Leaving Calorie Counting Behind

Obesity has become a global epidemic among human beings, affecting over 20% of the population of most western countries and 68% of the US population (1,2).  Research over the last decade has been suggesting that the cause of this current problem may not be simply overeating but a mismatch between the foods we ate as we evolved and the composition of the standard western diet now dominant in industrialized countries.  Modern processed convenience foods are extremely energy dense with very low dietary fiber content and thus are remarkably different from the low-energy high-fiber diet that early humans adapted to during millions of years of evolution.  Evidence illustrates that, for most of our history, humans ingested on average over 100 grams per day of dietary fiber.  Today, that amount has dwindled to an intake of only about 15 grams of daily fiber (3).  In our evolutionary past, food equaled fiber. When the digestive tract was full of high-fiber food, hormones were released that inhibited eating. Not eating meant less fiber in the gut, a drop in the hormone level and boosting of the appetite.  Tube feeding studies corroborate this idea, illustrating that the more “full” the gut is, the lower is the desire to eat (4).

When it comes to dietary fiber, we humans are unable to digest much of it on our own.  The fiber we eat travels through the long length of our digestive tract largely unchanged, adding bulk to the stool and preventing constipation.  This is only the beginning of the benefits that fiber offers, however.  To profit fully from dietary fiber, we rely on our gut microbiome, the community of microorganisms that live in the last section of our intestinal tract, the large intestine or colon.  It is these microbes that thrive on fibrous food, digest it through fermentation, producing short-chain fatty acids, the main ones of which are butyrate, propionate, and acetate.  These short-chain fatty acids are associated with lower rates of many chronic health problems such as cardiovascular disease, diabetes and metabolic syndrome and cancer and with decreased mortality from all causes (5,6).  It is these same short-chain fatty acids that affect appetite regulation by activating cell receptors, in turn causing the release of hormones that control our appetite (7)

It has only been recently recognized that the gut microbiome is deeply involved in food metabolism.  Human beings possess a large bundle of nerve fibers that stretch from the central nervous system (CNS), located in the brain and spinal cord, down into the enteric nervous system (ENS) which is imbedded in the lining of the gastrointestinal tract.  This collection of nerves is called the vagal nerve system.  Communication through this system allows the brain and the GI tract, along with its resident microbes, to team up in many of their activities, including regulation of the metabolism of carbohydrates, lipids and amino acids.  The short-chain fatty acids produced by gut microbes are an integral part of the means by which the gut and the brain communicate and they also exert major influences of their own on appetite control and eating behavior.  Short-chain fatty acids stimulate the production and release of leptin and other peptide hormones that are involved in appetite regulation (8).  In addition, neurons within the vagal nerve system create receptors for these hormones and other gut peptides.  When the receptors sense the presence of peptides, they transfer that information to the CNS which results in a complicated variety of reactions.  Surprisingly, these messages can travel in both directions – from the brain to the gut microbiota and from the gut microbiota to the brain (3,9).

Multiple research studies have examined the role that lack of fiber may play in the development of obesity.  For example, populations that follow a fiber-rich, traditional diet generally have low body weights and improved parameters of food metabolism.  The benefits of fiber in appetite control seem to spring from both from the way fiber physically fills the intestines and from the actions engendered by the short-chain fatty acids that are produced by gut microbes during fermentation of fiber from the diet (10).  High fiber diets have been shown to promote greater numbers of health-promoting microbes in the gut microbiome as well as to stimulate higher production of short-chain fatty acids and enhance the release of the hormones involved in appetite suppression (7).  In particular, the release of leptin, a well-studied hormone that suppresses the appetite, is significantly boosted by the short-chain fatty acids produced by gut microbes (11).

How much fiber is needed to affect food intake?  A 2015 study showed that small increases in dietary fiber are not sufficient to make a difference.  Appetite suppression occurred only with a daily fiber dose of 35 grams or more.  In addition, it is still unclear how long fiber ingestion needs to remain high to achieve better hunger control.  Some research has concluded that it takes from 3 to 12 months of continual daily high fiber consumption to improve short-chain fatty acid production and increase the release of appetite-controlling hormones.  Another study showed significant reduction of weight gain in overweight adults after a 24-week period of fiber supplementation.  Yet another observed that even one large dose of fiber has the ability to reduce energy intake at an ensuing buffet meal by about 14% through the production of the short-chain fatty acid, butyrate, by the gut microbiome (3).


Appetite Hormones

It’s time to examine more closely the substances produced by the body that can control appetite. There are a number of gut peptides that influence eating behaviour by sending signals through the vagus nerve system to an area of the brain called the hypothalamus (12).  Peptides are short chains of linked amino acids.  The gut peptides include the hormones leptin, insulin, ghrelin, cholecystokinin (CCK), Pancreatic Tyrosine Tyrosine (PYY3-36), GLP-1, oxyntomodulin, obestatin and nesfatin.  These hormones work to balance energy intake with energy expenditure.  Leptin, insulin and ghrelin have been the most extensively studied.  (1)


Leptin (aka the Satiety Hormone)

Leptin is an appetite-inhibiting hormone that is produced and released by adipose (fat) tissue. It communicates both with the brain to regulate food intake and energy expenditure, and with other areas of the body to adjust fat and carbohydrate metabolism. When we eat, we need to store some excess energy within our fat cells for future needs.  Once the fat cells are full enough, they release leptin into the bloodstream to signal the brain that enough food has been eaten.  Accordingly, appetite is lowered and metabolic rate rises, causing the burning of stored calories to help maintain energy balance.  Conversely, low levels of fat in tissues shrink leptin production and the brain reacts by increasing the appetite and reducing metabolism. (13,14)

Most humans can manufacture enough leptin.  However, a condition called leptin resistance can occur in which the body continues to produce leptin but the brain does not receive its signal.  Leptin resistance can be caused by a range of factors including low-grade inflammation, elevated free fatty acids ***  in the bloodstream and high production of leptin itself.  All these issues are present in obesity and when eating a diet low in fiber and high in saturated fat. (15)


***Free fatty acids are fats that have been released from their triglyceride storage form in the adipose (fat) tissue.  Their release occurs when working cells require more energy or simply as “spillover” of excess fat in overweight and obese individuals. Free fatty acids are single fatty acids that are bound to a component of the blood called albumin and travel freely through the bloodstream.  They can be saturated fats, trans fats, polyunsaturated and monounsaturated fats.  However, short-chain fatty acids produced by the gut microbiome are mostly metabolized as energy for the cells of the colon wall and are found in only very small amounts in the blood stream. (32,33,34)


It has been discovered that people suffering from obesity almost always have leptin resistance (16).  Because obese individuals have more fat cells, they produce more leptin.  Constant high leptin levels seem to render leptin receptors less sensitive to the hormone and thus blunt the strength of leptin’s signals to the brain.  Consequently, even though leptin is present in copious amounts, the appetite is not turned down at all but actually increases, causing over-consumption of food.  In addition, fat storage continues unabated, energy levels decline and the number of calories being burned at rest decrease, all in spite of the continuing presence of leptin.  Instead of weight loss, any weight that might have already been lost will be regained and, regrettably, even more weight on top of that (1,14,17,19,20).

Other factors that contribute to leptin resistance include stress, inflammation, excessive intake of refined carbohydrates, poor sleep and some unusual molecular and genetic mechanisms (21,22).


Ghrelin (aka the Hunger Hormone)

Ghrelin increases food intake.  It is produced by the stomach and exerts its effects through the vagal nerve system to stimulate the appetite, instigating the opposite effect to that of leptin.  Fiber has been found to be an important regulator of ghrelin levels (1,23).



Insulin is produced in the pancreas and is released in response to changes in energy intake. The actions of insulin mimic those of leptin, with higher levels decreasing food consumption and lower insulin levels increasing it.  Insulin signals also employ the vagal system and the hypothalamus to exert their effects (1,12).


What Happens When You Try to Lose Weight by Counting Calories? (2,15)

Weight management is more complex than simply calories in/calories out.  By concentrating on counting calories and not paying attention to the type of foods being ingested, weight loss is doomed to failure.  This is because the body has its own mechanisms for maintaining weight.


  • First of all, leptin resistance is almost always a factor in obesity, meaning that the brain will not receive leptin’s message that there is enough fat stored away for the future. Appetite will not be lessened and overeating results, further augmenting fat stores and promoting even more leptin production.


  • Studies show that, when faced with fewer calories being ingested, the body counters with adjustments to recover that energy. Missing calories are replaced over the next few meals by alterations in body physiology and changes in the nature of the subsequent food consumed so that the missing energy is eventually completely compensated for.  This can happen with no increase in the amount of food eaten.  Consumption of foods higher in calorie density rises and, at the same time, the body’s metabolic rate decreases.


  • In addition, the hormone ghrelin will be released to balance energy intake and expenditure. Ghrelin increases the appetite and can cause hunger that can become a constant urge.  Studies have shown that cutting only 10 calories daily in a diet can result in an appetite that will not be satisfied until those 10 daily calories are not only replaced but multiplied. (8,21).


  • Reducing calorie intake will reduce the energy expenditure of muscles. However, the resulting thriftier body responds by promoting higher deposition of body fat.


  • Even a year after dieting, hormonal mechanisms that stimulate the appetite remain high. The long-term consequences of low-calorie diets are that between one-third and two-thirds of dieters regain more weight than they lost initially.


  • The bottom line is that counting calories alone has only limited short-term influence on weight.



There is a better way to promote weight loss (10)

Here are some practical steps to take to achieve weight loss without counting calories.


  • Add more high-fiber foods to your diet every day. It appears that long-term ingestion of high amounts of fiber offers the best chance of realizing its benefits.  Fiber is the source of healthy short-chain fatty acids.  Fiber can also diminish leptin resistance and increase satiety by filling up the digestive tract (24).   Did you know that only plant-sourced foods contain fiber?  And that fiber is present in virtually all fruits, vegetables, legumes, grains, nuts and seeds.  Plant-sourced foods usually contain both soluble and insoluble types of fiber, both of which have many health bonuses including aiding in weight loss and protecting against obesity. (25,26)


  • Boosting ingestion of all kinds of plants in their whole form has other advantageous effects too. Whole plant-sourced foods are non-inflammatory which can help to reduce leptin resistance (27,28).  In addition, brand new research, from October 2021, reports that plant-derived foods are a source of many previously unknown peptides that have their own appetite-regulating effects and can link biochemically to the hypothalamus, the area of the brain that is involved in appetite regulation.  These peptides also have the ability to interact with the appetite-altering hormones that are produced in the body such as leptin and ghrelin. (1)


  • Avoid refined carbohydrates and processed foods. They lack fiber, cause increased inflammation and damage gut walls.  Such foods are also associated with high blood triglyceride levels.  Triglycerides are involved in both leptin and insulin resistance. (29)


  • Enjoy some form of exercise daily. Exercise can lower leptin resistance.  (30)


  • Try to improve your sleep by going to bed at the same time each night, early enough to get at least 6 to 7 hours of sleep. (31)



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2  Benton, D., Young, H.A. Reducing Calorie Intake May Not Help You Lose Body Weight. Perspect Psychol Sci. 2017; 12(5): 703-714. Doi:10.1177/1745691617690878.

3  Byrne, C., Chambers, E., Morrison, D. et al. The role of short chain fatty acids in appetite regulation and energy homeostasis. Int J Obes 2015; 39: 1331–1338.  Doi.org/10.1038/ijo.2015.84.

4  Poppitt, S.D., Shin, H.S., McGill, A.T., et al. Duodenal and ileal glucose infusions differentially alter gastrointestinal peptides, appetite response, and food intake: a tube feeding study. Am J Clin Nutr. 2017;106(3):725-735.

5  Aune, D., Giovannucci, E., Boffetta, P., Fadnes, L.T., Keum, N., Norat, T., Greenwood, D.C., Riboli, E., Vatten, L.J., Tonstad, S..  Fruit and vegetable intake and the risk of cardiovascular disease, total cancer and all-cause mortality-a systematic review and dose-response meta-analysis of prospective studies.  Int J Epidemiol. 2017 Jun 1;46(3):1029-1056.

6  Reynolds, A., Mann, J., Cummings, J., Winter, N., Mete, E., Te Morenga, L.  Carbohydrate quality and human health: a series of systematic reviews and meta-analyses.  Lancet. 2019 Feb 2;393(10170):434-445.

7  Frost, G.S., Walton, G.E., Swann, J.R., Psichas, A., Costabile, A., Johnson, L.P., et al.  Impacts of plant-based foods in ancestral hominin diets on the metabolism and function of gut microbiota in vitro.  mBio. 2014 May 20; 5(3): e00853-14. Doi: 10.1128/mBio.00853-14.

8  Al-Lahham, S.H., Roelofsen, H., Priebe, M., Weening, D. et al.  Regulation of adipokine production in human adipose tissue by propionic acid.  Eur J Clin Invest. 2010 May; 40(5): 401-407. Doi:10.1111/j.1365-2362.2010.02278.x.

9  Wang, S.-Z., Yu, Y.-J., Adeli, L.  Role of Gut Microbiota in Neuroendocrine Regulation of Carbohydrate and Lipid Metabolism via the Microbiota-Gut-Brain-Liver Axis.  Microorganisms. 2020 Apr; 8(4): 527.  Doi:10.3390/microorganisms8040527.

10  Sleeth, M.L., Thompson, E.L., Ford, H.E., Zac-Varghese, S.E.K., Frost, G.  Free fatty acid receptor 2 and nutrient sensing: a proposed role for fibre, fermentable carbohydrates and short-chain fatty acids in appetite regulation.  Nutr Res Rev. 2010 Jun; 23(1): 135-145. Doi: 10.1017/S0954422410000089.

11  Ryan, K.K., Seeley, R.J.  Food as a Hormone.  Science. 2013 Feb 22; 339(6122): 918–919.   Doi:10.1126/science.1234062.

12  Miller, G.D. Appetite Regulation: Hormones, Peptides, and Neurotransmitters and Their Role in Obesity.  Am J Lifestyle Med. 2017;13(6): 586-601.  doi:10.1177/1559827617716376.

13  Park, H.-K., Ahimab, R.S.  Leptin in the 21st Century. Physiology of leptin: energy homeostasis, neuroendocrine function and metabolism.  Metabolism January 2015; 64(1): 24-34. Doi.org/10.1016/j.metabol.2014.08.004.

14 Chan, J.L., Heist, K., DePaoli, A.M., Veldhuis, J.D., Mantzoros, C.S.  The role of falling leptin levels in the neuroendocrine and metabolic adaptation to short-term starvation in healthy men.   J Clin Invest . 2003 May; 111(9): 1409-1421. Doi: 10.1172/JCI17490.

15  Guyenet, S.J., Schwartz, M.W. Clinical review: Regulation of food intake, energy balance, and body fat mass: implications for the pathogenesis and treatment of obesity. J Clin Endocrinol Metab. 2012; 97(3): 745-755. Doi:10.1210/jc.2011-2525.

16  Izquierdo, A.G., Crujeiras, A.B., Casanueva, F.F., Carreira, M.C. Leptin, Obesity, and Leptin Resistance: Where Are We 25 Years Later? Nutrients. 2019; 11(11): 2704. Doi:10.3390/nu11112704.

17 Considine, R.V., Sinha, M.K., Heiman, M.L., Kriauciunas, A., Stephens, T.W., Nyce, M.R., Ohannesian, J.P., Marco,  C.C., McKee, L.J., Bauer, T.L. et al.  Serum immunoreactive-leptin concentrations in normal-weight and obese humans.  N Engl J Med. 1996 Feb 1; 334(5): 292-295. Doi:10.1056/NEJM199602013340503.

19  Jung, C.H., Kim, M.-S.  Molecular mechanisms of central leptin resistance in obesity.  Arch Pharm Res. 2013 Feb; 36(2): 201-207. Doi: 10.1007/s12272-013-0020-y.  Chang Hee Jung 1, Min-Seon Kim

20   Thaler, J.P., Yi, C.-X., Schur, E.A., Guyenet, S.J., Swang, B.H., Dietrich, M. O. et al.  Obesity is associated with hypothalamic injury in rodents and humans.  J Clin Invest. 2012 Jan 3; 122(1): 153–162.  Doi: 10.1172/JCI59660.

21  Zhou, Y., Rui, L. Leptin signaling and leptin resistance. Frontiers of Medicine. 2013; 7(2): 207-222.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4069066/

22  Obradovic, M., Sudar-Milovanovic, E., Soskic, S., et al.  Leptin and Obesity: Role and Clinical Implication.  Frontiers in Endocrinology. 2021; 12: 563.  Doi: 10.3389/fendo.2021.585887 .

23  St. Pierre, D.H., Rabasa-Lloret, R., Lavoie, M.-E., Karelis, A.D., Strycar, I., et al.  Fiber intake predicts ghrelin levels in overweight and obesepostmenopausal women.   European Journal of Endocrinology. 2009; 161: 65-72.

24  Zhang, R., Jiao, J., Zhang, W., Zhang, Z., Zhang, W., Qin, L. et al.  Effects of cereal fiber on leptin resistance and sensitivity in C57BL/6J mice fed a high-fat/cholesterol diet. Food & Nutrition Research. August 2016; 60(1): 31690.  Doi:10.3402/fnr.v60.31690.

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28 https://www.forksoverknives.com/health-topics/diet-and-inflammation

29  Banks, W.A., Farr, S., Salameh, T., Niehoff, Mm.L., Rhea, E.M., Morley, J. et al. Triglycerides cross the blood–brain barrier and induce central leptin and insulin receptor resistance. Int J Obes. 2018 Mar; 42(3): 391-397.  Doi: 10.1038/ijo.2017.231.

30  Ropelle, E., Flores, M., Cintra, D., Rocha, G., Pauli, J., Morari, J. et al. IL-6 and IL-10 Anti-Inflammatory Activity Links Exercise to Hypothalamic Insulin and Leptin Sensitivity through IKKβ and ER Stress Inhibition. PLoS Biology. 2010.  http://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.1000465

31  García-García, F., Juárez-Aguilar, E., Santiago-García, J., Cardinali, D.P. Ghrelin and its interactions with growth hormone, leptin and orexins: implications for the sleep-wake cycle and metabolism.   Sleep Med Rev. 2014 Feb; 18(1): 89-97. Doi: 10.1016/j.smrv.2013.04.003.

32  https://www.encyclopedia.com/sports/sports-fitness-recreation-and-leisure-magazines/free-fatty-acids-blood


34 Yip, W., Hughes, M.R., Li, Y., et al. Butyrate Shapes Immune Cell Fate and Function in Allergic Asthma. Front Immunol. February 2021; 12: 628453. Doi:10.3389/fimmu.2021.628453.



Promoting a healthy adventurous lifestyle powered by plants and the strength of scientific evidence.

My name is Debra Harley (BScPhm) and I welcome you to my retirement project, this website. Over the course of a life many lessons are learned, altering deeply-rooted ideas and creating new passions.


  1. Ruth Russell on March 25, 2022 at 12:32 pm

    Thanks Deb for your research here on fibre. I always learn something from your blogs. I never had trouble with my weight until I hit menopause. I’m always within the “normal” weight range but I definitely have more fat around my middle as an older adult.

    • Deb on March 30, 2022 at 11:06 am

      Hi Ruth, yes, age brings its challenges and one of them is maintaining your ideal weight. This one is made much easier by eating plant-based.

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