Following the children of depressed parents from childhood to adult life: A focus on mood and anxiety disorders.

Background: Parental depression increases risk for anxiety and depression in offspring. The transition from adolescence to adulthood is a common risk period for onset of such disorders. However, relatively few studies have considered development of these disorders from childhood to adulthood including multiple assessments during this transition period. Method: Offspring of depressed parents aged 9-17 years at baseline were followed prospectively for 13 years (n = 337). Average length of follow-up was 16 months between the first and second waves, 13 months between the second and third, and 8 years between the third and fourth. Current (3-month) psychopathology was assessed at each wave using diagnostic interviews. We derived estimates of 3-month prevalence, age at first diagnosis, course and comorbidity of disorders. Social functioning in adult life was assessed at the final wave and we assessed how prior and current disorder impacted adult functioning. Results: A quarter of young people met criteria for a mood disorder and a third for anxiety disorder at least once. Mood and anxiety disorder prevalence increased from 4.5% and 15.8% respectively in childhood (9-11 years) to 22.3% and 20.9% respectively by age 23-28. Increased prevalence across the transition from adolescence to adulthood was particularly marked in males, while prevalence increased earlier in adolescence in females. Age at first diagnosis varied widely (mood disorder mean = 16.5 years (range 9-26); anxiety disorder mean = 14.5 years (range 9-28)). Over half (52%) reported functional impairment in early adulthood, 31% harmful alcohol use, and 10% self-harm or a suicide attempt. Both previous and current mood or anxiety disorder were associated with functional impairment in early adulthood. Conclusions: There is a prolonged risk period for mood and anxiety disorders in this group, with prevalence peaking in early adulthood. This highlights the need for prolonged vigilance and effective targeted interventions in the offspring of depressed parents.

Developing and validating a prediction model of adolescent major depressive disorder in the offspring of depressed parents.

BACKGROUND: Parental depression is common and is a major risk factor for depression in adolescents. Early identification of adolescents at elevated risk of developing major depressive disorder (MDD) in this group could improve early access to preventive interventions. METHODS: Using longitudinal data from 337 adolescents at high familial risk of depression, we developed a risk prediction model for adolescent MDD. The model was externally validated in an independent cohort of 1,384 adolescents at high familial risk. We assessed predictors at baseline and MDD at follow-up (a median of 2-3 years later). We compared the risk prediction model to a simple comparison model based on screening for depressive symptoms. Decision curve analysis was used to identify which model-predicted risk score thresholds were associated with the greatest clinical benefit. RESULTS: The MDD risk prediction model discriminated between those adolescents who did and did not develop MDD in the development (C-statistic = .783, IQR (interquartile range) = .779, .778) and the validation samples (C-statistic = .722, IQR = -.694, .741). Calibration in the validation sample was good to excellent (calibration intercept = .011, C-slope = .851). The MDD risk prediction model was superior to the simple comparison model where discrimination was no better than chance (C-statistic = .544, IQR = .536, .572). Decision curve analysis found that the highest clinical utility was at the lowest risk score thresholds (0.01-0.05). CONCLUSIONS: The developed risk prediction model successfully discriminated adolescents who developed MDD from those who did not. In practice, this model could be further developed with user involvement into a tool to target individuals for low-intensity, selective preventive intervention.

Understanding de novo onset of anxiety during COVID-19: Pre-pandemic socio-emotional functioning in vulnerable children.

Background: There is a need to understand and mitigate the psychological impacts of the COVID-19 pandemic for children known to be vulnerable. Data from prior to the pandemic are required to provide robust assessments of the socio-emotional impacts of COVID-19 and identify those who are more vulnerable. Method: This study capitalises on an ongoing UK study of primary school children (4-8 years) identified prior to the pandemic as "at risk" for mental health problems by teachers. We collected mental health and social-emotional functioning data prior to the pandemic (Time 1) and re-assessed this cohort (N = 143) via researcher-led videocalls during lockdown (Time 2, summer 2020) and post-lockdown, 12 months later (Time 3; summer 2021). Results: Mental health problems, particularly clinically significant anxiety, increased from 34% to 43% during lockdown and to 48% post-lockdown. Parental mental health difficulties (anxiety and depression) were prevalent during lockdown (40%) but had decreased 1 year later (20%). Children who developed clinically significant anxiety during the pandemic had impaired socio-emotional functioning at Time 1 (i.e., impaired emotion recognition, low self-esteem and social problems) and a high proportion (44%) had no contact with any peers during lockdown, which may have contributed to their anxiety, especially their school anxiety. Conclusion: The pandemic appears to have exacerbated anxiety in already vulnerable children. A profile of socio-emotional problems identified a group of children who developed significant anxieties during the pandemic. These socio-emotional processes can be targeted for intervention to mitigate the negative mental health consequences of the pandemic and contribute to resilience in children.

The antecedents and outcomes of persistent and remitting adolescent depressive symptom trajectories: a longitudinal, population-based English study.

BACKGROUND: Depression often first emerges in adolescence and, for many, is a lifelong disorder. The long-term clinical course of depression is highly variable. We aimed to examine the adult outcomes of adolescent-onset trajectories of clinically significant depressive symptoms and to identify factors differentiating trajectories that persist and desist in adulthood. METHODS: We included participants from the English population-based Avon Longitudinal Study of Parents and Children with data on depressive symptoms. Self-reported depression symptoms were assessed on ten occasions when participants were age 10·5-25 years using the short Mood and Feelings Questionnaire, and major depressive disorder episodes were assessed at age 13·0 years, 15·0 years, 17·5 years, and 25·0 years. We characterised trajectories of depression symptoms using latent class growth analysis, for which we required depression data at least once from each of three key phases: ages 10·5-13·5 years; 16·5-18·5 years; and 21-25 years. We examined adult outcomes by assessing lifetime suicidal self-harm and functional impairment at age 24·0 years, and employment, education, and the self-reported Strengths and Difficulties Questionnaire at age 25·0 years. FINDINGS: We studied 4234 participants: 2651 (63%) female, 1582 (37%) male, and one individual with missing sex data. The mean age was 10·6 years (SD 0·2) at baseline and 25·8 years (SD 0·5) at the final timepoint. Data on ethnicity were not available in our data set. We identified four depression trajectory classes: adolescent-persistent depression with onset early in adolescence (7%, n≈279), adolescent-limited depression with onset later in adolescence and remittance by adult life (14%, n≈592), adult-increasing depression (25%, n≈1056), and stable-low levels of depression (54%, n≈2307). The adolescent-persistent class was associated with poor adult outcomes for functional impairment (62%), suicidal self-harm (27%), mental health difficulties (25%), and not being in education, employment, or training (16%). Adolescent-limited depression was associated with transient adolescent stress, but by early adulthood functional impairment and mental health difficulties were similar to the stable-low group. Major depressive disorder polygenic score (odds ratio [OR] 1·36, 95% CI 1·04-1·79), adolescent educational attainment (OR 0·47, 0·30-0·74), and any early childhood adversity (OR 2·60, 1·42-4·78), that persisted into adulthood (OR 1·60, 1·38-1·87) distinguished the adolescent-persistent and adolescent-limited groups. INTERPRETATION: The future course of adolescent depression can be differentiated by age at onset during adolescence, adolescent academic attainment, early and persistent adversity, and genetic loading. A detailed social and educational history could be helpful in making clinical decisions about the intensity of interventions for young people with clinically elevated depressive symptoms who seek help. FUNDING: Medical Research Council, Wolfson Centre for Young People's Mental Health, Wolfson Foundation.

The effect of amniotomy on urine protein creatinine ratio test accuracy.

Introduction: While the gold standard for evaluation of maternal urinary protein is a 24-hr urine collection, spot urine protein/creatinine ratio has been instituted as an alternative for quantification proteinuria. Though it seems intuitive to obtain a catheterized urine sample on patients with ruptured amniotic membranes, it is a common practice to forgo this step under the argument that there is no data to show its necessity. Data on the effect of amniotomy, spontaneous or artificial, on the accuracy of the protein/creatinine ratio are scant. The present study was designed to address this issue and objectively compare protein/creatinine ratio values on samples obtained from the same patient before and after amniotomy. Methods: We conducted a prospective non-interventional study. Women presenting in active labor or for labor induction with intact amnion were enrolled. Separate random catch urines for the protein/creatinine ratio were obtained prior to and immediately after spontaneous or assisted amniotomy. The urine samples were analyzed in the hospital chemistry department, and the results were compared. Results: Of the 137 patients consented, 63 had pre- and post-amniotomy protein/creatinine ratios collected. The mean age was 28.5±5.6 y, Gravidity 2.7±1.6, Gestational age 39.2±1.8 wks, and BMI 31.6±6.4 kg/m2. Comorbidities included gestational diabetes (5/63, 7.9%), chronic hypertension (3/63, 4.7%), and pre-eclampsia (5/63, 7.9%). Post-amniotomy protein/creatinine ratio was significantly higher than pre-amniotomy ratio (1.3±2.5 vs 0.34±0.83, p<0.001). In addition, the number of patients with protein/creatinine ratio greater than 0.3 was higher post-amniotomy than pre-amniotomy (41/63 vs 14/63, p<0.001). Conclusion: Amniotomy results in a false elevation of the protein/creatinine ratio in term patients. Urine samples should be obtained by catheterization in the setting of ruptured membranes to reduce falsely elevated results. Although the same can be assumed for other gestational ages, further studies including this population need to be conducted.