Proposal summaries
B1357 - Association of candidate genetic regions with the participation in excessive exercise - 24/05/2012
The overall aim of the study is to characterize the development of the excessive exercise and to identify the genetic basis of this phenotype. Genetic regions have been selected on the basis of mouse genetic mapping studies revealing genetic loci for baseline physical activity levels. Specific aim 1: Validation of association between genetic candidate regions and physical activity levels. Hypothesis 1: There is a significant association between genetic variation in candidate regions and the self-reported as well as objectively measured participation in EE. Specific aim 2: Assessing the developmental trajectories of EE in females in childhood and adolescence and their relation to BMI. Hypothesis 2: Participation in EE is a phenotype developing during adolescence and associated with lowered BMI.
B1373 - Combined parental postnatal depression and its effect on children a systematic review and meta-analysis - 24/05/2012
Aims: This systematic review aims to determine the prevalence of combined parental depression during the prenatal period and first year post-partum
Published and unpublished observational studies (cohort and cross-sectional studies) were included in the investigation if they reported the prevalence of combined parental depression during pregnancy and/or the first year postpartum. Studies were considered if they were published between January 1980 and December 2011.
Parents aged 15 to 50 years old, who had a primary diagnosis of depressive disorder according to DSM or ICD criteria assessed by a clinical interview, or who scored as depressed on a validated questionnaire, during pregnancy or within 1 year of the birth of their child were included.
Outcome measures
1. Prevalence of combined parental depressive disorder according to DSM or ICD criteria
2. Prevalence of heightened risk of depression according to a validated questionnaire (e.g. Edinburgh Postnatal Depression Scale or Beck Depression Inventory) simultaneously in both parents
Potential confounding variables:
Parental age/SES/eduction, study quality/calendar year/locality, measure of depression
As for ALSPAC data specifically, I would be interested in data on the number of couples assessed prenatally (at 18 weeks gestation), and postnatally (8 weeks and 8 months postpartum) in which both the mother and her partner scored more than 12 on the Edinburgh Postnatal Depression Scale (EPDS). Also, for reference, I would like to know the total number of couples assessed at these time points and numbers of mothers and partners individually scoring greater than 12 on the EPDS.
B1372 - Can hip DXA scans be used to identify genetic determinants of hip shape and osteoarthritis - 24/05/2012
Mutations resulting in hip dysplasia represent rare but important causes of hip osteoarthritis (OA). Commoner forms of genetic variation, with more subtle effects hip shape, may also contribute to hip OA. However, though several components of hip shape are associated with hip OA, rather than a causal role, these relationships may reflect altered hip modeling secondary to OA. The present proposal is intended to identify the major common genetic determinants of hip shape, thereby enabling (i) Mendelian Randomisation studies to examine causal pathways between hip shape and OA, and, in the case of shape parameters found to play a causal role, (ii) the identification of novel genetic risk factors for OA acting through specific alterations in hip shape. Exposure Variables: GWAS data imputed to latest version of Hapmap. Further analyses may be performed in relation to rare variants from exome sequence data in those participants involved in UK10K, and to methylation data in those included in ARIES.
B1371 - The Genome-Wide Association Study of Phenotypic Robustness in Human-a Canalization Study - 24/05/2012
Aims
Human phenotypes exhibit significant levels of variation among individuals. Recently, genome-wide association studies (GWAS) have been performed to identify the genetic loci that control these variations. Despite the success of GWAS to identify a set of genetic loci, it has become widely recognized that these loci cannot fully explain the variance of a phenotype. One possible explaination is that there is phenotypic stochastic noise which has not been taken into account in the typical GWAS. Normally, only one measurement of phenotype from each individual has been used in the typical GWAS which could be considered as the average phenotype of each individual. However, if we measure one phenotype several times in one individual, we will find that in some people the phenotype is relatively stable while in other people the phenotype is relatively variable. In other words, people show different levels of phenotypic robustness (canalization). The genetic control on phenotypic robustness has been reported in plants, yeast and mice. However, there is still scarce data in human.
Hypothesis
We hypothesized that genetic components controlling phenotype robustness may exist in humans. Since typical GWAS's focus on the genetic variation impact upon average phenotypes, the findings from genetic control on phenotype stochastic noise would improve our understanding on the genotype-phenotype relationship. In TwinsUK dataset, we observed different levels of phenotypic robustness on glucose and lipids across multiple measures on each individual. In the initial GWA analysis on glucose level robustness, we found a trend of association on several genetic loci across the genome. In order to verify our finding, we will request to use the ALSPAC data to perfrom GWA on glucose level robustness. Then we will perform meta-analysis using GWAS results from TwinsUK and ALSPAC. We will carry out genome-wide meta-analysis on lipids levels as well.
Request Data
Exposure variables
The genome-wide genotypes are considered as exposure variables. Both genotyped and imputed SNPs will be used for analysis. We suggest to employ the following threshold for quality control of the SNPs:
a. Call rate greater than = 95%
b. Minor Allele Frequency greater than =1%
c. For the imputed SNPs, MACH r2greater than =3 or IMPUTE prop infogreater than =0.4
d.HWE pvalue greater than 10e-6
Outcome variables
Glucose levels and lipids levels (including HDL/LDL cholesterol, triglyceride) will be used to generate outcome variables. The individuals with greater than =2 measurements will be included in the analysis. The standard deviation of multiple measurements of phenotypic levels in each individual will be used as outcome variables. Age of phenotype collection will be included in the analysis model as covariate.
B1370 - Exploration of Special Educational Needs in Preterm Infants - 24/05/2012
Aims
To explore what the discrepancies between date of birth and expected date of birth have on neuro-cognitive outcomes in preterm infants.
Hypotheses
It is well recognised that infants born preterm, both at extreme gestations (e.g. less tah 28 weeks) but also at more modest gestations (e.g. 32-36 weeks) have worse outcomes at school age, including cognition and school performance. While direct neurological injury is an important component of this (particularly in the extremely preterm group) the process of prematurity has consequences on the measurement of these age-dependent variables and the school processes that the infants go through.
In most work cognitive and school measures are measured when the infants reach a specified age, and are rarely corrected for any prematurity. In addition infant's born preterm are more likely to enter school a year earlier than if they had been born at term with potential impacts on their ability to perform at this level.
Methodology
We will assess the relative risk, and population impact of being born at different gestational ages compared to term infants. Gestational groups are anticipated to be less than 28 weeks, 28 to 32 weeks, 33 to 36 weeks and 37 to 42 weeks. Post term (greater than 42 week infants) will not be included. Associations of these gestational groups with the presence of special educational needs and cognition will be derived and an estimate of population impact calculated. Unadjusted and adjusted results will be derived consistent with previous work.
This will be done in three ways:
1) Matching each preterm infant with a term infant born in the same month and year.
2) Matching each preterm infant with a term infant with equivalent expected date of birth (month and year)
3) Matching each preterm infant with a term infant with equivalent expected date of birth (month and year) who also entered school in the same school year.
Exposure: Gestation
Outcomes: Special Educational Needs and Cognition
Confounders: Birth condition, growth, gender, parity, maternal hypertension, maternal pyrexia, mode of delivery, maternal age, socio-economic position, educational achievement, tenure, crowding index, ethnicity, place of birth
B1369 - Multiple Risk Behaviours in Adolescence association of outcomes at age 18 and risk behaviours at age 16 - 24/05/2012
We are requesting access to the age data on these variables at age 17-19 in order to undertake initial descriptive analyses of the all of outcomes at this age, followed by more complex analyses exploring the extent to which and ways in which these outcomes are associated with clusters of risk behaviours at age 15/16 identified using latent class analysis. Adjustment for missing data will be undertaken using multiple imputation techniques. The work is being undertaken as part of the DECIPHer programme of work on multiple risk behaviours in adolescence. The work is directed by a multi disciplinary group of researchers, led by Prof Rona Campbell and Prof Matt Hickman, with involvement from Dr Ruth Kipping, Dr Jon Heron and Dr Michele Smith. Dr Michele Smith will undertake the descriptive analysis and Dr Jon Heron will undertake the latent class analysis. Michele Smith is supported by Jon Heron and hence there is no need to incur the time (and therefore costs) of a data buddy to facilitate the use of the data.
B1368 - Gender inequalities in early life health outcomes are they important and can they be modified - 24/05/2012
Aims:
This project aims to quantify gender inequalities in pre-natal and neonatal health outcomes and examine whether the maternal environment modifies the risks. Hypothesis:The maternal environment and offspring gender modify each other's influence on key early life health outcomes. Our first objective is to quantify the degree of excess risk to males across several linked outcomes in early life. By undertaking a cohesive overview of existing databases, the work will identify whether gender imbalances are increasing or static, and whether patterns are consistent across countries. Our second objective is to review systematically the extent to which published studies and datas on the primary outcomes take account of gender as a potential modifier of the effect of treatments and risk factors, and to review their statistical power to detect interactions if they exist. Our final objective is to test the hypothesis that maternal environment (smoking, race, social class, maternal age, and economic deprivation) interacts with gender in determining the degree of risk of the outcomes.
B1367 - Genetic variants influencing lean mass and the muscle-bone unit in children and adolescents - 24/05/2012
Aim: Identify genetic variants influencing lean mass and the muscle-bone unit in children and
adolescents.
Hypothesis: Genetic variants influencing lean mass will be easier to detect in children and adolescents
where the noise introduced by environmental exposures and bone loss will be less pronounced than in
adult populations. We also expect that variants with pleiotropic effects on lean mass and BMD exist
given the common mesenchimal origin and the biological cross-talk between cells from both tissues, and
hope they can be identified applying a bivariate analysis.
Exposure Variable: Genome Wide Single Nucleotide Polymorphysms
Outcome variables: Bone Mineral Density and Lean Mass for both Total Body and site specific
measurements.
Confounding variables: The linear models used in the model need to be adjusted for base line
characteristics such as: Age, Gender, Height and Weight. As well as DXA derived variables as: Fat mass,
Bone Mineral Content (BMC) and Bone Area (BA) for Total body and site-specific measurements.
B1366 - Association between pubertal development and depressive symptoms in males from late childhood to early adulthood - 24/05/2012
AIMS / HYPOTHESES:
In comparison to the substantial body of research examining the link between pubertal development and depression in girls, the relationship between puberty and depression in boys is not well documented. There is a need to expand research in this area to advance understanding of the link between aspects of male pubertal development and the emergence of depression. The current study, based on a large contemporary birth cohort, will examine the association between pubertal development and levels of depressive symptoms in boys from early adolescence childhood into early adulthood. Using separate indicators of pubertal maturation, including Tanner pubic hair and genital stage, growth of axillary hair, voice changes and increase in height, we will examine whether non-normative timing of puberty (early or late relative to peers) at age 13 years is associated with increased levels of depressive symptoms at 13 - 18 years.
B1376 - Mother-to-Child transmissibility of metabolic health gestational diabetes and epigenetic modification - 24/05/2012
The Northern Finland Birth Cohort Project (NFBC, www.kelo.oulu.fi/NFBC), Avon Longitudinal Study on Parents and Children (ALSPAC) and other projects have identified several characteristics of the foetal environment (e.g. parental stress, smoking/drinking, obesity, excessive weight gain and other complications during pregnancy) that impact on intrauterine growth, preterm birth, the hypothalamo-pituitary-adrenal (HPA) axis, neonatal health and later morbidity. In the present proposal we will focus in one of the most important complications of pregnancy, gestational diabetes mellitus (GDM), a feasible "test exposure" because of complexities and unpredictable problems in these analyses, while proposing to create a more extensive data resource for future analyses of e.g. gestational hypertensive disorders, stress, obesity and weight gain during pregnancy as a collaborative effort. Intrauterine period is highly susceptible for the impact of environment. Epigenetic changes play likely a key role also in normal development.
B1358 - Bidirectional reciprocal genome-wide Mendelian Randomization of Maternal Smoking and Conduct Disorder/ADHD - 10/05/2012
Maternal smoking has been linked to a number of poor outcomes in offspring, including conduct disorder and attention-deficit hyperactivity disorder (1). This finding has been remarkably consistent and replicated across multiple studies (2, 3). However, it is uncertain whether this association is causal, or if it is due to maternal risk factors that predispose the mother and offspring to substance abuse in addition to these disorders (2). Several studies have found that a latent variable predisposing both mother and child to externalizing is a better model for the increase in risk (4, 5), while others have found that smoking during pregnancy has a direct, independent association with both ADHD and antisocial behavior (6-8). Overall, the results imply that maternal smoking may have a direct, causal effect on ADHD, but antisocial behavior, ADHD, and substance abuse share common risk factors that may account for some of this relationship.
Conduct disorder, ADHD, and substance abuse disorders all fall into the spectrum of externalizing, an empirically derived personality factor that accounts for their genetic and phenotypic overlap (9, 10). Previous studies have implied that the molecular basis for these disorders lies in dysfunction of the dopamine system (11), finding signification associations with dopaminergic genes (12, 13). Studies have also found interaction effects between maternal smoking and dopamine genes (14, 15). Again, the link could be causal, or due to indirect overlap of genetic risk.
We intend on performing Bidirectional reciprocal Mendelian Randomization analysis using genome-wide scores to disentangle the relationship between maternal smoking and conduct disorder/ADHD. We will use genome-wide meta-analyses of smoking, conduct disorder and ADHD supplied by other groups in order to construct genome-wide scores in ALSPAC mothers (smoking) and ALSPAC children (conduct disorder, ADHD). We will then perform bidirectional reciprocal Mendelian Randomization to attempt to inform on causality between these variables.
1. Weissman, M. M., Warner, V., Wickramaratne, P. J., & Kandel, D. B. (2002). Maternal smoking during pregnancy and psychopathology in offspring followed to adulthood. Journal of American Academy of Child and Adolescent Psychiatry, 38(7), 892-899.
2. Wakschlag, L. S., Pickett, K. E., Cook, E., Benowitz, N. L., Leventhal, B. L. (2002). Maternal Smoking During Pregnancy and Severe Antisocial Behavior in Offspring: A Review. American Journal of Public Health, 92(6), 966-974.
3. Langley, K., Rice, F., van den Bree, M. B., & Thapar, A. (2005). Maternal smoking during pregnancy as an environmental risk factor for attention deficit hyperactivity disorder behaviour. A review. Minerva Pediatrica,57(6), 359-371.
4. Silberg, J. L., Parr, T., Neale, M. C., Rutter, M., Angold, A., & Eaves, L. J. (2003). Maternal Smoking During Pregnancy and Risk to Boys' Conduct Disturbance: An Examination of the Causal Hypothesis. Biological Psychiatry, 53,130-135.
5. D'Onofrio, B. M., van Hulle, C. A., Waldman, I. W., Rodgers, J. L., Harden, K. P., Rathouz, P. J., & Lahey, B. B. (2008). Smoking during pregnancy and offspring externalizing problems: An exploration of genetic and environmental confounds. Development and Psychopathology, 20, 139-164.
6. Button, T. M. M., Thapar, A., McGuffin, P. (2005). Relationship between antisocial behaviour, attention-deficit hyperactivity disorder and maternal prenatal smoking. The British Journal of Psychiatry, 187, 155-160.
7. Nigg, J. T., Breslau, N. (2007). Prenatal Smoking Exposure, Low Birth Weight, and Disruptive Disorders. Journal of the American Academy of Child and Adolescent Psychiatry, 46(3), 362-369.
8. Thapar, A., Fowler, T., Rice, F., Scourfield, J., van den Bree, M. B., Thomas, H., Harold, G., Hay, D. (2003). Maternal Smoking During Pregnancy and Attention Deficit Hyperactivity Disorder Symptoms in Offspring. American Journal of Psychiatry, 160(11), 1985-1989.
9. Krueger, R. F., Markon, K. E., Patrick, C. J., Benning, S. D., & Kramer, M. D. (2007). Linking Antisocial Behavior, Substance Use, and Personality: An Integrative Quantitative Model of the Adult Externalizing Spectrum. Journal of Abnormal Psychology, 116(4), 645-666.
10. Krueger, R. F., Hicks, B. M., Patrick, C. J., Carlson, S. R., Iacono, W. J., McGue, M. (2002). Etiologic Connections Among Substance Dependence, Antisocial Behavior, and Personality: Modeling the Externalizing Spectrum. Journal of Abnormal Psychology, 111(3), 411-424.
11. Solanto, M. V. (2002). Dopamine dysfunction in AD/HD: integrating clinical and basic neuroscience research. Behavioural Brain Research, 130(1-2), 65-71.
12. Li, D., Sham, P. C., Owen, M. J., & He, L. (2006). Meta-analysis shows significant association between dopamine system genes and attention-deficit hyperactivity disorder (ADHD). Human Molecular Genetics, 15(14), 2276-2284.
13. Comings, D. E., Gade-Andavolu, R., Gonzalez, N., Wu, S., Muhleman, D., Blake, H., Dietz, G., Saucier, G., & MacMurray, J. P. (2000). Comparison of the role of dopamine, serotonin, and noradrenaline genes in ADHD, ODD and conduct disorder: multivariate regression analysis of 20 genes. Clinical Genetics, 57(3), 178-196.
14. Neuman, R. J., Lobos, E., Reich, W., Henderson, C. A., Sun, L., Todd, R. D. (2007). Prenatal smoking exposure and dopaminergic genotypes interact to cause a severe ADHD subtype. Biological Psychiatry, 61(12), 1320-1328.
15. Kahn, R. S., Khoury, J., Nichols, W. C., Lamphear, B. P. (2003). Role of dopamine transporter genotype and maternal prenatal smoking in childhood hyperactive-impulsive, inattentive, and oppositional behaviors. The Journal of Pediatrics, 143(1), 104-110.
B1349 - Nutritional determinants of slow growth in infancy - 10/05/2012
Infants showing slow growth in infancy compared to their peers have been identified in ALSPAC and their growth followed up to 13 years of age. This work has shown that if they grew slowly between birth and 8 weeks they then grew very fast between 8 weeks and 2 years with their growth in weight outstripping their growth in height. By 13 years they were very close in weight and height to their normal growing peers. A second group who grew slowly between 8 weeks and 9 months were very slow in catching up with their normal peers and remained much lighter and shorter at 13 years.ALSPAC has collected data on feeding behaviours, difficulties and foods and drinks consumed by these children at 4 weeks, 6 months, 15 months, 2 years and so on. These include breast and formula feeding as well as age of introduction of solid foods and other drinks. There are also questions about parental feeding practices including feeding on demand or by schedule, use of food as rewards and attitudes to feeding. On a 10% subsample of the children there are detailed diet diaries at 4, 8 and 18 months these give a great deal more information about types of foods fed and timing of meals and drinks. Two investigations will be carried out one into the early slow growing group and the other into the late slow growing group using the rest of the cohort as a comparison group. The reason for the division is that we have previously shown very different recovery growth patterns in these two groups and it important to determine if nutritional or behaviour differences are determining these differences in growth trajectory.
B1348 - The contribution to Nutritional Science of the first 21 years of the ALSPAC nutrition project - 10/05/2012
A review will be carried out to assess the scope of the impact on nutritional science of the nutritional data collected in ALSPAC and the publications arising from it. It will look first at what ALSPAC shows about the impact of diet in pregnancy and early childhood, feeding practices, habits and choices on growth, obesity development, mental development and future diet. Secondly it will look at mid childhood and adolescent diet and how this may be associated with genetic make-up, infant diet and parental diet and how it relates to later outcomes such as fat and lean mass, growth trajectories and obesity development. The proposed review of this work would aim to synthesise the finding so far and identify gaps that can be filled by further interrogation of the data. It will also identify areas where other studies could fill the gaps or confirm or refute the findings. The end of the first 21 years of ALSPAC is a timely opportunity to take stock of the contribution of the ALSPAC nutrition project to knowledge about human nutrition. This review will clarify the importance of this project and identify where future research in ALSPAC should be targeted to ensure that the data already collected and any future data will be fully exploited to add to evidence-based nutrition recommendations.
B1365 - Relationship between empirically-based candidate SNPs for major neuropsychiatric disease and quantitative trait variation - 10/05/2012
Aims- This project is designed to estimate the relationship between variation in SNPs recently identified as risk factors for major neuropsychiatric diseases and cognitive/behavioral phenotypes in the general population. The SNPs requested below were identified as candidates in the Psychiatric GWAS Consortium analyses. Hypotheses- Common genetic variants that have been associated with major neuropsychiatric diseases (e.g. schizophrenia, bipolar disorder) will be associated with a continuous shift towards impairment in the distribution of cognitive and behavioral abilities in the general population. For example, variation in SNPs associated with schizophrenia will predict mean differences in IQ in the general population.
B1347 - Does high protein intake in infancy associate with rapid growth beyond infancy - 10/05/2012
The prevalence of childhood overweight and obesity is increasing around the world. Childhood obesity has been shown to be related to adult obesity and other health related problems. Studies have reported that a high intake of protein in early life is related to rapid early growth which may be a risk factor for obesity in later childhood. In ALSPAC dietary information has been collected repeatedly from a 10% sub-sample of the ALSPAC cohort (around 1000 children) at the following ages: 8 months, 1 1/2 years, 3 1/2 years, 5, 7 & 10 years. All the dietary data have been coded and prepared and are ready for use. Children will be allocated to quintiles according to their protein intake at 8 months of age in the first instant. Foods will be investigated to ascertain the sources of the protein in the diet at 8 months and the degree of tracking of protein intakes will be assessed at 1.5, 3.5, 5.0, 7.5 & 10 years. The tracking of protein intakes from one age to the next will be assessed using a multinomial logistic regression to estimate the odds ratio for being in the highest quintile for protein at the each sequential
B1363 - Meta-analysis GWAS of urticaria - 10/05/2012
The ALSPAC analysis will contribute to a large-scale GWAS meta-analysis conducted within the EAGLE cohort. A case/control status of 'Urticaria ever' will be derived using the questions listed in the table above. This derived variable will then be used to conduct a case/control genome-wide association study within ALSPAC using the imputed genome-wide SNP data of the offspring. Summary results for each SNP will transferred to the meta-analysis team in Munich. No individual level data will be transferred. The team in Munich will meta-analyse the ALSPAC data along with several other cohorts from the EAGLE consortium.
B1362 - Reciprocal genome-wide Mendelian Randomization of smoking Body Mass Index and educational attainment - 10/05/2012
The aim of the project is to inform the relationship between smoking, BMI and educational attainment using bidirectional genome-wide Mendelian Randomization.
Required ALSPAC data: All available smoking and BMI data on the mothers and the children as well as educational attainment level of mother. Genome-wide SNP data will be required to calculate genome-wide allelic scores in the mothers and offspring.
B1345 - Replication of GWAS Signals from the ACCT cohort - 10/05/2012
Project title: Replication of GWAS signals for arterial stiffness in the ALSPAC study participants.
Outline: Stiffening of the aorta is an important independent risk factor for heart attack and stroke. It is also highly heritable but the genetics is complex, and little is currently known about the molecular pathways that bring the increase in stiffness about. In a recently completed genetic study (a GWAS) of aortic stiffness in young normotensives from the Anglo-Cardiff Collaborative Trial (ACCT), a number of genetic variants associated with aortic stiffness (pless than 10-8less than 10-6).
Aim: We specifically plan to validate 45 of these genetic variants identified in our GWAS in the ALSPAC study children who have had arterial stiffness assessments made; in particular measurements taken of their aortic pulse wave velocity (aPWV) and augmentation index during the screening.
We envisage that the findings will advance our understanding of the pathophysiology of stiffness and identify new drug targets to modulate it.
B1361 - Epigenetics of pre - and post-pubertal leukocytes - 10/05/2012
Aims: Compare methylome in normal white blood cells before and after puberty.
Hypothesis: Puberty is accompanied by characteristic changes in the epigenome that mediate greater leukocyte inflammatory responses in the post-pubertal age.
Variables: Normal males and females sampled and tested for DNA methylation at pre- (e.g. ~age 7) and post- pubertal ages (e.g. ~15 +).
The question: Why do children survive when adults do not? One aspect of the puberty transition is extraordinary but neglected: pre-pubertal children show a remarkable resistance to mortality from the same severe infections, sepsis and trauma that are otherwise commonly fatal in post-pubertal individuals (adults). Studying the biology behind resistance and how it is lost in the puberty transition could provide a treasure trove of insights into basic mechanisms and new leads for drugs.
The rationale: Blood leukocytes of children consistently produce less pro-inflammatory, and more anti-inflammatory cytokines than their adult counterparts. The natural resistance of children to mortality from influenza and other infections is lost at puberty, implying a hormonally-mediated (and deleterious) 'reprogramming' of the host response. Our central hypothesis is that a specific epigenetic program in leukocytes mediates the superior resistance of children to mortality.
Analysis plan: Given the overlap with longitudinal modelling of the HM450 ARIES data set, it is proposed that data for this project will be analysed in Bristol under the supervision of Caroline Relton by a visiting researcher from HSPH.
B1360 - The relationship between parental anxiety and child anxiety A longitudinal exploration of mediators and moderators - 10/05/2012
This study has two key aims. The first is to confirm, in a large, diverse, longitudinal sample, the relationship between maternal anxiety and offspring anxiety. Second, we will explore the environmental factors that mediate (or moderate) this relationship, using a series of structural equation models. As an ancillary aim, (to be conducted as a master's degree project) we will explore positive outcomes of childhood anxiety. Hypotheses: Analysis 1: Longitudinal relationship between maternal anxiety, child anxiety, parenting and attachment. Analysis 2: Longitudinal relationship between maternal anxiety, child anxiety and temperament. Analysis 3: Early infant temperament, parental beliefs and susequent child Analysis 4: A model of child anxiety Ancillary hypothesis. There will be some positive benefit to experiencing clinical levels of anxiety. In particular, we hypothesis that highly anxious individuals will experience fewer accidents, and fewer injuries to bones and teeth.