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Soy foods may contribute to the beneficial health effects of healthy plant-based diets on the risk to develop cardiovascular disease (CVD). However, their effects on vascular function have hardly been studied. To investigate longer-term effects of soy nut consumption on vascular function and cardiometabolic risk markers in healthy older men and women. Twenty-three healthy participants (age: 60–70 years; BMI: 20–30 kg/m2) participated in a randomized, controlled, single-blinded cross-over trial with an intervention (67 g/day of soy nuts providing 25.5 g protein and 174 mg isoflavones) and control period (no nuts) of 16 weeks, separated by eight weeks wash-out. Adults followed the Dutch food-based dietary guidelines. No serious adverse events were reported and the soy nut regime was well tolerated. Body weights remained stable during the whole study. A higher protein (3.1 energy percent [En%]) and a lower carbohydrate intake (2.0 En%) was observed during the intervention period. Total fat intake was comparable, but that of saturated (−1.3 En%), cis -monounsaturated (−1.5 En%) and cis -polyunsaturated fatty acids (+1.9 En%) differed. Serum isoflavone concentrations were higher after the intervention as compared with the control period (daidzein: 127.8 ng/mL; 95% CI: 74.3–181.3 ng/mL; p < 0.001 and genistein: 454.2 ng/mL; 95% CI: 266.6–641.8 ng/mL; p < 0.001). Brachial artery flow-mediated vasodilation was 1.48 percent points (pp; 95% CI: 0.08–2.89 pp; p = 0.040) higher following soy nut intake. The carotid artery reactivity response and arterial stiffness did not differ. Serum LDL-cholesterol was lower (0.17 mmol/L; 95% CI: 0.02–0.32 mmol/L; p = 0.027), while HDL-cholesterol and triacylglycerol concentrations were comparable. Mean arterial pressure (MAP) was lower (3 mmHg; 95% CI: 0–6 mmHg; p = 0.035). Longer-term soy nut intake as part of a healthy diet improved endothelial function, LDL-cholesterol concentrations and MAP levels, suggesting mechanisms by which an increased soy food intake beneficially affects CVD risk in older adults. Registered under ClinicalTrials.gov Identifier no. NCT03627637. [ABSTRACT FROM AUTHOR]

Background Effects of soy foods on cerebral blood flow (CBF)—a marker of cerebrovascular function—may contribute to the beneficial effects of plant-based diets on cognitive performance. Objectives We aimed to investigate longer-term effects of soy nut consumption on CBF in older adults. Changes in 3 different domains of cognitive performance were also studied. Methods Twenty-three healthy participants (age: 60–70 y; BMI: 20–30 kg/m2) participated in a randomized, controlled, single-blinded crossover trial with an intervention (67 g/d of soy nuts providing ∼25.5 g protein and 174 mg isoflavones) and control period (no nuts) of 16 wk, separated by an 8-wk washout period. Adults followed the Dutch food-based dietary guidelines. At the end of each period, CBF was assessed with arterial spin labeling MRI. Psychomotor speed, executive function, and memory were assessed using the Cambridge Neuropsychological Test Automated Battery (CANTAB). Results No serious adverse events were reported, and soy nut intake was well tolerated. Body weights remained stable during the study. Serum isoflavone concentrations increased (daidzein mean difference ± SD: 128 ± 113 ng/mL, P  < 0.001; genistein: 454 ± 256 ng/mL, P  < 0.001), indicating excellent compliance. Regional CBF increased in 4 brain clusters located in the left occipital and temporal lobes (mean ± SD increase: 11.1 ± 12.4 mL · 100 g−1 · min−1, volume: 11,296 mm3, P  < 0.001), bilateral occipital lobe (12.1 ± 15.0 mL · 100 g−1 · min−1, volume: 2632 mm3, P  = 0.002), right occipital and parietal lobes (12.7 ± 14.3 mL · 100 g−1 · min−1, volume: 2280 mm3, P  = 0.005), and left frontal lobe (12.4 ± 14.5 mL · 100 g−1 · min−1, volume: 2120 mm3, P  = 0.009) which is part of the ventral network. These 4 regions are involved in psychomotor speed performance, which improved as the movement time reduced by (mean ± SD) 20 ± 37 ms (P  = 0.005). Executive function and memory did not change. Conclusions Longer-term soy nut consumption may improve cerebrovascular function of older adults, because regional CBF increased. Effects may underlie observed improvements in psychomotor speed. This trial was registered at clinicaltrials.gov as NCT03627637. [ABSTRACT FROM AUTHOR]

Background Observed associations of high-protein diets with changes in insulin resistance are inconclusive. Objectives We aimed to assess associations of changes in both reported and estimated protein (PRep; PEst) and energy intake (EIRep; EIEst) with changes in HOMA-IR, glycated hemoglobin (HbA1c), and BMI (in kg/m2), in 1822 decreasing to 833 adults (week 156) with overweight and prediabetes, during the 3-y PREVIEW (PREVention of diabetes through lifestyle intervention and population studies In Europe and around the World) study on weight-loss maintenance. Eating behavior and measurement errors (MEs) of dietary intake were assessed. Thus, observational post hoc analyses were applied. Methods Associations of changes in EIEst, EIRep, PEst, and PRep with changes in HOMA-IR, HbA1c, and BMI were determined by linear mixed-model analysis in 2 arms [high-protein-low-glycemic-index (GI) diet and moderate-protein-moderate-GI diet] of the PREVIEW study. EIEst was derived from energy requirement: total energy expenditure = basal metabolic rate × physical activity level; PEst from urinary nitrogen, and urea. MEs were calculated as [(EIEst − EIRep)/EIEst] × 100% and [(PRep − PEst)/PEst] × 100%. Eating behavior was determined using the Three Factor Eating Questionnaire, examining cognitive dietary restraint, disinhibition, and hunger. Results Increases in PEst and PRep and decreases in EIEst and EIRep were associated with decreases in BMI, but not independently with decreases in HOMA-IR. Increases in PEst and PRep were associated with decreases in HbA1c. PRep and EIRep showed larger changes and stronger associations than PEst and EIEst. Mean ± SD MEs of EIRep and PRep were 38% ± 9% and 14% ± 4%, respectively; ME changes in EIRep and En% PRep were positively associated with changes in BMI and cognitive dietary restraint and inversely with disinhibition and hunger. Conclusions During weight-loss maintenance in adults with prediabetes, increase in protein intake and decrease in energy intake were not associated with decrease in HOMA-IR beyond associations with decrease in BMI. Increases in PEst and PRep were associated with decrease in HbA1c. This trial was registered at clinicaltrials.gov as NCT01777893. [ABSTRACT FROM AUTHOR]

Background: Weight loss has been associated with adaptations in energy expenditure. Identifying factors that counteract these adaptations are important for long-term weight loss and weight maintenance.Objective: The aim of this study was to investigate whether increased protein/carbohydrate ratio would reduce adaptive thermogenesis (AT) and the expected positive energy balance (EB) during weight maintenance after weight loss in participants with prediabetes in the postobese state.Methods: In 38 participants, the effects of 2 diets differing in protein/carbohydrate ratio on energy expenditure and respiratory quotient (RQ) were assessed during 48-h respiration chamber measurements ∼34 mo after weight loss. Participants consumed a high-protein (HP) diet (n = 20; 13 women/7 men; age: 64.0 ± 6.2 y; BMI: 28.9 ± 4.0 kg/m 2) with 25:45:30% or a moderate-protein (MP) diet (n = 18; 9 women/9 men; age: 65.1 ± 5.8 y; BMI: 29.0 ± 3.8 kg/m 2) with 15:55:30% of energy from protein:carbohydrate:fat. Predicted resting energy expenditure (REEp) was calculated based on fat-free mass and fat mass. AT was assessed by subtracting measured resting energy expenditure (REE) from REEp. The main outcomes included differences in components of energy expenditure, substrate oxidation, and AT between groups.Results: EB (MP = 0.2 ± 0.9 MJ/d; HP = -0.5 ± 0.9 MJ/d) and RQ (MP = 0.84 ± 0.02; HP = 0.82 ± 0.02) were reduced and REE (MP: 7.3 ± 0.2 MJ/d compared with HP: 7.8 ± 0.2 MJ/d) was increased in the HP group compared with the MP group (P < 0.05). REE was not different from REEp in the HP group, whereas REE was lower than REEp in the MP group (P < 0.05). Furthermore, EB was positively related to AT (rs = 0.74; P < 0.001) and RQ (rs = 0.47; P < 0.01) in the whole group of participants.Conclusions: In conclusion, an HP diet compared with an MP diet led to a negative EB and counteracted AT ∼34 mo after weight loss, in participants with prediabetes in the postobese state. These results indicate the relevance of compliance to an increased protein/carbohydrate ratio for long-term weight maintenance after weight loss. The trial was registered at clinicaltrials.gov as NCT01777893. [ABSTRACT FROM AUTHOR]

Background: Obesity and type 2 diabetes have been linked to alterations in food reward processing, which may be linked to insulin resistance. Objectives: In this clinical study, we investigated the respective contribution of insulin resistance, anthropometric measurements, and behavioral factors to brain reward activation in response to visual stimuli. Design: Food reward–related brain reward activation was assessed with functional magnetic resonance imaging in 39 overweight or obese individuals with impaired fasting glucose, impaired glucose tolerance, or both [22 women, 17 men; mean ± SD insulin sensitivity index (ISI): 2.7 ± 1.3; body mass index (BMI; kg/m²): 32.3 ± 3.7; body fat percentage: 40.5% ± 7.9%; fasting glucose: 6.3 ± 0.6 mmol/L]. Food and nonfood images were shown in a randomized block design. Brain activation (food compared with nonfood images) was correlated with anthropometric and behavioral variables. Behavioral variables included eating behavior [Three-Factor Eating Questionnaire (TFEQ)] and habitual physical activity (Baecke). Glucose and insulin concentrations, determined during an oral-glucose challenge, were used to assess the homeostatic model assessment for insulin resistance (HOMA-IR) and Matsuda ISI. Results: Food compared with nonfood brain activation was positively associated with HOMA-IR in the nucleus accumbens, right and left insula, and right cingulate gyrus (P < 0.005, corrected for multiple comparisons). TFEQ factor 2 was positively related to food compared with nonfood brain activation in the supramarginal gyrus (P < 0.005, corrected for multiple comparisons). Habitual physical activity during leisure time was negatively associated with food compared with nonfood brain activation in multiple regions associated with the attention and reward network (P < 0.005, corrected for multiple comparisons). Conclusions: Individuals with increased insulin resistance and emotional eating or disinhibition showed higher brain reactivity to food cues, which may imply changes in food preference and hyperphagia. Individuals with higher habitual physical activity showed less food reward–related brain activation. [ABSTRACT FROM AUTHOR]

Abstract: The increase in obesity, including childhood obesity, has developed over the same time period as the progressive decrease in self-reported sleep duration. Since epidemiological studies showed an inverse relationship between short or disturbed sleep and obesity, the question arose, how sleep duration and sleep quality are associated with the development of obesity. In this review, the current literature on these topics has been evaluated. During puberty, changes in body mass index (BMI) are inversely correlated to changes in sleep duration. During adulthood, this relationship remains and at the same time unfavorable metabolic and neuro-endocrinological changes develop, that promote a positive energy balance, coinciding with sleep disturbance. Furthermore, during excessive weight loss BMI and fat mass decrease, in parallel, and related with an increase in sleep duration. In order to shed light on the association between sleep duration, sleep quality and obesity, until now it only has been shown that diet-induced body-weight loss and successive body-weight maintenance contribute to sleep improvement. It remains to be demonstrated whether body-weight management and body composition improve during an intervention concomitantly with spontaneous sleep improvement compared with the same intervention without spontaneous sleep improvement. [Copyright &y& Elsevier]

Background: Flexibility of food reward-related brain signaling (FRS) between food and nonfood stimuli may differ between overweight and normal-weight subjects and depend on a fasted or satiated state. Objective: The objective was to assess this flexibility in response to visual food and nonfood cues. Design: Twenty normal-weight [mean ± SEM BMI (in kg/m²) = 22.7 ± 0.2; mean ± SEM age = 22.4 ± 0.4 y] and 20 overweight (BMI = 28.1 ± 0.3; age = 24.0 ± 0.7 y) participants completed 2 fMRI scans. Subjects arrived in a fasted state and consumed a breakfast consisting of 20% of subject-specific energy requirements between 2 successive scans. A block paradigm and a food > nonfood contrast was used to determine FRS. Results: An overall stimulus x condition x subject group effect was observed in the anterior cingulate cortex (ACC) (P < 0.006, F(1,38) = 9.12) and right putamen (P < 0.006, F(1,38) = 9.27). In all participants, FRS decreased from the fasted to the satiated state in the cingulate (P < 0.005, t(39) = 3.15) and right prefrontal cortex (PFC) (P < 0.006, f(39) = 3.00). In the fasted state, they showed FRS in the PFC (P < 0.004, t(39) = 3.17), left insula (P < 0.009, t(39)) = 2.95), right insula (P < 0.005, t(39) = 3.12), cingulate cortex (P < 0.004, f(39) = 3.21), and thalamus (P < 0.006, t = 2.96). In the satiated state, FRS was limited to the left insula (P < 0.005, r(39) = 3.21), right insula (P < 0.006, t(39) = 3.04), and cingulate cortex (P < 0.005, t(39) = 3.15). Regarding subject group, in the fasted state, FRS in the ACC was more pronounced in overweight than in normal-weight subjects (P < 0.005, F(1,38) = 9.71), whereas in the satiated state, FRS was less pronounced in overweight than in normal-weight subjects in the ACC (P < 0.006, F(1,38) = 9.18) and PFC (P < 0.006, F(1,38) = 8.86), which suggests lower inhibitory control in the overweight. Conclusion: FRS was higher in the overweight in the satiated state; however, when sufficiently satiated, the overweight showed decreased inhibitory control signalling, which facilitates overeating. This trial was registered in the Dutch clinical trial register as NTR2174. [ABSTRACT FROM AUTHOR]

Abstract: An increasing number of people report concerns about the amount of stress in their life. At the same time obesity is an escalating health problem worldwide. Evidence is accumulating rapidly that stress related chronic stimulation of the hypothalamic–pituitary–adrenal (HPA) axis and resulting excess glucocorticoid exposure may play a potential role in the development of visceral obesity. Since adequate regulation of energy and food intake under stress is important for survival, it is not surprising that the HPA axis is not only the ‘conductor’ of an appropriate stress response, but is also tightly intertwined with the endocrine regulation of appetite. Here we attempt to link animal and human literatures to tease apart how different types of psychological stress affect eating. We propose a theoretical model of Reward Based Stress Eating. This model emphasizes the role of cortisol and reward circuitry on motivating calorically dense food intake, and elucidating potential neuroendocrine mediators in the relationship between stress and eating. The addiction literature suggests that the brain reward circuitry may be a key player in stress-induced food intake. Stress as well as palatable food can stimulate endogenous opioid release. In turn, opioid release appears to be part of an organisms'' powerful defense mechanism protecting from the detrimental effects of stress by decreasing activity of the HPA axis and thus attenuating the stress response. Repeated stimulation of the reward pathways through either stress induced HPA stimulation, intake of highly palatable food or both, may lead to neurobiological adaptations that promote the compulsive nature of overeating. Cortisol may influence the reward value of food via neuroendocrine/peptide mediators such as leptin, insulin and neuropeptide Y (NPY). Whereas glucocorticoids are antagonized by insulin and leptin acutely, under chronic stress, that finely balanced system is dysregulated, possibly contributing to increased food intake and visceral fat accumulation. While these mechanisms are only starting to be elucidated in humans, it appears the obesity epidemic may be exacerbated by the preponderance of chronic stress, unsuccessful attempts at food restriction, and their independent and possibly synergistic effects on increasing the reward value of highly palatable food. [Copyright &y& Elsevier]

Background: The mechanism of protein-induced satiety remains unclear. Objective: The objective was to investigate 24-h satiety and related hormones and energy and substrate metabolism during a high-protein (HP) diet in a respiration chamber. Design: Twelve healthy women aged 18-40 y were fed in energy balance an adequate-protein (AP: 10%, 60%, and 30% of energy from protein, carbohydrate, and fat, respectively) or an HP (30%, 40%, and 30% of energy from protein, carbohydrate, and fat, respectively) diet in a randomized crossover design. Substrate oxidation, 24-h energy expenditure (EE), appetite profile, and ghrelin and glucagon-like peptide 1 (GLP-1) concentrations were measured. Results: Sleeping metabolic rate (6.40 ± 0.47 compared with 6.12 ± 0.40 MJ/d; P < 0.05), diet-induced thermogenesis (0.91 ± 0.25 compared with 0.69 ± 0.24 MJ/d; P < 0.05), and satiety were significantly higher, and activity-induced EE(1.68 ± 0.32 compared with 1.86 ± 0.41; P < 0.05), respiratory quotient (0.84 ± 0.02 compared with 0.88 ± 0.03; P < 0.0005), and hunger were significantly lower during the HP diet. There was a tendency for a greater 24-h EE during the HP diet (P = 0.05). Although energy intake was not significantly different between the diet groups, the subjects were in energy balance during the HP diet and in positive energy balance during the AP diet. Satiety was related to 24-h protein intake (r2 = 0.49, P < 0.05) only during the HP diet. Ghrelin concentrations were not significantly different between diets. GLP-1 concentrations after dinner were higher during the HP than during the AP diet (P < 0.05). Conclusion: An HP diet, compared with an AP diet, fed at energy balance for 4 d increased 24-h satiety, thermogenesis, sleeping metabolic rate, protein balance, and fat oxidation. Satiety was related to protein intake, and incidentally to ghrelin and GLP-1 concentrations, only during the HP diet. [ABSTRACT FROM AUTHOR]

To examine whether eating behavior and perceived stress predict the maintenance of self-reported dietary change and adherence to dietary instructions during an intervention. A secondary analysis of the behavior maintenance stage (6–36 months) of the 3-year PREVIEW intervention (PREVention of diabetes through lifestyle Intervention and population studies in Europe and around the World). Adults (n = 1,311) with overweight and prediabetes at preintervention baseline. Eating behavior (Three-Factor Eating Questionnaire), stress (Perceived Stress Scale), and dietary intake (4-day food records on 4 occasions) were reported. Associations between predictors and dietary outcomes were examined with linear mixed-effects models for repeated measurements. Eating behaviors and stress at 6 months did not predict the subsequent change in dietary outcomes, but higher cognitive restraint predicted lower energy intake, and both higher disinhibition and hunger predicted higher energy intake during the following behavior maintenance stage. In addition, higher disinhibition predicted higher saturated fat intake and lower fiber intake, and higher hunger predicted lower fiber intake. Stress was not associated with energy intake or dietary quality. Eating behaviors and stress were not consistently associated with adherence to dietary instructions. Higher cognitive restraint predicted lower energy intake (food quantity), but disinhibition and hunger were also associated with dietary quality. [ABSTRACT FROM AUTHOR]

The gut microbiota influences communication between the gastrointestinal tract and the brain (the gut–brain axis) in a bidirectional manner. Recent in vitro research and animal studies suggest a link between the gut microbiota and the regulation of satiety and energy intake via a variety of direct and indirect pathways. However, the contribution of gut microbial metabolites to these processes in humans remains unclear. Short-chain fatty acids (SCFAs) are the most commonly studied microbial metabolites, and prebiotic supplementation enhances their production by the gut microbiota. Analyzing evidence from human studies, focusing on prebiotic supplementation, gut microbial alterations, and changes in satiety-related parameters, might generate important insights into the links between the gut microbiota and satiety signaling in humans. Recent studies show a link between the gut microbiota and the regulation of satiety and energy intake, processes that contribute to the development and pathophysiology of metabolic diseases. However, this link is predominantly established in animal and in vitro studies, whereas human intervention studies are scarce. In this review we focus on recent evidence linking satiety and the gut microbiome, with specific emphasis on gut microbial short-chain fatty acids (SCFAs). Based on a systematic search we provide an overview of human studies linking the intake of prebiotics with gut microbial alterations and satiety signaling. Our outcomes highlight the importance of in-depth examination of the gut microbiota in relation to satiety and provide insights into recent and future studies in this field. [ABSTRACT FROM AUTHOR]