Even Modest Selenium Deficiency Harms Health

FRESNO, Calif. Modest selenium deficiency create mutations in selenium-dependent proteins that result in characteristics shared by age-related diseases including cancer, heart disease and loss of immune or brain function, according to researchers Joyce C. McCann and Bruce N. Ames at the Nutrition and Metabolism Center at Childrens Hospital Oakland Research Institute in Oakland, CA (FASEB J. 2011 25:1793-1814. DOI: 10.1096/fj.11-180885). This study and a previous one the researchers conducted on vitamin K show modest nutrient deficiencies can result in long-term health issues, and highlights how supplementation may reduce these implication.

McCann and Ames reported this study supports the triage theory, which proposes that modest deficiency of any vitamin or mineral could increase age-related diseases because vitamin- and mineral-dependent proteins required for short-term survival and/or reproduction (i.e., essential") are predicted to be protected over vitamin/mineral deficiency over other nonessential" vitamin/mineral-dependent proteins needed only for long-term health.

Ames explained the triage theory at last years Natural Health Research Institutes (NHRI) symposium on the cost effectiveness and safety of dietary supplements. He said evolution has trained our bodies to sacrifice long-term health to meet short-term needs for survival when diets are only modestly deficient in one or more vitamins and minerals (micronutrients), adding that science has taught us we need about 30 essential vitamins and minerals to survive, but most Americans are not getting enough for long-term health.

In this current study, they reviewed about half of the 25 known mammalian selenoproteins; all of those with mouse knockout or human mutant phenotypes that could be used as criteria for a classification of essential or nonessential. Five selenoproteins (Gpx4, Txnrd1, Txnrd2, Dio3 and Sepp1) were classified as essential and seven (Gpx1, Gpx 2, Gpx 3, Dio1, Dio2, Msrb1 and SelN) were classified as nonessential.

On modest selenium deficiency, nonessential selenoprotein activities and concentrations were preferentially lost, with one exception (Dio1 in the thyroid, which they predicted is conditionally essential). Mechanisms include the requirement of a special form of transfer RNA sensitive to Se deficiency for translation of nonessential selenoprotein messenger RNAs except Dio1. The same set of age-related diseases and conditions, including cancer, heart disease and immune dysfunction, are prospectively associated with modest selenium deficiency and also with genetic dysfunction of nonessential selenoproteins, suggesting that selenium deficiency could be a causal factor, a possibility strengthened by mechanistic evidence.