Male infertility is a frequent cause of childlessness, and, indeed, a comparison of the contributions to conception failure made by male and female factors shows them to be equally frequent. In practice, male infertility appears to be resistant to most treatments. However, the major reason for this may be that often attempts are carried out without knowing the cause of the problem. Unlike in women, obstructions and hormonal disorders are rare in male infertility. Rather, it would appear that sperm disorders are the most common cause, reflecting a variety of pathogenetic mechanisms. Defects in sperm morphology, defective sperm movement, deficient development or functional failure of the acrosome, and the excessive generation of reactive oxygen species are changes that are often seen in infertile semen, but little is known about their aetiology. In 5–10% of men being treated for infertilty, an autoimmune reaction against spermatozoa is observed. Although the correlation between the presence of systemic antisperm antibodies and fertility potential is poor, the appearance of sperm-bound antibodies of immunoglobulin class IgA in semen seems to be closely associated with infertility. Studies in laboratory animals and humans have shown that complementary adhesion molecules are located on the surface of oocytes and spermatozoa. These molecules interact and lead to gamete fusion. Abnormalities in these molecules on the sperm surface might be expected to contribute to male infertility. However, their clinical significance has not yet been documented, and the molecular basis of human gamete interaction is far from being understood. Therefore, the key to understanding male infertility may lie in basic research which directly targets the fundamental cellular and molecular biology of the human spermatozoon.

Consideration of the function of the epididymis has undergone profound changes over the last century during which it has moved from a largely neglected male reproductive organ to one that is an increasingly exploited source of sperm for assisted reproduction strategies. From histological studies in the lizard1 it was considered that, ‘…the cells lining the epididymal canal produce a material necessary for the spermatozoa during their passage through the organ …’ whereas a fertility study with guinea-pigs stated boldly that, ‘… changes undergone [by spermatozoa in the epididymis] are not conditioned by some specific action of epididymal secretion …’. The former view found favour in a review of the literature which concluded that, ‘… there are specific epididymal secretions necessary for sperm maturation and survival …’, although the nature of the secretions were not then known. However, this concept, currently held by most of those studying the epididymis of animals, was again contradicted on the basis of clinical work: ‘… it certainly is possible for sperm that have never passed through any length of the epididymis at all to mature on their own …’.

Follicle stimulating hormone (FSH) is a glycoprotein hormone secreted by the pituitary gland that, together with luteinizing hormone (LH), controls development, maturation and function of the gonad. Like the related hormones, LH, thyroid stimulating hormone (TSH) and human chorionic gonadotropin (hCG), FSH consists of two polypeptide chains, α and β, bearing carbohydrate moieties N-linked to asparagine (Asn) residues. The α subunit is common to all members of the glycoprotein hormone family, whereas the β subunit, although structurally very similar, differs in each hormone and confers specificity of action.

Late-onset or nonclassic hyperandrogenic congenital adrenal hyperplasia (CAH) is an attenuated deficiency of 21-hydroxylase, 3β-ol-hydroxysteroid dehydrogenase or 11β-hydroxylase which presents during childhood or adolescence and leads to an increased secretion of adrenal androgens. Many reviews of the genetic or hormonal characteristics of these syndromes have been published, but relatively little attention has been paid to the pathogenesis and treatment of hirsutism which, in most young women, is the main complaint. In fact, it is generally assumed that the hirsutism is strictly related to the increased secretion of adrenal androgens and that glucocorticoids are the treatment of choice. However, some recent studies have shown that the ovary contributes to the hyperandrogenism of these patients and some alternative therapies have been proposed. This forms the matter of the present review.

Epidemiological studies relating cigarette smoking to the ability to conceive and maintain a pregnancy provide information on the clinical significance of smoking on reproductive health. Cigarette smoking by females has significantly increased in the decades after World War II, and now has an average initiation at ages 18–20 years. Maternal smoking is a hazard to the general health, the reproductive health and the life of both mother and child. Gestational smoking renders the fetus a passive smoker. This can result in fetal and neonatal death and in reduced fecundity of adult daughters.