Tag: major depression

  • Psych Meds Are Not the Enemy. Bad Medicine Is

    Psych Meds Are Not the Enemy. Bad Medicine Is

    There is a dangerous difference between criticizing bad psychiatric practice and stigmatizing psychiatric illness.

    I have criticized aspects of psychiatry many times. I believe our field should be open to critique. We should question our prescribing habits. We should challenge lazy diagnosis. We should acknowledge when medications are used too quickly, continued too long, or substituted for the deeper work of psychotherapy, lifestyle change, social support, and careful clinical formulation.

    Psychiatry should never be above criticism.

    But criticism of psychiatric practice is not the same thing as denying the legitimacy of psychiatric illness.

    And right now, that line is being blurred.

    Serious Mental Illness Is Real

    One thing you will never hear me say is that psychiatric disease is not real.

    Schizophrenia is real.
    Bipolar disorder is real.
    Severe major depression is real.
    Catatonia is real.
    Psychotic depression is real.
    Obsessive-compulsive disorder can be profoundly disabling.
    Posttraumatic stress disorder can devastate a person’s life.

    These are not character flaws. They are not weakness. They are not simply failures of lifestyle, discipline, resilience, spirituality, or mindset.

    They are legitimate medical illnesses.

    That does not mean every painful experience is a disease. It does not mean every person who is grieving, anxious, overwhelmed, lonely, or struggling needs a diagnosis or a medication. In fact, one of the most important tasks in psychiatry is knowing the difference.

    Some people need medication.

    Some people need psychotherapy.

    Some people need sleep, exercise, nutrition, structure, social connection, housing, safety, meaning, accountability, or community.

    Many people need several of these at the same time.

    The goal is not to medicalize all suffering. The goal is to recognize real illness when it is present and treat it with the seriousness it deserves.

    The Problem Is Not “Medication”

    Psychiatric medications are often discussed as if they are inherently suspicious.

    But medication is not the enemy.

    Bad medicine is.

    A medication can be life-changing when used for the right condition, in the right person, at the right time, for the right reason.

    The same medication can be harmful when used carelessly, without a clear diagnosis, without follow-up, without discussion of risks and benefits, or without a plan for reassessment.

    That is not unique to psychiatry.

    Antibiotics can be lifesaving, but inappropriate antibiotic use causes harm. Opioids can be appropriate in some clinical contexts, but reckless prescribing devastated communities. Steroids can be powerful tools, but long-term unnecessary use can create major problems.

    The issue is not whether medications are “good” or “bad.”

    The issue is whether we are practicing medicine well.

    Deprescribing Matters, But It Is Not a Mental Health Policy

    Deprescribing is important.

    Every psychiatrist I know has experience reducing, simplifying, or stopping medications when the risks outweigh the benefits or when the original indication no longer makes sense.

    This is not a fringe idea. It is part of daily psychiatric practice.

    We stop medications that are not helping.
    We reduce unnecessary polypharmacy.
    We simplify regimens when possible.
    We monitor side effects.
    We reassess diagnoses.
    We talk with patients about what still makes sense.

    Good psychiatry includes deprescribing.

    But deprescribing alone will not solve the mental health crisis.

    People cannot deprescribe their way out of a lack of psychiatric beds. They cannot deprescribe their way out of months-long waitlists. They cannot deprescribe their way out of poverty, homelessness, trauma, addiction, loneliness, or a collapsing continuum of care.

    And they cannot deprescribe their way out of schizophrenia, mania, catatonia, psychotic depression, or severe melancholic depression.

    When we frame the mental health crisis primarily as a problem of overprescribing, we oversimplify a system failure.

    We ignore the shortage of psychiatrists. We ignore the lack of access to psychotherapy. We ignore inadequate visit times, fragmented care, insurance barriers, emergency departments boarding psychiatric patients for days, and the near disappearance of a true continuum of care.

    Those are not solved by telling people to take fewer medications.

    The Risk of Stigma Dressed Up as Reform

    My concern is not that we are talking about prescribing quality. We should be talking about that.

    My concern is that the rhetoric around psychiatric medications often sends a dangerous message to people who already feel ashamed.

    Many patients with serious mental illness already struggle with the idea of needing medication.

    They worry it means they are weak.
    They worry it means they are broken.
    They worry it means they are dependent.
    They worry it means they are not trying hard enough.
    They worry others will see them differently.

    When public conversations frame psychiatric medications as the central villain, those patients hear something very different from “we need better prescribing.”

    They hear:

    You are dependent.
    You are addicted.
    You are taking the easy way out.
    You should be able to fix this naturally.
    You are the problem.

    That is not empowerment.

    That is stigma.

    And for some patients, that stigma can be dangerous. It can lead people to stop medications abruptly, avoid treatment, disengage from care, relapse, or delay help until a crisis occurs.

    Of course patients should be informed. Of course they should understand risks and benefits. Of course they should have a voice in treatment decisions.

    But informed consent should not become fear-based messaging. And reform should not become another way of shaming people with serious psychiatric illness.

    Better Medicine Means Holding Two Truths

    The future of psychiatry depends on our ability to hold two truths at the same time.

    First, psychiatric illness is real and can be devastating.

    Second, psychiatry must be careful not to overdiagnose, overprescribe, or turn normal human suffering into lifelong pathology.

    Both truths matter.

    If we only emphasize the first, we risk medicalizing everything.

    If we only emphasize the second, we risk abandoning people with serious illness.

    Real psychiatric care lives in the tension between those truths.

    It requires humility. It requires careful diagnosis. It requires honest conversations about uncertainty. It requires medication when appropriate, psychotherapy when appropriate, lifestyle intervention when appropriate, social support when appropriate, neuromodulation when appropriate, and deprescribing when appropriate.

    It also requires us to say clearly that some people need medication, and that needing medication is not a moral failure.

    The Goal Is Better Medicine

    The goal is not to prescribe more.

    The goal is not to prescribe less.

    The goal is to prescribe better.

    Better diagnosis.
    Better informed consent.
    Better follow-up.
    Better access to psychotherapy.
    Better use of lifestyle interventions.
    Better systems of care.
    Better deprescribing when medications are no longer needed.
    Better protection for people whose medications are the reason they are alive, stable, working, parenting, studying, and functioning.

    We do not fix psychiatry by pretending psychiatric medications are always the answer.

    But we also do not fix psychiatry by pretending they are the enemy.

    Psych meds are not the enemy.

    Bad medicine is.

  • 🧠 New Research Alert! 🧠

    🧠 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

  • Can Creatine Boost Therapy for Depression? New Study Says Maybe!

    Can Creatine Boost Therapy for Depression? New Study Says Maybe!

    A recent 8-week double-blind, randomized, placebo-controlled trial investigated whether oral creatine monohydrate (5g/day) could enhance the effects of cognitive-behavioral therapy (CBT) in treating major depressive disorder (MDD)—especially in under-resourced areas where access to treatment is limited.

    🔬 Why Does This Matter?
    While CBT is a gold-standard therapy for depression, many patients do not achieve full remission. This study explored whether creatine—widely used for muscle and brain energy metabolism—could provide an extra boost to treatment.

    🧠 Key Findings:
    ✅ Participants receiving creatine + CBT had greater reductions in depression symptoms (measured by the Hamilton Depression Rating Scale) compared to those receiving placebo + CBT
    ✅ Reported improvements in mood, energy levels, and cognitive function
    ✅ Creatine was well-tolerated, with no significant safety concerns
    ✅ CBT was delivered once weekly by trained therapists

    ⚠️ Study Limitations:
    🔹 Small sample size—larger studies are needed to confirm these findings
    🔹 Short trial duration—long-term effects are still unknown
    🔹 Study population—results may not generalize to all individuals with MDD

    💡 What’s Next?
    If larger studies confirm these results, creatine could become an accessible, affordable adjunct to therapy, particularly in communities with limited mental health resources.

    What do you think? Could a common fitness supplement help improve mental health? Let’s discuss! ⬇️

    link to study: https://www.sciencedirect.com/science/article/pii/S0924977X24007405

  • Gepirone: A New Player in the Antidepressant Arena—Should We Care?

    Gepirone: A New Player in the Antidepressant Arena—Should We Care?

    Gepirone may have flown under the radar for many of us. I’ll admit, it didn’t generate much excitement on my end. However, it recently crossed a significant milestone: FDA approval as an antidepressant. But let’s not overlook its rocky path to getting there—a journey marked by hurdles and setbacks.

    The road to FDA approval for gepirone was anything but smooth. Its initial development began decades ago, but the approval process faced repeated delays and rejections. Questions about efficacy and study designs kept it in limbo for years. What ultimately got it across the finish line was a re-analysis of data demonstrating robust effects in specific populations, particularly those with significant depressive symptoms. This serves as a reminder that persistence and rigorous data reassessment can change the trajectory for medications once thought to have limited potential.

    Now that gepirone is finally available, the big question is: should we care? If so, where does it fit into our treatment algorithms for adult depression?

    With a mechanism targeting the serotonin 1A receptor as a partial agonist, gepirone offers a unique profile compared to SSRIs, SNRIs, and other standard antidepressants. Its anxiolytic effects may make it particularly appealing for patients with co-occurring anxiety. However, like any medication, it isn’t without its downsides.

    Potential side effects include nausea, dizziness, fatigue, and headache. These are generally mild, but it’s important to monitor for tolerability in sensitive patients. Gepirone also carries warnings about potential interactions with other serotonergic agents, raising the risk of serotonin syndrome. While this risk isn’t unique to gepirone, it’s a critical point to keep in mind when integrating it into a treatment plan.

    So, where does gepirone fit? Will it serve as a first-line option for certain patients, or will it find a niche role for those with specific tolerability issues or suboptimal responses to other antidepressants?

    I’d love to hear your thoughts. Is gepirone a tool worth adding to our arsenal, or just another option that might not shift the needle much in clinical practice?

  • 🧠 New Insights into Depression: How the Brain’s “Negativity Bias” Shapes Our Perceptions

    🧠 New Insights into Depression: How the Brain’s “Negativity Bias” Shapes Our Perceptions

    Did you know that in depression, the brain’s wiring can actually amplify negative experiences? Recent research from the Institut Pasteur and collaborators explored this phenomenon, finding that depression alters specific neurons in the amygdala. These changes can reduce activity in neurons that process positive stimuli while overactivating those that process negative stimuli. This “negativity bias” means people with depression often perceive even neutral events through a negative lens.

    In studies with mouse models of depression, activating neurons responsible for positive perceptions helped reduce depressive behaviors. This groundbreaking discovery could pave the way for new treatments aimed at rebalancing these circuits, especially for people who don’t respond to conventional therapies.

    By understanding depression’s effects on the amygdala, researchers hope to develop more targeted and effective therapies for those resistant to current treatments. This is a step toward a more personalized approach to mental health.

    link to the article: https://pmc.ncbi.nlm.nih.gov/articles/PMC10963437/

  • MAOIs: Mechanism of Action, Common Medications, and Side Effects

    MAOIs: Mechanism of Action, Common Medications, and Side Effects

    Mechanism of Action

    Monoamine oxidase inhibitors (MAOIs) are a class of medications primarily used to treat depression. They work by inhibiting the activity of monoamine oxidase enzymes (MAO-A and MAO-B). These enzymes are responsible for breaking down neurotransmitters such as serotonin, norepinephrine, and dopamine in the brain. By inhibiting these enzymes, MAOIs increase the levels of these neurotransmitters, which can help improve mood and alleviate depressive symptoms.

    Common Medications

    1. Phenelzine (Nardil)
    2. Tranylcypromine (Parnate)
    3. Isocarboxazid (Marplan)
    4. Selegiline (Emsam) – Available as a transdermal patch

    Side Effects

    MAOIs can have significant side effects and interactions, which is why they are often not the first choice for treating depression. Some common side effects include:

    1. Hypertensive Crisis: Consuming foods high in tyramine (such as aged cheeses, cured meats, and fermented products) can cause dangerously high blood pressure.
    2. Orthostatic Hypotension: A sudden drop in blood pressure when standing up, leading to dizziness or fainting.
    3. Insomnia: Difficulty falling or staying asleep.
    4. Weight Gain: An increase in body weight over time.
    5. Sexual Dysfunction: Decreased libido, erectile dysfunction, or difficulty achieving orgasm.
    6. Headaches: Frequent or severe headaches.
    7. Edema: Swelling, particularly in the lower limbs.
    8. Fatigue: General feeling of tiredness or lack of energy.
    9. Dry Mouth: Reduced saliva production, leading to a dry sensation in the mouth.

    Precautions

    • Dietary Restrictions: Due to the risk of hypertensive crisis, patients on MAOIs must follow strict dietary restrictions to avoid tyramine-rich foods.
    • Drug Interactions: MAOIs can interact with numerous medications, including over-the-counter drugs, other antidepressants, and certain pain medications, potentially leading to severe or life-threatening conditions.
    • Medical Monitoring: Regular monitoring by a healthcare professional is essential to manage and mitigate potential side effects and interactions.

    MAOIs can be effective for certain patients, particularly those who have not responded to other antidepressant treatments. However, their use requires careful management due to their side effect profile and interaction potential.

  • ECT Maintenance: To Continue or Not To Continue

    ECT Maintenance: To Continue or Not To Continue

    The article on Clinical Outcomes of Continuation and Maintenance Electroconvulsive Therapy (ECT) highlights the role of ECT in preventing relapses in patients with major depressive disorder. Continuation (C-ECT) and maintenance (M-ECT) ECT, when used after an initial successful acute ECT response, are shown to be effective in reducing the recurrence of mood disorders, particularly when combined with pharmacotherapy. Despite its proven benefits, this therapeutic approach is underutilized. Studies also suggest that C-ECT and M-ECT are well-tolerated with no significant cognitive decline​

    Link to the study: https://jamanetwork.com/journals/jamapsychiatry/article-abstract/2823669

  • Oral Extended-Release Ketamine: Beyond the Hype or Just Another Hope?

    Oral Extended-Release Ketamine: Beyond the Hype or Just Another Hope?

    Psychiatry’s fascination with ketamine continues, despite growing evidence that it may not be the miracle treatment some once hoped for. It’s clear that ketamine is not disease-modifying, meaning patients treated for depression with ketamine can still experience relapses. Even more concerning is that ketamine’s effects are short-lived, with the average time to relapse being just 2-4 weeks.

    This brings us to recent studies on oral extended-release ketamine for treatment-resistant depression (TRD). In a proof-of-concept study, twice-weekly dosing of extended-release ketamine showed statistically significant and clinically meaningful improvements in depressive symptoms. The treatment was generally well-tolerated, with a side effect profile that included reduced dissociation and sedation, though there were increases in blood pressure. Having a tablet form of ketamine could make the treatment more accessible, but it also raises concerns about potential abuse and diversion.

    In my view, this is another symptom management tool for patients with TRD. However, the challenge remains that patients will likely need to continue ketamine treatment long-term without a clear dosing regimen. Nonetheless, the results were promising enough to lead to a phase-3 trial using 180 mg doses twice daily.

    Link to article: https://www.nature.com/articles/s41591-024-03063-x

  • 20 Seconds or 60 Seconds: One Doubles Your Chances of Remission

    20 Seconds or 60 Seconds: One Doubles Your Chances of Remission

    In ECT, there’s a common saying that “nothing good happens after 1 minute.” However, recent data suggests that nothing good happens if a seizure lasts less than 20 seconds either. Patients whose seizures lasted 30 seconds or longer during their first ECT session were more than twice as likely to achieve remission by the end of treatment compared to those with seizures under 20 seconds. Seizure durations around one minute appeared to provide the best chances for remission.

  • Why People with Major Depression Don’t Get Better 

    Why People with Major Depression Don’t Get Better 

    When Someone does not experience remission from major depression, we need to ask ourselves why, and come up with new solutions. This discussion will focus on the treatment of these individuals by first explaining what symptoms predict poor response to treatment and what symptoms of major depression result in the most psychosocial dysfunction. 

    What Causes Functional Impairment in Major Depression 

    From the STAR*D study we know that only 50% of patients respond to the first antidepressant treatment and only 33% achieve remission. An important question is why, or more specifically what factors result in poor outcomes. 

    Contrary to popular belief the medications we use to treat depression work well for some neurovegetative symptoms. Symptoms such as sleep, and appetite improve but the most debilitating symptoms often remain. Consistently Anhedonia and concentration are rated by patients with depression as the most debilitating. These cognitive symptoms such as trouble concentrating, difficulty planning, and poor attention lead to dysfunction at home and work. 

    Cognitive Symptoms Impair Work Performance 

    We all need to work to live, and depression is a leading cause of disability and poor work performance worldwide. What we know is that subjective measures of cognitive dysfunction are a better predictor of workplace performance than total depression severity. Someone with more severe overall depression scores may perform better at work than someone with perceived cognitive dysfunction from depression. This is one possible reason for a lack of improvement as many treatments do not address cognitive symptoms. 

    Anhedonia makes everything Worse 

    Possibly the most debilitating symptom of depression is anhedonia. Anhedonia is defined as loss of interest in previously pleasurable activities. A strong predictor of poor antidepressant outcome is the loss of interest. Making anhedonia a primary target of treatment would be wise if we want to improve outcomes in depression. 

    We have additional evidence that indicates how important anhedonia is for psychosocial function. Functional improvement is strongly associated with improvement in anhedonia. The improvement in anhedonia had a larger effect on psychosocial function than overall symptomatic response. 

    Emotional Blunting Effects on Treatment Outcomes 

    While people do not want to be depressed, they also do not want to be emotionally dull. Unfortunately, we know that emotional blunting is reported in nearly half of all depressed patients on antidepressants. This appears to be common to all monoamine antidepressants with bupropion having the lowest reported risk. Emotional blunting cannot be totally accounted for as just a side effect of treatment, it’s also a symptom of depression. However, the point remains the same emotional blunting results in poorer quality of remission. 

    Doctors Are Too Medically Oriented

    The world of psychiatry is very different from other medical specialties. Psychiatry is really art based in science and if you try to approach mental health treatment from a strictly scientific basis you will never help anyone. When patients and physicians are asked to rank the symptoms of depression, they believe are most important, the lists do not match up. 

    Patients focus on restoration of positive affect by ranking things such as meaning and purpose in life, enjoyment in life, satisfaction with oneself as the top three most important things to address in depression. Clearly what should stand out to you here is that medication is unlikely to improve any of these factors. 

    Doctors rank depressed mood, hopelessness, and anhedonia as their top three symptoms to address. These symptoms are far better addressed by medication than the ones listed by patients although you could argue that hopelessness and anhedonia are difficult to treat with medication. 

    The effect of Loneliness on Health Outcomes

    I’ve talked about this before and it continues to be a major concern in our modern world. We are the most connected we have ever been as a society with the advent of social media and the internet, yet no one feels connected. This is an existential crisis for all of us and I haven’t heard many good solutions. Time and time again we go back to the same things such as the internet and social media to feel connected and they continue to let us down. Not only is this emotionally taxing, but it’s also effecting our physical health as well. Here is yet another example of something that is very important for depression treatment outcomes that medication cannot fix. 

    Conclusion

    What does this all mean? Should we stop attempting to use medication for the symptoms of depression? For me these findings indicate we need to screen more carefully for these specific symptoms that result in poor outcomes. We need to improve our psychosocial treatments to help people address ways to enhancing meaning and purpose in their lives. We need to recognize the limitations of medications. Medications have a place and do address some of the symptoms associated with depression, they just aren’t the ones patients believe are most important in their lives.