Shrinks In Sneakers

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  • The Silent Crisis: Physician Suicide in the United States

    The Silent Crisis: Physician Suicide in the United States

    I saw these magnets today on the refrigerator located in the physicians lounge and it seemed like a good reminder 

    In the U.S., an estimated 300-400 physicians die by suicide each year, a staggering rate far higher than that of the general population. This crisis, largely unspoken in healthcare settings, underscores the immense pressures physicians face daily. The high expectations, long hours, emotional exhaustion, and the stigma around seeking mental health support create a dangerous environment where burnout can quickly spiral into severe mental health struggles.

    Physicians are trained to endure, often putting others’ health before their own. But the costs of “pushing through” take a toll. Many feel they cannot safely reach out for help without risking their careers due to institutional stigma around mental health treatment. This cycle of isolation and suppressed emotion can lead to tragic outcomes.

    Organizations are beginning to address this issue by implementing wellness programs, peer support systems, and confidential mental health resources, but more systemic changes are needed. Reducing the stigma around mental health support, reforming punitive policies, and fostering a culture of openness in medicine could be life-saving.

    Physician suicide affects us all—it robs the healthcare system of dedicated professionals and leaves profound impacts on patients, families, and communities. It’s time to break the silence and actively support those who care for us.

  • Family Ties That Bind: When High Expressed Emotion Worsens Schizophrenia

    Family Ties That Bind: When High Expressed Emotion Worsens Schizophrenia

    In psychiatry we are always asking patients about social support. The presence or absence of social support can have a major impact on treatment response and ability to remain well once someone leaves the hospital. This usually includes support from family members and friends. 

    In 1956 the Medical Research Council Social Psychiatry (MRCSP) London conducted a study regarding the readmission of schizophrenic patients. The research revealed that patients who were stabilized symptomatically and functionally inpatient and subsequently discharged to live with their parents or wives were frequently readmitted for relapse of symptoms compared to those who were discharged to a sibling, or non-family environment. While family involvement is generally a protective factor that helps prevent things like suicide, there are some situations where the over involvement of family can complicate matters and even create worse outcomes.

    This usually occurs when a family has high expressed emotion. 

    Expressed emotion (EE) has consistently been shown to predict relapse in schizophrenia as well as other psychiatric disorders. Expressed emotion is a measure of the family environment that is based on how the relatives of a psychiatric patient spontaneously talk about the patient. 

    It measures 3 aspects of the family environment associated with high expressed emotion:

    1. Hostility (outward anger and frustration towards the patient because the family believes they are choosing to not get better) 
    2. Emotional over-involvement (This is where the family tries to solve all the problems for the patient taking away their ability to be self-reliant). 
    3. Critical comments (where the family views the mentally ill patient as lazy or selfish, not appreciating the difficulty of living with mental illness). 

    However, research has shown the following as indications of an environment with low expressed emotion: 

    1.    Positivity: (statements that express appreciation or support for the patient’s behavior and gives verbal and nonverbal reinforcement). 

    2.    Warmth: (kindness, concern and empathy expressed by the caregiver).

    There is such a thing as too much involvement on the part of the families which can lead to complicating family dynamics and exacerbation of an individual’s symptoms of mental illness. Interventions for improving outcomes include reducing contact with high EE caregivers and providing psychoeducation about EE to care givers. Bringing awareness to this behavior may help family members change. 

  • Breaking the Cycle: Effective Strategies to Prevent Self-Injurious Behavior (SIB)

    Breaking the Cycle: Effective Strategies to Prevent Self-Injurious Behavior (SIB)

    This post comes from another real-world case that I frequently encounter in clinical practice. Self-injurious behavior (SIB) is common in the inpatient care setting and the strategies to prevent it are mostly behavioral. Many patients and families are also looking for pharmacological options. Here are some of the more common options and recommendations for treating SIB.

    Behavioral Interventions

    1. Functional Behavior Analysis (FBA): Start with an FBA to understand why the self-injury is occurring (e.g., to gain attention, avoid demands, or self-soothe). This guides intervention planning.
    2. Positive Reinforcement and Skill Building: Reinforce alternative, adaptive behaviors that fulfill the same needs as self-injury, such as communication skills (e.g., teaching to request attention) or self-soothing techniques.
    3. Cognitive Behavioral Therapy (CBT): For individuals able to engage in talk therapy, CBT can address underlying thoughts and emotions driving SIB, such as distress intolerance, perfectionism, or negative self-beliefs.
    4. Dialectical Behavior Therapy (DBT): DBT is particularly effective for reducing SIB, especially in borderline personality disorder. It combines emotional regulation, mindfulness, and distress tolerance skills.
    5. Environmental Modifications: Minimizing triggers in the individual’s environment can help reduce occurrences. This might include changes in routines, avoiding overstimulation, or modifying demands.
    6. Applied Behavior Analysis (ABA): Techniques from ABA, like differential reinforcement of other behaviors (DRO) or non-contingent reinforcement (NCR), can reduce self-injury by decreasing its functional value.

    Pharmacological Interventions

    1. SSRIs (Selective Serotonin Reuptake Inhibitors): Useful if self-injury is driven by anxiety, depression, or obsessive-compulsive tendencies. SSRIs can help stabilize mood and reduce anxiety, lessening the need for SIB.
    2. Antipsychotics: Atypical antipsychotics, such as risperidone or aripiprazole, are sometimes effective, particularly in autism spectrum disorders or severe intellectual disabilities. However, weigh these benefits against side effects, especially for long-term use.
    3. Mood Stabilizers: Medications like lithium, lamotrigine, or valproate can help regulate mood fluctuations that contribute to SIB. Lithium, in particular, has shown effectiveness in reducing aggression and impulsivity.
    4. Naltrexone: This opioid antagonist can be effective in cases where SIB is hypothesized to release endogenous opioids, providing a calming effect.
    5. Beta-blockers (e.g., propranolol): In cases of high impulsivity or aggression linked to SIB, beta-blockers can reduce physiological arousal, lessening the drive for self-injury.
    6. Clonidine or Guanfacine: These medications, which target the noradrenergic system, can help reduce impulsivity and aggression in patients with ADHD or autism, indirectly lowering self-injury.

    Choosing the best approach depends on the individual’s specific triggers, co-occurring conditions, and underlying motivations for SIB. Integrating both behavioral and medication interventions, while monitoring closely for effectiveness and side effects, often yields the best outcomes.

  • Brighten Your Mood: Light Therapy to Combat Daylight Savings Blues!

    Brighten Your Mood: Light Therapy to Combat Daylight Savings Blues!

    With daylight savings time quickly approaching a summary of the randomized controlled trial evidence for light therapy in seasonal affective disorder (SAD), particularly in relation to daylight savings time seems appropriate this week. 

    Efficacy of Light Therapy for SAD

    Several randomized controlled trials have demonstrated the efficacy of light therapy for treating seasonal affective disorder:

    A meta-analysis of randomized controlled trials found that bright light treatment was associated with a significant reduction in depression symptom severity in SAD, with an effect size of 0.84 (95% CI: 0.60 to 1.08)

    Another meta-analysis revealed that dawn simulation light therapy was also effective for SAD, with an effect size of 0.73 (95% CI: 0.37 to 1.08)

    One study found that exposure to bright light (10,000 lux) for as little as 20-40 minutes could lead to significant improvements in mood scores in SAD patients

    Timing and Duration of Light Therapy

    Light therapy is typically administered daily for at least several weeks during the fall and winter months

    One study found that 40 minutes of exposure to 10,000 lux light resulted in greater improvement than 20 minutes, but was not significantly different from 60 minutes of exposure

    The rate of mood improvement was steepest during the first 20 minutes of light exposure

    Mechanisms and Considerations

    The efficacy of light therapy is thought to be related to its effects on circadian rhythms and neurotransmitters like serotonin

    Light boxes used for therapy should provide 10,000 lux of light and have screens that filter out UV rays

    Light therapy is generally recommended to be used within the first hour of waking up in the morning

    Limitations of Current Evidence 

    Many studies on light therapy for SAD have not used rigorous study designs

    There is limited research specifically examining the effects of light therapy in relation to daylight savings time changes.

    More long-term follow-up studies are needed to assess the safety and potential side effects of light therapy

    While the evidence supports the efficacy of light therapy for SAD, there is a need for more rigorous, large-scale randomized controlled trials to further establish its effectiveness, optimal timing, and duration, particularly in relation to daylight savings time changes. The current evidence suggests that light therapy can be an effective treatment option for SAD, with effects comparable to antidepressant medications

    Resources: 

    https://psychiatryonline.org/doi/10.1176/appi.ajp.162.4.656

    https://pmc.ncbi.nlm.nih.gov/articles/PMC2913518

    https://www.mayoclinic.org/diseases-conditions/seasonal-affective-disorder/in-depth/seasonal-affective-disorder-treatment/art-20048298

  • ADHD and Cannabis Use Disorder: Key Facts You Shouldn’t Ignore

    ADHD and Cannabis Use Disorder: Key Facts You Shouldn’t Ignore

    1. Prevalence and Patterns of Use

    People with ADHD have been shown to use cannabis at higher rates than those without ADHD. Studies indicate that adolescents and adults with ADHD are more likely to use cannabis, and they may start using it at a younger age. This may be due to self-medication attempts, as people with ADHD often report using cannabis to help with symptoms like impulsivity, anxiety, and sleep difficulties which seems like a bad idea to me but lets look at the reasons.

    2. Cannabis as a Self-Medication Attempt

    Some people with ADHD use cannabis in an attempt to self-manage their symptoms. Anecdotally, users report feeling more focused, relaxed, and less anxious, though the scientific evidence on cannabis’s effectiveness for ADHD symptom management is not robust. Studies show that while some ADHD symptoms like restlessness might feel alleviated short-term, long-term outcomes often do not show sustained benefit, and impairment can increase over time.

    3. Impact on ADHD Symptoms

    Research on cannabis’s effect on ADHD symptoms is mixed:

    • Impulsivity and Attention: Cannabis can impair attention, memory, and executive functioning, which are already areas of struggle for individuals with ADHD. Heavy cannabis use is associated with poorer performance on tasks measuring these cognitive domains.
    • Cognitive Function: Longitudinal studies have shown that chronic cannabis use can worsen cognitive functions over time, especially if use begins in adolescence. These cognitive impacts may compound ADHD-related deficits.
    • Motivation and Goal-Directed Behavior: Cannabis can affect motivation and goal-directed behavior, which can exacerbate some ADHD symptoms, particularly in individuals who already struggle with organization and task completion.

    4. ADHD as a Risk Factor for Cannabis Use Disorder

    Studies suggest that people with ADHD may be more prone to developing cannabis use disorder (CUD) compared to the general population. Traits like impulsivity and sensation-seeking, common in ADHD, may increase vulnerability to addiction. Additionally, the reinforcing effects of cannabis (e.g., reduction in perceived anxiety) may lead to increased use and dependency in those with ADHD.

    5. Genetic and Neurobiological Factors

    There is some evidence suggesting that the overlap between cannabis use and ADHD may have a genetic or neurobiological basis:

    • Genetic Overlap: Studies have found that genes linked to ADHD, particularly those affecting dopamine function, are also implicated in substance use disorders, including cannabis use disorder.
    • Endocannabinoid System: ADHD and cannabis use affect dopamine and endocannabinoid systems. Some research posits that dysregulation in these systems might underlie both the propensity for ADHD and substance use, but this remains an area for further research.

    6. Cannabis and Medication Interactions

    For those with ADHD taking stimulant medications, cannabis use can interfere with treatment. THC, the psychoactive component of cannabis, can interact with medications like methylphenidate or amphetamine-based treatments, potentially reducing their effectiveness or exacerbating side effects like anxiety and heart palpitations.

    7. Longitudinal and Population Studies

    Long-term studies generally show that early and heavy cannabis use is associated with worse outcomes for individuals with ADHD. These include lower academic achievement, increased rates of unemployment, and higher incidences of mental health issues, especially when cannabis use starts in adolescence.

    Summary

    While some people with ADHD report short-term symptom relief with cannabis, research shows that heavy, frequent use tends to worsen cognitive deficits associated with ADHD over time. Additionally, ADHD may predispose individuals to higher rates of cannabis use and a greater risk of developing cannabis use disorder. While cannabis might seem beneficial for symptom relief in the short term, its long-term use is generally not supported as an effective management strategy for ADHD.

  • Split or Stick? The Real Impact of Dividing Clozapine Doses

    Split or Stick? The Real Impact of Dividing Clozapine Doses

    This post comes from a recent discussion I had with my resident about the utility of splitting clozapine doses in a recent case we had.

    The evidence on splitting clozapine into multiple daily doses primarily stems from clinical observations and smaller studies rather than extensive, randomized controlled trials (RCTs). Since clozapine has a unique pharmacodynamic and pharmacokinetic profile, standardizing an RCT on dose splitting has been challenging.

    1. Clozapine’s Half-Life and Steady-State Concentration: Clozapine has a long half-life (averaging about 12 hours), meaning steady-state concentrations can be reached without strict multiple dosing. Many patients maintain stable blood levels with once-daily dosing, especially at lower doses.
    2. Dose Splitting and Side Effects: Some smaller studies and clinical observations suggest that splitting doses can help reduce peak plasma levels of clozapine, which can be associated with side effects like sedation, hypotension, and dizziness. In these cases, a split dosing regimen may improve tolerability, particularly in patients who experience significant sedation or orthostatic hypotension with a single daily dose.
    3. Metabolic Side Effects and Compliance: In cases where metabolic side effects are of concern, or in patients who may not tolerate high single doses well, dividing doses could help with tolerability, potentially improving compliance and minimizing adverse effects like sedation or metabolic impact.
    4. Seizure Risk: High plasma peaks with a single large dose may theoretically increase the risk of seizures, especially in patients on higher doses of clozapine. Dividing doses is sometimes recommended as a preventive measure to maintain a more consistent blood level, although robust RCT data supporting this specific benefit is lacking.

    While RCT evidence specifically on clozapine dose-splitting remains limited, clinical judgment, patient tolerance, and monitoring of therapeutic blood levels play essential roles in tailoring dose regimens.

  • Raising the Bar: Should Buprenorphine Doses Be Higher to Combat Opioid Use Disorder?

    Raising the Bar: Should Buprenorphine Doses Be Higher to Combat Opioid Use Disorder?

    The study “Association of Daily Doses of Buprenorphine With Urgent Health Care Utilization” explored how different buprenorphine doses affect emergency department (ED) and inpatient service use among individuals with opioid use disorder (OUD).

    1. Higher Doses Associated with Fewer Acute Care Visits: Patients receiving higher doses of buprenorphine (above 16 mg/day) had a longer time to ED or inpatient visits compared to those on lower doses (8-16 mg/day). Those on doses over 24 mg saw a significant reduction in the need for urgent care, particularly related to behavioral health crises.
    2. Implications for Fentanyl Users: The findings are particularly relevant for those using synthetic opioids like fentanyl, which often require higher doses of buprenorphine to manage withdrawal symptoms effectively. These higher doses may reduce acute care needs and improve overall treatment outcomes.
    3. Policy Considerations: The study highlights potential barriers, such as restrictive state laws or insurance limitations, that may prevent patients from accessing higher buprenorphine doses, which could limit effective treatment.

    These results suggest that modifying buprenorphine dosing guidelines could be beneficial, especially as the opioid crisis evolves with the prevalence of fentanyl​

    Link to article: https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2824049

  • Rethinking Antipsychotics: Is It Time to Hit Pause for Schizophrenia Patients

    Rethinking Antipsychotics: Is It Time to Hit Pause for Schizophrenia Patients

    The article “Deprescribing Antipsychotics in Patients with Schizophrenia: Findings from a Specialized Clinic” emphasizes a growing interest in reducing or discontinuing antipsychotic medications in patients with schizophrenia, particularly those stable on long-term treatment. While continuous antipsychotic use is common to prevent relapse, concerns about long-term side effects, such as metabolic give us pause and rise concerns. 

    Key Points:

    1. Benefits of Deprescribing:
      • Reduction in side effects such as weight gain and metabolic syndrome.
      • Potential reversal of tardive dyskinesia.
      • Empowering patients by involving them in shared decision-making, improving adherence and satisfaction.
    2. Risks:
      • The primary risk is relapse, with studies indicating relapse rates between 20-60% after discontinuation.
      • Relapse can lead to hospitalization, job loss, and disrupted relationships.
    3. Strategies for Safe Deprescribing:
      • Individualized Tapering: Gradual reduction in dose is essential, tailored to the patient’s specific needs and history.
      • Relapse Prevention: Engaging support systems (family, mental health teams), monitoring for early signs of relapse, and incorporating psychosocial interventions.
      • Ethical Considerations: Balancing patient autonomy with the duty to minimize harm is a challenge. Encouraging patient participation respects autonomy while ensuring they are aware of risks.

    Future Directions:

    • More research is needed on long-term outcomes of deprescribing, particularly in identifying which patients are the best candidates for safe withdrawal.
    • Clinical guidelines should better integrate recovery-oriented approaches with deprescribing efforts to strike a balance between risk mitigation and promoting patient empowerment​

    link to the article: https://www.cambridge.org/core/journals/psychological-medicine/article/deprescribing-antipsychotics-in-patients-with-schizophrenia-findings-from-a-specialized-clinic/DA2F622FFA9D26A1F119F4F9BC11F2E3

  • Liam Payne and Pink Cocaine: What You Need to Know About the Party Drug

    Liam Payne and Pink Cocaine: What You Need to Know About the Party Drug

    Pink cocaine, also known as tucibi or 2C-B, is a synthetic hallucinogen from the phenethylamine family, first synthesized in the 1970s. Despite the “cocaine” in its street name, it is chemically unrelated to cocaine. It usually comes in powder form but can also be found in tablets. It’s popular in party scenes for its euphoric and stimulant effects, which are often compared to a combination of MDMA and LSD.

    Key Points for Addiction Psychiatrists:

    1. Effects:
      • Euphoria, enhanced sensory perception, hallucinations.
      • At higher doses, it can cause anxiety, paranoia, and dissociation.
      • Effects can last from 4-8 hours depending on the dose and mode of administration (oral, nasal).
    2. Health Risks:
      • Cardiovascular issues, including hypertension and tachycardia.
      • Risk of psychosis and mood disorders, especially with repeated use.
      • Hyperthermia and dehydration, especially in party environments.
      • Possible neurotoxic effects, though research is limited.
    3. Addiction and Dependence:
      • While physical dependence is not common, psychological dependence can develop due to its euphoric effects.
      • Patients may use it in cycles with other substances (e.g., MDMA, alcohol), leading to polysubstance abuse.
    4. Withdrawal:
      • No specific withdrawal syndrome has been documented, but patients may experience depression, anxiety, and cravings after discontinuation.
      • Management may require addressing underlying mental health issues or substance use patterns.
    5. Treatment:
      • Cognitive-behavioral therapy (CBT) or motivational interviewing may help address compulsive use.
      • Monitor for concurrent use of other drugs, especially stimulants or hallucinogens, as polysubstance abuse is common.
      • Referral to harm-reduction programs may be beneficial for patients unwilling to quit completely.
    6. Legal Status:
      • It is illegal in most countries, classified as a Schedule I drug in the U.S. However, enforcement is inconsistent, and it continues to be accessible in underground markets.

    For addiction psychiatrists, it’s crucial to recognize tucibi use, especially in patients with party-drug histories. Understanding the psychological effects and potential for dependence will aid in developing a comprehensive treatment plan. Monitoring for concurrent substance use and educating patients on the risks is key.

  • Is Clozapine Disease Modifying?

    Is Clozapine Disease Modifying?

    This post comes from my real world experience with treating many patients with treatment resistant schizophrenia. I wanted to create a consolidated post that goes over what we know about the benefits of clozapine in schizophrenia treatment as well as what we do not know. Clozapine is unique among antipsychotics due to its superior efficacy in treatment-resistant schizophrenia (TRS), but whether it is disease-modifying remains debated.

    1. Superior Long-term Outcomes in TRS

    • Reduced Relapse Rates: Clozapine has been shown to reduce relapse rates more effectively than other antipsychotics. For instance, a large cohort study found lower rates of rehospitalization for patients on clozapine compared to those on other second-generation antipsychotics (SGAs). The lower relapse rates may suggest stabilization of disease progression.
    • Cognitive Benefits: Several studies report improvements or stabilization in cognitive function in patients on clozapine, which contrasts with the cognitive decline often observed in schizophrenia. The preservation or improvement in cognitive function could indicate a modification of disease trajectory.

    2. Impact on Mortality and Suicidality

    • Reduced Mortality: Long-term use of clozapine has been associated with lower mortality rates in schizophrenia, both due to reduced suicide risk and fewer overall medical complications compared to other antipsychotics.
    • Suicide Prevention: Clozapine is the only antipsychotic shown to significantly reduce suicidality in schizophrenia patients, which may point to broader effects on disease severity and progression.

    3. Neurobiological Effects

    • Neuroprotection: Preclinical and human imaging studies suggest clozapine might have neuroprotective properties. Some animal models and neuroimaging studies indicate that clozapine can increase neurogenesis, reduce oxidative stress, and potentially protect against the neurodegeneration associated with chronic schizophrenia.
    • Synaptic Remodeling: There is some evidence that clozapine might positively influence synaptic plasticity. Studies suggest it might normalize the synaptic dysfunction seen in schizophrenia, which could theoretically have a disease-modifying effect by restoring some aspects of brain connectivity and function.

    4. Delay in Onset of TRS

    • Intervention Timing: There is emerging evidence suggesting that earlier introduction of clozapine (when TRS is identified) might lead to better long-term functional outcomes. This hints that clozapine could modify the disease course if used earlier in resistant cases, though direct evidence of disease modification remains scarce.

    5. Chronicity and Brain Volume Loss

    • Potential for Reduced Brain Volume Loss: Some studies indicate that clozapine may be associated with less gray matter loss over time compared to other antipsychotics. This could imply a reduction in the neuroprogressive aspects of schizophrenia.

    Limitations in Evidence

    While clozapine shows many positive outcomes, definitive evidence proving it is “disease-modifying” remains elusive:

    • Lack of RCTs Focused on Disease Modification: Most clinical trials focus on symptomatic improvement rather than long-term neurobiological changes or functional outcomes.
    • Challenges in Measuring Disease Progression: Schizophrenia is a complex, heterogeneous disorder with no clear biomarkers for progression, making it difficult to measure whether clozapine alters the underlying disease process.

    In summary, while there is compelling evidence that clozapine leads to better long-term outcomes and may have neuroprotective effects, proving it as a true disease-modifying treatment in schizophrenia requires more robust, long-term studies focused specifically on changes in the disease course.