Presentation on theme: "Biological explanations to eating behaviour"— Presentation transcript:
1Biological explanations to eating behaviour Role of neural mechanismsBiological explanations to eating behaviourEvolutionary explanations
2Role of neural mechanisms in eating behaviour Eating behaviour = ingestive behaviourHomeostasisif we are hot – we sweatif we are dehydrated – thirstsIf we need food – hungerHomeostasis 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 eating behaviour.The process by which the body maintains a constant internal environment
3Body weightEach individual has a set point and their weight is regulated around that set pointBody regulates hunger based possibly onFat stores (lipostatic hypothesis)Glucose levels (glucostatic hypothesis)Cellular energy – adenosine trisophate (ATP) is a product of the breakdown of macronutrients (fats, carbohydrates and proteins) and considered important for the regulation and maintenance of homeostasis
4The hypothalamusPatient with tumours in the hypothalamus tend to become obeseMethods used to research hypothalamusLesioning in animalsInvestigation of feedingpatterns after brain damageEffects of neurotransmittersintroduced into parts of brainImpact of drugs on eatingUse of fMRI (FunctionalMagnetic Resonance Imaging)
5Dual-Centre Theory of feeding behaviour 2 areas of the hypothalamus involved in eating behaviourVentro Medial Hypothalamus (VMH) as a "satiety center"Lateral Hypothalamus (LH) as a "Hunger center".NOTE: VMH and LH are also called VMN and LN (N stands for NUCLEUS!!!)
6Dual-Centre Theory of feeding behaviour Hunger -> eating startsIncrease in blood glucose, decrease in ghrelin releaseVMH satiety centre activatedSatiety – feeding stops......Feelings of declining nutrient levelsLH feeding centre activated
7The lateral nucleus of the hypothalamus Contains the feeding centreThis initiates eating.It responds to decreased blood glucose and increase in ghrelin a hormone released from the stomach when it is empty.
8Ventro medial nucleus (VMN)of the hypothalamus Contains the satiety centre.This inhibits eating behaviour when we are full.Responds toan increase in blood glucose,a decrease in ghrelin and to CCK, a hormone released when food is detected in the duodenumleptin a long term satiety signal released by fat cells.
9Role of hypothalamus - evidence Aphagia (failure to eat when hungry) can be caused by damage to the LHRats whose VMH had been lesioned developed overeating and obesityHowever, Gold (1973) found that lesions restricted to the VMH alone did NOT result in hyperphagia and only produced overeating when they included other areas such as the parvoventricular nucleus!However, subsequent research has failed to replicate Gold’s findings...
10Role of ghrelin - evidence Cummings et al (2004) monitored PPs’ ghrelin levels every 5 minutesPPs 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 behaviourAO3: The study used a small sample limiting how far the findings can be generalised and 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)Ghrelin injections result in increased food intake in animalsGastric bands used in treating obesity reduce ghrelin secretion.
11Role of neurotransmitters 3 main neurotransmitters are found to influence appetite:Catecholamines (dopamine, norepinephrine, and epinephrine): sympathomimetic "fight-or-flight" hormones that are released by the adrenal glands in response to stressSerotonin: found extensively in the gastrointestinal tract, it activates the muscles used for feeding. Is also associated to aggression and “happiness”Peptides: short polymers formed from the linking, in a defined order, of α-amino acids
12Neurotransmitters that increase food intake Norepinephrine (NE) – injections of NE in hypothalamuscan stimulate feeding if injected into the paraventricular nucleusCan reduce feeding if injected into the perfornical areaNeuropeptide Y (33 amino acid peptide)– high concentrations in the paraventricular hypothalamus and perfornical hypothalamus.Rats injected with neuropeptide Y continue eating large amounts of food even when fullIt also seems to cause a preference for carbohydratesGalanin (29 amino acid peptide)- particularly found in the paraventricular hypothalamus.Injections of galanin into rats cause an increase of food intake and a preference for fats rather than carbohydrates
13Marie et al (2005) role of neuropeptide Y Genetically manipulated mice so that they did not produce neuropeptide YFound no subsequent decrease in their feeding behaviour!!However, injections of NPY cause hunger......May be due to an experimental artefact, because of the unexpected intake of NPY in experimental conditions (through injection)
14Neurotransmitters and modulators that decrease food intake Cholecystokinin (CCK) – endogenous 33 amino acid peptide that is released into bloodstream during mealsCauses reduction in appetite and satiationSuppresses weight gainBombesin – peptide found to reduce food intake in ratsCorticotropin-Releasing Hormone (CRH) – 41 amino acid peptide produced in the paraventricular hypothalamus and other regions of brain that reduces food intakeSerotonin (5HT) – neurotransmitter which decreases food intake.
15KEY WORDS – matching exercise HomeostasisNegative feedback loopSet pointLipostatic hypothesisGlucostatic hypothesisadenosine trisophate (ATP)Lateral NucleusVentro Medial NucleusGhrelinCCKLeptinNeuropeptide Y (NPY)
16Impact of drugs on eating behaviour Nicotine – decreases food intake.Smokers generally weigh 3 kg less than non-smokers (US Department of Health and Human Services, 1990)Ogden (1994) some dieters use smoking as a weight-loss strategy and those who stop smoking increase their calorie intake, especially from sweet foodsAmphetamines - have a dramatic suppressant impact on both subjective hunger and food intakeMarijuana – increases hunger and food intake
17Impact of drugs on eating behaviour Alcohol – influences food intake in contradictory waysSome studies indicate it can have a weak inhibitory effectOthers show it can stimulate hungerAnti-psychotic drugs – both lithium and chloropromazine cause considerable weight gainTricyclic anti-depressants – cause cravings for sweet food and weight gainSelective Serotonin Reuptake Inhibitors (SRRIs) – used for patients with depression, might promote weight loss...
18Impact of drugs on eating behaviour Analgesics – used for pain reliefNaloxone can trigger deceased food intakeMorphine has also a weak depressant effect on appetiteAppetite-suppressant drugshave a consistent depressant effect on hunger and reduce food intakeHave been removed from the market because linked to heart problems
19Does it increase or decrease hunger? MorphineAnti-psychotic drugsTricyclic anti-depressantsSelective Serotonin Reuptake Inhibitors (SRRIs)NaloxoneAlcoholAppetite-suppressant drugsDECREASEINCREASEINCREASEDECREASEDECREASEBOTH!DECREASE
20IDAs? issues debates approaches Ethical issues with non-human animals Is the biological approach reductionist?Free will vs determinism (can biological drives be overridden?)debatesCompare and contrast explanations to eating behaviourBiological,Learning (Behaviourist)CognitiveSocialapproachesIDAs?
21Evaluation of neural mechanisms and eating behaviour +Reflection on people’s experience of hunger\satiety+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 evidenceCumming et al, ghrelin
22Cont.-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 lack of generalisability -Highly controlled lab experiments may lack ecological validity -Physiological drives can be overriden (eg desire to loose weight; dislike of certain foods; fear of losing control; social cues to continue eating; food availability)
23Outline and evaluate the role of neural mechanisms involved in controlled eating and satiation(25 marks)AO1:Intro: homeostasis; negative feedback loop; set pointLipostatic and glucostatic hypothesesdescribe dual centre model (diagram will be also credited);Role of LH and VMH;neurotransmitters and hormones involved in eating regulation (ghrelin; CKK; leptin; norepinephrine; Neuropeptide Y...)AO2:research evidence for effects of hormones + contrasting evidence (eg Cummings et al, 2004 ghrelin AND Marie et, 2005 NEY al OR Gold, 1973 VMH lesioning) (4)Impact of drugs (eg alcohol, anti-depressants...) on appetite confirms biological basis of eating behaviourI: ethics with non-himan PPs; reductionismD: free will vs determinism; nature vs nurtureA: biological vs social, behaviourist, psychodynamicAO3Lack of ecological validityLack of generalisabilitySampling issues (eg Cummings et al, 2004)