Neural mechanisms, eating and satiation

What parts of the brain are invovled in us getting hungry and studies

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Homeostasis (AO1)

The homeostasis is the control over the body, to maintain certain things within the body (the internal conditions). A negetive feedback loop is used to maintain the internal conditions. There are set points in the brain and any deviation in the body will trigger mechanisms in the brain (e.g. lack of food will initiate the feeling of hunger). The set points are adaptive from our evolutionary past, the weight of our body is regulated around these points. 

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Hypothalamus (AO1)

The hypothalamus is in the brain and controls the feelings of hunger and satiation. In the 1950s there was a simple model that controlled food intake. It was suggested that one section of the brain was turned on i.e the 'hunger centre' and another turned hunger 'off' i.e. a satiety centre. 

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Hormones - Ghrelin and CCK (AO1)

When we are hungry the body releases a hormone called Ghrelin. When we're hungry the hypothalumus will cause ghrelin in the stomach to be released. The proportion of ghrelin released depends on how hungry we are. 

As food is digested another hormone is released called cholecystokinin (just remember CCK, none of us are going to remember the full name...). CCK is the opposite to ghrelin and triggers the feeling of satiety, so we stop eating.

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Dual centre model

Research has found that damage to the lateral hypothalamus (LH) in rats results in aphagia (decreased feeding). The stimulation of the LH stimulates eating, it is therefore suggested that the LH is the 'on'  switch for feeding.

A more complex theory have been made, which involves a neurotransmitter in the LH, called Neuropeptide Y (NPY). When rats were injected with NPY, they began to feed immediately, even after satiation (Wickens (2000)) Within a few days of injecting NPY, the rats were obese (Stanley et al (1986)).

Damage to the ventromedial hypothalamus (VMH) caused rats to overeat, this ins a condition called hyperphalgia. Stimulation to the VMH inhibits feeding. Damage to a control of feeding causes increased feeding and body weight. It has been concluded that the VMH is the 'satiety centre' and stops feeding. 

Damage to nerve fibers passing the VMH also damages other parts of the hypothalamus. The paraventricular nucleus (PVN) is believed to cause hyperphalgia (Gold (1973))

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Dual centre model diagram

Decline in glucose levels and increase in ahrelin =

activation of the hypothalamus =

feeling of hunger =

eating occurs =

rise in glucose levels CCK secreted, adhrelin decreases =

feeling satiation (full) =

eating inhibits =

activation of ventromedial hypothalamus =

back to the beginning 

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Neural mechanisms AO2

Homeostatic limitations

To be adaptive, our hunger mechanisms need to anticipate and prevent energy deficits, not just react to them. So the theory that we only react when the level of food in our body falls below the preferred level does not fit. If the system is adaptive, then it must have a buffer level, to maintain a level of energy above the needed level. This would therefore provide a buffer in case of future food deficits. 

Lateral hypothalamus

The theory that the LH is a 'on switch' is questioned. Damage to the LH decreases thirst and sex drive as well as hunger. There has also been found that other parts of the brain control hunger, not just the hypothalamus, but the LH is a important part in our eating behavior, it is not the 'eating centre' (Sakurai et al (1998))

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Neural mechanisms AO2

Neuropeptide Y

t has now been questioned if the NPY is mainly to influence feeding. Marie et al (2005) genetically engineered mice to not produce NPY and found no decrease in feeding. It has therefore been suggested that the increased feeding when mice wee injected with NPY may have been due to conditions of the experiment, not as a result in the injection of NPY.

Supporting evidence for ghrelin

Cummings et al monitored participants ghrelin levels every 5 mins, participants were required to assess their hunger every 30 mins. 5/6 participants had a significant correlation between ghrelin levels and the emptiness of the stomach. 

AO3

This is real life application, however the sample was biased, only made up of men, which restricts generalisability. Participants hunger can also be influenced. 

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Issues, debates and approaches (AO3)

Reductionism

This approach reduces everything to brain functions and ignores cultural, social and psychological factors. 

Determinism

Emphasises everything on nature and ignores freewill. Physiological drives such as diets can be ignored.

 Lab experiments and ecological validity

The highly controlled lab experiments decrease ecological validity, therefore limits the ability to apply the findings to real life. 

Ethical issues and generalisability of findings

There is problems with experimenting on rats and generalising results from rats to humans.

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