Presentation on theme: "Biological explanations to eating behaviour Role of neural mechanisms Evolutionary explanations."— Presentation transcript:
Biological explanations to eating behaviour Role of neural mechanisms Evolutionary explanations
Role of neural mechanisms in eating behaviour Eating behaviour = ingestive behaviour Homeostasis – if we are hot – we sweat – if we are dehydrated – thirsts – 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 eating behaviour. The process by which the body maintains a constant internal environment
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 (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
The hypothalamus Patient 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 Magnetic Resonance Imaging)
Dual-Centre Theory of feeding behaviour 2 areas of the hypothalamus involved in eating behaviour – Ventro 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!!!)
Dual-Centre Theory of feeding behaviour
The lateral nucleus of the 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.
Ventro medial nucleus (VMN)of the 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 CCK, a hormone released when food is detected in the duodenum – leptin a long term satiety signal released by fat cells.
evidence 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 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 such as the parvoventricular nucleus! However, subsequent research has failed to replicate Golds findings...
evidence Role of ghrelin - evidence Cummings et al (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 AO3: The study used a small sample limiting how far the findings can be generalised and it is likely that the participants 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 animals Gastric bands used in treating obesity reduce ghrelin secretion.
Role 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 stress – Serotonin: 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
Neurotransmitters that increase food intake Norepinephrine (NE) – injections of NE in hypothalamus – can stimulate feeding if injected into the paraventricular nucleus – Can reduce feeding if injected into the perfornical area Neuropeptide 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 full – It also seems to cause a preference for carbohydrates Galanin (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
Marie et al (2005) role of neuropeptide Y Genetically manipulated mice so that they did not produce neuropeptide Y Found 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)
Neurotransmitters and modulators that decrease food intake Cholecystokinin (CCK) – endogenous 33 amino acid peptide that is released into bloodstream during meals – Causes reduction in appetite and satiation – Suppresses weight gain Bombesin – peptide found to reduce food intake in rats Corticotropin-Releasing Hormone (CRH) – 41 amino acid peptide produced in the paraventricular hypothalamus and other regions of brain that reduces food intake Serotonin (5HT) – neurotransmitter which decreases food intake.
KEY WORDS – matching exercise Homeostasis Negative feedback loop Set point Lipostatic hypothesis Glucostatic hypothesis adenosine trisophate (ATP) Lateral Nucleus Ventro Medial Nucleus Ghrelin CCK Leptin Neuropeptide Y (NPY)
Impact 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 foods Amphetamines - have a dramatic suppressant impact on both subjective hunger and food intake Marijuana – increases hunger and food intake
Impact of drugs on eating behaviour Alcohol – influences food intake in contradictory ways – Some studies indicate it can have a weak inhibitory effect – Others show it can stimulate hunger Anti-psychotic drugs – both lithium and chloropromazine cause considerable weight gain Tricyclic anti-depressants – cause cravings for sweet food and weight gain Selective Serotonin Reuptake Inhibitors (SRRIs) – used for patients with depression, might promote weight loss...
Impact of drugs on eating behaviour Analgesics – used for pain relief – Naloxone can trigger deceased food intake – Morphine has also a weak depressant effect on appetite Appetite-suppressant drugs – have a consistent depressant effect on hunger and reduce food intake – Have been removed from the market because linked to heart problems
Does it increase or decrease hunger? Morphine Anti-psychotic drugs Tricyclic anti-depressants Selective Serotonin Reuptake Inhibitors (SRRIs) Naloxone Alcohol Appetite-suppressant drugs BOTH! INCREASE DECREASE
Ethical issues with non-human animals issues Is the biological approach reductionist? Free will vs determinism (can biological drives be overridden?) debates Compare and contrast explanations to eating behaviour Biological, Learning (Behaviourist) Cognitive Social approaches
Evaluation of neural mechanisms and eating behaviour +Reflection on peoples 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 evidence Cumming et al, ghrelin
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 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)
Outline and evaluate the role of neural mechanisms involved in controlled eating and satiation(25 marks) AO1: – Intro: homeostasis; negative feedback loop; set point – Lipostatic and glucostatic hypotheses – describe 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 behaviour – I: ethics with non-himan PPs; reductionism – D: free will vs determinism; nature vs nurture – A: biological vs social, behaviourist, psychodynamic AO3 – Lack of ecological validity – Lack of generalisability – Sampling issues (eg Cummings et al, 2004)