Addictions Case Study Part 1 Case Conceptualization

(Ksir, 2021)

Ksir, C. C. (2021-05-01). Drugs, Society, and Human Behavior, 18th Edition

Chapter 9

Alcohol

Alcoholic Beverages

Fermentation and Fermentation Products

Many thousands of years ago, Neolithic humans discovered “booze.” Beer and berry wine were known and used about 6400 bc and grape wine dates from 300 to 400 bc. Mead, which is made from honey, might be the oldest alcoholic beverage; some authorities suggest it appeared in the Paleolithic Age, about 8000 bc. Early use of alcohol seems to have been worldwide: Beer was drunk by the Native Americans whom Columbus met.

Fermentation forms the basis for all alcoholic beverages. Certain yeasts act on sugar in the presence of water, and this chemical action is fermentation. Yeast recombines the carbon, hydrogen, and oxygen of sugar into ethyl alcohol and carbon dioxide. Chemically, C6H12O6 (glucose) is transformed into C2H5OH (ethyl alcohol) + CO2 (carbon dioxide).

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Most fruits, including grapes, contain sugar, and the addition of the appropriate yeast (which is pervasive in the air wherever plants grow) to a mixture of crushed grapes and water will begin the fermentation process. The yeast has only a limited tolerance for alcohol; when the concentration reaches 15 percent, the yeast dies and fermentation ceases. While up to 15 percent is theoretically possible, in practice the standard alcohol content for wine is about 12 percent.

Cereal grains can also be used to produce alcoholic beverages. However, cereal grains contain starch rather than sugar, and before fermentation can begin the starch must be converted to sugar. This is accomplished by making malt, which contains enzymes that convert starch into sugar. In American beer the primary grain is barley, which is malted by steeping it in water and allowing it to sprout. The sprouted grain is then slowly dried to kill the sprout but preserve the enzymes formed during the growth. This dried, sprouted barley is called malt, and when crushed and mixed with water, the enzymes convert the starch to sugar. Only yeast is needed then to start fermentation. The lower sugar content of these grain-based beverages results in somewhat lower alcohol content: The typical American commercial beer contains about 4 percent alcohol, although some craft beers approach 10 percent.

Distilled Products

To obtain alcohol concentrations above 15 percent, distillation is necessary. Distillation is a process in which the solution containing alcohol is heated, and the vapors are collected and condensed into liquid form again. Alcohol has a lower boiling point than water, so there is a higher percentage of alcohol in the distillate (the condensed liquid) than there was in the original solution.

There is still debate over who discovered the distillation process and when the discovery was made, but many authorities place it in Arabia around ad 800. The term alcohol comes from an Arabic word meaning “finely divided spirit” and originally referred to that part of the wine collected through distillation—the essence, or “spirit,” of the wine. In Europe, only fermented beverages were used until the 10th century, when the Italians first distilled wine, thereby introducing “spirits” to the Western world. These new products were studied and used in the treatment of many illnesses, including senility. The initial feeling about their medicinal value is best seen in the Latin name given to these condensed vapors by a 13th-century French professor of medicine: aqua vitae, “the water of life.”

Europeans distilled wine into “brandywine” (derived from the Dutch term “burnt wine”), while the Irish and Scots distilled their malted-grain beverages (beer) into whiskey (the Gaelic term uisgebaugh also means “water of life”).

In the United States the alcoholic content of distilled beverages is indicated by the term proof. The percentage of alcohol by volume is one-half of the proof number: for instance, 90-proof whiskey is 45 percent alcohol. The word proof developed from a British Army procedure to gauge the alcohol content of distilled spirits before there were modern techniques. The liquid was poured over gunpowder and ignited. If the alcohol content was high enough, the alcohol would burn and ignite the gunpowder, which would go “poof” and explode. That was proof that the beverage had an acceptable alcohol content, about 57 percent. Typical distilled beverages sold commercially (whiskey, vodka, gin, etc.) range between 40 percent and 50 percent alcohol content (80 to 100 proof).

Beer Page 200

Beer is made by adding barley malt to other cereal grains, such as ground corn or rice. The enzymes in the malt change the starches in these grains into sugar; then the solids are filtered out before the yeast is added to the mash to start fermentation. Hops (dried blossoms from only the female hop plant) are added with the yeast to give beer its distinctive, pungent flavor.

Because most American beer is sold in bottles or cans, the yeast must be removed to prevent it from spoiling after packaging. This is usually accomplished by heating it (pasteurization), but some brewers use microfilters to remove the yeasts while keeping the beer cold. The carbonation is added at the time of packaging. Standard brands of commercial American beer contain about 4 percent alcohol.

If you were asked to produce a “light” beer, with fewer calories, a lighter taste, and less alcohol, what would you do—add water? That’s only part of the answer, because light beers have about 10 percent less alcohol and 25 to 30 percent fewer calories. The mash is fermented at a cooler temperature for a longer time, so that more of the sugars are converted to alcohol. Then the alcohol content is adjusted by adding water, resulting in a beverage with considerably less remaining sugar and only a bit less alcohol.

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A stronger beverage sold as malt liquor is made by added sugar or corn syrup to produce a beverage similar in alcohol content to wine (about 12 percent). Two years after Prohibition ended there were 750 U.S. brewers, but by 1941 that number had dwindled to 507. The U.S. brewing picture has changed dramatically since 1960. The first phase, during the 1960s and 1970s, saw the fairly rapid disappearance of many local or regional breweries and increasing dominance by a smaller number of national brands. These traditional brewers have continued to close, consolidate, or be acquired by larger companies, so that by 2006 there were only 20 of the traditional breweries still in operation. The American brewing business has become even more consolidated, and less American, in recent years. The large Milwaukee-based Miller brewing company had already been bought by the London corporation SAB, and Coors had merged with the Canadian brewer Molson, before the 2007 merger that formed MillerCoors, with joint headquarters in Denver and London. This consolidation was planned to compete better with the true giant of American brewers, St. Louis-based Anheuser-Busch. Then in 2008 Anheuser-Busch was acquired by the Belgian company InBev, which had previously acquired large brewing operations in both Brazil and China. So now two “American” brewers, each a wholly owned subsidiary of an international corporation, account for 60 percent of all the beer sold in the United States. Beginning in the early 1980s, small “craft” breweries began to appear, followed later by the appearance of microbreweries, or brewpubs, which make beer for sale only on the premises. The total number of these craft breweries is now over 14,500. The distinction between the large brewers and craft brewers is blurred, as both of the giants also now produce craft-like brands, and Yuengling, a craft brewer, is both the oldest and largest American-owned brewery.

Table 9.1 points out a couple of interesting things about beer sales in the United States. First, Anheuser-Busch continues to dominate the U.S. market, making six of the top-selling brands. Bud Light sells more than twice as much beer as its nearest competitor, Coors Light. The increasing share held by light beers is also reflected here, with former industry leader Budweiser slipping to fourth place and six of the top brands falling into the light category. The two U.S. giants, Anheuser-Busch and MillerCoors, battle to retain their market shares with expensive advertising campaigns as well as by introducing a variety of specialty products. Most recently these include various fruit-flavored beers and flavored seltzers with about 5 percent added alcohol.

Imported beers have become increasingly popular in the past 20 years. The largest-selling imported beers are Corona and Modelo Especial, both from Mexico. Imports now represent about 13 percent of total U.S. sales. The craft beers produced by new, small breweries combined with an increased variety of imports and no-alcohol beers add many new choices for the beer connoisseur, but Bud Light still dominates the mass market.

Wine Page 202

Wine is one of humankind’s oldest beverages, a drink that for generations has been praised as a gift from heaven and condemned as a work of the devil. Although a large volume of wine is now produced in mechanized, sterilized wine “factories,” many small wineries operate alongside the industry giants, and the tradition continues that careful selection and cultivation of grapevines, good weather, precise timing of the harvest, and careful monitoring of fermentation and aging can result in wines of noticeably higher quality.

There is a bewildering array of different types of wines, but the most common distinction is between red and white. The red color in red wines comes from the skin of red grapes. White wines can be made from white grapes or from red grapes if the skins are removed before fermentation. Wines are often named for the type of grape used to make them, or for one of the traditional European land areas known for producing a particular kind of wine.

Besides red versus white, another general distinction is dry versus sweet. The sweeter wines are likely to have a “heavier” taste overall, with the sweetness balancing out flavors that might be considered harsh in a dry wine.

Because carbon dioxide is produced during fermentation, it is possible to produce naturally carbonated sparkling wines by adding a small amount of sugar as the wine is bottled and then keeping the bottle tightly corked. French champagnes are made in this way, as are the more expensive American champagnes, which might be labeled “naturally fermented in the bottle,” or “methode Champagnoise.” A cheaper method is used on inexpensive sparkling wines: Carbon dioxide gas is injected into a generic wine during bottling. Champagnes vary in their sweetness, also, with brut being the driest. Sweet champagnes are labeled “extra dry.” The extra means “not,” as in extraordinary.

Most wines contain about 12 percent alcohol. It was discovered many years ago in Spain that if enough brandy is added to a newly fermented wine the fermentation will stop and the wine will not spoil (turn to vinegar). Sealing the wine in charred oak casks for aging further refined its taste, and soon sherry was in great demand throughout Europe. Other fortified wines, all of which have an alcohol content near 20 percent, include port, Madeira, and Muscatel.

Distilled Spirits

Although brandy, distilled from wine, was probably the first type of spirits known to Europeans, the Celts of Ireland and the Scottish highlands were distilling a crude beverage known as uisgebaugh before 1500. If you try to pronounce that, you’ll see that it was the origin of the word whiskey (spelled whisky in Scotland and Canada). Today’s Scotch whisky is distilled from fermented barley malt (a strong beer).

In the Americas, one of the early distillers who established a good reputation was Elijah Craig, a Baptist minister living in what was then Bourbon County, Kentucky. He began storing his whiskey in charred new oak barrels, originating a manufacturing step still used with American bourbon whiskeys.

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By the 17th century, improved distillation techniques had made possible the production of relatively pure alcohol. Today’s standard product from many large commercial distilleries is 95 percent pure ethyl alcohol (ethanol) (190 proof). Into the process goes whatever grain is available at a cheap price and tank loads of corn syrup or other sources of sugars or starches. Out the other end come grain neutral spirits, a clear liquid that is essentially tasteless (except for the strong alcohol taste), which might be sold in small quantities as Everclear or for use in medicine or research. More often, it is processed in bulk in various ways. For example, large quantities of ethanol are added to gasoline to produce a less polluting fuel, which also helps out the American farmer. Besides other industrial uses for ethanol, such as in cleaners and solvents, bulk grain neutral spirits are also used in making various beverages, including blended Scotch whiskies. One of the first beverages to be made from straight grain neutral spirits was gin. By filtering the distillate through juniper berries and then diluting it with water, a medicinal-tasting drink was produced. First called “jenever” by the Dutch and “genievre” by the French, the British shortened the name to “gin.” Gin became a popular beverage in England and now forms the basis for many an American martini.

Another major use for bulk grain neutral spirits is in the production of vodka. Many inexpensive vodkas are simply a mixture of grain neutral spirits and water, adjusted to the desired proof. More expensive vodkas are distilled to a lower proof and may retain more of the flavors of the original fermented grain or potatoes.

Source: Library of Congress Prints and Photographs Division [LC-USZC4-6495]

The proof at which distillation is carried out influences the taste and other characteristics of the liquor. When alcohol is formed, other related substances, known as congeners, are also formed. These may include alcohols other than ethanol, oils, and other organic matter. Luckily they are present only in small amounts, because some of them are quite toxic. Grain neutral spirits contain relatively few congeners and none of the flavor of the grains used in the mash. Whiskey is usually distilled at a lower proof, not more than 160, and thus the distillate contains more congeners and some of the flavor of the grain used. Whiskey accumulates congeners during aging, at least for the first 5 years, and the congeners and the grain used provide the variation in taste among whiskeys.

Until Prohibition almost all whiskey consumed in the United States was straight rye or bourbon manufactured in the United States. Prohibition introduced smuggled Canadian and Scotch whisky to American drinkers, and they liked them. World War II sent American men around the world, further exposing them to this different type of liquor. Scotch and Canadian whiskys are lighter than American straight whiskey, which means lighter in color and less heavy in taste. American blended whiskeys include a minimum of 20 percent straight whiskey along with neutral spirits and water, thus offering a lighter taste and color than straight whiskey. Seagram’s 7-Crown has been one of the most popular blended American whiskeys.

Liqueurs, or cordials, are similar in some ways to the fortified wines. Originally the cordials were made from brandy mixed with flavorings derived from herbs, berries, or nuts. After dilution with sugar and water, the beverages are highly flavored, sweet, and usually about 20 to 25 percent alcohol. Some of the old recipes are still closely guarded secrets of a particular group of European monks. The late 20th century saw an increase in popularity for these drinks, which are usually consumed in small amounts and have only about half the alcohol content of vodka or whiskey. Many new types were introduced, from Bailey’s Irish Cream to varieties of schnapps. Modern American peppermint, peach, and other types of schnapps are made from grain neutral spirits, which are diluted, sweetened, and flavored with artificial or natural flavorings.

Alcohol Use and “The Alcohol Problem”

Historians seem to agree that, at the time of America’s revolution against the English in the late 1700s, most Americans drank alcoholic beverages and most people favored these beverages compared with drinking water, which was often contaminated. The per-capita consumption of alcohol was apparently much greater than current levels, and little public concern was expressed. Even the early Puritan ministers, who were moralistic about all kinds of behavior, referred to alcoholic drink as “the Good Creature of God.” They denounced drunkenness as a sinful misuse of the “Good Creature” but clearly placed the blame on the sinner, not on alcohol itself.1

A new view of alcohol as the cause of serious problems began to emerge in America soon after the Revolution. That view took root and still exists as a major influence in American culture today. It is so pervasive that some people have a hard time understanding what is meant by the “demonization” of alcohol (viewing alcohol as a demon, or devil). The concept is important, partly because alcohol was the first psychoactive substance to become demonized in American culture, leading the way for similar views of cocaine, heroin, and marijuana in this century. We are referring to a tendency to view a substance as an active (sometimes almost purposeful) source of evil, damaging everything it touches. Whenever harmful consequences result from the use of something (firearms and nuclear energy are other possible examples), some people find it easiest to simply view that thing as “bad” and seek to eliminate it.

The Temperance Movement in America

The first writings indicating a negative view of alcohol itself are attributed to a prominent Philadelphia physician named Benjamin Rush, one of the signers of the Declaration of Independence. Rush’s 1784 pamphlet, “An Inquiry into the Effects of Ardent Spirits on the Mind and Body,” was aimed particularly at distilled spirits (ardent means “burning,” “fiery”), not at the weaker beverages, such as beer and wine. As a physician, Rush had noticed a relationship between heavy drinking and jaundice (an indicator of liver disease), “madness” (perhaps the delirium tremens of withdrawal, or perhaps what we now call Korsakoff’s psychosis), and “epilepsy” (probably the seizures seen during withdrawal). All of those are currently accepted and well-documented consequences of heavy alcohol use. However, Rush also concluded that hard liquor damaged the drinker’s morality, leading to a variety of antisocial, immoral, and criminal behaviors. Rush believed that this was a direct toxic action of distilled spirits on the part of the brain responsible for morality. Rush then introduced for the first time the concept of “addiction” to a psychoactive substance, describing the uncontrollable and overwhelming desires for alcohol experienced by some of his patients. For the first time this condition was referred to as a disease (caused by alcohol), and he recommended total abstinence from alcohol for those who were problem drinkers.1

Other physicians readily recognized these symptoms in their own patients, and physicians became the first leaders of the temperance movement. What Rush proposed, and most early followers supported, was that everyone should avoid distilled spirits entirely, because they were considered to be toxic, and should consume beer and wine in a temperate, or moderate, manner. Temperance societies were formed in many parts of the country, at first among the upper classes of physicians, ministers, and businesspeople. In the early 1800s, it became fashionable for the middle classes to join the elite in this movement, and hundreds of thousands of American businesspeople, farmers, lawyers, teachers, and their families “took the pledge” to avoid spirits and to be temperate in their use of beer or wine.

In the second half of the 19th century, things changed. Up to this time there had been little consumption of commercial beer in the United States. It was only with the advent of artificial refrigeration and the addition of hops, which helped preserve the beer, that the number of breweries increased. The waves of immigrants who entered the country in this period provided the necessary beer-drinking consumers. At first, encouraged by temperance groups that preferred beer consumption to the use of liquor, breweries were constructed everywhere. However, alcohol-related problems did not disappear. Instead, disruptive, drunken behavior became increasingly associated in the public’s mind with the new wave of immigrants—Irish, Italians, and eastern Europeans, more often Catholic than Protestant—and they drank beer and wine. Temperance workers now advocated total abstinence from all alcoholic beverages, and pressure grew to prohibit the sale of alcohol altogether.

Prohibition

It’s difficult now to imagine how important the issue of alcohol prohibition became in American society, but it was one of the major “culture war” issues for almost 100 years, from before the Civil War until the Great Depression of the 1930s. As political power swung back and forth, states would pass and then sometimes later repeal laws intended to restrict access to alcoholic beverages. The first state prohibition period began in 1851 when Maine passed its prohibition law. Between 1851 and 1855, 13 states passed statewide prohibition laws, but by 1868 nine had repealed them. The National Prohibition Party and the Woman’s Christian Temperance Union (WCTU), both organized in 1874, provided the impetus for the second wave of statewide prohibition, which developed in the 1880s. From 1880 to 1889 seven states adopted prohibition laws, but by 1896 four had repealed them.

In 1899, a group of educators, lawyers, and clergymen described the saloon as the “working-man’s club, in which many of his leisure hours are spent, and in which he finds more of the things that approximate luxury than in his home. . . .” They went on to say: “It is a centre of learning, books, papers, and lecture hall to them. It is the clearinghouse for common intelligence, the place where their philosophy of life is worked out, and their political and social beliefs take their beginnings.”2 Truth lay somewhere between those statements and the sentiments expressed in a sermon:

The liquor traffic is the most fiendish, corrupt and hell-soaked institution that ever crawled out of the slime of the eternal pit. It is the open sore of this land. . . . It takes the kind, loving husband and father, smothers every spark of love in his bosom, and transforms him into a heartless wretch, and makes him steal the shoes from his starving babe’s feet to find the price for a glass of liquor. It takes your sweet innocent daughter, robs her of her virtue and transforms her into a brazen, wanton harlot. . . .

The open saloon as an institution has its origin in hell, and it is manufacturing subjects to be sent back to hell.3

Prohibition was not just a matter of “wets” versus “drys” or a matter of political conviction or health concerns. Intricately interwoven with these factors was a middle-class, rural, Protestant, evangelical concern that the good and true life was being undermined by ethnic groups with a different religion and a lower standard of living and morality. One way to strike back at these groups was through prohibition. The temperance movement can be credited with strengthening the political power of women’s groups, such as the WCTU. Acting as protectors of the family, women marched, organized letter-writing campaigns, raised money, and had a major influence on decisions to outlaw the sale of alcohol, even though U.S. women did not attain the right to vote until 1920.

Between 1907 and 1919, 34 states enacted legislation enforcing statewide prohibition, whereas only 2 states repealed their prohibition laws. By 1917, 64 percent of the population lived in dry territory, and between 1908 and 1917 over 100,000 licensed bars were closed.

But a state prohibition law did not mean that the residents did not drink. They did, both legally and illegally. They drank illegally in speakeasies and other private clubs. They drank legally from a variety of the many patent medicines that were freely available. A few of the more interesting ones were Whisko, “a nonintoxicating stimulant” at 55 proof; Colden’s Liquid Beef Tonic, “recommended for treatment of alcohol habit” with 53 proof; and Kaufman’s Sulfur Bitters, which “contains no alcohol” but was in fact 20 percent alcohol (40 proof) and contained no sulfur.

In August 1917, the U.S. Senate adopted a resolution, authored by Andrew Volstead, that submitted the national prohibition amendment to the states. The U.S. House of Representatives concurred in December, and 21 days later, on January 8, 1918, Mississippi became the first state to ratify the 18th Amendment. A year later, January 16, 1919, Nebraska was the 36th state to ratify the amendment, and the deed was done.

As stated in the amendment, a year after the 36th state ratified it, national Prohibition came into effect—on January 16, 1920. The amendment was simple, with only two operational parts:

Section 1. After one year from the ratification of this article the manufacture, sale or transportation of intoxicating liquors within, the importation thereof into, or the exportation thereof from the United States and all territory subject to the jurisdiction thereof for beverage purposes is hereby prohibited.

Section 2. The Congress and the several States shall have concurrent power to enforce this article by appropriate legislation.

The beginning of Prohibition was hailed in a radio sermon by popular preacher Billy Sunday:

The reign of tears is over. The slums will soon be a memory. We will turn our prisons into factories and our jails into storehouses and corncribs. Men will walk upright now, women will smile, and the children will laugh. Hell will be forever for rent.1

The law did not result in an alcohol-free society, and this came as quite a surprise to many people. Apparently the assumption was that Prohibition would be so widely accepted that little enforcement would be necessary. Along with saloons, breweries, and distilleries, hospitals that had specialized in the treatment of alcohol dependence closed their doors, presumably because there would no longer be a need for them.

It soon became clear that people were buying and selling alcohol illegally and that enforcement was not going to be easy. The majority of the population might have supported the idea of Prohibition, but such a large minority insisted on continuing to drink that speakeasies, hip flasks, and bathtub gin became household words. Organized crime became both more organized and vastly more profitable as a result of Prohibition.

Prohibition Worked!

The popular conception is that Prohibition was a total failure, leading to its repeal. That is not the case. Prohibition did reduce overall alcohol intake. Hospital admissions for alcohol dependence and deaths from alcohol declined sharply at the beginning of Prohibition. But during the 1920s, it appears that the prohibition laws were increasingly violated, and the rates of alcohol dependence and alcohol-related deaths began to increase. However, even toward the end of the “noble experiment,” as Prohibition was called by its detractors, alcohol dependence and alcohol-related deaths were still lower than before Prohibition.

Prohibition Is Repealed

If Prohibition did reduce alcohol-related problems, why was it repealed? In 1926, the Association Against Prohibition was founded by a small group of America’s wealthiest men, including the heads of many of the largest corporations in America. Their primary concern seems to have been the income taxes they were paying. Historically, taxes on alcohol had been one of the primary sources of revenue for the federal government. The federal government relied heavily on alcohol taxes before the income tax was initiated in 1913. A major hope of the repeal supporters was that income taxes could be reduced. There was also fear that the widespread and highly publicized disrespect for the Prohibition law encouraged a sense of “lawlessness,” not just among the bootleggers and gangsters but also in the public at large. The Great Depression, which began in 1929, not only made more people consider the value of tax revenues but also increased fears of a generalized revolt. If Prohibition weakened respect for law and order, it had to go. Although women’s groups had played a big role in getting Prohibition passed and the WCTU lobbied against repeal, other women’s groups (again acting as protectors of the family) argued that Prohibition’s dangers were too great and supported repeal.

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The 18th Amendment was repealed by the 21st Amendment, proposed in Congress on February 20, 1933, and ratified by 36 states by December 5 of that year. So ended an era. The 21st Amendment was also short and sweet:

Section 1. The eighteenth article of amendment of the Constitution of the United States is hereby repealed.

Section 2. The transportation or importation into any State, Territory, or possession of the United States for delivery or use therein of intoxicating liquors, in violation of the laws thereof, is hereby prohibited.

When national Prohibition ended, America did not return overnight to the pre-1920s levels of alcohol consumption. Sales increased gradually until after World War II, at which point per-capita consumption was approximately what it had been before Prohibition. Thus, the prohibition of alcohol, much like the current prohibitions of marijuana and heroin, did work in that it reduced alcohol availability, alcohol use, and related problems. On the other hand, even at its best it did not allow us to close all the jails and mental hospitals, and it encouraged organized crime and created expensive enforcement efforts.

Regulation after 1933

After national Prohibition, control over alcohol was returned to the states. Each state has since had its own means of regulating alcohol. Although a few states remained dry after national Prohibition, most allowed at least beer sales. Thus, the temperance sentiment that beer was a safer beverage continued to influence policy. In many cases, beer containing no more than 3.2 percent alcohol by weight was allowed as a “nonintoxicating” beverage.

Over the years the general trend was for a relaxation of laws: States that did not allow sales of liquor became fewer until in 1966 the last dry state, Mississippi, became wet. The minimum age to purchase alcoholic beverages was set at 21 in all states except New York and Louisiana before 1970, when the national voting age was lowered to 18. During the 1970s, 30 states lowered the drinking age to 18 or 19. Per-capita consumption rates, which were relatively stable during the 1950s, increased steadily from 1965 through 1980. However, times changed; pushed by concerns over young people dying in alcohol-related traffic accidents, in the 1980s Congress authorized the Transportation Department to withhold a portion of federal highway funds for any state that did not raise its minimum drinking age to 21. In 1988, the final state raised its drinking age, making 21 the uniform drinking age all across the United States.

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Taxation

Federal taxes on alcoholic beverages are a significant means of gathering money for the federal government. Although most of the federal revenue comes from individual income taxes, taxes on alcohol produce about 1 percent of the total collections by the Internal Revenue Service ($10 billion in 2019). The states also collect over $6 billion each year in excise taxes and license fees for alcoholic beverages. When all these are added up, more than half the consumer’s cost for an average bottle of distilled spirits is taxes. In 2017, as part of the Tax Cuts and Jobs Act, alcohol taxes were reduced for small producers of all types of alcohol products. These reductions were temporary and are scheduled to go back to the old rates at the end of 2020.

Who Drinks? And Why?

Cultural Influences on Drinking

Comparing alcohol use in various cultures around the world allows us to look at ethnic and social factors that lead to differences in patterns of alcohol use. For example, both the Irish and the Russian cultures are associated with heavy drinking, especially of distilled spirits, and with high rates of intoxication and alcohol-related problems. By contrast, Mediterranean countries like Italy and Spain have been characterized by wine consumption, often in a family environment and associated with meals. In these cultures, children are introduced to wine drinking within the family at an early age, but drunkenness is discouraged. The most recent estimates from the World Health Organization indicate that total per-capita alcohol consumption is highest in Russia and several of the neighboring countries that were former members of the Soviet Union. Most western European countries drink about 80 percent as much compared to the leading countries, and Canada and the United States about 65 percent as much. The lowest-consuming countries are those with predominantly Muslim populations.4

It is important to note that the culture of “extreme drinking” does not necessarily correlate well with overall alcohol consumption. The French and Italians may drink wine in moderation with their meals and in family settings, but they manage to drink a lot of wine. Luxembourg, France, Ireland, and Italy are all among the top countries for total per-capita alcohol consumption, but the drinking patterns and alcohol-related problems vary considerably among these countries. It should be pointed out that these comparative statistics are based on reported sales, and Russia is not included because so much alcohol is sold on the black market in that country. As for beer consumption, the Czech Republic leads this list, followed by Austria and Germany with the United States in 20th place.5

Trends in U.S. Alcohol Consumption

Figure 9.1 shows trends in apparent alcohol consumption in the United States over more than two decades. This graph is based on the taxed sale of beer, wine, and spirits.6 For comparison purposes, each beverage is calculated in terms of the amount of pure alcohol consumed. The figure shows that overall alcohol consumption, which had been rising through most of the 1970s, peaked in 1981. Remember from Chapter 1 that this is about the same time that reported use of illicit drugs also reached a peak. The population consists of those age 14 and older, reflecting the long-known fact that the “drinking” population includes quite a few people who are not legally able to purchase alcohol. The last 20 years have seen a dramatic decline in beer consumption, with increased sales of wine and distilled spirits. There has been a steady growth in overall consumption in that same time period, but the latest figures are still about 15 percent lower than the peak consumption year of 1981.

Regional Differences in the United States

In the United States, about one-third of the adult population label themselves as abstainers. The two-thirds who use alcohol consume an amount that averages out to about three drinks per day. Most don’t drink anything near that amount—in fact, another consistent finding is that half the alcohol is consumed by about 10 percent of the drinkers.

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Whites are more likely to drink than Blacks, northerners more than southerners, younger adults more than older, Catholics and Jews more than Protestants, nonreligious more than religious, urban more than rural, large-city dwellers more than small-city residents, and college-educated people more than those with only a high-school or grade-school education.

Figure 9.2 shows estimated overall alcohol consumption combining beer, wine, and distilled spirits for each state, based on sales.6 New Hampshire has the highest per-capita sales, along with the District of Columbia. The District of Columbia is the leader in sales of wine, whereas New Hampshire and Nevada sell the most beer. Note the generally low consumption in the southern states and the generally higher consumption in the western states, with the notable exception of Utah, which has a large Mormon population. These differences in per-capita sales reflect differences in the degree of urbanization as well as some regional cultural differences. For example, the District of Columbia is completely urban, and a large proportion of the population of Nevada lives in either Las Vegas or Reno. The outlier is New Hampshire, a low-population state. However, it has low alcohol taxes and more than half of all sales are to out-of-state buyers. In fact, a decrease in the alcohol tax in Massachusetts had an impact on liquor sales in New Hampshire.7

Gender Differences Page 210

It will surprise no one that males are somewhat more likely to drink alcohol than females. The difference in proportions of those who have drunk alcohol in their lifetimes is not great, but 55 percent of males and 48 percent of females report current (past month) drinking. These results from the National Survey on Drug Use and Health are based on the U.S. population age 12 and older.8 When “binge” drinking is defined as having five or more drinks for males and four or more drinks for females on the same occasion, males are more likely than females to report binge drinking within the past 30 days (28 percent of males versus 21 percent of females). About 8 percent of males and 4 percent of females report “heavy” drinking, defined as binge drinking on five or more separate days during the past month. So, as we look at those who drink the most, as opposed to those who drink only occasionally, we find an increasing proportion of males among the heaviest drinkers.

Drinking among College Students

The college years have traditionally been associated with alcohol use, and in 2015 the proportion of drinkers was about 8 percent higher among 18- to 22-year-old college students than among others of that age (e.g., 58 percent of college students reported drinking within the past month, compared with 48 percent of other 18- to 22-year-olds in the National Survey on Drug Use and Health).8 Many campuses have banned the sale or advertising of alcohol. Many fraternities have banned keg parties and the use of alcohol during “rush,” partly out of concern for legal liability for the consequences if a guest becomes intoxicated and has an accident. Most colleges and universities have adopted a variety of prevention programs to reduce the negative consequences of excessive alcohol use (e.g., education about blood alcohol levels, screening for alcohol use when students go to the health service or counseling center, teaching about helping someone who has had too much alcohol). There is some evidence that these activities are helping. In 2019, about one-fourth of college students reported binge drinking, as defined by five or more drinks at a sitting. This is down from about 40 percent in 2000. Even more impressive is the decrease from 30 percent to 16 percent in those who reported driving after drinking.9

Alcohol Pharmacology

Absorption

Some alcohol is absorbed from the stomach, but the small intestine is responsible for most absorption. In an empty stomach, the overall rate of absorption depends primarily on the concentration of alcohol. Alcohol taken with or after a meal is absorbed more slowly because the food remains in the stomach for digestive action, and the protein in the food retains the alcohol with it in the stomach. Plain water, by decreasing the concentration, slows the absorption of alcohol, but carbonated liquids speed it up. The carbon dioxide acts to move everything quite rapidly through the stomach to the small intestine. It is because of this emptying of the stomach and the more rapid absorption of alcohol in the intestine that champagne has a faster onset of action than noncarbonated wine.

Distribution

The relationship between blood alcohol concentration (BAC) and alcohol intake is relatively simple and reasonably well understood. When taken into the body, alcohol is distributed throughout the body fluids, including the blood. However, alcohol does not distribute much into fatty tissues, so a 180-pound lean person will have a lower BAC than a 180-pound fat person who drinks the same amount of alcohol.

Table 9.2 demonstrates the relationships among alcohol intake, BAC, and body weight for hypothetical, average females and males. The chart distinguishes between the sexes because the average female has a higher proportion of body fat and therefore, for a given weight, has less volume in which to distribute the alcohol. Understanding this table and trying one of the blood alcohol calculators on the Internet (see the Targeting Prevention box on page 213) could reveal how much you can probably drink to avoid going above a specified BAC.

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Table 9.2 makes the simplifying assumption that all of the alcohol is absorbed quickly so that there is little opportunity for metabolism. If the 150-pound female had a tank of water weighing about 100 pounds (12.5 gallons, or 45 liters) and just dumped 1 ounce (28.3 g) into it and stirred it, the concentration would be about 0.6 g/liter, or 0.06 g/100 ml (0.06 percent). Figure 9.3 shows a schematic of such a tank. The 150-pound average male has a tank with more water in it, so his alcohol concentration after 1 ounce is about 0.05 percent. The major factor determining individual differences in BAC is the volume of distribution, so find your own weight on Table 9.2 and estimate how many drinks could be poured into your tank to obtain a BAC of 0.05 percent.

Notice that several beverages are equated to 0.5 ounce of absolute alcohol. A 12-ounce can or bottle of beer at about 4 percent alcohol contains 12 × 0.04 = 0.48 ounce of alcohol. The same amount is found in a glass containing about 4 ounces of wine at 12 percent alcohol, 1 ounce of 100-proof spirits, or 1.25 ounces of 80-proof spirits. Each of these can be equated as a standard “drink.”

We have not yet considered metabolism, but we can do so with one more simple calculation. Alcohol is removed by the liver at a constant rate of 0.25 to 0.30 ounce of ethanol per hour. Most people fall within this range no matter what their body size or drinking experience, unless they have consumed so much alcohol that the liver is damaged. To be on the safe side, estimate that you can metabolize about 0.25 ounce per hour, and note that this is one-half of one of our standard drinks (1 beer, 1 shot, or 1 glass of wine). Over the course of an evening, if your rate of intake equals your rate of metabolism, you will maintain a stable BAC. If you drink faster than one drink every 2 hours, your BAC will climb.

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Compared with men, women absorb a greater proportion of the alcohol they drink. Some metabolism of alcohol actually occurs in the stomach, where the enzyme alcohol dehydrogenase is present. Because this stomach enzyme is more active, on the average, in men than in women, women might be more susceptible to the effects of alcohol.10

Metabolism

Once absorbed, alcohol remains in the bloodstream and other body fluids until it is metabolized, and more than 90 percent of this metabolism occurs in the liver. A small amount of alcohol, less than 2 percent, is normally excreted unchanged—some in the breath, some through the skin, and some in the urine.

The primary metabolic system is a simple one: the enzyme alcohol dehydrogenase converts alcohol to acetaldehyde. Acetaldehyde is then converted fairly rapidly by aldehyde dehydrogenase to acetic acid. With most drugs a constant proportion of the drug is removed in a given amount of time, so that with a high blood level the amount metabolized is high. With alcohol, the amount that can be metabolized is constant at about 0.25 to 0.30 ounces per hour regardless of the BAC. The major factor determining the rate of alcohol metabolism is the activity of the enzyme alcohol dehydrogenase. Exercise, coffee consumption, and so on have no effect on this enzyme, so the sobering-up process is essentially a matter of waiting for this enzyme to do its job at its own speed.

Acetaldehyde might be more than just an intermediate step in the oxidation of alcohol. Acetaldehyde is quite toxic; though its blood levels are only one-thousandth of those of alcohol, this substance might cause some of the physiological effects now attributed to alcohol. One danger in heavy alcohol use might be in the higher blood levels of acetaldehyde.

The liver responds to chronic intake of alcohol by increasing the activity of metabolic enzymes (see Chapter 5). This gives rise to some interesting situations. In a person who drinks alcohol heavily over a long period, the activity of the metabolic enzymes increases. As long as there is alcohol in the system, alcohol gets preferential treatment and the metabolism of other drugs is slower than normal. When heavy alcohol use stops and the alcohol has disappeared from the body, the high activity level of the enzymes continues for 4 to 8 weeks. During this time, other drugs are metabolized more rapidly. To obtain therapeutic levels of other drugs metabolized by this enzyme system (e.g., the benzodiazepines), it is necessary to administer less drug to a chronic heavy drinker and more drug to one who has recently stopped drinking. Thus, alcohol increases the activity of one of the two enzyme systems responsible for its own oxidation. The increased activity of this enzyme is a partial basis for the tolerance to alcohol that is shown by heavy users of alcohol.

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Mechanism(s) of Action

Alcohol is like any other general anesthetic: It depresses the central nervous system. It was used as an anesthetic until the late 19th century, when nitrous oxide, ether, and chloroform became more widely used. However, it was not just new compounds that decreased the use of alcohol as an anesthetic; alcohol itself has some major disadvantages. In contrast to the gaseous anesthetics, alcohol metabolizes slowly. This gives alcohol a long duration of action that cannot be controlled. A second disadvantage is that the dose effective in surgical anesthesia is not much lower than the dose that causes respiratory arrest and death. Finally, alcohol makes blood slower to clot.

The exact mechanism for the CNS effect of alcohol is not clear. Until the mid-1980s, the most widely accepted theory was that alcohol acted on all neural membranes, perhaps altering their electrical excitability. However, with increased understanding of the role of the GABA receptor complex in the actions of other depressant drugs (see Chapter 7), researchers began to study the effects of alcohol on GABA receptors. As with the barbiturates and benzodiazepines, alcohol enhances the inhibitory effects of GABA at the GABA-A receptor. This would explain the similarity of behavioral effects among these three different kinds of chemicals. But alcohol has many other effects in the brain, so it has been very difficult to pin down a single mechanism. No matter what neurotransmitter or receptor or transporter is examined, alcohol appears to alter its function in some way. Because alcohol’s ability to enhance GABA inhibition at the GABA-A receptor occurs at very low doses, this mechanism probably has special importance. Remember that GABA is a widespread inhibitory neurotransmitter, so alcohol tends to have widespread inhibitory effects on neurons in the brain. At higher doses, alcohol also blocks the effects of the excitatory transmitter glutamate at some of its receptors, so this may enhance its overall inhibitory actions.

Alcohol also produces a variety of effects on dopamine, serotonin, and acetylcholine neurons, and researchers continue to explore these various actions with an eye to understanding not only the acute intoxicating effects of alcohol, but also the long-term changes that occur when the brain is exposed to alcohol on a chronic basis. One of the oldest and chemically simplest psychoactive drugs also seems to have the most complicated set of effects on the nervous system.

Behavioral Effects

At the lowest effective blood levels, complex, abstract, and poorly learned behaviors are disrupted. As the alcohol dose increases, better learned and simpler behaviors are also affected. Inhibitions can be reduced, with the result that the overall amount of behavior increases under certain conditions. Even though alcohol can result in an increase in activity, most scientists would not call alcohol a stimulant. Rather, the increased behavioral output is usually attributed to decreased inhibition of behavior.

If the alcohol intake is “just right,” most people experience euphoria, a happy feeling. Below a certain BAC there are no mood changes, but at some point we become uninhibited enough to enjoy our own “charming selves” and uncritical enough to accept the “clods” around us. We become witty, clever, and quite sophisticated, or at least it seems we are.

Another factor contributing to the feeling of well-being is the reduction in anxieties as a result of the disruption of normal critical thinking. The reduction in concern and judgment can range from not worrying about who’ll pay the bar bill to being sure that you can take that next curve at 60 mph.

These effects depend on the BAC—also called blood alcohol level (BAL).

Before suggesting relationships between BAC and behavioral change, two factors must be mentioned. One is that the rate at which the BAC rises is a factor in determining behavioral effects. The more rapid the increase, the greater the behavioral effects. Second, a higher BAC is necessary to impair the performance of a chronic, heavy drinker than to impair a moderate drinker’s performance.

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Performance differences might reflect only the extent to which experienced drinkers have learned to overcome the disruption of nervous system functioning. Another explanation might be that the CNS in the regular drinker develops a tolerance to alcohol. It is established that neural tissue becomes tolerant to alcohol, and tolerance can apparently develop even when the alcohol intake is well spaced over time.

Table 9.3 describes some general behavioral effects of increasing doses of alcohol. These relationships are approximately correct for moderate drinkers. There are some reports that changes in nervous system function have been obtained at concentrations as low as 0.03 to 0.04 percent.

The surgical anesthesia level and the minimum lethal level are perhaps the two least precise points in the table. In any case, they are quite close, and the safety margin is less than 0.1 percent blood alcohol. Death resulting from acute alcohol intoxication usually is the result of respiratory failure when the medulla is depressed.

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Scientific study of the behavioral effects of alcohol is made difficult by the importance of placebo effects. With a substance as pervasive as alcohol, we have a long history of learning about what to expect from this substance, even before taking a drink (and even for those who never drink). Culture passes along a rich set of ideas about how alcohol is supposed to affect people, and we need to be sure which of the many behavioral changes we see after people drink are actually due to the pharmacological effects of having alcohol in the system. A number of laboratory studies have focused on alcohol effects using the balanced placebo design. Half the study participants are given mixed drinks that contain alcohol, while the other half get similar-tasting drinks without alcohol. Each of those groups is divided in half, with some being told they are getting alcohol (whether they are or not) and others being told they are testing a nonalcohol drink. By analyzing the behavioral effects seen in the four conditions, it is possible to determine which effects are actually produced by alcohol and which by the belief that one has consumed alcohol (alcohol expectancy effects). Many of the effects on social behavior (increased laughter, talkativeness, flirtation) are strongly influenced by expectancy even when no alcohol has been consumed, whereas such things as impairment in reaction times and driving simulators result from actual alcohol consumption even when the participant is not aware of the alcohol in the drink. Clearly such studies are limited to the effects of fairly low doses, because if enough alcohol is consumed the participants can detect its effects.

Time-Out

Many of the effects experienced by drinkers are based on what they expect to happen, which interacts somewhat with the pharmacological effects of alcohol. One important component of alcohol use is that drinking serves as a social signal, to the drinker and others, indicating a “time-out” from responsibilities, work, and seriousness. Sitting down with a drink indicates “I’m off duty now” and “Don’t take anything I say too seriously.” One hypothesis is that alcohol induces a kind of social and behavioral myopia, or nearsightedness. After drinking, people tend to focus more on the here and now and to pay less attention to peripheral people and activities, and to long-term consequences.11 That might be why some people are more violent after drinking, whereas others become more helpful even if there is personal risk or cost involved. The idea is that alcohol releases people from their inhibitions, largely because the inhibitions represent concerns about what might happen, whereas the intoxicated individual focuses on the immediate irritant or the person who needs help right now.

Driving under the Influence

Attention was focused in the early 1980s on the large number of traffic fatalities involving alcohol. The total number of traffic fatalities in 1980 was over 50,000, but by 2019 that had dropped to just over 36,000, owing to safer cars and highways, seat belt laws, and decreases in driving while intoxicated.12 It is difficult to estimate exactly how many of those fatalities are caused by alcohol, but we can obtain some relevant information. Many states mandate that the coroner measure blood alcohol in all fatally injured drivers. Based on those measurements, estimates have been made of the number of alcohol-related traffic crash fatalities. From the peak of almost 60 percent in 1982, by 2018 the percentage had declined to less than 30 percent (see Figure 9.4).13

Several studies have demonstrated that the danger of combining alcohol with automobiles is dose-related. At a BAC of 0.08 percent the relative risk of being involved in a fatal crash is about three times as great as for a sober driver. A British study on younger, less experienced drivers (and drinkers) found that the relative risk at 0.08 percent was about five times as great. The risk rises sharply for all drivers with a BAC above 0.10. Similarly, the risk of involvement in a personal injury crash increases with BAC, as does the risk of involvement in a fatal pedestrian accident.

Other interesting facts have emerged from studies of alcohol and accidents. Alcohol-related traffic fatalities are not a random sample of all fatalities. Single-vehicle fatalities are more likely to involve alcohol than are multiple-vehicle fatalities. Alcohol-related fatalities are a greater proportion of the fatalities occurring during dark hours than of those occurring in daylight and are a greater proportion of fatalities occurring on the weekend than of those occurring during the week. Fatally injured drivers in accidents occurring between midnight and 3 am are eight times as likely to have a BAC above 0.08 percent as drivers in accidents occurring between 9 am and noon.12

When you hear that about 80 percent of all the fatally injured drivers who had been drinking were male, that sounds like a big difference, and it is. But it is important to remember that 70 percent of all fatally injured drivers are male, whether or not drinking is involved. That men are more likely to be involved in alcohol-related traffic fatalities reflects three important facts: Any given car is more likely to have a male than a female driver, men might take more chances when driving even when they’re sober, and male drivers are more likely than female drivers to have been drinking.

Who is responsible for all these alcohol-related traffic accidents? One question is whether there are certain individuals, such as problem drinkers, responsible for much of the drunk driving. Problem drinkers, although a relatively small fraction of the drinking population, are more likely on a given day to be driving around with a high BAC. On the other hand, 90 percent of the intoxicated drivers involved in fatal crashes have never been convicted of DUI in the past. Therefore, whereas individual problem drinkers cause more than their share of traffic accidents, the majority of alcohol-related traffic accidents are caused by individuals who have not been identified as problem drinkers. Anyone who drinks and drives is a potential threat.

Younger drivers have more than their share of alcohol-related accidents. The highest rate of alcohol involvement in traffic fatalities is among 21- to 24-year-olds. In 2015, almost 30 percent of the fatalities in this age group were alcohol-related.12

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What can be done about this problem? Current efforts focus mainly on three fronts: identifying repeat offenders and keeping them off the roads, publicizing in the mass media the dangers of drinking and driving, and targeting younger drinkers for special prevention efforts. Although it is impossible to determine the effectiveness of any one of these measures, Figure 9.4 indicates that the total effort has worked to reduce alcohol-related fatalities. In 2000, the U.S. Congress passed legislation requiring states to reduce the BAC for DUI conviction from 0.10 to 0.08.

What’s a safe BAC? If you are going to drink and want to remain in reasonable control of your faculties, you should probably stay below 0.05 percent. Individuals differ considerably in their sensitivities to alcohol, however, so the best rule is to learn about your own sensitivity and not to feel compelled to keep up with anyone else’s drinking. Alcohol-induced impairment is dose-related and depends on what you’re trying to do. Carrying on bar conversation places fewer demands on your nervous system than driving on a crowded freeway during rush hour, where any alcohol at all might interfere.

BAC gives a good estimate of the alcohol concentration in the brain, and the concentration of alcohol in the breath gives a good estimate of the alcohol concentration in the blood. The concentration in the blood is almost 2,100 times the concentration in air expired from the lungs, making breath samples accurate indicators of BAC. Such breath samples are easily collected by police and can be the basis for conviction as a drunk driver in most states.

Sexual Behavior

No psychoactive substance has been as closely linked to sexuality as alcohol. Movies tell us that a romantic occasion is enhanced with wine or champagne, and the use of sexual attraction in beer ads on television is so common we are barely aware of it. The association has been noted for generations—400 years ago Shakespeare wrote about alcohol in Macbeth:

“Lechery, sir, it provokes and unprovokes; it provokes the desire, but it takes away the performance.”

William Shakespeare, The Tragedy of Macbeth, 1606.

Was Shakespeare right? It certainly seems that alcohol does make people less inhibited, and more likely to desire sex, but can we demonstrate that this is a real effect? If so, how much of the enhancement of sexual interest after drinking is really due to the pharmacological effects of the alcohol, and how much is a placebo response based on our expectancies about alcohol’s effects? The importance of understanding alcohol’s ability to provoke desire is enormous. On one hand, many people of both sexes for many generations and across many cultures have viewed alcohol’s ability to enhance sexual interest and pleasure as a great benefit, and many will continue to do so. On the other hand, the use of alcohol is linked with risky sexual behavior (early sexual experience; unprotected sex) as well as with increased likelihood of sexual assault. The analogy to “playing with fire” is an apt one—under the right circumstances both fire and alcohol are beneficial, but both are risky and can lead to destructive outcomes.

And what about the other half of Shakespeare’s statement, that alcohol takes away the performance? Anecdotal evidence shows that men with high BACs are unable to attain or maintain an erection, and there is clinical evidence that chronic alcohol abuse can lead to more permanent impotence in men. But are these effects consistent, and are they limited to high doses or long-term exposure?

Human sexual response is complex, but we can somewhat artificially divide our questions about sexuality into psychological effects (ratings of sexual arousal or interest) versus physiological effects (measurements of penile tumescence or vaginal blood volume; measurements of time to orgasm). Also, we should assume that men and women may differ considerably with respect to both dimensions of sexuality and alcohol’s effects on them.

A review of the available literature on alcohol and sex points out some still unresolved questions, but also some reliable findings reported by different sets of researchers.14 First, both men and women tend to agree with the expectancy statements that alcohol enhances or disinhibits sexuality. In balanced-placebo laboratory experiments, men who had stronger expectancies that alcohol would enhance sexuality also reported experiencing more arousal after being given a placebo drink. Therefore, at least some of the subjective arousal that men experience after drinking is a psychological reaction to the belief that alcohol enhances sexuality. There have been fewer such experiments with women, and the results have been inconsistent.

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When men and women have been given alcohol in a laboratory setting and then exposed to erotic films, both sexes report more sexual arousal after alcohol, and there is a correlation between their ratings of feeling intoxicated and their self-reported arousal. These studies have not usually explored BACs above 0.15 percent, and most have used lower BACs. In men, physiological measures of penile tumescence are correlated with self-reports of arousal, whereas in women there is no consistent relation between self-reported arousal and vaginal blood volume.

Many studies have reported that alcohol reduces penile tumescence in men, sometimes even at fairly low doses. The long-standing assumption has been that this is a direct pharmacological effect on the physiological mechanisms responsible for penile erection. However, several studies have found no effect on this measure, even at fairly high doses. Studies on animals and on nocturnal penile tumescence in men who are asleep have generally not found that alcohol suppresses erection. Therefore, attention is now shifting to the idea that when men become less aroused at higher BACs it might be due to impaired attention to or processing of erotic information. Alcohol can also impair the ability to suppress an erection when men are instructed to avoid becoming aroused.

Several studies have reported that when men believe that a woman has been drinking, they rate her as being more interested in sex and more sexually available. A similar finding has been reported for women’s perceptions of men who have been drinking.

Surveys typically find that people are more likely to have sex on a date (including first dates) when they drink on that date. With respect to risky sex, both men and women given alcohol in laboratory situations report more willingness to engage in unprotected sex, and more agreement with justifications for not using condoms.

We know that alcohol is a frequent presence in sexual assaults, and laboratory studies on college students have reported some related findings. When a date rape scene is described to either men or women, less blame is assigned to the perpetrator if he has been described as drinking before the rape, and more blame is assigned to the victim if she has been described as drinking. Men are generally more aroused by nonviolent erotic films than by erotic films that contain violence, but after consuming alcohol in the laboratory, they were less discriminating and more likely to be aroused by the violent films.

Many of these effects of alcohol on sexual behavior are consistent with the alcohol myopia theory mentioned previously—alcohol impairs information processing in such a way that people are more likely to attend to what’s right in front of them at the time. In a conflicting sexual situation, the person affected by alcohol will be more likely to tend toward immediate gratification and less likely to be inhibited by concerns about outcomes that are uncertain or delayed.

Blackouts

Alcohol-induced blackouts are periods during alcohol use in which the drinking individual appears to function normally but later, when the individual is sober, he or she cannot recall any events that occurred during that period. The drinker might drive home or dance all night, interacting in the usual way with others. When the individual cannot remember the activities, the people, or anything else, that’s a blackout. Most authorities include it as one of the danger signs suggesting excessive use of alcohol. The limited amount of recent research on this topic is probably related to ethical concerns about giving such high doses of alcohol to experimental subjects. An article from 1884 titled “Alcoholic Trance” referred to the syndrome:

This trance state is a common condition in inebriety, where . . . a profound suspension of memory and consciousness and literal paralysis of certain brain-functions follow.

This trance state may last from a few moments to several days, during which the person may appear and act rationally, and yet be actually a mere automaton, without consciousness or memory of his actual condition.15

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Crime and Violence

Homicide

The correlation between alcohol use and homicides is well known to police and judicial systems around the world. A meta-analysis of 23 published reports from nine countries revealed apparent variation across countries, but overall just about half of those who committed homicide were “under the influence” of alcohol at the time.16 Previous studies have reported that a similar proportion of homicide victims had also been drinking just before they were killed. These data certainly imply that homicide is more likely to occur in situations in which drinking also occurs, but they leave open the question as to whether alcohol plays a causal role in homicides.

Assault and Other Crimes of Violence

As with homicide, studies of assault, spousal abuse, and child abuse reveal correlations with drinking: Heavier drinkers are more likely to engage in such behaviors, and self-reports by offenders indicate a high likelihood that they had been consuming alcohol before the violent act. However, scientists are still cautious in trying to determine how much of a causal role alcohol plays in such activity. For example, if fights are likely to occur when men get together in groups at night and drinking is likely to occur when men get together in groups at night, how much of a role does alcohol itself play in increasing the chances of violence? Similarly, if both heavy drinking and violent arguments are characteristics of dysfunctional family situations, how much of the ensuing family violence can be blamed on the use of alcohol? Unfortunately, it has proven difficult to perform controlled experimental studies on these complex problems, so the answers remain unclear.

Date Rape

In spite of widespread concern about drugs being slipped into someone’s drink, by far the most significant date rape drug is and always has been alcohol. For most college women who report having been sexually assaulted by a date, the assault happened after the woman had consumed alcohol.17 That is why many college campuses now combine sexual assault prevention education with alcohol education.

Suicide

Most studies show that alcohol is involved in about one-third of all suicides. Suicide attempts seem to have a different background than successful suicides, but alcohol abuse is second only to depression as the diagnosis in suicide attempters. The relationship between alcohol abuse and depression is a strong one and has been the subject of many studies. A study of almost 2,000 suicide attempts in Germany again found that acute alcohol consumption was present in about one-third of the cases, and in about one-sixth of the total cases the person could be diagnosed with an alcohol use disorder.18

Physiological Effects

Peripheral Circulation

One effect of alcohol on the CNS is the dilation of peripheral blood vessels. This increases heat loss from the body but makes the drinker feel warm. The heat loss and cooling of the interior of the body are enough to cause a slowdown in some biochemical processes. This dilation of peripheral vessels argues against giving alcohol to individuals in shock or extreme cold. Under these conditions, blood is needed in the central parts of the body, and heat loss must be diminished if the person is to survive.

Fluid Balance

One action of alcohol on the brain is to decrease the output of the antidiuretic hormone (ADH, also called vasopressin) responsible for retaining fluid in the body. It is this effect, rather than the actual fluid consumption, that increases the urine flow in response to alcohol. This diuretic effect can lower blood pressure in some individuals.

Hormonal Effects

Even single doses of alcohol can produce measurable effects on a variety of hormonal systems: Adrenal corticosteroids are released, as are catecholamines from the adrenal medulla, and the production of the male sex hormone testosterone is suppressed. It is not known what significance, if any, these effects have for occasional, moderate drinkers. However, chronic abusers of alcohol can develop a variety of hormone-related disorders, including testicular atrophy and impotence in men and impaired reproductive functioning in women.

Alcohol Toxicity

Alcohol consumption can result in toxicity, both acute and chronic. We have already discussed the problem of alcohol-related traffic accidents, which we would consider to be examples of acute behavioral toxicity. In a similar vein are other alcohol-related accidents and adverse effects, such as falls, drowning, cycling and boating accidents, and accidents associated with operating machinery. Although we know that alcohol increases the risk of injury and death for all these types of accidents, we are less certain about how many of these problems are actually caused by alcohol intoxication.

Alcohol Poisoning

As the DAWN data in Chapter 2 revealed, many drug-related deaths include alcohol in combination with some other substance, so it is difficult to know exactly how many overdose deaths are primarily due to alcohol versus another drug, or to the specific combination. But people also die from acute alcohol poisoning alone, and the Centers for Disease Control estimates that about 2,200 people die each year simply from drinking too much alcohol.19 Several well-publicized drinking deaths of young college students have occurred in recent years. These students had been drinking for many hours before their deaths, and as a result colleges and universities began reexamining their alcohol-use policies. Two pieces of advice are worth mentioning: (1) If one of your friends drinks enough to pass out, DO NOT simply leave her or him alone to sleep it off. The person should be placed on his or her side so that any vomit is less likely to be aspirated, and someone who is sober needs to monitor the person’s breathing until he or she can be aroused and begins to move. If this is not possible, take the victim to the emergency room. Don’t worry about getting in trouble for helping out a friend—the alternative can be much worse. (2) It is particularly dangerous to drink to the point of vomiting and then begin drinking again after vomiting. The vomiting reflex is triggered by rapidly rising BAC, usually above 0.12 percent. But the vomiting reflex is inhibited when the BAC rises above 0.20 or so, and it is then possible to continue drinking and reach lethal concentrations. See the Life Saver box on page 215 for more information on alcohol poisoning.

Hangover

The Germans call it “wailing of cats” (Katzenjammer), the Italians “out of tune” (stonato), the French “woody mouth” (gueule de boise), the Norwegians “workmen in my head” (jeg har tommeermenn), and the Swedes “pain in the roots of the hair” (hont i haret). Hangovers aren’t much fun. And they aren’t very well understood, either. Even moderate drinkers who only occasionally overindulge are well acquainted with the symptoms: upset stomach, fatigue, headache, thirst, depression, anxiety, and general malaise.

Some authorities believe that the symptoms of a hangover are the symptoms of withdrawal from a short- or long-term dependence on alcohol. The pattern certainly fits. Some people report continuing to drink just to escape the pain of the hangover. This behavior is not unknown to moderate drinkers, either: Many believe that the only cure for a hangover is some of “the hair of the dog that bit you”—alcohol. And it might work to minimize symptoms, because it spreads them out over a longer time. There is no evidence that any of the “surefire-this’ll-fix-you-up” remedies are effective. The only known cures are an analgesic for the headache, rest, and time.

Some hangover symptoms are probably reactions to congeners. Congeners are natural products of the fermentation and preparation process, some of which are quite toxic. Congeners make the various alcoholic beverages different in smell, taste, color, and, possibly, hangover potential.

Still other factors contribute to the trials and tribulations of the “morning after the night before.” Thirst means that the body has excreted more fluid than was taken in with the alcoholic beverages. However, this does not seem to be the only basis for the thirst experienced the next day. Another cause might be that alcohol causes fluid inside cells to move outside the cells. This cellular dehydration, without a decrease in total body fluid, is known to be related to, and might be the basis of, an increase in thirst.

The nausea and upset stomach typically experienced can most likely be attributed to the fact that alcohol is a gastric irritant. Consuming even moderate amounts causes local irritation of the mucosa lining the stomach. It has been suggested that the accumulation of acetaldehyde, which is quite toxic even in small quantities, contributes to the nausea and headache.

The best way to avoid a hangover is still to drink in moderation, regardless of the beverage.

Chronic Disease States

The relationship of alcohol use to many diseases has been studied extensively. As a general rule, heavy alcohol use, either directly or indirectly, affects every organ system in the body. The alcohol or its primary metabolite, acetaldehyde, can irritate and damage tissue directly. Because alcohol provides empty calories, many heavy drinkers do not eat well, and chronic malnutrition leads to tissue damage. Separating the effects of alcohol exposure from those of malnutrition relies to a great extent on experiments with animals. Some animals can be fed adequate diets and exposed to high concentrations of alcohol, whereas other animals are fed diets deficient in certain vitamins or other nutrients.

Brain Damage

Perhaps the biggest concern is the damage to brain tissue that is seen in chronic alcohol abusers. It has been reported for years that the brains of deceased heavy drinkers demonstrate an obvious overall loss of brain tissue: The ventricles (internal spaces) in the brain are enlarged, and the fissures (sulci) in the cortex are widened. Modern imaging techniques have revealed this tissue loss in living alcohol abusers as well. This generalized loss of brain tissue is probably a result of direct alcohol toxicity rather than malnutrition and is associated with alcoholic dementia, a global decline of intellect. Patients with this type of organic brain syndrome might have difficulty swallowing in addition to impaired problem solving, difficulty in manipulating objects, and abnormal electroencephalograms. Another classical alcohol-related organic brain syndrome has two parts, which so often go together that the disorder is referred to as Wernicke-Korsakoff syndrome. Wernicke’s disease is associated with a deficiency of thiamine (vitamin B1) and can sometimes be corrected nutritionally. The symptoms include confusion, ataxia (impaired coordination while walking), and abnormal eye movements. Most patients with Wernicke’s disease also exhibit Korsakoff’s psychosis, characterized by an inability to remember recent events or to learn new information. Korsakoff’s psychosis can appear by itself in patients who maintain adequate nutrition, and it appears to be mostly irreversible. There has been great controversy about the specific brain areas that are damaged in Wernicke-Korsakoff syndrome, as well as about the relationship between the two parts of the disorder.

Important practical questions include the following: Exactly how much alcohol exposure is required before behavioral and/or anatomical evidence can be found indicating brain damage? And how much of the cognitive deficit seen in alcoholic dementia can be reversed when drinking is stopped and adequate nutrition is given? Both questions have been the subject of several experiments. There is no definitive answer for the first question. Some of the studies on moderate drinkers have included individuals who consume up to 10 drinks per day! Most studies with lower cutoffs for moderate drinking have not found consistent evidence for anatomical changes in the brain. As for recovery, several studies have reported both behavioral improvement and apparent regrowth of brain size in chronic alcohol abusers after some months of abstinence. However, not all such studies find improvement, and some have found improvement in some types of mental tasks but not in others.

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Liver Disorders

Fatty acids are the usual fuel for the liver. When present, alcohol has higher priority and is used as fuel instead. As a result, fatty acids (lipids) accumulate in the liver and are stored as small droplets in liver cells. This condition is known as alcohol-related fatty liver, which for most drinkers is not a serious problem. If alcohol input ceases, the liver uses the stored fatty acids for energy. Sometimes the droplets increase in size until they rupture the cell membrane, causing death of the liver cells. Before the liver cells die, a fatty liver is completely reversible and usually of minor medical concern.

Sometimes, with prolonged or high-level alcohol intake, another phase of liver damage is observed. Alcoholic hepatitis is a serious disease and includes both inflammation and impairment of liver function. Usually this occurs in areas of the liver where cells are dead and dying, but it is not known if an increasingly fatty liver leads to alcoholic hepatitis. Alcoholic hepatitis does exist in the absence of a fatty liver, so this form of tissue damage might be due to direct toxic effects of alcohol.

Cirrhosis is the liver disease everyone knows is related to high and prolonged levels of alcohol consumption. It’s not easy to get cirrhosis from drinking alcohol—you have to work at it. Usually it takes about 10 years of steady drinking of the equivalent of a pint or more of whiskey a day. Not all cirrhosis is alcohol related, but a high percentage is, and cirrhosis is the seventh leading cause of death in the United States. In large urban areas it is the fourth or fifth leading cause of death in men aged 25 to 65. In cirrhosis, liver cells are replaced by fibrous tissue (collagen), which changes the structure of the liver (see Figure 9.5). These changes decrease blood flow and, along with the loss of cells, result in a decreased ability of the liver to function. When the liver does not function properly, fluid accumulates in the body, jaundice develops, and other infections or cancers have a better opportunity to establish themselves in the liver. Cirrhosis is not reversible, but stopping the intake of alcohol will retard its development and decrease the serious medical effects.

In drinkers with severely damaged livers, liver transplants have been quite successful—a 64 percent survival rate after 2 years. Most of these recipients do not resume drinking after the transplant.

Heart Disease

Another area of concern is the effect of alcohol on the heart and circulation. Heavy alcohol use is associated with increased mortality resulting from heart disease. Much of this is due to damage to the heart muscle (cardiomyopathy), but the risk of the more typical heart attack resulting from coronary artery disease also increases. Heavy drinkers are also more likely to suffer from high blood pressure and strokes. An interesting twist to this story is that several studies have found a lower incidence of heart attacks in moderate drinkers than in abstainers, and for several years this protective effect of moderate alcohol consumption and the possible mechanism for it have been discussed. It has been pointed out that the abstainers in such studies might include both abstaining alcohol abusers who once drank heavily and others who quit on their doctor’s advice because of poor health. However, studies that separate those who never drank from the “quitters” still report fewer heart attacks and lower overall mortality in moderate drinkers, with increased mortality for both abstainers and heavy drinkers. It has been proposed that alcohol increases high-density lipoproteins (HDL, sometimes called “good cholesterol”), some of which seem to protect against high blood pressure. The reduced blood clotting produced by alcohol could also play a role. There has been speculation that red wine might have better effects than other forms of alcohol due to the presence of antioxidants in the grapes from which the wine is made. But the scientific evidence supports only a beneficial effect of regular alcohol use, with an increased risk for those who “binge” drink (heavy use once a week or so).20

Cancer

Alcohol use is associated with cancers of the mouth, tongue, pharynx, larynx, esophagus, stomach, liver, lung, pancreas, colon, and rectum. There are many possible mechanisms for this, from direct tissue irritation to nutritional deficiencies to the induction of enzymes that activate other carcinogens. A particularly nasty interaction with cigarette smoking increases the incidence of cancers of the oral cavity, pharynx, and larynx. Also, suppression of the immune system by alcohol, which occurs to some extent every time intoxicating doses are used, probably increases the rate of tumor growth.

The Immune System

The immune deficits seen in chronic alcohol abusers are associated with at least some increase in the frequency of various infectious diseases, including tuberculosis, pneumonia, yellow fever, cholera, and hepatitis B. Alcohol use might be a factor in AIDS, for several reasons: Loss of behavioral inhibitions probably increases the likelihood of engaging in unprotected sex; alcohol could increase the risk of HIV infection in exposed individuals; and alcohol could suppress the immune system and therefore increase the chances of developing full-blown AIDS once an HIV infection is established. Although one epidemiological study did not find an acceleration of HIV-related disease in infected individuals who drank, heavy alcohol use is probably not a good idea for anyone who is HIV-positive.

There is no evidence that the occasional consumption of one or two drinks has overall negative effects on the physical health of most individuals. An important exception to this statement might be drinking during pregnancy.

Fetal Alcohol Syndrome

The unfortunate condition of infants born to alcohol-abusing mothers was noted in an 1834 report to the British Parliament: They have a “starved, shriveled, and imperfect look.” Until fairly recently most scientists and physicians believed that any effects on the offspring of heavy alcohol users were the result of poor nutrition or poor prenatal care. Those beliefs changed, however, when a 1973 report described eight children who displayed a particular pattern of craniofacial and other defects. All of these children had been born to alcohol-dependent mothers. This article was the first to describe the symptoms of fetal alcohol syndrome (FAS), a collection of physical and behavioral abnormalities that seems to be caused by the presence of alcohol during development of the fetus (see related photo). There are three primary criteria for diagnosing FAS, at least one of which must be present:

Growth retardation occurring before and/or after birth.

A pattern of abnormal features of the face and head, including small head circumference, small eyes, or evidence of retarded formation of the midfacial area, including a flattened bridge and short length of the nose and flattening of the vertical groove between the nose and mouth (the philtrum).

Evidence of CNS abnormality, including abnormal neonatal behavior, mental retardation, or other evidence of abnormal neurobehavioral development.

Each of these features can be seen in the absence of alcohol exposure, and other features might also be present in FAS, such as eye and ear defects, heart murmurs, undescended testicles, birthmarks, and abnormal fingerprints or palmar creases. Research also found a high frequency of various abnormalities of the eyes, often associated with poor vision. Thus, the diagnosis of FAS is a matter of judgment, based on several symptoms and often on the physician’s knowledge of the mother’s drinking history.

Many animal studies have been done in a variety of species, and they indicate that FAS is related to peak BAC and to duration of alcohol exposure, even when malnutrition is not an issue. In mice and other animal models, increasing amounts of alcohol yield an increase in mortality, a decrease in infant weight, and increased frequency of soft-tissue malformation. The various components of the complete FAS reflect damage occurring at different developmental stages, so heavy alcohol exposure throughout pregnancy is the most damaging situation, followed by intermittent high-level exposure designed to imitate binge drinking.

Not all infants born to drinking mothers show abnormal development. If they did, it would not have taken so long to recognize FAS as a problem. It is estimated that the overall rate of FAS in the general U.S. population is about 2 per 1,000 live births.21 Estimating the prevalence among problem drinkers or alcohol abusers is more of a problem. There is the difficulty not only of diagnosing FAS but also of diagnosing alcohol abuse. If the physician knows that the mother is a heavy drinker, this can increase the probability of noticing or diagnosing FAS, thus inflating the prevalence statistics among drinking mothers. FAS seems to occur in as many as 2 or 3 percent of births when the mothers are known to be problem drinkers, or at 10 times the rate in the general population. If all alcohol-related birth defects (referred to as fetal alcohol spectrum disorder, or FASD) are counted, the rate among heavy-drinking women is higher, from 80 to a few hundred per 1,000. Maternal alcohol abuse might be the most frequent known environmental cause of mental retardation in the Western world.

In addition to the risk of FAS, the fetus of a mother who drinks heavily has a risk of not being born at all. Spontaneous abortion early in pregnancy is perhaps twice as likely among the 5 percent of women who are the heaviest drinkers. The data on later pregnancy loss (stillbirths) are not as clearly related to alcohol for either animals or humans.

An important question, and one that can never be answered in absolute terms, is whether there is an acceptable level of alcohol consumption for pregnant women (see the Taking Sides box). The data on drinking during pregnancy rely on self-reports by the mothers, who are assumed to be at least as likely as everyone else to underreport their drinking. In addition, almost every study has used different definitions of heavy drinking, alcohol abuse, and problem drinking. The heaviest drinkers in each study are the most at risk for alcohol-related problems with their children, but we don’t really know if the large number of light or moderate drinkers are causing significant risks. Based on the dose-related nature of birth problems in animal studies, one might argue that any alcohol use at all produces some risk, but at low levels the increased risk is too small to be revealed except in a large-scale study. In 1981, the U.S. surgeon general recommended that “pregnant women should drink absolutely no alcohol because they may be endangering the health of their unborn children.” Maybe that went a bit too far. The bottom line is this: Scientific data do not demonstrate that occasional consumption of one or two drinks definitely causes FAS or other alcohol-related birth defects. On the other hand, neither do the data prove that low-level alcohol use is safe, nor do they indicate a safe level of use. Remember from Chapter 5 that it is not within the realm of science to declare something totally safe, so it will be impossible to ever set a safe limit on alcohol use. Most women decrease their alcohol use once they have become pregnant, and many decrease it further as pregnancy progresses.

Alcohol Dependence

Withdrawal Syndrome

The physical dependence associated with prolonged heavy use of alcohol is revealed when alcohol intake is stopped. The abstinence syndrome that develops is medically more severe and more likely to cause death than is withdrawal from opioid drugs. In untreated advanced cases, the mortality rate can be as high as one in seven. For that reason it has long been recommended that the initial period of detoxification (allowing the body to rid itself of the alcohol) be carried out in an inpatient medical setting, especially for people who have been drinking very heavily or have other medical complications.

The progression of withdrawal, the abstinence syndrome, has been described in the following way:

Stage 1: tremors, excessively rapid heartbeat, hypertension, heavy sweating, loss of appetite, and insomnia.

Stage 2: hallucinations—auditory, visual, tactile, or a combination of these; and, rarely, olfactory signs.

Stage 3: delusions, disorientation, delirium, sometimes intermittent and usually followed by amnesia.

Stage 4: seizure activity.

Medical treatment is usually sought in stage 1 or 2, and rapid intervention with a sedative drug, such as diazepam, will prevent stage 3 or 4 from occurring. The old term delirium tremens is used to refer to severe cases including at least stage 3.

Tremors are one of the most common physical changes associated with alcohol withdrawal and can persist for a long period after alcohol intake has stopped. Anxiety, insomnia, feelings of unreality, nausea, vomiting, and many other symptoms can also occur.

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The withdrawal symptoms do not develop all at the same time or immediately after abstinence begins. The initial signs (tremors, anxiety) might develop within a few hours, but the individual is relatively rational. Over the next day or two, hallucinations appear and gradually become more terrifying and real to the individual. One common feature of alcohol-withdrawal hallucinations includes the sensation of ants or snakes crawling on the skin. You might remember that this also occurs after high doses of stimulant drugs. In the context of alcohol withdrawal, it is an indication that the nervous system is rebounding from constant inhibition and is hyperexcitable.

Optimal treatment of patients during the early stages involves the administration of a benzodiazepine, such as chlordiazepoxide or diazepam (see Chapter 7). Because of the high degree of cross-dependence between alcohol and chlordiazepoxide, one drug can be substituted for the other and withdrawal continued at a safer rate.22

Some withdrawal symptoms can last for up to several weeks. Unstable blood pressure, irregular breathing, anxiety, panic attacks, insomnia, and depression are all reported during this period. These phenomena have been referred to as a protracted withdrawal syndrome, and they can trigger intense cravings for alcohol. Thus, some chronic drinkers might benefit from residential or inpatient treatment for up to 6 weeks, simply to prevent relapse during this critical period. Preventing relapse for longer periods is a more difficult task.

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Alcohol Use Disorder

Probably the most significant influence on American attitudes about alcoholism was a 75-year-old book called Alcoholics Anonymous. This book described the experiences of a small group of people who formed a society whose “only requirement for membership is a desire to stop drinking.” That society has now grown to include more than 2 million members in over a hundred countries. A central part of their belief system is that alcohol dependence is a progressive disease characterized by a loss of control over drinking and that the disease can never be cured. People who do not have the disease might drink and even become intoxicated, but they do not “lose control over alcohol.” There is a suspicion that the dependent drinker is different even before the first drink is taken. The only treatment is to arrest the disease by abstaining from drinking. This disease model of alcohol dependence has received support from many medical practitioners and has been endorsed by the American Medical Association and other professional groups. In one sense, this description of alcohol dependence as a disease is a reaction against long-held notions that excessive drinking is only a symptom of some other underlying pathology, such as depression, or some type of personality defect. Traditional psychoanalysts practicing many years ago might have treated alcohol abusers by trying to discover the unconscious conflicts or personality deficiencies that caused the person to drink. One important consequence of defining alcohol dependence as a primary disease is to recognize that the drinking itself might be the problem and that treatment and prevention should be aimed directly at alcohol abuse/dependence.

However, there are many scientific critics of the disease concept. If alcohol dependence is a disease, what is its cause? How are alcohol abusers different from others, except that they tend to drink a lot and have many alcohol-related problems? Although sequential stages have been described for this “progressive disease,” most individual drinkers don’t seem to fit any single set of descriptors. Some don’t drink alone, some don’t drink in the morning, some don’t go on binges, some don’t drink every day, and some don’t report strong cravings for alcohol. Experiments have shown that alcohol-dependent individuals do retain considerable control over their drinking, even while drinking—it’s not that they completely lose control when they start drinking, but they might have either less ability or less desire to limit their drinking because they do drink excessively. Although an “alcoholic personality” has been defined that characterizes many drinkers who enter treatment, the current belief is that these personality factors (impulsive, anxious, depressed, passive, dependent) reflect the years of intoxication and the critical events that led to the decision to enter treatment rather than preexisting abnormalities that caused the problem drinking.

The American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders23 is the closest thing there is to a single official, widely accepted set of labels for behavioral disorders, including substance use disorders (see Chapter 2). The DSM-5 lists 11 possible criteria for alcohol use disorder, including drinking more than intended, desire to cut down or stop, craving, drinking causing disruption of major life roles, social problems, giving up other activities, repeated hazardous use, tolerance, and withdrawal. The severity of the disorder is then ranked based on the number of these criteria, with six or more of the symptoms indicating a severe alcohol use disorder.

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Why are some people able to drink in moderation all their lives, whereas others repeatedly become intoxicated, suffer from alcohol-related problems, and continue to drink excessively? So far, no single factor and no combination of multiple factors has been presented that allows us to predict which individuals will become alcohol abusers. Multiple theories exist, including biochemical, psychoanalytic, and cultural approaches. At this period of scientific history, probably the most attention is being focused on understanding two types of factors: cognitive and genetic. Two important tools have been used in the cognitive research: the Alcohol Expectancy Questionnaire (asking people what effects they think alcohol has on people), and the balanced placebo design (p. 216).24 Both alcohol-dependent drinkers and social drinkers report more intoxication and consume more drinks when they are told the drinks have alcohol, regardless of the actual alcohol content. It is important that alcohol-dependent people actually given small amounts of alcohol (equivalent to one or two drinks) do not report becoming intoxicated and do not increase their drinking if they are led to expect that the drink contains no alcohol. Therefore, it would seem that, if alcohol abusers do lose control when they begin drinking, it might be because they have come to believe that they will lose control if they drink (this is sometimes referred to as the abstinence violation effect). These balanced placebo experiments have been replicated several times by others. The most obvious interpretation of such results is that alcohol use provides a social excuse for behaving in ways that would otherwise be considered inappropriate, and it is enough for one to believe that one has drunk alcohol for such behaviors to be released.

Considerable evidence supports the idea that some degree of vulnerability to alcohol dependence might be inherited. Alcohol dependence does tend to run in families, but some of that could be due to similar expectancies developed through similar cultural influences and children learning from their parents. Studies on twins provide one way around this problem. Monozygotic (one-egg, or identical) twins share the same genetic material, whereas dizygotic (two-egg, or fraternal) twins are no more genetically related than any two nontwin siblings. Both types of twins are likely to share very similar cultural and family learning experiences. If one adult twin is diagnosed as alcohol dependent, what is the likelihood that the other twin will also receive that diagnosis (are the twins concordant for the trait of alcohol dependence)? Almost all such studies report the concordance rate for monozygotic twins is higher than that for dizygotic twins, and in some studies it is as high as 50 percent. These results imply that inheritance plays a strong role but is far from a complete determinant of alcohol dependence. Another important type of study looks at adopted sons whose biological fathers were alcohol dependent. These reports consistently find that such adoptees have a much greater than average chance of becoming alcohol dependent, even though they are raised by “normal” parents. Although these studies again provide clear evidence for a genetic influence, most children of alcohol abusers do not become alcohol dependent—they simply have a statistically greater risk of doing so. For example, in one study, 18 percent of the adopted-away sons of alcohol-dependent drinkers became dependent on alcohol, compared with 5 percent of the adopted-away sons whose parents had not received the diagnosis.

Alcohol dependence is a complicated feature of human behavior, and even if genetic influences are critical, more than one genetic factor could be involved. Probably it is too much to hope that a single genetic marker will ever be found to be a reliable indicator of alcohol dependence in all individuals.

Summary

Alcohol is made by yeasts in a process called fermentation. Distillation is used to increase the alcohol content of a beverage.

Reformers first proposed temperate use of alcoholic beverages, and it was not until the late 1800s that alcohol sales were prohibited in several states.

National Prohibition of alcohol was successful in reducing alcohol consumption and alcohol-related problems, but it also led to increased law-breaking and a loss of alcohol taxes.

Alcohol use has decreased since 1980, and consumption varies widely among different cultural groups and in different regions of the United States.

Men are more likely than women to be heavy drinkers, and college students are more likely to drink than others of the same age.

Alcohol is metabolized by the liver at a constant rate, which is not much influenced by body size.

The exact mechanism(s) by which alcohol exerts its effects in the central nervous system is not known, but its interactions with the GABA receptor are probably important.

Knowing a person’s weight, gender, and the amount of alcohol consumed, one can estimate the blood alcohol concentration (BAC), and from that the typical effects on behavior.

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The balanced placebo design has helped to separate the pharmacological effects of alcohol from the effects of alcohol expectancies.

Alcohol tends to increase the user’s focus on the “here and now,” a kind of alcohol myopia.

Alcohol-related traffic fatalities have decreased considerably since 1980, but there are still thousands every year in the United States.

Alcohol appears to enhance interest in sex, but to impair physiological arousal in both sexes.

Alcohol use is statistically associated with homicide, assault, family violence, and suicide.

Chronic heavy drinking can lead to neurological damage, as well as damage to the heart and liver. However, moderate drinking has been associated with a decrease in heart attacks.

Fetal alcohol syndrome is seen in less than 10 percent of babies whose mothers drink heavily.

Withdrawal from heavy alcohol use can be life-threatening when seizures develop.

The notion that alcohol dependence is a disease in its own right goes back at least to the 1700s but did not become popular until Alcoholics Anonymous began to have a major influence in the 1940s and 1950s.

Although many studies have indicated a likely genetic influence on susceptibility to alcohol dependence, the exact nature and extent of this genetic link is not known.

Review Questions

1. What is the maximum percentage of alcohol obtainable through fermentation alone? What would that be in “proof”?

2. Did Prohibition reduce alcohol abuse?

3. In about what year did apparent consumption of alcohol reach its peak in the United States?

4. About how much more likely are men than women to engage in frequent heavy drinking?

5. About how many standard drinks can the typical human metabolize each hour?

6. For your own gender and weight, about how many standard drinks are required for you to reach the legal BAC limit for driving under the influence?

7. Alcohol enhances the action of which neurotransmitter at its receptors?

8. What is the typical behavior of a person with a BAC of 0.20 percent?

9. Describe the four groups in the balanced placebo design.

10. What term is used to describe the fact that drinkers tend to focus on the “here and now”?

11. About what proportion of U.S. traffic fatalities are considered to be alcohol related?

12. What is the role of expectancy in males’ increased interest in sex after drinking?

13. If alcohol did not actually increase violent tendencies, how might we explain the statistical correlation between alcohol and such things as assault and homicide?

14. Why is it dangerous to drink alcohol to “stay warm” in the winter?

15. If someone you know has drunk enough alcohol to pass out, what are two things you can do to prevent a lethal outcome?

16. Can brain damage be reversed if someone has been drinking heavily for many years?

17. About what percentage of the heaviest-drinking women will have children diagnosed with FAS?

18. What is the most dangerous withdrawal symptom from alcohol?

19. Did the early founders of AA view alcohol dependence as a disease?

20. If one identical twin is diagnosed with alcohol dependence, what is the likelihood that the other twin will also receive this diagnosis?

References

Lender, M. E. Drinking in America. New York: The Free Press, 1987.

Koren, J. Economic Aspects of the Liquor Problem. New York: Houghton Mifflin, 1899.

Clark, N. H. The Dry Years: Prohibition and Social Change in Washington. Seattle: University of Washington Press, 1965.

WHO Global Status Report on Alcohol and Health 2018. Available at www.who.int/publications/i/item/global-status-report-on-alcohol-and-health-2018

List of countries by beer consumption per capita. Retrieved from Wikipedia.com, June 29, 2020.

NIAAA Surveillance Report #115. Available at https://pubs.niaaa.nih.gov/publications/surveillance115/CONS18.pdf

“Mass. Alcohol Tax Cut Hurt Bottom Line at N. H. State-Owned Liquor Stores.” Concord Monitor, February 26, 2013.

Substance Abuse and Mental Health Services Administration. (2019). Results from the 2018 National Survey on Drug Use and Health. Available at http://www.samhsa.gov/data

American College Health Association. ACHA-NCHA Reference Group Data Report. Hanover, MD. American College Health Association, Spring 2019.

Frezza, M., and others. “High Blood Alcohol Levels in Women: The Role of Decreased Gastric Alcohol Dehydrogenase Activity and First-Pass Metabolism.” New England Journal of Medicine 322 (1990), p. 95.

Massa, A. A., O. S. Subramani, C. I. Eckhardt, and D. J. Parrott. “Problematic Alcohol Use and Acute Intoxication Predict Anger-Related Attentional Biases: A Test of the Alcohol Myopia Theory. Psychology of Addictive Behaviors 33 (2) (2019), pp. 139–43.

National Highway Traffic Safety Administration. (2019). Traffic Safety Facts: Alcohol-Impaired Driving, 2018 Data. NHTSA Publication DOT HS 812 864.

Insurance Information Institute. Facts and Statistics: Alcohol-Impaired Driving. Available at www.iii.org/fact-statistic/facts-statistics-alcohol-impaired-driving

George, W. H., and S. A. Stoner. “Understanding Acute Alcohol Effects on Sexual Behavior.” Annual Review of Sex Research 11 (2000), pp. 1053–2528.

Crothers, T. D. “Alcoholic Trance.” Popular Science 26 (1884), pp. 189, 191.

Kuhns, J. B., M. L. Exum, T. A. Clodfelter, and M. C. Bottia. “The Prevalence of Alcohol-Involved Homicide Offending: A Meta-Analytic Review.” Homicide Studies 18 (2014), pp. 251–70.

Krebs, C. P., and others. “College Women’s Experiences with Physically Forced, Alcohol- or Other Drug-Enabled, and Drug-Facilitated Sexual Assault before and since Entering College.” Journal of American College Health 57 (2009), pp. 639–49.

Boenisch, S., and others. “The Role of Alcohol Use Disorder and Alcohol Consumption in Suicide Attempts–A Secondary Analysis of 1921 Suicide Attempts.” European Psychiatry 25 (2010), pp. 414–20.

Centers for Disease Control and Prevention. “Vital Signs: Alcohol Poisoning Deaths.” Available at https://www.cdc.gov/vitalsigns/pdf/2015-01-vitalsigns.pdf

Britton, A. “Alcohol and Heart Disease.” British Medical Journal 341 (2010), pp. 1114–5.

Popova, S., S. Lange, C. Probst, N. Parunashvili, and J. Rehm. “Prevalence of Alcohol Consumption during Pregnancy and Fetal Alcohol Spectrum Disorders among the General and Aboriginal Populations in Canada and the United States.” European Journal of Medical Genetics, 60 (2017), pp. 32–48.

Sachdeva, A. “Alcohol Withdrawal Syndrome: Benzodiazepines and Beyond.” Journal of Clinical and Diagnostic Research, 9 (2015), pp. 1–7.

American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 5th ed. Washington, DC: American Psychiatric Association, 2013.

Kreusch, F., and others. “Assessing the Stimulant and Sedative Effects of Alcohol with Explicit and Implicit Measures in a Balanced Placebo Design.” Journal of Studies on Alcohol and Drugs 74 (2013), pp. 923–30.

Design Credits: (Drugs in the Media) ©Glow Images; (Targeting Prevention) ©Medioimages/Alamy; (Life Saver) ©McGraw Hill Education; (Taking Sides) ©McGraw Hill Education; (Focus on Treatment) ©dencg/Shutterstock.com

Do You Have a Drinking Problem?

This assessment was designed to be a simple and rapid way for a physician to interview a patient and get an initial indication of whether to suggest a more thorough assessment of alcohol use disorder. You can ask the questions about your own drinking.

Rapid Alcohol Problems Screen (RAPS 4)

1. During the last year have you had a feeling of guilt or remorse after drinking? [Remorse]

2. During the last year has a friend or a family member ever told you about things you said or did while you were drinking that you could not remember? [Amnesia]

3. During the last year have you failed to do what was normally expected from you because of drinking? [Perform]

4. Do you sometimes take a drink when you first get up in the morning? [Starter]

A “yes” answer to any one of these should cause you to reflect seriously on whether your drinking behavior is already on a dangerous path. If you answered “yes” to two or more, we suggest that you visit a professional counselor, psychologist, or physician who specializes in substance abuse, to discuss your drinking and get a more in-depth assessment.

C. J. Cherpitel, “A Brief Screening Instrument for Alcohol Dependence in the Emergency Room: The RAPS 4,” Journal of Studies on Alcohol, 61 (2000), pp. 447–9.