Male Contraceptives

MALE CONTRACEPTIVES

The only way to suppress male fertility by drugs is to inhibit spermatogenesis. Though considerable effort has been made in this direction and effective drugs have been found, no satisfactory/ acceptable solution is yet tangible. Reasons are—

1)    Complete suppression of spermatogenesis is relatively difficult without affecting other tissues: millions of spermatozoa are released at each ejaculation vs a single ovum per month in women.

2) Spermatogenesis takes 64 days. A drug which even completely inhibited spermatogenesis will take a long latent period to produce infertility. Similarly, return of fertility will be slow.

3)    Gonadotropin suppression inhibits testosterone secretion as well, resulting in loss of libido and impotence: unacceptable to all men and to most spouses.

4)    Risk of adverse effects.

5)  Most importantly—men don’t get pregnant: few would be ready to bear the contingency of regular medication so that their sexual partners do not become pregnant.

Drugs and approaches tried are—

1. Antiandrogens Act by direct action on testes; cause unacceptable loss of libido.

2. Estrogens and progestins Act by suppressing Gns— cause unacceptable feminization.

3. Androgens They inhibit Gns but have poor efficacy; combination with progestin is more efficacious, preserves libido, but is still not reliable.

4. Superactive Gn RH analogues They inhibit Gn release after continued action; also inhibit testosterone secretion— produce impotence, loss of libido.

5. Cytotoxic drugs Cadmium, nitrofurans and indoles suppress spermatogenesis, but are toxic, often produce irreversible action.

6. Gossypol It is a nonsteroidal compound, obtained from cotton seed; has been studied in China. It is effective orally—causes suppression of spermatogenesis in 99% men and reduces sperm motility—infertility develops after a couple of months; fertility is restored several months after discontinuation. However, about 10% men remain oligozoospermic for long periods after discontinuation. During treatment serum LH and testosterone levels do not change: libido and potency are not affected. It has no hormonal or antihormonal activity: mechanism of action is uncertain; probably involves direct toxicity on seminiferous epithelium.

Suggested dose is 20 mg/day for 2–3 months, followed by 40–60 mg/week.

Most important adverse effect is hypokalaemia (due to renal loss of K+) with its attendant muscular weakness (even paralysis). Other side effects are—edema, diarrhoea, breathlessness and neuritis.