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Glucose6-phosphate dehydrogenase deficiency is one of the most common enzyme defects in humans and it is highly prevalent among populations in malaria-endemic areas of sub-Saharan Africa and the Middle East where approximately up to 7.5% of people are affected (Nkhoma et al., 2009)

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The genetic correlates relate primarily to variants in the genes coding for transporters controlling plasma UA, yet such presumed functional variants will also influence, through the same proteins, the transport of UA into the brain and subsequently into neurons and glia, as described below

In addition, it is possible that evolution led to shared redox-sensing channels (e.g., Hyperkinetic and Shaker) to mechanically link sleep-active neurons and redox metabolism in order to more efficiently serve a common fundamental need