This post was written by one of our contributors; medical student w/ BSc in human nutrition + MSc in clinical and public health nutrition – Rebecca Fox.
We’ve all been there. It’s 11:00 am, and you’ve skipped breakfast rushing out the door (or running to your next zoom meeting #wfh), and that slightly painful grumbling feeling in your stomach starts to set in. You’re hungry! But why do we get hungry? and how does our body know that we haven’t eaten in a while?
At the core of it, our bodies require a certain amount of food energy to keep us going. The amount of energy each of us needs is unique to our own bodies and changes with time. However, balancing the amount of food we take in with the amount we expend is a tricky process involving coordinated regulation by the central nervous system (CNS), after receiving signals from:
- the Gastrointestinal tract (stomach and intestines)
- Body fat
These systems are all interconnected in one way or another by hormones, nerves and other cell signalling molecules that have the overall effect of either making us feel hungry or full by activating certain areas of the brain. The hypothalamus and brainstem are particularly important structures in the CNS and are the main regulators of both when and how much we eat. Within the hypothalamus there is a special group of neurons called the arcuate nucleus. Within this area, there are two types of neural cells that are part of regulating food intake. Specific neurons are involved in either turning off our hunger signals (i.e. telling us we are full), or turning them back on (telling us we’re hungry) (1). This part of the brain is sometimes referred to as being part of the “appetite center”. Both short term (i.e. between meals) and long term (i.e. how much energy we have stored as body fat) signals dictate our food intake behaviour.
So, how does this “appetite centre” work?
Well, the brain receives information about what’s going on in the gut in one of two ways:
1 – From nerve signals
2 -From molecules that circulate in the blood
First, let’s talk about the nerve connection between the gut and the brain. The vagus nerve is one of our cranial nerves (i.e. nerves coming directly from the brain rather than off of the spinal cord). It plays an important role in sensing what’s going on in the gastrointestinal tract (GIT) and carries that signal back to the brain. The GIT contains many different types of receptors that sense things such as stretching of the intestinal walls as well as changes in osmolarity and presence of nutrients inside the intestine that might be present following a meal. The vagus nerve then communicates with these gut receptors and relays their signals to the brainstem, which then communicate with the arcuate nucleus in the hypothalamus. These hypothalamic neurons then relay information to other parts of the brain to control whether or not we keep eating. For example, if the initial gut signals included things like lots of stretch in the intestinal walls (i.e. if food was present in the gut causing it to stretch out), it would trigger the vagus nerve to tell arcuate nucleus to send signals to the rest of the brain to reduce our food intake for the meantime, and increase the amount of energy we expend.
However, the vagus nerve isn’t the only thing signalling these hypothalamic neurons. Some molecules can also cross the blood-brain barrier and directly bind to the arcuate nucleus. It’s important to note that there are many signals all working together to regulate our hunger. Here’s a few of the major ones:
Major Hunger Signal:
When you haven’t eaten in a while, the gut releases a substance called ghrelin mainly from the stomach and small intestine. Ghrelin then makes its way back up to the brain and binds to receptors in the arcuate nucleus as well as on the vagus nerve which turns on hunger signals (2). It also stimulates the production of stomach acid as it gets your stomach ready to receive food.
Major Satiety Signals:
Leptin is a hormone released from our body fat (adipose tissue). It is secreted as a signal that we’ve had enough to eat for the meantime. When released, leptin binds directly to receptors in the hypothalamus inhibiting the “hunger” pathways and activating “fullness” pathways. Since leptin is secreted from adipose tissue, individuals who have higher amounts of body fat will secrete more leptin. However, for individuals with obesity, there may be problems with over secretion of leptin. As individuals with obesity have more adipose tissue, more leptin is secreted overall. However, their bodies may not be able to respond to the fullness signals that leptin normally provides. This may be one of the reasons why appetite control may be more difficult for individuals with obesity (3). Similarly, when we look at the effects of dieting on these hormones the opposite is true. A number of studies have shown that in healthy individuals, consuming a low calorie diet for even just a few weeks straight can decrease the amount of leptin circulating in our blood (4,5).
Insulin is a hormone secreted by beta cells of the pancreas. It acts on many different metabolic pathways throughout the body, particularly in glucose metabolism. However, in the central nervous system, insulin signals satiety by binding directly in the arcuate nucleus and directing satiety neurons (6).
During digestion, the carbohydrates, protein, and fat in our food are broken down into glucose, amino acids, and fatty acids. Aside from providing our bodies with energy, these amino acids, glucose molecules, and fatty acids also send signals to the brain to change the amount of food we eat using different mechanisms. Blood glucose concentrations rise after glucose is absorbed from the gut. This increase in blood glucose creates a feedback loop to the brain where glucose-sensitive neurons in the hypothalamus are either activated or inhibited (7). These neurons then help signal to the rest of the brain whether we should keep eating or stop. Similar brain regions have been identified that sense amino acids and fatty acids. Overall, when these neurons sense increased concentrations of glucose, amino acids, and fatty acids in our blood, the hypothalamus triggers a reduction in food intake in the short term (1).
Environmental Factors & Hunger
While our hardwired signalling molecules and nerves make up the majority of what signals hunger and satiety, there are a number of factors in our environment that change how hungry we get. For example, some individuals find that emotional stress can either increase or decrease hunger (8). This is thought to be a result of changes in cortisol levels, and changes in cardiovascular function during both short term and long-term stress. However, the exact mechanism of each of those factors in relation to hunger isn’t quite clear and appears to be associated more with the duration of stress (9, 10).
Or, as I’m sure you’ve experienced at one point or another, the sight and smell of food has a strong impact on how much you feel like eating. In fact, it has been shown that people’s sense of smell improves during fasting and declines when full (11). Similarly, it has been demonstrated that oral exposure of a food (i.e. how long something is in your mouth) can contribute to satiety through nutrient sensing systems (12). Lastly, researchers have also found that there is a significant increase in how much people salivate (and want to eat more) when certain food odors are present compared to others. Particularly, energy dense foods such as chocolate tend to make people salivate more than lower calorie food odors (13).
Overall, there are a variety of different body signals impacting hunger. Substances from the gastrointestinal tract, body fat, and pancreas indirectly tell our brain how much we should eat; while environmental factors such as stress, and how tasty our food smells also have a big impact on how hungry we get.
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