The taste of food is sensed by taste receptors on the tongue and the information is then passed on to the brain. Brala and Hagan (1983) found that sweet flavours made people feel hungrier and made them eat more. Rats were found to press bars to receive saccharin which is sweet but non-nutritious and over eat sugary foods if they are available to them (Morgan, 1965). Rolls et al. (1981) showed that people would eat a larger meal if more than one type of sandwich filling were available rather than only one.
The stomach was thought to contract when empty and when the stomach expands it is full and therefore the feeling of hunger disappears. Canon and Washburn (1912) tested this theory. Washburn swallowed a balloon that could be inflated inside his stomach. He recorded his hungry feeling and found that when the balloon was expanded the feelings of hunger disappeared. Morgan and Morgan (1940) and Grossman and Stein (1948) all found that hunger can still be felt when the vagus nerve has been cut. The vagus nerve is the nerve that carries impulses from the stomach/gastrointestinal tract to the brain. Signals from the gut to the brain can be sent via the circulatory system. People have also been found to still experience hunger even when the stomach has been removed (Janovitz, 1967). Cutting the conections between the gastrointestinal tract and the brain has little or no effect on food intake in both humans and non-humans (Pinel, 1993).
The brain, part of the central nervous system, is involved in the regulation of food and therefore feelings of hunger. The ventromedial hypothalamus has been found to function as an ‘off’ switch to tell us when to stop eating. Animals with damage to this area have been found to overeat and become obese, sometimes tripling their body weight (Hetherington and Ranson, 1940). Olds (1958) stimulated the ventromedial hypothalamus with electrodes and found that this decreased eating. When the animal is full then the VMH sends impulses to say that it is time to stop eating, if the VMH is destroyed then the signal is not sent and the animal does not stop eating therefore becoming obese.
The lateral hypothalamus is seen as the opposite, an ‘on’ switch. Animals who have damage to that area do not receive the signal to start eating and so they don’t and consequently starve to death (Anand and Brobeck, 1951). Hess 91954) found that stimulating this area caused the animal to eat compulsively.
The Glucostatic hypothesis says that the levels of glucose in the bloodstream determine how hungry we are. Neurons detect the level of glucose in the body, they are situated in the hypothalamus, the blood vessels and other organs. If the glucose level in the body drops and no more food is available then the liver releases more (this is stored in the liver in the form of glycogen). Louis-Sylvestre Le Magnen, (1980) found this when he studied rats. He found that blood glucose levels in rats fell by 6-8% before the start of a meal. A few minutes later the levels rose and another meal was not eaten until the levels began to fall again. Campfield et al. (1985) found that if glucose was injected into a rat before a meal than the meal was postponed.
The Lipostatic hypothesis (Nisbett, 1972) states that the body monitors food intake by detecting how much fat (lipid) there is in the blood. Everyone has a set body weight that they can not stray very far from. It has been shown that as the proportion of fats in the body decreases, hunger increases (Hoebel and Teitelbaum, 1966). According to Keesey (1966) when the body fat gets too low people start to eat and when it gets too high they stop eating. It has been proposed that the set point weight is determined at or soon after birth by the number of fat cells in the body. Weight is changed by the size of the fat cells. This hypothesis suggests that damage to the hypothalamus can indirectly shifty the body’s set point. Damage to the VMH move the point upwards so that they overeat and damage to the LH lower the set point so that the animal eats less and eventually nothing.
The glucostatic theory has some problems. Grossman and Grossman (1963) found that damage to other areas of the brain, not the hypothalamus, could also affect eating behaviour in animals. This suggests that there is more to regulating the hunger mechanism than just monitoring the levels of glucose in the blood. Carlson (1988) found that an animal that eats a meal low in carbohydrates but high in fats and protein still eats the same number of calories but the blood glucose levels drop. Therefore eating cannot be controlled solely by the blood glucose levels, if it was then the animal would be fat because it would overeat. Diabetics have high levels of blood glucose but they still experience hunger. It is therefore unlikely that the change in blood glucose levels are large enough and regular enough to explain eating behaviour fully.
The lipostatic and set point theory hypothesis has little evidence to support it. This study showed us that rats with VMH lesions and obese humans have similarities. Obese humans are not highly motivated to eat as would be expected. Teitelbaum (1955) suggests that the result of VMH lesions are to make the rat more sensitive to taste and smell and less responsive to the feelings of hunger. In obese humans it has been found that they pay less attention to hunger and eat according to availability of food and taste (Schachter et al. 1968). Obese humans are far less willing to find or prepare food in some way. Schachter (1971) put two groups in two rooms, an obese group and a control group. They both had equal numbers of shelled and unshelled nuts. The control group ate equal amounts of shelled and unshelled nuts, the obese group ignored the unshelled and ate only the shelled nuts.
Rats with LH damage have been able to be coaxed into eating and although they do not show any interest in food, they do not show interest in anything (Teitelbaum and Epstein, 1962). Therefore the idea of the LH being the ‘on’ switch is a little too simple and is a much more complex interaction of several systems together.
The nervous system’s involvement in the regulation of hunger is a little doubtful. The theories above have supporting and contradictory evidence. The ‘on/off’ model of the control of the hypothalamus is said to be too simple to control such a complicated and important mechanism in the body. There is evidently more to hunger than Canon and Washburn’s empty and full stomach hypothesis. The glucostatic theory leaves some questions unanswered and there are definite problems. The theories alone don’t seem to explain the complex mechanism of hunger control and regulation but an interaction of all of the theories may be a little closer to what really happens.
