We’ve all experienced that feeling of being completely full after a meal, yet still having room for dessert… maybe even craving a little something sweet. While you may have heard family members and friends refer to this gastronomic phenomenon as the “second stomach for dessert,” research scientists often use the term hedonic hunger, meaning the desire to consume foods for the purposes of pleasure and in the absence of physical hunger. Why does this happen? Let’s start by taking a look at the mechanisms involved in hunger and appetite control.

Regulation of food intake

Our digestive system is in constant communication with the brain, sending signals back and forth to ensure that we’re getting enough nutrients to meet our body’s needs. When our body senses an energy shortage, it sends out a variety of hunger signals that drive us to eat. A major player influencing our decision to start eating is a hormone called ghrelin. This “hunger hormone” is produced primarily by the cells lining the stomach to stimulate appetite in response to low energy or in anticipation of a meal. During a meal or snack, our body senses an increase in available energy and suppresses these hunger signals. At the same time, it starts to send out signals that we are full through the appetite-suppressing hormone leptin. In other words, our digestive system and our brain communicate about whether we have sufficient calories and respond accordingly by signaling us to eat or to stop eating. However, there are several factors that may cause us to eat in the absence of an energy need.

Gut hormones, including ghrelin, act as signals communicating between the brain and digestive tract. The brain matches these signals with information such as taste and smell stimuli, learned associations, pleasant sensations (hedonic) and energy needs to influence eating behavior. Brain region abbreviations: PFC, prefrontal cortex; NAc, nucleus accumbens; VTA, ventral tegmental area; Hypo, hypothalamus; NTS, nucleus tractus solitaries. Clemmensen et al., 2017, Cell.
Reward-based eating

Like many pleasurable behaviors, eating tasty food leads to the release of dopamine, a signaling molecule that plays an important role in feeling pleasure. While all tasty foods can cause a dopamine rush, sweet and fatty foods are highly pleasure-inducing. Over time, we develop associations between the stimuli linked to delicious foods, such as the sight, smell or even thoughts of these foods, with the rewarding feeling we get from the dopamine release. This process, called conditioning, can cause a dopamine surge in anticipation of a yummy treat, motivating us to eat. This phenomenon has been demonstrated in mice conditioned to receive a sweet reward (a 20% sucrose solution) after a five second audiovisual cue. In these conditioned mice, dopamine activity increased in response to the conditioned stimulus, as well as the sweet reward. Similarly, brain imaging studies in humans have shown that dopamine levels spike in response to the sight, smell and taste of food without actually consuming the food, which increases the desire to eat. Dopamine is so important in the motivation to eat that mice lacking the ability to produce dopamine die of starvation.

The “hunger hormone” ghrelin is also involved in our craving for desserts. Studies have shown that ghrelin shifts rodents’ preferences towards sweet and fatty foods even if they are not hungry. For example, rats that can’t respond to ghrelin signaling ate less of a cookie dough treat after a full meal compared to those that could. Similarly, mice that can’t produce the active ghrelin hormone eat less of a high-fat dessert after a full meal compared to mice that can. These studies reveal that ghrelin is involved in the drive to consume food for pleasure, even without the need for calories.

In a study by Thanarajah et al., milkshake consumption caused immediate dopamine release due to pleasant taste sensations, as well as delayed dopamine release that was likely due to signaling following food consumption (post-ingestive signaling). Image modified from Thanarajah et al, 2019, Cell Metabolism.
Sensory-specific satiety

Another important aspect involved in our desire to eat desserts on a full stomach is something called sensory-specific satiety, which occurs when a person is less eager to continue eating a food that they’ve already eaten compared to a “new” food. In one landmark study on sensory-specific satiety, participants received a four-course meal of either the same four dishes or four different dishes. The participants that received four different courses consumed 60% more calories compared to those that received four identical courses, primarily because of the perceived pleasantness of the new foods. In another study, participants were given fries and brownies to eat with or without condiments (such as ketchup and vanilla cream). They ate more and gave higher pleasure ratings when the food was accompanied with condiments. Essentially, when our brain has lost interest in a certain food we perceive a feeling of fullness, whereas our appetite returns when we’re given the option to try a new food or even a new flavor (such as adding ketchup to our fries). In terms of having room for dessert, our brains may be bored of the main dish, but dessert serves as a new stimulus, reactivating our desire to eat.

Exposure to new foods or flavors makes eating more pleasant and renews appetite, preventing sensory-specific satiety, the decline in satisfaction that occurs when continuing to eat the same food.
Image obtained from Pixabay.
Making room for dessert

When we’re presented with the option of dessert after a filling meal, reward-seeking behavior and sensory-specific satiety trick the brain into wanting more. These signals override the fact that we’re already full and don’t have a physiological need for calories. When simply thinking about food or visualizing food can influence the levels of signaling molecules like dopamine and appetite-related hormones like ghrelin, it’s not surprising that many find it hard to resist the temptation of dessert.


  • Cassondra Saande

    Cassondra Saande received her PhD in Nutritional Sciences from Iowa State University where she studied the impact of whole egg consumption on nutrient balance in metabolic disease. Her research interests include identifying strategies to optimize health and the prevention and treatment of chronic disease. You can find her on LinkedIn at https://www.linkedin.com/in/cassondrasaande.

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