research paper on depression in adolescence

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Child and Adolescent Depression: A Review of Theories, Evaluation Instruments, Prevention Programs, and Treatments

Elena bernaras.

1 Developmental and Educational Department, University of the Basque Country, Donostia/San Sebastián, Spain

Joana Jaureguizar

2 Developmental and Educational Psychology Department, University of the Basque Country, Lejona, Spain

Maite Garaigordobil

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.

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 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.

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

KR-20, Kuder-Richardson coefficient (formula 20); κ, Cohen's kappa reliability co-efficient; PPV, Positive predictive value; NPV, Negative predictive value; AUC, Area under the Receiver Operating Characteristic Curve (AUC) .

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

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.

School-based child and adolescent depression prevention programs.

Type: T, targeted; U, universal .

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.

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.

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

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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.

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*Correspondence: Joana Jaureguizar, [email protected]

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• Published: 07 August 2023

A global mental health approach to depression in adolescence

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Nature Mental Health volume  1 ,  pages 527–528 ( 2023 ) Cite this article

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Adolescence is one of the most important transition periods in life, in which self-esteem and identity are being shaped and individuals experience profound social and physical transformations. In recent years, a concerning increase in the prevalence of mental health disorders in adolescents has been documented, prompting the mental health research community to prioritize understanding the risks of developing psychiatric disorders as well as factors that might be protective. Nature Mental Health spoke about depression in adolescence with Christian Kieling , an associate professor of child and adolescent psychiatry at the School of Medicine at the Federal University of Rio Grande do Sul in Brazil. Kieling is leading an international project called ‘Identifying depression early in adolescence ( IDEA )’ that brings a global health approach to the topic.

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What Do We Know About Depression Among Youth and How Can We Make Progress Toward Improved Understanding and Reducing Distress? A New Hope

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This paper summarizes many findings about depression among children and adolescents. Depression is prevalent, highly distressing, and exerts considerable burden worldwide. Rates surge from childhood through young adulthood and have increased over the last decade. Many risk factors have been identified, and evidence-based interventions exist targeting mostly individual-level changes via psychological or pharmacological means. At the same time, the field appears stuck and has not achieved considerable progress in advancing scientific understanding of depression’s features or delivering interventions to meet the challenge of youth depression’s high and growing prevalence. This paper adopts several positions to address these challenges and move the field forward. First, we emphasize reinvigoration of construct validation approaches that may better characterize youth depression’s phenomenological features and inform more valid and reliable assessments that can enhance scientific understanding and improve interventions for youth depression. To this end, history and philosophical principles affecting depression’s conceptualization and measurement are considered. Second, we suggest expanding the range and targets of treatments and prevention efforts beyond current practice guidelines for evidence-based interventions. This broader suite of interventions includes structural- and system-level change focused at community and societal levels (e.g., evidence-based economic anti-poverty interventions) and personalized interventions with sufficient evidence base. We propose that by focusing on the FORCE (Fundamentals, Openness, Relationships, Constructs, Evidence), youth depression research can provide new hope.

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Introduction

Over the last several decades, a prodigious literature has amassed on depression in children and adolescents. Major and consequential epidemiological findings show that (1) depression exhibits high prevalence and is associated with substantial distress and burden around the world (World Health Organization [WHO], 2017 ); (2) rates surge six-fold from childhood through late adolescence with steady, persistent rates throughout adulthood (Hankin et al., 1998 , 2015 ); and (3) rates are increasing across generations, with current prevalence rates exceeding those seen just 10 years ago (Daly, 2022 ; Jorm et al., 2017 ). As such, public policy experts recommend annual screening of depression for individuals ages 12 and above (USPSTF, 2022 ). In an effort to better understand (and interrupt) the development of depression across childhood and adolescence, researchers have identified numerous risk and resilience factors that prospectively predict depression (Hankin & Cohen, 2020 ). Indicated or selective preventions can reduce the likelihood of future depression for youth Footnote 1 with elevated symptoms or risk factors (Cuijpers et al., 2021a , 2021b ). Moreover, there exist several evidence-based treatments, including psychotherapies and pharmacotherapies, each of which works generally equally well to relieve youth depression (Weersing et al., 2017 ). Table 1 enumerates what we know regarding risk factors for youth depression, and Table 2 summarizes knowledge of evidence-based interventions (treatments and preventions).

The field has accumulated an impressive corpus of knowledge. At the same time, however, it is an undeniable reality that many young people across the world continue to suffer from and with depression, and there is an urgent and critical need to address this suffering for as many people as possible. Consider global data, for example, which indicate that the age-standardized prevalence of depression increased by 4.2% from 1990 to 2013, whereas the prevalence of anxiety decreased by 0.5% over this same period (Global Burden of Disease Study, 2013 Collaborators, 2015 ). This depression rise has been accompanied by co-occurring increases in rates of treatment; yet, no country included in this global analysis showed diminished depression rates over this time period. Even with many empirically supported treatments, there has been little sustained progress in reducing depression’s burden, or decreasing depression-related distress and suffering since 1980s. What can be done to address clear gaps to reduce the considerable and highly consequential distress and burden associated with youth depression?

The purpose of this paper is to revisit and critically interrogate how and what we think we know about youth depression and its interventions. To this end, we review the sociohistorical context in which the phenomena termed “depression” were conceptualized and highlight the ways in which our academic notions and “best practice” assessment instruments both do and do not align with the symptoms and features of this depression construct. In a similar manner, we consider contemporary prevention and treatment strategies and provide rationale for expanding the range and scope of intervention efforts to more efficiently and effectively respond to youth depression and prioritize structural- and systems-level change.

Ultimately, we strive to provide A New Hope for advancing progress on youth depression. To this end we take some positions (admittedly ours) for what we believe are directions and priorities that hold promise for both improving the scholarly understanding of youth depression and reducing depression-related distress and burden worldwide. We believe meaningful progress can be made without unduly devoting more time, energy, and limited resources investigating primarily unproven biological and technological solutions (e.g., certain biomarkers, Joober, 2022 ; Kapur et al., 2012 ; Winter et al., 2022 ; or innovative pharmacotherapeutics, such as psilocybin or other psychedelics; McClure-Begley & Roth, 2022 ) in the hope that some kind of singular breakthrough will meet massive current needs and close the prevalence-intervention gap.

As Darth Vader famously said in the original Star Wars: A New Hope (episode IV), “Don’t be too proud of this technological terror you’ve constructed. The ability to destroy a planet, or even a whole system, is insignificant next to the power of the Force.” Our perspective and the main points we emphasize can be summarized by focusing on the power of the FORCE: Fundamentals are essential to ground clear thinking informed by humility, history, and philosophy; Openness is needed to explore new ideas with scientific rigor and transparency; Relationships matter for understanding and intervening in youth depression across all levels in social–ecological systems; Constructs are key in the conceptualization, measurement, and classification of depression; and Evidence must be collected and evaluated, grounded in construct validation with epistemic iteration, to ensure accurate, reliable, reproducible knowledge with scientific and practical utility.

In this paper, we have three main goals. First is to provide an overview of what the field knows about depression among youth, via Table 1 for depression risks across ecological levels and Table 2 for interventions. All of this knowledge is grounded in how depression as a construct is currently, and has historically, been conceptualized and measured. Our second goal is to reinvigorate serious academic progress focused on defining and explicating conceptually what depression is among youth as informed by developmental psychopathology. As we summarize in our historical review, necessary and important steps in the construct validation process (content conceptualization; measurement) were minimally engaged in the study of adult depression, and this incomplete conceptual understanding has carried forth in the study of depression among youth. Our final goal is to address immediate needs to reduce the prevalence and distress associated with youth depression. We propose ways for responding to unmet needs of youth at risk for and affected by depression, as well as their families and communities. We begin with an eye toward how we might improve the science of youth depression, with an emphasis on issues of methods, measures, and construct validity. We then propose directions to enhance interventions to alleviate the prevalence and distress of youth depression and suggest efforts that engage multiple ecological systems and stakeholders.

What Is Depression and What Do We Know About It?

For optimal conceptual clarity, we explain and unpack what we mean by specific terms, especially “depression,” among children and adolescents. We define the term “depression” as a construct, i.e., a complex concept intended to synthesize varied components into a cohesive “thing,” one which cannot be directly measured but is inferred from available data. This latent entity is capable of organizing features and processes that cannot be directly observed. We use the terminology of “constructs,” as is typical in psychological science (e.g., Borsboom et al., 2004 ; Cronbach & Meehl, 1955 ; Messick, 1987 ), and these constructs are defined and identified within their nomological networks (Cronbach & Meehl, 1955 ).

Tables 1 and 2 (and other exemplary expert reviews; e.g., Herrman et al., 2022 ; Thapar et al., 2022 ) synthesize the state of knowledge in depression among youth. This summary is based predominantly on modern DSM/ICD perspectives that have primarily conceived of depression as a categorical disorder with philosophical grounding in hard realism. Hard realism states that entities have real essences in nature that provide clear boundaries that separate and can categorize entities (Kendler et al., 2011 ). For example in the periodic table from chemistry, a paradigmatic example is gold as an element, in which gold’s 79 protons (its atomic number) constitute a real essence that separates this element from all other elements. Analogously for psychological disorders, such as depression, hard realism implies the existence of simple, unifying etiological causes (e.g., genetic or brain dysfunctions), and knowing depression’s essential causes enables clear categorization from other psychopathologies. Searching for biomarkers via novel, emerging technologies makes sense when depression is conceptualized through this lens of hard realism in which disorder is believed to be an essential kind. Yet, leading philosophical scholars cogently argue that psychopathological disorders, such as depression, are not essential kinds and do not possess any real essence. Instead, such philosophers assert that depression exhibits characteristics of either soft realism (e.g., as in the case of biological species) with fuzzy boundaries and conflicting conceptualizations, or as a practical kind, based on an instrumentalist approach to science that is pragmatic and avoids deep ontological claims (Kendler, 2022 ).

A Brief History of Depression Over Time: Classification and Its Discontents

What we know about youth depression is grounded in a set of assumptions (e.g., is depression of hard or soft realism, or a practical kind?) and a set of historical events occurring in a particular social–political context. These assumptions and history, both of which are rarely examined, have exerted outsized influence and largely set the mold in which the conceptual contours and measurement of today’s youth depression have been cast. Starting in the mid-late 1970s and persisting into the present, many key notions and assumptions about “what depression is” have largely been determined by particular clinical authorities, and their scholarly conceptions of depression have been concretized and operationalized in an interrelated set of systems and classifications, including the DSM and ICD. These official nosologies dominate how nearly all mental health scholars and applied workers across numerous disciplines think of depression, define it as a syndrome, picture and envision diagnosis, and use assessment instruments. These notions and assumptions then inform the measurements that comprise the data that formatively affect our body of knowledge regarding youth depression. As such, much of what we know about youth depression, including its prevalence and developmental trajectories, comorbidities, risks, and interventions are filtered through a particular contextual lens shaped by philosophical principles and specific historical events. Appreciation for this historical and philosophical undergirding can bring greater understanding of our present knowledge base, as summarized in Tables 1 and 2 .

In this section, we discuss how key historical events over the last century provided a particular context that affected who the field has regarded as primary clinical experts, and shaped how these authorities chose to conceptualize and operationalize depression via particular signs and symptoms. In contemporary research and practice, these authorities’ decisions have largely been uncoupled from the sociohistorical context in which they emerged, yet still these specialists and their beliefs continue to dominate our conceptual and applied understanding of depression (Kendler, 2017 ; Kendler et al., 2010 ). With the dominance of modern DSM in mind, consider the following observation noted by an eminent biological psychiatrist who values ongoing study of phenomenology in psychopathology:

DSM-III and its successors… became universally and uncritically accepted as the ultimate authority on psychopathology and diagnosis. DSM forms the basis for psychiatric teaching to both residents and undergraduates throughout most of the United States…. Because DSM is often used as a primary textbook or the major diagnostic resource in many clinical and research settings, students typically do not know about other potentially important or interesting signs and symptoms that are not included in the DSM…. Validity has been sacrificed to achieve reliability. DSM diagnoses have given researchers a common nomenclature—but probably the wrong one . (emphasis added; Andreasen, 2007 , p. 111).

Our perspective builds on others’ recent work in similar areas, including works emphasizing fundamental philosophical principles (e.g., Aftab et al., 2021 ; Kendler, 2022 ; Kendler and Zachar, 2019 ), historical overviews (e.g., Clark et al., 2017 ; Harrington, 2019 ), constructs (e.g., Bringmann et al., 2022 ; Hayden, 2022 ), and measurement (e.g., Fried et al., 2022 ; Haslbeck et al., 2021 ). We recommend to interested readers these excellent published pieces. Nearly all focus on adults. There exists far less literature pertaining to critical history and philosophy relevant for conceptualizing and measuring depression specifically among children and adolescents. This is a clear gap in the literature and field’s understanding, as such knowledge from adults should not be uncritically adopted in developmental downward extensions to children and adolescents. As we discuss later, these underexamined developmental downward applications of such fundamental concepts and principles can have unintended consequences when principles and practices are applied “top down” with less focus on complementary “bottom up” perspectives from phenomenological and developmental sciences.

The views and perspectives affecting depression’s definition and measurement result from a set of historical conditions that are deeply intertwined with changing political and institutional values and priorities. Funds for research and professional training in clinical psychology and psychiatry were first made possible by the passage of the American Mental Health Act in 1946, shortly after the end of World War II. Shortly thereafter, the National Institute of Mental Health (NIMH) was created with Robert Felix as its founding director, and they emphasized the social roots and consequences of mental health. At the point of its inception, the NIMH concentrated significantly more funds on research connecting mental illness with social determinants of health including poverty, social isolation, poor education, overcrowding, and violence compared with biological or medically focused risks and correlates. This history suggests that the contemporary, medicalized conceptualizations of depression were not a necessary, logical eventuality or even a product of naturalistic scientific progress.

Continuing this history and its impact on classification for psychopathologies, including depression, consider several well-intentioned changes implemented by the United States government and Food and Drug Administration (FDA) during the 1960s–1970s. Specifically, the Kefauver–Harris Amendment of 1962 required that medications needed to demonstrate empirical evidence for their safety and efficacy in terms of treating a specific disease in order to be sold. Then in the 1970s, the FDA mandated that efficacy testing of new drugs required controlled clinical trials. For the growing psychiatric pharmaceutical industry, these novel mandates introduced a new conundrum. If controlled clinical trials required diagnostically homogeneous patients, and no physiological tests existed to definitively establish the presence of psychopathology, how could researchers ensure that participants in a psychiatric clinical trial all share the same disorder? Herein laid the essential problem: No reliable psychiatric diagnostic classification system existed in the 1970s!

A predominant reason for poor reliability in psychiatric diagnosis was the dominance of psychodynamic paradigms in psychology and psychiatry during the 1960s and early 1970s. According to these psychodynamic theories, psychopathology reflects varied intrapsychic conflicts resulting from unconscious drives and impulses and disturbances in early psychosocial development. The leading psychodiagnostics manual in the 1960s–1970s—the Diagnostic and Statistical Manual, Second Edition ( DSM-II ; 1968 )—was an administrative manual grounded in abstract psychodynamic theory. There was little interest in the symptoms themselves and the ways in which they might be organized into coherent syndromes or disorders. Within psychodynamic practice and tradition, depression symptoms were conceptualized and explained as defense against anxiety (the core of all “psychoneurotic disorders”). In other words, psychodynamic conceptual models viewed depression as an expression to cope with underlying anxiety, rather than a phenomenon onto itself that required inquiry and understanding.

Yet, the novel FDA regulations of the 1970s required some simple, straightforward, and reliable way to assign individuals to homogenous groups of “depression” for the purpose of controlled efficacy studies. To continue to sell widely prescribed and used antidepressant medications to adults at that time (e.g., Elavil), pharmaceutical companies needed some means to create groups of homogeneous patients diagnosed with the same disorder (later to be named Major Depression Disorder; MDD, in DSM-III). This urgent press contributed to pressure for a psychiatric diagnostic classification that was first and foremost reliable . That is, clinicians needed to operationalize features of depression to reach adequate consensus on the presence and most observable properties of the phenomena, not its conceptual nature . Accordingly, the developers of the DSM-III endeavored to define mental disorders, including depression, “regardless of the cause,” so uniform diagnostic criteria were created with avowed agnosticism toward potential causal processes or underlying latent constructs that such criteria might be understood to represent. Footnote 2

Instrumental in the early development of an approach toward improving the reliability of classification of psychiatric disorders was a small group of clinical scholars (e.g., psychiatrists, psychologists) from the psychiatry department of the Washington University in St. Louis. This group of scholars, who were named “neo-Kraepelinians,” believed that the development of diagnostic criteria for the classification of mental illness was a valuable and legitimate enterprise. The neo-Kraepelinians thought that the abysmal inter-rater diagnostic agreement noted in voluminous studies from the 1970s could be solved via the creation of operationalized diagnostic criteria and the use of standardized symptom checklists. Feighner led the group in developing diagnostic criteria proposals and checklists (known as Feighner Criteria (Feighner et al., 1972 ), which influenced Research Diagnostic Criteria (RDC; Spitzer et al., 1975 ) and then ultimately the officially approved and recognized DSM-III (APA, 1980 ). In contrast to earlier versions of the DSM (I and II) which were guided by psychodynamic perspectives, the DSM-III aimed to inform the diagnosis of discrete disorders using observable symptom-based criterion, representing a radical shift in clinical approaches to diagnosis and classification. The practical operationalization system formally introduced by the DSM-III permitted researchers and clinicians to use a systematic approach to assemble potentially disparate symptoms into discrete diagnoses with improved reliability.

An important philosophical piece in this history of the early developments leading to DSM-III is that the neo-Kraepelinians intended the symptom criteria they proposed for each disorder (which were then instantiated into DSM-III) to represent a hypothetical diagnostic construct . The psychiatrists at Washington University did not intend nor believe that the symptom lists they proposed for each diagnosis were meant to sufficiently and literally constitute the disorder in an explicit one-to-one manner (Kendler, 2017 ). Rather, the influential neo-Kraepelinians believed that depression and other disorders are hypothetical constructs, so these psychiatrists also developed and proposed an initial set of validity criteria (known as “Robins & Guze criteria”; Robins & Guze, 1970 ). Their underlying assumptions for these validity criteria were grounded in a biological psychiatric medical model, not the psychodynamic theories still predominant in the 1970s, nor other possible conceptual frameworks (e.g., social determinants of health as originally supported by Robert Felix at the start of NIMH). Their views and decisions presumed that depression and other disorders are “essential kinds” in nature and were intended to mirror other medical disorders in other branches of medicine (Blashfield, 1984 ).

What relevance does this history have for the conceptual definition and measurement of the construct of depression today and going forward? This historical context provides the framing in which modern priorities, principles, and beliefs were first set, and understanding these prequels provides important background to explain how and why the dominant DSM/ICD became substantiated as the official classification system. Taken together with its implicit emphasis on essentialism and biological psychiatry, the modern DSM system and this biological framework have driven most basic and applied research since the early 1980s. This forms the bedrock foundation for most of the current knowledge on risks and interventions for depression among adults, adolescents, and children. The neo-Kraepelinians broke new ground by creating consistent symptom checklists intended first to increase reliability of psychopathological disorders conceived as discrete diagnoses. The shifting in the set of assumptions emphasizing biological predominance reflected the neo-Kraepelinians’ beliefs that psychiatry ought to investigate biological causes and treatments of discrete mental illnesses and should position itself as a modern, scientific branch of medicine. This small group of influential authorities at Washington University exerted a tremendous impact on DSM-III and subsequent nosological successors (e.g., currently DSM-5). For these reasons, it behooves us to understand how the neo-Kraepelinians’ assumptions and beliefs affected depression and other disorder definition, conceptualization, measurement, and then interpretation of data for eventual knowledge generation.

Also breaking from the predominant psychodynamic perspective, a few clinical scholars (e.g., Beck, Hamilton) in the mid-late 1960s developed standardized checklists to measure some depression symptoms with adults. These measures (Beck Depression Inventory; Hamilton Depression Rating Scale) reflect each author’s conceptualization of depression based on their observations of particular depression phenomena in different contexts and settings. Hamilton created the HDRS in 1960, for example, drawing on his knowledge and experience with already diagnosed severely depressed hospitalized inpatients, and he emphasized observable indicators such as psychomotor retardation (including slower speech) and weight loss relatively more so than self-reported symptoms. It is notable that the HDRS has remained the gold-standard depression clinical ascertainment for randomized control trials (RCTs) in adults over the last 60 years and is used in about 90% of antidepressant drug trials (Cipriani et al., 2018 ). The development of the HDRS can be contrasted with that of the Beck Depression Inventory (BDI), for instance, which was informed by Aaron Beck’s evolving cognitive theory of depression, and accordingly, placed relatively more emphasis on individuals’ self-reported affective and cognitive experiences.

These and other depression measures offer divergent conceptualizations of what the depression construct is. These differing conceptualizations were grounded in each clinical scholar’s own beliefs, phenomenological observations, and emphases, as well as the larger social and philosophical contexts in which these experts learned and worked. Given such widely divergent conceptual notions and histories, it therefore is not surprising to learn that empirical correlations among these and other depression scales are small to moderate (r’s ranging from 0.2 to 0.5). With this degree of small-to-moderate convergent validity, one cannot assume that different depression instruments equivalently assess the same construct of “depression.” With the discrepant conceptual and substantive content between different measures, the various depression assessments are not interchangeable. It is important to align practical, psychometric, and conceptual practices.

We need to be reminded that the ways in which we construe depression are a product of both the phenomenology and characteristics of depression as well as the limitations imposed by our theories and methods…. This has resulted in a situation where a great deal of what we think we know about depression in children and youth may not be about depression as such. (Hammen & Compas, 1994 , pp. 586–588)

When it comes to assessing depression among youth, the state of knowledge and measurement practice has lagged behind that of adult depression. Prior to Kovacs developing the Children’s Depression Inventory (as a downward extended youth-modification of the BDI) in 1977, for example, few scholars believed that children could be depressed. Indeed, the dominant beliefs and theories of the time held that (1) children are generally happy and show little persistent sadness, (2) youth lack mature social or emotional or cognitive structures deemed necessary for depression, and/or (3) kids manifest behavioral conduct problems (not primary depression-like symptoms as presenting problems or concerns) as a syndrome labeled “masked depression” (e.g., Cantwell, 1982; Strober & Werry, 1986 ). Even as youth depression slowly emerged as a topic of independent inquiry in the late 1970s, few developmental adaptations were considered. Indeed, when it came time to define the content, symptoms and criteria sets for childhood depression for DSM-III, historical writing suggests that key decisions were made based on predominantly entrenched beliefs around adult depression (Strober & Werry, 1986 ). It was largely assumed that youth depression comprised the same symptoms, expressed in the same way, as adult depression, and as a result, diagnostic criteria for depression among children and adolescents in DSM-III were asserted to be nearly the same as those for adults. Once the official psychiatric classification system authoritatively asserted this set of criteria defining depression in youth, the conceptual definition of youth depression as a construct as well as its measurement were established, and later reinforced and reified. Many youth depression assessments were created by translating adult conceptualizations and measurements downward to children and adolescents (e.g., Kendall et al., 1989 ; Klein et al., 2005 ; Weiss & Garber, 2003 ).

So much depends on how scientists conceptualize the problems they work on. Observations lead to interpretations. Interpretations become concepts. And concepts may become dogmas that feel so intuitive, so natural, that they are accepted without question. We should, from time to time, re-evaluate the core beliefs of our fields of study. (Rust & LeDoux, 2023 , p. 4)

We believe it is time to reconsider and revise (to the extent needed) how youth depression is conceptualized, rather than reflexively perpetuate the initial conceptual system of DSM-III that barely questioned and evaluated depression developmentally.

Construct Validity of Currently Oft-Used Depression Measures

As we elaborated in the previous section, the way in which depression is conceptually defined and measured today emerged as a function of a specific set of philosophical principles, scholars’ beliefs, and historical movements and events. In this section, we seek to describe how the field might move forward by re-energizing efforts toward construct validation. We argue that of the three phases of the construct validation process, the first two fundamental primary steps (i.e., defining the construct and operationally translating that conceptualization into reliable measurement, respectively) have historically been, and continue to be, overlooked. Reinvesting in these initial stages, especially of defining clearly the construct, can advance development and implementation of measures that adequately capture what depression is to the youth who experience it.

Implementing psychometrically sound measures starts with sufficient coverage of the key conceptual content. As there exist many ways to gauge construct validity, we focus here on internal structural aspects of depression assessments. Our review considers the degree to which the commonly used instruments may be covering and capturing important content, signs, symptoms, and features of the depression construct as phenomenologically observed and described by youth and other informants (e.g., caregivers, teachers, providers) with most direct access to children’s depression features.

Evidence to date suggests that DSM’s operationalization of the depression construct does not adequately capture and index many features of depression most salient to youth’s phenomenological experiences. For example, in large school-based community samples of Brazilian adolescents aged 14–16 years, researchers used network analyses of self-reported symptoms to evaluate the structure and centrality of depression symptoms to understand which symptoms tend to correlate with other another and are most densely connected with other symptoms (Manfro et al., 2021 ). Certain symptoms that are not captured in current DSM-based criteria, such as loneliness and self-hatred, were among the most interconnected, central, and frequently reported facets of depression, alongside DSM-based symptoms of sadness and worthlessness. These findings among a non-clinical sample of adolescents recruited from the general community align with research examining adult depressed patients, who endorse therapeutic priorities focused on improved self-esteem, as well as reduced loneliness and social isolation (Chevance et al, 2020 ). Manfro and colleagues’ network analysis also showed that hopelessness (not a core DSM MDD feature, but an accessory symptom in ICD-11) served as a highly central symptom of adolescent depression, consistent with adult work finding that hopelessness reliably differentiates depressed from non-depressed participants (McGlinchey et al., 2006 ). Surprisingly, anhedonia, one of the cardinal, criterial symptoms for MDD according to the DSM, was not highly interconnected with other depression symptoms.

This pattern of findings reinforces our proposition that the conceptualization of depression, as described by modern DSM (III through 5), insufficiently reflects the construct of depression as youth experience their symptoms. Moreover, the content of any given depression scale is often quite different from that of another. An analysis of eighteen youth depression instruments found that 52 separate symptoms were included, and these scales only comprised around 50% of the symptoms needed for MDD diagnosis according to DSM. Low content overlap was also observed across the measures, as only 29% of symptoms coincided across scales (Vilar et al., 2022 ). This heterogeneity of assessments extends to RCTs for adolescent depression treatment: 19 different outcome measures were used in 30 trials according to one recent review (Mew et al., 2020 ).

Understanding of the construct of depression as phenomenologically experienced by depressed individuals is underdeveloped. Recent qualitative research conducted among an international sample of depressed adults, as well as their providers and caregivers, indicates that features of mental/psychological pain (described often as “torture,” or “suffering”) were the most frequently endorsed and experienced, followed by anxiety and sadness (Chevance et al., 2020 ). It is notable, however, that none of the most commonly used depression assessments actually measure mental pain as a particularly important feature. Unfortunately, the commonly used depression measures do not cover some of this important phenomenological content that appears to comprise features of depression of primary concern to youth.

Applying the FORCE to Improve Understanding of Youth Depression

The conceptualization and measurement of depression has evolved over time, and contemporary notions of depression as a construct can be understood in the context of the theoretical, social, and political histories from which these notions emerged. Across all current measures of depression, there tends to be a central constellation of specific symptoms and features (e.g., hopelessness, sadness, apathy) that most likely captures core features of the depression construct and explains the moderate intercorrelations among measures. Also, the most used depression measures exhibit considerable heterogeneity in content coverage. Last, the most used measures do not capture important features of depression (e.g., mental pain) that figure prominently in individuals’ phenomenological experience. In our view, the construct of depression should not be defined merely, exclusively, and isomorphically in terms of the scales we use to measure it. Our proposed positions to improve the science of youth depression are organized in terms of the FORCE.

Fundamentals

Meaningful, replicable, and interpretable science, especially in applied areas like youth depression, requires reliable and valid measurement with clinical utility. Before investing further in advanced technologies and biological strategies to provide novel insights into the causes and correlates of youth depression—technologies and strategies that to date have yielded largely unreliable and inconsistent findings (e.g., Joober, 2022 ; Kapur et al., 2012 )—we encourage clinical researchers to consider the assumptions upon which measures and models are built and to re-engage with the fundamental (if often frustrating) challenge of articulating the parameters of the problems we are trying to understand. What are the core features of youth depression? What are the experiences youth describe? What does youth depression look like to parents and caregivers? How can these features inform our efforts to develop measures that facilitate enhanced understanding, as well as early detection and intervention? Meaningful progress can be made by producing and disseminating measures that are optimally valid, reliable, and culturally responsive for the needs of contemporary and future young people and those in their communities .

Revisiting these fundamentals will necessarily require openness. We must be open, for example, to embrace research paradigms that have not been mainstream approaches in clinical psychological science, such as qualitative methods aimed at enriching descriptive understanding of youth depression as observed and experienced by various stakeholders. We agree with Sir Michael Rutter who commented, “I think on the one hand you have to have quantitative analysis, but on the other hand qualitative research has a role to play as well, although I think it would be a mistake to say that simply counting quantities is an answer in itself. Understanding is definitely helped by qualitative studies” (Rutter & Werker, 2021 ). Indeed, as our history highlights, rich descriptive and exploratory work is fundamental to inform testable hypotheses and generate new knowledge that can advance the field.

We also encourage openness to novel conceptualizations of psychopathology that extend beyond current DSM-based nosologies. The Hierarchical Taxonomy of Psychopathology (HiTOP) Consortium (e.g., Kotov et al., 2021 ), for example, provides a promising framework that illustrates how the field can employ stages 1 and 2 of the construct validation process to better understand and organize surface-level signs and symptoms of youth depression, and reimagine the ways in which we conceptualize and structure psychopathology. HiTOP’s approach is focused on descriptive psychopathology and empirical analyses of surface-level phenomenological signs and symptoms. The HiTOP framework is consistent with many proposals in this position paper. HiTOP has begun to develop and test empirical measures using modern construct validation techniques, albeit largely with adults to date (e.g., Clark et al., 2023 ; Simms et al., 2022 ; Watson et al., 2022 ). Last, and importantly, HiTOP contains a committee and structure that formally, openly, and transparently considers and evaluates revisions to the organization and structural model based on ongoing research and evidence (Forbes et al., 2023 ; Kotov et al., 2022 ; Ringwald et al., 2021 ). HiTOP also includes a committee focused on developmental applications and considerations, and work in this developmental HiTOP committee is in progress (e.g., Nelson, et al., 2023 ).

Openness also extends to how we conduct our science. Values of transparency and principled, intentional decision-making are needed to guide construct validation efforts. Moreover, by engaging with science as an iterative, ultimately communal process by which knowledge is shared and collectivized, it is our hope that scholars motivated by open science practices might accelerate progress toward a more valid and reliable science of youth depression.

Relationships

Concretely illustrating such a communal process, the World Health Organizations’ (WHO) international process for depression instrument development provides an excellent example showing how interdisciplinary collaborations and conversations among different working groups can advance fundamental conceptual understanding of what constitutes the depression construct and how best to operationalize such information into measurement (e.g., Fulford & Sartorius, 2009 ; Sartorius et al., 1974 , 1980 ). In the 1970s, the WHO began work to create a standardized assessment that could be used around many countries to estimate adult depression prevalence worldwide. Doing so was an enormous, challenging task, especially because different countries had very different ways of defining and measuring adult depression, as there existed no uniform worldwide psychiatric classification system. As a result, the WHO realized that a necessary first step toward providing these essential epidemiological data was to develop an assessment tool that investigators around the world could agree on and then be used to reliably cover the main depression features across countries and cultures when implemented in the field worldwide. The WHO formalized regular international meetings with expert mental health workers from around the world who provided phenomenological summaries of depressed patients, and reviewed audio and video tapes of clients. These relatively inclusive, regular meetings enabled world-leading clinical scholars to generate the symptoms lists that were eventually included in the WHO’s depression checklist interview measure that was then used in the first international epidemiological study of depression. Also critical in the WHO’s process for creating their Schedule for Standardized Assessment of Depressive Disorders was their inclusion of a companion glossary that defined each symptom and provided clear criteria by which depression features could be rated reliably (Sartorius et al., 1983 ). This rich historical example of the construct validation process illustrates how conceptual content was developed for step 1 by cultivating relationships among experts around the world; it also demonstrates how these world experts invited many viewpoints and considered data to cull down items in step 2 of measure development. We propose that this process can be further enriched by the inclusion and formalization of relationships with non-psychiatric experts, such as youth, families, caregivers, and community partners and providers (broadly defined).

The cultivation and maintenance of collaborative intra- and inter-professional and personal relationships is vital to realizing the goals emphasized in this position paper. To improve content understanding of youth depression, for example, we must meaningfully and reciprocally engage with individuals who have experienced depression (either directly, in the case of youth, or indirectly, in the case of caregivers and providers), and reflect with humility in recognizing the bounds of our own expertise and construct-level understanding. A deeper conceptual understanding of youth depression can be enhanced through conversation and coordination with developmental scientists and others from interdisciplinary, allied fields.

We must also maintain critical and reflective relationships with ourselves and our histories (Rodriguez-Seijas et al., 2023 ). Psychological science and construct conceptualization do not emerge in an intellectual vacuum. They often reflect common sense folk accounts and ideas (Mandler & Kessen, 1959 ), which are then informed by specific theoretical paradigms, philosophical principles, and sociohistorical circumstances. Pausing for such reflection sets the stage to enable clinical scholars to interrogate assumptions undergirding work and examine the role our own preconceptions, paradigms, and positionality play in informing questions asked, methods employed, and interpretations made (Rodriguez-Seijas et al., 2023 ).

At the risk of belaboring the point, the production and dissemination of meaningful and impactful science depend on reliable and valid measures to assess conceptually based constructs. Understanding, detection, prevention, and intervention with respect to youth depression may be improved to the extent that the construct validation process is re-energized, and measurement efforts are reinvigorated. We believe that these goals are aligned with proposals and current efforts to use more ecologically valid digital phenotyping (e.g., sensors, smartphones, experience sampling methods) that enable youth and informants to monitor and rate their experience over time, contexts, and across units of analysis (e.g., Hitchcock et al., 2022 ). Deep phenotyping can provide enhanced information on sleep, various affects and emotions, reports of mental and physical pain, movement, exercise and activity, concentration and distraction, as well as social connection to ascertain what youth are doing (e.g., social media, games, substance use, etc.) and with whom (e.g., peers, family). Such efforts may have dual benefits for the future of the field. Deep phenotyping can both inform construct conceptualization, as well as facilitate the identification of ecologically valid, malleable targets and mechanisms to intervene on youth distress.

Progress in the conceptualization and measurement of youth depression must be based on strong evidence. Moreover, it is important that epistemic iteration drives knowledge generation so that the field’s evidence base dynamically evolves with the production of more developmentally and culturally informed measures. It will be important to engage diverse populations of youth, as well as their caregivers, teachers, and providers at each stage of the construct validation process. All involved should remain reflective and transparent about to whom and the extent to which evidence may generalize.

What Do We Know About Interventions for Youth Depression?

Efforts to improve the conceptualization and measurement of youth depression must occur alongside work to improve its detection, prevention, and treatment. Youth struggle with and from depression, and there continues to be need for better, more accessible interventions. Footnote 3 Thus, we shift attention to review what is known regarding evidence-based interventions for youth depression (see Table 2 ) before describing how the FORCE may be applied to propel the field forward.

In a meta-analysis summarizing treatment effects for youth interventions over the past 50 years, Weisz and colleagues (2017) reported an overall mean effect size (ES) = 0.46 compared to control condition for all youth mental health problems, indicating that treatments yield moderate improvements, on average, in youth mental health. Notably, however, treatments for youth depression, specifically, were found to be generally less effective in yielding symptom improvement (ES = 0.29) relative to interventions for anxiety (ES = 0.61) and other conditions. Moreover, after synthesizing the literature, Weisz and colleagues (2017) concluded that therapy effects have not improved over the past 50 years. Further, estimates indicate that fewer than 50% of depressed adolescents in the United States receive care for their symptoms (Avenevoli et al., 2015 ; Forman-Hoffman et al., 2016 ; Lu, 2019 ), and racial and ethnically minoritized youth encounter disproportionate barriers to mental health care relative to their non-Hispanic white peers (Alegría et al., 2008 ; Lu, 2019 ; Yeh et al., 2003 ). Globally, the WHO ( 2017 ) finds that mental health needs far exceed the availability of mental health workers around the world, with individuals in lower-resourced settings facing particular difficulty accessing adequate care.

Taken together, results of this work paint a sobering picture regarding the field’s present capacity to adequately respond to the challenges of youth depression: Treatments are (at least on average) only modestly effective in reducing symptoms and are only reaching a limited number of youth. Further complicating this picture, there are currently not enough well-trained mental health providers of evidence-based psychotherapy to meet the massive current or anticipated future needs. It is unlikely that the needs of distressed youth can be completely met even with an expanded base of well-trained mental health providers.

Psychopharmacological interventions are also commonly used to treat youth depression, and antidepressant medications have been approved by the FDA for the treatment of depression among adolescents ages 12 and older. The American Association of Child and Adolescent Psychiatry recommends the use of selective serotonin reuptake inhibitors (SSRIs), preferably fluoxetine, as a first-line treatment for depression (Walter et al., 2022 ). It is notable, however, that use of antidepressant medications can be associated with side effects and other risks. For example, the FDA issued a “black box” warning in 2004 cautioning that use of SSRIs among youth may increase the risk of suicidality.

Intervention efforts need not wait until youth experience the onset of a depressive disorder. Preventative interventions aim to reduce the likelihood that youth experience depression in the future and represent one means to proactively reduce youths’ prospective risk for depression-related suffering (Heckman, 2011 ; Lee et al., 2017 ; Mihalopoulos & Chatterton, 2015 ). Systematic and quantitative reviews reveal modest to small effects (pooled SMD = 0.16 [0.07–0.26]; Ormel et al., 2020 ) for psychological or educational interventions for preventing depression across multiple settings (e.g., schools, health care, community) and populations. Generally, effectiveness is higher for preventive interventions targeting youth at risk (selective) or with elevated subsyndromal depression (indicated). Estimates indicate that selective and indicated prevention reduce depression incidence by 20–25% (Ormel et al., 2020 ).

Universal prevention efforts exhibit much smaller effect sizes. Several school-based cognitive behavioral or interpersonal preventions show no meaningful effect on depression risk, on average (Caldwell et al., 2019 ; Cuijpers et al., 2021b ), indicating that some universal prevention efforts are ineffective for reducing risk among unselected youth. A recent large-scale universal prevention trial comparing mindfulness-based training to teaching as usual (TAU) with social–emotional learning among students ( n  = 8376) distributed across numerous British schools (84 schools) showed no average prevention effects on primary depression and wellbeing outcomes, and iatrogenic effects were observed in some schools such that TAU did better than mindfulness (Kuyken et al., 2022 ).

This summary illustrates both good and bad news regarding the state of intervention knowledge for youth depression. Encouragingly, some treatments such as cognitive behavioral therapy (CBT) and interpersonal psychotherapy (IPT) demonstrate efficacy as assessed via RCTs, and these have been designated “well-established” treatments for youth depression (see Weersing et al., 2017 ). The bad news is that the field has not progressed in terms of improving effectiveness, dissemination, or implementation of existing preventative and/or treatment interventions to address increasing mental health needs, especially rising prevalence depression rates among youth. One way to shrink depression prevalence is for clinical researchers to reduce the “quality gap” (Jorm et al., 2017 ). This will require providing preventative interventions and treatments that meet minimal standards of clinical practice guidelines and reducing barriers to evidence-based care for youth with highest needs and risk.

Additional gaps and particular limitations in the treatment outcome and prevention literatures also merit attention. Most RCTs, for example, have included predominantly non-Hispanic white youth, and culturally responsive interventions for racial and ethnically minoritized are relatively underfunded and understudied (Pina et al., 2019 ; Polo et al., 2019 ; Walter et al., 2022 ). Further, salient moderators and mediators of treatment response are poorly understood, even among “gold-standard” treatments (Walter et al., 2022 ). Without this knowledge, clinicians are limited in their abilities to select and individualize treatments to most efficiently and effectively meet individual patients’ specific needs. Additionally, many new treatments have been developed and refined over several decades, yet treatment efficacy has not followed suit and has not substantially improved (Holmes et al., 2018 ). Further, with respect to preventative interventions, most prevention trials have relatively short-term follow-ups (less than 1 year), and generally longer-term trials exhibit effect sizes that diminish over time (Caldwell et al., 2019 ; Cuijpers et al., 2021a , 2021b ; Gee et al., 2020 ; Merry et al., 2004 ). So, it remains relatively unclear how long prevention effects last. Overall, despite the field’s best efforts, interventions do not sufficiently map onto the needs of youth experiencing depression. Work remains to further improve interventions to reduce youth depression.

Fortunately, several developments leave us hopeful that significant progress may be made in the coming years. It is increasingly recognized, for instance, that interventions for youth internalizing problems are needed. For example, the Wellcome Trust launched a new priority mental health strategy emphasizing adolescent and young adult (14–24 years) depression and anxiety. Moreover, the United States Office of the Surgeon General ( 2021 ) Advisory on Protecting Youth Mental Health proposes and describes a multipronged, ecologically informed series of recommendations to circumvent youth risk for psychopathology and promote youth wellbeing aimed at both health care specialists (e.g., primary care providers) as well as naturalistic settings and supports (e.g., schools, community organizations, digital media, etc.). As we describe below, this kind of ecological approach is needed in the field of youth depression, as systems- and structure-level change will be essential to augment present evidence-based interventions to address the current prevalence–intervention gap.

There and Back Again: Historical Shifts Between Individual and Relational-Community Mental Health Approaches

We briefly summarize relevant policy and mental health events over the century that illustrate how psychiatry, psychology, and allied disciplines repeatedly (re-)learn the lesson and importance of keeping care within local communities and focusing on relationships. This short history reveals why it can be useful and worthwhile to revisit our field’s history to see what has worked, what has not, and how we can learn from this history and apply these lessons going forward.

Broadly reflecting the back-and-forth shifts emphasizing individually focused care to more relationally based interventions, consider large-scale mental health intervention experiences from military psychiatry. Throughout World War I experts believed the best approach was to move “shell-shocked” soldiers to far-away special hospitals for treatment, yet the affected suffering soldiers did not do well, their recovery was delayed, and some got worse. In contrast during World War 2, military psychiatry adopted more relational help and found that “shell-shocked” soldiers could be rehabilitated and “turned around” more quickly when treated near their platoon or local army communities to which they would then return. These military experiences providing mental health treatment for affected soldiers over decades show that a more locally focused, relational, community-based approach works (Glass, 1971 ).

Robert Felix, NIMH’s first director, was a proponent of this approach. In the Foreword to Caplan’s, 1964 Principles of Preventive Psychiatry emphasizing “community mental health,” Felix wrote, “This book… is a bible. It should be read by every psychiatric resident and mental health worker in training. Footnote 4 ” In 1963, President Kennedy signed the Mental Retardation Facilities and Community Mental Health Centers Construction Act. The idea was that the federal government would release money via block grants to states, which were supposed to build new community mental health centers to replace crumbling, aging, ineffective state mental institutions. However, state governments did not follow through as Congress intended. States did not invest their own funds and instead used federal block grants as a chance to downsize and economize. As a result, there was never sufficient resources and means for mental health system reform as recommended via integration with community mental health.

When major recession and stagflation hit in the 1970s, many adults with severe mental illness had been released from state inpatient hospitals, and numerous released patients faced barriers with the continuation of their psychotropic medication and other supportive therapies. Subsequently, many of these former patients became homeless due to lack of support systems from the community; several were subsequently incarcerated. Indeed, carceral systems, rather than supportive psychotherapeutic care settings, served as a common destination for individuals whose mental health needs remained unmet. Prisons became (and continue to serve) as America’s largest mental hospital system, especially for minoritized individuals and people of color. Today, Illinois Cook County jail, LA County Jail, and NY Rikers Island are the three largest mental health care providers in the United States.

We believe the youth depression field can learn from public health approaches that target modifiable social risk factors and social determinants of health. For example, consider public health efforts aimed at reductions for smoking, cardiovascular disease, and cancer mortality. These public health preventions have included multipronged, intensive programs aimed at both individual and structural targets (e.g., individual, school, curriculum, community) with enduring success (Office of the Surgeon General, 2020 ). Our review of depression facts and findings (Table 1 ) suggests many modifiable risk factors that can be targeted, ranging from the individual level (e.g., cognitive vulnerabilities, poor coping) to environmental and contextual stressors (e.g., peer victimization, childhood maltreatment) to political and structural violence and inequality (e.g., exposure to racism, poverty, armed conflict). Moreover, there exist transactions among individual (e.g., negative emotionality, cognitive vulnerabilities) and contextual risks (e.g., family conflict), such that these risks can mutually reinforce one another over time. As such, interventions can be enhanced by attending to opportunities to intervene at multiple ecological levels by cultivating and leveraging contextual supports to bolster the potential of well-validated individual-level preventions and treatments to allow children, families, and communities to thrive.

“A Matter of Political Will”

Before describing the way in which the FORCE may provide a helpful framework for guiding future work to alleviate youth depression, we echo that reducing mental health problems, including youth depression, is “all a matter of political will” (Jorm, 2014 , p. 800). Mental health workers and clinical scholars across disciplines will need to coordinate, collaborate, and convince politicians and policy makers of the evident truth that investing in proven depression interventions reduces suffering and shrinks disease burden. All too-frequently, the already too-limited funds for mental health services are among the first to be cut during economic challenges of recession or budget problems. Personalized prevention efforts represent one path forward; however, depression interventions will also need to expand beyond only the individual-level focus to effectively target social determinants of health and engage larger-scale, structural system levels. We suggest that additional improvement toward reducing depression can be made by both improving individual interventions and making structural changes.

Applying the FORCE to Improve the Prevention and Treatment of Youth Depression

In order for youth to benefit from depression prevention and treatment efforts, they must first and foremost have access to evidence-based care. Common barriers to care include structural factors (e.g., lack of financial resources or transportation, geographic restrictions, long waitlists, and limited providers), as well as social (e.g., mental health stigmatization) and intrapersonal factors (e.g., lack of confidence in treatment, low perceived need) (Andrade et al., 2014 ; Mojtabai et al., 2011 ). Structural racism and other forms of identity-based oppression as well as lack of provider cultural competence impose additional barriers for individuals with minoritized identities, including LGBTQIA + and transgender individuals, and folks of minoritized racial and ethnic identities (Castro-Ramirez et al., 2021 ; Romanelli & Hudson, 2017 ; Shipherd et al., 2010 ). Thus, addressing barriers to care is fundamental to improving outcomes for children and adolescents.

We are encouraged by several developments that seek to address barriers to care across ecological levels. At the policy level, the Mental Health Parity and Addiction Equity Act of 2008, which was expanded under the Affordable Care Act of 2010, mandated that most health insurance providers guarantee reasonable coverage for mental health care services (Block et al., 2020 ). Project AWARE (Advancing Wellness and Resilience in Education) is a federally funded program that supports the development of school-based prevention, screening, and early intervention services, incentivizing stakeholders to integrate evidence-based services in youths’ naturalistic settings. Moreover, state-level initiatives have been implemented to provide youth with accessible, free services, such as the “I Matter” program in Colorado which provides up to 6 sessions of free psychotherapy for youth 18 and under. Mental Health First Aid, a standardized educational program aimed at increasing mental health literacy and reducing mental health stigma, has been successfully implemented in more than 20 countries worldwide. Meta-analysis shows effectiveness for producing changes in mental health knowledge (ES = 0.56), attitudes (ES = 0.28), and behaviors (ES = 0.25) (Hadlaczky et al., 2014 ).

The growing ubiquity of digital technology also presents exciting opportunities to address barriers to care and increase access to evidence-based treatment. Telehealth technology, such as the use of videoconferencing software to deliver psychotherapy services, may allow providers to reach youth in rural or otherwise hard to reach locations and those youth who face transportation or other physical barriers to care (Myers & Comer, 2016; Nelson et al., 2003 , 2006 ). Text-messaging based interventions have also shown promise to promote treatment engagement and proactively address barriers to care among youth (Ridings et al., 2019 ; Suffoletto et al., 2021 ). Single-session inventions (SSIs) can be delivered asynchronously and in an anonymized manner. They represent another way to provide immediate service access for at-risk youth; SSIs are feasible and effective for reducing depression symptoms among diverse samples of adolescents (Schleider & Weisz, 2017 ). SSI proponents and researchers take care to note that these interventions are meant to motivate and supplement, not replace, comprehensive evidence-based therapies (Dobias et al., 2022 ; Schleider et al., 2022 ).

Addressing the unmet mental health needs of contemporary and future youth will require creativity, flexible thinking, and openness to new approaches and modalities. Doing more and better to address the needs for youth depression will also require openness (and additional training to enhance psychological scientists’ skills) to collaborate and consult with various stakeholders, community members, educational staff, allied health care professionals, and policy makers.

Ecological frameworks for dissemination and implementation emphasize that successful collaboration involves building on existing community strengths, knowledge, and resources to design and refine prevention and treatment strategies that are effective, sustainable, and culturally responsive (Atkins et al., 2015 , 2017 ; Mehta et al., 2019 ). Schools (e.g., Hoover & Bostic, 2021 ) and community mental health centers (e.g., Starin et al., 2014 ) are two clear examples of naturalistic settings in which psychologists can consult and collaborate with multidisciplinary teams to implement evidence-informed interventions for youth. Further, research indicates that digitally facilitated interventions are also enhanced when they feature human support (e.g., coaching) relative to a computer alone (Bennett et al., 2019 ; Ebert et al., 2016 ; Whittaker et al., 2017 ).

Relationships with natural helpers (i.e., non-professionals to whom community members appeal for both social and instrumental support; Israel, 1985 ) may also enhance efforts to respond to the challenge of youth depression, particularly among historically underserved and/or minoritized community members. Trained natural helpers (or “paraprofessionals”) can increase access via increased help-seeking and reduce barriers to care by offering community-based services from community insiders. Such trained natural helpers may be best equipped to respond to the particular cultural values and needs of the children and families they serve. This can be particularly important and valuable in low-resourced and/or historically minoritized settings, in which access to culturally responsive care may be limited and negative experiences within the health care system may be more likely (Jain, 2010 ). Psychologists can partner with community agencies and natural helpers to increase effectiveness of care for historically underserved children and families. These partnerships can improve child outcomes (Garcia et al., 2022 ). For example, psychologists actively collaborated with community agencies to gain insight into community values, norms, and concerns, and used trained natural helpers to provide in-home support to families of young children (age 2–8) enrolled in a course of clinic-based parent–child interaction therapy.

As innovative ways expand the scope and reach of clinical interventions, it will be important to integrate knowledge from ongoing construct validation work. With enhanced and updated understanding of the construct of depression, prevention and treatment strategies need to follow suit. For example, should conceptual and psychometric work show that mental pain is an important feature to include in measures of depression, then new and potentially promising avenues of intervention (e.g., treatments targeting pain alleviation and management for youth across settings and contexts) can be developed and examined. Of course, any enhanced conceptual clarity that may inform expansion or refinement depression interventions will require proper and rigorous evaluation with evidence.

Across ecological levels, prevention and treatment efforts should be informed by empirical evidence and not merely assumed to work. Additionally, applying extant research needs to consider the generalizability of findings and available evidence to samples and the larger population beyond the specific samples (see Simons et al., 2017 for excellent discussion on these “constraints on generalizability”). Interventions involve substantial resources (e.g., time, personnel, money), so knowing from evidence that particular interventions are not superior to control conditions (e.g., school-based cognitive behavioral universal preventions) is important for prioritizing valuable resources and directing policy recommendations toward efforts that do work. More concerningly, even well-intended and conceptualized efforts may be associated with iatrogenic effects. In their large study evaluating universal mindfulness interventions versus TAU in schools, for example, Kuyken et al. ( 2022 ) found iatrogenic effects due to mindfulness training in some schools. These surprising results reinforce the importance of evidence gathering and careful evaluation. In sum, evidence-based care remains essential to promoting wellbeing among youth and their families and prioritizing intervention efforts to those with the highest potential for success.

Next, we illustrate two examples of how principles of the FORCE can be used to advance efforts to reduce youth depression across ecological and structural levels.

Case Example 1: Alleviating Poverty to Alleviate Depression

Poverty, income, and food insecurity represent one key grouping of social determinants of health (cf., Lund et al., 2018 ) with clear implications for youth depression. Highlighting the promise of targeting the economic domain, a compelling recent review states that “we now know that loss of income causes mental illness” (Ridley et al., 2020 , p. 1). Ridley and colleagues’ summary also provides evidence supporting bidirectional causal relationships between poverty and mental illness, including depression.

Quasi-experimental evidence demonstrates the impressive benefits of providing families enhanced economic resources. As part of Covid-19 pandemic relief in July 2021, the US Government expanded temporarily a Child Tax Credit (CTC) so that additional economic funds (up to $3600 maximum per child from the previous CTC of $2000) were provided nearly universally (with few administrative burdens) to families via direct automatic monthly payments to family bank accounts. This expanded CTC was made available to a much wider pool of families relative to previous efforts. The July 2021 expansion made these direct economic benefits available to low-income and unemployed caregivers, who were previously ineligible for this economic support.

The net result of the expanded CTC was that child poverty was cut nearly in half, and food insecurity and insufficiency were reduced (Batra et al., 2023 ). These dramatic results were observed in only two years of increasing financial support to children and families. Comparable findings from another federal program to reduce poverty for low-income families, based on work with Earned Income Tax Credit (EITC), similarly showed outcomes including improved housing, higher family income, and better access to health care. These anti-poverty effects improved mental health especially for Black families (Batra & Hamad, 2021 ).

Results from a large serial cross-sectional study employing a quasi-experimental design showed that the July 2021 expanded CTC was linked with lower depression and anxiety symptoms among lower-income adults with children (Batra et al., 2023 ). More specifically, analyses compared internalizing symptom levels as measured from a baseline (prior to the initiation of the expanded CTC) to after infusion of these additional economic resources. Results showed that low-income caregivers with children reported approximately 13% reduction in clinically significant anxiety symptoms and 6% drop in clinically significant depression.

Additional findings from this expanded CTC study highlight policy implications. With increased financial resources from the expanded CTC, no change was found for average mental health care visits or psychiatric prescriptions. These results suggest that anxiety and depression symptoms can improve without families requiring use of additional mental health services. In other words, changing the circumstances of living can exert meaningful effects for individuals’ psychological symptoms even in the absence of direct psychotherapeutic intervention. Poverty is associated with greater exposure to trauma and violence, increased environmental stressors, worse physical health, and exposure to interpersonal discrimination and structural inequality. Improving safety, economic stability, and physical wellbeing within the family may be reasonably assumed to have downstream effects of lowering depression and co-occurring psychopathologies within families.

In summary, given strong evidence that broader systemic factors and social determinants are linked and appear to causally affect depression and other forms of youth psychopathology, multiple approaches are needed to reduce distress and relieve depression’s burden in addition to improving access to psychological interventions. Social determinants of mental health (e.g., poverty, health care access, food insecurity) are fundamental aspects of youths’ experience that can be addressed by building relationships with community advocates and policymakers to enact higher level economic policy. The recent CTC expansion provides important evidence demonstrating the salutary effects of direct economic interventions for family mental health.

Case Example 2: Personalizing Depression Preventions

Evidence-based reviews demonstrate that indicated and selective preventions are effective for decreasing incidence and risk for anxiety and depression among youth (Breedvelt et al., 2018 ; Caldwell et al., 2019 ; Moreno-Peral et al., 2017 ). While findings are mixed with strength of effectiveness for universal prevention depending on settings, contexts, delivery, and intervention modality, universal interventions can be combined and blended with targeted approaches for anxiety and depression. Parenting programs represent an excellent example of this approach and are among the most efficacious and cost-effective interventions to reduce the prevalence of youth mental health (Prinz & Shapiro, 2018 ). Parenting programs are acceptable to many caregivers, effective across diverse contexts, and can be applied with population-based approaches to achieve high dissemination. Economic analysis shows that parenting programs provide successful impact for family and offspring mental health that result in more savings economically from social service spending relative to the cost of implementing these universal, population-based programs (Washington State Institute for Public Policy, 2019 ).

Systems-contextual approaches, such as the parenting program Triple P, use a tiered approach to flexibly provide contextually sensitive, ecologically engaged, and developmentally appropriate parenting support in a manner that is feasible, scalable, and effective (Sanders & Mazzucchelli, 2022 ). One key explanation for the effectiveness of this program involves the flexible selection of appropriate evidence-based programs emerging from the central, unified theoretical framework to respond to the specific needs and priorities of particular target populations within a broader population-based service model (Sanders & Mazzucchelli, 2022 ). While universal, population-based programs such as Triple P achieve this component via flexible delivery and implementation of teaching particular parenting skills based on varying parenting needs and primary concerns, other options can include personalizing prevention in a manner that matches intervention selection to youth’s particular risks and needs.

Rather than providing a one-size-fits all approach via prevention delivery to all youth regardless of risks or strengths, more precise personalization can occur when evidence-based risk profiles identify individuals or subgroups for whom particular interventions may prove more efficacious. As our risk factor review in Table 1 illustrates, numerous risks could be examined and tested to inform such a risk profile with translation to impact prevention. Here, we provide one example (Hankin, 2020 ). A cognitive and interpersonal risk profile was developed based on foundational research over years of solid, replicable vulnerability research. This algorithm was then tested and evaluated in independent samples and shown to predict future occurrence of MDD (Hankin et al., 2018 ). This risk profile was used in a randomized trial, the Personalized Depression Project (PDP; Young et al., 2021 ), to evaluate the degree to which risk-informed personalized prevention can improve future depression reduction. Youth categorized as exhibiting high or low cognitive and interpersonal risks were randomized to receive an intervention that either matched their risk and best met their needs (e.g., high cognitive risk and low interpersonal risk received a cognitive behavioral program; high interpersonal risk and low cognitive risk received an interpersonal-based program) or mismatched (e.g., high cognitive risk and low interpersonal risk received the interpersonal-based program). Results showed that matched adolescents reported significantly fewer depression symptoms relative to mismatched youth over the 21-month study period, although no significant difference was observed for MDD onset (12% for matched vs 18.3% for mismatched). Additional outcome data for anxiety symptoms revealed that matched youth reported significant decrease in anxiety symptoms compared to mismatched adolescents from postintervention through 18-month follow-up (Jones et al., 2022 ). Last, matched youth experienced significantly fewer dependent stressors compared to non-matched adolescents over follow-up (Jones et al., 2023 ).

In summary, findings from PDP illustrate that openness to new modes of prevention that implement evidence-based approach to personalizing prevention efforts as informed by knowledge of the construct of depression to create health and risk profiles can work to enhance outcomes among youth. Future research is still needed to replicate these PDP findings and extend investigation to evaluate the extent to which the specific cognitive–interpersonal risk classification profile and its categorical cutoffs generalize to other adolescents in other settings and contexts for maximal clinical utility.

Clinical psychological scientific study of youth depression began in earnest in the late 1970s and has seen rapid expansion of inquiry and knowledge accumulation from the mid-1990s to the present. The field has produced impressive facts and findings regarding depression’s prevalence, course, patterning, risk and resilience factors, and interventions. As with all forms of scientific investigation, the validity and utility of this corpus of information on youth depression rests on foundational principles and frameworks that affect, and are affected by, how the construct of depression has been conceptually defined and assessed.

We provided a review of particular sociohistorical events and philosophical principles that help to contextualize how scholars and applied mental health workers have conceptualized and measured youth depression over theses decades. Given particular implicit assumptions affecting how key features of depression have been defined, which signs and symptoms have been predominantly included (as well as excluded), we advocated for a renewal in the refinement, revision, and reconceptualization of the depression construct among children and adolescents especially incorporating a developmentally informed perspective. We discussed modern principles of the construct validation process, including the first two steps of content definition and then measurement development. We encouraged depression experts and important stakeholders to engage in the back-and-forth iterative process involving these two construct validation steps to create living, ongoing measures of the youth depression construct that would be freely available for use and ongoing refinement. Research can then evaluate proposed newer measure(s) via the third step of construct validation in which associations between revitalized measurement instrument(s) and other external constructs (e.g., risk factors, intervention) are evaluated. Because these construct validation steps were not used in the development and testing of most currently and commonly used youth depression measures, our proposal to revisit and reconceptualize the depression construct in a developmentally sensitive manner holds promise for the field of youth depression to improve all aspects of basic scientific and applied knowledge.

At the same time, the considerable number of children and adolescents around the world experiencing elevated depression demands enhanced efforts to reduce the tremendously high distress and burden among youth. The current literature shows that the present suite of evidence-based depression interventions for children and adolescents demonstrate some efficacy and effectiveness in treating and preventing depression. However, these largely individually focused pharmacological and psychological interventions are not enough to meet the massive needs to seriously decrease the gulf between depression’s high prevalence and available implementations provided via trained mental health experts. We proposed more serious attention and focus to broaden interventions beyond the predominant individual level and expand efforts structurally across socio-ecological systems and levels. Such expanded approaches could include more universal efforts with supportive evidence, such as promoting positive parenting (e.g., Triple P), enhancing available resources (e.g., educational, health care), and financial supports to lift children and families out of poverty via government and legislative initiatives. Additionally, expanded universal preventions can be combined with more targeted, selective approaches that personalize depression interventions using risk-informed profiles to guide matching to evidence-based programs.

In closing, the field of youth depression has come a long way, amassed many impressive findings, and found ways to reduce depression symptoms and disorder. At the same time, rates of depression, distress, and burden continue to rise for children and adolescents, and this prevalence–intervention gap is widening. We believe there is a New Hope for the future of youth depression research that can rise to meet these challenges and offer avenues to reduce distress and burden around the world. With a clearer understanding of fundamentals (clear thinking informed by history and philosophy), openness to explore new ideas transparently using the scientific method, relationships with youth, families, and stakeholders most intimately acquainted with depression, constructs to guide conceptualization and measurement of youth depression’s signs and symptoms, and evidence collection and evaluation to ensure accurate and believable knowledge (the FORCE), we look forward to future advances that instill realistic hope and are poised to advance progress on youth depression.

Data Availability

There are no data collected or analyzed for this review, so there are no data to share.

In the context of the present paper, “youth” is used to refer to school-aged children and adolescents, specifically, as much of the evidence and empirical emphasis of the literature to date has focused on these periods of development. We wish to note, however, that the ideas and suggestions promulgated in this paper may provide meaningful directions for efforts to improve research and intervention efforts targeting earlier periods of development (e.g., infancy, preschool age). That is, fundamentals, openness, relationships, constructs, and evidence are essential to improving our understanding of and capacity to respond to the needs of vulnerable young people across the lifespan.

We will proceed to discuss several key events and players involved in the development of the model DSM as it relates to youth depression; however, for more information regarding the history of the DSM, we direct interested readers to several excellent reviews in this area (Blashfield, 1984 ; Blashfield et al., 2014 ; Clark, Cuthbert et al., 2017 ; Frances & Widiger, 2012 ; Horwitz; Kendler, 2016 , 2017 ; Wilson, 1993 ).

We use “intervention” to refer to both prevention and treatment efforts.

Contrast Dr. Felix, as the first NIMH director’s “bible” reference, to the most recent outgoing NIMH Director, Dr. Insel, saying DSM is not the “bible” of psychiatric classification.

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Benjamin L. Hankin acknowledges Grant funding support from NHLBI R01HL155744 and NIMH R01MH109662. Julianne M. Griffith acknowledges grant funding support from NSF GRPF 1000259217.

This work is supported by the National Heart, Lung, and Blood Institute (Grant No. 155744) and National Institute of Mental Health (Grant No. 109662) to Benjamin Hankin and National Science Foundation, 1000259217, Julianne Griffith

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Hankin, B.L., Griffith, J.M. What Do We Know About Depression Among Youth and How Can We Make Progress Toward Improved Understanding and Reducing Distress? A New Hope. Clin Child Fam Psychol Rev 26 , 919–942 (2023). https://doi.org/10.1007/s10567-023-00437-4

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Anxiety, Depression, and Suicide in Youth

• Ned H. Kalin , M.D.

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Anxiety disorders and depression are among the most common psychiatric illnesses affecting youth. Anxiety disorders typically begin in childhood, whereas the onset of depression frequently occurs later during adolescence or early adulthood. These illnesses are highly comorbid, with pathological anxiety regularly preceding the development of depression. The lifetime prevalence of anxiety disorders when assessed in adolescents is reported to be as high as 32% ( 1 ), whereas the estimated 12-month prevalence of major depression in adolescents is approximately 13% ( 2 ). Prior to adolescence, the incidence of these disorders is the same between boys and girls; however, as girls mature and go through puberty, they are approximately twice as likely as boys to be diagnosed with anxiety and major depression. In addition to causing considerable suffering and impaired functioning, when severe, these illnesses can be life threatening. Tragically, 6,200 suicide deaths were reported in 2017 among U.S. adolescents and young adults from 15 to 24 years of age ( 3 ), and suicide is the second leading cause of death among individuals 10–34 years of age ( 4 ).

As with other psychiatric illnesses, the risks for developing anxiety disorders and major depression are due to interactions between heritable and nonheritable factors. It is estimated that the heritability of anxiety and major depression is between 30% and 40%, leaving a considerable amount of the risk to potentially modifiable environmental factors. Genome-wide association studies with increasingly large sample sizes continue to identify genes that help explain a portion of the heritability for anxiety and depression ( 5 ). However, it is important to note that a recent study has provided evidence questioning the validity of previous findings that have linked a number of the familiar, “usual suspect” candidate genes (e.g., polymorphisms of the gene for the serotonin transporter protein) to be strongly associated with anxiety and depression ( 6 ). Early life trauma, neglect, inadequate parenting, and ongoing stress are among the environmental factors that contribute to the likelihood of developing anxiety, depression, and other stress-related disorders. Adolescence is a particularly vulnerable period, as the psychosocial challenges of adolescence converge with rapid and substantial developmental changes in the brain and in hormones. Prior to the onset of anxiety disorders and major depression, at-risk phenotypes or personality traits such as behavioral inhibition ( 7 ) and neuroticism ( 8 ), which are also partially heritable, can be identified and provide an opportunity for developing early intervention strategies for children at risk.

Two now classic clinical trials have evaluated the efficacy of selective serotonin reuptake inhibitors and cognitive therapies for the treatment of major depression and anxiety disorders in youth. The Treatment for Adolescents With Depression Study was a randomized 12-week trial involving 439 adolescents with major depression in which fluoxetine, cognitive-behavioral therapy (CBT), CBT plus fluoxetine, and placebo were compared ( 9 ). Results demonstrated that fluoxetine plus CBT and fluoxetine alone were significantly better than placebo, with the combination outperforming fluoxetine alone. CBT by itself did not statistically differ from placebo (fluoxetine plus CBT, 71% response; fluoxetine alone, 60.6% response; CBT alone, 43.2% response; placebo, 34.8% response). With continued treatment, rates of response remained high for up to 36 months ( 10 ). The Child/Adolescent Anxiety Multimodal Study was a randomized clinical trial comparing 14 CBT sessions with 12 weeks of sertraline plus CBT, sertraline alone, or placebo in 488 children and adolescents (7–17 years old) with separation anxiety disorder, generalized anxiety disorder, or social phobia ( 11 ). Results demonstrated that all therapies were more effective than placebo and that the combination of sertraline plus CBT was superior to the other active treatments (sertraline plus CBT, 80.7% response; CBT, 59.7% response; sertraline alone, 54.9% response; placebo, 23.7% response). Long-term follow-up of 319 of these children revealed that only 22% were in stable remission, whereas the remainder were either chronically ill or had relapsed ( 12 ). Taken together, these studies highlight the efficacy of relatively short-term interventions and point to the need for treatments that can fundamentally affect childhood developmental trajectories that will enable initial interventions to have long-lasting positive effects.

In this regard, a more complete understanding of the pathophysiology underlying anxiety disorders and major depression in youth is necessary to advance the development of new early intervention strategies. Neuroimaging studies suggest that anxiety and depression share alterations in the function of prefrontal-limbic circuits that underlie the adaptive regulation of emotion and the processing of anxiety ( 13 ), and studies also show alterations in reward-related processing to be associated with both anxiety and depression ( 14 , 15 ). However, to move beyond the associations between brain and behavior that have been identified with neuroimaging, preclinical studies are critical to elucidate potential mechanisms that underlie anxiety- and depression-related pathophysiology. For various reasons, developing valid preclinical animal models of depression has been challenging. In contrast, anxiety and fear can be effectively modeled in rodents and nonhuman primates ( 13 , 16 ), and such research has led to a deep understanding of the circuits, cells, and molecules that are mechanistically involved in mediating adaptive and pathological anxiety. The evolutionary expansion of the primate prefrontal cortex makes nonhuman primates particularly valuable for modeling human anxiety, as the expanded primate prefrontal cortex is prominently involved in mediating internal emotional experiences and cognitive processes that are unique to primate species and that, when aberrant, contribute to psychopathology.

The neural circuitry underlying fear and anxiety includes subcortical structures such as specific amygdala nuclei, the bed nucleus of the stria terminalis, the anterior hippocampus, and brainstem regions such as the periaqueductal gray ( 17 ). These subcortical regions, via their synaptic connectivity, work in concert with the ventromedial prefrontal cortex, the anterior insular cortex, the anterior cingulate cortex, and other regions of the posterior orbitofrontal cortex to regulate and process anxiety. In relation to major depression, the presence of anhedonia is a clinical feature that clearly distinguishes depression from anxiety. This diminished capacity to enjoy and engage with one’s world is in part mediated by altered function of the brain’s reward circuitry. For exam-ple, neuroimaging studies in adolescents with depression demonstrate altered reward-related responsivity of various components of this system, including the nucleus accumbens and striatum, as well as cortical regions such as the insular and the anterior cingulate cortices ( 14 ).

This issue of the Journal focuses on depression and anxiety during childhood and adolescence and importantly includes two articles that address mental health issues in disadvantaged youth living in poverty. We include four research articles that address critical treatment areas, including the use of CBT for treating childhood grief, ketamine for treatment-resistant adolescent depression, the use of neuroimaging in anxious youth to predict treatment response, and a preschool intervention for preventing psychopathology in disadvantaged children. Another article that is relevant to the health of disadvantaged and underresourced populations presents research that combines measures of inflammation with neuroimaging to better understand factors that may underlie physical health problems in children living in poverty. Other articles in this issue are focused on understanding underlying pathophysiology (capitalizing on neuroimaging data from the large Adolescent Brain Cognitive Development [ABCD] database), examining neuroimaging measures associated with suicidal thoughts, and examining reward-related neural processing in relation to disruptive behavior disorders.

Treating Prolonged Grief in Children and Adolescents

The loss of a loved one during childhood is traumatic and increases the risk to develop stress-related psychiatric illnesses such as depression and posttraumatic stress disorder (PTSD). Boelen and coauthors ( 18 ) present data from a randomized clinical trial comparing CBT aimed at coping with grief with an intervention employing supportive counseling in 134 children and adolescents who met criteria for prolonged grief disorder. Prolonged grief disorder, which was recently added to ICD-11, is defined by the presence of significant and interfering grief symptoms that last beyond the first 6 months after a loss. Although it is not in DSM-5, prolonged grief disorder is similar to the DSM-5 diagnosis of persistent complex bereavement disorder. In this study, each participant received nine sessions of the respective therapies, and their parents or caregivers received five therapy sessions focused on supporting their children and strengthening their relationship with their child. Results demonstrated that, when assessed at 3, 6, and 9 months posttreatment, both treatments had positive effects. However, the CBT group demonstrated greater decreases in grief symptoms at all posttreatment time points, and at 6 and 12 months, CBT considerably outperformed counseling in the domains of depression and PTSD symptoms. Margaret Crane and Lesley Norris, Ph.D. candidates, along with Dr. Philip Kendall from Temple University, contribute an editorial that speaks to moving beyond the findings presented in this study toward developing personalized treatment approaches for prolonged grief and modifying current treatment strategies to make them more widely accessible to suffering youth ( 19 ).

An Intervention in Children Living in Poverty Aimed at Reducing the Later Development of Psychopathology

Poverty is associated with numerous factors that are stressful and traumatic. To assess the extent to which an early school intervention can make a difference for impoverished children, Bierman et al. ( 20 ) report data from a randomized clinical trial examining the effects of an evidence-based intervention on the development of psychopathology, when assessed years later during adolescence. In this study, 356 4-year-old children from low-income families received an intervention consisting of a social-emotional learning program combined with an interactive reading program that was compared with usual educational practices. The children were recruited from three counties in Pennsylvania and came from families with a median annual income of $15,000. While differences between the interventions were not apparent when children were in the 7th grade, significant differences were observed when children reached 9th grade. For example, significantly fewer conduct problems, emotional symptoms, and peer problems were present in the 9th graders who, at 4 years of age, had participated in the social-emotional learning program. This study underscores the need to view the societal issue of poverty as stressful and traumatic, the disparities in health care associated with poverty, and the profound effects poverty can have on families and children. The findings are encouraging, with important public health implications, and clearly support early interventions aimed at promoting healthy social, emotional, and cognitive development in children facing the chronic adversity of growing up in poverty.

Enhanced Linkages Between Neural Activation and Inflammation in Impoverished Children

Miller and coauthors present data from a sample of early adolescents supporting an enhanced association between brain activation and peripheral inflammation that is selective to children living in poverty ( 21 ). The findings may shed light onto why underprivileged children have increased vulnerabilities to develop psychiatric and physical illnesses. The study was performed in 207 12- to 14-year-old children from the Chicago area who came from families across the socioeconomic spectrum. To explore a link between peripheral inflammation and neural function, the investigators correlated blood inflammatory markers (C-reactive protein, tumor necrosis factor-α, and interleukins-6, -8, and -10) with functional neuroimaging measures that assessed threat- and reward-related neural activation. First, the authors found that children living in poverty had higher levels of inflammation than children from higher socioeconomic backgrounds. In addition, the results demonstrated that in impoverished children, the inflammatory markers were positively correlated with both threat-related amygdala and reward-related striatal activation. The authors speculate that this enhanced coupling between neural and inflammatory processes may be due to the developmental impact of chronic adversity and may be a mechanism linking poverty to increased stress reactivity and illness. Interestingly, the positive relation between inflammatory markers and striatal activation was not in the predicted direction. Dr. Charles Nemeroff, from the University of Texas at Austin, contributes an editorial that emphasizes the deleterious effects of poverty on poor health and mental illness and further elaborates on the immune and neural alterations found in children who grow up in such impoverished and unfortunate conditions ( 22 ).

Neuroimaging Measures Are Not Good Predictors of Childhood Suicidal Ideation and Behavior

Vidal-Ribas and coworkers ( 23 ) use the large ABCD multimodal imaging database to comprehensively assess the usefulness of structural and functional brain measures in predicting childhood suicidal thoughts and behaviors. In a sample of 7,994 9- to 10-year-old children, the researchers found that 14.3% of the sample, or 1,140 children, had suicidal ideation or behaviors as reported by themselves or by caregivers. The occurrence of suicidal thoughts and behaviors was associated with increased levels of psychopathology and psychosocial adversity. Of the more than 5,000 statistical tests that were performed with multiple imaging measures (to assess cortical thickness, resting-state functional connectivity, and task-related functional activation), only one test survived correction for multiple comparisons. This finding revealed a relation between reduced thickness of the left bank of the superior temporal sulcus and caregiver-reported suicidal thoughts and behaviors. The authors draw the conclusion from these overall negative findings that current neuroimaging methods are not useful in reflecting the biological underpinnings of suicidal ideation and behavior in youth. In their editorial, Dr. Randy Auerbach from Columbia University and Drs. Henry Chase and David Brent from the University of Pittsburgh discuss the comprehensive and thorough nature of the study, the potential meaning of the superior temporal sulcus finding, and other critical aspects worth considering in future studies aimed at understanding the factors underlying youth suicide ( 24 ).

Reward-Related Functional Brain Alterations in Children With Disruptive Behavior Disorders and Callous-Unemotional Traits

Hawes et al. examine the extent to which children with disruptive behavior disorders (DBDs) (e.g., oppositional defiant disorder and conduct disorder) have alterations in neural responses to the anticipation and actual receipt of a reward ( 25 ). As in the Vidal-Ribas et al. study ( 23 ), these investigators used the ABCD neuroimaging database to provide a large sample size. Alterations in reward processing characterized by difficulties in delaying gratification and overvaluation of immediate rewards have been hypothesized to underlie externalizing phenotypes. In this study, reward-related brain activation in response to a monetary incentive delay task was examined in youth with DBDs who were subdivided into those with DBDs only (N=276) and those with DBDs with callous-unemotional traits (N=198), a characteristic that is more likely to be associated with antisocial behavior. The data from these children were compared with neuroimaging data from 693 typically developing youth. The children were, on average, 9.5 years old when studied. The findings from the study demonstrated that regardless of the presence of callous-unemotional traits, youth with DBDs exhibited decreased dorsal anterior cingulate activation in response to reward anticipation and increased orbitofrontal cortical and nucleus accumbens activation during reward receipt. Some neural activation differences between the DBD-only group and the DBD callous-unemotional trait group were also observed. Taken together, these findings shed light on the cortical control systems and subcortical reward-related neural substrates that may underlie the maladaptive behaviors characteristic of youth with DBDs.

Pretreatment Reward-Related Brain Activation Is Associated With Response to Psychotherapy in Youth With Anxiety Disorders

Sequeira and coworkers ( 26 ) explore the use of pretreatment functional imaging measures to predict treatment responses to psychotherapy in 9- to 14-year-old children with anxiety disorders (i.e., separation anxiety disorder, generalized anxiety disorder, or social anxiety disorder). Similar to other articles in this issue, this study probed reward-related brain activation. In this case, activation of brain regions encompassing the medial prefrontal cortex and the striatum was compared between the conditions of winning a reward relative to the experience of losing. The study included 50 children treated with 16 sessions of CBT, 22 children treated with child-centered therapy, and 37 healthy comparison youth. The intervention was effective, as 67% of the patients, regardless of treatment, responded to the intervention. Prior to treatment, greater activation of the medial prefrontal cortex was found in the patients with anxiety compared with the control subjects. However, the authors note that this difference in medial prefrontal activation could be accounted for by the co-occurrence of depressive symptoms in the anxiety group. Importantly, the authors found that as a group, treatment responders compared with nonresponders had increased pretreatment activation of regions encompassing the subgenual anterior cingulate cortex and the nucleus accumbens. These initial findings point to the potential importance of understanding reward-related brain systems in relation to psychotherapeutic outcomes in youth with anxiety. The authors speculate that increased striatal responsivity to rewards prior to treatment could be associated with increased motivation and engagement with therapy.

A Proof-of-Concept Trial Assessing Ketamine for Depression in Adolescents

Dwyer and colleagues ( 27 ) report the results of a small randomized double-blind single-dose crossover study in 17 adolescents with major depression who had not responded to at least one adequate trial of an antidepressant. In this trial, intravenous ketamine (0.5 mg/kg) or intravenous midazolam (0.045 mg/kg) was administered to each patient in a crossover design with a 2-week interval between treatments. Patients remained on their current psychiatric medications throughout the study. Sixteen patients completed both treatments, and the primary outcome was depression severity measured with the Montgomery-Åsberg Depression Rating Scale (MADRS) 24 hours after the infusion. Results demonstrated that 24 hours after infusion, ketamine had a significantly greater effect than midazolam in reducing depressive symptoms. For the midazolam infusion, the average pretreatment MADRS score was 31.88, and 24 hours later it was 24.13. For the ketamine infusion, the average pretreatment MADRS score was 30.56, and 24 hours later it was 15.44. Responders were defined by a 50% reduction in the MADRS score, and it was found that ketamine was associated with a response in 77% of the patients, with 35% of patients responding to midazolam (five of six of these participants also responded to ketamine). Compared with midazolam, the ketamine infusions were associated with reduced MADRS scores at all time points measured up to 14 days postinfusion. Ketamine was associated with dissociative side effects that were transient as well as with transient changes in blood pressure and heart rate. In their editorial ( 28 ), Drs. Parikh and Walkup from Northwestern University discuss the potential importance of this finding in relation to treating adolescent depression, but they also put into context such issues as the small sample size, the difficulty maintaining blinding because of ketamine’s dissociative effects, and concerns raised by others regarding the role of opiates in mediating ketamine’s effects in relation to its addiction potential ( 29 ).

Conclusions

Many psychiatric disorders have their origins early in life, which is clearly the case with anxiety and depression. In addition, the adolescent transition period is a time of increased risk during which psychiatric illnesses, especially depression, tend to emerge. Although there are adequate treatments for youth with anxiety and depressive disorders, many individuals do not respond to current treatments, and it is important to emphasize that many young people with psychiatric illnesses do not have access to available treatments. There is no question that we need better treatments and better access for children suffering from these disorders. This issue of the Journal highlights recent insights and clinical advances related to the treatment of anxiety disorders and major depression. Findings with the potential to directly affect the clinical care of youth include: demonstration of the efficacy of CBT in treating prolonged grief; early school socioemotional and cognitive interventions in disadvantaged children that prevent adolescent psychopathology; the rapid efficacy and safety of ketamine in reducing depressive symptoms in youth with treatment-resistant depression; and the promise of using functional neuroimaging to inform treatment choice and predict outcomes in youth with anxiety disorders. Other articles in this issue address pathophysiology, demonstrating increased coupling between brain and peripheral inflammatory markers in impoverished youth, altered reward-related brain activation in youth with DBDs, and a lack of association between structural and functional neuroimaging measures with suicidal ideation and behavior in youth. Continued research focused on a better understanding of the mechanisms underlying the early life risk to develop anxiety disorders and major depression is critical for the development of novel, improved treatment strategies. Efforts should be devoted to developing treatments that have the potential to positively affect the at-risk neurodevelopmental trajectories of vulnerable children. Such early life interventions provide the hope of moving beyond symptomatic treatment and toward prevention strategies.

Disclosures of Editors’ financial relationships appear in the April 2021 issue of the Journal .

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• Cited by None

• Anxiety Disorders
• Depressive Disorders
• Suicide and Self-Harm
• Child/Adolescent Psychiatry

• Open access
• Published: 17 April 2024

Potential of niacin skin flush response in adolescent depression identification and severity assessment: a case-control study

• Jie Feng 1 , 3   na1 ,
• Wenjiao Min 1 , 3   na1 ,
• Dandan Wang 4 ,
• Jing Yuan 2 , 3 ,
• Junming Chen 2 , 3 ,
• Lisha Chen 2 , 3 ,
• Wei Chen 2 , 3 ,
• Meng Zhao 5 ,
• Jia Cheng 2 , 3 ,
• Chunling Wan 4   na2 ,
• Bo Zhou 1 , 3   na2 ,
• Yulan Huang 1 , 3   na2 &
• Yaoyin Zhang 1 , 3  

BMC Psychiatry volume  24 , Article number:  290 ( 2024 ) Cite this article

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The diagnosis of adolescent Depressive Disorder (DD) lacks specific biomarkers, posing significant challenges. This study investigates the potential of Niacin Skin Flush Response (NSFR) as a biomarker for identifying and assessing the severity of adolescent Depressive Disorder, as well as distinguishing it from Behavioral and Emotional Disorders typically emerging in childhood and adolescence(BED).

In a case-control study involving 196 adolescents, including 128 Depressive Disorder, 32 Behavioral and Emotional Disorders, and 36 healthy controls (HCs), NSFR was assessed. Depressive symptoms were measured using the Patient Health Questionnaire-9 (PHQ-9) and anxious symptoms with the Generalized Anxiety Disorder 7-item scale (GAD-7). Pearson correlation analysis determined the relationships between NSFR and the severity of depression in DD patients. Receiver Operating Characteristic (ROC) was used to identify DD from BED integrating NSFR data with clinical symptom measures.

The adolescent Depressive Disorder group exhibited a higher rate of severe blunted NSFR (21.4%) compared to BED (12.5%) and HC ( 8.3%). Adolescent Depressive Disorder with psychotic symptoms showed a significant increase in blunted NSFR ( p  = 0.016). NSFR had negative correlations with depressive ( r = -0.240, p  = 0.006) and anxious ( r = -0.2, p  = 0.023) symptoms in adolescent Depressive Disorder. Integrating NSFR with three clinical scales improved the differentiation between adolescent Depressive Disorder and BED (AUC increased from 0.694 to 0.712).

The NSFR demonstrates potential as an objective biomarker for adolescent Depressive Disorder, aiding in screening, assessing severity, and enhancing insights into its pathophysiology and diagnostic precision.

Peer Review reports

Introduction

Major Depressive Disorder (MDD) presents a pressing challenge in adolescent mental health, with prevalence estimates for adolescent Depressive disorder (DD) as high as 25.2% [ 1 ]. This is particularly concerning in China, where up to 40.1% of high school students show depressive symptoms, and 8% exhibit severe depression [ 2 , 3 ]. Moreover, depression significantly contributes to adolescent suicide [ 4 ]. It is also linked to various adverse outcomes, such as academic and social difficulties, substance abuse, and self-harm [ 5 ].

The etiology of Adolescent Depressive Disorder (DD, ICD-10 F32) involves complex biological and psychosocial influences, leading to varied clinical presentations and treatment outcomes [ 6 , 7 ]. However, severe cases often go unrecognized or inadequately treated, with less than half diagnosed before adulthood [ 8 ].Current diagnostic methods, including structured interviews and scales, are inefficient and lack objective precision. Additionally, Behavioral and Emotional Disorders (BED, ICD-10 F98.9) typically emerging in childhood and adolescence present a spectrum of psychological symptoms overlapping with DD, challenging accurate diagnosis under ICD-10 guidelines. BED encompass a spectrum of emotional and behavioral challenges. This includes cases where children experience emotional distress, but do not meet the criteria for severe Depressive Disorder (DD), yet exhibit recurrent emotional issues and self-harm. BED also includes individuals with mood fluctuations and irritability that do not fit the diagnosis of bipolar disorder, as well as those with transient emotional downturns due to external factors, which improve once these influences subside [ 9 , 10 ]. This symptom overlap between BED and DD complicates differential diagnosis, underscoring the urgent need for unique biomarkers for accurate disorder identification [ 11 ].

Prior research highlights the potential of the Niacin Skin Flush Response (NSFR) in delineating adult patients with Schizophrenia and Affective Disorders from healthy controls, demonstrating a positive predictive value of 93.66% [ 12 ]. The Niacin Skin Flush Response (NSFR) displays a delayed response in adult depression, showing an inverse correlation with symptom severity as noted in previous studies [ 13 , 14 ].Similar patterns have been noted in pediatric psychiatric conditions [ 15 ]. Notably, Jinfeng Wang et al. reported attenuated NSFR in adolescent depression [ 16 ], underscoring its potential as a marker for Depressive Disorder (DD). However, further exploration is needed regarding the role of NSFR in diagnosing and differentiating Adolescent Depressive Disorder.

The Niacin Skin Flush Response (NSFR), associated with inflammation and oxidative stress, may indicate disruptions in arachidonic acid metabolism, potentially pointing to lipid imbalances in the brain that could be significant for understanding depressive disorders [ 16 , 17 ]. While existing biomarkers examine monoamine neurotransmission, immune inflammation, neuroplasticity, and neuroendocrine functions, focusing on protein dysfunction, NSFR stands out due to its specific metabolic insights [ 18 , 19 ]. Its non-invasiveness, ease of administration, and repeatability suggest it could offer valuable insights, particularly in adolescent depression [ 19 ].

Depressive Disorder (DD) with psychotic features(ICD-10 F32.3) is identified as a distinct subtype, highlighting the clinical need to distinguish between depressive disorders with varying presentations. Evidence shows the Niacin Skin Flush Response (NSFR) can discern adult schizophrenia from depression, with varying NSFR patterns correlated to psychiatric conditions [ 12 , 20 ]. This study probes NSFR’s viability as a biomarker to differentiate DD with and without psychotic symptoms((ICD-10 F32.0-F32.2) ), aiming to clarify DD subclassifications.

This study aims to evaluate the Niacin Skin Flush Response (NSFR) as a biological marker for adolescent Depressive Disorder (DD), with the objective of improving screening accuracy, assessing severity, classifying subgroups, and differentiating DD from BED.

Material and method

Participants.

Our study conducted from January to October 2023, at Sichuan Provincial People’s Hospital, Chengdu, China. Inclusion criteria :(1)Adolescents aged 12–18 years. (2)Adolescents were diagnosed with Depressive Disorder (ICD-10 F32) and Behavioral and Emotional Disorders (BED, ICD-10 F98.9) typically emerging in childhood and adolescence according to International Classification of Diseases, 10th (ICD-10). (3) Diagnosis confirmed via the Composite International Diagnostic Interview (CIDI) by two psychiatrists. (4)The Patient Health Questionnaire-9 (PHQ-9) Score ≥ 10. Exclusion criteria : Any participant with neurological diseases, brain injury, severe skin diseases, or immune diseases was excluded from this study. Those who used anti-inflammatory drugs within 2 weeks were also excluded.

The experimental group was assembled from a cohort of 208 adolescents admitted to the Child and Adolescent Psychiatry Inpatient Department, employing a randomized selection method on Tuesdays and Thursdays of each week. This group ultimately included 160 patients, comprising 128 individuals diagnosed with Depressive Disorder (ICD-10 F32) and 32 with Behavioral and Emotional Disorders typically emerging in childhood and adolescence (BED) (ICD10 F98.9). The Depressive Disorder was further stratified by the presence (ICD-10 F32.3) or absence (ICD-10 F32.0-F32.2) of psychotic symptoms. We excluded those 48 with Bipolar Disorder, Neuro-developmental disorders, Adjustment Disorder, Schizophrenia, Organic Mood Affective Disorder, Obsessive-Compulsive Disorder, PTSD, or Dissociative disorders. For healthy controls (HCs), 50 high school students were initially considered through targeted advertisements, with 36 ultimately selected post PHQ-9 screening and CIDI confirmation, ensuring no history of mental illness.

Before participation, comprehensive information about the study and testing procedures was provided to all participants. Their parents or legal guardians also received this information. Informed consents were then obtained from all participants and their legal guardians.

Assessment of niacin skin flush response (NSFR)

Methodology.

The Niacin Skin Flush Response (NSFR) of participants was evaluated using the Brain Aid Skin Niacin Response Test Instrument TY-AraSnap-H100, manufactured by Shanghai Tianyin Biological Technology Ltd., Shanghai, China. This instrument employs a transdermal delivery system involving a patch. The patch administers an aqueous solution of methyl nicotinate (AMN), which has a chemical formula of C7H7NO2 and a purity of 99%, as provided by Sigma-Aldrich. Furthermore, the patch’s unique design features six circular apertures that penetrate its sponge and adhesive layers. These apertures expose the filter paper layer beneath, which is specifically designed to facilitate the delivery of AMN.

A precise volume of the AMN solution was applied to the patch’s apertures. The solution came in varying concentrations: 60 mM, 20 mM, 6.67 mM, 2.22 mM, 0.74 mM, and 0.25 mM. After applying the solution, the patch was affixed to the volar aspect of the participant’s left forearm. It remained there for a standardized duration of one minute. Following this, the patch was carefully removed. A time-lapse photographic record was then established. Images were captured at ten-second intervals over a ten-minute period. These images documented the erythema response. From this process, a set of 60 photographs was obtained for each participant.

An initial photograph served as a baseline for comparative analysis. The instrument’s software then quantified the erythema at 59 time points. These points were under six different AMN concentrations. This process generated 354 measurements for each participant. The software analyzed the erythema surface area responses. It focused on the first quartile of AMN concentrations. This analysis helped determine the overall NSFR magnitude.

We lacked data specific to adolescents. Therefore, we used an adult-referenced model from the BrainAid database to evaluate adolescent NSFR. This database is accessible at http://brainaid.sjtu.edu.cn . The model is based on adult depression-related niacin patterns. It helped us classify adolescents’ niacin responses as either ‘blunted’ or ‘normal.’ We divided the ‘blunted’ responses into three categories: mild, moderate, and severe. This classification is crucial for analyzing how adolescent responses differ from adult patterns.

The Patient Health Questionnaire-9 (PHQ-9) was used as a validated instrument for assessing Depressive Disorder (DD) in adolescents. It consistently demonstrated high reliability, as evidenced by a Cronbach’s α coefficient ranging from 0.86 to 0.89. The PHQ-9’s sensitivity for evaluating depressive symptoms in adolescents was 89.5%, with a specificity of 77.5%, reflecting its performance in adult assessments [ 21 , 22 ]. This instrument assesses each of the nine DSM-5 depression criteria on a scale of“0”(not at all) to“3”(nearly every day). An example item from this tool is, ‘Over the last two weeks, how often have you been bothered by little interest or pleasure in doing things?’

The Generalized Anxiety Disorder 7-item scale (GAD-7) was a reliable measure for assessing anxiety symptoms in adolescents. A GAD-7 score of 10 or above demonstrated a sensitivity of 89% and a specificity of 82% for diagnosing Generalized Anxiety Disorder during psychiatric evaluations [ 23 ]. It effectively detected clinically significant anxiety symptoms in the adolescent population [ 24 ].The Chinese version of the GAD-7 exhibited commendable internal consistency, with a Cronbach’s α coefficient ranging from 0.93 to 0.95 [ 25 ]. An example item could be, “Over the last two weeks, how often have you been bothered by feeling nervous, anxious, or on edge?”

The Patient Health Questionnaire-15 (PHQ-15) was employed as an efficacious instrument for evaluating somatic symptoms, demonstrating a sensitivity of 80.2% and a specificity of 58.5% [ 26 , 27 ].The Chinese version of the PHQ-15 exhibited commendable internal consistency, with a Cronbach’s α coefficient of 0.83 [ 28 ]. A sample item from this tool might be, ‘In the last four weeks, how much have you been bothered by stomach pain?’

Statistical analysis

For this study, encompassing both binary and continuous variables, demographic characteristics across groups were analyzed using the Chi-square test for categorical variables and the Bonferroni correction for continuous measures. The Chi-square test assessed the distribution ratios of blunted Niacin Response and normal Niacin Response among individuals with adolescent DD, BED, and HC to evaluate the degree of NSFR impairment across different groups. The Mann-Whitney U test and Fisher’s Exact Test compared demographic features within the two adolescent DD subgroups. Parameters were estimated using the nonlinear least squares method. Pearson correlation analysis determined the relationships between NSFR and the severities of anxiety and depression in adolescent Depressive disorder (DD) patients. Receiver Operating Characteristic (ROC) curve analyses were then applied to gauge the efficacy of combined NSFR and symptom scores in differentiating between adolescent DD and BED. All statistical analyses were performed using R studio (Version 4.1.2). SPSS 27 and GraphPad Prism 8 with a P value of less than 0.05 denoting statistical significance and all probabilities calculated as two-tailed. In this research, we utilized the GPT-4 model for assisted writing, aiming to improve the logical structure and language expression of the paper. It is noteworthy that the entire generation process took place under the careful supervision of the authors.

Demographic characteristics

A total of 196 participants, aged between 12 and 18, were enrolled in this study.The mean age of the participants was 14.72 years, with females constituting 73.5% of the sample. Detailed data on BMI, Gender, smoking, drinking, and self-harm rates were presented in Table  1 . No significant differences were observed in gender, height, weight, or BMI between the adolescent DD, BED and HC group (all p  > 0.05). However, a statistically significant difference was noted in age between the groups ( p  < 0.05). Adolescent DD patients comprised 48.4% in junior high and 51.6% in high school. For those with BED, 68.8% were in junior high and 31.3% were in high school. All HCs were in their first year of high school. Furthermore, 37.5% of the adolescent DD patients had a family history of mental illness, 16.4% showed psychotic symptoms, 21.9% had comorbid anxiety disorders, and 2.3% had comorbid obsessive-compulsive disorder. Notably, 10.2% did not have thoughts of self-harm or suicide, whereas 89.8% did in the adolescent DD group. In the BED group, 43.8% had a family history of mental illness, 25% did not have self-harm or suicidal thoughts, and 75% did. Before admission, 63.1% of adolescent DD and BED were already undergoing treatment with selective serotonin reuptake inhibitors (SSRIs) for depression. The detailed information is delineated in Table  1 .

Increased prevalence of severe blunted niacin skin flush response in adolescent DD

In order to assess variations in NSFR across different disease cohorts and the healthy control (HC) group, chi-square tests were employed to analyze the distribution of normal to mild blunted NSFR (NMB) and moderate to severe blunted NSFR (MSB) within diverse subject groups. Comparative analysis with the BED group revealed a higher incidence of MSB subjects in adolescent DD group (21.4%) as opposed to the BED group (12.5%), with the HC group showing the lowest representation (8.3%) (refer to Fig.  1 ). While the chi-square test did not reach statistical significance ( p  = 0.136), our findings suggest an elevated proportion of moderate to severe blunted NSFR in the DD group compared to the HC group.

Distribution Proportion of NMB and MSB among Different Groups. Dark blue indicates the population with the normal to mild blunted NSFR, while light blue indicates the population with the moderate to severe blunted NSFR. Abbreviations: DD: Adolescence Depressive Disorder; BED: Behavioral and Emotional Disorders typically emerging in childhood and adolescence; HC: Healthy control; NSFR: Niacin Skin Flush Reaction, NMB: the normal to mild blunted NSFR, MSB: moderate to severe bunted NSFR.

Utilizing NSFR for subgroup classification in adolescent DD

Patients with Depressive Disorder (DD) were divided into two subgroups: those with and those without psychotic symptoms. Using Fisher’s Exact Test and the Mann-Whitney U test for comparative analysis, no significant differences were found between the groups in terms of gender, age, weight, height, or Body Mass Index (BMI), as well as the severity of depressive (PHQ-9) and somatic symptoms (PHQ-15). However, anxiety levels (GAD-7) were higher in the subgroup with psychotic features. This subgroup also showed a significantly heightened blunted NSFR ( p  = 0.016) when compared to those without psychotic symptoms (Fig.  2 ).

Heightened Blunted NSFR in DD with Psychotic Symptoms. Heightened blunted NSFR in adolescent DD with Psychotic Symptoms(PS) vs.Non-Psychotic Symptoms (NPS) ( p  = 0.016). NSFR: Niacin Skin Flush Reaction

NSFR assists in the differential diagnosis of adolescent DD

The ability of NSFR to distinguish between adolescent Depressive Disorder (DD) and Behavioral and Emotional Disorders (BED) was evaluated using a focused diagnostic model. This model, employing binary logistic regression with scale and NSFR data, aimed to differentiate DD from BED. Given the small sample size for BED, additional segmentation analysis is recommended. When only scale data were used, the diagnostic accuracy was modest, with an AUC of 0.694, which underscores the clinical symptoms’ overlap. The incorporation of NSFR data enhanced the diagnostic precision, elevating the AUC to 0.712 as depicted in Fig.  3 A&B. This increase demonstrates the effectiveness of NSFR in specifically distinguishing DD from BED.

NSFR and Scales Scoring Assisted Diagnosis of adolescent DD and BED.Biomarker for identification of adolescent DD and BED via niacin skin flushing response. ROC curves of the niacin-flushing degree for distinguishing DD from BED increased from 0.694 to 0.712 (Fig.  3 A&B). ROC: Receiver Operating Characteristic; AUC: Area Under Curve. NSFR: Niacin Skin Flush Reaction

NSFR exhibits strong association with clinical symptoms in adolescent DD

Pearson correlation analysis was conducted to investigate the relationship between Niacin Skin Flush Response (NSFR) and symptoms of depression, anxiety, and somatization. The findings revealed a notable negative correlation between NSFR and the severity of depressive symptoms (as measured by PHQ-9) in the DD group ( R =-0.240, p  = 0.006). Similarly, a significant negative association was identified between NSFR and anxiety severity (as assessed by GAD-7) ( R =-0.200, p  = 0.023) (Fig.  4 ). However, no significant relationship was detected with somatization symptoms ( R =-0.160, p  = 0.072). Intriguingly, these correlations were not observed in either the BED or HC group. This suggests a plausible hypothesis that the niacin acid phenotype of DD patients is uniquely influenced by their clinical symptoms.

Negative Correlation of NSFR with PHQ9 and GAD7 in adolescent DD. Note: The graph demonstrates that an increase in the severity of these symptoms correlates with a more pronounced blunting of Niacin Skin Flush Reaction (NSFR)

This study represents a pioneering effort to validate the Niacin Skin Flush Response (NSFR) as an objective biomarker for the precision diagnosis of adolescent Depressive Disorder (DD). Our primary findings revealed a higher prevalence of moderate to severe blunted NSFR among DD patients, with a heightened blunted NSFR in DD patients with psychotic symptoms. Furthermore, Our results revealed that an increase in the severity of depressive and anxious symptoms correlates with a more pronounced blunting of NSFR in adolescent DD group. Notably, the integration of NSFR with established clinical scales significantly improved the accuracy of differentiating DD from BED in adolescence.

Our study contributes to understanding NSFR as a potential biomarker for adolescent DD. It reveals a notably higher prevalence of moderate to severe blunted NSFR in DD (21.4%) compared to BED (12.5%) and healthy controls (8.3%). This result aligns with findings from Jinfeng Wang et al., who observed significant blunting and delay in NSFR in adolescent depression. Additionally, our study confirms the diagnostic value of NSFR. This is evidenced by AUC values of 0.719 and 0.721, demonstrating its high sensitivity in detecting adolescent DD [ 16 ]. Additionally, Qing et al.‘s work, which showed blunted NSFR across a spectrum of pediatric psychiatric disorders, further supports the biomarker’s broad applicability [ 15 ]. However, contrary to existing literature, our results did not confirm delays in NSFR typically associated with Depression, suggesting variability in NSFR response or potential age-related factors affecting the biomarker’s performance. While the proportion of blunted NSFR was higher in adolescent DD group, the lack of statistical significance necessitates cautious interpretation and underscores the need for further research with larger cohorts to validate these findings.

Our exploratory study represents the first to document a heightened blunted NSFR in adolescent DD patients with psychotic symptoms compared to those with non-psychotic symptoms. Clinically, psychotic features in depression introduce specific challenges, including a higher rate of recurrence, an elevated risk of suicide, and a potential increase in hospital admissions [ 29 , 30 , 31 ]. Pathophysiologically, a spectrum of susceptibility genes such as BDNF, DBH, DTNBP1, DRD2, DRD4, GSK-3beta, and MAO-A has been implicated [ 32 ]. Additionally, heightened HPA axis activity [ 33 ], and changes in the advanced associative regions of the frontal and insular cortices have been associated with an increased risk of psychotic manifestations in depression [ 34 ]. Our findings contribute a novel insight into the pathophysiological mechanisms underlying adolescent DD with psychotic symptoms. While our data indicate that NSFR maybe could assist in differentiating DD subtypes, these findings warrant cautious interpretation. The potential of NSFR as a non-invasive biomarker for stratifying patients according to psychotic symptomatology requires further validation.

Differentiating between adolescent DD and BED is a significant challenge in clinical practice [ 35 , 36 ]. When we combine the niacin phenotype with clinical symptoms, the differentiation improves. These symptoms are captured by PHQ-9, GAD-7, and PHQ-15 scales. This approach is more effective than using the scales alone. Using NSFR as a biological marker may further enhance the precision in distinguishing between DD and BED in adolescents.

This groundbreaking study has unveiled a novel negative correlation between the Niacin Skin Flush Response (NSFR) and the severity of depressive and anxiety symptoms as measured by the PHQ-9 and GAD-7 scales in adolescent Depressive Disorder (DD). Our results revealed that an increase in the severity of these symptoms correlates with a more pronounced blunting of NSFR. This finding is consistent with earlier studies [ 14 ].Previous research noted a significant link between reduced NSFR and depression symptoms. It also associated diminished NSFR with anxiety symptoms in adults. Furthermore, the research connected reduced NSFR with somatic complaints. These complaints include appetite loss and weight reduction in adults.These findings highlight the potential of NSFR as a valuable tool for assessing the severity of adolescent DD.

However, as indicated in Fig.  4 , we observed considerable variability in NSFR among individuals with similar levels of depressive severity. This variability could stem from the inherent heterogeneity in the etiology and clinical manifestations of adolescent DD, influenced by an interplay of biological and psychosocial factors [ 6 , 7 ]. Therefore, we postulate the presence of a distinct adolescent DD subgroup characterized by a significant phospholipid signaling defect, evident as abnormal NSFR responses [ 14 ]. Such a finding could offer new perspectives on the pathophysiological underpinnings of adolescent DD. It could also inform targeted therapeutic interventions, such as the application of Omega-3 fatty acids in depression management [ 37 ].

The Niacin Skin Flush Response (NSFR) is mediated by the PLA2-AA-COX2 pathway and its prostaglandin products [ 16 ]. Increased oxidative stress has been observed in Childhood and Adolescence with DD. This leads to enhanced PLA2 activity, resulting in the excessive breakdown of membrane phospholipids [ 17 ].. This process likely contributes to the diminished NSFR observed in these individuals. Furthermore, a significant decrease in free arachidonic acid (AA) levels in the red blood cell membranes of DD in childhood and adolescence has been reported [ 38 , 39 ], suggesting an AA turnover imbalance. These factors are associated with chronic inflammation. They may drive abnormal PLA2-AA-COX2 activity, culminating in niacin response blunting in DD.

Implications

Our study highlights the potential of NSFR in improving the identification and treatment of adolescent Depressive Disorder. Transcending traditional methods, NSFR provides an innovative and objective screening tool within schools, allowing for the rapid identification of depressive conditions among middle and high school students. This approach enhances detection accuracy and increases the rate of early diagnosis, significantly reducing the reliance on subjective self-reported assessments. Additionally, in clinical settings, NSFR provides an objective evaluation of the severity of depression in adolescents. Moreover, identifying adolescent DD patients with blunted NSFR responses could guide the targeted use of Omega-3 fatty acids in managing depression, suggesting a personalized approach to treatment.

Limitations

In our study’s limitations, the significant disparity in group size might have affected the statistical outcomes, including Cohen’s d values. Future research should ensure balanced group sizes to robustly validate NSFR’s role as a biomarker in adolescent DD. Additionally, with over half of the patients undergoing SSRI antidepressant treatment during NSFR assessment, it is imperative for subsequent studies to explore how these medications might affect NSFR results. Future research should focus on evaluating NSFR’s specificity and sensitivity in adolescent Depressive Disorder (DD) to establish its efficacy as a biological marker. Investigating NSFR’s role in longitudinal studies to monitor depressive disorder progression and its correlation with treatment outcomes is crucial. Expanding research to various populations will help determine NSFR’s generalizability as a biomarker. Additionally, exploring the molecular mechanisms linking NSFR to depression can provide deeper insights into its pathophysiology, enhancing our understanding and treatment of adolescent DD.

The NSFR maybe emerge as a promising objective biological marker for screening, severity assessment, subgroup classification, and differential diagnosis in adolescent DD. It unveils novel insights into the pathophysiological underpinnings of the disorder and may lead to advancements in precision diagnosis. However, the establishment of NSFR’s clinical utility necessitates further validation through rigorous studies. These should aim to determine the specificity and sensitivity of NSFR in the context of adolescent DD and evaluate its potential as a longitudinal measure of treatment efficacy (See Table 2 for detailed abbreviations.)

Data availability

Availability of data and materialsThe datasets generated during the current study are not publicly available due to the subjects’ privacy but are available from the corresponding author on reasonable request.

Abbreviations

Depressive Disorder

Behavioral and Emotional Disorders typically emerging in childhood and adolescence

Healthy control

Phospholipase A2

Arachidonic acid

Cyclooxygenase 2

Aqueous methyl nicotinate

Selective serotonin reuptake inhibitor

Niacin Skin Flush Reaction

the normal to mild blunted NSFR

moderate to severe bunted NSFR

DD with Psychotic Symptom

Non-Psychotic Symptoms

Receiver Operating Characteristic

Area Under Curve

Composite International Diagnostic Interview

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Acknowledgements

We want to express special gratitude to the participants and their families for their cooperation and patience across this study. We also thank the nursing staff of the Sichuan Provincial People’s Hospital for their help in data collection.

This study was supported by the Youth Fund Project of Sichuan Provincial Science and Technology Department (Number: 2022NSFSC1550).

Author information

Jie Feng and Wenjiao Min contributed equally to this work.

Chunling Wan, Bo Zhou and Yulan Huang are joint correspondence

Authors and Affiliations

Department of Psychosomatics, School of Medicine, Sichuan Provincial Center for Mental Health, Sichuan Provincial People’s Hospital, University of Electronic Science and Technology of China, No. 32, West second Section, 1st Ring Road, 610041, Chengdu, Sichuan, China

Jie Feng, Wenjiao Min, Bo Zhou, Yulan Huang & Yaoyin Zhang

Sichuan Provincial Center for Mental Health, Sichuan Academy of Medical Science & Sichuan Provincial People’s Hospital, No. 33, Section 2, Furong Avenue, Wenjiang District, 611135, Chengdu, Sichuan, China

Jing Yuan, Junming Chen, Lisha Chen, Wei Chen & Jia Cheng

Key Laboratory of Psychosomatic Medicine, Chinese Academy of Medical Sciences, Chengdu, China

Jie Feng, Wenjiao Min, Jing Yuan, Junming Chen, Lisha Chen, Wei Chen, Jia Cheng, Bo Zhou, Yulan Huang & Yaoyin Zhang

Bio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Ministry of Education, Shanghai Jiao To ng University, Shanghai, China

Dandan Wang & Chunling Wan

School of Nursing, Chengdu Medical College, Chengdu, China

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Contributions

Conception and design of the study: JF, DW, BZ, YZ. Acquisition and formal analysis of data: JF, WM, DW, YZ. Data curation: JF, DW, JY, JC, LC, WC, MZ, JC. Writing-original draft: JF. Writing-review & editing: JF, WM, DW, BZ, YH, YZ. Project administration: CW, BZ, YH, YZ. All authors read and approved the final manuscript.

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Correspondence to Yaoyin Zhang .

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The study was approved by the Medical Ethics Committee of Sichuan Provincial People’s Hospital (Approval No.2023KY223). All the research procedures involving human participants followed the Declaration of Helsinki in 1964 and its subsequent amendments. Written informed consent was obtained from all participants and a parent or legal guardian (if the participant is younger than 18 years old).

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Feng, J., Min, W., Wang, D. et al. Potential of niacin skin flush response in adolescent depression identification and severity assessment: a case-control study. BMC Psychiatry 24 , 290 (2024). https://doi.org/10.1186/s12888-024-05728-w

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DOI : https://doi.org/10.1186/s12888-024-05728-w

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• Niacin skin flush response
• Adolescent depressive disorder
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Study suggests adolescent stress may raise risk of postpartum depression in adults

by Johns Hopkins University

In a new study, a Johns Hopkins Medicine-led research team reports that social stress during adolescence in female mice later results in prolonged elevation of the hormone cortisol after they give birth. The researchers say this corresponds to the equivalent hormonal changes in postpartum women who were exposed to adverse early life experiences—suggesting that early life stress may underlie a pathophysiological exacerbation of postpartum depression (PPD).

The team's findings, published in Nature Mental Health , also suggest that current drug treatments for PPD in people may, in some cases, be less effective at targeting the relevant chemical imbalances in the brain, and that alternative methods may be more beneficial.

According to previous studies, an estimated one-third of psychiatric conditions fail to respond to current therapies, and "PPD is difficult to treat," says study senior author Akira Sawa, M.D., Ph.D., director of the Johns Hopkins Schizophrenia Center and professor of psychiatry, neuroscience, biomedical engineering, genetic medicine and pharmacology at the Johns Hopkins University School of Medicine. "The new study results add to evidence that patients with PPD are not all the same, and more individualized diagnosis and treatment—a precision medicine approach—is needed."

PPD, states the federal government's Office on Women's Health, is estimated to occur in 7% to 20% of all women, most commonly within six weeks of giving birth. Symptoms include feelings of sadness, anxiety, and fatigue, and can make it difficult to complete basic self-care tasks and care for the new baby.

The current first-line treatment for PPD is the use of a class of anti-depressant pills called selective serotonin reuptake inhibitors (SSRIs), but these are only effective in approximately half of all patients. SSRIs boost the effects of the natural brain chemical serotonin, one of many hormone-like substances that help control mood. Some patients also are treated with IV infusions of a different class of drugs that target GABAA, a brain chemical linked to nerve hyperactivity.

However, the calming infusions are costly (more than $30,000 for a single course of one such drug) and often require hospitalization. They are generally reserved for the most severe and resistant cases of PPD.

In the new study, the Johns Hopkins-led research team aimed to build on evidence that adverse life events may affect the likelihood and severity of PPD. Previous studies have shown that PPD is more prevalent in teens, and in urban populations.

Working with mice, the researchers first created four test groups: unstressed virgins, stressed virgins, unstressed mothers and stressed mothers. The stressed mice were subjected to social isolation in their adolescence, and all groups were tested for stress. At seven days postpartum, the stressed mothers showed decreased mobility and a decrease in sugar preference, both of which are considered markers for depression. This persisted for at least three weeks after delivery.

As the second and most critical step, the researchers tested plasma levels of several hormones and found the level of cortisol was increased in mothers both with and without adverse early life experiences. However, cortisol levels in unstressed mothers decreased to normal levels after delivery, while the levels in mothers with adverse early life experiences remained high for one to three weeks after birth. This finding, Sawa says, suggests a correlation between prolonged post-delivery elevation of cortisol and behavioral changes in postpartum mice who experienced social isolation in adolescence.

If these findings translate to humans, it could mean that a different kind of antidepressant, a glucocorticoid receptor (GR) antagonist, which blocks the effects of elevated cortisol, could be a novel treatment option for PPD. Mifepristone may be one such drug.

"Unfortunately, everyone knows someone who has suffered or currently suffers from PPD, and it has such a huge impact on both mother and baby," says Sawa. "The alternative line of treatment suggested by the mouse study—where the findings are consistent with those from our observational study in humans—might enable mothers to be treated at home and avoid separation from their babies, and target a different mechanism for depression that may be specific to PPD."

Plans are underway, Sawa says, to collect precise data on cortisol levels in people with PPD to determine if GR antagonists would be more beneficial than current treatments for some, and later, to conduct clinical trials with alternatives to SSRIs.

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• Open access
• Published: 02 October 2020

Depression in adolescence: a review

• Diogo Beirão   ORCID: orcid.org/0000-0001-5612-8941 1 ,
• Helena Monte 1 ,
• Marta Amaral 1 ,
• Alice Longras 1 ,
• Carla Matos 1 , 2 &
• Francisca Villas-Boas 1  

Middle East Current Psychiatry volume  27 , Article number:  50 ( 2020 ) Cite this article

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Depression is a common mental health disease, especially in mid to late adolescence that, due to its particularities, is a challenge and requires an effective diagnosis. Primary care providers are often the first line of contact for adolescents, being crucial in identifying and managing this pathology. Besides, several entities also recommend screening for depression on this period. Thus, the main purpose of this article is to review the scientific data regarding screening, diagnosis and management of depression in adolescence, mainly on primary care settings.

Comprehension of the pathogenesis of depression in adolescents is a challenging task, with both environmental and genetic factors being associated to its development. Although there are some screening tests and diagnostic criteria, its clinical manifestations are wide, making its diagnosis a huge challenge. Besides, it can be mistakenly diagnosed with other psychiatric disorders, making necessary to roll-out several differential diagnoses. Treatment options can include psychotherapy (cognitive behavioural therapy and interpersonal therapy) and/or pharmacotherapy (mainly fluoxetine), depending on severity, associated risk factors and available resources. In any case, treatment must include psychoeducation, supportive approach and family involvement. Preventive programs play an important role not only in reducing the prevalence of this condition but also in improving the health of populations.

Depression in adolescence is a relevant condition to the medical community, due to its uncertain clinical course and underdiagnosis worldwide. General practitioners can provide early identification, treatment initiation and referral to mental health specialists when necessary.

Adolescence is an important period in developing knowledge and skills, learning how to manage emotions and relationships and acquiring attributes and abilities for adulthood. Depression in adolescence is a common mental health disease with a prevalence of 4–5% in mid to late adolescence [ 1 ]. It is a major risk factor for suicide and can also lead to social and educational impairments. Consequently, identifying and treating this disorder is crucial.

General practitioners and primary care providers are frequently the first line of contact for adolescents in times of distress and can be crucial to identify mental health issues amongst these patients. They can facilitate early identification of depression, initiate treatment and refer the adolescents for mental health specialists [ 2 ]. It is vital to make a timely and accurate diagnosis of depression in adolescence and a correct differential diagnosis from other psychiatric disorders, due to the recurrent nature of this condition and its association with poor academic performance, functional impairment and problematic relationships with parents, siblings and peers. Furthermore, depression at this age is strongly related to suicidal ideation and attempts [ 2 ].

The US Preventive Services Task Force (USPSTF) recommends screening adolescents for depressive disorder by the General Practitioners [ 2 , 3 ]. Guidelines from the American Academy of Pediatrics (AAP) state that adolescent patients should be screened annually for depression in Primary Care with a formal self-report screening tool [ 4 ]. AAP recommends that Primary Care clinicians should evaluate for depression in those who screen positive on the screening tool, in those who present with any emotional problem as the chief complaint and in those in whom depression is highly suspected despite a negative screen result [ 4 ].

The present work consists of a review on the depression in the adolescent, summarizing data published in scientific papers in the last years, regarding the epidemiology of the disease, its pathogenesis and risk factors, screening and diagnosis tools and its management and treatment. Our research focused on research papers published between January 2010 and March 2020 in the area. Other research papers not included in this first search were included due to their interest and value to the subject. The keywords, used in different permutations and combinations, included the following: depression, adolescence, overview, pathophysiology, diagnosis and treatment.

Epidemiology

The prevalence of depression is significantly linked to age, being low in children (< 1%) and increasing throughout childhood and adolescence. Nevertheless, the prevalence of depression in adolescence varies significantly between studies and reports. A reported prevalence in Great Britain was 4%, whereas in the USA was 2.1% and in France was 11.0% [ 5 , 6 , 7 ]. Nevertheless, a systematic review from 2013 stated the life prevalence of depression varies from 1.1 to 14.6% [ 8 ].

A possible factor for the reported increase during adolescence is the set of social and biological changes characteristic of post-pubertal phase, such as enhanced social understanding and self-awareness, brain circuits changes involved in responses to reward and danger and increased reported stress levels [ 9 , 10 , 11 ].

Regarding differences between genders, while no significant differences are found in depression during childhood, depression during adolescence has a strong female preponderance, similar to adulthood [ 12 , 13 , 14 ]. This difference is still observed between distinct epidemiological and clinical samples and across various methods of assessment. As such, it is unlikely due to differences in help-seeking or reporting of symptoms and more closely tied to female hormonal changes, which suggests a direct link to hormone-brain relations [ 15 ].

Pathogenesis

Comprehension of the pathogenesis of depression in adolescents is a challenging task, due to its heterogeneous clinical presentation and diverse causes.

Putative risk factors, potentially modifiable during adolescence without professional intervention, are substance use (alcohol, cannabis and other illicit drugs, tobacco), diet and weight [ 16 ].

Alcohol use is known to have neurotoxic effects during this developmentally sensitive period. Cannabis and other illicit drugs can have an impact on serotonin and other neurotransmitters causing an increase in depressive symptoms. Furthermore, alcohol, cannabis and other illicit drug use have various deleterious social and academic consequences for the adolescent which could increase their risk for depression [ 16 ].

The relationship between tobacco use and depression is unclear. However, it has been proposed that this linkage may arise from the effects of nicotine on neurotransmitter activity in the brain, causing changes to neurotransmitter activity [ 17 ]. Overweight can have a negative impact on self-image which elevates the risk for depression. Moreover, depressed people may lead a less healthy lifestyle and suffer from deregulation in the stress response system, which may contribute to weight gain [ 16 ].

Association between depression and environmental factors, such as exposures to acute stressful events (personal injury, bereavement) and chronic adversity (maltreatment, family discord, bullying by peers, poverty, physical illness), has been subject of papers. Stressful life events seem more strongly associated with first onset rather than recurrence, and risk is considerably greater in girls and in adolescents who have multiple negative life events. The most important factors are chronic and severe relationship stressors [ 18 ]. A significant interaction was found between exposure to maternal threatening behaviours and deficits in emotional clarity in relation to depressive symptom severity [ 19 ].

Genetic factors can also play a very important role in the pathogenesis. Many reports suggest that a variant (5-HTTLPR) in the serotonin transporter gene might increase the risk of depression, but only in the presence of adverse life stressors or early maltreatment. The findings are less robust in adolescent boys than girls. This gene variant has also been reported to affect fear-related and danger-related brain circuitry, which is altered in depression. However, such findings seem to vary not only by genotype but also by age, sex, and severity of symptoms, and are also reliant on good quality measures of adversity and depression [ 18 , 20 ].

Two interrelated neural circuits and associated modulatory systems have been closely linked to risk for depression. One circuit connects the amygdala to the hippocampus and ventral expanses of the prefrontal cortex (PFC) and is linked to hypothalamic-pituitary-adrenal (HPA) axis activity. Disruption of this circuit links depression to stress-related enhancements in HPA-stress systems, such as higher than expected cortisol concentrations, and activity in the serotonergic system. Psychosocial stress, sex hormones and development have also been linked to changing activity in this circuit, with evidence that this circuit matures after adolescence. High concentrations of sex steroid receptors have been identified within this circuit and might provide a biological mechanism for why girls have higher risk of depression than boys. The other key circuit implicated in depression encompasses the striatum and its connection to both the PFC and ventral dopamine-based systems. Like the first circuit, this one also continues to mature through adolescence. Sex differences emerge in both circuits. Research into this reward circuit implies that reduced activity is linked with expression of and risk for depression. Reduced striatal and PFC activity during tasks involving rewards has been recorded both in individuals with major depression and in those with depressed parents. Both inherited factors and stress-related perturbations seem to contribute to these changes [ 18 , 21 ].

Temperament and character traits are also important factors in the pathogenesis of depression in adolescence. According to Cloninger, temperament is responsible for automatic and emotional responses to environmental stimuli and encompasses four dimensions: novelty seeking, exploratory activity, harm avoidance, reward dependence and persistence [ 22 ]. In contrast, character develops across the lifespan and is influenced by social and cultural experiences. Three dimensions are distinguished: self-directedness, cooperativeness and self-transcendence [ 23 ]. Studies showed that depressed patients present higher novelty seeking, harm avoidance and lower reward dependence, persistence, self-directedness and cooperativeness compared to healthy individuals [ 23 , 24 ].

Primary care providers are frequently the first contact during times of distress and can be crucial to identify mental health issues allowing for an earlier depression diagnosis, treatment and referral [ 2 ].

The symptoms can differ from the adult population. In comparison to it, adolescents tend to have more frequently somatic symptoms, anxiety, disruptive behaviour and personality disorders [ 25 ].

The fact that these symptoms are common in other disorders such as hypothyroidism, anaemia, sleep apnoea or other chronic diseases makes the diagnosis more challenging to establish in these subjects [ 26 ].

Screening tools

The screening of adolescents for depression is an essential tool for early detection of this disorder. USPSTF and AAP recommend the screening of adolescents in primary care settings [ 2 , 3 , 4 , 25 , 26 , 27 ].

The Beck Depression Inventory (BDI) and Patient Health Questionnaire for Adolescents (PHQ-A) are the most commonly used, outperforming other screening tools in the identification of major depressive disorder among adolescents [ 2 , 28 ].

Originally developed as a depression symptom rating scale for the adult population, BDI is widely used among adults and adolescents and mainly in research. It is a 21-item self-report measure of depressive symptoms, scored from “0” to “3”. Participants are asked to respond to each item based on their experiences within the past 2 weeks. The total score can range from 0 to 63, with higher scores meaning higher levels of depressive symptoms [ 29 ]. In primary care settings, an adapted version (BDI-PC) is often used, which consists of a 7-item self-report instrument, with a cut-off of 4 points for major depression [ 30 ]. Good performance has also been shown using BDI, with sensitivity ranging from 84 to 90% and specificity ranging from 81 to 86% [ 3 ].

The PHQ-A is the depression module of a 67-item questionnaire that can be used to screen for depression among adolescent primary care patients. Composed of 9 questions, it can be entirely self-administered by the patient and evaluates symptoms experienced in the 2 weeks prior. It measures functional impairment and inquiries about suicidal ideation and suicide attempts [ 31 ]. The PHQ-A study had the highest positive predictive value, as well as a sensitivity and specificity of 73% and 94%, respectively [ 3 ].

Diagnostic tools

Diagnosis of depression in adolescents is established through the criteria described in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) [ 32 ]. The evaluation of patients should be made through interviews, alone and with the patient’s family and/or caregivers and should include an assessment of functional impairment in different domains and other existing psychiatric conditions [ 4 ].

DSM-5 establishes the diagnosis of major depressive disorder as a period of at least 2 weeks during which there is a depressed mood or the loss of interest or pleasure in nearly all activities, and, additionally, at least four additional symptoms from a list that includes changes in weight, sleep disturbances, changes in psychomotor activity, fatigue, feelings of worthlessness or guilt, impaired concentration or ability to make decisions, or suicidal ideation. Additionally, it states that, in adolescents, depressed mood can be replaced by irritability or crankiness, a sign that can be neglected during assessment or by caregivers. This presentation should be differentiated from a pattern of irritability when frustrated [ 33 ]. Children diagnosed with disruptive mood dysregulation disorder, a new diagnosis referring persistent irritability and frequent episodes of extreme behaviour, typically develop unipolar depressive or anxiety disorders as they mature into adolescence [ 32 ]. Clinical presentation differs between genders, with female adolescents reporting feelings of sadness, loneliness, irritability, pessimism, self-hatred and eating disorders, while males present with somatic complaints, reduced ability to think or concentrate, lacking decision making skills, restlessness and anhedonia [ 34 , 35 ].

The severity of depressive disorders can be based on symptom count or intensity, and/or level of impairment. Mild depression can be defined as 5 to 6 symptoms that are mild in severity, with mild impairment in functioning. Severe depression exists when a patient experiences all depressive symptoms listed in the DSM-5 or severe impairment in functioning and, also, with at least 5 criteria and a specific suicide plan, clear intent or recent suicide attempt, psychotic symptoms or family history of first-degree relatives with bipolar disorder. Moderate depression falls between these two categories [ 4 ].

Differential diagnosis

Despite its well-defined diagnostic criteria, depression during adolescence can often be misdiagnosed, with the main differential diagnoses being adjustment disorder, dysthymic disorder, bipolar disorder and schizophrenia. However, it is crucial to establish the correct diagnosis as different psychiatric disorders involve distinct treatment and prognosis.

Adjustment disorder is classified as depressed mood in response to an identifiable psychosocial stressor. It arises within 3 months of the onset of a stressor and persists up to 6 months after stressor resolution. It is characterized by low mood, tearfulness, or hopelessness associated with a significant distress that exceeds what would be expected given the nature of the stressor, or impaired social or occupational functioning. On the other hand, dysthymic disorder is a pattern of chronic symptoms of depression that are present for most of the time on most days with a minimum duration of 1 year for children and adolescents [ 32 ].

Bipolar disorder and schizophrenia are much less common in adolescents compared to depression disorder. However, they have different prognosis and require different treatments. Consequently, when establishing the diagnosis of depressive disorder in adolescence, it is important to bear in mind that the first symptomatic episode may also represent the beginning of a bipolar disorder [ 36 , 37 ].

Management and treatment

The treatment of depression in adolescence can include psychotherapy, pharmacotherapy or both [ 38 ]. Treatment should be selected based on the severity of the condition, the preference of the patient/family, associated risk factors, family support and the availability of each therapy [ 39 , 40 ]. On first approach, it is essential to comprehensively explain the therapeutic strategy and involve both patients and family members to assure close follow-up of progress, treatment adjustment according to symptoms and prevention of relapse [ 41 ]. Adolescents with moderate to severe depression, substance abuse, psychiatric disorders, suicidal ideation or resistance to treatment should be referred for specialized evaluation [ 42 ].

Treatment may be divided into three phases: acute (obtain response and remission), continuation (consolidate the response) and maintenance (avoid recurrences) [ 39 ]. Each of them must include psychoeducation, supportive approach and family involvement [ 39 , 40 ].

In mild depression, psychotherapy may be the first option, complemented with pharmacotherapy if there is no response [ 42 , 43 ]. The AAP recommends starting with active support, symptom monitoring and close follow-up for 6–8 weeks [ 44 ]. These measures are also useful when patients refuse more interventional treatments. The National Institute for Health and Care Excellence (NICE) has a slightly stricter approach, in which it recommends psychotherapy after absence of improvement after 2 weeks of watchful waiting [ 45 ]. In adolescents with moderate to severe depression, treatment is based on combined psychotherapy and pharmacotherapy [ 42 , 43 ]. NICE recommends psychotherapy for the minimum of 3 months, followed by fluoxetine if necessary. AAP has a similar approach [ 44 , 45 ]. Other strategies such as physical exercise, sleep hygiene and adequate nutrition have been referred as treatment adjuvants [ 44 , 46 , 47 ].

Both NICE and AAP recommend treatment for at least 6 months after remission of symptoms to consolidate the response and prevent relapse (continuation phase). In addition, both organizations also recommend maintaining follow-up during 1 year or, in cases of recurrent depression, 2 years [ 44 , 45 ].

Psychotherapy

In this area, Cognitive Behavioural Therapy (CBT) and Interpersonal Therapy (IPT) have shown effectiveness [ 40 , 48 ].

CBT is a brief psychotherapy, carried out individually or in groups, based on the relationship between thoughts, feelings and behaviours [ 40 ]. CBT focuses on cognitive distortions associated with depressive mood and the development of behavioural activation techniques, coping strategies and problem solving [ 42 ]. When used in acute depression, it has been shown to have a moderate effect [ 40 ]. CBT seems to be useful in preventing relapses and suicidal ideation, in the treatment of resistant depression and in adolescents with long-term physical conditions [ 49 , 50 , 51 ]. Moreover, the combination of psychotherapy and pharmacotherapy, in particular fluoxetine, has shown promising results [ 52 ]. Within the different psychotherapy approaches, behavioural activation, challenging thoughts and involvement of caregivers have a higher success rate [ 53 ].

IPT assumes depression association with disruptive relationships, based on the negative impact of symptoms on interpersonal relationships and vice-versa [ 40 ]. This approach may be useful especially when there is a well-established relational factor as the cause of the depressive condition [ 54 ]. Most studies have compared only IPT with placebo groups or with other psychotherapy, showing favourable results for IPT [ 48 , 55 ].

Psychotherapy should be considered first line of treatment in adolescents afraid of or with contraindications for medication, with identified stress factors or those with poor response to other approaches [ 56 ]. There are no contraindications to psychotherapy, though it has a limited effect in cases of cognitive delay [ 40 ].

Pharmacotherapy

Even though psychotherapy is an important component, pharmacotherapy can be used as an addition. When psychotherapy is not available or cannot be applied, pharmacotherapy can be an alternative [ 39 , 41 ].

Fluoxetine is widely regarded as the first-line drug for this age group given its efficacy [ 2 , 38 , 57 , 58 , 59 ]. Besides fluoxetine, escitalopram has also shown to be particularly effective, especially for ages between 12 and 17 years [ 38 , 60 , 61 , 62 ]. The main side effects of selective serotonin receptor inhibitors (SSRIs) include abdominal pain, agitation, jitteriness, restlessness, diarrhoea, headache, nausea and changes in sleep patterns. However, these effects are dose dependent and tend to decrease over time [ 39 ].

Given the efficacy of fluoxetine and escitalopram, many studies have focused on other SSRIs, such as sertraline, citalopram, paroxetine and fluvoxamine. Citalopram must be carefully evaluated as side effects include prolongation of the QT interval, which can lead to arrhythmia [ 63 , 64 ]. Paroxetine and fluvoxamine are not commonly used due to a lack of efficacy in this age group [ 65 , 66 ]. Regarding serotonin noradrenaline receptor inhibitors (SNRIs), venlafaxine appears to have a similar efficacy to SSRIs in resistant depression and no significant differences in adverse effects [ 49 ]. However, because hypertension is a possible side effect, this parameter must be periodically evaluated [ 41 , 64 ]. In Table 1 , the main drugs used in the treatment of depression in adolescents are displayed.

Bupropion and duloxetine have also been studied as alternatives but the evidence of its use in adolescents is limited. Bupropion can be useful in the treatment of overweight patients or those who intend to quit smoking. The main side effects are insomnia, agitation and seizures [ 41 ]. Bupropion is contraindicated in patients suffering from eating disorders. Duloxetine can be used for comorbid depression and pain in adolescents [ 67 ].

Tricyclic antidepressants do not have any demonstrated benefit in the treatment of depression in adolescents [ 42 , 68 , 69 ]. This drug class has significant side effects such as dry mouth, orthostatic hypotension, tremors and vertigo and can increase PR interval and QRS duration. Moreover, it is highly lethal in overdose [ 69 ].

At the time of writing, only fluoxetine (ages 8 years and older) and escitalopram (ages 12 years and older) are approved by the Food and Drug Administration for the treatment of depression in children and adolescents [ 70 , 71 ].

Several studies suggest an association between antidepressants and increased suicidal risk [ 18 , 58 ]. However, the risks and benefits of this strategy should be evaluated. Adolescents should be closely monitored, and, if suicidal thoughts arise during treatment, parents should seek care as soon as possible, to adjust dosage, change antidepressant or discontinue it [ 42 ].

Finally, the treatment strategies proposed in this age group are illustrated in Fig. 1 .

Algorithm for the management and treatment of depression in adolescents

Prevention is crucial to depression management, consequence of the impact on the population and inequal quality health care access [ 72 ]. In addition, it prevents the onset of other possible comorbidities, as well as reduces the impact on the patient and their families [ 73 , 74 , 75 ].

It is important to understand which different risk factors and protective factors intervene in the development of the disease. The risk factors can be divided into specific and non-specific for depression. Regarding the specific ones, parent depression history increases the risk between 2 and 4 times [ 76 ]. Among the non-specific, poverty, domestic violence and child abuse also increase the risk. On the other hand, protective factors are good family support, emotional skills or coping ability [ 77 ].

Depression prevention can be divided into 3 types: universal, selective and indicated. Universal interventions target the adolescent population group in general. Selective interventions target adolescents who are at risk for developing depression. Finally, indicated interventions target adolescents with subclinical symptoms of depression [ 78 ].

With regard to universal interventions, the efficacy of prevention programs through therapy for problem solving and overcoming traumatic situations has been demonstrated in multiple studies [ 79 , 80 ]. Although it has been shown that adolescents under these programs experience decreased depressive symptoms, the long-term usefulness of these programs was not unanimous. The inclusion of parents to these programs provided no additional advantage [ 81 ]. Furthermore, no significant difference between adolescents who received an intervention program and those who did not was found, although improvements in school environment were reported [ 82 ].

Concerning selective interventions, interpersonal communication skills and optimistic thinking programs have shown to be effective in decreasing anxiety and depression [ 83 ]. Contrary to universal interventions, the inclusion of parents in programs was demonstrated as beneficial [ 83 , 84 , 85 ]. However, it had no benefit to adolescents, but improved the parents’ perception of children’s behaviour [ 86 ].

Finally, in indicated interventions, psychoeducation and skill development programs to overcome interpersonal issues and role disputes among adolescents have been carried out [ 87 , 88 ]. It was shown that symptoms improved significantly compared at the end of the program [ 87 ]. Additionally, the number of adolescents with suicidal ideations decreased.

Comparing different groups of programs, various meta-analyses have found that selective and indicated programs are more effective than universal ones [ 89 , 90 ]. These prevention programs are more effective when started between the ages of 11 and 15 [ 78 ]. However, their superiority is not unanimous [ 91 ].

Depression in adolescence can be a complex diagnosis and requires individual and oriented treatment. For this reason, early identification, treatment initiation and prompt referral to mental health specialists is crucial for the prognosis of these patients.

Due to the variety of its main clinical manifestations and the lack of diagnostic tests that fully and accurately establish the definite diagnosis, this process can be particularly challenging. Additionally, several differential diagnoses must be made to provide an accurate course of treatment.

Treatment options can include both psychotherapy (CBT or IPT) and pharmacotherapy. The most promising results are observed with the combination of psychotherapy and pharmacotherapy, mainly fluoxetine.

Nevertheless, the authors would like to highlight certain aspects that require improvement and implementation in daily practice in comparison with the presented recommendations in this publication. First, although Cognitive Behavioral Therapy is one of the most studied therapeutic orientations, the reproducibility of performance among professionals is limited and relies on the relationship established between the mental health professional and the patient, in a deeper way compared to pharmacotherapy. The scarce number of professionals and the absence of choice by the user may not allow the development of this interpersonal bond. This limitation is particularly important in the case of children and adolescents, who are in a period of transition in their physical and mental development, and whose psychological intervention can have a significant positive or negative impact with potential future repercussions. Second, most of the prevention programs described in the literature are not currently implemented. Finally, approaching the family environment is essential in the implementation of effective long-term therapeutic interventions, especially in the presence of a dysfunctional structure. Although recommended, its practical application is often difficult due to the need of active participation of family members, inside and outside the clinical office. Prevention, early diagnosis and treatment of depression in adolescence should be considered worldwide objectives, and the implementation of straightforward, effective and cost-conscious strategies for achieving such purposes is essential. Amongst these objectives, prevention is of utter importance and must be a priority when defining political strategies and governmental programs related to mental health.

Availability of data and materials

Not applicable.

Abbreviations

US Preventive Services Task Force

American Academy of Pediatrics

Prefrontal cortex

Hypothalamic-pituitary-adrenal

Beck Depression Inventory

Patient Health Questionnaire for Adolescents

Beck Depression Inventory for Primary Care

Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition

Cognitive Behavioral Therapy

Interpersonal Therapy

Selective Serotonin Reuptake Inhibitors

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The authors would like to thank Dilermando Sobral, MD, Sónia Almeida, MD and Paula Assunção, MD for their guidance.

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DB conceived the original idea of this work and took the lead in writing the manuscript. All authors contributed equally in the literature review and writing of the manuscript. DB was responsible for the section on epidemiology and comorbidities. HM was responsible for the sections on the background and pharmacological treatment. MA was responsible for the abstract, non-pharmacological treatment and the conclusion. AL was responsible for the sections on methods and pathogenesis. CM was responsible for the sections on diagnosis and background, and FVB for the section on prevention. DB and HM were responsible for the construction of the final version of the manuscript which was reviewed and approved by all co-authors.

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Beirão, D., Monte, H., Amaral, M. et al. Depression in adolescence: a review. Middle East Curr Psychiatry 27 , 50 (2020). https://doi.org/10.1186/s43045-020-00050-z

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Study suggests adolescent stress may raise risk of postpartum depression in adults

A johns hopkins medicine-led study suggests early-life stress may lead to prolonged elevation of the hormone cortisol after childbirth and in turn, postpartum depression.

By Michael E. Newman

A Johns Hopkins Medicine -led research team reports in a new study that social stress during adolescence in female mice later results in prolonged elevation of the hormone cortisol after they give birth. The researchers say this corresponds to the equivalent hormonal changes in postpartum women who were exposed to adverse early life experiences, suggesting that early life stress may underlie a pathophysiological exacerbation of postpartum depression (PPD).

The team's findings, first published online on April 11 in Nature Mental Health , also suggest that current drug treatments for PPD in people may, in some cases, be less effective at targeting the relevant chemical imbalances in the brain, and that alternative methods may be more beneficial.

According to previous studies, an estimated one-third of psychiatric conditions fail to respond to current therapies.

Image caption: Akira Sawa

Image credit : Johns Hopkins Initiative for Medical Innovation and NeuroDiscovery

"PPD is difficult to treat," says study senior author Akira Sawa , director of the Johns Hopkins Schizophrenia Center and professor of psychiatry, neuroscience, biomedical engineering, genetic medicine, and pharmacology at the School of Medicine. "The new study results add to evidence that patients with PPD are not all the same, and more individualized diagnosis and treatment—a precision medicine approach—is needed."

PPD is estimated to occur in 7% to 20% of all women, most commonly within six weeks of giving birth. Symptoms include feelings of sadness, anxiety, and fatigue, and can make it difficult to complete basic self-care tasks and care for the new baby.

The current first-line treatment for PPD is the use of a class of anti-depressant pills called selective serotonin reuptake inhibitors (SSRIs), but these are only effective in approximately half of all patients. SSRIs boost the effects of the natural brain chemical serotonin, one of many hormone-like substances that help control mood. Some patients also are treated with IV infusions of a different class of drugs that target GABAA, a brain chemical linked to nerve hyperactivity.

However, the calming infusions are costly (more than $30,000 for a single course of one such drug) and often require hospitalization. They are generally reserved for the most severe and resistant cases of PPD.

In the new study, the Johns Hopkins-led research team aimed to build on evidence that adverse life events may affect the likelihood and severity of PPD. Previous studies have shown that PPD is more prevalent in teens and in urban populations.

Working with mice, the researchers first created four test groups: unstressed virgins, stressed virgins, unstressed mothers and stressed mothers. The stressed mice were subjected to social isolation in their adolescence, and all groups were tested for stress. At seven days postpartum, the stressed mothers showed decreased mobility and a decrease in sugar preference, both of which are considered markers for depression. This persisted for at least three weeks after delivery.

As the second step, researchers tested plasma levels of several hormones and found the level of cortisol was increased in mothers both with and without adverse early life experiences. However, cortisol levels in unstressed mothers decreased to normal levels after delivery, while the levels in mothers with adverse early life experiences remained high for one to three weeks after birth. This finding, Sawa says, suggests a correlation between prolonged post-delivery elevation of cortisol and behavioral changes in postpartum mice who experienced social isolation in adolescence.

If these findings translate to humans, it could mean that a different kind of antidepressant, a glucocorticoid receptor (GR) antagonist, which blocks the effects of elevated cortisol, could be a novel treatment option for PPD. Mifepristone may be one such drug.

"Unfortunately, everyone knows someone who has suffered or currently suffers from PPD, and it has such a huge impact on both mother and baby," says Sawa. "The alternative line of treatment suggested by the mouse study—where the findings are consistent with those from our observational study in humans—might enable mothers to be treated at home and avoid separation from their babies, and target a different mechanism for depression that may be specific to PPD."

Plans are underway, Sawa says, to collect precise data on cortisol levels in people with PPD to determine if GR antagonists would be more beneficial than current treatments for some, and later, to conduct clinical trials with alternatives to SSRIs.

Along with Sawa, members of the study team from Johns Hopkins Medicine are Sedona Lockhart, Jennifer Payne , Gary Wand , Daniel Wood, and Kun Yang . Team members from the University of Alabama at Birmingham Heersink School of Medicine are study lead author Minae Niwa, Adeel Ahmed, Shin-ichi Kano, Kyohei Kin, and Jose Francis-Oliveira.

The study authors do not have financial or conflict-of-interest disclosures.

Posted in Health

Tagged mental health , maternal health

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Teen stress may raise risk of postpartum depression in adults

In a new study, a Johns Hopkins Medicine-led research team reports that social stress during adolescence in female mice later results in prolonged elevation of the hormone cortisol after they give birth. The researchers say this corresponds to the equivalent hormonal changes in postpartum women who were exposed to adverse early life experiences -- suggesting that early life stress may underlie a pathophysiological exacerbation of postpartum depression (PPD).

The team's findings, first published online Apr. 11, 2024, in Nature Mental Health , also suggest that current drug treatments for PPD in people may, in some cases, be less effective at targeting the relevant chemical imbalances in the brain, and that alternative methods may be more beneficial.

According to previous studies, an estimated one-third of psychiatric conditions fail to respond to current therapies, and "PPD is difficult to treat," says study senior author Akira Sawa, M.D., Ph.D., director of the Johns Hopkins Schizophrenia Center and professor of psychiatry, neuroscience, biomedical engineering, genetic medicine and pharmacology at the Johns Hopkins University School of Medicine. "The new study results add to evidence that patients with PPD are not all the same, and more individualized diagnosis and treatment -- a precision medicine approach -- is needed."

PPD, states the federal government's Office on Women's Health, is estimated to occur in 7% to 20% of all women, most commonly within six weeks of giving birth. Symptoms include feelings of sadness, anxiety, and fatigue, and can make it difficult to complete basic self-care tasks and care for the new baby.

The current first-line treatment for PPD is the use of a class of anti-depressant pills called selective serotonin reuptake inhibitors (SSRIs), but these are only effective in approximately half of all patients. SSRIs boost the effects of the natural brain chemical serotonin, one of many hormone-like substances that help control mood. Some patients also are treated with IV infusions of a different class of drugs that target GABAA, a brain chemical linked to nerve hyperactivity.

However, the calming infusions are costly (more than $30,000 for a single course of one such drug) and often require hospitalization. They are generally reserved for the most severe and resistant cases of PPD.

In the new study, the Johns Hopkins-led research team aimed to build on evidence that adverse life events may affect the likelihood and severity of PPD. Previous studies have shown that PPD is more prevalent in teens, and in urban populations.

Working with mice, the researchers first created four test groups: unstressed virgins, stressed virgins, unstressed mothers and stressed mothers. The stressed mice were subjected to social isolation in their adolescence, and all groups were tested for stress. At seven days postpartum, the stressed mothers showed decreased mobility and a decrease in sugar preference, both of which are considered markers for depression. This persisted for at least three weeks after delivery.

As the second and most critical step, the researchers tested plasma levels of several hormones and found the level of cortisol was increased in mothers both with and without adverse early life experiences. However, cortisol levels in unstressed mothers decreased to normal levels after delivery, while the levels in mothers with adverse early life experiences remained high for one to three weeks after birth. This finding, Sawa says, suggests a correlation between prolonged post-delivery elevation of cortisol and behavioral changes in postpartum mice who experienced social isolation in adolescence.

If these findings translate to humans, it could mean that a different kind of antidepressant, a glucocorticoid receptor (GR) antagonist, which blocks the effects of elevated cortisol, could be a novel treatment option for PPD. Mifepristone may be one such drug.

"Unfortunately, everyone knows someone who has suffered or currently suffers from PPD, and it has such a huge impact on both mother and baby," says Sawa. "The alternative line of treatment suggested by the mouse study -- where the findings are consistent with those from our observational study in humans -- might enable mothers to be treated at home and avoid separation from their babies, and target a different mechanism for depression that may be specific to PPD."

Plans are underway, Sawa says, to collect precise data on cortisol levels in people with PPD to determine if GR antagonists would be more beneficial than current treatments for some, and later, to conduct clinical trials with alternatives to SSRIs.

Along with Sawa, members of the study team from Johns Hopkins Medicine are Sedona Lockhart, Jennifer Payne, Gary Wand, Daniel Wood and Kun Yang. Team members from the University of Alabama at Birmingham Heersink School of Medicine are study lead author Minae Niwa, Adeel Ahmed, Shin-ichi Kano, Kyohei Kin and Jose Francis-Oliveira.

Funding for this research was provided by National Institutes of Health grants MH-092443, MH-094268, K99MH-094408, MH-105660, MH-107730, DA-040127, and MH-116869; the Brain and Behavior Research Foundation (formerly the National Alliance for Research on Schizophrenia and Depression); and other sources.

• Mental Health Research
• Teen Health
• Personalized Medicine
• Alternative Medicine
• Mental Health
• Adolescence
• Pituitary gland
• Growth hormone deficiency
• Stress (medicine)
• House mouse
• Double blind
• Menstrual cycle

Story Source:

Materials provided by Johns Hopkins Medicine . Note: Content may be edited for style and length.

Journal Reference :

• Minae Niwa, Sedona Lockhart, Daniel J. Wood, Kun Yang, Jose Francis-Oliveira, Kyohei Kin, Adeel Ahmed, Gary S. Wand, Shin-ichi Kano, Jennifer L. Payne, Akira Sawa. Prolonged HPA axis dysregulation in postpartum depression associated with adverse early life experiences: a cross-species translational study . Nature Mental Health , 2024; DOI: 10.1038/s44220-024-00217-1

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