Table of Contents
In the prior articles I discussed the primary components of homeostatic food intake regulation, including the hypothalamus and other intermediary brain centers that influence hunger signals. In this article I will discuss the hedonic considerations, which overlap with homeostatic considerations as many of the same brain regions are used. I will then demonstrate the higher brain centers that all of these intermediary centers influence for conscious decision-making choices regarding food intake.
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.
Note: Sensory input (such as sight or smell) does more than simply trigger signalling in various brain regions. It can also trigger the “cephalic phase response” prior to food consumption, which begins the processes of salivation, gastric acid secretion, and GI hormone release (ie, ghrelin and insulin). These signals are discussed in more depth later in this series.
Tip: Appetite disinhibition (ie, the probability of giving in to hedonic eating drive) may be a key mediator relating underlying genetic risk and obesity.(Brunner, 2021) Thus, people with obesity may find weight loss to be much easier if they work with people who are close to them to alter their local food environment to remove various hedonic-stimulating foods.
Cortical brain regions integrate all of the prior considerations
Thus far I have discussed:
- homeostatic food intake considerations
- hedonic food intake considerations
- the integral role of the hypothalamus and several intermediary brain centers
- the role of specific signaling molecules (such as NPY) and pathways (such as dopamine)
The remaining question is how does the brain tie all of this together? The following image demonstrates this, which should be examined from the bottom to the top.
You can access the article that published this image to read the caption. I will discuss the signals included in the bottom panel in the next article. Moving up, sensory signals go to the arcuate nucleus of the hypothalamus and the brainstem, where they are processed and interact with other hypothalamic nuclei as well as the thalamus. These various signals are then sent to other intermediary brain centers that govern hedonic eating, some of which are listed in the purple panel. Subsequently, all of this information is sent to the conscious processing cortical regions, using signaling including a variety of neurotransmitters from the hedonic pathways as well as orexigenic or anorexigenic hunger influences from the homeostatic-regulating brain centers. This culminates in conscious decision-making regarding eating.
Hedonic eating is stimulated by sensory information (such as smell and sight) as well as pleasant memories and feelings associated with eating highly palatable foods. This utilizes dopamine and other signaling pathways that are strengthened by hunger and promote increased desirable food intake. People with obesity may have blunted hedonic signaling when consuming these foods, thus triggering greater intake to generate the same pleasurable response.
To summarize how the full brain contributes to hunger and appetite:
- Peripheral signals and sensory information are processed in the hypothalamus and brainstem. Sensory information is further processed in the thalamus (with the exception of the sense of smell).
- The sensory information is further processed by intermediary brain centers as the hedonic system activates its various signaling pathways.
- All of this information from the homeostatic and hedonic structures and processes is transmitted to the higher central nervous system cortical structures, which assimilates all of the various signaling to generate the sensations of hunger, appetite, satiation, and satiety, strongly influencing your choice to consume or not consume food at any given time.
At this point I have discussed all of the primary brain considerations regarding hunger and appetite control. As mentioned previously, and as the above image demonstrates, peripheral signaling directly influences several brain regions. I will discuss these peripheral considerations next.
Click here to proceed to article 5 of this series, or jump around with the drop-down menu below.
- Archer N, Shaw J, Cochet-Broch M, Bunch R, Poelman A, Barendse W, Duesing K. Obesity is associated with altered gene expression in human tastebuds. Int J Obes (Lond). 2019 Jul;43(7):1475-1484. doi: 10.1038/s41366-018-0303-y. Epub 2019 Jan 29. PMID: 30696932.
- Brondel L, Quilliot D, Mouillot T, Khan NA, Bastable P, Boggio V, Leloup C, Pénicaud L. Taste of Fat and Obesity: Different Hypotheses and Our Point of View. Nutrients. 2022 Jan 27;14(3):555. doi: 10.3390/nu14030555. PMID: 35276921; PMCID: PMC8838004.
- Brunner EJ, Maruyama K, Shipley M, Cable N, Iso H, Hiyoshi A, Stallone D, Kumari M, Tabak A, Singh-Manoux A, Wilson J, Langenberg C, Wareham N, Boniface D, Hingorani A, Kivimäki M, Llewellyn C. Appetite disinhibition rather than hunger explains genetic effects on adult BMI trajectory. Int J Obes (Lond). 2021 Apr;45(4):758-765. doi: 10.1038/s41366-020-00735-9. Epub 2021 Jan 14. Erratum in: Int J Obes (Lond). 2021 Mar;45(3):711. PMID: 33446837; PMCID: PMC8005371.
- Hanßen R, Schiweck C, Aichholzer M, Reif A, Thanarajah SE. Food reward and its aberrations in obesity. Current Opinion in Behavioral Sciences. 2022;48. doi: 10.1016/j.cobeha.2022.101224.
- Stice E, Yokum S. Neural Vulnerability Factors That Predict Future Weight Gain. Curr Obes Rep. 2021 Dec;10(4):435-443. doi: 10.1007/s13679-021-00455-9. Epub 2021 Sep 30. PMID: 34591256.