AQA PSYCHOLOGY PSYA3: Neural Mechanisms in Eating Behaviour (Hunger and Satiety)

AQA A PSYCHOLOGY PSYA3.  Full essay plan for the Neural Mechanisms section in the Eating Behaviour Topic. Enjoy! :)

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Preview of AQA PSYCHOLOGY PSYA3: Neural Mechanisms in Eating Behaviour (Hunger and Satiety)

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Eating Behaviour ­ Neural Mechanisms Essay Plan
AO1 THE DUAL CENTRE MODEL OF FEEDING
All humans and mammals are Homeostatic (run our bodies on a constant state of balance).
"Feeding centre" in the brain is activated when we are hungry
"Satiety centre" in the brain is activated when we are full
Hypothalamus monitors and regulates our blood glucose levels and eating behaviour.
Blood glucose levels fall or Ghrelin levels increase Lateral Hypothalamus activated feeling of
hunger and therefore eat
Blood glucose levels falls or ghrelin levels decrease Ventromedial hypothalamus activated
feeling of satiety and therefore stop eating
AO2
Heatherton and Ranson (1942)
SUPPORT Lesions to the Ventromedial hypothalamus caused rats to become obese compared
to a control group. Theory that the Satiety centre in the brain was destroyed which led to
uncontrollable eating and an inability to feel full.
PROBLEMS There was an initial increase in weight but then stabilised. Suggesting there may be
another factor contributing to satiety. Also, these rats were more finicky about the food they would
eat e.g. if it was stale not expected behaviour.
Also, cannot generalise the findings to humans. Humans have more complex brain functioning
which might react differently to lesions.
Anand and Brobeck (1951)
SUPPORT ­ Lesions were produced in the Lateral Hypothalamus of rats caused them to develop
aphagia (complete loss of feeding behaviour) ­ to the point of starvation despite the availability of
food.
PROBLEMS ­ However, if this area was destroyed on one side, normal feeding persisted. This
small hypothalamic area is so precisely located that even lesions as much as 0.5mm away from it
do not disturb feeding ­ suggesting that it cannot really be described as a feeding "centre".
Also, cannot generalise to humans (see above).
Reductionism
Ignores other approaches such as behavioural explanations and biological rhythms.
Simplifies Neurological mechanisms are more complex than just the dual centre
model.
Example Rats are more active and feed more just after darkness falls. This is
controlled by a different part of the hypothalamus Suprachiasmatic Nucleus.
This suggests feeding involves more than just the LH and VH.
AO1 ­ GHRELIN
A hormone released when the stomach is empty that signals the hypothalamus to start eating. The
amount released is directly proportional to the emptiness of the stomach.
Increasing time from last meal Increasing hunger Increasing hormone Ghrelin released.
Ghrelin = HUNGER SIGNAL

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AO2
Goldstone (2010)
SUPPORT Found that people who skipped breakfast (e.g. with higher levels of Ghrelin in their
system) crave highcalorie foods more than low calorie foods.
Study include 3 separate visits where they either, they ate breakfast + received a shot of Ghrelin,
fasted and received a shot of Ghrelin or ate break fast + received a shot of salt water. They were
then shown a slideshow of different foods.…read more

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