5/17/2023 0 Comments Hedonic principleIt is generally agreed that hypo-functioning of brain reward circuitry can be an innate human characteristic determined by a concatenation of genetic effects that jointly contribute to a low activation potential. A chronic attenuation in the ability to experience reward–duly named anhedonia-was first described clinically in the late 19th century as a core feature of many psychiatric disorders including depression, schizophrenia, and drug withdrawal. Attempts to understand the biological basis of hedonic responsiveness has focused largely on the sensitivity, or arousability, of the mesocorticolimbic dopamine pathways. Natural rewards comprise all those incentives important for our survival like eating, reproduction, and mastery. Hedonic responsiveness is a highly heritable trait reflecting individual differences in the motivation to seek out rewarding stimuli in one’s environment, and in the capacity to experience pleasure from these events. Hedonic Responsiveness and Capacity for Reward In the former group, there was also a reduction in the view that obese individuals are mentally impaired, and a decrease in the participants’ fear of personal weight gain. However, other recent experimental research found that when a random selection of adult participants was presented with a food-addiction model of obesity with a focus on causal biological mechanisms, stigmatization and blame towards overweight individuals was reduced compared to ratings from another group of participants who were given a non-addiction model of obesity. According to this view, the pathology is the compulsive overeating it is not vitally related to the addictive quality of certain foods. In other words, food addiction is often perceived as a “problem of the mind” where the causes focus on eating as a personal choice and a coping mechanism for alleviating personal unhappiness. Interestingly, some public-perception evidence suggests that the notion of food addiction is more vulnerable to stigmatization than that of smoking or alcoholism, and that it tends to be viewed as a behavioral rather than a substance-related disorder. Even the tactility of certain foods in one’s mouth can be highly rewarding before they are even ingested. On the other hand, the very act of eating can be viewed as a potentially addictive behavior because of its ability to arouse all the senses in a highly pleasurable way, from the sounds and aromas of cooking, to the aesthetic appeal of visually colorful and attractively arranged food. Moreover, when taken in excess they can foster neuro-adaptations that promote compulsive intake, dependence, and cravings, in the same manner as addictive drugs. On the one hand, there is a growing acknowledgement that many processed foods-specifically those whose palatability is enriched by high levels of added sugar, fat, and salt-have properties similar to substances like cocaine, nicotine, and alcohol in their ability to perturb brain reward mechanisms (see ). This putative condition is unique, however, by straddling both substance-related and non-substance-related addiction disorders. The shift in psychiatric thinking, reflected in both these chapters of the DSM-5, may have contributed to a burgeoning clinical and preclinical interest in the topic of food addiction. In addition, our findings that the food-addiction group had significantly higher levels of hedonic responsiveness to food suggests that this bio-behavioral trait may foster a proneness to overeating, to episodes of binge eating, and ultimately to a compulsive and addictive pattern of food intake. The purpose of the study was therefore to test a model predicting that a stronger activation potential of opioid circuitry-as indicated by the functional A118G marker of the mu-opioid receptor gene-would serve as an indirect risk factor for food addiction via a heightened hedonic responsiveness to palatable food. While brain opioid signaling has also been strongly implicated in the control of food intake, there is no research examining this neural circuitry in the association with food addiction. What does exist has focused almost exclusively on dopaminergic reward pathways in the brain. Currently, there is little biologically-based research investigating the risk factors for food addiction. While food addiction has no formally-recognized definition, it is typically operationalized according to the diagnostic principles established by the Yale Food Addiction Scale-an inventory based on the symptom criteria for substance dependence in the DSM-IV.
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