Original Article | Published:

Integrative Biology

High sodium intake is associated with short leukocyte telomere length in overweight and obese adolescents

International Journal of Obesity volume 39, pages 12491253 (2015) | Download Citation

Abstract

Background/objectives:

Telomere shortening has an important role in cellular aging. However, the impact of high sodium intake, an important risk factor of age-related diseases, on telomere shortening remains unknown. Therefore, we examined the relationship between high dietary sodium intake and leukocyte telomere length (LTL), particularly in the context of obesity, as obesity increases salt sensitivity.

Subjects/methods:

LTL was determined by a quantitative polymerase chain reaction method in 766 adolescents aged 14–18 years (50% females, 49% African Americans). Dietary sodium intake was assessed by seven independent 24-h dietary recalls. We divided the sample into low sodium (mean 2388±522 mg per day) or high sodium groups (mean 4142±882 mg per day) based on the median value (3280.9 mg per day).

Results:

In the entire cohort, there was no significant association between sodium intake and LTL (r=−0.05, P=0.24). However, there was a significant interaction between sodium intake and obesity status (P=0.049). Further multiple linear regression analyses revealed that higher dietary sodium intake was associated with shorter LTL in the overweight/obese group (body mass index 85th percentile, β=−0.37, P=0.04), but not in the normal-weight group (β=0.01, P=0.93) after adjusting for multiple confounding factors. In the overweight/obese group, LTL was significantly shorter in the high sodium intake subjects vs low sodium intake subjects (1.24±0.22 vs. 1.32±0.20, P=0.02), but not the normal-weight group (1.29±0.24 vs 1.30±0.24, P=0.69).

Conclusions:

Higher dietary sodium intake is associated with shorter telomere length in overweight and obese adolescents.

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Acknowledgements

We thank all of the schools, adolescents and parents who participated in the study funded by National Institute of Health (HL064157).

Author information

Affiliations

  1. Georgia Prevention Institute, Department of Pediatrics, Medical College of Georgia, Georgia Regents University, Augusta, GA, USA

    • H Zhu
    • , J Bhagatwala
    • , N K Pollock
    • , S Parikh
    • , B Gutin
    • , J Thomas
    • , G A Harshfield
    •  & Y Dong
  2. Internal Medicine, Department of Medicine, Medical College of Georgia, Georgia Regents University, Augusta, GA, USA

    • J Bhagatwala
    •  & S Parikh
  3. Department of Physiology, Medical College of Georgia, Georgia Regents University, Augusta, GA, USA

    • I Stallmann-Jorgensen

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Competing interests

The authors declare no conflict of interest.

Corresponding author

Correspondence to H Zhu.

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DOI

https://doi.org/10.1038/ijo.2015.51

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