Summary: Suppressing bodily sensations tied to emotions—such as the tightness in the chest or a lump in the throat that comes with sadness—can impede recovery from depression and increase the risk of relapse.
Source: University of Toronto
Sadness often brings vivid bodily sensations—a constricted chest, teary eyes and a raw throat—that can feel both intense and unwelcome.
Norman Farb, an associate professor of psychology at the University of Toronto Mississauga, together with Zindel Segal, a distinguished professor of psychology specializing in mood disorders at U of T Scarborough, report that maintaining awareness of these sensory experiences during stressful moments is essential for long-term well-being, especially for people who have recovered from depression.
In the largest neuroimaging study to date examining psychotherapy to prevent relapse and recurrence of depression, the team found that people with a history of depression are more likely to reduce sensory processing when confronted with emotional stress.
Their findings further show that this sensory shutdown—turning down or ignoring bodily sensation when upset—is associated with a higher likelihood of depressive relapse.
“We naturally try to avoid feeling unpleasant things, but we rarely consider how choosing short-term relief can harm our long-term emotional health,” says Farb.
“Our results clarify why staying in touch with feeling matters. Emotional stress can blunt sensory experience, and reversing that inhibition is an important part of recovery.”
The study, published in NeuroImage: Clinical, was authored by Farb and Segal, along with Ph.D. student Philip Desormeau from U of T Scarborough’s clinical science program and Adam Anderson from Cornell University.
A total of 166 people who had remitted from depression but remained vulnerable to future episodes participated. They were randomized into two treatment arms: an eight-week cognitive therapy program emphasizing well-being, and mindfulness-based cognitive therapy.
Eighty-five participants underwent fMRI scanning between therapy sessions. During scans they watched a series of film clips: neutral content such as lifestyle TV segments for baseline measurement, followed by emotionally charged scenes from a dramatic film. The team then followed all participants with check-ins every two months for two years to track relapse.
Examining the brain scans revealed a striking pattern among those who later relapsed: their brains showed a stronger tendency to “shut down” sensory processing when exposed to sad or dysphoric material.
Importantly, the researchers observed that merely reporting greater sadness during the clips did not predict relapse. Instead, it was the degree to which that sadness coincided with reduced sensory activation that distinguished those who went on to relapse from those who did not.
“What predicted recurrence wasn’t how sad someone felt, but how much that sadness was accompanied by a sensory shutdown,” Farb explains.
When the brain suppresses sensory input during a negative mood, people are left mainly with their thoughts to interpret the situation. Thoughts alone can become narrow and self-reinforcing, trapping individuals inside an “echo chamber” of negative beliefs.
“Thoughts help us hold on to information, but they also require new sensory input to stay updated,” Farb says. “If sensory signals are inhibited, thoughts remain uncorrected and can spiral into worse mood states.”
Segal notes that everyday stressors—such as criticism at work or conflict with a partner—may seem minor, but for someone with a history of depression they can trigger feelings of inadequacy or worthlessness that are compounded when bodily sensations are ignored.
“These negative moods become entangled with self-critical thoughts and bodily sensations. If those sensations are suppressed, the thinking intensifies and can lead to deeper depressive responses,” Segal adds.
The authors suggest that assessing sensory inhibition could become a useful clinical marker to identify individuals at higher risk for relapse. Therapies could be adapted to train people in recovering from depression to notice and integrate bodily sensations throughout daily life, countering the tendency for negative moods to shut down sensation and lock in depressive thought patterns.
“We don’t have to wait until someone is in deep crisis, which demands extensive resources to reverse,” Farb says. “Monitoring for sensory avoidance offers an opportunity to intervene earlier—before job performance or caregiving responsibilities are affected.”
About this depression research news
Author: Kristy Strauss
Source: University of Toronto
Contact: Kristy Strauss – University of Toronto
Image: The image is in the public domain
Original Research: Open access.
“Static and treatment-responsive brain biomarkers of depression relapse vulnerability following prophylactic psychotherapy: Evidence from a randomized control trial” by Norman A.S. Farb et al. NeuroImage: Clinical
Abstract
Static and treatment-responsive brain biomarkers of depression relapse vulnerability following prophylactic psychotherapy: Evidence from a randomized control trial
Background
Neural reactivity to induced dysphoric mood reflects how distress can promote cognitive reactivity and sensory avoidance. Connecting these neural responses to clinical outcomes after recovery from Major Depressive Disorder enhances our understanding of relapse vulnerability and identifies targets for preventive interventions.
Methods
This prospective fMRI study examined the relationship between dysphoric reactivity and relapse after prophylactic psychotherapy. Remitted depressed outpatients (N = 85) were randomized to eight weeks of Cognitive Therapy with a Well-Being focus or Mindfulness-Based Cognitive Therapy. Participants were assessed before and after therapy and followed for two years to determine relapse. Neural responses consistent across assessments were considered static biomarkers of relapse, while changes in reactivity were treated as dynamic biomarkers.
Results
Dysphoric mood induction produced increased prefrontal activation and decreased sensory cortex activity. After controlling for prior episodes, current symptoms and medication, somatosensory deactivation predicted depression recurrence in a stable pattern that did not change with prophylactic treatment (HR 0.04, 95% CI [0.01, 0.14], p < .001). Treatment-related prophylaxis was associated with reduced activation in the left lateral prefrontal cortex (LPFC) (HR 3.73, 95% CI [1.33, 10.46], p = .013). The right LPFC, conversely, demonstrated dysphoria-evoked inhibitory connectivity with the right somatosensory biomarker.
Conclusions
These results support a two-factor model of relapse vulnerability: persistent patterns of dysphoria-induced sensory deactivation increase the risk of recurrence, while vulnerability can be mitigated by targeting prefrontal regions responsive to clinical intervention. Enhancing emotion regulation during remission may benefit from reducing dominant prefrontal cognitive processing in favor of greater sensory representation and integration.