Why am I so hungry?

 We’re going to go all sciency on you today, and discuss appetite in more detail than ‘I WANT CAKE.’


Appetite can be described as the drive or signalling system to eat and provide nourishment and energy for the body. Feeling satisfied by the food we eat has two distinct descriptors, satiation and satiety. Satiation is regarded as the complex processes that bring the act of eating to a halt, while satiety is the suppression of hunger and a maintained inhibition to eating for some time following consumption of food.


Appetite in the international textbook of obesity Blundell(2001) states that:


‘There are many reasons to believe that an adjustment to the expression of appetite is the best chance we have to prevent the persistent surfeit of energy consumed over energy expended which is currently characterising much of the world’s population.’


Whether we agree or not with the hypothesis of calories in-calories out, it is an interesting point that appetite controls our food intake & perhaps the main reason people do have a more extensive food intake due to constant or unsatisfied hunger.


The nervous system stimulates our eating behaviours. 


But if we choose to eat foods that boost blood sugar enormously, are laden with powerful flavour enhancers or stimulate our taste buds with generous levels of salt then our choices will further stimulate strong physical responses that the nervous system becomes accustomed to.


This, in turn, will increase the neural drive to return and eat those foods. If we eat low quality, calorie-dense, additive ridden food too often, it soon becomes our preference. 

We may even develop addictive behaviours because of the nerve pathways that are stimulated in the mesolimbic region of the brain, our neural reward centre.


Appetite or hunger provides a strong urge to eat that can be difficult to ignore. The body has developed tight regulatory systems to ensure we are driven to eat the necessary food to ensure survival.


Any attempt made to ignore appetite signals initially seem relatively easy, but as time passes the stimuli become stronger, and the need to eat increases to the point that almost any food will do providing the need can be satisfied. One of these drives to eat is our need to obtain energy to maintain physiological integrity.


This is often observed when hunger has reached a heightened intensity, and the resulting food characteristics often sought are sweet or fatty foods.



Appetite Control and Mechanisms


More than 24 hormones and gut peptides regulate hunger and appetite.


40 known neural receptor sites signal hunger or satiety


Neural stimuli trigger our behaviours & actions.


Each action, in turn, stimulates neurochemical responses which can drive our future behaviour and choices.


Food can stimulate addictive, food-driven behaviours. Therefore if we consider both those choices, we know food can encourage addictive food drive behaviours, because our brain starts to crave these neurochemicals to stimulate specific actions towards certain foods.


The need for energy is often cited as one of the main reasons that we develop hunger or appetite. Yet, despite this, some experts have said that diets with a low energy density are associated with higher levels of satiety (Bray & Popkin, 1998). Energy cannot be the only stimulus of appetite and hunger. Alongside the need for energy, science has identified a hormone involved in appetite mechanics called ghrelin.







Ghrelin is a hormone secreted from the stomach to stimulate the appetite.


Concentrations in the blood are highest before eating and the lowest post-meal. Ghrelin appears to have the ability to adapt to expected meal times. Research looking into differences in ghrelin related to the length of time between meals found that people who habitually waited a shorter time between breakfast and lunch had a rise in ghrelin before the meal. In those who waited significantly longer, the increase in ghrelin followed a similar pattern before the meal despite the more considerable time.


Levels decrease with nutrient intake, not because of the distension of the stomach. As we eat and eat a nutrient-dense meal, ghrelin levels will drop because of the nutrition in that meal.


Ghrelin has an inverse relationship with BMI, indicating that in thin people, ghrelin drives a need to eat more and generate a positive energy balance.


Weight loss in overweight people will, in turn, increase ghrelin levels and elevate hunger which may be a reason why weight loss can be challenging to maintain.


This has been noticed in low-calorie diets, when they decrease their intake & bodyweight decrease they begin to increase their appetite, and this is why people can fail as their hunger drives them to go back to their regular eating habit or binging. It may well be that the effects of ghrelin during weight loss are one of the reasons for that binging attitude.




Perhaps the most well known of these satiating mechanisms is a protein called leptin. Leptin levels in the blood have been found to correlate very closely to the standards of stored body fat.


It has been found that leptin is released by adipose tissue when the internal environment favours storage of fats within the adipose tissue. Leptin also brings about some reduction in food intake and a net increase in metabolic rate.


So, when someone eats some food & that food pushes the body during a period when its fat-storing, it is only right for the body to send a message via leptin to the brain to decrease food intake & increase metabolic rate so that this energy can be utilised & we don’t eat in excess.


After this discovery, leptin went through a period of real scientific interest in the hope that it may provide a truly viable solution to obesity. This enthusiasm was a little pre-emptive as it turned out that leptin had a dual role.


More recent findings have determined that when leptin levels are low, this facilitates a drive to eat described as ‘voracious food-seeking’ (Blundell, 2001).


This would be brought about, for example, by low-calorie diets & lose weight quickly; leptin levels will drop soon. These low levels will register with the brain & stimulate appetite, increasing that drive to eat.


It seems, therefore, that leptin may not be the ‘holy grail’ for managing obesity it was once considered. Its main role is now thought to be one of modulating long term energy stores.



Peptide YY


Peptide YY belongs to a set of compounds from the neuropeptide Y family.


It has been found to reduce food intake by as much as 30% in humans the following infusion into the blood at levels similar to those generally experienced after meal ingestion (Druce et al., 2004). It appears that PYY inhibits appetite by acting to the centre of the brain.


PYY is released shortly after food intake and seems to be stimulated mostly by carbohydrates and fat intake, to provide a sensation of fullness and satiety.




A powerful gut peptide from the gut into the circulation and again influences the hypothalamus.


Oxm is released Infusion of Oxm into the blood of humans lowers free food intake by 19% while also keeping the total calorie intake of the next 12 hours at a lower level.


Oxm use as an aid against obesity is effective in lowering total food intake and even positively influencing activity levels in overweight individuals (Wynne et al., 2006).




CCK also influences the hypothalamus but affects other brain areas such as the hindbrain.


Concentrations of CCK appear to be highest in the duodenum and first portion of the small intestine. Levels rise gradually between 10 and 30 minutes following the initiation of a meal and can remain elevated for as long as 3 to 5 hours (Moran and Kinzig, 2004).


Dietary fat and protein appear to be the most potent stimulators of CCK with carbohydrates having a significantly smaller influence. CCK has been found to aid digestion by stimulating pancreatic secretions to assist in enzymatic digestion and in stimulating the release of bile from the gall bladder to emulsify fats.


It has also been found to inhibit gastric emptying and to modify the speed at which digested food, called chime, moves through the intestine. CCK also plays a significant role in satiation and therefore, has been found in numerous studies to reduce the amount of food ingested and the time until hunger and appetite occur again.




The control of appetite is a very complex process, regulated by a myriad of neural and endocrine mechanisms.


This article has only discussed a handful of the better-known mechanisms. The body has developed such complexity surrounding food intake to ensure that its needs are catered for, both in energy and nutrient requirements.


Once again, this seems to question the simplistic concept that being overweight is simply about being lazy and overeating. The body has an intricate system of regulating food intake and also causing satiety and food inhibition!


These mechanisms are so accurately tuned that a typical, healthy male eats over 900,000 calories per year, while females eat more than 730,000 calories per year. Yet, after 365 days, these average individuals can remain the same weight and be just as healthy.


To accept that the primary cause of obesity is excessive appetite would be suggesting that we can ignore or override numerous controlling systems tuned with intricate sensitivity to be able to maintain the status quo. It is much more likely that there are multiple underlying factors at work, not just an excessive appetite.


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