To follow and predict the evolution of adiposity during growth, individual adiposity curves, assessed by the weight/height2 index, were drawn for 151 children from the age of 1 month to 16 yr. Adiposity increases during the 1st yr and then decreases. A renewed rise, termed here the adiposity rebound, occurs at about 6 yr. Individual weight/height2 curves may differ regarding their percentile range level and age at adiposity rebound. The present study shows a relationship between the age at adiposity rebound and final adiposity. An early rebound (before 5.5 yr) is followed by a significantly higher adiposity level than a later rebound (after 7 yr). This phenomenon is observed whatever the subject's adiposity at 1 yr. The present observations might be connected with the cellularity of adipose tissue.

Until quite recently, there has been a widespread belief in the popular media and scientific literature that the prevalence of childhood obesity is rapidly increasing. However, high quality evidence has emerged from several countries suggesting that the rise in the prevalence has slowed appreciably, or even plateaued. This review brings together such data from nine countries (Australia, China, England, France, Netherlands, New Zealand, Sweden, Switzerland and USA), with data from 467,294 children aged 2-19 years. The mean unweighted rate of change in prevalence of overweight and obesity was +0.00 (0.49)% per year across all age ×sex groups and all countries between 1995 and 2008. For overweight alone, the figure was +0.01 (0.56)%, and for obesity alone -0.01 (0.24)%. Rates of change differed by sex, age, socioeconomic status and ethnicity. While the prevalence of overweight and obesity appears to be stabilizing at different levels in different countries, it remains high, and a significant public health issue. Possible reasons for the apparent flattening are hypothesised.

Childhood obesity is an important public health problem, with a rapidly increasing frequency worldwide. Identification of critical periods for the development of childhood and adolescent obesity could be very useful for targeting prevention measures. Weight status in early childhood is a poor predictor of adult adiposity status, and most obese adults were not obese as children. We first proposed to use the body mass index (BMI) charts to monitor individual BMI development. The adiposity rebound (AR) corresponds to the second rise in BMI curve that occurs between ages 5 and 7 years. It is not as direct a measure as BMI at any age, but because it involves the examination of several points during growth, and because it is identified at a time when adiposity level clearly change directions, this method provides information that can help us understand individual changes and the development of health risks. An early AR is associated with an increased risk of overweight. It is inversely associated with bone age, and reflects accelerated growth. The early AR recorded in most obese subjects and the striking difference in the mean age at AR between obese subjects (3 years) and non-obese subjects (6 years) suggest that factors have operated very early in life. The typical pattern associated with an early AR is a low BMI followed by increased BMI level after the rebound. This pattern is recorded in children of recent generations as compared to those of previous generations. This is owing to the trend of a steeper increase of height as compared to weight in the first years of life. This typical BMI pattern (low, followed by high body fatness level) is associated with metabolic diseases such as diabetes and coronary heart diseases. Low body fatness before the AR suggests that an energy deficit had occurred at an early stage of growth. It can be attributable to the high-protein, low-fat diet fed to infants at a time of high energy needs, the former triggering height velocity and the latter decreasing the energy density of the diet and then reducing energy intake. The high-fat, low-protein content of human milk may contribute to its beneficial effects on growth processes. Early (pre-and postnatal) life is a critical period during which environmental factors may programme adaptive mechanisms that will persist in adulthood. Under-nutrition in fetal life or during the first years after birth may programme a thrifty metabolism that will exert adverse effects later in life, especially if the growing child is exposed to overnutrition. These observations stress the importance of an adequate nutritional status in childhood and the necessity to provide nutritional intakes adapted to nutritional needs at various stages of growth. Because the AR reflects particular BMI patterns, it is a useful tool for the paediatrician to monitor the child's adiposity development and for researchers to investigate the different developmental patterns leading to overweight. It contributes to the understanding of chronic disease programming and suggests ne...

Diet can affect cognitive ability and behaviour in children and adolescents. Nutrient composition and meal pattern can exert immediate or long-term, beneficial or adverse effects. Beneficial effects mainly result from the correction of poor nutritional status. For example, thiamin treatment reverses aggressiveness in thiamin-deficient adolescents. Deleterious behavioural effects have been suggested; for example, sucrose and additives were once suspected to induce hyperactivity, but these effects have not been confirmed by rigorous investigations. In spite of potent biological mechanisms that protect brain activity from disruption, some cognitive functions appear sensitive to short-term variations of fuel (glucose) availability in certain brain areas. A glucose load, for example, acutely facilitates mental performance, particularly on demanding, long-duration tasks. The mechanism of this often described effect is not entirely clear. One aspect of diet that has elicited much research in young people is the intake/omission of breakfast. This has obvious relevance to school performance. While effects are inconsistent in well-nourished children, breakfast omission deteriorates mental performance in malnourished children. Even intelligence scores can be improved by micronutrient supplementation in children and adolescents with very poor dietary status. Overall, the literature suggests that good regular dietary habits are the best way to ensure optimal mental and behavioural performance at all times. Then, it remains controversial whether additional benefit can be gained from acute dietary manipulations. In contrast, children and adolescents with poor nutritional status are exposed to alterations of mental and/or behavioural functions that can be corrected, to a certain extent, by dietary measures.

Several epidemiological studies have observed an inverse relationship between people's habitual frequency of eating and body weight, leading to the suggestion that a 'nibbling' meal pattern may help in the avoidance of obesity. A review of all pertinent studies shows that, although many fail to find any significant relationship, the relationship is consistently inverse in those that do observe a relationship. However, this finding is highly vulnerable to the probable confounding effects of post hoe changes in dietary patterns as a consequence of weight gain and to dietary under-reporting which undoubtedly invalidates some of the studies. We conclude that the epidemiological evidence is at best very weak, and almost certainly represents an artefact. A detailed review of the possible mechanistic explanations for a metabolic advantage of nibbling meal patterns failed to reveal significant benefits in respect of energy expenditure. Although some short-term studies suggest that the thermic effect of feeding is higher when an isoenergetic test load is divided into multiple small meals, other studies refute this, and most are neutral. More importantly, studies using whole-body calorimetry and doubly-labelled water to assess total 24h energy expenditure find no difference between nibbling and gorging. Finally, with the exception of a single study, there is no evidence that weight loss on hypoenergetic regimens is altered by meal frequency. We conclude that any effects of meal pattern on the regulation of body weight are liely to be mediated through effects on the food intake side of the energy balance equation. Meal frequency: Nibbling: Gorging: Energy balanceThe present paper reviews the epidemiological studies relating meal frequency to body weight, and attempts to integrate these with the results of physiological investigations on meal frequency and energy metabolism. The paper will focus exclusively on human subjects because, although there is a considerable literature describing the metabolic effects of differing meal patterns in experimental animals (Fabry & Tepperman, 1970;Adams & Morgan, 1981; Bellisle, 1995), there are important ecological differences between the natural feeding patterns of species, and because the human experimental data are adequate to answer the key questions relating to the efficiency of energy utilization in this context. EPIDEMIOLOGICAL ASSOCIATIONS BETWEEN HABITUAL MEAL FREQUENCY AND BODY WEIGHTThe extensive work of Fabry and co-workers (Fabry et al. , 1966Hejda & Fabry, 1964) was the first to demonstrate strong and reproducible inverse relationships between habitual meal frequency and body weight in human subjects. Results from their first large sample study involving 379 Czechoslovakian men aged 60-64 years are illustrated in Fig. 1. Both the proportion of overweight subjects and mean skinfold thicknesses were significantly inversely related to meal frequency. Similar trends were observed in a smaller sample of eighty-nine men aged 30-50 years (Hejda 8z .

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Human desire for sweet taste spans all ages, races, and cultures. Throughout evolution, sweetness has had a role in human nutrition, helping to orient feeding behavior toward foods providing both energy and essential nutrients. Infants and young children in particular base many of their food choices on familiarity and sweet taste. The low cost and ready availability of energy-containing sweeteners in the food supply has led to concerns that the rising consumption of added sugars is the driving force behind the obesity epidemic. Low-calorie sweeteners are one option for maintaining sweet taste while reducing the energy content of children’s diets. However, their use has led to further concerns that dissociating sweetness from energy may disrupt the balance between taste response, appetite, and consumption patterns, especially during development. Further studies, preferably based on longitudinal cohorts, are needed to clarify the developmental trajectory of taste responses to low-calorie sweeteners and their potential impact on the diet quality of children and youth.

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