Effects of Randomized Controlled Infancy-Onset Dietary Intervention on Leukocyte Telomere Length-The Special Turku Coronary Risk Factor Intervention Project (STRIP).

Niina Pitkänen,Frej Fyhrquist,Anna E Nyman,Outi J Saijonmaa,Hanna Lagström,Harri Niinikoski,Tapani Rönnemaa,Olli Simell,Antti Jula,Olli T Raitakari,Suvi P Rovio,Jorma S A Viikari,Katja Pahkala

doi:10.3390/nu13020318

Abstract

Reduced telomere length (TL) is a biological marker of aging. A high inter-individual variation in TL exists already in childhood, which is partly explained by genetics, but also by lifestyle factors. We examined the influence of a 20-year dietary/lifestyle intervention on TL attrition from childhood to early adulthood. The study comprised participants of the longitudinal randomized Special Turku Coronary Risk Factor Intervention Project (STRIP) conducted between 1990 and 2011. Healthy 7-month-old children were randomized to the intervention group (n = 540) receiving dietary counseling mainly focused on dietary fat quality and to the control group (n = 522). Leukocyte TL was measured using the Southern blot method from whole blood samples collected twice: at a mean age of 7.5 and 19.8 years (n = 232; intervention n = 108, control n = 124). Yearly TL attrition rate was calculated. The participants of the intervention group had slower yearly TL attrition rate compared to the controls (intervention: mean = −7.5 bp/year, SD = 24.4 vs. control: mean = −15.0 bp/year, SD = 30.3; age, sex and baseline TL adjusted β = 0.007, SE = 0.004, p = 0.040). The result became stronger after additional adjustments for dietary fat quality and fiber intake, serum lipid and insulin concentrations, systolic blood pressure, physical activity and smoking (β = 0.013, SE = 0.005, p = 0.009). A long-term intervention focused mainly on dietary fat quality may affect the yearly TL attrition rate in healthy children/adolescents.

Highlights

Telomeres are structures consisting of DNA sequence repeats and associated proteins that protect the ends of eukaryotic chromosomes
In contrast to the yearly telomere length (TL) attrition rate, the intervention did not have an effect on the change in the proportion of short telomeres, which may be explained by differences in biological mechanisms related to these two outcomes or by the small number of participants with short telomeres
A few other longitudinal studies have addressed the association between diet and change in TL, and they have mostly been conducted in adults

Summary

Introduction

Telomeres are structures consisting of DNA sequence repeats and associated proteins that protect the ends of eukaryotic chromosomes. Telomere length (TL) decreases progressively in most proliferating somatic cell types as a result of terminal DNA sequence loss associated with replication of linear chromosomes [1]. TL is maintained by the activity of telomerase, a ribonucleoprotein enzyme, which adds sequence repeats to the ends of chromosomes [1]. Substantial inter-individual variation exists and can be observed from birth/infancy [3,4,5]. Other predictors of the inter-individual variation in TL include paternal age, genetic factors and ethnicity [2,5,6,7,8]. One possible mechanism behind the link between lifestyle related risk factors and TL shortening may be inflammation and oxidative stress, that are associated with poor lifestyle and have, in addition to DNA replication, been related to accelerated shortening of telomeres [13,14]

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Conclusion