by Zijun Zhou, July 27, 2025

In the 21st century, social technology and cultural advances have brought new challenges. One of the most serious is drug addiction, now a major public health and social issue. The latest statistics from the Addiction Group (2024) show that nearly 50 million Americans suffer from a substance addiction or substance use disorder (SUD) each year, but less than 10% receive appropriate treatment. Further, more than 70% of alcohol-dependent people have never sought professional help. Addiction is also deeply intertwined with broader mental health challenges, including a significantly elevated risk for suicidality. While not all of the 13 million adults and 3.4 million adolescents in the United States affected by suicidal thoughts each year necessarily have a diagnosed substance use disorder, research robustly demonstrates that individuals with SUDs face a substantially increased risk of suicide mortality (Sugue, 2024). For example, a large case-control study conducted across eight integrated healthcare systems in the United States found that all categories of substance use disorders, including alcohol, tobacco, and other drug use disorders, were significantly associated with an increased risk of suicide mortality, even after controlling for comorbid mental health and physical health conditions. This methodological rigor is critical, as it provides strong evidence that Substance Use Disorder is not merely an epiphenomenon or symptom of other psychiatric conditions, but rather a powerful and independent driver of suicide risk. This finding offers a solid evidentiary foundation for the article’s central thesis: that addiction is itself a primary pathological process. The study emphasized that the risk is particularly pronounced for individuals with multiple substance use disorders, and that women face a relatively higher risk compared to men (Lynch et al., 2020). This strong association further underscores that substance use disorders likely contribute significantly to suicide risk, particularly among individuals experiencing suicidal ideation and broader mental health crises. Such findings emphasize the importance of addressing addiction as a critical public health concern.

Despite the mounting scientific evidence, a consensus on the nature of addiction remains elusive in both academic and public spheres. A landmark event in this debate occurred in 2014, when the esteemed journal Nature published an editorial, Animal farm, which claimed that the view of addiction as a brain disease was not particularly controversial, at least among scientists (Animal Farm, 2014). This assertion, however, provoked a swift and strong backlash, culminating in a letter signed by 94 international addiction scholars who contested this one-dimensional portrayal. They argued that substance abuse cannot be divorced from its social, psychological, cultural, political, legal and environmental contexts: it is not simply a consequence of brain malfunction. This public debate highlights the complexity of the issue. Therefore, this article’s support for the disease model is not intended to dismiss these vital critiques. Rather, it is to argue that, while fully acknowledging the importance of these psychosocial and environmental factors, the neuroadaptive changes that occur in the brain during addiction are so profound, pathological, and dysfunctional that the disease framework remains the most robust scientific model for understanding its compulsive nature and for guiding effective intervention.

Addiction is a chronic disease characterized by drug seeking and use that is compulsive or difficult to control despite harmful consequences (National Institute on Drug Abuse, 2018). Unlike the traditional concept of addiction as a weakness of will or an individual’s choice, the occurrence and development of addiction are driven by complex neurobiological mechanisms. These neurobiological mechanisms fundamentally undermine voluntary control by profoundly restructuring the brain’s reward system. This restructuring pathologically heightens the motivational value of the drug while diminishing the perceived value of natural rewards. As a result, the individual experiences intense, cue-driven cravings that can overwhelm rational thought. This is compounded by severe disturbances in emotion and stress regulation that create a deeply negative affective state during abstinence, driving a powerful compulsive need to use the drug to escape from this distress. These issues are further exacerbated by significant impairments in executive function, which compromise the prefrontal cortex’s ability to control impulses and weigh long-term consequences, weakening the brain’s inhibitory control system against relapse. The clinical manifestations of addiction are usually accompanied by tolerance and withdrawal symptoms, and its essence is continuous and repeated drug seeking and use. Tolerance and withdrawal symptoms may be present, and the essential elements include continuous and repeated drug seeking at the cost of normal rewards. It is not the result of one’s own choice.

Critics often argue that addiction is not a real disease because they believe that the brain is designed to change throughout life naturally. They support this by pointing out that the growth stages of children and adolescents and learning throughout adulthood are based on similar changes in the cerebral cortex and limbic system (Lewis, 2017). However, this view ignores the changes in brain structure and function that addiction demonstrably causes, which form the core basis for defining it as a disease. These extensive alterations exemplify an abnormal state affecting brain structure and function, accompanied by clear behavioral symptoms, consistent with established medical criteria for a disease (National Cancer Institute, 2011). Indeed, addiction manifests precisely through such pathological changes. For example, a defining feature of drug abuse is the pathological ‘hijacking’ of the brain’s natural reward system and emotional regulation circuits. This hijacking itself represents a fundamental disruption of normal brain function, an abnormal state directly initiated when all addictive drugs drastically increase dopamine release in key brain regions. Dopamine is the central neurotransmitter of the brain’s reward system and is primarily responsible for regulating feelings of pleasure, motivation, and reinforcement learning. However, a drug-induced surge in dopamine is not a physiological adaptation like normal learning, but rather an extreme and abnormal neurochemical event that profoundly alters neural circuits. In addictive behaviors, drugs cause a sharp rise in dopamine levels in key regions such as the nucleus accumbens and the striatum by stimulating dopamine neurons. This abnormal dopamine release alters neural circuits deep in the brain from the ventral tegmental area (VTA) to the nucleus accumbens. Further, it extends to regions such as the limbic system and orbitofrontal cortex (Leshner, 1997). Together, these regions regulate emotions, decision-making, and impulse control. Unlike the gradual changes of natural learning, this overwhelming, drug-induced flood of dopamine fundamentally corrupts the brain’s decision-making architecture, which is a hallmark of a disease state.

While these changes begin with the limbic system, the effects of addiction extend further to higher-order regulatory regions. The ventromedial prefrontal cortex (VMPC) in drug addicts exhibits significant functional impairments.The behavior of people with an addiction is highly similar to that of patients with VMPC damage: both groups often deny or are unaware of their problems (Bechara, 2005). Moreover, when faced with a choice that offers an immediate reward, they tend to ignore the possible long-term negative consequences, including the loss of their job, family, or even reputation. VMPC damage usually includes the medial parts of Brodmann Area (BA) 25, lower 24, 32, 11, 12, and 10. Although patients may retain normal intelligence, memory, and other cognitive functions, they show significant deficits in emotional and social behavior and long-term decision-making abilities, which is highly consistent with the characteristics of drug addiction (Bechara, 2005). Compared with non-addicts, drug addicts (such as cocaine-dependent individuals) have significantly lower resting-state functional connectivity (RSFC) between the frontal hemispheres. This change is particularly pronounced in areas related to the dorsal attention network, including bilateral prefrontal, medial prefrontal, and posterior parietal regions (Kelly et al., 2011). This weakening of RSFC reflects the persistent impairments in executive function, attention control, and behavioral regulation in people with an addiction. This not only makes them more prone to relapse in the face of environmental cues (for example, encountering people who used to take drugs together, going to places associated with past drug use, or seeing items and equipment related to drugs), but also weakens motivation for long-term goals and impulse control (Mennis et al., 2016).This phenomenon reveals that addiction is not only a functional abnormality of a single neural circuit but also the result of impaired collaboration among multiple brain regions.

From a neurobiological perspective, the development of addiction can be divided into three recurring stages: Binge and Intoxication, Withdrawal and Negative Affect, and Preoccupation and Anticipation. This cyclical model, driven by profound neural adaptations within specific neural circuits, clearly reveals the progressive pathophysiological process of addiction as a chronic, relapsing brain disease, rather than a simple issue of willpower or choice. Each stage involves the activation of specific neurobiological circuits and is accompanied by clinical and behavioral characteristics (Koob & Volkow, 2016; Volkow, Koob, & McLellan, 2022). Exploring each of these stages in turn reveals how the disease progresses and systematically hijacks the brain’s circuitry.

During the Binge and Intoxication stage, addictive substances significantly increase dopamine levels by triggering their release in the brain’s reward circuitry. This process bypasses natural reward mechanisms, directly stimulating dopamine transmission in key regions such as the nucleus accumbens and prefrontal cortex, resulting in reward effects from drug use that far exceed those of natural stimuli (Kalivas & O’Brien, 2008). This direct and overwhelming stimulation of the reward pathway represents an initial pathological transformation and an early manifestation of the disease state of addiction, as it disrupts the brain’s normal regulatory processes, disproportionately amplifying the incentive value of drugs. Dopamine signaling not only reinforces the immediate response to drugs but also links drug use to specific environmental cues through conditioned learning. As usage frequency increases, dopamine cells gradually become less responsive to the reward but more sensitive to cues predicting the reward, thereby intensifying drug cravings (Koob & Volkow, 2016). This neural adaptation marks a pathological hijacking, reflecting addiction as a disease where patients’ behavior is increasingly driven by external cues rather than autonomous choice. This neural adaptation marks a pathological hijacking, reflecting addiction as a disease where patients’ behavior is increasingly driven by external cues rather than autonomous choice, thereby setting the stage for the painful withdrawal of the second act.

The Withdrawal and Negative Affect stage is characterized by a critical shift from reward-system dominance to the recruitment of brain stress and antireward systems. This transition is initiated by counteradaptive mechanisms, specifically the opponent process, a neurobiological response that counteracts the drug’s initial rewarding effects. In addition, this process becomes dysregulated; it fails to return to its homeostatic baseline and instead establishes a new, pathological state known as allostasis (Koob & Le Moal, 2008). This allostatic state represents a chronic deviation of the brain’s reward set point, sustained by the extended amygdala’s overactivation of the antireward system (Koob & Le Moal, 2008). The hyperactivity of this system, mediated by neurotransmitters like corticotropin-releasing factor, is responsible for the profound negative emotional states of withdrawal, such as anxiety and irritability (Volkow, Koob, & McLellan, 2022). Consequently, the motivation for drug use is fundamentally altered. It shifts from a volitional act to seek pleasure to a compulsive behavior driven by the need to temporarily alleviate this persistent, aversive internal state (Koob & Volkow, 2016). This shift from choice to compulsion is a core pathological feature of the disease. At this juncture, the motivation for drug use has fundamentally shifted from chasing pleasure to escaping pain—a critical turning point that marks the transition from voluntary use to compulsion.

Regarding the Preoccupation and Anticipation stage, its core feature is dysfunction in the prefrontal cortex and its associated circuits. This stage is primarily associated with significant impairment in executive function, including reduced impulse control, self-regulation, and decision-making abilities. Due to abnormal regulation of dopamine and glutamate signaling in the prefrontal cortex, addicts struggle to resist impulses when exposed to drug-related cues. Additionally, prolonged drug use has led to significant neuroplastic changes in the brain. These changes are concentrated at the molecular level, such as the accumulation of deltaFosB and brain-derived neurotrophic factor (BDNF). These molecular-level changes not only reinforce compulsive drug-taking behavior but also significantly increase the risk of relapse (Kalivas & O’Brien, 2008). Research has shown that short-term withdrawal (e.g., 12 hours) significantly increases an individual’s reactivity to cues, accompanied by enhanced activation of the medial prefrontal cortex (mPFC) and orbitofrontal cortex (OFC). This change is associated with intense craving and withdrawal symptoms (Goldstein & Volkow, 2011; Volkow, Koob & McLellan, 2022). The effects of long-term abstinence on prefrontal cortex activity highlight the complexity of neuroadaptive changes in addiction. While some studies suggest reduced activity in certain prefrontal regions during prolonged abstinence, possibly due to adaptive behavioral strategies, the overarching pattern remains one of significant dysfunction. Such complexity underscores the difficulty addicts face in resisting drug-related cues, reinforcing the importance of understanding impaired cortical function in the chronic relapse cycle of addiction. Due to impaired executive function in the prefrontal cortex, addicts often struggle with decision-making to inhibit drug use, leading to a vicious cycle of repeated drug use. This significant functional impairment of the prefrontal cortex, including imbalances in neurochemical signaling and persistent molecular-level adaptive changes, constitutes the core pathological manifestation of addiction as a chronic brain disease. A key example of such a change is the accumulation of the protein deltaFosB, which acts as a long-lasting molecular switch that structurally rewires neural circuits to reinforce compulsive drug-seeking (Nestler et al., 2001). It directly undermines an individual’s ability to engage in rational assessment, inhibit inappropriate impulses, and maintain long-term goals, rendering self-control exceptionally challenging at the physiological level, thereby contributing to the chronic nature of the disease and its high relapse rate. At this point, the brain’s accelerator (the craving system) is stuck on full throttle, while the brakes (executive function) have failed, trapping the individual in a cycle of relapse that is physiologically difficult to escape.

The profound impact of environmental and social factors on the neurobiologically vulnerable individual—as underscored by the disease model of addiction—is vividly illustrated by the case of Vietnam War veterans. Vietnam War veterans experienced widespread heroin addiction due to the high levels of stress and availability of drugs in the war environment. However, after returning home, many were able to quit relatively successfully due to the disappearance of the war environment and related cues (Leshner, 1997). This case powerfully demonstrates the significant influence of social and environmental factors on addiction, highlighting the need for holistic treatment strategies that address not only neurobiology but also the psychological context in which addiction occurs.

While the end of the war created a positive environmental shift for many, more recently, the COVID-19 pandemic provided a stark counterexample of how social upheaval can catastrophically worsen the addiction crisis. In the wake of the pandemic, U.S. drug overdose deaths surged dramatically, increasing by over 30% in 2020 and surpassing 106,000 in 2021, with opioid-related fatalities showing the most significant rise (Tanz et al., 2022; Spencer et al., 2022). This trend was starkly illustrated at the state level; in New York, a recent report by the New York State Office of the State Comptroller (OSC) found that the increase in opioid overdose deaths in New York between 2019 and 2021 was approximately 68% (OSC, 2022). A perfect storm of factors drove this crisis. On one hand, the pandemic created a widespread mental health crisis, increasing feelings of anxiety, loneliness, and despair, which fueled the demand for substances. On the other hand, lockdowns and social distancing measures severely disrupted access to treatment and recovery support services, leaving vulnerable individuals isolated (Hulsey et al., 2020). This was compounded by an increasingly toxic illicit drug supply, where lethal synthetic opioids like fentanyl became more prevalent (Melamed et al., 2022). This modern-day example powerfully underscores the complex interplay between the neurobiological disease of addiction and large-scale environmental stressors. These cases powerfully illustrate a central tenet of the modern disease model: the neurobiological vulnerabilities established by the disease process are dramatically amplified or mitigated by the external environment. A purely neurobiological focus, therefore, is insufficient. A truly comprehensive strategy must be bimodal, simultaneously targeting the internal pathophysiology of the brain and the external social context of the individual.

Viewing addiction as a disease shapes healthcare policies, treatment approaches, and social attitudes, directly influencing societal outcomes. This disease-oriented perspective provides a clear scientific basis for developing effective treatment protocols, reducing stigma towards individuals with addiction, and guiding evidence-based policy-making. For instance, it supports legislative changes such as improved insurance coverage for addiction treatment and shifts from punitive measures toward rehabilitation. Economically, addiction imposes significant burdens on society; the annual social cost of tobacco, alcohol, and illicit drug abuse in the United States reaches approximately $700 billion (Volkow et al., 2022). This figure is projected to rise due to the ongoing opioid crisis, with opioid-related disorders and overdoses alone accounting for around $1.5 trillion in losses in 2020, including healthcare expenditures, lost productivity, and criminal justice expenses (Lines, 2024). Additionally, over 25% of arrests in the United States involve drug-related offenses (Lines, 2024). Addressing addiction comprehensively as a public health issue, then, is both economically and socially essential.

From a policy and legislative perspective, treating addiction as a disease has driven changes in healthcare and insurance systems. For example, the Mental Health and Substance Abuse Equity Act (MHPAEA) requires that substance abuse treatment be covered under the same insurance as general healthcare services. The implementation of this law has significantly improved patients’ access to treatment. Although there has been a slight increase in spending on substance abuse treatment per insured person, the impact on overall healthcare costs has been relatively small, demonstrating the economic viability and social value of insurance policies with equality at their core (Busch et al., 2014). Moreover, treating addiction is less costly and more effective than incarcerating addicts. Leaders in the police and justice sectors are increasingly recognizing that sending addicts to prison only perpetuates social problems, while directing resources to treatment and rehabilitation services can improve public safety (Williams, 2015). Despite its existence, enforcement has been challenging, leading to persistent coverage disparities. Federal agencies issued final rules in September 2024 to strengthen enforcement (U.S. Department of Labor, EBSA, 2024), but these new rules were immediately challenged by industry lawsuits, ultimately leading the agencies to suspend enforcement in May 2025 pending review (APASI, 2025). This policy uncertainty highlights the ongoing challenges of translating scientific consensus into stable and effective societal responses. Nevertheless, the view of addiction as a disease remains the fundamental driver for promoting fairer insurance coverage and shifting from punitive to rehabilitative criminal justice reforms.

Moreover, considering addiction as a disease may also reduce social stigma, so that more addicts can actively seek help rather than refusing treatment out of shame or fear. Currently, more than 70% of alcohol-dependent people have never sought professional help, and views of addiction as a moral failure or a weakness of the will undoubtedly exacerbate this phenomenon. In contrast, defining addiction as a disease can lead society to invest more resources in treatment, rehabilitation, and prevention services, rather than simply punitive policies. For example, the Patient Protection and Affordable Care Act (ACA) has promoted the inclusion of substance abuse services in basic health benefits, which has greatly improved the accessibility of addiction treatment, further illustrating the important guiding significance of the disease definition for public policy.

Viewing addiction as a disease provides the essential foundation for critical policy and social reforms. Such a perspective underscores the value of evidence-based treatment strategies over punitive approaches, which not only reduces stigma and encourages more individuals to seek necessary care but also promotes public safety by breaking the cycle of addiction-related crime. Ultimately, addressing addiction as a chronic disease rather than a moral failing allows for a more compassionate, effective, and economically sustainable societal response.

In summary, neurobiological evidence clearly indicates that addiction is a brain disease rather than a simple lack of willpower. Addictive substances create lasting changes in brain circuits, disrupting neurotransmitter regulation (e.g., dopamine) and impairing critical functions controlled by areas such as the prefrontal cortex. These persistent physiological alterations undermine self-control, rational decision-making, and the proper assessment of natural versus drug-induced rewards. However, this biological model is not deterministic; as the experiences of Vietnam veterans demonstrate, environmental context and social support are powerful modulators of these neurobiological vulnerabilities. The cyclical and relapsing nature of addiction underscores its chronicity and complexity. Just like other chronic diseases, a short-term cure is a relatively rare outcome; instead, relapses are more common. Recognizing addiction as a disease, one that involves a complex interplay of biology and environment, thus fosters deeper understanding and enables society to respond with greater empathy and effectiveness.

References:

APA Services Inc (APASI). (2025). Challenges to mental health parity law leave uncertainty for mental health and substance use disorder care.

APA Services (2025). https://www.apaservices.org/advocacy/news/challenges-mental-health-parity-law

Bechara, A. (2005). Decision making, impulse control and loss of willpower to resist drugs: A neurocognitive perspective. Nature Neuroscience, 8(11), 1458–1463. https://doi.org/10.1038/nn1584

Busch, S. H., Epstein, A. J., Harhay, M. O., Fiellin, D. A., Un, H., Leader, D., Jr., & Barry, C. L. (2014). The effects of federal parity on substance use disorder treatment. The American Journal of Managed Care, 20(1), 76–82.

Di Chiara, G. (2002). Nucleus accumbens shell and core dopamine: Differential role in behavior and addiction. Behavioural Brain Research, 137(1–2), 75–114. https://doi.org/10.1016/s0166-4328(02)00286-3

Goldstein, R. Z., & Volkow, N. D. (2011). Dysfunction of the prefrontal cortex in addiction: Neuroimaging findings and clinical implications. Nature Reviews Neuroscience, 12(11), 652–669. https://doi.org/10.1038/nrn3119

Hulsey, J., Mellis, A., & Kelly, B. (2020, September). COVID-19 pandemic impact on patients, families and individuals in recovery from substance use disorders. Addiction Policy Forum.

Kalivas, P. W. (2009). The glutamate homeostasis hypothesis of addiction. Nature Reviews Neuroscience, 10(8), 561–572. https://doi.org/10.1038/nrn2515

Kalivas, P. W., & O’Brien, C. (2008). Drug addiction as a pathology of staged neuroplasticity. Neuropsychopharmacology, 33(1), 166–180. https://doi.org/10.1038/sj.npp.1301564

Kelly, C., Zuo, X.-N., Gotimer, K., Cox, C. L., Lynch, L., Brock, D., Imperati, D., Garavan, H., Rotrosen, J., Castellanos, F. X., & Milham, M. P. (2011). Reduced interhemispheric resting state functional connectivity in cocaine addiction. Biological Psychiatry, 69(7), 684–692. https://doi.org/10.1016/j.biopsych.2010.11.022

Koob, G. F., & Le Moal, M. (2008). Addiction and the brain antireward system. Annual Review of Psychology, 59(1), 29–53. https://doi.org/10.1146/annurev.psych.59.103006.093548

Koob, G. F., & Volkow, N. D. (2016). Neurobiology of addiction: A neurocircuitry analysis. The Lancet Psychiatry, 3(8), 760–773. https://doi.org/10.1016/s2215-0366(16)00104-8

Leshner, A. I. (1997). Addiction is a brain disease, and it matters. Science, 278(5335), 45–47. https://doi.org/10.1126/science.278.5335.45

Lewis, M. (2017). Addiction and the brain: Development, not disease. Neuroethics, 10(1), 7–18. https://doi.org/10.1007/s12152-016-9293-4

Lines, L. (2024). Economic impact of addiction. EBSCO Information Services, Inc. https://www.ebsco.com/research-starters/economics/economic-impact-addiction

Lynch, F. L., Peterson, E. L., Lu, C. Y., Hu, Y., Rossom, R. C., Waitzfelder, B. E., Owen-Smith, A. A., Hubley, S., Prabhakar, D., Williams, L. K., Beck, A., Simon, G. E., & Ahmedani, B. K. (2020). Substance use disorders and risk of suicide in a general US population: A case control study. Addiction Science & Clinical Practice, 15(1), 14. https://doi.org/10.1186/s13722-020-0181-1

Melamed, O. C., deRuiter, W. K., Buckley, L., & Selby, P. (2022). Coronavirus disease 2019 and the impact on substance use disorder treatments. The Psychiatric Clinics of North America, 45(1), 95–107. https://doi.org/10.1016/j.psc.2021.11.006

Mennis, J., Stahler, G. J., & Mason, M. J. (2016). Risky substance use environments and addiction: A new frontier for environmental justice research. International Journal of Environmental Research and Public Health, 13(6), 607. https://doi.org/10.3390/ijerph13060607

National Cancer Institute. (2011). Disease. https://www.cancer.gov/publications/dictionaries/cancer-terms/def/disease

National Institute on Drug Abuse. (2018). Understanding drug use and addiction DrugFacts. https://nida.nih.gov/publications/drugfacts/understanding-drug-use-addiction Nestler, E. J., Barrot, M., & Self, D. W. (2001). ΔFosB: A sustained molecular switch for addiction. Proceedings of the National Academy of Sciences of the United States of America, 98(20), 11042–11046. https://doi.org/10.1073/pnas.191352698

Nature. (2014). Animal Farm. 506(7486), 5–5. https://doi.org/10.1038/506005a

New York State Office of the State Comptroller (OSC). (2022). Continuing crisis: Drug overdose deaths in New York. https://www.osc.ny.gov/reports/continuing-crisis-drug-overdose-deaths-new-york

Spencer, M. R., Miniño, A. M., & Warner, M. (2022). Drug overdose deaths in the United States, 2001–2021 (NCHS Data Brief No. 457).

Substance Abuse and Mental Health Services Administration. (2014). Leading change 2.0: Advancing the health of the nation 2015–2018.

Sugue, M. (2024). Current addiction statistics: 2024 data on substance abuse & trends. Addiction Group. https://www.addictiongroup.org/resources/addiction-statistics/

Tanz, L. J., Dinwiddie, A. T., Snodgrass, S., O’Donnell, J., Mattson, C. L., & Davis, N. L. (2022). A qualitative assessment of circumstances surrounding drug overdose deaths during the early stages of the COVID-19 pandemic(SUDORS Data Brief No. 2).

Volkow, N. D., Koob, G. F., & McLellan, A. T. (2022). Neurobiologic advances from the brain disease model of addiction. In Evaluating the brain disease model of addiction (pp. 25–34).

Routledge. U.S. Department of Labor, Employee Benefits Security Administration (EBSA). (2024). Statement regarding enforcement of the final rule on requirements related to MHPAEA. https://www.dol.gov/agencies/ebsa/laws-and-regulations/laws/mental-health-parity/statement-r egarding-enforcement-of-the-final-rule-on-requirements-related-to-mhpaea#t1

Williams, T. (2015). Police leaders join call to cut prison rosters. The New York Times. https://www.nytimes.com/2015/10/21/us/police-leaders-join-call-to-cut-prison-rosters.html