Differential effects of nutritive and non-nutritive sweet mouth rinsing on appetite in adults with obesity.

BACKGROUND: Excessive added sugar intake has been associated with obesity; however, the effect of dietary sweetness on energy intake (EI) and appetite in adults with and without obesity has not yet been determined. OBJECTIVE: To assess the effect of mouth rinses with and without energy and sweetness on measures of appetite, and to compare responses between subjects with body mass index (BMI) between 18.5 and 24.9 kg/m2 or ≥30 kg/m2. METHODS: In this randomized, double-blind crossover study, 39 subjects (age 23±5y; 17 male, 22 female; BMI 18.5-24.9 kg/m2: n = 21; ≥30 kg/m2: n = 18) performed modified sham-feeding (MSF) with a mouth rinse containing either sucrose, sucralose, maltodextrin, or water for 2min before expectorating the solution. Blood sampling and subjective appetite assessments occurred at baseline (-5) and 15, 30, 60, and 90min post-MSF. After, EI was assessed at a buffet meal and post-meal appetite ratings were assessed hourly for 3h. RESULTS: Post-MSF ghrelin increased for water vs. maltodextrin (water: p = 0.03). Post-MSF cholecystokinin increased following maltodextrin-MSF (p = 0.03) and sucralose-MSF (p = 0.005) vs. sucrose for those with BMI:18.5-24.9 kg/m2 only. There was greater post-MSF desire to eat in response to water vs. sucrose (p = 0.03) and reduced fullness with sucralose for those with BMI≥30 vs. 18.5-24.9 kg/m2 (p < 0.001). There was no difference in EI at the buffet meal by mouth rinse (p = 0.98) or by BMI (p = 0.12). However, there was greater post-meal fullness following sucralose-MSF vs. water (p = 0.03) and sucrose (p = 0.004) for those with BMI≥30 vs. 18.5-24.9 kg/m2. CONCLUSION: Sucralose rinsing led to greater cephalic phase CCK release in adults with a BMI:18.5-24.9 kg/m2 only; however, ghrelin responses to unsweetened rinses were energy-specific for all adults. As subsequent EI was unaffected, further investigation of cephalic phase appetite is warranted.

A 4-Week Pecan-Enriched Diet Improves Postprandial Lipid Peroxidation in Aging Adults.

Pecans are rich in bioactive compounds known to reduce oxidative stress and provide glucoregulatory benefits. Few studies assessing the effect of a pecan-enriched diet on such health outcomes suggest potential improvements to cardiometabolic health; however, this has not been studied in an older adult population. Thus, we aimed to examine the effect of daily pecan consumption for 4-weeks on fasting and postmeal antioxidant status, oxidative stress, and markers of glycemia in healthy aging adults. In this randomized, parallel, controlled trial, 41 healthy adults (50-75 years) either consumed 68 g of pecans/day (pecan; n = 21) or avoided all nuts (control; n = 20). At pre- (V1) and postintervention visits (V2), blood samples were obtained at fasting, and 30, 60, and 120 min following a high saturated fat meal to assess changes in malondialdehyde, which is a measure of lipid peroxidation, total antioxidant capacity (TAC), glucose, and insulin. Across the intervention, there were no differences in fasting or postprandial TAC, glucose, or insulin for pecan versus control. There was a trend for a difference in fasting lipid peroxidation from V1 to V2 by treatment (P = .06) driven by a slight reduction for pecan versus control (Δpecan: -2.0 ± 1.1 vs. Δcontrol: +0.6 ± 0.8 µM). In addition, postprandial lipid peroxidation was suppressed at V2 for pecan, and this was different from control (pecan areas under the curve (AUC): 10.6 ± 1.3 µM/h to 9.1 ± 1.2 µM/h vs. control AUC: 8.9 ± 1.3 µM/h to 9.2 ± 1.1 µM/h; P = .03). These findings suggest that a 1 month, pecan-enriched diet is protective against postmeal oxidative stress. Longer interventions or a diabetic population may be needed to observe glucoregulatory benefits. Clinical Trial Registration: NCT04385537.

A pecan-enriched diet reduced postprandial appetite intensity and enhanced peptide YY secretion: A randomized control trial.

BACKGROUND & AIMS: Tree nuts have been shown to have satiating qualities; however, little is known concerning the effect of pecans on measures of appetite. The purpose of this study was to examine the impact of a pecan-enriched diet on subjective, physiological, and direct measures of appetite in older adults. METHODS: This was a randomized, controlled trial in which healthy older adults (50-75 y) were randomized to either consume 68 g of pecans/day (pecan; n = 21) or avoid all nuts (control; n = 23) for 4 weeks. At pre- (V1) and post-diet (V2) visits body weight (BW) and body fat percentage (BF) were assessed and actual change in these outcomes for pecan were compared to theoretical changes if pecans were consumed without compensation. Subjective appetite was measured using visual analog scale (VAS), and blood was collected to assess changes in physiological appetite before and every 30 min for 4 h following a high-fat meal. Energy intake (EI) at a buffet meal was then assessed in the laboratory ("in-lab"). VAS assessments continued hourly for the next 7 h and EI ("at-home") was self-reported. RESULTS: BW and BF did not change for pecan or control across the intervention and theoretical change in BW (theoretical: 2.2 ± 0.1 vs. actual: 0.4 ± 0.2 kg; p < 0.0001) and BF (theoretical: 0.4 ± 0.04 vs. actual: 0.2 ± 0.2%; p < 0.0001) was significantly greater than actual change for pecan. From V1 to V2, there was an increase in fasting (pecan: 77.0 ± 4.6 to 93.5 ± 6.1 vs control: 76.0 ± 5.0 to 72.5 ± 5.0 pg/mL; p = 0.01) and postprandial peptide YY for pecan vs. control (p = 0.04); however, fasting and postprandial cholecystokinin and ghrelin did not differ (p > 0.05). There were no differences in the change in subjective appetite ratings at fasting, following the high-fat meal (in-lab), at-home, or across the full day between groups (p > 0.05 for all). However, there was a significant suppression of peak desire to eat ratings for pecan vs. control (pecan: 67.9 ± 4.6 to 57.1 ± 5.2 vs. control: 61.9 ± 4.2 to 60.6 ± 4.3 mm; p = 0.04). Combined, buffet meal, and at-home EI did not differ significantly within pecan and control; however, there was a trend (p = 0.11) for a between group difference in buffet meal EI driven by increased EI for control (+137 ± 86 kcal) vs. decreased EI for pecan (-45 ± 77 kcal). CONCLUSION: A 4-week pecan-enriched diet led to enhanced satietogenic metrics compared to a diet void of all nuts. As weight remained stable during the intervention, adding pecans to the daily diet may be beneficial to appetite control and weight maintenance in a healthy older population. TRIAL REGISTRATION INFORMATION: ClinicalTrials.gov: NCT04385537.

Pecan-enriched diet improves cholesterol profiles and enhances postprandial microvascular reactivity in older adults.

Pecan-enriched diets have been linked to improved lipid metabolism; however, the impact of pecans on vascular health has yet to be examined. We hypothesized that 4 weeks of a pecan-enriched diet would improve fasting and postprandial blood lipids and vascular function compared with a nut-free diet. In this randomized control study, 44 older adults (59 ± 6 years) consumed 68 g of pecans/d (pecan; n = 21) or avoided all nuts (control; n = 23) for 4 weeks. At pre- and post-diet visits, fasting and postprandial blood lipids, macrovascular (by flow-mediated dilation), and microvascular (tissue saturation index reactive hyperemia [RH] kinetics by continuous-wave near-infrared spectroscopy) function were assessed. From the pre- to post-diet visit, there were greater reductions in fasting total cholesterol (pecan: -14 ± 4.0 vs control: -0.2 ± 5.4 mg/dL; P = .04), low-density lipoprotein (LDL) cholesterol (pecan: -15 ± 3.7 vs control: +1.9 ± 4.4 mg/dL; P = .01), non-high-density lipoprotein cholesterol (pecan: -15 ± 3.6 vs control: -0.5 ± 4.8 mg/dL; P = .02), LDL particle number (pecan: -126 ± 51 vs control: +43 ± 42 nmol/L; P = .01), and LDL medium (pecan: -34 ± 13 vs control: +16 ± 11 nmol/L; P < .01), for pecan vs control. Further, postprandial triglyceride was suppressed for pecan (P = .01) compared with control (P = .78). Postprandial RH slope (P = .04) and RH time to half (P = .004) was different by group, driven by improvements in pecan vs control. However, fasting macro- and microvascular function was unaffected. Daily pecan consumption for 4 weeks improved fasting and postprandial blood lipids and microvascular reactivity in older adults. Because changes in microvascular function typically precipitate macrovascular changes, long-term pecan consumption may improve vascular health and reduce risk for cardiovascular events. This trial was registered at clinicaltrials.gov (NCT04385537).

Effect of Prior Exercise on Postprandial Lipemia: An Updated Meta-Analysis and Systematic Review.

The purpose of this systematic review was to synthesize the results from current literature examining the effects of prior exercise on the postprandial triglyceride (TG) response to evaluate current literature and provide future direction. A quantitative review was performed using meta-analytic methods to quantify individual effect sizes. A moderator analysis was performed to investigate potential variables that could influence the effect of prior exercise on postprandial TG response. Two hundred and seventy-nine effects were retrieved from 165 studies for the total TG response and 142 effects from 87 studies for the incremental area under the curve TG response. There was a moderate effect of exercise on the total TG response (Cohen's d = -0.47; p < .0001). Moderator analysis revealed exercise energy expenditure significantly moderated the effect of prior exercise on the total TG response (p < .0001). Exercise modality (e.g., cardiovascular, resistance, combination of both cardiovascular and resistance, or standing), cardiovascular exercise type (e.g., continuous, interval, concurrent, or combined), and timing of exercise prior to meal administration significantly affected the total TG response (p < .001). Additionally, exercise had a moderate effect on the incremental area under the curve TG response (Cohen's d = -0.40; p < .0001). The current analysis reveals a more homogeneous data set than previously reported. The attenuation of postprandial TG appears largely dependent on exercise energy expenditure (∼2 MJ) and the timing of exercise. The effect of prior exercise on the postprandial TG response appears to be transient; therefore, exercise should be frequent to elicit an adaptation.