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Hedonic hunger - A potential contributor to obesity
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Wednesday, 21 April, 2021, 16 : 00 PM [IST]
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Mounika Patiballa
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Introduction
Hedonic hunger is defined as the driver to consume highly palatable foods in the absence of physiological need for calories/ energy deprivation. Hedonic eating is more prevalent in women, when compared to men (Ewoldtet al., 2015). Hedonic hunger is equal to substance use/gambling. As substance users/gamblers are pre-occupied with their habits even, when they are not engaging in it. Likewise people with hedonic hunger experience frequent thoughts, feelings and urges about food in absence of energy deficiency.
Mechanism of food intake
Central and peripheral mechanism involved in maintenance of body homeostasis. The metabolic consequences of food are regulated by homeostatic functions and the hedonic consequences by reward functions. Hedonic and metabolic consequences are interdependent in that the hedonic value of food modulates caloric intake, and the metabolic status modulates hedonic processing. When a person is hungry, stomach increases the production of ghrelin and decreases leptin produced by adipose tissue, which indicates weight loss and signals hypothalamus to increase food intake.
In hypothalamus signals are received by neurons, i.e., accurate nucleus it’s a first order neuron it regulates appetite since peripheral adiposity factors act directly on these neurons. It contains agouti-related peptide (appetite activators) and pro –opiomelanocortin neuron (appetite inhibitor. Then information regarding food intake will pass to second order neuron (incharge of receiving information regarding food intake from AN) - paraventicular nucleus and lateral hypothalamus these signals further project into nucleus tractus solitary (brain stem), this then triggers ghrelin through vagus nerve to increase food intake and maintain homeostasis.
In hedonic hunger, presently due to highly availability of cheap, energy dense and palatable foods, it activates reward system in which sensory signals activate insula, when someone tastes opioids release from endocannobiniods, that activates mesolimibical system in brain that activates the neurotransmitter dopamine in ventral tegmental area to communicate with neurons in nucleus accumbens in order to elevate reward system and motivate to increase food intake. The obese state is associated with altered reward functions, but it is not clear whether these changes are the cause or consequence of obesity. Altered reward functions could cause obesity via increased intake of calories or fat, or alternatively, could result from consequences of the obese state, or could be a combination of both.
Measure of Hedonic Hunger - Power of Food Scale
The PFS questionnaire designed to measure individual difference in appetite motivation to eat high palatable foods & assesses the psychological impact of living in food-abundant environments. It measures appetite for, rather than consumption of, palatable foods, at three levels of food proximity (food available, food present, and food tasted). It does not include any items describing actual food consumption. It comprises 15 items re?ecting the responsiveness to the food environment grouped into 3 domains according to food proximity-
• Food available - food readily available in the environment but not physically present. Ex-“I ?nd myself thinking about food even when I’m not physically hungry”.
• Food present - food present but not tasted. Ex-“ If I see or smell a food I like, I get a powerful urge to have some”.
• Food tasted - food when ?rst tasted but not consumed. Ex- “When I eat delicious food I focus a lot on how good it tastes.”
For each item, subjects had to score their reactions on a 5-level scale: 1 = I don’t agree at all, 2 = I agree a little, 3 = I agree somewhat, 4 = I agree, and 5 = I strongly agree. Thus, each of the 3 domain scores was calculated to obtain an aggregated score.
Obesity phenotypes
• Hungry Brain – Its brains inability to determine when a meal is over, known as abnormal satiation or fullness. Ex – Leptin resistance, where leptin signal to brain is distracted, which increases fat cells but brain is starved. About 19 % fell into hungry brain category.
• Hungry Gut – the gut ability to not, eat in periods between meals is distracted. Some intestinal bacteria like blautia, ruminococcus, coprococcuscatus act as mini brain influencing the food cravings, through an axis of wrong communication with adipose tissue and triggers factor for insulin. About 20 min after meal, certain bacteria in gut send signal that had enough to eat by stimulating the release of hormone that has been linked to feeling of satiety, but if you don’t have diverse microbiota, other species become dominant. About 12 % fell in this category.
• Hedonic Eating - Drive to eat to obtain pleasure in the absence of an energy deficit. It contributes to about 25% of obesity.
• Slow Burn – Due to modern sedentary lifestyle energy expenditure doesn’t match to energy intake. It contributes to about 30% of obesity.
Metabolic obesity and hedonic obesity
Body weight is neither stationary nor changing unidirectional which usually oscillates up and down around set point. Two types of forces determine direction of weight change i.e., metabolic obesity develops when body weight set point become abnormally elevated, whereas hedonic obesity due to reward system that over rides homeostatic regulation. Metabolic and hedonic obesity as related to their respective mechanisms of weight gain. The homeostatic weight regulatory system located primarily in hypothalamus and brainstem accounts for weight regulation around a body weight set point. Deviation of body weight from this set point elicits a compensatory increase or decrease in food intake (cumulative over a long time period) and energy expenditure (both resting and non-resting) in an opposite direction in order to restore the previous body weight set point. Obesity results from an elevation of the metabolic set point that is characterised by an elevated body weight which is metabolically defended just as normal body weight is defended at its set point; we term an elevated body weight set point ‘metabolic obesity’. Hedonic eating is governed by the reward system to satisfy the need of pleasure and is non-homeostatic with regard to energy balance. Dysfunction of the reward system may lead to hedonic over-eating in susceptible individuals in the face of metabolic signals indicating an energy surplus, leading to sustained weight gain above the metabolic set point weight; we term this form of obesity ‘hedonic obesity’.
Hedonic hunger suppressor
• Thylakoids – These are pouches that are located in the chloroplast of green leaves. They have the ability to trigger satiety signals through body’s satiety system.
• Bariatric Surgery – A surgery that treats obesity, removes no fat tissue, instead, they change the stomach and intestine so that a person feels full more quickly, or absorbs fewer calories, or both. It also inhibits the reward mechanism in brain.
• Pharmacological interventions -Novel pharmacological interventions inhibit reward mechanism in brain. These explore targets relevant to addiction might lead the way to new anti-obesity drugs. It is even possible that future drugs initially developed for addiction treatment will have profound effects on body weight and obesity. Because eating is central to survival, the ability to selectively target hedonic eating, while leaving homeostatic feeding untouched is the ultimate goal in curbing the obesity epidemic.
• Optogenetic&chemogenetic manipulation -Optogenetics is a biological technique that involves the use of light to control neurons in reward system. Chemogenetics is the process in which macromolecules are used to altered reward pathways in brain (hedonic hotspots).
High hedonic foods – They contain lot of calories in small packs. Highly palatable foods that are combination of sugar, salt and fat. Ex-muffins, chocolates, chips, french fries, MSG and flavours. These are main types of trigger foods, this happens because they light up the pleasure centres in the brain.
Low hedonic foods – Thylakoids found in photosynthetic membranes of green leaves, these suppress hunger and promote satiety. Further decreases liking for fat and sweet foods. Fibre foods increase feeling of fullness, slow digest and increases satiety.
Application of hedonic hunger
Conclusion
Hedonic hunger contributes to about 25% of obesity phenotype. Recently due to modern environment, food industry expends tremendous effort to manipulate ingredients in products to enhance rewarding properties in brain, subsequently, motivates hedonic pathway that overrides homeostatic mechanisms to cause increase in body weight. Thus, assessment of hedonic hunger useful to further identify mediators of weight loss and novel therapeutic strategies for prevention of hedonic obesity and its related complications.
(The author is PhD scholar in food science and nutrition, University of Agricultural Sciences, GKVK, Bangalore)
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