Suchergebnisse

OBJECTIVE: The goals of this research was (1) to analyze the role of emotional eating behavior on weight-loss progression during a 30-week weight-loss program in 1,272 individuals from a large Mediterranean population and (2) to test for interaction between CLOCK 3111 T/C SNP and emotional eating behavior on the effectiveness of the weight-loss program. DESIGN AND METHODS: A total of 1,272 overweight and obese participants (BMI: 31±5 kg/m2), aged 20 to 65 years, attending outpatient weight-loss clinics were recruited for this analysis. Emotional eating behavior was assessed by the Emotional Eating Questionnaire (EEQ), a questionnaire validated for overweight and obese Spanish subjects. Anthropometric measures, dietary intake and weight-loss progression were assessed and analyzed throughout the 30-week program. Multivariate analysis and linear regression models were performed to test for gene-environment interaction. RESULTS: Weight-loss progression during the 30-week program differed significantly according to the degree of emotional eating behavior. Participants classified as 'very emotional eaters' experienced more irregular (P = 0.007) weight-loss, with a lower rate of weight decline (-0.002 vs. -0.003, P = 11), lost significantly less weight than those C carriers with a low emotional score (<11) (P = 0.005). CONCLUSIONS: Emotional eating behavior associates with weight-loss pattern, progression and total weight-loss. Additionally, CLOCK 3111 T/C SNP interacts with emotional eating behavior to modulate total weight loss. These results suggest that the assessment of this locus and emotional eating behavior could improve the development of effective, long-tern weight-management interventions. ; This study was supported by grants from the Tomas Pascual and Pilar Gomez-Cuetara Foundations, the Spanish Government of Science and Innovation (BFU2011-24720), and Seneca Foundation from the Government of Murcia (15123/PI/10). National Heart, Lung, and Blood Institute grants HL-54776, National Institute of Diabetes and Digestive and Kidney Diseases, Grant Number DK075030 and by contracts 53-K06-5-10 and 58-1950-9-001 from the US Departmentof Agriculture Research. ; Sí

The composition of the diet (what we eat) has been widely related to the microbiota profile. However, whether the timing of food consumption (when we eat) influences microbiota in humans is unknown. A randomized, crossover study was performed in 10 healthy normal-weight young women to test the effect of the timing of food intake on the human microbiota in the saliva and fecal samples. More specifically, to determine whether eating late alters daily rhythms of human salivary microbiota, we interrogated salivary microbiota in samples obtained at 4 specific time points over 24 h, to achieve a better understanding of the relationship between food timing and metabolic alterations in humans. Results revealed significant diurnal rhythms in salivary diversity and bacterial relative abundance (i.e., TM7 and Fusobacteria) across both early and late eating conditions. More importantly, meal timing affected diurnal rhythms in diversity of salivary microbiota toward an inverted rhythm between the eating conditions, and eating late increased the number of putative proinflammatory taxa, showing a diurnal rhythm in the saliva. In a randomized, crossover study, we showed for the first time the impact of the timing of food intake on human salivary microbiota. Eating the main meal late inverts the daily rhythm of salivary microbiota diversity which may have a deleterious effect on the metabolism of the host ; This work was supported by Spanish Government of Economy and Competitiveness (MINECO) Grants AGL2015-707487-P (to M.C.C.) and SAF2014-52480R; the European Regional Development Fund (ERDF); U.S. National Institutes of Health (NIH) National Institute of Diabetes and Digestive and Kidney Diseases Grants R01DK102696 and DK1-R01DK_105072-01A1 (to M.G.), and R01 DK099512 and R01DK105072 (to F.A.J.L.S.); and NIH National, Heart, Lung, and Blood Institute Grants R01 HL094806, R01 HL140574 and R01 HL118601 (to F.A.J.L.S.). F.A.J.L.S. has received speaker fees from Bayer Healthcare, Sentara Healthcare, Philips, and Kellogg Company. The remaining authors declare no conflicts of interest. ; Peer reviewed

The composition of the diet (what we eat) has been widely related to the microbiota profile. However, whether the timing of food consumption (when we eat) influences microbiota in humans is unknown. A randomized, crossover study was performed in 10 healthy normal-weight young women to test the effect of the timing of food intake on the human microbiota in the saliva and fecal samples. More specifically, to determine whether eating late alters daily rhythms of human salivary microbiota, we interrogated salivary microbiota in samples obtained at 4 specific time points over 24 h, to achieve a better understanding of the relationship between food timing andmetabolic alterations in humans. Results revealed significant diurnal rhythms in salivary diversity and bacterial relative abundance (i.e., TM7 and Fusobacteria) across both early and late eating conditions. More importantly, meal timing affected diurnal rhythms in diversity of salivary microbiota toward an inverted rhythm between the eating conditions, and eating late increased the number of putative proinflammatory taxa, showing a diurnal rhythm in the saliva. In a randomized, crossover study, we showed for the first time the impact of the timing of food intake on human salivary microbiota. Eating the main meal late inverts the daily rhythm of salivary microbiota diversity which may have a deleterious effect on the metabolism of the host. ; This work was supported by Spanish Government of Economy and Competitiveness (MINECO) Grants AGL2015-707487-P (to M.C.C.) and SAF2014-52480R; the European Regional Development Fund (ERDF); U.S. National Institutes of Health (NIH) National Institute of Diabetes and Digestive and Kidney Diseases Grants R01DK102696 and DK1-R01DK_105072-01A1 (to M.G.), and R01 DK099512 and R01DK105072 (to F.A.J.L.S.); and NIH National, Heart, Lung, and Blood Institute Grants R01 HL094806, R01 HL140574 and R01 HL118601 (to F.A.J.L.S.). ; Peer reviewed