Childhood emotion dysregulation mediates the relationship between preschool emotion labeling and adolescent depressive symptoms.

Deficits in emotion processing (e.g., emotion labeling and regulation) are widely implicated in depression risk. While prior literature documents these deficits in concurrence with depression, more research is needed to investigate emotion processing pathways of depression risk across development. The purpose of this study was to investigate if emotion processes (i.e., emotion labeling and emotion regulation/dysregulation) in early and middle childhood predict adolescent depressive symptom severity in a prospective sample. Data were analyzed from a longitudinal study of diverse preschoolers oversampled for depressive symptoms using measures of preschool emotion labeling of faces (i.e., Facial Affect Comprehension Evaluation), middle childhood emotion regulation and dysregulation (i.e., emotion regulation checklist), and adolescent depressive symptoms (i.e., PAPA, CAPA, and KSADS-PL diagnostic interviews). Multilevel models indicated that preschoolers with depression had similar development of emotion labeling in early childhood as peers. Mediation analyses revealed that deficits in preschool-aged anger and surprise labeling ability indirectly predicted higher adolescent depressive symptom severity through increased middle childhood emotion lability/negativity, not decreased emotion regulation. Adolescent depression may be predicted by an emotion processing pathway that spans from early childhood to adolescence, and findings may generalize to high risk for depression youth samples. Specifically, poor emotion labeling in early childhood may lead to increased childhood emotion lability/negativity, which increases the risk for adolescent depressive symptom severity. Findings may help identify specific emotion processing relations in childhood that increase the risk for depression and inform intervention aimed at improving preschoolers' anger and surprise labeling. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Associations Between Polygenic Scores for Cognitive and Non-cognitive Factors of Educational Attainment and Measures of Behavior, Psychopathology, and Neuroimaging in the Adolescent Brain Cognitive Development Study.

Background: Both cognitive and non-cognitive (e.g., traits like curiosity) factors are critical for social and emotional functioning and independently predict educational attainment. These factors are heritable and genetically correlated with a range of health-relevant traits and behaviors in adulthood (e.g., risk-taking, psychopathology). However, whether these associations are present during adolescence, and to what extent these relationships diverge, could have implications for adolescent health and well-being. Methods: Using data from 5,517 youth of European ancestry from the ongoing Adolescent Brain Cognitive DevelopmentSM Study, we examined associations between polygenic scores (PGS) for cognitive and non-cognitive factors and outcomes related to cognition, socioeconomic status, risk tolerance and decision-making, substance initiation, psychopathology, and brain structure. Results: Cognitive and non-cognitive PGSs were both positively associated with cognitive performance and family income, and negatively associated with ADHD and severity of psychotic-like experiences. The cognitive PGS was also associated with greater risk-taking, delayed discounting, and anorexia, as well as lower likelihood of nicotine initiation. The cognitive PGS was further associated with cognition scores and anorexia in within-sibling analyses, suggesting these results do not solely reflect the effects of assortative mating or passive gene-environment correlations. The cognitive PGS showed significantly stronger associations with cortical volumes than the non-cognitive PGS and was associated with right hemisphere caudal anterior cingulate and pars-orbitalis in within-sibling analyses, while the non-cognitive PGS showed stronger associations with white matter fractional anisotropy and a significant within-sibling association for right superior corticostriate-frontal cortex. Conclusions: Our findings suggest that PGSs for cognitive and non-cognitive factors show similar associations with cognition and socioeconomic status as well as other psychosocial outcomes, but distinct associations with regional neural phenotypes in this adolescent sample.

Contributions of socioeconomic status and cognition to emotion processes and internalizing psychopathology in childhood and adolescence: A systematic review.

This systematic review evaluated evidence from 25 manuscripts regarding three possible relationships of socioeconomic disadvantage (SESD) and cognition to emotion knowledge (EK), emotion regulation (ER), and internalizing psychopathology (IP) across development; a) independent contributions of disadvantage and cognition; b) cognition mediates relations of disadvantage; or c) cognition moderates' relations of disadvantage. Results support associations between SESD and cognition to emotion that differ by cognitive domain and developmental epoch. For EK, in early and middle childhood language and executive functions contribute to EK independent of SESD, and early childhood executive functions may interact with socioeconomic status (SES) to predict prospective EK. Regarding ER, language contributes to ER independent of SES across development and may mediate associations between SES and ER in adolescence. Regarding IP, SES, language, executive function, and general ability have independent contributions to IP across development; in adolescence executive function may mediate or moderate associations between SES and IP. Findings highlight the need for nuanced and developmentally sensitive research on the contributions of SESD and domains of cognition to emotion.

Phenome-wide Investigation of Behavioral, Environmental, and Neural Associations with Cross-Disorder Genetic Liability in Youth of European Ancestry.

Etiologic insights into psychopathology may be gained by using hypothesis-free methods to identify associations between genetic risk for broad psychopathology and phenotypes measured during adolescence, including both markers of child psychopathology and intermediate phenotypes such as neural structure that may link genetic risk with outcomes. We conducted a phenome-wide association study (phenotype n=1,269-1,694) of polygenic risk scores (PRS) for broad spectrum psychopathology (i.e., Compulsive, Psychotic, Neurodevelopmental, and Internalizing) in youth of PCA-selected European ancestry (n=5,556; ages 9-13) who completed the baseline and/or two-year follow-up of the ongoing Adolescent Brain Cognitive Development℠ (ABCD) Study. We found that Neurodevelopmental and Internalizing PRS were significantly associated with a host of proximal as well as distal phenotypes (Neurodevelopmental: 187 and 211; Internalizing: 122 and 173 phenotypes at baseline and two-year follow-up, respectively), whereas Compulsive and Psychotic PRS showed zero and one significant associations, respectively, after Bonferroni correction. Neurodevelopmental PRS were further associated with brain structure metrics (e.g., total volume, mean right hemisphere cortical thickness), with only cortical volume indirectly linking Neurodevelopmental PRS to grades in school. Genetic variation influencing risk to psychopathology manifests broadly as behaviors, psychopathology symptoms, and related risk factors in middle childhood and early adolescence.

Understanding Associations Between Race/Ethnicity, Experiences of Discrimination, and Psychotic-like Experiences in Middle Childhood.

OBJECTIVE: The present study aimed to examine factors that may account for race/ethnicity differences in psychotic-like experiences (PLEs) in a middle childhood sample, including evidence for experiences of discrimination as a psychosocial mediator of these differences. METHOD: In a sample of 9- to 10-year-olds (N = 10,839) from the Adolescent Brain Cognitive Development Study, we compared PLEs across racial/ethnic groups. We also examined whether experiences of discrimination indirectly linked racial/ethnic identity and PLEs and whether social support moderated this indirect association. RESULTS: Differences between racial/ethnic groups were found in the endorsement of PLEs, such that Black and Hispanic participants endorsed higher levels of PLEs compared with Asian, multiracial/multiethnic, and White participants. These differences were accounted for in part by experiences of discrimination, an indirect effect that was in turn attenuated by increased social support. CONCLUSION: This is the first study to suggest that the experience of discrimination may indirectly link the association between racial/ethnic differences and endorsement of PLEs using the Prodromal Questionnaire-Brief Child Version and additionally that social support may act as a moderator of this mediation. Results provide evidence that social inequities such as racial discrimination may contribute to increases in PLEs. These findings shed further light on the links between structural racism and mental health inequities for people in minoritized groups.

Trajectories of Suicidal Thoughts and Behaviors From Preschool Through Late Adolescence.

OBJECTIVE: Suicidal thoughts and behaviors (STBs) represent a significant and escalating public health concern in youth. Evidence that STBs can emerge in the preschool years suggests that some pathways leading to clinically significant STBs begin early in life. METHOD: This prospective longitudinal study examined the developmental trajectories of STBs in children from ages 3 to 17, oversampled for preschool-onset depression. RESULTS: Three unique trajectories of STBs across childhood and adolescence were identified: low class (n = 273) characterized by low rates of STBs, early-persistent class (n = 21) characterized by steadily increasing STBs, and late-onset class (n = 21) characterized by low rates of STBs through age 10 followed by a dramatic increase from ages 11 to 14 years. Preschool measures of depression symptoms, externalizing symptoms, impulsivity, and lower income relative to needs were associated with both high-risk STB classes. Both high-risk STB classes reported greater functional impairment, more externalizing symptoms, and more cumulative stressful life events in adolescence relative to the low class; the late-onset class also reported poorer academic functioning relative to both the early-persistent and low classes. CONCLUSION: A significant minority of this prospectively followed group of preschool children evidenced STBs by and/or after age 10. Although relatively rare before age 10, approximately half of the children who experienced STBs in adolescence first exhibited STBs in early childhood and comprised a trajectory suggesting increasing STBs. In contrast, approximately half of children first exhibited STBs in early adolescence. Early screening and identification of at-risk youth during both preschool and late childhood is important for early intervention regarding STBs.

Early Childhood Socioeconomic Status and Cognitive and Adaptive Outcomes at the Transition to Adulthood: The Mediating Role of Gray Matter Development Across Five Scan Waves.

BACKGROUND: Early low socioeconomic status (SES) is associated with poor outcomes in childhood, many of which endure into adulthood. It is critical to determine how early low SES relates to trajectories of brain development and whether these mediate relationships to poor outcomes. We use data from a unique 17-year longitudinal study with five waves of structural brain imaging to prospectively examine relationships between preschool SES and cognitive, social, academic, and psychiatric outcomes in early adulthood. METHODS: Children (n = 216, 50% female, 47.2% non-White) were recruited from a study of early onset depression and followed approximately annually. Family income-to-needs ratios (SES) were assessed when children were ages 3 to 5 years. Volumes of cortical gray and white matter and subcortical gray matter collected across five scan waves were processed using the FreeSurfer Longitudinal pipeline. When youth were ages 16+ years, cognitive function was assessed using the NIH Toolbox, and psychiatric diagnoses, high-risk behaviors, educational function, and social function were assessed using clinician administered and parent/youth report measures. RESULTS: Lower preschool SES related to worse cognitive, high-risk, educational, and social outcomes (|standardized B| = 0.20-0.31, p values < .003). Lower SES was associated with overall lower cortical (standardized B = 0.12, p < .0001) and subcortical gray matter (standardized B = 0.17, p < .0001) volumes, as well as a shallower slope of subcortical gray matter growth over time (standardized B = 0.04, p = .012). Subcortical gray matter mediated the relationship of preschool SES to cognition and high-risk behaviors. CONCLUSIONS: These novel longitudinal data underscore the key role of brain development in understanding the long-lasting relations of early low SES to outcomes in children.

Contributions from resting state functional connectivity and familial risk to early adolescent-onset MDD: Results from the Adolescent Brain Cognitive Development study.

BACKGROUND: Family history of Major Depressive Disorder (MDD) is a robust predictor of MDD onset, especially in early adolescence. We examined the relationships between familial risk for depression and alterations to resting state functional connectivity (rsFC) within the default mode network (wDMN) and between the DMN and the left/right hippocampus (DMN-LHIPP/DMN-RHIPP) to the risk for early adolescent MDD onset. METHODS: We examined 9403 youth aged nine to eleven from the Adolescent Brain Cognitive Development study. Depressive symptoms were measured with the parent-reported Child Behavior Checklist. Both youth and their parents completed the Kiddie Schedule for Affective Disorders and Schizophrenia, which provided MDD diagnoses. A family history screen was administered to determine familial risk for depression. Youth underwent a resting state functional magnetic resonance imaging scan, providing us with rsFC data. RESULTS: Negative wDMN rsFC was associated with child-reported current depression, both child- and parent-reported past depression, and parent-reported current depressive symptoms. No difference was found in wDMN, DMN-LHIPP or DMN-RHIPP rsFC in children with or without familial risk for depression. Familial risk for depression interacted with wDMN rsFC in association with child-reported past MDD diagnosis and parent-reported current depressive symptoms. LIMITATIONS: Information such as length of depressive episodes and age of onset of depression was not collected. CONCLUSIONS: Altered wDMN rsFC in youth at familial risk for depression may be associated with increased risk for MDD onset in adolescence, but longitudinal studies are needed to test this hypothesis.

Evidence for dissociable cognitive and neural pathways from poverty versus maltreatment to deficits in emotion regulation.

Poverty and threat exposure (TE) predict deficits in emotion regulation (ER). Effective cognitive ER (i.e., reappraisal) may be supported by: (1) cognitive processes implicated in generating and implementing cognitive reappraisal, supported by activation in brain regions involved in cognitive control (e.g., frontal, insular, and parietal cortices) and (2) emotion processing and reactivity, involving identification, encoding, and maintenance of emotional states and related variation in brain activity of regions involved in emotional reactivity (i.e., amygdala). Poverty is associated with deficits in cognitive control, and TE with alterations in emotion processing and reactivity. Our goal was to identify dissociable emotional and cognitive pathways to ER deficits from poverty and TE. Measures of cognitive ability, emotional processing and reactivity, ER, and neural activity during a sadness ER task, were examined from a prospective longitudinal study of youth at risk for depression (n = 139). Both cognitive ability and left anterior insula extending into the frontal operculum activity during a sadness reappraisal task mediated the relationship between poverty and ER. Emotion processing/reactivity didn't mediate the relationship of TE to ER. Findings support a cognitive pathway from poverty to ER deficits. They also underscore the importance of dissociating mechanisms contributing to ER impairments from adverse early childhood experiences.

Labeling Emotional Stimuli in Early Childhood Predicts Neural and Behavioral Indicators of Emotion Regulation in Late Adolescence.

BACKGROUND: Effective emotion regulation (ER) may be supported by 1) accurate emotion identification, encoding, and maintenance of emotional states and related brain activity of regions involved in emotional response (i.e., amygdala, ventral/posterior insula) and 2) cognitive processes that implement reframing, supported by activation in cognitive control brain regions (e.g., frontal, insular, and parietal cortices). The purpose of this project was to examine how emotion labeling ability in early childhood is related to ER concurrently and prospectively. METHODS: Data from a prospective longitudinal study of youths at risk for depression, including measures of emotion labeling (i.e., Facial Affect Comprehension Evaluation) and ER ability (i.e., Emotion Regulation Checklist) and strategy use (i.e., Cognitive Emotion Regulation Questionnaire, Children's Response Style Questionnaire), and functional magnetic resonance imaging data during a sadness ER task (N = 139) were examined. RESULTS: Findings from multilevel modeling and linear regression suggested that greater emotion labeling ability of more difficult emotions in early childhood was associated with enhanced parent-reported ER in adolescence, but not with a tendency to engage in adaptive or maladaptive ER strategies. Recognition of fear and surprise predicted greater activation in cortical regions involved in cognitive control during an ER of sadness task, including in the insula, anterior cingulate cortex, dorsal medial prefrontal cortex, and inferior frontal gyrus. CONCLUSIONS: These findings suggest that early ability to identify and label difficult facial emotions in early childhood is associated with better ER in adolescence and enhanced activity of cognitive control regions of the brain.

Testosterone and hippocampal trajectories mediate relationship of poverty to emotion dysregulation and depression.

There is robust evidence that early poverty is associated with poor developmental outcomes, including impaired emotion regulation and depression. However, the specific mechanisms that mediate this risk are less clear. Here we test the hypothesis that one pathway involves hormone mechanisms (testosterone and DHEA) that contribute to disruption of hippocampal brain development, which in turn contributes to perturbed emotion regulation and subsequent risk for depression. To do so, we used data from 167 children participating in the Preschool Depression Study, a longitudinal study that followed children from preschool (ages 3 to 5 y) to late adolescence, and which includes prospective assessments of poverty in preschool, measures of testosterone, DHEA, and hippocampal volume across school age and adolescence, and measures of emotion regulation and depression in adolescence. Using multilevel modeling and linear regression, we found that early poverty predicted shallower increases of testosterone, but not DHEA, across development, which in turn predicted shallower trajectories of hippocampal development. Further, we found that early poverty predicted both impaired emotion regulation and depression. The relationship between early poverty and self-reported depression in adolescence was explained by serial mediation through testosterone to hippocampus to emotion dysregulation. There were no significant interactions with sex. These results provide evidence about a hormonal pathway by which early poverty may contribute to disrupted brain development and risk for mental health problems later in life. Identification of such pathways provide evidence for potential points of intervention that might help mitigate the impact of early adversity on brain development.

Convergent Evidence for Predispositional Effects of Brain Gray Matter Volume on Alcohol Consumption.

BACKGROUND: Alcohol use has been reliably associated with smaller subcortical and cortical regional gray matter volumes (GMVs). Whether these associations reflect shared predisposing risk factors or causal consequences of alcohol use remains poorly understood. METHODS: Data came from 3 neuroimaging samples (N = 2423), spanning childhood or adolescence to middle age, with prospective or family-based data. First, we identified replicable GMV correlates of alcohol use. Next, we used family-based and longitudinal data to test whether these associations may plausibly reflect a predispositional liability for alcohol use or a causal consequence of alcohol use. Finally, we used heritability, gene-set enrichment, and transcriptome-wide association study approaches to evaluate whether genome-wide association study-defined genomic risk for alcohol consumption is enriched for genes that are preferentially expressed in regions that were identified in our neuroimaging analyses. RESULTS: Smaller right dorsolateral prefrontal cortex (DLPFC) (i.e., middle and superior frontal gyri) and insula GMVs were associated with increased alcohol use across samples. Family-based and prospective longitudinal data suggest that these associations are genetically conferred and that DLPFC GMV prospectively predicts future use and initiation. Genomic risk for alcohol use was enriched in gene sets that were preferentially expressed in the DLPFC and was associated with replicable differential gene expression in the DLPFC. CONCLUSIONS: These data suggest that smaller DLPFC and insula GMV plausibly represent genetically conferred predispositional risk factors for, as opposed to consequences of, alcohol use. DLPFC and insula GMV represent promising biomarkers for alcohol-consumption liability and related psychiatric and behavioral phenotypes.

The role of familial risk, parental psychopathology, and stress for first-onset depression during adolescence.

BACKGROUND: Adolescence represents a critical developmental period during which the initial onset of depression emerges. Family risk for depression is a salient risk factor for the initial onset of Major Depressive Disorder (MDD). We examined the effects of familial risk, stress, and behavior on the risk of developing first-onset depression. METHODS: Adolescents aged 12 to 15 with high (n = 166) or low (n = 159) familial risk for depression were assessed annually for up to five years. Stress was assessed using the Stressful Life Events Schedule and Childhood Trauma Questionnaire. The Kiddie Schedule for Affective Disorders and Schizophrenia-Present and Lifetime Version was administered to the adolescents and their parents to assess lifetime psychiatric conditions and diagnose MDD onset. Survival and path analyses were used in tandem to determine the risk for first-onset depression as well as the contributions of additional direct and indirect pathways to onset. RESULTS: High-risk adolescents were eight times more likely to develop first-onset depression compared with low-risk adolescents. The path analyses revealed that the presence of maternal behavioral disorders and increased recent life stress directly predicted an initial onset of MDD in high-risk adolescents. LIMITATIONS: The small samples used in this study limit the generalizability of these findings. CONCLUSIONS: Adolescents at high familial risk for depression had an increased risk for the emergence of first-onset depression during adolescence. Stress and maternal behavioral psychopathology directly contributed to depression onset independently of familial risk, while childhood trauma exerted an indirect effect on first-onset MDD through recent stress.

An epidemiological evaluation of trauma types in a cohort of deployed service members.

OBJECTIVE: Using Stein et al.'s (2012) categorization scheme for typing Criterion A events (i.e., Life Threat to Self, Life Threat to Other, Aftermath of Violence, Traumatic Loss, Moral Injury by Self, and Moral Injury by Other) and extending Litz et al.'s (2018) prior work, we investigated the prevalence of trauma types, prevalence of posttraumatic stress disorder within each trauma type, and associations between trauma types and behavioral and mental health outcomes for an epidemiological sample of service members. METHOD: Criterion A events coded by independent raters (kappas = .85-1.00) were used to determine prevalence rates and to conduct two path models examining all trauma types in relation to mental health outcomes. RESULTS: Consistent with prior research, we found events containing Life Threat to Self (51.1%) and Life Threat to Other (30.8%) to be most prevalent, and a majority of events (62.9%) were coded with one trauma type. Although least prevalent, Aftermath of Violence (12.0%) and Moral Injury by Self (4.8%) were most frequently and strongly associated with worse mental health outcomes. Path models predicted a very small amount of variance in continuous outcomes, thus limiting the interpretation of findings. CONCLUSION: More epidemiological research is needed to understand the role of trauma type in relation to mental health among nontreatment-seeking service members. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

Relative abundance of Akkermansia spp. and other bacterial phylotypes correlates with anxiety- and depressive-like behavior following social defeat in mice.

As discussion of stress and stress-related disorders rapidly extends beyond the brain, gut microbiota have emerged as a promising contributor to individual differences in the risk of illness, disease course, and treatment response. Here, we employed chronic mild social defeat stress and 16S rRNA gene metagenomic sequencing to investigate the role of microbial composition in mediating anxiety- and depressive-like behavior. In socially defeated animals, we found significant reductions in the overall diversity and relative abundances of numerous bacterial genera, including Akkermansia spp., that positively correlated with behavioral metrics of both anxiety and depression. Functional analyses predicted a reduced frequency of signaling molecule pathways, including G-protein-coupled receptors, in defeated animals. Collectively, our data suggest that shifts in microbial composition may play a role in the pathogenesis of anxiety and depression.

Correction: Comparative evaluation of a new magnetic bead-based DNA extraction method from fecal samples for downstream next-generation 16S rRNA gene sequencing.

[This corrects the article DOI: 10.1371/journal.pone.0202858.].

Paradoxical associations between familial affective responsiveness, stress, and amygdala reactivity.

Studies of early life extremes such as trauma, abuse, and neglect highlight the critical importance of quality caregiving in the development of brain circuits supporting emotional behavior and mental health. The impact of normative variability in caregiving on such biobehavioral processes, however, is poorly understood. Here, we provide initial evidence that even subtle variability in normative caregiving maps onto individual differences in threat-related brain function and, potentially, associated psychopathology in adolescence. Specifically, we report that greater familial affective responsiveness is associated with heightened amygdala reactivity to interpersonal threat, particularly in adolescents having experienced relatively low recent stress. These findings extend the literature on the effects of caregiving extremes on brain function to subtle, normative variability but suggest that presumably protective factors may be associated with increased risk-related amygdala reactivity. We consider these paradoxical associations with regard to studies of basic associative threat learning and further consider their relevance for understanding potential effects of caregiving on psychological development. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

Trajectories of Alcohol Initiation and Use During Adolescence: The Role of Stress and Amygdala Reactivity.

OBJECTIVE: Early alcohol use initiation predicts onset of alcohol use disorders in adulthood. However, little is known about developmental trajectories of alcohol use initiation and their putative biological and environmental correlates. METHOD: Adolescents (N = 330) with high or low familial loading for depression were assessed annually for up to 6 years. Data were collected assessing affective symptoms, alcohol use, and stress at each assessment. Adolescents also participated in a functional magnetic resonance imaging protocol that included measurement of threat-related amygdala and reward-related ventral striatum activity. RESULTS: Latent class analyses identified 2 trajectories of alcohol use initiation. Early initiators (n = 32) reported greater baseline alcohol use and rate of change of use compared with late initiators and/or current abstainers (n = 298). Early initiators reported higher baseline levels of stressful life events (p = .001) and exhibited higher amygdala (p = .001) but not ventral striatum activity compared with late initiators. Early initiators were 15.3 times more likely to have a full drink (p < .0001), 9.1 times more likely to experience intoxication (p < .0001), and 6.7 times more likely to develop an alcohol use disorder by 19 years of age compared with late initiators (p = .003). CONCLUSION: Adolescents on a trajectory of early alcohol use initiation have higher levels of stress, have increased threat-related amygdala activity, are more likely to consume a full standard alcoholic drink, are more likely to experience early intoxication, and are at a heightened risk for the onset of an alcohol use disorder.

Comparative evaluation of a new magnetic bead-based DNA extraction method from fecal samples for downstream next-generation 16S rRNA gene sequencing.

We are colonized by a vast population of genetically diverse microbes, the majority of which are unculturable bacteria that reside within the gastrointestinal tract. As affordable, advanced next-generation sequencing technologies become more widely available, important discoveries about the composition and function of these microbes become increasingly possible. In addition to rapid advancement in sequencing technologies, automated systems have been developed for nucleic acid extraction; however, these methods have yet to be widely used for the isolation of bacterial DNA from fecal samples. Here, we adapted Promega's Maxwell® RSC PureFood GMO and Authentication kit for use with fecal samples and compared it to the commonly used Qiagen QIAamp® PowerFecal® kit. Results showed that the two approaches yielded similar measures of DNA purity and successful next-generation sequencing amplification and produced comparable composition of microbial communities. However, DNA extraction with the Maxwell® RSC kit produced higher concentrations with a lower fecal sample input weight and took a fraction of the time compared to the QIAamp® PowerFecal® protocol. The results of this study demonstrate that the Promega Maxwell® RSC system can be used for medium-throughput DNA extraction in a time-efficient manner without compromising the quality of the downstream sequencing.