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Effect of a Personalized Diet to Reduce Postprandial Glycemic Response vs a Low-fat Diet on Weight Loss in Adults With Abnormal Glucose Metabolism and Obesity: A Randomized Clinical Trial.
Popp, CJ, Hu, L, Kharmats, AY, Curran, M, Berube, L, Wang, C, Pompeii, ML, Illiano, P, St-Jules, DE, Mottern, M, et al
JAMA network open. 2022;5(9):e2233760
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Postprandial glycaemic response (PPGR) to foods can be different from person to person. This could be the reason why people experience different weight loss outcomes with standardised diets such as a low glycaemic index diet, low-fat diet or a low carbohydrate diet. In this single-centre, population-based, randomised, blinded clinical trial, 204 participants with irregular glucose metabolism and obesity were randomised to consume either a low-fat or personalised diet for six months in combination with fourteen behavioural change counselling sessions. The participants in the personalised diet group received a colour-coded meal score to indicate their estimated PPGR for different foods. The results of this study showed no significant weight reduction in the personalised diet group compared to the low-fat diet. Further robust studies are required to develop appropriate precision nutrition interventions for weight loss and energy balance. However, healthcare professionals can use the results of this study to understand that both a low-fat diet and a personalised diet, coupled with behavioural counselling, may be effective in promoting weight loss in obese populations with irregular glucose metabolism.
Abstract
IMPORTANCE Interindividual variability in postprandial glycemic response (PPGR) to the same foods may explain why low glycemic index or load and low-carbohydrate diet interventions have mixed weight loss outcomes. A precision nutrition approach that estimates personalized PPGR to specific foods may be more efficacious for weight loss. OBJECTIVE To compare a standardized low-fat vs a personalized diet regarding percentage of weight loss in adults with abnormal glucose metabolism and obesity. DESIGN, SETTING, AND PARTICIPANTS The Personal Diet Study was a single-center, population-based, 6-month randomized clinical trial with measurements at baseline (0 months) and 3 and 6 months conducted from February 12, 2018, to October 28, 2021. A total of 269 adults aged 18 to 80 years with a body mass index (calculated as weight in kilograms divided by height in meters squared) ranging from 27 to 50 and a hemoglobin A1c level ranging from 5.7% to 8.0% were recruited. Individuals were excluded if receiving medications other than metformin or with evidence of kidney disease, assessed as an estimated glomerular filtration rate of less than 60 mL/min/1.73 m2 using the Chronic Kidney Disease Epidemiology Collaboration equation, to avoid recruiting patients with advanced type 2 diabetes. INTERVENTIONS Participants were randomized to either a low-fat diet (<25% of energy intake; standardized group) or a personalized diet that estimates PPGR to foods using a machine learning algorithm (personalized group). Participants in both groups received a total of 14 behavioral counseling sessions and self-monitored dietary intake. In addition, the participants in the personalized group received color-coded meal scores on estimated PPGR delivered via a mobile app. MAIN OUTCOMES AND MEASURES The primary outcome was the percentage of weight loss from baseline to 6 months. Secondary outcomes included changes in body composition (fat mass, fat-free mass, and percentage of body weight), resting energy expenditure, and adaptive thermogenesis. Data were collected at baseline and 3 and 6 months. Analysis was based on intention to treat using linear mixed modeling. RESULTS Of a total of 204 adults randomized, 199 (102 in the personalized group vs 97 in the standardized group) contributed data (mean [SD] age, 58 [11] years; 133 women [66.8%]; mean [SD] body mass index, 33.9 [4.8]). Weight change at 6 months was -4.31% (95% CI, -5.37% to -3.24%) for the standardized group and -3.26% (95% CI, -4.25% to -2.26%) for the personalized group, which was not significantly different (difference between groups, 1.05% [95% CI, -0.40% to 2.50%]; P = .16). There were no between-group differences in body composition and adaptive thermogenesis; however, the change in resting energy expenditure was significantly greater in the standardized group from 0 to 6 months (difference between groups, 92.3 [95% CI, 0.9-183.8] kcal/d; P = .05). CONCLUSIONS AND RELEVANCE A personalized diet targeting a reduction in PPGR did not result in greater weight loss compared with a low-fat diet at 6 months. Future studies should assess methods of increasing dietary self-monitoring adherence and intervention exposure. TRIAL REGISTRATION ClinicalTrials.gov Identifier: NCT03336411.
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Altered metabolic homeostasis is associated with appetite regulation during and following 48-h of severe energy deprivation in adults.
Karl, JP, Smith, TJ, Wilson, MA, Bukhari, AS, Pasiakos, SM, McClung, HL, McClung, JP, Lieberman, HR
Metabolism: clinical and experimental. 2016;65(4):416-27
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Intermittent periods of substantial energy deficit, common among military personnel, result in multiple endocrine and metabolic signals. To date, the association between metabolic and endocrine markers with appetite regulation remain controversial. Using a novel model, the aim of this crossover study was to determine the effects of severe energy deprivation on cognitive function, and explore the metabolic response and its impact on appetite regulation in 23 young adults. Following prescribed exercise, participants were randomised to consume an energy balanced or energy deficit diet. The findings of this study showed that during energy deprivation, metabolic homeostasis modulates appetite independent of diet volume. Though further studies are required, these results suggest that metabolic and endocrine signals are associated with adipose and lean tissue loss to restore energy balance.
Abstract
BACKGROUND Military personnel frequently endure intermittent periods of severe energy deficit which can compromise health and performance. Physiologic factors contributing to underconsumption, and the subsequent drive to overeat, are not fully characterized. This study aimed to identify associations between appetite, metabolic homeostasis and endocrine responses during and following severe, short-term energy deprivation. METHODS Twenty-three young adults (17M/6F, 21±3years, BMI 25±3kg/m(2)) participated in a randomized, controlled, crossover trial. During separate 48-h periods, participants increased habitual energy expenditure by 1647±345kcal/d (mean±SD) through prescribed exercise at 40-65% VO2peak, and consumed provided isovolumetric diets designed to maintain energy balance at the elevated energy expenditure (EB; 36±93kcal/d energy deficit) or to produce a severe energy deficit (ED; 3681±716kcal/d energy deficit). Appetite, markers of metabolic homeostasis and endocrine mediators of appetite and substrate availability were periodically measured. Ad libitum energy intake was measured over 36h following both experimental periods. RESULTS Appetite increased during ED and was greater than during EB despite maintenance of diet volume (P=0.004). Ad libitum energy intake was 907kcal/36h [95% CI: 321, 1493kcal/36h, P=0.004] higher following ED compared to following EB. Serum beta-hydroxybutyrate, free fatty acids, branched-chain amino acids, dehydroepiandrosterone-sulfate (DHEA-S) and cortisol concentrations were higher (P<0.001 for all), whereas whole-body protein balance was more negative (P<0.001), and serum glucose, insulin, and leptin concentrations were lower (P<0.001 for all) during ED relative to during EB. Cortisol concentrations, but not any other hormone or metabolic substrate, were inversely associated with satiety during EB (R(2)=0.23, P=0.04). In contrast, serum glucose and DHEA-S concentrations were inversely associated with satiety during ED (R(2)=0.68, P<0.001). No associations between physiologic variables measured during EB and ad libitum energy intake following EB were observed. However, serum leptin and net protein balance measured during ED were inversely associated with ad libitum energy intake following ED (R(2)=0.48, P=0.01). CONCLUSION These findings suggest that changes in metabolic homeostasis during energy deprivation modulate appetite independent of reductions in diet volume. Following energy deprivation, physiologic signals of adipose and lean tissue loss may drive restoration of energy balance. CLINICAL TRIALS REGISTRATION www.clinicaltrials.gov #NCT01603550.
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Effects of exercise on gut peptides, energy intake and appetite.
Martins, C, Morgan, LM, Bloom, SR, Robertson, MD
The Journal of endocrinology. 2007;193(2):251-8
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The impact of physical activity on weight loss is difficult to quantify as it involves both long-term and short-term mechanisms. It has been suggested that the deficit created by exercise may be partially compensated for by an increase in energy intake, resulting in no weight loss. The aim of this crossover study was to investigate the acute effects of exercise on energy intake, appetite, satiety and postprandial hormone levels in 12 healthy volunteers. This study indicates that while exercise increases subsequent energy intake, it produces a significant decrease in overall energy balance. The authors conclude that moderate-intensity exercise temporarily decreases hunger sensations and is able to produce a short-term negative energy balance.
Abstract
This study investigated the acute effects of exercise on the postprandial levels of appetite-related hormones and metabolites, energy intake (EI) and subjective measures of appetite. Ghrelin, polypeptide YY (PYY), glucagon-like peptide-1 (GLP-1) and pancreatic polypeptide (PP) were measured in the fasting state and postprandially in 12 healthy, normal-weight volunteers (six males and six females) using a randomised crossover design. One hour after a standardised breakfast, subjects either cycled for 60 min at 65% of their maximal heart rate or rested. Subjective appetite was assessed throughout the study using visual analogue scales and subsequent EI at a buffet meal was measured at the end (3-h post-breakfast and 1-h post-exercise). Exercise significantly increased mean PYY, GLP-1 and PP levels, and this effect was maintained during the post-exercise period for GLP-1 and PP. No significant effect of exercise was observed on postprandial levels of ghrelin. During the exercise period, hunger scores were significantly decreased; however, this effect disappeared in the post-exercise period. Exercise significantly increased subsequent absolute EI, but produced a significant decrease in relative EI after accounting for the energy expended during exercise. Hunger scores and PYY, GLP-1 and PP levels showed an inverse temporal pattern during the 1-h exercise/control intervention. In conclusion, acute exercise, of moderate intensity, temporarily decreased hunger sensations and was able to produce a short-term negative energy balance. This impact on appetite and subsequent energy homeostasis was not explained by changes in postprandial levels of ghrelin; however, 'exercise-induced anorexia' may potentially be linked to increased PYY, GLP-1 and PP levels.