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A unique resource of longitudinal childhood height data available in Finnish population cohorts was used to study the largely unknown genetic underpinnings of height growth. The partially correlated variants at LIN28B which influence the entire period of postnatal growth implied a critical role for LIN28B in the regulation of human growth.

Adult height is determined by genetic potential and by net nutrition, the balance between food intake and the demands on it, including the demands of disease, most importantly during early childhood. Historians have made effective use of recorded heights to indicate living standards, in both health and income, for periods where there are few other data. Understanding the determinants of height is also important for understanding health; taller people earn more on average, do better on cognitive tests, and live longer. This paper investigates the environmental determinants of height across 43 developing countries. Unlike in rich countries, where adult height is well predicted by mortality in infancy, there is no consistent relationship across and within countries between adult height on the one hand and childhood mortality or living conditions on the other. In particular, adult African women are taller than is warranted by their low incomes and high childhood mortality, not to mention their mothers' educational level and reported nutrition. High childhood mortality in Africa is associated with taller adults, which suggests that mortality selection dominates scarring, the opposite of what is found in the rest of the world. The relationship between population heights and income is inconsistent and unreliable, as is the relationship between income and health more generally. income | mortality | Africa | nutrition | childhood

Research indicates that there is a strong link between an individual's height and upward social mobility, creating a genetic propensity for tallness among those in higher social classes. Studies included paternal and maternal education, occupational status, and urban and rural residence localities.

A study of the heights of parents of children with growth hormone deficiency revealed that the mothers tended to be short in stature. However, it is not clear whether short stature of the mother is characteristic only for children with growth hormone deficiency or whether this feature occurs in other forms of short stature, such as that due to genetic causes or delayed growth. Previous studies examining the relation between heights of children and parents were conducted with normal children; consisted of small numbers of subjects; and did not compare heights of mothers and fathers. Consequently, the relation of heights of parents and children were assessed in 341 children with short stature of varying causes. The children were classified into three groups according to the cause of short stature: genetic short stature; delayed growth; and normal short stature or height in the 5th to 25th percentile of the growth curve. The average height of mothers of children with genetic short stature, 157.7 centimeters (cm), was less than the average height of mothers of children with delayed growth, 161.1 cm, or of mothers of children with normal short stature, 162.5 cm. (These heights are about 62, 63 and 64 inches, respectively.) The average height of fathers was similar for all groups. These findings indicate that the height of a child with genetic short stature is related more to the mother's height. This relation was not observed among children with short stature due to delayed growth. (Consumer Summary produced by Reliance Medical Information, Inc.)

The robust family based association test is used to test 18 single nucleotide polymorphisms and seven haplo-type blocks covering the full transcript length of the RANK gene. Study suggests that RANK polymorphisms contribute to adult height variation.

The effect of genetic and environmental factors on the association between self-reported height and education in Minnesota and Finland are studied. The data included 1598 twin pairs in Minnesota and 5454 twin pairs in Finland born between 1936 and 1955.

We examined sources of variability in stature, body mass, and body mass index (BMI) in families of black and white elementary schoolchildren from Philadelphia, Pennsylvania. The sample consisted of 445 black and 379 white children, 7-13 years old, and their parents (total n = 2016). The sample was distributed among 596 nuclear families, each representing an independent pedigree. Maximum-likelihood-based variance decomposition methods were used to simultaneously estimate ethnic group-specific effects of genes, sex, age by sex, and unmeasured environmental factors on stature, body mass, and BMI. Likelihood ratio tests were performed to assess the significance of [h.sup.2] estimates and differences in [Σ.sub.g] and [Σ.sub.e] between black and white families. Genes account for moderate proportions of the phenotypic variance ([h.sup.2]) of these traits in black and white children. In black and white children, respectively, [h.sup.2] estimates were 0.37 and 0.53 for stature, 0.37 and 0.31 for body mass, and 0.38 and 0.24 for BMI (p < 0.0005). Although the differences in [h.sup.2] between ethnic groups were not significant (stature, p = 0.23; body mass, p = 0.49; BMI, p = 0.14), black children exhibited a significantly greater total residual phenotypic standard deviation ([Σ.sub.e] and [Σ.sub.g]) in body mass and BMI and a significantly greater [Σ.sub.e] for stature compared with white children. The larger residual phenotypic variance in the black sample is likely due to exposure to unmeasured environmental factors that are not accounted for in this model. Given that [Σ.sub.g] for stature is not significantly different between ethnic groups, the slightly lower estimates in black children are due to the increased contribution of the environment to the phenotypic variance in this trait. KEY WORDS: GENETICS, HERITABILITY, OBESITY, BODY MASS INDEX, YOUTH, CHILDREN, Body mass index (BMI) is often used as a proxy measure for body fatness because it is correlated with body mass and percentage of body fat in the general population [...]

One of the largest-ever genome-wide association studies has identified 697 genetic variants for human height--several hundred more than a previous, smaller study. Peter Visscher of the University of Queensland in [...]

You can mainly blame--or thank--your genes for your height. But although an estimated 80% of the variability in height is thought to be down to genetic factors, pinpointing which genes [...]

Evolutionary models of sexual dimorphism link increased male size to male-male competition, while female size is tied to the nutritional requirements of reproduction. Molecular correlates of this model have not been explored. The androgen receptor gene, located on the X chromosome, mediates male reproductive development. Mutations of this gene interfere with virilization suggesting that this gene may be linked to the evolution of primate sexual dimorphism. A genetic mechanism for the evolution of dimorphism must account for the continuous inter-specific variation of dimorphism. Expansion of the tri-nucleotide CAG repeat in the androgen receptor gene is a possible mechanism for modulating dimorphism among primate species. The androgen receptor gene was sequenced from a convenience sample of Catarrhine primates including chimpanzee (n=6) gorilla (n=3), orangutan (n=l), gibbon (n=l), baboon (n=4), and macaque (n=3). The index of dimorphism was calculated as mean female weight divided by mean male weight for the species. Results show a negative correlation between repeat expansion and this index of dimorphism. This finding is consistent with a role for the expansion of this simple sequence repeat in the evolution of primate sexual dimorphism. Directional evolution toward an expanded CAG repeat has been proposed elsewhere. However, the causal link between the expanded tri-nucleotide repeat and several neuro-degenerative diseases indicates that excessive expansion has deleterious effects. One of the attractive features of this hypothesis is that it provides a genetic mechanism underlying variation in sexual dimorphism among species.