Mechanism of hunger or hunger motivation

1.3. Mechanism of hunger  or hunger motivation


1.Gastric Contractions

In 1912, Walter Cannon and A. L. Washburn conducted an experiment that revealed a close association between stomach contractions and hunger. Thus, it was proposed that hunger motivation is activated by the experience of stomach contractions. When the stomach is empty, contractions occur, these contractions are sensed by the organism and act as a signal that drives the organism to seek food. This finding was confirmed in subsequent experiments with other volunteers. Thus researchers began to believe that gastric activity was the basis for hunger.

However, later experiments showed that people report feeling hungry even after the nerves of the stomach had been severed, or when the stomach was entirely removed!!!


2.Blood Nutrient Levels

Most researchers today believe that levels of nutrients dissolved in the blood, or the rate at which they are used, activates hunger motivation.The homeostatic system of the body is believed to constantly strive to maintain the level of nutrients and the rate at which they are used, within certain limits.

Set Point: The system wherein weight is maintained when no effort is made to gain or lose weight. If the levels of nutrients or rate of use fall below the set-point, hunger drive is activated. When food is consumed, the blood levels of nutrients come back to the set-point level.

Three chemical substances are important in hunger motivation –

1) Glucose– Glucose is an important factor in hunger, probably because the brain is critically dependent on sugar for energy. One set of sugar receptors, located in the brain itself, triggers hunger when sugar levels fall too low. Another set of sugar receptors is in the liver, which stores excess sugar and releases it into the blood when needed. The sugar receptors in the liver signal the brain when its sugar supply falls, and this signal also can make you hungry.

2) Insulin-Insulin causes excess sugar in the blood to be stored in cells as fats and carbohydrates.  Insulin injections cause profound hunger because they lower blood sugar drastically.  Psychologist Judith Rodin has pointed out that, when we eat complex carbohydrates, such as cereals, bread, and pasta, insulin levels go up but then fall off gradually.  When we consume simple sugars such as candy bars and sweetened beverages, insulin levels rise and then fall off sharply. The consequence is that we are more likely to eat within the next several hours after eating simple sugars than after eating complex carbohydrates. And the food we eat at one meal often influences how much we will eat at our next meal. Thus consuming doughnuts and candy bars, which provide no nutritional value, sets up an ongoing sequence of what and how much we probably will crave the next time we eat.

3) Leptin– Leptin, a protein that is released by fat cells, decreases food intake and increases energy expenditure (Mito & others, 2004; Oberbauer & others, 2001).  The role of leptin in long-term satiety was discovered in a strain of ob mice, genetically obese mice (Campfield & others, 1995; Carlson, 2001). The ob mouse has a low metabolism, overeats, and gets extremely fat. Because of a genetic mutation, the fat cells of ob mice cannot produce leptin.  Leptin strongly affects metabolism and eating, acting as an antiobesity hormone (Misra & others, 2001).


3.Neurobiology of Hunger Motivation

The activity in two areas of the hypothalamus contributes to our understanding of hunger – lateral & ventromedial hypothalamus.  The lateral hypothalamus is involved in stimulating eating.  When it is electrically stimulated in a well-fed animal, the animal begins to eat.  And if this area of the hypothalamus is destroyed, even a starving animal will show no interest in food!

The ventromedial hypothalamus is involved in reducing hunger and restricting eating.  When this area of an animal’s brain is stimulated, the animal stops eating. When the area is destroyed, the animal eats profusely and quickly becomes obese (two to three times that of normal rats). There was an initial spurt of weight gain in these rats, after which they maintained their weight at a new point.

Some researchers are however challenging the role of these parts of the hypothalamus in hunger motivation.

    1. Firstly, other brain areas like the amygdala are more important in hunger and eating behavior.
    2. Secondly, the LH and VMH effects on eating are (wholly or at least partially) due to what happens in the nerve-fiber pathways which pass through the LH the VMH. Some researchers are however challenging the role of these parts of the hypothalamus hunger motivation.
    3. Thirdly, at least some of the effects of the LH lesions may be due to lowered levels of overall arousal and general neglect of sensory inputs (especially inputs from food); rather than lowering of hunger motivation specifically.


Current Position:

The current view is that the hypothalamus centres may be involved in –

    • monitoring the body’s nutrition supply
    • controlling metabolism &
    • perception of food-related stimuli

Thus, the LH and VMH lesions change the set-point around which the weight is regulated (LH lesions may lower the set-point, whereas VMH lesions may raise it).


Psycho-Social Factors Affecting Hunger Motivation

  • Taste, sight of food, color, presentation, ambience, health, mood-state, etc. influence hunger motivation especially in human beings.


Cessation of Eating – Satiety

Restoration of nutrient levels after consuming food takes hours. However, we stop eating long before this restoration occurs.

Experiments have suggested two mechanisms by which satiation may occur –

    1. Experiments have shown that the  stomach contains nutrient receptors which provide satiety and signal the organism to stop eating.
    2. Another signal may be provided by the hormone ‘cholecystokinin’ (CCK).


When injection of ‘Cholecystokinin’ (CCK) was administered to food-deprived rats who are eating, the rats stopped eating and started grooming and other behaviors that are characteristic of experience of satiety.

The neurotransmitter serotonin is partly responsible for the satiating effect of CCK, and serotonin antagonists have been used to treat obesity in humans.

Neural circuits involved in the action of such drugs may be in the brain stem, as well as the hypothalamus. The neural circuitry also extends to the cerebral cortex, where humans make decisions about whether to eat or not to eat.

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