Eating Disorders

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 syndrome.

What the Board expects you to know:

The Board 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 misunderstandings:

Differences between the two:

Explanations of eating disorders

You 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 advance.

You should all be familiar with the basic approaches to psychology by now. 

The 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. 

The 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. 

Medical Model

Genetic explanation

Genes for 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. 

Twin studies (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. 

Holland et al (1984):               

MZ twins: concordance rate 56%

DZ twins: concordance rate 7%

However, 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

The major 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!

When 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.

Finally, 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 genetic. 

Most research into specific genes has focused on the ones responsible for the production of serotonin (known to be linked to eating behaviour and to mood). 

Biochemical explanation

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. 

Research evidence

Fava et al (1989) found altered levels of serotonin and noradrenaline in anorexics. 

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. 

Brain structure

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.   

Evaluation

The 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.

But 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 the disorder. 

Overall evaluation of medical

It 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!