Stressful life events in early life and leukocyte telomere length in adulthood

Background: Exposure to stressful life events (SLEs) in early life is associated with higher rates of morbidity and mortality from age-related chronic disease. In this study, we considered whether these general patterns extend to leukocyte telomere length (TL), an indicator of cellular aging. We also explored potential subgroup variations by race and age. Methods: Using cross-sectional data from the Nashville Stress and Health Study (2011–2014), a probability sample of 1108 adults (558 blacks and 550 whites) ages 22–69, we tested whether SLEs experienced in early life were associated with shorter telomeres in adulthood. Leukocyte TL was measured using the monochrome multiplex quantitative polymerase chain reaction method with albumin as the single-copy reference sequence. An index of 32 potentially traumatic events experienced before the age of 18 was employed. An abbreviated index of seven events that are frequently used in telomere research was also employed. Results: The complete SLEs index was unrelated to TL in the full sample (b = −0.003; p = 0.058) and for blacks (b = −0.003; p = 0.28), whites (b = −0.004; p = 0.18), and adults aged 45 or older (b = 0.001; p = 0.68). The complete SLEs index was inversely associated with telomere length (b = −0.007; p = 0.002) for those adults under the age of 45. Each additional SLE experienced before the age of 18 was associated with a reduction in TL equivalent to one additional year of age. The association between the complete SLEs index and TL for those under the age of 45 was statistically different from those aged 45 or older (t = 2.02; p = 0.04). In no case, was the abbreviated SLEs index related to TL. Conclusion: This study confirms that the long-term health consequences of SLEs in early life can extend to shorter leukocyte telomeres in adults aged 22–44, but not adults aged 45–69. Our analyses also showed that the association between SLEs and TL is sensitive to the precise measurement of SLEs. We discuss the substantive and methodological implications of our findings for research on SLEs and cellular aging.