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.     

Size at birth, fat-free mass and resting metabolic rate in adult life.

Resting metabolic rate is an important predictor of obesity and is closely related to fat-free mass. There is evidence that fat-free mass may be partly determined during critical periods of growth before and after birth. The objective of this study was to examine the relationship between size at birth, childhood growth and fat-free mass and resting metabolic rate in adult life. 318 men and women with detailed records of body size at birth and growth during school years participated in the study. Fat-free mass correlated positively with birth weight among both sexes (r = 0.264, p < 0.001). Those having a higher birth weight had a higher fat-free mass at any adult BMI. Fat-free mass among men increased by 2.2 kg (95 % Cl 0.5 to 3.9; p = 0.01) for every kg increase in birth weight and by 1.5 kg (95 % Cl 1.3 to 1.7, p < 0.0001) for every kg/m(2) BMI in adult life. In women, fat-free mass increased by 2.7 kg (95 % Cl 1.6 - 3.9; p < 0.001) for every kg increase in birth weight and by 0.8 kg (95 % CI 0.7 to 1.0, p < 0.001) for every kg/m(2) of BMI in adult life. Height, weight and body mass index at each age from 7 to 15 years were also strongly, positively associated with fat-free mass. A negative correlation between birth weight and resting metabolic rate expressed per unit of fat-free mass (r = - 0.158; p < 0.001) was found. Fat-free mass may be determined during critical periods of muscle growth in utero and during childhood. The muscle tissue of people who had a lower birth weight is more metabolically active than those with a higher birth weight. This may protect them from the increased risk of obesity associated with low fat-free mass.     

The association between birth weight and visceral fat in middle-age adults

Objective: Low birth weight, a proxy for fetal underdevelopment, is associated with increased risk of developing type 2 diabetes during adulthood. Low birth weight is also associated with central obesity, but little is known about the association between birth weight and visceral adiposity. The purpose of this study is to test the hypothesis that lower birth weight is associated with increased amounts of visceral fat in middle‐age adults. Research Methods and Procedures: This is an observational study of 91 adults (58 men and 33 women) 40 ± 6 years of age (mean ± standard deviation). Ethnicity was either Japanese American (79%) or non‐Hispanic white (21%). Birth weight was obtained from State Departments of Health. Measurements included smoking status, BMI, and visceral (intra‐abdominal) fat measured by computed tomography. Results: Visceral fat was not associated with birth weight after adjustment for age, sex, ethnicity, BMI, or smoking status (p = 0.76). There was no evidence that the association between birth weight and visceral fat varied by age, sex, or ethnicity. Discussion: We found no evidence that low birth weight is associated with increased visceral fat in middle‐age adults     

Chronic maternal feed restriction impairs growth but increases adiposity of the fetal guinea pig

Small size at birth has been associated with an increased risk of central obesity and reduced lean body mass in adult life. This study investigated the time of onset of prenatally induced obesity, which occurs after maternal feed restriction, in the guinea pig, a species that, like the human, develops substantial adipose tissue stores before birth. We examined the effect of maternal feed restriction [70% ad libitum intake from 4 wk before to midpregnancy, then 90% until day 60 gestation (term approximately 69 days)] on fetal growth and body composition in the guinea pig. Maternal feed restriction reduced fetal (-39%) and placental (-30%) weight at 60 days gestation and reduced liver, biceps muscle, spleen, and thymus weights, relative to fetal weight, while relative weights of brain, lungs, and interscapular and retroperitoneal fat pads were increased. In the interscapular depot, maternal feed restriction decreased the volume density of multilocular fat and increased that of unilocular fat, resulting in an increased relative weight of interscapular unilocular fat. Maternal feed restriction did not alter the relative weight of perirenal fat or the volume density of adipocyte populations within the depot but increased unilocular lipid locule size. Maternal feed restriction in the guinea pig is associated with decreased weight of major organs, including liver and skeletal muscle, but increased adiposity of the fetus, with relative sparing of unilocular adipose tissue. If this early-onset obesity persists, it may contribute to the metabolic and cardiovascular dysfunction that these offspring of feed-restricted mothers develop as adults.     

Birth weight and body composition in overweight Latino youth: a longitudinal analysis

To examine the associations between birth weight and BMI, and total body composition, in overweight Latino adolescents. Two hundred and forty-two overweight Latino children (baseline age = 11.1 +/- 1.7 years; BMI >or= 85th percentile) were measured annually for up to 6 years (2.6 +/- 1.4 observations/child, total 848 visits). Birth weight and history of gestational diabetes were obtained by parental interview. Visceral fat and subcutaneous abdominal fat were assessed by magnetic resonance imaging, while total body fat, total lean tissue mass (LTM), trunk fat, and lean tissue trunk mass were measured by dual-energy X-ray absorptiometry. BMI and BMI percentile were calculated using the Centers for Disease Control and Prevention age appropriate cutoffs. Longitudinal linear mixed effects (LME) modeling was used to evaluate the influence of birth weight on subsequent changes in body composition and distribution of fat across puberty. Birth weight significantly predicted BMI (P < 0.001), total trunk fat (P < 0.001), total trunk LTM (P < 0.001), total fat mass (FM) (P < 0.001), and total LTM (P < 0.001), but not subcutaneous (P = 0.534) or visceral fat (P = 0.593) at age 11 years. Longitudinally, as participants transitioned into puberty, birth weight did not significantly predict any of the body composition or fat distribution measures (P > 0.05). Birth weight is significantly associated with increased adiposity and LTM and negatively associated with trunk fat mass and trunk lean mass at baseline; however these relationships did not predict rate of change of any of the variables as the children progress through adolescence.     

The relationship of birth weight with longitudinal changes in body composition in adult women

Most research on birth weight and adult health status has reported adult measures at a single time point. This study examined the relationship of self‐reported birth weight to longitudinal changes in adult body composition in 587 women of the Michigan Bone Health and Metabolism Study, followed from 1992 to 2007 and aged 24–50 years at baseline. Linear mixed models were used to estimate the association between three birth weight categories and women's 15‐year changes in adult weight, height, BMI, waist and hip circumference, waist‐to‐hip ratio, and fat, lean, and skeletal muscle mass. Body composition measures increased in all women over the 15‐year study period. At their adult baseline, high birth weight women weighed 13% more and had waist circumference and lean mass measures that were 5.51 cm and 3.91 kg larger, respectively, than normal birth weight women. No differences were observed in adult body composition between low and normal birth weight women and rates of change in the adult measures did not vary across the birth weight groups. Women heavier at birth continued to be heavier through adulthood, corroborating previous reports based on single measures of adult body composition. Research to address whether higher adult body composition in high birth weight women increases the longitudinal risk for obesity‐related chronic diseases is needed.     

Birth Weight,Adult Body Composition,and Subcutaneous Fat Distribution

Objectives: To investigate if birth weight is related to both body mass index (BMI) and distribution of subcutaneous fat at adult age. Research Methods and Procedures: A 9‐year longitudinal study was performed in 229 subjects (192 women) with ages ranging from 27 to 36 years. Birth weight was retrieved by a questionnaire, and adult weight, height, skinfold thicknesses, and waist‐to‐hip ratio (WHR) were repeatedly measured at mean ages 27, 29, 31, and 36 years. BMI, sum of four skinfolds (S4S), the ratio between two truncal skinfolds and S4S (SS/S4S), and the ratio between WHR and the cross‐sectional area of the left thigh were calculated with the available data. Results: The adjusted model showed that in women, birth weight was significantly negatively related to adult S4S [β = ?5.211; (?9.768 to ?0.654)], waist circumference [β = ?1.449; (?2.829 to ?0.069)], and SS/S4S ratio [β = ?3.579; (?5.296 to ?1.862)]. In men, a significant negative association was observed between birth weight and adult WHR [β = ?1.096; (?2.092 to ?0.100)] only. Other relationships showed, although not significantly, the same negative trend, namely that lower birth weight is related to higher adult body fat mass (S4S) and a more truncal subcutaneous fat distribution (SS/S4S). No associations were found between birth weight and either adult BMI or the cross‐sectional area of the thigh. Discussion: Lower birth weight is, in both adult men and women, related to a higher adult subcutaneous fat mass and a more truncal distribution of subcutaneous fat, indicating a higher risk for obesity.     

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.     

Obese children have higher arterial elasticity without a difference in endothelial function: the role of body composition

The childhood obesity epidemic is expected to increase cardiovascular disease risk, but the impact of obesity on vascular function in children is not fully understood. The purpose of this study was to determine the effect of obesity and maturation on vascular function in normal weight (BMI: 25-75 percentile) and obese (BMI: ≥95 percentile) children ages 8-18 years old. Large and small artery elasticity (LAEI and SAEI, respectively), measured by diastolic radial pulsewave contour analysis, and reactive hyperemia index (RHI), measured by peripheral arterial tonometry, were obtained, along with anthropometric and biochemical outcomes, in 61 normal weight and 62 obese children. SAEI and LAEI increased with age and were 30% and 18% higher, respectively, in obese children (P < 0.01). In contrast, reactive hyperemia increased with age in the normal weight group but did not differ between groups. Multivariate modeling was used to select variables that explained differences in vascular outcomes. The best model for LAEI in normal weight children was height alone (r(2) = 0.49), whereas for obese children the best model included height + fat mass (r(2) = 0.40). For SAEI, there were no significant models for normal weight children, but for obese children the best model included lean mass + fat mass (r(2) = 0.36). Obese children had greater lean and fat mass, and more advanced Tanner stages than their normal weight peers. The increased elasticity observed in obese children appears to reflect accelerated growth and maturation without affecting vascular reactivity measured by reactive hyperemia. Longitudinal follow up will be essential in determining effects on future vascular disease risk.     

Relationship Between Birth Weight and Body Composition,Energy Metabolism,and Sympathetic Nervous System Activity Later in Life

Objective: Epidemiological studies suggest that high birth weight might be associated with an increased risk of obesity later in life. Programming of metabolic, endocrine, and/or autonomic pathways during intrauterine development has been proposed to explain this association. Research Methods and Procedures: To determine the relationship between birth weight and body composition and energy metabolism later in life, we measured fat mass and fat‐free mass (hydrodensitometry or double‐energy X‐ray absorptiometry), 24‐hour energy expenditure, sleeping metabolic rate, and 24‐hour respiratory quotient (respiratory chamber) in 272 adult nondiabetic Pima Indians (161 males/111 females, age 25 ± 5 years, mean ± SD). In these subjects, birth weight varied over a wide range (2000 to 5000 g). Individuals known to be offspring of diabetic pregnancies were excluded. In 44 of the 272 subjects, muscle sympathetic nerve activity was assessed by microneurography. Results: Birth weight was positively correlated with adult height (r = 0.20, p < 0.001) and fat‐free mass (r = 0.21, p < 0.001), but not with fat mass (r = 0.01, not significant). Sleeping metabolic rate, adjusted for age, sex, fat‐free mass, and fat mass, was negatively related to birth weight (r = ?0.13, p < 0.05), whereas adjusted 24‐hour energy expenditure (r = 0.07, not significant) and 24‐hour respiratory quotient (r = ?0.09, not significant) were not. There was no relationship between birth weight and muscle sympathetic nerve activity (r = 0.12, not significant, n = 44). Discussion: In Pima Indians who are not offspring of diabetic pregnancies, high birth weight is associated with increased height and lean body mass, but not with increased adiposity later in life. Although high birth weight may be associated with relatively low resting energy expenditure, it is not associated with major abnormalities in 24‐hour energy metabolism or with low muscle sympathetic nerve activity later in life.     

Maternal obesity at conception programs obesity in the offspring

Risk of obesity in adult life is subject to programming during gestation. To examine whether in utero exposure to maternal obesity increases the risk of obesity in offspring, we developed an overfeeding-based model of maternal obesity in rats utilizing intragastric feeding of diets via total enteral nutrition. Feeding liquid diets to adult female rats at 220 kcal/kg(3/4) per day (15% excess calories/day) compared with 187 kcal/kg(3/4) per day for 3 wk caused substantial increase in body weight gain, adiposity, serum insulin, leptin, and insulin resistance. Lean or obese female rats were mated with ad libitum AIN-93G-fed male rats. Exposure to obesity was ensured to be limited only to the maternal in utero environment by cross-fostering pups to lean dams having ad libitum access to AIN-93G diets throughout lactation. Numbers of pups, birth weight, and size were not affected by maternal obesity. Male offspring from each group were weaned at postnatal day (PND)21 to either AIN-93G diets or high-fat diets (45% fat calories). Body weights of offspring from obese dams did not differ from offspring of lean dams when fed AIN-93G diets through PND130. However, offspring from obese dams gained remarkably greater (P < 0.005) body weight and higher % body fat when fed a high-fat diet. Body composition was assessed by NMR, X-ray computerized tomography, and weights of adipose tissues. Adipose histomorphometry, insulin sensitivity, and food intake were also assessed in the offspring. Our data suggest that maternal obesity at conception leads to fetal programming of offspring, which could result in obesity in later life.     

Associations of Maternal Diabetes During Pregnancy with Overweight in Offspring: Results from the Prospective TEDDY Study

Objective: This study aimed to determine the relationship between different forms of, and potential pathways between, maternal diabetes and childhood obesity at different ages. Methods: Prospective cohort data from The Environmental Determinants of Diabetes in the Young (TEDDY) study, which was composed of 5,324 children examined from 0.25 to 6 years of age, were analyzed. Cross‐sectional and longitudinal analyses taking into account potential confounders and effect modifiers such as maternal prepregnancy BMI and birth weight z scores were performed. Results: Offspring of mothers with gestational diabetes mellitus (GDM) or type 1 diabetes mellitus (T1DM) showed a higher BMI standard deviation score and increased risk for overweight and obesity at 5.5 years of age than offspring of mothers without diabetes. While these associations could be substantially explained by maternal prepregnancy BMI in offspring of mothers with GDM, significant associations disappeared after adjustment for birth weight z scores in offspring of T1DM mothers. Furthermore, overweight risk became stronger with increasing age in offspring of mothers with diabetes compared with offspring of mothers without diabetes. Conclusions: Maternal diabetes is associated with increased risk of offspring overweight, and the association appears to get stronger as children grow older. Indeed, intrauterine exposure to maternal T1DM may predispose children to later obesity through increased birth weight, while maternal BMI is more important in children exposed to GDM.     

Placental restriction of fetal growth reduces size at birth and alters postnatal growth, feeding activity, and adiposity in the young lamb

Intrauterine growth restriction (IUGR) is associated with accelerated growth after birth. Together, IUGR and accelerated growth after birth predict reduced lean tissue mass and increased obesity in later life. Although placental insufficiency is a major cause of IUGR, whether it alters growth and adiposity in early postnatal life is not known. We hypothesized that placental restriction (PR) in the sheep would reduce size at birth and increase postnatal growth rate, fat mass, and feeding activity in the young lamb. PR reduced survival rate and size at birth, with soft tissues reduced to a greater extent than skeletal tissues and relative sparing of head width (P < 0.05 for all). PR did not alter absolute growth rates (i.e., the slope of the line of best fit for age vs. parameter size from birth to 45 days of age) but increased neonatal fractional growth rates (absolute growth rate relative to size at birth) for body weight (+24%), tibia (+15%) and metatarsal (+18%) lengths, hindlimb (+23%) and abdominal (+19%) circumferences, and fractional growth rates for current weight (P < 0.05) weekly throughout the first 45 days of life. PR and small size at birth reduced individual skeletal muscle weights and increased visceral adiposity in absolute and relative terms. PR also altered feeding activity, which increased with decreasing size at birth and was predictive of increased postnatal growth and adiposity. In conclusion, PR reduced size at birth and induced catch-up growth postnatally, normalizing weight and length but increasing adiposity in early postnatal life. Increased feeding activity may contribute to these alterations in growth and body composition following prenatal restraint and, if they persist, may lead to adverse metabolic and cardiovascular outcomes in later life.     

Stability of the Association between Birth Weight and Childhood Overweight during the Development of the Obesity Epidemic

Objective: To assess whether changes in the birth weight distribution or changes in the association of birth weight with the later risk of childhood overweight have contributed to the development of the obesity epidemic. Research Methods and Procedures: A Danish population‐based cohort study of 124,615 girls and 128,346 boys (ages 6 to 13 years), born between 1936 and 1983, were studied. Birth weight and annual measurements of height and weight were obtained from school health records. Overweight was defined by BMI in relation to internationally accepted criteria. The relative risk of being overweight by birth weight was calculated separately for each age, sex, and time period. Results: The birth weight distribution remained relatively stable over time. Compared with children with a birth weight of 3.0 to 3.5 kg, the risk of overweight increased consistently with each increase in birth weight category among girls and boys and at all ages between 6 and 13 years. Furthermore, the association between birth weight and increased risk of overweight in childhood remained stable across a 48‐year period. Discussion: The increase in the prevalence of overweight could not be explained by time trends in the distribution of birth weight or by changes in the association between birth weight and the later risk of overweight over time. This implies that, unless the prenatal environment influences the later risk of overweight without increasing birth weight, the environmental influences contributing to the obesity epidemic in children of school age operate in the early postnatal period.     

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.     

Endocrine disrupting chemicals and the developmental programming of adipogenesis and obesity

Obesity and related disorders are a burgeoning public health epidemic, particularly in the U.S. Currently 34% of the U.S. population is clinically obese (BMI > 30) and 68% are overweight (BMI > 25), more than double the worldwide average and 10-fold higher than Japan and South Korea. Obesity occurs when energy intake exceeds energy expenditure; however, individuals vary widely in their propensity to gain weight and accrue fat mass, even at identical levels of excess caloric input. Clinical, epidemiological, and biological studies show that obesity is largely programmed during early life, including the intrauterine period. The environmental obesogen hypothesis holds that prenatal or early life exposure to certain endocrine disrupting chemicals can predispose exposed individuals to increased fat mass and obesity. Obesogen exposure can alter the epigenome of multipotent stromal stem cells, biasing them toward the adipocyte lineage at the expense of bone. Hence, humans exposed to obesogens during early life might have an altered stem cell compartment, which is preprogrammed toward an adipogenic fate. This results in a higher steady state number of adipocytes and potentially a lifelong struggle to maintain a healthy weight, which can be exacerbated by societal influences that promote poor diet and inadequate exercise. This review focuses on the developmental origins of the adipocyte, the relationship between adipocyte number and obesity, and how obesogenic chemicals may interfere with the highly efficient homeostatic mechanisms regulating adipocyte number and energy balance.     

Longitudinal study of body weight changes in children: who is gaining and who is losing weight

Cross-sectional studies have reported significant temporal increases in prevalence of childhood obesity in both genders and various racial groups, but recently the rise has subsided. Childhood obesity prevention trials suggest that, on average, overweight/obese children lose body weight and nonoverweight children gain weight. This investigation tested the hypothesis that overweight children lose body weight/fat and nonoverweight children gain body weight/fat using a longitudinal research design that did not include an obesity prevention program. The participants were 451 children in 4th to 6th grades at baseline. Height, weight, and body fat were measured at month 0 and month 28. Each child's BMI percentile score was calculated specific for their age, gender and height. Higher BMI percentile scores and percent body fat at baseline were associated with larger decreases in BMI and percent body fat after 28 months. The BMI percentile mean for African-American girls increased whereas BMI percentile means for white boys and girls and African-American boys were stable over the 28-month study period. Estimates of obesity and overweight prevalence were stable because incidence and remission were similar. These findings support the hypothesis that overweight children tend to lose body weight and nonoverweight children tend to gain body weight.     

Body adiposity and type 2 diabetes: increased risk with a high body fat percentage even having a normal BMI

Obesity is the major risk factor for the development of prediabetes and type 2 diabetes. BMI is widely used as a surrogate measure of obesity, but underestimates the prevalence of obesity, defined as an excess of body fat. We assessed the presence of impaired glucose tolerance or impaired fasting glucose (both considered together as prediabetes) or type 2 diabetes in relation to the criteria used for the diagnosis of obesity using BMI as compared to body fat percentage (BF%). We performed a cross-sectional study including 4,828 (587 lean, 1,320 overweight, and 2,921 obese classified according to BMI) white subjects (66% females), aged 18-80 years. BMI, BF% determined by air-displacement plethysmography (ADP) and conventional blood markers of glucose metabolism and lipid profile were measured. We found a higher than expected number of subjects with prediabetes or type 2 diabetes in the obese category according to BF% when the sample was globally analyzed (P < 0.0001) and in the lean BMI-classified subjects (P < 0.0001), but not in the overweight or obese-classified individuals. Importantly, BF% was significantly higher in lean (by BMI) women with prediabetes or type 2 diabetes as compared to those with normoglycemia (NG) (35.5 ± 7.0 vs. 30.3 ± 7.7%, P < 0.0001), whereas no differences were observed for BMI. Similarly, increased BF% was found in lean BMI-classified men with prediabetes or type 2 diabetes (25.2 ± 9.0 vs. 19.9 ± 8.0%, P = 0.008), exhibiting no differences in BMI or waist circumference. In conclusion, assessing BF% may help to diagnose disturbed glucose tolerance beyond information provided by BMI and waist circumference in particular in male subjects with BMI <25 kg/m(2) and over the age of 40.     

Gestational and early life influences on infant body composition at 1 year

Excess weight gain during both pre‐ and postnatal life increases risk for obesity in later life. Although a number of gestational and early life contributors to this effect have been identified, there is a dearth of research to examine whether gestational factors and weight gain velocity in infancy exert independent effects on subsequent body composition and fat distribution.

Objective:

To test the hypothesis that birth weight, as a proxy of prenatal weight gain, and rate of weight gain before 6 months would be associated with total and truncal adiposity at 12 months of age.

Design and Methods:

Healthy, term infants (N = 47) were enrolled in the study and rate of weight gain (g/day) was assessed at 0‐3 months, 3‐6 months, and 6‐12 months.

Results:

Total and regional body composition were measured by dual‐energy X‐ray absorptiometry (DXA) at 12 months. Stepwise linear regression modeling indicated that lean mass at 12 months, after adjusting for child length, was predicted by rate of weight gain during each discrete period of infancy (P < 0.05), and by maternal pre‐pregnancy BMI (P < 0.05). Total fat mass at 12 months was predicted by rate of weight gain during each discrete period (P < 0.01), and by older maternal age at delivery (P < 0.05). Trunk fat mass at 12 months, after adjusting for leg fat mass, was predicted by rate of weight gain from 0‐3 months and 3‐6 months (P < 0.05).

Conclusion:

Results suggest that growth during early infancy may be a critical predictor of subsequent body composition and truncal fat distribution.     

Are there sex differences in the prevalence of overweight and adiposity in elementary school children in Austria

Based on the data of 203 male and 179 female schoolchildren from Eastern Austria (Burgenland), aged between 6 and 10 years, sex typical differences in body composition (absolute and relative body fat, lean body mass) and weight status were analyzed. Body composition analyses were carried out by means of BIA method, weight status was estimated using BMI percentiles (BMI > 90th percentile defined overweight, BMI > 97th percentile defined obesity). Statistically significant sex differences were found for all body composition parameters, girls exhibited a significantly higher amount of absolute and relative body fat, whereas their male counterparts exhibited a significantly higher amount of lean body mass. Regarding weight status, no statistically significant sex differences were observable, however, a higher amount of girls could be classified as overweight or obese. Evolutionary and sociocultural explanations for these observations are discussed.