Transcript Psychoactive Drugs

PSYCHOACTIVE DRUGS
Hip and cool?
Faces of Meth
 Before
After (3 years later)
Faces of Meth
 Before
After (17 months later)
Faces of Meth
 Before
After (3 months later)
DSM Abuse/Dependence Categories
 5.1 Alcohol-Related Disorders
 5.2 Amphetamine (Or Amphetamine-Like) Related Disorders
 5.3 Caffeine-Related Disorders
 5.4 Cannabis-Related Disorders
 5.5 Cocaine-Related Disorders
 5.6 Hallucinogen-Related Disorders
 5.7 Inhalant-Related Disorders
 5.8 Nicotine-Related Disorders
 5.9 Opioid-Related Disorders
 5.10 Phencyclidine (Or Phencyclidine-Like)-Related Disorders
 5.11 Sedative-, Hypnotic-, or Anxiolytic-Related Disorders
 5.12 Polysubstance-Related Disorder
 5.13 Other (or Unknown) Substance-Related Disorder
Substance-related disorder
 Substance-related disorder
 Abuse of, or dependence on, a mood- or behavior-altering drug
 Substance: Anything that is ingested in order to produce a high, alter
one's senses, or otherwise affect functioning
 Characterized by
 Excessive use of habit forming substances
 The use of a substance for a reason other than which it was intended
or in a manner or in quantities other than directed
 Two general groups:
 Substance abuse
 Use interferes with social or occupational functioning
 Abuse may progress to dependence
 Substance dependence
 Compulsive abuse behavior
 Shows tolerance and withdrawal
DSM-IV definition: Substance abuse
 A maladaptive pattern of substance use leading to clinically
significant impairment or distress, as manifested by one or
more of the following in a 12-month period:
 failure to fulfill major role obligations at work, school, home
 e.g., repeated absences or poor work performance related to
substance use; substance-related absences, suspensions, or
expulsions from school; neglect of children or household
 use in situations in which it is physically hazardous
 e.g., driving an automobile or operating a machine
 substance-related legal problems
 e.g., arrests for substance-related disorderly conduct
 persistent or recurrent social or interpersonal problems
caused or exacerbated by the effects of the substance
 e.g., arguments with spouse or children, physical fights
DSM-IV definition: Substance dependence
(continued)
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Tolerance: a need for markedly increased amounts of the
substance to achieve intoxication or desired effect
Withdrawal: Physiological and psychological symptoms
associated with reduction in heavy substance use> Usually
exhibits 2 or more of the following symptoms:
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Sweating or rapid pulse Nausea or vomiting
Increased hand tremor Physical agitation
Insomnia
Anxiety
Transient visual, tactile, or auditory hallucinations or illusions
Grand mal seizures
DSM-IV definition: Substance dependence
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The substance is often taken in larger amounts or over a longer
period than was intended
There is a persistent desire or unsuccessful efforts to cut down or
control substance use
A great deal of time is spent in activities to obtain, use, or recover
from effects of the substance
Important social, occupational or recreational activities are given up
or reduced
Continued use despite knowledge of having a persistent or recurrent
physical or psychological problem that is likely to have been caused
or exacerbated by the substance
 e.g., illness, marital conflict, job problems
How Alcohol Works: Getting in
 About 20 percent of alcohol is
absorbed in your stomach
 The remaining 80 percent is
absorbed in your small intestine
 How quickly depends on
 the percent of the alcohol in the
drink
 vodka is absorbed faster than
beer because vodka has a
higher alcohol percentage
 how much you've just eaten
 a full stomach will slow down
alcohol absorption
How Alcohol Works: Getting out
 Where it goes: Kidneys, Lungs, Liver, Brain
 Kidneys and lungs remove about 10% of the alcohol
 which is why a breathalyzer test can be used to measure a person's
blood alcohol level)
 Liver breaks down 90% of the alcohol into acetic acid
 Blood alcohol concentration (BAC)
 The proportion of alcohol in your blood
 Goes up when the body is taking in alcohol faster than it can release it
 One ounce of alcohol will increase the average person's BAC roughly
0.03%
 BAC and the number of drinks consumed are not always accurate
indicators of the level of impairment
 There is much variation according to genetics, body weight, gender,
and body fat percentage
 Tolerance to alcohol varies from one person to another because of the
above factors and from adaptation to chronic alcohol use
How Alcohol Works: In your brain
 Alcohol alters amounts of neurotransmitters
 Causes sluggish movements and slurred speech by
 Increasing the effects of the inhibitory neurotransmitter
GABA
 Inhibiting the excitatory neurotransmitter glutamate
 Creates a feeling of pleasure by
 Increasing the amount of the dopamine in the brain's
reward center
How Alcohol Works: In your brain
 Alcohol affects multiple areas of the brain
 In the Cortex it affects our thought processes
 depresses behavioral inhibitions, causing less inhibition
 slows down the processing of information from the senses
 interferes with thought processes, making it difficult to think clearly
 In the Cerebellum it affects our kinesthetic senses
 interferes with the integration of information from movement and
balance sensory organs, resulting in staggering
 In the Hypothalamus and pituitary it influences our emotional
state
 Depresses nerve centers that control sexual arousal and performance
 Sexual urges may increase, but sexual performance will decreases
 In the Medulla it affects our vital life functions
 Induces sleepiness, slows breathing, and lowers body temperature
Stages of Alcohol Intoxication
 Euphoria (BAC = 0.03 to 0.12 percent)
 Become more self-confident, attention span shortens, flushed, judgment
reduced, trouble with fine movements
 Excitement (BAC = 0.09 to 0.25 percent)
 Become sleepy, have trouble understanding or remembering things,
uncoordinated balance and body movements
 Confusion (BAC = 0.18 to 0.30 percent)
 Become confused and emotional, dizzy and may stagger, slurred speech
 Stupor (BAC = 0.25 to 0.4 percent)
 Can barely move, stand or walk, may vomit, may lapse in and out of
consciousness
 Coma (BAC = 0.35 to 0.50 percent)
 They are unconscious, lower-than-normal body temperature, breathing is
slower and more shallow, heart rate may slow
 Death (BAC more than 0.50 percent)
 The person usually stops breathing and dies
Substance-related disorders
 People with substance-related disorders also
commonly suffer from other psychological
disorders, a condition known as comorbidity
 Substance abusers also likely to have:
 disruptive disorders (conduct or oppositional defiant
disorder, impulse-control disorders)
 mood disorders (e.g., depression, dysthymia)
 anxiety disorders (e.g., PTSD; social phobia)
Prevention
 Substance abuse and dependence tend to develop rapidly
following first use
 suggesting that a slim window of opportunity exists to
prevent substance disorders once drug use has begun
 Conclusions of a study by
 Reebye, P, Moretti, MM, and Lessard, JC (1995) Conduct
disorder and substance use disorder: comorbidity in a
clinical sample of preadolescents and adolescents.
Canadian Journal of Psychiatry, 40(6): 313-9.
Neural Basis of Drug Cravings
 Mesolimbic Dopamine Pathway = System of neurons connecting
– Ventral Tegmental Area (VTA)
• Activated by activities that
produce pleasure
• Also involved in security
motivation, avoidance, and fearconditioning, Seeking food and
companionship and avoiding
physical and psychological
discomfort and intoxication
– Nucleus accumbens (Nac)
• Key structure of the brain
responsible for reward,
motivation, and addiction
– Prefrontal cortex
• Regulates overall motivational salience and determines the
intensity of behavioral responding
Mesolimbic Pathway and Addictive Behavior
 Almost every drug abused by humans has been shown to
increase dopamine levels in the Mesolimbic Pathway
 Mesolimbic Pathway and Psychotic Behavior
 Abnormally high dopamine levels in the mesolimbic pathway are
strongly linked to psychosis and schizophrenia
 Responsible for psychotic affects of addictive drugs
 Mesolimbic Pathway and Creative Drive
 Moderate levels of dopamine in the mesolimbic pathway increases
general arousal and goal directed behaviors and decreases latent
inhibition; all three effects increase the creative drive of idea
generation
 Flaherty, A.W, (2005). "Frontotemporal and dopaminergic control of idea
generation and creative drive". Journal of Comparative Neurology 493 (1):
147-153.
Neural Basis of Drug Cravings
 Sustained dopamine release
 promotes drug-seeking behavior
 causes pathophysiological synapse changes along the
Mesolimbic Pathway, the prefrontal cortex, and nucleus
accumbens (brain damage)
 Hyperresponsive to stimuli predicting drug availability
 Reduced capacity to regulate neurotransmission
 Sources:
 Phillips, et al. (2003). Nature, 422, 614-818.
 The Neural Basis of Addiction: A Pathology of Motivation
and Choice. Peter W. Kalivas, Ph.D. and Nora D. Volkow,
M.D. Am J Psychiatry 162:1403-1413, August 2005.
Can Drugs Cause Brain Damage?
 Drugs that have been associated with brain damage or
cognitive impairments:
 Amphetamines
 MDMA (“ecstasy”): Serotonin neurons
 Methamphetamine: Dopamine neurons
 Cocaine:
 Blocks cerebral blood flow
 Phencyclidine (PCP or “angel dust”):
 Blocks NMDA receptors
 Drugs that have NOT been associated with long-lasting brain
damage
 LSD
 Marijuana
 Opiates
Psychoactive Drug
 A chemical substance that acts primarily upon the CNS where
it alters brain function, resulting in temporary changes in
perception, mood, consciousness, and behavior
 Most psychoactive drugs exert their effects by influencing
chemical reactions at synapses
 Agonist
 Substance that ENHANCES the function of a synapse
 Cause excessive release of a neurotransmitter
 Block re-uptake off a neurotransmitter
 Antagonist
 Substance that BLOCKS the function of a synapse
An Acetylcholine Synapse:
Example of Drug Action
Whole eggs, liver, beef steak, and
soy are among foods naturally rich
in choline
Black widow and cobra
venom & ACh: Paralysis
Botulinum toxin & ACh:
denervation and local paralysis
Nicotine & ACh: An increase in
conductance of the ion(s) for
which that channel is selective
Nerve agents
Pesticides
muscle relaxant, poison
Psychoactive drug classification
 One can classify a drug by it’s most pronounced behavioral or
psychoactive effect
 Sedative Hypnotics and Anti-anxiety Agents
 Antipsychotic Agents
 Antidepressants
 Mood Stabilizers
 Narcotic Analgesics
 Psychomotor Stimulants
 Psychedelics and Hallucinogens
Psychoactive drugs: Anti-anxiety
Agents and Sedative Hypnotics
 Central nervous system depressants
 They bind to GABA (inhibitory neurotransmitter) receptors
and increase its effect
 The GABAA Receptor Has Two Sites:
 Sedative-Hypnotic Site: Alcohol and barbituates
 Antianxiety Site: Benzodiazepines
Psychoactive drugs: Anti-anxiety Agents and
Sedative Hypnotics (continued)
 Barbituates
 Produce sedation and sleep (e.g., Phenobarbital, alcohol)
 Can also produce general anesthesia, coma, and death
 Used as an anesthetic
 Other uses: Replaced by benzodiazepines, which have
less potential for abuse and danger of lethal overdose
 Benzodiazepines
 Minor tranquilizers
 Antianxiety agents
 Drugs that reduce anxiety (e.g., Valium, Xanax)
 Used to treat anxiety, insomnia, agitation, seizures,
muscle spasms, and alcohol withdrawal
Psychoactive drugs: Anti-anxiety Agents and
Sedative Hypnotics (continued)
 Allopregnanolone
 Natural hormone (a neurosteroid) produced by pineal
gland
 Reduces anxiety and creates calm at times of stress
(conflicting evidence)
 Higher levels in women than in men
 Thought to make women more sensitive to alcohol than
men
 Associated with premenstrual symptoms
Psychoactive drugs: Antipsychotic
Agents
 Major Tranquilizers (Neuroleptic)
 Drugs used to treat psychosis - a loss of contact with
reality (hallucinations, delusions, disorganized thinking)
 Examples: schizophrenia, mania, and delusional disorder
 Blocks the D2 dopamine receptor
 The normal effect of dopamine release is reduced
 Mechanism of therapeutic action is still not understood
 Immediate effect of reducing motor activity
 After short period of use, there is a reduction in the
symptoms of schizophrenia
 Negative side effect: Dyskinesia (impaired control of
movement)
Psychoactive drugs: Examples of
Antipsychotic Agents
 Zyprexa - acute manic episodes and maintenance of
bipolar disorder
 Solian - positive (high dose) and negative (low dose)
symptoms of schizophrenia
 Seroquel - bipolar disorder, schizophrenia, and
chronic insomnia (low dose)
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Dopamine Hypothesis
of Schizophrenia
Proposal that schizophrenia
symptoms are due to excess
activity of the
neurotransmitter dopamine
 Evidence
 Antipsychotic drugs block
D2 receptors
 Amphetamine promotes
release of dopamine and
can also produce
symptoms similar to
schizophrenia
 But there is still no conclusive
evidence of dopamine-related
differences in the brains of
schizophrenic patients
Psychoactive drugs: Antidepressants
 Although antidepressants affect synapses very quickly, their
antidepressive actions take weeks to develop
 About 30% and 50% of patients with depression fail to respond to
antidepressants, suggesting that other neurotransmitters are likely
involved
 Antidepressant drugs tend to lose efficacy over the course of
treatment
 Therapeutic effects of antidepressants typically do not continue
once the course of medication ends
 Most antidepressants are known to produce tolerance
 They are not addictive, but can produce psychological withdrawl
 Virtually all major antidepressant drugs suppress REM sleep
 a common side effect of most antidepressants is an increase in vivid
dreams
Classes of Antidepressants
1. Monoamine Oxidase (MAO) Inhibitors
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Block the enzyme MAO from degrading
neurotransmitters such as dopamine, norepinephrine,
and serotonin
2. Tricyclic Antidepressants
 First-generation antidepressants with a chemical
structure characterized by three rings that block
serotonin, dopamine, and norepinephrine reuptake
transporter proteins
3. Second-Generation Antidepressants
 Action is similar to first-generation antidepressants, but is
more selective in its action on the serotonin reuptake
transporter proteins; also called atypical antidepressants
 Selective Serotonin Reuptake Inhibitors (SSRIs)
 Block the reuptake of serotonin into the presynaptic
terminal
Psychoactive drugs: Second-Generation
Antidepressants
 Action is similar to older (tricyclic) antidepressants, but with fewer
side effects
 Paroxetine (e.g. Paxil, Seroxat, Aropax) is a selective serotonin
reuptake inhibitor (SSRI)
 Used to treat the symptoms of depression, obsessive-compulsive disorder,
post-traumatic stress disorder, panic disorder, generalized anxiety
disorder, social phobia/social anxiety disorder, and premenstrual dysphoric
disorder
 Bupropion (e.g. Wellbutrin, Zyban) is a norepinephrine and
dopamine reuptake inhibitor (NRDI)
 Also used for smoking cessation, seasonal affective disorder, and
Attention Deficit Disorder
 Side effects: Nausea, diarrhea, headaches, sexual (loss of libido,
failure to attain an erection or reach orgasm, Bupropions may
increase libido slightly
The most commonly prescribed
antidepressants
 In the US in 2005:
 Sertraline (e.g. Zoloft, Lustral, Apo-Sertral, Asentra, Gladem, Serlift,
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Stimuloton)
Escitalopram (e.g. Lexapro, Cipralex)
Fluoxetine (e.g. Prozac, Sarafem, Fluctin, Fontex, Prodep, Fludep,
Lovan)
Venlafaxine (e.g. Effexor XR, Efexor)
Citalopram (e.g. Celexa, Cipramil, Talohexane)
Paroxetine (e.g. Paxil, Seroxat, Aropax)
Trazodone (e.g. Desyrel, Trazolan)
Amitriptyline (e.g. Elavil)
Bupropion (e.g. Wellbutrin, Zyban)
 The most commonly prescribed antidepressant in Germany is reported to
be concentrated extracts of hypericum perforatum (St John's Wort)
Psychoactive Drugs: Narcotic
Analgesics
 Drugs with sleep-inducing (narcotic) and pain-relieving
(analgesic) properties
 General effects of narcotic analgesics
 sedation, slowed reflexes, raspy speech, sluggish "rubber-
like" movements, slowed breathing, cold skin, and
possible vomiting
Psychoactive Drugs: Narcotic
Analgesics - Opiates
 Many of these drugs are derived from opium, an extract of
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the seeds of the opium poppy plant
Opiates are potentially addictive
Continued use of narcotic analgesics will build a tolerance
Pure opioids (from the plant)
 Codeine: ingredient of cough medicines and pain relievers
 Morphine: powerful pain reliever
Synthetic opioid
 Methadone
Psychoactive Drugs: Morphine
 Acts directly on the synapses of the nucleus accumbens to
relieve pain
 Morphine binds very strongly to the mu-opioid receptors
 Causes higher incidence of euphoria and dependence
(addiction) as compared to most other opioids
 Morphine has recently been found to be endogenously
produced by humans
 made by cells in the heart, pancreas and brain
Psychoactive Drugs: Narcotic
Analgesics
 Nalorphine and Naxolone
 Blocks the effects of morphine
 useful in reversing the effects of narcotic overdoses
 Heroin
 An opiate drug synthesized from morphine
 More fat soluble and penetrates the BBB faster than
morphine, therefore it produces very rapid pain relief
 Once in the brain, heroin is rapidly metabolizes back into
morphine
 the morphine molecule binds with opioid receptors and
produces the subjective effects of the heroin high
Psychoactive Drugs: Endorphins
 Peptide hormone that acts as a neurotransmitter and may be
associated with feelings of pain or pleasure
 produced by the pituitary gland and hypothalamus
 resemble opiates in their abilities to produce analgesia and
a sense of well-being
 Endorphins are released during stress, such as during long,
continuous workouts, when the level of intensity is between
moderate and high, and breathing is difficult
 Do endorphins cause the runner's high? …. not likely
 changes in mood state occur when people exercise on
opioid antagonists (e.g., Nalorphine)
 high appears to come from completing a challenge rather
than as a result of exertion
Psychoactive Drugs: Behavioral
Stimulants
 Stimulates the sympathetic nervous system to increase
motor behavior and elevate a person’s mood and level of
alertness by increasing synaptic activity of the monoamine
neurotransmitters:
 dopamine (primarily), norepinephrine and serotonin
 Physical effects: Overall agitation, prevents sleep, reduces
appetite, speeds up breathing and heart rate and widens the
pupils
Psychoactive Drugs: Behavioral Stimulants
 Low to moderate doses
 Induce wakefulness, increase activity, decrease appetite
 Produce feelings of euphoria, well-being and self-confidence
 Stereotypic behaviors - brief, repetitive actions (e.g., arranging of
objects, grooming, and persistent repetition of words)
 High doses
 Produce a psychosis (vivid hallucinations and paranoid ideation)
 Often indistinguishable from paranoid schizophrenia
 Can cause periods to become irregular or even stop in women
 Emotional effects:
 At first - feel more energetic, cheerful and confident
 Come down - feel sad, helpless, hopeless, nervous, angry, violent
 Regular users – psychotic symptoms (e.g., delusions, hallucinations, &
paranoia) that can develop into paranoid psychosis
Psychoactive Drugs: Behavioral
Stimulants
 Cocaine
 Obtained from the leaves of the coca plant
 Addictive
 Derivates such as Novocaine are used as local anesthetics
 Dopamine agonist: blocks the reuptake of dopamine
 Amphetamine
 Initially an asthma treatment
 Study aid
 Improvement of alertness and productivity
 Weight-loss aid
Psychoactive Drugs: Behavioral Stimulants
 Caffeine
 Inhibits the enzyme the normally breaks down the second messenger
cyclic AMP
 Increase in cAMP leads to an increase in glucose production within
cells, which makes more energy available and allows for higher rates
of cellular activity
 Results in increased activity of dopamine (causes stimulating effects)
and serotonin (to a lesser extent - causing positive changes in mood)
 Nicotine
 A cholinergic agonist -- it acts by stimulating nicotinic acetylcholine
receptors
 Low dose stimulation of the central nervous system is followed by
depression at high doses
 Chronic use of nicotine leads tolerance and dependence
Psychoactive Drugs: Speed Methamphetamine - Amphetamines
 Toxic effects on the brain
 A single high dose of meth has been shown to damage
nerve terminals in the dopamine-containing regions of the
brain
 As much as 50% of the dopamine-producing cells in the
brain can be damaged after prolonged exposure to
relatively low levels of speed
 Serotonin-containing nerve cells may be damaged even
more extensively
 Messes with every aspect of mood, emotion, sleep and
appetite
Long-term Use of Methamphetamine
Longterm Use of Methamphetamine
Meth-Mites
 Users develop obsessive itching and picking of the skin,
creating red, irritated, blotchy, and sometimes bloody sores
Psychoactive Drugs: Psychedelic Drugs
 Alter sensory perception and cognitive processes
 Range from seemingly non-toxic to extremely toxic
 Do NOT cause hallucinations
 Hallucinations are perceptions that have no basis in reality,
but that appear entirely realistic
 ”Hallucinations" induced by psychedelic drugs are more
accurately described as a modification of regular
perception
 the subject is usually quite aware of the illusory and
personal nature of their perceptions
Psychedelic Drugs: Four main types
 Acetylcholine psychedelics
 Norepinephrine psychedelics (e.g., mescaline)
 Tetrahydrocannabinol (THC): active ingredient in marijuana
 Serotonin psychedelics (e.g., lysergic acid diethylamide)
Psychedelic Drugs - Acetylcholine
psychedelics
 Examples: PCP, angel dust, crystal, dust, embalming fluid,
DOA, surfer; street K, special K
 Distort perception of sight and sound and produces feelings
of detachment (dissociation)
 Some effects include
 agitation, euphoria, disinhibition, rigidity, unable to speak,
unresponsive to pain, including unpredictable violent
reactions to environmental stimuli, Schizophrenia-like
psychotic states; Flashbacks
 Effects are directly caused by the toxicity to one's body
Psychedelic Drugs - Norepinephrine
psychedelics
 Examples: mescaline, DOM (also as STP), TMA, MDA, MDMA
(ecstasy),MMDA, DMA, and drugs from nutmeg (myristin
and elemicin)
 Mental Effects
 Sensation and perception impairment, loss of a sense of
time, disorganization of thought and psychotic reactions.
 Physical Effects
 Speed up the heartbeat and increase the blood pressure,
dilates pupils, increases blood sugar level, raise body
temperature, cause heavy perspiration and nausea.
 Large doses, mescaline lowers the blood glucose.
Psychedelic Drugs - Tetrahydrocannabinol
 Active ingredient in marijuana
 Low to medium use:
 Relaxation, reduced coordination and blood pressure,
disruption in attention, an altered sense of time and space.
 High use can cause:
 Depression, hallucinations, delusions, impaired memory,
disorientation, cancer.
 Unclear if it becomes addictive or causes long-term mental
abnormalities
 Lung cancer is high risk of regular use because there is a high
level of tar and other chemicals.
Psychedelic Drugs - Serotonin psychedelics
 Examples: LSD, Dimethyltryptamine (DMT), Psilocybin
(mushrooms that belong to the genera Psilocybe,
Panaeolus, andConocybe), psilocin, bufotenine Ololiuqui
(morning glory seeds) Harmine
 Alter mood and perception, paranoid ideation, depression,
undesirable hallucinations, and/or a confusional state
resembling a drug-induced dementia.
 Persistent flashbacks occur weeks/months after last drug
use
 Psychedelics can precipitate serious depressions, paranoid
behavior, or prolonged psychotic episodes.
Drugs, Experience, Context, and Genes
Tolerance
 How do we develop a tolerance to drugs such as alcohol?
 Metabolic Tolerance
 Changes in efficiency or capacity to metabolize ethanol resulting in a
decrease in the BAC following a given dose of alcohol
 Number of enzymes needed to break down alcohol may increase
 Cellular (Functional) Tolerance
 Activities of brain cells may adjust to minimize the effect of alcohol
 Characterized by a decrease in pharmacologic or physiologic
responsiveness upon alcohol exposure
 Hypothesized to be mediated by neuroadaptative changes in the CNS
 Learned Tolerance
 People can learn to cope with effects of alcohol and therefore may not
appear to be drunk
Drugs, Experience, Context, and Genes
Why Doesn’t Everyone Abuse Drugs?
 Genetics?
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Despite some evidence of a genetic contribution, no gene or set of genes
related to alcoholism have been found
 Any satisfactory explanation of drug abuse will require genetic and learning
components
 Personality Traits?
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Unusual risk-taking may be trait common to drug abusers
Low Frustration and Tolerance - impatient
Anxiety
Grandiosity - to hide feelings of low self-worth
Perfectionism - an idealist
Justification
Isolation and deep insecurity - loners
Exaggerates unpleasant interpersonal relationships
Impulsiveness
Defiance - a feeling that one does not fit into society
Dependence on other persons
Factors that influence drug
responsiveness
 Age:
 Older individuals are more sensitive to drugs
 Less effective barriers and less effective at eliminating
drugs
 Body Size:
 Smaller individuals are more sensitive to drugs
 Fewer body fluids to dilute drugs
 Sex
 Females are more sensitive to drugs
 Smaller than men on average
 Homones may also play a role