328I suggest the basis of the findings of McDonnell, et al., is increased dehydroepiandrosterone (DHEA).

In 1994, I first suggested that low DHEA is directly involved in initiation of oncogenes: “An Explanation of Cancer and the Increase in Cancer: High Testosterone, Low DHEA and Breast Cancer,” at: http://anthropogeny.com/A... which appeared first in publication: Annals of Internal Medicine 2005; 142: 471-472 .

It is my hypothesis that evolution selected dehydroepiandrosterone (DHEA) because it optimizes replication and transcription of DNA, that is, genes. Therefore, DHEA levels affect all tissues and all tissues compete for available DHEA, especially the brain. (I think evolutionary selection of DHEA produced mammalia. “Hormones in Mammalian Evolution,” Rivista di Biologia / Biology Forum 2001; 94: 177-184). DHEA naturally begins to decline around the ages of twenty to twenty-five, reaching very low levels in old age. When DHEA is low or decreasing, all tissues / genes are adversely affected.  Loss of DHEA is the cause of aging. Cancer initiation increases with age.

Vitamin D has been connected with DHEA. It is known that vitamin D receptors are involved in the synthesis of DHEA; it has been found to be involved in bone metabolism: “The study shows that the VDR gene predicts synthesis and/or metabolism of sexual steroid precursor DHEA in parallel with bone mineral density (BMD).” (Horm Metab Res. 2002 Mar;34(3):127-31) I think this relationship will exist in other tissues. Therefore, I suggest low vitamin D levels may be involved in low levels of DHEA.