neural mechanisms 2012
TRANSCRIPT
Biological
explanations
of eating
behaviourSpecification:
The role of neural
mechanisms involved in
controlling eating and
satiation
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?
Neural mechanisms in eating
and satiation
Homeostasis
Humans, along with all
mammals are
homeostatic animals, (we are designed to run our
bodies in a constant state
of balance)
Involves mechanisms that detect both the
state of the internal environment (e.g. Level
of nutrients) and correct the situation to
restore that environment to its optimal state
Our eating behaviour is a prime example of
this internal balance in that it is clear from
research that we have a “Feeding” centre
in the brain activated when we are hungry
and a “Satiety” centre activated when we
are full.
The body has evolved two separate systems
(both involving the hypothalamus)
Turning eating ON
- Lateral hypothalamus
Turning eating OFF
- Ventromedial
hypothalamus
The Dual Feeding System!
The control of eating and satiation
Among humans, glucose levels play the most
important part in producing feelings of hunger
**Hunger increases as glucose levels decrease**
**Satiation (fullness) increases as glucose levels
increase**
Decreasing glucose and
the Lateral Hypothalamus1. A decline in glucose levels
in the blood activates the
Lateral Hypothalamus.
2. Feelings of hunger
3. Individual searches for and
then consumes food
- Glucose levels rise again
Rising glucose and the
Ventromedial Hypothalamus1. A rise in glucose levels in the
blood activate the VMH
2. Feeling of satiation (fullness)
This inhibits further feeding
LH + NPY seem to control eating behaviour
In the 1950’s...
• Researchers found that damage to
the LH in rats caused aphagia(a failure to eat when hungry)
• Stimulation of the LH caused the
animal to want to feed
Neuropeptide Y (NPY) was also
found to be important in turning
eating on.
- When injected into the
hypothalamus of rats, NPY caused
them to start feeding, even when they
were full!
It was
concluded
therefore that
the LH was the
„ON‟ switch for
eating
behaviour
Repeated injections of
NPY caused obesity in a
matter of days
(Stanley 1986)
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)
AO1 – Neural mechanisms
involved in the control of eating....
LH NPYHigh levels of
Ghrelin
Cause Hunger
All switch eating ON
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
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 be a result of the experimental artefact, in
that the flood of NPY given to the rats during the
experimental manipulations could cause behaviour not like
that caused by normal amounts of the neurotransmitter
This shows that the relationship between NPY and feeding
behaviour remains unclear. Which means that we do not
know everything “as yet” about brain mechanisms which
control feeding behaviour.
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
Research into the role of
GhrelinCummings et al (2004)
A – To investigate changes in blood ghrelinlevels over time between meals
P – 6 male participants were allowed to eat lunch, ghrelin levels were monitored via blood samples taken every 5 minutes until the participant requested their evening meal. Participants assessed their degree of hunger every 30 minutes
F – Cummings found that ghrelin levels fell immediately after eating lunch and then slowly began to rise, peaking as participants requested their evening meal. In 5/6 participants ghrelin levels were closely correlated to their self-report feelings of hunger
C – The researchers concluded therefore that ghrelin directly reflects stomach emptiness and are closely related to subjective feelings of hunger.
Ghrelin therefore has a key role in appetite
signalling in humans
A03? IDEAs?
EvaluationGhrelin
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
(2004)
Sample
Bias?
Cummings
(2004)
Correlation?
Cummings
(2006)
Ethical
Issues
Cummings
(2004)
Ps were
isolated
from time &
social cues
Debates: DeterministicApproaches: Biological
Ignores other explanations (e.g.
evolutionary explanation)
Also, don‟t forget..AO3.. How
- ExtrapolationIssues:
Reductionist
Ethical issues
Question exercise
Outline the role of neural
mechanisms involved in
controlling eating behaviour
(8 marks)
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
The Ventromedial Hypothalamus• Researchers discovered that
damage to the VMH caused rats to overeat leading to a condition called hyperphagia.
• Stimulation of the VMH inhibits feeding
A02 - However...
Damage to the nerves passing
through the VMH causes damage
to another part of the
hypothalamus, the paraventricular
nucleus (PVN) – it is thought that
damage to the PVN alone causes
hyperphagia
It was
concluded
therefore that
the VMH was
the „OFF‟
switch for
eating
behaviour
A02
The PVN also
detects the specific
foods our body
needs (may be
responsible for
cravings)
EvaluationVentromedial 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
EvaluationVentromedial 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
However...
Further research has failed to replicate
Gold’s findings, demonstrating that
animals with VMH lesions ate
substantially more and gained more
weight compared to those with lesions
in other brain areas
The
reliability of
Gold’s
research
can be
questioned
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!
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.........
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
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!
AO2: An evaluation of the role of
Leptin in eating behaviour
Debates: DeterministicApproaches: Biological
Ignores other explanations (e.g.
evolutionary explanation)
Also, don‟t forget..AO3.. How
- ExtrapolationIssues:
Reductionist
Ethical issues
General EvaluationThe 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?
Diagram of the Dual Centre Model of Feeding
Feelings of hunger -feeding starts
Food intake, rise in
glucose levels and a
decrease in ghrelin
VMH satiety centre
satisfied
Satiety, feeling of fullness (feeding stops)
Signals of decline in nutrients
(decrease of glucose,
increase of ghrelin
LH feeding centre is activated