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.

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.

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.

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.

Short stature: does it matter? A review of the evidence.

Short stature is widely regarded to be a liability, but despite the importance commonly ascribed to the psychological impact of physique, there is a paucity of methodologically sound research on the topic. The question of growth hormone therapy for a short, but otherwise normal child is still controversial. The justification for such treatment will depend not only on whether a marked improvement in height can be achieved but also on whether short stature can be shown to be an appreciable handicap, either in childhood or later in life. There is some evidence, though much is anecdotal, to suggest that the short statured adult is disadvantaged both socially and economically. There are no conclusive data as yet, however, to suggest that short statured children, either before or during early adolescence have significantly lower scores on conventional psychometric testing than children of average stature. Possibly, the problems associated with short stature will only emerge in the older adolescent, but for the present, alternative, less expensive forms of treatment should be considered for those children apparently unable to cope.

Can we measure growth?

Poor installation and maintenance of height measuring equipment is a serious problem in the community. With care, however, height can be measured with sufficient precision (+/- 0.5 cm) to identify unusually short or tall stature. Height velocity, on the other hand, is liable to misinterpretation. It cannot be estimated with sufficient precision to identify abnormal growth in the short term. There is no correlation between two successive 12 month velocities. When a trend towards poor velocity is beyond all doubt then it will be apparent on the height chart alone. In addition, "poor" or "excessive" growth is conditional on the height of the child: short children do not grow at the same rate as tall. A diagnosis of abnormal growth requires long term monitoring and is best seen as a series of height measurements crossing the centiles on the height chart. Given the correct equipment and training, height or length can be measured with a fair degree of precision in the youngest of children. The earlier measurements begin, the sooner an abnormal pattern of growth will become evident. The regular monitoring of height should be standard practice and available to each and every child.

Normal growth in the short normal prepubertal child: the Wessex Growth Study.

OBJECTIVE: The study aimed at defining the normal rate of growth for short, prepubertal children, and comparing their pattern of growth with those of average stature. SETTING: Community based. DESIGN: Observation of an unselected population of 109 very short, normal prepubertal children (< 3rd height centile) and 107 controls matched for age and sex (10th to 90th centile). MAIN OUTCOME MEASURES: Height, velocity, change in height standard deviation score, from 6 to 9 years of age. RESULTS: The absolute mean rate of growth was significantly different between groups--short normal 5.3 cm/year, controls 5.9 cm/year--corresponding to velocities on the 25th and 50th centiles, respectively. The relative growth rates, however, as shown by the changes in height standard deviation score (short normal 0.10 (SD 0.22), controls 0.10 (SD 0.24) did not differ, and each group remained close to its original 3rd and 50th centiles. Two short children showed "catch up" growth after adoption, but, otherwise, the divergence from their original height centile was the same for short normal and control children. No social or biological factors were found to predict growth rate in the short normal children, and only target height in controls. "Normal" velocity is conditional on height. Short normal children do grow more slowly than children of average stature, but they do not necessarily grow more poorly. From 6 to 9 years of age they are no more likely to fall off their height centiles than children of average stature. The value of height monitoring at this age is questioned.

Short normal stature and psychosocial disadvantage: a critical review of the evidence.

Physicians and parents alike are under increasing pressure to identify and to treat short stature, but intervention implies the presence of some pathology, physical or psychological, that can be corrected. Where there is true GH deficiency, the argument for replacement is uncontroversial. It is less compelling where GH 'insufficiency' is diagnosed. In the case of the short, but otherwise normal, child the indications for therapy are even less clear. Short stature, per se, is clearly not a disease, in spite of the perception by some practitioners that the rate of growth of such children is abnormal. Short stature is, however, commonly perceived to be associated with social and psychological disadvantage, yet many of these misperceptions about short stature can be challenged. A critical review of the literature pertaining to the psychosocial correlates of short stature uncovers much flawed evidence. Most importantly, the belief, widely held by paediatricians, that short children are likely to be significantly disadvantaged, has been founded largely on data from clinic-referred samples. In such studies, children with real (or perceived) behavioural or academic problems are likely to be overly represented. Publications arising from such studies, however, inevitably lead to an increase in the demand for treatment both from and for those who previously had no such concern. In contrast, data from a well controlled, prospective population-based study suggest the essential normality of the short normal child. Parents and children alike should be reassured by these findings. In the absence of clear pathology, physical or psychological, GH therapy for short but otherwise normal children must therefore, in most cases, be deemed cosmetic, raising issues as to the ethics of so-called "plastic endocrinology".

Poor growth in school entrants as an index of organic disease: the Wessex growth study.

OBJECTIVE: To establish whether poor height or height velocity, assessed during the year of school entry, might identify children with previously undiagnosed organic disease. DESIGN: Observation of a total population and their case controls. SETTING: Community base. SUBJECTS: All 14,346 children in two health districts entering school during two consecutive years were screened for height by school nurses, and those whose height lay below the 3rd centile according to Tanner and Whitehouse standards (n = 180) were identified. After excluding 32 with known organic disease, five from ethnic minorities, and three who refused to take part, the remaining 140 short normal children were matched with 140 age and sex matched controls of average height (10th-90th centile) and their height velocities over 12 months measured. MAIN OUTCOME MEASURES: Height, height velocity, previously diagnosed organic disease, and organic disease diagnosed as a result of blood tests and specialist examination. RESULTS: Twenty five of the 180 short children (14%) were already known to have chronic organic disease which could explain their poor growth. Blood tests and specialist examination revealed a further seven with organic disease, which was acquired rather than congenital in three, and a second cause of short stature in one with known organic disease. These eight conditions had been missed at the school entry medical examination. The shorter the child, the more likely an underlying organic disorder, with seven of the 12 children whose heights were more than 3 standard deviations below the mean having some organic disease. Height velocity measured over 12 months, however, did not distinguish short normal children from those with disease or from their matched controls. CONCLUSIONS: Height, but not height velocity, is a useful index for identifying unrecognised organic disease at school entry. The shorter the stature the greater the prevalence of organic disease. The frequency of newly diagnosed remediable disease in this study (1 in 3-4000) is similar to that of neonatal hypothyroidism, which is routinely screened for. Routine investigation of all very short school entrants is recommended.

Are short normal children at a disadvantage? The Wessex growth study.

OBJECTIVE: To examine whether short stature through childhood represents a disadvantage at around 12 years. DESIGN: Longitudinal non-intervention study of the physical and psychological development of children recruited from the community in 1986-7 after entry into primary school at age 5-6 years; this is the second psychometric assessment made in 1994-5 after entry into secondary school at age 11-13 years. SETTING: Southampton and Winchester health districts. SUBJECTS: 106 short normal children (< 3rd centile for height when recruited) and 119 controls of average stature (10th-90th centile). MAIN OUTCOME MEASURES: Psychometric measures of cognitive development, self concept development, behaviour, and locus of control. RESULTS: The short children did not differ significantly from the control children on measures of self esteem (19.4 v 20.2), self perception (104.2 v 102.4), parents' perception (46.9 v 47.0), or behaviour (6.8 v 5.3). The short children achieved significantly lower scores on measures of intelligence quotient (IQ) (102.6 v 108.6; P < 0.005), reading attainment (44.3 v 47.9; P < 0.002), and basic number skills (40.2 v 43.5; P < 0.003) and displayed less internalisation of control (16.6 v 14.3; P < 0.001) and less satisfaction with their height (P < 0.0001). More short than control children, however, came from working class homes (P < 0.05). Social class was a better predictor than height of all measures except that of body satisfaction. Attainment scores were predicted by class and IQ together rather than by height. Height accounted for some of the variance in IQ and locus of control scores. CONCLUSIONS: These results provide only limited support for the hypothesis that short children are disadvantaged, at least up until 11-13 years old. Social class seems to have more influence than height on children's psychological development.

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.

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.

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.