Addiction Study Guide

📖 Core Concepts Addiction – a neuropsychological disorder marked by compulsive drug/behavior use despite harm; driven by brain reward circuitry. Substance vs. Behavioral Addiction – substance addictions involve drugs (e.g., alcohol, nicotine); behavioral addictions involve activities (e.g., gambling, internet). Reward System – mesolimbic pathway (VTA → nucleus accumbens) releases dopamine, creating “wanting” (incentive salience) and “liking” (pleasure). ΔFosB – a long‑lasting transcription factor that accumulates after repeated high‑dose drug or intense natural reward exposure; drives structural and functional changes underlying craving. Tolerance & Sensitization – tolerance = reduced effect with same dose; sensitization (reverse tolerance) = heightened effect with repeated exposure. DSM‑5 Severity – 2‑3 criteria = mild, 4‑5 = moderate, 6‑9 = severe (severe = “addiction”). Risk Factors – genetic (40‑60 % heritability), stress‑axis activation, early exposure, adverse childhood events, impulsivity, low socioeconomic status. Transtheoretical Model (Stages of Change) – precontemplation → contemplation → preparation → action → maintenance → relapse‑prevention; non‑linear. --- 📌 Must Remember Neurobiology: Dopamine surge in nucleus accumbens → craving; chronic use → down‑regulation of receptors, persistent cue‑induced wanting. ΔFosB: stable for 1‑2 months; overexpression → increased drug self‑administration; inhibition blocks addiction‑related plasticity. Diagnostic Threshold: ≥ 2 of 11 DSM‑5 criteria + functional impairment. Genetic Influence: 40‑60 % of alcoholism risk; similar for other drugs; Alpha‑5 nAChR gene linked to nicotine addiction. Stress‑Induced Relapse: Acute/chronic stress ↑ cortisol & CRF → heightened drug cue salience via amygdala activation. Treatment Core: Combine pharmacotherapy (e.g., buprenorphine, naltrexone) with behavioral therapy (CBT, mindfulness, contingency management). Screening Tools: CRAFFT (adolescents), TAPS, DAST‑10, ASSIST – each yields a risk score guiding further assessment. --- 🔄 Key Processes Drug Exposure → Dopamine Release VTA neurons fire → dopamine → nucleus accumbens (NAc). Reward Sensitization Repeated high dopamine → ↑ incentive salience of drug cues → craving. ΔFosB Accumulation Repeated exposure → transcription of ΔFosB in D1‑type medium spiny neurons → long‑term gene expression changes. Neuroadaptation Cycle ↑ dopamine → receptor down‑regulation → tolerance → increased drug use → further ΔFosB build‑up. Stress‑Relapse Loop Stress → HPA axis activation → cortisol/CRF ↑ → amygdala sensitization → cue‑induced craving → relapse. Stage‑Matched Intervention (Transtheoretical Model) Identify stage → apply stage‑appropriate strategy (e.g., motivational interviewing in contemplation, CBT in action). --- 🔍 Key Comparisons Substance vs. Behavioral Addiction Substance: chemical pharmacodynamics, physical dependence, withdrawal syndrome. Behavioral: no pharmacological agent, dependence manifested as compulsive engagement, no classic somatic withdrawal. Tolerance vs. Sensitization Tolerance: decreasing effect → need higher dose. Sensitization: increasing effect (often “reverse tolerance”) → heightened response to same dose. DSM‑5 vs. ICD‑11 Classification DSM‑5: single “substance use disorder” continuum; severity specifiers; only gambling listed as behavioral addiction. ICD‑11: separates “harmful use” and “dependence”; distinct codes for each; broader behavioral‑addiction category. Cue‑Induced “Wanting” vs. “Liking” Wanting: dopamine‑driven motivational drive, can rise even when pleasure (“liking”) drops. Liking: hedonic impact, mediated by opioid and other systems, often diminishes with chronic use. --- ⚠️ Common Misunderstandings “Addiction = Lack of Willpower.” – True addiction is a brain disorder with neuroadaptations; willpower alone cannot overcome it. “Tolerance always precedes dependence.” – Tolerance and dependence can develop independently; some drugs cause strong dependence with minimal tolerance. “Only illicit drugs cause addiction.” – Alcohol, nicotine, caffeine, and even highly palatable foods can produce addiction‑like neuroadaptations. “ΔFosB is only present in drug users.” – ΔFosB also rises after intense natural rewards (e.g., sexual activity, exercise). --- 🧠 Mental Models / Intuition “Hijacked Reward Highway” – Imagine the brain’s reward circuit as a highway; addictive substances repeatedly flood it with traffic (dopamine), causing the road to remodel (ΔFosB) and become permanently wider for that direction, making detours (alternative rewards) harder. “Stress as a Fuel Pump” – Stress adds extra fuel to the engine, accelerating the speed at which cues trigger craving. “Stage Ladder” – Visualize the Transtheoretical Model as a ladder; you may climb up, slip down, or step sideways—treatment must meet the person on the rung they occupy. --- 🚩 Exceptions & Edge Cases Behavioral Addiction Limited to Gambling (DSM‑5) – Other behaviors (e.g., internet gaming) are listed as “conditions for further study,” not formal diagnoses. Physical vs. Psychological Dependence – Some substances (e.g., cannabis) produce prominent psychological dependence with minimal somatic withdrawal. Genetic Influence Not Deterministic – High heritability does not guarantee addiction; environment can mitigate or exacerbate risk. --- 📍 When to Use Which Screening Tool Selection Adolescents: CRAFFT (quick, validated). General adult primary care: ASSIST (covers all substance classes). Focused drug‑specific assessment: DAST‑10 (drug abuse). Pharmacotherapy vs. Behavioral Therapy Severe opioid dependence: start medication‑assisted treatment (buprenorphine/naltrexone) + CBT. Mild‑moderate alcohol use disorder: motivational interviewing + brief CBT; consider pharmacologic adjuncts if cravings persist. Stage‑Matched Intervention Precontemplation: use psychoeducation & empathic listening. Contemplation: employ motivational interviewing to resolve ambivalence. Preparation/Action: implement CBT skills training, contingency management. --- 👀 Patterns to Recognize Cluster of DSM‑5 criteria – cravings + loss of control + continued use despite problems → indicates severe disorder. Stress‑Cue‑Craving Triad – recent stressor + drug‑related environmental cue → high relapse risk. ΔFosB‑Associated Behaviors – escalating use, increased drug‑seeking despite adverse consequences. Early Initiation + Family History – predicts higher treatment resistance and relapse rates. --- 🗂️ Exam Traps Confusing “Tolerance” with “Sensitization.” – Both involve repeated exposure but have opposite directions of effect. Assuming DSM‑5 includes all behavioral addictions. – Only gambling is officially listed; others are research‑only categories. Attributing “withdrawal” solely to physical symptoms. – Psychological withdrawal (anhedonia, anxiety) is equally diagnostic. Choosing “ΔFosB” as a short‑term marker. – It is a long‑lasting molecular switch, not a transient signal. Overlooking the role of glutamate – While dopamine gets most attention, glutamatergic projections from prefrontal cortex drive drug‑seeking and are essential in relapse pathways. ---