There are a
number of different eating disorders, the two best known being anorexia
nervosa (nervous loss of appetite) and bulimia nervosa (nervous hungry
ox!). Others include rumination syndrome (described as “effortless
regurgitation” of food), compulsive overeating and selective eating
Board expects you to know:
Psychological explanations of one eating disorder: for example,
nervosa, bulimia nervosa, obesity
Biological explanations, including neural and evolutionary
explanations, for one
eating disorder: for example, anorexia nervosa, bulimia nervosa,
only requires knowledge of one disorder and since anorexia nervosa (AN)
is the most widely researched, that’s the one we’ll chose. First of all
a few differences between AN and BN to clear up any possible
between the two:
of being fat
Binge eating followed by guilt.
Distorted body image
of control over eating
weight is less than 85% of normal
weight within 10% of normal
Amenorrhoea (cessation of periods)
Binge eating on average twice a week for 3 month period
Explanations of eating disorders
are already aware of the main approaches in psychology. We will look at
each in turn and see how they try to explain eating disorders. With a
little thought and imagination you should be able to predict these in
should all be familiar with the basic approaches to psychology by now.
Medical model looks for a physical cause to normal and abnormal
behaviour so considers genes, brain chemicals, brain structure and
infections. The medical model is the approach used by psychiatrists.
Psychological models include Psychodynamic, Behaviourist and Cognitive.
These believe behaviour is caused by unconscious conflicts, learning and
though processes respectively. Clinical psychologists adopt one or more
of these approaches when dealing with abnormal behaviour.
specific behaviours have not yet been identified, but anecdotally there
is a tendency for the disorders to run in families (like noses!). The
American Psychological Association (1994) found an increased incidence
in family members if first-degree relatives (parents and siblings) had
the disorder. Evidence suggests there is a four fold increase in
likelihood of developing a disorder if a close relative has one.
(compare concordance rates between MZ (identical twins) and DZ
(fraternal twins). If the concordance rate is higher for MZ than DZ it
is evidence for a genetic component.
concordance rate 56%
concordance rate 7%
twin studies like this pose a number of problems. On the face of it
they suggest a genetic cause. The more genes people share the more
likely they are to share the characteristic. One firm conclusion we can
draw of course is that anorexia is not entirely genetic otherwise there
would be 100% concordance in identical (MZ) twins. So even if there is
a genetic component other factors must also be at work
problem is in ruling out environmental factors. Not only do MZ twins
share the same genes they also share very similar environments, far more
so than DZ twins. MZ twins are often dressed similarly, have the same
friends, same interests, same teachers and so on. And of course they
are always the same sex, unlike DZ twins that can be brother and
sister. This last factor is particularly relevant when considering
eating disorders because of their much greater prevalence in girls of
the female gender!
considering genetic causation it is also worth mentioning that the
effect may not be direct. Perhaps genes are influencing a
characteristic which in turn is increasing the risk of eating
disorders. For example, as we’ll see with the cognitive model, many
anorexics have perfectionist personality traits and there is evidence to
suggest that this personality type is itself genetic.
Bachner-Melman et al (2007) found that three of the genes implicated in
AN are also associated with perfectionist personality.
Wade et al
(2008) also considered a genetic link with another personality traits
associated with anorexia, the need for order in their lives and the need
for praise and reward and found that these characteristics also tend to
run in families.
assuming AN has a genetic cause, how can we explain the huge increases
in reported cases in the past forty years and the incidence in certain
parts of the World only. This suggests cultural factors rather than
research into specific genes has focused on the ones responsible for the
production of serotonin (known to be linked to eating behaviour and to
My (and no
doubt your) favourite neurotransmitter seems to be the most likely
candidate since eating foods containing lots of starch are known to
increase levels of serotonin in the brain. Serotonin is
associated with happiness and better mood. Serotonin has been
implicated in both anorexia and bulimia and appears to suppress
appetite. Another neurotransmitter, noradrenaline appears to trigger
appetite. Though as you will all appreciate by now, nothing in the
brain is ever quite that simple.
As would be
expected, anorexics do have low levels of leptin, presumably because of
the very low levels of fat in their adipocytes.
Fava et al
(1989) found altered levels of serotonin and noradrenaline in
Similarly, recovered anorexics tend to have abnormal functioning of
serotonin and noradrenaline systems. However as with all correlational
evidence like this it is impossible to show cause and effect; i.e. it
could be the disorder that has caused the altered levels of chemicals.
Everyone’s favourite brain structure, the hypothalamus, is the most
likely candidate here, since, as we’ve seen already, it is known to be
involved with control of eating. The dual hypothalamic theory of eating
explains how the lateral hypothalamus (LH) and the ventromedial
hypothalamus (VMH) act to regulate our feeling of hunger and satiety.
It would seem possible therefore that problems with these structures may
cause abnormal patterns of eating, perhaps having the set-point for
hunger set too low.
Animals with damage to the hypothalamus often stop eating and will even
starve themselves to death.
hypothalamus controls hormones including those involved in the menstrual
cycle. One of the defining characteristics of anorexia is amenorrhoea.
Perhaps this is due to a fault with the endocrine system.
Nineteen-year-old anorexics typically have the hormone levels of the
average 9 year old.
post mortems on the brains of anorexics has not shown any damage to the
hypothalamus and even if it were present it would be difficult to prove
that the damage pre-dated the anorexia rather than arise as a symptom of
Overall evaluation of medical
seems likely that there are genetic influences predisposing some to a
greater risk of eating disorders. However, the extent of these
influences is difficult to disentangle from the effects of their
upbringing. Chemical and structural issues may be a contributory factor
too and there is evidence for both. However, as we shall see later in
the year when we look at depression, it is notoriously difficult to show
what came first… the chicken or the egg!