|J.M. Howard wrote: "It is my hypothesis that schizophrenia results from low dehydroepiandrosterone (DHEA) in utero / neonatal."|
Interesting. How does this notion reconcile low DHEA levels in twins discordant for schizophrenia? If low DHEA levels are found in utero, wouldn't both twins be affected?
Indeed, homocysteine has been found in many disorders and diseases. Do you think, reduced DHEA would also explain biopolar disorder?
DHEA for twins would be lower for both. Therefore, I would expect to find consequences of this effect. In fact, concordant and discordant twins with schizophrenia both show reduced brain
volume. I suggest this would be predicted by sharing of DHEA by twins (Biol Psychiatry. 2004 Sep 15;56(6):454-61). However, there are differences in volumes within the brains of those discordant, suggesting environmental influences, as the authors
of the citation suggest. It is my hypothesis that the in utero effects of low DHEA produce a brain
vulnerable to schizophrenia because of low maternal DHEA. Once born, an individual may or may not produce "normal" DHEA. Normal DHEA would protect from the reductions in DHEA in life caused by stressful events (environmental influences) and testosterone. However, since most schizophrenics do produce low DHEA, these events may trigger a decline in their already reduced brains which produces the symptoms of schizophrenia.
I have thought about bipolar disorder and suspect that DHEA may be involved. However, this one is difficult to put together. Homocysteine
levels have been found to be elevated in bipolar. High DHEA are connected with bipolar and lithium has been found to reduce DHEA in rat
brains. The connection may occur when depression occurs in bipolar. It is my hypothesis from 1985 that low DHEA results in depression and this has since been supported.