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Discuss two or more ways in which eating and satiation are controlled by neural mechanisms. (24)
Homeostasis is one explanation of how neural mechanisms control eating and satiation. According to
homeostasis, when a person's blood glucose level is low, the lateral hypothalamus is activated. This
creates a feeling of hunger which then makes us eat in order to raise our blood glucose levels. Once
these levels are raised, the ventromedial hypothalamus is activated, which triggers a feeling of
satiety to stop us eating. The process is repeated when our blood glucose levels drop again.
However, this can be said to be a limited explanation of eating and satiety. If a system is adaptive, it
needs to be able to anticipate and prevent low energy levels, not merely respond to them. It is not
adaptive for this system to only activate when our blood glucose levels are low, as we would not
have the energy needed to get food to raise our glucose levels. Due to our EEA, the system would
not have evolved in this way as it does not promote survival.
Despite this, the lateral hypothalamus has been shown to have an effect on our eating and satiation.
When it is damaged, it can result in a condition known as aphagia- a lack of eating. Stimulation of the
lateral hypothalamus results in the need to eat. The conclusion that can be drawn from this is that the
lateral hypothalamus is the `on switch' for eating behaviour.
However it may not be the lateral hypothalamus alone which is responsible for our eating behaviour.
The neurotransmitter NPY (neuropeptide Y) has also been shown to be important in eating. Wickens
injected NPY into the hypothalamus of rats and found that they would immediately feed even when
full. Stanley et al also found that repeated injections of NPY could cause obesity in a matter of days.
This research suggests that NPY also contributes to our eating behaviour, not the lateral
hypothalamus alone. This is a weakness of homeostasis, as it shows that there are factors that have
been missed out.
This research has a generalisability issue in that it was conducted using rats, so the findings may not
necessarily be as accurate when applied to humans. However, the brain structure of rats is similar to
the brain structure of humans, so it is likely that the findings have some value for us. It is the most
ethical method of study, as it uses a creature which is close to humanity without having to use an
It has also been found that damage to the lateral hypothalamus causes problems with thirst and sex
as well as with hunger, suggesting that it is not exclusively important to eating behaviour and there is
another influencing factor. Eating behaviour is also controlled by neural circuits in the brain, not just by
the hypothalamus. Sakuri et al suggested that the role of the lateral hypothalamus is important, but it
is not the eating centre, as was previously thought.
Wickens' findings that NPY influences eating behaviour are not necessarily reflected by other
research. Marie at al genetically manipulated mice so that they could not produce NPY, and found
that there was no decrease in their feeding behaviour. Hunger as a result of an injection of NPY is an
experimental artefact- it causes unusual behaviour which may not be seen with normal levels of NPY.
This research suggests that NPY does not necessarily influence our eating behaviour; therefore
neural mechanisms may not be the only influencing factor. The biological approach may not be able to
fully explain our eating behaviour.
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It has been suggested that the ventromedial hypothalamus is the `off switch' for hunger. Damage to
it results in hyperphagia- over eating. Stimulation to it causes inhibited eating. However, the
ventromedial hypothalamus may not be the only thing that affects satiety. Gold found that damage
to the paraventricular nucleus alone also causes hyperphagia, supporting this idea. The PVN detects
food our body needs and is responsible for cravings. This is another weakness of homeostasis, as it is
another missed factor.…read more