EATING: Factors influencing eating and neural mechanisms

Question 1

2 factors influencing attitudes to food and/or eating behaviour

Answer 1

1. Early Exposure

2. Stress

Question 2

3 elements of early exposure

Answer 2

• classical conditioning
• SLT
• mere exposure effect

Question 3

classical conditioning AO1

with example of positive and negative attitudes towards food

Answer 3

• 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

Question 4

classical conditioning A02

Answer 4

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

Question 5

Social learning theory AO1

Answer 5

• 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

Question 6

Social learning theory AO2: peer influence

Answer 6

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

Question 7

Social learning theory: parental influence

Answer 7

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

Question 8

Mere exposure effect AO1

Answer 8

• 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

Question 9

Mere exposure effect AO2

Answer 9

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

Question 10

Early exposure: practical applications

Answer 10

• peers and parents can model healthy eating behaviour

* keep exposing children to new food, will take 8-10 exposures to get over neophobia

Question 11

early exposure: IDA

Answer 11

• 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

Question 12

Stress introduction

Answer 12

• 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.

Question 13

stress model

Answer 13

Individual differences Model – Greeno and Wing

Question 14

3 elements of stress model

Answer 14

• external eaters
• emotional eaters
• restrained eaters

Question 15

external eaters

Answer 15

• 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

Question 16

emotional eaters

Answer 16

• 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

Question 17

restrained eaters

Answer 17

• 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

Question 18

Stress model IDA

Answer 18

• 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

Question 19

emotional eaters AO2

Answer 19

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.

Question 20

external eaters AO2

Answer 20

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

Question 21

Stress model: practical applications

Answer 21

• 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

Question 22

2 main neural mechanisms in the control of eating

Answer 22

• dual centre model of eating

- other neural mechanisms

Question 23

dual centre model of eating AO1

Answer 23

• 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

Question 24

dual centre model of eating: AO2

Answer 24

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

Question 25

dual centre model of eating: AO2 - NOT RESEARCH

Answer 25

• 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

Question 26

name the two ‘other neural mechanisms’

Answer 26

• ghrelin

- leptin

Question 27

ghrelin AO1

Answer 27

• = 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

Question 28

Ghrelin AO2

Answer 28

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

Question 29

leptin AO1

Answer 29

• = 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

Question 30

leptin AO2

Answer 30

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