What the board expects you to know:
Factors influencing attitudes to food and eating behaviour, for example,
cultural influences, mood and health concerns
Explanations for the success and failure of dieting
In modern times in the Western World we have come to take food very much
for granted. It is mostly cheap and plentiful. However, this is a
relatively new development. In relatively recent times and before the
onset of modern farming methods food could become scare. In the mid
nineteenth century (1845 to 1852) over a million people starved to death
in Ireland and another million or more emigrated (mostly to the USA) to
avoid starvation as a result of the Great Potato Famine.
This part of the topic considers factors that influence our attitudes to
food and covers issues such as mood, wealth, culture, social class,
health concerns and medical (mis) information. Based on the Board’s
specification we will group these under their chosen headings of
culture, mood and health concerns:
What is food?
Different cultures view different things as food. Our very idea of food
is to some extent determined by the culture in which we are brought up.
A few obvious examples for starters:
In the West we tend not to regard insects as food. In most parts of the
World insects are an important constituent of the diet.
Hindus do not consider the cow as food and Jews the pig.
We know the French see horses and frogs as food, whereas the British
In South America hamster is popular and in Korea a dog isn’t just for
So what determines and maintains these biases towards certain food
How various preferences originally came about is difficult to say,
though some may be practical; not eating pig in a hot climate and many
are undoubtedly religious. The Bible (Leviticus) lists many creatures
that can or cannot be eaten!
Maintenance of eating behaviour within a culture or society is easier to
As children we tend to eat what our parents eat, partly of course
because they prepare it for us. However, as we grow up we tend to
express a preference for similar foods to our parents. So here we have
SLT in action.
The media and advertising clearly have a huge impact too. In recent
years there has been concern about food advertising aimed at children
because of the possible harm it is doing to their health.
Advertising creates associations between food and good times or positive
outcomes: mealtimes with the oxo family, Special K and slim waistlines,
yoghurt and healthy guts and the less said about Hagan Das and its
associations the better
However, we create associations of our own. Some of these may be
positive, such as various lagers and drunken nights out or being curled
up in front of the fire on a cold night with a cup of Bovril (probably
less likely). Food is very susceptible to associations and for
excellent biological reasons. The first time I tasted whiskey (New
Years Eve 1979) I was ill the next day. In all fairness to the single
malt in question it was unlikely that the whiskey had been the trigger
for the next day’s events, rather the lager that had preceded it.
However, humans like all species, make very rapid associations between
food and illness. This can potentially be life-saving and is certainly
Garcia’s sickly rats
In a series of experiments on rats Garcia demonstrated on-trial
learning. He would give the rats novel solutions to taste (for example
saccharin). He would then expose the rats to radiation that would
subsequently make the rats sick. He found that even though the sickness
occurred many hours after the novel food had been tasted that the rats
still developed an immediate aversion to the substance. They seemed
predisposed to make associations between food and sickness and after
only one trial.
Points to bear in mind:
Usually with classical conditioning many trials are needed. Think of
Little Albert’s learned fear of white rats or Pavlov’s dogs learning to
associate food and bell. These rats only had to associate taste and
sickness once for the link to be made.
Up until Garcia it had also been assumed that the UCS (e.g. food) would
need to be presented at the same time as the CS (e.g. bell) for the
association to be made. Garcia showed that with food the CS (sickness)
may occur many hours after the initial presentation of the food and the
conditioning would still occur.
It is clear that this mechanism is biologically useful. Sickness can be
fatal. If an animal is sick after consuming a food stuff for the first
time it is best avoided in the future.
To this day I still find the smell of whiskey nauseating. The beer that
probably triggered the illness is still acceptable. I had many prior
experiences of consuming beer and had learned to associate this with
Schema for ‘food’
British troops expected something that looked like jam to be
sweet and fruity, not salty and fishy. Caviar therefore did not
fit their existing schemas for ‘food.’
Through experience we develop a template for what constitutes food.
During WW!! British troops were given caviar, much favoured by our
Soviet allies. Caviar, for the inexperienced is black, liquidy and is
spread on bread. The British Tommy had a schema for such a substance…
he called it ‘jam.’ Jam was sweet and contained blackberries or similar
juicy fruits. Caviar tasted salty and contained fish eggs. It didn’t
fit the Tommys’ schemas and this ‘fish jam’ was not viewed as food!
Culture doesn’t just determine what we eat, but also when we eat, where
we eat, how we eat and with what we eat:
Different cultures and nationalities eat at different times of the day.
In the UK we have an early breakfast, lunch around midday and an evening
dinner, unless we’re working class, in which case we have an earlier
dinner followed by tea! Mediterranean countries generally tend to eat
later, particularly the evening dinner which in some countries may not
be eaten until 10pm or later.
Research suggests eating together as a family can have a number of
benefits. The food tends to be healthier as we eat more servings of
essential foods such as fruit and vegetables and fewer unhealthy fatty
foods. Families that eat together are also more likely to eat
Where we eat
In the 1970s about a third of the family’s food budget was spent on
eating outside the home. By the 1990s this had risen to just under a
Eating out generally results in consumption of less healthy foods since
restaurants tend to offer fewer healthy options.
School meals were first introduced in the late nineteenth century and
were designed to combat malnutrition that was common in many of the
poorer children of the time. In the 1940s it was made compulsory for
schools to offer free meals to children from poorer backgrounds. From
then until the 1980s little changed. Few choices were available and the
fare tended to be pretty basic stuff. Spam fritters were a favourite at
my school (though probably not with the students) and desserts tended to
be stodgy affairs; lots of crumbles and steamed puddings with lashings
of lumpy pink custard! Don’t mention semolina!
Then in the 1980s the then Conservative Government under Maggie sold off
the council run kitchens to the lowest bidders. Those able to produce
the cheapest meals were awarded the contracts. Choice increased but
quality plummeted. Guidelines on nutritional value were relaxed and the
emphasis instead placed on fast, cheap and convenient. Then in 2004
Jamie Oliver attempted to rescue the situation by doing away with the
turkey twizzler and introducing salads. Unfortunately, although quality
has undoubtedly improved, over three quarters of secondary schools still
have vending machines offering less healthy options. Kubik et al
(2003) believes eating unhealthy food at school has an adverse effect on
our general eating habits and intake of healthy foods at home.
Eating at home continues to decline. When we do eat at home it is more
likely to be a pre-packed convenience meal that takes a few minutes in
the microwave. With most families now being one-parent or having both
parents working, time spent on preparation of fresh food has dropped
Supersizing began in the USA but has become popular in other Western
countries, particularly in the UK. In many fast food outlet the options
now may be limited to medium, large or extra large… small having gone
that way of the dodo.
As I write this…in the middle of a recession with food outlets declining
and many closing, the last twelve months has seen one noticeable
exception. New kid on the block, Taybarns, has bucked the trend and
shown a 3% increase in turnover. Taybarns is apparently based on the
American Golden Corral ‘all you can eat’ model. It offers a wide choice
of dishes based on a variety of cuisines. So as you move along the 34
metre serving area you can pick up Pizza, Mexican, Chinese, Indian… as
well as fish and chips. The controversial aspect however, is the ‘eat
as much as you like’ approach which is said to be encouraging greed and
obesity. Customers pay a flat rate of £5.99 (or £7.99 in the evening)
and can help themselves over and over again. The recorded average
number of platefuls eaten by Taybarns' customers is 3.37.
Young and Nestle (2002) reported that the average portion size of fries,
burgers and soft drinks had increased between 2 and 5 fold in the last
Some US restaurants even offer ‘BIG KID MEALS.’
Low mood can often result in comfort eating, although occasionally it
seems to have the opposite effect and can cause reduction of eating.
Garg et al (2007) got participants to watch a funny film (Sweet Home
Alabama) or a tear jerker (Love Story) whilst the researchers watched
the participants choice of snacks; either popcorn or grapes. Those
watching Love Story consumed a third more popcorn than the other group
whilst those watching Sweet Home Alabama ate more grapes.
Low mood seems also to influence binge eating behaviour. Davis et al
(1988) showed that low mood often preceded binge eating in bulimics.
The same seems to apply in those with no known eating disorder.
Students were asked to record their mood and eating habits over a two
week period. Days that included binge eating tended also to be days of
low mood, but significantly, binge eating did nothing to improve mood
afterwards. So although we may binge when down it seems to do little to
make us feel better.
Some studies go further and suggest that we often feel worse after binge
eating, presumably because of the guilt.
Michel (2007) studied 617 13 and 14 year old boys and girls and found
that negative moods (low mood and stress) were linked to emotional
eating. However, boys tended to eat when stressed, girls when feeling
low. Boys were also more likely to snack on healthier foods such as
Christensen and Brooks 2006 got men and women to read a happy or sad
short story and apply it to their own experiences. They were then asked
about their eating habits after such events. Both sexes said they would
eat more after a happy event, but only women said they were likely to
eat sweet foods following a sad event.
Of all the food stuffs associated with emotional or comfort eating the
most widely cited and studied has to be chocolate.
Although there may be psychological factors at work such as associating
chocolate with happiness (classical conditioning) and often seeing other
happy people eating ice cream and chocolate (SLT), many of the effects
can be explained using a bit of brain chemistry. So why attempt a dull
emotional answer when we can reduce it all to neurotransmitters and
Chocolate and serotonin?
The old explanation for carbohydrates and particularly chocolate,
increasing mood is that they increase our levels of serotonin (the
brain’s ‘happy’ chemical). Certainly, carbohydrates do result in
increased levels of an essential amino acid tryptophan in the brain.
Tryptophan is a precursor to serotonin (meaning it’s involved in the
production of serotonin). This would seem to make sense since
increasing carbohydrate intake would lead to increased levels of
However, although this works in the laboratory it doesn’t seem to work
in the human digestive system. The sticking point is protein. We tend
not to eat food stuffs in isolation. Chocolate is likely to be entering
the system at the same time as other food groups. Apparently even tiny
amounts of protein in the system will prevent this tryptophan effect.
A study of 300 pregnant women in Finland (2004) reported that those who
ate chocolate regularly whilst pregnant had given birth to happier
babies (assessed by their time spent smiling and laughing). This was
attributed to the chemical phenylethylamine
which is found in chocolate. Alongside caffeine and magnesium this has
been suggested as the possible feel-good chemical in chocolate.
However, many other foodstuffs contain greater amounts of these
chemicals than chocolate but without the same affect on mood. Even
Cadburys believe the effects of chocolate to be more psychological than
But there seems to be little question that chocolate does have a special
effect on our mood.
Macht and Dettmer (2006) gave women an apple, a chocolate bar or
nothing. They were then asked to complete questionnaires assessing
The chocolate and the apple both improved the mood of the women
and decreased their hunger. However, in addition to this many
of the women reported ‘joyous feelings’ and almost euphoric
symptoms that the apple simply couldn’t compete with.
Unfortunately, this often turned to guilt a short while later.
So how does chocolate produce this effect?
Chocolate and the endorphins
Chocolate seems to be one of those foods that ticks all the boxes… a
perfect storm of bitter-sweet taste, pleasant aroma, sexy texture and
that melt in the mouth quality. This results in pleasure and the
release of the brain’s natural opiates the endorphins. These are
associated with pleasure and even addictive behaviours.
How many of you can’t function until you’ve had your first or second
Smith et al (2003) found that two cups of coffee improved mood and
increased alertness, memory and other cognitive abilities. Its magical
abilities were attributed to its effect in maintaining the brain
chemical noradrenaline (NA), which is chemically similar to its sister
adrenaline and has very similar effects.
NA is a permissive amine, a group of chemicals (which include serotonin)
that are responsible for mood. We will consider them in more detail
when we look at depression after Christmas. This effect via NA may also
explain why we feel so tired when withdraw from caffeine, since we are
reducing the stimulating and arousing qualities of NA.
Some have argued that these effects are not necessarily caffeine causing
improvements in mood but merely reversing the harm done when caffeine
wasn’t present. For example, we feel better after that first coffee in
the morning because we are reversing the negative effects of twelve
hours or more without caffeine.
Is it psychological?
Rogers et al (1992) attribute at least some of caffeine’s effects to SLT.
From an early age many of us are exposed to parents unable to function
before coffee which produces expectations. We also see their improved
mood after their first cup.
Chicken or egg?
Certain foods seem to be capable of altering our mood, but it seems our
mood can also impact upon our taste and subsequently our eating
behaviour. Chemicals such as NA and serotonin lift our mood and alter
our taste perception. In effect, being in a good mood makes food taste
better, so for example our threshold for sweetness is lowered so foods
we would normally find bland suddenly appear sweet. This may also
explain why sometimes depression results in lowered appetite rather than
comfort eating. Lowered mood reduces our ability to taste and food
appears bland and unappetizing.
The UK’s Food Standard’s Agency (2007) questioned British children on
their attitudes to food and health.
42% had concerns about food-related diseases and about various food
issues relating to fat, sugar, salt etc.
95% believed that eating healthy foods would make them healthier
79% reported receiving information on healthy eating from school
Most realized the importance of eating five daily portions of fruit and
Given this understanding of nutrition it seems even more perplexing that
obesity in children is now running at 27% with 14% being classed as
Do health warnings work?
Westcombe and Wardle (1997) fibbed to thirty six 18 to 53 year olds.
They were given three cheeses, three yogurts and three tofu based dishes
to taste. Although all three of each category contained similar levels
of fat they were labeled differently as having either low, medium or
high fat content. The participants were asked to judge the items on
taste and asked how likely they would be to buy the products. Those who
had expressed concerns about their health were more likely to describe
the low fat products as slightly less tasty but would be more likely to
buy them. The researchers concluded that food advice labels were most
likely to influence those concerned about their health.
However, studies like this, based on self report are not always reliable
since they consider people’s opinions on how they would behave rather
than look at their behaviour directly.
Allen et al (2007) asked adolescents to select a fast food meal. They
were then presented with a 30 minute education video. When asked to
select a fast food meal afterwards they were more likely to go for a
healthier option than before.
Children were shown a video of Food Dudes eating good food and
battling against the Junk Punks. They were then offered
stickers and pens if they tried some fruit. This lead to
increased consumption of fruit and veg. which in some cases
lasted for the next 15 months.
Socio economic status
Dissatisfaction with body shape in children increases as SES increases.
Dombusch et al (1984) studied 7000 US children and found that the desire
to be thin (and hence diet) was much higher in children from higher SES
However, it needs to be added that other studies such as Story et al
(1995) found that wealthier children were generally happier with their
body shape. Others have found no relationship between social class and
This could in part be attributed to money. Generally the higher the
income of a family the better the diet (greater intake of protein,
calcium, iron, fruit and veg. and polyunsaturated fats). Lower income
families tend to eat more potatoes, saturated fats, sugars, jams and
less fruit and veg. (Xie et al 2003).
The better educated the parents the better the diet of their offspring.
Although education at school can influence later adult diet, generally
knowledge about nutrition does not equate to a good diet in practice.
Part of this failure to act on advice could be put down to mixed
messages from science and misinterpretation and distortion by the press
in their reporting of scientific advice. De Almeida et al (1997)
emphasized the importance of consistent and accurate messages when it
comes to food.
Food Standard’s Agency Report (2005)
People are increasingly concerned about their diet and health, according
to the Agency's fifth Consumer Attitudes Survey published today.
Salt levels are the top food concern, with fat and sugar also appearing
in the list of top five.
More people than ever before are checking food labels to find out how
much salt, fat and sugar is in the food. Over the past five years, among
people who check labels, the number of people who say they look for
nutritional details has risen to 75% in 2004, from just over half in
Gill Fine, Director of Consumer Choice and Dietary Health at the Food
Standards Agency said:
'Over the last five years the trend among consumers has been towards
healthier eating and an increase in demand for reliable and practical
information on all aspects of nutrition, food and health. People are
more worried about levels of salt, fat and sugar in food and the
accuracy of food labels, and less concerned about issues like BSE.
The Food Standards Agency has launched a new website - www.food.gov.uk/eatwell
- dedicated to providing reliable and practical advice on all aspects of
food, diet and health, as well as helpful tips on topics such as
understanding food labels.'
The level of concern about BSE has fallen by almost a quarter since
Other five year trends include: the number of people claiming to have
eaten five portions of fruit and vegetables the previous day has risen
from just over a quarter in 2000 to half of all consumers in 2004
knowledge of the '5 a day' message of eating fruit and vegetables has
increased from 43% in 2000, to 58% in 2004 concern about the safety of
raw beef has fallen dramatically, from over half of all consumers in
2000, to just over a third in 2004 concern about the accuracy of food
labeling has risen from 35% in 2000 to 44% in 2004
Why diets fail or
Dieting refers to the adopting of a particular diet in order to achieve
a particular purpose. Given the increase in levels of obesity in many
parts of the western world in the past four decades, most of today’s
diets have the sole purpose of losing weight.
BBC News website October 2007:
Between half and two-thirds of men and women in 63 countries across five
continents - not including the US - were overweight or obese in 2006.
The Circulation journal study included over 168,000 people evaluated by
a primary care doctor.
People who are overweight have a higher risk of heart disease, Type II
diabetes and other diseases including some cancers. The International
Day for the Evaluation of Obesity (IDEA) study looked at two measures of
fatness - waist circumference and a calculation called body mass index
A BMI (weight in kg divided by square of height in meters) of 18.5 to 25
is considered healthy.
A BMI over 25 is deemed overweight and greater than 30 is obese.
Just 7% of people in eastern Asia were obese, compared to 36% of people
seeing their doctors in Canada, 38% of women in Middle Eastern countries
and 40% in South Africa.
Canada and South Africa led in the percentage of overweight people, with
an average BMI of 29 among both men and women in Canada and 29 among
South African women.
A Foresight report released in the UK 2008 warned the government that it
must act to stop Britain "sleepwalking" into a crisis. The report,
which was the largest UK study into obesity, backed by the government
and compiled by 250 experts, said excess weight had become the norm in
our "obesogenic" society. By 2050 90% of today's children will be
overweight or obese, it predicted.
This section of the topic considers the reasons, biological and other,
why diets fail or succeed.
Most diets reduce the intake of calories and or fat. The simple belief
being that if you can reduce the intake of calories to below the number
of calories being burned off, weight loss will be inevitable. However,
research suggests that very often these low-cal diets actually increase
the calories consumed.
Pre-load taste tests
A common measure used to determine hoe much food people are consuming.
Typically participants are given a pre-load meal consisting of either a
high-calorie snack such as chocolate or cake or a low-calorie snack such
as a cracker.
Researchers then tell the participants that they are going to take part
in a taste test and left with a variety of foods to assess; such as
biscuits, snacks, ice cream. Participants are left to do this
(supposedly unobserved and in their own time) and asked to assess the
foods in terms of saltiness, sweetness etc. In fact this is a fib!
Researchers are only interested in the amount of food consumed.
Non-dieters tend to adjust for the earlier pre-load meal. If they
initially ate a high-cal snack they would consume fewer calories during
the taste test.
Dieters on the other hand would eat fewer calories if they had had the
low-cal snack but eat lots more if they had consumed the high calorie
The researchers conclude that dieters often eat less but on other
occasions over-compensate by binging, especially if they eat one
Does dieting increase food intake?
Klosges et al (1992) looked at the dieting habits of nearly 300 men and
women and found that although they often decrease calorie intake they
increase their consumption of fat.
Wardle and Beale (1988) went further and found that restraint causes
over-eating. Women were placed in one of three groups and tested at
regular intervals for seven weeks:
They found that dieters actually consumed the most. The pattern seemed
to be that generally they would eat less but then over-compensate and
binge on something until full resulting in a net increase in calories
compared to the other two groups.
explanations of failure of diets
Mood and displacement
Dieters, it seems, often over-eat to overcome the low mood, perhaps
brought on by dieting (a masking effect). Poliving and Herman told
participants they had either passed or failed a cognitive task. The
purpose being to alter their mood (increase or decrease respectively).
They were then provided with food, either in limited or plentiful
supply. It was found that those on diets would over-eat and then
attribute their low mood to the fact that they’d eaten too much. It was
concluded that dieters over-eat to move responsibility for their low
mood from the real cause, displacing it onto food instead.
Note: starting a new diet can, in itself, often improve mood.
Theory of ironic process (denial)
From one Freudian defence mechanism to another. Who says Freud got it
Basically the more you try not to think of something the more it
dominates your thoughts. Wegner et al (1987); participants were told
‘Not to think of a white bear’ or ‘Think of a white bear.’ Each time a
white bear entered their thoughts they had to ring a bell. Not
surprisingly those told not to think of the white bear rang the bell
more often. Trying not to think about food is a sure way of ensuring
we’ll think of little else. NB as we’ll see later, many anorexics love
cooking and talk of food incessantly.
All or Nothing theory
Likens dieting to quitting smoking or stopping drinking. Some people
struggle, others manage either or both with ease. The most successful
ones seem to be the ones that STOP completely rather than reduce
gradually. Clearly this strategy is not possible with food and may
explain why cutting calories is more difficult that quitting smoking.
The biology of diets
Generally speaking diets seem to produce short term results but fail in
the longer term with the dieter returning to or even exceeding their
starting weight. According to mark (2006), for a diet to work it must
address the biological mechanisms involved in weight regulation.
Two chemicals are crucial in regulating appetite and blood sugar.
Insulin is produced by the pancreas, helps to regulate blood sugar
levels and is an essential component of homeostasis. Obese people
become insensitive to insulin and as a result cannot deal with blood
sugar levels. Hence the link between obesity and diabetes. Apparently
regular exercise helps to reinstate insulin sensitivity enabling high
blood sugar levels to be lowered.
The neurotransmitter neuropeptide Y (NPY) produced by the hypothalamus
increases eating (by stimulating hunger) and decreases physical
activity. The hormone leptin (Greek for ‘thin’) binds with NPY neurons
and tells the brain that we’ve had enough to eat. Basically leptin
makes us feel full or sated and stops us eating more.
Low calorie diets reduce the levels of leptin resulting in higher levels
of NPY which in turn makes us feel hungry and triggers eating.
Leptin and obesity
In general, obese people have an unusually high circulating
concentration of leptin so we would expect them to eat less. However,
these people seem to be resistant to the effects of leptin, in much the
same way that people with
2 diabetes are
resistant to the effects of
insulin. The constantly high
concentrations of leptin from their fat stores result in leptin
desensitization. As a result the leptin doesn’t trigger that ‘full’
feeling as it does in people of normal weight.
Laposky et al (2007) believes that desensitivity to leptin is genetic.
If this is the case it would explain why people become obese in the
first place and why diets don’t work. The brain is simply not getting
the ‘full’ message to stop eating.
Although losing weight by dieting has benefits, such as lowered risk of
CHD and diabetes it does seem to have long term costs.
A large scale longitudinal study carried out over a 24 year period in
Finland looked at the health, weight and other records of 3000 people.
Those trying to lose weight or those who had gained weight were more
likely to die at a younger age.
Sorenson (2003) recommends that we don’t get obese in the first place.
Truby et al (2006) offers more hope!
They carried out a six month trial of four diets, including low fat and
low cal, on obese participants. This was done as part of a BBC
documentary. Participants were recruited by national
advertisements to take part in a reality TV series, BBC
Diet Trials, that urged them to "be a star in your own right
and lose weight." Participants were randomly assigned to one of
four diets: the Slim-Fast Plan, Weight Watchers Pure Points
Programme, Dr Atkins' New Diet Revolution, Rosemary Conley's
"Eat Yourself Slim" Diet and Fitness Plan, or to a control group
receiving usual care.
All had significantly reduced their weight by an average of 6Kg (4.5Kg
of which was fat tissue). After twelve months weight loss averaged 10%
of body weight. However, fewer than half of those who took part were
available for the 12 monthly follow up which reduces the reliability of
the study considerably.
Additionally only 15% of those assigned to the Atkins or Slim-Fast
programmes were still using them, compared with 35% of those
assigned to Rosemary Conley and Weight Watchers programmes.
So here we have examples of low cal diets reducing weight longer term
which seems to contradict the leptin theory.
However, there are some contributory factors to consider.
Typically with a diet all starts well. Early weight loss reinforces the
dieting behaviour and keeps us on track. Then we reach a plateau when
the downward spiral of weight loss falters. Here social support is
needed to maintain interest and motivation (which is why slimming clubs
can be so successful). In the Truby study, having your progress tracked
for a television programme would have been highly motivating so it’s
perhaps not surprising that the dieters were so successful.
As well as social support there are other social factors involved in our
ability to diet. It seems the amount we eat increases in proportion to
the number of people present. So better avoid large dinner parties or
other social gatherings.
Lichtman et al (1992) found that dieters do con themselves. Typically
they over-estimate the amount of exercise they take by about 50 % and
under-estimate their food intake by about the same amount.
Exercise alongside diet does seem to be crucial for long term success.
Miller et al (1997) carried out a meta-analysis of weight loss
programmes and found that by far the most successful were those
combining diet and regular exercise. Exercise not only burns off
calories it increases basal metabolic rate for 24 hours or longer after
the exercise has stopped.
The role of
neural mechanisms in eating behaviour
What the Board expects you to know:
The role of neural mechanisms involved in controlling eating
Evolutionary explanations of food preference
A word of warning at the outset: this is not an easy topic! Although
there is some overlap with biological explanations of dieting, covered
in the first booklet, there are lots of new ideas and brain structures
with odd names. However, I shall try to keep it as simple as possible
and progress in a logical manner. For those so-minded, there is lots of
other information out there with new research shedding more light on
this intriguing area of study.
The body needs neural mechanisms that motivate eating and stop us eating
when we are full. If the body responded directly to nutrients in the
bloodstream we would be eating for hours when hungry, since it takes at
least two hours for the simplest foods to pass from the stomach into the
Hunger monitors current needs, anticipates future needs and motivates
Satiety tells us when enough has been consumed and terminates eating.
Cannon (1927) believed hunger and satiety were governed by the stomach.
When full it would stretch and tell the brain to stop eating. One of
his co-workers Washburn, swallowed a balloon and inflated it inside his
own stomach. As predicted this stretched the stomach and apparently he
no longer felt hungry. However, this is a huge over-simplification.
Patients who have had surgical removal of the stomach still report
feelings of hunger and satiety despite nothing to stretch or contract.
Karl Lashley (1938) made the first significant advance when he
discovered the brain area seemingly responsible for eating behaviour.
He removed various areas from the brains of hungry rats and tested how
motivated they were to run a maze for food. Lashley concluded that the
hypothalamus seemed to be controlling eating behaviour. This should not
be a surprise to you seasoned psychologists. The hypothalamus has a
regulatory role in many human functions, such as stress, sleep,
temperature and anything to do with the endocrine system…basically
anything involving homeostasis.
This discovery eventually led to the dual hypothalamic control theory of
eating. Lots more on this later.
Regulation of blood glucose levels
Before proceeding further a few words (revision hopefully) of the
mechanisms involved in maintaining constant blood-sugar levels.
The main source of energy in the body is carbohydrate, in particular,
the simplest of sugars, glucose.
Following a meal, lots of glucose enters the bloodstream. For glucose
to be useful it needs to pass from the blood into the cells of the body
for the purpose of respiration. The hormone insulin, released from the
pancreas, in response to heightened blood sugar levels helps transfer
glucose from the blood into the cells and tissues of the body.
Any excess glucose is stored as glycogen, either in small quantities in
the muscles or in larger quantities in the liver. Glycogen provides a
store of energy that we can call upon when needed.
Later, as levels of blood-sugar start to drop, the hormone glucogon
breaks this glycogen down into glucose which can circulate in the blood
until needed by the tissues.
Well maintained levels of blood-glucose are essential. If they rise or
fall to far from the norm there are noticeable behavioural changes
within minutes and if no action is taken to address the issue coma can
When blood sugar is raised we store the excess.
This is called the ABSORTIVE PHASE.
When blood sugar drops due to use we refer to
this as the FASTING PHASE.
A drop in blood glucose alone however, doesn’t
seem to be enough to initiate eating.
It is sometimes likened to a petrol gauge that simply
warns us that we need to consider filling up soon.
thanks to homeostasis, blood sugar levels fluctuate very little.
They are tightly controlled by insulin and glucagons.
The Dual Hypothalamic Theory of Regulation of eating
Sounds complicated but it does exactly what it says on the tin. It
suggests that two areas (hence dual) of the hypothalamus work together
to regulate how hungry or sated we feel.
One part of the theory considers the role of sugars (glucostatic) and
the other considers the role of fats (lipostatic).
Key elements before we get down to the nitty-gritty: Involves sugar
levels, the lateral hypothalamus (LH) and creates the feeling of
hunger…so motivates eating behaviour.
Cells in the lateral hypothalamus (LH) detect glucose levels. When
these drop below a certain point the cells fire and initiate hunger and
the ‘feed me’ response!
I have been careful here in avoiding the phrase ‘blood sugar.’ It used
to be thought that levels of glucose in the blood were the crucial
trigger. Studies on rats showed that injections of glucose would
inhibit eating a hungry rat. However, blood sugar levels in untreated
diabetics can get frighteningly high, yet they still feel VERY hungry,
suggesting low blood sugar levels were not the cause of hunger.
Mayer (1951) realized that it was levels of glucose in the cells that
were important. This would explain the hunger felt by diabetics.
Although there blood sugar was sky-high since they weren’t producing
insulin this sugar could not escape into the cells where it was needed.
Hence low levels in the cells… hence the hunger.
Russek (1971) narrowed this down further when he discovered that
injecting glucose directly into the livers of starving animals would
stop them eating. It seems that the LH detects changes in glucose
levels in the liver. Messages being sent along the vagus nerve that
connects the two.
One small issue with the theory: severing the vagus nerve as happens
during liver transplants should stop us eating. It doesn’t!
Also Blass and Kraly (1974) found that lesions to the LH of rats didn’t
effect their eating behaviour, running counter to the research of
Apparently we all have a set point. Tennis players have many; well the
good ones do!
Set point refers to a body weight that we possess around which our
weight fluctuates within a narrow range. Our set point seems to be
determined by fat levels in the adipocytes of the body. Adipocyes are
fat cells and sometimes referred to as lipocytes. Set point theory
explains why when we diet and lose weight, we usually return to the
starting point when we give up. It’s the point at which our biology
Key elements: It involves fat levels, the ventromedial hypothalamus (VMH)
and acts to make us feel sated. It stops us eating.
Cells in the ventomedial hypothalamus (VMH) detect when fat levels in
the adipocytes fall.
Teitelbaum (1955) found that lesions to the VMH of rats caused
over-eating. Usually the VMH stops us eating…since these rats had a
damaged VMH they continued to eat and became hyperphagic.
This seems to occur in two stages.
Eat until obese
Eat to maintain this new obese weight (or new set point).
If the rats were starved and lost weight they would eat to regain the
new weight rather than the original weight.
Liebelt et al (1973) surgically removed the fat from the VMH-damaged
rats and the rats ate until the fat was replaced.
Reeve and Plum (1969) reported the results of a post-mortem on woman who
had doubled in weight in the previous two years. She was found to have
a tumour on her VMH.
Combining the two hypotheses
Glucostatic Hypothesis seems to control short term eating
Lipostatic Hypothesis seems to determine our longer term eating.
Additions to the basic dual hypothalamic model
Recently a third structure has been added to the model. The arcuate
nucleus, also located in the hypothalamus seems to be involved in the
regulation of eating behaviour. The arcuate nucleus produces various
chemicals, one of these being neuropeptide Y (NPY) that we looked at
with regard to slimming. NPY is a powerful stimulant to appetite.
Action of peptides:
basically a reminder of the biology looked at in dieting:
The neurotransmitter neuropeptide Y (NPY) produced by the hypothalamus
increases eating (by stimulating hunger) and decreases physical
activity. The hormone leptin binds with NPY neurons and tells the brain
that we’ve had enough to eat. Basically leptin makes us feel full or
sated and stops us eating more. Conversely a drop in fat levels stops
the secretion of leptin and the hypothalamus triggers eating.
In general, obese people have an unusually high circulating
concentration of leptin so we would expect them to eat less. However,
these people seem to be resistant to the effects of leptin, in much the
same way that people with
type 2 diabetes are
resistant to the effects of
insulin. The constantly high
concentrations of leptin from their fat stores result in leptin
desensitization. As a result the leptin doesn’t trigger that ‘full’
feeling as it does in people of normal weight.
However, other neuropeptides are also involved in regulating eating
Agouti-gene related peptide (AGRP) seems to be implicated too. If rats
are starved ten their levels of AGRP and NPY increase. Rats injected
with these two chemicals become very hungry. However, their effects
seem to be different:
NPY is fast acting but its effects are short-lived
AGRP on the other hand requires a gradual build up but its effects
can last for days.
One injection of AGRP can cause rats to over-eat for days afterwards.
The model therefore is complex and as present not fully understood.
Psychological factors and eating behaviour
There are a number of factors that can make us feel more or less
The mere smell of freshly baked bread or freshly brewed
coffee can instill a craving.
particularly relating to eating times can cause us to eat even
though we don’t feel hungry. This seems to be a particularly
powerful influence on people that are obese.
Stress and mood,
as we’ve seen in the first section can trigger either comfort eating
or sometimes can reduce appetite.
Clearly psychological factors as well as neural mechanisms are at work.
Evaluation of the model
The model cannot explain:
Why damage to the VMH of rats not only triggers eating behaviour but
also makes them fussy eaters. Usually a hungry rat will eat
anything it can get (provided it hasn’t made it ill in the past).
However, food soaked in a bitter chemical (quinine) is avoided by
rats with a damaged VMH. Usually hungry rats wouldn’t be bothered.
Rats with damage to their VMH will eat more provided the food is
easily accessible. For some reason they will not carry out tasks
such as lever-pressing to gain food; despite their hunger.
Something similar is evident in obese humans… according to Schacter
20 obese participants and 20 controls were asked to stand at a desk and
complete a questionnaire. The researcher ate an almond from a nearby
bag and politely tells the participants to help themselves while they
complete the questions.
The nuts are either shelled (no shell) or unshelled (still have their
The control group ate similar amounts of nuts regardless of whether or
not they had to shell them.
Of the obese group, 19 ate the shelled nuts (no work to do) whereas only
one ate the unshelled nuts (work required).
Schacter concluded that obese people are motivated to eat but only when
food is readily available.
Other evaluation points
The precise mechanisms by which leptin enters the brain is not clear.
Leptin is a large molecule and the brain has a ‘barrier’ that prevents
chemicals entering from the blood (the so-called ‘blood-brain barrier).
The arcuate nucleus which apparently has no barrier may be one possible
Biological rhythms have an impact on eating behaviour. We tend to feel
hungry at certain times of the day, regardless of what we’ve eaten
earlier. Rats tend to feel hungry just after darkness. This suggests a
link between the body clock and eating mechanisms but again the precise
link isn’t known; though the main clock is located in adjacent areas of
Blood glucose levels remain constant in a non-diabetic. It therefore
seems unlikely that changes in blood-sugar are needed to initiate hunger
or satiety. In fact this would seem counter-intuitive since increases
in insulin are needed to trigger hunger. Insulin levels increase
following a meal to deal with increased blood-sugar so hunger would be
triggered after eating! However, blood-sugar levels are not as
important as cellular sugar levels and especially levels of sugar in the
Evolutionary Explanations of Food Preferences
Darwin’s theory of natural selection states that individuals will behave
in such a way as to maximize their survival and their reproductive
potential. Individuals that survive to maturity and beyond are more
likely to produce offspring and be able to ensure the long term survival
of their young. In terms of evolutionary theory therefore, it pays to
In present day Western society food is plentiful, but it hasn’t always
been that way. In book one of this sequence I mentioned the Irish
potato famine when hundreds of thousands of people starved to death and
millions of others were forced to flee Ireland to find food. Stalin’s
farming policy in the Soviet Union after WWII ensured the deaths from
starvation of millions of Ukrainians and more recently there have been
famines in Africa.
In our not too distant past, food would often have been scarce. Binge
eating would therefore be adaptive. It may be a while before the next
meal. As a result piling on extra pounds would have been a useful
strategy for survival. Genes that made this behaviour more likely would
have made it to the next generation as their hosts (the humans with
those genes) would have been more likely to survive and reproduce.
Those that didn’t binge would die out and their genes would die with
Why the preference for a high fat diet?
Calories are essential for energy. Every cell in the body produces
energy by the process of respiration and respiration needs a constant
supply of glucose. A useful supply of sugars in times of hardship is
the body’s fat reserve that can be converted to glucose.
We seem to learn at a very young age which foods are high in calories
and we develop a taste for these. Fats are very useful for energy. A
given amount of fat contains about twice the calories of similar amounts
of protein or carbohydrate.
In our historical past, fats would have been relatively rare. As a
result fat would have been relished and cherished! Today, in contrast
fat is everywhere, but unfortunately we have not lost that preference
for it and as a result we consume it in huge and dangerous amounts.
Eaton and Konner (1985) described what they called their ‘Paleolithic
Diet’ that ancient man would have consumed. This comprised some meat,
fish, fatty oils, fruit and veg,
Fatty foods would have provided the calories along with vitamins A and D
whilst the fruit and veg would have provided a few carbohydrates and
vitamins B and C. Compared to modern diet however, carbohydrates would
have been in short supply.
Some believe this move away from our ancient diet with a much greater
reliance on carbs. Has led to increased incidence of hypertension, CHD
and obesity. Others however, such as Leonard (2002) believe that humans
have evolved to be flexible eaters and as a result can live in most
areas of the planet and vary what we eat.
Evidence for our ability to adapt diet
The Japanese diet is very high in starch (a complex carbohydrate) due to
their love of rice. The Japanese genome seems to have adapted to this
by producing extra copies of AMY1, a gene responsible for the production
of amylase (enzyme that digests starch). The Yakut or the Arctic, have
a low carb diet, preferring to indulge on the plentiful supplies of fish
in the area. These have fewer genes for the production of amylase.
Culture, therefore may be having an impact on human biology, as we adapt
to various diets due to the myriad of conditions in which we are capable
Why the preference for sweet foods?
In some ways the answer to this is obvious. Sweet indicates presence of
sugar which indicates calories needed for energy. Sweetness would be
associated with foods that are ripe and foods that are ripe are going to
contain more sugar. Rozin (1982) thinks this preference for sweetness
This would seem to be supported by the number of sweet receptors on the
human tongue, far more than for the other flavours such as bitter, sour,
salt and umami. People of all ages and of all cultures seem to prefer
sweet taste to any other, suggesting it is an inherited preference:
Meiselman et al (1989)
Bell et al (1973) gave sweet foods to Eskimos in Alaska. Under normal
conditions Eskimos have nothing sweet in their diet. However, the foods
were readily accepted despite their novel nature, again suggesting an
underlying human preference for sweet foods. Human babies also love
things that are sweet and will eat them the first time they are
fat and sugar. The foods we crave. The makers of Mr Porky pork
scratchings must find it difficult to advertise their mostly fat and
heavily salted pig rind sound healthy. The packets used to bear the
legend ‘High in energy!’ lol. Still TASTY tho
Evidence form pre-history
Modern researchers have a pretty good idea of what our ancestors ate.
Cave drawings, like the ones found in Lascaux in France depict food of
the day. Ancient skulls bear clues in the form of patterns of wear and
tear on the teeth and carbon and nitrogen isotopes which enable us to
judge the age of findings.
Ancient pre-hominids ate mostly wild plants and seeds with occasional
meat and bone marrow. Homo-Habilis (about 2.4 million years ago) was
living mostly on deer, birds, rabbits and fish supplemented by wild
plants. At this time our ancestors seemed to have been confined to East
Africa which was still largely forested. As the continent got drier the
forests gradually disappeared to be replaced by the grasslands and
savannahs we still see today. This meant food became more scarce which
is a double whammy, since it obviously means less food and longer trips
to find it, resulting in greater expenditure of calories.
Over the next million or so years as we evolved we grew in size…( I say
‘we’). This appears to be true of most species and is referred to as
Cope’s law. Mankind began to move north in search of more food (about 1
million years ago) and at about this time our brain began to increase
considerably in size. Clearly this has its advantages in terms of
intellect and problem solving but it also comes at a cost.
The human brain is very hungry. Despite it accounting for only about 2%
of body weight, it consumes about 25% of the body’s energy resources.
This might also explain the human fascination for high calorie food.
This combination of increase in body size, increase in brain size and
reduced levels of food caused a problem. As gorillas began to grow they
evolved to eat more. Modern gorillas spend much of their day chewing on
mostly non-nutritious plants. Early humans, like chimpanzees opted for
a more diverse diet that included more nutritious meat. MacArthur and
Plank (1966) proposed OFT (optimal foraging theory, not to be confused
with the Office for Fair Trading!
OFT basically states that species adopt a feeding system that maximizes
intake of calories with the loss of minimal calories. Basically species
live on the limit. Getting the balance wrong could be fatal.
At this stage we were still hunter-gatherers, out looking for food
rather than growing and rearing our own supplies. Modern day
hunter-gatherers such as the San of Namibia and Botswana, still acquire
about 60% of their energy intake from meat and milk. These modern
hunter-gatherers tend to be shorter and lighter than their urban cousins
but still need to consume far more calories due to the additional energy
expended in finding food.
Agriculture, which didn’t really begin until about 10,000 years
revolutionized the human diet and our food supply.
The ability to adapt our diet has been essential to the human migration
from the warmth of Africa to the cold of the Arctic north and the arid
heat of the deserts.
Cooked food and farming
The ability to use fire to cook food also had a big impact. Cooking
softens foods so that less damage is done to teeth during the chewing
process. It also releases some nutrients from foodstuffs and so eases
the demands on our digestive system. Apparently a cooked carrot is more
nutritious than one eaten raw. The cooking process makes the nutrients
more readily available. Wobber et al (2008) found that chimps, bonobos
and orangutans prefer some foods such as meat, sweet potatoes and
carrots that have been cooked rather than raw. However, with potatoes
and apples it made no difference if they’d been cooked or not.
Brewer (1978) had already shown that chimpanzees prefer seeds that have
been cooked by natural fires to ones that are raw. It seems likely that
the human preference for cooked food evolved long before we had learned
to control fire.*
The move from a hunter-gatherer existence to farming increased the
availability of food and also decreased the amount of energy expended in
Modern man not only consumes more calories due to the easy availability
of food but burns far fewer as our lives become more and more
sedentary. However, our propensity to over-eat and binge, perhaps
partly due to our inherited survival strategy ensures that we are
becoming increasingly obese. It is estimated that 75% of UK adults are
either overweight or obese.
The Family Tree:
Early Hominid: here we have the lovely Lucy**. Believed to have
lived 3.2 million years ago.
Homo Habilis: 2.4 million years ago to 1,5 million years ago
Homo Sapians: first appeared about 500,000 years ago
Why the preference for salty foods?
Salt is essential for the functioning of muscles and nerve cells (action
potentials and all that). Homeostasis keeps salt levels reasonably
constant. However, salt is not readily available naturally, so like fat
when it was found by our ancestors it would have been much prized, hence
the reason for us liking it so much. Some have suggested that our
desire for salt is innate, we do after all have salt receptors on the
However, unlike sweet, our taste for salt doesn’t seem to evolve until
we’re a few months old, suggesting a predisposition but with a learned
component. Not until the age of about 4 months does the taste seem to
develop and by the age of two years children will reject food that
they’re expecting to be salty that isn’t.
Food producers have been accused of taking advantage of our ancient
desire for salt by adding it in overly-liberal quantities in processed
Our successful ancestors would have been the ones wired to eat as much
as they could whenever they got the chance, literally not knowing when
the next meal would come. Today, we are in possession of those genes
that predispose us to binge, but unlike our ancient forerunners we don’t
need to go looking far for food, we don’t burn calories in our search
and the next meal is guaranteed at a certain time.
Other species that live where food is plentiful exert more self control
when it comes to food consumption. Forzono and Logue (1992) found a
positive correlation between food levels and self control. As food
supply drops so does a species ability to exert self-control, causing
them to binge. We were “created” for a time of little so have would
have benefited from little control. Today we are not cut out for a
World of plenty!
Rather than binging in times of plenty, a better approach would be
self-control. As we grow ever more obese we are putting our health at
greater risk. As with so many human characteristics, the biology
designed to preserve us is now putting us at risk.
*According to Greek legend fire was stolen from the Gods by Prometheus,
a Titan known for his intelligence. He carried the fire to Earth in a
giant fennel stalk and gave it to mankind. His punishment was severe!
Zeus had him tied to a rock in the Caucusus, where each day an eagle ate
out his liver. Over night it would grow back so the eagle could feast
again the next day.
** The skeleton of an ancient female Australopithecus was discovered in
Ethiopia in 1974. The anthropologists who discovered her called her
Lucy after playing the Beatle’s Lucy in the Sky with Diamonds’ over and
over in celebration! (Source: Wikipedia!).
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!
number of different explanations have been produced, but all have the
telltale influence of Freud et al.
Hilde Bruch has suggested a couple of ways in which
eating disorders may have originated:
Freud saw eating and sex as symbolically related. Girls
may link the fattening stomach caused by eating with that of pregnancy
at an unconscious level. Refusing to eat, therefore, could be seen as a
refusal to accept developing sexuality.
girl wants to remain immature so she doesn’t have to adopt the
responsibilities of the adult role. One way to achieve this is to stop
eating which helps to maintain the pre-pubescent shape and as we’ve
seen, can stop periods.
believes that this is a two way process, since the daughter can continue
to rely on the mother for security and the mother in turn is able to
keep their daughter safe and in the home.
However, as with all psychodynamic theories, Bruch’s ideas on oral
impregnation are unscientific and untestable. The unconscious forces
involved are hypothetical constructs that cannot be observed or measured
by any objective means.
Effective parents, according to Bruch, feed their
children when they’re hungry and comfort them when they’re anxious.
Ineffective parents, may mis-read the cues. When the
anxious child cries the mother might feed it, believing it to be hungry
and when it cries due to hunger she may comfort it believing it to be
anxious. This confuses the child about their own internal state and
their needs. It makes them dependent on others, for example to tell tem
when they’re hungry.
As it reaches adolescence it is expected to become
increasingly independent, but their uncertainty makes them fearful.
This results in a feeling of helplessness and not being in control of
their own body. The one thing they can control with certainty is their
Bruch (1975) found that many mothers of anorexic children
had admitted to anticipating the child’s hunger when they were young.
As a result the children had never experienced hunger. There is also
evidence that anorexics do rely too heavily on the views of others,
perhaps suggesting a perceived lack of self-control.
Minuchin believes that anorexics are products of enmeshment.
This is the tendency by some families to be over-protective of their
children and prevent any sort of independence. Families like this tend
to do everything together and as a result the child has no sense of its
own identity. One way the child can rebel is to stop eating.
Another feature of this kind of family is an inability to resolve
conflicts. This causes anxiety, (classic psychodynamic concept). In
order to deal with their anxiety, parents of the anorexic are able to
take on the role of caring for their ‘sick’ child.
Kalucy et al (1977) found that the families of anorexics tend to be
unable to resolve conflicts and blame others for their problems
(external locus of control).
However, whilst it is true that there is a lot of
conflict within the families of anorexic children we can’t be certain
that there is a cause and effect relationship. It is certainly true
that having an anorexic living in the house will cause tension and
families like the ones described above have presumably always existed
how can we use this model to explain the recent increases in the
incidence of eating disorders?
Looks at the
individual and society.
taught to be dominant and outwardly expressive. Girls on the
other hand are encouraged from an early age to be subservient
and self-critical. As a result, faced with a trauma in later
life boys are more likely take out their anger on others,
whereas girls are more likely to take it out on themselves by
abusing their bodies
need to be thin:
especially white, middle class men, hold power in Society and
they define the ideal image for women, for example through
advertising. Other examples include what is termed the 'gaze'
in films, i.e. the portrayal of life from a male perspective.
In films men tend to play the lead roles and usually the woman
is very much in a supporting role, often something pretty for
the male audience to look at! Feminists therefore suggest that
since women are unable to exercise power in other areas they
exercise it over their bodies.
also criticise the image of women portrayed to young girls.
Cartoon characters tend to be thin, I think of Penelope Pitstop
and Olive Oyle, you can probably think of contemporary
examples. Barbie and Cindy dolls are appallingly thin, and mis-shaped
if you imagine one blown up to real size. A thought experiment
for the boys. (Sorry, was forgetting this is a feminist
approach is based on the portrayal of women in the media, particularly
over the past thirty years. In this time, the ideal shape has shifted
from the rounded size 12/14 of the Sixties, as exemplified by Marilyn
Monroe, to the emaciated, twig like form of today, for example Kate Moss
and Posh Becks. (probably best not to quote the last bit, but you get
the idea!). This has led to women, particularly teenagers, dieting, and
the lay-persons idea of anorexia is the slimmers’ disease.
using the behaviourist model to explain any behaviour it is useful to
adopt Mowrer’s Two Stage Approach. This explains how a behaviour is
acquired and how it is later maintained.
Classical conditioning (or learning by association).
People are told they look good when they lose a little weight. Dieting
therefore becomes associated with feeling good about yourself. Eating
causes weight gain and as a result anxiety. As a result eating becomes
associated with anxiety. Or
Social Learning Theory
see others on television and in the media being rewarded for their thin
build. Successful women tend to be thin! Think of television
presenters, newsreaders, pop stars, actresses, celebrities, WAGS….
Girls, particularly are exposed to this vicarious reinforcement (the
rewarding of others) and imitate in order to be rewarded themselves.
Admiring glances and compliments following weight loss, act to reinforce
the dieting behaviour, so the weight loss continues. This is an example
of Thorndike’s Law of Effect which put into simple terms predicts that
of all behaviours performed, those that are rewarded are more likely to
worth mentioning that severe weight loss and abstinence from food also
punishes parents, which to the adolescent can be very rewarding in
with interests in areas with the most reward for weight loss are the
most likely to develop an eating disorder, for example dancers, gymnasts
etc. Garner et al (1987) found that 25% of a group of 11 to 14 year old
ballet dancers developed anorexia during a 2 year course.
the model would predict, anorexia is most common in Western Society
where slim is portrayed by the media as being attractive.
immigrants from societies where anorexia is rare settle in Western
society their chances of developing an eating disorder increases
significantly. For example Nasser (1986) compared the following:
50 Egyptian women at University in London with
Egyptian women at University in Cairo.
Findings. 12% of the London group developed an eating disorder during
their course. None of the Cairo group did!
some countries, particularly SE Asia, there are positive attitudes to
women being a larger shape. Here, there is an association of large with
health, attractiveness and fertility. As behaviourists would predict,
anorexia is rare, almost unheard of, in these cultures.
Similarly in China, where girls tend to be slimmer, there is an
association of thin and ill! Obesity is seen as a sign of prosperity
rather than in the West where it is seen as a sign of lack of
self-discipline. Again eating disorders are very rare.
Anorexia is a rare success story for the behaviourists. Their model can
explain some of the patterns that we see:
it has become so prevalent in recent years (as the portrayal of women in
the media has changed).
Why it is becoming increasingly prevalent in men (as the
portrayal of the ideal body shape for men becomes increasingly thinner).
there are cross-cultural differences such as its greater prevalence in
Western Society where the emphasis is on ‘thin is beautiful.’
not explain why anorexics continue to diet even after they stop
receiving compliments and are even told how awful they look.
not explain individual differences, i.e. why some people develop the
disorder and others with the same media pressures do not.
has obvious face validity as an explanation since we know from
research that anorexics typically have a distorted body image. The
cognitive approach to abnormal behaviour is based on distorted thinking
Evidence for distorted body image
Bemis-Vitouesk & Orimoto (1993) (no I didn't make it up, that is their
real names) found that anorexics consistently have a distorted body
image and believe that they must continually lose weight in order to be
in control of their bodies. Typical thoughts included: 'I must lose
more weight I am not yet thin.' Similarly, Garfinkel and Garner (1982)
found that anorexics overestimate their weight and body size.
Lovell et al (1997) found that people who had recovered from anorexia
nervosa two years earlier still had distorted body images and odd views
about food and other 'adolescent issues.'
However, yet again we have the issue of cause and effect. Do the
distorted ideas pre-date the onset of anorexia, so offer a possible
causal explanation, or do the distortions arise because of the anorexia?
Fairburn et al (1999) identified perfectionism and negative self-image
as the greatest risk factors in developing an eating disorder. It seems
likely that a combination of these two factors, distorted self-image and
desire to be perfect are the risk factors.
Halmi et al (2000) tested 322 anorexics on the
Multidimensional Perfectionism Scale and found
that they scored significantly higher than a control group. Furthermore
it was found that as levels of perfectionism increased so did the
severity of the anorexia.
However, the same study reported that perfectionism of
this sort tends to run in families, again providing support for the view
of a genetic component. Perhaps genes aren’t causing the anorexia
directly, merely increasing the risk of developing a personality type
that is a risk factor in anorexics.
Stroeber et al (2006) investigated the cases of anorexic
boys and girls being treated for eating disorders and found high levels
of perfectionism in their past (73% in girls and 50% of boys). But this
study by its nature is retrospective, with the patients and presumably
parents having to recall childhood events. However, if this were the
case it would suggest the perfectionism pre-dating the anorexia and
provide stronger evidence for a cause and effect relationship.
A suitable conclusion for an essay on explanations of
eating disorders requires a multi-perspective approach.
Diathesis refers to the genetic predisposition of some
people to develop the disorder. The medical model for anorexia, though
generally weak, clearly suggests a genetic element to the condition.
Evidence suggests that this may however, be indirect.
research has centred on the psychodynamic models which emphasises family
issues. A combination of behaviourist and cognitive seem to offer a
reasonable compromise with behaviourist explaining how the pressures to
be thin arise and the cognitive accounting for individual differences
that pre-dispose some to eating disorders but not others.
behaviourist-cognitive model also offers an explanation of depression.