Dehydroepiandrosterone sulphate (DHEAS) and unconjugated dehydroepiandrosterone (DHEA) have been determined in the blood serum of normal subjects of both sexes from 1 month to 100 years of age. In total, 92 girls, 49 boys, 211 women and 110 men were investigated. The effects of age and sex on the levels of the hormones were measured. DHEAS levels declined rapidly during the first year of life and were maintained at a minimum level for 5 years. They increased significantly from 6 to 7 years of age and reached maximum levels in women at about 24 years and in men at about 30 years of age. They then declined rapidly in both sexes but the fall which occurred after 50 and 60 years of age respectively was only moderate. Age-related unconjugated DHEA levels were different. After the first month of life DHEA levels were relatively high and declined more slowly. The minimum level was observed in girls between 5 and 7 years and in boys between 5 and 9 years of age. A significant rise then began and levels reached a maximum in women as well as in men at about 20 years of age. In men levels then declined up to the age of 80. In women the DHEA levels declined during the next 15 years and from approximately 36 years of age they again rose significantly up to a second peak. A mild but significant decline then resumed. There was a difference in the levels of DHEA and DHEAS depending on sex. Unlike DHEAS, unconjugated DHEA was higher in women than in men. However, this difference was significant only in some age groups: during puberty (between 11 and 15 years of age), in the premenopausal period (between 36 and 45 years of age) and in the older group (after 60 years of age). Age- and sex-related dependencies were different between DHEAS and DHEA. They indicate the possible variable secretion and dynamics of their (inter)conversion. We have concluded that DHEA measurements cannot be a substitute for DHEAS and vice versa.

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A neurodegenerative disease such as Alzheimer's disease (AD) is associated with significantly higher dehydroepiandrosterone (DHEA) levels in cerebrospinal fluid (CSF). Because the human brain is known to transform DHEA into DHEA sulfate (DHEAS), 7 alpha-hydroxy-DHEA, 7 beta-hydroxy-DHEA, and 16 alpha-hydroxy-DHEA, it is possible that DHEA accumulation in the brain results from a decreased production of such metabolites. To test this hypothesis, we have measured and compared CSF levels of DHEA, DHEAS, 7 alpha-hydroxy-DHEA, 7 beta-hydroxy-DHEA, and 16 alpha-hydroxy-DHEA in 14 patients with AD, 12 controls, and eight patients with another common dementia, vascular dementia (VD). Results indicated that DHEAS CSF levels were significantly decreased in AD and VD (P < 0.007), whereas other metabolite levels were not significantly changed. Use of steroid level ratios, such as DHEA/(7 alpha-hydroxy-DHEA + 7 beta-hydroxy-DHEA), 7 beta-hydroxy-DHEA/DHEA, and DHEAS/DHEA ratios, resulted in significant differences between diseased and control patients (P < 0.0003, P < 0.002, and P < 0.002, respectively). In addition, the 7 alpha-hydroxy-DHEA/7 beta-hydroxy-DHEA ratio was significantly different between AD and VD (P < 0.0001) and could be used for differentiating AD from VD. These results indicate that, in AD and VD, increased DHEA levels are not neuroprotective and are neither better sulfated nor better hydroxylated at the 7 alpha, 7 beta, and 16 alpha positions than in controls. The results also suggest that, in AD and VD brains, the sulfotransferase and the cytochromes P450 responsible for the 7 alpha-, 7 beta-, and 16 alpha-hydroxylations of DHEA are either present at lower levels or transformed through natural polymorphism into less-efficient enzymes.

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