Hyperglycaemia and central obesity disrupt conditioned pain modulation: A single-blind cross-over randomised controlled trial

Di Ye; Timothy J Fairchild; Lechi Vo; Peter D Drummond

doi:10.1016/j.jpain.2024.104553

Hyperglycaemia and central obesity disrupt conditioned pain modulation: A single-blind cross-over randomised controlled trial

J Pain. 2024 May 6:104553. doi: 10.1016/j.jpain.2024.104553. Online ahead of print.

Authors

Di Ye¹, Timothy J Fairchild², Lechi Vo¹, Peter D Drummond³

Affiliations

¹ School of Psychology and Centre for Healthy Ageing, College of Health and Education, Murdoch University, 90 South Street, Murdoch WA 6150, Australia.
² School of Allied Health and Centre for Healthy Ageing, College of Health and Education, Murdoch University, 90 South Street, Murdoch WA 6150, Australia.
³ School of Psychology and Centre for Healthy Ageing, College of Health and Education, Murdoch University, 90 South Street, Murdoch WA 6150, Australia. Electronic address: P.Drummond@murdoch.edu.au.

PMID: 38719155
DOI: 10.1016/j.jpain.2024.104553

Abstract

Hyperglycaemia and high adiposity are risk factors for pain in diabetes. To clarify these links with pain, the effects of a glucose load on sensory detection, pain sensitivity, conditioned pain modulation (primary aims), and autonomic and endothelial functions (secondary aims) were examined in 64 pain-free participants: 22 with normal adiposity (determined by dual-energy X-ray absorptiometry), 29 with high adiposity, and 13 with combined high adiposity and elevated glycated haemoglobin (HbA1c; including prediabetes and type 2 diabetes). Participants ingested either 37.5-g glucose or 200-mg sucralose (taste-matched) in the first session and crossed over to the other substance in the second session one month later. At baseline, painful temple cooling (the conditioning stimulus) inhibited pressure- and heat-pain in the ipsilateral arm (the test stimuli) immediately after cooling ceased (partial η²'s >.32). Glucose ingestion weakened pressure-pain inhibition irrespective of HbA1c levels (partial η² =.11). However, a larger reduction in pressure-pain inhibition after ingesting glucose was associated with a higher waist/hip ratio (r =.31), suggesting a role of central obesity. Heat-pain inhibition was absent at baseline in unmedicated participants with elevated HbA1c, and these participants reported more occlusion-induced pain after ingesting glucose (partial η²'s >.17). Glucose ingestion interfered with parasympathetic activity in all participants (partial η² =.11) but did not affect endothelial function (measured by reactive hyperaemia) or alter other sensations (e.g., feet vibration detection). The disruptive effect of hyperglycaemia on conditioned pain modulation increases in line with central obesity, which might facilitate pain in diabetes. PERSPECTIVE: Ingesting 37.5-g glucose (approximately 350-mL soft drink) interfered with pain modulation in pain-free adults with normal adiposity or with combined high adiposity and HbA1c levels. The interference was stronger alongside increasing central obesity, suggesting that controlling blood glucose and body fat mass might help preserve pain modulation.

Keywords: blood glucose; body fat; heart rate variability; pain modulation; reactive hyperaemia.