Handbook of the Medical Consequences of Alcohol and Drug Abuse

John Brick, John Brick

• Publisher: Routledge
• Year: 2012
• ISBN:
  9781136864575
• Edition: 2
• Topic: Medicine
• Subtopic: Medical Theory, Practice & Reference

The essential newly-expanded reference that needs to be on the desk of every health care professional who encounters substance abusers. Handbook of the Medical Consequences of Alcohol and Drug Abuse, Second Edition is the newly-updated classic reference text that provides even more detailed and expanded information on the pharmacological, toxicological, and neuropsychological consequences of alcohol and drug abuse. Eight new chapters of crucial information have been added. Written by leading experts in the fields of medical physiology, psychopharmacology, and neuropsychology, this valuable resource provides the detailed alcohol and drug information health professionals in all fields need to know. Handbook of the Medical Consequences of Alcohol and Drug Abuse, Second Edition greatly expands on the expert information provided in the first edition. This text provides reviews of the cardiovascular, neurological, pulmonary, gastrointestinal, psychological, and hepatic effects of commonly abused drugs. The book also provides in-depth explanations of the mechanisms by which these psychoactive drugs exert their biobehavioral effects as well as current thinking about—and definitions of—abuse, dependence, and alcohol/drug use. The Handbook of the Medical Consequences of Alcohol and Drug Abuse, Second Edition includes vital information on:

• alcohol, including definitions of alcohol use, abuse, and dependence
• the relationship between alcohol and accidental injuries, alcohol's effect on skeletal and major organ systems, and its effect on risk factors for certain cancers
• effects of alcohol and other drugs on neuropsychological function
• the effects of alcohol on neuron signaling, neurotransmitter function, and alcoholic brain damage and cognitive dysfunction
• fetal alcohol effects
• chronic effects of marijuana use on psychological and physical health, including a fair and balanced discussion of the medical marijuana issue
• the consequences of opiate abuse and methadone pharmacotherapy, including a comparison of the effects of methadone and heroin on organ systems
• cocaine's history, the various forms of the drug, and the adverse effects of cocaine on cardiovascular, neurologic, and pulmonary systems
• the medical consequences of inhalants ranging from benzene to xylene
• the prenatal effects of nicotine, cocaine, marijuana, and opiates
• terminology that appears in the current literature on alcohol

New topics in the Handbook of the Medical Consequences of Alcohol and Drug Abuse, Second Edition include chapters discussing:

• chemical dependency in psychiatric patients
• medical consequences of steroids
• OTC medications
• hallucinogens
• health effects of tobacco, nicotine, and exposure to tobacco smoke
• interactions of alcohol with other drugs and other medications
• periodontal effects of alcohol and drug abuse in the oral cavity
• imaging studies of structural brain changes

The Handbook of the Medical Consequences of Alcohol and Drug Abuse, Second Edition is an invaluable resource for physicians, scientists, nurses, psychologists, and alcohol and drug counselors.

Chapter 1

Characteristics of Alcohol: Definitions, Chemistry, Measurement, Use, and Abuse

Brick, John

We begin this textbook with an overview of alcohol, one of the oldest and most widely used psychoactive drugs on earth. In an effort to provide a foundation for the interpretation of terms related to alcohol and its use throughout this text and elsewhere, this introductory chapter will define alcohol both as a chemical and as a drug, explain the scientific notation for reporting alcohol in blood or serum, and present an overview of the use of alcohol: how we currently define alcohol use, abuse, and dependence in American society.

What is Alcohol?

The term “alcohol” is used to define several types of alcohol, including the three most common: ethyl alcohol (ethanol), methyl alcohol (methanol), and isopropyl alcohol (isopropanol). All alcohols have a similar chemical structure and contain a hydroxyl group, OH, attached to a saturated carbon molecule. Methyl alcohol, also known as methanol or wood alcohol, is so highly toxic that even small amounts (less than an ounce) may cause retinal damage. Methanol’s toxicity is the result of its metabolism to formaldehyde and then to formic acid, a cellular toxin that is about six times more poisonous than methanol. The accumulation of formic acid produces severe metabolic acidosis and more than 6 to 7 ounces of methanol are lethal for most adults.

Isopropyl alcohol, also known as isopropanol or common rubbing alcohol, is also highly toxic. Small amounts, as little as a few ounces, can cause permanent damage to the visual system, and 8 ounces is considered a lethal dose. Some alcoholics may consume methanol or isopropanol, intentionally or unknowingly, and of the three alcohols with potentially lethal consequences discussed here, methanol and isopropanol are the most dangerous.

The alcohol that is the subject of this review and the alcohol consumed as a beverage by most people, is ethanol, a clear, relatively odorless chemical. The lethal dose (LD:50) of acute ethanol is estimated to be a blood alcohol concentration of about 0.40 percent, although death may occur at higher or lower concentrations depending upon factors such as tolerance or the presence of other drugs. Given reasonable alcohol pharmacokinetics, a 150-pound male would reach LD:50 after consuming about four to five drinks per hour over a four-hour period. Sublethal doses are more insidious and are the primary focus of this review. Throughout this chapter and throughout this book, the term alcohol will be synonymous with ethanol.

Whether we are discussing alcohol as a chemical or psychoactive drug, alcohol is a relatively simple molecule, CH₃–CH₂–OH, formed during a process of fermentation that occurs when yeast combines with water and sugar. The yeast recombines carbon, hydrogen, oxygen, and water to form alcohol and carbon dioxide. Different types of alcoholic beverages are derived from the use of different fermenting ingredients. Wine manufacturing, for example, may utilize grapes, apricots, berries, and other fruits that are rich in sugars and provide the necessary oxygen for fermentation. Fermentation continues until a maximum alcohol concentration of about 15 percent is reached, at which point, the concentration of alcohol is so high the yeast dies. Beers are manufactured with a different source of sugar, namely, the starch found in cereal grains, which is enzymatically converted to sugar through a malting process. This process involves sprouting cereal, such as barley, in water. The dried sprouts are then mixed with water. The enzymes formed during sprouting convert starch to sugar, which allows fermentation to proceed. For beers, the process of fermentation is stopped when the alcohol concentration reaches about 3 to 6 percent by volume, although some specialty beers may contain significantly more alcohol. For wines, the process is stopped, or found to be self-limiting, at higher concentrations (typically 11-13 percent by volume). Distillation of fermented beverages allows exceptionally high alcohol concentrations (typically 50–60 percent by volume in some beverages and up to nearly 100 percent in other products) to be obtained.

The range of alcohol concentration in alcoholic beverages is determined by biological processes, manufacturing design, or some combination of the two. Alcoholic beverage contents are usually expressed as a percentage of alcohol by volume, as in the case of beers and wines, or as “proof,” an archaic term that is twice the alcohol concentration by volume. From a scientific perspective, the total amount of alcohol in a measured drink should be standardized so that for all practical purposes it is the same from drink to drink. However, the differences in alcohol concentrations among beverages may have medical consequences because of the direct action of alcohol on the tissues with which it comes in contact. The concentration of alcohol in beverages varies widely from about 3 percent in the case of light beers to about 50 percent or more in some liquors. Outside the laboratory, the amount of alcohol in a serving varies due to many factors (e.g., container or serving size, drink formulation, etc.). As alcohol absorption to maximum concentration in blood takes from about 30 to 90 minutes in most social-drinking cases, and total absorption takes even longer; beverage type and beverage concentration may be a factor in determining some of the medical consequences of alcohol use (Brick, 2006). Therefore, studies regarding the acute effects of alcohol should be conducted, and the results interpreted with this fact in mind.

Scientific Notation for Alcohol Concentrations

Throughout this book, alcohol concentrations are expressed using various scientific notations. When comparing the results within these chapters with other references, it may be necessary to convert from one scientific notation to another. The concentration of alcohol in blood, serum, water, or any other liquid is the quantity of absolute alcohol by weight in a fixed volume of fluid. When alcohol is measured in breath, most breath-testing instruments are calibrated to take a fixed breath sample size. Instruments are designed on the basis of certain physiological assumptions and calibrated so that the results are reported as whole blood equivalents (e.g., 0.10 percent). In some literature, alcohol concentrations are reported as grams/ 2,100 cc air, and in blood or other tissues or fluids, they are more commonly reported in milligrams per deciliter (mg/dl). In molecular biological studies of how alcohol affects tissues, alcohol is sometimes reported in millimolar concentrations (mM). In those studies, mg/dl alcohol = mM alcohol × 4.6 provides a good conversion to a more identifiable concentration. This will be helpful for interpreting some of the data presented in Chapter 5, for example, ethanol concentrations of more than 50 mM (about 230 mg/dl) affect certain brain receptors but in some neurons, concentrations of more than 100 mM (about 460 mg/dl) were necessary to inhibit certain neuronal actions. These are relatively high doses.

When alcohol is measured in blood, the reported blood alcohol concentration (BAC) is the amount of alcohol by weight in a fixed volume of blood, which is usually 100 ml in the United States. BAC is usually expressed in g/100 ml or mg/100 ml of whole blood or serum. The following BAC notations are identical with regard to the amount of alcohol expressed: 0.10 percent, 0.10 g percent, 0.10 g/100 ml, 0.10 g/dl, 100 mg/dl, 100 mg percent, 100 mg/100 cc or ml.

Clinical Measurement of Alcohol

Most hospital clinical laboratories measure alcohol in serum, rather than in whole blood. As alcohol is distributed throughout the water-containing compartments of the body including the blood, serum alcohol is not the equivalent of a blood alcohol concentration because serum contains more water than the whole blood from which it is derived. Therefore, the concentration of alcohol in whole blood is less than that of the serum in proportion to their respective water contents. This may have important implications for scientists comparing test results. Early studies reported that the plasma: whole blood ethanol ratio ranged from 1.10 to 1.35 with an average of 1.18 (Payne, Hill, and Wood, 1968). Payne’s average value of 1.18 has found acceptance in the literature (Baselt, 2000) and corresponds as well as our observations comparing serum alcohol measured by the alcohol dehydrogenase (ADH) method with gas chromatography analyses of the same sample (unpublished observations). Other studies suggest the ratio of serum: whole blood alcohol ranges from about 1.1 to 1.18 (Winek and Carfagna, 1987) to 1.25 (Hodgson and Shajani, 1985). Individual differences between subjects or within the same subject after some medical interventions, for example, may alter the water content of blood. Various mathematical models have been proposed when interpreting BACs particularly in patients with hemodilution or hemoconcentration (Brick, 2006; Brick and Erickson, 1999).

Defining Alcohol Use

Alcohol has been consumed for thousands of years, but the medical consequences of alcohol abuse have come to the attention of the medical/scientific community only in the last 150 years or so. Alcohol consumption and related problems have been well documented (Dufour, 1999). In the United States, for example, nearly half the adult population consumes alcohol, and alcohol-related medical problems account for a disproportionate number of hospital admissions. Data from the National Longitudinal Epidemiologic Survey indicate that nearly 9 percent of adults in the United States consume, on average, more than two drinks per day (Dawson et al., 1995), and the results of an ongoing national survey of high school students recently reported that among twelfth graders, about 3 percent consume alcohol daily and about half of them had consumed alcohol within the last month of the survey (Johnston, O’Malley, and Bachman, 1999). The use of alcohol and other drugs also has a profound economic impact. Estimates place the cost of addiction at more than $200 billion per year from the effect of alcohol on families and society through lost wages, absent or ineffectual parental models, and shared exposure to high risks and resulting injuries associated with intoxication.

Alcohol use is not always associated with deleterious medical consequences. In fact, some research suggests that alcohol use under some conditions is beneficial to health. How alcohol exerts such biphasic effects has been the subject of considerable research and debate. However, we can define alcohol use in two ways: first, through current definitions of use, abuse, and dependence and, second, by defining what constitutes “a drink.” The social use of alcohol is now generally described as a cold beer after a ball game, a glass of wine with meals, or a glass of champagne at festive occasions. Alcohol consumption is often defined as drug abuse (or misuse) whenever it places the drinker or others affected by the drinker’s behavior at increased risk for injury. The term “moderate” drinking is sometimes used by clinicians, and often used by laypersons, to describe consumption that is neither abusive nor very infrequent, or that describes a constellation of behavioral or other factors that differentiate it from “light” or “heavy.” However, these terms are relative. For example, a “moderate” drinker may drink heavily (e.g., more than six drinks a day on some days) but not be classified as a “heavy” drinker. On the other hand, the U.S. Department of Agriculture (USDA) and the U.S. Department of Health and Human Services in the Dietary Guidelines for Americans defines moderate drinking as one drink per day or less for women and two or fewer drinks per day for men (USDA, 1995). In addition, the National Institute on Alcohol Abuse and Alcoholism (NIAAA, 2000) further recommends that people aged 65 and older limit their consumption of alcohol to one drink per day. The terms light, moderate, and heavy should be interpreted carefully based on the operational definition of the study as the definitions of these terms vary. Similarly, there is considerable variation in terms of defining “a drink” (Case, Destefano, and Logan, 2000; Kerr et al., 2005).

The Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) (American Psychiatric Association, 1994) defines two types of problem drinkers: (1) abusers, who intentionally drink too much, too often, and make wrong choices about their use of alcohol, and (2) dependent users (i.e., alcoholics), who lack control over their use of alcohol in lifestyle situations in which abusers would generally stop drinking. Voluntary alcohol abuse is a significant problem that contributes to accidents, medical expenses, lost productivity, family problems, and, of course, a host of direct and indirect medical consequences. Drug dependence, whether the drug is alcohol or some other psychoactive substance, is a brain disease caused by a neurochemical imbalance. The addict has no control of his or her alcohol or other drug use (see Erickson and Wilcox, 2001, for a review). Both types of drinkers are overly represented as inpatients and as patients in hospital emergency rooms.

What Constitutes a Drink?

We can also define what is meant by a drink by standardizing this definition across beverage types so that the interpretation is meaningful and useful. Many epidemiological and empirical research studies define alcohol consumption in terms of the number of drinks consumed or the number of grams of absolute alcohol. Often the precise definition of what constitutes a drink is not included in studies or the range of definitions makes it difficult to compare results across studies. Equating commonly consumed beverages, a drink can be defined as 1.5 ounces of 80-proof alcohol, 5 ounces of 12 percent wine, or a 12-ounce standard beer (~4.8 percent v/v) (Brick, 2006). Each of these contains approximately 14 grams of alcohol, 0.6 ounces of absolute alcohol, and about 100 kilocalories. Outside of the laboratory, a mixed drink may contain more or less than 1.5 ounces of 80-proof alcohol (or the equivalent) and wine may be served in volumes larger or smaller than 5 ounces. Similarly, the concentration of alcohol in beers varies from an average of about 3.8 percent (v/v) for “light” beers to about 5 percent (v/v) for most beers. Imported or specialty beers may contain significantly more alcohol by volume (Case et al., 2000).

Regardless of the type of alcoholic beverage consumed, it is the psychoactive drug ethanol that produces the effects on the brain, virtually all cells within the body, and behavior. The degree of those effects is determined by the concentration, amount, and time of consumption, bioavailability due to factors such as absorption and biotransformation of alcohol, and drinking experience. All of these factors ultimately result in the exposure and response of various cells to concentrations of alcohol.

References

American Psychiatric Association (1994). Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition. Washington, DC: American Psychiatric Association.

Baselt, R.C., ed. (2000). Disposition of Toxic Drugs and Chemicals in Man. Foster City, CA: Chemical Toxicology Institute.

Brick, J. (2006). Standardization of alcohol calculations in research. Alcoholism Clinical and Experimental Research 30(8).

Brick, J. and Erickson, C. (1999). Drugs, the Brain, and Behavior: The Pharmacology of Abuse and Dependence. Binghamton, NY: The Haworth Medical Press, p. 67.

Case, G.A., Destefano, S., and Logan, B.K. (2000). Tabulation of alcohol content of beer and malt beverages. Journal of Analytical Toxicology 24:202–210.

Dawson, D.A., Grant, B.F., Chou, S.P., and Pickering, R.P. (1995). Subgroup variation in U.S. drinking patterns: Results of the 1992 national longitudinal alcohol epidemiologic study. Journal of Substance Abuse 7(3):331–344.

Dufour, M.C. (1999). What is moderate drinking? Alcohol Research & Health: Winter 1999. Available at: http://www.findarticles.com/p/articles/mim()CXH/is123/ai57050104. Accessed January 18, 2006.

Erickson, C. and Wilcox, R. (2001). Neurobiological causes of addiction. Journal of Social Work Practice in the Addictions 1(3):7–22.

Hodgson, B.T. and Shajani, N.K., (1985). Distribution of ethanol: Plasma to the whole blood rations. Canadian Society of Forensic Science Journal 18:73

Johnston, L.D., O’Malley, P.M., and Bachman, J.G. (1999). Drug trends in 1999 are mixed. Retrieved from the University of Michigan Web site: http://www.monitoringthefuture.org.

Kerr, W.C., Greenfield, T.K., Tujague, J., and Brown, S.E. (2005). A drink is a drink? Variation in the amount of alcohol contained in beer, wine and spirits drinks in the US methodological sample. Alcoholism Clinical and Experimental Research 29(1):2015–2021.

National Institute on Alcohol Abuse and Alcoholism (2000). Tenth Special Report to the U.S. Congress on Alcohol and Health. Washington, DC: U.S. Department of Health and Human Services.

Payne, J.P., Hill, D.W., and Wood, D.G.L. (1968). Distribution of ethanol between plasma and erythrocytes in whole blood. Nature 217:963–964.

Pieters, J., Wedel, M., and Schaafsma, G. (1990). Parameter estimation in a threecompartment model for blood alcohol curves. Alcohol and Alcoholism 25:17–24.

U.S. Department of Agriculture and U.S. Department of Health and Human Services (1995). Home and Garden Bulletin No. 232, Fourth Edition. Washington, DC: U.S. Department of Agriculture.

Winek, C.L. and Carfagna, M. (1987). Comparison of plasma, serum and whole blood ethanol concentrations. Journal of Analytical Toxicology 11:267–278.

Chapter 2

Medical Consequences of Acute and Chronic Alcohol Abuse

Brick, John

Introduction and Overview

More has been written about alcohol and its diverse effects tha...