Archived Comments for:
A systematic review of the incidence of schizophrenia: the distribution of rates and the influence of sex, urbanicity, migrant status and methodology
It is my hypothesis that schizophrenia results from low dehydroepiandrosterone (DHEA) in utero and/or early infancy. I suggest low DHEA results in reduced growth and development of affected structures which are vulnerable later in life to events which reduce DHEA availability. Cortisol and testosterone should adversely affect DHEA. This combination of an associated stressful event (cortisol) and puberty (testosterone) around the time of the beginning of the natural decline of DHEA, around age twenty, may explain a preponderance of onset of schizophrenia in the late teens and early twenties. (DHEA is low in schizophrenia. DHEA is known to positively affect growth of neuronal structures.)
My principal hypothesis is that DHEA was selected by evolution because DHEA optimizes replication and transcription of DNA. Therefore, all tissues, especially the brain, are affected by levels of DHEA. Subordinately, the other major, adrenal steroid hormone, cortisol, evolved to counteract the effects of DHEA and produces the “fight or flight” mechanism. Too much cortisol will adversely affect neural structures poorly developed by low DHEA. (It is known that excessive cortisol over prolonged periods damages neural structures.) Testosterone interferes with availability of DHEA and this adversely affects neural structures which have developed poorly because of low DHEA.
I recently had the necessity to explain seasonal affective disorder (SAD) (depression) of winter. In so doing, I found that testosterone interferes with the conversion of DHEAS (sulfate), the reserve form of DHEA, to DHEA, the active form. It is also my hypothesis (1985) that depression may result from low DHEA in vulnerable individuals. (It has since been determined that DHEA is low in depression and that the ratio of cortisol to DHEA is involved.) Testosterone increases in fall and winter, therefore, the conversion of DHEAS to DHEA is reduced by testosterone during these seasons. This may explain SAD.
A study in 2003 reported that “Only male cases of schizophrenia and schizophreniform disorder showed a significant seasonal distribution to dates of onset of symptoms, with a peak in August (winter).” (Psychol Med. 2003 Jan;33(1):163-7). I suggest the same mechanism is occurring in this study as in SAD but is affecting different liabilities produced during growth and development of the brain. That is, it is testosterone, the increase in testosterone in winter, and the effects of testosterone on the conversion of DHEAS to DHEA that are causing the “significant seasonal” peak of schizophrenia in the winter.
With the foregoing in mind, I suggest the other categories associated with increased schizophrenia may also reflect higher levels of testosterone.
This may be due to testosterone
28 April 2004
This may be due to testosterone.
It is my hypothesis that schizophrenia results from low dehydroepiandrosterone (DHEA) in utero and/or early infancy. I suggest low DHEA results in reduced growth and development of affected structures which are vulnerable later in life to events which reduce DHEA availability. Cortisol and testosterone should adversely affect DHEA. This combination of an associated stressful event (cortisol) and puberty (testosterone) around the time of the beginning of the natural decline of DHEA, around age twenty, may explain a preponderance of onset of schizophrenia in the late teens and early twenties. (DHEA is low in schizophrenia. DHEA is known to positively affect growth of neuronal structures.)
My principal hypothesis is that DHEA was selected by evolution because DHEA optimizes replication and transcription of DNA. Therefore, all tissues, especially the brain, are affected by levels of DHEA. Subordinately, the other major, adrenal steroid hormone, cortisol, evolved to counteract the effects of DHEA and produces the “fight or flight” mechanism. Too much cortisol will adversely affect neural structures poorly developed by low DHEA. (It is known that excessive cortisol over prolonged periods damages neural structures.) Testosterone interferes with availability of DHEA and this adversely affects neural structures which have developed poorly because of low DHEA.
I recently had the necessity to explain seasonal affective disorder (SAD) (depression) of winter. In so doing, I found that testosterone interferes with the conversion of DHEAS (sulfate), the reserve form of DHEA, to DHEA, the active form. It is also my hypothesis (1985) that depression may result from low DHEA in vulnerable individuals. (It has since been determined that DHEA is low in depression and that the ratio of cortisol to DHEA is involved.) Testosterone increases in fall and winter, therefore, the conversion of DHEAS to DHEA is reduced by testosterone during these seasons. This may explain SAD.
A study in 2003 reported that “Only male cases of schizophrenia and schizophreniform disorder showed a significant seasonal distribution to dates of onset of symptoms, with a peak in August (winter).” (Psychol Med. 2003 Jan;33(1):163-7). I suggest the same mechanism is occurring in this study as in SAD but is affecting different liabilities produced during growth and development of the brain. That is, it is testosterone, the increase in testosterone in winter, and the effects of testosterone on the conversion of DHEAS to DHEA that are causing the “significant seasonal” peak of schizophrenia in the winter.
With the foregoing in mind, I suggest the other categories associated with increased schizophrenia may also reflect higher levels of testosterone.
Competing interests
None declared