DHEA secretion and age

In humans and in some non-human primates the secretion of DHEA(S) shows a characteristic pattern throughout the life cycle (Orentreich etal. 1984;Palmert etal. 2001; Reiter et al. 1977) (Fig. 19.1). DHEA(S) is secreted in high quantities by the fetal zone of the adrenal cortex, leading to high circulating DHEAS levels at birth. As the fetal zone involutes, a sharp fall in serum DHEA(S) concentrations is observed post partum to almost undetectable levels after the first months of life.

Levels remain very low until they gradually increase between the sixth and tenth years of age owing to increasing DHEA(S) production by the zona reticularis, a phenomenon termed adrenarche (Reiter et al. 1977; Sklar et al. 1980). DHEA(S) concentrations peak during the third decade, followed by a steady decline with advancing age so that levels during the eighth and ninth decade are only 10-20% of those in young adults (Orentreich et al. 1992). This decline has been termed "adrenopause" in spite of unchanged or even increased cortisol secretion (Laughlin and Barrett-Connor 2000). The age-related decline in DHEA(S) levels shows high interindividual variability and is associated with a reduction in size of the zona reticularis (Parker Jr. etal. 1997). DHEA secretion follows a diurnal rhythm similar to that of cortisol while DHEA(S) does not vary throughout the day. Liu et al. (1990) observed an age-associated attenuation of the diurnal rhythm and the pulse amplitude of DHEA secretion. Moreover, the ACTH-induced increase in DHEA secretion is reduced in elderly subjects (Parker Jr. et al. 2000), whereas the cortisol response to an ACTH challenge is constant or even increased. There is a clear gender difference in DHEA(S) concentrations with lower DHEAS concentrations in adult women compared to men (Orentreich etal. 1984). The physiological basis for this gender difference is not fully clear. However, while some of the circulating DHEA in males is contributed by the testes (Nieschlag etal. 1973; Zappulla etal. 1981) no such contribution from the ovaries is found, although they may indirectly affect DHEA(S) levels (Cumming etal. 1982).

There is also a clear genetic component to circulating DHEA(S) levels which vary significantly in different populations (Khaw 1996). Moreover, the high interindividual variability in any group of similar age is apparently in part inherited and serum DHEAS has thus been reported to be a specific individual marker (Thomas etal. 1994).

19.3 Epidemiology

There is some gender effect of high DHEAS levels in epidemiologic studies: Barrett-Connor et al. (1986) reported an inverse correlation between DHEAS levels and death from any cause for men (>50 years of age) but not for women (Barrett-Connor and Khaw 1987; Barrett-Connor and Goodman-Gruen 1995). In a prospective cohort study in 622 subjects of 65 years and older mortality at two and four years was associated with low serum DHEAS at baseline in men but not in women (Berr et al. 1996). Similarly in a recent report including men (n = 963) andwomen (n = 1171) >65 years of age, all cause and cardiovascular disease mortality were highest in the lowest DHEAS quartile for men. Again no significant association of circulating DHEAS and mortality was found for women (Trivedi and Khaw 2001). In addition, Mazat et al. (2001) found no association between mortality and DHEAS levels in women, whereas in men the relative risk of death was 1.9 (p < 0.01) for those with the lowest concentrations of DHEAS. Accordingly, in a study of healthy very old men (90-106 years) low DHEAS concentrations were associated with poor functional status (Ravaglia et al. 1996). This sex difference observed in many (but not all) studies could be explained, in part, by sex-specific differences in bioconversion of DHEA(S) (Arlt etal. 1998; 1999b) (see below).

In addition, low DHEAS levels may be a non-specific marker of poor health status and thereby associated with an increased risk of severe illness and death. Low DHEA(S) concentrations have been found in systemic lupus erythematosus, dementia, breast cancer and rheumatoid arthritis and there is an inverse relationship between serum DHEAS levels and severity of disease (Deighton etal. 1992). Chronic disease often leads to a shift of intra-adrenal biosynthesis away from DHEA(S) production favoring cortisol secretion (Parker etal. 1985). Thus, low DHEAS levels may indicate the presence of a not yet apparent disease, which determines a future risk of morbidity or even mortality.

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