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 衰老是阿尔茨海默病 (AD) 的主要危险因素，阿尔茨海默病是痴呆症的最常见形式 是美国发病率和死亡率增长最快的原因之一。 AD 的危险因素出现 中年时期，与心脑血管疾病类似。对此，强化 大弹性动脉（即主动脉和颈动脉）和脑灌注不足会随着年龄的增长而发生， 与年龄相关的认知障碍有关，主要是通过将破坏性压力波传递给 脑血管系统，导致脑血管功能障碍和神经元损伤。中年的影响 不良的生活习惯进一步加剧了大脑血管的变化，包括食用 含有大量添加糖的饮食（例如，含有大量糖分的超加工食品） 果糖）。虽然确切机制尚不清楚，但高糖饮食与血浆升高有关 甘油三酯（TG），可能会通过以下方式加剧与年龄相关的动脉功能障碍和记忆障碍 机制涉及全身炎症增加。我们的横截面初步数据表明 血浆 TG 与动脉僵硬度增加、脑血管功能降低、血压降低密切相关。 记忆分数和海马体完整性下降，海马体是一种对于编码和记忆至关重要的大脑结构。 回忆往事；然而，目前尚不清楚这些因素如何受到添加物消耗的影响。 糖。该项目的目的是为添加糖之间的因果关系建立初步证据 中年成年人的摄入量以及对血管和大脑健康的不利变化。我们的中心假设是过量 添加糖的摄入会导致海马体结构和功能的减少，尽管对海马体的不利变化 动脉通过涉及增加血浆TG和全身炎症的机制。我们将进行一次 随机、单盲、控制喂养研究，以确定食用低含量饮食的影响 （总能量摄入的 5%）与高添加糖（总能量摄入的 25%）各 10 天，测量结果为 大弹性动脉僵硬度、脑血管功能和海马结构与功能。预期的 结果是添加糖摄入量与血管和大脑减少之间存在因果关系的证据 通过涉及增加 TG 和炎症的机制发挥作用。该项目生成的数据 将支持未来的 NIH R01 提案，进行一项旨在降低添加糖摄入量的随机对照试验 中年成年人。