduced motility and increased abnormal morphology) of unknown cause is common and the need for treatment is felt by patients and doctors alike. As a result, a variety of empirical, non-specific treatments have been used in an attempt to improve semen characteristics and fertility. The administration of anti-oestrogens is a common treatment because anti oestrogens interfere with the normal negative feedback of sex steroids at hypothalamic and pituitary levels in order to increase endogenous gonadotropin-releasing hormone secretion from the hypothalamus and FSH and LH secretion directly from the pituitary. In turn, FSH and LH stimulate Leydig cells in the testes, and this has been claimed to lead to increased local testosterone production, thereby boosting spermatogenesis with a possible improvement in fertility. There may also be a direct effect of anti-oestrogens on testicular spermatogenesis or steroidogenesis. This review considers the available evidence of the effect of both Clomiphene citrate and tamoxifen, both of which have a predominant anti-oestrogenic effect, for idiopathic oligo and/or asthenospermia.
OBJECTIVES:
The objective was to assess the effects of treating subfertile men with anti-oestrogens (clomiphene or tamoxifen) on pregnancy rates among couples where subfertility has been attributed to idiopathic oligo- and/or asthenospermia.
SEARCH STRATEGY:
The Cochrane Subfertility Review Group specialised register of controlled trials was searched".
SELECTION CRITERIA:
Randomised trials of anti-oestrogen therapy for 3 months or more compared to placebo or no placebo for subfertile males among couples where subfertility is attributed to male factor.
DATA COLLECTION AND ANALYSIS:
Data were extracted independently by two reviewers. Any differences were resolved with a third reviewer.
MAIN RESULTS:
Ten studies involving 738 men were included. Five of the trials did not specify method of randomisation. Anti-oestrogens had a positive effect on endocrinal outcomes, such as serum testosterone levels. In trials with secure randomisation there was no difference in the pregnancy rate between the anti-oestrogen groups and the control groups (odds ratio 1.26, 95% confidence interval 0.99 to 1.56). The overall pregnancy rate for these five trials was 15.4% compared to the spontaneous rate of 12.5% in the control groups. These odds increased to 1.56 (95% confidence interval 0.99 to 2.19) when all 10 trials were included, but this result is likely to be artificially inflated.
REVIEWER'S CONCLUSIONS:
Anti-oestrogens appear to have a beneficial effect on endocrinal outcomes, but there is not enough evidence to evaluate the use of anti-oestrogens for increasing the fertility of males with idiopathic oligo-asthenospermia.
Tamoxifen treatment of oligozoospermia: a re-evaluation of its effects including additional sperm function tests.
Abstract
Because of previous contradictory results, we reevaluated the effects of tamoxifen on 29 men presenting with idiopathic oligozoospermia. To determine whether a possible increase in sperm concentration might be correlated with an improvement of sperm quality, the hamster ovum penetration (HOP) test and the hypo-osmotic swelling (HOS) test were included as additional tests of sperm function. Patients were treated with tamoxifen (20 mg/day) for 3 months. From 4 weeks until the end of the study, tamoxifen had a significant effect (P < 0.001) on blood levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone (T), and estradiol (E2). Prolactin (PRL) concentrations were not altered significantly (P > 0.05). There was no significant improvement (P > 0.05) of conventional semen parameters (volume, concentration, motility, morphology), and of HOP and HOS test results. The lack of correlation between a rise in hormone levels and improvement of sperm quality suggests that tamoxifen is of questionable value in men with idiopathic oligozoospermia.
Human Chorionic and Menopausal Gonadotropin (hCG/hMG) treatment has had the best success at bringing back spermatogenesis
Although, your condition is not at the level of being azoospermic, I believe that hMG, or a combination of hCG and hMG, make for the best PCT after any androgen cycle.
Successful treatment of anabolic steroid-induced azoospermia with human chorionic gonadotropin and human menopausal gonadotropin.
Abstract
OBJECTIVE:
To document for the first time the successful treatment using human chorionic gonadotropin (hCG) and human menopausal gonadotropins (hMG) of anabolic steroid-induced azoospermia that was persistent despite 1 year of cessation from steroid use.
DESIGN:
Clinical case report.
SETTINGS:
Tertiary referral center for infertility.
PATIENT(S):
A married couple with primary subfertility secondary to azoospermia and male hypogonadotropic hypogonadism. The husband was a bodybuilder who admitted to have used the anabolic steroids testosterone cypionate, methandrostenolone, oxandrolone, testosterone propionate, oxymetholone, nandrolone decanoate, and methenolone enanthate.
INTERVENTION(S):
Twice-weekly injections of 10,000 IU of hCG (Profasi; Serono) and daily injections of 75 IU of hMG (Humegon; Organon) for 3 months.
MAIN OUTCOME MEASURE(S):
Semen analyses, pregnancy.
RESULT(S):
Semen analyses returned to normal after 3 months of treatment. The couple conceived spontaneously 7 months later.
CONCLUSION(S):
Steroid-induced azoospermia that is persistent after cessation of steroid use can be treated successfully with hCG and hMG.
hCG may be enough to bring back spermatogenesis. hCG mimics LH almost identically, and how it stimulates FSH production is beyond me, but they have had a lot success with it.
Anabolic steroid induced hypogonadism treated with human chorionic gonadotropin.
Abstract
A case is presented of a young competitive body-builder who abused anabolic steroid drugs and developed profound symptomatic hypogonadotrophic hypogonadism. With the help of prescribed testosterone (Sustanon) he stopped taking anabolic drugs, and later stopped Sustanon also. Hypogonadism returned, but was successfully treated with weekly injections of human chorionic gonadotropin for three months. Testicular function remained normal thereafter on no treatment. The use of human chorionic gonadotropin should be considered in prolonged hypogonadotrophic hypogonadism due to anabolic steroid abuse.
Maintenance of spermatogenesis in hypogonadotropic hypogonadal men with human chorionic gonadotropin alone.
Abstract
OBJECTIVE:
It is generally accepted that both gonadotropins LH and FSH are necessary for initiation and maintenance of spermatogenesis. We investigated the relative importance of FSH for the maintenance of spermatogenesis in hypogonadotropic men.
SUBJECTS AND METHODS:
13 patients with gonadotropin deficiency due to idiopathic hypogonadotropic hypogonadism (IHH), Kallmann syndrome or pituitary insufficiency were analyzed retrospectively. They had been treated with gonadotropin-releasing hormone (GnRH) (n=1) or human chorionic gonadotropin/human menopausal gonadotropin (hCG/hMG) (n=12) for induction of spermatogenesis. After successful induction of spermatogenesis they were treated with hCG alone for maintenance of secondary sex characteristics and in order to check whether sperm production could be maintained by hCG alone. Serum LH, FSH and testosterone levels, semen parameters and testicular Volume were determined every three to six Months.
RESULTS:
After spermatogenesis had been successfully induced by treatment with GnRH or hCG/hMG, hCG treatment alone continued for 3-24 Months. After 12 Months under hCG alone, sperm counts decreased gradually but remained present in all patients except one who became azoospermic. Testicular Volume decreased only slightly and reached 87% of the Volume achieved with hCG/hMG. During treatment with hCG alone, FSH and LH levels were suppressed to below the detection limit of the assay.
CONCLUSION:
Once spermatogenesis is induced in patients with secondary hypogonadism by GnRH or hCG/hMG treatment, it can be maintained in most of the patients qualitatively by hCG alone, in the absence of FSH, for extended periods. However, the decreasing sperm counts indicate that FSH is essential for maintenance of quantitatively normal spermatogenesis.
I hope this helps.
