Childhood intelligence and adult obesity

Objective: Recent studies conclude childhood intelligence has no direct effect on adult obesity net of education, but evolutionary psychological theories suggest otherwise. Design and Methods: A population (n = 17,419) of British babies has been followed since birth in 1958 in a prospectively longitudinal study. Childhood general intelligence is measured at 7, 11, and 16, and adult BMI and obesity are measured at 51. Results: Childhood general intelligence has a direct effect on adult BMI, obesity, and weight gain, net of education, earnings, mother's BMI, father's BMI, childhood social class, and sex. More intelligent children grow up to eat more healthy foods and exercise more frequently as adults. Conclusion: Childhood intelligence has a direct effect on adult obesity unmediated by education or earnings. General intelligence decreases BMI only in adulthood when individuals have complete control over what they eat.     

Selective Leptin Insensitivity and Alterations in Female-Reproductive Patterns Linked to Hyperleptinemia during Infancy

The dramatic increase in the prevalence of childhood obesity worldwide makes the investigation of its early developmental stages and effective prevention strategies an urgent issue. CCK₁ deficient OLETF rats are a model of obesity previously used to study the early phases of this disorder. Here, we exposed wild type (LETO) females to an early obesogenic environment and genetically obese OLETF females to a lean postnatal environment, to assess long term alterations in leptin sensitivity, predisposition to diet induced obesity and adult female health. We found that genetically lean females reared by obese mothers presented early postnatal hyperleptemia, selectively reduced response to leptin and sensitivity to diet induced obesity when exposed to a high palatable diet as adults. The estrous cycle structure and intake profile were permanently disrupted, despite presenting normal adiposity/body weight/food intake. Genetically obese females reared by lean dams showed normalized early levels of leptin and reduced body weight, food intake and body fat at adulthood; normalized estrous cycle structure and food intake across the cycle, improved hormonal profile and peripheral leptin sensitivity and a remarkable progress in self-control when exposed to a high fat/palatable diet. Altogether, it appears that the early postnatal environment plays a critical role in determining later life coping with metabolic challenges and has an additive effect on the genetic predisposition that makes OLETF females morbidly obese as adults. This work also links, for the first time, alterations in the leptin system during early development to later life abnormalities related to female reproduction and health.     

Socioeconomic position at different stages of the life course and its influence on body weight and weight gain in adulthood: a longitudinal study with 13-year follow-up

Socioeconomic inequalities in body weight have been demonstrated in numerous cross-sectional studies; however, little research has investigated these inequalities from a life course and longitudinal perspective. We examined the association between child- and adulthood socioeconomic position (SEP) and BMI and overweight/obesity in 1991 (baseline) and changes in BMI and the prevalence of overweight and obesity between 1991 and 2004. Data from the 1991 and 2004 waves of the longitudinal Dutch GLOBE study were used. Participants (n = 1,465) were aged 40-60 years at baseline. BMI was calculated from self-reported height and weight collected by postal questionnaire. Retrospective recall of father's occupation was used as childhood socioeconomic indicator, and adulthood SEP was measured by the occupation of the main income earner of the household. The findings showed that among women, childhood SEP exerted a greater influence on body weight than SEP in adulthood: at baseline, women from disadvantaged backgrounds in childhood had a higher BMI and were more likely to be overweight or obese, and they gained significantly more weight between baseline and follow-up. In contrast, adult SEP had a greater impact than childhood circumstances on men's body weight: those from disadvantaged households had a higher mean BMI and were more likely to be overweight or obese at baseline, and they gained significantly more weight between 1991 and 2004. The findings suggest that exposure to disadvantaged circumstances at critically important periods of the life course is associated with body weight and weight gain in adulthood. Importantly, these etiologically relevant periods differ for men and women, suggesting gender-specific pathways to socioeconomic inequalities in body weight in adulthood.     

Parental care in childhood and obesity in adulthood: a study among twins

The purpose of the study was to examine if parental antipathy and neglect during childhood were associated with obesity in adulthood. From the Danish Twin Registry (DTR) 146 adult same-sexed twin pairs discordant for BMI were identified. Criteria for being discordant were that one of the twins should have a BMI between 20 and 25 kg/m(2) (normal weight) and the co-twin a BMI ≥30 kg/m2 (obesity). In total 236 out of 289 (81.7%) eligible twin individuals participated in an interview and a physical examination. A part of the Childhood Experience of Care and Abuse, the parental care and neglect questionnaire, by Bifulco et al., was used to assess perceived parental antipathy and neglect. Data were analyzed by means of intrapair comparisons. Our results showed that recalled maternal antipathy (P = 0.04) and maternal neglect (P = 0.01) were both associated with adult obesity. Paternal neglect and antipathy were not related with adult obesity. The study demonstrates that experience in childhood maternal antipathy and neglect may contribute to the development of obesity at age 20 and later in adulthood.     

Size at birth, postnatal growth and risk of obesity

Epidemiological studies over the last 15 years have shown that size at birth, early postnatal catch-up growth and excess childhood weight gain are associated with an increased risk of adult cardiovascular disease and type 2 diabetes. At the same time, rising rates of obesity and overweight in children, even at pre-school ages, have shifted efforts towards the identification of very early factors that predict risk of subsequent obesity, which may allow early targeted interventions. Overall, higher birth weight is positively associated with subsequent greater body mass index in childhood and later life; however, the relationship is complex. Higher birth weight is associated with greater subsequent lean mass, rather than fat mass. In contrast, lower birth weight is associated with a subsequent higher ratio of fat mass to lean mass, and greater central fat and insulin resistance. This paradoxical effect of lower birth weight is at least partly explained by the observation that infants who have been growth restrained in utero tend to gain weight more rapidly, or 'catch up', during the early postnatal period, which leads to increased central fat deposition. There is still debate as to whether there are critical early periods for obesity: does excess weight gain during infancy, childhood or even very early neonatal life have a greater impact on long-term fat deposition and insulin resistance? Early identification of childhood obesity risk will be aided by identification of maternal and fetal genes that regulate fetal nutrition and growth, and postnatal genes that regulate appetite, energy expenditure and the partitioning of energy intake into fat or lean tissue growth.     

Neonatal exposure to leptin augments diet-induced obesity in leptin-deficient Ob/Ob mice

Objective: Epidemiological evidence has revealed that undernutrition in utero is closely associated with obesity and related detrimental metabolic sequelae in adulthood. Recently, using a wild‐type (wt) mouse model in which offspring were exposed to intrauterine undernutrition (UN offspring), we reported that the premature leptin surge during neonatal growth promotes lifelong changes in energy regulating circuitry in the hypothalamus, thus playing an important role in the development of pronounced obesity on a high‐fat diet (HFD) in adulthood. Here, we further evaluate the essential involvement of leptin in the developmental origins of obesity using leptin‐deficient ob/ob mice. Methods and Procedures: We assessed the progression of obesity on an HFD in adult leptin‐deficient ob/ob male mice that were exposed to intrauterine undernutrition by maternal food restriction (ob/ob UN offspring) or to leptin treatment during the neonatal period; this treatment is comparable to the premature leptin surge observed in the wt‐UN offspring. Results: On an HFD, the body weight of the male ob/ob UN offspring paralleled that of the ob/ob offspring exposed to normal intrauterine nutrition (ob/ob NN offspring). In contrast, early exposure to leptin in the ob/ob NN offspring during early neonatal growth reproduced the development of pronounced obesity on an HFD in adulthood. Discussion: The presence of leptin and associated energy regulation are indispensable in the acceleration of obesity on an HFD caused by undernutrition in utero. The premature leptin surge plays an essential role in the developmental origins of obesity as a programming signal during the early neonatal period.     

Young adult weight trajectories through midlife by body mass category

Objective : To estimate the expected weight gain through midlife for those in a given BMI category in young adulthood. Design and Methods : Group‐based trajectory modeling and National Longitudinal Survey of Youth 1979 data from 1990 to 2008 were used to quantify weight trajectories through midlife for 10,038 young adult men and women stratified by BMI category. Logistic regression was used to assess the association of trajectory membership with obesity‐related conditions (hypertension, diabetes, arthritis) in middle age. Results : Annual weight gain averaged 0.53 kg (1.17 lb) across the entire sample. However, there was considerable variation by and within BMI categories. More than 98% of men and 92% of women were on upward‐sloping trajectories, generally moving into a higher BMI category by middle age. Those who experienced early and rapid weight gain during young adulthood were most likely to be on a steeper trajectory and had greater risks for obesity‐related conditions. Conclusion : This study points to the health and weight benefits of entering young adulthood with a normal BMI, but further reveals that this is no guarantee of maintaining a healthy weight through midlife. For those who are young adults today, weight maintenance is unlikely to occur without significant environmental or technical innovation.     

Racial Differences in the Tracking of Childhood BMI to Adulthood

Objective: The possibility that there are racial differences in the patterns of BMI (kilograms per meter squared) change throughout life has not been examined. For example, the high prevalence of obesity among black women could result from a higher prevalence of obesity among black girls or because normal‐weight black girls experience larger BMI increases in adolescence or adulthood than do their white counterparts. Therefore, we examined the tracking of childhood BMI into adulthood in a biracial (36% black) sample. Research Methods and Procedures: Five‐ to 14‐year‐old children (2392) were followed for (mean) 17 years. Childhood overweight was defined as BMI ≥ 95th percentile, and adult obesity was defined as BMI ≥ 30 kg/m². Results: The tracking of childhood BMI differed between whites and blacks. Among overweight children, 65% of white girls vs. 84% of black girls became obese adults, and predictive values among boys were 71% (whites) vs. 82% (blacks). These racial differences reflected contrasting patterns in the rate of BMI change. Although the initial BMI of black children was not higher than that of white children, BMI increases with age were larger among black girls and overweight black boys than among their white counterparts. In contrast, relatively thin (BMI < 50th percentile) white boys were more likely to become overweight adults than were their black counterparts. Discussion: These findings emphasize the black/white differences in BMI changes with age. Because of the adult health consequences of childhood‐onset obesity, early prevention should be given additional emphasis.     

Hypothalamic Neuroendocrine Circuitry is Programmed by Maternal Obesity: Interaction with Postnatal Nutritional Environment

Objective

Early life nutrition is critical for the development of hypothalamic neurons involved in energy homeostasis. We previously showed that intrauterine and early postnatal overnutrition programmed hypothalamic neurons expressing the appetite stimulator neuropeptide Y (NPY) and suppressor proopiomelanocortin (POMC) in offspring at weaning. However, the long-term effects of such programming and its interactions with post-weaning high-fat-diet (HFD) consumption are unclear.

Research Design and Methods

Female Sprague Dawley rats were exposed to chow or HFD for 5 weeks before mating, throughout gestation and lactation. On postnatal day 1, litters were adjusted to 3/litter to induce postnatal overnutrition (vs. 12 in control). At postnatal day 20, half of the rats from each maternal group were weaned onto chow or HFD for 15 weeks. Hypothalamic appetite regulators, and fuel (glucose and lipid) metabolic markers were measured.

Results

Offspring from obese dams gained more weight than those from lean dams independent of post-weaning diet. Maternal obesity interacted with post-weaning HFD consumption to cause greater levels of hyperphagia, adiposity, hyperlipidemia, and glucose intolerance in offspring. This was linked to increased hypothalamic NPY signaling and leptin resistance in adult offspring. Litter size reduction had a detrimental impact on insulin and adiponectin, while hypothalamic NPY and POMC mRNA expression were suppressed in the face of normal energy intake and weight gain.

Conclusions

Maternal obesity, postnatal litter size reduction and post-weaning HFD consumption caused obesity via different neuroendocrine mechanims. There were strong additive effects of maternal obesity and post-weaning HFD consumption to increase the metabolic disorders in offspring.     

Fat Feeding of Rats During Pubertal Growth Leads to Neuroendocrine Alterations in Adulthood

Juvenile obesity is a rising epidemic due largely to consumption of caloric dense, fat-enriched foods. Nevertheless, literature on fat-induced neuroendocrine and metabolic disturbances during adolescence, preceding obesity, is limited. This study aimed to examine early events induced by a fat diet (45% calories from saturated fat) in male rats fed the diet during the pre- and post-pubertal period. The neuroendocrine endpoints studied were the levels of circulating leptin, insulin and corticosterone, as well as their receptors in the hypothalamus and hippocampus. Hormonal levels were determined by radioimmunoassay and receptors’ levels by western blot analysis. Leptinemia was increased in pubertal rats and in adult rats fed the fat diet from weaning to adulthood, but not in those fed from puberty to adulthood. Modifications in the developmental pattern from puberty to adulthood were observed for most of the brain receptors studied. In adult animals fed the fat diet from weaning onwards, the levels of leptin receptors in the hypothalamus and glucocorticoid receptors in the hippocampus were decreased compared to chow-fed controls. Switching from fat to normal chow at puberty onset restored the diet-induced alterations on circulating leptin, but not on its hypothalamic receptors. These data suggest that when a fat-enriched diet, resembling those consumed by many teenagers, provided in rats during pubertal growth, it can longitudinally influence the actions of leptin and corticosterone in the brain. The observed alterations at a preobese state may constitute early signs of the disturbed energy balance toward overweight and obesity.     

Preventing excessive weight gain in adolescents: interpersonal psychotherapy for binge eating

The most prevalent disordered eating pattern described in overweight youth is loss of control (LOC) eating, during which individuals experience an inability to control the type or amount of food they consume. LOC eating is associated cross-sectionally with greater adiposity in children and adolescents and seems to predispose youth to gain weight or body fat above that expected during normal growth, thus likely contributing to obesity in susceptible individuals. No prior studies have examined whether LOC eating can be decreased by interventions in children or adolescents without full-syndrome eating disorders or whether programs reducing LOC eating prevent inappropriate weight gain attributable to LOC eating. Interpersonal psychotherapy, a form of therapy that was designed to treat depression and has been adapted for the treatment of eating disorders, has shown efficacy in reducing binge eating episodes and inducing weight stabilization among adults diagnosed with binge eating disorder. In this paper, we propose a theoretical model of excessive weight gain in adolescents at high risk for adult obesity who engage in LOC eating and associated overeating patterns. A rationale is provided for interpersonal psychotherapy as an intervention to slow the trajectory of weight gain in at-risk youth, with the aim of preventing or ameliorating obesity in adulthood.     

Weight Status Continuity and Change From Adolescence to Young Adulthood: Examining Disease and Health Risk Conditions

This study examined weight status during adolescence and young adulthood, and young adult health condition diagnosis. Data are from 10,439 African‐American, Hispanic, and white men and women participating in the National Longitudinal Study of Adolescent Health during Waves 1 (adolescence: ages 12–19) and 3 (young adulthood: ages 19–26). Categories were created differentiating individuals based on their weight status during adolescence and young adulthood: (i) obese during adolescence and young adulthood (i.e., continuously obese), (ii) obese during adolescence only, (iii) obese during young adulthood only, and (iv) never obese. Multilevel random intercept regression models were used to examine the impact of obesity category, sex, and race/ethnicity on young adult asthma, diabetes, high cholesterol, and high blood pressure. Continuous obesity increased the likelihood for young adult disease and health risk conditions compared to individuals who were never obese. Obesity isolated to adolescence (Wave 1) increased the likelihood for high cholesterol and high blood pressure, whereas obesity isolated to young adulthood (Wave 3) also increased the likelihood for diabetes—all increases were relative to nonobese weight status during both periods. Associations varied in direction and degree when sex and race/ethnicity were considered. Findings clarify some of the mixed understandings regarding the associations between age of onset and stability of obesity, and health outcomes with important public health implications. Although results indicate obesity isolated to a single developmental period does have health repercussions, obesity experienced continuously during adolescence and young adulthood greatly intensified risk across all health conditions.     

Maternal nutrition and the programming of obesity

The increasing incidence of obesity in the developed and developing world in the last decade has led to a need to define our understanding of the physiological mechanisms which can predispose individuals to weight gain in infancy, childhood and adulthood. There is now a considerable body of evidence which has shown that the pathway to obesity may begin very early in life, and that exposure to an inappropriate level of nutrition during prenatal and/or early postnatal development can predispose individuals to obesity in later life The brain is at the heart of the regulation of appetite and food preferences, and it is increasingly being recognised that the development of central appetitive structures is acutely sensitive to the nutritional environment both before and immediately after birth. This review will summarise the body of work which has highlighted the critical role of the brain in the early origins of obesity and presents some perspectives as to the potential application of these research findings in the clinical setting.     

Metabolic Consequences and Vulnerability to Diet-Induced Obesity in Male Mice under Chronic Social Stress

Social and psychological factors interact with genetic predisposition and dietary habit in determining obesity. However, relatively few pre-clinical studies address the role of psychosocial factors in metabolic disorders. Previous studies from our laboratory demonstrated in male mice: 1) opposite status-dependent effect on body weight gain under chronic psychosocial stress; 2) a reduction in body weight in individually housed (Ind) male mice. In the present study these observations were extended to provide a comprehensive characterization of the metabolic consequences of chronic psychosocial stress and individual housing in adult CD-1 male mice. Results confirmed that in mice fed standard diet, dominant (Dom) and Ind had a negative energy balance while subordinate (Sub) had a positive energy balance. Locomotor activity was depressed in Sub and enhanced in Dom. Hyperphagia emerged for Dom and Sub and hypophagia for Ind. Dom also showed a consistent decrease of visceral fat pads weight as well as increased norepinephrine concentration and smaller adipocytes diameter in the perigonadal fat pad. On the contrary, under high fat diet Sub and, surprisingly, Ind showed higher while Dom showed lower vulnerability to obesity associated with hyperphagia. In conclusion, we demonstrated that social status under chronic stress and individual housing deeply affect mice metabolic functions in different, sometime opposite, directions. Food intake, the hedonic response to palatable food as well as the locomotor activity and the sympathetic activation within the adipose fat pads all represent causal factors explaining the different metabolic alterations observed. Overall this study demonstrates that pre-clinical animal models offer a suitable tool for the investigation of the metabolic consequences of chronic stress exposure and associated psychopathologies.     

Psychological workload and weight gain among women with and without familial obesity

Objective : High job demands and low job influence may be associated with subsequent weight gain. Predisposition to obesity may further modify such associations. The purpose of the study was to determine whether familial predisposition to obesity modified associations between psychological workload and 6‐year weight changes among nurses. Research Methods and Procedures : A total of 6404 Danish nurses 45 to 65 years old, who belonged to the workforce in both 1993 and 1999, answered a questionnaire on psychological workload, body weight, and familial obesity. Women were considered to be predisposed to obesity if they were overweight and had at least one obese parent. Parents’ body shape was reported using pictograms. Results : An increased psychological workload, reflected by high job demands and low influence in job, was associated with an increased body weight. This was particularly the case for nurses being predisposed to obesity, suggesting a synergy between familial obesity predisposition and the psychological workload environment. An interaction test among job demands, familial predisposition to obesity, and weight gain on adjusted data was made. The test showed p = 0.05. The adjusted interaction test among influence in job, familial predisposition to obesity, and weight gain showed p = 0.02. Predisposed nurses who were busy in their job gained 4.4 kg, whereas other nurses gained only 3.2 kg during the 6 years. Similarly, nurses predisposed to obesity with low influence in job had a higher body weight gain (5.4 vs. 3.2 kg) compared with other nurses. Discussion : High psychological workload due to high job demands and low influence in job seems to predict weight gain in general and, in particular, among those nurses with a familial predisposition to obesity.     

FTO influences on longitudinal BMI over childhood and adulthood and modulation on relationship between birth weight and longitudinal BMI

SNP rs9939609 within the fat mass and obesity associated gene (FTO) is strongly associated with adult body mass index (BMI). However, influences of FTO on longitudinal BMI change from childhood to adulthood have not been examined. Knowledge is limited on FTO, modulating the association between birth weight and longitudinal change of BMI. This longitudinal study examined SNPs of FTO in 658 white subjects from childhood (3–17 years) to adulthood (18–45 years). No significant associations of FTO SNPs with either birth weight or longitudinal BMI over childhood were noted after multiple-test adjustment. However, three SNPs (rs9939609, rs17820875 and rs860713) with different inheritance patterns were identified to be associated with longitudinal BMI over adulthood after Bonferroni adjustment (P = 5.3 × 10⁻⁵, 2.0 × 10⁻⁴ and 0.001). In addition, interactions were discovered between birth weight and SNPs of rs17820875 (P = 0.001) and rs860713 (0.002). A negative association between birth weight and adult BMI were found in risk genotype AG of rs17820875 and GG of rs860713 in contrast to positive associations in other genotypes. These findings led to the conclusion that lower birth weight predisposes to higher adult BMI depending on FTO risk genotypes. Our studies underscore the importance of FTO influences on obesity and provide insights into the evolution of the long-term burden of obesity.     

Folate depletion during pregnancy and lactation reduces genomic DNA methylation in murine adult offspring

The developmental origins of adult health and disease (DOHaD) hypothesis that argues for a causal relationship between under-nutrition during early life and increased risk for a range of diseases in adulthood is gaining epidemiological support. One potential mechanism mediating these effects is the modulation of epigenetic markings, specifically DNA methylation. Since folate is an important methyl donor, alterations in supply of this micronutrient may influence the availability of methyl groups for DNA methylation. We hypothesised that low folate supply in utero and post-weaning would alter the DNA methylation profile of offspring. In two separate 2 × 2 factorial designed experiments, female C57Bl6/J mice were fed low- or control/high-folate diets during mating, and through pregnancy and lactation. Offspring were weaned on to either low- or control/high-folate diets, resulting in 4 treatment groups/experiment. Genomic DNA methylation was measured in the small intestine (SI) of 100-day-old offspring. In both experiments, SI genomic DNA from offspring of low-folate-fed dams was significantly hypomethylated compared with the corresponding control/high folate group (P = 0.009/P = 0.006, respectively). Post-weaning folate supply did not affect SI genomic DNA methylation significantly. These observations demonstrate that early life folate depletion affects epigenetic markings, that this effect is not modulated by post-weaning folate supply and that altered epigenetic marks persist into adulthood.     

Adult socioeconomic,educational, social,and psychological outcomes of childhood obesity: a national birth cohort study

Objectives To assess adult socioeconomic, educational, social, and psychological outcomes of childhood obesity by using nationally representative data.Design 1970 British birth cohort.Participants 16 567 babies born in Great Britain 5-11 April 1970 and followed up at 5, 10, and 29-30 years.Main outcome measures Obesity at age 10 and 30 years. Self reported socioeconomic, educational, psychological, and social outcomes at 30 years. Odds ratios were calculated for the risk of each adult outcome associated with obesity in childhood only, obesity in adulthood only, and persistent child and adult obesity, compared with those obese at neither period.Results Of the 8490 participants with data on body mass index at 10 and 30 years, 4.3% were obese at 10 years and 16.3% at 30 years. Obesity in childhood only was not associated with adult social class, income, years of schooling, educational attainment, relationships, or psychological morbidity in either sex after adjustment for confounding factors. Persistent obesity was not associated with any adverse adult outcomes in men, though it was associated among women with a higher risk of never having been gainfully employed (odds ratio 1.9, 95% confidence interval 1.1 to 3.3) and not having a current partner (2.0, 1.3 to 3.3).Conclusions Obesity limited to childhood has little impact on adult outcomes. Persistent obesity in women is associated with poorer employment and relationship outcomes. Efforts to reduce the socioeconomic and psychosocial burden of obesity in adult life should focus on prevention of the persistence of obesity from childhood into adulthood.     

The “Long-arm” of chronic conditions in childhood: Evidence from Canada using linked survey-administrative data

The objective of this study was to investigate the relationship between health conditions in childhood (ages 4–11), and health and socioeconomic outcomes in adulthood (ages 21–33). This study takes advantage of a new linkage between the National Longitudinal Survey of Children and Youth (NLSCY) and administrative tax data from the T1 Family File (T1FF) from Statistics Canada. The NLSCY includes rich longitudinal information on child development, while the T1FF includes administrative tax information on each child in adulthood (e.g., income, social assistance). The primary measures of child health relate to the diagnosis of a chronic condition, affecting the child’s physical or mental/developmental health. The results suggest that mental/developmental health conditions in childhood more negatively influence adult health and socioeconomic conditions, compared to physical health conditions. Interaction models reveal modest heterogenous effects; for example, there is some evidence of a cushioning effect from higher household income in childhood, as well as an exacerbating negative effect from lower birth weight for mental/developmental health conditions. Using a covariate decomposition approach to explore underlying pathways, the results reveal that associations between health in early life and outcomes in adulthood are partially explained by differences in cognitive skills (i.e., mathematics test scores) in adolescence (ages 16–17). Results may encourage policy investments to mitigate the occurrence of health conditions in childhood and to ensure timely access to educational supports and health services for children with chronic conditions.     

The Relationship of Rapid Weight Gain in Infancy to Obesity and Skeletal Maturity in Childhood

Objective: Children with birth weight appropriate for gestational age (AGA) who also demonstrate rapid weight gain in infancy have a greater risk of being overweight or obese during childhood. A concurrent advancement in skeletal maturity would account for their greater size and would, therefore, not necessarily pose a threat of greater risk during adolescence and early adulthood. This study aims to determine whether children with rapid weight gain during infancy have advanced skeletal maturity during childhood. Research Methods and Procedures: One hundred and ninety‐three African children (boys = 108; girls = 85) of normal birth weight and gestational age were assessed from birth to 9 years. Body composition was assessed at 9 years of age by whole‐body DXA, and skeletal maturity was assessed using the Tanner‐Whitehouse II technique. Rapid weight gain in infancy was defined as a +0.67 change in weight‐for‐age Z‐score between birth and 2 years. Results: Rapid weight gain was experienced by over 20% of the sample. Children with rapid weight gain were significantly lighter at birth and significantly taller, heavier, and fatter throughout childhood. Chronological age and Tanner‐Whitehouse II technique skeletal ages at 9 years were not significantly different between groups or between sexes within groups. Discussion: Because AGA children with rapid weight gain have a greater risk of overweight and obesity but are not advanced in skeletal maturity, later adolescent adjustments toward average weight and fatness values are unlikely. The identification and monitoring of such children is of importance in reducing their risk of morbidity.