The Association Between Detailed Obesity Measurements and Peripheral Neuropathy in Persons With Diabetes.
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| Title: | The Association Between Detailed Obesity Measurements and Peripheral Neuropathy in Persons With Diabetes. |
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| Authors: | Reynolds, Evan L. (AUTHOR), Russman, David (AUTHOR), Baskozos, Georgios (AUTHOR), Feldman, Eva L. (AUTHOR), Bennett, David L. (AUTHOR), Callaghan, Brian C. (AUTHOR) |
| Source: | European Journal of Neurology. Dec2025, Vol. 32 Issue 12, p1-15. 15p. |
| Subjects: | Obesity, Diabetes, Peripheral neuropathy, Bioelectric impedance, Diabetic neuropathies, Anthropometry |
| Abstract: | Background: Obesity increases the risk of diabetic peripheral neuropathy (DPN). However, past studies have typically assessed obesity using anthropometric measurements. Our primary aim determined associations between detailed obesity measurements, DPN, and painful DPN (pDPN). Our secondary aim compared the discriminatory capabilities of these measurements. Methods: We performed a cross‐sectional study of persons with diabetes. Obesity was assessed using anthropometrics, bioelectrical impedance (BIA), abdominal MRIs (aMRI), and/or dual x‐ray absorptiometry (DEXA). Obesity measurements were categorized as measuring general, central, or peripheral obesity, or the central‐peripheral obesity ratio. DPN was defined as Michigan Neuropathy Screening Instrument questionnaire ≥ 4. Within this group, pDPN was defined as bilateral foot pain in the prior 3 months. Areas under receiver operating characteristic curves (AUC) determined discriminatory capabilities of obesity measurements for DPN, stratified by sex. Results: We identified 7090 persons with diabetes that completed DPN assessments (mean age: 58.4, 39.6% female), of which 100.0% completed anthropometrics, 98.4% completed BIA, 3.9% completed aMRI, and 2.3% completed DEXA. 1271 (17.9%) had DPN with 28.1% experiencing pDPN. Logistic regression revealed 13/13 anthropometric, 27/29 BIA, 21/34 DEXA, and 8/14 aMRI measurements associated with DPN, but none associated with pDPN. For males, median AUCs for DPN were similar regardless of location (central: 0.88, 0.89, general: 0.89, peripheral: 0.88, central–peripheral ratio: 0.87), whereas for females, central obesity (0.92) had the largest AUC for DPN, followed by general (0.88), peripheral (0.84), and central–peripheral obesity ratio (0.78). Conclusions: Obesity is associated with DPN, but not pDPN. For males, obesity distribution did not differentially discriminate DPN, whereas for females, central obesity best discriminated DPN. [ABSTRACT FROM AUTHOR] |
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| Database: | Psychology and Behavioral Sciences Collection |
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| Abstract: | Background: Obesity increases the risk of diabetic peripheral neuropathy (DPN). However, past studies have typically assessed obesity using anthropometric measurements. Our primary aim determined associations between detailed obesity measurements, DPN, and painful DPN (pDPN). Our secondary aim compared the discriminatory capabilities of these measurements. Methods: We performed a cross‐sectional study of persons with diabetes. Obesity was assessed using anthropometrics, bioelectrical impedance (BIA), abdominal MRIs (aMRI), and/or dual x‐ray absorptiometry (DEXA). Obesity measurements were categorized as measuring general, central, or peripheral obesity, or the central‐peripheral obesity ratio. DPN was defined as Michigan Neuropathy Screening Instrument questionnaire ≥ 4. Within this group, pDPN was defined as bilateral foot pain in the prior 3 months. Areas under receiver operating characteristic curves (AUC) determined discriminatory capabilities of obesity measurements for DPN, stratified by sex. Results: We identified 7090 persons with diabetes that completed DPN assessments (mean age: 58.4, 39.6% female), of which 100.0% completed anthropometrics, 98.4% completed BIA, 3.9% completed aMRI, and 2.3% completed DEXA. 1271 (17.9%) had DPN with 28.1% experiencing pDPN. Logistic regression revealed 13/13 anthropometric, 27/29 BIA, 21/34 DEXA, and 8/14 aMRI measurements associated with DPN, but none associated with pDPN. For males, median AUCs for DPN were similar regardless of location (central: 0.88, 0.89, general: 0.89, peripheral: 0.88, central–peripheral ratio: 0.87), whereas for females, central obesity (0.92) had the largest AUC for DPN, followed by general (0.88), peripheral (0.84), and central–peripheral obesity ratio (0.78). Conclusions: Obesity is associated with DPN, but not pDPN. For males, obesity distribution did not differentially discriminate DPN, whereas for females, central obesity best discriminated DPN. [ABSTRACT FROM AUTHOR] |
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| ISSN: | 13515101 |
| DOI: | 10.1111/ene.70447 |
