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Causes and Risk Factors of Depression

Nancy Schimelpfening, MS is the administrator for the non-profit depression support group Depression Sanctuary. Nancy has a lifetime of experience with depression, experiencing firsthand how devastating this illness can be.

Carly Snyder, MD is a reproductive and perinatal psychiatrist who combines traditional psychiatry with integrative medicine-based treatments.

Verywell / Joshua Seong

Common Causes of Depression

• Family History & Genetics
• Brain & Body Causes
• Lifestyle Causes
• Next in Depression Guide How Depression Is Diagnosed According to the DSM-5

If you or a loved one are struggling with depression, contact the Substance Abuse and Mental Health Services Administration (SAMHSA) National Helpline at 1-800-662-4357 for information on support and treatment facilities in your area. 

For more mental health resources, see our National Helpline Database .

Depression is one of the most common mental disorders in the United States. It can affect anyone at almost any age, but what causes depression in some people is not always known . Potential depression causes can include genetics, brain chemistry, life events, medical conditions, and lifestyle factors.

The Centers for Disease Control and Prevention reported that approximately 1 in 5 U.S. adults have received a depression diagnosis in their lifetime. The World Health Organization estimates that 5% of men and 9% of women experience depressive disorders in any given year.

This article discusses common causes of depression. It covers the genetic, biological, and environmental factors that can play a role in the condition.

Researchers suspect there are actually many different causes of depression and that it is not always preventable. Factors that can contribute to depression include:

• Brain chemistry
• Certain medical conditions
• Substance use
• Poor nutrition

Depression does not have a single cause. There are many factors that play a role in increasing the risk that a person will develop the condition. Women experience depression at higher rates than men (10.5% of women vs. 6.2% of men), which experts suggest may be due to hormonal factors.

Family History and Genetics

A family history of depression may increase your risk of developing the condition. You are more likely to experience symptoms of depression if others in your family also have depression or another type of mood disorder . Estimates suggest that depression is approximately 40% determined by genetics.

Twin, adoption, and family studies have linked depression to genetics. While studies suggest that there is a strong genetic component, researchers are not yet certain about all the genetic risk factors for depression.

Studies show that having a parent and grandparent with depression doubles the risk of having the condition.

It is still unclear exactly which genes play a role in depression, but researchers do know that there are many different genes that can play a role. By better understanding how they function, gene researchers hope to be able to create more effective treatments.

It is important to remember that no single cause of depression acts in isolation. Genetics may increase your risk and environmental influences may then determine how likely you are to develop depression. 

Brain and Body Causes of Depression

Some causes of depression are related to the brain and body. These can raise your risk for depression.

Brain Chemistry Imbalances

One potential biological cause of depression is an imbalance in the neurotransmitters which are involved in mood regulation. Certain neurotransmitters, including dopamine, serotonin , and norepinephrine, play an important role in mood.

Neurotransmitters are chemical substances that help different areas of the brain communicate with each other. When certain neurotransmitters are in short supply, it may lead to the symptoms we recognize as clinical depression.

This theory of depression suggests that having too much or too little of certain neurotransmitters causes, or at least contributes to, depression.

While this explanation is often cited as a major cause of depression, it remains unproven and many experts believe that it doesn't paint a complete picture of the complex factors that contribute to the condition.

Medications to treat depression often focus on altering the levels of certain chemicals in the brain. Some of these treatments include selective serotonin reuptake inhibitors (SSRIs) , serotonin-norepinephrine reuptake inhibitors (SNRIs), monoamine oxidase inhibitors (MAOIs), and tricyclic antidepressants (TCAs).

Physical Health and Certain Medical Conditions

You may be more likely to experience symptoms of depression if you have a chronic illness, sleep disorder, or thyroid condition. Depression rates also tend to be higher among people who have chronic pain, diabetes, multiple sclerosis, and cancer.

The mind and the body are linked. If you are experiencing a physical health problem, you may discover changes in your mental health as well. 

Illness is related to depression in two ways. The stress of having a chronic illness may trigger an episode of major depression. In addition, certain illnesses, such as thyroid disorders, Addison's disease, and liver disease, can cause depression symptoms.

Female Sex Hormones

It has been widely documented that women experience major depression about twice as often as men. Because of the incidence of depressive disorders peaks during women's reproductive years, it is believed that hormonal risk factors may be at play.

Women are especially prone to depressive disorders during times when their hormones are in flux, such as around the time of their menstrual period , pregnancy, childbirth, and perimenopause. The risk of depression declines after menopause.

Hormone fluctuations caused by childbirth and thyroid conditions can also contribute to depression. Postpartum depression may occur after childbirth and is believed to result from the rapid hormonal changes that take place immediately after giving birth.

Some Common Causes of Depression

Lifestyle causes of depression.

There are also a number of lifestyle factors that can play a role in causing depression. While many of the risk factors for depression, such as sex or family history, cannot be changed, people have much more control over lifestyle factors.

Circadian Rhythm Disturbances

One type of depression, called seasonal affective disorder  (officially known as major depressive disorder with seasonal pattern) is believed to be caused by a disturbance in the normal circadian rhythm of the body.

Light entering the eye influences this rhythm. During the shorter days of winter, when people may spend limited time outdoors, this rhythm may become disrupted.

People who reside in colder climates where there are short, dark days may be at the highest risk. 

In addition to disruptions in circadian rhythm, reduced sunlight can also lead to a drop in serotonin levels in the brain, which may influence mood. Seasonal changes can also alter melatonin levels in the body, which can disrupt sleep and contribute to mood changes.

While you cannot control seasonal shifts, there are steps you can take to minimize the effect these changes have on your mental health. Light therapy, spending more time outdoors, eating a healthy diet, and exercising regularly may help combat seasonal depression.

Poor Nutrition

A poor diet can contribute to depression in several ways. A variety of vitamin and mineral deficiencies are known to cause symptoms of depression. In addition, diets high in sugar have been associated with depression.

Some studies have found that diets either low in omega-3 fatty acids or with an imbalanced ratio of omega-6 to omega-3 fats are associated with increased rates of depression.

Stressful life events, which overwhelm a person's ability to cope, can also be a cause of depression. Researchers suspect high levels of the hormone cortisol, which are secreted during periods of stress , may affect the neurotransmitter serotonin and contribute to depression.

Grief and Loss

Following the loss of a loved one, people who are grieving experience many of the same symptoms of depression. Trouble sleeping, poor appetite, and a loss of pleasure or interest in activities are a normal response to loss.

The symptoms of grief are expected to subside over time. But when symptoms get worse, grief may turn into depression.

Substance Use

Drug and alcohol use can contribute to depressive disorders. But even some prescription drugs have been linked to depression.

Some drugs that have been found to be associated with depression include anticonvulsants, statins, stimulants, benzodiazepines, corticosteroids, and beta-blockers. It's important to review any medications that you've been prescribed and to speak with your physician if you are feeling depressed.

Centers for Disease Control and Prevention.  National, State-Level, and County-Level Prevalence Estimates of Adults Aged ≥18 Years Self-Reporting a Lifetime Diagnosis of Depression — United States, 2020 .

National Institute of Mental Health. Major depression .

Lohoff FW. Overview of the genetics of major depressive disorder . Curr Psychiatry Rep . 2010;12(6):539-546. doi:10.1007/s11920-010-0150-6

National Institute of Mental Health. Chronic illness & mental health .

Weissman MM, Berry OO, Warner V. A 30-year study of 3 generations at high risk and low risk for depression . JAMA Psychiatry . 2016;73(9):970-977. doi:10.1001/jamapsychiatry.2016.1586

Ng E, Browne CJ, Samsom JN, Wong AHC. Depression and substance use comorbidity: What we have learned from animal studies . Am J Drug Alcohol Abuse . 2017;43(4):456-474. doi:10.1080/00952990.2016.1183020

Yang L, Zhao Y, Wang Y, et al. The effects of psychological stress on depression .  Curr Neuropharmacol . 2015;13(4):494-504. doi:10.2174/1570159x1304150831150507

Knüppel A, Shipley MJ, Llewellyn CH, Brunner EJ. Sugar intake from sweet food and beverages, common mental disorder and depression: Prospective findings from the Whitehall II study .  Sci Rep . 2017;7(1):6287. doi:10.1038/s41598-017-05649-7

Larrieu T, Layé S. Food for mood: Relevance of nutritional omega-3 fatty acids for depression and anxiety .  Front Physiol . 2018;9:1047. doi:10.3389/fphys.2018.01047

Zisook S, Shear K. Grief and bereavement: What psychiatrists need to know .  World Psychiatry . 2009;8(2):67-74. doi:10.1002/j.2051-5545.2009.tb00217.x

Qato, DM, Ozenberger, K, Olfson, M.  Prevalence of prescription medications with depression as a potential adverse effect among adults in the United States . JAMA.  2018;319(22):2289-2298. doi:10.1001/jama.2018.6741

Aziz R, Steffens D. What are the causes of late-life depression? . Psychiatr Clin North Am . 2013;36(4):497-516. doi:10.1016/j.psc.2013.08.001

Wigner P, Czarny P, Galecki P, Su KP, Sliwinski T. The molecular aspects of oxidative & nitrosative stress and the tryptophan catabolites pathway (TRYCATs) as potential causes of depression .  Psychiatr Res . 2018;262:566-574. doi:10.1016/j.psychres.2017.09.045

By Nancy Schimelpfening Nancy Schimelpfening, MS is the administrator for the non-profit depression support group Depression Sanctuary. Nancy has a lifetime of experience with depression, experiencing firsthand how devastating this illness can be.  

Causes of Depression

Reviewed by Psychology Today Staff

As common as depression is—about one person in 10 experiences depression in any given year—it still eludes complete understanding. The trigger for depression can be almost any negative experience or hardship. Triggers can be external—losing a parent (especially when young), losing a job or developing a debilitating disease—or they can be internal and invisible, such a brooding over that most common of experiences, a failed relationship. People differ in their susceptibility, both by virtue of the biological heritage, their parenting heritage, their styles of thinking, the coping skills they acquire or deliberately cultivate, and the degree to which situations afford them the ability to control their fate.

On This Page

• What are the most common causes of depression?
• Does depression have some hidden trigger?
• Can stress bring on depression?
• How do thinking styles influence depression?
• Do adverse experiences always result in depression?
• How does perfectionism lead to depression?
• How does learned helplessness contribute to depression?
• What is the role of inflammation in depression?
• How does loneliness lead to depression?
• What happens in the brain with depression?
• Are there risk factors for depression?
• If my mother or father was depressed will I be depressed?
• How is depression related to anxiety?
• Why are rates of depression rising?
• Are women more susceptible to depression than men?

Studies consistently show that depression is most associated with the number of stressors experienced in life, and the effect is cumulative—the more stresses that accrue over time, the greater the likelihood of getting depressed. The loss of an important relationship by death or divorce is experienced by most people as a major stress requiring significant adjustment.

Loneliness is both a physical and emotional stressor, and rates of loneliness, known to be high among the elderly, are sharply rising among the young, who increasingly report having no close friends. Job loss or the threat of job loss are almost invariably sources of constant worry. In the absence of a wide array of coping skills, even minor bumps on life’s journey can become significant stressors.

Although depression most often arises in response to some kind of defeat, depression can seem to arise out of the blue, for no obvious reason. It may even arise when life appears to be going extremely well. What is often hidden from conscious awareness are basic beliefs about life and love and work, or ways of explaining life’s twists and turns, many of which are learned at home in the early years of life.

Additionally, people may reach goals they’ve pursued for a long time, and find that they don’t deliver the emotional rewards they secretly or openly expected. In such cases, people may feel they don’t have the right to be depressed and may even feel ashamed of being depressed. Cognitive behavioral therapy is highly effective at unearthing and correcting such problematic views.

Studies show that one factor consistently associated with depression is the number and degree of major stresses experienced in life. Poverty, for example, is a significant, enduring stressor, not easily modifiable, highly linked to depression risk. But to a degree still under study, attitude plays a major role in the perception of stress.

Some stress is necessary to keep people alert. It isn’t just that situations differ in the degree to which they stress human systems; much depends on how people regard some situations—say, taking final exams. People who see stress as a challenge rather than as a plague recruit positive rather than negative emotions. What’s more, they do not experience the harmful effects of stress hormones on body and brain.

Brooding over mistakes or unpleasant experiences, jumping to catastrophic conclusions from one or two setbacks, overgeneralizing from limited evidence—all are errors of thinking, or cognitive distortions, strongly linked to depression.

Such thinking mires the brain in negativity and, if unchecked, breed self-doubt and hopelessness. What’s more, studies show that negative thinking styles such as catastrophizing actually change physiology. Researchers have found that they enhance reactivity to painful stimulation and raise levels of the stress hormone cortisol and of pro-inflammatory agents in the blood. The inflammatory response brings on behavioral changes commonly associated with both sickness and depression—fatigue, slow reaction time, cognitive sluggishness, and loss of appetite.

Research documents that there is a strong relationship between adverse experience in childhood —such as verbal or physical abuse or household dysfunction caused by a mentally ill parent—and the lifetime risk of depression. Studies show that verbal abuse more than doubles the lifetime risk of depression. Adverse experiences are a significant source of stress.

But whether they summon resources for successful coping or lead to despair depends in part on the situation and in part on the person. A child facing verbally or physically abusive treatment at home or school who has no means of escaping continuing injury is at elevated risk for developing depression. Situations may not be subject to change—but attitudes, interpretation, and meaning of experience are always under individual control and can confer resistance to depression and other disorders..

Perfectionism is like an endless negative report card. Those in its grip don’t just hold high standards for themselves, they are perpetual self-critics, always judging themselves harshly. They focus on the very thing they most want to avoid—negative evaluation and failure. Perfectionism keeps people completely self-absorbed, always finding fault with themselves, a mindset that prevents them from taking on potentially-rewarding challenges.

Even when perfectionists complete a task, they cannot enjoy a sense of achievement; relentless concern with mistakes leads them to be haunted with uncertainty about their performance. The constant negative focus leads to a negatively distorted view of themselves, self-doubt, and feelings of inadequacy and worthlessness. Perfectionists are vulnerable to depression because their self-worth is contingent on fully achieving goals—a condition that, by definition, they can never meet.

Learned helplessness is a state of mind in which people come to believe (often through experiences of childhood abuse or neglect) that they have no way of escaping difficult or painful circumstances and therefore exert no effort to change distressing situations even when it is possible to do so. The resulting passivity can keep people from taking any measures to avoid a problem or to help themselves when one arises, or to seek help from others, compounding their own suffering and precipitating such feelings as hopelessness that are the hallmarks of depression. Because the helplessness is learned, the belief that no action matters can be unlearned; part of the cure is also gaining a realistic understanding of what can and can’t be controlled in life.

There is growing evidence that depression gives rise to inflammation and the inflammatory response creates or exacerbates depression. Neuroscientists know that there is lots of crosstalk in the brain between neural circuits and inflammatory pathways. Negative thoughts are a source of psychological pain.

Like all signs of injury, pain mobilizes various immune cells to help subdue the source, and that mobilization creates inflammation. Stress is known to activate an inflammatory response. The presence of inflammatory cells in the brain may be one reason many drug treatments for depression fail; they do not target inflammation.

Loneliness assaults the body and mind in multiple ways. By itself, it is felt as a major stress, and is linked to the release of stress hormones, which are known to impair such brain operations as learning and memory retrieval. What’s more, loneliness magnifies the perception of all other stresses. It diminishes functioning of the immune system and readily leads to inflammation, a known pathway to depression.

The emotional discomfort of loneliness makes us feel sad, and sadness saps our energy and slows functioning of all body systems. Companionship is such a powerful buffer to all human difficulty that loneliness is said to have even more of a detrimental effect on health than cigarette smoking.

Many people believe that depression is caused by a “chemical imbalance” in the brain. Experts explain that depression is far more complex and that it is unproductive to think of depression as a brain disease that is primarily biological.

Instead, depression can be viewed as a behavioral shutdown in response to overwhelmingly negative situations in which you have little personal control, lack resources for dealing with them, and have little comfort in the way of social support. The response is reflected in many operations of the brain, such as difficulty with memory, sluggishness of thinking, inability to feel pleasure, loss of appetite and interest in sex, and heightened perception of pain.

Neuroimaging studies indeed show changes in brain function among depressed people, and they are generally associated with impairments of connectivity among brain areas that normally work together. Studies also show that such changes are reversible as depression lifts.

While genetics is believed to confer some susceptibility, there is no single gene or set of genes implicated; so far, it appears that a very large number of genes—likely modifiable by diet or behavior—each contributes a very tiny degree of vulnerability that could precipitate depression under conditions of stress. People can also be at risk of depression because of their personality attributes, particularly if they have a tendency to worry a lot, have low self-esteem, are perfectionists, are sensitive to personal criticism, or are self-critical and negative. Of the Big Five personality dimensions, the one most consistently associated with depression susceptibility is the trait of neuroticism. It denotes the degree to which the negative affect system is readily activated. People high in trait neuroticism are inclined to find experiences distressing, to worry, and to doubt themselves disproportionate to the circumstances they are in. In addition, studies indicate that women are at especially high risk for depression after divorce and men are at high risk following following financial, occupational, or legal problems.

Depression can be transmitted in families in several ways. Parents and children may share an array of genes that create susceptibility to depression. Even more subtly, parents may engage in depressive thinking and explanatory styles that children acquire unwittingly in the air they breathe every day at home while growing up.

There is considerable evidence that when mothers of young children are depressed, they fail to engage with their children. As a result, babies do not acquire the strong emotional bond that enables them to grow, to withstand stress, to develop emotional regulation, and to become responsive to others. Treating depressed mothers is often the best way to treat problems in children.

Depression and anxiety are considered two faces of the same coin. Both involve brooding over experience—in depression, things that happened in the past; in anxiety, things that might happen in the future. Depression is also thought to result from sustained anxiety . More than half of all people with major depression also suffer from persistent anxiety. The two conditions share many symptoms, including insomnia, difficulty concentrating, negative thinking, and loss of appetite. Many treatments that relieve depression also relieve anxiety.

Depression rates are rising especially among the young . While the lifetime risk of depression is approximately 20 percent, for the general population the highest rates currently occur among young adults, those between the ages of 18 and 29, while individuals over 65 have the lowest rates.

Experts cite several reasons why the young are especially susceptible. They range from social factors, such as decreasing availability of meaningful work, to individual factors, such as lack of coping skills due to overprotective parenting. Cultural factors figure in, too. An increased concern with safety and decreased tolerance for risk has curtailed the opportunities children have for free play , in which children experience joy, gain friends and learn social skills, and discover how to exercise control over their own life.

Around the world, women are 1.7 times more likely to develop depression than are men, and the difference in susceptibility emerges in adolescence. Among younger women, the gender gap in depression is even greater, although before puberty, males and females have equal rates of depression. Studies pinpoint social and cultural reasons as well as biological ones.

Women more often experience internalizing symptoms, reflected in physical pain and other somatic complaints, social withdrawal, and self-blame, while men present with externalizing behaviors, reflected in irritability, anger, aggression, and substance use. In addition, childbirth is associated with a particular form of depression ; susceptibility is thought to be related in part to the rapid hormonal shifts that occur postpartum in combination with the vastly increased demands of new motherhood.

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• Systematic Review
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• Published: 20 July 2022

The serotonin theory of depression: a systematic umbrella review of the evidence

• Joanna Moncrieff 1 , 2 ,
• Ruth E. Cooper 3 ,
• Tom Stockmann 4 ,
• Simone Amendola 5 ,
• Michael P. Hengartner 6 &
• Mark A. Horowitz 1 , 2  

Molecular Psychiatry volume  28 ,  pages 3243–3256 ( 2023 ) Cite this article

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A Correspondence to this article was published on 16 June 2023

A Comment to this article was published on 16 June 2023

The serotonin hypothesis of depression is still influential. We aimed to synthesise and evaluate evidence on whether depression is associated with lowered serotonin concentration or activity in a systematic umbrella review of the principal relevant areas of research. PubMed, EMBASE and PsycINFO were searched using terms appropriate to each area of research, from their inception until December 2020. Systematic reviews, meta-analyses and large data-set analyses in the following areas were identified: serotonin and serotonin metabolite, 5-HIAA, concentrations in body fluids; serotonin 5-HT 1A receptor binding; serotonin transporter (SERT) levels measured by imaging or at post-mortem; tryptophan depletion studies; SERT gene associations and SERT gene-environment interactions. Studies of depression associated with physical conditions and specific subtypes of depression (e.g. bipolar depression) were excluded. Two independent reviewers extracted the data and assessed the quality of included studies using the AMSTAR-2, an adapted AMSTAR-2, or the STREGA for a large genetic study. The certainty of study results was assessed using a modified version of the GRADE. We did not synthesise results of individual meta-analyses because they included overlapping studies. The review was registered with PROSPERO (CRD42020207203). 17 studies were included: 12 systematic reviews and meta-analyses, 1 collaborative meta-analysis, 1 meta-analysis of large cohort studies, 1 systematic review and narrative synthesis, 1 genetic association study and 1 umbrella review. Quality of reviews was variable with some genetic studies of high quality. Two meta-analyses of overlapping studies examining the serotonin metabolite, 5-HIAA, showed no association with depression (largest n  = 1002). One meta-analysis of cohort studies of plasma serotonin showed no relationship with depression, and evidence that lowered serotonin concentration was associated with antidepressant use ( n  = 1869). Two meta-analyses of overlapping studies examining the 5-HT 1A receptor (largest n  = 561), and three meta-analyses of overlapping studies examining SERT binding (largest n  = 1845) showed weak and inconsistent evidence of reduced binding in some areas, which would be consistent with increased synaptic availability of serotonin in people with depression, if this was the original, causal abnormaly. However, effects of prior antidepressant use were not reliably excluded. One meta-analysis of tryptophan depletion studies found no effect in most healthy volunteers ( n  = 566), but weak evidence of an effect in those with a family history of depression ( n  = 75). Another systematic review ( n  = 342) and a sample of ten subsequent studies ( n  = 407) found no effect in volunteers. No systematic review of tryptophan depletion studies has been performed since 2007. The two largest and highest quality studies of the SERT gene, one genetic association study ( n  = 115,257) and one collaborative meta-analysis ( n  = 43,165), revealed no evidence of an association with depression, or of an interaction between genotype, stress and depression. The main areas of serotonin research provide no consistent evidence of there being an association between serotonin and depression, and no support for the hypothesis that depression is caused by lowered serotonin activity or concentrations. Some evidence was consistent with the possibility that long-term antidepressant use reduces serotonin concentration.

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Introduction.

The idea that depression is the result of abnormalities in brain chemicals, particularly serotonin (5-hydroxytryptamine or 5-HT), has been influential for decades, and provides an important justification for the use of antidepressants. A link between lowered serotonin and depression was first suggested in the 1960s [ 1 ], and widely publicised from the 1990s with the advent of the Selective Serotonin Reuptake Inhibitor (SSRI) antidepressants [ 2 , 3 , 4 ]. Although it has been questioned more recently [ 5 , 6 ], the serotonin theory of depression remains influential, with principal English language textbooks still giving it qualified support [ 7 , 8 ], leading researchers endorsing it [ 9 , 10 , 11 ], and much empirical research based on it [ 11 , 12 , 13 , 14 ]. Surveys suggest that 80% or more of the general public now believe it is established that depression is caused by a ‘chemical imbalance’ [ 15 , 16 ]. Many general practitioners also subscribe to this view [ 17 ] and popular websites commonly cite the theory [ 18 ].

It is often assumed that the effects of antidepressants demonstrate that depression must be at least partially caused by a brain-based chemical abnormality, and that the apparent efficacy of SSRIs shows that serotonin is implicated. Other explanations for the effects of antidepressants have been put forward, however, including the idea that they work via an amplified placebo effect or through their ability to restrict or blunt emotions in general [ 19 , 20 ].

Despite the fact that the serotonin theory of depression has been so influential, no comprehensive review has yet synthesised the relevant evidence. We conducted an ‘umbrella’ review of the principal areas of relevant research, following the model of a similar review examining prospective biomarkers of major depressive disorder [ 21 ]. We sought to establish whether the current evidence supports a role for serotonin in the aetiology of depression, and specifically whether depression is associated with indications of lowered serotonin concentrations or activity.

Search strategy and selection criteria

The present umbrella review was reported in accordance with the 2009 PRISMA statement [ 22 ]. The protocol was registered with PROSPERO in December 2020 (registration number CRD42020207203) ( https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=207203 ). This was subsequently updated to reflect our decision to modify the quality rating system for some studies to more appropriately appraise their quality, and to include a modified GRADE to assess the overall certainty of the findings in each category of the umbrella review.

In order to cover the different areas and to manage the large volume of research that has been conducted on the serotonin system, we conducted an ‘umbrella’ review. Umbrella reviews survey existing systematic reviews and meta-analyses relevant to a research question and represent one of the highest levels of evidence synthesis available [ 23 ]. Although they are traditionally restricted to systematic reviews and meta-analyses, we aimed to identify the best evidence available. Therefore, we also included some large studies that combined data from individual studies but did not employ conventional systematic review methods, and one large genetic study. The latter used nationwide databases to capture more individuals than entire meta-analyses, so is likely to provide even more reliable evidence than syntheses of individual studies.

We first conducted a scoping review to identify areas of research consistently held to provide support for the serotonin hypothesis of depression. Six areas were identified, addressing the following questions: (1) Serotonin and the serotonin metabolite 5-HIAA–whether there are lower levels of serotonin and 5-HIAA in body fluids in depression; (2) Receptors - whether serotonin receptor levels are altered in people with depression; (3) The serotonin transporter (SERT) - whether there are higher levels of the serotonin transporter in people with depression (which would lower synaptic levels of serotonin); (4) Depletion studies - whether tryptophan depletion (which lowers available serotonin) can induce depression; (5) SERT gene – whether there are higher levels of the serotonin transporter gene in people with depression; (6) Whether there is an interaction between the SERT gene and stress in depression.

We searched for systematic reviews, meta-analyses, and large database studies in these six areas in PubMed, EMBASE and PsycINFO using the Healthcare Databases Advanced Search tool provided by Health Education England and NICE (National Institute for Health and Care Excellence). Searches were conducted until December 2020.

We used the following terms in all searches: (depress* OR affective OR mood) AND (systematic OR meta-analysis), and limited searches to title and abstract, since not doing so produced numerous irrelevant hits. In addition, we used terms specific to each area of research (full details are provided in Table  S1 , Supplement). We also searched citations and consulted with experts.

Inclusion criteria were designed to identify the best available evidence in each research area and consisted of:

Research synthesis including systematic reviews, meta-analysis, umbrella reviews, individual patient meta-analysis and large dataset analysis.

Studies that involve people with depressive disorders or, for experimental studies (tryptophan depletion), those in which mood symptoms are measured as an outcome.

Studies of experimental procedures (tryptophan depletion) involving a sham or control condition.

Studies published in full in peer reviewed literature.

Where more than five systematic reviews or large analyses exist, the most recent five are included.

Exclusion criteria consisted of:

Animal studies.

Studies exclusively concerned with depression in physical conditions (e.g. post stroke or Parkinson’s disease) or exclusively focusing on specific subtypes of depression such as postpartum depression, depression in children, or depression in bipolar disorder.

No language or date restrictions were applied. In areas in which no systematic review or meta-analysis had been done within the last 10 years, we also selected the ten most recent studies at the time of searching (December 2020) for illustration of more recent findings. We performed this search using the same search string for this domain, without restricting it to systematic reviews and meta-analyses.

Data analysis

Each member of the team was allocated one to three domains of serotonin research to search and screen for eligible studies using abstract and full text review. In case of uncertainty, the entire team discussed eligibility to reach consensus.

For included studies, data were extracted by two reviewers working independently, and disagreement was resolved by consensus. Authors of papers were contacted for clarification when data was missing or unclear.

We extracted summary effects, confidence intervals and measures of statistical significance where these were reported, and, where relevant, we extracted data on heterogeneity. For summary effects in the non-genetic studies, preference was given to the extraction and reporting of effect sizes. Mean differences were converted to effect sizes where appropriate data were available.

We did not perform a meta-analysis of the individual meta-analyses in each area because they included overlapping studies [ 24 ]. All extracted data is presented in Table  1 . Sensitivity analyses were reported where they had substantial bearing on interpretation of findings.

The quality rating of systematic reviews and meta-analyses was assessed using AMSTAR-2 (A MeaSurement Tool to Assess systematic Reviews) [ 25 ]. For two studies that did not employ conventional systematic review methods [ 26 , 27 ] we used a modified version of the AMSTAR-2 (see Table  S3 ). For the genetic association study based on a large database analysis we used the STREGA assessment (STrengthening the REporting of Genetic Association Studies) (Table  S4 ) [ 28 ]. Each study was rated independently by at least two authors. We report ratings of individual items on the relevant measure, and the percentage of items that were adequately addressed by each study (Table  1 , with further detail in Tables  S3 and S4 ).

Alongside quality ratings, two team members (JM, MAH) rated the certainty of the results of each study using a modified version of the GRADE guidelines [ 29 ]. Following the approach of Kennis et al. [ 21 ], we devised six criteria relevant to the included studies: whether a unified analysis was conducted on original data; whether confounding by antidepressant use was adequately addressed; whether outcomes were pre-specified; whether results were consistent or heterogeneity was adequately addressed if present; whether there was a likelihood of publication bias; and sample size. The importance of confounding by effects of current or past antidepressant use has been highlighted in several studies [ 30 , 31 ]. The results of each study were scored 1 or 0 according to whether they fulfilled each criteria, and based on these ratings an overall judgement was made about the certainty of evidence across studies in each of the six areas of research examined. The certainty of each study was based on an algorithm that prioritised sample size and uniform analysis using original data (explained more fully in the supplementary material), following suggestions that these are the key aspects of reliability [ 27 , 32 ]. An assessment of the overall certainty of each domain of research examining the role of serotonin was determined by consensus of at least two authors and a direction of effect indicated.

Search results and quality rating

Searching identified 361 publications across the 6 different areas of research, among which seventeen studies fulfilled inclusion criteria (see Fig.  1 and Table  S1 for details of the selection process). Included studies, their characteristics and results are shown in Table  1 . As no systematic review or meta-analysis had been performed within the last 10 years on serotonin depletion, we also identified the 10 latest studies for illustration of more recent research findings (Table  2 ).

Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA) flow diagramme.

Quality ratings are summarised in Table  1 and reported in detail in Tables  S2 – S3 . The majority (11/17) of systematic reviews and meta-analyses satisfied less than 50% of criteria. Only 31% adequately assessed risk of bias in individual studies (a further 44% partially assessed this), and only 50% adequately accounted for risk of bias when interpreting the results of the review. One collaborative meta-analysis of genetic studies was considered to be of high quality due to the inclusion of several measures to ensure consistency and reliability [ 27 ]. The large genetic analysis of the effect of SERT polymorphisms on depression, satisfied 88% of the STREGA quality criteria [ 32 ].

Serotonin and 5-HIAA

Serotonin can be measured in blood, plasma, urine and CSF, but it is rapidly metabolised to 5-hydroxyindoleacetic acid (5-HIAA). CSF is thought to be the ideal resource for the study of biomarkers of putative brain diseases, since it is in contact with brain interstitial fluid [ 33 ]. However, collecting CSF samples is invasive and carries some risk, hence large-scale studies are scarce.

Three studies fulfilled inclusion criteria (Table  1 ). One meta-analysis of three large observational cohort studies of post-menopausal women, revealed lower levels of plasma 5-HT in women with depression, which did not, however, reach statistical significance of p  < 0.05 after adjusting for multiple comparisons. Sensitivity analyses revealed that antidepressants were strongly associated with lower serotonin levels independently of depression.

Two meta-analyses of a total of 19 studies of 5-HIAA in CSF (seven studies were included in both) found no evidence of an association between 5-HIAA concentrations and depression.

Fourteen different serotonin receptors have been identified, with most research on depression focusing on the 5-HT 1A receptor [ 11 , 34 ]. Since the functions of other 5-HT receptors and their relationship to depression have not been well characterised, we restricted our analysis to data on 5-HT 1A receptors [ 11 , 34 ]. 5-HT 1A receptors, known as auto-receptors, inhibit the release of serotonin pre-synaptically [ 35 ], therefore, if depression is the result of reduced serotonin activity caused by abnormalities in the 5-HT 1A receptor, people with depression would be expected to show increased activity of 5-HT 1A receptors compared to those without [ 36 ].

Two meta-analyses satisfied inclusion criteria, involving five of the same studies [ 37 , 38 ] (see Table  1 ). The majority of results across the two analyses suggested either no difference in 5-HT 1A receptors between people with depression and controls, or a lower level of these inhibitory receptors, which would imply higher concentrations or activity of serotonin in people with depression. Both meta-analyses were based on studies that predominantly involved patients who were taking or had recently taken (within 1–3 weeks of scanning) antidepressants or other types of psychiatric medication, and both sets of authors commented on the possible influence of prior or current medication on findings. In addition, one analysis was of very low quality [ 37 ], including not reporting on the numbers involved in each analysis and using one-sided p-values, and one was strongly influenced by three studies and publication bias was present [ 38 ].

The serotonin transporter (SERT)

The serotonin transporter protein (SERT) transports serotonin out of the synapse, thereby lowering the availability of serotonin in the synapse [ 39 , 40 ]. Animals with an inactivated gene for SERT have higher levels of extra-cellular serotonin in the brain than normal [ 41 , 42 , 43 ] and SSRIs are thought to work by inhibiting the action of SERT, and thus increasing levels of serotonin in the synaptic cleft [ 44 ]. Although changes in SERT may be a marker for other abnormalities, if depression is caused by low serotonin availability or activity, and if SERT is the origin of that deficit, then the amount or activity of SERT would be expected to be higher in people with depression compared to those without [ 40 ]. SERT binding potential is an index of the concentration of the serotonin transporter protein and SERT concentrations can also be measured post-mortem.

Three overlapping meta-analyses based on a total of 40 individual studies fulfilled inclusion criteria (See Table  1 ) [ 37 , 39 , 45 ]. Overall, the data indicated possible reductions in SERT binding in some brain areas, although areas in which effects were detected were not consistent across the reviews. In addition, effects of antidepressants and other medication cannot be ruled out, since most included studies mainly or exclusively involved people who had a history of taking antidepressants or other psychiatric medications. Only one meta-analysis tested effects of antidepressants, and although results were not influenced by the percentage of drug-naïve patients in each study, numbers were small so it is unlikely that medication-related effects would have been reliably detected [ 45 ]. All three reviews cited evidence from animal studies that antidepressant treatment reduces SERT [ 46 , 47 , 48 ]. None of the analyses corrected for multiple testing, and one review was of very low quality [ 37 ]. If the results do represent a positive finding that is independent of medication, they would suggest that depression is associated with higher concentrations or activity of serotonin.

Depletion studies

Tryptophan depletion using dietary means or chemicals, such as parachlorophenylalanine (PCPA), is thought to reduce serotonin levels. Since PCPA is potentially toxic, reversible tryptophan depletion using an amino acid drink that lacks tryptophan is the most commonly used method and is thought to affect serotonin within 5–7 h of ingestion. Questions remain, however, about whether either method reliably reduces brain serotonin, and about other effects including changes in brain nitrous oxide, cerebrovascular changes, reduced BDNF and amino acid imbalances that may be produced by the manipulations and might explain observed effects independent of possible changes in serotonin activity [ 49 ].

One meta-analysis and one systematic review fulfilled inclusion criteria (see Table  1 ). Data from studies involving volunteers mostly showed no effect, including a meta-analysis of parallel group studies [ 50 ]. In a small meta-analysis of within-subject studies involving 75 people with a positive family history, a minor effect was found, with people given the active depletion showing a larger decrease in mood than those who had a sham procedure [ 50 ]. Across both reviews, studies involving people diagnosed with depression showed slightly greater mood reduction following tryptophan depletion than sham treatment overall, but most participants had taken or were taking antidepressants and participant numbers were small [ 50 , 51 ].

Since these research syntheses were conducted more than 10 years ago, we searched for a systematic sample of ten recently published studies (Table  2 ). Eight studies conducted with healthy volunteers showed no effects of tryptophan depletion on mood, including the only two parallel group studies. One study presented effects in people with and without a family history of depression, and no differences were apparent in either group [ 52 ]. Two cross-over studies involving people with depression and current or recent use of antidepressants showed no convincing effects of a depletion drink [ 53 , 54 ], although one study is reported as positive mainly due to finding an improvement in mood in the group given the sham drink [ 54 ].

SERT gene and gene-stress interactions

A possible link between depression and the repeat length polymorphism in the promoter region of the SERT gene (5-HTTLPR), specifically the presence of the short repeats version, which causes lower SERT mRNA expression, has been proposed [ 55 ]. Interestingly, lower levels of SERT would produce higher levels of synaptic serotonin. However, more recently, this hypothesis has been superseded by a focus on the interaction effect between this polymorphism, depression and stress, with the idea that the short version of the polymorphism may only give rise to depression in the presence of stressful life events [ 55 , 56 ]. Unlike other areas of serotonin research, numerous systematic reviews and meta-analyses of genetic studies have been conducted, and most recently a very large analysis based on a sample from two genetic databanks. Details of the five most recent studies that have addressed the association between the SERT gene and depression, and the interaction effect are detailed in Table  1 .

Although some earlier meta-analyses of case-control studies showed a statistically significant association between the 5-HTTLPR and depression in some ethnic groups [ 57 , 58 ], two recent large, high quality studies did not find an association between the SERT gene polymorphism and depression [ 27 , 32 ]. These two studies consist of  by far the largest and most comprehensive study to date [ 32 ] and a high-quality meta-analysis that involved a consistent re-analysis of primary data across all conducted studies, including previously unpublished data, and other comprehensive quality checks [ 27 , 59 ] (see Table  1 ).

Similarly, early studies based on tens of thousands of participants suggested a statistically significant interaction between the SERT gene, forms of stress or maltreatment and depression [ 60 , 61 , 62 ], with a small odds ratio in the only study that reported this (1.18, 95% CI 1.09 to 1.28) [ 62 ]. However, the two recent large, high-quality studies did not find an interaction between the SERT gene and stress in depression (Border et al [ 32 ] and Culverhouse et al.) [ 27 ] (see Table  1 ).

Overall results

Table  3 presents the modified GRADE ratings for each study and the overall rating of the strength of evidence in each area. Areas of research that provided moderate or high certainty of evidence such as the studies of plasma serotonin and metabolites and the genetic and gene-stress interaction studies all showed no association between markers of serotonin activity and depression. Some other areas suggested findings consistent with increased serotonin activity, but evidence was of very low certainty, mainly due to small sample sizes and possible residual confounding by current or past antidepressant use. One area - the tryptophan depletion studies - showed very low certainty evidence of lowered serotonin activity or availability in a subgroup of volunteers with a family history of depression. This evidence was considered very low certainty as it derived from a subgroup of within-subject studies, numbers were small, and there was no information on medication use, which may have influenced results. Subsequent research has not confirmed an effect with numerous negative studies in volunteers.

Our comprehensive review of the major strands of research on serotonin shows there is no convincing evidence that depression is associated with, or caused by, lower serotonin concentrations or activity. Most studies found no evidence of reduced serotonin activity in people with depression compared to people without, and methods to reduce serotonin availability using tryptophan depletion do not consistently lower mood in volunteers. High quality, well-powered genetic studies effectively exclude an association between genotypes related to the serotonin system and depression, including a proposed interaction with stress. Weak evidence from some studies of serotonin 5-HT 1A receptors and levels of SERT points towards a possible association between increased serotonin activity and depression. However, these results are likely to be influenced by prior use of antidepressants and its effects on the serotonin system [ 30 , 31 ]. The effects of tryptophan depletion in some cross-over studies involving people with depression may also be mediated by antidepressants, although these are not consistently found [ 63 ].

The chemical imbalance theory of depression is still put forward by professionals [ 17 ], and the serotonin theory, in particular, has formed the basis of a considerable research effort over the last few decades [ 14 ]. The general public widely believes that depression has been convincingly demonstrated to be the result of serotonin or other chemical abnormalities [ 15 , 16 ], and this belief shapes how people understand their moods, leading to a pessimistic outlook on the outcome of depression and negative expectancies about the possibility of self-regulation of mood [ 64 , 65 , 66 ]. The idea that depression is the result of a chemical imbalance also influences decisions about whether to take or continue antidepressant medication and may discourage people from discontinuing treatment, potentially leading to lifelong dependence on these drugs [ 67 , 68 ].

As with all research synthesis, the findings of this umbrella review are dependent on the quality of the included studies, and susceptible to their limitations. Most of the included studies were rated as low quality on the AMSTAR-2, but the GRADE approach suggested some findings were reasonably robust. Most of the non-genetic studies did not reliably exclude the potential effects of previous antidepressant use and were based on relatively small numbers of participants. The genetic studies, in particular, illustrate the importance of methodological rigour and sample size. Whereas some earlier, lower quality, mostly smaller studies produced marginally positive findings, these were not confirmed in better-conducted, larger and more recent studies [ 27 , 32 ]. The identification of depression and assessment of confounders and interaction effects were limited by the data available in the original studies on which the included reviews and meta-analyses were based. Common methods such as the categorisation of continuous measures and application of linear models to non-linear data may have led to over-estimation or under-estimation of effects [ 69 , 70 ], including the interaction between stress and the SERT gene. The latest systematic review of tryptophan depletion studies was conducted in 2007, and there has been considerable research produced since then. Hence, we provided a snapshot of the most recent evidence at the time of writing, but this area requires an up to date, comprehensive data synthesis. However, the recent studies were consistent with the earlier meta-analysis with little evidence for an effect of tryptophan depletion on mood.

Although umbrella reviews typically restrict themselves to systematic reviews and meta-analyses, we aimed to provide the most comprehensive possible overview. Therefore, we chose to include meta-analyses that did not involve a systematic review and a large genetic association study on the premise that these studies contribute important data on the question of whether the serotonin hypothesis of depression is supported. As a result, the AMSTAR-2 quality rating scale, designed to evaluate the quality of conventional systematic reviews, was not easily applicable to all studies and had to be modified or replaced in some cases.

One study in this review found that antidepressant use was associated with a reduction of plasma serotonin [ 26 ], and it is possible that the evidence for reductions in SERT density and 5-HT 1A receptors in some of the included imaging study reviews may reflect compensatory adaptations to serotonin-lowering effects of prior antidepressant use. Authors of one meta-analysis also highlighted evidence of 5-HIAA levels being reduced after long-term antidepressant treatment [ 71 ]. These findings suggest that in the long-term antidepressants might produce compensatory changes [ 72 ] that are opposite to their acute effects [ 73 , 74 ]. Lowered serotonin availability has also been demonstrated in animal studies following prolonged antidepressant administration [ 75 ]. Further research is required to clarify the effects of different drugs on neurochemical systems, including the serotonin system, especially during and after long-term use, as well as the physical and psychological consequences of such effects.

This review suggests that the huge research effort based on the serotonin hypothesis has not produced convincing evidence of a biochemical basis to depression. This is consistent with research on many other biological markers [ 21 ]. We suggest it is time to acknowledge that the serotonin theory of depression is not empirically substantiated.

Data availability

All extracted data is available in the paper and supplementary materials. Further information about the decision-making for each rating for categories of the AMSTAR-2 and STREGA are available on request.

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There was no specific funding for this review. MAH is supported by a Clinical Research Fellowship from North East London NHS Foundation Trust (NELFT). This funder had no role in study design, data collection, data analysis, data interpretation, or writing of the report.

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Joanna Moncrieff & Mark A. Horowitz

Research and Development Department, Goodmayes Hospital, North East London NHS Foundation Trust, Essex, UK

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Ruth E. Cooper

Psychiatry-UK, Cornwall, UK

Tom Stockmann

Department of Dynamic and Clinical Psychology, and Health Studies, Faculty of Medicine and Psychology, Sapienza University of Rome, Rome, Italy

Simone Amendola

Department of Applied Psychology, Zurich University of Applied Sciences, Zurich, Switzerland

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JM conceived the idea for the study. JM, MAH, MPH, TS and SA designed the study. JM, MAH, MPH, TS, and SA screened articles and abstracted data. JM drafted the first version of the manuscript. JM, MAH, MPH, TS, SA, and REC contributed to the manuscript’s revision and interpretation of findings. All authors had full access to all the data in the study and had final responsibility for the decision to submit for publication.

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All authors have completed the Unified Competing Interest form at http://www.icmje.org/coi_disclosure.pdf (available on request from the corresponding author). SA declares no conflicts of interest. MAH reports being co-founder of a company in April 2022, aiming to help people safely stop antidepressants in Canada. MPH reports royalties from Palgrave Macmillan, London, UK for his book published in December, 2021, called “Evidence-biased Antidepressant Prescription.” JM receives royalties for books about psychiatric drugs, reports grants from the National Institute of Health Research outside the submitted work, that she is co-chairperson of the Critical Psychiatry Network (an informal group of psychiatrists) and a board member of the unfunded organisation, the Council for Evidence-based Psychiatry. Both are unpaid positions. TS is co-chairperson of the Critical Psychiatry Network. RC is an unpaid board member of the International Institute for Psychiatric Drug Withdrawal.

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Moncrieff, J., Cooper, R.E., Stockmann, T. et al. The serotonin theory of depression: a systematic umbrella review of the evidence. Mol Psychiatry 28 , 3243–3256 (2023). https://doi.org/10.1038/s41380-022-01661-0

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Published : 20 July 2022

Issue Date : August 2023

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Etiology of Depression: Biological and Environmental Factors in the Development of Depression

• Yiwen Hu Bishop Strachan School
• Dr. Robert Clark Mentor, University of Califonia San Diego

While depression affects 300 million people worldwide and is one of the most significant contributors to suicide, the mechanisms behind its onset remain unclear. This paper summarizes and discusses several biological and environmental factors that lead to the development of depression in an effort to demonstrate the intricate relationship between the various factors. First, an examination of the roles genetics and the external environment play in depression’s occurrence is considered by comparing adoption studies. In the next section, biological mechanisms of depression, such as alterations in neurotransmitter systems and brain networks, are explored in an analysis of previous studies and by identifying areas that require further investigation. A discussion is included of how several environmental factors, including urbanization and childhood trauma, elevate the risk of depression in certain individuals along with genetic factors. The conclusion encapsulates how various factors interact with one another and calls for further research on the precise mechanisms behind the onset of depressive symptoms. This approach is crucial for understanding the cause of depression and improvements in its treatment. 

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What is depression?

Depression (also known as major depression, major depressive disorder, or clinical depression) is a common but serious mood disorder. It causes severe symptoms that affect how a person feels, thinks, and handles daily activities, such as sleeping, eating, or working.

To be diagnosed with depression, the symptoms must be present for at least 2 weeks.

There are different types of depression, some of which develop due to specific circumstances.

• Major depression includes symptoms of depressed mood or loss of interest, most of the time for at least 2 weeks, that interfere with daily activities.
• Persistent depressive disorder (also called dysthymia or dysthymic disorder) consists of less severe symptoms of depression that last much longer, usually for at least 2 years.
• Perinatal depression is depression that occurs during pregnancy or after childbirth. Depression that begins during pregnancy is prenatal depression, and depression that begins after the baby is born is postpartum depression.
• Seasonal affective disorder is depression that comes and goes with the seasons, with symptoms typically starting in the late fall or early winter and going away during the spring and summer.
• Depression with symptoms of psychosis is a severe form of depression in which a person experiences psychosis symptoms, such as delusions (disturbing, false fixed beliefs) or hallucinations (hearing or seeing things others do not hear or see).

People with  bipolar disorder  (formerly called manic depression or manic-depressive illness) also experience depressive episodes, during which they feel sad, indifferent, or hopeless, combined with a very low activity level. But a person with bipolar disorder also experiences manic (or less severe hypomanic) episodes, or unusually elevated moods, in which they might feel very happy, irritable, or “up,” with a marked increase in activity level.

Other depressive disorders found in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5-TR)   include disruptive mood dysregulation disorder (diagnosed in children and adolescents) and premenstrual dysphoric disorder (that affects women around the time of their period).

Who gets depression?

Depression can affect people of all ages, races, ethnicities, and genders.

Women are diagnosed with depression more often than men, but men can also be depressed. Because men may be less likely to recognize, talk about, and seek help for their feelings or emotional problems, they are at greater risk of their depression symptoms being undiagnosed or undertreated.

Studies also show higher rates of depression and an increased risk for the disorder among members of the LGBTQI+ community.

What are the signs and symptoms of depression?

If you have been experiencing some of the following signs and symptoms, most of the day, nearly every day, for at least 2 weeks, you may have depression:

• Persistent sad, anxious, or “empty” mood
• Feelings of hopelessness or pessimism
• Feelings of irritability, frustration, or restlessness
• Feelings of guilt, worthlessness, or helplessness
• Loss of interest or pleasure in hobbies and activities
• Fatigue, lack of energy, or feeling slowed down
• Difficulty concentrating, remembering, or making decisions
• Difficulty sleeping, waking too early in the morning, or oversleeping
• Changes in appetite or unplanned weight changes
• Physical aches or pains, headaches, cramps, or digestive problems without a clear physical cause that do not go away with treatment
• Thoughts of death or suicide or suicide attempts

Not everyone who is depressed experiences all these symptoms. Some people experience only a few symptoms, while others experience many. Symptoms associated with depression interfere with day-to-day functioning and cause significant distress for the person experiencing them.

Depression can also involve other changes in mood or behavior that include:

• Increased anger or irritability
• Feeling restless or on edge
• Becoming withdrawn, negative, or detached
• Increased engagement in high-risk activities
• Greater impulsivity
• Increased use of alcohol or drugs
• Isolating from family and friends
• Inability to meet the responsibilities of work and family or ignoring other important roles
• Problems with sexual desire and performance

Depression can look different in men and women. Although people of all genders can feel depressed, how they express those symptoms and the behaviors they use to cope with them may differ. For example, men (as well as women) may show symptoms other than sadness, instead seeming angry or irritable. And although increased use of alcohol or drugs can be a sign of depression in anyone, men are more likely to use these substances as a coping strategy.

In some cases, mental health symptoms appear as physical problems (for example, a racing heart, tightened chest, ongoing headaches, or digestive issues). Men are often more likely to see a health care provider about these physical symptoms than their emotional ones.

Because depression tends to make people think more negatively about themselves and the world, some people may also have thoughts of suicide or self-harm.

Several persistent symptoms, in addition to low mood, are required for a diagnosis of depression, but people with only a few symptoms may benefit from treatment. The severity and frequency of symptoms and how long they last will vary depending on the person, the illness, and the stage of the illness.

If you experience signs or symptoms of depression and they persist or do not go away, talk to a health care provider. If you see signs or symptoms of depression in someone you know, encourage them to seek help from a mental health professional.

If you or someone you know is struggling or having thoughts of suicide, call or text the 988 Suicide and Crisis Lifeline   at 988 or chat at 988lifeline.org   . In life-threatening situations, call 911 .

What are the risk factors for depression?

Depression is one of the most common mental disorders in the United States . Research suggests that genetic, biological, environmental, and psychological factors play a role in depression.

Risk factors for depression can include:

• Personal or family history of depression
• Major negative life changes, trauma, or stress

Depression can happen at any age, but it often begins in adulthood. Depression is now recognized as occurring in children and adolescents, although children may express more irritability or anxiety than sadness. Many chronic mood and anxiety disorders in adults begin as high levels of anxiety in childhood.

Depression, especially in midlife or older age, can co-occur with other serious medical illnesses, such as diabetes, cancer, heart disease, chronic pain, and Parkinson’s disease. These conditions are often worse when depression is present, and research suggests that people with depression and other medical illnesses tend to have more severe symptoms of both illnesses. The Centers for Disease Control and Prevention (CDC)  has also recognized that having certain mental disorders, including depression and schizophrenia, can make people more likely to get severely ill from COVID-19.

Sometimes a physical health problem, such as thyroid disease, or medications taken for an illness cause side effects that contribute to depression. A health care provider experienced in treating these complicated illnesses can help determine the best treatment strategy. 

How is depression treated?

Depression, even the most severe cases, can be treated. The earlier treatment begins, the more effective it is. Depression is usually treated with psychotherapy , medication , or a combination of the two.

Some people experience treatment-resistant depression, which occurs when a person does not get better after trying at least two antidepressant medications. If treatments like psychotherapy and medication do not reduce depressive symptoms or the need for rapid relief from symptoms is urgent, brain stimulation therapy  may be an option to explore.

Quick tip : No two people are affected the same way by depression, and there is no "one-size-fits-all" treatment. Finding the treatment that works best for you may take trial and error.

Psychotherapies

Several types of psychotherapy (also called talk therapy or counseling) can help people with depression by teaching them new ways of thinking and behaving and helping them change habits that contribute to depression. Evidence-based approaches to treating depression include cognitive-behavioral therapy (CBT) and interpersonal therapy (IPT). Learn more about psychotherapy .

The growth of telehealth for mental health services , which offers an alternative to in-person therapy, has made it easier and more convenient for people to access care in some cases. For people who may have been hesitant to look for mental health care in the past, virtual mental health care might be an easier option.

Medications

Antidepressants are medications commonly used to treat depression. They work by changing how the brain produces or uses certain chemicals involved in mood or stress. You may need to try several different antidepressants before finding the one that improves your symptoms and has manageable side effects. A medication that has helped you or a close family member in the past will often be considered first.

Antidepressants take time—usually 4–8 weeks—to work, and problems with sleep, appetite, and concentration often improve before mood lifts. It is important to give a medication a chance to work before deciding whether it’s right for you. Learn more about mental health medications . 

New medications, such as intranasal esketamine , can have rapidly acting antidepressant effects, especially for people with treatment-resistant depression. Esketamine is a medication approved by the U.S. Food and Drug Administration (FDA)  for treatment-resistant depression. Delivered as a nasal spray in a doctor’s office, clinic, or hospital, it acts rapidly, typically within a couple of hours, to relieve depression symptoms. People who use esketamine will usually continue taking an oral antidepressant to maintain the improvement in their symptoms.

Another option for treatment-resistant depression is to take an antidepressant alongside a different type of medication that may make it more effective, such as an antipsychotic or anticonvulsant medication. Further research is needed to identify the role of these newer medications in routine practice.

If you begin taking an antidepressant, do not stop taking it without talking to a health care provider . Sometimes people taking antidepressants feel better and stop taking the medications on their own, and their depression symptoms return. When you and a health care provider have decided it is time to stop a medication, usually after a course of 9–12 months, the provider will help you slowly and safely decrease your dose. Abruptly stopping a medication can cause withdrawal symptoms.

Note : In some cases, children, teenagers, and young adults under 25 years may experience an increase in suicidal thoughts or behavior when taking antidepressants, especially in the first few weeks after starting or when the dose is changed. The FDA advises that patients of all ages taking antidepressants be watched closely, especially during the first few weeks of treatment.

If you are considering taking an antidepressant and are pregnant, planning to become pregnant, or breastfeeding, talk to a health care provider about any health risks to you or your unborn or nursing child and how to weigh those risks against the benefits of available treatment options.

To find the latest information about antidepressants, talk to a health care provider and visit the FDA website  .

Brain stimulation therapies

If psychotherapy and medication do not reduce symptoms of depression, brain stimulation therapy may be an option to explore. There are now several types of brain stimulation therapy, some of which have been authorized by the FDA to treat depression. Other brain stimulation therapies are experimental and still being investigated for mental disorders like depression.

Although brain stimulation therapies are less frequently used than psychotherapy and medication, they can play an important role in treating mental disorders in people who do not respond to other treatments. These therapies are used for most mental disorders only after psychotherapy and medication have been tried and usually continue to be used alongside these treatments.

Brain stimulation therapies act by activating or inhibiting the brain with electricity. The electricity is given directly through electrodes implanted in the brain or indirectly through electrodes placed on the scalp. The electricity can also be induced by applying magnetic fields to the head.

The brain stimulation therapies with the largest bodies of evidence include:

• Electroconvulsive therapy (ECT)
• Repetitive transcranial magnetic stimulation (rTMS)
• Vagus nerve stimulation (VNS)
• Magnetic seizure therapy (MST)
• Deep brain stimulation (DBS)

ECT and rTMS are the most widely used brain stimulation therapies, with ECT having the longest history of use. The other therapies are newer and, in some cases, still considered experimental. Other brain stimulation therapies may also hold promise for treating specific mental disorders.

ECT, rTMS, and VNS have authorization from the FDA to treat severe, treatment-resistant depression. They can be effective for people who have not been able to feel better with other treatments; people for whom medications cannot be used safely; and in severe cases where a rapid response is needed, such as when a person is catatonic, suicidal, or malnourished.

Additional types of brain stimulation therapy are being investigated for treating depression and other mental disorders. Talk to a health care provider and make sure you understand the potential benefits and risks before undergoing brain stimulation therapy. Learn more about these brain stimulation therapies .

Natural products

The FDA has not approved any natural products for treating depression. Although research is ongoing and findings are inconsistent, some people use natural products, including vitamin D and the herbal dietary supplement St. John’s wort, for depression. However, these products can come with risks. For instance, dietary supplements and natural products can limit the effectiveness of some medications or interact in dangerous or even life-threatening ways with them.

Do not use vitamin D, St. John’s wort, or other dietary supplements or natural products without talking to a health care provider. Rigorous studies must be conducted to test whether these and other natural products are safe and effective.

Daily morning light therapy is a common treatment choice for people with seasonal affective disorder (SAD). Light therapy devices are much brighter than ordinary indoor lighting and considered safe, except for people with certain eye diseases or taking medications that increase sensitivity to sunlight. As with all interventions for depression, evaluation, treatment, and follow-up by a health care provider are strongly recommended. Research into the potential role of light therapy in treating non-seasonal depression is ongoing.

How can I find help for depression?

A primary care provider is a good place to start if you’re looking for help. They can refer you to a qualified mental health professional, such as a psychologist, psychiatrist, or clinical social worker, who can help you figure out next steps. Find tips for talking with a health care provider about your mental health.

You can learn more about getting help on the NIMH website. You can also learn about finding support  and locating mental health services  in your area on the Substance Abuse and Mental Health Services Administration (SAMHSA) website. 

Once you enter treatment, you should gradually start to feel better. Here are some other things you can do outside of treatment that may help you or a loved one feel better:

• Try to get physical activity. Just 30 minutes a day of walking can boost your mood.
• Try to maintain a regular bedtime and wake-up time.
• Eat regular, healthy meals.
• Break up large tasks into small ones; do what you can as you can. Decide what must get done and what can wait.
• Try to connect with people. Talk with people you trust about how you are feeling.
• Delay making important decisions, such as getting married or divorced, or changing jobs until you feel better. Discuss decisions with people who know you well.
• Avoid using alcohol, nicotine, or drugs, including medications not prescribed for you.

How can I find a clinical trial for depression?

Clinical trials are research studies that look at new ways to prevent, detect, or treat diseases and conditions, including depression. The goal of a clinical trial is to determine if a new test or treatment works and is safe. Although people may benefit from being part of a clinical trial, they should know that the primary purpose is to gain new scientific knowledge so that others can be better helped in the future.

Researchers at NIMH and around the country conduct many studies with people with and without depression. We have new and better treatment options today because of what clinical trials have uncovered. Talk to a health care provider about clinical trials, their benefits and risks, and whether one is right for you.

To learn more or find a study, visit:

• Clinical Trials – Information for Participants : Information about clinical trials, why people might take part in a clinical trial, and what people might experience during a clinical trial
• Clinicaltrials.gov: Current Studies on Depression   : List of clinical trials funded by the National Institutes of Health (NIH) being conducted across the country
• Join a Study: Depression—Adults : List of studies currently recruiting adults with depression being conducted on the NIH campus in Bethesda, MD
• Join a Study: Depression—Children : List of studies currently recruiting children with depression being conducted on the NIH campus in Bethesda, MD
• Join a Study: Perimenopause-Related Mood Disorders : List of studies on perimenopause-related mood disorders being conducted on the NIH campus in Bethesda, MD
• Join a Study: Postpartum Depression : List of studies on postpartum depression being conducted on the NIH campus in Bethesda, MD

Where can I learn more about depression?

Free brochures and shareable resources.

• Chronic Illness and Mental Health: Recognizing and Treating Depression : This brochure provides information about depression for people living with chronic illnesses, including children and adolescents. It discusses signs and symptoms, risk factors, and treatment options.
• Depression : This brochure provides information about depression, including different types of depression, signs and symptoms, how it is diagnosed, treatment options, and how to find help for yourself or a loved one.
• Depression in Women: 4 Things to Know : This fact sheet provides information about depression in women, including signs and symptoms, types of depression unique to women, and how to get help.
• Perinatal Depression : This brochure provides information about perinatal depression, including how it differs from “baby blues,” causes, signs and symptoms, treatment options, and how to find help for yourself or a loved one.
• Seasonal Affective Disorder : This fact sheet provides information about seasonal affective disorder, including signs and symptoms, how it is diagnosed, causes, and treatment options.
• Seasonal Affective Disorder (SAD): More Than the Winter Blues : This infographic provides information about how to recognize the symptoms of SAD and what to do to get help.
• Teen Depression: More Than Just Moodiness : This fact sheet is for teens and young adults and provides information about how to recognize the symptoms of depression and what to do to get help.
• Digital Shareables on Depression : These digital resources, including graphics and messages, can be used to spread the word about depression and help promote depression awareness and education in your community.

Federal resources

• Depression   (MedlinePlus - also en español  )
• Moms’ Mental Health Matters: Depression and Anxiety Around Pregnancy   ( Eunice Kennedy Shriver National Institute of Child Health and Human Development)

Research and statistics

• Journal Articles   : This webpage provides articles and abstracts on depression from MEDLINE/PubMed (National Library of Medicine).
• Statistics: Major Depression : This webpage provides the statistics currently available on the prevalence and treatment of depression among people in the United States.
• Depression Mental Health Minute : Take a mental health minute to watch this video on depression.
• NIMH Experts Discuss the Menopause Transition and Depression : Learn about the signs and symptoms, treatments, and latest research on depression during menopause.
• NIMH Expert Discusses Seasonal Affective Disorder : Learn about the signs and symptoms, treatments, and latest research on seasonal affective disorder.
• Discover NIMH: Personalized and Targeted Brain Stimulation Therapies : Watch this video describing repetitive transcranial magnetic stimulation and electroconvulsive therapy for treatment-resistant depression. Brain stimulation therapies can be effective treatments for people with depression and other mental disorders. NIMH supports studies exploring how to make brain stimulation therapies more personalized while reducing side effects.
• Discover NIMH: Drug Discovery and Development : One of the most exciting breakthroughs from research funded by NIMH is the development of a fast-acting medication for treatment-resistant depression based on ketamine. This video shares the story of how ketamine infusions meaningfully changed the life of a participant in an NIMH clinical trial.
• Mental Health Matters Podcast: Depression: The Case for Ketamine : Dr. Carlos Zarate Jr. discusses esketamine—the medication he helped discover—for treatment-resistant depression. The podcast covers the history behind the development of esketamine, how it can help with depression, and what the future holds for this innovative line of clinical research.

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• Depression (major depressive disorder)
• What is depression? A Mayo Clinic expert explains.

Learn more about depression from Craig Sawchuk, Ph.D., L.P., clinical psychologist at Mayo Clinic.

Hi, I'm Dr. Craig Sawchuk, a clinical psychologist at Mayo Clinic. And I'm here to talk with you about depression. Whether you're looking for answers for yourself, a friend, or loved one, understanding the basics of depression can help you take the next step.

Depression is a mood disorder that causes feelings of sadness that won't go away. Unfortunately, there's a lot of stigma around depression. Depression isn't a weakness or a character flaw. It's not about being in a bad mood, and people who experience depression can't just snap out of it. Depression is a common, serious, and treatable condition. If you're experiencing depression, you're not alone. It honestly affects people of all ages and races and biological sexes, income levels and educational backgrounds. Approximately one in six people will experience a major depressive episode at some point in their lifetime, while up to 16 million adults each year suffer from clinical depression. There are many types of symptoms that make up depression. Emotionally, you may feel sad or down or irritable or even apathetic. Physically, the body really slows down. You feel tired. Your sleep is often disrupted. It's really hard to get yourself motivated. Your thinking also changes. It can just be hard to concentrate. Your thoughts tend to be much more negative. You can be really hard on yourself, feel hopeless and helpless about things. And even in some cases, have thoughts of not wanting to live. Behaviorally, you just want to pull back and withdraw from others, activities, and day-to-day responsibilities. These symptoms all work together to keep you trapped in a cycle of depression. Symptoms of depression are different for everyone. Some symptoms may be a sign of another disorder or medical condition. That's why it's important to get an accurate diagnosis.

While there's no single cause of depression, most experts believe there's a combination of biological, social, and psychological factors that contribute to depression risk. Biologically, we think about genetics or a family history of depression, health conditions such as diabetes, heart disease or thyroid disorders, and even hormonal changes that happen over the lifespan, such as pregnancy and menopause. Changes in brain chemistry, especially disruptions in neurotransmitters like serotonin, that play an important role in regulating many bodily functions, including mood, sleep, and appetite, are thought to play a particularly important role in depression. Socially stressful and traumatic life events, limited access to resources such as food, housing, and health care, and a lack of social support all contribute to depression risk. Psychologically, we think of how negative thoughts and problematic coping behaviors, such as avoidance and substance use, increase our vulnerability to depression.

The good news is that treatment helps. Effective treatments for depression exist and you do have options to see what works best for you. Lifestyle changes that improve sleep habits, exercise, and address underlying health conditions can be an important first step. Medications such as antidepressants can be helpful in alleviating depressive symptoms. Therapy, especially cognitive behavioral therapy, teaches skills to better manage negative thoughts and improve coping behaviors to help break you out of cycles of depression. Whatever the cause, remember that depression is not your fault and it can be treated.

To help diagnose depression, your health care provider may use a physical exam, lab tests, or a mental health evaluation. These results will help identify various treatment options that best fit your situation.

Help is available. You don't have to deal with depression by yourself. Take the next step and reach out. If you're hesitant to talk to a health care provider, talk to a friend or loved one about how to get help. Living with depression isn't easy and you're not alone in your struggles. Always remember that effective treatments and supports are available to help you start feeling better. Want to learn more about depression? Visit mayoclinic.org. Do take care.

Depression is a mood disorder that causes a persistent feeling of sadness and loss of interest. Also called major depressive disorder or clinical depression, it affects how you feel, think and behave and can lead to a variety of emotional and physical problems. You may have trouble doing normal day-to-day activities, and sometimes you may feel as if life isn't worth living.

More than just a bout of the blues, depression isn't a weakness and you can't simply "snap out" of it. Depression may require long-term treatment. But don't get discouraged. Most people with depression feel better with medication, psychotherapy or both.

Depression care at Mayo Clinic

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Although depression may occur only once during your life, people typically have multiple episodes. During these episodes, symptoms occur most of the day, nearly every day and may include:

• Feelings of sadness, tearfulness, emptiness or hopelessness
• Angry outbursts, irritability or frustration, even over small matters
• Loss of interest or pleasure in most or all normal activities, such as sex, hobbies or sports
• Sleep disturbances, including insomnia or sleeping too much
• Tiredness and lack of energy, so even small tasks take extra effort
• Reduced appetite and weight loss or increased cravings for food and weight gain
• Anxiety, agitation or restlessness
• Slowed thinking, speaking or body movements
• Feelings of worthlessness or guilt, fixating on past failures or self-blame
• Trouble thinking, concentrating, making decisions and remembering things
• Frequent or recurrent thoughts of death, suicidal thoughts, suicide attempts or suicide
• Unexplained physical problems, such as back pain or headaches

For many people with depression, symptoms usually are severe enough to cause noticeable problems in day-to-day activities, such as work, school, social activities or relationships with others. Some people may feel generally miserable or unhappy without really knowing why.

Depression symptoms in children and teens

Common signs and symptoms of depression in children and teenagers are similar to those of adults, but there can be some differences.

• In younger children, symptoms of depression may include sadness, irritability, clinginess, worry, aches and pains, refusing to go to school, or being underweight.
• In teens, symptoms may include sadness, irritability, feeling negative and worthless, anger, poor performance or poor attendance at school, feeling misunderstood and extremely sensitive, using recreational drugs or alcohol, eating or sleeping too much, self-harm, loss of interest in normal activities, and avoidance of social interaction.

Depression symptoms in older adults

Depression is not a normal part of growing older, and it should never be taken lightly. Unfortunately, depression often goes undiagnosed and untreated in older adults, and they may feel reluctant to seek help. Symptoms of depression may be different or less obvious in older adults, such as:

• Memory difficulties or personality changes
• Physical aches or pain
• Fatigue, loss of appetite, sleep problems or loss of interest in sex — not caused by a medical condition or medication
• Often wanting to stay at home, rather than going out to socialize or doing new things
• Suicidal thinking or feelings, especially in older men

When to see a doctor

If you feel depressed, make an appointment to see your doctor or mental health professional as soon as you can. If you're reluctant to seek treatment, talk to a friend or loved one, any health care professional, a faith leader, or someone else you trust.

When to get emergency help

If you think you may hurt yourself or attempt suicide, call 911 in the U.S. or your local emergency number immediately.

Also consider these options if you're having suicidal thoughts:

• Call your doctor or mental health professional.
• Contact a suicide hotline.
• In the U.S., call or text 988 to reach the 988 Suicide & Crisis Lifeline, available 24 hours a day, seven days a week. Or use the Lifeline Chat . Services are free and confidential.
• U.S. veterans or service members who are in crisis can call 988 and then press “1” for the Veterans Crisis Line . Or text 838255. Or chat online .
• The Suicide & Crisis Lifeline in the U.S. has a Spanish language phone line at 1-888-628-9454 (toll-free).
• Reach out to a close friend or loved one.
• Contact a minister, spiritual leader or someone else in your faith community.

If you have a loved one who is in danger of suicide or has made a suicide attempt, make sure someone stays with that person. Call 911 or your local emergency number immediately. Or, if you think you can do so safely, take the person to the nearest hospital emergency room.

More Information

Depression (major depressive disorder) care at Mayo Clinic

• Male depression: Understanding the issues
• Nervous breakdown: What does it mean?
• Pain and depression: Is there a link?

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It's not known exactly what causes depression. As with many mental disorders, a variety of factors may be involved, such as:

• Biological differences. People with depression appear to have physical changes in their brains. The significance of these changes is still uncertain, but may eventually help pinpoint causes.
• Brain chemistry. Neurotransmitters are naturally occurring brain chemicals that likely play a role in depression. Recent research indicates that changes in the function and effect of these neurotransmitters and how they interact with neurocircuits involved in maintaining mood stability may play a significant role in depression and its treatment.
• Hormones. Changes in the body's balance of hormones may be involved in causing or triggering depression. Hormone changes can result with pregnancy and during the weeks or months after delivery (postpartum) and from thyroid problems, menopause or a number of other conditions.
• Inherited traits. Depression is more common in people whose blood relatives also have this condition. Researchers are trying to find genes that may be involved in causing depression.
• Marijuana and depression
• Vitamin B-12 and depression

Risk factors

Depression often begins in the teens, 20s or 30s, but it can happen at any age. More women than men are diagnosed with depression, but this may be due in part because women are more likely to seek treatment.

Factors that seem to increase the risk of developing or triggering depression include:

• Certain personality traits, such as low self-esteem and being too dependent, self-critical or pessimistic
• Traumatic or stressful events, such as physical or sexual abuse, the death or loss of a loved one, a difficult relationship, or financial problems
• Blood relatives with a history of depression, bipolar disorder, alcoholism or suicide
• Being lesbian, gay, bisexual or transgender, or having variations in the development of genital organs that aren't clearly male or female (intersex) in an unsupportive situation
• History of other mental health disorders, such as anxiety disorder, eating disorders or post-traumatic stress disorder
• Abuse of alcohol or recreational drugs
• Serious or chronic illness, including cancer, stroke, chronic pain or heart disease
• Certain medications, such as some high blood pressure medications or sleeping pills (talk to your doctor before stopping any medication)

Complications

Depression is a serious disorder that can take a terrible toll on you and your family. Depression often gets worse if it isn't treated, resulting in emotional, behavioral and health problems that affect every area of your life.

Examples of complications associated with depression include:

• Excess weight or obesity, which can lead to heart disease and diabetes
• Pain or physical illness
• Alcohol or drug misuse
• Anxiety, panic disorder or social phobia
• Family conflicts, relationship difficulties, and work or school problems
• Social isolation
• Suicidal feelings, suicide attempts or suicide
• Self-mutilation, such as cutting
• Premature death from medical conditions
• Depression and anxiety: Can I have both?

There's no sure way to prevent depression. However, these strategies may help.

• Take steps to control stress, to increase your resilience and boost your self-esteem.
• Reach out to family and friends, especially in times of crisis, to help you weather rough spells.
• Get treatment at the earliest sign of a problem to help prevent depression from worsening.
• Consider getting long-term maintenance treatment to help prevent a relapse of symptoms.
• Brown AY. Allscripts EPSi. Mayo Clinic, Rochester, Minn. Nov. 17, 2016.
• Research report: Psychiatry and psychology, 2016-2017. Mayo Clinic. http://www.mayo.edu/research/departments-divisions/department-psychiatry-psychology/overview?_ga=1.199925222.939187614.1464371889. Accessed Jan. 23, 2017.
• Depressive disorders. In: Diagnostic and Statistical Manual of Mental Disorders DSM-5. 5th ed. Arlington, Va.: American Psychiatric Association; 2013. http://www.psychiatryonline.org. Accessed Jan. 23, 2017.
• Depression. National Institute of Mental Health. https://www.nimh.nih.gov/health/topics/depression/index.shtml. Accessed Jan. 23, 2017.
• Depression. National Alliance on Mental Illness. http://www.nami.org/Learn-More/Mental-Health-Conditions/Depression/Overview. Accessed Jan. 23, 2017.
• Depression: What you need to know. National Institute of Mental Health. https://www.nimh.nih.gov/health/publications/depression-what-you-need-to-know/index.shtml. Accessed Jan. 23, 2017.
• What is depression? American Psychiatric Association. https://www.psychiatry.org/patients-families/depression/what-is-depression. Accessed Jan. 23, 2017.
• Depression. NIH Senior Health. https://nihseniorhealth.gov/depression/aboutdepression/01.html. Accessed Jan. 23, 2017.
• Children’s mental health: Anxiety and depression. Centers for Disease Control and Prevention. https://www.cdc.gov/childrensmentalhealth/depression.html#depression. Accessed. Jan. 23, 2017.
• Depression and complementary health approaches: What the science says. National Center for Complementary and Integrative Health. https://nccih.nih.gov/health/providers/digest/depression-science. Accessed Jan. 23, 2017.
• Depression. Natural Medicines. https://naturalmedicines.therapeuticresearch.com/databases/medical-conditions/d/depression.aspx. Accessed Jan. 23, 2017.
• Natural medicines in the clinical management of depression. Natural Medicines. http://naturaldatabase.therapeuticresearch.com/ce/CECourse.aspx?cs=naturalstandard&s=ND&pm=5&pc=15-111. Accessed Jan. 23, 2017.
• The road to resilience. American Psychological Association. http://www.apa.org/helpcenter/road-resilience.aspx. Accessed Jan. 23, 2017.
• Simon G, et al. Unipolar depression in adults: Choosing initial treatment. http://www.uptodate.com/home. Accessed Jan. 23, 2017.
• Stewart D, et al. Risks of antidepressants during pregnancy: Selective serotonin reuptake inhibitors (SSRIs). http://www.uptodate.com/home. Accessed Jan. 23, 2017.
• Kimmel MC, et al. Safety of infant exposure to antidepressants and benzodiazepines through breastfeeding. http://www.uptodate.com/home. Accessed Jan. 23, 2017.
• Bipolar and related disorders. In: Diagnostic and Statistical Manual of Mental Disorders DSM-5. 5th ed. Arlington, Va.: American Psychiatric Association; 2013. http://www.psychiatryonline.org. Accessed Jan. 23, 2017.
• Hirsch M, et al. Monoamine oxidase inhibitors (MAOIs) for treating depressed adults. http://www.uptodate.com/home. Accessed Jan. 24, 2017.
• Hall-Flavin DK (expert opinion). Mayo Clinic, Rochester, Minn. Jan. 31, 2017.
• Krieger CA (expert opinion). Mayo Clinic, Rochester, Minn. Feb. 2, 2017.
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Depression and Its Causes in the Modern Society Essay

Various people have different opinions when it comes to analyzing the quality of life in the 21 st century. According to popular opinions, modern life is an easy affair that has a ton of conveniences for 21 st century human beings. Modern people are able to cure most diseases and lead easier lives as compared to those individuals who lived in the past. Consequently, it is expected that the people who live in the modern times would have high levels of happiness.

However, the list of the leading problems for the 21 st century humanity includes global warming, conflict, cancer, and depression. The inclusion of depression in this list negates the possibility of the 21 st century man being the ‘happiest among them all’. Depression has become a pandemic in the modern times. In addition, depression is currently responsible for increased drug abuse, conflict, and suicide rates. Therefore, it is important to examine what has contributed to the high instances of depression in modern times.

Studies indicate that women are at a higher risk of developing depression than men are. For instance, statistics indicate that while about twenty-five percent of American women suffer from depression, only about twelve percent of men suffer from similar predicaments (Galambos, Leadbeater and Barker 16). The higher instances of depression among women can be explained using a number of reasons including the lifestyle of the modern woman and her role in the society. The modern woman is a career woman, a caregiver, a mother, a businesswoman, a wife, a housekeeper, and a political leader among others.

In the past, the role of a woman was restricted to domestic chores and procreation. The increased pressures that have been piled upon the modern woman might explain why depression is more prevalent among women. The increased dimensions of pressure among the modern women might also help to explain why the rest of the population is depressed. The modern life presents individuals with endless possibilities and this piles pressure on the people who are forced to make tough decisions about their lives. Moreover, modern women have to deal with other external pressures such as marital strain, hormonal changes, and hereditary deficiencies.

Another cause of depression in the modern society involves low self-esteem. In the modern society wealth, career success, and political power are often flaunted for all to see. There are displays of wealth in the media and all other possible avenues. The blatant displays of success and good fortune are likely to become a constant bother to individuals with low self-esteem.

In addition, the modern society is more materialistic than most of the others that existed in the past. For instance, a good number of depression cases involve individuals losing their jobs, houses, and companies (Brown and Harris 45). In the past, there were other social descriptors that were strong enough to rival wealth. People who do not believe that they are good enough to find their own success can easily fall into depression cycles.

The social fabric of the modern society has deteriorated and this has made personal struggles difficult to handle. In the past, the social fabric was intact and problems were handled in a more communal manner than they are dealt with today. Today, people find themselves deserted when they are dealing with difficult life events such as childhood traumas, divorces, and bereavement.

Lack of social and moral support whenever people are dealing with personal issues is a common cause of depression. In addition, there are various genetic predispositions that increase instances of depression among individuals. However, individuals who are predisposed to depression can avoid suffering from this condition by investing in social capital.

There is a complicated relationship between alcohol and substance abuse on one hand, and depression on the other. It is difficult to establish if alcohol is the source of depression or vice versa. For instance, people who take up social drinking might end up depressed while sufferers of depression are likely to turn to drugs and alcohol for comfort.

Nevertheless, alcohol is a known cause of depression especially in cases that involve genetic predispositions. On the other hand, people who seek to lessen their burdens by turning to alcohol and other drugs often end up with chronic cases of depression. Experts have described alcohol as “a depressant which increases a person’s chances of developing depression” (Klein and Wender 18).

There are various causes of depression in the modern society. However, the general consensus is that depression is easily aggravated by a combination of factors. Women are at a higher risk of suffering from depression than men. The modern society’s promotion of displays of affluence is also another factor that is likely to cause depression among individuals with low self-esteem.

The institution of the modern society also discourages individuals from sharing their problems with other members of their societies. The lack of social dependence among individuals is a known cause of depression in the modern society. Alcohol is another known cause of depression in the modern society. The future society will continue to deal with various scopes of depression. Meanwhile, it is up to the current society to institute measures to curb runaway depression.

Works Cited

Brown, George, and Tirril Harris. Social origins of depression , New York: Routledge, 2012. Print.

Galambos, Nancy, Bonnie Leadbeater, and Erin Barker. “Gender differences in and risk

factors for depression in adolescence: A 4-year longitudinal study.” International Journal of Behavioral Development 28.1 (2008): 16-25. Print.

Klein, Donald F., and Paul H. Wender. Understanding depression: A complete guide to

its diagnosis and treatment , Oxford: Oxford University Press, 2005. Print.

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Home — Essay Samples — Nursing & Health — Depression — Depression And Its Main Causes

Depression and Its Main Causes

• Categories: Cognitive Behavioral Therapy Depression Mental Health

About this sample

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Published: Jan 28, 2021

Words: 1373 | Pages: 3 | 7 min read

• Beyondblue. (n.d.). Retrieved from https://www.beyondblue.org.au/the-facts/depression/treatments-for-depression/psychological-treatments-for-depression
• Hannibal, J. (2012). Psychology for the IB diploma. Oxford: Oxford University Press, 149-61.
• Harvard Health Publishing. (n.d.). What causes depression? Retrieved from https://www.health.harvard.edu/mind-and-mood/what-causes-depression
• Lyness, D. (Ed.). (2016, August). Why Do People Get Depressed? (for Teens). Retrieved from https://kidshealth.org/en/teens/why-depressed.html
• Morin, A., & Lcsw. (n.d.). How Many People Are Actually Affected by Depression Every Year? Retrieved from https://www.verywellmind.com/depression-statistics-everyone-should-know-4159056
• Schimelpfening, N., & Gans, S. (n.d.). Why Some People Are More Prone to Depression Than Others. Retrieved from https://www.verywellmind.com/why-are-some-people-more-prone-to-depression-1067622

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Your chance of acceptance, your chancing factors, extracurriculars, college essay on depression.

I've been dealing with depression for a while and I feel like it's played a big part in shaping who I am today. Is it a good idea to write my college essay about it? Will admissions officers view it negatively? Any insights would be appreciated.

Writing about depression in your college essay can be a powerful and meaningful way to share your personal experiences and reflect on your growth. However, it's essential to approach the topic thoughtfully and carefully, as mental health is a sensitive subject.

1. Focus on growth and resilience: Instead of primarily describing your struggles with depression, emphasize how you've navigated those challenges and grown as a result. Discuss coping strategies, support systems, and other positive changes you've made that have helped you move forward.

2. Show self-awareness: Demonstrate an understanding of your situation and acknowledge your progress, while still recognizing that recovering from depression is an ongoing journey. This can give college admissions officers a sense of maturity and emotional intelligence on your part.

3. Keep it relevant to your college goals: Connect your experiences with depression to your educational and career aspirations. Perhaps overcoming depression has influenced your choice of major, or it has motivated you to engage in volunteer work or other extracurricular activities.

4. Seek feedback from trusted individuals: Ask someone you trust, like a teacher or counselor, to review your essay and provide input. Their perspectives can ensure that you're discussing depression sensitively and that your essay is appropriate for college admissions officers.

5. Be cautious of oversharing: While it's important to be genuine and authentic, avoid revealing deeply personal or disturbing details about your mental health struggles. Some admissions officers may not be comfortable with this level of disclosure, and it could overshadow your accomplishments and other positive aspects of your application.

In summary, writing about depression in your college essay is a personal choice. If you can present your experiences in a thoughtful, growth-focused manner, and connect your journey to your future goals, then it may be a powerful and effective essay topic. However, always consider seeking feedback from trusted individuals to ensure you are addressing the topic appropriately.

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