ABSTRACT
Favism was known to affect more males than females, and it also seemed to be confined to certain families. The studies have shown that almost all cases of favism and primaquine sensitivity possess a gene that produces a deficiency of glucose-6-phosphate dehydrogenase (G6PD) activity. Female heterozygotes for the G6PD deficiency alleles have a variable amount of enzyme activity. Since males have only one allele for a sex-linked locus, the frequency of males with the G6PD deficiency would be the same as the frequency of the deficiency allele in the population. The electrophoretic variants of G6PD have been shown to be sex-linked. Each area with high G6PD-deficiency frequencies seems to have its own variant that causes the deficiency. The data for the linkage of G6PD-deficiency alleles with other sex-linked loci in different human populations seem to result in different X-chromosome maps.
