Multivitamins Linked to Younger Biological Age

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New research shows the cells of multivitamin users may have a younger biological age than cells from non-users.
Researchers led by Honglei Chen, M.D., Ph.D. from the National Institute of Environmental Health Sciences, a division of the National Institutes of Health, looked at the length of telomeres, DNA sequences at the end of chromosomes that shorten as cells replicate and age.

The ageing and lifespan of normal, healthy cells are linked to the so-called telomerase shortening mechanism, which limits cells to a fixed number of divisions. During cell replication, the telomeres function by ensuring the cell's chromosomes do not fuse with each other or rearrange, which can lead to cancer. With each replication the telomeres shorten, and when the telomeres are totally consumed, the cells are destroyed. Previous studies have also reported that telomeres are highly susceptible to oxidative stress.

Dr. Chen and his co-workers noted that telomere length may therefore be a marker of biological ageing, and that multivitamins may beneficially affect telomere length via modulation of oxidative stress and chronic inflammation.

The scientists analyzed multivitamin use and nutrient intakes, as well as telomere length of 586 women aged between 35 and 74 in the Sister Study. A 146-item food-frequency questionnaire was used to determine multivitamin use and nutrient intakes. Compared to non-multivitamin users, the researchers noted that the telomeres were on average 5.1% longer for daily multivitamin users.


“To our knowledge, this was the fist epidemiologic study of multivitamin use and telomere length,” wrote Dr. Chen and his co-workers. “Regular multivitamin users tend to follow a healthy lifestyle and have a higher intake of micronutrients, which sometimes makes it difficult to interpret epidemiologic observations on multivitamin use. Further investigation would be needed to understand the role of multivitamin use and telomere length and its implication in the etiology of chronic diseases.”

American Journal of Clinical Nutrition 89(6):1857-1863, 2009

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