Background: Osteoporosis is a skeletal disease associated with high morbidity, mortality and increased economic costs. Early prevention during adolescence appears to be one of the most beneficial practices. Exercise is an effective approach for developing bone mass during puberty, but some sports may have a positive or negative impact on bone mass accrual. Plyometric jump training has been suggested as a type of exercise that can augment bone, but its effects on adolescent bone mass have not been rigorously assessed. The aims of the PRO-BONE study are to: 1) longitudinally assess bone health and its metabolism in adolescents engaged in osteogenic (football), non-osteogenic (cycling and swimming) sports and in a control group, and 2) examine the effect of a 9 month plyometric jump training programme on bone related outcomes in the sport groups.
Methods/Design: This study will recruit 105 males aged 12-14 years who have participated in sport specific training for at least 3 hours per week during the last 3 years in the following sports groups: football (n=30), cycling (n=30) and swimming (n=30). An age-matched control group (n=15) that does not engage in these sports more than 3 hours per week will also be recruited. Participants will be measured on 5 occasions: 1) at baseline; 2) after 12 months of sport specific training where each sport group will be randomly allocated into two sub-groups: intervention group (sport + plyometric jump training) and sport group (sport only); 3) exactly after the 9 months of intervention; 4) 6 months following the intervention; 5) 12 months following the intervention. Body composition (dual energy X-ray absorptiometry, air displacement plethysmography and bioelectrical impedance), bone stiffness index (ultrasounds), physical activity (accelerometers), diet (24 h recall questionnaire), pubertal maturation (Tanner stage), physical fitness (cardiorespiratory and muscular) and biochemical markers of bone formation and resorption will be measured at each visit.
Discussion: the PRO-BONE study is designed to investigate the impact of osteogenic and non-osteogenic sports on bone development in adolescent males during puberty, and how a plyometric jump training programme is associated with body composition parameters.

Abstract
. Background
. International guidelines for physical activity recommend at least 150 min per week of moderate-to-vigorous physical activity (MVPA) for adults, including those with cardiac disease. There is yet to be consensus on the most appropriate way to categorise raw accelerometer data into behaviourally relevant metrics such as intensity, especially in chronic disease populations. Therefore the aim of this study was to estimate acceleration values corresponding to inactivity and MVPA during daily living activities of patients with heart failure (HF), via calibration with oxygen consumption (VO2) and to compare these values to previously published, commonly applied PA intensity thresholds which are based on healthy adults.
.
. Methods
. Twenty-two adults with HF (mean age 71 ± 14 years) undertook a range of daily living activities (including laying down, sitting, standing and walking) whilst measuring PA via wrist- and hip-worn accelerometers and VO2 via indirect calorimetry. Raw accelerometer output was used to compute PA in units of milligravity (mg). Energy expenditure across each of the activities was converted into measured METs (VO2/resting metabolic rate) and standard METs (VO2/3.5 ml/kg/min). PA energy costs were also compared with predicted METs in the compendium of physical activities. Location specific activity intensity thresholds were established via multilevel mixed effects linear regression and receiver operator characteristic curve analysis. A leave-one-out method was used to cross-validate the thresholds.
.
. Results
. Accelerometer values corresponding with intensity thresholds for inactivity (< 1.5METs) and MVPA (≥3.0METs) were > 50% lower than previously published intensity thresholds for both wrists and waist accelerometers (inactivity: 16.7 to 18.6 mg versus 45.8 mg; MVPA: 43.1 to 49.0 mg versus 93.2 to 100 mg). Measured METs were higher than both standard METs (34–35%) and predicted METs (45–105%) across all standing and walking activities.
.
. Conclusion
. HF specific accelerometer intensity thresholds for inactivity and MVPA are lower than previously published thresholds based on healthy adults, due to lower resting metabolic rate and greater energy expenditure during daily living activities for HF patients.
.
. Trial registration
. Clinical trials.gov NCT03659877, retrospectively registered on September 6th 2018.
.

OBJECTIVES: to describe differences in bone outcomes according to biological age in male athletes participating in osteogenic (OS) or non-osteogenic (NOS) sports. DESIGN: Longitudinal (12-months). METHODS: 104 adolescents (12-14years) were measured at baseline and after 1y: OS group (n=37 football or soccer players) and NOS group (n=39 swimmers, n=28 cyclists). Years from peak height velocity (PHV, -2 to +2) was used as a maturational landmark. Bone mineral content (BMC) was assessed using DXA. Hip structural analysis estimated cross-sectional area (CSA), cross-sectional moment of inertia (CSMI) and section modulus (Z) at the femoral neck (FN). Trabecular bone score (TBS) estimated lumbar spine (LS) texture. Quantitative ultrasound measured bone stiffness. Multilevel regression models adjusted by hours of training were fitted. RESULTS: Compared to NOS, OS had significantly greater total body (less head) BMC from PHV to +2years from PHV (from 9.5% to 11.3%, respectively); LS BMC from -1years from PHV to PHV (from 9.8% to 9.9%); hip BMC (from 11.6% to 22.9%), FN BMC (from 12.0% to 15.9%), TBS (from 4.2% to 4.8%) and stiffness index (from 11.9% to 23.3%) from -1years from PHV to +2years from PHV; and CSA (from 8.4% to 18.8%), Z (from 5.5% to 22.9%) and CSMI (from 10.6% to 23.3%) from -2years from PHV to +2years from PHV. There was a significant trend for the between-group differences to increase with biological age except for LS BMC and TBS. CONCLUSIONS: These findings underline the differential bone response to different sports throughout the years surrounding PHV in male adolescent athletes. CLINICAL TRIAL REGISTRATION: ISRCTN17982776.

OBJECTIVES: Research investigating the longitudinal effects of the most popular sports on bone development in adolescent males is scarce. The aim is to investigate the effect of 12-month participation in osteogenic and non-osteogenic sports on bone development. DESIGN: a 12-month study was conducted in adolescent males involved in football, swimming and cycling and compared with an active control group. METHODS: 116 adolescent males (13.1±0.1years at baseline): 37 footballers, 37 swimmers, 28 cyclists and 14 active controls were followed for 12 months. Bone mineral content (BMC) was measured by dual-energy X-ray absorptiometry, and bone stiffness was measured by quantitative ultrasound. Bone outcomes at 12 months were adjusted for baseline bone status, age, height, lean mass and moderate to vigorous physical activity. RESULTS: Footballers had higher improvement in adjusted BMC at the total body, total hip, shaft, Ward's triangle, legs and bone stiffness compared to cyclists (6.3-8.0%). Footballers had significantly higher adjusted BMC at total body, shaft and legs compared to swimmers (5.4-5.6%). There was no significant difference between swimmers and cyclists for any bone outcomes. Swimming and cycling participation resulted in non-significant lower bone development at most sites of the skeleton compared to controls (-4.3 to -0.6%). CONCLUSIONS: Football participation induces significantly greater improvements in BMC and bone stiffness over 12 months compared to cycling and swimming. CLINICAL TRIAL REGISTRATION: ISRCTN17982776.

AIM: This study investigated the associations between fitness indices and bone outcomes in young males. METHODS: Data were collected between autumn and winter 2014-2015 on 121 males with a mean age of 13.1 ± 0.1 years: 41 swimmers, 37 footballers, 29 cyclists and 14 nonathletes. Participants were recruited from athletic clubs and schools across South West England. Lean mass, areal bone mineral density and hip structural estimates were measured using dual-energy X-ray absorptiometry. The relationships between bone outcomes and the vertical jump, standing long jump and the 20-m shuttle run test were analysed using three regression models: model 1 was adjusted by age and stature, model 2 added vigorous physical activity and model 3 then added lean mass. RESULTS: the boys' performance in the vertical jump and standing long jump was positively associated with the majority of bone outcomes in models 1 and 2, but most of these disappeared in model 3. The 20-m shuttle run test was positively associated with most bone outcomes in all three models. Lean mass played a key role in the association between muscular fitness and bone outcomes. CONCLUSION: Vigorous physical activity did not explain the associations between fitness and bone outcomes, but lean mass did.

BACKGROUND: Diabetes is closely linked to obesity, and obesity rates climb during adolescence for reasons that are not clear. Energy efficiency is important to obesity, and we describe a temporary but substantial fall in absolute energy expenditure, compatible with improved energy efficiency, during the rapid growth phase of puberty. METHODS: in a longitudinal cohort study lasting 10 years, we measured voluntary energy expenditure as physical activity (PA) by accelerometry, involuntary energy expenditure as resting energy expenditure (REE) by oxygen consumption, body mass index (BMI) and body composition by dual energy X-ray absorptiometry annually on 10 occasions from 7 to 16 years in the 347 children of the EarlyBird study. We used mixed effects modelling to analyse the trends in REE and their relationship to BMI, lean mass (LM), fat mass (FM), age, PA and pubertal stage. RESULTS: Relative REE and total PA fell during puberty, as previously described, but the longitudinal data and narrow age-range of the cohort (s.d.±4m) revealed for the first time a substantial fall in absolute REE during the period of maximum growth. The fall became clearer still when adjusted for FM and LM. The fall could not be explained by fasting insulin, adiponectin, leptin, luteinising hormone or follicle stimulating hormone. CONCLUSIONS: There appears to be a temporary but substantial reduction in energy expenditure during puberty, which is unrelated to changes in body composition. If it means higher energy efficiency, the fall in REE could be advantageous in an evolutionary context to delivering the extra energy needed for pubertal growth, but unfavourable to weight gain in a contemporary environment.

Background: Mothers often do not realize when their child is overweight. We aimed to compare mothers' perceptions of children's weight before and during puberty, and to explore factors at 7 years predicting recognition of overweight at 16 years. Methods: Mothers of 237 children (136 boys) from the EarlyBird study estimated their own weight category and that of their child aged 7 years and 16 years. The children estimated their own weight category at 16 years. Annual measures: body mass index standard deviation score (BMIsds), per cent fat, physical activity. Pubertal development assessed by age at peak height velocity (APHV). Maternal measures: BMI, education, socio-economic status. Results: at 7 years 21% of girls and 16% of boys were overweight or obese, rising to 27% and 22% respectively at 16 years. The accuracy of the mother's perception of her child's weight category improved from 44% at 7 years to 74% at 16 years, but they were less able to judge overweight in sons than daughters. The mothers' level of concern about overweight was greater for girls than boys, and increased for girls (52% mothers of overweight/obese girls were worried at 7 years, 62% at 16 years), but remained static in the boys (42% vs. 39%). Over 80% of the youngsters realized when they were overweight, but 25% normal-weight girls also classed themselves as overweight. Only BMI predicted a mother's ability to correctly perceive her child's weight. Neither her awareness, nor concern, about the child's weight at 7 years had any impact on the trajectory of the child's BMI from 7 years to 16 years. Conclusions: Parents are central to any successful weight reduction programme in their children, but will not engage while they remain ignorant of the problem. Crucially, any concern mothers may have about their child's excess weight at 7 years appears to have no impact on subsequent weight change.

BACKGROUND: Mothers often do not realize when their child is overweight. We aimed to compare mothers' perceptions of children's weight before and during puberty, and to explore factors at 7 years predicting recognition of overweight at 16 years. METHODS: Mothers of 237 children (136 boys) from the EarlyBird study estimated their own weight category and that of their child aged 7 years and 16 years. The children estimated their own weight category at 16 years. Annual measures: body mass index standard deviation score (BMIsds), per cent fat, physical activity. Pubertal development assessed by age at peak height velocity (APHV). MATERNAL MEASURES: BMI, education, socio-economic status. RESULTS: at 7 years 21% of girls and 16% of boys were overweight or obese, rising to 27% and 22% respectively at 16 years. The accuracy of the mother's perception of her child's weight category improved from 44% at 7 years to 74% at 16 years, but they were less able to judge overweight in sons than daughters. The mothers' level of concern about overweight was greater for girls than boys, and increased for girls (52% mothers of overweight/obese girls were worried at 7 years, 62% at 16 years), but remained static in the boys (42% vs. 39%). Over 80% of the youngsters realized when they were overweight, but 25% normal-weight girls also classed themselves as overweight. Only BMI predicted a mother's ability to correctly perceive her child's weight. Neither her awareness, nor concern, about the child's weight at 7 years had any impact on the trajectory of the child's BMI from 7 years to 16 years. CONCLUSIONS: Parents are central to any successful weight reduction programme in their children, but will not engage while they remain ignorant of the problem. Crucially, any concern mothers may have about their child's excess weight at 7 years appears to have no impact on subsequent weight change.

INTRODUCTION: Contemporary adolescents are deemed inactive, especially girls, but whether for biological reasons associated with their maturation, changes in their behavior or because of environmental constraints, is uncertain. We examined the trends in physical activity (PA) in relation to both biological and environmental factors in an attempt to establish what drives activity patterns from childhood through adolescence. METHODS: Physical activity (7-d Actigraph accelerometry) was measured annually from 5 to 15 yr in a single cohort of some 300 UK children. Total PA (TPA; in-school and out-of-school separately and combined as whole day) and intensity-specific PA (sedentary, light, and moderate-and-vigorous [MVPA]) were analyzed. Biological age (years before/after measured peak height velocity) and pubertal stage (self-reported pubic hair development-Tanner staging) were also measured as was socioeconomic status (postcode-derived index of multiple deprivation [IMD]). RESULTS: Total PA was stable from 5 to 8 yr (trend P = 0.10) but fell progressively from 9 to 15 yr (by approximately 30% in girls and approximately 20% in boys, both P < 0.001; sex interaction, P < 0.01). Half of this fall was attributable to light intensity PA and only a quarter to MVPA. The decline in PA was related similarly to chronological and biological age, whereas pubertal stage explained the more rapid PA decline in girls (puberty-adjusted sex interaction, P = 0.51). Total PA fell to the same extent for in-school and out-of-school settings (both P < 0.001), and for lower and higher IMD areas (both P < 0.001). Total PA tracked moderately to strongly from childhood into adolescence (r = 0.58; P < 0.001). CONCLUSIONS: the adolescent decline in PA is consistent across different environmental settings, attributable to falls in light-intensity/habitual activity and influenced by puberty, suggesting that the inactivity of adolescence may, in part, be under biological control.

AIMS/HYPOTHESIS: the aim of this work was to test whether the mid-adolescent peak in insulin resistance (IR) and trends in other metabolic markers are influenced by long-term exposure to physical activity. METHODS: Physical activity (7 day ActiGraph accelerometry), HOMA-IR and other metabolic markers (glucose, fasting insulin, HbA1c, lipids and BP) were measured annually from age 9 years to 16 years in 300 children (151 boys) from the EarlyBird study in Plymouth, UK. The activity level of each child was characterised, with 95% reliability, by averaging their eight annual physical activity measures. Age-related trends in IR and metabolic health were analysed by multi-level modelling, with physical activity as the exposure measure (categorical and continuous) and body fat percentage (assessed by dual-energy X-ray absorptiometry) and pubertal status (according to age at peak height velocity and Tanner stage) as covariates. RESULTS: the peak in IR at age 12-13 years was 17% lower (p < 0.001) in the more active adolescents independently of body fat percentage and pubertal status. However, this difference diminished progressively over the next 3 years and had disappeared completely by the age of 16 years (e.g. difference was -14% at 14 years, -8% at 15 years and +1% at 16 years; 'physical activity × age(2), interaction, p < 0.01). Triacylglycerol levels in girls (-9.7%, p = 0.05) and diastolic blood pressure in boys (-1.20 mmHg, p = 0.03) tended to be lower throughout adolescence in the more active group. CONCLUSIONS/INTERPRETATION: Our finding that physical activity attenuates IR during mid-adolescence may be clinically important. It remains to be established whether the temporary attenuation in IR during this period has implications for the development of diabetes in adolescence and for future metabolic health generally.

Objective: an HbA1c threshold of ≥6.5% has recently been adopted for the diagnosis of diabetes in adults, and of ≥5.7% to identify adults at risk. Little, however, is known of HbA1c's behaviour or diagnostic value in youth. Our aim was to describe the course of HbA1c during childhood, and its association with fasting glucose. Research Design and Methods: HbA1c and glucose were measured every year in a cohort of 326 healthy children (162 boys) from 5 to 15years. Mixed effects modelling was used to establish the determinants of HbA1c and its development over time. ROC analysis was used to determine the diagnostic value of HbA1c in the 55 individuals who showed impaired fasting glucose (IFG-glucose ≥5.6mmol/L). Results: Glucose rose progressively from 4.3mmol/L at 5years to 5.1mmol/L at 15years, and although there were positive associations between HbA1c and glucose, from 10 to 13 years, HbA1c fell while glucose continued to rise. IFG developed in 55 children, but HbA1c exceeded 5.7% in only 16 of them. The maximum area under the ROC curve was 0.71 at the age of 14 (p

Lifestyle interventions to improve health in young children tend to target areas of relative deprivation, but the evidence for so doing is largely historical. Accordingly, we have re-examined the link between deprivation, obesity and metabolic risk in contemporary UK children. Using a postcode-based index of multiple deprivation (IMD), we assessed 269 children from the community-based EarlyBird Study, attending 53 schools representing a wide socio-economic range. Annual measures of fatness from 5 to 8 yr included body mass index (BMI), waist circumference (WC), and sum of five skinfolds (SSF). A metabolic risk score, based on blood pressure, lipids and insulin resistance, was derived from annual fasting blood samples. There were no significant associations between deprivation and any measure of adiposity in girls (all p > 0.37). In boys, there was a weak but consistently inverse relationship between deprivation and WC (r = -0.19, p = 0.03) and BMI (r = -0.14, p = 0.09) at 8 yr. Changes in adiposity over 3 yr were unrelated to deprivation in boys. In girls there was a slight but significant increase in SSF only (1 mm/yr per 20 IMD units, p = 0.001). Importantly, in both genders, metabolic risk score was unrelated to deprivation throughout (r values -0.05 to -0.13, all p > 0.12), as was change in metabolic risk (all p > 0.30). Our data do not support the assumption that obesity, metabolic disturbance and thus risk of type 2 diabetes are more prevalent among poorer children. In today's increasingly obesogenic environment, youngsters from all backgrounds appear to be vulnerable, with population-wide implications for public health spending, and the prevention of diabetes in contemporary youth.

The early environment, acting via epigenetic processes, is associated with differential risk of cardiometabolic disease (CMD), which can be predicted by epigenetic marks in proxy tissues. However, such measurements at time points disparate from the health outcome or the environmental exposure may be confounded by intervening stochastic and environmental variation. To address this, we analyzed DNA methylation in the peroxisome proliferator-activated receptor γ coactivator 1α promoter in blood from 40 children (20 boys) collected annually between 5 and 14 years of age by pyrosequencing. Body composition was measured annually by dual X-ray absorptiometry, physical activity by accelerometry, and pubertal timing by age at peak high velocity. The effect of methylation on transcription factor binding was investigated by electrophoretic mobility shift assays. Seven cytosine guanine dinucleotide (CpG) loci were identified that showed no significant temporal change or association with leukocyte populations. Modeling using generalized estimating equations showed that methylation of four loci predicted adiposity up to 14 years independent of sex, age, pubertal timing, and activity. Methylation of one predictive locus modified binding of the proadipogenic pre-B-cell leukemia homeobox-1/homeobox 9 complex. These findings suggest that temporally stable CpG loci measured in childhood may have utility in predicting CMD risk.

WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT: Both negative and positive associations have been reported between body fat and bone density. Extra mechanical loading from excess fat may lead to greater bone mass. Excess ectopic fat may lead to bone demineralisation through inflammatory pathways. WHAT THIS STUDY ADDS: Longitudinally collected data from narrow-angle beam densitometry gives a novel insight into bone growth through adolescence. There is no evidence of a deleterious effect of body fat on children's growing bones after adjustment for height and age. Body fat, mediated by puberty, is associated with larger bones in boys and bones that are both denser and larger in girls. OBJECTIVE: Bone growth is an important determinant of peak bone mass and fracture risk, but there is limited data on the impact of fat-on-bone development at a time when childhood obesity is reaching epidemic proportions. Accordingly, we explored the effect of body fat (BF) on bone growth over time in the context of age, pubertal tempo and gender. METHOD: a cohort of 307 children was measured biannually from 9-16 years for height and weight, and every 12 months for percent BF, bone area (BA), bone mineral content and areal bone mineral density (aBMD) by dual-energy X-ray absorptiometry. Pubertal tempo was determined quantitatively by age at peak height velocity. RESULTS: Percent BF increased and then fell in the boys, but increased throughout in the girls. aBMD and BA increased in both genders (P 

Objective: Impaired fasting glucose (IFG) is a predictor of future diabetes and is increasingly common in children, but the extent to which it results from excess insulin demand or failure of supply is unclear. Our aim was to compare the behaviour of insulin sensitivity and beta-cell function in children who developed IFG with those whose glucose levels remained within the normal range. Methods: We examined trends in fasting glucose, insulin sensitivity (HOMA-S) and beta-cell function (HOMA-B) in 327 healthy children annually from 5 to 15 yr, and the parents at baseline. Results: Fifty-five children showed IFG, mostly after age 11 yr. Fasting glucose rose progressively and was higher throughout in those who developed IFG compared with those who did not (p < 0.001). Beta-cell function was lower from the age of 5 yr in those who developed IFG (p = 0.006), but there was no difference in BMI (p = 0.71). A difference in insulin sensitivity was revealed on adjustment for covariates (p = 0.03). Glucose was higher (p < 0.001), beta-cell function lower (p = 0.01), and insulin sensitivity the same (p = 0.86) in the mothers of children who showed IFG, compared with those who did not. Conclusions: IFG is common in contemporary children, and appears to be related to a defect in beta-cell function already present at 5 yr. Similar findings in the mothers of IFG children suggest that the beta-cell defect may be transmissible. © 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

OBJECTIVE: Impaired fasting glucose (IFG) is a predictor of future diabetes and is increasingly common in children, but the extent to which it results from excess insulin demand or failure of supply is unclear. Our aim was to compare the behaviour of insulin sensitivity and beta-cell function in children who developed IFG with those whose glucose levels remained within the normal range. METHODS: We examined trends in fasting glucose, insulin sensitivity (HOMA-S) and beta-cell function (HOMA-B) in 327 healthy children annually from 5 to 15 yr, and the parents at baseline. RESULTS: Fifty-five children showed IFG, mostly after age 11 yr. Fasting glucose rose progressively and was higher throughout in those who developed IFG compared with those who did not (p < 0.001). Beta-cell function was lower from the age of 5 yr in those who developed IFG (p = 0.006), but there was no difference in BMI (p = 0.71). A difference in insulin sensitivity was revealed on adjustment for covariates (p = 0.03). Glucose was higher (p < 0.001), beta-cell function lower (p = 0.01), and insulin sensitivity the same (p = 0.86) in the mothers of children who showed IFG, compared with those who did not. CONCLUSIONS: IFG is common in contemporary children, and appears to be related to a defect in beta-cell function already present at 5 yr. Similar findings in the mothers of IFG children suggest that the beta-cell defect may be transmissible.

BACKGROUND: Despite the health risks, physical inactivity is common. Identifying the correlates of physical activity to inform the design of interventions to reduce the disease burden associated with physical inactivity is a public health imperative. Rural adults have a unique set of characteristics influencing their activity behaviour, and are typically understudied, especially in England. The aim of this study was to identify the personal, social, and environmental correlates of physical activity in adults living in rural villages. METHODS: the study used baseline data from 2415 adults (response rate: 37.7%) participating in the first time period of a stepped-wedge cluster randomised trial, conducted in 128 rural villages from south-west England. Data collected included demographic characteristics, social factors, perception of the local environment, village level factors (percentage male, mean age, population density, Index of Multiple Deprivation, and sport market segmentation), and physical activity behaviour. Random effects ("multilevel") logistic regression models were fitted to the binary outcome whether individuals met physical activity guidelines, and random effects linear regression models were fitted to the continuous outcome MET-minutes per week leisure time physical activity, using the personal, social, environmental, and village-level factors as predictors. RESULTS: the following factors both increased the odds of meeting the recommended activity guidelines and were associated with more leisure-time physical activity: being male (p = 0.002), in good health (p < 0.001), greater commitment to being more active (p = 0.002), favourable activity social norms (p = 0.004), greater physical activity habit (p < 0.001), and recent use of recreational facilities (p = 0.01). In addition, there was evidence (p < 0.05) that younger age, lower body mass index, having a physical occupation, dog ownership, inconvenience of public transport, and using recreational facilities outside the local village were associated with greater reported leisure-time physical activity. None of the village-level factors were associated with physical activity. CONCLUSIONS: This study adds to the current literature on the correlates of physical activity behaviour by focusing on a population exposed to unique environmental conditions. It highlights potentially important correlates of physical activity that could be the focus of interventions targeting rural populations, and demonstrates the need to examine rural adults separately from their urban counterparts.

OBJECTIVE: Insulin resistance (IR) is associated with diabetes. IR is higher during puberty in both sexes, with some studies showing the increase to be independent of changes in adiposity. Few longitudinal studies have reported on children, and it remains unclear when the rise in IR that is often attributed to puberty really begins. We sought to establish from longitudinal data its relationship to pubertal onset, and interactions with age, sex, adiposity, and IGF-1. RESEARCH DESIGN AND METHODS: the EarlyBird Diabetes study is a longitudinal prospective cohort study of healthy children aged 5-14 years. Homeostasis model assessment (HOMA-IR), skinfolds (SSF), adiposity (percent fat, measured by dual-energy X-ray absorptiometry), serum leptin, and IGF-1 were measured annually in 235 children (134 boys). Pubertal onset was adduced from Tanner stage (TS) and from the age at which luteinizing hormone (LH) first became serially detectable (≥0.2 international units/L). RESULTS: IR rose progressively from age 7 years, 3-4 years before TS2 was reached or LH became detectable. Rising adiposity and IGF-1 together explained 34% of the variance in IR in boys and 35% in girls (both P < 0.001) over the 3 years preceding pubertal onset. The contribution of IGF-1 to IR was greater in boys, despite their comparatively lower IGF-1 levels. CONCLUSIONS: IR starts to rise in mid-childhood, some years before puberty. Its emergence relates more to the age of the child than to pubertal onset. More than 60% of the variation in IR prior to puberty was unexplained. The demography of childhood diabetes is changing, and prepubertal IR may be important.

BACKGROUND/AIMS: the concept of the 'thin-fat' Indian baby is well established, but there is little comparative data in older children, and none that examines the metabolic correlates. Accordingly, we investigated the impact of body composition on the metabolic profiles of Asian Indian and white U.K. children. METHODS: Body mass index (BMI), waist circumference, sum of four skin-folds, % body fat (by dual-energy X-ray absorptiometry), glucose, insulin, insulin resistance (Homeostasis Model Assessment), trigylcerides, cholesterol [total, low-density lipoprotein, high-density lipoprotein {HDL}, total/HDL ratio] and blood pressure (systolic, diastolic and mean arterial) were measured in 262 white Caucasian children from Plymouth, U.K. (aged 6.9 ± 0.2 years, 57% male), and 626 Indian children from rural villages around Pune, India (aged 6.2 ± 0.1 years, 53% male). RESULTS: Indian children had a significantly lower BMI (boys: -2.1 kg m(-2) , girls: -3.2 kg m(-2) , both P 

Objective: to determine whether, and to what extent, physical activity interventions affect the overall activity levels of children. Design: Systematic review and meta-analysis. Data sources: Electronic databases (Embase, Medline, PsycINFO, SPORTDiscus) and reference lists of included studies and of relevant review articles. Study selection: Design: randomised controlled trials or controlled clinical trials (cluster and individual) published in peer reviewed journals. Intervention: incorporated a component designed to increase the physical activity of children/adolescents and was at least four weeks in duration. Outcomes: measured whole day physical activity objectively with accelerometers either before or immediately after the end of the intervention period. Data analysis: Intervention effects (standardised mean differences) were calculated for total physical activity, time spent in moderate or vigorous physical activity, or both for each study and pooled using a weighted random effects model. Meta-regression explored the heterogeneity of intervention effects in relation to study participants, design, intervention type, and methodological quality. Results: Thirty studies (involving 14 326 participants; 6153 with accelerometer measured physical activity) met the inclusion criteria and all were eligible for meta-analysis/meta-regression. The pooled intervention effect across all studies was small to negligible for total physical activity (standardised mean difference 0.12, 95% confidence interval 0.04 to 0.20; P

OBJECTIVE: the objective of this study was to establish the extent to which parental factors influence the metabolic health of their offspring. DESIGN: the study was designed as a prospective longitudinal cohort study SUBJECTS: the study's subjects were 226 healthy trios from a 1995 to 1996 birth cohort randomly recruited in the city of Plymouth, UK MEASUREMENTS: Body mass index (BMI) and metabolic z-score (derived from natural log HOMA-IR, triglycerides, total/high-density lipoprotein cholesterol ratio), measured at nine annual time points, from 5 to 13 years. RESULTS: As expected, the metabolic z score was closely related to BMI in both genders and at all ages (r = 0.40-0.57, P 

OBJECTIVE: Several studies suggest that taller children may be wrongly labelled as 'overweight' because body mass index (BMI) is not independent of height (Ht) in childhood, and recommend adjustment to render the index Ht independent. We used objective measures of %body fat and hormonal/metabolic markers of fatness to investigate whether BMI and the corresponding fat mass index (FMI) mislead in childhood, or whether taller children really are fatter. DESIGN: Longitudinal observational study measuring children annually from age 7 to 12 years. SUBJECTS: Two hundred and eighty healthy children (56% boys) from the EarlyBird study. MEASUREMENTS: BMI (body mass (BM)/Ht(2)), FMI (fat mass (FM)/Ht(2)), %body fat ((FM/BM) × 100, where FM was measured by dual-energy X-ray absorptiometry), fasting leptin (a hormonal measure of body fatness) and insulin resistance (a metabolic marker derived from the validated homeostasis model assessment program for insulin resistance--HOMA2-IR) were all analysed in relation to Ht. Alternative Ht-independent indices of BM and FM were compared with BMI and FMI as indicators of true fatness and related health risk. RESULTS: BMI and FMI correlated with Ht at each annual time point (r~0.47 and 0.46, respectively), yet these correlations were similar in strength to those between Ht and %fat (r~0.47), leptin (r~0.41) and insulin resistance (r~0.40). Also, children who grew the most between 7 and 12 years showed greater increases in BMI, FMI, leptin and insulin resistance (tertile 1 vs 3, all p

The objective of the present study was to explore the consistency of dietary choices made by children as they grow up. The dietary habits of 342 healthy children were reported annually from 5 to 13 years on a forty-five-item FFQ and analysed by factor analysis. The same two principal dietary patterns--'Healthy' and 'Unhealthy'--emerged each year, and their consistency was assessed using Tucker's congruence coefficient (φ). Individual dietary z-scores for both of these patterns were then calculated every year for each child, and their consistency was measured by Pearson's correlation coefficient (r). Linear mixed-effects modelling was used to investigate individual trends and to quantify reliability of the individual dietary z-scores. Dietary patterns were moderately consistent and systematic over time (0·65 ≤ φHealthy ≤ 0·76; 0·62 ≤ φUnhealthy ≤ 0·78). Individual choices were also consistent year-on-year (0·64 ≤ rHealthy ≤ 0·71; 0·57 ≤ rUnhealthy ≤ 0·68). Reliability rose from 70 % with a single measure to over 90 % with four consecutive measures. The quality of diet diminished over time in 29 % of the children and improved in only 14 %. Dietary habits appear to be set early and seldom improve spontaneously.

OBJECTIVE: to investigate the direction of causality in the association between adiposity and insulin resistance in children. METHODS: Body composition by DEXA, and insulin resistance by HOMA-2 IR were measured annually in 238 children aged from 7-13 years. Longitudinal modelling was used to establish whether baseline and/or trends in adiposity were associated with change in IR or whether, conversely, baseline and/or trends in IR were associated with change in adiposity. RESULTS: Baseline adiposity was associated with change in IR in the short-term (p < 0.001) but less so in the long-term (p < 0.09) in both genders. Baseline IR was not associated with short-term change in adiposity in either gender (p > 0.42). In the long-term, baseline IR appeared to be positively associated with change in adiposity in boys (p = 0.02) but inversely associated with change in adiposity (the higher the baseline IR, the lower the gain in %fat) in girls (p < 0.001). CONCLUSIONS: the dominant direction of causality appears to be from adiposity to insulin resistance. In boys, adiposity appears to be both a cause and an effect of IR in the long term. In girls, however, higher insulin resistance appeared to limit further gain in body fat in the long term, an observation consistent with insulin desensitization as an adaptive response to weight gain.

OBJECTIVE: to establish in children whether inactivity is the cause of fatness or fatness the cause of inactivity. DESIGN: a non-intervention prospective cohort study examining children annually from 7 to 10 years. Baseline versus change to follow-up associations were used to examine the direction of causality. SETTING: Plymouth, England. PARTICIPANTS: 202 children (53% boys, 25% overweight/obese) recruited from 40 Plymouth primary schools as part of the EarlyBird study. MAIN OUTCOME MEASURES: Physical activity (PA) was measured using Actigraph accelerometers. The children wore the accelerometers for 7 consecutive days at each annual time point. Two components of PA were analysed: the total volume of PA and the time spent at moderate and vigorous intensities. Body fat per cent (BF%) was measured annually by dual energy x ray absorptiometry. RESULTS: BF% was predictive of changes in PA over the following 3 years, but PA levels were not predictive of subsequent changes in BF% over the same follow-up period. Accordingly, a 10% higher BF% at age 7 years predicted a relative decrease in daily moderate and vigorous intensities of 4 min from age 7 to 10 years (r=-0.17, p=0.02), yet more PA at 7 years did not predict a relative decrease in BF% between 7 and 10 years (r=-0.01, p=0.8). CONCLUSIONS: Physical inactivity appears to be the result of fatness rather than its cause. This reverse causality may explain why attempts to tackle childhood obesity by promoting PA have been largely unsuccessful.

The role of resting energy expenditure (REE) in the development of obesity in children is controversial. Our aim was to test the hypothesis that REE has a meaningful impact on change in weight or body composition in healthy children. Resting energy expenditure by indirect calorimetry and body composition by dual-energy x-ray absorptiometry were measured in 236 children (131 boys) on 7 annual occasions (7-13 years). The effect of REE at 7 years on change in weight and body composition was analyzed using linear mixed effects models. In neither sex was there an interaction between REE at 7 years and change in weight (P >. 9). There were weak associations between REE at 7 years and change in body composition in boys but not in girls: for a 418 kJ (100 kcal) lower REE at 7 years, an increase in rate of change in fat mass of approximately 0.1 kg/y and in percentage of fat of 0.2% per year and a decrease in fat-free mass of 0.1 kg/y. Change in REE during follow-up was not significantly associated with body composition changes in either sex (P >. 06). Thus, REE has little impact on the wide variation in weight gain at this age; although in boys, some fat was simply exchanged for lean, the effect was small. Resting energy expenditure does not appear to provide an explanation for childhood obesity.

OBJECTIVES: to explore the activitystat hypothesis in primary school children by asking whether more physical activity (PA) in school time is compensated for by less PA at other times. STUDY DESIGN: Observational, repeated measures (four consecutive occasions over a 12-month period). SETTING: South-west England. PARTICIPANTS: a total of 206 children (115 boys, aged 8-10 years) from 3 primary schools (S1, S2 and S3), which recorded large differences in PA during school time. MEASUREMENTS: Total PA (TPA) and its moderate-and-vigorous component were recorded weekly by accelerometry, in school and out of school, and adjusted for local daily rainfall and daylight hours. Habitual PA was assessed by linear mixed-effects modelling on repeated measures. RESULTS: S1 children recorded 64% more in-school PA, but S2 and S3 children compensated with correspondingly more out-of-school PA, so that TPA between the three schools was no different: 35.6 (34.3-36.9), 37.3 (36.0-38.6) and 36.2 (34.9-37.5) Units, respectively (P=0.38). CONCLUSIONS: the PA of children seems to compensate in such a way that more activity at one time is met with less activity at another. The failure of PA programmes to reduce childhood obesity could be attributable to this compensation.

OBJECTIVE: Height, body fat and body mass index (BMI) are correlated in children, so we hypothesized that the gender-assortative associations in BMI recently reported in contemporary children might extend to their height and body fat. DESIGN: Prospective longitudinal cohort study. SUBJECTS: a total of 226 healthy trios (mother, father and child) from a 1995?1996 birth cohort randomly recruited in the city of Plymouth, UK. MEASUREMENTS: Height, weight, and BMI (kg/m(2)) were measured in each of the parents and, in addition, sum of five skin-folds (SF) in their children at 5, 6, 7 and 8 y. RESULTS: BMI and SF were strongly height-dependent in the children by 8 y (r = 0.41-0.56). SF was gender-assortative insofar as the mean SF was significantly greater in the daughters (but not the sons) of obese mothers (obese vs. normal weight: +2.5 cm p < 0.001) and in the sons (but not the daughters) of obese fathers (obese vs. normal: +1.3 cm p < 0.001). As expected, offspring height correlated with that of their parents, but overweight/obese children were systematically taller than normal weight children (boys: +1.02 SDS, girls: +1.14 SDS, p < 0.01), and this difference was independent of parental height or BMI. CONCLUSIONS: Height is transmitted by both parents, and the body fat of overweight/obese children largely by the same-sex parent, but the extra height associated with more fat in the child is unrelated to the height or weight of either parent. The secular trend in height among contemporary children may simply reflect their rising body fat. Excess fat is unhealthy, so the trend in height may not be healthy either.

BACKGROUND & AIMS: in adults, adjustments in resting energy expenditure (REE) are used to defend energy balance against disturbance caused by over-and under-nutrition, and may be linked to changes in insulin resistance and leptin. Little is known of these associations in children. Our aim was to test the hypothesis that long-term weight gain in children is met with adaptive changes in resting energy expenditure, mediated by insulin resistance and/or leptin. METHODS: REE by indirect calorimetry, anthropometry, body composition by DEXA, insulin resistance (HOMA-IR) and serum leptin were measured annually in 232 children from the age of 7-10 y. RESULTS: REE rose from 7 to 10 y, and the rise exceeded that predicted by the concurrent rise in fat and fat-free mass by 184 kcal/day in the boys and by 160 kcal/day in the girls. However, there were no significant relationships in either gender between this 'excess' rise in REE and change in body composition (r < or = 0.08, p > or = 0.42). The rise in both boys and girls was associated with, but not explained by, a rise in insulin resistance (p < or = 0.002). There was no association with serum leptin (p > or = 0.32). CONCLUSIONS: the data do not support the hypothesis of adaptive changes in REE in pre-pubertal children, and insulin resistance explains very little of the pre-pubertal rise in REE. The rise in REE beyond that explained by changes in body composition may reflect an increase in energy requirements prior to puberty.

Voss LD, Hosking J, Metcalf BS, Jeffery AN, Frémeaux AE, Wilkin TJ. Metabolic risk in contemporary children is unrelated to socio-economic status: longitudinal study of a UK urban population (EarlyBird 42). Lifestyle interventions to improve health in young children tend to target areas of relative deprivation, but the evidence for so doing is largely historical. Accordingly, we have re-examined the link between deprivation, obesity and metabolic risk in contemporary UK children. Using a postcode-based index of multiple deprivation (IMD), we assessed 269 children from the community-based EarlyBird Study, attending 53 schools representing a wide socio-economic range. Annual measures of fatness from 5 to 8 yr included body mass index (BMI), waist circumference (WC), and sum of five skinfolds (SSF). A metabolic risk score, based on blood pressure, lipids and insulin resistance, was derived from annual fasting blood samples. There were no significant associations between deprivation and any measure of adiposity in girls (all p > 0.37). In boys, there was a weak but consistently inverse relationship between deprivation and WC (r = -0.19, p = 0.03) and BMI (r = -0.14, p = 0.09) at 8 yr. Changes in adiposity over 3 yr were unrelated to deprivation in boys. In girls there was a slight but significant increase in SSF only (1 mm/yr per 20 IMD units, p = 0.001). Importantly, in both genders, metabolic risk score was unrelated to deprivation throughout (r values -0.05 to -0.13, all p > 0.12), as was change in metabolic risk (all p > 0.30). Our data do not support the assumption that obesity, metabolic disturbance and thus risk of type 2 diabetes are more prevalent among poorer children. In today's increasingly obesogenic environment, youngsters from all backgrounds appear to be vulnerable, with population-wide implications for public health spending, and the prevention of diabetes in contemporary youth.

BACKGROUND: Few weight management clinics have access to indirect calorimetry with which to measure energy expenditure. Instead, they use energy expenditure prediction equations, which were not designed for use in obesity. We aimed to establish the extent to which such equations overestimate and underestimate resting energy expenditure (REE) in overweight and obese individuals. METHODS: We compared the Schofield, Harris & Benedict, James & Lean and World Health Organisation (WHO) REE prediction equations with the clinical gold standard of indirect calorimetry in 28 males and 168 females, with a mean (SD) age of 28.9 (6.4) years and body mass index (BMI) of 19-67 kg m(-2). RESULTS: the mean REE estimated by indirect calorimetry, and the Schofield, Harris & Benedict, James & Lean and WHO equations were 8.09, 8.30, 8.09, 8.37 and 8.23 MJ day(-1) (1934, 1983, 1933, 2001 and 1966 kcal day(-1)), respectively. Although rising BMI exerted only a small effect on the mean differences between indirect calorimetry and the predicted REE [Schofield: +272 kJ (+65 kcal)/10 units BMI, P = 0.02; Harris & Benedict: +42 kJ (+10 kcal)/10 units BMI, P = 0.69; James & Lean: +217 kJ (+52 kcal) 10 units BMI, P = 0.06 and WHO: +42 kJ (+10 kcal) BMI, P = 0.11], the variance among overweight and obese patients of BMI >25 was substantially higher compared to that among normal weight subjects of BMI

OBJECTIVE: to look for same-sex (gender assortative) association of body mass index (BMI) in healthy trios (mother, father and child) from a contemporary birth cohort, which might imply shared environment rather than shared genes because selective mother-daughter and father-son gene transmission is not a common Mendelian trait. DESIGN: Prospective (longitudinal) cohort study with four annual time points, from 5 to 8 years. SUBJECTS: 226 healthy trios from a 1995 to 1996 birth cohort randomly selected in the city of Plymouth, UK. MEASUREMENTS: Average BMI of the two parents and maternal/paternal BMI separately related to the BMI-SDS (standard deviation score) of all offspring and to the BMI-SDS of the sons and the daughters separately. RESULTS: There were big differences in BMI-SDS among the daughters grouped according to mothers' category of BMI (effect size 1.37 SDS), but not their sons (effect size 0.16 SDS, gender interaction P

BACKGROUND: Early weight gain (0-5 years) is thought to be an important contributor to childhood obesity and consequently metabolic risk. There is a scarcity of longitudinal studies in contemporary children reporting the impact of early weight gain on metabolic health. OBJECTIVE: We aimed to assess the impact of early weight gain on metabolic health at 9 years of age. METHOD: Two hundred thirty-three children (134 boys, 99 girls) with a gestational age of >37 weeks were assessed at birth, 5 years of age, and 9 years of age. Measures included weight SD scores at each time point and excess weight gained (Delta weight SD score) between them. The outcome measure included composite metabolic score (sum of internally derived z scores of insulin resistance, mean blood pressure, triglyceride level, and total cholesterol/high-density lipoprotein cholesterol ratio). RESULTS: Weight SD score increased by 0.29 SD score in girls and 0.26 SD score in boys from 0 to 5 years of age and by 0.03 SD score in girls and 0.11 SD score in boys from 5 to 9 years of age. Weight SD score correlated poorly to moderately before 5 years of age but strongly after 5 years of age. Birth weight SD score predicted (girls/boys) 2.4%/0% of the variability in composite metabolic score at 9 years of age. Adding Delta weight SD score (0-5 years old) contributed (girls/boys) 11.2%/7.0% to the score, and adding Delta weight SD score (5-9 years old) additionally contributed (girls/boys) 26.4%/16.5%. Importantly, once weight SD score at 9 years of age was known, predictive strength was changed little by adding Delta weight SD score. CONCLUSIONS: Most excess weight before puberty is gained before 5 years of age. Weight at 5 years of age bears little relation to birth weight but closely predicts weight at 9 years of age. Single measures of current weight are predictive of metabolic health, whereas weight gain within a specific period adds little. A single measure of weight at 5 years of age provides a pointer to future health for the individual. If metabolic status at 9 years of age means future risk, diabetes/cardiovascular prevention strategies might better focus on preschool-aged children, because the die seems to be largely cast by 5 years of age, and a healthy weight early in childhood may be maintained at least into puberty.

BACKGROUND: the role of the autonomic nervous system in the complex link between insulin resistance and cardiovascular risk remains unclear. Increased sympathetic nervous system activity has been implicated in the pathophysiology of insulin resistance but is confounded by a number of factors. METHODS: We have therefore examined the relationship among cardiac autonomic control, insulin resistance, habitual physical activity, resting energy expenditure (REE), and anthropometric variables in a subset (107 boys, 101 girls, age 9 +/- 0.25 yr) of the EarlyBird cohort. Cardiac autonomic activity was assessed using time domain and power spectral density analysis methods of heart rate variability. Insulin resistance was measured using homeostasis model assessment of insulin resistance (HOMA2-IR). RESULTS: Girls, in comparison to boys, showed significantly higher resting heart rate and lower systolic blood pressure (BP); were more insulin resistant; undertook less physical activity, and had lower fat-free mass and REE. Increasing fasting insulin and increasing insulin resistance were associated with increasing BP. CONCLUSION: the data suggest early gender differences in predictors of cardiac autonomic control. Pubertal staging was not undertaken in this study, and we plan to evaluate this in future studies to further clarify these associations.

OBJECTIVE - Recent evidence suggests that, in children, traditional markers of metabolic disturbance are related only weakly to physical activity. We therefore sought to establish the corresponding relationships with newer metabolic markers. RESEARCH DESIGN AND METHODS - This was a nonintervention longitudinal study of 213 healthy children recruited from 54 schools in Plymouth, U.K. MTI accelerometers were used to make objective 7-day recordings of physical activity at ages 5 ± 0.3 (mean ± SD), 6, 7, and 8 years. Overall physical activity was taken as the average of the four annual time points. The metabolic markers at 8 years were adiponectin, leptin, high-sensitivity C-reactive protein (hsCRP), and insulin resistance (homeostasis model assessment). Potential confounders included percent body fat measured by dual-energy X-ray absorptiometry and diet measured by food frequency questionnaire. RESULTS - Whereas physical activity did not correlate with insulin resistance (r = -0.01), leptin (r = +0.04), or hsCRP (r = +0.01) independently of percent body fat, it did correlate with adiponectin, but inversely (r = -0.18, P = 0.02). This unexpected inverse relationship was strongest among the less active children (physical activity < median: r = -0.30, P = 0.01) but negligible in the more active children (physical activity > median: r = +0.04, P = 0.76). Adiponectin was significantly higher (0.52 SD, P < 0.01) in the least active tertile compared with the other two tertiles. Insulin resistance, however, did not differ across the physical activity tertiles (P = 0.62). CONCLUSIONS - Adiponectin levels in children are highest among those who are least active, but their insulin resistance is no different. Adiponectin has a known insulin-sensitizing effect, and our findings are consistent with a selective effect at low levels of physical activity. © 2009 by the American Diabetes Association.

Adiponectin, a hormone produced and secreted by adipocytes, is present in circulation in high circulating concentrations, suggesting an important physiological role. An indirect regulator of glucose metabolism, adiponectin increases insulin sensitivity, improves glucose tolerance and inhibits inflammation. Plasma adiponectin relates inversely to adiposity and, importantly, reflects the sequelae of accumulation of excess adiposity. The role of adiponectin in adults has been explored in detail. Studies in children are now available and, given the increasing rates of childhood obesity, it is important to establish the role of adiponectin in mediating insulin resistance and cardiovascular disease in this age group. This paper reviews the regulation of adiponectin, its effect on body mass, glucose metabolism and cardiovascular risk in infants, children and adolescents. It demonstrates clear links between adiponectin and features of the metabolic syndrome in obese children and adolescents. However, adiponectin's role as a predictor of metabolic dysfunction in healthy, normal-weight youngsters is less clear.

BACKGROUND: Rising levels of childhood obesity have led to an increasing number of Government sponsored initiatives attempting to stem the problem. Much of the focus to date has been on physical activity and out-of-school activity in particular. There is an assumption that children from low-income families suffer most where there is a lack of structured physical education in school. Accordingly, provision of additional facilities for sport and other forms of active recreation tend to target areas of socio-economic deprivation. AIM: We have assessed the relationship between parental income, the use of out-of-school sports facilities and the overall physical activity of young children across a wide socio-economic range. METHODS: Total weekly physical activity was measured, objectively, over 7 days both at 7 years and 8 years in a healthy cohort of 121 boys and 93 girls using actigraph accelerometers. Questionnaires were used to establish parental income and parents reported the child's weekly use of out-of-school facilities for structured physical activity. RESULTS: Children from low-income families attended significantly fewer sessions of structured out-of-school activities than those from wealthier families (r = 0.39), with a clear dose-response relationship across income groups. Nevertheless, total physical activity, measured objectively over seven continuous days, showed no relationship between parental income and the mean activity level of the children (r = -0.08). Nor did we find a relationship between parental income and time spent in higher intensity activity (r = -0.04). CONCLUSION: Social inequality appears to have little impact on physical activity in young children. Those from poorer families make less use of facilities for structured activity out-of-school but they nevertheless record the same overall level of activity as others. What they lack in opportunity they appear to make up in the form of unstructured exercise. Improving provision for sport may not lead to the expected rise in activity levels in young children.

BACKGROUND: the emergence of type 2 diabetes in young populations has mirrored a rising prevalence of obesity and insulin resistance during childhood and adolescence. At the same time, the role of adipokines as links between obesity and insulin resistance is becoming more appreciated. We sought to establish age- and sex-specific distributions of metabolic correlates of insulin resistance in healthy prepubertal children. METHODS: We collected fasting blood samples from a contemporary cohort of 307 British children at ages 5, 6, 7, and 8 years and measured insulin, glucose, triglycerides, total and HDL cholesterol, urate, glycohemoglobin, sex hormone-binding globulin (SHBG), leptin, and adiponectin. We used homeostasis model assessment (HOMA 2) to estimate insulin sensitivity (HOMA-%S) and beta-cell function (HOMA-%B). Anthropometric measures included body mass index. RESULTS: Body mass index increased from age 5 to 8 years (P < 0.001). HOMA-%B decreased (P < 0.001) and HOMA-%S increased (P < 0.05), but glucose also increased (P < 0.001) whereas glycohemoglobin decreased (P < 0.001). Consistent with the rise in insulin sensitivity, HDL cholesterol increased (P < 0.001) and triglycerides decreased (NS), whereas adiponectin decreased (P = 0.02). The patterns were similar in boys and girls, although girls were less insulin sensitive throughout. Accordingly, triglycerides tended to be higher in the girls, and HDL cholesterol and SHBG lower. CONCLUSIONS: the metabolic disturbances associated with insulin resistance appear to be more advanced in girls. Markers of metabolic health improve in both sexes from 5 to 8 years, despite rising adiposity.

BACKGROUND: in the UK and USA, government guidelines for childhood physical activity have been set (> or =60 min/day at > or =3 metabolic equivalents of thermogenesis (METs)), and body mass index (BMI) chosen as the outcome measure. AIM: to determine the extent to which physical activity at the government-recommended intensity is associated with change in body mass/fat and metabolic health in pre-pubertal children. METHODS: Non-intervention longitudinal study of 113 boys and 99 girls (born 1995/96) recruited from 54 schools. Physical activity (Actigraph accelerometers), changes in body mass (raw and age/gender-standardised BMI), fatness (skin-fold thickness and waist circumference) and metabolic status (insulin resistance, triglycerides, cholesterol/HDL ratio and blood pressure - separately and as a composite metabolic z score) were measured on four annual occasions (5, 6, 7 and 8 years). RESULTS: Mean physical activity did not change over time in either sex. Averaging the 7-day recordings from four time points rather than one increased the reliability of characterising a child's activity from 71% to 90%. Some 42% of boys and 11% of girls met the guideline. There were no associations between physical activity and changes in any measurement of body mass or fatness over time in either sex (eg, BMI standard deviation scores: r = -0.02, p = 0.76). However, there was a small to moderate inverse association between physical activity and change in composite metabolic score (r = -0.19, p

OBJECTIVE. Serum adiponectin levels are inversely related to adiposity and resting energy expenditure (REE) in adults yet may protect against excess weight gain. Little is known of these associations in children, in whom obesity is rising. The aim of this study was therefore to investigate the relationships between REE, adiponectin and weight gain in young children. METHODS. Adiponectin by ELISA, REE by indirect calorimetry, fat-free mass (FFM) and fat mass (FM) by DEXA were measured at 6.9 years, and repeated one year later in 151 healthy children, aged 7.9±0.3 years. RESULTS. There were no significant correlations between REE and adiponectin at 6.9 years or at 7.9 years (boys r=-0.02, p=0.88 and r=0.05, p=0.69, respectively; girls r=-0.11, p=0.35 and r=0.05, p=0.70, respectively). There was no link between REE at 6.9 years and subsequent weight gain or adverse change in body composition (all r0.08). Similarly, there were no correlations between adiponectin and weight change, but there was a significant inverse association between adiponectin at 6.9 years and FFM gain in boys (r=-0.27, p=0.02). CONCLUSIONS. The relationship between adiponectin and REE has yet to appear in young children. REE is not a significant predictor of future weight gain or adverse change in body composition and, although the period of follow-up was limited, adiponectin seems unlikely to confound such a relationship in healthy young children.

Background: Rising obesity has been observed in all age groups. Anthropometric cut-points have been used to predict metabolic risk in children, although they are not based on known outcomes. Aim: We examined the trends, associations and predictions of metabolic health from anthropometry in prepubertal children. Method: Three hundred and seven healthy children were examined annually between 5 and 8 yr. Measures: height, weight, body mass index (BMI), sum of skinfold thickness at five sites (SSF) and waist circumference (WC). Outcome measures: homeostasis model assessment of insulin resistance (HOMA-IR), high-density lipoprotein cholesterol (HDL-C) and triglycerides (TG). Results: Two hundred and thirty-one [131 boys (B) and 100 girls (G)] children had complete data sets at all four time points. (i) all measures of adiposity rose from 5 to 8 yr (BMI - B: +3.4%, G: +5.7%; WC - B: +10.4%, G: +11.8%; SSF - B: +23.3%, G: +30.7%, all p < 0.001). HOMA-IR unexpectedly fell (B: -16.6%, p = 0.01; G: -32.5%, p < 0.001). This fall was significant between 5 and 6yr in both genders (5-6 yr - B: -17.8%, p < 0.001; G: -20.0%, p = 0.002) and between 6 and 7yr in girls only (6-7 yr - B: -10.8%, p=0.12; G: -19.2%, p = 0.001). HDL-C rose (B: +17.8%, G: +17.1%, both p < 0.001) and TG fell (B: -4.8%, p = 0.16; G: -11.6%, p = 0.006). (ii) Correlations between insulin resistance (IR) and anthropometry were poor at 5 yr but strengthened by 8 yr (BMI - B: r = 0.20/0.38, G: r = 0.28/0.49; WC - B: r = 0.25/0.40, G: r = 0.32/0.58; SSF - B: r=0.11/0.36, G: r = 0.18/0.53). (iii) in girls, but not boys, adiposity at 5yr predicted IR better at 8yr (BMI - r2 = 0.17; WC - r2 = 0.28; SSF - r2 = 0.17, all p < 0.001) than it did at 5 yr (BMI - r2 = 0.08, p

BACKGROUND: Rising obesity has been observed in all age groups. Anthropometric cut-points have been used to predict metabolic risk in children, although they are not based on known outcomes. AIM: We examined the trends, associations and predictions of metabolic health from anthropometry in prepubertal children. METHOD: Three hundred and seven healthy children were examined annually between 5 and 8 yr. MEASURES: height, weight, body mass index (BMI), sum of skinfold thickness at five sites (SSF) and waist circumference (WC). OUTCOME MEASURES: homeostasis model assessment of insulin resistance (HOMA-IR), high-density lipoprotein cholesterol (HDL-C) and triglycerides (TG). RESULTS: Two hundred and thirty-one [131 boys (B) and 100 girls (G)] children had complete data sets at all four time points. (i) all measures of adiposity rose from 5 to 8 yr (BMI - B: +3.4%, G: +5.7%; WC - B: +10.4%, G: +11.8%; SSF - B: +23.3%, G: +30.7%, all p < 0.001). HOMA-IR unexpectedly fell (B: -16.6%, p = 0.01; G: -32.5%, p < 0.001). This fall was significant between 5 and 6 yr in both genders (5-6 yr - B: -17.8%, p < 0.001; G: -20.0%, p = 0.002) and between 6 and 7 yr in girls only (6-7 yr - B: -10.8%, p = 0.12; G: -19.2%, p = 0.001). HDL-C rose (B: +17.8%, G: +17.1%, both p < 0.001) and TG fell (B: -4.8%, p = 0.16; G: -11.6%, p = 0.006). (ii) Correlations between insulin resistance (IR) and anthropometry were poor at 5 yr but strengthened by 8 yr (BMI - B: r = 0.20/0.38, G: r = 0.28/0.49; WC - B: r = 0.25/0.40, G: r = 0.32/0.58; SSF - B: r = 0.11/0.36, G: r = 0.18/0.53). (iii) in girls, but not boys, adiposity at 5 yr predicted IR better at 8 yr (BMI - r(2 )= 0.17; WC - r(2 )= 0.28; SSF - r(2 )= 0.17, all p < 0.001) than it did at 5 yr (BMI - r(2 )= 0.08, p < 0.01; WC - r(2 )= 0.10, p < 0.01; SSF - r(2 )= 0.03, p = 0.07). CONCLUSIONS: Cross-sectional association cannot indicate direction of trend or predict the future. Predicting metabolic health from anthropometric measures in prepubertal children requires longitudinal data, tracking variables from childhood into adulthood. Until the data set reaches adulthood, it is probably not safe to make recommendations on which children to 'target' or whether early intervention would be of benefit.

Fasting glucose is associated with future risk of type 2 diabetes and ischemic heart disease and is tightly regulated despite considerable variation in quantity, type, and timing of food intake. In pregnancy, maternal fasting glucose concentration is an important determinant of offspring birth weight. The key determinant of fasting glucose is the enzyme glucokinase (GCK). Rare mutations of GCK cause fasting hyperglycemia and alter birth weight. The extent to which common variation of GCK explains normal variation of fasting glucose and birth weight is not known. We aimed to comprehensively define the role of variation of GCK in determination of fasting glucose and birth weight, using a tagging SNP (tSNP) approach and studying 19,806 subjects from six population-based studies. Using 22 tSNPs, we showed that the variant rs1799884 is associated with fasting glucose at all ages in the normal population and exceeded genomewide levels of significance (P=10-9). rs3757840 was also highly significantly associated with fasting glucose (P=8x10-7), but haplotype analysis revealed that this is explained by linkage disequilibrium (r2=0.2) with rs1799884. A maternal a allele at rs1799884 was associated with a 32-g (95% confidence interval 11-53 g) increase in offspring birth weight (P=.002). Genetic variation influencing birth weight may have conferred a selective advantage in human populations. We performed extensive population-genetics analyses to look for evidence of recent positive natural selection on patterns of GCK variation. However, we found no strong signature of positive selection. In conclusion, a comprehensive analysis of common variation of the glucokinase gene shows that this is the first gene to be reproducibly associated with fasting glucose and fetal growth.

BACKGROUND: High birth weight predicts subsequent obesity, but paradoxically, a reduced risk of subsequent cardiovascular disease compared with low birth weight. This apparent paradox might be explained if high birth weight programmed a greater proportion of subsequent lean mass, which carries less cardiovascular risk than fat tissue. AIM: the aim of this study was to test the hypothesis that the direct correlation between birth weight and subsequent body mass index (BMI) represents an association between birth weight and lean tissue, and to assess the metabolic impact of this relationship. METHODS: a total of 234 healthy prepubertal children (133 boys, 101 girls, mean age 5.9 yr +/- 0.3 standard deviation) were studied. Birth weights were obtained from maternity records. Lean mass was measured by bioelectrical impedance. Anthropometric measures included height, weight (BMI), waist circumference, and subcutaneous fat mass (FM). Insulin resistance was assessed by the homeostasis model method. Metabolic correlates of insulin resistance included total and high-density lipoprotein cholesterol, triglycerides, and sex-hormone-binding globulin. RESULTS: Birth weight correlated significantly with lean mass in boys (r = 0.41, p < 0.001) and girls (r = 0.27, p < 0.01). Adjusting for BMI did not improve the correlation further. After adjustment for FM, lean mass correlated inversely with triglycerides in boys only (r = -0.41, p < 0.01). Birth weight correlated inversely with triglycerides in boys (r = -0.18, p < 0.05); after adjustment for lean mass, this correlation was not significant. INTERPRETATION: in boys, the relationships between birth weight, triglycerides, and lean mass are consistent with the hypothesis. Overall, our findings provide limited evidence in support of the argument that higher birth weight predicts lower metabolic risk because it marks programming of more lean mass.

The International Obesity TaskForce has published paediatric cutoffs from the age of 2 years for overweight and obesity, based on adult thresholds. We question their rationale. The adult cutoffs were based on known health risk; the children's were not. Data from the EarlyBird Study show that BMI category for overweight and obesity in young children are poor markers of insulin resistance and, by implication, of metabolic risk and diabetes. Moreover, BMI is known to track poorly from early childhood to adulthood. We know even less about the tracking of insulin resistance and other indices of metabolic risk from the earliest years. Until we understand more about which children acquire such risk factors, any such thresholds for overweight and obesity should be used with caution in the very young, as they may unnecessarily stigmatise the heavier child.

OBJECTIVE: the aim of this study was to evaluate whether adaptive responses made to the uterine or very early infant environment are affecting the current metabolic health of young children in the United Kingdom. METHODS: Participants were 300 healthy children and their parents from the EarlyBird Diabetes Study cohort. Children were recruited from randomly selected schools at 5 years of age. Retrospective measures were maternal prepregnancy weight (n = 230), maternal fasting glucose levels at 28 weeks of pregnancy (n = 27), birth weight, and infant weight at ages 3 and 6 weeks. Prospective measures were insulin resistance, height, weight, and percentage of body fat (sum of 5 skinfold measurements) at ages 5, 6, 7, and 8 years. RESULTS: Maternal third-trimester fasting glucose levels were associated positively with birth weight but were not associated with either weight or insulin resistance for the same children at 8 years. Birth weight was unrelated to insulin resistance at 8 years. There were no relationships between weight change in the first weeks of life and weight, percentage of fat, or insulin resistance at 8 years. Longer breastfeeding correlated inversely, although weakly, with percentage of body fat for boys only. Current weight was correlated with insulin resistance at 8 years. CONCLUSIONS: for these contemporary children, neither the gestational environment nor early postnatal growth predicted insulin resistance, which was best predicted by current weight. There was no evidence that predictive adaptive responses made by the fetus or infant affected the child's weight or insulin resistance later in childhood.

BACKGROUND: the APOA5 gene variants, -1131T>C and S19W, are associated with altered triglyceride concentrations in studies of subjects of Caucasian and East Asian descent. There are few studies of these variants in South Asians. We investigated whether the two APOA5 variants also show similar association with various lipid parameters in Indian population as in the UK white subjects. METHODS: We genotyped 557 Indian adults from Pune, India, and 237 UK white adults for -1131T>C and S19W variants in the APOA5 gene, compared their allelic and genotype frequency and determined their association with fasting serum triglycerides, total cholesterol, HDL and LDL cholesterol levels using univariate general linear analysis. APOC3 SstI polymorphism was also analyzed in 175 Pune Indian subjects for analysis of linkage disequilibrium with the APOA5 variants. RESULTS: the APOA5 -1131C allele was more prevalent in Indians from Pune (Pune Indians) compared to UK white subjects (allele frequency 20% vs. 4%, p = 0.00001), whereas the 19W allele was less prevalent (3% vs. 6% p = 0.0015). Patterns of linkage disequilibrium between the two variants were similar between the two populations and confirmed that they occur on two different haplotypes. In Pune Indians, the presence of -1131C allele and the 19W allele was associated with a 19% and 15% increase respectively in triglyceride concentrations although only -1131C was significant (p = 0.0003). This effect size was similar to that seen in the UK white subjects. Analysis of the APOC3 SstI polymorphism in 175 Pune Indian subjects showed that this variant is not in appreciable linkage disequilibrium with the APOA5 -1131T>C variant (r2 = 0.07). CONCLUSION: This is the first study to look at the role of APOA5 in Asian Indian subjects that reside in India. The -1131C allele is more prevalent and the 19W allele is less prevalent in Pune Indians compared to UK Caucasians. We confirm that the APOA5 variants are associated with triglyceride levels independent of ethnicity and that this association is similar in magnitude in Asian Indians and Caucasians. The -1131C allele is present in 36% of the Pune Indian population making it a powerful marker for looking at the role of elevated triglycerides in important conditions such as pancreatitis, diabetes and coronary heart disease.

Foot-to-foot bioelectrical impedance analysis (BIA) is simple and non-invasive, making it particularly suitable for use in children. There is insufficient evidence of the validity of foot-to-foot BIA compared with dual-energy X-ray absorptiometry (DEXA) as the criterion method in healthy young children. Our objective was to assess the validity of foot-to-foot BIA against DEXA in a large cohort of healthy young children. Body composition was measured by foot-to-foot BIA and DEXA in 203 children (mean age 8.9 (SD 0.3) years). Bland-Altman and simple linear regression analyses were used to determine agreement between methods. BIA overestimated fat-free mass by a mean of 2.4% in boys and 5.7% in girls, while fat mass was underestimated by 6.5% in boys and 10.3% in girls. The percentage fat recorded by BIA was, accordingly, also lower than by DEXA (boys 4.8%; girls 12.8%). In boys, however, there were correlations between the size of the difference between methods and the size of the measure under consideration such that in smaller boys fat-free mass was underestimated (r-0.57; P

OBJECTIVE: There is currently wide interest in the physical activity of children, but little understanding of its control. Here, we use accelerometers to test the hypothesis that habitual activity in young children is centrally, rather than environmentally, regulated. By central regulation we mean a classic biological feedback loop, with a set-point individual to the child, which controls his/her activity independently of external factors. DESIGN: Non-intervention, observational and population-based, set in the home and at school. RESULTS: Girls were systematically less active than boys, and both weekday/weekend day and year-on-year activities were correlated (r=0.43-0.56). A fivefold variation in timetabled PE explained less than 1% of the total variation in physical activity. The activity cost of transport to school was only 2% of total activity, but over 90% of it was recovered elsewhere in the day. The weekly activity recorded by children in Plymouth was the same (to within

Rare mutations in the glucokinase (GCK) gene cause fasting hyperglycemia and considerably influence birth weight when present in a mother or her offspring. The role of common variation of GCK is uncertain. A polymorphism at position -30 of the GCK beta-cell-specific promoter, present in 30% of the population, has been variably associated with type 2 diabetes and diabetes-related quantitative traits. Using 1,763 U.K. Caucasian normoglycemic adult subjects, we demonstrated that the a allele at GCK(-30) is associated with a 0.06-mmol/l increase in fasting plasma glucose (FPG) (P = 0.003). The a allele was also associated with an increase in FPG in 755 women who were 28 weeks pregnant (0.075 mmol/l, P = 0.003). We then went on to analyze the effect of GCK(-30) on birth weight using 2,689 mother/child pairs. The presence of the a allele in the mother was associated with a 64-g (25-102 g) increase in offspring birth weight (P = 0.001). We did not detect a fetal genotype effect. The increase in offspring birth weight in the 30% of mothers carrying an a allele at GCK(-30) is likely to reflect an elevated FPG during pregnancy. This study establishes that common genetic variation, in addition to rare mutations and environmental factors, can affect both FPG and birth weight.

OBJECTIVE: Recent studies of type 2 diabetes in young populations consistently show a predominance of affected girls over boys. Girls are more insulin resistant than boys. We aimed in the present report to establish how much of the sex difference in insulin resistance is intrinsic. METHODS: EarlyBird is a community-based, nonintervention cohort study of 307 healthy children from school entry at age 5 years. It asks the question: which children are insulin resistant and why? Anthropometric measures, physical activity, resting energy expenditure, and insulin resistance and its metabolic correlates were measured. RESULTS: at 5 years, insulin resistance was 35% higher in girls than in boys. Girls carried 26% more subcutaneous fat despite similar body weights. However, after correcting for anthropometric variables and physical activity, girls remained 33% more insulin resistant than boys. Triglycerides were significantly higher in girls, and high-density lipoprotein cholesterol and sex hormone-binding globulin were significantly lower. CONCLUSIONS: Sex-linked genes may account for the intrinsic sex difference observed. These genes may have an important impact on the development of insulin resistance and the metabolic syndrome and may help to explain the female preponderance of type 2 diabetes in children. Their identification may also help in understanding the pathogenesis of insulin resistance.

The insulin gene variable number of tandem repeats minisatellite (INS-VNTR) class III allele is associated with altered fetal growth, type 2 diabetes risk (especially when paternally inherited), and insulin and IGF2 gene expression. Further studies are needed to establish the role of the INS-VNTR in fetal growth and assess whether its effects depend on the parent of origin. We analyzed the INS-VNTR-linked -23 Hph1 polymorphism in 2283 subjects, comprising 1184 children and 1099 parents. There were no differences (P < 0.05) in birth weight between offspring of the three genotypes: III/III (n = 108) vs. I/I (n = 558), effect size, -8 g (P = 0.87); and I/III (n = 464) vs. I/I, effect size, -19 g (P = 0.54). We observed no differences in head circumference [III/III (n = 95) vs. I/I (n = 470), effect size, -0.14 cm; P = 0.31] or birth length. No differences were observed when stratifying by postnatal growth realignments [nonchangers III/III (n = 37) vs. I/I (n = 170), effect size, -43 g; P = 1.00] or by parent of origin of the class III allele (presence of paternal III allele effect size, -15 g; P = 0.74). INS-VNTR was nominally associated (P < 0.05) with body mass index and insulin resistance, but not with beta-cell function, in young adults. In the largest study to date, we found a lack of support for a role for INS-VNTR in fetal growth and nominal association with type 2 diabetes-related intermediate traits.

BACKGROUND: Insulin resistance is believed to be the process underlying type 2 diabetes and premature cardiovascular disease. We have established that a relation between body mass and insulin resistance calculated by homeostasis model assessment (HOMA-IR) exists by 5 y of age in contemporary UK children. Resting energy expenditure (REE) is variable among individuals and is one of many factors controlling body mass. OBJECTIVE: the objective was to investigate the relations between REE, body mass, and HOMA-IR in young children. DESIGN: EarlyBird is a nonintervention prospective cohort study of 307 healthy 5-y-olds that asks the question: Which children develop insulin resistance and why? REE by indirect calorimetry and HOMA-IR were measured in addition to total body mass, fat-free mass (FFM) by bioimpedance, body mass index (BMI; in kg/m(2)), and skinfold thickness when the mean age of the cohort was 5.9 +/- 0.2 y. RESULTS: Whereas the BMI of the boys was lower than that of the girls (x +/- SD: boys, 15.9 +/- 1.9; girls, 16.5 +/- 1.9; P = 0.03), their REE was higher by 6% (x +/- SD: 4724 +/- 615 compared with 4469 +/- 531 kJ/d; P = 0.002). This difference persisted after adjustment for FFM and other anthropometric variables (P = 0.04). In boys, there was a weak, although significant, inverse correlation between REE and HOMA-IR, independent of fat mass and FFM (boys: r = -0.21, P = 0.03; girls: r = 0.12, P = 0.34). CONCLUSION: There is a sex difference in REE at 6 y of age that cannot be explained by body composition. The difference appears to be intrinsic, and its contribution to sex differences in adiposity and HOMA-IR in children merits further exploration.

OBJECTIVE: to explore relationships between maternal pre-pregnancy weight, third trimester glucose, baby birth weight, weight and metabolic health of the mother and child 5 years after birth. DESIGN: an observational study set within a non-intervention, longitudinal cohort study looking at insulin resistance in children. SETTING: a teaching hospital in the south west of the United Kingdom. PARTICIPANTS: 300 mothers and their five-year-old children from randomly selected Plymouth schools, stratified according to socioeconomic status. MEASUREMENTS: were obtained from obstetric records maternal pre-pregnant weight, random and fasting third trimester blood glucose, baby birth weight. Five years later the following measurements were made of the mother and child: height, weight, glucose and insulin resistance. FINDINGS: five years after the pregnancy, 33% of the mothers were overweight, with an additional 19% obese. In the children 13% of boys were overweight (4% obese), and in the girls, 26% were overweight (5% obese). In the five-year-old children, weight (r=0.28, p

For a decade or more, poor nutrition during gestation, expressed as low weight at birth, was held to be the factor responsible for insulin resistance later in life. Birth weights, however, are rising and insulin resistant states, such as diabetes mellitus, faster still. Alternative explanations are needed to explain insulin resistance in contemporary industrialised populations. EarlyBird is a non-intervention prospective cohort study that asks the question 'Which children develop insulin resistance, and why?' it is unique in taking serial blood samples from a young age with which to monitor the behaviour of insulin resistance and its metabolic correlates. This, the baseline report of the EarlyBird Study, describes the rationale, design and methodology of the study, and the profile of the population at entry. It situates the anthropometric, physical activity and dietary status of the EarlyBird children and provides a detailed metabolic profile of the British 5 year-old in the year 2000.

Accelerometers revealed a fivefold variation in physical activity among healthy 5 year old children. They singled out habitually inactive children, most of them girls, who did little, whether at school or over the weekend. Accelerometers are of potential value in identifying, from an early age, children at risk of becoming obese.

The increasing incidence of type 2 diabetes worldwide is causing concern. Genetic and environmental influences have been put forward to explain the origins of this disease, but perhaps the most convincing contributory factor is high body weight. The authors review the literature on the subject to identify some of the predisposing factors influencing healthcare practitioners' concerns about the issue.

PURPOSE: to evaluate the technical performance of the CSA accelerometer-based activity monitor. METHODS: Twenty-three CSA monitors were subjected to intra- and inter-instrument variability tests by controlled trials using a motorized turntable. The CSA monitor measures change in acceleration, and precision was tested by producing sinusoidal variations in speed around two fixed baseline speeds (fast and medium). The angle of the monitor to the line of force along the radius of the turntable was varied using tilted blocks. Three sets of tests were carried out. 1. Intra-instrument variability: seven monitors were tested three times in each of the four quadrants. 2. All 23 monitors were used for inter-instrument tests. 3. The effects of tilt at 15 degrees, 30 degrees, and 45 degrees were carried out on six monitors. RESULTS: Intra-instrument coefficients of variation (CV) never exceeded 2% for fast or medium speed and achieved "between run" intra-class correlation coefficients (ICC) of 0.92 and 0.84 respectively. There were no significant differences between the monitors in terms of repeatability (fast: = 0.97, medium: = 0.77). Although there were significant differences between monitors in terms of mean score, inter-instrument variability did not exceed 5% at either speed. Inter-batch ICCs ranged from 0.87 to 0.98 for fast and from 0.71 to 0.99 for medium. The angle test results corresponded closely to those predicted theoretically, with a loss in mean score of only 6% when the monitor was tilted from 0 degrees to 15 degrees. CONCLUSION: the CSA monitor provides a precise tool for measuring changes in acceleration in laboratory settings. Technically, the device performs well, and is likely to prove a useful tool in the assessment of physical activity in children and adults.

For more than a decade, the fetal programming hypothesis has taught that insulin resistance and its associated metabolic disturbances result from poor gestational environment, for which low birth weight is a surrogate. Low birth weight, however, is now uncommon in industrialized societies. We have investigated the relevance of birth weight, "catch-up" weight, and current weight to insulin resistance in 300 contemporary British children. Insulin resistance at 5 years was not related to birth weight but was correlated with current weight and weight catch-up in both sexes, more strongly so in girls (r = 0.33, P < 0.001 vs. r = 0.18, P = 0.03), who were intrinsically more insulin-resistant than boys. Weight change merely co-correlated with current weight (r = 0.67, P < 0.01 in both sexes) and did not improve on the prediction of insulin resistance. Most important, insulin resistance at 5 years was the same in children of heavier birth weight, whose weight SD score had not changed, as in those of lighter birth weight, matched for current weight, who had experienced so-called catch-up (boys 0.89 and 0.88 units, respectively, P = 0.96; girls 1.26 and 1.13 units, P = 0.41). Insulin resistance in contemporary children seems to be a function of excess current weight rather than of low birth weight or change in weight.