Substance Use and Sexual Dysfunction: Definitions and Causes

Substance abuse

A pattern of behavior in which a person relies on a drug excessively and chronically, damaging relationships, affecting work functioning, and/or putting self or others in danger.

Substance dependence

A more advanced pattern of substance use in which a person abuses a drug and centers their life around it; may include tolerance and withdrawal.

Tolerance

The need for increasing doses of a drug to achieve the same effect, a sign of dependence.

Withdrawal

Unpleasant and sometimes dangerous symptoms that occur when a person stops or cuts down on drug use.

Depressants

Drugs that slow the activity of the central nervous system (CNS), reduce tension and inhibitions, and may impair judgment, motor activity, and concentration. Includes alcohol, sedative-hypnotics, and opioids.

Alcohol (mechanism)

Ethyl alcohol is absorbed into the bloodstream through the stomach lining; it acts as a GABA agonist, blocking messages between neurons, initially relaxing the drinker and then impairing judgment, coordination, memory, and reaction time.

Why women become more intoxicated than men on equal doses of alcohol

Women have less alcohol dehydrogenase, an enzyme that metabolizes alcohol in the stomach before it enters the bloodstream.

Sedative-hypnotic (anxiolytic) drugs

Drugs that produce feelings of relaxation and drowsiness; at low doses they are calming (sedative); at high doses they induce sleep (hypnotic). Includes barbiturates and benzodiazepines.

Barbiturates - danger of dependence

The lethal dose remains the same even as tolerance to the sedative effects builds; withdrawal can cause life-threatening convulsions.

Opioids

A class of depressants including natural (opium, morphine, codeine), semi-synthetic (heroin, oxycodone), and synthetic (methadone, fentanyl) compounds that bind to opioid receptors, producing a "rush" of warmth followed by hours of pleasurable "high."

Fentanyl

A potent synthetic opioid 100× more potent than morphine and 50× more potent than heroin; the deadliest drug type, accounting for ~72% of overdose deaths. Naloxone (Narcan) can reverse overdose if given in time.

Stimulants

Substances that increase CNS activity, raising blood pressure, heart rate, and alertness. The four most common are cocaine, amphetamines, caffeine, and nicotine.

Cocaine (mechanism)

The most powerful natural stimulant; increases dopamine, norepinephrine, and serotonin by blocking reuptake to presynaptic neurons, producing a euphoric rush and decreased appetite.

Cocaine intoxication

High doses of cocaine can cause mania, paranoia, impaired judgment, hallucinations, and delusions (cocaine-induced psychotic disorder); "crashing" follows as effects subside.

Amphetamines

Lab-manufactured stimulants (e.g., methamphetamine) that increase energy and alertness and suppress appetite; tolerance builds rapidly, and stopping causes serious depression and extended sleep.

Caffeine

The world's most widely consumed stimulant; releases dopamine, serotonin, and norepinephrine; intoxication possible with >2-3 cups of brewed coffee; withdrawal causes headaches, depression, anxiety, and fatigue.

Hallucinogens (psychedelics)

Drugs that produce powerful changes in sensory perception ("trips"). Include natural forms (mescaline, psilocybin) and synthetic forms (LSD, MDMA/Ecstasy).

LSD - mechanism and effects

Binds to serotonin receptors controlling visual info and emotions; produces hallucinogen intoxication (hallucinosis) within 2 hours—altered perceptions, hallucinations, synesthesia, and strong emotions lasting ~6 hours.

Synesthesia

A crossing of the senses (e.g., "seeing" sounds or "hearing" colors) that can occur under LSD intoxication.

Flashbacks

Recurrences of hallucinogen-induced perceptual disturbances that can happen a year or more after last drug use; a danger associated with hallucinogens.

Cannabis

Drugs derived from the hemp plant, including marijuana and hashish; the major active ingredient is THC (tetrahydrocannabinol); produces a mixture of hallucinogenic, depressant, and stimulant effects.

Cannabis intoxication

At low doses: joy and relaxation; at high doses: odd visual experiences, changes in body image, and hallucinations; some users become anxious or suspicious.

THC potency over time

1969 cannabis was ~1% THC; today's flower is >15%; concentrates (wax, shatter) can be 60-90% THC.

Long-term effects of early high-dose THC exposure

Disrupts neural connections in the prefrontal cortex (PFC), causing lasting issues with memory, learning, executive function, and emotional regulation; also linked to schizophrenia/psychosis, cardiovascular problems, and depression/anxiety.

Polydrug use

Using more than one drug at a time; can produce synergistic or antagonistic effects.

Synergistic drug effect

When two drugs multiply each other's effects; the combined impact is greater than the sum of each alone. Example: mixing alcohol, barbiturates, and opioids (all depressants) can severely depress the CNS and cause death.

Antagonistic drug effect

When drugs with opposite effects are combined; stimulants taken with depressants may build up lethal levels because stimulants slow the liver's metabolism of the depressants.

Sociocultural causes of substance disorders

Living in stressful socioeconomic conditions or in environments where substance use is valued or accepted.

Psychodynamic cause of substance disorders

Powerful unmet dependency needs traced to early childhood (lack of nurturing).

Cognitive-behavioral cause of substance disorders

Conditioned rewarding effects lead to increased dose and frequency of use.

Biological cause of substance disorders

Disrupted neurotransmitter functioning (especially dopamine); genetic predisposition; activation of the brain's reward pathway (VTA → nucleus accumbens → medial PFC).

Behavioral strategies for substance use disorders

Contingency management, aversion therapy, covert sensitization, Behavioral Self-Control Training (BSCT), and Relapse-Prevention Training (RPT).

BSCT (Behavioral Self-Control Training)

Clients track their own use and triggers, learn coping strategies, set limits on use, and build relaxation, coping, and problem-solving skills.

RPT (Relapse-Prevention Training)

Clients plan ahead for high-risk situations to prevent returning to substance use; used especially for alcohol and other drug abuse.

Biological treatments for substance disorders

Detoxification (gradual or with antagonist drugs like naltrexone); drug maintenance programs (e.g., methadone for opioid dependence); both require psychotherapeutic maintenance.

Sexual dysfunctions

Disorders in which people cannot respond normally in key areas of sexual functioning; typically distressing and may cause frustration, guilt, low self-esteem, and interpersonal problems.

Four phases of the human sexual response cycle

Desire → Excitement → Orgasm → Resolution. Sexual dysfunctions affect one or more of the first three phases.

Hypoactive sexual desire disorder

Characterized by a lack of interest in sex and little sexual activity; affects ~16% of men and ~33% of women.

Sexual aversion disorder

Total aversion to or disgust of sex; sexual advances may sicken, repulse, or frighten the person; more common in women.

Biological causes of desire disorders

Hormone abnormalities, chronic illness, certain medications (e.g., oral contraceptives, some psychotropics, narcotics).

Psychological causes of desire disorders

Anxiety, depression, OCD, anger, fears, negative attitudes, or traumatic memories.

Sociocultural causes of desire disorders

Situational pressures such as divorce, death of a loved one, relationship problems, or past sexual trauma.

Female sexual arousal disorder

Repeated inability to maintain proper lubrication or genital swelling during sexual activity; affects >10% of women; often co-occurs with orgasmic disorder.

Male erectile disorder (ED)

Repeated inability to attain or maintain an adequate erection during sexual activity; affects ~10% of men.

Performance anxiety and the spectator role

A cognitive explanation for ED: after initial erectile failure, a man becomes a fearful observer of his own performance rather than a participant, creating a self-perpetuating cycle of dysfunction.

Rapid/premature ejaculation

Persistent orgasm and ejaculation with little sexual stimulation; linked to anxiety, hurried masturbation, serotonin receptor abnormalities, or heightened penile sensitivity.

Male orgasmic disorder

Repeated inability to reach orgasm or very delayed orgasm after normal sexual excitement; causes include performance anxiety, low testosterone, neurological issues, and SSRIs.

Female orgasmic disorder

Persistent delay or absence of orgasm following normal sexual excitement; affects ~25% of women; linked to depression, trauma, relationship stress, and sometimes illness or medications.

Vaginismus

Involuntary contractions of the outer vaginal muscles, potentially preventing intercourse; understood as a learned fear response; treated with muscle control exercises and gradual behavioral exposure.

Dyspareunia

Severe genital pain during sexual activity; affects ~14% of women and ~3% of men; usually has a physical cause (e.g., injury from childbirth); treated by identifying and addressing the specific cause.

Masters and Johnson's sex therapy (1970)

Revolutionized treatment of sexual dysfunctions; a short-term (15-20 sessions), multidimensional approach addressing specific sexual problems rather than broad personality issues.

Key features of modern sex therapy

Mutual responsibility for the problem, sexual education, attitude change, elimination of performance anxiety and the spectator role, improving communication, addressing lifestyle and medical factors.

Treatment for erectile disorder

Reducing performance anxiety (e.g., sensate-focus, tease technique); biological options include Viagra (sildenafil), gels, penile injections, vacuum erection device (VED), or penile implant surgery.

Treatment for premature ejaculation

Behavioral techniques: stop-start (pause) procedure and the squeeze technique; also serotonin-enhancing antidepressants (e.g., fluoxetine) to delay ejaculation.

Treatment for female arousal/orgasmic disorders

Cognitive-behavioral techniques, self-exploration, body awareness enhancement, directed masturbation training, and psychoeducation; hormone therapy or Viagra tried but not consistently helpful.

Gender Dysphoria

A persistent feeling of having been assigned to the wrong biological sex; formerly called Gender Identity Disorder (GID) in DSM-IV; associated with anxiety, depression, and sometimes suicidal ideation. Treatment may include hormones and/or surgery.

The first phase of sex therapy

Addressing communication issues

Psychosis

A state defined by a loss of contact with reality in which the ability to perceive and respond to the environment is significantly disturbed; can be substance-induced or caused by brain injury, but most commonly appears as schizophrenia.

Schizophrenia - demographics

Equally common in men and women, but male symptoms tend to be more severe; found across all socioeconomic groups but more frequently in lower levels (stress of poverty; "downward drift" theory).

Positive symptoms of schizophrenia

"Pathological excesses" - bizarre additions to behavior. Include delusions, disordered thinking/speech (loose associations, neologisms, perseveration, clang), heightened perceptions, hallucinations, and inappropriate affect.

Delusions

Faulty interpretations of reality; types include delusions of persecution, reference, grandeur, and control.

Loose associations (derailment)

A positive symptom of schizophrenia: rapidly shifting from one unrelated topic to another within speech.

Neologisms

A positive symptom of schizophrenia: made-up words that have meaning only to the speaker (e.g., "This desk is a cramstile").

Perseveration

Repeating words or statements again and again; a positive symptom of schizophrenia.

Clang

Speaking in rhymes; a positive symptom of schizophrenia (e.g., "Well, hell, it's well to tell").

Hallucinations

Sensory perceptions that occur in the absence of external stimuli; the most common type in schizophrenia is auditory, but they can be tactile, somatic, visual, gustatory, or olfactory.

Types of hallucinations

Auditory (most common), visual, tactile, somatic, gustatory (taste), and olfactory (smell).

Inappropriate affect

Displaying emotions that are unsuited to the situation; a positive symptom of schizophrenia.

Negative symptoms of schizophrenia

"Pathological deficits" - characteristics that are lacking. Include poverty of speech (alogia), diminished emotional expression (blunted/flat affect), anhedonia, loss of volition, ambivalence, and social withdrawal.

Alogia (poverty of speech)

Long pauses before responding, failure to answer, or reduced quantity/content of speech; a negative symptom of schizophrenia.

Anhedonia

A general lack of pleasure or enjoyment; a negative symptom of schizophrenia.

Loss of volition

Feeling drained of energy and interest; inability to start or follow through on a course of action; a negative symptom of schizophrenia.

Psychomotor symptoms of schizophrenia

Awkward movements, repeated grimaces, and odd gestures; extreme forms are called catatonia (stupor, rigidity, posturing, excitement).

Catatonia

An extreme form of psychomotor disturbance in schizophrenia involving stupor, rigidity, unusual posturing, or frenzied excitement.

Three phases of schizophrenia

Prodromal (mild, beginning symptoms), Active (symptoms fully apparent), and Residual (return to prodromal level). One-quarter fully recover; three-quarters have ongoing residual problems.

Factors predicting better recovery from schizophrenia

High premorbid functioning, disorder triggered by identifiable stressor, abrupt onset, and later onset (middle age).

DSM-5 diagnosis of schizophrenia

Signs persist ≥6 months; at least 2 symptoms present for ≥1 month (at least one must be a positive symptom); must show deterioration in work, social relations, or self-care.

Type I vs. Type II schizophrenia

Type I: dominated by positive symptoms; better premorbid adjustment, later onset, more likely to improve, linked to biochemical abnormalities. Type II: dominated by negative symptoms; linked to structural brain abnormalities.

Dopamine hypothesis

The leading biochemical explanation for schizophrenia: certain dopamine neurons fire too often, producing symptoms. Evidence includes antipsychotics blocking D2 receptors (causing Parkinsonian side effects) and excessive stimulants or L-Dopa causing psychosis.

Genetic factors in schizophrenia

General population risk: 1%; second-degree relatives: 3%; first-degree relatives: 10%; identical twins: 48%; fraternal twins: 17%. Schizophrenia is considered polygenic.

Brain structure abnormalities in schizophrenia (Type II)

Enlarged ventricles, smaller temporal and frontal lobes, and abnormal blood flow; may reflect poor development or damage in those regions.

Viral hypothesis of schizophrenia

Prenatal viral exposure may cause biochemical and structural brain abnormalities; supported by higher rates of schizophrenia in people born in winter and whose mothers had influenza during pregnancy.

Diathesis-stress model of schizophrenia

People with a biological predisposition will develop schizophrenia only when certain environmental stressors or events trigger the disorder.

Schizophrenogenic mother theory

An early psychodynamic view that cold, domineering, uninterested mothers caused schizophrenia in their children; now discredited.

Double-bind hypothesis

A sociocultural explanation: parents send mutually contradictory messages so the child cannot avoid displeasing them, contributing to schizophrenia.

Expressed emotion

A family pattern of frequent criticism, hostility, and intrusion; people with schizophrenia in high-expressed-emotion families have relapse rates ~4× higher than those in supportive families.

Social labeling and schizophrenia

Sociocultural theorists argue that the schizophrenia diagnosis itself can become a self-fulfilling prophecy once a person is labeled for failing to conform to behavioral norms.

Milieu therapy

A humanistic institutional approach promoting productive activity, self-respect, and individual responsibility; one of two approaches developed in the 1950s that brought hope to chronic patients.

Token economy

A behavioral institutional approach that rewards adaptive behavior with tokens (exchangeable for privileges); improved personal care and self-image, but raised issues of human rights and whether symptoms were cured or merely masked.

Conventional (typical) antipsychotic drugs (neuroleptics)

First-generation antipsychotics developed from phenothiazines in the 1950s-1980s; reduce positive symptoms in ≥65% of patients; more effective for positive than negative symptoms; maximum improvement within 6 months.

Extrapyramidal effects

Movement side effects of conventional antipsychotics due to reduced dopamine in the basal ganglia/substantia nigra; include Parkinsonian symptoms (tremor, rigidity), dystonia, and akathisia. Can sometimes be treated with anti-Parkinsonian drugs.

Dystonia

Bizarre, involuntary movements of the face, neck, tongue, and back; an extrapyramidal side effect of conventional antipsychotics.

Akathisia

Extreme restlessness, agitation, and discomfort in the limbs; an extrapyramidal side effect of conventional antipsychotics.

Tardive dyskinesia

A serious side effect of conventional antipsychotics appearing up to a year after starting medication; involves involuntary writhing or tic-like movements of the mouth, lips, tongue, legs, or body; affects >10% of users; difficult or impossible to eliminate.

Neuroleptic malignant syndrome

A severe, potentially fatal reaction to conventional antipsychotics (affects ~1% of patients, especially elderly); symptoms include muscle rigidity, fever, altered consciousness, and autonomic dysfunction; treated by stopping the drug and using dopamine-enhancing medications.

Atypical (second-generation) antipsychotics

Newer antipsychotics more effective than conventional drugs, especially for negative symptoms; cause fewer extrapyramidal side effects; risks include agranulocytosis (potentially fatal drop in white blood cells) and high cost.

Agranulocytosis

A potentially fatal drop in white blood cells; a serious risk associated with atypical antipsychotic medications.

Cognitive-behavioral therapy for schizophrenia

Provides education about biological causes of hallucinations; helps clients track their own symptoms; challenges inaccurate beliefs about hallucinations and delusions; helps clients cope and gain a greater sense of control.

Family therapy for schizophrenia

Addresses family stress and expressed emotion; creates realistic expectations; provides psychoeducation; connects families with support groups; reduces relapse risk.

Social therapy for schizophrenia

Addresses practical difficulties: advice, problem solving, social skills training, medication management, employment counseling, financial assistance, and housing; research shows it reduces rehospitalization.