What causes it?
Energy intake and body weight (i.e. energy expenditure) is thought to be tightly regulated by the body and the nervous system, and should, theoretically, fluctuate only within a narrow range. The current epidemic of obesity and the rise in the Metabolic Syndrome, and other chronic diseases (e.g. type-2 diabetes, cardiovascular and neurodegenerative diseases) challenge this theory at its core.
One of the most apparent reason is the sheer availability of food all around us, day and night, let it be the fresh and shinny (waxed) fruits and vegetables neatly presented in the front of a grocery store, the delicious smell from a food outlet, or the convenience of affordable fast-food, which may override any regulatory processes we posses, made worse by, for example, a poster in the street or an ad on TV.
How curious it is that after watching an ad about popcorn, we feel like having a large bowl, when seconds earlier, we did not even think about food at all.
Is, then, hunger an adaptable and subjective feeling?
Throughout history, with only a few real periods of abundance, the human body has developed mechanisms to protect itself from energy deficits. This is why the body is so efficient in storing energy as fat rather than muscle (1 g of fat = 9 kcal, 1 g of protein = 4 kcal).
Our body has yet to develop a mechanism for excess consumption of food.
Many theories have, therefore, surfaced in the world of science.
In 1953, GC Kennedy developed the Lipostatic Theory: a theory that body fat is the key to regulate our eating pattern. When we eat, blood sugar level rise, then fall. From this point, free fatty acids are released by fat cells into the blood, asking the brain to stimulate hunger.
Another key role of fat cells in regulating hunger is by releasing leptin. The circulating leptin level serves as a gauge for energy reserves and directs the central nervous system to adjust food intake and energy expenditure accordingly. Leptin exerts immediate effects by acting on the brain to regulate appetite and metabolism. Higher level of Leptin in the blood triggers hunger and reduce energy expenditure.
Leptin also interacts with the dopamine system, which is involved in motivation for and reward of feeding, and parts of the brain to contribute to satiety (see illustration below).
Figure 1. Kelesidis, T. et al. (2010. p. 93).
Another theory, the Aminostatic Theory, suggests that the brain monitors amino acid levels in the blood. When levels are low the brain triggers the feeling of hunger.
Many amino acids are precursors of hormones or neurotransmitters, which include histamine and serotonin. Serotonin release (mainly produced in the gut) may help decrease food intake by communicating with the brain.
The issue here is that all chemically-synthesised protein found in our food today may not be recognised by the brain and may alter the feeling of satiety.
The Thermostatic Theory relies on the knowledge that digestion generates heat, especially the liver, and the increase in heat may inhibit further food intake.
Lastly, the Hepatostatic Theory accepts that the liver and its metabolic processes, during fasting states (between meals) are involved in the feeling of hunger.
An overwhelmed or overworked liver may prevent food intake, or force the body to reject food. This is the main reason why some people cannot physically have breakfast in the morning.
Toxins, the liver has to process assure their excretion out of the body, include: alcohol, pesticides and other insecticides residues present in our food, colouring, certain preservatives, prescription or recreative drugs, chemicals from the environment (car/plane fumes, cigarette smoke, and any other form of pollution), but also toxins generated by metabolic processes of the body itself.
Despite that there is not one common consensus on all these theories — or if these mechanisms are working together to control hunger —, they are all supported by a great amount of evidence; however, they all fail to explain why food intake varies greatly between two individuals of the same height and weight, and similar physical activity. This leads to suggest that there is not such a tight control after all between energy intake and body weight.
The composition of our food and drinks today, often refined and highly-processed, may play a role in satiety. Since most of the nutrients are missing, mostly removed or destroyed by the processing methods. This may lead to extended hunger phases and an increase in food intake (cravings ⇔ snacking).
Eating is also regulated by many complex interactions between hormones, the brain, each of our organs, and environmental factors, but also, and most importantly, by our emotions, which acts positively, or negatively, on our eating behaviours.
To conclude, it may be that when we feel hungry we are not and that when we should eat we do not feel hungry in the slightest. For example, having three set meal a day may be too difficult to control hunger and many people eat their lunch even though they do not feel they want to eat at that time. This acts on satiety and delayed hunger, leading to snacking on high-caloric foods, and stimulants, later on in the day.
Some people wish they never had to eat, when others feel they cannot stop eating. Some others binge on food and/or purge themselves in all the ways they know.
Some more feel they have complete control of their body and so dictate when they should eat and what they should eat. This also opens a window of understanding on the new growing wave of malnutrition in our Western part of the world.
Chronic, overwhelming stress, anxiety and depression are not only increasing causes for obesity but also malnutrition, contributing to the rise in most chronic metabolic diseases.
It may be that we should only eat when we are hungry, but, obviously, for many people this is not an advice to give, and so hunger — and feeding behaviour — is truly a personal thing.
Kelesidis, T. et al. (2010). Narrative Review: The Role of Leptin in Human Physiology: Emerging Clinical Applications. Annals of internal medicine. 152 (2), pp. 93–100. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2829242/pdf/nihms176732.pdf. Last accessed 14 September 2018
Drewnowski, A. (2003). The role of energy density. Lipids. 38 (2), pp. 109–115.
Korek, E. et al. (2013). Hormonal regulation of appetite. Medycyna Ogólna i Nauki o Zdrowiu (General Medicine and health Sciences). 19 (2), pp. 211–217.
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