Proposal summaries
B913 - Modelling the effects of residential mobility on children and young people - 23/11/2009
(No proposal received).
B914 - To determine if the omega-3 intake and blood status at various stages influence the adolescents drinking - 21/11/2009
This proposal builds on studies already completed or ongoing within ALSPAC regarding essential fatty acid status and behavioural outcomes during development. Several levels of data predict that greater omega-3 fatty acid intake and greater serum status will be beneficial in protecting individuals from developing substance misuse disorders, in particular alcohol misuse. We have reported that deficient omega-3 intake during pregnancy increases risk for low verbal IQ, suboptimal motor development and suboptimal social interactions. These parameters have been described as early markers of an adverse developmental trajectory.
In addition, a phenotype characterized by a low level of response to first exposures to alcohol has been well characterized in the ALSPAC cohort by Marc Schuckit and shown to be predictive of alcohol misuse at age 15. A plausible biological mechanism partially underlying this phenotype is hyper activity of the endocannabinoid system because it is associated with increased tolerance to alcohol and lower levels of response in both animal models and pilot clinical studies. Endocannabinoids are produced from phosholipid precursors in membranes and are comprised of arachidonic acid, an omega-6 essential fatty acid. We have demonstrated in animal studies that dietary depletion of omega-3 fatty acids causes reciprocal replacement with omega-6 fatty acids in phospholipids which, in turn, causes 2-3 fold greater endocannabinoid activity in liver and brain.
Aims: Determine if essential fatty status of RBC's during pregnancy, or in umbilical serum, or in 7 or 13 year old serum samples predict parameters of alcohol use or pheonotypic response to alcohol, throughout development.
Long chain essential fatty acid status is determined by a combination of direct dietary intakes and genetic variation in the FADS 1-2 gene complex, which enzymes that desaturate short chain precursors to long chain polyunsaturates. Thus, these determinants of serum essential fatty acid composition will be examined as predictive determinants of the parameters of alcohol use and response. These genetic variants are currently being examined as determinants of serum and maternal RBC fatty acid composition. Potential confounders including parameters of social, educational, smoking and nutritional status will be examined.
All data are or will be available, with the exception of fatty acid levels at age 13.We assume plasma will be available at this stage and a request has gone to the SR.If approved, the plasma will be assayed for fatty acid composition using the automated robotic high-throughput methodology established by the Section of Nutritional Neurosciences, NIAAA. NIH for the n = 4,090 umbilical cord and n = 6,500 7 year old serum samples.Validation of a method of high-throughput quantitative analysis of endocannabinoids in 250 ul of plasma is currently underdevelopment in this laboratory.If validated, endocannabinoid measures, in addition to the fatty acid compositional measures will be added to the rich ALSPAC database.
B915 - Data cleaning of diet diaries at 10 13 years - 18/11/2009
(No proposal received).
B907 - The relationship between insulin levels and skeletal development in ALSPAC - 16/11/2009
Background
Based on the positive association which we previously found between total body fat mass and bone mass as measured in ALSPAC children at age 10, we postulated that fat mass exerts a positive influence on bone mass accrual in childhood (1). A subsequent mendelian randomisation study in which genetic markers of obesity were used as instrumental variables supported a causal relationship between fat mass and bone mass accrual (2). In a recent study where we examined the relationship between fat mass and cortical bone geometry by pQCT, higher fat mass was associated with a greater overall cross section of bone, but reduced expansion of the inner surface, of which the latter effect was particularly marked in females (A Sayers et al, submitted for publication).
The biological pathways by which fat mass stimulates bone mass accrual in childhood are currently unclear, but may involve factors related to insulin resistance (3). For example, adiponectin is thought to be inversely related to insulin resistance, fat mass and BMD. However, in a recent study based on ALSPAC, whereas adiponectin was inversely related to a range of measures of skeletal development, this association only explained a relatively small proportion of the relationship between fat mass and bone development (A Sayers et al, submitted for publication). In terms of alternative pathways by which fat mass stimulates bone mass accrual in childhood, the insulin/IGF1 axis is another good candidate. IGF1 is known to increase overall bone cross section by stimulating periosteal bone growth in animal models (4). We also previously observed a positive relationship between IGF-1 and BMD measures at age 10 in the children in focus subgroup (J Tobias unpublished observations).
Aims and methods
We aim to establish whether insulin levels, as measured in children at age 16 (TF3) are related to bone mass accrual and cortical geometry as assessed at the same age. If a positive association is observed as expected, we will go on to determine whether this relationship helps to explain associations between the same skeletal parameters and fat mass and adiponectin as previously described. Insulin levels at age 16 will be analysed in relation to bone mass as measured by total body DXA scans at the same age, as will related factors such as fasting blood sugar and lipid levels measured at the same time. We will analyse relationships between total body less head bone mineral content, bone area, bone mineral density and bone mineral content adjusted for bone area. We will also investigate associations with indices of cortical geometry derived from pQCT scans of the mid tibia. Assuming positive associations are observed, we will then examine whether associations between fat mass and bone mass can be explained by those with insulin, by comparing fat-bone mass associations with or without adjustment for insulin. Equivalent analyses will be performed for adiponectin, with the exception that for these analyses, adiponectin levels will consist of those measured at age 10.
B906 - Prevalence course and age of onset of anxiety disorders in longitudinal samples - 16/11/2009
The project follows on from a systematic review of published longitudinal data appertaining to the prevalence, course and onset of anxiety disorders in childhood and adolescence submitted as part of a doctoral thesis to the University of Manchester (Gallagher, 2008). From the limited published data in the field this review concluded that it was likely that many adult anxiety disorders had their onset in childhood and adolescence, and that childhood anxiety was as prevalent as anxiety disorders in adulthood, yet receives only a small proportion of the research attention, despite a lack of specific developmentally appropriate treatment models. Due to the scarcity of published data on diagnosed anxiety disorders in these populations, these conclusions could not be sufficiently substantiated.
The current project has secured access to large longitudinal data sets from Germany and the US that have not yet been fully analysed in terms of prevalence, course and age at onset of anxiety disorders. Once these datasets are fully analysed then this data will be used in a metaanalysis to determine at what age onset of each anxiety disorder is most likely, whether early onset confers greater risk for later disorders, and in samples which have data into adulthood what proportion of adults had their first onset in childhood or adolescence.
The data requested from ALSPAC would therefore include diagnostic status according to the DAWBA at age 7, 10 and 13(14). These data would be analysed to generate prevalence rates, new onset and continuity of disorders across the three follow ups. The combination of mother and child response (if available) will be dictated in part by the methods used in existing data sets as this will then be compared to data from two published data sets and the two data sets that we have analysed. This information will also be statistically combined in order to generate mean prevalence and median age at onset for anxiety disorders across the samples. As the ALSPAC data is currently collected into adolescence it would not be suitable for inclusion in the final metaanalysis examining age at onset of adult disorders. However, this data will add to the current proposal in two major areas. 1) Longitudinal data from Britain was not previously included due to a lack of published data and ALSPAC data will give insight into patterns of the development of anxiety in a British population. 2) Only one of the other studies included has collected data before the age of 11, the inclusion of prevalenc data for seven year olds will add to the understanding of the course from childhood into adolescence.
B908 - Genetics of Osteoarthritis - ARCOGEN study - 15/11/2009
Osteoarthritis is the most common form of arthritis and has a huge clinical and economic impact. The disease has a complex aetiology but genetic factors play an important role in pathogenesis. Identification of the loci that predispose to OA susceptibility will lead to a much better understanding of the cause of the disease as well as identifying new molecular targets for therapeutic intervention. Alleles that predispose to OA could also be used, in individual cases, to determine prognosis and the response to surgical or drug treatments.
We have undertaken a genome-wide association study for OA susceptibility alleles in a large collaborative study of 8000 OA cases involving 5 UK centres using Illumina's 610K array. Analysis of the first 4000 cases was performed using publically available common control sets from circa 5000 UK individuals from the 1958 British Birth Cohort (58BC), the UK Blood Service collection of the Wellcome Trust Case Control Consortium and the TwinsUK. In the second stage of the study we need additional UK controls preferably analysed using the same platform. We have obtained permission to use non overlapping sets of 58BC (2500 samples) typed by the T1D Geneetic Consortium and TwinsUK (2000 samples). To further increase the control sample we seak permission to include the genotypic data of the 3000 ALSPAC samples profiled with the 317K and 660K arrays at the Sanger Institute. The genotypic data are available at the Sanger Institute and therefore there is no need to resend. Analyses may require to correct for height and weight and therefore we are requesting this data for the oldest available age. Genotypic data will be used as common controls in the main discovery GWA analysis as well as part of further meta-analyses of other OA scans.
We would like to request
Sex Child
Body weight Child Clinic latest age
Height Child '' latest age
Genotypes (317K or 660K array) Child ''
B905 - CORNET a consortium to identify genes influencing variation in plasma cortisol - 15/11/2009
Variations in morning plasma cortisol are associated with quantitative traits including blood pressure and glucose, serum lipid profile, mood and memory. Morning plasma cortisol is a heritable trait but little is known of the genes that contribute. To identify such genes we have undertaken cortisol measurements and genome wide association studies (GWAS) in ~3000 participants from 3 cohorts. Initial results are promising, identifying two loci in which the top hit SNPs are associated with cortisol to pless than 10-8. We have therefore established the CORtisol NETwork (CORNET) in order to: (i) extend GWAS with morning cortisol to n=10,000; (ii) genotype top hit SNPs in at least two replication cohorts, in which additional measurements of dynamic control of cortisol are available; and (iii) resequence loci around top hits to identify rarer variants contributing to cortisol variation. The results will provide novel insights into pathways leading to cardiometabolic and neuropsychiatric disease.
B904 - The effects of common genetic variation in the thyroid hormone pathway on growth and development - 07/11/2009
We intend to analyse the genotypes TSH-R, PDE8B and DIO1 and their phenotypic effects on bone and neurological and emotional development in the entire ALSPAC cohort, as genotype data are already available from previous work on childhood growth. We will also use GWA data to assess the phenotypic effects of other SNPs known to be reasonable thyroid related candidates, but which do not satisfy strict thresholds for "genomewide significance".
B902 - Mechanisms linking early nutrition growth and ageingthe role of DNA methylation LINKED TO B0903 and 0921 - 04/11/2009
The influence of early nutrition and growth on ageing processes and the role of DNA methylation in mediating this will be explored by integrating transcriptomic and epigenomic profiling of a rodent model and two human cohorts. Information arising from these analyses will be replicated in several human cohorts of different age strata inclduing ALPSAC.
As outlined above, quantitative DNA methylation analysis will be undertaken on one or more platforms. DNA quantity and volme will therefore need to be stipulated when the platform is confirmed but will be in line with requirements already familiar to the ALSPAC lab team as the platforms are those used for MRC CAiTE pilot epigenetics work. Assays will be multiplxed where possible and DNA used for multiple assays from the same bisulphite conversion where ever possible.
The possible range of phenotypic data required is outlined above and will be specified once the discovery phase of the proposed project has been completed and any associations between DNA methylation and phenotypic traits have been confirmed in the discovery cohorts.
Exposure data requested will include birth weight, growth during infancy (conditional weight; birth to 3 months, 6 months and 12 months) .
Data requested may include existing DNA methylation information held by ALSPAC at the time the project comes online, including that generated by CAiTE epigenetics pilot work or proposed human methylation 27K array analysis.
B899 - Developmental origins of bone phenotypes - 02/11/2009
There is increasing evidence for a developmental origin of bone mass and skeletal development. Peak bone mass, together with later life bone mass loss, is a major determinant of osteoporosis risk in later life.(1) Lower birth weight and earlier gestational age are associated with reduced bone mineral density (BMD) and bone mineral content (BMC) in infancy, childhood and adulthood and with adult fracture risk in a number of studies.(2-5) These findings have led to the exploration for modifiable pre-natal risk factors that affect later bone health.
Maternal pregnancy diet/nutrition and offspring bone health
Variation in maternal vitamin D during pregnancy has been positively associated with offspring total and spinal BMC and with total BMD in a small study (N=198) from the Southampton Women's Survey.(6) In ALSPAC (N=6995) maternal UVB exposure in pregnancy (used as proxy for vitamin D level (7)) is related to bone size at mean age 9.9 years independently of height and lean mass.(8) We will further explore maternal vitamin D in pregnancy with offspring bone phenotypes as agreed with ALSPAC exec. as part of the MRC Vitamin D grant (DAL PI) and so this is not discussed further in this application.
Whilst other constituents of maternal diet/nutrition (other than vitamin D) have been implicated in offspring bone health, a detailed analysis in ALSPAC suggested that variation in folate intake during pregnancy was the only important predictor of future offspring BMC after adjustment for child size and other potential convariables.(9) In a separare ALSPAC publication the child's own C667T MTHFR genotype was found to be associated with spinal BMD at mean age 9.9 years, with each additional T allele of that variant being associated with a 0.10SD decrease in spinal BMD on average (but with no association to total body bone phenotypes).(10) There was some evidence in that study that this association was considerably weakened in children whose mother's diet during pregnancy, and whose own diet in childhood was high in vitamin B, suggesting that high levels of homocysteine adversely affect accrual of trabecuar bone.
Maternal smoking in pregnancy
In the Southamton Women's Survey (N=145 and in later study = 841) maternal smoking in pregnancy was associated with decreased whole body BMC at birth,(11,12) and in the Tasmanian Infant Health Survey (N=330) maternal smoking in pregnancy was associated with reduced size adjusted bone mass at the lumbar spine and femoral neck (but not whole body) at mean age 8 years in children who were born at term.(13) The association of maternal smoking in pregnancy with offspring bone phenotypes has not been examined in detail in the ALSPAC cohort, to our knowledge, though in one publication concerned with diet and bone phenotypes it was noted (but results not presented) that maternal smoking was not associated with DXA determined bone phenotypes at age 9.9 years.(9) Any association of maternal pregnancy smoking with offspring bone phenotypes might be due to intrauterine mechanisms or might be due to the association of maternal smoking in pregnancy with other lifestyle characteristics, that are shared by the offspring (including earlier initiation of smoking) that affect bone development (though for associations with bone phenotype at birth this is unlikely). One way of exploring this that has been used in ALSPAC with other offspring outcomes is to compare the association of maternal smoking in pregnancy with offspring bone phenotype to that of paternal smoking in pregnancy to bone phenotype; a stronger maternal association would be expected if intrauterine mechanisms are important.
Maternal adiposity and weight gain in pregnancy
In the Southampton Women's Survey (N=841) independent predictors of whole body bone area and BMD included maternal own birthweight, height and triceps skinfold thicknes in pregancy.(12) One conclusion of this study was that offspring of women with greater fat stores in pregnancy had better bone development and greater BMC at birth. They speculated that maternal fat stores might influence intrauterine bone mineral acrual through several mechanisms including effects on nutrient availability and endocrine factors such as leptin and oestrogen. The latter would be influenced in pregnancy by both maternal adiposity pre-pregnancy and greater acquisition of fat during pregnancy. This potential advantage of greater maternal fat stores in pregnancy requires further exploration since other studies suggest that greater maternal adiposity in pregnancy might be detremental to offspring future cardiovascular and metabolic risk.(13) As with other phenotypes comparing maternal pre-pregnancy adiposity associations to those of paternal prepregnancy adiposity associations can help to distinguish intrauterine mechanisms from shared familial genetic and lifestyle characteristics.
Given that much of the work to date on potential modifiable pre-natal influences on offspring bone phenotypes has come from the Southampton Women's Survey with a relatively small sample size and with general non-specificity (variation in associations with different bone phenotypes) there is a need for further exploration of this area. This is particulalry important with respect to maternal adiposity and fat stores in pregnancy where associations with potential advantages for bone health may be in the opposite direction to those for cardiovascular health.
Objectives
1. To examine the association of maternal smoking in pregnancy with offspring bone phenotypes and compare these associations with equivalent associations for paternal smoking in pregancy
2. To examine the association of maternal pre-pregnancy BMI with offspring bone phenotypes and compare these associations with equivalent associations for paternal prepregancy BMI
3. To examine the associations of maternal gestational weight gain with offspring bone phenotype
Methods
All applicants will contribute to the analysis protocol. DAL will compile a dataset. CM will complete analyses with supervision from DAL. All applicants will contribute to interpretation of results and writing of papers.
References
1. Hernande CJ, et al. Osteoporosis Int 2003;14:843-847
2. Jones G, Dwyer T. Calcif Tissue Int 2000;67:304-308
3. Yarbrough DE, et al. Osteoporosi Int 2000;11:626-630
4. Dennison EM, et al. Pediatric Research 2005;57:582-86
5. Cooper C, et al. Osteoporosis Int 2001;12:623-629
6. Javaid MK, et al. Lancet 2006;367:36-43
7. Sayers A, et al. IJE; 2009 doi:10.1093/ije/dyp237
8. Sayers A & Tobias JH. J Clin Endocrinol Metab 2009;94:765-771
9. Tobias JH, et al. Osteoporos Int 2005;16:1731-1741
10. Steer CD, et al. J Bone & Mineral Res 2009;24:117-124
11. Godfrey K, et al. J Bone & Mineral Res 2001;9:1694-1703
12. Harvey K, et al. J Developmental Origins of Health & Disease 2009, in press
13. Jones G, et al. J Bone & Mineral Res 1999;14:146-151
14. Viswanthan M et al. Evidence Report/Technology Assessment No. 168. AHRQ Publication No. 08-E009 ed. Rockville, MD: Agency for Healthcare Research and Quality, 2008.
B916 - 10000 UK genome sequences accessing the role of rare genetic variants in health disease - 01/11/2009
The 10,000 UK Genome Sequence project is an expansion on the GWAS (common gene variant) studies that we have already performed on our twin cohort. Our primary objective is to investigate in a systematic genome-wide fashion the contribution of low frequency and rare genetic variants to medical traits, based on genome-scale sequencing of phenotyped samples. We will study multiple groups of related phenotypes so as to explore rare variants in different types of disease process, and add exomes from extreme sample sets to increase power and compare clinical extreme to population cohort designs. The sequence data set we generate will provide a public genotype resource an order of magnitude deeper than available currently that will empower future human genetic research in the UK and beyond.
We do not plan to do provide the twins with the results of their genetic data, which is in keeping with the procedures we have maintained in our previous genetic projects.
B900 - Increasing the breadth of understanding about the factors that affect pupil attainment - 30/10/2009
DCSF has exploited the National Pupil Database to investigate the kinds of things that are related to pupils' attainment. The PLASC variables have allowed the department to disentangle the effects of, say, ethnicity, gender and SEN status. However, the range of data available for use in this way is rather narrow, and the same kind of information is generally available every year. With only NPD available, it was not possible to examine the effects of other factors about which information is not collected, or to assess the extent to which the effects of the NPD variables appear inflated due to the lack of this other information. Further, there is still a large unexplained variation at pupil level which it is presumed must be partly due to those variables we don't have information for.
Schools Analysis and Research Division has formed a new team which has among its responsibilities the task of investigating other data sources which can broaden the Department's understanding of what affects attainment. This team has done some work using other longitudinal data sources where factors such as parental education, material deprivation and family composition have been unpicked in terms of their influence on raw GCSE scores and also on progression from Key Stage 2 to Key Stage 4. It has also been possible to look at how important each of these factors is in terms of explaining gaps in attainment and progression between certain groups of pupils. For example, by combining the effects of different levels of aspirations with the prevalence of each level amongst both Free School Meal pupils and their counterparts, it is possible to attribute some of the FSM gap to aspirations. Doing the same for other factors allows comparison of the relative sizes of the contributions to the gaps.
Given that ALSPAC has also been matched into NPD, it offers two key things that the other data sources have not been able to provide, and which would enable similar work to be carried out and provide answers to similar questions. First, there is a wide range of other data collected, such as birth weights, handedness and child development scores. These would allow us to look at the relative importance of these factors in explaining gaps in attainment and progression alongside the other family and school factors available on NPD. Second, the young people involved in ALSPAC have had information collected about them from before birth, and should all have completed Key Stage Four. This gives a huge depth of information about the individuals as well as breadth. It would enable analysis of the factors that contribute to earlier attainment than has been looked at so far, Key Stage Two results, and allow greater likelihood of attributing causality, as it will allow factors from an earlier age to be taken into account.
Indeed, analysis could look separately at attainment at Key Stage Two, attainment at Key Stage Four and progression between the two, using data collected at ages appropriate for each part. Results from this work would be used to inform policy development inEngland, particularly on narrowing the attainment gap between disadvantaged children and others. Analysis would be carried out internally by government statisticians using the GSS code of practice. Results may be published as departmental research reports, possibly alongside similar analysis from other sample data sources.
B898 - Replication study A common variant on chromosome 11q13 is associated with atopic dermatitis - 26/10/2009
Common variant (rs7927894) has a reasonably strong effect on atopic dermatitis [1]. We propose two
analyses: 1) to look at the association of this genetic variant with atopic dermatitis in ALSPAC and 2) to look at the association of this genetic variant with asthma, given the effect of filaggrin on asthma.
References
[1] Gordillo et al. A common variant on chromosome 11q13 is associated with atopic dermatitis Nat Genet. 2009 May;41(5):596-601.
B897 - Family and social influences on the development of sexual behaviour in childhood and adolescence - 26/10/2009
Romantic and sexual relationships that begin at a relatively young age are associated with an increased risk of maladaptive outcomes [1] and an adverse influence on relationship skills and sexual functioning in later life [2]. In the UK, teenage girls are at high risk of acquiring sexually transmitted infections with various pathological outcomes. More than one in four young adults in the UK now report sexual activity before their 16th birthday [3] with a mean age of sexual debut of 14 years for both boys and girls [4]. In Wales, boys and girls report a mean age of debut of 12 and 13 years respectively [5].
An "integrative model" of predictors of initiation of sexual activity in adolescence concluded that a variety of factors predicted and influenced intention to initiate sexual activity [6]. These included parental involvement in the child's life, supervision and the quality of the parent-child relationship, perceived peer norms and parental attitudes towards sex. Adolescents who experience efficient and effective parental monitoring are less likely to be involved in early sexual activity than those exposed to authoritarian or permissive monitoring [1]. There is also an association between deviant peer relationships and risky sexual activity [2] and there is evidence that risky behaviours cluster together so that individuals develop "health-compromising lifestyles" [3]. Biological factors are also associated with sexual activity with an association betweeen early puberty and early sexual debut [4] and this has been linked to family structure and the presence or otherwise of the father [5]. Adolescents whose families are in lower socio-economic groups are at increased risk of risky sexual behaviour, teenage pregnancy and also sexually transmitted infections[6, 7] However, much of the research from which these conclusions were drawn was undertaken with convenience samples and high risk or clinical groups rather than national cohorts and recommendations have been made for more research using large representative cohorts in order to improve the generalisability of results.
The aim of this study is to examine the relationship between family and social relationships in late childhood and adolescence and both early or otherwise risky sexual activity for both girls and boys in a British population birth cohort.
Methods
Study population
The Avon Longitudinal Study of Parents and Children (ALSPAC: see www.alspac.bris.ac.uk) is a population-based study which has been described in detail elsewhere (Golding, Pembrey, & Jones, 2001). All pregnant women living in one of three Bristol-based health districts (EDD April 1991 - December 1992) were invited to take part in the study; 14,541 mothers enrolled and 13,988 infants were still alive at their first birthday.
Measurement of romantic and sexual behaviour
Romantic and sexual behaviour in the ALSPAC chort has been measured since age 11 using an adapted version of the Adolescent Sexual Activity Index [8]. This measure is administered via a computer assisted interview and asks whether romantic or sexual behaviour has been experienced, whether it was with a same- or opposite sex partner and whether drugs and / or alcohol had been used prior to the event. Each question also includes several items which are designed to assess sexual competence as described by Wellings, 2001 [9] including perceived regret and contraceptive use.
Measurement of parent-child and peer relationships
Parent-child relationships have been measured in a variety of ways across the whole span of the ALSPAC study. Some of these items (measured from infancy onwards through early and middle childhood) fit with concepts of parenting and parent-child relationship which are discussed in the literature eg measures of warmth and support, control and rejection [10] whereas others measure active aspects of the parent-child relationship such separation anxiety (infancy and childhood) and parental monitoring measured from 12 years onwards [11]. Aspects of the parent-child relationship were observed by a third-party during the completion of an interactive task between parent and child using the etch-a-sketch task at 10 and 12 years.
Potential confounders
Family and parent measures: Child age was recorded at the 9-year clinic and mother's age at the birth of the study child has also been recorded. Mother's education level was recorded in the 32-week ante-natal questionnaire and was categorised into none / Certificate of Secondary Education (CSE - a national school exam taken at 16 years), vocational, O level (a national school exam taken at 16 years but higher than CSE), A level (a national school exam taken at 18 years) or degree. Both the mother's occupation and that of her partner were also recorded at this time and these data were used to allocate the family to a social class group (classes I to V with class III split into non-manual and manual) using the 1991 Office for Population Cencuses and Surveys classification. Questions about the early sexual experience of each parent were asked in the 18- and 32-week antenatal questionnaire (mother) and in the 8-month questionnaire (father) and questions about parents' perceptions of their own childhood and the bond they shared with their own parents were asked ante-natally and at 33 months. Items about the quality of the marital relationship including the bond between parents as well as previous marriages and aggression within the relationship have been asked regularly since recrutiment into the cohort together with items about spiritual outlook and religious affiliation. Depression and anxiety have been measured regularly across the life of the cohort using both the Edinburgh post-natal depression scale and the Crown-Crisp Experiential Index. Parental locus of control was also asked at 12 years.
Child behaviour: Measures of child behaviour include the revised Rutter Behaviour Scale [12], the SDQ [13] and the DAWBA [14] - each is measured at least twice giving a choice of measures of social, behavioural and emotional development over time. The Moods and Feelings questionnaire [15] has also been adminsitered regularly from 7 years onwards. Life events have also been measured in data from the study child from 18 months onwards [16] and risky health behaviours including alcohol, tobacco and illicit substance use have been measured from 3 years onwards; anti-social behaviour was first measured at 8 years. Sensation seeking behaviour [17] has also been measured from 11 years onwards.
Biological measures: measures of puberty (Tanner staging) have been measured regularly from 97 months onwards.
Analyses
The opportunity to use data from the ALSPAC cohort to examine the influence of family and social relationships on romantic and sexual activity in adolescence means that both descriptive and inferential analyses can be undertaken to both provide an overview of relationships between all of these factors but we will also be able to start to examine causal relationships - the availability of prospective family data from infancy means that regressional analyses and structural equation modelling can be employed to determine both risk and adaptive factors which influence the development of sexual behaviour in late childhood and adolescence.
References
[1] Rai AA, Stanton B, Wu Y, Li XM, Galbraith J, Cottrell L, et al. Relative influences of perceived parental monitoring and perceived peer involvement on adolescent risk behaviors: An analysis of six cross-sectional data sets. Journal of Adolescent Health. 2003;33:108-18.
[2] Ary DV, Duncan TE, Duncan SC, Hops H. Adolescent problem behaviour: the influence of parents and peers. Behaviour Research and Therapy. 1999;37:217-30.
[3] Jessor R. New Perspectives on Adolescent Risk Behvaiour. Cambridge: Cambridge University Press 1998.
[4] Brooks-Gunn J, Furstenberg Jr FF. Adolescent sexual behaviour. American Psychologist. 1989;44(2):249-57.
[5] O'Connor TG, Dunn J, Jenkins JM, Pickering K, Rasbash J. Family settings and children's adjustment: differential adjustment within and across families. British Journal of Psychiatry. 2001;179:110-5.
[6] Kotchick BA, Shaffer A, Forehand R. Adolescent sexual risk behavior: a multi-system perspective. Clinical Psychology Review. 2001;21(4):493-519.
[7] Teenage Pregnancy. Report. London: Social Exclusion Unit; 1999 June. Report No.: Cm 4342.
[8] Hansen WB, Paskett ED, Carter LJ. The adolescent sexual activity index (ASAI): a standardised strategy for measuring interpersonal heterosexual behaviours among youth. Health Education Research. 1999;14(4):485-90.
[9] Wellings K, Nanchahal K, Macdowall W, McManus S, Erens B, Mercer CH, et al. Sexual behaviour in Britain: Early heterosexual experience. Lancet (North American Edition). 2001;358(9296):1843-50.
[10] Repetti RL, Taylor SE, Seeman TE. Risky families: family social environments and the mental and physical health of offspring. Psychological Bulletin. 2002;128(2):330-66.
[11] Stattin H, Kerr M. Parental monitoring: A reinterpretation. Child Development. 2000 Jun-Aug;71(4):13.
[12] Elander J, Rutter M. Use and development of the Rutter parent's and teachers's scales. International Journal of Methods in Psychiatric Research. 1996;6:63-78.
[13] Goodman R. Psychometric properties of the Strengths and Difficulties Questionnaire. Journal of the American Academy of Child Psychiatry. 2001;40(11):1337-45.
[14] Goodman R, Ford T, Richards H, Gatward R, Meltzer H. The Development and Well-being Assessment: description and initial validation of an integrated assessment of child and adolescent psychopathology. Journal of Child Psychology & Psychiatry. 2000;41:645-55.
[15] Angold A, Costello AJ, Messer SC, Pickles A, Winder F, Silver D. The development of a short questionnaire for use in epidemiological studies of depression in children and adolescents. International Journal of Methods in Psychiatric Research. 1995;5:1-12.
[16] Coddington RD. The significance of life events as etiologic factors in the diseases of children. Journal of Psychosomatic Research. 1972;16:7-18.
[17] Arnett J. Sensation seeking: a new conceptualisation and a new scale. Personality and Individual Differences. 1994;16(2):289-96.
B896 - Associations between the parent-child relationship and the health related outcomes for children - 26/10/2009
Various aspects of the relationship between parent and child influence the child's social and emotional development [1, 2] and there is increasing evidence that specific aspects of the parent-child relationship are also associated with general physical health both in childhood and in adulthood with more negative relationships being associated with poorer general health outcomes [3-6]. Relationships between parenting and more specific conditions such as obesity and oral health are also reported. An increased risk of obesity has been shown to be associated with parenting styles which might be considered authoritarian ie low warmth and high control or "demandingness" [7, 8] and there is some emerging work on similar associations between parenting and oral health in childhood [9-11]. There is also evidence parenting is socially patterned and that parenting changes over time as a function of changes in sociodemographic factors eg changes in the mother's health, the availability of social support and also (to a lesser extent) changes in financial circumstance; deterioration in these sociodemographic factors is associated with a reduced (less warm and supportive) parenting score over time whereas improvements in maternal health specifically are associated with an increased (more warm and supportive) parenting score. These changing relationships may in part explain some of the social patterning which can be observed in inequalities in child health.
Parent-child relationships have been classified and measured in a variety of ways but key aspects which are proving to be robust are the mother's (or main carer's) sensitivity towards and attunement to the needs of the child [12], different parenting styles [13], discipline [14] and also specific aspects of the parent-child relationship such as maternal warmth and support and hostility towards / rejection of the child [15]. As well as the provision of sustenance and stimulation, children also need their parents or carers to provide support, structure and supervision if they are to develop optimally [16]. Research has shown that parent-child relationships which are warm and supportive are associated with positive child social, emotional and physical outcomes [15, 16] whereas cold, neglecting relationships between parent and child increase the risk of problematic outcomes [3].
The aim of this proposal is to examine aspects of the parent-child relationship which have been measured over time in the ALSPAC cohort and to investigate their associations with and ability to predict child health outcomes both generally [6] and with regard to specific outcomes such as obesity and oral health. We are also interested to determine further the role of sociodemographic factors on parenting and child health outcomes. In particular we plan to investigate whether the warmth, support and control between parent and child are associated with specific conditions such as obesity and oral health but we would also like to investigate whether we can replicate a study undertaken on the NICHD Study of Early Child Care to determine the extent to which parenting mediates the detectable effects of socioeconomic risk on health in childhood [4].
Methods
Study Population: The Avon Longitudinal Study of Parents and Children (ALSPAC: see www.alspac.bris.ac.uk) cohort is ideally placed to investigate these relationships as it has various measures of child health and also measures of the parent-child relationship and associated socio-demographic factors over time. ALSPAC is a population-based study which has been described in detail elsewhere ([17].
Measures of Health: Measures of health include maternal assessment of the child's general health (annually), number of physical symptoms in the last 12 months (annually) and also more specific measures such as DXA estimates of fat and muscle which are available at several timepoints between 9 and 17 years years. Oral health is measured via maternal report throughout childhood with questions on brushing teeth, visits to the dentist etc and via child report at 8 and 10 years. Actual observations of child dentition are also available for a subsample of the cohort in early childhood and a questionnaire about oral health is currently being administered to the cohort (age 17). Measures of the parent-child relationship include measures of attachment which have been collected between 18 months and 6 years, measures of warmth and support as well as of control, hostility and resentment (available in early childhood at eight and 33 months) and also measures of physical discipline (shouting, smacking etc) which have been collected regularly between 18 months and 6 years.
Potential confounders: A report by Waylen and Stewart-Brown [18] has shown that the sociodemographic factors associated with parenting include maternal age and education level, maternal physical and mental health (measured annually), social support and financial circumstance. Variables such as the presence of the mother's romantic partner (measured at each time point) and also ethnic group should also be accounted for.
Other possible confounders include child gender, age and birth weight / length and also gestational age; a second measure of infant weight and length collected at eight months in order to develop a measure of early rapid weight gain (models of growth have also been developed using study data); food frequency questionnaires at various ages, dietary intake of different food types including sweets and chocolate measured from 6 months onwards by maternal report and also child self-report at 10 years and diet diaries completed at 7, 10 and 13 years; the mother's occupation and that of her partner, maternal height and pre-pregnancy (used to calculate maternal BMI), maternal tobacco use both during and after pregnancy; the amount of time the child spends watching TV / playing outside or with other children (from early childhood onwards).
References
[1] Maccoby EE, Martin JA, Hetherington EM. Socialization in the context of the family: parent-child interaction. In: Anonymous, ed. Mussen Manual of Child Psychology. New York: Wiley 1983:1--102.
[2] Patterson G, DeBaryshe B, al e. A developmental perspective on antisocial behaviour. American Journal of Psychology. 1989;44:329-35.
[3] Repetti RL, Taylor SE, Seeman TE. Risky families: family social environments and the mental and physical health of offspring. Psychological Bulletin. 2002;128(2):330-66.
[4] Belsky J, Bell B, Bradley RH, Stallard N, Stewart-Brown SL. Socioeconomic risk, parenting during the preschool years and child health age 6 years. Eur J Public Health. 2007 January 12, 2007:ckl261.
[5] Stewart-Brown S, Fletcher L, Wadsworth MEJ. Parent-child relationships and health problems in adulthood in three UK national birth cohorts. European Journal of Public Health. 2005;15(6):640-6.
[6] Waylen A, Stallard N, Stewart-Brown S. Parenting and health in mid-childhood: a longitudinal study. Eur J Public Health. 2008;18(3):300-5.
[7] Rhee KE, Lumeng JC, Appugliese DP, Kaciroti N, Bradley RH. Parenting styles and overweight status in first grade. Pediatrics. 2006;117(6):2047-54.
[8] Ambrosini G, Oddy W, Robinson M, O'Sullivan T, Hands B, de Klerk N, et al. Adolescent dietary patterns are associated with lifestyle and family psycho-social factors. Public Health Nutrition. 2009;12(10):1807-15.
[9] Law CS. The impact of changing parenting styles on the advancement of pediatric oral health. J Calif Dent Assoc. 2007;35(3):192-7.
[10] Amin M, Harrison R. Understanding parents' oral health behaviors for their young children. Qualitative Health Research. 2008;19(1):116-27.
[11] Astrom A. Parental influences on adolescents' oral health behavior: two year follow-up of the Norwegian Longitudinal Health Behavior Study participants. European Journal of Dental Sciences. 1998;106:922-30.
[12] Ainsworth MDS, Bell SM, Stayton DJ, Schaffer H. Individual differences in strange-situation behaviour of one-year olds. In: Anonymous, ed. The origins of human social relations. New York: Academic Press 1971.
[13] Baumrind D. Current patterns of parental authority. Developmental Psychology. 1971;4(2):1-103.
[14] Gershoff ET. Corporal punishment by parents and associated child behaviors and experiences: A meta-analytic and theoretical review. Psychological Bulletin. 2002 Jul;128(4):539-79.
[15] Barber BK, Stolz HE, Olsen JA. Parental support, psychological control and behavioural control: assessing relevance across time, culture and method. Report. Oxford, UK: Society for Research in Child Development; 2005.
[16] Bradley R, Caldwell BM. Caregiving and the regulation of child growth and development: describing proximal aspects of the caregiving system. Developmental Review. 1995;15:38-85.
[17] Golding J, Pembrey M, Jones R. ALSPAC--the Avon Longitudinal Study of Parents and Children. I. Study methodology. Paediatr Perinat Epidemiol. 2001;15(1):74-87.
[18] Waylen A, Stewart-Brown S. Parenting in ordinary families: diversity, complexity and change. York: Joseph Rowntree Foundation; 2008.
B895 - Is there a relationship between the movies people watch and their involvement in risky or delinquent behaviour - 26/10/2009
One of the ways in which children learn is by modelling the behaviour of others [1]. While there is an abundance of research examining the influence of family and friends on behaviour, there is increasing evidence that exposure to risky or delinquent behaviour in the media (via video games, television programmes, films and music) is associated with increased risky and delinquent behaviours such as early sexual activity, substance use, aggressive behaviour, suicide, unhealthy eating habits and poor school performance in childhood and adolescence [2]. Given that exposure to television and movies is ubiquitous, it is important to examine associations such as these within longitudinal, prospective cohorts in order to determine exactly what the relationships are.
Research has shown that exposure to depictions of alcohol use and cigarette smoking in movies is associated with actual alcohol and tobacco use [3-5] and there is also evidence that exposure to violence in the media predicts violence and general aggression [6] and results in desensitization to real life violence [7]. Exposure to violence in the media has been reported to explain around 10% of the variance in real-life violence [2]. There is also evidence that exposure to "sexy" media is associated with precocious sexual activity in adolescence and increased likelihood of teenage pregnancy [8, 9]. However, other risk factors are also associated with delinquent behaviour in childhood and adolescence (apart from exposure to violence) including reduced academic ability and achievement, psychopathic tendencies and psychopathology / emotional disorder [6].
Unfortunately the majority of research to date has been carried out in North America which limits the generalisability of the conclusions. The aim of this proposal therefore is to examine the relationships between media exposure and a range of risky and delinquent behaviours in a UK cohort while controlling for a range of for individual, family and enviromental variables which may confound these relationships. In so doing we will compliment the work which has already been undertaken by Professor Jim Sargent from the USA.
Methods
Study Population: The Avon Longitudinal Study of Parents and Children (ALSPAC: see www.alspac.bris.ac.uk) is a population-based study which has been described in detail elsewhere (Golding, Pembrey, & Jones, 2001). All pregnant women living in one of three Bristol-based health districts in the United Kingdom (EDD April 1991 - December 1992) were invited to take part in the study; in total 14,541 mothers enrolled and 13,988 infants were still alive at their first birthday.
Measures
Media exposure: items about television and movie exposure have been asked at various stages throughout the duration of the cohort. In childhood and early adolescence, time spent watching television and attempts to model oneself on characters (height, weight, hair colour etc) from television have been administered and in the 15+ clinic adolescents were asked which movies they had seen from a list which had been coded for risky / delinquent behaviours.
Risky / delinquent behaviours
Items asking study participants about tobacco, alcohol and substance use have been administered repeatedly since late childhood / early adolescence as have items about romantic and sexual behaviours. Although there appear to be no items relating to exposure to violence per se, questionnaires about anti-social behaviour and being the victim / perpetrator of bullying have also been asked on a regular basis. Items about eating patterns were asked in the 16+ child completed questionnaire.
Potential confounders
The comprehensive nature of the ALSPAC cohort means that a variety of potentially confounding factors are available for use in the analyses. Variables measured repeatedly over late childhood and adolescence which comprise individual characteristics include the age and sex of the young person, their academic ability, measures of affect (Moods and Feelings questionnaire) and psychopathology (DAWBA). Family variables include family type and structure, family adversity, parental involvement in anti-social or delinquent behaviours / dealings with the police and environmental or contextual variables include feelings of security in the neighbourhood (14 years) and also questions about peer relationships asked at various times throughout late childhood / adolescence.
Analysis
The opportunity to use data from the ALSPAC cohort to examine relationships between media exposure (movie and TV viewing ) and risky / delinquent behaviour in adolescence means that both descriptive and inferential analyses can be undertaken to both provide an overview of relationships between these factors and will also provide an opportunity to begin to examine causal relationships.
References
[1] Bandura A, Ross D, Ross SA. Imitation of film mediated aggressive models. Journal of Abnormal and Social Psychology. 1963;63:3-11.
[2] Strasburger VC. Children, adolescents and the media: what we know, what we don't know and what we need to find out (quickly!). Archives of Disease in Childhood. 2009;94(9):655-7.
[3] Dal Cin S, Worth K, Gerrard M, Gibbons F, Stoolmiller M, Wills T, et al. Watching and drinking: expectancies, prototypes, and friends' alcohol use mediate the effect of exposure to alcohol use in movies on adolescent drinking. Health Psychology. 2009;28(4):475-83.
[4] Tanski S, Stoolmiller M, Dal Cin S, Worth K, Gibson J, Sargent J. Movie character smoking and adolescent smoking: who matters more, good guys or bad guys? Pediatrics. 2007;124:135-43.
[5] Heatherton T, Sargent J. Does watching smoking in movies promote teenage smoking? Current Directions in Psychological Science. 2009;18(2):63-7.
[6] Boxer P, Huesmann LR, Bushman BJ, O'Brien M, Moceri D. The Role of Violent Media Preference in Cumulative Developmental Risk for Violence and General Aggression. Journal of Youth and Adolescence. 2009;38(3):417-28.
[7] Anderson CA, Carnagey NL. Causal effects of violent sports video games on aggression: Is it competitiveness or violent content? Journal of Experimental Social Psychology. 2009;45(4):731-9.
[8] Collins RL, Elliott MN, Berry SH, Kanouse DE, Hunter SB. Entertainment television as a healthy sex educator: The impact of condom-efficacy information in an episode of Friends. Pediatrics. 2003;112(5):1115-21.
[9] Chandra A, Martino SC, Collins RL, Elliott MN, Berry SH, Kanouse DE, et al. Does Watching Sex on Television Predict Teen Pregnancy? Findings From a National Longitudinal Survey of Youth. Pediatrics. 2008;122(5):1047-54.
B894 - Human Development Epigenetics and Ageing - 23/10/2009
-Mapping the epigenetic signature of nutritional state and socioeconomic positioning early in life
-Mapping the trajectories of epigenetic signatures at different time points in life and defining their association with nutrition and socioeconomic positioning at the different time points
-Mapping association between epigenetic signatures early in life and throughout life and longevity, define the functional genomic circuitries affected by epigenetic programming early in life that affect longevity.
Our understanding of the process of aging has advanced dramatically in the last decade as a result of elegant genetic work in model organisms, yeast, nematodes and mice. Although the process of aging has its unique characteristics in different branches of the phylogenic tree, common rules have emerged that could now be translated and tested in humans. One of the first principles is the inverse relationship between calorie intake and longevity in organism from different branches of the phylogenic tree. The molecular pathways mediating this involve the insulin response pathway. The second principle is the discovery of the involvement of a class of NAD dependent histone deacetylases the Sirtuins in longevity. Although these HDACs have non-histone targets as well as histone targets the involvement of an HDAC enzyme, alludes to an epigenetic pathway. Indeed elegant genetic analysis by in yeast has linked Sir2 and chromatin modification at telomeres, Sir 2 opposes replicative aging in yeast by maintaining low H4K16 acetylation at telemore elements. Interestingly the activity of Sir2 is dependent and sensitive metabolite in the cell NAD+, thus connecting this epigenetic process with cellular metabolism. The third principle is that the process of aging involves a systemic deregulation of gene expression suggesting a system wide genome wide rearrangement of control of gene expression. Aging seems to represent itself as a component of the normal trajectory of development from conception to death. Longevity is not just determined by the normal process of aging but it is mainly delineated by susceptibility to common adult onset disease such as cardiovascular, metabolic, cancer and mental and cognitive decline. These diseases involve as well system-wide changes in gene expression that affect critical gene-expression circuitries. Animal work from our lab as well as other laboratories suggests that there is an early developmental origin to late onset disease. Thus, adverse exposures early in life will be memorized and appear as adult onset disease that will affect longevity and shorten the life span. Epidemiological data in humans strongly suggests that poverty early in life as well as metabolic disruptions such as nutritional restriction during gestation as well as poverty during the perinatal period increase vulnerability to adult onset diseases including obesity, cardiovascular disease and autoimmune disease.
The critical question is mechanism: How are these early life experiences memorized in the genome so that they trigger disease during adulthood? Indeed can some be triggered by life experiences in the previous generation(s)?
B890 - The associations between early sleep patterns and later risks of Autism and ADHD - 19/10/2009
The children within ALSPAC with diagnoses of ASD and ADHD have been identified from 3 independent sources: (a) the clinical records of all children in the cohort investigated for a suspected developmental disorder by a multi-disciplinary assessment (b) the national educational database in England (PLASC) which identified all children in state schools (over 90% of children) who were needing special educational provision in 2003 and c) the Development and Well Being assessment (DAWBA), applied in the ALSPAC 9 yr research clinic. A total of 86 children were identified with ASD and 175 with ADHD by 11 years of age.
ALSPAC has repeatedly asked questions about children's sleep patterns from birth through to adolescence. A multi disciplinary ALSPAC sleep interest group (Alan Emond, Peter Fleming, Pete Blair, Esther Crawley, Raghu Lingam, Paul Gringras, Nicola Scott and John Henderson) have been overseeing the data. Now that the 16 year old data is available, the dataset is complete through childhood and can be used to answer four crucial sleep-related health questions:
1. What are 'normal' sleep patterns of children in the UK?
We will describe sleep patterns from birth to 16, using latent class analyses and trajectory modelling, and then explore the impact of factors such as co-sleeping, social adversity, parental smoking and alcohol use. This will cover areas including:
Are poor sleepers in infancy, still poor sleepers in adolescence? What impact does social adversity have on sleep patterns?
2. What is the association between short-sleepers and ADHD?
The association between decreased sleep time in infancy and later diagnoses of ADHD is unclear.(1) ALSPAC data allows us to define all the short sleepers in infancy including those that drop their daytime nap early, and then follow-up those children that eventually receive a diagnosis of ADHD. This 'chicken and egg' question could help to provide an early marker of ADHD, help understand causes of ADHD and offer a potential target for early treatment.
3. Is there an association between long-term iron stores, sleep disturbance and ADHD?
Low iron stores, as measured by peripheral ferritin levels have been associated with both restless sleep, and symptoms of ADHD.( 2) The extent of this relationship is still unknown. If it is real, then one would expect increased numbers of children with ADHD to have lower levels of ferritin. Sleep, ferritin levels and ADHD have already been measured within ALSPAC offering a chance to explore another potentially treatable cause of ADHD.
4. What is the relationship between sleep disturbance, breast-feeding and autistic spectrum disorders?
Exciting new genetic research has suggested physiological reasons why sleep problems are so much more common in children with autism than in the general population. (3) Dr Gringras has proposed that due to certain hormones related to early brain development, theoretically, it is non-breast fed infants that should be at increased risk for sleep disorders and autism. ALSPAC, through its questions on early feeding, sleep and later diagnoses of autism has already gathered the data necessary to explore this fascinating question with potentially huge public health implications.
Variables required
In addition to the sleep variables to which we already have access , we are requesting questionnaire data:
1.developmental diagnoses from the IDI database-11 yrs
2. DAWBA data- 7,10 yrs
3.SDQ data-4,6,8, 9, 11yrs
4. SCDC data- 4.5, 6.5, 7.5 yrs
5. IQ data- 8 yrs
6. lab data: ferritins from CIF- 8months,18 months
Project team
The analyses will be supervised by Prof Alan Emond and Dr Paul Gringras, supported by the ALSPAC sleep interest group.
The ALSPAC database is huge, and we a will need a considerable amount of statistical support as this will be the first time all ALSPAC sleep data will have been divided into latent classes, to track each individual child's sleep history and find common patterns. Dr Pete Blair, a senior research statistician at Bristol University, has already worked with aspects of the ALSPAC data and been part of many key publications. His familiarity with the data is a huge advantage, as is his interest in childhood sleep. Pete will be undertaking the analyses, assisted by academic F2 trainee Dr Joanna Humphries.
Whilst Prof Emond, Dr Gringras and the rest of the sleep interest group already have enough ring-fenced academic time to carry out the above work without funding, none of them have Dr Blair's statistical expertise or familiarity with the ALSPAC dataset. We are requesting funding from The Guys Hospital Charitble Trust for Dr Blair's salary for 6 months and a small 'data buddy' fee to gain access to all the cleaned ALSPAC variables required. The only non-pay resources requested are the travel costs associated with meetings of the researchers in London and Bristol. No overheads are included.
The interpretation and writing up of the results will be undertaken by the ALSPAC sleep interest group within existing academic sessions.
REFERENCES
1.Gringras P. Sleep disorders and ADHD. In Taylor, E editor. ADHD. Mackeith Press 2007
2.Konofal E, Lecendreux M, Deron J, Marchand M, Cortese S,Zaim M, Mouren MC, Arnulf I. Effects of iron supplementation on attention deficit hyperactivity disorder in children.
Pediatr Neurol 2008;38:20-26.
3.J Melke, H Goubran Botros, P Chaste, C Betancur, G Nygren, H Anckarsa , M Rastam,O Stahlberg, IC Gillberg, R Delorme, N Chabane, M-C Mouren m,Simeoni, F Fauchereau, CM Durand, F Chevalier, Drouot, C Collet,J-M Launay M Leboyer C Gillberg T Bourgeron and the PARIS study. Abnormal melatonin synthesis in autism spectrum Disorders. Molecular Psychiatry (2008) 13, 90-98
B891 - Fathers social interventions and childrens well-being - 16/10/2009
The proposed fellowship's main substantive aim is to explore the potential for social interventions with fathers to enhance the emotional well-being of children. Social interventions with fathers are developing fairly rapidly in the UK and elsewhere but the evidence base is slender. (Note that the term 'fathers' is being used here in an inclusive sense, to include social fathers and step fathers as well as biological ones). The proposed fellowship's research programme has three main research questions:
1. How do the social, attitudinal and behavioural characteristics of fathers interact with the emotional well-being of children over time? (and how can this knowledge inform interventions?)
2. What kinds of social interventions are currently being used by practitioners who see themselves as successfully engaging fathers?
3. Can social interventions with fathers improve the emotional well-being of children?
There are three proposed studies which relate to these three questions. Studies 2 and 3 focus directly on social interventions with fathers, relate to research questions 2 and 3 and do not involve ALSPAC data. Study 1 involves analysis of ALSPAC. It relates to research question 1 above and will help to set the context for research on social interventions.
Study 1 uses ALSPAC data to explore associations between children's emotional well-being and the social, behavioural and attitudinal characteristics of fathers. The study will include consideration of which characteristics of fathers are associated with increased or decreased risk of emotional distress in children and any evidence about fathers' contact with helping professionals. It will include examination of whether associations differ in sons and daughters and are independent of maternal influences. There has already been some analysis of ALSPAC data on depression in fathers and absent fathers (e.g Dunn et al, 2004; Ramchandani et al 2008). The current proposal is to examine associations between children's emotional well-being and fathers' attitudes, domestic behaviour and social support (including from professionals), since these are especially relevant to social interventions. Data analysis will involve appropriate multivariable linear and logistic regression modelling to investigate the impact of confounding on observed associations; missing data techniques will be used to assess the impact of missing data as appropriate. The intention is not to replicate the now considerable evidence about father involvement, but to inform social interventions with fathers by identifying the social circumstances and attitudinal and behavioural profiles of fathers which are associated with greater risk of emotional distress in children as well as the characteristics of fathers which seem to be protective factors over time for the maintenance of children's emotional well-being. Much of the existing evidence for a positive impact of father involvement only considers fathers as an undifferentiated category.
The proposed fellowship has been adopted as a DECIPHer study. DECIPHer is the Centre for the Development and Evaluation of Complex Interventions for Public Health Improvement, which involves Cardiff, Bristol and Swansea universities and is funded by the UK Clinical Research Collaboration.
The fellowship application can include the costs of ALSPAC data preparation.
References
Dunn J, Cheng H, O'Connor TG, Bridges L. (2004) Children's perspectives on their relationships with their nonresident fathers: influences, outcomes and implications. Journal of Child Psychology and Psychiatry, 45:553-566.
Ramchandani PG, Stein A, O`Connor TG, Heron J, Murray L, Evans J, (2008) Depression in men in the postnatal period and later child psychopathology: a population cohort study. Journal of the American Academy of Child and Adolescent Psychiatry, 47 (4): 390-8.
B888 - Re-introduction of pet ownership questions to the ALSPAC questionnaire PART OF B719 PROJECT - 12/10/2009
The beneficial effect of pet ownership on the physical, social and psychological health of people has been well documented (Friedmann, 1995; Headey, 2003; Katcher, 1981; Katcher & Friedmann, 1982; McNicholas et al., 2005). Contact with companion animals during childhood is likely to have effects on child development , and therefore ownership of pets (and the different types) is also likely to be of significance to child development.
Most studies of health benefits of pets are cross-sectional. Consequently it is difficult to determine whether these health benefits result from pet ownership or whether it is healthier people who choose to own pets. The relatively few longitudinal studies indicate the direction of causality is from pet to owner (Serpell 1991; Headey & Grabka 2007). Longitudinal national representative surveys in Germany and Australia show that pet owners make about 15% fewer annual doctor visits than non-owners (Headey & Grabka 2007). The relationship remains statistically significant after controlling for gender, age, marital status, income and other variables associated with health.
Pet ownership data was collected from the ALSPAC cohort up to age 10 years. This was using the carer questionnaire. At gestation, and 8 months, the number of cats, dogs, rabbits, rodents, birds and other pets were collected. This was then expanded to include categories fish, tortoises and turtles, and any remaining pet types as 'other pets', for the rest of the data collection. These data were collected at 21, 33, 47, 85, 97 and 122 months.
Our team at Liverpool University are currently using the ALSPAC data to explore if there is any association between pet ownership, and obesity, using measures of BMI, fatness and physical activity. This project is funded by WALTHAM(registered trademark) . The data is currently limited to up to 10 years, but it is plausible to consider that there may also be interesting effects beyond this time. In fact, the teenage years may be particularily important in relation to pet ownership, as this is a time when children become more independent and responsible, and for example may walk their dog on their own. For this reason we propose that questions on pet ownership be re-introduced to ALSPAC data collection. The data will be of use not only to researchers interested in obesity and physical activity, but those interested in the effects of the human-companion animal bond in relation to many different aspects of physical and psychological health and development.
To our knowledge, there have been no detailed longitudinal studies decribing pet ownership trends during childhood and teenage years, despite the knowledge that pets, in particular dogs, are more likely to be found in households with school age children that those without (Westgarth et.al., 2007). It is thought that pet ownership is associated with factors such as household type and socioeconomic status, and so there is high potential for confounding in studies of health-related factors. In addition, the factors associated seem to vary with specific pet type, and so the effects of, for example, cat, dog, and small animal ownership need to be investigated separately (Westgarth et.al., In Press). For these reasons it is well worth fully characterising aspects of pet ownership in childhood years using a large and detailed resource such as ALSPAC.
Our proposal to re-introduce pet ownership questions back into the ALSPAC questionnaire at 18 years can be done in a number of formats.
1) Firstly, we would like to re-introduce the basic questions relating to pet ownership, namely - Do you own a pet? And how many cats, dogs, rabbits, rodents, birds, fish, tortoises and terrapins, and other pets, do you own?
2) Because there is a data gap from age 10 to 18, we also propose attempting to inform this gap by asking children to recall whether they owned pets at age 14, and which types. We do not imagine recall bias to be a significant problem, because we imagine that people can reliably remember whether or not they owned a type of pet. They may not be able to recall 'numbers of' a particular pet as accurately though, and therefore a simple indication of pet type is probably most appropriate.
3) Because we have reliable pet ownership information up to 10 years, it would be possible to test the validity of asking respondents to recall pet ownership, by asking them what types of pet they owned up to 10 years old, and then checking this against the data already collected. Surveys of pet ownership are often cross-sectional and ask respondents to recall previous pet ownership, and so a measure of the validity of such an approach would be extremely useful in the field of Human-Animal Interaction research. It would also inform the results from 2) above.
4) The data on pet ownership in the ALSPAC resourse is limited, albeit of large numbers. This would be an opportunity to further explore particular aspects and attitudes relating to pet ownership, that may further elucidate any impact that pet ownership has on health.
In particular:
How much the child is involved in the day-to-day responsibilities and care of the pet.
For example, if they own a dog, do they walk it and how often. This can be compared with the reported frequency of activities such as walking from all children, in particular those not owning a dog.
If they own a dog, what breed, and size of dog.
Measures of attachment to the pet (measured using a published and validated pet attachment scale), as this may affect the impact of owning a pet on a particular individual.
WALTHAM(registered trademark) is a leading scientific authority in pet nutrition and well-being. For almost 50 years they have researched the nutritional and behavioural needs of companion animals and their benefits to humans. In 2008, WALTHAM(registered trademark) formed a public-private partnership with the National Institutes of Health (NIH) in the USA to encourage research in the field of HAI and to help grow the field. In particular they acknowledged the uses of birth cohort studies such as ALSPAC. Sandra McCune directs the Human-Animal Interaction research programme at the WALTHAM(registered trademark) Centre for Pet Nutrition where she manages a large portfolio of HAI research projects. WALTHAM(registered trademark) has identified the role of pets in physical activity and obesity as a research priority for the programme and are keen to support this study.
References
Friedmann, E. (1995). The role of pets in enhancing human well-being: physiological effects. In The Waltham Book of Human-Animal Interaction: Benefits and Responsibilities of Pet Ownership, pp. 33-53. Edited by I. Robinson. Oxford: Elsevier Science Ltd.
Headey, B. (2003). Pet ownership: good for health? Medical Journal Of Australia 179, 460-461.
Headey, B & Grabka, M.W. (2007) Pets and human health in Germany and Australia: National Longitudinal results. Social Indicators Research (2007) 80: 297-311.
Katcher, A. H. (1981). Interactions between people and their pets: form and function. In Interrelations between people and pets, pp. 41-67. Edited by B. Fogle. Springfield: Charles C. Thomas.
Katcher, A. H. & Friedmann, E. (1982). Potential health value of pet ownership. California Veterinarian 36, 9-13.
McNicholas, J., Gilbey, A., Rennie, A., Ahmedzai, S., Dono, J.-A. & Ormerod, E. (2005). Pet ownership and human health: a brief review of evidence and issues. BMJ 331, 1252-1254.
Serpell,J. (1991) Beneficial effects of pet ownership on some aspects of human health and behaviour Journal of the Royal Society of Medicine Volume 84 December: 717-720
Westgarth, C., Pinchbeck, G. L., Bradshaw, J. W., Dawson, S., Gaskell, R. M. & Christley, R. M. (2007). Factors associated with dog ownership and contact with dogs in a UK community. BMC Vet Res 3, 5.
Westgarth, C., Pinchbeck, G. L., Bradshaw, J. W., Dawson, S., Gaskell, R. M. & Christley, R. M. (In Press). Factors associated with cat ownership in a UK community. Vet Record.