What is in the best interests of a child, and could that ever include interventions that we might regard as prima facie detrimental to a child’s physical well-being? This question is raised a fortiori by growth attenuation treatments in children with severe neurological disorders causing extreme developmental delay. I argue that two principles that provide guidance in generating a conception of best interests for each individual child yield the right results in such cases. The principles are as follows: the potentiality principle, whereby every child should be able to develop its potential and is entitled to receive certain help in doing so, and the principle of psychosomatic harmony, whereby every human being is entitled to treatment that is appropriate to or enables a life in which mind and body are in tune with each other. These principles indicate a certain response to what we can call Ashley-type cases and admit certain caveats.

The high prevalence of obesity is a major public health issue and contributes to the ‘double burden’ of disease in developing countries. Early exposure to poor nutrition may cause metabolic adaptations that, when accompanied by exposure to ‘affluent’ nutrition, may increase the risk for obesity and other metabolic disorders. The aim of this study was to determine differences in energy metabolism and nutritional status between normal-height and growth-retarded North Korean children living in South Korea. A total of 29 children were recruited and underwent measurements of resting energy expenditure (REE), respiratory quotient (RQ), anthropometrics and dietary intake. There was no difference in REE or any assessment of obesity between the growth-retarded and normal-height children. Children who were classified as growth retarded (HAZ<−1.0) or stunted (HAZ<−2.0) had a significantly higher RQ (β=0.036 or 0.060, respectively, P=0.018 or 0.016), independent of sex, age, fat-free mass, fat mass and food quotient, compared with children with normal height. The results from this study, the first from an Asian population, add to the growing body of literature suggesting that undernutrition early in life results in adaptations in energy metabolism that favor fat deposition, increasing the risk of stunted children becoming overweight or obese later in life. Continued research on this topic is warranted, given the continued rise in the prevalence of the double burden in transitional countries.

We have reported that blood pressure was elevated in 3-month-old rats whose mothers were Fe-restricted during pregnancy. These animals also had improved glucose tolerance and decreased serum triacylglycerol. The aim of the present study was to determine whether these effects of maternal nutritional restriction, present in these animals at 3 months of age, can be observed in the same animals in later life. Pulmonary and serum angiotensin converting enzyme (ACE) concentrations were also measured to investigate whether the renin–angiotensin system was involved in the elevation of blood pressure observed in the offspring of Fe-restricted dams. Systolic blood pressure was higher in the offspring of Fe-restricted dams at 16 months of age. Heart and kidney weight were increased as a proportion of body weight in the offspring of Fe-restricted dams. The pulmonary ACE concentration was not significantly different between the groups. The serum ACE concentration was significantly elevated in the offspring of Fe-restricted dams at 3 but not 14 months of age. There was a strong correlation between serum ACE levels at 3 and 14 months of age. Glucose tolerance and serum insulin were not different between the maternal diet groups. Serum triacylglycerol tended to be lower in the offspring of Fe-restricted dams. There were no differences in serum non-esterified fatty acids or serum cholesterol between the maternal diet groups. This study provides further evidence that maternal nutrition has effects on the offspring that persist throughout life. At 16 months of age, the elevation of blood pressure in Fe-restricted offspring does not appear to be mediated via changes in ACE levels. Both cardiac hypertrophy and decreased serum triacylglycerol have also been observed in Fe-restricted fetuses, suggesting that these changes may be initiated in utero.

To examine the possibility that there is an early sensitive period for the effects of malnutrition on cognitive development, three groups of children (N = 197) were recruited from a birth cohort with known growth characteristics in south-west Ethiopia (N = 1563). All had initial weights [ges ]2500g. Early growth falterers dropped in weight below the third centile (z<−1·88) of the NCHS/WHO reference population in the first 4 months. Late growth falterers were children not in the first group whose weights were below the third centile at 10 and 12 months. Controls were a stratified random sample with weights above the third centile throughout the first year. All children were tested blind at 2 years using the Bayley Scales of Infant Development, adapted for use in Ethiopia. Mean (SD) scores on the psychomotor scale were 10·2 (3·7) in the controls, 6·6(4·2) in the early growth falterers, and 8·5(4·3) in the late growth falterers. For the mental scale they were 28·9(5·8), 22·6(6·2), and 26·6(6·1) respectively. Both overall differences were statistically significant at p<·001, and planned comparisons between the control and the combined growth faltering groups, and between the early and later growth faltering groups, showed that each difference was statistically significant for both scales. However, early weight faltering was associated with weight at the time of testing (r = .33), which was associated with scores both on the psychomotor (r = .53) and the mental scale (r = .49). After taking weight at the time of testing into account there was no additional effect attributable to the timing of growth faltering. In this population, therefore, early malnutrition does not have specific adverse effect beyond the contribution that it makes to enduring malnutrition over the first 2 years.

The developmental sequelae of infant failure to thrive (FTT) were examined in an unreferred group of 6-year-olds with a history of severe nonorganic growth retardation, sampled from a 1-year birth cohort in an inner-city area of South London. Children who failed to thrive in infancy (weight below the third centile for at least 3 months) and their pairwise matched comparisons were originally studied at 15 months, and 42 cases and 42 controls (89.5% of the sample) were followed up. At 6 years, previously growth-retarded children were considerably smaller than matched comparisons, in terms of body mass index (BMI), and height and weight for age z scores. History of FTT explained substantial variance in weight and BMI at 6 years, with maternal height also contributing to variation in height for age. Child cognitive functioning at 6 years was examined using the McCarthy Scales: cases had more limited quantitative and memory skills than comparisons, but there was no intergroup variation in general cognitive performance. In contrast to analyses of physical development, failure to thrive did not account for cognitive functioning; maternal IQ was the sole significant predictor of performance on all indices of child cognitive abilities. At 15 months, earlier growth faltering was linked to limitations in mental development, but these findings were not confirmed by the follow-up data: the timing of FTT was not related to cognitive abilities at 6 years. Results correspond to past research indicating that nonorganic failure to thrive is associated with persistent limitations in physical stature. There was little evidence of cognitive disadvantage for case group children at school age, suggesting that the adverse effects of early malnutrition on cognitive functioning appear to diminish over time.

Recently a type of growth failure (Hyperphagic Short Stature) has been described, in which there is potentially reversible severe impairment of growth hormone secretion, in association with excessively high levels of psychosocial stress. This condition is a variant of the disorder formerly known as Psychosocial Dwarfism. In the present study we compared children with Hyperphagic Short Stature (N=25, aged 9.04 years±3.78, 72% male) and a closely matched sample with normal height, drawn from comparably stressful family circumstances (N=25, aged 10.61±3.04, 60% male). Measures of the psychosocial environment, anthropometry, and developmental history from infancy were obtained. Many symptoms thought previously to be characteristics of psychosocial dwarfism were found to be nonspecific stress responses. Hypotonia (p<.05), enuresis/encopresis (p<.01), and sleep cycle disruption (p<.05) did differentiate the groups. Growth, appetite, and sleep are all influenced by hypothalamic nuclei, suggesting hypothalamic pathology could account for most of the clinical features of Hyperphagic Short Stature.

In order to examine the mechanism whereby stunted children have poor developmental levels, we compared the behaviour of stunted (N=78) and nonstunted (N=26) children aged 12 to 24 months, and examined the relationship of their behaviour to their developmental levels. The effect of nutritional supplementation with or without psychosocial stimulation on the stunted children's behaviour was also examined. The children were observed at home during 4 days over a period of 6 months. The stunted children showed significantly more apathy, and less enthusiasm and variety in exploring, were less happy and more fussy. Caretakers' vocalisations to them were less warm or instructive. Stunted children's activity level, exploratory and happy behaviours were predictive of change in developmental levels measured on the Griffiths Scales, from enrolment to 12 and 24 months later. Supplementation predicted mental age at 12 and 24 months after enrolment, however, it had no significant effect on behaviour.

The effect(s) of finite exposure(s) to 22.0 °C on embryo weight gain, 3rd tarsus length, transfer of lipid from the yolk and uptake of specific lipid components by the liver, were measured in the chick embryo. Embryo growth was completely suspended over the period of temperature reduction, but resumed unimpaired when the optimum temperature of 37.5 °C was restored. Two successive periods of embryonic exposure to 22.0 °C (36 h at d 3 followed by 24 at d 10) were additive in their effect on growth retardation. Embryos subjected to temperature reductions on d 3 of incubation displayed significant changes in lipid concentrations and polyunsaturated fatty acid profiles within the liver when measured at d 18 of incubation. Yolk lipid uptake was significantly reduced but not suspended by embryonic exposure to 22.0 °C. It is suggested that the observed suspension of embryonic development was the result of a temperature dependent reduction in metabolism according to a Q10∼2, which is typical of an ectothermic organism.

Twenty-two twin pregnancies each with one growth-retarded and one normal twin fetus were examined to determine the effects of fetal growth retardation on the maturation of the adrenal gland with respect to cortisol and dehydroepiandrosterone sulphate (DHEAS). The growth-retarded twin fetuses (IUGR) had lower umbilical arterial concentrations of DHEAS than their siblings (IUGR 5.25 ± 2.4; non-IUGR 6.51 ± 2.9 μmol/l; p < 0.01), whereas cortisol concentrations were not statistically different (no labor, IUGR 1,134 ± 751, non-IUGR 1,140 ± 958 μmol/l; labor IUGR 2,062 ± 929, non-IUGR 1,609 ± 469 μmol/l). These data suggest that while the definitive zone of the fetal adrenal is as well-developed as in non-growth-retarded twins, the fetal zone shows reduced secretory capacity of Δ5-steroids. This supports the hypothesis that in growth retardation the adrenal gland shows features of increased maturation.

Sixteen pairs of term discordant twins (weight discrepancy of more than 20% when the, lighter twin was compared to the heavier) were evaluated at birth. Weight, length, head circumference, anterior fontanel area, and combined ossification of the knee epiphyses were measured, and ponderal index (weight/length ratio) calculated. The most severely growth retarded infants had markedly decreased ossification and larger anterior fontanels.

Eleven pairs had physical measurements at one year of age. With individual exceptions, the lighter twins at birth remained smaller in all dimensions. Despite these persistent differences between twin pairs, the values for length at one year of age were within normal limits for both the heavier and lighter twins. Infants without ossification at birth had a greater incremental linear growth by one year than those infants with ossification.