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Social and cognitive functioning, urbanicity and risk for schizophrenia

  • Mark Weiser (a1), Jim van Os (a2), Abraham Reichenberg (a3), Jonathan Rabinowitz (a4), Daniella Nahon (a5), Efrat Kravitz (a6), Gad Lubin (a7), Moti Shmushkevitz (a7), Haim Y. Knobler (a7), Shlomo Noy (a8) and Michael Davidson (a8)...
Abstract
Background

Previous work suggests that the association between urbanicity and schizophrenia may be greatest in those with pre-existing vulnerability.

Aims

To test for synergism in risk of schizophrenia between population density and a combined exposure of poor premorbid social and cognitive functioning.

Method

For 371 603 adolescent males examined by the Israeli Draft Board on social and cognitive functioning, data on population density of place of residence and later hospitalisation for schizophrenia were obtained from population-based registries.

Results

There was an interaction between population density (five levels) and poor premorbid social and cognitive functioning (interaction χ2=4.6, P=0.032). The adjusted increase in cumulative incidence associated with one unit change in population density was 0.10% in the vulnerable group (95% CI 0.019–0.18, P=0.015), nine times larger than that in the non-vulnerable group (0.011%, 95% CI 0.0017–0.020, P=0.021).

Conclusions

Risk of schizophrenia may increase when people with a genetic liability to the disorder, expressed as poor social and cognitive functioning, need to cope with city life.

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Copyright
Corresponding author
Mark Weiser, MD, Department of Psychiatry, Sheba Medical Center, Tel-Hashomer, Israel 52621. Email: mweiser@netvision.net.il
Footnotes
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Declaration of interest

None.

Footnotes
References
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  • ISSN: 0007-1250
  • EISSN: 1472-1465
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Social and cognitive functioning, urbanicity and risk for schizophrenia

  • Mark Weiser (a1), Jim van Os (a2), Abraham Reichenberg (a3), Jonathan Rabinowitz (a4), Daniella Nahon (a5), Efrat Kravitz (a6), Gad Lubin (a7), Moti Shmushkevitz (a7), Haim Y. Knobler (a7), Shlomo Noy (a8) and Michael Davidson (a8)...
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eLetters

This could be due to testosterone.

James M. Howard, Biologist
04 October 2007

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 bycortisol and testosterone reduce both function and tissue maintenance. Schizophrenics are characterized by low DHEA.

A report comparing rural areas and a large city found that testosterone is higher in the large city (Folia Histochem Cytobiol. 2001;39 Suppl 2:38-9). I suggest the findings of Weiser, et al., may be explained by increased testosterone in urban areas, perhaps accentuated byincreased population density within an urban area.
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Conflict of interest: None Declared

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