GAD runs in families and is six times more common in the children of someone with the condition.

While anxiety arose as an adaptation, in modern times it is almost always thought of negatively in the context of anxiety disorders. People with these disorders have highly sensitive systems; hence, their systems tend to overreact to seemingly harmless stimuli. Sometimes anxiety disorders occur in those who have had traumatic youths, demonstrating an increased prevalence of anxiety when it appears a child will have a difficult future. In these cases, the disorder arises as a way to predict that the individual’s environment will continue to pose threats.

Several studies aim to understand the long-term mental health consequences of SAD. SAD contributed to vulnerability and acted as a strong risk factor for developing other mental disorders in people aged 19–30. Specifically disorders including panic disorder and depressive disorders were more likely to occur. Other sources also support the increased likelihood of displaying either of the two psychopathologies with previous history of childhood SAD.

Discomfort from separations in children from ages 8 to 14 months is normal. Children oftentimes get nervous or afraid of unfamiliar people and places but if the behavior still occurs after the age of 6 and if it lasts longer than four weeks, the child might have Separation Anxiety Disorder.

About 4% of children have the disorder. Separation Anxiety Disorder is very treatable especially when caught early on with medication and behavioral therapies. Helping children with separation anxiety to identify the circumstances that elicit their anxiety (upcoming separation events) is important. A child's ability to tolerate separations should gradually increase over time when he or she is gradually exposed to the feared events. Encouraging a child with separation anxiety disorder to feel competent and empowered, as well as to discuss feelings associated with anxiety-provoking events promotes recovery.

Children with separation anxiety disorder often respond negatively to perceived anxiety in their caretakers, in that parents and caregivers who also have anxiety disorders may unwittingly confirm a child's unrealistic fears that something terrible may happen if they are separated from each other. Thus, it is critical that parents and caretakers become aware of their own feelings and communicate a sense of safety and confidence about separation.

At a low level, anxiety is not a bad thing. In fact, the hormonal response to anxiety has evolved as a benefit, as it helps humans react to dangers. Researchers in evolutionary medicine believe this adaptation allows humans to realize there is a potential threat and to act accordingly in order to ensure greatest possibility of protection. It has actually been shown that those with low levels of anxiety have a greater risk of death than those with average levels. This is because the absence of fear can lead to injury or death. Additionally, patients with both anxiety and depression were found to have lower morbidity than those with depression alone. The functional significance of the symptoms associated with anxiety includes: greater alertness, quicker preparation for action, and reduced probability of missing threats. In the wild, vulnerable individuals, for example those who are hurt or pregnant, have a lower threshold for anxiety response, making them more alert. This demonstrates a lengthy evolutionary history of the anxiety response.

It has been shown that there is a two to threefold greater risk of having social phobia if a first-degree relative also has the disorder. This could be due to genetics and/or due to children acquiring social fears and avoidance through processes of observational learning or parental psychosocial education. Studies of identical twins brought up (via adoption) in different families have indicated that, if one twin developed social anxiety disorder, then the other was between 30 percent and 50 percent more likely than average to also develop the disorder. To some extent this 'heritability' may not be specific – for example, studies have found that if a parent has any kind of anxiety disorder or clinical depression, then a child is somewhat more likely to develop an anxiety disorder or social phobia. Studies suggest that parents of those with social anxiety disorder tend to be more socially isolated themselves (Bruch and Heimberg, 1994; Caster et al., 1999), and shyness in adoptive parents is significantly correlated with shyness in adopted children (Daniels and Plomin, 1985).

Growing up with overprotective and hypercritical parents has also been associated with social anxiety disorder. Adolescents who were rated as having an insecure (anxious-ambivalent) attachment with their mother as infants were twice as likely to develop anxiety disorders by late adolescence, including social phobia.

A related line of research has investigated 'behavioural inhibition' in infants – early signs of an inhibited and introspective or fearful nature. Studies have shown that around 10–15 percent of individuals show this early temperament, which appears to be partly due to genetics. Some continue to show this trait into adolescence and adulthood, and appear to be more likely to develop social anxiety disorder.

Social anxiety disorder is known to appear at an early age in most cases. Fifty percent of those who develop this disorder have developed it by the age of 11, and 80% have developed it by age 20. This early age of onset may lead to people with social anxiety disorder being particularly vulnerable to depressive illnesses, drug abuse and other psychological conflicts.

When prevalence estimates were based on the examination of psychiatric clinic samples, social anxiety disorder was thought to be a relatively rare disorder. The opposite was found to be true; social anxiety was common, but many were afraid to seek psychiatric help, leading to an underrecognition of the problem.

The National Comorbidity Survey of over 8,000 American correspondents in 1994 revealed 12-month and lifetime prevalence rates of 7.9 percent and 13.3 percent, respectively; this makes it the third most prevalent psychiatric disorder after depression and alcohol dependence, and the most common of the anxiety disorders. According to U.S. epidemiological data from the National Institute of Mental Health, social phobia affects 15 million adult Americans in any given year. Estimates vary within 2 percent and 7 percent of the U.S. adult population.

The mean onset of social phobia is 10 to 13 years. Onset after age 25 is rare and is typically preceded by panic disorder or major depression. Social anxiety disorder occurs more often in females than males. The prevalence of social phobia appears to be increasing among white, married, and well-educated individuals. As a group, those with generalized social phobia are less likely to graduate from high school and are more likely to rely on government financial assistance or have poverty-level salaries. Surveys carried out in 2002 show the youth of England, Scotland, and Wales have a prevalence rate of 0.4 percent, 1.8 percent, and 0.6 percent, respectively. In Canada, the prevalence of self-reported social anxiety for Nova Scotians older than 14 years was 4.2 percent in June 2004 with women (4.6 percent) reporting more than men (3.8 percent). In Australia, social phobia is the 8th and 5th leading disease or illness for males and females between 15–24 years of age as of 2003. Because of the difficulty in separating social phobia from poor social skills or shyness, some studies have a large range of prevalence. The table also shows higher prevalence in Sweden.

According to research by RM Carney et al., any history of child depression influences the occurrence of adolescent cardiac risk factors, even if individuals no longer suffer from depression. They are much more likely to develop heart disease as adults.

According to research conducted by Laura P. Richardson et al., major depression occurred in 7% of the cohort during early adolescence (11, 13, and 15 years of age) and 27% during late adolescence (18 and 21 years of age). At 26 years of age, 12% of study members were obese. After adjusting for each individual's baseline body mass index (calculated as the weight in kilograms divided by the square of height in meters), depressed late adolescent girls were at a greater than 2-fold increased risk for obesity in adulthood compared with their non-depressed female peers (relative risk, 2.32; 95% confidence interval, 1.29-3.83). A dose-response relationship between the number of episodes of depression during adolescence, and risk for adult obesity was also observed in female subjects. The association was not observed for late adolescent boys or for early adolescent boys or girls.

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.

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.

The etiology of PMDD is still an active area of research. While the timing of symptoms suggests hormonal fluctuations as the cause of PMDD, a demonstrable hormonal imbalance in people with PMDD has not been identified. In fact, levels of reproductive hormones in people with and without PMDD are indistinguishable. It is instead hypothesized that people with PMDD are more sensitive to normal levels of hormone fluctuations, predominantly estrogen and progesterone which produces biochemical events in the nervous system that cause the premenstrual symptoms. These symptoms are more predominant in people who have a predisposition to the disorder.

While the etiology of the PMDs is still under investigation, it is apparent that these disorders are biologically driven and are not simply psychological or cultural phenomena. PMDD is found in people worldwide, indicating a biological basis. Most psychologists infer that this disorder is caused by both reaction to hormone influx and genetic components. There is evidence of heritability of premenstrual symptoms not accounted for by family environment suggesting a genetic component to PMDD; however, which genes are involved is a broader question that is still being investigated. Environmental stress can also be a large contributor to triggering PMDD. While there is likely a genetic component to PMDs, the environment must also be considered. Genetics do not operate in a vacuum, and environmental effects such as stress, hormonal fluctuation, and epigenetics likely play a role as well. History of traumatic stress has been associated with PMDD.

"At least three-quarters of patients with dysthymia also have a chronic physical illness or another psychiatric disorder such as one of the anxiety disorders, cyclothymia, drug addiction, or alcoholism". Common co-occurring conditions include major depression (up to 75%), anxiety disorders (up to 50%), personality disorders (up to 40%), somatoform disorders (up to 45%) and substance abuse (up to 50%). People with dysthymia have a higher-than-average chance of developing major depression. A 10-year follow-up study found that 95% of dysthymia patients had an episode of major depression. When an intense episode of depression occurs on top of dysthymia, the state is called "double depression."

20-30% of people who menstruate experience symptoms severe enough to meet PMS criteria and 3-8% of people who are of reproductive age meet the PMDD criteria.

Bipolar depression, anxiety disorders, and other Axis I disorders are more common in people with PMDD than in the general population. In people with PMDD, there is a 50-78% lifetime incidence of various psychiatric disorders such as generalized anxiety disorder, seasonal affective disorder and major depressive disorder.

The symptoms in which coincide with mood disorders, such as major depressive disorder or bipolar disorder, may worsen during the premenstrual period and thus may mimic PMDD. This phenomenon is known as premenstrual exacerbation (PME) and refers to the worsening of mood disorder symptoms during the premenstrual phase. An estimated 40% of people who seek treatment for PMDD are found to not have PMDD, but rather a PME of an underlying mood disorder.

Medical personnel can avoid misdiagnosis by having people seeking treatment for PMDD use a daily charting method to record their symptoms. Daily charting helps distinguish when mood disturbances are experienced and allows PMDD to be distinguished from other mood disorders. With PMDD, mood symptoms are present only during the luteal phase, or last two weeks, of the menstrual cycle. While PMDD mood symptoms are of a cyclical nature, other mood disorders are variable or constant over time. Although the medical community lacks a consensus on the most efficient instrument by which to confirm a PMDD diagnosis, several well-validated scales for recording premenstrual symptoms include the Calendar of Premenstrual Experiences (COPE), Daily Record of Severity of Problems (DRSP), and Prospective Record of the Severity of Menstruation (PRISM).

PMDD mood symptoms are only present in people who are menstruating. Thus, symptoms do not occur during pregnancy and after menopause. Other mood disorders typically persist across all reproductive life events and are independent of a person's menstrual cycle or lack thereof.

In addition to AXIS I disorders, several other medical illnesses such as chronic fatigue syndrome, fibromyalgia, irritable bowel syndrome and migraine disorder may present symptoms similar or identical to those of PMDD. Clinicians must distinguish between PMDD and other medical and/or psychiatric conditions.

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.

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.

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.

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.

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.

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.

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.

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.

Minor depressive disorder, also known as minor depression, is a mood disorder that does not meet the full criteria for major depressive disorder but at least two depressive symptoms are present for two weeks. These symptoms can be seen in many different psychiatric and mental disorders, which can lead to more specific diagnoses of an individual's condition. However, some of the situations might not fall under specific categories listed in the "Diagnostic and Statistical Manual of Mental Disorders". Minor depressive disorder is an example of one of these nonspecific diagnoses, as it is a disorder classified in the DSM-IV-TR under the category Depressive Disorder Not Otherwise Specified (DD-NOS). The classification of NOS depressive disorders is up for debate. Minor depressive disorder as a term was never an officially accepted term, but was listed in Appendix B of the DSM-IV-TR. This is the only version of the DSM that contains the term, as the prior versions and the most recent edition, DSM-5, does not mention it.

A person is considered to have minor depressive disorder if they experience 2 to 4 depressive symptoms, with one of them being either depressed mood or loss of interest or pleasure, during a 2-week period. The person must not have experienced the symptoms for 2 years and there must not have been one specific event that caused the symptoms to arise. Although not all cases of minor depressive disorder are deemed in need of treatment, some cases are treated similarly to major depressive disorder. This treatment includes cognitive behavioral therapy (CBT), anti-depressant medication, and combination therapy. A lot of research supports the notion that minor depressive disorder is an early stage of major depressive disorder, or that it is simply highly predictive of subsequent major depressive disorder.

Depression may also be iatrogenic (the result of healthcare), such as drug induced depression. Therapies associated with depression include interferon therapy, beta-blockers, Isotretinoin, contraceptives, cardiac agents, anticonvulsants, antimigraine drugs, antipsychotics, and hormonal agents such as gonadotropin-releasing hormone agonist.

Estimates of the numbers of people suffering from major depressive episodes and Major Depressive Disorder (MDD) vary significantly. In their lifetime, 10% to 25% of women, and 5% to 12% of men will suffer a major depressive episode. Fewer people, between 5% and 9% of women and between 2% and 3% of men, will have MDD, or full-blown depression. The greatest differences in numbers of men and women diagnosed are found in the United States and Europe. The peak period of development is between the ages of 25 and 44 years. Onset of major depressive episodes or MDD often occurs to people in their mid-20s, and less often to those over 65. Prepubescent girls and boys are affected equally. The symptoms of depression are the same in both children and adolescents though there is evidence that their expression within an individual may change as he or she ages.

In a National Institute of Mental Health study, researchers found that more than 40 percent of people with post-traumatic stress disorder suffered from depression 4 months after the traumatic event they experienced.

Cultural factors can influence the symptoms displayed by a person experiencing a major depressive episode. The values of a specific culture may also influence which symptoms are more concerning to the person or and their friends and family. It is essential that a trained professional knows not to dismiss specific symptoms as merely being the "norm" of a culture.

Women who have recently given birth may be at increased risk for having a major depressive episode. This is referred to as postpartum depression and is a different health condition than the baby blues, a low mood that resolves within 10 days after delivery.

Major depressive episodes may show comorbidity (association) with other physical and mental health problems. About 20-25% of individuals with a chronic general medical condition will develop major depression. Common comorbid disorders include: eating disorders, substance-related disorders, panic disorder, and obsessive-compulsive disorder. Up to 25% of people who experience a major depressive episode have a pre-existing dysthymic disorder.

Some persons who have a fatal illness or are at the end of their life may experience depression, although this is not universal.