1. Biological
explanations
of eating
behaviour
Specification:
The role of neural
mechanisms involved in
controlling eating and
satiation

2. How do we know when it is time
to eat?
• Hunger is activated by both
environmental and biological
factors.
This topic looks at biological
mechanisms involved in
eating.
•What makes us feel hungry?
•What tells us to stop eating
when we are full?

3. Neural mechanisms in eating
and satiation
Involves mechanisms that detect both the
Homeostasis state of the internal environment (e.g. Level
of nutrients) and correct the situation to
Humans, along with all restore that environment to its optimal state
mammals are Our eating behaviour is a prime example of
homeostatic animals, this internal balance in that it is clear from
(we are designed to run our research that we have a “Feeding” centre
bodies in a constant state in the brain activated when we are hungry
of balance) and a “Satiety” centre activated when we
are full.
The body has evolved two separate systems
The Dual Feeding System!
(both involving the hypothalamus)
Turning eating OFF
Turning eating ON
- Ventromedial
- Lateral hypothalamus
hypothalamus

4. The control of eating and satiation
Among humans, glucose levels play the most
important part in producing feelings of hunger
Decreasing glucose and
Rising glucose and the
the Lateral Hypothalamus
Ventromedial Hypothalamus
1. A decline in glucose levels
1. A rise in glucose levels in the
in the blood activates the
blood activate the VMH
Lateral Hypothalamus.
2. Feeling of satiation (fullness)
2. Feelings of hunger
3. Individual searches for and
This inhibits further feeding
then consumes food
- Glucose levels rise again
**Hunger increases as glucose levels decrease**
**Satiation (fullness) increases as glucose levels
increase**

5. LH + NPY seem to control eating behaviour
In the 1950’s...
• Researchers found that damage to
the LH in rats caused aphagia It was
(a failure to eat when hungry) concluded
• Stimulation of the LH caused the therefore that
the LH was the
animal to want to feed
„ON‟ switch for
eating
Neuropeptide Y (NPY) was also behaviour
found to be important in turning
eating on. Repeated injections of
NPY caused obesity in a
matter of days
- When injected into the (Stanley 1986)
hypothalamus of rats, NPY caused
them to start feeding, even when they
were full!

6. What does this suggest about the
neural mechanisms of the LH in
controlling eating behaviour?
* It suggests that the LH is the main feeding centre
in rats and that the LH triggers feeding in response
to signals from the body.
* It also suggests that NPY is also important in
triggering the feeding response.
* The LH and NPY therefore turn feeding ON! (not
off)

7. AO1 – Neural mechanisms
involved in the control of eating....
High levels of
LH NPY Ghrelin
Cause Hunger
All switch eating ON

8. AO2: An evaluation of the role of the LH
in eating behaviour
Damage to the LH causes deficits in other aspects of
behaviour (e.g. Thirst and sex). Therefore LH does not only
control hunger.
More recent research has shown that eating behaviour is
controlled by neural circuits that run through the brain, not
just the hypothalamus
This shows that although LH undoubtedly plays an important
role in the control of eating behaviour, it may not, as
previously thought, be the brain’s sole feeding centre
Sakurai et al, 1998

9. AO2: An evaluation of the role of
Neuropeptide Y in eating behaviour
Recent research on NPY has cast doubt on whether its
normal function is to influence feeding behaviour
Marie et al (2005) genetically manipulated mice so that they
did not make NPY. They found no subsequent decrease in
their feeding behaviour
This suggests that the hunger stimulated by the injections of
NPY may actually thea result of the experimental artefact, in
This shows that be relationship between NPY and feeding
that the floodremains given to the ratsmeans the we do not
behaviour of NPY unclear. Which during that
experimental manipulations about brain mechanisms which
know everything “as yet” could cause behaviour not like
control feeding behaviour.
that caused by normal amounts of the neurotransmitter

10. Hormone - Ghrelin
• Ghrelin is a hormone that is released from
an empty stomach
• The amount of ghrelin released is directly
proportional to the emptiness of the
stomach
i.e. As the time from the last meal increases
and we feel hungrier, so ghrelin secretion
is increased
Ghrelin is the hunger signal

11. Research into the role of
A03? Ghrelin IDEAs?
F – Cummings al (2004)
Cummings et found that ghrelin levels fell
immediately after eating lunch and then
– To investigate changes in blood ghrelin
A slowly began to rise, peaking as participants
levels over time between meals
requested their evening meal. In 5/6
P participants ghrelin levels were closely eat
– 6 male participants were allowed to
correlated to their self-report feelings of
lunch, ghrelin levels were monitored via
hunger
C blood samples taken every 5 minutesthat
– The researchers concluded therefore until
the participant reflects stomach emptiness
ghrelin directly requested their evening
meal. Participants assessed their degree
and are closely related to subjective feelings
of hunger. every 30 minutes
hunger
Ghrelin therefore has a key role in appetite
signalling in humans

12. Evaluation
Ghrelin
Further research conducted by Cummings (2006) has found
that injections of ghrelin increases food intake in both animals
and humans
This provides biological evidence of the link between the
hormone ghrelin and the beginning of eating, satiety and
overeating.
Cummings
Cummings Cummings
Cummings (2004)
(2004) (2006)
(2004) Ps were
isolated
Sample Ethical
Correlation? from time &
Bias? Issues
social cues

13. Approaches: Biological
Debates: Deterministic
Ignores other explanations (e.g.
evolutionary explanation)
Also, don‟t forget..AO3.. How
Issues: - Extrapolation
Reductionist
Ethical issues

14. Question exercise
Outline the role of neural
mechanisms involved in
controlling eating behaviour
(8 marks)

15. Mind map
Make sure you construct a
mind map to organise the
AO1; AO2; AO3 and IDEAs
for the role of neural
mechanisms involved in
eating behaviours

16. The Ventromedial Hypothalamus
• Researchers discovered that
damage to the VMH caused rats to
overeat leading to a condition called It was
hyperphagia. concluded
therefore that
• Stimulation of the VMH inhibits the VMH was
feeding the „OFF‟
switch for
A02 - However... eating
Damage to the nerves passing behaviour
through the VMH causes damage
A02
to another part of the The PVN also
hypothalamus, the paraventricular detects the specific
nucleus (PVN) – it is thought that foods our body
needs (may be
damage to the PVN alone causes responsible for
hyperphagia cravings)

17. Evaluation
Ventromedial Hypothalamus
Extensive research has supported the finding that
lesions/damage to the VMH results in hyperphagia and
obesity
Shows that the VMH plays an important part in signalling to
an individual when it’s necessary for them to cease eating
Hetherington & Ranson conducted research and reported
that lesions to the VMH caused rats to become dramatically
obese
Supporting the idea that if the VMH (satiety centre) is
destroyed it can lead to uncontrolled eating

18. Evaluation
Ventromedial Hypothalamus
Gold (1973) found lesions/damage to the VMH alone did not
result in hyperphagia and only produced over eating when
other areas (such as the PVN) was also damaged
Suggesting that the VMH doesn’t appear to control
hunger/satiety alone
The
However...
reliability of
Further research has failed to replicate Gold’s
Gold’s findings, demonstrating that research
can be
animals with VMH lesions ate
questioned
substantially more and gained more
weight compared to those with lesions
in other brain areas

19. The role of Leptin
• Leptin is a fat hormone
• It is secreted into the blood stream to
signal to the brain (via the hypothalamus)
that calorie storage is high.
• Basically telling the brain that the body has
sufficient fat stored
The body releases more leptin as more fat is
stored – how should the body respond to this?
STOP EATING!

20. Therefore..Low levels of Leptin
also cause us to feel hungry
* When people don’t eat enough food, fat is used
up, the fat cells cease to secrete leptin.
* Leptin levels in the blood fall – the
hypothalamus detects the drop in leptin levels
and generates a feeling of hunger to increase
eating.
In summary.........

21. AO2: An evaluation of the role of
Leptin in eating behaviour
Support for the role of leptin in eating behaviour comes from
conducting experiments using ‘ob’ mice (a stain of mice that
are genetically obese).
Studies have demonstrated that these mice are missing the
gene that produces leptin. They therefore eat continually.
(remember, low levels of leptin are thought to cause hunger)
Furthermore, injections of leptin into the ob mice stop them
eating so much and their weight eventually returns to normal
This shows that there appears to be a strong link in the
relationship between low levels of leptin and over-eating

22. AO2: An evaluation of the role of
Leptin in eating behaviour
However, some
humans who are
overweight have a
leptin deficiency but
most actually have
increased levels of
leptin!

23. Approaches: Biological
Debates: Deterministic
Ignores other explanations (e.g.
evolutionary explanation)
Also, don‟t forget..AO3.. How
Issues: - Extrapolation
Reductionist
Ethical issues

24. General Evaluation
The role of neural mechanisms are still unclear,
exactly how ghrelin and leptin reach their targets
in the brain is not fully clear, both are large
peptides what do not cross the blood brain barrier
easily
Influence of biological rhythms, research has
shown that rats become more active and start to
eat soon after darkness descends. This and
similar rhythms are controlled by another area of
the hypothalamus (the SCN)
IDEA - Alternative approach – what other factors
influence your hunger levels everyday?

25. Diagram of the Dual Centre
Model of Feeding
Feelings of
hunger -
feeding
starts
Food intake,
rise in
LH feeding
glucose levels
centre is
and a
activated
decrease in
ghrelin
Signals of
decline in
nutrients VMH satiety
(decrease of centre
glucose, satisfied
increase of
ghrelin
Satiety,
feeling of
fullness
(feeding
stops)