What is the debate?
It is questionable whether neural mechanisms are sufficient in themselves to explain human eating behaviour.
Outline the Dual Centre Model
According to the Dual Centre Model of eating, there are two neural mechanisms responsible for eating behaviour/ The lateral hypothalamus is thought to be responsible for feelings of hunger and the ventromedial hypothalamus is thought to be responsible for feelings of satiation. Together they work to maintain energy homeostasis. Neuropeptide Y (NPY) is a protein produced by the arcuate nucleus of the hypothalamus. When deprived of food, levels of NPY increase, signalling feelings of hunger in the lateral hypothalamus. Ghrelin is a hormone secreted from the stomach at it empties. The amount of ghrelin release is directly proportional to the emptiness of the stomach. Therefore, as time passes from our last meal, ghrelin levels increase, signalling feelings of hunger in the lateral hypothalamus. Cholecystokinin (CCK) is a gut peptide which is secreted from the duodenum when food passes from the stomach into the small intestine. Whilst it is responsible for the digestion of fat and protein, CCK also signals satiety in the ventromedial hypothalamus. Leptin is a hormone released by specialised fat cells in the bloodstream, called adipocytes. After eating, leptin levels reach their lipostatic set point (an individual threshold indicating energy homeostasis), which signals satiety in the ventromedial hypothalamus.
Evidence to support DCM
Strong evidence to support the role of biological factors in eating behaviour comes from Lashley, who found that damage to the rats lateral hypothalamus cause aphagia (loss of feeding behaviour) and damage to the ventromedial hypothalamus caused hyperphagia (increased feeding behaviour). This shows that there are two centres that control eating behaviour, the lateral hypothalamus causes feelings of hunger and the ventromedial hypothalamus caused feelings of satiation.
Evidence to support NPY
Strong evidence for the role of Neuropeptide Y comes from Lee and Stanley, who found that micro injections into the lateral hypothalamus with Neuropeptide Y caused hyperphagia in animals and repeated injections lead to severe obesity. This shows that NPY signals feelings of hunger in the lateral hypothalamus, however, too much of this protein can cause us to over eat because of excessive feelings of hunger.
Give evidence for Ghrelin
Weak evidence to support the role of Ghrelin in the lateral hypothalamus comes from Cummings, who found that Ghrelin levels fell immediately after eating (reading lowest after 70 minutes), but then rose steadily until participants reported they were hunger. Five out of six participants' ghrelin levels were strongly positively correlated with feelings of hunger. Cummings also found that injections of ghrelin increase food intake and body weight in humans and animals. This shows that ghrelin levels increase as the stomach empties, signalling feelings of hunger in the lateral hypothalamus and without it we wouldn’t feel hungry, but too much of the hormone, food intake increases as we wouldn’t feel full.
Give evidence for CCK
Strong evidence to support the role of CCK in the ventromedial hypothalamus comes from Smith, who found that injections of CCK caused a reduction in meal size in animals and humans. This shows that the addition of CCK causes a stronger signal to the ventromedial hypothalamus for satiety and therefore we feel full much quicker Further strong evidence to support the role of CCK in the ventromedial hypothalamus comes from Smith, who found that animals with a genetic mutation that eliminates their CCK became obese. This shows that the removal of CCK causes no signal to the ventromedial hypothalamus and therefore we will not feel full.
Give evidence for leptin
Convincing evidence to support the role of Leptin in the ventromedial hypothalamus comes from Carlson, who found that mice with a genetic deficiency showed hyperphagia (excessive eating) causing them to be obese. He also found that when given regular Leptin injections the mice began to eat normally again until their weight returned to normal. This shows that when leptin levels reach their lipostatic set point it signals satiety in the ventromedial hypothalamus so we stop eating, therefore without we wouldn’t receive those signals and would over eat.
Give a criticism of neural mechanisms
Being from the biological approach neural mechanisms in eating behaviour can be criticised for being simplistic because they propose a purely biological cause for hunger, which ignores psychological hunger (where the individual thinks that need food, even though it is not biologically necessary). In this way the biological approach ignores the environmental cues which still stimulate the lateral hypothalamus to make us feel hungry, such as stress, the availability of rich foods, of the smell of food, all of which have been shown to stimulate hunger in the lateral hypothalamus.
What is the conclusion?
Whilst it is clear that neural mechanisms are fundamental in the control of eating behaviour, it is clear that the biological approach is not sufficient in itself to explain eating because it ignores a range of environmental influences of our eating behaviour.