Food groups such as whole grains, nuts, fish, fruit, and vegetables and prudent dietary patterns rich in these foods were inversely associated with several age-related diseases and total rate of mortality (14
). Those associations could reflect effects of diet on the aging process. It was suggested that telomere length, or more precisely, the rate of telomere shortening, may be a better marker of the biological aging process than chronologic age itself (1
). Therefore, we hypothesized that dietary intake of specific foods and patterns of dietary intake would be associated with telomere length in a manner consistent with reported associations between diet and inflammation, chronic diseases, and rate of mortality. Our data showed an inverse association between consumption of the food group processed meat and telomere length, but other food groups and dietary patterns were not associated with telomere length.
Our finding that processed meat consumption was associated with shorter telomeres is consistent with studies showing associations between greater intake of processed meat and risk of cancer (47
) and diabetes (48
) and with studies showing associations between red meat intake and CVD (51
), all diseases with frequencies that increase with age. The difference in telomere length (T/S ratio) between the highest and lowest quartiles of processed meat intake (0.017) corresponds to a 3.4-y age difference (with the use of our sample-specific estimates). Within our sample, a 1-y difference in age corresponded to a 0.005 smaller T/S ratio, consistent with previous reports (6
). The observed association between processed meat intake and telomere length was independent of intake of other food groups. Constituents of processed meat that may accelerate the aging process include saturated fat, sodium, nitrates and nitrites, cholesterol, and iron (55
). Interestingly, red meat was not similarly associated with telomere length. Red meat has shown variable associations with rates of morbidity and mortality, which may be due to differences in preparation methods and cut of meat consumed (percentage of fat or lean) (56
). Such variables are not measured well (or at all) by FFQ and, therefore, could not be investigated in our sample.
On the basis of the hypothesis that inflammation partly mediates telomere shortening (57
), we hypothesized that the dietary patterns of fats and processed meat and of whole grains and fruit would be associated with shorter and longer telomeres, respectively. We previously reported strong associations between these empirical dietary patterns and markers of inflammation in the larger MESA cohort (32
). The finding that the dietary pattern typified by high consumption of processed meat (fats and processed meat) was not associated with telomere length is somewhat surprising in light of the observed association between intake of processed meat and telomere length. It is possible that the absence of association is due to a dilution effect by other food groups not associated with telomere length but included in dietary pattern score computation. Although not among the food groups we identified for investigation a priori, intake of added fats and oils (the highest loading food group on this dietary pattern) was not associated with telomere length, nor was intake of salty snacks, fried potatoes, or desserts, other important contributors to scores on this dietary pattern.
Although telomere length or attrition was associated with several environmental factors (13
), telomere length is also under genetic control (12
) and shows interindividual variation beginning at birth (60
). Thus, an ideally designed study would be able to take into account these inherent differences or, alternatively, measure within-person change in telomere length over a period of several years, preferably during the exposure periods in question. Our investigation was cross-sectional; therefore, we were not able to take into account intrinsic differences in telomere length, nor were we able to investigate changes in telomere length over time within participants. Such interindividual variations may have limited our ability to detect associations between telomere length and dietary factors.
Although we adjusted for demographic and lifestyle factors previously shown to be associated with telomere length, residual confounding remains a possibility. For example, persons of lower SES may be more likely to consume processed meat because of lower cost. Low SES may lead to greater life stress, which was associated with shorter telomeres (54
). However, our data were adjusted for educational status and were not changed if also adjusted for family income (proxies for SES). Low energy intake was hypothesized to increase longevity (61
); however, we observed no association between total energy intake and telomere length (data not shown), and the association between processed meat intake and telomere length was independent of total energy intake. Although adjustment for demographics, lifestyle factors, energy intake, and other food groups did not attenuate the association between shorter telomere length and greater intake of the food group processed meat, it remains possible that processed meat intake is serving as a marker of other lifestyle, dietary behaviors, or both that confound or mediate the association. We made every effort to measure these covariates accurately, but residual confounding in studies of this nature is, to some degree, unavoidable.
Two important limitations remain to be addressed. First, our sample size was relatively small, which may have limited our ability to detect small associations were they truly present. Second, it is possible that the statistically significant association we observed between processed meat intake and telomere length was a result of chance. We chose not to modify our criteria for statistical significance to account for multiple hypotheses testing, although we did study several food groups and 2 dietary patterns. We felt that an exploratory approach was justified, given the limited amount of research in this area and that we identified the food groups and dietary patterns of interest a priori. Furthermore, in the sample free of diabetes, the fully adjusted association between processed meat consumption and telomere length would remain significant (P = 0.002) even if we applied the conservative Bonferroni's correction (0.004 = 0.05/13 tests for 13 foods groups), and the association would be marginally significant in the larger group including participants with prevalent diabetes (P = 0.006).
In conclusion, in this cross-sectional study of 840 white, African American, and Hispanic adults we found little evidence of expected associations between telomere length and dietary intake of specific food groups and dietary patterns. However, we did observe a significant association between high intake of processed meat and shorter telomeres, deserving of further investigation in larger longitudinal studies with baseline and repeat measures of telomere length.