University of Udine, Clinica Neurologica, Department of Experimental and Clinical Medical Sciences, Italy.
University of Trieste, Clinica Medica, Department of Medical, Surgical and Health Sciences, Italy.
Clin Nutr. 2015 Dec;34(6):1189-94. doi: 10.1016/j.clnu.2014.12.007. Epub 2014 Dec 23.
The correlation between Parkinson disease and malnutrition is well established, however a protein-restricted diet is usually prescribed because of potentially negative interactions between dietary amino acids and l-dopa pharmacokinetics. This strategy could increase the risk of further nutritional deficits.
A monocentric, prospective, randomized, double-blind pilot study was performed on two groups of Parkinson-affected, protein-restricted, patients: Intervention (n = 7; amino acid supplementation twice daily) and Placebo (n = 7; placebo supplementation twice daily). At enrolment, after 3- and 6-month supplementation, neurological evaluations (UPDRS III, Hoenh-Yahr scale, l-dopa equivalent dose assessment) were performed and blood sample was collected to define insulin sensitivity (QUICKI index) and oxidative stress (oxidized and reduced glutathione). Repeated measure ANCOVA was applied to define time effect and time × treatment interaction.
Participants were comparable at baseline for all assessed parameters. Neurological outcomes and l-dopa requirement were comparable in both group after 6-month of supplementation, without time × treatment interaction. The decrease in insulin sensitivity, as assessed by QUICKI index, observed after 6 months in both groups, was greater in Placebo than in Intervention (time effect p < 0.001; time × treatment interaction p = 0.01). Moreover, despite no changes in total erythrocyte glutathione concentrations, oxidized glutathione levels decreased by 28 ± 17% in the Intervention while increased by 55 ± 38% in Placebo (time effect p = 0.05; time × treatment interaction p = 0.05), after 6-month supplementation.
Amino acid supplementation, assumed with shrewd temporal distribution, did not show detrimental effects on neurological and pharmacological control in protein-restricted Parkinson-affected patients, chronically treated with l-dopa. Furthermore, daily amino acid supplementation partially counteracted insulin resistance development and the loss in antioxidant availability.
帕金森病与营养不良之间存在相关性,这一点已得到充分证实,但是由于饮食氨基酸与左旋多巴药代动力学之间可能存在潜在的相互作用,通常会开出限制蛋白质的饮食处方。这种策略可能会增加进一步出现营养不足的风险。
对两组接受蛋白质限制治疗的帕金森病患者进行了一项单中心、前瞻性、随机、双盲的初步研究:干预组(n = 7;每天两次补充氨基酸)和安慰剂组(n = 7;每天两次补充安慰剂)。在入组时、补充 3 个月和 6 个月后进行神经学评估(UPDRS III、Hoenh-Yahr 量表、左旋多巴等效剂量评估),并采集血样以确定胰岛素敏感性(QUICKI 指数)和氧化应激(氧化和还原型谷胱甘肽)。应用重复测量方差分析来确定时间效应和时间 × 治疗的相互作用。
在所有评估参数方面,两组患者在基线时均具有可比性。补充 6 个月后,两组患者的神经学结果和左旋多巴需求均无差异,且无时间 × 治疗的相互作用。在补充 6 个月后,两组的 QUICKI 指数均观察到胰岛素敏感性下降,安慰剂组的下降幅度大于干预组(时间效应 p < 0.001;时间 × 治疗的相互作用 p = 0.01)。此外,尽管总红细胞谷胱甘肽浓度没有变化,但干预组的氧化型谷胱甘肽水平下降了 28 ± 17%,而安慰剂组则增加了 55 ± 38%(时间效应 p = 0.05;时间 × 治疗的相互作用 p = 0.05)。
在长期接受左旋多巴治疗的蛋白质限制帕金森病患者中,假设以巧妙的时间分布给予氨基酸补充剂,不会对神经和药物控制产生不良影响。此外,每天补充氨基酸部分抵消了胰岛素抵抗的发展和抗氧化剂供应的损失。