# Emotional Blunting in Hong Kong Patients with Major Depressive Disorder Treated with Vortioxetine: A Naturalistic Observational Study

**Authors:** Yanni Ip Chi Kwan, C. S. Fung, Sharon K. W. Lee, Vivian W. Y. Lui, Calvin P. W. Cheng

PMC · DOI: 10.3390/biomedicines14020270 · Biomedicines · 2026-01-26

## TL;DR

This study examines how vortioxetine affects emotional blunting in Hong Kong patients with depression over eight weeks.

## Contribution

It provides new evidence on vortioxetine's impact on emotional blunting in a real-world clinical setting.

## Key findings

- Emotional blunting decreased from 91.9% at baseline to 73.3% at week 8.
- Depressive symptoms, cognitive dysfunction, and fatigue also improved significantly.
- Anhedonia scores decreased but were not statistically significant.

## Abstract

Background/Objectives: Major Depressive Disorder (MDD) affects over 280 million people worldwide and is a leading cause of disability. Emotional blunting—characterized by a numbing or flattening of emotions—is a significant yet often underrecognized symptom that impairs daily functioning and interpersonal relationships in patients with MDD. It remains unclear whether emotional blunting results primarily from the disorder itself or from antidepressant treatments, especially selective serotonin reuptake inhibitors (SSRIs) and serotonin–norepinephrine reuptake inhibitors (SNRIs). Vortioxetine, a multimodal antidepressant approved for MDD, may help alleviate emotional blunting by modulating neurotransmitters differently than SSRIs. This study investigates the severity of emotional blunting among Hong Kong MDD patients and explores the changes in this symptom with the use of vortioxetine, while also considering anhedonia as a related dimension of reward processing. Methods: This naturalistic, longitudinal observational study in Hong Kong enrolled adults (aged 18 and above) clinically diagnosed with MDD who were initiating vortioxetine treatment for emotional blunting. Patient inclusion was based on independent prescribing decisions by psychiatrists, with informed consent obtained. Data collection comprised one intake interview and the administration of four self-report questionnaires—ODQ, PHQ-9, PDQ-D, SDS, MFI, and SHAPS—at baseline, week 1, week 4, and week 8. Demographic and clinical history data were also recorded. Questionnaires were completed online or via phone, over a study duration of approximately two months. Results: The prevalence of emotional blunting, estimated by the proportion of patients with an ODQ score at or above the clinical cut-off (≥50), was 91.9% at baseline, decreasing to 85.5% at week 1, 77.7% at week 4, and 73.3% at week 8. Significant improvements were also observed in depressive symptoms, cognitive dysfunction, functional impairment, pleasure experience, and fatigue. Conclusions: In this naturalistic observational cohort of patients with MDD who were prescribed vortioxetine, self-reported emotional blunting, depressive symptoms, cognitive dysfunction, functional impairment, and fatigue decreased over eight weeks. Anhedonia scores (SHAPS) decreased to non-significant levels, and clinician-rated Clinical Global Impression scores confirmed a significant reduction in illness severity.

## Linked entities

- **Chemicals:** vortioxetine (PubChem CID 9966051)
- **Diseases:** Major Depressive Disorder (MONDO:0002009)

## Full-text entities

- **Genes:** HTR7 (5-hydroxytryptamine receptor 7) [NCBI Gene 3363] {aka 5-HT7}, HTR3A (5-hydroxytryptamine receptor 3A) [NCBI Gene 3359] {aka 5-HT-3, 5-HT3A, 5-HT3R, 5HT3R, HTR3}, SLC6A4 (solute carrier family 6 member 4) [NCBI Gene 6532] {aka 5-HTT, 5-HTTLPR, 5HTT, HTT, OCD1, SERT}, HTR1B (5-hydroxytryptamine receptor 1B) [NCBI Gene 3351] {aka 5-HT-1B, 5-HT-1D-beta, 5-HT1B, 5-HT1DB, HTR1D2, HTR1DB}, HTR1D (5-hydroxytryptamine receptor 1D) [NCBI Gene 3352] {aka 5-HT1D, HT1DA, HTR1DA, HTRL, RDC4}
- **Diseases:** Deficit (MESH:D009461), MDD (MESH:D003865), Emotional Blunting (MESH:D014949), vomiting (MESH:D014839), cognitive dysfunction (MESH:D003072), nausea (MESH:D009325), Depression (MESH:D003866), FAST (MESH:C563832), cognitive symptoms (MESH:D019954), Fatigue (MESH:D005221), mental disorders (MESH:D001523), impairment (MESH:D060825), diminished motivation (MESH:D015354), anxiety (MESH:D001007), impaired daily functioning (MESH:D020773), injury to (MESH:D014947), inflammatory (MESH:D007249), Anhedonia (MESH:D059445)
- **Chemicals:** agomelatine (MESH:C084711), GABA (MESH:D005680), norepinephrine (MESH:D009638), DA (MESH:D004298), serotonin (MESH:D012701), PDQ (MESH:C061077), acetylcholine (MESH:D000109), Vortioxetine (MESH:D000078784), celecoxib (MESH:D000068579), histamine (MESH:D006632), SNRIs (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

7 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12937620/full.md

## References

37 references — full list in the complete paper: https://tomesphere.com/paper/PMC12937620/full.md

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Source: https://tomesphere.com/paper/PMC12937620