Abstract
Objective
The bidirectional relationships between family functioning and adolescent depressive and anxiety disorders have been documented. However, categorical diagnostic criteria for these disorders often mask the high variability of symptom severity across individuals sharing the same diagnoses. Accounting for such heterogeneity, this study examined the associations between domains of family functioning and depression, anxiety, and anhedonia symptoms from the adolescent perspective using a dimensional approach.
Method
Semistructured diagnostic interviews and self-reported measures for depression, anxiety, and anticipatory and consummatory anhedonia were used to evaluate adolescents. Participants’ perception of 7 aspects of family life was assessed with the Family Assessment Device. Bivariate assessments of associations between family subscales and symptom severity scores were conducted. Subsequently, regression models were employed to investigate these relationships while adjusting for age, sex, race, ethnicity, and multiple comparisons.
Results
Data from 79 adolescents (15.0 ± 1.84 years old; 61.8% biologically female) were analyzed, including 59 participants with psychopathology and 19 control participants. Adolescents with psychiatric symptoms perceived lower levels of family Problem Solving, Communication, and General Functioning relative to control participants. Depression severity was associated with Problem Solving, Communication, Roles, Affective Responsiveness, and General Functioning. Anxiety was associated with Problem Solving, Roles, and General Functioning. These relationships remained significant following adjustments for covariates and multiple comparisons correction. Anhedonia subconstructs and perceived family functioning associations were not as robust, suggesting a different etiological pathway.
Conclusion
These findings support the intertwined relationships between adolescent mood and anxiety processes and perceived family functioning factors. Future studies should examine larger samples and incorporate parents’ perspectives.
Diversity & Inclusion Statement
We worked to ensure sex and gender balance in the recruitment of human participants. We worked to ensure that the study questionnaires were prepared in an inclusive way. We worked to ensure race, ethnic, and/or other types of diversity in the recruitment of human participants. One or more of the authors of this paper self-identifies as a member of one or more historically underrepresented sexual and/or gender groups in science. We actively worked to promote sex and gender balance in our author group. We actively worked to promote inclusion of historically underrepresented racial and/or ethnic groups in science in our author group. While citing references scientifically relevant for this work, we also actively worked to promote sex and gender balance in our reference list. While citing references scientifically relevant for this work, we also actively worked to promote inclusion of historically underrepresented racial and/or ethnic groups in science in our reference list. The author list of this paper includes contributors from the location and/or community where the research was conducted who participated in the data collection, design, analysis, and/or interpretation of the work.
Key words: adolescence, anhedonia, anxiety, depression, family functioning
Plain language summary
This study examined biobehavioral factors in 79 participants in relation to the trajectory of adolescent depression with a focus on the associations between domains of family functioning and depression, anxiety, and anhedonia symptoms from the adolescent perspective. Adolescent depression and anxiety severity, but not anhedonia, were significantly associated with lower perception of family functioning across various domains. The findings suggest that clinical interventions which enhance each family member’s understanding of others’ perspectives may help strengthen family functioning.
Adolescence is a developmental period highly vulnerable to biopsychosocial stressors and onset of neuropsychiatric illness.1,2 These psychiatric conditions may impact an adolescent’s interactions with their social environment and family.3 In less supportive family environments, teens endorse worse depressive symptoms2,4 and more suicide attempts.5,6 In parallel, adolescents with depression and anxiety disorders and their parents report more severe family dysfunction and conflicts compared with controls.7,8 Prior studies using a wide range of instruments across diverse populations yielded convergent findings linking family functioning and categorical depressive and anxiety disorders in adolescence. Adolescents with major depressive disorder (MDD) perceive low levels of general family functioning, communicative interactions, supportive behaviors, problem-solving abilities, and affect regulations, although there is mixed evidence on whether their parents share these perceptions.7,9, 10, 11, 12 Adolescents with anxiety disorders report parental overinvolvement in addition to low family general functioning, cohesiveness, and support.13, 14, 15 Notably, altered family processes specific to affective domains have been consistently linked to adolescent MDD, but not anxiety disorders. Further, depression and anxiety comorbidity in youth appears to be associated more strongly with family dysfunction than either condition alone.7,11,16 As such, the relationship between family function and internalizing disorders is thought to be bidirectional,14,17 and maintaining healthy family functioning shows great promise in easing psychiatric burden for adolescents and their families.18 Additionally, as family functioning is often inconsistently perceived by all family members,19,20 it is crucial to examine the adolescent perception of family functioning with their psychopathology taken into context.
However, a common limitation of family functioning studies in adolescents is the comparison of participants with categorical psychiatric diagnoses relative to controls without psychiatric diagnoses.21, 22, 23, 24 This categorical approach does not account for clinical phenotypic intervariability and masks the heterogeneity of mood and anxiety conditions.25 For example, to be diagnosed with MDD based on criteria in the DSM-5,26 an adolescent must endorse at least 5 symptoms, one of which must be a core symptom of depressed mood, irritable mood, or anhedonia. Critically, despite being a core symptom of MDD, anhedonia has been shown to be neurobiologically dissociable from overall depression.27 Recent evidence further suggests the distinction between motivational and experiential aspects of anhedonia, conceptualized as anticipatory and consummatory anhedonia.28,29 Yet, whether anhedonia subconstructs relate to family functioning remains unclear.
To address the knowledge gap, we sought to investigate the relationships between family functioning from the adolescent perspective and affective symptomatology. The current study sample was drawn from our prospective research program examining biobehavioral factors in relation to adolescent depression trajectory and comprised clinically healthy adolescents and adolescents presenting predominantly with internalizing conditions. We focused on symptoms of depression, anxiety, and anticipatory and consummatory anhedonia, as they often co-occur but likely represent distinct underlying mechanisms.27,29, 30, 31 The Family Assessment Device (FAD)32 capturing 7 complementary family domains was administered to systemically evaluate adolescent perception of family functioning. Notably, we investigated associations between symptoms and family domains dimensionally, treating variables of interest as continuous. Our hypotheses of this dimensional investigation were built upon convergent findings from prior reports examining family functioning perception in adolescent depressive and anxiety psychopathologies as determined by categorical diagnostic criteria. Specifically, we developed the following hypotheses:
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1.
Depression severity would be associated with FAD-indexed domains of General Functioning, Problem Solving, Communication, Roles, Affective Involvement, Affective Responsiveness, and Behavior Control, which resembled convergent reports in adolescents with MDD.7,9, 10, 11, 12
-
2.
Anxiety severity would be associated with a more restricted set of family domains, namely, General Functioning, Problem Solving, Communication, Roles, and Behavior Control, corresponding to prior findings in adolescents with anxiety disorders.13, 14, 15
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3.
Anhedonia subconstructs isolated from overall depression severity would not be related to perceived family functioning due to their strong neurobiological bases,27,33, 34, 35 likely independent of family factors.
Method
Participant Recruitment and Initial Assessments
Our research program recruits participants through community advertisements and referrals from physicians across the New York metropolitan area. The FAD was incorporated into our ongoing laboratory procedures and has not been previously examined with constructs not described in this article. Therefore, in this investigation, we included only participants with available FAD.
Our research protocol was approved by the institutional review boards of the institutions at which the study was conducted. Before all study procedures, adolescents younger than 18 years old provided signed informed assent, and their accompanying parent or legal guardian provided informed consent. Adolescents age 18 years and older provided signed informed consent. Next, a trained child and adolescent psychiatrist, clinical psychologist, or social worker evaluated each adolescent using the Schedule for Affective Disorders and Schizophrenia for School-Age Children–Present and Lifetime Version for Children (K-SADS-PL).36 The parent or legal guardian was interviewed separately. The K-SADS-PL is a well-validated semistructured diagnostic interview to detect past and current psychiatric disorders in pediatric populations. Most items on the K-SADS-PL are rated on a scale of 0 to 3 points, with a score of 0 indicating unavailable information, a score of 1 indicating absence of symptoms, a score of 2 indicating subthreshold symptom presentation, and a score of 3 indicating threshold symptom presentation. The K-SADS-PL comprises 6 components: Unstructured Introductory Interview, Diagnostic Screening Interview, Supplement Completion Checklist, Diagnostic Supplements, Summary Lifetime Diagnosis Checklist, and Children’s Global Assessment Scale. The first 2 components allow for rapport building and screening of past and current psychiatric symptoms. If the respondent’s answers in the Diagnostic Screening Interview suggest psychopathology that warrants further assessment, the interviewing clinician conducts corresponding supplement sections. An interview with each respondent takes approximately 75 to 90 minutes. Following the interviews, the clinician combines the child self-reports, parent reports of observable behaviors, and summary ratings to determine psychiatric diagnostic profiles.
In our research protocol, the clinician wrote a comprehensive clinical report after finalizing the K-SADS-PL ratings for each case. If participants endorsed substantial symptoms indicating psychopathology based on the K-SADS-PL, regardless of meeting the diagnostic criteria for any disorder per DSM-IV37 or DSM-5,26 they were classified into the clinical group. This approach allowed us to capture a diverse range of transdiagnostic clinical phenotypes. Otherwise, participants were considered healthy controls (HC).
Inclusion and Exclusion Criteria
We excluded participants with a current or past diagnosis of schizophrenia, pervasive development disorder, or substance use disorder. We also excluded any participants with neurological disorders potentially contributing to the psychiatric presentation and participants with an estimated IQ less than 80 based on the Kaufman Brief Intelligence Test.38 While psychotropic medication use was not exclusionary, most of our study sample was psychotropic medication–free for 2 weeks before assessments. For the HC group, additional exclusion criteria included any current or past psychiatric diagnosis or treatment.
Additionally, all participants were required to complete a thorough medical assessment including medical history, blood draws, urine toxicology screen, and urine pregnancy test (if biologically female). Blood samples were sent for a comprehensive metabolic panel, complete blood count, thyroid function tests, and liver function tests. Participants were excluded if pregnant or determined to have an acute and/or chronic medical illness after their medical history and test results were reviewed by a physician in our research group.
Dimensional Measures of Mood and Anxiety Symptoms
To capture mood and anxiety symptoms dimensionally, we used self-rated scales established in adolescent populations.39, 40, 41 Specifically, participants reported depression severity with the Beck Depression Inventory (BDI),39 which includes 21 multiple-choice statements on various depressive symptoms. Each statement provides 4 answer choices corresponding to scores of 0 to 3. The possible score range for the BDI is 0 to 63, with higher scores indicating more severe depression. The 39-item self-rated Multidimensional Anxiety Scale for Children (MASC)40 was used to quantify anxiety severity. For each item, there are 4 choices: “never true about me,” “rarely true about me,” “sometimes true about me,” and “often true about me.” These choices correspond to scores of 0, 1, 2, and 3, respectively, summing to a possible score range of 0 to 117 for the MASC. As anhedonia is a complex clinical phenomenon, representing deficits across various reward processes with distinct neurobiological mechanisms,42,43 we measured anhedonia with the 18-item, self-reported Temporal Experience of Pleasure Scale (TEPS),41 which differentiated anticipatory pleasure (TEPS-A; 10 items) from consummatory pleasure (TEPS-C; 8 items). Each item is scored from 1 to 6 as follows: 1 = “very false for me”; 2 = “moderately false for me”; 3 = “slightly false for me”; 4 = “slightly true for me”; 5 = “moderately true for me”; 6 = “very true for me.” The score ranges for TEPS-A and TEPS-C are 10 to 60 and 8 to 48, respectively. By design, the TEPS does not have a total score (ie, the summation of TEPS-A and TEPS-C); therefore, we did not include a total TEPS score in our analyses. In contrast to the BDI and MASC, lower TEPS scores indicate higher levels of anhedonia. As these scales probe symptom severity dimensionally, we expected some HC to report nonpathological symptom levels, resulting in scores higher than the minimum value of each scale (see Figures S1 and S2, available online).
Family Functioning Assessment
Adolescents self-reported their perception of family functioning by completing the FAD,32 which captures clinically relevant dimensions of family functioning.19,20,44 The FAD comprises 60 items and is divided into 7 subscales: Problem Solving, ability to resolve problems together while maintaining effective family functioning (6 items); Communication, clarity and directedness in information exchange between family members (9 items); Roles, efficacy in allocating and conducting family tasks (11 items); Affective Responsiveness, ability to express appropriate positive and/or negative emotions across settings (6 items); Affective Involvement, interests and concerns for each other within the family unit (7 items); Behavior Control, maintenance of standard behaviors in the family (9 items); and General Functioning, overall family health or pathology independent of the remaining scales (12 items). These subscales assess corresponding family dimensions theorized in the McMaster Model of Family Functioning.32 Because of its high reliability, internal consistency across various family types, and ability to differentiate healthy and dysfunctional family factors,32,45 the FAD has been used in multiple clinical populations.19,20
Each statement about family life on the FAD can be rated by participants as “strongly agree,” “agree,” “disagree,” or “strongly disagree.” Each answer is scored from 1 to 4 as follows: 1 = “strongly agree”; 2 = “agree”; 3 = “disagree”; 4 = “strongly disagree.” For the 35 statements that describe unhealthy family functioning, the scores are inverted by subtracting the score from 5. The questionnaire is scored by adding the responses in each subscale and dividing by the number of items in the subscale. The subscale scores can range from 1 to 4, with lower scores representing healthy family functioning and higher scores representing family dysfunction.32 For missing data, if more than 60% was completed, scales were scored pro rata. For each subscale, there is a traditional clinical cutoff point of 1.90 to 2.30 depending on the scale.32 However, in line with the dimensional approach, we treated subscale scores to be on a continuum.
Statistical Analyses
Statistical analyses were jointly performed in MATLAB R2022a (MathWorks Inc., Natick, Massachusetts; normality tests, bivariate analyses, and multiple comparison correction) and SAS 9.4 (SAS Institute Inc., Cary, North Carolina; linear regression models). We first assessed the normality of continuous variables using the Lilliefors test.46 To determine potential differences in characteristics between the clinical and HC groups, we employed the 2-sample t-test or Mann-Whitney U test for continuous variables and χ2 test or Fisher exact test for categorical variables. Group comparisons across the 7 family functioning subscales and 4 symptom measures were conducted using 2-sample t-tests or Mann-Whitney U tests.
Primary Analyses
To capture the full ranges of symptom severity and degrees of family function, we included the whole sample (N = 76). Associations between each symptom and family functioning domain were assessed with Pearson or Spearman correlations. If a correlation was significant at α = .05, linear regression models were used to control for age, biological sex, race, and ethnicity. Additionally, if either anticipatory or consummatory anhedonia was significantly associated with a family subscale, we further adjusted for depression severity. Race and ethnicity were combined and categorized into Hispanic, non-Hispanic Black, and non-Hispanic White/other groups. Correction for multiple comparisons was conducted using the false discovery rate method,47 with results considered significant at false discovery rate–corrected pFDR < .05. See Table S1, available online, for all linear regression models conducted in this study.
Secondary Analyses
As clinical participants (n = 59) perceived higher family dysfunction in Problem Solving, Communication, and General Functioning compared to HC (Table 1), we conducted a set of secondary analyses restricting the aforementioned analytical procedures to only the clinical group.
Table 1.
Demographic and Clinical Characteristics of Study Participants
| Measure | Whole sample (N = 76) |
Clinical group (n = 59) |
HC Group (n = 17) |
p | |||
|---|---|---|---|---|---|---|---|
| Mean | (SD) | Mean | (SD) | Mean | (SD) | ||
| Demographics | |||||||
| Age, y | 15.03 | (1.84) | 15.10 | (1.85) | 14.76 | (1.82) | .54 |
| % | % | % | |||||
| Sex, female | 61.84 | 64.41 | 52.94 | .39 | |||
| Race and ethnicity | .12 | ||||||
| Hispanic | 42.10 | 47.46 | 23.23 | — | |||
| Non-Hispanic Black | 28.95 | 23.73 | 47.36 | — | |||
| Non-Hispanic White/othera | 28.95 | 28.81 | 29.41 | — | |||
| Mean | (SD) | Mean | (SD) | Mean | (SD) | ||
| Clinical profile | |||||||
| BDI | 14.00 | (13.43) | 17.24 | (13.53) | 2.76 | (2.91) | 1.92 × 10−6∗ |
| MASC | 45.83 | (19.77) | 50.78 | (18.49) | 28.94 | (14.11) | 2.29 × 10−5∗ |
| TEPS-A | 44.54 | (8.22) | 43.49 | (8.28) | 48.18 | (7.07) | .03∗ |
| TEPS-C | 33.39 | (7.40) | 33.14 | (7.29) | 34.29 | (7.91) | .59 |
| % | % | % | |||||
| Psychotropic medication–freeb | 93.42 | 91.53 | 100 | .21 | |||
| n | n | n | |||||
| Most common DSM diagnoses | |||||||
| Mood disorders | 41 | 41 | 0 | — | |||
| Anxiety disorders | 45 | 45 | 0 | — | |||
| ADHD | 19 | 19 | 0 | — | |||
| ODD | 9 | 9 | 0 | — | |||
| PTSD | 5 | 5 | 0 | — | |||
| % | % | % | |||||
| Comorbidityc | 57.89 | 74.58 | 0 | — | |||
| Mean | (SD) | Mean | (SD) | Mean | (SD) | ||
| Perception of family functioning profile | |||||||
| Problem solving | 2.15 | (0.53) | 2.23 | (0.54) | 1.88 | (0.35) | 7.82 × 10−3∗ |
| Communication | 2.34 | (0.40) | 2.39 | (0.40) | 2.18 | (0.37) | .046∗ |
| Roles | 2.31 | (0.42) | 2.34 | (0.41) | 2.20 | (0.44) | .17 |
| Affective responsiveness | 2.45 | (0.53) | 2.46 | (0.53) | 2.38 | (0.56) | .41 |
| Affective involvement | 2.48 | (0.57) | 2.50 | (0.53) | 2.40 | (0.71) | .86 |
| Behavior control | 2.14 | (0.50) | 2.13 | (0.48) | 2.15 | (0.60) | .92 |
| General functioning | 2.21 | (0.56) | 2.30 | (0.59) | 1.91 | (0.34) | 1.14 × 10−3∗ |
Note: Mean (SD) values are reported for all continuous variables, including age, 4 symptom scales, and 7 family functioning domain subscales. Reported p values are of appropriate bivariate tests comparing the clinical (participants with psychiatric symptoms and/or diagnoses) and HC groups. Boldface indicates significant p values. There were no missing data except for the MASC score of 1 clinical participant. ADHD = attention-deficit/hyperactivity disorder; BDI = Beck Depression Inventory; HC = healthy control; MASC = Multidimensional Anxiety Scale for Children; ODD = oppositional defiant disorder; PTSD = posttraumatic stress disorder; TEPS-A = Temporal Experience of Pleasure Scale–Anticipatory; TEPS-C = Temporal Experience of Pleasure Scale–Consummatory.
“Other” participants were those who identified as Asian or other racial backgrounds. No participant included in this study identified as American Indian, Alaskan, or Native Hawaiian/other Pacific Islander.
Defined as not taking any psychotropic medication for 2 weeks before assessments.
Defined as having at least 2 DSM diagnoses.
p < .05.
Results
Demographic and Clinical Characteristics
We studied 76 adolescents, including 59 adolescents who endorsed predominantly mood and anxiety symptoms and 17 HC. Clinical participants and HC did not differ on demographic traits. Demographic and clinical characteristics of our study sample are presented in Table 1.
Symptom Severity Score Distribution
There was a high variability of symptom severity across the whole sample and, importantly, within each group, with HC also exhibiting a range of symptom levels (Figure 1). Relative to HC, clinical participants reported significantly higher BDI and MASC scores and lower TEPS-A scores, corresponding respectively to higher severity of depression, anxiety, and anticipatory anhedonia at the group level.
Figure 1.
Whole-Sample Distributions of Clinical Symptoms and Family Functioning Domains
Note:The solid line of each plot shows the median value, and the dashed lines indicate the 25th and 75th percentile values. Blue and red dots represent individual data points from HC and clinical participants, respectively. BDI = Beck Depression Inventory; FAD = Family Assessment Device; HC = healthy control; MASC = Multidimensional Anxiety Scale for Children; TEPS-A = Temporal Experience of Pleasure Scale–Anticipatory; TEPS-C = Temporal Experience of Pleasure Scale–Consummatory. Plots were made with GraphPad Prism 9.
Family Functioning Score Distribution
Clinical participants perceived lower family functioning in Problem Solving, Communication, and General Functioning, but there were no group differences in perception of the other 4 family domains.
Relationships Between Family Functioning and Affective Symptomatology
Five of 7 family domains (Problem Solving, Communication, Roles, Affective Responsiveness, and General Functioning) significantly correlated with symptom severity (Table 2). As no significant correlations were detected between any symptoms and Affective Involvement and Behavior Control, these family domains were excluded from further analysis with linear regression modeling.
Table 2.
Correlations Between Each Family Functioning Domain and Clinical Symptoms
| BDI | MASC | TEPS-A | TEPS-C | |
|---|---|---|---|---|
| Problem solving | 0.50∗∗ | 0.36∗ | −0.34∗ | −0.18 |
| Communication | 0.36∗ | 0.21 | −0.24∗ | −0.29∗ |
| Roles | 0.36∗ | 0.35∗ | −0.25∗ | −0.17 |
| Affective responsiveness | 0.27∗ | 0.11 | −0.15 | −0.21 |
| Affective involvement | 0.10 | 0.18 | 0.04 | −0.05 |
| Behavior control | 0.16 | 0.20 | −0.09 | −0.07 |
| General functioning | 0.46∗∗ | 0.30∗ | −0.33∗ | −0.24∗ |
Note: Depending on the normality of each variable, Pearson r or Spearman ρ were computed. Negative values of anhedonia estimates are expected due to the TEPS scoring system (lower scores reflecting more severe anhedonia). Boldface indicates significant values. BDI = Beck Depression Inventory; MASC = Multidimensional Anxiety Scale for Children; TEPS-A = Temporal Experience of Pleasure Scale–Anticipatory; TEPS-C = Temporal Experience of Pleasure Scale–Consummatory.
∗p < .05; ∗∗p < .001.
Linear regression models further confirmed significant relationships between the 5 family domains and affective symptoms while controlling for age, biological sex, race, ethnicity, and multiple comparisons (Table 3):
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•
Depression: Among the symptoms, depression was found to be associated with the greatest number of family domains, including Problem Solving, Communication, Roles, Affective Responsiveness, and General Functioning.
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•
Anxiety: Anxiety severity was significantly associated with family Problem Solving, Roles, and General Functioning.
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•
Anhedonia: In unadjusted models, anticipatory anhedonia was associated with family Problem Solving, Roles, and General Functioning, while consummatory anhedonia was associated with Communication. However, after adjusting for multiple comparisons and depression severity, these associations were no longer significant.
Table 3.
Linear Regression Models Associating Symptoms and Family Domains
| β ± SE | puncorrected | pFDR | |
|---|---|---|---|
| FAD: problem solving | |||
| TEPS-A | −.019 ± .008 | .026∗ | .101 |
| TEPS-A, controlling for BDI | −.004 ± .009 | .683 | .691 |
| BDI | .017 ± .004 | 1.12 × 10−4∗∗ | 1.24 × 10−3∗ |
| BDI, controlling for TEPS-A | .016 ± .005 | 1.59 × 10−3∗ | 3.77 × 10−3∗ |
| MASC | .012 ± .003 | 2.88 × 10−4∗∗ | 8.64 × 10−4∗∗ |
| FAD: communication | |||
| TEPS-A | −.013 ± .006 | .051 | .101 |
| TEPS-A, controlling for BDI | −.003 ± .007 | .636 | .691 |
| TEPS-C | −.015 ± .006 | .018∗ | .073 |
| TEPS-C, controlling for BDI | −.011 ± .006 | .083∗ | .110 |
| BDI | .011 ± .003 | 1.71 × 10−3∗ | 3.77 × 10−3∗ |
| BDI, controlling for TEPS-A | .010 ± .004 | .013∗ | .014∗ |
| BDI, controlling for TEPS-C | .009 ± .003 | 7.25 × 10−3∗ | 9.97 × 10−3∗ |
| FAD: roles | |||
| TEPS-A | −.014 ± .007 | .045∗ | .101 |
| TEPS-A, controlling for BDI | −.003 ± .007 | .691 | .691 |
| BDI | .012 ± .003 | 7.36 × 10−4∗∗ | 3.77 × 10−3∗ |
| BDI, controlling for TEPS-A | .011 ± .004 | 6.36 × 10−3∗ | 9.97 × 10−3∗ |
| MASC | .009 ± .003 | 7.90 × 10−4∗∗ | 1.19 × 10−3∗ |
| FAD: affective responsiveness | |||
| BDI | .011 ± .004 | .011∗ | .013∗ |
| FAD: general functioning | |||
| TEPS-A | −.019 ± .009 | .033∗ | .101 |
| TEPS-A, controlling for BDI | −.007 ± .010 | .495 | .691 |
| TEPS-C | −.017 ± .009 | .052 | .103 |
| TEPS-C, controlling for BDI | −.011 ± .009 | .198 | .198 |
| BDI | .015 ± .005 | 1.64 × 10−3∗ | 3.77 × 10−3∗ |
| BDI, controlling for TEPS-A | .013 ± .005 | .017∗ | .017∗ |
| BDI, controlling for TEPS-C | .013 ± .005 | 5.54 × 10−3∗ | 9.97 × 10−3∗ |
| MASC | .010 ± .003 | 2.17 × 10−3∗ | 2.17 × 10−3∗ |
Note: All reported models were adjusted for age, sex, race, and ethnicity. Multiple comparison correction for FDR was applied to p values of each symptom of interest across the models in which it was included. Negative values of anhedonia estimates are expected due to the TEPS scoring system (lower scores reflecting more severe anhedonia). Boldface indicates significant values. BDI = Beck Depression Inventory; FAD = Family Assessment Device; MASC = Multidimensional Anxiety Scale for Children; TEPS-A = Temporal Experience of Pleasure Scale–Anticipatory; TEPS-C = Temporal Experience of Pleasure Scale–Consummatory.
∗p < .05 or pFDR < .05; ∗∗p < .001 or pFDR < .001.
Clinical Group Findings
The results remained consistent with whole-group analyses, with 2 exceptions. First, although no association between anhedonia subconstructs and family domains in the whole-group analysis survived multiple comparison correction, more severe consummatory anhedonia was significantly linked to perceived lower family communication at false discovery rate–corrected pFDR < .05. Additionally, we detected more severe anxiety being associated with worse family Behavior Control. Details of the clinical group’s results are in Tables S4 and S5, available online.
Discussion
The present study investigated adolescent perception of family functioning in relation to depression, anxiety, and anhedonia symptom severity in a demographically and clinically diverse sample of adolescents. As expected, we documented high symptom variability in our sample, including in the HC group. Despite significant differences in depression, anxiety, and anticipatory anhedonia scores between HC and clinical participants as detected by statistical tests, group-level data distribution showed that many HC participants reported similar symptom severity as clinical participants. Similarly, there was a wide range of perceptions of family functioning in each domain. Except for 3 domains, group differences between HC and clinical participants in perceiving family functioning were nonsignificant. These results could be related to the high inter-variability among the clinical and HC participants, emphasizing the importance of a dimensional investigative approach that subsequently revealed significant relationships. In support of our first and second hypotheses, family domains of Problem Solving, Roles, and General Functioning were associated with both depression and anxiety symptoms. Depression severity was additionally associated with Affective Responsiveness and Communication. In contrast, the lack of significant associations between depression severity and family Affective Involvement or Behavior Control, as well as anxiety severity and Communication or Behavior Control, did not support our first and second hypotheses. Supporting our third hypothesis, there was minimal relation between anhedonia subconstructs and perception of family functioning independent of overall depression severity.
Mood and anxiety symptoms among adolescents both can affect and can be affected by perceptions of family functioning. Here, we discuss our cross-sectional findings within this bidirectional framework, focusing on the perspective of adolescents on various dimensions of family functioning in the context of their internalizing symptomatology. Further, we speculate about the underlying internal and environmental vulnerability factors that may influence the detected relationships.
Our observation that greater depression severity was associated with worse perceptions of family Problem Solving, Communication, Roles, Affective Responsiveness, and General Functioning aligns with and further expands upon the literature. Using the FAD subscales, Tamplin and Goodyer12 observed that adolescents with lower mood perceived worse family Roles and General Functioning. Relatedly, although they did not assess children’s perception of the family, Stein et al.10 used the FAD to compare parents of children with MDD with parents of children without depression. The authors reported greater family dysfunction across 4 family dimensions in the depressed group: Roles and Affective Involvement appeared more unhealthy to mothers, whereas Behavior Control and General Functioning were of significant concern to fathers.10 Taken together, although these studies separately examined perception of family function of depressed adolescents vs parents of children with depression, their findings on the influence of the child’s depression on Roles and General Functioning converge with our findings. Notably, we detected significant relationships between depression and 3 family domains (Problem Solving, Communication, Affective Responsiveness) not previously reported. In contrast to Stein et al.,10 we did not detect an association between depression severity and Affective Involvement. These divergent findings possibly stem from how adolescent depression is assessed across studies; here, we employed the BDI, a well-validated dimensional measure capturing depression severity. This method thus allowed us to examine the wide range of depression severity in our sample. Importantly, by further isolating depression from anhedonia, a cardinal symptom of depression, we infer that cognitive and somatic symptoms other than anhedonia might contribute more strongly to disruptions in how adolescents perceived family dynamics.
Further, our analyses showed more severe anxiety being linked to worse perception of family Problem Solving, Roles, and General Functioning. Moreover, the relationship between anxiety and Behavior Control emerged only when examined in the clinical group, suggesting higher sensitivity to family behaviors among adolescents with psychopathology. Interestingly, prior evidence shows greater degrees of family dysfunction as experienced by adolescents with mood and anxiety comorbidities compared with adolescents with only 1 diagnosis,7,11 further emphasizing the need to disentangle links between varied symptoms and disparate elements of family function. Some studies showed that adolescents with comorbid MDD and generalized anxiety disorder reported worse family dysfunction compared with adolescents with either diagnosis alone or no diagnosis.7,16 Building upon the critical insights into the role of family functioning in adolescent mood and anxiety disorders from these studies, our dimensional approach accounting for demographic traits revealed specific relationships between adolescent perception of diverse aspects of family functioning and depression and anxiety symptomatology that cut across categorical diagnoses. Broadly, our findings support the notion that depressive and anxiety symptoms may negatively bias how adolescents view their family. The other direction is also likely, in which perceived family dysfunctions may induce or exacerbate depressive and anxiety symptoms in youth. Over time, these 2 directions may perpetuate a cycle, potentiating family conflicts as parents attempt to lessen their children’s symptoms and experience frustrations when their efforts appear unfruitful.48
Anhedonia is considered a core symptom of depression and likely reflects a depression subtype with more debilitating consequences.33, 34, 35 Although some studies suggest a possible link between adolescent anhedonia and family functioning,49,50 family functioning was reported by caregivers only, and anhedonia was not captured with a standardized measure. Thus, by parsing anhedonia into its anticipatory and consummatory components and relating them to adolescent-rated family subscales, we provide novel insights into whether anhedonia subconstructs and perceived family dysfunction influence each other. Though none of the relationships between anhedonia and family dimensions survived multiple comparison, we observed a general trend of worse anticipatory anhedonia relating to perceived worse family Problem Solving, Roles, and General Functioning. Further, more severe consummatory anhedonia was implicated in lower perception of family Communication within the clinical group. However, when anhedonia and depression were concurrently examined in the same linear regression model, only depression was found to be significantly associated with the family domains of interest. The overall lack of association between anhedonia subconstructs and perception of family functioning after adjusting for depression severity is in line with the lack of prior data for relations between anhedonia and family factors in the literature and reinforces the neurobiological basis of anhedonia.27,33, 34, 35 In line with the bidirectional framework, we speculate from our data that anhedonia represents psychopathological disruptions minimally influenced by perceived family functioning and that depressive symptoms other than anhedonia may be more sensitive to family factors.
Although we did not have data on these constructs, attachment styles, reflective functioning, and family compositions are possible vulnerability factors underlying an adolescent’s internalizing psychopathology and view of family functions. Insecure attachment to primary caregivers has been shown to be a risk factor for depression and anxiety in adolescents and influence their perceived autonomy within the family.51,52 Higher levels of avoidant attachment and youth-reported dysfunctional family interactions have also been linked to more depressive symptomatology.53 Further, relative to adolescents who never attempted suicide, those who had attempted suicide were more likely to be diagnosed with MDD and anxiety disorders and reported lower attachment to parents, along with lower family cohesion and adaptability.6 Apart from nonsecure attachment, deficits in reflective functioning—the capacity to understand mental states of the self and others—may also underlie internalizing symptomatology and distorted family functioning perception in youth. Relative to controls, adolescents with internalizing symptoms in inpatient and community samples demonstrated lower reflective functioning, which may compromise their ability to accurately assess family relationships and quality.54, 55, 56 Indeed, interventions aimed at increasing adolescent and parental reflective functioning, notably mentalization-based therapy, have been shown to improve adolescent secure attachment and social-emotional development,57,58 supporting the mediating effects of reflective functioning and attachment styles on adolescent symptomatology and perceived family factors. Relatedly, family composition may shape family perception and experiences of symptoms among adolescents. Disrupted family structures due to parental divorce and becoming adjusted to a stepparent have been linked to adolescent depression.8,59 Relative to adolescents living with 2 biological parents, adolescents in single-mother families are more likely to develop depressive symptoms and externalizing disorders.60,61 However, disrupted family structures may not substantially impact depressive and anxiety symptoms in adolescents if they perceive high parental social support62 and family emotional bonding,63 as well as when an empathic parenting style, devoid of excessive intrusion and infantilization, is employed.8 Taken together, these underlying factors and their interactions can modulate associations between adolescent perception of family dynamics and affective symptomatology.
Healthy family functioning has been documented to play a role in improving outcomes for adolescents with mood and anxiety conditions. Previous data suggest that positive parent–child relationships may serve as a protective buffer during stressful life events that otherwise would worsen depression and anxiety throughout childhood.64 Importantly, altered affective processes might influence adolescents with internalizing symptoms to view family functioning through a more negative lens. Particularly, adolescents experiencing lower mood and self-esteem perceived worse family functioning in a dose-dependent fashion, yet their symptoms did not appear to affect their parents’ reports on family functioning.12 Taken together with our current study, targeting the adolescent perception on family functioning is a promising therapeutic approach.
This study has several limitations. First, the FAD was not corroborated by additional family members. Although this limited our ability to assess different perceptions within the family unit, our focus remained on the adolescent’s own view on family factors and how they relate to internal experiences of depression and anxiety. Second, our study is cross-sectional, limiting our ability to explore the trajectory of family functioning perception in parallel with changes of symptoms in adolescents over time. Third, although our study is among the few that incorporated demographic covariates into our analyses, we did not account for other potential confounders, such as socioeconomic status, family history of psychiatric illness, and history of trauma. Overall, future investigations should thoroughly measure psychosocial stressors and other family-related constructs, including attachment styles, reflective functioning, and family structures, to delineate their influences on adolescent perception of family functioning in psychopathology contexts.
In conclusion, a major strength of our study is the inclusion of adolescents presenting with a wide range of symptomatology regardless of categorical diagnoses, allowing for assessment over a clinical spectrum from subthreshold syndromes to severe illness. By using a dimensional approach and rigorous statistical methodology correcting for possibly confounding demographic traits and multiple comparisons, we isolated distinct relationships between multiple aspects of family functioning as perceived by adolescents and their levels of internalizing symptoms. As such, our findings elaborate the complex link between adolescent perception of family elements and affective symptomatology beyond psychiatric diagnoses. We hence advocate for clinical interventions that enhance each family member’s understanding of perspectives of others, which hold great promise in improving how adolescents with psychiatric conditions view the family, while supporting parents in the pursuit of alleviating their children’s symptoms. Altogether, such interventions can produce synergistic effects and ultimately help strengthen the family unit.
CRediT authorship contribution statement
Tram N.B. Nguyen: Writing – review & editing, Writing – original draft, Visualization, Validation, Software, Resources, Project administration, Methodology, Investigation, Funding acquisition, Formal analysis, Data curation, Conceptualization. Aaron B. Chance: Writing – review & editing, Writing – original draft, Validation, Project administration, Methodology, Investigation, Data curation, Conceptualization. Chloe Roske: Writing – review & editing, Validation, Project administration, Methodology, Investigation. Emily Chase: Writing – review & editing, Writing – original draft, Validation, Project administration, Methodology, Investigation, Data curation, Conceptualization. Tamar B. Rubinstein: Writing – review & editing, Validation, Project administration, Methodology, Investigation, Funding acquisition. Amanda Zayde: Writing – review & editing, Validation, Project administration, Methodology, Investigation. Wenzhu B. Mowrey: Writing – review & editing, Writing – original draft, Validation, Software, Project administration, Methodology, Investigation, Formal analysis. Vilma Gabbay: Writing – review & editing, Writing – original draft, Validation, Supervision, Resources, Project administration, Methodology, Investigation, Funding acquisition, Data curation, Conceptualization.
Footnotes
This project was funded by the National Institutes of Health (NIH) under Award Numbers F30DA056227 to T.N.B.N.; K23AR080803 to T.B.R.; P30AI124414, RM1DA055437, R01DA054885, R21MH126501, R01MH120601, R21MH121920, R01MH128878, and R01MH126821 to V.G. (principal investigator [PI]). T.N.B.N. was additionally supported by NIH grants UL1TR001073 (Clinical Research Training Program; PIs: Harry Shamoon and Marla J. Keller), T32GM007288 (Medical Scientist Training Program; PI: Myles H. Akabas), and TL1TR002557 (PI: Paul R. Marantz). The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.
The research was performed with permission from the institutional review boards at all involved institutions.
Consent has been provided for descriptions of specific patient information.
This work has been previously posted on a preprint server: https://doi.org/10.21203/rs.3.rs-3645454/v1.
Data Sharing: Data that support the findings of this study are available upon reasonable request from the corresponding author. The data are not publicly available as not all participants consented to the public sharing of their individual data.
Wenzhu B. Mowrey served as the statistical expert for this research.
The authors thank the children and families who participated in the study.
Disclosure: Tram N.B. Nguyen, Aaron B. Chance, Chloe Roske, Emily Chase, Tamar B. Rubinstein, Amanda Zayde, Wenzhu B. Mowrey, and Vilma Gabbay have reported no biomedical financial interests or potential conflicts of interest.
Supplemental Material
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