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.

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.

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 %.

The exact cause of the disorder remains unknown, and relatively few studies have focused exclusively on the etiology of schizophreniform disorder. Like other psychotic disorders, a diathesis–stress model has been proposed, suggesting that some individuals have an underlying multifactorial genetic vulnerability to the disorder that can be triggered by certain environmental factors. Schizophreniform disorder is more likely to occur in people with family members who have schizophrenia or bipolar disorder.

Studies suggest that the prevalence of paraphrenia in the elderly population is around 2-4%.

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.

Schizophreniform disorder is equally prevalent among men and women. The most common ages of onset are 18–24 for men and 18–35 for women. While the symptoms of schizophrenia often develop gradually over a period of years, the diagnostic criteria for schizophreniform disorder require a much more rapid onset.

Available evidence suggests variations in incidence across sociocultural settings. In the United States and other developed countries, the incidence is low, possibly fivefold less than that of schizophrenia. In developing countries, the incidence is substantially higher, especially for the subtype "With Good Prognostic Features". In some of these settings schizophreniform disorder may be as common as schizophrenia.

According to the Mayo Clinic, it is best to start receiving treatment for paranoid schizophrenia as early as possible and to maintain the treatment throughout life. Continuing treatment will help keep the serious symptoms under control and allow the person to lead a more fulfilling life. This illness is typically unpreventable.

It has a strong hereditary component with a first degree parent or sibling. There is some possibility that there are environmental influences including "prenatal exposure to a viral infection, low oxygen levels during birth (from prolonged labor or premature birth), exposure to a virus during infancy, early parental loss or separation, and verbal, physical or sexual abuse in childhood". Eliminating any of these factors could help reduce an individual's future risk of developing paranoid schizophrenia.

A combination of genetic and environmental factors are believed to play a role in the development of schizoaffective disorder.

Viewed broadly then, biological and environmental factors interact with a person's genes in ways which may increase or decrease the risk for developing schizoaffective disorder; exactly how this happens (the biological mechanism) is not yet known. Schizophrenia spectrum disorders, of which schizoaffective disorder is a part, have been increasingly linked to advanced paternal age at the time of conception, a known cause of genetic mutations. The physiology of people diagnosed with schizoaffective disorder appears to be similar, but not identical, to that of those diagnosed with schizophrenia and bipolar disorder; however, human neurophysiological function in normal brain and mental disorder syndromes is not fully understood.

While paraphrenia can occur in both men and women, it is more common in women, even after the difference has been adjusted for life expectancies. The ratio of women with paraphrenia to men with paraphrenia is anywhere from 3:1 to 45:2

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.

Various psychoactive substances (both legal and illegal) have been implicated in causing, exacerbating, or precipitating psychotic states or disorders in users, with varying levels of evidence. This may be upon intoxication, for a more prolonged period after use, or upon withdrawal. Individuals who have a substance induced psychosis tend to have a greater awareness of their psychosis and tend to have higher levels of suicidal thinking compared to individuals who have a primary psychotic illness. Drugs commonly alleged to induce psychotic symptoms include alcohol, cannabis, cocaine, amphetamines, cathinones, psychedelic drugs (such as LSD and psilocybin), κ-opioid receptor agonists (such as enadoline and salvinorin A) and NMDA receptor antagonists (such as phencyclidine and ketamine).

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.

Those suffering from post-schizophrenic depression are also commonly at risk for suicidal tendencies. There is a trend correlated between suicide and post-schizophrenic depression according to Mulholland and Cooper's research in "The Symptoms of Depression in Schizophrenia and its Management." Furthermore, depression and schizophrenia have both been studied individually to try to determine if there is a correlation, and research has indicated that there is a very strong tendency for people with depression or schizophrenia to attempt suicide. Statistically, out of all patients suffering from schizophrenia, "10%...commit suicide. Depressed patients with schizophrenia are at a particularly high risk for suicide the first few months after diagnosis and after hospital discharge." Risk factors increasing the chance of suicide are, from highest to lowest, previous depressive orders, previous suicide attempts, drug abuse, and several other factors. Surprisingly, the suicide risk actually decreased with the presence of hallucinations. "The ICD-10 Classification of MEntal and Behavioural Disorders" officially recognizes suicide as being a prominent aspect of post-schizophrenic depression. Because of this drastic increase in suicide, it can be difficult to study post-schizophrenic depression as many of its victims tragically take their own lives.

There is no clear cause to how certain patients with schizophrenia develop post-schizophrenic depression while others may surpass this stage. However, there are a few theories as to possible causes. Those suffering from post-schizophrenic depression often suffer from social isolation due to their illness, which may increase depression levels. There is strong evidence of stigma-related isolation against those suffering from mental illnesses in a variety of societies, especially those with schizophrenia as they are often viewed as dangerous and unpredictable. Because of this isolation and studies linking social isolation and depression, it is possible that patients under these stigmas eventually develop post-schizophrenic depression. Depression in patients with schizophrenia may also be caused by substance abuse, which is fairly common among those suffering from schizophrenia, as depressants such as alcohol and cannabis can relax the patient. Furthermore, with what little information is currently known about post-schizophrenic depression, the onset may be caused by not giving patients with schizophrenia antipsychotic medications. After being taken off of antipsychotic medication, schizophrenic patients' antidepressant medication had to be increased, while those under antipsychotic medication reported suffering fewer depressive symptoms, further giving reason to believe that a lack of antipsychotic medication in earlier stages of schizophrenia may lead to post-schizophrenic depression. However, some psychology professionals still push for the reduction of neuroleptic drugs, as there is a popular belief that post-schizophrenic depression is caused by neuroleptic treatment. Therapists are also believed to engage the depression in people with schizophrenia, having given too much psychotherapy after the patient had overcome their schizophrenic symptoms. Schizophrenia itself should not be overlooked as a key player in causing post-schizophrenic depression, though. A study done over a two-year time period shadowing patients with schizophrenia and monitoring their depression was unable to locate possible triggers such as the ones previously listed, so it is possible the nature of schizophrenia itself is the primary cause of post-schizophrenic depression.

Paranoid schizophrenia is an illness that typically requires lifelong treatment with neuroleptics to allow someone to have a relatively stable and normal lifestyle. In order to be successfully treated, a person with schizophrenia should seek help from family or primary care doctors, psychiatrists, psychotherapists, pharmacists, family members, case workers, psychiatric nurses, or social workers, provided he or she is not unable to do so, due to many people with schizophrenia having the inability to accept their condition. Non-compliance with neuroleptics may also occur if the patient considers the side effects (such as extrapyramidal symptoms) to be more debilitating than the condition itself. The main options that are offered for the treatment of paranoid schizophrenia are the following: neuroleptics, psychotherapy, hospitalization, electroconvulsive therapy, and vocational skills training.

There are many different types of disorders that have similar symptoms to paranoid schizophrenia. There are tests that psychiatrists perform to achieve a correct diagnosis. They include "psychiatric evaluation, in which the doctor or psychiatrist will ask a series of questions about the patient's symptoms, psychiatric history, and family history of mental health problems; medical history and exam, in which the doctor will ask about one's personal and family health history and will also perform a complete physical examination to check for medical issues that could be causing or contributing to the problem; laboratory tests in which the doctor will order simple blood and urine tests can rule out other medical causes of symptoms".

There are side effects associated with antipsychotic medication. Neuroleptics can cause high blood pressure and high cholesterol. Many people who take them exhibit weight gain and have a higher risk of developing diabetes.

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 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.

Neuroleptic-induced deficit syndrome (NIDS) is a psychopathological syndrome that develops in some patients who take high doses of an antipsychotic for an extended time. It is most often caused by high-potency typical antipsychotics, but can also be caused by high doses of many atypicals, especially those closer in profile to typical ones (that have higher D dopamine receptor affinity and relatively low 5-HT serotonin receptor binding affinity), like risperidone and amisulpride.

It has possibly the earliest onset compared to all other schizophrenias, considered to begin in some within childhood. Symptoms of "schizophrenia" "simplex" include an absence of will, impoverished thinking and flattening of affect. There is a gradual deterioration of functioning with increased amotivation and reduced socialization. It is considered to be rarely diagnosed and is a schizophrenia without psychotic symptoms.

In a study of patients in a Massachusetts hospital, persons suffering with "simple schizophrenia" were found to make attempts at reality fulfillment with respect to the more primitive needs; tending toward the achievement of fulfillment of these needs rather than engaging in fantasy as is typically found as a reaction to environmental stimuli by the psychotic person.

In psychiatry, thought broadcasting is the belief that others can hear or are aware of an individual's thoughts. This differs from telepathy in that the thoughts being broadcast are thought to be available to anybody.

Thought broadcasting can be a positive symptom of schizophrenia. Thought broadcasting has been suggested as one of the first rank symptoms (Schneider's first-rank symptoms) believed to distinguish schizophrenia from other psychotic disorders.

In mild manifestations, a person with this thought disorder may doubt their perception of thought broadcasting. When thought broadcasting occurs on a regular basis, the disorder can affect behavior and interfere with the person's ability to function in society. According to an individual's personality this is considered to be a severe manifestation of thought broadcasting that is usually indicative of schizophrenia.

Simple-type schizophrenia is a sub-type of schizophrenia as defined in the International Classification of Diseases . It is not included in the current "Diagnostic and Statistical Manual of Mental Disorders" (DSM-5). Simple-type schizophrenia is characterized by negative ("deficit") symptoms, such as avolition, apathy, anhedonia, reduced affect display, lack of initiative, lack of motivation, low activity; with absence of hallucinations or delusions of any kind.

Disorganized schizophrenia, also known as hebephrenia or hebephrenic schizophrenia, is a subtype of schizophrenia, although it is not recognized in the latest version of the "Diagnostic and Statistical Manual of Mental Disorders". It's recognized only in the 10th revision of the International Statistical Classification of Diseases and Related Health Problems (ICD-10).

Disorganized schizophrenia is thought to be an extreme expression of the "disorganization syndrome" that has been hypothesized to be one aspect of a three-factor model of symptoms in schizophrenia, the other factors being "reality distortion" (involving delusions and hallucinations) and "psychomotor poverty" (lack of speech, lack of spontaneous movement and various aspects of blunting of emotion).

Tardive psychosis is a term for a hypothetical form of psychosis, proposed in 1978. It was defined as a condition caused by long term use of neuroleptics, noticeable when the medication had become decreasingly effective, requiring higher doses, or when not responding to higher doses.

Evaluation suggests that tardive psychosis as a whole is a combination of "several different and not necessarily correlated phenomena related to neuroleptic treatment of schizophrenia."

Some articles equate tardive psychosis to supersensitivity psychosis. However, descriptions of symptoms of the latter do not match the former. Specific supersensitivity psychosis articles only address psychotic episodes in the wake of psychotic medication withdrawal associated with Clozapine. They do not mention medication resistance, which is the cornerstone of tardive psychosis theory.

A hypothetical condition related to tardive psychosis, tardive dysmentia, has also been questioned.