Age 23 years + oral health questionnaire in Avon Longitudinal Study of Parents and Children.
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ABSTRACT:
SUBMITTER: Dudding T
PROVIDER: S-EPMC5941244 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Background: Early life experiences can have a significant impact on an individual's later behaviour, the way they view the world, their beliefs and their success at forming strong interpersonal relationships. These factors may subsequently influence the way that the individual may parent their children, which in turn may have an effect on their child's behaviour, mental health and world view. Research has linked early traumatic life experiences in the parent's childhood to disorganised attachment to their own child. In this paper we describe the data collected from parents enrolled in the Avon Longitudinal Study of Parents and Children (ALSPAC) on traumatic events experienced during their childhood, so that it can act as a resource for researchers in the future when considering outcomes on the adult, their children and grandchildren. Methods: Data were collected via multiple questionnaires completed by parents enrolled into the ALSPAC study. During pregnancy and post-delivery, questionnaires were administered between 1990 and 1992 via post to the study mothers and their partners. Data were collected on life events including bereavement, sexual abuse, physical abuse, abandonment, neglect, memories of childhood and accidents. Other reports of traumatic events in childhood were reported by parents using free text. This can be made available to researchers for coding on request.
| S-EPMC7199499 | biostudies-literature
Project description:Cardiometabolic disease risk begins in early life and tracks through the life course. As described in "Sex-specific trajectories of measures of cardiovascular health during childhood and adolescence: a prospective cohort study" (O'Keeffe et al., 2018), we modelled sex-specific change in 11 key measures of cardiovascular health from birth/early childhood to age 18 years in a British birth cohort study, the Avon Longitudinal Study of Parents and Children (ALSPAC). In this article, we describe the data used in these analyses. Risk factors measured included BMI, fat and lean mass, blood pressure and blood-based biomarkers. Data are from several sources including cord blood at birth, clinic assessments, routine health records, questionnaires and nuclear magnetic resonance spectroscopy. Outcomes were measured over varying time spans from birth or mid-childhood to age 18 and with different numbers of repeated measures per outcome. Analyses were performed using fractional polynomial and linear spline multilevel models. Further information can be found in O'Keeffe et al. (2018).
| S-EPMC6389726 | biostudies-literature
Project description:Summary The Avon Longitudinal Study of Children and Parents (ALSPAC) was established to understand how genetic and environmental characteristics influence health and development in parents and children. All pregnant women resident in a defined area in the South West of England, with an expected date of delivery between 1st April 1991 and 31st December 1992, were eligible and 13761 women (contributing 13867 pregnancies) were recruited. These women have been followed over the last 19-22 years and have completed up to 20 questionnaires, have had detailed data abstracted from their medical records and have information on any cancer diagnoses and deaths through record linkage. A follow-up assessment was completed 17-18 years postnatal at which anthropometry, blood pressure, fat, lean and bone mass and carotid intima media thickness were assessed, and a fasting blood sample taken. The second follow-up clinic, which additionally measures cognitive function, physical capability, physical activity (with accelerometer) and wrist bone architecture, is underway and two further assessments with similar measurements will take place over the next 5 years. There is a detailed biobank that includes DNA, with genome-wide data available on >10000, stored serum and plasma taken repeatedly since pregnancy and other samples; a wide range of data on completed biospecimen assays are available. Details of how to access these data are provided in this cohort profile.
| S-EPMC3600619 | biostudies-literature
Project description:Antibodies against pathogens provide information on exposure to infectious agents and are meaningful measures of past and present infection. Antibodies were measured in the plasma of children that are the offspring in a population-based birth cohort, the Avon Longitudinal Study of Parents and Children (ALSPAC). Plasma was collected during clinics at age 5, 7, 11 and 15 years. The antigens examined include: fungal ( Saccharomyces cerevisiae); protozoan ( Toxoplasma gondii and surface antigen 1 of T. gondii); herpes viruses (cytomegalovirus, Epstein-Barr virus, herpes simplex virus type 1); common colds (influenza virus subtypes H1N1 and H3N2); other antigens (measles); animal (feline herpes virus, Theiler's virus); bacteria ( Helicobacter pylori); dietary antigens (bovine casein alpha protein, bovine casein beta protein). Alongside the depth of data available within the ALSPAC cohort, this longitudinal resource will enable the investigation of the association between infections and a wide variety of outcomes.
| S-EPMC6124408 | biostudies-literature
Project description:Background: Exposure to adverse childhood experiences (ACEs) is a risk factor for poor later life health. Here, we describe the ACE variables measured in the children of the Avon Longitudinal Study of Parents and Children (ALSPAC) study, and a method used to derive summary measures and deal with missing data in them. Methods: The ALSPAC data catalogue (59 608 variables) was searched in September 2017 for measures on adversity exposure between birth and 18 years. 6140 adversity questions were then screened for conforming to our ACE definitions and suitability for dichotomisation. This screening identified 541 questions on ten 'classic' ACEs (sexual, physical or emotional abuse, emotional neglect, substance abuse by the parents, parental mental illness or suicide attempt, violence between parents, parental separation, bullying and parental criminal conviction) and nine additional ACEs (bond between parent and child, satisfaction with neighbourhood, social support for the parent, social support for the child, physical illness of a parent, physical illness of the child, financial difficulties, low social class and violence between child and partner). These were used to derive a binary construct for exposure to each ACE. Finally, as cumulative measures of childhood adversity, different combinations of the 19 ACE constructs were summed to give total adversity scores. An appropriate strategy for multiple imputation was developed to deal with the complex patterns of missing data. Results: The ACE constructs and ACE-scores for exposure between birth and 16 years had prevalence estimates that were comparable to previous reports (for instance 4% sexual abuse, 18% physical abuse, 25% bullied, 32% parental separation). Conclusions: ACE constructs, derived using a pragmatic approach to handle the high dimensional ALSPAC data, can be used in future analyses on childhood adversity in ALSPAC children.
| S-EPMC6281007 | biostudies-literature
Project description:BackgroundThe relationships between offspring depression profiles across adolescence and different timings of parental depression during the perinatal period remain unknown.AimsTo explore different timings of maternal and paternal perinatal depression in relation to patterns of change in offspring depressive mood over a 14 year period.MethodData were obtained from the Avon Longitudinal Study of Parents and Children (ALSPAC). Parental antenatal depression (ANTD) was assessed at 18 weeks gestation, and postnatal depression (PNTD) at 8 weeks postpartum. Population-averaged trajectories of offspring depressive symptoms were estimated using the Short Mood and Feelings Questionnaire (SMFQ) on nine occasions between 10 and 24 years of age.ResultsFull data were available for 5029 individuals. Offspring exposed to both timings of maternal depression had higher depressive symptoms across adolescence compared with offspring not exposed to ANTD or PNTD, characterised by higher depressive symptoms at age 16 (7.07 SMFQ points (95% CI = 6.19, 7.95; P < 0.001)) and a greater rate of linear change (0.698 SMFQ points (95% CI = 0.47, 0.93; P = 0.002)). Isolated maternal ANTD and to a lesser extent PNTD were also both associated with higher depressive symptoms at age 16, yet isolated maternal PNTD showed greater evidence for an increased rate of linear change across adolescence. A similar pattern was observed for paternal ANTD and PNTD, although effect sizes were attenuated.ConclusionsThis study adds to the literature demonstrating that exposure to two timings of maternal depression (ANTD and PNTD) is strongly associated with greater offspring trajectories of depressive symptoms.
| S-EPMC8485341 | biostudies-literature
Project description:ObjectiveTo investigate whether (1) maternal psychosocial stress (depression/anxiety) during pregnancy is associated with offspring vascular function and (2) whether any association differs depending on the gestational timing of exposure to stress. We also investigated whether any association is likely to be due to intrauterine mechanisms by (3) comparing with the association of paternal stress with offspring vascular function and (4) examining whether any prenatal association is explained by maternal postnatal stress.Methods and resultsAssociations were examined in a UK birth cohort, with offspring outcomes (systolic and diastolic blood pressure, SBP and DBP, endothelial function assessed by brachial artery flow-mediated dilatation (FMD); arterial stiffness assessed by carotid to radial pulse wave velocity (PWV), brachial artery distensibility (DC), and brachial artery diameter (BD) assessed at age 10-11 years (n?=?4,318). Maternal depressive symptoms and anxiety were assessed at 18 and 32 weeks gestation and 8 months postnatally. Paternal symptoms were assessed at week 19. With the exception of DBP and BD, there were no associations of maternal depressive symptoms with any of the vascular outcomes. Maternal depressive and anxiety symptoms were associated with lower offspring DBP and wider BD, though the latter attenuated to the null with adjustment for confounding factors. Paternal symptoms were not associated with offspring outcomes. Maternal postnatal depressive symptoms were associated with lower offspring SBP.ConclusionsWe found no evidence to support the hypothesis that maternal stress during pregnancy adversely affects offspring vascular function at age 10-12 years via intrauterine mechanisms.
| S-EPMC4230381 | biostudies-literature
Project description:BACKGROUND AND AIMS:Familial hypercholesterolaemia (FH) is an autosomal-dominant disease with frequency of 1/500 to 1/250 that leads to premature coronary heart disease. New approaches to identify FH mutation-carriers early are needed to prevent premature cardiac deaths. In a cross-sectional study of the Avon Longitudinal Study of Parents and Children (ALSPAC), we evaluated the biochemical thresholds for FH screening in childhood, and modelled a two-stage biochemical and sequencing screening strategy for FH detection. METHODS:From 5083 ALSPAC children with cholesterol measurement at age nine years, FH genetic diagnosis was performed in 1512 individuals, using whole-genome or targeted sequencing of known FH-causing genes. Detection rate (DR) and false-positive rate (FPR) for proposed screening thresholds (total-cholesterol > 1.53, or LDL-C > 1.84 multiples of the median (MoM)) were assessed. RESULTS:Six of 1512 sequenced individuals had an FH-causing mutation of whom five had LDL-C > 1.84 MoM, giving a verification-bias corrected DR of 62.5% (95% CI: 25-92), with a FPR of 0.2% (95% CI: 0.1-0.4). The DR for the TC cut-point of 1.53 MoM was 25% (95% CI: 3.2-65.1) with a FPR of 0.4% (95% CI: 0.2-0.6). We estimated 13 of an expected 20 FH mutation carriers (and 13 of the 20 parental carriers) could be detected for every 10,000 children screened, with false-positives reliably excluded by addition of a next generation sequencing step in biochemical screen-positive samples. CONCLUSIONS:Proposed cholesterol thresholds for childhood FH screening were less accurate than previously estimated. A sequential strategy of biochemical screening followed by targeted sequencing of FH genes in screen-positive children may help mitigate the higher than previously estimated FPR and reduce wasted screening of unaffected parents.
| S-EPMC5414415 | biostudies-literature
Project description:Depression during adolescence is associated with a number of negative outcomes in later life. Research has examined the longitudinal nature of adolescent depression in order to identify patterns of depressive mood, the early antecedents and later consequences. However, rich longitudinal data is needed to better address these questions. The Avon Longitudinal Study of Parents and Children (ALSPAC) is an intergenerational birth cohort with nine repeated assessments of depressive symptoms throughout late childhood, adolescence and young adulthood. Depressive symptoms are measured using the Short Mood and Feelings Questionnaire (SMFQ). Many studies have used ALSPAC to examine the longitudinal nature of depressive symptoms in combination with the wealth of early life exposure and later outcome data. This data note provides a summary of the SMFQ data, where the data are stored in ALSPAC, the characteristics and distribution of the SMFQ, and highlights some considerations for researchers wanting to use the SMFQ data in ALSPAC.
| S-EPMC6764237 | biostudies-literature
Project description:We established air pollution modelling to study particle (PM10) exposures during pregnancy and infancy (1990-1993) through childhood and adolescence up to age ~15?years (1991-2008) for the Avon Longitudinal Study of Parents And Children (ALSPAC) birth cohort. For pregnancy trimesters and infancy (birth to 6?months; 7 to 12?months) we used local (ADMS-Urban) and regional/long-range (NAME-III) air pollution models, with a model constant for local, non-anthropogenic sources. For longer exposure periods (annually and the average of birth to age ~8 and to age ~15?years to coincide with relevant follow-up clinics) we assessed spatial contrasts in local sources of PM10 with a yearly-varying concentration for all background sources. We modelled PM10 (?g/m3) for 36,986 address locations over 19?years and then accounted for changes in address in calculating exposures for different periods: trimesters/infancy (n?=?11,929); each year of life to age ~15 (n?=?10,383). Intra-subject exposure contrasts were largest between pregnancy trimesters (5th to 95th centile: 24.4-37.3??g/m3) and mostly related to temporal variability in regional/long-range PM10. PM10 exposures fell on average by 11.6??g/m3 from first year of life (mean concentration?=?31.2??g/m3) to age ~15 (mean?=?19.6??g/m3), and 5.4??g/m3 between follow-up clinics (age ~8 to age ~15). Spatial contrasts in 8-year average PM10 exposures (5th to 95th centile) were relatively low: 25.4-30.0??g/m3 to age ~8?years and 20.7-23.9??g/m3 from age ~8 to age ~15?years. The contribution of local sources to total PM10 was 18.5%-19.5% during pregnancy and infancy, and 14.4%-17.0% for periods leading up to follow-up clinics. Main roads within the study area contributed on average ~3.0% to total PM10 exposures in all periods; 9.5% of address locations were within 50?m of a main road. Exposure estimates will be used in a number of planned epidemiological studies.
| S-EPMC5907299 | biostudies-literature