Fetal and infant growth and cardiovascular risk factors in women.

OBJECTIVE--To examine whether cardiovascular risk factors in women are related to fetal and infant growth. DESIGN--Follow up study of women born 1923-30 whose birth weights and weights at one year were recorded. SETTING--Hertfordshire. SUBJECTS--297 women born and still living in East Hertfordshire. MAIN OUTCOME MEASURES--Plasma glucose and insulin concentrations during a standard oral glucose tolerance test; fasting plasma proinsulin and 32-33 split proinsulin concentrations; blood pressure; fasting serum total, low density lipoprotein and high density lipoprotein cholesterol, triglyceride, and apolipoprotein A I and B concentrations; and plasma fibrinogen and factor VII concentrations. RESULTS--Fasting plasma concentrations of glucose, insulin, and 32-33 split proinsulin fell with increasing birth weight (P = 0.04, P = 0.002, and P = 0.0002 respectively, when current body mass index was allowed for). Glucose and insulin concentrations 120 minutes after an oral glucose load showed similar trends (P = 0.03 and P = 0.02). Systolic blood pressure, waist:hip ratio, and serum triglyceride concentrations also fell with increasing birth weight (P = 0.08, P = 0.07, and P = 0.07 respectively), while serum high density lipoprotein cholesterol concentrations rose (P = 0.04). At each birth weight women who currently had a higher body mass index had higher levels of risk factors. CONCLUSION--In women, as in men, reduced fetal growth leads to insulin resistance and the associated disorders: raised blood pressure and high serum triglyceride and low serum high density lipoprotein cholesterol concentrations. The highest values of these coronary risk factors occur in people who were small at birth and became obese. In contrast with men, low rates of infant growth did not predict levels of risk factors in women.     

Low birth weight for gestational age associates with reduced glucose concentrations at birth, infancy and childhood

BACKGROUND/AIMS: Our aim was to investigate glucose homeostasis, insulin sensitivity and insulin-like growth factor (IGF) system status in children born small for gestational age (SGA). METHODS: A case-control study was carried out at birth, infancy and childhood, comparing SGA with children appropriate for gestational age strictly matched for age, gender, pubertal status and body mass index. Ninety newborns, 52 infants, and 68 children were studied. Fasting insulin (I(F)), fasting glucose (G(F)) to I(F) ratio (G(F)/I(F)), the homeostasis model assessment of insulin sensitivity, the quantitative insulin sensitivity check index, insulinogenic index and the triglyceride/high-density lipoprotein-cholesterol ratio were measured. IGF-I, IGF-binding protein-3 and the IGF-I/IGF-binding protein-3 molar ratio were assessed. RESULTS: Glucose concentrations were lower in SGA newborns (p < 0.0001), infants (p = 0.01), and children (p = 0.001). Birth weight correlated with glucose levels at birth (r = 0.59, p < 0.0001), 12 months (r = 0.29, p = 0.04) and childhood (r = 0.44, p < 0.0001). CONCLUSION: Our results provide evidence for a developmental adaptation of glucose metabolism in SGA children leading to reduced glucose concentrations.     

Sequelae of syndrome X in children born small for gestational age

OBJECTIVE: Low birth weight is associated with the presence of syndrome X in adults. We studied the components of this syndrome in prepubertal children born SGA (small for gestational age) and children born AGA (appropriate for gestational age). METHODS: Twenty-nine SGA children, age (mean +/- SD) 9.1 +/- 1.1 years and 24 AGA children, age 9.0 +/- 1.1 years were studied. Fasting serum lipid concentrations were determined. A hyperinsulinemic euglycemic clamp was performed to measure insulin sensitivity. Ambulatory monitoring was performed to obtain 24-hour recordings of blood pressure. RESULTS: Prepubertal SGA children are less insulin sensitive and have a higher nighttime systolic blood pressure (SBP) after correction for BMI than children born AGA. No differences were found in lipid concentrations between the 2 groups. CONCLUSIONS: Not all components of syndrome X can yet be found in 9-year-old children born SGA; follow-up of this cohort is required.     

Fetal and infant growth and impaired glucose tolerance at age 64.

OBJECTIVE--To discover whether reduced fetal and infant growth is associated with non-insulin dependent diabetes and impaired glucose tolerance in adult life. DESIGN--Follow up study of men born during 1920-30 whose birth weights and weights at 1 year were known. SETTING--Hertfordshire, England. SUBJECTS--468 men born in east Hertfordshire and still living there. MAIN OUTCOME MEASURES--Fasting plasma glucose, insulin, proinsulin, and 32-33 split pro-insulin concentrations and plasma glucose and insulin concentrations 30 and 120 minutes after a 75 g glucose drink. RESULTS--93 men had impaired glucose tolerance or hitherto undiagnosed diabetes. They had had a lower mean birth weight and a lower weight at 1 year. The proportion of men with impaired glucose tolerance fell progressively from 26% (6/23) among those who had weighted 18 lb (8.16 kg) or less at 1 year to 13% (3/24) among those who had weighed 27 lb (12.25 kg) or more. Corresponding figures for diabetes were 17% (4/23) and nil (0/24). Plasma glucose concentrations at 30 and 120 minutes fell with increasing birth weight and weight at 1 year. Plasma 32-33 split proinsulin concentration fell with increasing weight at 1 year. All these trends were significant and independent of current body mass. Blood pressure was inversely related to birth weight and strongly related to plasma glucose and 32-33 split proinsulin concentrations. CONCLUSIONS--Reduced growth in early life is strongly linked with impaired glucose tolerance and non-insulin dependent diabetes. Reduced early growth is also related to a raised plasma concentration of 32-33 split proinsulin, which is interpreted as a sign of beta cell dysfunction. Reduced intrauterine growth is linked with high blood pressure, which may explain the association between hypertension and impaired glucose tolerance.     

Metabolic aspects of insulin resistance in individuals born small for gestational age

Numerous studies have shown an association between low weight at birth and being born small for gestational age (SGA) on the one hand and risk of developing insulin resistance and type 2 diabetes on the other. Our studies in twins have indicated a non-genetic age-dependent origin of insulin resistance and type 2 diabetes associated with being born SGA. In order to gain insight into the molecular metabolic defects and mechanisms linking SGA with insulin resistance and type 2 diabetes, we performed a series of experiments in young and elderly twins, and, in particular, in young men (aged 19-23 years) with a weight at birth at term in the lowest 10th percentile with no family history of diabetes. The control group included age-matched men with birth weights at term in the upper normal range. While body mass index and waist-to-hip ratios were similar in the individuals born SGA and controls, dual-energy X-ray absorptiometry studies documented a higher degree of abdominal obesity in the men who had a low weight at birth. Using the gold standard hyperinsulinaemic-euglycaemic clamp technique combined with glucose tracers and studies of forearm glucose uptake, we found an impairment of insulin-stimulated glycolytic flux and reduced forearm (muscle) glucose uptake in the face of normal whole-body glucose uptake. In addition, we found a significantly decreased insulin secretion rate during oral glucose ingestion after correction for insulin action (disposition index), a paradoxical enhanced insulin suppression of hepatic glucose production and lower fasting plasma glycerol levels, suggesting impaired lipolysis. Finally, analysis of skeletal muscle biopsies showed reduced muscle expression of several key proteins involved in insulin signalling and glucose transport, including protein kinase C-zeta, the two subunits of phosphoinositol 3-kinase (i.e., p85alpha and p110beta) and the insulin-sensitive glucose transporter, Glut-4, in individuals of low birth weight. In conclusion, being born SGA and of low birth weight is associated with type 2 diabetes in a non-genetic manner, and programming of muscle insulin action and signalling represents an early mechanism responsible for this association.     

Impact of birth weight and early infant weight gain on insulin resistance and associated cardiovascular risk factors in adolescence

Background

Low birth weight followed by accelerated weight gain during early childhood has been associated with adverse metabolic and cardiovascular outcomes later in life. The aim of this study was to examine the impact of early infant weight gain on glucose metabolism and cardiovascular risk factors in adolescence and to study if the effect differed between adolescents born small for gestational age (SGA) vs. appropriate for gestational age (AGA).

Methodology/Principal Findings

Data from 30 SGA and 57 AGA healthy young Danish adolescents were analysed. They had a mean age of 17.6 years and all were born at term. Data on early infant weight gain from birth to three months as well as from birth to one year were available in the majority of subjects. In adolescence, glucose metabolism was assessed by a simplified intravenous glucose tolerance test and body composition was assessed by dual-energy X-ray absorptiometry. Blood pressures as well as plasma concentrations of triglycerides and cholesterol were measured. Early infant weight gain from birth to three months was positively associated with the fasting insulin concentration, HOMA-IR, basal lipid levels and systolic blood pressure at 17 years. There was a differential effect of postnatal weight gain on HOMA-IR in AGA and SGA participants (P for interaction = 0.03). No significant associations were seen between postnatal weight gain and body composition or parameters of glucose metabolism assessed by the simplified intravenous glucose tolerance test. In subgroup analysis, all associations with early infant weight gain were absent in the AGA group, but the associations with basal insulin and HOMA-IR were still present in the SGA group.

Conclusion

This study suggests that accelerated growth during the first three months of life may confer an increased risk of later metabolic disturbances – particularly of glucose metabolism – in individuals born SGA.     

Effect of parental anthropometric parameters on neonatal birth weight and birth length

Data on 550 healthy pregnant women, 550 healthy fathers and their healthy term neonates born from singleton pregnancies (37(+0) through 41(+6) week) during a one-year period were reviewed. Maternal mean age was 27.7 +/- 9.37 years, mean pregestational weight 64.0 +/- 9.50 kg, mean gestational weight gain 15.4 +/- 4.33 kg, mean height 169.7 +/- 5.81 cm, and mean gestational age 40.1 +/- 0.95 weeks. Paternal mean age was 31.4 +/- 6.22 years, mean weight 84.6 +/- 10.35 kg, and mean height 182.8 +/- 6.84 cm. Mean birth weight was 3,709.8 +/- 500.48 g and 3,562.5 +/- 443.02 g, and mean birth length 51.5 +/- 1.91 cm and 50.7 +/- 1.62 cm in male and female newborns, respectively, yielding a birth weight greater by 147.3 g and birth length by 0.8 cm in the former. Study variables showed statistically significant correlations: maternal age contributed to the significant correlation between maternal weight and parity, maternal pregestational weight, weight at delivery, gestational weight gain and body height correlated significantly with neonatal birth weight and birth length, gestational age correlated significantly with neonatal weight and length (p = 0.01 all), parity had no major impact (p > 0.05). Paternal height and weight correlated significantly with neonatal birth weight and birth length (p = 0.01). Study results pointed to a significant correlation of maternal pregestational weight, gestational weight gain and body height, and of paternal weight and height with the neonate birth weight and birth length.     

Prematurity and insulin sensitivity

Premature infants of low and extremely low birth weight represent a challenge for neonatal intensive care units and paediatricians. These neonates may be at increased risk of insulin resistance and diabetes perinatally and during childhood. During the first week of postnatal life, infants born prematurely are at risk of abnormalities in glucose homeostasis. Additionally, there are major differences in their glucose/insulin homeostasis compared with infants born at term. Preterm infants are at risk of hypoglycaemia, due to decreases in deposits of glycogen and fat that occur during the third trimester, and also to transient hyperinsulinaemia. Hyperglycaemia may also be observed in preterm infants during the perinatal period. These infants are unable to suppress glucose production within a large range of glucose and insulin concentrations, insulin secretory response is inappropriate, insulin processing is immature and there is an increased ratio of the glucose transporters Glut-1/Glut-2 in fetal tissues, which limits sensitivity and hepatocyte reaction to increments in glucose/insulin concentration during hyperglycaemia. In addition, increased concentrations of tumour necrosis factor alpha present in intrauterine growth retardation (IUGR) and induce insulin resistance. It has been proposed that the reduced insulin sensitivity may result from adaptation to an adverse in utero environment during a critical period of development. We have investigated postnatal insulin resistance in 60 children born with very low birth weight and either small for gestational age or at an appropriate size for gestational age. This study showed that IUGR, rather than low birth weight itself, was associated with increased fasting insulin levels. As poor fetal growth may be associated with the development of obesity, type 2 diabetes and the metabolic syndrome in later life, it is important that we continue to increase our understanding of the effects of IUGR on postnatal growth and metabolism.     

Hyperinsulinemia in pre- and post-pubertal children born small for gestational age

BACKGROUND: Reduced fetal growth is a potential risk factor for development of metabolic abnormalities in later life. The relationship between low birthweight and impaired glucose tolerance, type 2 diabetes and insulin resistance in adulthood has been well documented. PURPOSE: Assuming that fetal undernutrition is associated with insulin resistance in middle age, we elected to study whether this process may already be present in young adults and adolescents born small for gestational age (SGA). SUBJECTS AND METHODS: Children born in Vall d'Hebron Hospital Infantil, Barcelona, between 1986 and 1989 and between 1978 and 1983 with birthweights below the third centile for the local standard values, were invited to participate in the present study. Of those, 51 (22 girls and 29 boys) were pre-pubertal with 9.4 +/- 0.2 years of age and 49 (29 girls and 20 boys ) were post-pubertal, with 17.3 +/- 0.3 years of age. All patients underwent a standard, 2-hour oral glucose tolerance test. Insulin and glucose responses were compared with our previously published data in control children with normal birthweight. RESULTS: The insulin response at 30 min after glucose load was significantly higher (p < 0.001) in pre- and post-pubertal girls and boys formerly SGA than in controls. In addition, the girls also had a higher insulin response at 60 and 120 min. Mean serum insulin (MSI), the area under the insulin curve during the glucose challenge, was statistically increased in pre- and post-pubertal boys and girls born SGA when compared to controls. CONCLUSION: The presence of high insulin levels after an oral glucose challenge in children and adolescents born SGA might be considered as an early marker of subsequent insulin resistance in adulthood. Furthermore, our population offers the opportunity to study the natural course of hyperinsulinemia and its outcome. Follow-up of this cohort may be helpful in distinguishing a subset of young children and adolescents in whom therapeutic intervention could be done.     

Size at birth,maternal nutritional status in pregnancy,and blood pressure at age 17: population based analysis.

OBJECTIVE: To assess the effect of size at birth, maternal nutrition, and body mass index on blood pressure in late adolescence. DESIGN: Population based analysis of birth weight corrected for gestational age, mother''s weight before pregnancy and weight gain in pregnancy, obtained from the Jerusalem perinatal study, and blood pressure and body mass index at age 17, available from military draft records. SETTING: Jerusalem, Israel. SUBJECTS: 10,883 subjects (6684 men and 4199 women) born in Jerusalem during 1974-6 and subsequently drafted to the army. MAIN OUTCOME MEASURES: Systolic and diastolic blood pressures measured at age 17 and their correlation with birth weight, size at birth, mother''s body mass index and weight gain during pregnancy, and height and weight at age 17. RESULTS: Systolic and diastolic blood pressures were significantly and positively correlated with body weight, height, body mass index at age 17, and with mother''s body weight and body mass index before pregnancy, but not with birth weight or mother''s weight gain in pregnancy. CONCLUSION: Variables reflecting poor intrauterine nutrition, including low maternal body mass index before pregnancy, poor maternal weight gain in pregnancy, and being born small for gestational age, were not associated with a higher blood pressure in late adolescence.     

Adult height distribution in subjects born small for gestational age

The aim of the study was to investigate the post-natal growth of subjects born small for gestational age (SGA) by describing adult height distribution and by testing the effects of parental, neonatal and pregnancy-related parameters on the risk for adult short stature. The study population was made of adults selected on birth data from a maternity registry and born either small (SGA, n = 734, birth weight < 10th percentile) or appropriate for gestational age (AGA, n = 886, 25th < birth weight < 75th percentile) in whom anthropometric parameters were measured at 22 years of age. The SGA group demonstrated significantly reduced body size in comparison to the AGA group with a mean loss of 0.7 standard deviation (SD) in adult height. The frequency of adult short stature (< -2 SD) was 10.3% in the SGA group vs. 2.4% in the AGA group (p = 0.0001), adult height < -2.5 SD was observed in only 3.7% of the SGA group. Maternal (OR = 0.31 (0.16-0.62), p = 0.0001) and paternal (OR = 0.45 (0.31-0.67), p = 0.0001) heights and subjects birth length (OR = 0.78 (0.62-0.99), p = 0.04) significantly influenced the risk of adult short stature. In summary, post-natal growth defect remains moderate in the majority of subjects born SGA and < 4% only will end up with severe short stature requiring GH therapy according to most current recommendations. The role of parental height and birth length suggests that adult short stature in SGA subjects results at least in some cases from a familial and likely genetic growth disorder with antenatal onset.     

Sex of preceding sibling and anthropometrics of subsequent offspring at birth and in young adulthood: A population‐based study in Sweden

In many mammal species with sexual dimorphism producing sons is energetically more demanding to the mother than producing daughters. Although some studies in humans have suggested that offspring born after a brother have a smaller birth weight and adult height when compared with those born after a sister, little is known about this intergenerational cost of producing sons. We aimed to study whether the sex of preceding sibling is associated with anthropometrics of the subsequent child at birth and in young adulthood. This population‐based study was carried out on two data sets derived from the Swedish registers. Information on birth weight and length was obtained for 752,723 children of both sexes. Adult weight, height and muscle strength were available for 506,326 men. Multiple linear regression analyses showed that boys and girls born after a brother were, respectively, 18 and 9 g lighter and 0.08 and 0.03 cm (P < 0.001) shorter at birth than those born after a sister. Adjustment for gestational age decreased the magnitude of the associations [10 g and 0.04 cm (P < 0.001) in men and nonsignificant estimates in women], suggesting that part of the lower mean birth weight and length of individuals born after a brother was due to a shorter gestation. In young adulthood, men with a preceding brother showed 0.16 kg more in weight, 0.3% higher body mass index (P < 0.001) and a trend towards reduced height and muscle strength. Our results suggest that even though the sex of the previous child is associated with the anthropometrics of the subsequent child, the effect sizes are very small questioning whether this mechanism has adaptive value in contemporary humans. Am J Phys Anthropol 154:471–478, 2014. © 2014 Wiley Periodicals, Inc.     

Prematurity--another example of perinatal metabolic programming?

Low birth weight is associated with both later adult diseases such as type 2 diabetes mellitus and a number of metabolic abnormalities, the foremost of which is insulin resistance. Indeed the link between an adverse perinatal environment, manifested by low birth weight, and adult life pathology may be an early, permanent reduction in insulin sensitivity. A reduction in insulin sensitivity has been demonstrated in small for gestational age (SGA), term subjects from childhood through to adulthood. Less is known about children born premature into an adverse neonatal environment. We present data demonstrating that premature infants also have metabolic abnormalities similar to those observed in term, SGA children and that these occur irrespective of whether they are SGA or appropriate for gestational age (AGA).     

Reference values for height, weight and body mass index of German born Turkish children

Turkish children and adolescents born in Northern Europe grow different from native Northern European children, but reference values for height, weight and BMI for these children do not exist. With this study, we intend to provide growth standards for German born Turkish children. Data were obtained from 797 Turkish children and adolescents born in Germany age 0-25.8 years (males), respectively 0-18.3 years (females). We generated synthetic reference values for height, weight, and BMI. The results show that Turkish children and adolescents are heavier after the age of 6 years, and that they remain short after puberty. Eighteen year old Turkish men, and 15-year-old Turkish women are shorter (males 175.2 cm vs. 180.4 cm, p < 0.05; females 159.3 cm vs. 165.0 cm, p < 0.05), and heavier than Germans. Six out of 53 young Turkish men and 9 out of 100 young Turkish women were obese. Twelve out of 53 young Turkish men (23%) and 18 out of 100 young Turkish women (18%) have fallen below the 3rd centile for height. It can be concluded that growth of Turkish children and adolescents born in Germany significantly differs from native children. Reference LMS values for body height, weight and BMI of German born Turkish boys and girls are presented.     

Decreasing Birth Weight Is Associated with Adverse Metabolic Profile and Lower Stature in Childhood and Adolescence

Objective

We aimed to evaluate the association of birth weight SDS with insulin resistance, blood pressure, and auxology in children and adolescents born 23–42 weeks of gestation.

Methods

We studied 143 singleton children and adolescents aged 9.3 ± 3.3 years (range 2.0–17.9 years). Clinical assessments included insulin resistance measured by HOMA2-IR, auxology, and blood pressure from sphygmomanometer measurements. Continuous associations were examined, and stratified analyses carried out. For the latter, participants were divided into those of below-average birth weight (BABW, <0 SDS) and above-average birth weight (AABW, ≥0 SDS).

Results

Irrespective of gestational age, lower birth weight SDS was associated with progressively greater HOMA2-IR (p<0.0001) and higher fasting insulin concentrations (p<0.0001). Decreasing birth weight SDS was associated with higher systolic (p = 0.011) and diastolic (p = 0.006) blood pressure. Lower birth weight SDS was also associated with decreasing stature (p<0.010). The BABW group was ~40% more insulin resistant than AABW participants (p = 0.004), with the former also displaying fasting insulin concentrations 37% higher (p = 0.004). BABW participants were 0.54 SDS shorter than those of higher birth weight (p = 0.002). On average, BABW participants had not met their genetic potential, tending to be shorter than their parents (p = 0.065). As a result, when corrected for parents'' heights, BABW participants were 0.62 SDS shorter than those born of higher birth weight (p = 0.001). Sub-group analyses on participants born appropriate-for-gestational-age (n = 128) showed that associations of birth weight SDS with both insulin resistance and stature remained (although attenuated).

Conclusion

Decreasing birth weight SDS (even within the normal range) is associated with adverse metabolic profile and lower stature in children and adolescents.     

Association of low birth weight with beta cell function in the adult first degree relatives of non-insulin dependent diabetic subjects.

OBJECTIVE--To examine the relation between birth weight and beta cell function in the first degree relatives of non-insulin dependent diabetic subjects. DESIGN--Cross sectional study of 101 adults of known birth weight from 47 families which had at least one member with non-insulin dependent diabetes. SUBJECTS--101 white adults aged mean 43 (SD 7) years. SETTING--Oxfordshire, England. MAIN OUTCOME MEASURES--Glucose tolerance was measured by continuous infusion glucose tolerance test. beta cell function and insulin sensitivity were calculated from the fasting plasma glucose and insulin concentrations with homeostasis model assessment. beta cell function was standardised to allow for the confounding effects of age and obesity. RESULTS--Twenty seven subjects had non-insulin dependent diabetes, 32 had impaired glucose tolerance, and 42 were normoglycaemic. Birth weight correlated with the beta cell function of the complete cohort (rs = 0.29, p = 0.005), the non-insulin dependent diabetic subjects (rs = 0.50, p = 0.023), and the non-diabetic subjects (rs = 0.29, p = 0.013). The non-insulin dependent diabetic (n = 27) and the non-diabetic (n = 74) subjects had similar mean (inter-quartile range) centile birth weight 50% (19%-91%), and 53% (30%-75%) respectively. Non-insulin dependent diabetic subjects had significantly lower beta function than the non-diabetic subjects: 69% (48%-83%) v 97% (86%-120%), p < 0.001. CONCLUSIONS--The cause of the association between low birth weight and reduced beta cell function in adult life is uncertain. Impaired beta cell function in non-insulin dependent diabetic subjects was not accounted for by low birth weight, and genetic or environmental factors are likely to be necessary for development of diabetes.     

Intrauterine growth pattern and risk of childhood onset insulin dependent (type I) diabetes: population based case-control study.

OBJECTIVE: To investigate whether prenatal growth affects the risk of development of childhood onset insulin dependent (type I) diabetes mellitus. DESIGN: Population based case-control study. SETTING: Data from a nationwide childhood diabetes case register were linked with data from the nationwide Swedish Medical Birth Registry. SUBJECTS: Data from a total of 4584 diabetic children born after 1973 and diagnosed with diabetes from 1978 to 1992 were studied. For each child with insulin dependent diabetes three control children were randomly selected from among all infants born in the same year and at the same hospital as the proband. MAIN OUTCOME MEASURES: Birth weight, gestation, maternal age and parity, number of previous spontaneous abortions, and sex specific birth weight by gestational week expressed as multiples of the standard deviation (SD). RESULTS: There was a clear trend in the odds ratio for childhood onset diabetes according to SD of birth weight. The odds ratio (95% confidence interval) for small for gestational age after stratification for maternal age, parity, smoking habits, and maternal diabetes was 0.81 (0.65 to 0.99) and for large for gestational age after similar stratification was 1.20 (1.02 to 1.42). CONCLUSIONS: Intrauterine conditions that affect prenatal growth seem also to affect the risk of development of childhood diabetes in the way previously described for postnatal growth: a poor growth decreases and an excess growth increases the risk. The mechanism for this association is unclear.     

Chromosomal region 13q21q31 and heterochrony of development

If the theory of evolution is now largely accepted, there are still many debates on the mechanisms of evolution, including human evolution. One of these mechanisms is heterochrony of development including progenesis and neoteny. We report on a patient who could be an example of human progenesis. This boy was born prematurely, after a cesarian section for preeclampsia. Family history was unremarkable. He walked unaided when he was 2.5 years old. At 5 years of age height was 95 cm (< 3rd centile), weight 18.6 kg (40th centile) and OFC 54 cm (98th centile is 53 cm). He had a macropenis. He attended elementary school. However, at 9 years of age he had to have special education. Puberty occurred when he was 8 years old. At 14 years of age height was 141 cm (3rd centile is 144 cm), weight 32.5 kg (3rd centile) and OFC 55.5 cm (75th centile). At physical examination he had hypertelorism, narrow forehead, short philtrum, retromicrognathia, large and low set ears, hyperlaxity, overcrowed teeth, dorsal kyphosis, and macropenis. Karyotype showed a deletion 13q21q31. The deletion was de novo and pure. In conclusion this case with sexual precocity and small final stature could be an example of progenesis, rising the question of the presence of a critical region for human evolution within chromosomal region 13q21q31.     

Waist circumference cutoff points in school-aged Chinese Han and Uygur children

Objective: To examine the distribution of age‐ and gender‐specific waist circumference (WC) and to identify optimal cutoffs for predicting cardiovascular (CV) risk factors in Chinese Han and Uygur children. Methods and Procedures: In total 4,224 Han and Uygur children aged 7–18 were randomly selected from schools in Urumqi city, China. WC, height, and weight were accurately measured in all subjects. Blood pressure, fasting lipids, glucose, and insulin were determined in 258 overweight/obese children and 370 age‐, gender‐, and ethnicity‐matched normal‐weight controls selected from the same study sample. LMS (lambda‐mu‐sigma) method was used to construct WC centile curves. Optimal WC cutoffs were determined by comparing the performance of five sets of WC cutoffs in predicting CV risk factors. Results: Han boys and girls had higher WC at all percentiles and ages except for girls over the age of 16. Uygur girls also showed a greater increase in WC corresponding with age (2.1 cm/year vs. 1.6 cm/year for the median) than Han girls. Compared with the other four sets of cutoffs, the 85th WC percentile showed the best combination of sensitivity (81.0%) and specificity (71.4%). The two sets of WC cutoffs constructed by allowing centile curves passing through the adult cutoffs for central adiposity using the fitted LMS curves provided poor sensitivities in predicting the presence of cluster of CV risk factors. Discussion: The growth pattern of WC varies with gender and ethnicity. The 85th percentile of WC is an appropriate cutoff for Chinese Han and Uygur children in the prediction of CV risks.