The genetic consequences of our sweet tooth

  • Published 2009

Abstract

she has a complete set of teeth free of decay. Like many patients with HFI, this individual is homozygous for a point mutation (A149P) that interferes with the catalytic action of aldolase B on the specific metabolite of exogenous fructose, fructose-1-phosphate4 (FIG. 1a). Individuals that are heterozygous for mutations in aldolase B show no symptoms of disease; they have no resting biochemical phenotype and manifest no obvious advantage. The A149P mutation seems to have had an ancient common origin on an ancestral HAPLOTYPE5 and therefore spread, presumably by GENETIC DRIFT, in the absence of long-term selection, through the populations of Europe. Studies in Switzerland and the United Kingdom have shown that HFI occurs with an estimated birth frequency of ~1 in 20,000 — indeed, heterozygotes for the A149P allele alone occur at almost polymorphic frequency (>1 in 100) in the general population1,4–7. Although HFI has a long history in the human population, the disease itself has only recently risen to prominence. As I describe below, changes in our lifestyle — specifically, our overconsumption of sugars — lie at the heart of this rise to prominence. A massive agro-industrial effort, based historically on former sugar colonies, now meets global demand for these commodities — but the consequences for human health extend well beyond HFI.

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Cite this paper

@inproceedings{2009TheGC, title={The genetic consequences of our sweet tooth}, author={}, year={2009} }