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.

According to a substantial amount of epidemiology studies conducted, women are twice as likely to develop certain mood disorders, such as major depression. Although there is an equal number of men and women diagnosed with bipolar II disorder, women have a slightly higher frequency of the disorder.

In 2011, mood disorders were the most common reason for hospitalization among children aged 1–17 years in the United States, with approximately 112,000 stays. Mood disorders were top principal diagnosis for Medicaid super-utilizers in the United States in 2012. Further, a study of 18 States found that mood disorders accounted for the highest number of hospital readmissions among Medicaid patients and the uninsured, with 41,600 Medicaid patients and 12,200 uninsured patients being readmitted within 30 days of their index stay—a readmission rate of 19.8 per 100 admissions and 12.7 per 100 admissions, respectively. In 2012, mood and other behavioral health disorders were the most common diagnoses for Medicaid-covered and uninsured hospital stays in the United States (6.1% of Medicaid stays and 5.2% of uninsured stays).

A study conducted in 1988 to 1994 amongst young American adults involved a selection of demographic and health characteristics. A population-based sample of 8,602 men and women ages 17–39 years participated. Lifetime prevalence were estimated based on six mood measures:

1. major depressive episode (MDE) 8.6%,

2. major depressive disorder with severity (MDE-s) 7.7%,

3. dysthymia 6.2%,

4. MDE-s with dysthymia 3.4%,

5. any bipolar disorder 1.6%, and

6. any mood disorder 11.5%.

The exact cause of cyclothymia is unknown. It is known that major depression, bipolar disorder, and cyclothymia often occur together within families. There may be a genetic component to cyclothymia: In one study, it was found that an individual is 2–3 times more likely to have the disorder if an identical twin is affected.

It is also believed that a person suffering with PTSD may experience similar shifts in mood based on how many flashbacks they've been dealing with.

Depressed mood can be the result of a number of infectious diseases, nutritional deficiencies, neurological conditions and physiological problems, including hypoandrogenism (in men), Addison's disease, Cushing's syndrome, hypothyroidism, Lyme disease, multiple sclerosis, Parkinson's disease, chronic pain, stroke, diabetes, and cancer.

Meta-analyses show that high scores on the personality domain neuroticism is a strong predictor for the development of mood disorders. A number of authors have also suggested that mood disorders are an evolutionary adaptation. A low or depressed mood can increase an individual's ability to cope with situations in which the effort to pursue a major goal could result in danger, loss, or wasted effort. In such situations, low motivation may give an advantage by inhibiting certain actions. This theory helps to explain why negative life incidents precede depression in around 80 percent of cases, and why they so often strike people during their peak reproductive years. These characteristics would be difficult to understand if depression were a dysfunction.

A depressed mood is a predictable response to certain types of life occurrences, such as loss of status, divorce, or death of a child or spouse. These are events that signal a loss of reproductive ability or potential, or that did so in humans' ancestral environment. A depressed mood can be seen as an adaptive response, in the sense that it causes an individual to turn away from the earlier (and reproductively unsuccessful) modes of behavior.

A depressed mood is common during illnesses, such as influenza. It has been argued that this is an evolved mechanism that assists the individual in recovering by limiting his/her physical activity. The occurrence of low-level depression during the winter months, or seasonal affective disorder, may have been adaptive in the past, by limiting physical activity at times when food was scarce. It is argued that humans have retained the instinct to experience low mood during the winter months, even if the availability of food is no longer determined by the weather.

Much of what we know about the genetic influence of clinical depression is based upon research that has been done with identical twins. Identical twins both have exactly the same genetic code. It has been found that when one identical twin becomes depressed the other will also develop clinical depression approximately 76% of the time. When identical twins are raised apart from each other, they will both become depressed about 67% of the time. Because both twins become depressed at such a high rate, the implication is that there is a strong genetic influence. If it happened that when one twin becomes clinically depressed the other always develops depression, then clinical depression would likely be entirely genetic.

Bipolar disorder is also considered a mood disorder. In the case of bipolar disorder several causes have been considered as possible, please see the wikipedia page Bipolar disorder for more details on the most common attributed causes. Recently, apart of the recent knowledge, it is hypothesized and there is evidence that bipolar disorder might be caused by mitochondrial dysfunction or mitochondrial disease.

Studies have shown that those who fall into minorities due to either their gender identity or sexual orientation (such as those that identify as LGBT), are more prone to depression.

There are no known biological causes that apply consistently to all cases of dysthymia, which suggests diverse origin of the disorder. However, there are some indications that there is a genetic predisposition to dysthymia: "The rate of depression in the families of people with dysthymia is as high as fifty percent for the early-onset form of the disorder". Other factors linked with dysthymia include stress, social isolation, and lack of social support.

In a study using identical and fraternal twins, results indicated that there is a stronger likelihood of identical twins both having depression than fraternal twins. This provides support for the idea that dysthymia is in part caused by heredity.

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.

Winter depression is a common slump in the mood of some inhabitants of most of the Nordic countries. It was first described by the 6th century Goth scholar Jordanes in his "Getica" wherein he described the inhabitants of Scandza (Scandinavia). Iceland, however, seems to be an exception. A study of more than 2000 people there found the prevalence of seasonal affective disorder and seasonal changes in anxiety and depression to be unexpectedly "low" in both sexes. The study's authors suggested that propensity for SAD may differ due to some genetic factor within the Icelandic population. A study of Canadians of wholly Icelandic descent also showed low levels of SAD. It has more recently been suggested that this may be attributed to the large amount of fish traditionally eaten by Icelandic people, in 2007 about 90 kilograms per person per year as opposed to about 24 kg in the US and Canada, rather than to genetic predisposition; a similar anomaly is noted in Japan, where annual fish consumption in recent years averages about 60 kg per capita. Fish are high in vitamin D. Fish also contain docosahexaenoic acid (DHA), which help with a variety of neurological dysfunctions.

Cyclothymia (), also called cyclothymic disorder, is a type of chronic mood disorder widely considered to be a more chronic but milder or subthreshold form of bipolar disorder. Cyclothymia is characterized by numerous mood swings, with periods of hypomanic symptoms that do not meet criteria for a manic episode, alternating with periods of mild or moderate symptoms of depression that do not meet criteria for a major depressive episode.

An individual with cyclothymia may feel stable at a baseline level but experience a noticeable shift to an emotional high during subthreshold hypomanic episodes of elation or euphoria, with symptoms similar to those of mania but less severe, and often cycle to emotional lows with moderate depressive symptoms. To meet the diagnostic criteria for cyclothymia, a person must experience this alternating pattern of emotional highs and lows for a period of at least two years with no more than two consecutive symptom-free months. For children and adolescents, the duration must be at least one year.

The diagnosis of cyclothymia is rare compared to other mood disorders. Diagnosis of cyclothymia entails the absence of any major depressive episode, manic episode or mixed episode, which would qualify the individual for diagnosis of other mood disorders. When a major episode manifests after an initial diagnosis of cyclothymia, the individual may qualify for a diagnosis of bipolar I or bipolar II disorder. Although estimates vary greatly, 15–50% of cases of cyclothymia later advance to the diagnostic criteria for bipolar I and/or bipolar II disorder (with cyclothymic features). Although the emotional highs and lows of cyclothymia are less extreme than those of bipolar disorder and generally do not cause the same conditions, the symptomatology, longitudinal course, family history and treatment response of cyclothymia are consistent with bipolar spectrum.

Lifetime prevalence of cyclothymic disorder is 0.4–1%. Frequency appears similar in men and women, though women more often seek treatment. People with cyclothymia during periodic hypomania (euphoria) tend to feel an inflated self-worth, self-confidence and elation, often with rapid speech, racing thoughts, not much need to sleep, increased aggression and impulsive behavior, showing little regard for consequences of decisions—but may sometimes be somewhat, fully or hyper-productive for a period of several days at a time.

In many species, activity is diminished during the winter months in response to the reduction in available food, the reduction of sunlight (especially for diurnal animals) and the difficulties of surviving in cold weather. Hibernation is an extreme example, but even species that do not hibernate often exhibit changes in behavior during the winter. Presumably, food was scarce during most of human prehistory, and a tendency toward low mood during the winter months would have been adaptive by reducing the need for calorie intake. The preponderance of women with SAD suggests that the response may also somehow regulate reproduction.

Various proximate causes have been proposed. One possibility is that SAD is related to a lack of serotonin, and serotonin polymorphisms could play a role in SAD, although this has been disputed. Mice incapable of turning serotonin into N-acetylserotonin (by serotonin N-acetyltransferase) appear to express "depression-like" behavior, and antidepressants such as fluoxetine increase the amount of the enzyme serotonin N-acetyltransferase, resulting in an antidepressant-like effect. Another theory is that the cause may be related to melatonin which is produced in dim light and darkness by the pineal gland, since there are direct connections, via the retinohypothalamic tract and the suprachiasmatic nucleus, between the retina and the pineal gland. Melatonin secretion is controlled by the endogenous circadian clock, but can also be suppressed by bright light.

One study looked at whether some people could be predisposed to SAD based on personality traits. Correlations between certain personality traits, higher levels of neuroticism, agreeableness, openness, and an avoidance-oriented coping style, appeared to be common in those with SAD.

Globally dysthymia occurs in about 105 million people a year (1.5% of the population). It is slightly more common in women (1.8%) than in men (1.3%). The lifetime prevalence rate of dysthymia in community settings appears to range from 3 to 6% in the United States. However, in primary care settings the rate is higher ranging from 5 to 15 percent. United States prevalence rates tend to be somewhat higher than rates in other countries.

Depressive personality disorder (also known as melancholic personality disorder) is a controversial psychiatric diagnosis that denotes a personality disorder with depressive features.

Originally included in the American Psychiatric Association's DSM-II, depressive personality disorder was removed from the DSM-III and DSM-III-R. Recently, it has been reconsidered for reinstatement as a diagnosis. Depressive personality disorder is currently described in Appendix B in the DSM-IV-TR as worthy of further study. Although no longer listed as a personality disorder, the diagnosis is included under the section “personality disorder not otherwise specified”.

While depressive personality disorder shares some similarities with mood disorders such as dysthymia, it also shares many similarities with personality disorders including avoidant personality disorder. Some researchers argue that depressive personality disorder is sufficiently distinct from these other conditions so as to warrant a separate diagnosis.

Socioeconomic status has also been looked at as a potential cause for personality disorders. There is a strong association with low parental/neighborhood socioeconomic status and personality disorder symptoms. In a recent study comparing parental socioeconomic status and a child's personality, it was seen that children who were from higher socioeconomic backgrounds were more altuistic, less risk seeking, and had overall higher IQs. These traits correlate with a low risk of developing personality disorders later on in life. In a study looking at female children who were detained for disciplinary actions found that psychological problems were most negatively associated with socioeconomic problems. Furthermore, social disorganization was found to be inversely correlated with personality disorder symptoms.

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 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.

Individual differences in women's estrogen cycles may be related to the expression of BPD symptoms in female patients. A 2003 study found that women's BPD symptoms were predicted by changes in estrogen levels throughout their menstrual cycles, an effect that remained significant when the results were controlled for a general increase in negative affect.

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.

Child abuse and neglect consistently show up as risk factors to the development of personality disorders in adulthood. A study looked at retrospective reports of abuse of participants that had demonstrated psychopathology throughout their life and were later found to have past experience with abuse. In a study of 793 mothers and children, researchers asked mothers if they had screamed at their children, and told them that they did not love them or threatened to send them away. Children who had experienced such verbal abuse were three times as likely as other children (who did not experience such verbal abuse) to have borderline, narcissistic, obsessive-compulsive or paranoid personality disorders in adulthood. The sexually abused group demonstrated the most consistently elevated patterns of psychopathology. Officially verified physical abuse showed an extremely strong correlation with the development of antisocial and impulsive behavior. On the other hand, cases of abuse of the neglectful type that created childhood pathology were found to be subject to partial remission in adulthood.

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.

Reported prevalence of STPD in community studies ranges from 0.6% in a Norwegian sample, to 4.6% in an American sample. A large American study found a lifetime prevalence of 3.9%, with somewhat higher rates among men (4.2%) than women (3.7%). It may be uncommon in clinical populations, with reported rates of 0% to 1.9%.

Together with other Cluster A personality disorders, it is also very common among homeless people.

A University of Colorado Colorado Springs study comparing personality disorders and Myers-Briggs Type Indicator types found that the disorder had a significant correlation with the Introverted (I), Intuitive (N), Thinking (T), and Perceiving (P) preferences.

Genetic

Schizotypal personality disorder is widely understood to be a "schizophrenia spectrum" disorder. Rates of schizotypal personality disorder are much higher in relatives of individuals with schizophrenia than in the relatives of people with other mental illnesses or in people without mentally ill relatives. Technically speaking, schizotypal personality disorder may also be considered an "extended phenotype" that helps geneticists track the familial or genetic transmission of the genes that are implicated in schizophrenia. But there is also a genetic connection of STPD to mood disorders and depression in particular.

Social and environmental

There is now evidence to suggest that parenting styles, early separation, trauma/maltreatment history (especially early childhood neglect) can lead to the development of schizotypal traits. Neglect or abuse, trauma, or family dysfunction during childhood may increase the risk of developing schizotypal personality disorder. Over time, children learn to interpret social cues and respond appropriately but for unknown reasons this process does not work well for people with this disorder.

Schizotypal personality disorders are characterized by a common attentional impairment in various degrees that could serve as a marker of biological susceptibility to STPD. The reason is that an individual who has difficulties taking in information may find it difficult in complicated social situations where interpersonal cues and attentive communications are essential for quality interaction. This might eventually cause the individual to withdraw from most social interactions, thus leading to asociality.

In general, atypical depression tends to cause greater functional impairment than other forms of depression. Atypical depression is a chronic syndrome that tends to begin earlier in life than other forms of depression—usually beginning in the teenage years. Similarly, patients with atypical depression are more likely to suffer from personality disorders and anxiety disorders such as borderline personality disorder, avoidant personality disorder, generalized anxiety disorder, obsessive-compulsive disorder, and bipolar disorder.

Recent research suggests that young people are more likely to suffer from hypersomnia while older people are more likely to suffer from polyphagia.

Medication response differs between chronic atypical depression and acute melancholic depression. Some studies suggest that the older class of antidepressants, monoamine oxidase inhibitors (MAOIs), may be more effective at treating atypical depression. While the more modern SSRIs and SNRIs are usually quite effective in this illness, the tricyclic antidepressants typically are not. The wakefulness-promoting agent modafinil has shown considerable effect in combating atypical depression, maintaining this effect even after discontinuation of treatment. Antidepressant response can often be enhanced with supplemental medications, such as buspirone, bupropion, or aripiprazole. Psychotherapy, whether alone or in combination with medication, is also an effective treatment.

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