Opparounds

The Reinforcement Effect of Social Media Likes in Depression

Mirea D-M, Chen S, Ding J, et al. · JAMA Psychiatry · September 2026

This study examined more than 17 million posts from 7,736 X (Twitter) users across three independent datasets to test whether depression changes how strongly people respond to social approval online. Reinforcement was operationalized simply: how much did receiving likes on one day predict posting again the next day.

Across all three samples, users with a depression diagnosis or higher depressive symptoms showed a stronger reinforcement effect from likes than non-depressed users -- not a blunted one. A preregistered replication tied the effect specifically to a transdiagnostic anxious-depression factor, while a separate compulsivity factor predicted behavioral persistence independent of likes received.

Read the paper →  doi:10.1001/jamapsychiatry.2026.1430

A Randomized Controlled Trial Testing the Effects of Sequential Psychotherapy in Depression: Changing Therapist, or Both Therapist and Method?

Miggiels M, ten Klooster PM, Beekman A, Bremer S, Dekker J, Van HL, van Dijk MK · Journal of Affective Disorders · February 2026

Dutch investigators randomized 163 adults with major depressive disorder who had not responded to an initial 16-session course of CBT or short-term psychodynamic supportive psychotherapy to one of three second-phase strategies: continue with the same therapist and method, switch to a new therapist but keep the method, or switch both therapist and method.

All three groups improved modestly on the IDS-SR by the end of the second phase (mean change -5.23, Cohen's d = 0.29), but there was no significant difference between strategies in symptom reduction, response, or remission rates.

Read the paper →  doi:10.1016/j.jad.2025.120556

Vortioxetine's CYP2D6 Problem Doesn't Show Up Until You Look for It

Vortioxetine is metabolized almost entirely through CYP2D6, and the FDA label reflects it plainly: in confirmed CYP2D6 poor metabolizers, steady-state plasma concentrations run roughly twice those seen in normal metabolizers on the same dose, and the maximum recommended dose drops from 20 mg to 10 mg daily. The same halving applies whenever you add a potent CYP2D6 inhibitor -- bupropion, fluoxetine, paroxetine -- regardless of the patient's own genotype, because the inhibitor phenocopies a poor metabolizer within days.

The trap is that vortioxetine's side-effect profile is nonspecific enough (nausea, dizziness) that clinicians often chase the dose upward before recognizing an exposure problem, since nothing about the presentation screams "genotype." A patient who is intolerant at 10 mg but never actually reached 10-mg-equivalent exposure at a "standard" 20 mg dose is not treatment-resistant -- they were probably overdosed by pharmacokinetics before they were ever adequately assessed at the right exposure. Check the med list for a CYP2D6 inhibitor before concluding vortioxetine failed.

An Enactment Is Data, Not a Failure of Technique

An enactment is not a lapse in neutrality to feel guilty about -- it is the relationship acting out something that cannot yet be said. The patient's transference and the therapist's countertransference combine into a mutually constructed scene: a session runs long, a boundary gets stretched, a joke lands wrong and the therapist responds in kind.

The old technical advice was to avoid enactments entirely through vigilant neutrality; the more useful modern stance is that they are unavoidable and diagnostically rich, because the patient's core relational pattern is usually invisible until it is being lived out between two people rather than described by one. The technical task is not prevention but recognition and use: noticing you have been pulled into a role, tolerating it long enough to understand what it is communicating, then naming the enactment itself -- the fact that something happened between you -- before interpreting what it means.