Melatonin supplementation and the effects on clinical and metabolic status in Parkinson's disease: A randomized, double-blind, placebo-controlled trial

Abstract

ObjectiveThis study was performed to evaluate the impact of melatonin supplementation on clinical and metabolic profiles in people with Parkinson's disease (PD). MethodsThis randomized, double-blind, placebo-controlled clinical trial was conducted among 60 patients with PD. Participants were randomly divided into two groups to intake either 10 mg melatonin (two melatonin capsules, 5 mg each) (n = 30) or placebo (n = 30) once a day, 1 h before bedtime for 12 weeks. ResultsMelatonin supplementation significantly reduced the Unified Parkinson's Disease Rating Scale (UPDRS) part I score (β −2.33; 95% CI, −3.57, −1.09; P < 0.001), Pittsburgh Sleep Quality Index (PSQI) (β −1.82; 95% CI, −3.36, −0.27; P = 0.02), Beck Depression Inventory (BDI) (β −3.32; 95% CI, −5.23, −1.41; P = 0.001) and Beck Anxiety Inventory (BAI) (β −2.22; 95% CI, −3.84, −0.60; P = 0.008) compared with the placebo treatment. Compared with the placebo, melatonin supplementation resulted in a significant reduction in serum high sensitivity C-reactive protein (hs-CRP) (β −0.94 mg/L; 95% CI, −1.55, −0.32; P = 0.003) and a significant elevation in plasma total antioxidant capacity (TAC) (β 108.09 mmol/L; 95% CI, 78.21, 137.97; P < 0.001) and total glutathione (GSH) levels (β 77.08 μmol/L; 95% CI, 44.29, 109.86; P < 0.001). Additionally, consuming melatonin significantly decreased serum insulin levels (β −1.79 μIU/mL; 95% CI, −3.12, −0.46; P = 0.009), homeostasis model of assessment-insulin resistance (HOMA-IR) (β −0.47; 95% CI, −0.80, −0.13; P = 0.007), total- (β −13.16 mg/dL; 95% CI, −25.14, −1.17; P = 0.03) and LDL- (β −10.44 mg/dL; 95% CI, −20.55, −0.34; P = 0.04) compared with the placebo. ConclusionsOverall, melatonin supplementation for 12 weeks to patients with PD had favorable effects on the UPDRS part I score, PSQI, BDI, BAI, hs-CRP, TAC, GSH, insulin levels, HOMA-IR, total-, LDL-cholesterol, and gene expression of TNF-α, PPAR-γ and LDLR, but did not affect other metabolic profiles.