Polyneuropathy and Nutrition
October 1, 2017 3 minutes read
By Michael Rubin, MD
Professor of Clinical Neurology, Weill Cornell Medical College
Dr. Rubin reports no financial relationships relevant to this field of study.
SYNOPSIS: Other than the identification of a specific vitamin or essential element deficiency, overall nutritional status does not appear to play any role in the development of idiopathic neuropathies in adults.
SOURCE: Visser NA, Notermans NC, de Vries JHM, et al. The role of nutrition as risk factor for polyneuropathy: A case-control study. J Peripher Nerv Syst 2017; Aug 8. doi: 10.1111/jns.12233. [Epub ahead of print].
Despite in-depth evaluations, a cause is never determined in about 33% of patients with polyneuropathy. Most such patients are older than 50 years of age; usually present with the insidious onset of slowly progressive sensory symptoms including tingling, numbness, burning, or aching discomfort, generally with preserved strength; and often demonstrate an axonal polyneuropathy on electrodiagnostic studies. Implicated, but unproven, are multiple etiologies including abdominal obesity, hypertension, lipid abnormalities, glucose intolerance, or oxidative stress. Visser et al addressed the question regarding polyneuropathy — variously referred to as chronic idiopathic axonal polyneuropathy (CIAP), chronic sensory polyneuropathy, chronic polyneuropathy of undetermined cause, chronic idiopathic polyneuropathy of the elderly, and unclassified peripheral neuropathy — Is nutrition a risk factor for developing polyneuropathy?
The study included all patients referred to the Department of Neurology, University Medical Center Utrecht Neuromuscular Outpatient Unit in The Netherlands, and diagnosed with CIAP between Oct. 1, 2008, and July 1, 2012. Controls for the study were healthy individuals participating in a prospective, population-based amyotrophic lateral sclerosis study in The Netherlands. Patients were excluded if they had a history of diabetes or consumed ≥ 10 g/day of alcohol. All patients underwent a standardized clinical evaluation for polyneuropathy, including history and physical examination, laboratory studies encompassing vitamin levels, lipid profile, celiac serologic screening, nerve conduction studies, and, where indicated, genetic testing, lumbar puncture, chest radiograph, and magnetic resonance imaging. To address nutritional factors, a validated 199-item food frequency questionnaire was completed by patients and controls, covering their intake over the prior month. Enrollees were contacted by phone, where necessary, to supply missing data or clarify inconsistencies. Statistical analyses comprised chi-square testing, Student’s t-test, Mann-Whitney U test, and multivariate binary logistic regression analysis, applying the Benjamini-Hochberg procedure, where necessary, to adjust uncorrected P values.
Among 318 CIAP patients and 636 controls, the mean age of onset was 59.1 years, with 73% demonstrating sensory CIAP and 27% having sensorimotor CIAP. No association with CIAP risk was found with respect to the intake of 28 different nutrients, including carbohydrates, protein, fat, fiber, vitamins, minerals, glutamate, or phytoestrogens, regardless of moderate alcohol intake. Patients with CIAP who drank alcohol had a lower intake of vitamin B2 (riboflavin) and carbohydrates, compared to those with CIAP who did not drink, but B2 levels were not measured and thus its role in the etiology of polyneuropathy could not be addressed. Overall, no difference was found between the two groups regarding energy or nutrient intake, allowing for the conclusion that poor nutrition does not appear to be a risk factor for CIAP.
COMMENTARY
These investigators examined nutrition in otherwise normal persons and found that it played no role in the development of CIAP. However, multiple nutritional deficiencies likely play a central role in the development of neuropathy in patients with a history of alcohol abuse, bariatric surgery, gastrectomy, and anorexia. Both acute and chronic neuropathies have been described in these instances, and nutritional deficiency must be considered in their differential diagnosis, which also includes immune, toxic, infectious, and metabolic etiologies. Appropriate measurements of these various nutrients in the blood should be undertaken before any vitamin or nutritional supplements are prescribed.
Other than the identification of a specific vitamin or essential element deficiency, overall nutritional status does not appear to play any role in the development of idiopathic neuropathies in adults.
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