Summary: For decades, the mental health field has operated on a half-truth: that curing depression means removing sadness. A new study argues that the most dangerous part of depression isn’t negative emotion, it’s the absence of positive emotion, known as anhedonia.
Affecting 90% of patients, anhedonia is a primary predictor of suicide and chronic illness. The researchers have introduced Positive Affect Treatment (PAT), a 15-session therapy that ignores “fixing” sadness and instead focuses exclusively on rebuilding the brain’s capacity for joy, motivation, and reward.
Key Facts
- The Treatment Gap: Conventional therapies focus on reducing negative symptoms (anxiety, sadness, fear). PAT shifts the focus to “positive affect,” targeting the brain’s reward system directly.
- Paradoxical Healing: In clinical trials, patients who received PAT improved in both positive and negative measures, even though negative emotions were never addressed during the sessions.
- Hopelessness vs. Helplessness: Lead researcher Alicia E. Meuret distinguishes between the two: “Helplessness” still contains a drive to change; “Hopelessness” (anhedonia) is the belief that nothing can change.
- The Power of Savoring: PAT utilizes specific exercises like “savoring,” gratitude, and loving-kindness to retrain how the brain anticipates and learns from rewarding events.
- Superior Outcomes: In a trial of 98 adults, PAT outperformed conventional therapies in overall clinical status, proving more effective at reducing suicidal behavior and relapse risks.
Source: SMU
Most people know depression as a disorder of sadness. But for millions of patients, the most debilitating feature is something else entirely: the reduced ability or inability to feel positive emotions.
Anhedonia affects nearly 90% of people with major depression. It predicts a longer, more severe course of illness, undermines recovery and is a substantial predictor of suicidal behavior. Anhedonia also appears in anxiety disorders, PTSD, substance use disorders and schizophrenia, yet most conventional treatments do not address it.
For decades, treatment has focused almost entirely on reducing negative emotions, leaving anhedonia largely unaddressed. Patients themselves actually view restoring positive emotion as their primary goal, even more than reducing negative symptoms.
A new study in JAMA Network Open by SMU psychologists Alicia E. Meuret and Thomas Ritz and Michelle G. Craske at UCLA suggests targeting positive emotions directly is a more powerful treatment approach. The research is the culmination of more than a decade of clinical trials examining Positive Affect Treatment, or PAT, a 15-session psychotherapy designed to rebuild patients’ capacity for joy, purpose, motivation and reward.
“There’s a difference between feeling helpless and feeling hopeless,” said Meuret, who leads the Anxiety and Depression Research Center at SMU. “When you feel helpless, you still have the drive and the will to want to change things. When people feel hopeless, they don’t believe anything will change. That’s what anhedonia can look like, and taking away negative emotions doesn’t fix it.”
Targeting the brain’s reward system
PAT was developed to directly target the brain’s reward system, which governs how people anticipate, experience, and learn from positive events. The therapy retrains what researchers describe as the brain’s “positive system” through exercises that re-engage patients with rewarding activities, redirect attention toward positive experiences, and build practices such as gratitude, savoring, and loving-kindness.
Unlike conventional treatments that address negative emotions directly, PAT focuses exclusively on positive affect. That distinction makes its results more striking: patients improved on both positive and negative measures despite the treatment never targeting negativity at all.
In a randomized controlled trial of 98 adults with severe anhedonia, depression and anxiety, PAT produced greater improvements in overall clinical status than a conventional therapy targeting negative affect, an advantage that held at one-month follow-up.
Patients also showed significant reductions in depression and anxiety symptoms. Researchers identified modulation of reward and threat processes as a central mechanism driving those gains.
Reducing key risk factors in depression and anxiety
Targeting impaired reward processing, the researchers concluded, is essential for reducing key risk factors in depression and anxiety, including suicidality and relapse.
“It’s not enough to take away the bad,” Meuret said. “Treatment needs to ask: Is this activity meaningful to you? Will it give you joy or a sense of accomplishment? Does it foster connection?”
The study used 9 measures to track changes in reward sensitivity across three domains: reward anticipation and motivation, response to reward attainment, and reward learning, in addition to 5 threat processing measures, drawn from self-report, behavioral tasks, and physiological assessments. Six of seven self-reported reward and threat measures mediated clinical outcomes. Behavioral and physiological measures did not show the same effect.
Study co-authors include David Rosenfield and Emily Wang of SMU; and Christina Hough of UCLA.
Key Questions Answered:
A: Negative and positive emotions aren’t two sides of a single see-saw; they are controlled by different systems in the brain. You can stop a car from sliding backward (removing negative affect) without ever putting it in “drive” (activating the positive system).
A: PAT uses reward learning. By repeatedly engaging in meaningful activities and intentionally “savoring” even tiny positive moments, patients can slowly rebuild the neural pathways that govern anticipation and motivation. It’s like physical therapy for the brain’s reward center.
A: No, but it means we should stop treating them as the only goals. For patients with severe anhedonia, restoring a sense of accomplishment and connection is often the only way to break the cycle of “hopelessness” that leads to long-term disability and suicide.
Editorial Notes:
- This article was edited by a Neuroscience News editor.
- Journal paper reviewed in full.
- Additional context added by our staff.
About this depression research news
Author: Alicia E. Meuret
Source: SMU
Contact: Alicia E. Meuret – SMU
Image: The image is credited to Neuroscience News
Original Research: Closed access.
“Positive Affect Treatment for Depression, Anxiety, and Low Positive Affect” by Alicia E. Meuret, David Rosenfield, Emily Wang, Christina M. Hough, Thomas Ritz, and Michelle G. Craske. JAMA Network Open
DOI:10.1001/jamanetworkopen.2026.7403
Abstract
Positive Affect Treatment for Depression, Anxiety, and Low Positive Affect
Importance
Targeting impaired reward processing that underlies anhedonia and diminished positive affect is essential for reducing key risk factors in depression and anxiety, including suicidality and relapse. However, mechanistic research in this area remains limited.
Objectives
To assess whether a novel psychosocial intervention engages reward systems more than a mechanistically distinct comparison therapy, and whether alterations in reward and threat processing differentially mediate clinical outcomes.
Design, Setting, and Participants
This was an assessor-blinded, parallel-group, multisite, 2-arm randomized clinical superiority trial. Study recruitment was from December 2021 to January 2024, with final assessment in July 2024. Participants were recruited from academic outpatient treatment centers in Los Angeles, California, and Dallas, Texas, and included treatment-seeking adults with severely low positive affect and moderate to severe depression or anxiety that was functionally impairing. Analyses were conducted with intent-to-treat principles.
Intervention
Participants underwent 15 weekly individual therapy sessions of positive affect treatment (PAT) or negative affect treatment (NAT).
Main Outcomes and Measures
Clinical status was self-reported positive affect (using the Positive and Negative Affect Schedule–Positive subscale), interviewer-rated anhedonia (embedded within the Structured Clinical Interview for the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition), and self-reported depression and anxiety (using the Depression, Anxiety, and Stress Scale). Target measures were 14 self-reported, behavioral, and physiological measures of reward anticipation-motivation, response to reward attainment, reward learning, and threat. Analyses included mixed-effects multilevel models.
Results
In total, 98 participants (mean [SD] age, 32.8 [12.2] years; 65 [66.3%] female) were randomized to receive PAT (n = 51) or NAT (n = 47). Multivariate multilevel model analyses of the 3 clinical status variables as a multivariate outcome showed that clinical status improved more with PAT than NAT (b = −0.06 [95% CI, −0.11 to −0.01]; t3039 = 2.43; P = .02; d = 0.27) and that PAT had better (higher) scores on clinical status than NAT at the 1-month follow-up (b = −0.21 [95% CI, −0.41 to −0.02]; t3039 = 2.11; P = .04; d = 0.21). Improvements in reward anticipation-motivation (b = 0.02 [95% CI, 0.01-0.03]; t1307 = 4.36; P < .001; d = 0.40) and reward attainment (b = 0.04 [95% CI, 0.01-0.06]; t1405 = 3.16; P = .002; d = 0.18) targets were comparable for PAT and NAT. Of 7 reward and threat self-reported target measures, 6 mediated improvements in clinical status, but none of the behavioral or physiological measures did. There was limited evidence for moderated mediation.
Conclusions and Relevance
In this randomized clinical trial of 98 adults with severely low positive affect, depression, and anxiety, findings suggested that modulation of reward and threat processes was a central mechanism of therapeutic improvement, with a reward-focused intervention producing superior clinical outcomes.
Trial Registration
ClinicalTrials.gov Identifier: NCT05203861
