Discuss neural mechanisms involved in the control of eating behaviour. (8 marks + 16 marks)

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Discuss neural mechanisms involved in the control of eating behaviour.0
(8 marks + 16 marks)
Homeostasis is the biological process involving neural mechanisms that detect the state of the
environment inside the body and also correct it to restore that environment to its optimal state.
The body has evolved two homeostatic mechanisms to regulate food intake which are both
dependent on glucose levels.
Hunger increases as glucose levels decrease. This decline activates the lateral hypothalamus resulting
in feelings of hunger. This causes the individual to search for and consume food, causing glucose
levels to rise again. This then activates the ventromedial hypothalamus leading to feelings of
satiation and a cessation of feeding.
There are however limitations to a homeostatic explanation because for a homeostatic hunger
mechanism to be truly adaptive, it must anticipate and prevent energy deficits, rather than just react
to them- because our ancestors in the wild would never know when their next meal would come so
should be constantly on the lookout.
The claim that feelings of hunger and eating behaviour are only triggered when energy levels fall
below their optimal level is inconsistent with the harsh environment in which this mechanism would
have developed. A buffer against a lack of future food availability would have been necessary in such
circumstances, therefore the homeostatic theory is an incomplete explanation on its own.
Evolutionary theorists offer an alternative explanation. They propose that the primary influence for
hunger and eating is not homeostasis, but food's positive-incentive value, i.e. people eat because
they develop a taste for foods that promote their survival, such as a preference for meat high in
nutrients as opposed to low-nutrient foods such as grass.
However, this explanation doesn't necessarily apply to modern-day humans because humans would
otherwise choose to eat much healthily than they do (e.g. fruit and vegetables instead of fatty food),
therefore the evolutionary explanation is low in mundane realism because it doesn't apply to modern
humans.
Instead, the role of the hypothalamus is involved in the control of eating behaviour.
Research into the lateral hypothalamus (LH) found that damage to the LH in rats causes aphasia
(absence of eating), whilst stimulation of the LH elicits feeding behaviour. The opposing
consequences of the LH led researchers to conclude that they had discovered the `on' switch for
eating behaviour.
Stanley et al found a neurotransmitter in the LH called neuropeptide Y which is important in turning on
eating behaviour. When injected into the LH of rats it causes them to immediately start feeding, even
when satiated, and repeated injections of the neural mechanism caused obesity in rats in a few days.
However, refuting evidence comes from Marie et al who genetically manipulated mice so that they
did not produce the neurotransmitter, yet there was no subsequent decrease in their feeding
behaviour to suggest the neuropeptide Y is not linked to eating.
Though, Marie's research was on genetically manipulated mice that may not perform in the same way
once their biology has been modified, thus making her study low in internal validity which doesn't
support her research as refuting evidence. In addition, a mouse's anatomy is completely different to
the physiology of a human, therefore the conclusions drawn can't be generalised across species
making them low in external validity.

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Real world applications have arisen from the LH explanation because Yang et al found that
Neuropeptide Y is also produced by abdominal fat. This leads to a vicious cycle where the
neurotransmitter produced in the brain leads to more eating and the production of more fat cells,
which in turn leads to the production of more neurotransmitters.…read more

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