People with serious mental illness (SMI) are over-represented throughout the US criminal justice system. To address this issue, forensic assertive community treatment has recently emerged as a best-practice intervention. Also known as forensic ACT, ForACT, or most commonly as “FACT,” forensic assertive community treatment is an adaptation of the assertive community treatment (ACT) model. Unlike ACT, however, FACT is purposefully designed to prevent arrest and incarceration among people with SMI who have histories of involvement with the criminal justice system (i.e., “justice-involved” individuals). Although FACT was recognized as a best practice by the Substance Abuse and Mental Health Services Administration (SAMHSA) in 2019, FACT teams vary widely in their structure and daily operations. This lack of a standard FACT model continues to impede FACT program implementation and outcomes research. This article begins with a review of FACT origins, followed by a discussion of what we know (and do not know) about FACT operation and effectiveness. Based on the authors’ experience, the article then discusses key components of FACT and concludes with a discussion of current challenges and research recommendations for FACT model development.

Increasing numbers of Americans are affected by serious mental illness and severe substance use disorders. While funding has increased for the treatment of these conditions in recent years, increases in service needs have outstripped resources. Further, too often those living with these conditions are incarcerated, held for inordinate periods without treatment in emergency departments, and/or relegated to the streets as part of the burgeoning numbers of homeless in the United States. These conditions require innovative approaches to care that should include integrated medical care and community resources to decrease isolation and to improve the response to crises as they occur. There are numerous opportunities already in place that, used appropriately, can improve outcomes for some of our most vulnerable people and will improve community living for all. This perspective describes available resources that can better address the mental health and substance use crisis facing the American people.

Cannabis has a long history as a medicine and was a part of medical practice until the late 19th century. The discovery of cannabidiol (CBD) and ∆9-tetrahydrocannabinol (THC) in the mid-20th century, and then the various components of the endocannabinoid system (ECS) over the following decades has again brought cannabis back into the public eye as a potential therapeutic agent. At present, cannabis is being used in the community across the world for both recreational and medical purposes. In the case of medical usage, it may be prescribed by a medical doctor or purchased either legally or illicitly for medical purposes such as symptom relief. Evidence for cannabis as a medicine is still an emerging field, and while potential mechanisms of action for a variety of conditions have been elucidated, including cancer, epilepsy, and chronic pain, high-quality randomized controlled trials in humans are still lacking. Despite popular beliefs, cannabis, like all other medicines, has potential benefits and harms, and long-term consumption of cannabis, even for medical reasons, may not be risk-free. In addition, consumption via modes of administration such as smoking or using a bong may increase the risk of negative health outcomes.

Anxiety disorders, characterized by excessive fear and behavioral disturbances, are among the most prevalent psychiatric conditions, yet treatment options remain suboptimal for many patients. Clonidine, an alpha-2 adrenergic receptor agonist, has shown potential anxiolytic effects and may address treatment-resistant cases. This review explores the efficacy, safety, and mechanism of clonidine as a pharmacological option for anxiety disorders, with emphasis on its role in modulating noradrenergic dysfunction and its potential synergistic effects with existing therapies. A literature review was conducted to evaluate clinical studies, case reports, and comparative trials on clonidine’s use in anxiety disorders, focusing on its pharmacological profile, efficacy, and tolerability. Evidence suggests clonidine may reduce anxiety symptoms, particularly in treatment-resistant cases and specific populations, such as pediatric patients and those with comorbid psychiatric disorders. Its mechanism involves modulating norepinephrine release and glutamatergic pathways. Case studies and small trials highlight its potential in reducing cognitive symptoms of anxiety, but inconsistencies in efficacy and side effects, including sedation and hypotension, were noted. Comparative studies suggest clonidine may have similar efficacy to SSRIs in some cases but lack large-scale validation. Clonidine presents as a promising pharmacotherapeutic option for anxiety disorders, particularly in cases resistant to conventional treatments or in patients with contraindications to other typical medications. Its mechanism of action, tolerability, and potential synergistic effects with existing therapies underscore the need for continued exploration and clinical trials to establish its optimal role in anxiety disorder management.

Parkinson’s disease (PD) is a severe neurodegenerative disorder characterized by prominent motor and non-motor (e.g., cognitive) abnormalities. Notwithstanding Food and Drug Administration (FDA)-approved treatments (e.g., L-dopa), most persons with PD do not adequately benefit from the FDA-approved treatments and treatment emergent adverse events are often reasons for discontinuation. To date, no current therapy for PD is disease modifying or curative. Glucagon-like peptide-1 receptor agonists (GLP-1RAs) are central nervous system (CNS) penetrant and have shown to be neuroprotective against oxidative stress, neuroinflammation, and insulin resistance, as well as promoting neuroplasticity. Preclinical evidence suggests that GLP-1RAs also attenuate the accumulation of α-synuclein. The cellular and molecular effects of GLP-1RAs provide a basis to hypothesize putative therapeutic benefit in individuals with PD. Extant preclinical and clinical trial evidence in PD provide preliminary evidence of clinically meaningful benefit in the cardinal features of PD. Herein, we synthesize extant preclinical and early-phase clinical evidence, suggesting that GLP-1RAs may be beneficial as a treatment and/or illness progression modification therapeutic in PD.

Suicide accounts for over 700,000 deaths per year globally and remains a public health priority. Evidence suggests that sleep-related interventions may be effective in reducing depressive symptom severity and suicidal thoughts in patients diagnosed with depression and comorbid insomnia. This study aims to systematically review the efficacy of sedative-hypnotics and/or cognitive behavioral therapy for insomnia (CBT-I) on measures of suicidality.

In accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, PubMed, Medline, Cochrane Library, Embase, Scopus, and Web of Science were searched from inception to July 30, 2024. Studies were included if they (1) were randomized controlled trials (RCTs) and (2) reported on suicide-related measures associated with sleep interventions as a primary outcome, secondary outcome, or a safety measure. We endeavored to define and operationalize suicidality as suicidal ideation (SI), suicide attempts (SA), and suicide completion (SC). In cases where study authors failed to separate these three dimensions, the term “suicidality” was applied.

Eighteen studies were identified meeting inclusion criteria, comprised of studies investigating benzodiazepines (n = 2), Z-drugs (n=4), orexin receptor antagonists (ORAs) (n=8), and CBT-I (n=4). Zolpidem reduces SI as well as insomnia (linear association = 0.12, p<0.05) as evidenced by improvement on both the Columbia-Suicide Severity Rating Scale (C-SSRS) and the Scale for Suicide Ideation (SSI). ORAs were not associated with either an increase or decrease in suicidality. CBT-I alleviates SI in patients with insomnia (t = −3.35, p<0.05).

Effectively treating insomnia is associated with reduced SI. Available evidence suggests that Food and Drug Administration (FDA)-approved sedative-hypnotics do not increase the risk of suicidality.

In recent times, several longitudinal studies aimed at clarifying whether cannabis use during adolescence might play a causal role in the subsequent risk of developing bipolar disorder have been published. Although their methodological heterogeneity precludes any meta-analytic approaches, evidence from these studies can be systematically evaluated using the Bradford Hill criteria. A biological gradient is supported by evidence on the dose–response relationship between exposure severity and outcome. As such, the effect of cannabis use on bipolar disorder onset is likely to be strong, coherent, plausible, and based on a clear temporality. In addition, some analogies can be hypothesized between studies testing the possible causal role of cannabis in the development of bipolar disorder and those is schizophrenia. Cannabis may represent a precipitating agent inducing bipolar disorder in a multicausal model of individual vulnerability. However, this relationship seems to be only partially consistent and nonspecific, and the experimental evidence is strongly suggestive but, as yet, inconclusive. Nevertheless, in summary, it seems there is sufficient support for the hypothesis that cannabis use during adolescence may play a causal role in bipolar disorder, although further studies are needed to consolidate the evidence.

Ketamine, originally synthesized in 1962, has gained increasing attention due to its rapid and sustained antidepressant effects in treatment-resistant depression (TRD). Unlike traditional antidepressants, ketamine acts on multiple neurotransmitter systems, including NMDA receptor antagonism and AMPA receptor potentiation, offering a novel mechanism for mood regulation. Beyond psychiatry, ketamine remains a valuable anesthetic and analgesic agent with applications in acute and chronic pain management. Its anti-inflammatory, neuroprotective, and potential antitumor properties further underscore its versatility in clinical medicine. Despite its therapeutic promise, ketamine poses challenges due to its dissociative and hallucinogenic effects, contributing to widespread recreational use. Chronic misuse is associated with adverse health outcomes, including bladder dysfunction and hepatobiliary complications. As a result, ketamine has been subject to increasing regulatory scrutiny, balancing its medical utility with concerns about abuse potential. The rediscovery of ketamine’s antidepressant effects in the early 2000s has revolutionized psychiatric treatment, particularly in TRD and suicidality. Recent studies have also explored its efficacy in bipolar depression, posttraumatic stress disorder, obsessive-compulsive disorder, and substance use disorders, expanding its therapeutic applications. Additionally, ongoing research aims to elucidate its long-term effects and optimize dosing regimens to maximize clinical benefits while minimizing risks. This review highlights ketamine’s multifaceted pharmacological properties, its evolution from an anesthetic to a novel psychiatric treatment, and its broader medical applications. As research advances, a comprehensive understanding of ketamine’s mechanisms and clinical implications will be crucial for optimizing its therapeutic potential while mitigating its risks.

Stimulants that act on the central nervous system have been used since antiquity for ritual and other uses. Organic chemistry techniques, especially those developed in Germany in the late 1800s, resulted in the isolation and structural determination of several important stimulants. Synthetic pathways for amphetamine and related stimulants were developed in the first half of the 19th century, and these new drugs were widely marketed. Awareness of abuse potential emerged soon after but was contested. Stimulants have been used to counteract fatigue and promote wakefulness during military operations, as well as to treat sleep disorders, since the 1930s. Methylphenidate was approved to treat children with behavioral problems in 1962, predating the recognition of attention deficit hyperactivity disorder (ADHD). Stimulant abuse became a political concern in the post-war period, initially with the use of “pep-pills” by long-haul truck drivers and later as drug dealing became common in night clubs, with new laws limiting availability passed in the early 1960s. They have also been used to increase athletic and cognitive performance. Stimulants are still first-line therapies for ADHD and some sleep disorders; however, newer-generation drugs have been developed with better safety profiles and lower abuse potential. Illicit stimulant use continues to be common in many countries.