Maternal mindful eating as a target for improving metabolic outcomes in pregnant women with obesity.

BACKGROUND: Maternal diet and eating behaviors have the potential to influence the metabolic milieu in pregnancies complicated by obesity, with implications for the developmental programming of offspring obesity. Emerging evidence suggests that mindfulness during eating may influence metabolic health in non-pregnant populations, but its effects in the context of pregnancy is less well understood. This study explored the individual and combined effects of mindful eating and diet quality on metabolic outcomes among pregnant women with obesity. METHODS: In 46 pregnant women (body mas index >30 kg/m2) enrolled in the MomEE observational study, mindful eating (Mindful Eating Questionnaire, MEQ) and energy-adjusted dietary inflammatory index (DII, from 7 days of food photography) was assessed at two time points and the mean pregnancy values computed. Rate of gestational weight gain (GWG) and fat mass gain per week were determined from measured weight and body composition using a three-compartment method, respectively, at each assessment. Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) and ghrelin concentrations were determined from fasting blood samples in late gestation (35-37 weeks). Linear regression was used to examine the association of the MEQ and its subscales (where higher values indicate more mindful eating) with metabolic outcomes, adjusting for covariates: maternal age, pregravid body mass index, race, parity, DII. The effects of the MEQ*DII interaction was also tested. RESULTS: Total MEQ scores were not associated with rate of weight or fat mass gain, although greater distracted eating behavior was associated with greater adiposity gain (weight and fat mass). Mindful eating was inversely associated with insulin resistance, although this was attenuated to non-significance after additional adjustment for GWG. Total MEQ and the external eating subscale was significantly inversely associated with fasted ghrelin, such that less tendency to eat under the influence of external cues was associated with lower ghrelin concentrations. After false discovery rate adjustment for multiple testing, only the association of the total MEQ and external eating subscale with ghrelin levels trended towards significance. The DII was not associated with MEQ scores or outcome variables, nor did it moderate the effect of MEQ on any of the outcomes. CONCLUSION: This study generates early evidence to suggest that mindful eating holds potential as a tool to improve metabolic health outcomes in pregnant women with obesity, although further research is required on this topic. Prenatal lifestyle interventions should consider including mindfulness during eating to determine its efficacy for reducing adverse pregnancy and offspring health outcomes associated with maternal obesity.

Behavioral Determinants of Objectively Assessed Diet Quality in Obese Pregnancy.

Interventions to promote healthy pregnancy in women with obesity by improving diet quality have been widely unsuccessful. We hypothesized that diet quality is determined by eating behaviors, but evidence in women with obesity is lacking. We evaluated diet quality and eating behavior in 56 women with obesity (mean ± SEM, 36.7 ± 0.7 kg/m2, 46% White, 50% nulliparous) early in pregnancy (14.9 ± 0.1 weeks). Diet quality was objectively assessed with food photography over six days and defined by Healthy Eating Index. Eating behaviors were assessed by validated questionnaires. Women reported consuming diets high in fat (38 ± 1% of energy) and the HEI was considered "poor" on average (46.7 ± 1.3), and for 71% of women. Diet quality was independently associated with education level (p = 0.01), food cravings (p < 0.01), and awareness towards eating (p = 0.01). Cravings for sweets and fast foods were positively correlated with respective intakes of these foods (p < 0.01 and p = 0.04, respectively), whereas cravings for fruits and vegetables did not relate to diet intake. We provide evidence of the determinants of poor diet quality in pregnant women with obesity. Based on this observational study, strategies to improve diet quality and pregnancy outcomes are to satisfy cravings for healthy snacks and foods, and to promote awareness towards eating behaviors.

The effects of polyphenol supplementation on adipose tissue morphology and gene expression in overweight and obese humans.

Dietary polyphenols have beneficial effects on adipose tissue mass and function in rodents, but human studies are scarce. In a randomized, placebo-controlled study, 25 (10 women) overweight and obese humans received a combination of the polyphenols epigallocatechin-gallate and resveratrol (282 mg/d, 80 mg/d, respectively, EGCG+RES, n = 11) or placebo (PLA, n = 14) supplementation for 12 weeks. Abdominal subcutaneous adipose tissue (SAT) biopsies were collected for assessment of adipocyte morphology and micro-array analysis. EGCG+RES had no effects on adipocyte size and distribution compared with PLA. However, we identified pathways contributing to adipogenesis, cell cycle and apoptosis were significantly downregulated by EGCG+RES versus PLA. Furthermore, EGCG+RES significantly decreased expression of pathways related to energy metabolism, oxidative stress, inflammation, and immune defense as compared with PLA. In conclusion, the SAT gene expression profile indicates a reduced cell turnover after 12-week EGCG+RES in overweight-obese subjects. It remains to be elucidated whether these alterations translate into long-term metabolic effects.

Global testing of shifts in metabolic phenotype.

INTRODUCTION: Current metabolomics approaches to unravel impact of diet- or lifestyle induced phenotype variation and shifts predominantly deploy univariate or multivariate approaches, with a posteriori interpretation at pathway level. This however often provides only a fragmented view on the involved metabolic pathways. OBJECTIVES: To demonstrate the feasibility of using Goeman's global test (GGT) for assessment of variation and shifts in metabolic phenotype at the level of a priori defined pathways. METHODS: Two intervention studies with identified phenotype variations and shifts were examined. In a weight loss (WL) intervention study obese subjects received a mixed meal challenge before and after WL. In a polyphenol (PP) intervention study obese subjects received a high fat mixed meal challenge (61E% fat) before and after a PP intervention. Plasma samples were obtained at fasting and during the postprandial response. Besides WL- and PP-induced phenotype shifts, also correlation of plasma metabolome with phenotype descriptors was assessed at pathway level. The plasma metabolome covered organic acids, amino acids, biogenic amines, acylcarnitines and oxylipins. RESULTS: For the population of the WL study, GGT revealed that HOMA correlated with the fasting levels of the TCA cycle, BCAA catabolism, the lactate, arginine-proline and phenylalanine-tyrosine pathways. For the population of the PP study, HOMA correlated with fasting metabolite levels of TCA cycle, fatty acid oxidation and phenylalanine-tyrosine pathways. These correlations were more pronounced for metabolic pathways in the fasting state, than during the postprandial response. The effect of the WL and PP intervention on a priori defined metabolic pathways, and correlation of pathways with insulin sensitivity as described by HOMA was in line with previous studies. CONCLUSION: GGT confirmed earlier biological findings in a hypothesis led approach. A main advantage of GGT is that it provides a direct view on involvement of a priori defined pathways in phenotype shifts.

Combined epigallocatechin-3-gallate and resveratrol supplementation for 12 wk increases mitochondrial capacity and fat oxidation, but not insulin sensitivity, in obese humans: a randomized controlled trial.

BACKGROUND: The obese insulin-resistant state is characterized by impairments in lipid metabolism. We previously showed that 3-d supplementation of combined epigallocatechin-3-gallate and resveratrol (EGCG+RES) increased energy expenditure and improved the capacity to switch from fat toward carbohydrate oxidation with a high-fat mixed meal (HFMM) test in men. OBJECTIVE: The present study aimed to investigate the longer-term effect of EGCG+RES supplementation on metabolic profile, mitochondrial capacity, fat oxidation, lipolysis, and tissue-specific insulin sensitivity. DESIGN: In this randomized double-blind study, 38 overweight and obese subjects [18 men; aged 38 ± 2 y; body mass index (kg/m(2)): 29.7 ± 0.5] received either EGCG+RES (282 and 80 mg/d, respectively) or placebo for 12 wk. Before and after the intervention, oxidative capacity and gene expression were assessed in skeletal muscle. Fasting and postprandial (HFMM) lipid metabolism was assessed by using indirect calorimetry, blood sampling, and microdialysis. Tissue-specific insulin sensitivity was assessed by a hyperinsulinemic-euglycemic clamp with [6,6-(2)H2]-glucose infusion. RESULTS: EGCG+RES supplementation did not affect the fasting plasma metabolic profile. Although whole-body fat mass was not affected, visceral adipose tissue mass tended to decrease after the intervention compared with placebo (P-time × treatment = 0.09). EGCG+RES supplementation significantly increased oxidative capacity in permeabilized muscle fibers (P-time × treatment < 0.05, P-EGCG+RES < 0.05). Moreover, EGCG+RES reduced fasting (P-time × treatment = 0.03) and postprandial respiratory quotient (P-time × treatment = 0.01) compared with placebo. Fasting and postprandial fat oxidation was not significantly affected by EGCG+RES (P-EGCG+RES = 0.46 and 0.38, respectively) but declined after placebo (P-placebo = 0.05 and 0.03, respectively). Energy expenditure was not altered (P-time × treatment = 0.96). Furthermore, EGCG+RES supplementation attenuated the increase in plasma triacylglycerol concentrations during the HFMM test that was observed after placebo (P-time × treatment = 0.04, P-placebo = 0.01). Finally, EGCG+RES had no effect on insulin-stimulated glucose disposal, suppression of endogenous glucose production, or lipolysis. CONCLUSION: Twelve weeks of EGCG+RES supplementation increased mitochondrial capacity and stimulated fat oxidation compared with placebo, but this did not translate into increased tissue-specific insulin sensitivity in overweight and obese subjects. This trial was registered at clinicaltrials.gov as NCT02381145.

A 3-day EGCG-supplementation reduces interstitial lactate concentration in skeletal muscle of overweight subjects.

Green tea, particularly epigallocatechin-3-gallate (EGCG), may affect body weight and composition, possibly by enhancing fat oxidation. The aim of this double-blind, randomized placebo-controlled cross-over study was to investigate whether 3-day supplementation with EGCG (282 mg/day) stimulates fat oxidation and lipolysis in 24 overweight subjects (age = 30 ± 2 yrs, BMI = 27.7 ± 0.3 kg/m(2)). Energy expenditure, substrate metabolism and circulating metabolites were determined during fasting and postprandial conditions. After 6 h, a fat biopsy was collected to examine gene expression. In 12 subjects, skeletal muscle glycerol, glucose and lactate concentrations were determined using microdialysis. EGCG-supplementation did not alter energy expenditure and substrate oxidation compared to placebo. Although EGCG reduced postprandial circulating glycerol concentrations (P = 0.015), no difference in skeletal muscle lipolysis was observed. Fasting (P = 0.001) and postprandial (P = 0.003) skeletal muscle lactate concentrations were reduced after EGCG-supplementation compared to placebo, despite similar tissue blood flow. Adipose tissue leptin (P = 0.05) and FAT/CD36 expression (P = 0.08) were increased after EGCG compared to placebo. In conclusion, 3-day EGCG-supplementation decreased postprandial plasma glycerol concentrations, but had no significant effects on skeletal muscle lipolysis and whole-body fat oxidation in overweight individuals. Furthermore, EGCG decreased skeletal muscle lactate concentrations, which suggest a shift towards a more oxidative muscle phenotype.