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  • 1. Biological explanations to eating behaviour Role of neural mechanisms Evolutionary explanations
  • 2. Answer the following - • Did you have breakfast this morning? • Why did you stop eating the food? • What are your favourite foods? Why? • How do you feel after a large meal?
  • 3. Role of neural mechanisms in eating behaviour • Eating behaviour = ingestive behaviour • Homeostasis – if we are hot – we sweat – if we are dehydrated – thirsty – If we need food – hunger • Homeostasis is maintained via a negative feedback loop: this assumes that all body variables have a set point (or range) • The digestive tract and the hypothalamus play a significant role in homeostasis in eating behaviour. The process by which the body maintains a constant internal environment
  • 4. Homeostasis • Involves mechanisms that can detect and correct. • Detect – check whether the body has enough nutrients (internal environment) • Correct – restore the body to its optimal state. • Body evolved 2 separate systems in order to cope with the time lag between restoring equilibrium and body registering their effect. • Turning eating on and turning eating off!
  • 5. GLUCOSE LEVELS Decrease in glucose levels As glucose levels decrease hunger levels increase Increase in glucose levels means satiation reached. Activates this area – feel hungry. Individual searches for food and eats Increase in glucose levels Activates this area – feeling of satiation – inhibits further feeding
  • 6. Body weight • Each individual has a set point and their weight is regulated around that set point • Body regulates hunger based possibly on – Fat stores – Glucose levels – Cellular energy
  • 7. Dual-Centre Theory of feeding behaviour • 2 areas of the hypothalamus involved in eating behaviour – Ventro Medial Hypothalamus (VMH) as a "satiety centre" = full up! – Lateral Hypothalamus (LH) as a "Hunger centre". • NOTE: VMH and LH are also called VMN and LN sometimes
  • 8. Dual-Centre Theory of feeding behaviour
  • 9. The lateral hypothalamus • Contains the feeding centre • This initiates eating. • It responds to decreased blood glucose and increase in ghrelin a hormone released from the stomach when it is empty.
  • 10. Ventro medial hypothalamus • Contains the satiety centre. • This inhibits eating behaviour when we are full. • Responds to – an increase in blood glucose, – a decrease in ghrelin and to release of CCK, a hormone released when food is detected in the duodenum – leptin a long term satiety signal released by fat cells.
  • 11. The hypothalamus – research evidence comes from… • Case studies -patients with tumours in the hypothalamus tend to become obese • Methods used to research hypothalamus – Lesioning in animals – Investigation of feeding patterns after brain damage – Effects of neurotransmitters introduced into parts of brain – Impact of drugs on eating – Use of fMRI (Functional MRI scans)
  • 12. Role of hypothalamus - evidence • Aphagia (failure to eat when hungry) can be caused by damage to the LH. • Rats whose VMH had been lesioned developed overeating and obesity • Wickens (2000) Rats: Injected with NPY = became obese! • However, Gold (1973) found that lesions restricted to the VMH alone did NOT result in hyperphagia and only produced overeating when they included other areas.
  • 13. Hetherington and Ranson (1942) The VMH Rat Made lesions on an area of the VMH (part of the hypothalamus) in rats. Caused the rats to overeat and be dramatically obese. This lesion destroyed a centre that is vital for the control of feeding behaviour. Its destruction led to an increase in feeding and body weight. It was assumed that this was a satiety centre – which is normally activated when the animal is full at the end of the meal. Satiety – the feeling or state of being fully satisfied. Satiety centres function is to stop feeding
  • 14. The role of the hypothalamus - evaluation Is it really the ‘ON’ switch?? Damage to LH also affects thirst and sex drives. Recent research suggests eating is more widely spread It is thought that the hypothalamus plays a role but it is not solely responsible
  • 15. Ao2 Role of ghrelin - evidence • Cummings (2004) monitored PPs’ ghrelin levels every 5 minutes • PPs had to assess their level of hunger every 30 mins. • In 5 of the 6 participants there was a significant correlation between ghrelin levels, emptiness of the stomach and hunger. • The results support the theory of the role of ghrelin in eating behaviour • In addition ghrelin injections result in increased food intake in animals • Gastric bands used in treating obesity reduce ghrelin secretion. • However: The study used a small sample limiting how far the findings can be generalised. • It is likely that the participant’s subjective judgements of hunger were influenced by expectations of food based on meal times (cultural factors rather than biological factors)
  • 16. Role of neurotransmitters Neurotransmitters that increase food intake • Neuropeptide Y–Rats injected with neuropeptide Y continue eating large amounts of food even when full – It also seems to cause a preference for carbohydrates
  • 17. Ao2 Supporting evidence: Marie et al (2005) role of neuropeptide Y • Injections of NPY in mice cause hunger... • However: Genetically manipulated mice so that they did not produce neuropeptide Y. Found no subsequent decrease in their feeding behaviour!!
  • 18. Neurotransmitters and modulators that decrease food intake • (CCK) –released into bloodstream during meals – Causes reduction in appetite. – Suppresses weight gain
  • 19. Evaluation of neural mechanisms and eating behaviour ++Insight into brain chemicals – could be used to develop medical interventions to help change what we eat +Provides explanation of some differences in eating behaviour +Studies such as those involving lesions to the LH and VMH in rats have supported the role of the hypothalamus in regulating eating behaviour +Studies involving electrical stimulation of these centres have confirmed their role in feeding and satiety. +Such studies provide sound scientific evidence but there is the issue of extrapolating finding from rats to humans. +Research evidence • Cumming et al, 2004 - ghrelin
  • 20. Cont. -Reductionism: focus exclusively on biological aspects of hunger and satiety -Biological determinism: focus exclusively on the role of nature and no space left to choice and cultural and social influences -there is substantial and convincing evidence that social, cultural and psychological factors affect our eating behaviours as is evident from psychological explanations of eating disorders -Use of animals in research implies a lack of generalisability- we must be cautious of findings -Highly controlled lab experiments may lack ecological validity -Physiological drives can be overriden (eg desire to lose weight; dislike of certain foods; fear of losing control; social cues to continue eating; food availability)
  • 21. • Ethical issues with non-human animalsissues • Is the biological approach reductionist? • Free will vs determinism (can biological drives be overridden?) debates • You contrast explanations to eating behaviour • Biological, • Learning (Behaviourist) • Cognitive • Social approaches