Schizophrenia has no single cause. It develops from a combination of genetic vulnerability, brain chemistry, early life experiences, and environmental exposures, with heritability estimated at about 77%. The condition affects roughly 1 in 300 people worldwide, and understanding the risk factors helps explain why some people develop it while others with similar backgrounds do not.
Family History and Genetic Risk
Having a first-degree relative (a parent or sibling) with schizophrenia is the single strongest known risk factor. It increases your likelihood of developing the condition by roughly 7 to 9 times compared to the general population. In large Nordic studies, 10 to 14% of people diagnosed with schizophrenia had a family history of the disorder, compared to about 1% of people without it.
The genetic contribution is substantial but not deterministic. Twin studies place heritability at around 77%, meaning genetics account for most of the variation in who develops the disorder. Shared environment, such as growing up in the same household, accounts for another 10% or so. But even among identical twins who share all their DNA, if one twin has schizophrenia the other develops it only about half the time. That gap points to the importance of everything else on this list.
Age, Sex, and Onset Patterns
Schizophrenia typically appears in late adolescence or early adulthood, but the timing differs between men and women. Men tend to develop symptoms 3 to 4 years earlier than women, with peak incidence between ages 20 and 29. Women show two peaks: one between 20 and 39, and a second wave around perimenopause. The later female peak may be linked to declining estrogen levels, which appear to have a protective effect earlier in life.
Men also tend to experience more prominent negative symptoms (flat emotional expression, social withdrawal, reduced motivation), while women more often show mood-related symptoms like depression and emotional instability. Men generally have worse functioning before the illness begins, even though they may perform better on certain cognitive tasks like visual memory and attention.
Advanced Paternal Age
The age of the father at conception is an independent risk factor. In a landmark Israeli birth cohort study, children born to fathers aged 50 or older had roughly triple the risk of schizophrenia compared to children of fathers in their early twenties. Across multiple studies, every 10-year increase in paternal age has been associated with close to a 90% increase in risk. Some research has found up to a fivefold increase for the oldest fathers.
The leading explanation involves new genetic mutations that accumulate in sperm over a man’s lifetime. Unlike eggs, which are formed before birth, sperm cells divide continuously, and each division introduces a small chance of copying errors. By age 50, a man’s sperm has undergone far more divisions than at age 25, increasing the odds of spontaneous mutations in genes related to brain development.
Prenatal Infections and Complications
What happens during pregnancy matters. Maternal infections during pregnancy are a well-documented risk factor, with different infections carrying different levels of risk. Rubella exposure during pregnancy is the most dramatic: about 20% of prenatally exposed children went on to develop schizophrenia in adulthood, representing a 10 to 20-fold increase. Influenza during the first trimester is associated with a 7-fold increase, and toxoplasmosis (a parasitic infection often spread through undercooked meat or cat litter) roughly doubles the risk.
The infections themselves may not be the direct culprit. Instead, the mother’s immune response appears to be the key mechanism. When the body fights an infection, it produces signaling molecules called cytokines. Researchers have found that mothers whose children later developed schizophrenia had nearly twice the normal levels of one such molecule (interleukin-8) during the second trimester. These immune signals can cross the placenta and potentially disrupt fetal brain development during critical windows.
Birth complications add further risk. Oxygen deprivation during delivery, low birth weight, and maternal high blood pressure during pregnancy are each associated with a 1.5 to 3 times greater likelihood of schizophrenia. Oxygen deprivation specifically has been linked to earlier onset of the disorder.
Childhood Trauma
Traumatic experiences in childhood are now recognized as a prominent risk factor. High rates of early trauma, including physical abuse, sexual abuse, neglect, and emotional maltreatment, are consistently found in people with psychotic disorders. A meta-analysis estimated that childhood adversity accounts for about 33% of the population-level risk for psychosis, meaning that if childhood trauma could be eliminated entirely, roughly a third of cases might be prevented.
One particularly revealing line of evidence comes from sibling studies. When researchers compared people with schizophrenia to their siblings (who share 50% of their genes), the diagnosed individuals reported significantly more childhood trauma. Since both siblings carry similar genetic vulnerability, the difference in trauma exposure may help explain why one developed the disorder and the other did not. The relationship also follows a dose-response pattern: more severe or prolonged trauma correlates with more severe psychotic symptoms later.
The biological pathway likely involves chronic stress reshaping the brain’s stress response system. Prolonged early trauma can dysregulate the hormonal stress axis, alter neurotransmitter function, and damage the hippocampus, a brain region critical for memory and emotional regulation.
Cannabis Use in Adolescence
Cannabis use, particularly heavy use during adolescence, is one of the most significant modifiable risk factors. A meta-analysis found that the most frequent cannabis users had nearly four times the odds of developing a psychotic disorder compared to non-users. But the age of use matters enormously. Cannabis use during adolescence specifically was associated with an 11-fold increase in risk of psychotic disorders. When researchers looked only at cases severe enough for hospitalization or emergency visits, the risk jumped to nearly 27 times higher.
The adolescent brain is still undergoing major development, particularly in areas involved in reasoning, impulse control, and filtering sensory information. Cannabis affects the same signaling systems that coordinate this development, which may explain why teenage use carries far greater risk than adult use. The relationship appears to be dose-dependent: the more frequently someone uses cannabis during this window, the higher the risk.
Urban Living and Migration
Growing up in a city roughly doubles the risk of schizophrenia compared to growing up in a rural area. A large Danish study found approximately a two-fold increase among people born in the capital versus rural regions. Importantly, follow-up research clarified that it is being raised in an urban area, not simply being born in one, that drives the risk. The more years spent in a densely populated environment during childhood and adolescence, the greater the likelihood of developing the disorder. The population-level impact is considerable: urban upbringing accounts for an estimated 30% of schizophrenia cases in some populations.
Migration is another social risk factor with striking numbers. First-generation immigrants have roughly 2.7 times the risk of schizophrenia compared to the native-born population. For second-generation immigrants, the risk is even higher at about 4.5 times. Migrants from developing countries and those who experience racial discrimination face the greatest increases. The pattern suggests that social stress, marginalization, and the experience of being an outsider play a meaningful role, rather than something inherent to the act of moving.
Brain Chemistry Changes
At the biological level, two chemical signaling systems in the brain are most consistently implicated. The first involves dopamine, a messenger molecule tied to motivation, reward, and the ability to distinguish meaningful signals from background noise. Brain imaging consistently shows that people with schizophrenia produce and release excess dopamine in a deep brain region called the striatum. This overactivity may explain hallucinations and delusions: the brain essentially flags irrelevant stimuli as deeply significant.
The second system involves glutamate, the brain’s primary excitatory messenger. Drugs that block a specific glutamate receptor can produce the full range of schizophrenia symptoms in healthy people, including hallucinations, flattened emotions, and cognitive difficulties. Current models suggest the two systems are connected. When glutamate receptors malfunction on certain inhibitory brain cells, it removes a natural brake on dopamine production, leading to the excess dopamine activity seen in imaging studies. Genetic and environmental risk factors for schizophrenia appear to converge on disrupting both of these systems, which helps explain why so many different risk factors can lead to a similar set of symptoms.