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Addiction isn't just about willpower or "bad choices"—it's a complex interplay of neurobiology, learning, cognition, and social context that fundamentally alters motivated behavior. You're being tested on your ability to explain why people become addicted and how different theoretical frameworks account for the transition from casual use to compulsive drug-seeking. These theories connect directly to core physiology concepts: reward circuitry, neurotransmitter systems, homeostatic regulation, and the neural basis of learning and memory.
The AP exam loves questions that ask you to compare theoretical perspectives or apply them to case scenarios. Don't just memorize theory names—know what mechanism each theory emphasizes (dopamine deficiency vs. sensitization vs. opponent processes) and whether it focuses on biological vulnerability, psychological factors, or social influences. Understanding these distinctions will help you tackle both multiple-choice comparisons and FRQ prompts asking you to evaluate addiction from multiple perspectives.
These theories emphasize that some individuals are neurobiologically predisposed to addiction before they ever encounter a substance. The focus is on inherited differences in brain chemistry and reward processing that create unequal vulnerability.
Compare: Genetic Predisposition Theory vs. Reward Deficiency Syndrome—both emphasize biological vulnerability, but Genetic Predisposition focuses on inherited risk factors while Reward Deficiency specifies the mechanism (dopamine hypofunction). If an FRQ asks you to explain biological bases of addiction, Reward Deficiency gives you the more specific neural explanation.
These theories explain how the brain changes in response to repeated substance exposure. The key concept is that chronic drug use fundamentally alters neural circuitry, creating new motivational states that perpetuate use.
Compare: Opponent Process Theory vs. Allostatic Model—both explain the shift from pleasure-seeking to pain-avoidance, but Opponent Process focuses on hedonic dynamics (pleasure vs. displeasure) while the Allostatic Model emphasizes stress system involvement and the concept of a shifting set point. The Allostatic Model is more comprehensive but Opponent Process is more testable in simple scenarios.
These theories focus on how experience shapes addiction through conditioning, sensitization, and observational learning. The brain doesn't just adapt—it learns to associate cues, contexts, and behaviors with drug effects.
Compare: Incentive-Sensitization Theory vs. Social Learning Theory—Incentive-Sensitization explains individual neural changes that maintain addiction, while Social Learning explains how addiction begins through environmental exposure. Use Incentive-Sensitization for questions about craving and relapse; use Social Learning for questions about initiation and prevention.
These theories emphasize the role of thoughts, beliefs, and psychological needs in addiction. Mental processes mediate the relationship between biology, environment, and addictive behavior.
Compare: Self-Medication Hypothesis vs. Cognitive-Behavioral Model—both are psychological theories, but Self-Medication emphasizes why people start using (to address pre-existing distress) while Cognitive-Behavioral focuses on what maintains use (thought patterns and behavioral chains). Treatment implications differ: Self-Medication suggests treating underlying conditions; CBT targets addiction-specific cognitions.
| Concept | Best Examples |
|---|---|
| Biological vulnerability | Genetic Predisposition Theory, Reward Deficiency Syndrome |
| Dopamine system dysfunction | Reward Deficiency Syndrome, Neuroadaptation Theory |
| Homeostatic dysregulation | Opponent Process Theory, Allostatic Model |
| Learning and conditioning | Incentive-Sensitization Theory, Social Learning Theory |
| Wanting vs. liking dissociation | Incentive-Sensitization Theory |
| Psychological coping | Self-Medication Hypothesis, Cognitive-Behavioral Model |
| Executive function impairment | Dual Process Model, Neuroadaptation Theory |
| Environmental/social factors | Social Learning Theory, Allostatic Model |
Which two theories both emphasize dopamine system dysfunction but differ in whether they focus on pre-existing deficits versus changes caused by drug use?
A patient reports that they no longer enjoy using their substance but feel intense cravings when exposed to drug-related cues. Which theory best explains this dissociation, and what key distinction does it make?
Compare and contrast Opponent Process Theory and the Allostatic Model: What common phenomenon do both explain, and how do their proposed mechanisms differ?
An FRQ asks you to explain why someone with a history of childhood trauma might be more vulnerable to addiction. Which theory provides the most direct explanation, and what is its central claim?
How would a Dual Process Model theorist explain why an individual continues using substances despite knowing the negative consequences and genuinely wanting to quit?