1. Eating Behaviour Unit PSYA3 Miss Bird

2. What will we cover in this topic? 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. What we have covered Where we are now

3. RECAP: Dual-control theory 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.

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

5. Set point theory Support for the dual-control theory  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 and weight control are the result of a balance between these two parts of the hypothalamus.

6. RESEARCH Support for dual-control theory Last lesson we looked at research to support the role of the lateral hypothalamus (LH) in initiating feelings of hunger and eating.

7. Ghrelin 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.

8. 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. 1.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. 2.Quaade (1971) – successfully lesioned the LH of obese patients to reduce eating behaviour. If LH was stimulated electrically they reported feeling hungry.

9. Neuropeptide Y  Neurotransmitter found in the hypothalamus.  Important in turning on eating - increased levels promotes increases in food intake and weight.  When NPY 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).

10. RESEARCH Support for dual-control theory This lesson we will look at research to support the role of the ventromedial hypothalamus (VMH) in initiating feelings of satiety and stopping eating.

11. 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 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).

12. 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.

13. The role of Leptin  The hormone leptin is secreted by adipose (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.

14. Research into the role of Leptin 1.Read the research in your booklets and fill in the missing gaps. 2.Read the evaluation points for the role of leptin and highlight the key points. Be prepared to feedback to the class. You have 10 minutes

15. Evaluation 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. Insight into brain chemicals may be used to develop medical interventions to help change what we eat (e.g. obese patients). 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. 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.

16. 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).

17. 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.

18. IDA Reductionism – biological explanation only focuses on limited factors which can be used to explain eating behaviour. 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. Biological approach – cannot provide full explanation as it ignores the role of nurture. (Nature vs. Nurture).

19. 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 brain chemicals may be used to develop medical interventions to help change what we eat and manage our weight (e.g. obese patients).

20. Homework Due in Tuesday 9 th April 1.Complete the 24-mark past-exam question: Discuss neural mechanisms involved in the control of eating behaviour (Jan 2012). 2.Research neural control of cognitive factors in eating behaviour including the role of the amygdala and the inferior frontal cortex (page 88 of third edition textbook). 3.Update key terms table with today’s lesson content.