The effect of dietary added sugar intake on cerebrovascular function and brain health
Date
2023
Authors
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Publisher
University of Delaware
Abstract
Alzheimer’s disease (AD) is the most common form of dementia and the fifth leading cause of death in the United States. AD shares many of the same modifiable risk factors as cardiometabolic diseases, which includes aberrant blood lipids such as increased blood triglycerides (TGs), which are associated with reduced brain tissue microstructural integrity and poor memory performance. Additionally, a high consumption of added sugars typically from a Western diet, is associated with elevated cardiometabolic parameters that likely contribute to cognitive aging. Increased added sugar intake acutely raises blood TGs and uric acid and is associated with reduced peripheral vascular endothelial function via the production of reactive oxygen species (ROS). Limited research suggests that acute added sugar intake may be associated with reduced cerebral blood flow. As such, repetitive acute insults to the cerebrovasculature from increased added sugar consumption may result in long-term reductions in brain tissue properties through sustained reductions in cerebrovascular function. OBJECTIVES: To evaluate the associations among habitually elevated blood lipids, acute dietary added sugar intake, cerebrovascular function, and brain tissue viscoelastic properties in humans through the following aims: 1) Determine whether habitually elevated blood lipids are cross-sectionally associated with lower hippocampal (HC) tissue properties and assess whether this relation is moderated by cerebrovascular function. 2) Determine whether acute consumption of a high-sugar (HS) meal is associated with a transient reduction in cerebrovascular function, brain tissue properties and cognitive (executive) function compared to a low-sugar (LS) meal, and assess whether these reductions are correlated to an increase in blood lipids, uric acid and markers of ROS. HYPOTHESES: 1) Elevated blood lipids will be associated with lower HC tissue properties and this relation will be mediated by reduced cerebrovascular function. 2) Acute consumption of a HS meal will be associated with a transient reduction in cerebrovascular function, brain tissue properties and cognitive (executive) function compared to a LS meal, and these reductions will be correlated to an increase in blood lipids, uric acid and markers of ROS. METHODS: Healthy young and mid-life adults were enrolled in a randomized-controlled crossover trial that consisted of a single meal high in added sugars (HS: 61 g) and a single meal low in added sugars (LS: 16 g). Serum lipids and uric acid were assessed at baseline and 3 hours postprandial following both meals. ROS levels were measured as superoxide concentration and assessed with electron paramagnetic resonance. Cerebral perfusion and cerebrovascular reactivity to hypercapnia was assessed using arterial-spin labeling coupled with prospective end-tidal targeting. Brain tissue viscoelastic properties were assessed using magnetic resonance elastography. RESULTS: Twenty-two participants [9M/13F, age: 4812 y (range: 30-64 y), BMI: 24.72.8 kg/m2, BP: 11611/736 mmHg) were included in this study. Baseline LDL-C was significantly associated with HC stiffness (r=-0.42, p=0.049) while baseline TG was significantly associated with HC damping ratio (r=0.46, p=0.04). These associations were not mediated by cerebrovascular function. Serum TG concentration was higher following both meals (Time: p<0.0001; Meal: p=0.29; Interaction: p=0.07) where the increase tended to be greater following the HS meal (p=0.06). Serum uric acid concentration was reduced following both meals (Time: p<0.0001; Meal: p=0.80; Interaction: p=0.0003) and the reduction was greater following the HS meal (p<0.001). ROS concentration was reduced following both meals (Time: p=0.002; Meal: p=0.14; Interaction: p=0.32). There was no significant change in cerebrovascular function following either meal. Whole brain damping ratio was higher (Time: p=0.0007; Meal: p=0.55; Interaction: p=0.21) and HC stiffness was lower (Time: p=0.02; Meal: p=0.11; Interaction: p=0.095) following both meals. In a subset of participants, executive function increased following both meals, whereas participants’ measures of attention and inhibitory control were increased following the HS meal and was decreased following the LS meal. CONCLUSIONS: Habitually elevated LDL-C and TGs are associated with a reduction in brain tissue properties, however, this association is not mediated by a reduction in cerebrovascular function. Habitually elevated LDL-C and TGs are associated with a reduction in brain tissue properties, however, this association is not mediated by a reduction in cerebrovascular function. Acute high dietary added sugar intake tends to lead to a greater increase in serum TG concentration and a greater reduction in serum uric acid concentration. There is also a reduction in postprandial ROS concentration following both meals. Brain tissue properties, but not cerebrovascular function, are reduced following both meals, regardless of added sugar content.
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Keywords
Added sugars, Blood lipids, Brain tissue viscoelastic properties, Cerebrovascular function, Brain health