Sex-specific impulsivity, but not other facets of executive function, predicts fat and sugar intake two-years later amongst adolescents with a healthy weight: Findings from the ABCD study.

During adolescence, processes that control food intake (executive functions [EF]) undergo extensive refinement; underlying differences in EF may explain the inability to resist overeating unhealthy foods. Yet, overeating fat and sugar also causes changes to EF and cognition but disentangling these relationships has been difficult, as previous studies included youth with obesity. Here, amongst youth initially of a healthy weight, we evaluate whether 1) sex-specific underlying variation in EF/cognition at 9/10-years-old predict fat/sugar two-years later (Y2) and 2) if these relationships are moderated by body mass index (BMI), using linear mixed effects models (controlled for puberty, caregiver education; random effect: study site). Data were leveraged from Adolescent Brain Cognitive Development Study (n = 2987; 50.4% male; 15.4% Latino/a/x; 100% healthy weight at baseline; 12.4% overweight/obese by Y2, data release 4.0). EF and cognition (e.g., inhibition, cognition, motor, memory, impulsivity) were assessed with the NIH toolbox, Rey Auditory Verbal Learning Task, Little Man Task, the BIS/BAS, and UPPS-P. A saturated fat/added sugar (kcals) composite score was extracted from the validated Kids Food Block Screener. For males, greater baseline impulsivity (e.g., Positive Urgency, Lack of Planning and Perseverance) and reward (e.g., Fun seeking, Drive) was related to greater Y2 intake. For both sexes, greater baseline Negative Urgency and higher BMI was related to greater Y2 intake. No other relationships were observed. Our findings highlight a phenotype that may be more at risk for weight gain due to overconsumption of fat/sugar. Thus, prevention efforts may wish to focus on impulsive tendencies for these foods.

Associations between community-level patterns of prenatal alcohol and tobacco exposure on brain structure in a non-clinical sample of 6-year-old children: a South African pilot study.

The current small study utilised prospective data collection of patterns of prenatal alcohol and tobacco exposure (PAE and PTE) to examine associations with structural brain outcomes in 6-year-olds and served as a pilot to determine the value of prospective data describing community-level patterns of PAE and PTE in a non-clinical sample of children. Participants from the Safe Passage Study in pregnancy were approached when their child was ∼6 years old and completed structural brain magnetic resonance imaging to examine with archived PAE and PTE data (n = 51 children-mother dyads). Linear regression was used to conduct whole-brain structural analyses, with false-discovery rate (FDR) correction, to examine: (a) main effects of PAE, PTE and their interaction; and (b) predictive potential of data that reflect patterns of PAE and PTE (e.g. quantity, frequency and timing (QFT)). Associations between PAE, PTE and their interaction with brain structural measures demonstrated unique profiles of cortical and subcortical alterations that were distinct between PAE only, PTE only and their interactive effects. Analyses examining associations between patterns of PAE and PTE (e.g. QFT) were able to significantly detect brain alterations (that survived FDR correction) in this small non-clinical sample of children. These findings support the hypothesis that considering QFT and co-exposures is important for identifying brain alterations following PAE and/or PTE in a small group of young children. Current results demonstrate that teratogenic outcomes on brain structure differ as a function PAE, PTE or their co-exposures, as well as the pattern (QFT) or exposure.

The impact of prenatal alcohol and/or tobacco exposure on brain structure in a large sample of children from a South African birth cohort.

BACKGROUND: Neuroimaging studies have emphasized the impact of prenatal alcohol exposure (PAE) on brain development, traditionally in heavily exposed participants. However, less is known about how naturally occurring community patterns of PAE (including light to moderate exposure) affect brain development, particularly in consideration of commonly occurring concurrent impacts of prenatal tobacco exposure (PTE). METHODS: Three hundred thirty-two children (ages 8 to 12) living in South Africa's Cape Flats townships underwent structural magnetic resonance imaging. During pregnancy, their mothers reported alcohol and tobacco use, which was used to evaluate PAE and PTE effects on their children's brain structure. Analyses involved the main effects of PAE and PTE (and their interaction) and the effects of PAE and PTE quantity on cortical thickness, surface area, and volume. RESULTS: After false-discovery rate (FDR) correction, PAE was associated with thinner left parahippocampal cortices, while PTE was associated with smaller cortical surface area in the bilateral pericalcarine, left lateral orbitofrontal, right posterior cingulate, right rostral anterior cingulate, left caudal middle frontal, and right caudal anterior cingulate gyri. There were no PAE × PTE interactions nor any associations of PAE and PTE exposure on volumetrics that survived FDR correction. CONCLUSION: PAE was associated with reduction in the structure of the medial temporal lobe, a brain region critical for learning and memory. PTE had stronger and broader associations, including with regions associated with executive function, reward processing, and emotional regulation, potentially reflecting continued postnatal exposure to tobacco (i.e., second-hand smoke exposure). These differential effects are discussed with respect to reduced PAE quantity in our exposed group versus prior studies within this geographical location, the deep poverty in which participants live, and the consequences of apartheid and racially and economically driven payment practices that contributed to heavy drinking in the region. Longer-term follow-up is needed to determine potential environmental and other moderators of the brain findings here and assess the extent to which they endure over time.

Combined Face-Brain Morphology and Associated Neurocognitive Correlates in Fetal Alcohol Spectrum Disorders.

BACKGROUND: Since the 1970s, a range of facial, neurostructural, and neurocognitive adverse effects have been shown to be associated with prenatal alcohol exposure. Typically, these effects are studied individually and not in combination. Our objective is to improve the understanding of the teratogenic effects of prenatal alcohol exposure by simultaneously considering face-brain morphology and neurocognitive measures. METHODS: Participants were categorized as control (n = 47), fetal alcohol syndrome (FAS, n = 22), or heavily exposed (HE) prenatally, but not eligible for a FAS diagnosis (HE, n = 50). Structural brain MRI images and high-resolution 3D facial images were analyzed using dense surface models of features of the face and surface shape of the corpus callosum (CC) and caudate nucleus (CN). Asymmetry of the CN was evaluated for correlations with neurocognitive measures. RESULTS: (i) Facial growth delineations for FAS, HE, and controls are replicated for the CN and the CC. (ii) Concordance of clinical diagnosis and face-based control-FAS discrimination improves when the latter is combined with specific brain regions. In particular, midline facial regions discriminate better when combined with a midsagittal profile of the CC. (iii) A subset of HE individuals was identified with FAS-like CN dysmorphism. The average of this HE subset was FAS-like in its facial dysmorphism. (iv) Right-left asymmetry found in the CNs of controls is not apparent for FAS, is diminished for HE, and correlates with neurocognitive measures in the combined FAS and HE population. CONCLUSIONS: Shape analysis which combines facial regions with the CN, and with the CC, better identify those with FAS. CN asymmetry was reduced for FAS compared to controls and is strongly associated with general cognitive ability, verbal learning, and recall in those with prenatal alcohol exposure. This study further extends the brain-behavior relationships known to be vulnerable to alcohol teratogenesis.

Volume changes and brain-behavior relationships in white matter and subcortical gray matter in children with prenatal alcohol exposure.

Children with prenatal alcohol exposure (PAE) may have cognitive, behavioral and brain abnormalities. Here, we compare rates of white matter and subcortical gray matter volume change in PAE and control children, and examine relationships between annual volume change and arithmetic ability, behavior, and executive function. Participants (n = 75 PAE/64 control; age: 7.1-15.9 years) each received two structural magnetic resonance scans, ~2 years apart. Assessments included Wechsler Intelligence Scale for Children (WISC-IV), the Child Behavior Checklist and the Behavior Rating Inventory of Executive Function. Subcortical white and gray volumes were extracted for each hemisphere. Group volume differences were tested using false discovery rate (q < 0.05). Analyses examined group-by-age interactions and group-score interactions for correlations between change in volume and raw behavioral scores. Results showed that subjects with PAE had smaller volumes than control subjects across the brain. Significant group-score interactions were found in temporal and parietal regions for WISC arithmetic scores and in frontal and parietal regions for behavioral measures. Poorer cognitive/ behavioral outcomes were associated with larger volume increases in PAE, while control subjects generally showed no significant correlations. In contrast with previous results demonstrating different trajectories of cortical volume change in PAE, our results show similar rates of subcortical volume growth in subjects with PAE and control subjects. We also demonstrate abnormal brain-behavior relationships in subjects with PAE, suggesting different use of brain resources. Our results are encouraging in that, due to the stable volume differences, there may be an extended window of opportunity for intervention in children with PAE.

The role of testosterone and estradiol in brain volume changes across adolescence: a longitudinal structural MRI study.

It has been postulated that pubertal hormones may drive some neuroanatomical changes during adolescence, and may do so differently in girls and boys. Here, we use growth curve modeling to directly assess how sex hormones [testosterone (T) and estradiol (E2)] relate to changes in subcortical brain volumes utilizing a longitudinal design. 126 adolescents (63 girls), ages 10 to 14, were imaged and restudied ∼2 years later. We show, for the first time, that best-fit growth models are distinctly different when using hormones as compared to a physical proxy of pubertal maturation (Tanner Stage) or age, to predict brain development. Like Tanner Stage, T and E2 predicted white matter and right amygdala growth across adolescence in both sexes, independent of age. Tanner Stage also explained decreases in both gray matter and caudate volumes, whereas E2 explained only gray matter decreases and T explained only caudate volume decreases. No pubertal measures were related to hippocampus development. Although specificity was seen, sex hormones had strikingly similar relationships with white matter, gray matter, right amygdala, and bilateral caudate volumes, with larger changes in brain volume seen at early pubertal maturation (as indexed by lower hormone levels), followed by less robust, or even reversals in growth, by late puberty. These novel longitudinal findings on the relationship between hormones and brain volume change represent crucial first steps toward understanding which aspects of puberty influence neurodevelopment.

Longitudinal mapping of cortical change during early adolescence associated with prenatal tobacco and/or alcohol exposure in the Adolescent Brain Cognitive Development Study.

Importance: The effects of prenatal alcohol (PAE) and tobacco exposure (PTE) on adolescent neuroanatomical development are typically evaluated cross-sectionally. It is unclear if observed effects persist throughout life or reflect different developmental trajectories. Objective: To determine how PAE and PTE are associated with cortical structure and development across two timepoints in early adolescence. Design: Observational, longitudinal analyses of data within the Adolescent Brain Cognitive Development Study. Setting: 21 study sites in the United States. Participants: 5,417 youth participants, aged ~9-12 years old. Exposures: PAE and PTE based on caregiver (self) reports of alcohol/tobacco use during pregnancy, before and after pregnancy recognition. Main Outcomes and Measures: Cortical thickness (mm) and cortical surface area (mm2) measured approximately 2 years apart in early adolescence, across 68 bilateral cortical regions. Results: At baseline data collection, youth participants were ~9.9 years old (SD=0.6). At the second neuroimaging appointment, youth participants were ~11.9 years old (SD=0.6). When modelling cortical thickness, we controlled for individuals' whole-brain volume; when modelling cortical surface area, individuals' total surface area. Cortical thickness generally declined with age. Cortical surface area either expanded or contracted with age, depending on region. PAE had minimal effects on cortical structure (main effects) and development (PAE×Age interactions). PTE had robust effects on cortical thickness and was associated with faster rates of cortical thinning in several regions within the frontal lobe. Post hoc analyses on (1) the effects of PTE for those who continued tobacco use after pregnancy recognition and (2) the effects of PTE in those who did not also use alcohol revealed weaker effects. Conclusions and Relevance: PTE had robust effects on neuroanatomical structure and longitudinal development, particularly cortical thickness. Analyzing developmental cortical trajectories informs how PTE and/or PAE not only affects cortical structure but how it develops long after those prenatal exposures occurred. Future analyses involving cotinine biomarkers of PTE would enhance the temporal resolution of the ABCD Study®'s PTE-related queries of tobacco use before and after learning of the pregnancy.

Socioeconomic Disadvantage and Youth Mental Health During the COVID-19 Pandemic Lockdown.

Importance: Adolescence is a period in which mental health problems emerge. Research suggests that the COVID-19 lockdown may have worsened emotional and behavioral health. Objective: To examine whether socioeconomic status was associated with mental health outcomes among youths during the COVID-19 pandemic. Design, Setting, and Participants: The Adolescent Brain Cognitive Development (ABCD) Study is a multisite 10-year longitudinal study of youth neurocognitive development in the US. Recruitment was staggered where the baseline visit (ages 9 to 10 years) occurred from 2016 to 2018, and visits occurred yearly. The COVID-19 lockdown halted research collection during the 2-year follow-up visits (ages 11 to 12 years), but eventually resumed. As some youths already underwent their 2-year visits prior to lockdown, this allowed for a natural experiment-like design to compare prepandemic and intrapandemic groups. Thus, data were gathered from the 1-year follow-up (pre-COVID-19 lockdown for all youths) and the 2-year follow-up, of which a portion of youths had data collected after the lockdown began, to compare whether a period of near social isolation was associated with mental health symptoms in youths. The prepandemic group consisted of youths with a 2-year follow-up visit collected prior to March 11, 2020, and the intrapandemic group had their 2-year follow-up visit after lockdown restrictions were lifted. Main Outcomes and Measures: Assessments included measures on income-to-needs ratio (INR; derived from total household income), the Child Behavior Checklist (a measure of mental health symptomology), and the Family Environmental Scale. Results: The final sample included 10 399 youths; 3947 (52.3%) were male; 2084 (20.3%) were Latinx/Hispanic; 6765 (66.0%) were White; 4600 (44.2%) reported caregiver education levels below a 4-year college degree; and 2475 (26.2%) had INR either below 100% (indicating poverty) or between 100% and less than 200% (near poverty). Among youths in the intrapandemic group, worse mental health symptoms (eg, more total problems, greater depression, and greater anxiety) over time were associated with being from a household with higher socioeconomic status (eg, when comparing individuals who differed by 1 unit on INR between prepandemic and intrapandemic groups from 1-year to 2-year follow-up, their expected difference in total problems score was 0.79 [95% CI, 0.37-1.22]; false discovery rate-corrected P < .001). Conclusions and Relevance: This cohort study found that the COVID-19 lockdown was associated with disproportionately negative mental health outcomes among youths from higher socioeconomic status backgrounds. Although this study does not shed light on the direct mechanisms driving these associations, it does provide some support for positive outcomes for youths. Future studies are needed to understand whether these associations persist over longer periods of time.

Smaller subcortical volume relates to greater weight gain in girls with initially healthy weight.

OBJECTIVE: Among 3614 youth who were 9 to 12 years old and initially did not have overweight or obesity (12% [n = 385] developed overweight or obesity), we examined the natural progression of weight gain and brain structure development during a 2-year period with a high risk for obesity (e.g., pre- and early adolescence) to determine the following: 1) whether variation in maturational trajectories of the brain regions contributes to weight gain; and/or 2) whether weight gain contributes to altered brain development. METHODS: Data were gathered from the Adolescent Brain Cognitive Development (ABCD) Study. Linear mixed-effects regression models controlled for puberty, caregiver education, handedness, and intracranial volume (random effects: magnetic resonance scanner [MRI] scanner and participant). Because pubertal development occurs earlier in girls, analyses were stratified by sex. RESULTS: For girls, but not boys, independent of puberty, greater increases in BMI were driven by smaller volumes over time in the bilateral accumbens, amygdala, hippocampus, and thalamus, right caudate and ventral diencephalon, and left pallidum (all p < 0.05). CONCLUSIONS: The results suggest a potential phenotype for identifying obesity risk because underlying differences among regions involved in food intake were related to greater weight gain in girls, but not in boys. Importantly, 2 years of weight gain may not be sufficient to alter brain development, highlighting early puberty as a critical time to prevent negative neurological outcomes.

A longitudinal study of the long-term consequences of drinking during pregnancy: heavy in utero alcohol exposure disrupts the normal processes of brain development.

Exposure to alcohol in utero can cause birth defects, including face and brain abnormalities, and is the most common preventable cause of intellectual disabilities. Here we use structural magnetic resonance imaging to measure cortical volume change longitudinally in a cohort of human children and youth with prenatal alcohol exposure (PAE) and a group of unexposed control subjects, demonstrating that the normal processes of brain maturation are disrupted in individuals whose mothers drank heavily during pregnancy. Trajectories of cortical volume change within children and youth with PAE differed from those of unexposed control subjects in posterior brain regions, particularly in the parietal cortex. In these areas, control children appear to show a particularly plastic cortex with a prolonged pattern of cortical volume increases followed by equally vigorous volume loss during adolescence, while the alcohol-exposed participants showed primarily volume loss, demonstrating decreased plasticity. Furthermore, smaller volume changes between scans were associated with lower intelligence and worse facial morphology in both groups, and were related to the amount of PAE during each trimester of pregnancy in the exposed group. This demonstrates that measures of IQ and facial dysmorphology predict, to some degree, the structural brain development that occurs in subsequent years. These results are encouraging in that interventions aimed at altering "experience" over time may improve brain trajectories in individuals with heavy PAE and possibly other neurodevelopmental disorders.

Abnormal cortical thickness alterations in fetal alcohol spectrum disorders and their relationships with facial dysmorphology.

Accumulating evidence from structural brain imaging studies on individuals with fetal alcohol spectrum disorder (FASD) has supported links between prenatal alcohol exposure and brain morphological deficits. Although global and regional volumetric reductions appear relatively robust, the effects of alcohol exposure on cortical thickness and relationships with facial dysmorphology are not yet known. The structural magnetic resonance imaging data from 69 children and adolescents with FASD and 58 nonexposed controls collected from 3 sites were examined using FreeSurfer to detect cortical thickness changes across the entire brain in FASD and their associations with facial dysmorphology. Controlling for brain size, subjects with FASD showed significantly thicker cortices than controls in several frontal, temporal, and parietal regions. Analyses conducted within site further revealed prominent group differences in left inferior frontal cortex within all 3 sites. In addition, increased inferior frontal thickness was significantly correlated with reduced palpebral fissure length. Consistent with previous reports, findings of this study are supportive of regional increases in cortical thickness serving as a biomarker for disrupted brain development in FASD. Furthermore, the significant associations between thickness and dysmorphic measures suggest that the severity of brain anomalies may be reflected by that of the face.

Relating neighborhood deprivation to childhood obesity in the ABCD study: Evidence for theories of neuroinflammation and neuronal stress.

OBJECTIVE: We evaluated whether relationships between area deprivation (ADI), body mass index (BMI) and brain structure (e.g., cortical thickness, subcortical volume) during preadolescence supported the immunologic model of self-regulation failure (NI) and/or neuronal stress (NS) theories of overeating. The NI theory proposes that ADI causes structural alteration in the brain due to the neuroinflammatory effects of overeating unhealthy foods. The NS theory proposes that ADI-related stress negatively impacts brain structure, which causes stress-related overeating and subsequent obesity. METHOD: Data were gathered from the Adolescent Brain Cognitive Development Study (9 to 12 years old; n = 3,087, 51% male). Linear mixed-effects models identified brain regions that were associated with both ADI and BMI; longitudinal associations were evaluated with mediation models. The NI model included ADI and BMI at 9 to 10 years old and brain data at 11 to 12 years old. The NS model included ADI and brain data at 9 to 10 years old and BMI at 11 to 12 years old. RESULTS: BMI at 9 to 10 years old partially mediated the relationship between ADI and ventral diencephalon (DC) volume at 11 to 12 years old. Additionally, the ventral DC at 9 to 10 years old partially mediated the relationship between ADI and BMI at 11 to 12 years old, even in youth who at baseline, were of a healthy weight. Results were unchanged when controlling for differences in brain structure and weight across the 2-years. CONCLUSION: Greater area deprivation may indicate fewer access to resources that support healthy development, like nutritious food and nonstressful environments. Our findings provide evidence in support of the NI and NS theories of overeating, specifically, with greater ADI influencing health outcomes of obesity via brain structure alterations. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Variation in executive function relates to BMI increases in youth who were initially of a healthy weight in the ABCD Study.

OBJECTIVE: The study aim was to determine whether (A) differences in executive function (EF) and cognition precede weight gain or (B) weight gain causes changes to EF and cognition. METHODS: Data were gathered from the Adolescent Brain Cognitive Development (ABCD) Study (release 4.0; ages 9-12 years old [N = 2794]; 100% had healthy weight at baseline [i.e., 9/10 years old], 12.4% had unhealthy weight by ages 11/12 years). EF and cognition were assessed across several domains (e.g., impulsivity, inhibitory control, processing speed, memory); BMI was calculated from height and weight. Nested random-effects mixed models examined (A) BMI ~ EF × Time (i.e., variation in EF/cognition precedes weight gain) and (B) EF ~ BMI × Time (weight gain causes changes to EF/cognition) and controlled for sex, puberty, and caregiver education; random effects were site and subject. RESULTS: Variation in impulsivity, memory, learning, and processing speed was associated with greater increases in BMI trajectories from 9 to 12 years old. Weight gain was associated with a decrease in inhibitory control, but no other associations were observed. CONCLUSIONS: Underlying variation in EF and cognition may be important for weight gain, but 2 years of weight gain may not be enough to have clinical implications for EF and cognition beyond inhibitory control. These findings suggest that more attention should be paid to the inclusion of EF programs in obesity prevention efforts.

Longitudinal assessment of brain structure and behaviour in youth with rapid weight gain: Potential contributing causes and consequences.

OBJECTIVE: Independent of weight status, rapid weight gain has been associated with underlying brain structure variation in regions associated with food intake and impulsivity among pre-adolescents. Yet, we lack clarity on how developmental maturation coincides with rapid weight gain and weight stability. METHODS: We identified brain predictors of 2-year rapid weight gain and its longitudinal effects on brain structure and impulsivity in the Adolescent Brain Cognitive DevelopmentSM Study®. Youth were categorized as Healthy Weight/Weight Stable (WSHW , n = 527) or Weight Gainers (WG, n = 221, >38lbs); 63% of the WG group were healthy weight at 9-to-10-years-old. RESULTS: A fivefold cross-validated logistic elastic-net regression revealed that rapid weight gain was associated with structural variation amongst 39 brain features at 9-to-10-years-old in regions involved with executive functioning, appetitive control and reward sensitivity. Two years later, WG youth showed differences in change over time in several of these regions and performed worse on measures of impulsivity. CONCLUSIONS: These findings suggest that brain structure in pre-adolescence may predispose some to rapid weight gain and that weight gain itself may alter maturational brain change in regions important for food intake and impulsivity. Behavioural interventions that target inhibitory control may improve trajectories of brain maturation and facilitate healthier behaviours.

Contextualizing the impact of prenatal alcohol and tobacco exposure on neurodevelopment in a South African birth cohort: an analysis from the socioecological perspective.

Background: Alcohol and tobacco are known teratogens. Historically, more severe prenatal alcohol exposure (PAE) and prenatal tobacco exposure (PTE) have been examined as the principal predictor of neurodevelopmental alterations, with little incorporation of lower doses or ecological contextual factors that can also impact neurodevelopment, such as socioeconomic resources (SER) or adverse childhood experiences (ACEs). Here, a novel analytical approach informed by a socio-ecological perspective was used to examine the associations between SER, PAE and/or PTE, and ACEs, and their effects on neurodevelopment. Methods: N = 313 mother-child dyads were recruited from a prospective birth cohort with maternal report of PAE and PTE, and cross-sectional structural brain neuroimaging of child acquired via 3T scanner at ages 8-11 years. In utero SER was measured by maternal education, household income, and home utility availability. The child's ACEs were measured by self-report assisted by the researcher. PAE was grouped into early exposure (<12 weeks), continued exposure (>=12 weeks), and no exposure controls. PTE was grouped into exposed and non-exposed controls. Results: Greater access to SER during pregnancy was associated with fewer ACEs (maternal education: ß = -0.293,p = 0.01; phone access: ß = -0.968,p = 0.05). PTE partially mediated the association between SER and ACEs, where greater SER reduced the likelihood of PTE, which was positively associated with ACEs (ß = 1.110,p = 0.01). SER was associated with alterations in superior frontal (ß = -1336.036, q = 0.046), lateral orbitofrontal (ß = -513.865, q = 0.046), caudal anterior cingulate volumes (ß = -222.982, q = 0.046), with access to phone negatively associated with all three brain volumes. Access to water was positively associated with superior frontal volume (ß=1569.527, q = 0.013). PTE was associated with smaller volumes of lateral orbitofrontal (ß = -331.000, q = 0.033) and nucleus accumbens regions (ß = -34.800, q = 0.033). Conclusion: Research on neurodevelopment following community-levels of PAE and PTE should more regularly consider the ecological context to accelerate understanding of teratogenic outcomes. Further research is needed to replicate this novel conceptual approach with varying PAE and PTE patterns, to disentangle the interplay between dose, community-level and individual-level risk factors on neurodevelopment.

Family- and neighborhood-level environmental associations with physical health conditions in 9- and 10-year-olds.

OBJECTIVE: To determine how environmental factors are associated with physical health conditions in 9- to 10-year-old participants in the Adolescent Brain Cognitive Development (ABCD) Study, and how they are moderated by family-level socioeconomic status (SES). METHOD: We performed cross-sectional analyses of 8,429 youth participants in the ABCD Study, in which nine physical health conditions (having underweight or overweight/obesity, not participating in sports activities, short sleep duration, high sleep disturbances, lack of vigorous and strengthening-related physical activity, miscellaneous medical problems, and traumatic brain injury) were regressed on three environmental factors [neighborhood disadvantage (area deprivation index [ADI]), risk of lead exposure, and concentrations of particulate matter 2.5 (PM2.5)] and their interaction with family-level SES (i.e., parent-reported annual household income). Environmental data were geocoded to participants' primary residential addresses at 9- to 10-year-olds. RESULTS: Risk of lead exposure and ADI were positively associated with the odds of having overweight/obesity, not participating in sports activity, and short sleep durations. ADI was also positively associated with high sleep disturbances. PM2.5 was positively associated with the odds of having overweight/obesity and reduced vigorous physical activity. Family-level SES moderated relationships between ADI and both underweight and overweight/obesity, with high SES being associated with more pronounced changes given increased ADI. CONCLUSIONS: Policymakers and public health officials must implement policies and remediation strategies to ensure children are free from exposure to neurotoxicant and environmental factors. Physical health conditions may be less of a product of an individual's choices and more related to environmental influences. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Callosal thickness reductions relate to facial dysmorphology in fetal alcohol spectrum disorders.

BACKGROUND: Structural abnormalities of the corpus callosum (CC), such as reduced size and increased shape variability, have been documented in individuals with fetal alcohol spectrum disorders (FASD). However, the regional specificity of altered CC structure, which may point to the timing of neurodevelopmental disturbances and/or relate to specific functional impairments, remains unclear. Furthermore, associations between facial dysmorphology and callosal structure remain undetermined. METHODS: One hundred and fifty-three participants (age range 8 to 16) including 82 subjects with FASD and 71 nonexposed controls were included in this study. The structural magnetic resonance imaging data of these subjects was collected at 3 sites (Los Angeles and San Diego, California, and Cape Town, South Africa) and analyzed using classical parcellation schemes, as well as more refined surface-based geometrical modeling methods, to identify callosal morphological alterations in FASD at high spatial resolution. RESULTS: Reductions in callosal thickness and area, specifically in the anterior third and the splenium, were observed in FASD compared with nonexposed controls. In addition, reduced CC thickness and area significantly correlated with reduced palpebral fissure length. CONCLUSIONS: Consistent with previous reports, findings suggest an adverse effect of prenatal alcohol exposure on callosal growth and further indicate that fiber pathways connecting frontal and parieto-occipital regions in each hemisphere may be particularly affected. Significant associations between callosal and facial dysmorphology provide evidence for a concurrent insult to midline facial and brain structural development in FASD.

Neural correlates of socioeconomic status in the developing human brain.

Socioeconomic disparities in childhood are associated with remarkable differences in cognitive and socio-emotional development during a time when dramatic changes are occurring in the brain. Yet, the neurobiological pathways through which socioeconomic status (SES) shapes development remain poorly understood. Behavioral evidence suggests that language, memory, social-emotional processing, and cognitive control exhibit relatively large differences across SES. Here we investigated whether volumetric differences could be observed across SES in several neural regions that support these skills. In a sample of 60 socioeconomically diverse children, highly significant SES differences in regional brain volume were observed in the hippocampus and the amygdala. In addition, SES × age interactions were observed in the left superior temporal gyrus and left inferior frontal gyrus, suggesting increasing SES differences with age in these regions. These results were not explained by differences in gender, race or IQ. Likely mechanisms include differences in the home linguistic environment and exposure to stress, which may serve as targets for intervention at a time of high neural plasticity.

Thinning of sensorimotor cortices in children with Tourette syndrome.

The basal ganglia portions of cortico-striato-thalamo-cortical (CSTC) circuits have consistently been implicated in the pathogenesis of Tourette syndrome, whereas motor and sensorimotor cortices in these circuits have been relatively overlooked. Using magnetic resonance imaging, we detected cortical thinning in frontal and parietal lobes in groups of Tourette syndrome children relative to controls. This thinning was most prominent in ventral portions of the sensory and motor homunculi that control the facial, orolingual and laryngeal musculature that is commonly involved in tic symptoms. Correlations of cortical thickness in sensorimotor regions with tic symptoms suggest that these brain regions are important in the pathogenesis of Tourette syndrome.

Access to quality health resources and environmental toxins affect the relationship between brain structure and BMI in a sample of pre and early adolescents.

Background: Environmental resources are related to childhood obesity risk and altered brain development, but whether these relationships are stable or if they have sustained impact is unknown. Here, we utilized a multidimensional index of childhood neighborhood conditions to compare the influence of various social and environmental disparities (SED) on body mass index (BMI)-brain relationships over a 2-year period in early adolescence. Methods: Data were gathered the Adolescent Brain Cognitive Development Study® (n = 2,970, 49.8% female, 69.1% White, no siblings). Structure magnetic resonance imaging (sMRI), anthropometrics, and demographic information were collected at baseline (9/10-years-old) and the 2-year-follow-up (11/12-years-old). Region of interest (ROIs; 68 cortical, 18 subcortical) estimates of cortical thickness and subcortical volume were extracted from sMRI T1w images using the Desikan atlas. Residential addresses at baseline were used to obtain geocoded estimates of SEDs from 3 domains of childhood opportunity index (COI): healthy environment (COIHE), social/economic (COISE), and education (COIED). Nested, random-effects mixed models were conducted to evaluate relationships of BMI with (1) ROI * COI[domain] and (2) ROI * COI[domain] * Time. Models controlled for sex, race, ethnicity, puberty, and the other two COI domains of non-interest, allowing us to estimate the unique variance explained by each domain and its interaction with ROI and time. Results: Youth living in areas with lower COISE and COIED scores were heavier at the 2-year follow-up than baseline and exhibited greater thinning in the bilateral occipital cortex between visits. Lower COISE scores corresponded with larger volume of the bilateral caudate and greater BMI at the 2-year follow-up. COIHE scores showed the greatest associations (n = 20 ROIs) with brain-BMI relationships: youth living in areas with lower COIHE had thinner cortices in prefrontal regions and larger volumes of the left pallidum and Ventral DC. Time did not moderate the COIHE x ROI interaction for any brain region during the examined 2-year period. Findings were independent of family income (i.e., income-to-needs). Conclusion: Collectively our findings demonstrate that neighborhood SEDs for health-promoting resources play a particularly important role in moderating relationships between brain and BMI in early adolescence regardless of family-level financial resources.