Transcript EATING BEHAVIOUR - Caroline Chisholm School

Eating behaviour
 You will be able to:
 Understand the role of neural mechanisms involved in
controlling eating and satiation
 Evaluate research into the mechanisms of eating and
satiation
 Discuss neural mechanisms
involved in the control of eating
behaviour.
 (8 marks + 16 marks)
 Eating behaviour covers all aspects of normal eating behaviour and
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eating disorders.
However candidates are likely to focus on hypothalamic feeding and
satiety centres and the dual centre model of feeding regulation.
This model also involves the role of hormones such as CCK, leptin and
ghrelin. As long as the role of hormones is explicitly linked to neural
mechanisms in the brain this approach is fully acceptable. Descriptive
terms such as ‘neurotransmitter’ would also be sufficient as a link to
neural mechanisms eg in relation to neuropeptide Y and serotonin.
Answers that focus, for instance, on eating disorders, should be
assessed on the degree to which neural (brain) mechanisms are
involved.
There are no partial performance criteria on this question. It is hard to
imagine an answer considering a single mechanism, but any such
answer would be limited and unlikely to move beyond Basic.
 The biology of eating behaviour is very complicated.
 You need a basic knowledge of the need for control of
food intake and body weight, and some of the key
processes involved.
 Focus =
 The key centres in the hypothalamus need signals to
tell them when to start and when to stop feeding.
 You should be able to outline at least two of these
signals.
 Hetherington and Ranson (1942)
 Lesions in the hypothalamus of the brain in rats
caused the rats to overeat and become obese.
 The lesion was in the ventromedial nucleus of the
hypothalamus and the rat became known as
 The VMH rat.
 Found that a lesion in the lateral hypothalamus (LH)
led to a loss of feeding in rats known as
 Aphagia
 They assumed the function of the LH was to stimulate
feeding in hungry rats.
 The lesion destroyed a vital centre for the control of
feeding behaviour.
 Its destruction led to an increase in feeding and body
weight.
 Hetherington and Ranson assumed this was a ‘satiety
centre’.
 They assumed it was normally activated when the
animal was full and its function was to inhibit feeding.
 Later studies confirmed previous findings.
Rise in glucose,
decrease in ghrelin
release
Hunger – feeding
starts
VMH satiety
centre activated
Lateral
hypohtalamus
(LH) feeding
centre activated
Satiety, feeding
stops
Signals of
declining nutrient
levels, decrease in
blood sugar,
increase in ghrelin
release
 The dual model is confirmed by much research but the
pathways are very complex.
 In Western countries we usually eat to a schedule. The
digestive system starts preparing itself by releasing
saliva and enzymes just before a meal time (Pinel,
2007). This represents a learned response, anticipating
the presence of food.
 Even when we’re
not really hungry,
we can be tempted
by some things.
 The empty
stomach sends
signals to the
brain to start
eating.
 An important role
is played by a
hormone –
 Grehlin
 Ghrelin is a hormone
that signals the
hypothalamus to
stimulate feeding.
 The amount released is
directly proportional to
the emptiness of the
stomach.
 As the time from the last
meal increases so ghrelin
secretion is increased.
 Injections of ghrelin
increase food intake and
body weight in animals
and humans
(Cummings, 2006).
 Gastric bands used to
treat obesity reduce
ghrelin secretion from
the stomach.
 Cummings (2006)
found that ghrelin
acts directly on the
brain mechanisms of
feeding behaviour,
including the
hypothalamus.
 Investigated changes in
blood ghrelin levels over
time between meals.
 6 participants ate lunch.
 Their ghrelin levels were
measured from blood
samples taken every 5
minutes until they
requested their evening
meal.
 Participants assessed
their hunger every 30
minutes.
 Ghrelin levels fell
immediately after eating
lunch
 The lowest level was after
about 70 minutes.
 Then they slowly began
to rise
 Peaking as participants
requested their evening
meal.
 Ghrelin levels positively
correlated with the
degree of hunger
reported in 5 out of the 6
participants.
 Conclusion – ghrelin
levels directly reflect
stomach emptiness and
are closely related to
feelings of hunger.
 This
supports a
role for
ghrelin in
signalling
appetite in
humans.
 Leptin is a hormone
released from fatty
(adipose) tissue.
 It acts as an indicator
of body weight to
hypothalamic
mechanisms
controlling long-term
food intake.