Brain and Other Responses in Hedonic Hunger
The desire to eat is controlled by two different mechanisms, the body’s homeostatic, or energy balance, system and its hedonic, or pleasure, system.1
The homeostatic system is controlled by communication between the hypothalamus and brainstem in the brain and the digestive system to ensure that the body’s energy needs are met. Different regions in the brain mediate hedonic hunger. 1,2 These “pleasure” regions respond to foods, drugs of abuse, and sex in similar manners, seeking reward and rarely sending a strong “stop” signal.
Hedonic Hunger and the Brain
The hippocampus, amygdala, ventral pallidum, nucleus accumbens (NAc), and orbitofrontal cortex areas of the brain influence hedonic hunger,1 which includes the “liking” and “wanting” of food. The NAc and ventral pallidum play particularly prominent roles in this reward system, as they house both dopamine and opioid signaling. These hedonic “hotspots” can be overactive in some people.
Functional magnetic resonance imaging (fMRI) is used as a tool for monitoring activation of different areas of the brain in response to stimuli. It frequently is used to compare subjective reports of food-related pleasure with brain activity. In one study, those who drank a liter of chocolate milk reported less pleasure and this was accompanied by a drop in activation in certain brain areas.3 High calorie foods have been shown by fMRI to increase activity in the hedonic sections of the brain, particularly when food previously has been restricted.
While all people have a pleasure region in the brain, it has been observed that in obesity, there is a greater response to food cues than if at a healthy weight. Research suggests that the appetite-suppressing portions of the brain in obesity may be less inhibited after eating.1
The Neurotransmitter Dopamine Plays a Prominent Role
Dopamine participates in the homeostatic regulation of eating, but its hedonic effects are more prominent. Dopamine signals the desire to seek out rewards, including palatable foods, and fMRI studies verify that dopamine correlates more strongly with wanting than liking a reward.4 With repeated exposure to a reward such as palatable food, hedonic centers of the brain can become desensitized to dopamine.
Hedonic Hunger and Metabolic Responses
The various metabolic hormones associated with hunger and satiety act directly on both homeostatic and hedonic brain receptors. Ghrelin is the primary hormone that signals hunger. Insulin, glucagon, and amylin from the pancreas and leptin and adiponectin from adipose tissue all signal satiety. Metabolic signals affect dopamine activation and therefore the brain’s reward system. In healthy weight individuals, a rise in leptin and insulin signals satiety and reduces dopaminergic signaling; in contrast, calorie restriction increases signaling and desire for reward. When leptin is chronically elevated in obesity, brain receptors may stop responding to leptin, much as body cells become resistant to elevated insulin levels, and this impacts response to dopamine.1 Desire for reward increases as a means to elevate dopamine levels.
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2Vucetic Z, Reyes TM. Central dopaminergic circuitry controlling food intake and reward: implications for the regulation of obesity Wiley Interdiscip Rev Syst Biol Med. 2010 Sep-Oct; 2(5):577-93.
3Kringelbach ML, O’Doherty J, Rolls ET Andrews C.Activation of the human orbitofrontal cortex to a liquid food stimulus is correlated with its subjective pleasantness Cereb Cortex. 2003; 13:1064–71.
4Berridge KC, Ho CY, Richard JM, DiFeliceantonio AG. The tempted brain eats: pleasure and desire circuits in obesity and eating disorders Brain Res. 2010 Sep 2; 1350:43-64.