An article published online  in 2008 in the Proceedings of the National Academy of Sciences reported that human cells grown in a magnesium deficient environment undergo accelerated senescence (aging).

Studies have indicated that increased cellular senescence can lead to tissue damage and promote the development of diseases associated with aging. Aging-related diseases, including cardiovascular disease, hypertension, diabetes, osteoporosis, and some cancers have all been linked with magnesium inadequacy, a condition that is estimated to affect half of the population in the United States.

David W. Killilea and Bruce N. Ames, PhD of Children’s Hospital Oakland Research Institute in California cultured human fibroblasts, which are cells that provide a structural framework for many tissues, in magnesium deficient media to which magnesium was added to provide 13 percent, 50 percent or 100 percent of the magnesium level in normal human serum. Although there was no decrease in cell viability, cells in the reduced magnesium media appeared to undergo accelerated senescence. An increased loss of population doublings was shown to be associated with decreased magnesium exposure, as well as an increase in beta-galactosidase activity, which is a senescence-associated biomarker. The deficient cells also underwent an increased loss of telomere length compared with cells cultured in normal magnesium conditions. Telomeres are DNA sequences that cap the ends of chromosomes, which shrink with age. Telomere malfunction has been associated with aging and the development of cancer.

According to the authors, the mechanism supporting magnesium deficiency’s effect on cellular senescence may involve an increase in oxidative stress levels which damages telomeres. Supplemental antioxidant vitamins C and E, as well as niacinamide have all been shown to slow telomere shortening in human cell cultures.

“The long-term consequence of inadequate magnesium availability in human fibroblast cultures was accelerated cellular senescence,” Drs Killilea and Ames conclude, “which may be a mechanism through which chronic magnesium inadequacy could promote or exacerbate age-related disease.”