BIOLOGICAL EXPLANATIONS OF EATING
BEHAVIOUR
To read up on biological explanations of eating behaviour, refer to pages 199–208 of
Eysenck’s A2 Level Psychology.
Ask yourself
 How is eating behaviour related to hunger?
 How is eating behaviour not related to hunger? Do we eat when we’re not
hungry?
 How might the lifestyle of our evolutionary ancestors have shaped the way
we eat?
What you need to know
NEURAL MECHANISMS INVOLVED IN
CONTROLLING EATING AND
SATIATION
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Hunger, satiety, and the brain
The role of hormones
EVOLUTIONARY EXPLANATIONS OF
FOOD PREFERENCE
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Research evidence for and against
evolutionary explanations
NEURAL MECHANISMS INVOLVED IN CONTROLLING EATING AND SATIATION
Hunger, Satiety, and the Brain
There are key centres in the brain that control hunger: these are the neural
mechanisms involved in the drive to eat (hunger) and the feeling of fullness that
switches off the hunger drive (satiety).
RESEARCH EVIDENCE FOR NEURAL MECHANISMS
 Research by de Araujo et al. (2006, see A2 Level Psychology pages 199–200)
focuses on the lateral hypothalamus, orbitofrontal cortex, insular cortex, and
amygdala. de Araujo et al. planted electrodes in these areas in rat brains so
that they could monitor the excitation during periods of feeding and satiety.
They found that they could identify individual neurons that were activated
during different phases of the feeding cycle (see the diagram at the top of
page 200 of A2 Level Psychology).
 Two significant eating control centres are in the hypothalamus. One is in the
lateral hypothalamus (or LH), also know as the “start” switch, the other is in
the ventro-medial hypothalamus (or VMH), also known as the “stop” switch.
The parietal and temporal cortex are also involved with hunger and the
prefrontal cortex is involved with satiety.
 Research from the 1940s onwards showed that lesioning (i.e. destroying)
tiny areas in the LH in rats, dogs, and other mammals led to a loss of interest
in food and eating, the animals seemingly unaware that they were starving
themselves. Whereas the opposite happened with lesions to the VMH as this
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led to the animals concerned eating voraciously, so they became obese. This
suggested that the LH initiates eating behaviour (hence the “start” switch)
and the VMH stops this behaviour (hence the “stop” switch).
Another neural mechanism is interconnected with the stomach. The stomach
sends nerve impulses to the brain, stretch receptors in the stomach walls
send signals via the vagus nerve to the hypothalamus, and these stimulate
feelings of satiety. However, there is a time delay between the arrival of the
food into the stomach and these messages being sent, and so this is why we
are advised to eat slowly, because eating too quickly could mean going past
the satiety point without the brain realising it; whereas slower eating allows
the gut time to communicate with the brain.
The Role of Hormones
Hormones such as insulin and leptin are also involved in eating behaviour. Leptin
acts upon various hypothalamic areas and seems to inhibit the release of another
neurochemical, neuropeptide Y, which is the neurotransmitter stimulating hunger
and eating behaviour. Thus, low levels of leptin will increase hunger and eating
behaviour. Blood glucose imbalances as a result of insulin insensitivity are also
linked to either increased or decreased eating behaviour.
RESEARCH EVIDENCE FOR THE ROLE OF HORMONES
 Blood glucose levels affect hunger. When glucose levels were lowered in rats
or in humans, appetite increased; when they were raised, appetite faded
away (Smith & Campfield, 1993; Lavin et al., 1996, see A2 Level Psychology
page 201).
 Animal studies showed that when blood insulin levels were low the animals
ate much more than usual, whereas injections of moderate levels of insulin
seemed to reduce appetite, probably by reducing hunger (Rosenzweig,
Breedlove, & Leiman, 2002, see A2 Level Psychology page 201).
 Licinio et al. (2004, see A2 Level Psychology page 201) researched three
adults from the same Turkish family to demonstrate that when they were
given leptin supplements body weight and eating behaviour became normal.
 London (2007, see A2 Level Psychology page 201) showed some sustained
structural changes in the cortex with the same leptin supplements of those
three adults. London continued to research these three family members who
had no leptin production of their own. Thus, investigation of the neural
circuits for leptin action using fMRI imaging was possible. Neural activity was
measured in the absence of leptin and then in the presence of leptin to
identify the brain areas leptin acted upon. The results were reduced activity
in the insular, parietal, and temporal cortices, and increased brain activity in
the prefrontal cortex after the leptin treatment. This fits in with the insular,
parietal, and temporal cortex areas being concerned with hunger but the
prefrontal areas being concerned with satiety, and so leptin decreases eating
behaviour (see diagram in A2 Level Psychology page 202).
 Ravussin et al.’s (1997, see A2 Level Psychology page 202) longitudinal study
investigated the Pima Indians, a population prone to obesity. Two weight-
matched groups (i.e. participants matched based on their weight) were
studied over 3 years and it was found that mean plasma leptin
concentrations were lower in the group that gained weight than in the group
that did not gain weight. This confirms leptin’s influence on appetite and
weight gain.
RESEARCH EVIDENCE AGAINST BIOLOGICAL EXPLANATIONS
 Lesions have a wider effect. In criticism of the conclusions from brainlesioning studies, Logue (2004, see A2 Level Psychology page 200) and others
have pointed out that lesions could affect far more neurons and neural
activity than that of the cell bodies in the destroyed area because nerve fibres
may be damaged in nearby areas.
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The delayed signaling between stomach and brain is challenged by Johnstone
et al.’s (2006, see A2 Level Psychology page 202) study on the drive to eat.
They used rats on a strict and regular diet where food was presented for 2
hours a day. Brain activity was analysed when fasting, when anticipating
feeding, and when actually feeding. The results showed that appetitestimulating neurons start firing off before feeding starts in anticipation of the
food. Also appetite-suppressing neurons started to activate as soon as food
was being eaten. Thus, this seems to contradict the research on the time
delay between food entering the stomach and the brain receiving this
information. However, extrapolation is clearly an issue (see below).
EVALUATION OF NEURAL MECHANISMS AND THE ROLE OF HORMONES
 The role of cognition is ignored. The neurons with cell bodies in the LH or
VMH could be affected by sensory input relayed from other areas, in
particular the frontal cortex. This is supported by the fact that we all have
food preferences, and so cognition also plays a part in eating and stopping
eating; these behaviours are not just automatic stimulus–response drives.
Thus, hunger, eating, and satiety are not just a result of biological processes,
and the LH and VMH control system is far from a set of simple on–off
switches.
 Extrapolation. The influence of cognition is true of animals as well as
humans, but more so in humans due to the greater role of cognition in human
behaviour, and so this leads to the issue of extrapolation from animal
research as findings on animals may lack generalisability to humans. It
cannot be assumed that what is true of animals is the same for the far more
complex human brain.
 Individual differences. There are wide individual differences showing that
the biological mechanisms do not work in a uniform way. Horvath (2005, see
A2 Level Psychology page 201) suggests that each person has their individual
set point (a balance between hunger and satiety) as a result of genetic factors
and early nutritional experience. Thus, if the set point is nearer to hunger,
then that person might have a tendency to eat more and be overweight,
whereas if the balance point is nearer satiety then that person will eat less
and will be unlikely to be overweight. This may well be true but it doesn’t
account for people who can eat large amounts and not put on weight, nor
whether this set point can change, for example with the season (we tend to
eat more during the winter) or mood (comfort eating). Also the Prisoners of
War released from the German concentration camps were all severely
underweight and so everyone can lose weight, it is not a physiological
impossibility.
 Cause and effect and direction of effect. The roles of neural mechanisms
and hormones in eating behaviour are unclear because it is not clear whether
it is their dysfunction that causes abnormal eating behaviour or whether the
eating behaviour causes the neural mechanism dysfunction or hormonal
imbalance. Furthermore, because the real-life cases of brain damage provide
only correlational evidence we cannot establish cause and effect (i.e. that
neural damage causes abnormal eating behaviour), conclusions are limited to
association.
 Mundane realism. Clearly the lesioning of the VMH and LH shows damage
to these areas can cause dysfunctional eating behaviour but this does not
mean this is the direction of effect in real life. Thus, the findings may lack
generalisability to real life and so have limited external validity.
 Sample bias. The sample sizes of the research, e.g. the three family members
in the leptin research, mean the research is unrepresentative of the general
population. We cannot generalise from such research and so it lacks
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population validity as we cannot be sure how true the findings are for other
populations.
Increased understanding and positive applications. Research is
beginning to show how the hormones interact with the brain centres, and
this increased understanding offers the possibility of positive applications in
terms of treatment for obesity. The leptin supplements used by Licinio et al.
(2004, see A2 Level Psychology page 201) are one example of how this has
already begun. However, if this was joined up with the action of PYY (peptide
tyrosine tyrosine) then perhaps even more effective treatments can be
developed.
EVOLUTIONARY EXPLANATIONS OF FOOD PREFERENCE
Evolutionary explanations focus on what factors could have been adaptive, i.e. what
could have been advantageous and so helped our evolutionary ancestors survive
and reproduce in the EEA (evolutionary environment of adaptation). Food
preferences may have been adaptive, for example, being omnivorous (eat plants and
animals) would be more adaptive than being either herbivorous (plant eating) or
carnivorous (meat eating) as eating both animals and plants affords a greater food
range and this would increase chances of survival and consequently reproduction.
In harsh conditions there would be a fine line between the energy expended in
hunting for and gathering food, and the energy and nutrients gained from the food.
Foods rich in energy and nutrients would be more likely to have a positive energy
balance, i.e. the energy from the food outweighs that used to find it. This may
explain the universal human preference for foods rich in protein, fat, oils, and sugar,
and this suggests that these preferences are genetic, innate, and hard-wired into us.
RESEARCH EVIDENCE FOR EVOLUTIONARY EXPLANATIONS OF FOOD PREFERENCE
 Fats and oils contain twice as many calories as carbohydrates or proteins.
This would suggest that a preference and searching for fatty foods would
have been adaptive for our ancestors.
 Protein-rich foods would also have been necessary for health as these are
needed to repair and build body tissue, especially in pregnant or lactating
(breast-feeding) women.
 Eaton and Konner (1985, see A2 Level Psychology page 204) suggest humans
have a genetically controlled preference for fatty, meaty foods and this is
evident in the “paleolithic diet” of meat, fish, and fatty/oily foods plus fruits
and vegetables, which has been put forward as the only healthy way for
humans to eat. Fatty foods have fat-soluble vitamins such as vitamin D and so
they are sources of more than just calories. Eaton and Konner suggest
carbohydrates give empty calories because they do not contain many other
vitamins and link the high-carbohydrate content of the modern diet to
serious health issues such as hypertension, coronary heart disease, and
obesity.
 Evidence for the types of food eaten by our evolutionary ancestors takes a
number of forms: cave drawings and paintings show people out hunting and
gathering food; tooth-wear patterns from skulls can be analysed to give
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insight into the types of food eaten; there is also evidence from buried refuse
heaps as radioactive isotope analysis can reveal how long ago the food
refuse, such as bone and shell fragments and seed cases, was thrown away.
The early hominids, or australopithecines, ate wild plant food and
occasionally scavenged animal carcasses for meat and bone marrow, etc.
About 2.4 million years ago the first of our Homo group emerged: Homo
habilis, who ate a wide variety of animals including deer, birds, rabbits, fish,
and shellfish, as well as wild plants (O’Neill, 2008).
As Homo sapiens emerged, Africa’s climate was changing and the
environment was drying out. This meant searching for food would be harder
and take more time and energy. It is estimated that the modern huntergatherers travelled up to 8 miles per day for food and that they obtained an
average of 40–60% of their dietary energy from animal foods such as meat
and milk. The latest techniques for analysing carbon and nitrogen isotopes in
hominid bones show that these ancestral types were already obtaining
almost all of their dietary protein from animals.
The australopithecines’ (our earliest evolutionary ancestor) brains averaged
400 cm3, whereas our brains are on average 1,350 cm3. The larger brain is a
very energy-expensive structure, though it forms only 2% of our body mass it
consumes 20–25% of our energy and nutrient resources. Hence, the
evolution of brain size may have driven our preference for energy-dense
foods.
RESEARCH EVIDENCE AGAINST EVOLUTIONARY EXPLANATIONS OF FOOD PREFERENCE
 In contradiction to the view that humans need a very specific diet for optimal
health is the view that humans have evolved to be flexible eaters (Leonard,
2002, see A2 Level Psychology page 204).
EVALUATION OF EVOLUTIONARY EXPLANATIONS OF FOOD PREFERENCE
 Starch digestion is probably not linked to brain size. Perry et al. (2007)
claimed the ability to obtain energy from starch drove brain development.
But this seems unlikely as the fire needed to cook such food was a relatively
recent development, only about 500,000 years ago, whereas rapid brain
growth precedes this, so the two factors are not clearly associated.
 Research evidence. Evolution is accepted by the scientific community as
fact. There is evidence of the gradual change of evolution, such as changes in
anatomy, in particular brain size that necessitated an increase in meat
consumption. However, we cannot be sure of the exact processes of evolution
because the theory is post hoc (made up after the event) and so we have to
rely on fossils and other sources of incomplete evidence. This means we have
only patchy evidence because it is difficult to obtain evidence on specific
diets.
 Scientific criticisms. The lack of evidence means that evolutionary
explanations lack scientific validity because they can neither be verified nor
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falsified and so do not meet Popper’s criterion of science, that the theory can
be tested and rejected.
Face validity. The linking of food preferences to the EEA and the adaptive
behaviours of our evolutionary ancestors makes sense. It is highly plausible
that we have a strong preference for high-fat foods because these increased
our chances of survival in the harsh conditions experienced by our
evolutionary ancestors.
Determinism. Evolutionary theories are considered deterministic because
they suggest that genes control behaviour, which ignores the free will of the
individual, i.e. their ability to control their own behaviour.
Reductionism. Evolutionary theories are reductionist as they focus on one
factor only, the gene, when other emotional, social, cognitive, behavioural,
and developmental factors are highly relevant to food preferences. They are
oversimplified accounts at best, which is illustrated by the fact that eating is
not just about survival.
Nature/nurture. The evolutionary explanations overemphasise the role of
nature and ignore nurture. It is not a question of nature or nurture, as
indisputably an interactionist perspective must be taken.
Multi-perspective. Evolutionary explanations need to be considered in
combination with other explanations. Both biological and psychological
factors interact in eating behaviour and so a compromise position such as the
diathesis–stress model is needed, which accounts for the influence of genetic
predisposition and experience.
NOTE: the generic criticisms given in the last evaluation section before this one also
apply, e.g. scientific criticisms, reductionism, determinism, and nature/nurture.
SO WHAT DOES THIS MEAN?
It is obvious that when the hunter-gatherers moved from a nomadic existence to a
settled agrarian one that efforts to forage were reduced. However, the preference
for energy-dense and nutrient-dense foods seems to have evolved because our
ancestors required much higher energy consumption. Consequently, our desire for
fatty, creamy, or sweet foods may be innate, i.e. genetically hard-wired into us, so we
eat more than we need. This may explain the obesity epidemic of today’s society
because now more than ever we lead sedentary lives and so many of us eat more
than our energy requirements and the unnecessary calories are stored as body fat.
OVER TO YOU
1(a). Describe the neural mechanisms involved in hunger and satiety. (9 marks)
(b). Discuss the evolutionary explanations of food preference. (16 marks)