Infancy Weight Research Articles

Association of Weight Gain in Infancy and Early Childhood with Metabolic Risk in Young Adults

Early postnatal life has been suggested as an important window during which risks for long-term health may be influenced. The aim of this study was to examine the independent associations between weight gain during infancy (0-6 months) and early childhood (3-6 yr) with components of the metabolic syndrome in young adults. This was a prospective cohort study (The Stockholm Weight Development Study). The study was conducted in a general community. Subjects included 128 (54 males) singletons, followed from birth to 17 yr. None of these young adults met the full criteria for the metabolic syndrome. We therefore calculated a continuous clustered metabolic risk score by averaging the standardized values of the following components: waist circumference, blood pressure, fasting triglycerides, high-density lipoprotein cholesterol, glucose, and insulin level. Clustered metabolic risk at age 17 yr was predicted by weight gain during infancy (standardized beta = 0.16; P < 0.0001) but not during early childhood (standardized beta = 0.10; P = 0.23), adjusted for birth weight, gestational age, current height, maternal fat mass, and socioeconomic status at age 17 yr. Further adjustment for current fat mass and weight gain during childhood did not alter the significant association between infancy weight gain with the metabolic risk score (standardized beta = 0.20; P = 0.007). Rapid weight gain during infancy (0-6 months) but not during early childhood (3-6 yr) predicted clustered metabolic risk at age 17 yr. Early interventions to moderate rapid weight gain even at very young ages may help to reduce adult cardiovascular disease risks.

Rapid infancy weight gain and subsequent obesity: Systematic reviews and hopeful suggestions

In a systematic review, we identified 21 separate studies with data on the association between rapid infancy weight gain, up to age 2 y, and subsequent obesity risk. Uniformly all studies reported significant positive associations. We transformed the reported effect sizes to a standard infancy weight gain exposure, and found that further differences in study design accounted for much of the variation in risk. An accompanying paper by Melinda Yeung reminds us that there are benefits of postnatal catch-up growth in certain populations, and suggests that genetic and nutritional factors could moderate the unhealthy translation of rapid infancy weight gain to visceral fat and insulin resistance. Further evidence is needed, and we will need to rigorously test the benefits and risks of any interventions. However, the concept of "healthy" rapid catch-up infancy growth is an attractive prospect. Rapid infancy weight gain is consistently associated with increased subsequent obesity risk, but the predictive ability of different weight gain cut-offs needs to be tested.

Maternal perceptions of her child’s body weight in infancy and early childhood and their relation to body weight status at age 7

Maternal perception of her child's weight status has been hypothesised to affect a child's weight development. The aim of this analysis was to determine in how far the maternal weight perception of her child's weight at different ages is related to its future body weight status. Longitudinal data on body weight, height and skinfolds from the Dortmund Nutritional and Anthropometric Longitudinally Designed Study were used to determine the risk of being overweight at age 7. Complete data on anthropometry, maternal weight perception and confounding variables were available for 253 children. Maternal weight perception assessments at age 6 months, 12 months, 2 years and 4 years of age were related to body weight status as well as changes in body mass index standard deviation score (BMI-SDS) and skinfold SDS between age at assessment and age 7. With respect to the risk of being overweight at age 7, no independent effect of maternal perception was found. When changes in anthropometric measures were considered, it could be observed that children whose weight was considered too low gained more weight until age 7, and those who were considered to be too heavy lost more weight as compared to the children whose weight was considered to be just right. Among infants aged 6 months who were above the 85th percentile, maternal misperception appeared to promote an unfavourable weight development. These latter results support the hypothesis that maternal weight perception might affect a child's weight development. As our data suggest, this effect might begin to operate already in infancy.

Early and late weight gain and the timing of puberty

Nutrition is an important regulator of the tempo of growth and obesity is usually associated with tall childhood stature and earlier pubertal development. Several longitudinal studies have demonstrated that timing of puberty is most closely linked to infancy weight gain: suggesting an early window for programming of growth and development. Earlier puberty in the UK MRC 1946 birth cohort was related to smaller size at birth and rapid growth between 0 and 2 years. Rapid early weight gain leads to taller childhood stature and higher insulin-like growth factor I (IGF-I) levels, possibly through early induction of growth hormone (GH) receptor numbers, and such children are also at risk of childhood obesity. In the Avon Longitudinal Study of Parents and Children, rapid infancy weight gain was associated with increased risk of obesity at 5 and 8 years, with evidence of insulin resistance, exaggerated adrenarche and reduced levels of sex hormone binding globulin (SHBG). Potentially the elevated IGF-I and adrenal androgen levels, increased aromatase activity and increased ‘free’ sex steroid levels consequent to lower SHBG levels could all promote activity of the GnRH pulse generator. In addition obese children have higher leptin levels, a proven permissive factor in initiating LH pulsatility. Obesity could also affect the rate of progression through puberty as nutrition and SHBG may act respectively as an accelerator and brake on peripheral sex steroid action. Early weight gain and early pubertal development might also be associated with loss of the pubertal growth spurt perhaps through obesity-related suppression of GH secretion. Trans-generational recurrence of low birth weight, early catch-up weight gain, earlier menarche, and shorter adult stature have been observed in women, and could contribute to the strong heritability in age at menarche.

Adult Consequences of Fetal Growth Restriction

Low birthweight in relation to the length of gestation, is now known to be associated with increased rates of coronary heart disease and the related disorders stroke, hypertension and type 2 diabetes. These associations extend across the whole range of birthweight, which implies that normal variations in nutrient delivery to the fetus have profound long-term effects. The associations are thought to reflect the body's plasticity during development, by which its structure and function can be permanently changed by the intra uterine and early post natal environment. Slow growth during infancy and rapid weight gain after the age of two years exacerbate the effect of slow fetal growth. Cardiovascular disease and type 2 diabetes arise through a series of interactions between environmental influences and the pathways of development that precede them.

The Insulin Gene Variable Number of Tandem Repeat: Associations and Interactions with Childhood Body Fat Mass and Insulin Secretion in Normal Children

Polymorphism at the insulin gene (INS) variable number of tandem repeat (VNTR) shows variable associations with childhood body mass index (BMI) in different populations. The objective of this study was to observe INS VNTR associations with body composition and insulin secretion in children. The study was designed as a prospective birth cohort study. A total of 947 children genotyped for the INS VNTR participated. Main outcome measures were whole body dual x-ray emission absorptiometry at 9 yr to estimate height-corrected fat mass index (FMI), truncal FMI, and fat-free mass, and insulin secretion after oral glucose at 8 yr. Homozygous III/III children had higher BMI (P = 0.020), FMI (P = 0.015), and truncal FMI (P = 0.022) at 9 yr than class I bearers, but no difference in fat-free mass (P = 0.23). Gain in weight sd score between birth and 3 yr was associated positively with BMI, FMI, and truncal FMI in class I bearers, but not in III/III children (p-interaction with genotype = 0.009-0.066). INS VNTR genotype was not associated overall with insulin secretion at 8 yr (P = 0.64), but class I bearers showed a stronger positive correlation between insulin secretion and BMI at 8 yr (regression coefficient +/- se, 0.26 +/- 0.05; P < 0.0001) than III/III children (-0.10 +/- 0.07; P = 0.48) (p-interaction = 0.003). We clarified that the overall association between INS VNTR class III/III genotype and larger BMI in this population relates to fat mass, but not fat-free mass. In contrast, among the subgroup of children who showed rapid infancy weight gain, class I bearers tended to have larger BMI and fat mass than III/III children. This genetic interaction could relate to insulin secretion, which, in class I bearers, increased more rapidly with overweight and obesity.

Lipid Profile and Carotid Intima-Media Thickness in a Prospective Cohort of Very Preterm Subjects at Age 19 Years: Effects of Early Growth and Current Body Composition

Cardiovascular disease (CVD) risk is associated with prenatal and infancy growth. However, the relative importance of these time periods for the CVD risk is uncertain. To elucidate this, we tested in a very preterm cohort the effects of birth weight for gestational age and weight gain between birth and 3 mo post-term (early postnatal weight gain) and between 3 mo and 1 y post-term (late infancy weight gain) on the lipid profile and carotid intima-media thickness (CIMT) at age 19 y. A less favorable lipid profile was strongly associated with higher current body mass index (BMI), greater waist circumference, and greater absolute fat mass. CIMT was positively associated with current height, and with low-density lipoprotein (LDL) cholesterol and apolipoprotein B (ApoB) levels, and LDL/high-density lipoprotein (HDL) cholesterol and ApoB/apolipoprotein AI (ApoAI) ratios. Lipid profile and CIMT were unrelated to gestational age, birth weight standard deviation score (SDS) and early postnatal weight gain. CIMT was positively associated with late infancy weight gain, but the relationship disappeared after correction for current height. Our findings in 19 y olds born very preterm argue for an effect of current body composition, rather than of early growth, on the CVD risk. Attempts to reduce the CVD risk in this specific population should focus on weight reduction in young adulthood rather than on optimizing the early growth pattern.

Preterm birth and later insulin resistance: effects of birth weight and postnatal growth in a population based longitudinal study from birth into adult life

An increased risk of type 2 diabetes mellitus is associated with low birthweight after full-term gestation, including amplification of this risk by weight gain during infancy and adult body composition. Premature birth is also associated with insulin resistance, but studies conducted so far have not provided follow-up into adulthood. We studied the effects of (1) lower birthweight (as standard deviation score [SDS]) and infancy weight gain on insulin resistance in 19-year-olds born before 32 weeks of gestation, and (2) the interaction between lower birthweight SDS and infancy weight gain, as well as between lower birthweight and adult body composition, on insulin resistance. This was a prospective follow-up study in 346 subjects from the Project on Preterm and Small-for-gestational-age infants cohort, in whom fasting glucose, insulin and C-peptide levels were measured at 19 years. Insulin resistance was calculated with homeostatic modelling (homeostatic model assessment for insulin resistance index [HOMA-IR]). Birthweight SDS was unrelated to the outcomes. Rapid infancy weight gain until 3 months post-term was weakly associated with higher insulin level (p=0.05). Adult fatness was positively associated with insulin and C-peptide levels and HOMA-IR (all p<0.001). On these parameters, there was a statistical interaction between birthweight SDS and adult fat mass (p=0.002 to 0.03). In subjects born very preterm, rapid infancy weight gain until 3 months predicted higher insulin levels at 19 years, but the association was weak. Adult obesity strongly predicted higher insulin and C-peptide levels as well as HOMA-IR. The effect of adult fat mass on these parameters was dependent on its interaction with birthweight SDS.

Growth and cognitive function of Indonesian children: zero-inflated proportion models

This is a study of the cognitive function of Indonesian children. The cognitive function assessment consisted of 17 items and the number of correct answers a child could score therefore ranged between 0 and 17. In this upper bounded situation, a zero-inflated binomial model and a zero-inflated beta-binomial model were considered. The purpose of the analysis was to examine whether the growth status in infancy and at the age of 7 years was related to the cognitive function of the children. The four regression models proposed by Lucas, Fewtrell and Cole were fitted, i.e. an 'early model' relating early body size to the outcome, a 'later model' relating later body size to the outcome, a 'combined model' including both early and later anthropometry measures, and an 'interaction model' further including an interaction term calculated as the product of early and later body size. It was found that social variables predicted the probability of zero-inflation, while weight-for-age at 7 years predicted the proportion of correct answers. The results do not support the existence of a critical window of cognitive development in infancy. Rather they suggest that it is the lack of catch-up growth after poor growth in infancy that is hazardous, and that childhood weight gain is influential regardless of weight in infancy.

Review: developmental origins of osteoporotic fracture

Osteoporosis is a major cause of morbidity and mortality through its association with age-related fractures. Although most effort in fracture prevention has been directed at retarding the rate of age-related bone loss and reducing the frequency and severity of trauma among elderly people, evidence is growing that peak bone mass is an important contributor to bone strength during later life. The normal patterns of skeletal growth have been well characterised in cross-sectional and longitudinal studies. It has been confirmed that boys have higher bone mineral content (BMC), but not volumetric bone density, than girls. Furthermore, there is a dissociation between the peak velocities for height gain and bone mineral accrual in both genders. Puberty is the period during which volumetric density appears to increase in both axial and appendicular sites. Many factors influence the accumulation of bone mineral during childhood and adolescence, including heredity, gender, diet, physical activity, endocrine status, and sporadic risk factors such as cigarette smoking. In addition to these modifiable factors during childhood, evidence has also accrued that fracture risk might be programmed during intrauterine life. Epidemiological studies have demonstrated a relationship between birth weight, weight in infancy, and adult bone mass. This appears to be mediated through modulation of the set-point for basal activity of pituitary-dependent endocrine systems such as the HPA and GH/IGF-1 axes. Maternal smoking, diet (particularly vitamin D deficiency), and physical activity also appear to modulate bone mineral acquisition during intrauterine life; furthermore, both low birth size and poor childhood growth are directly linked to the later risk of hip fracture. The optimisation of maternal nutrition and intrauterine growth should also be included within preventive strategies against osteoporotic fracture, albeit for future generations.

Developmental Origins of Osteoporotic Fracture: the Role of Maternal Vitamin D Insufficiency1-4

Osteoporosis is a major cause of morbidity and mortality through its association with age-related fractures. Although most efforts in fracture prevention have been directed at retarding the rate of age-related bone loss and reducing the frequency and the severity of trauma among elderly people, evidence is growing that peak bone mass is an important contributor to bone strength during later life. The normal patterns of skeletal growth have been well characterized in cross-sectional and longitudinal studies. It has been confirmed that boys have higher bone-mineral content, but not volumetric bone density, than girls. Furthermore, there is a disassociation between the peak velocities for height gain and bone mineral accrual in both genders. Puberty is the period during which volumetric density appears to increase in both axial and appendicular sites. Many factors influence the accumulation of bone mineral during childhood and adolescence, including heredity, gender, diet, physical activity, endocrine status, and sporadic risk factors (e.g., cigarette smoking). In addition to these modifiable factors during childhood, evidence has also accrued that fracture risk might be programmed during intrauterine life. Epidemiological studies have demonstrated a relationship between birthweight, weight in infancy, and adult bone mass. This appears to be mediated through modulation of the set-point for basal activity of endocrine systems such as the GH/IGF-1 and parathyroid hormone/vitamin D axes. Maternal vitamin D insufficiency is associated with reduced bone mineral acquisition during intrauterine and early postnatal life. Furthermore, both low birth size and poor childhood growth are directly linked to the later risk of hip fracture. The optimization of maternal nutrition and intrauterine growth should also be included within preventive strategies against osteoporotic fracture, albeit for future generations.

Weight Gain in the First Week of Life and Overweight in Adulthood

Successful prevention of obesity and related cardiovascular risk factors requires a clear understanding of its determinants over the life course. Rapid infancy weight gain is associated with childhood obesity, whereas low infancy weight is associated with coronary heart disease. Our aim was to identify during which periods in infancy weight gain is associated with adult obesity. A cohort of European American formula-fed subjects, measured on 7 occasions during infancy as part of several infant formula studies, were contacted at age 20 to 32 years, when they reported usual adult weight and height. A life-course plot was used to identify critical periods of weight gain associated with adulthood overweight (body mass index > or =25 kg/m2). These associations were tested with logistic regressions. Data were available for 653 subjects (72% of eligible subjects). Approximately 32% of them were overweight adults. The period between birth and age 8 days was identified as potentially critical. After adjustment for important confounding factors, weight gain during the first week of life was associated with adulthood overweight status (OR for each 100-g increase 1.28, 95% CI 1.08 to 1.52), as was weight gain during the first 112 days of life (OR 1.04, 95% CI 1.01 to 1.08). Similar results were obtained after standardization with z scores from a reference population. In formula-fed infants, weight gain during the first week of life may be a critical determinant for the development of obesity several decades later. These results contribute to the understanding of chronic disease programming and suggest new approaches to obesity prevention.

Associations between prenatal and infancy weight gain and BMI, fat mass, and fat distribution in young adulthood: a prospective cohort study in males and females born very preterm

Increasing evidence indicates that adult body composition is associated with prenatal and infancy weight gain, but the relative importance of different time periods has not been elucidated. The objective was to study the association between prenatal, early postnatal, and late infancy weight gain and body mass index (BMI), fat mass, and fat distribution in young adulthood. We included 403 men and women aged 19 y from a Dutch national prospective follow-up study who were born at <32 wk of gestation. BMI, waist circumference, and waist-to-hip ratio SD scores and subscapular-to-triceps ratio, percentage body fat, fat mass, and fat-free mass at age 19 y were studied in relation to birth weight SD scores, weight gain from preterm birth until 3 mo postterm (early postnatal weight gain), and weight gain from 3 mo until 1 y postterm (late infancy weight gain). Birth weight SD scores were positively associated with weight, height, BMI SD scores, and fat-free mass at age 19 y but not with fat mass, percentage body fat, or fat distribution. Early postnatal and late infancy weight gain were positively associated with adult height, weight, BMI, waist circumference SD scores, fat mass, fat-free mass, and percentage body fat but not with waist-to-hip ratio SD scores or subscapular-to-triceps ratio. In infants born very preterm, weight gain before 32 wk of gestation is positively associated with adult body size but not with body composition and fat distribution. More early postnatal and, to a lesser extent, late infancy weight gain are associated with higher BMI SD scores and percentage body fat and more abdominal fat at age 19 y.

The Developmental Origins of Adult Disease

Low birthweight is now known to be associated with increased rates of coronary heart disease and the related disorders stroke, hypertension and non-insulin dependent diabetes. These associations have been extensively replicated in studies in different countries and are not the result of confounding variables. They extend across the normal range of birthweight and depend on lower birthweights in relation to the duration of gestation rather than the effects of premature birth. The associations are thought to be consequences of developmental plasticity, the phenomenon by which one genotype can give rise to a range of different physiological or morphological states in response to different environmental conditions during development. Recent observations have shown that impaired growth in infancy and rapid childhood weight gain exacerbate the effects of impaired prenatal growth. A new vision of optimal early human development is emerging which takes account of both short and long-term outcomes.

The developmental origins of chronic adult disease

Low birthweight is now known to be associated with increased rates of coronary heart disease and the related disorders stroke, hypertension and non-insulin-dependent diabetes. These associations have been extensively replicated in studies in different countries and are not the result of confounding variables. They extend across the normal range of birthweight and depend on lower birthweights in relation to the duration of gestation rather than the effects of premature birth. The associations are thought to be consequences of developmental plasticity, the phenomenon by which one genotype can give rise to a range of different physiological or morphological states in response to different environmental conditions during development. Recent observations have shown that impaired growth in infancy and rapid childhood weight gain exacerbate the effects of impaired prenatal growth. Coronary heart disease and the disorders related to it arise through a series of interactions between environmental influences and the pathways of development that preceded them. These diseases are the product of branching pathways of development in which the branchings are triggered by the environment before and after birth.

The developmental origins of well-being.

Low birthweight is now known to be associated with increased rates of coronary heart disease and the related disorders, stroke, hypertension and adult-onset diabetes. These associations have been extensively replicated in studies in different countries and are not the result of confounding variables. They extend across the normal range of birthweight and depend on lower birthweights in relation to the duration of gestation rather than the effects of premature birth. The associations are thought to be consequences of developmental plasticity, the phenomenon by which one genotype can give rise to a range of different physiological or morphological states in response to different environmental conditions during development. Recent observations have shown that impaired growth in infancy and rapid childhood weight gain exacerbate the effects of impaired prenatal growth. A new vision of optimal early human development is emerging, which takes account of health and well-being throughout life.

Small size at birth and greater postnatal weight gain: relationships to diminished infant lung function.

Recent evidence suggests that impaired lung development is linked with diminished lung function and an increased risk of chronic obstructive airway disease in adulthood. To examine environmental influences on early lung development, we measured lung function in 131 normal-term infants aged 5-14 weeks. Adjusting for age at measurement, FEV at 0.4 seconds fell by 4.4% for each standard deviation decrease in birth weight (p = 0.047); when adjusted for FVC, FEV at 0.4 seconds was not related to birth weight but fell by 3.2% per standard deviation increase in infant weight gain (p = 0.001). Age- and sex-adjusted total respiratory system compliance fell by 7.0% per standard deviation decrease in birth weight (p < 0.001) but was not related to infant weight gain. In univariate analyses, age-adjusted forced expiratory flow at functional residual capacity was not related to birth weight, but decreased by 11.0% per standard deviation increase in infant weight gain (p = 0.007). The respiratory rate rose by 5.1% per standard deviation increase in infant weight gain (p = 0.001). Lung function measurements were not related to infant feeding. The observations suggest that lower rates of fetal growth and higher rates of early infancy weight gain are associated with impaired lung development.

The developmental origins of osteoporotic fracture.

Undernutrition and other adverse influences arising in fetal life or immediately after birth have a permanent effect on body structure, physiology and metabolism. Evidence is now accumulating from human studies that programming of bone growth might be an important contributor to the later risk of osteoporotic fracture. Body weight in infancy is a determinant of adult bone mineral content, as well as of the basal levels of activity of the GH/IGF-1 and HPA axes, and recent work has suggested a central role for vitamin D. Epidemiological studies have suggested that maternal smoking and nutrition during pregnancy influence intrauterine skeletal mineralization. Finally, childhood growth rates have been directly linked to the risk of hip fracture many decades later. Further work is needed to use this approach to develop novel therapeutic and preventative strategies to reduce the burden of osteoporotic fractures in the population.

Birth weight, growth and feeding in infancy: relation to serum lipid concentration in 12-month-old infants.

To assess the effects of birth size, growth and feeding in infancy on serum lipids in 12-month-old infants. A longitudinal observation study on infants' consumption and growth. Food and growth records were made every month. At 6, 9 and 12 months, food records were weighed to calculate intake. Serum total cholesterol (TC), high-density lipoprotein-cholesterol (HDL), low-density lipoprotein (LDL) -cholesterol and triglyceride concentrations were analysed at 12 months. Birth and growth information was gathered from maternity wards and healthcare centres in Iceland and food consumption data at home. Randomly selected newborns (n=180) according to the mother's domicile and 77% (n=138) participated, of them 75% (n=103), came in for blood sampling. Among boys, a 1 kg higher birth weight resulted in a 0.79 mmol/l higher TC (P=0.005), but nonsignificant after adjustment for growth. Duration of breastfeeding was related to LDL-cholesterol (B=0.06 +/-0.02, P=0.020, adj. R(2)=0.039), adjusting for gender. Independent of size at birth and breastfeeding, increase in length from 6 to 12 months and in weight from birth to 12 months were negatively related to TC (B=-0.455+/-0.156, P=0.008 and B=-1.086+/-0.474, P=0.032, respecitvely) in boys. PUFA was the strongest nutrient variable predicting TC (B=0.332, adj. R(2)=0.24, P>0.001). Cod liver oil consumption increased both TC and LDL-cholesterol in girls (B=0.141+/-0.051, P=0.008 and B=0.112+/-0.047, P=0.021, respectively). Slower growth of high birth weight infants and breastfeeding contributes to higher TC concentration at the age of 12 months. Nutrient intake in infancy also affects lipid profile. The effect of birth weight, growth and nutrient intake in infancy on lipid profile is different for boys and girls.

Association of birth weight and breast-feeding with coronary heart disease risk factors at the age of 6 years

Background and Aim: It has been shown that early growth and nutrition affect health in childhood and later life. The aim of this study was to assess the association of birth weight and breast-feeding in infancy with body mass index (BMI) and serum lipids at the age of six years. The contributions of current macronutrient intake, maternal age and BMI were assessed. Methods and Results: This was a longitudinal observational study of 120 randomly chosen children whose birth weight and duration of breast-feeding had been recorded. At the age of six years, their weight and height, and serum cholesterol (total, LDL and HDL) and triglyceride levels were measured at healthcare centres in Iceland. Dietary intake at six years was estimated using 3-day weighed food records. The duration of breast-feeding negatively correlated with BMI in 6-year-old boys (B=−0.19±0.07, p=0.011) but not in girls; after adjusting for maternal BMI, the relationship in boys was of borderline significance ( p=0.087). The 6-year-old boys who had been breast-fed for <6 months had a significantly higher BMI (18.0 ± 2.5 kg/m 2) than those breast-fed for 8–9 months (15.8 ± 1.2 kg/m 2, p=0.006) or ≥10 months (15.7 ± 1.2 kg/m 2, p=0.005). A longer duration of breast-feeding was related to higher HDL-cholesterol levels in 6-year-old girls (B=0.03±0.01, p=0.032), but not boys. Birth weight was not related to BMI or serum lipid levels at the age of 6 years. Conclusion: In this high birth weight population, a longer duration of breast-feeding may be effective in preventing childhood overweight, at least among boys. Breast-feeding also seems to be related to an improved lipid profile in girls.