New genetic variants of decreased TBG binding capacity observed in our studies are described and discussed in relation to previously reported variant types. Although single factor inheritance may explain the strikingly different phenotypes found in X-linked variants it cannot explain the wide variation discerned in the majority of individuals in our control population or the phenomenon of nonpentrance in one of our families. TBG binding capacity may be a polygenic trait with many loci contributing to the observed phenotypes.
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