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Keypoint: First-degree relatives of individuals with TRD are 7.47 times more likely to develop TRD than individuals without a family history. Patients with a family history of treatment resistant depression (TRD) are at increased risk for antidepressant resistance and suicide mortality, relative to those without family history. These findings indicate that TRD treatment options beyond antidepressant monotherapy may be necessary for this patient population, according to results published in JAMA Psychiatry. In Major Depressive Disorder (MDD), combining or altering depression treatments earlier may be beneficial, given the clinical significance of a family history of treatment-resistant depression (TRD) for antidepressant resistance and increased suicide mortality, according to study results published Previous studies suggest that major depressive disorder (MDD) and TRD have a genetic component and may be transmitted across families. Although there is evidence that patients with TRD face increased mortality risks, relatively little is known about whether first-degree relatives are also at increased risk of mortality. The current study sought to explore the susceptibility to TRD within families and its association with treatment and mortality outcomes. Investigators conducted a cohort study using data from the Taiwan national health insurance database between January 2003 and December 2017. The investigators identified individuals with MDD (using International Classification of Diseases [ICD] codes) and defined TRD as failure to respond to 3 different antidepressants, validated via prescription records. Once the TRD cohort was determined, the investigators identified first-degree relatives (n=34,467). Additionally, the investigators created a 1:4 comparison group (n=137,868) of first-degree relatives of individuals without TRD, matched by age, sex, and kinship. Overall, 533,302 individuals were diagnosed with MDD and 21,046 had TRD. A total of 172,335 first-degree relatives (48.75% women) were included for analysis, of whom 34,467 were in the TRD relatives cohort and 137,868 were in the control cohort. On average, individuals were 22.9 (SD, 18.1) years of age at the beginning of follow-up. Relative to the control group, first-degree relatives of individuals with TRD had lower monthly incomes (P <.001), more physical comorbidities (P <.001), and a greater proportion lived outside of urban areas (P =.004). In a model adjusting for sex, birth year, comorbidities, income, urbanization, and more stringent TRD inclusion criteria, the investigators found that first-degree relatives of individuals with TRD had an increased risk of all-cause mortality (adjusted risk ratio[aRR], 1.21) and suicide mortality (aRR, 2.72). Results of the model also indicated a significantly elevated risk for developing TRD (aRR, 7.47), MDD (aRR, 3.57), bipolar disorder (aRR, 3.36), obsessive-compulsive disorder (aRR, 2.85), anxiety (aRR, 2.57), autism spectrum disorder (aRR, 2.35), attention-deficit/hyperactivity disorder (aRR, 2.22), and schizophrenia (aRR, 2.15). These mortality and psychiatric disorder risks remained robust even when excluding first-degree relatives who were themselves diagnosed with TRD. “Family history of TRD is a clinical risk factor due to its association with increased suicide mortality and resistance to antidepressant treatment; therefore, more intensive depression treatments, such as add-on pharmacotherapy or nonpharmacotherapy might be considered earlier,” the investigators concluded. A major study limitation is the strict definition of treatment-resistant depression, which may limit the generalizability of the study findings. Note: This article originally appeared on Psychiatry Advisor

Keypoint: Second-generation long-acting injectable antipsychotics reduce the risk for hospitalization among patients with first-episode psychosis and co-occurring cannabis use disorder. Clozapine, oral aripiprazole, and long-acting injectable (LAI) formulations of risperidone, aripiprazole, and paliperidone decrease the risk for hospitalization due to psychotic relapse among patients with first-episode psychosis (FEP) and comorbid cannabis use disorder (CUD). These findings from a nationwide cohort study were published in Schizophrenia Bulletin. Although cannabis use following a FEP event is associated with elevated psychotic symptom severity and more relapses, up to 50% of individuals with FEP have comorbid CUD. Yet, no nationwide studies have evaluated real-world outcomes of antipsychotic treatments among individuals with FEP and CUD. To address this knowledge gap, investigators used data from Swedish national registers to evaluate the efficacy of antipsychotics in reducing the risk for hospitalization among patients with FEP and co-occurring CUD. The primary exposure was dispensations of antipsychotic medications for FEP between 2005 and 2021 to individuals (N=1820) aged 16 to 64 years with co-occurring CUD diagnosed between 2006 and 2021. The primary study outcomes were hospitalization due to psychotic disorder, any psychiatric disorder, and/or any substance use disorder – confirmed via International Classification of Diseases, Tenth Revision (ICD-10), codes. Of the 1820 individuals included for analysis, 84.73% were boys and men, 43.57% achieved a medium level of education, and 55.55% earned income from work. On average, individuals were 26.8 (SD, 8.3) years of age. At the time of FEP, 33.9% of individuals had a diagnosis of harmful cannabis use, 32.4% had cannabis-induced psychosis, 20.6% had cannabis dependence, and 13.1% had other cannabis-related diagnoses. Most individuals were hospitalized for psychotic relapse (61%), any psychiatric diagnosis (76%), and any SUD (63%) during a mean follow-up of 6.13 years. The investigators found that the risk for hospitalization due to psychotic relapse was significantly lower among individuals who used LAI risperidone (hazard ratio [HR], 0.40), LAI aripiprazole (HR, 0.42), clozapine (HR, 0.43), LAI paliperidone (HR, 0.46), polytherapy (HR, 0.60), aripiprazole (HR, 0.61), and olanzapine (HR, 0.80). The risk for hospitalization was not decreased with LAI olanzapine, quetiapine, or risperidone. Overall, the use of any antipsychotic was associated with a 33% reduction of psychotic relapse risk (HR, 0.67), relative to non-use. When evaluating the risk for hospitalization for any psychiatric disorder, HRs were significantly lower among individuals who used LAI paliperidone (HR, 0.43), clozapine (HR, 0.44), LAI aripiprazole (HR, 0.45), LAI risperidone (HR, 0.53), polytherapy (HR, 0.69), aripiprazole (HR, 0.73), and olanzapine (HR, 0.83). Similarly, LAI olanzapine, quetiapine, and risperidone were not associated with significantly lower risk. For hospitalization due to any SUD, clozapine (HR, 0.14), LAI risperidone (HR, 0.33), LAI paliperidone (HR, 0.37), LAI aripiprazole (HR, 0.58), polytherapy (HR, 0.67), and olanzapine (HR, 0.82) were associated with decreased risk. The investigators concluded, “[T]hese findings encourage the early use of [second-generation antipsychotic] LAIs as an important secondary prevention strategy to reduce rates of hospitalization in FEP patients with comorbid CUD.” This study was limited by not having access to data about cannabis use trajectories, however, 63.6% of the study population were re-diagnosed with CUD during follow-up. Note: This article originally appeared on Psychiatry Advisor

Keypoint: OnTrackNY (OTNY) piloted its Cognitive Health Toolkit to implement cognitive health services in large systems of care. The implementation of cognitive health services in large systems of care is possible with the help of training programs, quality assurance monitoring, and improvement activities, according to new research published in Schizophrenia Bulletin. Although a wealth of research indicates a critical need for improved cognitive support services, there have been relatively few large-scale efforts that systematically address cognitive health needs in systems of care. To address this gap between research and practice, the current study aimed to evaluate and outline the necessary adaptations for effective implementation of cognitive health services in routine clinical settings within larger systems of care. Investigators evaluated the implementation of cognitive health services within the OnTrackNY (OTNY) network of clinics that deliver Coordinated Specialty Care programs in New York state. OnTrack Central coordinated with local agencies and team leaders to govern the implementation process, and a Cognitive Health Toolkit was developed to facilitate the systematic assessment and integration of cognitive health interventions. The investigators evaluated the program via quality assurance monitoring from 2019 through 2022. The primary outcomes of interest included the use of the cognitive health screening tool, rates of self-reported and/or clinician-reported cognitive health needs, and participant interest in addressing cognitive health. OnTrack Central provided 18 OTNY teams with the Cognitive Health Toolkit and these teams received training on screening participants for cognitive health needs and providing participants with relevant psychoeducation and skills training. In the first full year of implementation, the use of cognitive health screening tools was 53.9% – although these rates varied from 8.3% to 100% across the OTNY network. Among participants who were screened in 2019, 95.5% were identified via self- report and/or clinician-report, with clinicians identifying cognitive health needs (68.4%) more frequently than participants (52.4%). Of those who were referred for the service based on an identified cognitive health need, 92.2% received a standardized neurocognitive assessment battery and 78.4% initiated cognitive remediation sessions. The investigators noted that before the development and implementation of the Cognitive Health Toolkit, there was significant variability in the methods used to assess cognitive health needs across OTNY teams, and the methods used were not always evidence-based. Additionally, the investigators found that the organizational infrastructure of OTNY facilitated the implementation of a standardized approach for cognitive health services throughout the larger system. The investigators concluded, “Our experience speaks to the need for a flexible, person-centered service model and a comprehen­sive, responsive system of implementation support to en­able the start-up, evolution, and improvement of cognitive health services within large systems of care.” Note: This article originally appeared on Psychiatry Advisor

Keypoint: Established focal neuromodulation therapies are generally considered safe from a cognitive standpoint. Focal neuromodulation therapies for psychiatric and neurological conditions are not generally associated with adverse cognitive effects, according to a review published in Nature Reviews Psychology. In fact, focal direct-to-brain neuromodulation has the potential to improve aspects of cognition by treating the underlying disorder. Health care providers and researchers are increasingly using focal neuromodulation therapies – such as transcranial magnetic stimulation (TMS), deep brain stimulation (DBS), and ablative techniques – to disrupt aberrant brain networks that contribute to clinical symptoms in neurological and psychiatric disorders. However, there is still concern that these approaches may also negatively affect normative cognitive processes. To address these concerns, investigators from Sunnybrook Research Institute in Canada conducted a systematic review to assess the effects of repetitive TMS, DBS, and ablative techniques on cognition among patients with major depressive disorder (MDD), obsessive-compulsive disorder (OCD), schizophrenia, Parkinson disease (PD), essential tremor, and Alzheimer disease (AD). Most studies employing repetitive TMS target the dorsolateral prefrontal cortex with the motivation of improving executive function. This treatment approach has been granted regulatory approval for use by the United States Food and Drug Administration (FDA) for treatment-resistant MDD. The body of research about repetitive TMS indicated that this approach likely did not impair cognition among patients with MDD, treatment-resistant OCD, schizophrenia, PD, or AD. Some studies reported improvements in cognition, however, the studies had conflicting findings and differing lengths of follow-up. Deep brain stimulation is an invasive modality that involves implanting electrodes unilaterally or bilaterally into target regions or fiber tracts. The implanted electrodes are connected to a power stimulator implanted in the chest. The FDA approved this technique for the treatment of PD and essential tremor and has regulatory approval by the US FDA for the treatment of OCD. In general, no evidence indicated that DBS changed or improved cognition among patients with MDD or OCD. However, some evidence indicated verbal fluency declined among patients with PD and essential tremor. In AD there was limited evidence supporting the use of DBS to slow cognitive decline. Ablative techniques involve surgically creating focal lesions in the brain. Some examples of lesional techniques include radiofrequency ablation, Gamma Knife radiosurgery, and magnetic-resonance-guided focused ultrasound. Ablative techniques are not associated with substantial impairments to cognition among patients with MDD, OCD, PD, and essential tremor. However, the risk for post-operative cognitive decline was lower after magnetic resonance-guided focused ultrasound relative to other approaches. Review authors concluded, “Overall, clinicians and patients can be reassured that the neuromodulation therapies used to treat the psychiatric and neurological conditions discussed in this Review do not generally cause cognitive impairment.” The review authors noted that cognitive effects were often assessed as a secondary outcome which may have decreased the power for the studies to detect cognitive changes. In addition, many studies had small sample sizes, lacked a control group, and did not have long-term follow-up data to evaluate outcomes after a sufficient amount of time. Note: This article originally appeared on Psychiatry Advisor

Magnetic seizure therapy (MST) offers similar efficacy as electroconvulsive therapy (ECT) in treating bipolar mania in adults, with significantly fewer adverse effects on language abilities, new research suggests. The randomized clinical trial is the first to study the efficacy of MST for acute manic symptoms. Investigators found that most participants had good response rates with both therapies, but those in the MST group showed superior preservation of language abilities than those in the ECT group. "These findings suggest that MST is associated with a high response rate and fewer cognitive impairments in bipolar mania, and that it might be an alternative therapy for the treatment of bipolar mania," lead investigator Shan Chen, MMed, of the Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China, and colleagues wrote. The study was published online on April 29 in JAMA Network Open. First MST Trial Pharmacotherapy is regarded as first-line treatment for bipolar mania, with ECT as a second-line option for patients with inadequate response to first-line monotherapy, the authors wrote. However, the use of ECT to treat bipolar mania is limited by several adverse effects, including cognitive impairment and stigma. Previous research showed that MST is associated with symptom improvement in patients with treatment-resistant depression and schizophrenia, but its efficacy for acute bipolar mania had not been studied. The therapy uses magnetic pulses, rather than electrical currents, while patients are under general anesthesia. Magnetic pulses are not impeded by the skull and thus can be targeted over the cortical region to minimize or possibly prevent adverse cognitive effects. For the trial, 48 patients with bipolar mania received either ECT (mean age, 32 years; 60% men) or MST (mean age, 35 years; 68% men). Participants completed two or three sessions of the interventions per week for a total of eight to 10 sessions. Mania symptoms were measured with the Young Mania rating Scale (YMRS), administered before and after MST and ECT, with a reduction in the total score as the primary outcome. A response to treatment was defined as > 50% reduction in the total YMRS score from baseline. Patients' depressive symptoms were assessed using the Montgomery-Åsberg Depression Rating Scale (MADRS), and neurocognitive function was assessed using the Repeatable Battery for the Assessment of Neuropsychological Status. Age, sex, years of education, marital status, YMRS, and MADRS scores at baseline did not differ between the two groups. Language Preserved With MST At baseline, the daily chlorpromazine-equivalent doses of atypical antipsychotics were significantly higher in the MST group (P = .02). But after treatment, the daily doses were comparable between the groups (P = .86), and the increase in daily doses was significantly greater in the ECT group (P = .02). Both groups had a high response rate to treatment, with no significant differences between the two (95% with ECT vs 86% with MST; P = .67). There was also no significant difference between groups in reduction of mania symptoms or in neurocognitive function. Patients receiving ECT had worse language performance after treatment compared to baseline (P = .045), while people in the MST group had no significant changes. These findings are similar to those found in previous studies in major depressive disorder and schizophrenia, investigators noted. Patients in the MST group had shorter seizures (mean duration, 10 seconds vs 37 seconds, respectively), and neither group reported any serious adverse effects. Limitations included the lack of precise sample size estimation for a noninferiority design and a small sample size. Moreover, the researchers did not restrict the use of concomitant psychotropic medication during either intervention, and the daily chlorpromazine-equivalent doses were initially higher in the MST vs the ECT group, so the effects of medication on the outcomes cannot be excluded. More Study Needed In an accompanying editorial, Axel Nordenskjöld, MD, PhD, of the Universitetssjukhuset Örebro, Örebro, Sweden, and coauthors noted that ECT involves a "trade-off, where more intensive stimuli result in more intense seizures, stronger clinical effects, and more cognitive adverse effects." However, he added the trade-off may be necessary because stronger clinical effects are usually the goal in the treatment of severe mania. "Magnetic seizure therapy has been introduced as a more tolerable form of convulsive therapy. It has been claimed that the cognitive adverse effects may be reduced compared with standard ECT, while the clinical effects are similar," the authors wrote. "If this is true, MST may be an improvement over ECT. However, so far, there are not enough data to support the claim, and the field has been mistaken before." While these and other findings on MST suggest the therapy could be an alternative for ECT, "it is important to stress that the evidence on the effectiveness and safety profile of MST is still limited," the authors wrote. The small number of participants and the shorter seizure duration with MST are two issues that would need to be addressed in future trials, they added. "If it becomes less complicated to produce adequate seizures using MST in the future, it may come to be regarded as an alternative and equivalent form of convulsive therapy to ECT," the commentary authors wrote. "Then, we can worry less about whether the electromagnetic field is produced by electrodes or coils and put more emphasis on the quality of the seizure." This work was supported by grants from STI2030-Major Projects, the Science and Technology Commission of Shanghai Municipality, the National Natural Science Foundation of China, the Clinical Research Center at Shanghai Mental Health Center, the Shanghai Clinical Research Center for Mental Health, the Shanghai Talented Youth Program, and the Shanghai Municipal Education Commission-Gaofeng Clinical Medicine. The study authors and Nordenskjöld reported no relevant financial relationships. The other editorial coauthors' disclosures are listed on the original paper. Note: This article originally appeared on Medscape

Keypoint: Individuals with long COVID are about twice as likely to experience depression, anxiety, sleep issues, and cognitive impairment, relative to controls. Adults with long COVID are about twice as likely to experience psychiatric symptoms than their peers without long COVID, according to study results published in JAMA Network Open. However, patients with long COVID report cost-related barriers to accessing mental health care. Previous research indicates that individuals with long COVID can experience psychiatric symptoms like depression, anxiety, sleep difficulties, fatigue, cognitive difficulties, and post-traumatic stress disorder. However, it has been difficult to establish the prevalence of these conditions thus far, given how recently the condition was identified. To evaluate the prevalence of psychiatric symptoms, uptake of mental health treatment, and barriers to treatment among people experiencing long COVID, researchers analyzed data from the National Health Interview Study (NHIS) – a nationwide cross-sectional survey conducted between October 2023 and February 2024. Respondents were classified as having symptomatic long COVID if they reported a previous SARS-CoV-2 infection, had new symptoms that persisted for more than 3 months following infection, and had active symptoms at the time of the survey. The researchers used self-reported answers to survey questions to evaluate mental health treatment, cost-related barriers to care, and secondary psychiatric outcomes (ie, sleep difficulties, cognitive difficulties, fatigue), while the primary psychiatric symptoms of interest (ie, depression and anxiety) were measured using the 8-item Patient Health Questionnaire (PHQ-8). A total of 25,122 respondents were included for analysis. The median age of participants was 46 years, 50.2% were women, and 19.3% had long COVID. Individuals with long COVID were more likely to be women, non-Hispanic White, and have multiple comorbidities, but less likely to have been vaccinated. Relative to adults without long COVID, individuals experiencing long COVID were significantly more prone to: moderate to severe depression symptoms (adjusted odds ratio [aOR], 1.96; 95% CI, 1.51-2.55), anxiety symptoms (aOR, 2.21; 95% CI, 1.53-3.19), sleep difficulties (aOR, 1.95; 95% CI, 1.65-2.29), cognitive issues (aOR, 2.04; 95% CI, 1.66-2.50), and disabling fatigue (aOR, 1.85; 95% CI, 1.20-2.86). Despite the increased burden of these psychiatric symptoms, treatment uptake for mental health concerns within the previous 12 months did not significantly differ between individuals with long COVID and those without (28.2% vs 34.9%; AOR, 1.02; 95% CI, 0.66-1.57). Furthermore, individuals with long COVID who were experiencing symptoms of depression or anxiety were more likely to cite cost-related barriers to accessing mental health counseling or therapy (AOR, 2.12; 95% CI, 1.65-2.73). Sensitivity analyses reaffirmed these findings across various subgroups and measures, emphasizing the need to address mental health challenges, particularly among individuals with long COVID. The researchers concluded, “At the individual level, clinicians should be aware that people with [long COVID] are about twice as likely to report psychiatric symptoms and consider routine screening for these symptoms. At the health system level, it may be useful for health care leaders to prioritize the inclusion of affordable mental health supports when designing care pathways for [long COVID].” Study limitations include a lack of information regarding the timing or duration of participants’ psychiatric symptoms relative to COVID-19 diagnosis and an inability to determine whether psychiatric distress is a risk factor for long COVID due to the cross-sectional study design. Note: This article originally appeared on Psychiatry Advisor

CONFERENCE REPORTER There has been an increasingly crucial role of mental health in the world of sports, with more athletes and teams recognizing the importance of addressing mental health concerns. Sports and performance psychiatry is a subspecialty of psychiatry with a rapidly increasing presence and prevalence. This subspecialty focuses on the diagnosis, treatment, and prevention of mental health diagnoses in athletes, coaches, and sports teams. Up until last year, there was no formal credentialing body in the United States to certify psychiatrists practicing in this subspecialty. In 2023, the American Board of Sports & Performance Psychiatry (ABSPP) was formed by 7 board-certified psychiatrists: Brook Choulet, MD; Mark Allen, MD; Thomas Horn, DO; Ankur Desai, MD; Amanda Klass, DO; Rolando Gonzalez, MD; and Tia Konzer, DO. ABSPP’s mission is to empower and credential sports and performance psychiatrists who demonstrate excellence in the comprehensive care of athletes and performers, fostering mental well-being and optimal performance. Through the certification of board-certified sports and performance psychiatrists, ABSPP aims to enhance the mental health and well-being of athletes, performers, executives, and individuals striving for peak performance in their personal and professional lives. Five of the 7 board members held a session at the 2024 American Psychiatric Association Annual Meeting this year on Saturday, May 4th, titled “Sports Psychiatry: An Overview from the American Board of Sports & Performance Psychiatry.” This was held as a Coffee & Conversations session, where thought leaders in their respective fields present for 30 minutes. Sports psychiatry has been an increasingly popular topic and the session truly exemplified this. With over 100 individuals in attendance, the excitement in the session was palpable. There were several questions surrounding how to get involved in the field as well as interest from early career psychiatrists. David R. McDuff, MD, an advisor to the ABSPP and cochair of the Mentorship Committee, was in attendance as well. The ABSPP provided a high-level overview on the 3 pathways towards board-certification, which include an experienced sports psychiatrist pathway, a sports psychiatry diploma or certificate pathway, and a general psychiatrist board-certification pathway. During the presentation, the board of directors also provided additional information on some key aspects of sports psychiatry. Some of these key aspects include a focus on mental health treatment, performance optimization, psychological impact of injury and rehabilitation, stress management, team dynamics, and support during career transitions and retirement. Overall, sports psychiatry aims to promote mental wellness, resilience, and performance excellence in athletes, coaches, and sports organizations. It recognizes the integral relationship between mental health and athletic success, emphasizing the importance of holistic care to achieve peak performance.

PHOENIX — There is a high prevalence of emotional and physical burden associated with being a Mohs surgeon, particularly among women and younger surgeons, according to new findings. In addition, most surgeons did not feel prepared to manage or prevent these symptoms. "Our study highlights the need to implement ergonomic training and emotion-focused coping skills, as part of fellowship training and the continuing medical education curriculum, to alleviate and prevent emotional burnout," said lead author Eduardo A. Michelen-Gómez, MD, a dermatology resident at the University of Puerto Rico School of Medicine, San Juan, Puerto Rico. "This interaction also must be designed to cater to generation and sex specific needs." Michelen-Gómez presented the findings at the American College of Mohs Surgery (ACMS) 2024 Annual Meeting. Mohs is a demanding procedure that involves repetitive motion, strict attention to detail, and high practice efficiency, all of which must be balanced with the need to prioritize patient safety and well-being. "All of these factors predispose Mohs surgeons to be at an increased risk of physical and emotional stress," he said. Despite these concerns, however, the literature is limited concerning work-associated stressors among Mohs surgeons. To further explore this issue, Michelen-Gómez and colleagues conducted a survey study of ACMS members to investigate not only the prevalence of emotional and physical stressors associated with being a Mohs surgeon but also what specific actions physicians were taking to prevent and/or treat these stressors. They designed a 21-question cross-sectional electronic survey that was sent to all active ACMS members in 2023. Outcomes evaluated were gender, years of practice, concern for and prevalence of occupational musculoskeletal disorders, emotional stress and burnout, and surgeon's knowledge and training to manage these symptoms. A total of 473 Mohs surgeons responded. High Prevalence of Injury and Burnout "Almost 90% of respondents reported moderate to severe concern for occupational musculoskeletal injuries," said Michelen-Gómez. "The prevalence of these injuries was 68%, with neck injuries being the most common complaint. Of the entire cohort, 67% have adopted ergonomic practices patterns." Female surgeons had a higher prevalence of musculoskeletal injuries than men, and there was no correlation between years of practice and prevalence of these injuries. Their results also showed that 70% of respondents reported experiencing psychological and emotional stress or burnout associated with being a Mohs surgeon. The cause of emotional stress differed between men and women. "In males, the most common cause was patient care–related anxiety, while in females, it was finding an adequate work-life balance," he said. Surgeons with fewer years of experience were more likely to experience emotional stress (P = .01), and female surgeons had a higher prevalence of burnout and musculoskeletal disorders (71.0% and 71.4%, respectively) than male surgeons (67.7% and 65.2%, respectively). To prevent or manage musculoskeletal injury, respondents reported using interventions such as physical therapy, yoga/stretching/Pilates, massage therapy, cupping, and using a physical trainer. Specific actions for preventing or managing emotional stress and burnout included engaging with a therapist, working with a life coach, practicing meditation or mindfulness, journaling, relying on religion or spirituality, and exercise. However, among those who reported musculoskeletal disorders or emotional stress, only 40.56% and 46.67%, respectively, felt they had sufficient knowledge and the resources to manage them appropriately. "In addition, we found a positive correlation between the development of psychological stress and physical issues," said Michelen-Gómez. Future studies can include determining the most effective methods to address the emotional and physical stressors of practicing Mohs Surgery." Note: This article originally appeared on Medscape

Keypoint: Elevated levels of high-density lipoprotein may be protective against psychiatric disorder risk. Carbohydrate and lipid metabolism may play a role in the development of depression, anxiety, and stress-related disorders, according to study results published in JAMA Network Open. Depression, anxiety, and stress-related disorders are highly prevalent mental health issues and have been commonly associated with cardiometabolic dysfunction. However, research on the relationship between glucose or lipid biomarkers and these disorders has yielded inconsistent results and the directionality of this association remains unclear. To this aim, investigators conducted a longitudinal population-based cohort study to assess how carbohydrate, lipid, and apolipoprotein metabolism may affect the risk of developing depression, anxiety, and stress-related disorders. Investigators used data collected in Sweden between January 1, 1985, and December 31, 1996, from the Apolipoprotein-Related Mortality Risk (AMORIS) cohort. The investigators identified participants aged 16 years and older who underwent routine health screenings in an occupational setting, had no psychiatric disorders at baseline, and had at least 1 biomarker measured during the recruitment period. The primary outcomes of interest were incident cases of depression, anxiety, or stress disorders – confirmed via International Classification of Diseases codes – following enrollment in the AMORIS study. The investigators assessed 211,200 participants and matched each case with up to 10 controls based on birth year, sex, and enrollment year. On average, participants were 42.1 (SD, 12.6) years of age at first biomarker measurement and 42% of individuals were women. Over a 21-year follow-up, 16,256 people were diagnosed with depression, anxiety, or stress-related disorders, for an incidence rate of 36.4 per 10,000 person-years. The investigators found that psychiatric disorder risk was higher among those with elevated glucose (hazard ratio [HR], 1.30; 95% CI, 1.20-1.41) and triglyceride levels (HR, 1.15; 95% CI, 1.10-1.20). Conversely, elevated levels of high-density lipoprotein lowered psychiatric disorder risk (HR, 0.88; 95% CI, 0.80-0.97). These results did not differ significantly between men and women and remained robust in sensitivity analyses. These findings indicate that individuals diagnosed with depression, anxiety, or stress-related disorders exhibited elevated levels of glucose, triglycerides, and total cholesterol up to 20 years before their diagnosis. “These results add further evidence of the association between cardiometabolic health and psychiatric disorders and potentially advocate for a closer follow-up of individuals with metabolic dysregulations for prevention and early diagnosis of psychiatric disorders,” the investigators concluded. Study limitations include potential biases due to recruitment through employment-related health screenings, which may restrict the generalizability of findings beyond the study population. Note: This article originally appeared on Psychiatry Advisor

Keypoint: Long-term use of antidepressants is not associated with dementia risk. Antidepressant medication use is not associated with long-term cognitive decline, brain atrophy, or dementia risk, according to results from a prospective cohort study published in Alzheimer’s and Dementia. Although antidepressants are used widely and have become more frequently used among older adults, the long-term effects of antidepressant use on cognition and dementia remain uncertain. To address this knowledge gap, investigators analyzed data from the Rotterdam Study – an ongoing prospective population-based cohort study that began in 1990 and evaluated participants every 4 years at a dedicated research center. The investigators included participants (N=5511) who were 60 years of age and older, attended a follow-up examination at a dedicated research center between 2002 and 2008, and had no indication of cognitive impairment at baseline. All participants underwent cognitive assessments and magnetic resonance imaging (MRI), and the investigators used pharmacy records to identify antidepressant medication use between 1991 and baseline (eg, between 2002 and 2008). The primary outcomes of interest were incident dementia (diagnosed between baseline and 2018), changes in cognition, and brain atrophy. On average, participants were 70.6 (SD, 7.6) years of age and had a body mass index (BMI) of 27.7 (SD, 4.2) kg/m2. Overall, 57.5% were women, 49.7% used benzodiazepines, 16.7% of participants had used antidepressants in the 10 years before baseline, 4.1% continued to use antidepressants at baseline, and 1.6% used antipsychotic medications. Medication use at baseline was more common among women than men (20.8% vs 11.7%), among individuals with lower education, and among individuals aged 80 years and older than among those aged 45 to 50 years (5.4% vs 2.1%), respectively. Among the cohort that used antidepressants, 33% only used tricyclic antidepressants (TCAs), 36% used serotonin reuptake inhibitors, 5% used other types, and 25% used a combination of antidepressants. During a mean follow-up of 10.2 years, 11.6% of individuals developed incident dementia. The investigators found that dementia risk was not significantly associated with overall antidepressant use. However, after stratifying by type of antidepressant, dementia risk was elevated among individuals who had ever used TCAs (adjusted hazard ratio [aHR], 1.36; 95% CI, 1.01-1.83). The increased risk tended to be associated with shorter-term use (aHR, 1.43; 95% CI, 1.00-2.04) and not with longer-term use (aHR, 1.26; 95% CI, 0.78-2.02) of TCAs. The investigators did not observe a relationship between antidepressant use and cognition at baseline or with a decline in global cognitive performance over time. However, antidepressant use was associated with a slower reduction in Purdue Pegboard Test performance over time (b, 0.010; 95% CI, 0.002-0.018). Similarly, no relationships between antidepressant use and brain volume at baseline or with changes in brain volume over time were observed. Study authors concluded, “[A]ntidepressant use was not associated with long-term adverse effects on dementia risk, cognitive decline, or brain atrophy in older individuals without clear signs of cognitive impairment.” This study may have been limited by excluding individuals with Mini-Mental State Examination (MMSE) scores of less than 26 at baseline. Note: This article originally appeared on Psychiatry Advisor

KEY POINTS Mitochondria are first responders to every change in your environment and activity. Metabolic activity makes the brain especially vulnerable to oxidative damage. Because mitochondria are involved in all you think and dream and do, any malfunction can have major effects. Your brain is a metabolically fierce organ, punching way above its weight of two pounds to consume 20 to 25 percent of the body’s fuel supply. The brain’s energy-making machinery, centered in mitochondria, is powering your ability to see this page, decode the symbols, take in the information, and maybe even store some of it in memory. Given the outsize energy demands of the brain, it is intensely populated with mitochondria, likely thousands of them per neuron. The evidence is accumulating that the many ways they function, and the many possibilities for dysfunction, are the common source of all mental health disorders. Descendants of an ancient bacterium that made its way into an equally ancient single-cell organism and worked out a cooperative living agreement—an event that likely happened two billion years ago—mitochondria are essential for producing energy, although that is by no means all they do. The energy mitochondria produce not only sustains life but enables adaptation to challenges. Mitochondria respond very quickly to your needs: They’re there for your muscles when you climb a hill or ride a bike. You can’t make a decision, answer a question, or laugh at a punch line without a blast of energy in your brain. The sensitivity of mitochondria to environmental needs makes them a critical nexus for our adaptation to the ever-changing demands of the inner and outer environment. That same sensitivity also may make them especially vulnerable to assault from an array of environmental perturbations. That vulnerability is what makes mitochondrial dysfunction a prime contender as the source of psychiatric disorders. As the descendants of once-independent organisms, mitochondria retain some autonomy; for example, they have their own DNA, something that helps mitochondria respond quickly to local energy demands without having to first consult the nuclear DNA. It also allows mitochondria to multiply on their own. Unprotected by telomeres, mitochondrial DNA is especially vulnerable to damage, which can significantly affect energy production capacity. And because of the outsize importance of mitochondria to brain activity, even small changes in mitochondrial function can have big effects. Research increasingly ties mitochondria dysfunction to a wide range of mental health conditions, from developmental disorders such as autism to psychiatric ills such as depression, bipolar disorder, and schizophrenia, to neurodegenerative disorders such as Alzheimer’s and Parkinson’s diseases. Mitochondria as the Master Regulator Beyond energy production, mitochondria play an essential role in the production and regulation of neurotransmitters, including serotonin, dopamine, and that all-purpose brake on neural excitability, GABA. Mitochondria are key regulators of hormones, including cortisol, essential to the stress response, and the hormones of reproduction: estrogen, testosterone, and progesterone. Mitochondria are epigenetic forces, regulating the expression of cellular genes, turning them on and off. They appear to be the ultimate responders to adversity. Everything they do has a profound impact on cognition and all other mental processes. Many roads point to mitochondria as the hub of what goes wrong in psychiatric and neurodegenerative disorders. What Goes Wrong There are many ways the function of mitochondria can be impaired. A major one is oxidative stress. ATP, derived from the breakdown of glucose, is the molecule that mitochondria produce for power, drawing on the energy contained in its chemical bonds. In the constant production of ATP, some electrons go rogue and create free radicals of oxygen, also called reactive oxygen species, (ROS). Free radicals can damage DNA, proteins, and other important cellular components. Oxidative stress describes the condition within cells when the free radicals of oxygen released in ordinary activity outnumber the antioxidants available to neutralize them and protect against the damage they can do. Because it is so metabolically active consuming so much oxygen for its constant activity, the brain is particularly susceptible to oxidative stress. In fact, the relentless accumulation of oxidative stress in all cells is why we age. Prolonged oxidative stress erodes the efficiency and activity of mitochondria, and it can damage mitochondrial genes. Another pathway to problems is poor garbage removal. All cells engage in a process of self-maintenance and self-renewal, called autophagy, by which worn-out or damaged parts are broken down and removed, and reusable elements are upcycled into new cells. Autophagy keeps cells in working order. Mitophagy is the process of upkeep and rejuvenation of mitochondria, and, given the demands on mitochondria, meticulous housekeeping is essential to the viability and function of their host brain cells. Mitochondria are normally capable of swiftly meeting energy demands by increasing their number, a process called mitochondrial biogenesis. A change in biogenesis can also impair mitochondrial function. Mitochondrial dysfunction from any cause not only leads to a decrease in ATP levels and energy production and an increase in the generation of ROS but it can also lead to inflammation. If, because of reduced mitochondrial function, defective mitochondria are not removed by mitophagy, they can release their contents, setting off inflammatory processes. Fatigue, Worry, and More When Mitochondria Malfunction The malfunction of mitochondria leads to a lack of brain energy that affects every aspect of brain operations. It is a source of fatigue. It is a cause of all degrees of cognitive sluggishness and impairment; it undermines cognitive flexibility, by which we adapt to life’s ever-changing circumstances. It impedes the most energy-intensive of operations, executive function, affecting everything from attentional focus and decision-making to impulse control, emotion regulation, and memory. Those negative thoughts and worries that play on repeat in our head? It takes lots of mental energy to keep them from taking over. Imaging studies of the brain, such as functional magnetic resonance imaging (fMRI), are essentially studies of brain metabolism. They measure changes in cerebral blood flow to meet the demands of neural activity. The last few decades have provided overwhelming evidence that in every mental disorder, there are disturbances in cerebral blood flow that show up on imaging studies; that is, there are irregularities of brain metabolism, which is centered in mitochondria. In some cases, specific brain regions are overactive, in others some regions are underactive. In all cases, mitochondria are implicated. A Link to Insulin There is more evidence that malfunctioning mitochondria cause mental illness. Metabolic disorders such as obesity and cardiac disease are extremely common in the U.S. According to the Centers for Disease Control and Prevention, more than 40 percent of U.S. adults are obese. And more than 35 percent have anxiety, depression, or both. The incidence of mental disorders among those with metabolic disorders is two to three times greater than normal. Those with mental disorders have two to three times greater chances of developing obesity and diabetes. Both kinds of disorders share a common cause: impaired mitochondrial function. Obesity, for example, is commonly accompanied by insulin resistance. Insulin is an important regulator of metabolism as well as a signaling molecule: Insulin resistance not only influences glucose metabolism and energy production but also, for example, alters dopamine dynamics, affecting reward and motivational networks in the brain, and is linked to both anxiety and depression. The evidence is mounting that mental illness is, first and foremost, a consequence of metabolic malfunction. That same knowledge is also paving the way for a whole new approach to treating mental distress. Note: This article originally appeared on Psychology Today

May is Mental Health Awareness Month, an important opportunity to recognize the needs of those with mental health issues and the ways in which those who struggle with them, both affected individuals and loved ones, can access help. Unfortunately, the mental health-related information and advice that circulates in May is often overwhelmingly focused on short-term mental health conditions like anxiety and depression, issues that today are highly treatable and far less stigmatized than they were even a few years ago. However, there is a small subset of those experiencing mental health issues that are often overlooked, even during Mental Health Awareness Month. This includes the 10 million adults in the US living with serious mental illness, meaning a mental, behavioral or emotional disorder resulting in serious functional impairment, which substantially interferes with or limits one or more major life activities. Serious mental health diagnoses include schizophrenia, bipolar disorder, major depression, acute anxiety and related illnesses. As a mental health attorney who counsels families of loved ones with serious mental health issues, I always seek to advocate for these individuals, whose needs and realities too often go unseen and/or are misunderstood. With that in mind, and in honor of Mental Health Awareness Month, I’m sharing the following 10 often-overlooked realities of those struggling with serious mental illness. These include: They often lack insight into their condition, which can make it challenging for them to accept they have a mental illness and need treatment. This reality is a major factor in the debate regarding involuntary treatment versus personal autonomy. Among those creating and reforming policies affecting those with serious mental illness, insight must always be top of mind. They are statistically more likely to be the victims of crime than perpetrators. Such a tragic reality is well worth reiterating given the enormous spotlight on occasions in which those suffering from mental illness have been involved in incidents of violence, often provoking feelings of fear and prejudice. They are overrepresented among our nation’s homeless population and among those incarcerated. Since the large-scale closing of state-run mental health facilities, a vast number of mentally ill individuals have found themselves living on the streets or in jail, where they lack needed medication and other forms of treatment, and the stability often required to make clinical progress. But serious mental illness does not equal homelessness. They are entitled to mental health care under the federal Mental Health Parity and Addiction Equity Act, which requires insurance coverage for mental health and substance use disorder treatment to be “no more restrictive” than coverage for physical health conditions. Yet despite these laws, our healthcare system is rife with persistent bias against mental health, adding challenges to individuals and families coping with diagnoses. They are further entitled to Social Security Disability Insurance (SSDI) and Supplemental Security Income (SSI) to help cover the costs of their basic needs. To qualify, a person’s mental illness must be severe enough to prevent them from performing substantial gainful activity (SGA) for at least 12 months or result in death. They are too often left out of today’s discourse concerning mental health and mental wellness. Not just during Mental Health Awareness Month but all year long, those struggling with serious mental illness simply aren’t part of the ongoing dialogue that routinely emphasizes help like self-care. They will likely require lifelong care. While there is often hope and progress for those experiencing serious mental illness, no cure exists, meaning they and their loved ones live with diagnoses all their lives. They often have family members who urgently need respite to take care of their own needs and those of other loved ones. Our country’s dire lack of mental health treatment and supportive housing has put family members on the front lines, all but forcing them to make enormous sacrifices in order to protect the health and wellness of their loved ones. They are represented across all demographics. Like all mental health issues, serious mental health illness does not discriminate, but generally first surfaces in young people ages 18-22 across racial identities, socioeconomics, geographies, etc. They, along with their families, often require legal advocacy to best ensure someone with their best interests at heart is involved in their treatment plan. The mental health legal system is notoriously complex, frequently necessitating the involvement of attorneys with real expertise in how to navigate it. While the complexities inherent in serious mental health illnesses—and the fear often surrounding them—make the conditions incredibly challenging to discuss, silence does a tremendous disservice to those who are contending with these conditions day in and day out. This May, let’s make sure our conversations include those with these hard-to-discuss, challenging issues so that they, and their families, know they aren’t alone. Note: This article originally appeared on Psychology Today