Written by Susan Sweeny Johnson, PhD. Recommended daily amounts (RDAS) of vitamins and minerals based on the minimum amounts necessary to prevent deficiency diseases is insufficient, instead it should also be based on DNA damage.

Historically, the government has recommended daily amounts (RDAs) of vitamins and minerals based on the minimum amounts necessary to prevent deficiency diseases. Over the last couple of decades, however, researchers have seen that larger amounts of vitamins and minerals are necessary to prevent or reduce DNA damage which causes longer term health consequences. This editorial review suggests that improvements in assaying DNA damage provide a more accurate method of determining optimal amounts of vitamin and minerals in the body than that which has been available in the past. Because human populations vary in the way they absorb and metabolize vitamins and minerals, subpopulations should also be considered when establishing dietary guidelines.

Pro-vitamins such as lycopene, lutein, astaxanthin and zeaxanthin consistently protect genomes against DNA damage (1) but vitamin A carotenoids]can both protect DNA and cause damage possibly because they can function as oxidants (2).

Niacin is involved in the function of some enzymes necessary for DNA repair, but no human studies have been done to clearly determine optimal amounts. The authors state that some human population groups are well below the amounts suggested by animal studies, and supplementation in these cases may be beneficial.

Folate and vitamin B12 work together to maintain nuclear and mitochondrial genome stability. Low folate levels result in an increase of mistakes in copying DNA which leads to breaking of the strands and deletions in mitochondrial DNA (3). There is some evidence that low folate levels could reduce telomere length which in turn reduces the lifetime of the DNA (4). Since individuals vary in ability to absorb and metabolize these vitamins, the amount and type of folate and B12 recommended for supplementation must be determined for these subpopulations.

Choline is involved folate metabolism and deficiency impairs folate metabolism which in turn causes the same miscopying of DNA as previously mentioned. As with folate and B12, individuals vary in their ability to absorb and metabolize choline. (4)

Vitamin D seems to play a role in protection against DNA damage and oxidation in animal studies but there are limited human studies to date.

Biotin plays a role in protection again DNA damage (5) but because it is made in human intestines by bacteria, supplementation guidelines are difficult to establish. More studies are needed on the variations of gut flora in disease states and different population groups.

CoQ10 plays an important role in the electron transport chain in mitochondria and is a powerful antioxidant.  Although animal studies have demonstrated the beneficial effects of supplementation on genome integrity, more dose-response studies in humans are necessary to establish optimal amounts necessary to prevent DNA damage. (6)

Minerals necessary in small amounts are often toxic in larger amounts. Iron, selenium and zinc seem to cause chromosome breakage and other DNA destruction in high concentrations although they are protective at optimal, intermediate levels.  The optimal levels of these minerals seem to vary with individual genotype and may also vary with age. (7-9)

Since the integrity of each individual’s genome is sensitive to their vitamin and mineral status, dietary recommendations for intake of vitamins and minerals should be based on DNA damage prevention rather than only  on avoidance of deficiency diseases.  More human studies looking at the dose dependent effect of vitamin and mineral levels alone and in conjunction with each other on genome stability should be performed to establish more accurate supplementation recommendations.  In addition, individual metabolic variations should be taken into account. (2,10)

Source: Ferguson, Lynnette R., and Michael F. Fenech. “Vitamin and minerals that influence genome integrity, and exposure/intake levels associated with DNA damage prevention.” (2012): 1-3.

 © 2012 Elsevier B.V. All rights reserved.

Posted May 1, 2012.

References:

  1. [2] A, Azqueta, A.R. Collins, Carotenoids and DNA damage, Mutat. Res., in press.
  2. [21] M.F. Fenech, Dietary reference values of individual micronutrients and nutri- omes for genome damage prevention: current status and a road map to the future, Am. J. Clin. Nutr. 91 (May (5)) (2010) 1438S–1454S.
  3. M.F. Fenech, Folate (vitamin B9) and vitamin B12 and their function in the maintenance of nuclear and mitochondrial genome integrity, Mutat. Res., in press.
  4. [5] B. van Ommen, A. El-Sohemy, J. Hesketh, J. Kaput, M. Fenech, C. Evelo, H.J. McArdle, J. Bouwman, G. Lietz, J.C. Mathers, S. Fairweather-Tait, H. van Kranen, R. Elliott, S. Wopereis, L.R. Ferguson, C. Méplan, G. Perozzi, L. Allen, D. Rivero, The Micronutrient Genomics Project Working Group, The micronutrient genomics project: creating a community driven knowledge base for micronutrient research, Genes Nutr. 5 (4) (2010 Dec) 285–296.
  5. J. Zempleni, D. Camara Teixeira, T. Kuroishi, E.L. Cordonier, S. Baier, Biotin requirements for DNA damage, Mutat. Res., in press.
  6. C. Schmelzera, F. Döring, Micronutrient special issue: coenzyme Q10 require- ments for DNA damage prevention, Mutat. Res., in press.
  7. L.R. Ferguson, N. Karunasinghe, S. Zhu, A.H. Wang, Selenium and its’ role in the maintenance of genomic stability.
  8. R. Sharif, P. Thomas, P. Zalewski, M. Fenech, The role of zinc in genomic stability, Mutat. Res., in press.
  9. N. Karunasinghe, D.Y. Han, S.T. Zhu, J. Yu, K. Lange, H. Duan, R. Medhora, N. Singh, J. Kan, W. Alzaher, B. Chen, S. Ko, C.M. Triggs, L.R. Ferguson, Serum selenium and single-nucleotide polymorphisms in genes for selenoproteins: relationship to markers of oxidative stress in men from Auckland, New Zealand, Genes Nutr. (December) (2011) (Epub ahead of print) PubMed PMID 22139612.
  10.  L.R. Ferguson, M. Philpott, Nutrition and mutagenesis, Annu. Rev. Nutr. 28 (2008) 313–329.