Neural mechanisms in eating behaviour

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Discuss the role of neural mechanisms in eating and satiation (24 Marks)
Homeostatic mechanisms maintain a consistent natural environment for the body. Thus
food intake is regulated to maintain normal levels and a set weight for individuals. The body
has evolved two separate systems, one for turning on eating and one for turning it off. A
decline in glucose levels in the blood activates a part of the brain called the Lateral
Hypothalamus, resulting in feelings of hunger. The Lateral Hypothalamus is known as the
`start' switch. A neurotransmitter found in the hypothalamus known as neuropeptide Y
(NPY) and may be particularly important in turning on eating. When injected into the
stomachs of rats this immediately causes them to eat even when full (Wickens 2000). As a
result of activation of the LH the individual searches for and consumes food. As a result
glucose levels rise again. The ventromedial hypothalamus (VMH) is now important for
turning off eating ­ this is the stop switch that activates feelings of satiation. A rise in
glucose activates the VMH, leading to feelings of satiation and inhibiting further eating.
Another area of the brain ­ the amygdala ­ may be responsible for neural control of the
cognitive factors relating to food- in particular how we select food on the basis of previous
experience ­ for example we walk past a curry house and feel hungry, even though we have
eaten. This is supported by Rolls and Rolls who found that surgically removing the amygdala
of rats would cause them to consume both familiar and novel foods indiscriminately
whereas untouched rats would initially avoid novel foods and consume only familiar foods.
There is considerable research evidence for the role of neural mechanisms in hunger and
satiety. Researchers have found for example that damage to the lateral hypothalamus in
rats caused a condition called aphagia (absence of eating). They also found that stimulation
of the LH results in feeding behaviour. Also, repeated injections of NPY into the
hypothalamus of rats produce obesity in just a few days ( Stanley et al. 1986). In contrast
researchers also discovered that damage to the VMH caused rats to overeat ­ hyperphagia.
Stimulation of the VMH led to feeding being inhibited. However, damage to the nerve fibres
passing through the VMH tends to also damage another area of the hypothalamus, the PVN
(Paraventricular Nucleus) and it is now believed that damage to the PVN alone could cause
hyperphagia (Gold 1973). The PVN also detects the specific foods our bodies need and may
be responsible for cravings. However more recent research has failed to replicate Gold's
studies, with most research showing that compared to lesions in other brain areas such as
the PVN, animals with VMH lesions ate substantially more and gained more weight.
There are limitations of the homeostatic explanation. For the hunger mechanism to be
adaptive it must anticipate and prevent deficits in energy, rather than just react to them.
This mechanism would work only where resources are constantly in supply­ in times of
famine people would need to overeat to survive. For homeostasis to be adaptive it must
promote consumption that maintains bodily resources well above the optimal level to act as
a buffer against future lack of food availability.

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The view that the LH served as an on switch for eating turned out to also be problematic.
Damage to the LH causes deficits to other aspects of behaviour ­ not just eating. Ghrelin
and libido for example may also be affected. Also more recent research has shown that
eating behaviour is controlled by neural circuits that run throughout the brain, and not just
by hypothalamus.…read more

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Grade A AQA A…read more


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