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https://www.psychiatrictimes.com/view/the-diy-psychiatry-movement-potential-threat-to-patient-welfare-and-wellbeing?ekey=RUtJRDpFOTIxNUQyMy03MkY0LTREOEUtQjRBRi1GNEI1RjcyQ0M4ODM%3D&utm_campaign=%25%25emailname&utm_medium=email&_hsenc=p2ANqtz-8yCipP-nw0j59WZH_2ST3hCXfsyUzy_m1fOJLsQtfxV3EqpNigpbIHRyE9XvVPRUSNEPp4UuTMqehDDvuSaH7TDVvPlg&_hsmi=360390508&utm_source=hs

The “DIY” Psychiatry Movement: A Potential Threat to Patient Welfare and Well-Being
Author(s)Katherine Ponte, JD, MBA, Joseph F. Goldberg, MD

COMMENTARY

There has been a surge of attention in the popular media about patients with serious mental illness (SMIs) moving away from traditional psychiatric treatment as a result of dissatisfaction and disaffection with traditional care by mental health experts.1 (See related article Deprescribing: Does the Term Belong in the Psychiatric Lexicon?) Proponents of a do-it-yourself (DIY) approach to managing one’s conditions without professional oversight frequently espouse disbelief that psychotropic medications ease suffering and save lives, claiming that they instead pose more harm than good. The public DIY discourse has included mutual aid platforms2 and services3 offered by people with lived experience who encourage patients to self-educate and procure information from other people with lived experience—not from clinicians—turning to their peers not merely as a support but as a kind of ersatz management approach.

To date, there has been surprisingly little commentary or rebuttal from the patient, caregiver, and practitioner communities in response to the DIY movement, which does not necessarily reflect the views of all or even many people with lived experience. Thus, this collaborative response—coauthored by an individual with SMI lived experience (KP) and a clinical psychopharmacologist (JFG)— aims to provide insight about the merits and shortcomings of DIY mental health management as well as to offer guidance to patients and practitioners about strengthening their collaborative work and minimizing the risk for patient estrangement.

DIY: Born From Paternalistic Medicine

What is meritorious about the arguments raised in the DIY movement? Perhaps most importantly it validates and acknowledges the sentiments of patients who feel disenfranchised from their own care. For example, during KP’s initial 10 years of treatment, there was little if any discussion about diagnosis or medication options, treatment goals or rationales, risks, alternatives, or possible adverse medication consequences beyond a cursory review. Perhaps reflecting the experience of other individuals with SMIs, questions about treatment were essentially deflected, discouraged, dismissed, or reframed as proof of impaired insight about the nature or gravity of a clinical condition.

Nowadays, such paternalistic medicine4 has come under fire for posing ethical conflicts (eg, lack of informed consent). More enlightened thinking has led to the rejection of paternalism (as well as a redirected focus toward patient-centered outcomes research, eg, www.pcori.org). It has also given way to what some authors have called the “new age of patient autonomy.”5

Importantly, for perhaps many people with lived experience, the heritage of paternalistic medicine has left an indelible mark that undermines basic trust in both experts and mainstream treatment, laying a foundation for the DIY movement. Indeed, DIY approaches to mental health self-management carry forth an anti-paternalism message. It can: polarize patients and clinicians; reinforce stigma; rob people of a sense of hope and recovery through effective treatment; and capitalize on individuals’ fears of exploitation. The movement can play on patients’ insecurities, discontent, and feelings of injustice, utterly undermining any spirit of collaboration that otherwise defines the backbone of all good psychiatric treatment: the therapeutic alliance.

Here lies perhaps the most hazardous aspect of rejecting mainstream treatment in favor of a DIY approach: the potential for clinical worsening without professional supervision and oversight. Patients who take matters into their own hands because they are unhappy with their treatment run the risk of clinical deterioration, relapse, disability, displacement from their home environments, and suicide.

Largely absent from the DIY management approach is any suggestion that proper care involves a collaborative endeavor between patient and prescriber. The DIY mindset seems to assume that clinicians could not become stronger allies in the shared effort to manage SMIs and medication adverse events, combat stigma, and help patients strive toward recovery in the fullest sense.

Finding a Happy Medium

A potential compromise could combine mutual aid and peer support, such as that offered by much-needed peer specialists, while developing a strong collaborative relationship with a prescribing clinician. Moreover, the peer support community’s sense of empowerment could help patients appreciate the value of shared decision making and inspire them to pursue a treatment relationship in which their needs are heard, their concerns are addressed, and they are invested in the treatment approach.

For KP, strength and courage from peer support empowered her to persistently advocate for her concerns with her provider. This support ultimately led her to seek a new health care professional when her existing clinician refused her request to taper a medication that had marked adverse events. As a result of her proactive stance, she became more engaged and invested in her care, which set the stage for the path to recovery.6,7

Similarly, it would greatly enhance anti-DIY sentiments if more clinicians adopted a recovery-oriented approach—one that prioritizes the patient’s desired quality of life as opposed to merely managing symptoms. This approach may require clinicians to take calculated risks to help patients achieve the lives they envision.

In KP’s situation, her current provider immediately addressed longstanding concerns that her previous clinician would not acknowledge or address. The positive outcomes were nearly immediate and, consequently, she has been thriving without relapse since 2016.

The Importance of Shared Decision Making

Shared decision-making remains an underutilized modality that significantly improves treatment adherence, outcomes, and patient satisfaction.8 It is a collaborative process in which the patient defines their treatment objectives, the clinician presents options based on their expertise and evidence-based medicine, and together they partner to determine the best course of action.

When patients feel heard and supported in shaping their care, they are more likely to positively receive the treatment that allows them to live their best lives, adhere to treatment, and experience greater satisfaction. Unfortunately, too often patients feel unheard—both by their providers and by families who defer entirely to clinical authority. This dynamic can strain relationships between caregivers and patients, ultimately hindering recovery. And, although current attention is focused on deprescribing, similar attention should be paid to decisions surrounding prescribing agents. Shared decision-making benefits both strategies.

Although patients and medical professionals are often siloed, integrating lived experience into medical research is becoming more common. This approach leads to more relevant studies, improved outcomes, and greater patient engagement and empowerment, highlighting the power of collaboration in health care.

The Allure and Downfall of DIY

The idea of purposefully shunning medication can project a kind of anti-establishmentarian allure. In some circles, deliberately foregoing medication for an SMI can be perceived as portraying resilience and an indomitable spirit (ie, like riding a motorcycle without a helmet). However, that mindset also can reinforce denial and may prevent individuals from considering medication that could alleviate their symptoms and distress.

The DIY approach also runs the risk of promoting medication shaming—making patients feel judged, guilty, or criticized about taking medicines. This, in turn, can drive feelings of failure and foster alienation from treatment, as opposed to the feelings of strength and power over one’s situation when getting proper clinical support. The resulting guilt and shame may also drive a sense of secrecy and fear of harsh reprisals from caregivers or judgmentalism from providers. Overcoming these challenges can be formidable, especially for people who have endured long-term distress from persistent symptoms or disabilities.

If the patient, caregiver, and clinician communities remain silent about the double-edged sword of DIY approaches, that complicity could have many negative consequences: increased widespread deterioration of the doctor-patient relationship (not just in psychiatry, but perhaps in other areas of health care as well); and increased polarization and divisiveness within the mental health community. It could also popularize the abandonment of appropriate care and add to the already alarming escalation of suicide completion rates.9

Moreover, the medication journey for most people with lived experience is highly individualized and vulnerable to misinformation or influential contrarians. Sole reliance on the lived experience of peers, who have their own unique circumstances, incurs potential risk to patient safety and well-being.

Concluding Thoughts

Given these issues and our collaborative care experiences, we offer a list of thoughts and suggestions for fostering a more collaborative approach between patients and their clinicians to use as a guide (Table).

True collaboration between a patient and their clinician is—or should be—a covenant whose sanctity becomes the cornerstone of effective treatment. The growing specter of the DIY movement should be a wake-up call to stakeholders about threats to the integrity of the therapeutic alliance and the need for all parties to work together to safeguard that collaboration.

Ms Ponte is a mental health advocate, author, lived experience recovery coach, and thought leader happily living in recovery from severe bipolar I disorder with psychosis. Dr Goldberg is a clinical professor of psychiatry at The Icahn School of Medicine at Mount Sinai in New York, NY and president of the American Society of Clinical Psychopharmacology.

References

1. Barry E. Leading a Movement Away From Psychiatric Medication. The New York Times. March 24, 2025. Accessed April 7, 2025. https://www.nytimes.com/2025/03/17/health/laura-delano-psychiatric-meds.html

2. Your life. Your story. You choose. The Inner Compass. Accessed April 7, 2025. https://www.theinnercompass.org

3. Delano L. Psychiatric treatment can be limiting. Are you ready to forge a different path? Accessed April 7, 2025. https://www.lauradelano.com/fortify-focus

4. De M. Defining paternalism in medicine. Virtual Mentor. 2004;6(2): virtualmentor.2004.6.2.fred1-0402.

5. Kilbride MK, Joffe S. The new age of patient autonomy: implications for the patient-physician relationship. JAMA. 2018;320(19):1973-1974.

6. Ponte K, Goncalves I. Loving Someone with a Serious Mental Illness: Caring for Your Loved One and Yourself on the Journey to Mental Health Recovery. New Harbinger Publications;2025.

7. Ponte K. Your Mental Health Recovery Workbook. Trigger Publishing; 2023

8. Tian CY, Wong E L-Y, Qiu H, et al. Patient experience and satisfaction with shared decision-making: a cross-sectional study. Patient Educ Couns. 2024;129:108410.

9. Suicide Data and Statistics. Centers for Disease Control and Prevention. March 26, 2025. Accessed April 11, 2025. www.cdc.gov/suicide/facts/data.html

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What’s Your New Name?
November 20, 2024
by Oneka McClellan

"And you will be given a new name by the LORD’s own mouth.” Isaiah 62:2c (NLT)

In the Bible, renaming was a sacred act. It signified that God wanted to change the direction of a person’s life so they could step into His purpose for them.  In Genesis 17:5-6, God spoke to the father of our faith, Abram: “… I am changing your name. It will no longer be Abram. Instead, you will be called Abraham, for you will be the father of many nations. I will make you extremely fruitful. Your descendants will become many nations, and kings will be among them!” (NLT).

Genesis 17:15-16 says, “Regarding Sarai, your wife her name will no longer be Sarai. From now on her name will be Sarah. And I will bless her and give you a son from her! Yes, I will bless her richly, and she will become the mother of many nations. Kings of nations will be among her descendants” (NLT).

“Abram” means “exalted father.” “Abraham” means “father of multitudes.” God was saying to Abram, Not only are you going to be a father, but you’ll be a father to many I’m changing the course of your life! As for Sarah, God changed her name’s meaning from “my princess” to “princess of all.”

You might be carrying all sorts of names today hurtful names from childhood or labels forced on you now. No matter what names you’re carrying, when you accept Christ as your Savior, God has unique, beautiful and wholly true names for you. As God told His people in Isaiah 62:2c, “You will be given a new name by the LORD’s own mouth.”

This is how the God of the universe sees you:

    Loved (Jeremiah 31:3).

    Saved (Ephesians 2:8).

    Redeemed (Galatians 3:13).

    Chosen (1 Peter 2:9).

    Right with God (2 Corinthians 5:21).

    Belonging to God (Isaiah 43:1).

    Daughter of God (Romans 8:16).

    Light of the world (Matthew 5:14).

    Overcomer (1 John 5:4).

These are just a few of the incredible names God has given you!  Sometimes we assume our names can’t change until we live in a new identity. But God changed Abraham and Sarah’s names years before their circumstances changed. Your identity is true and God’s vision for you is real even if you can’t see it exhibited in your current circumstances.  It’s time for us to say, “I’m God’s chosen daughter. He has a plan and purpose for my life. He’s bigger than my circumstances, my thoughts, and the labels the world puts on me. He has given me a brand-new name.”

If you’ve been a slave to your old mindsets or ways of living, God is ready to fill your heart with freedom and truth. He’s erasing those labels, lies and weights that enslave you. When we embrace our God-given names and own our God-given identity, we encourage those around us to do the same. Because God has called us each by name and what beautiful names they are!

https://www.psychiatrictimes.com/view/when-the-fog-doesnt-lift-targeting-cognitive-dysfunction-in-depression?ekey=RUtJRDpFOTIxNUQyMy03MkY0LTREOEUtQjRBRi1GNEI1RjcyQ0M4ODM%3D&utm_campaign=emailname&utm_medium=email&_hsenc=p2ANqtz-_xqo8-8CeBzYeWDGgKMFPVpW-BIgDnf6ko0TaLLwjQGKQ0vb6ccG8oYj-GJ50rniPmNQno5-Pd4OZ_ZlKIZegxCPSSCQ&_hsmi=360069957&utm_source=hs

Publication|Articles|March 24, 2025

Psychiatric Times
Vol 42, Issue 3

When the Fog Doesn’t Lift: Targeting Cognitive Dysfunction in Depression
Author(s)Susannah Murphy, DPhil, MA, MSc

Cognitive symptoms affect between 85% and 94% of patients with major depressive disorder. Despite this prevalence, cognitive dysfunction often remains undertreated and inadequately addressed in routine clinical practice.

SPECIAL REPORT: COGNITION

Clinical Vignette

“Sarah,” a 42-year-old marketing executive, presented with a major depressive episode of moderate severity. After 6 months of treatment with sertraline, her mood had significantly improved. She was sleeping well, had regained her appetite, and reported feeling much more positive about life. However, during follow-up, she expressed ongoing concerns about things at work.

“I can’t seem to keep up anymore,” she explained. “I make mistakes I never used to make, and I can’t focus during important meetings. Even though I do not feel as depressed, my mind feels foggy, and I am forgetting important details.”

Despite achieving remission of core depressive symptoms, Sarah’s persistent cognitive difficulties were threatening her career advancement and contributing to diminished self-esteem. Her case illustrates the common challenge of residual cognitive dysfunction even after successful treatment of mood symptoms in depression.

Incomplete Remission

Cognitive symptoms affect between 85% and 94% of patients with major depressive disorder (MDD), making them nearly ubiquitous in the clinical presentation.1 Despite this prevalence, cognitive dysfunction often remains undertreated and inadequately addressed in routine clinical practice. Growing evidence suggests that problems with cognition are a distinct clinical dimension of depression that are independent from mood symptoms and that may need targeted clinical management.

While diagnostic manuals emphasize problems in concentration, depression is associated with impairments across a much broader range of cognitive domains, including executive function, memory, processing speed, and attention.2 The degree of cognitive dysfunction has been shown to be associated with several clinical features, including severity of depression, age of onset, psychiatric comorbidity, educational background, and number of previous episodes. Cognitive dysfunction has been shown to be more pronounced in patients with recurrent depression.3,4

A particularly concerning aspect of depression treatment is the high rate of incomplete remission, especially regarding cognitive symptoms. Evidence shows that over 70% of patients who respond to selective serotonin reuptake inhibitor (SSRI) treatment continue to experience significant cognitive impairments, even when their mood symptoms have improved.5 These residual symptoms, particularly in domains of memory, concentration, attention, and executive function, present a substantial clinical challenge.

The consequences of untreated cognitive dysfunction are far-reaching. Ongoing cognitive problems are known to be a risk factor for subsequent relapse.6 These symptoms also significantly impact patients’ psychosocial functioning, often presenting greater barriers to occupational recovery than mood symptoms alone. Quality of life measures consistently show that cognitive difficulties interfere with workplace performance, social relationships, and daily functioning, even in patients whose emotional symptoms have improved with treatment.7,8

Current Pharmacological Approaches

Current treatments for depression, whether medication or therapy, produce only minimal improvements in cognitive function. A recent review highlighted that 95% of cognitive problems show little or no meaningful improvement after treatment.9 While a patient’s mood might get better, their ability to think clearly, remember information, and focus on tasks often remains impaired. This analysis also highlighted that with each episode of depression, some cognitive problems may worsen. Like scratches on a record, these scar effects are particularly noticeable in areas like sustained attention and verbal memory. This suggests that early intervention might be crucial in preventing long-term cognitive decline.

There is currently a lack of pharmacological treatments approved by the US Food and Drug Administration (FDA) to treat the cognitive symptoms of depression. SSRIs, while demonstrating reliable efficacy for core depressive symptoms, have shown limited impact on cognitive dysfunction. Meta-analyses of SSRI trials typically demonstrate small effect sizes for cognitive improvement.10,11 However, most benefits appear secondary to mood improvement rather than direct procognitive effects, and many studies do not appropriately control for nonspecific effects that can affect cognitive task performance, such as practice and learning. One large-scale study with a healthy control group (to control for nonspecific effects of repeated testing) reported no significant effect of 8 weeks of antidepressant treatment with sertraline, venlafaxine, or escitalopram on standardized assessments of cognition.12 Taken together, this evidence suggests that traditional SSRI treatment may be insufficient to address the full spectrum of cognitive deficits in MDD.

The multimodal antidepressant vortioxetine appears to have a more direct effect on cognitive symptoms and is the only medicine indicated by the FDA for the treatment of cognition in depression. As well as inhibiting serotonin reuptake, vortioxetine directly modulates serotonin modulator activity (acting as an antagonist at 5-HT3A, 5-HT7, and 5-HT1D receptors, a partial agonist at 5-HT1B receptors, and a full agonist at 5-HT1A receptors). Clinical trials have demonstrated vortioxetine’s ability to improve executive function and learning and memory, with particularly well-replicated effects on the Digit Symbol Substitution Test (a general measure of cognitive impairment that is not specific to any one cognitive domain).13,14 Importantly, path analyses suggest that vortioxetine’s cognitive benefits are, in part, independent of its antidepressant effects, suggesting direct procognitive properties. The magnitude of these effects appears more robust than those observed with conventional SSRIs, although head-to-head comparisons have suggested that its clinical superiority in the treatment of cognitive symptoms is marginal at best.15,16

Beyond serotonin, there is some evidence that modulators of dopamine (eg, bupropion, modafinil), glutamate (eg, ketamine), and acetylcholine (eg, donepezil) may have some positive effects on cognition in individuals with depression, although the extent to which these effects are independent from broader symptomatic improvements is not clear.17

Future Treatment of Symptoms

The development of treatments that effectively target both mood and cognitive symptoms is now recognized as essential for achieving successful long-term remission and functional recovery in depression. More selective targeting of specific serotonin receptors may hold promise in the development of novel treatments. In particular, there is ongoing interest in the potential of selective agonists of the 5-HT1A and 5-HT4 and selective antagonists of the 5-HT6 and 5-HT7 receptors. While there is promising evidence of this potential from animal studies and healthy volunteer studies, clinical evidence is still sparse. There are also some promising novel treatment targets in the pipeline, but they have not yet been tested in placebo-controlled randomized clinical trials in patients, including creatine, α2-adrenergic receptor antagonists, glucagon-like peptide-1 agonists, GABAB receptor agonists, and histamine H3 receptor antagonists.17 Finally, there are a range of nonpharmacological approaches to the treatment of cognition that may hold utility as stand-alone or adjunctive treatment approaches, including neurostimulation (transcranial magnetic stimulation, transcranial direct-current stimulation), cognitive remediation, and physical exercise.18 With renewed interest in this area, and a growing recognition of cognition as a neurobiologically and clinically distinct feature of MDD, there is genuine potential for improving the treatment of cognitive impairment in depression in the future.

Dr Murphy is an associate professor in the Department of Psychiatry at the University of Oxford. Murphy has received consultancy fees from Zogenix, Sumitomo Dainippon Pharma, UCB Pharma, and Janssen Pharmaceuticals. She holds grant income from UCB Pharma, Janssen Pharmaceuticals, and ADM.

References

1. Conradi HJ, Ormel J, de Jonge P. Presence of individual (residual) symptoms during depressive episodes and periods of remission: a 3-year prospective study. Psychol Med. 2011;41(6):1165-1174.

2. Rock PL, Roiser JP, Riedel WJ, Blackwell AD. Cognitive impairment in depression: a systematic review and meta-analysis. Psychol Med. 2014;44(10):2029-2040.

3. Varghese S, Frey BN, Schneider MA, et al. Functional and cognitive impairment in the first episode of depression: a systematic review. Acta Psychiatr Scand. 2022;145(2):156-185.

4. Semkovska M, Quinlivan L, O’Grady T, et al. Cognitive function following a major depressive episode: a systematic review and meta-analysis. Lancet Psychiatry. 2019;6(10):851-861.

5. McClintock SM, Husain MM, Wisniewski SR, et al. Residual symptoms in depressed outpatients who respond by 50% but do not remit to antidepressant medication. J Clin Psychopharmacol. 2011;31(2):180-186.

6. Maeshima H, Baba H, Satomura E, et al. Residual memory impairment in remitted depression may be a predictive factor for recurrence. J Clin Psychiatry. 2016;77(2):247-251.

7. Knight MJ, Air T, Baune BT. The role of cognitive impairment in psychosocial functioning in remitted depression. J Affect Disord. 2018;235:129-134.

8. Knight MJ, Lyrtzis E, Baune BT. The association of cognitive deficits with mental and physical quality of life in major depressive disorder. Compr Psychiatry. 2020;97:152147.

9. Ahern E, White J, Slattery E. Change in cognitive function over the course of major depressive disorder: a systematic review and meta-analysis. Neuropsychol Rev. Published online February 5, 2024.

10. Baune BT, Renger L. Pharmacological and non-pharmacological interventions to improve cognitive dysfunction and functional ability in clinical depression – a systematic review. Psychiatry Res. 2014;219(1):25-50.

11. Keefe RSE, McClintock SM, Roth RM, et al. Cognitive effects of pharmacotherapy for major depressive disorder: a systematic review. J Clin Psychiatry. 2014;75(8):864-876.

12. Shilyansky C, Williams LM, Gyurak A, et al. Effect of antidepressant treatment on cognitive impairments associated with depression: a randomised longitudinal study. Lancet Psychiatry. 2016;3(5):425-435.

13. McIntyre RS, Lophaven S, Olsen CK. A randomized, double-blind, placebo-controlled study of vortioxetine on cognitive function in depressed adults. Int J Neuropsychopharmacol. 2014;17(10):1557-1567.

14. McIntyre RS, Florea I, Tonnoir B, et al. Efficacy of vortioxetine on cognitive functioning in working patients with major depressive disorder. J Clin Psychiatry. 2017;78(1):115-121.

15. Nierenberg AA, Loft H, Olsen CK. Treatment effects on residual cognitive symptoms among partially or fully remitted patients with major depressive disorder: a randomized, double-blinded, exploratory study with vortioxetine. J Affect Disord. 2019;250:35-42.

16. Vieta E, Sluth LB, Olsen CK. The effects of vortioxetine on cognitive dysfunction in patients with inadequate response to current antidepressants in major depressive disorder: a short-term, randomized, double-blind, exploratory study versus escitalopram. J Affect Disord. 2018;227:803-809.

17. Colwell MJ, Tagomori H, Chapman S, et al. Pharmacological targeting of cognitive impairment in depression: recent developments and challenges in human clinical research. Transl Psychiatry. 2022;12(1):484.

18. Pan Z, Park C, Brietzke E, et al. Cognitive impairment in major depressive disorder. CNS Spectr. 2019;24(1):22-29.