Locus of control (LOC) measures an individual׳s expectancy regarding their ability to affect what happens to them based on their behavior. Those with an internal LOC (ILOC) believe their own behavior influences what happens to them. Those with an external LOC (ELOC) perceive that what happens to them is beyond their control (i.e. determined by luck, fate, chance or powerful others) [1]. A vast amount of research (mainly cross-sectional) suggests that an ELOC is associated with many adverse personal, social, academic and health outcomes. LOC data were uniquely collected prenatally from over 12,000 pregnant women and their partners enrolled in the Avon Longitudinal Study of Parents and Children (ALSPAC). The LOC measure used was a shortened version of the adult version of the Nowicki-Strickland Internal-External locus of control scale. This was administered to the mothers within self-completion questionnaires at three-time points: during pregnancy, at 6 and at 18 years post-partum. In parallel, self-completion questionnaires containing the same LOC questions were completed by their partners during pregnancy, at 6 and 20 years later. ALSPAC LOC data are unique in that they measured orientation over time and on a much larger sample of respondents than is usual. We describe the scale used, why it was chosen and how individual scores changed over time.
Background: Data from epidemiology have consistently highlighted a disparity between the true prevalence of childhood psychiatric disorders and their recognition as defined by receiving a clinical diagnosis. Few studies have looked specifically at the level of unidentified autistic spectrum disorder (ASD) in the population. Method: Logistic regression was used to determine the behavioural traits associated with receiving a diagnosis of ASD using data from the Avon Longitudinal Study of Parents and Children (ALSPAC). A composite score was derived to measure levels of autistic traits; undiagnosed children with scores matching those diagnosed with ASD were identified. Levels of educational provision beyond that provided by standard schooling were examined. Results: Fifty‐five percent of children with autistic traits at the same levels as those who had an autism diagnosis had not been identified as needing extra support from education or specialised health services. Of those who were identified as having special needs, 37.5% had been formally diagnosed with an ASD. For children with impairment at the same level as that associated with Asperger’s syndrome, 57% had no special provision at school, and were not accessing specialised health services. Twenty‐six percent of those who did have special provision at school had an ASD diagnosis. Conclusions: The results suggest that there may be a substantial proportion of children on the autistic spectrum who are never identified by services.
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 13 761 women (contributing 13 867 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 >10 000, 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.
A method is proposed for identification of cases of sudden infant death syndrome (SIDS) from information available on death certificates. Deaths at ages between 7 days and 2 years, referred to a coroner, having certain specified causes of death codes, identified 160 of 169 cases of SIDS confirmed as such by a pathologist. The sensitivity of the method was 94% and the specificity was 97%.
Apolipoprotein E (APOE) genotype (ε2/ε3/ε4: rs429358 ε4 allele; rs7412 ε2 allele) is strongly associated with both lipid levels and Alzheimer's disease. Although there is also evidence of milder cognitive impairment in later life in carriers of the APOE ε4 allele, there have been few studies investigating the impact of APOE genotype on cognitive function in children.We determined APOE genotype in 5995 children from the Avon Longitudinal Study of Parents and Children and investigated associations between APOE genotype and plasma lipids (at age 9), IQ (at age 8), memory (at ages 8 and 10), and performance in school attainment tests (at ages 7, 11, and 14).Observed genotype group counts were consistent with Hardy-Weinberg equilibrium (χ(2)p value = .84). There were strong relationships between APOE genotype and low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and triglycerides, which follow the same patterns as in adults. There was no strong evidence to suggest that APOE genotype was associated with IQ (all p values ≥ .46), memory function (p ≥ .35), or school attainment test results (p ≥ .28).Although APOE genotype does have strong associations with lipid levels in childhood, there does not seem to be meaningful effects on cognitive performance, suggesting that any detrimental effects of the ε4 allele on cognitive function are not important until later life.
Two previous studies have suggested that higher prenatal selenium exposure may decrease the risk of wheezing in early childhood. We aimed to test whether higher maternal selenium status in pregnancy is associated with a decreased risk of childhood asthma, and whether this association is modified by glutathione peroxidase (GPX) 4 genotype. In the Avon Longitudinal Study of Parents and Children (ALSPAC) we analysed associations between maternal blood concentrations of selenium during pregnancy and childhood asthma (n=2409) and wheezing (n=2438) at 7 years of age. We also explored interactions between maternal selenium and GPX4 genotype (rs713041) on these outcomes. After controlling for confounders, maternal blood selenium concentration was not associated with offspring asthma or wheezing overall. When we stratified by child GPX4 genotype, maternal selenium was not associated with these outcomes in children who carried the C allele of rs713041, however, in children who were homozygous for the minor T allele, maternal selenium was negatively associated with asthma (adjusted odds ratio per doubling concentration 0.15 (95% CI: 0.04 to 0.63), P=0.010) and wheezing (OR 0.16 (0.04 to 0.66), P=0.011), P interaction 0.059 and 0.013, respectively. Conversely, children of mothers in the bottom quintile for blood selenium concentration were more likely to have asthma than children of mothers with higher selenium status, but only if the children were homozygous for the T allele of rs713041 (OR 2.40 (1.07 to 5.41)). Higher maternal selenium status in pregnancy is associated with a decreased risk of asthma in offspring who are homozygous for the T allele of the rs713041 polymorphism of GPX4 .
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