There is growing evidence that lifestyle factors, such as your diet and your physical activity, can influence your DNA damage levels. For example, exhaustive exercise has been shown to induce DNA damage through the production of reactive oxygen species. Additionally, antioxidants, micronutrients, and vitamins from your diet can influence DNA damage levels. Below is a select list of scientifiic peer-reviewed articles showing just a few examples. Please note that Exogen does not endorse any specific diet, activity, or product that may be listed.

Selected Scientific Peer-Reviewed Articles

  • Ames et al., “DNA damage from micronutrient deficiencies is likely to be a major cause of cancer.Mutat Res, 2001.
    “A deficiency of any of the micronutrients: folic acid, Vitamin B12, CVitamin B6, niacin, Vitamin C, Vitamin E, iron, or zinc, mimics radiation in damaging DNA by causing single- and double-strand breaks, oxidative lesions, or both.”
  • Toden et al., “High red meat diets induce greater numbers of colonic DNA double-strand breaks than white meat in rats: attenuation by high-amylose maize starch.Carcinogenesis, 2007.
    “Both red and white meat increased colonocyte SSB (single-strand breaks) and DSB (double-strand breaks) dose dependently but damage was greater with red meat… Dietary RS (resistant starch) protects against this damage and also against loss of the mucus barrier, probably through increased butyrate production.”
  • Quiles et al., “Coenzyme Q supplementation protects from age-related DNA double-strand breaks and increases lifespan in rats fed on a PUFA-rich diet.Exp Gerontol, 2004.
    “Supplemented animals showed higher concentration of coenzyme Q10 in liver mitochondria, lower levels of DNA double-strand breaks in peripheral blood lymphocytes.” 
  • Kuefner et al., “Effect of antioxidants on X-ray-induced y-H2AX foci in human blood lymphocytes: preliminary observations.Radiology, 2012.
    “The tested formulation of antioxidants significantly reduced formation of γ-H2AX and 53BP1 foci (measured DNA double-strand breaks) after irradiation at a radiologic radiation dose typical for computed tomographic imaging.”
  • Gill et al., “Watercress supplementation in diet reduces lymphocyte DNA damage and alters blood antioxidant status in healthy adults.” Am J Clin Nutr, 2007.
    “Watercress supplementation was associated with reductions in basal DNA damage, in basal plus oxidative purine DNA damage, and in basal DNA damage in response to ex vivo hydrogen peroxide challenge.”
  • Mastaloudis et al., “Endurance exercise results in DNA damage as detected by the comet assay.Free Radic Biol Med, 2004.
    “Ultramarathon (50 km) resulted in DNA damage as shown by the comet assay and antioxidant (1000 mg vitamin C and 400 IU RRR-a-tocopheryl acetate) seemed to enhance recovery in women but not in men.”
  • Møller et al., “Acute hypoxia and hypoxic exercise induce DNA strand breaks and oxidative DNA damage in humans.” FASEB J, 2001.
    “The subjects had more DNA strand breaks in altitude hypoxia than at sea level. The level of DNA strand breaks further increased immediately after exercise in altitude hypoxia… DNA strand breaks and oxidative DNA damage are probably produced by reactive oxygen species, generated by leakage of the mitochondrial respiration or during a hypoxia-induced inflammation. Furthermore, the presence of DNA strand breaks may play an important role in maintaining hypoxia-induced inflammation processes. Hypoxia seems to deplete the antioxidant system of its capacity to withstand oxidative stress produced by exhaustive exercise
  • Neubauer et al., “Exercise-induced DNA damage: is there a relationship with inflammatory responses.Exerc Immunol Rev, 2008.
    “Both a systemic inflammatory response as well as DNA damage has been observed following exhaustive endurance exercise.” “The most conclusive picture that emerges from available data is that oxidative stress seems to be the main link between exercise-induced inflammation and DNA damage.”
  • Fogarty et al., “Exercise-induced lipid peroxidation: Implications for deoxyribonucleic acid damage and systemic free radical generation.Environ Mol Mutagen, 2011.
    “These findings identify lipid-derived free radical species as possible contributors to peripheral mononuclear cell DNA damage in the human exercising model. This damage occurs in the presence of lipid oxidation but in the absence of any change to protein carbonyl concentration. The significance of these findings may have relevance in terms of immune function, the aging process, and the pathology of carcinogenesis.”