One thing we all have in common is that we eat! And I am sure that most of us enjoy it too.
Although major energy deficits clearly increase hunger and eating, they are not a common factor in the eating behavior of people like us, who live in food replete societies. I will tell you which factors determine what we eat, influence when we eat, and how much we eat.
Factors that determine what we eat
Certain tastes have high positive incentive value for all members of a species. Most humans have a special fondness for sweet, fatty, and salty tastes. This taste preference is adaptive because in nature sweet and fatty tastes are typically characteristic of high-energy foods rich in vitamins and minerals, and salty tastes are characteristic of sodium rich foods. In contrast, bitter tastes, for which most humans have an aversion, are often associated with toxins. Each of us has the ability to also learn specific taste preferences and aversions. Humans and other animals learn what to eat from their conspecifics. In humans, many food preferences are culturally specific. For example, in some cultures, non toxic insects are considered a delicacy.
Animals select diets which provide all the vitamins and minerals they need. When an animal is deficient in sodium, it develops an immediate and compelling preference for the taste of sodium salt. When an animal is deficient in a certain vitamin or mineral other than sodium, it will learn to consume foods rich in the missing nutrient by experiencing their positive effects. Dietary deficiencies are prevalent in our society. One reason for this is manufacturers produce foods that have the tastes humans prefer but lack many of the nutrients needed to maintain health. The number of different substances consumed each day by most people in industrialised societies is immense, and this makes it difficult for their bodies to learn which foods are beneficial and which are not.
Factors that influence when we eat
The key to understanding hunger is to appreciate that eating meals stresses the body. Before a meal, the body’s energy reserves are in reasonable homeostatic balance; then, as a meal is consumed, there is a major homeostasis-disturbing influx of fuels into the bloodstream. The body does what it can to defend its homeostasis. At the first indication that a person will soon be eating, for example, when the usual mealtime approaches, the body enters the cephalic phase and takes steps to soften the impact of the impending homeostasis disturbing influx by releasing insulin into the blood and reducing blood glucose. The strong feelings of hunger experienced at mealtimes are not cries from your body for food, they are the sensations of your body’s preparations for the expected homeostasis disturbing meal. Mealtime hunger is caused by the expectation of food, not by an energy deficit.
In one experiment, rats were presented with six meals per day at irregular intervals, and the impending delivery of each meal was singled with a buzzer and light conditioned stimulus. This conditioning procedure was continued for 11 days. Throughout the ensuing test phase of the experiment, the food was continuously available. Despite the fact the subjects were never deprived during the test phase, the rats starter to eat each time the buzzer and light were presented, even if they had recently completed a meal. This Pavlovian conditioning experiment, provides strong support for the view that hunger is often caused by the expectation of food, not by a deficit in energy.
Factors that influence how much we eat
The motivational state that causes us to stop eating a meal when there is food remaining is satiety. Satiety mechanisms play a major role in determining how much we eat. Food in the gut and glucose entering the blood can induce satiety signals, which inhibit subsequent consumption. These signals depend on both volume and nutritive density (calories per unit volume) of the food.
Sham eating indicates that satiety signals from the gut or blood are not necessary to terminate a meal. In sham eating experiments, food is chewed and swallowed by the subjects, but rather than passing down the subject’s oesophagus into the stomach, it passes out of the body through an implanted tube. Because sham eating adds no energy to the body, set point theories predict that all sham eaten meals should be huge. But this is not the case. Satiety is a function of previous experience, not the current increases in the body’s resources. This is shown in sham meals eaten by rats, in which the first sham meal of rats sham eating their usual diet is the same size as previous normal meals. However, after the first few sham meals, rats begin to sham eat larger meals.
Small amounts of food consumed before a meal actually increase hunger rather than reduce it. This is the appetiser effect. Presumably, it occurs because the consumption of food is particularly effective in eliciting cephalic phase responses. Many experiments have shown that the amount of consumption is influenced by serving size. The larger the serving size, the more we tend to eat. Feelings of satiety also depend on whether we are eating alone or with others. People consume more when eating with others.
The number of different tastes available at each meal has a major effect on meal size. It appears that signals from taste receptors produce an immediate decline in the positive-incentive value of similar tastes and that signals associated with the post ingestive consequences of eating produce a general decrease in the positive incentive value of all foods. The phenomenon of sensor specific satiety has two adaptive consequences. First it encourages the consumption of a varied diet, If there was no sensory specific satiety a person would tend to eat his or her preferred food and nothing else, and the result would be malnutrition. Second, sensory specific satiety encourages animals that have access to a variety of foods to eat a lot. An animal that has eaten its fill of one food will often begin eating again if it encounters a different one. Therefore, animals are encouraged to take full advantage of times of abundance, which are all too rare in nature.
There has been an interest in the role of the hypothalamus in hunger and eating. This was stimulated by the discovery of hunger (increase appetite) and satiety (decrease appetite) peptides. Peptides are short chains of amino acids that can function as hormones and neurotransmitters. They are the chemicals released by the gastrointestinal tract and stomach which send signals to the brain. The sheer number of these peptides indicates that the neural system that controls eating likely reacts to many different signals, not just to one or two (e.g., not just to glucose and fat). Many of the hunger and satiety peptides have receptors in the hypothalamus, and this has renewed interest in the role of they hypothalamus in hunger and eating.
So, now you have an overview of some of what can influence eating, can you identify what influences you?