Life events that occur during adulthood are defined as particularly significant experiences that result in substantial changes to personal circumstances. These changes may be positive or they may be negative changes and can occur across all aspects of life, including health, education, employment, relationships, bereavement, housing, legal, and financial issues.

What is the evidence for adult life events as risk factors for schizophrenia?

Moderate quality evidence finds a medium-sized increase in recent adverse life events in people with psychosis compared to people without psychosis, measured between 3 months and 3.6 years prior. There was a small association between increased rates of neighbourhood crime and increased rates of psychosis.

Moderate to low quality evidence suggests a small increase in prevalence, and a medium to large increase in incidence of subclinical psychotic symptoms in people reporting prior exposure to stress and trauma. There was a medium-sized increase in perceived stress, but not adverse events, in people at ultra high-risk for psychosis; those with attenuated psychotic symptoms or brief and limited intermittent psychotic symptoms, genetic risk, and functional deterioration.

April 2022

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Childhood adversities encompass a range of childhood experiences, including loss of a close relative, parental separation, bullying, physical abuse, sexual abuse, emotional abuse, and neglect. The nature, timing, severity, and duration of exposure are likely to influence mental health, however any evidence that childhood adversity directly causes psychosis or schizophrenia is controversial. Firstly, psychotic disorders may be secondary to comorbid affective, substance use, personality, or post-traumatic stress disorders, all of which have been linked to early adversities, and all are common in those with a psychotic mental illness. Another difficulty is accurately measuring childhood adversity, as it is dependent on assessment of the experiences via information collected retrospectively. This is particularly problematic if having a psychotic disorder impacts on memory recall.

What is the evidence for childhood adversity?

Moderate to high quality evidence found a small to medium-sized increased risk of schizophrenia and other psychotic disorders following exposure to childhood adversities (abuse, neglect, bullying, or parental loss) compared to people without exposure to childhood adversities. Rates of childhood sexual abuse in people with psychosis was approximately 26.3%, childhood physical abuse was approximately 38.8%, and childhood emotional abuse was approximately 34%. Rates were highest in older studies, in studies with more females, in studies with older patients, and in studies of patients with comorbid substance abuse.

In people with a psychotic disorder, exposure to any childhood adversity was associated with more severe symptom severity and poor cognition. For increased positive symptoms, there were small associations with sexual abuse, physical abuse, emotional abuse, and emotional neglect, and no association with physical neglect. For increased negative symptoms, there were small associations with sexual abuse, physical abuse, physical neglect, and emotional neglect, and no association with emotional abuse. For increased depression, there were small to medium-sized associations with sexual abuse, physical abuse, emotional abuse, emotional neglect, and physical neglect.

Compared to people with anxiety disorders, there was a medium-sized increased risk of childhood adversity in people with schizophrenia. Compared to people with dissociative disorders or post-traumatic stress disorder, there was a large decreased risk of childhood adversity in people with schizophrenia. There were no differences in rates of childhood adversity between people with schizophrenia and people with depressive disorders or affective psychosis.

Moderate to low quality evidence finds mediation and moderating effects of other life events and stressors, social defeat, loneliness, and social support on the relationship between childhood adversity and psychosis. Mediation, but not moderating effects were found for negative cognitive schemas about the self, the world and others, attachment style and parental bonding, mood symptoms, emotional dysregulation, post-traumatic stress disorder, and dissociation. Mediators are mechanisms through which the relationship may be at least partly explained, while moderators were factors that changed the relationship.

April 2022

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Exposure to environmental toxins can cause problems to both physical and mental health. Pollutants of main public health interest involve organic and elemental carbons, metals such as lead, polycyclic aromatic hydrocarbons, carbon monoxide, ozone, nitrogen dioxide, sulphur dioxide, and perchloroethylene commonly used in dry cleaning. Being born or raised in an urban environment has been related to a higher incidence of schizophrenia, and air pollution could be one of the explanatory factors.

What is the evidence for environmental toxins as a risk factor for schizophrenia?

Moderate to low quality evidence suggests exposure to high levels of air pollution may be associated with increased risk for schizophrenia. Prenatal and early childhood exposure to perchloroethylene may also be associated with increased risk of schizophrenia.

April 2022

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Some ethnic groups may show more or less risk for schizophrenia than other ethnic groups. Incidence refers to how many new cases there are per population in a specified time period, while prevalence refers to how many existing cases there are at a particular point in time. Differences in the incidence and prevalence across various ethnic groups can provide clues to possible causes of schizophrenia.

What is the evidence for ethnicity as a risk factor for schizophrenia?

Moderate to high quality evidence suggests the incidence of any psychotic disorder is greater in ethnic minority groups living in the UK or the Netherlands than in the majority population in those areas. The incidence of psychotic disorders in ethnic minority groups is highest in areas with low own-group ethnic density than in areas with high own-group ethnic density. There was also a small increase in the prevalence and incidence of subclinical psychotic symptoms in people from ethnic minority groups. Small effects showed increased rates of psychotic symptoms and experiences in people with high perceived ethnic discrimination.

For schizophrenia in particular, there is a large increased risk in black Caribbean and black African migrants living in the UK, and also in their descendants and a medium-sized increased risk for Asian migrants compared to the white British population. In the USA, moderate quality evidence found a medium-sized increased risk of schizophrenia in Black people compared to White people. This effect was largest in studies with more males, more White participants, more young participants, in studies conducted in hospital and military settings, and in studies conducted in the Midwest, Southeast or national/multistate USA settings.

April 2022

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Familial expressed emotion involving hostility, emotional over-involvement and critical comments has been associated with increased psychotic relapse in people with schizophrenia, so these traits may contribute to the development of psychotic symptoms in vulnerable individuals. Negative parental affective style involving guilt induction, over-intrusiveness and personal criticism, and a lack of clarity in communication may also contribute to increased risk of schizophrenia.

April 2022

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Consumption of a balanced diet during childhood aids the development of a healthy brain. This may act as a preventative factor for the development of schizophrenia in adulthood. In contrast, poor diet in childhood may increase the risk of developing the disorder.

What is the evidence on famine?

Moderate quality evidence suggests a small increased risk of schizophrenia in adulthood after exposure to famine in utero and/or childhood. This result was observed in regional China only as no reviews were found that assessed other regions.

April 2022

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Many disorders are the result of interaction between susceptibility genes and environmental influences. One example is cardiovascular disease; people with a family history of cardiovascular disease are more susceptible to heart problems, and environmental influences, such as diet, can increase this risk. Schizophrenia is also a complex disorder that can arise from both genetic and environmental influences, although heritability estimates are around 80%.

What is the evidence for genetic and non-genetic risk?

Moderate to high quality evidence found large increased risk of schizophrenia in people with one or two first-degree relatives with schizophrenia compared to people without a relative with schizophrenia. Moderate quality evidence from twin studies suggests genetic effects contributing to risk of schizophrenia are much higher than environmental effects, although both factors are involved. Genetic risk scores for schizophrenia are associated with increased symptoms of schizophrenia, particularly negative and disorganised symptoms.

Moderate to low quality evidence suggests a medium increase in prevalence rates of subclinical psychotic symptoms in people with a family history of mental illness. There is a large increased risk of schizophrenia in offspring of people with schizophrenia compared to offspring of people with no mental disorder. There is no increased risk of depression, anxiety, disruptive disorders, substance use disorder, or attention deficit hyperactivity disorder in offspring of people with schizophrenia. There is high familial coaggregation of schizophrenia and bipolar disorder, with first-degree relatives of people with schizophrenia or bipolar disorder showing an increased risk of developing either disorder.

April 2022

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Increased exposure to infections prior to the onset of schizophrenia has been recognised, which suggests infections may be involved in its aetiology. Potential mechanisms for this association include direct impacts of infections on the brain, immune activation, inflammatory cytokines, and alterations in the gut microbiota. This topic summarises the available evidence for the risk of developing schizophrenia following exposure to infectious agents, both before and after birth. For further information, please also see the maternal illness, infectious agents and immunological changes topics.

What is the evidence for infectious agents as risk factors for schizophrenia?

Moderate to high quality evidence found a small increased risk of schizophrenia in people exposed to childhood infections, particularly central nervous system viral infections. The effect sizes increased with increasing number of hospitalisations and decreased with increasing age of exposure (up to 10 years old).

Moderate quality evidence from prospective cohort studies, but not retrospective case-control studies, showed a small but significant association between gastroenteritis exposure and later development of schizophrenia. There was also a small increase in Toxoplasma gondii antibodies found before the development of schizophrenia. Toxoplasma gondii is a parasitic protozoa, hosted by domestic cats and other warm-blooded animals, including humans.

Moderate to high quality evidence suggests a small increased risk of psychotic disorders (mostly schizophrenia spectrum or non-affective psychosis) following exposure to herpes simplex type 2 in utero. Lower quality evidence suggests exposure to toxoplasma gondii or genitourinary infections in utero may also be associated with increased risk of psychotic disorders. No significant risk was found following exposure to herpes simplex type 1, influenza (in any trimester), or cytomegalovirus in utero.

April 2022

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For some time, researchers have observed variations in population rates of schizophrenia, with rates changing depending on the time and place of birth. For example, the prevalence rate in a given population may be increased if birth was at a higher latitude with a cooler climate. These variables are also related to variances in diet, precipitation, sun exposure, socioeconomic status and genetic factors, as well as age and gender differences. Therefore the observed relationships between rates of schizophrenia and higher latitude and cooler climates may have several related explanations.

What is the evidence for latitude, climate and winter birth?

Moderate to high quality evidence finds a small relationship between winter or winter/spring births and increased risk for schizophrenia in the Northern Hemisphere. High quality evidence also finds a small relationship between winter/spring births and subclinical psychotic symptoms in children in Japan and the U.K.

Moderate quality evidence finds a small effect of increased prevalence of schizophrenia with increased latitude and decreased annual mean daily temperature in the Northern Hemisphere. Moderate to low quality evidence finds this association is greatest in people with older fathers at birth (over 45 years old), and in disadvantaged ethnic minority groups.

Moderate to high quality evidence finds a small effect of increased rates of deficit schizophrenia (predominately negative symptoms) in offspring born in the summer months of June and July in the Northern Hemisphere.

April 2022

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Being married can increase the extent and intensity of relationships, as well as increase feelings of reciprocity and sharing; all of which have been linked to a decreased risk of developing schizophrenia. Conversely, being married can increase stress, particularly if there are problems in the marriage, and stress has been linked to an increased risk of schizophrenia.

What is the evidence for marital status?

Moderate quality evidence suggests a small increased rate of subclinical psychotic symptoms in people who are not married compared to people who are married. There is also increased rates of single status in people with ultra high-risk mental states (attenuated, brief or limited intermittent psychotic symptoms).

April 2022

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