Selenium (Se) is an essential element for humans and livestock. A total of 25 genes encoding selenoproteins
have been identified in humans, including iodothyronine deiodinases, thioredoxin reductases, glutathione
peroxidases, and a range of other selenoproteins (e.g. SelP, SelM, SelT)1. These proteins have critical roles in
thyroid functioning, cell proliferation and survival through redox homeostasis, antioxidant defence and the
immune response. When Se intake is suboptimal, the selenoprotein status of people decreases and there are
increased risks of adverse health effects. At extremely low Se intake levels (where habitual intakes for adults are
,20 mg Se d21), clinical deficiency disorders have been reported including Keshan disease (a cardiomyopathy)
and Kashin-Beck disease (an osteoarthropathy). Where habitual intakes for adults are less than those needed for
maximal expression of glutathione peroxidase, typically at least 40 mg Se d21, there is an increased risk of health
disorders, including cardiovascular disorders, impaired immune functions, and some cancers1. The relationships
between Se intake, Se status in terms of selenoprotein expression and health outcomes have still to be fully
resolved2,3. These uncertainties are reflected in the wide range of Dietary Reference Intake (DRI) levels in different
countries1. Some DRIs are set to reduce risks of overt deficiency (i.e. recommending intakes of ,40 mg Se d21),
although most countries have recommended intake levels of 50–70 mg Se d21. As high habitual levels of Se intake
are potentially toxic (.400–900 mg Se d21), care must be taken in setting DRIs and recommending dietary
supplementation.
Selenium intake in human populations is derived primarily from dietary sources and can be determined from
direct dietary analyses or surveys and food composition tables. Reported Se intakes range from 3 to
7000 mg Se d21 globally4 due to differing dietary preferences and the levels of plant available Se in the soil on
which crops are grown for consumption1,4–7. Populations in many European countries and elsewhere have intakes
,50 mg Se d21, which are likely to be suboptimal in terms of selenoprotein expression2. Higher dietary Se intake
levels (.150 mg Se d21) occur in Se-rich (seleniferous) environments (e.g. parts of China, India, North America,
and Venezuela) and where seafood-based diets containing high concentrations of Se are prevalent (e.g. notably in
parts of Greenland and Japan). Selenium intake from water and air is usually insignificant, except where environmental
Se concentrations are high due to natural or anthropogenic factors.