The act of eating and drinking is innate, it is one of the few things we know how to do from the moment we are born. Eating is integral to life, and for most, this is obvious because if we don’t eat we die. Quite ironically though, it is the act of eating to excess that contributes to hundreds of thousands of deaths worldwide, a global issue that is in serious need of a fix. Whatever that ‘fix’ may be, isn’t going to come easy, but what I can do is shed some light on why the average Joe can eat and eat, and yet STILL feel hungry a few minutes after. Let’s look a little deeper…
The digestive tract
Everything we eat passes through the digestive tract (unless you have digestive issues), so it stands to reason that the digestive tract, or the gastrointestinal tract to use its technical name plays a significant role in appetite. The presence of food and drink in the digestive tract i.e. the stomach and intestine, can affect a person’s appetite via the physical space it occupies and the pressure it exerts. This is known as gastrointestinal distention, you know, that sometimes uncomfortable bloating you might feel after a large portion of carbs for example.
This leads onto a hormonal message
This physical message is then accompanied by a hormonal (chemical) message that signals the body to stop eating. The first hormone on the scene is cholecystokinin (CCK). CCK is released from the duodenum and jejunum within 15mins of consuming food and signals the body to STOP eating. The intestine has receptors in the lining of the walls that can recognise specific macronutrients (protein, carbs and fat), so it clearly has a part to play on satiety i.e. feeling full. Following on from CCK, the body releases other hormones such as glucagon-like-peptide-1 and 2 (GLPs) and glucose-dependant insulinotropic polypeptide (GIP). These are all believed to play a role in orchestrating the feeling of fullness, and are key to appetite control.
One of the most well- known appetite suppressing hormones is leptin, which since its discovery in 1994 has been at the forefront of weight loss investigations because of its ability to reduce food intake, body weight, and increase energy expenditure in both rodents and humans. A crude explanation is that people who are low in, or non- receptive to leptin become obese, whilst people who have higher levels of leptin are more likely to be slim. However (this is where it gets confusing), leptin is secreted by white fat cells, consequently people with higher levels of white fat are going to have higher levels of leptin, and yet remain overweight. The reason for this is something known as leptin sensitivity, in other words, these individuals have higher levels of leptin but it has little to no effect on their appetite.
Insulin is synonymous with blood sugar control, and to the general person, is usually associated with nothing more than diabetes. Yes insulin is an important factor in diabetes, but its function is more diverse than that. Insulin has a similar role to that of leptin but albeit to a slightly lesser degree. When we consume food or drink, the protein and carbohydrate present signals to the islets of langerhans in the pancreas to secrete insulin. Insulin then serves to act as a key that unlocks the muscle and bodily tissue so that it can absorb the nutrients for energy. Insulin is also thought to stimulate the synthesis and secretion of leptin from white fat cells via a process known as the adipo- insular axis, a process designed to control nutrient balance. This is orchestrated according to leptin levels, so the more leptin secreted leads to less insulin secreted which often results in reduced insulin sensitivity and increased fat mass. Being overweight can be somewhat of a vicious circle if not controlled, and one of the best ways of doing this is via the diet.
So why is my appetite stuck on repeat?
It could be for a number of reasons, but they usually all go back to the composition of one’s diet, and the amount of it they consume. The amount of carbs (for example) a person consumes can have profound effects on their appetite and weight. This is because of a chain reaction of hormonal shifts that include CCK, leptin and insulin, and the hunger promoting hormone ghrelin. Carbohydrates are not the villain, but the amounts we consume of the fast releasing sugary kinds can be. The problem with consuming too many sugary foods is that they are very easy to digest and absorb from the intestine, consequently CCK and insulin responses are very fast which in turn cause an aggressive attack on the sugar that enters your blood. The sugar in your blood is diverted to your muscles and bodily tissue to where it can be used for energy, but the problem with the abrupt removal of sugar from your blood is that blood sugar levels actually drop too low! This compensatory drop in blood sugar leads to a low feeling, and another compensatory release of the appetite stimulating hormone ghrelin. Ghrelin is important, however ghrelin levels stay elevated for longer than they should in the obese. So you see, in order to reduce unwanted hunger pangs you have to break the chain somewhere. Losing weight is very important, but it’s very difficult if you can’t get that appetite under control. One of the best ways to do it is to stick to complex carbs when you can, and if you have to consume simple, quick releasing carbs, then do so alongside or near to another meal that contains protein, fat and fibre to help regulate the otherwise aggressive hormonal response that follows refined, simple sugar.
If your hunger seems to be stuck on repeat then break the chain of events, starting with simple carbs. Minimise simple, refined carbs and stick to complex starchy carbs such as sweet potato and brown rice, and combine these with a high protein and moderate fat ratio. Breaking the chain will help you lose some weight initially, the weight loss will improve hormonal control, and the improved hormonal control will reduce hunger pangs and encourage a more efficient satiety mechanism.
Perry, B. and Wang, Y. (2012). Appetite regulation and weight control: the role of gut hormones. Nature. Retrieved 24th November, 2014, from http://www.nature.com/nutd/journal/v2/n1/full/nutd201121a.html
Kieffer, T, J. Habener, J, F. (2000). The adipoinsular axis: effects of leptin on pancreatic beta-cells. American Journal Physiology Endocrinology Metabolism. Retrieved 24th November, 2014, from http://www.ncbi.nlm.nih.gov/pubmed/10644531