<unk>  is described as a neurodevelopmental disorder with no precise boundary, or single cause, and is thought to develop from gene–environment interactions with involved vulnerability factors. The interactions of these risk factors are complex, as numerous and diverse insults from conception to adulthood can be involved. A genetic predisposition on its own, without interacting environmental factors, will not give rise to the development of<unk> . The genetic component means that prenatally brain development is disturbed, and environmental influence affects the postnatal development of the brain. Evidence suggests that genetically susceptible children are more likely to be vulnerable to the effects of environmental risk factors. Genetic Estimates of the heritability of<unk>  are between 70% and 80%, which implies that 70% to 80% of the individual differences in risk to<unk>  is associated with genetics. These estimates vary because of the difficulty in separating genetic and environmental influences, and their accuracy has been queried. The greatest risk factor for developing<unk>  is having a first-degree relative with the disease (risk is 6.5%); more than 40% of identical twins of those with<unk>  are also affected. If one parent is affected the risk is about 13% and if both are affected the risk is nearly 50%. However, the DSM-5 indicates that most people with<unk>  have no family history of psychosis. Results of candidate gene studies of<unk>  have generally failed to find consistent associations, and the genetic loci identified by genome-wide association studies explain only a small fraction of the variation in the disease. Many genes are known to be involved in<unk> , each with small effect and unknown transmission and expression. The summation of these effect sizes into a polygenic risk<unk> ore can explain at least 7% of the variability in liability for<unk> . Around 5% of cases of<unk>  are understood to be at least partially attributable to rare copy-number variations (CNVs); these structural variations are associated with known genomic disorders involving deletions at 22q11.2 (DiGeorge syndrome) and 17q12 (17q12 microdeletion syndrome), duplications at 16p11.2 (most frequently found) and deletions at 15q11.2 (Burnside-Butler syndrome). Some of these CNVs increase the risk of developing<unk>  by as much as 20-fold, and are frequently comorbid with autism and intellectual disabilities. The genes CRHR1 and CRHBP are associated with the severity of suicidal behavior. These genes code for stress response proteins needed in the control of the HPA axis, and their interaction can affect this axis. Response to stress can cause lasting changes in the function of the HPA axis possibly disrupting the negative feedback mechanism, homeostasis, and the regulation of emotion leading to altered behaviors. The question of how<unk>  could be primarily genetically influenced, given that people with<unk>  have lower fertility rates, is a paradox. It is expected that genetic variants that increase the risk of<unk>  would be selected against due to their negative effects on reproductive fitness. A number of potential explanations have been proposed, including that alleles associated with<unk>  risk confers a fitness advantage in unaffected individuals. While some evidence has not supported this idea, others propose that a large number of alleles each contributing a small amount can persist. A meta-analysis found that oxidative DNA damage was significantly increased in<unk> . Environmental Environmental factors, each associated with a slight risk of developing<unk>  in later life include oxygen deprivation, infection, prenatal maternal stress, and malnutrition in the mother during prenatal development. A risk is also associated with maternal obesity, in increasing oxidative stress, and dysregulating the dopamine and serotonin pathways. Both maternal stress and infection have been demonstrated to alter fetal neurodevelopment through an increase of pro-inflammatory cytokines. There is a slighter risk associated with being born in the winter or spring possibly due to vitamin D deficiency or a prenatal viral infection. Other infections during pregnancy or around the time of birth that have been linked to an increased risk include infections by Toxoplasma gondii and Chlamydia. The increased risk is about five to eight percent. Viral infections of the brain during childhood are also linked to a risk of<unk>  during adulthood. Adverse childhood experiences (ACEs), severe forms of which are classed as childhood trauma, range from being bullied or abused, to the death of a parent. Many adverse childhood experiences can cause toxic stress and increase the risk of psychosis. Chronic trauma can promote lasting inflammatory dysregulation throughout the nervous system. It is suggested that early stress may contribute to the development of<unk>  through these alterations in the immune system.<unk>  was the last diagnosis to benefit from the link made between ACEs and adult mental health outcomes. Living in an urban environment during childhood or as an adult has consistently been found to increase the risk of<unk>  by a factor of two, even after taking into account drug use, ethnic group, and size of social group. A possible link between the urban environment and pollution has been suggested to be the cause of the elevated risk of<unk> . Other risk factors of importance include social isolation, immigration related to social adversity and racial discrimination, family dysfunction, unemployment, and poor housing conditions. Having a father older than 40 years, or parents younger than 20 years are also associated with<unk> . It has been suggested that apart from gene-environment interactions, environment-environment interactions also be taken into account as each environmental risk factor on its own is not enough. Substance use About half of those with<unk>  use recreational drugs, including cannabis, tobacco, and alcohol excessively. Use of stimulants such as amphetamine and cocaine can lead to a temporary stimulant psychosis, which presents very similarly to<unk> . Rarely, alcohol use can also result in a similar alcohol-related psychosis. Drugs may also be used as coping mechanisms by people who have<unk> , to deal with depression, anxiety, boredom, and loneliness. The use of cannabis and tobacco are not associated with the development of cognitive deficits, and sometimes a reverse relationship is found where their use improves these symptoms. However, substance use disorders are associated with an increased risk of suicide, and a poor response to treatment. Cannabis-use may be a contributory factor in the development of<unk> , potentially increasing the risk of the disease in those who are already at risk. The increased risk may require the presence of certain genes within an individual. Its use is associated with doubling the rate. The use of more potent strains of cannabis having a high level of its active ingredient tetrahydrocannabinol (THC), increases the risk further. One of these strains is well known as skunk.
Schizophrenia
Delusional disorder
Disorganized schizophrenia
Schizoaffective disorder
Simple-type schizophrenia
Autism
Schizophreniform disorder
Bipolar disorder