Telomere shortening unrelated to smoking, body weight, physical activity, and alcohol intake: 4,576 general population individuals with repeat measurements 10 years apart

Abstract

Cross-sectional studies have associated short telomere length with smoking, body weight, physical activity, and possibly alcohol intake; however, whether these associations are due to confounding is unknown. We tested these hypotheses in 4,576 individuals from the general population cross-sectionally, and with repeat measurement of relative telomere length 10 years apart. We also tested whether change in telomere length is associated with mortality and morbidity in the general population. Relative telomere length was measured with quantitative polymerase chain reaction. Cross-sectionally at the first examination, short telomere length was associated with increased age (P for trend across quartiles = 3 × 10(-77)), current smoking (P = 8 × 10(-3)), increased body mass index (P = 7 × 10(-14)), physical inactivity (P = 4 × 10(-17)), but not with increased alcohol intake (P = 0.10). At the second examination 10 years later, 56% of participants had lost and 44% gained telomere length with a mean loss of 193 basepairs. Change in leukocyte telomere length during 10 years was associated inversely with baseline telomere length (P<1 × 10(-300)) and age at baseline (P = 1 × 10(-27)), but not with baseline or 10-year inter-observational tobacco consumption, body weight, physical activity, or alcohol intake. Prospectively during a further 10 years follow-up after the second examination, quartiles of telomere length change did not associate with risk of all-cause mortality, cancer, chronic obstructive pulmonary disease, diabetes mellitus, ischemic cerebrovascular disease, or ischemic heart disease. In conclusion, smoking, increased body weight, and physical inactivity were associated with short telomere length cross-sectionally, but not with telomere length change during 10 years observation, and alcohol intake was associated with neither. Also, change in telomere length did not associate prospectively with mortality or morbidity in the general population.

Figure 1. Telomere length in basepairs as a function of age in years at the 1991–1994 examination.

Linear regression is shown in equation and as a grey line. N = number of participants. P-value and R² are for the correlation from the linear regression. Statistical tests were two-sided.

Figure 2. Absolute change in basepairs during 10 years observation. N = number of participants.

Figure 3. 10 year change in telomere length in basepairs or percent as functions of telomere length at the 1991–1994 examination.

Linear regressions are shown in equations and as grey lines. N = number of participants. P-value and R² are for the correlation from the linear regression. Statistical tests were two-sided.

Figure 4. All-cause mortality by quartiles of telomere length at the 1991–94 examination (left) and at the 2001–03 examination (right).

Hazard ratios were adjusted for covariates obtained at the date of examination; age, gender, current smoking, daily tobacco consumption, body mass index, heavy alcohol intake, and physical inactivity. Numbers of participants were all available participants with measured telomere lengths (1991–94; 9250, 2001–03; 5843). Follow-up began the day of the 1991–94 (for the 9250 participants examined in 1991–94) or the 2001–03 (for the 5843 participants examined in 2001–03) examination.