Leukocyte Telomere Length in 13-to 16-Year-Old Adolescents

Telomeres are long lengths of TTAGGG repeats, which cap the end of the chromosomes and protect them from degradation and fusion. By undergoing erosion with each replicative cycle, telomeres chronicle the replicative history of human somatic cells in vitro and in vivo. Cross-sectional studies in adults have described complex associations between leukocyte telomere lengths (LTLs) and clusters of traditional cardiovascular (CV) risk factors, including dyslipidemia, hypertension, diabetes mellitus, obesity, and smoking. Furthermore, shorter LTL has been associated with subclinical and clinical markers of atherosclerosis. The biological basis for these associations, however, remains unclear. Inflammation, a novel risk factor for CV disease, has been suggested as a common driver of both atherosclerosis and an increased rate of LTL shortening. A chronic inflammatory exposure may play a key role in coronary artery disease and other manifestations of atherosclerosis. Immune cells dominate early atherosclerotic plaques, their effector molecules accelerate progression of the lesions, and activation of inflammation can elicit acute coronary syndromes. Indeed, inflammatory markers such as C-reactive protein (CRP) and fibrinogen may improve the CV risk stratification compared with that provided by traditional CV risk factors (eg, cholesterol, smoking, diabetes mellitus). Simultaneously, a chronic increase in the systemic inflammatory burden could enhance the rate of telomere attrition in peripheral leukocytes by increasing the number of cell replications and by exposing the telomere sequences to higher levels of oxidative stress. In adult cross-sectional studies, it is difficult to explore the biological origins of the association between LTL and CV disease because of the long-term exposure of patients to a variable level of CV risk factors. In contrast, in the young, there is a considerably lower risk factor burden as well as a shorter exposure period, and this provides the opportunity to study early biological mechanisms that may account for the adult association between LTL and CV disease. We, therefore,