I suggest type 2 diabetes is part of a syndrome which includes obesity, increased infections, negative metabolic findings, etc. This syndrome is caused by disruptions in availability of dehydroepiandrosterone (DHEA). Vitamin D3 may help increase intracellular availability of DHEA.

It is my hypothesis that human evolution is driven by increases in testosterone levels. ("Androgens in Human Evolution," Rivista di Biologia / Biology Forum 2001; 94: 345-362. If your library does not subscribe to "Rivista ... ," you may find this at: http://anthropogeny.com/A... .) Periodically in humans, I think, testosterone increases to such levels that testosterone causes negative consequences by disturbing the testosterone to dehydroepiandrosterone (DHEA) ratios. I think this is occurring at this time; the manifestations of this are all increasing simultaneously at this time. My explanation of human evolution is based on increased availability of DHEA caused by increases in androgen receptors stimulated by increased testosterone.

Testosterone and DHEA work together to increase DHEA availability. This is a balance, too much testosterone actually reduces DHEA availability; this would manifest during youth. Increased testosterone during evolution also causes the biological secular trend, the increase in size and earlier puberty in children. This is caused by an earlier, higher testosterone peak which causes an earlier decline of testosterone in adulthood. Since testosterone is involved in intracellular DHEA, this earlier decline of testosterone reduces DHEA for all tissues. This is the cause of the syndrome which includes type 2 diabetes and is increasing at this time. A case may be made in the medical literature that low testosterone of adulthood is involved in the onset of type 2 diabetes.

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.

Vitamin D3 may increase intracellular DHEA levels which would ameliorate the effects of low DHEA identified as type 2 diabetes. I suggest this explains the findings of Park, et al.,