EATING: Factors influencing eating and neural mechanisms Flashcards
2 factors influencing attitudes to food and/or eating behaviour
- Early Exposure
2. Stress
3 elements of early exposure
- classical conditioning
- SLT
- mere exposure effect
classical conditioning AO1
with example of positive and negative attitudes towards food
- Learning food preferences through association
- Associate NS with an UCS
- E.g: fun/games at b-day party (UCS) + birthday cake (NS) → pleasant feelings (UCR) → CR
- UCS paired with NS
- Also leads to aversive attitudes to food
- E.g. bacterial poison (UCS) + food that contains it (NS) → UCR → CR as associate the food with the poison/being ill, avoid it in the future
classical conditioning A02
Garcia et al
• Fed flavoured water to lab rats
• Several hours later, rats were injected with substance that made them ill
• Poison (UCS) + water (NS) → UCR
• Later rats when offered flavoured water, didn’t drink it
• - However, rats’ eating still far less complex than humans, who eat also for cognitive and social, as well as biological and learning reasons.
• - Well controlled experiment
Social learning theory AO1
- Learning food preferences through observation
- Pay attention to role models, observe eating behaviour, retain memory of this, likely to imitate if results in positive rewards i.e. parents/peers enjoy certain foods
Social learning theory AO2: peer influence
Birch et al
- Changing children’s preferences
• Children seated at lunch next to a child who preferred a different veg (peas and carrots used)
• Children showed a shift in the preference, backed up through follow-up assessment several weeks later
Social learning theory: parental influence
Ogden et al
• Reported consistent correlations between parents and children in snack-food intake and eating motivations
• - non-experimental research – cannot establish cause and effect
Mere exposure effect AO1
- the more exposed we are the something, the more familiar we become to it, resulting in the attitude towards it
- if exposed to new foods, likely to have a negative attitude towards it
Mere exposure effect AO2
Birch and Marlin
• 2 year old children introduced to novel foods over 6 weeks
• condition 1, food presented 20x
• condition 2, food presented 10x
• condition 3, food presented 5x
• found it took 8-10 exposures before food preferences shifted significantly
• + well operationalized
• - mere exposure won’t get one to like everything
Early exposure: practical applications
- peers and parents can model healthy eating behaviour
* keep exposing children to new food, will take 8-10 exposures to get over neophobia
early exposure: IDA
- early exposure environmental
- based on behaviourist and social learning theories – nurture
- ignores nature and biological influences
- very determinist – might act as a justification for unhealthy eating behaviour
Stress introduction
- When stressed, may favour certain types of foods over others/change the amount we eat
- Stress affects individuals differently, depending on: biology e.g. gender, early experience e.g. MEE, CC, SLT and cognitions e.g. attitudes, beliefs
- IDA: Holistic account of interaction, sometimes between nature and nurture.
stress model
Individual differences Model – Greeno and Wing
3 elements of stress model
- external eaters
- emotional eaters
- restrained eaters
external eaters
- eat in response to environmental cues
- when food is available, not when hungry, eat in response to food cues e.g. sight/smell
- more likely to increase food intake when stressed as long as food is available
emotional eaters
- fail to distinguish between feelings and hunger
- when anxious or emotionally aroused, misinterpret emotion as hunger
- may be due to inconsistent parenting
- increase food intake when stressed as experience anxiety as hunger
restrained eaters
- deliberately try to limit their food intake e.g. diet, using will power to supress food intake
- will power undermined by stress
- people who have to try hard to control eating increase eating when stressed
- people who do not have to try hard are unaffected by stress
Stress model IDA
• provides justification for eating healthy foods as very deterministic
• GP should say eating behaviour is a consequence of free will – so able to change behaviour
- external/emotional fairly vague - not as helpful as more reductionist ideas e.g. SLT or biologocal reasons
emotional eaters AO2
Oliver et al
• Condition 1 – stress – 4 min speech to prepare
• Condition 2 – control – listened to piece of neutral text
• Physiological measures and self-report used to assess: appetite for range of foods immediately before meal, food intake during meal
• Did not alter food intake but emotional eaters had more sweet and high-fat foods, more ‘energy-dense’ meal
• Amount of stress doesn’t affect eating habits – depends on individual differences
• Women: more stress-related eating (i.e. emotional eating, where anxiety confused with hunger) than men. Supports IDM, as effect of stress different by gender.
• + Controlled experiment
• + well operationalised objective measures.
• - Demand characteristics if ppts guessed aim of the study from appetite assessment.
external eaters AO2
Conner et al
• Ppts kept daily record of no. and severity of daily hassles and no. of snacks consumed over 7 days
• 33 female, 27 male students
• Questionnaire assessing whether: restrained/emotional/external
• Ppts that scored highly on measures of external eating, significant positive relationship between hassles and snacking (not for emotional/restrained)
• - Non-experimental – no cause → effect
• - Questionnaires – social desirability and records may not cover secret eating
Stress model: practical applications
- a consequence of own free will
- surround external eaters with healthy food, avoid lots of exposure to food, work hard to regulate the times they eat at
2 main neural mechanisms in the control of eating
- dual centre model of eating
- other neural mechanisms
dual centre model of eating AO1
- eating behaviour controlled by two main nuclei in hypothamulus
- blood glucose levels increase, sensed by hypothamulus, VHM = ventro-medial hypothamulus, satiety reached/feeling full, reduced food intake, reduction in blood glucose levels
- blood glucose levels fall, sensed by hypothamulus, lateral hypothamulus activated aka feeding centre, feel hunger, signals food intake, blood glucose levels rise
dual centre model of eating: AO2
Hetherington and Ranson
• lesions damaged VHM
• rats overate → obese
• so VHM under normal conditions acts as satiety centre
• lesion had prevented signals being sent – rats didn’t feel full
Anand and Brobeck
• lesion caused a loss of eating behaviour when added to lateral hypothamulus
• loss of feeding = aphagia
• this area is the hunger centre under normal conditions
More research
• later studies confirmed this: electrical stimulation of VMH inhibited feeding and stimulation of LH produced feeding, confirming normal functions
dual centre model of eating: AO2 - NOT RESEARCH
• using animals as research participants
o brain physiology similar but humans have ability to override neural impulses
o human eating behaviour is more complex: social influence, health awareness, emotional eating
• too simplistic – see other neural mechanisms
o brain is not an ‘island’
o key ‘messengers’ are hormones
o travel in bloodstream, diffuse into brain, act on synapses
o ‘feedback’ from body
o dual centre model too reductionist and simplistic to explain eating behaviour
o neural mechanisms can not control eating on their own: ghrelin and leptin
name the two ‘other neural mechanisms’
- ghrelin
- leptin
ghrelin AO1
- = a hormone released from the empty stomach that signals the hypothamulus to stimulate feeding
- stimulates receptors in the arcuate nucleus, part of the hypothamulus
- arcuate nucleus has neurons reaching into both lateral and ventromedial hypothamulus
- counteracts, switching off receptor sites in the VHM, preventing brain activity that would supress hunger drives
- stimulates, switching on receptors in the LH, stimulating brain activity that creates hunger drives
Ghrelin AO2
Cummings
• 6 participants allowed to eat lunch
• ghrelin levels were monitored from blood samples taken every 5 mins until ppts requested their evening meal
• ppts assessed degree of hunger every 30mins
• levels fell immediately after lunch, lowest after 70mins, then slowly began to rise peaking as ppts requested their evening meals
• 5/6 ppts, ghrelin levels closely correlated with the degree of hunger reported by the ppts
Lutter
• starved mice for 4 days
• ghrelin levels increased
• levels also increased when mice were stressed: shows that food, hunger, stress and anxiety seem to be associated
• + used to support link between stress and increased food intake (comfort eating)
• - use of animals may leaf to unwarranted extrapolation and ethical issues
leptin AO1
- = a hormone released from fatty (adipose) tissue. It acts as an indicator of body weight to hypothalamic mechanisms controlling long-term food intake
- binds to receptors in the arcuate nucleus part of the hypothamulus
- arcuate nucleus has neurons reaching into both LH and VHM
- counteracts, switching off receptor sites in the LH, preventing brain activity that would otherwise create hunger drives
- enhances, switching on receptors in the VHM, stimulating brain activity that suppresses hunger
leptin AO2
Carlson
• obese mice that had a mutation – were without the gene that produced leptin
• so their hypothamulus does not receive a signal to stop eating and so they eat continuously and become obese
• when injected with leptin, weight went back to normal
• would therefore seem to be a potential treatment for human obesity as we would expect overweight humans to have low levels of leptin in their bloodstream, but majority have normal leptin levels, problem is that the brain mechanisms controlling feeding behaviour are insensitive to the effects of leptin/or other neural mechanisms override the leptin signals
