Introduction
In this blog post, we’re going to look at how our body uses its internal signals that come from food ingestion, into a behavioral response. While external signals from the environment modulate our approach responses, the internal signals modulate the rewarding aspects of the ingested food object. These signals represent a complex interplay of feedback loops going from our brain sites to many different tissues involved in digestion, nutrient extraction, and hormonal responses. It is based on these feedback signals, that associations between cause and effect are being formed between the perceived (food) item i.e. cue and its reward. This eventually establishes a so-called motivational magnet which modulates the behavior response, when the same (or similar) cue is perceived again.
Two-types of responses
On a very basic level, ingested food can evoke either a positive or negative response. Positive responses facilitate further ingestion, while negative decrease it. Both responses can be perceived from the facial expression and other bodily responses (when looking at the higher-order mammalian species). An example of a positive response would be an increased rate of ingestion, while a negative response would be in a form of object avoidance, gag reflex stimulation, and sickness. Responses to basic tastes are native, however, they can be changed through exposure and positive reinforcement. Still, the main aim of these responses is to prevent inappropriate food ingestion and facilitate the ingestion of rewarding ones.
Food Related Interoception
When ingested, food travels through various sites of our periphery, such as the mouth, throat, stomach, and our gut. With the presence of food at each site, specific signaling molecules are evoked and interpreted (depending on what has been ingested). In the mouth, most of the behavior is regulated through structural and taste analysis. Here we see native responses to tastes (sour, bitter, sweet, salty, and umami) which informs the organism about food being appropriate for ingestion [1]. If one had a bad experience with a particular feature (taste, smell, and or structure) of the food avoidance or even a gag reflex is evoked to prevent the same bad experience to repeat itself. The negative association is called conditioned taste aversion – CTA. If food however is appropriate for digestion, nutrient specific signaling molecules are being stimulated in later downstream parts of digestion (stomach and the gut). Hormones like gastrin, secretin, cholecystokinin – CCK, guanylin are the most prevalent. They make sure that food is being correctly digested by influencing the activity of other digestive organs. Similarly, in the process of nutrient absorption, extracted nutrients are transmitted to our blood, where another set of signaling molecules are evoked. Hormones like insulin, growth hormone, ghrelin, that evoke a response on the periphery to deal with nutrient partitioning and to the nervous system to modulate further behavior. The behavior is modulated by integrating the current state of the organism and the hormonal response from the ingested food (this can be however skewed with high rewarding food and substances). This process is called alliesthesia [2]–[4]. It is this mechanism that opens up the Pandoras’ box of integrating the signaling molecules coming from the aforementioned periphery, at the central nervous system that later form an appropriate response.
Integration of peripheral signals in the brain
While the periphery evokes and produces the signaling molecules, it is at the brain site where these signals are interpreted so that they modulate the behavioral response. The signaling molecules primarily provide information about the current state of the organism, especially in relation to energy reserves i.e. hunger or satiety. Based on the state of metabolism, different brain activity can be observed while food is being ingested. Regions like the hippocampus, parahippocampus, amygdala in anterior cingulate gyrus express a lower activity in the state of satiety, while the regions of the insula, thalamus, and substantia nigra are significantly more active in the state of hunger [5]. This shows that based on the particular metabolic state, different processing and response initiation are being evoked at the brain site. In [5], the researches also found a difference in brain activation, based on the nutrients ingested as well, which provides an explanation of reward processing and value estimation.
Modulating behavior based on Interoception
As we described in the previous two sections, signals between the periphery and the central nervous systems integrate together to evoke a response. Research looking at the effect of the state of the metabolism in relation to the response modulation has demonstrated response modulation at all of the sites, where food travels through. It has been shown that chewing speed is influenced by the state of satiety (short term satiety) as well as the state of total body fat reserves (long term satiety). Later in the digestion route, the fullness of the stomach modulates how much the organism desires further ingestion of food [6]. Connected with a feedback loop, the food from the stomach is being moved to the next stage of digestion inside the intestines. The movement of broken-down food from the stomach to the intestines is performed until a threshold of nutrients has been accumulated in the first part of the duodenum [7]. Once the food hits the duodenum and nutrient absorption is on the schedule, the body switches its dominance from the sympathetic to the parasympathetic nervous system. This shifts the metabolism into extracting nutrients and consequently downregulates other metabolic processes. In that state, other hormones are required to process and store the absorbed nutrients in the blood. Hormones like insulin, glucagon, and leptin play a key role in this signaling mechanism, which predominantly define the state of satiety. Once the dominance of the parasympathetic nervous system has been established, we stop eating and feel the need to rest and relax.
Conclusion
Signals coming from the inside of our body as food is consumed, digested, and absorbed provide the physiological aspect of food perception. Those signaling molecules flow through the bloodstream into the brain, which then provides an appropriate behavioral response. As we described before, the interplay and interconnection include a vast array of brain regions such as the insula, amygdala, cingulate cortex, hippocampus, and thalamus. And it is this vast connection between the periphery and the brain regions that give us an understanding as to how much food influences our behavior.
References
[1] K. L. Mueller, M. A. Hoon, I. Erlenbach, J. Chandrashekar, C. S. Zuker, and N. J. P. Ryba, “The receptors and coding logic for bitter taste,” Nature, vol. 434, no. 7030, pp. 225–229, Mar. 2005, doi: 10.1038/nature03352.
[2] J. E. Blundell and D. G. Freeman, “Sensitivity of Stimulus-Induced-Salivation (SIS), Hunger Ratings and Alliesthesia to a Glucose Load: SIS as a Measure of Specific Satiation,” Appetite, vol. 2, no. 4, pp. 373–375, Dec. 1981, doi: 10.1016/S0195-6663(81)80025-6.
[3] M. Cabanac and L. Lafrance, “Duodenal preabsorptive origin of gustatory alliesthesia in rats,” Am. J. Physiol. – Regul. Integr. Comp. Physiol., vol. 263, no. 5, pp. R1013–R1017, Nov. 1992.
[4] M. Cabanac and L. Lafrance, “Postingestive alliesthesia: The rat tells the same story,” Physiol. Behav., vol. 47, no. 3, pp. 539–543, Mar. 1990, doi: 10.1016/0031-9384(90)90123-L.
[5] L. Haase, B. Cerf-Ducastel, and C. Murphy, “Cortical activation in response to pure taste stimuli during the physiological states of hunger and satiety,” NeuroImage, vol. 44, no. 3, pp. 1008–1021, Feb. 2009, doi: 10.1016/j.neuroimage.2008.09.044.
[6] J. A. Deutsch, “The role of the stomach in eating,” Am. J. Clin. Nutr., vol. 42, no. 5, pp. 1040–1043, Nov. 1985, doi: 10.1093/ajcn/42.5.1040.
[7] I. Rønnestad, Y. Akiba, I. Kaji, and J. D. Kaunitz, “Duodenal luminal nutrient sensing,” Curr. Opin. Pharmacol., vol. 19, pp. 67–75, Dec. 2014, doi: 10.1016/j.coph.2014.07.010.