Vol. 24, No.

0145-6008/00/2401-0072$0300/0
ALCOHOL
ISM CLINICAL
AND EXPERIMFNI
A I RESEARCII

January 2000

Alcohol Consumption, Alcohol Dependence, and

All-Cause Mortality
Deborah A. Dawson

Background:This study examined the effects of alcohol consumption and DSM-IV alcohol dependence
on the risk of mortality.
Methods: Data from the 1988 National Health Interview Survey Alcohol Supplement were matched to
the National Death Index for the years 1988 to 1995 (baseline n = 37,682 U.S. adults age 2 2 5 linked to
3,586 deaths). All mortality analyses were based on proportional hazards models that adjusted for age, sex,
raceiethnicity, marital status, education, income, labor force status, body mass index, smoking status, and
poor health indicators at baseline.
Results: When dependence was not considered and all past-year abstainers were used as the reference
group, both light and moderate drinkers exhibited a reduced risk of mortality, with hazards ratios of 0.76
(0.68-0.84) and 0.84 (0.74-0.96). Heavy drinkers had about the same risk of dying as did past-year
abstainers, and very heavy drinkers had an increased risk that was not significant (OR = 1.17, CI =
0.93-1.47). When lifetime abstainers were used as the reference category, the protective effect of moderate
drinking fell short of significance, and there were nearly significant increased risks among former drinkers
and vety heavy drinkers. When dependence was considered, light and moderate drinkers without dependencc had a reduced mortality risk regardless of reference group, and there was no significant effect among
heavy or very heavy drinkers without dependence. Among dependent drinkers, there was no protective
effect of light or moderate drinking, and very heavy drinkers had a significantly increased risk (OR = 1.56
relative to past-year abstainers and 1.65 relative to lifetime abstainers).
Conclusions: Because alcohol dependence nullifies the protective effect of light and moderate drinking,
it is important to understand its role as an independent risk factor for mortality. Differences between
dependent and nondependent drinkers who drank comparable amounts suggest that this risk may result
from longer and heavier drinking histories before baseline, more severe health problems at baseline, more
heavy episodic drinking, and, possibly, differences in beverage preference.
Key Words: Mortality, Consumption, Dependence, Alcoholism.

H E ASSOCIATION BETWEEN alcohol consumption

and all-cause mortality has been studied extensively.
Although the findings of past research have been inconsistent, the bulk of studies have found a J-shaped curve (see
reviews in Anderson 1994; Poikolainen, 1995.) That is,
relative to abstainers, light to moderate drinkers have demonstrated a reduced risk of mortality whereas heavy drinkers have demonstrated an increased risk of mortality. Recent literature supporting a J-shaped curve between alcohol
consumption and all-cause mortality includes studies conducted in a number of countries. Yuan et al. (1997), who
followed 18,244 Chinese men age 45 to 64 years for 6 years,
found a significant reduction in mortality at a consumption
level of 1 to 14 drinks per week, a nonsignificant reduction

From the Division of Biometry and Epidemiology, National Institute on

Alcohol Abuse & Alcoholism, National Institutes of Health, Bethesda,
Maryland.
Received for publication March 31, 1999; accepted October 20, 1999.
Reprint requests: Deborah A. Dawson, Ph. D., NIAAAIDBE, W i k o Bldg.,
Suite 514, 6000 Executive Blvd. MSC 7003, Bethesda, MD 20892-7003; Fax:
301-443-8614; E-mail: ddawson@willco.niaaa.nih.gov
Copyright 0 2000 by the Research SocieQ on Alcoholism.
72

at 15 to 28 drinks per week, and an increase in risk at more

than 28 drinks per week (all relative to lifetime abstainers).
In the Copenhagen city heart study, which followed 13,285
Danish men and women between the ages of 30 and 79 for
10 to 12 years, GronbEk et al. (1994) found that individuals
consuming 1 to 6 drinks per week had the lowest mortality
levels, with significantly increased risks among baseline
abstainers and those consuming more than 42 drinks per
week. A sample of 12,321 British male physicians who were
followed for 13 years indicated that the lowest mortality
rates occurred among those consuming 8 to 14 standard
drink units per week and that mortality among those consuming 1 to 14 units per week was significantly lower than
mortality among baseline abstainers (Doll et al., 1994). A
French sample of 34,014 middle-aged men followed for an
average of 9.3 years similarly reported the lowest mortality
rates among those consuming 22 to 54 g of ethanol (roughly
1-2.5 drinks) per day (Renaud et al., 1998).
Other recent studies have reported nonsignificant
J-shaped mortality curves. In a registry-based sample of
9,057 Swedish adult twins followed from 1975 to 1992
(Andreasson and Brandt, 1997), the lowest mortality rates
Alcohol Clin Exp Re,, Vol 24, No 1, 2000. pp 72-81

73

ALCOHOL CONSUMPTION, DEPENDENCE, AND ALL-CAUSE MORTALITY

were among those consuming 1 to 250 g (1-11 drinks) per

month; however, the increased risk of death among abstainers (OR = 1.2) was not significant. Two other recent small
prospective studies have reported similar findings of a nonsignificant J-shaped curve (Cullen et al., 1993; Keil et al.,
1997), and a Dutch study that examined frequency but not
quantity of drinking reported a nonsignificant reduction in
risk among occasional, frequent, and daily drinkers compared to nondrinkers (Berberian et al., 1994). Studies such
as these neither support nor contradict the J-shaped curve
at the individual study level; however, they contribute to
the significant J-shaped curve that has resulted when data
are combined across surveys in meta-analyses (Duffy, 1995:
Holman et al., 1996). When Holman et al. reanalyzed 16
studies of mostly European populations, they found that
relative to abstainers, men drinking <3.0 and women drinking <2.0 standard drinks per day had lower risks of allcause mortality.
Studies of U.S. mortality have been mixed in support of
the J-shaped curve. Studies that have confirmed this pattern of association include the American Cancer Society
Prospective Study (Boffetta and Garfinkel, 1990; Thun et
al., 1997), the Kaiser Permanente Study (Klatsky et al.,
1992), the US. Physicians Health Study (Camargo et al.,
1997), and the Honolulu Heart Study (Chyou et al., 1997;
Kagan et al., 1981); however, the Framingham and Albany
studies (Gordon and Doyle, 1987 ; Gordon and Kannel,
1983) failed to find any significant relationship between
alcohol and all-cause mortality. In recent meta-analyses of
primarily U.S. data sets, a nonsignificant J-shaped curve
was found among women, but among men, the odds ratios
were lower for abstainers than light drinkers-significantly
so in youth samples and nonsignificantly so in adult samples
(Fillmore et al., 1998; Leino et al., 1998). Although none of
the follow-up studies of the National Health and Nutrition
Examination Survey have found a significant J-shaped association for the adult population as a whole (Davis et al.,
1994; Rehm and Sempos, 1995), Serdula et al. (1995) did
find a weak but significant J-shaped curve among adults 40
years of age and older at baseline. In addition, Rehm and
Sempos (1995) found a nonsignificant U-shaped association among men and women age 60 years and older at
baseline, and Davis et al. found a nonsignificant J-shaped
association among men age 45 to 64 and women age 45 to
54.
Far less is known about alcohol dependence as a risk
factor for all-cause mortality, despite many studies that
have examined mortality patterns and risk factors among
alcoholics (e.g., Bunn et al., 1994; Callahan and Tierney,
1995; Hampl and Hajin, 1992; Langle et al., 1993; Lewis et
al., 1995; Spinatsch, 1992; Wells and Walker, 1990) and the
proportion of deaths attributable to alcohol use disorders
(e.g.,Romelsjo et al., 1993). Most of the prospective studies
that have compared mortality rates among alcoholics and
nonalcoholics have been based on medical samples. For
example, in a recent study of 649 patients with head and

neck cancers, both alcoholism and a history of alcoholrelated systemic conditions were positively associated with
the risk of dying (Deleyiannis et al., 1996), and a study of
patients receiving inpatient treatment for alcohol problems
found that they were almost 10 times as likely to have died
over a 10 year follow up period as were matched community controls (Finney and Moos, 1991). In a rare study using
a representative population sample of Norwegian military
conscripts followed for 40 years, Rossow and Amundsen
(1 997) found that alcohol abusers had an excess mortality
risk of 3.3 compared to nonabusers.
No study to date has evaluated the independent effects
of both alcohol dependence and volume of ethanol intake
as predictors of all-cause mortality. Thus, the existing literature does not indicate the extent to which the increase in
mortality risk among heavy drinkers is based on the experience of dependent drinkers- drinkers whose risk of dying
may be affected by deleterious drinking patterns and comorbid mental and physical conditions that augment the
simple effects of their volume of consumption. This paper
represents an attempt to bridge these two branches of
mortality research. In this study I examined deaths over a
7.5 year follow-up period among a representative sample of
U.S. adults interviewed in 1988 as part of the US. National
Health Interview Survey, using both volume of ethanol
intake and alcohol dependence as predictors of the risk of
dying. Additionally, I controlled for a variety of preexisting
conditions that might bias estimates of the association between alcohol consumption and mortality; evaluated the
effects of using lifetime as opposed to baseline abstainers as
the reference group for the mortality estimates; examined
the effects of prior intake level among former drinkers; and
incorporated data on -episodic heavy drinking to obtain
better estimates of volume of intake than can be derived
solely from questions on usual frequency and quantity of
intake. Finally, I examined factors beyond volume of consumption that may account for any residual difference in
mortality risk between dependent and nondependent
drinkers. These include length of drinking history, consumption during period of heaviest drinking, episodic
heavy drinking, beverage preference, and degree of health
impairment at baseline.
METHODS
Sample

For this analysis, data from the 1988 National Health Interview Survey
(NHIS) were linked with death records for the period 1988 to 1995 (the
most recent year available) to examine the associations between alcohol
consumption and mortality risk. The 1988 NHIS was based on a nationally
representative sample of the household population residing in the contiguous United States. Within each sample household, a randomly chosen
adult 18 years of age or over was selected to respond a variety of supplemental questionnaires that were attached to the basic 1988 NHIS. These
included one supplement devoted to alcohol and another that obtained
smoking history. A total of 43,763 adults 18 years of age and over responded to both of these supplemental surveys, 86% of those who were
eligible.

74

Linkage with death records was performed by the National Center for
Health Statistics, based on identifiers collected at the time of the NHIS
interview, such as the respondents social security number (SSN), date of
birth, and so forth. These identifiers were combined in various ways to
produce 12 alternative criteria for selecting a possible match with a death
record, for example, (1) SSN plus first name both match, (2) SSN plus last
name both match, (3) month and year of birth and first and last names all
match, and so forth. All cases that met even 1of the 12 criteria for a match
were assigned to one of five classes, ordered by the certainty of the match.
In the first class, where there were matches on SSN, first, middle, and last
names, sex, state of birth, and month and year of birth (i.e., on all
matching data), every match was considered to be a true match, that is, an
actual death. In the fifth class, where the SSN was known but did not
match, all matches were considered to be false matches. In the intervening
three classes, a score was devised to represent the probability of a true
match. This score was a weighted function of the 12 matching criteria, with
positive weights used for criteria that were met and negative weights for
criteria that were not met. A cutoff level was then selected within each
class to maximize the proportion of records correctly classified and minimize the number of records incorrectly classified. Using two large national population surveys where longitudinal follow-up provided an indcpendent ascertainment of vital status (i.e., of whether the respondent was
dead or alive at the end of the follow-up period), this matching procedure
yielded accurate matches for 94% of female respondents and 97% of male
respondents (National Center for Health Statistics, 1997).
When the NHIS sample was matched with death records for 1988 to
1995, approximately one third of all potential matches fell below the
required cutoff and were treated as nondeaths. Cases with insufficient
linkage data were removed from the sample, leaving a total of 42,910 cases
with linked alcohol, smoking, and mortality data. These cases were reweighted to match the original 1988 NHIS poststratification estimates of
the adult population by age, sex, and race (Massey et al., 1989).
This analysis was restricted to the 37,682 cases where the respondents
were 25 years of age or older at baseline. Younger respondents, many of
whom were below the legal drinking age when originally interviewed, were
excluded from the analysis to minimize the possibility that baseline drinking habits would differ substantially from those over the follow-up period
and to facilitate comparisons with other surveys of adult samples. The
total number of deaths among the analytical sample was 3,586, or 9.5% of
all cases. This corresponds to a weighted mortality estimate of 8.3%, with
the differential reflecting the oversampling of Blacks, whose mortality
rates were higher than those of non-Blacks.
Measures
The 1988 NHIS collected detailed information on alcohol intake from
individuals who were classified as past-year drinkers. These were individuals who in screening reported having had at least 12 alcohol drinks in the
year preceding interview. Other categories of drinkers defined by the
screening questions were lifetime abstainers (drank less than 12 drinks in
their lives), lifetime infrequent drinkers (drank 12 or more drinks in their
lives but never drank 12 or more drinks in any one year), and former
drinkers (drank 12 or more drinks in at least 1 year, but not the year
preceding interview). In this analysis, lifetime abstainers were assumed to
have consumed no drinks in the year preceding interview. Lifetime infrequent drinkers and former drinkers were asked how many drinks they had
consumed in the preceding year (range = 0-11). This number was converted to an average daily ethanol intake by assuming a standard drink size
of 0.54 oz of ethanol (the mean drink size reported by this sample) and
dividing by 365.
Past-year drinkers were asked how often they usually drank (no time
reference period specified, recorded in exact number of days per week,
month, or year) and how many drinks they usually consumed on those
days. They also were asked whether they had consumed any alcohol in the
2 weeks preceding the interview and the date of their last drink. For a 2
week reference period (either the 2 weeks preceding interview or the most
recent 2 weeks in which a drink was consumed), they were asked number

DAWSON

of drinking days, usual quantity of drinks per drinking day, and usual drink
size in separate series of questions for beer, wine, and liquor. Based on
these data, usual volume of intake was ascertained in one of three ways:
(1) For individuals who provided detailed 2 week data and whose lasr
drink occurred during the 2 wceks immediately preceding the interview
(80.8% of all past-year drinkers), annual volume of ethanol intake was
calculated as the product of annualized frequency (26 times the 2 week
frequency) times quantity of drinks per drinking day times drink size in
ounces times an ethanol conversion factor of 0.045 for beer, 0.121 for
wine, and 0.409 for liquor (DISCUS, 1985; Kling, 1989; Modern Brewery
Age, 19Y2; Turner, 1990; Williams et al., 1993). These volumes were
summed across beverage type and divided by 365 to yield average daily
ethanol intake. Because interviewing was conducted continuously
throughout the year, the estimation of annual intake from a 2 week
reference period should not entail any seasonal bias.
(2) For the 1.5% of past-year drinkers who had missing data for the 2
week reference period but did provide usual frequency and quantity of
drinks (no time reference period specified), average daily ethanol intake
was estimated as the product of this annualized frequency and quantity
(assuming 0.54 oz of ethanol per drink), divided by 365.
(3) For the 17.7% of past-year drinkers who provided detailed 2 week
data but whose most recent drink was not consumed during the 2 weeks
immediately preceding the interview, multiplying the 2 week consumption
levels times 26 would have overestimated of annual frequency of drinking.
Moreover, the date of last drink was missing for more than two thirds of
these individuals. After comparing the results of various ways to estimate
annual intake volume for these drinkers, I decided to multiply their 2 week
consumption times 13 to obtain annual frequency, which was multiplied,
as in (I), by number of drinks, drink size, and the appropriate ethanol
conversion factor and then summed across beverages. In essence, these
individuals were assumed to drink half as frequently as those whose last
drink had been consumed in the 2 weeks preceding the interview. This
resulted in a volume of at least 13 drinks in the past year, which ensured
that they met the threshold of >12 drinks required to be defined as a
past-year drinker. When this approach was compared to the alternative of
constructing an estimate based on usual frequency and quantity of drinking, as in method 2, the cases were evenly divided in terms of which
approach yielded the highest volume estimate. The median value of the
ratio of the estimates yielded by these two approaches was 1.01.
Past-year drinkers also were asked the past-year frequencies of consuming 2 5 and 2 9 drinks on a single day (with the difference between the
two representing the frequency of drinking 5-8 drinks). If one of these two
frequencies was missing, it was imputed on the basis of the other nonmissing frequency. If both were missing, they were imputed on the basis of
average daily ethanol intake. Consumption on these heavy drinking days
was incorporated into an adjusted estimate of average daily ethanol intake
by replacing the unadjusted average daily intake with an intake of 3.24 oz
(6 standard drinks) on days of consuming 5 to 8 drinks and an intake of
6.48 oz (12 standard drinks) on days of consuming 2 9 drinks and then
recalculating the daily average. (If this reduced average daily intake, the
original value was retained.) This adjusted average daily ethanol intake
formed the basis for the categories of past-year consumption that were
used in this analysis:
Both current and former drinkers were asked frequency of drinking and
usual quantity of drinks consumed during their period of heaviest drinking. Again assuming a standard drink size of 0.54 oz ethanol, these
variables were multiplied together to estimate average daily ethanol intake
during the period of heaviest consumption. This intake was categorized by
using the same categories and definitions as listed previously for past-year
consumption, to describe the drinking categories of former drinkers.
Alcohol dependence was classified in accordance with the DSM-IV
criteria (American Psychiatric Association, 1994) and was measured using
a set of 17 symptom item indicators taken from a larger list of 41
alcohol-related problems. (Although the list of indicators was designed
before the publication of the DSM-IV criteria, it contained items that
were sufficient to generate DSM-IV diagnoses.) To be classified with
alcohol dependence, an individual had to meet three or more of the seven

ALCOHOL CONSUMPTION, DEPENDENCE, AND ALL-CAUSE MORTALITY

75

Table 1. Number and Characteristicsof Adults Age 25 and Older, By Drinking Status at Baseline

Number of

cases at
baseline
Total
Past-year abstainers
Lifetime abstainers
Lifetime infrequent drinkers
Former drinkersa
Light/moderateb
Heavyhery heavyb
Past-year drinkers
Lightd
Moderated
Heavy*
Very heavyd

37,682
19,102
7,148
4,579
7,375
4,999
1,335
18,580
9,557
6,422
1,402
1,086

Distribution
of cases at
baseline

100.0 (0.0)
49.5 (0.4)
17.8 (0.3)
11.8 (0.2)
19.9 (0.3)
15.5 (0.2)
4.4 (0.1)
50.5 (0.4)
26.0 (0.3)
17.6 (0.3)
3.9 (0.1)
3.0 (0.1)

Average daily ethanol

intake during year
preceding baseline
0.32 (0.1)
<0.01 (<0.01)
0.00 (0.00)
<0.01 (<0.01)
<0.01 (<0.01)
<0.01 (<0.01)
10.01 (<0.01)
0.63 (0.01)
0.10 (<0.01)
0.60 (<0.01)
1.67 (0.01)
4.04 (0.09)

% With

alcohol

% Dying

dependence in

in follow-

year preceding
baseline

interval

4.6 (0.1)
0.0 (0.0)
0.0 (0.0)
0.0 (0.0)
0.0 (0.0)
0.0 (0.0)
0.0 (0.0)
9.1 (0.3)
2.4 (0.2)
10.2 (0.4)
24.4 (1.4)
42.4 (1.6)

8.3 (0.2)
11.3 (0.2)
11.5 (0.4)
9.4 (0.5)
12.2 (0.4)
10.7 (0.5)
13.5 (1.0)
5.5 (0.2)
4.8 (0.2)
5.3 (0.3)
6.3 (0.7)
10.0 (1.O)

UP

~~

Note: Figures in parentheses are standard errors of estimates.

a Including those with unknown volume of consumption during period of heaviest drinking.

Based on intake level during period of heaviest drinking.

Including those with unknown volume of consumption during year preceding baseline interview.
Based on intake level during year preceding baseline interview.
DSM-IV criteria for dependence: ( I ) tolerance: (2) withdrawal (including
relief or avoidance of withdrawal); (3) persistent desire or unsuccessful
attempts to cut down on or stop drinking; (4) much time spent drinking,
obtaining alcohol, or recovering from its effects; ( 5 ) reduction or cessation
of important activities in favor of drinking; (6) impaired control over
drinking; and (7) continued use despite physical or psychological problems
caused by drinking. Criteria not associated with duration qualifiers were
considered to be satisfied if an individual reported one or more positive
symptoms of the criterion during the past year. Criteria with duration
qualifiers were considered to be satisfied if a person reported two or more
symptoms during the past year or one symptom that occurred at least two
times during the past year. To be consistent with the syndromal definition
of the withdrawal criterion, two or more positive symptoms were required
in addition to satisfaction of the duration qualifier.
I constructed a dichotomous measure of poor health at baseline to
control for the potentially confounding effect of health-related selectivity
into the categories of lifetime abstainers and former drinkers. The latter
was coded positively if the respondent reported any of six preexisting
major health problems (heart disease, arteriosclerosis, hypertension, diabetes, liver disease, or cancer), major limitations of activity, or selfperceived fair or poor health status. The health problems were ascertained
by the question, Tell me whether or not you have ever had any of the
following conditions and did not stipulate whether the condition was
diagnosed by a doctor. Individuals were coded as having a major limitation
of activity if they were unable to perform their main activity (e.g., work,
housework, school attendance) because of an impairment or health problem. The response options for the question on health status (Would you
say your health in general is . . .) were excellent, very good, good, fair, or
poor.

Analysis
The 1988 NHIS used a complex, multistage sampling design (Massey et
al., 1989) that featured selection of primary sampling units with probability
proportional to size and oversampling of the Black population. To account
for these design features in estimating confidence intervals for the hazards
ratios and descriptive statistics, I generated all of the results presented in
this paper using SUDAAN software (Shah et al., 1997), which uses
Taylor-series linearization techniques to adjust variance estimates for
complex sample design characteristics.
Mortality hazard rate ratios (HRRs) were derived from multivariate
proportional hazards models assuming discrete time intervals. Intervals
were measured in months between the date of interview (estimated from
the processing quarter and week) and either the date of death (taken from
the death certificate) or December 1995, the end of the linkage period and

the date by which nondeaths were considered to be censored from further

observation. All models controlled for the following characteristics measured at baseline: age, sex, raceiethnicity (Black and Hispanic, each versus
White), marital status (married and formerly married, each versus never
married), educational attainment (high school graduate and college graduate, each versus non-high school graduate), income, labor force participation, body mass index (<21 and 235, each versus 21-34.9), smoking
status (current and former, each versus never), and a dichotomous measure of poor health at baseline.

RESULTS

Data collected in the 1988 NHIS revealed that half

(49.5%) of adults 25 years of age and over were past-year
abstainers who had consumed fewer than 12 drinks in the
year preceding the interview (Table 1). These included
17.8% who were lifetime abstainers (i.e., who had consumed fewer than 12 drinks in their lifetimes), 11.8% who
were lifetime infrequent drinkers (i.e., who had never consumed 2-12 drinks in any one year), and 19.9% who were
former drinkers. Former drinkers were subdivided into
those who had been light or moderate drinkers during their
period of heaviest drinking (15.5%) and those who had
been heavy or very heavy drinkers (4.4%). The remaining
half (50.5%) were past-year drinkers who had consumed at
least 12 drinks in the preceding year, including 26.0% light
drinkers, 17.6% moderate drinkers, 3.9% heavy drinkers,
and 3.0% very heavy drinkers.
Past-year abstainers had an average daily ethanol intake
of (0.01 oz for the year preceding the interview. (For
lifetime abstainers, past-year consumption was assumed to
be zero; lifetime infrequent drinkers and former drinkers
reported an average of two to three drinks per year.)
Among past-year drinkers, the average daily ethanol intake
for the year preceding interview varied from 0.10 oz. (one
or two drinks per week) among light drinkers to 4.04 (seven
to eight drinks per day) among very heavy drinkers. Pastyear abstainers were not asked the symptom item indicators
for past-year alcohol dependence; all were assumed to be

DAWSON

76

Table 2. Adjusteda Mortality Hazard Rate Ratios (HRRs) for Adults Age 25 and
Older by Drinking Status at Baseline

Past year abstainers

Lifetime abstainers
Lifetime infrequent drinkers
Former drinkers
Lightlmoderate
Heavyhery heavyb
Past-year drinkers
Light
ModerateC
HeavyC
Very heavyC

Table 3. Adjusted Mortality Hazard Rate Ratios (HRRs) for Adults Age 25 and
Older By Drinking Status and DSM-IV Alcohol Dependence at Baseline

Model 1

Model 2

Model 1

Model 2

HRR 95% CI

HRR 95% CI

HRR 95% CI

HRR 95% CI

1.OO (Reference)

1.OO (Reference)

0.93 (0.82 -1.06)

1.09 (0.97 -1.24)

1.I 8 (0.99 -1.42)

0.76 (0.68 -0.84)

0.84 (0.74 -0.96)
0.94 (0.73 -1.19)
1.I7 (0.93 -1.47)

0.78 (0.69 -0.89)

0.88 (0.76 -1.01)
0.98 (0.76 -1.26)
1.23 (0.96 -1.56)

a Adjusted for age, sex, racekthnicity, marital status, education, income, labor
force participation, body mass index, and smoking status.
Based on intake during period of heaviest drinking.
Based on intake during year preceding baseline interview.

negative for dependence during that time period. Among

past-year drinkers, the proportions classified with dependence rose from 2.4% of light drinkers to 42.4% of very
heavy drinkers.
The proportions of individuals dying between 1988 and
1995 were highest for past-year abstainers (11.3%). Among
these, former drinkers were the most likely to have died
(12.2%), especially those who had been heavy or very heavy
drinkers (13.5%), whereas lifetime infrequent drinkers
were the least likely to have died (9.4%). Past-year very
heavy drinkers also were among those with the highest
mortality levels, with 10.0% having died. There were few
significant differences in the proportions dying among
these groups. However, all exhibited higher levels of mortality than did light to heavy past-year drinkers. Among
these, the proportions dying varied from 4.8% of the light
drinkers to 6.3% of the heavy drinkers. Thus, the crude
mortality data revealed a U-shaped pattern with respect to
volume of ethanol intake at baseline.
Table 2 presents mortality hazard rate ratios adjusted for
demographic and socioeconomic characteristics, body mass
index, smoking history, and poor health at baseline. The
first model used all past-year abstainers (i.e., lifetime abstainers, lifetime infrequent drinkers and former drinkers)
as the reference category against which the mortality risks
of past-year drinkers were measured. The results of this
model indicated a protective effect of both light drinking
(HRR = 0.76, CI = 0.68-0.84) and moderate drinking
(HRR = 0.84, CI = 0.74-0.96). Heavy drinking did not
significantly affect mortality (HRR = 0.94, CI = 0.731.19). The effect of very heavy drinking suggested a slight
increased risk, but it was not statistically significant
(HRR = 1.17, CI = 0.93-1.47). Thus, even after adjustment for a variety of potential confounders, the adjusted
mortality figures continued to exhibit a U-shaped pattern,
with a suggestion of a J-shaped increase in risk at the
heaviest intake levels.
As indicated in model 2, switching to lifetime abstainers
as the reference group yielded few significant changes in

Past year abstainers

Lifetime abstainers
Lifetime infrequent drinkers
Former drinkers
Light/moderateb
Heavyhery heavyb
Past-year drinkers
Not dependent
LightC
Moderate
Heavy
Very heavy
Dependent
LightC
Moderate
HeavyC
Very heavyC

1.OO (Reference)

1.OO (Reference)
0.93 (0.82 -1.06)

1.09 (0.97 -1.24)

1.I 8 (0.99 -1.42)

0.75 (0.67 -0.84)

0.82 (0.72 -0.94)
0.88 (0.69 -1.12)
1.02 (0.80 -1.30)

0.78 (0.69 -0.88)

0.86 (0.79 -0.93)
0.92 (0.69 -1.23)
1.07 (0.98 -1 .I 7)

1.15 (0.87 -7.52)

I .26 (0.95 -1.67)
1.35 (0.75 -1.92)
1.56 (1.17 -2.08)

1.20 (0.89 -1.61)

1.32 (1.01 -1.72)
1.42 (0.96 -2.10)
1.65 (1.38 -1.98)

a Adjusted for age, sex, race/ethnicity,marital status, education. income, labor

force participation, body mass index, and smoking status.
Based on intake during period of heaviest drinking.
Based on intake during year preceding baseline interview.

these findings. The most important change was that the

protective effect of moderate drinking fell just short of
significance (HRR = 0.88, CI = 0.76-1.01) when compared to lifetime abstention. In addition, former drinkers
demonstrated an increased risk that fell short of significance but showed a clear dose response, varying from 1.09
for former light or moderate drinkers to 1.18 for former
heavy or very heavy drinkers. When all former drinkers
were combined (data not shown), they had a significantly
increased risk of mortality relative to lifetime abstainers
(HRR = 1.21, CI = 1.09-1.35). (This hazard rate ratio
exceeds that for either of the former drinking groups shown
in Table 2 because of the exceptionally high mortality rates
among former drinkers whose level of intake during their
period of heaviest drinking was unknown.)
To examine how alcohol dependence would affect the
mortality risks associated with different consumption levels
(Table 3), a dichotomous measure of past-year dependence
was added to the proportional hazards models. In both
models, dependence exerted a significant positive effect on
the risk of mortality (HRR = 1.53 in model 1 and 1.54 in
model 2, data not shown). Rather than create separate
categorical measures for dependent and nondependent
drinkers at each volume level, I constructed models to test
for interactions between dependence and volume of intake.
Because tests revealed no significant interactions between
the categorical consumption measures and dependence, I
calculated hazard rate ratios for dependent individuals by
exponentiating the sum of the parameters for their respective consumption levels and dependence; those for nondependent individuals were calculated by exponentiating the
parameters for their consumption levels alone. This approach resulted in fewer model parameters and smaller
confidence intervals than would have been obtained with
separate categorical measures of volume for dependent and

77

ALCOHOL CONSUMPTION, DEPENDENCE, AND ALL-CAUSE MORTALITY

Table 4. Characteristics of Past-Year Drinkers Age 25 and Older, by Drinking Status and DSM-IV Alcohol Dependence at Baseline: Standardized for Age and Sex
Light drinkers
Dependent

Heavy drinkers

Very heavy drinkers

Nondependent

Dependent

Moderate drinkers
Nondependent

Dependent Nondependent

Dependent Nondependent

0.10 (<0.01)
50.0 (0.7)
1.9 (<0.1)
0.5 (<0.1)
0.1 ( i O . 1 )
40.9 (0.5)
29.5 (0.5)
29.6 (0.5)

0.67 (0.02)
145.2 (5.9)
3.7 (0.2)
10.9 (0.9)
3.0 (0.5)
54.8 (3.7)
13.9 (1.7)
31.2 (3.3)

0.59 (<0.01)
182.1 (2.0)
2.5 (<0.1)
5.1 (0.2)
0.8 (<0.1)
46.8 (0.7)
23.2 (0.6)
30.0 (0.6)

1.64 (0.01)
1.69 (0.05)
268.9 (4.6)
227.7 (8.7)
4.3 (0.2)
3.5 (0.1)
25.5 (1.2)
38.5 (2.8)
5.5 (0.6)
8.3 (0.8)
46.8 (1.7)
56.0 (3.0)
16.1 (4.6)
18.8 (1.5)
27.9 (4.6)
34.3 (1.6)

3.82 (0.12)
4.60 (0.25)
292.6 (6.7)
298.5 (5.9)
5.0 (0.2)
6.7 (0.5)
128.7 (11.1) 86.1 (6.4)
28.0 (2.8)
70.4 (10.9)
52.0 (2.6)
56.1 (3.4)
9.1 (3.5)
10.6 (1.8)
37.4 (2.5)
34.8 (4.3)

3.10 (0.50)
1.88 (0.07)
290.4 (4.8)
292.1 (6.7)
7.3 (1.0)
5.0 (0.3)
19.4 (0.2)
18.9 (0.3)

4.70 (0.40)
2.86 (0.1 1)
330.3 (5.2)
318.6 (5.8)
6.1 (0.2)
9.8 (0.7)
19.0 (0.4)
17.3 (0.4)

~~

Past year consumption

Average daily intake
Frequency of drinking
Quantity per drinking day
Days drank 2 5 drinks
Days drank 2 9 drinks
% Intake in beer
% Intake in wine
% Intake in liquor
Period of heaviest drinkinq
Average daily intake
Frequency of drinking
Quantity per drinking day
Age at first drink
Past-year health indicators
Bed days
% Hospitalized
% In poor health
% With major limitations
% With preexisting conditions

0.13
64.3
3.5
1.8
0.4
51.1
9.2
39.7

(<0.01)
(6.4)
(0.3)
(0.2)
(0.1)
(3.1)
(1.6)
(2.9)

1.68 (0.19)
171.2 (8.9)
5.6 (0.4)
18.9 (0.2)
6.9
11.9
3.7
8.9
31.7

(1.3)
(2.6)
(1.5)
(2.2)
(3.3)

0.64 (0.02)
113.4 (1.4)
3.1 ((0.1)
20.3 (0.1)
4.1
6.9
2.0
3.7
29.0

(0.2)
(0.3)
(0.2)
(0.2)
(0.5)

1.95(0.15)
1.15(0.03)
236.1 (10.6) 220.3 (2.1)
5.6 (0.3)
3.8 (0.1)
18.4 (0.2)
19.6 (0.1)
8.7
9.5
3.2
6.7
36.3

(2.3)
(1.6)
(1.0)
(1.7)
(4.0)

4.1
7.0
1.5
2.8
28.2

(0.3)
(0.4)
(0.2)
(0.2)
(0.6)

18.2
16.1
13.8
10.2
40.8

(10.2)
(1.3)
(1.5)
(4.6)
(3.6)

2.8
6.4
1.0
2.5
32.5

(0.3)
(1.3)
(0.3)
(0.5)
(1.8)

11.4
18.1
13.9
6.5
56.2

(3.5)
(4.1)
(3.2)
(1.3)
(2.3)

4.8
8.9
2.7
4.3
34.7

(0.8)
(1.8)
(0.8)
(1.0)
(3.2)

Note: Figures in parentheses are standard errors of estimates.

Both consumption level and dependence were tested for

nondependent drinkers. The hazard rate ratios for nondependent drinkers remained essentially the same as in the interaction with some of the model covariates previously
earlier models that ignored dependence. For dependent demonstrated to modify their effects, namely age, sex,
drinkers, though, there was no longer any protective effect smoking status, and baseline poor health. There was some
of light or moderate drinking. In fact, dependent drinkers evidence of interaction between light drinking and male
exhibited an increased mortality risk at all consumption gender, but this result was not consistent across models and
levels, although not a consistently significant increase. Rel- was of a marginal significance level given the number of
ative to all past-year abstainers, the increase in risk was tests performed. However, being 65 years of age or older at
significant only for very heavy dependent drinkers (HRR = baseline and being a former or current smoker showed a
1.56, CI = 1.17-2.08). Relative to lifetime abstainers, the strong and consistent negative interaction with very heavy
increase was significant for both moderate drinkers drinking. When these interactions were tested simulta(HRR = 1.32, CI = 1.01-1.72) and very heavy dependent neously, the age interaction failed to retain its significance,
drinkers (HRR = 1.65, CI = 1.38-1.98). Although the but smoking status remained a significant effect modifier.
estimated effect for heavy drinkers lay between these two Among individuals who never smoked, there was a signif(HRR = 1.42), as would be expected given a dose response icantly increased risk of mortality associated with very
heavy drinking, whereas among lifetime smokers the effect
relationship, it fell just short of significance.
By controlling for broadly defined poor health at base- remained nonsignificant (data not shown). This interaction
line, the models whose results were summarized in Tables did not affect the impact of including alcohol dependence
2 and 3 treated poor health as a potential confounder of the as a predictor. That is, dependent individuals remained
associations of consumption and dependence with mortal- more at risk of dying than those without dependence irreity as opposed to an intervening variable linking them. If spective of smoking status.
To identify factors that might explain why dependent
some aspects of poor health at baseline were actually the
result of prior alcohol consumption and/or dependence, drinkers did not experience any reduction in mortality from
that is, diseases that were part of the causal chain between light and moderate drinking and why nondependent drinkconsumption and death, then this adjustment would lead to ers did not experience any increase in mortality from very
overly conservative estimates of the true mortality hazards heavy drinking, I compared various drinking pattern and
associated with alcohol consumption and dependence health measures for dependent and nondependent drinkers
(Poikolainen, 1995). To assess the impact of making this (Table 4). All data were standardized by age and sex (Shah
adjustment for poor health, I re-ran the models excluding et al., 1997) to account for the confounding effect of dethis covariate. The changes in the model parameters were pendent drinkers being predominantly young and male,
small, well within sampling error and inconsistent in direc- characteristics that in and of themselves are strongly assotion (data not shown). Thus, the inclusion of poor health as ciated with drinking patterns and morbidity. In terms of
an adjustment factor in this analysis did not seem to have past-year consumption, dependent drinkers drank a greater
much effect on the magnitude of the hazard rate ratios for volume of ethanol than nondependent drinkers in all but
the heavy drinking category. Although their frequency of
consumption and dependence.

DAWSON

78

drinking was greater only among moderate and heavy

drinkers, their quantity of drinks per drinking day was
consistently higher across volume categories, as were their
frequencies of drinking five or more and nine or more
drinks.
Considering the period of heaviest drinking, dependent
drinkers reported volumes of consumption that were 1.6 to
2.6 times greater than those of their nondependent counterparts. Again, this difference was driven more by differentials in the quantity consumed per drinking day than in
the overall frequency of drinking. Dependent drinkers also
started drinking at a younger age, meaning that they had
experienced a slightly longer exposure to ethanol at any
given age.
In terms of health, dependent drinkers reported more
days spent in bed due to poor health and a higher prevalence of hospitalization in the year preceding the NHIS
interview. The measure of baseline poor health that was
used as a control in this analysis was based on three components: reporting health as fair or poor (as opposed to
good, very good, or excellent), reporting major limitation of
activity, and/or reporting any of six preexisting medical
conditions. Among heavy and very heavy drinkers, those
with dependence were more likely than those without dependence to report being in poor health or to report preexisting conditions. Among light to heavy drinkers, those
with dependence were more likely to report major limitation of activities. Thus, within the control for poor health
that was used in this analysis, dependent drinkers seem
more likely than nondependent drinkers to have experienced multiple and more serious indicators.
DISCUSSION

This analysis of prospective data from a sample of U.S.

adults 25 years of age and older at baseline indicated that
alcohol consumption and alcohol dependence exerted significant and independent effects on the risk of all-cause
mortality over a 7.5 year follow-up period. Considered
separately, the effect of consumption was a U-shaped
curve, with a near-significant increase in mortality among
the heaviest drinkers, and the effect of dependence was
positive and independent of volume of consumption. Together, these findings revealed that among nondependent
drinkers, light and moderate drinking was protective and
heavier drinking did not significantly affect the risk of
dying; among dependent drinkers, the effect of alcohol
consumption was never protective and often increased the
risk of death. These findings indicate the importance of
considering dependence in addition to consumption when
interpreting the implications of drinking for all-cause mortality. Although the possibility of greater underreporting of
consumption among dependent drinkers cannot be ruled
out, this studys comparison of dependent and nondependent drinkers suggested several alternative reasons for the
positive mortality risk associated with alcohol dependence.

First, the comparison of dependent and nondependent

drinkers suggested that the frequency of heavy episodic
drinking may be positively associated with all-cause mortality. This would be expected for mortality from external
causes such as injuries, but this study, in which external
causes contributed only 5% of all deaths during the observation period, suggests that heavy drinking occasions may
increase the risk of other types of death as well. This finding
is supported by the recent meta-analyses conducted by
Leino et al. (1998) and Fillmore et al. (1998), which found
higher all-cause mortality hazard rate ratios associated with
heavy quantity of intake per drinking day than with high
frequency of drinking. Similarly, a recent analysis by Kauhanen et al. (1997) found that men whose usual intake was
six or more beers per drinking day had a higher risk of
all-cause mortality than those whose usual intake was three
or fewer beers, even after adjusting for the higher overall
volume of intake of the former. Heavy episodic drinking is
not limited to dependent drinkers, and this aspect of drinking pattern should be investigated in conjunction with volume of intake for all drinkers.
Second, the comparison of dependent and nondependent drinkers suggested that drinking at baseline may not
fully capture the harm or benefits conferred by earlier
patterns of drinking. When available, drinking history (to
at least distinguish former drinkers from lifetime abstainers) and measures of lifetime or heaviest intake and
lifetime dependence might explain mortality risks that
seem contradictory in light of baseline consumption patterns. In this study, former drinkers exhibited a mortality
risk that increased with their level of heaviest intake and
that fell just short of being significantly higher than that
for lifetime abstainers. In this sense, their risk curve
paralleled that for dependent drinkers, suggesting that
prior dependence may have been a factor in many former
drinkers decisions to stop drinking. (In a prospective
study of U.S. medical patients between the ages of 55
and 65, Mertens et al., 1996, found that fully two thirds
of baseline abstainers had former alcohol problems.)
Studying both baseline and prior consumption levels
(i.e., drinking trajectories) and the incidence and remission of dependence among all drinkers, not just former
drinkers, might provide additional insights into how
drinking and mortality are linked.
In a related point, it has been argued (e.g., Shaper, 1990)
that the inclusion of former drinkers in the reference category of baseline abstainers might bias findings because of
the possibility of drinking cessation having been linked to
health problems associated with the risk of dying. Using the
drinking history obtained in the NHIS, I was able to determine that the distinction between baseline and lifetime
abstinence as the reference group against which consumption levels were assessed was of limited importance in this
U.S. sample of adults 25 years of age and older. It had only
a small effect on the magnitudes of the hazard rate ratios
for different consumption levels but did make a difference

ALCOHOL CONSUMPTION, DEPENDENCE, AND ALL-CAUSE MORTALITY

in whether some of the ratios with borderlinep values could

be considered significant.
It is possible that with a larger sample or a longer
follow-up period, the choice of reference group might make
the difference between a U-shaped and J-shaped curve for
all-cause mortality; that is, it might affect whether the
increased risk among the heaviest drinking group(s) is significant or not. Given the near-significant increased risk of
mortality among former drinkers compared to lifetime abstainers, the choice of reference group also might be more
important in populations where former drinkers make up a
larger proportion of baseline abstainers, that is, where
lifetime abstinence is less common. This is by no means
certain, though, because the probability of lifetime abstainers being selected with respect to poor health, social isolation, or other mortality risk factors is likely to be greater
when abstinence is less common.
A third point suggested by the comparison of dependent
and nondependent drinkers has to do with baseline health
indicators. Although this studys control for baseline poor
health was intended to rule out this factor as a confounder
of the effect of dependence, there were many differences in
severity not captured by the baseline measure used. It is
likely that even more differences would have been documented if the NHIS had collected information on comorbid
psychiatric and drug use disorders that are known to be
disproportionately prevalent among individuals with alcohol dependence (Grant and Harford, 1995; Kessler et al.,
1994; Merikangas and Gelernter, 1990; Regier et al., 1990)
or on illness-related stressors and associated coping responses (Mertens et al., 1996). Although this study found
little change in the effects of consumption and dependence
when baseline health was excluded as a control, the impact
of including versus excluding it might have been greater
had a more sensitive health measure or measures been
used.
In any event, the decision about whether to adjust mortality hazards estimates for baseline health should not be
made on empirical grounds but rests on the extent to which
baseline health problems are considered to have resulted
from prior alcohol consumption. The best possible solution
would be to measure both the direct effects of consumption
at baseline and the indirect effects of prior consumption
through their effect on baseline health. Thus baseline conditions not attributable to prior consumption would be
retained as controls, and those resulting from prior consumption would be treated as intervening variables., Even
this optimal approach fails to capture changes in drinking
that may occur between the baseline measure and the end
of the observation period, illustrating the limits of estimating the mortality risks associated with alcohol consumption
from data taken at a single time point.
Finally, the comparison of dependent and nondependent
drinkers revealed that at light and moderate consumption
levels, dependent drinkers consumed significantly less of
their overall ethanol intake in the form of wine. In view of

19

studies that have found a protective effect of light or moderate wine consumption (a finding that is by no means
consistent across studies; see White, 1996), this suggests
that beverage preference might be another factor associated with dependence being a positive risk factor for mortality.
The ranges of ethanol intake at which this study found
protective and risky effects with respect to all-cause
mortality were in line with those reported in other studies. For example, both the meta-analysis by Holman et al.
(1996) and the large-scale American Cancer Society prospective study (Thun et al., 1997) found that the increase
in mortality risk did not begin until an average of four or
more drinks per day were consumed, the same level at
which this study found the first significant and nearsignificant increased risks. However, in both the studies
by Thun et al. and Holman et al., this finding was restricted to specific subpopulations, individuals age 30 to
59 with low cardiovascular risk in the former case and
men in the latter case.
Holman et al. found a lower threshold for increased
risk among women (with a significantly increased risk at
intake levels of more than drinks per day) that was not
supported in this study. Although I did not a priori
stratify the sample by age and sex, I tested for and failed
to detect any significant interaction between sex and the
volume of intake consumption levels. (The only nearsignificant interaction with sex suggested a less strongly
protective effect of light drinking among male compared
to female drinkers, and no impact on the risk at the
heavy drinking level of approximately two to four drinks
per day that distinguished men and women in the study
by Holman et al.) Additional research is needed to clarify whether the risky volume thresholds do indeed differ
for men and women. Gender differentials in the selectivity of drinking and in sensitivity to reporting baseline
health conditions need to be examined. It is also important to adjust volume measures for atypical heavy drinking, as was done in this study, and to test for the significance of any differences in threshold rather than
assuming that a stratified analysis is justified.
These findings may not be generalizable to populations other than that used for analysis, which consisted of
U.S. adults 25 years of age and over. All-cause mortality
curves reflect the curves for the most common causes of
death, which vary substantially by age and among cultures with different diets and social practices. For the
study sample, coronary heart disease was the primary
cause of death, and its J-shaped association with alcohol
consumption has been widely documented. Populations
where mortality is predominantly associated with infectious diseases or external causes such as accidents and
suicide-and these populations include U.S. adolescents
and young adults as well as the populations of many
developing countries-cannot be assumed to experience

DAWSON

80

alcohol-related mortality risks comparable to those described in this study.

REFERENCES
American Psychiatric Association (1994) Diagnostic and Statistical Manual
of Mental Disorders. 4th ed. American Psychiatric Association, Washington, DC.
Andcrson P (1994) Are there net health benefits from moderate drinking?
All-cause mortality. Contemp Drug Probl 21:143-161.
Andreasson S, Brandt L (1997) Mortality and morbidity related to alcohol.
Alcohol Alcohol 32:173-178.
Berberian KM, van Dujin CM, Hoes AW, Valkenburg HA, Hofman A
(1994) Alcohol and mortality: Results from the EPOZ follow-up study.
Eur J Epidemiol 10:587-593.
Boffetta P, Garfinkel L (1990) Alcohol drinking and mortality among men
enrolled in an American Cancer Society prospective study. EpidemiolOW 1~347-348.
Bunn JY, Booth BM, Cook CA, Blow FC, Fortney JC (1994) Relationship
between mortality and intensity of inpatient alcoholism treatment. Am J
Public Health 84:211-214.
Callahan CM, Tierney WM (1995) Health services use and mortality
among older primary care patients with alcoholism. J Am Geriatr Soc
43:1378-1 383.
Camargo CA, Hennekens CH, Gaziano JM, Glynn RJ, Manson JE,
Stampfer MJ (1997) Prospectivc study of moderate alcohol consumption and mortality in US male physicians. Arch Intern Med 157:79-85.
Chyou P-H, Burchfiel CM, Yano K, Sharp DS, Rodriguez BL, Curb JD,
Nomura AMY (1997) Obesity, alcohol consumption, smoking and mortality. Ann Epidemiol 7:311-317.
Cullen KJ, Knuiman MW, Ward NJ (1993) Alcohol and mortality in
Brusselton, Western Australia. Am J Epidemiol 137:242-248.
Davis MA, Ncuhaus JM, Moritz DJ, Lein D, Barclay JD, Murphy SP
(1994) Health behaviors and survival among middle-aged and older
men and women in the NHANES I epidemiologic follow-up study. Prev
Med 23:369-376.
Deleyiannis FWB, Thomas DB, Vaughan TJ, Davis S (1996) Alcoholism:
Independent predictor of survival in patients with head and neck cancer.
J Natl Cancer Inst 88542-549.
DISCUS (Distilled Spirits Council of the United States) (1985) Annual
Statistical Review 19841198.5. Distilled Spirits Industry, Washington, DC.
Doll R, Peto R, Hall E, Wheatley K, Gray R (1994) Mortality in relation
to consumption of alcohol: 13 years observations on male British
doctors. Br Med J 309:911-918.
Duffy JC (1995) Alcohol consumption and all-cause mortality. Int J
Epidemiol 24:lOO-105.
Fillmore KM, Golding JM, Graves KL, Kniep S, Leino EV, Romelsjo A,
Shoemaker C, Ager CR, Allebeck P, Ferrer H (1998) Alcohol consumption and mortality: 111. Studies of female populations. Addiction 93:
219 -229.
Finney JW, Moos RH (1991) Long-term course of alcoholism: I. Mortality, relapse and remission rates and comparisons with community controls. J Stud Alcohol 53:44-54.
Gordon T, Doyle J (1987) Drinking and mortality. Am J Epidemiol
125:263-270.
Gordon T, Kannel WB (1983) Drinking habits and cardiovascular disease:
The Framingham Study. Am Heart J 105:667-673.
Grant BF, Harford TC (1995) Comorbidity between DSM-IV alcohol use
disorders and major depression: Results of a national survey. Drug
Alcohol Depend 39:197-206.
Gronhaek M, Deis A, Sorensen TIA, Becker U, Borch-Johnsen K, Miiller
C, Schnohr P, Jensen G (1994) Influence of sex, age, body mass index,
and smoking on alcohol intake and mortality. Br Med J 308:302-306.
Hampl K, Hajin J (1992) Mortality of alcohol abusers, in 36th International
Congress on Alcohol and Drug Dependence, vol 2; pp 1146-1 152, International Congress on Alcohol and Drug Dependence, Glasgow, Scotland.

Holman CD, English DR, Milne E, Winter MG (1996) Meta-analysis of

alcohol and all-cause mortality: A validation of NHMRC recommendations. Med J Aust 164:141-145.
Kagan A, Yano K, Rhodcs G, McGee DL (1981) Alcohol and cardiovascular disease: The Hawaiian experience. Circulation 64(Suppl 111):2731.
Kauhanen J, Kaplan GA, Goldberg DE, Salonen JT (1997) Beer binging
and mortality: Results from the Kuopio ischemic heart disease risk
factor study, a prospective population based study. Br Med J 3152346851.
Keil U, Chambless LE, Doring A, Filipiak B, Sticber J (1997) The relation
of alcohol intake to coronary heart disease and all-cause mortality in a
beer-drinking population. Epidemiology 8:150-156.
Kessler RC, McGonagle KA, Zhao S, Nelson CB, Hughes M, Eshlenian S,
Wittchen H-U, Kendler K (1994) Lifetime and 12-month prevalence of
DSM-111-R psychiatric disorders in the United States: Results from the
National Comorbidity Survey. Arch Gen Psychiatry 51:s-19.
Klatsky AL, Armstrong MA, Friedman GD (1 992) Alcohol and mortality.
Ann Intern Med 117:646-654.
Kling W (1989) Measurement of ethanol consumed in distilled spirits.
J Stud Alcohol 501456-460.
Langle G, Mann K, Mundle G, Schied HW (1993) Ten years after: The
post-treatment course of alcoholism. Eur Psychiatry 8:95-100.
Leino EV, Romelsjo A, Shoemaker C, Ager CR, Allebeck P, Fcrrer H,
Fillmore KM, Golding JM, Graves KL, Kniep S (1998) Alcohol consumption and mortality: 11. Studies of male populations. Addiction
93205-21 8.
Lewis CE, Smith E, Kercher C, Spitznagel E (1995) Assessing gender
interactions in the prediction of mortality in alcoholic men and women:
A 20-year follow-up study. Alcohol Clin Exp Res 19:1162-1172.
Massey JT, Moore TF, Parsons V, Tadros W (1989) Design and estimation from the National Health Interview Survey, 1985-1994. National
Center for Health Statistics, Vital Health Stat 2(110):1-33.
Merikangas KR, Gelernter CS (1990) Comorbidity for alcoholism and
depression. Psychiatr Clin North Am 13:613-632.
Mertens JR, Moos RH, Brennan PL (1996) Alcohol consumption, life
context, and coping predict mortality among late-middle aged drinkers
and former drinkers. Alcohol Clin Exp Res 20:313-319.
Modern Brewery Age (1992) Beer analysis. Modern Brewery Age 43(37):
52-53.
National Center for Health Statistics (1 997) National Health Interview
Survey Multiple Cause of Death Public Use Data File. National Center for
Health Statistics, Centers for Disease Control, Hyattsville, MD.
Poikolainen K (1995) Alcohol and mortality: A review. J Clin Epidemiol
48:455-465.
Regier DA, Farmer ME, Rae DS, Locke BZ, Keith SJ, Judd LL, Goodwin
FK (1 990) Comorbidity of mental disorders with alcohol and other drug
abuse. Results from the Epidemiologic Catchment Area (ECA) Study.
J A M 26412511-2518.
Rehm J, Sempos CT (1995) Alcohol consumption and all-cause mortality.
Addiction 90:471-480.
Renaud SC, GuCguen R, Schenker J, dHoutaud A (1998) Alcohol and
mortality in middle-aged men from Eastern France. Epidemiology
9:184-188.
Romelsjo A, Karlsson G, Henningsohn L, Jakobsson SW (1993) Prevalence of alcohol-related mortality in both sexes: Variation between
indicators, Stockholm 1987. Am J Public Health 832338-844.
Rossow I, Amundsen A (1997) Alcohol ahuse and mortality: A 40-year
prospective study of Norwegian conscripts. Soc Sci Med 44:261-267.
Serdula MY, Koong S-L, Williamson DF, Anda RF, Madans JH, Kleinman JC, Byers T (1995) Alcohol intake and subsequent mortality:
Findings from the NHANES I follow-up study. J Stud Alcohol 56:233239.
Shah BV, Barnwell BG, Bieler GS (1997) SUDAAN Users Manual. Release 7:5., Research Triangle Institute, Research Triangle Park, NC.

ALCOHOL CONSUMPTION, DEPENDENCE, AND ALL-CAUSE MORTALITY

Shaper AG (1990) Alcohol and mortality: A review of prospective studies.

Br J Addict 85:837-847.
Spinatsch M (1992) Prediction of long-term outcome of male alcoholics
after inpatient treatment: The case of a clinical population in Germanspeaking Switzerland. Int J Addict 27:1087-1103.
Thun MJ, Peto R, Lopez A, Monaco JH, Henley SJ, Heath CW, Doll R
(1997) Alcohol consumption and mortality among middle-aged and
elderly U.S. adults. N Engl J Med 337:1705-1714.
Turner C (1990) How much alcohol is in a standard drink? An analysis of
125 studies. Br J Addict 85:1171-1175.
Wells JE, Walker ND (1990) Mortality in a follow-up study of 616

81

alcoholics admitted to an inpaticnt alcoholism clinic 1972-1976. N Z

Med J 103:l-3.
Yuan J-M, Ross RK, Gao Y-T, Henderson BE, Yu MC (1997) Follow up
study of moderate alcohol intake and mortality among middle-age men
in Shanghai, China. Br Med J 314:18-23.
White IR (1996) The cardioprotective effects of moderate alcohol consumption. Br Med J 312:1179-1180.
Williams GD, Clem D, Dufour M (1993) Apparent Per Capita Alcohol
Consumption: National, State, and Regional Trends, 1977-1991. Alcohol
Epidemiologic Data System (AEDS) Report No. 27. National Institute
on Alcohol Abuse and Alcoholism, Rockville, MD.