It is my hypothesis that DHEA was selected by evolution because it optimizes replication and transcription of DNA. Therefore, all tissues rely on DHEA for optimal function. DHEA naturally begins to decline around age twenty, reaching very low levels in old age. (This past week, it was reported that measurable mental decline actually begins in the twenties).
It follows that genes rely on DHEA levels for optimal function. As DHEA begins to decline, genes which are not "optimal," themselves, may begin to fail to express optimally as DHEA declines. I suggest this is the reason for an early "hump" in the chart of mortality and morbidity that occurs before the late "hump" which typifies old age. This includes many diseases which may be most dramatically exemplified by Parkinson's, Huntington's, and Alzheimer's diseases, to mention some of the brain-related diseases which, I think, are produced by the early loss of DHEA and malfunctioning genes.
The findings of Brown, et al., may be explained by the foregoing. That is, some surgeries may be required because of abnormalities of growth and development and "wear and tear." These may not be directly due to loss of DHEA of old age. However, many hospitalizations of old age, I suggest, are due to the loss of DHEA and, therefore, represent a failure of availability of DHEA as genes fail to operate. While surgery is known to temporarily reduce DHEA, which may trigger a "rebound," hospitalizations for "failure of available DHEA" will not produce a rebound.
None declared