The effects of added sugar intake on brain blood flow and hippocampal function in midlife adults

添加糖摄入量对中年成年人脑血流量和海马功能的影响

• 批准号: 10271700
• 负责人: Christopher Martens
• 金额: $ 34.5万
• 依托单位: UNIVERSITY OF DELAWARE
• 依托单位国家: 美国
• 财政年份: 2016
• 资助国家: 美国
• 起止时间: 2016-05-15 至 2026-05-31
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/10271700
• 关键词: Adipose tissue; Adult; Age-associated memory impairment; Aging; Alzheimer' s Disease; Alzheimer' s disease risk; Aorta; Arteries; Attenuated; Blood Pressure; Blood Vessels; Brain; Buffers; Cardiovascular Diseases; Cardiovascular Physiology; Carotid Arteries; Centers of Research Excellence; Cerebrovascular Circulation; Cerebrovascular Disorders; Cerebrovascular system; Chronic; Clinical; Cognitive aging; Consumption; Cross-Over Studies; Data; Dementia; Development; Diet; Dietary intake; Disease; Endothelium; Energy Intake; Energy-Generating Resources; Environmental Risk Factor; Food; Fructose; Functional disorder; Future; Glucose; Glycogen; Habits; Health; Health Policy; Heart; Hippocampus (Brain); Hour; Human; Hypercapnia; Hypertension; Hypertriglyceridemia; Impairment; Inflammation; Ingestion; Intake; Life Style; Link; Liver; Magnetic Resonance Elastography; Measures; Mediating; Memory; Memory Loss; Memory impairment; Modeling; Morbidity - disease rate; Nerve Degeneration; Neurons; Outcome; Oxidative Stress; Pathologic; Pathology; Performance; Plasma; Preparation; Process; Public Health; Randomized; Randomized Controlled Trials; Risk; Risk Factors; Serum; Single-Blind Study; Structure; Sweetening Agents; Testing; Tissues; Triglycerides; Ultrasonography; United States; United States National Institutes of Health; Very low density lipoprotein; abeta deposition; age related; arterial stiffness; brain health; brain tissue; cardiometabolic risk; cardiovascular health; cardiovascular risk factor; cerebral hypoperfusion; cerebrovascular; feeding; high risk; lipid biosynthesis; memory recall; middle age; mortality; neuron loss; nutritional guideline; pressure; sugar; systemic inflammatory response; transmission process; viscoelasticity; western diet

ABSTRACT Aging is the primary risk factor for Alzheimer's disease (AD) which is the most common form of dementia and among the fastest growing causes of morbidity and mortality in the United States. The risk factors for AD emerge during midlife and are similar to cardiovascular and cerebrovascular diseases. In this regard, stiffening of the large elastic arteries (i.e., the aorta and carotid arteries) and cerebral hypoperfusion occur with aging and are linked to age-related cognitive impairment, primarily through the transmission of damaging pressure waves to the cerebral vasculature, resulting in cerebrovascular dysfunction and neuronal damage. The impact of midlife vascular changes on the brain are further exacerbated by poor lifestyle habits, including the consumption of a diet that contains high amounts of added sugar (e.g., from ultra-processed foods containing high amounts of fructose). While the exact mechanisms are not known, a high sugar diet is associated with elevated plasma triglycerides (TGs), which may exacerbate age-related arterial dysfunction and memory impairment through a mechanism involving increased systemic inflammation. Our cross-sectional preliminary data suggest that plasma TGs are strongly associated with increased arterial stiffness, reduced cerebrovascular function, lower memory scores and decreased integrity of the hippocampus, a brain structure that is critical for encoding and recalling memories; however, it remains unknown how these factors are influenced by the consumption of added sugars. The purpose of this project is to establish preliminary evidence for a causal link between added sugar intake and adverse changes to vascular and brain health in midlife adults. Our central hypothesis is that excess added sugar intake causes reductions and hippocampal structure and function though adverse changes to arteries via a mechanism involving increased plasma TGs and systemic inflammation. We will conduct a randomized, single-blind, controlled-feeding study to determine the effects of consuming a diet containing low (5% of total energy intake) vs. high (25% of total energy intake) added sugar for 10-days each on measures of large elastic artery stiffness, cerebrovascular function and hippocampal structure and function. The expected outcome is evidence of a causal relation between added sugar intake and reductions in vascular and brain functions through a mechanism involving increased TG's and inflammation. The data generated from this project will support a future NIH R01 proposal for a randomized controlled trial aimed at lowering added sugar intake in mid-life adults.

抽象的 衰老是阿尔茨海默氏病（AD）的主要危险因素，这是最常见的痴呆症形式和 美国发病率和死亡率最快的原因之一。 AD出现的风险因素 在中年期间，类似于心血管和脑血管疾病。在这方面，僵硬 大型弹性动脉（即主动脉和颈动脉）和脑灌注不足，随着衰老而发生，并且是 与年龄相关的认知障碍有关，主要是通过将破坏压力波传播到 脑脉管系统，导致脑血管功能障碍和神经元损伤。中年的影响 不良的生活方式习惯进一步加剧了大脑的血管变化，包括消费 含有大量添加糖的饮食（例如，来自含有大量的超级加工食品 果糖）。虽然确切的机制尚不清楚，但高糖饮食与血浆升高有关 甘油三酸酯（TGS），可能会加剧与年龄相关的动脉功能障碍和记忆障碍 涉及增加全身炎症的机制。我们的横断面初步数据表明 血浆TG与动脉刚度的增加密切相关，脑血管功能降低，较低 记忆评分和降低海马的完整性，这是一种对编码和编码至关重要的大脑结构 回忆回忆；但是，尚不清楚这些因素如何受到添加的消费的影响 糖。该项目的目的是建立添加糖之间因果关系的初步证据 中年成年人的血管和脑健康的摄入量和不利变化。我们的中心假设是 添加的糖摄入导致减少和海马结构和功能，尽管不良变化 通过涉及血浆TGS和全身性炎症的机制进行的动脉。我们将进行 随机，单盲，受控喂养研究，以确定食用含有低饮食的影响 （占总能量摄入量的5％）与高（总能量摄入的25％）添加了10天的糖 大动脉刚度，脑血管功能以及海马结构和功能。预期 结果证明了添加的糖摄入量与血管和大脑减少之间的因果关系 通过涉及增加TG和炎症的机制来功能。该项目生成的数据 将支持未来的NIH R01提案，用于一项旨在降低添加糖摄入量的随机对照试验 中年成年人。