It has been suggested that iron overload, which indicates the accumulation of iron, generates cellular reactive oxygens and causes peroxide damages to the body. Such oxidative stresses, in a broader context, are also caused by lifestyles such as alcohol consumption and smoking. However, there are limited data on the association between these lifestyle factors and internal iron overload. In present study, we evaluated associations between lifestyle factors, such as smoking status, alcohol consumption, and physical activity, and serum markers of iron overload. In a population-based cross-sectional study including 2,347 Korean men and women aged 49–79 years, we assessed serum transferrin saturation (TSAT) levels and defined iron overload as TSAT levels > 50% for men and > 45% for women. After excluding persons with chronic diseases and iron deficiency, multivariate odds ratio (OR) and its 95% confidence interval (CI) were estimated to evaluate associations between lifestyle factors and iron overload in 1,973 participants. In all participants, we examined a significantly positive association between heavy alcohol consumption (> 30 g/day) and iron overload; heavy drinkers showed 1.6-fold higher OR (95% CI, 1.11–2.36) than non-drinkers. Stratified analysis by sex showed that this association was significant only among men. In addition, we observed a potential association between heavy smoking > 10 cigarettes/day and iron overload (p = 0.07). In stratified analysis by sex, we examined a significant association between smoking and iron overload only among women; former or current smokers had 1.9-fold higher OR (95% CI, 1.01–3.63) than never-smoker. Our findings suggest that heavy alcohol consumption and smoking may worsen iron accumulation in the body.
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Folate, vitamin B12, and homocysteine (HCY) are involved in the metabolism of nucleic acid precursors and it has been hypothesized that they also influence telomere length, a biomarker of aging. However, previous studies have reported inconsistent findings, and data for older adults are limited. Our study aimed to evaluate associations between leukocyte telomere length (LTL) and serum folate, vitamin B12, and HCY levels among adults aged 55 years and over. In a cross-sectional study in 798 men and women aged 55-79 years, serum folate, vitamin B12, and HCY levels were measured using chemiluminescent immunometric assays, and relative LTL was assessed using quantitative real-time polymerase chain reaction. To evaluate associations between LTL and serum folate, vitamin B12, and HCY levels, multiple linear regression models were used. In multiple models adjusted for age, sex, serum high sensitive C-reactive protein (hs-CRP) levels, and other potential confounding factors, we found no association between LTL and serum folate, vitamin B12, and HCY levels. However, we did find a significant inverse association between HCY levels and LTL in participants with serum hs-CRP levels of ≥ 2 mg/L (p < 0.05). Moreover, there was a trend toward an association between HCY and vitamin B12 levels in these individuals (p = 0.08). In those with serum hs-CRP levels of < 2 mg/L, HCY was inversely associated with vitamin B12 levels (p < 0.001) and had no association with LTL. Our findings suggest that increased serum HCY levels, when combined with the presence of systemic inflammation, may play a role in accelerating biological aging.
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