Hunger is the physiological need to eat food. Satiety is the absence of hunger and the sensation of feeling full. While it’s good to be hungry from time-to-time, being constantly hungry indicates that something is amiss. The feeling of hunger and satiety is caused by various types of hormones secreted by different organs in your body.
Over-production or under-production of these hormones upsets the balance of the digestive system and it is important that they function optimally. Here are eight hormones that influence hunger and ways to ensure their ideal performance.
Insulin, a hormone secreted by the pancreas, is released when blood sugar levels rise. It prevents the fat cells from being broken down. The main effect of insulin is to make us store fat. A high-sugar meal, such as bread, pasta, or breakfast cereals, can cause a drastic increase in your blood sugar levels. This results in the pancreas releasing insulin
The best way to prevent hypoglycemia from making you hungry is to consume foods that don’t shoot up your blood sugar. Reducing or avoiding sugar and simple carbohydrates can keep your blood sugar levels stabilized. It is important to reduce fructose, which increases insulin levels and is linked to insulin resistance. Regular exercise helps to burn glycogen reserves and increases insulin activity in skeletal muscles.
Cortisol is the stress hormone produced by the adrenals when the body is under stress. Sleep deprivation or chronic stress increases the cortisol levels in our body. An elevated cortisol level constantly keeps our appetite high.1 Chronically elevated levels of cortisol are known to cause overeating and weight gain.
High levels of cortisol are also directly linked to abdominal fat in women. The ideal method to reduce stress is to practice regular meditation, breathing exercises, physical activity, and quality sleep. Consuming three balanced meals every day consisting of fiber, protein, greens, and healthy fat can help beat stress and reduce cortisol levels.
Leptin is another hunger hormone that is released from the fat cells. Leptin has the opposite effect of ghrelin. Its secretion sends a signal to the brain to stop eating and prevents you from overeating. The main purpose of leptin is to prevent us from gaining weight.2
New research shows that eating a diet high in sugar and simple carbohydrates can block the effects of leptin. The simple carbs raise our triglyceride levels, which in turn, blocks leptin signaling to the brain.3
The best method to make our brains to sense leptin and stop feeling constantly hungry is to reduce sugar and simple carbohydrates in our diets. It is important to avoid inflammatory foods, like seed oils, and instead, consume omega-3 fatty acids. Good sleep is also crucial, as sleep deprivation is linked to reduced leptin levels.
When your stomach is empty, the gastrointestinal tract releases ghrelin. And when your stomach is stretched, its secretion stops. Ghrelin levels are
The best way to suppress ghrelin secretion is to ensure that low-calorie fibrous foods or water is present in your stomach during meal times. A sumptuous salad or even a glass of water can quickly stop the body from production ghrelin.
5. Neuropeptide Y (NYP)
Neuropeptide Y is a powerful brain neurotransmitter considered as a hunger hormone that compels us to eat. In a 1985 study, researchers injected male rats with neuropeptide Y. Within minutes of the injection, the male rats became obsessed with food and lost all interest in sex. Even though a willing sexual mate was readily available, the male rats injected with neuropeptide Y craved for food more than sex.4
Studies show that neuropeptide Y is released in response to stress as well as a high-sugar, high-fat diet.5 Interestingly, intermittent fasting has been shown to lower neuropeptide Y levels.6 The best way to lower neuropeptide Y levels is to minimize or avoid unhealthy fats and sugar, manage stress, and practice intermittent fasting after consulting your physician.
6. Peptide YY (PYY)
Insulin resistance and chronically elevated blood sugar levels impair the secretion of PYY. When the blood sugar level is balanced, it increases PYY response and production. Protein-based foods increase PYY concentrations and foods rich in fiber increases PYY production.
7. Cholecystokinin (CCK)
Cholecystokinin, a hormone produced by the duodenum (the first section of the small intestine), stimulates gallbladder contraction and plays a role in the control of appetite. It also stimulates pancreatic and gastric acid secretion and controls nutrient delivery to the small intestine by inhibiting food intake and gastric emptying.8.
In one study, cholecystokinin induced satiety by interacting through CCK-1 receptors located in the hind region of the brain. Elevated cholecystokinin levels decreased appetite and reduced intestinal inflammation caused by parasites and bacterial toxins. By regulating orexigenic pathways in the body, cholecystokinin may help control appetite-related disorders such as obesity and bulimia.9
An over-production of cholecystokinin due to irritable bowel syndrome (IBS) can make you feel deprived of energy. The direct interaction of CCK and dietary protein contributes to satiety response. Fat triggers the release of this hormone and fiber doubles its production.
8. Glucagon-Like Peptide-1 (GLP-1)
Glucagon-like peptide 1 (GLP-1) is an amino acid peptide hormone produced in the intestinal epithelial endocrine L-cells. It is secreted when food enters the intestines and signals our brain indicating that the stomach is full.10
However, chronic inflammation can reduce its production, which prevents satiety signaling making you constantly hungry. Avoiding inflammatory foods and instead consuming probiotics, leafy green vegetables, and high-protein foods increase GLP-1 production.
|↑1||Abraham, SB1, D. Rubino, N. Sinaii, S. Ramsey, and L. K. Nieman. “Cortisol, obesity, and the metabolic syndrome: A cross‐sectional study of obese subjects and review of the literature.”
|↑2||Wabitsch, Martin, Jan-Bernd Funcke, Belinda Lennerz, Ursula Kuhnle-Krahl, Georgia Lahr, Klaus-Michael Debatin, Petra Vatter, Peter Gierschik, Barbara Moepps, and Pamela Fischer-Posovszky. “Biologically inactive leptin and early-onset extreme obesity.” New England Journal of Medicine 372,
|↑3||Veyrat-Durebex, Christelle, Anne-Laure Poher, Aurélie Caillon, Emmanuel Somm, Philippe Vallet, Yves Charnay, and Françoise Rohner-Jeanrenaud. “Improved leptin sensitivity as a potential candidate responsible for the spontaneous food restriction of the Lou/C rat.” PloS one 8, no. 9 (2013): e73452.|
|↑4||CLARK, JOHN T., PUSHPA S. KALRA, and SATYA P. KALRA. “Neuropeptide Y stimulates feeding but inhibits sexual behavior in rats.”
|↑5||Paternain, L., M. A. Batlle, A. L. De la Garza, F. I. Milagro, J. A. Martinez, and J. Campion. “Transcriptomic and epigenetic changes in the hypothalamus are involved in an increased susceptibility to a high-fat-sucrose diet in prenatally stressed female rats.” Neuroendocrinology 96, no. 3 (2012): 249-260.|
|↑6||Marks, Jonathan L., Mu Li, Michael Schwartz, Daniel Porte, and Denis G. Baskin. “Effect of fasting on regional levels of neuropeptide Y mRNA and insulin receptors in the rat hypothalamus: An autoradiographic study.” Molecular and Cellular Neuroscience 3, no. 3 (1992): 199-205.|
|↑7||Cahill, Farrell, Yunqi Ji, Danny Wadden, Peyvand Amini, Edward Randell, Sudesh Vasdev, Wayne Gulliver, and Guang Sun. “The association of serum total peptide YY (PYY) with obesity and body fat measures in the CODING study.” PLoS One 9, no. 4 (2014): e95235.|
|↑8||Dockray, Graham J. “Cholecystokinin.” Current Opinion in Endocrinology, Diabetes and Obesity 19, no. 1 (2012): 8-12.|
|↑9||Chandra, Rashmi, and Rodger A. Liddle. “Cholecystokinin.” Current Opinion in Endocrinology, Diabetes and Obesity 14, no. 1 (2007): 63-67.|
|↑10||Holst, Jens Juul. “The physiology of glucagon-like peptide 1.” Physiological reviews 87, no. 4 (2007): 1409-1439.|