Zusammenfassung der Ressource
Biological explanations of eating behaviour
- Neural mechanisms
- Homeostasis
- Eating
- Increase BGL
- VMH activated
- Satiety
- Eating stops
- Decrease BGL
- LH activated
- Hunger
- Hetherington & Ranson - VMH
lesions made rats over eat
- Han & Lin - lesioned VMH
then force fed rats. Lesion
didn't cause overeating higher
set point already reached
- Anand & Brobeck - LH lesions
stopped eating behaviour
- Neither killed rats, must have
been stopped somehow -
dual control theory
- LH lesions lower set
point VMH lesions raise it
- set point theory
- Powley & Keesey - starved rats
and lesioned LH. Lesion didn't stop
eating, lower point already reached
- Insulin & Glucagon maintain BSL.
Bloodstream fat -> adipose tissue
- Role of the hypothalamus
- PYY - screted
after meals,
suggests fullness
- Ghrelin - secreted by
stomach, suggests hunger
- Also activates NPY neurones
- Marie et al - manipulated mice
so NPY neurones not created,
no change in feeding behaviour
- Leptin levels increase
when plenty of adipose
- Insulin & Leptin reduced,
NPY neurones stimulate
orexigenic neurones
- LH stimulated - starting eating
- Insulin & Leptin increased,
POMC neurones stimulate
anorexigenic neurones
- VMH stimulated - eating
stops
- NPY produced
by abdominal fat.
Vicious cycle
where NPY
causes more
eating, producing
more fat cells
- Individuals at risk of
increased NPY treated
to prevent obesity
- Gold - VMH
lesions only
produced
overeating when
including PVN
- Findings not
replicated in
humans
- In animals PVN lesion lead
to increased feeding. In
humans PVN detects food we
need, may cause cravings
- Neural control
- Amygdala used to select
food based on experience
- Rolls & Rolls - surgically
removed rats amygdala,
they ate novel and familiar
foods, unlike normal rats
- Can explain the
behaviour of
Klüver–Bucy suffers
who have an eat
anything attitude,
including non food
items. Food cues no
longer represent
reward
- Inferior frontal cortex recieves
messages from the olfactory bulb
- Kolb & Wishaw - damage
caused decreased eating
due to less sensory
information affecting taste
- Evolutionary explanations
of food preference
- EEA - the environment where
a species first evolved
- Adaptations to environment
shaped food preferences
- Humans lived in hunter gather
society with preference for
easy high calorie food
- Men: Hunters.
Women: childcare
and foraging
- Low cholesterol
preference not from
EEA. No advantages
- Stanford - Chimps (mostly starved)
go for the fattiest part of meat
- Abrams - All
human
societies show
preference for
animal fat.
Universal
adaptation
- Taste preference
- Meat - packed with nutrients -
catalyst for brain growth.
Supplied AA and minerals
- Adapted for meat - larger
than average duodenum,
for protein breakdown
- Fatty foods - provided
energy for survival
- Distaste for sour -
associated with
gone off food -
source of bacteria
- Taste aversion -
evolutionary
advantage
- Garcia et al - rats made ill
by radiation after eating
Saccharin (sweetener).
Aversion developed from
association
- Eating poison and being
sick makes you unlikely
to eat the same food in
the future. Hard to shift
- Neese & Williams - Children's taste
aversion to broccoli & brussels
sprouts understood as they contain
chemicals toxic to children
- The medicine effect -
preference developed for
food eaten just before
overcoming illness
- Assocaited with
feeling better
- Food neophobia - evolutionary
tendency to avoid new foods
- Frost -
Greater liking
for familiar
foods
- Bernstein & Webster -
chemotherapy
patients given novel
ice cream before
treatment. Aversion
developed
- Hospitals now give patients
novel and familiar foods
- Cooking
- Wrangham et al - food
cooking started 500,000 years
ago. Good way to kill bacteria
- Lucas et al - cooking
made food easier to chew,
molar size decreased
- Embryo protection hypothesis -
morning sickness occurs in early stage
of pregnancy during organ development
- Buss - Coffee, tea, meat
& eggs most avoided
- Most common
sources of bacteria