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The notion that the environment can adversely affect male reproductive development and/or function is not an idea that most clinicians take seriously. There are probably good practical reasons for this stance; for example, few clinicians will have encountered patients in whom reproductive dysfunction was diagnosed as being altered by some environmental factor. Does this mean that such causes are rare or does it mean that they go unrecognized? Unfortunately, we probably still lack sufficient understanding to definitively answer this question, but hopefully this chapter will address it.

When viewed from an evolutionary perspective, it is clear that the environment and reproductive function are inextricably linked, as evidenced by the fact that the majority of mammals (seasonal breeders) exhibit seasonal hypogonadism and infertility under the influence of daylight length and other environmental cues (1). Humans are not seasonal breeders, but as we undoubtedly have seasonally breeding ancestors somewhere in our evolutionary past, residues of such effects are likely, as discussed later in this chapter. Perhaps the most important lesson is that seasonal breeding evolved to ensure that offspring are born at the optimum time of year for survival, which usually equates to the availability of a good food supply. Thus, environmental factors, of which daylight is the most invariable, were adopted as cues to regulate function of the reproductive system—this seems to work primarily via central regulation of the hypothalamic-pituitary axis (2). However, effects of the environment on reproduction are far more pervasive than this. The well-established relationship between food intake/energy balance and onset of puberty/maintenance of menstrual cycling in females is another example (3), and the mechanisms by which these effects occur are now being established (e.g., leptin). These examples remind us that we have evolved to be in tune with our environment, and, if we accept this premise, we must

From: Male Hypogonadism: Basic, Clinical, and Therapeutic Principles Edited by: S. J. Winters © Humana Press Inc., Totowa, NJ

also recognize that when our environment or lifestyle change dramatically, there may be health consequences. The major changes in Western diet (increased intake of refined carbohydrates and diary products/fats) and lifestyle (e.g., widespread artificial light and increased sedentary habits) during the last century are, therefore, certain to have had some impact, but the extent to which these changes may have affected our general or reproductive health is unclear, with the notable exception of obesity and obesity-related disorders.

In the past decade, the specter of more widespread environmental adverse effects on male reproductive function have arisen, fueled by the possibility of falling sperm counts and increase in other male reproductive disorders (4,5). Although this is a somewhat controversial topic, some aspects, such as the increase in incidence of testicular germ cell cancer during the past 50 yr or so, are beyond dispute. This increase must have a lifestyle/environmental cause, and the various possibilities are outlined here. There are strong beliefs that testis cancer may be the tip of an iceberg, signaling us about a more fundamental underlying syndrome of disorders (testicular dysgenesis syndrome) that may have a common origin in fetal life during the sexual differentiation process (6). Much of this is still hypothesis, but the evidence in its favor continues to grow. True or not, this hypothesized syndrome has played an important part in opening our eyes to the importance of fetal and neonatal life in setting up the reproductive system for adulthood more than a decade later. This reality is still not taken seriously by many, yet it is in step with thinking in other areas of medicine in which the fetal origins of adult disease are recognized increasingly as being of major importance (7). This puts the spotlight on the pregnant woman and, with the dramatic changes that have been occurring in women's lifestyles in the past two decades or so, it is inevitable that this must have lifelong consequences for the fetus. These may be good or bad, but if they adversely affect the reproductive health of the offspring (3), such effects can remain hidden for 30 or more years, with the result that recognition of the effect and its cause are made extremely difficult.

Finally, the media have made great play of the supposed dangers to the reproductive health of humans and wildlife from so-called endocrine disruptors. This is a broad and complex area with much controversy and uncertainty, but whether endocrine disruptors exert any significant effect on our reproductive health remains to be established (4,5,8). However, we must recognize that manmade products such as dichlorodiphenyl-trichloroethene (DDT) and polychlorinated biphenyls (PCBs), which undoubtedly exert a range of biological effects in wildlife, persist in us all and are, to some extent, passed from one generation to the next via breast milk and the food chain. These and numerous other manmade chemicals are part of our everyday environment, and it is more likely than not that some of these compounds will have a biological effect on some of us. Such effects may be beneficial, adverse, or benign.

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