Several studies have shown that the risk of suicide is higher in patients who suffer from Bipolar II than those who suffer from Bipolar I, and especially higher than patients who suffer from major depressive disorder.

In results of a summary of several lifetime study experiments, it was found that 24% of Bipolar II patients experienced suicidal ideation or suicide attempts compared to 17% in Bipolar I patients and 12% in major depressive patients. Bipolar disorders, in general, are the third leading cause of death in 15- to 24-year-olds. Bipolar II patients were also found to employ more lethal means and have more complete suicides overall.

Bipolar II patients have several risk factors that increase their risk of suicide. The illness is very recurrent and results in severe disabilities, interpersonal relationship problems, barriers to academic, financial, and vocational goals, and a loss of social standing in their community, all of which increase the likelihood of suicide. Mixed symptoms and rapid-cycling, both very common in Bipolar II, are also associated with an increased risk of suicide. The tendency for Bipolar II to be misdiagnosed and treated ineffectively, or not at all in some cases, leads to an increased risk.

As a result of the high suicide risk for this group, reducing the risk and preventing attempts remains a main part of the treatment; a combination of self-monitoring, close supervision by a therapist, and faithful adherence to their medication regimen will help to reduce the risk and prevent the likelihood of a completed suicide.

Comorbid conditions are extremely common in individuals with BP-II. In fact, individuals are twice as likely to present a comorbid disorder than not. These include anxiety, eating, personality (cluster B), and substance use disorders. For bipolar II disorder, the most conservative estimate of lifetime prevalence of alcohol or other drug abuse disorders is 20%. In patients with comorbid substance abuse disorder and BP-II, episodes have a longer duration and treatment compliance decreases. Preliminary studies suggest that comorbid substance abuse is also linked to increased risk of suicidality.

Bipolar disorder can cause suicidal ideation that leads to suicidal attempts. Individuals whose bipolar disorder begins with a depressive or mixed affective episode seem to have a poorer prognosis and an increased risk of suicide. One out of two people with bipolar disorder attempt suicide at least once during their lifetime and many attempts are successfully completed. The annual average suicide rate is 0.4 percent, which is 10–20 times that of the general population. The standardized mortality ratio from suicide in bipolar disorder is between 18 and 25. The lifetime risk of suicide has been estimated to be as high as 20 percent in those with bipolar disorder.

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%.

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 causes of bipolar disorder likely vary between individuals and the exact mechanism underlying the disorder remains unclear. Genetic influences are believed to account for 60–80 percent of the risk of developing the disorder indicating a strong hereditary component. The overall heritability of the bipolar spectrum has been estimated at 0.71. Twin studies have been limited by relatively small sample sizes but have indicated a substantial genetic contribution, as well as environmental influence. For bipolar disorder type I, the rate at which identical twins (same genes) will both have bipolar disorder type I (concordance) is estimated at around 40 percent, compared to about 5 percent in fraternal twins. A combination of bipolar I, II, and cyclothymia similarly produced rates of 42 percent and 11 percent (identical and fraternal twins, respectively), with a relatively lower ratio for bipolar II that likely reflects heterogeneity. There is overlap with major (unipolar) depression and if this is also counted in the co-twin the concordance with bipolar disorder rises to 67 percent in identical twins and 19 percent in fraternal twins. The relatively low concordance between fraternal twins brought up together suggests that shared family environmental effects are limited, although the ability to detect them has been limited by small sample sizes.

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.

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.

The cause of major depressive disorder is unknown. The biopsychosocial model proposes that biological, psychological, and social factors all play a role in causing depression. The diathesis–stress model specifies that depression results when a preexisting vulnerability, or diathesis, is activated by stressful life events. The preexisting vulnerability can be either genetic, implying an interaction between nature and nurture, or schematic, resulting from views of the world learned in childhood.

Childhood abuse, either physical, sexual or psychological are all risk factors for depression, among other psychiatric issues that co-occur such as anxiety and drug abuse. Childhood trauma also correlates with severity of depression, lack of response to treatment and length of illness. However, some are more susceptible to developing mental illness such as depression after trauma, and various genes have been suggested to control susceptibility.

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.

The 5-HTTLPR, or serotonin transporter promoter gene's short allele has been associated with increased risk of depression. However, since the 1990s results have been inconsistent, with three recent reviews finding an effect and two finding none. Other genes that have been linked to a GxE interaction include CRHR1, FKBP5 and BDNF, the first two of which are related to the stress reaction of the HPA axis, and the latter of which is involved in neurogenesis.

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.

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.

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.

Information on the condition, importance of regular sleep patterns, routines and eating habits and the importance of compliance with medication as prescribed. Behavior modification through counseling can have positive influence to help reduce the effects of risky behavior during the manic phase. Additionally, the lifetime prevalence for bipolar I disorder is estimated to be 1%.

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.

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.

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.

The cause (etiology) of RBD is unknown, but recent findings may suggest a link between RBD and bipolar disorders, pointing to the importance of genetic factors. A small sub-group of patients with RBD has temporal lobe epilepsy.

There are a number of biological features that may distinguish psychotic depression from non-psychotic depression. The most significant difference may be the presence of an abnormality in the hypothalamic pituitary adrenal axis (HPA). The HPA axis appears to be dysregulated in psychotic depression, with dexamethasone suppression tests demonstrating higher levels of cortisol following dexamethasone administration (i.e. lower cortisol suppression). Those with psychotic depression also have higher ventricular-brain ratios than those with non-psychotic depression.

The lifetime prevalence of RBD has been estimated at 2.6 to 10.0%, and the one-year prevalence at 5.0-8.2%. The World Health Organization project on "Psychological problems in general health care", which was based on primary care samples, reported a one-year prevalence of 3.7 – 9.9%. However none of these studies differentiate between RBD with and without a history of other mood disorders (e.g. major depression). DSM-IV field trial estimated the life-time of RBD only to be about 2%.

While the causes of PPD are not understood, a number of factors have been suggested to increase the risk:

- Prenatal depression or anxiety

- A personal or family history of depression

- Moderate to severe premenstrual symptoms

- Maternity blues

- Birth-related psychological trauma

- Birth-related physical trauma

- Previous stillbirth or miscarriage

- Formula-feeding rather than breast-feeding

- Cigarette smoking

- Low self-esteem

- Childcare or life stress

- Low social support

- Poor marital relationship or single marital status

- Low socioeconomic status

- Infant temperament problems/colic

- Unplanned/unwanted pregnancy

- Elevated prolactin levels

- Oxytocin depletion

Of these risk factors, formula-feeding, a history of depression, and cigarette smoking have been shown to have additive effects.

These above factors are known to correlate with PPD. This correlation does not mean these factors are causal. Rather, they might both be caused by some third factor. Contrastingly, some factors almost certainly attribute to the cause of postpartum depression, such as lack of social support.

Not surprisingly, women with fewer resources indicate a higher level of postpartum depression and stress than those women with more resources, such as financial. Rates of PPD have been shown to decrease as income increases. Women with fewer resources may be more likely to have an unintended or unwanted pregnancy, increasing risk of PPD. Women with fewer resources may also include single mothers of low income. Single mothers of low income may have more limited access to resources while transitioning into motherhood.

Studies have also shown a correlation between a mother's race and postpartum depression. African American mothers have been shown to have the highest risk of PPD at 25%, while Asian mothers had the lowest at 11.5%, after controlling for social factors such as age, income, education, marital status, and baby's health. The PPD rates for First Nations, Caucasian and Hispanic women fell in between.

Sexual orientation has also been studied as a risk factor for PPD. In a 2007 study conducted by Ross and colleagues, lesbian and bisexual mothers were tested for PPD and then compared with a heterosexual sample group. It was found that lesbian and bisexual biological mothers had significantly higher Edinburgh Postnatal Depression Scale scores than did the heterosexual women in the sample. These higher rates of PPD in lesbian/bisexual mothers may reflect less social support, particularly from their families of origin and additional stress due to homophobic discrimination in society.

A correlation between postpartum thyroiditis and postpartum depression has been proposed but remains controversial. There may also be a link between postpartum depression and anti-thyroid antibodies.

Bipolar I disorder (BD-I; pronounced "type one bipolar disorder") is a bipolar spectrum disorder characterized by the occurrence of at least one manic or mixed episode. Most patients also, at other times, have one or more depressive episodes, and all experience a hypomanic stage before progressing to full mania.

It is a type of bipolar disorder, and conforms to the classic concept of manic-depressive illness, which can include psychosis during mood episodes. The difference with bipolar II disorder is that the latter requires that the individual must never have experienced a full manic or mixed-manic episode - only less severe hypomanic episode(s).

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.

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.