Abstract

The notion of food “addiction” often focuses on the overconsumption of sweet tasting foods or so-called sugar “addiction”. In the extreme, some have suggested that sugar and sweet tastes elicit neural and behavioral responses analogous to those observed with drugs of abuse. These concepts are complicated by the decades long uncertainty surrounding the validity and reproducibility of functional magnetic resonance imaging (fMRI) methodologies used to characterize neurobiological pathways related to sugar and sweet taste stimuli. There are also questions of whether sweet taste or post-ingestion metabolic consequences of sugar intake would lead to addiction or excessive caloric intake. Here, we present a focused narrative review of literature related to the reward value of sweet taste which suggests that reward value can be confounded with the construct of “addictive potential”. Our review seeks to clarify some key distinctions between these constructs and questions the applicability of the addiction construct to human over-eating behaviors. To adequately frame this broad discussion requires the flexibility offered by the narrative review paradigm. We present selected literature on: techniques used to link sugar and sweet tastes to addiction neurobiology and behaviors; sugar and sweet taste “addiction”; the relationship of low calorie sweetener (LCS) intake to addictive behaviors and total calorie intake. Finally, we examined the reward value of sweet tastes and contrasted that with the literature describing addiction. The lack of reproducibility of fMRI data remains problematic for attributing a common neurobiological pathway activation of drugs and foods as conclusive evidence for sugar or sweet taste “addiction”. Moreover, the complicated hedonics of sweet taste and reward value are suggested by validated population-level data which demonstrate that the consumption of sweet taste in the absence of calories does not increase total caloric intake. We believe the neurobiologies of reward value and addiction to be distinct and disagree with application of the addiction model to sweet food overconsumption. Most hypotheses of sugar “addiction” attribute the hedonics of sweet foods as the equivalent of “addiction”. Further, when addictive behaviors and biology are critically examined in totality, they contrast dramatically from those associated with the desire for sweet taste. Finally, the evidence is strong that responses to the palatability of sweets rather than their metabolic consequences are the salient features for reward value. Thus, given the complexity of the controls of food intake in humans, we question the usefulness of the “addiction” model in dissecting the causes and effects of sweet food over-consumption.

Highlights

  • Many studies in animals with a focus on the dopamine system underlie the hypothesis that the abuse potential from sweet or fatty foods is analogous to abuse seen in drug addiction. While both foods and drugs have shared brain reward pathways, food intake is extensively controlled by numerous other systems not currently recognized as related to addiction

  • Attributing the negative addictive qualities of drugs of abuse to foods may be appealing but does not necessarily lead to a greater understanding of interventions that are likely to be effective in reducing excessive food intake

  • Focusing on particular nutrients such as sugars or any stimulus of sweet taste and suggesting avoiding these foods is not likely to be a useful strategy for dealing with the present rates of overweight and obesity

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Summary

Introduction

Public Health 2021, 18, 9791 and compulsive These similarities do not, mean that the processes underlying overeating and drug addiction are the same, nor that it is appropriate to characterize overeating as food “addiction”. Various gut peptides such as CCK interact with gastric distension to effect changes in food intake [4,6,9,10,11] To date, these controls have not been implicated in models of addiction [12,13,14,15]. The necessity of distinguishing between habit and palatability as separate determinants of food choice was first pointed out by Paul Thomas Young [35] Confusing these fundamental food choice concepts and related underlying neurobiology with “addiction” confounds scientific study design and potential interventions addressing overeating and obesity. Supporting this narrative, we applied the search terms “sweet taste reward and food addiction” and “hedonics of sweet taste and food addiction” to PubMed and Google Scholar

Insights from Animal Studies
Food “Addiction” in Humans
Issues with fMRI Studies
Findings
Conclusions
Full Text
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