M.1. Group design: Study involved a randomized controlled design;
M.2. Independent variable defined: Treatment manuals or logical equivalent were used for the treatment;
M.3. Population clarified: Conducted with a population, treated for specified problems, for whom inclusion criteria were clearly delineated;
M.4. Outcomes assessed: Reliable and valid outcome assessment measures gauging the problems targeted (at a minimum) were used;
M.5. Analysis adequacy: Appropriate data analyses were used, and sample size was sufficient to detect expected effects.
The criteria for including a trial in the present review were: (a) that the mean age of participants was between 12 and 18 years old; (b) a primary diagnosis of depression; (c) randomized controlled trial; (d) valid and reliable depression assessment measures; (e) comparison of at least one psychological treatment with another psychological, pharmacological, and/or placebo treatment, and/or waitlist (WL); and (f) publication in a peer-reviewed journal; (g) between 1980 and September 2020.
Exclusion criteria were: (a) mean age of participants was less than 12 or more than 18 years; (b) depressive symptomatology only, without a diagnosis of depression; (c) open trial or case study; (d) trials testing medication alone; (e) preventive interventions; and (f) publication in media other than peer-reviewed journals (handbooks, conference proceedings, etc.); (g) prior to 1980 or after September 2020.
We used several strategies to identify trials: (a) searches in the PsycINFO, PubMed, ERIC, Web of Science and CSIC-ISOC databases; (b) websites of institutions: Division 53. Society of Clinical Child and Adolescent Psychology, of the American Psychological Association (APA) (Retrieved 13 April 2021 from https://effectivechildtherapy.org/concerns-symptoms-disorders/ ); National Institute for Health and Care Excellence (NICE) (Retrieved 13 April 2021 from https://www.nice.org.uk/guidance/ng134 ); National Health System (Sistema Nacional de Salud, SNS) of Spain (Retrieved 13 April 2021 from https://portal.guiasalud.es/gpc/depresion-infancia/ ); and (c) the retrieval of primary studies from systematic reviews and meta-analyses.
We identified 123 potential trials, published between 1986 and 2020, of which 96 were excluded [ 13 , 16 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 , 47 , 48 , 49 , 50 , 51 , 52 , 53 , 54 , 55 , 56 , 57 , 58 , 59 , 60 , 61 , 62 , 63 , 64 , 65 , 66 , 67 , 68 , 69 , 70 , 71 , 72 , 73 , 74 , 75 , 76 , 77 , 78 , 79 , 80 , 81 , 82 , 83 , 84 , 85 , 86 , 87 , 88 , 89 , 90 , 91 , 92 , 93 , 94 , 95 , 96 , 97 , 98 , 99 , 100 , 101 , 102 , 103 , 104 , 105 , 106 , 107 , 108 , 109 , 110 , 111 ] (see Table 2 ). The main reason for exclusion was that they were prevention rather than treatment trials, mostly with indicated samples (adolescents with depressive symptoms, but without a diagnosis of depression). Other reasons for exclusion were the mean age of participants below 12 years (preadolescents) or above 18 years (youths), noncompliance with methodological standards (e.g., nonrandom assignment, open trial), and recruitment of heterogeneous samples with depression or other disorders. The 27 selected adolescent depression treatment trials [ 14 , 112 , 113 , 114 , 115 , 116 , 117 , 118 , 119 , 120 , 121 , 122 , 123 , 124 , 125 , 126 , 127 , 128 , 129 , 130 , 131 , 132 , 133 , 134 , 135 , 136 , 137 ] resulted in 46 studies in which a psychological treatment was compared with another psychological or pharmacological treatment, or with an active control or WL condition. CBT was the most investigated treatment with 22 trials (81%). Research on other treatments is rather scarce, with four trials of family therapy (FT), three of interpersonal therapy (IPT), and a single trial of psychoanalytic therapy (PT).
Trials excluded from the current review.
Year | Author(s) | Treatment Condition(s) | Reason(s) for Exclusion |
---|---|---|---|
1986 | Reynolds and Coats [ ] | CBT Pleasant Activities + Cognitive Techniques CBT Progressive Relaxation WL | Indicated prevention: BDI ≥ 12, RADS ≥ 72, BID ≥ 20 (two adolescents BID = 18) |
1990 | Kahn et al. [ ] | CBT CWD-A CBT Progressive Relaxation CBT Self–Modeling WL | Indicated prevention: BID ≥ 20 |
1991 | Fine et al. [ ] | CBT Social Skills ST Therapeutic and Mutual Support | No random assignment in the strictest sense |
1994 | Lewinsohn et al. [ ] | CBT CWD-A Parents and Adolescents CBT CWD-A Adolescents WL | Not published in a peer-reviewed journal |
1994 | Mufson et al. [ ] | IPT for Adolescents | Open clinical trial |
1994 | Reed [ ] | CBT Structured Learning Therapy Attention-Placebo | Only holistic clinical judgments of improvement were used as outcome assessment measure |
1995 | Clarke et al. [ ] | CBT Adolescent Coping with Stress Course TAU | Indicated prevention: CES-D ≥ 24 |
1996 | Kroll et al. [ ] | CBT Continuation Therapy | Historical Control Condition |
1996 | Lewinsohn et al. [ ] | CBT CWD-A Parents and Adolescents CBT CWD-A Adolescents WL | The same trial as Lewinsohn et al. [ ] (This trial was excluded from the count of studies) |
1997 | Feehan and Vostanis [ ] | CBT Placebo | The same trial as Vostanis et al. [ ] |
1998 | Ackerson et al. [ ] | CBT Book “Feeling Good” Delayed-Treatment Condition | Indicated prevention: CDI ≥ 10, HRSD ≥ 10 |
2001 | Clarke et al. [ ] | CBT Adolescent Coping with Stress Course TAU | Selective prevention: Adolescent offspring of depressed parents |
2001 | Santor and Kusumakar [ ] | IPT for Adolescents | Open clinical trial |
2003 | Puskar et al. [ ] | CBT Teaching Kids to Cope TAU | Indicated prevention: RADS > 60 |
2003 | Roberts et al. [ ] | CBT PRP Usual Health Education | Preadolescents: M age = 11.9, range: 11–13. Indicated prevention: CDI = 10 (mean) |
2004 | Kerfoot et al. [ ] | CBT brief TAU | Indicated prevention: MFQ ≥ 23 |
2004 | Szigethy et al. [ ] | CBT PASCET-Physical Illness | Open trial |
2005 | Asarnow et al. [ ] | CBT Quality Improvement Intervention and/or Medication TAU | 57.4% no diagnosis of depression (depressive symptoms) |
2005 | Jeong et al. [ ] | Dance Movement Therapy WL | Indicated prevention: High depression score (Beckman Depression Inventory) |
2005 | Kowalenko et al. [ ] | CBT Adolescents Coping with Emotions WL | Indicated prevention: CDI ≥ 18 Trial was randomized at the school level |
2006 | Sanford et al. [ ] | FT Psychoeducation + TAU TAU | Diagnosis of depression in the last 6 months 28.9% no depression diagnosis at baseline |
2006 | Sheffield et al. [ ] | CBT Universal Intervention CBT Indicated Intervention CBT Universal + Indicated Intervention No Intervention Condition | Universal and/or indicated prevention |
2006 | Young et al. [ ] | IPT Adolescent Skills Training School Counseling | Indicated prevention: 16 ≤ CES-D ≤ 39 75.6% no depression diagnosis |
2007 | Bolton et al. [ ] | IPT Group Creative Play Intervention WL | Indicated prevention: APAI ≥ 32 Adolescents with symptoms of depression, anxiety, and conduct problems |
2007 | Riggs et al. [ ] | CBT + Placebo Fluoxetine + Placebo | Adolescents with a primary diagnosis of substance use disorder |
2007 | Szigethy et al. [ ] | CBT PASCET-Physical Illness TAU | Indicated prevention: CDI ≥ 9 |
2007 | Trowell et al. [ ] | PT Focused Individual Psychodynamic Therapy FT Systems Integrative Familiar Therapy | Preadolescents: M age = 11.7 |
2008 | Bahar et al. [ ] | Problem-Based Group Therapy Occupational Therapy | Semi-experimental study. Selective prevention: Students, six months after an earthquake |
2008 | Connell and Dishion [ ] | FT Adolescent Transitions Program School-As-Usual Control | Selective prevention |
2008 | Rosselló et al. [ ] | CBT Individual CBT Group IPT Individual IPT Group | 34% no diagnosis of depression (CDI ≥ 13) |
2008 | Stice et al. [ ] | CBT Brief Adolescent Coping with Stress Course CBT Book “Feeling Good” Group Supportive–Expressive Intervention Assessment–Only Control Condition | MDD excluded (depressive symptoms) |
2009 | Garber et al. [ ] | CBT TAU | Indicated and selective prevention: Adolescents with depressive symptoms, offspring of depressed parents |
2009 | O’Kearny et al. [ ] | CBT MoodGYM Internet Program Usual curriculum | Universal prevention: All year 10 girls attending a single sex school |
2009 | Weisz et al. [ ] | CBT PASCET TAU | Preadolescents: M age = 11.8, range: 8–15 |
2010 | Diamond et al. [ ] | FT Attachment-Based Family Therapy TAU Enhanced | Heterogeneous sample: 39.4% MDE, 7.6% Dd, 66.7%% AD, 57.6% ED |
2010 | Dobson et al. [ ] | CBT Adolescent Coping with Stress Course Attention-Placebo “Let’s Talk” | MDD or Dd excluded (depressive symptoms) |
2010 | Young et al. [ ] | IPT Adolescent Skills Training School counseling | Indicated prevention: 16 ≤ CESMD ≤ 39 82.5% no depression diagnosis |
2011 | Hayes et al. [ ] | CBT Acceptance and Commitment Therapy TAU | 26.4% no diagnosis of depression (out the clinical range for depression) |
2011 | Stallard et al. [ ] | CBT CD-ROM “Think, Feel, Do” WL | Depressive or anxious symptoms |
2012 | Fleming et al. [ ] | CBT SPARX Computerized Program WL | Indicated prevention: CDRS-R ≥ 30 |
2012 | Gillham et al. [ ] | CBT PRP Parents and Adolescents CBT PRP Adolescents School-As-Usual Control | Indicated prevention: CDI = 11.1 (mean) |
2012 | Kauer et al. [ ] | CBT Mobile Phone Self-Monitoring Program Attention-Placebo | Youth: M age > 18, range 14–24 Indicated prevention: KPDS > 16 |
2012 | Merry et al. [ ] | CBT SPARX Computerized program TAU | Symptoms of mild to moderate depressive disorder |
2012 | Stallard et al. [ ] | CBT Resourceful Adolescent Program Usual School Provision Attention-Placebo | Indicated prevention: SMFQ ≥ 5 |
2013 | Carrion et al. [ ] | CBT Behavioral, Cognitive and Insight Techniques WL | Selective prevention: Adolescents exposed to interpersonal violence |
2013 | Horigian et al. [ ] | FT Brief Strategic Family Therapy TAU | Selective and indicated prevention |
2013 | Listug-Lunde et al. [ ] | CBT CWD-A Culturally Modified Version TAU | Students with depressive symptoms |
2013 | McCarty et al. [ ] | CBT Positive Thoughts and Action ST Individual Support Program | Indicated prevention: MFQ ≥ 14 |
2013 | Nöel et al. [ ] | CBT “Talk’n’ Time” WL | Selective prevention: Rural preadolescent girls |
2013 | Shirk et al. [ ] | CBT Cognitive Restructuring, Relaxation, Behavioral Activation, Interpersonal Problem Solving | Open clinical trial |
2013 | Stikkelbroek et al. [ ] | CBT Individual Program “D(o)epression Course” TAU | Project to study effectiveness of CBT for adolescent depression |
2014 | Chen et al. [ ] | CBT Program “Children and Disaster: Teaching Recovery Techniques” ST Listening, reflection, and empathy techniques No Intervention Condition | Selective prevention: Adolescents who lost at least one parent in an earthquake |
2014 | Richardson et al. [ ] | CBT Reaching Out to Adolescents in Distress and/or Medication TAU | 39.6% no diagnosis of depression (depressive symptoms) |
2014 | Rohde et al. [ ] | FT Followed by CBT CBT Followed by FT Coordinated FT and CBT | Selective and indicated prevention: Adolescents with comorbid depressive disorders (54% MDD, 18% Dd) |
2014 | Stasiak et al. [ ] | CBT CD-ROM “The Journey” Attention-Placebo: Computerized Psychoeducation | Indicated prevention: CDRS-R ≥ 30, RADS-2 ≥ 76 |
2014 | Wijnhoven et al. [ ] | CBT PRP WL | Indicated prevention: CDI ≥ 16 |
2015 | Compas et al. [ ] | CBT Family Group Written Information | Selective prevention: Preadolescents (M age = 11.5) of parents with depression |
2015 | Dietz et al. [ ] | IPT Family-Based CCT Child-Centered Therapy (Rogerian model) | Preadolescents: M age = 10.8, range: 7–12 |
2015 | Rickhi et al. [ ] | Spirituality Informed e-Mental Health Intervention WL | M age > 18, range: 13–24 Inclusion criteria: Suspicion they might be suffering from depression |
2015 | Smith et al. [ ] | CBT Stressbusters Computerized Program WL | Indicated prevention: MFQ ≥ 20 |
2016 | Bella-Awusah et al. [ ] | CBT WL | Indicated prevention: BDI-II ≥ 18 Trial was randomized at the school level |
2016 | Chu et al. [ ] | CBT Transdiagnostic Behavioral Activation WL | Principal diagnosis: 17.1% depression, 82.9% anxiety disorder |
2016 | De Voogd et al. [ ] | Active Online Emotional Working Memory Training Placebo Online Emotional Working Memory Training | Symptoms of anxiety and depression |
2016 | Fristad et al. [ ] | Omega-3 Polyunsaturated Fatty Acids (Ω3) Psychoeducational Psychotherapy (PEP) Ω3 + PEP | Preadolescents: M age = 11.6, range: 7–14 |
2016 | Gaete et al. [ ] | CBT Normal teaching activities at school | Indicated prevention: BDI-II ≥ 10 (boys), BDI-II ≥ 15 (girls) |
2016 | Goossens et al. [ ] | CBT Preventure Program No Intervention Condition | Selective prevention: Adolescents who drink alcohol |
2016 | Ip el al. [ ] | CBT Grasp the Opportunity Website Attention control: An Anti-Smoking Website | Indicated prevention: 11 < CES-D < 41 |
2016 | Jacob and de Guzman [ ] | CBT Based-Bibliotherapy Intervention No Intervention Condition | Indicated prevention: BDI-II > 14, AADS > 61, KADS-11 > 12 |
2016 | Jacobs et al. [ ] | CBT Rumination-Focused Assessment Only Control | Adolescents at risk for depressive relapse |
2016 | McCauley et al. [ ] | CBT Behavior Activation EBP-D | Diagnosis of depression or CDRS-R ≥ 45 |
2016 | Poppelaars et al. [ ] | CBT PRP (Dutch version: Op Volle Kracht) CBT SPARX Computerized Program CBT PRP + SPARX Monitoring Control Condition | Indicated prevention: RADS-2 ≥ 59 |
2016 | Rice et al. [ ] | Omega-3 Polyunsaturated Fatty Acids + CBT Cognitive Behavioral Case Management Paraffin Oil Placebo + CBT Cognitive Behavioral Case Management | Project “The Fish Oil Youth Depression Study (YoDA-F)”. Young: Age range 15–25 |
2016 | Schleider and Weisz [ ] | Single-Session Teaching Growth Personality Mindsets ST | Symptoms of anxiety and depression: RCADS-P T-score ≥ 60 |
2016 | Takagaki et al. [ ] | CBT Behavioral Activation No Intervention Condition | Indicated prevention: BDI-II ≥ 10 M age = 18.2; range: 18–19 |
2017 | Barry et al. [ ] | CBT Group Coaching Intervention No Intervention Condition | Indicated prevention: CES-DC ≥ 15 Not published in a peer-reviewed journal |
2017 | Ehrenreich-May et al. [ ] | CBT UP-A WL | Principal diagnosis: 21.6% MDD, 3.9% Dd, 2.9% DD NOS, 41.2% GAD, 31.4% SP |
2017 | Ranney et al. [ ] | TBI Motivational Interviewing CBI Motivational Interviewing TAU Enhanced | Indicated (CES-D-10 = 13.2 mean) and selective prevention: Adolescents presenting to Emergency Department at Level 1 |
2017 | Shomaker et al. [ ] | CBT Mindfulness: “Learning to BREATHE” CBT Blues Program | Indicated (CES-D ≥ 16) and selective prevention: Adolescent girls at risk for type 2 diabetes |
2017 | Tompson et al. [ ] | CBT Family-Focused Treatment for Child Depression ST Individual | Preadolescents: M age = 10.8, range: 7–14 |
2017 | Wright et al. [ ] | CBT Stressbusters Computerized Program Attention Control: Accessing Low Mood Self-Help Websites | Indicated prevention: MFQ ≥ 20 |
2018 | Bai et al. [ ] | CBT Behavioral Health Intervention TAU Enhanced | 48% no diagnosis of depression (CES-D = 20.1, mean). Adolescents with health risk behaviors |
2018 | Díaz-González et al. [ ] | CBT Mindfulness-Based Stress Reduction TAU | Adolescents attending Mental Health Services: 11.3% MDD, 21.3% AD, 67.5% Other disorders |
2018 | Högberg and Hällström [ ] | CBT Systematised Mood-Regulation TAU | Symptoms of depression tested with SMFQ |
2018 | Jensen-Doss et al. [ ] | CBT UP-A + YOQ TAU + YOQ TAU | Adolescents with significant symptoms of anxiety or depression: CSR ≥ 4 |
2018 | Singhal et al. [ ] | CBT Coping Skills Program Interactive Psychoeducation | Indicated prevention: 14 ≤ CDI ≤ 24 Trial was randomized at the school level |
2018 | Topooco et al. [ ] | CBT Internet-Based Attention-Placebo | 24.3% no diagnosis of depression (depressive symptoms only) |
2019 | Brown et al. [ ] | CBT DISCOVER ‘How to Handle Stress” WL | 27.33% depression ‘cases’ 48.7% anxiety ‘cases’ |
2019 | Davey et al. [ ] | CBT + Fluoxetine CBT + Pills Placebo | M age = 19.6; range: 15–25 |
2019 | Diamond et al. [ ] | FT Attachment-Based ST Nondirective | Indicated prevention: BDI-II > 20 41.2% MDD, 3.9% Dd, 46.9% AD |
2019 | Grupp-Phelan et al. [ ] | STAT-ED Motivational Interviewing TAU Enhanced | Selective prevention: Suicidal adolescents (ASQ) |
2019 | Idsoe et al. [ ] | CBT Adolescent Coping with Depression Course TAU | Indicated prevention: CES-D ≥ 28 |
2019 | Sánchez-Hernández et al. [ ] | CBT Smile Program No Intervention condition | Indicated prevention: CDI > 10 |
2020 | García-Escalera et al. [ ] | CBT Internet UP-A WL | Universal prevention |
2020 | Osborn, Rodriguez et al. [ ] | SI Single-Session Digital Intervention Digital Study Skills Condition | Universal prevention |
2020 | Osborn, Venturo-Conerly et al. [ ] | Shamiri Intervention: Growth-Mindset Module + Gratitude Module + Value Affirmations Module Study Skills Condition | Indicated prevention: PHQ-8 ≥ 28 (depression), GAD-7 ≥ 10 (anxiety) |
2020 | Osborn, Wasil et al. [ ] | Shamiri Intervention: Growth-Mindset Module + Gratitude Module + Value Affirmations Module Study Skills Condition | Indicated prevention: 37.3% adolescents reported moderately severe-to-severe depressive symptoms, 92.2% moderate-to-severe anxiety symptoms |
AADS = Asian Adolescent Depression Scale; AD = Anxiety Disorder; APAI = Acholi Psychosocial Assessment Instrument; ASQ = Ask Suicide Screening Questions; BDI = Beck Depression Inventory; BID = Bellevue Index of Depression; CBI = Computer-delivered Brief Intervention; CBT = Cognitive Behavioral Therapy; CDI = Children’s Depression Inventory; CDRS-R = Children’s Depression Rating Scale-Revised; CES-D(C) = Center for Epidemiological Studies-Depression Scale (for Children); CSR = Clinical Severity Rating; CWD-A = Coping with Depression Course for Adolescents; DD = Depressive Disorder; Dd = Dysthymic Disorder; EBP-D = Evidence-Based Practice for Depression; ED = Externalizing Disorder; FT = Family Therapy; GAD(-7) = Generalized Anxiety Disorder (Screener-7); HRSD = Hamilton Rating Scale for Depression; IPT = Interpersonal Therapy; KADS-11 = Kutcher Adolescent Depression Scale; KPDS = Kessler Psychological Distress Scale; MDD = Major Depression Disorder; MDE = Major Depression Episode; NOS = Not Otherwise Specified; PASCET = Primary and Secondary Control Enhancement Training; PEPT = Psychoeducational Psychotherapy; PHQ-8 = Patient Health Questionnaire-8-item version; PT = Psychodynamic Therapy; PRP = Penn Resiliency Program; RADS = Reynolds Adolescent Depression Scale; RCADS-P = Revised Child Anxiety and Depression Scale-Parent Form; SI = Shamiri Intervention; (S)MFQ = (Short) Mood and Feelings Questionnaire; SPARX = Smart, Positive, Active, Realistic, X-factor thoughts; ST = Supportive Therapy; STAT-ED = Suicidal Teens Accessing Treatment After an Emergency Department Visit; TAU = Treatment As Usual; TBI = Therapist-delivered Brief Intervention; UP-A = Unified Protocol for the Treatment of Emotional Disorders in Adolescents; WL = Wait-list Condition; YOQ = Youth Outcomes Questionnaire.
The 27 RCTs reviewed involved 3501 adolescents, mean age 15 years, 66.6% girls, from families with varied socioeconomic status and structure, and of diverse ethnicity (see Table 3 ). The adolescents had major depressive disorder (87.4%) and/or persistent depressive/dysthymic disorder (10%), unspecified depressive disorder (0.9%), or another depressive disorder (5%). In ten trials, with 1391 participants, suicidality was reported: 36.8% of adolescents had current suicidal ideation and/or 35% had a history of suicide attempts. In sixteen trials with 2483 adolescents, a wide range of comorbid disorders were reported: 43.1% anxiety disorders, 28.3% disruptive and conduct disorders, 17% attention deficit hyperactivity disorder, and 26.6% had other disorders. The trial by Szigethy and colleagues [ 130 ] departs from the above, because the comorbidity of the participating children and adolescents was inflammatory bowel disease, Crohn’s disease (75%) or ulcerative colitis (25%).
Sociodemographic and clinical characteristics of the participants in trials included in the current review.
Year | Authors | N | Mean Age (Range) | Gender Female | Family Demographics | Ethnicity | Diagnosis | Suicidality | Comorbidity |
---|---|---|---|---|---|---|---|---|---|
1990 | Lewinsohn et al. [ ] | 59 | 16.2 (14–18) | 61% | 40.7% Both parents 52.5% One parent 6.8% Neither parent | 49% MDD 7% mDD 44% IDD | 40% HSA | ||
1996 | Vostanis et al. [ ] | 57 | 12.7 (8–17) | 56.1% | 50.9% Both parents 29.8% Single parent 7% Adoptive parents 12.3% Others | 87.7% White 8.8% Asian 3.5% Black | 29.8% MDD 54.4% mDD 15.8 Dd | 45.6% OAD or SAD 19.3% ODD or CD | |
1996 | Wood et al. [ ] | 53 (48) | 14.2 (9–17) | 68.8% | 91.5% MDD 27% EDD | 56% OAD 23% CD | |||
1997 | Brent et al. [ ] | 107 | 15.6 (13–18) | 75.7% | 57% Both parents | 83.2 White | 77.6% MDD 22.4% MDD + Dd | 36.4% CSI 23.4% HSA | 31.8% AD 20.6% DBD |
1999 | Clarke et al. [ ] | 123 (96) | 16.2 (14–18) | 70.8% | 43.8% Both parents | 76% MDD 12.5% Dd 11.5% MDD + Dd | 23.6% AD | ||
1999 | Mufson et al. [ ] | 48 | 15.8 (12–18) | 70.9% | 68.8% One parent | 70.8% Hispanic | 79% MDD 21% MDD + Dd | 42.5% CSI 27.5% HSA | 88% AD |
1999 | Rosselló and Bernal [ ] | 71 | 14.7 (13–18) | 54% | 24% MDD 76% MDD + Dd | ||||
2002 | Clarke et al. [ ] | 88 | 15.3 (13–18) | 69.3% | 82.7% Parent female 4.6% Parent minority 77% Parents married 23.3% Parent college graduate 74.7% Employed | 9.1% Minority | 93.2% MDD 3.4% Dd 1.1% NOS BD | 22.7% PTSD 18.2% ODD 4.5% SA 2.3% NOS Ed | |
2002 | Diamond et al. [ ] | 32 | 14.9 (13–17) | 78% | 80% One parent 69% < USD 30,000 annual income 34% ≤ USD 20,000 annual income | 69% African American 31% White | 100% MDD | ||
2004 | Mufson et al. [ ] | 63 | 15.1 (12–18) | 84.1% | 69.8% One parent | 71.4% Hispanic | 50.8% MDD 17.5% Dd 14.3% ADDM 11.1% NOS DD 6.3% dD | 33.3% CSI 11.1% HSA | |
2004 | Rohde et al. [ ] | 93 | 15.1 (13–17) | 48.4% | 15.1% Both biological parents 14.8% Parent with bachelor’s degree or higher | 80.6% White | 100% MDD | 39.8% HSA | 100% CD |
2004 | TADS [ ] | 439 | 14.6 (12–17) | 54.4% | 41% One parent USD 50,000–74,000 modal family income | 73.8% White 12.5% Black 8.9% Hispanic | 100% MDD 10.5% Dd | 27.4% AD, 23.5% DB, 13.7% ADHD, 4.3% Others | |
2005 | Clarke et al. [ ] | 152 | 15.3 (12–18) | 77.6% | 13.8% Minority | 100% MDD | |||
2006 | Melvin et al. [ ] | 73 | 15.3 (12–18) | 65.8% | 58.5% Secondary school 41.5% Tertiary school | 60.3% MDD 23.3% Dd 16.4% NOS DD | 37% AD 26% PCRP 8.2% CD/ODD 15% Others | ||
2007 | Goodyer et al. [ ] | 208 | 14 (11–17) | 74% | 100% MDD 0.5% Dd | 44.2% SP, 38% OCD, 37.5% PTSD, 31.2% AP, 28.4% SAD, 22.6% sP | |||
2008 | Brent et al. [ ] | 334 | 15.9 (12–18) | 69.8% | USD 61,000 median family income | 82.9% White 17.1% Other Ethnicity | 100% MDD 29.3% Dd | 23.7% HSA | 36.4% AD 15.6% ADHD 9.9% ODD/CD |
2013 | Alavi et al. [ ] | 30 | 16.1 (12–18) | 90% | 100% MDD | 100% HSA | |||
2013 | Israel and Diamond [ ] | 20 | 15.6 (13–17) | 55% | 100% MDD | 85% ID 55% ED 40% Ap | |||
2014 | Shirk et al. [ ] | 43 | 15.5 (13–17) | 83.7% | 49% Non-Hispanic Caucasian 38% African American 33% Hispanic | 81.4% MDD 7% Dd 11.6% NOS DD | 46% PTSD 14% SA | ||
2014 | Szigethy et al. [ ] | 217 | 14.3 (9–17) | 51% | 89.4% White 10.6% Black | 63.1% MDD 36.9% mDD | 74.2% Cd 25.8% UC | ||
2015 | Kobak et al. [ ] | 65 | 15.4 (12–17) | 66.2% | 41.5% Caucasian 36.9% African American 4.6% American Indian 1.5% Asian, 7.7% Biracial, 7.7% Others | 47.7% MDD 30.8% PDD 4.6% MDD and PDD 7.7% NOS DD | |||
2016 | Charkhandeh et al. [ ] | 188 | (12–17) 12.8% 12–13 36.7% 14–15 50.5% 16–17 | 53.7% | 86.2% Both parents 8.5% Only mother 3.2% Only father 2.1% None 30.9% > USD 800 68.6% < USD 800 | 100% MDD | |||
2016 | Clarke et al. [ ] | 212 | 14.7 (12–18) | 68.4% | $64,073 average family income | 16% Hispanic 11.8% Minority | 100% MDD | ||
2016 | Yang et al. [ ] | 45 | 15 (12–18) | 55.6% | 100% Chinese population | 100% DD | 24.4% CSI/HSA | ||
2017 | Goodyer et al. [ ] | 470 (465) | 15 (11–17) | 74.8% | 84.5% White | 100% MDD | 34.4% HSA | 12% ODD/CD | |
2018 | Poole et al. [ ] | 64 | 15.2 (12–18) | 73.4% | 37.5% Married 37.5% Divorced 17.9% Single 19% USD 0–20,000 36% USD 20,000–50,000 21% USD 50,000–80,000 24% > USD 80,000 | 100% MDD, mDD or Dd | |||
2019 | Esposito-Smythers et al. [ ] | 147 | 14.9 (12–18) | 76.2% | 85.5% White 2.1% Black/African American 2.8% Asian/Pacific Islander 9.7% Multiracial | 89.1% MDD 10.9 Dd or NOS DD | 65.5% HSA | 39.6% GAD, 26.6% ADHD, 22.2% SAD, 18.8% ODD/CD, 18.3 PTSD |
a,b Data from a completers or from b intent-to-treat. AD = Anxiety Disorder; ADDM = Adjustment Disorder with Depressed Mood; ADHD = Attention Deficit Hyperactivity Disorder; AP = Agoraphobia; Ap = Attention Problems; BD = Bipolar Disorder; BN = Bulimia Nervosa; CD = Conduct Disorder; Cd = Crohn’s Disease; CSI = Current Suicidal Ideation; DB(D) = Disruptive Behavior (Disorder); DD = Depressive Disorder; Dd = Dysthymic Disorder; dD = Double Depression; DS = Depressive Symptomatology; ED = Externalizing Disorder; Ed = Eating Disorder; EDD = Endogenous Depression Disorder (RCD); GAD = Generalized Anxiety Disorder; HAS = History of Suicide Attempt; ID = Internalizing Disorder; IDD = Intermittent Depressive Disorder (RDC); MDD = Major Depression Disorder (DSM); mDD = Minor Depression Disorder (RDC); MDE = Major Depression Episode; NOS = Not Otherwise Specified; OAD = Overanxious Disorder; OCD = Obsessive Compulsive Disorder; ODD = Oppositional Defiant Disorder; PCRP = Parent–Child Relational Problem; PDD = Persistent Depressive Disorder; PTSD = Posttraumatic Stress Disorder; SA(D) = Substance Abuse (Disorder); SAD = Separation Anxiety Disorder; SP = Social Phobia; sP = Specific Phobia; SU(D) = Substance Use (Disorder); UC = Ulcerative Colitis.
Considering the large number of studies of CBT and the fact that definitions of evidence-based treatment emphasize the accumulation of positive findings, we focused on the analysis of trials with positive effects. Table 4 presents the RCTs that evaluated treatments for depression in adolescents included in the current review.
Adolescent depression treatment outcome of trials included in the current review.
Year | Authors | Treatment Conditions | Sessions | Measures (Sources) | Posttreatment | Follow-Up | |||
---|---|---|---|---|---|---|---|---|---|
Improvement | Effect Size | Response Rate | |||||||
1990 | Lewinsohn et al. [ ] | CBT Parent and Adolescent CBT Adolescent WL | 14 two-hour group over 7 weeks | CES-D (A) BDI (A) CBCL-D (P) | CBT (PA) ≥ CBT (A) > WL | CES-D: 1.51 PA, 1.18 A BDI: 1.48 PA, 0.94 A CBCL-D: 1.35 PA, -0.13 A | Loss of Diagnosis CBT (PA): 47.6% CBT (A): 42.9% WT: 5.3% | 24 months Improvement was maintained | |
1996 | Vostanis et al. [ ] | CBT PL | 9 individual biweekly | MFQ (A, P) | CBT = PL | MFQ: 0.05 A, 0.51 P | Loss of Diagnosis CBT: 87% PL: 75% | 9 months (recovered) 86% CBT, 75% PL 24 months 74.1% CBT, 85% PL | |
1996 | Wood et al. [ ] | CBT RT Progressive Relaxation | 8 individual weekly | MFQ-C (A, P) | CBT > RT | MFQ: N/A A, 0.41 P | MFQ-C Clinical Significance CBT: 75% RT: 33% | 3 months: = −0.06 6 months: = 0.14 | |
1997 | Brent et al. [ ] | CBT FT Systemic and Behavioral NDST | 12–16 individual over 12–16 weeks | K-SADS (C) BDI (A) | CBT > FT = NDST | K-SADS: 0.45 CBT, 0.14 FT BDI: 0.41 CBT, 0.07 FT | Loss of Diagnosis + BDI < 9 (3 Sessions) CBT: 82.9% FT: 67.7% NDST: 57.6% | 12 months (recovered) 96.7% (rapid responders), 68.7% (initial non-responders) 24 months (recovered) No between-group differences | |
1999 | Clarke et al. [ ] | CBT Parent and Adolescent CBT Adolescent WL | 16 two-hour group over 8 weeks | HRSD (C) BDI (A) CBCL-D (P) | CBT (PA) = CBT (A) > WL | HRSD: 0.14 PA, 0.52 A BDI: 0.24 PA, 0.58 A CBCL-D: −0.43 PA, −0.47 A | Loss of Diagnosis CBT (PA): 68.8% CBT (A): 64.9% WT: 48.1% | 12 months (recovered) 100% booster, 50% assessment 24 months (recovered) 100% booster, 90% assessment | |
1999 | Mufson et al. [ ] | IPT CM | 12 45 min individual weekly | HRSD (C) BDI (A) | IPT > CM | HRSD: 0.66 BDI: 0.66 | HRSD ≤ 6 IPT: 75% CM: 46% | Not reported | |
1999 | Rosselló and Bernal [ ] | CBT IPT WL | 12 one-hour individual weekly | CDI (A) | CBT = IPT > WL | CDI: 0.35 CBT, 0.76 IPT | CDI < 12 CBT: 76% IPT: 89% WL: 66% | 3 months CBT = IPT | |
2002 | Clarke et al. [ ] | CBT + TAU TAU | 16 two-hour group over 8 weeks | HRSD (C) CES-D (A) CBCL-D (P) | CBT = TAU | HRSD: 0.10 CES-D: 0.20 CBCL-D: −0.24 | Few or no Depressive Symptoms ≥ 8 Weeks CBT: 31.6% TAU: 29.8% | 12 months (recovered) 71.1% CBT, 82.1% TAU 89.5% CBT, 92.3% TAU | |
2002 | Diamond et al. [ ] | FT Attachment-based WL | 12 60–90 min family group weekly | HRSD (C) BDI (A) | FT > WL | HRSD: 0.64 BDI: 0.77 | Loss of Diagnosis FT: 81% WL: 47% | 6 months (recovered) 87% FT | |
2004 | Mufson et al. [ ] | IPT TAU | 12 35 min individual over 16 weeks | HRSD (C) BDI (A) | IPT > TAU | HRSD: 0.50 BDI: 0.37 | HRSD ≤ 6 IPT: 50% TAU: 34% | Not reported | |
2004 | Rohde et al. [ ] | CBT LST | 16 two-hour group over 8 weeks | HRSD (C) BDI-II (A) | CBT > LST | HRSD: 0.39 BDI-II: 0.17 | Loss of Diagnosis CBT: 38.6% LST: 19.1% | 6 months (recovered) 54% CBT, 60% LST 12 months (recovered) 63% CBT, 63% LST | |
2004 | TADS [ ] | CBT Fluoxetine CBT + Fluoxetine Pill Placebo | 15 50–60 min individual over 12 weeks | CDRS-R (C) RADS (A) | CBT + FL > FL > CBT = PL | CDRS-R: −0.03 CBT, 0.68 FL, 0.98 CBT+FL RADS: −0.10 CBL, 0.50 FL, 0.82 | CGI ≤ 2 CBT + FL: 71% FL: 60.6% CBT: 43.2% PL: 34.8% | Not reported | |
2005 | Clarke et al. [ ] | CBT Brief + SSRI (TAU) SSRI (TAU) | 5–9 one-hour individual | HRSD (C) CES-D (A) CBCL-D (P) | CBT + SSRI ≥ SSRI | HRSD: 0.05 CES-D: 0.17 CBCL-D: 0.09 | No CMDE CBT + SSRI: 77% SSRI: 72.1% | 12 months (recovered) 80.3% CBT + SSRI, 94.2% SSRI | |
2006 | Melvin et al. [ ] | CBT Sertraline CBT + Sertraline | 12 50 min individual weekly | RADS (A) | CBT > SER CBT + SER = CBT CBT + SER = SER | CBT vs. SER: 0.42 CBT vs. CBT + SER: 0.33 SER vs. CBT + SER: −0.07 | Full Remission MDD CBT: 86% SER: 46% | 6 months (recovered) CBT = SER = CBT + SER | |
2007 | Goodyer et al. [ ] | CBT + SSRI + TAU SSRI + TAU | 19 55 min individual over 28 weeks | CDRS-R (C) MFQ (A) | CBT + SSRI + TAU = SSRI + TAU | CDRS-R: −0.11 MFQ: −0.22 | CGI ≤ 2 CBT + SSRI + TAU: 53.1% SSRI + TAU: 60.7% | Not reported | |
2008 | Brent et al. [ ] | CBT + SSRI SSRI CBT + Venlafaxine Venlafaxine | 12 60–90 min individual weekly | CDRS-R (C) BDI (A) | CBT + SSRI or Venlafaxine > SSRI = Venlafaxine | CBT vs. Medication: 0.09 CDRS-R, −0.05 BDI CBT vs. SSRI: 0.07 CDRS-R, 0.04 BDI CBT vs. Venlafaxine: 0.01 CDRS-R, −0.10 BD | CGI ≤ 2 CBT: 59% Medication: 47.6% | 15 months (recovered) 89% without MDD | |
2013 | Alavi et al. [ ] | CBT + TAU TAU | 12 individual weekly | BDI (A) | CBT > TAU | BDI: 2.88 | BDI Decrement CBT: 54% TAU: −0.1% | Not reported | |
2013 | Israel and Diamond [ ] | FT Attachment-based TAU | 12–16 family group weekly | HRSD (C) BDI-II (A) | FT > TAU | HRSD: 1.10 BID-II: 0.80 | HRSD < 9 FT: 27% TAU: 11% | Not reported | |
2014 | Shirk et al. [ ] | CBT Interpersonal Trauma TAU | 12 individual weekly | BDI-II (A) | CBT = TAU | BDI-II: −0.95 | Loss of Diagnosis CBT: 50.0% TAU: 48.0% | 1 month BDI-II: = −2.98 | |
2014 | Szigethy et al. [ ] | CBT PASCET NDST Supportive listening | 12 45 min individual weekly | CDRS-R (C) | CBT = NDST | CDRS-R: 1.31 CBT, 1.30 NDST | CDRS-R ≤ 28 CBT: 67.7% NDST: 63.2% | Not reported | |
2015 | Kobak et al. [ ] | CBT Technology-assisted TAU | 12 weeks | QIDS (A) | CBT = TAU | QIDS: 0.08 | CGI ≤ 2 CBT: 71.4% TAU: 60% | Not reported | |
2016 | Charkhandeh et al. [ ] | CBT Reiki WL | 24 90 min individual over 12 weeks | CDI (A) | CBT > Reiki > WL | CBT vs. Reiki: 1.11 CBT vs. WL: 2.03 Reiki vs. WL: 0.76 | CDI Decrement CBT: 32.4% Reiki: 12.2% WL: 0% | Not reported | |
2016 | Clarke et al. [ ] | CBT Brief Individual + TAU TAU | 5–9 individual | CDRS-R (C) CES-D (A) | CBT > TAU | CDRS-R: 0.60 CES-D: 0.37 | Loss of Diagnosis CBT: 31.3% TAU: 12.1% | 24 months CBT: 88.9% TAU: 78.8% | |
2016 | Yang et al. [ ] | CBT ABM Placebo ABM | 8 individual over 2 weeks + 4 individual over 2 weeks | K-SADS (C) HRSD (C) CES-D (A) | ABM > PL | K-SADS: 0.60 HRSD: 0.63 CES-D: 0.07 | Loss of Diagnosis ABM: 87% PL: 59% | 12 months CES-D: = 0.94 | |
2017 | Goodyer et al. [ ] | CBT PT Short-term BPI | 20 over 30 weeks 28 over 30 weeks 12 over 20 weeks | MFQ (A) | CBT = PT CBT and PT = BPI | CBT vs. PT: 0.16 CBT vs. BPI: 0.40 PT vs. BPI: 0.25 | Loss of Diagnosis CBT: 69% PT: 64% BPI: 56% | 12 months CBT: 74% PT: 73% BPI: 71% | 20 months CBT: 75% PT: 85% BPI: 73% |
2018 | Poole et al. [ ] | FT Best Mood Program TAU PAST Program | 8 two-hour family group | SMFQ (A) | FT = TAU | SMFQ: 0.07 | SMFQ Decrement FT: 29.6% TAU: 23.8% | 3 months = −1.02 | |
2019 | Esposito-Smythers et al. [ ] | CBT Family-focused TAU Enhanced | 0–6 months: weekly (A), biweekly (P) 6–9 months: biweekly (A), biweekly-monthly (P) 9–12 months: monthly (A, P) | K-SADS (C) CDI-2 (A) | CBT = TAU | CDI-2: 0.06 | Loss of Diagnosis CBT: 79% TAU: 86.4% | 6 months CBT: 72.6% TAU: 87.5% CDI-2: = −0.56 |
A = Adolescent; ABM = Attention Bias Modification; BA = Behavioral Activation; BDI = Beck Depression Inventory; BPI = Brief Psychosocial Intervention; C = Clinician; CBCL-D: Child Behavior Checklist-Depression; CBT = Cognitive Behavioral Therapy; CDI = Children’s Depression Inventory; CDRS-R = Children’s Depression Rating Scale-Revised; CES-D = Center for Epidemiological Studies-Depression Scale; CGI = Clinical Global Impressions; CM = Clinical Monitoring; CMDE = Current Major Depressive Episode; EBP-D = Evidence-Based Practice for Depression; FL = Fluoxetine; FT = Family Therapy; HRSD = Hamilton Rating Scale for Depression; IPT = Interpersonal Therapy; K-SADS = Kiddie School Age Schedule for Affective Disorders and Schizophrenia; LST = Life Skills Tutoring; MDD = Major Depression Disorder; NDST = Non-Directive Supportive Therapy; P = Parents; PASCET = Primary and Secondary Control Enhancement Training; PAST = Parenting Adolescents Support Training; PL = Placebo; PT = Psychoanalytic Therapy; QIDS = Quick Inventory of Depressive Symptomatology; RADS = Reynolds Adolescent Depression Scale; RT = Relaxation Training; SER = Sertraline; (S)MFQ(-C) = (Short) Mood and Feelings Questionnaire (-Child); SSRI = Selective Serotonin Reuptake Inhibitor; TAU = Treatment As Usual; WL = Wait-list Condition.
The first trials compared CBT with another psychological treatment, with active controls, or WL. Approximately fifteen years ago, research began to investigate the effectiveness of CBT combined with antidepressants; additionally, WL was used less and was replaced by treatment as usual (TAU).
Lewinsohn and colleagues [ 14 ] conducted a pioneering trial with two objectives: (1) to test the efficacy of the Coping With Depression Course for Adolescents (CWD-A) [ 138 ], the main components of which were social skills, pleasant activities, relaxation training, cognitive restructuring, conflict resolution, and relapse prevention; and (2) to test whether parental involvement enhanced treatment efficacy. Adolescents in CWD-A recovered significantly from depressive episodes and reduced their depressive symptoms, depressive cognitions, and anxiety significantly more than those in WL; improvement was maintained at a two-year follow-up. There was a trend in favor of the parent-involved group over the adolescent-only group; a significant difference between the two treatment groups was obtained on the depression, internalizing problems, and externalizing problems subscales of the Child Behavior Checklist [ 139 ] completed by the parents.
In a replication of the pioneering trial by Lewinsohn et al. [ 14 ], Clarke and colleagues [ 115 ] found that the recovery rate of treated adolescents was significantly higher than WL (66.7% versus 48.1%), an improvement confirmed by self-report of depression and clinician-rated global functioning. There were no differences, however, between the parent-and-adolescent group and adolescent alone group. Immediately after the post-treatment assessment, they introduced the novelty of randomly reassigning treated adolescents to three new conditions during the 24-month follow-up: (1) assessments every 4 months with booster sessions; (2) only assessments every 4 months; and (3) only assessments every 12 months. The booster sessions did not reduce the recurrence rate at follow-up, but they did appear to accelerate the recovery of adolescents who remained depressed at the end of the acute phase. A significant difference was also found for externalizing behaviors between adolescents who had received booster sessions and those who had only been assessed; participants who were evaluated quarterly outperformed those assessed annually on parental reports of depression and internalizing behaviors.
Rohde and colleagues [ 121 ] evaluated the effectiveness of the CWD-A course in depressed adolescents with comorbid conduct disorder, recruited from a juvenile justice department, compared with life skills tutoring (LST) that included current events review, life skills training (e.g., filling out a job application or renting an apartment), and academic tutoring. At the end of treatment, the rate of recovery from depression was significantly higher in CWD-A (39%) than in LST (19%), and depressive symptoms reduced more, according to adolescent self-report and clinician assessment. There also was an improvement in social functioning; the between-group difference in conduct disorder was not significant, however. The rate of recovery from depression was the same in both groups one year later (63%).
Clarke and colleagues [ 133 ] examined the feasibility of a brief CBT intervention in primary care with adolescents who had declined or discontinued treatment with antidepressants. In the first session of the acute phase, the adolescent and therapist together chose one of two program modules: cognitive restructuring or behavioral activation, which was implemented over four sessions. If, at the end of the first module, the adolescent was almost or completely recovered, they could end the intervention; if not, they were encouraged to continue with the other module. During the continuation phase, the adolescent had up to six optional treatment contacts. Recovery rates from depression in the follow-up period were significantly higher for CBT plus TAU than for TAU alone: 69.7% versus 43.4% (week 26), 79.8% versus 68.7% (week 52), 86.9% versus 75.8% (week 78), and 88.9% versus 78.8% (week 104). Median recovery time was 22.6 weeks for CBT plus TAU and 30 weeks for TAU alone. Compared with TAU alone, the reduction in clinician-rated and adolescent-reported depressive symptoms, reduction in dysfunctional thoughts and complaints, and improvements in global functioning and quality of life were superior for CBT plus TAU in the first year of follow-up, although not in the second year. The rate of psychiatric hospitalizations was also significantly lower for CBT plus TAU during the first year of follow-up.
In a replication of the initial trial of Reynolds and Coats [ 13 ] with depressed adolescents, Wood and colleagues [ 113 ] compared a program composed of Beck’s cognitive therapy [ 140 ], interpersonal problem solving, sleep hygiene, and pleasant activities, with another active treatment for depression and comorbid symptoms. Adolescents in the multicomponent program improved significantly more in depression and self-esteem and were more satisfied with the treatment than those who received only progressive relaxation training [ 141 ]. Both groups improved in anxiety, but not in antisocial behavior. At follow-up, the between-group difference narrowed, partly because of the high relapse rate in the CBT group and partly because the adolescents in the relaxation group continued to recover.
Brent and colleagues [ 114 ] tested the efficacy of a protocol that included Beck’s cognitive therapy [ 142 ], problem solving, emotion regulation, and social skills, with a mixed-modality of family therapy (FT) based on behavioral and systemic approaches, and with non-directive supportive therapy (NDST). Only 17.1% of the adolescents in the CBT group were still depressed at the end of treatment, whereas 32.3% and 42.4% of the FT and NDST groups, respectively, still had major depressive disorder (MDD); the difference was significant only with NDST. CBT showed significantly higher remission rates, defined as the absence of depression and a score < 9 on the Beck Depression Inventory [ 143 ] for at least three consecutive sessions, than the other treatments: 64.7% (CBT) versus 37.9% (FT) and 39.4% (NDST). CBT also outperformed the other treatments in the reduction in clinician-rated depressive symptomatology and in the credibility of the therapy. Finally, CBT was better than FT in adolescent-reported depressive symptoms.
Alavi and colleagues [ 127 ] evaluated the effectiveness of a CBT protocol for Suicide Prevention, developed by Stanley and colleagues [ 144 ], with the aim of decreasing suicidal ideation and hopelessness in depressed adolescents, who had had at least one suicide attempt in the previous quarter. In the initial phase of the treatment, which was conducted over three sessions, vulnerability factors and triggering events of suicidal crises were analyzed (i.e., chain analysis), coping strategies, and sources of support were provided (i.e., safety planning), the nature of suicide was explained together with the need to monitor potential lethal means (i.e., psychoeducation), the adolescent’s personal reasons for living were discussed (i.e., building hope), and a functional analysis of the problem was conducted (i.e., case conceptualization). The middle phase, sessions 4–9, included individual and family modules on behavioral activation, emotion regulation, cognitive restructuring, problem solving, and assertiveness. The three sessions of the final phase were devoted to relapse prevention. At the end of treatment, there were significant differences between youths in CBT versus those in the control condition on measures of depression, suicidal ideation, and hopelessness. Scores on these variables decreased between 54% and 77% in CBT, whereas they did not change in the condition that received only routine psychiatric intervention, including medication.
Charkhandeh and colleagues [ 132 ] compared CBT with the Reiki method of alternative medicine and WL. The goals of CBT were to modify distorted perceptions, learn problem-solving, acquire coping skills, and motivate behavior through enjoyable activities. At the conclusion of treatment, CBT had reduced depressive symptoms significantly more than either the Reiki method or WL.
Finally, we reviewed an RCT by Yang and colleagues [ 134 ] that compared active training in attentional bias modification (ABM) with placebo training. Although the treatment was very different from usual CBT, we included the trial because ABM is a specific target of cognitive therapy [ 142 ]. In the active condition, adolescents completed the neutral phase of ABM in eight sessions (320 trials per session), over two weeks, to shift their attention from sad words to neutral words. Nine weeks later, the positive phase of ABM took place in four sessions (480 trials per session), over two weeks, to redirect the attention from neutral words to positive words. The placebo condition used identical tasks but gave equal attention to sad and neutral words. After the neutral phase, a significantly higher proportion of adolescents in active ABM did not meet diagnostic criteria for MDD compared to placebo ABM (87% and 59%, respectively). The between-group difference was not maintained at the 7- or 11-week follow-ups, however. Active ABM also reduced clinician-rated depressive symptoms and attentional bias more than placebo ABM. At the 12-month follow-up, adolescents reported significantly fewer depressive and anxiety symptoms with active ABM as compared to placebo ABM.
The Treatment for Adolescents with Depression Study (TADS) Team [ 122 ] conducted one of the largest adolescent depression RCTs to assess the effectiveness of CBT and/or fluoxetine versus pharmacological placebo. The starting dose of fluoxetine and placebo was 10 mg/day, which was increased to 20 mg/day at week 1 and, if necessary, up to 40 mg/day at week 8. The initial phase of CBT (sessions 1–6) included psychoeducation, mood monitoring, pleasant activities, social problem-solving, and cognitive restructuring. The middle phase (sessions 7–12) addressed adolescents’ social skill deficits, including problems with social engagements, communication, negotiation, compromise, and assertion. In the final phase (sessions 13–15), two sessions were held with the parents alone to provide psychoeducation, and one to three sessions were held with the parents and the adolescent, focused on the concerns of both parties. The combined treatment of CBT plus fluoxetine significantly reduced depressive symptoms as assessed by the clinician more than separate psychological and pharmacological treatments and/or the placebo. Treatment response at week 12, defined as being much or very much improved, was more positive in the combined treatment (71%) and fluoxetine alone (60.6%) than in CBT alone (43.2%) or the placebo (34.8%). Suicidal ideation decreased in all four groups, although the reduction was greater in the combined treatment. The authors concluded that the combination of CBT with fluoxetine offered the best balance between benefit and risk and adding CBT to medication enhanced safety.
In another combined treatment trial, Clarke and colleagues [ 123 ] asked whether the adjunct of a brief CBT intervention based on cognitive restructuring and/or behavioral activation would increase the effectiveness of selective serotonin reuptake inhibitor (SSRI) administered as TAU in a health maintenance organization. The acute phase CBT program was the same as previously described [ 133 ] and its duration varied depending on the adolescent’s degree of recovery. During the continuation phase of CBT, the therapist made six brief check-in telephone calls to the adolescent at one, two, three, five, seven and nine months after completing treatment. Adolescents in the SSRI condition could receive any other treatment from the health maintenance organization and/or other outside services. Over one year, Clarke et al. conducted four follow-up assessments, at weeks 6, 12, 26, and 52, and found that CBT had significant benefits for mental health status. There was a reduction in outpatient visits and in the number of days on all types of medication and a marginally significant difference in depressive symptoms and externalizing problems as reported by adolescents.
Melvin and colleagues [ 124 ] compared the combination of CBT and sertraline with CBT alone and sertraline alone. CBT consisted of the CWD-A adapted for individual use in therapy. The initial dose of sertraline was 25 mg/day. After the first week, the dose was adjusted depending on clinical response. If adverse effects occurred, the medication was halved during several days for one week, after which time it was increased again to 25 mg/day. Conversely, if no adverse effects were observed during the first week, the dose was doubled (i.e., 50 mg/day). Subsequently, the dose was increased by 25 mg to a maximum of 100 mg/day, depending on clinical response and tolerance. The most frequent adverse effects of sertraline were fatigue (31.1%), difficulty concentrating (24.4%), and insomnia (22.2%). The highest response to treatment was obtained in the CBT alone group (86%), and the lowest in the sertraline alone group (46%). The probability of occurrence of depression at post-treatment was significantly lower in the CBT alone group than in the sertraline alone group, whereas the combined treatment did not differ from either treatment alone. At the six-month follow-up, there were no differences between the groups. Thus, in contrast to the short-term findings of the TADS Team [ 122 ], the advantage of the combined treatment in this study was less evident.
In the Treatment of SSRI-Resistant Depression in Adolescents (TORDIA) trial, Brent and colleagues [ 126 ] compared the combination of CBT and an SSRI or venlafaxine with these drugs given separately to adolescents who had previously failed to respond to SSRI treatment. All participants’ parents, regardless of treatment group, received family psychoeducation about depression. The CBT included cognitive restructuring, behavioral activation, emotion regulation, social skills, and problem solving. The alternative SSRIs were paroxetine, citalopram, or fluoxetine, with a daily dose of 10 mg per day the first week, 20 mg per day in weeks 2–6, with an option to increase to 40 mg per day if there was no improvement. The starting dose of venlafaxine was 37.5 mg, which was increased by that same amount over the next three weeks (i.e., 75, 112.5, and 150 mg), with the possibility of reaching a maximum dose of 225 mg daily in the sixth week. CBT plus any antidepressant showed a significantly higher response rate than any medications alone; the effects of the various medications did not differ from each other. There were no differences between treatments on clinician-rated or adolescent-reported depressive symptoms, suicidal ideation, rate of related harm, or any other negative events. Adverse effects of medication, such as increased diastolic blood pressure and pulse or skin problems, were more frequent with venlafaxine.
In the late 1990s, Mufson and colleagues [ 116 ] adapted the therapy developed by Klerman and colleagues [ 145 ], used to treat depression in adults, for the treatment of adolescents. The modification addressed common developmental issues in adolescence such as separation from parents, conflict with parental authority, exploration of dyadic interpersonal relationships, experience of the death of a family member or friend, and peer pressure. A specific area was added for single-parent families. The control condition was clinical monitoring, in which the therapist was limited to checking depressive symptoms and school attendance, assessing suicide risk, and practicing active listening, refraining from counseling, or providing skills training. Adolescents in both groups could contact the therapist if they felt worse (“call-me-if-you-need-me”). At the end of treatment in the intention-to-treat sample, 75% of the IPT adolescents had recovered from depression, scoring 6 or less on the Hamilton Rating Scale for Depression [ 146 ], whereas only 46% improved in the control condition. In addition, for youth in the IPT, there was a significantly greater reduction in depressive symptoms based on the clinician ratings and adolescent’s self-report, better overall social functioning with friends and with their partner, and greater interpersonal problem-solving skills, compared to youth in the control condition.
Rosselló and Bernal [ 117 ] evaluated the effectiveness of IPT and CBT compared with WL. The IPT used in this study was also an adaptation of the original model of Klerman and colleagues [ 145 ]. IPT was carried out in three blocks of four sessions each. The goals of sessions 1–4 were to elicit information about the adolescent’s depression, present the therapy, assess interpersonal relationships, identify core issues such as grief, interpersonal disputes, role transitions, and interpersonal deficits, establish a treatment plan, and explain what was expected of the adolescent in therapy. In sessions 5–8, they worked on selected interpersonal issues, monitoring depressive feelings, facilitating a positive therapeutic relationship, and preventing parental interference in the treatment. Sessions 9–12 discussed feelings related to separation, the treatment was reviewed, and the adolescents’ interpersonal competence was acknowledged. The CBT was based on Lewinsohn’s behavioral therapy [ 147 , 148 ], and Beck’s [ 142 ] and Ellis’ [ 149 , 150 ] cognitive therapy, the main components being cognitive restructuring, pleasant activities, and social skills. At both post-treatment and the three-month follow-up, adolescents that received treatment showed significantly fewer depressive symptoms than those who did not; there was no difference between IPT and CBT; and self-esteem and social adjustment improved with IPT compared with WL. No differences in these variables were found between IPT and CBT, nor between CBT and WL.
In 2004, the Mufson team [ 120 ] evaluated the effectiveness of IPT compared with TAU, from school-based health clinic clinicians. IPT was implemented as described in the manual by Weissman and colleagues [ 151 ], similar to those in the earlier trial by the Mufson team [ 116 ]. Most of the adolescents in the TAU group received individual psychotherapy–supportive counseling. At the conclusion of treatment, youth in the IPT showed significantly fewer clinician-rated depressive symptoms, better global and social functioning, greater clinical improvement, and a greater decrease in severity than TAU.
The trial by Brent and colleagues [ 114 ], described earlier, included an FT condition. In the first phase of treatment, based on Alexander and Parsons’ [ 152 ] functional FT, the therapist addressed the concerns raised by the family and reframed issues to optimize treatment engagement and identify dysfunctional behavior patterns. During the second phase, adapted from Robin and Foster’s [ 153 ] problem-solving model, family members focused on communication, negotiation, and conflict resolution skills, as well as on the modification of inappropriate family relationship patterns. The protocol included psychoeducation on depression and the developmental and educational aspects of depression, and emphasized skills building and positive practice in sessions and at home. FT was significantly inferior to CBT and did not differ from NDST in the remission rate of depression. There also was a smaller reduction in depressive symptoms, as assessed by clinician ratings and adolescent report, for those in FT compared to CBT; the latter treatment seemed more credible to parents.
Diamond and colleagues [ 119 ] contrasted attachment-based FT with a minimal contact WL control. The therapy consisted of five tasks aimed at repairing attachment and promoting autonomy. The Relational Reframing Task replaced a focus on “fixing” the adolescent with one of improving family relationships and addressing parental criticism and hostility with the aim of reducing blame and increasing mutual respect. The Adolescent Alliance-Building Task sought to create a bond to increase motivation and treatment engagement, explore family conflicts that damage trust, and prepare to discuss these issues with parents. The Parent Alliance-Building Task explored the parent’s current stressors and history of attachment failures, as well as promoted an authoritative educational style. The Attachment Task was initiated when the adolescent expressed anger about core conflicts, usually related to betrayal, abandonment, or abuse, such that parental remorse promoted adolescent forgiveness. The Competence-Promoting Task fostered the adolescents’ relationships and success outside the home (e.g., school, peers, work); with attachment recovered, the family became the secure base from which the adolescents could explore their emerging autonomy. At post-treatment, 81% of the adolescents who had received FT did not meet criteria for MDD, in contrast to 47% on the WL. FT also achieved a significantly greater reduction in depressive and anxiety symptoms and family conflict. Of the 15 cases evaluated at six-months follow-up, 13 adolescents (87%) were free of depression.
In a Norwegian pilot study with a small sample, Israel and Diamond [ 128 ] implemented the protocol of the previous trial [ 119 ]. The control condition was individually dispensed treatment in outpatient clinics. FT reduced depressive symptoms significantly more than TAU when assessed by the clinician, but not by adolescent self-report.
Pool and colleagues [ 136 ] compared the BEST MOOD program [ 154 ], which incorporates elements of attachment theory, such as parental sensitivity, grief responses, and understanding of frightening or stressful family environments, with the Parenting Adolescents Support Training (PAST) program [ 155 ], a control condition similar to TAU. The first four BEST MOOD sessions were held with parents only and included strategies for engaging the child in the program, stress reduction techniques, psychoeducation on family and adolescent development, family unity, parent–child communication, and parental self-care. The adolescent and siblings joined the therapy in the final four sessions devoted to clarifying the family roles, addressing loss and trauma, improving communication patterns, implementing behavioral activation techniques with the adolescent, and promoting positive family rituals. Improvement in depressive symptoms was similar in the two groups at post-treatment, d = 0.83 and d = 0.80, BEST MOOD and PAST, respectively, and at three-months follow-up, d = 0.46 and d = 0.51, BEST MOOD and PAST, respectively. There was no difference between the programs in the other variables including emotional symptoms, alcohol consumption, efficacy, dependence, and self-criticism. The only positive effect of BEST MOOD was the greater reduction in symptoms of depression and stress in the parents at the three-month follow-up.
The IMPACT trial [ 135 ] is the only one psychoanalytic therapy (PT) compared to CBT and a brief psychosocial intervention control condition. The short-term PT was based on close observation of the relationship which the adolescent established with the therapist. The therapist approached therapy as the task of understanding the adolescent’s feelings and life difficulties. The therapist was nonjudgmental and non-inquisitive and conveyed the value of self-understanding. The CBT focused on modifying behaviors and information processing biases through collaborative empiricism between the therapist and the adolescent. The brief psychosocial intervention control condition emphasized the importance of psychoeducation about depression, in addition to goal-focused and action-oriented interpersonal activities but did not include either self-understanding or cognitive change. There was no significant difference in adolescent-reported depressive symptoms between short-term PT and CBT, or between short-term PT and CBT versus the control condition, at either the conclusion of treatment (week 36) or at follow-up (week 86).
The first review that applied the Criteria for Empirically Supported Treatments [ 156 ] to evaluate the efficacy of psychological treatments [ 157 ] identified seven trials on adolescent depression, and considered CWD-A to be the only treatment that had achieved probable efficacious status, based on the two trials by the research team of Lewinsohn [ 14 , 25 ], which demonstrated the superiority of CBT over WL. This paucity of results is understandable, considering that when the review was published in 1998, barely three years had elapsed since the development of the classification criteria for evidence-based therapy.
A subsequent review published in 2008 [ 158 ] revealed the growing number of adolescent depression trials produced in one decade. They examined 18 new trials plus two published in 1996 [ 112 , 113 ], which had not been included in the earlier review, and concluded that CBT and IPT were well-established treatments, because there were at least two RCTs showing that they were superior to another treatment or to an active control condition.
A third 2016 review [ 159 ], collected on the website of the Society of Clinical Child and Adolescent Psychology, Division 53 of the American Psychological Association, on evidence-based mental health treatment for depression (Retrieved 13 April 2021 from https://effectivechildtherapy.org/concerns-symptoms-disorders/disorders/sadness-hopelessness-and-depression/ ), re-evaluated the 27 trials from the previous reviews—of which it eliminated six trials mainly for methodological reasons—additionally, it identified 14 new trials, confirming the well-established treatment status of CBT and IPT. The novelty was the addition of FT as a possibly efficacious treatment, because in the two trials by the research team of Diamond, FT was superior to an active control [ 128 ] and WL [ 119 ].
These reviews included treatment trials with clinical samples and prevention trials with subclinical samples. In the current review, we focused only on trials involving adolescents with a diagnosis of depression; that is, 18 of the previous trials, to which we added 9 more that were new or were not included [ 127 , 128 , 131 , 132 , 133 , 134 , 135 , 136 , 137 ] in the aforementioned reviews.
The body of research generated by CBT is far superior to that of other therapies. Six trials [ 13 , 14 , 19 , 23 , 25 , 114 ] in the 1998 review [ 157 ] included at least one CBT group, which was the only probably efficacious treatment. However, CBT is the first psychological treatment that, as early as the 1990s, achieved the status of a well-established treatment, because two trials conducted by independent research teams revealed that CBT was more effective than progressive relaxation training [ 113 ], FT, and NDST [ 114 ]. The discrepancy in evaluation is explained by the fact that the 1998 review did not include the study by Wood and colleagues [ 113 ]. The 2008 review [ 158 ] added fifteen trials, ten treatment [ 112 , 113 , 115 , 117 , 118 , 121 , 122 , 123 , 124 , 125 ] and five prevention [ 27 , 28 , 34 , 36 , 38 ], corroborating the well-established treatment status achieved by CBT in 1997. The 2016 review [ 159 ] updated the review of evidence-based treatments, removing five of the twenty-one previous trials and adding ten trials published between 2008 and 2014. They assigned well-established treatment status to individual CBT and to group CBT, possibly efficacious status to CBT using bibliotherapy, and experimental status to technology-assisted CBT.
We identified 96 CBT trials, of which we included 22 ( Table 4 ) and excluded 74 ( Table 2 ). Independent research teams have shown that CBT, applied individually, is superior to FT and NDST [ 114 ], relaxation training [ 113 ], the Reiki method [ 132 ], TAU [ 127 , 133 ], psychological placebo [ 134 ], and WL [ 117 , 132 ]. With respect to medication, CBT is more effective than sertraline [ 124 ]; when combined with fluoxetine, it is more effective than fluoxetine or a pharmacological placebo [ 122 ]; when combined with SSRI, CBT is more effective than an SSRI or venlafaxine (an SNRI) [ 123 , 126 ]; and when combined with venlafaxine, CBT is more effective than an SSRI or venlafaxine [ 126 ], making CBT a well-established treatment. Three trials by the same research team of Clarke, Rohde, Lewinsohn, and colleagues have shown that CBT, applied in a group setting, is superior to life skills tutoring [ 121 ] and WL [ 14 , 115 ], making it a probably efficacious treatment.
In recent years, there has been an increase in CBT programs via the internet (iCBT), computer (cCBT), or other devices such as cell phones [ 49 , 55 , 56 , 58 , 59 , 70 , 75 , 82 , 95 , 101 ], although these have been prevention trials with universal or indicated samples. One study [ 134 ] used a computer to present the stimulus words of an attention redirection task, although such attentional bias modification training is not really comparable to the usual technology-assisted CBT, of which we found only one trial with depressed adolescents [ 131 ]. Although this online intervention achieved greater improvement on all measures, including depressive symptoms, the difference with TAU was not significant. Similarly, CBT trials using bibliotherapy [ 27 , 47 , 83 ] were with indicated samples for prevention; thus, these modalities remain in the experimental phase.
The only study included in the 1998 review [ 157 ] was the open trial by Mufson and colleagues [ 21 ] which involved 14 adolescents with depression, making IPT an experimental treatment up to that date. The 2008 review [ 158 ] identified three RCTs of IPT applied individually and one applied in a group setting. In the trial by Rosselló and Bernal [ 117 ], IPT was equivalent to CBT; CBT had previously achieved well-established status and was superior to WL.
In the trials by Mufson’s team, IPT was superior to clinical monitoring [ 116 ] and TAU [ 120 ]. In another trial by Mufson’s team, group IPT was more effective than school counseling [ 39 ]. Thus, individual IPT was considered to be a well-established treatment, because in at least two trials, conducted by different research teams, it proved to be as effective as a well-established treatment and superior to other treatments, whereas group IPT remains an experimental treatment.
The 2016 review [ 159 ] added two new trials conducted by the same two research teams. In the second trial by Rosselló’s team [ 46 ], IPT was shown to be a robust treatment, both individually and in groups, although the reduction in depressive symptoms and internalizing and externalizing behaviors, as well as the improvement in self-concept, were significantly lower than with CBT. In a new trial by Mufson’s team [ 53 ], IPT was superior to school counseling in reducing depressive symptoms and improving global functioning. Thus, individual IPT was judged to be a well-established treatment and group IPT was a probably efficacious treatment.
We identified ten IPT trials, of which seven were excluded because they were indicated to be prevention [ 39 , 40 , 53 ] or open-label trials [ 21 , 29 ], or involved preadolescents [ 73 ]. The exclusion of the most recent trial by Rosselló’s team [ 46 ] could be debatable; one out of three adolescents was selected by the clinical interviewer’s judgment based on the degree of impairment and two out of three met the criteria for MDD; this exclusion, however, does not affect the evaluation of IPT because it was significantly inferior to CBT. Of the remaining three trials, the first RCT by Mufson’s team [ 116 ] compared IPT with clinical monitoring, an “ethical WL condition” (p. 574), which consisted of three monthly 30 min sessions, with an option for a second session within the month. In contrast, IPT included 12 weekly 45 min sessions, i.e., psychological attention time was up to six times longer in the active treatment than in the control condition.
Despite these concerns, individual IPT maintains the status of a well-established treatment for adolescent depression because there are at least two RCTs, conducted by independent research teams, in which it was as effective as CBT [ 117 ], a treatment of proven efficacy, and superior to TAU [ 120 ]. In contrast, group IPT would be in the experimental phase because the trials of Mufson’s team [ 39 , 53 ] were indicated prevention, as was that of Bolton [ 40 ], who selected adolescent survivors of war and displaced persons in northern Uganda.
In the 1998 review [ 157 ], only the trial by Brent and colleagues [ 114 ] applied an FT protocol, which was inferior to CBT and did not differ from NDST; therefore, it was an experimental treatment. The 2008 review [ 158 ] included two new trials. In the first trial, attachment-based FT [ 119 ] was shown to be superior to WL, but in the second trial, psychoeducation-based FT [ 37 ] did not differ significantly from TAU; thus, FT was rated to be an experimental treatment. The 2016 review [ 159 ] incorporated two new trials [ 51 , 69 ], plus a third one [ 43 ] in which they analyzed childhood depression. The two adolescent trials, one by Diamond and colleagues [ 51 ] and one by Rohde and colleagues [ 69 ], failed to find a significant reduction in depressive symptoms between FT and control conditions; thus, it did not change the possibly efficacious status.
In the current review, we excluded seven of the ten FT trials identified because the samples did not meet our inclusion criteria. In the trial by Sanford and colleagues [ 37 ], not all adolescents met criteria for MDD; the trial by Trowell and colleagues [ 43 ] involved children and adolescents with a mean age of less than 12 years; the trial by Connell and Dishion [ 45 ] included high-risk adolescents based on parent and teacher reports of emotional or behavioral problems. Participants in the trial by Diamond and colleagues [ 51 ] had suicidal ideation and a major depressive episode, anxiety, attention deficit hyperactivity disorder, oppositional defiant or conduct disorders. Horigian and colleagues [ 62 ] included participants who were in substance use treatment and had symptoms of depression and anxiety. Rohde and colleagues [ 69 ] studied adolescents with comorbid substance abuse and depressive disorders. In the sample of Diamond and colleagues [ 104 ], participants were adolescents with suicidal ideation and depressive or anxiety disorders. Although in the trials by Sanford and colleagues [ 37 ] and Rohde and colleagues [ 69 ], a significant percentage of the adolescents had a depressive disorder 71% and 72%, respectively, there was no significant difference in depression measures between FT and the groups with which they were compared. Disparate results were obtained in the four trials included in the current review. In the two trials of Diamond’s team, FT was superior to TAU [ 128 ] and WL [ 119 ], although in the other trials no difference was found with TAU [ 136 ] or supportive therapy, and FT was inferior to CBT [ 114 ]; thus, the status of FT as possibly efficacious did not change.
Of the three reviews prior to ours, only the most recent one, in 2016 [ 159 ], included a trial of PT [ 43 ], that focused on individual psychodynamic psychotherapy. PT did not differ from system integrative FT. Therefore, PT was judged to be an experimental treatment for child and adolescent depression. We excluded the study by Trowell and colleagues [ 43 ] from the present review because it included children and adolescents aged 9 to 15 years old, and therefore aligned better with other trials of treating depression in children. We did identify one new RCT [ 135 ], in which short-term PT was no more effective than either CBT, or a brief psychosocial intervention. The absence of significant differences in outcome suggests that short-term PT is only experimental treatment at this time.
In the more than thirty years since the 1986 Reynolds and Coats trial [ 13 ], a wealth of data has been accumulated on the treatment of depression in adolescents, which justifies moderate optimism about the future. In this review, we used the conservative criteria for selecting trials that involved adolescents diagnosed with depression and focused primarily on improvements in depression. Table 5 presents the categorization of each treatment for depression in adolescents based on these criteria. Thus, our results differed somewhat from previous reviews [ 157 , 158 , 159 ]. We confirmed that individual CBT and individual IPT are well-established psychological treatments for depression in adolescents; CBT reached level 1 in 1997 [ 113 , 114 ] and IPT did so years later in 2004 [ 117 , 120 ]. In contrast, group CBT, and especially group IPT, were repositioned at lower levels in our review because group application was more frequent in preventive trials. Rosselló and colleagues [ 46 ] analyzed the efficacy of individual and group formats of both therapies in a sample of 112 Puerto Rican adolescents with depressive symptoms. Both formats reduced depressive symptoms from pre- to post-treatment, 9.98 units on the Children’s Depression Inventory (CDI) [ 160 ] with the individual format ( d = 1.30) and 7.33 units ( d = 1.22) with the group format. Similarly, in CBT, the reduction in depressive symptoms on the CDI was 10.58 units ( d = 1.50), and for IPT it was 6.9 units ( d = 1.33). CBT showed significantly greater improvement than IPT in depressive symptoms, self-concept, and internalizing and externalizing problems. In contrast, there was no statistical difference between the individual and group formats in any of the outcomes assessed. Clinical improvement, defined as a cut-off score of 12 on the CDI, was similar for both therapies: 62% in CBT and 57% in IPT.
Evidence base for adolescent depression treatment.
Review | Level 1 Well-Established | Level 2 Probably Efficacious | Level 3 Possibly Efficacious | Level 4 Experimental | Level 5 Questionable Efficacy |
---|---|---|---|---|---|
1998 | Group CBT | Individual IPT FT | |||
2008 | Group CBT Individual IPT | Individual CBT | Group IPT FT | ||
2016 | Individual CBT Group CBT Individual IPT | Group IPT | Bibliotherapy CBT FT | Technology-assisted CBT | |
Current | Individual CBT Individual IPT | Group CBT | FT | Bibliotherapy CBT Technology-assisted CBT Group IPT Short-term PT |
CBT = Cognitive Behavioral Therapy; FT = Family Therapy; IPT = Interpersonal Therapy; PT = Psychoanalytic Therapy.
O’Shea and colleagues [ 161 ] conducted an IPT-only trial with a sample of 39 adolescents, aged 13 to 19 years old, from the metropolitan area of Brisbane, Australia. Intention-to-treat analyses indicated a significant improvement in depression with both individual and group modalities, which was maintained at 12-months follow-up, although there was no significant difference between individual and group administration. These data suggest that group CBT and group IPT may work well, but the paucity of trials with clinical samples prevents according them superior status.
FT was upgraded from an experimental treatment to probably efficacious in 2013 [ 119 , 128 ], although this qualification should be scrutinized further in the future, because the only two trials of FT with a positive effect on adolescent depression were conducted with small samples by the same research team.
The present review is an important update due to the addition of the 2017 trial of short-term PT as an evidence-based therapy. In the IMPACT trial [ 135 ], conducted with the largest sample to date, at 36 weeks from baseline, short-term PT achieved an improvement of large magnitude ( d = 1.40), which was maintained at 86 weeks follow-up ( d = 1.77). Moreover, PT was not inferior to the improvement obtained with CBT at 36 weeks ( d = 1.70) or at 86 weeks ( d = 1.80). It will be important to replicate these findings in future randomized controlled trials, and demonstrate that the CBT and short-term PT, as conducted in this setting, are superior to an active control condition.
Thus, having treatments with demonstrated efficacy that work well for treating depression in adolescents, such as CBT and IPT, or that may be promising such as FT or short-term PT, is cause for cautious optimism. Several issues, however, limit total enthusiasm, but provide directions for continued progress in future research.
Firstly, in several trials, the improvement achieved with psychological treatments did not differ from that obtained with the control condition. An explanation for the absence of statistically significant differences could be, together with the high rate of response to placebo and spontaneous recovery from depression in adolescents, the nature of the control conditions used. For ethical reasons, WL is used less and less and, faced with the difficulty of finding a psychological placebo, TAU often is the control condition of choice. Over time, the quality of routine care provided in mental health clinics has improved considerably. Therefore, TAU should be considered more of an active treatment than a “no” or limited treatment control condition in RCTs on evidence-based therapy [ 162 ].
Secondly, a significant percentage of adolescents do not respond to treatment. Except for the trial by Esposito-Smythers and colleagues [ 137 ] with depressed adolescents with suicidal crises and concurrent risk factors, where flexible treatment was offered over one year, in the remaining 26 RCTs reviewed here, the response rate at post-treatment ranged from 27% to 29% in FT [ 128 , 136 ], to 86% to 89% in CBT and IPT [ 112 , 117 , 124 , 134 ], with an average of 60.9% across all studies. Why was a higher overall success rate not obtained? One salient predictor of poor response to treatment is comorbid anxiety disorders [ 163 , 164 , 165 ]. As such, transdiagnostic interventions are a possibly useful alternative. Ehrenreich-May and colleagues [ 91 ] implemented the Unified Protocol for the Treatment of Emotional Disorders in Adolescents (UP-A) with 51 adolescents with at least one primary diagnosis of generalized anxiety disorder (41.2%), social phobia (31.4%), major depression (21.6%) or other disorders (35.2%) and comorbid diagnoses. The core modules were: (a) knowledge of behaviors and emotions; (b) emotional awareness; (c) flexibility of thinking; (d) emotional exposure; and (e) maintenance of improvement. Additional modules included: (a) strengthening motivation; (b) coping with difficulties; and (c) parental education about the emotional adolescent. Transdiagnostic treatment significantly outperformed WL on all outcome measures at post-treatment. Sandín and colleagues [ 166 ] adapted the protocol for internet-based application (iUP-A), facilitating its implementation. Using the transdiagnostic protocol, Group Behavioral Activation Therapy (GBAT), based on live anti-avoidance exposure, Chu and colleagues [ 77 ] achieved a marginally significant reduction in the remission rate of the main diagnosis: 57.1% GBAT versus 28.6% WL.
Thirdly, specific treatment effects tend to fade over time [ 167 ]. Due to spontaneous recovery, most depressive episodes remit in 7–9 months in clinical samples [ 168 ], rather than worsening in treated adolescents. The course of depression is often chronic, with periods of remission; however, depression in adolescents is also recurrent between 46% and 63% [ 169 ]. Therefore, a relapse prevention component in the acute phase of treatment and booster sessions during the maintenance phase should be encouraged.
A fourth important question is to what degree should parents be involved in the treatment of depression in adolescents. Studies by Lewinsohn’s team [ 14 , 115 ] have not reliably shown the superiority of including parents. Spirito and colleagues [ 170 ] used a CBT protocol similar to that used in the TORDIA trial [ 126 ], with 24 dyads of adolescents with a suicidal history and a current major depressive episode and parents with a current or past major depressive episode. They hypothesized that treatment would be more effective if delivered jointly to the adolescent and parents than to the adolescent alone. The parent–adolescent group was significantly superior in reducing the depressive symptoms in both members of the dyad, especially the parents, at the end of the maintenance phase (24 weeks). There were no differences between groups at follow-up (48 weeks). Suicidal ideation was equally reduced in both groups during the acute and maintenance phases of treatment, and this improvement continued at follow-up. Interestingly, however, satisfaction with treatment was lower in the conjoint group; two adolescents were described by their therapist as oppositional and sessions with the family were needed to address parent–child conflict. Another adolescent reported abuse in the family and had to be hospitalized mid-treatment. In the absence of conclusive data and the higher cost of the involving parents in therapy, including parents in treatment of depression in adolescents needs further study and should be viewed with caution.
Additionally, the pharmacological treatment of adolescent depression is not without controversy. In 2006, Hammad and colleagues [ 171 ] conducted a meta-analysis with data from 4582 pediatric patients, who had participated in 24 trials—of which 16 dealt with MDD, including the multicenter TADS study—and reported that suicidality increased in pediatric patients treated with antidepressants by 1–3%. Consequently, the Food and Drug Administration (FDA) issued a “black box” warning about prescribing such medication to persons under 24 years of age [ 87 ]. Considering the concern raised and the response rate to antidepressants of approximately 60% [ 172 ], the first option for treating depression in adolescents will likely be psychological [ 173 ]. If the circumstances make combined treatment advisable, then the indicated drug is fluoxetine, in accordance with the indications of the U.S. FDA, the European Medicines Agency, and the Spanish Agency of Medicines and Health Products.
There is still a long way to go, but more than three decades of research have left us with two well-established and well-functioning psychological treatments for depression in adolescents: CBT and IPT. Other treatments, FT and short-term PT, require further RCTs to replicate the positive preliminary findings. Transdiagnostic protocols, delivery of therapy through information and communication technologies, and indicated prevention programs are currently expanding lines of research.
In conclusion, the first-line psychological treatments for depression in adolescents are individual CBT and individual IPT. The present review has been limited to adolescents with depressive disorders, excluding those with depressive symptoms; thus, it would be interesting to review the indicated prevention trials, especially considering that many of the excluded trials ( Table 2 ) obtained positive results.
Conceptualization, J.M., Ó.S.-H., J.G., J.P.E., and M.O.; methodology, J.M., Ó.S.-H., J.G., J.P.E., and M.O.; validation, J.M., Ó.S.-H., J.G., J.P.E., and M.O.; formal analysis, J.M., Ó.S.-H., J.G., J.P.E., and M.O.; investigation, J.M., Ó.S.-H., J.G., J.P.E., and M.O.; data curation, J.M., Ó.S.-H., J.G., J.P.E., and M.O.; writing—original draft preparation, J.M., Ó.S.-H., J.G., J.P.E., and M.O.; writing—review and editing, J.M., Ó.S.-H., J.G., J.P.E., and M.O.; visualization, J.M., Ó.S.-H., J.G., J.P.E., and M.O.; supervision, J.M., Ó.S.-H., J.G., J.P.E., and M.O.; project administration, J.M., Ó.S.-H., J.G., J.P.E., and M.O. All authors have read and agreed to the published version of the manuscript.
This research received no external funding.
Not applicable.
Data availability statement, conflicts of interest.
The authors declare no conflict of interest.
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Data were compiled from the final master file of the Québec Longitudinal Study of Child Development (1998–2019), Gouvernement du Québec, Institut de la Statistique du Québec (Quebec Institute of Statistics). Details on the scales used and scoring are found in the Methods section and Table 1. NEET indicates not being in education, employment, or training; OR, odds ratio; and SES, socioeconomic status.
a NA (not applicable) represents variables that were not kept in the final model because they did not reach statistical significance.
b Factors remaining significant ( P < .05) after applying Bonferroni adjustment.
eTable 1. MIA and SBQ Depression Symptoms Items
eFigure. Correlation Plot of All Depression Symptoms Scores
eTable 2. Comparison of Included and Excluded Participants for Each Outcome
eTable 3. Estimated Coefficients (β or OR) Associated With an Increased Risk of Reporting Impaired Adult Outcomes
eTable 4. Estimated Coefficients (β or OR) of Unadjusted and Adjusted Depression Symptoms at Every Time Point Associated With an Increased Risk of Reporting Impaired Adult Outcomes
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Psychogiou L , Navarro MC , Orri M , Côté SM , Ahun MN. Childhood and Adolescent Depression Symptoms and Young Adult Mental Health and Psychosocial Outcomes. JAMA Netw Open. 2024;7(8):e2425987. doi:10.1001/jamanetworkopen.2024.25987
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Question Are depression symptoms during childhood and adolescence associated with poor mental health and psychosocial outcomes in young adulthood?
Findings In this cohort study using a representative population-based Canadian birth cohort of 2120 infants, depression symptoms during adolescence (ages 13 to 17 years) were associated with higher levels of depression symptoms and perceived stress in early adulthood (at ages 20 and 21 years), while both middle-childhood (ages 7 to 12 years) and adolescent depression symptoms were associated with decreased social support for participants at age 21 years, independent of early risk factors. There were no associations of depression symptoms with binge drinking; not being in education, employment, or training; or experiencing online harrasment.
Meaning The findings of this study underscore the importance of screening children and adolescents for depression, which may reduce depression symptoms and compromised psychosocial functioning in young adulthood.
Importance Depression is a leading cause of disability. The timing and persistence of depression may be differentially associated with long-term mental health and psychosocial outcomes.
Objective To examine if depression symptoms during early and middle childhood and adolescence and persistent depression symptoms are associated with impaired young adult outcomes independent of early risk factors.
Design, Setting, and Participants Data for this prospective, longitudinal cohort study were from the Québec Longitudinal Study of Child Development, a representative population-based Canadian birth cohort. The cohort consists of infants born from October 1, 1997, to July 31, 1998. This is an ongoing study; data are collected annually or every 2 years and include those ages 5 months to 21 years. The end date for the data in this study was June 30, 2019, and data analyses were performed from October 4, 2022, to January 3, 2024.
Exposures Depression symptoms were assessed using maternal reports in early childhood (ages 1.5 to 6 years) from 1999 to 2004, teacher reports in middle childhood (ages 7 to 12 years) from 2005 to 2010, and self-reports in adolescence (ages 13 to 17 years) from 2011 to 2015.
Main Outcomes and Measures The primary outcome was depression symptoms at age 20 years, and secondary outcomes were indicators of psychosocial functioning (binge drinking; perceived stress; not being in education, employment, or training; social support; and experiencing online harrasment) at age 21 years. All outcomes were self-reported. Adult outcomes were reported by participants at ages 20 and 21 years from 2017 to 2019. Risk factors assessed when children were aged 5 months old were considered as covariates to assess the independent associations of childhood and adolescent depression symptoms with adult outcomes.
Results The cohort consisted of 2120 infants. The analytic sample size varied from 1118 to 1254 participants across outcomes (56.85% to 57.96% female). Concerning the primary outcome, adjusting for early risk factors and multiple testing, depression symptoms during adolescence were associated with higher levels of depression symptoms (β, 1.08 [95% CI, 0.84-1.32]; P < .001 unadjusted and Bonferroni adjusted) in young adulthood. Concerning the secondary outcomes, depression symptoms in adolescence were only associated with perceived stress (β, 3.63 [95% CI, 2.66-4.60]; P < .001 unadjusted and Bonferroni adjusted), while both middle-childhood (β, −1.58 [95% CI, −2.65 to −0.51]; P = .003 unadjusted and P < .001 Bonferroni adjusted) and adolescent (β, −1.97 [95% CI, −2.53 to −1.41]; P < .001 unadjusted and Bonferroni adjusted) depression symptoms were associated with lower levels of social support. There were no associations for binge drinking; not being in education, employment, or training; or experiencing online harrasment.
Conclusions and Relevance In this cohort study of Canadian children and adolescents, childhood and adolescent depression symptoms were associated with impaired adult psychosocial functioning. Interventions should aim to screen and monitor children and adolescents for depression to inform policymaking regarding young adult mental health and psychosocial outcomes.
Depression is a leading contributor to global disease burden. 1 A nationally representative US study of 2016 data found that 3.2% of children and adolescents (ages 3 to 17 years) were depressed and that prevalence rates tended to increase with age. 2 The timing of depression onset and symptom persistence may differentially impact an individual’s functioning. Longitudinal and meta-analytic evidence suggest that depression symptoms during adolescence are associated with mental health problems and impaired functioning in adulthood. 3 - 7
Because available studies do not often examine depression symptoms during childhood, it is not yet clear whether symptoms occurring during early (ages 1.5 to 6 years) and middle (ages 7 to 12 years) childhood and adolescence (ages 13 to 17 years) are independently associated with adult mental health and psychosocial outcomes. Additionally, focusing on 1 developmental period precludes the examination of whether individuals with persistent symptoms are at higher risk for worse outcomes later in life. This omission has implications for prioritizing the allocation of support to individuals who are most at risk. 8 Moreover, most studies focus on mental health as the primary outcome, thus overlooking the association of depression symptoms with pertinent psychosocial outcomes. 9 Therefore, it is important to examine a broad range of outcomes to understand the associations of depression symptoms with overall functioning in adulthood to inform policymaking. 9
Previous studies have investigated the associations of the timing of depression symptoms with adult outcomes. 8 , 10 A study examining trajectories of depression symptoms from ages 10.5 to 25 years found that individuals with persistent early-onset depression symptoms during adolescence were associated with poorer mental health and work and educational outcomes in early adulthood. 8 Another study found that depression during childhood and adolescence was associated with physical and mental health problems, risky behaviors, and problems in psychosocial functioning in adulthood. 10 Importantly, individuals who had adolescent-onset vs childhood-onset depression and individuals with depressive symptomatology across childhood and adolescence had worse outcomes in adulthood. 10
A limitation of the existing literature is that studies have often not considered a broad range of confounding factors. 10 Several factors, including being female, having a limited-income background, being exposed to parental psychopathology, and experiencing problematic family relationships, are known risk factors for depression symptoms and impaired adult functioning. 11 - 15 Therefore, it is important to consider these and other confounding factors to obtain an accurate estimate of the associations of childhood and adolescent depression symptoms with adult outcomes. 10
The objective of this study was to examine the associations of depression symptoms in early and middle childhood with depression symptoms (primary outcome) and psychosocial outcomes (secondary outcome) in young adulthood. Our hypothesis for the current study was that childhood and adolescent depression symptoms would be associated with primary and secondary outcomes in early adulthood, but no a priori hypotheses were made about the associations of childhood and adolescent depression symptoms on any specific adult outcome.
Data for this cohort study were drawn from the ongoing Québec Longitudinal Study of Child Development (QLSCD), a large, representative population-based birth cohort conducted by the Institut de la Statistique du Québec in Canada. The cohort in the QLSCD consisted of 2120 infants born from October 1, 1997, to July 31, 1998 (see the cohort profile for more information on the overall cohort 16 ). The end date for the data in this study was June 30, 2019. Baseline characteristics were assessed when children were aged 5 months old by trained research assistants during interviews held at participants’ homes or using mailed questionnaires. Depression symptoms during early childhood (ages 1.5 to 6 years) were reported by children’s mothers, from 1999 to 2004 and during middle childhood (ages 7 to 12 years) by teachers, from 2005 to 2010, whereas adolescent depression symptoms were self-reported by participants at ages 13, 15, and 17 years from 2011 to 2015. Adult outcomes were reported by participants at ages 20 and 21 years from 2017 to 2019 using online questionnaires. Informed written consent was obtained by all participating families (and teachers) at each assessment point. Participants consented to data collection from age 18 years onward. Ethics were approved by the health research ethics committees of the Institut de la Statistique du Québec and the Sainte-Justine Hospital Research Centre. This study adhered to the Strengthening the Reporting of Observational Studies in Epidemiology ( STROBE ) reporting guideline for standard reporting in cohort studies. 17
The primary outcome of the present study was depression symptoms assessed at age 20 years. The secondary outcomes were indicators of psychosocial functioning (binge drinking; perceived levels of stress; not being in education, employment, or training [NEET] status; social support; and experiencing online harrasment at age 21 years.
We examined the independent and joint associations of depression symptoms in early and middle childhood and adolescence with young adult outcomes. Based on prior evidence, a broad range of covariates were adjusted for in the analyses. The early-childhood depression symptoms were reported when children were 1.5, 2.5, 3.5, 4.5, and 5, and 6 years of age, and middle-childhood symptoms when children were aged 7, 8, 10, and 12 years using items from the Social Behavior Questionnaire (SBQ 18 ). The SBQ integrates items from the Rutter Children’s Behaviour Questionnaire, 19 the Child Behavior Checklist, 20 the Ontario Child Health Study scales, 21 and the Preschool Behavior Questionnaire. 22 Mothers and teachers ranked the frequency with which children experienced different dimensions of depression (eg, unhappy, sad, or depressed or lacked energy) on a scale from 0 (never) to 2 (often), with higher scores indicating more depression. Given our focus on depression symptoms, we used 5 SBQ items that were similar to the items used to assess depression in adolescence (ages 13-17 years) and young adulthood (ages 18-24 years) (eTable 1 in Supplement 1 ). The internal consistency of these items ranged from 0.19 (95% CI, 0.14-0.25) to 0.63 (95% CI, 0.60-0.65).
To create childhood depression variables, we first calculated the mean scores, separately, of mother-reported and teacher-reported depression symptoms. To account for variation in the measures used to assess depression symptoms across developmental periods, we identified children in the top quintile of mother-reported and teacher-reported depression symptom scores. These variables were used as binary indicators of early-childhood (mother-reported) and middle-childhood (teacher-reported) depression symptoms, in which 1 indicated children rated in the top quintile of depression symptoms by mothers and teachers, respectively, and 0 indicated all other children.
Adolescents self-reported their depression symptoms using the SBQ at age 13 years and at ages 15 and 17 years (α = 0.90), using the Mental Health and Social Inadaptation Assessment for Adolescents. 23 We first calculated the mean of depression symptoms at ages 15 and 17 years using the Mental Health and Social Inadaptation Assessment for Adolescents and then identified participants in the top quintile of this mean score. We then identified participants in the top quintile of depression symptoms at age 13 years. The final variable was binary, with 1 indicating adolescents rated in the top quintile of depression symptoms at ages 13 or 15 and 17 years and 0 indicating all other children. To examine correlations between depression scores reported by different informants across different ages, we used the Spearman correlation coefficient. This test was used due to the nonnormal distribution of depression scores.
Outcomes in young adulthood were self-reported only at ages 20 and 21 years. At age 20 years, participants reported their depression symptoms using the Center for Epidemiologic Studies Depression (CES-D) scale, 24 a validated and widely used measure of depression symptoms in adults. Psychosocial outcomes were reported at age 21 years. Perceived levels of stress in the past month were assessed using the Perceived Stress Scale. 25 Social support was assessed using the validated short version of the Social Provisions Scale. 26 Experiencing online harrasment was assessed using a single item asking about the frequency (never, once, sometimes, often, or very often) with which the participant had been harrased (eg, insults, threats) over the internet or by telephone in the past year. We created a binary variable with 1 for participants who indicated being harrased at least once and 0 otherwise. Binge drinking was also assessed with a single item asking how often participants had consumed 4 (for females) or 5 (for males) or more drinks on a single occasion in the past year. Participants’ NEET status was determined using 2 items asking about their current studies and employment. Participants who indicated that they were not in school, in training, or employed were classified as NEET.
We searched previous literature for variables that could confound associations between depression symptoms and each of the adult outcomes. Different covariates were used in different models, as each outcome was included in a separate model. All of the following covariates were assessed at baseline when children were aged 5 months old: family socioeconomic status (derived from parental educational and occupational status and household income), maternal and paternal depression symptoms (based on the CES-D scale 24 ) and antisocial behavior in their adolescence and adulthood (assessed with 5 binary questions on conduct problems based on Diagnostic and Statistical Manual of Mental Disorders [Fourth Edition] 27 criteria), maternal employment status, maternal substance use during pregnancy (ie, tobacco, alcohol, or an illegal drug), in-home observations of mother and child interactions (stimulation and verbalization) using the Home Observation Measurement of the Environment, 28 self-reported maternal and paternal parenting practices (self-efficacy, reactive hostility, overprotection, affection, warmth, and parental impact) using the Parental Cognitions and Conduct Toward the Infant Scale, 29 and the child’s sex. Family functioning was assessed using the Family Dysfunction Scale, in which scores range from 0 to 10.00, with higher scores indicating higher levels of family dysfunction. 30
Data analysis was performed from October 4, 2022, to January 3, 2024. We estimated the association of early and middle childhood and adolescent depression symptoms with each adult outcome in separate regression models that were adjusted for the relevant covariates. Linear regression models were used for continuous outcomes (depression, perceived stress, and social support) and logistic regressions for binary outcomes (experiencing online harrasment, binge drinking, and NEET status). We also tested the interactions of depression symptoms in early childhood, middle childhood, and adolescence in each model. The interactions between depression symptoms in early childhood and at other time points were not significant and were therefore dropped from the models. Given the use of multiple testing, we present both the unadjusted and adjusted (Bonferroni-corrected) P values for all models; the Bonferroni correction was used for the final model of each outcome. A 2-sided P < .05 was considered significant.
Participants were included in analyses if they had available data for at least 1 time point for depression symptoms in early or middle childhood and adolescence and 1 adult outcome. The excluded and analytic samples significantly differed in baseline characteristics; we therefore used inverse probability weighting, in which weights represent the probability of being included in an analytic sample, in all analyses. 31 The comparison of each analytic sample with the excluded sample on the variables used for weighting is presented in eTable 2 in Supplement 1 . Missing data for covariates, ranging from 4.89% to 5.19% depending on the sample, were handled using multiple imputation by a chained equation (n = 50 imputed datasets). Statistical analyses were performed using R, version 4.2.3 (R Project for Statistical Computing). 32
Among the 2120 infants in the cohort, the analysis sample size varied from 1118 to 1254 across outcomes and included 648 to 713 females (56.85% to 57.96%) and 470 to 541 males (42.04% to 43.14%) ( Table 1 ). Participants who experienced high depression symptoms in adolescence were more likely to experience depression symptoms in young adulthood (β, 1.08 [95% CI, 0.84-1.32]; P < .001 unadjusted and Bonferroni adjusted) and to report higher levels of perceived stress (β, 3.63 [95% CI, 2.66-4.60]; P < .001 unadjusted and Bonferroni adjusted) after adjusting for covariates ( Figure and eTable 3 in Supplement 1 ). Depression symptom scores were created in the cohort of 2120 infants, including the mean, SD, range, and cutoff scores for children and adolescents in the top quintile in each developmental period (early childhood: mean [SD] score, 1.18 [0.87; range, 0-7.14]; middle childhood: mean [SD] score, 1.88 [1.54; range, 0-10.00]; adolescence: mean [SD] score, 3.62 [2.08; range, 0-10.00]) ( Table 2 ). The correlations between depression scores across different ages are presented in the eFigure in Supplement 1 . Depression symptoms’ correlation coefficients were greater when reported by the same informant compared with coefficients between informants.
High depression symptoms in middle childhood were not associated with higher levels of depression symptoms (β, 0.43 [95% CI, −0.03 to 0.90]; P = .07) and perceived stress (β, 1.90 [95% CI, 0.03-3.77]; P = .05) in young adulthood; these results remained nonsignificant after adjusting for multiple testing (depression symptoms: β, 0.43 [95% CI, −0.03 to 0.90]; P = .11 and perceived stress: β, 1.90 [95% CI, 0.03-3.77]; P = .10) (eTable 3 in Supplement 1 ). A similar pattern was observed between high depression symptoms in adolescence and NEET status in young adulthood, in which the statistical significance (β, 2.46 [95% CI, 1.09-5.56]; P = .03) did not survive the Bonferroni correction ( P = .06) (eTable 3 in Supplement 1 ).
The only outcome with which high depression symptoms in middle childhood and adolescence were associated was social support ( Figure and eTable 3 in Supplement 1 ). Participants in middle childhood (β, −1.58 [95% CI, −2.65 to −0.51]; P = .003 unadjusted and P < .001 Bonferroni adjusted) and adolescents (β, −1.97 [95% CI, −2.53 to −1.41]; P < .001 unadjusted and Bonferroni adjusted) who experienced more depression symptoms reported lower levels of social support in young adulthood. The interaction between high depression symptoms in middle childhood and adolescence was not significant, suggesting that the independent associations of depression symptoms in each period were more relevant than the cumulative experience of high depression symptoms ( Figure and eTable 3 in Supplement 1 ). We found no association between high depression symptoms across developmental periods with any outcome. The experience of high depression symptoms across (early and middle) childhood and adolescence was not associated with binge drinking, NEET status, or experiencing online harrasment ( Figure and eTable 3 in Supplement 1 ). To test whether the associations of depression symptoms with adult outcomes were mediated by depression symptoms at a later point, we conducted simple regression analyses between depression symptoms in each developmental period and adult outcomes to ensure that the impact of childhood depression symptoms was not overshadowed by later depression symptoms (eTable 4 in Supplement 1 ). As almost all of the results were not significant, it appeared that the association of childhood depression symptoms with adult outcomes was not masked by later depression symptoms, and therefore, we did not test mediation models.
In this cohort study using prospective longitudinal data from children, adolescents, and adults aged 1.5 to 21 years, we found that depression symptoms during adolescence were associated with increased depression symptoms at age 20 years and perceived stress at age 21 years, adjusting for covariates and multiple testing. Additionally, depression symptoms during adolescence were associated with compromised psychosocial outcomes at age 21 years, but the result was nonsignificant after correcting for multiple testing. Social support was the only outcome for which depression symptoms during middle childhood and adolescence had an association that persisted after adjusting for covariates and multiple testing. Depression symptoms were not associated with experiencing online harrasment, NEET status, or binge drinking.
Being in the top quintile of depression symptoms in adolescence was associated with a 1-point increase on the CES-D scale, an association that corresponds with a medium effect size (Cohen d = 0.5) and is thus relevant from a population and clinical perspective. These findings provide some support for the stability of depression symptoms and are consistent with previous research suggesting that depression symptoms during adolescence increase the risk of mental health problems in emerging adulthood. 7 Additionally, in our study, young adults who experienced depression symptoms during adolescence self-reported increased perceived stress at age 21 years, independent of early risk factors. One explanation for this finding is that the experience of depression symptoms may have contributed to cognitive vulnerabilities and the perception of events as more stressful. Alternatively, it could be that young adults may have experienced stressful life circumstances at the time of the assessment or that structural or social determinants not captured at birth may have contributed to depression symptoms. 33 - 35 Notably, these results were not significant for childhood depression symptoms, suggesting that the associations were confined to adolescent depression symptoms. However, it is worth mentioning that adolescence and adult depression symptoms were measured with self-reports, which may have reflected common rater bias, while early- and middle-childhood depression symptoms were measured with mothers’ (early childhood) and teachers’ (middle childhood) reports, which may have reflected measurement and rater difference. 36
The experience of depression symptoms in middle childhood and adolescence was associated with decreased social support at age 21 years. There were no significant interactions, suggesting that the independent associations of depression symptoms in each developmental period were more relevant than the cumulative experience of high depression symptoms. This finding is consistent with a previous study’s finding that adolescent depression symptoms were associated with lower social support in early adulthood 37 and adds to the existing literature by showing that the experience of depression symptoms during middle childhood (ages 7 to 12 years) may be independently associated with diminished social support. This is a concerning finding, as it implies that young adults may go through life transitions (eg, family and career) without adequate social support. 38 Similarly, they may be reluctant to access support provided by health services. 37 , 38 Future research should examine why this occurs and if the associations of childhood vs adolescent depression with social support have distinct environmental and genetic causes.
While no firm conclusions can be made about the timing (childhood vs adolescence) of depression symptoms and its prospective associations with adult outcomes, it appears that depression symptoms during adolescence were associated with a broader range of adult outcomes (depression symptoms, perceived stress, and social support) compared with depression symptoms during childhood (social support only). There was no evidence that individuals with persistently elevated depression symptoms relative to peers had worse adult outcomes. Except for social support, young adults whose depression symptoms did not persist beyond childhood showed no other impairments, suggesting that it was depression symptoms in adolescence that were associated with adult outcomes. However, this finding should be interpreted with caution because the association may be an artifact of the fact that depression symptoms were reported by different informants at different ages with different measures. 36
The onset and course of depression symptoms were not captured in this study. Future studies should examine trajectories of depression symptoms and their prospective associations with adult outcomes. Moreover, the overall low internal consistency of depression items in early childhood, reported by mothers and teachers, has to be considered, as it indicates a potential lack of validity of depression measures. There were no data on whether participants were treated with antidepressant medication or psychological therapy, which may have impacted depression symptoms and adult outcomes. Exposure variables during adolescence and outcomes in early adulthood were assessed using self-reports, which may have inflated associations between variables (eg, individuals experiencing depression being more vulnerable to negative self-perceptions). 39 , 40 However, different reporters (mothers, teachers) were used to measure depression symptoms across childhood, and self-reports are reliable for internalizing problems. 41 , 42
The findings have implications for mental health interventions. It is of clinical importance to identify children and adolescents experiencing depression early to decrease depression symptoms and prevent compromised functioning. Our findings suggest that mental health interventions including interpersonal/social components may improve psychosocial functioning in adulthood. Furthermore, some of the early risk factors we considered showed associations with adverse adult outcomes. Thus, mental health interventions that address exposure to early adversity or trauma could be beneficial to children and adolescents experiencing depression symptoms. 43 Last, mental health interventions should identify and monitor children and adolescents experiencing subclinical symptoms as our findings suggest that individuals who had increased depression symptoms during childhood or adolescence experienced adverse outcomes in young adulthood.
The findings of this cohort study suggest that both childhood and adolescent depression symptoms may be associated with adverse psychosocial outcomes, while adolescent depression symptoms were associated with depression symptoms and perceived stress in young adulthood independent of early risk factors. Interventions should aim to screen and monitor children and adolescents for depression to inform policymaking regarding young adult mental health and psychosocial outcomes.
Accepted for Publication: May 21, 2024.
Published: August 8, 2024. doi:10.1001/jamanetworkopen.2024.25987
Open Access: This is an open access article distributed under the terms of the CC-BY License . © 2024 Psychogiou L et al. JAMA Network Open .
Corresponding Author: Marilyn N. Ahun, PhD, Department of Medicine, Faculty of Medicine and Health Sciences, McGill University, 5252 Boulevard de Maisonneuve, Montréal, H4A 3S5, Quebec, Canada ( [email protected] ).
Author Contributions: Drs Navarro and Ahun had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis. Drs Psychogiou and Navarro were co–first authors.
Concept and design: Psychogiou, Navarro, Côté, Ahun.
Acquisition, analysis, or interpretation of data: All authors.
Drafting of the manuscript: Psychogiou, Ahun.
Critical review of the manuscript for important intellectual content: Navarro, Orri, Côté, Ahun.
Statistical analysis: Navarro, Orri, Ahun.
Obtained funding: Côté.
Administrative, technical, or material support: Côté.
Conflict of Interest Disclosures: None reported.
Funding/Support: The Québec Longitudinal Study of Child Development (QLSCD) was supported by funding from the Ministère de la Santé et des Services Sociaux, the Ministère de la Famille, Ministère de l’Éducation et de l’Enseignement Supérieur, the Lucie and André Chagnon Foundation, the Institut de Recherche Robert-Sauvé en Santé et en Sécurité du Travail, the Research Centre of the Sainte-Justine University Hospital, the Ministère du Travail, de l’Emploi et de la Solidarité Sociale, and the Institut de la Statistique du Québec. Additional funding was received by the Fonds de Recherche du Québec-Santé, the Fonds de Recherche du Québec-Société et Culture, the Social Science and Humanities Research Council of Canada, and the Canadian Institutes of Health Research.
Role of the Funder/Sponsor: The funders had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication.
Data Sharing Statement: See Supplement 2 .
Additional Contributions: We are grateful to the children and parents of the QLSCD and the participating teachers and schools.
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Molecular Psychiatry volume 27 , pages 315–327 ( 2022 ) Cite this article
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Depression onset peaks during adolescence and young adulthood. Current treatments are only moderately effective, driving the search for novel pathophysiological mechanisms underlying youth depression. Inflammatory dysregulation has been shown in adults with depression, however, less is known about inflammation in youth depression. This systematic review identified 109 studies examining the association between inflammation and youth depression and showed subtle evidence for inflammatory dysregulation in youth depression. Longitudinal studies support the bidirectional association between inflammation and depression in youth. We hypothesise multiple inflammatory pathways contributing to depression. More research is needed on anti-inflammatory treatments, potentially tailored to individual symptom profiles.
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This work was funded by a Wellcome Trust Mental Health Priority Area ‘Active Ingredients’ commission awarded to LS at Orygen. LS is supported by a NHMRC Career Development Fellowship (1140764), and the Dame Kate Campbell Fellowship from the Faculty of Medicine, Dentistry and Health Sciences at The University of Melbourne. CGD is supported by an NHMRC Career Development Award (141738). MB is supported by a NHMRC Senior Principal Research Fellowship (1156072). FL is supported by ZonMw: The Netherlands Organisation for Health Research and Development (project number: 636310017).
These authors contributed equally: Yara J. Toenders, Liliana Laskaris.
Orygen, Parkville, VIC, Australia
Yara J. Toenders, Liliana Laskaris, Michael Berk & Lianne Schmaal
Centre for Youth Mental Health, The University of Melbourne, Parkville, VIC, Australia
Department of Psychiatry, The University of Melbourne, Melbourne, VIC, Australia
Christopher G. Davey & Michael Berk
IMPACT—the Institute for Mental and Physical Health and Clinical Translation, School of Medicine, Barwon Health, Deakin University, Geelong, VIC, Australia
Michael Berk
Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville, VIC, Australia
Department of Psychiatry, Amsterdam UMC, Department of Amsterdam Public Health Research Institute and Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam, Netherlands
Yuri Milaneschi, Femke Lamers & Brenda W. J. H. Penninx
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The literature search was conducted by YJT and LL, and this process was supervised by LS. All authors contributed to writing and reviewing of the paper.
Correspondence to Lianne Schmaal .
Competing interests.
MB is a co-inventor of two provisional patents regarding the use of NAC and related compounds for psychiatric indications, which, while assigned to the Mental Health Research Institute, could lead to personal remuneration upon a commercialisation event. MB has served as a speaker for Astra Zeneca, Bristol Myers Squibb, Eli Lilly, Glaxo SmithKline, Janssen Cilag, Lundbeck, Merck, Pfizer, Sanofi Synthelabo, Servier, Solvay, and Wyeth; and has served as a consultant to Astra Zeneca, Bristol Myers Squibb, Eli Lilly, Glaxo SmithKline, Janssen Cilag, Lundbeck Merck, and Servier. BP has received (non-related) research funding from Jansen Research and Boehringer Ingelheim. The other authors report no competing interests.
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Toenders, Y.J., Laskaris, L., Davey, C.G. et al. Inflammation and depression in young people: a systematic review and proposed inflammatory pathways. Mol Psychiatry 27 , 315–327 (2022). https://doi.org/10.1038/s41380-021-01306-8
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DOI : https://doi.org/10.1038/s41380-021-01306-8
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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.
Understanding depression in adolescents: a dynamic psychosocial web of risk and protective factors.
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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.
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 ).
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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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Department of Psychology, University of Illinois Urbana Champaign, 603 E. Daniel Street, Champaign, IL, 61820, USA
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For this review and position paper, Benjamin L. Hankin developed the primary ideas, conducted literature searches, wrote the first manuscript draft, and revised the work. Julianne M. Griffith conducted literature searches, and wrote and revised the work. Both authors read and approved the final manuscript.
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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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DOI : https://doi.org/10.1007/s10567-023-00437-4
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SHELLEY S. SELPH, MD, MPH, AND MARIAN S. MCDONAGH, PharmD
Am Fam Physician. 2019;100(10):609-617
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The prevalence of major unipolar depression in children and adolescents is increasing in the United States. In 2016, approximately 5% of 12-year-olds and 17% of 17-year-olds reported experiencing a major depressive episode in the previous 12 months. Screening for depression in adolescents 12 years and older should be conducted annually using a validated instrument, such as the Patient Health Questionnaire-9: Modified for Teens. If the diagnosis is confirmed, treatment should be initiated for persistent, moderate, and severe depression. Active support and monitoring may be sufficient for mild, self-limited depression. For more severe depression, evidence indicates greater response to treatment when psychotherapy (e.g., cognitive behavior therapy) and an antidepressant are used concurrently, compared with either treatment alone. Fluoxetine and escitalopram are the only antidepressants approved by the U.S. Food and Drug Administration for treatment of depression in children and adolescents. Fluoxetine may be used in patients older than eight years, and escitalopram may be used in patients 12 years and older. Monitoring for suicidality is necessary in children and adolescents receiving pharmacotherapy, with frequency of monitoring based on each patient's individual risk. The decision to modify treatment (add, increase, change the medication or add psychotherapy) should be made after about four to eight weeks. Consultation with or referral to a mental health subspecialist is warranted if symptoms worsen or do not improve despite treatment and for those who become a risk to themselves or others.
The prevalence of depression is increasing among youth in the United States. The 2005 to 2014 National Surveys on Drug Use and Health, which included 172,495 adolescents 12 to 17 years of age, found that the percentage of adolescents who experienced one or more major depressive episodes in the previous 12 months increased from 9% in 2005 to 11% in 2014. 1 In 2016, this percentage was approximately 13% (5% in 12-year-olds, 13% in 14-year-olds, and 17% in 17-year-olds), and although 70% of youths experienced severe impairment from depression, only about 40% received treatment. 1 Treatment rates have changed little since 2005, raising concern that adolescents are not receiving needed care for depression. 1
, | Recommendation from evidence-based guidelines | |
– | Evidence from response in placebo arms of trials and recommendation from consensus guidelines | |
, – | Consistent evidence from several randomized trials | |
, – | Evidence from several randomized trials and systematic reviews |
Increased risk of depression in children and adolescents may be due to biologic, psychological, or environmental factors ( Table 1 ) . 2 – 34 In children 12 years and younger, depression is slightly more common in boys than in girls (1.3% vs. 0.8%). 35 However, after puberty, adolescent girls are more likely to experience depression. 35
Being overweight Chronic illness (e.g., lupus, diabetes mellitus, asthma) – Early puberty (girls) Family history of depression Female sex , High-functioning autism , LGBTQ identified Polymorphisms in the serotonin, dopamine, or monoamine oxidase genes | Body dissatisfaction and early dieting , , ; sweetened beverage consumption Dysfunctional emotional regulation Internet gaming disorder or video game addiction , Less attachment to parents and peers, or problems with peers – , Low self-esteem and lack of self-kindness , Negative thinking and recall styles , Other mental health and behavior problems, including previous depression and cannabis or tobacco use – , , Problematic use of social media (e.g., Facebook) Worried about school grades or standardized testing | Academic difficulties Being victimized or bullied or witnessing violence , , , ; physical, sexual, or emotional abuse or neglect , Exposure to natural disasters , Few opportunities for physical activity and sports ; low physical activity ; greater than two hours per day of leisure-time screen use Foreign born or perceived discrimination , Loss of a loved one Low socioeconomic status , , , Parental rejection or low parental involvement , , Poor family functioning or caretaker depression , , |
The U.S. Preventive Services Task Force (USPSTF) recommends screening children and adolescents 12 to 18 years of age for major depressive disorder with adequate systems in place to ensure accurate diagnosis, effective treatment, and appropriate follow-up. 36 The American Academy of Family Physicians supports the USPSTF recommendation. 37 In 2018, the American Academy of Pediatrics endorsed the Guidelines for Adolescent Depression in Primary Care (GLAD-PC), which recommends screening adolescents 12 years and older annually for depressive disorders using a self-report screening tool. 38 , 39
There are various instruments to screen adolescents for depression. One popular instrument for use in primary care is the Patient Health Questionnaire-9: Modified for Teens (also called PHQ-A) for patients 11 to 17 years of age. The PHQ-A is shown in Figure 1 and Table 2 , along with four questions not used in scoring that address suicidality, dysthymia, and severity of depression. 40 , 41
Scoring is easy but involves thinking about several different aspects of depression. | |
To use the PHQ-9 as a diagnostic aid for major depressive disorder: answers are needed. | |
To use the PHQ-9 to screen for all types of depression or other mental illness: answers should be followed by a clinical interview. | |
To use the PHQ-9 to aid in the diagnosis of dysthymia: | |
To use the PHQ-9 to screen for suicide risk: | |
To use the PHQ-9 to obtain a total score and assess depressive severity: | |
0 to 4 | No or minimal depression |
5 to 9 | Mild depression |
10 to 14 | Moderate depression |
15 to 19 | Moderately severe depression |
20 to 27 | Severe depression |
The presenting sign of major depressive disorder may be insomnia or hypersomnia; weight loss or gain; difficulty concentrating; loss of interest in school, sports, or other previously enjoyable activities; increased irritability; or feeling sad or worthless. 42 To distinguish between normal grief, such as after the loss of a loved one, and a major depressive episode, it may be helpful to determine whether the predominant symptom is a sense of loss or emptiness (more typical of grief) vs. a persistent depressed mood with the inability to anticipate future enjoyable events (more typical of depression). 42
When a child or adolescent screens positive using a formal screening tool, such as the PHQ-A, or when he or she presents with symptoms indicating a possible depressive disorder, the primary care physician should assess whether the symptoms are a result of a major depressive episode or another condition that could present with similar symptoms. To diagnose major depressive disorder, criteria from the Diagnostic and Statistical Manual of Mental Disorders , 5th ed. (DSM-5), must be met and not explained by substance abuse, medication use, or other medical or psychological condition. 42 The full DSM-5 criteria are available at https://www.aafp.org/afp/2018/1015/p508.html#afp20181015p508-t6 . Some children may develop a cranky mood or irritability rather than sadness.
Medical conditions that may present similarly to depression include hypothyroidism, anemia, autoimmune disease, and vitamin deficiency. Laboratory tests that may be helpful in ruling out common medical conditions that could be mistaken for depression include complete blood count; comprehensive metabolic profile panel; an inflammatory biomarker, such as C-reactive protein or erythrocyte sedimentation rate; thyroid-stimulating hormone; vitamin B 12 ; and folate.
Other psychological conditions that may present similarly to major depressive disorder include persistent depressive disorder (also called dysthymia) and disruptive mood dysregulation disorder. If a child or adolescent has a depressed mood for more days than not for at least one year, the diagnosis may be persistent depressive disorder, which is often treated the same as a major depressive episode (e.g., antidepressants, psychotherapy). 42 If a child or adolescent is predominantly angry with temper outbursts, the diagnosis may be disruptive mood dysregulation disorder or posttraumatic stress disorder. 42
Symptoms of bipolar disorder, eating disorders, and conduct disorders may also overlap with major depressive disorder. Children and adolescents may have more than one psychiatric diagnosis concurrently, such as comorbid depression and anxiety. According to the Centers for Disease Control and Prevention, 74% of children three to 17 years of age who have depression also have anxiety, and 47% of children with depression also have a behavior problem. Therefore, a thorough assessment is needed, with possible mental health consultation or referral.
Suicide is the second leading cause of death for people 10 to 24 years of age after unintentional injury. 43 Depression is a risk factor for suicide, but at-risk youth can be easily missed without specific suicide screening. In one study, nurses in a pediatric emergency department used the Ask Suicide-Screening Questions (ASQ) tool to assess suicide risk in 970 adolescents who presented with psychiatric problems. 44 Of those who screened positive, 53% did not present with suicide-related problems. The sensitivity and specificity for a return visit to the emergency department because of suicidality within six months were 93% and 43%, respectively, for a positive predictive value of 10% and a negative predictive value of 99%. 44 The ASQ screening test is shown in Figure 2 . 45 The complete ASQ toolkit is available at https://www.nimh.nih.gov/research/research-conducted-at-nimh/asq-toolkit-materials/index.shtml#outpatient .
The GLAD-PC guidelines recommend that primary care physicians counsel families and patients about depression and develop a treatment plan that includes setting specific goals involving functioning at home, at school, and with peers. 38 For example, a treatment plan might include treating others with respect, attending family meals, keeping up with schoolwork, and spending time in activities with supportive peers. Additionally, a safety plan should be established that limits access to lethal means, such as removing firearms from the home or locking them up. It should also provide a way for the patient to communicate during an acute crisis (e.g., providing phone numbers for people to contact if suicidal thoughts occur, creating a list of coping skills, educating the parents on how to recognize if the patient is a risk to self or others). 38 If the danger of suicide becomes imminent, psychiatric evaluation in a hospital emergency department or psychiatry crisis clinic is needed.
For mild depression, which may be short-lived, primary care physicians should consider active support such as counseling about depression and treatment options, facilitating caregiver/patient depression self-management, and monitoring the patient every week or two for six to eight weeks before initiating pharmacotherapy and/or psychotherapy. 46 – 50 According to the DSM-5, although the symptoms of mild depression are distressing, they are manageable and result in only minor impairment in functioning, whereas severe depression causes more seriously distressing, unmanageable symptoms that greatly impact functioning. See Figure 3 for a suggested approach to the management of depression in children and adolescents. 43 , 50
Treatment options for children and adolescents with depression include psychotherapy and anti-depressants. Cognitive behavior therapy (CBT) is a form of talk therapy that focuses on changing behaviors by correcting faulty or potentially harmful thought patterns and generally includes five to 20 sessions. Whereas CBT focuses on cognition and behaviors, interpersonal psychotherapy concentrates on improving interpersonal relationships and typically includes around 12 to 16 sessions.
Fluoxetine (Prozac) and escitalopram (Lexapro) are the only two medications approved by the U.S. Food and Drug Administration to treat major depressive disorder in children and adolescents. Fluoxetine is approved for patients eight years and older, and escitalopram is approved for patients 12 years and older. There are concerns of increased suicidality with the use of fluoxetine and escitalopram in this population. 51 Although there were no suicides in trials of children and adolescents taking antidepressants, suicidal thoughts and behaviors were increased compared with placebo (4% vs. 2%). 51 Children and adolescents who are taking these medications should be monitored for suicidality. The frequency of monitoring should be based on the individual patient's risk (e.g., weekly monitoring at treatment onset, monthly monitoring in a child showing steady improvement on antidepressants).
Three systematic reviews of randomized controlled trials including children and adolescents with major depressive disorder support the use of fluoxetine as the first-line antidepressant medication. 52 – 54 Two reviews also support the use of escitalopram as initial therapy. 52 , 54 However, the effects of fluoxetine and escitalopram as monotherapy were often similar to placebo, depending on the outcome measured. Tricyclic antidepressants, other selective serotonin reuptake inhibitors, and serotonin-norepinephrine reupta ke inhibitors have not been shown to be effective in treating depression in children and adolescents. 46 , 52 – 54 If neither fluoxetine nor escitalopram is effective and antidepressant therapy is desired, referral to a child or adolescent psychiatrist is recommended.
Evidence is mixed for the use of CBT as monotherapy in children and adolescents with depression. A systematic review for the USPSTF found no benefit of CBT on remission or recovery and inconsistent effects on symptoms, response, and functioning. 54 One trial of youth with major depression who declined antidepressants found that compared with self-selected treatment as usual, 12 weeks of CBT was associated with shorter time to treatment response and remission and improved depression scores through week 52 but not in weeks 53 to 104. 55 In children and adolescents with subclinical depression, one systematic review (19 trials) found moderate-quality evidence that CBT is associated with a small effect on depressive symptoms vs. waitlist or no treatment. 56
Evidence from a good-quality randomized trial suggests that adolescents are most likely to achieve remission with 12 weeks of combined therapy with fluoxetine and CBT (37%; number needed to treat = 4) compared with either therapy alone (23% with fluoxetine; number needed to treat = 11; 16% with CBT) or placebo (17%). 47 , 57 Suicidality declined with duration of treatment for all therapies, but the decline was less steep for fluoxetine alone (26.2% at baseline to 13.7% at week 36) vs. combination therapy (39.6% to 2.5%) and CBT alone (25.2% to 3.9%). 47 , 57
In another trial of adolescents who achieved at least a 50% decrease in depression scores following six weeks of fluoxetine treatment, those who were randomized to receive the addition of CBT to fluoxetine therapy for six months were less likely to relapse at 78 weeks compared with continued fluoxetine monotherapy (36% vs. 62%). 58
Children and adolescents with moderate or severe depression or persistent mild depression should be treated with fluoxetine or escitalopram in conjunction with CBT or other talk therapy. 47 , 57 – 59 If combination therapy is not used, monotherapy with an antidepressant or psychotherapy is recommended, although the likelihood of benefit is lower. 46 , 52 – 56
One trial found that early reassessment of depression is valuable. 43 In this study, all youth received interpersonal psychotherapy and were randomized to a four- or eight-week follow-up assessment for treatment modification. If additional treatment was needed because of inadequate response, patients were further randomized to add-on fluoxetine or more intense (twice weekly) psychotherapy. Those who were reassessed at four weeks improved the most at 16 weeks (a difference of 5.7 points on the Hamilton Rating Scale for Depression; scores on this scale can range from 0 to 58 points, with a score of 0 to 7 considered normal and a score of 20 associated with moderate depression; P < .05). Additionally, those who began add-on fluoxetine at four weeks had better posttreatment depression scores than those who began intense interpersonal psychotherapy at eight weeks, although there was no difference in global assessment scores between the two groups.
Treatment duration for talk therapy in adolescents with unipolar depression is typically six months or less, but longer treatment may be necessary. Although good evidence regarding the duration of medication treatment in adolescents with depression is lacking, the GLAD-PC guidelines recommend continuing medication for one year beyond the resolution of symptoms. 50
If a child or adolescent does not improve after initial treatment for depression, the primary care physician may add, change, or increase a medication and may consider referral for psychotherapy. Referral to a licensed mental health professional is appropriate at any point in the treatment process. However, if the depression does not improve or the child deteriorates even with treatment, consultation with or referral to a child or adolescent psychiatrist is necessary.
This article updates previous articles on this topic by Clark, et al. 60 ; Bhatia and Bhatia 61 ; and Son and Kirchner . 62
Data Sources: We conducted general and targeted searches using Essential Evidence Plus, Ovid Medline, PubMed, the Cochrane Database of Systematic Reviews, the U.S. Preventive Services Task Force, the Agency for Healthcare Research and Quality, and UpToDate, including the key words children or adolescents with depression. Search dates: November 2018 to January 2019, and September 27, 2019.
The authors thank Alycia Brown, MD, for her review of the manuscript and Ngoc Wasson, MPH, and Chandler Weeks, BS, for help with formatting the manuscript.
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People who develop depression experience a maelstrom of emotions as they struggle to understand what is happening to them. While the experience has been comparatively well documented in older adults, much less is known about the depression experience and responses of young people. In this study, we aimed to explore the experience of young people diagnosed with depression. Twenty-six young people were recruited from a youth mental health service. A qualitative interpretative design was used, incorporating semi-structured, audio-recorded interviews. Results provided four overlapping themes, reflecting the young people's difficulties in coming to terms with, and responding in self-protective, harmful and at times life-threatening ways to their depression: (1) struggling to make sense of their situation; (2) spiralling down; (3) withdrawing; and (4) contemplating self-harm or suicide. Study conclusions are that young people faced considerable difficulties coming to terms with, and responding to, depression. Improving young people's understanding of depression and its treatment, reducing community stigma and providing accessible and youth-focused services remain important targets for intervention. It is also important to improve mental health literacy in the community to increase awareness of depression and how mental health professionals, including nurses, respond effectively to the young person.
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Large study highlights interplay between the brain and environment in the transition to adolescence
Shanice Harris
Journal: Proceedings of the National Academy of Sciences (PNAS)
EVANSTON, Ill. --- While the mental health crisis has touched the lives of young people across a broad age spectrum, new Northwestern University research has found that the presence of difficult social environments and the absence of positive social environments predicted greater increases in depressive symptoms in youth, aged 9-11, over a two-year period. In addition to environment, left hippocampal volume amplified the social context effects, suggesting that youth with a larger left hippocampus experience greater increases in Major Depressive Disorder (MDD) symptoms in challenging social spaces.
“Our research has implications not only for future research, but we also hope it increases awareness among parents, educators, mental health professionals and policy makers,” said co-lead author Claudia Haase, associate professor of human development and social policy at Northwestern’s School of Education and Social Policy (SESP). “Over the years, the pendulum has swung back and forth between some researchers and practitioners emphasizing the role of nature and others emphasizing the role of nurture. And we have come to really appreciate that we need to look at both and their interplay together.”
The study, publishing tomorrow (September 3) in Proceedings of the National Academy of Sciences (PNAS), underscores the importance of families, peers and schools in the development of depression during adolescence, and how variation in neural structure can amplify or diminish sensitivity to their environment.
The study was first authored by Matías Martínez, doctoral student at SESP, with senior co-authors Haase and Yang Qu, associate professor of human development and social policy at SESP. Titled “Depressive symptoms during the transition to adolescence: Left hippocampal volume as a marker of social context sensitivity,” additional authors include Tianying Cai; Beiming Yang; Zexi Zhou; Stewart Shankman; and Vijay A. Mittal.
“Our study emphasizes the importance of paying attention to individual differences and how some people are more sensitive to social environments than others,” Qu said. “We should never assume that the same environment will have the same impact for everyone. There is no one size fits all.”
Since neuroscience has seen major developments over the past few years, the researchers focused on brain-based sensitivity in the development of depressive symptoms. “Previous studies have focused on physiological processes or genetic variants, but with the development of neuroscience, now we can look at how the brain can play a role in the sensitivity to environments,” Martinez said. “There's a longstanding debate on whether some individuals are more or less sensitive to environments and in this study, we focused on sensitivity to social experiences, both negative and positive.”
The results concluded that the left hippocampus — a region of the brain that is primarily associated with memory, learning and how humans experience the world around them — plays an important role in whether a person becomes depressed if they find themselves in a challenging social space. A larger hippocampus would result in an individual being better able to remember an experience or recall a memory.
“It is one of the most plastic regions of the brain,” Martinez said. “It's very responsive to the environment, especially in a person’s early years. Our findings show that this brain region is playing a role in making youth more sensitive to difficult environments and to the absence of positivity in their life experiences — leading to depression symptoms.”
That area of the brain being larger in a child could result in that child having more sensitivity to social experiences — family conflicts, primary caregiver’s depressive symptoms, peer victimization, parental warmth and prosocial school environment — into adolescence.
“Some people tend to assume that we are ‘born this way’ when it comes to the human brain. But the more we learn about the brain, the more scientists have come to understand how open and malleable our brains are, not just in infancy but across the life span,” Haase said. “Our brains can change in response to the environments we find ourselves in — and studies show that this is certainly the case for the hippocampus as a brain region.”
The researchers examined two-year longitudinal data from the Adolescent Brain Cognitive Development study. The study — one of the largest studies in the U.S. conducted by 21 research sites across the country — aims to follow a diverse sample of 11,800 kids aged 9-11 over a 10-year period to observe their cognitive, brain, social and emotional development over time.
“The ABCD study is phenomenal, and we are deeply indebted to the National Institutes of Health and all the researchers involved for making this possible, and, of course, to all the youth and their families who are participating,” Qu said. “It’s the largest long-term study of brain development and child health in the United States.”
The data revealed a stronger association between socio-experiential environments and MDD symptoms for youth with a larger left hippocampal volume and no differences in MDD symptoms between individuals with different sizes of left hippocampus at low levels of negative and high levels of positive context exposure.
What’s next
The researchers are hoping the study helps parents, teachers and policymakers better understand and support youth’s mental health during adolescence. Martinez is hoping their expanded research can better explain how children in difficult social environments adapt to their surroundings in the long term.
“The ABCD study is such a comprehensive project that will continue to follow youth development for many more years,” Martinez said. “It will be exciting to examine what the interplay between exposure to different environments, hippocampal volume and depressive symptoms looks like as our youth navigate their teenage years.”
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IMAGES
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COMMENTS
Sara, a 35-year-old married female. Sara was referred to treatment after having a stillbirth. Sara showed symptoms of grief, or complicated bereavement, and was diagnosed with major depression, recurrent. The clinician recommended interpersonal psychotherapy (IPT) for a duration of 12 weeks. Bleiberg, K.L., & Markowitz, J.C. (2008).
For a diagnosis, an adolescent must have at least 5 symptoms, which must include at least one of either of the first 2 symptoms, for at least 2 weeks. 3. Symptoms of dysthymic disorder in adolescents. Depressed or irritable mood must be present for most of the day, more days than not, for at least 1 year.
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.
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 ...
Certain profiles of depression are more com-mon in adolescence than in adulthood. Although depressed mood is the most common symptom in adolescents and adults with major depressive disorder ...
Depression can be familial, and the risk of depressive disorders extends across generations. In a multigenerational study, children with depressed parents and depressed grandparents had the ...
2. Psychological Treatments for Depression in Adolescents. The criteria for including a trial in the present review were: (a) that the mean age of participants was between 12 and 18 years old; (b) a primary diagnosis of depression; (c) randomized controlled trial; (d) valid and reliable depression assessment measures; (e) comparison of at least one psychological treatment with another ...
Key Points. Question Are depression symptoms during childhood and adolescence associated with poor mental health and psychosocial outcomes in young adulthood?. Findings In this cohort study using a representative population-based Canadian birth cohort of 2120 infants, depression symptoms during adolescence (ages 13 to 17 years) were associated with higher levels of depression symptoms and ...
Depression rates in young people have risen sharply in the past decade, especially in females, which is of concern because adolescence is a period of rapid social, emotional, and cognitive development and key life transitions. Adverse outcomes associated with depression in young people include depression recurrence; the onset of other psychiatric disorders; and wider, protracted impairments in ...
The current study is a small-scale, exploratory study, in which we carried out semi-structured interviews with six adolescents with depression entering outpatient psychotherapy in Germany. In addition to the experience of depression, we studied the expectations of therapy that will be published elsewhere ( Weitkamp, Klein, Wiegand-Grefe ...
In total, 109 studies on inflammation in youth depression were identified by our systematic literature search, including case (MDD) versus control studies, studies investigating associations ...
Background: Problem-solving training is a common ingredient of evidence-based therapies for youth depression and has shown effectiveness as a versatile stand-alone intervention in adults. This scoping review provided a first overview of the evidence supporting problem solving as a mechanism for treating depression in youth aged 14 to 24 years.
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 ...
To overcome this gap in research, we use the NIMH CAT-D cohort, a longitudinal case control study that started pre-pandemic. As part of the CAT-D study, state-of-the-art diagnostic interviews were conducted with each participant, and standardized questionnaires were administered to youths and their parents/caretakers on a regular basis.
The prevalence of major unipolar depression in children and adolescents is increasing in the United States. In 2016, approximately 5% of 12-year-olds and 17% of 17-year-olds reported experiencing ...
Background: 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 ...
Study conclusions are that young people faced considerable difficulties coming to terms with, and responding to, depression. Improving young people's understanding of depression and its treatment, reducing community stigma and providing accessible and youth-focused services remain important targets for intervention.
IPT-A is an empirically supported psychosocial intervention for adolescents suffering from a depressive episode. It is delivered as an individual psychotherapy with a minimum of parental involvement. The following case study illustrates the principal strategies and techniques of IPT-A.
In this study, we aimed to explore the experience of young people diagnosed with depression. Twenty-six young people were recruited from a youth mental health service. A qualitative interpretative design was used, incorporating semi-structured, audio-recorded interviews. Results provided four overlapping themes, reflecting the young people's ...
parental depression.[12-14] In Puerto Rican youth, nonresponse to psychotherapy for depression has been associated with lower self-concept and more internaliz-ing behavior[15] in press. This case study aims to explore variables associated with a partial or limited treatment response to CBTand illustrate the challenges
The study — one of the largest studies in the U.S. conducted by 21 research sites across the country — aims to follow a diverse sample of 11,800 kids aged 9-11 over a 10-year period to observe their cognitive, brain, social and emotional development over time.
case study #1: the depressed teen 9 to provide emotional support to youth and their families. Positive social relationships outside one's immediate family are a protective factor against developing emotional problems like depression in at-risk youth (Huntley and Phelps, 1990). treatMent by Mental health specialists
This case study provides further support to the recommendations mentioned above that investigators have offered along this line in the treatment of youth depression. 2, 7, 9, 32, 33 Also, identifying the characteristics associated with treatment response in the initial stages of treatment can help inform treatment planning in terms of selection ...
Background: Tall ship sail training, a form of outdoor adventure education, has historically been used with youth to build competency in seamanship and social and emotional skills. However, there is a void in the literature documenting precise program models connected to specific goals. Purpose: This paper presents a case study of the Shenandoah Model of sail training.
A plan aiming to streamline clinical trial reporting procedures in some circumstances is now out for consultation. Medsafe is seeking public feedback on a series of proposed updates to the regulatory guidelines for people conducting clinical trials for medicines and medical devices.