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.

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.

Risk factors for mental illness include genetic inheritance, such as parents having depression, or a propensity for high neuroticism or "emotional instability".

In depression, parenting risk factors include parental unequal treatment, and there is association with high cannabis use.

In schizophrenia and psychosis, risk factors include migration and discrimination, childhood trauma, bereavement or separation in families, and abuse of drugs, including cannabis, and urbanicity.

In anxiety, risk factors may include family history (e.g. of anxiety), temperament and attitudes (e.g. pessimism), and parenting factors including parental rejection, lack of parental warmth, high hostility, harsh discipline, high maternal negative affect, anxious childrearing, modelling of dysfunctional and drug-abusing behaviour, and child abuse (emotional, physical and sexual).

Environmental events surrounding pregnancy and birth have also been implicated. Traumatic brain injury may increase the risk of developing certain mental disorders. There have been some tentative inconsistent links found to certain viral infections, to substance misuse, and to general physical health.

Social influences have been found to be important, including abuse, neglect, bullying, social stress, traumatic events and other negative or overwhelming life experiences. For bipolar disorder, stress (such as childhood adversity) is not a specific cause, but does place genetically and biologically vulnerable individuals at risk for a more severe course of illness. The specific risks and pathways to particular disorders are less clear, however. Aspects of the wider community have also been implicated, including employment problems, socioeconomic inequality, lack of social cohesion, problems linked to migration, and features of particular societies and cultures.

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.

Another theory is that there may be shared risk factors that can lead to both substance abuse and mental illness. Mueser hypothesizes that these may include factors such as social isolation, poverty, lack of structured daily activity, lack of adult role responsibility, living in areas with high drug availability, and association with people who already misuse drugs.

Other evidence suggests that traumatic life events, such as sexual abuse, are associated with the development of psychiatric problems and substance abuse.

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.

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.

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.

Correlations of mental disorders with drug use include cannabis, alcohol and caffeine, use of which appears to promote anxiety. For psychosis and schizophrenia, usage of a number of drugs has been associated with development of the disorder, including cannabis, cocaine, and amphetamines. There has been debate regarding the relationship between usage of cannabis and bipolar disorder.

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.

The alleviation of dysphoria theory suggests that people with severe mental illness commonly have a negative self-image, which makes them vulnerable to using psychoactive substances to alleviate these feelings. Despite the existence of a wide range of dysphoric feelings (anxiety, depression, boredom, and loneliness), the literature on self-reported reasons for use seems to lend support for the experience of these feelings being the primary motivator for drug and alcohol misuse.

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.

Premorbidity refers to the state of functionality prior to the onset of a disease or illness. It is most often used in relation to psychological function (e.g. premorbid personality or premorbid intelligence), but can also be used in relation to other medical conditions (e.g. premorbid lung function or premorbid heart rate).

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.

Major Depression is a mental disorder characterized by an all-encompassing low mood accompanied by low self-esteem, and loss of interest or pleasure in normally enjoyable activities.Nearly 5 million of the 31 million Americans who are 65 years or older are clinically depressed, and 1 million have major depression. Approximately 3 percent of healthy elderly persons living in the community have major depression. Recurrence may be as high as 40 percent. Suicide rates are nearly twice as high in depressed patients as in the general population. Major depression is more common in medically ill patients who are older than 70 years and hospitalized or institutionalized. Severe or chronic diseases associated with high rates of depression include stroke (30 to 60 percent), coronary heart disease (8 to 44 percent), cancer (1 to 40 percent), Parkinson's disease (40 percent), Alzheimer's disease (20 to 40 percent), and dementia (17 to 31 percent).

Minor depression is a clinically significant depressive disorder that does not fulfill the duration criterion or the number of symptoms necessary for the diagnosis of major depression. Minor depression, which is more common than major depression in elderly patients, may follow a major depressive episode. It also can be a reaction to routine stressors in older populations. Fifteen to 50 percent of patients with minor depression develop major depression within two years.

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.

The causes of PTSD are: Natural or human disasters, war, serious accident, witness of violent death of others, violent attack, being the victim of sexual abuse, rape, torture, terrorism or hostage taking.

Predisposing factors

The predisposing factors are: Personality traits and Previous history of Psychiatric illness.

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.

Delusional disorders are uncommon in psychiatric practice, though this may be an underestimation due to the fact that those afflicted lack insight and thus avoid psychiatric assessment. The prevalence of this condition stands at about 24 to 30 cases per 100,000 people while 0.7 to 3.0 new cases per 100,000 people are reported every year. Delusional disorder accounts for 1–2% of admissions to inpatient mental health facilities. The incidence of first admissions for delusional disorder is lower, from 0.001–0.003%.

Delusional disorder tends to appear in middle to late adult life, and for the most part first admissions to hospital for delusional disorder occur between age 33 and 55. It is more common in women than men, and immigrants seem to be at higher risk.

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.

Underlying causes may include:

- Han (a Korean culture-related depressive sentiment related to hard life and social unfairness resulting not only from a tragic collective national history, but also from personal traumas)

- prior instances of major depressive disorder

- prior instances of anxiety disorder

- prior instances of adjustment disorder

- prior instances of other somatoform disorders

- repression of feelings of anger/resentment arising from past events

Triggering causes are typically external events, including:

- familial stressors, e.g. spousal infidelity or conflict with in-laws

- witnessing acts/actions/phenomena that conflict with one's own moral and/or ethical principles

The syndrome itself is believed to be the result of the continued repression of feelings of anger without addressing their source. In holistic medicine the containment of anger in hwabyung disturbs the balance of the five bodily elements, resulting in the development of psychosomatic symptoms such as panic, insomnia, and depression after a long period of repressed feelings.

It is possible that hormonal imbalances such as those around the time of menopause may also be an underlying cause of hwabyung in middle-aged women, the most often-diagnosed demographic.

The terms "nervous breakdown" and "mental breakdown" have not been formally defined through a medical diagnostic system such as the DSM-5 or ICD-10, and are nearly absent from current scientific literature regarding mental illness. Although "nervous breakdown" is not rigorously defined, surveys of laypersons suggest that the term refers to a specific acute time-limited reactive disorder, involving symptoms such as anxiety or depression, usually precipitated by external stressors. Many health experts today refer to a nervous breakdown as a "modern mental health crisis."

Specific cases are sometimes described as a "breakdown" only after the emotional and physical demands on a person's life are so great as to prevent him or her from performing activities of daily living or, less strictly, only when those demands prevent him/her from performing his/her familial or occupational duties.

Nervous breakdowns are often caused by serious ongoing mental health disorders.

Disorders that cause injury or damage to the brain and contribute to OBS include, but are not limited to:

- Alcoholism

- Alzheimer's Disease

- Attention deficit/hyperactivity disorder

- Autism

- Concussion

- Encephalitis

- Epilepsy

- Fetal alcohol syndrome

- Hypoxia

- Parkinson's disease

- Intoxication/overdose caused by drug abuse including alcoholism

- Sedative hypnotic dependence and drug abuse

- Intracranial hemorrhage/trauma

- Korsakoff Syndrome

- Mastocytosis

- Meningitis

- Psychoorganic syndrome

- Stroke/transient ischemic attack (TIA)

- Withdrawal from drugs, especially sedative hypnotics, e.g. alcohol or benzodiazepines

Other conditions that may be related to organic brain syndrome include: clinical depression, neuroses, and psychoses, which may occur simultaneously with the OBS.