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Background: Maternal depression is a major determinant of offspring mental health. Yet, little is understood about how the duration and timing of maternal depression shapes youth risk for depressive symptoms, which if understood could inform when best to intervene. This study aimed to determine how the timing and duration of maternal depression was related to offspring depression in emerging adulthood, and if these associations varied by sex. Methods: We analysed data from the Avon Longitudinal Study of Parents and Children (a prenatal cohort in the Avon area of England, 1991–2003), n = 3,301. We applied the structured lifecourse modelling approach to maternal depression (assessed at 13 points from prenatal period to adolescence) and emerging adult depressive symptoms (age 21). Lifecourse models assessed were accumulation (sum of timepoints when maternal depression was reported), sensitive periods (each period assessed as one during which maternal depression has a stronger effect) and instability (frequent fluctuations in maternal depression). Results: Female adolescents (n = 2,132) had higher SMFQ scores (mean = 6.15, SD = 5.90) than males (n = 1,169, mean = 4.87, SD = 4.82). Maternal depression was most common in the infancy period (21.2% males; 21.4% females). For males, accumulation was the most appropriate lifecourse model; for each additional period of maternal depression, depressive symptoms in emerging adulthood increased by 0.11 (95% CI: 0.07, 0.15, one‐sided p value ≤.001). For females, exposure to maternal depression was associated with increasing depressive symptoms in emerging adulthood, with the largest effect in mid‐childhood (increase of 0.27 units, 95% CI 0.03–0.50, p =.015 for difference between mid‐childhood and other time‐periods) and a smaller, equal effect at all other time‐periods (increase of 0.07 units per time‐period, 95% CI: 0.03–0.12, p =.002). Conclusions: This study highlights the importance of ongoing maternal depression for the development of depression in offspring through to emerging adulthood. Because long‐term exposure to maternal depression was particularly important, early interventions are warranted. [ABSTRACT FROM AUTHOR]

Background: Psychological resilience – positive psychological adaptation in the context of adversity – is defined and measured in multiple ways across disciplines. However, little is known about whether definitions capture the same underlying construct and/or share similar correlates. This study examined the congruence of different resilience measures and associations with sociodemographic factors and body mass index (BMI), a key health indicator. Methods: In a cross-sectional sample of 1429 African American adults exposed to child maltreatment, we derived four resilience measures: a self-report scale assessing resiliency (perceived trait resilience); a binary variable defining resilience as low depression and posttraumatic stress (absence of distress); a binary variable defining resilience as low distress and high positive affect (absence of distress plus positive functioning); and a continuous variable reflecting individuals' deviation from distress levels predicted by maltreatment severity (relative resilience). Associations between resilience measures, sociodemographic factors, and BMI were assessed using correlations and regressions. Results: Resilience measures were weakly-to-moderately correlated (0.27–0.69), though similarly patterned across sociodemographic factors. Women showed higher relative resilience, but lower perceived trait resilience than men. Only measures incorporating positive affect or resiliency perceptions were associated with BMI: individuals classified as resilient by absence of distress plus positive functioning had lower BMI than non-resilient (β = −2.10, p = 0.026), as did those with higher perceived trait resilience (β = −0.63, p = 0.046). Conclusion: Relatively low congruence between resilience measures suggests studies will yield divergent findings about predictors, prevalence, and consequences of resilience. Efforts to clearly define resilience are needed to better understand resilience and inform intervention and prevention efforts. [ABSTRACT FROM AUTHOR]

Pet ownership is common. Growing evidence suggests children form deep emotional attachments to their pets. Yet, little is known about children's emotional reactions to a pet's death. The goal of this study was to describe the relationship between experiences of pet death and risk of childhood psychopathology and determine if it was "better to have loved and lost than never to have loved at all". Data came from the Avon Longitudinal Study of Parents and Children, a UK-based prospective birth cohort (n = 6260). Children were characterized based on their exposure to pet ownership and pet death from birth to age 7 (never loved;loved without loss; loved with loss). Psychopathology symptoms at age 8 were compared across groups using multivariable linear regression. Psychopathology symptoms were higher among children who had loved with loss compared to those who had loved without loss (β = 0.35, p = 0.013; 95% CI = 0.07, 0.63), even after adjustment for other adversities. This group effect was more pronounced in males than in females. There was no difference in psychopathology symptoms between children who had loved with loss and those who had never loved (β = 0.20, p = 0.31, 95% CI = −0.18–0.58). The developmental timing, recency, or accumulation of pet death was unassociated with psychopathology symptoms. Pet death may be traumatic for children and associated with subsequent mental health difficulties. Where childhood pet ownership and pet bereavement is concerned, Tennyson's pronouncement may not apply to children's grief responses: it may not be "better to have loved and lost than never to have loved at all". [ABSTRACT FROM AUTHOR]

Introduction: Childhood adversities have been shown to increase psychopathology risk, including depression. However, the specific impact of childhood emotional neglect on later depression has been understudied. Moreover, few studies have investigated relational protective factors that may offset the risk of depression for children who experienced emotional neglect. Analyzing data (n = 3,265) from the Avon Longitudinal Study of Parents and Children (ALSPAC) study, a longitudinal birth cohort of children born to pregnant women residing in Avon, UK from 1990 to 1992, we assessed the prospective relationship between childhood emotional neglect and depressive symptoms in late adolescence, and tested whether peer social support in mid-adolescence moderates this relationship. Methods: Childhood emotional neglect, defined as the absence of parental attention and support, was measured across seven assessments from age 8 to 17.5. Peer social support was measured at age 15. Depressive symptoms were measured at age 18. We analyzed the associations between emotional neglect and depressive symptoms, and between peer support and depressive symptoms, and also tested interactive effects of peer support on the association between emotional neglect and depressive symptoms. Results: Higher levels of emotional neglect were associated with increased depressive symptoms at 18. Conversely, strong peer social support was associated with reduced depressive symptoms, though no significant interaction with emotional neglect was detected. Conclusion: Although childhood emotional neglect is a risk factor for later depression, our results suggest that strong peer social support at age 15 may generally reduce the risk of depressive symptoms by the time children reach late adolescence. Fostering strong peer support in youth may help offset depression risk for all youth, even among those who have experienced emotional neglect. [ABSTRACT FROM AUTHOR]

Background: Early‐onset depression during childhood and adolescence is associated with a worse course of illness and outcome than adult onset. However, the genetic factors that influence risk for early‐onset depression remain mostly unknown. Using data collected over 13 years, we examined whether polygenic risk scores (PRS) that capture genetic risk for depression were associated with depressive symptom trajectories assessed from childhood to adolescence. Methods: Data came from the Avon Longitudinal Study of Parents and Children, a prospective, longitudinal birth cohort (analytic sample = 7,308 youth). We analyzed the relationship between genetic susceptibility to depression and three time‐dependent measures of depressive symptoms trajectories spanning 4–16.5 years of age (class, onset, and cumulative burden). Trajectories were constructed using a growth mixture model with structured residuals. PRS were generated from the summary statistics of a genome‐wide association study of depression risk using data from the Psychiatric Genomics Consortium, UK Biobank, and 23andMe, Inc. We used MAGMA to identify gene‐level associations with these measures. Results: Youth were classified into six classes of depressive symptom trajectories: high/renitent (27.9% of youth), high/reversing (9.1%), childhood decrease (7.3%), late childhood peak (3.3%), adolescent spike (2.5%), and minimal symptoms (49.9%). PRS discriminated between youth in the late childhood peak, high/reversing, and high/renitent classes compared to the minimal symptoms and childhood decrease classes. No significant associations were detected at the gene level. Conclusions: This study highlights differences in polygenic loading for depressive symptoms across childhood and adolescence, particularly among youths with high symptoms in early adolescence, regardless of age‐independent patterns. [ABSTRACT FROM AUTHOR]

Objective: Efforts to prevent depression, the leading cause of disability worldwide, have focused on a limited number of candidate factors. Using phenotypic and genomic data from over 100,000 UK Biobank participants, the authors sought to systematically screen and validate a wide range of potential modifiable factors for depression.Methods: Baseline data were extracted for 106 modifiable factors, including lifestyle (e.g., exercise, sleep, media, diet), social (e.g., support, engagement), and environmental (e.g., green space, pollution) variables. Incident depression was defined as minimal depressive symptoms at baseline and clinically significant depression at follow-up. At-risk individuals for incident depression were identified by polygenic risk scores or by reported traumatic life events. An exposure-wide association scan was conducted to identify factors associated with incident depression in the full sample and among at-risk individuals. Two-sample Mendelian randomization was then used to validate potentially causal relationships between identified factors and depression.Results: Numerous factors across social, sleep, media, dietary, and exercise-related domains were prospectively associated with depression, even among at-risk individuals. However, only a subset of factors was supported by Mendelian randomization evidence, including confiding in others (odds ratio=0.76, 95% CI=0.67, 0.86), television watching time (odds ratio=1.09, 95% CI=1.05, 1.13), and daytime napping (odds ratio=1.34, 95% CI=1.17, 1.53).Conclusions: Using a two-stage approach, this study validates several actionable targets for preventing depression. It also demonstrates that not all factors associated with depression in observational research may translate into robust targets for prevention. A large-scale exposure-wide approach combined with genetically informed methods for causal inference may help prioritize strategies for multimodal prevention in psychiatry. [ABSTRACT FROM AUTHOR]

Background: Low maternal vitamin D levels [serum 25-hydroxyvitamin D (25(OH)D)] during pregnancy have been linked to offspring neuropsychiatric outcomes such as schizophrenia and autism, but studies on depression are lacking. We examined the association between maternal vitamin D status during pregnancy and offspring depression during childhood and adolescence and investigated whether any associations were modified by offspring genetic risk for depression.Methods: Mother-singleton birth offspring pairs in the Avon Longitudinal Study of Parents and Children (ALSPAC) that had maternal 25(OH)D measurements, offspring genetic data, and offspring depression measures collected in childhood (mean age=10.6 years; n = 2938) and/or adolescence (mean age=13.8 years; n = 2485) were included in the analyses. Using multivariable logistic regression, we assessed associations between maternal vitamin D status and offspring polygenic risk score (PRS) for depression on childhood/adolescent depression risk.Results: There was no evidence for an association between maternal vitamin D status during pregnancy and offspring depression in childhood (p = 0.72) or adolescence (p = 0.07). Offspring depression PRS were independently associated with childhood depression (p = 0.003), but did not interact with maternal vitamin D status. These results were robust to adjustments for potential confounders and different cut-offs for vitamin D insufficiency/deficiency.Limitations: 25(OH)D measurements were only available at a single time point during pregnancy.Conclusion: These findings suggest that maternal vitamin D status during pregnancy does not affect an offspring's risk for early life depression. [ABSTRACT FROM AUTHOR]

Background: Physical activity is increasingly recognized as an important modifiable factor for depression. However, the extent to which individuals with stable risk factors for depression, such as high genetic vulnerability, can benefit from the protective effects of physical activity, remains unknown. Using a longitudinal biobank cohort integrating genomic data from 7,968 individuals of European ancestry with high-dimensional electronic health records and lifestyle survey responses, we examined whether physical activity was prospectively associated with reduced risk for incident depression in the context of genetic vulnerability.Methods: We identified individuals with incident episodes of depression, based on two or more diagnostic billing codes for a depressive disorder within 2 years following their lifestyle survey, and no such codes in the year prior. Polygenic risk scores were derived based on large-scale genome-wide association results for major depression. We tested main effects of physical activity and polygenic risk scores on incident depression, and effects of physical activity within stratified groups of polygenic risk.Results: Polygenic risk was associated with increased odds of incident depression, and physical activity showed a protective effect of similar but opposite magnitude, even after adjusting for BMI, employment status, educational attainment, and prior depression. Higher levels of physical activity were associated with reduced odds of incident depression across all levels of genetic vulnerability, even among individuals at highest polygenic risk.Conclusions: Real-world data from a large healthcare system suggest that individuals with high genetic vulnerability are more likely to avoid incident episodes of depression if they are physically active. [ABSTRACT FROM AUTHOR]

Background: This study aimed to determine whether there were sensitive periods when a first exposure to trauma was most associated with emotion dysregulation symptoms in adulthood.Methods: Adult participants came from a public urban hospital in Atlanta, GA (n = 1944). Lifetime trauma exposure was assessed using the Traumatic Events Inventory (TEI). Multiple linear regression models were used to assess the association between the developmental timing of first trauma exposure, classified as early childhood (ages 0-5), middle childhood (ages 6-10), adolescence (ages 11-18), and adulthood (ages 19+), on adult emotion dysregulation symptoms, measured using the abbreviated Emotion Dysregulation Scale.Results: Participants exposed to trauma at any age had higher emotion dysregulation scores than their unexposed peers. However, participants first exposed to child maltreatment or interpersonal violence during middle childhood had higher emotion dysregulation scores relative to those first exposed during other developmental stages; these developmental timing differences were detected even after controlling for sociodemographic factors, exposure to other trauma, and frequency of exposure to trauma. Further, after controlling for current psychiatric symptoms, the effect of other interpersonal trauma exposure in middle childhood was diminished and first exposure to other interpersonal violence in early childhood was associated with significantly lower emotion dysregulation symptoms.Limitations: Limitations of this study include the use of retrospective reports and absence of complete information about trauma severity or duration.Conclusion: These findings should be replicated in other population-based samples with prospective designs to confirm the importance of developmental timing of trauma on later emotion dysregulation. [ABSTRACT FROM AUTHOR]

Background Trauma exposure is a known risk factor for psychopathology. However, the impact of the developmental timing of exposure remains unclear. This study examined the effect of age at first trauma exposure on levels of adult depressive and posttraumatic stress disorder (PTSD) symptoms. Methods Lifetime trauma exposure (including age at first exposure and frequency), current psychiatric symptoms, and sociodemographic information were collected during interviews with adults participating in a study at a public urban hospital in Atlanta, GA. Multiple linear regression models assessed the association between timing of first trauma exposure, classified as early childhood (ages 0–5), middle childhood (ages 6–10), adolescence (ages 11–18), and adulthood (ages 19+), on adult psychopathology in 2892 individuals. Results Participants exposed to trauma (i.e., child maltreatment, other interpersonal violence, non-interpersonal violence, and other events) at any age had higher depressive and PTSD symptoms compared to their unexposed peers. However, participants first exposed to child maltreatment during early childhood had depression and PTSD symptoms that were about twice as high as those exposed during later developmental stages. This association was detected even after controlling for sociodemographic characteristics, exposure to other trauma types, and frequency of exposure. Participants first exposed during middle childhood to other interpersonal violence also had depressive symptoms scores that were about twice as high as those first exposed during adulthood. Conclusions Trauma exposure at different ages may differentially impact depressive and PTSD symptoms in adulthood. More detailed examination of timing of trauma exposure is warranted to aid in identifying sensitive periods in development. [ABSTRACT FROM AUTHOR]

Background: Genome-wide association studies (GWAS) have made little progress in identifying variants linked to depression. We hypothesized that examining depressive symptoms and considering gene-environment interaction (GxE) might improve efficiency for gene discovery. We therefore conducted a GWAS and genome-wide by environment interaction study (GWEIS) of depressive symptoms.Methods: Using data from the SHARe cohort of the Women's Health Initiative, comprising African Americans (n = 7,179) and Hispanics/Latinas (n = 3,138), we examined genetic main effects and GxE with stressful life events and social support. We also conducted a heritability analysis using genome-wide complex trait analysis (GCTA). Replication was attempted in four independent cohorts.Results: No SNPs achieved genome-wide significance for main effects in either discovery sample. The top signals in African Americans were rs73531535 (located 20 kb from GPR139, P = 5.75 × 10(-8) ) and rs75407252 (intronic to CACNA2D3, P = 6.99 × 10(-7) ). In Hispanics/Latinas, the top signals were rs2532087 (located 27 kb from CD38, P = 2.44 × 10(-7) ) and rs4542757 (intronic to DCC, P = 7.31 × 10(-7) ). In the GEWIS with stressful life events, one interaction signal was genome-wide significant in African Americans (rs4652467; P = 4.10 × 10(-10) ; located 14 kb from CEP350). This interaction was not observed in a smaller replication cohort. Although heritability estimates for depressive symptoms and stressful life events were each less than 10%, they were strongly genetically correlated (rG = 0.95), suggesting that common variation underlying self-reported depressive symptoms and stressful life event exposure, though modest on their own, were highly overlapping in this sample.Conclusions: Our results underscore the need for larger samples, more GEWIS, and greater investigation into genetic and environmental determinants of depressive symptoms in minorities. [ABSTRACT FROM AUTHOR]

Depression is one of the most prevalent, disabling, and costly mental health conditions in the United States and also worldwide. One promising avenue for preventing depression and informing its clinical treatment lies in uncovering the genetic and environmental determinants of the disorder aswell as their interaction (GE). The overarching goal of this review article is to translate recent findings fromstudies of genetic association and GE related to depression, particularly for readers without in-depth knowledge of genetics or geneticmethods. The review is organized into threemajor sections. In the first, we summarize what is currently known about the genetic determinants of depression, focusing on findings from genome-wide association studies (GWAS). In the second section, we review findings from studies of GE, which seek to simultaneously examine the role of genes and exposure to specific environments or experiences in the etiology of depression. In the third section, we describe the challenges to genetic discovery in depression and promising strategies for future progress. [ABSTRACT FROM AUTHOR]

Background Beginning in adolescence, females are at significantly higher risk for depression than males. Despite substantial efforts, gaps remain in our understanding of this disparity. This study tested whether gender differences in adolescent-onset depression arise because of female's greater exposure or sensitivity to violence. Methods Data came from 5,692 participants in the National Comorbidity Survey Replication. Trained interviewers collected data about major depression and participants' exposure to four types of interpersonal violence (physical abuse, sexual assault, rape, and witnessing violence) using a modified version of the Composite International Diagnostic Interview. We used discrete time survival analysis to investigate gender differences in the risk of adolescent onset depression. Results Of the entire sample, 5.7% met DSM- IV criteria for depression by age 18; 5.8% of the sample reported being physically abused, 11.7% sexually assaulted, 8.5% raped, and 13.2% witnessed violence by age 18 . Females had 1.51 times higher odds of depression by age 18 than males. Exposure to all types of violence was associated with an increased odds of depression in both the past year and the years following exposure. Adjusting for exposure to violence partially attenuated the association between gender and depression, especially for sexual assault (odds ratio [ OR] attenuated = 1.28; 15.23%) and rape ( OR attenuated = 1.32; 12.59%). There was no evidence that females were more vulnerable to the effects of violence than males. Discussion Gender differences in depression are partly explained by females' higher likelihood of experiencing interpersonal violence. Reducing exposure to sexual assault and rape could therefore mitigate gender differences in depression. [ABSTRACT FROM AUTHOR]

Background: Depression is a major public health problem among youth, currently estimated to affect as many as 9% of US children and adolescents. The recognition that both genes (nature) and environments (nurture) are important for understanding the etiology of depression has led to a rapid growth in research exploring gene-environment interactions (GxE). However, there has been no systematic review of GxE in youth depression to date. Methods: The goal of this article was to systematically review evidence on the contribution of GxE to the risk of child and adolescent depression. Through a search of PubMed and PsycINFO databases to 1 April 2010, we identified 20 candidate gene-environment interaction studies focused on depression in youth (up to age 26) and compared each study in terms of the following characteristics: research design and sample studied; measure of depression and environment used; genes explored; and GxE findings in relation to these factors. Results: In total, 80% of studies ( n = 16) found at least one significant GxE association. However, there was wide variation in methods and analyses adopted across studies, especially with respect to environmental measures used and tests conducted to estimate GxE. This heterogeneity made it difficult to compare findings and evaluate the strength of the evidence for GxE. Conclusions: The existing body of GxE research on depression in youth contains studies that are conceptually and methodologically quite different, which contributes to mixed findings and makes it difficult to assess the current state of the evidence. To decrease this heterogeneity, we offer 20 recommendations that are focused on: (a) reporting GxE research; (b) testing and reporting GxE effects; (c) conceptualizing, measuring and analyzing depression; (d) conceptualizing, measuring and analyzing environment; (e) increasing power to test for GxE; and (f) improving the quality of genetic data used. Although targeted to GxE research on depression, these recommendations can be adopted by GxE researchers focusing on other mental health outcomes. [ABSTRACT FROM AUTHOR]

Objective: To test the hypothesis that a structured aerobic exercise regimen would decrease the severity of depressive symptoms in people with traumatic brain injury (TBI) who reported at least mild depression severity at baseline. Design: Prospective, randomized, controlled trial. Setting: Community gymnasium. Participants: Subjects with a history of a prior TBI (6 months to 5 years post-injury), recruited from the community. Inclusion criteria included scoring ≥5 on the Patient Health Questionnaire-9. Subjects were excluded if they were non-English speakers, had a medical condition precluding exercise, had suicidal ideation, regularly exercised, or could not use standard aerobic exercise equipment. Intervention: Weekly supervised exercise sessions over a 10-week period consisted of education, warm-up, 30 minutes of aerobic exercise, and cool down. The exercise intensity was adjusted to reach a heart rate goal of 60% of the participant''s estimated maximal heart rate. Main Outcome Measurement: Beck Depression Inventory (BDI) comparing exercise to control groups. Post hoc analyses compared groups exercising ≥90 minutes or <90 minutes per week. Results: Between-group comparisons at 10 weeks revealed no difference between groups on the BDI (P = .250). For the groups divided by minutes exercised per week, the high-activity group had significantly better depression scores than those in the low-activity group (P = .033). Conclusions: Although there was no statistically significant difference between the treated and the control group on mood after intervention, those persons with TBI who recounted higher levels of exercise per week also reported less depression and improved sleep, community participation, and overall quality of life. [Copyright &y& Elsevier]

The prevalence of depression is higher in individuals with autoimmune diseases, but the mechanisms underlying the observed comorbidities are unknown. Shared genetic etiology is a plausible explanation for the overlap, and in this study we tested whether genetic variation in the major histocompatibility complex (MHC), which is associated with risk for autoimmune diseases, is also associated with risk for depression. We fine-mapped the classical MHC (chr6: 29.6–33.1 Mb), imputing 216 human leukocyte antigen (HLA) alleles and 4 complement component 4 (C4) haplotypes in studies from the Psychiatric Genomics Consortium Major Depressive Disorder Working Group and the UK Biobank. The total sample size was 45,149 depression cases and 86,698 controls. We tested for association between depression status and imputed MHC variants, applying both a region-wide significance threshold (3.9 × 10−6) and a candidate threshold (1.6 × 10−4). No HLA alleles or C4 haplotypes were associated with depression at the region-wide threshold. HLA-B*08:01 was associated with modest protection for depression at the candidate threshold for testing in HLA genes in the meta-analysis (odds ratio = 0.98, 95% confidence interval = 0.97–0.99). We found no evidence that an increased risk for depression was conferred by HLA alleles, which play a major role in the genetic susceptibility to autoimmune diseases, or C4 haplotypes, which are strongly associated with schizophrenia. These results suggest that any HLA or C4 variants associated with depression either are rare or have very modest effect sizes. [ABSTRACT FROM AUTHOR]

Objective: The study aims to evaluate the association between exposure to childhood adversity and insomnia, with an emphasis on the role of adversity type, timing, and accumulation (i.e., the number of specific types of adversities the child reported being exposed to).Methods: Our analytic sample comprised 9582 adolescents from the National Comorbidity Survey Replication Adolescent Supplement (NCS-A), a nationally representative population-based sample. We examined the association between 18 different types of retrospectively reported adversities (capturing interpersonal violence, accidents and injuries, social network or witnessing events, and other adverse events) and risk of self-reported past-year insomnia. We also examined whether the age at first exposure to adversity was associated with the risk of insomnia, and whether exposure to a greater number of different types of adversities (ie, accumulation) conferred an elevated risk of insomnia. In addition, we performed a sensitivity analysis excluding adolescents with a past-year diagnosis of major depression, dysthymia, post-traumatic stress disorder (PTSD), or generalized anxiety disorder.Results: Almost one-third of adolescents reported insomnia, with a higher prevalence among girls and those from racial/ethnic minority groups. Adolescents exposed to at least one childhood adversity of any type (59.41%) were more likely than their nonexposed peers to experience insomnia (across adversities, prevalence ratios (PRs) ranged from 1.31 to 1.89). Risk of insomnia differed based on the age at first exposure to adversity as well as the type of adversity. Adolescents exposed to a greater number of different types of adversities had a higher risk of insomnia compared to those experiencing fewer adversities. These results were similar, by and large, to those obtained after excluding adolescents with at least one of the four past-year psychiatric disorders.Conclusions: Exposure to adversity confers an elevated risk of insomnia. This association varied by type, timing, and accumulation of exposure and did not appear to be driven by psychiatric disorders. Given the well-documented physical and mental health consequences of insomnia, such findings further support the need for practitioners to screen children for exposure to childhood adversity and insomnia symptoms. [ABSTRACT FROM AUTHOR]