Appetite Vs. Social Media

We all know that social media gives us dopamine rushes. But, did you know that those dopamine rushes can influence how our appetite is regulated? By viewing appetizing food-related Reels or TikToks, our brain’s reward centers are activated and increase our hunger and likelihood of impulsive eating. As a result, our appetites are becoming more and more dysregulated, inconsistent, and intense because of social media.

Figure 1. Food content on social media platforms like Instagram and TikTok is ubiquitous. (LaRose, n.d.).

Many of us have been there: the late night scrolling session turned into uncontrollable cravings, scrumptious meals appearing after every swipe. The visual stimulation of food triggers what is known as hedonic hunger, which is a pleasure-based desire to eat palatable, visually appealing foods even when our true physiological hunger is low.

This brings us to another significant distinction we must make: the difference between hunger and appetite. They are NOT the same things. Hunger, as alluded to before, is the physical need for food (regulated entirely homeostatically), whereas appetite is the desire for food (regulated both homeostatically and non-homeostatically). Appetite, unlike hunger, is also influenced by psychological and environmental cues, not only biological ones (The Difference Between, n.d.).

To understand more why our appetite is so malleable because of social media influence, we must understand 1) the regulatory psychobiological system called the satiety cascade and 2) how external cues trigger hedonic responses in our body.

What is the Satiety Cascade?

The satiety cascade is the biological systems that causes hunger. However, instead of getting lost in the biological complexities of the system, for initial simplicity purposes it is easier to think about the satiety cascade through how we feel before, during, and after meal cycles. Dr. Lucy Chambers, a corresponding author in the British Nutrition Foundation, neatly maps out this cycle in her article “Food texture and the satiety cascade” (Chambers, 2016). She includes a graphic demonstrating that the cycle begins when a person eats food. In the diagram below, this phase is indicated by “Food choice” to show that food has been consumed. The next phase, satiation, is the immediate fullness after eating the meal. Satiety, the third phase to be distinguished from satiation, is the long-term suppression of appetite until the next meal (Chambers, 2016). Think of this cycle as a bucket of water with a leak at the bottom. When you eat, you fill the bucket with water, the first 5% leaked out is satiation, where you still feel full after a meal. Then, satiety is the rest of the water that is leaked out from the bucket until you hit a threshold where your body tells you to eat, or fill your bucket again.

Figure 2. Schematic of the cycle of food consumption (indicated as "Food choice"), satiation, and satiety. Note that satiation occurs directly after a meal (short-term) while satiety is the prolonged period between meals where one does not feel hungry (long-term) (Chambers, 2016).

Biological Features of the Satiety Cascade

Now that the satiety cascade system is more familiar, we can now jump into the various biological factors that regulate the satiety cascade cycle. Both satiation and satiety are controlled by many sensory, cognitive, and hormonal signals within the body. However, they differ in that satiation is regulated by gastric and intestinal mechanisms while satiety is governed by episodic and tonic signals (Beneham, 2009).

Satiation

Diving first into satiation activation, most people recognize that the physical fullness of the stomach, or gastric distension, can cause one to feel full. The reason is because gastric distension causes mechanical stretching of the stomach, which activates stretch receptors or mechanoreceptors. In turn, the mechanoreceptors trigger the vagus nerve to send messages to the brainstem and hypothalamus to reduce the desire to eat (Borer, 2023). Pairing synergistically with gastric distention is the hormone cholecystokinin (CKK) that slows the emptying of the stomach, prolonging gastric distention, strengthening vagus nerve signals to further reduce food consumption (Kissileff et al., 2003).

Figure 3. Gastric distention (stomach expansion) triggers mechanoreceptors to send signals to the brain via the vagus nerve to trigger the feeling of fullness. Cholecystokinin (CKK) assists in the process by slowing down gastric emptying, intensifying the signals from the vagus nerve (Nässel & Wu, 2022).

Satiation also increases due to signals from the intestinal lining and initial digestion/absorption process. When food moves out of the stomach into the small intestine. The small intestine then breaks down carbohydrates, fats, and proteins into their respective components: sugars, fatty acids, and amino acids, respectively (Beneham, 2009).

Satiety

Episodic Signals

The intestines are where satiation seamlessly transitions into satiety. As mentioned earlier, satiety consists of both episodic and tonic signals. Episodic signals take place in response to eating food (which can be remembered by responses caused by episodes of food eating). Gut hormones’ effects on appetite are part of these episodic signals. One of the primary signals happens while digesting proteins, carbohydrates, and fats. Digestion significantly suppresses the levels of ghrelin, or the hormone attributed to increasing hunger, signaling to the brain that one is full. Unlike ghrelin, glucagon-like peptide 1 (GLP-1), responsible for gastric emptying, increases insulin levels for blood sugar level control, reduces hunger, and releases in response to nutrient absorption. Peptide YY (PYY), is another player in gut signaling as it slows digestion and for prolonged nutrient absorption (Gomez & Greeley, 2013). As with ghrelin inhibition, and GLP-1 elevation, and PPY increases, episodic signals play a key role in maintaining long-term satiety and hunger suppression.

Figure 4. Schematic of how ghrelin, GLP-1, and PYY work together to regulate satiety. Ghrelin increases gastric emptying and hunger. However, because digestion inhibits ghrelin production (as seen with the red line with a horizontal end below ghrelin), then gastric emptying is slowed, and we feel full. Glucagon-like peptide 1 (GLP-1) and peptide YY (PYY) both work to inhibit gastric emptying, amplifying the feeling of fullness (Steinert et al., 2017).

Tonic Signals

Tonic signals are another major distinction between satiation and satiety. Tonic signals serve as a communication pipeline between the brain and body that relays information about fat storage so that energy expenditure and intake are balanced. Leptin, a peptide hormone, is released from fat cells. It directly binds to hypothalamus receptors to inhibit hunger-activating neurons while stimulating satiety-activating neurons (Kharbanda et al., 2022). An analogy for leptin would be an inventory manager for a store. The inventory manager keeps track of if there are enough items in stock (sufficient fat storage), and once the shelves hit max capacity (max fat storage), the manager stops ordering more goods from the supplier (turns hunger off).

Additionally, insulin, a metabolic hormone released from the pancreas that controls blood sugar levels, is a substantial influencer of appetite. Insulin reduces the brain’s dopaminergic reward system to continue eating food. Insulin also decreases the tastiness of food that the brain perceives, and removes strong hedonic temptation to prevent intaking more food (Hallschmid et al., 2021).

Figure 5. Leptin and insulin work in tandem to create the feeling of fullness through tonic signaling. On the way, they bind to hypothalamic receptors (leptin to ObRb and insulin to IR). Since leptin and insulin are both at high concentrations after consuming food, they excite appetite-suppressing neurons (POMC) while inhibiting appetite-stimulating ones (NPY) (Thon et al., 2016).

HEDONIC RESPONSES

Now that the satiety cascade has been covered, it is now time to discuss the second key component of appetite. Before learning about how hedonic tendencies influence appetite control, it is first important to understand the psychology behind why humans can be so easily guided by hedonic responses. In psychology, hedonic theory is the concept that individuals strive to seek the experience that maximizes pleasure and minimizes displeasure (Zenko & Ladwig, 2024). Physiologically speaking, hedonic actions are often bound to the brain’s reward pathways, powered by dopamine (wanting) and opioids (pleasure) which can be reinforced by repetition (Finlayson & Dalton, 2012). If hedonic habits can be perpetuated by patterns, then there is no wonder that they can also be influenced by emotional, social, environmental, behavioral, and cultural norms. Recircling back to social media, which relates to all five of these influences, it is also no surprise that social media is one of today’s most potent dysregulators of appetite (Dumlu Bi̇lgi̇n et al., 2024). In fact, social media does what most hedonic influences can do to appetite: disrupt the satiety cascade to favor eating even when not physically hungry, shifting the primary reason for consuming food from nourishment to palatability. Neurologically speaking, eating hedonically can increase ghrelin levels and endocannabinoids (Monteleone et al., 2012), which enhance reward pathways and disrupt appetite regularity (Endocannabinoids, n.d.).

Key Takeaways

Hedonic eating, as most actions, are not harmful in moderation. That being said, it is important to recognize the causes of appetite-influencing stimuli like social media. If left unchecked, social media and other stimuli like food advertisements, availability, and social pressures, may cause fluctuating meal-times, intensify cravings, increased anxiety, lower self-esteem, and other nutritional problems. Learning about appetite’s mechanisms and patterns may also assist in understanding our own bodies. By becoming aware of our body’s tendencies and habits, it may also bring clarity to other aspects of life. To re-emphasize, hedonic eating, as many other things, is not to be antagonized. Rather, it is important to find balance between control and indulgence, as should be done in all aspects of life.

References

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17. Zenko, Z., & Ladwig, M. A. (2024, December 14). 12.3: Hedonic Theory. Medicine LibreTexts. https://med.libretexts.org/Bookshelves/Sports_and_Exercise/Essentials_of_Exercise_and_Sport_Psychology__-_An_Open_Access_Textbook_(Zenko_and_Jones)/12%3A_Affective_Responses_to_Exercise-_Measurement_Considerations_for_Practicing_Professionals/12.03%3A_Hedonic_Theory

Thumbnail image: (LaRose, n.d.)