Assessing the Effect of Plant-Based Mince on Fullness and Post-Prandial Satiety in Healthy Male Subjects.

This study aimed to assess the effect of substituting plant-based mince for beef mince in a standard pasta meal on the amount consumed and on objective and subjective measures of post-prandial satiety. Healthy, adult males (n = 24) consumed a pasta lunch meal containing either plant-based or beef mince at separate visits, and the amount consumed measured at each visit. Perceptions of hunger, fullness and satisfaction were recorded and blood samples collected before and for 3 h after eating, when a buffet meal was provided. Participants consumed 586 kJ less of the pasta meal prepared with plant-based mince compared to beef mince (p < 0.05). Energy intake at the buffet meal and measures of fullness, satiety and satisfaction after the pasta meal were not different between plant and beef mince (p > 0.05). Post-prandial Glucagon-Like Peptide-1 (GLP-1), but not insulin or leptin concentrations, were lower after the plant-based pasta meal (p < 0.05). Our results suggest that the pasta meal containing plant-based mince was more satiating than an equivalent meal prepared with beef mince, and that this was not associated with greater energy intake at a subsequent meal occasion. Further studies that evaluate the longer-term effects of replacing meat with plant-based mince on energy intakes and explore the mechanisms underlying the lower consumption of the plant-based mince meal would be valuable.

Krill oil improved osteoarthritic knee pain in adults with mild to moderate knee osteoarthritis: a 6-month multicenter, randomized, double-blind, placebo-controlled trial.

BACKGROUND: Osteoarthritis (OA) is a major cause of chronic pain and disability worldwide. Treatment generally focuses on symptom relief through nonsteroidal anti-inflammatory drugs (NSAIDs) and analgesics, which may incur side effects. Krill oil, rich in anti-inflammatory long-chain (LC) omega-3 ( ω-3) PUFAs and astaxanthin, may be a safe and effective alternative treatment. OBJECTIVES: This study sought to investigate the effects of a commercially available krill oil supplement on knee pain in adults with mild to moderate knee OA. Secondary outcomes were knee stiffness; physical function; NSAID use; Omega-3 Index; and lipid, inflammatory, and safety markers. METHODS: Healthy adults (n = 235, 40-65 y old, BMI >18.5 to <35 kg/m2), clinically diagnosed with mild to moderate knee OA, regular knee pain, and consuming <0.5 g/d LC ω-3 PUFAs, participated in a 6-mo double-blind, randomized, placebo-controlled, multicenter trial. Participants consumed either 4 g krill oil/d (0.60 g EPA/d, 0.28 g DHA/d, 0.45 g astaxanthin/d) or placebo (mixed vegetable oil). Knee outcomes were assessed using the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) numeric scale (normalized to scores of 0-100). Outcomes were assessed at baseline, 3 mo, and 6 mo. RESULTS: Omega-3 Index increased with the krill oil supplement compared with placebo (from 6.0% to 8.9% compared with from 5.5% to 5.4%, P < 0.001). Knee pain score improved in both groups with greater improvements for krill oil than for placebo (difference in adjusted mean change between groups at 6 mo: -5.18; 95% CI: -10.0, -0.32; P = 0.04). Knee stiffness and physical function also had greater improvements with krill oil than with placebo (difference in adjusted mean change between groups at 6 mo: -6.45; 95% CI: -12.1, -0.9 and -4.67; 95% CI: -9.26, -0.05, respectively; P < 0.05). NSAID use, serum lipids, and inflammatory and safety markers did not differ between groups. CONCLUSIONS: Krill oil was safe to consume and resulted in modest improvements in knee pain, stiffness, and physical function in adults with mild to moderate knee OA.This trial was registered at clinicaltrials.gov as NCT03483090.

Substitution of Refined Conventional Wheat Flour with Wheat High in Resistant Starch Modulates the Intestinal Microbiota and Fecal Metabolites in Healthy Adults: A Randomized, Controlled Trial.

BACKGROUND: Resistant starch (RS) confers many health benefits, mostly through the microbial production of SCFAs, but foods containing appreciable RS are limited. High-amylose wheat (HAW) is high in RS and lowers the glycemic response of foods, but whether it can improve gastrointestinal health measures is unknown. OBJECTIVES: The objective of this study was to determine whether daily consumption of HAW food products improved markers of gastrointestinal health in healthy men and women compared with similar foods made from conventional wheat. METHODS: Eighty healthy adults (47 women and 33 men) were enrolled in a 4-arm parallel, randomized-controlled, double-blind trial. After a 2-wk low-dietary fiber run-in period, they were randomly allocated to 1 of 4 treatment groups: low-amylose wheat (LAW)-refined (LAW-R), LAW-wholemeal (LAW-W), HAW-refined (HAW-R), and HAW-wholemeal (HAW-W) and consumed the assigned test bread (160 g/d) and biscuits (75 g/d) for 4 wk. Fecal biochemical markers were measured at baseline and 4 wk. Microbial abundance and diversity were quantified using 16S ribosomal RNA sequencing and perceived gut comfort by a semiquantitative questionnaire completed at baseline, 2 wk, and 4 wk. RESULTS: HAW showed similar effects on fecal output and excretion of total SCFA compared with LAW, but changes were observed in secondary measures for the refined treatment groups. At 4 wk, the HAW-R group had 38% higher fecal butyrate excretion than the LAW-R group (P < 0.05), and higher fecal SCFA-producing bacteria, Roseburia inulinivorans (P < 0.001), than at baseline. In comparison with baseline, LAW-R increased fecal p-cresol concentration, and fecal abundance of a p-cresol-producing bacterium, Clostridium from the Peptostreptococcaceae family, but both were reduced by HAW-R. Amylose level did not affect measures of fecal consistency or adversely affecting digestive comfort. CONCLUSIONS: Increasing RS intake of healthy adults by substituting refined conventional wheat with refined HAW modulates fecal metabolites and microbes associated with gastrointestinal health.This trial was registered at anzctr.org.au as ACTRN12618001060235.

Eucaloric diets enriched in palm olein, cocoa butter, and soybean oil did not differentially affect liver fat concentration in healthy participants: a 16-week randomized controlled trial.

BACKGROUND: Effects of dietary fat quality on liver fat remain to be elucidated. Inconsistent evidence may be influenced by fatty acid saturation, chain-length, and regio-specificity within triacylglycerol (TAG) molecules. OBJECTIVES: We aimed to compare eucaloric diets enriched in palm olein (POo), cocoa butter (COB), and soybean oil (SBO) on liver fat concentration in healthy participants. Secondary outcomes included visceral (VAT) and abdominal subcutaneous (aSCAT) adipose tissue, plus other obesity and cardiometabolic health outcomes. METHODS: Eighty-three healthy participants (20-45 y, BMI 18.5-27.5 kg/m2) commenced and 64 completed a 16-wk randomized parallel intervention, preceded by a 2-wk run-in. Participants consumed identical eucaloric background diets differing in test fats [contributing 20% total energy intake (%E)], providing 33%E total fat with the following ratios for PUFAs/SFAs/MUFAs: POo, 4.2/13.5/15%E; SBO, 14.4/8.8/9.4%E; COB, 2.3/19.5/11%E. Liver fat and abdominal adiposity were measured at weeks 0 and 16 using 1H-magnetic resonance spectroscopy/imaging; all other outcomes were measured at 0, 4, 8, 12, and 16 wk. RESULTS: Fat quality did not affect liver fat concentration, VAT, aSCAT, obesity indexes, blood pressure, liver enzymes, leptin, or fasting glucose. Body fat mass decreased with SBO and COB compared with POo. SBO decreased serum total cholesterol (TC), LDL cholesterol, and TC:HDL cholesterol relative to POo [estimated marginal mean (95% CI) differences: -0.57 (-0.94, -0.20) mmol/L; -0.37 (-0.68, -0.07) mmol/L; and -0.42 (-0.73, -0.11) mmol/L, respectively]. No diet differences were observed on HDL cholesterol, TAG, apoA1, apoB, apoB:apoA1, or fecal free fatty acids (FFAs), except for lower FFA pentadecanoic acid (15:0) with COB than with SBO and POo. CONCLUSIONS: In healthy adults, when consumed as part of eucaloric typical Australian diets, 3 different dietary fat sources did not differentially affect liver fat concentration and amounts of adipose tissue. Effects on serum lipids were inconsistent across lipid profiles. The findings must be confirmed in metabolically impaired individuals before recommendations can be made.

Fatty acid regio-specificity of triacylglycerol molecules may affect plasma lipid responses to dietary fats-a randomised controlled cross-over trial.

BACKGROUND/OBJECTIVES: Hypercholesterolaemic effects of saturated fatty acids (SFA) may be influenced not only by the chain length, but also by their specific location within the triacylglycerol (TAG) molecule. We examined the hypothesis that dietary fats rich in SFA, but containing mostly unsaturated fatty acids in the sn-2 position with most SFA in sn-1 and -3 (palm olein [PO] and cocoa butter [CB]) will have similar serum lipid outcomes to unsaturated olive oil (OO). SUBJECTS/METHODS: Thirty-eight participants (20-40 yr, 18.5- ≤ 27.5 kg/m2) completed a 4-week randomised 3 × 3 crossover feeding intervention, preceded by 2-week run-in and separated by 2-week washout periods. Background diet contained 35 percentage of total energy (%E) fat, 18%E protein, 48%E carbohydrates, differing in test fats only (palm olein (PO), CB, OO; 20%E). Total cholesterol (TC)/high density lipoprotein cholesterol (HDL-C) ratio and related variables; TC, HDL-C, low density lipoprotein cholesterol (LDL-C), TAG, apoA1, ApoB, ApoA1 (apolipoprotein A1)/ApoB (apolipoprotein B), lipoprotein (a) (Lp(a)), NEFA, LDL sub-fractions, were assessed pre- and post-intervention. Data were analysed using mixed effects longitudinal models with a P-value < 0.05 considered significant. RESULTS: Changes in plasma fatty acids (P < 0.05) confirmed compliance; C18:1 increased with OO compared to PO and CB; C16:0 decreased with OO and C18:0 increased following CB. No differences were seen for TC/HDL-C (mean [95%CI] change for PO, 0.08[0.00, 0.15] mmol/L; CB, 0.06 [-0.05, 0.16] mmol/L; and OO, -0.01 [-0.15, 0.13] mmol/L; P = 0.53] or any other parameter including LDL sub-fractions. OO decreased IDL-A compared to PO (-2.2 [-4.31, -0.21] mg/dL, P = 0.03). CONCLUSION: In healthy young participants, plasma lipid responses to PO and CB, enriched in SFA but having primarily unsaturated fatty acid in the sn-2 position of TAG, did not differ from OO.

Telomere shortening in elderly individuals with mild cognitive impairment may be attenuated with ω-3 fatty acid supplementation: a randomized controlled pilot study.

OBJECTIVES: Excessive shortening of the telomeric ends of chromosomes is a marker of accelerated aging. Oxidative stress and nutritional deficiency may influence this process. The aim of this study was to investigate the effect of ω-3 polyunsaturated fatty acid (ω-3 PUFA) supplementation on telomeric shortening in elderly individuals with mild cognitive impairment (MCI). METHODS: Thirty-three adults ages > 65 y with MCI were randomized to receive a supplement rich in the long-chain ω-3 PUFAs eicosapentaenoic acid (EPA; 1.67 g EPA + 0.16 g docosahexaenoic acid DHA/d; n = 12) or DHA (1.55 g DHA + 0.40 g EPA/d; n = 12), versus ω-6 PUFA linoleic acid (LA; 2.2 g/d; n = 9) for 6 mo. RESULTS: The intervention did not show an increase in telomere length with treatment and there was a trend toward telomere shortening during the intervention period. Linear mixed modeling produced a robust model although statistically underpowered. Telomere shortening was greatest in the LA group (d = 0.21) than in the DHA (d = 0.12) and EPA groups (d = 0.06). Increased erythrocyte DHA levels were associated with reduced telomere shortening (r = -0.67; P = 0.02) in the DHA group. CONCLUSION: Telomeric shortening may be attenuated by ω-3 PUFA supplementation, requiring further investigation in larger samples.

Chronic alcohol exposure induces genome damage measured using the cytokinesis-block micronucleus cytome assay and aneuploidy in human B lymphoblastoid cell lines.

Excessive alcohol consumption is associated with an increased risk of a variety of cancers. The specific association between alcohol consumption and increased risk of breast cancer has been a consistent finding in numerous studies to date; however, the biological mechanism remains unknown. One possibility is that alcohol induces chromosome instability and aneuploidy events commonly seen in cancer. The cytokinesis-block micronucleus cytome assay was used to assess the ability of alcohol to induce DNA damage and aneuploidy in two human B lymphoblastoid cell lines--WIL2-NS and GM13705. The cells were treated chronically with physiologically relevant levels of alcohol (0.36 and 1.35% v/v) for a period of 6 weeks. Results demonstrate that in these cell lines, chronic treatment with alcohol induces micronuclei, nucleoplasmic bridges and nuclear buds, indicative of the various genome damaging events of chromosome loss and breakage, asymmetric chromosome rearrangement and gene amplification, respectively. Using chromogenic in situ hybridisation, we measured chromosome 17 aneuploidy in these cell lines. Results from this assay indicate that chronic treatment of alcohol induces aneuploidy (measured as chromosome 17 aneuploidy) in both cell lines. The results from this study support the hypothesis that alcohol is a probable cause of cancer initiation by inducing chromosomal instability and aneuploidy, which may be a result of multiple indirect mechanisms.

Application and adaptation of the in vitro micronucleus assay for the assessment of nutritional requirements of cells for DNA damage prevention.

DNA damage is a fundamental cause of developmental and degenerative diseases. The in vitro cytokinesis-block micronucleus cytome (CBMN-Cyt) assay is an established comprehensive method for assessing cytostasis and chromosome stability in cells. Originally developed to study the acute effects of single environmental genotoxicants, creative applications and adaptations to the basic protocol have allowed its use in evaluating the impacts of dietary micronutrients and micronutrient combinations (nutriomes) on DNA damage. In this review, we examine some of these studies and the important findings they have generated with respect to nutrient/nutrient, nutrient/genotype and nutrient/genotoxicant interactions, as well as assessment of the carcinogenic (or protective) potential of whole dietary patterns. In addition, we outline current knowledge gaps and technical limitations and propose future adaptations to enhance the applicability of the CBMN-Cyt method for in vivo predictions.

High-protein/high red meat and high-carbohydrate weight-loss diets do not differ in their effect on faecal water genotoxicity tested by use of the WIL2-NS cell line and with other biomarkers of bowel health.

The impact of popular weight-loss diets with different macronutrient profiles on bowel health in humans has not been previously assessed. The aim of this study was to investigate whether a high-protein/high red meat (HP) diet influences faecal water genotoxicity and other standard biomarkers of bowel health differently compared with a high-carbohydrate (HC) diet. Thirty-three male subjects were randomly assigned to a HP (35% protein, 40% carbohydrate) or HC (17% protein, 58% carbohydrate) isocaloric energy-restricted dietary intervention consisting of 12 weeks intensive weight loss followed by weight maintenance for up to 52 weeks. Faecal samples were collected at 0, 12 and 52 weeks. Faecal water genotoxicity was assessed in the WIL2-NS human B lymphoblastoid cell line by means of the cytokinesis-block micronucleus cytome assay. Average weight loss after 12 weeks was 9.3 ± 0.7kg for both diets, with no further change in weight at 52 weeks. Two-way ANOVA showed a significant effect with time (P<0.001) but not diet for total DNA damage, with a reduction in genotoxicity after 12 weeks intensive weight loss, and a subsequent increase after 9 months weight maintenance to levels not significantly different from baseline. There was no significant effect for time or diet on faecal pH, short-chain fatty acid excretion, phenol or p-cresol. Results suggest that HP and HC weight-loss diets may modify the carcinogenic profile of the bowel contents such that weight loss may exert a beneficial effect by reducing genotoxic load in the short term; however, these results require verification against a non-weight-loss control.

High protein-high red meat versus high carbohydrate weight loss diets do not differ in effect on genome stability and cell death in lymphocytes of overweight men.

The importance of diet in DNA damage prevention is well established; however, the comparison of weight loss diets with different micronutrient and macronutrient profiles on genome stability in peripheral blood lymphocytes (PBLs) has not been studied. This study tested the hypothesis that genome stability in PBLs of overweight men who consume a high protein-high red meat (HP) weight loss diet is different from that of overweight men who consume a high carbohydrate (HC) weight loss diet. Thirty-three male subjects were randomly assigned to an HP or HC isocaloric energy-restricted dietary intervention for 12 weeks intensive weight loss and weight maintenance up to 52 weeks. Blood samples were collected at 0, 12 and 52 weeks. DNA damage in PBLs was assessed using the cytokinesis-block micronucleus cytome (CBMN-Cyt) assay. Average weight loss after 12 weeks was 9.3 +/- 0.7 kg for both diets, with no further change at 52 weeks. Two-way analysis of variance showed no time or diet effect on micronucleus frequency (chromosome loss/breaks). There was a significant trend with time (P = 0.03) but not diet, for reduction of nuclear buds (gene amplification). There was a positive trend with time for increased nucleoplasmic bridges (chromosome rearrangement) (P = 0.051). Necrosis and apoptosis both significantly decreased with time (P = 0.037 and P = 0.007, respectively) with no diet effect. There was no significant effect of time or diet for nuclear division index, a biomarker of immune response. The results suggest that the effect of the HP weight loss diet on DNA damage measured using the CBMN-Cyt assay in PBLs was not different from that observed for the HC weight loss diet.