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1.
Appetite control: hormones or diet strategies?
Freire, RH, Alvarez-Leite, JI
Current opinion in clinical nutrition and metabolic care. 2020;(5):328-335
Abstract
PURPOSE OF REVIEW Appetite control results from metabolic, behavioral, and environmental factors that influence hunger and the desire to eat. We summarize the latest advances in the hormonal and nutritional strategies to control appetite and reduce hunger. RECENT FINDINGS The fed-hunger-state is regulated by central and peripheric hormones, which modulate energy balance. Leptin, insulin, ghrelin, peptide YY (PYY), and other gut-derived peptides represent the main appetite controllers. The role of orexins, obestatin, and liver-expressed antimicrobial peptide 2 has been uncovered recently. New insights have demonstrated the role of hippocampal activity as a possible mechanism of action. Glucagon-like peptide 1 (GLP1) receptor agonists are well known agents controlling appetite. Association of GLP1 receptor agonist, PYY, or glucose-dependent insulinotropic polypeptide agonists have been tested as new approaches. Appetite-control hormones have also risen as factors involved in the efficacy of bariatric procedures. High-protein, ketogenic diet, and intermittent fasting have been described as nutritional strategies to reduce appetite, although the physiological mechanism and long-term safety remains unclear. SUMMARY Appetite control has been an important target for the treatment of obesity and associated disorders. New studies have demonstrated promising adoption of dietary approaches, hormone-based drugs, and bariatric surgery to control energy intake. Further research will establish a significant association, benefits, and safety of these new therapies.
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Responsive versus scheduled feeding for preterm infants.
Watson, J, McGuire, W
The Cochrane database of systematic reviews. 2016;(8):CD005255
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Abstract
BACKGROUND Feeding preterm infants in response to their hunger and satiation cues (responsive, cue-based, or infant-led feeding) rather than at scheduled intervals might enhance infants' and parents' experience and satisfaction, help in the establishment of independent oral feeding, increase nutrient intake and growth rates, and allow earlier hospital discharge. OBJECTIVES To assess the effect of a policy of feeding preterm infants on a responsive basis versus feeding prescribed volumes at scheduled intervals on growth rates, levels of parent satisfaction, and time to hospital discharge. SEARCH METHODS We used the standard search strategy of the Cochrane Neonatal Review group to search the Cochrane Central Register of Controlled Trials (CENTRAL 2016, Issue 1), MEDLINE via PubMed (1966 to 17 February 2016), Embase (1980 to 17 February 2016), and CINAHL (1982 to 17 February 2016). We also searched clinical trials' databases, conference proceedings, and the reference lists of retrieved articles for randomised controlled trials and quasi-randomised trials. SELECTION CRITERIA Randomised controlled trials (RCTs) or quasi-RCTs that compared a policy of feeding preterm infants on a responsive basis versus feeding at scheduled intervals. DATA COLLECTION AND ANALYSIS Two review authors assessed trial eligibility and risk of bias and undertook data extraction independently. We analysed the treatment effects in the individual trials and reported the risk ratio and risk difference for dichotomous data and mean difference (MD) for continuous data, with respective 95% confidence intervals (CIs). We used a fixed-effect model in meta-analyses and explored the potential causes of heterogeneity in sensitivity analyses. We assessed the quality of evidence at the outcome level using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach. MAIN RESULTS We found nine eligible RCTs including 593 infants in total. These trials compared responsive with scheduled interval regimens in preterm infants in the transition phase from intragastric tube to oral feeding. The trials were generally small and contained various methodological weaknesses including lack of blinding and incomplete assessment of all randomised participants. Meta-analyses, although limited by data quality and availability, suggest that responsive feeding results in slightly slower rates of weight gain (MD -1.36, 95% CI -2.44 to -0.29 g/kg/day), and provide some evidence that responsive feeding reduces the time taken for infants to transition from enteral tube to oral feeding (MD -5.53, 95% CI -6.80 to -4.25 days). GRADE assessments indicated low quality of evidence. The importance of this finding is uncertain as the trials did not find a strong or consistent effect on the duration of hospitalisation. None of the included trials reported any parent, caregiver, or staff views. AUTHORS' CONCLUSIONS Overall, the data do not provide strong or consistent evidence that responsive feeding affects important outcomes for preterm infants or their families. Some (low quality) evidence exists that preterm infants fed in response to feeding and satiation cues achieve full oral feeding earlier than infants fed prescribed volumes at scheduled intervals. This finding should be interpreted cautiously because of methodological weaknesses in the included trials. A large RCT would be needed to confirm this finding and to determine if responsive feeding of preterm infants affects other important outcomes.
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Understanding eating in the absence of hunger among young children: a systematic review of existing studies.
Lansigan, RK, Emond, JA, Gilbert-Diamond, D
Appetite. 2015;:36-47
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Abstract
BACKGROUND Eating in the Absence of Hunger (EAH), or consuming highly palatable foods when satiated, is one behavioral pathway that may lead to childhood obesity. EAH is an objective, laboratory-based measure. A more comprehensive understanding of potential determinants of EAH could inform childhood obesity programs outside of a laboratory setting. OBJECTIVE Systematic review of EAH experiments to identify individual, familial, and societal-level correlates of EAH among children 12 years of age or younger. DESIGN 1487 studies were retrieved from five electronic databases (Medline [PubMed], Web of Science, Cochrane Library, CINAHL, PsycINFO). Eligible studies were those that measured EAH as initially operationalized in a laboratory setting enrolling children ≤12 years or reporting age-specific results for children ≤12 years. Only articles written in English were included. RESULTS 12 cross-sectional, six prospective, and one behavioral-intervention studies were included in the review. EAH was observable among boys and girls; absolute levels of EAH increased with age; and maternal feeding styles were associated with EAH among girls. The most consistent evidence supported increased levels of EAH among overweight and obese versus normal weight children, both cross-sectionally and prospectively. Two studies supported a genetic component to EAH. CONCLUSIONS Studies enrolling independent samples support a positive association between weight status and EAH among children; studies addressing causality are needed. Other various individual, genetic, and familiar characteristics were associated with EAH, yet studies among more heterogeneous sample populations are needed to confirm findings. Studies addressing societal-level factors related to EAH were absent.
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4.
Responsive versus scheduled feeding for preterm infants.
Watson, J, McGuire, W
The Cochrane database of systematic reviews. 2015;(10):CD005255
Abstract
BACKGROUND Feeding preterm infants in response to their hunger and satiation cues (responsive, cue-based, or infant-led feeding) rather than at scheduled intervals might enhance infants' and parents' experience and satisfaction, help in the establishment of independent oral feeding, increase nutrient intake and growth rates, and allow earlier hospital discharge. OBJECTIVES To assess the effect of feeding preterm infants on a responsive basis versus feeding prescribed volumes at scheduled intervals on growth, duration of hospital stay, and parental satisfaction. SEARCH METHODS We used the standard search strategy of the Cochrane Neonatal Review Group. This included searches of the Cochrane Central Register of Controlled Trials (CENTRAL, The Cochrane Library, Issue 9, 2015), MEDLINE (1966 to September 2015), EMBASE (1980 to September 2015), and CINAHL (1982 to September 2015), conference proceedings, previous reviews, and trial registries. SELECTION CRITERIA Randomised controlled trials (RCTs) or quasi-RCTs that compared a policy of feeding preterm infants on a responsive basis versus feeding at scheduled intervals. DATA COLLECTION AND ANALYSIS Two review authors assessed trial eligibility and risk of bias and undertook data extraction independently. We analysed the treatment effects in the individual trials and reported the risk ratio and risk difference for dichotomous data and mean difference (MD) for continuous data, with respective 95% confidence intervals (CIs). We used a fixed-effect model in meta-analyses and explored the potential causes of heterogeneity in sensitivity analyses. MAIN RESULTS We found nine eligible RCTs including 593 infants in total. These trials compared responsive with scheduled interval regimens in preterm infants in the transition phase from intragastric tube to oral feeding. The trials were generally small and contained various methodological weaknesses including lack of blinding and incomplete assessment of all randomised participants. Meta-analyses, although limited by data quality and availability, suggest that responsive feeding results in slightly slower rates of weight gain (MD -1.4, 95% CI -2.4 to -0.3 g/kg/day), and provide some evidence that responsive feeding reduces the time taken for infants to transition from enteral tube to oral feeding (MD -5.5, 95% CI -6.8 to -4.2 days). The importance of this finding is uncertain as the trials did not find a strong or consistent effect on the duration of hospitalisation. None of the included trials reported any parent, caregiver, or staff views. AUTHORS' CONCLUSIONS Overall, the data do not provide strong or consistent evidence that responsive feeding affects important outcomes for preterm infants or their families. Some evidence exists that preterm infants fed in response to feeding and satiation cues achieve full oral feeding earlier than infants fed prescribed volumes at scheduled intervals. However, this finding should be interpreted cautiously because of methodological weaknesses in the included trials. A large RCT would be needed to confirm this finding and to determine if responsive feeding of preterm infants affects other important outcomes.
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Modulation of hunger and satiety: hormones and diet.
Feinle-Bisset, C
Current opinion in clinical nutrition and metabolic care. 2014;(5):458-64
Abstract
PURPOSE OF REVIEW To highlight recent research developments relating to the effects of, and interactions between, hormones and diet, as well as underlying mechanisms, on appetite, energy intake and body weight. For this purpose, clinically relevant English language articles were reviewed from October 2012 to April 2014. RECENT FINDINGS The mechanisms underlying nutrient-induced energy intake suppression differ between dietary protein and lipid. High-fat, energy-dense diets compromise the satiating effects of gut hormones, and, therefore, promote further overconsumption. These effects are mediated by changes in the signalling in both peripheral and central pathways, and may only be partially reversible by dietary restriction. Additional factors, including probiotics, meal-related factors (e.g., eating speed and frequency), circadian influences and gene polymorphisms, also modify energy intake and eating behaviour. SUMMARY Research continues to unravel the pathways and mechanisms underlying the nutrient-induced and diet-induced regulation of energy intake, as well as the changes, both peripherally and in the central nervous system, brought about by the consumption of high-fat, energy-dense diets. Much further work is required to translate this knowledge into novel, and effective, approaches for the management and treatment of obesity and associated metabolic disorders.
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Regulating satiety in bulimia nervosa: the role of cholecystokinin.
Hannon-Engel, S
Perspectives in psychiatric care. 2012;(1):34-40
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PURPOSE Individuals with bulimia nervosa (BN) report altered perceptions in hunger, fullness, and satiety. This article reviews the role of cholecystokinin (CCK), a satiety-producing hormone, in the regulation of binge eating in those who suffer from BN. CONCLUSION Studies have shown that CCK is decreased in individuals with BN when compared with healthy controls. Decreased CCK functioning may contribute to impaired satiety and thus binge eating in this patient population. Depending on the macronutrient composition of food choices, CCK release can be differentially influenced. For instance, protein is a potent stimulator of a CCK response. Eating more protein-rich meals increases the release of CCK, increasing satiety and ending a meal. PRACTICE IMPLICATIONS Knowledge of CCK functioning and the utility of manipulating the macronutrient composition of meals may inform standard behavioral treatment strategies for those who suffer from BN.
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Review article: the role of gastric motility in the control of food intake.
Janssen, P, Vanden Berghe, P, Verschueren, S, Lehmann, A, Depoortere, I, Tack, J
Alimentary pharmacology & therapeutics. 2011;(8):880-94
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BACKGROUND From a classical point of view, gastric motility acts to clear the stomach between meals, whereas postprandial motility acts to provide a reservoir for food, mixing and grinding the food and to assure a controlled flow of food to the intestines. AIM: To summarise findings that support the role of gastric motility as a central mediator of hunger, satiation and satiety. METHODS A literature review using the search terms 'satiety', 'satiation' and 'food intake' was combined with specific terms corresponding to the sequence of events during and after food intake. RESULTS During food intake, when gastric emptying of especially solids is limited, gastric distension and gastric accommodation play an important function in the regulation of satiation. After food intake, when the stomach gradually empties, the role of gastric distension in the determination of appetite decreases and the focus will shift to gastric emptying and intestinal exposure of the nutrients. Finally, we have discussed the role of the empty stomach and the migrating motor complex in the regulation of hunger signals. CONCLUSIONS Our findings indicate that gastric motility is a key mediator of hunger, satiation and satiety. More specifically, gastric accommodation and gastric emptying play important roles in the regulation of gastric (dis)tension and intestinal exposure of nutrients and hence control satiation and satiety. Correlations between gastric accommodation, gastric emptying and body weight indicate that gastric motility can also play a role in the long-term regulation of body weight.
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Hunger and thirst: issues in measurement and prediction of eating and drinking.
Mattes, RD
Physiology & behavior. 2010;(1):22-32
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Associations between hunger and eating and between thirst and drinking are generally weak. This stems, in part, from limitations in the measurement of these sensations which generally rely on temporal, motivational, metabolic and/or self-reported descriptive indices. Each is critically reviewed. Also problematic is the fact that the deterministic depletion-repletion concept of ingestive behavior fails to account for influences of a multitude of contravening cognitive, social, sensory and logistical factors. Although hunger and thirst serve some parallel purposes, sharp distinctions are also present with health implications. Of particular note are the observations that thirst ratings are higher and more stable over the day compared to hunger and thirst may be more motivating to drink than hunger is to eat. Coupling these observations with evidence that beverages have limited satiety value, they pose particular challenges and opportunities. Beverages can facilitate the delivery of nutrients to those desiring or requiring them, but also to those where they are not desired or required. The benefits and risks are a function of their use rather than their inherent properties.
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Is glycemic index of food a feasible predictor of appetite, hunger, and satiety?
Niwano, Y, Adachi, T, Kashimura, J, Sakata, T, Sasaki, H, Sekine, K, Yamamoto, S, Yonekubo, A, Kimura, S
Journal of nutritional science and vitaminology. 2009;(3):201-7
Abstract
This review assesses the feasibility of using glycemic index (GI) as a predictor of appetite, hunger and satiety by surveying published human intervention studies. We also discuss the relationship between GI and two appetite/satiety control hormones, leptin and ghrelin. Ingestion of high-GI food increased hunger and lowered satiety in short-term human intervention studies. This effect may be attributed to the rapid decline in blood glucose level following a hyperinsulinemic response caused by a sharp and transient increase in blood glucose level that occurs after the ingestion of high-GI food, which is defined as the glucostatic theory. However, appetite, hunger and satiety after the ingestion of foods with varying GI were inconsistent among long-term human intervention studies. From the few relevant long-term studies available, we selected two recent well-designed examples for analysis, but they failed to elicit clear differences in glycemic and insulinemic responses between high- and low-GI meals (consisting of a combination of different foods or key carbohydrate-rich foods incorporated into habitual diets). One of the reasons that these studies could not predict glycemic response to mixed meals is presumably that the GI of each particular food was not reflected in that of the mixed meals as a whole. Thus, it is difficult to conclude that the GI values of foods or mixed meals are a valid long-term predictor for appetite, hunger and satiety. Both insulin and insulin-mediated glucose uptake and metabolism in adipose tissue affect blood leptin concentration and its diurnal pattern. Circulating ghrelin level is suppressed by carbohydrate-rich meals, presumably via glycemia and insulinemia. Accordingly, low-GI foods may not necessarily increase satiety or suppress appetite and/or hunger because of the lack of insulin-mediated leptin stimulation and ghrelin suppression. However, insulin-mediated leptin stimulation and ghrelin suppression per se is not consistent among studies; thus we were not able to identify a clear relationship among GI, satietogenic leptin, and appetitic ghrelin.
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Neurophysiology of hunger and satiety.
Smith, PM, Ferguson, AV
Developmental disabilities research reviews. 2008;(2):96-104
Abstract
Hunger is defined as a strong desire or need for food while satiety is the condition of being full or gratified. The maintenance of energy homeostasis requires a balance between energy intake and energy expenditure. The regulation of food intake is a complex behavior. It requires discrete nuclei within the central nervous system (CNS) to detect signals from the periphery regarding metabolic status, process and integrate this information in a coordinated manner and to provide appropriate responses to ensure that the individual does not enter a state of positive or negative energy balance. This review of hunger and satiety will examine the CNS circuitries involved in the control of energy homeostasis as well as signals from the periphery, both hormonal and neural, that convey pertinent information regarding short-term and long-term energy status of the individual.