Can eating more fiber result in eating fewer calories?
How to Suppress Your Appetite and Naturally Boost GLP-1
Below is an approximation of this video’s audio content. To see any graphs, charts, graphics, images, and quotes to which Dr. Greger may be referring, watch the above video.
About 20 years ago there was a discovery that would forever change our ideas about fiber: our gut bacteria eat the fiber we eat to produce important signaling compounds called short-chain fatty acids. But before I get carried away, a little science lesson to frame the discovery.
Cells are the fundamental unit of life. We’re composed of trillions of them. They communicate with each other through receptors on the surface of our cells. That’s how many hormones work; it’s like a lock and key. Hormones are signaling messengers, each with a unique shape. When released into the bloodstream, they circulate throughout the body until they find a receptor they can fit into. Once the key is in the lock, it can turn on or off a whole series of reactions in the target cell.
The largest family of cell receptors is known as G protein-coupled receptors (GPCRs). More than a third of the drugs currently on the market work by plugging into these receptors. That’s how drugs like antihistamines work. We’ve discovered hundreds of different GPCRs, but remarkably, we don’t yet know what many of them do. We have the lock; we just don’t know what key fits. Accordingly, they’re called “orphan” receptors.
Two of these mystery receptors, known only as GPR43 and GPR41, were found heavily expressed throughout the body in our immune and fat cells, and in our gut, muscles, and heart. We knew they must be vital, but we didn’t know what activated them until 2003, when they were “deorphanized” (that’s actually what scientists call it). The keys that fit into those important locks were the short-chain fatty acids that our gut bacteria make when we feed them fiber.
This is how our gut bacteria may communicate with us. Renamed free fatty acid receptors, their existence is now considered crucial insight into how fiber could play such an important role in so many of our chronic diseases.
Hormones are defined as signaling messengers produced in one organ that circulate through the bloodstream and have a regulatory effect on another organ. So, these short-chain fatty acids can be considered hormones. It’s just that the organ that produces them is our microbiome, the bacteria that populate our gut. They can’t make these hormones, though, without fiber.
What do the free fatty acid receptors on our fat cells do? Remember leptin, the hormone produced by fat cells that helps tell our brain how to regulate our body weight? Short-chain fatty acids stimulate the production of leptin. This can be demonstrated in a petri dish with individual fat cells or by using fatty tissue samples removed during surgery. Drip on some short-chain fatty acids, and leptin production almost doubles.
Leptin is an “anorectic” hormone, so-called because it generates a loss of appetite and weight, but it does so over the long term. Leptin levels slowly rise as the volume of body fat gradually increases. There are other anorectic hormones that instead work rapidly, signaling our brain on more of a meal-to-meal basis. Two of these short-term appetite suppressants are PYY and GLP-1, which are both secreted by specialized L cells that line our colon. Guess what receptors are crowded all over their surface? Free fatty acid receptors.
Drip some short-chain fatty acids onto L cells, and they start churning out PYY and GLP-1. You can do this in a petri dish or in a person, either by infusing their rectums with a short-chain fatty acid enema, or the old-fashioned way by feeding people fiber––or even better, fiber-rich foods, like this whole-rye kernel wheat bread. These hormones then get released into the bloodstream where they can shoot up into the appetite center of our brain and turn down our cravings.
The flipside is ghrelin, the so-called hunger hormone. Ghrelin levels rise in our blood before a meal to stimulate our appetite, and fall down again once we eat before slowly building back up to drive us back to the kitchen. But four hours after eating just 24 grams of fiber, people’s ghrelin levels are suppressed as much as if they had just had 500 calories worth of food. Longer studies show similar effects. For example, 11- and 12-year-old children with overweight or obesity who were randomized to increased fiber intake for 16 weeks ended up eating hundreds of fewer calories of a buffet meal compared to the placebo control group.
Please consider volunteering to help out on the site.
- Koh A, De Vadder F, Kovatcheva-Datchary P, Bäckhed F. From Dietary Fiber to Host Physiology: Short-Chain Fatty Acids as Key Bacterial Metabolites. Cell. 2016;165(6):1332-1345.
- O'Connor CM, Adams JU. Essentials of Cell Biology. 2010.
- Hauser AS, Attwood MM, Rask-Andersen M, Schiöth HB, Gloriam DE. Trends in GPCR drug discovery: new agents, targets and indications. Nat Rev Drug Discov. 2017;16(12):829-842.
- Layden BT, Angueira AR, Brodsky M, Durai V, Lowe WL Jr. Short chain fatty acids and their receptors: new metabolic targets [published correction appears in Transl Res. 2013 Oct;162(4):269]. Transl Res. 2013;161(3):131-140.
- Kumari M, Kozyrskyj AL. Gut microbial metabolism defines host metabolism: an emerging perspective in obesity and allergic inflammation. Obes Rev. 2017;18(1):18-31.
- Brown AJ, Goldsworthy SM, Barnes AA, et al. The Orphan G protein-coupled receptors GPR41 and GPR43 are activated by propionate and other short chain carboxylic acids. J Biol Chem. 2003;278(13):11312-11319.
- Ang Z, Ding JL. GPR41 and GPR43 in Obesity and Inflammation - Protective or Causative?. Front Immunol. 2016;7:28.
- Kaji I, Karaki S, Kuwahara A. Short-chain fatty acid receptor and its contribution to glucagon-like peptide-1 release. Digestion. 2014;89(1):31-36.
- McKenzie CI, Mackay CR, Macia L. GPR43 - A Prototypic Metabolite Sensor Linking Metabolic and Inflammatory Diseases. Trends Endocrinol Metab. 2015;26(10):511-512.
- Soliman MM, Ahmed MM, Salah-Eldin AE, Abdel-Aal AA. Butyrate regulates leptin expression through different signaling pathways in adipocytes. J Vet Sci. 2011;12(4):319-323.
- Al-Lahham SH, Roelofsen H, Priebe M, et al. Regulation of adipokine production in human adipose tissue by propionic acid. Eur J Clin Invest. 2010;40(5):401-407.
- Schwartz MW, Morton GJ. Obesity: keeping hunger at bay. Nature. 2002;418(6898):595-597.
- Helander HF, Fändriks L. The enteroendocrine "letter cells" - time for a new nomenclature?. Scand J Gastroenterol. 2012;47(1):3-12.
- Freeland KR, Wolever TM. Acute effects of intravenous and rectal acetate on glucagon-like peptide-1, peptide YY, ghrelin, adiponectin and tumour necrosis factor-alpha. Br J Nutr. 2010;103(3):460-466.
- Greenway F, O'Neil CE, Stewart L, Rood J, Keenan M, Martin R. Fourteen weeks of treatment with Viscofiber increased fasting levels of glucagon-like peptide-1 and peptide-YY. J Med Food. 2007;10(4):720-724.
- Sandberg JC, Björck IM, Nilsson AC. Rye-Based Evening Meals Favorably Affected Glucose Regulation and Appetite Variables at the Following Breakfast; A Randomized Controlled Study in Healthy Subjects. PLoS One. 2016;11(3):e0151985.
- Canfora EE, Jocken JW, Blaak EE. Short-chain fatty acids in control of body weight and insulin sensitivity. Nat Rev Endocrinol. 2015;11(10):577-591.
- Tarini J, Wolever TM. The fermentable fibre inulin increases postprandial serum short-chain fatty acids and reduces free-fatty acids and ghrelin in healthy subjects. Appl Physiol Nutr Metab. 2010;35(1):9-16.
- Hume MP, Nicolucci AC, Reimer RA. Prebiotic supplementation improves appetite control in children with overweight and obesity: a randomized controlled trial. Am J Clin Nutr. 2017;105(4):790-799.
Motion graphics by Avo Media
Below is an approximation of this video’s audio content. To see any graphs, charts, graphics, images, and quotes to which Dr. Greger may be referring, watch the above video.
About 20 years ago there was a discovery that would forever change our ideas about fiber: our gut bacteria eat the fiber we eat to produce important signaling compounds called short-chain fatty acids. But before I get carried away, a little science lesson to frame the discovery.
Cells are the fundamental unit of life. We’re composed of trillions of them. They communicate with each other through receptors on the surface of our cells. That’s how many hormones work; it’s like a lock and key. Hormones are signaling messengers, each with a unique shape. When released into the bloodstream, they circulate throughout the body until they find a receptor they can fit into. Once the key is in the lock, it can turn on or off a whole series of reactions in the target cell.
The largest family of cell receptors is known as G protein-coupled receptors (GPCRs). More than a third of the drugs currently on the market work by plugging into these receptors. That’s how drugs like antihistamines work. We’ve discovered hundreds of different GPCRs, but remarkably, we don’t yet know what many of them do. We have the lock; we just don’t know what key fits. Accordingly, they’re called “orphan” receptors.
Two of these mystery receptors, known only as GPR43 and GPR41, were found heavily expressed throughout the body in our immune and fat cells, and in our gut, muscles, and heart. We knew they must be vital, but we didn’t know what activated them until 2003, when they were “deorphanized” (that’s actually what scientists call it). The keys that fit into those important locks were the short-chain fatty acids that our gut bacteria make when we feed them fiber.
This is how our gut bacteria may communicate with us. Renamed free fatty acid receptors, their existence is now considered crucial insight into how fiber could play such an important role in so many of our chronic diseases.
Hormones are defined as signaling messengers produced in one organ that circulate through the bloodstream and have a regulatory effect on another organ. So, these short-chain fatty acids can be considered hormones. It’s just that the organ that produces them is our microbiome, the bacteria that populate our gut. They can’t make these hormones, though, without fiber.
What do the free fatty acid receptors on our fat cells do? Remember leptin, the hormone produced by fat cells that helps tell our brain how to regulate our body weight? Short-chain fatty acids stimulate the production of leptin. This can be demonstrated in a petri dish with individual fat cells or by using fatty tissue samples removed during surgery. Drip on some short-chain fatty acids, and leptin production almost doubles.
Leptin is an “anorectic” hormone, so-called because it generates a loss of appetite and weight, but it does so over the long term. Leptin levels slowly rise as the volume of body fat gradually increases. There are other anorectic hormones that instead work rapidly, signaling our brain on more of a meal-to-meal basis. Two of these short-term appetite suppressants are PYY and GLP-1, which are both secreted by specialized L cells that line our colon. Guess what receptors are crowded all over their surface? Free fatty acid receptors.
Drip some short-chain fatty acids onto L cells, and they start churning out PYY and GLP-1. You can do this in a petri dish or in a person, either by infusing their rectums with a short-chain fatty acid enema, or the old-fashioned way by feeding people fiber––or even better, fiber-rich foods, like this whole-rye kernel wheat bread. These hormones then get released into the bloodstream where they can shoot up into the appetite center of our brain and turn down our cravings.
The flipside is ghrelin, the so-called hunger hormone. Ghrelin levels rise in our blood before a meal to stimulate our appetite, and fall down again once we eat before slowly building back up to drive us back to the kitchen. But four hours after eating just 24 grams of fiber, people’s ghrelin levels are suppressed as much as if they had just had 500 calories worth of food. Longer studies show similar effects. For example, 11- and 12-year-old children with overweight or obesity who were randomized to increased fiber intake for 16 weeks ended up eating hundreds of fewer calories of a buffet meal compared to the placebo control group.
Please consider volunteering to help out on the site.
- Koh A, De Vadder F, Kovatcheva-Datchary P, Bäckhed F. From Dietary Fiber to Host Physiology: Short-Chain Fatty Acids as Key Bacterial Metabolites. Cell. 2016;165(6):1332-1345.
- O'Connor CM, Adams JU. Essentials of Cell Biology. 2010.
- Hauser AS, Attwood MM, Rask-Andersen M, Schiöth HB, Gloriam DE. Trends in GPCR drug discovery: new agents, targets and indications. Nat Rev Drug Discov. 2017;16(12):829-842.
- Layden BT, Angueira AR, Brodsky M, Durai V, Lowe WL Jr. Short chain fatty acids and their receptors: new metabolic targets [published correction appears in Transl Res. 2013 Oct;162(4):269]. Transl Res. 2013;161(3):131-140.
- Kumari M, Kozyrskyj AL. Gut microbial metabolism defines host metabolism: an emerging perspective in obesity and allergic inflammation. Obes Rev. 2017;18(1):18-31.
- Brown AJ, Goldsworthy SM, Barnes AA, et al. The Orphan G protein-coupled receptors GPR41 and GPR43 are activated by propionate and other short chain carboxylic acids. J Biol Chem. 2003;278(13):11312-11319.
- Ang Z, Ding JL. GPR41 and GPR43 in Obesity and Inflammation - Protective or Causative?. Front Immunol. 2016;7:28.
- Kaji I, Karaki S, Kuwahara A. Short-chain fatty acid receptor and its contribution to glucagon-like peptide-1 release. Digestion. 2014;89(1):31-36.
- McKenzie CI, Mackay CR, Macia L. GPR43 - A Prototypic Metabolite Sensor Linking Metabolic and Inflammatory Diseases. Trends Endocrinol Metab. 2015;26(10):511-512.
- Soliman MM, Ahmed MM, Salah-Eldin AE, Abdel-Aal AA. Butyrate regulates leptin expression through different signaling pathways in adipocytes. J Vet Sci. 2011;12(4):319-323.
- Al-Lahham SH, Roelofsen H, Priebe M, et al. Regulation of adipokine production in human adipose tissue by propionic acid. Eur J Clin Invest. 2010;40(5):401-407.
- Schwartz MW, Morton GJ. Obesity: keeping hunger at bay. Nature. 2002;418(6898):595-597.
- Helander HF, Fändriks L. The enteroendocrine "letter cells" - time for a new nomenclature?. Scand J Gastroenterol. 2012;47(1):3-12.
- Freeland KR, Wolever TM. Acute effects of intravenous and rectal acetate on glucagon-like peptide-1, peptide YY, ghrelin, adiponectin and tumour necrosis factor-alpha. Br J Nutr. 2010;103(3):460-466.
- Greenway F, O'Neil CE, Stewart L, Rood J, Keenan M, Martin R. Fourteen weeks of treatment with Viscofiber increased fasting levels of glucagon-like peptide-1 and peptide-YY. J Med Food. 2007;10(4):720-724.
- Sandberg JC, Björck IM, Nilsson AC. Rye-Based Evening Meals Favorably Affected Glucose Regulation and Appetite Variables at the Following Breakfast; A Randomized Controlled Study in Healthy Subjects. PLoS One. 2016;11(3):e0151985.
- Canfora EE, Jocken JW, Blaak EE. Short-chain fatty acids in control of body weight and insulin sensitivity. Nat Rev Endocrinol. 2015;11(10):577-591.
- Tarini J, Wolever TM. The fermentable fibre inulin increases postprandial serum short-chain fatty acids and reduces free-fatty acids and ghrelin in healthy subjects. Appl Physiol Nutr Metab. 2010;35(1):9-16.
- Hume MP, Nicolucci AC, Reimer RA. Prebiotic supplementation improves appetite control in children with overweight and obesity: a randomized controlled trial. Am J Clin Nutr. 2017;105(4):790-799.
Motion graphics by Avo Media
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How to Suppress Your Appetite and Naturally Boost GLP-1
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Content URLDoctor's Note
For more on fiber, check out:
- Is Fiber an Effective Anti-Inflammatory?
- The Five-to-One Fiber Rule
- Juicing Removes More Than Just Fiber
For more on GLP-1, see my book OZEMPIC: Risks, Benefits, and Natural Alternatives to GLP-1 Weight-Loss Drugs.
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