Epidemiology

The median lifetime morbid risk for schizophrenia is 7.2 per 1000 people.[7] The male-to-female risk ratio is 1.4:1.[8][9] A connection may exist between later onset in females and higher pre-morbid functioning. It appears that the incidence and prevalence of schizophrenia vary depending on race and geographic location.[10] Patients with schizophrenia have a higher mortality than the general population due to physical illness (e.g., cardiovascular diseases and cancers), accidents, and suicide.[11][12][13]

The age of onset is usually <25 years for males and <35 years for females. It has been reported that more affected people are born in the winter versus the spring or summer seasons, but these data are controversial.[14][15] Additionally, a higher disease incidence has been reported in urban and low-income populations when compared with rural and higher-income groups.[8] The incidence and prevalence appears to increase over time.[16] There is a reported higher incidence in migrant populations, which appears to persist into the second generation.[17][18] While the prevalence of psychotic disorders in the 10- to 18-year-old age group is relatively low at around 0.4%, the prevalence of schizophrenia in 10- to 18-year-olds hospitalised for psychiatric causes is 25%, with an exponential increase over the adolescent years.[19]

Cognitive deficits tend to precede the development of schizophrenia, persist for the whole duration of illness, and be closely tied to functional outcomes.[3]

Risk factors

The closer the family relationship to an affected relative, the higher the risk.[34]

There appears to be a significant increase in the risk of schizophrenia in children of fathers age ≥30 years.[35]

This includes fetal growth retardation, maternal infection, blood group incompatibilities, perinatal hypoxia, and premature delivery.[36]

Heavy marijuana use may increase both the vulnerability to schizophrenia and the likelihood of developing the disorder (odds ratio of around 2.2 to 2.8).[37][38][39][40][41][42] Cannabis use following onset of first-psychosis is associated with both an increased risk of relapse and non-adherence with antipsychotic medication. The results of one prospective analysis suggest that up to 36% of the negative effects of continued cannabis use in patients with psychosis are due to a reduction in concordance with medication.[43]

A longitudinal, long-term follow-up cohort study looked at adolescents at ultra-high risk of developing psychosis. Low IQ was the single neurocognitive factor that discriminated the ultra-high risk patients who developed psychosis from those who did not, and from controls.[44]

Soft neurological signs (minor abnormalities in motor performance on clinical examination; for example, rigidity, gait imbalance, tremor) differentiate individuals at ultra-high risk for psychosis. These signs also correlate with an increase over time in the severity of negative symptoms.[45][46][47]

Evidence suggests a link between psychological stressors and disease onset.[48]

Connected with an increased risk of psychosis in adulthood.[49]

The evidence is debatable.[50]

Outcome of schizophrenia has been inversely correlated with mean daily temperatures.[10]

There is a reported higher incidence in migrant populations, which appears to persist into the second generation.[17][18]

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