Child and Adolescent Drug and Substance Abuse

A Comprehensive Reference Guide

Louis A. Pagliaro, Ann Marie Pagliaro

• Publisher: Routledge
• Year: 2019
• Print ISBN:
  9781138542143
• eBook ISBN:
  9781351009461
• Topic: Psychology
• Subtopic: Addiction in Psychology
• Index: Psychology

By offering unique analysis and synthesis of theory, empirical research, and clinical guidance in an up-to-date and unbiased context, this book assists health and social care professionals in understanding the use of drugs and substances of abuse by children and adolescents.

A comprehensive reference for health and social care professionals, the book identifies and corrects related false narratives and, with the use of the authors' combined experience of over 70 years of clinical and academic experience in drug and substance abuse, provides current pharmacotherapeutic and psychotherapeutic approaches for the treatment of alcohol or other dependence or use disorders among children and adolescents. The book also provides a useful reference for identifying brand/trade and street names of the drugs and substances of abuse commonly used by children and adolescents. Also included is a comprehensive, cross-referenced subject index.

Clear, comprehensive, accessible, and fully referenced, this book will be an invaluable resource for professionals and students who aim to treat children and adolescents. Child and Adolescent Drug and Substance Abuse is the 19th clinical pharmacology and therapeutic text that the Pagliaros have written over the past 40 years and is the sixth that deals exclusively with drug and substance abuse.

1

Alcohol

Alcohol―whether provided by an older sibling, stolen from a parent’s liquor supplies, purchased at a corner liquor store with a false I.D. or obtained by paying an adult standing outside of a liquor store, for a “six-pack” of beer—is widely used and abused by adolescents and young adults in the U.S. Whereas children often take a sip of a can of beer, while delivering it to a thirsty parent, “just to see what it tastes like,” adolescents and young adults often drink large amounts of beer and other alcoholic beverages in small groups or at parties and celebrations to:

1. Achieve a desired dose-dependent disinhibition euphoria;
2. Attain a sense of well-being;
3. Be like “everyone else,” whose “parents let them do it;”
4. Decrease social and sexual inhibitions;
5. Fit in with peers;
6. “Just have fun;”
7. Relieve anxiety, tension, or stress—to “cope” with “life’s pains, disappointments, and impossible tasks.”¹

Unfortunately, the abuse of alcohol is associated with more harm than all of the other drugs and substances of abuse—combined.

In this chapter, we present and discuss alcohol with attention to its pharmacology—“pharmacodynamics” (i.e., mechanism of action); “pharmacokinetics” (i.e., absorption, distribution, metabolism, and excretion); and related undesired, or harmful, effects and toxicities. Also included in the pharmacology section are alcohol: drug–drug interactions; overdosage; and effects when used by adolescent girls and young women during pregnancy and lactation. We then present and discuss child alcohol exposure and patterns of adolescent and young adult alcohol use in the U.S., during the new millennium. The chapter concludes with a thorough discussion of the assessment, diagnosis, and treatment of alcohol dependence or use disorder (AUD) among children and adolescents.²

Pharmacologically, alcohol is classified as a psychodepressant that belongs to the “sedative-hypnotic” subclass, which also includes the prescription sedative-hypnotics (e.g., benzodiazepines; z-drugs).³ However, we decided to separate alcohol from the prescription sedative-hypnotics and discuss it in its own chapter. There are several reasons for this decision, including the:

• Long history of medical and personal use of alcohol in the U.S.;
• Identification of alcohol as a neurotoxin in humans;
• Discontinued medical use of alcohol as a “psychostimulant” during the last century;
• Cultural inculcation of alcohol into social gatherings, parties, and celebrations in the U.S.;
• Potential for significant alcohol-related physical, mental, and social harm, including severe and irreversible teratogenic effects—Fetal Alcohol Syndrome/Spectrum Disorder (FAS/FASD)—when used by adolescent girls and young women during pregnancy;
• Use of alcohol, in the U.S., as a “rite of passage” from adolescence to adulthood;
• Current use of alcohol by more than 80% of adolescents and young adults in the U.S.

We begin with an overview and discussion of the pharmacology of alcohol.

Pharmacology

In this section we highlight the: basic chemistry; pharmacodynamics, or mechanism of action; pharmacokinetics; drug–drug interactions; and undesired, or harmful, effects and toxicities associated with alcohol use. Also discussed is alcohol overdosage and alcohol use during pregnancy and lactation.

Chemistry

In the scientific discipline of chemistry, “alcohol” is defined as any organic compound to which a hydroxyl (-OH) functional group is bound to a carbon atom. However, popularly it refers to beverage alcohol―ethyl alcohol or ethanol (Figure 1.1). Throughout this reference text, we use the word, “alcohol,” to refer exclusively to beverage alcohol.

Figure 1.1 Chemical Structure of Alcohol

Beverage alcohol⁴ is a colorless, flammable, and volatile liquid that is produced by fermenting various carbohydrate foodstuffs, including fruits, grains, and vegetables with the use of yeasts.^{5, 6} Like other sedative-hypnotics, alcohol produces a progressive dose-related depression of the central nervous system (CNS) that ranges from mild sedation to deep sleep. Coma may rarely occur and can be fatal. These psychodepressant effects are generally predictable and depend on three major factors:

1. “Type” of the alcoholic beverage ingested (e.g., beer versus whiskey);
2. “Proof” (i.e., the equivalent to double the percentage concentration of the alcoholic beverage—for example, 40 proof indicates 20% alcoholic concentration);
3. “Amount” of the alcoholic beverage ingested (e.g., one can of beer or a six-pack of beer) per unit of time (e.g., hour, day, or week).

For further information regarding these factors, see the related discussion in the later section, “Blood Alcohol Concentrations.”

Pharmacodynamics: Mechanism of Action and Blood Alcohol Concentrations

Common Misbelief: Alcohol is mostly used and abused for its psychostimulant actions.

Mechanism of Alcohol Actions

As recently as the last century, alcohol was considered to be a “psychostimulant” that was commonly used for such desired effects as to “have fun” and to “warm-up after coming in from the cold.” It also was medically used for a variety of indications, including reviving someone who has fainted and treating the fatigue and weakness associated with cachexia. Although this belief was supported by lay and medical observations that drinking too much often resulted in such behaviors as taking off one’s clothes and dancing naked on a table in a favorite bar or getting into a violent bar fight, alcohol possesses no psychostimulant actions (see the following subsection, “Blood Alcohol Concentrations”).

Empirical findings in support of the psychodepressant actions of alcohol include the observation that as more alcohol is consumed during a drinking episode, drinkers do not become more wakeful, they become drowsier and, inevitably, uniformly fall asleep.

The exact mechanism of action by which alcohol depresses the entire CNS remains a mystery. However, research over the last several decades has resulted in two major plausible theories:

1. Alcohol readily crosses the blood-brain barrier disrupting the function of brain membrane lipids and glucose metabolism;
2. Alcohol acts at two specific receptor sites in the brain—gamma aminobutyric acid (GABA_A) receptor sites and N-methyl-D-aspartate (NMDA) receptor sites (e.g., Brower, 2001; Gonzales & Jaworski, 1997; Pagliaro & Pagliaro, 2009; Peoples, Li, & Weight, 1996).

While either theory may contribute to alcohol’s actual mechanism of action, research in glucose metabolism supports the first theory, which also explains alcohol’s effects on learning and memory. Research in support of the second theory suggests that alcohol acts to enhance GABAergic inhibition primarily by modifying the membrane environment of the GABA_A receptor complex. This action significantly increases the affinity of the GABA_A receptor complex for both endogenous (e.g., GABA) and exogenous sedative-hypnotics (e.g., barbiturates and benzodiazepines), thus, enhancing GABAergic inhibition.⁷

In addition, alcohol appears to inhibit the activity of glutamate, which is a naturally occurring excitatory neurotransmitter that functions largely at the NMDA receptors—as well as AMPA receptors and metabotropic glutamate receptors (mGluRs) (Gonzales & Jaworski, 1997). The regular, long-term use of alcohol results in “up-regulation of the NMDA receptors.” The NMDA receptor has been posited, based on data obtained from laboratory animal studies, to play a significant role in both: (1) alcohol-induced neurotoxicity; and (2) the alcohol withdrawal syndrome, particularly the occurrence of withdrawal-related seizures (Chang-Mu, Jen-Kun, & Shing-Hwa, 2010; Charlton, Sweetnan, & Fitzgerald, 2002; Hoffman, 1995; Hoffman & Tabakoff, 1994). (For further related discussion of the GABA_A receptor complex, see Chapter 6, “Prescription Sedative-Hypnotics.”)

Additionally, other factors have been identified as contributing to both the pharmacological and toxicological effects related to alcohol use and withdrawal (Vezali Costardi, Teruaki Nampo, & Lourenco Silva, 2015). For example—regarding the serotonergic system:⁸ (1) serotonin release and transmission are increased in the CNS by the acute administration of alcohol; (2) regular long-term, or chronic, use of alcohol leads to adaptive changes to the serotonin 5-HT₂ receptor (e.g., “up-regulation” or an increase in the number of 5-HT₂ receptors); and (3) serotonin levels are reduced during alcohol withdrawal (Lovinger, 1997; Tollefson, 1989).

Blood Alcohol Concentrations

Regardless of the actual mechanism of action, BACs that are associated with the amount of alcohol ingested during a drinking episode highly correlate with the direct and progressive depression of the CNS (Pagliaro & Pagliaro, 2009).⁹ (See Table 1.1)

Table 1.1 Blood Alcohol Concentration (BAC) and Associated Physical and Mental Effects among Adolescents and Young Adults^{10, 11}

BAC (gram % or grams per 100 ml)	Physical Effects	Mental Effects
0.01 to 0.03	Generally, normal appearance	Generally, normal behavior
0.03 to 0.06	Feel warm and relaxed with mild impairment of coordination and diminished ability to perform fine motor tasks	Mild euphoria (e.g., feelings of intense excitement and happiness) with decreased inhibitions and increased sociability and talkativeness Mild decreases in alertness and concentration
0.06 to 0.08	Increasing loss of coordination with a slight loss of both balance and speaking ability	Mild impairment of reasoning and memory with intensification of emotions Increased disinhibition euphoria with apparent “stimulant effect” on behavior and extroversion Lowered interest in sex
0.08 to 0.10	Mild imp...

Table of contents

• Cover
• Half Title
• Title Page
• Copyright Page
• Dedication
• Table of Contents
• List of Illustrations
• About the Authors
• Acknowledgements
• Preface and Introduction
• Epigraph
• 1. Alcohol
• 2. Amphetamines and Cocaine
• 3. Caffeine and Nicotine
• 4. Cannabis and Other Psychodelics
• 5. Prescription Opiate Analgesics and Heroin
• 6. Prescription Sedative-Hypnotics
• Index