Reduction of Pressure Pain Sensitivity as Novel Non-pharmacological Therapeutic Approach to Type 2 Diabetes: A Randomized Trial
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Reduction of Pressure Pain Sensitivity as Novel Non-pharmacological Therapeutic Approach to Type 2 Diabetes : A Randomized Trial. / Faber, Jens; Eldrup, Ebbe; Selmer, Christian; Pichat, Caroline; Hecquet, Sofie Korsgaard; Watt, Torquil; Kreiner, Svend; Karpatschof, Benny; Gyntelberg, Finn; Ballegaard, Soren; Gjedde, Albert.
In: Frontiers in Neuroscience, Vol. 15, 613858, 2021.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Reduction of Pressure Pain Sensitivity as Novel Non-pharmacological Therapeutic Approach to Type 2 Diabetes
T2 - A Randomized Trial
AU - Faber, Jens
AU - Eldrup, Ebbe
AU - Selmer, Christian
AU - Pichat, Caroline
AU - Hecquet, Sofie Korsgaard
AU - Watt, Torquil
AU - Kreiner, Svend
AU - Karpatschof, Benny
AU - Gyntelberg, Finn
AU - Ballegaard, Soren
AU - Gjedde, Albert
PY - 2021
Y1 - 2021
N2 - Background: Autonomic nervous system dysfunction (ANSD) is known to affect glucose metabolism in the mammalian body. Tradition holds that glucose homeostasis is regulated by the peripheral nervous system, and contemporary therapeutic intervention reflects this convention.Objectives: The present study tested the role of cerebral regulation of ANSD as consequence of novel understanding of glucose metabolism and treatment target in type 2 diabetes (T2D), suggested by the claim that the pressure pain sensitivity (PPS) of the chest bone periosteum may be a measure of cerebral ANSD.Design: In a randomized controlled trial of 144 patients with T2D, we tested the claim that 6 months of this treatment would reduce PPS and improve peripheral glucose metabolism.Results: In the active treatment group, mean glycated hemoglobin A1c (HbA1c) declined from 53.8 to 50.5 mmol/mol (intragroup p = 0.001), compared with the change from 53.8 to 53.4 mmol/mol in the control group, with the same level of diabetes treatment but not receiving the active treatment (between group p = 0.036). Mean PPS declined from 76.6 to 56.1 units (p <0.001) in the active treatment group and from 77.5 to 72.8 units (p = 0.02; between group p <0.001) in the control group. Changes of PPS and HbA1c were correlated (r = 0.37; p <0.001).Conclusion: We conclude that the proposed approach to treatment of T2D is a potential supplement to conventional therapy.
AB - Background: Autonomic nervous system dysfunction (ANSD) is known to affect glucose metabolism in the mammalian body. Tradition holds that glucose homeostasis is regulated by the peripheral nervous system, and contemporary therapeutic intervention reflects this convention.Objectives: The present study tested the role of cerebral regulation of ANSD as consequence of novel understanding of glucose metabolism and treatment target in type 2 diabetes (T2D), suggested by the claim that the pressure pain sensitivity (PPS) of the chest bone periosteum may be a measure of cerebral ANSD.Design: In a randomized controlled trial of 144 patients with T2D, we tested the claim that 6 months of this treatment would reduce PPS and improve peripheral glucose metabolism.Results: In the active treatment group, mean glycated hemoglobin A1c (HbA1c) declined from 53.8 to 50.5 mmol/mol (intragroup p = 0.001), compared with the change from 53.8 to 53.4 mmol/mol in the control group, with the same level of diabetes treatment but not receiving the active treatment (between group p = 0.036). Mean PPS declined from 76.6 to 56.1 units (p <0.001) in the active treatment group and from 77.5 to 72.8 units (p = 0.02; between group p <0.001) in the control group. Changes of PPS and HbA1c were correlated (r = 0.37; p <0.001).Conclusion: We conclude that the proposed approach to treatment of T2D is a potential supplement to conventional therapy.
KW - type 2 diabetes
KW - glucose homeostasis
KW - glucose control
KW - HbA1c
KW - autonomic dysfunction
KW - non-pharmacological intervention
KW - pressure pain sensitivity
KW - lateral hypothalamus
U2 - 10.3389/fnins.2021.613858
DO - 10.3389/fnins.2021.613858
M3 - Journal article
C2 - 33776633
VL - 15
JO - Frontiers in Neuroscience
JF - Frontiers in Neuroscience
SN - 1662-4548
M1 - 613858
ER -
ID: 259257850