Brad S. Metcalf

Effectiveness of intervention on physical activity of children: systematic review and meta-analysis of controlled trials with objectively measured outcomes (EarlyBird 54)

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<0.01) and small for moderate or vigorous activity (0.16, 0.08 to 0.24; P<0.001). Meta-regression indicated that the pooled intervention effect did not differ significantly between any of the subgroups (for example, for total physical activity, standardised mean differences were 0.07 for age <10 years and 0.16 for ≥10 years, P=0.19; 0.07 for body mass index across the entire range and 0.22 for exclusively overweight/obese children, P=0.07; 0.12 for study duration ≤6 months and 0.09 for >6 months, P=0.71; 0.15 for home/family based intervention and 0.10 for school based intervention, P=0.53; and 0.09 for higher quality studies and 0.14 for lower quality studies, P=0.52). Conclusions This review provides strong evidence that physical activity interventions have had only a small effect (approximately 4 minutes more walking or running per day) on children’s overall activity levels. This finding may explain, in part, why such interventions have had limited success in reducing the body mass index or body fat of children.

Contribution of Early Weight Gain to Childhood Overweight and Metabolic Health: A Longitudinal Study (EarlyBird 36)

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 (Δ 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 Δ weight SD score (0–5 years old) contributed (girls/boys) 11.2%/7.0% to the score, and adding Δ 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 Δ 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.

Fatness leads to inactivity, but inactivity does not lead to fatness: a longitudinal study in children (EarlyBird 45)

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.

Variation in physical activity lies with the child, not his environment: evidence for an 'activitystat' in young children (EarlyBird 16)

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 <0.3%) as that recorded independently in Glasgow, 800 km away. Total daily activity was unrelated to time reportedly spent watching TV.Interpretation:The correlations within groups and the similarities between them suggest that physical activity in children is under central biological regulation. There are implications both for public health planners and for the potentially novel signalling pathways involved.

A Common Haplotype of the Glucokinase Gene Alters Fasting Glucose and Birth Weight: Association in Six Studies and Population-Genetics Analyses

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.

Contribution of timetabled physical education to total physical activity in primary school children: cross sectional study.

A recent survey of children at primary schools in England found a marked decline in timetabled physical education between 1994 and 1999.1 Sport England expressed concern about the impact of competing priorities, such as numeracy and literacy, on curricular physical education and concluded that children from poorer backgrounds would be worst affected. We used accelerometers to measure the impact of timetabled physical education at school on overall physical activity in children. We monitored physical activity during waking hours for seven days using accelerometers (Manufacturing Technology, Fort Walton Beach, FL2) in 215 children (120 boys and 95 girls aged 7.0-10.5 (mean 9.0) years) from three schools with different sporting facilities and opportunity for physical education in the curriculum. School 1, a private preparatory school with some boarding pupils, had extensive facilities and 9.0 hours a week of physical education in the curriculum. School 2, a village school awarded Activemark gold status …

Physical activity at the government-recommended level and obesity-related health outcomes: a longitudinal study (Early Bird 37)

Background: In the UK and USA, government guidelines for childhood physical activity have been set (⩾60 min/day at ⩾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<0.01). Mixed effects modelling showed that the improvement in metabolic score among the more active compared to the less active children was linear with time (−0.08 z scores/year, p = 0.001). Conclusions: In children, physical activity above the government-recommended intensity of 3 METs is associated with a progressive improvement in metabolic health but not with a change in BMI or fatness. Girls habitually undertake less physical activity than boys, questioning whether girls in particular should be encouraged to do more, or the recommendations adjusted for girls.

Age Before Stage: Insulin Resistance Rises Before the Onset of Puberty: A 9-year longitudinal study (EarlyBird 26)

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.

The impact of school-time activity on total physical activity: the activitystat hypothesis (EarlyBird 46).

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.

Adiponectin in childhood

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, adiponectins role as a predictor of metabolic dysfunction in healthy, normal-weight youngsters is less clear.