Satiety is the sensation of fullness experienced between meals. For instance, after lunch, our satiety peaks and gradually diminishes over time. If there are no snacks in between, it hits a low point before dinner. After dinner, satiety returns to a high level. A related but distinct concept is satiation, which pertains to how much we need to eat in one meal to feel “satisfied” and subsequently stop eating. Several factors influence satiation, including the taste and appeal of the food. However, satiety affects satiation for the same individual consuming the same type of food. This article does not delve into satiation but focuses on satiety.
Satiety has long-term implications for the calories we consume, impacting not only weight loss but also our overall health. Various non-communicable diseases and autoimmune-related conditions are linked to calorie intake. Reducing calorie intake can mitigate the risk of conditions like diabetes and cardiovascular diseases. Weight loss can play a role in managing psoriasis, and dietary adjustments serve as a starting point for interventions in rheumatoid arthritis. Cortisol and certain psychiatric medications are associated with weight gain, and effectively managing calorie intake can help mitigate the metabolic stress and side effects caused by these medications.
The Influence of Satiety and Eating on Endocrine and Neural Signals
The mechanisms governing eating and satiety within the human body are complex. In addition to the involvement of various hormones, these hormones possess receptors in distinct organs, and diverse feedback mechanisms further complicate any attempts to intervene in satiety regulation. Below, we provide a brief overview of several common mechanisms and hormones that play a role in satiety regulation.
Anorexigenic hormones from the gastrointestinal tract induce satiety. These hormones encompass cholecystokinin (CCK), glucagon-like peptide-1 (GLP-1), and peptide YY (PYY). Conversely, orexigenic hormones, such as ghrelin, stimulate appetite. These hormones have receptors in both the central nervous system and the sympathetic nervous system. The hypothalamus assumes a pivotal role in the central control of appetite, with contributions from other regions as well [1].
Blood Glucose and Insulin: Traditionally, blood glucose levels have been considered a factor influencing our eating behaviors, known as the glucostatic hypothesis. However, recent discoveries of various gastrointestinal hormones have posed challenges to this hypothesis. Nevertheless, insulin, responsible for regulating blood sugar, possesses receptors in the hypothalamus and can directly curb appetite or indirectly impact it by affecting leptin [2].
Cholecystokinin (CCK): CCK is a gastrointestinal hormone that enhances satiety and reduces food intake when released by intestinal endocrine cells in response to fat consumption. CCK also has receptors in the vagal nerve and nodose ganglia, contributing to heightened satiety and decreased food consumption [3].
Glucagon and GLP-1: Glucagon is a hormone secreted by pancreatic alpha cells, alongside insulin. It promotes satiety. GLP-1 is secreted by L cells in the distal intestine and proximal colon, also enhancing satiety. Both hormones are released in response to food intake and possess appetite-suppressing effects. GLP-1, due to its release in the distal intestine, exerts a delayed effect, continuing to suppress appetite for several hours after a meal. GLP-1 receptor agonists have been employed as weight loss and blood sugar-lowering medications in recent years.
Peptide YY (PYY): PYY is another hormone produced by the distal intestine and colon that enhances satiety and reduces food intake. Similar to GLP-1, it exerts a delayed effect on appetite suppression, maintaining elevated concentrations for several hours after a meal. PYY serves as a significant gastrointestinal hormone that hinders subsequent meal consumption.
Ghrelin: Ghrelin, secreted by the stomach, has the opposite effect of the gastrointestinal hormones mentioned earlier. Upon reaching the hypothalamus in the central nervous system, ghrelin stimulates our appetite.
Leptin: Leptin is primarily secreted by adipose tissue and regulates energy homeostasis in the body. The more fat cells a person has, the more leptin they produce. Leptin is believed to regulate appetite by influencing the central nervous system when it crosses the blood-brain barrier. In theory, as individuals become more obese, they should produce more leptin and consume less food. Unfortunately, a condition known as leptin resistance has been observed in obese individuals, where they exhibit high levels of leptin but reduced sensitivity of the central nervous system to it.
Impact of Composition of Macronutrients
The combination of different macronutrients can impact satiety. A 2016 UK study with 65 participants found that those on a high-fat, low-carb (HFLC) diet reported weaker satiety than those on a low-fat, high-carb (LFHC) diet with the same calorie intake [4]. Additionally, in ad libitum conditions, HFLC dieters consumed more daily calories than LFHC dieters [5].
Long-term studies offer different insights from short-term ones. In a 2015 year-long trial with 148 obese participants, those on a low-carb, high-fat diet experienced increased satiety due to significant changes in peptide YY levels. This suggests that sticking to a long-term low-carb diet can boost satiety [6].
Protein, among the three macronutrients, has a notable effect on satiety even when calorie intake remains the same [7].
In a 1999 study, participants were given either a high-carb, high-protein diet (29% protein, 61% carbs, 10% fat) or a high-fat diet (9% protein, 30% carbs, 61% fat). The high-protein, high-carb diet resulted in sustained satiety levels over 24 hours [8].
In a 2005 study, 19 participants consumed the same calories and 50% carbohydrate intake but followed either a high-protein diet (30% protein, 20% fat) or a high-fat diet (15% protein, 35% fat) for two weeks. The high-protein diet led to increased satiety, reducing daily calorie intake by an average of 441 calories [9]. This suggests that a high-protein diet may enhance central nervous system sensitivity to leptin, increasing the feeling of fullness.
Protein increases satiety by triggering anorexigenic hormones like CCK, GLP-1, and PYY. In a 2013 trial with 25 participants, higher protein intake boosted these hormones, leading to a 19% increase in satiety and a 26% drop in post-meal calorie intake [10].
A 2018 study involving 35 participants found that different protein sources (meat, legumes, or eggs) didn’t significantly affect satiety when calorie and macronutrient ratios were identical [11].
In a 2020 Danish study with 28 diabetic patients, a high-protein low-carb diet reduced overall and postprandial blood sugar levels by 13% and 60%, respectively. It increased insulin by 235% and subjective fullness by 18%, with no significant impact on GLP-1, PYY, and CCK [12].
Quality Carbs: Resistant Starch and Dietary Fiber
Opting for high-quality carbohydrates, like low glycemic index (GI) resistant starches, can boost satiety and support overall health [13]. A 2003 study revealed that resistant starch delays hunger, reduces calorie intake, and aids weight management. These foods maintain satiety for up to 2-3 hours [14].
In a 2013 study, 12 obese men consumed low-GI resistant starch and high-GI refined carbs. Refined carbs caused a 2.4x spike in blood sugar levels, followed by increased hunger and brain activity, driving further eating [15]. This suggests refined carbs lead to rapid blood sugar drops, triggering hunger and the brain’s reward system.
In a 2015 trial, whole wheat pasta with dietary fiber maintained higher post-meal blood sugar levels, reducing the urge to eat afterward [16].
In a 2018 study comparing whole wheat pasta to regular pasta, participants reported increased fullness and reduced cravings 4-8 hours after eating whole wheat pasta. Blood tests showed smaller blood sugar fluctuations with whole wheat foods, and ghrelin (an orexigenic hormone) increased less while PYY (an anorexigenic hormone) increased more [17].
In a 2017 trial, adding fiber to meatballs increased satiety by 11-13% and reduced calorie intake by 15-17% [18]. In a 2014 trial, adding bran to sausages was most effective at increasing satiety, while adding bran to bread slightly increased satiety but less than bran in sausages [19].
Healthy Snacks – Eat to Lose Body Fat
Many people turn to snacks between meals, and the choice of snacks may impact satiety without affecting body weight.
Higher protein snacks delayed dinner by 60 minutes, while high-carb and high-fat snacks delayed it by 34 and 25 minutes, respectively, aligning with previous findings on protein’s satiety benefits [20].
In a 2014 trial, participants consumed high-protein yogurt, high-fat cookies, and high-fat chocolate as snacks. The study found that high-protein yogurt induced the strongest feeling of fullness, leading to a reduction in calorie intake during subsequent dinners [21].
Nuts are a healthy snack choice. Pistachios do not lead to weight gain and improved waist size and biomarkers [22-23]. Almonds increased fullness and reduced calorie intake in a 2015 study [24]. A 2017 trial with mixed nuts showed a 1.7% body fat reduction, no change in weight, and improved metabolic parameters [25].
In a 2019 trial, obese participants snacking on mixed nuts felt fuller and had reduced ghrelin levels, while those snacking on bread had higher insulin and blood sugar levels. Mixed nuts seem better for obesity [26-27].
Fruits reduce calorie intake. In a 2015 study, mixed berries led to fewer calories consumed later [28].
In a 2019 crossover trial, orange juice with added pulp reduced post-meal blood sugar, increased insulin, and enhanced fullness compared to regular orange juice. It also boosted GLP-1 [29].
Dried prunes provided greater fullness than bread in two studies, one involving 45 participants and another with 19 females in 2010 [30-31].
Lifestyle for Losing Weight
Can eating while working affect satiety? In a 2019 crossover trial with 43 participants, eating pizza while working over lunch didn’t change food intake but significantly lowered satiety, suggesting “working meals” impact post-meal fullness [32].
Stress and sleep quality matter for satiety. A 2015 study followed 30 Cushing’s syndrome (high cortisol level) patients before and after cortisol normalization, finding increased satiety with normalized cortisol levels [33].
A 2013 study of 75 obese participants showed that those with shorter daily sleep had lower satiety scores [34]. In a 2017 crossover trial, sleep restriction, including delayed bedtime and early waking, boosted appetite [35].
Chewing food thoroughly increases satiety by triggering gut hormone secretion, reducing calorie intake [36]. Alcohol consumption boosts appetite, as shown in a 2019 meta-analysis [37]. Smoking can suppress appetite, but quitting may lead to weight gain, requiring dietary control to prevent overeating. Brain imaging studies reveal shared brain regions involved in smoking and eating, related to memory, motivation, and reward mechanisms [38].
The relationship between exercise and satiety is complex. Moderate to high-intensity aerobic exercise has been shown to exert an acute effect of increasing anorexigenic hormones (PYY and GLP-1) and reduce orexigenic hormones (ghrelin), enhancing satiety during exercise. Chronic exercise effects on satiety are less consistent; some studies suggest increased appetite, while others suggest a decrease. Long-term exercise impacts leptin and insulin secretion, often reducing their levels. Gender plays a role, with females more prone to overeating due to exercise, potentially offsetting weight loss benefits. However, both genders may increase food intake by about 30% to compensate for calories burned. While findings on exercise and satiety vary, exercise contributes to calorie deficit and overall health, emphasizing its importance despite mixed results on satiety [39-41].
Summary
The gastrointestinal tract, adipose tissue, and various organs in the body can secrete different hormones that promote or inhibit eating, affecting when we feel the need to eat our next meal and the calories we consume:
Different foods and lifestyle habits impact the secretion of calories that promote or inhibit eating, affecting satiety.
High-protein foods provide greater satiety compared to fats and carbohydrates.
Diets rich in dietary fiber, including whole grains and fruits and vegetables, offer higher levels of satiety.
Adding dietary fiber to meat can also increase satiety.
While snacking can easily increase calorie intake, high-protein, nuts, fruits, and dried fruits as snacks do not affect body weight and enhance satiety compared to processed carbohydrate-based snacks.
Lifestyle factors such as inadequate sleep and stress affect satiety.
Chewing increases satiety, and increasing chewing frequency can enhance satiety and reduce calorie intake with other aspects of the diet remaining constant.
Alcohol consumption encourages us to eat more, and quitting smoking requires careful calorie control; otherwise, smoking cessation may lead to excessive calorie intake.
Exercise, especially short-term effects of aerobic exercise, increases satiety, but long-term effects can lead to calorie compensation, affecting weight loss results. Nevertheless, exercise is overall beneficial for health.
References:
[1] Gut-Brain Interrelationships and Control of Feeding Behavior, https://themedicalbiochemistrypage.org/gut-brain-interrelationships-and-control-of-feeding-behavior/
[4] Hopkins, M. et al. (2016). Differing effects of high-fat or high-carbohydrate meals on food hedonics in overweight and obese individuals. The British journal of nutrition, 115(10), 1875–1884. https://doi.org/10.1017/S0007114516000775
[5] Patel, K. (2021), Does eating a higher carb diet make you more full?, https://examine.com/nutrition/high-carb-high-satiety/#:~:text=Carbohydrates%20and%20fat%20deliver%20the%20same%20amount%20of,appears%20to%20be%20due%20to%20calorie-density%20and%20palatability.%E3%80%81,
[7] Paddon-Jones, D. et al. (2008). Protein, weight management, and satiety. The American journal of clinical nutrition, 87(5), 1558S–1561S. https://doi.org/10.1093/ajcn/87.5.1558S
[8] Westerterp-Plantenga, et al. (1999). Satiety related to 24 h diet-induced thermogenesis during high protein/carbohydrate vs high fat diets measured in a respiration chamber. European journal of clinical nutrition, 53(6), 495–502. https://doi.org/10.1038/sj.ejcn.1600782
[10] Belza, A. et al. (2013). Contribution of gastroenteropancreatic appetite hormones to protein-induced satiety. The American journal of clinical nutrition, 97(5), 980–989. https://doi.org/10.3945/ajcn.112.047563
[13] Roberts S. B. (2003). Glycemic index and satiety. Nutrition in clinical care : an official publication of Tufts University, 6(1), 20–26.
[14] Anderson, G. H., & Woodend, D. (2003). Effect of glycemic carbohydrates on short-term satiety and food intake. Nutrition reviews, 61(5 Pt 2), S17–S26. https://doi.org/10.1301/nr.2003.may.S17-S26
[15] Lennerz, B. S. et al. (2013). Effects of dietary glycemic index on brain regions related to reward and craving in men. The American journal of clinical nutrition, 98(3), 641–647. https://doi.org/10.3945/ajcn.113.064113
[17] Costabile, G. et al. (2018). Subjective satiety and plasma PYY concentration after wholemeal pasta. Appetite, 125, 172–181. https://doi.org/10.1016/j.appet.2018.02.004
[19] Vuholm, S. et al. (2014). Appetite and food intake after consumption of sausages with 10% fat and added wheat or rye bran. Appetite, 73, 205–211. https://doi.org/10.1016/j.appet.2013.09.028
[20] Marmonier, C. et al. (2000). Effects of macronutrient content and energy density of snacks consumed in a satiety state on the onset of the next meal. Appetite, 34(2), 161–168. https://doi.org/10.1006/appe.1999.0302
[22] Wang, X. et al. (2012). Effects of pistachios on body weight in Chinese subjects with metabolic syndrome. Nutrition journal, 11, 20. https://doi.org/10.1186/1475-2891-11-20
[23] Gulati, S. et al. (2014). Effects of pistachio nuts on body composition, metabolic, inflammatory and oxidative stress parameters in Asian Indians with metabolic syndrome: a 24-wk, randomized control trial. Nutrition (Burbank, Los Angeles County, Calif.), 30(2), 192–197. https://doi.org/10.1016/j.nut.2013.08.005
[25] Njike, V. Y. et al. (2017). Snacking, Satiety, and Weight: A Randomized, Controlled Trial. American journal of health promotion : AJHP, 31(4), 296–301. https://doi.org/10.4278/ajhp.150120-QUAN-676
[27] Ortinau, L. C. et al. (2014). Effects of high-protein vs. high- fat snacks on appetite control, satiety, and eating initiation in healthy women. Nutrition journal, 13, 97. https://doi.org/10.1186/1475-2891-13-97
[28] James, L. J. et al. (2015). An afternoon snack of berries reduces subsequent energy intake compared to an isoenergetic confectionary snack. Appetite, 95, 132–137. https://doi.org/10.1016/j.appet.2015.07.005
[30] Farajian, P. et al. (2010). Short-term effects of a snack including dried prunes on energy intake and satiety in normal-weight individuals. Eating behaviors, 11(3), 201–203. https://doi.org/10.1016/j.eatbeh.2010.02.004
[31] Furchner-Evanson, A. et al. (2010). Type of snack influences satiety responses in adult women. Appetite, 54(3), 564–569. https://doi.org/10.1016/j.appet.2010.02.015
[33] Geer, E. B. et al. (2016). A prospective study of appetite and food craving in 30 patients with Cushing’s disease. Pituitary, 19(2), 117–126. https://doi.org/10.1007/s11102-015-0690-1
[34] McNeil, J. et al. (2013). Short sleep duration is associated with a lower mean satiety quotient in overweight and obese men. European journal of clinical nutrition, 67(12), 1328–1330. https://doi.org/10.1038/ejcn.2013.204
[35] McNeil, J. et al. (2017). The effects of partial sleep restriction and altered sleep timing on appetite and food reward. Appetite, 109, 48–56. https://doi.org/10.1016/j.appet.2016.11.020
[36] Miquel-Kergoat, S. et al. (2015). Effects of chewing on appetite, food intake and gut hormones: A systematic review and meta-analysis. Physiology & behavior, 151, 88–96. https://doi.org/10.1016/j.physbeh.2015.07.017
[38] Chao, A. M. et al. (2019). Tobacco Smoking, Eating Behaviors, and Body Weight: A Review. Current addiction reports, 6, 191–199. https://doi.org/10.1007/s40429-019-00253-3
[40] Stubbs, R. J. et al. (2002). The effect of graded levels of exercise on energy intake and balance in free-living women. International journal of obesity and related metabolic disorders : journal of the International Association for the Study of Obesity, 26(6), 866–869. https://doi.org/10.1038/sj.ijo.0801874
[41] Whybrow, S. et al. (2008). The effect of an incremental increase in exercise on appetite, eating behaviour and energy balance in lean men and women feeding ad libitum. The British journal of nutrition, 100(5), 1109–1115. https://doi.org/10.1017/S000711
