Department of Nutrition and Dietetics, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam Public Health research institute, PO Box 7057, 1007 MB, Amsterdam, The Netherlands.
Alzheimer Center Amsterdam, Department of Neurology, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, PO Box 7057, 1007 MB, Amsterdam, The Netherlands.
Alzheimers Res Ther. 2020 Sep 26;12(1):116. doi: 10.1186/s13195-020-00687-2.
Malnutrition is common in patients with Alzheimer's disease (AD) dementia and mild cognitive impairment (MCI) and is associated with institutionalization and increased mortality. Malnutrition is the result of a negative energy balance, which could be due to reduced dietary intake and/or higher energy expenditure. To study underlying mechanisms for malnutrition, we investigated dietary intake and resting energy expenditure (REE) of patients with AD dementia, MCI, and controls. In addition, we studied associations of global cognition (Mini-Mental State Examination (MMSE)) and AD biomarkers with dietary intake and REE.
We included 219 participants from the NUDAD project, 71 patients with AD dementia (age 68 ± 8 years, 58% female, MMSE 24 ± 3), 52 with MCI (67 ± 8 years, 42% female, MMSE 26 ± 2), and 96 controls (62 ± 7 years, 52% female, MMSE 28 ± 2). We used a 238-item food frequency questionnaire to assess dietary intake (energy, protein, carbohydrate, and fat). In a subgroup of 92 participants (30 patients with AD dementia, 22 with MCI, and 40 controls) we measured REE with indirect calorimetry. Between-group differences in dietary intake and REE were tested with ANOVAs. In the total sample, linear regression analyses were used to explore potential associations of MMSE score and AD biomarkers with dietary intake and REE. All analyses were adjusted for age, sex, education, and body mass index or fat-free mass.
Patients with AD dementia and MCI did not differ from controls in total energy intake (1991 ± 71 and 2172 ± 80 vs 2022 ± 61 kcal/day, p > 0.05) nor in protein, carbohydrate, or fat intake. Patients with AD dementia and MCI had a higher REE than controls (1704 ± 41 and 1754 ± 47 vs 1569 ± 34 kcal/day, p < 0.05). We did not find any association of MMSE score or AD biomarkers with dietary intake or REE.
We found a higher REE, despite similar energy intake in patients with AD and MCI compared to controls. These findings suggest that elevated metabolism rather than reduced energy intake explains malnutrition in AD. These results could be useful to optimize dietary advice for patients with AD dementia and MCI.
阿尔茨海默病(AD)痴呆和轻度认知障碍(MCI)患者中普遍存在营养不良的情况,且与住院和死亡率增加有关。营养不良是能量负平衡的结果,可能是由于饮食摄入减少和/或能量消耗增加所致。为了研究营养不良的潜在机制,我们研究了 AD 痴呆、MCI 和对照组患者的饮食摄入和静息能量消耗(REE)。此外,我们还研究了整体认知(简易精神状态检查(MMSE))和 AD 生物标志物与饮食摄入和 REE 的相关性。
我们纳入了 NUDAD 项目的 219 名参与者,其中 71 名为 AD 痴呆患者(年龄 68±8 岁,58%为女性,MMSE 为 24±3),52 名为 MCI 患者(67±8 岁,42%为女性,MMSE 为 26±2),96 名为对照组(62±7 岁,52%为女性,MMSE 为 28±2)。我们使用包含 238 种食物的食物频率问卷来评估饮食摄入(能量、蛋白质、碳水化合物和脂肪)。在 92 名参与者(30 名 AD 痴呆患者、22 名 MCI 患者和 40 名对照组)的亚组中,我们使用间接测热法测量了 REE。使用方差分析测试了组间饮食摄入和 REE 的差异。在总样本中,使用线性回归分析来探讨 MMSE 评分和 AD 生物标志物与饮食摄入和 REE 的潜在相关性。所有分析均针对年龄、性别、教育程度以及体重指数或去脂体重进行了调整。
AD 痴呆和 MCI 患者的总能量摄入(1991±71 和 2172±80 与 2022±61kcal/天,p>0.05)和蛋白质、碳水化合物或脂肪摄入均与对照组无差异。AD 痴呆和 MCI 患者的 REE 高于对照组(1704±41 和 1754±47 与 1569±34kcal/天,p<0.05)。我们未发现 MMSE 评分或 AD 生物标志物与饮食摄入或 REE 之间存在任何相关性。
尽管 AD 和 MCI 患者的能量摄入与对照组相似,但我们发现 REE 较高。这些发现表明,代谢升高而不是能量摄入减少解释了 AD 中的营养不良。这些结果可能有助于优化 AD 痴呆和 MCI 患者的饮食建议。