An update of the Swedish reference standards for weight, length, and head circumference at birth, for each week of gestational age, is presented. It is based on the total Swedish cohorts of infants born 1977-1981 (n = 475,588). A "healthy population" (79%) was extracted, using prospectively collected data. Weekly (28-42 weeks) grouped data for length and head circumference were well approximated by the normal distribution, but the distributions for birthweight were positively skewed. The original skewed distributions for birthweight were transformed, using the square root, resulting in distributions close to the Gaussian. For smoothing purposes, the weakly values for the mean and the standard deviation were both fitted by a third degree polynomial function. These functions also make possible the calculation of the continuous variable, standard deviation score, for individual newborn infants as well as a comparison of distributions between groups of infants. The reference values and charts presented here have two major advantages over the current Swedish ones: the sample size used is now sufficiently large at the lower gestational ages, so that empirically found variations can be used, and the skewness of the birth weight distribution has been taken into account. The use of the reference standards presented here improves and facilitates evaluation of size deviation at birth.
While previous research has suggested that body thinness is related to subsequent linear growth in children, it is unclear whether thinness at birth is related to linear growth in newborns and catch-up growth in small-forgestational age newborns. Drawing on data from a longitudinal growth study of 3,650 full-term Swedish babies, this study examines linear growth from birth to 6 months of age in three groups of newborns with short ( 2 SDS) body length for gestational age. Among infants short at birth, the Benn Index (kg/m2.69) at birth was not related to the odds of short stature ( 0.10). Nonetheless, the Benn Index was positively related to growth velocity in the first 6 months of life in the short (p = 0.060), appropriate (p
Body mass index (BMI) is an important indicator of nutritional status. Many studies have been done to present BMI reference values in centile values rather than mean and SD values since its statistical distribution is positively skewed. Both height and weight growth charts are usually available in terms of mean and 1, 2 and 3 SD around the means; it would be of clinical value to produce BMI reference charts in a similar way. The aim of this work was to derive the mean and +/- 1, 2 and 3 SD BMI reference ranges as a supplement to the BMI centile reference values published previously for the same group of Swedish children. The method was based on an age-dependent Box transformation, and the beta-value was given as a third-degree polynomial function over the paediatric age. The BMI reference values can be given from mathematical functions in addition to values for specific ages. Conclusion: The BMI reference values and charts derived as described effectively reflect the nature of the variant age-dependent positive skewed statistical distribution of BMI values in the population, and can serve as a valid supplementary tool in the evaluation of growth and nutrition during paediatric years.
A large number of studies have documented a strong correlation between size at birth and subsequent height, although the reported incidence of catch-up growth and consequently the impact on final height has varied with time and between countries. These variations may be real, but could also be related to a number of methodological problems. The aim of this study was to explore two important aspects related to postnatal growth after disturbed fetal growth: first, the definition of small for gestational age (SGA), including the selection of cut-off points in defining shortness; and, secondly, the importance of the general socio-economic status of the population with regard to the incidence of growth faltering in early life. Data were analysed from two longitudinal population-based studies, one from Sweden and one from Hong Kong. Of the Swedish cohort, 3.8% had a birth length below -2 SD scores; in the Hong Kong population the corresponding value was 11.9% (Swedish reference values were used in both studies). The following conclusions were made. Size at birth is important for postnatal growth, and the difference in length at birth of 9-10 cm between the two extreme birth length subgroups remains, on average, until maturity. This seems to be true for the two study populations with different degrees of socio-economic development. However, the rate of catch-up growth is highly dependent on the definition of SGA, on the rate of catch-up growth in early life and on the incidence of growth faltering between 6 and 18 months of age.
Target height, the genetic potential in stature, is commonly estimated by the corrected midparental height (CMH) method. A new model for estimating target height has recently been introduced based on a large, Swedish, population-based study. The aim of this study was to compare the validity of the two methods for estimating target height in Hong Kong Chinese children. The Hong Kong Chinese were more than 10 cm shorter than the Swedes in stature. The secular increase in height over the two generations, however, was 4.2-4.8 cm for the Hong Kong Chinese, much larger than that of the Swedes (0.7-1.0 cm). The two populations are thus at different stages in the secular trend. The new model derived from Swedish population for estimating target height was shown to be applicable to Hong Kong Chinese children; the mean of residual final height values was close to zero (-0.15 cm, p = 0.74). However, the mean of residual final height was significantly above the expected value of zero (4.5 cm, p
Previous growth studies have not explored how different growth phases-the fetal, infancy, childhood, and puberty phases-interact with each other in the development of adult shortness. In this paper, the authors attempt to describe the importance of each growth phase for adult shortness and the effect of growth in one phase on other, subsequent phases. The authors analyzed data from a longitudinal population-based growth study of 2,850 healthy, full term Swedish children born between 1973 and 1975. The height values were transformed into a centimeter score (CMS) by subtracting the raw values from the reference mean values for a particular age and sex. Subnormal growth in any growth phase, as defined by a decrease of 3 CMS or more during a growth phase, was associated with significant increased risk for final heights below 0, -6, and -12 CMS. For children with subnormal growth during one, two, and three phases, the percentages for final height below -12 CMS (a standard deviation score of approximately -2) were 0.5%, 9.4%, and 75%, respectively. Most children (57/62) with a final height below -12 CMS had subnormal growth in two or three phases. Height gains during the four growth phases were interdependent. The infancy phase was negatively associated with fetal growth (r = -0.33, p
OBJECTIVES: This study was designed to explore whether the influence of subnormal growth in fetal, infancy, childhood and pubertal phases on adult short stature was the same when comparing privileged and underprivileged populations. METHODS: Data came from two longitudinal growth studies: 1) Hong Kong Chinese children who were born in 1967 (n = 132), and 2) the comparatively more privileged Swedish children who were born in 1973-1975 (n = 2,850). RESULTS: 68% of Hong Kong Chinese children had two or more growth phases subnormal, much higher than the 12.4% for Swedish children. 42.4% of Hong Kong Chinese were short at final height, much higher than the 2.2% for Swedish children. Subnormal growth in any growth phase was associated with an increased risk of adult short stature in both series (p0.05) in the pooled data. CONCLUSIONS: The impact of subnormal growth in any phase on adult shortness is similar in privileged and underprivileged populations. The much higher prevalence of subnormal growth and consequently adult short stature in developing countries is likely mainly attributable to adverse extrinsic or environmental influences.
We describe spontaneous longitudinal growth in girls with Turner's syndrome (TS), using the infancy-childhood-puberty (ICP) growth model. Length/height during the first 12 years of life was studied in 58 Swedish girls with TS. Their mean length at birth was 47.8 cm (SDS -1.4) and mean height at 12.0 years of age 127.3 cm (SDS -3.0). A clear age-dependent subnormality was observed in the change in length-height SDS (delta SDS). Mean delta SDS values at ages 0.0 to 0.5 and 3.0 to 6.0 years were normal. In contrast, the mean delta SDS at ages 0.5 to 3.0 and 6.0 to 12.0 years were subnormal. The onset of the childhood growth component (normally located between 0.5 and 1.0 year of age) was, on the average, delayed by 0.28 year. This accounts for the subnormality of delta SDS at 0.5 to 3.0 years of age. About 50% of the variation in height at 12.0 years of age, as determined by a multiple linear regression analysis, was significantly explained by length at 0.5 year of age, age at the onset of the childhood component, and delta SDS at 6.0 to 12.0 years of age.
Linear growth during the first three years of life can be represented mathematically in terms of the "ICP-growth model", using a combination of a quickly decelerating Infancy component with the addition of a slowly decelerating Childhood component, the latter acting from the second half of the first postnatal year. The growth pattern for supine length of four children with growth hormone (GH) deficiency is related here to the first two components of this growth model. Basically, all four infants displayed a pattern in line with the exponential shape of the Infancy component to the age when GH therapy was initiated. This observation indicates the existence of the Infancy component as it has been adopted for the ICP-model, and also that it represents the part of postnatal linear growth which seems to be independent of GH. The onset of the Childhood component in healthy subjects has been observed as an abrupt increase in growth rate during the second half of the first year of life. A similar abrupt increase was observed in this study at the time of the initiation of GH therapy (16-27 months). This observation gives some further empirical support to the hypothesis that the child's age at onset of the Childhood component defines the as yet undetermined age at which GH begins to exert a significant influence on linear growth. ICP-based growth charts provide an improved instrument for early detection of GH deficiency.