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THE MITIGATING EFFECTS OF ADDICTION AND HIGH POTENCY STIMULANT USE ON CRIMINAL BEHAVIOR
As an expert with experience dealing with individuals who have addictive disease and their families, I am aware of a number of preconceptions that lay individuals, like jurors, may have regarding the disease of addiction. The lay perception is fourfold. First, many lay individuals believe that choosing to take drugs is the result of a character flaw. Therefore, moral significance may be attached to the decision to start taking drugs. Second, many individuals believe that the decision to take a drug on any single occasion is a choice the abuser makes. Therefore, in the common understanding the decision to take the drug is always a volitional act. Third, lay individuals believe that a user is still capable of rational thinking and volitional acts at the time of the crime, so that the fact of intoxication does not matter in their thinking about an individual's culpability. Fourth and finally, many lay individuals believe that a drug user many choose to quit at any point, so that moral significance is attached to the user's inability to just quit using drugs. Expert testimony regarding the disease of addiction must address these preconceptions. A drug is a pleasure producing chemical. (We refer only to psychoactive drugs; those drugs, both legal and illicit, that affect brain chemistry.) "Drugs" activate or imitate chemical pathways in the brain associated with feelings of well-being, pleasure, and euphoria. In order for a drug to have abuse potential, it must interact with specific brain chemistry in the reward and pleasure centers of the brain. The research is clear that methamphetamine, cocaine, alcohol, heroin and nicotine, all have an essentially similar mechanism of action through the neruotransmitters, dopamine and endorphin. While all drugs of abuse affect brain function through the action of dopamine, some drugs are more powerful, some are less powerful, some are sedating and some are excitatory. (reference/footnote: A summary of research findings is available in Blum K, Cull JG, Braverman ER, Comings DE. Reward deficiency syndrome. American Scientist 1996;84:132-145.) Pleasure serves to reward the completion of instinctive drives. Higher organisms have inherent "instincts" that drive them to seek/obtain food, seek/obtain water, seek/ have sex, seek/make shelter, and protect their young. Each drive/instinct has two aspects: First, if the drive is frustrated or cannot be met, the organism experiences dysphoria, anxiety, irritability, and anger. Second, if the drive is achieved, there is a complex interaction of neurotransmitters that leads to the release of dopamine and endorphins; the individual is rewarded or feels pleasure for completing the instinctive drive. Instincts are very powerful. When someone is under the pressure of an instinct, when a drive state is active, behavior is less voluntary; in other words, it is driven behavior. (reference/footnote: A summary of research findings is available in Wise RA. The neurobiology of craving: implications for the understanding and treatment of addiction. Journal of Abnormal Psychology 1988;97:118-32.) In 1954 Dr. James Olds, a psychologist, discovered that parts of the brain, when stimulated, produce a sensation of pleasure; these are the reward/pleasure centers of the brain. (reference: Olds J. Pleasure centers in the brain. Scientific American 1956;195:105-116.) When these parts of the brain are very strongly stimulated, the effect is euphoria, extreme pleasure. The reward/pleasure centers of the brain are closely attached to the parts of the brain that generate instinctive behavior. Each drive state is specifically located in the brain; attached to each part is a connection to the reward/pleasure centers of the brain called the dopamine/endorphin reward pathway. Drugs activate or imitate the chemical messengers (neurotransmitters) in the brain associated with feelings of well-being, pleasure and euphoria. A psychoactive drug activates the reward/pleasure centers of the brain. Drugs by-pass instinctual drives, but stimulate the release of specific neurotransmitters, dopamine and endorphins, in the reward/pleasure centers of the brain. Drugs go directly into the reward/pleasure centers of the brain and activate them. The individual does not have to work or have food or have sex, just use the drug. The release of neurotransmitters is much greater in drug stimulated states than in response to naturally occurring instinctive drives. Drugs of abuse modify the neurochemistry of pleasure. the euphoric "high" is produced by augmenting dopamine and endorphin function in the reward/pleasure centers of the brain. Generally, the intensity of the high is related to the degree to which reward circuits are activated. In addition to receptor binding properties of the drugs themselves, "pharmacokinetic" properties of the drugs have a major role in determining how high the "high" will be. Drugs that are delivered to the brain in high concentrations in a short time concentrate the "high;" the dopamine and endorphin generated by the drug are abruptly dumped in the reward/pleasure centers proportional to the sudden appearance of high concentrations of the drug. (Figure 1). The resultant "rush" of euphoria is intensely pleasurable, and likely to lead to loss of control over use of the drug more quickly than with low intensity drugs such as marijuana or alcohol. The release of dopamine is experienced as excited euphoria; release of endorphins is experienced as calm euphoria. Intensity of the high is one aspect of the drug's addictive potential. The other major aspect of addictive potential is the damage these extraordinary rushes do to the reward/pleasure centers themselves. Neuroadaptation is the process by which receptors in the reward/pleasure centers adapt to the high concentrations of dopamine and endorphins produced by the drugs. The receptors become insensitive to normal neurotransmitter levels. When the user stops and the high concentrations of dopamine and endorphin plummet, the reward/pleasure centers do not function. This process, called tolerance, is analogous to the deafness produced by exposure to loud sound, the pleasure centers "neuroadapt" to the high intensity stimulation. The user finds that s/he has to use more and more and more of the drug to get the same pleasure once obtained from a low dose of the drug. Tolerance to the drug effects is the result of neuroadaptation. A second problem with psychoactive drugs is more subtle, but probably more dangerous; drugs injure sobriety. Drugs damage the ability of the user to experience normal pleasure, to get normal enjoyment from the activities of daily life. Consequently, daily life becomes rather empty, and the user pulls away from the activities s/he formerly enjoyed. In a manner of speaking, it is as if the drug has "deafened" the pleasure centers, and the user no longer hears the amount of pleasure they would get from a walk with a friend or playing a game of ball or playing with their child. The user's normal mental state changes from feeling okay to feeling empty or bored or flat. The name for this feeling is dysphoria. High potency drugs: cocaine, heroin and methamphetamine, substantially injure the reward/pleasure centers so that the sober state of somebody who has been using a high potency drug is not normal. The sober state is dysphoric. The dysphoria activates the drive to use drugs. The individual's goal in using the drug changes from seeking euphoria to avoiding dysphoria; for most addicts the goal is simply to feel normal. After this change occurs the drug seeking/using behavior becomes less and less voluntary. The user becomes addicted to the drug in the most literal sense of the word, neurologically they have developed a new instinct (drive.) Over time that instinct (drive) becomes more powerful than any of the other instincts: seek/obtain food, seek/obtain water, seek/ have sex, seek/make shelter, and protect their young. An example of this can be found in a research study by ______ He started an intravenous line. in a rat, and let the rat bump up against a button. Each time the rat pressed the button, it received a dose of cocaine. The rat used the cocaine around the clock, about every 20-25 minutes, around the clock without sleep. The rat did not stop for food; it did not stop for fluids; it did not stop for sex. The rat was given an electric shock and did not get out of harm's way. The rat used the cocaine until it died. For drug addicts sobriety undergoes dramatic changes: in particular, the loss of ability to experience pleasure (dysphoria, anhedonia), inability to mobilize energy (anergia), and the appearance of extreme high levels of craving for the drug. Under unstimulated conditions, the user instead feels as if s/he was experiencing an unmet instinctive drive: dysphoria, anxiety, anger, frustration, and craving. The injury caused by receptor insensitivity leads the user to feel, when sober, the opposite of feeling high. For the user, sobriety becomes the opposite of euphoria. Both the length of use and the intensity of the drug are factors predicting the extent of the injury and the persistence of these distressing symptoms. When the drug is removed and the pleasure centers are unstimulated, the individual goes as low as they had been high. So, if the user spent a lot of time being very intoxicated, very high, when s/he tries to stop, clinically, most high intensity drug users experience significant symptoms, such as anxiety and insomnia, for up to a year or more. In 1980 the course of human history shifted when an ancient drug, cocaine, became a "high intensity" drug by becoming smokeable. That historical shift is now reinforced by the introduction of smokeable forms of two other highly addictive drugs, methamphetamine and heroin. In this context, "high intensity" refers not to the use of large amounts or frequent use, but rather to the intensity of the euphoric "high" induced by the drug. Users of these high intensity drugs are quite different from low intensity users of the same drugs, e.g., snorting or eating. For many of these users, sobriety itself becomes so unpleasant and dysfunctional that the risk of relapse is heightened. Use of high intensity drugs produces higher amounts of direct toxic injury to mental health, and the symptoms of an associated or underlying mental health disorder will be dramatically exacerbated.
DEFINITION OF ADDICTION The classic definition of addiction has four criteria, meaning that to diagnose addiction or drug dependence, four criteria must be met. Addiction is a disease of compulsion. Behavior that is compulsive is not voluntary. Therefore, addiction to any substance, such as methamphetamine or alcohol, is defined by loss of control; the user can't not do it; s/he is compelled to use. Compulsion is not rational; one does not plan to be compulsive. A person becomes an addict when they can no longer control their use. The central issue, the basic issue in addiction, is control. The issue is not getting sick when you stop. It is a control issue. An addict is someone who cannot control their use, the more addicted, the less control. A late stage addict will use unto death. S/he will not be able to stop until either something happens or they die. Therefore, compulsion or loss of control is the center piece of the disease.
Most persons have lost control at one time or another, that does not make the person an addict. The second characteristic of addictive disease is continued use despite adverse consequences. An addict is someone who uses even though s/he knows it is causing problems; an addict is someone who, even though they are experiencing job problems or emotional problems or their emotional or spiritual life is in trouble, continues to use the drug. The disease of addiction is not staged on the basis of how much the individual uses or how long s/he has used. Addiction is staged by the number of adverse consequences someone has had, and the severity of those consequences. Someone can be quite young and be a late stage addict because they have sustained serious problems and despite the severe problems s/he continues to use. The fourth symptom of the disease is denial. Denial is a distortion of perception caused by craving. The user, under the pressure of intense craving, is temporarily blinded to the risks and consequences of their drug use. In the face of terrible trouble, even in the face of health problems, craving for the drug blinds the addict. Thinking is distorted. The craving state is a true distortion of thought. The individual cannot see the consequences of what they are doing, and their behavior in the denial state is driven, allowing behaviors that would otherwise be morally or socially unacceptable to them. An analogy would be to someone being very hungry and having not eaten for three or four days. Under those conditions, someone who has never committed a crime or done any theft at all may break their own rules, violate their own standards, and thieve for food. When the craving builds up, the addict loses control over their behavior, and they really cannot see what they are doing. Physical dependence is a separate phenomenon from addiction. Physical dependence, such as alcohol dependence, is characterized by tolerance: the need for increasing amounts of alcohol to achieve intoxication or desired effect, or markedly diminished effect with continued use of the same amount of alcohol, and withdrawal as manifested by either the characteristic alcohol withdrawal syndrome when use is abruptly discontinued or resolution of the symptoms if a closely related substance is taken. As recently as twenty years ago people were taught there were two kinds of addiction, psychological addiction and physical addiction. These terms are outmoded. What was once called psychological addiction is the disease of addiction, including compulsive use, continued use despite adverse consequences, drug craving, and denial (distorted thinking in the presence of craving.) The American Psychiatric Association in the DSM IV uses the diagnostic term drug dependence to define the disease of addiction . What was once called physical addiction is now called physical dependence. Physical dependence is a separate phenomenon from drug dependence. Drug dependence means the individual cannot control his/her use of substances in the face of adverse consequences driven by craving and denial. Physical dependence means the individual becomes physically ill when use of the substance is discontinued; that is called withdrawal or the abstinence syndrome. The process is one of tolerance to the drug and the physiological need to use more to achieve the same effect. Many individuals have both the disease of addiction and physical dependence. If an individual is physically dependent, the appearance of withdrawal symptoms dramatically activates the drive to use. When the individual experiences withdrawal, drug craving becomes extremely intense, and commonly the individual will lose control.
BIO-PSYCHO-SOCIAL MODEL: PREDISPOSITION TO ADDICTION Addiction is a disease for which there is a known genetic predisposition. The first observation that alcohol runs in the family was in the book of Ecclesiastes in the bible. Dr. Alverez: you take 100 kids from the age of 9 or 10 and follow them long enough, you will observe that about 94 percent of kids will go through a period of time, usually adolescence or where they try to experiment or use drugs and alcohol. If you follow that group, 94 percent of whom tried drugs and alcohol, and follow that group, the next thing you will observe is that 80 percent of the people, all of whom tried it, will move through that period of experimentation and be okay, meaning they do not develop symptoms of the disease of addiction. They will have the ability to refuse drugs and alcohol. They will be able to moderate their use, and they will be able to control their use. Twenty percent get stuck, and in the research studies, the national prevalence of the disease of addiction is about one in five people, about 20 percent of Americans at some point in their life-time will meet criteria for diagnosis of the disease of addiction. So choice is present in most people at the onset of the experimentation time, but what we know is that some people usually on the basis of some predisposition ultimately lose control and are unable to exercise choice. For many years observers have noted that alcoholism runs in families. Over the past 90 years, more than 100 studies have shown that alcoholism is three to five times as frequent in the parents, siblings, and children of alcoholics as in the general population. More than 50 percent of persons who have addictive disease have a parent or grandparent with the disease. Children of alcoholic parents are four times as likely to become alcoholic themselves, whereas children who are raised by alcoholic adoptive parents are no more likely to become alcoholic themselves than other children. Sons of alcoholic fathers have between four and nine times the rate of alcoholism found in other males. Children of alcoholics are likely to become alcoholic even when raised in non-alcohol using homes. Numerous twin studies have shown that about 80% of drinking behavior (and smoking behavior) can be explained by inheritance. If an identical twin drinks alcoholically, the chances are about 80% that his (or her) twin also drinks alcoholically, even if they were adopted by separate non-drinking parents at birth. (kaprio j, koskenvuo m, langinvainio h, et al. Genetic influences on use and abuse of alcohol: a study of 5638 adult Finnish twin brothers. Alcoholism: clinical and experimental research 1987;11:349-56.) In genetically predisposed individuals, alcoholism develops at a younger age. Also, the course of the addictive disease is more severe. Koston showed that the sons of alcoholics (not themselves alcoholic) have decreased "sensitivity" to alcohol and drugs (the threshold for effect is higher.) These sons also had a prolonged response to drugs and alcohol, more rapid acquisition of tolerance, greater "rebound" effect (withdrawal) after stopping, and excess risk of toxic effects of alcohol, especially in the liver, brain, and pancreas. Once individuals are drug involved, they are at higher risk of losing control over use. Similarly, they are at increased risk of losing control when using other psychoactive drugs. (kosten tr. Neurobiology of abused drugs. Journal of nervous and mental disease 1990;178:217-27.) To understand what is inherited by individuals at risk of developing addictive disease requires an understanding of the role of neruotransmitters in generating the drug "high." In order for a drug to make the user "high" (to cause euphoria,) it has to activate the pleasure centers. Activating the pleasure centers means that the drug causes the release of neurotransmitters, the chemicals that the cells and the brain use to talk with each other. The neurotransmitters that must be activated to achieve a "high" are dopamine and/or endorphin. All drugs of abuse, in order to be a drug of abuse, augment dopamine function. Endorphins are the body's natural opiates. When the individual exercises hard, just to the point of physical pain, and then, there is a sudden feeling of exhilaration, the pain ebbs and energy increases; this is an example of endorphin release. That feeling is the result of the explosive release of endorphin in the pleasure centers of the brain. Endorphin is not just released under conditions of pleasure. The condition of pain, when the individual feels pain, what is perceived is actually less than it would have been because at the onset of a pain signal the brain also releases endorphins to reduce that pain. Dr. Caroline Gianoloukis was the first person to develop the technology to measure endorphins. She has published a series of papers to show that people who were born in families in which there's a high prevalence of alcoholism and drug addiction have about half as much endorphin as people who do not have that family background. Another group of investigators, including Doctor Kenneth Blum, Professor of Pharmacology at the University of Texas, has investigated the neurotransmitter, dopamine. Dr. Blum has published a series of studies to show that in some individuals with normal dopamine production, about one third fewer dopamine receptors are present. Some people appear to inherit both deficits, in other words, less endorphin and less dopamine, and those are the very most severely affected of all. Some people appear to just inherent just one deficit or the other. The younger the onset and the more explosive the alcohol/drug use, that group of persons tends to have the deficit, resulting in a dopamine system that is blunted. (Adapted from blum k, cull jg, braverman er, comings de. Reward deficiency syndrome. American scientist. 1996;84:132-145.) Dr. Blum calls this Reward Deficiency Syndrome. Individuals with Reward Deficiency Syndrome have been shown to have a specific chromosome sequence (predominantly the a1, d2 allele.) Persons with this chromosome sequence have 20% to 30% fewer reward (d2) receptors. Individuals with the a1 allele have a 74% increase in risk of having one or more of the reward deficiency syndrome disorders: substance abuse, compulsive disorder, attention deficit disorder. Insufficient dopamine receptors are what these disorders have in common. These individuals are hyperactive; they have to stimulate themselves constantly to feel normal. Once they discover drugs and alcohol, they tend to rely on the drugs or alcohol for the stimulation. And the tragedy of that is that the drugs further injure their dopamine endorphin systems resulting in cumulative damage. Every single time a reward deficient individual uses drugs, the tremendous difference between being high and being sober increases, and sobriety becomes less tolerable and more difficult. Sobriety becomes empty, hollow and dysphoric. The individual becomes anxious and irritable; they just feel bad all the time. At the same time it is perfectly clear to the individual that if they used a drug or alcohol, they would feel better. The studies of Dr. Shuckit, University of California, San Diego, have shown exactly what is inherited by individuals with addictive disease. In eloquent research he showed that one of the clinical manifestations of not having enough endorphin or dopamine receptors is that the individual with this background has a blunted response to the drug. This individual requires approximately twice as much alcohol/drug to get high as somebody without the background. Even though the individual gets pleasure that they had not felt before, they have to use considerably more alcohol/drug to get that pleasure. The other problem is that the individual with that genetic background acquires tolerance to alcohol/drugs much more quickly. For example, a young man who does not have a family background at the onset of his drinking experience, typically requires the equivalent of three beers to get high, to get a buzz. Someone with the genetic background of insufficient endorphin or dopamine receptors to get the same degree of high would have to drink about six beers. If you follow the two individuals, one of whom has the background, one of whom does not, at the end of a year of drinking tolerance will have occurred in both. At the end of a year of drinking, the individual without the genetic background who started drinking three beers to get high, now requires six beers to get high. The person with the genetic background who had needed six beers at the onset of drinking to get high now requires 18 beers to get high. Tolerance develops much more quickly in the at risk indvidual. Also, the rebound effect, the damage to the pleasure centers is much worse. In people with the genetic background, it's a setup for the development of addictive disease. In clinical terms this means that these individuals do not realize that their ability to experience pleasure is blunted until they discover a drug or alcohol. Then, they experience pleasure that heretofore, they did not know existed. They experience pleasure and reward that they had not previously experienced. It is very hard for these "reward deficient" individuals to go back to sobriety because they love the sensation that they get when they use. In that group of people there's a large portion of young onset, heavy drinkers, heavy drug using individuals. If the drug is around, those individuals have very frequent relapse problems. In retrospective studies childhood trauma, including emotional neglect, physical abuse, and especially unwanted sexual contact prior to age 13, are reported more frequently by individuals with addictive disease than by the non-addict population. Helplessness is the belief that one's situation is inevitable and unchangeable. When no one helps the child or tries to protect the child from trauma, when no help is available, the child develops a sense of helplessness that is well known to be associated with subsequent drug abuse. Finkelhor's population surveys in New England revealed that between l in 5 to 1 in 4 women had an "unwanted sexual contact" prior to the age of 13. Similar studies reveal that about 1 in 7 to 1 in 5 men had an "unwanted sexual contact" prior to the age of 13. In the studies of Rohsenow (l988), 71% to 90% of women in in-patient treatment for addiction reported a history of childhood sexual abuse. In these same Rohsenow studies, 23% to 42% of men being treated for addiction reported a history of childhood sexual abuse. (Rohsenow DJ, Corbett R, Devine D. Molested as children: A hidden contribution to substance abuse? Journal of Substance Abuse Treatment 1988;5:13-18.) Neglect is another kind of trauma for the child resulting in hopelessness, the feeling that no help is available. A substance abusing family is itself a highly traumatizing environment. There is a core feeling of danger for children in a substance abusing family. The children are unsupervised, neglected, subjected to more physical abuse, and may grow up in an atmosphere of violence. As a child there is little the individual can do to protect himself or others from the trauma, contributing to a lifelong sense of hopelessness. Children who live in severely traumatizing environments often develop chronic symptoms of Post Traumatic Stress Disorder (PTSD) leading to increased risk of drug and alcohol abuse. The essential feature of this disorder is the development of characteristic symptoms (intense fear, helplessness, or horror (or in children the response must involve disorganized or agitated behavior.) The symptoms, lasting more than one month, follow exposure to an extreme traumatic stressor involving direct personal experience of an event that involves actual or threatened death or serious injury or threat to one's physical integrity; or witnessing an event that involves death, injury or threat to the physical integrity of another person or learning about unexpected or violent death, serious harm, or threat of death or injury experienced by a family member or other close associate. The stressor producing this syndrome would be markedly distressing to almost anyone. The characteristic symptoms involve re-experiencing the traumatic event, avoidance of stimuli associated with the event or numbing of general responsiveness, and increased arousal. The diagnosis is not made if the disturbance lasts less than one month. (DSM IV.p.424) Long-term studies of war veterans who show symptoms of PTSD document that such individuals run a high risk of developing dependence on alcohol or other drugs. These traumatized men used alcohol and street drugs to control their insomnia, nightmares, hyperarousal, intrusive symptoms, and irritability, all of which can be consequences of the experience of trauma. A similar process is experienced by children who grow up in traumatizing environments.
MENTAL ILLNESS AND ADDICTION Dr. Khantzian (1985) studied 133 narcotic addicts: 93% met the criteria for one or more psychiatric disorders; of these 77% met criteria for diagnosis on Axis I, almost all of whom were diagnosed with major depression. Sixty five percent met criteria for diagnosis of a personality disorder on Axis II. A major feature of the diagnosed personality disorders was "negative mood" or "dysphoric affect," such as narcissistic and borderline personality disorders. Dr. Hesselbrock (l985) studied hospitalized alcoholics. Seventy seven percent met criteria for Axis I and/or Axis II psychopathology. Significantly, symptoms of mental illness preceded substance abuse, and the course of mental illness was exacerbated by the substance abuse. Individuals with mental illness symptoms started using alcohol/drugs earlier, progressed more rapidly in the disease of addiction, and were less successful in treatment. Clinical criteria for considering a dual diagnosis (addiction plus mental illness) are (1) onset of addictive disease in early or mid-adolescence, (2) indiscriminate polysubstance use, (3) frequent relapse despite engagement in treatment, (4) client states s/he dislikes sobriety, and (5) mental health symptoms worsen over time.
Environment helps shape the drug experience in two ways: set and setting. Set is defined as the individual's beliefs, attitudes and state of mind at the time of use. Setting is defined as the physical and social environment within which drug use occurs. User set and setting are shaped by both prescriptions and proscriptions of an individual's culture and social group. The individual's values and the rules of conduct influence the response one will have to the use of alcohol or any drug. (Beck, 1994, p28) The drug of choice, itself, contributes to the progression of addictive disease because some drugs are more potent than others. High potency drugs lead to the more rapid acquisition of tolerance forcing the user to escalate the dose to maintain the euphoric drug effect. Using an inadequate dose causes drug withdrawal; symptoms occur if the amount used is less than the tolerance level. Thus, the potency of the drug predicts the risk of developing physical dependence. Physical dependence occurs when the user gets sick or suffers withdrawal if the drug is abruptly discontinued. For example, "moonshine" whiskey, the home-brewed liquor that is available in the rural South is an extremely high potency alcohol. The route of drug administration also affects the drug using experience. The use of methamphetamine by nasal insufflation, snorting, leads very slowly to physical dependence because the amount of drug entering the body is less and the speed of administration is relatively slow. Intravenous use of methamphetamine leads to physical dependence with six to eight weeks because the route of administration is faster and more efficient. Intravenous use, like inhalation, smoking, produces an immediate, intense euphoria called a rush which prompts the user to try and recapture the euphoric feeling with subsequent use. An enabling system protects the user from the consequences of his drug use and therefore, exacerbates the symptoms of the disease. Some environments foster drug use because of the drug's availability and the lack of intervention in the using behavior.
Stimulant OVERVIEW Because cocaine and methamphetamine are so potent a small amount of the drug can cause dramatic effects. Even in very low doses, these stimulants produce a variety of significant physiological responses that are a consequence of the increase of epinephrine (adrenaline) in the system: pulse and blood pressure increase; the pupils dilate, and finally, body temperature rises. Stimulants increased motor and speech activity as well as nervousness and irritability. Alertness and excitement increase, and consequently, in high doses the drug produces prolonged periods of wakefulness, even when the individual is physiologically exhausted. (footnote: The DSM IV defines amphetamine intoxication (DSM IV 292.89) as A. Recent use of amphetamine or a related substance such as methamphetamine, and B. Clinically significant maladaptive behavioral or psychological changes (e.g., euphoria or affective blunting; changes in sociability; hypervigilance; interpersonal sensitivity; anxiety, tension, or anger; stereotyped behaviors; impaired judgment; or impaired social or occupational duration that developed during, or shortly after use, and C. Two (0r more) of the following developing during, or shortly after use 1. tachycardia or bradycardia 2. pupillary dilation 3. elevated or lowered blood pressure 4. perspiration or chills 5. nausea or vomiting 6. evidence of weight loss 7. psychomotor agitation or retardation 8. muscular weakness, respiratory depression, chest pain, or cardiac arrhythmia 9. confusion, seizures, dyskinesias, dystonias, or coma, and D. Symptoms not due to a general medical condition and are not better accounted for by another mental disorder. Diagnostic and Statistical Manual of Mental Disorders. 4th ed. Washington, DC: American Psychiatric Association, 1994. p.207-8.) If a strong stimulant, such as methamphetamine is used occasionally, the body has time to recover, and rest returns the body to a normal energy balance. If the stimulant is used over a long period of time or large quantities are consumed or both, the body becomes tolerant to the high stimulant levels; that is a high stimulant level becomes "normal," and the absence of the high stimulant level feels bad or dysphoric. Additionally, because the body is not allowed normal rest periods, the effects of exhaustion and starvation exaggerate the negative feelings. Methamphetamine use was prevalent after World War II; thereafter, the drug became the province of motorcycle gang members who cooked (manufactured) it, distributed it, and used it. Beginning in l988, reports of a new form of the drug appeared. This new form or methamphetamine was termed "ice" or "crystal meth." Prior to this time, the chemical basis for amphetamines was P-2-P. The P-2-P synthesis yields equal amounts of two forms of amphetamine, D-methamphetamine and L-methamphetamine. Of great significance, D-methamphetamine is of higher potency than L-methamphetamine because it enters the brain far more readily. The new methamphetamine, the "ice" or "crystal meth" form, is synthesized from ephedrine, and the product of this synthesis is pure, 100% D-methamphetamine. Crystallized to reduce impurities, the resultant drug is readily smoked. It should be viewed as the methamphetamine cousin to crack cocaine. Easily smoked, and producing an intense "high," it is remarkably addicting. The damage done to sobriety by this drug is catastrophic. Significantly, a large fraction of users will develop severe mental health problems, including toxic psychosis, that complicate treatment. In Southern California methamphetamine usually referred to as crystal; in Hawaii the drug is called ice. On the east coast, especially the southeast, the drug is called meth. Formerly, in the sixties the drug was called speed. There are old terms from the old eras of methamphetamine abuse, such as the biker era when it was called crank or go fast. Although there are many different names, but it is all the same drug. Beginning in Hawaii, California and the Southwest, the use d-methamphetamine is spreading epidemically. This epidemic differs from all previous drug epidemics in one major regard; this is the first recognized rural drug epidemic. D-methamphetamine is cooked in small labs that are easily hidden. After synthesis, the drug is distributed under the cover of the migrant worker streams. The principal areas of use are small farming communities throughout the Northwest, Midwest, and increasingly the Southeast.
PATTERNS OF USE BINGE CYCLE is the most common pattern of stimulant drug abuse. During the binge the drug is used regularly over a period of hours to days to achieve and maintain the drug high. The drug is usually smoked or injected intravenously. During the binge the individual's entire focus is drug use. The loss of control over use is progressive and the binge usually ends when the user has no more drug left. Distinct phases are recognized in the stimulant binge cycle. RUSH. The rush is the initial response the abuser feels when smoking or injecting cocaine or amphetamine and is the aspect of the drug that abusers do not experience when the drug is snorted or ingested orally. During the rush, the abuser's heartbeat races and metabolism, blood pressure, and pulse soar. The rush associated with crack cocaine lasts for approximately 2 to 5 minutes, as long as 20 minutes with methamphetamine. The reason for the rush is that the drug, when smoked or injected, triggers the adrenal gland to release a hormone call epinephrine (adrenaline) which puts the body in a battle mode, fight or flight. In addition, the physical sensation that the rush gives the abuser most likely results from the explosive release of dopamine in the pleasure center of the brain. HIGH. The rush is followed by the high, sometimes called the shoulder. During the high, the abuser often feels aggressively smarter and becomes argumentative, often interrupting other people and finishing their sentences. BINGE. The binge is the continuation of the high. The abuser maintains the high by smoking more cocaine or methamphetamine. The user is attempting to re-capture the "rush" of euphoria produced by the initial inhalation. Each time the abuser smokes or injects more of the drug a smaller euphoric rush than the initial rush is experienced until, finally there is no rush and no high. During the binge, the abuser becomes hyperactive both mentally and physically. Because there is rapid acquisition of tolerance (the process of neuroadaptation that forces the user to escalate the dose to maintain the euphoric drug effect.) and because failure to use more is associated with increasingly distressing symptoms of dysphoria, hysteria, paranoia, and agitation, the user continues smoking to avoid the distressing symptoms of "coming down.". The usual cocaine binge lasts 12 to 24 hours; methamphetamine binges last 24 to 72 hours. TWEAKING. Tweaking occurs at the end of the binge when nothing the abuser does will take away the feeling of emptiness and "dysphoria." including taking more crack cocaine. Tweaking is very uncomfortable, and the user often takes a depressant to ease the bad feeling. The most popular depressant is alcohol.. Tweaking is the most dangerous stage of the binge cycle because of the potential for violence. If alcohol is used to ease the discomfort, the threat to others intensifies. During the tweak the abuser can appear normal. In fact, unlike a person intoxicated on alcohol with glassy eyes, slurred speech, and difficulty even standing up, a tweaker appears "super-normal." The tweaker's eyes are clear, speech is concise, and body movement is quick and jerky. A tweaker can look directly at the observer and lie. With a closer look the observer will notice that the eyes are moving about ten times faster than normal and may roll.. Speech is quick, often the voice is steady with a slight quiver to it. The individual's movements are often exaggerated secondary to over stimulation; thinking is scattered and subject to paranoid delusions. Once bingeing has started, there is little that will interrupt it except for depleted stores of the drug. Typically, this necessitates brief interruptions of the binge to seek out more drug. It should be emphasized that once a binge pattern is initiated, subsequent drug use is not volitional, voluntary behavior. Rather, a binge is the typical event in stimulant addiction, a pattern of compulsive use that should be viewed as a complete loss of control over behavior. Laboratory animals provided with unlimited access to cocaine will continue to use it to the exclusion of food, water, sex, sleep, and will in fact die of cocaine intoxication in about 10 days. An extreme example of this behavior is illustrated by the "toss-up," a woman willing to exchange sex for drugs in a continuous, compulsive manner (men also engage in this behavior.) CRASH To a binge abuser, the crash means an incredible amount of sleep. The body's epinephrine has been depleted, and the body uses the crash to replenish its supply. During the crash the abuser sleeps deeply, appearing almost lifeless, and poses a threat to no one. However, the effects of sleep deprivation compound the cognitive and behavioral consequences of stimulant use. Research studies document that sleep-deprived persons develop perceptual distortions, temporal disorganization and recent memory impairment. The ability to concentrate on a task requiring sustained attention decreases. Decreased ability to concentrate results in decreased accuracy of task performance. The crash can last 1 to 3 days or longer. Upon awakening users report feeling relatively normal. (footnote: The DSM IV defines stimulant withdrawal (DSM IV 292.0) as A. Cessation or reduction in use that has been heavy and prolonged, and B. Dysphoric mood and two (or more) of the following physiological changes, developing within hours to days after cessation or deduction in use: 1. fatigue 2. vivid, unmpleasant dreams 3. insomnia or hypersomnia 4. increased appetite 5. psychomotor retatdation or agitation, and C. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning, and D. Symptoms not due to a general medical condition and are not better accounted for by another mental disorder. Diagnostic and Statistical Manual of Mental Disorders. 4th ed. Washington, DC: American Psychiatric Association, 1994. p.209.)
HIGH INTENSITY USE Methamphetamine levels are difficult, if not impossible, to interpret, and therefore of little clinical value. Long-term methamphetamine use sets in train a complicated series of interactions affecting both blood levels and behavioral responses. As is true in cases of cocaine abuse, death may be associated with very low or very high levels. Unlike alcohol, but like cocaine, blood levels do not correlate well with impairment. Since tolerance occurs, very high levels should not be surprising (6 references dated form 1963-1984) (1996 Karch, p.204) Karch in The Pathology of Drug Abuse 2nd ed. summarizing the results of a 1989 study by Suzuki notes "Daily oral dosing with methamphetamine appears to have little effect on either metabolism or peak blood levels. When a group of six volunteers was given 10mg of methamphetamine/day for two weeks, there was no evidence for any change in the rate of metabolism or in peak blood levels, which remained between 25-50 ng/mL." (1996 Karch, p.206) Therefore, the actual reported blood value is of little significance nor does a high value correlate with the presence of intoxication, psychosis or delirium. After the individual stops using a stimulant drug and goes throught the sleep (crash) phase, a period of relative normalacy occurs. However, within seven to ten days symptoms of withdrawal develop. This abstinence or withdrawal syndrome has three primary symptoms: anergia: decreased physical and psychic energy; anhedonia: inability to experience pleasure, boredom: in contrast to the intense euphoria of the drug experience, and craving for the drug. Two types of drug craving are recognized. Endogenous "comes from within" or background craving which is characterized by feelings of dysphoria, anergia, anhedonia. The most problematic craving is environmentally cued timulated by persons, places, things that the indiviudal associates with his/her specific drug using experiences. This type of craving is immediate, catastrophic, and overwhelming.(reference: Wise RA. The neurobiology of craving: implications for the understanding and treatment of addiction. Journal of Abnormal Psychology 1988;97:125.) In the context of environmentally cued craving the individual often loses control and returns to drug use despite terrible adverse consequences.
DEFINITION TOXIC PSYCHOSIS Stimulant Psychosis is characterized by delusions usually of the paranoid type and/or hallucinations usually auditory, occurring in the absence of intact reality testing, sometimes with disorganization of speech and behavior. Stimulant Psychosis can be expected to have several substantive effects on behavior; these can include euphoria or affective blunting, changes in sociability, hyper vigilance, interpersonal sensitivity, anxiety, tension, or anger, stereotyped (repetitive) behaviors, impaired judgment, or impaired social or occupational functioning. Cognitive abilities are similarly affected, including paranoia and hallucinations, compounding the severe irritability and poor impulse control. In short, a person intoxicated by high potency stimulants will be impaired in all areas of mental function. As a consequence of the drug-induced psychotic state, the individual is unable to separate fact from fantasy (psychosis), and is subject to irrational fear (paranoia) that can trigger responsive (and impulsive) behavior from him. Events occur, and behaviors are seen that would not occur if it were not for stimulant intoxication. Because of the paranoid delusions, the stereotyped compulsive behavior and the occurrence of visual and auditory hallucinations, methamphetamine intoxication has been compared to paranoid schizophrenia. A number of studies have shown that the biochemical effects of methamphetamine on the brain closely resemble those of paranoid schizophrenia. Besides inducing a psychotic episode in a healthy person, methamphetamine can also hasten such episodes in individuals with underlying psychiatric illnesses. In such users the liability for psychosis lasts well beyond the time that the user has methamphetamine in his system. The initial onset of psychotic symptoms in the stimulant drug user is a sentinel event because once psychosis develops, further use of these drugs, even in small amounts, will result in the prompt return of the psychotic symptoms. Stimulant psychosis requires medical management and often hospitalization. Between episodes of use the psychotic symptoms tend to subside and eventually resolve.. Delirium is a disturbance of consciousness manifested by a reduced clarity of awareness of the environment or more simply, delirium is a confusional state. There is impairment in the ability of the individual to focus, sustain, or shift attention. Interference with thought develops and the individual becomes disoriented to time and place. Perceptual disturbances appear including misinterpretation of events, illusions, and hallucinations. Thoughts skip and race, and information in the environment is misinterpreted (in particular, information is misinterpreted to mean that the individual is under threat). Though memory is not particularly affected, during the delirium the individual reacts to cues and stimuli in an exaggerated, overreacting, and excessive fashion. (footnote: The DSM IV defines a substance-induced delirium as A. Disturbance of consciousness (reduced clarity of awareness of the environment) with reduced ability to focus, sustain, or shift attention, and B. Change in cognition (disorientation, memory impairment, language disturbance, or perceptual disturbance (illusions or hallucinations,), and C. Rapid onset and fluctuating course during the day, and D. Evidence of causation by a physiologic condition (e.g., medical illness, intoxication or withdrawal.). Diagnostic and Statistical Manual of Mental Disorders. 4th ed. Washington, DC: American Psychiatric Association, 1994. p.131.) Often the appearance of drug-induced psychosis includes episodes of violence. Amphetamine-related violence is typically impulsive, not planned, and the degree of violence is greater than that which was expected from the actions of the intoxicated individual. In a methamphetamine intoxicated person, for example, the rate of thought is extremely fast, and there is little ability to ponder the consequences or reasonableness of behavior. By virtue of methamphetamine intoxication, such individuals are unable to premeditate or form specific intent; malice should be viewed as arising from the extreme irritability and distorted perceptions created by the drug. A person under the influence of a methamphetamine psychosis can experience his delusions as terrifying and overwhelming. In one case from the literature, a man who under the influence of methamphetamine believed that he would be killed unless he murdered the person he thought was persecuting him. Under this delusion he went out with his knife and killed a passerby he thought was a "hit man" who had been sent to murder him. An extensive review of amphetamines and violence was published in 1978: (Reference: Asnis SF and Smith RC. Amphetamine abuse and violence. Journal of Psychedelic Drugs. 1978;10:371-7) While the (drug) culture provides an awareness that paranoid reactions are drug related, individuals on extended runs of speed who have concurrently used barbiturates and alcohol frequently lose their insight into the delusional nature of their thinking and strike out against those whom they perceive to be plotting against them. Because many stimulant abusers carry knives or guns, the result is may be unprovoked and senseless violence against totally innocent strangers. (Reference: Asnis SF and Smith RC. Amphetamine abuse and violence. Journal of Psychedelic Drugs. 1978;10:374) Unfortunately, Once an individual has experienced methamphetamine psychosis, the likelihood of recurrence is substantial. (footnote: The National Center for Drug Intelligence has published a guide for law enforcement, health and welfare personnel, and others who work with individuals who may be suffering from stimulant psychosis. This informational booklet gives specific advise for approaching an individual 'under the influence' of stimulants and/or who is paranoid. Potter MJ. Effects of D-Methamphetamine: Baseline Assessment. Johnstown, PA: National Drug Intelligence Center, 1996. KEEP A SOCIAL DISTANCE-preferably a 7 to 10 foot radius. Once a person has been identified as a potential tweaker, never try to manage the situation alone. Call for help. DO NOT SHINE BRIGHT LIGHTS AT HIM/HER. The tweaker is already paranoid, and if blinded by a bright light the likelihood of violence increases. SLOW YOUR SPEECH AND LOWER THE PITCH OF YOUR VOICE. A tweaker already hears sounds at a fast pace and in a high pitch. A side effect of the drug is a constant electrical buzzing sound in the background. SLOW YOUR MOVEMENTS. This will decrease the odds that the tweaker will misinterpret your physical actions. KEEP YOUR HANDS VISIBLE. Because the tweaker is already paranoid, if you place your hands where s/he cannot see them, s/he might feel threatened and could become violent. KEEP THE TWEAKER TALKING. A tweaker who falls silent can be extremely dangerous. Silence often means that the paranoid thoughts have overtaken reality. Anyone on the scene can become part of the tweaker's paranoid delusions. Another consequence of long-term stimulant use is sleep deprivation which also leads to profound psychological disturbances in the user. Sleep-deprived persons develop perceptual distortions, temporal disorganization, and memory impairment for recent events. Ability to concentrate on a task requiring sustained attention is decreased resulting in decreased accuracy of task performance. In studies of sleep-deprived medical personnel, there are reports of difficulty in thinking, depression, and hyper-irritability. Sleep deprivation also caused ideas of reference (false, personalized interpretation of events,) depersonalization (feeling that one is an outside observer of one's own mental processes,) and derealization (feeling that objects in the external world are unreal.) Sleep deprived individuals show changes in their speech patterns which are described as slower, softer and containing repetitions, unexpected breaks in rhythm, unfinished statements, mispronunciations, and omissions of syllables. Indeed, international attention has been focused on the practice of obtaining confessions from suspects after depriving them of sleep. Amnesty International and others have documented that sleep-deprived individuals fail to appreciate the significance of their statements, and are extremely suggestible, often offering to confess to a crime in order to be allowed to sleep.
OVERVIEW OF ALCOHOL ABUSE Because of the way it works in the brain, alcohol also produces disinhibition in behavior. Behavioral disinhibition causes varying effects in different individuals, and in different settings. In one setting the intoxicated individual may feel happy or euphoric, in another setting he might feel withdrawn, in another, angry and violent. The intoxicated person has a labile affect; that is, he is vulnerable to external stimuli and may be moody and withdrawn one moment and angry the next. He has little understanding or cognitive insight as to why he behaves the way he does. In the early stages of intoxication there's a phenomenon in which the rational, reasonable part of the brain goes to sleep first. The frontal lobes of the brain where cognition or though occurs, are the most sensitive to alcohol. The frontal lobes are responsible for reasoning, logic, ethics and values. Deep in the brain there is a set of structures that are constantly generating emotions: rage, lust, fear, anger. In the normal non-intoxicated person the reasoning part of the brain balances off the emotional part; that is inhibition. When the individual drinks alcohol in particular, the reasoning part of the brain is sedated, depressed, and literally the raw emotions are left without controls, that is called alcohol disinhibition. Behavioral disinhibition causes varying effects in different individuals, and in different settings. In one setting the intoxicated individual may feel happy or euphoric, in another setting he might feel withdrawn, in another, angry and violent. The intoxicated person has a labile affect; that is, he is vulnerable to external stimuli and may be moody and withdrawn one moment and angry the next. He has little understanding or cognitive insight as to why he behaves the way he does. Loss of inhibition is that state where the individual's ability to draw upon their morals or values, their logic, their reasoning is impaired. They cannot inhibit themselves; they cannot stop doing what their emotions tell them to do. Consequently, the individual can become giddy, dangerous or violent. Most people in our culture know when someone is severely intoxicated, they are not in their right mind. With higher doses of alcohol disorientation increases; impairment of judgment and distortion of thought increase in severity. As the user's blood alcohol level increases the individual becomes progressively incapacitated; first fine motor function, and then, gross motor function is affected. The consequence of very high doses of alcohol in the body is the suppression of respiration and finally, death. (footnote: In a widely available book reviewing the effects of psychoactive drugs, Inaba DS, Cohen WE. Uppers, downers, all-arounders. 2nd ed. Ashland, OR: CNS Productions, 1989, revised 1993 the effects of alcohol on the individual are summarized: 1. The concentration of alcohol in each kind of beverage depends on the length of fermentation, the type of fruit or vegetable used, the percent of additives used, and the amount of distillation. . . . Alcohol, as a cause of death, includes half of all murders (particularly family violence) and a fourth of all suicides. 2. The reason for alcohol's disinhibiting effect is its action on the higher centers of the brain's cortex. It disrupts the chemical balance controlling reasoning and judgment. Then it acts on the lower centers of the limbic system that rule mood and emotion. 3. The suppression of our inhibitions can fool us because along with his apparent emotional stimulation comes a physical depression. The more alcohol that is drunk, the freer the user feels but, the blood pressure is lowered, motor reflexes are slowed, digestion becomes poor, body heat is lost, and sexual excitement is diminished. 4. Alcohol is one of the few drugs that the body metabolizes at a defined, continuous rate, based upon a person's body weight, amount of alcohol drunk, the time that has passed since the last drink, and to a lesser extent the tolerance to alcohol that has come from years of drinking. Thus, we can usually predict the amount of alcohol that will be circulating through the body and brain, and how long it will take to be metabolized by the liver and eliminated via urination, sweating, and breathing. 5. The ability to tolerate alcohol depends mostly on the liver. Thus, as we drink over a period of time, the liver adapts and changes. It creates more enzymes to handle the protoplasmic poison, alcohol. Unfortunately, since liver cells are also being destroyed by the drinking and by the natural aging process, the liver eventually becomes less able to handle the alcohol. A condition known as reverse tolerance occurs. So, a drinker who could handle two fifths of whiskey at the age of 30 will get drunk on half a pint of wine at the age of 40. (Inaba and Cohen 1989 pp.123-5) There are additional important facts about the degradation of alcohol in the human body. Following ingestion, alcohol is eliminated from the body at a fairly regular rate equal to 0.02 percent decrease per hour. The rate of elimination is increased in chronic alcohol users 0.03 percent per hour because of an increase the amount of the enzyme which is required for the metabolism of alcohol. The absence of food in the stomach also increases the rate of elimination. With acute alcohol intoxication nerve cell damage is reversible. However, long term chronic alcohol ingestion may irreversibly destroy nerve cells leading to permanent impairment of cognition, memory, and motor control. Chronic use of alcohol can also produce a specific dementia called "Korsakoff's syndrome." Additionally, since alcoholics frequently fail to eat properly, vitamin deficiencies result and other neurological problems associated with malnutrition occur. The long term consumption of alcohol has psychological consequences for the user. The impact of alcoholism on a young person's development is profound. Chronic intoxication among adults usually causes them to regress in psychological sophistication. Adolescent alcoholics fail to develop the true confidence and independence which teenagers must achieve to become functioning adults. Instead, alcoholic adolescents look mature, but their personalities stagnate at an earlier stage of development. Alcoholic adolescents are plagued by an inner sense of low self worth and vulnerability. There is a vicious cycle among young alcoholics. They hid from feelings by continuing to drink, which produces increasing low self-worth and vulnerability, which are temporarily forgotten by more drinking. At some point the child's body becomes a man's body, but the personality is still adolescent. Prolonged use of alcohol produces anxiety and depression. All of the symptoms associated with depression and anxiety: insomnia, irritability, palpitations often appear. Drinking temporarily relieves these symptoms increasing the difficulty of maintaining sobriety in the long term user. Drinking alcohol also exacerbates any pre-existing mood disorder: depression and/or anxiety, from which the individual suffered. Alcohol occasionally produces amnesia or blackouts. This phenomenon was described by Donald Goodwin, M.D. in a widely available government publication in 1971. The amnesia is anterograde: a failure to make new memories. During a blackout, the individual has relatively intact remote and immediate memory, but experiences a specific short-term memory deficit for which he is unable to recall events that happened 5 or 10 minutes before. Because other intellectual faculties are well preserved, they can perform complicated acts and appear normal to the casual observer. According to Dr. Goodwin, blackouts probably represent impaired consolidation of new information rather than repression motivated by a desire to forget events that happened while drinking. The amnesia may be brief or may last for hours. Without intact memory of the event, the user may unconsciously fill the gaps by confabulation: untrue experiences that the individual believes. Amnesic episodes are more common among chronic users than among those who only occasionally drink to excess. In the "blacked out" state the user does not simply "forget;" rather, the individual has impaired consolidation of new information resulting in vague, brief, and inconsistent memories of an event. These memory fragments cannot be retrieved later, except possibly during a period of intoxication, because the learning experience is state-specific. Often the individual simply has no memory of the experience (impaired consolidation of new information) and will never be able to recall the event. In a study of five men who committed violent acts during amnesic episodes, Wolf provided clinical confirmation of the amnesic process. In this study five men each of whom had committed a homicide after a period of drinking and who claimed that he could not remember the killing were studied. Researchers gave the men alcohol to try to induce another blackout. The testers noted that several hours into the drinking episode the emotional affect of each of the five men abruptly changed and became hostile and violent. Some of the men reported having violent feelings. Additionally, during the period of memory loss, each of the five men focused on some emotionally laden theme that related to his personal or cultural identity. Researchers could not distract the individuals from the theme. Each man experienced these themes with overwhelming intensity during the blackout, yet none of them could remember such feelings and themes the next day. The disinhibiting effects of alcohol, which continue during amnesic episode, intensify the responses to intact long term memories and the associated emotional affect. Therefore, if the user recalls being attacked, he may respond violently to the perceived threat, but be unable to recall or explain later why he did what he did. (Reference: Wolf AS. Homicide and Blackout in Alaskan Natives. Journal of Studies on Alcohol 1980;41:456-62.) How does addiction to methamphetamine and alcohol affect physical and/or mental function? Alcohol is often used concurrently with stimulant drugs: cocaine or methamphetamine. The alcohol is used to counter the side effects of the stimulant when the user is ready to end the binge. The stimulant user is particularly likely to drink alcohol during the period when he is tweaking. The user who drinks alcohol anticipates that the alcohol will have an antagonistic effect on the stimulant; he anticipates that the sedating effect of alcohol will neutralize or reduce the undesirable effects of the stimulant. However, the combination of alcohol and methamphetamine is not fully antagonistic. In fact, alcohol can produce synergistic effects when taken with methamphetamine. Because alcohol slows the process in the body by which methamphetamine is metabolized, simultaneous use of the two drugs initially increases the concentration of methamphetamine in the brain. Additionally, the behavioral effects of alcohol, disinhibition, mood lability, and impaired judgment are enhanced by methamphetamine. Therefore, the individual who uses methamphetamine and alcohol together is more irritable, more labile and less behaviorally inhibited. The chronic user rebounds from upper to downer and back again using ever increasing amounts of each drug to counter the inevitable withdrawal from the other. Where methamphetamine goes, violence follows. It is built into the basic action of methamphetamine; it is not a side effect. The use of methamphetamine leads to belligerent aggressive behavior. If someone is also intoxicated from alcohol, the combination of the loss of reasoning in the face of a driven emotion can lead to violent behavior and does lead to violent behavior.
What is the effect of methamphetamine and alcohol on the individual's ability to waive his/her rights under Miranda v. California to refuse to speak to law enforcement officers?
HEROIN New users, people who would never consider using heroin because of fear of needles, are experimenting with the drug in the new smokeable form, in the woefully mistaken beliefs that it is not habit forming if smoked and overdose does not occur when heroin is smoked. Although the risk of overdose is somewhat less for heroin smokers, overdoses do occur. Development of physical dependence may occur more slowly with heroin smokers than with intravenous users, but smoking heroin offers absolutely no protection against addiction to this high potency drug.
MARIJUANA one way of taking methamphetamine isto smoke it either in nicotine cigarettes or marijuana joints.does that magnify the effect of the methamphetamine upon the user? in practice the methamphetamine is so much stronger than the marijuana. however, there is some magnifying effect. the effect of methamphetamine is so overwhelming that the additional effect would not be great.
a person who is ingesting alcohol enough that he's intoxicated or she's intoxicated, add to that marijuana that's laced with the methamphetamine, and we're at the point of intoxication, how would you describe that kind of person in terms of his performance or his behavior? the main determinants in addition to the effect of the drug, the determinants of what someone experiences depends as on two additional variables. one is their mind-set. if they were in a good mood when they started to become intoxicated, that good mood may expand and they may become giddy or silly or belligerent or euphoric. if they're in a bad mood or fatigued or tired when they start to become intoxicated, they can become mean, become aggressive, and do become belligerent, aggressively belligerent. the other determinant how someone acts or what happens to them is the setting that they are in. one is their mind-set. the other is the setting. so if someone is in a setting where everybody is having a good time, the likelihood is that the drug will act to help them have a good time. but if someone is in a situation that's upsetting or frightening or dangerous, their experience of those things will be magnified and accelerated.
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