Advanced

A Swedish National Prospective and Co-relative Study of School Achievement at Age 16, and Risk for Schizophrenia, Other Nonaffective Psychosis, and Bipolar Illness.

Kendler, Kenneth S; Ohlsson, Henrik LU ; Mezuk, Briana; Sundquist, Kristina LU and Sundquist, Jan LU (2016) In Schizophrenia Bulletin 42(1). p.77-86
Abstract
While cognitive ability is inversely associated with risk for schizophrenia (SZ), the association is less clear with other nonaffective psychoses (ONAP) and bipolar illness (BPI). Using national Swedish hospital registry data, we examined the prospective relationship between school achievement (SA) and development of SZ, ONAP, and BPI in 1800643 adolescents born 1972-1990. We used Cox proportional hazard and co-relative control models to predict onset of SZ, ONAP, and BPI from standardized SA scores at age 16. The hazard ratio (HRs; and 95% CIs) for first onset of SZ as a function of SA was 0.66 (0.64-0.68) for both sexes. For ONAP, the HRs equaled 0.66 (0.64-0.68) for males and 0.72 (0.70-0.75) for females. For BPI, parallel HRs were 0.81... (More)
While cognitive ability is inversely associated with risk for schizophrenia (SZ), the association is less clear with other nonaffective psychoses (ONAP) and bipolar illness (BPI). Using national Swedish hospital registry data, we examined the prospective relationship between school achievement (SA) and development of SZ, ONAP, and BPI in 1800643 adolescents born 1972-1990. We used Cox proportional hazard and co-relative control models to predict onset of SZ, ONAP, and BPI from standardized SA scores at age 16. The hazard ratio (HRs; and 95% CIs) for first onset of SZ as a function of SA was 0.66 (0.64-0.68) for both sexes. For ONAP, the HRs equaled 0.66 (0.64-0.68) for males and 0.72 (0.70-0.75) for females. For BPI, parallel HRs were 0.81 (0.78-0.84) and 0.71 (0.70-0.73). The association between SA and risk was stronger in the lower vs the higher ranges of SA. In most analyses, moderate increases in risk were observed at the highest levels of SA, with the strongest evidence for females and risk of ONAP. Co-relative control analyses indicated that common genetic or familial-environmental effects only marginally confounded these associations. Consistent with prior studies, these results have 3 major implications for neurodevelopmental models: (1) adolescent cognitive deficits that increase risk are not the result of prodromal changes,( 2) individual specific environmental exposures are largely responsible for the association between low SA and psychosis risk, and (3) neurodevelopmental disturbances (as indicated by low SA) are not unique to SZ but also occur in ONAP and to a lesser degree BPI. (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Schizophrenia Bulletin
volume
42
issue
1
pages
77 - 86
publisher
Oxford University Press
external identifiers
  • pmid:26231719
  • wos:000368629000012
  • scopus:84954341835
ISSN
1745-1701
DOI
10.1093/schbul/sbv103
language
English
LU publication?
yes
id
1328e065-42db-40ae-98a0-18d61f75d8c5 (old id 7845102)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/26231719?dopt=Abstract
date added to LUP
2015-09-05 11:59:48
date last changed
2017-11-12 03:06:58
@article{1328e065-42db-40ae-98a0-18d61f75d8c5,
  abstract     = {While cognitive ability is inversely associated with risk for schizophrenia (SZ), the association is less clear with other nonaffective psychoses (ONAP) and bipolar illness (BPI). Using national Swedish hospital registry data, we examined the prospective relationship between school achievement (SA) and development of SZ, ONAP, and BPI in 1800643 adolescents born 1972-1990. We used Cox proportional hazard and co-relative control models to predict onset of SZ, ONAP, and BPI from standardized SA scores at age 16. The hazard ratio (HRs; and 95% CIs) for first onset of SZ as a function of SA was 0.66 (0.64-0.68) for both sexes. For ONAP, the HRs equaled 0.66 (0.64-0.68) for males and 0.72 (0.70-0.75) for females. For BPI, parallel HRs were 0.81 (0.78-0.84) and 0.71 (0.70-0.73). The association between SA and risk was stronger in the lower vs the higher ranges of SA. In most analyses, moderate increases in risk were observed at the highest levels of SA, with the strongest evidence for females and risk of ONAP. Co-relative control analyses indicated that common genetic or familial-environmental effects only marginally confounded these associations. Consistent with prior studies, these results have 3 major implications for neurodevelopmental models: (1) adolescent cognitive deficits that increase risk are not the result of prodromal changes,( 2) individual specific environmental exposures are largely responsible for the association between low SA and psychosis risk, and (3) neurodevelopmental disturbances (as indicated by low SA) are not unique to SZ but also occur in ONAP and to a lesser degree BPI.},
  author       = {Kendler, Kenneth S and Ohlsson, Henrik and Mezuk, Briana and Sundquist, Kristina and Sundquist, Jan},
  issn         = {1745-1701},
  language     = {eng},
  number       = {1},
  pages        = {77--86},
  publisher    = {Oxford University Press},
  series       = {Schizophrenia Bulletin},
  title        = {A Swedish National Prospective and Co-relative Study of School Achievement at Age 16, and Risk for Schizophrenia, Other Nonaffective Psychosis, and Bipolar Illness.},
  url          = {http://dx.doi.org/10.1093/schbul/sbv103},
  volume       = {42},
  year         = {2016},
}