Transcript Eating Behaviour - Home

Eating Behaviour
Unit PSYA3
Miss Bird
What will we cover in this topic?
Eating
behaviour
Factors influencing attitudes to food and eating behaviour. For
example: 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 eating
Evolutionary explanations of food preference.
behaviour
In relation to either anorexia nervosa or bulimia nervosa:
Eating
disorders
Psychological explanations.
Biological explanations, including neural and evolutionary
explanations.
What we have covered
Where we are now
RECAP: Dual-control
theory
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.
RECAP: Dual-control theory
Eating
Increase in
blood glucose
Ventromedial
hypothalamus
activated
Hunger
Lateral
hypothalamus
activated
Decrease in
blood glucose
Satiety
Eating stops
Set point theory
Support for the dual-control theory
 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 and weight control are the result of a
balance between these two parts of the hypothalamus.
RESEARCH
Support for dual-control theory
Last lesson we looked at research to
support the role of the lateral
hypothalamus (LH) in initiating feelings
of hunger and eating.
Ghrelin
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.
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.
Neuropeptide Y
 Neurotransmitter found in the hypothalamus.
 Important in turning on eating - increased levels
promotes increases in food intake and weight.
 When NPY 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).
RESEARCH
Support for dual-control theory
This lesson we will look at research to
support the role of the ventromedial
hypothalamus (VMH) in initiating feelings
of satiety and stopping eating.
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
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.
The role of Leptin
 The hormone leptin is secreted by adipose (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.
Research into the role of
Leptin
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.
Be prepared to feedback to the class.
You have 10 minutes
Evaluation
 There are individuals who have a genetic leptin deficiency who are
correlated with being obese.
 Humans are biological organisms and our eating behaviour relies
on our biological systems. Insight into brain chemicals may be
used to develop medical interventions to help change what we eat
(e.g. obese patients).
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.
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.
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).
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
Reductionism – biological explanation only focuses
on limited factors which can be used to explain
eating behaviour. 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.
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 positiveincentive value.
Real-world applications of research - insight into brain
chemicals may be used to develop medical interventions
to help change what we eat and manage our weight
(e.g. obese patients).
Homework
Due in Tuesday 9th April
1. Complete the 24-mark past-exam question:
Discuss neural mechanisms involved in the
control of eating behaviour (Jan 2012).
2. Research neural control of cognitive factors in
eating behaviour including the role of the
amygdala and the inferior frontal cortex (page
88 of third edition textbook).
3. Update key terms table with today’s lesson
content.