alcohol consumption and hypertension - NCBI

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John Wiley and Sons, 1981. 4. US Department of Health, Education, and .... Epidemiology of. Hypertension. New York: Grune & Stratton, 1967, pp 255-. 288. 45.


Alcohol abuse and hypertension are two important health concerns for the general US population. A review of the literature indicates, however, that black Americans are at greater risk of experiencing primary and secondary health and behavioral problems associated with these two concerns. Empirical evidence exists suggesting a relationship between alcohol consumption and hypertension and its related sequelae. Although the correlation is not of a dose-effect nature, the results of numerous longitudinal and other studies have suggested a positive relationship. Various implications exist in the treatment, control, and prevention of hypertension for highrisk groups. For example, existing health-care protocols may be modified for regular screening and monitoring of "excessive" alcohol

From the Department of Sociology, Howard University, Washington, DC. Dr. Livingston is at present a postdoctoral fellow, Department of Behavioral Science and Health Education, School of Hygiene and Public Health, Johns Hopkins University, Baltimore, Maryland. Requests for reprints should be addressed to Dr. Ivor L. Livingston, 14659 Tynewick Terrace, Silver Spring, MD 20906.

consumption patterns, especially of hypertensive and borderline hypertensive patients. Whenever possible, health-care counseling and education should be a necessary adjunct to treatment and prevention efforts to better control hypertension in the black community.

The notion that alcohol consumption may be related to hypertension is not new. It is over 65 years since Lian1 published a report on the prevalence of hypertension in relation to the drinking habits of French army officers. However, empirical study of the relationship between alcohol consumption and hypertension has not been as vigorously pursued as might be expected, given the benefits that could accrue from such a documented relationship. Neglect has been so complete that it has been said that no mention has been made of an alcohol-hypertension relationship in any of the standard textbooks on hypertension.2 This paper attempts to selectively review evidence that substantiates a relationship between alcohol consumption and hypertension. Before such evidence is examined, a brief overview of the indi-




vidual areas of alcohol use and abuse and hypertension will be presented. The review will, among other things, emphasize prevention and treatment implications for hypertension in high-risk groups. Black Americans have disproportionate prevalence rates (ie, compared with white Americans) for both alcoholism and hypertension. Focusing on blacks as a representative at-risk group in the US population, the paper will conclude with the importance of the suggested implications of an alcohol-hypertension relationship for them as a target group in the prevention and management of hypertension.

ALCOHOL ABUSE It has been stated that alcohol abuse is perhaps the number one problem in the United States today.3 Approximately 100 million Americans, or 68 percent of the population 18 years and older, are social drinkers. Of this number, 10 million either have a serious drinking problem or are chronic alcoholics.4 Alcohol contributes to more than 50 percent of all traffic accidents and causes more than 28,000 fatalities, as well as a huge number of injuries and immeasurable property damage each year.5 On a physiological basis, long-term drinking may eventuate in cancer, heart disease, and cirrhosis of the liver.3 Data have shown that alcohol can cause birth defects and mental impairment in offspring of mothers who drink while pregnant. A unique pattern of dysmorphology with mental impairment occurs in some offspring of women who consume alcohol heavily; this condition has been called the fetal alcohol syndrome.6 Alcoholism is a considerable problem for black Americans, ranking as the number one mental health problem in the black urban community.7 Studies indicate that blacks have a higher prevalence rate of alcoholism than their white counterparts. For example, Bailey and co-workers,8 in a study of an urban residential area, reported that the prevalence of alcoholism was 19 per 1,000. Blacks had a higher rate (men, 37 per 1,000; women, 20 per 1,000) than whites (men, 31 per 1,000; women, 5 per 1,000). There was a tendency for alcoholics to be concentrated among the group 130

with the least education. Also, alcoholics reported lower personal earnings, poorer housing, greater occupational and residential mobility, and more chronic illnesses than adults in general. Viamontes and Powell9 studied 100 black and 100 white male alcoholics who were hospitalized. Although both groups were from low socioeconomic backgrounds, blacks reported earlier drinking than whites and earlier loss of control over drinking. Drinking began for blacks at approximately 15.7 years, whereas for whites it was 19.0 years. Blacks reported on the average "loss of control" at 28.5 years, whereas whites reported "loss of control" at 32.9 years. The effect of early drinking and greater chronicity of alcoholism has had a tremendous impact on blacks, especially the young black male, in terms of accidents, criminal assaults, other conflicts, and homicides.'0 It has been reported that alcohol-related homicide rates are higher for black males under 30 years of age than for white males of the same age." Black Americans also suffer disproportionately by having higher rates of cancer,'2"13 obstructive pulmonary disease and severe malnutrition, 4 intestinal disaccharidase activities,'5 birth defects,'6 hypertension risk,'7 and cirrhotic deaths.'8"19 Closer scrutiny of these health problems highlights the severity of alcohol-related illness in black Americans. For example, although cirrhotic mortality rates have generally declined each year since peaking in 1973, they are still disproportionately high among black Americans.'9 According to the National Institute on Alcohol Abuse and Alcoholism (NIAAA),'9 some cities report the cirrhotic mortality rate among black males, aged 25 to 34 years, to be 10 times higher than that for white males of the same age. Other reports suggest that when ages are taken into consideration, the cirrhotic mortality rate for black Americans is nearly twice that for white Americans.'8

PREVALENCE OF HYPERTENSION Hypertension, or high blood pressure, is a mass public health problem in the United States. It is said that, depending on the criteria used to define it, hypertension affects 23 to 60 million Ameri-



cans.20 Approximately 35 million Americans have definite high blood pressure (ie, blood pressure of 160/95 mmHg or greater); another 25 million are estimated to have borderline hypertension (ie, blood pressure of 140/90 to 159/94 mmHg).21 Taken together, these figures represent approximately one fourth of the entire US population.21 Nearly 90 percent of all hypertension is diagnosed as "essential." Essential hypertension, ie, hypertension of unknown etiology,22 can be controlled but not cured.23 It should be stated, however, that control of hypertension has been shown to be effective in delaying cardiovascular and cerebrovascular sequelae and prolonging life.24'25 The prevalence of hypertension increases with advancing age, and serious side effects are associated with uncontrolled hypertension. For example, high blood pressure is the single greatest risk factor for stroke,26 and a contributing factor in at least one third of all coronary cases.27'28 Compared with the general US population, black Americans are disproportionately afflicted with both hypertension and alcoholism.29 It was aptly suggested by the Fourth Special Report to the United States Congress on Alcohol and Health19 that the rate of hypertension is further complicated by drinking. Hypertension is of particular concern for black Americans. Data derived from the National Health Survey and other reports show that the prevalence of hypertension is twice as high among blacks as compared with whites for both sexes and for all age groups.3G32 The destructive sequelae of hypertension are disproportionately reflected in the black population. For example, death rates for cardiovascular disease are about two times higher for black women than for white women and are approximately 30 percent higher for black men than white men. The race differentials vary according to age, with greater variations occurring at younger ages than at older ages.31'32 It has been reported that, with age adjustment to the US population, the incidence of stroke is 5.8 per 1,000 among black men and women, with rates of 4.7 for white men and 1.2 for white women.33 The pattern of target organ damage likely in the black hypertensive is somewhat different from damage in the white hypertensive. For example, black hypertensives are more likely than white hypertensives to show electrocardiographic

and radiographic evidence of left ventricular enlargement.34'35

ALCOHOL-HYPERTENSION RELATION Issues Influencing Study The general relationship of alcohol to cardiovascular disorders has interested researchers for centuries. According to Klatsky and colleagues,'7 however, investigators have failed to recognize that the relation of alcohol habits to each cardiovascular condition (eg, cardiomyopathy, angina pectoris, myocardial infarction, sudden cardiac death, or hypertension) consists of features unique to each condition and, as such, must be considered separately. In the case of the alcohol-hypertension relation, a major obstacle to establishing a more definitive association has been the difficulty of differentiating the effects of alcohol from other life-style components. For example, heavy drinkers are more likely to smoke than teetotallers and light drinkers, and, depending on race and sex, may weigh more. 17'36-39 Heavy drinkers tend to be older, and their patterns of physical activity, dietary preferences, and use of stimulants may be somewhat different from those of teetotallers.40 It has been long thought that in healthy human beings alcohol doses equivalent to two-to-five ordinary drinks (ie, 30 to 75 mL of alcohol) produce slightly increased heart rate, blood pressure (systolic and diastolic), and cardiac output.41 It has been suggested, however, that blood pressure elevation in persons who use large amounts of alcohol may be due primarily to alcohol withdrawal than direct alcohol action.42 Although controlling for various confounders is a major issue in assessing the alcohol-hypertension relation, perhaps it is controlling for physiological confounders that is the most difficult. It is unclear how much of blood pressure change and elevation is the direct effect of alcohol in the circulatory system and how much is caused by indirect nervous system regulation. It has been suggested in the case of severe intoxification that the nervous system predominates in contributing to low blood pressure, slow heart rate, and ultimately, death from cardiac standstill.43




Documentation of Alcohol-Hypertension Relation Notwithstanding the potentially obscuring effects of various confounders, several studies have reported significant associations between alcohol consumption and hypertension. Examples of such studies include a prospective epidemiological investigation,44-46 a case control study of "problem drinkers,"47 and a study of twins.48 Epidemiological studies have been conducted to assess the alcohol-hypertension relation. The largest population-based study of this kind, involving 83,000 individuals, was conducted by Klatsky and co-workers'7 at Kaiser Permanente in California. The results of the study indicated that men and women who consumed three or more drinks per day (ie, approximately 45 grams or more of ethanol) had higher mean systolic blood pressures and a substantially higher prevalence of hypertension than the controls. Perhaps of greater importance was their finding that the association of drinking and blood pressure was independent of the customary confounders of age, sex, race, smoking, coffee use, former heavy drinking, educational attainment, and adiposity. Other studies (eg, Stokes et a149) have shown by statistical comparisons and multiple-regression analysis that associations between alcohol consumption and blood pressure can be discerned independent of the aforementioned confounders. The findings of Klatsky and colleagues'7 concurred with the results of other studies (eg, Kannel and Sorlie,45 Clark et a146), suggesting that individuals who had one or two drinks per day had approximately the same or slightly lower blood pressure than teetotallers. In addition, it was reported that males and females who took three or more drinks daily had higher systolic and diastolic blood pressures than nondrinkers. These relationships were again independent of the sociodemographic and behavioral confounders previously mentioned. Klatsky et al'7 also reported a "threshold" effect; the blood pressure relationship was positive up to six or eight drinks a day for whites and Asians, and up to three to five drinks a day in blacks. Among black men and women who had three or more drinks daily, the prevalence of hypertension (ie, defined as blood pressure of 160/95 mmHg or higher) was increased by about 50 percent. Other studies (eg, Kannel and Sorlie45) have 132

also reported a threshold effect associated with the alcohol-hypertension relation. In still another study49 involving 21,000 clients of a health-screening service, when partial regression coefficients obtained by multiple regression analysis were used to adjust for differences in age, adiposity, and smoking habit, a constant and proportionate elevation of blood pressure with increasing alcohol consumption was found, from low levels of consumption (ie, 1 to 6 drinks per week) up to about 500 g per week (ie, 7 drinks per day).50 A study by Arkwright and co-workers38 contributed additional evidence for an alcohol-hypertension relation. Using a population of 491 employed males between the ages of 20 to 45, this study sought to assess the relationship between alcohol consumption and blood pressure while controlling for various confounders such as age, obesity, cigarette smoking, and physical activity. The results revealed that average weekly alcohol consumption correlated with systolic blood pressure (r = 0.18), but not with diastolic blood pressure. Contrary to other reports,17,45'46 systolic blood pressure increased progressively with increasing alcohol consumption without obvious threshold effect. In moderate and heavy drinkers (ie, 53 percent of the population studied), the prevalence of systolic hypertension (ie, 140 mmHg) was four times that of teetotallers. This alcohol-systolic blood pressure relation was again independent of the aforementioned confounding factors. ,

Possible Explanations Direct action on the central nervous system seems the most common explanation for the alcohol-hypertension relation. In vulnerable individuals, alcohol may have a sustained pressor action by interfering with central inhibitory pathways controlling vasomotor centers (analogous to alcohol's action on higher cortical function, which leads to loss of emotional control). Pressor effects might then be mediated by neural and humoral mechanisms similar to those in acute "stress" reaction induced by alcohol.51'52 Reports of intervention studies have also contributed information on a paradoxical relationship between alcohol consumption and hypertension. Henningsen et al53 reported a decrease in blood pressure following alcohol withdrawal, indicating



ASSOCIATION, VOL. 77, NO. 2, 1985


that reduction or cessation of antihypertensive drug treatment might be possible in alcoholic hypertensive patients. In another study, Saunders et al51 observed 132 alcoholic patients whose daily consumption exceeded 80 grams. They reported a significant correlation between blood pressure and mean daily alcohol intake and between the level of blood pressure and the severity of alcohol withdrawal symptoms. In most patients blood pressure fell to normal after abstinence, remaining so for at least a year in those who continued to abstain, but rising in those who started to drink again. Arkwright and colleagues,38 believed that because alcohol has widespread biologic effects, its action on blood pressure control mechanisms may be multiple and complicated by interactions with other factors. Therefore, the central pressor influence of alcohol may be countered to some extent by its action as a peripheral vasodilator, perhaps accounting for its effect predominately on systolic rather than diastolic pressure in the relatively young population.54 The finding that blood pressure returns to normal with abstinence suggests that alcohol-induced elevations are not fixed and do not necessarily lead to a continuing rise of blood pressure over a long period of time. Longitudinal studies of factors associated with blood pressure increases over a well-defined follow-up period suggest that alcohol is not a major cause of the increases.55 This finding, however, cannot be taken as an indication of fewer long-term sequelae in patients with alcoholinduced hypertension, because the age-specific death rate is high in heavy drinkers, and a direct relationship with the higher blood pressure in alcoholics has been reported in other studies.56

IMPLICATIONS Although this paper attests that both alcohol abuse and hypertension are important fields of inquiry, the author believes that hypertension should be the outcome phenomenon of interest. Health care providers and other related personnel should become more cognizant of various treatment, management, and prevention implications associated with hypertension, especially for black Americans. As US blacks exhibit a disproportionate prevalence of both alcoholism10 and hyper-

tension,29 health-care information disseminated in the black community regarding the control of hypertension by a monitoring of alcohol consumption should have a corollary effect of controlling alcohol and its related problems in the black community. An inverse relationship has been reported between socioeconomic position and elevated blood pressure57'58; it is, therefore, imperative that the information, whether patient-oriented or communityoriented, be directed especially to blacks of low income and education, who are at greatest risk. Whatever the approach, blacks should be informed of important facts concerning hypertension.59 It is also necessary for health information to be distributed in communities in a manner that will facilitate the greatest amount of attitude change in the desired direction.57 Pharmacological treatmern of hypertension can substantially reduce the occurrence of cardiovascular25'60 and cerebrovascular mortality and morbidity in the general population. According to Saunders et al,2 cerebrovascular disease represents a major complication of hypertension and is the leading cause of death in heavy drinkers. Kozararevic et al6l reported that, although alcohol consumption was inversely related to coronary heart disease, the overall risk of dying increased with alcohol intake due to stroke. The control of hypertension would result in the reduction of stroke (which takes a heavy toll on the black population33) and other hypertension-related sequelae. It is known, however, that there are various disincentives associated with the current treatments for hypertension that could contribute to a lack of better control. Some disincentives are the large number of potential subjects, high cost of long-term therapy, drug side effects, behavioral repercussions of using medication on a continuing basis, and noncompliance with prescribed medication.62 As the alcohol-hypertension relation becomes more definitive and health care providers more aware of the disincentives associated with the current pharmacological treatment of hypertension, there should be a more vigorous effort to ascertain what factors affect the alcoholhypertension relation. Possible associative factors that could be explored are sociopsychological stress,63 hereditary predilection for both alcohol and hypertension, and alcohol withdrawal (which




is associated with increased heart rate and blood pressure in some heavy drinkers).42 Diagnosticians, health educators, counselors, and related personnel should be aware of factors that could influence the alcohol-hypertension relation. For example, it has been reported that many features of alcohol withdrawal are suggestive of a hyperadrenergic state64 and can be controlled by beta-adrenergic blocking drugs.65 It has also been suggested that excessive sodium ingestion from alcoholic drinks, such as beer, may also be implicated.66 Routine screening of the at-risk black, in clinics, hospitals, or health fairs, for "appreciable levels" of alcohol consumption becomes even more significant in view of reports that a sustained reduction in blood pressure has been seen in response to abstinence from alcohol, ie, even in patients who had previously required anti-hypertensive drugs.51 Saunders et al5' reported that strict abstinence from alcohol may not be necessary, but it is advisable to limit alcohol intake to not more than 20 to 30 grams per day. This latter point is crucial because treatment with anti-hypertensive drugs is usually of no avail while patients continue to drink heavily.53'67 Irrespective of the possible effect that other factors may have on the hypertension, the effects of alcohol alone warrant a modification in approach regarding the treatment, control, and prevention of hypertension, especially for the high-risk black population. Screening for "excessive" drinking, especially in hypertensive patients, must now become an essential and routine part of the healthcare provider protocol in the black community and elsewhere. It is hoped that a greater appreciation of the implications associated with the alcoholhypertension relation will, with other past and future endeavors, serve to make hypertension less of a public health problem, especially for black community residents.

Literature Cited 1. Lian C. L'alcoolisme cause d'hypertension arterielle. Bull Acad Nati Med (Paris) 1915; 74:525-528. 2. Saunders JB, Beeves DG, Patton A. Alcohol and hypertension. Circulation 1982; 65:1038-1039.


3. Sorochan WD. Promoting Your Health. New York: John Wiley and Sons, 1981. 4. US Department of Health, Education, and Welfare. Blood Pressure of Adults by Race and Area, United States, 1960-1962. National Health Survey, National Center for Health Statistics, series 11, No. 5, 1964. 5. Hafen BQ. Alcohol: The Crutch That Cripples. New York: West Publishing, 1977. 6. Jones KL, Smith DW. The fetal alcohol syndrome. Teratology 1975; 12(1):1-10. 7. Yamamoto J, Steinberg A. Ethnic, racial, and social class factors in mental health. J Natl Med Assoc 1981; 73: 231-240. 8. Bailey MB, Haberman PW, Alskne H. The epidemiology of alcoholism in an urban residential area. Q J Studies Alcohol 1965; 26(1):19-40. 9. Viamontes JA, Powell BJ. Demographic characteristics of black and white male alcoholics. Int J Addiction 1974; 9:489-494. 10. National Institute on Alcohol Abuse and Alcoholism. Biomedical Consequences of Alcohol Use and Abuse and Social Implications of Alcohol Abuse. Fourth Special Report for the US Congress on Alcohol and Health, Rockville, Md, 1981. 11. Harper FD. Alcohol use among North American blacks. In: Israel Y, Glaser FB, Kalant H, et al, eds. Research Advances in Alcohol and Drug Problems, vol 4. New York: Plenum Press, 1977, pp 349-366. 12. Keller AZ. Liver cirrhosis, tobacco, alcohol, and cancer among blacks. JAMA 1978; 70:575-580. 13. Tuyns AJ. Alcohol and cancer. Alcohol Health and Research World 1978; 2(4):20-31. 14. Moore MA, Merson MH, Charache P, Sherpard RH. Characteristics and mortality of outpatients' acquired pneumonia. Johns Hopkins Med J 1977; 140(1):9-14. 15. Perlow W, Baraona E, Lieber CS. Symptomatic intestinal disaccharidase deficiency in alcoholics. Gastroenterology 1977; 72(4):180-200. 16. Raftos J. The difficult hypertensive. Drugs 1976; 11:55. 17. Klatsky AL, Friedman GD, Siegelaub AB, Gerard MJ. Alcohol consumption and blood pressure. N EngI J Med 1977; 296:1194-1200. 18. Alcohol Epidemiologic Data Systems (AEDS). Cirrhosis of the Liver Mortality in the United States, Each State and County, and Selected SMSAs. US Alcohol Epidemiologic Data Reference Manual, Section 2. Rockville, Md: National Institute on Alcohol Abuse and Alcoholism, December 1980. 19. National Institute on Alcohol Abuse and Alcoholism. Biomedical Consequences of Alcohol Use and Abuse and Social Implications of Alcohol Abuse. Fourth Special Report to the US Congress on Alcohol and Health, Rockville, Maryland, 1981. 20. Rice DP, Kleinman JC. National health data for policy planning. Health Policy Educ 1980; 1:129-141. 21. Hamburg DA, Elliott GR, Parron DL. Health and Behavior: Frontiers of Research in the Behavioral Sciences. Washington, DC: National Academy Press, 1982. 22. Weiner H. Essential Hypertension. Psychobiology of Human Disease. New York: Elsevier, 1979. 23. Stamler J, Schoenberger JA, Shekelee RB, Stamler R. The Problem and Challenge. In the Hypertension Handbook. West Point, Pa: Merck & Co, 1974. 24. Veterans Administration Cooperative Study Group on Antihypertensive Agents. Effects of treatment on morbidity in hypertension: II. Results in patients with blood pressure averaging 90 through 1 14 mmHg. JAMA 1970; 213:



1143-1152. 25. Hypertension Detection and Follow-up Program Cooperative Group. Five-year findings of the Hypertension Detection and Follow-Up Program. JAMA 1979; 242:25622577. 26. Kaplan NM. Clinical Hypertension. New York: Medicom, 1973. 27. Kannel WB, Schwartz MJ, McNamara PM. Blood pressure and risk of coronary disease: The Framingham Study. JAMA 1969; 54:43-52. 28. Kannel WB, Castelli WP, McNamara PM, et al. Role of blood pressure in the development of congestive heart failure: The Framingham Study. N Engl J Med 1972; 16: 781-787. 29. Shade BJ, Nichols BL. Ethnic stress: Some sociological and intracultural aspects. In: Day S, ed. Life Stress, a Comparison to the Life Sciences. New York: Van Nostrand Reinhold Co, 1982. 30. US Department of Health, Education, and Welfare. Blood Pressure of Adults by Race and Area, United States, 1960-1962. National Health Survey, National Center for Health Statistics, series 11, No. 5, 1964. 31. McDonough JR, Garrison GE, Hames CG. Blood pressure and hypertensive disease among Negroes and whites. Ann Intern Med 1964; 61:208-228. 32. Comstock GW. An epidemiologic study of blood pressure levels in a biracial community in the southern United States. Am J Hygiene 1957; 65:271-278. 33. Heyman A, Karp HR, Heyden S. Cerebrovascular disease in the biracial population of Evans County, Georgia. Arch Intern Med 1978; 128:949-956. 34. Cassel JC. Review of 1960 through 1962 cardiovascular disease prevalence study. Arch Intern Med 1971; 128: 890-895. 35. Hypertension Detection and Follow-Up Program Cooperative Group. Sex and race difference in end organ damage among 10,940 hypertensives, abstracted. Am J Cardiol 1978; 41:402. 36. Gyntelberg F, Meyer J. Relationship between blood pressure and physical fitness, smoking and alcohol consumption in Copenhagen males aged 40-59. Acta Med Scand 1974; 195:375-380. 37. Dyer AR, Stamler J, Paul 0, et al. Alcohol consumption, cardiovascular risk factors and mortality in two Chicago epidemiologic studies. Circulation 1977; 56:10671074. 38. Arkwright PD, Beilin LJ, Rouse I, et al. Alcohol: Effect on blood pressure and predisposition to hypertension. Clin Sci 1981; 61:3735-3755. 39. Mitchell Pi, Morgan MJ, Boadle DJ, et al. Role of alcohol in the aetiology of hypertension. Med J Aust 1980; 2:198-200. 40. Stokes GS. Hypertension and alcohol: Is there a link? Chronic Dis 1982; 35:759-762. 41. Biomedical consequences of alcohol use and abuse. Alcohol Health and Research World 1981; 5:10-23. 42. Wallace R. Alcohol Consumption and Hypertension. Paper presented at the 20th Annual Conference on Cardiovascular Epidemiology, San Diego, 1980. 43. Eliaser M, Giansiracusa FJ. The heart and alcohol. California Med 1956; 84:234-236. 44. Dawber TR, Kannel WB, Kagan A. Environmental factors in hypertension. In: Stamler J, ed. Epidemiology of Hypertension. New York: Grune & Stratton, 1967, pp 255288. 45. Kannel WB, Sorlie P. Hypertension in Framingham. In: Paul 0, ed. Epidemiology and Control of Hypertension.

New York: Stratton Intercontinental Medical, i974, pp 553592. 46. 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 1967; 20:571-581. 47. D'Alonzo CN, Pell S. Cardiovascular disease among problem drinkers. J Occup Med 1968; 10:344-350. 48. Mryhed M. Alcohol consumption in relation to factors associated with ischemic heart disease. Acta Med Scand (suppl) 1974; 1-93. 49. Stokes G, MacCarthy P, Frost G, et al. Management of hypertension newly detected by health screening. Med J Aust 1981; 1:527-531. 50. Cooke KM, Frost GW, Thornell IR, Stokes GS. Alcohol consumption and blood pressure. Survey of the relationship at a health screening clinic. Med J Aust 1982; 1:207. 51. Saunders, JB, Beeves, DG, Patton A. Alcohol-induced hypertension. Lancet 1981; 2:653-656. 52. Ogata M, Mendelson JH, Mellon NK, Majchrowicz E. Adult function and alcoholism. II. Catecholamines. Psychosom Med 1971; 159:83-89. 53. Henningsen NC, Ohlsson 0, Mattiasson I, et al. Hypertension levels, serum gamma glutamyl transpeptidase and degree of blood pressure control in middle-aged males. Acta Med Scand 1980; 207:245-251. 54. Primary Prevention of Essential Hypertension: Report of a WHO Scientific Group. Technical Report Series 686, WHO, Geneva, 1983. 55. Svardsudd K. Factors associated with the initial blood pressure level and with the subsequent blood pressure increase in a longitudinal population study. The study of men born in 1913. Eur Heart J 1980; 1:345-354. 56. Dawber TR. Environmental factors in hypertension. In: Stamler T, et al, eds. The Epidemiology of Hypertension: Proceedings of an International Symposium. New York: Grune & Stratton, 1967. 57. Livingston I. The importance of socio-psychological stress in the interpretation of the race-hypertension association. J Humanity Soc (in press). 58. Cooper R, Steinhauer M, Miller W, et al. Racism, society, and disease: An exploration of the social and biological mechanisms of differential mortality. Int J Health Serv 1981; 11(3):389-415. 59. Livingston I. Beliefs concerning hypertension: An exploratory study of awareness in the black community. Western J Black Studies 1983; 7(4):198-205. 60. Report of the management committee. The Australian therapeutic trial in mild hypertension. Lancet 1980; 1:1261-1267. 61. Kozararevic DJ, McGee D, Vojvodic N, et al. Frequency of alcohol consumption and morbidity and mortality. Lancet 1980; 1:613. 62. Sackett DL. The hypertensive patient: Compliance with therapy. Can Med Assoc J 1979; 121 :12-14. 63. Livingston I. Stress and hypertension: A relationship reconsidered. Urban Health 1982; 10(3):102-111. 64. Carlsson C, Haggendahl J. Arterial noradrenaline levels after ethanol withdrawal. Lancet 1967; 11:889-890. 65. Zilm DH, Sellers EM, MacLeod SM, Degani H. Propranolol effect on tremor in alcohol withdrawal. Ann Intern Med 1975; 83:234-236. 66. Beard JP, Knott DH. Fluid and electrolyte balance during acute withdrawal in chronic alcohol patients. JAMA 1968; 204:135-139. 67. Ichinotsubo D, MacKinnon A, Liu C, et al. Mutagenicity of nitrosated cimetidines. Carcinogenesis 1981; 2: 261-264.



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