Shrinks In Sneakers

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  • A Time for Gratitude

    A Time for Gratitude

    Thanksgiving is the perfect opportunity to pause and reflect on the many blessings in our lives. In today’s fast-paced, hyper-connected world, it’s all too easy to fall into the trap of comparison—looking at what others have and wishing we were in their shoes. This mindset often leaves us feeling inadequate, overlooking the beauty of what we already possess.

    But life’s true treasures aren’t found in material possessions or social status—they’re in the little moments that bring us peace, joy, and connection. A quiet morning with the sun streaming through your window. Sharing a cup of coffee and conversation with your significant other. The gift of a healthy body that carries you through each day. The clarity of mind to appreciate it all.

    Today, let’s take a step back from the noise and truly embrace the small things that make life meaningful. Let’s spend time with friends and family, cherishing the laughter, love, and warmth they bring. Let’s acknowledge the present moment and express gratitude for all we have right now—not what we hope to gain tomorrow, but what fills our lives with richness today.

    So, as we gather around the table, let’s give thanks not just for the feast before us but for the everyday blessings that sustain us. May this day remind us to carry gratitude in our hearts, not just on Thanksgiving but throughout the year.

    Happy Thanksgiving to all!

  • Establishing Routine in Bipolar Disorder: A Guide to Social Rhythm Therapy

    Establishing Routine in Bipolar Disorder: A Guide to Social Rhythm Therapy

    Bipolar disorder thrives on disruption, and life can quickly spiral when daily rhythms are inconsistent. Social Rhythm Therapy (SRT) is a powerful, evidence-based approach that helps stabilize mood by anchoring routines. Here’s how it works and why it matters:

    What is Social Rhythm Therapy?
    SRT focuses on regulating daily activities to stabilize the body’s internal clock (circadian rhythms). It combines behavioral strategies with insights into mood patterns, encouraging patients to establish predictable schedules for sleep, meals, social interactions, and exercise.

    Why Does It Work?
    Our biological clocks are sensitive to disruptions. Irregular sleep or eating patterns can trigger mood episodes in bipolar disorder. By synchronizing daily activities with natural rhythms, SRT reduces these disruptions, promoting emotional stability and resilience.

    Core Elements of SRT:

    1. Monitor Social Rhythms: Start by logging your daily activities to identify patterns and areas of inconsistency.
    2. Set Regular Sleep-Wake Times: Consistent sleep routines are the cornerstone of SRT. Aim to go to bed and wake up at the same time every day—even on weekends.
    3. Structure Key Activities: Schedule meals, exercise, and social time at consistent times.
    4. Track Moods: Pair activity tracking with mood journaling to understand how routines impact emotional states.
    5. Anticipate Disruptions: Plan ahead for potential schedule changes (e.g., travel or holidays) to minimize their effects.

    Practical Tips for Success:

    • Start Small: Introduce one new routine at a time to avoid feeling overwhelmed.
    • Enlist Support: Share your goals with friends or family who can help keep you accountable.
    • Be Flexible: Life happens—don’t strive for perfection, but prioritize getting back on track.
    • Combine with Other Treatments: SRT complements medications and psychotherapy, creating a well-rounded treatment plan.

    In my practice, I’ve seen patients experience fewer mood episodes and greater confidence in managing their disorder when they commit to SRT. Establishing a routine isn’t just about organization—it’s about reclaiming control and fostering stability in an unpredictable world.

    If you or someone you know is living with bipolar disorder, consider incorporating Social Rhythm Therapy into their care plan. Small changes can lead to significant improvements in mood and quality of life.

  • Breaking the Benzodiazepine Cycle: Why Long-Term Use Isn’t the Answer to Anxiety

    Breaking the Benzodiazepine Cycle: Why Long-Term Use Isn’t the Answer to Anxiety

    It never ceases to astonish me when I encounter a young patient who has been prescribed 2 mg of alprazolam daily for years under the guise of treating an “anxiety disorder.” The situation becomes even more concerning when they’re simultaneously taking 30 mg of Adderall. Discussing the risks of long-term benzodiazepine use or proposing an evidence-based tapering plan over 6–12 months often elicits a defensive or negative reaction. However, I make it a point to emphasize that my approach is rooted in evidence and science, which do not support the long-term use of benzodiazepines for anxiety disorders. As clinicians, we have a responsibility to address this widespread prescribing practice, educate patients about the associated risks, and prioritize safer, evidence-based treatments.

    RCT Evidence

    1. Duration of Trials:
      • Most RCTs investigating BZDs in anxiety disorders are short-term, typically lasting 4–12 weeks. Very few extend beyond 6 months, leading to a scarcity of long-term controlled data.
    2. Efficacy:
      • BZDs, such as diazepam, alprazolam, and clonazepam, are effective in the short term for managing anxiety symptoms in generalized anxiety disorder (GAD), panic disorder (PD), and social anxiety disorder (SAD).
      • Studies often show comparable short-term efficacy between BZDs and SSRIs or SNRIs, though BZDs act faster.
    3. Tapering and Relapse:
      • Long-term RCTs involving tapering strategies suggest that discontinuation often leads to relapse of anxiety symptoms, which can complicate the interpretation of their role in maintaining anxiety control versus masking symptoms.
      • Some studies (e.g., long-term diazepam use in GAD) found sustained symptom relief in individuals maintained on the medication compared to those tapered off, but these are limited and subject to biases such as withdrawal effects.
    4. Combination with Other Treatments:
      • Some RCTs have explored BZDs as adjunctive therapy, particularly during the initiation of antidepressants, to mitigate early anxiety exacerbation. Long-term data, however, are sparse, and most combination studies focus on the acute phase.

    Concerns with Long-Term Use:

    1. Tolerance and Dependence:
      • Long-term BZD use is associated with tolerance (requiring higher doses for the same effect) and dependence, with withdrawal symptoms often mimicking anxiety.
      • This complicates distinguishing between anxiety relapse and withdrawal during tapering in long-term trials.
    2. Cognitive Effects:
      • Chronic BZD use is linked to potential cognitive impairment, particularly in attention and memory, which may persist even after discontinuation.
    3. Risk of Misuse:
      • Prolonged use carries a risk of misuse, particularly in populations with comorbid substance use disorders.
    4. Lack of Evidence-Based Guidelines:
      • While short-term efficacy is well-documented, there is insufficient RCT evidence to strongly support long-term BZD use as a monotherapy for anxiety disorders.

    Clinical Implications:

    • Indications for Long-Term Use:
      • Long-term use may be justified in select patients, such as those who fail other treatments, have contraindications to antidepressants, or require intermittent use for episodic anxiety (e.g., situational SAD).
    • Guidelines and Best Practices:
      • Professional guidelines typically recommend using BZDs as a short-term bridge or for situational anxietywhile prioritizing SSRIs, SNRIs, or CBT for long-term management.
      • If BZDs are used long-term, clinicians should aim for the lowest effective dose, regularly reassess the risk-benefit ratio, and educate patients about dependence.
  • Clozapine: Unlocking Relief for Negative Symptoms in Schizophrenia

    Clozapine: Unlocking Relief for Negative Symptoms in Schizophrenia

    Clozapine has been studied extensively in schizophrenia, particularly for treatment-resistant cases. Its role in managing negative symptoms (e.g., apathy, alogia, anhedonia, social withdrawal) has been investigated in various randomized controlled trials (RCTs).

    RCT Evidence for Clozapine in Negative Symptoms

    1. Clozapine vs. Typical Antipsychotics
      • Several studies have shown clozapine’s superiority over first-generation antipsychotics (FGAs) like haloperidol in reducing negative symptoms.
      • Example: A landmark RCT (Kane et al., 1988) demonstrated that clozapine not only reduced positive symptoms but also had beneficial effects on negative symptoms, potentially due to its unique pharmacology (e.g., serotonin-dopamine antagonism, NMDA receptor modulation).
    2. Clozapine vs. Other Atypical Antipsychotics
      • Mixed Results: Some RCTs suggest that clozapine is more effective than other atypical antipsychotics (e.g., risperidone or olanzapine) in improving negative symptoms, while others show no significant difference.
      • A meta-analysis of head-to-head RCTs found that while clozapine had modest effects on negative symptoms, differences between it and other atypicals were small.
    3. Clozapine in Primary Negative Symptoms
      • Challenges: True primary negative symptoms (not secondary to positive symptoms, sedation, or depression) are challenging to isolate in trials.
      • Some RCTs highlight that clozapine’s effects on negative symptoms might be indirect, mediated by improvements in positive symptoms, cognitive function, or overall social functioning.
    4. Adjunctive Therapies
      • RCTs combining clozapine with adjuncts like antidepressants (e.g., fluvoxamine) or cognitive enhancers (e.g., aripiprazole, NMDA modulators) have been conducted. While adjunctive strategies show promise, the evidence remains preliminary and inconsistent.

    Potential Mechanism

    Clozapine’s effects on negative symptoms may be attributed to:

    • Serotonin-Dopamine Antagonism: Improved dopamine transmission in the mesocortical pathway.
    • Glutamatergic Modulation: Effects on NMDA and AMPA receptors.
    • Anti-inflammatory Properties: Reduced neuroinflammation may play a role in symptom improvement.
    • Sedation Reduction: Lower propensity for extrapyramidal side effects compared to FGAs.

    Limitations of Evidence

    • Heterogeneity: Most RCTs mix patients with primary and secondary negative symptoms, confounding results.
    • Measurement Challenges: The assessment of negative symptoms in trials is often subjective and prone to bias.
    • Indirect Effects: Improvements may stem from reductions in positive symptoms or cognitive enhancements rather than direct action on negative symptoms.

    Key Takeaway

    Clozapine shows some benefit for negative symptoms, particularly when compared to FGAs and in cases with secondary negative symptoms. However, its effects on primary negative symptoms are modest, and it is generally not considered the first-line choice for this domain of schizophrenia. Adjunctive approaches or newer agents might offer additional promise.

  • Psychiatry: Ahead of the Curve on Singulair’s Neuropsychiatric Risks

    Psychiatry: Ahead of the Curve on Singulair’s Neuropsychiatric Risks

    Psychiatry is often criticized for being “late to the table” when it comes to recognizing the broader impacts of medical treatments. However, in the case of Singulair (montelukast), psychiatry has been aware of its potential neuropsychiatric effects for quite some time.

    Singulair, widely used for asthma and allergic rhinitis, has long been associated with side effects such as mood changes, anxiety, depression, and even suicidality. This connection has been documented for years, yet the broader medical community and regulatory bodies have taken time to fully address these risks.

    Recently, the FDA issued a new warning aimed at heightening awareness of montelukast’s neuropsychiatric side effects. This update emphasizes the importance of assessing the risk-benefit ratio, particularly for patients with mild conditions where alternative treatments may suffice.

    Psychiatry’s Role

    Psychiatrists have long recognized and documented cases where montelukast seemed to exacerbate or trigger psychiatric symptoms. Many of us have seen patients whose mood instability or new-onset anxiety correlated with starting the medication, leading to its discontinuation and subsequent symptom improvement.

    Why This Matters

    This development underscores the value of psychiatry’s vigilance in identifying patterns that might initially go unnoticed in other fields. It’s also a reminder of the importance of collaboration between specialties to ensure patient safety.

    Key Takeaways:

    • Patients and families: Be aware of the potential neuropsychiatric side effects of montelukast. Monitor mood, sleep, and behavior changes closely, especially in children.
    • Clinicians: Always evaluate the necessity of montelukast in mild cases and consider alternatives when possible. Open conversations with patients about these risks can be life-saving.
    • Psychiatrists: Continue advocating for the recognition of neuropsychiatric risks in non-psychiatric medications. Our input is crucial in ensuring patient safety.

    Psychiatry wasn’t late to this table. In fact, we may have set it.

  • Abrupt Discontinuation of Buprenorphine and Risk of Psychosis: Clinical Considerations

    Abrupt Discontinuation of Buprenorphine and Risk of Psychosis: Clinical Considerations

    This post is inspired by a real case from my practice involving a patient with no significant past psychiatric history but a strong history of substance use, including opioids and cocaine. The patient had been on buprenorphine maintenance therapy for several decades, providing stability in their recovery. However, following an abrupt discontinuation of buprenorphine, the patient developed acute psychotic symptoms. This case highlights an uncommon but important phenomenon clinicians should be aware of when managing buprenorphine discontinuation, especially in individuals with a history of substance use.

    Emerging evidence suggests that abrupt discontinuation of buprenorphine may induce psychosis in some individuals, though this appears to be a relatively uncommon occurrence. Here are the key findings:

    Documented Cases

    • New-onset psychotic symptoms have been reported after sudden cessation of buprenorphine in patients with no prior psychosis.
    • Common symptoms include auditory hallucinations, paranoid ideation, and delusions of reference.
    • Psychotic symptoms typically emerge within days to weeks after discontinuation.

    Potential Mechanisms

    1. Loss of buprenorphine’s antipsychotic effects through kappa-opioid receptor antagonism.
    2. Interaction between neurobiological vulnerabilities and the stress of withdrawal.
    3. Possible unmasking of latent psychotic disorders.

    Risk Factors

    • History of substance use.
    • Early adverse life events.
    • Underlying psychiatric conditions (e.g., bipolar disorder).

    Outcomes and Management

    • Symptoms may resolve in weeks to months, though some cases persist longer.
    • Reintroduction of buprenorphine has led to symptom remission in some cases, suggesting a causal relationship.
    • Gradual tapering of buprenorphine might mitigate this risk, though more research is needed.

    Clinical Implications

    Clinicians should remain vigilant when discontinuing buprenorphine, especially in individuals with risk factors for psychosis. A gradual tapering strategy is recommended to reduce potential risks, though further studies are necessary to guide best practices.

    Understanding this phenomenon highlights the importance of individualized care when managing buprenorphine discontinuation in vulnerable populations.

  • Bupropion and Bipolar Depression: Good Idea or Bad Idea 

    Bupropion and Bipolar Depression: Good Idea or Bad Idea 

    Bupropion, an atypical antidepressant with dopaminergic and noradrenergic activity, has been evaluated for use in bipolar depression through several studies, including double-blind, randomized controlled trials (RCTs).

    1. Sachs et al. (2007) – In this multicenter trial, 179 patients with bipolar disorder (bipolar I or II) and depressive episodes were randomized to receive either bupropion, sertraline, or venlafaxine as adjunctive therapy to mood stabilizers (e.g., lithium, valproate) over 26 weeks. The study found that bupropion had a similar efficacy profile to the other antidepressants, with a response rate of about 40%. Importantly, bupropion had a relatively low rate of inducing manic or hypomanic episodes, which was around 7%, lower than venlafaxine but comparable to sertraline.
    2. El-Mallakh et al. (2008) – This smaller study focused on the use of bupropion in bipolar II depression. It suggested that bupropion can effectively reduce depressive symptoms without significantly increasing the risk of switching to mania, although the study size was limited, and larger trials were recommended.
    3. Systematic Reviews and Meta-analyses – A review by Gijsman et al. (2004) included a number of RCTs that assessed antidepressants in bipolar depression. While bupropion was included, the overall conclusion was that the risk of treatment-emergent affective switch (TEAS) was lower compared to tricyclic antidepressants, but comparable to other selective serotonin reuptake inhibitors (SSRIs). However, bupropion was noted for having a more favorable side effect profile, especially concerning sexual dysfunction and weight gain.

    In general, while double-blind RCTs suggest that bupropion can be effective for bipolar depression, its most notable benefit is its relatively low risk of triggering manic episodes compared to other antidepressants. The data supports its use as an adjunct to mood stabilizers, but careful monitoring is still necessary with a mood stabilizing agent in place, as switching to mania, though less frequent, remains a risk.

  • Antidepressants and School Shootings: Debunking Ungrounded Claims in a Complex Crisis

    Antidepressants and School Shootings: Debunking Ungrounded Claims in a Complex Crisis

    In times of societal turmoil, it’s natural for people to search for reasons behind tragedies. However, as scientists and clinicians, it’s our duty to address myths with evidence and guide public discourse toward meaningful solutions. Linking antidepressants to school shootings oversimplifies a multifaceted problem, diverts attention from real issues, and perpetuates harmful misconceptions.

    Understanding the Evidence

    1. FDA Warnings and Black Box Labeling

    • In 2004, the FDA introduced black-box warnings on antidepressants, citing an increased risk of suicidal thoughts and behaviors in individuals under 25 during the early stages of treatment.
    • While well-intentioned, this warning has inadvertently reduced antidepressant use in some cases, leading to untreated depression and potentially worse outcomes.

    2. Aggression and Behavioral Changes

    • Rare case reports describe paradoxical effects like increased irritability or aggression, but these reports are anecdotal and often involve patients who may have undiagnosed conditions, such as bipolar disorder.
    • Case reports represent the lowest level of scientific evidence. They highlight rare phenomena but cannot establish causation.

    3. Lack of Causal Evidence

    • Comprehensive studies and meta-analyses have consistently failed to find a causal link between antidepressants and violent behavior.
    • On a broader scale, antidepressant use is associated with reduced rates of violent crime and suicide, underscoring their therapeutic benefits in managing mental health conditions.

    4. School Shootings: A Multifactorial Crisis

    • These tragic events are exceedingly rare and result from a confluence of factors, including access to firearms, social isolation, trauma, and untreated psychiatric illnesses.
    • Simplistic narratives blaming antidepressants ignore the broader societal and systemic issues at play.

    5. Public Concern and Media Narratives

    • High-profile cases have sometimes involved individuals prescribed antidepressants. However, media narratives often amplify anecdotal links without rigorous scientific backing, fueling public fears unnecessarily.

    Current Recommendations

    • Clinicians continue to weigh the risks and benefits of antidepressants, particularly in younger populations, while emphasizing close monitoring during treatment initiation.
    • Effective treatment typically combines medication with psychotherapy, a holistic approach proven to reduce risks and improve outcomes.

    Call to Action

    Rather than succumbing to fear-driven narratives, we must focus on evidence-based solutions for mental health care, responsible gun ownership, and addressing social determinants of violence. Antidepressants save lives when used appropriately and should not be scapegoated for society’s broader challenges.

    By addressing myths with facts, we can foster more informed and productive discussions on preventing violence and supporting mental health.

  • Hallucinogens: A Trip Not Everyone Should Take

    Hallucinogens: A Trip Not Everyone Should Take

    The recent JAMA Psychiatry study, Emergency Department Visits Involving Hallucinogen Use and Risk of Schizophrenia Spectrum Disorder, explored a notable increase in emergency department (ED) visits related to hallucinogen use, with a focus on potential links to the onset of schizophrenia spectrum disorders.

    Key Findings:

    1. Rise in Hallucinogen-Related ED Visits:
      • The number of ED visits due to hallucinogens, including LSD, psilocybin, and MDMA, has significantly risen, particularly among younger populations. This aligns with changing perceptions of these substances in some parts of society.
    2. Connection to Schizophrenia Spectrum Disorders:
      • Individuals who presented at EDs for hallucinogen-related issues were found to have a higher risk of later developing schizophrenia spectrum disorders. The study suggests a potential association between hallucinogen use and triggering or exacerbating underlying psychiatric vulnerabilities.
    3. Demographic Insights:
      • The rise in hallucinogen use and related health complications appears to disproportionately affect young adults and men. These groups may face greater risks due to higher consumption rates and potential genetic predispositions to mental health disorders.
    4. Clinical Implications:
      • Emergency physicians and mental health professionals are encouraged to screen for hallucinogen use during ED visits, particularly in individuals showing early signs of psychosis. Early identification and intervention may help mitigate long-term mental health outcomes.

    This study emphasizes the importance of public health strategies addressing hallucinogen use, including education on potential risks and the establishment of protocols to identify and treat associated psychiatric conditions.

    Link to the article: https://jamanetwork.com/journals/jamapsychiatry/article-abstract/2825649

  • Beyond Blood Sugar: GLP-1 Agonists Show Promise in Cutting Alcohol Cravings

    Beyond Blood Sugar: GLP-1 Agonists Show Promise in Cutting Alcohol Cravings

    Recent research in JAMA and JCI Insight on repurposing GLP-1 receptor agonists, particularly semaglutide and liraglutide, for Alcohol Use Disorder (AUD) shows promise.

    1. Mechanism of Action: Semaglutide and liraglutide, commonly used to manage diabetes and obesity, activate the GLP-1 receptor, which plays a role in satiety and reward pathways. This activation has shown to suppress the rewarding effects of alcohol, aligning with existing data on the overlap between mechanisms regulating food intake and addictive behaviors.
    2. Preclinical Findings: In rodent models, semaglutide reduced alcohol intake in a dose-dependent manner, with promising results across both binge drinking and alcohol-dependent models. Compared to other GLP-1 agonists, semaglutide’s potent binding and prolonged action make it a strong candidate for further study.
    3. Clinical Potential: The findings provide a foundation for testing semaglutide in clinical trials for people with AUD, where it could potentially serve as an alternative to traditional treatments by targeting alcohol cravings and reducing consumption patterns in those with AUD.

    The promising preclinical data suggests that further investigation could potentially lead to semaglutide as a viable treatment for AUD, adding to the treatment options for substance use disorders that overlap with metabolic disorders. This research is ongoing, and clinical trials may help solidify its role in AUD treatment in the future.