Other Lifestyle Dietary Factors Affecting the Adult Male

The preceding section dealing with scrotal temperature obviously applies as much to sedentary lifestyles outside, as well as inside, of the workplace. Probably the most important other factors are dietary habits, particularly obesity and alcohol intake, smoking, stress, and recreational/sporting drug use.

Unlike the well-established relationship between caloric intake and maintenance of menstrual cycles in women, there is no such clear relationship in men regarding sperm production and semen quality. However, obesity in men is clearly associated with a fall in total testosterone levels, and this may be severe in massively obese individuals (57-60). One large study found no clear relationship between dietary factors and testosterone levels (60), but one smaller study showed a positive relationship to carbohydrate intake (59). Protein and fiber intake may also affect testosterone bioavailability via effects on sex hormone-binding globulin (SHBG) (61). There is a well-established relationship between obesity, insulin resistance, and SHBG secretion (62,63), but probably the most important pathways by which obesity affects testosterone levels are at the hypothalamic-pituitary level (57) and/or at the testicular level (64). The latter study, as well as animal studies, have indicated a role for leptin in directly suppressing testosterone production by Leydig cells, so the inverse relationship between leptin and testosterone levels in obese and nonobese men (64,65) is perhaps indicative of cause and effect. For certain, there is an intriguing relationship emerging between sex steroids (particularly estradiol), fat stores/obesity, insulin resistance, and leptin levels (63,65-67), but the precise cascade of events is unclear (see Chapter 17). Once this is better understood, it will hopefully shed more light on the relationship between increased abdominal obesity and lowering of testosterone levels with aging in men, as well as the ethnic differences in testosterone/SHBG/insulin levels and their relationship to adiposity and disease risk (63).

Increased rates of smoking and alcohol intake are found in infertile couples (68). Moreover, it is accepted that the normal testis is poised on the brink of hypoxia because of its unusual anatomy (69), so, in theory, smoking is likely to compromise normal tes-ticular function because it lowers the oxygen-carrying capacity of the blood. However, evidence to support this prediction is equivocal at best. Although smoking may sometimes emerge from epidemiology studies as a risk factor for low sperm counts or altered sperm morphology, this is an inconsistent finding (70-72). Nevertheless, effects of male smoking on outcome of in vitro fertilization (IVF) have been reported (73), as have effects on sperm morphology (74) and DNA damage (75). Smoking may be associated with increased, rather than decreased, total (but not free) testosterone levels, probably through effects on SHBG (59,76), and some (77), but not all (76), studies have reported higher estradiol levels in smokers. There is no consistent relationship between moderate alcohol intake and sperm counts in men (59,78), but heavy alcohol intake is consistently associated with lowered testosterone levels (79,80).

Stress arising for various reasons is frequently (81-83), but not always (84), associated with decrements in semen quality, with effects on both sperm counts and sperm motility. The mechanisms behind such changes are unclear. Stress is also widely considered to be associated with lowered testosterone levels in men, but the evidence to support this view is equivocal (85-88). However, there is little doubt that the hypothal-amic-pituitary-gonadal and hypothalamic-pituitary-adrenal axes exhibit cross-talk at various levels (88), so that effects of stress on sex steroids and vice versa are expected.

Although Western men are generally less physically active today than they were 30 or so years ago, for those who do participate in sports, they are far more competitive today, and this has led to use of performance-enhancing drugs, the most common being anabolic androgenic steroids (89-91). Outside of sports, the same drugs are used for improving physique and body image (see Chapter 16). New male contraceptive approaches also rely on systemic androgen administration (usually in combination with a progestogen) and, depending on the dose administered, it is well established that this will suppress production of endogenous testosterone and, hence, interfere with sperm production (92). Similarly, individuals who use anabolic steroids are clearly at risk of hypogonadism (90,93-95), but this is dependent on factors such as type of steroid, dose administered, and, perhaps, administration duration (96). It is not clear how prevalent such hypogonadism may be, because much of the anabolic steroid use is

Cryptorchidism Human Males

Fig. 3. Schematic diagram to illustrate the cellular basis and general pathways via which the disorders that comprise testicular dysgenesis syndrome (TDS) are likely to arise in the human. Abnormal testicular cell differentiation/function is an integral part of this syndrome of disorders, but several pathways might lead to this occurrence, including genetic, environmental, and/or lifestyle factors. Note also that the resultant disorders that arise because of TDS occur with differing frequency, varying from quite common (reduced sperm production, cryptorchidism) to rare (testis germ cell cancer). Note also that some of the disorders may occur for reasons other than TDS (e.g., low sperm counts). TDS may be associated with subnormal testosterone production and/or action, but note that neither the Sertoli cells nor germ cells are targets for testosterone action in fetal life (104).

Fig. 3. Schematic diagram to illustrate the cellular basis and general pathways via which the disorders that comprise testicular dysgenesis syndrome (TDS) are likely to arise in the human. Abnormal testicular cell differentiation/function is an integral part of this syndrome of disorders, but several pathways might lead to this occurrence, including genetic, environmental, and/or lifestyle factors. Note also that the resultant disorders that arise because of TDS occur with differing frequency, varying from quite common (reduced sperm production, cryptorchidism) to rare (testis germ cell cancer). Note also that some of the disorders may occur for reasons other than TDS (e.g., low sperm counts). TDS may be associated with subnormal testosterone production and/or action, but note that neither the Sertoli cells nor germ cells are targets for testosterone action in fetal life (104).

clandestine, but clinicians faced with athletic young men with hypogonadism should always consider this possibility. Similar awareness should be practiced for other nons-teroidal drugs, because we live in an age when use of a range of these recreational drugs is widespread, and some of these may adversely affect testosterone levels and/or sperm production (97-100). Finally, vigorous exercise, such as long-distance running, may result in temporary suppression of testosterone levels in men and minor decrements in semen quality, but the changes are by no means as pronounced as the antireproductive effects that can occur in female athletes (101,102).

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