Types of Addiction: Causes, Signs, and Treatment

There are two major types of addiction comprising of substance use disorders, and behavioral addictions.

Drug addiction covers alcohol, opioids, stimulants, and sedatives, and behavioral addictions, including gambling disorder and compulsive sexual behaviour.

Both categories produce the same neurological signature. Repeated use permanently alters the mesolimbic dopamine pathway, shifting the brain from voluntary use to compulsive, loss-of-control seeking.

The inability to stop is not a character flaw. It reflects measurable changes in prefrontal cortex function, dopamine receptor density, and neuroadaptive stress-system recruitment.

Identifying which type of addiction is present is the first clinical step toward choosing the right level of care.

• According to SAMHSA’s 2023 National Survey on Drug Use and Health, approximately 48.7 million Americans aged 12 or older met DSM-5 criteria for a substance use disorder in the past year. Fewer than 13% of those individuals received any form of specialty addiction treatment.
• The American Society of Addiction Medicine classifies addiction as a chronic brain disease defined by compulsive drug seeking, continued use despite harmful consequences, and lasting neurobiological changes in the brain’s reward and motivation circuits.
• Genetic factors account for 40 to 60% of individual vulnerability to substance use disorder, according to the National Institute on Drug Abuse, with environmental exposures and co-occurring mental health conditions compounding that inherited risk.
• The DSM-5-TR places both substance use disorders and gambling disorder within the “Substance-Related and Addictive Disorders” chapter, recognizing their shared dopaminergic mechanisms as the basis for applying the same diagnostic framework to both categories.
• Evidence-based treatment including medically supervised detox, medications for opioid use disorder (MOUD), and structured residential and step-down programming produces significantly better long-term recovery outcomes than unassisted cessation attempts.

What Is Addiction? The DSM-5 Definition Explained

The DSM-5-TR classifies addiction as substance use disorder: a chronic brain disease defined by a pathological pattern of use that produces clinically significant impairment across four diagnostic domains.

The 11 DSM-5 Diagnostic Criteria

The DSM-5 replaced the older “abuse” and “dependence” labels with a single unified diagnosis graded by criteria count. Severity specifiers are assigned as follows:

• Mild substance use disorder: 2 to 3 criteria met within 12 months
• Moderate substance use disorder: 4 to 5 criteria met within 12 months
• Severe substance use disorder: 6 or more criteria met within 12 months

The 11 criteria span four diagnostic domains:

• Impaired control: Taking more than intended, repeated failed attempts to cut back, excessive time spent obtaining or recovering from use, and persistent cravings
• Social impairment: Failing major obligations at work, school, or home; continued use despite interpersonal conflict; and withdrawal from previously valued activities
• Risky use: Repeated use in physically hazardous situations and continued use despite recognizing a recurring problem the substance is directly causing
• Pharmacological indicators: Tolerance, defined as requiring markedly increased amounts for the same effect, and withdrawal, defined as characteristic symptoms upon cessation or dose reduction

One critical clinical clarification for the pharmacological domain:

• Tolerance and withdrawal do not count toward a substance use disorder diagnosis when they occur solely in the context of appropriately prescribed, medically supervised treatment

Substance Addictions vs Behavioural Addictions

The DSM-5-TR organizes addiction within the “Substance-Related and Addictive Disorders” chapter under two distinct categories:

Substance use disorders recognized in DSM-5-TR include:

• Alcohol use disorder (AUD): The most prevalent substance use disorder in the US, affecting approximately 29.5 million Americans annually, with withdrawal that can produce life-threatening seizures and delirium tremens
• Opioid use disorder (OUD): Encompasses prescription opioids, heroin, and illicit fentanyl and fentanyl analogs, which now drive the majority of overdose deaths nationally
• Stimulant use disorder: A unified DSM-5-TR category covering both cocaine use disorder and amphetamine-type stimulant use disorder based on their shared dopaminergic dysregulation mechanisms
• Cannabis use disorder: First formally recognized in DSM-5, including a cannabis withdrawal syndrome reported in approximately 34% of frequent users upon cessation
• Sedative, hypnotic, or anxiolytic use disorder: Covers benzodiazepines, Z-drugs, and barbiturates; associated with life-threatening withdrawal requiring medically supervised tapering for safe discontinuation

Behavioral addictions formally recognized in DSM-5-TR include:

• Gambling disorder: The only non-substance behavioral addiction with full DSM-5-TR diagnostic status, sharing nine of the 11 substance use disorder criteria through shared mesolimbic reward mechanisms
• Internet gaming disorder: Listed in DSM-5-TR Section III as requiring additional research before formal diagnostic criteria can be finalized

How Addiction Rewires the Brain

All types of addiction, whether driven by substances or behaviors, dysregulate the mesolimbic dopamine pathway and produce converging neurobiological adaptations that explain compulsive use and the profound difficulty of stopping without clinical support.

The Mesolimbic Dopamine Pathway and Reward Circuit

The mesolimbic pathway is the brain’s core reward and motivation circuit. Every addictive substance activates it far above natural reward thresholds. Key structures and their functions in addiction development:

• Ventral tegmental area (VTA): The origin of dopamine projections activated by all drugs of abuse; sends dense projections to the nucleus accumbens and prefrontal cortex that generate the brain’s primary reward and motivation signals
• Nucleus accumbens (NAc): The primary dopamine target; the shell processes incentive salience, the compulsive motivational “wanting” signal that encodes drug cues, while the core drives habit formation and automated drug-seeking behavior
• Prefrontal cortex (PFC): Mediates executive function, impulse control, and top-down inhibition of reward-seeking circuits; chronic drug exposure impairs PFC metabolic activity, producing the hypofrontality documented by Volkow and Goldstein’s PET and fMRI studies
• Extended amygdala: Mediates the dysphoria and anxiety of withdrawal and craving through stress-system neurotransmitters including corticotropin-releasing factor (CRF) and dynorphin; its progressive recruitment explains the shift from pleasure-seeking to compulsion
• Supraphysiological dopamine surges: Drugs of abuse flood the nucleus accumbens with dopamine at two to ten times the concentrations produced by natural rewards, pathologically encoding drug-associated cues as compulsive motivational targets through incentive sensitization

Neuroadaptation, Tolerance, and the Wanting-Liking Dissociation

Repeated supraphysiological dopamine surges trigger compensatory neuroadaptations that sustain compulsive use long after initial pleasure has diminished.

Within-system neuroadaptations that drive tolerance and anhedonia:

• D2 receptor downregulation: Chronic drug exposure reduces dopamine D2 receptor density in the striatum, blunting responsiveness to all rewards including non-drug pleasures and generating the pervasive anhedonia characteristic of active addiction
• Tolerance via receptor depletion: The brain requires progressively larger doses to achieve the original effect because fewer D2 receptors are available to respond to dopamine signaling
• Incentive sensitization: Drug-associated environmental cues trigger exaggerated dopamine release even as the drug itself produces diminishing hedonic pleasure, producing the wanting-without-liking paradox Robinson and Berridge documented

Between-system neuroadaptations that drive compulsion and negative reinforcement:

• Hypofrontality: Reduced prefrontal cortex metabolic activity impairs the top-down inhibitory control over drug-seeking that enables voluntary cessation; neuroimaging evidence shows partial normalization following sustained abstinence
• Extended amygdala CRF recruitment: Chronic drug exposure recruits corticotropin-releasing factor, dynorphin, and norepinephrine stress systems in the extended amygdala, generating hyperkatifeia: the intensified dysphoria, irritability, anhedonia, and anxiety that Koob named from the Greek for intense dejection
• Wanting-liking dissociation: Sensitized mesolimbic circuits drive compulsive craving for the substance while D2 receptor downregulation simultaneously eliminates the pleasure it once produced, creating the clinical reality of compulsive use without enjoyment

Koob’s Three-Stage Addiction Cycle

Koob’s three-stage model, the dominant NIDA and NIAAA framework for addiction, describes how the motivational driver shifts from pleasure-seeking to compulsion as the disorder progresses.

The three stages and their neurobiological bases:

• Stage 1, binge/intoxication: Dopamine-mediated positive reinforcement; the person uses to experience the reward produced by nucleus accumbens activation at supraphysiological thresholds
• Stage 2, withdrawal/negative affect: Extended amygdala activation produces hyperkatifeia; the person uses primarily to relieve the persistent negative emotional baseline rather than to achieve pleasure, shifting motivation from positive to negative reinforcement
• Stage 3, preoccupation/anticipation: Prefrontal cortex-driven cue reactivity activates compulsive drug-seeking through incentive salience mechanisms that operate independently of conscious desire to use

The critical allostatic consequence of repeated cycles:

• Allostatic load accumulation: Koob and Le Moal’s allostatic framework describes how each cycle shifts the brain’s hedonic set point further below its natural baseline, making abstinence itself aversive until neurobiological recovery occurs through sustained treatment

Types of Addiction: Substances, Behaviors, and Risks

Each addiction category produces distinct risk profiles, withdrawal timelines, overdose patterns, and treatment requirements that directly determine the appropriate clinical level of care.

Addiction Type Comparison: Withdrawal Risk and Treatment Approach

Opioid and Depressant Addictions

Opioids and CNS depressants produce physical dependence through receptor mechanisms that generate medically serious withdrawal and the highest overdose mortality rates of any substance class.

• Opioid use disorder: Chronic mu-opioid receptor activation produces tolerance requiring escalating doses and a withdrawal-driven negative reinforcement cycle mediated by locus coeruleus noradrenergic hyperactivity. MOUD with buprenorphine or methadone directly targets the receptor mechanisms driving craving, withdrawal severity, and compulsive seeking.
• Heroin addiction: Heroin crosses the blood-brain barrier faster than morphine due to higher lipophilicity, producing rapid onset and severe physical dependence within weeks of regular use. Overdose risk is amplified by illicit supply frequently adulterated with fentanyl analogs.
• Fentanyl addiction: Illicit fentanyl is a synthetic opioid 50 to 100 times more potent than morphine; according to the CDC, it now drives more than 70% of all US overdose deaths. Medically supervised detox with MOUD initiation is essential before any step-down in level of care.
• Benzodiazepine addiction: Benzodiazepines produce physical dependence through GABA-A receptor downregulation at the chloride ionophore complex, generating a withdrawal syndrome that can produce life-threatening tonic-clonic seizures upon abrupt cessation. Medically supervised tapering with gradual receptor resensitization is the clinically indicated detox approach.
• Alcohol addiction: Alcohol use disorder produces a withdrawal syndrome mechanistically identical to benzodiazepine withdrawal through GABA-A rebound hyperexcitation, with delirium tremens and generalized seizures emerging in severe cases 24 to 96 hours after last use. The CIWA-Ar protocol is the validated tool guiding medical detox and symptom-triggered medication dosing.

Stimulant and Other Substance Addictions

Stimulant use disorders produce dopaminergic dysregulation with high psychiatric comorbidity. While physical withdrawal is not medically dangerous, the prolonged dysphoria and anhedonia of stimulant withdrawal drive high relapse rates without structured clinical support.

• Cocaine addiction: Cocaine simultaneously blocks dopamine, norepinephrine, and serotonin reuptake transporters, producing rapid euphoria followed by a severe dopamine-depleted crash. Chronic cocaine use reduces striatal dopamine transporter density, producing the anhedonia that CBT and contingency management directly target.
• Methamphetamine addiction: Methamphetamine depletes striatal dopamine stores rather than simply blocking reuptake, reducing dopamine transporter density by up to 50% with heavy long-term use per NIDA PET imaging data. Extended residential treatment allows partial dopaminergic system restoration through sustained abstinence.
• Marijuana addiction: Cannabis use disorder develops in approximately 9% of all users and up to 17% of those who begin use before age 18. DSM-5-recognized cannabis withdrawal produces irritability, insomnia, and appetite disruption beginning within 72 hours of cessation in physically dependent users.
• Polysubstance use disorder: Polysubstance use disorder, diagnosed when two or more concurrent substance use disorders are present, increases overdose risk through synergistic CNS depression. Multiple withdrawal syndromes with different onset timelines must be managed simultaneously during detox.

Behavioral and Process Addictions

Behavioral addictions activate the mesolimbic dopamine pathway through the same mechanisms as substances, producing shared features of tolerance, cue-driven craving, impaired control, and withdrawal-equivalent distress.

• Gambling disorder: The only behavioral addiction with full DSM-5-TR diagnostic status, gambling disorder shares nine of the 11 substance use disorder criteria including tolerance, withdrawal-equivalent restlessness, and persistent failed attempts to stop. CBT and motivational interviewing are the primary evidence-based treatments.
• Sex addiction: Compulsive sexual behavior disorder, as classified in ICD-11, involves failed attempts to control repetitive sexual behaviors despite significant distress and functional impairment. Neuroimaging-confirmed incentive salience patterns are comparable to drug-seeking, and treatment adapts CBT, motivational interviewing, and group therapy from validated addiction frameworks.

Signs of Addiction: Physical, Behavioral, and Psychological

Addiction produces identifiable warning signs across physical, behavioral, and psychological domains, with specific emergency presentations requiring immediate medical intervention.

Common Signs of Addiction

Early and moderate-severity signs of substance use disorder and behavioral addiction span multiple functional domains.

Physical warning signs include:

• Tolerance development: Requiring progressively larger amounts to achieve the original effect, reflecting D2 receptor downregulation and reduced reward circuit sensitivity
• Withdrawal on cessation: Physical or psychological symptoms including anxiety, tremor, insomnia, nausea, and diaphoresis appearing when use is reduced or stopped, reflecting neuroadaptive changes that now require the substance to maintain equilibrium
• Physical health deterioration: Unintended weight loss or gain, neglected personal hygiene, frequent illness, and visible substance-specific organ damage accumulating with duration of active use

Behavioral warning signs include:

• Loss of control over use: Consistently consuming more than intended or for longer than intended despite repeated failed efforts to cut back
• Time consumed by use: Spending a significant portion of daily life obtaining, using, or recovering from the effects of the substance or behavior
• Abandoning valued activities: Withdrawing from occupational responsibilities, interpersonal relationships, or recreational activities that previously held importance

Psychological warning signs include:

• Persistent craving: Recurrent strong urges to use, particularly in response to drug-associated environmental cues that trigger incentive salience responses through sensitized mesolimbic circuits
• Continued use despite harm: Recognizing that a recurring physical, psychological, or social problem is being caused by use and continuing despite that awareness
• Failed abstinence attempts: Repeated genuine efforts to stop or significantly reduce use that consistently fail despite motivation to change

Severe Symptoms and When to Seek Emergency Help

The following presentations are medical emergencies requiring immediate 911 contact or emergency department evaluation.

Life-threatening substance use emergencies include:

• Respiratory depression or arrest: Slow, shallow, or stopped breathing following opioid or combined CNS depressant use; administer naloxone (Narcan) immediately and call 911 before any other action
• Tonic-clonic seizures: Grand mal seizures occurring during alcohol or benzodiazepine withdrawal, typically beginning 24 to 72 hours after last use and potentially progressing to status epilepticus without medical intervention
• Delirium tremens: Hallucinations, extreme agitation, hyperthermia, and autonomic instability occurring 48 to 96 hours into alcohol withdrawal; carries a mortality rate of 5 to 15% without medical treatment
• Loss of consciousness or unresponsiveness: Following any drug combination or suspected overdose, regardless of which substance is involved
• Severe chest pain or cardiac arrhythmia: Cocaine and methamphetamine induce coronary vasospasm and catecholamine surge that can precipitate myocardial infarction in users of any age

Naloxone (Narcan) reverses opioid-induced respiratory depression within minutes. Call 911 immediately after administration and remain with the person until emergency services arrive.

Long-Term Effects of Untreated Addiction

Untreated substance use disorders produce progressive neurological, organ-system, and psychiatric damage that worsens with each additional year of active use.

Long-term consequences across organ systems and neurological function:

• Neurological: Persistent hypofrontality reducing executive function and impulse control; alcohol use disorder-related Wernicke-Korsakoff syndrome from thiamine deficiency; methamphetamine-induced dopaminergic dysregulation producing long-term anhedonia and cognitive impairment even after cessation
• Cardiovascular: Alcohol use disorder-associated dilated cardiomyopathy; cocaine-induced coronary vasospasm and accelerated atherosclerosis; methamphetamine-associated cardiomyopathy; opioid injection use transmitting endocarditis-causing bacteria to cardiac valves
• Hepatic: Alcohol use disorder progressing from hepatic steatosis to fibrosis to irreversible cirrhosis; opioid injection drug use transmitting hepatitis C through shared injection equipment
• Psychiatric: Co-occurring major depressive disorder, post-traumatic stress disorder, anxiety disorders, and bipolar disorder each independently worsen substance use disorder prognosis when left untreated; dual diagnosis treatment addressing both conditions simultaneously is the standard of care

What Causes Addiction: Risk Factors and Vulnerability

No single factor predicts who will develop addiction; risk accumulates across genetic, neurobiological, developmental, and environmental domains and requires a comprehensive biopsychosocial assessment to understand in each individual case.

Genetic and Neurobiological Risk Factors

Heritable biological factors account for the single largest share of addiction vulnerability.

Key genetic risk factors include:

• Heritability of 40 to 60%: NIDA confirms genetic factors account for 40 to 60% of individual vulnerability to substance use disorder, operating through multiple gene-environment interaction pathways affecting reward sensitivity, stress reactivity, and impulse control
• First-degree family history: First-degree relatives with substance use disorder substantially increase neurobiological vulnerability through shared genetic architecture affecting the mesolimbic dopamine system and stress-response circuits
• D2 receptor gene polymorphisms: Variants in DRD2 and DRD4 genes affect striatal dopamine D2 receptor density, directly influencing reward pathway responsiveness and cross-substance addiction risk
• Alcohol metabolism gene variants: Polymorphisms in ALDH2 and ADH1B alter ethanol metabolism rates, modifying physiological sensitivity to alcohol’s reinforcing effects and alcohol use disorder vulnerability

Environmental and Psychological Risk Factors

Environmental exposures and co-occurring psychiatric conditions interact with genetic vulnerability to determine addiction onset and severity.

High-risk environmental and psychological factors include:

• Early trauma and adverse childhood experiences (ACEs): Higher ACE scores correlate with substantially elevated substance use disorder risk; childhood trauma activates the extended amygdala CRF stress systems that sustain the withdrawal and negative affect stage of addiction
• Co-occurring mental health conditions: Major depressive disorder, PTSD, generalized anxiety disorder, and attention-deficit/hyperactivity disorder each independently increase substance use disorder risk through shared neurobiological vulnerabilities and self-medication mechanisms
• Early age of first use: Beginning alcohol or cannabis use before age 15 increases lifetime substance use disorder probability two to four times compared to initiation after age 21, per NIDA data
• Social and community risk factors: Peer substance use, community-level drug availability, housing instability, and absence of protective social support consistently predict substance use disorder onset across major epidemiological studies
• Chronic stress and unmet mental health needs: Chronic stress activates corticotropin-releasing factor pathways in the extended amygdala, sensitizing the neural circuits that drive the withdrawal and negative affect stage and increasing vulnerability to both initiation and relapse

How Addiction Is Treated: The ASAM Continuum of Care

Effective addiction treatment follows the ASAM continuum, with placement calibrated to withdrawal severity, the specific substances involved, the presence of co-occurring mental health conditions, and the individual’s medical and social context.

Medical Detox

Medical detox provides 24-hour supervision to manage withdrawal safely and initiate the physiological stabilization required before residential treatment can begin.

Core components of evidence-based medical detox include:

• Continuous medical monitoring: Vital signs, neurological status, and validated withdrawal severity scoring using the CIWA-Ar for alcohol withdrawal and the COWS scale for opioid withdrawal guide real-time medication adjustments
• Symptom-targeted pharmacotherapy: Benzodiazepine tapers for alcohol and sedative withdrawal, buprenorphine induction for opioid withdrawal, and clonidine for noradrenergic storm suppression reduce both withdrawal severity and acute medical risk
• MOUD initiation during opioid detox: Buprenorphine induction during opioid detox reduces withdrawal severity, suppresses craving, and significantly lowers 30-day relapse and overdose mortality compared to detox without pharmacological support
• Safety monitoring for severe complications: Medical detox environments are equipped to manage tonic-clonic seizures, delirium tremens, and cardiac complications that can emerge during alcohol and benzodiazepine withdrawal without warning

Residential Treatment

Residential treatment provides 24-hour structured programming in a therapeutic environment, addressing the psychological and neurobiological mechanisms of addiction alongside continued medical management.

What residential treatment delivers:

• Daily evidence-based therapy: Six or more hours of individual and group therapy per day incorporating CBT, DBT, trauma-focused modalities including EMDR, and motivational interviewing
• Dual diagnosis treatment: Simultaneous psychiatric care addressing co-occurring mental health conditions that sustain substance use disorder through shared neurobiological pathways and independently worsen relapse risk when untreated
• Relapse prevention skill-building: Structured rehearsal of coping strategies for cue-induced craving, hyperkatifeia management, and high-risk situations that activate the preoccupation and anticipation stage of Koob’s addiction cycle
• Medication management: Continuation of MOUD, psychiatric medication stabilization, and management of substance-related medical complications throughout the residential stay

PHP, IOP, and Outpatient Step-Down Programs

ASAM criteria define a structured continuum of step-down care following residential treatment, calibrated to declining acuity and increasing independence.

Step-down levels by clinical intensity:

• PHP (Partial Hospitalization Program): 20 or more structured clinical hours per week; participants reside off-site in sober living or home environments while attending intensive daily programming
• IOP (Intensive Outpatient Program): 9 or more clinical hours per week; supports return to occupational and educational responsibilities while maintaining therapeutic continuity
• Outpatient: Weekly group or individual therapy sessions providing maintenance support and relapse prevention monitoring for clients at lower acuity
• Alumni and continuing care: Structured peer-support and alumni programming and ongoing monitoring that extend recovery support beyond formal treatment and address the chronic, relapsing nature of substance use disorder long-term

Evidence-Based Therapies for Substance Use Disorder

Multiple psychosocial interventions carry strong empirical support for substance use disorder treatment across substance and behavioral addiction categories.

Tier 1 evidence-based therapies include:

• Cognitive Behavioral Therapy (CBT): Targets the maladaptive cognitions and conditioned behavioral responses sustaining substance use; directly modifies the prefrontal cortex-mediated appraisal patterns driving cue-induced craving and relapse
• Dialectical Behavior Therapy (DBT): Addresses the emotion dysregulation underlying both substance use disorders and co-occurring borderline personality disorder through structured skills training in distress tolerance, interpersonal effectiveness, and emotion regulation
• Motivational Interviewing (MI): A directive, client-centered counseling approach that resolves ambivalence about behavioral change by evoking the person’s own intrinsic motivation for recovery rather than imposing external pressure
• Contingency Management: An operant conditioning approach using positive reinforcement for verified abstinence; carries the strongest evidence base for stimulant use disorder and consistently improves treatment engagement and retention across substance categories
• Eye Movement Desensitization and Reprocessing (EMDR): Processes the traumatic memory networks that activate extended amygdala stress circuitry and maintain the addiction cycle through trauma-driven relapse and craving

Medications for Opioid and Alcohol Use Disorder

FDA-approved pharmacological treatments are the standard of care for opioid use disorder and alcohol use disorder, reducing mortality significantly when combined with psychosocial treatment.

FDA-approved medications by substance and mechanism:

• Buprenorphine (Suboxone, Subutex): A partial mu-opioid agonist that reduces cravings and withdrawal without producing full euphoria; now the frontline MOUD for opioid use disorder per current SAMHSA treatment guidelines
• Methadone: A full opioid agonist dispensed through licensed Opioid Treatment Programs; over 50 years of evidence supports its effectiveness for severe opioid use disorder presentations with high-complexity medical histories
• Naltrexone (Vivitrol): An opioid receptor antagonist that blocks all opioid-mediated euphoria; available as a once-monthly injection for opioid use disorder and as a daily oral medication or injection for alcohol use disorder
• Acamprosate: Modulates GABA and glutamate neurotransmitter activity to reduce protracted alcohol withdrawal symptoms and craving in patients who have completed detox; FDA-approved for sustained alcohol use disorder recovery
• Disulfiram: Inhibits aldehyde dehydrogenase, producing an aversive acetaldehyde-mediated reaction to alcohol consumption; used as a deterrent adjunct for motivated patients with alcohol use disorder

Addiction Treatment at New Spirit Recovery

New Spirit Recovery provides medically supervised, dual-diagnosis addiction treatment across the full ASAM continuum at facilities in Tarzana, Northridge, and Encino, California, with same-day assessments available.

Detox Program

New Spirit Recovery’s detox program provides 24-hour nursing coverage and physician oversight throughout the full withdrawal period, integrating MOUD protocols and individual therapy from the first day of care. Medical detox at New Spirit Recovery is designed to stabilize both substance withdrawal and co-occurring psychiatric symptoms before transitioning clients into residential programming.

Residential Treatment Program

Residential treatment at New Spirit Recovery delivers a minimum of six structured clinical hours per day, seven days a week. Programming incorporates CBT, DBT, somatic therapy, art therapy, and the proprietary Rewired curriculum developed by co-founder Erica Spiegelman. Each treatment plan is individualized based on the specific substance or behavioral addiction, co-occurring diagnoses, and clinical acuity at intake.

Dual Diagnosis Treatment

New Spirit Recovery’s dual diagnosis program delivers simultaneous evidence-based treatment for substance use disorders and co-occurring conditions including major depressive disorder, PTSD, anxiety disorders, bipolar disorder, borderline personality disorder, and dissociative disorders. Dr. Patrick Lockwood, licensed clinical psychologist and Cal Lutheran University professor, provides on-site consultation, treatment planning, and clinical supervision across 12 or more hours per week.

Step-Down Programming

Step-down programming at New Spirit Recovery transitions clients through PHP, IOP, and outpatient levels with coordinated sober living arrangements at each stage. The model directly addresses the chronic, relapsing nature of substance use disorder by ensuring clinical support and accountability extend well beyond acute residential care.

Medication-Assisted Treatment

New Spirit Recovery’s medication-assisted treatment program provides buprenorphine induction and continuation, naltrexone administration, and access to the full range of FDA-approved medications for both opioid use disorder and alcohol use disorder across all levels of care from detox through outpatient.

Veterans Program

New Spirit Recovery’s veterans program provides specialized clinical programming for active-duty service members and veterans, including trauma-informed therapy adapted for combat-related PTSD, military-specific cue-reactivity patterns, and moral injury. Clinicians with military trauma specialization provide dedicated weekly sessions tailored to veteran-specific substance use disorder presentations.

Frequently Asked Questions

What is addiction?

Addiction, clinically diagnosed as substance use disorder under the DSM-5-TR, is a chronic brain disease defined by compulsive use of a substance or engagement in a rewarding behavior despite harmful consequences. It reflects measurable neurobiological changes in the mesolimbic dopamine pathway, prefrontal cortex function, and extended amygdala stress-system reactivity that clinical treatment directly targets.

Is addiction a disease or a choice?

Addiction is classified as a chronic brain disease by the American Society of Addiction Medicine, NIDA, and the American Psychiatric Association. Initial use involves voluntary choice, but repeated use produces D2 receptor downregulation, hypofrontality, and extended amygdala stress-system recruitment that progressively impair voluntary control, making cessation without clinical support comparable to managing any other chronic disease without treatment.

What are the most common types of addiction?

Alcohol use disorder is the most prevalent substance use disorder in the US, affecting approximately 29.5 million Americans annually. Opioid use disorder, stimulant use disorder covering cocaine and methamphetamine, cannabis use disorder, and benzodiazepine use disorder are the next most common substance categories. Gambling disorder is the most clinically recognized behavioral addiction with full DSM-5-TR diagnostic status.

What are the early signs of addiction?

Early signs include developing tolerance to the substance, spending increasing time obtaining or using it, failing to meet major role obligations at work or home, withdrawing from previously valued activities, and continuing use despite recognizing a recurring problem it is causing. Two or more of these signs within 12 months meet the DSM-5-TR threshold for mild substance use disorder.

What causes addiction?

Addiction develops through the interaction of genetic vulnerability (40 to 60% of risk per NIDA), early substance exposure, co-occurring mental health conditions, and environmental stressors that activate extended amygdala stress circuits. No single cause explains addiction universally; effective treatment simultaneously addresses the biological, psychological, and social factors contributing to each individual’s presentation.

Can addiction be cured?

Addiction cannot be permanently cured the way an acute infection resolves, but it is effectively managed through evidence-based treatment. NIDA reports that long-term relapse rates for substance use disorders are comparable to those of other chronic diseases including hypertension and type 2 diabetes, with sustained recovery achievable through ongoing clinical support and structured continuing care.

What is the difference between addiction and physical dependence?

Physical dependence refers to the physiological adaptation that produces tolerance and withdrawal when a substance is reduced or stopped; it can develop with medications taken as prescribed. Addiction involves the loss of control, compulsive seeking, and continued use despite consequences that reflect mesolimbic and prefrontal cortex neuroadaptations extending far beyond simple physical dependence.

References

1. Substance Abuse and Mental Health Services Administration. (2024). 2023 National Survey on Drug Use and Health: Key substance use and mental health indicators in the United States. SAMHSA. https://www.samhsa.gov/data/report/2023-nsduh-annual-national-report

2. National Institute on Drug Abuse. (2023). Drug misuse and addiction. NIDA. https://nida.nih.gov/publications/drugs-brains-behavior-science-addiction/drug-misuse-addiction

3. National Institute on Drug Abuse. (2022). Understanding drug use and addiction DrugFacts. NIDA. https://nida.nih.gov/publications/drugfacts/understanding-drug-use-addiction

4. National Institute on Drug Abuse. (2020). Drugs, brains, and behavior: The science of addiction. NIDA. https://nida.nih.gov/publications/drugs-brains-behavior-science-addiction/drugs-brain

5. Koob, G. F., & Volkow, N. D. (2016). Neurobiology of addiction: A neurocircuitry analysis. The Lancet Psychiatry, 3(8), 760-773.

6. American Psychiatric Association. (2022). Diagnostic and statistical manual of mental disorders (5th ed., text rev.). American Psychiatric Publishing.

7. Volkow, N. D., Koob, G. F., & McLellan, A. T. (2016). Neurobiologic advances from the brain disease model of addiction. New England Journal of Medicine, 374(4), 363-371.

8. Substance Abuse and Mental Health Services Administration. (2023). Medications for opioid use disorder: Treatment improvement protocol (TIP) 63. SAMHSA. https://store.samhsa.gov/product/tip-63-medications-opioid-use-disorder/PEP21-02-01-002