Timing Of Adiposity Rebound Research Articles

Metabolic trade-offs in childhood: Exploring the relationship between language development and body growth.

During human childhood, brain development and body growth compete for limited metabolic resources, resulting in a trade-off where energy allocated to brain development can decrease as body growth accelerates. This preregistered study explores the relationship between language skills, serving as a proxy for brain development, and body mass index at three distinct developmental stages, representing different phases of body growth. Longitudinal data from 2002 children in the EDEN mother-child cohort were analyzed using structural equation modeling. Our findings reveal a compelling pattern of associations: girls with a delayed adiposity rebound, signaling slower growth rate, demonstrated better language proficiency at ages 5-6. Importantly, this correlation appears to be specific to language skills and does not extend to nonverbal cognitive abilities. Exploratory analyses show that early environmental factors contributing to enhanced cognitive development, such as higher parental socio-economic status and increased cognitive stimulation, are positively associated with both language skills and the timing of adiposity rebound in girls. Overall, our findings lend support to the existence of an energy allocation trade-off mechanism that appears to prioritize language function over body growth investment in girls.

Low testosterone at age 31 associates with maternal obesity and higher body mass index from childhood until age 46: A birth cohort study.

Low testosterone (T) levels in men associate with increased risks of obesity, type 2 diabetes, metabolic syndrome, and cardiovascular diseases. However, most studies are cross-sectional with follow-up-time<10 years, and data on early growth are limited. To compare prenatal factors and body mass index (BMI) development from birth to age 46 in relation to low T at age 31. Men with low T (T<12.1nmol/L, n=132) and men with normal T at age 31 (n=2561) were derived from the Northern Finland Birth Cohort 1966. Prenatal factors, longitudinal weight and height data from birth to age 14, and cross-sectional weight and height data at ages 31 and 46, and waist-hip-ratio (WHR) and T levels at age 31 were analyzed. Longitudinal modeling and timing of adiposity rebound (AR, second BMI rise at age 5-7 years) were calculated from fitted BMI curves. Results were adjusted for mother's pre-pregnancy BMI and smoking status, birth weight for gestational age, alcohol consumption, education level, smoking status, and WHR at age31. Neither gestational age nor birth weight was associated with low T at age 31; however, maternal obesity during gestation was more prevalent among men with low T (9.8%vs. 3.5%, adjusted aOR: 2.43 [1.19-4.98]). Men with low T had earlier AR (5.28vs. 5.82, aOR: 0.73 [0.56-0.94]) and higher BMI (p<0.001) from AR onward until age 46. Men with both early AR and low T had the highest BMI from AR onward. In men, maternal obesity and early weight gain associate with lower T levels at age 31, independently of adulthood abdominal obesity. Given the well-known health risks related to obesity, and the rising prevalence of maternal obesity, the results of the present study emphasize the importance of preventing obesity that may also affect the later reproductive health of the offspring.

Investigation of umbilical cord serum miRNAs associated with childhood obesity: A pilot study from a birth cohort study.

We investigated umbilical cord serum microRNA (miRNA) profiles to identify biomarkers of a risk for obesity later in life. Participating children were divided into high‐ and low‐risk groups of obesity based on the timing of adiposity rebound and the body mass index (BMI) at 5 years and randomly selected from each group for this study. 3D‐Gene® Human miRNA Oligo Chip was performed using cord serum in five children of both groups. The most relevant miRNAs were confirmed in 33 children of the groups using the TaqMan® microRNA assay. We detected five cord serum miRNAs differentially expressed in children at high risk of obesity compared with the levels in children at low risk, namely, miR‐516‐3p and miR‐130a‐3p with increased levels and miR‐1260b, miR‐4709‐3p, and miR194‐3p with decreased levels. This study provides the first identification of altered umbilical cord serum miRNAs in childhood obesity.

Timing of Adiposity Rebound and Determinants of Early Adiposity Rebound in Korean Infants and Children Based on Data from the National Health Insurance Service.

Adiposity rebound (AR) is defined as the second rise in the body mass index (BMI) usually occurring in early childhood. This study aimed to investigate the timing of AR and the factors determining early AR (EAR) by tracking BMI patterns using large-scale longitudinal nationwide data (n = 142,668; 73,389 boys and 69,279 girls) over seven time periods (4–6, 9–12, 18–24, 30–36, 42–48, 54–60, and 66–71 months). The average BMI rebound indicating AR was found before the age of 5 years (6th time period, 54–60 months). Interestingly, children experiencing BMI rebound during the 4th to 6th time periods showed a small increase in the proportion of underweight in the 2nd time period, but a dramatically higher proportion of underweight during the corresponding time period, similar to M-shaped patterns. In contrast, overweight or obese children in the above group showed opposite W-shaped patterns. The parameters predicting the risk of EAR are diverse for each time period by sex. Adequate breastfeeding before the age of 1 year, adequate diet, and reduced sugar-sweetened beverage consumption after the age of 1 year were important for reducing EAR. This study presents for the first time, the timing of AR and the major determinants of EAR among Korean infants and children based on large-scale nationwide data.

Adiposity rebound may be a predictive index of body size for adolescents—Based on retrospective cohort data in a Japanese rural area

BackgroundWe aimed to examine whether the timing of adiposity rebound (AR) could be a predictive index of body size in Japanese adolescents. MethodsThe longitudinal individual data of 1438 Japanese children, including 714 boys and 724 girls born between 2001 and 2007, were obtained from child health check-ups conducted at ages 1.5, 2, 3, and 5 years, and then yearly after the age of 6 years. We examined whether the timing of AR could be used to estimate the body size at 14 years of age. ResultsThe AR had a normal distribution with a mean occurrence at age 6–7 years. The odds ratio of having obesity at age 14 were 8.32 for boys and 4.81 for girls, whereas boys and girls with later AR at the same age had a relative risk of thinness of 6.27 and 8.14, respectively. The probability that children with an early AR (i.e., <6 years old) would be obese was nearly 40%. Similar to obesity, the probability of thinness at 14 years remained approximately 8% for both sexes. ConclusionsThe findings suggest that early AR could raise the risk of obesity, and AR could later raise the risk of thinness. However, both probabilities of AR timing as predictors of adolescent weight status may only be about 10%–20%. This study cannot clearly determine whether the results were influenced by other factors after controlling for the timing of AR. Future studies that also consider lifestyle and genetic factors are warranted.

Body mass index trajectories and adiposity rebound during the first 6 years in Korean children: Based on the National Health Information Database, 2008-2015.

We analyzed the nationwide longitudinal data to explore body mass index (BMI) growth trajectories and the time of adiposity rebound (AR). Personal data of 84,005 subjects born between 2008 and 2012 were obtained from infant health check-ups which were performed at 5, 11, 21, 33, 45, 57, and 69 months. BMI trajectories of each subject were made according to sex and the timing of AR, which was defined as the lowest BMI occurred. Subjects were divided according to birth weight and AR timing as follows: very low birth weight (VLBW), 0.5 kg ≤ Bwt ≤ 1.5 kg; low birth weight (LBW), 1.5 kg < Bwt ≤ 2.5 kg; non-LBW, 2.5 kg < Bwt ≤ 5.0 kg; very early AR, before 45 months; early AR, at 57 months; and moderate-to-late AR, not until 69 months. Median time point of minimum BMI was 45 months, and the prevalence rates of very early, early, and moderate-to-late AR were 63.0%, 16.6%, and 20.4%, respectively. BMI at the age of 57 months showed a strong correlation with AR timing after controlling for birth weight (P < 0.001). Sugar-sweetened beverage intake at 21 months (P = 0.02) and no-exercise habit at 57 months (P < 0.001) showed correlations with early AR. When VLBW and LBW subjects were analyzed, BMI at 57 months and breastfeeding at 11 months were correlated with rapid weight gain during the first 5 months (both P < 0.001). Based on this first longitudinal study, the majority of children showed AR before 57 months and the degree of obesity at the age of 57 months had a close correlation with early AR or rapid weight gain during infancy.

The adiposity rebound in the 21st century children: meaning for what?

With the increase in the prevalence of overweight and obesity worldwide, early adiposity rebound, which is known to have a strong association with obesity, has recently been a focus of research. Early adiposity rebound is conventionally known to have a close relationship with non-communicable diseases. However, novel insights into early adiposity rebound have implied an acceleration of growth and puberty, which is directly reflected in the trends in the timing of adiposity rebound, in the 21st century compared with in the past. Furthermore, the observation that lean mass changes rather than fat mass changes show a more similar pattern to body mass index trajectories is interesting. In this article, the later outcomes and risk factors of early adiposity rebound are briefly summarized, and the current trends in the timing of adiposity rebound and novel insights into its relationship with body composition are reviewed.

The association between overweight and internalizing and externalizing behavior in early childhood

ObjectiveThe aim of this study was to examine bidirectional associations between overweight and behavior problems during early childhood taking into account the adiposity rebound, which is the turning point in the nonlinear development of Body Mass Index in early childhood. MethodsLongitudinal data from 6624 Dutch children in the Generation R Study were used to analyze the association between measured overweight and scores on the internalizing and externalizing scale of the Child Behavior Checklist between one-and-a-half, three and six years. The adiposity rebound was determined for each child by estimating the lowest point in their growth curve. Cross-lagged modeling was used to test (bi)directional associations. ResultsBoth body mass and behavior problems were modest to highly stable from age one-and-a-half to six years. Externalizing and internalizing behavior were both associated with later overweight, although effect sizes were small (βs ranged between 0.06 and 0.07, ps < 0.05). No significant associations in the other direction were found. Controlling for adiposity rebound did not change the pattern of associations. There was a moderating effect of gender, and ethnicity, and timing of adiposity rebound. ConclusionBehavior problems in early childhood may put children at risk for overweight at a later age. This implies that young children with behavior problems may benefit from careful monitoring of eating behavior and weight development. Future studies should take the adiposity rebound into account.

The effects of pre-pregnancy BMI and maternal factors on the timing of adiposity rebound in offspring.

To assess the effect of pre-pregnancy body mass index (BMI), gestational weight gain (GWG), and other maternal factors on the timing of adiposity rebound (AR). In this study, 594 mothers (mothers who do not have diabetes and not underweight) from the longitudinal Growth and Obesity Chilean Cohort Study self-reported their weights at the beginning and end of their pregnancies, and their heights were measured. Pre-pregnancy BMI was categorized as normal weight, overweight, or obesity, and GWG was assessed according to Institute of Medicine guidelines. For children, weight and height measurements from 0 to 3 years were retrieved from records, and they were measured from age 4 to 7 years. BMI curves from 0 to 7 years were used to estimate the age at AR, which was categorized as early (<5 years), intermediate (5-7 years), or late (>7 years). The associations between pre-pregnancy BMI and GWG and early AR were tested using logistic regression models. In total, 33% of the mothers had excess pre-pregnancy weight, 31.2% exceeded Institute of Medicine recommendations, and 45% of children had early AR. The pre-pregnancy BMI and parity were associated with earlier AR (OR = 1.07, 95% CI = 1.02-1.11; OR = 0.86; 95% CI = 0.74-0.99, respectively), but GWG was unrelated. These results suggest that preventive strategies for promoting normal pre-pregnancy BMI, especially in women's first pregnancies, could delay the timing of AR, with protective metabolic effects on offspring.

Timing of adiposity rebound and adiposity in adolescence.

To investigate associations between timing of adiposity rebound (AR; the period in childhood where BMI begins to increase from its nadir) and adiposity (BMI, fat mass) at age 15 years in the Avon Longitudinal Study of Parents and Children (ALSPAC). The sample consisted of 546 children with AR derived in childhood and BMI and fat mass index (FMI; fat mass measured by dual-energy radiograph absorptiometry/height in m(2)) measured at 15 years. Multivariable linear regression models were based on standardized residuals of log BMI and log FMI to allow comparison of regression coefficients across outcomes. There were strong dose-response associations between timing of AR and both adiposity outcomes at 15 years independent of confounders. BMI was markedly higher in adolescence for those with very early AR (by 3.5 years; β = 0.70; 95% confidence interval [CI]: 0.33-1.07; P ≤ .001) and was also higher for those with early AR (between 3.5 and 5 years; β = 0.34; 95% CI: 0.08-0.59; P = .009) compared with those with later AR (>5 years) after full adjustment for a range of potential confounders. Similar magnitudes of association were found for FMI after full adjustment for confounders (compared with later AR: very early AR β = 0.74; 95% CI: 0.34-1.15; P ≤ .001; early AR β = 0.35; 95% CI: 0.07-0.63; P = .02). Early AR is strongly associated with increased BMI and FMI in adolescence. Preventive interventions should consider targeting modifiable factors in early childhood to delay timing of AR.

Factors affecting the timing of adiposity rebound

Background The age of adiposity rebound (AR), when body mass index (BMI) starts to rise after infancy, is thought to be an origin of obesity in later life. We have already reported that children who exhibited an earlier AR were associated with the higher BMI value and atherogenic metabolic status at 12 years of age. We investigated which factors influenced on an earlier AR, birth weight, initial feeding, family history, meals or exercise.

Polyunsaturated fatty acid content of mother’s milk is associated with childhood body composition

The consumption of polyunsaturated fatty acids has changed, and the prevalence of adiposity has increased over the past 30 y. A decrease of n-3 polyunsaturated fatty acid content in breast milk has been suggested to be a contributing factor. The objective of this study was to investigate the relationship between docosahexaenoic acid (DHA) content and n-6/n-3 polyunsaturated fatty acid ratio in breast milk, body composition, and timing of adiposity rebound in children. In the Copenhagen Prospective Study on Asthma in Childhood birth cohort, breast milk fatty acid profile was determined in 281 mothers and BMI development was prospectively followed up to the age of 7 y in 222 children. Age and BMI at adiposity rebound were registered. Furthermore, fat mass determination by dual energy X-ray absorptiometry was performed in 207 children at 6-9 y of age. There was a significant association between breast milk DHA and BMI from 2 to 7 y, fat mass, and, for the girls, age at adiposity rebound. No associations were found between the breast milk n-6/n-3 polyunsaturated fatty acid ratio and body composition. Early intake of DHA may have an effect on body composition. Dietary habits of lactating mothers could contribute to the increased prevalence of obesity in Western societies.

Role of Birth Weight and Postnatal Growth on Pulse Wave Velocity in Teenagers

Low birth weight and accelerated postnatal growth appear to play a significant role in the pathogenesis of hypertension and cardiovascular disease in adulthood. The aim of the present study was to characterize the factors determining pulse wave velocity (PWV) in teenagers and, in particular, to verify the relationship with birth weight, postnatal growth, timing of adiposity rebound, lifestyle, and hemodynamic parameters. Carotid-femoral and carotid-radial pulse wave velocities of 558 healthy teenagers (age range: 16.2-19.9 years) were determined by means of a PulsePen tonometer. Birth weight and gestational age were obtained from obstetrical records, and data regarding postnatal growth were obtained from pediatric clinical records. No change in aortic PWV was found in association with birth weight, postnatal growth, and timing of adiposity rebound. However, the study showed a strong association between accelerated growth from 0 to 12 months and carotid-radial PWV (trend: p = .02). Subjects with birth weight values <2,500 g showed higher values of upper limb PWV (p < .05) and higher values of diastolic and mean arterial pressure (p < .05). Stepwise regression analysis revealed that mean arterial pressure, age, and height were the main independent factors determining aortic PWV in this young population. These results suggest that there is no linear correlation between birth weight and hemodynamic parameters in teenagers; however, subjects characterized by very low birth weight and accelerated postnatal weight gain appear to demonstrate increased upper limb PWV and diastolic and mean arterial pressure values.

Estimation for the Time of Adiposity Rebound in Korean Children and the Effects of Breast Feeding on BMI before Adiposity Rebound

연구배경: 조기 지방증 반등은 생애 후기 비만의 위험을 증가시킨다. 한국 아동의 지방증 반등 시기를 추정하고, 모유수유가 지방증 반등시기 이전의 체질량지수에 미치는 영향을 분석하여 보다 어린 시기에 비만을 예방할 수 있 는 조기중재를 위한 기반이 되고자 본 연구를 시행하였다. 방법: 보건복지부의 2005년 소아·청소년 신체계측 및 혈압측정 조사의 원자료를 이용하였다. 자료분석방법은 지 방증 반등시기 추정 및 모유수유가 체질량지수에 미치는 영향을 알아보기 위하여 STATA 11 프로그램을 이용하여 분위회귀분석을 실시하였다. 결과: 지방증 반등시기 추정 결과 남아는 52개월(4.3세)에 도달하고 그 때의 평균 체질량지수는 15.78이며, 여아 의 경우 56개월(4.7세)에 도달하며 평균 체질량지수는 15.58이었고, 여아가 남아보다 지방증 반등시기가 늦게 나타 났으며 동시에 그 점에서의 평균 체질량지수도 낮았다. 지방증 반등 시기 이전에 모유수유가 체질량지수에 미치는 영향은 남아의 경우 50백분위에서는 체질량지수의 감소효과가 없었고 95백분위에서만 0.19의 감소효과가 있었다. 여아의 경우는 50백분위에서 0.07 감소하는 효과가 있었고 95백분위에서 0.23 감소하여, 50백분위에 비하여 체지 방 감소 효과가 약 3.3배 더 크다고 추정되었다. 결론: 한국아동의 지방증 반등시기는 약 만 4세 정도이며, 따라서 만 4세 이전의 체질량지수에 대한 관심이 요구 된다. 모유수유 효과는 정상체중아보다는 비만아동에게서 더 높게 나타났으므로 과체중 및 비만의 위험이 있는 아 동 즉 부모가 비만한 경우나 저출생체중아로 태어난 아동에게 모유수유를 더 권장해야 할 것으로 생각된다. ꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏ 중심단어: 지방증 반등, 한국 아동, 조기중재, 비만, 분위회귀분석

Patterns of Growth Associated With the Timing of Adiposity Rebound

This study was undertaken to evaluate the effects of age of adiposity rebound (AR) on measures of fat mass between ages 7 and 11 years, maturity, and adiposity in 458 children from a birth cohort studied to age 26 years. Patterns of growth between ages 3 and 26 years and changes in fat mass index between 7 and 11 years in groups with early (<5.5 years for boys and <5 years for girls), average (between 5.5 and 7.5 years for boys and between 5 and 7 years for girls), and late AR (> or =7.5 years for boys and > or =7 years for girls) are described. The mean z-scores for BMI, height, and weight increased between age 3 years and adolescence in the early-rebound group and decreased in the late-rebound group. The differences were maintained until adulthood for BMI and weight. Disproportionately high increases in fat mass index during growth (7-11 years), more advanced bone age in boys at age 7 years, and earlier menarche in girls were evident in the early-rebound group. The relative risks at 26 years of being overweight (BMI 25-29.9 kg/m(2)) and obese (BMI > or =30 kg/m(2)) were 2.70 (95% confidence interval (CI): 1.55, 4.66) and 5.91 (95% CI: 3.03, 11.55) respectively, using the average group as the reference. The corresponding relative risks for adult waist girths exceeding international cut points were 2.12 (95% CI: 1.09, 4.13) and 3.32 (95% CI: 1.46, 7.54). Thus, early rebound is associated with increased depositions of fat in middle childhood, and risks associated with early rebound persist at least until early adulthood.

Physical activity, sedentary behaviour and energy balance in the preschool child: opportunities for early obesity prevention

Prevalence of obesity in preschool children has increased dramatically in recent years. The preschool years (age 3-6 years) have been regarded as critical for the programming of energy balance, via the concept of early 'adiposity rebound'. Children who undergo early adiposity rebound are at increased risk of later obesity. Recent evidence suggests that associations between timing of adiposity rebound and later obesity may not reflect programming, but might denote that 'obesogenic' growth trajectories are often established by the preschool period. Studies of objectively-measured physical activity and sedentary behaviour in preschool children show that levels of physical activity are typically low and sedentary behaviour high. The review of evidence presented here is supportive of the hypothesis that physical activity is protective against obesity in the preschool period, and that sedentary behaviour, particularly television viewing, is obesogenic. Definitive evidence on dose-response relationships between physical activity, sedentary behaviour and obesity remain unclear. Dose-response evidence could be obtained fairly readily by intervention and longitudinal observational studies that use accelerometry in preschool children. The generalisability of much of the evidence base is limited and there is a need for research on the influence of physical activity and sedentary behaviour in the preschool years in the aetiology of obesity in the developing world.

Obesity and Attenuated Adiposity Rebound in Children with Congenital Hypothyroidism. Normalization of BMI Values in Adolescents

An earlier adiposity rebound, suggestive of adult obesity, has been reported in children with congenital hypothyroidism. We undertook this study to evaluate the effect of congenital hypothyroidism on: 1) the timing of adiposity rebound, 2) the long-term prognosis of BMI status, and 3) the factors potentially affecting adiposity in subjects with congenital hypothyroidism. We found that in children with congenital hypothyroidism the BMI values were higher during the first years of life compared to normal population, but subsequently normalized. After the initial rise of BMI, the decline (nadir) and subsequent rise (adiposity rebound), usually occurring in normal children at an age greater than 30 months, was less evident in our group of children with congenital hypothyroidism. The severity of hypothyroidism affected BMI values at 6 and 12, but not at 36 months of age. In conclusion, in children with congenital hypothyroidism, 1) the high BMI values in early childhood normalize in adolescence, and 2) the normally expected BMI fluctuations during the first years of life are attenuated. These findings constitute indirect evidence that thyroid function during fetal and neonatal life affects BMI status during the first years of life.

Critical periods in human growth and their relationship to diseases of aging.

It has long been recognized that there are "critical periods" during mammalian development when exposure to specific environmental stimuli are required in order to elicit the normal development of particular anatomical structures or their normal functioning. The responses of the organism to these stimuli depend on a specific level of anatomical maturation and a state of rapid anatomical and/or functional change. This discussion of critical periods in growth is not confined to the classic definition of a narrow time frame of development during which a particular environmental threshold or limit must exist for normal growth and function to ensue. Using both auxological and epidemiological approaches, we suggest a lifespan perspective which encompasses accumulating and interacting risks that are manifest from prenatal life onward. By understanding the process of growth development, and by scrutinizing the growth process, early variations that lead to later disease can be identified. Here we review a significant amount of the evidence that links exposure during growth to later morbidity and mortality. The fetus appears to respond to insults during the prenatal period through the process of "programming," which has short-term survival advantages but may have a long-term disadvantage in that it is associated with cardiovascular disease, hypertension, type II diabetes, and later obesity. Low birth weight combined with rapid postnatal growth during infancy also appears to be associated, for instance, with later childhood and adult sequelae in terms of glucose tolerance and obesity. Independent of birth weight, the timing of adiposity rebound during mid-childhood also predicts later obesity. The timing, magnitude, and duration of adolescent growth and maturationare associated with critical body composition changes, including the normal acquisition of body fat and bone mineralization. In particular, the acquisition of appropriate peak bone mass is critical in determining the later risk of osteoporosis. A putative causal mechanism linking early growth variation to later chronic disease risk through telomeric attrition is discussed. The obligatory loss of telomeric DNA with each cell division serves as a mitotic clock and marks the rate of growth and repair processes in the cell. Although much more work is required, existing studies support the notion that telomere shortening is not only a clock of cellular division, but also marks relative growth rate, as well as contributing to common degenerative processes of aging through its impact on cellular senescence.

Childhood weight, stature, and body mass index among never overweight, early-onset overweight, and late-onset overweight groups.

To determine the effects of timing of onset of overweight (OW) on childhood anthropometric adiposity levels using long-term serial data from the Fels Longitudinal Study. OW was defined as body mass index (BMI; kg/m(2)) >25, and the age at first measurement of BMI >25 was the age of onset of OW. Early onset of OW (early-OW) and late onset of OW (late-OW) were defined as having onset of OW before and after 25 years of age, respectively, whereas never OW (never-OW) was defined as never having a BMI >25. Subjects consisted of 67 males and 47 females in early-OW groups, 62 males and 48 females in late-OW groups, and 80 males and 114 females in never-OW groups. Levels of weight and BMI in early-OW males and females were significantly greater than those in never-OW and late-OW males and females beginning at the time of adiposity rebound, which generally occurs between 4 and 8 years of age. Median BMI and weight patterns between never-OW and late-OW males were similar throughout childhood. However, significant differences in median levels of BMI for never-OW and late-OW females began at 11 years of age, although onset of OW was not until >25 years of age in the latter group. For both males and females, adiposity rebound is likely an effective time in a child's development to detect and initiate prevention for childhood and early adulthood onset of OW. Although later-onset OW needs additional study, puberty seems to be a critical phase in the development of later adult onset of OW in females.

Obesity in 21-hydroxylase deficient patients

OBJECTIVESTo evaluate the natural history and timing of adiposity rebound (nadir of body mass index (BMI)) in children with congenital adrenal hyperplasia 21-hydroxylase deficiency (CYP21).STUDY DESIGNA retrospective mixed longitudinal study.METHODSHeight...