DO GEOLOGIC FACTORS CONTROL DIETARY SE DEFICIENCY AFFECTING ETIOLOGY OF VIRAL INFECTIOUS DISEASES (VIDs)

The Oldfield map (2002) of regions low in geologic Se bioavailability was overlain with etiological origins of various diseases. Resulting correlations were stark: pandemic influenzas (1957 Asian, 1968 Hong Kong, Avian H5N1) and SARS originated in east central China “Guangdong” and Hubei Provinces, respectively; whereas, HIV and Ebola hemorrhagic fever originated in west central Sub-Saharan Cameroon and Gabon, respectively. Each of these diseases is viral in origin and is infectious.

Commonality of micronutrient deficiency was suggested when Beck et al. (>1994) found that humans deficient in essential Se were susceptible to enterovirus, and benign forms of that virus mutated to virulence under Se-deficient host conditions. Further, Broome et al. (2004) determined individuals with <1µMol Se/L blood were susceptible to poliovirus, had decreased immune response to poliovirus vaccination, and that poliovirus had increased mutation rates under low-Se host conditions; however, Se supplementation of the low Se status population raised immune response and lowered number of viral mutations.

In this project, literature indicates blood Se levels in China and SSA can fall substantially below 1 µMol/L requisite for full expression of immune system regulation: east central China, 0.18-.32 µMol Se/L; Nigeria, 0.73; DRC, 0.28-.62; Burundi, 0.2; Zambia, 0.49; and Malawi, 0.57; compared to US average of 1.5 µMol Se/L blood. These data suggest constraints, possibly geological, which limit dietary 47 mcg Se/d necessary to achieve 1µMol Se/L blood for immunocompetence and VID inhibition.