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A psycho-genetic study of hedonic responsiveness in relation to "food addiction".

Davis C, Loxton NJ - Nutrients (2014)

Bottom Line: What does exist has focused almost exclusively on dopaminergic reward pathways in the brain.Results confirmed these relationships.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.

View Article: PubMed Central - PubMed

Affiliation: School of Kinesiology & Health Sciences, 343 Bethune College, York University, 4700 Keele Street, Toronto, ON M3J 1P3, Canada. cdavis@yorku.ca.

ABSTRACT
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. Currently, there is little biologically-based research investigating the risk factors for food addiction. What does exist has focused almost exclusively on dopaminergic reward pathways in the brain. 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. 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. Results confirmed these relationships. 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.

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Related in: MedlinePlus

Model predicting that the OPRM1 A118G genetic marker will relate to the hedonic-responsiveness composite variable, which in turn will be positively associated with YFAS symptom scores.
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nutrients-06-04338-f001: Model predicting that the OPRM1 A118G genetic marker will relate to the hedonic-responsiveness composite variable, which in turn will be positively associated with YFAS symptom scores.

Mentions: The current study is the first to examine a biological indicator of brain opioid functioning in the risk profile for YFAS food addiction. Specifically, the purpose was to test the indirect-effects model illustrated in Figure 1. Specifically, we predicted that a stronger activation potential of opioid circuitry in the common reward pathway-as indicated by the GG polymorphism of the functional A118G marker of MOR-would serve as a risk factor for food addiction. The mechanism of conduction was hypothesized to be an indirect relationship via a heightened hedonic responsiveness to palatable food. Specifically, the GG genotype would be associated with greater hedonic responsiveness, modeled as a composite variable with three separate indicators–viz. hedonic eating, food cravings, and a preference for sweet and fatty foods. In turn, hedonic responsiveness was predicted to correlate positively with symptoms of food addiction as indicated by scores on the YFAS.


A psycho-genetic study of hedonic responsiveness in relation to "food addiction".

Davis C, Loxton NJ - Nutrients (2014)

Model predicting that the OPRM1 A118G genetic marker will relate to the hedonic-responsiveness composite variable, which in turn will be positively associated with YFAS symptom scores.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4210920&req=5

nutrients-06-04338-f001: Model predicting that the OPRM1 A118G genetic marker will relate to the hedonic-responsiveness composite variable, which in turn will be positively associated with YFAS symptom scores.
Mentions: The current study is the first to examine a biological indicator of brain opioid functioning in the risk profile for YFAS food addiction. Specifically, the purpose was to test the indirect-effects model illustrated in Figure 1. Specifically, we predicted that a stronger activation potential of opioid circuitry in the common reward pathway-as indicated by the GG polymorphism of the functional A118G marker of MOR-would serve as a risk factor for food addiction. The mechanism of conduction was hypothesized to be an indirect relationship via a heightened hedonic responsiveness to palatable food. Specifically, the GG genotype would be associated with greater hedonic responsiveness, modeled as a composite variable with three separate indicators–viz. hedonic eating, food cravings, and a preference for sweet and fatty foods. In turn, hedonic responsiveness was predicted to correlate positively with symptoms of food addiction as indicated by scores on the YFAS.

Bottom Line: What does exist has focused almost exclusively on dopaminergic reward pathways in the brain.Results confirmed these relationships.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.

View Article: PubMed Central - PubMed

Affiliation: School of Kinesiology & Health Sciences, 343 Bethune College, York University, 4700 Keele Street, Toronto, ON M3J 1P3, Canada. cdavis@yorku.ca.

ABSTRACT
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. Currently, there is little biologically-based research investigating the risk factors for food addiction. What does exist has focused almost exclusively on dopaminergic reward pathways in the brain. 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. 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. Results confirmed these relationships. 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.

Show MeSH
Related in: MedlinePlus