Awareness of body weight by mothers and their children: repeated measures in a single cohort (EarlyBird 64).

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.

Body fat in children does not adversely influence bone development: a 7-year longitudinal study (EarlyBird 18).

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 < 0.001). Greater BF was associated with higher aBMD and BA in girls (P < 0.001), but only BA in boys (P < 0.001). The extra aBMD associated with increased BF was greater in older girls. The rise in aBMD and BA was associated with earlier puberty in both genders (P < 0.001). The impact of BF on aBMD was greater in later puberty in girls (0.0025 g cm(-2) per 10% BF at 10 years versus 0.016 g cm(-2) per 10% BF at 14 years, P < 0.001). CONCLUSION: Greater BF is associated with larger bones, but also denser bones in girls. The effects of fat and puberty are complex and gender specific, but BF of contemporary UK children does not appear to be deleterious to bone quality.

Differences in body composition and metabolic status between white U.K. and Asian Indian children (EarlyBird 24 and the Pune Maternal Nutrition Study).

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 < 0.001), waist circumference (P < 0.001) and skin-fold thickness (P < 0.001) than white U.K. children, yet their % body fat was higher (boys +4.5%, P < 0.001, girls: +0.5%, P = 0.61). Independently of the differences in age and % body fat, the Indian children had higher fasting glucose (boys +0.52 mmol L(-1) , girls +0.39 mmol L(-1) , both P < 0.001), higher insulin (boys +1.69, girls +1.87 mU L(-1) , both P < 0.01) and were more insulin resistant (boys +0.25, girls +0.28 HOMA-IR units, both P < 0.001). CONCLUSIONS: The 'thin-fat' phenotype observed in Indian babies is also apparent in pre-pubertal Indian children who have greater adiposity than white U.K. children despite significantly lower BMIs. Indian children are more insulin resistant than white U.K. children, even after adjustment for adiposity.

The contribution of parental BMI to the metabolic health of their offspring: a longitudinal cohort study (EarlyBird 55).

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 < 0.001). Accordingly, there were large and significant differences in the metabolic z-score between children categorized as normal weight or overweight/obese. At 13 years, for example, the metabolic z score of the overweight/obese girls was 14-fold greater than that of the normal-weight girls (P < 0.001). However, parental BMI and metabolic status had little effect on these differences. Indeed, mixed effects modelling showed that, as the child's BMI increased, so the influence of parental factors became less relevant. Time-lag analyses confirmed that weight gain preceded metabolic disturbances in the children. CONCLUSION: The impact of obesity on the metabolic health of contemporary children is a function of their own weight gain, rather than that of their parents, and is therefore potentially preventable.

The convergence of type 1 and type 2 diabetes in childhood: the accelerator hypothesis.

It seems likely that type 1 and type 2 diabetes lie at different points of the same spectrum, separated by the misunderstanding that one belongs to childhood and the other to adulthood. The spectrum is that of tempo--the rate at which beta cell function is lost over time. A combination of beta cell up-regulation (insulin demand, largely determined by obesity) and the genetically-determined immune response to it ('autoimmunity') determines tempo, ranging from slow to fast with every variant in between. There is good evidence that people who go on to develop type 1 (fast) diabetes are, like those who develop type 2 (slow diabetes), insulin resistant, and overwhelming evidence that body mass plays a key role. The prevention of type 1 diabetes may lie in weight restriction from an early age.

Can we modulate physical activity in children? No.

Intuition tells us that physical activity is central to weight reduction in obese children. Evidence, on the other hand, suggests that increases in physical activity are difficult to achieve in the short term, and may not be possible in the long term. One explanation could be an 'activitystat', a feedback loop in the child's brain that controls physical activity according to a set point. This brief article, which argues that it may not be possible to modulate the activity of children, reviews the principles of feedback control as they apply to physical activity, discusses evidence for its central control, and demonstrates how a physical activity control loop might operate to defend the set point. Studies restricted to objective measurement suggest that the physical activity of children varies in a systematic, rather than random manner. It varies little from environment to environment, from year to year or from place to place. Where children undertake more activity at one time of day, they appear to compensate at another. Systematic variation of this kind implies control, and the control of physical activity appears to lie with the child, not with his environment. Perturbation (temporary change in response to disturbance) during short-term physical activity interventions may be mistaken for modulation (permanent change in set point), a fundamentally different response. Perturbation lasts no longer than the disturbance that causes it, and there is little evidence that interventions raise activity long term, if at all.

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.

BMI was right all along: taller children really are fatter (implications of making childhood BMI independent of height) EarlyBird 48.

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<0.05). BMI and FMI explained ~20% more of the variation in %fat, ~15% more in leptin and ~10% more in insulin resistance than the respective Ht-independent reformulations (BM/Ht(3.5) and FM/Ht(7), both p<0.001). CONCLUSION: Taller children really are fatter than their shorter peers, have higher leptin levels and are more insulin resistant. Attempts to render indices of BM or FM independent of Ht in children seem inappropriate if the object of the index is to convey health risk.

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.

Reliability of energy expenditure prediction equations in the weight management clinic.

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 <25, on whom the equations were based. The estimated REE by Schofield for an individual of BMI 35 kg m(-2), for example, could lie anywhere from 2.78 MJ (661 kcal) above the indirect calorimetry value to 2.59 MJ (618) kcal below it. CONCLUSIONS: Prediction equations offer a quick assessment of energy needs for hypocaloric diets although, in reality, they run the random risk of excessive restriction or further weight gain.

The accelerator hypothesis: a review of the evidence for insulin resistance as the basis for type I as well as type II diabetes.

Although some 40 years have passed since type I diabetes was first defined, its cause remains unknown. The autoimmunity paradigm of immune dysregulation has not offered an explanation for its rising incidence, nor means of preventing it, and there is arguably good reason to consider alternatives. The accelerator hypothesis is a singular, unifying concept that argues that type I and type II diabetes are the same disorder of insulin resistance, set against different genetic backgrounds. The hypothesis does not deny the role of autoimmuniy, only its primacy in the process. It distinguishes type I and type II diabetes only by tempo, the faster tempo reflecting the more susceptible genotype and (inevitably) earlier presentation. Insulin resistance is closely related to the rise in overweight and obesity, a trend that the hypothesis deems central to the rising incidence of all diabetes in the developed and developing world. Rather than overlap between the two types of diabetes, the accelerator hypothesis envisages overlay-each a subset of the general population differing from each other only by genotype. Indeed, it views type I and type II diabetes as a continuum, where the infinitely variable interaction between insulin resistance and genetic response determines the age at which beta-cell loss becomes critical. Adult diabetes is not viewed as an entity, but rather as diabetes presenting in adulthood. Childhood diabetes, similarly, is diabetes presenting in childhood. The increasing incidence of both is primarily the result of lifestyle change and the rise in body weight that has resulted.

Assortative weight gain in mother-daughter and father-son pairs: an emerging source of childhood obesity. Longitudinal study of trios (EarlyBird 43).

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<0.004), and among the sons grouped according to their fathers' BMI (effect size 1.28 SDS), but not their daughters (effect size 0.17, gender interaction P=0.02). Children whose same-sex parents were of normal weight, weighed either close to (girls+0.20 BMI-SDS) or less than (boys,-0.34 BMI-SDS) children of 20 years ago, and did not change from 5 to 8 years. In contrast, the risks of obesity at 8 years were 10-fold greater (girls 41%, P<0.001) or sixfold greater (boys 18%, P<0.05) if the same-sex parent was obese. Longitudinal linear mixed effects (multilevel) modelling showed a marked influence of maternal and paternal BMI on the rate of weight gain, which was unaffected by birth weight of the child. We report perhaps the largest effect sizes so far recorded in childhood obesity. CONCLUSIONS: Childhood obesity today seems to be largely confined to those whose same-sex parents are obese, and the link does not seem to be genetic. Parental obesity, like smoking, might be targeted in the interests of the child.

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 (> 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<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.

Children from low-income families have less access to sports facilities, but are no less physically active: cross-sectional study (EarlyBird 35).

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.

Changing perspectives in diabetes: their impact on its classification.

Type 1 and type 2 diabetes are usually regarded as distinct disorders, but the convergence of their phenotypes over recent years, the relationship of body weight to the risk of type 1 diabetes, the diminishing importance of the type 1 susceptibility genes and the finding of autoantibodies in patients with type 2 diabetes, invite a different interpretation. The possibility that type 1 and type 2 diabetes, rather than being different, are merely poles of a single spectrum, where variation in the tempo of beta cell loss determines age at onset and symptoms at presentation, has important implications. Correct classification is crucial because it directs appropriate treatment and, where available, prevention. This article argues that type 1 diabetes is currently misclassified, provides evidence that insulin resistance drives type 1 diabetes as it does type 2, and proposes how the 'accelerator hypothesis' can be tested in a randomised controlled trial, which could demonstrate, for the first time, the safe and effective prevention of type 1 diabetes.

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.