Nutrients for DNA Damage and Repair: Spotlight on Telomere Health

Deoxyribonucleic acid (DNA) damage in the body is responsible for both normal aging and the emergence of different health conditions.1 Certain lifestyle choices, such as unprotected exposure to ultraviolet radiation or consuming unhealthy foods, can increase the amount of DNA damage incurred daily.2 Making lifestyle changes, such as improving one’s diet, may therefore have the potential to slow down aging and minimize disease onset by limiting or reversing DNA damage.

In the body, double-stranded DNA molecules coil around histone proteins to form chromosomes, which carry genomic information between cells.3 Individual chromosomes are capped at both ends by regions of repetitive DNA sequences known as telomeres, which protect the ends of chromosomes from fraying or becoming entangled with each other.4 In young cells, the enzyme telomerase keeps telomeres from wearing down; as cells continue to divide, however, there is no longer enough telomerase to go around, and telomeres become increasingly shorter until the cell can no longer divide successfully, at which point it dies.4 Shorter telomeres may predispose individuals to a variety of diseases, including cancer, and a greater risk of mortality.5 Telomere shortening is a natural part of the aging process, and inflammation may exacerbate the rate of telomere attrition, which leads to telomere dysfunction-mediated cellular senescence to further accelerate the aging process;6 it has also been postulated that telomere shortening may promote inflammation,7 leading to a potential feedback loop between the two phenomena. 

Research suggests that diet can influence telomere length, although different macro- and micronutrients may have variable effects depending in part on their pro- or anti-inflammatory potential. It has been reported that dietary fiber is protective against high levels of C-reactive protein (CRP), a marker of acute inflammation,8 and more fiber appears to be good for telomere health.9 Cereal fiber, relative to vegetable and fruit fiber, has shown a more consistent association with lower inflammation,10 and other research has concluded that cereal dietary fiber intake in particular is positively linked to leukocyte telomere length.11 

Meanwhile, different types of fat seem to impact telomere length in different ways. Saturated fat and telomere length are negatively correlated.12,13 Monounsaturated fatty acids collectively seem to have either a negative12 or no association13 with lymphocyte telomere length. Meanwhile, the reported effects of polyunsaturated fatty acids, although potentially positive overall,12 are more complex: while the intake of linoleic acid (found in vegetable oils, nuts, seeds, meats, and eggs) was inversely associated with leukocyte telomere length,11 that of another polyunsaturated fatty acid, arachidonic acid, was positively correlated with leukocyte telomere length.12 In another study, blood levels of marine omega-3 fatty acids, another kind of polyunsaturated fatty acid, were also found to be inversely associated with the rate of leukocyte telomere shortening over a period of five years—that is, higher levels of docosahexaenoic acid (DHA) and eicosapentaenoic acid (EHA) helped to slow down leukocyte telomere shortening over time.14 It is important to note, however, that this study was conducted in a population of 608 outpatients with stable coronary artery disease,14 and other research has suggested that the relationship between telomere shortening and macronutrients can be complicated by disease. Using data from the United States (US) National Health and Nutrition Examination Survey (NHANES), investigators in one study found that telomere length was positively correlated with high-density lipoprotein (HDL) cholesterol levels in individuals without diabetes, hypertension, coronary atherosclerotic heart disease, or hyperuricemia, yet the same relationship could not be identified in individuals with these conditions, which the authors attributed to the presence of HDL cholesterol dysfunction in these diseases.15 

Other conditions, such as persistent high cholesterol (dyslipidemia), may also correlate with accelerated shortening of telomere length over time;16 indeed, it is suggested that high serum lipid concentrations may be associated with systemic inflammation and atherosclerosis, which could lead to oxidative stress, resulting in telomere shortening and dysfunction.17,18 In this vein, some research has suggested that antioxidant intake may positively influence telomere length. One study of Spanish children and adolescents found a positive correlation between the general dietary total antioxidant capacity and telomere length after adjustment for age and energy intake.19 Other studies have also linked specific antioxidants to longer telomeres, including minerals, such as zinc and selenium;20,21 vitamins C and E;22,23 and carotenoids, such as lutein, zeaxanthin, and alpha- and beta-carotene.24,25 However, one study determined that gamma-tocopherol (a form of vitamin E), found in nuts, vegetable oils, and seeds, but not alpha-tocopherol (another form of vitamin E), negatively impacted telomere length, with adults in the 75th percentile of gamma-tocopherol showing 2.8 to 3.4 years of greater cellular aging than those at the 25th percentile, depending on the covariates in the model.26 The choice of antioxidant may therefore matter with regard to telomeric effects.

Consumption of sugar-sweetened beverages (SSBs) like soda and sports drinks have also been linked to shortened telomeres,27 while the intake of 100-percent fruit juice may help to ensure longer telomeres.28 Although it was unclear what the SSBs in question were sweetened with, other research contends that fructose, found in fruit juice, may lead to lower blood glucose and insulin concentrations29 than either glucose or sucrose. The consumption of 100-percent fruit juice may also impart beneficial effects of phytochemicals and micronutrients (e.g., antioxidant vitamins) to balance out the negative effect of its sugar content.30 However, other research contends that greater intakes of both total and added fructose are significantly associated with shorter relative telomere length,31 and the intake of 100-percent fruit juice in the aforementioned study28 led to only a marginal association with longer telomeres. Telomere shortening has also been linked to elevated fasting glucose, hemoglobin A1c (HbA1c), and Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) values,32,33 which can be indicators of progression toward diabetes, and patients with diabetes have shorter telomeres compared to healthy individuals.34 Insulin resistance itself, the hallmark of diabetes, induces inflammation,35 which has been linked to telomere shortening. As such, minimizing the consumption of all sugars may help to prevent accelerated telomere shortening.

Research on the link between protein intake and telomere length is limited; however, greater protein intake supports a lower-calorie diet,36 helping to minimize inflammation.37 Importantly, though, the source of the protein might matter; for example, the consumption of red meat27 and particularly processed meats27,38,39 has been inversely linked to telomere shortening. Although the trend may be linked to greater concentrations of certain nutrients, such as saturated fat, processed meat also contains high concentrations of advanced glycation end-products and nitrosamines that may promote inflammation and oxidative stress.38,40 Moreover, considering for a moment other types of DNA damage, an analysis of tumors from patients with colorectal cancer revealed a specific “alkylating” pattern of DNA damage attributed to the production of certain compounds in the body following the consumption of red and processed meat,41 and the intake of heterocyclic amines, a kind of carcinogen formed when meat, poultry, or fish is cooked at high temperatures, has also been suggested to result in DNA alkylation through their bioactivation upon consumption into reactive species.42,43 As such, it is recommended to limit intake of animal products, especially processed meats, to avoid DNA damage, including telomere shortening. 

Ultra-processed food, which typically contains greater amounts of saturated and trans fats, sugar, and salt—all of which trigger inflammation44—has been linked to shorter telomeres. A population of elderly Spanish individuals with the greatest consumption of ultra-processed food demonstrated almost twice the odds of having short telomeres, compared to those with the lowest consumption.45 Beneficial nutrients are also typically stripped away during the industrial processes used to produce ultra-processed foods, and research suggests that deficiencies in folate, niacin, iron, and zinc as well as vitamins B12, B6, C, and E can mimic the DNA-damaging effects of radiation by causing single- and double-strand breaks, oxidative lesions, or both.46 

Conversely, the Mediterranean diet in particular might support longer leukocyte telomeres;47,48 one study of individuals at high risk for cardiovascular disease observed longer telomeres at baseline in participants with a more anti-inflammatory diet (lowest Dietary Inflammatory Index score) and, following a five-year intervention with the Mediterranean diet, longitudinal analyses suggested that a diet with greater anti-inflammatory potential could significantly slow down the rate of telomere shortening.49 In other research comparing two major dietary patterns—“the prudent dietary pattern,” which was characterized by a high intake of whole grains, fish and seafood, legumes, vegetables, and seaweed, and the “Western dietary pattern,” which was characterized by a high intake of refined grain, red meat or processed meat, and sweetened carbonated beverages—the “prudent dietary pattern” was found to be positively associated with leukocyte telomere length, while an inverse trend was observed for the association between the “Western dietary pattern” and leukocyte telomere length.27

Finally, one study contended that the very act of cooking foods—including vegetables—at high temperatures might result in DNA mutations, abasic sites, or double-strand breaks by way of metabolic salvage; its authors noted distinct differences in the level of damage according to time and type of cooking, with roasting (220°C) causing more damage to food than boiling (100°C).43 However, the authors of this study stress that more research is necessary.

Editor’s notes. Although telomeres exist in all cells, leukocyte telomere length is the measure most commonly used in telomere length research.

Please discuss any health concerns, including those regarding your diet, with your primary care physician.

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