Introduction:
The aging process in children and adolescents is accelerated resulting in the premature development of “adult” diseases such as hypertension and diabetes. Telomere shortening plays a key role in human aging; identifying factors that regulate this process is important for developing effective lifestyle interventions so as to prevent and treat age-associated diseases.
In vitro
and
in vivo
studies demonstrate that high salt content markedly decreases life span, and accelerates cellular aging through increased DNA breakage. However, the effect of high salt diet on telomere length, a marker of biological aging, remains unknown. Therefore, we aimed to test the hypothesis that high dietary sodium intake is inversely associated with leukocyte telomere length, especially in the context of obesity.
Methods:
Leukocyte telomere length (T/S ratio) was assessed by a quantitative polymerase chain reaction method in 766 adolescents aged 14-18 years (50% female, 49% African Americans). Diet was assessed with three to seven 24-h recalls, and physical activity was determined by accelerometry. Participants were classified according to low vs. high sodium intake (below or above the median), and according to weight status (normal vs. overweight/obese). Analysis of covariance and linear regression analyses were used to determine the effects of sodium intake and weight status on leukocyte telomere length.
Results:
After controlling for age, sex, race, energy intake, Tanner stage, and vigorous physical activity, a statistically significant sodium intake by weight status interaction was observed, such that leukocyte telomere length was significantly shorter in the high sodium intake vs. low sodium intake subjects from the overweight/obese group (1.24 ± 0.22 vs. 1.32 ± 0.21, p=0.02), but not the normal weight group (1.29 ± 0.24 vs. 1.30 ± 0.24, p=0.69). Consistent with the low vs. high sodium intake group data, multiple linear regression analyses, adjusting for age, sex, race, energy intake, Tanner stage and vigorous physical activity, revealed that higher dietary sodium intake was associated with shorter leukocyte telomere length in the overweight/obese group (β=-0.37, p=.045), but not the normal weight group.
Conclusion:
High dietary sodium intake is associated with shorter telomere length in overweight and obese adolescents suggesting that high sodium intake and obesity may act synergistically to accelerate cellular aging. Longitudinal studies are warranted to determine the synergistic effect of high sodium intake and obesity on telomere shortening over time.
Physical Activity, Physical Fitness, and Leukocyte Telomere Length
