Childhood Growth Rate Research Articles

Short stature due to intrauterine growth retardation. Clinical and hormonal-metabolic features, possibilities of growth-stimulating therapy

The article presents data about short stature due to intrauterine development delay. This type of short stature - separate nosology, unites children born small for gestation age. The majority of them in the first years of life have accelerated growth rates, allowing the child to normalize their weight-growth indicators and catch up in the development of peers. In the absence of an accelerated growth rates, children have a high risk of lagging behind in physical development throughout childhood, achieving low final growth and becoming short adults. In addition, the fact of birth with small body sizes is associated with a number of hormonal and metabolic features, a risk of metabolic syndrome in adult years.It is assumed that the absence of postnatal growth acceleration is due to various damages to the GH-IGF1 axis (partial GH deficiency, partial resistance to GH, partial resistance to IGF1). Growth hormone therapy, initiated early in life, is able to normalize growth rates in childhood and ultimately significantly improve or normalize the final growth of short stature children born small for gestational age.

Maternal Sedentary Behavior and Physical Activity across Pregnancy and Early Childhood Growth.

Background: Evidence suggests in utero exposures are related to lifespan health of the offspring. Whether maternal activity profile during pregnancy impacts offspring health remains unknown. Methods: This follow-up study recruited mothers with objectively measured sedentary behavior (SED) and moderate-to-vigorous intensity physical activity (MVPA) from a previous cohort study. Maternal activity was analyzed across pregnancy (trajectory groups) and continuously by trimester. Offspring anthropometrics up to 24 months were abstracted from medical records (n = 62). Outcomes included childhood growth rate (incremental rate of BMI z-score change up to 24 months) and rapid growth (increased BMI z-score >0.67 at 12 months). Associations of maternal activity with growth rate were examined using mixed linear models and rapid growth using generalized linear models. Results: Forty percent of participants were in the high SED and 20% in the high MVPA trajectories during pregnancy. Higher SED, across pregnancy [slope (95% confidence interval; CI): 0.080 (0.024-0.061) ΔBMI z-score/month] and in the first trimester [standardized beta; std β (95% CI): 0.017 (0.007-0.026)], was related to accelerated growth rate. Higher MVPA, in the second and third trimesters, was associated with accelerated growth rate [std β (95% CI): trimester 2: 0.013 (0.002-0.024) and trimester 3:0.011 (0.003-0.020)] and greater risk of rapid growth [risk ratio (95% CI): trimester 2: 1.25 (1.009-1.555) and trimester 3: 1.25 (1.056-1.475)]. Conclusions: These findings add to growing evidence on the deleterious effects of high SED during pregnancy. The increased risk for accelerated growth with higher MVPA elicits further investigation. Overall, maternal activity profile shows promise as a modifiable behavior to improve intergenerational health.

Feeding Preterm Infants Today for Later Metabolic and Cardiovascular Outcomes

Preterm birth continues to contribute disproportionately to neonatal morbidity and subsequent physical and neurodevelopmental disabilities. Epidemiologic studies have described additional long-term health consequences of preterm birth such as an increased risk of hypertension and insulin resistance in adult life. It is not known whether the influence of infant and childhood growth rates and early nutrition on long-term outcomes is the same or different among preterm infants and neonates with intrauterine growth restriction. Our goal is to review the effects of fetal growth, postnatal growth, and early nutrition on long-term cardiovascular and metabolic outcomes in preterm infants. Present evidence suggests that even brief periods of relative undernutrition during a sensitive period of development have significant adverse effects on later development. Our review suggests that growth between birth and expected term and 12-18 months post-term has no significant effect on later blood pressure and metabolic syndrome, whereas reduced growth during hospitalization significantly impacts later neurodevelopment. In contrast, growth during late infancy and childhood appears to be a major determinant of later metabolic and cardiovascular well being, which suggests that nutritional interventions during this period are worthy of more study. Our review also highlights the paucity of well-designed, controlled studies in preterm infants of the effects of nutrition during hospitalization and after discharge on development, the risk of developing hypertension, or insulin resistance.

Developmental origins of cardiovascular risk in Jamaican children: The Vulnerable Windows Cohort Study

Both intra-uterine and early childhood development contribute to the risk of developing CVD in adult life. We therefore evaluated the maternal, placental, fetal, birth, infant and childhood determinants of cardiovascular risk in a cohort of Afro-Jamaican children. The Vulnerable Windows Cohort is a longitudinal survey of 569 mothers and their offspring recruited from the first trimester. The offspring's anthropometry was measured at birth, at 6 weeks, every 3 months to 1 year and then every 6 months. At mean age 11.5 years, fasting blood was sampled for glucose, insulin and lipids. Analyses were confined to 296 women and their offspring who had complete data. Waist circumference (WC) was related to maternal weight and BMI, placental weight and to the size of the offspring in utero, at birth and the rate of growth in childhood (P < 0.05). Total cholesterol, TAG and glucose concentrations were unrelated to maternal, placental, fetal, neonatal and childhood measurements. Fasting insulin and homeostasis model assessment of insulin resistance were related to maternal weight and BMI (P < 0.05), but not after adjusting for WC. HDL-cholesterol was inversely related to placental and birth weight, and inversely related to weight and BMI throughout childhood (P < 0.001), but not after adjusting for WC. Systolic blood pressure was directly related to maternal weight, child's height, weight and BMI (P < 0.05), but not after adjustment for WC. Systolic blood pressure and fasting glucose concentration were inversely related to birth weight in boys but directly associated in girls. We concluded that maternal anthropometry during pregnancy, fetal size, and childhood growth rate contribute to cardiovascular risk factors in childhood.

Brief communication: Tissue isotopic enrichment associated with growth depression in a pig: Implications for archaeology and ecology

Stressors such as fasting or poor diet quality are thought to potentially alter the nitrogen and carbon isotopic values of animal tissues. In this study, we demonstrate an inverse correlation between growth rate and multiple tissue enrichment of delta(15)N, delta(13)C, and, to a lesser degree, delta(18)O in a juvenile pig. A more complex pattern is observed with respect to tissue deltaD and growth rate. The observed association between growth rate and tissue isotopic fractionation has important implications for paleodietary and migratory reconstructions of archaeological populations that may have been affected by famine, malnutrition, seasonal variation in food availability, and/or other factors that can affect childhood growth rates.

Early development and osteoporosis and bone health.

Osteoporosis is a skeletal disorder characterized by low bone mass and micro-architectural deterioration of bone tissue with a consequent increase in bone fragility and susceptibility to fracture. 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 growth hormone/insulin-like growth factor-1 (GH/IGF-1) and hypothalamo-pituitary-adrenal (HPA) axes, and recent work has suggested a central role for vitamin D. Epidemiological studies have shown that maternal smoking and nutrition during pregnancy influence intrauterine skeletal mineralization. Childhood growth rates have been directly linked to the risk of hip fracture many decades later, and now evidence is emerging from experimental animal studies that support these observational data. Recent studies have also highlighted epigenetic phenomena as potential mechanisms underlying the findings from epidemiological studies.

The Women’s Health Initiative Randomized Controlled Dietary Modification Trial: a post-mortem

Ecological correlations derived from national mortality data and case-control studies have suggested a positive relation between dietary fat and risk of breast cancer. However, in the many large prospective studies that have been conducted more recently, little or no association has been found between total fat intake and breast cancer incidence. The recently released results from the Women's Health Initiative Fat Reduction Trial found no significant effect of a low-fat diet on risk of breast cancer or total cancer incidence. However, methodologic limitations of this trial, particularly low compliance with the dietary intervention, make these data difficult to interpret, and in the end this massive trial contributes little to our understanding of the role of fat intake in the risk of breast cancer. A substantial body of available evidence now suggests that the percentage of energy derived from fat intake during midlife does not appear to be an important risk factor for breast cancer and is not the primary reason for the large international differences in disease incidence. Diet has a major impact on breast cancer risk, mainly mediated through childhood growth rates and weight gain in later life. Minimizing weight gain during midlife or weight loss after menopause reduces the risk of postmenopausal breast cancer. Massive randomized trials of behavior change to prevent cancer will usually not be a good investment, as clear answers are unlikely. The best information on prevention by diet and lifestyle will generally come from long-term prospective studies combined with controlled trials of intermediate endpoints.

Relationship between household wealth inequality and chronic childhood under-nutrition in Bangladesh

BackgroundHousehold food insecurity and under-nutrition remain critically important in developing countries struggling to emerge from the scourge of poverty, where historically, improvements in economic conditions have benefited only certain privileged groups, causing growing inequality in health and healthcare among the population.MethodsUtilizing information from 5,977 children aged 0-59 months included in the 2004 Bangladesh Demographic and Health Survey , this study examined the relationship between household wealth inequality and chronic childhood under-nutrition. A child is defined as being chronically undernourished or whose growth rate is adversely stunted, if his or her z-score of height-for-age is more than two standard deviations below the median of international reference. Household wealth status is measured by an established index based on household ownership of durable assets. This study utilized multivariate logistic regressions to estimate the effect of household wealth status on adverse childhood growth rate.ResultsThe results indicate that children in the poorest 20% of households are more than three time as likely to suffer from adverse growth rate stunting as children from the wealthiest 20% of households (OR=3.6; 95% CI: 3.0, 4.3). The effect of household wealth status remain significantly large when the analysis was adjusted for a child's multiple birth status, age, gender, antenatal care, delivery assistance, birth order, and duration that the child was breastfed; mother's age at childbirth, nutritional status, education; household access to safe drinking water, arsenic in drinking water, access to a hygienic toilet facility, cooking fuel cleanliness, residence, and geographic location (OR=2.4; 95% CI: 1.8, 3.2).ConclusionThis study concludes that household wealth inequality is strongly associated with childhood adverse growth rate stunting. Reducing poverty and making services more available and accessible to the poor are essential to improving overall childhood health and nutritional status in Bangladesh.

Growth of Jersey Schoolchildren During the 1940-1945 German Occupation: Comparison with Schoolchildren on Mainland Britain

The 1940-45 German occupation of the Channel Islands was accompanied by a gradual deterioration in food availability and culminated in a nine-month siege with severe food shortages after supplies from France were cut off following the liberation of Normandy in 1944. The aim of this study was to compare the growth rates of schoolchildren resident on one of the Channel Islands (Jersey) with children growing up on mainland Britain. Secondary analyses were conducted on published data describing the growth of approximately 3500 schoolchildren resident on Jersey throughout the occupation, 10,000-15,000 London schoolchildren, and about 5000 children evacuated from mainland cities to "residential camp schools" in rural areas. A comparison of age- and sex-adjusted average annual growth rates between 1940 and 1943 confirmed that 8 1/2 - 12 1/2-year-old children on Jersey gained 28.2-33.1% less weight and 23.6-26.5% less height per year than children on the mainland. Because food shortages on Jersey intensified after 1943 (when the mid-occupation growth measurements had been recorded), growth rates toward the end of the occupation (in 1944 and early 1945) are likely to have been even worse than those observed between 1940 and 1943. As such, these analyses provide a somewhat conservative estimate of the decline in childhood growth rates that occurred on Jersey during the 1940-45 German occupation.

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.

Maternal height, childhood growth and risk of hip fracture in later life: a longitudinal study.

Although measures to enhance bone mineralization during childhood and adolescence are widely incorporated into preventive programmes against osteoporotic fracture, there are no published data directly linking growth rates in childhood with the risk of later hip fracture. We addressed this issue in a unique Finnish cohort in whom birth and childhood growth data were linked to later hospital discharge records. This permitted follow-up of 3639 men and 3447 women who were born in Helsinki University Central Hospital between 1924 and 1933, who went to school in Helsinki and still lived in Finland in 1971. Body size at birth was recorded and an average of 10 measurements were obtained of height and weight throughout childhood. We identified 112 subjects (55 men and 57 women) who sustained a hip fracture during 165 404 person-years of follow-up. After adjustment for age and sex in a proportional hazards model, we identified two major determinants of hip fracture risk: tall maternal height (p < 0.001) and a low rate of childhood growth (height, p = 0.006; weight, p = 0.01). The hazard ratio for hip fracture was 2.1 (95% CI 1.2-3.5) among men and women born to mothers taller than 1.61 m, when compared with those whose mothers were shorter than 1.54 m. The ratio was 1.9 (95% CI 1.1-3.2) among those whose rate of childhood height gain was below the lowest quartile for the cohort, compared with those whose growth rate was above the highest quartile. The effects of maternal height and childhood growth rate were statistically independent of each other, and remained after adjusting for socioeconomic status. The patterns of childhood growth that predicted future hip fracture differed between boys and girls. In boys, there was a constant deficit in height and weight between ages 7 and 15 years among those later sustaining fractures; in girls, there was a progressively increasing deficit in weight but a delayed height gain among those later sustaining fractures. This epidemiologic study provides the first direct evidence that a low rate of childhood growth is a risk factor for later hip fracture. Whether reduced growth rate is a consequence of childhood lifestyle, genetic background or intrauterine hormonal programming, the data support measures to optimize childhood growth as part of preventive strategies against osteoporotic fracture in future generations.

Prepubertal stature and blood pressure in early old age

AIMSTo test the hypothesis that childhood growth rate is a marker for formation of control mechanisms that influence blood pressure in early old age.METHODSData are from a sample of 149...

Regular fluctuations in growth hormone (GH) release determine normal human growth.

Growth hormone (GH) is the principal hormone associated with growth through childhood, but in a normal child the amount of GH secretion does not appear to be critical in the generation of normal growth rates. We have assessed the relationship between growth and urinary GH (uGH) output in a longitudinal study of 29 healthy prepubertal schoolchildren (13 male, 16 female; age 5.7-7.8 years) over 1 year. Height and uGH were measured three times a week. Individual height velocity curves were derived using non-linear regression. Growth was expressed in terms of the total increment over the year (DeltaHt, cm), height velocity standard deviation score (HVSDS) and the average size of individual growth spurts. Urinary GH data (ng) were expressed as a weekly average. Mean uGH did not correlate with stature or growth over the year. However, the coefficient of variation of uGH was correlated with height standard deviation score (HtSDS, r = 0.38, P< 0.05), while the relative constancy of short-term change in uGH (coefficient of incremental change, DeltaINC) was inversely correlated with DeltaHt (r = - 0.44) and HVSDS (r = - 0.42, both P< 0.05) but not with HtSDS. DeltaINC was also inversely correlated with the average size of individual growth spurts derived from the height velocity curves (r = - 0.45, P< 0.05). Using time series analysis to identify rhythms in uGH excretion, a positive correlation was found between the magnitude of rhythms of a period of 2 to 4 weeks and HtSDS (r = 0.40, P< 0.05). These data demonstrate that variability in GH is a more important determinant of normal childhood growth rate than the amount of GH alone. Stature is correlated to the overall variability in GH release, while increment in height and the magnitude of individual growth spurts are influenced by the constancy of the GH profile. This would imply that once the GH dose has been replaced in GH deficiency, optimal growth could only be achieved by varying the pattern of GH administration.

Nutrition and cancer.

Evidence from both animal and epidemiologic studies indicate that throughout life excessive energy intake in relation to requirements increases risk of human cancer. Rapid growth rates in childhood lead to earlier age at menarche, which in turn increases risk of breast cancer, and accumulation of body fat in adulthood in related to cancers of the colon, kidney, and endometrium as well as postmenopausal breast cancer. Higher intake of vegetables and fruits has been associated with lower risks of many cancers. The constituents responsible for these apparent protective effects remain uncertain, although evidence supports a contribution of folic acid. Recent evidence suggests that the percentage of energy from fat in the diet is not a major cause of cancers of the breast or colon. Higher intake of meat and dairy products has been associated with greater risk of prostate cancer, which may be related to their saturated fat content. Also, red meat consumption has been associated with risk of colon cancer in numerous studies, but this appears to be unrelated to its fat content. Excessive consumption of alcohol increases risks of upper gastrointestinal tract and even moderate intake appears to increase cancers of the breast and large bowel. Although many details remain to be learned, evidence is strong that remaining physically active and lean throughout life, consuming an abundance of fruits and vegetables, and avoiding high intakes of red meat, foods high in animal fat, and excessive alcohol will substantially reduce risk of human cancer.

Childhood weight and growth rate as predictors of adult mortality.

The effect of rate of growth and relative weight in childhood on adult mortality was studied among 13,146 persons whose weights and heights were measured between the ages of 5 and 18 years in Hagerstown, Maryland, during the period 1933-1945. Relative weight was defined internally, age- and sex-specific Z-scores for height and weight were calculated using national standards, and height and weight velocities were measured as annual increments. Associations between growth parameters (pre- and postpubertal) and mortality through 1985 were investigated in subjects who matched the 1963 and 1975 private health censuses of Washington County, Maryland, using a nested case-control design. Odds ratios of mortality increased linearly with prepubertal relative weight (p less than 0.05 for both sexes combined) and with postpubertal relative weight in females (p less than 0.01). The associations between growth velocities or attained height with mortality tended to be inverse, although not statistically significant. These results are compatible with the existence of positive associations of overweight in school-age children with long-term mortality and seem to allay fears that harm could come from increased growth rates in childhood. Without jeopardizing growth, the avoidance of overweight in childhood might reduce mortality in middle age.

Glycogen debranching enzyme deficiency: Long‐term study of serum enzyme activities and clinical features

In glycogen storage disease type III (glycogen debranching enzyme (DE) deficiency), the activities of serum alanine aminotransferase, aspartate aminotransferase and lactate dehydrogenase may be strikingly elevated during childhood but are low during adult life. To determine the pattern of the elevated serum enzyme activities in relationship to diet, the biochemical subtype and clinical symptoms, 13 patients with DE deficiency were studied. Activities of serum aspartate and alanine transaminases, lactate dehydrogenase, and alkaline phosphatase were markedly elevated during infancy. Continued elevation of enzyme activities during childhood appeared to be related to DE deficiency in liver, but unrelated to DE deficiency in muscle. Activity elevations correlated inconsistently with diet and poorly with childhood growth rate or the presence of hypoglycaemia. The serum enzyme activities declined around puberty concomitantly with a decrease in liver size. Although periportal fibrosis and micronodular cirrhosis indicated the presence of hepatocellular damage during childhood, the decline in serum enzyme activities with age and the absence of overt hepatic dysfunction suggest that the fibrotic process may not always progress.