psychology research articles on depression

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• June 01, 2024 | VOL. 181, NO. 6 CURRENT ISSUE pp.461-564
• May 01, 2024 | VOL. 181, NO. 5 pp.347-460
• April 01, 2024 | VOL. 181, NO. 4 pp.255-346
• March 01, 2024 | VOL. 181, NO. 3 pp.171-254
• February 01, 2024 | VOL. 181, NO. 2 pp.83-170
• January 01, 2024 | VOL. 181, NO. 1 pp.1-82

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Insights and Advances Into Treatments for Major Depression

• Ned H. Kalin , M.D.

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This issue of the Journal is broadly focused on mood disorders, with an emphasis on understanding how treatments for major depressive disorder may work and how the efficacy of current neuromodulation and antidepressant medication treatment strategies can be enhanced. The issue begins with an overview by Drs. Manish Jha and Sanjay Matthew on treatment-resistant depression ( 1 ); they focus on augmentation strategies with atypical antipsychotic medications as well as other new treatment strategies. This issue also includes 1) a study that starts to provide a genetic framework for understanding heterogeneity in bipolar disorder as characterized by the number of depressive and manic episodes an individual experiences; 2) the long-term relation, and interaction, between different degrees of alcohol use and depression; 3) a study that characterizes functional brain connectivity changes associated with treatment outcomes for cognitive behavioral therapy versus antidepressant medication; and 4) two studies aimed at optimizing treatment outcomes for depressed patients: one addressing the utility of using functionally defined dorsolateral prefrontal cortex coordinates for transcranial magnetic stimulation treatment, the other presenting clinical trial data assessing the efficacy of cariprazine as an adjunctive treatment to enhance antidepressant responses in patients with major depression.

Bipolar Illness Life Course Heterogeneity in Relation to Polygenic Risk Scores

At the individual level, there is marked heterogeneity in the life course of bipolar illness, as it is characterized by varying admixtures of depressive, manic, and mixed episodes. Hasseris et al. ( 2 ) use polygenic risk scores (PRS) for bipolar disorder, major depression, and schizophrenia to help understand the factors underlying this heterogeneity. For this analysis the investigators used data from a sample of 2,705 genotyped individuals drawn from the Integrative Psychiatric Research Case Cohort (iPSYCH2015) who were diagnosed with bipolar disorder at a hospital in Denmark. Individuals were included in the study if they had their first documented episode between 10 and 35 years of age, and the median age of follow-up was 5 years after initial diagnosis. As has been reported in other studies, PRS for bipolar disorder, major depression, and schizophrenia were significantly intercorrelated with each other. The authors also found that the bipolar and schizophrenia PRS were significantly correlated with an individual’s number of affective episodes regardless of polarity. In relation to manic episodes, both bipolar and schizophrenia PRS were related to the number of episodes, whereas the depression PRS were associated with depressive and mixed episodes and negatively associated with manic episodes. The researchers also examined PRS in relation to psychotic symptoms and in these analyses found that the bipolar PRS were associated with both psychotic and nonpsychotic manic episodes, the schizophrenia PRS were only associated with psychotic manic episodes, and the major depression PRS were associated with a reduced likelihood of psychotic symptoms regardless of episode polarity. These findings are interesting because they begin to help explain the genetic differences that are related to the likelihood of experiencing depression, mania, and mixed episodes in the context of a life course of bipolar disorder. In an editorial ( 3 ), Dr. John Kelsoe from the University of California San Diego discusses the genetic findings from this paper in relation to other clinical and treatment outcome data that are associated with bipolar disorder heterogeneity. He also provides a valuable discussion on the use of PRS in psychiatry and their potential limitations.

The Longitudinal Relationship Between Alcohol Use and Depressive Symptoms

Visontay et al. ( 4 ) use a large longitudinal database along with a statistical approach that allows for making assumptions related to causality to understand the association between different amounts of alcohol consumption and depressive symptoms. Data drawn from the National Longitudinal Survey of Youth 1979 came from 5,667 participants beginning at ages 29–37. Longitudinal data up until age 41–49 were available from 3,593 of the participants. At different time points, participants’ alcohol use was assessed and characterized as abstinent (no drinking), occasional consumption (less than 1 day/week; no heavy episodic drinking), moderate consumption (greater than or equal to 1 day/week with no more than seven drinks/week for women and no more than 14 drinks/week for men; no heavy episodic drinking), and consumption above guidelines (greater than or equal to 1 day/week and more than seven drinks/week for women and 14 drinks/week or more for men; and/or heavy episodic drinking). Depression symptoms were derived from the Centre for Epidemiological Studies-Depression Scale short form. Using analytic methods that incorporate marginal structural models, significant protective effects were observed for the consistent occasional and consistent moderate alcohol drinkers such that, compared with abstainers, they were likely to have lower depression scores at 50 years of age. In contrast, when compared with abstainers the consistent above-guideline drinkers were found to have nonsignificantly higher depression symptoms. Similar findings were observed when categorical analyses were performed in relation to the likelihood of individuals having syndromal depression. The authors point out that these findings are consistent with previous reports and with the statistical method used they assert that the results may provide support for a statistically based causal relation between different amounts of alcohol use and depression. Dr. Edward Nunes from Columbia University contributes an editorial ( 5 ) that further discusses the intertwined relation between depression and alcohol use and more specifically addresses the clinical relevance of the findings from this paper.

Functional Brain Changes Associated With the Successful Treatment of Depression With CBT or Antidepressants

Both antidepressants and cognitive behavioral therapy (CBT) are effective treatments for major depression and evidence supports that they are most effective when combined. While the specific mechanisms underlying the efficacy of these treatments are not understood, they are hypothesized to, in part, be due to the modification of different neural pathways. In this regard, Dunlop and colleagues ( 6 ) use resting-state functional MRI to assess brain changes associated with remission from major depression. A primary goal of the study was to compare changes in brain activity between psychotherapeutic and psychopharmacologic interventions. The study used resting-state functional connectivity (RSFC) data from 131 individuals collected at the beginning and end of a randomized clinical trial in which treatment-naive depressed patients received either 16 weeks of CBT, duloxetine 30–60 mg/day, or escitalopram 10–20 mg/day. Seed-based analyses were performed to assess RSFC using a posterior cingulate cortex seed for the default mode network, dorsolateral prefrontal cortex seed for the executive control network, anterior insular cortex seed for the salience network, and subgenual cingulate cortex seed for the affective network. Data from the two antidepressant medication treatment groups were combined in the analysis. First, shared brain changes in remitters were assessed across all treatment groups (N=64 of 131), and next data from antidepressant remitters (N=45 of 91) were compared with data from CBT remitters (N=19 of 40). Across both treatments, remitters (Hamilton Depression Score [HAM-D] ≤ 7), and nonresponders (≥50% reduction HAM-D) demonstrated significantly decreased RSFC between the subgenual anterior cingulate and motor cortices. Numerous differential changes in RSFC were detected when comparing CBT with antidepressant medication remitters involving connectivity patterns of the executive control network, the affective network, and the salience network. For example, when using the dorsolateral prefrontal cortex as a seed, its connectivity with the left inferior parietal lobule increased in CBT remitters and decreased in antidepressant remitters. Likewise, when using the subgenual cingulate cortex seed, increased connectivity with the posterior insula was observed in the CBT responders, whereas decreased connectivity occurred in the antidepressant responders. In the discussion section, the authors emphasize the finding that CBT remitters, and not antidepressant remitters, showed increased connectivity between the executive control network and attention-related regions. In an editorial ( 7 ), Dr. Stephen Strakowski from Indiana University discusses the difficulties in replicating findings in studies of this nature and cautions the reader to consider the findings as preliminary. He also highlights the potential importance and veracity of the findings defining the functional brain changes that are associated with successful CBT treatment.

Assessing the Utility of Functional Connectivity Measures in Directing rTMS Targeting for Treating Depression

The subgenual anterior cingulate cortex (sgACC) serves as an integrative hub between regulatory prefrontal cortical regions and emotion-related limbic structures, such as the amygdala, and altered sgACC function has often been associated with depression. Furthermore, this region has also been used as a deep brain stimulation target for the treatment of refractory depression. In relation to repetitive transcranial magnetic stimulation (rTMS), a number of studies, yielding somewhat mixed results, have assessed the value of using negative functional connectivity measures between the left dorsolateral prefrontal cortex (dlPFC) stimulation site and sgACC as a means to improve rTMS targeting. Elbau et al. ( 8 ) present data from a large sample, 295 participants, with the goal of further understanding the extent to which individualized functional connectivity measures between the left dlPFC stimulation site and sgACC predict treatment outcomes. The resting functional MRI data used for the analyses came from a sample of individuals with treatment-resistant depression that previously participated in a noninferiority clinical trial designed to compare 10Hz rTMS to theta burst TMS ( 9 ). It is important to note that the same neuroanatomical coordinates for the left dlPFC TMS stimulation site were used across all the subjects, and this was based on neuroanatomical coordinates from an earlier study that linked functional connectivity measures to optimal outcomes. In other treatment studies, individualized dlPFC stimulation sites are selected based on the dlPFC region that is most negatively functionally coupled to sgACC ( 10 ). The current study is distinguished by its large sample, and the thorough analytic approach that was used, which included electric field modeling to estimate the actual subregions of dlPFC in which electrical changes were induced. The authors found that pretreatment individual differences in negative functional coupling between the dlPFC stimulation site and sgACC accounted for 3% of the variance in treatment outcomes. While this is a considerably smaller effect than previously reported, it is important to consider that the method used here did not prospectively select the dlPFC site that was most functionally connected with sgACC. It is interesting that the strongest effects for the predictive value of the functional coupling between the stimulation site and sgACC were found to be in a subgroup of patients that had a distinct breathing pattern characterized as “burst breathing.” Burst breathing, which is associated with a pattern of BOLD signal fluctuations across the brain, also has distinct impacts on resting connectivity that differ from individuals that typically engage in other forms of breathing such as deep breathing ( 11 ). In their editorial ( 12 ), Dr. Noah Phillips from Brown University and Dr. Shan Siddiqi from Harvard Medical School discuss this finding in relation to earlier work and comment on important methodological issues as they relate to the small but significant predictive effect that was observed.

A Double-Blind Randomized Clinical Trial Assessing the Efficacy of Cariprazine as an Adjunctive Treatment for Major Depression

Sachs and colleagues ( 13 ) report data from a Phase III study that is aimed at assessing the extent to which cariprazine is an effective add-on treatment for individuals with major depression that have not responded to their current treatment. This study builds on earlier studies with cariprazine and on studies demonstrating the efficacy of other atypical antipsychotic medications as adjunctive treatments for major depressive disorder, some of which have received FDA approval (i.e., aripiprazole, quetiapine, and brexpiprazole). Cariprazine was also recently approved by the FDA as an adjunctive treatment for major depression and is also approved for treating schizophrenia and bipolar disorder (mania, depression, and mixed). Cariprazine has multiple neurochemical effects, including acting as a partial agonist at the D 3 , D 2 , and 5-HT1 A receptors with highest selectivity for D 3 . It also acts as a 5-HT 2B and 5-HT 2A partial antagonist. In this 6-week, double-blind study, patients with major depression remained on their antidepressant treatment and also received either placebo, cariprazine 1.5 mg/day, or cariprazine 1.5 mg for 2 weeks and then increased to 3 mg/day. A total of 751 patients were included in the modified intention-to-treat analysis. In relation to the primary outcome measure, change in Montgomery-Asberg Depression Rating Scale (MADRS), cariprazine 1.5mg/d resulted in significantly greater decreases when compared with placebo; however the effects of the 3.0 mg/day dose were not statistically significant. The effect of the 1.5 mg/day dose was found to be significant after 2 weeks of drug administration. Change in the Clinical Global Inventory scale was used as the secondary outcome measure and while both doses of cariprazine were associated with greater reductions than placebo, neither reached statistical significance. Regarding response and remission rates, the 1.5-mg dose of cariprazine demonstrated significantly greater response rates compared with placebo (≥50% MADRS reduction: cariprazine=44.0%, placebo=34.9%) whereas no significant differences were found for remission rates (MADRS≤10: 25.2% versus 23.3%, respectively. Among the side effects, the cariprazine-treated patients experienced more akathisia (3mg group– 7.9%, 1.5mg group −5.2% compared to placebo group-0.8%). In an editorial ( 14 ), Dr. Michael Thase from the University of Pennsylvania discusses the specific findings related to cariprazine as well as the overall utility of second-generation antipsychotics in treating depression.

Conclusions

Major depression is very common with profound deleterious consequences at individual and societal levels in terms of suffering, disability, increased medical morbidity and mortality, and suicide. We clearly need better treatments for major depression as our current treatments are ineffective or intolerable for numerous individuals. This issue of the Journal brings together papers that are focused on how we can better understand mood disorders and improve the efficacy of our treatments. From these papers we learn: 1) by using polygenic risks scores we can begin to understand the heterogeneity in the course of bipolar disorder; 2) that moderate alcohol intake may be associated with a decreased risk of depression whereas the opposite may be the case with excessive alcohol use; 3) that remission in depressed patients treated with CBT or antidepressants is associated with shared and distinct patterns of treatment-associated change in functional connectivity between specific brain networks; 4) the value of using functional connectivity measures between the dlPFC and sgACC to predict and enhance rTMS treatment outcomes; and 5) the potential efficacy of adjunctive cariprazine treatment, in addition to other atypical antipsychotic medications, for patients not responding to their antidepressant treatment.

The papers in this issue of the Journal are helping to move us in the direction of improving our interventions for depression by building on and attempting to optimize existing treatment strategies. Continued neuroscientific investigations linked with clinical translational efforts are imperative to deepen our understanding of the mechanisms underlying mood disorders with the hope of developing more effective treatments that are directly aimed at these mechanisms.

Disclosures of Editors’ financial relationships appear in the April 2022 issue of the Journal .

1. Jha MK, Mathew SJ : Pharmacotherapies for treatment-resistant depression: how antipsychotics fit in the rapidly evolving therapeutic landscape . Am J Psychiatry 2023 ; 180:190–199 Abstract ,  Google Scholar

2. Hasseris S, Albiñana C, Vilhjalmsson BJ, et al. : Polygenic risk and episode polarity among individuals with bipolar disorder . Am J Psychiatry 2023 ; 180:200–208 Abstract ,  Google Scholar

3. Kelsoe JR : Polygenic polarity in bipolar disorder . Am J Psychiatry 2023 ; 180:177–178 Google Scholar

4. Visontay R, Mewton L, Slade T, et al. : Moderate alcohol consumption and depression: a marginal structural model approach promoting causal inference . Am J Psychiatry 2023 ; 180:209–217 Abstract ,  Google Scholar

5. Nunes EV : Alcohol and the etiology of depression . Am J Psychiatry 2023 ; 180:179–181 Abstract ,  Google Scholar

6. Dunlop BW, Cha J, Choi KS, et al. : Shared and unique changes in brain connectivity among depressed patients after remission with pharmacotherapy versus psychotherapy . Am J Psychiatry 2023 ; 180:218–229 Link ,  Google Scholar

7. Strakowski SM : Applying functional imaging to clinical practice: are we making progress toward its promise? Am J Psychiatry 2023 :180:182–184 Abstract ,  Google Scholar

8. Elbau IG, Lynch CJ, Downar J, et al. : Functional connectivity mapping for rTMS target selection in depression . Am J Psychiatry 2023 ; 180:230–240 Link ,  Google Scholar

9. Blumberger DM, Vila-Rodriguez F, Thorpe KE, et al. : Effectiveness of theta burst versus high-frequency repetitive transcranial magnetic stimulation in patients with depression (THREE-D): a randomised non-inferiority trial . Lancet 2018 ; 391:1683–1692 Crossref , Medline ,  Google Scholar

10. Lynch CJ, Silver BM, Dubin MJ, et al. : Prevalent and sex-biased breathing patterns modify functional connectivity MRI in young adults . Nat Commun 2020 ; 11:5290 Crossref , Medline ,  Google Scholar

11. Cole EJ, Phillips AL, Bentzley BS, et al. : Stanford Neuromodulation Therapy (SNT): a double-blind randomized controlled trial . Am J Psychiatry 2022 ; 179:132–141 Link ,  Google Scholar

12. Siddiqi SH, Philip NS : Hitting the target of image-guided psychiatry? Am J Psychiatry 2023 ; 180:185–187 Abstract ,  Google Scholar

13. Sachs GS, Yeung PP, Rekeda L, et al. : Adjunctive cariprazine for the treatment of patients with major depressive disorder: a randomized, double-blind, placebo-controlled phase 3 study . Am J Psychiatry 2023 ; 180:241–251 Link ,  Google Scholar

14. Thase ME : A new option for depressed patients who do not respond to antidepressant medications . Am J Psychiatry 2023 ; 180:188–189 Abstract ,  Google Scholar

• Cited by None

• Depressive Disorders
• pharmacotherapy
• neurostimulation
• antidepressants

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Depression articles from across Nature Portfolio

Depression refers to a state of low mood that can be accompanied with loss of interest in activities that the individual normally perceived as pleasurable, altered appetite and sleep/wake balance. Its severe form, major depression is classified as a mood disorder.

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Dissociable effects of dopaminergic medications on depression symptom dimensions in Parkinson disease

In this Article, the authors investigate dissociable effects of dopaminergic medications and different depression symptom dimensions in patients with Parkinson disease, suggesting a role for dopamine agonists as a potential treatment.

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MDMA therapy for PTSD rejected by FDA panel

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Overcoming depression: How psychologists help with depressive disorders

Depression is extreme sadness or despair that lasts more than days and affects people in different ways. Fortunately, depression is highly treatable.

Everyone experiences sadness at times. But depression is something more. Depression is extreme sadness or despair that lasts more than days. It interferes with the activities of daily life and can even cause physical pain. Fortunately, depression is highly treatable.

Depression, also known as major depressive disorder or clinical depression, is one of the most common mental disorders in the United States. In 2020, an estimated 21 million adults in the U.S.—about 8.4% of all U.S. adults—had at least one major depressive episode , according to the National Institute of Mental Health (NIMH).

Understanding depression

Depression affects different people in different ways, but most of them experience some combination of the following symptoms:

• Prolonged sadness or feelings of emptiness
• Feelings of helplessness or hopelessness
• Feelings of guilt or worthlessness
• Anger and irritability
• Restlessness
• Difficulty concentrating
• Changes in sleep patterns
• Appetite changes
• Chronic pain, headaches, or stomachaches
• Loss of interest in activities
• Withdrawal from friends and family
• Thoughts of death or suicide

Depression is caused by a combination of genetic, biological, psychological, social, and environmental factors. People who have a family history of depression, and people with serious chronic diseases such as heart disease or cancer, are at an increased risk of depression. Major life changes, trauma, and stress can also bring about an episode of depression, although some episodes of depression begin without any obvious external cause.

Treatment for depression

Depression isn’t a sign of weakness. It’s not something you can just “snap out of.” It’s an illness that requires professional treatment. Yet with the right care, people can feel better.

Antidepressant medications can be helpful for reducing depression symptoms in some people, especially in people with severe depression. Psychotherapy is also an effective treatment, either alone or in combination with medications. The benefits of psychotherapy may have an enduring effect that protects against symptoms returning even after treatment is ended.

Seeing a psychologist about depression

Licensed psychologists are highly trained mental health professionals with experience in helping patients recover from depression. Several different approaches to psychotherapy have been shown to help individuals recover from depression, especially those with mild to moderate depression. Psychotherapy can help people with depression to:

• Pinpoint life events that contribute to their depression and help them find ways to change, accept or adapt to those situations
• Set realistic goals for the future
• Identify distorted thought processes or unhelpful behaviors that contribute to feelings of hopelessness and helplessness
• Develop skills to cope with symptoms and problems, and identify or prevent future episodes of depression

Two of the most common evidence-based therapies for depression are cognitive behavioral therapy and interpersonal therapy.

• Cognitive behavioral therapy (CBT) is a type of therapy in which patients learn to identify and manage negative thought and behavior patterns that can contribute to their depression. CBT helps patients identify unhelpful or negative thinking, change inaccurate beliefs, change behaviors that might make depression worse, and interact with others in more positive ways.
• Interpersonal therapy (IPT) is a form of therapy in which patients learn to improve their relationships with others by better expressing their emotions and solving problems in healthier ways. IPT helps patients resolve or adapt to troubling life events, build social skills, and organize their relationships to increase support for coping with depressive symptoms and life stressors.

There is no one “right” approach to therapy. Therapists work closely with their patients to create tailored treatment plans to address their unique needs and concerns. Psychotherapy can help patients learn ways to better cope with stress and manage their symptoms of depression. These strategies can lead to recovery and enable patients to function at their best.

To find a licensed psychologist in your area, use our Psychologist Locator .

Depression in children and adolescents

Depression is common in adolescents. In 2020, an estimated 4.1 million children age 12–17 in the U.S. (about 17% of 12–17 year olds in the U.S.) had at least one major depressive episode, according to NIMH.

Adolescents are often moody. But if your child is extremely irritable, has ongoing problems with motivation, or has persistent sadness that lasts two weeks or more, it’s a good idea to have him or her evaluated for depression.

While antidepressant medications can be effective for children and adolescents, they can have side effects in young people, including an increased risk of suicidal thoughts. For that reason, many parents and health care providers prefer to try treating children with psychotherapy first. Both CBT and IPT are effective treatments for young people with depression. Studies also show that a combination of antidepressant medication and cognitive behavior therapy is highly effective in treating youth depression.

The good news is that most kids recover from depression. Still, research shows that people who have depression as children are at a higher risk of having a recurrence later in adolescence or adulthood. Both CBT and IPT can help kids recognize the signs of a depressive episode, so that they can monitor their symptoms and get help quickly if they experience a recurrence.

APA gratefully acknowledges Laura Mufson, PhD, Lynn Bufka, PhD, and C. Vaile Wright, PhD, for contributing to this fact sheet.

Recommended Reading

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• Seasonal affective disorder: More than the winter blues
• Clinical Practice Guideline for the Treatment of Depression Across Three Age Cohorts
• How to find help through seeing a psychologist

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REVIEW article

Child and adolescent depression: a review of theories, evaluation instruments, prevention programs, and treatments.

• 1 Developmental and Educational Department, University of the Basque Country, Donostia/San Sebastián, Spain
• 2 Developmental and Educational Psychology Department, University of the Basque Country, Lejona, Spain
• 3 Personality, Evaluation and Psychological Treatments Department, University of the Basque Country, Donostia/San Sebastián, Spain

Depression is the principal cause of illness and disability in the world. Studies charting the prevalence of depression among children and adolescents report high percentages of youngsters in both groups with depressive symptoms. This review analyzes the construct and explanatory theories of depression and offers a succinct overview of the main evaluation instruments used to measure this disorder in children and adolescents, as well as the prevention programs developed for the school environment and the different types of clinical treatment provided. The analysis reveals that in mental classifications, the child depression construct is no different from the adult one, and that multiple explanatory theories must be taken into account in order to arrive at a full understanding of depression. Consequently, both treatment and prevention should also be multifactorial in nature. Although universal programs may be more appropriate due to their broad scope of application, the results are inconclusive and fail to demonstrate any solid long-term efficacy. In conclusion, we can state that: (1) There are biological factors (such as tryptophan—a building block for serotonin-depletion, for example) which strongly influence the appearance of depressive disorders; (2) Currently, negative interpersonal relations and relations with one's environment, coupled with social-cultural changes, may explain the increase observed in the prevalence of depression; (3) Many instruments can be used to evaluate depression, but it is necessary to continue to adapt tests for diagnosing the condition at an early age; (4) Prevention programs should be developed for and implemented at an early age; and (5) The majority of treatments are becoming increasingly rigorous and effective. Given that initial manifestations of depression may occur from a very early age, further and more in-depth research is required into the biological, psychological and social factors that, in an interrelated manner, may explain the appearance, development, and treatment of depression.

Introduction

Depression is the principal cause of illness and disability in the world. The World Health Organization (WHO) has been issuing warnings about this pathology for years, given that it affects over 300 million people all over the world and is characterized by a high risk of suicide (the second most common cause of death in those aged between 15 and 29) [ World Health Organization (WHO), 2017 ]. Studies on the child population which use self-reports to evaluate severe symptoms of depression, specifically the Children's Depression Inventory (CDI, Kovacs, 1992 ) and the Children's Depression Scale (CDS, Lang and Tisher, 1978 ), have observed prevalence rates of, for example, 4% in Spain ( Demir et al., 2011 ; Bernaras et al., 2013 ), 6% in Finland ( Puura et al., 1997 ), 8% in Greece ( Kleftaras and Didaskalou, 2006 ), 10% in Australia ( McCabe et al., 2011 ), and 25% in Colombia ( Vinaccia et al., 2006 ). The main classifications of mental disorders are the Diagnostic and Statistical Manual of Mental Disorders, DSM-5 ( American Psychiatric Association, 2014 ), published by the American Psychiatric Association, which has become a key reference in clinical practice, and version 10 of the International Classification of Diseases (ICD-10, 1992), published by the WHO, which classifies and codifies all diseases, although initially its aim was to chart mortality rates. The new ICD-11 classification will be presented for approval to Member States at the World Health Assembly in May 2019, and is expected to come into effect on January 1, 2022 [ World Health Organization (WHO), 2018 ]. The two classifications offer different categorizations of depressive disorders, although certain similarities do exist, and it should be borne in mind also that both have been criticized for hardly distinguishing at all between child and adult depression.

Throughout history, there have been many different explanatory theories of depression. Biological and psychological theories are the ones which have mainly tried to explain the origin of this mental disorder. Biological theories have, from a variety of different perspectives, postulated that depression may occur due to noradrenalin deficits (e.g., Schildkraut, 1965 ; Narbona, 2014 ), endocrine disorders (e.g. Birmaher et al., 1996 ), sleep-related disorders (e.g., Sivertsen et al., 2014 ; Pariante, 2017 ), alterations in brain structure ( Whittle et al., 2014 ), or the influence of genetics ( Scourfield et al., 2003 ). Psychological theories have attempted to explain depression on the basis of psychoanalysis and, more specifically, in terms of attachment theories (e.g., Bowlby, 1976 ; Ainsworth et al., 1978 ; Blatt, 2004 ; Bigelow et al., 2018 ), behavioral models (e.g., Skinner, 1953 ; Ferster, 1966 ; Lewinsohn, 1975 ), cognitive models (e.g., Seligman, 1975 ; Abramson et al., 1978 ; Beck, 1987 ), the self-control model (e.g., Rehm, 1977 ; Rehm et al., 1979 ), interpersonal theory (e.g., Markowitz and Weissman, 1995 ; Milrod et al., 2014 ), stressful life events (e.g., Reinherz et al., 1993 ; Frank et al., 1994 ), and sociocultural models (e.g., Lorenzo-Blanco et al., 2012 ; Chang et al., 2013 ; Reeves et al., 2014 ).

Evaluating depression accurately has been another concern upon which psychology has focused, with attention being centered specifically around diagnosing this pathology in childhood and adolescence. Although many diagnostic instruments have been developed and validated, mainly for the adolescent and adult stages of life, it is still difficult to find diagnostic tests for evaluating depression in children. Preventing depression is another aspect to which much importance is attached by the World Health Organization (WHO) (2017) , which argues that school programs, interventions aimed at parents and specific exercises for the elderly population help reduce the prevalence of this pathology. Depression prevention programs do exist, but they are mainly targeted at adolescents and very few focus on children under the age of 10.

The treatment of depression is another aspect that should not be overlooked. In 2016, the WHO and the World Bank announced that investing in the treatment of depression and anxiety leads to four-fold returns, since these pathologies cost the global economy one trillion US dollars each year. Furthermore, they claimed that humanitarian emergencies and conflicts highlight a pressing need to broaden current therapeutic options. In this sense, the multiple different explanatory theories of depression have given rise to a plethora of different treatments (psychotherapeutic, behavioral, cognitive-behavioral, interpersonal, etc.) which are currently being analyzed with a high degree of precision and scientific rigor.

In light of the different aspects related to depression outlined above, the present study has the following aims: (1) To analyze the construct of depression offered by the two main mental disorder classifications (DSM-5 and ICD-10); (2) To provide an overview of the main explanatory theories of depression; (3) To outline the child and adolescent depression evaluation instruments most commonly used in scientific literature; (4) To provide a brief overview of child and adolescent depression prevention programs in the school environment; and (5) To describe the most scientifically rigorous and effective clinical treatments for this mental disorder.

The databases used for carrying out the searches were PubMed, PsycINFO, Web of Science, Scopus, Science Direct and Google Scholar, along with a range of different manuscripts. With the constant key word being depression, the search for information cross-referenced a series of other key words also, namely: childhood, adolescence, explanatory theories, etiology, evaluation instruments, prevention programs, and treatment. Searches were conducted for information published between 1970 and 2017.

Thus, first we describe the construct of depression and summarize the main explanatory theories. Next, we present the main evaluation instruments used to measure child and adolescent depression and report the results of a bibliographical review of prevention programs in school settings. Finally, we outline the main clinical treatments used nowadays to treat child and adolescent depression.

The Construct of Depression: DSM-5 and ICD-10

Depression features in both of the two most important global classifications: the DSM-5 and the ICD-10. As stated earlier in the introduction, the new ICD-11 classification will be presented for approval to Member States at the World Health Assembly in May 2019, and is expected to come into effect on January 1, 2022. The presentation of the new classification in 2019 will enable countries to plan for its implementation, prepare the necessary translations and train professionals accordingly [ World Health Organization (WHO), 2018 ]. In texts published by WHO collaborators ( Luciano, 2017 ), it has been suggested that the ICD-11 will include mood disorders within the mental and behavioral disorder category. However, until the final version is published, this information cannot be fully verified.

The two classifications (DSM-5 e IDC-10) offer different categorizations of depressive disorders, as shown in Table 1 . The WHO includes depressive disorders in the mood disorders category, although this review only focuses on Sections F32, F33, F34, and F38, which include the most frequent depressive disorders and which, in turn, contain subsections that will be further specified later on.

Table 1 . Depressive disorders according to the DSM-5 and the ICD-10.

According to the DSM-5, depressive disorders all have one common feature, namely the presence of sad, empty or irritable mood, accompanied by somatic and cognitive changes that significantly affect the individual's capacity to function (DSM-5). They may become a serious health problem if allowed to persist for long periods of time and occur with a moderate-to-severe degree of intensity. One important consequence of depression is the risk of suicide, which is, according the World Health Organization (WHO) (2017) , the second most common cause of death among young people aged between 15 and 29.

The main novelty offered by the DSM-5 in its section on depressive disorders is the introduction to Disruptive mood dysregulation disorder (which should not be diagnosed before the age of 6 or after the age of 18). This disorder is characterized by severe recurrent temper outbursts manifested verbally (e.g., verbal rages) and/or behaviorally (e.g., physical aggression toward people or property). These outbursts often occur as the result of frustration and in order to be considered a diagnostic criterion must be inconsistent with the individual's developmental level, occur three or more times per week for at least a year in a number of different settings (at home, at school, etc.) and be severe in at least one of these. This disorder was added to the DSM-5 due to doubts arising in relation to how to classify and treat children presenting with chronic persistent irritability as opposed to other related disorders, specifically pediatric bipolar disorder. The prevalence of this disorder has been estimated at between 2 and 5%, with male children and teenage boys being more likely to suffer from it than their female counterparts.

Major Depressive Disorder

Major depressive disorder is characterized by a depressed mood most of the day, nearly every day, although in children and adolescents this mood may be irritable rather than depressed. The disorder causes a markedly diminished interest or pleasure in all, or almost all, activities most of the day, nearly every day, significant weight loss or gain, insomnia or hypersomnia, psychomotor agitation or retardation, fatigue or loss of energy, feelings of worthlessness, or excessive or inappropriate guilt, diminished ability to think or concentrate, recurrent thoughts of death, recurrent suicidal ideation without a specific plan, or a suicide attempt or a specific plan for committing suicide. These symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning. In the United States, the 12-month prevalence is ~7%, although it is three times higher among those aged between 18 and 29 than among those aged 60 or over. Moreover, the prevalence rates for women are ~1.5–3 times higher than for men.

Persistent Depressive Disorder (Dysthymia)

Persistent depressive disorder (dysthymia) is a consolidation of DSM-5-defined chronic major depressive disorder and dysthymic disorder, and is characterized by a depressed mood for most of the day, for more days than not, for at least 2 years. In children and adolescents, mood can be irritable and duration must be at least 1 year. The DSM-5 specifies that patients presenting symptoms that comply with the diagnostic criteria for major depressive disorder for 2 years should also be diagnosed with persistent depressive disorder. When the individual in question is experiencing a depressive mood episode, they must also present at least two of the following symptoms: poor appetite or overeating, insomnia or hypersomnia, low energy or fatigue, low self-esteem, poor concentration, or difficulty making decisions and feelings of hopelessness. The prevalence of this disorder in the United States is 0.5%.

Premenstrual Dysphoric Disorder

The diagnostic criterion for premenstrual dysphoric disorder states that, in the majority of menstrual cycles, at least five symptoms must be present during the last week before the start of menstruation, and individuals should start to feel better a few days later, with all symptoms disappearing completely or almost completely during the week after menstruation. The most important characteristics of this disorder are affective lability, intense irritability or anger, or increased interpersonal conflicts, markedly depressed mood and/or over-excitation, and symptoms of anxiety which may be accompanied by behavioral and somatic symptoms. Symptoms must be present during most menstrual cycles during the past year and must negatively affect occupational and social functioning. The most rigorous estimations of the prevalence of this disorder claim that 1.8% of women comply with the criterion but have no functional impairment, while 1.3% comply with the criterion and suffer functional impairment and other concomitant symptoms of another mental disorder.

Substance/Medication-Induced Depressive Disorder

Substance/medication-induced depressive disorder is characterized by the presence of the symptoms of a depressive disorder, such as major depressive disorder, induced by the consumption, inhalation or injection of a substance, with said symptoms persisting after the physiological effects or the effects of intoxication or withdrawal have disappeared. Some medication may generate depressive symptoms, which is why it is important to determine whether the symptoms were actually induced by the taking of the drug or whether the depressive disorder simply appeared during the period in which the medication was being taken. The prevalence of this disorder in the United States is 0.26%.

Depressive Disorder Due to Another Medical Condition

Depressive disorder due to another medical condition is characterized by the appearance of a depressed mood and a markedly diminished interest or pleasure in all activities within the context of another medical condition. The DSM-5 offers no information about the prevalence of this disorder.

The category Other specified depressive disorder is used when the symptoms characteristic of a depressive disorder appear and cause significant distress or impairment in social, occupational or other areas of functioning but do not comply with all the criteria of any depressive disorder, and the clinician opts to communicate the specific reason for this. In the Other unspecified depressive disorder category , on the other hand, the difference is that the clinician prefers not to specify the reason why the presentation fails to comply with all the criteria of a specific disorder and includes presentations about which there is insufficient information for giving a more specific diagnosis.

In the ICD-10, depressive disorders are included within the mood disorders category. The following disorders are analyzed below: single depressive episode, recurrent depressive disorder, and persistent mood (affective) disorders.

Single Depressive Episode

The classification Single depressive episode distinguishes between depressive episodes of varying severity: mild, moderate, and severe without psychotic symptoms. Characteristics common to all of them include lowering of mood, reduction of energy, and decrease in daily activity. There is a loss of interest in formerly pleasurable pursuits, a decrease in the capacity for concentration, and an increase in tiredness, even during activities requiring minimum effort. Changes occur in appetite, sleep is disturbed, self-esteem and self-confidence drop, ideas of guilt or worthlessness are present and the symptoms vary little from day to day. In its mildest form, two or three of the symptoms described above may be present, and the patient is able to continue with most of their daily activities. When the episode is moderate, four or more of the symptoms are usually present and the patient is likely to have difficulty continuing with ordinary activities. In its most severe form, several of the symptoms are marked and distressing, typically loss of self-esteem and ideas of worthlessness or guilt. Suicidal thoughts and acts are common and a number of somatic symptoms are usually present. If the depressive episode is with psychotic symptoms, it is characterized by the presence of hallucinations, delusions, psychomotor retardation, or stupor so severe that ordinary social activities are impossible; there may be danger to life from suicide, dehydration, or starvation.

Recurrent Depressive Disorder

Recurrent depressive disorder is characterized by repeated episodes of depression similar to those described above for single depressive episodes without mania. There may be brief episodes of mild mood elevation and over activity (hypomania) immediately after a depressive episode, sometimes precipitated by antidepressant treatment. The more severe forms of this disorder are very similar to manic-depressive depression, melancholia, vital depression, and endogenous depression. The first episode may occur at any age, from childhood to old age. The onset may be either acute or insidious and can last from a few weeks to many months. Recurrent depressive disorder can be mild or moderate, but in neither of these is there any history of mania. This section also includes recurrent depressive disorder currently in remission, in which the patient may have had two or more depressive episodes in the past, but has been free from depressive symptoms for several months.

Persistent Mood [Affective] Disorders

Persistent mood [affective] disorders are persistent and usually fluctuating disorders in which the majority of episodes are not sufficiently severe to warrant being diagnosed as hypomanic or mild depressive episodes. Since they last for many years and affect the patient's normal life, they involve considerable distress and disability. This section also includes cyclothymia and dysthymia. Cyclothymia is a persistent instability of mood involving numerous periods of depression and mild elation, none of which are sufficiently prolonged to justify a diagnosis of bipolar affective disorder or recurrent depressive disorder. This disorder is frequently found among the relatives of patients with bipolar affective disorder and some patients with cyclothymia eventually develop bipolar affective disorder. For its part, dysthymia is a chronic depression of mood, lasting at least several years, which is not sufficiently severe, or in which individual episodes are not sufficiently prolonged, to justify a diagnosis of mild, moderate, or severe recurrent depressive disorder.

Other Mood (Affective) Disorders

Finally, other mood (affective) disorders include any mood disorders that do not fall into the categories described above because they are not of sufficient severity or duration. They may be single, recurrent (brief), or specified episodes.

The manifestations and symptoms of depression vary in accordance with age and level of development. However, it is clear that the DSM-5 and the ICD-10 do not distinguish between adult and child depression, although by including disruptive mood dysregulation disorder, the DSM-5 does take into account the fact that children and young people aged between 7 and 18 may express their distress in other ways, through chronic, severe, and recurrent irritability manifested verbally and/or behaviorally. Similarly, major depressive disorder specifies that in children the mood may be irritable rather than depressed. However, no distinctions of this kind are found in the ICD-10, an absence which may lead to the faulty inference that the characteristics of child and adolescent depression are similar to those of adult depression.

Explanatory Theories of Depression

Depressive disorders cannot be explained by any single theory, since many different variables are involved in their onset and persistence. The principal biological and psychological theories were therefore taken as the main references for this section. Subsequently, the contributions made by each of these theories regarding depression were studied by conducting searches in PubMed, Web of Science, Science direct, and Google Scholar. With the constant key words being depression, child depression and adolescent depression, the search for information cross-referenced a series of other key words also in accordance with the specific theory in question. Due to the importance of some seminal works in relation to the development of psychological theories of depression, certain authors have remained key references for decades. A total of 64 bibliographical references were used. The following is a summary of the various explanations for the onset of depression, according to the different theoretical frameworks.

Biological Theories

If a mood disorder cannot be explained by family history or stressful life events, then it may be that the child or adolescent in question is suffering from a neurological disease. In such a case, depressive symptoms may manifest early in children and adolescents as epileptic syndromes, sleep disorders, chronic recurrent cephalalgias, several neurometabolic diseases, and intracranial tumors ( Narbona, 2014 ).

Noradrenalin Deficit

Serotonin is a monoamine linked to adrenaline, norepinephrine, and dopamine which plays a key role, particularly in the brain, since it is involved in important life regulation functions (appetite, sleep, memory, learning, temperature regulation, and social behaviors, etc.), as well as many psychiatric pathologies ( Nique et al., 2014 ). Serotonin modulates neuroplasticity, particularly during the early years of life, and dysfunctions in both systems contribute to the physiopathology of depression ( Kraus et al., 2017 ). MRI tests in animals have revealed that a reduction in neuron density and size, as well as a reduction in hippocampal volume among depressive patients may be due to serotonergic neuroplasticity changes. Branchi (2011) , however, argues that improving serotonin levels may increase the likelihood of both developing and recovering from the psychopathology, and underscores the role played by the social environment in this process. In this sense, Curley et al. (2011) point out that the quality of the social environment may influence the development and activity of neural systems, which in turn have an impact on behavioral, physiological, and emotional responses.

Endocrine Alterations

Age-related changes and the presence of biological risk factors, including endocrine, inflammatory or immune, cardiovascular and neuroanatomical factors, make people more vulnerable to depression ( Clarke and Currie, 2009 ). Indeed, some studies suggest that depression may be linked to endocrine alterations: nocturnal cortisol secretions ( Birmaher et al., 1996 ), nocturnal growth hormone secretion ( Ryan et al., 1994 ), thyroid stimulating hormone secretion ( Puig-Antich, 1987 ), melatonin and prolactin secretions ( Waterman et al., 1994 ), high cortisol levels ( Herane-Vives et al., 2018 ), or decreased growth hormone production ( Dahl et al., 2000 ). Puberty and the accompanying hormonal and physical changes require special attention because it has been proposed that they could be associated with an increased incidence of depression ( Reinecke and Simons, 2005 ).

Sleep Disorders

Sleep problems are often associated with situations of social deprivation, unemployment, or stressful life events (divorce, bad life habits, or poor working conditions) ( Garbarino et al., 2016 ). It also seems, however, that sleep disorders are linked to the development of depression. This relationship occurs as a result of how insufficient sleep affects the hippocampus, heightening neural sensitivity to excitotoxic insult and vulnerability to neurotoxic challenges, resulting in a net decrease in gray matter in the hippocampus in the left orbitofrontal cortex ( Novati et al., 2012 ).

For their part, Franzen and Buysse (2008) state that bidirectional associations between sleep disturbances (particularly insomnia) and depression make it more difficult to distinguish cause-effect relations between them. It is therefore unclear whether depression causes sleep disturbances or whether chronic sleep disturbances lead to the appearance of depression. What does seem clear, however, is that treating sleep disturbances (both insomnia and hypersomnia) may help reduce the severity of depression and accelerate recovery ( Franzen and Buysse, 2008 ).

Longitudinal studies have identified insomnia as a risk factor for the onset or recurrence of depression in young people and adults ( Sivertsen et al., 2014 ). In comparison with the non-clinical population, depressed children and adolescents report both trouble sleeping and longer sleep duration ( Accardo et al., 2012 ).

For their part, Foley and Weinraub (2017) observed that, among preadolescent girls, early and later sleep problems directly or indirectly predicted a wide variety of social and emotional adjustment disorders (depressive symptoms, low school competence, poor emotion regulation, and risk-taking behaviors).

Altered Neurotransmission

Studies conducted over the past 20 years have shown that increased inflammation and hyperactivity of the hypothalamic–pituitary–adrenal (HPA) axis may explain major depression ( Pariante, 2017 ). Some of the pathophysiological mechanisms of depression include altered neurotransmission, HPA axis abnormalities involved in chronic stress, inflammation, reduced neuroplasticity, and network dysfunction ( Dean and Keshavan, 2017 ). Other studies report alterations in the brain structure: smaller hippocampus, amygdala, and frontal lobe ( Whittle et al., 2014 ). Nevertheless, the underlying molecular and clinical mechanisms have yet to be discovered ( Pariante, 2017 ). Major depressive disorder in children and adolescents has been associated with increased intracortical facilitation, a direct neurophysiological result of excessive glutamatergic neurotransmission. However, contrary to the findings in adults with depression, no deficits in cortical inhibition were found in children and adolescents with major depressive disorder ( Croarkin et al., 2013 ).

Genetic Factors

Other studies have highlighted the importance of genetics in the onset of depression (40%) ( Scourfield et al., 2003 ). It is important to recognize that a genetic predisposition to an excessive amygdala response to stress, or a hyperactive HPA axis (moderate hyperphenylalaninemia) due to stress during early childhood may trigger an excessive effect or alter an otherwise healthy psychological system ( Dean and Keshavan, 2017 ). Kaufman et al. (2018) support a potential role for genes related to the homeobox 2 gene of Orthodenticle (OTX2) and to the OTX2-related gene in the physiopathology of stress-related depressive disorders in children. Furthermore, genetic anomalies in serotonergic transmission have been linked to depression. The serotonin-linked polymorphic region (5-HTTLPR) is a degenerate repeat in the gene which codes for the serotonin transporter (SLC6A4). The s/s genotype of this region is associated with a reduction serotonin expression, in turn linked to greater vulnerability to depression ( Caspi et al., 2010 ).

For their part, Oken et al. (2015) claim that psychological disturbances may trigger changes in physiological parameters, such as DNA transcription, or may result in epigenetic modifications which alter the sensitivity of the neurotransmitter receptor.

Psychological Theories

This section outlines the different psychological theories which have attempted to explain the phenomenon of depression. Depression is a highly complex disorder influenced by multiple factors, and it is clear that no single theory can fully explain its etiology and persistence. It is likely that a more eclectic outlook must be adopted if we are to make any progress in determining the origin, development, and maintenance of this pathology.

Attachment-Informed Theories

Attachment theory was the term used by Bowlby (1976) to refer to a specific conceptualization of human beings' propensity to establish strong and long-lasting affective ties with other people. Bowlby (1969 , 1973) proposes that consistency, nurturance, protectiveness, and responsiveness in early interactions with caregivers contribute to the development of schemas or mental representations about the relationships of oneself with others, and that these schemas serve as models for later relationships. Bowlby's ethological model of attachment postulates that vulnerability to depression stems from early experiences which failed to satisfy the child's need for security, care and comfort, as well as from the current state of their intimate relations ( Bowlby, 1969 , 1973 , 1988 ). Adverse early experiences can contribute to disturbances in early attachments, which may be associated with vulnerability for depression ( Cummings and Cicchetti, 1990 ; Joiner and Coyne, 1999 ). Associations between insecure attachment among children and negative self-concept, sensitivity to loss, and an increased risk of depression in childhood and adolescence have been reported ( Armsden et al., 1990 ; Koback et al., 1991 ; Kenny et al., 1993 ; Roelofs et al., 2006 ; Allen et al., 2007 ; Chorot et al., 2017 ). Relationships between secure attachment and depression seem also to be mediated by the development of maladaptive beliefs or schemas ( Roberts et al., 1996 ; Reinecke and Rogers, 2001 ).

Thus, attachment theory has become a useful construct for conceptualizing many different disorders and provides valuable information for the treatment of depression ( Reinecke and Simons, 2005 ).

Ainsworth described three attachment styles, in accordance with the child's response to the presence, absence, and return of the mother (or main caregiver): secure, anxious-avoidant, and anxious-resistant ( Ainsworth et al., 1978 ). The least secure attachment styles may give rise to traumatic experiences during childhood, which in turn may result in the appearance of depressive symptoms.

Similarly, Hesse and Main (2000) argued that the central mechanism regulating infant emotional survival was proximity to attachment figures, i.e., those figures who help the child cope with frightening situations. Using Ainsworth's strange situation procedure, Main (1996) found that abused children engaged in more disorganized, disruptive, aggressive, and dissociative behaviors during both childhood and adolescence. Main (1996) also found that many people with clinical disorders have insecure attachment and that psychological-disoriented and disorganized children are more vulnerable.

For his part, Blatt (2004) explored the nature of depression and the life experiences which contribute to its appearance in more depth, identifying two types of depression which, despite a common set of symptoms, nevertheless have very different roots: (1) anaclitic depression, which arises from feelings of loneliness and abandonment; and (2) introjective depression, which stems from feelings of failure and worthlessness. This distinction is consistent with psychoanalytical formulations, since it considers defenselessness/dependency and desperation/negative feelings about oneself to be two key issues in depression.

Brazelton et al. (1975) found that at age 3 weeks, babies demonstrate a series of interactive behaviors during face-to-face mother-infant interactions. These behaviors were not found to be present in more disturbed interactions, which may trigger infant anxiety.

In a longitudinal study focusing on the relationship between risk of maternal depression and infant attachment behavior, Bigelow et al. (2018) analyzed babies at age 6 weeks, 4 and 12 months, finding that mothers at risk of depression soon after the birth of their child may have difficulty responding appropriately to their infant's attachment needs, giving rise to disorganized attachment, with all the psychological consequences that this may involve. Similarly, Beeghly et al. (2017) found that among infants aged between 2 and 18 months, greater maternal social support was linked to decreasing levels of maternal depressive symptoms over time, and that boys were more vulnerable than girls to early caregiving risks such as maternal depression, with negative consequences for mother-child attachment security during toddlerhood.

Authors such as Shedler and Westen (2004) have attempted to find solutions to the problems arising in relation to the DSM diagnostic categories, developing the Shedler Westen Assessment Procedure (SWAP-200) to capture the wealth and complexity of clinical personality descriptions and to identify possible diagnostic criteria which may better define personality disorders.

For their part, Ju and Lee (2018) argue that peer attachment reduces depression levels in at-risk children, and also highlight the curative aspect of attachment between adolescent peers.

Behavioral Models

The first explanations proposed by this model argued that depression occurs due to the lack of reinforcement of previously reinforced behaviors ( Skinner, 1953 ; Ferster, 1966 ; Lewinsohn, 1975 ), an excess of avoidance behaviors and the lack of positive reinforcement ( Ferster, 1966 ) or the loss of efficiency of positive reinforcements ( Costello, 1972 ). A child with depression initially receives a lot of attention from his social environment (family, friends…), and behaviors such as crying, complaints or expressions of guilt are reinforced. When these depressive behaviors increase, the relationship with the child becomes aversive, and the people who used to accompany the child avoid being with him, which contributes to aggravating his depression ( Lewinsohn, 1974 ). Low reinforcement rates can be explained by maternal rejection and lower parental support ( Simons and Miller, 1987 ), by a lower rate of reinforcement offered to their children by mothers of depressed children ( Cole and Rehm, 1986 ), or by low social competence ( Shah and Morgan, 1996 ).

Depression is mainly a learned phenomenon, related to negative interactions between the individual and his or her environment (e.g., low rate of reinforcement or unsatisfactory social relations). These interactions are influenced by cognitions, behaviors and emotions ( Antonuccio et al., 1989 ).

Cognitive Models

The attributional reformulation of the learned helplessness model ( Abramson et al., 1978 ) and Beck's cognitive theory ( Beck et al., 1979 ) are the two most widely-accepted cognitive theories among contemporary cognitive models of depression ( Vázquez et al., 2000 ).

Learned helplessness is related to cognitive attributions, which can be specific/global, internal/external, and stable/unstable ( Hiroto and Seligman, 1975 ; Abramson et al., 1978 ). Global attribution implies the conviction that the negative event is contextually consistent rather than specific to a particular circumstance. Internal attribution is related to the belief that the aversive situation occurs due to individual conditions rather than to external circumstances. Stable attribution is the belief that the aversive situation is unchanging over time ( Miller and Seligman, 1975 ). People prone to depression attribute negative events to internal, stable and global factors and make external, unstable, and specific attributions for success ( Abramson et al., 1978 ; Peterson et al., 1993 ), a cognitive style also present in children and adolescents with depression ( Gladstone and Kaslow, 1995 ).

The Information Processing model ( Beck, 1967 ; Beck et al., 1979 ) postulates that depression is caused by particular stresses that evoke the activation of a schema that screens and codes the depressed individual's experience in a negative fashion ( Ingram, 1984 , p. 443). Beck suggests that this distortion of reality is expressed in three areas, which he calls the “cognitive triad”: negative views about oneself, the world and the future as a result of their learning history ( Beck et al., 1983 ). These beliefs are triggered by life events which hold special meaning for the subject ( Beck and Alford, 2009 ).

Self-Control Model

This theory assumes that depression is due to deficits in the self-control process, which consists of three phases: self-monitoring, self-evaluation, and self-administration of consequences ( Rehm, 1977 ; Rehm et al., 1979 ). In the self-monitoring phase, individuals attend only to negative events and tend to recognize only immediate, short-term consequences. In the self-evaluation phase, depressed individuals establish unrealistic evaluation criteria and inaccurately attribute their successes and failures. If self-evaluation is negative, in the self-administration of consequences phase the individual tends to engage very little in self-reinforcement and very frequently in self-punishment.

Both Rehm's self-control model ( Rehm, 1977 ) and Bandura's conception of child depression ( Bandura, 1977 ) assume that children internalize external control guidelines. These guidelines are related to family interaction patterns and both may contribute to the etiology or persistence of depression in children.

In a study conducted with children aged between 8 and 12 years, Kaslow et al. (1988) found that depressed children had a more depressive attributional style and more self-control problems.

Interpersonal Theory

This model, which is closely linked to attachment theories, aims to identify and find solutions for an individual's problems with depression in their interpersonal functioning. It suggests that the difficulties experienced are linked to unresolved grief, interpersonal disputes, transition roles and interpersonal deficits ( Markowitz and Weissman, 1995 ).

Milrod et al. (2014) argue that pathological attachment during early childhood has serious consequences for adults' ability to experience and internalize positive relationships.

Similarly, various different studies have highlighted the fact that one of the variables that best predicts depression in children is peer relations ( Bernaras et al., 2013 ; Garaigordobil et al., 2017 ).

Stressful Life Events

Studies focusing on the adult population have reported that between 60 and 70% of depressed adults experienced one or more stressful events during the year prior to the onset of major depression ( Frank et al., 1994 ). In children and adolescents, modest associations have been found between stressful life events and depression ( Williamson et al., 1995 ). For their part, Shapero et al. (2013) found that people who had suffered severe emotional abuse during childhood experienced higher levels of depressive symptoms when faced with current stressors. Sokratous et al. (2013) argue that the onset of depression is not only triggered by major stressful events, but rather, minor life events (dropping out of school, your father losing his job, financial difficulties in the family, losing friends, or the illness of a family member) may also influence the appearance of depressive symptoms.

Events such as the loss of loved ones, divorce of parents, mourning or exposure to suicide (either individually or collectively) have all been associated with the onset of depression in childhood ( Reinherz et al., 1993 ). Factors such as a history of additional interpersonal losses, added stress factors, a history of psychiatric problems in the family and prior psychopathology (including depression) increase the risk of depression in adolescents ( Brent et al., 1993 ). Birmaher et al. (1996) found that prior research into stressful life events in relation to early-onset depression had been based on data obtained from self-reports, making it difficult to determine the causal relationship, since events may be both the cause and consequence of depression.

However, not everyone exposed to this kind of traumatic experience becomes depressed. Personality and the moment at which events occur are both involved in the relationship between depression and stressful life events, although biological factors such as serotonergic functioning ( Caspi et al., 2010 ) also exert an influence.

Sociocultural Models

These models postulate that cultural variables are responsible for the appearance of depressive symptoms. These variables are mainly acculturation and enculturation. In acculturation, structural changes are observed (economic, political, and demographic), along with changes in people's psychological behavior ( Casullo, 2001 ). Some studies link increased suicide rates with economic recession ( Chang et al., 2013 ; Reeves et al., 2014 ). Enculturation occurs when the older generation invites, induces or forces the younger generation to adopt traditional mindsets and behaviors.

In an attempt to better understand the influence of culture and family on depressive symptoms, Lorenzo-Blanco et al. (2012) tested an acculturation, cultural values and family functioning model with Hispanic students born in the United States. The results revealed that both family conflict and family cohesion were related to depressive symptoms.

Another study carried out with girls aged 7–10 years ( Evans et al., 2013 ) observed that internalizing an unrealistically thin ideal body predicted disordered eating attitudes through body dissatisfaction, dietary restraint and depression.

Finally, the importance of family interactions in the onset of depressive symptoms cannot be overlooked. Parenting style has been identified as a key factor in children's and adolescents' psychosocial adjustment ( Lengua and Kovacs, 2005 ). Parental behavior has been studied from two different perspectives: warmth and control. Warmth is linked to aspects such as engagement and expression of affection, respect, and positive concern by parents and/or principal caregivers ( Rohner and Khaleque, 2003 ). In this sense, prior studies have identified a significant association between parental warmth and positive adjustment among adolescents ( Barber et al., 2005 ; Heider et al., 2006 ). Rohner and Khaleque (2003) argue that children's psychological adjustment is closely linked to their perception of being accepted or rejected by their principal caregivers, and other studies have found that weaker support from parents is associated with higher levels of depression and anxiety among adolescents ( Yap et al., 2014 ).

Similarly, Jaureguizar et al. (2018) found that a low level of perceived parental warmth was linked to high levels of clinical and school maladjustment, and that the weaker the parental control, the greater the clinical maladjustment. These authors also found that young people with negligent mothers and authoritarian fathers had higher levels of clinical maladjustment.

In short, according to the different theories, depression may be due to (1) biological reasons; (2) insecure attachment; (3) lack of reinforcement of previously-reinforced behaviors; (4) negative interpersonal relations and relations with one's environment and the resulting negative consequences; (5) attributions made by individuals about themselves, the world and their future; and (6) sociocultural changes. It is likely that no single theory can fully explain the genesis and persistence of depression, although currently, negative interpersonal relations and relations with one's environment and sociocultural changes (economic, political, and demographic) may explain the observed increase in the prevalence of depression.

Evaluation Instruments

Many different evaluation instruments can be used to measure child and adolescent depression. Tables 2 , 3 outline the ones most commonly used in scientific literature. Table 2 summarizes the main self-administered tests that specifically measure child and adolescent depression, while Table 3 presents tests that measure child and adolescent depression among other aspects (i.e., broader or more general tests). Finally, Table 4 summarizes the main hetero-administered psychometric tests for assessing this pathology.

Table 2 . Self-administered psychometric tests designed specifically for evaluating child and adolescent depression.

Table 3 . Self-administered general psychometric tests which, among other variables, also assess child and adolescent depression.

Table 4 . Hetero-administered psychometric tests for assessing child and adolescent depression.

As shown in the tables above, there are several self-administered instruments that can be used with children from age 6 to 7 onwards, although their duration should be taken into consideration in order to avoid overtiring subjects. While it is clear that an effort has been made to design shorter measures (compare, for example, the 66 items of the CDS with the 16 items of the longest version of the KADS), the duration of the test should not be the only aspect taken into account when selecting an evaluation instrument.

One of the most widely used instruments to measure child depression in the scientific literature is the Children's Depression Inventory-CDI ( Kovacs, 1985 ), which is based on the Beck Depression Inventory-BDI ( Beck and Beamesderfer, 1974 ). Thus, it is based on Beck's cognitive theory of depression. Following this same theoretical line, the Children's Depression Scale-CDS ( Lang and Tisher, 1978 ) was designed, but in this case, this instrument was not created based on another instrument previously designed for adult population (as in the case of the CDI), but instead from its beginnings, it was conceived exclusively to assess child depression. Chorpita et al. (2005) explain that the CDI measures a broader construct of negative affectivity rather than depression as a separate construct, and that it may be useful for screening for trait dimensions or personality features, whereas other instruments, such as the Revised Child Anxiety and Depression Scale-RCADS ( Chorpita et al., 2000 ), measure a specific clinical syndrome.

Table 2 describes many other instruments that are very useful as screening tests for depression and depressive disorder, such as the Center for Epidemiological Studies Depression Scale for Children-CES-DC ( Weissman et al., 1980 ) (based on the Center for Epidemiological Studies Depression Scale for Adults, CES-D; Radloff, 1977 ), the Mood and Feelings Questionnaire-MFQ ( Angold et al., 1995 ), or the Depression Self-Rating Scale for Children-DSRS ( Birleson, 1981 ). This last one, for example, is useful to measure moderate to severe depression in childhood and is based on the operational definition of depressive disorder, that is, a specific affective-behavior pattern that implies an impairment of a child's or adolescent's ability to function effectively in his/her environment ( Birleson, 1981 ).

The cognitive and affective component of depression is the one that is most present in the instruments described in Table 2 . In fact, for example, the Short Mood and Feelings Questionnaire (SMFQ) includes the cognitive and affective items from the original MFQ item pool, in addition to some items related to tiredness, restlessness, and poor concentration ( Angold et al., 1995 ). In the SMFQ, more than half of the items from the MFQ were removed, and even so, high correlations between the MFQ and the SMFQ were found ( Angold and Costello, 1995 ), which may be indicating that the really important items were the cognitive and affective items that were maintained. Reynolds et al. (1985) defended that children could accurately report their cognitive and affective characteristics, so “ if one wishes to know how a child feels, ask the child” ( Reynolds et al., 1985 , p. 524).

Depending on the specific aim of the evaluation or research study, a broader diagnostic measure, such as those outlined in Table 3 , may also provide valuable information. Finally, it is worth noting that only two hetero-administered instruments were found for teachers, with all others being clearly oriented toward the clinical field. In this sense, special emphasis should be placed on the need to develop valid and reliable instruments for teachers, since they may be key agents for detecting symptoms among their students. While it is important to train teachers in this sense, it is also important to provide them with instruments to help them assess their students. The instruments that are currently available have produced very different results as regards their correlation with students' self-reported symptoms, although in general, teachers tend to underestimate their students' depressive symptoms ( Jaureguizar et al., 2017 ).

Child and Adolescent Depression Prevention Programs in the School Environment

Extant scientific literature was reviewed in order to summarize the main depression prevention programs for children and adolescents in school settings. The databases used for conducting the searches were PubMed, PsycINFO, Web of Science, Scopus, Science Direct, and Google Scholar, along with a range of different manuscripts. With the constant key word being depression, the search for information cross-referenced a series of other key words also, namely: “child* OR adolescent*,” “prevent*program,” and “school OR school-based.” Searches were conducted for information published between January 1, 1970 and December 31, 2017.

First, articles were screened (i.e., their titles and abstracts were read and a decision was made regarding their possible interest for the review study). The inclusion criteria were that the study analyzed all the research subjects of the review study (depression, childhood, or adolescence and prevention programs in school settings), that study participants were aged between 6 and 18, that the study was published in a peer-reviewed journal and that it was written in either English or Spanish. Review studies and their references were also analyzed. Studies focusing mainly on psychiatric disorders other than depression were excluded.

Finally, 39 studies were selected for the review, which explored 8 prevention programs that are outlined in Table 5 . In general terms, child depression prevention programs are divided into two main categories: universal programs for the general population, and targeted programs aimed at either the at-risk population or those with a clear diagnosis. Although scientific literature reports that targeted programs obtain better outcomes than universal ones, the latter type nevertheless offer certain advantages, since they reach a larger number of people without the social stigma attached to having been specially selected ( Roberts et al., 2003 ; Huggins et al., 2008 ). Thus, the ideal context for instigating universal child depression prevention programs is the school environment.

Table 5 . School-based child and adolescent depression prevention programs.

Table 5 outlines the most important child depression prevention programs carried out in the school context. They are all cognitive-behavioral programs implemented either by psychologists or teachers with specialist training, consisting of between 8 and 15 sessions. Only a few universal programs designed to prevent the symptoms of depression focus on younger children, since most are targeted mainly at the adolescent population ( Gillham et al., 1995 ; Barrett and Turner, 2001 ; Farrell and Barrett, 2007 ; Essau et al., 2012 ; Gallegos et al., 2013 ; Rooney et al., 2013 ). Indeed, in the present review, only four universal child depression prevention programs were found that were aimed at a younger age group (between 8 and 12): the Penn Resiliency Program, FRIENDS, the Aussie Optimism Program, and FORTIUS (see Table 5 ).

As shown in the table, the results of the various programs outlined are not particularly positive, since on many occasions the effects (if there are any) are not sustained over time or are limited in scope (being dependent on who applies the program or on the sex of the participant, etc.). Nor is the distinction between universal and targeted programs particularly clear as regards their effects, since although targeted programs may initially appear to be more effective, their impact is not found to be sustained in the long term.

Greenberg et al. (2001) argue that researchers should explain whether their prevention programs focus on one or various microsystems (basically family and school), mesosystems or exosystems, etc. (following the model described by Bronfenbrenner, 1979 ), or are centered exclusively on the individual and his or her environment, since this will influence the results reported. These same authors conclude that programs focused exclusively on children and adolescents themselves are less effective than those which aim to “educate” subjects and bring about positive changes in their family and school environments.

As Calear and Christensen (2010) point out in their review, some authors suggest that the fact that some targeted programs are aimed at people with high levels of depressive symptoms entails a broader range of possibilities for change; however, this does not help us understand why these changes are not sustained over time. Thus, further research is required in this field in order to identify what specific components of those programs observed to be effective actually have a positive impact on the level of depressive symptoms, how these programs are developed, who implements them and whether or not their effects are sustained in the short, medium, and long term.

Clinical Treatments for Depression

In order to draft this section, a search was conducted for the most commonly-used therapies with proven efficacy for treating depression. The databases used were PubMed, Web of Science, Science direct, and Google Scholar. The key words used in the search were treatment, depression, child depression, and adolescent depression. A total of 30 bibliographic references were used in the drafting of this summary, including the major contribution made by The American Psychological Association's Society of Clinical Psychology ( American Psychological Association, Society of Clinical Psychology (APA), 2017 ) regarding the most effective psychological methods for treating depression.

Although the World Health Organization (WHO) (2017) claims that prevention programs reduce the risk of suffering from depression, it has yet to be ascertained what type of programs and what contents are the most effective. The WHO also states that there are effective treatments for moderate and severe depression, such as psychological treatments (behavioral activation, cognitive behavioral therapy, and interpersonal psychotherapy) and antidepressant drugs (although it also warns of adverse effects), as well as psychosocial treatments for cases of mild depression. Moreover, a study conducted with adolescents by Foster and Mohler-Kuo (2018) found that the combination of cognitive-behavioral therapy and fluoxetine (antidepressant drug) was more effective than drug therapy alone.

The efficacy of treatment with antidepressants has been called into question for some years now. Iruela et al. (2009) claim that tricyclic antidepressants (imipramine, clomipramine, amitriptyline) are not recommended in childhood and adolescence since no benefits other than the placebo effect have been proven and furthermore, they generate major side effects due to their cardiotoxicity. They are therefore particularly dangerous in cases of attempted suicide. These same authors also advise against the use of monoamine oxidase inhibitors (MAOIs) due to dietary restrictions, interactions with other medication and the lack of clinical trials with sufficiently large groups which guarantee their efficacy. SSRIs or serotonergic antidepressants are the ones that have been most extensively studied in this population. The most effective is fluoxetine, the use of which is recommended in association with cognitive psychotherapy for cases of moderate and severe child depression.

On another hand, Wagner and Ambrosini (2001) analyzed the efficacy of pharmacological treatment in children and adolescents and stated that, at best, antidepressant therapy for depressed youth was moderately effective. Peiró et al. (2005) indicate that there is a great debate about the safety of selective serotonin reuptake inhibitors (SSRIs) in childhood. SSRIs, except for fluoxetine in the United States, have never been authorized by any agency for use in children or adolescents, mainly because of the risk of suicide to which they are associated. In 1991, the Food and Drugs Administration (FDA) claimed that there was insufficient evidence to confirm a causal association between SSRIs and suicide. Vitiello and Ordoñez (2016) conducted a systematic review of the topic and found more than 30 controlled clinical trials in adolescents and a few studies with children. Most studies found no differences between studies that administered drugs and those that used placebo, but they did find fluoxetine to be effective. They noted that antidepressants increased the risk of suicide (suicidal ideation and behaviors) compared to studies that had used placebos. The authors recommend using antidepressants with caution in young people and limiting them to patients with moderate to severe depression, especially when psychosocial interventions are not effective or are not feasible.

As regards the effectiveness of psychodynamic treatments, Luyten and Blatt (2012) advocate the inclusion of psychoanalytic therapy in the treatment of child, adolescent and adult depression. After conducting a review of both the theoretical assumptions of psychodynamic treatments of depression and the evidence supporting the efficacy of these interventions, these authors concluded that brief psychoanalytic therapy (BPT) is as effective in treating depression as other active psychotherapeutic treatments or pharmacotherapy, and its effects tend to be maintained in the longer term. They also observed that the combination of BPT and medication obtained better results than medication alone. Longer-term psychoanalytic treatment (LTPT) was found to be effective for patients suffering from chronic depression and co-morbid personality problems. Together, the authors argue, these findings justify the inclusion of psychoanalytic therapy as a first-line treatment in adult, child, and adolescent depression.

In a qualitative study carried out by Brown (2018) on parents' expectations regarding the recovery of their depressed children, a direct relationship was observed between said expectations and type of attachment. Parents who remained more passive and expected expert helpers to fix their child experienced reduced hope months after finishing the program. However, when parents changed their interactions with their child and adopted more positive expectations regarding their cure, they felt a more sustained sense of hope. Moreover, when parents themselves participated in therapy sessions, as part of their child's treatment, they felt greater hope and effectiveness in contributing to their child's recovery.

The American Psychological Association's Society of Clinical Psychology [ American Psychological Association, Society of Clinical Psychology (APA), 2017 ] has published a list of psychological treatments that have been tested with the most scientific rigor and which, moreover, have been found to be most effective in treating depression. These treatments are as follows:

– Self-Management/Self-Control Therapy ( Kanfer, 1970 ). Depression is due to selective attention to negative events and immediate consequences of events, inaccurate attributions of responsibility for events, insufficient self-reinforcement, and excessive self-punishment. During therapy, the patient is provided with information about depression and taught skills they can use in their everyday life. This 10-session program can be delivered either in group or individual formats, at any age.

– Cognitive Therapy ( Beck, 1987 ). Individuals suffering from depression are taught cognitive and behavioral skills to help them develop more positive beliefs about themselves, others, and the world. Méndez (1998) argues that therapists working with depressed children should pursue three changes: (1) Learn to value their own feelings; (2) Replace behaviors which generate negative feelings with more appropriate behaviors; and (3) Modify distorted thoughts and inaccurate reasoning. The number of sessions varies between 8 and 16 in patients with mild symptoms. Those with more severe symptoms show improvement after 16 sessions.

– Interpersonal Therapy ( Klerman et al., 1984 ). García and Palazón (2010) identified four typical focal points for tension in depression, related to loss (complicated mourning), conflicts (interpersonal disputes), change (life transitions), and deficits in relations with others (interpersonal deficits), which generate and maintain a depressive state. It uses certain behavioral strategies such as problem solving and social skills training and lasts between 12 and 16 sessions in the most severe cases, and between 3 and 8 sessions in milder cases.

– Cognitive Behavioral Analysis System of Psychotherapy ( McCullough, 2000 ). This therapy combines components of cognitive, behavioral, interpersonal, and psychodynamic therapies. According to McCullough (2003) , it is the only therapy developed specifically to treat chronic depression. Patients undergoing this therapy generate more empathic behaviors and identify, change and heal interpersonal patterns related to depression. Patients are recommended to combine the therapy with a regime of antidepressant medication.

– Behavior Therapy/Behavioral Activation (BA) ( Martell et al., 2013 ). Depression prompts sufferers to disengage from their routines and become increasingly isolated. Over time, this isolation exacerbates their depressive symptoms. Depressed individuals lose opportunities to be positively reinforced through pleasant experiences or social activities. The therapy aims to increase patients' chances of being positively reinforced by increasing their activity levels and improving their social relations. The therapy usually lasts between 20 and 24 sessions, with the brief version consisting of between 8 and 15 sessions.

– Problem-Solving Therapy ( Nezu et al., 2013 ). The aim is to enhance patients' personal adjustment to their problems and stress using affective, cognitive, and behavioral strategies. The therapy usually comprises around 12 sessions, although substantial changes are generally observed from the fourth session onwards. This therapy is widely used in primary care. It is an adaptation that is easy to apply in general medicine by personnel working in those contexts, and can be completed in around 6 weeks ( Areán, 2000 ).

The treatments that, according to the American Psychological Association, Society of Clinical Psychology (APA) (2017) , have modest research support and could be used with children are as follows:

– Rational Emotive Behavioral Therapy ( Ellis, 1994 ). This short-term, present-focused therapy works on changing the thinking which contributes to emotional and behavioral problems using an active-directive, philosophical and empirical intervention model. Using the A-B-C model (A: events observed by the individual; B: Individual's interpretation of the observed event; C: Emotional consequences of the interpretations made), the aim is to bring about the cognitive restructuring of erroneous thoughts, so as to replace them with more rational ones. The most commonly used techniques are cognitive, behavioral, and emotional.

– Self-System Therapy ( Higgins, 1997 ). Depression occurs as the result of the individual's chronic failure to achieve their established goals. During therapy, patients review their situation, analyze their beliefs and, on the basis of the results, alter their regulation style and move toward a new vision of themselves. Therapy generally consists of between 20 and 25 sessions.

– Short-Term Psychodynamic Therapy ( Hilsenroth et al., 2003 ). The aim of this therapy is to help patients understand that past experiences influence current functioning, and to analyze affect and the expression of emotion. The therapy focuses on the therapeutic relationship, the facilitation of insight, the avoidance of uncomfortable topics and the identification of core conflictual relationship themes. It is usually combined with pharmacological treatment to alleviate depressive episodes.

– Emotion-Focused Therapy (emotion regulation therapy or Greenberg's experiential therapy) ( Greenberg, 2004 ). According to Greenberg et al. (2015) , this therapy combines elements of client-based practices ( Rogers, 1961 ), Gestalt therapy ( Perls et al., 1951 ), the theory of emotions and a dialectic-constructivist meta-theory. The aim is to create a safe environment in which the individual's anxiety is reduced, thereby enabling them to confront difficult emotions, raising their awareness of said emotions, exploring their emotional experiences in more depth and identifying maladaptive emotional responses. The therapy is delivered in 8–20 sessions.

– Acceptance and Commitment Therapy ( Hayes, 2005 ). This theory has become increasingly popular over recent years and is the contextual or third-generation therapy that is supported by the largest body of empirical evidence. It is based on a realization of the importance of human language in experience and behavior and aims to change the relationship individuals have with depression and their own thoughts, feelings, memories, and physical sensations that are feared or avoided. Strategies are used to teach patients to decrease avoidance and negative cognitions, and to increase focus on the present. The aim is not to modify the content of the patient's thoughts, but rather to teach them how to change the way they analyze them, since any attempt to correct thoughts may, paradoxically, only serve to intensify them ( Hayes, 2005 ).

Ferdon and Kaslow (2008) , for their part, in a theoretical review of the treatment of depression in children and adolescents, concluded that the cognitive-behavioral-therapy-based specific programs of the Penn Prevention program meet the criteria to conduct effective interventions in children with depression. In adolescent depression, the cognitive-behavioral therapy and the Interpersonal Therapy–Adolescent seem to have a well-established efficacy. Weersing et al. (2017) , in this same line, state that, although the efficacy of treatments in children is rather weak, cognitive-behavioral therapy is probably the most effective therapy. They also confirm that, in depressed adolescents, cognitive behavioral therapy, and interpersonal psychotherapy are appropriate interventions.

There are other studies also which focus on treatments for depression in childhood. For example, Crowe and McKay (2017) carried out a meta-analysis of the effects of Cognitive Behavioral Therapy (CBT) on children suffering from anxiety and depression, concluding that CBT can be considered an effective treatment for child depression. According to these authors, the majority of protocols for children have been adapted from protocols for adults, and the most common techniques are psychoeducation, self-monitoring, identification of emotions, problem solving, coping skills, and reward plans. Similarly, cognitive strategies include the identification of cognitive errors, also known as cognitive restructuring. In another meta-analysis conducted to analyze the efficacy and acceptability of CBT in cases of child depression, Yang et al. (2017) observed that, in comparison with the control groups that did not receive treatment, the experimental groups showed significant improvement, although they also pointed out that the relevance of this finding was limited due to the small size of the trial groups.

Another study carried out in Saudi Arabia concluded that student counseling in schools may help combat and directly reduce anxiety and depression levels among Saudi children and adolescents ( Alotaibi, 2015 ).

Family-based treatment may also be effective in treating the interpersonal problems and symptoms observed among depressed children. The data indicate that the characteristics of the family environment predict recovery from persistent depression among depressed children ( Tompson et al., 2016 ). In this sense, Tompson et al. (2017) compared the effects of a family-focused treatment for child depression (TCF-DI) with those of individual supportive psychotherapy among children aged 7–14 with depressive disorders. The results revealed that incorporating the family into the therapy resulted in a significant improvement in depressive symptoms, global response, functioning, and social adjustment.

To conclude this section, it can be stated that treatment for depression should be multifactorial and should bear in mind the personal characteristics of the patient, their coping strategy for problems, the type of relationship they have with themselves and the type of relationship they establish with their environment (friends, school, family, etc.). Thus, in order for the individual to attain the highest possible level of psychological wellbeing, attention should focus on both these and other related aspects.

Conclusions

The present review aims to shed some light on the complex and broad-ranging field of child and adolescent depression, starting with a review of the construct itself and its explanatory theories, before continuing on to analyze existing evaluation instruments, the main prevention programs currently being implemented and the various treatments currently being applied. All these aspects are intrinsically linked: how the concept is defined depends on the explanatory variables upon which said definition is based, and this in turn influences how we measure it and the variables we define as being key elements for its prevention and treatment.

It is interesting to note the low level of specificity of both the construct itself and the explanatory theories offered by child and adolescent psychology, which suggest that child depression can be understood on the basis of the adult version of the pathology. This may well be a basic error in our approach to depression among younger age groups. The fact that universal prevention programs specifically designed for children are obtaining only modest results may indicate that we have perhaps failed to correctly identify the key variables involved in the genesis and maintenance of child and adolescent depression.

The review of current child and adolescent depression prevention programs revealed that the vast majority coincide in adopting a cognitive-behavioral approach, with contents including social skills and problem solving training, emotional education, cognitive restructuring, and strategies for coping with anxiety. These contents are probably included because they are important elements in the treatment of depression, as shown in this review. But if their inclusion is important and effective in the treatment of depression, why do they not seem to be so effective in preventing this pathology? There are probably many factors linked to prevention programs which, in one way or another, influence their efficacy: who implements the program and what prior training they receive; the characteristics of the target group; group dynamics; how sessions are run; how the program is evaluated; and if the proposed goals are really attained (e.g., training in social skills may be key, but perhaps we are not training students correctly). Moreover, in universal prevention programs carried out in schools, the intervention focuses on students themselves rather than adopting a more holistic approach, as recommended by certain authors such as Greenberg et al. (2001) . But, if we accept that depression is multifactorial and that risk and protection factors may be found not only in the school environment but also in the family and social contexts, should prevention not also be multifactorial?

There is therefore still much work to be done in order to fully understand child and adolescent depression and its causes, and so design more effective evaluation instruments and prevention and treatment programs. Given the important social and health implications of this disorder, we need to make a concerted effort to further our research in this field.

Author Contributions

MG designed the study and wrote the protocol. EB and JJ conducted literature review and provided summaries of previous research studies, and wrote the first draft of the manuscript. All authors contributed to and have approved the final manuscript.

The Research Project was sponsored by the Alicia Koplowitz Foundation, with grant number FP15/62.

Conflict of Interest Statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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Keywords: depression, adolescent, child, instruments, prevention, treatment

Citation: Bernaras E, Jaureguizar J and Garaigordobil M (2019) Child and Adolescent Depression: A Review of Theories, Evaluation Instruments, Prevention Programs, and Treatments. Front. Psychol. 10:543. doi: 10.3389/fpsyg.2019.00543

Received: 13 March 2018; Accepted: 25 February 2019; Published: 20 March 2019.

Reviewed by:

Copyright © 2019 Bernaras, Jaureguizar and Garaigordobil. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY) . The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Joana Jaureguizar, [email protected]

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

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Personal Health

The Devastating Ways Depression and Anxiety Impact the Body

Mind and body form a two-way street.

By Jane E. Brody

It’s no surprise that when a person gets a diagnosis of heart disease, cancer or some other life-limiting or life-threatening physical ailment, they become anxious or depressed. But the reverse can also be true: Undue anxiety or depression can foster the development of a serious physical disease, and even impede the ability to withstand or recover from one. The potential consequences are particularly timely, as the ongoing stress and disruptions of the pandemic continue to take a toll on mental health .

The human organism does not recognize the medical profession’s artificial separation of mental and physical ills. Rather, mind and body form a two-way street. What happens inside a person’s head can have damaging effects throughout the body, as well as the other way around. An untreated mental illness can significantly increase the risk of becoming physically ill, and physical disorders may result in behaviors that make mental conditions worse.

In studies that tracked how patients with breast cancer fared, for example, Dr. David Spiegel and his colleagues at Stanford University School of Medicine showed decades ago that women whose depression was easing lived longer than those whose depression was getting worse. His research and other studies have clearly shown that “the brain is intimately connected to the body and the body to the brain,” Dr. Spiegel said in an interview. “The body tends to react to mental stress as if it was a physical stress.”

Despite such evidence, he and other experts say, chronic emotional distress is too often overlooked by doctors. Commonly, a physician will prescribe a therapy for physical ailments like heart disease or diabetes, only to wonder why some patients get worse instead of better.

Many people are reluctant to seek treatment for emotional ills. Some people with anxiety or depression may fear being stigmatized, even if they recognize they have a serious psychological problem. Many attempt to self-treat their emotional distress by adopting behaviors like drinking too much or abusing drugs, which only adds insult to their pre-existing injury.

And sometimes, family and friends inadvertently reinforce a person’s denial of mental distress by labeling it as “that’s just the way he is” and do nothing to encourage them to seek professional help.

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In Sight: The Biological Diagnosis of Depression and Anxiety

The science of psychiatry is gaining on the daunting complexity of the brain..

Updated June 20, 2024 | Reviewed by Hara Estroff Marano

• What Is Depression?
• Find counselling to overcome depression
• Diagnostic models in psychiatry are largely based on clinical experience, with some statistical modeling.
• Scientific biomedical models are necessary to advance understanding of mental illness.
• Understanding the biology of mental illness will allow development of better treatments.
• Personalized analysis of brain networks holds promise for people suffering from depression and anxiety.

According to the World Health Organization (WHO), clinical depression affects nearly 300 million people worldwide. The Centers for Disease Control (CDC) estimates that 20 million or more people in the U.S. have depression at any given time, while more than 18 percent of U.S. adults report depression at some point in their lives and .more than 12 percent of adults report significant feelings of anxiety .

Treatment for depression is of limited effectiveness; only 30-40 percent of those initially treated experience full resolution of symptoms, or remission. What's more, studies show, successive efforts to achieve remission are less and less effective.

Understanding the underlying biology of depression, anxiety, and related conditions such as post- traumatic stress disorder ( PTSD ) is necessary for making correct diagnosis and planning effective treatment. But especially in psychiatry, given the complexities of the brain, diagnosis and treatment are not yet well-grounded in biological understanding.

Medical treatment is ideally based on a number of factors, including knowledge of the disease process, the ability to make accurate diagnoses, and an understanding of how individual factors affect treatment planning and outcome. The National Institutes of Health started the BRAIN Initiative (Brain Research Through Advancing Innovative Neurotechnologies) in 2013, calling for neuroscience -based models of disease and health. Understanding the causal factors of disease suggests the levers clinicians can manipulate to provide the most effective treatment possible.

Toward a More Scientific Psychiatry

Psychiatric diagnosis in the United States is currently based on the Diagnostic and Statistical Manual of Mental Disorders (DSM-5). Although efforts have been made to improve its approach with more specific criteria for mental illness based on statistics and available data, the DSM is not firmly scientifically based. For the vast majority of illnesses described, the diagnostic criteria say little to nothing about the cause of the disease; instead, they primarily reflect long-observed clinical patterns, rendering the DSM a work in progress and of less-than-desirable utility for diagnosis and treatment.

Not all causes of psychiatric disease are strictly biological. For example, inheriting a genetic predisposition to depression—and many genes contribute–does not invariably lead to depression. It’s highly likely that social and family factors can also bring on depression—not being productive or social, for example. Current treatments for depression often address biological and social factors, but there is as yet no standard biological testing for depression nor any clear framework for scientifically based treatment.

DSM 5 identifies several subtypes of depression, all based on clinical observation and statistical analysis. With unipolar depression (as contrasted with bipolar disorder ), subtypes include atypical and melancholic, and specifiers include severity of symptoms as well as presence or absence of psychotic features. Diagnosis is made by reviewing clinical presentation and history, whether informally through clinical interview or formally via structured, guided interview and review of accompanying information. The same approach applies to anxiety disorders, including generalized anxiety, social anxiety , panic disorder, and obsessive-compulsive disorder, as well as to stress-related disorders such as PTSD. The disorders may be divided into subtypes by specifiers, but a true medical-scientific framework is lacking.

Biotyping Depression and Anxiety

A recent study of brain networks in depression and anxiety reported in Nature Medicine (2024) is an important step toward establishing an empirical model of "biotypes",; it echoes prior work on depression 3 and brain-based personality research 4 . Researchers Tozzi and colleagues used functional magnetic resonance imaging (fMRI) to look at brain activity in more than 1,000 people with depression and anxiety, measuring “task-free” brain activity. They repeated imaging in a subset of patients who received psychotherapy or pharmacotherapy or underwent a variety of activities. During the imaging, subjects were shown a variety of stimuli—such as sad, threatening, or happy faces—and were asked to perform a variety of cognitive and attention tasks. Cluster analysis was used to identify underlying biotypes based on brain circuit dysfunction, sometimes referred to as “dysconnectivity” in brain networks. Treatment would, therefore, restore "euconnectivity".

Notably, the study was transdiagnostic: Given how much depression an anxiety overlap, the study didn't assume they are separate disorders. The analysis was unbiased by preconceived diagnostic models. Participants included those diagnosed with various conventional disorders, including major depression, generalized anxiety, panic disorder, social anxiety, PTSD, obsessive-compulsive disorder,. Some patients met criteria for more than one diagnosis.

Six underlying biotypes of depression and anxiety were identified among participants with clinically-significant symptoms. Their labels are complicated, based on activity levels in key brain networks: default mode, or resting state (D); salience, or what stands out as important (S); and attentional (A). In addition to connectivity patterns, research looked at such key factors as negative emotional circuitry in response to sadness and threat (conscious and unconscious ), positive emotion circuits, and cognitive circuits. There were no sex differences in response patterns, and minimal differences in age.

• Biotype D C+ S C+ A C+ . This cluster showed hyperconnectivity among all three networks. This biotype had slow responses identifying sad faces and increased errors in executive function tasks. The response to behavior coaching for wellness was strong.
• Biotype A C− . This cluster had less connectivity in the attention network, less severe stress compared with other biotypes, and relatively little dysfunction in cognitive control, with faster responses on cognitive measures but more errors, as well as faster priming when viewing threatening faces. Response to behavioral coaching was less robust.
• Biotype NS A+ P A+ . This cluster had elevated activity during conscious processing of emotions, with sadness evoking greater negative circuit activity and happiness more positive. This group also experienced more severe anhedonia —inability to enjoy things—and greater ruminative brooding.
• Biotype C A+ . This group showed increased cognitive control under specific conditions. This cluster also showed greater anhedonia, greater anxious arousal, negative bias , and dysregulation in response to threat. Cognitive errors were high, especially with sustained attention. This biotype had a better response to the antidepressant venlafaxine, a serotonin-norepinephrine reuptake inhibitor (SNRI) commonly prescribed.
• Biotype NTC C- C A− . This small group was characterized by loss of functional connectivity in negative emotion circuits during conscious processing of threatening faces and by reduced activity in cognitive control circuits. This cluster had less ruminative brooding and faster reaction times to sad faces.
• Biotype D X S X A X N X P X C X . This small group did not show significant circuit dysfunction. There were slower reaction times to implicit threat.

Implications

While not ready for standard clinical use, the study results build on prior work demonstrating that brain network analysis holds promise for developing biologically based diagnostic testing for depression, anxiety, and stress-related disorders. The study also provides initial proof of concept that psychiatric biotyping could be used in the selection of treatments, with some biotypes responding better to medication and others to psychotherapeutic interventions.

Clearly, more work is needed before such models of illness can underpin diagnosis and treatment. Given the complexity of the human experience, it's important to recognize that many of the causes of mental illness are likely to be social or circumstantial, external to the individual. More debatable is how to distinguish psychology from neuroscience, mind from brain, without becoming neuroreductionistic. Personalized scientific approaches to psychiatry on a par with other medical disciplines remain largely aspirational, but current approaches are likely to move the needle.

1. An important clarification about how the word “causal” is being used here–it is being used to refer to the causes of the problems in the present moment, the precise factors in the complex system which maintain the status quo of health and illness. Notably, we are not necessarily talking about the historical causes–what started the process in motion may not be what is currently causing it to persist. This is a mathematic definition of causality.

2. Causal discovery has been used to look at PTSD among police officers using a process called Protocol for Computation Causal Discovery in Psychiatry (PCCDP). Saxe and colleagues (2020) reviewed a large data set from over 200 police officers. They identified 83 causal pathways with 5 causes: changes (single-nucleotide polymorphisms–SNPs) in histidine decarboxylase and mineralocorticoid receptor genes involved with stress-response, acoustic startle to low perceived threat during training, peritraumatic distress to incident exposure in the first year of service, and general symptom severity during training after one year of service. This study is a proof-of-concept for using causal discovery to identify points for intervention, and clearly could be used preventively–for example, identifying trainees with those features and responding accordingly.

3. Four Biotypes of Depression

4. Brainprint of Basic Mental Activity

WHO Depression Fact Sheet

CDC Depression Prevalence 2020

CDC Anxiety

NIH Brain Initiative

Saxe GN, Bickman L, Ma S, Aliferis C. Mental health progress requires causal diagnostic nosology and scalable causal discovery. Front Psychiatry. 2022 Nov 15;13:898789. doi: 10.3389/fpsyt.2022.898789. PMID: 36458123; PMCID: PMC9705733.

Saxe GN, Ma S, Morales LJ, Galatzer-Levy IR, Aliferis C, Marmar CR. Computational causal discovery for post-traumatic stress in police officers. Transl Psychiatry. 2020 Aug 11;10(1):233. doi: 10.1038/s41398-020-00910-6. PMID: 32778671; PMCID: PMC7417525.

Tozzi, L., Zhang, X., Pines, A. et al. Personalized brain circuit scores identify clinically distinct biotypes in depression and anxiety. Nat Med (2024). https://doi.org/10.1038/s41591-024-03057-9

Grant Hilary Brenner, M.D., a psychiatrist and psychoanalyst, helps adults with mood and anxiety conditions, and works on many levels to help unleash their full capacities and live and love well.

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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 fact sheet provides information about the link between depression and chronic disease. It describes what a chronic disease is, symptoms of depression, and treatment options, and presents resources to find help for yourself or someone else.
• 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.

Last Reviewed: March 2024

Unless otherwise specified, the information on our website and in our publications is in the public domain and may be reused or copied without permission. However, you may not reuse or copy images. Please cite the National Institute of Mental Health as the source. Read our copyright policy to learn more about our guidelines for reusing NIMH content.

6 distinct forms of depression identified by AI in brain study

A new analysis of the brains of 800 people has revealed that there may be six distinct types of depression, with potential implications for treatment.

Scientists have identified six biologically distinct forms of depression , which could explain why some people don't respond to traditional treatments for the condition, such as antidepressants and talk therapy. 

In a new study, researchers analyzed brain scans of more than 800 patients who'd been diagnosed with depression and anxiety. These scans were taken as the patients were resting and while they were engaged in different tasks designed to test how their brains functioned. 

Specifically, the team compared the brains of the patients, looking for differences in the activity of specific regions and the connections between them. These brain "circuits" had previously been identified as being implicated in depression. They include the frontoparietal network, which is associated with goal-driven behavior , and the default mode network, which is tied to daydreaming . 

Using a type of artificial intelligence (AI) known as machine learning, the team was able to categorize the patients into specific groups based on their brain scans. Patients within each group differed in terms of their symptoms and their ability to complete certain tasks, the team found. They described their findings in a paper published Monday (June 17) in the journal Nature Medicine . 

For instance, patients who had high activity in regions of the brain associated with processing emotions were more likely to display feelings of anhedonia — the inability to experience pleasure — than other patients. They also performed worse than the others on tasks that assessed their executive function, or capacity to focus and manage activities. 

Related: 'Scent therapy' helps unlock memories in people with depression, trial finds

Despite being grouped under the same umbrella term of major depressive disorder (MDD), not everyone experiences depression in exactly the same way, Leanne Williams , co-senior study author and a professor of psychiatry and behavioral sciences at Stanford University, told Live Science. 

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To be officially diagnosed with MDD, a patient must have experienced at least five of nine possible symptoms of depression — such as depressed mood, insomnia and fatigue — for at least two weeks. However, this leaves a lot of possible symptom combinations. 

A better understanding of the biological reasons for a particular symptom of depression may help patients feel like they're understood and may help reduce any stigma associated with their condition, Williams said. 

In a separate analysis, the team found that three of the six subtypes that they'd identified showed signs that they were either more or less likely to respond to specific treatments. For example, patients who had high activity in cognitive regions of the brain responded better to an antidepressant called venlafaxine, commonly marketed under the brand name Effexor, than other subtypes did. 

This knowledge could be clinically useful, as up to a third of people with depression don't respond to any form of treatment. Meanwhile, it can take weeks or months to determine if antidepressants, for instance, will have an effect on a particular patient's symptoms. 

"To see that we can predict better outcomes on specific treatments really makes it [this work] really worthwhile," Williams said. 

This is an "extraordinary" study, Greg Siegle , a professor of psychiatry at the University of Pittsburgh, who was not involved in the research, told Live Science in an email. 

The idea that neuroimaging-derived subtypes of depression could have important clinical differences and potentially different treatment responses could be a critical step in moving towards personalized care, he said. 

— 'Smoothness' in parts of brain's surface may boost risk of depression, study suggests

— Psychedelics may treat depression by invading brain cells

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The researchers now plan to test their approach on more people. They'd also like to look at the response of each subtype to other treatment options.  

The hope is that someday, doctors might be able to match patients to the type of treatment that is most likely to work for them based on their subtype, Williams said. 

Emily is a health news writer based in London, United Kingdom. She holds a bachelor's degree in biology from Durham University and a master's degree in clinical and therapeutic neuroscience from Oxford University. She has worked in science communication, medical writing and as a local news reporter while undertaking journalism training. In 2018, she was named one of MHP Communications' 30 journalists to watch under 30. ( [email protected] ) 

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Parental attachment and depression in vocational college students: a moderated mediation model of resilience and subjective well-being

• Published: 21 June 2024

Cite this article

• Shuwei Hao   ORCID: orcid.org/0000-0002-5867-1275 1  

Based on theoretical and empirical research on subjective well-being and resilience, the present study constructs a moderated mediation model to explore their role in parental attachment and depression among vocational college students. A cross-sectional study was conducted with a sample of 1055 vocational college students in Beijing, China. Results indicated that insecure parental attachment significantly positively predicts depression and negatively predicts subjective well-being. Moreover, subjective well-being acts as a mediator between parental attachment and depression. More importantly, resilience can moderate not only the direct path of parental attachment to depression, but also the indirect path by the first half of the subjective well-being mediator path. The present findings provide novel insights into the understanding of depression through attachment theory and positive psychology, suggesting that interventions targeting parental attachment and resilience hold promise for reducing depression in vocational college students.

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Acknowledgements

This work was supported by the Major Projects of Beijing Municipal Science & Technology Commission [D151100002315004]. Thanks to prof. Rengang Wu, the recipient of the Foundation, and Dr. Honghong Xu for their support and help in this study.

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Hao, S. Parental attachment and depression in vocational college students: a moderated mediation model of resilience and subjective well-being. Curr Psychol (2024). https://doi.org/10.1007/s12144-024-06234-8

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The Nature of Clinical Depression: Symptoms, Syndromes, and Behavior Analysis

In this article we discuss the traditional behavioral models of depression and some of the challenges analyzing a phenomenon with such complex and varied features. We present the traditional model and suggest that it does not capture the complexity of the phenomenon, nor do syndromal models of depression that dominate the mainstream conceptualization of depression. Instead, we emphasize ideographic analysis and present depression as a maladaptive dysregulation of an ultimately adaptive elicited emotional response. We emphasize environmental factors, specifically aversive control and private verbal events, in terms of relational frame theory, that may transform an adaptive response into a maladaptive disorder. We consider the role of negative thought processes and rumination, common and debilitating aspects of depression that have traditionally been neglected by behavior analysts.

As the field of clinical behavior analysis grows, it will benefit from analyses of increasingly complex and common clinical phenomena, especially those with significant public health implications. One such phenomenon is clinical depression, considered to be the “common cold” of outpatient populations. Up to 25 million people in the United States alone meet criteria for some type of depressive disorder in a given year (M. B. Keller, 1994 ). Depressive disorders also result in considerable financial expenditure including time spent away from the workplace and an increase in health care costs. Based on broad measures that include work absenteeism, treatment costs, and other factors, the annual economic cost of depressive disorders in the United States may be over $40 billion ( Antonouccio, Thomas, & Danton, 1997 ). Suicide is the ultimate cost.

Perhaps nowhere in clinical psychology is the medicalization of behavioral problems more complete than with depression. Depression is largely seen by the general public and mainstream media as a neuropsychiatric illness (e.g., Wingert & Kantrowitz, 2002 ) with a fluctuating course that is best described in disease-state terms such as disorder, episodes, remission, recovery, relapse , and recurrence ( Frank et al., 1991 ). An additional assumption is that this disorder may be diagnosed and labeled using the symptom checklists of the standard diagnostic system, the Diagnostic and Statistical Manual of Mental Disorders ( DSM-IV-TR ; American Psychiatric Association, 2000 ). The basic ontological assumption is that depression is an illness that occurs episodically and can be described adequately in medical terms. Thus, more depression is treated in primary care than in any other mental health or health care setting ( Kessler, McGonagle, Swartz, Blazer, & Nelson, 2003 ; Shapiro, 1984 ), and guidelines for treatment in these settings recommend antidepressant treatment without specialty referral unless the patient has complicating factors such as comorbid substance use or suicide risk ( Schulberg, Katon, Simon, & Rush, 1998 ). Even in these cases, specialty referral is first to psychiatry for medication management, and only a small number of individuals diagnosed with depression will be seen by a clinical psychologist, much less a behaviorally oriented practitioner.

A hallmark of behavior analysis has been its condemnation of the misappropriation of lay terms as scientific, technical terms (e.g., Skinner, 1945 ). The first task is precise specification of the behavioral phenomena invoked by the term. There are several obstacles to achieving this precision with the term depression, which have been excellently presented for the term anxiety by Friman, Hayes, and Wilson (1998) . The case for depression is quite similar. First, the term depression was never meant as a technical term and actually has a metaphorical, idiomatic basis. Second, our psychiatric nomenclature and mainstream usage of the term suggest that depression is an empirical phenomenon with an essential composition. To a behavior analyst, the term depression is not a technical term, does not precisely map onto any empirical or behavioral phenomena, and has no essential composition. Thus, given the exhaustive medicalization of the phenomenon of depression, there exists an immense gap between a behavioral analysis of depression and mainstream usage of it as a medical term with its various associations and meanings.

Behavior-analytic writings on clinical depression (e.g., Dougher & Hackbert, 1994 , 2000 ; Ferster, 1973 ; Lewinsohn, 1974 ; see Eifert, Beach, & Wilson, 1998 , for an alternative, paradigmatic behavioral model) have been illuminative but sparse. Although research on depression has outpaced research on virtually every other disorder by psychiatric and cognitive-behavioral researchers, behavior analysts have been alarmingly silent. There are undoubtedly many reasons for this silence (e.g., a lack of training programs that focus on behavior analysis and traditional psychopathology and more reinforcement for studying familiar topics). More relevant to the current paper is the possibility that the exhaustive medicalization of the term; the wealth of non-behavior-analytic research data on biology and genetics, personality, and cognitive factors; and the emphasis on private events in depression—on how depression feels and on changing that feeling—may function to evoke avoidance in behavior analysts.

This is unfortunate, because behavior analysis can not only provide an integrative view of depression, taking into consideration genetics, biology, enduring patterns of responding labeled personality , verbal (“cognitive”) behavior, and private events, but it can do so with a theoretical consistency and pragmatic utility unmatched by other theoretical systems. In this paper we attempt to start at the beginning, with a discussion of what depression is to a behavior analyst and how this contrasts with mainstream usage of the term as a medical syndrome. We review the traditional operant model of depression that emphasized reductions in behavior as a response to environmental events. We then tackle several areas of inquiry important to an understanding of depression that have traditionally been neglected by behavior analysts, including private events and the role of verbal behavior in depression. We see this not as completing a behavioral analysis but as a reminder of the importance of idiographic, functional analyses of specific individuals for this complex phenomenon.

What Is Depression? Tacting Depression and Its Symptoms

We describe depression in radical behavioral terms, emphasizing the occasions on which the term is used and deemphasizing any underlying unitary disease, physiological, or emotional state to which the term refers. Depression comes from the late Latin word depressare and the classical Latin word deprimere . Deprimere literally means “press down”; de translates into “down” and premere translates into “to press.” In essence, the term appears to denote a feeling of heaviness, of being “pressed down,” that is also referred to as “sad,” “blue,” or simply “down.” Depression also refers to a depressed topography or the fact of being pressed down. Depression as a referent to mood or emotional state appeared as early as 1665 and merely meant a lowering of mood or spirits ( Simpson & Weiner, 1989 ). Thus, the core experience of depression appears to be a private event tacted as depressed or in psychiatric terms as dysphoric . However, a minority of individuals will meet criteria for depression and deny depressed mood or present with irritable mood instead. These individuals may have deficits in accurate tacting of private experience, or they may represent diagnostic Type II errors and should not be classified as depressed.

It is important not to associate what is tacted as depression with a specific pattern of physiological responding or reify it as a particular emotional state. The antecedent conditions and underlying physiologies associated with the experience of depression may vary widely, and no core composition can be assumed. Emotional states such as sadness are simply co-occurring behavioral responses (elicited unconditioned reflexes, conditioned reflexes, operant predispositions) that appear to be integrated because the behaviors are occasioned by common discriminanda and are controlled by common consequences ( Skinner, 1953 ). For example, a child with overbearing parents experiences an emotional state of sadness and a co-occurring behavioral response of crying when her parents criticize her. The crying is negatively reinforced when her parents comfort her and stop criticizing her, which may also result in a change of her emotional state.

The particular quality of an emotional state labeled depression should vary with the characteristics of the environmental triggers. For example, private events labeled as depressed may be associated with overworking and receiving little reinforcement for long stretches of time or with grieving the death of a loved partner. In each case the underlying physiology is presumably different, but the experienced phenomena may be sufficiently similar to prompt the tact. More specific discrimination training may be useful (e.g., the first situation may be better labeled as burned out and the second as grieving ) but given the problems associated with training the tacting of private events ( Moore, 1980 ) it is not clear that an individual will be able to make these discriminations reliably.

The psychiatric nomenclature emphasizes this core experience and several additional symptoms. Depressed mood or dysphoria is the primary feature of major depressive disorder (MDD), the most common depressive diagnosis. In addition to this core experience, there are several other symptoms of MDD, including loss of interest in activities, sleep and appetite changes, guilt and hopelessness, fatigue, restlessness, concentration problems, and suicidal ideation. As discussed in detail below, the medical model holds that this constellation of symptoms represents a syndrome, but complexity is immediately introduced because the presence and nature of these symptoms vary considerably across clients ( Líndal & Stefánsson, 1991 ). For example, some clients experience vegetative symptoms of depression (decreased appetite and insomnia) whereas, less commonly, others experience reversed vegetative symptoms of increased appetite and hypersomnia. Similarly, psychomotor retardation is more common and agitation is less common, and both may be demonstrated by the same individual at different times.

To account for this complexity, DSM-IV-TR has parsed depression into various additional categories, each with similar and overlapping characteristics, and there are an increasing number of diagnostic categories of depressive disorders or problems involving sad or irritable affect. In fact, Appendix B of DSM-IV-TR lists 17 proposed disorders for further study, six of which deal with disorders of mood. Although detailed review of these subcategories is outside the purview of this paper, it should be noted that although there may indeed be different syndromes with different etiologies and treatment implications, a behavior-analytic view holds that the current proliferation of depressive disorders is largely unnecessary. We see not several distinct disorders but a phenomenon of depression with great variability in time course, symptom severity, and correlated conditions. All the disorders share a depressed mood symptom that parallels the core experience of the problem, and all share several additional criteria with MDD, often differing only in duration or number of symptoms. From an idiographic behavior-analytic perspective, there exists not one or three or several depressive disorders—there are as many depressive disorders as there are depressed individuals.

The constellation of depressive disorders with shared characteristics suggests that the tact depression involves a variety of public and private antecedent stimulating events that vary from occasion to occasion but have sufficient overlapping properties to occasion consistent usage of the term. We view the diversity of additional symptoms represented by these disorders as consistent with the diversity of environmental causes of depression, physiological states labeled depression , and psychological responses to the environmental causes and physiological states. Thus, no overarching depressive syndromes are posited or assumed at this point. Nonetheless, commonalities in history, environmental antecedents, and symptom presentation exist and may guide treatment decisions.

Thus, our understanding of depression must allow for the great variety of stimulus conditions that occasion use of the term. We can discard several classes of use that we can simply label as incorrect. For example, an individual learning a foreign language may simply state the wrong word. Likewise, a person may be diagnosed with depression but later it is determined that the person has a large cancerous tumor that is causing the symptoms. Although a complete behavioral analysis must account for these usages, they are not interesting from a clinical standpoint. More important are instances in which the term is not used but could be. For example, a person visits a psychologist and complains of several symptoms of depression but not depressed mood. Another person would label the private experience as “depressed,” but the current client did not develop adequate private stimulus control over the experience. The psychologist performs a diagnostic interview, and the client falls one symptom short of the diagnosis of MDD. In this case it is advantageous to consider the person depressed even though it is possible that neither the psychologist nor the client will use the term.

Traditional Behavioral Models of Depression

Skinner wrote very little on depression; when he did, he emphasized overt behavior rather than the core affective experience, in line with an operant rather than respondent model. For example, in 1953 he wrote,

If we remove a man from his characteristic surroundings, a large part of his social behavior cannot be emitted and may therefore become more and more probable: he will return to his old surroundings whenever possible and will be particularly “sociable” when he does so. Other parts of his behavior become strong because they are automatically reinforced under the prevailing deprivation; he will talk to anyone who will listen about his old surroundings, his old friends, and what he used to do. This is all a result of deprivation. But nostalgia is also an emotional condition in which there is a general weakening of other forms of behavior—a “depression,” which may be quite profound. We cannot classify this as the result of deprivation because the behavior which is thus affected has not been specifically restrained. (p. 165)

Three aspects of this passage are noteworthy. First, as Skinner typically did, by placing the term depression in quotes he was careful to avoid giving it any special status other than that of a verbal description. As discussed above, this practice of placing such terms in quotes may be awkward and tiresome but serves as a reminder that certain assumptions are not to be made when using them. The quotes also serve as a reminder of an important verbal quality to the term, discussed below. Second, Skinner described the core experience as an “emotional condition,” suggesting an elicited component. Consistent with an operant model, he did not elaborate on this point and instead focused on overt behavioral reductions. Third, Skinner highlighted the centrality of reduced positive reinforcement in depression. Simply put, social behavior depends on a reinforcing environment; change the environment so that responses do not yield reinforcement and one reduces the behavior.

This notion became the foundation of Lewinsohn's (1974) theory and dominated the behavioral literature for several decades. Lewinsohn described depression as characterized primarily by a low rate of response-contingent positive reinforcement (RCPR). In a nutshell, Lewinsohn emphasized environmental events that produce losses of major sources of RCPR, such as a divorce or the loss of a job, and social skills deficits that limit an individual's ability to reobtain RCPR once it has been lost. Thus, his model focused on the behavioral reductions often seen in depression. Lewinsohn assumed the core experience to be an elicited by-product of these situations, but he did not detail this process. Other symptoms of depression (e.g., fatigue, somatic symptoms, and cognitive symptoms) were assumed to be evoked or to be secondary elaborations of other symptoms.

We hold that Lewinsohn's (1974) characterization of the core affective experience of depression as an elicited by-product of losses of or reductions in positive reinforcement is fundamental to understanding depression. Some cases of depression clearly are described best by Lewinsohn's model, such as single, discrete episodes of depression with clear environmental precipitants and with symptom profiles that emphasize behavioral reductions that resolve when the environments are reinstated. For example, a person may become depressed after a divorce or loss of job, and the depression resolves when the person finds a new relationship partner or a new job. With cases of chronic depression, Lewinsohn's model emphasizes persistently insufficient levels of reinforcement and social skills deficits that prevent the individual from changing the situation, and this model also seems to be adequate for some cases. For example, a person who becomes depressed after a divorce, resulting in a net reduction in positive reinforcement, and does not have adequate social skills for initiating new romantic relationships will likely become chronically depressed until the necessary social skills are learned.

All of this is nothing new. However, Lewinsohn's (1974) model vastly underestimated the variety and complexity of factors that can reduce behavior. Indeed, the field of behavior analysis, if nothing else, has demonstrated functional processes that can increase or decrease behavior. All functional processes that decrease behavior are potentially relevant, if the behavioral reductions produced are large and generalized and a dysphoric reaction occurs concomitant with the behavioral reductions. For example, extreme persistent and uncontrollable punishment may lead to substantial behavioral reductions, elicited negative affect, and depression as per Seligman's early learned helplessness model ( Overmier & Seligman, 1967 ).

Further consideration of this complexity is provided by Hopko, Lejuez, Ruggiero, and Eifert (2003) and Lejuez, Hopko, and Hopko (2001) , who analyzed depression in terms of the matching law ( Herrnstein, 1970 ). Briefly, this suggests that the behavioral reductions seen in depression are not accurately seen as the simple product of reductions in positive reinforcement but rather as the product of ratios of reinforcement for depressed relative to nondepressed (or healthy) behavior. In other words, the sum total of reinforcement available in a person's environment must be taken into consideration, not just reinforcement for target behaviors. As a simple example, a depressed person may not get out of bed due to loss of a job (loss of positive reinforcer for getting out of bed), but positive reinforcers for staying in bed (e.g., spouse who now takes care of the person or makes the person breakfast) must also be considered. The bottom line is that the situation is complicated, and nothing less than a complete functional analysis of the individual's environment is required if one is to attempt a full functional analysis of depression.

Aversive Control in Depression

Skinner also suggested that depression may be an emotional response to aversive controlling practices, especially aversive social control (1953, pp. 360–363). Similarly, Ferster (1973) suggested that depression is characterized as much by increased escape and avoidance repertoires as by reduced positive repertoires. In fact, research indicates that more cases of depression are characterized by the accrual of multiple chronic mild stressors, such as work-related stress, homemaking demands, and financial trouble than by major losses such as divorce or the loss of a job ( Billings & Moos, 1984 ; Kessler, 1997 ; Mazure, 1998 ; Monroe & Depue, 1991 ; Paykel, 1982 ). In these cases we suggest that the core elicited affective experience of depression is as much a product of increased aversive control as it is reduced appetitive control.

It is important to recognize, however, that the two sources of control are often intimately related. Ferster (1973) suggested that the depressed escape and avoidance repertoire is largely passive, which also leads to a decrease in positive reinforcement relative to what an active repertoire would provide. For example, consider a client who stayed in bed all day and did not go to work, thereby avoiding a stressful meeting with his boss where he believed he was going to be reprimanded. Staying in bed successfully avoids this outcome, but it also prevents contact with other contingencies that might function to ameliorate depression—for example, if the client was wrong and no reprimand was forthcoming. Similarly, an individual with social phobia, which is highly comorbid with depression ( Mineka, Watson, & Clark, 1998 ), may be negatively reinforced by successfully avoiding situations that may result in social humiliation or embarrassment, but avoidance of such situations also reduces opportunities for contact with positive social reinforcement. In other words, an increase in aversive social control here almost guarantees a decrease in appetitive social control. These aversive environments evoke and maintain behavior that is immediately effective as a response to these contingencies but maladaptive over the long term in that access to positive reinforcers is diminished.

Such aversive situations may elicit anxiety rather than depression per se, but the point is that a repertoire characterized by excessive escape and avoidance behavior (and elicited affect labeled anxiety ) will undoubtedly result in decreased contact with positive reinforcement (and elicited affect labeled depression ) over time. Thus, anxiety should precede and then become comorbid with depression, and this pattern appears to characterize many comorbid cases ( Mineka et al., 1998 ). In fact, the well-established comorbidity of anxiety and depressive disorders should be a function of the degree to which anxious avoidance also results in a loss of positive reinforcement. Hayes, Wilson, Gifford, Follette, and Strosahl (1996) have provided a convincing review showing that avoidance may underlie a host of psychological problems, including depression, and the specific relation between avoidance and depression has received empirical support as well (reviewed by Ottenbreit & Dobson, 2004 ). Finally, research indicates that over the course of treatment for social phobia, change in anxiety predicts change in depression, but change in depression does not predict change in anxiety ( Moscovitch, Hofmann, Suvak, & In-Albon, 2005 ), suggesting that symptoms of depression are at least partially maintained by a social environment that has aversive functions.

To summarize our analysis to this point, there are many pathways to depression. Depression is not a precise, technical term and has no essential composition. It is not a syndrome. The term refers to a chronic experience of feeling sad or down and to associated symptoms that vary widely. This symptomatic heterogeneity is due to the heterogeneity of historical and environmental controlling variables. That said, some processes may be more common in depression, and awareness of these processes would help to limit what could be a vast assessment of many potentially irrelevant variables ( Hayes & Follette, 1992 ). Two broad processes have been highlighted here: (a) losses of, reductions in, or persistently insufficient levels of positive reinforcement as per Lewinsohn (1974) , and (b) increases in environmental aversive control (negatively reinforcing and punishment contingencies). When chronic, both processes may be seen as functioning as enduring motivating operations for depression ( Dougher & Hackbert, 2000 ). Of course, multiple sources of control are probable.

An Adaptive Syndrome or Maladaptive Response? Genetics and Evolutionary Theories

In contrast to an idiographic functional analysis of depression, the medical disease model posits that depression is a syndrome or multiple syndromes and one inherits risk for this syndromal response. The model relies to a considerable degree on research indicating at least some genetic involvement in depression ( Wallace, Schneider, & McGuffin, 2002 ). However, the family, twin, and adoption studies on which this conclusion is based point to a larger environmental contribution than genetic contribution in all but the most severe cases of depression ( Wallace et al., 2002 ). Furthermore, researchers and theorists from a variety of perspectives have highlighted methodological flaws and unsubstantiated assumptions of this research ( Ceci & Williams, 1999 ; Hayes, 1998 ; Turkheimer, 1998 ) that have the collective effect of lowering heritability estimates even further as well as questioning their very basis. Nonetheless, it seems likely that some inherited vulnerability to depression exists in some cases, and a full behavior-analytic account can include this possibility.

A typical behavioral argument against the medical disease model of depression is to accept that depression is a syndrome but posit that it is adaptive, the product of contingencies of survival ( Skinner, 1953 ). In fact, many evolutionary explanations for depression have been offered (e.g., Bowlby, 1980 ; Gilbert, 1992 ; Leahy, 1997 ; Price, Sloman, Gardner, Gilbert, & Rohde, 1994 ; P. J. Watson & Andrews, 2002 ; see McGuire & Troisi, 1998 , for a review), and such evolutionary accounts are important to consider and are consistent with behavioral theory ( Corwin & O'Donohue, 1995 ). There are three broad themes under which these theories fall: resource conservation, social competition, and attachment ( Allen & Badcock, 2003 ).

Theories of resource conservation posit that depression permits the conservation of resources and disengagement from unsuccessful goal-directed activity by decreasing appetite, energy levels, and motivation ( Leahy, 1997 ; Nesse, 2000 ). For instance, when in a new environment with unknown contingencies, such as traveling to a foreign country, one is more likely to be functioning in a way to avoid negative reinforcement or punishment while trying to learn the rules of the new environment. If one were to engage in a goal-directed activity, such as trying to obtain a job, one would likely not be successful. Social-competition theories view depression as a deescalation or yielding reaction to a defeat. This is said to be adaptive because it signals submission to the victor and allows acceptance of social subordination and the avoidance of unnecessary conflict ( Price, 1967 , 1998 ; Price et al., 1994 ). An example of this can be seen in a boxing match, when one fighter is knocked down for a full 10 counts. The loser typically displays behaviors including sloped posture, decreased eye contact, and avoidance (all depressed behaviors) as opposed to getting back up and continuing to fight. Finally, attachment theories of the adaptive nature of depression claim that a depressive reaction is an adaptive response to the loss of interpersonal relationships that helps to maintain the proximity of caregivers or reestablish an attachment by signaling a need for assistance from others and eliciting that assistance ( Averill, 1968 ; Bowlby, 1980 ; Frijda, 1994 ). This can easily be seen by a lost boy in a busy mall. When the child begins to cry, passersby typically attend to him, try to find the boy's parents, and comfort him during the search.

We suggest that depression is neither a syndrome nor adaptive. Any theory of depression as an adaptive syndrome has to overcome two primary hurdles inherent in the phenomenon. First, given the variability in symptom profiles in depression, one has to pick which set of symptoms of depression comprises the syndrome, or alternately posit multiple syndromes with different symptom sets (M. C. Keller & Nesse, 2006 ). For example, are both melancholic and atypical depression adaptive syndromes? Given that some of symptoms associated with melancholic depression (insomnia and loss of appetite) are the opposite of those associated with atypical depression (hypersomnia and increased appetite), it is impossible for the same theory to account for both presentations.

Second, the nature and chronicity of depressive symptoms seem to be maladaptive. For example, a transient sad mood in response to a loss certainly seems adaptive in that it elicits empathy and evokes helping behaviors in others. If this is true, then such an affective respondent reaction may have evolved due to contingencies of survival. It would be expected to have certain losses as antecedents and to resolve when support is acquired. However, in clinical depression the sad mood is often chronic and unresponsive to helping behaviors. In fact, although the evolutionary account suggests that the response should garner social support, research is clear that depressive behaviors result in decreased social support ( Coyne, 1976 ; Gotlib & Lee, 1989 ; Joiner & Metalsky, 2001 ) and worse psychosocial functioning in general ( Barnett & Gotlib, 1988 ). Suicide is another example. Although suicidal gestures may be seen as operant attempts to garner support ( Linehan, 1993 ), completed suicide is difficult to conceive of as an operant (i.e., learned) behavior ( Hayes, Strosahl, & Wilson, 1999 ) and is clearly not adaptive in terms of survival.

A more likely scenario is that depression itself is not adaptive, but the core experience represents a variation of an adaptive affective response ( Nettle, 2004 ; also see Nesse, 2000 ). In other words, the capability to experience moderate low mood or sadness in appropriate situations (but not become clinically depressed) may have many of the same short-term benefits that have been used to support the claim that depression is adaptive. Support for this view comes from personality researchers, who have posited the temperamental trait of negative affectivity as a trait that is selected for and normally distributed ( Nettle, 2004 ; D. Watson & Clark, 1984 ), and considerable research suggests that this trait may be a vulnerability factor for both depression and anxiety (L. A. Clark & Watson, 1991 ; L. A. Clark, Watson, & Mineka, 1994 ).

Although the notions of temperament or traits are unnecessary, it is reasonable to suggest that there may be a range in the duration and magnitude of affective reactions that are adaptive. A depressed individual could represent a deviation from that range in that he or she experiences negative affect longer and to a greater extent in response to an environmental event. In other words, the propensity to experience mild and appropriate levels of negative affect may be adaptive and thus appear on a continuum; those at one of the extreme ends of this continuum may be quite sensitive to fluctuations in reinforcement contingencies, suffer from chronic negative affect, and be at risk for clinical depression.

It is important to remember that we are proposing a scenario in which there is a genetic contribution to the likelihood of the core affective experience in depression but the remaining symptoms are potentially free to vary and should be described in terms of antecedents and consequences. Of course, there may be an adaptive, normally distributed range in the sensitivity of these additional behaviors (e.g., sleep) to environmental stimuli that represent separate inherited vulnerabilities. This view of depression is consistent with recent biological findings that suggest that depression is likely a product of multiple genes and a complex gene–environment interaction ( Wallace et al., 2002 ), as well as neuroscientific findings of mixed and variable structural and functional abnormalities in several brain regions, with few depressed individuals displaying the complete package of deficits, leading researchers to conclude that depression refers to a heterogeneous group of disorders as well ( Davidson, Pizzagalli, Nitschke, & Putnam, 2002 ). Thus, other scientific fields are taking tentative steps away from a syndromal view of depression and toward an idiographic analysis.

The Shift From Adaptive to Maladaptive Behavior

As discussed above, elicited affective experiences are normal, adaptive, and not disordered. Depression appears to be a maladaptive dysregulation or extension of this adaptive experience. Genetic vulnerabilities aside, it is important to identify the historical and environmental processes responsible for this shift from a normal, adaptive experience of elicited affect to a disordered experience of depression.

Obviously, chronically maladaptive environments may produce chronically maladaptive behavior. Perhaps the simplest and ultimate example of this is a concentration camp ( Frankel, 1984 ). Such an environment, almost completely lacking in positive reinforcers and abundant in stable and salient aversive stimuli, may result in rather consistent depressed behavior and negative affect. However, it is safe to say that most depressed people do not live in such environments. Processes through which environments characterized by variable positive and negative reinforcers and punishers result in relatively stable experiences of depression need to be identified. For example, consider a person who has a handful of close friends with whom she interacts with on a regular basis, men who are showing interest in her romantically, good career prospects including an upcoming promotion (all opportunities for positive reinforcement), but still cannot sleep at night and considers herself to be depressed. The question remains, why do so many people engage in repertoires that are more consistent with impoverished environments than with those environments in which they live? Below we consider two processes: avoidance of aversive private events and the role of verbal behavior.

Avoidance of Private Events

Two similar processes by which an adaptive elicited response can lead to chronic and maladaptive depression in the absence of chronically maladaptive environments recently have been proposed and linked to treatment techniques: Martell, Addis, and Jacobson's (2001) theory behind behavioral activation (BA) and Hayes et al.'s (1999) model of experiential avoidance for acceptance and commitment therapy (ACT). The two models differ in several respects (see Kanter, Baruch, & Gaynor, 2006 , for a full comparison).

Both models argue that problematic avoidance in depression is not always a response to the environment per se, but is a response to the core aversive experience of depression (which is in turn a response to the environment). Both models suggest that the core affective experience, once elicited, may play a functional role in maintaining, exacerbating, and creating the additional symptoms of depression. Specifically, if we allow that the initial elicited private response is functionally aversive, it may evoke behavior designed to avoid and escape the private response. For example, after a difficult breakup, a man may experience an increase in feelings of anxiety and negative self-referential thoughts. Although this individual now may avoid public stimuli based on formal stimulus properties (e.g., romantic relationships), he also may avoid the newly elicited thoughts and feelings in a variety of ways (e.g., heavy drinking). The key to understanding how this applies to depression is the notion that avoidance of private events, even when it works in the short term, produces additional long-term problems. In the example above, the man feels better in the short run after drinking, but the long-term consequences would likely include an even more impoverished environment. Through this process, flexible repertoires of problem solving and repertoires based on stable positive reinforcement are either extinguished, depotentiated, or never developed.

BA interventions have focused on disrupting how aversive private events can function as discriminative stimuli or motivating operations for avoidance behavior. For example, consider a client who stayed in bed all day because she felt depressed and thereby was able to avoid the additional stress and fatigue associated with her unpleasant work situation. Although she may experience her work situation as aversive to some extent at all times, the heaviness and fatigue experienced upon awakening in the morning and tacted as “feeling depressed” may signal that working would be experienced as especially aversive on that particular day. According to BA, staying in bed in this situation is negatively reinforced through avoidance of an especially aversive work day. However, it creates more long-term problems and solves none in that it does nothing to address the aversive work situation proactively ( Kanter et al., 2006 ).

ACT offers additional theoretical elaborations that suggest a more prominent role for verbal behavior in avoidance processes. First, ACT suggests that experiential avoidance repertoires are maintained over long periods of time because they are rule governed or verbally controlled ( Hayes & Ju, 1998 ). In other words, individuals develop rules that dictate experiential avoidance, and these rule-governed avoidance repertoires may persist in the face of histories of reinforcement to the contrary. For example, a depressed man may tell himself, “If bad things happen in my life, I will take it like a man.” Such self-talk may lead to denial of certain private events such as sadness or grief (e.g., after his father died) despite an environment that would shape more effective behavior (e.g., a loving wife who wants to discuss his feelings), were it not for verbal control.

There may in fact be no way to distinguish a rule-governed avoidance repertoire (i.e., ACT) from a directly conditioned avoidance repertoire (i.e., BA) in a clinical setting, in that the topographies may look similar, the relevant reinforcement histories are distal, and reporting on them accurately will be unreliable. At issue is the degree to which a depressed individual's avoidance is rule governed. In fact, Rehm (1979 , 1989) has argued that depressed individuals demonstrate deficits in the ability to generate and follow rules, and his self-management therapy program attempts to improve self-monitoring, self-evaluation, and self-reinforcement skills. In accord with these views are findings that depressed individuals demonstrate increased self-reported preferences for immediate over delayed reinforcement compared to nondepressed individuals, suggesting less rule following in depressed individuals ( Rehm & Plakosh, 1975 ). Two additional studies have shown that dysphoric individuals demonstrate greater schedule sensitivity and less rule-governed behavior compared to nondepressed individuals ( Baruch, Kanter, Busch, Richardson, & Barnes-Holmes, 2007 ; Rosenfarb, Burker, Morris, & Cush, 1993 ). However, these studies demonstrate significant variability in schedule sensitivity, and McAuliffe (2003) found the opposite (increased rule-governed behavior in depressed adolescents), again highlighting the need for idiographic analysis and acknowledging both increased rule-governed behavior and decreased rule-governed behavior to be problematic in depression.

To reiterate the important themes at this point, it bears repeating that an idiographic analysis is required. Some cases of depression may be adequately conceptualized in terms of Lewinsohn's (1974) traditional model of reductions in response-contingent positive reinforcement, whereas others may be more accurately conceptualized in terms of ACT's or BA's models of avoidance. In both the traditional model and the new conceptualizations, the core experience is seen as an elicited response to environmental events that produce reductions in positive reinforcement. However, the new conceptualizations speculate how one's reaction to that experience may in fact perpetuate and exacerbate it, and in some cases this may be the case.

The Functions of Private Events in Behavior Analysis

Allowing that a private response is functionally aversive creates some problems for behavior analysis. Simply put, the classic exhortation to focus functional analyses on manipulable environmental variables may lead some to conclude that private events are simple respondent by-products and have no functional value. This stance on the nonfunctional value of private events is one of the great perplexities of behavior analysis. It is a perplexity because, to most humans, thoughts and emotions—as we have come to label them—are not only felt quite strongly at times but it feels as if they control our behavior ( Schnaitter, 1978 ). This is especially true regarding avoidance behavior, which is often described as negatively reinforced by a reduction in aversive emotional experience (e.g., Barlow, 2002 ). In other words, it seems as if we avoid not only the conditions that occasion depression but also feeling depression itself. It may have been behavior analysts' rigid adherence to this simple view of private events, which runs counter to common sense for many researchers, therapists, and clients, that bolstered the cognitive revolution and the subsequent obsolescence of behavioral approaches to treatment of depression, as well as adult outpatient psychotherapy in general, which is dominated by “feeling” talk.

Skinner presented a much more nuanced and complex view. On the one hand, he consistently defined reinforcers and discriminative stimuli as environmental stimuli on pragmatic rather than ontological grounds ( Skinner, 1945 , 1953 ). Simply put, reinforcers are labeled as such only if functional analysis has determined, or at least in principle could determine, that a manipulable event evidences such a function. Private events in general are not manipulable in this sense and thus have been typically defined as dependent rather than independent variables. Put differently, Skinner consistently argued that emotions are not causes.

However, in other places Skinner allowed private events to participate, partially, in the control of behavior. For example, he wrote,

Emotional responses may be interpreted as in part an escape from the emotional components of anxiety. Thus we avoid the dentist's office, not only because it precedes painful stimulation and is therefore a negative reinforcer, but because, having preceded such stimulation, it arouses a complex emotional condition which is also aversive. The total effect may be extremely powerful. (1953, p. 179)

In this example, the emotional components of anxiety clearly have taken on functional stimulus properties. Likewise, Skinner's analysis of self-knowledge (1957, 1974) depended heavily on the supposition that private events exert discriminative control over tacting. In this case, the use of the term private event rather than private behavior may have been Skinner's acknowledgment of the complexity, but the complexity is not resolved simply by changing the term. In these cases, although the private events in question are assumed to have acquired at least partial control over other behavior, environmental variables are important for the historical development of the control (see also Hayes & Brownstein, 1986). For example, in the case of the tact of “sad,” the private stimulation involved is seen as the discriminative stimulus for the resulting tact, and that stimulation has obtained functional significance through social mediation ( Moore, 1980 ). Thus, it is consistent with behavior analysis (or at least, with behavior analysis's inconsistency) to allow functionally salient private events to evoke avoidance behavior.

The Role of Verbal Behavior in Depression

Perhaps the biggest obstacle for traditional behavioral theorists to overcome when discussing depression is the role of language. In general, an extremely large and unquestionable body of research establishes the presence of negative cognitive content during depressive episodes, leading cognitive researchers to assume a causal role for cognition in depression (D. A. Clark, Beck, & Alford, 1999 ). Although longitudinal research has failed to establish negative cognitive biases as independent predictors of depression ( Ingram, Miranda, & Segal, 1998 ), it is clear that thinking influences feeling on a moment-to-moment basis. Cognitive researchers see this influence as sufficiently causal, but behavior analysts instead search for environmental conditions responsible for such behavior–behavior relations ( Hayes & Brownstein, 1986 ). Regardless, it is clear that negative thinking predominates in many depressions, and such thinking may elicit aversive affect.

Research on stimulus equivalence (e.g., Sidman, 1994 ) readily accounts for the relation between cognition and mood. Simply put, through participation in equivalence relations with nonverbal stimuli, verbal stimuli may obtain eliciting functions. Although there are many examples of this effect, perhaps the clearest example is work by Dougher and colleagues on the transfer of aversive elicitation and avoidance functions through equivalence classes. Using match-to-sample procedures, Dougher, Augustson, Markham, Greenway, and Wulfert (1994) taught 8 subjects two four-member equivalence classes, paired one member of one class with electric shock, and then demonstrated transfer of elicited arousal to other members of the class that had not been directly paired with the shock. Augustson and Dougher (1997) subsequently demonstrated that avoidance responding similarly transfers through equivalence classes. After pairing one member of one class with shock, subjects were taught that they could avoid this member by repeatedly pressing a key on the keyboard. Subjects then demonstrated transfer of avoidance response functions to other class members.

Growing research on relational frame theory (RFT; Hayes, Barnes-Holmes, & Roche, 2001 ) extends these findings. According to RFT, verbal behavior (including thinking) is technically seen as the behavior of framing events relationally: responding to one stimulus in terms of its given or inferred relation to other stimuli. For example, a woman caught speeding receives a ticket. If that person thinks that people who get speeding tickets are bad drivers, she may then consider herself a bad driver. RFT views equivalence as just one type of relation (i.e., sameness ) and views deriving relations among stimuli in the absence of direct conditioning as a generalized operant ( Barnes-Holmes & Barnes-Holmes, 2000 ).

Responding in accordance with other derived relations has also been demonstrated, including relations of sameness, opposition , and difference ( Roche & Barnes, 1996 , 1997 ; Steele & Hayes, 1991 ; Whelan & Barnes-Holmes, 2004 ), more than and less than ( Dymond & Barnes, 1995 ; O'Hora, Roche, Barnes-Holmes, & Smeets, 2002 ; Whelan, Barnes-Holmes, & Dymond, 2006 ), and before and after ( O'Hora, Barnes-Holmes, Roche, & Smeets, 2004 ; see also Barnes & Roche, 1996 ; Hayes & Barnes, 1997 ). Evidence is mounting that these relations may result in the transformation of functions in accordance with the relations trained, akin to the transfer of function seen with equivalence relations (for a review, see Dymond & Rehfeldt, 2001 ). Thus if that same woman who received a speeding ticket has a history of avoiding authority figures who reprimanded her in the past (e.g., teachers and supervisors), she may then begin to avoid police officers as well. These stimulus functions may be quite arbitrary and unrelated to current environmental features. Thus, the behavior of relational framing has a potentially transformative effect on the environment; environmental stimuli that would otherwise control behavior may not do so and new stimuli, idiosyncratic to the individual's verbal learning history, may exert control.

The importance of these findings to depression, and other psychological disorders, cannot be overstated. To the extent that stimulus equivalence and RFT present a behavior-analytic model of language and cognition, these theories provide behavior analysts with a vocabulary and theory with which cognitive variables can be conceptualized and understood. Negative self-statements so often seen in depression acquire their meanings and functions through transformations of function that occur in relational framing. For verbal stimuli to obtain these specific functions, previous specific-exemplar training involving the specific stimuli participating in relational frames is not necessary. All that is necessary is a history that establishes relational framing as a generalized operant and a history in which the specific stimuli at issue are related in a relational network.

There appear to be two uses of the term relational network , and a brief diversion on this issue is necessary because one of the usages may be potentially confusing to behavior analysts. First, a relational network may refer to a sentence or another unit of speech that sets the context for relational activity ( Barnes-Holmes, Hayes, Dymond, & O'Hora, 2001 )—there is no issue with this usage. Second, a relational network may be used to graphically depict the full set of relations between specific stimuli and the transformations of function that are relevant to a particular stimulus. Such networks are often displayed in RFT or stimulus equivalence experiments to depict the specific relations trained, but a network may also be employed more loosely when the history can only be assumed. For example, Blackledge (2003) displayed a network to account for a person taking a walk in the woods that elicits fear due to a verbal history in which it was learned that snakes are to be found in woods. This usage bears considerable resemblance to nonbehavioral entities such as schemas and requires clarification. One has to be careful to maintain that the network, unlike a schema, is the not the cause of behavior. The network is a description of a history, and it is this history, along with the current environmental and verbal events, that functions as the cause. The history is described in terms of a network to emphasize how the functions of any term in the network may be transformed in accordance with the network, but such transformations are a product of a history of verbal behavior described as a network, not the network per se. It is easy to lose sight of behavior analysis at this point; thus, it is important to remember that these functions of relational framing were obtained through a history of interaction with the social and verbal community. Historical environmental factors result in the transformation and reduction of control by the current environment. These effects are easily described in terms of relational networks and stimulus functions that are transformed across members of the network.

The important point is that verbal behavior can dysregulate and extend normal adaptive experiences of aversive elicitation into disordered experiences. Consider an individual who has received a poor work evaluation. This naturally elicits aversive affect that, if transient, can be considered normal and adaptive. However, this individual may begin to think about the event, and the content of thinking will be a complex product of multiple historical and current antecedents. Given a history that has established high-strength relational networks of “loss,” “failure,” “helplessness,” or similar networks, a transient setback such as a poor job evaluation can become functionally overwhelming. The key point is that the core experience of depression, the elicited affect, was normal and adaptive without verbal elaboration. With verbal elaboration, however, the experience is magnified and extended, and may become disordered.

Examples of verbal elaborations of potentially normal experiences abound in the clinical literature on depression. In fact, cognitive therapy for depression ( Beck, Rush, Shaw, & Emery, 1979 ) assumes challenging these unrealistic verbal elaborations to be the primary task of therapy. Discussion of whether such cognitive interventions are successful, for the reasons cognitive therapists say they are, is beyond the scope of this paper. Rather, we simply highlight the finding that many depressed individuals appear to have become depressed in the absence of environmental histories that would indicate such a response to be adaptive, and point to verbal behavior to account for the elaboration of such histories into a disorder. Language vastly expands the range of situations that can function as depression-eliciting and depression-maintaining stimuli, because the functions of the stimuli largely may be determined by one's idiosyncratic verbal learning history.

As an example, a depressed individual may respond to all social events as participating in a verbal relation with a host of other aversive stimuli (e.g., the words fake, small-talk, embarrassment, boring, stressful, idiot, foolish, exposed and the words for a range of aversive private sensations germane to escape, panic, etc.). Although another individual may respond to the relation between the stimuli party and stressful on occasion, there is flexibility in responding based on other historical and contextual features. For the depressed individual, however, this verbal class may be so well formed through a fairly idiosyncratic history of verbal and nonverbal pairings of these stimuli, and so negatively reinforced through past derived escape and avoidance experiences, that there may be few or no contexts in which the term party does not elicit the functions of other aversive stimuli or function as a derived discriminative stimulus for escape or avoidance. This rigid avoidance repertoire vastly narrows the range of behavioral options available and most likely will lead to rather stable reductions in response-contingent social reinforcement.

The Function of Rumination

In addition to negative cognitive content in depression, research clearly identifies a particular ruminative cognitive style in depression. In fact, a ruminative cognitive style predicts the onset ( Just & Alloy, 1997 ; Nolen-Hoeksema, 2000 ), length ( Umberson, Wortman, & Kessler, 1992 ), and severity ( Nolen-Hoeksema, Parker, & Larson, 1994 ) of depressive episodes. Depressed individuals may spend long periods of time “lost in thought,” rehashing events of the day and stewing over problems; this leads to increased negatively biased thoughts, poor problem solving, inhibition of operant behavior, impaired concentration, increased stress, and increased problems ( Lyubomirsky & Tkach, 2004 ). A complete behavioral analysis of depression needs to account for the relation between negative cognitive content and depressed mood as well as the function of rumination.

An appreciation of the somewhat unique features of verbal behavior in terms of antecedent and consequential control provides some insight into the function of rumination in depression. First, it bears repeating that thinking, like any behavior, is under the control of multiple and complex historical and situational stimuli. Consider a depressed student attending a lecture in a class in which she is doing poorly. She is having a hard time keeping up with the professor, and thoughts about her poor performance on the last test occur. The initial stimuli for such thoughts are obvious. As this continues, it is common that this student may end up thinking about a completely different topic, with unexpected twists and turns in thought, arriving at thoughts that she will never get her degree, that there must be something wrong with her brain, and that she is a complete failure. She now begins to think about a negative interaction with a friend the previous day, and thinks that her friendship was never genuine, that she is a failure as a friend as well as in school, and so forth. These twists and turns may increasingly be under the stimulus control of previous thoughts and decreasingly under the control of the current external environment. As described by RFT, the contextual cues that occasion relational framing and its content may themselves be relational and arbitrary in nature; thus, other than previous verbal behavior (which may be private), little environmental support is necessary to occasion verbal behavior and control its content. This in fact is consistent with Skinner's (1953) account. As Skinner put it, “The speaker's own verbal behavior automatically supplies stimuli for echoic, textual, or intraverbal behavior, and these in turn generate stimuli for further responses” (p. 439). He referred to such a thinking process as a “simple soliloquy” and noted, “Regardless of the respectability of the connections, such a ‘train of thought’ … is scarcely to be distinguished from a ‘flight of ideas’” (p. 439). We may refer to such thinking instead as rumination.

The question of reinforcing variables for such behavior remains. RFT suggests that verbal behavior occurs so frequently and relentlessly because of a history of reinforcement provided by the wider community for coherence or sense making in one's verbal behavior (see Hayes et al., 1999 ). It is argued that during early language-training experiences, the verbal behavior of the speaker is evaluated for coherence by the verbal community and is differentially reinforced. Over time, these processes (the verbal behavior, its evaluation in terms of coherence, and its reinforcement) become covert and automatic so that the derivation and rehearsal of coherent verbal relations becomes self-reinforcing (see Barnes-Holmes et al., 2001 ). Skinner (1953) highlighted that thinking is productive, in that it has an effect on the thinker and is reinforcing because it does so. Both processes are undoubtedly applicable. We would like the depressed student to think about her class performance and the poor friend interaction in such a way that it leads to improved performances and interactions in the future, but in many cases it does not. More likely is an avoidance function—the rumination may function to reduce the anxiety about the class performance and the interaction without increasing the anxiety of dealing with the problems in the moments they occur. As long as the cognitive solutions make sense and reduce anxiety, the rumination may continue, even if it is ultimately unproductive.

Accepting that sense making is reinforcing, one may still argue that the content of rumination often does not make sense and should not be reinforcing. In the current example, one poor performance in a class does not make one a failure as a student, and one poor friend interaction does not make one a failure as a friend. Indeed, pointing out that such content is not logical and is not evidence based is the hallmark of cognitive therapy ( Beck et al., 1979 ). However, to a behavior analyst sense making is idiographic and occurs in the context of the individual's unique history and experiences. For this individual, we would expect a history in which other negative experiences were interpreted as evidence of complete failure by caregivers and important others, or something similar ( Bolling, Kohlenberg, & Parker, 2000 ). The current context also plays a role: The negative affect of depression provides a context in which interpretations of failure make sense, and the interpretation of friendship failure makes sense given the previous interpretation of school failure.

An important point is that as this individual continues to ruminate, the class lecture is continuing and the student is now largely divorced from contact with any potentially external controlling variables. Thus, verbal behavior, when it occurs, may be quite relentless in overpowering, transforming, and reducing environmental control. As seen in the example of rumination, if the aforementioned student continues ruminative thought throughout her class period she would not be engaged in class discussions and would therefore miss any opportunities of praise or encouragement from the professor. She may also miss necessary information for her next assignment, thereby not only reducing her rate of receiving response-contingent reinforcement but also increasing the likelihood of punishment through a lowered grade. After leaving class and realizing this mistake, she may continue to ruminate now about her difficulty in lecture as well as her previous interaction, which results in further attentional distancing from her immediate environment and additional negative affect.

Summary and Conclusions

There are many pathways to depression. Depression is not a precise, technical term, has no essential composition, and is not a syndrome. The term refers to a core experience of feeling sad or down and to associated symptoms that vary widely. This symptomatic heterogeneity is due to the heterogeneity of historical antecedents and consequences. The core experience may be seen as an elicited by-product of losses of, reductions in, or persistently insufficient levels of positive reinforcement. However, Lewinsohn (1974) , with his focus on environments characterized directly by losses of response-contingent positive reinforcement, presented a fairly unitary operant model that obscured the heterogeneity of depressive symptom profiles. Given the ubiquity of depression and the diversity of its symptom presentations, both reductions in positive reinforcement and increases in aversive control may function as enduring motivating operations ( Dougher & Hackbert, 2000 ). Of course, multiple sources of control are probable. Thus, idiographic assessment is required to determine both the relative importance of positive and aversive control and to determine specific target variables for any given individual. Clinical behavior analysts treating depression would be well served to engage in detailed, idiographic, and historical functional assessments that inform treatment course and technique.

We argue that a modern behavioral account of depression must incorporate controlling variables at both environmental and interoceptive levels, with a recognition of the role of avoidance and verbal behavioral processes. We have emphasized that the core experience of depression is a private event—elicited negative affect that is felt and tacted in a variety of ways. This affect itself is not problematic and is in fact adaptive, but it becomes chronic, maladaptive, or dysregulated through environmental and learned behavioral processes. A key process may be avoidance: Responses to the original private events that function to avoid or escape the event may be negatively reinforced and establish a cycle of increasing negative affect and avoidance, a vicious spiral into depression.

Verbal processes may be particularly important as well, in that research on stimulus equivalence and RFT clearly demonstrates how private stimulus events can be transformed and elaborated when related verbally to other events. Thus, stimulus events that would not otherwise function to elicit depressive affect may come to do so through verbal processes, already aversive stimuli may become more so through verbal processes, and verbal processes may establish avoidance and other dysfunctional responses to such stimuli that otherwise would not be established. Rumination—a hallmark feature of depression—is an example of how verbal behavioral processes may result in negative reinforcement through reducing contact with the current physical environment but exacerbate depressive functioning. Behavior-analytic research on the role of verbal processes in depression is in its infancy, but as research in these areas continues to accumulate, analyses of complex phenomena such as depression may benefit greatly.

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