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Reduction of Pressure Pain Sensitivity as Novel Non-pharmacological Therapeutic Approach to Type 2 Diabetes: A Randomized Trial

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@article{cd6e7bf0832a43758b042f3e0cebb3e0,
title = "Reduction of Pressure Pain Sensitivity as Novel Non-pharmacological Therapeutic Approach to Type 2 Diabetes: A Randomized Trial",
abstract = "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.Clinical Trial Registration: www.clinicaltrials.gov (NCT03576430).",
keywords = "autonomic dysfunction, glucose control, glucose homeostasis, HbA1c, lateral hypothalamus, non-pharmacological intervention, pressure pain sensitivity, type 2 diabetes",
author = "Jens Faber and Ebbe Eldrup and Christian Selmer and Caroline Pichat and Hecquet, {Sofie Korsgaard} and Torquil Watt and Svend Kreiner and Benny Karpatschof and Finn Gyntelberg and S{\o}ren Ballegaard and Albert Gjedde",
note = "Funding Information: This work was supported by the Johan Schr{\o}ders Erhvervs-og Familiefond, and Innovation Fund Denmark (Grant Reg. No: 8062-00554B). Funding Information: We are thankful to the staff of the Metabolic Ward O4 at Department of Medicine, Endocrine Unit, Herlev and Gentofte Hospital, for their very valuable contribution concerning the practical issues: Louise Holmberg Storck, Ulla Kjaerulff-Hansen, Marianne S?rensen, Helle R. Christensen, and Syela Azemovski; statistician Tobias Wirenfeldt Klausen for performing the statistical analyses. We also thank Christian Erik Ballegaard for research assistance. Funding. This work was supported by the Johan Schr?ders Erhvervs-og Familiefond, and Innovation Fund Denmark (Grant Reg. No: 8062-00554B). Publisher Copyright: {\textcopyright} Copyright {\textcopyright} 2021 Faber, Eldrup, Selmer, Pichat, Hecquet, Watt, Kreiner, Karpatschof, Gyntelberg, Ballegaard and Gjedde. Copyright: Copyright 2021 Elsevier B.V., All rights reserved.",
year = "2021",
month = mar,
day = "11",
doi = "10.3389/fnins.2021.613858",
language = "English",
volume = "15",
journal = "Frontiers in Neuroscience",
issn = "1662-4548",
publisher = "Frontiers Research Foundation",

}

RIS

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, Søren

AU - Gjedde, Albert

N1 - Funding Information: This work was supported by the Johan Schrøders Erhvervs-og Familiefond, and Innovation Fund Denmark (Grant Reg. No: 8062-00554B). Funding Information: We are thankful to the staff of the Metabolic Ward O4 at Department of Medicine, Endocrine Unit, Herlev and Gentofte Hospital, for their very valuable contribution concerning the practical issues: Louise Holmberg Storck, Ulla Kjaerulff-Hansen, Marianne S?rensen, Helle R. Christensen, and Syela Azemovski; statistician Tobias Wirenfeldt Klausen for performing the statistical analyses. We also thank Christian Erik Ballegaard for research assistance. Funding. This work was supported by the Johan Schr?ders Erhvervs-og Familiefond, and Innovation Fund Denmark (Grant Reg. No: 8062-00554B). Publisher Copyright: © Copyright © 2021 Faber, Eldrup, Selmer, Pichat, Hecquet, Watt, Kreiner, Karpatschof, Gyntelberg, Ballegaard and Gjedde. Copyright: Copyright 2021 Elsevier B.V., All rights reserved.

PY - 2021/3/11

Y1 - 2021/3/11

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.Clinical Trial Registration: www.clinicaltrials.gov (NCT03576430).

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.Clinical Trial Registration: www.clinicaltrials.gov (NCT03576430).

KW - autonomic dysfunction

KW - glucose control

KW - glucose homeostasis

KW - HbA1c

KW - lateral hypothalamus

KW - non-pharmacological intervention

KW - pressure pain sensitivity

KW - type 2 diabetes

UR - http://www.scopus.com/inward/record.url?scp=85103329240&partnerID=8YFLogxK

U2 - 10.3389/fnins.2021.613858

DO - 10.3389/fnins.2021.613858

M3 - Journal article

C2 - 33776633

AN - SCOPUS:85103329240

VL - 15

JO - Frontiers in Neuroscience

JF - Frontiers in Neuroscience

SN - 1662-4548

M1 - 613858

ER -

ID: 67032981