Statural Growth Research Articles

Body Stature Growth Trajectories during Childhood and the Development of Myopia

Stature at a particular age can be considered the cumulative result of growth during a number of preceding growth trajectory periods. We investigated whether height and weight growth trajectories from birth to age 10 years were related to refractive error at ages 11 and 15 years, and eye size at age 15 years. Prospective analysis in a birth cohort. Children participating in the Avon Longitudinal Study of Parents and Children (ALSPAC) U.K. birth cohort (minimum N = 2676). Growth trajectories between birth and 10 years were modeled from a series of height and weight measurements (N = 6815). Refractive error was assessed by noncycloplegic autorefraction at ages 11 and 15 years (minimum N = 4737). Axial length (AXL) and radius of corneal curvature were measured with an IOLMaster (Carl Zeiss Meditec, Welwyn Garden City, U.K.) at age 15 years (minimum N = 2676). Growth trajectories and an allelic score for 180 genetic variants associated with adult height were tested for association with refractive error and eye size. Noncycloplegic autorefraction at ages 11 and 15 years, and AXL and corneal curvature at age 15 years. Height growth trajectory during the linear phase between 2.5 and 10 years was negatively associated with refractive error at 11 and 15 years (P<0.001), but explained <0.5% of intersubject variation. Height and weight growth trajectories, especially shortly after birth, were positively associated with AXL and corneal curvature (P<0.001), predicting 1% to 5% of trait variation. Height growth after 2.5 years was not associated with corneal curvature, whereas the association with AXL continued up to 10 years. The height allelic score was associated with corneal curvature (P = 0.03) but not with refractive error or AXL. Up to the age of 10 years, shared growth mechanisms contribute to scaling of eye and body size but minimally to the development of myopia. The author(s) have no proprietary or commercial interest in any materials discussed in this article.

Familial short stature and intrauterine growth retardation associated with a novel mutation in the IGF‐I receptor (IGF1R) gene

IGF-I is essential for normal human growth and mediates its effects through the IGF1R. IGF1R mutations have been associated with varying degrees of intrauterine and postnatal growth retardation. To identify IGF1R gene mutations in a short-statured family with intrauterine growth retardation and microcephaly. Direct DNA sequencing was used to identify IGF1R mutations. Multiplex ligation-dependent probe amplification analyses were performed for deletions and duplications of all IGF1R exons. Functional studies were conducted to assess mutation pathogenicity. A novel heterozygous IGF1R missense mutation in exon 7 (c.A1549T, p.Y487F) was identified in a short-statured girl with severe prenatal growth retardation and microcephaly. The same mutation was also identified in her mother, who presented prenatal and postnatal growth failure, and her short-statured maternal grandmother, both of whom exhibited microcephaly. The index case showed a partial response to rhGH. Functional studies performed in dermal fibroblasts from the index case and her mother showed normal IGF-I binding; however, IGF-I activation of intracellular signalling measured as AKT and extracellular signal-regulated kinase phosphorylation was markedly reduced, with patients' values being lower than those of her mother. IGF-I stimulation of DNA synthesis was significantly reduced compared with controls. Our results show a novel missense mutation in the IGF1R gene (c.A1549T, p.Y487F) associated with prenatal and postnatal growth failure and microcephaly in the context of familial short stature. The functional studies are in line with the inactivation of one copy of the IGF1R gene with variable expression within the same family.

A cross sectional study of socio-demographic determinants of anaemia in adolesecent boys of urban slum area in south India

Background: Adolescence a period of transition between childhood and adulthood is a significant period of human growth and maturation. The term “adolescence” has been defined by WHO as those including between 10 to 19 years. During this period, more than 20% of the total growth in stature and 50% of adult bone mass are achieved and iron requirement increases dramatically in both adolescent boys and girls. Available literature from India confirms that anaemia is common among adolescent girls but there is a paucity of information on status of anaemia among adolescent boys and most of the studies are based on school – going population and are not from the community. Materials and methods: The present cross-sectional study was conducted in 440 Adolescent boys aged 10 to 19 years residing in the registered families in the urban slum area of Andhra Pradesh. Results: The prevalence of anemia in adolescent boys aged 10 to 19 years were found to be 36.14%. The various sociodemographic determinants which were found to be statistically significant in boys includes type of family , socioeconomic status, adolescents educational status, H/o of malaria infection, habit of taking meal. Conclusion: Iron supplements have to be provided to the adolescent boys also as in our country, most of the National programmes related to supplementary nutrition are focusing only on adolescent girls, but none of the programmes include adolescent boys.

Update on Statural Growth and Pubertal Development in Obese Children

Childhood obesity is a growing and alarming problem, associated with several short-term and long-term metabolic and cardiovascular complications. In addition, it has also been suggested that excess adiposity during childhood influences growth and pubertal development. Several studies have shown that during pre-pubertal years, obese patients present higher growth velocity and that this pre-pubertal advantage tends to gradually decrease during puberty, leading to similar final heights between obese and non-obese children. Excess body weight might also influence pubertal onset, leading to earlier timing of puberty in girls. In addition, obese girls are at increased risk of hyperandrogenism and polycystic ovary syndrome. In boys, a clear evidence does not exist: some studies suggesting an earlier puberty associated with the obesity status, whereas other have found a delayed pubertal onset. Overall, the existing evidence of an association between obesity and modification of growth and pubertal patterns underlines a further reason for fighting the epidemics of childhood obesity.

Sotos syndrome is associated with deregulation of the MAPK/ERK-signaling pathway.

Sotos syndrome (SoS) is characterized by tall stature, characteristic craniofacial features and mental retardation. It is caused by haploinsufficiency of the NSD1 gene. In this study, our objective was to identify downstream effectors of NSD1 and to map these effectors in signaling pathways associated with growth. Genome-wide expression studies were performed on dermal fibroblasts from SoS patients with a confirmed NSD1 abnormality. To substantiate those results, phosphorylation, siRNA and transfection experiments were performed. A significant association was demonstrated with the Mitogen-Activated Protein Kinase (MAPK) pathway. Members of the fibroblast growth factor family such as FGF4 and FGF13 contributed strongly to the differential expression in this pathway. In addition, a diminished activity state of the MAPK/ERK pathway was demonstrated in SoS. The Ras Interacting Protein 1 (RASIP1) was identified to exhibit upregulated expression in SoS. It was shown that RASIP1 dose-dependently potentiated bFGF induced expression of the MAPK responsive SBE reporter providing further support for a link between NSD1 and the MAPK/ERK signaling pathway. Additionally, we demonstrated NSD1 expression in the terminally differentiated hypertrophic chondrocytes of normal human epiphyseal growth plates. In short stature syndromes such as hypochondroplasia and Noonan syndrome, the activation level of the FGF-MAPK/ERK-pathway in epiphyseal growth plates is a determining factor for statural growth. In analogy, we propose that deregulation of the MAPK/ERK pathway in SoS results in altered hypertrophic differentiation of NSD1 expressing chondrocytes and may be a determining factor in statural overgrowth and accelerated skeletal maturation in SoS.

Do Class III patients have a different growth spurt than the general population?

Understanding the timing and length of the growth spurt of Class III prognathic patients is fundamental to the strategy of interceptive orthopedic orthodontics as well as to the timing of orthognathic surgery. Consequently, this study was undertaken to determine whether there are any significant differences in the stature growth pattern of Class III subjects compared with non-Class III subjects and the general population. Twelve-year longitudinal stature growth data were collected for 402 randomly selected adolescents in the general population, 55 Class III mandibular prognathic patients, and 37 non-Class III patients. The growth data were analyzed by using the traditional linear interpolation method and nonlinear growth functions. The 6 stature growth parameters were measured: age at takeoff, stature at takeoff, velocity at takeoff, age at peak height velocity, stature at peak height velocity, and velocity at peak height velocity. Comparisons in the stature growth parameters and 15 cephalometric variables among the general population, Class III subjects, and non-Class III subjects were made with multivariate analysis. Patients with Class III prognathism did not have different growth parameters compared with Class II subjects or the general population. This study does not allow meaningful conclusions with regard to the relationship of mandibular size and stature growth pattern. The application of nonlinear growth curves vs the traditional linear interpolation method was also discussed.

Diurnal cortisol rhythms and child growth: Exploring the life history consequences of HPA activation among the Tsimane'

Although psychosocial stress has also been implicated as a contributor to growth failure by imposing energetic constraints during development, the direct physiological pathways by which these life history trade-offs are imposed are not well understood. This study explores associations between diurnal cortisol rhythms and differential patterns of linear child growth among the Tsimane, a horticulturalist and foraging society in the Bolivian Amazon. Waking and bedtime salivary cortisol samples (n = 243) were collected from 53 Tsimane' children ages 1.6-6 over 3 days as part of a larger study of developmental trajectories in hypothalamic-pituitary-adrenal axis dynamics. Anthropometric measurements and survey data were collected in conjunction with the Tsimane' Amazonian panel study (TAPS). Among children under the age of 6, diurnal rhythms in stunted versus nonstunted children vary dramatically: stunted children display elevated cortisol at both the AM (P = 0.03) and PM (P = 0.02) collection points. Multilevel regression analysis demonstrates an inverse relationship between cortisol and height-for-age z-score status (P = 0.00), which is mediated, in part, by infection (P = 0.00), and is strongest among male children (n.s.). Moreover, the poorest statural growth is exhibited among children with high cortisol living in more acculturated Tsimane' communities, a proxy for a more adverse developmental milieu. This study reports a small, but significant, life history cost of elevated diurnal cortisol rhythms on linear growth among Tsimane' children, and provides critical insight into the developmental origins of health differentials among an indigenous Amazonian population experiencing rapid lifestyle changes.

CHARACTERIZATION OF SOMATIC HYBRIDS SOLANUM BULBOCASTANUM + DIHAPLOID SOLANUM TUBEROSUM

A total of 45 somatic hybrids of S. bulbocastanum 8003 (2n=2x=24, cytoplasmic type Wγ; blb 8003) and dihaploid S. tuberosum 243 (2n=2x=24, cytoplasmic type Tβγ; tbr dh 243) generated by protoplast fusion were acclimatised and 36 recovered. Most of the somatic hybrids exhibited morphological abnormalities and a reduced growth stature. Five hybrids were intermediately dwarfed and two were tbr like. Eight somatic hybrids initiated flowering but only three generated the complete flower structure. The flowers produced less pollen with 10% fertility. The female fertility was strongly reduced. The vegetative growth phase was delayed and tubers yield was reduced. Three somatic hybrids had good tuber productivity but still lower than the tbr parent. A laboratory test with Phytophthora infestans infection showed that 33 lines were as resistant as parent blb 8003. An effect of the cytoplasm composition on the resistance level was not detected. Hybrids with different cytoplasm composition (Tβγ, Wβγ, WTβγ) showed a similar response to P. infestans infection. On the basis of the evaluation, seven perspective somatic hybrids were selected as suitable for potato breeding programme. The protoplast fusion turned out to be a suitable tool for creation of new breeding materials of Solanum genera.

A Characteristic Cognitive and Behavioral Pattern as a Clue to Suspect Klinefelter Syndrome in Prepubertal Age

Klinefelter syndrome (KS) with the classic 47,XXY karyotype is the most frequent chromosomal aneuploidy, with a prevalence of 1 in 700 men; although the classic clinical picture is well-known and easily recognizable, most patients remain undiagnosed. The rate of diagnosis during childhood is extremely low, and only 10% of cases are identified before puberty, with a subsequent rate of ascertainment during lifetime of 25%. The low rate of timely diagnosis is because most of the classical signs and symptoms of androgen deficiency appear in mid- to late adolescence but it is important to recognize that adult men with KS may show a great variability in clinical and physical features. A common, often underappreciated, element in young boys and children with KS is the characteristic cognitive and behavioral pattern. We describe 2 patients who were diagnosed at 7.1 and 10 years through a characteristic neurocognitive profile. Both of them showed low-normal scores when evaluated by tests of general intelligence and a behavioral profile characterized by immaturity, low self-esteem, and learning disabilities. Clinical examination showed tall stature and progressive growth acceleration between 5 and 7 years, and one of them had hypoplastic scrotum with monolateral cryptorchidism. To achieve the goal of an early diagnosis of KS, it is necessary to increase medical awareness of the disease and, in particular, to augment pediatricians' knowledge that during prepubertal age pathognomonic clinical features of KS are often lacking but a characteristic cognitive and behavioral pattern is commonly present.

Vitamin D, tuberculin skin test conversion, and latent tuberculosis in Mongolian school-age children: a randomized, double-blind, placebo-controlled feasibility trial

By modulating immune function, vitamin D might increase innate immunity and inhibit the growth of initial bacterial invasion and protect against tuberculosis infection. We examined the effect of vitamin D supplementation on tuberculin skin test (TST) conversion. A double-blind, placebo-controlled study was conducted in 120 Mongol schoolchildren. We estimated the prevalence of latent tuberculosis infection at baseline and examined the effect of vitamin D (800 IU/d) on serum concentrations of 25-hydroxyvitamin D [25(OH)D] and TST conversion. At baseline, the mean (±SD) 25(OH)D concentration was 7 ± 4 ng/mL, and all concentrations were <20 ng/mL. Vitamin D supplementation increased serum 25(OH)D by a mean of 12.7 ng/mL compared with placebo (P < 0.0001). At baseline, 16 children in the vitamin D group and 18 in the placebo group were TST positive (P = 0.7). Over 6 mo, TSTs converted to positive in 5 (11%) children receiving vitamin D compared with 11 (27%) receiving placebo (RR: 0.41; 95% CI: 0.16, 1.09; P = 0.06). Only one TST conversion occurred among those whose serum 25(OH)D concentration increased to >20 ng/mL, whereas 8 TST conversions occurred in those whose final 25(OH)D concentration remained <10 ng/mL (P = 0.05). The mean increase in stature was 2.9 ± 1.6 cm in the vitamin D group and 2.0 ± 1.7 cm in the placebo group (95% CI: 2.16, 2.81; P < 0.003). Vitamin D supplementation for 6 mo had significant favorable effects on serum 25(OH)D concentrations and on growth in stature. A trend was seen toward fewer TST conversions in the vitamin D group. This trial was registered at clinicaltrials.gov as NCT01244204.

La talla de los europeos, 1700-2000: ciclos, crecimiento y desigualdad

This article explores secular changes in the biological well-being of Europeans and relationships between economic growth and human development. With male height data of military recruitment and several national surveys on health and height-by-age data from the European Community Panel, heights trends in the last three centuries are reconstructed. The results show, on the one hand, the strong growth of the European population stature from the 1850s onwards, after a period of height deterioration with unequal intensity in the majority of countries between 1750 and 1850. On the other hand, it shows the persistence of territorial disparities in height since the eighteenth century. It demontrates the inequality was mainly associated to long-term environmental and socioeconomic factors. It concluded that the fantastic height increase was a physiological revolution linked to processes of economic growth, industrialization and urbanization, but mainly to improvements in nutrition, income, education, and public health.

Systematics and ecology of the Australasian genus Empodisma (Restionaceae) and description of a new species from peatlands in northern New Zealand

The genus Empodisma comprises two species that are ecologically important in wetland habitats. Empodisma gracillimum is restricted to south-western Australia, whereas Empodisma minus is found in Tasmania, eastern Australia and New Zealand. We sequenced three cpDNA genes for 15 individuals of Empodisma sampled from throughout the range of the species. The results support an Australian origin for Empodisma sometime during the late Oligocene to early Miocene with more recent dispersal, colonization and diversification in New Zealand. We recovered six genetically distinct maternal lineages: three Empodisma gracillimum haplotypes corresponding to the three accessions in our analysis, a wide-ranging Empodisma minus haplotype found in eastern Australia and Tasmania, an Empodisma minus haplotype found in New Zealand from Stewart Island to approximately 38° S latitude on the North Island, and a distinct haplotype restricted to the North Island of New Zealand north of 38° S latitude. The Eastern Australian and New Zealand haplotypes of Empodisma minus were supported by only one cpDNA gene, and we felt the relatively minor morphological differences and the small amount of genetic divergence did not warrant taxonomic recognition. However, we recommend that the northern New Zealand haplotype should be recognized as the new species Empodisma robustum and provide descriptions and a key to the species of Empodisma. Monophyly of Empodisma robustum is supported by all three cpDNA genes. Empodisma robustum can be distinguished from Empodisma gracillimum and Empodisma minus by its robust growth stature and distinct ecology. It is typically eliminated by fire and re-establishes by seed (seeder strategy), whereas Empodisma minus and Empodisma gracillimum regrow after fire (sprouter strategy).

Secular Trend in Height Mirrors Socio-economic Changes:A Study of Adolescent Population From Zagreb, Croatia

The aim of this study was to examine the height in adolescent population of Zagreb (15-19 years) and to evaluate possible impact of war on secular changes from 1990 to 2010. Randomly selected adolescents of both sexes were surveyed three times in that period, in 1990, 1997 and in 2010. Mean heights were compared between sexes as well as between surveys using the One-way ANOVA. ANOVA Tukey HDS post hoc test was used to determine which survey differed from the others. A trend of decline in height was present in all five female age groups. However, the differences were significant only for 15-year-olds, when comparing 1990 to 2010 survey (p=0.007). The total mean height in girls, over the 20-year-period, decreased by 17.4 mm (p<0.001). In contrast to that, boys´ height did not change in a 20-year period. When put in a broader socio-economic context, the decline in height detected in 1997 might be a result of the worsening of living conditions during and after the Croatian War of Independence (1991-1995). However, regardless of economic stability that was established after the war, the mean age-at-menarche in 2010 declined in comparison to both 1990 and 1997, causing an earlier halt in the growth of long bones and shorter stature. These results are in concordance with recent hypothesis (Dubois et al. 2012) that the influence of the environment on height is less evident in boys than in girls.

Growth in children receiving contemporary disease specific therapy for Crohn's disease

IntroductionIt is unclear whether recent therapeutic advances have improved the growth of children with Crohn's disease (CD).AimTo assess the frequency of short stature and poor growth and their relationship to...

Growth hormone regimens in Australia: analysis of the first 3 years of treatment for idiopathic growth hormone deficiency and idiopathic short stature

To investigate response to growth hormone (GH) in the first, second and third years of treatment for all idiopathic GH-deficient (GHD) and idiopathic short stature (ISS) patients in Australia. Eligibility for subsidized GH treatment in Australia is determined on auxological criteria for the indication of Short Stature and Slow Growth (SSSG), which includes ISS (SSSG-ISS). The biochemical GHD (BGHD, peak GH < 10 mU/l) and SSSG indications are treated similarly: starting dose of 4·5 mg/m(2)/week with provision for incremental dosing. Some ISS patients were specifically diagnosed with familial short stature (SSSG-FSS). Responses for each year of treatment for BGHD, SSSG-ISS and SSSG-FSS cohorts were compared in relation to influencing variables and with international benchmarks. The effect of incremental dosing was assessed. Australian BGHD, SSSG-ISS and SSSG-FSS patients who had completed 1, 2, or 3 years of treatment and were currently receiving GH. Growth hormone dose, change in height-standard deviation score (ΔSDS) and growth velocity (GV). First-year response was 2-3 times greater than that in subsequent years: ΔSDS(1st year) = 0·92, 0·50 and 0·46 for BGHD, SSSG-ISS and SSSG-FSS, respectively. Responses were similar to international reports and inversely related to age at commencement of GH. First-year GV-for-age for BGHD patients was similar to international standards for idiopathic GHD. However, girls had an inferior response to boys when treatment commenced at <6 years of age. First-year GV-for-age for SSSG-ISS/FSS patients was less than ISS standards. Dose increments attenuated the first- to second-year decline in response to BGHD but marginally improved the responses for SSSG-ISS/FSS. The Australian auxology-based GH programme produces comparable responses to international programmes. A lower starting dose is offset by the initiation of treatment at younger ages. Incremental dosing does not appear optimal. A first-year dose of 6·4-6·9 mg/m(2)/week for GHD and 8·9 mg/m(2)/week for ISS with early commencement of GH treatment may be most efficacious.

Differences between Neandertal and modern human infant and child growth models

Studying the emergence of distinctive human growth patterns is essential to understanding the evolution of our species. The large number of Neandertal fossils makes this species the best candidate for a comparative study of growth patterns in archaic and modern humans. Here, Neandertal height growth during infancy and early childhood is described using a mathematical model. Height growth velocities for individuals five years old or younger are modelled as age functions based on different estimates of height and age for a set of ten Neandertal infants and children. The estimated heights of each Neandertal individual are compared with those of two modern human populations based on longitudinal and cross-sectional data. The model highlights differences in growth velocity during infancy (from the age of five months onward). We find that statural growth in Neandertal infants is much slower than that seen in modern humans, Neandertal growth is similar to modern humans at birth, but decreases around the third or fourth month. The markedly slower growth rates of Neandertal infants may be attributable to ontogenetic constraints or to metabolic stress, and contribute to short achieved adult stature relative to modern humans.

Determination of Bone Age in Pediatric Patients with Crohnʼs Disease Should Become Part of Routine Care

Impaired growth and delayed puberty are common in pediatric Crohn's disease (CD). Bone age (BA) is important for interpretation of statural growth. Our aims were to 1) determine the distribution of BA-Z scores; 2) identify clinical factors associated with BA-Z scores; and 3) compare anthropometric Z scores based on chronological age (CA) (CA-Z) versus BA-Z in pediatric CD. CD patients ≤ CA 15 in females and 17 years in males were enrolled in a cross-sectional study. BA was determined with left hand/ wrist x-ray. In all, 49 patients (65% male; 84% Caucasian; mean CA 13 years) examined between January 2007 and July 2009 qualified for the study. Mean BA-Z score was -1.40 ± 1.50 (standard deviation). 41% had BA-Z score < -2.0. Mean BA-Z scores were lower in females (P = 0.02), Caucasians (P = 0.006), Tanner stage 1-3 children (P = 0.004), and patients with colonic disease (P = 0.0006), past corticosteroid exposure (P = 0.01), current azathioprine/6-mercaptopurine treatment (P = 0.003), or lower height (P = 0.006), weight (P < 0.001), or body mass index (BMI) (P = 0.01) CA-Z scores. Mean height, weight, and BMI BA-Z scores were 0.73 units (P < 0.0001), 0.51 units (P < 0.0001), and 0.23 units (P < 0.0001) greater than mean height, weight, and BMI CA-Z scores. Low BA occurs frequently in CD. Determination of BA should become the standard of care in pediatric CD patients, allowing clinically meaningful interpretation of growth in the context of skeletal maturation, leading to improved treatment recommendations, as growth is a dynamic marker of disease status. Prospective longitudinal studies are required to clarify determinants of BA and patterns of BA advancement in CD.

Growth hormone treatment of skeletal dysplasia

It seems that recombinant human growth hormone (rhGH) therapy can lead to increased growth in just about any child with (or without) chronic disease. An exception to this has been one of the more common skeletal dysplasias achondroplasia. Attempts at achieving enhanced growth in children with this disorder have not been successful.Achondroplasia is caused by a mutation in the FDFR3 gene. There is a phenotypically very similar condition, hypochrondroplasia, which is actually associated with a different mutation in this same gene. In this issue of The Journal, Rothenbuhler et al provide an interim report of a trial of rhGH in 6 children with hypochondroplasia. This is an important report for a couple of reasons. First of all, the authors used a dosing regimen for the rhGH that was titrated to achieve preset goal levels of insulin-like growth factor 1 in each patient. Unlike the situation with achondroplasia, all of these children had improved statural growth and improvement in body proportion during this first period of treatment. The second important take-home message from this report is the potential need for mutation analysis in children with suspected achondroplasia. Because the disorder may not be differentiated from hypochondroplasia clinically, and the two disorders appear to differ in their responsiveness to growth hormone, making the correct diagnosis may be extremely important for the child's ultimate outcome.Article page 849▶ It seems that recombinant human growth hormone (rhGH) therapy can lead to increased growth in just about any child with (or without) chronic disease. An exception to this has been one of the more common skeletal dysplasias achondroplasia. Attempts at achieving enhanced growth in children with this disorder have not been successful. Achondroplasia is caused by a mutation in the FDFR3 gene. There is a phenotypically very similar condition, hypochrondroplasia, which is actually associated with a different mutation in this same gene. In this issue of The Journal, Rothenbuhler et al provide an interim report of a trial of rhGH in 6 children with hypochondroplasia. This is an important report for a couple of reasons. First of all, the authors used a dosing regimen for the rhGH that was titrated to achieve preset goal levels of insulin-like growth factor 1 in each patient. Unlike the situation with achondroplasia, all of these children had improved statural growth and improvement in body proportion during this first period of treatment. The second important take-home message from this report is the potential need for mutation analysis in children with suspected achondroplasia. Because the disorder may not be differentiated from hypochondroplasia clinically, and the two disorders appear to differ in their responsiveness to growth hormone, making the correct diagnosis may be extremely important for the child's ultimate outcome. Article page 849▶

Ancient‐to‐modern secular changes in Korean stature

Statural growth in human populations is a sensitive indicator of socio-economic well-being, and improvements in socio-economic status are reflected in secular increases in adult height. In the present study, we investigated the statures of historical Korean societies to show how stature changed over time. Applying Fujii's equation, derived from modern Japanese, to the measurement of femora removed from 15th- to 19th-century Joseon tombs, the average heights of Korean adults during the Joseon dynasty were estimated to be 161.1 ± 5.6 cm and 148.9 ± 4.6 cm for males and females, respectively. Plotting statures for successive historical societies against time revealed that Korean heights remained relatively unchanged through to the end of the 19th century, a pattern that differs from that seen in many Western countries in which stature transiently decreases after the Middle Ages. In contrast, a sharp increase in Korean stature was observed at the beginning of the 20th century, similar to trends seen in other nations (although exact timing varies in different countries). There were no accompanying changes of stature sexual dimorphism. The data reported in this study reflect the unique historical experience of Korea; the relative isolation of Joseon society, the late onset of modernization (at the end of the 19th century), and the later occurrence of industrialization (during the 1960s).

Thyroid autoimmunity in 72 children with type 1 diabetes mellitus: relationship with pancreatic autoimmunity and child growth

The aim of this study was to assess the association between pancreatic and thyroid autoimmunity (TA) and determine impact of thyroid antibodies on statural growth. Seventy-two children with type 1 diabetes mellitus (TIDM) and no clinical evidence of thyroid disorders were evaluated: glycated haemoglobin (A1c), thyroid peroxidase antibodies (TPOAb), glutamic acid decarboxylase antibody (GADA), tyrosine phosphatase antibodies (IA2A), and thyroid-stimulating hormone (TSH). The score of standard deviation for height (SDS) was calculated. There were 72 patients, 38 (52.7%) boys and 34 (47.2%) girls, with a mean age of 10.89 +/- 4.26 years and a mean duration of T1DM of 3.41 +/- 2.56 years. TPOAb were present in 23.6% of patients; 12.5% of subjects were positive for GADA and 41.6% for IA2A. Patients with TA had more prevalent GADA and IA2A (23.5% vs. 9%, p < 0.001, and 58.8% vs. 36.3%, p < 0.001, respectively). A1c was higher in patients with TA (9.7% +/- 2.05% vs. 8.6% +/- 2.11%, p = 0.05). TA was associated with lower SDS (0.26 vs. 0.98, p = 0.043). TSH was higher in patients with TA (3.39 vs. 2.15 microU/mL, p < 0.05). Logistic regression analysis revealed that a negative SDS for height was independently associated with duration of diabetes (p = 0.049) and TSH (p = 0.027) but not with birth weight, A1c, and TPOAb. In conclusion, TA was found in 23.6% TIDM children. Patients with TA had significantly higher prevalence of GADA and IA2A and significantly higher A1c vs. patients without TA. Our data suggest significant association between TA and height in children with T1DM. SDS was independently associated with diabetes duration and TSH.