- Created by: Mindy Dhanda
- Created on: 23-02-15 15:58
Biological explanations of eating behaviour
Neural mechanisms :Neurotransmitters,hormones, brain structures.
Research into neural mechanisms involved in controlling eating behaviour has been carried out on animals based on the principle that their neural systems are similar to those of humans.
Research has suggested that the hypothalamus plays a key role in controlling eating behaviour. Much research has used precise methods of studying the brain, in particular the hypothalamus to determine its role in eating.
Lesion: When a small inscision or cut is made to certain areas of the brain in order to see the effects of that brain area.
Stimulation: Where an electrical impulse is sent through the brain to temporarily increase activity.
The hypothalamus has been identified as a key brain area involved in controlling eatinf behaviour and is often referred to as the 'hunger centre' of the brain. It has been suggested that the hypothalamus acts like a 'thermostat' to initiate or stop eating. Different parts of the hypothalamus have been identified as being responsible for different aspects of eating behaviour.
Dual- control theory of eating behaviour (homeostatic view of hunger and satiety)- According to the dual control theory of eating behaviour when blood glucose levels are decreased the lateral hypothalamus is activated.When this happens an individual is likely to experience feelings of hunger and so therefore will start eating is response to this hunger. Eating will result in an increase of blood glucose levels which will then activate the ventromedial hypothalamus. As a result of this activation an individual will experience satiety and will stop eating.
Set Point theory of eating behaviour suggests that the LH and VMH function in response to a set point. i.e. biologically- determined. The hypothalamic systems work together to maintain a reasonably constant level of satiety by switching on and off eating behaviour appropriately.This info regarding satiation comes from changes in blood glucose levels.Therefore food intake and weight control are the result of a balance between these two groups of the hypathalamus.
The role of the stomach in eating behaviour ...
Supporting the role of the hypothalamus in eating behaviour - When you eat food arrives in the stomach
It is broken down by digestive enzymes into nutrients, Key nutrient is glucose
glucose travels to cells as engery and to liver/fat cells
blood glucose levels monitored by sensors in the liver and hypothalamus
when blood glucose levels decrease:
1) liver converts stored nutrients back to glucose 2)LH activated = hunger and eating initiated
Liver and LH work together to increase blood glucose levels.
Lutter el al- suggestsed GHRELIN is an important hormone that indicates whether or not we are hungry. Ghrelin is produced and released by the stomach and travels to the LH. The LH has receptors for ghrelin and signals the body of hunger.Therefore when food is eaten the secretion of ghrelin stops.
Role of the Lateral hypathalamus
There is supporting research for the LH and the dual control theory of eating.
- Damage to the LH leads to undereating and weight loss, because the person no longer feels hungry and this loss of appetitie helps them to lose weight.
- Stimulation of LHproduces feels of hunger and initiates feeding behaviour.
Anand and Brobeck (1951) - rats with lesions to the LH showed aphagia and starved to death.
Quuade (1971) - successfully lesioned the LH of obese patients to reduce eating behaviour. If the LH was stimulated they reported feeling hungry.
- Damage to the LH causes deficits in other aspects of behaviour (e.g. thirst and temperature) not just hunger.
- Recent research has shown eating behaviour is controlled by neural circuits that run throughout the brain not just by the hypathalamus.
Neuropeptide Y (NPY) is a neurotransmitter found in the hypathalamus(LH). It has been suggested that it plays an improtant role in turnining on eating as increased levels promote increases in food intake and weight. When injected into the hypothalamus of rats, NPY causes them to immediately begin feeding (even when full) and produces obesity is just a few days. (Stanley et al 1986; Wickens 2000).
This can be seen as a potential treatment for anorexia.
AO2 The VMH
There is research to support the role of the ventromedial hypathalamus(VMH) and therefore the dual control theory, in initiating feelings of satiety and stopping eating.
Suggested that the VMH is the satiety centre of the brain, therefore responsible for turning off eating behaviour. Research has shown that lesions or tumours in the VMH lead to hyperphagia (overeating) and weight gain. Research has also shown that stimulation to the VMH inhibits eating.
Hetherington and Ranson (1942) - rats with lesions to the VMH would overeat until they became grossly fat.
Reeves and Plum (1969)- carried out a post mortem on a patient who had doubled her weight in two years and found a tumour on her VMH suggesting that this had impaired the sensation of satiety,
Evaluation of research into the VMH
- suggested that damage to the nerve fibres passing through the VMH tends to also damage another area of the hypothalamus called the paraventricular nucleus (PVN)
- It has been suggested that it is damage PVN alone that causes hyperphagia (Gold 1973)
- Gold (1973) found that lesions restricted to the VMH alone did not result in hyperphagia abd only resulted in overeating when they included other brain areas such as the PVN.
- However subsequent research has failed to replicate Gold's findings with most studies showing that, compared to lesions in other brain areas, animals with VMH lesions eat more and gain more weight.
The hormone leptin is secreted by fat tissue and travels via the bloodstream to the hypathalamus where it binds to certain receptors.Leptin acts to decrease food intake. Leptin also works opposite to ghrelin. The role of ghrelin is to send signals that the body is full, it also has specific roles in the regulation of energy expenditure and food intake.
Leptin and Obesity
Research with mice has shown that some mice receice two copies of the gene for obesity (ob).The ob/ob mice have a tendency to overeat, especially foods high in fat or sugar. Zhang et al (1994) discovered that ob/ob mice have defective genes for the protein leptin is normally produced by fat tissue and secreted into the bloodstream where it travels to the brain and to other tissues, causing fat loss and decreased appetite. In ob/ob mice this processs does not happen. Injecting ob/ob mice with leptin dramatically reduces the amount of food eaten and results in a decrease in body weight. Leptin treatment for obese human patients is still in its infancy but research in genetics has made it possible to identify a predisposition to obesity.
The strengths and weaknessess of leptin
Strenths of leptin research-
There are individuals who have a genetic leptin deficiency who are correlated with being obese
Humans are biological organisms and our eating behaviour relies on our biological systems. Insights into brain chemicals may be used to develop medical interventions to help change what we eat.
If it was this simple obese people could just be injected with leptin to reduce weight . However it is not the case that all obese people have low levels of leptin; some have normal or even high levels. It could be that for these people their brain mechanisms are failing to recognise leptin.
The biological approach is reductionist, focusing only on biological systems regulating food intake and body weight. It ignored psychological, cultural and social factors that can influence our eating behaviour.
The role of serotonin
It has a chamical influence on satiation(similar to leptin)
However increased activity of serotonin in the medial hypothalamus has been associated with decreased food intake. This suggests that it is not just VMH that plays a role in stopping eating but also the MH as well as chemicl influences.
Reductionist- Could be argued that dualo control theory is reductionist because it ignored the role of neurotransmitters in influencing eating behaviour such as serotonin and leptin. It oversimplifies a complex behaviour explaining it with one area of the brain. This criticism of the theory suggests that the theory is a weak theory to explain eating behaviours.