I would be very interested to examine the association between physical activity and birth weight (continuous variable, low birth weight (less than 2500 grammes), SGA (less than the 10the percentile [the question is which standards tot use), gestational age (continuous variable), preterm birth (less than 37 weeks). Firstly, I would like to analyse the univariate association between the abovementioned factors and the aforementioned outcome measures. Secondly I would like tot do a multivariate analysis looking at physical activity and the aforementioned outcome measures, thereby adjusting for variables that emerged forom the univariate analysis as statistically significantly associated the outcome.

Obesity among American children has reached epidemic proportions. 34.8% of children in the 2003-2004 National Health and Nutrition Examination Survey (NHANES) sample were at risk for overweight (greater than 85%ile Body Mass Index, or BMI) or overweight (greater than 95%ile BMI) (37). Childhood obesity is an extremely strong predictor of adult obesity, poor cardiovascular health and a number of significant and lifelong health problems that manifest during childhood (38). Childhood obesity is thus extremely costly to society, reducing quality of life and burdening our health care system.

Though the epidemic of childhood obesity is widely recognized, the future consequences of overweight and at risk of overweight for the current generation of American children are not known. Preventing adult obesity by preventing or reversing childhood obesity may represent a major cost-effective strategy to improve present and future health in America, but no study has predicted future prevalence of obesity (and associated increases in cardiovascular and other morbidities) if additional efforts are not devoted to its prevention or reversal.

Aim 1 of this research proposal is therefore to apply data from longitudinal cohort studies on the tracking of obesity, the existing literature on the comorbidities associated with childhood obesity, and extant federal databases (NHANES, National Longitudinal Survey of Youth, Medical Expenditure Panel Survey and the National Hospital Discharge Survey) to predict the health and economic consequences of obesity in present and future cohorts of American children. Markov processes will be developed to describe each of the transitional probabilities of obesity over the lifespan, and multi-variable sensitivity analysis using Monte Carlo simulation will also be employed to develop a range that most accurately describes the possible consequences of childhood obesity.

Childhood obesity at its most basic level represents an imbalance between dietary intake and physical activity. Poor diet and physical inactivity are the leading etiologic factors of childhood obesity in America. In its report Preventing Childhood Obesity: Health in the Balance, the Institute of Medicine has identified a variety of promising approaches in childhood and adolescence to reducing morbidity of childhood obesity (39). Resources to combat childhood obesity are limited, and thus the most cost-effective interventions should be applied in order to reduce morbidity from childhood obesity, yet no study has systematically evaluated the relative cost-effectiveness of strategies to reduce morbidity from childhood obesity.

In Aim 2 of this research proposal, I will use data from the Iowa Bone Development Study to quantify the potential impact of various changes in diet and physical activity on future risk of obesity. I will then apply a decision-analytic model that compares the scenario in which no intervention is applied with the scenario in which an intervention that reduces children's television viewing, increases physical activity or improves diet is applied across the appropriate age cohort(s). The goal will be to assess the potential cost-effectiveness and cost-benefit profile of effective interventions identified by the Cochrane Group (40) that could reduce morbidity from childhood obesity by reducing children's television viewing, increasing physical activity or improving diet.

Traditional pediatric disease prevention has focused on identification of individual risk factor-disease relationships, and development of effective interventions to reduce risk. By executing the proposed research plan, I will become expert in the application of mathematical modeling and economic analysis to the design and evaluation of evidence-based interventions against obesity and other chronic childhood diseases and in the effective translation of science into evidence-based prevention.

There is currently much discussion as to whether exposure to the chemicals used in swimming pools early in a child's life is responsible for the initiation of symptoms of asthma in susceptible children. The main evidence for this comes from Belgium, and there have not been studies in Britain to our knowledge. There is some anxiety at DfES concerning the validity of these results, particularly since it is government policy that all primary school children learn to swim as part of the current curriculum.

ALSPAC did not ask about swimming directly in early parental questionnaires, but did ask about activities with the child undertaken with the mother and with the father at various time points. Reports of swimming would occur as text.

In order to assess the feasibility of undertaking a study of swimming in ALSPAC we therefore propose coding the activities undertaken with the child over time. This would allow us then to undertake power calculations to ascertain the appropriateness of carrying out a detailed analysis of the ALSPAC asthma data in this regard.

To this end we have managed to obtain a promise of £3500 - which I anticipate will cover the costs of JG coding all the activities over the pre-school and possibly the primary school period, and the computing team adding the data to the SPSS built files. The funders are the Amateur Swimming Association and the Pool Water Treatment Group, with some help possibly from DfES.'

In Western countries, there are no cohorts of childhood refraction data large enough to provide the statistical power to detect subtle genetic effects (e.g. QTL controlling less than 5% of the variation in the trait phenotype). This study will provide complementary information to a moderately sized study (1400 children) in Asia, in which refraction data has been collected, and selected SNP genotyping is planned. This work will also provide preliminary data to inform a future genomewide association studies for refractive error in this cohort.

No outline received

(No outline received).

No outline received

Background: It has been clear for some years now: overweight and obesity are a major problem for public health in developed and developing countries [WHO World Health Report 2002]. Changes in both physical activity levels and nutrition have contributed to this problem. These changes are partly due to changes in economic standards, culture and social norms, as well as to changes in our environment. Cars, computers, escalators, and remote controls have all made their entry in our lives in the past century. The discussion about whether and to what extent we can compensate and manage these changes, and what impact this would have on overweight and obesity prevalence, is ongoing. Changes in our environment have not been limited to the places where we live and work.

Because expectant mothers today are different from those who lived a century ago (for example they are generally fatter and less physically active during pregnancy [Kramer 2002]), the intrauterine environment has also changed over time. These changes in the intrauterine environment are reflected in the fact that birth weight increased between 1978-1996, with a corresponding drop in small-for-gestational age (SGA) babies and increase in large-for-gestational-age (LGA) babies [Kramer 2002].

The importance of birth weight for the development of chronic disease later in life was first recognised by Barker [1995]. His hypothesis was that SGA babies were at increased risk for cardiovascular disease later in life. Hence, the attention was at first predominantly on SGA babies. However, more recently, LGA babies have been found to be at risk as well. In addition to the fact that giving birth to an LGA baby is a risk for complications during childbirth [e.g. Oral 2001], these babies have disproportionately more fat in childhood. Hammami et al. [2001] have shown that body weight and length are the dominant predictors of body composition in LGA and appropriate-for-gestational age (AGA) neonates. They also found that LGA neonates have significantly higher proportions of total body fat and bone mineral content, but lower lean body mass as a percent of body weight. In contrast, Hediger et al. did not find a surfeit of fatness in infants born LGA within the first years after birth [Hediger 1998], but found an increase in fatness at the triceps and subscapular sites at 3 years of age [Hediger 1999]. Rogers et al. [2006] found that an increased relative weight-for-height at birth was associated with increased fat mass. Based on these findings, it seems that prevention of LGA births could be important in the prevention of overweight and obesity and related health problems later in life.

Several researchers have shown that increased maternal body mass index (BMI) is partly responsible for the rise in proportion of LGA births over time [Kramer 2002; Surkan 2004], and it is consistently related to the risk of LGA births [Orskou 2003; Schaefer- Graf 2002 & 2003]. Other lifestyle factors reducing the risk of LGA births are smoking and caffeine intake during pregnancy [Orskou 2003]. Since levels of smoking are falling in most Western countries, this may also contribute to a higher number of LGA babies [Kramer 2002].

Maternal glucose tolerance is another strong determinant of LGA birth. Women with gestational diabetes (GDM) have a strongly increased risk of giving birth to a LGA baby [Schaefer-Graf 2002 & 2003]. Not only is their risk of an LGA birth higher, the consequences of LGA are more pronounced in babies whose mothers had GDM. Evidence suggests that the increase in fat mass in LGA babies [Hediger 1998; Hammami 2001] is larger in LGA babies following GDM pregnancies, than in LGA babies whose mothers had normal glucose tolerance [Hammami 2001; Vohr 1997 & 1999]. Moreover, Vohr et al. have shown that fat mass in LGA children whose mothers had GDM was higher than in LGA babies from 'control' women, even at 7 years of age [Vohr 1999]. In addition to this increased adiposity, they also found that LGA babies of GDM mothers also had higher blood pressure and higher levels of serum glucose at 4-7 years of age. Adverse effects of LGA births also include a higher risk for the development of insulin intolerance and obesity during childhood [Strauss 1997].

In relation to maternal physical activity, Alderman et al. [1998] have shown that moderate or vigorous physical activity for two hours per week or more in any month of pregnancy is associated with decreased risk of LGA birth, but has no significant effect on risk of SGA birth or length of gestation. They postulate that this effect may be due to beneficial effects on glucose tolerance. If so, physical activity may not only reduce the risk of LGA birth, but may also reduce the associated increase in adiposity. This effect may be more pronounced in babies born to GDM mothers. However, the role of physical activity during pregnancy on fat distribution in infancy has not been studied to date. Given the strong influence of physical activity on glucose metabolism, this relationship is very plausible.

No outline received