Alcohol Consumption and Cardiovascular Diseases

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In any population survey or epidemiological study, the complex nature of drinking behavior also gives rise to problems of measurement. Respondents differ in the types of beverage they drink, the amounts of each beverage they drink on occasions of drinking, and their frequency of drinking. Within individual considerations raise further complications. The same person drinking the same beverage on different occasions may drink different amounts, while in consecutive weeks an individual may undertake different numbers of drinking occasions which may involve the use of different beverages. When assessing the various methods in use to measure alcohol consumption, it is important to bear in mind that in epidemiological research the most important aspect is the classification of respondents by individual levels of consumption (Wilke, 1994). This is necessary to examine the relationship between individual experience of disease and consumption, and, in the population, is essential to the calculation of attributable risk. About 85% of all US residents have had an alcohol-containing drink at least once in their lives and about 51% of US adults are current users of alcohol (Death Statistics for Types of Alcohol Abuse 2005).

A subcategory of cardiovascular mortality which has been linked with alcohol consumption is a hypertensive disease. A recent review of population studies ( MacMahon, 1987) considered 30 cross-sectional studies and noted that the majority of these reported small but significant elevation of blood pressure in consumers of around 35 units per week or more. In 40% of studies, non-drinkers had higher blood pressures than moderate consumers (Death Statistics for Types of Alcohol Abuse 2005). The author concluded that the long-term effects of restriction of alcohol intake as a public health measure to reduce levels of hypertension required further investigation using long-term controlled trials, particularly among moderate consumers. It is clear from experimental work that there is a causal effect of alcohol on blood pressure among subjects with normal blood pressure and that on the restriction of alcohol intake blood pressure rapidly returns to normal (Ammerman, 1999).

Although the relation between alcohol and cerebrovascular disease has been moderately frequently researched, few studies have given adequate attention to quantifying alcohol consumption and estimating the risk at different levels. There seems to be a consensus medical opinion that alcohol is implicated in both ischaemic and hemorrhagic stroke, but the mechanisms may be different in the two cases (Chafetz and Demone 1962). The statistical evidence is only persuasive in the case of hemorrhagic stroke for men at high levels of consumption (Ammerman 1999). For women, few of whom have very high consumption, there is little statistical evidence. At low levels of consumption, there is some evidence that alcohol is associated with a lower risk of stroke as compared with zero consumption. The studies prove an effect of heavy alcohol on cerebral blood flow and indicate that even low alcohol concentrations can produce spasms in isolated arteries, while high concentrations will cause ruptures of blood vessels Alcohol has been shown to affect blood platelet metabolism and function and hence coagulability (Ammerman, 1999). “The effect of alcohol is also likely to be mediated by blood levels of HDL and LDL cholesterol which respectively rise and fall with increasing intake. This may account for the apparent protective effect of low alcohol consumption on non-haemorrhagic strokes” (Chafetz and Demone 1962, p. 65). Reduced coagulability is potentially harmful in hemorrhagic stroke, although it could be of benefit in coronary heart disease.

The most important risk factor for stroke is hypertension and, as seen in the previous section, heavy drinking is known to be a risk factor for hypertension. Even when hypertension is controlled for statistically, heavy drinking remains significantly associated with an increased risk of hemorrhagic stroke; hence other mechanisms are likely to exist. It is noted that strokes among alcoholics seem to be precipitated during the intoxication itself rather than in the withdrawal syndrome (Death Statistics for Types of Alcohol Abuse 2005). Biochemical markers of alcohol intake have been studied has been reported as showing a very high association with stroke. There is also an association between acute alcohol intake and atrial fibrillation which is an established precursor of thromboembolic stroke Altogether, despite quite a large number of studies, the possible mechanisms linking acute alcohol intake with stroke are not well understood, and this is acknowledged in the literature (Chafetz and Demone 1962).

In any attempt to answer the question of how much risk of stroke is alcohol-related, the role of confounding variables must be considered. For example, smoking is generally thought to be a risk factor for stroke, but, as it is highly associated with drinking, estimates of the risk attributable to drinking will vary depending on whether smoking, is or is not adjusted for (Jackson et al 1991). If one adjusts for smoking, the alcohol-relative risk will attempt to estimate the increased risk for a person consuming at a given level compared with a person consuming no alcohol, assuming both smoke the same amount (Death Statistics for Types of Alcohol Abuse 2005). At extreme smoking levels, such a comparison could be rather hypothetical, as it is rare for zero alcohol consumption to be combined with high smoking, or high alcohol with non-smoking. It is also quite likely that for individuals a change in drinking behavior would be accompanied by a change in smoking behavior so that any increased or decreased risk could not be assigned uniquely to one or another factor. In the absence of an understanding of causal mechanisms, there is no unique statistical estimate of the risk attributable to alcohol. If smoking is adjusted for, there is likely to be an underestimation of the true alcohol effect; if it is not adjusted for, overestimation is likely to result (Goodlett et al 1999).

The reason alcohol is filling is that it shares another characteristic of food: Like meat, fruit, or milk, it must go through the process of digestion, or oxidation. The process begins in the stomach, where the stomach muscles start a churning movement not only helps get the digestive fluids secreted by the stomach lining to the food but also gets some of the oxygen in the body to the food. The oxygen combines with the food, burns off its chemical ingredients, and turns it into carbon dioxide and water (Death Statistics for Types of Alcohol Abuse 2005). Most foods are oxidized slowly and in successive stages, first in the stomach and small intestine, allowing the various nutrients in the food to be absorbed slowly into the bloodstream for distribution to the parts of the body where they are needed (Jackson et al 1991). Because of the small size of the ethyl alcohol molecule, alcohol begins to oxidize immediately. It is absorbed into the lining of the stomach and small intestine virtually unchanged in form. Instead of being acted upon by the stomach, it acts on the stomach walls. Large amounts of alcohol over years damage the stomach lining and cause the stomach muscles to lose tone. The liver accepts some more alcohol for oxidation and sends the rest on to the heart again. This process continues until the alcohol is completely oxidized. Meanwhile, alcohol, like actual foods, has reached every part of the body. The difference is that while real foods travel throughout the body in oxidized or digested form, alcohol passes through the various organs in unoxidized form (Kelly and Edwards 1998). While the stomach and liver suffer most from excessive amounts of alcohol, no part of the body is unaffected. One of the first effects a drinker notice is a warm, flushed feeling. This is because the blood vessels in the skin enlarge. Small doses of alcohol cause an increase in blood pressure and an increased heart rate. But this condition does not last long. Alcohol slows down the heart rate, causing less blood to be pumped throughout the system. Thus, alcohol is not beneficial to a very cold person. It is bad for the person because it slows the circulation rather than increases it and lowers the body temperature. In extreme cases, the cardiac nerves are paralyzed, causing instant death. Alcohol abuse contributes to a variety of heart diseases, the primary cause of death nationally. Chronic heavy drinking causes the walls of the blood vessels to thicken, which accounts for the swollen, red appearance of the noses and faces of many alcoholics. This slows down the passage of blood through the vessels and thus hinders the carrying of nutritional materials to the body cells (Wilke, 1994).

In sum, alcohol heavy use can lead to cardiovascular diseases and mortality. Researchers explain the extremely strong inverse relationship with a slight upturn in risk for the heaviest drinkers among the other, initially ill, respondents in terms of self-selection. Those who are most ill and therefore most at risk drink the least — because they are ill. The upturn in risk among the heaviest drinkers in this group is explained as an effect of their consumption. While the data for the initially ill group are also consistent with a protective effect of drinking among men with cardiovascular diagnoses, they maintain that such an interpretation does not accord with information concerning changes in drinking habits.

References

Ammerman, R.T. (1999). Prevention and Societal Impact of Drug and Alcohol Abuse. Mahwah, New Jersey London.

Chafetz, M. E., Demone J. W. Jr. (1962). Alcoholism and Society, Harold W. Oxford University Press.

Death Statistics for Types of Alcohol Abuse. (2005). Web.

Goodlett, Ch. R., Hannigan, J. H., Spear, L. P. (1999). Alcohol and Alcoholism: Effects on Brain and Development, Lawrence Erlbaum Associates.

Jackson R., Scragg R. and Beaglehole R. (1991) “Alcohol consumption and risk of coronary heart disease”, British Medical Journal 303: 211-16.

Kelly, K. J. Edwards, R.W. (1998). Image Advertisements for Alcohol Products: Is Their Appeal Associated with Adolescents’ Intention to Consume Alcohol? Adolescence, 33 (1), p.47-51.

Wilke, D. (1994). Women and Alcoholism: How a Male-as-Norm Bias Affects Research, Assessment, and Treatment. Health and Social Work, 19, p. 29.

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Alcohol Consumption and Cardiovascular Diseases

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