Magnesium Research


Long term magnesium supplementation influences favourably the natural evolution of neuropathy in Mg‐depleted type 1 diabetic patients (T1dm) Volume 17, issue 2, June 2004


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Department Diabetology, Metabolism and Clinical nutrition, University Hospital Antwerp, Belgium

Chronic Mg depletion in T1dm has been linked to polyneuropathy (PNP). Short term Mg supplementation has suggested a decrease in pathological EMG signs typical for PNP. The aim of this study is to determine if long term supplementation under stable metabolic control can normalize the Mg status and influence the natural evolution of PNP. 110 T1dm (60 M,50 W) with chronic Mg depletion (erythrocyte Mg < 2.3 mMol\l) were randomised to receive 300 mg Mg++ daily or no supplement for a period of 5 years. Follow‐up was organized by the same diabetologist: HbA1c, renal function and Mg status every 3 months, electromyography (EMG) and clinical neurological control with staging every year. Drop‐out was decided for recurrent DKA, diseases or drugs interfering with Mg status or side‐effects of Mg treatment. 97 patients (53 M,44 W) finished the study: 49 (27 M,22W) were supplemented (group A) and 48 (26 M,22 W) served as controls (group B). At the start there were no significant differences between both groups. HbA1c after 5 years (A:7.80% sd 0.80, B:7.75% sd 0.75) was not significantly different from the start. Erythrocyte Mg (Mg rbc) rose significantly (p < 0.0001) in group A to normal levels but remained low in group B. Staging of PNP after 5 years shows a decrease in 39%, statu quo in 49% and a worsening in 12% in group A and 8,31 and 61% respectively in group B (Fisher Exact test: p < 0.0001). Normalization of EMG signs was only seen in incipient PNP. Logistic regression analysis shows that longer duration of diabetes (p < 0.006) and low Mgrbc (p < 0.05) are the major determinants of PNP evolution. Under stable metabolic control long term Mg supplementation is able to restore a normal Mg status and influence favourably the natural evolution of PNP as compared to non supplemented T1dm controls.