Map of U.S. states which have passed laws allowing the formation of benefit corporations:
Passed into law. No existing law. Bill failed a vote in the state's legislature.
In business, particularly in United States corporate law, a benefit corporation (or in some states, a public benefit corporation) is a type of for-profit corporate entity
whose goals include making a positive impact on society. Laws
concerning conventional corporations typically do not define the "best
interest of society", which has led to the belief that increasing shareholder value (profits and/or share price) is the only overarching or compelling interest of a corporation. Benefit corporations explicitly specify that profit is not their only goal. An ordinary corporation may change to a benefit corporation merely by stating in its approved corporate bylaws that it is a benefit corporation.
A company chooses to become a benefit corporation in order to
operate as a traditional for-profit business while simultaneously
addressing social, economic, and/or environmental needs. For example, a 2013 study done by MBA students at the University of Maryland showed that one main reason businesses in Maryland had chosen to file as benefit corporations was for community recognition of their values. A benefit corporation's directors and officers operate the business
with the same authority and behavior as in a traditional corporation,
but are required to consider the impact of their decisions not only on
shareholders but also on employees, customers, the community, and the
local and global environment. For an example of what additional impacts
directors and officers are required to consider, view the Maryland Code §
5-6C-07 – Duties of director. The nature of the business conducted by
the corporation does not affect its status as a benefit corporation.
Instead, it provides a justification for including public benefits in
their missions and activities.
The benefit corporation legislation ensures that a director is
required to consider other public benefits in addition to profit,
preventing shareholders from using a drop in stock value as evidence for
dismissal or a lawsuit against the corporation. Transparency provisions
require benefit corporations to publish annual benefit reports of their
social and environmental performance using a comprehensive, credible,
independent, and transparent third-party standard. However, few of the
states have included provisions for the removal of benefit corporation
status or fines if the companies fail to publish benefit reports that
comply with the state statutes.
Although approximately 36 jurisdictions now authorize the
creation of benefit corporations, outside of those jurisdictions there
are no legal standards that define what constitutes a benefit
corporation. With jurisdictions that recognize this form of business, a benefit
corporation is intended "to merge the traditional for-profit business
corporation model with a non-profit model by allowing social
entrepreneurs to consider interests beyond those of maximizing
shareholder wealth." In jurisdictions where regulations have not been enacted, a benefit
corporation need not be certified or audited by the third-party
standard. Instead, it may use third-party standards solely as a rubric to measure its own performance.
Some research suggests a possible synergy between a benefit corporation and employee ownership.
History
United States
In April 2010, Maryland became the first U.S. state to pass benefit corporation legislation. As of March 2018, 36 states and Washington, D.C., have passed legislation allowing for the creation of benefit corporations: and enhance corporate responsibility.
Connecticut's benefit corporation law is the first to allow
"preservation clauses", which allow the corporation's founders to
prevent it from reverting to a 'For Profit' entity at the will of their
shareholders.
Public benefit LLCs
A subset of benefit corporation, the public benefit LLC, allows for limited liability companies the same opportunities afforded to corporations under a state's benefit corporation law.
Some states have passed legislation for creating social purpose
corporations (SPCs), which are more flexible in their legal requirements
and responsibilities compared to benefit corporations.
Low-profit limited liability companies (L3Cs) were created to comply with the Internal Revenue Service
(IRS) program-related investments (PRIs) rules (26 U.S.C. §
170(c)(2)(B)) which allow most typically private foundations the ability
to maintain tax-exempt status through investments in qualifying
businesses and/or charities. They blend aspects of law regarding limited
liability companies with aspects of non-profit law, but remain
for-profit companies for tax purposes.
In May 2018, the leader of the British Columbia Green Party introduced a bill to amend the Business Corporations Act to permit the incorporation of "benefit companies" in British Columbia.[17]
On June 30, 2020, British Columbia became the first province in Canada
to offer the option of incorporating as a benefit company.
Colombia
In 2018, Colombia introduced benefit corporation legislation.
Israel
Israeli law defines a public benefit company in chapter 9 of its
Companies Law, with the current definition stemming from a 2007
amendment. Public benefit companies may only draw their stated goals
from a closed list codified in law, and are prohibited from distributing
dividends.
Italy
In December 2015, the Italian Parliament passed legislation recognizing a new kind of organization, named Società Benefit, which was directly modeled after benefit corporations in the United States.
United Kingdom
In the United Kingdom, Community Interest Companies
(CIC) were introduced in 2005, intended "for people wishing to
establish businesses which trade with a social purpose..., or to carry
on other activities for the benefit of the community".
Differences from traditional corporations
Historically, U.S. corporate law has not been structured or tailored
to address the situation of for-profit companies that wish to pursue a
social or environmental mission. While corporations generally have the ability to pursue a broad range
of activities, corporate decision-making is usually justified in terms
of creating long-term shareholder value.
The idea that a corporation has as its purpose to maximize financial gain for its shareholders was first articulated in Dodge v. Ford Motor Co. in 1919. Over time, through both law and custom, the concept of "shareholder primacy" has come to be widely accepted. This was reaffirmed in 2010 for Delaware corporations by the case eBay Domestic Holdings, Inc. v. Craig Newmark, et al., 3705-CC,
61 (Del. Ch. 2010)., in which the Delaware Chancery Court stated that a
non-financial mission that "seeks not to maximize the economic value of
a for-profit Delaware corporation for the benefit of its stockholders"
is inconsistent with directors' fiduciary duties. However, the fiduciary
duties do not list profit or financial gains specifically, and to date
no corporate charters have been written that identify profit as one of
those duties.
In the ordinary course of business, decisions made by a
corporation's directors are generally protected by the business judgment
rule, under which courts are reluctant to second-guess operating
decisions made by directors. In a takeover or change of control
situation, however, courts give less deference to directors' decisions
and require that directors obtain the highest price in order to maximize
shareholder value in the transaction. Thus a corporation may be unable
to maintain its focus on social and environmental factors in a change of
control situation because of the pressure to maximize shareholder
value.
Mission-driven businesses, impact investors, and social
entrepreneurs are constrained by this legal framework, which is not
equipped to accommodate for-profit entities whose mission is central to
their existence.
Even in states that have passed "constituency" statutes, which
permit directors and officers of ordinary corporations to consider
non-financial interests when making decisions, legal uncertainties make
it difficult for mission-driven businesses to know when they are allowed
to consider additional interests. Without clear case law, directors may
still fear civil claims if they stray from their fiduciary duties to
the owners of the business to maximize profit.
By contrast, benefit corporations expand the fiduciary duty of
directors to require them to consider non-financial stakeholders as well
as the interests of shareholders. This gives directors and officers of mission-driven businesses the
legal protection to pursue an additional mission and consider additional
stakeholders.The enacting state's benefit corporation statutes are placed within
existing state corporation codes so that the codes apply to benefit
corporations in every respect except those explicit provisions unique to
the benefit corporation form.
Provisions
Typical major provisions of a benefit corporation are:
Shall have the right to name specific public benefit purposes
The creation of public benefit is in the best interests of the benefit corporation.
Accountability
Directors' duties are to make decisions in the best interests of the corporation
Directors and officers shall consider effect of decisions on
shareholders and employees, suppliers, customers, community, environment
(together the "stakeholders")
Transparency
Shall publish annual Benefit Report in accordance with
recognized third party standards for defining, reporting, and assessing
social and environmental performance
Benefit Report delivered to: 1) all shareholders; and 2) public website with exclusion of proprietary data
Right of action
Only shareholders and directors have right of action
Right of action can be for 1) violation of or failure to pursue
general or specific public benefit; 2) violation of duty or standard of
conduct
Change of control/purpose/structure
Shall require a minimum status vote which is a 2/3 vote in most states, but slightly higher in a few states
Benefit corporations are treated like all other corporations for tax purposes.
Benefits
Benefit corporation laws address concerns held by entrepreneurs who
wish to raise growth capital but fear losing control of the social or
environmental mission of their business. In addition, the laws provide
companies the ability to consider factors other than the highest
purchase offer at the time of sale, in spite of the ruling on Revlon, Inc. v. MacAndrews & Forbes Holdings, Inc.
Chartering as a benefit corporation also allows companies to
distinguish themselves as businesses with a social conscience, and as
one that aspires to a standard they consider higher than profit-maximization for shareholders. Yvon Chouinard, founder of Patagonia,
has written "Benefit corporation legislation creates the legal
framework to enable companies like Patagonia to stay mission-driven
through succession, capital raises, and even changes in ownership, by
institutionalizing the values, culture, processes, and high standards
put in place by founding entrepreneurs."
Oregon House Bill 3572, signed by the governor of Oregon in July 2023, allows public contracting agencies to award contracts to benefit
corporations if the cost of the goods and services is not more than 5%
higher than that available from another company.
Benefit corporation vs. certified benefit corporation
There is a difference between being filing as a benefit corporation in a state, and being a certified benefit corporation also known as a B Corporation. B Corporations voluntarily promise to run their firm with social and environmental causes as a concern. To receive their certification from B Lab they must score a minimum of
80 out of 200 on a survey called the B impact assessment. Next, they will have to pass through an audit process. Finally, the firms wishing to remain certified will be required to pay an annual fee to B Lab. Furthermore, companies will pledge to incorporate as a benefit corporation before their re-certification.
Benefit corporations and cooperatives
Benefit corporations are not synonymous with cooperatives,
which are a type of corporate governance in which the governance and
shares are equally held by their members, such as all employees or all
consumers. However, a benefit corporation may also be organized as a
cooperative or vice versa.
Taxation
A public benefit corporation is a legal entity that is organized and taxed as either an S corporation or C corporation.
An S or C corporation will not change its tax status upon transferring
to a public benefit corporation, while an LLC, partnership or sole
proprietorship will have to. While public benefit corporations are taxed
the same as their underlying corporation status, there is added benefit
to taxation on charitable contributions. If a firm makes donations to a
qualifying non-profit, the charitable contributions receive a
tax-deductible status. This will lower a firm's taxes compared to a
typical C-corporation that is not donating money and only focusing on
short term profits.
Possible incentives to change to a benefit corporation
Reorganizing as a public benefit corporation affords a corporation's
directors and founders protection from shareholder lawsuits when
pursuing decisions that benefit the public at the expense of short-term
profits. Furthermore, firms that transition typically experience advantages in
retaining employees, increasing their customer loyalty and attracting
prospective talent that will mesh well into the company culture.
Transition process
Changing status to a public benefit corporation requires several
steps. First, the firm should choose one or more specific public benefit
projects that it will pursue. Next, the articles of incorporation
should be amended to state at the beginning that the firm is a public
benefit corporation. The term public benefit corporation (PBC) or
another abbreviation may be added to the entity's name if the founders
choose. Finally the share certificates that are issued by the entity
should state that the firm is a public benefit corporation. A
shareholder vote is required to amend the articles which must include
"non-voting" shares. The vote must gain a two-thirds majority to pass,
depending on the Articles of Incorporation. Shareholders should be notified early that dissenter's rights apply.
Dissenter's rights mean that those that vote against the amendment and
qualify, may require the company to buy back their shares at fair value
before the change. Firms making the transition should also perform a "due diligence
review" of their business contracts, affairs and status in order to
avoid any unforeseen liability associated with changing the form of the
entity.
The transition process is different state by state but for
Colorado it is as follows. First, the firm must prepare the
aforementioned amended articles. Then, they also amend their bylaws and
assign responsibilities to the board of directors. Next, the amendments
must be approved by the directors before going to a shareholder vote.
Finally they file the amended articles of incorporation with the
secretary of the state.
If the prior entity is an LLC or partnership there is an extra
step required. For these entities the articles of incorporation
themselves and the related bylaws must first be prepared and filed with
the state secretary. Only then will it be possible to merge or
transition the previous form into the benefit corporation.
Investor and consumer preferences
According to William Mitchell Law Review
journal, about 68 million US customers have a preference for making
decisions about their purchases based on a sense of environmental or
social responsibility. Some individuals even go as far as using their purchases to "punish"
companies for bad corporate behavior when it pertains to environmental
or social cause. Others do the opposite, and use their purchasing power to reward firms
that they believe are doing social or environmental good. The Mitchell Law Review
also states that around 49% of Americans have at some point in time
boycotted firms whose behavior they see as "not in the best interest of
society." Recent research also suggests that when variables like price and
quality are held constant, 87% of customers would switch from a less
socially responsible brand to a more socially responsible competitor.
The diagnosis of major depressive disorder is based on the
person's reported experiences, behavior reported by family or friends,
and a mental status examination. There is no laboratory test for the disorder, but testing may be done to rule out physical conditions that can cause similar symptoms. The most common time of onset is in a person's 20s, with females affected about three times as often as males. The course of the disorder varies widely, from one episode lasting months to a lifelong disorder with recurrent episodes.
Major depressive disorder is believed to be caused by a combination of genetic, environmental, and psychological factors, with about 40% of the risk being genetic. Risk factors include a family history of the condition, major life changes, childhood traumas, environmental lead exposure, certain medications, chronic health problems, and substance use disorders. It can negatively affect a person's personal life, work life, or
education, and cause issues with a person's sleeping habits, eating
habits, and general health.
A person having a major depressive episode usually exhibits a low mood, which pervades all aspects of life, and an inability to experience pleasure in previously enjoyable activities. Depressed people may be preoccupied with or ruminate over thoughts and
feelings of worthlessness, inappropriate guilt or regret, helplessness
or hopelessness.
Other symptoms of depression include poor concentration and memory, withdrawal from social situations and activities, reduced sex drive, irritability, and thoughts of death or suicide. Insomnia is common; in the typical pattern, a person wakes very early and cannot get back to sleep. Hypersomnia, or oversleeping, can also happen, as well as day-night rhythm disturbances, such as diurnal mood variation. Some antidepressants may also cause insomnia due to their stimulating effect. In severe cases, depressed people may have psychotic symptoms. These symptoms include delusions or, less commonly, hallucinations, usually unpleasant. People who have had previous episodes with psychotic symptoms are more likely to have them with future episodes.
A depressed
person may report multiple physical symptoms such as fatigue, headaches,
or digestive problems; physical complaints are the most common
presenting problem in developing countries, according to the World Health Organization's criteria for depression. Appetite often decreases, resulting in weight loss, although increased appetite and weight gain occasionally occur.
Major depression significantly affects a person's family and personal relationships, work or school life, sleeping and eating habits, and general health. Family and friends may notice agitation or lethargy. Older depressed people may have cognitive symptoms of recent onset, such as forgetfulness, and a more noticeable slowing of movements.
Depressed children may often display an irritable rather than a depressed mood; most lose interest in school and show a steep decline in academic performance. Diagnosis may be delayed or missed when symptoms are interpreted as "normal moodiness". Elderly people with depression may not present with classical depressive symptoms. Diagnosis and treatment is further complicated in that the elderly are often simultaneously treated with a number of other drugs, and often have other concurrent diseases.
A cup analogy demonstrating the diathesis–stress model that under the same amount of stressors, person 2 is more vulnerable than person 1, because of their predisposition.
The etiology of depression is not yet fully understood. 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. American psychiatrist Aaron Beck suggested that a triad of automatic and spontaneous negative thoughts about the self, the world or environment, and the future may lead to other depressive signs and symptoms.
Genes play a major role in the development of depression. Family and twin studies suggest that genetic factors account for nearly
40% of the variation in risk for major depressive disorder. Like most
psychiatric disorders, major depression is likely shaped by a
combination of many individual genetic influences. In 2018, a genome-wide association study discovered 44 genetic variants linked to risk for major depression; a 2019 study found 102 variants in the genome linked to depression. However, it appears that major depression is less heritable compared to bipolar disorder and schizophrenia.Research focusing on specific candidate genes has been criticized for its tendency to generate false positive findings. There are also other efforts to examine interactions between life stress and polygenic risk for depression.
Other health problems
Depression can also arise after a chronic or terminal medical condition, such as HIV/AIDS or asthma, and may be labeled "secondary depression".It is unknown whether the underlying diseases induce depression through
effect on quality of life, or through shared etiologies (such as
degeneration of the basal ganglia in Parkinson's disease or immune dysregulation in asthma). Depression may also be iatrogenic (the result of healthcare), such as drug-induced depression. Therapies associated with depression include interferons, beta blockers, isotretinoin, contraceptives, cardiac agents, anticonvulsants, and hormonal agents. Celiac disease is another possible contributing factor.
Substance use in early age is associated with increased risk of developing depression later in life. Depression occurring after giving birth is called postpartum depression and is thought to be the result of hormonal changes associated with pregnancy. Seasonal affective disorder, a type of depression associated with seasonal changes in sunlight, is thought to be triggered by decreased sunlight. Vitamin B2, B6 and B12 deficiency may cause depression in females.
A 2025 study found that, among more than 172,500 adults in the UK aged 39 and older, those with a history of depression experienced the onset of chronic illnesses approximately 30% earlier than those without depression.
Adverse childhood experiences (incorporating childhood abuse, neglect and family dysfunction) markedly increase the risk of major depression, especially if more than one type. Childhood trauma also correlates with severity of depression, poor responsiveness to treatment and length of illness. Some are more susceptible than others to developing mental illness such
as depression after trauma, and various genes have been suggested to
control susceptibility. Couples in unhappy marriages have a higher risk of developing clinical depression.
There appears to be a link between air pollution and depression and suicide. There may be an association between long-term PM2.5 exposure and depression, and a possible association between short-term PM10 exposure and suicide.
In a review, people who lived alone were found to have a 42% greater risk of depression.
Evolutionary explanations propose that low mood may sometimes represent an adaptive response, such as conserving energy during adverse circumstances or promoting rumination on complex problems. Other models emphasize the potential social functions of depressive
symptoms, including signaling a need for support. Recent reviews
highlight both the heuristic value and limitations of these perspectives, noting that empirical support remains mixed.
The pathophysiology of depression is not completely understood, but current theories center around monoaminergic systems, the circadian rhythm, immunological dysfunction, HPA-axis dysfunction, and structural or functional abnormalities of emotional circuits.
Derived from the effectiveness of monoaminergic drugs in treating
depression, the monoamine theory posits that insufficient activity of
monoamine neurotransmitters is the primary cause of depression. Evidence for the monoamine theory comes from multiple areas. First, acute depletion of tryptophan—an amino acid and a necessary precursor of the monoamine serotonin—can
cause depression in those in remission or relatives of people who are
depressed, suggesting that decreased serotonergic neurotransmission is
important in depression. Second, the correlation between depression risk and polymorphisms in the 5-HTTLPR gene, which codes for serotonin receptors, suggests a link. Third, decreased size of the locus coeruleus, reduced activity of tyrosine hydroxylase, increased density of alpha-2 adrenergic receptors, and evidence from rat models suggest decreased adrenergic neurotransmission in depression. Furthermore, decreased levels of homovanillic acid, altered response to dextroamphetamine, responses of depressive symptoms to dopamine receptor agonists, decreased dopamine receptor D1 binding in the striatum, and polymorphism of dopamine receptor genes implicate dopamine, another monoamine, in depression. Lastly, increased activity of monoamine oxidase, an enzyme that degrades monoamines, has been associated with depression. However, the monoamine theory is inconsistent with observations that
serotonin depletion does not cause depression in healthy persons, that
antidepressants instantly increase levels of monoamines but take weeks
to work, and the existence of atypical antidepressants which can be
effective despite not targeting this pathway.
One proposed explanation for the therapeutic lag, and further
support for the deficiency of monoamines, is that a desensitization of self-inhibition in raphe nuclei by the increased serotonin, mediated by antidepressants, occurs before the therapeutic efficacy of the drugs can be realized.[86] However, disinhibition of the dorsal raphe
has been proposed to occur as a result of decreased serotonergic
activity in tryptophan depletion, resulting in a depressed state
mediated by increased serotonin. Further countering the monoamine
hypothesis is the fact that rats with lesions of the dorsal raphe are
not more depressive than controls; the finding of increased jugular 5-HIAA in people who are depressed that normalized with selective serotonin reuptake inhibitor (SSRI) treatment, and the preference for carbohydrates in people who are depressed. Already limited, the monoamine hypothesis has been further oversimplified when presented to the general public. A 2022 review found no consistent evidence supporting the serotonin hypothesis linking serotonin levels and depression.
HPA-axis abnormalities have been suggested in depression given the association of CRHR1 with depression and the increased frequency of dexamethasone test
non-suppression in people who are depressed. However, this abnormality
is not adequate as a diagnosis tool because its sensitivity is only 44%. These stress-related abnormalities are thought to be the cause of
hippocampal volume reductions seen in people who are depressed. Furthermore, a meta-analysis yielded decreased dexamethasone suppression, and increased response to psychological stressors. Further abnormal results have been obscured with the cortisol awakening response, with increased response being associated with depression.
There is also a connection between the gut microbiome and the central nervous system, otherwise known as the Gut–Brain axis, which is a two-way communication system between the brain and the gut. Experiments have shown that microbiota
in the gut can play an important role in depression, as people with MDD
often have gut-brain dysfunction. One analysis showed that those with
MDD have different bacteria in their guts. Bacteria Bacteroidetes and Firmicutes were most affected in people with MDD, and they are also impacted in people with irritable bowel syndrome (IBS). Another study showed that people with IBS have a higher chance of developing depression, which shows the two are connected. There is even evidence suggesting that altering the microbes in the gut can have regulatory effects on developing depression.
Theories unifying neuroimaging
findings have been proposed. The first model proposed is the
limbic-cortical model, which involves hyperactivity of the ventral
paralimbic regions and hypoactivity of frontal regulatory regions in
emotional processing. Another model, the cortico-striatal model, suggests that abnormalities of the prefrontal cortex in regulating striatal and subcortical structures result in depression. Another model proposes hyperactivity of salience structures in identifying negative stimuli and hypoactivity of cortical regulatory structures resulting in a negative emotional bias and depression, consistent with emotional bias studies.
The newer field of psychoneuroimmunology, the study between the immune system and the nervous system and emotional state, suggests that cytokines may impact depression.
Immune system abnormalities have been observed, including increased levels of cytokines—cells produced by immune cells that affect inflammation—involved in generating sickness behavior, creating a pro-inflammatory profile in MDD. Some people with depression have increased levels of pro-inflammatory
cytokines and some have decreased levels of anti-inflammatory cytokines. Ketamine infusion may rapidly reduce depressive symptoms in
treatment-resistant depression by modulating proinflammatory cytokines. With this, in MDD, people will more likely have a Th1-dominant
immune profile, which is a pro-inflammatory profile. This suggests that
there are components of the immune system affecting the pathology of
MDD.
Another way cytokines can affect depression is in the kynurenine pathway, and when this is overactivated, it can cause depression. This can be due to too much microglial activation and too little astrocytic activity. When microglia get activated, they release pro-inflammatory cytokines that cause an increase in the production of COX2. This, in turn, causes the production of PGE2, which is a prostaglandin, and this catalyzes the production of indolamine, IDO. IDO causes tryptophan to get converted into kynurenine, and kynurenine becomes quinolinic acid. Quinolinic acid is an agonist for NMDA receptors,
so it activates the pathway. Studies have shown that the post-mortem
brains of patients with MDD have higher levels of quinolinic acid than
people who did not have MDD. With this, researchers have also seen that
the concentration of quinolinic acid correlates to the severity of
depressive symptoms.
A diagnostic assessment may be conducted by a suitably trained general practitioner, or by a psychiatrist or psychologist, who records the person's current circumstances, biographical history,
current symptoms, family history, and alcohol and drug use. The
assessment also includes a mental state examination,
which is an assessment of the person's current mood and thought
content, in particular the presence of themes of hopelessness or pessimism, self-harm or suicide, and an absence of positive thoughts or plans. Specialist mental health services are rare in rural areas, and thus diagnosis and management is left largely to primary-care clinicians. This issue is even more marked in developing countries. Rating scales
are not used to diagnose depression, but they provide an indication of
the severity of symptoms for a time period, so a person who scores above
a given cut-off point can be more thoroughly evaluated for a depressive
disorder diagnosis. Several rating scales are used for this purpose; these include the Hamilton Rating Scale for Depression, the Beck Depression Inventory or the Suicide Behaviors Questionnaire-Revised.
Primary-care physicians
have more difficulty with underrecognition and undertreatment of
depression compared to psychiatrists. These cases may be missed because
for some people with depression, physical symptoms often accompany
depression. In addition, there may also be barriers related to the
person, provider, or the medical system. Non-psychiatrist physicians
have been shown to miss about two-thirds of cases, although there is
some evidence of improvement in the number of missed cases.
A doctor generally performs a medical examination and selected
investigations to rule out other causes of depressive symptoms. These
include blood tests measuring TSH and thyroxine to exclude hypothyroidism; basic electrolytes and serum calcium to rule out a metabolic disturbance; and a full blood count including ESR to rule out a systemic infection or chronic disease. Adverse affective reactions to medications or alcohol misuse may be ruled out, as well. Testosterone levels may be evaluated to diagnose hypogonadism, a cause of depression in men. Vitamin D levels might be evaluated, as low levels of vitamin D have been associated with greater risk for depression. Subjective cognitive complaints appear in older depressed people, but they can also be indicative of the onset of a dementing disorder, such as Alzheimer's disease. Cognitive testing and brain imaging can help distinguish depression from dementia. A CT scan can exclude brain pathology in those with psychotic, rapid-onset or otherwise unusual symptoms. No biological tests confirm major depression. In general, investigations are not repeated for a subsequent episode unless there is a medical indication.
Under mood disorders, ICD-11 classifies major depressive disorder as either single episode depressive disorder (where there is no history of depressive episodes, or of mania) or recurrent depressive disorder (where there is a history of prior episodes, with no history of mania). ICD-11 symptoms, present nearly every day for at least two weeks, are a depressed mood or anhedonia,
accompanied by other symptoms such as "difficulty concentrating,
feelings of worthlessness or excessive or inappropriate guilt,
hopelessness, recurrent thoughts of death or suicide, changes in
appetite or sleep, psychomotor agitation or retardation, and reduced
energy or fatigue." These symptoms must affect work, social, or domestic activities. The
ICD-11 system allows further specifiers for the current depressive
episode: the severity (mild, moderate, severe, unspecified); the
presence of psychotic symptoms (with or without psychotic symptoms); and
the degree of remission if relevant (currently in partial remission,
currently in full remission). These two disorders are classified as "Depressive disorders", in the category of "Mood disorders".
According to DSM-5, at least one of the symptoms is either
depressed mood or loss of interest or pleasure. Depressed mood occurs
nearly every day as subjective feelings like sadness, emptiness, and
hopelessness or observations made by others (e.g. appears tearful). Loss
of interest or pleasure occurs in all, or almost all activities of the
day, nearly every day. These symptoms, as well as five out of the nine
more specific symptoms listed, must frequently occur for more than two
weeks (to the extent in which it impairs functioning) for the diagnosis. Major depressive disorder is classified as a mood disorder in the DSM-5. The diagnosis hinges on the presence of single or recurrent major depressive episodes. Further qualifiers are used to classify both the episode itself and the course of the disorder. The category Unspecified Depressive Disorder is diagnosed if the depressive episode's manifestation does not meet the criteria for a major depressive episode.
A major depressive episode is characterized by the presence of a severely depressed mood that persists for at least two weeks. Episodes may be isolated or recurrent and are categorized as mild (few
symptoms in excess of minimum criteria), moderate, or severe (marked
impact on social or occupational functioning). An episode with psychotic
features—commonly referred to as psychotic depression—is automatically rated as severe. If the person has had an episode of mania or markedly elevated mood, a diagnosis of bipolar disorder is made instead. Depression without mania is sometimes referred to as unipolar because the mood remains at one emotional state or "pole".
Bereavement
is not an exclusion criterion in the DSM-5, and it is up to the
clinician to distinguish between normal reactions to a loss and MDD.
Excluded are a range of related diagnoses, including dysthymia, which involves a chronic but milder mood disturbance; recurrent brief depression, consisting of briefer depressive episodes; minor depressive disorder, whereby only some symptoms of major depression are present; and adjustment disorder with depressed mood, which denotes low mood resulting from a psychological response to an identifiable event or stressor.
Subtypes
The DSM-5 recognizes six further subtypes of MDD, called specifiers, in addition to noting the length, severity and presence of psychotic features:
"Melancholic depression"
is characterized by a loss of pleasure in most or all activities, a
failure of reactivity to pleasurable stimuli, a quality of depressed
mood more pronounced than that of grief or loss, a worsening of symptoms in the morning hours, early-morning waking, psychomotor retardation, excessive weight loss (not to be confused with anorexia nervosa), or excessive guilt.
"Atypical depression" is characterized by mood reactivity (paradoxical anhedonia) and positivity, significant weight gain or increased appetite (comfort eating), excessive sleep or sleepiness (hypersomnia),
a sensation of heaviness in limbs known as leaden paralysis, and
significant long-term social impairment as a consequence of
hypersensitivity to perceived interpersonal rejection.
"Catatonic depression"
is a rare and severe form of major depression involving disturbances of
motor behavior and other symptoms. Here, the person is mute and almost
stuporous, and either remains immobile or exhibits purposeless or even
bizarre movements. Catatonic symptoms also occur in schizophrenia or in manic episodes, or may be caused by neuroleptic malignant syndrome.
"Depression with anxious
distress" was added into the DSM-5 as a means to emphasize the common
co-occurrence between depression and anxiety, as well as the risk of
suicide of depressed individuals with anxiety.
"Depression with peri-partum
onset" refers to the intense, sustained and sometimes disabling
depression experienced by women after giving birth or while a woman is
pregnant. DSM-IV-TR used the classification "postpartum depression", but
this was changed not to exclude cases of depressed women during
pregnancy. Depression with peripartum onset has an incidence rate of
3%–6% among new mothers. The DSM-5 mandates that to qualify as
depression with peripartum onset, onset occurs during pregnancy or
within one month of delivery.
"Seasonal affective disorder"
(SAD) is a form of depression in which depressive episodes come on in
the autumn or winter, and resolve in spring. The diagnosis is made if at
least two episodes have occurred in colder months with none at other
times, over a two-year period or longer.
To confirm major depressive disorder as the most likely diagnosis, other potential diagnoses must be considered, including dysthymia, adjustment disorder with depressed mood, or bipolar disorder.
Dysthymia is a chronic, milder mood disturbance in which a person
reports a low mood almost daily over a span of at least two years. The
symptoms are not as severe as those for major depression, although
people with dysthymia are vulnerable to secondary episodes of major
depression (sometimes referred to as double depression). Adjustment disorder with depressed mood
is a mood disturbance appearing as a psychological response to an
identifiable event or stressor, in which the resulting emotional or
behavioral symptoms are significant but do not meet the criteria for a
major depressive episode.
Other disorders need to be ruled out before diagnosing major
depressive disorder. They include depressions due to physical illness, medications, and substance use disorders. Depression due to physical illness is diagnosed as a mood disorder due to a general medical condition. This condition is determined based on history, laboratory findings, or physical examination. When the depression is caused by a medication, non-medical use of a psychoactive substance, or exposure to a toxin, it is then diagnosed as a specific mood disorder (previously called substance-induced mood disorder).
Screening and prevention
Preventive efforts may result in decreases in rates of the condition of between 22% and 38%. Since 2016, the United States Preventive Services Task Force
(USPSTF) has recommended screening for depression among those over the
age of 12, provided that it would be diagnosed accurately, treated
efficiently, and followed-up as needed;though a 2005 Cochrane review found that the routine use of screening questionnaires has little effect on detection or treatment. Screening the general population is not recommended by authorities in
the UK or Canada for similar reasons, citing insufficient data.
Behavioral interventions, such as interpersonal therapy and cognitive behavioral therapy, are effective at preventing new-onset depression. Because such interventions appear to be most effective when delivered
to individuals or small groups, it has been suggested that they may be
able to reach their large target audience most efficiently through the
Internet.
The Netherlands's mental health care system
provides preventive interventions, such as the "Coping with Depression"
course (CWD) for people with sub-threshold depression. The course is
claimed to be the most successful of psychoeducational interventions for
the treatment and prevention of depression (both for its adaptability
to various populations and its results), with a risk reduction of 38% in
major depression and an efficacy as a treatment comparing favorably to
other psychotherapies.
The most common and effective treatments for depression are
psychotherapy, medication, and electroconvulsive therapy (ECT); a
combination of treatments is the most effective approach when depression
is resistant to treatment. American Psychiatric Association
treatment guidelines recommend that initial treatment should be
individually tailored based on factors including severity of symptoms, co-existing disorders, prior treatment experience, and personal preference. Options may include pharmacotherapy, psychotherapy, exercise, ECT, transcranial magnetic stimulation (TMS) or light therapy. Antidepressant
medication is recommended as an initial treatment choice in people with
mild, moderate, or severe major depression, and is often given to
people with severe depression unless ECT is planned. There is evidence that collaborative care by a team of health care
practitioners produces better results than routine single-practitioner
care.
Psychotherapy is the treatment of choice (over medication) for people under 18; and cognitive behavioral therapy (CBT), third-wave CBT and interpersonal therapy may help prevent depression. The UK National Institute for Health and Care Excellence
(NICE) 2004 guidelines indicate that antidepressants should not be used
for the initial treatment of mild depression because the risk–benefit ratio
is poor. The guidelines recommend that antidepressant treatment in
combination with psychosocial interventions should be considered:
For people with a history of moderate or severe depression
For those with mild depression that has been present for a long period
As a second-line treatment for mild depression that persists after other interventions
As a first-line treatment for moderate or severe depression.
Treatment options are more limited in developing countries, where
access to mental health staff, medication, and psychotherapy is often
difficult. Development of mental health services is minimal in many
countries; depression is viewed as a phenomenon of the developed world
despite evidence to the contrary, and not as an inherently
life-threatening condition. There is insufficient evidence to determine the effectiveness of psychological versus medical therapy in children.
Physical exercise is one recommended way to manage mild depression.
Physical exercise has been found to be effective for major
depression, and may be recommended to people who are willing, motivated,
and healthy enough to participate in an exercise program as treatment. It is equivalent to the use of medications or psychological therapies in most people. In older people it does appear to decrease depression. Sleep and diet may also play a role in depression, and interventions in
these areas may be an effective add-on to conventional methods. In studies, smoking cessation has benefits in depression.
Talking therapy
(psychotherapy) can be delivered to individuals, groups, or families by
mental health professionals, including psychotherapists, psychiatrists,
psychologists, clinical social workers,
counselors, and psychiatric nurses. A 2012 review found psychotherapy
to be better than no treatment but not better than other treatments. With more complex and chronic forms of depression, a combination of medication and psychotherapy may be used. There is moderate-quality evidence that psychological therapies are a useful addition to standard antidepressant treatment of treatment-resistant depression in the short term. Psychotherapy has been shown to be effective in older people. Successful psychotherapy appears to reduce the recurrence of depression
even after it has been stopped or replaced by occasional booster
sessions.
The most-studied form of psychotherapy for depression is CBT,
which teaches clients to challenge self-defeating, but enduring, ways of
thinking (cognitions) and change counter-productive behaviors. CBT can
perform as well as antidepressants in people with major depression. CBT has the most research evidence for the treatment of depression in
children and adolescents, and CBT and interpersonal psychotherapy (IPT)
are preferred therapies for adolescent depression. In people under 18, according to the National Institute for Health and Clinical Excellence, medication should be offered only in conjunction with a psychological therapy, such as CBT, interpersonal therapy, or family therapy. Several variables predict success for cognitive behavioral therapy in
adolescents: higher levels of rational thoughts, less hopelessness,
fewer negative thoughts, and fewer cognitive distortions. CBT is particularly beneficial in preventing relapse. Cognitive behavioral therapy and occupational programs (including
modification of work activities and assistance) have been shown to be
effective in reducing sick days taken by workers with depression. Several variants of cognitive behavior therapy have been used in those with depression, the most notable being rational emotive behavior therapy, and mindfulness-based cognitive therapy. Mindfulness-based stress reduction programs may reduce depression symptoms. Mindfulness programs also appear to be a promising intervention in youth. Problem solving therapy, cognitive behavioral therapy, and interpersonal therapy are effective interventions in the elderly.
Psychoanalysis is a school of thought, founded by Sigmund Freud, which emphasizes the resolution of unconscious mental conflicts. Psychoanalytic techniques are used by some practitioners to treat clients presenting with major depression. A more widely practiced therapy, called psychodynamic psychotherapy,
is in the tradition of psychoanalysis but less intensive, meeting once
or twice a week. It also tends to focus more on the person's immediate
problems, and has an additional social and interpersonal focus. In a meta-analysis of three controlled trials of Short Psychodynamic
Supportive Psychotherapy, this modification was found to be as effective
as medication for mild to moderate depression.
The remote provision of psychotherapy, through media such as telephone and video, can make treatment for depression more available and accessible. The administration of treatments, such as CBT, via telehealth may provide a viable alternative to face-to-face care.
Sertraline (Zoloft) is used primarily to treat major depression in adults.
Conflicting results have arisen from studies that look at the
effectiveness of antidepressants in people with acute, mild to moderate
depression. A review commissioned by the National Institute for Health and Care Excellence (UK) concluded that there is strong evidence that SSRIs, such as escitalopram, paroxetine, and sertraline, have greater efficacy than placebo
on achieving a 50% reduction in depression scores in moderate and
severe major depression, and that there is some evidence for a similar
effect in mild depression. Similarly, a Cochrane systematic review of clinical trials of the generic tricyclic antidepressantamitriptyline concluded that there is strong evidence that its efficacy is superior to placebo. Antidepressants work less well for the elderly than for younger individuals with depression.
To find the most effective antidepressant medication with minimal
side-effects, the dosages can be adjusted, and if necessary,
combinations of different classes of antidepressants can be tried.
Response rates to the first antidepressant administered range from 50%
to 75%, and it can take at least six to eight weeks from the start of
medication to improvement. Antidepressant medication treatment is usually continued for six to
nine months after remission, to minimize the chance of recurrence, and
even up to two years of continuation is recommended.
SSRIs are the primary medications prescribed, owing to their relatively mild side-effects, and safety. People who do not respond to one SSRI can be switched to another antidepressant, and this results in improvement in almost 50% of cases. Another option is to augment the atypical antidepressant bupropion to the SSRI as an adjunctive treatment. Venlafaxine, an antidepressant with a different mechanism of action, may be modestly more effective than SSRIs. However, venlafaxine is not recommended in the UK as a first-line
treatment because of evidence suggesting its risks may outweigh
benefits, and it is specifically discouraged in children and adolescents as it increases the risk of suicidal thoughts or attempts.
Hypericum perforatum
(St. John's wort) has approval in the European Union as an herbal
product for the treatment of mild to moderate depressive episodes
(according to ICD-10) and for the short-term treatment of symptoms in mild depression. It is more effective than placebo
and as effective as standard antidepressants, including SSRIs, for mild
to moderate depression, with some evidence suggesting fewer adverse effects and lower discontinuation rates.
Electroconvulsive therapy, ketamine, esketamine, and psilocybin
are the most effective and safe first-line treatments for
treatment-resistant depression, with esketamine and psilocybin showing
slightly lower tolerability.
A nasal spray form of esketamine was approved in the US by the FDA in March 2019 for use in treatment-resistant depression when combined with an oral antidepressant. It was approved as monotherapy for treatment-resistant depression in adults in January 2025. Ketamine and esketamine offer rapid-acting, non-monoaminergic treatment
options for adults with treatment-resistant depression, but questions
remain about their safety, optimal use, and implementation in clinical
practice. Racemic ketamine, especially at higher doses, may have greater and more sustained antidepressant effects than esketamine.
For children and adolescents with moderate-to-severe depressive disorder, fluoxetine seems to be the best treatment (either with or without cognitive behavioural therapy) but more research is needed to be certain. Sertraline, escitalopram, duloxetine might also help in reducing symptoms. Some antidepressants have not been shown to be effective. Medications are not recommended in children with mild disease.
There is also insufficient evidence to determine effectiveness in those with depression complicated by dementia. Any antidepressant can cause low blood sodium levels; nevertheless, it has been reported more often with SSRIs. It is not uncommon for SSRIs to cause or worsen insomnia; the sedating atypical antidepressantmirtazapine can be used in such cases.
Irreversible monoamine oxidase inhibitors,
an older class of antidepressants, have been plagued by potentially
life-threatening dietary and drug interactions. They are still used only
rarely, although newer and better-tolerated agents of this class have
been developed. The safety profile is different with reversible monoamine oxidase inhibitors, such as moclobemide, where the risk of serious dietary interactions is negligible and dietary restrictions are less strict.
It is unclear whether antidepressants affect a person's risk of suicide. For children, adolescents, and probably young adults between 18 and 24 years old, there is a higher risk of both suicidal ideations and suicidal behavior in those treated with SSRIs. For adults, it is unclear whether SSRIs affect the risk of suicidality. One review found no connection; another an increased risk; and a third no risk in those 25–65 years old and a decreased risk in those more than 65. A black box warning
was introduced in the United States in 2007 on SSRIs and other
antidepressant medications due to the increased risk of suicide in
people younger than 24 years. Similar precautionary notice revisions were implemented by the Japanese Ministry of Health.
Other medications and supplements
The combined use of antidepressants plus benzodiazepines
demonstrates improved effectiveness when compared to antidepressants
alone, but these effects may not endure. The addition of a
benzodiazepine is balanced against possible harms and other alternative
treatment strategies when antidepressant mono-therapy is considered
inadequate.
For treatment-resistant depression, adding on the atypical antipsychoticbrexpiprazole for short-term or acute management may be considered. Brexpiprazole may be effective for some people; however, the evidence
as of 2023 supporting its use is weak and this medication has potential
adverse effects including weight gain and akathisia. Brexpiprazole has not been sufficiently studied in older people or children and the use and effectiveness of this adjunctive therapy for longer term management is not clear.
Nonsteroidal anti-inflammatory drugs (NSAIDs) and cytokine inhibitors may be effective in treating depression. For instance, celecoxib, an NSAID, is a selective COX-2 inhibitor; COX-2 is an enzyme that helps in the production of pain and inflammation. In recent clinical trials, this NSAID has been shown helpful with
treatment-resistant depression as it helps inhibit proinflammatory
signaling.
Statins,
which are anti-inflammatory medications prescribed to lower cholesterol
levels, have also been shown to have antidepressant effects. When
prescribed for patients already taking SSRIs, this add-on treatment was
shown to improve anti-depressant effects of SSRIs when compared to the
placebo group. With this, statins have been shown to be effective in
preventing depression in some cases too.
There is insufficient high-quality evidence to suggest omega-3 fatty acids are effective in depression. There is limited evidence that vitamin D supplementation is of value in
alleviating the symptoms of depression in individuals who are vitamin
D-deficient.
Lithium has long been used to augment antidepressants. Lithium augmentation is much more effective than placebo and has proven
efficacy in treating major depressive disorder in multiple randomized controlled trials. Lithium dramatically lowers the risk of suicide in people with
depression. The risk of suicide is reduced by 87% in people with
depression or bipolar disorder who take lithium. In addition to lowering the risk of suicide, lithium also lowers the
risk of mortality from all causes in people with depression or bipolar
disorder. One disadvantage of lithium therapy is that occasional blood tests are usually prescribed to monitor lithium levels.
Low-dose thyroid hormone may be added to existing antidepressants to treat persistent depression symptoms. Limited evidence suggests stimulants, such as amphetamine and modafinil, may be effective in the short term, or as adjuvant therapy.Also, it is suggested that folate supplements may have a role in depression management. There is tentative evidence for benefit from testosterone in males.
Electroconvulsive therapy
Electroconvulsive therapy (ECT) is a standard psychiatric treatment in which seizures are electrically induced in a person with depression to provide relief from psychiatric illnesses. ECT is used with informed consent as a last line of intervention for major depressive disorder. A round of ECT is effective for about 50% of people with
treatment-resistant major depressive disorder, whether it is unipolar or
bipolar. Follow-up treatment is still poorly studied, but about half of people who respond relapse within twelve months. Aside from effects in the brain, the general physical risks of ECT are similar to those of brief general anesthesia. Immediately following treatment, the most common adverse effects are confusion and memory loss. ECT is considered one of the least harmful treatment options available for severely depressed pregnant women.
A usual course of ECT involves multiple administrations,
typically given two or three times per week, with a total of six to
twelve treatments. ECT is administered under anesthesia with a muscle relaxant. Electroconvulsive therapy can differ in its application in three ways:
electrode placement, frequency of treatments, and the electrical
waveform of the stimulus. These three forms of application have
significant differences in both adverse side effects and symptom
remission. After treatment, drug therapy is usually continued, and some
people receive maintenance ECT.
Transcranial magnetic stimulation (TMS) or deep transcranial magnetic stimulation (dTMS) is a noninvasive method used to stimulate small regions of the brain. TMS was approved by the FDA for treatment-resistant major depressive disorder (trMDD) in 2008. While TMS is widely considered safe and effective for treating MDD, its
actual efficacy and tolerability vary across populations, with high
heterogeneity, small-study effects, and widespread bias in the evidence. The American Psychiatric Association, the Canadian Network for Mood and Anxiety Disorders, and the Royal Australia and New Zealand College of Psychiatrists have endorsed TMS for trMDD. Transcranial direct current stimulation
(tDCS) is another noninvasive method used to stimulate small regions of
the brain with a weak electric current. Several meta-analyses have
concluded that active tDCS was useful for treating depression.
There is a small amount of evidence that sleep deprivation may improve depressive symptoms in some individuals, with the effects usually showing up within a day. This effect is
usually temporary. Besides sleepiness, this method can cause a side
effect of mania or hypomania. There is insufficient evidence for reiki and dance movement therapy in depression. Cannabis is specifically not recommended as a treatment.
The microbiome of people with major depressive disorder differs from that of healthy people, and probiotic and synbiotic treatment may achieve a modest depressive symptom reduction. With this, fecal microbiota transplants
(FMT) are being researched as add-on therapy treatments for people who
do not respond to typical therapies. It has been shown that the
patient's depressive symptoms improved, with minor gastrointestinal
issues, after a FMT, with improvements in symptoms lasting at least 4
weeks after the transplant.
Prognosis
Studies have shown that 80% of those with a first major depressive episode will have at least one more during their life, with a lifetime average of four episodes. Other general population studies indicate that around half those who
have an episode recover (whether treated or not) and remain well, while
the other half will have at least one more, and around 15% of those
experience chronic recurrence. Studies recruiting from selective inpatient sources suggest lower
recovery and higher chronicity, while studies of mostly outpatients show
that nearly all recover, with a median episode duration of 11 months.
Around 90% of those with severe or psychotic depression, most of whom
also meet criteria for other mental disorders, experience recurrence. Cases when outcome is poor are associated with inappropriate treatment,
severe initial symptoms including psychosis, early age of onset,
previous episodes, incomplete recovery after one year of treatment,
pre-existing severe mental or medical disorder, and family dysfunction.
A high proportion of people who experience full symptomatic
remission still have at least one symptom not fully resolved after
treatment. Recurrence or chronicity is more likely if symptoms have not fully resolved with treatment. Current guidelines recommend continuing antidepressants for four to
six months after remission to prevent relapse. Evidence from many randomized controlled trials
indicates continuing antidepressant medications after recovery can
reduce the chance of relapse by 70% (41% on placebo vs. 18% on
antidepressant). The preventive effect probably lasts for at least the
first 36 months of use.
Major depressive episodes often resolve over time, whether or not
they are treated. Outpatients on a waiting list show a 10%–15%
reduction in symptoms within a few months, with approximately 20% no
longer meeting the full criteria for a depressive disorder. The median duration of an episode has been estimated to be 23 weeks, with the highest rate of recovery in the first three months. According to a 2013 review, 23% of untreated adults with mild to
moderate depression will remit within 3 months, 32% within 6 months and
53% within 12 months.
Ability to work
Depression may affect people's ability to work. The combination of
usual clinical care and support with return to work (like working less
hours or changing tasks) probably reduces sick leave by 15%, and leads
to fewer depressive symptoms and improved work capacity, reducing sick
leave by an annual average of 25 days per year. Helping depressed people return to work without a connection to
clinical care has not been shown to have an effect on sick leave days.
Additional psychological interventions (such as online
cognitive behavioral therapy) lead to fewer sick days compared to
standard management only. Streamlining care or adding specific providers
for depression care may help to reduce sick leave.
Life expectancy and the risk of suicide
Depressed individuals have a shorter life expectancy than those without depression, in part because people who are depressed are at risk of dying of suicide. About 50% of people who die of suicide have a mood disorder
such as major depression, and the risk is especially high if a person
has a marked sense of hopelessness or has both depression and borderline personality disorder. About 2%–8% of adults with major depression die by suicide. In the US, the lifetime risk of suicide associated with a diagnosis of
major depression is estimated at 7% for men and 1% for women, even though suicide attempts are more frequent in women.
Depressed people also have a higher rate of dying from other causes. There is a 1.5- to 2-fold increased risk of cardiovascular disease,
independent of other known risk factors, and is itself linked directly
or indirectly to risk factors such as smoking and obesity. People with
major depression are less likely to follow medical recommendations for
treating and preventing cardiovascular disorders, further increasing
their risk of medical complications. Cardiologists may not recognize underlying depression that complicates a cardiovascular problem under their care.
Major depressive disorder affected approximately 163 million people in 2017 (2% of the global population). The percentage of people who are affected at one point in their life
varies from 7% in Japan to 21% in France. In most countries the number
of people who have depression during their lives falls within an 8%–18%
range. Lifetime rates are higher in the developed world (15%) compared to the developing world (11%).
In the United States, 8.4% of adults (21 million individuals)
have at least one episode within a year-long period; the probability of
having a major depressive episode is higher for females than males
(10.5% to 6.2%), and highest for those aged 18 to 25 (17%). 15% of adolescents, ages 12 to 17, in America are also affected by depression, which is equal to 3.7 million teenagers. Among individuals reporting two or more races, the US prevalence is highest. Out of all the people suffering from MDD, only about 35% seek help from a professional for their disorder.
Major depression is about twice as common in women as in men,
although it is unclear why this is so, and whether factors unaccounted
for are contributing to this. The relative increase in occurrence is related to pubertal development
rather than chronological age, reaches adult ratios between the ages of
15 and 18, and appears associated with psychosocial more than hormonal
factors. In 2019, major depressive disorder was identified (using either the DSM-IV-TR or ICD-10) in the Global Burden of Disease Study as the fifth most common cause of years lived with disability and the 18th most common for disability-adjusted life years.
People are most likely to develop their first depressive episode
between the ages of 30 and 40, and there is a second, smaller peak of
incidence between ages 50 and 60. The risk of major depression is increased with neurological conditions such as stroke, Parkinson's disease, or multiple sclerosis, and during the first year after childbirth (postpartum depression). It is also more common after cardiovascular illnesses, and is related more to those with a poor cardiac disease outcome than to a better one. Depressive disorders are more common in urban populations than in rural
ones and the prevalence is increased in groups with poorer
socioeconomic factors, such as homelessness. Depression is common among those over 65 years of age and increases in frequency beyond this age. The risk of depression increases in relation to the frailty of the individual. Depression is one of the most important factors which negatively impact quality of life in adults, as well as the elderly. Both symptoms and treatment among the elderly differ from those of the rest of the population.
Major depression was the leading cause of disease burden
in North America and other high-income countries, and the
fourth-leading cause worldwide as of 2006. In the year 2030, it is
predicted to be the second-leading cause of disease burden worldwide
after HIV/AIDS, according to the WHO. Delay or failure in seeking treatment after relapse and the failure of
health professionals to provide treatment are two barriers to reducing
disability.
Comorbidity
Major depression frequently co-occurs with other psychiatric problems. The 1990–92 National Comorbidity Survey (US) reported that half of those with major depression also have lifetime anxiety and its associated disorders, such as generalized anxiety disorder. Anxiety symptoms can have a major impact on the course of a depressive
illness, with delayed recovery, increased risk of relapse, greater
disability and increased suicidal behavior. Depressed people have increased rates of alcohol and substance use, particularly dependence, and around a third of individuals diagnosed with attention deficit hyperactivity disorder (ADHD) develop comorbid depression. Post-traumatic stress disorder and depression often co-occur. Depression may also coexist with ADHD, complicating the diagnosis and treatment of both. Depression is also frequently comorbid with alcohol use disorder and personality disorders. Depression can also be exacerbated during particular months (usually winter) in those with seasonal affective disorder. While overuse of digital media has been associated with depressive symptoms, using digital media may also improve mood in some situations.
Depression and pain
often co-occur. One or more pain symptoms are present in 65% of people
who have depression, and anywhere from 5% to 85% of people who are
experiencing pain will also have depression, depending on the setting—a
lower prevalence in general practice, and higher in specialty clinics.
Depression is often underrecognized, and therefore undertreated, in
patients presenting with pain. Depression often coexists with physical disorders common among the elderly, such as stroke, other cardiovascular diseases, Parkinson's disease, and chronic obstructive pulmonary disease.
The Ancient Greek physician Hippocrates described a syndrome of melancholia (μελαγχολία, melankholía)
as a distinct disease with particular mental and physical symptoms; he
characterized all "fears and despondencies, if they last a long time" as
being symptomatic of the ailment. It was a similar but far broader concept than today's depression;
prominence was given to a clustering of the symptoms of sadness,
dejection, and despondency, and often fear, anger, delusions and
obsessions were included.
Diagnoses of depression go back at least as far as Hippocrates.
The term depression itself was derived from the Latin verb deprimere, meaning "to press down". From the 14th century, "to depress" meant to subjugate or to bring down in spirits. It was used in 1665 in English author Richard Baker'sChronicle to refer to someone having "a great depression of spirit", and by English author Samuel Johnson in a similar sense in 1753. The term also came into use in physiology and economics. An early usage referring to a psychiatric symptom was by French psychiatrist Louis Delasiauve
in 1856, and by the 1860s it was appearing in medical dictionaries to
refer to a physiological and metaphorical lowering of emotional
function. Since Aristotle,
melancholia had been associated with men of learning and intellectual
brilliance, a hazard of contemplation and creativity. However, by the
19th century, this association has largely shifted and melancholia
became more commonly linked with women.
Although melancholia remained the dominant diagnostic term, depression gained increasing currency in medical treatises and was a synonym by the end of the century; German psychiatrist Emil Kraepelin may have been the first to use it as the overarching term, referring to different kinds of melancholia as depressive states. Freud likened the state of melancholia to mourning in his 1917 paper Mourning and Melancholia. He theorized that objective loss, such as the loss of a valued relationship through death or a romantic break-up, results in subjective loss as well; the depressed individual has identified with the object of affection through an unconscious, narcissistic process called the libidinal cathexis of the ego.
Such loss results in severe melancholic symptoms more profound than
mourning; not only is the outside world viewed negatively but the ego
itself is compromised. The person's decline of self-perception is revealed in his belief of his own blame, inferiority, and unworthiness. He also emphasized early life experiences as a predisposing factor. Adolf Meyer put forward a mixed social and biological framework emphasizing reactions in the context of an individual's life, and argued that the term depression should be used instead of melancholia. The first version of the DSM (DSM-I, 1952) contained depressive reaction and the DSM-II (1968) depressive neurosis,
defined as an excessive reaction to internal conflict or an
identifiable event, and also included a depressive type of
manic-depressive psychosis within Major affective disorders.
The term unipolar (along with the related term bipolar) was coined by the neurologist and psychiatrist Karl Kleist, and subsequently used by his disciples Edda Neele and Karl Leonhard.
The term major depressive disorder was introduced by a
group of US clinicians in the mid-1970s as part of proposals for
diagnostic criteria based on patterns of symptoms (called the "Research
Diagnostic Criteria", building on earlier Feighner Criteria), and was incorporated into the DSM-III in 1980. The American Psychiatric Association added "major depressive disorder" to the Diagnostic and Statistical Manual of Mental Disorders (DSM-III), as a split of the previous depressive neurosis in the DSM-II, which also encompassed the conditions now known as dysthymia and adjustment disorder with depressed mood. To maintain consistency the ICD-10 used the same criteria, with only
minor alterations, but using the DSM diagnostic threshold to mark a mild depressive episode, adding higher threshold categories for moderate and severe episodes. The ancient idea of melancholia still survives in the notion of a melancholic subtype.
The new definitions of depression were widely accepted, albeit
with some conflicting findings and views. There have been some continued
empirically based arguments for a return to the diagnosis of
melancholia. There has been some criticism of the expansion of coverage of the
diagnosis, related to the development and promotion of antidepressants
and the biological model since the late 1950s.
The term depression is used in a number of different ways. It is often used to mean this syndrome but may refer to other mood disorders
or simply to a low mood. People's conceptualizations of depression vary
widely, both within and among cultures. "Because of the lack of
scientific certainty," one commentator has observed, "the debate over
depression turns on questions of language. What we call it—'disease,'
'disorder,' 'state of mind'—affects how we view, diagnose, and treat
it." There are cultural differences in the extent to which serious
depression is considered an illness requiring personal professional
treatment, or an indicator of something else, such as the need to
address social or moral problems, the result of biological imbalances,
or a reflection of individual differences in the understanding of
distress that may reinforce feelings of powerlessness, and emotional
struggle.
Cultural dimension
Cultural differences contribute to different prevalence of symptoms. In their article, "Do the Chinese somatize
depression? A cross-cultural study", Parker and others discuss the
cultural differences in prevalent symptoms of depression between individualistic and collectivistic cultures. The authors reveal that individuals with depression in collectivistic cultures tend to present more somatic symptoms and less affective symptoms compared to those in individualistic cultures. The finding suggests that individualistic cultures' "warranting" or validating
of one's expression of emotions explains this cultural difference since
collectivistic cultures see this as a taboo against the social
cooperation it deems one of the most significant values.
Stigma
Historical figures were often reluctant to discuss or seek treatment for depression due to social stigma
about the condition, or due to ignorance of diagnosis or treatments.
Nevertheless, analysis or interpretation of letters, journals, artwork,
writings, or statements of family and friends of some historical
personalities has led to the presumption that they may have had some
form of depression. People who may have had depression include English
author Mary Shelley, American-British writer Henry James, and American president Abraham Lincoln. Some well-known contemporary people with possible depression include Canadian songwriter Leonard Cohen and American playwright and novelist Tennessee Williams. Some pioneering psychologists, such as Americans William James and John B. Watson, dealt with their own depression.
In 1998, the Norwegian PM Kjell Magne Bondevik publicly announced he would take a leave of absence in order to recover from a depressive episode.
There has been a continuing discussion of whether neurological
disorders and mood disorders may be linked to creativity, a discussion
that goes back to Aristotelian times. British literature gives many examples of reflections on depression. English philosopher John Stuart Mill
experienced a several-months-long period of what he called "a dull
state of nerves", when one is "unsusceptible to enjoyment or pleasurable
excitement; one of those moods when what is pleasure at other times,
becomes insipid or indifferent". He quoted English poet Samuel Taylor Coleridge's
"Dejection" as a perfect description of his case: "A grief without a
pang, void, dark and drear, / A drowsy, stifled, unimpassioned grief, /
Which finds no natural outlet or relief / In word, or sigh, or tear." English writer Samuel Johnson used the term "the black dog" in the 1780s to describe his own depression, and it was subsequently popularized by British Prime Minister Sir Winston Churchill, who also had the disorder. Johann Wolfgang von Goethe, in his Faust, Part One, published in 1808, has Mephistopheles assume the form of a black dog, specifically a poodle.
Social stigma of major depression is widespread, and contact with
mental health services reduces this only slightly. Public opinions on
depression treatment vary. While some remain skeptical about
antidepressants, recent studies show a more balanced view. Many patients
recognize their benefits but have concerns about side effects and
personality changes. In the UK, the Royal College of Psychiatrists and the Royal College of General Practitioners conducted a joint Five-year Defeat Depression campaign to educate and reduce stigma from 1992 to 1996; a MORI study conducted afterwards showed a small positive change in public attitudes to depression and treatment.
While serving his first term as Prime Minister of Norway, Kjell Magne Bondevik
attracted international attention in August 1998 when he announced that
he was suffering from a depressive episode, becoming the
highest-ranking world leader to admit to suffering from a mental illness
while in office. Upon this revelation, Anne Enger
became acting Prime Minister for three weeks, from 30 August to 23
September, while he recovered from the depressive episode. Bondevik then
returned to office. Bondevik received thousands of supportive letters,
and said that the experience had been positive overall, both for himself
and because it made mental illness more publicly acceptable.
