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PAPERS: JEAN THÉBERGE, KATE E. WILLIAMSON, NAOKO AOYAMA, DICK J. DROST, RAHUL MANCHANDA, ASHOK K. MALLA, SANDRA NORTHCOTT, RAVI S. MENON, RICHARD W. J. NEUFELD, NAGALINGAM RAJAKUMAR, WILLIAM PAVLOSKY, MARIA DENSMORE, BETSY SCHAEFER, and PETER C. WILLIAMSON Longitudinal grey-matter and glutamatergic losses in first-episode schizophrenia The British Journal of Psychiatry 2007; 191: 325-334 [Abstract] [Full text] [PDF]

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This could be explained by DHEA levels during schizophrenia.

James M. Howard   (12 October 2007)

This could be explained by DHEA levels during schizophrenia. 12 October 2007
James M. Howard, Biologist independent Send letter to journal: Re: This could be explained by DHEA levels during schizophrenia. jmhoward{at}anthropogeny.com James M. Howard	It is my hypothesis that schizophrenia results from reduced fetal brain growth and development due to low maternal DHEA. This underdevelopment is exposed later in life by hormones that interfere with DHEA availability, that is, cortisol and testosterone, along with the natural decline of DHEA that begins around age twenty. Therefore, schizophrenia often occurs following a stressful event (cortisol) in the late teens or early twenties (testosterone and loss of DHEA) or later in life as DHEA reaches very low levels. This loss of DHEA and antagonism by cortisol and testosterone reduce both function and tissue maintenance. Schizophrenics are characterized by low DHEA. Even though DHEA is low in schizophrenia, prior to the onset of schizophrenia sufficient DHEA exists for total brain function. However, as DHEA availability is reduced, triggering prodromal symptoms, reduced social / behavioral function is reduced. As this occurs, use of DHEA by frontal areas is reduced. I suggest this, initially, increases availability of DHEA for midbrain structures which increases their function. I suggest this increase in function of midbrain structures is the basis of positive symptoms. As brain function declines, the brain reduces stimulation of DHEA so DHEA ultimately declines. I suggest loss of DHEA increases negative symptoms. As stated earlier, I suggest testosterone reduces DHEA; negative symptoms are increased by testosterone in male schizophrenics (Psychoneuroendocrinology. 2007 May;32(4):385-91). It is known that DHEA promotes presynaptic glutamate release (Neuropharmacology. 2007 Mar;52(3):966-74). I suggest the foregoing explanation of schizophrenia may explain the findings of Theberge, et al. That is, DHEA availability is initially increased for midbrain structures as frontal use of DHEA decreases followed by gradual decline of overall DHEA which would initially increase glutamate levels followed by a subsequent decline in glutamate levels.