Brain and Other Responses in Hedonic Hunger

 

Article By: The Weight Watchers Research Department   Print   Email

 

The desire to eat is controlled by two different mechanisms, the body’s homeostatic, or energy balance, system and its hedonic, or pleasure, system.

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 signalling. 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 litre 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 centres 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 signalling; in contrast, calorie restriction increases signalling 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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