47. Alcohol

Epidemiology of Alcohol Use and Alcohol-related Disease Conditions

Alcoholic beverages and the problems they engender have been familiar fixtures in human societies since the beginning of recorded history. Because alcohol is causally related to more than 60 International Classification of Diseases codes (Rehm, Room, Graham, and others 2003), disease outcomes are among the most important alcohol-related problems. Depending on the pattern of consumption, alcohol is also protective against diseases, most important among them, coronary heart disease (Rehm, Sempos, and Trevisan 2003). However, the net effect is negative, and 4 percent of the global burden of disease is attributable to alcohol, or about as much death and disability globally as is attributable to tobacco and hypertension (Ezzati and others 2002; WHO 2002). Alcohol thus constitutes a serious public health problem (Room, Babor, and Rehm 2005). Evidence-based preventive measures are available at both the individual and the population levels, with alcohol taxes, restrictions on alcohol availability, and drinking-and-driving countermeasures among the most effective policy options (Babor and others 2003). This chapter reviews the cost-effectiveness of different interventions in developing regions of the world.

Dimensions of Alcohol Related to Disease

The relationship between alcohol consumption and health and social outcomes is complex and multidimensional (Rehm and others 2004). As figure 47.1 shows, alcohol consumption is linked to acute and long-term health and social consequences through three intermediate mechanisms—toxic and beneficial biochemical effects, intoxication, and dependence (Babor and others 2003; Rehm, Room, Graham, and others 2003)—as follows:
[Figure 47.1]

• Toxic and beneficial biochemical effects. These effects of alcohol consumption may influence chronic disease in either beneficial or harmful ways. Accepted beneficial effects include the influence of moderate drinking on coronary heart disease through reduction of plaque deposits in arteries, protection against blood clot formation, and promotion of blood clot dissolution (Zakhari 1997). Examples of harmful effects include increased risk for high blood pressure and for liver damage (Rehm, Room, Graham, and others 2003) and direct toxic effects on acinar cells triggering pancreatic damage (Apte, Wilson, and Korsten 1997) or hormonal disturbances (Emanuele and Emanuele 1997). These are just examples, because alcohol exposure is associated with a multitude of toxic effects on different organs.

• Intoxication. Alcohol intoxication is a powerful mediator for acute health outcomes, such as accidental or intentional injuries or deaths, although intoxication can also be implicated in chronic health and social problems and in certain forms of heart disease. The subjective feeling of intoxication is mainly caused by the effects of alcohol on the central nervous system, and these effects are felt and can be measured even at light to moderate consumption levels (Eckardt and others 1998).

• Dependence. Alcohol dependence is a clinical disorder in its own right, but it is also a powerful mechanism sustaining alcohol consumption and mediating its impact on both chronic and acute physiological and social consequences of alcohol (Drummond 1990). In the quantitative analyses reported in this chapter, alcohol dependence—and alcohol-use disorders (AUDs) in general—will be considered only as a health outcome related to high-risk alcohol use.

This chapter, including the section on the cost-effectiveness of interventions, focuses primarily on health consequences, although later it briefly discusses the social consequences of high-risk drinking and recommended interventions. The epidemiological calculations are taken from Ezzati and others' (2002) comparative risk analysis (CRA) and the World Health Organization (WHO) assessment of the global burden of disease (WHO 2002). (For further information, see Mathers and others 2003; Rehm, Rehn, and others 2003; Rehm, Room, Graham, and others 2003; Rehm, Room, Monteiro and others 2003; Rehm and others 2004). The CRA defines alcohol exposure using two measures: the average volume of alcohol consumption and patterns of drinking (figure 47.1). It then relates these exposure measures to disease outcomes.

The average volume of consumption has been the conventional measure of exposure in alcohol epidemiology (Bruun and others 1975) and has been linked to many disease categories following the seminal work of English and others (1995; see also Rehm, Room, Graham, and others 2003). Patterns of drinking have been linked mainly to two categories of disease outcome: acute effects of alcohol (such as accidental and intentional injuries) and cardiovascular outcomes (mainly coronary heart disease). The CRA defines patterns of drinking primarily in terms of high-risk drinking occasions and also in terms of drinking in public settings and the proportion of drinking that occurs outside of meals (for further details, see Rehm and others 2004).

Epidemiology of High-Risk Alcohol Use

The intervention analyses presented in this chapter focus on average high-risk drinking, although patterns of drinking were also incorporated into the disease burden calculations. High-risk drinking is defined in sex-specific terms as drinking 20 grams per day or more of pure alcohol on average for females and 40 grams per day or more of pure alcohol on average for males (a bottle of table wine contains about 70 grams of pure alcohol). This definition of high-risk drinking is fairly standard in alcohol epidemiology and was first introduced by English and others (1995) on the basis of Australian guidelines. Originally, English and others (1995) used two categories: hazardous drinking (defined as drinking between 20 and 40 grams per day of pure alcohol on average for females and between 40 and 60 grams per day of pure alcohol for males) and harmful drinking (defined as drinking 40 grams per day or more of pure alcohol on average for females and 60 grams per day or more of pure alcohol on average for males). These categories have been used in almost every comprehensive meta-analysis on alcohol and disease since 1995 (see Rehm, Room, Graham, and others 2003for an overview). However, critics asserted that the terms hazardous drinking and harmful drinking were not neutral; thus, the CRA uses drinking categories II and III, referring to the term high-risk drinking when both categories are considered together. High-risk drinking thresholds differ by sex because the risk for chronic disease is related to lower volumes of drinking for women than for men; thus, the thresholds for high-risk drinking were set to reflect an approximately similar risk of chronic disease.

Table 47.1 shows the distribution of high-risk drinking by age and by World Bank region. The table excludes the Middle East and North Africa because prevalence rates of high-risk drinking are considerably lower than 1 percent and this situation is unlikely to change in the near future.

Calculating the burden of high-risk alcohol use that is avertable by means of effective interventions requires additional epidemiological data—in particular, rates of incidence to and remission from high-risk alcohol use and the relative fatality of high-risk alcohol users compared with non-high-risk alcohol users. We derived remission rates from studies of natural recovery from alcohol problems, which found an average of 10.9 years to remission (Sobell, Ellingstad, and Sobell 2000), with an adjustment of plus 20 percent for older age groups and minus 20 percent for younger age groups. We set the relative risk of mortality for high-risk alcohol users age 15 to 44 at 2.5 and the relative risk for older age groups at 1.3 for men and 1.4 for women (Gmel, Gutjahr, and Rehm 2003; Rehm, Gutjahr, and Gmel 2001). Using WHO disease-modeling software, we derived an internally consistent epidemiological profile of current high-risk alcohol use in each region, including specifications of incidence and the relative risk of mortality, with currently observed rates of prevalence, remission, and risk of mortality as inputs. A final input parameter is the disability level for high-risk alcohol use, which we estimated at 0.154 (where zero equals no disability); this is a weighted average based on the severity breakdown of high-risk drinkers from the CRA (80 percent category II, or hazardous; 20 percent category III, or harmful). The preference values for these health states of 0.11 and 0.33, respectively, are derived from Stouthard, Essink-Bot, and Bonsel (2000).

Relationship between High-Risk Drinking and AUDs

Assessing the relationship between high-risk drinking and AUDs is not a straightforward exercise. Even though high-risk drinking over a long period entails the risk of AUDs, that all people with AUDs are also high-risk drinkers does not automatically follow. First, neither the definition of alcohol dependence nor WHO's (1993) definition of harmful use includes actual consumption levels. An individual is considered dependent if at least three of the following criteria apply:

• strong desire or compulsion to take the substance

• impaired control and physiological withdrawal if the substance is reduced or ceased

• tolerance to the effects of the substance

• preoccupation with use of the substance

• persistent use despite clear evidence of harmful consequences.

By contrast, harmful alcohol use is defined as a pattern of use that is causing damage to physical or mental health. Thus, whereas many of these criteria are associated with high-risk alcohol use, no strict classificatory rule indicates that people with AUDs are a subcategory of high-risk drinkers.

Second, the prevalence of AUDs is often derived from surveys, where the operationalization usually requires that three symptoms be present in a lifetime and at least one of these criteria be present within the past 12 months (see, for example, Demyttenaere and others 2004, table 2). Thus individuals may be categorized as alcohol dependent even if they are currently abstaining from alcohol.

Third, qualitative studies across a wide range of cultures have found that the criteria used for diagnosing AUDs often have different meanings and implications in different cultural settings (Room and others 1996; Schmidt and Room 1999). For instance, in the United States over the past decade, the level of reported AUDs increased despite decreases in high-risk drinking (Grant and others 2004). This fact has been explained in terms of changes in drinking norms and social attitudes during a period when the United States has become a "drier" culture. Thus, the measurement of AUDs is quite complex and culturally dependent. Moreover, AUDs are only one outcome of alcohol consumption and, in many parts of the world, not the most important one. As a result, we decided to focus on high-risk alcohol consumption rather than AUDs.

Relationship between Alcohol Use and Disease Categories

The exact procedures for quantifying the risk of disease attributable to alcohol are described in detail elsewhere (Rehm, Room, Graham, and others 2003; Rehm and others 2004). For most chronic disease categories, investigators have derived alcohol-attributable fractions of disease by combining prevalence and relative risk estimates based on meta-analyses (Corrao and others 2000; English and others 1995; Gutjahr, Gmel, and Rehm 2001; Ridolfo and Stevenson 2001; Single and others 1996, 1999). For depression, we drew alcohol-attributable fractions from mental health surveys, looking at the rates of comorbidity and the order of onset of depression and alcohol disorders. For coronary heart disease, we modeled the interaction of average volumes and patterns of drinking based on multilevel analyses that include temporal information as covariates (Gmel, Rehm, and Frick 2003; Rehm and others 2004). For the final estimates, we based alcohol-attributable fractions on these multilevel results for all countries, except for developed countries with relatively favorable drinking patterns (Australia, Japan, and countries in North America and Western Europe), which are not discussed here because the focus is on developing countries. For injuries, we took a similar multilevel approach to quantify the interaction of the average volume of consumption and patterns of drinking in determining alcohol-attributable fractions (Rehm and others 2004).

Thus the analysis includes the following major disease categories:

• chronic disease

• cancer (mouth and oropharyngeal, esophageal, liver, female breast)

• neuropsychiatric diseases (AUDs, unipolar major depression, epilepsy)

• diabetes

• cardiovascular diseases (hypertensive diseases, coronary heart disease, stroke)

• gastrointestinal diseases (cirrhosis of the liver)

• conditions arising during the perinatal period (low birthweight)

• injury

• unintentional injury (motor vehicle accidents, drowning, falls, poisonings, other unintentional injuries)

• intentional injury (self-inflicted injuries, homicide, other intentional injuries).

We did not include other disease categories that are clearly alcohol-related, such as fetal alcohol syndrome, because the current analysis was based on the CRA and was, thus, limited to the global burden-of-disease categories.

Social Determinants of Exposure and Risk

Alcohol-specific risks to health are in part determined and modified by social determinants. For example, Harrison and Gardiner (1999) find that for men age 25 to 69 in England and Wales in 1988-94, those in the lowest socioeconomic status category, unskilled labor, had a 15-fold greater risk for alcohol-related mortality than professionals in the highest category had. These differences cannot be explained by the overall volume of drinking, which actually tended to be greater for those in higher socioeconomic groups. Rather, the differences can be explained by the fact that more of the drinking of those in lower socioeconomic status categories is in high-risk patterns; that is, depending on the use values for drinking in the culture, poor drinkers may see little point in wasting resources on drinking that is not to intoxication. Poorer drinkers are also likely to be less protected physically and socially from possible harm arising from drinking, such as injuries and chronic and infectious diseases. Makela (1999) finds that multiple dimensions of socioeconomic status are required to capture all the adverse interactions of socioeconomic status with alcohol-related mortality.

A critical macroeconomic question is how a country's level of economic development is related to alcohol-related risks to health. The impact of alcohol on disease and mortality may be more potent in countries with greater poverty and nutritional deficiencies (Isichei, Ikwuagu, and Egbuta 1993; Room and others 2002, 119-30). However, most of the risk relationships between alcohol and disease have been derived from studies in established market economies, and the extent of systematic research is currently insufficient to allow quantification of this phenomenon. As a result, the estimated disease burden cited here may be considered as a lower-bound estimate of the actual alcohol-attributable disease burden in developing countries.