Avon Longitudinal Study Of Parents Research Articles

Childhood Adversity and Incident Psychotic Experiences in Early Adulthood: Cognitive and Psychopathological Mediators.

Childhood adversity is often described as a potential cause of incident psychotic experiences, but the underlying mechanisms are not well understood. We aimed to examine the mediating role of cognitive and psychopathological factors in the relation between childhood adversity and incident psychotic experiences in early adulthood. We analyzed data from the Avon Longitudinal Study of Parents and Children, a large population-based cohort study. Childhood adversity was measured prospectively from birth to age 11 years, mediators (anxiety, depression, external locus of control [LoC], negative symptoms) were assessed at approximately 16 years of age, and incident psychotic experiences were assessed at ages 18 and 24 years. Mediation was examined via the counterfactual g-computation formula. In total, 7% of participants had incident suspected or definite psychotic experiences in early adulthood. Childhood adversity was related to more incident psychotic experiences (ORadjusted = 1.34, 95% CI = 1.21; 1.49), and this association was partially mediated via all mediators examined (proportion mediated: 19.9%). In separate analyses for each mediator, anxiety, depression, external LoC, and negative symptoms were all found to mediate the link between adversity and incident psychotic experiences. Accounting for potential confounders did not modify our results. Our study shows that cognitive biases as well as mood symptomatology may be on the causal pathway between early-life adversity and the development of psychotic experiences. Future studies should determine which mediating factors are most easily modifiable and most likely to reduce the risk of developing psychotic experiences.

Childhood Gender Nonconformity and Parental Maltreatment as Mediators of Sexual Orientation Disparities in Childhood Emotional and Behavioral Difficulties.

The mechanisms underlying sexual orientation differences in psychopathology originating in childhood remain understudied since sexual orientation does not directly manifest in childhood. This study tested whether childhood gender nonconformity and parental maltreatment before age 6years 9months partly explained sexual orientation disparities in the developmental trajectories of emotional and behavioral difficulties from age 6years 9months to 11years 8months. The Avon Longitudinal Study of Parents and Children was used (2182 boys and 2422 girls, Mage = 15.5, 90% White). After controlling for early life factors, non-heterosexual boys and girls displayed significantly greater emotional and behavioral difficulties than their heterosexual counterparts at all three ages. There was a sex difference in the mediating effects. For girls, sexual orientation disparities in childhood emotional and behavioral difficulties were partially explained by childhood gender nonconformity. For boys, sexual orientation disparities in childhood emotional and behavioral difficulties were partially explained by a path through greater childhood gender nonconformity, leading to increased risk of being the targets of parental maltreatment. Childhood gender nonconformity, parental maltreatment, and other early life factors only partially explain sexual orientation disparities in childhood emotional and behavioral difficulties. The mediating effects of childhood gender nonconformity and parental maltreatment on the association between sexual orientation and childhood emotional and behavioral difficulties differ between the sexes.

Mediating effect of fat mass, lean mass, blood pressure and insulin resistance on the associations of accelerometer-based sedentary time and physical activity with arterial stiffness, carotid IMT and carotid elasticity in 1574 adolescents

This study examined the mediating effect of total body fat mass, lean mass, blood pressure (BP) and insulin resistance on the associations of sedentary time (ST), light physical activity (LPA) and moderate-to-vigorous PA (MVPA) with carotid-femoral pulse wave velocity (cfPWV), carotid intima-media thickness (cIMT) and carotid elasticity in 1574 adolescents from the Avon Longitudinal Study of Parents and Children birth cohort, UK. ST, LPA and MVPA were assessed with ActiGraph accelerometer. ST and LPA were sex-categorised in tertiles as low (reference), moderate and high, while MVPA was categorised as <40 min/day (reference), 40–<60 min/day and ≥60 min/day. cfPWV, cIMT and carotid elasticity were measured with Vicorder and ultrasound. Fat mass and lean mass were assessed with dual-energy X-ray absorptiometry and homeostatic model assessment of insulin resistance (HOMA-IR) was computed. Mediation analyses structural equation models and linear mixed-effect models adjusted for cardiometabolic and lifestyle factors were conducted. Among 1574 adolescents [56.2% female; mean (SD) age 15.4 (0.24) years], 41% males and 17% females accumulated ≥60 min/day of MVPA. Higher ST was associated with lower cIMT partly mediated by lean mass. Higher LPA (standardized β = −0.057; [95% CI −0.101 to −0.013; p = 0.014]) and the highest LPA tertile were associated with lower cfPWV. BP had no significant mediating effect movement behaviour relations with vascular indices. Lean mass partially mediated associations of higher MVPA with higher cIMT (0.012; [0.007–0.002; p = 0.001], 25.5% mediation) and higher carotid elasticity (0.025; [0.014–0.039; p = 0.001], 28.1% mediation). HOMA-IR mediated the associations of higher MVPA with higher carotid elasticity (7.7% mediation). Engaging in ≥60 min/day of MVPA was associated with higher carotid elasticity. In conclusion, higher LPA was associated with lower arterial stiffness, but higher MVPA was associated with thicker carotid wall explained by higher lean mass.

Maternal experienced bereavement and offspring mental health in early adulthood: the role of modifiable parental factors.

It is estimated that 78% of children experience the death of a close friend or family member by 16 years of age, yet longitudinal research examining the mental health outcomes of wider experiences of bereavement is scarce. We conducted a longitudinal investigation of the association between maternal experienced bereavement before the age of 11 years and offspring depressive and anxiety disorders at age 18 and examined moderation of this association by modifiable parental factors. We analysed data from the Avon Longitudinal Study of Parents and Children, a UK-based birth cohort, including 9,088 child participants with data available on bereavement. Bereavement was measured via maternal report at eight timepoints until children were 11 years. Offspring depressive and anxiety-related disorders were self-reported at 18 years old using the Clinical Interview Schedule-Revised (CIS-R). The potential moderating roles of maternal anxiety, maternal depression, parental monitoring, positive parenting and negative parenting practices were examined. Maternal experienced bereavement was not associated with depression or anxiety-related disorders in early adulthood among offspring. In addition, no support was found for negative parenting practices, parental monitoring or maternal anxiety and depression as moderators of the relationship between maternal experienced bereavement and offspring mental health problems at 18 years old. Findings in relation to the moderating role of positive parenting practices were inconsistent. Findings suggest that a large number of children are exposed to maternal experienced bereavement. We found no evidence that maternal experienced bereavement during childhood increases the risk for offspring psychiatric disorders in early adulthood. Several methodological considerations prudent to bereavement research are discussed.

Releasing synthetic data from the Avon Longitudinal Study of Parents and Children (ALSPAC): Guidelines and applied examples

The Avon Longitudinal Study of Parents and Children (ALSPAC) is a prospective birth cohort. Since its inception in the early 1990s, the study has collected over thirty years of data on approximately 15,000 mothers, their partners, and their offspring, resulting in over 100,000 phenotype variables to date. Maintaining data security and participant anonymity and confidentiality are key principles for the study, meaning that data access is restricted to bona fide researchers who must apply to use data, which is then shared on a project-by-project basis. Despite these legitimate reasons for restricting data access, this does run counter to emerging best scientific practices encouraging making data openly available to facilitate transparent and reproducible research. Given the rich nature of the resource, ALSPAC data are also a valuable educational tool, used for teaching a variety of methods, such as longitudinal modelling and approaches to modelling missing data. To support these efforts and to overcome the restrictions in place with the study’s data sharing policy, we discuss methods for generating and making openly available synthesised ALSPAC datasets; these synthesised datasets are modelled on the original ALSPAC data, thus maintaining variable distributions and relations among variables (including missing data) as closely as possible, while at the same time preserving participant anonymity and confidentiality. We discuss how ALSPAC data can be synthesised using the ‘synthpop’ package in the R statistical programming language (including an applied example), present a list of guidelines for researchers wishing to release such synthesised ALSPAC data to follow, and demonstrate how this approach can be used as an educational tool to illustrate longitudinal modelling methods.

Later eating rhythm measured in children at 7 years of age in the ALSPAC cohort

Later eating rhythm (LER) refers to later timing, greater energy intake (EI), and higher frequency of eating occasions (meal/snack) in the evening. The significance of LER in child health is becoming increasingly recognised. However, the lack of consensus regarding the definition of LER makes it challenging to fully comprehend its role. This data note describes LER variables derived in the Avon Longitudinal Study of Parents and Children (ALSPAC). ALSPAC is an ongoing birth cohort which enrolled 14,541 pregnant women living in Avon, UK, with an expected date of delivery between April 1991 and December 1992. When children were aged 7 years, parents completed a structured 3-day food diary, recording all foods/drinks consumed over 3 days (preferably 1 weekend day and 2 weekdays). Data was available for 7,285 children (50.1% response rate). A subsample of 4,869 children had exact time of eating occasions added to the existing database, which only included broad indications of eating timing based on 2-7 hour long meal slots. 13 LER variables were derived for the entire week and weekdays/weekend days separately. These comprise: 1) eating around individual bedtime (yes/no); 2) eating around average bedtime (yes/no); 3) time of evening main meal (hrs:mins); 4) time of last eating occasion (hrs:mins); 5) EI in the evening (percentage of total daily energy intake, %TDEI); 6) EI within 2hrs before bedtime (%TDEI); 7) EI for evening main meal (%TDEI); 8) EI for evening snacks (%TDEI); 9) eating over 30% of total daily energy intake after 18:00 (yes/no); 10) eating over 25% of total daily energy intake within 2hrs before bedtime (yes/no); 11) eating frequency after 17:00 (number of eating occasions); 12) regularity of dinner (number of days having dinner); 13) frequency of evening snacks (number of days having evening snacks). We describe the derivation, prevalence and inter-corelations between LER variables.

Life course plasma metabolomic signatures of genetic liability to Alzheimer’s disease

Mechanisms through which most known Alzheimer’s disease (AD) loci operate to increase AD risk remain unclear. Although Apolipoprotein E (APOE) is known to regulate lipid homeostasis, the effects of broader AD genetic liability on non-lipid metabolites remain unknown, and the earliest ages at which metabolic perturbations occur and how these change over time are yet to be elucidated. We examined the effects of AD genetic liability on the plasma metabolome across the life course. Using a reverse Mendelian randomization framework in two population-based cohorts [Avon Longitudinal Study of Parents and Children (ALSPAC, n = 5648) and UK Biobank (n ≤ 118,466)], we estimated the effects of genetic liability to AD on 229 plasma metabolites, at seven different life stages, spanning 8 to 73 years. We also compared the specific effects of APOE ε4 and APOE ε2 carriage on metabolites. In ALSPAC, AD genetic liability demonstrated the strongest positive associations with cholesterol-related traits, with similar magnitudes of association observed across all age groups including in childhood. In UK Biobank, the effect of AD liability on several lipid traits decreased with age. Fatty acid metabolites demonstrated positive associations with AD liability in both cohorts, though with smaller magnitudes than lipid traits. Sensitivity analyses indicated that observed effects are largely driven by the strongest AD instrument, APOE, with many contrasting effects observed on lipids and fatty acids for both ε4 and ε2 carriage. Our findings indicate pronounced effects of the ε4 and ε2 genetic variants on both pro- and anti-atherogenic lipid traits and sphingomyelins, which begin in childhood and either persist into later life or appear to change dynamically.

Measures of puberty in the Avon Longitudinal Study of Parents and Children (ALSPAC) offspring cohort

Background When studying the development of children through the preteen years into adolescence, it is often important to link features of their physical and mental health to the stage of puberty at the time. This is complex since individuals vary substantially in the ages at which they reach different pubertal milestones. Methods The Avon Longitudinal Study of Parents and Children (ALSPAC) is an ongoing longitudinal cohort study based in southwest England that recruited over 14000 women in pregnancy, with expected dates of delivery between April 1991 and December 1992. From 1999, information on puberty was collected using a number of different methods : (a) A series of annual questionnaires were administered when the index children were aged between eight and 17 years; these were mainly concerned with the physical changes associated with puberty; (b) identification of the age at peak height growth using the SITAR methodology; and (c) retrospective information from the girls on their age at onset of menstruation (menarche). Results The advantages and disadvantages of each method are discussed. Conclusions The data are available for analysis by interested researchers.

Genetic influences on sibling bullying and mental health difficulties.

Sibling bullying is associated with mental health difficulties; both in the short and long term. It is commonly assumed that sibling bullying leads to mental health difficulties but additional explanations for the relationship between the two are seldom investigated. To address this gap in knowledge, we used a genetically sensitive design with data from the Avon Longitudinal Study of Parents and Children (maximum N = 3,959, 53% female). At ages 11-13 years, individuals self-reported their involvement in sibling bullying, as a victim and perpetrator, and parents reported on their child's mental health difficulties. Polygenic scores, indices of genetic risk for psychiatric disorders (major depressive disorder and attention deficit hyperactivity disorder) were computed using children's genetic data. Regression and structural equation models were fitted to the data. Sibling bullying, victimisation and perpetration, and polygenic scores both predicted mental health difficulties in an additive manner but there was no interaction between them. Polygenic scores for mental health difficulties were also associated with sibling bullying. These findings suggest that sibling bullying, victimisation and perpetration, is associated with mental health difficulties, even after accounting for some genetic effects. Additionally, the relationship between sibling bullying and mental health difficulties may be, at least partly, due to shared genetic aetiology. One possibility is that genetic risk for mental health difficulties influences the onset of mental health difficulties which in turn make children more susceptible to sibling bullying.

Inflammation proteomics datasets in the ALSPAC cohort

Proteomics is the identification, detection and quantification of proteins within a biological sample. The complete set of proteins expressed by an organism is known as the proteome. The availability of new high-throughput proteomic technologies, such as Olink Proteomic Proximity Extension Assay (PEA) technology has enabled detailed investigation of the circulating proteome in large-scale epidemiological studies. In particular, the Olink® Target 96 inflammatory panel allows the measurement of 92 circulating inflammatory proteins. The Avon Longitudinal Study of Parents and Children (ALSPAC) is a prospective population-based cohort study which recruited pregnant women in 1991-1992 and has followed these women, their partners, and their offspring ever since. In this data note, we describe the newly-released proteomic data available in ALSPAC. Ninety-two proteins were analysed in 9000 blood plasma samples using the Olink® Target 96 inflammatory panel. Samples were derived from 2968 fasted mothers (mean age 47.5; Focus on Mothers 1 (FOM1)), 3005 non-fasted offspring at age 9 (Focus@9) and 3027 fasted offspring at age 24 (Focus@24). Post sample filtering, 1834 offspring have data at both timepoints and 1119 of those have data from their mother available. We performed quality control analyses using a standardised data processing workflow (metaboprep) to produce a filtered dataset of 8983 samples for researchers to use in future analyses. Initial validation analyses indicate that IL-6 measured using the Olink® Target 96 inflammatory panel is highly correlated with IL-6 previously measured by clinical chemistry (Pearson’s correlation = 0.77) and we are able to reproduce the reported positive correlation between body mass index (BMI) and IL-6. The pre-processing and validation analyses indicate a rich proteomic dataset to further characterise the role of inflammation in health and disease.

Child hyperactivity, mother-child negativity, and sibling dyad negativity: A transactional family systems approach.

Attention-deficit/hyperactivity disorder (ADHD) is among the most common mental disorders in children and adolescents. While most studies in this field have focused on the genetic and neurobiological underpinnings of the disorder, research focusing on the family environment as a critical context contributing toward the manifestation and maintenance of child ADHD symptoms is still less extensive. Therefore, the aim of this study was to examine longitudinal and bidirectional associations between child hyperactivity, mother-child negativity, and sibling dyad negativity. Data were analyzed of up to 4,429 children from the Avon Longitudinal Study of Parents and Children, a nationally representative prospective birth cohort study in the United Kingdom, at three time points (T1-T3, children aged 4, 7, and 8 years). At baseline (T1, n = 4,063), the child sample (98.8% White ethnic background) composed of 51.6% males. Child hyperactivity symptoms, mother-child negativity, and sibling dyad negativity were examined based on maternal reports. The random intercepts cross-lagged panel model was adopted to parcel out between-family differences from within-family fluctuations and test bidirectional associations. On the between-family level, families with higher child hyperactivity reported higher mother-child and sibling dyad negativity. On the within-family level, unidirectional spillover processes between sibling dyad negativity and mother-child negativity as well as between mother-child negativity and child hyperactivity emerged. Future work in the area of child hyperactivity should implement a transactional family systems approach incorporating both parent-child and sibling subsystems. Interventions to reduce negative interactions between parents and hyperactive children may offer promising improvements in child symptoms and thus alleviate family burden. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Maternal religiosity and adolescent mental health: A UK prospective cohort study

BackgroundPrevious research has examined associations between parental religiosity and offspring mental health, but findings are inconsistent, and few studies have focused on late adolescence when mental health problems are more common. This study examines the prospective relationship between maternal religiosity and offspring mental health in late adolescence. MethodsWe used data from the Avon Longitudinal Study of Parents and Children to examine the prospective association between latent classes of maternal religiosity (Highly Religious, Moderately Religious, Agnostic, Atheist) and self-reported mental health problems including common mental disorders, ICD 10 depression, depressive symptoms, generalised anxiety symptoms, self-harm acts, self-harm thoughts, and disordered eating outcomes at age 17–18 years (n = 7714). We used multivariable logistic regression analysis adjusted for maternal mental health, maternal adverse childhood experiences, and socioeconomic variables. ResultsCompared with adolescent offspring of parents in the Agnostic class, offspring of the Atheist class had increased odds of depressive symptoms ((1.31[1.03,1.67]) and offspring of the Highly Religious class had increased odds of self-harm thoughts (1.43[1.04,1.97]). There was also weak evidence (95 % confidence intervals crossed the null) of increased odds of depression in the offspring of Moderately religious and Highly religious classes (1.26 [0.97,1.65], and 1.30 [0.99,1.70], respectively)) and self-harm acts in the offspring of the Highly religious class (1.31[0.98,1.74]). There was no evidence of associations with the disordered eating outcomes or generalised anxiety disorder symptoms. ConclusionsWe found evidence that adolescents whose mothers are Atheist, Moderately Religious, and Highly Religious are more likely to have depressive symptoms than those whose mothers are Agnostic. There was also evidence for an increased likelihood of self-harm (thoughts and acts) amongst adolescents of Highly Religious parents. Further research is needed to examine possible mechanisms that could explain these observed associations as well as a repetition of our analyses in a non-UK sample.

Confirmation of COVID-19 infection status and reporting of Long COVID symptoms in a population-based birth cohort: No evidence of a nocebo effect.

Some patients with COVID-19 develop symptoms after the acute infection, known as 'Long COVID'. We examined whether or not confirmation of COVID-19 infection status could act as a nocebo, using data from questionnaires distributed to the Avon Longitudinal Study of Parents and Children cohort. We examined associations between confirmation of COVID-19 infection status (confirmed by a positive test vs unconfirmed) and reporting of Long COVID symptoms. We explored the roles of sex and anxiety as potential moderators. There was no clear evidence of a strong association between confirmation of COVID-19 infection status and the Long COVID composite score, physical or psychological symptoms or duration of symptoms. There was no clear evidence of moderation by sex or anxiety. We therefore found no evidence of a nocebo effect. Our data suggest that this psychological mechanism does not play a role in the medical symptomatology experienced by patients with Long COVID.

Hypertensive disorders of pregnancy and midlife maternal cognition in a prospective cohort study.

Hypertensive disorders of pregnancy (HDP) are associated with an increased risk of cardiovascular disorders, with recent evidence linking pre-eclampsia with vascular dementia. We examined associations of HDP with cognitive performance measured in midlife, in a prospective cohort study, the Avon Longitudinal Study of Parents and Children. Six cognitive function domains were measured 20 years after pregnancy at a mean age of 51 years. The cognition tests were repeated at clinics in the following two years. Cognitive function domains measured were immediate and delayed verbal episodic memory, working memory, processing speed, verbal intelligence, and verbal fluency. Exposures were pre-eclampsia, gestational hypertension (GH), and a combined category of any HDP, all compared to normotensive pregnancy. Of 3393 pregnancies included in the analysis, GH was experienced by 417 (12.3%) and pre-eclampsia by 57 (1.7%). GH was associated with lower verbal episodic memory, in the delayed logic memory test (-0.16 SDs; 95% CI -0.30, -0.03; p=.015) and there was weak evidence of an association with the immediate logic memory test (-0.13 SDs; -0.27, 0.001; p=.058). However, we did not see steeper declines by age for women with GH and there was no evidence of associations with other cognitive domains or for pre-eclampsia with any domains. Results were not substantially changed after controlling for midlife blood pressure. Our findings suggest that a history of GH is associated with slightly reduced episodic memory 20 years after pregnancy, but we found no evidence of a quicker age-related decline compared to women with normotensive pregnancies.

Maternal Pregnancy and Pre-Pregnancy Weight and Behavioural Outcomes in Children.

Reported associations of pre-pregnancy weight and/or gestational weight gain with offspring behavioural outcomes are inconsistent. Using data from the Avon Longitudinal Study of Parents and Children (ALSPAC), this study aimed to examine these associations at five developmental stages between the ages of 3 and 16. Over 6800 mother-offspring pairs at age 3 and 3925 pairs at age 16 were included. Pre-pregnancy underweight was associated with a 22% increased risk of total behavioural difficulties (OR = 1.22, 95% CI 1.02-1.45). In separate analyses using the SDQ subscales, pre-pregnancy underweight was linked to a 37% (OR = 1.37, 95% CI 1.14-1.65) and 33% (OR = 1.33, 95% CI 1.01-1.76) increased risk of emotional symptoms and prosocial behaviour problems over time, respectively. While pre-pregnancy overweight was associated with an 11% (OR = 1.11, 95% CI 1.03-1.20) and 18% (OR = 1.18, 95% CI 1.03-1.36) increased risk of conduct and peer relationship problems, respectively, pregnancy obesity was associated with a 43% increased risk of emotional problems (OR = 1.43, 95% CI 1.16-1.77). We found no evidence of associations between gestational weight gain and child behaviour except for a reduced risk in prosocial behaviour problems (OR = 0.82, 95% CI 0.70-0.96). Our findings provide insights into the link between preconception BMI and child behaviour, underscoring the necessity for further research to validate these associations and elucidate underlying mechanisms.

Associations of childhood diet quality scores with arterial stiffness and carotid artery intima-media thickness in adolescence/early adulthood: findings from the ALSPAC cohort.

This study examined the relationship between childhood diet quality and arterial stiffness and thickness during adolescence/early adulthood. Participants were from the Avon Longitudinal Study of Parents and Children (ALSPAC) with dietary data at ages 7, 10 and 13 years and pulse wave velocity (PWV) and carotid intima-media thickness (cIMT) at ages 17 and/or 24 years. Diet quality (DQ) was assessed using five scores: a children's Mediterranean-style diet (C-rMED) Z-score, a children's Dietary Inflammatory Z-score (C-DIS), a DASH diet Z-score, a children's Eatwell Guide (C-EWG) Z-score reflecting UK dietary guidelines and a data-driven obesogenic Z-score. Adjusted regression models examined the associations between DQ scores at 7-13 years and PWV and cIMT at 17 and 24 years. In adjusted models, a high v. low Obesogenic Z-score at 7 and 10 years was associated with higher PWV at 17: β 0.07 (95 % CI 0.01, 0.13) and β 0.10 (95 % CI 0.04, 0.16), respectively. A high v. low C-rMED Z-score at 7 years was associated with lower PWV at 17 (β -0.07; 95 % CI -0.14, -0.01). A high (more anti-inflammatory) vs low C-DIS Z-score at 10 years was associated with a lower PWV at 17 years: β -0.06 (95 % CI -0.12, -0.01). No other associations were observed. In conclusion, an Obesogenic dietary pattern in childhood (7-10 years) was related to increased arterial stiffness, while Mediterranean-style and anti-inflammatory diets were related to decreased arterial stiffness in adolescence. This highlights the importance of establishing healthy dietary habits early in life to protect against vascular damage.

Exploring the associations between adverse childhood experiences (ACEs) and adolescent cancer risk behaviours in the ALSPAC cohort

BackgroundSome modifiable risk factors for cancer originate during adolescence. While there is evidence indicating relationships between adverse childhood experiences and health risk behaviours generally, little is known about how childhood adversity influences the engagement of adolescents in cancer risk behaviours. This study aimed to determine the relationship between adverse childhood experiences and adolescent cancer risk behaviours.MethodsData were collected prospectively from birth to age 18 years on children born to mothers enrolled into the Avon Longitudinal Study of Parents and Children (ALSPAC) cohort study. Multivariable linear regression models assessed relationships of a composite exposure measure comprised of adverse childhood experiences (total number of childhood adversities experienced from early infancy until age 9 years) with multiple cancer risk behaviours. The latter was expressed as a single continuous score for tobacco smoking, alcohol consumption, obesity, unsafe sex, and physical inactivity, at ages 11, 14, 16 and 18 years. Analysis was carried out on the complete case and imputation samples of 1,368 and 7,358 participants respectively.ResultsAll adolescent cancer risk behaviours increased in prevalence as the adolescents grew older, except for obesity. Each additional adverse childhood experience was associated with a 0.25 unit increase in adolescent cancer risk behaviour (95% CI 0.16–0.34; p < 0.001). Individually, parental substance misuse (β 0.64, 95% CI 0.25–1.03, p < 0.001) and parental separation (β 0.56, 95% CI 0.27–0.86, p < 0.001) demonstrated the strongest evidence of association with engagement in adolescent cancer risk behaviour.ConclusionChildhood adversity was associated with a greater degree of engagement in adolescent cancer risk behaviours. This finding demonstrates the need for targeted primary and secondary prevention interventions that reduce engagement across multiple cancer risk behaviours for children and adolescents who have experienced adversity in childhood, such as parental substance misuse and separation, and reduce exposure to adversity.

DEXA-based Fat Mass with the Risk of Worsening Insulin Resistance in Adolescents: A 9-Year Temporal and Mediation Study.

Surrogate measures of childhood and adolescent obesity have impaired the understanding of body composition's relationship with insulin resistance in the young population. We aim to examine the longitudinal associations of directly measured total fat mass, trunk fat mass, and lean mass with the risk of hyperglycaemia, hyperinsulinemia, and insulin resistance from ages 15-24 years, the mediation path through which lipids and inflammation influence insulin resistance and whether increased fat mass temporally precede insulin resistance. We studied 3160 adolescents from the Avon Longitudinal Study of Parents and Children (ALSPAC), UK birth cohort, who had complete dual-energy Xray absorptiometry measure and fasting blood samples at age 15 years and repeated measures at ages 17- and 24-years clinic visit. Fasting glucose >6.1 mmol/L, insulin >11.78 mU/L, and homeostatic model assessment for insulin resistance (HOMA-IR) ≥75th percentile were categorized as hyperglycaemia, hyperinsulinemia, and high insulin resistance, respectively. Longitudinal associations were examined with generalized logit-mixed effect models, whilst mediation and temporal path analyses were examined using structural equation models, adjusting for cardiometabolic and other lifestyle factors. Among 3160 participants (51% female), fat mass and lean mass increased linearly in both males and females while glucose, insulin, and HOMA-IR had a U-shaped course from age 15 through 24 years. After full adjustment, each 1 kg cumulative increase in total fat mass [odds ratio 1.12 (95% confidence interval 1.11-1.13)] and trunk fat mass [1.21 (1.19-1.23)] from ages 15 through 24 years were associated with a progressively worsening risk of high insulin resistance as well as hyperglycaemia and hyperinsulinemia. The association of increased total fat mass with increased insulin resistance was partly mediated by triglycerides (9% mediation). In the temporal path analysis, higher total fat mass at age 15 years was associated with higher insulin resistance at 17 years, but not vice versa. Higher total fat mass at 17 years was bi-directionally associated with higher insulin resistance at 24 years. Mid-adolescence may be an optimal time for interrupting the worsening fat mass-insulin resistance pathologic cycle and attenuating the risk of progressively worsening metabolic dysfunction before young adulthood.

Parental and child genetic burden of glycaemic dysregulation and early-life cognitive development: an Asian and European prospective cohort study

Insulin resistance and glucose metabolism have been associated with neurodevelopmental disorders. However, in the metabolically more susceptible Asian populations, it is not clear whether the genetic burden of glycaemic dysregulation influences early-life neurodevelopment. In a multi-ethnic Asian prospective cohort study in Singapore (Growing Up in Singapore Towards healthy Outcomes (GUSTO)), we constructed child and parental polygenic risk scores (PRS) for glycaemic dysregulation based on the largest genome-wide association studies of type 2 diabetes and fasting glucose among Asians. We found that child PRS for HOMA-IR was associated with a lower perceptual reasoning score at ~7 years (β = −0. 141, p-value = 0.024, 95% CI −0. 264 to −0. 018) and a lower WIAT-III mean score at ~9 years (β = −0.222, p-value = 0.001, 95% CI −0.357 to −0.087). This association were consistent in direction among boys and girls. These inverse associations were not influenced by parental PRS and were likely mediated via insulin resistance rather than mediators such as birth weight and childhood body mass index. Higher paternal PRS for HOMA-IR was suggestively associated with lower child perceptual reasoning at ~7 years (β = −0.172, p-value = 0.002, 95% CI −0.280 to −0.064). Replication analysis in a European cohort, the Avon Longitudinal Study of Parents and Children (ALSPAC) birth cohort, showed that higher child PRS for fasting glucose was associated with lower verbal IQ score while higher maternal PRS for insulin resistance was associated with lower performance IQ score in their children at ~8.5 years. In summary, our findings suggest that higher child PRS for HOMA-IR was associated with lower cognitive scores in both Asian and European replication cohorts. Differential findings between cohorts may be attributed to genetic and environmental factors. Further investigation of the functions of the genetic structure and ancestry-specific PRS and a more comprehensive investigation of behavioural mediators may help to understand these findings better.

The dietary approaches to stop hypertension (DASH) dietary pattern in childhood in relation to cardiometabolic risk in adolescence and early adulthood in the ALSPAC birth cohort.

To investigate the relationship between the dietary approaches to stop hypertension (DASH)-style dietary patterns in childhood and cardiometabolic risk (CMR) in adolescence/early adulthood. Data were obtained from the Avon Longitudinal Study of Parents and Children (ALSPAC) prospective cohort. Diet diary data collected at 7, 10 and 13 years were used to calculate DASH-style diet scores (DDS). Multivariable linear regression models were used to investigate the associations between the DDS at 7, 10 and 13 years and CMR scores, calculated at 17 and 24 years. The ALSPAC cohort included children born in south-west England in 1991-1992. Children with complete dietary, covariate and cardiometabolic data at 17 (n 1,526) and 24 years (n 1,524). A higher DDS at 7 and 10 years was negatively associated with CMR scores at 17 years (β = -0·64 (95 % CI -1·27, -0·006), Ptrend=0·027 for fifth v. first DDS quintile at 7 years; β = -0·73 (95 % CI -1·35, -0·12) and Ptrend=0·037 for fifth v. first DDS quintile at 10 years) and at 24 years (β = -0·92 (95 % CI -1·49, -0·34) Ptrend = 0·001 for fifth v. first DDS quintile at 7 years; β = -0·60 (95 % CI -1·20, -0·05) Ptrend = 0·092 for fifth v. first DDS quintile at 10 years). No associations were found between the DDS at 13 years and CMR score at 17 and 24 years. Greater adherence with a DASH-style diet during childhood was associated with better cardiometabolic health in adolescence/adulthood in the ALSPAC cohort. The components of the DASH diet could be recommended to improve children's cardiometabolic health.