The “Ketogenic Diet” still has the word “diet.” Dieting is a dreaded word for most since we know the process is typically accompanied by hunger and cravings. For the traditional diet, success is dependent on an individual’s ability to manage hunger and stay on course with their diet. Once someone has finished their standard diet, maintaining progress depends on their ability to not want to eat every piece of junk food in sight that they have been craving for so long. Well, what if there was a diet that would prevent you from experiencing intense hunger pains during and after dieting? This is where the ketogenic diet may be able to help.

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The Brain and Hunger

To understand how the ketogenic diet can impact our hunger, it is first important to understand how the body regulates appetite. The brain plays a significant role in regulating our appetite. To put this more simply, our brain tells our body when we need more food or when we have enough food. However, this mechanism is not fully functional in all individuals. It is thought that obese individuals may have impaired satiety signaling which can lead to increased caloric intake. The hypothalamus of the brain is our center for hunger/satiety (fullness) control. The foods we eat as well as the hormonal responses in our body can interact with this portion of the brain and cause us to feel either hungry or full. One of the oldest theories on how this is regulated is the glucostatic theory (1). This theory states that as our blood glucose decreases, as it does between meals, receptors in our brain receive signals to stimulate appetite. The other macronutrients as well as total calorie intake have also been studied as potential appetite regulators. Other systems of our body can also interact with our brain to signal appetite such as our endocrine system. Our endocrine system can regulate appetite in the short term by sending hormones to the brain following a meal and in the long term by sending hormones to the brain that reflect our body fat percentage. There is also growing evidence that our gut and gastrointestinal tract can regulate our appetite by interacting with our brain through several proposed mechanisms (involving ghrelin, amylin, pancreatic polypeptide, and peptide YY).

Dieting and Hunger

Numerous studies have demonstrated that as we decrease our caloric intake, our perceived hunger increases (2). The same is true following weight loss. The theory is that as we decrease our calorie intake and lose weight, our body stimulates appetite hormones to facilitate the regain of weight to maintain homeostasis (3). Some studies have even found that following weight loss, hunger can remain elevated for a year or even longer (3). This is one of the primary reasons why staying on track with a diet or maintaining your weight loss following a diet can be so tough.

Hormones and Hunger

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Two important hormones responsible for regulating appetite are leptin and ghrelin. Leptin, which is produced mainly by adipose tissue, is released following increases in body fat percentage or increases in food intake. Once released into the bloodstream it possesses the ability to cross the blood brain barrier and communicate the body’s energy status to the hypothalamus. When leptin reaches the hypothalamus it essentially says that we have enough body fat, which in the healthy individual leads to a decrease in food intake and an increase in energy expenditure (4). To simplify all of this, in a properly functioning individual, as we are on the verge of increasing our body fat stores, our fat cells will release leptin to tell our body to decrease food intake and increase activity. It has been demonstrated also that an increase in leptin can lead to weight loss (5)!

Ghrelin, on the other hand, is a hormone secreted by the stomach. The secretion of ghrelin is dependent on the nutritional state of our body. Prior to eating, our body has elevated levels of ghrelin, which also act on the hypothalamus but in this case telling us that it is time to eat. Following the consumption of food, in healthy individuals, ghrelin levels decrease. This is essentially to tell our body that we have consumed food and we no longer need to eat. Interestingly, it has been demonstrated that ghrelin and leptin can interact with each other. For example, when leptin is secreted from adipose tissue, ghrelin secretion by the stomach is suppressed. For these reasons, leptin and ghrelin have been noted as the key regulators of our hunger levels.

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The Ketogenic Diet and Hunger

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Typically, the ketogenic diet is accompanied with a drop in caloric intake; however, it is often reported that despite this drop in calories, individuals on a ketogenic diet experience a decrease in their perceived hunger (6). There are multiple ketogenic diet studies that allow subjects to eat as much ketogenic food as they want as long as carbohydrates are restricted. Many of these studies have found that the subjects voluntarily consume less food (7,8,9,10). These studies display that the ketogenic diet is not only causing greater weight loss (11) but also a greater perceived rate of fullness (6). So, what makes the ketogenic diet different? There are several theories that you may have heard on why this may occur. The simple fact that fat is more nutrient dense than the other macronutrients (9 calories per gram compared to 4 calories per gram for carbs and protein) is one proposed reason for improvements with appetite. While this theory does hold some truth as reasons why ketogenic dieters may experience more satiety (fullness), this may not be the only mechanism at work!

Ketones and Hunger

Studies are starting to find that it may be ketones themselves that are leading to changes in appetite regulation. Several studies have found that severe calorie restriction (under 800 calories/day) can lead to changes in perceived hunger similar to those experienced on the ketogenic diet (12). All of these studies demonstrate ketosis occurring to some degree as a result of the extreme calorie restriction. This offers reason to consider ketosis as a primary factor for appetite regulation. But what is it that ketones are doing that allow for appetite suppression?

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One major mechanism likely lies within stabilizing blood glucose. As we enter ketosis, we prevent our body from having drastic changes in blood sugar, which could result in improved hunger signaling. Another key mechanism may lie within ghrelin. Being in a state of ketosis can suppress the weight-loss-induced rise in ghrelin (13, 14). This is key to successful weight loss because it prevents our body from telling us we need to eat more. Additionally, we know that ghrelin and leptin interact with each other, so if the ketogenic diet is impacting one, it is likely that it is also impacting the other.

Between the effects that ketones can have on hormone levels and blood sugar levels we can see why the ketogenic diet may be a great choice for those interested in weight loss. But it turns out that there are even more reasons why ketosis may be an effective method. In a recent study (15), it was found that ketones may have the ability to interact with our brain through an additional mechanism to regulate our hunger levels! If you have read some of the previous articles on the physiology of ketosis, then you probably know that ketones are a produced as a result of increased fat oxidation in the liver due to energy and/or carbohydrate restriction. What most people do not know is that ketones can also be produced in the astrocytes of the hypothalamus. An astrocyte is a cell of the central nervous system that has a wide range of functions. Ketones produced by astrocytes come from the fat we get in our diet rather than the fat from our adipose tissue. Once these ketones are produced, they can be taken up by the neurons of the hypothalamus, which are energy-sensing neurons. Just as in normal ketone body metabolism, once taken in by these cells, ketones are used to produce energy. In a study conducted by Le Foll, it was found that this ATP (energy) production from ketones possessed the ability to override a protein referred to as CD36. To prevent this from getting too complicated, just know that CD36 acts as a fatty acid sensor for the hypothalamus. The overriding of this protein has been shown to lead to a short-term decrease in food intake. This suggests that a high fat diet can also control our food intake in the short term!

There are many other theories behind the satiating effect of a ketogenic diet that we did not touch on, such as its effect on other hormones as well as the gut microbiome. One of the biggest limitation to a ketogenic diet is that people often do not stick to the diet long enough to experience the changes in hunger. When we first begin fasting or restricting carbohydrates, our body produces something called adiponectin, which can stimulate increased food intake (16). However, following adherence to the low carb lifestyle, this subsides. The main take home is if you allow yourself to become adapted to the ketogenic diet, you are likely to experience positive changes in your appetite, which can allow for a much better overall lifestyle!

Keto Conclusions

  • Dieting typically leads to an increase in hunger during and after the diet.
  • Hunger is controlled by the interaction between hormones and the brain.
  • Standard dietary protocols often lead to impaired hormone function that causes our increase in hunger.
  • The ketogenic diet has been shown to ameliorate these hunger symptoms by suppressing hunger hormones.
  • Increased fat in the diet can allow ketones to be produced in the brain that can control hunger through additional mechanisms.
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References

  1. Mayer, J. (1955). Regulation of energy intake and the body weight: the glucostatic theory and the lipostatic hypothesis. Annals of the New York Academy of sciences, 63(1), 15-43.
  2. Doucet, E., Imbeault, P., St-Pierre, S., Almeras, N., Mauriege, P., Richard, D., & Tremblay, A. (2000). Appetite after weight loss by energy restriction and a low-fat diet-exercise follow-up. International journal of obesity, 24(7), 906-914.
  3. Sumithran, P., Prendergast, L. A., Delbridge, E., Purcell, K., Shulkes, A., Kriketos, A., & Proietto, J. (2011). Long-term persistence of hormonal adaptations to weight loss. New England Journal of Medicine, 365(17), 1597-1604.
  4. Schwartz, M. W., Peskind, E., Raskind, M., Boyko, E. J., & Porte, D. (1996). Cerebrospinal fluid leptin levels: relationship to plasma levels and to adiposity in humans. Nature medicine, 2(5), 589-593.
  5. Heymsfield, S. B., Greenberg, A. S., Fujioka, K., Dixon, R. M., Kushner, R., Hunt, T., ... & McCamish, M. (1999). Recombinant leptin for weight loss in obese and lean adults: a randomized, controlled, dose-escalation trial. Jama, 282(16), 1568-1575.
  6. McClernon, F. J., Yancy, W. S., Eberstein, J. A., Atkins, R. C., & Westman, E. C. (2007). The Effects of a Low‐Carbohydrate Ketogenic Diet and a Low‐Fat Diet on Mood, Hunger, and Other Self‐Reported Symptoms. Obesity, 15(1), 182-182.
  7. Johnstone, A. M., Horgan, G. W., Murison, S. D., Bremner, D. M., & Lobley, G. E. (2008). Effects of a high-protein ketogenic diet on hunger, appetite, and weight loss in obese men feeding ad libitum. The American journal of clinical nutrition, 87(1), 44-55.
  8. Yancy, W. S., Olsen, M. K., Guyton, J. R., Bakst, R. P., & Westman, E. C. (2004). A low-carbohydrate, ketogenic diet versus a low-fat diet to treat obesity and hyperlipidemiaA randomized, controlled trial. Annals of internal medicine, 140(10), 769-777.
  9. Brehm, B. J., Seeley, R. J., Daniels, S. R., & D’alessio, D. A. (2003). A randomized trial comparing a very low carbohydrate diet and a calorie-restricted low fat diet on body weight and cardiovascular risk factors in healthy women. The Journal of Clinical Endocrinology & Metabolism, 88(4), 1617-1623.
  10. Boden, G., Sargrad, K., Homko, C., Mozzoli, M., & Stein, T. P. (2005). Effect of a low-carbohydrate diet on appetite, blood glucose levels, and insulin resistance in obese patients with type 2 diabetes. Annals of internal medicine, 142(6), 403-411.
  11. Shai I, Schwarzfuchs D, Henkin Y, Shahar DR, Witkow S, Greenberg I et al. Weight loss with a low-carbohydrate, mediterranean, or low-fat diet. N Engl J Med 2008; 359: 229–241.
  12. Asher, R. C., Burrows, T. L., & Collins, C. E. (2013). Very low‐energy diets for weight loss in adults: A review. Nutrition & Dietetics, 70(2), 101-112.
  13. Sumithran, P., Prendergast, L. A., Delbridge, E., Purcell, K., Shulkes, A., Kriketos, A., & Proietto, J. (2013). Ketosis and appetite-mediating nutrients and hormones after weight loss. European journal of clinical nutrition, 67(7), 759-764.
  14. Ratliff, J., Mutungi, G., Puglisi, M. J., Volek, J. S., & Fernandez, M. L. (2009). Carbohydrate restriction (with or without additional dietary cholesterol provided by eggs) reduces insulin resistance and plasma leptin without modifying appetite hormones in adult men. Nutrition research, 29(4), 262-268.
  15. Le Foll, C., & Levin, B. E. (2016). Fatty acid-induced astrocyte ketone production and the control of food intake. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 310(11), R1186-R1192.
  16. Valassi, E., Scacchi, M., & Cavagnini, F. (2008). Neuroendocrine control of food intake. Nutrition, Metabolism and Cardiovascular Diseases, 18(2), 158-168.