Neural mechanism in eating and satiation (24 marks)

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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.

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. Although the LH undoubtedly plays an important role in controlling eating behaviour, it may not be as previously thought the brain’s `eating centre’ (Sakurai et al. 1998).

Recent research on the role of neuropeptide Y (NPY) has also cast doubt on whether its normal function is to influence feeding behaviour. Marie et al genetically manipulated mice so that they did not make NPY. They found no subsequent decrease in their feeding behaviour. The researchers suggest that the hunger stimulated by injections of NPY may actually be an experimental artefact, in that the flood of NPY during experimental manipulations could cause behaviour not like that caused by normal amounts of the neurotransmitter.

The homeostatic explanation does not take individual differences into account. Biological mechanisms may not work in the same way in every individual. Horvarth (2005) suggests that every individual has their own set point (balance between hunger and satiety) as a result of genetic factors and early nutritional experience. Also hunger and eating may not be under purely neural control. Recent research in Texas (Lutter et al. 2008) has shown that the body produces extra quantities of the hormone ghrelin in response to stress. This is part of the body’s natural defence against stress as it reduces depressive and anxious behaviours. However ghrelin boosts appetite- leading to increased comfort eating. An application of this is of course that blocking the body’s
response to ghrelin may help those whose comfort eating has led to obesity.

A great deal of the research done on neural mechanisms has been done using rats which means it is difficult to extrapolate to humans. Rats do not have a functioning prefrontal cortex like humans do and this is what helps humans make judgements so it is difficult to say how far studies using animals can support the role of neural mechanisms in humans.

The neural explanation of eating and satiation is reductionist as it reduces our desire for food and our desire to stop eating down to mechanisms in the hypothalamus and neurotransmitters alone. There is plenty of evidence that there are social, cultural and psychological factors such as mood that affects our eating patterns and this explanation does not consider these. For example research into mood has shown that we crave junk food when feeling low (Garg et al.) Of course a positive side of this reductionism is that drug treatments may be developed to help those who over-eat. However, a more holistic view of our eating behaviours rather than one considering only nature rather than nurture must be preferable. The explanation is also biologically determinist and leaves no room for free will or personal choice – many people clearly eat above their required normal requirements whereas others are able to discipline themselves and this cannot be explained by the hypothalamus alone.

19/24 Grade A AQA A

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