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"Hyperphagia"
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The hunger habit : why we eat when we're not hungry and how to stop
\"A program proven to heal our relationship with food and our bodies from New York Times bestselling author of Unwinding Anxiety. Anyone who struggles with overeating knows what it's like to feel out of control-and to feel the guilt attached to it. While ordinary anxiety feels like something that happens to us, the siren song of food cravings feels like something we should be able to control. The result is a toxic cocktail of shame and self-loathing that makes it impossible to change our behavior. The Hunger Habit is based on Judson Brewer's deeply researched plan proven to help us understand what is going on in our brains so that we can heal the shame and overcome overeating. The step-by-step program focuses on the power of awareness-there is no willpower, calorie-counting, or restricted eating. Setbacks are a good thing! The key is to learn how to work with our brains rather than to fight cravings, and to adopt an attitude of self-kindness rather than self-judgment. Grounded in cutting-edge neuroscience, The Hunger Habit is both accessible and compassionate. It will finally help you break out of food jail and reclaim your life\"-- Provided by publisher.
Book
Probiotic supplementation prevents high-fat, overfeeding-induced insulin resistance in human subjects
The purpose of the present study was to determine whether probiotic supplementation (Lactobacillus casei Shirota (LcS)) prevents diet-induced insulin resistance in human subjects. A total of seventeen healthy subjects were randomised to either a probiotic (n 8) or a control (n 9) group. The probiotic group consumed a LcS-fermented milk drink twice daily for 4 weeks, whereas the control group received no supplementation. Subjects maintained their normal diet for the first 3 weeks of the study, after which they consumed a high-fat (65 % of energy), high-energy (50 % increase in energy intake) diet for 7 d. Whole-body insulin sensitivity was assessed by an oral glucose tolerance test conducted before and after overfeeding. Body mass increased by 0·6 (se 0·2) kg in the control group (P< 0·05) and by 0·3 (se 0·2) kg in the probiotic group (P>0·05). Fasting plasma glucose concentrations increased following 7 d of overeating (control group: 5·3 (se 0·1) v. 5·6 (se 0·2) mmol/l before and after overfeeding, respectively, P< 0·05), whereas fasting serum insulin concentrations were maintained in both groups. Glucose AUC values increased by 10 % (from 817 (se 45) to 899 (se 39) mmol/l per 120 min, P< 0·05) and whole-body insulin sensitivity decreased by 27 % (from 5·3 (se 1·4) to 3·9 (se 0·9), P< 0·05) in the control group, whereas normal insulin sensitivity was maintained in the probiotic group (4·4 (se 0·8) and 4·5 (se 0·9) before and after overeating, respectively (P>0·05). These results suggest that probiotic supplementation may be useful in the prevention of diet-induced metabolic diseases such as type 2 diabetes.
Journal Article
Loss-of-function mutations in MRAP2 are pathogenic in hyperphagic obesity with hyperglycemia and hypertension
The G-protein-coupled receptor accessory protein MRAP2 is implicated in energy control in rodents, notably via the melanocortin-4 receptor1. Although some MRAP2 mutations have been described in people with obesity1–3, their functional consequences on adiposity remain elusive. Using large-scale sequencing of MRAP2 in 9,418 people, we identified 23 rare heterozygous variants associated with increased obesity risk in both adults and children. Functional assessment of each variant shows that loss-of-function MRAP2 variants are pathogenic for monogenic hyperphagic obesity, hyperglycemia and hypertension. This contrasts with other monogenic forms of obesity characterized by excessive hunger, including melanocortin-4 receptor deficiency, that present with low blood pressure and normal glucose tolerance4. The pleiotropic metabolic effect of loss-of-function mutations in MRAP2 might be due to the failure of different MRAP2-regulated G-protein-coupled receptors in various tissues including pancreatic islets.
Journal Article
Intranasal Carbetocin Reduces Hyperphagia, Anxiousness, and Distress in Prader-Willi Syndrome: CARE-PWS Phase 3 Trial
Abstract
Context
Prader-Willi syndrome (PWS) is a rare genetic disorder characterized by endocrine and neuropsychiatric problems including hyperphagia, anxiousness, and distress. Intranasal carbetocin, an oxytocin analog, was investigated as a selective oxytocin replacement therapy.
Objective
To evaluate safety and efficacy of intranasal carbetocin in PWS.
Design
Randomized, double-blind, placebo-controlled phase 3 trial with long-term follow-up.
Setting
Twenty-four ambulatory clinics at academic medical centers.
Participants
A total of 130 participants with PWS aged 7 to 18 years.
Interventions
Participants were randomized to 9.6 mg/dose carbetocin, 3.2 mg/dose carbetocin, or placebo 3 times daily during an 8-week placebo-controlled period (PCP). During a subsequent 56-week long-term follow-up period, placebo participants were randomly assigned to 9.6 mg or 3.2 mg carbetocin, with carbetocin participants continuing at their previous dose.
Main outcome measures
Primary endpoints assessed change in hyperphagia (Hyperphagia Questionnaire for Clinical Trials [HQ-CT]) and obsessive-compulsive symptoms (Children's Yale-Brown Obsessive-Compulsive Scale [CY-BOCS]) during the PCP for 9.6 mg vs placebo, and the first secondary endpoints assessed these same outcomes for 3.2 mg vs placebo. Additional secondary endpoints included assessments of anxiousness and distress behaviors (PWS Anxiousness and Distress Behaviors Questionnaire [PADQ]) and clinical global impression of change (CGI-C).
Results
Because of onset of the COVID-19 pandemic, enrollment was stopped prematurely. The primary endpoints showed numeric improvements in both HQ-CT and CY-BOCS which were not statistically significant; however, the 3.2-mg arm showed nominally significant improvements in HQ-CT, PADQ, and CGI-C scores vs placebo. Improvements were sustained in the long-term follow-up period. The most common adverse event during the PCP was mild to moderate flushing.
Conclusions
Carbetocin was well tolerated, and the 3.2-mg dose was associated with clinically meaningful improvements in hyperphagia and anxiousness and distress behaviors in participants with PWS.
Clinical Trials Registration Number
NCT03649477
Journal Article
Dietary Intake and Eating Behaviours of Obese New Zealand Children and Adolescents Enrolled in a Community-Based Intervention Programme
Describes dietary intake and eating behaviours of obese children and adolescents in NZ. Determines how these differ in Indigenous versus non-Indigenous children at enrolment in an obesity programme. Source: National Library of New Zealand Te Puna Matauranga o Aotearoa, licensed by the Department of Internal Affairs for re-use under the Creative Commons Attribution 3.0 New Zealand Licence.
Journal Article
Obesity-programmed mice are rescued by early genetic intervention
Obesity is a chronic metabolic disorder affecting half a billion people worldwide. Major difficulties in managing obesity are the cessation of continued weight loss in patients after an initial period of responsiveness and rebound to pretreatment weight. It is conceivable that chronic weight gain unrelated to physiological needs induces an allostatic regulatory state that defends a supranormal adipose mass despite its maladaptive consequences. To challenge this hypothesis, we generated a reversible genetic mouse model of early-onset hyperphagia and severe obesity by selectively blocking the expression of the proopiomelanocortin gene (Pomc) in hypothalamic neurons. Eutopic reactivation of central POMC transmission at different stages of overweight progression normalized or greatly reduced food intake in these obesity-programmed mice. Hypothalamic Pomc rescue also attenuated comorbidities such as hyperglycemia, hyperinsulinemia, and hepatic steatosis and normalized locomotor activity. However, effectiveness of treatment to normalize body weight and adiposity declined progressively as the level of obesity at the time of Pomc induction increased. Thus, our study using a novel reversible monogenic obesity model reveals the critical importance of early intervention for the prevention of subsequent allostatic overload that auto-perpetuates obesity.
Journal Article
Proopiomelanocortin Deficiency Treated with a Melanocortin-4 Receptor Agonist
Absence of proopiomelanocortin results in early-onset obesity, hyperphagia, hypopigmentation, and hypocortisolism. Two affected patients received setmelanotide, a new melanocortin-4 receptor agonist, which led to sustainable reduction of hunger and substantial weight loss.
Melanocyte-stimulating hormone, which is produced from proopiomelanocortin, plays a pivotal role in the regulation of satiety and energy expenditure. In the hypothalamic leptin–melanocortin signaling pathway, melanocyte-stimulating hormone transmits the anorexic effect of leptin through the melanocortin-4 receptor.
1
Patients with a mutation in the gene encoding proopiomelanocortin (
POMC
), a very rare condition, have early-onset obesity due to severe hyperphagia as a result of the lack of hypothalamic melanocyte-stimulating hormone. Furthermore, the lack of melanocyte-stimulating hormone at the melanocortin-1 receptor in melanocytes and hair follicles may lead to pale skin and red hair. In addition, affected persons have secondary hypocortisolism . . .
Journal Article
Food addiction and obesity: unnecessary medicalization of hedonic overeating
The concept of food addiction as an explanation for the rise in obesity has become increasingly popular. In this Opinion article, Graham Finlayson critically evaluates the food addiction hypothesis and highlights several problems with its use.
The concept of addiction is loaded with connotations and is often used for its political as much as its medical utility. The scientific case for 'food addiction' as a clinical phenotype currently rests on its association with generic diagnostic criteria for substance-related disorders being applied to everyday foods and eating-related problems. This has fused the concept of obesity with addiction regardless of whether it fits the definition. The hedonic, or reward, system can account for the ingestion of foods and drugs, confirming that they share neural substrates that differentiate liking and wanting. These are normal processes that are recruited for natural homeostatic behaviours and can explain the phenomenon of hedonic overeating as a consequence of human motivation pushed to extremes by an obesogenic environment. Food addiction constitutes a medicalization of common eating behaviours, taking on the properties of a disease. The use of this medical language has implications for the way in which society views overeating and obesity.
Journal Article
Overeating Saturated Fat Promotes Fatty Liver and Ceramides Compared With Polyunsaturated Fat: A Randomized Trial
Saturated fatty acid (SFA) vs polyunsaturated fatty acid (PUFA) may promote nonalcoholic fatty liver disease by yet unclear mechanisms.
To investigate if overeating SFA- and PUFA-enriched diets lead to differential liver fat accumulation in overweight and obese humans.
Double-blind randomized trial (LIPOGAIN-2). Overfeeding SFA vs PUFA for 8 weeks, followed by 4 weeks of caloric restriction.
General community.
Men and women who are overweight or have obesity (n = 61).
Muffins, high in either palm (SFA) or sunflower oil (PUFA), were added to the habitual diet.
Lean tissue mass (not reported here). Secondary and exploratory outcomes included liver and ectopic fat depots.
By design, body weight gain was similar in SFA (2.31 ± 1.38 kg) and PUFA (2.01 ± 1.90 kg) groups, P = 0.50. SFA markedly induced liver fat content (50% relative increase) along with liver enzymes and atherogenic serum lipids. In contrast, despite similar weight gain, PUFA did not increase liver fat or liver enzymes or cause any adverse effects on blood lipids. SFA had no differential effect on the accumulation of visceral fat, pancreas fat, or total body fat compared with PUFA. SFA consistently increased, whereas PUFA reduced circulating ceramides, changes that were moderately associated with liver fat changes and proposed markers of hepatic lipogenesis. The adverse metabolic effects of SFA were reversed by calorie restriction.
SFA markedly induces liver fat and serum ceramides, whereas dietary PUFA prevents liver fat accumulation and reduces ceramides and hyperlipidemia during excess energy intake and weight gain in overweight individuals.
Journal Article
The gliotransmitter ACBP controls feeding and energy homeostasis via the melanocortin system
Glial cells have emerged as key players in the central control of energy balance and etiology of obesity. Astrocytes play a central role in neural communication via the release of gliotransmitters. Acyl-CoA binding protein (ACBP)-derived endozepines are secreted peptides that modulate the GABAA receptor. In the hypothalamus, ACBP is enriched in arcuate nucleus (ARC) astrocytes, ependymocytes and tanycytes. Central administration of the endozepine octadecaneuropeptide (ODN) reduces feeding and improves glucose tolerance, yet the contribution of endogenous ACBP in energy homeostasis is unknown. We demonstrated that ACBP deletion in GFAP+ astrocytes, but not in Nkx2.1-lineage neural cells, promoted diet-induced hyperphagia and obesity in both male and female mice, an effect prevented by viral rescue of ACBP in ARC astrocytes. ACBP-astrocytes were observed in apposition with proopiomelanocortin (POMC) neurons and ODN selectively activated POMC neurons through the ODN-GPCR but not GABAA, and supressed feeding while increasing carbohydrate utilization via the melanocortin system. Similarly, ACBP overexpression in ARC astrocytes reduced feeding and weight gain. Finally, the ODN-GPCR agonist decreased feeding and promoted weight loss in ob/ob mice. These findings uncover ACBP as an ARC gliopeptide playing a key role in energy balance control and exerting strong anorectic effects via the central melanocortin system.
Journal Article