Background: Limited and inconsistent research findings exist about the effect of dietary protein intake on indexes of sleep.Objective: We assessed the

Age-related increases in intermuscular adipose tissue (IMAT) impair muscle quality, decrease functional capacity, and promote several cardiometabolic and inflammatory disorders. Whether these age-related alterations in muscle composition improve by consuming a high-protein (HP) diet with whole eggs are unclear. This parallel-design, randomized-controlled trial assessed the effects of a 12-week eucaloric HP diet with three whole eggs per day (1.4 g protein kg⁻¹ day⁻¹) versus a normal-protein diet void of eggs (NP, 0.8 g protein kg⁻¹ day⁻¹) on muscle composition (IMAT), cardiometabolic health, and systemic inflammation in older adults with overweight or obesity (12 men and 10 women; age 70 ± 5 years, BMI 31.3 ± 3.2 kg/m², mean ± SD). No changes in muscle composition were observed over time, independent of protein intake. Total body weight was reduced in both groups (−3.3 ± 1.2%) and lean mass was preserved only with the HP diet. LDL concentration and hip circumference decreased only with the NP diet, while MCP-1 and HsCRP concentrations increased over time in both groups. A HP diet with whole eggs promotes lean mass retention with modest weight loss, but does not positively influence muscle composition, cardiometabolic health or systemic inflammation, compared to a NP diet void of eggs.

Limited evidence suggests that consuming a higher-protein diet during weight loss improves subjective indices of sleep in overweight and obese adults. We sought to a priori assess the effects of consuming the recommended versus a higher protein Healthy US-Style Eating Pattern during energy-restriction on sleep quality indices. Using a randomized, parallel study design, 51 adults (mean ± SEM age: 47 ± 1 y; BMI: 32.6 ± 0.5 kg/m2) consumed a controlled USDA Healthy US-Style Eating Pattern containing 750 kcal/d less than their estimated energy requirement for 12 wk. Participants were randomly assigned to consume either 5 or 12.5 oz-equivalent (eq)/d of protein foods. The additional 7.5 oz-eq/d came from animal-based protein sources and displaced primarily grains. Objective (wrist-worn actigraphy) and subjective (Pittsburgh Sleep Quality Index, Epworth Sleepiness Scale) sleep quality indices were measured at baseline, week 6, and week 12. Among all participants, body mass decreased (-6.2 ± 0.4 kg). Dietary protein intake did not affect any objective or subjective sleep quality outcomes measured (repeated measures ANOVA). Over time, objective measures of time spent in bed, time spent sleeping, sleep onset latency, and time awake after sleep onset did not change; however, sleep efficiency improved (1 ± 1%; P = 0.027). Subjectively, global sleep scores [GSS: -2.7 ± 0.4 arbitrary units (au)] and daytime sleepiness scores (-3.8 ± 0.4 au; both P < 0.001) improved over time. The GSS improvement transitioned the participants from being categorized with "poor" to "good" sleep (GSS: >5 compared with ≤5 au of a 0-21 au scale; baseline 7.6 ± 0.4 au, week 12: 4.8 ± 0.4 au). Although objective sleep quality may not improve, adults who are overweight or obese and poor sleepers may become good sleepers while consuming either the recommended or a higher-protein energy-restricted Healthy US-Style Eating Pattern. This trial was registered at clinicaltrials.gov as NCT03174769.

Colorectal disturbances encompass a variety of disorders that impact the colon and rectum, such as colitis and colon cancer. Butyrate, a short-chain fatty acid, plays a pivotal role in supporting gut health by nourishing colonocytes, promoting barrier function, modulating inflammation, and fostering a balanced microbiome. Increasing colorectal butyrate concentration may serve as a critical strategy to improve colon function and reduce the risk of colorectal disturbances. Butyrylated high-amylose maize starch (HAMSB) is an edible ingredient that efficiently delivers butyrate to the colon. HAMSB is developed by esterifying a high-amylose starch backbone with butyric anhydride. With a degree of substitution of 0.25, each hydroxy group of HAMSB is substituted by a butyryl group in every four D-glucopyranosyl units. In humans, the digestibility of HAMSB is 68% (w/w), and 60% butyrate molecules attached to the starch backbone is absorbed by the colon. One clinical trial yielded two publications, which showed that HAMSB significantly reduced rectal O⁶-methyl-guanine adducts and epithelial proliferation induced by the high protein diet. Fecal microbial profiles were assessed in three clinical trials, showing that HAMSB supplementation was consistently linked to increased abundance of Parabacteroides distasonis. In animal studies, HAMSB was effective in reducing the risk of diet- or AOM-induced colon cancer by reducing genetic damage, but the mechanisms differed. HAMSB functioned through affecting cecal ammonia levels by modulating colon pH in diet-induced cancer, while it ameliorated chemical-induced colon cancer through downregulating miR19b and miR92a expressions and subsequently activating the caspase-dependent apoptosis. Furthermore, animal studies showed that HAMSB improved colitis via regulating the gut immune modulation by inhibiting histone deacetylase and activating G protein-coupled receptors, but its role in bacteria-induced colon colitis requires further investigation. In conclusion, HAMSB is a food ingredient that may deliver butyrate to the colon to support colon health. Further clinical trials are warranted to validate earlier findings and determine the minimum effective dose of HAMSB.