Short guide to hunger and satiety

my 8 tips to feel full after eating and satisfied longer

Do you find it difficult to stop eating? Or do you feel full at the end of the meal but the sense of satiety weans off in no time?

In this article, we are going to explore the concepts of satiation and satiety, what regulates these feelings and what you can do to feel full and satiated until the next meal! And if you’re not interested in the geeky part, you can jump straight to my tips!

If you are instead…let’s dive in and talk about how the body’s appetite control system is regulated!

Photo by James Barker on Unsplash

Let’s get started with some definitions: satiation and satiety, in fact, are not exactly the same thing. Satiation is the signal that causes you to stop eating, while satiety is the feeling of fullness and satisfaction in between meals. And both these feelings are of course important when it comes to determining how much you eat and how you feel.

The feelings of hunger, satiation and satiety are regulated by multiple and complex mechanisms and hormones. These are not fully known yet and are an area of ongoing research.

We start from the top. Up in our brains, there are two regions in the hypothalamus that control feeding. They receive information from the nervous and hormonal systems and bring about a response in terms of feelings of hunger and satiation/satiety. Many mechanisms and hormones are at play. We’ll explore just a few here.

What happens when we eat and what leads us to stop eating?

Short term signals leading to meal termination

Presence of food in the stomach When food enters our stomach, the volume of the stomach increases and the stretch is sensed by the nervous system, which signals the brain we are eating. This acts as the first satiation signal.

Interesting note: Fat tends to spend the longest time in the stomach (compared to carbohydrates and proteins) and furthermore its presence in the small intestine slows down gastric emptying, helping us feel satiated for a longer time.

Release of Cholecystokinin (CCK) As explained in the blog post on gallbladder health, the composition of the partly digested food entering the small intestine from the stomach (chyme) determines the release of some hormones in the small intestine.

One of them is called CCK and is released in the duodenum (the first part of the small intestine) in response to the presence of fat and protein in the chyme. CCK not only stimulates the gallbladder to release its bile content, but it also has an effect on receptors on the vagus nerve (the main nerve connecting gut and brain) that transports the signal to the brain to inhibit food consumption.

Interesting note: An impaired release of CCK may play a role in eating disorders.

Release of Glucagon-like Peptide-1 (GLP-1) GLP-1 is another hormone that is released in the small intestine in response to a nutrient load - glucose, protein, fatty acids and bile acids are triggers for GLP-1 release -, most likely under the mediation of the vagus nerve. GLP-1 has effects on satiation and satiety through actions in the gut and the brain: it delays gastric emptying and gut motility and acts also at the brain level on the areas involved with regulation of feeding [1].

The sensitivity to the short-term signals above, involved in satiation and meal termination, is also affected by the long-term signals described below [2].

What happens in between meals? Long-term signals.

Also in between meals, several hormones and mechanisms are at play. The first two we are going to explore are ghrelin, the so-called hunger hormone and leptin, commonly defined as the satiety hormone. I also touched on these hormones in the blog post on blood sugar balance in connection with the effects of sleep on ghrelin and leptin. Sleep timing, duration and quality, in fact, have an effect on the release or timing of release of ghrelin and leptin.

Ghrelin Ghrelin is our hunger hormone and its suppression is relevant to the onset of the satiety feeling. It is primarily produced by the stomach but also by the intestines and kidneys. When our stomach is empty, ghrelin is secreted in the blood stream and it reaches the hypothalamus, where it signals a feeling of hunger. When the stomach is full, on the contrary, the serum levels of ghrelin decrease, thus decreasing the feeling of hunger.

What are some factors influencing ghrelin levels/release?

• Fibres and protein are the most helpful in keeping ghrelin levels in check [3,4].

• High protein breakfasts were found to decrease post-prandial ghrelin levels over time more strongly compared to high carb breakfasts (and to reduce gastric emptying too) [5]!

• Eating slowly by chewing more was found to result in lower ghrelin concentrations after meals [6].

• Fructose increases the ghrelin response and decreases the activation of brain satiety centres [7] (see also effect on leptin resistance in the next section).

• As mentioned in the blood sugar article, sleep affects ghrelin production: less sleep, more ghrelin, more hunger (particularly appetite for high carbohydrate foods) [8]!

Interesting note: when we try to restrict caloric intake very fast, ghrelin kicks in, making weight loss be much more of a struggle.

Would you like some help discovering how your breakfast affects your symptoms? Let me help you with my “after-breakfast body check-in” (FREE pdf guide) and receive guidance on identifying what YOUR ideal breakfast is! Leptin Leptin is an appetite-suppressing hormone. It is produced by the adipose tissue and secreted into the circulatory system, through which it travels to the hypothalamus where it provides information on the availability of body fat. Leptin levels are also influenced by the circadian rhythm and quality and duration of sleep (see also previous blog post on blood sugar balance)

Interesting note: it is possible to become resistant to the effects of leptin and when this happens the hunger mechanism is not stopped leading the brain to think we are starving and making us feel even hungrier. Leptin resistance typically occurs in obese people and is common in people with weight-loss resistance. Chronic, low-grade inflammation contributes to leptin resistance [9].

What are some factors influencing leptin levels?

• Fructose decreases circulating leptin levels [10] and was found to induce leptin resistance in animal studies [11] This is one more reason to avoid fructose without its fibre packaging (e.g. straight fructose or high fructose corn syrup!).

• As already mentioned, leptin levels are dependent on the quantity and quality of sleep. So taking care of your sleep is important for feeling satiated too!

Other hormones Peptide YY (PYY) is yet another hormone involved in both satiation and satiety. Its secretion in the large intestine is strongly stimulated by dietary fats, proteins and fibres. PYY slows gastric emptying and promotes digestive activities [12]. It acts as an appetite-suppressant, countering the effects of ghrelin.

Insulin also has an appetite-suppressing effect. It is secreted by the pancreas in response to an increase in glucose in the blood stream and in healthy people it stabilises blood sugar levels by driving glucose into the cells.

When it comes to hunger and insulin, the effects of imbalanced blood sugar (the blood sugar roller coaster) needs to be considered. Depending on our own individual response, a meal high in refined carbohydrates, which is digested very rapidly, might cause a spike in blood sugar and a following spike of insulin, which might then plummet the blood sugar. We are then at the “bottom of the blood sugar roller coaster”, and we commonly feel an urgent need to eat to bring the blood glucose back to a good level.

Interesting note: it is possible to become insulin resistant too. When this happens, glucose does not easily get into the cells. The feedback to the brain is then compromised and we actually feel the need for more food.

Knowing all this, what can we do to influence our appetite and have more control on how much we eat and how long we feel satiated after eating?

Here my 8 tips to feel full after eating, and satisfied longer.

1. Eat your proteins – to stimulate CCK and keep ghrelin levels in check.
   

2. Don’t skip the (good) fat – to slow gastric emptying and stimulate CCK.
   

3. Load up on veggies – they take space in your stomach, giving you a feeling of fullness, while being loaded with nutrients, low caloric, blood sugar safe and microbiota-friendly!
   

4. Ban fructose (outside of its fibre package)! – e.g. high fructose corn syrup and fructose sweeteners.
   

5. Eat slowly and chew more – for the effects on post-prandial levels of ghrelin (decreased) [13], CCK, PYY and GLP -1 (increased) [6, 13].
   

6. Eat until you feel 80% full. – It takes some time before getting the satiation feeling.
   

7. Eat mindfully and avoid distractions while eating – not only will you enjoy your meal more and digest it better, you’ll also experience satiation better [14].
   

8. Mind your sleep – for its effects on ghrelin and leptin (as well as on insulin sensitivity and blood sugar regulation).

Do you have questions or would you like to know more? Comment below or contact me directly!

Or are you ready to go further and would like to receive 1:1 support with me?

Get in touch for a free 20-minute functional nutrition and lifestyle consultation and let’s find out how I can further support your healing journey.

References

[1] Shah, Meera, and Adrian Vella. “Effects of GLP-1 on appetite and weight.” Reviews in endocrine & metabolic disorders vol. 15,3 (2014): 181-7.

[2] de Graaf, Cees et al. “Biomarkers of satiation and satiety.” The American journal of clinical nutrition vol. 79,6 (2004): 946-61.

[3] St-Pierre, David H et al. “Fiber intake predicts ghrelin levels in overweight and obese postmenopausal women.” European journal of endocrinology vol. 161,1 (2009): 65-72.

[4] Koliaki, Chrysi et al. “The effect of ingested macronutrients on postprandial ghrelin response: a critical review of existing literature data.” International journal of peptides vol. 2010 (2010): 710852.

[5] Blom, Wendy A M et al. “Effect of a high-protein breakfast on the postprandial ghrelin response.” The American journal of clinical nutrition vol. 83,2 (2006): 211-20.

[6] Li, Jie et al. “Improvement in chewing activity reduces energy intake in one meal and modulates plasma gut hormone concentrations in obese and lean young Chinese men.” The American journal of clinical nutrition vol. 94,3 (2011): 709-16.

[7] Lowette, Katrien et al. “Effects of high-fructose diets on central appetite signaling and cognitive function.” Frontiers in nutrition vol. 2 5. 4 (2015).

[8] Leproult, Rachel, and Eve Van Cauter. “Role of sleep and sleep loss in hormonal release and metabolism.” Endocrine development vol. 17 (2010): 11-21.

[9] Zhou, Yingjiang, and Liangyou Rui. “Leptin signaling and leptin resistance.” Frontiers of medicine vol. 7,2 (2013): 207-22.

[10] Teff, Karen L et al. “Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women.” The Journal of clinical endocrinology and metabolism vol. 89,6 (2004): 2963-72.

[11] Shapiro, Alexandra et al. “Fructose-induced leptin resistance exacerbates weight gain in response to subsequent high-fat feeding.” American journal of physiology. Regulatory, integrative and comparative physiology vol. 295,5 (2008): R1370-5.

[12] Wilde, Peter J. “Eating for life: designing foods for appetite control.” Journal of diabetes science and technology vol. 3,2 366-70. 1 Mar. 2009.

[13] Kokkinos, Alexander et al. “Eating slowly increases the postprandial response of the anorexigenic gut hormones, peptide YY and glucagon-like peptide-1.” The Journal of clinical endocrinology and metabolism vol. 95,1 (2010): 333-7.

[14] Brunstrom, Jeffrey M, and Gemma L Mitchell. “Effects of distraction on the development of satiety.” The British journal of nutrition vol. 96,4 (2006): 761-9.