Transcript Eating Behaviour - Beauchamp College

Eating Behaviour
PSYA3
Miss Bird
AQA A Specification
Factors influencing attitudes to food and eating behaviour. For example:
Eating behaviour cultural influences; psychological influences (mood); and social
influences (health concerns/media).
Explanations for the success and failure of dieting.
Neural mechanisms involved in controlling eating behaviour.
Biological
explanations of Evolutionary explanations of food preference.
eating behaviour
In relation to either anorexia nervosa or bulimia nervosa:
Eating disorders
Psychological explanations.
Biological explanations, including neural and evolutionary explanations.
Neural mechanisms in eating
behaviour (biological)
What are neural mechanisms?
Different brain components (neurons, neurotransmitters,
hormones and brain regions).
We are going to look at the influence of these different brain
components on eating behaviour.
Research into neural
mechanisms
 Much research into neural mechanisms in eating behaviour
has been carried out on animals based on the principle that
their neural systems are similar to those of humans.
 Research suggests that the hypothalamus plays a key role
in eating behaviour.
 Much research has used precise methods of studying the
brain to examine the role of the hypothalamus in eating.
 These include lesions and stimulation – what do these
terms mean?
The hypothalamus
 Referred to as the ‘hunger centre’ of the brain.
 Main area associated with hunger and satiation.
 Acts like a ‘thermostat’ to initiate or stop eating
behaviour.
 Different parts of the hypothalamus are responsible for
different aspects of eating (i.e. hunger and satiation).
A01: Dual-control theory
Homeostatic view of hunger and satiety
What is homeostasis?
Involves mechanisms to detect state of internal environment
(the body) and restore to its optimal state e.g. temperature.
Proposes that the body has two separate systems; one for
turning eating ‘on’ and one for turning eating ‘off.’
Lateral hypothalamus (LH) –feeding centre, stimulates eating
behaviour.
Ventromedial hypothalamus (VMH) – satiety centre, stops
eating behaviour.
A01: Dual-control theory
Eating
Increase in blood
glucose
Ventromedial
hypothalamus
activated
Hunger
Lateral
hypothalamus
activated
Decrease in blood
glucose
Satiety
Eating stops
Independent task
• In your booklets write an A01 descriptive
paragraph of the dual-control theory of
eating behaviour.
• Use your diagram to help you.
• 5 minutes!
A01: Dual-control theory
When blood glucose levels decrease the lateral hypothalamus
(LH) is activated in the brain resulting in feelings of hunger and an
increase in appetite.
This motivates the individual to search for and consume food,
which causes blood glucose levels to increase again.
This rise in blood glucose levels activates the ventromedial
hypothalamus which leads to feelings of satiation (fullness) and
stops eating by decreasing appetite.
A01: Set point theory of
eating behaviour
 Suggests that the LH and the VMH function in response to a
set point – an optimal weight (biologically determined
standard) that the body seeks to maintain.
 The hypothalamic systems work together to maintain a
reasonably constant level of satiety (fullness) by ‘switching
on’ and ‘switching off’ eating behaviour appropriately.
 This information comes from changes in blood glucose levels.
 Therefore food intake/consumption and weight control are
the result of a balance between these two parts of the
hypothalamus.
A01: The role of the stomach in
eating behaviour
 Food arrives in the stomach.
 Broken down by digestive enzymes
into nutrients.
 Key nutrient is glucose (source of
immediate fuel for the body and
brain).
 Glucose travels to cells as energy and
to liver/fat cells (stored as nutrients).
 Blood glucose levels monitored by
sensors in the liver and the
hypothalamus.
A01: The role of the stomach in
eating behaviour
When blood glucose levels decrease: -
1.Liver converts stored nutrients back to glucose.
2.LH activated = hunger and eating initiated.
LIVER + LH work together to INCREASE BLOOD GLUCOSE LEVELS.
Glucostatic theory – changes in the supply of glucose available to cells (detected by
the liver) that sends signals to the hypothalamus which helps control eating
behaviour.
Independent task
• 10 minutes in silence to read
over/revise/summarise on A4 paper, the
A01 descriptive information on biological
explanations of eating behaviour.
• Then...QUIZ!
QUIZ /9
1. Give 2 examples of neural mechanisms. (2)
2.What is a lesion? (1)
3.What is stimulation? (1)
4.Which key brain area plays a role in eating behaviour?
(1)
5.When activated, which part of this brain area is said to
result in feelings of hunger? (1)
6.When activated, which part of this brain area is said to
result in feelings of satiation? (1)
7.What is satiation? (1)
8.Which simple sugar plays a key role in the dual-control
theory? (1)
A02: Supporting research for the role
of the stomach in eating
Lutter et al (2008)
 Ghrelin is an important hormone that indicates whether or not we
are hungry.
 It is produced and released by the stomach and travels to the LH.
 The LH has receptors for ghrelin and signals the body of hunger.
 When food is eaten the secretion of ghrelin stops.
 Hormonal levels of ghrelin increase before meals and decrease
after.
 Support for the role of hormones/brain areas in controlling
eating behaviour.
A02: Supporting evidence
We now need to look at research to support the
dual-control theory of eating behaviour.
First we are going to look at research to support
the role of the lateral hypothalamus (LH) in
initiating feelings of hunger resulting in eating.
P.E.E.L (A02)
• P: There is research to support the dual-control theory of
eating behaviour, particularly the role of the lateral
hypothalamus in stimulating eating behaviour.
• E: Research by _____________ has shown...
• E: This suggests/shows...
• L: This supporting research evidence by _____________
suggests that the dual-control theory is a valid biological
explanation of eating behaviour.
Supporting research for LH
 Damage to the LH leads to undereating and weight loss.
 Stimulation of the LH produces feelings of hunger and initiates
feeding behaviour.
1. Anand and Brobeck (1951) – rats with lesions to the LH
showed aphagia (they stopped eating even when palatable
food was readily available) and starved to death.
2. Quaade (1971) – successfully lesioned the LH of obese
patients to reduce eating behaviour. If LH was stimulated
electrically they reported feeling hungry.
Refer to evaluation in booklets re. lesions.
Neuropeptide Y
 Neurotransmitter found in the hypothalamus.
 Important in turning on eating - increased levels promotes
increases in food intake and weight.
 When injected into the hypothalamus of rats, NPY causes
them to immediately begin feeding even when full and
produces obesity in just a few days (Stanley et al, 1986;
Wickens, 2000).
 Practical applications: Potential treatment for anorexia?
IDA
Any ideas of issues, debates or approaches that you
could apply to what we have covered so far?
Something to think about…
Is it ethical to test on animals?
Can results from research on animals be generalised to humans?
A02: Supporting evidence
We now need to look at research to support the
role of the ventromedial hypothalamus (VMH) in
initiating feelings of satiety and stopping eating.
P.E.E.L (A02)
• P: There is research to support the dual-control theory of
eating behaviour, particularly the role of the
ventromedial hypothalamus in stopping eating
behaviour.
• E: Research by _____________ has shown...
• E: This suggests/shows...
• L: This supporting research evidence by _____________
suggests that the dual-control theory is a valid biological
explanation of eating behaviour.
Supporting research for VMH
Satiety centre, ‘stops eating’
 Research has shown that lesions or tumours in the VMH
lead to hyperphagia (overeating) and weight gain.
 Research has also shown that stimulation to the VMH
inhibits (i.e. stops) eating.
Hetherington and Ranson (1942) – rats with lesions to the
VMH would overeat until became grossly fat (hyperphagia).
Reeves and Plum (1969) carried out a post-mortem on a
patient who had doubled her weight in two years and found
a tumour on her VMH suggesting that this had impaired the
sensation of satiety (fullness).
Evaluation of research into the VMH
 Suggested that damage to the nerve fibres passing through the
VMH tends to also damage another area of the hypothalamus
called the paraventricular nucleus (PVN).
 It has been suggested that it is damage to the PVN alone that
causes hyperphagia (Gold, 1973).
 Found that lesions restricted to the VMH alone did not result in
hyperphagia and only resulted in overeating when they included
other brain areas such as the PVN.
 However subsequent research has failed to replicate Gold’s
findings with most studies showing that, compared to lesions in
other brain areas, animals with VMH lesions eat more and gain
more weight.
A02: The role of Leptin
 The hormone leptin is secreted by fat tissue and travels via
the bloodstream to the hypothalamus where it binds to
certain receptors.
 Leptin acts to decrease food intake.
 Leptin works opposite of Ghrelin.
 Role of Ghrelin = signals the body that it is hungry.
 Role of Leptin = signals the body that it is full.
 Also has specific roles in the regulation of energy
expenditure and food intake.
Independent tasks
1. Read the research in your booklets and fill in
the missing gaps.
2. Read the evaluation points for the role of
leptin and highlight the key points.
You have 10 minutes
A02: Evaluation
There are individuals who have a genetic leptin
deficiency who are diagnosed as being obese.
Humans are biological organisms and our eating
behaviour relies on our biological systems. Insight
into biological mechanisms may be used to develop
medical interventions to help change what we eat
and manage weight (e.g. obese patients).
A02: Evaluation
X If it was this simple obese people could just be injected with
leptin to reduce weight. However it is not the case that all
obese people have low levels of leptin or a leptin deficiency.
X The biological approach is reductionist, focusing only on
biological systems regulating food intake and body weight.
It ignores psychological, cultural and social factors that can
influence our eating behaviour.
A02: The role of Serotonin
Serotonin is a neurotransmitter.
It has a chemical influence on satiation (similar to Leptin).
However increased activity of serotonin in the medial
hypothalamus (MH) has been associated with decreased food
intake.
This suggests that it is not just the VMH that plays a role in
‘stopping eating’ but also the MH as well as chemical influences
(leptin and serotonin).
Suggests a more complex interaction of many neural
mechanisms working together to control eating behaviour.
IDA
In pairs, discuss and make notes on any issues, debates or
approaches that you could apply to the dual-control theory
of eating behaviour and associated research.
Something to think about…






Reductionism.
Determinism.
Biological approach (nature vs. nurture).
Ethical issues.
Evolutionary approach?
Real-world applications.
IDA
Reductionist – biological explanations only focus on limited
factors which can be used to explain eating behaviour e.g. specific
brain area, hormone, NT. It pays no attention to psychological,
cultural and social factors that influence our eating behaviour.
Deterministic – damage to the LH, VMH, or lack of leptin can
result in disordered eating – ignores free will (cognition).
Biological approach – cannot provide full explanation as it ignores
the role of nurture. (Nature vs. Nurture).
IDA
Ethical issues – is it ethical to test on animals? Much of the
research is on mice/rats. Based on principle that brain systems
similar to humans but to what extent can findings be
generalised?
Ignores evolutionary approach – suggest primary stimulus for
hunger and eating is food’s positive-incentive value.
Real-world applications of research - insight into neural
mechanisms may be used to develop medical interventions to
help change what we eat and manage our weight (e.g. obese
patients).
Homework
1. Complete the table of key terms for biological
explanations of eating behaviour in your booklets.
2. Complete essay structure and IDA gap fill task in booklet.
3. Revision aid for this section of the topic –
mindmap/revision notes/cue cards.
4. TEST NEXT WEEK.