Randomized single-blind trial demonstrates that self-acupressure increases beta-endorphin and relieves symptoms in multiple sclerosis, indicating a potential neurochemical mechanism for relief.
BACKGROUND: Multiple sclerosis (MS) is associated with neurochemical alterations, cognitive impairment, and patient-reported symptoms that substantially affect quality of life. Although self-acupressure has shown promise for symptom management, its effects on neuropeptides and cognition remain unclear. This study aimed to evaluate the effects of self-acupressure on beta-endorphin, hypocretin, cognition, and patient-reported outcome measures in individuals with MS. METHODS: A single-center, randomized, single-blind controlled trial was conducted in Türkiye. Ninety-two participants with MS were randomly assigned to an intervention group receiving an 8-week self-acupressure program or a control group receiving standard care. Eighty-two participants completed the study. Primary outcomes were changes in serum beta-endorphin and hypocretin levels. Secondary outcomes included cognitive performance, pain, fatigue, depressive symptoms, and health-related quality of life. RESULTS: Compared with the control group, the intervention group demonstrated a significantly greater increase in beta-endorphin levels (mean change: 56.7 vs. 12.5; P <0.001), whereas no significant between-group difference was observed for hypocretin levels ( P =0.685). Cognitive performance did not differ significantly between groups. However, the intervention group showed significantly greater improvements in pain ( P <0.001), fatigue ( P <0.001), depressive symptoms ( P =0.002), and health-related quality of life ( P =0.016). CONCLUSION: Self-acupressure improved several patient-reported outcomes and increased beta-endorphin levels in people with MS but had no significant effect on hypocretin levels or cognitive performance. These findings support self-acupressure as a feasible complementary nursing intervention for symptom management in MS and suggest that beta-endorphin may represent a potential biological mechanism underlying its therapeutic effects.
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Demir et al. (2026) studied this question.
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