© International Epidemiological Association 2001
International Journal of Epidemiology 2001;30:766–770
Printed in Great Britain
Body weight, alcohol consumption and liver
enzyme activity—a 4-year follow-up study
Duk-Hee Lee,a Myung-Hwa Hab and David C Christianic
Background This prospective study was performed in order to investigate the effect of baseline
body mass index (BMI), BMI changes, baseline alcohol consumption, and changes
in alcohol consumption on liver enzyme activity.
Methods
This study population consisted of 6846 male workers in a steel manufacturing
company who had undergone health examinations in 1994 and 1998.
Results
The risk for elevated both aspartate aminotransferase (AST) and alanine aminotransferase (ALT) values over the four years increased with the baseline BMI and
BMI changes, but not with alcohol consumption. Compared with the subject BMI
,20, the adjusted odds ratios (OR) for those with baseline BMI 20–21.9, 22–24.9,
25– were 1.2, 1.6, 1.7 in AST and 1.4, 2.4, 2.8 in ALT, respectively. Compared with
subjects who either lost or maintained their weight, the adjusted OR for men
with slight, moderate, and heavy weight gain were 1.7, 2.6, 6.8 in AST and 2.4,
3.9, 11.3 in ALT, respectively. However gamma-glutamyl transferase (GGT) was
associated with BMI changes and baseline alcohol consumption, not with baseline BMI and changes in alcohol consumption. Compared with subjects who lost
or maintained weight, the adjusted OR for men with slight, moderate, and heavy
weight gain were 2.4, 4.4 and 8.5, respectively. In comparison with non-drinkers,
the adjusted OR for light, moderate and heavy drinkers were 1.8, 2.1 and 5.8,
respectively.
Conclusion
These data suggest that body weight, rather than alcohol consumption, may be the
major factor in determining the serum level of liver enzymes. Even when body
weight was not generally considered to be overweight, slight to moderate gains
in weight were associated with increases in serum liver enzymes.
Keywords
Liver enzymes, body weight, alcohol consumption, aspartate aminotransferase,
alanine aminotransferase, gamma-glutamyl transferase
Accepted
10 April 2001
Alcohol is one of the factors most frequently associated with
increased liver enzyme and the association between alcohol
intake and alcohol-induced liver disease is well known. The
Italian Dionysos study showed that alcohol was suspected to
be the cause in 23% of all cases of liver disease, with a dosedependent increase in the risk of developing liver disease.1,2
Conversely, two studies from Japan did not show a strong
relationship between alcohol consumption and serum liver
enzymes; specifically, aspartate aminotransferase (AST) and
alanine aminotransferase (ALT).3,4
a Department of Preventive Medicine, College of Medicine, Kosin University,
34 Amnam-Dong, Suh-Gu, Pusan, Korea, 602–702. E-mail: ducky@ns.
kosinmed.or.kr
b Health Care Center, Pohang Steel Company, Pohang, Korea.
c Department of Environmental Health, Harvard School of Public Health,
Boston, MA, USA
Obesity has also been identified as an important factor
known to contribute to raised levels of serum liver enzyme
in several cross-sectional studies.5–8 In the Dionysos study,9
it appeared that obesity rather than alcohol abuse was the
main cause of raised values of ALT and the presence of fatty
liver.
There have been a few studies evaluating the effects of the
changes of alcohol consumption or the changes of body mass
index (BMI) on the level of liver enzymes in a prospectively
systematic way among apparently healthy people.10–13 In these
studies, the effect of the changes of alcohol consumption was
very weak on liver enzyme, in comparison to that of the BMI
change. This is an apparently surprising result given the strong
association between alcohol consumption and serum liver
enzymes consistently reported in many cross-sectional studies
from western countries.1,2 Some clinical-based studies14–16
have also showed that the effect of weight loss seemed to be
766
BODY WEIGHT, ALCOHOL AND LIVER ENZYMES
more crucial in normalizing the liver enzyme than reduced
alcohol consumption.
However, one study which analysed liver enzymes separately
showed that the effect of body weight or alcohol consumption
could be different depending upon which liver enzyme is
assessed.10 In addition, most studies10–13 published to date have
usually focused on moderate or severe obesity, defined as a BMI
.25. The aim of this prospective study was to investigate the
association of baseline BMI, BMI changes, baseline alcohol
consumption, and changes in alcohol consumption on serum
liver enzyme activity in male workers, most of whom were in a
normal range of BMI at baseline, at a large steel company in the
Republic of Korea.
Methods
Study population
All workers in this company are required to have an annual
health check-up consisting of clinical and laboratory measurements. Throughout 1994, health check-ups were performed
between 9:00 a.m. and noon after an overnight fast, in a health
care centre at the factory. Male workers between 25 and 50 years
old without definite liver disease or hepatitis B antigen were
eligible for follow-up for this study. Of the 11 867 men who
met these criteria, 8553 men (72.1% follow-up rate) were reexamined in 1998. Among these subjects, 8445 men without
diseases requiring continuous medication became the base population for a cross-sectional analysis. For the incidence analysis,
subjects with abnormal levels of liver enzyme activity at
baseline defined as an AST over 33 U/L, ALT over 35 U/L, or
gamma glutamyl transferase (GGT) over 50 U/L, were excluded.
After all exclusions, 6846 men were included in the incidence
analyses.
Measurement
Information on lifestyle factors including cigarette smoking,
alcohol consumption, exercise, and medical history were obtained
by self-reported questionnaires. Each year, all workers were
asked to complete the same, or slightly modified, questionnaire.
For each questionnaire, changes spotted by a computerized data
system (which contained information from previous years)
were confirmed by a nurse in a direct interview.
The workers were asked how many times per week or per
month they consumed alcohol and the typical quantities consumed. They were asked to estimate the amount in terms
of soju, a popular Korean liquor. Based on this information
the amount of alcohol consumed per week was calculated.
All subjects were divided into four groups by the baseline
amount of alcohol consumption (non-drinker; light drinker,
1–180 g/week; moderate drinker, 181–360 g/week; heavy
drinker, 361+ g/week). The population was stratified into four
groups by changes in alcohol consumption (decreased, no
change, increased 1–90 g/week, increased 91+ g/week). The
BMI value, defined as weight (kg)/height (m2), was used as a
weight index; and during weighing, almost all subjects wore the
standard company uniform. Subjects were classified into four
groups according to baseline BMI or BMI change, respectively.
The criteria for the former were: ,20 kg/m2; 20–21.9 kg/m2;
22–24.9 kg/m2; and >25 kg/m2. Criteria for the latter were:
weight loser or maintainer, <0 kg/m2 or 0 kg/m2; slight weight
767
gainer, 0.1–1.0 kg/m2; moderate weight gainer, 1.1–2.0 kg/m2;
heavy weight gainer, .2.0 kg/m2.
Venous blood samples were obtained from a cubital vein after
overnight 12 hours fasting. The serum samples were kept at 4°C
and analysed within 48 hours. Laboratory tests were performed
with an automatic analyser (Hitachi 7170, Japan) by optimized
methods based on the recommendations of the Korean Society
for Clinical Chemistry, at 37°C. Our normal ranges (U/L) for
men were as follows: AST <33; ALT <35; GGT <50.
Statistical analyses
The relationship between alcohol consumption and BMI, and
the prevalence and incidence of elevated liver enzyme were
analysed by multiple logistic regression, using the SAS statistical
program, version 6.12. In the incidence analyses, we included
four main variables (baseline BMI, baseline alcohol consumption,
BMI change, change in alcohol consumption), covariates (age,
cigarette smoking [pack-years], exercise [frequency/week], baseline AST or ALT or GGT [baseline for the dependent variable]),
and interaction terms between main factors. There were no
interaction terms that reached statistical significance; therefore,
these terms were dropped from the final model. We included
baseline AST or ALT or GGT as covariates because amounts of
changes of these enzymes during 4 years were dependent upon
the baseline value of these enzymes. Those with relatively high
values of serum liver enzymes at baseline, although in normal
range, tended to increase more than those with low values. In
the prevalence analyses, two main variables (baseline BMI, baseline alcohol consumption) and covariates (age, cigarette smoking [pack-years], exercise [frequency/week]) were included in
the final model. The P-values used are two-sided, and values
,0.05 were regarded as statistically significant.
Results
Baseline characteristics (Table 1)
Table 1 shows the baseline characteristics of the subjects. The
mean age of the subjects was 38.3 years and 84.2% of subjects
Table 1 Baseline characteristics of the cohort (n = 8436)
Characteristics
Age (years)
BMIa (kg/m2)
Mean (range)
38.3 (25–50)
22.6 (13.3–32.3)
% overweight (ù25)
Alcohol (g/week)
Smoking (pack-years)
Physical activity(frequency/week)
ASTa(U/L)
15.8
131.7 (0–900)
13.7 (0–50)
0.9 (0–7)
23.5 (9–150)
Geometric mean
22.2
% elevated AST
ALTa(U/L)
7.8
24.2 (2–331)
Geometric mean
20.1
% elevated ALT
GGTa(U/L)
15.6
16.8 (1–271)
Geometric mean
12.2
% elevated GGT
4.4
a Abbreviations: BMI, body mass index; AST, aspartate aminotransferase;
ALT, alanine aminotransferase; GGT, gamma-glutamyl transferase.
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INTERNATIONAL JOURNAL OF EPIDEMIOLOGY
Table 2 Adjusteda odds ratio (aOR) of prevalence of elevated liver enzyme by body mass index (BMI) and alcohol consumption at baseline
(n = 8436)
ASTb
Variables
BMIb
ALTb
GGTb
Categories
n
aOR
–19.9
1168
1.0
20–21.9
2333
1.7
(1.1–2.5)
1.8
(1.3–2.4)
1.7
22–24.9
3598
2.9
(2.0–4.1)
5.0
(3.7–6.8)
4.5
(2.3–8.5)
25–
1337
7.2
(4.9–10.4)
14.2
(10.4–19.4)
12.6
(6.6–24.1)
Alcohol (g/week)
95% CI
aOR
95% CI
1.0
aOR
95% CI
1.0
1.0
(0.8–3.5)
0
1507
1.0
1–180
5590
1.1
(0.9–1.4)
0.9
(0.8–1.1)
1.0
2.1
181–360
1087
1.1
(0.8–1.5)
0.7
(0.6–0.9)
3.1
(2.0–4.9)
361–
252
1.3
(0.8–2.1)
0.8
(0.5–1.1)
5.9
(3.5–10.0)
(1.4–3.1)
a Adjusted for baseline age, cigarette smoking, exercise.
b Abbreviations: AST, aspartate aminotransferase; ALT, alanine aminotransferase; GGT, gamma-glutamyl transferase.
were within the normal range of BMI. The prevalence of
elevated liver enzyme at baseline was 7.8% in AST, 15.6% in
ALT, and 4.4% in GGT.
GGT were as follows: 2.1 (95% CI : 1.4–3.1) for light drinkers,
3.1 (95% CI : 2.0–4.9) for moderate drinkers, 5.9 (95% CI :
3.5–10.0) for heavy drinkers.
Cross-sectional analyses (Table 2)
Incidence analyses (Table 3)
The prevalence of elevated liver enzyme showed clear doseresponse relationships with BMI in 1994 for all three liver
enzymes. Compared with those with BMI ,20, the adjusted odds
ratios for BMI 20–21.9, 22–24.9, 25 or more were as follows:
1.7 (95% confidence interval [CI] : 1.1–2.5), 2.9 (95% CI :
2.0–4.1), 7.1 (95% CI : 4.9–10.4) in AST, respectively; 1.8
(95% CI : 1.3–2.4), 5.0 (95% CI : 3.7–6.8), 14.2 (95% CI :
10.4–19.4) in ALT, respectively; and 1.7 (95% CI : 0.8–3.5),
4.5 (95% CI : 2.3–8.5), 12.6 (95% CI : 6.6–24.1) in GGT,
respectively. GGT also showed a dose-response relationship
with the amount of alcohol consumption, however, AST and
ALT showed little or no statistically significant relationship. In
comparison with non-drinkers, the adjusted odds ratios in
During the follow-up periods 4.3%, 14.1% and 2.6% of the
subjects developed abnormal liver enzyme levels of AST, ALT
and GGT, respectively. The risk of developing both abnormal
AST and abnormal ALT values increased with baseline BMI
and the increase BMI. The magnitude of the effect of the
change in body weight was much larger than that of baseline body weight. Compared with subjects with BMI ,20,
the adjusted odds ratios for men with baseline BMI 20–21.9,
22–24.9, 25– were as follows: 1.2 (95% CI : 0.8–1.8), 1.6 (95% CI :
1.1–2.4), 1.7 (95% CI : 1.0–2.8) in AST, respectively; 1.4 (95% CI :
1.0–1.9), 2.4 (95% CI : 1.8–3.2), 2.8 (95% CI : 2.0–4.0) in ALT,
respectively. Compared with the weight losers or maintainers,
the adjusted odds ratios for slight weight gainers, moderate
Table 3 Adjusteda odds ratios (aOR) of incidence of elevated liver enzyme by baseline body mass index (BMI), BMI change, baseline alcohol
consumption, and change in alcohol consumption (n = 6846)
ASTb
Variables
Baseline BMI
BMI change
Baseline alcohol (g/week)
Alcohol change (g/week)
ALTb
GGTb
Categories
n
aOR
–19.9
1067
1.0
20–21.9
2083
1.2
(0.8–1.8)
1.4
(1.0–1.9)
0.8
(0.4–1.7)
22–24.9
2882
1.6
(1.1–2.4)
2.4
(1.8–3.2)
1.2
(0.6–2.4)
25–
814
1.7
(1.0–2.8)
2.8
(2.0–4.0)
0.8
(0.4–1.8)
<0
2518
1.0
0.1–1.0
2194
1.7
(1.2–2.5)
2.4
(2.0–2.9)
2.4
1.1–2.0
1597
2.6
(1.9–3.7)
3.9
(3.2–4.9)
4.4
(2.7–7.1)
2.1–
537
6.8
(4.6–10.0)
11.3
(8.6–14.8)
8.5
(4.6–15.7)
95% CI
aOR
95% CI
1.0
aOR
95% CI
1.0
1.0
1.0
1.0
(1.5–3.9)
0
1258
1.0
1–180
4544
1.1
(0.8–1.6)
1.0
(0.8–1.3)
1.0
1.8
181–360
852
1.5
(0.9–2.4)
1.2
(0.8–1.6)
2.1
(0.9–4.8)
361–
192
1.7
(0.8–3.4)
1.3
(0.8–2.1)
5.8
(2.3–14.7)
1.0
(0.9–3.7)
0
2204
1.0
,0
2772
0.8
(0.6–1.1)
1.1
(0.9–1.3)
0.6
(0.4–1.0)
1–90
1213
0.8
(0.6–1.2)
1.0
(0.8–1.2)
1.2
(0.7–2.0)
91–
657
1.2
(0.8–1.8)
0.9
(0.7–1.1)
1.5
(0.9–2.5)
a Adjusted for baseline age, cigarette smoking, exercise, AST or ALT or GGT (baseline for the dependent variable).
b Abbreviations: AST, aspartate aminotransferase; ALT, alanine aminotransferase; GGT, gamma-glutamyl transferase.
1.0
BODY WEIGHT, ALCOHOL AND LIVER ENZYMES
weight gainers, and heavy weight gainers were as follows: 1.7
(95% CI : 1.2–2.5), 2.6 (95% CI : 1.9–3.7), 6.8 (95% CI : 4.6–10.0)
in AST, respectively; 2.4 (95% CI : 2.0–2.9), 3.9 (95% CI :
3.2–4.9), 11.3 (95% CI : 8.6–14.8) in ALT, respectively. However, baseline alcohol consumption and the change of alcohol
consumption did not show any notable relationship with either
AST or ALT, even though there was a slight relationship with
baseline alcohol consumption.
GGT showed a marked difference from both AST and ALT with
regard to alcohol consumption and/or BMI. There were clear
dose-response relationships with BMI changes and baseline
alcohol consumption, but not baseline BMI and the changes
of alcohol consumption, even though the changes of alcohol
consumption affected slightly the incidence of abnormal GGT.
Compared with weight losers or maintainers, the adjusted
odds ratios for slight weight gainers, moderate weight gainers,
and heavy weight gainers were 2.4 (95% CI : 1.5–3.9), 4.4
(95% CI : 2.7–7.1) and 8.5 (95% CI : 4.6–15.7), respectively. In
comparison with non-drinkers, the adjusted odds ratios were
1.8 (95% CI : 0.9–3.7) for light drinkers, 2.1 (95% CI : 0.9–4.8)
for moderate drinkers, and 5.8 (95% CI : 2.3–14.7) for heavy
drinkers.
Discussion
We explored the relationships between BMI and alcohol
consumption, and the prevalence and/or incidence of abnormal
serum liver enzyme activity in both cross-sectional and prospective designs. First, serum activity of both AST and ALT showed
strong dose-response relationships with body weight rather
than with alcohol consumption. In particular, the association of
enzymes with BMI changes was much stronger than that with
baseline BMI. Regarding alcohol consumption, there was only
a weak relationship with baseline alcohol consumption and
no relationship with the changes of alcohol consumption. A
second major finding was that serum GGT activity was related
to both the baseline amount of alcohol consumed and the
changes of body weight, while there were only weak or no
relationships with the changes of alcohol consumption and the
baseline BMI.
Several cross-sectional and clinical studies5–8 have shown
consistently that the increased serum activity of various liver
enzymes is related to overweight or obesity. The results of a few
prospective studies10,12,14–16 also confirmed this association.
However, earlier studies usually focused on moderate or severe
obesity with BMI .25. In this prospective study, higher levels
of adiposity as assessed by baseline BMI and BMI change
were monotonically related to an increase in the incidence
of elevated serum liver enzymes, especially AST and ALT, even
though most of our subjects had a BMI within the normal
range. Our study allows a more precise quantification of the
dose-response relationship than has been possible previously
due to the large sample size. Also, we explored the association
of baseline BMI and BMI change simultaneously and showed
that the effect of BMI change was a more important factor in
developing abnormal liver enzymes than was baseline BMI. To
our knowledge, this is the first study to report these findings.
Among our subjects, those with higher baseline BMI tended
to experience an increase in body weight less than those
with lower baseline BMI. Hence, one of these factors should be
769
considered as a confounder when interpreting associations with
the other. Although Bruns et al.10 assessed the effect of body
weight change, they did not consider these two covariates concurrently as possible confounders.
Among liver enzymes, the serum activities of ALT were more
clearly related to BMI than were the other enzymes. These
findings were similar to those observed in other studies.7,9,10
On the basis of such observations, Wejstal et al.17 suggested that
ALT values should be corrected for body weight, especially when
ALT measurements are used as a surrogate test in screening
for non-A, non-B hepatitis. According to another study,18 AST
values also should be corrected for body weight because in various animal species, ranging from mice to cattle, the expected
enzymatic activity can be expressed as a function of a power of
the weight.
AST and ALT had a surprisingly weak or non-existent relationship with alcohol consumption in both the cross-sectional and
longitudinal analyses in our study; although the relationship
between alcohol consumption and GGT was clear, as expected.
The studies9,10,19 from western countries reported that the
magnitude of the effect of alcohol consumption was similar to,
or slightly smaller than, that of obesity. This could be because
the total alcohol consumption in our subjects might have been
lower than in other studies. Alternatively, Asians may be less
sensitive to alcohol than Caucasians. Studies3,4 from Japan also
reported that alcohol consumption was not significantly related
to ALT or AST.
The Serum GGT level showed a strong relationship only
with BMI change, but not baseline BMI. The importance of BMI
change means that the effects of adiposity might be temporary.
A 7-year longitudinal population study from Norway also showed
that the change in BMI was the single strongest determinant of
change in GGT.12 Our study suggested that liver enzymes could
be influenced by a slight weight change even within normal range.
One of the most interesting findings of this study was that
GGT showed a relationship only with baseline alcohol consumption, not change in alcohol consumption, the opposite finding
to the relationship observed for BMI. As far as we know, though,
there has been no previous study exploring the relationships
between both baseline and the changes of alcohol consumption,
and liver enzyme concurrently, the results of some studies support our finding. As a screening test for alcoholism and alcohol
abuse, the sensitivity of GGT has been considered to be acceptable, but its specificity is poor.20 In contrast to this, GGT has
been found to have reasonable specificity but low sensitivity
to changes in alcohol consumption.21 The Tromsø study12 in
Norway also reported a strong relationship between alcohol consumption and GGT in a cross-sectional setting, but a surprisingly
weak association between the changes of alcohol consumption
and the changes of GGT in longitudinal analyses. They interpreted
this as reflecting the imprecision of their alcohol questions,
which may have introduced random measurement errors that
obscured the true changes in alcohol consumption. However,
our result suggested that it could be a real association. Some
investigators22,23 have suggested that elevated GGT activity in
drinkers is probably related more closely to the biological effects
of alcohol than to the amount of alcohol consumption.
In conclusion, these data indicate that body weight rather than
alcohol consumption may be the major factor in determining
the level of liver enzyme, though some ethnic differences may
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INTERNATIONAL JOURNAL OF EPIDEMIOLOGY
need to be taken into consideration. In particular, even slight or
moderate gains in weight, and levels of body weight not generally
considered to be overweight, were associated with increases of
liver enzyme. With regard to the alcohol consumption, further
study is needed to clarify the reason for the small effect of
changes in alcohol consumption on GGT.
KEY MESSAGES
•
The risk for elevated both aspartate aminotransferase (AST) and alanine aminotransferase (ALT) values increased
with the baseline BMI and BMI changes, but not with alcohol consumption.
•
Gamma-glutamyl transferase (GGT) was associated with BMI changes and baseline alcohol consumption, not
with baseline BMI and changes in alcohol consumption.
•
Body weight, rather than alcohol consumption, may be the major factor in determining the serum level of liver
enzymes.
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