Figure 1.

Dynamic distributed neurobehavioural vulnerability model of eating behaviour in obesity.

Bold lines represent exaggerated appetite-related signals, broken lines represent impaired appetite-related signals, and grey dotted lines represent functional interactions between brain areas. For example, satiety signalling from homeostatic areas seems to be impaired (e.g. delayed fMRI inhibition response in hypothalamus) while hunger signals from emotion/memory areas and sensory/motor areas seem to be heightened (e.g. greater activation in amygdala, hippocampus, insula and precentral gyrus in response to food cues), in obese individuals. The functioning of the neurobehavioural system depends on genetic, biological and environmental influences, as well as cognitions, emotions and persistent patterns of behaviour (as well as interactions between these factors). To take a specific example, the role of reward areas may depend on dietary behaviour and genetic factors. For example, long-term exposure to highly palatable high-calorie foods may lead to decreased reward activation following food intake, but increased reward activation following food cues, in obese individuals. Alternatively, individuals with a genetic reward deficit may show decreased reward activation to both intake and cues. Both routes may cause individuals to compensate by over-eating. There is also evidence that the recruitment of cognitive control areas varies between obese individuals, depending on their habitual level of cognitive and/or behavioural dietary restraint. The areas included in this diagram are distributed all over the brain and interact with each other (i.e. functional connectivity), producing the complex and variegated phenotypes associated with common, multifactorial forms of obesity.