EFFECT OF ORAL ZINC SUPPLEMENTATION ON PHASE ANGLE AND BIOIMPEDANCE VECTOR ANALYSIS IN PATIENTS WITH DUCHENNE MUSCULAR DYSTROPHY
Zinc; Bioelectrical Impedance; Cell membrane; Duchenne Muscular Dystrophy; Dietary Supplements.
Zinc is one of the most abundant micronutrients in the human body, playing an important role in the stabilization of structural membranes, integrity and cellular functionality. The literature indicates that oral zinc supplementation offered to healthy children is positively associated with an increase in the phase angle (PA) value and improvement in bioelectrical impedance vector analysis (BIVA). However, there is a lack of studies involving zinc supplementation and its effects on cellular integrity and functionality in people with neurodegenerative diseases, such as Duchenne muscular dystrophy (DMD). This is a neurodegenerative disease that compromises the structure of the muscle membrane, causing loss of muscle mass and strength. Therefore, the objective of this thesis was to evaluate the changes in the PA and BIVA results in patients with DMD after oral zinc supplementation. To achieve this objective, a clinical trial was conducted including 33 boys diagnosed with DMD, aged between 5.6 and 24.5 years. They were grouped according to age (G1, G2 and G3) and supplemented with zinc orally. Before supplementation, the mean serum zinc concentration was 74 μg/dL (12.0) and 29% of the participants had concentrations below the reference value. The baseline values of the parameters of PA, resistance (R) and reactance (Xc) were 2.59° (0.84°), 924.36 (212.31) Ω and 39.64 (8.41) Ω, respectively. After supplementation, an increase in R and a decrease in PA and lean mass proportional to age were observed, in addition to a negative correlation (r = −0.614; p < 0.001) between age and PA. The mean cell mass assessed by BIVA in G1 was greater than that of G3 (p = 0.012). However, no significant differences were found between the groups in serum zinc levels or in bioelectrical impedance parameters after supplementation. We conclude that this population is at risk of zinc deficiency and that the dose of supplementation offered was not sufficient to alter serum zinc and PA values or improve BIVA. Considering the depth and detail of the approach on the functions of zinc and the pathophysiology of DMD, this may serve as a basis for the development and implementation of strategies to prevent and correct zinc deficiency in this population, in addition to encouraging other future studies with higher and safer doses of zinc supplementation