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Mikkel Arendt, Raben Rosenberg, Leslie Foldager, Gurli Perto, and Povl Munk-Jørgensen
Cannabis-induced psychosis and subsequent schizophrenia-spectrum disorders: follow-up study of 535 incident cases
The British Journal of Psychiatry 2005; 187: 510-515 [Abstract] [Full text] [PDF]
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[Read eLetter] This could be due to lower DHEA...
James M. Howard   (6 December 2005)

This could be due to lower DHEA... 6 December 2005
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James M. Howard,
biologist
independent

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Re: This could be due to lower DHEA...

jmhoward{at}anthropogeny.com James M. Howard

It is my hypothesis that schizophrenia begins with interference of the actions of, or simply low, DHEA in utero. This produces reduced growth and development of the brain. This is the "early lesion." Later in life, the hormones cortisol and testosterone act to reduce the availability / action of DHEA. This often occurs around the time when DHEA begins to naturally decline, in the late teens or early twenties. These combine to reduce function and structure of the parts of the brain affected in schizophrenia; symptoms and anatomy show decline. Hence, schizophrenia is often associated with a stressful event, cortisol, follows puberty in both sexes, but affects males more, and occurs when DHEA declines. DHEA has been found to be low in schizophrenia.

DHEA utilizes androgen receptors. One study examining the "anti- androgenic effects" of cannabis found interference of androgens (dihydrotestosterone) with androgen receptors (Endocrinology 1980; 107: 848-50). I suggest cannbis use may adversely affect growth and development of the brain by interferring with the effects of DHEA via androgen receptors. This explanation may explain the findings of Arendt, et al.