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INTRODUCTION: Epigenetic aging, a marker of biological aging measured by DNA methylation, may be affected by behaviors, including sleep and physical activity. However, investigations of physical activity and sleep with epigenetic aging among pediatric populations are scant and have not accounted for correlated behaviors. METHODS: The study population included 472 Mexico City adolescents (52% female). Blood collection and 7-day wrist actigraphy (Actigraph GTX-BT) occurred during a follow-up visit when participants were 14.5 (2.09) years. Leukocyte DNA methylation was measured with the Infinium MethylationEPIC array after bisulfite conversion, and 9 epigenetic clocks were calculated. Sleep vs wake time was identified through a pruned dynamic programing algorithm, and physical activity was processed with Chandler cut-offs. Kmeans clustering was used to select actigraphy-assessed physical activity and sleep behavior clusters. Linear regression analyses were used to evaluate adjusted associations between the clusters and epigenetic aging. RESULTS: There were 3 unique clusters: "Short sleep/high sedentary behavior", "Adequate sleep duration and late timing/low moderate or vigorous physical activity (MVPA)", and "Adequate sleep duration/high MVPA". Compared to the "Adequate duration/high MVPA", adolescents with "Adequate duration and late sleep timing/low MVPA" had more accelerated aging for the GrimAge clock (ß = 0.63;95% CI 0.07, 1.19). In pubertal-stratified analyses, more mature adolescents in the "Adequate duration and late sleep timing/low MVPA group" had accelerated epigenetic aging. In contrast, females in the "Short sleep/high sedentary" group had decelerated epigenetic aging for the Wu pediatric clock. CONCLUSIONS: Associations between behavior clusters and epigenetic aging varied by pubertal status and sex. Contrary results in the Wu clock suggest the need for future research on pediatric-specific clocks.

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BACKGROUND: The COVID-19 pandemic has not only caused tremendous loss of life and health but has also greatly disrupted the world economy. The impact of this disruption has been especially harsh in urban settings of developing countries. We estimated the impact of the pandemic on the occurrence of food insecurity in a cohort of women living in Mexico City, and the socioeconomic characteristics associated with food insecurity severity. METHODS: We analyzed data longitudinally from 685 women in the Mexico City-based ELEMENT cohort. Food insecurity at the household level was gathered using the Latin American and Caribbean Food Security Scale and measured in-person during 2015 to 2019 before the pandemic and by telephone during 2020-2021, in the midst of the pandemic. Fluctuations in the average of food insecurity as a function of calendar time were modeled using kernel-weighted local polynomial regression. Fixed and random-effects ordinal logistic regression models of food insecurity were fitted, with timing of data collection (pre-pandemic vs. during pandemic) as the main predictor. RESULTS: Food insecurity (at any level) increased from 41.6% during the pre-pandemic period to 53.8% in the pandemic stage. This increase was higher in the combined severe-moderate food insecurity levels: from 1.6% pre-pandemic to 16.8% during the pandemic. The odds of severe food insecurity were 3.4 times higher during the pandemic relative to pre-pandemic levels (p<0.01). Socioeconomic status quintile (Q) was significantly related to food insecurity (Q2 OR = 0.35 p<0.1, Q3 OR = 0.48 p = 0.014, Q4 OR = 0.24 p<0.01, and Q5 OR = 0.17 p<0.01), as well as lack of access to social security (OR = 1.69, p = 0.01), and schooling (OR = 0.37, p<0.01). CONCLUSIONS: Food insecurity increased in Mexico City households in the ELEMENT cohort as a result of the COVID-19 pandemic. These results contribute to the body of evidence suggesting that governments should implement well-designed, focalized programs in the context of economic crisis such as the one caused by COVID-19 to prevent families from the expected adverse health and well-being consequences associated to food insecurity, especially for the most vulnerable.

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PURPOSE: Early school start times could adversely impact adolescent sleep duration. They could also impact other behaviors like diet and physical activity, either directly or indirectly through effects on sleep. We examined whether the double school shift system was associated with sleep, diet, and physical activity behaviors among Mexican adolescents. METHODS: The analytic sample included 305 Mexican adolescents from a cohort study (on average 14.53 ± 1.75 years old and 51% male). Sleep and physical activity were measured with wrist actigraphy, while diet and other lifestyle behaviors were assessed with questionnaires. Regression analyses were conducted to compare lifestyle behaviors between the morning and afternoon school shifts, adjusting for potential confounders. RESULTS: Adolescents attending the morning school shift (44%) had pronounced differences in sleep compared to those attending afternoon shift, including a 1.77-hour shorter sleep duration on weekdays (95% CI -1.55, -2.00), a 0.40-hour longer sleep duration on weekends (95% CI 0.10, 0.70), higher social jetlag (1.07 hours with a 95% CI of 0.87, 1.27), and an earlier chronotype. Morning shift students also had 0.85 hours longer sedentary time (95% CI 0.61, 1.10) and higher consumption of a meat and starchy food dietary pattern. Among boys only, morning shift was associated with a lower likelihood of smoking and higher consumption of a breakfast pattern. DISCUSSION: Overall, attending a morning school shift was associated with shorter sleep, more social jetlag, greater sedentary time, and higher consumption of a meat and starchy diet. However, among boys, a few healthier behaviors were observed for the morning versus afternoon shift.

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Numerous studies have established associations between single nucleotide polymorphisms (SNPs) and various behavioral and neurodevelopmental conditions. This study explores the links between SNPs in candidate genes involved in central nervous system (CNS) physiology and their implications for the behavioral and emotional aspects in children and teenagers. A total of 590 participants, aged 7-15 years, from the Early Life Exposures In Mexico To Environmental Toxicants (ELEMENT) cohort study in Mexico City, underwent genotyping for at least one of 15 CNS gene-related SNPs at different timepoints. We employed multiple linear regression models to assess the potential impact of genetic variations on behavioral and cognitive traits, as measured by the Behavioral Assessment System for Children (BASC) and Conners parent rating scales. Significant associations were observed, including the rs1800497 TC genotype (ANKK1) with the Cognitive Problems/Inattention variable (p value = 0.003), the rs1800955 CT genotype (DDR4) with the Emotional Lability Global index variable (p value = 0.01), and the rs10492138 GA and rs7970177 TC genotypes (GRIN2B) with the Depression variable (p values 0.007 and 0.012, respectively). These finds suggest potential genetic profiles associated with "risk" and "protective" behaviors for these SNPs. Our results provide valuable insights into the role of genetic variations in neurobehavior and highlight the need for further research in the early identification and intervention in individuals at risk for these conditions.

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OBJECTIVE: To investigate the longitudinal association between breastfeeding duration and cardiometabolic health, using repeated measures study design among children and adolescents. STUDY DESIGN: This study included 634 offsprings aged 10 to 21 years (52% female) from the Early Life Exposure in Mexico to Environmental Toxicants birth cohort followed up to four time points during adolescence. Breastfeeding duration was prospectively quantified using questionnaires during early childhood. Cardiometabolic risk factors, body composition, and weight-related biomarkers were assessed as outcomes during adolescent follow-up visits. Sex-stratified linear mixed-effects models were used to model the association between quartiles of breastfeeding duration and outcomes, adjusting for age and additional covariates. RESULTS: Median breastfeeding duration was 7 months (minimum = 0, maximum = 36). Boys in the second quartile (median breastfeeding = 5 months) had lower total fat mass % (ß (SE) -3.2 (1.5) P = .037), and higher lean mass % (3.1 (1.6) P = .049) and skeletal muscle mass % (1.8 (0.8) P = .031) compared with the reference group (median breastfeeding = 2 months). A positive linear trend between breastfeeding duration and trunk lean mass % (0.1 (0.04) P = .035) was found among girls. No association was found with other cardiometabolic indicators. CONCLUSION: Despite sex-specific associations of breastfeeding duration with body composition, there was a lack of substantial evidence for the protective effects of breastfeeding against impaired cardiometabolic health during adolescence among Mexican youth. Further longitudinal studies with a robust assessment of breastfeeding are recommended.

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Purpose: The purpose of this study was to determine the association between prenatal and early life exposure to lead and the presence of molar hypomineralization (MH) in a group of Mexican children. Methods: A subset of participants of the Early Life Exposure in Mexico to Environmental Toxicants (ELEMENTS) cohort study was examined for the presence of molar hypomineralization using European Academy of Pedi- atric Dentistry (EAPD) criteria. Prenatal lead exposure was assessed by K-ray fluorescence measurements of patella and tibia lead and by maternal blood lead levels by trimester and averaged over trimesters. Postnatal exposure was assessed by levels of maternal blood lead at delivery and child blood lead at 12 and 24 months. Results: A subset of 506 subjects from the ELEMENT cohorts (nine to 18 years old) were examined for MH; 87 subjects (17.2 percent) had MH. Maternal blood lead levels in the third trimester (odds ratio [OR] equals 1.08; 95 percent confidence interval [95% CI] equals 1.02 to 1.15) and averaged over three trimesters (OR equals 1.10; 95% CI equals 1.02 to 1.19) were significantly associated with MH status. None of the maternal bone lead or the child's blood lead parameters was significantly associated with the presence of MH (P>0.05). Conclusions: This study documents a significant association between prenatal lead exposure especially in late pregnancy and the odds of molar hypomineralization.

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INTRODUCTION: During adolescence, dairy product intake has shown conflicting associations with metabolic syndrome (MetS) components, which are risk factors for cardiovascular disease (CVD). This study aims to investigate the association between plasma fatty acids (FAs) C15:0, C17:0, and t-C16:1n-7, as biomarkers of dairy intake, with MetS and its components in Mexican adolescents. METHODS: A sample of 311 participants from the Early Life Exposure in Mexico City to Environmental Toxicants (ELEMENT) cohort was included in this cross-sectional analysis. FA concentrations were measured in plasma as a percentage of total FA. We used quantile regression models stratified by sex to evaluate the association between FA quantiles and MetS components, adjusting for age, socioeconomic status (SES), sedentary behavior, BMI z-score, pubertal status, and energy intake. RESULTS: We found significant associations between dairy biomarkers and the median of MetS variables. In females, t-C16:1n-7 was associated with a decrease of 2.97 cm in WC (Q4 vs. Q1; 95% CI: -5.79, -0.16). In males, C15:0 was associated with an increase of 5.84 mm/Hg in SBP (Q4 vs. Q1; CI: 1.82, 9.85). For HDL-C, we observed opposite associations by sex. C15:0 in males was associated with decreased HDL-C (Q3 vs. Q1: ß = -4.23; 95% CI: -7.98, -0.48), while in females, C15:0 and t-C16:1n-7 were associated with increased HDL-C (Q3 vs. Q1: ß = 4.75; 95% CI: 0.68, 8.82 and Q4 vs. Q1: ß = 6.54; 95% CI: 2.01, 11.07), respectively. Additionally, in both sexes, different levels of C15:0, C17:0, and t-C16:1n-7 were associated with increased triglycerides (TG). CONCLUSION: Our results suggest that adolescent dairy intake may be associated in different directions with MetS components and that associations are sex-dependent.

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BACKGROUND: Epidemiological studies on children and adults have linked toxicants from plastics and personal care products to metabolic disruption. Yet, the impact of endocrine-disrupting chemicals (EDCs) on adolescent metabolic syndrome (MetS) risk during early and mid-adolescence is unclear. METHODS: To examine the links between exposure to EDCs and MetS risk and its components, cross-sectional data from 344 Mexican youth in early-to-mid adolescence (10-17 years) were analyzed. Urinary biomarker concentrations of phthalates, phenol, and paraben analytes were measured from a single spot urine sample collected in 2015; study personnel obtained anthropometric and metabolic measures. We examined associations between summary phthalates and metabolites, phenol, and paraben analytes with MetS risk z-scores using linear regression, adjusted for specific gravity, sex, age, pubertal status, smoking, alcohol intake, physical activity level, and screen time. As a secondary aim, mediation analysis was conducted to evaluate the role of hormones in the association between summary phthalates with lipids and MetS risk z-scores. RESULTS: The mean (SD) age was 13.2 (1.9) years, and 50.9% were female. Sex-stratified analyses revealed associations between summary phthalates and lipids ratio z-scores, including Σ DEHP [ß = 0.21 (95% CI: 0.04, 0.37; p < 0.01)], phthalates from plastic sources (Σ Plastic) [ß = 0.22 (95% CI: 0.05, 0.39; p < 0.01)], anti-androgenic phthalates (Σ AA) [ß = 0.22 (95% CI: 0.05, 0.39; p < 0.01)], and individual phthalate metabolites (MEHHP, MEOHP, and MECPP) among males. Among females, BPA [ß = 0.24 (95% CI: 0.03, 0.44; p < 0.05)] was positively associated with lipids ratio z-score and one phenol (2,5 DCP) [ß = 0.09 (95% CI: 0.01, 0.18); p < 0.05)] was associated with increased waist circumference z-score. Results showed no evidence of mediation by hormone concentrations in the association between summary phthalates with lipids ratio or MetS risk z-scores. CONCLUSION: Higher EDC exposure was positively associated with serum lipids during adolescence, particularly among males.

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Endocrine-disrupting chemicals (EDCs) may impact sleep during the menopausal transition by altering sex hormones. However, these studies are scarce among Latin American women. This investigation utilized cross-sectional and retrospective data from midlife women enrolled in the Early Life Exposure in Mexico to Environmental Toxicants (ELEMENT) study to examine associations between exposure to EDCs (phthalates, phenols, and parabens) and sleep health measures. For cross-sectional analyses, single spot urine samples were collected between 2017-2019 from a pilot sample of women (N = 91) of midlife age to estimate the urinary concentration of individual phthalates, phenols, and parabens and to calculate the summary concentration of phthalate mixtures. Seven-day nightly sleep duration, midpoint, and fragmentation were obtained from wrist-actigraphy devices and estimated from the actigraphy data using a pruned dynamic programming algorithm. Self-reported poor sleep quality was assessed by one item from the Pittsburgh Sleep Quality Index (PSQI). We examined associations between urinary summary phthalate mixtures, phthalate metabolites, phenol, and paraben analytes with each sleep measure using linear or logistic (to compute odds of poor sleep quality only) regression models adjusted for specific gravity, age, and socioeconomic status. We ran similar regression models for retrospective analyses (N = 74), except that urine exposure biomarker data were collected in 2008 when women were 24-50 years old. At the 2017-2019 midlife visit, 38% reported poor sleep quality. Cross-sectionally, EDCs were associated with longer sleep duration, earlier sleep timing, and more fragmented sleep. For example, every 1-unit IQR increase in the phenol triclosan was associated with a 26.3 min per night (95% CI: 10.5, 42.2; P < 0.05) longer sleep duration and marginally associated with 0.2 decimal hours (95% CI: -0.4, 0.0; P < 0.10) earlier sleep midpoint; while every 1-unit IQR increase in the phthalate metabolite MEHP was associated with 1.1% higher sleep fragmentation (95% CI: 0.1, 2.1; P < 0.05). Retrospective study results generally mirrored cross-sectional results such that EDCs were linked to longer sleep duration, earlier sleep timing, and more fragmented sleep. EDCs were not significantly associated with odds of self-reported poor sleep quality. Results from cross-sectional and retrospective analyses revealed that higher exposure to EDCs was predictive of longer sleep duration, earlier sleep timing, and more fragmented sleep among midlife women.

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DNA methylation (DNAm) is a plausible mechanism underlying cardiometabolic abnormalities, but evidence is limited among youth. This analysis included 410 offspring of the Early Life Exposure in Mexico to Environmental Toxicants (ELEMENT) birth cohort followed up to two time points in late childhood/adolescence. At Time 1, DNAm was quantified in blood leukocytes at long interspersed nuclear elements (LINE-1), H19, and 11ß-hydroxysteroid dehydrogenase type 2 (11ß-HSD-2), and at Time 2 in peroxisome proliferator-activated receptor alpha (PPAR-α). At each time point, cardiometabolic risk factors were assessed including lipid profiles, glucose, blood pressure, and anthropometry. Linear mixed effects models were used for LINE-1, H19, and 11ß-HSD-2 to account for the repeated-measure outcomes. Linear regression models were conducted for the cross-sectional association between PPAR-α with the outcomes. DNAm at LINE-1 was associated with log glucose at site 1 [ß = -0.029, p = 0.0006] and with log high-density lipoprotein cholesterol at site 3 [ß = 0.063, p = 0.0072]. 11ß-HSD-2 DNAm at site 4 was associated with log glucose (ß = -0.018, p = 0.0018). DNAm at LINE-1 and 11ß-HSD-2 was associated with few cardiometabolic risk factors among youth in a locus-specific manner. These findings underscore the potential for epigenetic biomarkers to increase our understanding of cardiometabolic risk earlier in life.

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Maternal diet during pregnancy has been associated with obesity among offspring. The extent to which trimester-specific dietary patterns are associated with markers of adiposity during adolescence remains unclear. We examined associations between prenatal diet patterns with adolescent offspring measures of adiposity and adipokines in 384 mother-adolescent dyads from the Mexico City ELEMENT cohort. Trimester-specific diet patterns were derived from principal component analysis of food frequency questionnaire data. Adolescent anthropometry and serum leptin and adiponectin were measured at 10-17 years. Three maternal diet patterns were identified: Prudent Diet (PD), high in fish and vegetables, the High Meat and Fat Diet (HMFD), high in pork and processed meats, and the Transitioning Mexican Diet (TMD), high in corn tortillas and sugar-sweetened beverages. Multiple linear regression was used to estimate sex-stratified associations among quartiles of diet patterns with adiposity and adipokines, adjusting for maternal marital status, education, and parity. First trimester TMD was associated with greater anthropometric measures and higher leptin in females, while third trimester HMFD was associated higher body fat percentage, triceps thickness, waist circumference, and leptin, but lower adiponectin among males. Contrary to expectation, there were positive associations between the trimester 1 PD pattern and anthropometric measurements in females, and for trimester 2 HMFD and TMD patterns with adipokines among males. Findings suggest maternal diet patterns may influence offspring adiposity markers during adolescence in a sex-specific manner.

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INTRODUCTION: Emerging research has shed light on the potential impact of environmental toxicants on sleep health, however, it remains unclear if these associations exist during adolescence and whether associations differ by sex. This study aimed to examine associations between phthalates, parabens, and phenols on adolescent sleep health using cross-sectional data from 470 participants from the Early Life Exposures in Mexico to Environmental Toxicants (ELEMENT) study. MATERIAL AND METHODS: In 2015, spot urine samples were analyzed for exposure biomarkers of 14 phthalate metabolites, seven phenol, and four paraben analytes. Over seven consecutive days, sleep duration, midpoint, and fragmentation were assessed with wrist-actigraphy. We examined associations between summary phthalates, individual phthalate metabolites, and phenol and paraben analytes with mean weekday sleep duration, midpoint, and fragmentation using linear regression models adjusted for specific-gravity and sex, age, pubertal status, smoking and alcohol behavior, physical activity, and screen time. RESULTS: Mean (SD) age was 13.8 (2.1) years; 53.5 % were female. Σ Plastic - summary measure for toxicants from plastic sources - and Σ DEHP and its metabolites, were associated with longer sleep duration in the unstratified sample. To illustrate, every 1-unit log increase in Σ DEHP was associated with 7.7 min (95 % CI: 0.32, 15.1; p < 0.05) longer duration. Summary measures of toxicants from plastic sources, personal care products, anti-androgenic toxicants, and multiple individual phthalates, phenols, and parabens were associated with later midpoint. The midpoint associations were largely female-specific. There were no associations with sleep fragmentation. CONCLUSIONS: Higher EDC exposure may be related to longer sleep duration and later sleep timing during adolescence, and associations may vary by toxicant and according to sex.

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BACKGROUND: Sedentary behavior is a modifiable risk factor for cardiometabolic health; however, the assessment of total sedentary time may not capture youth's highly active and interrupted activity patterns. This study examined the associations between sedentary activity patterns and cardiometabolic risk factors among Mexican youth, who have a disproportionate burden of metabolic diseases, using a repeated measure design out of a longitudinal data. METHODS: 570 subjects in the Early Life Exposure in Mexico to ENvironmental Toxicants (ELEMENT) birth cohort, who were followed up to three-time points during adolescence, were included. Bout duration, and frequency and percentages of waking time spent in specific intensities of activity, were quantified using ActiGraph wGT3X-BT wrist accelerometers. Self-reported questionnaires were used to query the usual duration of different sedentary behaviors. Outcomes were fasting lipid profile, markers for glucose homeostasis, anthropometry, and blood pressure. Associations were modeled using linear mixed-effects models, and isotemporal substitution approach was additionally used to assess the effect of replacing objectively assessed sedentary activity with other activity intensities, adjusting for potential confounders. RESULTS: Each hour of self-reported screen-based time was positively associated with diastolic blood pressure (mm Hg) [ß = 0.30, 95% confidence interval (95% CI) = 0.10, 0.51], and an hour of other sedentary time was associated with log serum glucose (mg/dL) [ß = 0.01, 95% CI = 0.004, 0.017]. Substitution models showed that replacing 5% of sedentary time with moderate to vigorous physical activity (MVPA) was associated with lower waist circumference (cm) [ß = - 1.35, 95% CI = - 1.91, - 0.79] and log serum triglycerides (mg/dL) [ß = - 0.11, 95% CI = - 0.18, - 0.03]. Substituting one uninterrupted sedentary bout with light activity was associated with lower insulin (µIU/mL) [ß = - 0.06, 95% CI = - 0.10, - 0.02]. CONCLUSIONS: Sedentary time was associated with cardiometabolic risk factors in Mexican youth in a context-specific manner. Replacing sedentary time with higher intensities was associated with improvements in some cardiometabolic markers.

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BACKGROUND AND AIM: An association between lead (Pb) exposure and antisocial behaviors has been documented, but findings have been inconclusive. We aimed to estimate the association between prenatal, early childhood, and preadolescent/adolescent (periadolescent) Pb exposure and aggression and conduct problems in periadolescent residents of Mexico City. METHODS: Using information from the ELEMENT cohort study, we assessed prenatal Pb exposure through maternal patella Pb (MPPb) measurement during the puerperium, early childhood (birth to 5 years of age) exposure through a cumulative blood lead index (CBLI), and periadolescent exposure through a blood Pb (BPb) measurement concurrent with the evaluation of the outcomes. Outcomes were assessed during periadolescence using the parent-reported scales of aggression and conduct problems of the Behavioral Assessment System for Children-2nd version (BASC-2). We modeled the association between Pb exposure at each stage and each outcome (defined as a T-score ≥60 in the corresponding behavioral scale) using logistic regression, adjusting for sex, maternal age at delivery, maternal education, and household socioeconomic status (SES). The differential effect by sex was assessed with an interaction term in the models. RESULTS: 743, 704, and 595 participants were respectively eligible for inclusion in final models of prenatal, early childhood, and periadolescent Pb exposure. Median Pb exposure at each stage was 9.9 µg/g for MPPb (prenatal), 5.19 µg/dl for CBLI (early childhood), and 2.62 µg/dl for concurrent BPb (periadolescence). 12 % of participants met the criterion for aggression, and 15 % for conduct problems. In adjusted models, a one interquartile range increase in MPPb increased the odds of conduct problems (OR:1.31; 95 % CI: 1.01, 1.70) and aggression (OR=1.24; 95 % CI: 0.93, 1.65) during periadolescence. Pb exposure during early childhood or periadolescence was not associated with either outcome. We found no evidence of interactions by sex. CONCLUSIONS: Exposure to Pb during the prenatal stage was associated with aggression and conduct problems during periadolescence.

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OBJECTIVE: To evaluate whether sleep duration, timing, and variability were associated with inflammatory cytokines in a cohort of Mexico City adolescents. METHODS: The analytic sample comprised >500 adolescents who were part of an ongoing longitudinal study in Mexico City. At two time points during mid-to-late puberty (average age 14, n = 391) and late-to-post puberty (average age 16, n = 345), adolescents completed a follow-up visit that included 7-day wrist actigraphy and clinical assessment of plasma inflammatory cytokines (high-sensitivity C-reactive protein, Interleukin 1ß, Interleukin 6, and Tumor Necrosis Factor ɑ). Sleep characteristics included weekday and weekend sleep duration and midpoint (median of bed and wake time), as well as sleep variability (SD of sleep duration across 7 days) and social jetlag (midpoint difference from weekdays to weekends). At each time point, multivariable linear regression models were run with log inflammatory levels as the outcome and categories of sleep characteristics as predictors, while adjusting for potential confounders (specific to each model). Analyses were run unstratified and sex-stratified. RESULTS: In the mid-to-late pubertal visit, weekday sleep duration was inversely associated with natural log hs-CRP after adjustment (Q4 vs Q1: ß = -0.41, 95% Confidence Interval (CI) -0.81 to -0.01) and later sleep midpoint was positively associated with log hs-CRP (Q4 vs Q1: ß = 0.55, 95% CI 0.13 to 0.97). Sleep duration variability was associated with higher IL-1ß among boys, while in girls social jetlag was associated with higher IL-1ß and weekend sleep duration was inversely associated with IL-6. At the late-to-post pubertal visit, there were few associations except for a positive association between weekday sleep duration and hs-CRP among boys (ß = 0.60, 95% CI 0.04 to 1.16) and a non-linear positive association between social jetlag and hs-CRP among girls (ß = 0.80, 95% CI 0.22 to 1.37 comparing 2 to 3 h of social jetlag vs <1 h). CONCLUSION: Later timing, shorter duration, and inconsistency of sleep were related to higher levels of inflammatory biomarkers, but associations were more evident at the mid-to-late pubertal visit than the late-to-post pubertal visit.

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Epidemiological studies assessing prenatal fluoride exposure and anthropometry at birth are scarce, inconsistent and with methodological limitations. The aim of this study was to evaluate associations between maternal urinary fluoride (MUF) at each trimester of pregnancy and birth weight and length in 536 mother-child pairs in the Early Life Exposures in Mexico to Environmental Toxicants (ELEMENT) cohort study. MUF (mg/L) was measured using microdiffusion/fluoride-specific electrode from at least one trimester of pregnancy. Non-linear associations were assessed through segmented regression models (MUF and birth weight Z-score) and we used linear regression models for MUF and birth length Z-score. Models were adjusted for potential confounders including urinary creatinine concentrations as a covariate. Non-creatinine adjusted MUF levels at each trimester of pregnancy were 0.81, 0.86, and 0.82 mg/L, mean concentrations for first, second and third trimester, respectively. For birth weight, we identified a MUF breakpoint at 0.99, 0.68 and 0.58 mg/L, for first, second and third trimester of pregnancy, respectively. In the first trimester, an increase of 1 mg/L in MUF concentrations ≥0.99 mg/L was associated with an increase in weight Z-score at birth (ß = 0.79; 95% CI: 0.10, 1.48; p = 0.02). Second trimester MUF (≥0.68 mg/L) was marginally associated with birth weight decrease (ß = -0.25; 95% CI: -0.55, 0.04; p = 0.09) and third trimester MUF (≥0.58 mg/L) was significantly associated with birth weight decrease (ß = -0.33; 95% CI: -0.63, -0.03; p = 0.03). We observed a linear and significant association between MUF and Z-score of length at birth only for the first trimester of pregnancy (ß = 0.55; 95% CI: 0.07, 1.04; p < 0.02). Prenatal fluoride exposure was associated with birthweight z-score with different susceptibility windows. Our findings reinforce the hypothesis that maternal fluoride exposure may affect birth anthropometry.

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INTRODUCTION: Heavy metals such as Lead (Pb) and Mercury (Hg) can affect adipose tissue mass and function. Considering the high prevalence of exposure to heavy metals and obesity in Mexico, we aim to examine if exposure to Pb and Hg in adolescence can modify how fat is accumulated in early adulthood. METHODS: This study included 100 participants from the ELEMENT cohort in Mexico. Adolescent Pb and Hg blood levels were determined at 14-16 years. Age- and sex-specific adolescent BMI Z-scores were calculated. At early adulthood (21-22 years), fat accumulation measurements were performed (abdominal, subcutaneous, visceral, hepatic, and pancreatic fat). Linear regression models with an interaction between adolescent BMI Z-score and Pb or Hg levels were run for each adulthood fat accumulation outcome with normal BMI as reference. RESULTS: In adolescents with obesity compared to normal BMI, as Pb exposure increased, subcutaneous (p-interaction = 0.088) and visceral (p-interaction < 0.0001) fat accumulation increases. Meanwhile, Hg was associated with subcutaneous (p-interaction = 0.027) and abdominal (p-interaction = 0.022) fat deposition among adolescents with obesity. CONCLUSIONS: Heavy metal exposure in adolescence may alter how fat is accumulated in later periods of life.

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Changes in consumption of sugar sweetened beverage (SSBs) have been associated with increased body mass index (BMI), but little work has evaluated the effect on waist circumference (WC) and body fat percentage during adolescence, a period characterized by rapid growth and change in dietary behaviors. We examined the relationship of changes in SSB intake and changes in adiposity over two years in 464 Mexican adolescents. Food frequency questionnaires were used to sum intake of regular soda, coffee with sugar, tea with sugar, sweetened water with fruit, chocolate milk, corn atole, and a sweetened probiotic milk beverage. Linear regression models were used to estimate the associations of changes in SSBs with changes in BMI, body fat percentage, and WC, adjusting for sex, socioeconomic status, screen time, physical activity, age, and change in age. Adolescents who increased their daily SSB intake by >2 serving had a −2.72% higher body fat percentage (95% CI: 0.61, 4.82); a 1−2 serving increase was associated with a 2.49 cm increase (95% CI: 0.21, 4.76) in WC compared with those with no change in intake. Within an adolescent sample, changes in SSB intake were related to concomitant changes in body fat percentage and WC, but not BMI.

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BACKGROUND: Maternal diet during gestation has been linked to infant sleep; whether associations persist through adolescence is unknown. OBJECTIVES: We explored associations between trimester-specific maternal diet patterns and measures of sleep health among adolescent offspring in a Mexico City birth cohort. METHODS: Data from 310 mother-adolescent dyads were analyzed. Maternal diet patterns were identified by principal component analysis derived from FFQs collected during each trimester of pregnancy. Sleep duration, midpoint, and fragmentation were obtained from 7-d actigraphy data when adolescents were between 12 and 20 y old. Unstratified and sex-stratified association analyses were conducted using linear regression models, adjusted for potential confounders. RESULTS: Mean ± SD age of offspring was 15.1 ± 1.9 y, and 52.3% of the sample was female. Three diet patterns were identified during each trimester of pregnancy: the Prudent Diet (PD), high in lean proteins and vegetables; the Transitioning Mexican Diet (TMD), high in westernized foods; and the High Meat & Fat Diet (HMFD), high in meats and fat products. Mean ± SD sleep duration was 8.5 ± 1.5 h/night. Most associations were found in the third trimester. Specifically, PD maternal adherence was associated with shorter sleep duration among offspring (-0.57 h; 95% CI: -0.98, -0.16 h, in the highest tertile compared with the lowest) and earlier sleep midpoint among females (-0.77 h; 95% CI: -1.3, -0.26 h). Adherence to the HMFD and TMD was nonlinearly associated with less fragmented sleep, with the latter only evident among females. CONCLUSIONS: Findings indicate that maternal dietary patterns, especially during the third trimester of pregnancy, may have long-term impacts on offspring sleep.

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There is limited evidence for the effects of diet on cardiometabolic profiles during the pubertal transition. We collected repeated measures of diet quality and cardiometabolic risk factors among Mexican youth. This analysis included 574 offspring of the Early Life Exposure in Mexico to Environmental Toxicants (ELEMENT) birth cohort followed up to three time points. Dietary Approaches to Stop Hypertension (DASH), alternate Mediterranean Diet (aMedDiet), and Children's Dietary Inflammatory Index (C-DIITM) scores were computed from food frequency questionnaires. Higher DASH and aMedDiet scores reflect a higher diet quality, and lower C-DII scores reflect an anti-inflammatory diet. Cardiometabolic risk factors were lipid profile, glucose homeostasis, blood pressure, and waist circumference. Linear mixed models were used between quartiles of each diet score and outcomes. Compared to the first quartile, the fourth DASH quartile was inversely associated with log serum insulin (µIU/mL) [ß = -0.19, p = 0.0034] and log-Homeostatic Model Assessment of Insulin Resistance [ß = -0.25, p = 0.0008]. Additionally, log serum triglycerides (mg/dL) was linearly associated with aMedDiet score [ß = -0.03, p = 0.0022]. Boys in the highest aMedDiet quartile had higher serum high-density lipoprotein cholesterol (mg/dL) [ß = 4.13, p = 0.0034] compared to the reference quartile. Higher diet quality was associated with a better cardiometabolic profile among Mexican youth.

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