Co-evolution of glucose-6-phosphate dehydrogenase deficiency and quinine taste sensitivity.

We hypothesized that 'quinine' taste sensitivity functions to regulate the intake of bitter-tasting, naturally occurring antimalarial substances of plant origin, and that this genetic trait has co-evolved with the G6PD locus. This hypothesis was tested by evaluating taste sensitivity to quinine sulphate and sodium chloride among 17 G6PD-deficient and 25 G6PD-normal African American subjects 14-40 years of age. There was no significant difference in mean 'quinine' taste sensitivity between the two groups, although there was a trend towards greater 'quinine' taste acuity among the G6PD-deficient subjects. A larger study sample would provide a fairer test of the hypothesis.