Alcohol, Tobacco, and Hypertension
GARY D. FRIEDMAN, M.D.,
M.S.,
ARTHUR L. KLATSKY,
M.D.,
AND A.B. SlEGELAUB, M.S.
Downloaded from http://hyper.ahajournals.org/ by guest on June 15, 2017
SUMMARY In many studies of diverse populations it has been found that persons drinking relatively large amounts of alcohol tend to have higher blood pressures. In the Kaiser-Permanente study of
about 87,000 persons, this alcohol-blood pressure association was not attributable to demographic
characteristics, adiposity, reported salt use, smoking, or coffee consumption, nor could it be explained
by underreporting of alcohol consumption. If the relationship is a causal one, the pathogenesis is not
yet established; direct mechanisms or the effects of withdrawal from alcohol are possible explanations.
The Kaiser-Permanente data suggest that about 5% of hypertension in the general population may be
due to the consumption of three or more alcoholic drinks per day. Alcohol use shows a positive relation
to some sequelae of hypertension but not others; the outstanding exception is coronary heart disease
which is negatively related to alcohol intake, probably through different mechanisms. In most studies,
cigarette smokers have shown similar or slightly lower blood pressures than nonsmokers. The degree
to which this is due to the thinner body build of smokers, on the average, is not well established; nor is
the degree to which a stronger negative relation of smoking to blood pressure might be masked by
concomitant alcohol use. (Hypertension 4 (supp III): IIM43-III-150, 1982)
KEY WORDS
• blood pressure • ethanol • epidemiology • cigarette smoking
T
HE relation of alcohol use to hypertension and to
other forms of cardiovascular disease has become
a major question for both medical and public
health research in recent years. Cigarette smoking is associated with alcohol use in our society. Since cigarette
smoking has pharmacological effects that might be expected to influence blood pressure, the question of a
smoking-blood pressure association also deserves
exploration.
In this investigation we consider:
1. The epidemiological evidence linking alcohol use
to blood pressure
2. The associated or potentially confounding factors
that must be considered
3. Possible mechanisms or explanations involved in
the alcohol-hypertension link
4. The effects of alcohol on the outcomes of hypertension
5. Potential public health implications
6. The relation between smoking and blood pressure.
From the Department of Medical Methods Research and the
Department of Medicine (Oakland), Kaiser-Permanente Medical
Care Program, Oakland, California.
Supported by a grant from the U.S. Brewers Association, Contract No. NOl-CP-05681 from the National Cancer Institute, and
the Community Services Program of Kaiser Foundation Hospitals.
Address for reprints: Dr. Gary D. Friedman, 3451 Piedmont
Avenue, Oakland, California 94611.
Alcohol and Hypertension:
Epidemiologic Evidence
It has been found in many studies, both in this country
and in others, that persons in the higher range of alcohol
consumption tend to have higher blood pressures.'"10 We
shall not present a complete review of the literature,
but a few examples will be illustrative.
The well-known Framingham study has involved a
careful initial evaluation and long-term follow-up of
over 5000 middle-aged men and women, initially aged
30-59 years. Although the overall correlation between
alcohol intake and blood pressure in this study population was small, the prevalence of hypertension, defined as a systolic pressure > 160 ordiastolic 2= 95 mm
Hg, was about twice as high among persons drinking
60 ounces or more of ethyl alcohol per month as among
those drinking less than 30 ounces per month. These
lighter drinkers had slightly lower blood pressures than
nondrinkers. 1
In a study of 922 "problem drinkers" among employees of the E.I. du Pont de Nemours and Co., Inc.,
and matched comparison subjects consisting of nondrinkers and moderate drinkers, hypertension defined
as above was over twice as frequent in the problem
drinkers. Interestingly, the relation appeared to be partially reversible in that recovered problem drinkers had
a lower prevalence of hypertension than those whose
drinking problem was current. 3
111-143
1-144
PERSPECTIVES IN HYPERTENSION
SUPPL III, HYPERTENSION, VOL. 4, No 5, SEPTEMBER-OCTOBER 1982
Downloaded from http://hyper.ahajournals.org/ by guest on June 15, 2017
A different type of study population in a different
setting consisted of 70 male twin pairs in Sweden who
were discordant for drinking, i.e., either only one twin
in each pair used substantial amounts of alcohol, or
one twin drank much more than the other. Here again
the users of more alcohol had higher casual and basal
blood pressures on the average than their co-twins.
Although most of the twins were dizygotic, the findings suggested at least some independence of the alcohol-blood pressure relation from genetic factors.4
On the other side of the world, 85 active working
men in Tasmania10 showed a direct correlation of both
systolic and diastolic blood pressures with alcohol consumption up to 240 g/week. Multivariate analysis
showed alcohol consumption to be an important predictive variable for blood pressure.
To our knowledge, our own cross-sectional investigation of this question has involved the largest study
group, 87,000 ambulatory adult subscribers to the Kaiser-Permanente Medical Care Program, a prepaid
health care plan.9 Our subjects lived in the San Francisco Bay area and received a multiphasic health checkup
between 1964 and 1968 at the program's medical center in Oakland or San Francisco. In this checkup, alcohol use data (as assessed by questionnaire) was computer-stored along with many other health-related
variables including blood pressure measured by an
automated device." The study population was characterized by ethnic and socioeconomic diversity.12
Figure 1 shows the age-adjusted mean systolic and
diastolic blood pressure in each race-sex group accord-
ing to usual number of drinks per day as reported on
questionnaire. Among both men and women, there
was a steady rise in blood pressure as consumption
increased beyond two drinks per day except among
blacks where the maximum blood pressure was usually
found in the three- to five-drink category. Among the
women of all races, there was a clear tendency for
consumers of two or fewer drinks per day to have
lower blood pressures than nondrinkers. In general,
the trends in systolic pressure were more pronounced
than those in diastolic pressure.
Not shown in figure 1 was a further breakdown of
the 6 + drink group into a 6-8 drink and 9 + drink
subgroup. The 9 + subgroup was relatively small and
did not show an increase in mean blood pressure beyond that of the 6-8 drink subgroup.
We also determined the prevalence of hypertension
in each alcohol consumption category (fig. 2), again
using the 160/95 breakpoint. In white men and women, the prevalence of hypertension was approximately
twice as great in the 6 + drink group as in the combined two or fewer and nondrinking categories.
Among blacks, the 3 + drink group had an approximately 50% higher prevalence of hypertension.
Potentially Confounding Factors
Adiposity
Adiposity has proven to be an important predictor or
determinant of hypertension. It is one of the first characteristics that should come to mind when trying to
1 5 0
i
I r
Yellow
o 140
O)
X
130
E
E
T99%
CONFIDENCE
£ 120
I 90
o
o
• MEN
— o WOMEN
[LIMITS
80
C
o
£
I
70
0
$2
J
I
3-5 *6
I
0
J
$2
I
3-5
*6
0
$2
3-5 >
Alcohol consumption (Usual number of drinks per day)
FIGURE 1. Age-adjusted mean systolic and diastolic blood pressure according to reported alcohol consumptioi
by race and sex. (Reproduced, by permission, from the New England Journal of Medicine (see ref. 9).
ALCOHOL, TOBACCO, AND HYPERTENSION/FWed/nan et al.
60
justed
50
40
cent (Age
o
i
i
I
r
Systolic blood pressure
>160 mm Hg
•
•
O
•
BUCK WOMEN
BLACK MEN
WHITE WOMEN
WHITE MEN
III-145
\
\
i
r
Diastolic blood pressure
_ >95 mm Hg
1
99%
CONFIDENCE
LIMITS
30
20
10 -
BD--
Downloaded from http://hyper.ahajournals.org/ by guest on June 15, 2017
I
I
0
«2
3-5
£6
0
I
<2
3-5
-*6
Alcohol consumption (Usual number of drinks per day)
FIGURE 2. Age-adjusted percentages with elevated systolic and diastolic blood pressure among black and white
men and women, according to reported alcohol consumption. (Reproduced, by permission, from the New England
Journal of Medicine (see ref. 9).
explain an association between the ingestion of any
item and hypertension. In this conference concerned
with aspects of nutrition in relation to blood pressure,
we should always ask ourselves whether a higher level
of intake of any particular item might be merely an
index for higher overall food intake in relation to energy expenditure, rather than the culprit itself. On the
other hand, since the relation of obesity to blood pressure is not fully understood, we should also be open to
the possibility that obesity is a marker for the consumption of one or more of the key substances that
raise blood pressure.
At any rate, we did subdivide our study population
into thirds according to their body mass (Quetelet)
index (wt/ht2). In each tertile of adiposity, the association of alcohol intake with mean blood pressure was
apparent (fig. 3).
Reported Indiscriminate Salt-Shaker Use
An item on the multiphasic questionnaire read as
follows: "Do you usually salt your food before tasting
it?" It is debatable whether " y e s " answers always
represent higher levels of salt intake, but lacking salt
excretion measurements we felt that, on the average,
people who affirmed this behavior ingested more salt
than those who denied it. We also found that there was
a strong association of " y e s " answers to this question
with alcohol intake. Among subjects subdivided by
their answers to this salt intake question, the relation of
alcohol intake to blood pressure persisted (fig. 4). It
can be seen that not only did this questionnaire item
fail to explain away the alcohol-blood pressure relation
but it has no discriminating ability for blood pressure
level.
Other Characteristics
As has been shown, the alcohol-blood pressure relation was present in each race and sex, and our data
were age-adjusted. Thus, the demographic characteristics of age, sex, and race were not responsible for the
observed correlation. We also subdivided the study
group by smoking habits and coffee consumption, two
characteristics associated with alcohol use; we found
that the alcohol-blood pressure relation persisted.
Possible Explanations
Underreporting Alcohol Use
We bring up underreporting of alcohol consumption
as a potential source of bias, first to dispense with it as
soon as possible, since it is repeatedly and incorrectly
cited as a reason for disbelief of our findings. We all
know that some persons consuming relatively large
quantities of alcohol are embarrassed by this and report
lesser amounts. But what kind of bias does this introduce into our studies?
Let us first consider the hypothetical case in which
there is no real relation of alcohol use to blood pressure. For simplicity we will assume that there are only
two categories of drinkers, heavy and light. If, because
of false reporting, some truly heavy drinkers are incorrectly placed in the light category, the mean blood
III-146
PERSPECTIVES
150
IN H Y P E R T E N S I O N
r
S U P P L III, H Y P E R T E N S I O N , V O L 4 , N o 5 , S E P T E M B E R - O C T O B E R 1 9 8 2
I
I
White Women
i
White Men
140
ID
CD
130
E
E
ADIPOSITY1 /NDEX
120
o HIGHEST THIRD
90
9 MIDDLE THIRD
_ J 99% CONFIDENCE
LIMITS
I
3-5
I
^6
• LOWEST THIRD
"O
o
_°
M ^--5^JL.
80
Downloaded from http://hyper.ahajournals.org/ by guest on June 15, 2017
c
o
a>
70
_L
0
I
^2
I
3-5
I
?6
I
0
I
^2
Alcohol consumption (Usual number of drinks per day)
FIGURE 3. Age-adjusted mean systolic and diastolic blood pressure according to degree of adiposity: white men
and women. (Reproduced, by permission, from the New England Journal of Medicine (see ref. 9).
pressure of the heavy group will not change, and since
heavy drinkers incorrectly placed in the light drinking
category had the same blood pressure as the light
drinkers, the mean blood pressure of the light drinking
group will not change. Thus, the heavy and light drinking groups will have the same mean blood pressure
_- 150
-o
S.
I
I
White Men
I
even after some of the truly heavy drinkers put themselves in the light drinking group. Only if false reporting is associated with low blood pressure, which to our
knowledge has never been demonstrated, would this
kind of misclassification produce as an artifact the
association that has been observed.
I
i
r
White Women
O 140
d)
o>
<
130
E
E
120
90
• SALT FOOD BEFORE TASTING
o D O N O T SALT FOOD
BEFORE TASTING
I 99% CONFIDENCE LIMITS
_
o
_2 80
Id
c
o
<u
70
I
I
I
I
I
I
I
0
$2
3-5
^6
0
$2
3-5
£
Alcohol consumption (Usual number of drinks per day)
FIGURE 4. Age-adjusted mean systolic and diastolic blood pressure according to whether the subjects (white
men and women) salt their food before tasting it.
ALCOHOL, TOBACCO, AND HYPERTENSlOWFrieclman et al.
Downloaded from http://hyper.ahajournals.org/ by guest on June 15, 2017
Now consider there to be a true difference in blood
pressure between heavy and light drinkers. If some
heavy drinkers erroneously put themselves in the light
drinking category, the reported light drinkers will become more like the remaining reported heavy drinkers.
That is, the apparent difference between the two
groups will be reduced.
Thus, if any bias is introduced by the underreporting
of alcohol consumption, this will not be in the direction of creating an association with blood pressure that
is not really there, but will rather be to reduce a true
association. We wish that many of those who raise this
question would not just assume that large population
studies relying on questionnaire assessments of alcohol use are invalid, but would follow the results of the
likely reporting errors to their logical conclusion.
We believe that in our relatively nonjudgmental
medical setting, the degree of underreporting is not
great. Our questionnaire data produced an alcoholdrinking distribution similar to that observed in a national survey based on careful personal interviews.13
For those who still do not believe that what people
say is valid unless backed up by laboratory data, there
is an interesting recent report from Belgium of a study
of blood pressure in over 9000 men who not only
reported their alcohol consumption but also had measurements of gamma-glutamyl transpeptidase, a biochemical index of alcohol consumption. Both the consumption reported and the enzyme measure were
associated with blood pressure.14 Two studies from the
Glasgow, Scotland area in 1977 also showed associations of liver function test abnormalities with hypertension and there was evidence that alcohol consumption was the common explanatory factor.5-6
Ill-147
became normotensive when the withdrawal symptoms
cleared. After discharge, blood pressure rose only in
those who started drinking again. These investigators
suggested that alcohol-related hypertension may be the
result of the alcohol-withdrawal syndrome possibly
due to increased "noradrenergic" activity. Thus, we
can now see that the withdrawal question is really
twofold. One question has to do with whether the alcohol-blood pressure association is really an artifact:
Could it be that alcohol drinkers do not really have
higher blood pressures most of the time, but only when
they are temporarily in a state of withdrawal at medical
examinations? The second question is: Given a true
association, is withdrawal the underlying mechanism?
It may be that withdrawal does raise blood pressure
both acutely as in the detoxification ward, and, of
greater concern, chronically through the long-term effects of repeated transient blood pressure increases
leading to sustained hypertension. This should be a
fruitful area of clinical research in the years to come.
Psychological Stress
It is also reasonable to ask whether psychological or
emotional stress is not the underlying factor. Perhaps
this leads both to increased alcohol intake and to raised
blood pressure. This is an area in need of further investigation. If it turns out that emotional factors are important in producing sustained blood pressure elevations in the general population, the role of alcohol in
this outcome would still need to be defined. Is increased alcohol use merely a marker for psychological
problems, having no direct effect on blood pressure, or
does emotional stress raise blood pressure, at least in
part, through an intervening pharmacological effect of
alcohol?
Withdrawal
Another question that has been raised is whether the
higher blood pressures in drinkers are largely due to
withdrawal from alcohol rather than alcohol itself. It
may be that a substantial number of heavy drinkers
abstain from alcohol for a day or so in preparation for
our multiphasic checkup or the other study examinations that have found this association. We agree that
this is an important question that has not yet been
answered. For example, the Lipid Research Clinics'5
presented preliminary data purportedly supporting the
withdrawal hypothesis; drinkers who, in a separate
dietary recall, reported drinking alcohol during the
prior 24 hours had slightly higher blood pressures than
drinkers of similar amounts who denied intake in the
prior 24 hours (difference not statistically significant).
It is not clear to us that the former group was more
withdrawn from alcohol than the latter when
examined.
The withdrawal issue was put into sharper focus by
the study of Saunders et al. '6 of 96 alcoholics admitted
to medical wards in Birmingham, England, for detoxification. At the time 48% were hypertensive and the
blood pressure level was related to the severity of alcohol-withdrawal symptoms. Most of the hypertensives
Possible Direct Mechanisms
The acute effects of small doses of ethanol (in the
range of 30 to 75 ml of alcohol or 2/2 to 6 ounces of 80
proof liquor), were studied decades ago.17 These produce a slight transient increase in heart rate and cardiac
output with some increase in blood pressure, particularly systolic. Significant effects on blood pressure are
not always found, however.18 Although cutaneous vascular resistance decreases, producing a flushed appearance, there is little change in total peripheral resistance
because of a compensatory vasoconstriction in the viscera. Large doses, sufficient to produce central respiratory depression, also depress the cardiovascular system leading to hypotension and bradycardia through a
combination of reflex mechanisms and myocardial effects. The chronic physiologic effects of alcohol are
not well understood and need further study. At this
stage it is difficult to muster physiological evidence
either to support or refute the notion that chronic alcohol use raises blood pressure. Possible mechanisms
that have been suggested are those mediated by the
central or autonomic nervous systems, direct effects on
the heart or blood vessels, chronic increases in corticosteroid levels, and a chronic hypermetabolic state.
1-148
PERSPECTIVES IN HYPERTENSION
SUPPL III, HYPERTENSION, VOL 4, No 5, SEPTEMBER-OCTOBER 1982
Downloaded from http://hyper.ahajournals.org/ by guest on June 15, 2017
Alcohol and the Outcomes of Hypertension
Two of the main complications of hypertension,
coronary heart disease and stroke, have been studied in
relation to alcohol consumption. The results have been
of great interest in recent years, particularly for coronary disease. Most of these studies have found a negative association between alcohol use and coronary
heart disease. This may at first seem surprising when it
is remembered that alcohol is positively associated
with two major coronary risk factors, cigarette smoking and hypertension. There are various epidemiologic
methods for dissecting out relationships, and when
these are applied the confounding effects of smoking
and hypertension can be removed.
First, consider the outcome of our study of four
groups of multiphasic examinees. We attempted to
match each of the 2084 persons in our original large
study group who reported six or more drinks per day
with one who drank three to five drinks per day, one
who drank two or fewer drinks per day and a nondrinker. Matching was for age, sex, race, cigarette
smoking, and date of examination.19 Hospital followup was accomplished by computer search of magnetic
tapes containing the 1971-1976 hospital records of all
hospitalizations in our prepaid plan in Northern
California.
The incidence of hospitalization for hypertension,
all coronary heart disease, acute myocardial infarction
and stroke, according to alcohol category, is shown in
table 1. The trend of hospitalization for hypertension
generally corresponded to that which we observed for
hypertension at the multiphasic examination in our
cross-sectional data. An inverse relation was observed
for coronary disease and one of its major components,
acute myocardial infarction. For stroke the correlation
with alcohol consumption was direct, as it was for
hypertension itself.
We also performed a mortality follow-up on the
same subjects.20 Here the trends for death from complications of hypertension were not as simple as they
were for hospitalization. For coronary heart disease,
there was a U-shaped curve with the highest death rate
observed in the nondrinkers and the lowest in the twoor-fewer drink group. For stroke, the curve was an
inverted U with the highest death rate in the 3-5 drink
group and the lowest in both the zero and 6 + drink
groups. In another mortality study that we conducted,
in which the primary focus was on smoking,21 alcohol
drinking was positively correlated with total mortality
but showed a slight negative correlation with mortality
from coronary heart disease that was not statistically
significant.
The Honolulu Heart Program, which has been
studying men of Japanese birth or ancestry, also found
an inverse correlation of alcohol consumption with the
incidence of and mortality from coronary heart disease.22 This persisted when cigarette smoking, relative
weight, and other important coronary risk factors were
included in a multivariate analysis. The Honolulu
group subdivided their stroke incidence and mortality
data into hemorrhagic and thromboembolic categories.
TABLE 1. Incidence of Hospitalization for Selected Cardiovascular Conditions in Relation to Reported Alcohol Consumption
Reported no. ofdrinks per day
Person years of
observation.
1971-1976
Number of persons
hospitalized
Hypertension
Coronary heart
disease
Acute myocardial
infarction
Stroke
Incidence: persons
hospitalized
per 1000
person-years
Hypertension
Coronary heart
disease
Acute myocardial
infarction
Stroke
0
$ 2
3-5
6+
8436
8610
8244
7920
33
40
47
59
112
84
80
74
54
26
46
36
31
33
33
29
3.9
4.6
5.7
7.4
13.3
9.8
9.7
9.3
6.4
3.1
5.3
3.4
4.4
3.8
4.2
4.2
Alcohol consumption showed a clear positive correlation with the subsequent development of hemorrhagic
stroke but not with the thromboembolic variety. It
seems reasonable to interpret this as reflecting the
more exclusive relation to hypertension of hemorrhagic than of thromboembolic stroke. Although blood
pressure is important in thrombotic strokes, alcohol's
metabolic effects may exert a counterbalancing protective influence against the occlusive atherosclerotic
process as it might for coronary heart disease. The
Honolulu investigators suggested that the stronger relation to hemorrhagic stroke was not entirely explained
by effects of alcohol on blood pressure.
Although population studies have suggested a negative relation and possibly protective effect of use of
small or intermediate amounts of alcohol against coronary heart disease,2-1"27 the finding is not unanimous
with respect to heavier drinking. Most contrasting evidence comes from studies of so-called "problem
drinkers," those whose alcohol consumption is relatively quite high and associated with antisocial behavior or difficulties in employment. Problem drinkers
studied have been identified among U.S. employees of
a public utility7 and a chemical company3 and among
Swedish twins27 and a population sample in Sweden.28
Unfortunately, many of these studies did not control
for cigarette smoking. There may be other reasons for
this contradiction yet to be identified. In studies of the
outcome of alcohol drinking we advocate classifying
the subjects by amount of alcohol consumed per day or
other time interval whenever possible and avoiding
judgmental terms such as "heavy," "moderate," or
ALCOHOL, TOBACCO, AND HYPERTENSION/Fnerf/na/i et al.
"excessive." Presence or absence of problem behavior is also a characteristic worth noting whenever
possible.
variation among different age-sex groups. For example, in our study group about 25% of the white men in
their fifties drank three or more drinks per day. Given
the same relative risk of 1.5, their population attributable risk would be 11%, or over twice as great as for all
subjects combined. Finally, any underestimation of
drinking habits would make these estimates conservative by reducing apparent relative risks.
Downloaded from http://hyper.ahajournals.org/ by guest on June 15, 2017
Potential Public Health Implications
If we assume that it will eventually be shown that
alcohol does raise blood pressure chronically, it is
worthwhile considering what proportion of hypertension would be due to alcohol ingestion. We can do this
in two ways. First, we can determine the proportion of
alcohol drinkers who have hypertension because of
alcohol, and, second, we can determine the proportion
of the entire population who have hypertension because of alcohol.
Altogether, persons drinking three or more drinks
per day have a relative risk (r) of having hypertension
of about 1.5 compared to persons drinking two or
fewer (including none) drinks per day. The fraction of
disease in the 3 + drinkers that is attributable to
drinking, assuming causality, may be estimated29 by
the expression
Cigarette Smoking and Blood Pressure
Experimental studies on man and animals have
shown that an acute effect of smoking or nicotine administration is to produce small increases in blood
pressure and heart rate, presumably due to the resulting
release of catecholamines.31 Nevertheless, most epidemiologic studies have shown that the blood pressure
of cigarette smokers is similar to or even slightly lower
than that of nonsmokers.31 Perhaps some of this has to
do with the fact that cigarette smokers tend to be thinner than nonsmokers, but it should also be remembered
that smokers tend to consume more alcohol than nonsmokers, so that a blood-pressure-lowering effect of
cigarette smoking, if actually present, might be
masked as a result.
Our own data33 support the paucity of a relation
between smoking and blood pressure (table 2). The
mean diastolic blood pressure was 1 mm Hg higher in
nonsmokers than smokers in each sex-race group.
Among women, the mean systolic measure was 1 or 2
mm hg higher in nonsmokers; among men, it was 1 or
2 mm Hg lower in nonsmokers. In comparing persons
who quit with persons who persisted in cigarette smoking, the mean blood pressure changes between successive examinations snowed only small disparities that
were in different directions in various race-sex
groups.33 To better assess the net chronic effects of
smoking on blood pressure, more studies are needed in
which the associated factors, alcohol use and body
build, are taken into account.
Of interest is the possibility that chewing tobacco
may have a different effect on blood pressure than
smoking it. In a study of male college students in
Texas,34 22 tobacco chewers had mean systolic and
diastolic pressures respectively, 9 and 4 mm Hg higher
than 69 nonchewers of tobacco (p < 0.01). Drinking
habits were not mentioned. If we may conclude by
briefly digressing from science to esthetics, it is reassuring to note that California, not Texas, is the main
source of social trends among U.S. youth.
, which in this case equals
= _ . Thus, also assuming reversability, about
1.5
3
one-third of hypertensives among these heavier drinkers might benefit if they drank two or fewer drinks
per day. From the population standpoint, with p being
the proportion of the population drinking three or
more drinks per day, which in our group was about
10%, the fraction of hypertension attributable to this
level of drinking is estimated30 by the expression
p(r - 1)
0.1(1.5 - 1)
_
,
n .
——
—=—
1 = n0.05.
Thus, aboutt
pr + (l - p)
0.15 + 0.9
5% of the hypertension in our study group might be
due to increased alcohol intake. If one has the courage
to generalize these estimates, then perhaps over 1 million cases of hypertension in the United States are due
to higher levels of alcohol use.
It should be emphasized that the calculations above
are based on the assumption, not fully proven, that
alcohol is a cause of hypertension rather than being
associated in a secondary way. Furthermore, the fact
that alcohol may have an opposite effect on a major
outcome of hypertension, i.e., coronary disease, must
also be factored into estimates of public health effects.
Further, this estimate of the so-called population attributable risk is an average; there would be marked
—
TABLE 2.
111-149
Age-Adjusted Mean Blood Pressure (mm Hg) by Race, Sex, and Smoking Status
Black \vomen
White women
Black: men
White men
S
N
S
N
S
N
S
N
1000
1546
4359
7956
765
376
3268
2819
Systolic BP
136
137
128
130
141
140
135
133
Diastolic BP
87
88
80
81
86
87
80
81
Total number
S = smokers; N = nonsmokers; BP = blood pressure.
Ill-150
P E R S P E C T I V E S IN H Y P E R T E N S I O N
S U P P L III, HYPERTENSION, V O L 4 , N o 5 , S E P T E M B E R - O C T O B E R
References
Downloaded from http://hyper.ahajournals.org/ by guest on June 15, 2017
1. Kannel WB, Sorlie P: Hypertension in Framingham. In: Epidemiology and Control of Hypertension, edited by Paul O.
New York: Stratton, 1974, pp 553-92
2. Clark VA, Chapman JM, Coulson AH: Effects of various
factors on systolic and diastolic blood pressure in the Los
Angeles Heart Study. J Chronic Dis 20: 571, 1967
3. D'Alonzo CA, Pell S: Cardiovascular disease among problem
drinkers. J Occup Med 10: 344, 1968
4. Myrhed M: Blood pressure. In Alcohol consumption in relation to factors associated with ischemic heart disease. Acta
Med Scand (suppl) 567: 40, 1974
5. Ramsay LE: Liver dysfunction in hypertension. Lancet 2: 111,
1977
6. Beevers DG: Alcohol and hypertension. Lancet 2: 114, 1977
7. Dyer A, Stamler J, Paul O, Berkson DM, Lepper MH,
McKean H, Shekelle RB, Lindberg HA, Garside D: Alcohol,
cardiovascular risk factors, and mortality in two Chicago epidemiologic studies. Circulation 56: 1067, 1977
8. Mathews JD: Alcohol use, hypertension and coronary heart
disease. Clin Sci Mol Med (suppl) 51: 661, 1976
9. Klatsky AL, Friedman GD, Siegelaub AB, Gerard MJ: Alcohol consumption and blood pressure: Kaiser-Permanente multiphasic health examination data. N Engl J Med 296: 1194,
1977
10. Mitchell PI, Morgan MJ, Boadle DJ. Batt JE, Marstrand JL,
McNeil HP, Middleton C, Rayner K, Lickiss JN: Role of
alcohol in the aetiology of hypertension. Med J Aust 2: 198,
1980
11. Collen MF, Davis LS: The multitest laboratory in health care. J
Occup Med 11: 355, 1969
12. Weissman A, Anderson R: Characteristics of health plan membership. In: The Kaiser-Permanente Medical Care Program: A
Symposium, edited by Somers AR. New York: The Commonwealth Fund, 1971, pp 33-43
13. Cahalan D, Cisin IH, Crossley HM: American Drinking Practices. New Haven: Yale University Press, 1969
14. Geboers J, Bellens A, Kesteloot H: Alcohol, gamma-glutamyl-transpeptidase and blood pressure (abstr). CVD Epidemiology Newsletter (American Heart Association) No 31, p
40, January, 1982
15. Wallace RB. Lynch CF. Pomrehn PR, Criqui MH, Heiss G:
Alcohol and hypertension: epidemiologic and experimental
considerations. Circulation 64 (suppl III): 111-41, 1981
16. Saunders JB, Beevers DG, Paton A: Factors influencing blood
pressure in chronic alcoholics. Clin Sci 57: 295s, 1979
17. Grollman A: The influence of alcohol on the circulation. Q J
Stud Alcohol 3: 5, 1942
18. Ramsay LE: Alcohol use and hypertension. Practical Cardiolo-
1982
gy 5: 27, 1979
19. Klatsky AL, Friedman GD, Siegelaub AB: Alcohol use and
cardiovascular disease: the Kaiser-Permanente experience.
Circulation 64 (suppl III): 111-32, 1981
20. Klatsky AL, Friedman GD, Siegelaub AB: Alcohol and mortality: a ten-year Kaiser-Permanente experience. Ann Intern
Med 95: 139, 1981
21. Friedman GD, Dales LG, Ury HK: Mortality in middle-aged
smokers and nonsmokers. N Engl J Med 300: 213, 1979
22. Kagan A, Yano K, Rhoads GG, McGce DL: Alcohol and
cardiovascular disease: the Hawaiian experience. Circulation
64 (suppl III): 111-27, 1981
23. Klatsky AL, Friedman GD, Siegelaub AB: Alcohol consumption before myocardial infarction: results from the Kaiser-Permanente epidemiologic study of myocardial infarction. Ann
Intern Med 8 1 : 294, 1974
24. Stason WB, Neff RK, Miettinen OS, Jick H: Alcohol consumption and nonfatal myocardial infarction. Am J Epidemiol
104: 603, 1976
25. Barboriak JJ, Rimm AA, Anderson AJ, SchmidhofferM.Tristani FE: Coronary artery occlusion and alcohol intake. Br
Heart J 39: 239, 1977
26. Hennekens CH, Rosner B, Cole DS: Daily alcohol consumption and fatal coronary heart disease. Am J Epidemiol 107:
196, 1978
27. Friberg L, Cederlof R, Lorich U, Lundman; T, de Faire U:
Mortality in twins in relation to smoking habits and alcohol
problems. Arch Environ Health 27: 294, 1973
28. Wilhelmsen L, Wedel H, Tibblin G: Multivariate analysis of
risk factors for coronary heart disease. Circulation 48: 950.
1973
29. Cole P, MacMahon B: Attributable risk percent in case-control
studies. Br J Prev Soc Med 25: 242, 1971
30. Levin ML. The occurrence of lung cancer in man. Acta Univ
Int Cancer 9: 531, 1953
31. United States Department of Health, Education, and Welfare;
Public Health Service: Smoking and Health: A Report of the
Surgeon General. DHEW Publication No (PHS) 79-50066.
Washington, DC: Government Printing Office 1979, pp 4-57,
4-58
32. Friedman GD, Siegelaub AB, Dales LG, Seltzer CC: Characteristics predictive of coronary heart disease in exsmokers before they stopped smoking: comparison with persistent smokers and nonsmokers. J Chronic Dis 32: 175, 1979
33. Friedman GD, Siegelaub AB: Changes after quitting cigarette
smoking. Circulation 61: 716, 1980
34. Squires WG, Bischoff S, Drummond D, HartungGH, Brandon
TA, Wasmund D: Blood pressure characteristics of oral
smokeless tobacco users (abstr). CVD Epidemiology Newsletter, American Heart Association No 31, p 44, January, 1982
Alcohol, tobacco, and hypertension.
G D Friedman, A L Klatsky and A B Siegelaub
Hypertension. 1982;4:III143
doi: 10.1161/01.HYP.4.5_Pt_2.III143
Downloaded from http://hyper.ahajournals.org/ by guest on June 15, 2017
Hypertension is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright © 1982 American Heart Association, Inc. All rights reserved.
Print ISSN: 0194-911X. Online ISSN: 1524-4563
The online version of this article, along with updated information and services, is located on the
World Wide Web at:
http://hyper.ahajournals.org/content/4/5_Pt_2/III143
Permissions: Requests for permissions to reproduce figures, tables, or portions of articles originally published in
Hypertension can be obtained via RightsLink, a service of the Copyright Clearance Center, not the Editorial
Office. Once the online version of the published article for which permission is being requested is located, click
Request Permissions in the middle column of the Web page under Services. Further information about this
process is available in the Permissions and Rights Question and Answer document.
Reprints: Information about reprints can be found online at:
http://www.lww.com/reprints
Subscriptions: Information about subscribing to Hypertension is online at:
http://hyper.ahajournals.org//subscriptions/