Eating Behaviour PSYA3 Miss Bird

Biological explanations of eating behaviour AQA A Specification   Eating behaviour Factors influencing attitudes to food and eating behaviour. For example: cultural influences; psychological influences (mood); and social influences (health concerns/media). Explanations for the success and failure of dieting. Biological explanations of eating behaviour Neural mechanisms involved in controlling eating behaviour. Evolutionary explanations of food preference. Eating disorders In relation to either anorexia nervosa or bulimia nervosa: Psychological explanations. Biological explanations, including neural and evolutionary explanations.

Neural mechanisms in eating behaviour (biological) What are neural mechanisms? Different brain components (neurons, neurotransmitters, hormones and brain regions). We are going to look at the influence of these different brain components on eating behaviour.

Research into neural mechanisms Much research into neural mechanisms in eating behaviour has been carried out on animals based on the principle that their neural systems are similar to those of humans. Research suggests that the hypothalamus plays a key role in eating behaviour. Much research has used precise methods of studying the brain to examine the role of the hypothalamus in eating. These include lesions and stimulation – what do these terms mean?

The hypothalamus Referred to as the ‘hunger centre’ of the brain. Main area associated with hunger and satiation. Acts like a ‘thermostat’ to initiate or stop eating behaviour. Different parts of the hypothalamus are responsible for different aspects of eating (i.e. hunger and satiation).

A01: Dual-control theory Homeostatic view of hunger and satiety What is homeostasis? Involves mechanisms to detect state of internal environment (the body) and restore to its optimal state e.g. temperature. Proposes that the body has two separate systems; one for turning eating ‘on’ and one for turning eating ‘off.’ Lateral hypothalamus (LH) –feeding centre, stimulates eating behaviour. Ventromedial hypothalamus (VMH) – satiety centre, stops eating behaviour.

A01: Dual-control theory Eating Increase in blood glucose Ventromedial hypothalamus activated Satiety Hunger Lateral hypothalamus activated Decrease in blood glucose Eating stops

Independent task In your booklets write an A01 descriptive paragraph of the dual-control theory of eating behaviour. Use your diagram to help you. 5 minutes!

A01: Dual-control theory When blood glucose levels decrease the lateral hypothalamus (LH) is activated in the brain resulting in feelings of hunger and an increase in appetite. This motivates the individual to search for and consume food, which causes blood glucose levels to increase again. This rise in blood glucose levels activates the ventromedial hypothalamus which leads to feelings of satiation (fullness) and stops eating by decreasing appetite.

A01: Set point theory of eating behaviour Suggests that the LH and the VMH function in response to a set point – an optimal weight (biologically determined standard) that the body seeks to maintain. The hypothalamic systems work together to maintain a reasonably constant level of satiety (fullness) by ‘switching on’ and ‘switching off’ eating behaviour appropriately. This information comes from changes in blood glucose levels. Therefore food intake/consumption and weight control are the result of a balance between these two parts of the hypothalamus.

A01: The role of the stomach in eating behaviour Food arrives in the stomach. Broken down by digestive enzymes into nutrients. Key nutrient is glucose (source of immediate fuel for the body and brain). Glucose travels to cells as energy and to liver/fat cells (stored as nutrients). Blood glucose levels monitored by sensors in the liver and the hypothalamus.

A01: The role of the stomach in eating behaviour When blood glucose levels decrease: - Liver converts stored nutrients back to glucose. LH activated = hunger and eating initiated. LIVER + LH work together to INCREASE BLOOD GLUCOSE LEVELS. Glucostatic theory – changes in the supply of glucose available to cells (detected by the liver) that sends signals to the hypothalamus which helps control eating behaviour.

Independent task 10 minutes in silence to read over/revise/summarise on A4 paper, the A01 descriptive information on biological explanations of eating behaviour. Then...QUIZ!

QUIZ /9 Give 2 examples of neural mechanisms. (2) What is a lesion? (1) What is stimulation? (1) Which key brain area plays a role in eating behaviour? (1) When activated, which part of this brain area is said to result in feelings of hunger? (1) When activated, which part of this brain area is said to result in feelings of satiation? (1) What is satiation? (1) Which simple sugar plays a key role in the dual-control theory? (1)

A02: Supporting research for the role of the stomach in eating Lutter et al (2008) Ghrelin is an important hormone that indicates whether or not we are hungry. It is produced and released by the stomach and travels to the LH. The LH has receptors for ghrelin and signals the body of hunger. When food is eaten the secretion of ghrelin stops. Hormonal levels of ghrelin increase before meals and decrease after. Support for the role of hormones/brain areas in controlling eating behaviour.

A02: Supporting evidence We now need to look at research to support the dual-control theory of eating behaviour. First we are going to look at research to support the role of the lateral hypothalamus (LH) in initiating feelings of hunger resulting in eating.

P.E.E.L (A02) P: There is research to support the dual-control theory of eating behaviour, particularly the role of the lateral hypothalamus in stimulating eating behaviour. E: Research by _____________ has shown... E: This suggests/shows... L: This supporting research evidence by _____________ suggests that the dual-control theory is a valid biological explanation of eating behaviour.

Supporting research for LH Damage to the LH leads to undereating and weight loss. Stimulation of the LH produces feelings of hunger and initiates feeding behaviour. Anand and Brobeck (1951) – rats with lesions to the LH showed aphagia (they stopped eating even when palatable food was readily available) and starved to death. Quaade (1971) – successfully lesioned the LH of obese patients to reduce eating behaviour. If LH was stimulated electrically they reported feeling hungry. Refer to evaluation in booklets re. lesions.

Neuropeptide Y Neurotransmitter found in the hypothalamus. Important in turning on eating - increased levels promotes 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 in just a few days (Stanley et al, 1986; Wickens, 2000). Practical applications: Potential treatment for anorexia?

IDA Any ideas of issues, debates or approaches that you could apply to what we have covered so far? Something to think about… Is it ethical to test on animals? Can results from research on animals be generalised to humans?

A02: Supporting evidence We now need to look at research to support the role of the ventromedial hypothalamus (VMH) in initiating feelings of satiety and stopping eating.

P.E.E.L (A02) P: There is research to support the dual-control theory of eating behaviour, particularly the role of the ventromedial hypothalamus in stopping eating behaviour. E: Research by _____________ has shown... E: This suggests/shows... L: This supporting research evidence by _____________ suggests that the dual-control theory is a valid biological explanation of eating behaviour.

Supporting research for VMH Satiety centre, ‘stops eating’ 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 (i.e. stops) eating. Hetherington and Ranson (1942) – rats with lesions to the VMH would overeat until became grossly fat (hyperphagia). 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 (fullness).

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 to the PVN alone that causes hyperphagia (Gold, 1973). Found that lesions restricted to the VMH alone did not result in hyperphagia and 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.

A01: The role of Leptin The hormone leptin is secreted by fat tissue and travels via the bloodstream to the hypothalamus where it binds to certain receptors. Leptin acts to decrease food intake. Leptin works opposite of Ghrelin. Role of Ghrelin = signals the body that it is hungry. Role of Leptin = signals the body that it is full. Also has specific roles in the regulation of energy expenditure and food intake.

Independent tasks Read the research in your booklets and fill in the missing gaps. Read the evaluation points for the role of leptin and highlight the key points. You have 10 minutes

A02: Evaluation There are individuals who have a genetic leptin deficiency who are diagnosed as being obese. Humans are biological organisms and our eating behaviour relies on our biological systems. Insight into biological mechanisms may be used to develop medical interventions to help change what we eat and manage weight (e.g. obese patients).

A02: Evaluation X 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 or a leptin deficiency. X The biological approach is reductionist, focusing only on biological systems regulating food intake and body weight. It ignores psychological, cultural and social factors that can influence our eating behaviour.

A02: The role of Serotonin Serotonin is a neurotransmitter. It has a chemical influence on satiation (similar to Leptin). However increased activity of serotonin in the medial hypothalamus (MH) has been associated with decreased food intake. This suggests that it is not just the VMH that plays a role in ‘stopping eating’ but also the MH as well as chemical influences (leptin and serotonin). Suggests a more complex interaction of many neural mechanisms working together to control eating behaviour.

IDA In pairs, discuss and make notes on any issues, debates or approaches that you could apply to the dual-control theory of eating behaviour and associated research. Something to think about… Reductionism. Determinism. Biological approach (nature vs. nurture). Ethical issues. Evolutionary approach? Real-world applications.

IDA Reductionist – biological explanations only focus on limited factors which can be used to explain eating behaviour e.g. specific brain area, hormone, NT. It pays no attention to psychological, cultural and social factors that influence our eating behaviour. Deterministic – damage to the LH, VMH, or lack of leptin can result in disordered eating – ignores free will (cognition). Biological approach – cannot provide full explanation as it ignores the role of nurture. (Nature vs. Nurture).

IDA Ethical issues – is it ethical to test on animals? Much of the research is on mice/rats. Based on principle that brain systems similar to humans but to what extent can findings be generalised? Ignores evolutionary approach – suggest primary stimulus for hunger and eating is food’s positive-incentive value. Real-world applications of research - insight into neural mechanisms may be used to develop medical interventions to help change what we eat and manage our weight (e.g. obese patients).

Homework Complete the table of key terms for biological explanations of eating behaviour in your booklets. Complete essay structure and IDA gap fill task in booklet.