The 72-year-old woman sitting in front of me had spent nearly a decade anxious. Not ordinary stress, not fleeting worry, but the kind of chronic physiologic anxiety that hijacks sleep, amplifies rumination, tightens the chest, and slowly shrinks a person’s world. For over eight years, she had been treated with escalating doses of bupropion, eventually reaching 450 mg daily, the maximum recommended dose. And I found myself returning to a question I believe psychiatry urgently needs to revisit: At what point do we stop and reconsider the original formulation?

Not because bupropion is a bad medication. In many cases, it is an excellent one. I prescribe it often. For the right patient, it can be transformative, improving motivation, energy, concentration, and hypersomnia. It can be particularly helpful in patients with unipolar depression characterized by low drive and psychomotor slowing, and it is sometimes used off-label in ADHD when stimulant treatment is not appropriate.

But pharmacology matters.

Bupropion is a norepinephrine-dopamine reuptake inhibitor. It is activating. In the wrong nervous system, especially at higher doses, that same activation can worsen anxiety, insomnia, agitation, and relentless rumination.

Within one week of beginning a slow taper off bupropion and initiating a very low dose of sertraline, the patient noticed something surprising. Her mind was quieter. Not cured, not transformed overnight, just quieter.

And before the sertraline had even reached a therapeutic dose, an unsettling possibility emerged: What if the treatment itself had become part of the clinical picture?

I wish this were an isolated case. It is not. I see many patients arriving after years of increasingly complex psychiatric interventions, carrying not only diagnoses, but the physiologic consequences of treatment itself.

One woman in her thirties with Bipolar I came to me after years of care within some of the most respected academic psychiatric systems in California. She had developed diabetes after prolonged exposure to second-generation antipsychotics. She now carried chronic kidney disease and hypothyroidism after years of lithium treatment with inadequate surveillance and management. She also developed tardive dyskinesia.

This was not the result of negligent or malicious clinicians. That is what makes these cases harder to discuss honestly. These patients were treated by intelligent, well-trained physicians working within highly regarded systems. Many of the medications prescribed were clinically defensible at one point in time.

But somewhere along the way, reassessment stopped.

I think often about another patient, a man in his early forties who came to me carrying diagnoses of depression, anxiety, ADHD, cognitive dysfunction, and “brain fog.” By the time I met him, he was taking high-dose gabapentin, an SNRI, and an SSRI, in addition to Adderall BID. He was exhausted all the time. He could not work consistently. His thinking felt slow and cloudy. He described feeling disconnected from himself, unable to access motivation or clarity.

And I remember wondering something deceptively simple: How do we distinguish psychiatric illness from medication burden when the two begin to overlap?

Gabapentin can absolutely be useful in select patients. I prescribe it myself in carefully chosen situations. But at 2400 mg daily, cognitive slowing, sedation, fatigue, and brain fog are hardly surprising physiologic possibilities.

Yet somewhere along the way, the side effects themselves appeared to have become folded back into the diagnostic narrative. Fatigue became depression. Cognitive slowing became labeled as part of his ADHD. Emotional flattening became treatment resistance.

And because the patient had lived in this medicated state for years, another problem emerged: He no longer remembered what his baseline nervous system felt like before the regimen.

That may be one of the quietest tragedies in modern psychiatry. Not simply polypharmacy itself, but the gradual loss of reference points. Patients adapt to chronic medication effects so slowly that neither they nor their clinicians can always distinguish illness progression from iatrogenic burden anymore.

And I increasingly believe psychiatry does not merely have a prescribing problem. It has a reassessment problem.

Modern psychiatry often operates under immense pressure: short visits, escalating acuity, limited access to psychotherapy, overloaded systems, insurance constraints, and patients arriving in profound distress asking for relief now. In that environment, medication changes can become reactive rather than reflective.

A patient remains anxious? Increase the dose. Still not sleeping? Add another medication. Mood unstable? Add an augmenting agent. Now there are side effects? Add another medication to manage those.

Over time, treatment plans can acquire a kind of clinical momentum that becomes difficult to interrupt. Each medication may have made sense at the moment it was introduced. Yet years later, some clinicians hesitate to step back and ask the larger question: Does this entire formulation still make biologic and clinical sense?

That question matters because psychiatric symptoms do not exist in isolation from physiology. Sometimes anxiety is activation. Sometimes fatigue is metabolic dysfunction. Sometimes cognitive impairment is polypharmacy. Sometimes agitation is akathisia. Sometimes emotional blunting is over-sedation. Sometimes worsening depression is inflammatory, endocrine, neurologic, or medication-induced. And sometimes “treatment resistance” is actually treatment mismatch.

Medications should exist within a broader framework of ongoing clinical curiosity. Not just “Is the patient symptomatic?” but “Does the treatment still fit the patient sitting in front of us today?”

Because patients change. Physiology changes. Nervous systems change. Medical comorbidities emerge. And medications themselves can alter the very biology we are attempting to stabilize.

Psychiatry desperately needs more humility around long-term treatment trajectories. We need to normalize periodic diagnostic and pharmacologic reassessment, especially in patients accumulating medical complexity, metabolic burden, neurologic symptoms, or diminishing quality of life. We should be asking not only whether a medication once made sense, but whether it still does.

Because sometimes the most dangerous phrase in medicine is: “The patient has been stable on this regimen for years.”

Carrie Friedman is a dual board-certified psychiatric and family nurse practitioner and the founder of Brain Garden Psychiatry in California. She integrates evidence-based psychopharmacology with functional and integrative psychiatry, emphasizing root-cause approaches that connect neuro-nutrition and gut–brain science, metabolic psychiatry, immunology, endocrinology, and mind–body lifestyle medicine. Carrie’s clinical focus bridges conventional psychiatry with holistic strategies to support mental health through nutrition, physiology, and sustainable lifestyle interventions. Her professional writing explores topics such as functional medicine, autism, provider well-being, and medical ethics.