Association of alcohol consumption and aortic calcification in healthy men aged 40–49 years for the ERA JUMP Study

Hemant Mahajan, Jina Choo, Kamal Masaki, Akira Fujiyoshi, Jingchuan Guo, Takashi Hisamatsu, Rhobert Evans, Siyi Shangguan, Bradley Willcox, Tomonori Okamura, Abhishek Vishnu, Emma Barinas-Mitchell, Vasudha Ahuja, Katsuyuki Miura, Lewis Kuller, Chol Shin, Hirotsugu Ueshima, Akira Sekikawa

Research output: Contribution to journalArticle

Abstract

Background and aims Several studies have reported a significant inverse association of light to moderate alcohol consumption with coronary heart disease (CHD). However, studies assessing the relationship between alcohol consumption and atherosclerosis have reported inconsistent results. The current study was conducted to determine the relationship between alcohol consumption and aortic calcification. Methods We addressed the research question using data from the population-based ERA-JUMP Study, comprising of 1006 healthy men aged 40–49 years, without clinical cardiovascular diseases, from four race/ethnicities: 301 Whites, 103 African American, 292 Japanese American, and 310 Japanese in Japan. Aortic calcification was assessed by electron-beam computed tomography and quantified using the Agatston method. Alcohol consumption was categorized into four groups: 0 (non-drinkers), ≤1 (light drinkers), >1 to ≤3 (moderate drinkers) and >3 drinks per day (heavy drinkers) (1 drink = 12.5 g of ethanol). Tobit conditional regression and ordinal logistic regression were used to investigate the association of alcohol consumption with aortic calcification after adjusting for cardiovascular risk factors and potential confounders. Results The study participants consisted of 25.6% nondrinkers, 35.3% light drinkers, 23.5% moderate drinkers, and 15.6% heavy drinkers. Heavy drinkers [Tobit ratio (95% CI) = 2.34 (1.10, 4.97); odds ratio (95% CI) = 1.67 (1.11, 2.52)] had significantly higher expected aortic calcification score compared to nondrinkers, after adjusting for socio-demographic and confounding variables. There was no significant interaction between alcohol consumption and race/ethnicity on aortic calcification. Conclusions Our findings suggest that heavy alcohol consumption may be an independent risk factor for atherosclerosis.

Original languageEnglish
Pages (from-to)84-91
Number of pages8
JournalAtherosclerosis
Volume268
DOIs
Publication statusPublished - 2018 Jan 1

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Alcohol Drinking
Atherosclerosis
Confounding Factors (Epidemiology)
X Ray Computed Tomography
Asian Americans
African Americans
Coronary Disease
Japan
Ethanol
Cardiovascular Diseases
Logistic Models
Odds Ratio
Demography
Light
Research
Population

Keywords

  • Alcohol
  • Aorta
  • Atherosclerosis
  • Calcification
  • Men

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

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Association of alcohol consumption and aortic calcification in healthy men aged 40–49 years for the ERA JUMP Study. / Mahajan, Hemant; Choo, Jina; Masaki, Kamal; Fujiyoshi, Akira; Guo, Jingchuan; Hisamatsu, Takashi; Evans, Rhobert; Shangguan, Siyi; Willcox, Bradley; Okamura, Tomonori; Vishnu, Abhishek; Barinas-Mitchell, Emma; Ahuja, Vasudha; Miura, Katsuyuki; Kuller, Lewis; Shin, Chol; Ueshima, Hirotsugu; Sekikawa, Akira.

In: Atherosclerosis, Vol. 268, 01.01.2018, p. 84-91.

Research output: Contribution to journalArticle

Mahajan, H, Choo, J, Masaki, K, Fujiyoshi, A, Guo, J, Hisamatsu, T, Evans, R, Shangguan, S, Willcox, B, Okamura, T, Vishnu, A, Barinas-Mitchell, E, Ahuja, V, Miura, K, Kuller, L, Shin, C, Ueshima, H & Sekikawa, A 2018, 'Association of alcohol consumption and aortic calcification in healthy men aged 40–49 years for the ERA JUMP Study', Atherosclerosis, vol. 268, pp. 84-91. https://doi.org/10.1016/j.atherosclerosis.2017.11.017
Mahajan, Hemant ; Choo, Jina ; Masaki, Kamal ; Fujiyoshi, Akira ; Guo, Jingchuan ; Hisamatsu, Takashi ; Evans, Rhobert ; Shangguan, Siyi ; Willcox, Bradley ; Okamura, Tomonori ; Vishnu, Abhishek ; Barinas-Mitchell, Emma ; Ahuja, Vasudha ; Miura, Katsuyuki ; Kuller, Lewis ; Shin, Chol ; Ueshima, Hirotsugu ; Sekikawa, Akira. / Association of alcohol consumption and aortic calcification in healthy men aged 40–49 years for the ERA JUMP Study. In: Atherosclerosis. 2018 ; Vol. 268. pp. 84-91.
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abstract = "Background and aims Several studies have reported a significant inverse association of light to moderate alcohol consumption with coronary heart disease (CHD). However, studies assessing the relationship between alcohol consumption and atherosclerosis have reported inconsistent results. The current study was conducted to determine the relationship between alcohol consumption and aortic calcification. Methods We addressed the research question using data from the population-based ERA-JUMP Study, comprising of 1006 healthy men aged 40–49 years, without clinical cardiovascular diseases, from four race/ethnicities: 301 Whites, 103 African American, 292 Japanese American, and 310 Japanese in Japan. Aortic calcification was assessed by electron-beam computed tomography and quantified using the Agatston method. Alcohol consumption was categorized into four groups: 0 (non-drinkers), ≤1 (light drinkers), >1 to ≤3 (moderate drinkers) and >3 drinks per day (heavy drinkers) (1 drink = 12.5 g of ethanol). Tobit conditional regression and ordinal logistic regression were used to investigate the association of alcohol consumption with aortic calcification after adjusting for cardiovascular risk factors and potential confounders. Results The study participants consisted of 25.6{\%} nondrinkers, 35.3{\%} light drinkers, 23.5{\%} moderate drinkers, and 15.6{\%} heavy drinkers. Heavy drinkers [Tobit ratio (95{\%} CI) = 2.34 (1.10, 4.97); odds ratio (95{\%} CI) = 1.67 (1.11, 2.52)] had significantly higher expected aortic calcification score compared to nondrinkers, after adjusting for socio-demographic and confounding variables. There was no significant interaction between alcohol consumption and race/ethnicity on aortic calcification. Conclusions Our findings suggest that heavy alcohol consumption may be an independent risk factor for atherosclerosis.",
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AU - Mahajan, Hemant

AU - Choo, Jina

AU - Masaki, Kamal

AU - Fujiyoshi, Akira

AU - Guo, Jingchuan

AU - Hisamatsu, Takashi

AU - Evans, Rhobert

AU - Shangguan, Siyi

AU - Willcox, Bradley

AU - Okamura, Tomonori

AU - Vishnu, Abhishek

AU - Barinas-Mitchell, Emma

AU - Ahuja, Vasudha

AU - Miura, Katsuyuki

AU - Kuller, Lewis

AU - Shin, Chol

AU - Ueshima, Hirotsugu

AU - Sekikawa, Akira

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N2 - Background and aims Several studies have reported a significant inverse association of light to moderate alcohol consumption with coronary heart disease (CHD). However, studies assessing the relationship between alcohol consumption and atherosclerosis have reported inconsistent results. The current study was conducted to determine the relationship between alcohol consumption and aortic calcification. Methods We addressed the research question using data from the population-based ERA-JUMP Study, comprising of 1006 healthy men aged 40–49 years, without clinical cardiovascular diseases, from four race/ethnicities: 301 Whites, 103 African American, 292 Japanese American, and 310 Japanese in Japan. Aortic calcification was assessed by electron-beam computed tomography and quantified using the Agatston method. Alcohol consumption was categorized into four groups: 0 (non-drinkers), ≤1 (light drinkers), >1 to ≤3 (moderate drinkers) and >3 drinks per day (heavy drinkers) (1 drink = 12.5 g of ethanol). Tobit conditional regression and ordinal logistic regression were used to investigate the association of alcohol consumption with aortic calcification after adjusting for cardiovascular risk factors and potential confounders. Results The study participants consisted of 25.6% nondrinkers, 35.3% light drinkers, 23.5% moderate drinkers, and 15.6% heavy drinkers. Heavy drinkers [Tobit ratio (95% CI) = 2.34 (1.10, 4.97); odds ratio (95% CI) = 1.67 (1.11, 2.52)] had significantly higher expected aortic calcification score compared to nondrinkers, after adjusting for socio-demographic and confounding variables. There was no significant interaction between alcohol consumption and race/ethnicity on aortic calcification. Conclusions Our findings suggest that heavy alcohol consumption may be an independent risk factor for atherosclerosis.

AB - Background and aims Several studies have reported a significant inverse association of light to moderate alcohol consumption with coronary heart disease (CHD). However, studies assessing the relationship between alcohol consumption and atherosclerosis have reported inconsistent results. The current study was conducted to determine the relationship between alcohol consumption and aortic calcification. Methods We addressed the research question using data from the population-based ERA-JUMP Study, comprising of 1006 healthy men aged 40–49 years, without clinical cardiovascular diseases, from four race/ethnicities: 301 Whites, 103 African American, 292 Japanese American, and 310 Japanese in Japan. Aortic calcification was assessed by electron-beam computed tomography and quantified using the Agatston method. Alcohol consumption was categorized into four groups: 0 (non-drinkers), ≤1 (light drinkers), >1 to ≤3 (moderate drinkers) and >3 drinks per day (heavy drinkers) (1 drink = 12.5 g of ethanol). Tobit conditional regression and ordinal logistic regression were used to investigate the association of alcohol consumption with aortic calcification after adjusting for cardiovascular risk factors and potential confounders. Results The study participants consisted of 25.6% nondrinkers, 35.3% light drinkers, 23.5% moderate drinkers, and 15.6% heavy drinkers. Heavy drinkers [Tobit ratio (95% CI) = 2.34 (1.10, 4.97); odds ratio (95% CI) = 1.67 (1.11, 2.52)] had significantly higher expected aortic calcification score compared to nondrinkers, after adjusting for socio-demographic and confounding variables. There was no significant interaction between alcohol consumption and race/ethnicity on aortic calcification. Conclusions Our findings suggest that heavy alcohol consumption may be an independent risk factor for atherosclerosis.

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