Eur. J. Epidemiol. 0392-2990

December 1988, p. 477-481

Vol. 4, No. 4

ALCOHOL CONSUMPTION AND BLOOD PRESSURE.

AN ITALIAN STUDY

M. PERITI *~, A. SALVAGGIO, G. QUAGLIA, L. DI MARZIO

*Clinica Medica Generale Universitgt degli Studi di Milano Ospedale "L. Sacco " Via G.B. Grassi 74, 20157 Milano, Italy

**Centro diagnostico Italiano via Saint Bon, 20 Milano, Italy

Key words: Alcohol - Blood

We studied the relationship between alcohol consumption and arterial pressure in 1190 subjects of both sexes aged between 18 and 63 years who were examined during the course of a program of preventive medicine organized by Centro Diagnostico Italiano. In 711 subjects who were not requested to alter their usual alcohol consumption we found a significant relationship between alcohol consumption and systolic arterial pressure, b+SE(b), 4.6 --+ 2.1 mmHg/100 g ethanol/day. In particular, males who were heavy drinkers (>_ 50 g_ethanol/day) presented significantly higher systolic pressure levels than the other men, d_+_SE(d), 3.7 ± 1.6 mmHg, whereas no significant differences were observed among the various classes of women subdivided according to alcohol intake (only 4.6% of the women consumed > 50 g ethanol/day). On the other hand, in 479 subjects who were requested to abstain from alcohol consumption during the three days preceding the examination, no significant relation was found between alcohol intake and arterial pressure. The difference between the systolic pressure levels of the male heavy drinkers and those of the male moderate and non-drinkers was only 0.1 mmHg. Excessive alcohol consumption, in this case, mainly in the form of wine, was therefore associated with higher systolic pressure levels. However, it seems that abstaining from alcohol for even a brief period may modify this relation considerably.

INTRODUCTION MATERIALS AND METHODS

Numerous studies have shown an association between regular alcohol consumption and elevated arterial pressure levels. Arterial pressure also appears to be strongly influenced by occasional alcohol intake, and even brief periods of abstinence seem capable of determining significant variations in pressure levels (15).

In the present study we examined the association between alcohol consumption and arterial pressure in 1190 Italians of both sexes. Some of the blood pressure readings were made after three days' abstinence from alcohol in order to identify effects unrelated to occasional consumption of alcohol or its abrupt suspension.

1 Corresponding author.

We studied the possible association between alcohol and arterial pressure in two groups of employees of companies which had agreed to an annual program of preventive medicine with Centro Diagnostico Italiano. Group I consisted of 711 subjects (473 male, 238 female) whose habitual alcohol intake was not restricted in any way.

The 479 subjects (381 male, 98 female) of group II were requested to abstain from alcohol consumption during the three days preceding examination, in order to evaluate, in parallel and independently, the hypothesis of a persistent elevation of arterial pressure related to habitual alcohol consumption. On a random basis, all the employees of a given company were either asked or not asked to abstain from alcohol for

477

Periti M. et al. Eur. J. Epidemiol.

three days, as part of the preventive medicine program.

The subjects of both groups were all voluntary participants in the study, and constituted 85% and 75% respectively of the subjects invited to take part.

The examinations of the subjects in both groups were performed by medical and paramedical personnel unaware of the aim of the study. Each subject underwent a physical examination during the course .of which an 18-page questionnaire was compiled. Blood pressure, anthropometric measure- ments, ECG and chest X-ray were also obtained, and some instrumental tests and laboratory tests were performed. Age and weight characteristics of the two groups of subjects studied are reported in Table 1. Weight is expressed as percentage of ideal weight (13).

Arterial pressure was measured with the subject in the supine position using a Riva-Rocci sphygmo- manometer with mercury column and standard cuff. Diastolic pressure was measured on the basis of disappearance of sound (Korotkoffs phase V). Three measurements were taken and the lowest recorded.

TABLE 1. - Characteristics of the study groups.

Group I Group II*

Men + women

number of subjects 711 479

age (years): mean 41.6 38.6

SD 9.9 9.5

range 18- 63 18- 62

weight % mean** 104.3 103.5

range 93 - 185 89 - 156

Men

number of subjects 473 381

age (years): mean 42.6 40.0

SD 10.0 9.2

weight % 104.5 103.5

Women

number of subjects 238 98

age (years): mean 38.9 32.7

SD 9.2 8.3

weight % 103.9 103.2

* Studied after three days' abstinence from alcohol. ** Calculated after logarithmic transformation to % of ideal weight.

478

The values found in the two groups are shown in Table 2.

Three items on the questionnaire were designed to investigate the form of the alcohol consumed: wine, beer or spirits.

The answers were expressed in fractions of a liter for wine and beer, and in number of glasses/day for spirits (30 ml/glass for strong liquors, 50 ml/glass for the others). The quantities of alcoholic beverages consumed were converted to grams of ethanol using Mallor's nomogran (12).

The subjects were subdivided according to their alcohol intakes as follows: non-drinkers, moderate drinkers (1-50 g ethanol/day), heavy drinkers (> 50 g ethanol/day).

The percentages of subjects in each of the above categories are shown in Table 2.

Multiple regression analysis was performed on the data with the subjects studied subdivided into classes (analysis of co-variance) (3, 19). The F tests were reported considering degrees of freedom as the denominator. P > 0.05 was considered significant. As a correction variable for the weight of the subjects studied, we used the logarithm of the percentage weight, and correction for weight refers to the logarithm of percentage weight.

TABLE 2. - Systolic (SBP) and diastolic (DBP) blood pressure and alcohol consumption in the subjects studied according to sex.

Men Women

Group I Number of subjects:

SBP (mmHg): mean

SD

DBP (mmHg): mean

SD

alcohol (g/day):

Group II Number of subjects:

SBP (mmHg): mean

SD

DBP (mmHg): mean

SD

alcohol (g/day):

473 238

134.7 128.3

17.1 14.2

87.4 83.8

9.8 8.4

0 16.9% 38.3%

1-50 54.8% 57.1%

>50 28.3% 4.6%

381 98

130.9 119.4

13.1 9.6

82.6 75.9

8.1 6.7

0 24.9% 46.9%

1-50 46.2% 46.0%

>50 28.9% 7.1%

Vol. 4, 1988 Alcohol and blood pressure in Italy

RESULTS

Systol ic arterial pressure (SBP) - group I

There was a linear correlation between alcohol consumption and SBP after correction for sex, age, weight, cigarette consumption (two rariables: _< 20 and > 20 cigarettes/day) and coffee (number of cups/day). SBP was increased by 4.6 ___ 2.1 mmHg/100 g ethanol/ day (F = 4.92, 1 df, P = 0.027), b _ SE(b).

Males who were heavy drinkers presented significantly higher systolic levels, after correction for age and weight, than the other men: d + SE(d), 3.7 _ 1.6 mmHg (F = 5.20, 1 df, P = 0.024). No significant differences were found in systolic levels among the women subdivided according to alcohol intake (Table 3). The low SBP observed in the female heavy drinkers refers to only 11 subjects and may be interpreted as a chance fluctuation; it was not significantly different from the SBP of the other women.

Diastof ic arterial pressure (DBP) - group I

No significant linear correlation was found between alcohol consumption expressed in grams of ethanol per day and DBP after correction for sex, age, weight, cigarette and coffee consumption: 2.3 ___ 1. 2 mmHg/100 g ethanol/day (F = 3.44, 1 df, P = 0.065). We observed no significant differences among DBP levels in males or females of the various alcohol consumption categories (Table 3).

Systolic a n d diastolic arterial pressure - group 11

We found no linear correlation between alcohol consumption expressed in grams of ethanol per day and either SBP or DBP after correction for sex, age, weight, cigarette and coffee consumption: SBP, 1.3 _ 2.0 mmHg/100 g ethanol/day (F = 0.42, 1 dr, P = 0.525); DBP, 0.5 _+ 1.3 mmHg/100 g ethanol/day (F = 0.15, 1 df, P = 0.703). No important differences were noted among the SBP and DBP levels of the men and

TABLE 3. - Systolic (SBP) and diastolic (DBP) arterial pressure of subjects studied according to ethanol consumption. The data are corrected for age and weight by analysis of co-variance.

Ethanol (g/day) 0 1-50 >50

Group I men Number of subjects: 80 259 134

SBP (mmHg): mean 124.8 123.1 127.2

SE 1.8 1.0 1.4

DPB (mmHg): mean 80.6 81.1 82.6

SE 1.0 O.6 0.8

w o m e n Number of subjects: 91 136 11 SBP (mmHg): mean 117.2 117.4 112.7

SE 1.3 1.1 3.9

DPB (mmHg): mean 79.6 79.6 79.1

SE 0.8 0.7 2.4

Group II men Number of subjects: 95 176 110

SBP (mmHg): mean 122.7 123.9 123.3

SE 1.2 0.9 1.1

DPB (mmHg): mean 78.5 79.4 78.9

SE 0.8 0.6 0.7

women Number of subjects: 46 45 7 SBP (mrnHg): mean 117.6 117.3 117.3

SE 1.4 1.4 3.6

DPB (mmHg): mean 75.1 77.3 73.0

SE 1.0 1.0 2.5

479

Periti M. et al. Eur. J. Epidemiol.

women in the various alcohol consumption categories (Table 3).

In particular, the SBP of the male heavy drinkers was only 0.1 ___ 0.8 mmHg higher than that of the other men, which is obviously not significant (F = 0.01, 1 df, P = 0.922). For the men in group I the difference between the heavy drinkers and the others was 3.7 ___ 1.6 mmHg, whereas for group II it was 0.1 ___ 0.8 mmHg, i.e. a difference of 3.6 ___ 1.8 mmHg which was significant at G test for differences between coefficients of regression (5). The differences between heavy drinkers and the other subjects were coefficients relating to binary (dummy) variables which considered classification of the subjects based on alcohol consumption (G --~ X? = 3.90, ldf, P = 0.049).

DISCUSSION

In 1974 Kannel and Sorlie (8), analyzing the data collected in the Framingham study, were already reporting a "modest but significant relationship of systolic pressure to alcohol intake independent of associated weight".

Subsequently Klatsky et al. (9) reported an increase o f > 5 mmHg in the systolic blood pressure of subjects who drink more than three glasses of spirits daily. These findings have recently been confirmed by other investigators, including Criqui et al. (5) and Mac Mahon et al. (11).

In the present study alcohol seemed to produce a hypertensive effect in males of limited duration, apparently without inducing irreversible modifications in pressure levels.

An earlier study performed on heavy drinkers (15) also showed a drop in pressure levels observed after a period of abstinence. In another study on heavy drinkers (17) the pressure level observed after a period of abstinence during hospitalization remained low two months after discharge in the subjects who did not start drinking again, whereas they increased in those who did.

Arkwright et al. compared the arterial pressures of lifelong non-drinkers and previously heavy drinkers who had stopped drinking, and did not find any significant differences (1).

Similarly, moderate drinkers with hypertension, who alternated three days of alcohol consumption with three days of abstinence, showed not only significant increases in both systolic and diastolic blood pressure during the period in which alcohol was consumed but also significant reductions during the periods of abstinence (16). Thus most of the studied cited (15-17) showed only a decrease of pressure levels following a short period in which alcohol consumption was suspended, but not the absence of a residual effect.

On the other hand, Arkwright's study (1) suggests that alcohol does not have a residual hypertensive effect although it did not provide precise information on the pattern of arterial pressure with time (alcohol

consumption was suspended spontaneously at an unspecified time before the pressure levels were recorded).

It must also be noted that the alcohol consumed by the subjects we studied was prevalently in the form of wine, a drink whose hypertensive effect has been questioned (5). Our results, however, indicate that wine, like spirits (5, 8, 9, 11) and beer (4), is capable of increasing blood pressure levels. Therefore, the hypertensive effect of ethanol would seem to be due to the quantity consumed and not to other qualities of the beverages.

There is still no clear explanation for the relationship between chronic alcohol consumption and arterial pressure. Some authors have attributed the effect of alcohol on blood pressure to elevated plasma catecholamine levels (14) and some to elevated cortisolemia (18, 20). Others, however, have not found modifications in either catecholamine or cortisol levels (2). Recently a low alpha-adrenergic response was observed following regular consumption of alcohol, hypothetically attributable to increased adrenergic activity (7).

Independently of the pathogenetic mechanism involved, alcohol appears to be a moderately important risk factor for hypertension. Although the modifications of the pressure levels associated with alcohol consumption are modest, they are capable of changing the classification, according to severity of hypertension, of a large number of subjects. It has also been hypothesized that the hypertension related to alcohol consumption may cause an increase in the mortality and morbidity for cerebrovascular accidents (6, 10).

Therefore, abstinence from alcohol or at least a reduced intake is recommendable, combined or not with pharmacologic treatment.

In our opinion alcohol consumption is an impor- tant variable to be considered in all epidemiologic studies on hypertension. In view of the apparent transience of the effect of alcohol on blood pressure, it might be preferable to investigate recent alcohol consumption.

However, if effects secondary to a persistent increase of pressure values are studied (e.g. organ damage), it might be more useful to considerer overall alcohol consumption. It also seems important to us that cigarette consumption be investigated, in addition to alcohol consumption, since in our study heavy alcohol consumption (over 50 g ethanol/day) was signficantly more frequent in the heavy smokers (over 20 cigarettes/day) regardless of their sex (males: X ~ = 26.78, 1 df, P <0.001; females: X ~ = 5.79, I df, P = 0.014) (Table 4).

In conclusion, it seems that excessive alcohol consumption, in any form, including wine, may determine significant elevations of arterial pressure. Furthermore, our data suggest that abstaining from alcohol even for only brief periods may be able to significantly modify, and perhaps nullify, the effects exerted by alcohol on arterial pressure.

480

Vol. 4, 1988 Alcohol and blood pressure in Italy

TABLE 4. - Percentage of non-smokers and smokers of up to and over 20 cigarettes/day according to alcobol consumption (subjects in groups I and II are considered together).

Non Smokers < 20 Smokers > 20 smokers cig./day cig./day

men

women

Number of subjects:

Alcohol (g/day):

Number of subjects:

Alcohol (g/day):

497 242 116

0 22.9% 17.3% 15.5%

1-50 53.9% 51.6% 35.3%

>50 23.1% 30.9% 49.1%

185 131 20

0 42.1% 41.2% 40.0%

1-50 52.9% 56.4% 45.0%

>50 4.8% 2.2% 15.0%

REFERENCES

1. Arkwright P.D., Beilin L.J., Rouse I., Armstrong B.K. and Vandongen R. 1982: Effects of alcohol use and other aspects of lifestyle on blood pressure levels and prevalence of hypertension in a working population. Circulation 66: 60-66.

2. Arkwright P.D., Bei#n L.J., Vandongen R et aL (1982): The pressor effect of moderate alcohol consumption in man: a search for mechanism. Circulation 66: 515- 519.

3. Armitage P. (1971): Statistical methods in medical research. Wiley, New York.

4. Cairns V., Keil U., Kleinbaum D., Doering A. and Stieber J. (1984): Alcohol consumption as a risk factor for high blood pressure. Munich Blood Pressure Study. Hypertension 6: 124-131.

5. Criqui M.H., Wallace R.B., Mishkel M. et al. (1981): Alcohol consumption and blood pressure. The Lipid Research Clinics Prevalence Study. Hypertension 3: 557-565.

6. Gill J.S., Zezulka A. V., Shipley L.J., Gill S.K., Beevers D.G. (1986): Stroke and alcohol consumption. N. Engl. J. Med. 315: 1041-1046.

7. Hones L.G., Reid J.L. (1985): Decreased vascular responsiveness to noradrenaline following regular ethanol consumption. Br. J. Clin. Pharmaco120: 669- 674.

8. Kannel W.B., Sorlie P. (1974): Hypertension in Framingham, epidemiology and control of hypertension. Edited by O. Paul. New York, Stratton Intercontinental Medical Book Corporation, pp. 553- 592.

9. Klatsky A.L., Friedman G.D., Siegelaub A.B. and GOrard M.J. (1977): Alcohol consumption and blood pressure. Kaiser - permanente Multiphasic Health Examination Data. N. Engl. J. Med. 296: 1194-1200.

481

10. Kozarerevic D., Mc Gee D., Vojvodic N. et al. (1980): Frequency of alcohol consumption and morbidity and mortality. The Yugoslavia cardiovascular disease study. Lancet i: 613-616.

11. Mac Mahon S.W., Blaeket R.B., Macdonald G.J. and Hall W. (1984): Obesity, alcohol consumption and blood pressure in Australian men and women. The National Heart Foundation of Australia Risk Factor Prevalence Study. J. Hypertension 2: 85-91.

12. Mallor C.S. (1970): Nomogram for calculating mass of alcohol in different beverages. Brit. Med. J. 3: 703.

13. Metropolitam Life Insurance Company (1959): New weight standards for men and women. Stat. Bull Metropol. Life Ins Co 40: 1-4.

14. Ogaia M., Mendelson J.H., Mello N.K., Majachrowicz E.H. (1971): Adrenal function and alcoholism. II. Catecholamines. Psycosom Med. 33: 154-180.

15. Potter J.F, Barman L.T., Saunders J.B., Ingram M.C. and Beevers D.G. (1983): Blood pressure and pressor mechanisms during alcohol withdrawal. J. of Hypertension 1 (suppl. 2): 97-99.

16. Potter J.F., Beevers D.G. (1984): Pressor effect of alcohol in hypertension. Lancet i: 119-122.

17. Saunders J.B., Beevers D.G., Paton A. (1981): Alcohol- induced hypertension. Lancet ii: 653-656.

18. Smalls A.G., Kloppenborg P. W., Njo K.T. et al. (1976): Alcohol-induced Cushingoid syndrome. Br. Med. J. 2: 1298.

19. Snedecor G.W., Cochran W.G. (1980): Statistical methods. 7th ed., Iowa State University Press, Ames, pp. 388-391.

20. Stokes P.E. (1973): Adrenocortical activation in alcoholics during chronic drinking. Ann. N.Y. Acad Sci 215: 77-83.