The heritability of human height

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Publicado em Fri May 18 16:09:27 GMT-03:00 2012
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The heritability of human height Bruce Weir

#28;The heritability of human height

Dr. Bruce Weir,
Professor and Chair, of the Department of Biostatistics,
University of Washington in Seattle.



In 1886 Francis Galton published data on heights for people and their parents. He showed that people#25;s heights tended to be closer to the population mean height than was the average of their parents#25; heights, introducing the concept of #28;regression to the mean.#29; He went on to show that the relationship between the heights of pairs of people depends on the degree of relatedness between the pair. His work was replicated by Karl Pearson in 1903, three years after the rediscovery of Mendel#25;s Laws and #28;in the present controversial phase of the theory of heredity.#29; With the introduction of quantitative genetic models (and the analysis of variance) by R.A. Fisher in 1918 we now express the correlation in heights for pairs of people in terms of their relatedness and the heritability of height. Heritability of a trait is the portion of variance in trait values that has an (additive) genetic component. By measuring heights on pairs of people of known family relatedness, geneticists have estimated the heritability of human height to be about 0.80. The recent flurry of genome-wide association studies has revealed many genetic markers, SNPs, as - associated with height #19; a 2010 publication listed 135 from a meta-analysis of 133,653 heights. However, these SNPs collectively accounted for only 10% of the variation in height and the search began for the #28;missing heritability.#29; Using data from the GENEVA pro ject that have been processed in our department, P.M. Visscher has extended the early work of Galton, Pearson and Fisher by using all the SNPs scored in a genome-wide scan, and by using measures of relatedness estimated from these SNPs instead of being inferred from family history. He could account for 45% of the variation. I will explain his approach (Yang et al., Nature Genetics 43:519#19;525, 2011) and suggest ways to account for the remaining 35%.