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Smoking and schizophrenia in population cohorts of Swedish women and men: a prospective co-relative control study.

ABSTRACT: The purpose of this study was to clarify the causes of the smoking-schizophrenia association.Using Cox proportional hazard and co-relative control models, the authors predicted future risk for a diagnosis of schizophrenia or nonaffective psychosis from the smoking status of 1,413,849 women and 233,879 men from, respectively, the Swedish birth and conscript registries.Smoking was assessed in women at a mean age of 27 and in men at a mean age of 18. The mean age at end of follow-up was 46 for women and 26 for men. Hazard ratios for first-onset schizophrenia were elevated both for light smoking (2.21 [95% CI=1.90-2.56] for women and 2.15 [95% CI=1.25-3.44] for men) and heavy smoking (3.45 [95% CI=2.95-4.03] for women and 3.80 [95% CI=1.19-6.60] for men). These associations did not decline when schizophrenia onsets 3-5 years after smoking assessment were censored. When age, socioeconomic status, and drug abuse were controlled for, hazard ratios declined only modestly in both samples. Women who smoked into late pregnancy had a much higher risk for schizophrenia than those who quit early. Hazard ratios predicting nonaffective psychosis in the general population, in cousins, in half siblings, and in full siblings discordant for heavy smoking were, respectively, 2.67, 2.71, 2.54, and 2.18. A model utilizing all relative pairs predicted a hazard ratio of 1.69 (95% CI=1.17-2.44) for nonaffective psychosis in the heavy-smoking member of discordant monozygotic twin pairs.Smoking prospectively predicts risk for schizophrenia. This association does not arise from smoking onset during a schizophrenic prodrome and demonstrates a clear dose-response relationship. While little of this association is explained by epidemiological confounders, a portion arises from common familial/genetic risk factors. However, in full siblings and especially monozygotic twins discordant for smoking, risk for nonaffective psychosis is appreciably higher in the smoking member. These results can help in evaluating the plausibility of various etiological hypotheses for the smoking-schizophrenia association.

SUBMITTER: Kendler KS

PROVIDER: S-EPMC4651774 | biostudies-literature | 2015 Nov

REPOSITORIES: biostudies-literature

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Smoking and schizophrenia in population cohorts of Swedish women and men: a prospective co-relative control study.

Kendler Kenneth S KS Lönn Sara Larsson SL Sundquist Jan J Sundquist Kristina K

The American journal of psychiatry 20150605 11

<h4>Objective</h4>The purpose of this study was to clarify the causes of the smoking-schizophrenia association.<h4>Method</h4>Using Cox proportional hazard and co-relative control models, the authors predicted future risk for a diagnosis of schizophrenia or nonaffective psychosis from the smoking status of 1,413,849 women and 233,879 men from, respectively, the Swedish birth and conscript registries.<h4>Results</h4>Smoking was assessed in women at a mean age of 27 and in men at a mean age of 18. ...[more]

PMID: 26046339

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Project description:Importance:Associations between childhood infection, IQ, and adult nonaffective psychosis (NAP) are well established. However, examination of sensitive periods for exposure, effect of familial confounding, and whether IQ provides a link between childhood infection and adult NAP may elucidate pathogenesis of psychosis further. Objectives:To test the association of childhood infection with IQ and adult NAP, to find whether shared familial confounding explains the infection-NAP and IQ-NAP associations, and to examine whether IQ mediates and/or moderates the childhood infection-NAP association. Design, Setting, and Participants:Population-based longitudinal cohort study using linkage of Swedish national registers. The risk set included all Swedish men born between 1973 and 1992 and conscripted into the military until the end of 2010 (n?=?771?698). We included 647?515 participants in the analysis. Measurement of Exposures:Hospitalization with any infection from birth to age 13 years. Main Outcomes and Measures:Hospitalization with an International Classification of Diseases diagnosis of NAP until the end of 2011. At conscription around age 18 years, IQ was assessed for all participants. Results:At the end of follow-up, the mean (SD) age of participants was 30.73 (5.3) years. Exposure to infections, particularly in early childhood, was associated with lower IQ (adjusted mean difference for infection at birth to age 1 year: -1.61; 95% CI, -1.74 to -1.47) and with increased risk of adult NAP (adjusted hazard ratio for infection at birth to age 1 year: 1.19; 95% CI, 1.06 to 1.33). There was a linear association between lower premorbid IQ and adult NAP, which persisted after excluding prodromal cases (adjusted hazard ratio per 1-point increase in IQ: 0.976; 95% CI, 0.974 to 0.978). The infection-NAP and IQ-NAP associations were similar in the general population and in full-sibling pairs discordant for exposure. The association between infection and NAP was both moderated (multiplicative, ??=?.006; SE?=?0.002; P?=?.02 and additive, ??=?.008; SE?=?0.002; P?=?.001) and mediated (??=?.028; SE?=?0.002; P?<?.001) by IQ. Childhood infection had a greater association with NAP risk in the lower, compared with higher, IQ range. Conclusions and Relevance:Early childhood is a sensitive period for the effects of infection on IQ and NAP. The associations of adult NAP with early-childhood infection and adolescent IQ are not fully explained by shared familial factors and may be causal. Lower premorbid IQ in individuals with psychosis arises from unique environmental factors, such as early-childhood infection. Early-childhood infections may increase the risk of NAP by affecting neurodevelopment and by exaggerating the association of cognitive vulnerability with psychosis.

Project description:Importance:Glucosinolates, a group of phytochemicals abundant in cruciferous vegetables, may have cardioprotective properties. However, no prospective study has evaluated the association of intake of glucosinolates with the risk of coronary heart disease (CHD). Objective:The objective of the study was to evaluate the association between the intake of glucosinolates and incident CHD in US men and women. Design:Prospective longitudinal cohort study. Setting:Health professionals in the USA. Participants:We followed 74,241 women in the Nurses' Health Study (NHS; 1984-2012), 94,163 women in the NHSII (1991-2013), and 42,170 men in the Health Professionals Follow-Up Study (1986-2012), who were free of cardiovascular disease and cancer at baseline. Exposure:Glucosinolate intake was assessed using validated semi-quantitative food frequency questionnaires at baseline and updated every 2-4 years during follow-up. Main outcome measures:Incident cases of CHD were confirmed by medical record review. Results:During 4,824,001 person-years of follow-up, 8,010 cases of CHD were identified in the three cohorts. After adjustment for major lifestyle and dietary risk factors of CHD, weak but significantly positive associations were observed for glucosinolates with CHD risk when comparing the top with bottom quintiles (hazard ratio [HR]:1.09; 95% CI: 1.01, 1.17; Ptrend<0.001). Higher intakes of three major subtypes of glucosinolates were consistently associated with a higher CHD risk, although the association for indolylglucosinolate did not achieve statistical significance. Regarding cruciferous vegetable intake, participants who consumed one or more servings per week of Brussels sprouts (HR: 1.16; 95% CI: 1.06, 1.26; P<0.001) and cabbage (HR: 1.09; 95% CI: 1.02, 1.17; P=0.009) had a significantly higher CHD risk than those who consumed these cruciferous vegetables less than once per month. Conclusion and relevance:In these three prospective cohort studies, dietary glucosinolate intake was associated with a slightly higher risk of CHD in US adults. These results warrant replications in further studies including biomarker-based studies. Further studies are needed to confirm these findings and elucidate mechanistic pathways that may underlie these associations.

Dataset Information

Smoking and schizophrenia in population cohorts of Swedish women and men: a prospective co-relative control study.

Publications

Smoking and schizophrenia in population cohorts of Swedish women and men: a prospective co-relative control study.

Similar Datasets

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