Alcohol and Alcoholism Vol. 47, No. 3, pp. 282–287, 2012 doi: 10.

1093/alcalc/ags019
Advance Access Publication 26 February 2012

CLINICAL ASPECTS
Association of Alcohol Consumption with Lipid Profile in Hypertensive Men
Hyejin Park1 and Kisok Kim2, *
1
Department of Epidemiology and Health Promotion, Kyungpook National University, Daegu 702-701, Republic of Korea and 2Department of Pharmacy,
Keimyung University, Daegu 704-701, Republic of Korea
*Corresponding author: Tel.: +82-53-580-5932; Fax: +82-53-580-5164; E-mail: kimkisok@kmu.ac.kr

(Received 14 April 2011; accepted 8 January 2012)

Abstract — Aims: Alcohol consumption is known to be closely related with alterations in blood lipid levels as well as in blood
pressure. The objective of this study was to evaluate the association between alcohol consumption and blood lipid levels in hyperten-
sive men. Methods: A cross-sectional study involving participants (n = 2014) aged 20–69 years from the Korea National Health and
Nutrition Examination Survey, 1998–2009. Demographic characteristics, dietary intake and medical history were obtained from the
participants by questionnaire, and lipid levels were determined by analysis of blood samples. Results: After adjusting for demograph-
ic and dietary factors, alcohol consumption was negatively associated with risk of low high-density lipoprotein cholesterol [HDL-C;
odds ratio (OR): 0.29, 95% confidence interval (CI): 0.22–0.40 in heavy (≥30 g/day) drinkers; P for trend <0.001], whereas the risk
of high triglycerides increased with increasing alcohol consumption (OR: 2.04, 95% CI: 1.53–2.72 in heavy drinkers; P for trend
<0.001). However, the OR of high non-HDL-C and the ratio of high triglycerides to HDL-C did not change significantly with an in-
crease in alcohol consumption. Conclusion: These data suggest that alcohol consumption differentially affected lipid measures
according to the amount of alcohol intake in hypertensive men.

INTRODUCTION hypertension, may represent an important and potentially

The consumption of alcoholic beverages is associated with
an elevated incidence of many diseases, including metabolic
syndrome and cardiovascular disease (Clerc et al., 2010;
Wakabayashi, 2010a). Interestingly, epidemiological data
from the general population have shown that the effect of
alcohol on many diseases has a biphasic pattern, depending
on the amount of alcohol consumed, such that the incidence
of coronary heart disease is known to be lowered by moder-
ate alcohol consumption and increased by high alcohol
consumption (Corrao et al., 2000; Meister et al., 2000).
Although the detailed mechanism of these biphasic effects
still remains to be determined, alcohol is known to have dif-
ferential effects on the metabolism of high-density lipopro-
tein cholesterol (HDL-C), low-density lipoprotein cholesterol
(LDL-C) and triglycerides (Wannamethee and Shaper, 1992;
Zilkens et al., 2003), as well as on blood pressure
(Panagiotakos et al., 2007). Additionally, the associations
between alcohol consumption and the risk of cardiovascular
disease, including myocardial infarction and coronary heart
disease, are mediated, in large part, by the differential influ-
ence on the levels of HDL-C and LDL-C (Gaziano et al.,
1993; Savolainen and Kesäniemi, 1995).
Consequently, many epidemiological studies have focused
on the relationship between alcohol consumption and
blood lipid concentrations within specific population groups.
However, findings on the association between alcohol and
the lipid profile or the odds ratio (OR) for dyslipidaemia
measures have been less consistent, owing partially to differ-
ences in race/ethnicity or concurrent disease state of partici-
pants in each study (Fan et al., 2008; Bellary et al., 2010;
Roy et al., 2010; Wakabayashi, 2010b). Despite both blood
pressure and lipid profile being important factors in the
pathogenesis of cardiovascular disease, alcohol consumption
is known to be differentially associated with blood pressure
and lipid levels (Ohta et al., 2009; Zhang et al., 2011).
Additionally, although underlying disease, such as
modifiable component of the lipid profile, few studies have
examined the correlation between alcohol consumption and
dyslipidaemia profiles in hypertensive men, based on a na-
tionwide survey. Thus, the aim of the present study was to
investigate this association in Korean men with hypertension,
using Korea National Health and Nutrition Examination
Survey (KNHANES) data from 1998 to 2009.
METHODS
Subjects
This study was based on the KNHANES 1998–2009, which
included a health and nutrition survey and a medical examin-
ation. The sample for KNHANES was selected using a strati-
fied multistage cluster sampling design with proportional
allocation, based on the National Census Registry. In total,
2200 sampling units, each of which contained about 23
households, were randomly sampled. From selected samples,
2014 men with hypertension (aged 20–69 years) were
included in this study. Based on data from the health
check-up, hypertensive individuals were identified as having
a systolic blood pressure ≥140 mmHg, a diastolic blood pres-
sure ≥90 mmHg or taking medication for hypertension.
Data collection and biochemical measurements
The KNHANES included well-established questions to deter-
mine the demographic and socioeconomic characteristics of
the subjects. These included questions on age, sex, education
level, income, smoking habits, alcohol consumption, exercise
and medical history. Daily energy and nutrient intakes were
assessed using a 24-h recall method and a food-intake fre-
quency method. Height and weight were measured with the
participant wearing light clothing and no shoes. Body mass
index (BMI) was then calculated as weight (kg) divided by
the square of height (m2). Blood pressure was measured with
a mercury sphygmomanometer (Baumanometer; WA Baum

© The Author 2012. Medical Council on Alcohol and Oxford University Press. All rights reserved
 Alcohol and lipid profile in hypertensive men
Co., Inc., Copiague, NY, USA) after the subject had rested
for 5 min in a sitting position.
Blood samples were collected by venipuncture after 10–
12 h of fasting. Total cholesterol, HDL-C and triglycerides
were measured by enzymatic methods with commercially
available kits. Non-HDL-C was calculated as total choles-
terol minus HDL-C. All blood analyses were carried out
within 2 h of blood sampling by a laboratory certified by the
Korean Ministry of Health and Welfare.
The study protocol was approved by the Korean Ministry
of Health and Welfare and was conducted in accordance
with the Ethical Principles for Medical Research Involving
Human Subjects, as defined by the Helsinki Declaration.
Study participants provided written informed consent.
Variable definitions
Alcohol consumption was assessed by questioning the sub-
jects about their drinking behavior during the month before
the interview. The subjects were asked about their average
frequency and amount of alcoholic beverage intake. The
average amount and number of alcoholic beverages con-
sumed was converted into the amount of pure alcohol
consumed per day. For the analysis, the subjects were cate-
gorized into five groups according to average daily alcohol
consumption: none, 0.1–4.9, 5.0–14.9, 15.0–29.9 and ≥30 g
alcohol/day. Dyslipidaemia included three lipid abnormal-
ities: decreased HDL-C levels, increased non-HDL-C and
increased triglyceride levels. According to the cutoff values
for plasma lipids as established by the Adult Treatment
Panel III guidelines published by the US National Institutes
of Health (National Cholesterol Education Program, 2002),
we defined low HDL-C level as <40 mg/dl for men and <50
mg/dl for women, a high non-HDL-C level as ≥160 mg/dl
and a high triglyceride level as ≥150 mg/dl. Additionally, the
ratio of triglycerides to HDL-C was used as a measure of
dyslipidaemia because a ratio greater than 3.8 is known to
correlate with the LDL-C phenotype B, which is a reliable
predictor for the risk of cardiovascular disease (Hanak et al.,
2004; Welsh et al., 2010).
As a covariate, education was categorized as less than a
high school diploma, high school diploma and college or
higher. Cigarette smoking status was defined as never, occa-
sional or frequent. The occasional smoking category
included former smokers and those who smoked less than
one cigarette per day and frequent smoking category
included participants whose average daily smoking was more
than one cigarette. Income was calculated by dividing the
square root of household size by the monthly household
income, according to the method of the Organization for
Economic Co-operation and Development. Income was cate-
gorized by quartiles, based on the income of all Korean
households.
Statistical analysis
We calculated the frequency and percentage or mean and
standard deviation where appropriate for demographic char-
acteristics to describe the sample population by categories of
alcohol consumption. Estimate statements in linear regression
models were used to determine the adjusted mean and 95%
confidence intervals (CI) of each of the lipid measures with
increasing alcohol consumption. For triglyceride level, based
283
on a normal probability plot, geometric means were used to
improve the approximation of a normal distribution.
Logistic regression models were used to estimate the
adjusted OR and 95% CI of dyslipidaemia among partici-
pants who consumed higher levels of alcohol compared with
the reference group (those consuming no alcohol). A result
was considered to be statistically significant if the 95% CI
did not include one. The presence of a linear trend was
evaluated by defining a linear contrast in each of the linear
and logistic regression models. All statistical analyses were
conducted using the SAS software (ver. 9.1; SAS Institute,
Inc., Cary, NC, USA).
RESULTS
The basic characteristics and outcomes of the study partici-
pants sorted by intake of alcohol are presented in Table 1.
As alcohol consumption increased, participants were more
likely to be young and smokers. Additionally, consumption
of alcohol correlated positively with the intake of energy
(P < 0.001). However, other demographic variables, includ-
ing BMI, education level, income, regular physical exercise,
and percentage of fat intake, were not significantly associated
with increased consumption of alcohol.
Age-adjusted mean HDL-C levels were higher among par-
ticipants consuming higher amounts of alcohol: 41.5 (95%
CI: 40.2–42.7) mg/dl among non-drinkers, 42.9 (95% CI:
41.5–44.3) mg/dl among those consuming 0.1–4.9 g/day of
alcohol, 47.6 (95% CI: 45.3–50.0) mg/dl among those con-
suming 5.0–14.9 g/day, 46.7 (95% CI: 44.1–49.3) mg/dl
among those consuming 15.0–29.9 g/day and 48.7 (95% CI:
46.5–50.9) mg/dl among those consuming 30.0 g/day or
more (P for trend <0.001; Fig. 1a). Adjusted mean
non-HDL-C levels were 149.0 (95% CI: 145.0–152.9) mg/dl
among non-drinkers, 142.5 (95% CI: 137.5–147.5) mg/dl
among participants consuming 0.1–4.9 g/day of alcohol,
136.1 (95% CI: 129.9–142.2) mg/dl among those consuming
5.0–14.9 g/day, 136.8 (95% CI: 130.2–143.3) mg/dl among
those consuming 15.0–29.9 g/day and 136.1 (95% CI:
130.4–141.8) mg/dl among those consuming 30.0 g/day or
more (P for trend = 0.005; Fig. 1b). Among these same
alcohol consumption groups, adjusted geometric mean trigly-
ceride levels were 124.8 (95% CI: 118.1–132.0), 125.1 (95%
CI: 117.2–133.5), 127.0 (95% CI: 117.4–137.4), 131.4 (95%
CI: 118.7–145.4) and 150.1 (95% CI: 137.9–163.4), respect-
ively (P for trend <0.001; Fig. 1c).
Table 2 shows the prevalence and ORs for lipid measures
associated with alcohol consumption. The prevalence of a
low HDL-C level decreased with increasing consumption of
alcohol (P for trend <0.001). Compared with non-drinking
participants, the adjusted ORs were 0.67 (95% CI: 0.51–
0.88) among those consuming 0.1–4.9 g/day of alcohol, 0.58
(95% CI: 0.44–0.77) among those consuming 5.0–14.9 g/
day, 0.49 (95% CI: 0.36–0.68) among those consuming
15.0–29.9 g/day and 0.29 (95% CI: 0.22–0.40) among those
consuming 30.0 g/day or more (P for trend <0.001).
However, the trends in prevalence and adjusted ORs for
high non-HDL-C were not significantly related with increas-
ing intake of alcohol after adjusting for age (model 1) or for
all other potential covariates, such as BMI, education,
income, cigarette consumption, physical exercise, energy
284 Park and Kim
Table 1. Demographic characteristics by categories of alcohol consumption among hypertensive men

Alcohol consumption (g/day)

Characteristic None (n = 491) 0.1–4.9 (n = 418) 5.0–14.9 (n = 404) 15.0–29.9 (n = 303) ≥30.0 (n = 398) Pa

Mean age (SD) 59.4 (13.4) 55.3 (14.6) 51.9 (14.1) 51.9 (13.8) 53.3 (13.3) <0.001
BMI, kg/m2 (SD) 24.5 (3.2) 24.6 (3.1) 24.5 (3.2) 24.5 (3.3) 24.4 (3.2) 0.351
Education (%) 0.461
<High school 272 (55.4) 177 (42.3) 153 (37.9) 119 (39.3) 204 (51.3)
High school 116 (23.6) 132 (31.6) 129 (31.9) 99 (32.7) 124 (31.2)
>High school 103 (21.0) 109 (26.1) 122 (30.2) 85 (28.1) 70 (17.6)
Income, US$/month (SD) 1336.4 (1256.7) 1580.6 (1375.7) 1678.1 (1442.0) 1715.2 (1314.9) 1423.7 (1333.9) 0.137
Cigarette smoker (%) <0.001
Never 139 (28.3) 87 (20.8) 73 (18.1) 46 (15.2) 33 (8.3)
Occasional 206 (42.0) 183 (43.8) 154 (38.1) 116 (38.3) 133 (33.4)
Frequent 146 (29.7) 148 (35.4) 177 (43.8) 141 (46.5) 232 (58.3)
Regular exercise (%) 229 (46.6) 209 (50.0) 188 (46.5) 150 (49.5) 162 (40.7) 0.104
Energy intake, kcal/day (SD) 2001.9 (770.9) 2053.9 (731.8) 2156.2 (845.3) 2234.9 (867.8) 2268.8 (920.7) <0.001
Fat intake, % of energy (SD) 14.5 (7.8) 14.7 (7.4) 16.3 (8.5) 15.4 (8.3) 15.1 (8.8) 0.147

P determined by analysis of variance test or Mantel–Haenszel χ2 test.

a

Fig. 1. Age-adjusted levels of mean HDL-C (a), mean non-HDL-C (b) and geometric mean triglycerides (c) by level of alcohol consumption among
hypertensive men. Error bar indicates 95% CIs.

Table 2. Prevalence and adjusted OR (95% CI) of dyslipidaemia measures by alcohol consumption among hypertensive men

Alcohol consumption (g/day)

Dyslipidaemia measure None (n = 491) 0.1–4.9 (n = 418) 5.0–14.9 (n = 404) 15.0–29.9 (n = 303) ≥30.0 (n = 398) P for trend

Low HDL-C
Prevalence, % 51.1 40.7 36.6 32.7 24.1 <0.001
OR (95% CI)
Model 1 1.00 (reference) 0.66 (0.51–0.86) 0.56 (0.43–0.74) 0.47 (0.35–0.64) 0.31 (0.23–0.41) <0.001
Model 2 1.00 (reference) 0.67 (0.51–0.88) 0.58 (0.44–0.77) 0.49 (0.36–0.68) 0.29 (0.22–0.40) <0.001
High non-HDL-C
Prevalence, % 35.6 36.8 34.4 32.3 32.7 0.175
OR (95% CI)
Model 1 1.00 (reference) 1.03 (0.78–1.35) 0.89 (0.67–1.17) 0.79 (0.58–1.08) 0.81 (0.61–1.07) 0.312
Model 2 1.00 (reference) 1.02 (0.77–1.35) 0.88 (0.66–1.18) 0.81 (0.59–1.12) 0.80 (0.59–1.07) 0.380
High triglycerides
Prevalence, % 38.5 38.3 47.5 51.2 59.3 <0.001
OR (95% CI)
Model 1 1.00 (reference) 0.94 (0.72–1.23) 1.30 (0.99–1.70) 1.48 (1.10–1.99) 2.11 (1.61–2.78) <0.001
Model 2 1.00 (reference) 0.97 (0.73–1.29) 1.35 (1.02–1.79) 1.62 (1.19–2.21) 2.04 (1.53–2.72) <0.001
High triglycerides-HDL-C ratio
Prevalence, % 40.7 37.6 42.6 42.2 46.2 0.044
OR (95% CI)
Model 1 1.00 (reference) 0.84 (0.64–1.11) 1.00 (0.76–1.31) 0.97 (0.72–1.30) 1.15 (0.88–1.51) 0.304
Model 2 1.00 (reference) 0.85 (0.64–1.12) 1.03 (0.77–1.36) 1.02 (0.75–1.40) 1.10 (0.83–1.46) 0.509

OR, odds ratio; CI, confidence interval.

Model 1: adjusted for age. Model 2: adjusted for model 1 + BMI, education, income, cigarette smoking status, physical activity, total energy intake and fat
intake.
 Alcohol and lipid profile in hypertensive men
intake and fat intake (model 2). Meanwhile, prevalence and
adjusted ORs for high triglyceride levels positively correlated
with increasing alcohol consumption (P for trend <0.001).
Adjusted ORs of high triglyceride levels among these same
consumption groups were 0.97 (95% CI: 0.73–1.29), 1.35
(95% CI: 1.02–1.79), 1.62 (95% CI: 1.19–2.21) and 2.04
(95% CI: 1.53–2.72), respectively, compared with the non-
drinking group.
The prevalence of a high ratio of triglycerides to HDL-C
correlated significantly with alcohol consumption (P for
trend = 0.044). However, there was no statistically significant
trend in ORs with greater intake of alcohol after adjusting
for potential covariates.
DISCUSSION
Although the association between alcohol consumption and
blood pressure or metabolic syndrome is well known
(Puddey et al., 1985; Ascherio et al., 1992; Yoon et al.,
2004), the effect of alcohol on lipid profiles among hyperten-
sive patients is less clear. In the present nationwide cross-
sectional study in hypertensive men aged 20–69 years, drin-
kers with heavier alcohol consumption tended to be current
smokers and to have high energy intakes. These results are
consistent with those of other epidemiological studies among
the general population, which have reported that heavy
alcohol consumption was associated with increased preva-
lence of smoking and high energy intake (Gaziano et al.,
1993; Beulens et al., 2007).
The associations between alcohol intake and higher
HDL-C levels and lower non-HDL-C levels are well estab-
lished (Gaziano et al., 1993; Ellison et al., 2004; Yoon et al.,
2004; Kabagambe et al., 2005; Wakabayashi, 2010a). The
results of the present study in hypertensive men also showed
a clear dose-dependent relationship between alcohol and
HDL-C and non-HDL-C levels. Furthermore, age-adjusted
geometric mean triglyceride levels showed a linear relation-
ship with increased alcohol consumption. However, the rela-
tionship between alcohol consumption and triglyceride levels
in the general population were not consistent among different
racial/ethnic groups. In many epidemiological studies, in-
cluding those performed in Europeans (Foerster et al., 2009;
Hansel et al., 2010) and the Japanese (Wakabayashi, 2010a,
b), the relationship was more J-shaped, with light alcohol
drinking associated with a decrease in blood triglyceride
level and heavy drinking associated with an increase. On the
other hand, some results, including those from Turkish men,
showed a linear increase in triglycerides with an increase in
alcohol intake.
There are many epidemiological studies on the relationship
between alcohol consumption and the risk of dyslipidaemia
in various general populations. Previous studies in Japanese
adults, as well as in Korean adults, showed that ORs for low
HDL-C and high triglycerides decreased linearly with
increasing alcohol consumption (Yoon et al., 2004;
Wakabayashi, 2010a,b). Moreover, in a study in Greece,
alcohol drinking was associated with lower risk of low
HDL-C (Athyros et al., 2007). However, although results
from a US white population also showed a linear decrease of
risk for high LDL-C, no significant relationship between
alcohol consumption and the risk of low HDL-C level or the
285
risk of high triglycerides was observed (Gaziano et al.,
1993). This discrepancy may due to differences in mean ages
of the study populations; the US population was older than
the others studied, including ours. Another possible explan-
ation may be a difference in race/ethnicity, because genetic
factors are known to play an important role in lipid metabol-
ism (López et al., 2008). Indeed, genetic factors are known
to play a major role as determinants of HDL-C, with esti-
mates of hereditability varying from ~ 40–60% (Hamsten
et al., 1986; Cohen et al., 1994; Guerra et al., 1997). Another
important confounding factor may be the existence of con-
current diseases exacerbated by chronic alcohol drinking,
such as hypertension. In this study among hypertensive men,
after adjusting for covariates, ORs for low HDL-C linearly
decreased with increasing alcohol consumption.
Additionally, ORs for high triglycerides showed J-shaped
relationships with alcohol consumption. Indeed, alcohol con-
sumption has been reported to have a J- or U-shaped rela-
tionship with cardiovascular disease, including coronary
artery disease, stroke and myocardial infarction (Mukamal
and Rimm, 2001; Reynolds et al., 2003; Yusuf et al., 2004).
Although the mechanism of these J-shaped effects of alcohol
on many diseases has not been fully determined, this result
suggests that an alteration in triglycerides metabolism may
play an important role in this biphasic effect in hypertensive
men. However, ORs for high non-HDL-C and high
triglycerides-HDL-C ratio were not significantly associated
with the amount of alcohol consumption.
Given that low HDL-C, high non-HDL-C, high triglycer-
ides and high ratio of triglyceride to HDL-C are important
risk factors for cardiovascular disease (Gordon et al., 1989;
Carey et al., 2010), the results of our study suggest that,
among hypertensive men, beneficial effects of light alcohol
consumption on the development of cardiovascular diseases
are associated with decreased ORs of both low HDL-C and
high triglycerides, whereas the harmful effects of heavy
alcohol consumption are due to an increase in triglyceride
levels. Because the J-shaped association between alcohol
consumption and blood pressure is well known (Zhang
et al., 2009), our findings suggest that light alcohol con-
sumption (0.1–4.9 g/day) has beneficial effects for hyperten-
sive patients in lowering the risk of dyslipidaemia as well as
decreasing blood pressure.
Our study has several limitations. Because the study used
a cross-sectional design, the results only indicate associations
and cannot be used to determine causality. Additionally, self-
reports of alcohol consumption and 24-h dietary recall may
lead to misclassification and measurement error (Day et al.,
2004). Furthermore, though medications for hypertension
may affect the metabolism of alcohol and lipids (Nandeesha
et al., 2009), we were unable to determine how the associa-
tions of alcohol with lipid measures may be modified by
antihypertensive drug. We were unable to classify the partici-
pants based on severity and duration of hypertension. Thus,
this deficiency may have led to a dilution of the findings of
this study. As lipid profile may be influenced by the type of
alcoholic beverages and drinking frequency (Foerster et al.,
2009; Hiramine et al., 2011), another limitation is that we
did not determine drinking patterns, such as binge drinking
and were not able to analyze by beverage type. Despite these
limitations, this study has several major strengths. To our
knowledge, this study is the first reported to assess the
286 Park and Kim
association between alcohol consumption and lipid profile
among hypertensive men using nationally representative
data. Another strength is that this study was able to control
for several important confounding variables, including
energy intake and fat intake.
CONCLUSIONS
In 2014 hypertensive men, higher consumption of alcohol
was associated with a decreased risk of low HDL-C and a
J-shaped increase in risk of high triglycerides. However, the
risk of a high non-HDL-C and a high triglyceride to HDL-C
ratio were not significantly associated with alcohol consump-
tion. Our results suggest that the beneficial effects of alcohol
among hypertensive men may be attributable to the lowered
risk of low HDL-C, whereas the harmful effect of alcohol
may be attributable to increased triglyceride levels.
Moreover, light alcohol consumption may be helpful for
hypertensive men to alleviate the risk of dyslipidaemia.
AUTHORS’ ROLES
H.P. contributed to the study design, analysis and interpret-
ation of data and review the literatures. K.K. designed the
study and study’s analytic strategy, prepared the manuscript
and involved in final approval of the revised manuscript.
Conflict of interest statement. The authors declare no conflict
of interest.
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