This article is part of Understanding Addiction: A Psychiatry-Informed Foundation & Medication-Assisted Treatment & Harm Reduction Psychiatry, a series that explains the neuroscience, psychology, and clinical realities behind substance use disorders.
A PMHNP Perspective on Why Cravings Happen — and How We Treat Them
Understanding Craving Neurobiology and Medication Options
One of the most harmful myths in addiction is the belief that cravings mean someone “isn’t trying hard enough.”
From a Psychiatric Mental Health Nurse Practitioner (PMHNP) perspective, cravings are not a failure of motivation or character — they are predictable neurochemical events driven by measurable changes in the brain.
Cravings arise from alterations in:
- the reward system (dopamine)
- the stress system (cortisol, norepinephrine)
- learning and memory circuits
- environmental and emotional conditioning
- disrupted glutamate signaling
Understanding the neurobiology of cravings allows clinicians to treat addiction more effectively — and allows patients to release shame and engage in evidence-based care.
What Are Cravings — Clinically Speaking?
Cravings are involuntary brain-driven urges to use a substance, even when a person intellectually wants to stop.
Clinically, cravings are:
- neurologically generated
- stress-responsive
- cue-conditioned
- strengthened by trauma
- intensified by withdrawal
- not a conscious decision
From a PMHNP standpoint, cravings signal brain dysregulation, not poor willpower.
Why Cravings Feel So Overwhelming
Patients often tell PMHNPs:
- “It feels like my brain is hijacked.”
- “I know better, but my body doesn’t.”
- “The urge feels urgent and panicked.”
- “I feel unsafe when cravings hit.”
This is because cravings activate survival circuits, not rational thought.
Cravings are not thoughts — they are physiological alarms.
Why Medication Alone Is Not Enough
From a PMHNP lens, medications reduce neurobiological pressure — but they work best when combined with:
- psychotherapy (CBT, DBT, MI)
- trauma-informed care
- sleep stabilization
- stress regulation
- nutrition
- structured routines
The Neurobiology of Cravings (PMHNP Breakdown)
Dopamine Dysregulation (Reward System)
Repeated substance use floods the brain with dopamine far beyond natural levels.
Over time, the brain adapts by:
- reducing dopamine receptor sensitivity
- decreasing baseline dopamine production
- requiring stronger stimulation for relief
This leads to:
- anhedonia (inability to feel pleasure)
- compulsive seeking
- “using just to feel normal”
National Institute on Drug Abuse – Drugs, Brains, and Behavior
Cue-Induced Craving (Conditioned Learning)
Cravings become conditioned responses, not conscious thoughts.
Triggers include:
- people
- places
- smells
- emotions
- time of day
- stress
- trauma reminders
The hippocampus and amygdala store these associations, creating automatic craving loops.
Stress System Hyperactivation
Chronic substance use sensitizes the amygdala.
This causes:
- exaggerated stress responses
- anxiety-driven cravings
- relapse during emotional distress
- urgency to “escape” discomfort
Stress becomes one of the most powerful relapse drivers, especially in trauma-exposed patients.
Glutamate Dysregulation (Learning & Relapse)
Glutamate governs learning, memory, and habit formation.
In addiction:
- glutamate signaling becomes dysregulated
- cue-response loops strengthen
- relapse risk increases even after abstinence
This explains why cravings can resurface months or years later.
Medication Options PMHNPs Use to Treat Cravings
One of the most important roles of a PMHNP is selecting craving-targeted pharmacotherapy based on diagnosis, neurobiology, and comorbid conditions.
Naltrexone (Oral & Vivitrol)
Mechanism:
- Opioid receptor antagonist
- Blocks reward from alcohol and opioids
Clinical benefits:
- Reduces alcohol cravings
- Blunts euphoric reinforcement
- Decreases relapse risk
Best for:
- Alcohol Use Disorder (AUD)
- Opioid Use Disorder (OUD) after detox
Acamprosate
Mechanism:
- Modulates glutamate and GABA balance
- Stabilizes post-acute withdrawal
Clinical benefits:
- Reduces baseline cravings
- Improves emotional regulation
- Supports abstinence maintenance
Best for:
Patients with anxiety-driven cravings
Alcohol Use Disorder
Buprenorphine (Suboxone)
Mechanism:
- Partial mu-opioid agonist
- Strong craving suppression
- Ceiling effect reduces overdose risk
Clinical benefits:
- Stabilizes reward system
- Prevents withdrawal
- Restores daily functioning
Best for:
- Moderate–severe Opioid Use Disorder
Gabapentin (Off-Label)
Mechanism:
- Modulates calcium channels
- Reduces hyperexcitability
Clinical use:
- Anxiety-driven cravings
- Protracted withdrawal
- Sleep disturbance
Best for:
Patients with comorbid anxiety
Mild–moderate AUD
Topiramate (Off-Label)
Mechanism:
- Reduces dopamine signaling
- Enhances GABA activity
Clinical benefits:
- Decreases craving intensity
- Reduces impulsive use
Best for:
Stimulant cravings (select cases)
Alcohol Use Disorder
What Happens to Cravings Over Time?
With treatment:
- dopamine pathways recalibrate
- stress reactivity decreases
- conditioned responses weaken
- emotional regulation improves
- cravings become less frequent and less intense
Cravings are not permanent — but untreated neurobiology prolongs them.
If cravings feel overwhelming, exhausting, or frightening, please know this:
Cravings are treatable neurobiological events — not personal failures. With the right combination of psychiatric care, medication, and support, relief is possible. You deserve treatment that understands your brain — not just your behavior.
No. Cravings decrease as brain chemistry stabilizes and conditioning weakens.
It depends on diagnosis:
Naltrexone for AUD/OUD
Acamprosate for alcohol abstinence
Buprenorphine for OUD
No. Cravings are signals — not commands.
Yes. Trauma sensitizes the stress system, increasing craving intensity.
Not everyone — but many benefit significantly when medications are appropriately matched.
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