Evidence for sugar addiction: Behavioral and neurochemical effects of intermittent, excessive sugar intake
TL;DR: The evidence supports the hypothesis that under certain circumstances rats can become sugar dependent and may translate to some human conditions as suggested by the literature on eating disorders and obesity.
About: This article is published in Neuroscience & Biobehavioral Reviews.The article was published on 2008-01-01 and is currently open access. It has received 1171 citations till now. The article focuses on the topics: Addiction & Food addiction.
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TL;DR: Overconsumption of palatable food triggers addiction-like neuroadaptive responses in brain reward circuits and drives the development of compulsive eating, demonstrating that common hedonic mechanisms may underlie obesity and drug addiction.
Abstract: We found that development of obesity was coupled with emergence of a progressively worsening deficit in neural reward responses. Similar changes in reward homeostasis induced by cocaine or heroin are considered to be crucial in triggering the transition from casual to compulsive drug-taking. Accordingly, we detected compulsive-like feeding behavior in obese but not lean rats, measured as palatable food consumption that was resistant to disruption by an aversive conditioned stimulus. Striatal dopamine D2 receptors (D2Rs) were downregulated in obese rats, as has been reported in humans addicted to drugs. Moreover, lentivirus-mediated knockdown of striatal D2Rs rapidly accelerated the development of addiction-like reward deficits and the onset of compulsive-like food seeking in rats with extended access to palatable high-fat food. These data demonstrate that overconsumption of palatable food triggers addiction-like neuroadaptive responses in brain reward circuits and drives the development of compulsive eating. Common hedonic mechanisms may therefore underlie obesity and drug addiction.
1,317 citations
TL;DR: Imaging studies show that obese subjects might have impairments in dopaminergic pathways that regulate neuronal systems associated with reward sensitivity, conditioning and control, and it is postulated that this could also be a mechanism by which overeating and the resultant resistance to homoeostatic signals impairs the function of circuits involved in reward sensitivity.
1,099 citations
Cites background from "Evidence for sugar addiction: Behav..."
...Interestingly, in rodents that have been exposed to diets rich in sugar, a pharmacological challenge with naloxone (opiate antagonist drug devoid of effects in control rats) elicits an opiate withdrawal syndrome similar to that observed in animals that have been chronically exposed to opioid drugs [42]....
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TL;DR: The Yale Food Addiction Scale (YFAS) is a sound tool for identifying eating patterns that are similar to behaviors seen in classic areas of addiction, and predicted binge-eating behavior above and beyond existing measures of eating pathology, demonstrating incremental validity.
1,049 citations
Additional excerpts
..., withdrawal, tolerance, dopaminergic downgrading) (Avena et al., 2008; Johnson & Kenny, 2010)....
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TL;DR: It is argued that the phenomenology of effort can be understood as the felt output of these cost/benefit computations of the costs and benefits associated with task performance and motivates reduced deployment of these computational mechanisms in the service of the present task.
Abstract: Why does performing certain tasks cause the aversive experience of mental effort and concomitant deterioration in task performance? One explanation posits a physical resource that is depleted over time. We propose an alternative explanation that centers on mental representations of the costs and benefits associated with task performance. Specifically, certain computational mechanisms, especially those associated with executive function, can be deployed for only a limited number of simultaneous tasks at any given moment. Consequently, the deployment of these computational mechanisms carries an opportunity cost-that is, the next-best use to which these systems might be put. We argue that the phenomenology of effort can be understood as the felt output of these cost/benefit computations. In turn, the subjective experience of effort motivates reduced deployment of these computational mechanisms in the service of the present task. These opportunity cost representations, then, together with other cost/benefit calculations, determine effort expended and, everything else equal, result in performance reductions. In making our case for this position, we review alternative explanations for both the phenomenology of effort associated with these tasks and for performance reductions over time. Likewise, we review the broad range of relevant empirical results from across sub-disciplines, especially psychology and neuroscience. We hope that our proposal will help to build links among the diverse fields that have been addressing similar questions from different perspectives, and we emphasize ways in which alternative models might be empirically distinguished.
895 citations
TL;DR: It is argued that a biological approach to psychiatry based on 'neurocognitive endophenotypes', whereby changes in behavioural or cognitive processes are associated with discrete deficits in defined neural systems, has important implications for the future classification of psychiatric disorders, genetics and therapeutics.
802 citations
References
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TL;DR: Findings in this work indicate that dopaminergic neurons in the primate whose fluctuating output apparently signals changes or errors in the predictions of future salient and rewarding events can be understood through quantitative theories of adaptive optimizing control.
Abstract: The capacity to predict future events permits a creature to detect, model, and manipulate the causal structure of its interactions with its environment. Behavioral experiments suggest that learning is driven by changes in the expectations about future salient events such as rewards and punishments. Physiological work has recently complemented these studies by identifying dopaminergic neurons in the primate whose fluctuating output apparently signals changes or errors in the predictions of future salient and rewarding events. Taken together, these findings can be understood through quantitative theories of adaptive optimizing control.
8,163 citations
"Evidence for sugar addiction: Behav..." refers background in this paper
...The NAc is important for several components of ‘‘reward’’ including food seeking and reinforcement of learning, incentive motivation, stimulus salience and signaling a stimulus change (Bassareo and Di Chiara, 1999; Berridge and Robinson, 1998; Salamone, 1992; Schultz et al., 1997; Wise, 1988)....
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TL;DR: S sensitization of incentive salience can produce addictive behavior even if the expectation of drug pleasure or the aversive properties of withdrawal are diminished and even in the face of strong disincentives, including the loss of reputation, job, home and family.
6,783 citations
"Evidence for sugar addiction: Behav..." refers background in this paper
...This is important since enhanced mesolimbic dopaminergic neurotransmission plays a major role in the behavioral effects of sensitization as well as cross-sensitization (Robinson and Berridge, 1993), and may contribute to addiction and comorbidity with polysubstance abuse....
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...This opioid–palatability link is further characterized by theories in which the reinforcing effect is dissociated into a dopaminergic system for incentive motivation and an opioid ‘‘liking’’ or ‘‘pleasure’’ system for hedonic responses (Berridge, 1996; Robinson and Berridge, 1993; Stein, 1978)....
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...Drug-induced sensitization may play a role in the enhancement of drug self-administration and is implicated as a factor contributing to drug addiction (Robinson and Berridge, 1993)....
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TL;DR: A model is described that delineates the roles of individual hormonal and neuropeptide signalling pathways in the control of food intake and the means by which obesity can arise from inherited or acquired defects in their function.
Abstract: New information regarding neuronal circuits that control food intake and their hormonal regulation has extended our understanding of energy homeostasis, the process whereby energy intake is matched to energy expenditure over time. The profound obesity that results in rodents (and in the rare human case as well) from mutation of key signalling molecules involved in this regulatory system highlights its importance to human health. Although each new signalling pathway discovered in the hypothalamus is a potential target for drug development in the treatment of obesity, the growing number of such signalling molecules indicates that food intake is controlled by a highly complex process. To better understand how energy homeostasis can be achieved, we describe a model that delineates the roles of individual hormonal and neuropeptide signalling pathways in the control of food intake and the means by which obesity can arise from inherited or acquired defects in their function.
6,178 citations
TL;DR: The most prominent contributors to mortality in the United States in 1990 were tobacco, diet and activity patterns, alcohol, microbial agents, toxic agents, firearms, sexual behavior, motor vehicles, and illicit use of drugs.
Abstract: Objective. —To identify and quantify the major external (nongenetic) factors that contribute to death in the United States. Data Sources. —Articles published between 1977 and 1993 were identified through MEDLINE searches, reference citations, and expert consultation. Government reports and compilations of vital statistics and surveillance data were also obtained. Study Selection. —Sources selected were those that were often cited and those that indicated a quantitative assessment of the relative contributions of various factors to mortality and morbidity. Data Extraction. —Data used were those for which specific methodological assumptions were stated. A table quantifying the contributions of leading factors was constructed using actual counts, generally accepted estimates, and calculated estimates that were developed by summing various individual estimates and correcting to avoid double counting. For the factors of greatest complexity and uncertainty (diet and activity patterns and toxic agents), a conservative approach was taken by choosing the lower boundaries of the various estimates. Data Synthesis. —The most prominent contributors to mortality in the United States in 1990 were tobacco (an estimated 400000 deaths), diet and activity patterns (300 000), alcohol (100 000), microbial agents (90 000), toxic agents (60 000), firearms (35 000), sexual behavior (30 000), motor vehicles (25 000), and illicit use of drugs (20 000). Socioeconomic status and access to medical care are also important contributors, but difficult to quantify independent of the other factors cited. Because the studies reviewed used different approaches to derive estimates, the stated numbers should be viewed as first approximations. Conclusions. —Approximately half of all deaths that occurred in 1990 could be attributed to the factors identified. Although no attempt was made to further quantify the impact of these factors on morbidity and quality of life, the public health burden they impose is considerable and offers guidance for shaping health policy priorities. (JAMA. 1993;270:2207-2212)
5,468 citations
TL;DR: A novel test for the selective identification of anxiolytic and anxiogenic drug effects in the rat is described, using an elevated + -maze consisting of two open arms and two enclosed arms, which showed that behaviour on the maze was not clearly correlated either with exploratory head-dipping or spontaneous locomotor activity.
5,391 citations
"Evidence for sugar addiction: Behav..." refers background in this paper
...This test has been extensively validated for both general anxiety (Pellow et al., 1985) and anxiety induced by drug withdrawal (File and Andrews, 1991)....
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