chapter2 note - CHAPTER 2 HEREDITY ENVIRONMENT PSYCHOACTIVE...

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Unformatted text preview: CHAPTER 2 HEREDITY, ENVIRONMENT, PSYCHOACTIVE DRUGS CHAPTER OVERVIEW This chapter examines the routes that drugs take to the brain and the ways in which they affect brain chemis- try. Psychoactive drugs affect both the old (primitive) brain and new brain particularly the re- ward/reinforcement center. Drugs cause their effects by mimicking or modifying neurotransmitters and other brain chemicals. An individual’s drug tolerance, tissue dependence, withdrawal, and metabolism determine additional effects. Besides the desired effects of drugs, undesirable side effects also occur. The level of drug use, from absti— nence, experimentation, and social/recreational use to habituation, abuse, and addiction, depends not only on the amount, frequency, and duration of drug use but on a person’s susceptibility to take psychoactive sub- stances compulsively as determined by heredity and environment. All these factors cause alterations in brain chemistry that can affect a person from a few hours to a lifetime. Many of these alterations can be seen with the assistance of new imaging techniques such as SPECT, MRI, and PET brain scans. SHORT CHAPTER OUTLINE ' HOW PSYCHOACTIVE DRUGS AFFECT US I. HOWDRUGS GET TO THE BRAIN A. ROUTES OF ADMINISTRATION & DRUG ABSORPTION 1. Inhaling 2. Injecting 3. Mucous Membrane Absorption 4. Oral Ingestion 5. Contact Absorption B. DRUG DISTRIBUTION 1. The Blood-Brain Barrier II. THE NERVOUS SYSTEM A. PERIPHERAL NERVOUS SYSTEM B. CENTRAL NERVOUS SYSTEM C. OLD BRAIN-NEW BRAIN 1. Old Brain 2. New Brain D. THE REWARD/REIN- FORCEMENT CENTER 1. Nucleus Accumbens 2. Satiation Centers E. ON/OFF SWITCHES F. MORALITY & THE REWARD/REIN F ORCE- MENT CENTER G. NEUROANATOMY 12 1. Nerve Cells H. NEUROTRANSMITTERS & RECEPTORS 1 . Maj or Neurotransrrntters 2. Advanced Neurochemistry 3. Agonist & Antagonist III. PHYSIOLOGICAL RESPONSES T 0 DR U GS A. TOLERANCE 1. Kinds of Tolerance B. TISSUE DEPENDENCE C. PSYCHOLOGICAL DEPENDENCE & THE REWARD/REINFORCING ACTION OF DRUGS D. WITHDRAWAL 1. Kinds of Withdrawal IV. BASIC PHARMACOLOGY A. METABOLISM & EXCRETION FROM EXPERIMENTA- TION TO ADDICTION V. DESIRED EFFECTS VS. SIDE EFFECTS A. DESIRED EFFECTS B. SIDE EFFECTS C. POLYDRUG ABUSE VI. LEVELS OF USE A. ABSTINENCE B. EXPERIMENTATION C. SOCIAL/RECREATIONAL D. HABITUATION E. DRUG ABUSE F. ADDICTION VII. THEORIES OF ADDICTION A. ADDICTIVE DISEASE MODEL B. BEHAVIORAL/ENVIRON- MENTAL MODEL C. ACADEMIC MODEL D. DIATHESIS-STRESS THEORY OF ADDICTION VIII. HEREDI T Y, EN VIRON- MENT, PSYCHOACTIVE DRUGS, & COMPULSIVE BEHA VI ORS A. HEREDITY 1. Twin & Retrospective Studies 2. Alcoholism-Associated Genes B. ENVIRONMENT 1. Environment & Brain Development C. PSYCHOACTIVE DRUGS D. COMPULSIV E BEHAVIORS IX. ALCOHOLICMICE & S OBER MICE X. COMPULSION CURVES XL CONCLUSIONS EXTENDED CHAPTER OUTLINE HOW PSYCHOACTIVE DRUGS AFFECT US Drug research has shifted from “Why do we crave a drug?” to “Why can’t we stop craving a drug?” (p. 43) I. HOWDRUGS GET TO THE BRAIN This is determined by the route of administration, the speed of the effects, and the action of the drugs on nerves and neurotransmitters. (p. 43) A. Routes of administration, from most rapid to the slowest, are the following: 1. Inhaling allows the vaporized drug to enter the lungs, the heart, and then the brain in about 7—10 seconds. (p. 44) 2. Injecting puts a drug directly into a vein (ef- fects in 15—30 seconds), into muscles, or under the skin (effects in 3—5 minutes for the last two methods). (p. 44) 3. Snorting and mucosal exposure. Drugs like cocaine and heroin, which are snorted, are absorbed through mucous membranes in the nasal passages. Other drugs like chopped coca leaves or tobacco snuff are placed un- der the tongue on the gums (effects in 3—5 minutes). (p. 45) 4. Oral ingestion. Drugs like codeine pass into the stomach and then into the small intestine where they are absorbed by capillaries in the intestinal walls. (p. 45) 5. Contact & transdermal absorption. Expo- sure puts drugs like LSD into the system through the eye or like nicotine via saturated adhesive patches next to the skin. (p. 45) B. Drug distribution. Drugs circulate through the bloodstream to the rest of the body where they will cause an effect, be ignored, be absorbed, or be biotransformed. Distribution depends on the drug itself and on the blood volume of the per- son taking it (6—8 quarts in an adult). In general the less a person weighs, the less blood to dilute the drug. A drug takes effect in 10—15 seconds after entering the bloodstream and has its great- est effects on the brain and spinal cord. (p. 45) 1. The blood-brain barrier. The walls of the capillaries that form a protective shield around the nerve cells of the central nervous system (CNS) and guard against toxins, vi- ruses, and bacteria can be penetrated by psy- choactive drugs. This penetration happens because psychoactive drugs are fat-soluble and the brain and its barrier are fatty. (p. 46) II. THE NERVOUS SYSTEM The nervous system is composed of the central nervous system and the peripheral nervous system. (p. 46) A. The peripheral nervous system is further di— vided into the autonomic nervous system, which controls involuntary functions such as circulation, digestion, and respiration, and the somatic nervous system, which transmits sen- sory messages from the environment to the central nervous system. (p. 47) B. The central nervous system (brain and spinal chord) is the message center, receiving, ana- lyzing, and responding to messages from the peripheral and autonomic nervous systems. Drugs alter information sent, disrupt the proc- essing of the information, and disrupt the com- mands sent back through the body. (p. 47) C. The old brain-new brain, a useful division based on anatomy, function, and location, helps us understand how psychoactive drugs work, especially when these concepts are put in an adaptive evolutionary framework. (p. 47) 1. The old brain, consisting of the brain stem, cerebellum, and mesocortex, regulates physiologic functions, experiences basic emotions and cravings, and imprints survival memories. (p. 48) 2. The new brain, which allows us to reason, speak, create, and remember, consists of the neocortex and processes the information from the old brain. Craving often is located in the old brain and is a powerful primitive impulse that can override the rationality of the new brain. (p. 48) D. The reward/reinforcement center is that part of the old brain that encourages a human being to remember and repeat an action that promotes survival. It is also affected by drugs and is thus responsible for craving. Drugs act on the re- ward pathway to trigger craving for euphoria or pain relief. This center is also called the E. G. 14 “mesolimbic dopaminergic reward pathway.” (13- 49) l. The nucleus accumbens is a small group of nerve cells called the “medial forebrain bun- dle.” It is a powerful motivator (reinforcer). Many psychoactive drugs stimulate this re- ward/reinforcement center and the longer the use, the stronger is the “do it again” message. (p. 49) 2. The satiation center is crucial in keeping craving and satiation in balance. When the reward/reinforcement center is activated by refined psychoactive drugs, the impact is so strong that they can imprint the emotional memory of euphoria or pain relief more deeply than most natural survival memories. This can induce strong cravings when im— printed memories are activated. Because the reward/reinforcement center is so connected with the physiologic regulatory center of the body, drugs strongly affect physiologic functions like heart rate and respiration. Psychoactive drugs hijack these mecha- nisms. (p. 50) On/off switches. Research is looking at why we can’t stop craving drugs and a number of theories about how drugs disrupt the on/of switches of the reward/reinforcement and satia- tion centers. These include, among others, the on/off switches becoming stuck or being ig- nored or overridden. Behavioral addictions also disrupt the on/off switches. (p. 50) Morality & the reward/reinforcement center. Since the reward/reinforcement center and the rest of the primal brain react more quickly and intensely than the neocortex, it takes a powerful conscious effort to override cravings and de- sires from the old brain even when reason tells us those feelings are antisurvival. Almost all theologies teach that one must resist most pri— mal cravings in order to live a moral life. (p. 51) Neuroanatomy 1. Nerve cells, consisting of dendrites, the cell body, the axon, and terminals, transmit im- pulses by sending neurochemicals (called “neurotransmitters”) across the synaptic gap between the nerve cells or neurons. These neurotransmitters move from holding sacs (vesicles) in one nerve cell, across the syn— aptic gap, slot into receptor sites, trigger an impulse, and then move back to the sending cell. There are rapid signals for reflex reac- tions and slower signals to allow time for thought. (p. 51) H. Neurotransmitters & receptors. The discov- ery of endorphins and enkephalins, the body’s own opioids (endogenous opioids) gave an un— derstanding of how drugs work. Exogenous opioids are external opioid drugs such as heroin and morphine. Psychoactive drugs cannot cre- ate sensations or feelings that don’t have a natu- ral counterpart in the body. (pp. 53—54) 1. Major neurotransmitters are acetylcholine (ACh); norepinephrine 01E) and epineph- rine (E); dopamine (DA); histamine; seroto- nin (5-HT); enkephalins, endorphins and dynorphins; GABA; glycine; glutamic acid (glutamate, glutamine); substance P; anan— damide; corticotrophins (ACTH, cortisone), nitric oxide (NO), and adenosine. Besides these, at least 100 more have been discov- ered. (p. 54) 2. Advanced neurochemistry. When a neuro- transmitter slots into a receptor, it causes an ion molecular gate to open allowing sodium, potassium, or chloride ionic electrical charges in or out. Excitatory neurotransmit- ters increase cell firings by opening the gate and allowing positive sodium ions in. In- hibitory neurotransmitters reduce cell firings by allowing negative ions in and pushing positive ions out. The process where the neurotransmitter directly affects electrical transmission in the receiving neuron is called the “first messenger system.” If the received neurotransmitters cause other bio- logical or chemical changes that then affect the electrical transmission, it is called a “second messenger system.” If a cell senses there are too many transmitters, it will de- crease the number of receptor sites to slow down transmission (down regulation). If there are too few, the opposite occurs (up regulation). (pp. 55—56) 3. Agonist & antagonist. Drugs disrupt neural message transmission. Agonists are those drugs that enhance neural signals whereas antagonists block neural signals. Drugs work in a number of ways: they imitate neuro- transmitters, prevent their reabsorption, re- lease them, force the release of excessive Immmmmmm amounts, or slow their action. Some stimu— lants release stimulating neurotransmitters. Depressants inhibit release of pain- transmitting neurotransmitters or force the release of inhibiting neurotransmitters. Psy- chedelics alter or confuse messages. (p. 56) III. PHYSIOLOGICAL RESPONSES T 0 DR U GS It is the way in which psychoactive drugs interact with neurotransmitters, nerve cells, and other tis- sues that helps determine how drugs affect people and why it is difficult to control their levels of use. (p. 57) A. Tolerance results from the body’s attempt to eliminate a drug that it treats as a toxin. With continued drug use, the body tries to neutralize the toxic effects, requiring larger amounts of the drugs to achieve the original effects. The degree of tolerance depends on amount, dura- tion, and frequency of use and an individual’s chemistry and state of mind. (p. 57) 1. Kinds of tolerance Dispositional tolerance is the speeding up of metabolism to handle the drug. Pharmacodynamic tolerance results from the desensitization of nerve cells to the ac- tion of a drug. Behavioral tolerance is the adjustments the brain makes in behavior to cope with the effects of a drug. Reverse tolerance is the greater sensitivity to a drug that grows as the body’s ability to metabolize a drug decreases. Acute tolerance is the body’s immediate resistance to the effects of a drug. Select tolerance means that tolerance de- velops to some effects of a drug but not others resulting in potentially fatal side ef- fects as larger doses are needed to achieve a high. Inverse tolerance (kindling) is the greater sensitivity to a drug because the body has learned how to anticipate and intensify the pleasurable effects of the drug. (p. 58) B. Tissue dependence is the biological adaptation of the body to a drug such that the body comes to depend on the drug to stay in balance. With— out the drug, withdrawal effects develop. (p. 59) C. Psychological dependence & the reward- reinforcing action of drugs result from the ac- tion of drugs on brain chemistry. Pleasurable effects of drugs virtually hypnotize the user into continual use. (p. 59) . Withdrawal is marked by the unpleasant ef- fects that follow the cessation of drug use as the body attempts to restore its chemical balance. Withdrawal effects can be severe; fear of their severity is a motive to keep abusing drugs. (p. 6.0) 1. Kinds of withdrawal Nonpurposive withdrawal is the series of unpleasant or even life-threatening physio- logical effects that accompanies cessation of drug use by an addict. (p. 60) Purposive withdrawal is either the ma— nipulative counterfeiting of withdrawal symptoms by the abuser or the self-inducing of expected symptoms. (p. 60) Protracted withdrawal (environmental triggers & cues) is the flashback or recur— rence of addiction withdrawal symptoms that trigger heavy craving for a drug long after detoxification. The craving can be trig- gered by a sensation associated with prior use and can be strong enough to cause re- lapse. (p. 61) IV. BASIC PHARMACOLOGY A. Metabolism & excretion. Metabolism is the ability of the body to process, use, and inacti- vate drugs or food—the neutralization proc— ess—while excretion is the process of elimi- nating those substances from the body. The chief organ of metabolism is the liver. Meta— bolic rates vary according to age, race, heredity, gender, general health, emotional state, the presence of other drugs in the system, weight, tolerance, and exaggerated or allergic re- sponses. (p. 61) FROM EXPERIMENTATION TO ADDICTION V. DESIRED EFFECTS VS. SIDE EFFECTS A. Desired effects include satisfying curiosity, getting high, self-medicating, gaining self- confidence, increasing energy, relieving pain, controlling anxiety, obliging friends, gaining 15 social confidence, relieving boredom, altering consciousness, coping with isolation or other personal problems, gaining a competitive edge, or seeking oblivion. (p. 61) B. Side effects include those undesirable effects that accompany drug use, ranging from mild to moderate to dangerous to fatal. These physical and mental effects along with social side effects are some of the main problems with psychoac— tive drugs. Users hope to take enough of a drug to get its effects without triggering the side ef- fects. (p. 63) C. Polydrug abuse, the combination of more than one abused drug, complicates treatment. People resort to polydrug use to replace the desired drug when it is not available, to get different feelings, to give the body a rest from a usual drug, to enhance the effects of a drug, to gain different effects, to switch drugs, or to counter- act the effects of a drug. (p. 64) VI. LEVELS OF USE These levels are one benchmark for deciding whether use of a drug is accelerating or has be- come problematic. Amount, frequency, and dura- tion help gauge the levels of use as does an as- sessment of the impact the drug has on a person’s life. Except for abstinence, the following levels should be seen as indistinct phases shading off into one another and varying from person to person. (p. 64) A. Abstinence means not using drugs except acci- dentally. With true abstinence, drug craving cannot develop no matter how high a hereditary and environmental predisposition exists. (p. 65) B. Experimentation is the infrequent use of a drug to satisfy curiosity. Only a few exposures occur and no pattern of use develops. Never- theless, problematic consequences can develop, even from experimentation, if the user is preg- nant, is driving, has a physical or mental illness, is an addict, has an allergic reaction, or has 1e- gal problems. (p. 65) C. Social/recreational use is an irregular pattern of use with small impact on a person’s life un- less the unintended consequences listed above develop. (p. 65) D. Habituation is a regular pattern of use and loss of some control over a drug but with minimal harmful consequences. (p. 65) 16 E. Drug abuse is continued use of drugs despite negative consequences. (p. 65) F. Addiction is compulsive use marked by preoc- cupation with the drug, severe negative conse- quences, denial, and relapse following with- drawal. Addiction also means loss of control and total focus on drug use. (p. 66) VII. T HEORIES 0F ADDICTION In the DSM-I V-T R, substance-related disorders are divided into substance use disorders and substance- induced disorders. Substance use disorders are then divided into substance dependence and substance abuse. Substance-induced disorders include condi- tions that are caused by use of specific substances, such as intoxication, withdrawal, delirium, etc. Theories of addiction focus on the environment, the host (the drug user), and the agent (the drug it— self) and the interactions between them. (p. 66) A. The addictive disease model, or medical model, holds that addiction is a chronic, pro- gressive, relapsing, incurable, and potentially fatal disease. It is triggered by drug use that re- acts to biochemical and neurological irregulari- ties. This model sees heredity as more impor- tant than environmental influences in moving a susceptible host into drug abuse. Addiction is characterized by impulsive use, loss of control, repeated attempts at abstinence, continuation of abuse despite negative consequences, and com- plications resulting from abuse. (p. 67) B. The behavioral/environmental model sees environmental and developmental influences as paramount in leading a person into drug abuse. Stress, anger, and peer pressure are some of the causal influences. (p. 67) C. The academic model sees addiction as occur- ring when the body adapts to the toxic effects of drugs. Given enough of a drug, a person will become addicted. The process is characterized by tolerance, tissue dependence, withdrawal syndrome, and psychic dependence. (p. 68) D. The diathesis—stress theory of addiction posits a predisposition or vulnerability to develop ad— diction based on genetic and environmental in- fluences combined with the availability of drugs or the practice of certain behaviors. (p. 68) VIII. HEREDI T Y, ENVIRONMENT, PSYCHOACTIVE DRUGS, & C OMPULSI VE BEHA VIORS Current addiction research indicates that the causes of drug addiction are a combination of three fac- tors: heredity, environment, and the use of psy- choactive drugs. (p. 68) frequent, or prolonged use can modify many of the same nerve cells and neurochemistry that are affected by heredity and environment. This influences not only the person’s reaction to those substances when they are used but also the level at which they are used. (p. 71) . Compulsive behaviors such as gambling, com- A. Heredity passes on a susceptibility to alcohol- ism, drug addictions, and other compulsive be- haviors from generation to generation. There are more than 100 genes that have been associ- ated with drug abuse. (p. 68) 1. Twin & retrospective studies have shown that identical twins, separated at birth and adopted into separate families, show more characteristics of their birth parents than of their adoptive parents with respect to alco— holism. Males are 34% more likely to be al- coholic than non-alcoholic if one parent is alcoholic, 400% more likely if both parents are alcoholic, and 900% more likely if both parents and a grandparent are alcoholic. (p. 68) 2. The alcoholism-associated gene (DRDzAI allele gene) was found in twice the number of severe alcoholics than in social drinkers or abstainers (70% vs. 30%). People with this gene, a so-called compulsivity gene, are more susceptible to alcoholism, addiction, and other compulsive behaviors. (p. 69) . Environment. interactions with the environ- ment, particularly home environment, actually make new nerve cell connections and alter the neurochemistry a person is born with thereby helping to determine how that person will use psychoactive drugs. (p. 69) 1. Environment & brain development. Envi- ronment helps mold the 100 trillion connec- tions between brain cells especially during the first 10 years of life. Addicts in treat- ment demonstrate high levels of childhood abuse both physical and emotional. Envi- ronment can increase the susceptibility to drug use and abuse in formative years and through social attitudes and practices. Trau- matic experiences and stress can also have lasting effects, making people more suscep- tible to drug abuse. (p. 69) C. Psychoactive drugs can cause addiction, even in individuals who were not made susceptible by their heredity or environment. Excessive, pulsive sex, and eating disorders are actual dys- functions of brain chemistry in the same way that drugs disrupt brain chemistry. These com- pulsive behaviors are different from obsessive- compulsive disorder (OCD). With compulsive behaviors there is an experience of pleasure as- sociated with the action whereas with OCD ac- tions are not associated with pleasure. (p. 72) IX. ALCOHOLIC MICE & SOBER MICE A classic experiment with mice demonstrated that mice bred as alcoholics, mice injected with alco- hol, mice subjected to stress, and in another ex- periment, mice nutritionally deprived all increased alcohol use to alcoholic levels. The experiments indicate that heredity, drugs, stress, and diet re- striction can lead to alcohol addiction. In addition analysis of the brains of the four groups of mice showed approximately the same alteration of brain chemistry. (p. 72) X. COMPULSION CURVES These curves are a way of indicating the interplay of heredity, environment, and drug use in pro- ducing compulsive use of alcohol and other drugs. 0 Hereditary susceptibility to avoid, use, or abuse drugs varies from individual to individ— ual depending on inherited brain structure and neurochemical composition. 0 Environmental factors, including childhood abuse, environmental stress, or nutritional re- strictions, can also increase susceptibility to habituation, abuse, and addiction. 0 Drug use can move people further along the compulsion curve, depending on the strength of the drug, amount, frequency, and duration of use. 0 Long~term or heavy drug use might take those with low susceptibility 10 years or more of heavy drinking to become alcoholics. It might take someone with high susceptibility less than a year. 17 0 It is somewhat unclear exactly what happens if 7. someone abstains after heavy drug use but indications are that many who have been ad— dicted will have a higher susceptibility than they had before they relapsed the last time. 8 0 Recovery from addiction is possible if stress is reduced and alternative coping strategies are adopted but any use will lead to rapid relapse. (p. 73) XI. CONCLUSIONS The interrelations of heredity, environment, psy- choactive drugs, and compulsive behaviors require 1 that any study of addiction should focus on the to— tality of people’s lives. (p. 76) DISCUSSION TOPICS 1. Discuss the differences among different meth- 2. ods of drug use and the factors that make some- one choose one method or another. 2. Talk about which human functions are con- trolled by the old brain and why they are. 3. Discuss why the reward/reinforcement center came to exist in animals and human beings and how it is a survival trait. 4. Describe how a message is sent from a sensa- tion to the brain and back again to another part of the body. 5. List and discuss natural activities that will have an effect similar to various psychoactive drugs. 6. Discuss how a desired effect of a drug can also be an unwanted effect in a different situation (e.g., a painkiller such as codeine deadens pain but also can cause drowsiness that could inter- fere with one’s ability to do certain kinds of work.) 18 Think about substances you eat or drink and how your capacity for use (tolerance) may have increased and then compare that to the increase in tolerance for psychoactive drugs. . Choose some activity you or a friend pursue to excess and describe the process that might have occurred from experimenting with the behavior, up through the levels of use, to addiction. CRITICAL THINKING AND CLASS EXERCISES . Have several students discuss which neuro- transmitter is most responsible for their person- ality. Then talk about someone else in the class they know, choosing a neurotransmitter that best describes their basic personality. Divide the class into five groups and ask each group to extemporize a conversation about how they might go about finding a drug if they were a. experimenters b. social/recreational users c. habitual users (1. abusers e. addicted. . Have students ask some friends or a parent to describe exactly how they feel physically and mentally after a cup of coffee (stimulant), after a cigarette (stimulant), and after drinking alco- hol. Then discuss reactions such as heart rate, alertness, physical coordination, clarity of thought, and problem-solving abilities. . Ask students to make a list with two columns, heredity and environment. Then have them list five factors under heredity and five under envi- ronment that might make them more suscepti- ble to drug abuse and five that would make them less susceptible. ...
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This note was uploaded on 04/13/2008 for the course BIO 1033 taught by Professor Joel.martinez,jr.,ph.d. during the Fall '04 term at The University of Texas at San Antonio- San Antonio.

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chapter2 note - CHAPTER 2 HEREDITY ENVIRONMENT PSYCHOACTIVE...

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