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The genetic consequences of our sweet tooth

Nature Reviews Genetics volume 3, pages 481–487 (2002)Cite this article

Abstract

First reported in 1956, hereditary fructose intolerance (HFI) illustrates vividly how interactions between genes and nutrients can influence taste preferences; the disease also reflects the ascendancy of sucrose and fructose as energy sources and as the world's principal sweeteners. However, HFI is not the only genetic ill to have emerged from our obsession with sugar: the slave trade, which had such a key part in the development of the sugar industry, also included major genetic consequences in its haunting legacy.

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Figure 1: Metabolic defect in hereditary fructose intolerance.
Figure 2: World production of raw sugar.
Figure 3: Sources of sugar.

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Author information

Authors and Affiliations

  1. Department of Medicine, University of Cambridge, Level 5, Addenbrooke's Hospital, Cambridge, CB2 2QQ, UK

    Timothy M. Cox

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  1. Timothy M. Cox
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DATABASES

LocusLink

aldolase B

G6PD

Sac/Tas1r3

TAS1R3

OMIM

glucose 6-phosphate dehydrogenase deficiency

hereditary fructose intolerance

non-insulin-dependent (type II) diabetes mellitus

phenylketonuria

sickle cell anaemia

FURTHER INFORMATION

Encyclopedia of Life Sciences

Fructose metabolism disorders

Glossary

ACIDOSIS

An excess of acid in the body fluids as a primary disturbance of hydrogen ion metabolism.

CENTRIFUGAL SUGAR

An industrial term for the product of modern sugar factories; commercial sugar is described as raw sugar if it is >96% sucrose and further refining generates the pure product. The terms 'centrifugal' and 'non-centrifugal' distinguish between the products of modern and traditional methods of manufacture: they refer to the methods used to separate sucrose crystals from the molasses.

FRUCTOSAEMIA

The presence of fructose in the blood.

GENETIC DRIFT

The random changes in allele frequency that occur because genes that appear in offspring are not a perfectly representative sample of the parental genes (for example, as occurs in small populations).

GLUCAGON

A pancreatic hormone released from the islets of Langerhans. It stimulates the formation of glucose, especially by activating liver phosphorylase, through the hormone-sensitive adenyl cyclase signalling pathway. Phosphorylase is the rate-limiting enzyme for the breakdown of glycogen.

HAPLOTYPE

An experimentally determined profile of genetic markers that are present on a single chromosome of any given individual.

HYPERMAGNESAEMIA

A high plasma concentration of ionized magnesium.

HYPERURICAEMIA

A high plasma-urate concentration.

HYPOGLYCAEMIA

A low blood-glucose concentration.

SICKLE CELL TRAIT

Heterozygosity for the inherited β-globin variant, HbS; the individual does not have sickle cell disease.

β-THALASSAEMIA

A group of inherited blood diseases caused by reduced synthesis of β-globin polypeptide chains.

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Cox, T. The genetic consequences of our sweet tooth. Nat Rev Genet 3, 481–487 (2002). https://doi.org/10.1038/nrg815

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