Environmental factors associated with the development of schizophrenia include the living environment, drug use, and prenatal stressors.

Maternal stress has been associated with an increased risk of schizophrenia, possibly in association with reelin. Maternal Stress has been observed to lead to hypermethylation and therefore under-expression of reelin, which in animal models leads to reduction in GABAergic neurons, a common finding in schizophrenia. Maternal nutritional deficiencies, such as those observed during a famine, as well as maternal obesity have also been identified as possible risk factors for schizophrenia. Both maternal stress and infection have been demonstrated to alter fetal neurodevelopment through pro-inflammatory proteins such as IL-8 and TNF.

Parenting style seems to have no major effect, although people with supportive parents do better than those with critical or hostile parents. Childhood trauma, death of a parent, and being bullied or abused increase the risk of psychosis. Living in an urban environment during childhood or as an adult has consistently been found to increase the risk of schizophrenia by a factor of two, even after taking into account drug use, ethnic group, and size of social group. Other factors that play an important role include social isolation and immigration related to social adversity, racial discrimination, family dysfunction, unemployment, and poor housing conditions.

It has been hypothesized that in some people, development of schizophrenia is related to intestinal tract dysfunction such as seen with non-celiac gluten sensitivity or abnormalities in the intestinal flora. A subgroup of persons with schizophrenia present an immune response to gluten different from that found in people with celiac, with elevated levels of certain serum biomarkers of gluten sensitivity such as anti-gliadin IgG or anti-gliadin IgA antibodies.

About half of those with schizophrenia use drugs or alcohol excessively.

Amphetamine, cocaine, and to a lesser extent alcohol, can result in a transient stimulant psychosis or alcohol-related psychosis that presents very similarly to schizophrenia. Although it is not generally believed to be a cause of the illness, people with schizophrenia use nicotine at much higher rates than the general population.

Alcohol abuse can occasionally cause the development of a chronic, substance-induced psychotic disorder via a kindling mechanism. Alcohol use is not associated with an earlier onset of psychosis.

Cannabis can be a contributory factor in schizophrenia, potentially causing the disease in those who are already at risk. The increased risk may require the presence of certain genes within an individual or may be related to preexisting psychopathology. Early exposure is strongly associated with an increased risk. The size of the increased risk is not clear, but appears to be in the range of two to three times greater for psychosis. Higher dosage and greater frequency of use are indicators of increased risk of chronic psychoses.

Other drugs may be used only as coping mechanisms by individuals who have schizophrenia, to deal with depression, anxiety, boredom, and loneliness.

Approximately three percent of people who are suffering from alcoholism experience psychosis during acute intoxication or withdrawal. Alcohol related psychosis may manifest itself through a kindling mechanism. The mechanism of alcohol-related psychosis is due to the long-term effects of alcohol resulting in distortions to neuronal membranes, gene expression, as well as thiamin deficiency. It is possible in some cases that alcohol abuse via a kindling mechanism can cause the development of a chronic substance induced psychotic disorder, i.e. schizophrenia. The effects of an alcohol-related psychosis include an increased risk of depression and suicide as well as causing psychosocial impairments.

According to some studies, the more often cannabis is used the more likely a person is to develop a psychotic illness, with frequent use being correlated with twice the risk of psychosis and schizophrenia. While cannabis use is accepted as a contributory cause of schizophrenia by some, it remains controversial, with pre-existing vulnerability to psychosis emerging as the key factor that influences the link between cannabis use and psychosis. Some studies indicate that the effects of two active compounds in cannabis, tetrahydrocannabinol (THC) and cannabidiol (CBD), have opposite effects with respect to psychosis. While THC can induce psychotic symptoms in healthy individuals, CBD may reduce the symptoms caused by cannabis.

Cannabis use has increased dramatically over the past few decades whereas the rate of psychosis has not increased. Together, these findings suggest that cannabis use may hasten the onset of psychosis in those who may already be predisposed to psychosis. High-potency cannabis use indeed seems to accelerate the onset of psychosis in predisposed patients. A 2012 study concluded that cannabis plays an important role in the development of psychosis in vulnerable individuals, and that cannabis use in early adolescence should be discouraged.

Schizophrenia disorders in children are rare. Boys are twice as likely to be diagnosed with childhood schizophrenia. There is often an disproportionately large number of males with childhood schizophrenia, because the age of onset of the disorder is earlier in males than females by about 5 years. People have been and still are reluctant to diagnose schizophrenia early on, primarily due to the stigma attached to it.

While very early-onset schizophrenia is a rare event, with prevalence of about 1:10,000, early-onset schizophrenia is manifests more often with an estimated prevalence of 0.5 %.

For women taking psychiatric medication, the decision as to whether continue during pregnancy and whether to take them while breast feeding is difficult in any case; there is no data to guide this decision with respect to preventing postpartum psychosis. There is no data to guide a decision as to whether women at high risk for postpartum psychosis should take antipsychotic medicine to prevent it. For women at risk of postpartum psychosis, informing medical care-givers, and monitoring by a psychiatrist during pregnancy, in the perinatal period, and for a few weeks following delivery, is recommended.

For women with known bipolar disorder, taking medication during pregnancy roughly halves the risk of a severe postpartum episode, as does starting to take medication immediately after the birth.

A clear causal connection between drug use and psychotic spectrum disorders, including schizoaffective disorder, has been difficult to prove. In the specific case of marijuana or cannabis, however, evidence supports a link between earlier onset of psychotic illness and cannabis use. The more often cannabis is used, particularly in early adolescence, the more likely a person is to develop a psychotic illness, with frequent use being correlated with double the risk of psychosis and schizoaffective disorder. A 2009 Yale review stated that in individuals with an established psychotic disorder, cannabinoids can exacerbate symptoms, trigger relapse, and have negative consequences on the course of the illness. While cannabis use is accepted as a contributory cause of schizoaffective disorder by many, it remains controversial, since not all young people who use cannabis later develop psychosis, but those who do use cannabis have an increased odds ratio of about 3.

There is evidence that the two major component cannabinoids in cannabis have different effects: tetrahydrocannabinol (THC), which causes a "high," may increase propensity to psychosis; while cannabidiol (CBD), which doesn't cause a "high" and may have neuroprotective effects—that is, reduce psychosis and have mood stabilizing effects.

About half of those with schizoaffective disorder use drugs or alcohol excessively. There is evidence that alcohol abuse via a kindling mechanism can occasionally cause the development of a chronic substance induced psychotic disorder, i.e. schizoaffective disorder. There is little evidence to suggest that psychotic individuals choose specific drugs to self-medicate; there is some support for the hypothesis that they use drugs to cope with unpleasant states such as depression, anxiety, boredom and loneliness.

Amphetamine, cocaine, and to a lesser extent alcohol, can result in psychosis that presents clinically like psychosis in schizoaffective disorder. It is well understood that methamphetamine and cocaine use can result in methamphetamine or cocaine-induced psychosis that may persist even when users remain abstinent. Alcohol-induced psychosis can also persist during abstinence, though it appears to do so at a lower rate, than when it is being abused.

Although it is not generally believed to be a cause of the illness, people with schizoaffective disorder use nicotine at much greater rates than the general population.

There is no known single cause or causes of schizophrenia, however, it is a heritable disorder.

Several environmental factors, including perinatal complications and prenatal maternal infections could cause schizophrenia. These factors in a greater severity or frequency could result in an earlier onset of schizophrenia. Maybe a genetic predisposition is a important factor too, familial illness reported for childhood-onset schizophrenic patients.

Women with a history of bipolar disorder, schizophrenia, prior episode of postpartum psychosis, or a family history of postpartum psychosis are at high risk; about 25-50% of women in this group will have postpartum psychosis. around 37% of women with bipolar disorder have a severe postpartum episode. Women with a prior episode of postpartum psychosis have about a 30% risk of having another episode in the next pregnancy. For a woman with no history of mental illness who has a close relative (a mother or sister) who had postpartum psychosis, the risk is about 3%. There may be a genetic component; while mutations in chromosome 16 and in specific genes involved in serotoninergic, hormonal, and inflammatory pathways have been identified, none had been confirmed as of 2014.

Family history of affective psychosis, prenatal depression, and autoimmune thyroid dysfunction also increase the risk of postpartum psychosis.

About half of women who experience postpartum psychosis had no risk factors. Many other potential factors like pregnancy and delivery complications, caesarean section, sex of the baby, length of pregnancy, changes in psychiatric medication, and psychosocial factors have been researched and no clear association has been found; the only clear risk factor identified as of 2014 was that postpartum psychosis happens more often to women giving birth for the first time, than to women having second or subsequent deliveries, but the reason for that was not known. There may be a role for hormonal changes that occur following delivery, in combination with other factors; there may be a role changes in the immune system as well.

The exact incidence and prevalence of brief psychotic disorder is not known, but it is generally considered uncommon. Internationally, it occurs twice as often in women than men, and even more often in women in the United States. It typically occurs in the late 30s and early 40s. The exact cause of brief psychotic disorder is not known. One theory suggests a genetic link, because the disorder is more common in people who have family members with mood disorders, such as depression or bipolar disorder. Another theory suggests that the disorder is caused by poor coping skills, as a defense against or escape from a particularly frightening or stressful situation. These factors may create a vulnerability to develop brief psychotic disorder. In most cases, the disorder is triggered by a major stress or traumatic event. Childbirth may trigger the disorder in some women. Approximately 1 in 10,000 women experience brief psychotic disorder shortly after childbirth. There are general medical causes of brief psychosis that should also be considered when being evaluated. Post-natal depression, HIV and AIDS, malaria, syphilis, Alzheimer's disease, Parkinson's disease, hypoglycaemia (an abnormally low level of glucose in the blood), lupus, multiple sclerosis, brain tumor and PANS.

Schizoaffective disorder is estimated to occur in 0.5 to 0.8 percent of people at some point in their life. It is more common in women than men; however, this is because of the high concentration of women in the depressive subcategory, whereas the bipolar subtype has a more or less even gender distribution.

There is limited evidence that caffeine, in high doses or when chronically abused, may induce psychosis in normal individuals and worsen pre-existing psychosis in those diagnosed with schizophrenia.

Various triggers have been associated with switching from euthymic or depressed states into mania. One common trigger of mania is antidepressant therapy. Studies show that the risk of switching while on an antidepressant is between 6-69% percent. Dopaminergic drugs such as reuptake inhibitors and dopamine agonists may also increase risk of switch. Other medication possibly include glutaminergic agents and drugs that alter the HPA axis. Lifestyle triggers include irregular sleep wake schedules and sleep deprivation, as well as extremely emotional or stressful stimuli.

Various genes that have been implicated in genetic studies of bipolar have been manipulated in preclinical animal models to produce syndromes reflecting different aspects of mania. CLOCK and DBP polymorphisms have been linked to bipolar in population studies, and behavioral changes induced by knockout are reversed by lithium treatment. Metabotropic glutamate receptor 6 has been genetically linked to bipolar, and found to be under-expressed in the cortex. Pituitary adenylate cyclase-activating peptide has been associated with bipolar in gene linkage studies, and knockout in mice produces mania like-behavior. Targets of various treatments such as GSK-3, and ERK1 have also demonstrated mania like behavior in preclinical models.

Mania may be associated with strokes, especially cerebral lesions in the right hemisphere.

Deep brain stimulation of the subthalamic nucleus in Parkinson's Disease has been associated with mania, especially with electrodes placed in the ventromedial STN. A proposed mechanism involves increased excitatory input from the STN to dopaminergic nuclei.

A paranoid reaction may be caused from a decline in brain circulation as a result of high blood pressure or hardening of the arterial walls.

Drug-induced paranoia, associated with amphetamines, methamphetamine and similar stimulants has much in common with schizophrenic paranoia; the relationship has been under investigation since 2012. Drug-induced paranoia has a better prognosis than schizophrenic paranoia once the drug has been removed. For further information, see Stimulant psychosis and Substance-induced psychosis.

Based on data obtained by the Dutch NEMISIS project in 2005, there was an association between impaired hearing and the onset of symptoms of psychosis, which was based on a five-year follow up. Some older studies have actually declared that a state of paranoia can be produced in patients that were under a hypnotic state of deafness. This idea however generated much skepticism during its time.

Social circumstances appear to be highly influential on paranoid beliefs. Based on data collected by means of a mental health survey distributed to residents of Ciudad Juárez, Chihuahua (in Mexico) and El Paso, Texas (in the United States), paranoid beliefs seem to be associated with feelings of powerlessness and victimization, enhanced by social situations. Potential causes of these effects included a sense of believing in external control, and mistrust which can be strengthened by lower socioeconomic status. Those living in a lower socioeconomic status may feel less in control of their own lives. In addition, this study explains that females have the tendency to believe in external control at a higher rate than males, potentially making females more susceptible to mistrust and the effects of socioeconomic status on paranoia.

Emanuel Messinger reports that surveys have revealed that those exhibiting paranoia can evolve from parental relationships and dis-trustworthy environments. These environments could include being very disciplinary, stringent, and unstable. It was even noted that, "indulging and pampering (thereby impressing the child that he is something special and warrants special privileges)," can be contributing backgrounds. Experiences likely to enhance or manifest the symptoms of paranoia include increased rates of disappointment, stress, and a hopeless state of mind.

Discrimination has also been reported as a potential predictor of paranoid delusions. Such reports that paranoia seemed to appear more in older patients who had experienced higher levels of discrimination throughout their lives. In addition to this it has been noted that immigrants are quite susceptible to forms of psychosis. This could be due to the aforementioned effects of discriminatory events and humiliation.

The condition is rare, with only 80 established cases reported in medical literature and incomplete evidence of a further 200.

Brief reactive psychosis generally follows a recognisably traumatic life event like divorce or homelessness, but may be triggered by any subjective experience which appears catastrophic to the person affected.

Among such stressors are the death of a loved one, professional loss such as unexpectedly losing one's job or otherwise becoming unemployed, or serious adverse changes in the patient's personal life, such as the breakdown of their family through divorce, etc.

It must be emphasised that this is by no means an exhaustive list of stressful life events, because the events which trigger brief reactive psychosis tend, due to the individualistic nature of human psychology, to be extremely personalized. BRP may be the first breakdown for someone with a chronic psychiatric disorder but only time will tell whether the disorder will be brief or lifelong, whether BRP or a chronic condition that is controlled well enough by medication that symptoms do not return.

Chronic abuse of methylphenidate can also lead to psychosis. Psychotic symptoms from methylphenidate can include hearing voices, visual hallucinations, urges to harm oneself, severe anxiety, mania, grandiosity, paranoid delusions, confusion, increased aggression, and irritability.

In the ICD-10 there are several disorders with the manic syndrome: organic manic disorder (), mania without psychotic symptoms (), mania with psychotic symptoms (), other manic episodes (), unspecified manic episode (), manic type of schizoaffective disorder (), bipolar affective disorder, current episode manic without psychotic symptoms (), bipolar affective disorder, current episode manic with psychotic symptoms ().

The theoretical tardive psychosis is distinct from schizophrenia and induced by the use of current (dopaminergic) antipsychotics by the depletion of dopamine and related to the known side effect caused by their long-term use, tardive dyskinesia.

In addition to dopaminergic upregulation in the nigrostriatal tracts, many investigators have suggested that dopaminergic upregulation may occur in mesolimbic or mesocortical tracts, leading to a worsening of psychosis beyond the original level. This phenomenon has been called 'tardive psychosis' or 'supersensitivity psychosis'.

Tardive psychosis was researched in 1978 and 1989, and sporadic research continues. Some studies have found it to be associated with psychotic depression and potentially, dissociation. For people with any tardive conditions clozapine remains an option but since it can create blood dyscrasias, which require frequent blood work, as well as other severe side effects, it is used increasingly less in clinical practice. Although tardive psychosis continues to be studied, it still has not been established as a fact but it is known that the study classes of antipsychotics such as the NMDA receptor modulators (glutamate antagonists) in not creating tardive dyskinesia will not create this condition.

Many things can cause temporary psychosis. Environmental triggers, such as losing a loved one, are known to contribute, as may excessive stress, or the interaction of strong social demands with a pre-existing vulnerability of self.

Other causes that have been identified include lack of sleep, fever, brain damage, and even hypnosis. War/battlefield experience may also trigger a psychotic break: when reality becomes unbearable, the mind temporarily breaks with it. Parenthood may occasionally set off a psychotic break in men, as may giving birth in women who have previously denied their pregnancy.

Several types of psychoactive drugs have been shown to correlate with psychotic breaks. The compulsive drug user may find their ego dissociating in a psychotic break if habituation means the drug can no longer fulfill its defensive function.

The disorder is characterized by a sudden onset of psychotic symptoms, which may include delusions, hallucinations, disorganized speech or behavior, or catatonic behavior. The symptoms must not be caused by schizophrenia, schizoaffective disorder, delusional disorder or mania in bipolar disorder. They must also not be caused by a drug (such as amphetamines) or medical condition (such as a brain tumor). The term bouffée délirante describes an acute nonaffective and nonschizophrenic psychotic disorder, which is largely similar to DSM-III-R and DSM-IV brief psychotic and schizophreniform disorders.

Symptoms generally last at least a day, but not more than a month, and there is an eventual return to full baseline functioning. It may occur in response to a significant stressor in one's life, or in other situations where a stressor is not apparent, including in the weeks following birth. In diagnosis, a careful distinction is considered for culturally appropriate behaviors, such as religious beliefs and activities. It is believed to be connected to or synonymous with a variety of culture-specific phenomena such as latah, koro, and amok.

There are three forms of brief psychotic disorder:

1. Brief psychotic disorder with a stressor, such as a trauma or death in the family.

2. Brief psychotic disorder without a stressor, there is no obvious stressor.

3. Brief psychotic disorder with postpartum onset. Usually occurs about four weeks after giving birth.

Hyperreligiosity may be associated with epilepsy — in particular temporal lobe epilepsy involving complex partial seizures — mania, frontotemporal lobar degeneration, Anti-NMDA receptor encephalitis, hallucinogen related psychsis and psychotic disorder. In persons with epilepsy episodic hyperreligosity may occur ictally or postictally, but is usually a chronic personality feature that occurs interictally. Hyperrelgiosity was associated in one small study with decreased right hippocampal volume. The medial prefrontal cortex may play a role in controlling religiousness, and dysfunction may lead to hyperreligiosity. Increased activity in the left temporal regions of hyperreligiosity in psychotic disorders. Pharmacological evidence points towards dysfunction in the ventral dopaminergic pathway.

A psychotic break occurs when a person experiences an episode of acute primary psychosis, generally for the first time, though it may also be after a significant symptom-free period.

Psychotic symptoms tend to develop after an individual has already had several episodes of depression without psychosis. However, once psychotic symptoms have emerged, they tend to reappear with each future depressive episode. The prognosis for psychotic depression is not considered to be as poor as for schizoaffective disorders or primary psychotic disorders. Still, those who have experienced a depressive episode with psychotic features have an increased risk of relapse and suicide compared to those without psychotic features, and they tend to have more pronounced sleep abnormalities.

The families of those who have experienced psychotic depression are at increased risk for both psychotic depression and schizophrenia.

Most patients with psychotic depression report having an initial episode between the ages of 20 and 40. Over a lifetime, it appears that patients with psychotic depression experience an average of 4 to 9 episodes. As with other depressive episodes, psychotic depression tends to be episodic, with symptoms lasting for a certain amount of time and then subsiding. While psychotic depression can be chronic (lasting more than 2 years), most depressive episodes last less than 24 months. Unlike psychotic disorders such as schizophrenia and schizoaffective disorder, patients with psychotic depression generally function well between episodes, both socially and professionally.