Binge Eating and Hormonal Regulation: Emotional Hunger

For our entire evolution, we were like any other species on this planet in constant search of food. We were not obese but in a state of constant hunger and constant physical activity. This was the case for all of our ancestor species and that means the time period of 50 million years.

Technological progress that happened in the last couple of hundreds of years didn’t change our body physiology. It is an abrupt shift in evolutional terms. The feeling of constant fullness, on the other hand, is not natural, and it is an example of maladaptation. Our hominin ancestors and even homo sapiens dint have technology and food on every corner. Hunger is a normal feeling and it is a normal feeling for every animal. Because of our evolutionary conditioning and the way our brain works, people even if we are on a restrictive diet cannot deal with the feeling of constant hunger. We want to have a feeling of fullness and there is nothing we can do about it. So here comes caffeine, hunger suppressors of different kinds and medicine and surgeries, and so on.

In an evolutionary sense, this is protective behavior, because there is an extreme scarcity of food, bingeing as much as we possibly can is a good survival strategy. But what happens when we have an overabundance of food and we never had that abundance during our entire existence including our direct ancestor species. Our evolution didn’t begin with the modern human species we have just become a little smarter. Most of our genes and the body are the same, especially in basic survival mechanisms that didn’t have to change for millions of years.

All of this would not have to be an issue but obesity is everything but a cosmetic issue. Most people do understand this but are unable to do anything about it because of fear of starvation. This fear is instinctive and it would override any logical behavior and in reality, we would always overeat. Weight gain comes slowly and in a prolonged period. Even if we gain just a little on a monthly basis, in time this little would be too much.

When an individual starts to have a restrictive diet the instinctive fear of starvation will have an impact on behavior and more than just in the psychological way. It will trigger different pathways in the brain that are responsible for appetite control, fear, reward mechanism (how much pleasure we get from pleasurable experiences), and most of our brain functioning. And this will not stop when we go off the diet but will continue as a never-ending story. It is a so-called “yo-yo” effect. Even since a Minnesota starvation experiment (Kelesidis et al., 2010) scientists have been aware of the full scope of effects that a restrictive diet can have on someone’s behavior.

The way that the brain works is by the “carrot and a stick” mechanism. Number one would be the avoidance of pain, and when pain is avoided pleasure-seeking comes into play.

The more pain the stronger behavioral changes. The problem is until the pain is removed the pleasure-seeking does not exist. For example, people in the Minnesota starvation experiment after a period of time couldn’t think of anything else except food. They could not take the pain of constant hunger. After they were given food the fear of starvation never went away and they were overeating and binging as much as they could and have become obese in a very short period. But this behavior exists just to a smaller extent in everyday “normal” behavior. The most normal feeling of hunger had become much more pronounced because today we cannot deal with hunger because we have never experienced the real level of starvation. That is the reason why most of us cannot really cope well with dieting because we do not have tolerance for pain anymore. And even if we do, the normal response of the brain will be to go into survival avoidance of pain mode and cut off all pleasure-seeking behavior until the hunger is removed. It is not possible to be in a state of hunger and enjoy life. Especially because now we are removed from our natural environment and we have supernormal stimuli everywhere. Even a normal feeling of hunger is something that we cannot take as a normal feeling anymore.

Our behavior has been conditioned in such a way that our brain has down-regulated its pleasure response. For example, this happens to heroin addicts. Heroin is one of the strongest drugs in existence. It gives a lot of pleasure. But in time addicts will become more tolerant of the effects of it to some extent because their brain adapts. The same thing has happened in our modern society. Our brain has to some extent adapted to supernormal stimuli from food and hunger has become a much more pronounced feeling than it would be in normal animal species. Because of lack of scarcity food is not as a big reward as it used to be especially because of unnaturally high concentrations and combinations of energy sources that do not exist in nature.

Extracted sugar and extracted fat do not exist in nature and it is digested much quicker than in normal circumstances from whole food sources giving us a dopamine high. Especially the combination of sugar and fat (Zhang et al., 2005). This combination does not exist in nature. Because of this dieting has become a form of addiction much more than it would be in a natural environment.

The result of this is that we have become obese and there is nothing we can do about it. Today nearly 70% of American adults are either overweight or obese.

Actually, even anorexia nervosa patients are victims of the same maladaptation. It is not a psychological issue it is conditioned behavior of pleasure and pain reward mechanisms. In anorexia patients, there is also malfunction but in the opposite direction. When they refeed themselves, their plasma leptin concentration will increase rapidly and reach roughly normal levels long before normal weight is achieved (Obradovic et al., 2021). Thus keeping them anorexic. They experience hunger much less than someone that does not have this condition. Excessive leptin production and its effect on the feeling of fullness could play a permissive role in the pathogenesis of this condition.

Leptin is the satiety hormone, and it is opposed by the actions of another hormone named ghrelin, the hunger hormone. Both hormones act on the receptors in the brain to regulate appetite (Zhang et al., 2017). When people think that their conscious mind will have an impact on their behavior I always asked them to do an experiment and try to keep their breath. After a minute or so there will be pain singling and the unconscious part of the brain will override our behavior. The signal is due to the fact that the brain is dying and no matter what, you have to take oxygen in or die. We will gasp for breath no matter how strongly we resist. This is a reason that someone can drown in 20 seconds if panic kicks in. The same behavior changes affect our day-to-day behavior in regard to the water we drink, the air we breathe and the food we eat.

The balance of these two hormones is necessary to achieve an overall energy balance in the body. In obesity, a decreased sensitivity to leptin occurs (Anderberg et al., 2016). This is a big problem that will result in a brain’s inability to detect satiety despite high energy stores in the rest of the body. Why does this happen? The basis for leptin resistance in obese human subjects is unknown. If leptin levels remain persistently raised due to overeating, there may be a downregulation of the leptin receptors and hence decreased sensitivity to the hormone. In humans, and actually in any other animal low leptin levels induced by a low-calorie diet resulted in a decrease in plasma leptin concentration triggering high levels of constant hunger. This may explain the high failure rate of dieting. Low leptin levels are likely to be a powerful stimulus to weight gain.

In the case of obesity, the standard regulatory system will tell the brain that we have fat deposits stored for an extended period and that we can endure little hunger. The problem is that we could never become fat due to scarcity, so we never developed an adaptation to the abundance of food. Our mind still thinks that if we do not eat all that we can we will starve to death in the upcoming drought.

References:

1. Kelesidis, T., Kelesidis, I., Chou, S., & Mantzoros, C. S. (2010). Narrative review: the role of leptin in human physiology: emerging clinical applications. Annals of internal medicine, 152(2), 93–100. https://doi.org/10.7326/0003-4819-152-2-201001190-00008
2. Zhang, F., Chen, Y., Heiman, M., & Dimarchi, R. (2005). Leptin: structure, function and biology. Vitamins and hormones, 71, 345–372. https://doi.org/10.1016/S0083-6729(05)71012-8
3. Obradovic, M., Sudar-Milovanovic, E., Soskic, S., Essack, M., Arya, S., Stewart, A. J., Gojobori, T., & Isenovic, E. R. (2021). Leptin and Obesity: Role and Clinical Implication. Frontiers in endocrinology, 12, 585887. https://doi.org/10.3389/fendo.2021.585887
4. Zhang, Y., & Chua, S., Jr (2017). Leptin Function and Regulation. Comprehensive Physiology, 8(1), 351–369. https://doi.org/10.1002/cphy.c160041
5. Anderberg, R. H., Hansson, C., Fenander, M., Richard, J. E., Dickson, S. L., Nissbrandt, H., Bergquist, F., & Skibicka, K. P. (2016). The Stomach-Derived Hormone Ghrelin Increases Impulsive Behavior. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 41(5), 1199–1209. https://doi.org/10.1038/npp.2015.297
6. Kalm, L. M., & Semba, R. D. (2005). They starved so that others be better fed: remembering Ancel Keys and the Minnesota experiment. The Journal of nutrition, 135(6), 1347–1352. https://doi.org/10.1093/jn/135.6.1347
7. Tobey J. A. (1951). The Biology of Human Starvation. American Journal of Public Health and the Nations Health, 41(2), 236–237.[PubMed]
8. Howick, K., Griffin, B. T., Cryan, J. F., & Schellekens, H. (2017). From Belly to Brain: Targeting the Ghrelin Receptor in Appetite and Food Intake Regulation. International journal of molecular sciences, 18(2), 273. https://doi.org/10.3390/ijms18020273
9. Müller, M. J., Enderle, J., Pourhassan, M., Braun, W., Eggeling, B., Lagerpusch, M., Glüer, C. C., Kehayias, J. J., Kiosz, D., & Bosy-Westphal, A. (2015). Metabolic adaptation to caloric restriction and subsequent refeeding: the Minnesota Starvation Experiment revisited. The American journal of clinical nutrition, 102(4), 807–819. https://doi.org/10.3945/ajcn.115.109173
10. Dulloo A. G. (2021). Physiology of weight regain: Lessons from the classic Minnesota Starvation Experiment on human body composition regulation. Obesity reviews : an official journal of the International Association for the Study of Obesity, 22 Suppl 2, e13189. https://doi.org/10.1111/obr.13189
11. LASKER G. W. (1947). The effects of partial starvation on somatotype: an analysis of material from the Minnesota starving experiment. American journal of physical anthropology, 5(3), 323–341. https://doi.org/10.1002/ajpa.1330050305
12. Dulloo, A. G., Jacquet, J., & Girardier, L. (1996). Autoregulation of body composition during weight recovery in human: the Minnesota Experiment revisited. International journal of obesity and related metabolic disorders : journal of the International Association for the Study of Obesity, 20(5), 393–405.[PubMed]
13. Keys et al. (1950) “The Biology of Human Starvation (2 volumes)”. University of Minnesota Press.

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