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In adolescence, caffeinated beverage consumption is negatively associated with cognitive functioning. The default mode network and dorsal attention network are anticorrelated brain systems that are essentially implicated in attention. Despite the importance of the anticorrelation of default mode network - dorsal attention network on cognitive functioning, no studies have examined the association between this anticorrelation and recent caffeine consumption among youths. This study analyzed baseline data from the Adolescent Brain Cognitive Development℠ Study, the largest longitudinal study examining brain development and adolescent health in the United States, to explore the associations between caffeinated beverage consumption and the strength of anticorrelation between the default mode network - dorsal attention network. A total of N = 4,673 early adolescents (average age 9.9 years, standard deviation = 0.6) had self-report data for two caffeine variables: [a] last 24-hour caffeinated beverage consumption (Yes/No) and [b] weekly caffeinated beverage consumption (continuous). A mixed-effects model was fitted with default mode network - dorsal attention network anticorrelation strength as the outcome. Most of the baseline ABCD sample did not consume a caffeinated beverage in the last 24 hours (n = 3,910; 83.7%). Controlling for covariates (age, attention problems, BMI, family, head motion, MRI scanner, and sex), neither the caffeinated beverage variables nor their interaction were statistically significant. Our study findings identified that approximately 16% of our sample consumed caffeine in the last 24 hours prior to the magnetic resonance imaging scan. We did not find caffeine to impact the default mode network - dorsal attention network anticorrelation strength in this sample. This study may guide the interpretation of functional magnetic resonance imaging results among adolescents who consume caffeinated beverages.

To determine the effect of the introduction of low dose computed tomography screening in 2013 on lung cancer stage shift, survival, and disparities in the stage of lung cancer diagnosed in the United States. Quasi-experimental study using Joinpoint modeling, multivariable ordinal logistic regression, and multivariable Cox proportional hazards modeling. US National Cancer Database and Surveillance Epidemiology End Results program database. Patients aged 45-80 years diagnosed as having non-small cell lung cancer (NSCLC) between 1 January 2010 and 31 December 2018. Annual per cent change in percentage of stage I NSCLC diagnosed among patients aged 45-54 (ineligible for screening) and 55-80 (potentially eligible for screening), median all cause survival, and incidence of NSCLC; multivariable adjusted odds ratios for year-to-year changes in likelihood of having earlier stages of disease at diagnosis and multivariable adjusted hazard ratios for changes in hazard of death before versus after introduction of screening. The percentage of stage I NSCLC diagnosed among patients aged 55-80 did not significantly increase from 2010 to 2013 (from 27.8% to 29.4%) and then increased at 3.9% (95% confidence interval 3.0% to 4.8%) per year from 2014 to 2018 (from 30.2% to 35.5%). In multivariable adjusted analysis, the increase in the odds per year of a patient having one lung cancer stage lower at diagnosis during the time period from 2014 to 2018 was 6.2% (multivariable adjusted odds ratio 1.062, 95% confidence interval 1.048 to 1.077; P<0.001) higher than the increase in the odds per year from 2010 to 2013. Similarly, the median all cause survival of patients aged 55-80 did not significantly increase from 2010 to 2013 (from 15.8 to 18.1 months), and then increased at 11.9% (8.9% to 15.0%) per year from 2014 to 2018 (from 19.7 to 28.2 months). In multivariable adjusted analysis, the hazard of death decreased significantly faster after 2014 compared with before 2014 (P<0.001). By 2018, stage I NSCLC was the predominant diagnosis among non-Hispanic white people and people living in the highest income or best educated regions. Non-white people and those living in lower income or less educated regions remained more likely to have stage IV disease at diagnosis. Increases in the detection of early stage disease in the US from 2014 to 2018 led to an estimated 10 100 averted deaths. A recent stage shift toward stage I NSCLC coincides with improved survival and the introduction of lung cancer screening. Non-white patients and those living in areas of greater deprivation had lower rates of stage I disease identified, highlighting the need for efforts to increase access to screening in the US.

Effect sizes are commonly interpreted using heuristics established by Cohen (e.g., small: r = .1, medium r = .3, large r = .5), despite mounting evidence that these guidelines are mis-calibrated to the effects typically found in psychological research. This study’s aims were to 1) describe the distribution of effect sizes across multiple instruments, 2) consider factors qualifying the effect size distribution, and 3) identify examples as benchmarks for various effect sizes. For aim one, effect size distributions were illustrated from a large, diverse sample of 9/10-year-old children. This was done by conducting Pearson’s correlations among 161 variables representing constructs from all questionnaires and tasks from the Adolescent Brain and Cognitive Development Study® baseline data. To achieve aim two, factors qualifying this distribution were tested by comparing the distributions of effect size among various modifications of the aim one analyses. These modified analytic strategies included comparisons of effect size distributions for different types of variables, for analyses using statistical thresholds, and for analyses using several covariate strategies. In aim one analyses, the median in-sample effect size was .03, and values at the first and third quartiles were .01 and .07. In aim two analyses, effects were smaller for associations across instruments, content domains, and reporters, as well as when covarying for sociodemographic factors. Effect sizes were larger when thresholding for statistical significance. In analyses intended to mimic conditions used in “real-world” analysis of ABCD data, the median in-sample effect size was .05, and values at the first and third quartiles were .03 and .09. To achieve aim three, examples for varying effect sizes are reported from the ABCD dataset as benchmarks for future work in the dataset. In summary, this report finds that empirically determined effect sizes from a notably large dataset are smaller than would be expected based on existing heuristics.

Attention-deficit/hyperactivity disorder (ADHD) is a common chronic neurobehavioral disorder related to clinically significant levels of inattention, hyperactivity, and/or impulsivity. ADHD begins in childhood and symptoms persist into adulthood for the majority of those with the disorder. Associated features of ADHD include emotion dysregulation and cognitive impairments, which contribute to the considerable functional impairments in this disorder. Current approved treatments are reasonably effective; however, a significant need remains for new pharmacotherapies, both for individuals who do not achieve a full therapeutic response and for symptoms that are under-treated including cognition and emotion regulation. The striking relationship between ADHD and cigarette smoking and the known effects of nicotine on cognition has spurred research into the therapeutic potential of nicotinic agents for ADHD. Although there are no approved medications for ADHD that target nicotinic acetylcholine receptor (nAChR) function, results from many trials of nicotinic drugs are available and reviewed in this article. ADHD symptoms were reduced in the majority of published studies of nicotine and novel α4β2 nicotinic agonists in adult ADHD. The drugs were generally well tolerated, with mild to moderate side effects reported, which were largely consistent with cholinergic stimulation and included nausea, dizziness, and gastrointestinal distress. Within-subject crossover study designs were used in the majority of positive studies. This design may be particularly useful in ADHD trials because it minimizes variability in this notoriously heterogeneous diagnostic group. In addition, many studies found evidence for a beneficial effect of nicotinic stimulation on cognitive and emotional domains. Thus, targeting nAChRs in ADHD appears to have a modest clinical benefit in adult ADHD. Continued refinement of nAChR agonists with greater specificity and fewer side effects may lead to even more effective nAChR agonists for ADHD. Future clinical trials in ADHD should include direct measures of neuropsychological performance and emotion regulation.

Attention deficit/hyperactivity disorder is associated with numerous neurocognitive deficits, including poor working memory and difficulty inhibiting undesirable behaviors that cause academic and behavioral problems in children. Prior work has attempted to determine how these differences are instantiated in the structure and function of the brain, but much of that work has been done in small samples, focused on older adolescents or adults, and used statistical approaches that were not robust to model overfitting. The current study used cross-validated elastic net regression to predict a continuous measure of ADHD symptomatology using brain morphometry and activation during tasks of working memory, inhibitory control, and reward processing, with separate models for each MRI measure. The best model using activation during the working memory task to predict ADHD symptomatology had an out-of-sample R2 = 2% and was robust to residualizing the effects of age, sex, race, parental income and education, handedness, pubertal status, and internalizing symptoms from ADHD symptomatology. This model used reduced activation in task positive regions and reduced deactivation in task negative regions to predict ADHD symptomatology. The best model with morphometry alone predicted ADHD symptomatology with an R2 = 1% but this effect dissipated when including covariates. The inhibitory control and reward tasks did not yield generalizable models. In summary, these analyses show, with a large and well-characterized sample, that the brain correlates of ADHD symptomatology are modest in effect size and captured best by brain morphometry and activation during a working memory task.

In structural neuroimaging studies, reduced cerebral cortical thickness in orbital and ventromedial prefrontal regions is frequently interpreted as reflecting an impaired ability to downregulate neuronal activity in the amygdalae. Unfortunately, little research has been conducted in order to test this conjecture. We examine the extent to which amygdalar reactivity is associated with cortical thickness in a population-based sample of adolescents. Data were obtained from the IMAGEN study, which includes 2,223 adolescents. While undergoing functional neuroimaging, participants passively viewed video clips of a face that started from a neutral expression and progressively turned angry, or, instead, turned to a second neutral expression. Left and right amygdala ROIs were used to extract mean BOLD signal change for the angry minus neutral face contrast for all subjects. T1-weighted images were processed through the CIVET pipeline (version 2.1.0). In variable-centered analyses, local cortical thickness was regressed against amygdalar reactivity using first and second-order linear models. In a follow-up person-centered analysis, we defined a \"high reactive\" group of participants based on mean amygdalar BOLD signal change for the angry minus neutral face contrast. Between-group differences in cortical thickness were examined (\"high reactive\" versus all other participants). A significant association was revealed between the continuous measure of amygdalar reactivity and bilateral ventromedial prefrontal cortical thickness in a second-order linear model (p < 0.05, corrected). The \"high reactive\" group, in comparison to all other participants, possessed reduced cortical thickness in bilateral orbital and ventromedial prefrontal cortices, bilateral anterior temporal cortices, left caudal middle temporal gyrus, and the left inferior and middle frontal gyri (p < 0.05, corrected). Results are consistent with non-human primate studies, and provide empirical support for an association between reduced prefrontal cortical thickness and amygdalar reactivity. Future research will likely benefit from investigating the degree to which psychopathology qualifies relations between prefrontal cortical structure and amygdalar reactivity.

Exposure to maltreatment during childhood is associated with structural changes throughout the brain. However, the structural differences that are most strongly associated with maltreatment remain unclear given the limited number of whole-brain studies. The present study used machine learning to identify if and how brain structure distinguished young adults with and without a history of maltreatment. Young adults (ages 18–21, n = 384) completed an assessment of childhood trauma exposure and a structural MRI as part of the IMAGEN study. Elastic net regularized regression was used to identify the structural features that identified those with a history of maltreatment. A generalizable model that included 7 cortical thicknesses, 15 surface areas, and 5 subcortical volumes was identified (area under the receiver operating characteristic curve = 0.71, p < 0.001). Those with a maltreatment history had reduced surface areas and cortical thicknesses primarily in fronto-temporal regions. This group also had larger cortical thicknesses in occipital regions and surface areas in frontal regions. The results suggest childhood maltreatment is associated with multiple measures of structure throughout the brain. The use of a large sample without exposure to adulthood trauma provides further evidence for the unique contribution of childhood trauma to brain structure. The identified regions overlapped with regions associated with psychopathology in adults with maltreatment histories, which offers insights as to how these disorders manifest.

Impulsivity is a known risk factor for the development of substance use disorders and other psychiatric conditions that is influenced by both genetics and environment. Although research has linked parental mental health to children's impulsivity, potential mediators of this relationship remain understudied. The current investigation leverages the large national Adolescent Brain Cognitive Development (ABCD) Study to assess the mediating role of family conflict - an important social context for youth development - in the relationship between parental mental health and youth impulsivity. Data were from the first three annual waves of the ABCD study (Baseline  = 11,876 children,  = 9.9 years; 48% female; 52% White). Parental mental health conditions were self-reported internalizing, externalizing, and total problems. Youth completed the family conflict scale, and Urgency, Planning (lack of), Perseverance (lack of), Sensation Seeking, and Positive Urgency (UPPS-P) scale to measure impulsivity. To determine if within-family change in conflict from baseline to year 1 explained changes in the strength of relations between baseline parental mental health and year 2 youth impulsivity, longitudinal causal mediation analyses were conducted, controlling for demographic factors (i.e., age, sex, race, household income, parental education, marital status), as well as baseline levels of family conflict and outcomes. Separate mediation models were run for each mental health condition and each UPPS-P subscale. Above and beyond bivariate relations, longitudinal mediation models, which included covariates, showed family conflict significantly ( s < 0.001) mediated relations between all three parental mental health conditions and all but one (i.e., sensation seeking) UPPS-P subscales. The proportion mediated through family conflict for internalizing problems and total problems on facets of impulsivity (except sensation seeking) ranged from 9% (for lack of perseverance) to 17% (for lack of planning). Proportion mediated via family conflict for externalizing problems on youth's impulsivity (except sensation seeking) was slightly higher, ranging between 13% (lack of perseverance) to 21% (lack of planning). Family conflict may be an important intergenerational factor linking parental mental health and youth's impulsivity. Addressing parental mental health and family conflict may help curb increased impulsivity in youth, and in turn reduce adolescent substance use disorders.