6 Hunger and Satiety Hormones and How to Control Them

This article is based on scientific studies: see references

Hunger Hormones | Ghrelin | Leptin | NPY | PYY | GLP-1 | CCK | Regulate Appetite | Control Hunger | Increase Satiety | Conclusion | FAQ | Studies

You’ve come to the right place if you want to understand why you sometimes still feel hungry after eating.

This article will look deeper into our bodies to see which hormones can trigger sensations of hunger and satiety.

Armed with essential knowledge about hunger and satiety hormones, we’ll further derive natural ways to control appetite.

What are Hunger and Satiety Hormones?

Hormones are chemical messengers that provide authoritative signals to regulate hunger, satiety, thirst, body temperature, or even bodyweight (Starka et al. 20201).

With the help of a control center in the brain, the hypothalamus, the hormone system is significantly involved in regulating bodily functions to remain in a healthy balance.

Eating behavior is also coordinated with the help of the hypothalamus, which acts as a control center for appetite (Austin et al. 20092).

Hunger and satiety hormones sometimes tell the brain how much energy you have already consumed and how much you still need.

The goal is energy homeostasis: the balance between energy production (metabolism) and energy consumption by cells (Vergara et al. 20193).

This article reviews the major hormones involved in balancing hunger and satiety.

In addition to the chemical messengers on this list, other hormones and neurotransmitters exist that can influence appetite regulation.

However, the following hormones are the best researched to understand how they affect our food intake.

In addition, sufficient research exists regarding these six hunger and satiety hormones to infer the influence of modern lifestyle factors on hormone balance.

For this reason, we can also derive how we can naturally regulate these hormones.

First among them is the essential initiator of appetite.

Hunger Hormone Ghrelin

Ghrelin is better known as the hunger hormone. And for a good reason. Ultimately, ghrelin is the only neurotransmitter outside the central nervous system that triggers appetite (Austin et al. 20094).

The body releases ghrelin in response to an empty stomach to tell you to eat again shortly (Klok et al. 20075).

Additionally, the reward center in your brain is stimulated to make food more interesting to you (Müller et al. 20156).

After a meal, on the other hand, ghrelin levels are low. When the stomach is full, there is no longer a need for food intake.

A healthy ghrelin level correlates negatively with body fat, i.e., it is higher in lean individuals and lower in obese individuals (Austin et al. 20097).

However, in obese people, ghrelin levels do not always decrease as they should after a meal. Because they continue to feel hungry, these people risk overeating (Klok et al. 20078).

Consequently, an imbalance in ghrelin secretion can lead to weight gain. Conversely, ghrelin balance must function properly to lose weight successfully.

Satiety Hormone Leptin

Leptin is the counterpart of the hunger hormone ghrelin. Accordingly, it is also known as the satiety hormone.

Unlike ghrelin, leptin has to do directly with body fat. It is the fat cells themselves that produce the hormone.

When you eat, and your fat cells determine that you’ve put in enough energy, they release leptin, which signals the brain to stop eating.

If your leptin levels are low, on the other hand, your brain receives the message that fat stores are empty, which in turn triggers hunger (Friedman et al. 19989).

Consequently, leptin is responsible for regulating the total amount of stored energy in the body. Hence, leptin levels correlate positively with your body fat (Austin et al. 200910).

When the signaling to regulate body fat stops working correctly, it is called leptin resistance.

When the body is constantly flooded with high amounts of leptin, it becomes less responsive to the hormonal signal over time. Therefore, leptin sensitivity decreases.

In short, with leptin resistance, your brain takes longer to recognize that you’re already full.

The result can be overeating, weight gain, obesity, and other metabolic disorders (Myers et al. 201011).

Leptin resistance is associated with chronic inflammation, obesity, cardiovascular disease, insulin resistance, and type 2 diabetes (Martin et al. 200812).

Researchers hypothesize that excessive levels of the storage hormone insulin, which is also instrumental in weight gain, cause leptin resistance (Lustig et al. 200413).

The more you eat those foods that stimulate insulin secretion, the worse leptin or insulin resistance can become.

Hormones control hunger in men and women

Other Satiety and Hunger Hormones

In addition to the well-known satiety hormone leptin, three other well-researched hormones inhibit appetite. And these are all mainly produced in your intestine.

In addition, researchers revealed a fascinating hormone that initiates hunger in your brain. Since it interacts closely with the primary hunger and satiety hormones, let’s look at the neurotransmitter in detail.

Neuropeptide Y

With neuropeptide Y (NPY), we move into the central nervous system. There it is the most abundant peptide.

NPY is primarily found in the hypothalamus and is both a hormone and a neurotransmitter. Moreover, NPY is considered the most potent appetite-stimulating compound in the human body.

Every other hunger or satiety hormone regulates food intake by acting on NPY in the hypothalamus. While leptin suppresses NPY activity, ghrelin stimulates it (Austin et al. 200914).

Accordingly, elevated NPY increases food cravings, predominantly carbohydrates (Beck 200615).

For this reason, like ghrelin, we can refer to it as a hunger hormone.

In addition to hunger, NPY stimulates fat storage and weight gain via the central nervous system while decreasing sex drive, locomotion, energy expenditure, and body temperature (Minor et al. 200916).

Moreover, stress increases NPY levels in fat cells, contributing to abdominal fat storage (Kuo et al. 200717).

However, elevated NPY levels make sense as a stress response because NPY has stress-reducing, anxiety-relieving, and neuroprotective properties, according to researchers at the University of Graz, Austria (Reichmann et al. 201618).

You may have also heard that researchers have found that many living things can live at least 33% longer if they eat less (McDonald et al. 201019).

Because NPY acts as the primary hunger signal in this context, researchers suspect it plays an essential role in extending lifespan (Minor et al. 200920).

Peptide YY

Like NPY, peptide YY (PYY) is a crucial brain-gut peptide. Therefore, the actions of both peptides are closely related to appetite regulation and the development of obesity (Wu et al. 201921).

PYY is produced in the intestine after eating. Here, the amount secreted is proportional to the fat ingested with food (Pironi et al. 199322).

It enters the hypothalamus in the brain via the bloodstream, reducing appetite (Wu et al. 201923).

Hence, it is a satiety hormone.

According to studies, individuals with obesity exhibited attenuated peptide YY responses after eating, leading to uncontrolled overeating (Zwirska-Korczala et al. 200724).

Therefore, adequate PYY levels are essential in reducing increased food intake, especially after extensive exercise (Zouhal et al. 201925).

In addition, researchers at Oxford have found that obese individuals do not already have high fasting PYY levels, but chronic overeating elevates them.

According to the researchers, this suggests a protective mechanism against excessive food intake and other satiety hormones (Cahill et al. 201126).

Glucagon-Like Peptide-1

The next satiety hormone, glucagon-like peptide-1 (GLP-1), is secreted along with PYY in the gut in response to nutrient intake.

Its main functions are to keep blood glucose levels stable and produce a feeling of satiety (Müller et al. 201927).

This hormone could also help weight loss and reduce body mass index (BMI) or waist circumference in overweight adults (Zhang et al. 201528).

Moreover, researchers explain the reduced hunger and increased satiety after gastric bypass surgery by an increased GLP-1 response to food intake (Morinigo et al. 200629).

The beneficial effects of GLP-1 make this hormone an exciting candidate for the treatment of obesity, diabetes, and neurodegenerative diseases (Müller et al. 201930).

Research suggests that people with obesity may experience problems with GLP-1 signaling (Anandhakrishnan et al. 201631).

As with the other appetite hormones, this suggests a possible type of GLP-1 resistance. This decreasing GLP-1 sensitivity may also explain the elevated fasted plasma GLP-1 levels in obese children and adults (Stinson et al. 202132).

Cholecystokinin

The last in our series of satiety hormones is cholecystokinin (CCK). Also, cells in the gut produce CCK in response to a meal.

CCK is the first gut hormone known to affect appetite (Gibbs et al. 197333). It is closely related to the primary satiety hormone leptin in this context.

On the one hand, CCK promotes leptin secretion (Konturek et al. 200134). On the other hand, leptin enhances CCK-induced satiety (Peters et al. 200635).

An elevated CCK level can be detected in the human body approximately 15 minutes after eating (Liddle et al. 198536).

In addition to satiety, cholecystokinin also plays an essential role in the following processes in the body (Okonkwo et al. 202137):

  • Inhibition of gastric acid secretion and release of digestive enzymes
  • Contraction of the gallbladder and regulation of bile acid
  • Regulation of gastric emptying
  • Energy production, protein synthesis, and cell growth

Our bodies produce CCK when we consume protein or fat (Dockray et al. 201238). As a result, food intake and, in particular, our cravings for sugar and carbohydrates are reduced (Lieverse et al. 199539).

Recent research suggests that obese people develop a type of CCK resistance. Reduced sensitivity to the hormone makes them more likely to overeat, which may contribute to the progression of CCK resistance (Cawthon et al. 202140).

How to Regulate Appetite Naturally

Even though science is still far from being able to fully explain all the hormones surrounding hunger and their complex interplay, tips can be derived for sustainable satiety.

We cannot completely control our appetite, but we can bring our modern lifestyle and thus our hormone balance back into the equilibrium that nature originally intended.

How to Control Hunger Hormones

Ghrelin is the essential circulating hunger hormone in the body, closely related to NPY, the primary hunger hormone in the central nervous system.

Together they initiate hunger while being influenced by other peripheral hormones.

Although ghrelin stimulates appetite, you should by no means consider taking ghrelin blockers. Ghrelin is also vital for learning, memory, gastric acid secretion, sleep-wake cycles, and reward behavior and should not be artificially unbalanced (Müller et al. 201541).

Instead, studies show that the eating behavior itself can curb the release of hunger hormones.

1. Focus Protein-Rich Foods

According to an Oxford study that compared the consumption of a high-protein meal with a high-carbohydrate meal, protein consumption can significantly lower ghrelin levels in the body (Blom et al. 200642).

Similarly, in Oxford, researchers found that reducing protein in the diet caused a more significant release of NPY and more body fat (White et al. 199443).

2. Increase Intake of Healthy Fats

High levels of NPY fuel carbohydrate cravings. In contrast, fat consumption inhibits NPY activity more than other macronutrients, which may reduce cravings (Beck 200644).

To summarize, natural foods high in fat and protein are excellent choices to curb appetite.

In addition to fattier cuts of meat, fatty fish, such as salmon or mackerel, is ideal, as its omega-3 fatty acids can further support satiety (Parra et al. 200845).

3 Avoid Fructose

The supposed fruit sugar is often marketed as healthy, which it is not. Fructose is the sweet molecule besides glucose in conventional table sugar. Therefore, a piece of dextrose (glucose) is not distinctively sweet because it lacks fructose.

Metabolic researchers have found that diets high in fructose can increase ghrelin levels, causing obesity (Teff et al. 200446).

Accordingly, the sweet molecule fuels cravings and promotes changes in the brain’s reward system, leading to overconsumption.

In addition, fructose causes the development of new fat and insulin resistance in the liver, leading to chronic metabolic diseases such as fatty liver and type 2 diabetes.

These effects on the liver become easier to understand when we realize that fructose is closely related to alcohol and can cause the same diseases.

The fermentation of fructose produces ethanol – alcohol. The main difference is that fructose is 100% metabolized in the liver and not in the brain, sparing sensations of intoxication and hangovers (Lustig 201347).

In addition, fructose significantly affects the satiety hormone leptin, as we will see shortly.

Sugar increases the hunger hormone ghrelin and decreases the satiety hormone leptin

How to Increase Satiety Hormones

Sustained satiety goes far beyond a short-term feeling of fullness due to stomach distension. Since the essential satiety hormones have been more adequately researched, we can draw meaningful conclusions about which meals make us feel full in the long term and which do not.

Interesting starting points also already exist regarding the influences of other lifestyle factors such as exercise and sleep on our satiety hormones. According to science, here are the best tips to increase those hormones that cause satiety.

1. Reduce Carbs

This first point may sound like old news, yet it cannot be repeated often enough. The industrialization of food production has creepily, yet significantly, increased carbohydrate consumption over the decades.

Refined carbohydrates like sugar can turn off the leptin receptors in the brain, so you need longer or higher levels of leptin to get full (Shapiro et al. 200848).

To summarize, added sugar in foods makes you hungry for more.

In this regard, the fructose in sugar is more dangerous than other carbohydrates when it comes to developing leptin resistance and obesity (Shapiro et al. 200849).

Therefore, it is advisable to avoid high fructose concentrations such as in high-fructose corn syrup, agave syrup, candy, and other processed foods.

Moreover, carbohydrate-rich meals not only stimulate the satiety hormone PYY the least, but their level also decreases rapidly afterward. In contrast, PYY continues to rise for hours after high-fat and high-protein meals (Lomenick et al. 200950).

For this reason, processed carbohydrates such as those in cookies or other baking goods do not keep you full for long. Moreover, they promote inflammation in the body (Buyken et al. 201451).

And inflammation is not only often associated with obesity, but it inhibits the release of GLP-1, thereby inhibiting satiety (Gagnon et al. 201552).

2. Prefer Natural Fats to Seed Oils

Refined seed oils, such as soybean, sunflower, or canola oil, are just as pro-inflammatory as refined carbohydrates (Marchix et al. 201553).

And like sugars, they are found in a wide variety of highly processed foods today.

In contrast, extra virgin olive oil could increase GLP-1 levels (Bodnaruc et al. 201654).

Furthermore, consumption of natural fats in extra virgin olive oil, grass-fed butter, or grass-fed beef supports CCK production, thereby maintaining satiety longer (Dockray et al. 201255).

Although fat is more nutritious than carbohydrates, excessive fat consumption does not lead to leptin resistance (Dirlewanger et al. 200056).

Moreover, the secretion of the satiety hormone PYY increases proportionally to the amount of fat consumed via diet (Pironi et al. 199357).

In short, a high-fat, low-carbohydrate diet such as the keto diet is ideal for increasing satiety and avoiding cravings.

3. Eat Enough Protein

Like healthy fats, protein increases the release of satiety hormones in the gut.

Accordingly, one study found that a high-protein diet, as opposed to a high-carbohydrate diet, can help increase CCK levels and thus feelings of satiety (Chungchunlam et al. 201558).

Similarly, protein-rich foods can increase GLP-1 levels (Gillespie et al. 201559). In particular, collagen, the essential protein for skin, hair, bone, and joints, promotes satiety via GLP-1 (Rubio et al. 200860).

In terms of PYY, high-protein meals satiate even more effectively than high-fat meals (Lomenick et al. 200961).

4. Get Regular, Quality Sleep

Here is the evidence if you’ve ever heard that sleep is vital for weight loss.

Among many other essential tasks, sleep helps you use leptin properly. Researchers have found that shorter sleep results in lower levels of the satiety hormone leptin in the body (Spiegel et al. 200462).

A brand new study even states that sleep deprivation can lead to obesity and subsequently type 2 diabetes by impairing leptin regulation, as it increases appetite and food intake (Mosavat et al. 202163).

Furthermore, studies consistently show that sleep deprivation leads to increased ghrelin levels and decreased leptin (Cooper et al. 201864).

A recent review of 21 studies involving 2,250 individuals concluded that reduced sleep duration is associated with increased ghrelin levels, whereas sleep disturbance affects leptin and ghrelin levels (Lin et al. 202065).

Consequently, sleep hygiene significantly affects the regulation of appetite. To avoid the risk of increasing your body mass index, you should regularly get more than 7 hours of quality net sleep per night (Cooper et al. 201866).

5. Don’t Rely on Exercise Alone

It is true that exercise helps increase leptin sensitivity, increasing the hormone’s perception and, therefore, satiety (Kang et al. 201367).

However, overall, study results are mixed regarding the effects of exercise on hunger and satiety hormones.

While individuals of average weight can increase their PYY levels with exercise, overweight individuals achieved this result only with long-term training for at least 32 weeks (Jones et al. 200968).

In contrast, there is evidence that high-intensity interval training (HIIT) or the combination of aerobic and strength training could increase CCK levels (Zouhal et al. 201969).

On the other hand, intense training could not affect NPY levels to the extent that weight loss could result (Khajehnasiri et al. 201970Benite-Ribeiro et al. 201671).

However, do not forget that exercise promotes hunger. And for some people, this compensatory effect of food intake is even more significant than it should be (Melanson et al. 201372).

Accordingly, exercise is not the tool of choice for regulating appetite. If the necessary dietary intervention is not provided, athletic ambitions can backfire by craving foods that reduce satiety, promoting overeating in the long run.

Do You Regulate Appetite, or Do Hormones Control You?

Hunger is not a bad feeling per se. Instead, hunger and satiety are standard physiological signals that keep us alive and contribute to the body’s optimal functioning.

Our lifestyle, marked by psychological stress and changes in food production, affects the natural balance of hunger and satiety hormones.

Although appetite and the hormones involved in it represent a complex interplay that we do not yet understand precisely, research has yielded revealing results in recent years.

Highly processed foods with refined carbohydrates and added sugars contribute to our feeling more hungry in the long term.

In particular, the fructose in sugar inhibits satiety signals and fuels cravings (Shapiro et al. 200873).

In contrast to these processed carbohydrates, natural fatty acids and proteins can contribute to lasting satiety and lower inflammation levels.

As a result, we get a low-carbohydrate, high-fat diet that relies on natural protein sources such as fatty fish.

Accordingly, brand-new studies highlight that such ketogenic diets prevent an increase in the hunger hormone ghrelin, which is otherwise seen after weight loss, and instead reduce feelings of hunger (Deemer et al. 202074).

In a direct comparison with a low-fat, high-carbohydrate (LFHC) diet, a low-carb, high-fat (LCHF) diet significantly increased satiety after it released 55% more PYY in the gut (Essah et al. 200775).

In addition to diet, sleep is the second major factor that can help curb appetite via healthy hormone balance. Therefore, you should always prioritize regular, quality sleep.

According to science, intermittent fasting is an effective way to increase sleep quality, REM sleep, and balance in as little as two weeks (Michalsen et al. 200376).

Learn how to successfully integrate fasting into your daily routine in my new book: Intermittent Fasting 101: The Science-Backed Beginner’s Guide to Lose Weight Without Dieting and Working Out.

Hunger and Satiety Hormones FAQ

Which hormones are involved in hunger and satiety?

The hormones ghrelin, leptin, neuropeptide Y, peptide YY, GLP-1, and CCK are involved in hunger and satiety.

Which hormones increase hunger?

The hormones ghrelin and neuropeptide Y increase hunger.

What is the satiety hormone called?

The satiety hormone is called leptin.

How can I control my hunger hormones?

You can control your hunger hormones by reducing carbohydrates and sugar while increasing protein and fat intake.

Studies click to expand!

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