Visscher of the Queensland Institute of Medical Research in Australia recently reported that the heritability of height is 80 percent, based on 3, pairs of Australian twins and siblings.
This estimate is considered to be unbiased, as it was based on a large population of twins and siblings and a broad survey of genetic markers. In the U. These estimates are well supported by another study of 8, pairs of Finnish twins, in which the heritability was 78 percent for men and 75 percent for women.
Other studies have shown height heritability among whites to be even higher than 80 percent. Because different ethnic populations have different genetic backgrounds and live in different environments, however, height heritability can vary from one population to another, and even from men to women. In Asian populations, the heritability of height is much lower than 80 percent.
For example, in Miao-Xin Li of Hunan Normal University in China and his colleagues estimated a height heritability of 65 percent, based on a Chinese population of families. In African populations, height heritability is also lower: 65 percent for the population of western Africa, according to a study by D. Roberts, then at Newcastle University in England, and colleagues.
Such diversities in heritability are mainly due to the different genetic background of ethnic groups and the distinct environments climates, dietary habits and lifestyle they experience. Heritability allows us to examine how genetics directly impact an individual's height. For example, a population of white men has a heritability of 80 percent and an average height of centimeters roughly five feet, 10 inches.
If we meet a white man in the street who is cm six feet tall, the heritability tells us what fraction of his extra height is caused by genetic variants and what fraction is due to his environment dietary habit and lifestyle. The man is five centimeters taller than the average. Thus, 80 percent of the extra five centimeters, or four centimeters, is due to genetic variants, whereas one centimeter is due to environmental effects, such as nutrition.
Heritability can also be used to predict an individual's height if the parents' heights are known. Descriptive statistics of height by age and sex for the pooled data all cohorts together and by geographic-cultural region are presented in Table 1. When comparing geographic-cultural regions, mean height was tallest in Europe, somewhat shorter in North-America and Australia and shortest in East-Asia at all ages in boys and girls.
The variation of height showed a less clear pattern but was generally greatest in North-America and Australia and lowest in East-Asia. The proportion of environmental variation shared by co-twins was greatest at age 1 0.
Accordingly, heritability was lowest at age 1 0. The proportion of height variation explained by environmental factors unique to each twin individual, which also includes measurement error, did not show any clear age pattern and was largely similar at all ages 0. In spite of the observed sex differences in the relative variance components at most of ages See Supplementary Table S2 , the age pattern was generally similar in boys and girls; the biggest sex-differences were found in late adolescence when the heritability estimates were slightly greater in boys.
The point estimates for the genetic correlations within opposite-sex DZ pairs were generally lower than 0. Univariate models for height were then conducted separately in the three geographic-cultural regions. Only the estimates of additive genetic factors are presented in Fig. The three geographic-cultural regions showed the general trend of increasing proportion of additive genetic factors with age during childhood. Explained by its largest sample size, the pattern in Europe was practically the same to that observed for all cohorts together, but with slightly greater heritability estimates at most ages.
In North-America and Australia and East-Asia, heritability estimates in childhood were generally somewhat lower than in Europe. In spite of the roughly similar age patterns, the proportions of height variation explained by genetic and environmental factors were different between the geographic-cultural regions See Supplementary Table S2. The Chinese National Twin Registry was excluded from these analyses because the heritability estimates in that cohort were substantially lower than in other East-Asian cohorts.
When data from this cohort was included in the analyses for East-Asia, the proportion of genetic factors decreased and common environmental factors increased considerably; the change in heritability estimates was from 0. Finally, we studied how age modifies the genetic and environmental variances of height by using gene-age interaction analysis, with data pooled across all age groups. When stratified by geographic-cultural region, genetic variation was largest in North-America and Australia, somewhat lower in Europe and lowest in East-Asia, particularly for boys.
The pattern of genetic variance increasing to a maximum and thereafter decreasing was consistent across the regions. Unique environmental variation showed a similar pattern and magnitude in the three geographic-cultural regions. When comparing sexes, in Europe and North-America and Australia there was a trend toward a greater genetic variation for boys than for girls, which increased with age.
Change of additive genetic dash line , common environmental solid line and unique environmental dot line variance with increasing age in quadratic gene-environment interaction model in Europe, North America and Australia and East Asia.
The present study of , paired measurements from 86, complete twin pairs in 20 countries revealed that environmental factors shared by co-twins contribute to the inter-individual variation in height from infancy to early adulthood. The relative proportion of common environmental factors was greatest during the first years of life, representing almost half of the variation at age 1 and decreased over childhood and adolescence.
The interpretation of these results, however, deserves some caution. It has been questioned whether twin studies are suitable for estimating heritability of height in infancy, since early growth patterns in twins differ considerably from singleton growth patterns Prenatal environmental factors can act very differently on MZ twins leading to differences in body size within pairs the most extreme case is the twin-to-twin transfusion syndrome.
This is an important issue because in the classical twin design heritability is estimated by comparing the resemblance of MZ and DZ twin pairs and thus body size differences in MZ pairs will result in lower heritability estimates. Since children may take several years to fully catch-up after birth, the high proportion of height variation explained by the shared environment in infancy may still reflect these prenatal environmental factors.
Among other possible explanations, it might be that the shared environment represents the effects of gestational age or the effects of the higher measurement error correlated in twins at earlier ages. Studies have shown that the secular trend in adult height occurs during the first two years of life mainly due to increases in leg length A plausible explanation is that the period of most rapid growth, when the effect of an adverse environment is strongest, coincides with the period when most growth takes place in the long bones of the legs Multinational studies analyzing the genetic and environmental influences on body length segments, particularly leg length, are thus needed to disentangle the aetiology of total height variation.
The small but considerable effect of unique environment on height variation, very similar across ages, may partly be due to measurement error, which is modelled as part of unique environmental factors. However, it is likely that it also reflects real environmental factors, for example, different exposure to childhood diseases.
Given the rapid growth that occurs in infancy, childhood and adolescence, in this individual-based pooled analysis we analyzed the heritability of height in one year age groups. We found that genetic contributions increase over childhood with heritability estimates in the range of previous studies in children and adults 15 , 16 , 18 , 20 , GWA studies have identified many common genetic variants for adult height.
The most recent GWA meta-analysis in , individuals of European ancestry identified genome-wide significant SNPs in loci that together explained one-fifth of the heritability for adult height However, much less is known on the genetics of height in children.
Van der Valk et al. The pattern of total height variation across ages was largely driven by genetic variance. After that point, even if mean height continued to increase, genetic variance started to decrease in such a way that in late adolescence the magnitude was similar to that before pubertal events start. Adolescence is characterized by the onset of puberty and the occurrence of growth spurts. In this study, twins within age groups are at various stages of puberty.
In addition to the substantial heritability reported for pubertal timing 32 , a genome-wide genetic correlation 0. In fact, a genome-wide association meta-analysis showed that five loci associated with pubertal timing impacted multiple aspects of growth, both before and during puberty Therefore, it is possible that some of the genetic variance in height at these ages is confounded with genetic variance in pubertal events.
In spite of the largely similar age patterns observed in boys and girls, boys showed somewhat greater heritability estimates and genetic variation, especially in late adolescence. Moreover, some studies have shown a sex-specific genetic effect on height variation in adolescents 19 and adults It is clear that both of the sex chromosomes are implicated in determining mean height.
Short stature has been demonstrated in females with Turner syndrome who have only one X chromosome 35 and taller stature seen in XYY men compared with XY men However, sex chromosomes have also been associated with height variation; for example, Gudbjartsson et al. Comparison between geographic-cultural regions showed that mean height was greatest in Europe, somewhat shorter in North-America and Australia and shortest in East-Asia, but total variance was largest in North-America and Australia.
Accordingly, genetic variation was also greatest in North-America and Australia and lowest in East-Asia. However, the relative proportions of additive and environmental variations were more similar in the different geographic-cultural regions. These results are consistent with a previous comparative twin study which found that the mean and variance of height were larger in Caucasian than in East-Asian populations in adolescence, but the heritability estimates were still at the same level An important proportion of the differences in total variances between geographic-cultural regions were attributable to genetic differences.
It may be that allelic frequencies and effects of the genes involved in height vary between Europeans, North-Americans and Australians and East-Asians, leading to differences in genetic variation between the three population groups.
However, a major part of the differences in genetic variation may also be because of gene-environment interactions modelled as part of the additive genetic component in our model. That is, the higher genetic variation observed in Caucasians could arise because there is a set of genes expressed more strongly in Western environments.
For example, a study of adults of Japanese descent living in the United States and native Japanese found that Japanese men and women were shorter than Japanese-Americans, suggesting that environmental factors play a role in physical growth Analyzing this question in detail would require collection of twins or GWA studies in unrelated individuals with East-Asian origin living in a Western environment.
However, our study found that shared environmental variance also differed between geographic-cultural regions. The lower shared environmental variance observed in East Asian girls and greater in North-America and Australia during childhood may reflect cultural differences in terms of nutrition and other environmental resources. It is also important to note that we limited our East-Asian cohorts to affluent East-Asian populations including the Shandong and Guangdong provinces but excluding poorer areas of China.
As reported previously, the heritability estimates of height were considerably lower and common environmental estimates higher in the poorer areas 40 , which may indicate larger differences between families in nutrition and infection history in these areas of China. This emphasizes the need to collect data on twins living under different environmental exposures.
Twin participants are from 20 different countries, thereby making it possible to stratify the analyses by regions representing different ethnicities and environments. Important advantages of individual-based data are better opportunities for statistical modelling and lack of publication bias.
However, our study also has limitations. The equal-environment assumption, upon which twin methodology is based, assumes that MZ and DZ twins are equally exposed to environmental factors relevant to the outcome. If equal-environment assumption is violated, it should be seen as differences in variances between MZ and DZ twins, but we did not find such evidence. In the classical twin design phenotypic assortment increases DZ correlations and thus inflates the common environmental component when not accounted for in the modelling.
Assortative mating is well recognized for height and when the potential underestimation of heritability estimates was corrected using a sample of twins and their parents 41 , these authors showed that doing so increased the heritability estimates from 0.
In our database we do not have information on parental height and thus could not take into account assortative mating, which may thus explain part of the shared environmental variation. A recent study showed that increased homozygosity, which is influenced by inbreeding, was associated with decreased height and that the effect sizes were similar across different continental groups and populations with different degrees of genome-wide homozygosity These authors thus suggested that homozygosity, rather than confounding as a result of environmental or additive genetic effects, directly contributes to phenotypic variance Further, most of the height measures were self-reported 43 , which are prone to error and can bias our analyses toward lower heritability estimates and higher estimates of unique environmental effects.
This demonstrates the need for new data collections in these regions. Worthwhile objectives for future research are to study whether the same genetic and environmental factors contributing to height variation operate throughout time or new genes or new environmental factors start to operate at different ages and to analyze the heritability of growth in height.
Serious diseases can also negatively affect growth, especially if they occur in childhood; celiac disease , bone disease, such as rickets and juvenile osteoporosis, and anemia are all examples. Although an unhealthy diet and serious illness in childhood can lead to a shorter stature, research suggests that genetic coding is far more influential.
In a study published in the journal Genetics , Hsu showcased the importance of genes in the determination of height. Along with colleagues, he used machine learning and computer algorithms to analyze close to half a million genomes of people living in the United Kingdom. After crunching the numbers, the team was able to accurately predict a person's height and bone density from just their genes. Moreover, genetic mutations and hormonal imbalances have also been linked to short stature, including dwarfism, a condition in which a person stands at 4 feet, 10 inches centimeters tall or less.
Dwarfism can be split into two subtypes. First, there's what is known as disproportionate dwarfism, which is when some parts of the body are small, but others are either of average or above-average size. On the flip side, a poor diet could lead to a shorter stature compared to your parents. Children of a poor socioeconomic status may be at risk of a lack of access to nutrition, along with poor access to adequate health care.
This, in turn, can contribute to a shorter height. You may notice that boys grow slower than girls at first, due to differences in puberty milestones.
Overall though, adult males tend to be an average of 14 centimeters 5. During puberty, hormones are essential for regulating body growth. These include thyroid hormones, human growth hormones, and sex hormones such as testosterone and estrogen. Any abnormalities in these hormones could alter growth as well as your overall height.
Children who develop hypothyroidism low thyroid or pituitary gland disorders may experience shorter than average height compared to their parents. Rarely, hormonal disorders can contribute to being taller than normal. For example, gigantism is caused by too many human growth hormones produced by pituitary gland tumors. For example, achondroplasia dwarfism is a rare bone growth disorder that runs in families. Another congenital disorder that can cause short stature is known as Turner syndrome.
This rare condition causes delays in puberty. Other congenital disorders lead to a taller than normal stature. These include Marfan and Klinefelter syndromes.
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