Hedonic hunger

Last updated

Hedonic hunger or hedonic hyperphagia is the "drive to eat to obtain pleasure in the absence of an energy deficit". [1] Particular foods may have a high "hedonic rating" [2] or individuals may have increased susceptibility to environmental food cues. [3] Weight loss programs may aim to control or to compensate for hedonic hunger. [4] Therapeutic interventions may influence hedonic eating behavior. [5]

Contents

Background

Although hunger may arise from energy or nutrient deficits, as would be expected in the set-point theories of hunger and eating, hunger may arise more commonly from anticipated pleasure of eating, [4] consistent with the positive-incentive perspective. [3] [6] [7] Gramlich distinguished the overeating responses to these stimuli as homeostatic hyperphagia and hedonic hyperphagia respectively. [8] Accordingly, hunger and eating are subject to feedback control from homeostatic, hedonic, and cognitive processes. [9] Although these mechanisms interplay and overlap to some extent, [3] [9] they can nonetheless be individually separated. [9] [10] Thus, the positive-incentive perspective suggests that eating is similar to sexual behavior: humans engage in sexual behavior, not because of an internal deficit, but because they have evolved in a way that makes them crave it.[ citation needed ] High calorie foods have had intrinsic reward value throughout evolution. [11] [12] The presence of desirable (or "hedonic") food, or the mere anticipation of it, makes one hungry. [13] The psychological effects of hedonic hunger may be the appetitive equivalent of hedonically driven activities such as recreational drug use and compulsive gambling. [3] [14] [15] Susceptibility to food cues can lead to overeating in a society of readily available calorie dense, inexpensive foods. [1] Such hedonistic eating overrides the body's ability to regulate consumption with satiety. [16] While there is a breadth of evidence for hedonic hunger, this topic is not without controversy. For example, recent evidence suggests that there is no relationship between milkshake liking and body mass index (BMI). [17]

A related phenomenon, specific appetite, also known as specific hunger, is conceptually related to, but distinct from, hedonic hunger. Specific appetite is a drive to eat foods with specific flavors or other characteristics: in usage, specific appetite has put greater emphasis on an individual who adaptationally learns a particular appetite behavior rather than an evolutionarily innate, hedonic appetite preference.

Food variability

A "hedonic rating" of foods reflects those individuals are more likely to eat even though they aren't hungry. [10] [18] [19] For example, functional magnetic resonance imaging (fMRI) scanning suggests that fed rats show a high preference for a mixture of fat and carbohydrate in the form of potato chips compared to their standard chow or single macronutrient foods. [20] When binge eating occurs without the presence of energy deprivation, researchers think it is due to frequent exposure to palatable food. [1] Another study evaluated how hedonic ratings of individual foods aggregate into the food components of particular types of meals, and related preferences to overall dietary intake. [21]

Interpersonal variability

Individuals may have increased hedonic hunger susceptibility to environmental food cues. [2] Genetic variability may influence hedonic hyperphagia. [10] [16] Variation in hedonic hunger levels from person to person may be key in determining success in weight loss tactics and a person's ability to cope with tempting foods that are readily available. To assess this, a Power of Food Scale (PFS) has been developed that quantifies a person's appetitive anticipation (not consumption). [1] [3] [22] [23] Binge-eaters, obese individuals and those with eating disorders such as anorexia nervosa scored higher than restrictive type and normal weight college students. [1] A decrease in PFS score leads to better success in weight loss. [2]

Food reinforcement

The reinforcing value of food refers to how hard someone is willing to work to obtain food. [24] Food reinforcement is influenced by several factors including food palatability, food deprivation, and food variety. It is also motivated by concerns about fullness (expected satiation) and the hunger that might be experienced in the intervening period between meals (expected satiety). The effector mechanisms of food reinforcement depend on dopaminergic activity in the brain. [24]

Treatment

Conceptually, weight loss programs might target control of hedonic hunger. [4] [10] Specific research to determine what diet techniques would be most beneficial for those with an increased hedonic hunger would help people modify their immediate availability of food or its palatability. [3] For example, whole grain popcorn may be a better choice than potato chips due to a lower calorie load and an increased sense of satiety. [25] Adding dietary fiber to foods and beverages increases satiety and reduces energy intake at the next meal. [26] Low-energy-density foods with high satiating power may be useful tools for weight management. [27] Satiety has been found to be greater with yogurt beverages than fruit juice, and was equal with low-energy-density yogurt with inulin and high-energy-density yogurt. [27] People with high PFS scores may do better with meal replacement products. [2] [28]

Medications may affect hedonic eating behavior. Glucagon-like peptide-1 (GLP1) agonists, such as exenatide and liraglutide, which are used for diabetes, may help suppress food reward behavior. [5] Inhibition of dopamine transport within the brain increases dopamine concentrations, which can reduce energy intake. [24] Despite theoretical underpinnings, opiate antagonists as single agents have generally not shown substantial clinical benefit. [16] [29] [30] However, preliminary data has suggested synergistic effects with concurrent targeted therapy of opiate receptors and either dopamine or cannabinoid receptors. [16]

Bariatric surgery of various types may influence hedonic hunger [31] [32] [33] particularly if accompanied by counseling interventions that reduce automatic hedonic impulses. [34] These surgeries may work in part by modifying the production of gastrointestinal hormones, particularly by increasing glucagon-like peptide-1 and peptide YY (PYY); [31] [35] reduction of ghrelin has been inconsistent. [31]

The physiological mechanisms

Hedonic hunger show a positive correlation between plasma of the endocannabinoid 2-arachidonoyl glycerol (2-AG) and ghrelin during hedonic, but not nonhedonic, eating and the consumption of food for pleasure is characterized by increased peripheral levels of both peptides. And this two endogenous rewarding chemical signals influences food intake and, ultimately, body mass. [36]

See also

Related Research Articles

<span class="mw-page-title-main">Eating</span> Ingestion of food

Eating is the ingestion of food. In biology, this is typically done to provide a heterotrophic organism with energy and nutrients and to allow for growth. Animals and other heterotrophs must eat in order to survive — carnivores eat other animals, herbivores eat plants, omnivores consume a mixture of both plant and animal matter, and detritivores eat detritus. Fungi digest organic matter outside their bodies as opposed to animals that digest their food inside their bodies.

Appetite is the desire to eat food items, usually due to hunger. Appealing foods can stimulate appetite even when hunger is absent, although appetite can be greatly reduced by satiety. Appetite exists in all higher life-forms, and serves to regulate adequate energy intake to maintain metabolic needs. It is regulated by a close interplay between the digestive tract, adipose tissue and the brain. Appetite has a relationship with every individual's behavior. Appetitive behaviour also known as approach behaviour, and consummatory behaviour, are the only processes that involve energy intake, whereas all other behaviours affect the release of energy. When stressed, appetite levels may increase and result in an increase of food intake. Decreased desire to eat is termed anorexia, while polyphagia is increased eating. Dysregulation of appetite contributes to anorexia nervosa, bulimia nervosa, cachexia, overeating, and binge eating disorder.

<span class="mw-page-title-main">Ghrelin</span> Peptide hormone involved in appetite regulation

Ghrelin is a hormone primarily produced by enteroendocrine cells of the gastrointestinal tract, especially the stomach, and is often called a "hunger hormone" because it increases the drive to eat. Blood levels of ghrelin are highest before meals when hungry, returning to lower levels after mealtimes. Ghrelin may help prepare for food intake by increasing gastric motility and stimulating the secretion of gastric acid.

Satiety is a state or condition of fullness gratified beyond the point of satisfaction, the opposite of hunger. Following satiation, satiety is a feeling of fullness lasting until the next meal. When food is present in the GI tract after a meal, satiety signals overrule hunger signals, but satiety slowly fades as hunger increases.

<span class="mw-page-title-main">Agouti-related peptide</span> Mammalian protein found in Homo sapiens

Agouti-related protein (AgRP), also called agouti-related peptide, is a neuropeptide produced in the brain by the AgRP/NPY neuron. It is synthesized in neuropeptide Y (NPY)-containing cell bodies located in the ventromedial part of the arcuate nucleus in the hypothalamus. AgRP is co-expressed with NPY and acts to increase appetite and decrease metabolism and energy expenditure. It is one of the most potent and long-lasting of appetite stimulators. In humans, the agouti-related peptide is encoded by the AGRP gene.

<span class="mw-page-title-main">Peptide YY</span> Peptide released from cells in the ileum and colon in response to feeding

Peptide YY (PYY), also known as peptide tyrosine tyrosine, is a peptide that in humans is encoded by the PYY gene. Peptide YY is a short peptide released from cells in the ileum and colon in response to feeding. In the blood, gut, and other elements of periphery, PYY acts to reduce appetite; similarly, when injected directly into the central nervous system, PYY is also anorexigenic, i.e., it reduces appetite.

Night eating syndrome (NES) is an eating disorder, characterized by a delayed circadian pattern of food intake. Although there is some degree of comorbidity with binge eating disorder, it differs from binge eating in that the amount of food consumed in the night is not necessarily objectively large nor is a loss of control over food intake required. It was originally described by Albert Stunkard in 1955 and is currently included in the other specified feeding or eating disorder category of the DSM-5. Research diagnostic criteria have been proposed and include evening hyperphagia and/or nocturnal awakening and ingestion of food two or more times per week. The person must have awareness of the night eating to differentiate it from the parasomnia sleep-related eating disorder (SRED). Three of five associated symptoms must also be present: lack of appetite in the morning, urges to eat at night, belief that one must eat in order to fall back to sleep at night, depressed mood, and/or difficulty sleeping.

<span class="mw-page-title-main">Growth hormone secretagogue receptor</span> Protein-coding gene in the species Homo sapiens

Growth hormone secretagogue receptor(GHS-R), also known as ghrelin receptor, is a G protein-coupled receptor that binds growth hormone secretagogues (GHSs), such as ghrelin, the "hunger hormone". The role of GHS-R is thought to be in regulating energy homeostasis and body weight. In the brain, they are most highly expressed in the hypothalamus, specifically the ventromedial nucleus and arcuate nucleus. GSH-Rs are also expressed in other areas of the brain, including the ventral tegmental area, hippocampus, and substantia nigra. Outside the central nervous system, too, GSH-Rs are also found in the liver, in skeletal muscle, and even in the heart.

<span class="mw-page-title-main">Palatability</span>

Palatability is the hedonic reward provided by foods or fluids that are agreeable to the "palate", which often varies relative to the homeostatic satisfaction of nutritional and/or water needs. The palatability of a food or fluid, unlike its flavor or taste, varies with the state of an individual: it is lower after consumption and higher when deprived. It has increasingly been appreciated that this can create a hunger that is independent of homeostatic needs.

In biology, energy homeostasis, or the homeostatic control of energy balance, is a biological process that involves the coordinated homeostatic regulation of food intake and energy expenditure. The human brain, particularly the hypothalamus, plays a central role in regulating energy homeostasis and generating the sense of hunger by integrating a number of biochemical signals that transmit information about energy balance. Fifty percent of the energy from glucose metabolism is immediately converted to heat.

An orexigenic, or appetite stimulant, is a drug, hormone, or compound that increases appetite and may induce hyperphagia. This can be a medication or a naturally occurring neuropeptide hormone, such as ghrelin, orexin or neuropeptide Y, which increases hunger and therefore enhances food consumption. Usually appetite enhancement is considered an undesirable side effect of certain drugs as it leads to unwanted weight gain, but sometimes it can be beneficial and a drug may be prescribed solely for this purpose, especially when the patient is suffering from severe appetite loss or muscle wasting due to cystic fibrosis, anorexia, old age, cancer or AIDS. There are several widely used drugs which can cause a boost in appetite, including tricyclic antidepressants (TCAs), tetracyclic antidepressants, natural or synthetic cannabinoids, first-generation antihistamines, most antipsychotics and many steroid hormones. In the United States, no hormone or drug has currently been approved by the FDA specifically as an orexigenic, with the exception of Dronabinol, which received approval for HIV/AIDS-induced anorexia only.

Hunger is a sensation that motivates the consumption of food. The sensation of hunger typically manifests after only a few hours without eating and is generally considered to be unpleasant. Satiety occurs between 5 and 20 minutes after eating. There are several theories about how the feeling of hunger arises. The desire to eat food, or appetite, is another sensation experienced with regard to eating.

<span class="mw-page-title-main">Weight management</span> Techniques for maintaining body weight

Weight management refers to behaviors, techniques, and physiological processes that contribute to a person's ability to attain and maintain a healthy weight. Most weight management techniques encompass long-term lifestyle strategies that promote healthy eating and daily physical activity. Moreover, weight management involves developing meaningful ways to track weight over time and to identify ideal body weights for different individuals.

Research into food choice investigates how people select the food they eat. An interdisciplinary topic, food choice comprises psychological and sociological aspects, economic issues and sensory aspects.

<span class="mw-page-title-main">Sensory-specific satiety</span>

Sensory specific satiety is a sensory hedonic phenomenon that refers to the declining satisfaction generated by the consumption of a certain type of food, and the consequent renewal in appetite resulting from the exposure to a new flavour or food. The phenomenon was first described in 1956 by the French physiologist Jacques Le Magnen. The term "sensory specific satiety" was coined in 1981 by Barbara J. Rolls and Edmund T. Rolls. The concept illustrates the role of physical stimuli in generating appetite and, more specifically, explains the significance of taste, or food flavour in relation to hunger. Besides conditioned satiety and alimentary alliesthesia, it is one of the three major phenomena of satiation. An Ingestive Classics paper on the topic has been written in conversation with Barbara J. Rolls

Ingestive behaviors encompass all eating and drinking behaviors. These actions are influenced by physiological regulatory mechanisms; these mechanisms exist to control and establish homeostasis within the human body. Disruptions in these ingestive regulatory mechanisms can result in eating disorders such as obesity, anorexia, and bulimia.

Satiety value is the degree at which food gives a human the sense of food gratification, the exact contrast feeling of hunger. The concept of the Satiety Value and Satiety Index was developed by Australian researcher and doctor, Susanna Holt. Highest satiety value is expected when the food that remains in the stomach for a longer period produces greatest functional activity of the organ. Limiting the food intake after reaching the satiety value helps reduce obesity problems.

Emotional eating, also known as stress eating and emotional overeating, is defined as the "propensity to eat in response to positive and negative emotions". While the term commonly refers to eating as a means of coping with negative emotions, it sometimes include eating for positive emotions, such as overeating when celebrating an event or to enhance an already good mood.

Expected satiety is the amount of relief from hunger that is expected from a particular food. It is closely associated with expected satiation which refers to the immediate fullness that a food is expected to generate.

<span class="mw-page-title-main">Hyperpalatable food</span> Food that triggers the brains reward system

Hyperpalatable food (HPF) combines high levels of fat, sugar, sodium, or carbohydrates to trigger the brain's reward system, encouraging excessive eating. The concept of hyperpalatability is foundational to ultra-processed foods, which are usually engineered to have enjoyable qualities of sweetness, saltiness, or richness. Hyperpalatable foods can stimulate the release of metabolic, stress, and appetite hormones that play a role in cravings and may interfere with the body's ability to regulate appetite and satiety.

References

  1. 1 2 3 4 5 Witt AA, Lowe MR (2014). "Hedonic Hunger and Binge Eating Among Women with Eating Disorders". International Journal of Eating Disorders. 47 (3): 273–80. doi:10.1002/eat.22171. PMID   24014479.
  2. 1 2 3 4 Theim KR, Brown JD, Juarascio AS, Malcom RR, O'Neil PM. Relations of hedonic hunger and behavioral change to weight loss among adults in a behavioral weight loss program utilizing meal-replacement products. Behav Modif. 2013; 37(6): 790-805.
  3. 1 2 3 4 5 6 Lowe, MR; Butryn, ML (Jul 24, 2007). "Hedonic hunger: a new dimension of appetite?". Physiology & Behavior. 91 (4): 432–9. doi:10.1016/j.physbeh.2007.04.006. PMID   17531274. S2CID   10704679.
  4. 1 2 3 Yu, Y-H.; Vasselli, J. R.; Zhang, Y.; Mechanick, J. I.; Korner, J.; Peterli, R. (February 2015). "Metabolic vs. hedonic obesity: a conceptual distinction and its clinical implications". Obesity Reviews. 16 (3): 234–247. doi:10.1111/obr.12246. PMC   5053237 . PMID   25588316.
  5. 1 2 Skibicka, KP (Oct 14, 2013). "The central GLP-1: implications for food and drug reward". Frontiers in Neuroscience. 7: 181. doi: 10.3389/fnins.2013.00181 . PMC   3796262 . PMID   24133407.
  6. ↑ Berridge K. C. (2004). "Motivation concepts in behavioral neuroscience". Physiology & Behavior. 81 (2): 179–209. doi:10.1016/j.physbeh.2004.02.004. PMID   15159167. S2CID   14149019.
  7. ↑ Booth D. A. (1981). "The physiology of appetite". British Medical Bulletin. 37 (2): 135–140. doi:10.1093/oxfordjournals.bmb.a071690. PMID   7032646.
  8. ↑ Gramlich, L; Zeman M; Sharma AM. (2010). "25". Evidence-Based Gastroenterology and Hepatology Chapter 25. Edited by McDonald JWD, Burroughs AK, Feagan BG, Fennerty MB (3rd ed.). John Wiley & Sons. ISBN   978-1-4443-4780-7.
  9. 1 2 3 Hall, KD; Hammond, RA; Rahmandad, H (Jul 2014). "Dynamic interplay among homeostatic, hedonic, and cognitive feedback circuits regulating body weight". American Journal of Public Health. 104 (7): 1169–75. doi:10.2105/ajph.2014.301931. PMC   4056226 . PMID   24832422.
  10. 1 2 3 4 Yeomans, MR; Blundell, JE; Leshem, M (Aug 2004). "Palatability: response to nutritional need or need-free stimulation of appetite?". British Journal of Nutrition. 92 (Suppl 1): S3-14. doi: 10.1079/bjn20041134 . PMID   15384315.
  11. ↑ Keen-Rhinehart, E; Ondek, K; Schneider, JE (Nov 15, 2013). "Neuroendocrine regulation of appetitive ingestive behavior". Frontiers in Neuroscience. 7: 213. doi: 10.3389/fnins.2013.00213 . PMC   3828638 . PMID   24298235.
  12. ↑ Van Schooten, WC; Ottenhoff, TH; Klatser, PR; Thole, J; De Vries, RR; Kolk, AH (Jun 1988). "T cell epitopes on the 36K and 65K Mycobacterium leprae antigens defined by human T cell clones". European Journal of Immunology. 18 (6): 849–54. doi:10.1002/eji.1830180604. PMID   2454825. S2CID   24172351.
  13. ↑ Pinel, John P.J. (2006). Biopsychology (6th ed.). Boston: Pearson A and B. ISBN   0-205-42651-4.
  14. ↑ Haskins, SC; Klide, AM (Mar 1992). "Anesthesia for very old patients". Veterinary Clinics of North America: Small Animal Practice. 22 (2): 467–9. doi:10.1016/s0195-5616(92)50673-8. PMID   1585606.
  15. ↑ Stice, E; Figlewicz, DP; Gosnell, BA; Levine, AS; Pratt, WE (Nov 2013). "The contribution of brain reward circuits to the obesity epidemic". Neuroscience & Biobehavioral Reviews. 37 (9 Pt A): 2047–58. doi:10.1016/j.neubiorev.2012.12.001. PMC   3604128 . PMID   23237885.
  16. 1 2 3 4 Reid, C; Davis C. (2011). Targeting the opioid system: an effective therapy for obesity? in Anti-Obesity Drug Discovery and Development, Volume 1. Edited by Atta-ur-Rahman, Choudhary MI. page 186-199. Bentham Science Publishers. ISBN   978-1-60805-163-2.
  17. ↑ Wall, K (May 12, 2020). "No evidence for an association between obesity and milkshake liking". International Journal of Obesity. 44 (8): 1668–1677. doi:10.1038/s41366-020-0583-x. PMC   7387147 . PMID   32398755.
  18. ↑ McBride R. L. (1986). "Hedonic rating of food: single or side-by-side sample presentation?". International Journal of Food Science & Technology. 21 (3): 355–363. doi:10.1111/j.1365-2621.1986.tb00414.x.
  19. ↑ Kozak, M; Cliff, MA (Aug 2013). "Systematic comparison of hedonic ranking and rating methods demonstrates few practical differences". Journal of Food Science. 78 (8): S1257-63. doi: 10.1111/1750-3841.12173 . PMID   23815796.
  20. ↑ Hoch, T; Pischetsrieder, M; Hess, A (2014). "Snack food intake in ad libitum fed rats is triggered by the combination of fat and carbohydrates". Frontiers in Psychology. 5: 250. doi: 10.3389/fpsyg.2014.00250 . PMC   3978285 . PMID   24744741.
  21. ↑ Johnson SL, Boles RE, Burer KS (2014). "Using participant hedonic ratings of food images to construct data driven food groupings". Appetite. 79: 189–196. doi:10.1016/j.appet.2014.04.021. PMC   4104662 . PMID   24769294.
  22. ↑ Lowe, MR; Butryn, ML; Didie, ER; Annunziato, RA; Thomas, JG; Crerand, CE; Ochner, CN; Coletta, MC; Bellace, D; Wallaert, M; Halford, J (Aug 2009). "The Power of Food Scale. A new measure of the psychological influence of the food environment". Appetite. 53 (1): 114–8. doi:10.1016/j.appet.2009.05.016. PMID   19500623. S2CID   20751745.
  23. ↑ Cappelleri, JC; Bushmakin, AG; Gerber, RA; Leidy, NK; Sexton, CC; Karlsson, J; Lowe, MR (Aug 2009). "Evaluating the Power of Food Scale in obese subjects and a general sample of individuals: development and measurement properties". International Journal of Obesity. 33 (8): 913–22. doi: 10.1038/ijo.2009.107 . PMID   19506564.
  24. 1 2 3 Epstein, LH; Leddy, JJ (Jan 2006). "Food reinforcement". Appetite. 46 (1): 22–5. doi:10.1016/j.appet.2005.04.006. PMID   16257474. S2CID   7031327.
  25. ↑ Nguyen, V; Cooper, L; Lowndes, J; Melanson, K; Angelopoulos, TJ; Rippe, JM; Reimers, K (Sep 14, 2012). "Popcorn is more satiating than potato chips in normal-weight adults". Nutrition Journal. 11: 71. doi: 10.1186/1475-2891-11-71 . PMC   3502142 . PMID   22978828.
  26. ↑ Perrigue, M; Carter, B; Roberts, SA; Drewnowski, A (Nov–Dec 2010). "A low-calorie beverage supplemented with low-viscosity pectin reduces energy intake at a subsequent meal". Journal of Food Science. 75 (9): H300-5. doi:10.1111/j.1750-3841.2010.01858.x. PMID   21535604.
  27. 1 2 Perrigue, MM; Monsivais, P; Drewnowski, A (Nov 2009). "Added soluble fiber enhances the satiating power of low-energy-density liquid yogurts". Journal of the American Dietetic Association. 109 (11): 1862–8. doi:10.1016/j.jada.2009.08.018. PMID   19857627.
  28. ↑ Paolini, BM; Laurienti, PJ; Norris, J; Rejeski, WJ (2014). "Meal replacement: calming the hot-state brain network of appetite". Frontiers in Psychology. 5: 249. doi: 10.3389/fpsyg.2014.00249 . PMC   3971177 . PMID   24723901.
  29. ↑ Peciña, S; Berridge, KC (Dec 14, 2005). "Hedonic hot spot in nucleus accumbens shell: where do mu-opioids cause increased hedonic impact of sweetness?". The Journal of Neuroscience. 25 (50): 11777–86. doi: 10.1523/jneurosci.2329-05.2005 . PMC   6726018 . PMID   16354936.
  30. ↑ Berridge, KC; Ho, CY; Richard, JM; DiFeliceantonio, AG (Sep 2, 2010). "The tempted brain eats: pleasure and desire circuits in obesity and eating disorders". Brain Research. 1350: 43–64. doi:10.1016/j.brainres.2010.04.003. PMC   2913163 . PMID   20388498.
  31. 1 2 3 Schultes, B; Ernst, B; Wilms, B; Thurnheer, M; Hallschmid, M (Aug 2010). "Hedonic hunger is increased in severely obese patients and is reduced after gastric bypass surgery". The American Journal of Clinical Nutrition. 92 (2): 277–83. doi: 10.3945/ajcn.2009.29007 . PMID   20519559.
  32. ↑ Ullrich, J; Ernst, B; Wilms, B; Thurnheer, M; Hallschmid, M; Schultes, B (2013). "The hedonic drive to consume palatable foods appears to be lower in gastric band carriers than in severely obese patients who have not undergone a bariatric surgery". Obesity Surgery. 23 (4): 474–9. doi:10.1007/s11695-012-0818-6. PMID   23179243. S2CID   207304613.
  33. ↑ Ullrich, J; Ernst, B; Wilms, B; Thurnheer, M; Schultes, B (2013). "Roux-en Y gastric bypass surgery reduces hedonic hunger and improves dietary habits in severely obese subjects". Obesity Surgery. 23 (1): 50–5. doi:10.1007/s11695-012-0754-5. PMID   22941334. S2CID   207304509.
  34. ↑ Husted, M; Ogden, J (2014). "Emphasising Personal Investment Effects Weight Loss and Hedonic Thoughts about Food after Obesity Surgery". Journal of Obesity. 2014: 810374. doi: 10.1155/2014/810374 . PMC   4060496 . PMID   24987525.
  35. ↑ Ashrafian, H; le Roux, CW (Jul 14, 2009). "Metabolic surgery and gut hormones - a review of bariatric entero-humoral modulation". Physiology & Behavior. 97 (5): 620–31. doi:10.1016/j.physbeh.2009.03.012. PMID   19303889. S2CID   19940122.
  36. ↑ Monteleone, Palmiero; Piscitelli, Fabiana; Scognamiglio, Pasquale; Monteleone, Alessio Maria; Canestrelli, Benedetta; Di Marzo, Vincenzo; Maj, Mario (2012-06-01). "Hedonic eating is associated with increased peripheral levels of ghrelin and the endocannabinoid 2-arachidonoyl-glycerol in healthy humans: a pilot study". The Journal of Clinical Endocrinology and Metabolism. 97 (6): E917–924. doi: 10.1210/jc.2011-3018 . ISSN   1945-7197. PMID   22442280.
This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.