An important component of addiction is reward. The brain’s reward system processes information about natural rewards such as eating and sex. Addictive chemical substances of abuse such as alcohol effectively hijack this system, and it has been suggested that obesity-promoting foods may also do this.
One theory of food reward neurobiological components: ‘liking’, ‘wanting’ and ‘learning’, phenomena that can be applied as readily to natural as to artificial rewards. ‘Liking’ is the hedonic component that reflects the immediate experience or anticipation of pleasure, for example, from the oral stimulation of eating a pleasurable food. ‘Wanting’ is the reward-seeking (or motivation) component that results in increased appetite, food cravings and other behaviours associated with increased motivation to obtain food. While ‘liking’ and ‘wanting’ are closely associated, it is clear from individuals with chemical drug addiction that motivated reward-seeking activity can occur in the absence of pleasure. Although it remains much debated as to whether there is a sufficient evidence base for food addiction, there are indications that the ‘wanting’ and ‘liking’ of obesogenic foods can also be dissociated, for example, in individuals with binge eating disorders.
The rewarding value attributed to a given food can be rather subjective, influenced not only by food palatability and availability but also by individual genetic/trait/psychosocial differences. In a recent report, it has even been suggested that for some individuals, exercise increases the rewarding value of food and hence, diminishes the impact of exercise on fat loss. Obese individuals may have allostatic changes in the hedonic set point for food and hence, attribute inappropriate rewarding values to foods. For example, according to the reward hyperfunction model of obesity, over-consumption could reflect a heightened responsiveness of the reward circuits to rewarding foods. This would be rather analogous to the enhanced responsiveness of the reward circuits to addictive drugs in susceptible individuals. Supportively, obese individuals self-report increased pleasure and displayed stronger reinforcement from eating high-fat and high-sugar foods than lean individuals. Alternatively (or perhaps additionally), it has been suggested that over-eating, like gambling or substance use disorder, could reflect a reward deficiency syndrome, the consequences of which would be to increase motivation to obtain the reward, in this case for food. Consistent with this, animals fed rewarding diets (eg high fat feeding or saccharine-enhanced chow) appear to have reduced sensitivity to psychostimulant rewards. It seems rather likely, as is the case for chemical drug addiction, that individuals predisposed to obesity may exhibit increased hedonic drives during early stages of the disease but, with increased exposure to rewarding foods, their hedonic value wanes while the motivational drives to obtain reward increase (ie increased eating to compensate for an increasing hedonic reward deficit). Individuals that have a tendency to over-eat, show an increased activity in brain areas associated with reward when shown appetizing compared with bland foods.More direct evidence for an altered reward mechanism in obese individuals is provided from studies examining the brain response to food intake or visual food cues. Those pathways responding to food intake are likely involved in the oral pleasure experience of eating. It has been shown that individuals that have a tendency to over-eat, show an increased activity in brain areas associated with reward when shown appetizing compared with bland foods. Obese individuals have a greater striatal response to visual food cues relative to lean individuals. By contrast, the striatal response to actual food intake was actually reduced in obese individuals. Collectively, these data suggest that obese individuals differ from lean individuals in reward processing; conceivably, the reduced activity of pathways involved in ‘liking’ is compensated for by a heightened activity of pathways involved in incentive motivation (‘wanting’). Consistent with this hypothesis, obese individuals have been shown to have reduced dopamine receptor D2 availability in the striatum relative to lean individuals. A decrease in D2 receptor availability, in other contexts, such as chemical drug addiction, has been thought to reflect increased dopamine release (ie increased activity of pathways involved in incentive motivation). Indeed, according to this model problematic over-eating would be driven by a hypofunction of the reward mechanism that compensates for a hedonic reward deficit.
There are indications that the successful weight loss outcome of gastric bypass surgery, may reflect changes in the hedonic set point for food. Patients that have undergone this bariatric surgery not only make healthier food choices but also have an altered attitude to (and desire for) food. Moreover, recent studies in rats that have undergone this surgery reveal an altered food reward behavior. After surgery, these rats show a suppressed preference/acceptance of high fat food together with a restoration of normal “wanting” and “liking” responses, effects that likely reflect an altered gut-reward signalling mechanism.