Why diets fail or succeed

Neural mechanisms in eating behaviour

Evolutionary explanations

Eating Disorders

Eating behaviour

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:

Cultural Influences

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 don’t

In South America hamster is popular and in Korea a dog isn’t just for Christmas (dinner)!

So what determines and maintains these biases towards certain food stuffs?

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 explain. 

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 J

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 life-promoting.

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 pleasant outcomes. 

Schema 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:

Mealtimes

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 breakfast.

Where we eat

Restaurant

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 half. 

Eating out generally results in consumption of less healthy foods since restaurants tend to offer fewer healthy options. 

School

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.

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 significantly.

Large portion….’yes!’

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 few decades. 

Some US restaurants even offer ‘BIG KID MEALS.’

Mood

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.

Sex differences

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 fruit.

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. 

Chocolate

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 brain chemistry? J

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 serotonin.

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 neurochemical. 

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 their mood.

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. 

Caffeine

How many of you can’t function until you’ve had your first or second coffee?

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. 

Health concerns

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 veg. 

Given this understanding of nutrition it seems even more perplexing that obesity in children is now running at 27% with 14% being classed as clinically obese.

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.

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 families. 

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 body dissatisfaction.

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).

Education

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 2000.

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 2000.

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 succeed

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 or BMI.

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.

The future:

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.

Restraint Theory

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 snack. 

The researchers conclude that dieters often eat less but on other occasions over-compensate by binging, especially if they eat one unhealthy meal.

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:

1. Diet
2. Exercise
3. Control

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.

Other 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 all wrong? J

Basically the more you try not to think of something the more it dominates your thoughts.  Wegner et al (1987); participants were told either:

‘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

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. 

Leptin

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 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. 

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

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 bloodstream. 

Hunger monitors current needs, anticipates future needs and motivates eating

Satiety tells us when enough has been consumed and terminates eating.

Early theories

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 result.

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. Note:  thanks to homeostasis, blood sugar levels fluctuate very little.  They are tightly controlled by insulin and glucagons.

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). 

The Glucostatic Hypothesis

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 others.

Set Point

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 feels ‘comfortable.’

Lipostatic Hypothesis

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. 

1. Eat until obese
2. 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.

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 behaviour.

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 hungry. 

• The mere smell of freshly baked bread or freshly brewed coffee can instill a craving.
• Habits, 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:

1. 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.
2. 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 (1971)

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 hard coating).

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 route.

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 the hypothalamus. 

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 liver. 

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 be healthy. 

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 them. 

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 of thriving.

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 is innate. 

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 encountered.

 Salt, 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 J

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 finding it. 

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:

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 tongue. 

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 foods.

Conclusions

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!). 

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!

Psychological explanations

Psychodynamic

A 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:

Oral impregnation:

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.  The 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.

Bruch 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. 

Ineffective parenting

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 eating.

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. 

Enmeshment

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. 

Evidence

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 conflict.

Since 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?

Behaviourist explanation

The 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. 

When 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. 

Acquisition

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 (neo-behaviourist)

We 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. 

Maintenance

Operant conditioning

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 be repeated. 

It is worth mentioning that severe weight loss and abstinence from food also punishes parents, which to the adolescent can be very rewarding in itself.

Evidence

Girls 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.

As the model would predict, anorexia is most common in Western Society where slim is portrayed by the media as being attractive.

When 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

·         60 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!

In 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. 

Evaluation

Anorexia is a rare success story for the behaviourists.  Their model can explain some of the patterns that we see:

·         Why 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).

·         Why there are cross-cultural differences such as its greater prevalence in Western Society where the emphasis is on ‘thin is beautiful.’

But

Does not explain why anorexics continue to diet even after they stop receiving compliments and are even told how awful they look.

Does not explain individual differences, i.e. why some people develop the disorder and others with the same media pressures do not.

Cognitive explanation

This 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 and perception.

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?

Perfectionist personality

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.

Evidence

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. 

Diathesis stress

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. 

Much 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. 

This behaviourist-cognitive model also offers an explanation of depression.