Neural Mechanisms in Eating Behaviour - Building Block

This is another building block for the third topic in the Eating unit. I didn't feel as confident with this one when it came to the exam because the biological stuff can be quite difficult to grasp completely sometimes, but the studies are more memorable than the ones in the textbook and if I was given this question, I think I would have been okay :)

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Building block: Neural Mechanisms in Eating Behaviour
AO / IDA Content of paragraph
AO1 The body aims to keep its state constant and in balance by carefully
monitoring its processes.
Glucostatic Homeostasis is the process of adjusting and rebalancing in order to achieve
Hypothesis balance. EG. In order to keep body temperature at thirty seven degrees, the
(Homeostasis) body shivers and sweats.
In terms of eating, blood glucose levels must be maintained at a correct level,
and the depletion and repletion of glucose forms the basis of the glucostatic
hypothesis.
AO1 The model is cyclic and represents the prompts we receive to start and eating.
When we are hunger, we eat until our blood glucose rises. This activates the
Glucostatic ventromedial hypothalamus which signals satiation and causes us to stop
Hypothesis eating.
Model After a number of hours, the blood sugar begins to decrease and this
activates the lateral hypothalamus, triggering feelings of hunger so we start to
eat again.
AO2 When the lateral hypothalamus in rats is damaged, results in aphagia (absence
of eating) due to it recognising hunger and triggering eating.
Support from When damage to ventromedial hypothalamus, results in hyperphagia
Rats (overeating) as it triggers you to stop eating.
Shows the hypothalamus is involved in the control of eating.
AO2 Frayn ­ found that glucose levels remain fairly constant throughout the day in
healthy individuals.
Challenge Things like insulin and other homeostatic processes prevent glucose
fluctuation, as changes in glucose can be dangerous and affect brain function,
leading to a coma.
This challenges the glucostatic hypothesis.
AO2 Rozin et al. ­ gave two densely amnesic patients meals continuously.
Found amnesics will eat meals one after another without registering fullness.
Importance of Challenges the glucostatic hypothesis, as they would otherwise stop eating
Memory like `normal' people s they would feel hungry and full like everyone else due to
glucose.
IDA Glucostatic hypothesis is reductionist ­ it alone cannot account for the
control of meal initiation and termination.
Reductionism Other factors, like memory and learning, needs to be taken into account.
Breaking something complex down into something too simple.

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Building block: Hormonal Mechanisms in Eating Behaviour
AO1 Hormones are released into the blood and travel to the brain, where they
influence appetite.
Ghrelin and Ghrelin ­ has a short-term effect that encourages eating. This is produced by
Laptin the intestine and stimulates feelings of hunger.
Leptin ­ long-term influence that suppresses eating. Released by fat tissue
and travels to the hypothalamus, decreasing appetite and leading to fat loss.…read more

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