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Jordan Peterson Shares How To HEAL From Emotional Trauma Great video about dealing from emotional trauma

The similarities in clinical phenotypes between PBD and ADHD may be caused by decreased gray matter volumes in the insula and anterior cingulate cortex seen in both conditions. Pediatric bipolar disorder (PBD) and attention-deficit/hyperactivity disorder (ADHD) were found to have both shared and distinct alterations in gray matter volumes (GMVs). These findings from a systematic review and meta-analysis were published in the Journal of the American Academy of Child & Adolescent Psychiatry. Among children, PBD and ADHD frequently co-occur and can affect similar cognitive and affective functions. However, both conditions also have unique, non-overlapping characteristics (eg, PBD typically affects executive functioning whereas ADHD affects attention and working memory). To compare the underlying neurobiological bases of these 2 conditions, investigators searched publication databases from inception through January 2022 for neuroimaging studies that compared PBD or ADHD groups to healthy controls in order to identify common and distinct neural substrates. A total of 42 articles were included for analysis, of which 32 assessed ADHD and 10 investigated PBD. The pooled sample size comprised 1333 cases with ADHD and 1308 controls and 268 cases with PBD and 385 controls, respectively. The patient groups with PBD and ADHD comprised 51% and 21% girls (P <.001) and they were 16.2 and 12.8 years of age (P <.001) on average, respectively. The control groups for both conditions were age- and gender-matched with cases. The investigators found shared GMV changes among the ADHD and PBD groups, with decreased volumes in the right insula (peak coordinates: 50, -4, 0; z=1.615; cluster size=100) and right anterior cingulate cortex (peak coordinates: 2, 26, -14; z=1.683; cluster size=22). These areas correspond with the functions of emotion processing and attention, respectively. In comparing PBD and ADHD cases, the PBD group had smaller GMVs than cases with ADHD in the right inferior frontal gyrus (peak coordinates: 52, 20, 26; z=1.682; cluster size=835), left orbitofrontal cortex (peak coordinates: 0, 24, -26; z=1.664; cluster size=261), and left hippocampus (peak coordinates: -20, -14, -10; z=1.517; cluster size=188). Conversely, cases with ADHD had greater GMV decreases than cases with PBD in the left precentral gyrus (peak coordinates: -40, -8, 56; z= -2.017; cluster size=158), left inferior frontal gyrus (peak coordinates: -26, 16, -24; z= -2.081; cluster size=59), and right superior frontal gyrus (peak coordinates: 26, 68, 0; z= -1.950; cluster size=28). When compared with controls, PBD cases had reduced GMVs in the left orbitofrontal cortex, left amygdala, and right inferior frontal gyrus. Cases with PBD had larger GMV in the left hippocampus associated with increasing age (R2, 0.276; P <.001) and boys had greater GMV abnormalities in the left hippocampus relative to girls. Cases with ADHD had decreased GMVs in the right anterior cingulate cortex, right insula, left precentral gyrus, and left inferior frontal gyrus and increased GMV in the bilateral thalamus relative to controls. Smaller GMV in the left inferior frontal gyrus was observed with increasing age among cases relative to controls (R2, 0.392; P <.001). Study authors concluded, “Overlapping anatomic substrates may account for similarities in the clinical presentation of PBD and ADHD, while disorder-differentiating regional alterations may account for the greater affective disturbances in PBD and greater neurocognitive and motor function disturbances in ADHD.” These study findings may be limited by the use of peak coordinate data instead of raw brain map data. Disclosure: Multiple study authors declared affiliations with biotech, pharmaceutical, and/or device companies. Please see the original reference for a full list of disclosures. This article originally appeared on Psychiatry Advisor

A "global human energy crisis" is coming. How can emotional intelligence help us navigate it? Are you and your team burned out? Increased rates of burnout impact the well-being of providers and the quality of care for patients. In a recent study, the American Medical Association reports half of physicians now experience aspects of burnout. Research at Six Seconds shows we are headed to a “global human energy crisis” with far-reaching implications for the entire health care system. What can disrupt burnout? Primary care physicians and other clinicians and health care providers can develop measurable skills of emotional intelligence to improve their well-being and workplace performance. Mental Health is a Workplace Issue Frontline health care workers were some of the hardest hit by the pandemic. In addition to tremendous workload, the added mental health effects of fear and uncertainty depleted people and the consequences of prolonged stress on the system have arrived. As World Health Organization Director General Tedros Adhanom Ghebreyesus said in March 2021, the pandemic has a long-term emotional impact: “When there is mass trauma, it affects communities for many years to come.” The effects of burnout are both personal and professional. In health care, emotional depletion is linked to higher turnover, more absenteeism, more errors and accidents, and an increase in unhealthy coping strategies (such as substance abuse). Mind Share Partners’ Mental Health at Work Report shows massive increases in mental health burdens at work, with 84% of respondents stating work has a negative effect on their mental health. The Workforce Institute at UKG found people’s supervisors had as much mental health impact as a spouse – and more than a therapist. Whether you’re in a formal role of leader, such as a private practice or supervising others in a hospital, you hold a position of leadership. In that position, your choices, your role-modeling, your interactions have a direct impact on others’ mental health and well-being. A Surprising Myth: Burnout is Not About Overwork Burnout is the feeling of being utterly depleted, unmotivated and detached from one’s work. As defined by the World Health Organization, burnout is: Physical and emotional exhaustion Depersonalization / detachment / cynicism Decline in sense of personal accomplishment Burnout’s causes are deeply linked to basic emotional needs like belonging, purpose, recognition and autonomy. Research backs this up. In a recent JAMA Network Open original investigation, physician burnout is connected to professional fulfillment. This study ranked at the most burned out and disconnected physicians by specialty. The results may surprise you (Figure 1). Do You Recognize Burnout? In this model (Figure 2) adapted from Freundenberger’s development of burnout research, we can see how burnout behaviors build and reinforce a cycle of overwork, degraded relationships and mental health issues. What are the key causes of burnout? Research has identified the following four factors: A perceived lack of control or autonomy Insufficient reward or recognition A perceived lack of social support / community A perceived lack of meaning / purpose While the burnout numbers are alarming, they should be a call to action: Clinicians and staff members are adversely affected by the increased emotional turmoil, and to meet this challenge, new skills are required. Emotional Intelligence for Health Care Providers Emotional intelligence has a mitigating effect on burnout for health care workers. In a 2022 cross-sectional public health study, researchers found “improving the emotional intelligence of health care staff has practical significance in reducing the level of job burnout directly and will reduce the incidence of burnout by reducing the frequency of violence (especially for emotional exhaustion and depersonalization).” How does emotional intelligence support health care professionals? We spoke with Carlos A. Pellegrini MD, FACS, executive coach, former chief medical officer of UW Medicine, and current chair of the Joint Commission. He points out that emotional intelligence is integral to a physician’s work: “The practice of medicine today requires clear, constant, and concise communications with the patients and with all other care providers.This starts with introspection – knowing and understanding our own emotions. That in turn, allows us to choose how we interact with them, to share and to give ourselves, and that elicits a need for all others to “give” (knowledge, skills, expertise) and share their emotions with us.The pursuit of excellence in medicine is tied to the emotional intelligence of the provider.” Five Ways to Reverse Burnout in Your Workplace The link between mental health and work led the U.S. Surgeon General, Vice Admiral Vivek Murthy, MD, MBA, to release the “Surgeon General’s Framework for Mental Health and Well-Being,” which offers useful broad structure. Based on that framework, here are five key areas to activate: Protection from harm: Take your share of the responsibility for mental health and well-being. That doesn’t mean taking all the share – but being clear that as a leader, you have some work to do in this area. Connection and community: Focus on building a positive, inclusive workplace where people feel a sense of belonging. By putting just a little more attention on relationships, physicians have a tremendous opportunity to shape the culture in your practice or team. Relationships are the number one driver of sustainable mental health (and, research on social determinants of health suggest this is true for physical health as well) – and on retaining and engaging employees. Work-life harmony: Set and respect boundaries, but also recognize autonomy. In the hierarchical nature of health care businesses, physicians sometimes overuse authority which diminishes autonomy. That has a deleterious effect on mental health, and on performance. Mattering at work: Build connection between routine tasks and the meaningful mission. When people can connect the dots between the work they do and the positive impact it has, this meaning at work can mitigate stress. Opportunity for growth: Learning brings a sense of accomplishment. Physicians can do this for themselves by engaging in meaningful learning, and support team members by teaching, mentoring, and offering quality feedback. Healthy Minds, Healthy Workplaces, Healthy People When health care organizations prioritize their own people, they create better results. In a case study using emotional intelligence in preventing burnout, the chief medical officer at Shirley Ryan AbilityLab, Dr. James Sliwa, stresses that the state-of-the-art facilities can only be used at full potential when the doctors and nurses who fill the building are flourishing and motivated. “The physical space is a manifestation of the people who work in it, and how they work together,” says Dr. Sliwa. “And research shows that emotional intelligence is a critical factor in people’s ability to regulate themselves and work effectively with others.” As individuals we are each responsible for our own wellness and we are also an integral part of an organizational system or institution. When we raise awareness and participate in positive practices to support emotional intelligence we can disrupt the cycle of burnout and influence a supportive work environment for all. Note: This article originally appeared in Medical Economics®.

SPECIAL REPORT: TREATMENT-RESISTANT DEPRESSION When initial treatments for depression do not work, patients often feel responsible. They blame themselves, feel stigmatized, and think they are not trying hard enough. Family relationships and work suffer. Life becomes still more constricted and cold. Suicide risk is an ongoing concern. Thus, patients who suffer from treatment-resistant depression (TRD) need and deserve the full range of the best available treatments. An oft-neglected treatment for TRD, both in research studies and in clinical practice, is evidence-based psychotherapy. Indeed, many definitions of TRD focus on medications and somatic treatments and do not even consider psychotherapies. There is a solid research base for the effectiveness of varied psychologically based antidepressant treatments in general. A meta-analysis of 101 studies and more than 11,000 patients found that several psychotherapies are as effective as medication for adult depression, and that combining psychotherapy and pharmacotherapy provides greater effects than either treatment alone. Some evidence indicates that psychotherapy may yield greater durability of treatment gains than pharmacotherapy and that sequential treatment with medication followed by psychotherapy extends durability. In a meta-analysis of 21 studies specifically targeting TRD, psychotherapy added to treatment as usual (TAU) was more effective than TAU alone.9 Another meta-analysis of 18 studies of psychotherapy for treatment nonresponders for any mood or anxiety disorder showed that psychotherapy decreased symptoms and improved quality of life. Among the psychotherapies investigated for TRD, multiple randomized controlled trials have demonstrated the effectiveness of cognitive behavior therapy (CBT) and mindfulness-based cognitive therapy. Other therapies that have fared well in general antidepressant studies but have not had extensive testing for TRD effectiveness include interpersonal psychotherapy (IPT) and brief psychodynamic psychotherapy. Although more research is needed, available evidence suggests that psychotherapy is well worth considering as part of a comprehensive approach to TRD. Key Principles for TRD Several identified mediators of TRD are problems psychotherapy typically addresses. Building hope, resolving interpersonal difficulties, normalizing negative affects instead of regarding them as bad feelings, generating positive attributions, teaching problem-solving, and behavioral activation are the bread and butter of CBT and IPT treatment. Many such targets may not fully respond to somatic interventions. In addition, individuals with chronic depression may have had the illness since childhood or early adult life, and therefore not have developed necessary psychological and social skills that psychotherapy can help them learn. When residual symptoms such as depressed mood or anxiety persist despite medication, evidence-based psychotherapy may reduce these and increase the likelihood of recovery. The therapeutic alliance deserves particular attention in work with patients who have long-standing illness. Acknowledgement of the demoralization and hopelessness that often accompany TRD may improve the relationship with the patient. The scientific literature is rife with implications that treatment resistance means “the patient failing the treatment” when, in fact, it is the other way around. Many patients (and, on occasion, their families) have the sense that there is no hope for a good life. Because such beliefs can counteract recovery, the therapist needs to convey a message of respect for the patient’s efforts and an attitude that one can live a meaningful and productive life, even with residual depressive symptoms. CBT for TRD CBT for TRD focuses on labeling hopelessness a belief and highlighting every new accomplishment as due to efforts by the patient to gradually improve a sense of self-efficacy. Another important aspect of CBT for TRD is helping patients to recognize when they begin to engage in the thinking associated with a negative mood state. Patients may then learn to employ tools that help them disengage from those overlearned mental habits—using thought records, activity scheduling, or mindfulness. Considering these thoughts as a depression mindset that occurs after stressors and can be managed without accelerating a negative mood can be a powerful tool in helping patients with TRD. Planning and managing activity are very important for patients with TRD. Often patients avoid rewarding and meaningful activities because of negative predictions about the outcome. Behavioral activation therapy, employed alone or as part of CBT, encourages the patient to experiment with small increments of activity in pursuit of meaningful goals or potential sources of enjoyment to increase positive affect. In addition, it provides a normalizing rationale for lack of motivation and illustrates the consequences of inactivity.12 Patients can learn to recognize and manage ruminative negative thinking and boost positive moods by augmenting behavioral activation with tools taught in psychotherapy to help them anticipate positive experiences and attend to positive emotions. IPT for TRD IPT focuses on patient emotions and their link to environmental circumstances and relationships.14 Acute treatment is time-limited, typically 12 weekly sessions. The IPT therapist helps the patient define depression as a temporary, treatable (if, for TRD, difficult-to-treat) illness that is not the patient’s fault. This maneuver helps to distinguish the disorder from the patient’s sense of self and relieves guilt. As in CBT, the patient has depression rather than being the depression. Exploring patient history, including previous treatments, yields a therapeutic focus for acute IPT treatment: complicated grief following death of a significant other; a role dispute or struggle with a significant other; a role transition or major life upheaval. The goal of acute treatment is to resolve this crisis. IPT sessions focus on recent interpersonal encounters and how the patient felt during them and handled them. Evoked feelings are explored as useful signals about the environment rather than the bad personal qualities patients often perceive them to be. Normalizing negative affects like anger removes an uncomfortable internal pressure and helps the patient gauge how to read and handle situations more effectively. Role play promotes assertiveness and the use of anger as self-defense in confrontations. No homework is assigned: patient autonomy and the pressure of the time limit determine when the patient acts on items learned in treatment. If IPT, with or without pharmacotherapy, yields acute response or remission, continuation IPT is often warranted to further strengthen functioning and forestall relapse. Short-term psychodynamic psychotherapies have been manualized, tested, and shown to benefit patients with major depression.16 So has brief supportive psychotherapy.17 All these treatments deserve further research, although the National Institute of Mental Health has unfortunately lost interest in funding clinical trials. Concluding Thoughts Patients with TRD live with an ongoing, debilitating disorder for this all-too-frequent condition. Although effective psychotherapy is not a panacea, it deserves more attention as an important contributor to the relief of TRD than it currently receives as well as an increased focus for research for more effective treatments.

Treatment with antidepressants results in a modest improvement in social functioning for patients with MDD. Antidepressants are associated with a small, but significant, improvement in social functioning (SF) for patients with major depressive disorder (MDD), as described in a systematic review and meta-analysis published in Psychotherapy and Psychosomatics. Many psychiatric disorders are associated with reduced sociability, which greatly impacts quality of life. Normative SF majorly contributes to a healthy life and well-being, and as such, is an important outcome in the treatment of psychiatric disorders. To evaluate the existing body of evidence regarding antidepressants and SF, investigators from the University of Cologne, Cologne, Germany, searched publication databases for relevant studies published through December 2022. The investigators selected a total of 39 publications covering 40 randomized controlled trials (RCTs) that investigated the efficacy of antidepressants compared with placebo for the treatment of MDD and measured SF as an outcome. The studies were published between 1995 and 2020 and were designed to evaluate primary depression (RCTs=27) or comorbid depression (k=13). The most common instruments for assessing SF were the Short Form Health Survey (SF-36), Social Role Functioning subsection; the Social Adaptation Self-Evaluation Scale (SASS); Work and Social Adjustment Scale (WSAS); and Activities of Daily Living for Mild Cognitive Impairment, Activities of Daily Living Scale (ADCS-ADL). "Since fulfilling social obligations is of enormous importance to patients, the field needs to increase its efforts in finding means beyond antidepressant drugs to help our patients live a successful social life." Across all studies analyzed, a total of 10,537 patients were randomly assigned to receive antidepressants and 6049 received placebo. The study participants were aged 46.8 years, on average, and 64.2% were women. In their meta-analysis, the investigators found a significant effect of antidepressants on SF relative to placebo for both primary (standardized mean difference [SMD], 0.25; 95% CI, 0.21-0.30; I2, 39%; P =.02) and comorbid (SMD, 0.24; 95% CI, 0.10-0.37; I2, 75%; P <.001) depression. When studies were stratified by risk for bias, the SMD of antidepressants on SF among patients with primary depression was 0.32 (95% CI, 0.24-0.40; I2, 35%) among studies with low risk for bias, compared with 0.23 (95% CI, 0.18-0.28; I2, 27%) for studies with high or uncertain risk for bias. Conversely, for comorbid depression, the SMD of antidepressants on SF did not have an effect in studies with low risk for bias 0.04 (95% CI, -0.16 to 0.24; I2, 0%) compared with 0.29 (95% CI, 0.13-0.44; I2, 79%) for studies with high or uncertain risk for bias. Notably, antidepressants’ impact on SF was correlated with improvements in depression (r =0.67; P <.001) and quality of life (r =0.63; P <.001). The investigators posit that this association suggests a construct overlap or redundancy in the measurement of these factors. Study authors concluded, “Since fulfilling social obligations is of enormous importance to patients, the field needs to increase its efforts in finding means beyond antidepressant drugs to help our patients live a successful social life.” This analysis may be limited by the stratification of studies by primary or comorbid depression status, which was a deviation from the original study design protocol. References: Kremer S, Wiesinger T, Bschor T, Baethge C. Antidepressants and social functioning in patients with major depressive disorder: systematic review and meta-analysis of double-blind, placebo-controlled RCTs.

The prevalence of e-cigarette use during late pregnancy among US adolescents has significantly increased, but does not elevate small-for-gestational-age birth risk. The prevalence of e-cigarette use during late pregnancy has increased among adolescents from 2016 to 2021, according to study results published in JAMA Network Open. Particularly, White adolescents were the most likely to use e-cigarettes during pregnancy, relative to other races/ethnicities. However, unlike combustible cigarettes, e-cigarette use did not significantly elevate the risk for small-for-gestational-age (SGA) births. Although the popularity of e-cigarettes has increased among adolescents in the United States, little is known about the prevalence of e-cigarette use among pregnant adolescents. Thus, researchers conducted a cohort study of data from the 2016 to 2021 Pregnancy Risk Assessment Monitoring System (PRAMS). This dataset used a mixed-mode approach to collect information on maternal behaviors, attitudes, and experiences throughout the perinatal period and covers approximately 83% of all US births. Participants self-reported their e-cigarette and combustible cigarette use. The researchers then categorized participants into the following groups: adolescents who abstained from both, exclusive e-cigarette users, exclusive combustible cigarette users, and individuals who engaged in dual use of both cigarette types. Additionally, SGA birth was defined as a weight below the 10th percentile for the corresponding sex and gestational duration, in accordance with the established criteria by the World Health Organization. A total of 10,428 adolescents, aged 10 to 19 years, who were pregnant between 2016 to 2021 were included in the final analysis. At baseline, 27.3% of individuals were aged 10 to 17 years and 72.7% were aged 18 to 19 years. By self-reported race/ethnicity, 58.9% of individuals identified as White, 23.3% as Black, and 69.8% as non-Hispanic. The researchers observed a significant increase in the weighted prevalence of pregnant women exclusively using e-cigarettes during late pregnancy (the last 3 months of gestation), from 0.8% in 2016 to 4.1% in 2021 (P =.001). In contrast, the prevalence of exclusive combustible cigarette use declined from 9.2% in 2017 to just 3.2% in 2021(P <.001). Dual use of both cigarette types did not significantly differ across the time period, fluctuating between 0.6% and 1.6% (P =.38). In 2021, the prevalence of cigarette use during late pregnancy among adolescents was highest for exclusive e-cigarette use (4.1%), then exclusive cigarette use (3.2%), and lastly dual use of both cigarette types (1.1%). Further, White adolescents had the highest prevalence of exclusive e-cigarette use (2.7%) and exclusive cigarette use (9.8%), compared to other race/ethnicity groups. Relative to pregnant adolescents who did not use cigarettes, the risk for SGA birth was not significantly elevated among adolescents who solely used e-cigarettes during late pregnancy (adjusted odds ratio [aOR], 1.68; 95% CI, 0.89-3.18) or adolescents who had dual use of both cigarette types (aOR, 1.68; 95% CI, 0.79-3.53). However, adolescents with exclusive use of combustible cigarettes had double the risk for SGA birth compared to nonusers (24.6% vs 12.9%; aOR, 2.51; 95% CI, 1.79-3.52). Study authors concluded, “In this cohort study of US pregnant adolescents, there was an increase in e-cigarette use and a decrease in cigarette use during late pregnancy from 2016 to 2021.” These study findings may be limited by recall bias, the potential confounding factors when distinguishing between cannabis and nicotine inhalation devices, and a lack of information on secondhand smoke exposure during pregnancy. Disclosure: One study author declared affiliations with biotech, pharmaceutical, and/or device companies. Please see the original reference for a full list of authors’ disclosures. This article originally appeared on Psychiatry Advisor

MDMA-assisted therapy for PTSD led to significant self-experience improvements, even after controlling for CAPS-5 score changes. In study findings published in PLOS One, 3,4-methylene-dioxymethamphetamine (MDMA)-assisted therapy for post-traumatic stress disorder (PTSD) had a positive effect on transdiagnostic mental processes of self-experience. Given that these processes are often associated with poor treatment outcomes, psychedelic agents that target these psychological capacities could lead to major improvements in PTSD symptomatology. Based on its positive performance with significant and sustained reductions in PTSD symptoms and acceptable safety profiles, the Food and Drug Administration (FDA) has designated MDMA-assisted therapy as a breakthrough therapy for PTSD. Studies involving healthy volunteers have demonstrated a positive effect of MDMA on self-regulatory capacities and self-compassion. Therefore, researchers assessed exploratory data from a randomized, double-blind, placebo-controlled study comparing the safety and efficacy of MDMA-assisted therapy to therapy with placebo among participants with severe PTSD. Treatment effects for self-experience were compared across scales of alexithymia, self-compassion, and an inventory of altered self-capacities. The study sample consisted of 90 participants with severe PTSD, as confirmed via the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) criteria and the Clinician-Administered PTSD Scale for DSM-5 (CAPS-5). Among the participants, 64.4% were women, 80.3% were White, and 92.7% were non-Hispanic or Latino. All participants underwent 3 preparation therapy sessions prior to experimental assignments, which consisted of 3 separate 8-hour experimental sessions, spaced about 4 weeks apart, of either MDMA-assisted therapy or therapy with placebo. The dosage was 80 mg + 40 mg MDMA HCl for the first experimental session and increased to 120 mg + 60 mg MDMA HCl in the second and third sessions. Relative to therapy with placebo, the group receiving MDMA-assisted therapy showed significantly greater improvements in all self-experience measures, except for the altered self-capacity factor of identity diffusion (P =.08). The MDMA-assisted therapy resulted in greater improvements in alexithymia (P =.0002), self-compassion (P <.0001), and most altered self-capacity factors, compared to placebo. However, upon adjusting for changes in CAPS-5 scores, only the improvements in self-compassion remained statistically significant (unadjusted for CAPS-5 change, P <.0001; adjusted for CAPS-5 change, P =.0076). In addition to the main treatment effects, the researchers evaluated interactions between treatment groups and the baseline categories. Participants with greater baseline alexithymia experienced a greater reduction in CAPS-5 scores in the MDMA-assisted therapy group, with a decrease of 16.16 (95% CI, -28.80 to -7.52). Additionally, when compared to individuals in the placebo group who had high baseline alexithymia, there were significantly greater improvements in CAPS-5 scores for participants in the MDMA-assisted therapy group with both low (P =.02) and high (P <.0001) baseline alexithymia. These findings indicate that MDMA has a significant impact on the regulation of emotions and self-experience measures, particularly alexithymia and self-compassion. Study authors concluded, “MDMA may be particularly effective for enhancing treatment efficacy by improving a range of problems with self-experience that are associated with treatment resistance.” The study results may be limited by a lack of information on outcomes of trust and intimacy, an inability to control for age and type of trauma exposure, and the homogenous demographics that may not reflect an epidemiologically representative PTSD population. This article originally appeared on Psychiatry Advisor

Regular THC use in adolescence is not a benign activity—it can have life-changing consequences. Here’s what you need to know. Although an epidemic of mental disorders in youth has been widely acknowledged, the role of cannabis has largely been ignored. Opioid and alcohol use disorders have long been recognized as substantial risks to the adolescent population, but the negative effects of cannabis tend to be overlooked. Although adolescents do not die from cannabis overdoses as they may from opiate overdoses, cannabis presents a significant danger. Tetrahydrocannabinol (THC), the euphoria-inducing cannabinoid in cannabis, is toxic to the adolescent brain, which is not fully developed until the age of 25 years. This toxicity is present even with non-disordered use (cannabis use that does not meet the DSM 5-TR criteria for a substance use disorder) and can lead to increased susceptibility to mental illness. Despite this evidence, we are seeing an increase in adolescent cannabis use. In 2019, 37% of US high school students reported use of cannabis in the past year, and 22% reported use in the past 30 days.3 Additionally, an increase in cannabis use has been observed in younger youth, with increased use observed in middle school. Increased THC Potency Not only is the frequency of cannabis use increasing, but so is the potency of THC in cannabis. Various preparations account for this increase. Cannabis plants have been bred to enrich THC and to decrease cannabidiol (CBD). Analysis of more than 38,000 cannabis samples seized by the US Drug Enforcement Administration (DEA) between 1995 and 2014 showed an average increase in THC from 4% in 1995 to 12% in 2014. This trend has continued over the past 9 years. Concentrated THC oil from buds called “wax” is 50% THC. With the increased use of vaping, adolescents can expose themselves to the very high levels of THC, as the concentration of THC in vaping cartridges can be as high as 80% to 90%. There is a paucity of literature on how high concentration of THC achieved through vaping impacts the developing brains of adolescents. Normal Brain Development A detailed examination of the neurodevelopment of the adolescent brain provides a hypothesis as to how THC can cause significant negative effects. In infancy, neurons are disparate and unconnected but begin connecting and forming synapses at an enormous rate, with 2 million synapses being formed every second up to age 2 years. At that time, the process of pruning ensues so that half of the hundred trillion synapses formed will disappear. A second period of overproduction of synapses, especially in the prefrontal cortex, occurs at the time of puberty, and pruning continues for the following 10 years. In addition, neurogenesis in the dentate gyrus of the hippocampus has a peak value near puberty. Pruning allows the brain to remove synapses that are no longer being utilized, providing much-needed space in the limited cranium for increased synaptogenesis to maximize the efficiency of developing brain circuits. During puberty, this surge in synaptogenesis occurs in the prefrontal cortex, which controls attention, impulsivity, emotional regulation, and recognition of possible consequences of one’s actions. This is followed by more pruning until full maturation is achieved at the age of 25 years. Possible Consequences of THC Use in Adolescence If something were to hinder the brain from strengthening neuronal connections or to alter their morphology during adolescence, those connections may become disrupted for the rest of that individual’s life. It is well established that THC interferes with the functioning of the endogenous cannabinoid anandamide, a retrograde neurotransmitter that modulates the release of other synaptic chemicals. The addition of THC to the developing brain may have major detrimental effects on the large-scale changes in neural connections occurring during this time. These developing neuro-networks, which are highly influenced by hormones and the environment, would make the developing adolescent brain vulnerable to THC. In particular, the prefrontal cortex seems to be susceptible to these changes, which could be the explanation for some of the long-term symptoms associated with chronic cannabis use. One of the most significant of these symptoms involves impairment of cognition including working memory, attention, information processing, judgment, and decision making. A New Zealand prospective study showed that regular cannabis use before the age of 18 years correlated with the loss of 5 to 8 IQ points at 20-year follow-up. These results were not confirmed by a subsequent twin study, but they did demonstrate that regular use of cannabis impaired academic functioning and subsequent socioeconomic levels. The investigators hypothesized that common vulnerability factors may make some individuals more prone to both cannabis use and negative outcomes. Impaired cognition, especially with executive function problems and poor school performance, occurs with acute cannabis use. It is unclear whether this returns to a normal level if cannabis use is stopped. Clinical experience has shown that some adolescents develop acute psychosis from smoking cannabis, which often recurs if they resume using cannabis again after remission of the first psychotic episode. Follow-up studies have shown that cannabis use increases the risk of the future development of schizophrenia. Regular cannabis use in adolescence also increases risk of depression, suicide attempts, anxiety, and gastrointestinal problems. Observations in Our Treatment Program In our adolescent substance abuse intensive outpatient program, during 2020 and 2021, approximately 40% of teens reported that cannabis was their drug of choice. Most of them begin by smoking cannabis once or twice a week, along with drinking some alcohol, and then progressed to vaping highly concentrated THC oils. When they reached the point of smoking and vaping 3 to 4 times a week, their schoolwork declined and cannabis use became the focus of their lives. In our clinical experience, almost every adolescent acknowledges that cannabis causes short-term memory loss. Comorbid attention-deficit/hyperactivity disorder (ADHD), anxiety, depression, and suicidal ideation often become more severe in adolescents who use cannabis. Cannabis appears to impair the prefrontal cortex’s ability for them to recognize their impairments. This becomes a major problematic issue in their treatment. It often takes 3 or 4 weeks of THC abstinence before the adolescent acknowledges the negative effects that cannabis has caused. Many adolescents and young adults with opiate use disorder attempt to use cannabis as a harm reduction means to prevent relapse to opiates. Our experience is that the high from using cannabis increases urges and cravings for opiates and can lead to opiate relapse. The Need for Early Intervention Many adolescents with psychiatric disorders including ADHD, anxiety, depression, and posttraumatic stress disorder (PTSD) will smoke or vape THC in order to feel better with the unfortunate outcome that a significant number of them will become addicted. This presents unique problems for treatment because adolescents will often participate in psychosocial and pharmacological treatments but resist stopping THC use. This in turn leads to negative cognitive and motivational effects that interfere with treatments such as cognitive behavioral therapy (CBT) and dialectical behavior therapy (DBT). Efforts to decrease or eliminate cannabis use may make a significant difference in treatment response. Educating adolescents as to the negative effects of THC as well as how long it stays in the brain (a single ingestion lasts a week, while regularly ingested THC will last a month) can be helpful. We ask the adolescents to commit to 30 days without cannabis to see for themselves how different and clearheaded they feel. If possible, family therapy with parents learning to set appropriate limits can help. Recovery groups may give needed support. There is a paucity of pharmacological studies of antidepressants in this population, with efficacy over placebo not developing until week 13 in 1 study. Significantly, in this study, both groups continued to smoke large amounts of cannabis. From a psychodynamic viewpoint, adolescence is a time of learning to develop the ego strategies to deal with anxiety, loss, and disappointment. If adolescents use THC to cope with these normal developmental challenges, these basic ego factors may be stunted, and this can contribute to them becoming more narcissistic and less empathic young adults. Concluding Thoughts The possible effects of THC on the adolescent brain are often not acknowledged in clinical and research studies. Studies on the marked increase of emotional problems in youth often explore important issues contributing to youth mental health crises such as the influence of psychosocial stressors, social media, bullying, trauma, and the lack of school attendance during the COVID-19 pandemic. This occurs despite growing literature that supports the fact that heavy THC use during brain development increases the risk of psychotic episodes, and negatively impacts cognition, emotional functioning, and school performance. Clinicians need to ask every adolescent, especially those with emotional challenges, about the role that cannabis plays in their life and educate them on the negative impact it may have on their brain development and treatment. Parents, adolescents, teachers, and health care providers need to become aware that regular THC use in adolescence is not a benign activity and can have life-changing consequences. In addition, legislatures and voters need to recognize that THC can be toxic to adolescent brain functioning. Note: This article originally appeared on Psychiatric Times

Among patients with Alzheimer disease, light therapy led to significant improvements in sleep quality, depression, and agitation. Light therapy significantly improved sleep and psychobehavioral outcomes among patients with Alzheimer disease (AD), according to a systematic review and meta-analysis published in PLoS One. The primary treatment for AD is pharmacologic therapy which may alleviate some AD-induced cognitive and memory impairment but are neither curative nor halt disease progression. These medications are associated with side effects including poor appetite, diarrhea, and hallucinations. Increasing attention has been paid to photobiomodulation as a potential nonpharmacologic treatment option, however, no systematic evaluation of the efficacy of light therapy in AD has been performed. Researchers from Weifang Medical University in China searched publication databases through December 2022 for randomized controlled trials evaluating phototherapy in AD. This analysis had 12 outcomes of interest: Sleep efficiency, Interdaily stability, Interdaily variability, Pittsburgh Sleep Quality Index (PSQI), Relative amplitude, Wake after sleep onset (WASO), Alzheimer’s Disease Assessment Scale-Cognitive subscale (ADAS-cog), Cohen-Mansfield Agitation Inventory (CMAI), Cornell Scale for Depression in Dementia (CSDD), Zarit Caregiver Burden Interview (ZBI), Neuropsychiatric Inventory (NPI), and Mini-Mental State Examination (MMSE). A total of 15 studies comprising 598 patients with AD were included in this analysis. The studies were published between 2005 and 2022 and were conducted in 7 countries across North America, Europe, and Asia. The studies recruited patients with mild to moderate AD (n=9) or moderate to severe AD (n=6). The interventions involved light therapy (n=11) or light therapy devices (n=4). Light therapy was associated with significant improvements to: Interdaily stability (mean difference [MD], -0.04; 95% CI, -0.05 to -0.03; I2, 0%; P <.00001), Interdaily variability (MD, -0.07; 95% CI, -0.10 to -0.05; I2, 48%; P <.00001), ADAS-cog scores (MD, -0.46; 95% CI, -0.66 to 0.25; I2, 89%; P <.00001), CMAI scores (MD, -3.97; 95% CI, -5.09 to 2.84; I2, 0%; P <.00001), and CSDD scores (MD, -2.55; 95% CI, -2.98 to -2.12; I2, 0%; P <.00001). Relative to usual care, light therapy improved sleep efficacy (MD, -2.42; 95% CI, -3.37 to -1.48; I2, 60%; P <.00001) and PSQI scores (MD, -1.73; 95% CI, -2.00 to -1.45; I2, 0%; P <.00001). Light therapy also reduced caregiver burden according to the ZBI (MD, -3.57; 95% CI, -5.28 to -1.87; I2, 0%; P <.00001) and psychobehavioral symptoms according to the NPI (MD, -3.07; 95% CI, -4.14 to -2.00; I2, 79%; P <.00001). No significant effect of light therapy was observed for: Relative amplitude (MD, -0.06; 95% CI, -0.14 to 0.01; P =.10), WASO (MD, -20.38; 95% CI, -41.88 to 1.13; P =.06), or MMSE scores (MD, 0.44; 95% CI, -0.71 to 1.59; P =.45). This analysis was limited by pooling data from patients with different AD severity. “[L]ight therapy significantly improved sleep and psychobehavioral symptoms in patients with AD. These findings combined with its low side effects suggest the role of light therapy as a promising treatment for AD,” the researchers concluded. This article originally appeared on Neurology Advisor

Although there has been a substantial increase in awareness—and, I hope, understanding—of depression, there has been far less public discussion of the challenges that clinicians face in the management of this condition and of the challenges that many patients face getting better. The public are increasingly aware that there are a range of antidepressant medications, and that some of these have problematic adverse effects. However, there has been far less public discussion about the frequent problems of therapeutic nonresponse and how we go about addressing these from a clinical perspective. I wrote Curing Stubborn Depression: Emerging & Breakthrough Therapies for Treatment-Resistant Depression1 to try to help fill this information gap. The book is aimed at patients, interested members of the general public, and potentially non-psychiatry clinicians (other doctors and health workers) interested in the management of patients with mood disorders. The book aims to make clear that response to antidepressant treatments, be they pharmaceutical or psychological, is not always simple, straightforward, or immediate: and that many patients will struggle to get better with standard treatments. But the book also emphasizes that the story is not all negative. There are a range of existing and emerging therapies that offer hope to many of these patients for improved treatment outcomes. The book begins with an overview of depression and a description of the standard pharmaceutical and psychotherapeutic approaches that are most commonly used in its management. It then continues with a chapter exploring what should be considered when initial therapy is not working; how the diagnosis and potential presence of comorbidity should be thought about and addressed; and what second-, third-, and fourth-line pharmacotherapy options tend to look like. This includes a discussion about treatment doses, augmentation, and other strategies. The book then addresses a range of lesser-known but increasingly important and prominent therapies. Chapters address the use of electroconvulsive therapy (ECT), repetitive transcranial magnetic stimulation (rTMS), transcranial direct current stimulation, bright light therapy, deep brain stimulation, ketamine, and the emerging field of psychedelic-assisted psychotherapy. Across these chapters, brief clinical vignettes are used to highlight important aspects of the treatments or areas of research being discussed. These are taken directly from my clinical experience over the years, managing patients with these modalities in clinical practice and in research trials. The history and context of the therapeutic area under discussion are addressed in each chapter, along with some of the controversies and challenges that have emerged over time. There is an intent that some of these chapters will open the eyes of patients to the availability, efficacy, and tolerability of novel treatments such as rTMS, which are underused in certain areas of clinical practice. The book ends with a series of practical suggestions for patients beginning, or who have already embarked on, the journey of treatment for depression. It includes what these patients should expect when being assessed, what to anticipate when commencing treatment, and the sorts of important questions to explore with their treating clinicians. The book aims to help them become actively engaged in their treatment, to understand what is being proposed, and to understand this, as well as the alternatives, in a way that allows them to make meaningfully considered decisions. As such, I am hoping to make our patients more genuine participants and drivers of their care—to be able to work with their treating clinicians in an informed and up-to-date manner. In particular, I hope the book encourages individuals with depression to “set the bar high” in regard to their treatment and recovery. Ultimately, the goal of treatment should be not just an improvement in symptoms but meaningful wellness. The pathway to this end may be a challenging one, but it is possible for many—if not most—individuals to get there. If these individuals are stuck in treatment (if, for example, they have been taking a medication for some time without optimal response), they should advocate for change and should have an expectation of fully engaged and proactive therapy. I wrote this book because of the patients who have been coming to me for help for many years. Because of the patients who have been treated with 3 or 4 selective serotonin reuptake inhibitors (SSRIs) in a row, but nothing else. Because of those who were prescribed a single antidepressant that was not working for months, if not years, at a time. Because of those who spent many hours in psychotherapy, but probably only received some form of supportive counseling despite the fact that they continued to suffer the travails of their condition. Because of those who had been told that “rTMS is a sham” or that “all ECT will do is cause brain damage.” There are many fantastic doctors and therapists out there helping patients with depression who provide excellent all-around care. However, there are also some who remain quite conservative and limited in their scope of practice, who predominantly practice psychopharmacology or psychotherapy, and who are not willing or able to recommend or discuss other treatment options. All patients with depression deserve to understand all of their treatment options and to be able to weigh how these options may or may not be relevant to them. These patients also deserve some sense of hope for the future, and I hope Curing Stubborn Depression can provide some of both to them.

Benzodiazepine treatment during pregnancy is associated with a significantly elevated risk for miscarriage. Benzodiazepine use during pregnancy is associated with an increased risk for miscarriage, according to new research published in JAMA Psychiatry. Health care professionals should carefully consider the risk-benefit ratio when considering benzodiazepine treatment for pregnant individuals. Although benzodiazepines can cross the placental barrier and may potentially impact fetal development, they are still used to treat psychiatric and sleep disorders in pregnancy. Studying the effect of benzodiazepines on pregnancy outcomes is challenging as pregnant women are often precluded from randomized clinical trials and confounding factors can bias results in observational studies. The current study aimed to quantify the risk for miscarriage associated with benzodiazepine use during pregnancy, using a case-time-control design that accounts for confounders. This nationwide, population-based study was conducted in Taiwan using pregnancy data from the National Health Insurance (NHI) database from 2002 to 2019 and the National Birth Certificate Application (BCA) database from 2004 to 2018. Researchers employed a case-time-control design to investigate the association between benzodiazepine use during pregnancy and the risk for miscarriage, comprising 2 analyses: a case-crossover analysis and an exposure time-trend control crossover analysis. The researchers used a conditional logistic model to estimate the odds ratios (ORs) of miscarriage. Overall, the study included 3,067,122 pregnancies among 1,957,601 women (mean age=30.61; SD, 5.91). Of those pregnancies, 136,134 (4.4%) resulted in miscarriage. The researchers then matched the case group of individuals who experienced miscarriage with controls (based on age, psychiatric medical conditions, lifestyle factors, chronic comorbidities, medication use, and health care utilization), resulting in 134,864 pairs of pregnant women. Among the cases cohort, 1502 pregnant women were exposed to benzodiazepines during the risk period only (1 to 28 days before miscarriage), and 2806 were exposed during the reference period only (181 to 208 days before the last menstrual period). Case-time-control ORs confirmed that exposure to benzodiazepines was associated with an increased risk for miscarriage (OR, 1.69; 95% CI, 1.52-1.87). Further, subgroup analyses revealed a dose-response association between benzodiazepine exposure and miscarriage, with the OR increasing from 1.61 (95% CI, 1.43-1.82) for low-dose exposure to 1.86 (95% CI, 1.53-2.25) for high-dose exposure. This nationwide case-time-control study revealed that benzodiazepine use during pregnancy was associated with an approximately 70% increased risk for miscarriage, even after accounting for measurable confounders. Study authors concluded, “Prescribing benzodiazepines should only be considered following a comprehensive evaluation of the potential benefits and risks for both the mother and the child.” The primary limitation of the study is the potential bias resulting from the use of birth certificate-based and claims-based databases for pregnancy and benzodiazepine exposure measures. This article originally appeared on Psychiatry Advisor

Delerium is tied to a significantly increased risk for dementia and death in older adults, with men at particular risk, new research showed. Incident dementia risk was more than three times higher in those who experienced just one episode of delirium, with each additional episode linked to a further 20% increase in dementia risk. The association was strongest in men. Patients with delirium also had a 39% higher mortality risk than those with no history of delirium. "We have known for a long time that delirium is dangerous, and this provides evidence that it's even more dangerous than perhaps we had appreciated," study investigator Emily H. Gordon, MBBS, PhD, a geriatrician and senior lecturer at the University of Queensland, Brisbane, Australia, told Medscape Medical News. "But we also know delirium is preventable. There are no excuses anymore; we really need to work together to improve the hospital system, to implement what are known to be effective interventions," she added. Close Matching Prior studies that suggested an association between delirium and dementia were relatively small with short follow-up and varied in their adjustment for confounders. They also didn't account for the competing risk for death, researchers noted. Investigators used a linked New South Wales (NSW) statewide dataset that includes records of care episodes from all NSW hospitals as well as personal, administrative, clinical, and death information. The study included an eligible sample of 626,467 older adults without dementia at baseline with at least one hospital admission between 2009 and 2014. For these patients, researchers calculated a hospital frailty risk score and collected other information including primary diagnosis and mean length of hospital stay and stay in the intensive care unit. From diagnostic codes, they categorized patients into no delirium and delirium groups and determined the number of delirium episodes. Investigators matched patients in the delirium group to patients with no delirium according to characteristics with potential to confound the association between delirium and risk for dementia, including age, gender, frailty, reason for hospitalization, and length of stay in hospital and intensive care. The matched study sample included 55,211 (mean age, 83 years) each in the delirium and the no delirium groups. Despite matching, the length of hospital stay for the index episode was longer for the delirium group than the no delirium group (mean, 9 days vs 6 days). The primary outcomes were death and incident dementia, determined via diagnostic codes. During a follow-up of 5.25 years, 58% of patients died, and 17% had a new dementia diagnosis. Among patients with at least one episode of delirium, the rate of incident dementia was 3.4 times higher than in those without delirium. After accounting for the competing risk for death, incident dementia risk remained three times higher among the delirium group (hazard ratio [HR], 3.00; 95% CI, 2.91-3.10). This association was stronger for men than women (HR, 3.17 and 2.88, respectively; P = .004). Sex Differences The study is thought to be the first to identify a difference between sexes in dementia risk and delirium, Gordon said. It's possible delirium in men is more severe in intensity or lasts longer than in women, or the male brain is, for whatever reason, more vulnerable to the effects of delirium, said Gordon. But she stressed these are only theories. Investigators also found a mortality rate 1.4 times higher in the delirium group vs those without delirium, equating to a 39% increased risk for death (HR, 1.39; 95% CI, 1.37-1.41). The risk was similar for men and women (interaction P = .62). When researchers categorized delirium by number of episodes, they found each additional episode was associated with a 10% increased risk for death (HR, 1.10; 95% CI, 1.09-1.12). In addition to its large size, long follow-up, and close matching, what sets this new study apart from previous research is it accounted for the competing risk for death, said Gordon. "This is really important because you're not going to get dementia if you die, and in this population, the rate of death is incredibly high," Gordon said. "If we just assume people who died didn't get dementia, then that screws the results." Causal Link? For those who experienced at least one episode of delirium within the first 12 months, each additional episode of delirium was associated with a 20% increased risk for dementia (HR, 1.20; 95% CI, 1.18-1.23). That dose-response association suggests a causal link between the two, Gordon said. "The number one way to prove causality is to do a randomized controlled trial," which isn't feasible with delirium, she said. "By demonstrating a dose-response relationship suggests that it could be a causal pathway." Exact mechanisms linking delirium with dementia are unclear. Delirium might uncover preexisting or preclinical dementia, or it might cause dementia by accelerating underlying neuropathologic processes or de novo mechanisms, the authors noted. Study limitations included the potential for residual confounding from unmeasured variables in the matching criteria. Delirium and dementia diagnoses depended on clinical coding of medical information recorded in the administrative dataset, and under-coding of dementia during hospitalization is well-recognized. Although the study controlled for length of stay in hospital and in intensive care, this may not have fully captured differences in severity of medical conditions. Data about the duration and severity of delirium episodes were also unavailable, which limited the dose-response analysis. Commenting on the findings for Medscape Medical News, Christopher Weber, PhD, Alzheimer's Association as director of Global Science Initiatives, said the results are consistent with other research on the association between delirium and incidents of dementia. The increased risk for dementia following delirium in males is "an interesting finding," said Weber. "This suggests a need for more research to understand the impact of sex differences in delirium, as well as research to see if preventing incidents of delirium could ultimately reduce rates of dementia." The study received support from the National Health and Medical Research Council: Partnership Centre for Health System Sustainability. Gordon and Weber reported no relevant conflicts of interest. Note: This article originally appeared on Medscape Medical News