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 analysisIntervention 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). ConclusionsThis 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. IntroductionPhysical activity is associated with many health benefits, 1-3 but most children fail to meet national recommendations. [4][5][6] Prevention of obesity in particular is thought to be one of the benefits to being more active, and accordingly most interventions aimed at reducing childhood obesity incorporate a physical activity component. Observational studies consistently show that greater activity is associated (r~−0.2) with lower body mass index and girth, 7-11 yet physical activity int...

Diabetes is currently of two types. Type I (insulin-dependent) diabetes mellitus is an autoimmune disorder of childhood, characterised by acute onset, ketoacidosis and insulin dependency. Type II diabetes is a metabolic disorder of middle-life, slow in onset and non-insulin-dependent.The definitions need urgent revision. More than half of the patients with Type I diabetes present in adulthood, when their onset is slow and many do not develop acidosis or require insulin for many years [1]. Type II diabetes occurs in teenagers [2], sometimes with keto-acidosis [3], and insulin-dependency frequently ensues given time. Clinically, there is little other than tempo to distinguish two types of diabetes. The HypothesisThe`Accelerator Hypothesis' argues that Type I and Type II diabetes are one and the same, distinguishable only by their rate of beta cell loss and the accelerators responsible. The first accelerator, a constitutionally (intrinsically) high rate of beta-cell apoptosis, is necessary for diabetes to develop but in itself rarely Diabetologia (2001) AbstractBlood glucose concentrations are controlled by a loop incorporating two components, the beta cells which secrete insulin and the insulin-sensitive tissues (liver, muscle, adipose) which respond to it. Loss of blood glucose control might result from failure of the beta cells to secrete insulin, resistance of the tissues to its action, or a combination of both. The distinctions between Type I (insulin-dependent) and Type II (non-insulin-dependent) diabetes mellitus are becoming increasingly blurred both clinically and aetiologically, where beta-cell insufficiency is the shared characteristic. The`Accelerator Hypothesis' identifies three processes which variably accelerate the loss of beta cells through apoptosis: constitution, insulin resistance and autoimmunity.None of the accelerators leads to diabetes without excess weight gain, a trend which the`Accelerator Hypothesis' deems central to the rising incidence of both types of diabetes in the industrially developed world. Weight gain causes an increase in insulin resistance, which results in the weakening of glucose control. The rising blood glucose (glucotoxicity) accelerates beta-cell apoptosis directly in all and, by inducing beta-cell immunogens, further accelerates it in a subset genetically predisposed to autoimmunity. Rather than overlap between two types of diabetes, the`Accelerator Hypothesis' envisages overlay. Body mass is central to the development and rising incidence of all diabetes. Only tempo distinguishes the`types'. The control of weight gain, and with it insulin resistance, could be the means of minimising both.

This randomized, double-masked, placebo-controlled trial evaluated the safety, tolerability and effects on bone mineral density (BMD) of alendronate in a large, multinational population of postmenopausal women with low bone mass. At 153 centers in 34 countries, 1908 otherwise healthy, postmenopausal women with lumbar spine BMD 2 standard deviations or more below the premenopausal adult mean were randomly assigned to receive oral alendronate 10 mg (n = 950) or placebo (n = 958) once daily for 1 year. All patients received 500 mg elemental calcium daily. Baseline characteristics of patients in the two treatment groups were similar. At 12 months, mean increases in BMD were significantly (p

Obesity is a serious public health concern. More than half of British adults are overweight, and obesity among preschool children has increased by an alarming 70% in the past generation.1 2 We aimed to explore parents' awareness of overweight and obesity in themselves and their children, and their degree of concern about weight. Participants, methods, and resultsWe studied 277 healthy randomly recruited children (mean age 7.4 years) and parents from the EarlyBird study.3 Overweight and obesity were defined as body mass index at least 25 and 30 in adults, and at least 91st and 98th centiles of the UK 1990 body mass index reference curves for children. 4 Before we weighed them, parents completed a written questionnaire asking them to estimate their own and their child's weight on a five point scale ranging from "very underweight" to "very overweight." Responses indicating level of concern about weight were similarly ranked from "very worried about underweight" to "very worried about overweight."Children and parents were significantly heavier than UK norms (table): 52/277 (19%) children, 141/273 (52%) mothers, and 165/230 (72%) fathers were overweight (including obese). Among overweight parents, 40% mothers (45% fathers) judged their own weight "about right" and 27% (61%) were unconcerned about their weight.Only a quarter of parents recognised overweight in their child. Even when obese, 33% mothers (57% fathers) saw their child's weight as "about right." Parents were less likely to identify overweight in sons than daughters: only 27% of overweight or obese boys were classified as at least "a little overweight," compared with 54% of overweight girls (P = 0.01). More mothers than fathers correctly assessed their child's weight (84% v 76%, P = 0.06).Maternal weight status did not affect mothers' awareness of their chidren's weight: 82% of overweight mothers were correct compared with 82% of normal weight mothers (P = 0.50). However, only 74% overweight fathers were correct compared with 85% normal weight fathers (P = 0.08).More than half of the parents of obese children expressed some degree of concern about their child's weight, but only a quarter were even "a little worried" if their child was overweight. Most parents (86%) who were unaware that their child was overweight, were also unconcerned about their child's weight. One in ten parents expressed some concern about underweight in normal weight children.Prevalence of overweight in parents in the highest and lowest socioeconomic groups did not differ-59% in classes I and II were overweight compared with 62% in classes VI, VII, and VIII (P = 0.63; National Statistics Socioeconomic Classification 2001). Neither was there a difference in correct perception of the child's weight between socioeconomic groups (78% v 82%, P = 0.34).

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.

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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 CAPN10, the gene encoding the ubiquitously expressed cysteine protease calpain-10, has been associated with type 2 diabetes in Mexican Americans and in two northern-European populations, from Finland and Germany. We have studied CAPN10 in white subjects of British/Irish ancestry, using both family-based and case-control studies. In 743 sib pairs, there was no evidence of linkage at the CAPN10 locus, which thereby excluded it as a diabetes-susceptibility gene, with an overall sib recurrence risk, lambda(S), of 1.25. We examined four single-nucleotide polymorphisms (SNP-44, -43, -19, and -63) previously either associated with type 2 diabetes or implicated in transcriptional regulation of calpain-10 expression. We did not find any association between SNP-43, -19, and -63, either individually or as part of the previously described risk haplotypes. We did, however, observe significantly increased (P=.033) transmission of the less common C allele at SNP-44, to affected offspring in parents-offspring trios (odds ratio 1.6). An independent U.K. case-control study and a small discordant-sib study did not show significant association individually. In a combined analysis of all U.K. studies (P=.015) and in combination with a Mexican American study (P=.004), the C allele at SNP-44 is associated with type 2 diabetes. Sequencing of the coding region of CAPN10 in a group of U.K. subjects revealed four coding polymorphisms-L34V, T504A, R555C, and V666I. The T504A polymorphism was in perfect linkage disequilibrium with the diabetes-associated C allele at SNP-44, suggesting that the synthesis of a mutant protein and/or altered transcriptional regulation could contribute to diabetes risk. In conclusion, we were not able to replicate the association of the specific calpain-10 alleles identified by Horikawa et al. but suggest that other alleles at this locus may increase type 2 diabetes risk in the U.K. population.