We say we care about mental health in America

We say we care about mental health in America.
But the data—and my front-line experience—say otherwise.

We are overmedicating, underfunding, and pathologizing poverty, trauma, and stress.
Instead of addressing why people are sick, we throw pills at symptoms.

🧠 In my latest article for Psychiatric Times, I make the case that we’ve built a system that profits off disease—not health.
We’re not solving the problem. We’re institutionalizing it.

If we want to make America healthy again, we need to stop doing the wrong things.

👉 Read the full piece here: https://www.psychiatrictimes.com/view/if-we-want-to-make-america-healthy-again-we-are-doing-the-wrong-thing

Is Antidepressant Withdrawal Overhyped? What the Evidence Really Says

In my clinical practice, I’ve often found myself scratching my head over the narrative surrounding antidepressant withdrawal.

I’m not denying that withdrawal is real—it is. And for a small subset of patients, it can be quite distressing. But what I am saying is this: it’s not nearly as common, dramatic, or dangerous as some online circles and sensational stories would have you believe.

I’ve seen countless patients abruptly stop antidepressants and experience no withdrawal symptoms. I’ve also aggressively tapered antidepressants in patients with bipolar disorder to prevent mood destabilization—again, with little to no evidence of withdrawal. This isn’t a one-off observation. It’s a consistent clinical pattern I’ve noted for years. So, I asked myself: What does the data actually say?

The Evidence

A 2024 meta-analysis published in JAMA Psychiatry examined 49 randomized controlled trials and finally gave us some clarity.

The results?
✅ People discontinuing antidepressants reported on average just one more symptom than those who either continued medication or discontinued a placebo.
✅ The most commonly reported symptoms in the first two weeks were dizziness, nausea, vertigo, and nervousness—exactly what I’ve seen clinically.
✅ Critically, the average number of symptoms fell below the threshold for what’s considered a clinically significant discontinuation syndrome.
✅ There was no link between discontinuation and worsening depression, suggesting that if mood symptoms return, it’s likely a relapse—not withdrawal.

Why This Matters

There are vocal groups online—often with clear anti-psychiatry agendas—who focus exclusively on rare, severe cases of withdrawal and present them as the norm. The goal is simple: to scare people away from psychiatry and evidence-based treatment using emotional testimonials instead of clinical reality.

Let’s be honest—those cases do exist, but they are not representative of what most patients experience.

As clinicians, we should remain cautious and responsible. Yes, we should taper medications thoughtfully. Yes, we should prepare patients for the possibility of withdrawal symptoms. But we also shouldn’t scare them into avoiding treatment—or make them feel trapped on medications for life.

Bottom Line

Antidepressant withdrawal can happen. It can be uncomfortable. But it’s rarely severe and almost never dangerous. The fear around it has been overstated by those with an ax to grind. We owe it to our patients to treat based on evidence, not anecdotes.

🧠 Blog Post: The Dark Mirror—How Screen Time Drains Our Mental Health

It’s no secret that screen time affects our mental health—but we still underestimate just how deeply it cuts.

As a psychiatrist, I find myself glued to my phone far more than I’d like. I’m not scrolling TikTok—I’m answering emails, responding to messages, and compulsively checking patient updates. Yet, even in this “productive” digital use, I feel drained. The compulsion to keep checking leaves me feeling hollow and anxious.

Now imagine that same digital pull in the hands of a developing mind.

A recent study in JAMA examined over 4285 adolescents and found a clear link: teens with high levels of addictive digital media use were significantly more likely to report depression, anxiety, and suicidal thoughts.

The connection isn’t surprising. Much of what’s consumed online isn’t educational or uplifting—it’s filtered perfection, highlight reels, and influencer fantasy. The more time spent scrolling, the easier it is to feel like you’re falling behind in life, socially or emotionally.

It’s telling that Steve Jobs famously limited his own children’s access to screens, despite pioneering the very technology we now feel chained to.

This isn’t about demonizing devices—it’s about reclaiming our attention and protecting mental space, especially for young people.

We need digital hygiene just like we need physical hygiene. That means:

  • Setting screen-time boundaries
  • Promoting offline connection
  • Reframing how we compare ourselves to curated content

Mental health isn’t just shaped in the therapy room—it’s shaped by the world we scroll through every day.

Mirtazapine: A unique tool in the antidepressant toolbox

Mirtazapine isn’t your typical SSRI—and that’s exactly why it can be useful in the right context.

✅ When to consider mirtazapine:

  • Depression with insomnia
  • Poor appetite or weight loss
  • Concern about sexual side effects
  • Patients struggling with GI intolerance to SSRIs

⚠️ When to avoid it:

  • Obesity or metabolic syndrome
  • Risk of daytime sedation
  • Orthostatic hypotension history

Mechanistically, it’s a noradrenergic and specific serotonergic antidepressant (NaSSA). It works via alpha-2 autoreceptor blockade, enhancing 5-HT1A transmission while avoiding 5-HT2/3 activity—translating to fewer GI and sexual side effects.

💡 Pro tip:
Sedation is dose-dependent and paradoxical:
Lower doses (7.5–15 mg) = more sedation
Higher doses (30–45 mg) = less sedation

In short, mirtazapine shines in cases where sleep, appetite, or tolerability limit other antidepressants—but use it strategically.

Avoid Tianeptine: FDA Alerts Consumers to Risks

The U.S. Food and Drug Administration (FDA) has issued a critical health warning about the growing availability of tianeptine, a dangerous, unapproved substance being sold as a dietary supplement under names like Zaza, Tianna Red, Pegasus, and others.

Commonly referred to as “gas station heroin”, tianeptine mimics opioid-like effects and is being sold in convenience stores, gas stations, smoke shops, and online—posing serious health risks to the public.

⚠️ Why This Matters:

Tianeptine is not approved for any medical use in the U.S. Despite this, it is widely marketed for supposed benefits like mood enhancement, anxiety relief, or cognitive boost. These claims are not supported by clinical evidence, and the risks are significant.

🩺 Serious Health Risks Associated With Tianeptine:

⚠️ Death, particularly when combined with alcohol or other substances

⚠️ Respiratory depression (slow or stopped breathing)

⚠️ Seizures

⚠️ Loss of consciousness

⚠️ Confusion and agitation

⚠️ Opioid-like withdrawal symptoms

🛑 What You Can Do:

Report adverse reactions to the FDA via MedWatch: https://www.fda.gov/medwatch

Avoid any products labeled as containing tianeptine.

Do not trust unregulated supplements marketed for mental clarity or energy.

📌 Quick Summary:

  • Tianeptine = dangerous, unapproved opioid-like drug
  • Sold as a supplement under names like Zaza or Tianna Red
  • Linked to seizures, coma, and death
  • Avoid these products and warn others
  • Report side effects to the FDA MedWatch Program

The Importance of Distinguishing Suicidal Behaviors

This is the subject of a recent discussion I had with a colleague regarding the differences between a suicide attempt and a suicide gesture. Though these terms are sometimes used interchangeably in casual conversation or even in clinical documentation, they carry fundamentally different meanings—both in terms of patient risk and in how we, as clinicians, should respond.

Our conversation emerged from a case involving a patient with borderline personality disorder who presented to the emergency department after ingesting a small quantity of over-the-counter medication. The intent was unclear. Was this a serious attempt to end her life? Or was it a gesture—an act of desperation without the intention to die, but rather to communicate emotional distress?

The question is not academic. Our interpretation of the event determines our risk formulation, our documentation, our treatment planning, and even how we communicate with the patient and their support system. Yet, it is precisely in these gray areas that clinicians often struggle, and where outdated or stigmatizing language can do real harm.

Defining the Terms: Clinical and Functional Differences

suicide attempt refers to an act of self-harm with at least some intent to die. The degree of lethality may vary, but what distinguishes an attempt is that the individual believed the act could result in death and engaged in it with that goal in mind—even if ambivalence was present. The National Institute of Mental Health (NIMH) and the Columbia-Suicide Severity Rating Scale (C-SSRS) define this with some specificity: any potentially self-injurious behavior with non-zerointent to die, regardless of outcome.

In contrast, a suicidal gesture is a behavior that mimics suicidal behavior or appears life-threatening but is typically not intended to be fatal. The function is often communicative or affect-regulating rather than aimed at death. Classic examples include superficial wrist-cutting, ingesting a sub-lethal dose of medication, or tying a noose but not tightening it. These acts often occur in interpersonal contexts and can be seen as efforts to signal pain, elicit help, or assert control in the face of perceived abandonment.

Why the Distinction Matters

It might be tempting to dismiss suicidal gestures as “attention-seeking” or “manipulative,” but this framing is both clinically dangerous and ethically fraught. Individuals who engage in gestures often experience intense psychological suffering, and repeated gestures are a well-established risk factor for future suicide attempts and completed suicide.

From a risk assessment standpoint, gestures should be taken seriously, especially when they become part of a pattern. While the intent to die may not be present in a given gesture, intent can shift quickly, particularly in individuals with mood disorders, personality pathology, or under the influence of substances.

From a treatment perspective, understanding the function of the behavior—whether it is to relieve affective tension, to communicate distress, or to punish oneself—is crucial to tailoring interventions. For instance, dialectical behavior therapy (DBT) explicitly targets self-harm and suicidal gestures as part of its hierarchy of treatment priorities, recognizing the urgency and potential danger of these behaviors even when lethality is low.

Conclusion: Clarify, Don’t Categorize

Ultimately, the conversation with my colleague reminded me that the real clinical challenge is not to label a behavior as a suicide attempt or a gesture, but to understand its meaning in the life of the patient. Both require empathy, structure, and a willingness to engage with complexity. Whether a patient wants to die or wants their suffering to be seen and acknowledged, both deserve serious clinical attention.

By sharpening our definitions and approaching these behaviors with nuance, we can better serve patients in crisis and avoid the pitfalls of assumptions—especially in emotionally charged clinical environments like emergency rooms, inpatient units, or high-acuity outpatient settings.

EMA Warns of Suicidal Ideation from Finasteride

In a significant update to its safety guidance, the European Medicines Agency (EMA) has officially recognized suicidal ideation as a potential side effect of finasteride. The EMA is urging healthcare professionals to advise patients to stop treatment and seek medical help if they experience depressed mood, depression, or suicidal thoughts while taking the drug.

This decision follows a growing number of reports linking finasteride, particularly in younger men using it for androgenic alopecia (male pattern baldness), to neuropsychiatric side effects. While previous warnings have addressed sexual dysfunction, this marks a critical shift in regulatory focus to mental health.

💊 What Is Finasteride?

Finasteride is a 5α-reductase inhibitor used to treat:

  • Benign prostatic hyperplasia (BPH) in a 5 mg daily dose (Proscar)
  • Male pattern baldness (androgenic alopecia) in a 1 mg daily dose (Propecia)

It works by inhibiting the conversion of testosterone to dihydrotestosterone (DHT)—a potent androgen implicated in hair loss and prostate growth.

⚠️ The EMA’s Updated Warning

The EMA’s Pharmacovigilance Risk Assessment Committee (PRAC) reviewed post-marketing surveillance data and published literature and concluded that:

“There is sufficient evidence to support a causal relationship between finasteride and the risk of suicidal ideation.”

Key recommendations:

  • Suicidal ideation will be added to the drug’s product information as a potential adverse effect.
  • Healthcare professionals should proactively inform patients about this risk.
  • Patients should be advised to discontinue treatment immediately and seek medical advice if they experience changes in mood or mental health.

🧠 Possible Mechanisms Behind Finasteride’s Psychiatric Effects

The exact mechanisms linking finasteride to depression and suicidality remain unclear, but several biological hypotheseshave been proposed:

1. Neurosteroid Depletion

Finasteride inhibits 5α-reductase, which not only converts testosterone to DHT but also helps produce neurosteroids like allopregnanolone and tetrahydrodeoxycorticosterone (THDOC).

  • These neurosteroids have potent GABAergic activity, contributing to anxiolytic and antidepressant effects.
  • Inhibition leads to decreased GABA-A receptor modulation, potentially increasing anxiety, depression, and suicidal thoughts.

2. Hypothalamic-Pituitary-Adrenal (HPA) Axis Dysregulation

Altered steroid metabolism may dysregulate the HPA axis, increasing cortisol levels, a well-known biomarker of depression and suicidal behavior.

3. Persistent Epigenetic Changes

Some animal and human data suggest that finasteride may induce long-lasting changes in gene expression related to stress response and mood regulation, even after discontinuation—supporting the idea of post-finasteride syndrome (PFS).

4. Neuroinflammation

Reduced neurosteroids may increase neuroinflammatory signaling, a growing area of interest in the neurobiology of depression and suicidality.

🧾 Final Thoughts

The EMA’s announcement is a sobering reminder that drugs affecting hormonal pathways can have wide-reaching systemic effects, including on the brain. With better awareness, screening, and patient education, we can minimize harm and support individuals who may be at risk.

Why CBT Reigns as the Top Therapy for Mental Health

🧠💡 CBT Confirmed—Again: Landmark Meta-Analysis Reinforces Clinical Value Across Diagnoses
A massive meta-analysis in JAMA Psychiatry (2025) reaffirms what many of us observe in day-to-day care: Cognitive Behavioral Therapy (CBT) is one of the most effective, versatile, and enduring treatments for adult psychiatric conditions.

🔬 Study at a Glance

  • Pooled data from hundreds of RCTs
  • Assessed CBT’s efficacy across depression, anxiety disorders, PTSD, and eating disorders
  • Found significant, lasting effects across diagnostic categories
  • Highlighted condition-specific variation in effect sizes, but overall CBT consistently outperformed inactive controls

📚 Real-World Relevance
Imagine a patient with chronic panic disorder who’s failed two SSRI trials and prefers non-pharmacologic interventions. CBT remains a frontline solution—equally relevant for the young adult with bulimia or the veteran with PTSD. These aren’t just data points—they’re the cases we see every day.

🔄 How Does CBT Stack Up Against Other Therapies?
While the study primarily focused on CBT, it reinforces existing literature suggesting that CBT often matches or outperforms alternative modalities like psychodynamic therapy or interpersonal therapy in short-term efficacy—especially when structure, time-limited treatment, and measurable goals are critical.

🛠 Implications for Clinical Practice
✅ Why prioritize CBT?

  • It’s highly adaptable
  • Supported across diverse populations
  • Scalable via group therapy, digital tools, and telehealth

🚧 Barriers to Access:

  • Limited availability of trained therapists
  • Insurance coverage gaps
  • Patient preference for “talk therapy” without structure

✅ Strategies to Overcome Them:

  • Integrate CBT-informed principles into brief med management visits
  • Refer to digital CBT platforms when face-to-face access is limited
  • Advocate for reimbursement parity and expanded training programs

📎 Bottom Line
This study isn’t just academic—it’s a call to action. Prioritizing CBT in treatment planning can lead to better outcomes, broader reach, and more durable recovery. As clinicians, it’s on us to ensure our systems support its accessibility.

📖 Full Article:
https://jamanetwork.com/journals/jamapsychiatry/article-abstract/2832696

🧠 Esketamine + Antidepressants in TRD: Does the Combo Matter?

📢 New data from a real-world study of 50,000+ patients with treatment-resistant depression (TRD) published in JAMA Psychiatry:

📌 Study Question:
Does combining esketamine with an SSRI or SNRI affect long-term outcomes in TRD?

📊 Key Findings (5-Year Follow-Up):

  • ✅ Esketamine + SNRI:
     ↘️ Lower all-cause mortality
     ↘️ Fewer hospitalizations
     ↘️ Reduced depressive relapse
  • ✅ Esketamine + SSRI:
     ↘️ Lower incidence of suicide attempts
  • 🔒 Overall: Low rates of adverse outcomes in all groups

💡 Clinical Implications:

  • Not all combinations are equal—pairing matters.
  • Esketamine + SNRI may be preferred for reducing relapse/mortality
  • Esketamine + SSRI may be considered in patients at risk for suicide
  • Personalized treatment decisions can enhance outcomes in TRD

🔍 More than symptom relief—it’s about survival, stability, and safety.

🧠 New Research Alert! 🧠

A study in JAMA Psychiatry explores how functional MRI (fMRI) biomarkers can help distinguish major depressive disorder (MDD) 😔 from healthy individuals. Researchers found that regional homogeneity (ReHo) patterns in the brain are a more reliable marker for MDD than traditional structural MRI 🏗️.

🔬 Why does this matter?
👉 Better Diagnostics: fMRI could lead to more objective ways to diagnose depression, reducing reliance on self-reporting.
👉 Early Detection: One day, brain scans 🏥 might help identify people at risk before symptoms fully develop.
👉 Personalized Treatment: Understanding individual brain patterns could help guide targeted interventions like therapy or medication.

Could brain scans be the future of depression diagnosis? 🤔 Drop your thoughts below! ⬇️

📖 Read more: jamanetwork.com

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