Alcohol consumption and aortic arch calcification in an older Chinese sample: The Guangzhou Biobank Cohort Study
Introduction
A J-shape association between alcohol consumption and cardiovascular diseases has been reported in epidemiological studies. Western studies showed that people who drink moderately, i.e., ≤2 drinks/day, tend to have a lower risk of coronary heart disease and atherosclerosis [1], [2], [3], [4], whereas those who drink heavily are prone to increased risk of pancreatitis, liver disease and breast and other cancer. Alcohol drinking is also associated with coronary calcification as measured by computed tomography [5], [6], [7]. However, this association has not been studied in Chinese population, and the limited evidence to date on Western populations is conflicting [5], [6], [7]. The explanation is not clear. We have previously reported that moderate alcohol drinkers had very similar level of fasting glucose, but higher HDL cholesterol than never drinkers in the Guangzhou Biobank Cohort Study (GBCS) [8]. We have also found that excessive alcohol drinking is associated with higher fasting glucose and elevated blood pressure, and alcohol sensitivity may aggravate the effect of drinking on blood pressure [8], [9]. We thus hypothesized that excessive drinking is associated with increased risk of aortic arch calcification (AAC), which is common in older Chinese [10].
In Western populations, AAC is independently associated with the development of coronary heart disease [11] and has a high specificity for detection of severe coronary atherosclerosis [12]. Recent cross-sectional and prospective studies in Japanese have confirmed that AAC assessed by chest X-ray has a high validity and reproducibility, and is a strong independent predictor of cardiovascular events beyond traditional risk factors including endothelial dysfunction [13], [14]. These results have suggested that AAC plays an important role in risk stratification of further cardiovascular events. We have reported that active and passive smoking were associated with both presence and severity of AAC in a dose–response pattern using the GBCS data [10], [15]. Our literature search found no data on alcohol drinking and AAC in observational or interventional studies. We hereby present the first report in participants from the GBCS.
Section snippets
Methods
Detailed information on GBCS has been described elsewhere [16], [17]. Briefly, the GBCS is a population-based cohort study that recruited Guangzhou permanent residents aged from 50 to 85 years. Participants were randomly selected from a large social and welfare association which was aligned with the municipal government: the “Guangzhou Health and Happiness Association for the Respectable Elders” (GHHARE), which included more than 95,000 permanent Guangzhou residents [16]. People who were 50 to 85
Results
The prevalence of AAC increased with increasing age in both sexes, from 18.0% to 45.3% then to 65.8% in women, and 18.5%, 36.2% and 57.7% in men aged 50–59, 60–69 and 70+, respectively (P for trend in both women and men < 0.001). Although overall more males had AAC, after adjusting for age, women had higher prevalence of AAC than men (44.1% (95% confidence interval (CI) 43.4–44.8) vs. 37.8% (95% CI 36.7–38.8), P < 0.001). In 7945 men, 52.3% were never drinkers, 23.0% were occasional drinkers,
Discussion
To the best of our knowledge, this is the first study showing a significant association between alcohol drinking and AAC in men, with a clear dose–response relation between frequency or quantity of drinking and presence as well as severity of AAC. The association remained significant after adjusting for many potential confounders, and was not mediated by HDL-cholesterol or blood pressure. We found that excessive alcohol drinking was associated with AAC in men, and different alcoholic beverage
Funding
This work was supported by the University of Hong Kong Foundation for Educational Development and Research, Hong Kong; the Guangzhou Public Health Bureau and the Guangzhou Science and Technology Bureau, Guangzhou, China; The University of Birmingham, UK; and the Guangdong Natural Science Foundation of China, Guangdong, China (grant number: 9451062001003477).
Acknowledgements
The Guangzhou Biobank Cohort Study investigators include: the Guangzhou No. 12 Hospital: WS Zhang, M Cao, T Zhu, B Liu, CQ Jiang (Co-PI); The University of Hong Kong: GN Thomas, CM Schooling, SM McGhee, GM Leung, TH Lam (Co-PI); The University of Birmingham: P Adab, KK Cheng (Co-PI).
The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology.
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