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

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

GROUP FOR THE ADVANCEMENT OF PSYCHIATRY, COMMITTEE ON WORK & ORGANIZATIONS

Work is central to many people’s lives. The average person spends one-third of their adult life working, yet psychiatrists may neglect work when assessing a patient’s well-being. We address drug use, family life, and psychiatric symptoms, but may not fully appreciate how those factors are relevant to our patient’s work.

Nonetheless, work is tied to the surge in mental health concerns precipitated by the coronavirus disease 2019 (COVID-19) pandemic. As we consider anxiety, depression, substance use, spousal and child abuse, and loneliness, all of which have been found to increase following disasters, we must not forget how the pandemic is affecting our workforce. For instance, during this time of increased social isolation, employers have been using video technology to maintain a sense of connectedness among their employees. This very much reflects the centrality of work to mental health and social cohesion.

Psychiatrists will find it difficult to ignore the centrality of work over the coming months, as the the pandemic has led to a surge in unemployment not seen since the Great Depression. Individuals filed more than 58 million initial unemployment benefit claims between March 14 and August 22, 2020, and economists 

When a patient loses their job, a psychiatrist must respond actively and swiftly. Employment fulfills essential biological, psychological, and social needs. It is the means by which we sustain ourselves, comprises a large part of our identity and social community, and determines how we spend most of our waking hours. As such, job loss is profoundly disorienting, challenging the very meaning and purpose of life. It directly affects self-esteem and perceptions of self-worth, precipitates anxiety, and increases the chance of physical and mental illness.

 Unemployment is associated with lower motivation, and an increased risk of substance abuse and suicide.

 This is compounded by the loss of structure and shared experience that work typically confers. Thus, job loss generally leads to a loss of well-being.

When a patient loses their job, the psychiatrist has 4 tasks: (1) triage and treat imminent emergencies; (2) treat acute or latent psychiatric symptoms medically or psychotherapeutically; (3) support the patient by helping them to recognize vulnerability, identify feelings, and enhance personal support systems; and (4) prompt the patient to realistically 

Treating emergencies and psychiatric disorders, as well as discussing the effects of job loss on personal and interpersonal variables can lead to improvement. Clinicians can do this informally or psychotherapeutically. Helping the patient identify their social support systems and how to use them can be helpful. As with any episode of clinically significant depression, anxiety, or psychosis, medication may be indicated.

Returning to work is the ultimate goal for the majority of our patients. To evaluate job prospects realistically, psychiatrists should take a work history once the initial crisis and reactions have been explored. Assessing a work history is not typically taught during residency training and is often not part of a clinical interview. However, a work history provides important information about a patient’s functionality (

 questions help patients identify what they wish to do for future employment, including a change in career. Expectations, skills, and qualifications can be realistically assessed by discussing patient responses. The psychiatrist can serve as a sounding board for the patient’s ideas and help the patient cultivate adaptive perceptions, expectations, and realistic future plans.

How do psychiatrists carry out this function? Perhaps the most important principle to consider is their role in serving as a source of reality testing and as a means of integrating the self. By listening to the patient’s occupational hopes and integrating these with the current reality and the work history, the psychiatrist can explore what is possible in a career. The psychiatrist and the patient may uncover a wider range options for work than the patient would discover in isolation.

It is clear that the pandemic will continue to affect the economy, the job market, and work. It is likely that many aspects of work—such as where, how, and for whom it is conducted—will change, and many changes will persist beyond the pandemic. We may wish to recall that our society, economy, and work situations were far from perfect prior to the pandemic; perhaps the crisis can be reframed as an opportunity for our patients to seek healthier and more meaningful work situations.

Job loss is likely to affect far more people than 

 itself. Psychiatrists are uniquely positioned to sustain the unemployed individual’s sense of efficacy, identity, and purpose during these difficult times. By understanding and supporting our patients, we can help them avoid the downward spiral of helplessness and despair that can otherwise follow job loss.

Dr Morrison is an assistant clinical professor of psychiatry at Chicago Medical School in Illinois. Dr Brown is a department psychiatrist at Boston Police Department in Massachusetts. Dr Sassano-Higgins is an adjunct professor of psychiatry at the University of Southern California, and chair of the Committee on Work & Organizations for the Group for the Advancement of Psychiatry. Dr VanDercar is a forensic psychiatry fellow at the University Hospitals Cleveland Medical Center and Case Western Reserve University School of Medicine in Ohio. Dr Long is the president-elect for the Group for the Advancement of Psychiatry. Dr White is an adjunct voluntary faculty member at Northwell Health System in New York City, New York. 

1. Galea S, Merchant RM, Lurie N. The mental health consequences of COVID-19 and physical distancing: the need for prevention and early intervention. JAMA Intern Med. 2020;180(6):817-818.

2. Chiwaya N, J Wu. The coronavirus has destroyed the job market in every state. NBC News. Updated August 27, 2020. Accessed November 30, 2020. 

https://www.nbcnews.com/business/economy/unemployment-claims-state-see-how-covid-19-has-destroyed-job-n1183686

3. Jin RL, Shah CP, Svoboda TJ. The impact of unemployment on health: a review of the evidence. 

5. Lee AM, Wong JGW, McAlonan GM, et al. Stress and psychological distress among SARS survivors 1 year after the outbreak. 

6. Darity WA Jr. Employment discrimination, segregation, and health. 

7. Kawohl W, Nordt C. COVID-19, unemployment, and suicide. 

8. Stam K, Sieben I, Verbakel E, de Graaf PM. Employment status and subjective well-being: the role of the social norm to work. 

9. Committee on Psychiatry in Industry, Group for the Advancement of Psychiatry. Job loss, a psychiatric perspective. 

Unemployment is associated with an array of social and psychological complexities, directly affecting patients' self-esteem and perceptions of self-worth. When a patient loses their job, the psychiatrist has 4 tasks.

My Patient Lost Their Job…Now What? 

-from the photograph “Stark Tree, 1956,”
by Wynn Bullock

Fall arrived too early, swamp maples ablaze
in August, Summer Rose apples withered
by drought, smoke from California fires graying
Berkshire sky to winter, and two hundred thousand

of us killed by virus, our landscape as foreign
as Bullock’s silhouettes of two hills and a valley
filled with moonlit fog, one stark tree
in the foreground, tortured limbs

and spiny black branches, a vulture’s nest
woven into the highest fork, threatening sky
with a faceless full moon glowing through a cloud
contorted like the tree, mist riding wind

with its damp smell of decay, inhuman
forces hard at work in their own time and place.
-Richmond, Massachusetts, 9/22/20

 has been writing a poem about his experience of being a doctor every month for the past 23 years in 

 in a column called “Poetry of the Times.” He is instructor in psychiatry, University of Massachusetts Medical School, Worcester, MA. ❒

A faceless full moon glowing through a cloud, contorted like the tree . . .  

Two Hundred Thousand

Decades of research have investigated inflammation and mental illness, suggesting that there is a robust and complex link. However, the link lacks diagnostic specificity and varies considerably among individuals, and with each stage of illness. Chronic, low-grade 

appears to precede the initial illness episode, at least in some individuals.

 Drugs that modulate the immune system may also affect an individual’s mood and have possible psychiatric adverse effects (AEs). Perhaps the best example is that interferon-α treatment of hepatitis C precipitates depressive episodes.

 is associated with reduction in inflammatory markers.

Statins are best known as competitive inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase. Statin treatment results in lower low-density lipoprotein cholesterol levels and in benefits to cardiovascular health. Statins also have anti-inflammatory mechanisms of action, including T-cell downregulation, suppression of cytokines, production of chemokines and C-reactive protein, and downregulation of transcription factors.3 In a post hoc, pooled analysis (N = 969) of data collected at baseline and at a 1-year follow-up from a study of patients with acute coronary syndrome, statin treatment was shown to reduce levels of interleukin (IL)-6 and IL-18. Raised levels of these cytokines appeared to predict depression after acute coronary syndrome.

Many epidemiological studies have shown that 

 is associated with a lower risk for depression (

 A population cohort study (N = 4,607,990) using Swedish national registry data investigated the relationship between statin use and the development of depression. The use of any statin was associated with an 8% decrease in risk for depression (odds ratio [OR], 0.92) compared with individuals who did not use statins.

 Elsewhere, in a cohort of individuals 55 years and older (N = 2804), statin use was associated with decreased depression (OR, 0.71).

 However, no association between statin use and depression was determined in an analysis of data from 19,114 individuals, most of whom were 70 years and older, of whom 5987 used statins.

Evidence from clinical trials suggests that, adjuvant to treatment with antidepressants, some statins are associated with better treatment outcomes. A 

 showed that treatment with lovastatin, atorvastatin, and simvastatin, adjunctive to antidepressant treatment, was superior to treatment with a placebo adjunctive to antidepressant treatment for improving depression (indexed by the Hamilton Depression Rating Scale).

 More recently, the results of a trial of rosuvastatin for young individuals with depression indicated that rosuvastatin failed to beat the placebo on the primary outcome, but it was positive on a number of secondary outcome measures, leaving the benefit uncertain.

A trial comparing simvastatin (n = 33) with placebo (n = 33) in participants with schizophrenia treated with risperidone found significantly higher reduction in the first group in negative symptom scores (P = .003) and total score (P = .001). These results measured the time period from baseline to week 8, using the Positive and Negative Syndrome Scale (PANSS).

 Simvastatin did not significantly differ from placebo for treating schizophrenia in an underpowered study (N = 36).

Two meta-analyses of statin add-on therapy in the antipsychotic treatment of schizophrenia have been conducted. 

 identified 5 randomized controlled trials (N = 236) showing improvement of PANSS total score, but not of PANSS subscale scores.

 The meta-analysis included studies of atorvastatin, lovastatin, pravastatin, and simvastatin. Risperidone was used in 3 studies; antipsychotic use was varied or not reported for 2 studies. 

 identified 6 randomized controlled trials (N = 339) showing benefit for improvement of PANSS positive and negative subscales.

 The meta-analysis by Shen et al included all 5 trials from the Nomura et al meta-analysis plus an additional trial of simvastatin versus placebo.

 have been associated with an increased risk for cardiovascular disease (CVD), independent of psychotropic medication use. This comorbidity is bidirectional, since depression is a common outcome after myocardial infarction and is also associated with higher comorbidity and mortality.

 In this context, treatment with statins may have an important dual purpose, with benefits to both mental and cardiovascular health. Evidence from a nested case-control study has shown that exposure to statins and aspirin is associated with a reduced risk of de novo major depression.

Preliminary studies suggest that adjuvant treatment with a statin may be beneficial for patients who are also prescribed psychotropic drugs for depression and schizophrenia.

Psychiatric Times Vol 38, Issue 1

Improving Care in Teens With Opioid Use Disorder

Benzodiazepine Use and the Risk of Dementia

My Patient Lost Their Job…Now What?

Two Hundred Thousand

The Psychiatric Potential of Statins

A Quick Primer on the Serendipity of Psychopharmacological Development

Microglial Involvement With Psychiatric Diseases

Post-COVID Stress Disorder: Another Emerging Consequence of the Global Pandemic

The Psychiatric Pipeline: 10 Agents to Watch

New Beginnings, New Promises