Hedonic Eating and Cortical Brain Contributions to Decision-Making

Hedonic eating

As mentioned previously, the hedonic system entails food cravings or desires and appetite for specific food items even when not necessarily hungry, generally with the expectation of some type of reward (ie, a pleasant taste in the mouth) after consumption. This is influenced by the hypothalamus but also involves several other brain areas discussed previously including the nucleus accumbens (“NAc”), the amygdala, and the ventral tegmental area (“VTA”), among others (such as the insula and various cortical regions). Several neurotransmitters are involved (ie, dopamine, serotonin, opioids, and cannabinoids) as are several neuropeptides (ie, ghrelin, leptin, and orexin). The hedonic system as a whole increases the incentive value of palatable food cues.

The following image demonstrates the widespread locations of sensory input and processing as well as the primary hedonic centers collating this information to generate pleasurable sensations, emotions, and memories associated with highly desirable foods.

Influence of dopamine

Dopamine is the primary neurotransmitter mediating the activity of the hedonic system, with dopaminergic projections across several brain regions including the VTA and NAc mentioned above and other centers such as the paraventricular nucleus of the hypothalamus and the amygdala. Various peripheral hormones such as ghrelin, insulin, leptin, and PYY can interact with dopaminergic neurons of the VTA and project to various locations involved in hedonic food intake regulation. Considering the function and complexity of all of these different brain regions, dopamine can mediate interactions between the hedonic drive to eat, your emotional state, and homeostatic food intake regulation.

Collectively, these processes trigger reward responses associated with emotions and memory that influence and potentially interfere with homeostatic energy balance considerations. Highly palatable food intake increases the release of dopamine in the NAc, which stimulates the hedonic system and generates a rewarding sensation, making you more prone to consume that food again. This hedonic signaling strengthens with food restriction, as does sweet & salty taste sensation in general; thus, when an individual has more signals increasing general hunger they will be more susceptible to the pleasurable sensations of eating highly palatable foods. Additionally, simply visualizing highly palatable food cues can induce a strong response in brain regions involved in reward and cognitive control, making you more prone to consuming these foods.

Opioids and endocannabinoids

Dopamine is not the only neurotransmitter involved; opioid and cannabinoid signaling are also utilized. These more directly correlate with “liking” of food and reinforce stimulation of the amygdala, potentiating pleasure-driven food intake, though some endocannabinoid-like molecules can also influence satiation. The opioid circuitry in particular has significant roles in food reward and incentivizing the motivational value of specific food-related cues while the endocannabinoid system can increase overall appetite. Some of the hedonic brain circuits utilizing these signaling pathways overlap with brain circuits activated in drug addiction; while “food addiction” is controversial, the overlap of relevant brain regions does indicate some addiction-like properties to the consumption of highly palatable foods.

In the last article I included an image demonstrating widespread dopamine and serotonin pathways in the brain; this distribution seems to be surpassed by opioids, which have many different signaling roles. This is shown in the following figure, with the distribution measured by using PET radioligands.

Relationship with obesity

So how does all of this contribute to or correlate with obesity?

• People with obesity may have increased activation of several of these brain areas when presented with images of highly palatable foods.^{(Brondel, 2022)}
  • Furthermore, the magnitude of this response even in people without obesity correlates with increased weight gain in subsequent months.
• Additionally, defective leptin signaling associated with obesity in the VTA can result in continued activation of food reward signals.
• This is compounded by the fact that sweet taste more so than the other basic tastes (which are umami, bitter, sour, and salt) activates reward areas, leading to greater desire for their consumption.
• However, obesity is associated with decreased gene expression in taste buds in several genes related to taste^{(Archer, 2019)}, and this may extend to the taste of fat itself when fat consumption is increased. Similarly, there is a decrease in dopaminergic D2 receptors as well as μ-opioid receptors in several of the involved brain regions in people with obesity.
  • Therefore, people with obesity have on average a lesser magnitude of pleasurable sensations when consuming highly palatable foods, requiring greater total consumption to generate the same rewarding sensation.

Much of these altered appetite and feeding characteristics between people with and without obesity seems related to dopamine signaling in the brain.^{(Hanßen, 2022)} The effect of some of these differences in the neurologic aspects of food intake were summarized in a review that discussed evidence supporting various neural vulnerability theories contributing to the development and maintenance of a state of obesity^{(Stice, 2021)}:

• • Incentive Sensitization Theory: Repeated associations between hedonic pleasure from the intake of high-calorie foods and their cues results in hyper-responsivity of the brain reward regions to these cues via conditioning -> this can thus lead to cravings and overeating.
  • Reward Surfeit Theory: People with greater activation of the brain reward regions to food taste are at increased risk of overeating and weight gain.
  • Inhibitory Control Deficit Theory: There is increased risk of overeating due to decreased inhibitory control when encountering food cues; thus there is a higher immediate reward bias to palatable food consumption.
  • Reward Deficit Theory: People with a lower sensitivity to dopamine-based reward regions overeat to compensate for this reward deficiency; this seems to be a consequence rather than a cause of obesity.