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Ylitalo, K., W. Herman, and Sioban D. Harlow. 2013. "Serial anthropometry predicts peripheral nerve dysfunction in a community cohort." Diabetes/Metabolism Research and Reviews, 29(2): 145-51.
BACKGROUND: Obesity is a risk factor for glucose intolerance, but the independent role of obesity in the development of peripheral neuropathy is unclear. This study assessed the impact of body size trajectories on prevalent nerve dysfunction in community-dwelling women with and without glucose intolerance. METHODS: Annual (1996-2008) anthropometric measures of weight, height, waist circumference and body mass index [BMI, weight (kg)/height (m(2) )] were assessed in the Study of Women's Health Across the Nation - Michigan site. Glucose intolerance was defined annually on the basis of current use of diabetes medications, self-reported diabetes diagnosis and, when available, fasting glucose. Peripheral nerve dysfunction in 2008 was defined as abnormal monofilament testing or >/=4 symptoms or signs. Linear mixed models were used to determine trajectories of anthropometry by subsequently identified nerve dysfunction status. RESULTS: Mean BMI was 32.4 kg/m(2) at baseline, and 27.8% of the women had nerve dysfunction in 2008. BMI, weight and waist circumference increased over time. Women who would have nerve dysfunction were significantly larger than women without dysfunction, independent of glucose intolerance. At mean baseline age of 46, BMI, weight and waist circumference differed significantly (p-value < 0.01) by subsequent nerve dysfunction status, independent of glucose intolerance and hypertension. These body size differences were maintained but not exacerbated over time. CONCLUSIONS: Peripheral nerve dysfunction is prevalent among community-dwelling women. Twelve years before the nerve assessment, anthropometry differed between women who would and would not have nerve dysfunction, differences that were maintained over time. Obesity deserves attention as an important and potentially modifiable risk factor for peripheral nerve dysfunction. Copyright (c) 2012 John Wiley & Sons, Ltd.
PMCID: PMC3565056. (Pub Med Central)