In the midst of a nationwide opioid epidemic, there is a population that is largely being ignored. According to a large cohort study, only a small percentage of teens receive proper aftercare following near-fatal overdoses. 

 examined data from more than 4 million Medicaid enrollees (N = 4,039,216) and found that only 1 in 54 youths aged 13 to 22 years received evidence-based pharmacotherapy after an overdose. Unfortunately, it appears that proper care in this patient population is given in very few cases (

 invited lead author Rachel H. Alinsky, MD, MPH, to share insights from the study. Alinsky is an adolescent medicine and addiction medicine fellow at 

Johns Hopkins University School of Medicine

: Your research highlights the need for quality treatment, especially for younger patients. What insights can you provide about interventions and obstacles to treatment?

We need to find effective interventions that can link adolescents and young adults directly into treatment after an opioid overdose. We also need to evaluate the barriers to accessing care at the time of overdose (such as insurance restrictions, lack of community providers or treatment centers, and stigma), and find strategies to mitigate these barriers. System-level changes are necessary, such as targeting federal funding for research and treatment for youth, decreasing insurance barriers, and increasing the availability of youth-serving physicians and addiction treatment centers.

 In the study, you and your colleagues noted, “Nonfatal opioid overdose may be a critical touch point when youths who have never received a diagnosis of opioid use disorder can be engaged in treatment.” Is that because these youths have hit rock bottom?

In the addiction treatment field, we do not abide by that old adage—that people have to hit rock bottom before they are ready to get treatment. That is somewhat of a myth. What we are trying to emphasize in our article is that overdose is a particularly crucial time when we can draw someone into treatment because they are presenting into the medical setting, seeing doctors, and we have this opportunity to interact with them and offer them treatment. Coming into the emergency department with an overdose may be the only time this person is sitting face-to-face with a doctor, and we want to capitalize on this opportunity to offer the best care we can to the patient.

Of course, that does not mean they did not want treatment a month ago or a week ago—they very well might have wanted treatment but did not know how to access it in our very difficult-to-navigate addiction treatment system. So when the patient is physically with us after an overdose, we have the chance to help them gain access to lifesaving treatment.

PT: What are the key takeaway points from the study?

Prior to this study, we knew that teens and young adults were about one-tenth as likely as adults to receive treatment for opioid use disorder in general.

 And while we knew that more than 4000 adolescents and young adults between the ages of 15 and 24 die from an 

 very little was known about health care use following nonfatal opioid overdose in youth. We were interested in figuring out the extent to which adolescents and young adults are receiving evidence-based treatment after a nonfatal opioid overdose.

We found that fewer than 1 in 50 adolescents and young adults who had an opioid overdose received the standard-of-care medication treatment that is recommended by the American Academy of Pediatrics.

 We also found that youths with opioid overdose have a 

; more than 8% of youths with heroin overdose experience another overdose within 3 months.

When an adolescent or young adult goes to the hospital with an emergency, you expect them to get the treatment they need. But here we see that less than 2% are getting that treatment, which would not be acceptable for any other medical condition. In pediatrics, it would be unacceptable if only 1 in 50 youths with asthma [received] the standard treatment when they came into the emergency department, or if 1 in 50 youths with diabetes [received] the standard treatment when they were hospitalized with diabetic ketoacidosis. Pediatricians would not find that treatment gap acceptable. Yet this is where we are now with the treatment for youths who have an opioid overdose—and we need to do better for them.

Additionally, with such high rates of recurrent overdose, it is even more important to get these youths into effective treatment as soon as possible, so we can try to prevent another overdose.

Finally, prescribing practices should be closely monitored in young people; they are a critically neglected patient population when it comes to addiction monitoring. As verified in an earlier study of 2,752,612 adolescents: “Safe opioid prescribing practices are critical to mitigate the risk of prescription opioid overdose in adolescents and young adults.”

PT: What are the key issues in recognizing opioid use disorder in youth?

The diagnosis of opioid use disorder is straightforward and is based on how many criteria an individual meets from a set of 11 criteria defined in DSM-5. In the case of youths who are presenting with opioid overdose, there is a chance that clinicians may view this as a standalone incident, and not recognize it as a manifestation of an adolescent’s underlying opioid use disorder. Thus, clinicians should be thinking about, and evaluating for, opioid use disorder in any youths that present with an overdose. Clinicians should probe for issues such as taking the opioid in larger amounts than intended, unsuccessful efforts to cut down use, cravings, recurrent use despite failure to fulfill obligations at school or home, or recurrent use in physically hazardous situations.

In terms of treatment, psychiatrists and other providers should offer medication for opioid use disorder as first-line treatment, consistent with recommendations from the 

. These medications include buprenorphine, methadone, and naltrexone. Pharmacological interventions can be combined with behavioral health services such as therapy or counseling. The provider will need to determine the level of care that will best support the patient in their current stage of treatment—inpatient hospitalization, residential treatment, intensive outpatient, or outpatient treatment.

We know that medication is effective and lifesaving for opioid use disorder; large studies in adults have found that medication cuts the risk of death in half.6,7 We also know that youths who are on medication stay in treatment longer.8 Because so few youths actually ever receive this effective addiction treatment, an overdose can be an ideal opportunity to link someone into care who has not been able to access it previously.

How can clinicians advise their patients and families on finding the most appropriate care?

Patients and their parents can advocate for treatment by asking their doctors about treatment when they are in the emergency department with an overdose. Some emergency departments have programs where patients can immediately start on medication treatment; the programs can then link them to a provider in the community. These programs have been shown to be extremely effective, with much higher rates of individuals entering and staying in treatment than if someone is simply handed a phone number to call to set up treatment.9 If that sort of linkage is not available, families should ask to be referred so their teen or young adult can receive treatment in their community as soon as possible.

Clinicians or patients and families who want to find available treatment resources within their community can use the treatment locator provided by the Substance Abuse and Mental Health Services Administration (

). Here you can enter your zip code and find all the available addiction treatment centers, sorting by services offered. It is also possible to specifically look for buprenorphine prescribers or methadone programs from that web page.

1. Alinsky RH, Zima BT, Rodean J, et al. 

Receipt of addiction treatment after opioid overdose among Medicaid-enrolled adolescents and young adults

2. Chua KP, Brummett CM, Conti RM, Bohnert A. 

Association of opioid prescribing patterns with prescription opioid overdose in adolescents and young adults

3. Overdose death rates. National Institute on Drug Abuse. Updated March 10, 2020. Accessed November 30, 2020, 2020. 

https://www.drugabuse.gov/related-topics/trends-statistics/overdose-death-rates

4. Committee on Substance Use and Prevention. Medication-assisted treatment of adolescents with opioid use disorders. 

5. Feder KA, Krawczyk N, Saloner B. Medication-assisted treatment for adolescents in specialty treatment for opioid use disorder.

6. Larochelle MR, Bernson D, Land T, et al. Medication for opioid use disorder after nonfatal opioid overdose and association with mortality: a cohort study. 

7. Medications for Opioid Use Disorder Save Lives. The National Academies Press. Accessed November 30, 2020. 

http://www.nationalacademies.org/hmd/Reports/2019/medications-for-opioid-use-disorder-save-lives.aspx

8. Hadland SE, Bagley SM, Rodean J, et al. Receipt of timely addiction treatment and association of early medication treatment with retention in care among youths with opioid use disorder. 

9. D’Onofrio G, O’Connor PG, Pantalon MV, et al. Emergency department-initiated buprenorphine/naloxone treatment for opioid dependence: a randomized clinical trial. 

Articles

With opoid use disorder, a tiny fraction of young patients are getting treatment, which would not be acceptable for any other medical condition. 

Improving Care in Teens With Opioid Use Disorder

 in patients with schizophrenia that can adversely affect treatment response and functional outcomes.

 for significant pro-cognitive effects for antipsychotics and other pharmacologic approaches.

 Therefore, treatment of cognitive impairment in schizophrenia represents a tremendous area of unmet need.

Regarding non-pharmacological treatments, there has been significant research on the 

 on brain structure and functional performance.

 A meta-analysis found that aerobic exercise exerted a positive effect on global cognition and some cognitive domains, but not others, in patients with schizophrenia, but findings are limited by small samples, as well as variable types and intensity of exercise and study designs.

 performed a 12-week randomized controlled trial of the effects of aerobic walking on cognitive function in patients with schizophrenia, and whether the intensity of aerobic walking is associated with changes in cognition. Patients were randomized 1:1 based on age and sex to usual treatment with antipsychotics with or without aerobic walking. Inclusion criteria were aged 20 to 60 years, DSM-5 diagnosis of schizophrenia, stable antipsychotic dose for at least 1 month, Positive and Negative Syndrome Scale (PANSS) total score < 95, no history of major physical illness, and no physical disability that caused difficulty walking.

The program comprised 150 minutes/week of outdoor walking, typically divided over 3 to 5 sessions and each with a 5-minute warm-up, followed by a 5-minute cool-down. Transportation was provided to the exercise sessions if needed. Participants wore a Fitbit to monitor heart rate and exercise intensity. Research staff supervised each participant and provided guidance based on heart rate. The patients could rest if needed. Participants were stratified into high- and low-intensity groups based on the average in-session heart rate reserve. 

 was evaluated with the Brief Assessment of Cognition in Schizophrenia (BACS).

Data were analyzed using intention-to-treat and per-protocol analyses. Multivariate general linear model repeated measures were used to investigate the effects of time, group, and the time x group interaction on cognition, controlling for illness duration. The authors randomized 67 patients to treatment-as-usual (TAU, n = 34) or aerobic walking (n = 33) who completed the baseline assessment. Thirty-three patients in the TAU and 31 in the 

The mean age was 42 years; mean BMI was 27; mean PANSS total score was 79; and 42% were male. Importantly, at baseline, subjects in the aerobic walking group scored approximately 0.5 standard deviations lower on global cognition than the TAU group. The mean duration of aerobic walking was 129 minutes/week. Eleven patients achieved high-intensity walking and 22 maintained low-intensity. In the entire intent-to-treat sample, the authors found a trend for a group effect for greater improvement in verbal fluency in the aerobic walking group. They also found a significant group effect on attention and processing speed in high- versus low-intensity aerobic walking.

The authors stated that theirs was the first trial of the effects of 

 intensity on cognitive function in schizophrenia. The majority (> 90%) of patients completed the trial, with a mean of 3 days of exercise per week, suggesting that this intervention is feasible and acceptable to patients, and that supervision and transportation are associated with retention. Study limitations include the modest sample size (especially the high-intensity group) and relatively short study duration, as well as the inability for blinding to the intervention.

“Mrs M” is a 48-year-old Black woman with a history of chronic schizophrenia. During hospitalization for an episode of illness exacerbation, her antipsychotic medication was changed. Over the next 4 months, she gained approximately 50 lb. Mrs M declined to lower the dose of her antipsychotic or change medications because of her clinical improvement and worry about risk of another illness relapse. However, she was receptive to the recommendation for increased physical activity for weight loss. Mrs M started walking with a neighbor friend for about 30 minutes at a moderate pace at least 3 times per week. Over the next year, she lost 36 pounds. Although there were no clinically appreciable changes in her cognitive function, she reported “feeling better” as a result of her exercise regimen.

A supervised aerobic walking program involving moderate-intensity exercise is feasible and acceptable in patients with schizophrenia. Higher intensity aerobic exercise may have modest pro-cognitive effects in these patients.

is professor in the Department of Psychiatry and Health Behavior, Augusta University, Augusta, Georgia. He is on the Editorial Board and serves as the schizophrenia section chief for 

The author reports that he receives research support from Augusta University, the National Institute of Mental Health, the Brain and Behavior Research Foundation, and the Stanley Medical Research Institute.

1. Hoe M, Nakagami E, Green MF, Brekke JS. 

The causal relationships between neurocognition, social cognition and functional outcome over time in schizophrenia: a latent difference score approach.

Pharmacological cognitive enhancement in schizophrenia

The magic of movement; the potential of exercise to improve cognition

4. Firth J, Stubbs B, Rosenbaum S, et al. Aerobic exercise improves cognitive functioning in people with schizophrenia: a systematic review and meta-analysis. 

Effects of aerobic walking on cognitive function in patients with schizophrenia: a randomized controlled trial

Schizophrenia is associated with cognitive impairment, and treatment of cognitive dysfunction in these patients represents an area of unmet need. What is the role of exercise?

Exercise and Cognition in Schizophrenia: Is There a Link?

Counter-intuitive as it may sound, happiness is a skill, and it can be practiced like a sport or musical instrument. In this Mental Health Minute, Richard J. Davidson, PhD, discusses his latest research on well-being, published in the 

Proceedings of the National Academy of Sciences

is the founder and director of the Center for Healthy Minds at the University of Wisconsin-Madison.

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A meeting with the Dalai Lama sends a researcher on a new path. 

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is an award-winning author and speaker who has devoted his career to neuroscience and brainwave entrainment. As the founder of BrainTap® Technologies, Dr Porter has emerged as a leader in the digital health and wellness field. BrainTap’s digital tools and mind development apps using proprietary algorithms that have made tremendous advances in mastering peak performance and bettering mental, physical, and emotional health. BrainTap has been praised for helping people improve mental clarity, sleep quality, energy levels.

Check out Dr Porter’s website, YouTube Channel, or follow him @BrainTapTech on Facebook, Instagram, and Twitter. You can also download the BrainTap Pro app for Free in the AppStore or on Google Play. (There are tons of free sessions available!)

Patrick Porter, PhD, has unique insight into the mindfulness health trend and how to use it. He is sharing try-at-home mental wellness tips for people of all ages & strategies people can use to manifest mindfulness and promote wellness in the new year.

. You can also download the BrainTap Pro app for Free in the

. (There are tons of free sessions available!)

The pandemic brought mindfulness to the masses as it created a rare opportunity for us all to breathe, reflect, and focus on the most important aspects of life.

Surviving Brain Versus Thriving Brain

Leslie Citrome, MD, MPH, talks about asenapine, or SECUDADO, the first-and-only transdermal patch formulation for the treatment of adults with schizophrenia approved by the U.S. Food and Drug Administration.

Read more about the asenapine transdermal system 

. Alternatively, visit the product website 

is Clinical Professor of Psychiatry and Behavioral Sciences at New York Medical College.

The first-and-only transdermal patch for adults with schizophrenia offers a new treatment. 

The Asenapine Transdermal System

Dr Bennett is a psychologist in the Department of Psychiatry and Behavioral Sciences, Cleveland Clinic Akron General, Akron, OH.

Available evidence indicates that benzodiazepines are commonly used to treat various disorders including anxiety, insomnia, agitation, alcohol withdrawal, and seizures.

 of benzodiazepine use among older adults in the United States is approximately 8.7%

; but it has been noted that approximately 44% of the prescriptions for benzodiazepine among older adults are potentially inappropriate.

2019 American Geriatrics Society Beers Criteria

 identifies benzodiazepines as potentially inappropriate medications for use among older adults.

) Factors associated with long-term use of benzodiazepines include the following: female sex, a diagnosis of Alzheimer disease (AD), schizophrenia, bipolar disorder, depression, coronary artery disease, and asthma/chronic obstructive pulmonary disease.

 is known to be associated with poor outcomes.

 One study found that benzodiazepine use was associated with greater risk for hospitalizations, emergency department visits, outpatient visits, and higher health care costs.

 Another study found the overdose death rate increased due to benzodiazepine use from 0.58 to 3.07 per 100,000 adults between 1996 and 2013.

 Benzodiazepines use is also associated with an increased risk of falls among older adults.

 Additionally, the use of benzodiazepines is associated with a 60% to 80% increase in the risk of traffic accidents.

 The co-ingestion of benzodiazepines and alcohol is associated with a 7.7-fold increased risk for traffic accidents.

Now, there is also emerging evidence that the use of 

 may increase the risk for developing dementia among older adults.

 This review evaluates the evidence from the literature on the association between benzodiazepine use and the risk for developing dementia.

A review of the literature indicates that there is a total of 15 studies that have evaluated the association between benzodiazepine use and the development of dementia.

 Four of the 15 studies were published prior to 2010

 and 11 of the studies were published since 2010.

Although there are no randomized controlled trials (RCTs) looking at the association between benzodiazepine use and the risk for dementia, 6 prospective cohort studies,

 and 1 retrospective cohort study18 explore the relationship. Two studies had both a prospective cohort and a case control component.

 Three of the studies were conducted in France,

 and 1 each in Sweden,14 the United States,

Of the 15 studies, 8 showed a positive association between benzodiazepine use and the development of dementia.

 Of these 8 studies, 2 were prospective cohort studies,

 had a prospective cohort and a case control arm to the study.

Four studies found benzodiazepines were not associated with the development of dementia.

 The negative studies included 2 case control studies,

 and 1 study that had a prospective cohort and a case control arm.

 One study found that previously using benzodiazepines was associated with the development of dementia, but current use was not.

 The other study found that short-term use of benzodiazepines was associated with the development of dementia, but long-term use was not.

 Finally, 1 prospective cohort study found that the use of benzodiazepines had a protective effect against the development of dementia.

More than half of the studies (8 out of 15, 53%) identified in the literature search showed a positive association between benzodiazepine use and the development of dementia. It is unclear whether there is any significant difference between men and women. This is true with higher doses; when the duration of use is shorter; for current users; for shorter-acting drugs; and study design (eg, cohort studies). (see 

Despite the evident association between benzodiazepine use and the development of dementia, a causality cannot be established, as none of the identified studies were RCTs.

Three important reviews have evaluated the association between benzodiazepine use and the development of dementia.

 In the first review, the investigators evaluated 3 studies that found an increased risk of cognitive decline among those using benzodiazepine, and 2 studies that found a lower risk of cognitive decline in former or ever users of benzodiazepines, and 2 studies that found no association between the use of benzodiazepines and the development of dementia.

 In another review that evaluated 10 studies, the investigators found that 9 studies showed an increased risk of dementia among those who used of benzodiazepines.

 The investigators opined that the risk of dementia increases with cumulative doses of medication, longer treatment duration, and when long-acting agents are used. In the third review that evaluated data from 11 studies, the investigators 

 positive association between benzodiazepine use and the development of dementia from 9 studies.

 One study found a protective effect for benzodiazepine use, and 1 study found no effect for benzodiazepine use and the development of dementia.

Three recent meta-analyses evaluated the risk of developing dementia among individuals who use benzodiazepines.

, which included data from 6 studies, the investigators found the pooled adjusted risk ratios (aRRs) for the development of dementia was 1.49 for those who have used benzodiazepines, 1.55 for those who recently benzodiazepines, and 1.55 for those who have previously used benzodiazepines, when compared with never users of benzodiazepines.

 The researchers stated the risk for dementia increased by 22% for every additional 20 defined daily doses of the drug per year (aRR=1.22).

that included data from 10 studies found the odds for developing dementia was higher by 78% among users those who were using benzodiazepines when compared to those who were not (OR=1.78)

 The investigators found a higher association when the studies were from Asia (OR=2.40), and a moderate association when the studies were from North America and Europe (OR=1.49).

 that included data from 12 prospective and retrospective cohort studies and case-control studies found that benzodiazepines can be a risk factor for the development of dementia (OR=1.38).

 The investigators concluded that the current evidence lacks the power to differentiate between the risks for the development of AD versus vascular dementias (VD), the risks when using long-acting versus short-acting benzodiazepines, and the risks based on the duration and the doses of the drugs that are used.

 Carl Salzman, MD, provided a counterpoint to the question on whether benzodiazepines cause AD.

 Salzman stated that “there is little doubt that benzodiazepines like other sedative hypnotics may be associated with impaired cognition which is usually mild and dose-dependent.” He reported that the usual recommendations include only short half-life benzodiazepines at low doses and, if clinically possible, for brief periods of time. Salzman opined that future studies are needed regarding benzodiazepines’ and other medications’ possible associations with the development of late-life cognitive disorders. Until then, he advised that we must assume that the appropriate use of benzodiazepines will not lead to the development of AD. One caution with this editorial is that it cites a limited number of studies evaluating the association benzodiazepines and AD, and it is difficult to develop any definitive conclusions based on these studies.

The available evidence for the association between benzodiazepine use and the development of dementia should be evaluated based on the heterogeneity between the studies and limitations of each of these studies. These studies were conducted in different countries and had differing methodologies. In addition, many studies did not control for confounding variables including educational attainment, the presence of depression, anxiety, insomnia, and alcohol use. Also, 4 studies used the older DSM III-R criteria for the diagnosis of the dementia, causing concerns regarding the validity of the diagnosis. It is unclear whether the observed association between the use of benzodiazepines and the development of dementia is really a causal effect, or the result of unmeasured confounding variables, as none of these studies were RCTs.

 occurs when a pharmaceutical agent has been inadvertently prescribed for an early manifestation of a disease that has not yet been diagnostically detected. A prolonged lag phase between the first appearance of brain pathology associated with dementias, the development of clinical symptoms that may be risk factors for dementias including anxiety and depression, and the actual clinical diagnosis of dementia has led to investigators citing protopathic bias or “reverse causality” as the main area of controversy regarding the association between benzodiazepine use and the development of dementia.

 To prove a definitive association between benzodiazepine use and the development of dementia, the studies would have to be approximately 3 decades long given the prolonged life course of neurodegenerative disorders like dementias.

There are 3 possible mechanisms that have been postulated for the association between benzodiazepine use and the development of dementia.

 For one, benzodiazepines possibly decrease activity of β-amyloid precursor protein-cleaving enzyme 1 (BACE-1) and c-secretase activity, thus promoting β-amyloid accumulation in the brain. Secondly, astrocytes near the β-amyloid accumulation in the brain secreting γ-aminobutyric acid (GABA), thereby promoting the negative cognitive effects of benzodiazepines. Finally, benzodiazepines may reduce the cognitive reserves by lowering brain activation levels.

Available evidence indicates a positive association between the use of benzodiazepines and the development of dementia, although causality cannot be inferred from this data. Despite the lack of evidence proving causality, the association between benzodiazepine use and the 

 is a major cause for concern given the prevalence benzodiazepine use among older adults. The prescription of benzodiazepines to older adults must be carefully reviewed given the lack of data regarding their long-term efficacy and their significant adverse effects including the risk for developing dementia.

is the chairman of the department of psychiatry and behavioral sciences, Cleveland Clinic Akron General, Akron, OH.

is a psychologist in the Department of Psychiatry and Behavioral Sciences, Cleveland Clinic Akron General, Akron, OH

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript.

1. Lader M. Benzodiazepines revisited--will we ever learn? 

3. Dionne PA, Vasiliadis HM, Latimer E, Berbiche D, Preville M. Economic impact of inappropriate benzodiazepine prescribing and related drug interactions among elderly persons. 

4. By the 2019 American Geriatrics Society Beers Criteria® update expert panel. 

American Geriatrics Society 2019 updated AGS Beers Criteria® for potentially inappropriate medication use in older adults

5. Taipale H, Koponen M, Tanskanen A, et al. Long-term use of benzodiazepines and related drugs among community-dwelling individuals with and without Alzheimer disease. 

6. Bachhuber MA, Hennessy S, Cunningham CO, Starrels JL. Increasing benzodiazepine prescriptions and overdose mortality in the United States, 1996-2013. 

7. Díaz-Gutiérrez MJ, Martínez-Cengotitabengoa M, Sáez de Adana E, et al. 

Relationship between the use of benzodiazepines and falls in older adults: a systematic review

8. Dassanayake T, Michie P, Carter G, Jones A. Effects of benzodiazepines, antidepressants and opioids on driving: a systematic review and meta-analysis of epidemiological and experimental evidence. 

9. Verdoux H, Lagnaoui R, Begaud B. Is benzodiazepine use a risk factor for cognitive decline and dementia? A literature review of epidemiological studies. 

Benzodiazepines and risk of Alzheimer disease

11. Bocti C, Roy-Desruisseaux J, Hudon C, Roberge P. Benzodiazepine and dementia: a time for reflection. 

12. Fastbom J, Forsell Y, Winblad B. Benzodiazepines may have protective effects against Alzheimer disease. 

13. Lagnaoui R, Bégaud B, Moore N, et al. Benzodiazepine use and risk of dementia: a nested case-control study. 

14. Lagnaoui R, Tournier M, Moride Y, et al. 

The risk of cognitive impairment in older community-dwelling women after benzodiazepine use

15. Wu CS, Wang SC, Chang IS, Lin KM. The association between dementia and long-term use of benzodiazepine in the elderly: nested case-control study using claims data.

16. Wu CS, Ting TT, Wang SC, et al. Effect of benzodiazepine discontinuation on dementia risk.

17. Gallacher J, Elwood P, Pickering J, et al. Benzodiazepine use and risk of dementia: evidence from the Caerphilly Prospective Study (CaPS). 

18. Chen PL, Lee WJ, Sun WZ, etal. Risk of dementia in patients with insomnia and long-term use of hypnotics: a population-based retrospective cohort study. 

19. Billioti de Gage S, Bégaud B, Bazin F, et al. Benzodiazepine use and risk of dementia: prospective population based study. 

20. Billioti de Gage S, Moride Y, Ducruet T, et al. Benzodiazepine use and risk of Alzheimer disease: case-control study. 

21. Imfeld P, Bodmer M, Jick SS, Meier CR. 

Benzodiazepine use and risk of developing alzheimer disease or vascular dementia: a case-control analysis

22. Shash D, Kurth T, Bertrand M, et al. Benzodiazepine, psychotropic medication, and dementia: a population-based cohort study.

23. Gray SL, Dublin S, Yu O, et al. Benzodiazepine use and risk of incident dementia or cognitive decline: prospective population based study. 

24. Biétry FA, Pfeil AM, Reich O, et al. Benzodiazepine use and risk of developing alzheimers disease: A case-control study based on Swiss claims data. 

25. Nafti M, Sirois C, Kröger E, et al. Is benzodiazepine use associated with the risk of dementia and cognitive impairment-not dementia in older persons? The Canadian study of health and aging. A

26. Osler M, Jørgensen MB. Associations of benzodiazepines, z-drugs, and other anxiolytics with subsequent dementia in patients with affective disorders: a nationwide cohort and nested case-control study. 

27. Verdoux H, Lagnaoui R, Begaud B. Is benzodiazepine use a risk factor for cognitive decline and dementia? A literature review of epidemiological studies. 

28. Billioti de Gage S, Pariente A, Bégaud B. Is there really a link between benzodiazepine use and the risk of dementia?

29. Pariente A, de Gage SB, Moore N, Bégaud B. 

The benzodiazepine-dementia disorders link: current state of knowledge

Association between benzodiazepine use and dementia: a meta-analysis

31. Islam MM, Iqbal U, Walther B, et al. 

Benzodiazepine use and risk of dementia in the elderly population: a systematic review and meta-analysis

32. Lucchetta RC, da Mata BPM, Mastroianni PC. 

Association between development of dementia and use of benzodiazepines: a systematic review and meta-analysis.

Do benzodiazepines cause alzheimer disease?

Nearly half of the prescriptions for benzodiazepine among older adults are potentially inappropriate, so how best to do no harm?

Benzodiazepine Use and the Risk of Dementia

H. Steven Moffic, MD, discusses the APA's apology for internal and external racism. 

is an award-winning psychiatrist who has specialized in the cultural and ethical aspects of psychiatry. A prolific writer and speaker, he received the one-time designation of being a Hero of Public Psychiatry from the Assembly of the American Psychiatric Association in 2002. He has recently been leading Tikkun Olam advocacy movements on climate instability, burnout, Islamophobia, and anti-Semitism for a better world. He serves on the Editorial Board of

Apologies are a psychological process. H. Steven Moffic, MD, talks about an important apology this week. 

Let the Sunshine in: APA's Racism Apology

Medical Marijuana and Mental Health: Cannabis Use in Psychiatric Practice

Poll

As our knowledge about herbal cannabis, the endocannabinoid system, and cannabinoid pharmacology expands, should psychiatrists discuss these issues with their patients?

Discussions With Patients: Medical Marijuana

by Devon Price, PhD; New York: Atria Books, 2021.

Editor's Note: As clinicians who treat mental illness, we have undoubtedly seen individuals who are labeled “lazy.” Some of our patients who are suffering the most may be those who have labeled themselves lazy. Fortunately, for those of us who chastise ourselves for taking even a moment away from work to focus on ourselves, and for our patients who cudgel themselves too, 

. Dr Price, a social psychologist and professor at Loyola University of Chicago’s School of Continuing and Professional Studies, recently sat for an interview, conducted via Zoom, on the topic of laziness. The interview will hopefully whet the appetite to read and recommend this truly helpful book.

Q: When I heard that you had written a book about the concept of laziness, the first question that came into my mind was: have you ever been called lazy?

A. I have only ever called myself lazy. I think I have absolutely been a workaholic in the way that I think a lot of academics are trained to be. You get this idea that you need to have a full course load, you need to be doing service to the university, you need to be doing research. And you need to be a self-starter if you want to have even a prayer of a career. They kind of drill that into you even as an undergrad. I think I have always had that bug in the back of my brain telling me that I was not doing enough. Many of us feel pressure to be a self-made individual and to be very individualistic and successful. So I am someone who has not been called lazy too often, because I have been able to check off a lot of society’s little boxes that make you look like a good little worker bee.

Patients and care providers often call themselves lazy. But what are the clinical consequences and cultural meanings of this term? 

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Exercise and Cognition in Schizophrenia: Is There a Link?

Can Happiness Be Taught?

Surviving Brain Versus Thriving Brain

The Asenapine Transdermal System

Benzodiazepine Use and the Risk of Dementia

Let the Sunshine in: APA's Racism Apology

Discussions With Patients: Medical Marijuana

Laziness Does Not Exist

Can Existential Issues Really Be Divorced From Clinical Practice? From Our Readers

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Moral Duty Beyond Prescribing Medications

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