Search

Summary: Background: Gestational weight gain (GWG) has been associated with the accumulation of body fat in offspring, but little is known about the intergenerational relationship. Objective: To assess the effect of GWG in grandmothers and mothers on the child's body mass index (BMI). Methods: This is a sub‐study nested in the 1993 Pelotas (Brazil) Birth Cohort at 22 years follow‐up visit. We calculated the BMI‐for‐age z‐score (BAZ) and evaluated overweight (>2 SD in ≤5 years of age and >1 SD for >5 years of age for BAZ). Grandmothers' and mothers' GWG were calculated as the difference between weight in the beginning of pregnancy and the last recorded weight before delivery. We standardized the GWG by adjusting for pre‐gestational BMI. We also categorized GWG as adequate, excessive, or insufficient, in accordance with the Institute of Medicine (2009). Linear and logistic regressions stratified by child's age (≤2 years; 2.01‐5 years; >5 years) were used. Structural equations were modelled to calculate the total, indirect, and direct effects of grandmothers' and mothers' GWG on children's BAZ. Results: Nine hundred and forty‐six out of 1113 children evaluated were 5 years of age or under. There was an indirect effect (through maternal birthweight, maternal pre‐gestational BMI, maternal GWG, and child birthweight) of grandmother GWG on grandchild BAZ, from 2.01 to 5 years of age [β = 0.12 95%CI: 0.04‐0.20 (P < 0.01)]. Maternal GWG directly increased the child's BAZ at >5 years of age [β = 0.34 95%CI: 0.15‐0.53 (P < 0.001)]. Conclusions: GWG's effect on BMI does seem to be transmitted across three generations. Managing this will require health education during the gestational period for women and their families. [ABSTRACT FROM AUTHOR]

Background and Aims: Longitudinal cohort studies examining different generations can explain how health problems can be transmitted through genetic and environmental mechanisms and their effects on the health of offspring. This study aimed to present the design and to describe the characteristics of the baseline sample of a second generation cohort. Methods: The 93Cohort‐II is a dynamic prospective cohort composed of a second generation from the original 1993 Pelotas Birth Cohort (offspring), whose parents had their last follow‐up at 22 years old. Biological parents were asked to answer questions addressing the type of birth, general health status, family composition, dietary habits, breastfeeding habits, and child‐caregiver(s), among others, and the children's anthropometric measurements were evaluated. Results: Of 1650 children identified, 1212 were evaluated (response rate, 73.4%), and 21 died before the baseline assessment. The age of the offspring ranged from 0 to 10 years (mean [±SD], 2.9 ± 2.1 years); most children (65.6%) lived with both parents and were born to young mothers and poor families. One‐third of the children were breastfed until 6 months of age, one‐half were born by cesarean section, 63.9% had used medication in the previous 15 days, 26.4% experienced hospitalization at least once since birth, and 14% had no updated vaccination; asthma/bronchitis (20.4%) and bronchiolitis (13.4%) were the most frequently reported diseases. More than 60% consumed ultra‐processed foods, and the prevalence of overweight among those <5 and ≥6 years of age was 10.2% and 18.9%, respectively. The mean total Child Behavior Checklist score was 44.1 ± 23.61 (≥16 months), and the mean intellectual quotient score in children ≥6 years of age was 97.9 ± 15.4. Conclusion: Despite the difficulties in conducting intergenerational cohort studies, the results of the present investigation provide evidence supporting the feasibility of performing these types of studies in middle‐income countries. [ABSTRACT FROM AUTHOR]

Objective: This study aimed to assess the association between adverse childhood experiences (ACEs) and adiposity in adolescents from two cohorts in different socioeconomic contexts.Methods: Data from the Avon Longitudinal Study of Parents and Children (ALSPAC, United Kingdom) and the 1993 Pelotas Cohort (Brazil) were used. Six ACEs were assessed in both cohorts up to age 15. At 15 years, body mass index (BMI) and waist circumference (WC) were measured, and at 18 years, BMI, fat mass index, and android fat percentage were assessed.Results: Few associations were observed between ACEs and adiposity at 15 years, and they were not consistent across cohorts. For adiposity at age 15 in ALSPAC, physical abuse had a positive association with WC, and domestic violence had a positive association with both WC and BMI. A dose-response relationship between the ACE score and both WC and BMI at 15 years was observed in ALSPAC. In the 1993 Pelotas Cohort, the associations found in crude analysis were no longer evident after adjustment.Conclusions: This study found some evidence of an association between an ACE score and adiposity in adolescence in a United Kingdom cohort but no evidence of association in a Brazilian cohort. Residual confounding or context-specific relationships could explain the different pattern of associations. [ABSTRACT FROM AUTHOR]

Background Many low- and middle-income countries have high levels of violence. Research in high-income countries shows that risk factors in the perinatal period are significant precursors of conduct problems which can develop into violence. It is not known whether the same early influences are important in lower income settings with higher rates of violence. This study compared perinatal and sociodemographic risk factors between Brazil and Britain, and their role in explaining higher rates of conduct problems and violence in Brazil. Methods Prospective population-based birth cohort studies were conducted in Pelotas, Brazil ( N = 3,618) and Avon, Britain ( N = 4,103). Eleven perinatal and sociodemographic risk factors were measured in questionnaires completed by mothers during the perinatal period. Conduct problems were measured in questionnaires completed by mothers at age 11, and violence in self-report questionnaires completed by adolescents at age 18. Results Conduct problems were predicted by similar risk factors in Brazil and Britain. Female violence was predicted by several of the same risk factors in both countries. However, male violence in Brazil was associated with only one risk factor, and several risk factor associations were weaker in Brazil than in Britain for both females and males. Almost 20% of the higher risk for conduct problems in Brazil compared to Britain was explained by differential exposure to risk factors. The percentage of the cross-national difference in violence explained by early risk factors was 15% for females and 8% for males. Conclusions A nontrivial proportion of cross-national differences in antisocial behaviour are related to perinatal and sociodemographic conditions at the start of life. However, risk factor associations are weaker in Brazil than in Britain, and influences in other developmental periods are probably of particular importance for understanding male youth violence in Brazil. [ABSTRACT FROM AUTHOR]

Background We examined the associations of maternal age with low birthweight ( LBW) and preterm birth in four cohorts from a middle- and a high-income country, where the patterning of maternal age by socio-economic position ( SEP) is likely to differ. Methods Population-based birth cohort studies were carried out in the city of Pelotas, Brazil in 1982, 1993, and 2004, and in Avon, UK in 1991 [ Avon Longitudinal Study of Parents and Children ( ALSPAC)]. Adjustment for multiple indicators of SEP were applied. Results Low SEP was associated with younger age at childbearing in all cohorts, but the magnitudes of these associations were stronger in ALSPAC. Inverse associations of SEP with LBW and preterm birth were observed in all cohorts. U-shaped associations were observed between maternal age and odds of LBW in all cohorts. After adjustment for SEP, increased odds of LBW for young mothers (<20 years) attenuated to the null but remained or increased for older mothers (≥35 years). Very young (<16 years) maternal age was also associated with both outcomes even after full SEP adjustment. SEP adjusted odds ratio of having a LBW infant in women <16 years and ≥35 years, compared with 25-29 years, were 1.48 [95% confidence interval ( CI) 1.00, 2.20] and 1.66 [95% CI 1.36, 2.02], respectively. The corresponding results for preterm birth were 1.80 [95% CI 1.23, 2.64)] and 1.38 [95% CI 1.15, 1.67], respectively. Conclusion Confounding by SEP explains much of the excess risk of LBW and preterm among babies born to teenage mothers as a whole, but not for mothers aged <16 or ≥35 years. Given that the proportion of women becoming pregnant at <16 years is smaller than for those ≥35 years, the population burden is greater for older age. [ABSTRACT FROM AUTHOR]

Background: The study of gene-environment interactions (G × E) is one of the most promising strategies to uncover the origins of mental disorders. Replication of initial findings, however, is essential because there is a strong possibility of publication bias in the literature. In addition, there is a scarcity of research on the topic originated from low- and middle-income countries (LMIC). The aim of this study was to replicate G × E hypotheses for externalizing problems among adolescents in a middle-income country. Methods: As part of the Pelotas 1993 Birth Cohort Study, 5,249 children were enrolled at birth and followed up to the age of 15 years, with an 85.7% retention rate. We sought an interaction between the homozygosity of the 10-repeat allele at the dopamine transporter ( DAT1) gene and prenatal maternal smoking in the development of hyperactivity problems during adolescence assessed by the Strengths and Difficulties Questionnaire. We also tested for an interaction between the uVNTR polymorphism at the monoamine oxidase A ( MAOA) and the experience of childhood maltreatment in the occurrence of conduct problems among adolescent boys. Results: Although there was a clear association between prenatal maternal smoking and hyperactivity scores in adolescence ( p < 0.001), no main genetic or interaction effects for the DAT1 gene were detected. Similarly, childhood maltreatment showed to be associated with conduct problems among boys ( p < 0.001), with no observable main genetic or interaction effects for the MAOA gene. Conclusions: In the largest mental health G × E study performed in a LMIC to date, we did not replicate previous positive findings from the literature. Despite the presence of main environmental effects, there was no evidence of effect modification by genotype status. Additional replication efforts to measure G × E are needed to better understand the origins of mental health and illness, especially in LMIC. [ABSTRACT FROM AUTHOR]

Objective: To investigate the main dental caries life course determinants and predictors of dental caries at age 12. Methods: This study was nested in a population-based birth cohort started in 1993 in Pelotas, Brazil. A sample of 359 children was followed-up. Dental examinations and interviews were performed at 6 and at 12 years old. Dental caries (DMFT) at 12 years old was the outcome. Exploratory variables included socioeconomic and demographic variables at birth, children’s nutritional and development characteristics, primary dental caries, oral health related behaviors and dental service use at age 6 and 12. Poisson regression was used in order to provide relative risk ratio estimates. Attributable risk or etiology fraction and population attributable risk for both main early life variables were calculated. Dental caries prediction (DMFT ≥ 1) at 12 years old was tested using logistic regression analyses. Results: Children who presented height-for-age deficit at 12 months (RR 1.50 CI: 95% = 1.03–2.18), children who showed a DMFT of 1–3 and 4–19 at 6 years (RR = 2.01; CI: 95% = 1.33–3.03, and RR = 2.66; CI: 95% = 1.81–2.53, respectively) and those children aged 12 in the highest tertile of proportion of teeth experiencing gingival bleeding (RR = 1.58; CI: 95% = 1.11–2.24) presented a higher level of dental caries at age 12. Attributable risk for dental caries at age 12 were 79.1% and 74.2% for deficit in height for age at 12 months and for primary dental caries at age 6 years respectively; population attributable risk for dental caries at age 12 were 3.1% for deficit in height for age at 12 months and 64.9% for primary dental caries at age 6. The level of accuracy in predicting dental caries at age 12 by using life course socioeconomic, behavioral and clinical data was modest. Conclusions: The results of this study support the hypothesis linking social, biological and behavioral exposures and dental caries at 12 years old. In addition, the findings reinforce the lack of accuracy of dental caries predictors therefore limiting the individuals high-risk approach as a public health strategy. [ABSTRACT FROM AUTHOR]

This study estimated the lifetime prevalence of toothache at ages 6 and 12 yr, the prevalence of toothache during the last month, and their association with social, behavioural and clinical exposures in the course of life of 339 12-yr-old children from a birth cohort in Pelotas, Brazil. Exploratory variables were collected in the perinatal study and during several follow-up studies. Prevalence ratios were calculated using Poisson regression, following a hierarchical conceptual model. The lifetime prevalence of toothache at ages 6 and 12 yr were 39% [95% confidence interval (CI) = (34;45)] and 63% [95% CI = (58;69)], respectively. Toothache during the last month was reported by 11% [95% CI = (8;15)]. Children who did not live with their biological father at birth, and children with higher dmf-t counts, reported a higher lifetime prevalence of toothache at age 6 yr. Children experiencing poverty between ages 0 and 4 yr, with higher dmf-t and DMF-T indexes presented a greater lifetime prevalence of toothache at 12 yr. Toothache within the last month was more likely to be reported by girls and by children who did not live with their biological father at birth. Preventive strategies should be implemented in early stages of the life cycle, taking into account the socio-economic and family context in which pain mostly occurs. [ABSTRACT FROM AUTHOR]

Background Emotional disorders are risk factors for atherosclerosis and consequent cardiovascular disease. However, it is not clear whether emotional symptoms (ESs) have direct effects on cardiovascular disease. The aim of the present study is to investigate the effects of early ESs on carotid atherosclerosis in young adults. Methods and Results We tested the association between expression of ESs at 11 and 15 years of age and carotid intima-media thickness at 18 years of age in the 1993 Pelotas Birth Cohort (N=5249, n=4336 with complete mental health data). ES s were assessed using the Strengths and Difficulties Questionnaire. Propensity score weighting procedure was run using generalized boosted regression model to adjust for potential confounding between exposure and outcome. We also tested whether traditional cardiovascular risk factors could mediate this relationship. Adjusted high expression of ESs , both at 11 and 15 years of age, led to mean increases in carotid intima-media thickness of 1.84 and 2.58 μm, respectively, at 18 years of age (both P<0.001). Longitudinal effects of ESs on atherosclerosis were direct and not significantly mediated by traditional cardiovascular risk factors. Male sex at age 15 years significantly enhanced the effects of ESs on carotid intima-media thickness at age 18 years ( P<0.001 for interaction): although high expression of ESs led to mean increases of 1.14 μm in females ( P<0.05), it led to mean increases of 5.83 μm in males ( P<0.001). Conclusions In this large birth cohort, expression of ESs in adolescence was longitudinally associated with a higher carotid intima-media thickness in young adults. The association is direct and not mediated by traditional cardiovascular risk factors. Interactions by sex might have important implications for designing future interventions.