What the board expects you to know:
Introduction
In modern times in the Western World we have come to take food very much for granted. Because of the development of industrial scale farming techniques food is mostly cheap and plentiful. However, this is a relatively new development. In the mid nineteenth century Ireland was part of the British Empire. Being one of closest neighbours we used Ireland to produce plentiful supplies of beef to satisfy our increasing taste for the product. As a result once pastoral land was replaced with arable. The Irish, famed for their love of potatoes were also largely dependent upon the common spud but now had less land on which to grow them. Then in 1844 potato blight arrived, probably from the USA. In 1845, 75% of the potato crop failed and one million people starved to death. A further one million emigrated to other parts of the World to avoid starvation. Despite this, the Irish government still continued exports to the rest of the UK!
Food has also been used as a weapon, most notably by Joseph Stalin. Having come to power in the Soviet Union following the death of Lenin, Stalin was fearful that Ukraine would seek independence and Russia would lose access to a ‘warm water naval base’ on the Black Sea. To control the Ukrainian population Stalin collectivised (nationalized essentially) all privately owned farms in Ukraine. A particular target were those owned by the Kulaks, seen as the wealthier middle class Ukrainians. These were thrown onto the streets, losing their houses and all their possessions. Stalin then imposed very tight export controls on the produce of the farms insisting that most was exported to Russia for sale onto other parts of the World for profit. Ukrainians found hording food were shot. Too little food was left in the country to feed the population. In 1933 it is estimated that 25,000 Ukrainians a day were starving to death. The final death toll will never be known but it is thought that Stalin managed to kill between seven and eleven million Ukrainians by controlling their food supply. Three million of the dead are thought to have been children.
Further back in our evolutionary past, as we were evolving on the plains of Africa, there would have been intermittent times of famine and plenty. Those predisposed by their genetics to lay down fat supplies during times of plenty would have been more likely to survive and pass on their genes to the next generation. The skinny ones amongst us would have died. It would have been Survival of the Fattest!
In a modern World, with plentiful supplies of cheap and nutritious food, those predisposed to weight gain and fat storage now appear at a disadvantage. The same mechanisms that motivated us to eat as much as possible are now creating the obesity pandemic. People are dying of obesity-related disorders. Meanwhile the Western media glorifies the size zero female body shape fueling body dis-satisfaction and low self-esteem for millions of women who are driven to extreme measures to lose weight, mostly without success. Welcome to Eating Behaviour.
Evolutionary explanations of food choice
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 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.
Evidence form pre-history
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. 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.
- Explanations for food preferences: the evolutionary explanation, including reference to neophobia and taste aversion; the role of learning in food preference, including social and cultural influences.
- Neural and hormonal mechanisms involved in the control of eating behaviour, including the role of the hypothalamus, ghrelin and leptin.
- Biological explanations for anorexia nervosa, including genetic and neural explanations.
- Psychological explanations for anorexia nervosa: family systems theory, including enmeshment, autonomy and control; social learning theory, including modelling, reinforcement and media cognitive theory, including distortions and irrational beliefs.
- Biological explanations for obesity, including genetic and neural explanations.
- Psychological explanations for obesity, including restraint theory, disinhibition and the boundary model. Explanations for the success and failure of dieting
Introduction
In modern times in the Western World we have come to take food very much for granted. Because of the development of industrial scale farming techniques food is mostly cheap and plentiful. However, this is a relatively new development. In the mid nineteenth century Ireland was part of the British Empire. Being one of closest neighbours we used Ireland to produce plentiful supplies of beef to satisfy our increasing taste for the product. As a result once pastoral land was replaced with arable. The Irish, famed for their love of potatoes were also largely dependent upon the common spud but now had less land on which to grow them. Then in 1844 potato blight arrived, probably from the USA. In 1845, 75% of the potato crop failed and one million people starved to death. A further one million emigrated to other parts of the World to avoid starvation. Despite this, the Irish government still continued exports to the rest of the UK!
Food has also been used as a weapon, most notably by Joseph Stalin. Having come to power in the Soviet Union following the death of Lenin, Stalin was fearful that Ukraine would seek independence and Russia would lose access to a ‘warm water naval base’ on the Black Sea. To control the Ukrainian population Stalin collectivised (nationalized essentially) all privately owned farms in Ukraine. A particular target were those owned by the Kulaks, seen as the wealthier middle class Ukrainians. These were thrown onto the streets, losing their houses and all their possessions. Stalin then imposed very tight export controls on the produce of the farms insisting that most was exported to Russia for sale onto other parts of the World for profit. Ukrainians found hording food were shot. Too little food was left in the country to feed the population. In 1933 it is estimated that 25,000 Ukrainians a day were starving to death. The final death toll will never be known but it is thought that Stalin managed to kill between seven and eleven million Ukrainians by controlling their food supply. Three million of the dead are thought to have been children.
Further back in our evolutionary past, as we were evolving on the plains of Africa, there would have been intermittent times of famine and plenty. Those predisposed by their genetics to lay down fat supplies during times of plenty would have been more likely to survive and pass on their genes to the next generation. The skinny ones amongst us would have died. It would have been Survival of the Fattest!
In a modern World, with plentiful supplies of cheap and nutritious food, those predisposed to weight gain and fat storage now appear at a disadvantage. The same mechanisms that motivated us to eat as much as possible are now creating the obesity pandemic. People are dying of obesity-related disorders. Meanwhile the Western media glorifies the size zero female body shape fueling body dis-satisfaction and low self-esteem for millions of women who are driven to extreme measures to lose weight, mostly without success. Welcome to Eating Behaviour.
Evolutionary explanations of food choice
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 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.
Evidence form pre-history
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. 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. |
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. Fat can store twice as many calories per unit weight than proteins are carbohydrates. If food was scarce it would literally have been survival of the fattest!
We seem to learn at a very young age which foods are high in calories and we develop a taste for these. Gibson and Wardle (2001) found that the calorific value of food was the best predictor of whether or not a child would like that food. 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.
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.
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. This suggests a biological/genetic predisposition to sweet tastes and seems to rule out a learned response. Again a genetic predisposition is evidence of evolutionary pressure to like sweet foods. Sugar placed on the tongues of newborn babies produces positive facial expressions again suggesting the preference for sweet is there at birth (Steiner 1977).
Zhao et al (2008) identified two specific genes, T1r2 and T1r3 which code for sweet receptors on the tongue. The fact that these genes exist and have been maintained within the population again provide powerful biological evidence for an adaptive preference for sweet foods.
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)
Finally, humans go to extreme lengths and risk danger to secure sweet food. Members of the Bayaka Pygmy tribe of Africa climb high trees and suffer stings from hundreds of angry bees to provide this sweet food for their families. (BBC’s Human Planet).
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. By four months of age, children being breastfed (which contains very low levels of salt) prefer cereals that are salty. Suggesting that not until this age 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. The fact that this is universal again suggests evolutionary/biological mechanisms at work.
People with natural sodium deficiency find salt even more palatable than the rest of us and eat it in larger quantities when available. Dudley et al (2008) found that ants living further inland with less salty soils prefer salty foods to sweet. Again these studies suggest that we instinctively know that we need salt and have developed mechanisms that ensure we get sufficient. Apparently Scottish deer risk death on British roads by licking surfaces that have been gritted with rock salt in the winter months. However, in humans there are large individual differences which might not be expected from an evolutionary-driven behavior.
Why we eat meat
Gorillas are herbivores, chimpanzees and orangutans eat a little meat most modern day humans eat lots. Why this disparity?
Meat does bring advantages. It is high in energy, courtesy of the fat content, high in protein so is ideal for growth and repair and contains lots of vitamins and minerals, particularly the organs such as heart, liver and kidney. It is also available all-year-round which would have been a major advantage to our ancestors who would have had limited means of storing food for the winter months. Our switch from mainly vegetarian to an omnivorous diet has been used by some to explain the growth of the human brain. Not only is meat high in nutritional value it also meant we didn’t need to spend so much time each day eating. This freed up time for social activities encouraging brain development.
However, hunting for meat is a dangerous activity and burns lots of calories. Eating meat also increases risk of food poisoning and other infections, for example HIV.
Dunn (1990) argues that we didn’t evolve to eat meat but happened upon it when other food became scarce. In fact humans are not like other carnivores who relish raw meat and little else. We prefer it cooked and accompanied by other food groups. Children show no immediate desire to eat meat. Parents have to introduce their offspring to meat gradually which suggests it’s a learned rather than innate behavior.
Evidence for our ability to adapt our 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.
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.
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.
Neophobia
This refers to a general unwillingness to eat novel foods and is especially prevalent in the young of humans and non-human animals alike. New foods could be toxic and cause illness or death. Neophobia therefore would be an obvious adaptive process making survival more likely. In humans it develops at about the age of two, just as children are starting to explore their environment unsupervised by parents who up until this age would have been able to regulate their offspring’s intake of food.
Taste aversion
According to very famous psychologist Martin Seligman, we learn some associations faster than others. For example, we very quickly learn to be fearful of spiders and snakes. A few electric shocks on seeing either and we become phobic. Trying to teach people to be scared of flowers or houses using the same procedure is practically impossible. It’s as though we are hard-wired by our biology to make certain associations (via classical conditioning) than we are others. This again would be of evolutionary advantage. Being fearful of spiders and snakes in our distant past would have been adaptive.
It seems the same process occurs with food. Novel food that makes us sick is immediately avoided in future. It’s called one-trial learning.
Garcia’s sickly rats
In a series of experiments on rats Garcia demonstrated one-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.
Evaluation of Evolutionary Model
The model suggests our food preferences have evolved to help us survive a difficult evolutionary past. Some recent research has suggested alternative beneficiaries to our eating habits: gut microbes. The importance of these for the human diet cannot be over-stated. Our symbiotic relationship with gut microbes is crucial to our digestion of food.
However, some such as de Weerth et al (2013) think gut microbes may be controlling our eating behavior for their own benefit. An example would be gut microbes causing cholic and pain in infants. Cholic causes the child to cry and as a result it gets fed. Of course mum is also inadvertently feeding the microbes. All part of the ‘clever’ ploy.
The ability to taste bitterness is obviously adaptive, acting as a warning to protect against consumption of toxic food. However, some people are born without the inability to detect bitterness. This is difficult to explain in evolutionary terms as it would seem to put them at a disadvantage. An alternative theory could be the protective role played by some bitter foods such as green tea, against certain cancers. Those without the receptors are more likely to consume these and benefit from the protection they offer.
Learning and Food Preferences
Classical Conditioning (flavour-flavour learning)
As already mentioned, we have an innate preference for sweet foods. As a result if we sweeten novel foods such as yogurt, tea and coffee we very quickly learn to like them. Over time and with repeated exposure to the tastes we learn to appreciate these foods for themselves and eventually like them without the need for added sweetness.
In fact, this is similar to Garcia’s rats but in reverse. However, when a new food is paired with something unpleasant the association is far stronger and can last a lifetime.
Classical conditioning may also be responsible on a different level. Certain foods become associated with certain occasions. Chocolate is the obvious example. From a young age we learn to associate it with celebrations: birthdays, Easter, Christmas, weddings. This may explain part of its universal appeal. However, it doesn’t seem to have worked with Brussel sprouts!
Operant Conditioning
One we would all be familiar with as children. For example, parents’ attempts to get us to eat healthy foods such as vegetables by offering rewards such as ice-cream afterwards. Generally with limited success.
Social Learning Theory (SLT)
We learn about eating behavior from watching others. Pretty obvious really. As children we eat food that is prepared by our parents. We learn to eat the foods that they eat. Again it could be argued that this is of survival value. Our parents are more experienced at earing food, they already know what’s good, what’s bad and what’s ugly. By copying parents we tasty foods that are good for us and we avoid toadstools and poisonous berries.
Peers
Birch (1980) sat children next to groups of other children during school lunches. The other children were chosen so they had different tastes in vegetables to the participants. After only a few days the children were starting to switch their veg eating to match those around them. ISI or NSI? A few weeks later, these altered tastes still persisted, suggesting ISI and internalization. (Bit of social influence revision J).
Media and advertising
A major, long-running news item in recent years, the role of advertising targeting children and encouraging them to eat unhealthy sugar-packed, carb-loaded, muffin-top causing foods. In recent years some of this advertising has been banned, however, it does highlight the power of SLT in determining what we eat.
Boyland et al (2007)
Fifty nine children aged between 9 and 11 were shown episodes of Scooby Doo preceded by advertisements for products such as chocolate, sweets, savoury snacks and soft drinks. After the cartoon children were offered a selection of five products to eat: Cadbury chocolate buttons, Haribo Starmix sweets, Walkers ready salted crisps and Quaker Snack-a-Jacks). Researchers then measured their total intake. The results were compared with the food consumed by the same children who were shown ten toy commercials around a cartoon on another occasion.
After watching the snack advertisements total food consumption by normal weight children rose by 84 per cent by 101 per cent for children who were overweight. Obese children ate 134 per cent more after seeing the food advertising, compared to the TV session with cartoons and commercials for toys. Importantly, the increase in the intake of food was not directly related to the brand that was featured in the advertising.
In 2007 advertisements for junk food around the time of children’s TV programmes were banned and in 2008 this was extended to programmes were children up to the age of 15 make up a high proportion of the viewers.
In other, similar research, Emma Boyland has also shown that children that watch more than three hours of television each day are more susceptible to the effects of advertising and are more likely to suffer from obesity.
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
Evaluation
Not all of the effects of SLT are equal. Parents and peers do appear to be far more influential than mere advertising. Hare-Brun et al (2011) studies a group of 8 to 10 year old Dutch children. Those who watched the most television were most likely to have the unhealthiest diets. Think of other possible reasons for this association!
Six years later in a follow up the effect was much weaker. As we get older peers become far more power influential in determining our eating behavior.
Culture
According to Rozin, culture is the most powerful determinant of food choice. It’s difficult to disagree with this conclusion. Culture determines not only what we see as food, for example horse, dog, insects, pig but also what constitutes a meal, the time of day we eat it, what we eat it with, how much of it we eat and the order in which we eat it.
The traditional British Sunday roast is a perfect example. Travel along the Algarve or Mediterranean coast on a Sunday afternoon and every other bar will be packed with holiday makers and ex-pats* tucking into roast meat, two veg, roast potatoes, Yorkshire pudding and lashings of gravy. All very British.
In Northern Europe we traditionally eat all parts of an animal. As well as the muscular tissue of popular farm creatures in the form of beef, pork and lamb we also relish their organs in the form of steak and kidney, haggis, liver and bacon. If anyone’s risked the ‘elephants foot’ at a kebab shop, goodness only knows what combination of mechanically-recovered, flavoured and artificially coloured animal parts you’ve imbibed.
In other parts of the World food is very different. Most parts of the World, even the USA don’t have quite the same taste for offal. Japanese love their raw fish, carefully cut. Koreans famously eat dog, most parts of Africa and Asia eat insects. South Americans love their guinea pigs.
Chinese culture
The Chinese idea of a meal is subtly different to the Western idea. The Chinese have two complimenting components to their main course. A bowl of rice or noodles that provide the complex carbohydrates and an accompanying dish of meat and vegetables. This is in contrast to western meals were the main course tends to be unitary with meat being the crucial component around which the rest of the meal revolves.
Mealtime is also a different experience being more communal (in line with the more collectivist nature of Chinese culture). Usually each person at the table is provided with their own dish of rice or noodles and the rest of the meal arrives on communal, help yourself dishes, what we in the west call ‘family style.’ The Chinese also think it poor practice to eat alone. Often when I was in Beijing waiting staff would sit opposite me in restaurants in order to keep me company whilst I ate. Desserts are rare, but soups have become more commonplace, thanks to the increasing influence of Western culture. Accompanying drinks such as water or juice are seen as inappropriate as they are thought to curb the process of digestion. Tea on the other hand is often served as it seen as an aid to digestion.
Classical Conditioning (flavour-flavour learning)
As already mentioned, we have an innate preference for sweet foods. As a result if we sweeten novel foods such as yogurt, tea and coffee we very quickly learn to like them. Over time and with repeated exposure to the tastes we learn to appreciate these foods for themselves and eventually like them without the need for added sweetness.
In fact, this is similar to Garcia’s rats but in reverse. However, when a new food is paired with something unpleasant the association is far stronger and can last a lifetime.
Classical conditioning may also be responsible on a different level. Certain foods become associated with certain occasions. Chocolate is the obvious example. From a young age we learn to associate it with celebrations: birthdays, Easter, Christmas, weddings. This may explain part of its universal appeal. However, it doesn’t seem to have worked with Brussel sprouts!
Operant Conditioning
One we would all be familiar with as children. For example, parents’ attempts to get us to eat healthy foods such as vegetables by offering rewards such as ice-cream afterwards. Generally with limited success.
Social Learning Theory (SLT)
We learn about eating behavior from watching others. Pretty obvious really. As children we eat food that is prepared by our parents. We learn to eat the foods that they eat. Again it could be argued that this is of survival value. Our parents are more experienced at earing food, they already know what’s good, what’s bad and what’s ugly. By copying parents we tasty foods that are good for us and we avoid toadstools and poisonous berries.
Peers
Birch (1980) sat children next to groups of other children during school lunches. The other children were chosen so they had different tastes in vegetables to the participants. After only a few days the children were starting to switch their veg eating to match those around them. ISI or NSI? A few weeks later, these altered tastes still persisted, suggesting ISI and internalization. (Bit of social influence revision J).
Media and advertising
A major, long-running news item in recent years, the role of advertising targeting children and encouraging them to eat unhealthy sugar-packed, carb-loaded, muffin-top causing foods. In recent years some of this advertising has been banned, however, it does highlight the power of SLT in determining what we eat.
Boyland et al (2007)
Fifty nine children aged between 9 and 11 were shown episodes of Scooby Doo preceded by advertisements for products such as chocolate, sweets, savoury snacks and soft drinks. After the cartoon children were offered a selection of five products to eat: Cadbury chocolate buttons, Haribo Starmix sweets, Walkers ready salted crisps and Quaker Snack-a-Jacks). Researchers then measured their total intake. The results were compared with the food consumed by the same children who were shown ten toy commercials around a cartoon on another occasion.
After watching the snack advertisements total food consumption by normal weight children rose by 84 per cent by 101 per cent for children who were overweight. Obese children ate 134 per cent more after seeing the food advertising, compared to the TV session with cartoons and commercials for toys. Importantly, the increase in the intake of food was not directly related to the brand that was featured in the advertising.
In 2007 advertisements for junk food around the time of children’s TV programmes were banned and in 2008 this was extended to programmes were children up to the age of 15 make up a high proportion of the viewers.
In other, similar research, Emma Boyland has also shown that children that watch more than three hours of television each day are more susceptible to the effects of advertising and are more likely to suffer from obesity.
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
Evaluation
Not all of the effects of SLT are equal. Parents and peers do appear to be far more influential than mere advertising. Hare-Brun et al (2011) studies a group of 8 to 10 year old Dutch children. Those who watched the most television were most likely to have the unhealthiest diets. Think of other possible reasons for this association!
Six years later in a follow up the effect was much weaker. As we get older peers become far more power influential in determining our eating behavior.
Culture
According to Rozin, culture is the most powerful determinant of food choice. It’s difficult to disagree with this conclusion. Culture determines not only what we see as food, for example horse, dog, insects, pig but also what constitutes a meal, the time of day we eat it, what we eat it with, how much of it we eat and the order in which we eat it.
The traditional British Sunday roast is a perfect example. Travel along the Algarve or Mediterranean coast on a Sunday afternoon and every other bar will be packed with holiday makers and ex-pats* tucking into roast meat, two veg, roast potatoes, Yorkshire pudding and lashings of gravy. All very British.
In Northern Europe we traditionally eat all parts of an animal. As well as the muscular tissue of popular farm creatures in the form of beef, pork and lamb we also relish their organs in the form of steak and kidney, haggis, liver and bacon. If anyone’s risked the ‘elephants foot’ at a kebab shop, goodness only knows what combination of mechanically-recovered, flavoured and artificially coloured animal parts you’ve imbibed.
In other parts of the World food is very different. Most parts of the World, even the USA don’t have quite the same taste for offal. Japanese love their raw fish, carefully cut. Koreans famously eat dog, most parts of Africa and Asia eat insects. South Americans love their guinea pigs.
Chinese culture
The Chinese idea of a meal is subtly different to the Western idea. The Chinese have two complimenting components to their main course. A bowl of rice or noodles that provide the complex carbohydrates and an accompanying dish of meat and vegetables. This is in contrast to western meals were the main course tends to be unitary with meat being the crucial component around which the rest of the meal revolves.
Mealtime is also a different experience being more communal (in line with the more collectivist nature of Chinese culture). Usually each person at the table is provided with their own dish of rice or noodles and the rest of the meal arrives on communal, help yourself dishes, what we in the west call ‘family style.’ The Chinese also think it poor practice to eat alone. Often when I was in Beijing waiting staff would sit opposite me in restaurants in order to keep me company whilst I ate. Desserts are rare, but soups have become more commonplace, thanks to the increasing influence of Western culture. Accompanying drinks such as water or juice are seen as inappropriate as they are thought to curb the process of digestion. Tea on the other hand is often served as it seen as an aid to digestion.
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.
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.
For health information to be effective it needs to be seen as reliable and reputable. Information coming from sources perceived as unreliable or information that is confused or contradictory is likely to be ignored. All too often health messages on food are mixed, such as the benefits of drinking 4 litres of water per day, the danger of eggs and the risks and benefits of alcohol are all likely to leave the public confused and less trusting in scientific advice
For health information to be effective it needs to be seen as reliable and reputable. Information coming from sources perceived as unreliable or information that is confused or contradictory is likely to be ignored. All too often health messages on food are mixed, such as the benefits of drinking 4 litres of water per day, the danger of eggs and the risks and benefits of alcohol are all likely to leave the public confused and less trusting in scientific advice
Cognitive theory of food preference
|
|
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!
|
Anorexia Nervosa
What the Board expects you to know:
Biological explanations for anorexia nervosa, including genetic and neural explanations.
Psychological explanations for anorexia nervosa: family systems theory, including enmeshment, autonomy and control; social learning theory, including modelling, reinforcement and media; cognitive theory, including distortions and irrational beliefs
Clinical Characteristics of Anorexia Nervosa (DSM-V)
- Persistent restriction of energy intake leading to significantly low body weight (in context of what is minimally expected for age, sex, developmental trajectory, and physical health).
- Either an intense fear of gaining weight or of becoming fat, or persistent behaviour that interferes with weight gain (even though significantly low weight).
- Disturbance in the way one's body weight or shape is experienced, undue influence of body shape and weight on self-evaluation, or persistent lack of recognition of the seriousness of the current low body weight.
Subtypes:
Anorexia Nervosa Binge / Purge
The individual suffering from anorexia nervosa binge / purge type, will purge when he or she eats. This is typically a result of the overwhelming feelings of guilt a sufferer would experience in relation to eating; they compensate by vomiting, abusing laxatives, or excessively exercising.
Restrictive Anorexia Nervosa
In this form of anorexia nervosa, the individual will fiercely limit the quantity of food consumed, characteristically ingesting a minimal amount that is well below their body’s caloric needs, effectively slowly starving him or herself.
Though two classifications of anorexia nervosa exist, both types exhibit similar symptoms, such as irrational fear of weight gain and abnormal eating patterns.
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. A newer and developing branch also considers evolutionary causation. The medical model is the approach used by psychiatrists.
The Psychological models include Psychodynamic (family Systems Theory), Behaviourist and Cognitive. These believe behaviour is caused by unconscious conflicts, learning and thought processes respectively. Clinical psychologists adopt one or more of these approaches when dealing with abnormal behaviour so tend to use psychoanalysis, CBT or similar talking therapies.
Biological 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):
The study looked at 34 pairs of twins (30 female and 4 male). Unlike in earlier studies were determining the real nature (MZ or DZ) was an issue, here the researchers took blood tests. In each case at least one of the twins in each pair had a diagnosis of anorexia nervosa and over a period of time, interviews were carried out o check incidence in the other twin.
MZ twins: concordance rate 56%
DZ twins: concordance rate 7%
However, it is worth pointing out that this is a very small sample size. By the time the twins had been divided into MZ and DZ, the researchers found 9 out 0f 16 MZ showed con concordance for AN compared to only 1 of the 14 DZ.
This is a quasi experiment and lacks control. The researchers could not rule out environmental factors as a possible cause of the higher incidence in MZ twins.
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!
Other studies
As well as twin studies, some research as looked at the incidence of eating disorders, particularly AN within families. Strober et al (2000) interviewed over 1800 first degree relatives of people diagnosed with eating disorders and compared this with relatives of those with no such diagnosis.
Anorexia was almost unheard of in the control group. However it was 11 times more likely in females related to others with anorexia.
Unlike twin studies this research clearly benefits in terms of numbers, with a huge sample size. This makes it much easier to generalise to the population as a whole. However, yet again it would not be possible to rule out environmental factors. Recent research (November 2010) carried out by Sugar magazine for the BBC showed the extent to which a mother’s eating behaviour can influence that of her daughter. According to the survey about 15% of teenage girls admit to dieting on a regular basis. This rises to 30% if their mothers regularly change their eating habits.
Candidate Genes
There have been a number of attempts to isolate specific genes that might be responsible for the predisposition to AN. Research has centred on an area of chromosome 1 (Kaye et al 2000). This research found that a number of anorexics and close family members had markers on chromosome 1. However, it is not possible to isolate specific genes, just the possibility that a number of genes may be causing a predisposition to developing AN. And as mentioned below, the link may not be a direct causal one, but instead it could be indirect, for example a gene predisposing an individual to a particular personality type or pattern of anxiety that makes AN more likely.
More recently Scott-Van Zeeland et al (2014) CARRIED OUT A GENE SEQUENCING STUDY ON OVER 1200 ANOREXICS. Only one out of a possible 152 genes studied showed any correlation with anorexia. It coded for an enzyme involved in the metabolism of cholesterol. This would make sense since many anorexics with the most sever symptoms have very high levels of cholesterol.
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.
As well as twin studies, some research as looked at the incidence of eating disorders, particularly AN within families. Strober et al (2000) interviewed over 1800 first degree relatives of people diagnosed with eating disorders and compared this with relatives of those with no such diagnosis.
Anorexia was almost unheard of in the control group. However it was 11 times more likely in females related to others with anorexia.
Unlike twin studies this research clearly benefits in terms of numbers, with a huge sample size. This makes it much easier to generalise to the population as a whole. However, yet again it would not be possible to rule out environmental factors. Recent research (November 2010) carried out by Sugar magazine for the BBC showed the extent to which a mother’s eating behaviour can influence that of her daughter. According to the survey about 15% of teenage girls admit to dieting on a regular basis. This rises to 30% if their mothers regularly change their eating habits.
Candidate Genes
There have been a number of attempts to isolate specific genes that might be responsible for the predisposition to AN. Research has centred on an area of chromosome 1 (Kaye et al 2000). This research found that a number of anorexics and close family members had markers on chromosome 1. However, it is not possible to isolate specific genes, just the possibility that a number of genes may be causing a predisposition to developing AN. And as mentioned below, the link may not be a direct causal one, but instead it could be indirect, for example a gene predisposing an individual to a particular personality type or pattern of anxiety that makes AN more likely.
More recently Scott-Van Zeeland et al (2014) CARRIED OUT A GENE SEQUENCING STUDY ON OVER 1200 ANOREXICS. Only one out of a possible 152 genes studied showed any correlation with anorexia. It coded for an enzyme involved in the metabolism of cholesterol. This would make sense since many anorexics with the most sever symptoms have very high levels of cholesterol.
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). More on this to follow: |
|
Biochemical explanation
Serotonin
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. However, it is important to bear in mind that brain chemicals like serotonin are simply messengers. They allow information to pass across a synapse. The precise effect they have depends more upon the information the nerve fibres are carrying. In some pathways of the brain, serotonin is associated with higher levels of anxiety.
Warning: different text books offer different explanations about how serotonin may be involved in anorexia. One thing that is certain, the relationship is complex. The simplest explanation I could find is:
1. Some anorexics seem to have an over-production of serotonin that results in high levels of anxiety.
2. Tryptophan is an essential amino acid that is essential for the production of serotonin.
3. By restricting diet, anorexics lower or even stop intake of tryptophan so serotonin cannot be produced.
4. This lowers their level of anxiety.
However, the nervous system compensates for the drop in serotonin levels by becoming more sensitive to the small amount available (the opposite of desensitisation we saw with leptin in obese patients). The brain develops additional serotonin receptors.
When the anorexic patient does eat, serotonin is produced which now has a much greater effect on the brain creating very high levels of anxiety. The anorexic therefore continues to restrict their diet in an attempt to keep anxiety levels low.
Bailer and Kaye found that serotonin levels return to normal in short term recovering anorexics. However, in long term recovery serotonin levels rise significantly above normal. This suggests that higher levels of serotonin in some anorexics are an underlying issue and may well have existed prior to the development of the disorder. This is good evidence that increased levels may be a cause and not just a symptom of anorexia.
However, as with all things in the brain the situation is never this simple. SSRIs such as Prozac have been used effectively to treat some patients with anorexia. They work by increasing the brains levels of serotonin. This model would predict that increased levels of serotonin would make the symptoms worse.
A study at Mawdsley Hospital in London found that anorexic patients are twice as likely to have a genetic variations in their serotonin receptors. This may predispose them to higher levels of serotonin resulting in their heightened anxiety.
Evidence
Ursula Bailer (2005) used brain scans on women who had recently recovered from various forms of anorexia nervosa and compared these to a control group of women who had never experienced an eating disorder. Those recovering from AN were found to have significantly higher levels of serotonin in the hypothalamic area. Additionally, those suffering the highest levels of anxiety had the highest levels of all. Bailer suggests a possible link between heightened levels of serotonin and anxiety with the anxiety then triggering anorexia.
Dopamine
Lowered levels of dopamine seem to be associated with anorexia nervosa.
Researchers usually measure levels of HVA (a breakdown product of dopamine) to gauge levels of circulating dopamine in the nervous system. HVA levels are lower in anorexics and crucially, also lower in recovered anorexics. This again suggest that lowered levels may actually be a cuse rather than just a symptom of anorexia since it seems to be ever-present.
Eating food, being a pleasurable activity for most of us, releases dopamine in the reward centres of the brain and therefore results in pleasure.
Bailer et al (2012) gave amphetamines to both anorexics and non-anorexics. Amphetamine results in increased dopamine levels.
In non-anorexics the amphetamine caused extreme pleasure, bordering on euphoria, as would be expected. In anorexics it created feelings of extreme anxiety.
Since eating increases levels of dopamine it seems anorexics learn to associate eating food with anxiety so avoid it.
Other chemicals?
Cortisol, the so-called stress hormone is known to suppress appetite. However, levels of cortisol seem to occur AFTER the onset of anorexia, seemingly ruling it out as a causal factor.
Nothing in the brain is this simple however. Fava et al (1989) found altered levels of serotonin and noradrenaline in anorexics and recent research has implicated serotonin, noradrenaline and dopamine in the pathways of the VMH and LH.
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.
|
Returning briefly to Ursula Bailer, in 2010 she has implicated the reward centres of the brain (more on these when we consider addiction). She showed images of women of various shapes to either severe anorexics or controls whilst they laid in a scanner. Images of underweight women triggered activity in the anorexics reward centres compared to more average images in non-anorexics. So yet again, trying to pin anorexia down in the brain is a complex task. Welcome to the Pleasuredome |
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!
Medical model and ethics
If it could be shown that anorexia was genetic or due to brain chemistry it would remove the guilt from parents who may consider themselves and their child-rearing skills responsible for the disorder. However, knowing there may be a genetic cause could lead to genetic testing in parents and additional anguish that offspring may grow up to develop the disorder.
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!
Medical model and ethics
If it could be shown that anorexia was genetic or due to brain chemistry it would remove the guilt from parents who may consider themselves and their child-rearing skills responsible for the disorder. However, knowing there may be a genetic cause could lead to genetic testing in parents and additional anguish that offspring may grow up to develop the disorder.
Evolutionary Explanations of Anorexia
Note: this is not mentioned on the AQA specification
A new idea for most of you I guess, but if like the biological model, we assume a possible genetic predisposition or causation we also need to consider the biological merit of that disorder. Otherwise why would seemingly maladaptive behaviours such as anorexia remain within the gene pool? Surely they would have been selected against. We shall consider two possibilities, but with a distinct emphasis on the former and more convincing:
1. The Adapted to Flee (famine) Hypothesis (Guisinger 2003)
Shan Guisinger’s AFFH seems to have gained much greater recognition in the past few years. Whilst treating anorexic girls Guisinger noticed two modal ages around which time girls seemed most susceptible to developing anorexia. The first of these was around the age of fourteen, the other around eighteen. What she found particularly curious about the fourteen year olds was that few of them reported being on a diet or having any desire to lose weight. Despite this, they were losing weight and showing many other of the signs of anorexia such as hyperactivity and body dysmorphia, whilst denying that there was a problem.
Girls at this age are, apparently, at their leanest. They tend to have a lower BMI than at any other age in their life. She hypothesised that dropping below a certain body weight, or body fat content may trigger the disorder. This would be like crossing a biological threshold. Above it and the person remains anorexia-free, below it and the body switches to anorexic mode. Typically, a period of stress or illness, or perhaps developing an interest in sport may then tip the already lean teenager below this threshold.
It’s important to emphasise that for Guisinger, anorexia is not a choice, it is not a reaction to family tensions nor is it a desperate attempt to get attention or exert control over parents. It is very much a biological response caused by body weight falling below a set point. The other danger age is around eighteen. Guisinger believes at this age, dieting or exercise is most likely to cause the initial loss in weight that triggers anorexia.
The evolutionary aspect
If Guisinger is right, and some people have a biological mechanism that triggers starvation, the obvious question is why has it evolved? At first glance it would be counter-productive from an adaptive standpoint. Behaviours that result in death or reduce reproductive chances tend not to be favoured by natural selection!
Guisinger thought back to our distant evolutionary past and considered the conditions of the early humans in Africa. Droughts and famines would have been frequent. We know that early hominids had to migrate thousands of miles to find food. Guisinger believes that if she is correct then the following should all be identifiable:
1. Adaptive
Think what we’re like when we’re hungry. Our mood drops, we become lethargic (presumably to save calories), we lack motivation and we become obsessed with thoughts of food. In times of severe drought/famine these behaviours would be counter-productive. Lethargy would not help us find food.
Anorexics on the other hand are unfazed by hunger. They ignore food even when it is plentiful. They deny the evidence of their emaciated bodies (body dysmorphia) and remain highly motivated. In fact, they become hyperactive, restless and seem to be full of energy.
These people would have been ideal people to have around. Survivors that could help motivate others in the migration needed to find new food supplies.
Dysmorphia and denial
Having individuals that remained optimistic and highly motivated despite appalling weight loss would confer an advantage on the whole group. Again this is not new. Lasegue (1873) reported the ‘inexhaustible optimism’ of anorexics. This could be due to the release of opiates resulting in euphoria. The body dysmorphia and refusal to accept severe illness appears to be a cultural constant and common amongst all anorexics past and present, suggesting a biological/genetic underpinning.
Hyperactivity
DSM IV dropped this from their primary symptoms of anorexia, making it secondary to weight loss below 85% of normal body weight. Many suggest this was a mistake. Kron et al (1987) point out that although it may not be an ever-present symptom in all anorexics, it is always present at some point. Guisinger likens it to a kind of migratory restlessness. Many species experience bouts of extreme restlessness prior to migration. It is best reported in the zugunrhue of birds.
Note: this is not mentioned on the AQA specification
A new idea for most of you I guess, but if like the biological model, we assume a possible genetic predisposition or causation we also need to consider the biological merit of that disorder. Otherwise why would seemingly maladaptive behaviours such as anorexia remain within the gene pool? Surely they would have been selected against. We shall consider two possibilities, but with a distinct emphasis on the former and more convincing:
1. The Adapted to Flee (famine) Hypothesis (Guisinger 2003)
Shan Guisinger’s AFFH seems to have gained much greater recognition in the past few years. Whilst treating anorexic girls Guisinger noticed two modal ages around which time girls seemed most susceptible to developing anorexia. The first of these was around the age of fourteen, the other around eighteen. What she found particularly curious about the fourteen year olds was that few of them reported being on a diet or having any desire to lose weight. Despite this, they were losing weight and showing many other of the signs of anorexia such as hyperactivity and body dysmorphia, whilst denying that there was a problem.
Girls at this age are, apparently, at their leanest. They tend to have a lower BMI than at any other age in their life. She hypothesised that dropping below a certain body weight, or body fat content may trigger the disorder. This would be like crossing a biological threshold. Above it and the person remains anorexia-free, below it and the body switches to anorexic mode. Typically, a period of stress or illness, or perhaps developing an interest in sport may then tip the already lean teenager below this threshold.
It’s important to emphasise that for Guisinger, anorexia is not a choice, it is not a reaction to family tensions nor is it a desperate attempt to get attention or exert control over parents. It is very much a biological response caused by body weight falling below a set point. The other danger age is around eighteen. Guisinger believes at this age, dieting or exercise is most likely to cause the initial loss in weight that triggers anorexia.
The evolutionary aspect
If Guisinger is right, and some people have a biological mechanism that triggers starvation, the obvious question is why has it evolved? At first glance it would be counter-productive from an adaptive standpoint. Behaviours that result in death or reduce reproductive chances tend not to be favoured by natural selection!
Guisinger thought back to our distant evolutionary past and considered the conditions of the early humans in Africa. Droughts and famines would have been frequent. We know that early hominids had to migrate thousands of miles to find food. Guisinger believes that if she is correct then the following should all be identifiable:
- The core symptoms are adaptive
- Anorexia should be in evidence throughout human history
- Food refusal should be present in other species following times of famine or following a drop in body weight
1. Adaptive
Think what we’re like when we’re hungry. Our mood drops, we become lethargic (presumably to save calories), we lack motivation and we become obsessed with thoughts of food. In times of severe drought/famine these behaviours would be counter-productive. Lethargy would not help us find food.
Anorexics on the other hand are unfazed by hunger. They ignore food even when it is plentiful. They deny the evidence of their emaciated bodies (body dysmorphia) and remain highly motivated. In fact, they become hyperactive, restless and seem to be full of energy.
These people would have been ideal people to have around. Survivors that could help motivate others in the migration needed to find new food supplies.
Dysmorphia and denial
Having individuals that remained optimistic and highly motivated despite appalling weight loss would confer an advantage on the whole group. Again this is not new. Lasegue (1873) reported the ‘inexhaustible optimism’ of anorexics. This could be due to the release of opiates resulting in euphoria. The body dysmorphia and refusal to accept severe illness appears to be a cultural constant and common amongst all anorexics past and present, suggesting a biological/genetic underpinning.
Hyperactivity
DSM IV dropped this from their primary symptoms of anorexia, making it secondary to weight loss below 85% of normal body weight. Many suggest this was a mistake. Kron et al (1987) point out that although it may not be an ever-present symptom in all anorexics, it is always present at some point. Guisinger likens it to a kind of migratory restlessness. Many species experience bouts of extreme restlessness prior to migration. It is best reported in the zugunrhue of birds.
|
2. Evidence from history
We have already seen that Lasegue was recording cases of anorexia in the nineteenth century but there are many reported cases long before this. In the fifteenth century 85 women were canonised by the Roman Catholic church for their piousness and ability to, miraculously, live on so little food. Right: Eva Vliegen (actually a Protestant rather than Catholic) Born in 1575 in what would be modern day Netherlands. In her teens she began to refuse food and in her early 20s began what she claimed would be a 34 year fast. It was believed that she could live on the fragrance of flowers. Today Eva would be seen as anorexic. At the time her behaviour was seen as miraculous. |
|
3. Presence in other species
It isn’t only humans that have had to endure starvation. We would therefore expect to see similar patterns of behaviour in other species. Bell (1985) reported refusal of food in some lab rats following a period of starvation. Yet again we have the scenario were a period of hunger results in the animal not eating when food becomes available.
Many species reduce their eating or stop altogether during migration.
Some species of domestic pig, bred for their lean meat provide a very good model for Guisinger’s theory. Bred to be low in fat they are similar to Guisinger’s fourteen year old girls. 6% of these pigs go on to develop ‘wasting pig syndrome.’ The main symptom, as the name suggests being extreme weight loss but also restlessness. According to farmers the trigger for the disorder seems to be a period of stress caused by separation or bullying from other pigs. This results in additional weight loss that then triggers the cessation in eating.
It isn’t only humans that have had to endure starvation. We would therefore expect to see similar patterns of behaviour in other species. Bell (1985) reported refusal of food in some lab rats following a period of starvation. Yet again we have the scenario were a period of hunger results in the animal not eating when food becomes available.
Many species reduce their eating or stop altogether during migration.
Some species of domestic pig, bred for their lean meat provide a very good model for Guisinger’s theory. Bred to be low in fat they are similar to Guisinger’s fourteen year old girls. 6% of these pigs go on to develop ‘wasting pig syndrome.’ The main symptom, as the name suggests being extreme weight loss but also restlessness. According to farmers the trigger for the disorder seems to be a period of stress caused by separation or bullying from other pigs. This results in additional weight loss that then triggers the cessation in eating.
Psychological explanations
Family System’s Theory: 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:
Ineffective parenting
As was popular with early psychological theory, this branch of psychodynamic theory places the blame on the family and in particular, long suffering mum!
Hilde Bruch believed that disturbed mother-child interactions led to ego deficiencies in the child resulting in a lack of autonomy and self-control. According to Bruch, effective parents attend to their children’s needs attentively. When the child cries they are able to distinguish between its cries of hunger and its cries for attention.
Ineffective parents on the other hand, misread the cues. They feed the child when it’s anxious and comfort the child when it’s hungry. As a result the child grows up feeling confused about its own internal needs and unable to recognise its own emotions. This confusion and uncertainty leads to the child being over-reliant on its parents and a failure to develop self-reliance and autonomy. Think back to Jahoda’s Deviation from Ideal Mental Health at AS.
On reaching adolescence, when usually they would be expected to develop greater independence, they feel restrained, fearful and helpless. This, again according to Bruch, results in a perceived lack of control over their body, resulting in restricted eating; the one thing they feel that they can control.
Evidence
Bruch herself interviewed the mothers of 51 anorexic girls. Most reported anticipating their children’s needs rather than allowing them to act for themselves. The mothers of bulimics often reported mistaking low mood for hunger and the need to eat.
Minuchin et al (1978) reported four characteristics often present in the families of anorexics:
Family System’s Theory: 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:
Ineffective parenting
As was popular with early psychological theory, this branch of psychodynamic theory places the blame on the family and in particular, long suffering mum!
Hilde Bruch believed that disturbed mother-child interactions led to ego deficiencies in the child resulting in a lack of autonomy and self-control. According to Bruch, effective parents attend to their children’s needs attentively. When the child cries they are able to distinguish between its cries of hunger and its cries for attention.
Ineffective parents on the other hand, misread the cues. They feed the child when it’s anxious and comfort the child when it’s hungry. As a result the child grows up feeling confused about its own internal needs and unable to recognise its own emotions. This confusion and uncertainty leads to the child being over-reliant on its parents and a failure to develop self-reliance and autonomy. Think back to Jahoda’s Deviation from Ideal Mental Health at AS.
On reaching adolescence, when usually they would be expected to develop greater independence, they feel restrained, fearful and helpless. This, again according to Bruch, results in a perceived lack of control over their body, resulting in restricted eating; the one thing they feel that they can control.
Evidence
Bruch herself interviewed the mothers of 51 anorexic girls. Most reported anticipating their children’s needs rather than allowing them to act for themselves. The mothers of bulimics often reported mistaking low mood for hunger and the need to eat.
Minuchin et al (1978) reported four characteristics often present in the families of anorexics:
- Enmeshment: described as a transactional style, with lots of family involvement in each other’s affairs. These families tended to lack privacy and there was a blurring of the boundaries between family and self. They would often speak on one another’s behalf.
- Over-protection: parents are over-nurturing and allow child far too little freedom and independence.
- Rigidity: the family strives to retain the status quo and avoids change of any sort (Daily Mail reader alert!). This can create numerous issues in the teenage years when the child expects more independence (Blinder et al 1988)
- Avoidance of conflict and lack of conflict resolution. This results in a build-up of unresolved conflict. Classic psychodynamic territory.
1. Enmeshment
There has long been a perceived association between anorexia and family dynamics. Gull in the 19th century suggested that anorexic girls should be removed from the family unit for their own protection. Similar ideas were applied to conditions such as autism and schizophrenia with the psychopathogenic mother seen as being particularly to blame.
As far as anorexia is concerned there is obvious face validity here. Anorexics tend to be young teenagers. Young teenagers tend to be within a family setting. However, to what extent does this relationship really exist, and if it does exist, is it causal? That is, to what extent are the families of anorexics merely reacting to the extreme behaviour of the child?
According to enmeshment, the family spends too much time together and interfere too much in one another’s lives. There is a blurring of self-identity with everyone being so inter-connected. The teenage girl struggles to assert her own identity and especially her independence from her mother. She soon realises that given the intrusive nature of the family dynamics that it will not be possible and exerts her self identity by not eating.
The research
There has been lots of research into the family dynamics of anorexic children but with very different findings.
In a review of the literature, Yager found contradictory results. Anecdotal studies describing the mothers of anorexics as rejecting, but sometimes over-bearing. However, according to his research there were some general traits:
Evidence
Minuchin looked at 45 families, 11 of which contained an anorexic child. Each was rated on the four characteristics above. They found the more dysfunctional the family the higher they tended to score with anorexic families scoring the highest of all.
However, the researchers did not report the operationalisation of the traits making this study impossible to scientifically verify.
Conflicting evidence
Sonne et al (1981) compared anorexic girls with groups of emotionally disturbed inpatients and outpatients at a local clinic. They found that the anorexics tended to be the least enmeshed, with very little parental intrusion. What they did find was that the girls tended to be very controlling towards their parents, compared to the other groups.
However, the study did support Minuchin’s views on conflict avoidance, particularly in the mother-daughter relationship.
However, the groups were small, eleven anorexics, making it difficult to generalise, particularly given the big individual differences found in families.
Although this study is seen as being more scientific, with better operationalization of the characteristics, Sonne believes that her operationalization of enmeshment differed from that of Minuchin. In other words, they were probably not measuring the same thing!
Over-protection
This is obsessive nurturing within the family in an attempt to protect it from external threats. Mothers may devote themselves almost sacrificially to protecting their daughter.
Rigidity
The family lacks flexibility and has very set ways of dealing with issues. This is fine until there is a change in circumstances within the family and it is unable to adapt and respond. Relating this to the daughter: if she seeks greater independence the mother refuses to allow this and does all in her power to prevent it.
Conflict avoidance
There is no discussion of crucial issues, fearing that disagreements, arguments and conflict may be the result. As a result serious issues are never resolved but instead are allowed to simmer and build up.
According to Minuchin all three of the above feed into Hilde Bruch’s concept of autonomy and control:
Autonomy and Control
According to Bruch, the mother is over-bearing and protective. She won’t allow the daughter the independence she needs and this causes confusion resulting in:
Body dysmorphia
Inability to identify internal states such as hunger
A feeling of loss of control
Outcome
The daughter takes control of the one thing still available to her: eating. She notices the effect this has on her parents as the weight loss starts to become visible and realises that she can regain control through restricting her diet.
Evaluation
A Portuguese study found no evidence for enmeshment and rigidity in anorexic patients. However, unlike most studies that have used observational techniques, this one assessed enmeshment and rigidity using self-report techniques. Given the nature of the traits being assessed this may not be the most valid measure since people are not likely to be entirely truthful.
This study also highlights a more serious issue with psychodynamic theories and measuring hypothetical constructs such as enmeshment. They are not easily to operationalise and pin down. As a result objective measures are almost impossible. Different researchers, using different techniques are going to come to different conclusions.
Practical Applications
Treatments based on FST have had some success in treating anorexia. It has been used to encourage greater cooperation within families and to encourage anorexics to seek out more interactions with people outside the family unit. Robin et al (1995) used the techniques on eleven anorexics for a period of 16 months. After that time six were reportedly recovered. A year later, a further three had recovered. However, this study was not blind. Those assessing recovery were aware of the patients who had been receiving the treatment. This introduces possible bias and reduces internal validity.
There has long been a perceived association between anorexia and family dynamics. Gull in the 19th century suggested that anorexic girls should be removed from the family unit for their own protection. Similar ideas were applied to conditions such as autism and schizophrenia with the psychopathogenic mother seen as being particularly to blame.
As far as anorexia is concerned there is obvious face validity here. Anorexics tend to be young teenagers. Young teenagers tend to be within a family setting. However, to what extent does this relationship really exist, and if it does exist, is it causal? That is, to what extent are the families of anorexics merely reacting to the extreme behaviour of the child?
According to enmeshment, the family spends too much time together and interfere too much in one another’s lives. There is a blurring of self-identity with everyone being so inter-connected. The teenage girl struggles to assert her own identity and especially her independence from her mother. She soon realises that given the intrusive nature of the family dynamics that it will not be possible and exerts her self identity by not eating.
The research
There has been lots of research into the family dynamics of anorexic children but with very different findings.
In a review of the literature, Yager found contradictory results. Anecdotal studies describing the mothers of anorexics as rejecting, but sometimes over-bearing. However, according to his research there were some general traits:
- Mums tended to focus too much attention on the child.
- They tended to have very high expectations and foster ambition.
- They tended to have a lack of intimate friends, meaning that often the child (usually daughter) was their main confidante. This created issues with separation later in adolescence.
Evidence
Minuchin looked at 45 families, 11 of which contained an anorexic child. Each was rated on the four characteristics above. They found the more dysfunctional the family the higher they tended to score with anorexic families scoring the highest of all.
However, the researchers did not report the operationalisation of the traits making this study impossible to scientifically verify.
Conflicting evidence
Sonne et al (1981) compared anorexic girls with groups of emotionally disturbed inpatients and outpatients at a local clinic. They found that the anorexics tended to be the least enmeshed, with very little parental intrusion. What they did find was that the girls tended to be very controlling towards their parents, compared to the other groups.
However, the study did support Minuchin’s views on conflict avoidance, particularly in the mother-daughter relationship.
However, the groups were small, eleven anorexics, making it difficult to generalise, particularly given the big individual differences found in families.
Although this study is seen as being more scientific, with better operationalization of the characteristics, Sonne believes that her operationalization of enmeshment differed from that of Minuchin. In other words, they were probably not measuring the same thing!
Over-protection
This is obsessive nurturing within the family in an attempt to protect it from external threats. Mothers may devote themselves almost sacrificially to protecting their daughter.
Rigidity
The family lacks flexibility and has very set ways of dealing with issues. This is fine until there is a change in circumstances within the family and it is unable to adapt and respond. Relating this to the daughter: if she seeks greater independence the mother refuses to allow this and does all in her power to prevent it.
Conflict avoidance
There is no discussion of crucial issues, fearing that disagreements, arguments and conflict may be the result. As a result serious issues are never resolved but instead are allowed to simmer and build up.
According to Minuchin all three of the above feed into Hilde Bruch’s concept of autonomy and control:
Autonomy and Control
According to Bruch, the mother is over-bearing and protective. She won’t allow the daughter the independence she needs and this causes confusion resulting in:
Body dysmorphia
Inability to identify internal states such as hunger
A feeling of loss of control
Outcome
The daughter takes control of the one thing still available to her: eating. She notices the effect this has on her parents as the weight loss starts to become visible and realises that she can regain control through restricting her diet.
Evaluation
A Portuguese study found no evidence for enmeshment and rigidity in anorexic patients. However, unlike most studies that have used observational techniques, this one assessed enmeshment and rigidity using self-report techniques. Given the nature of the traits being assessed this may not be the most valid measure since people are not likely to be entirely truthful.
This study also highlights a more serious issue with psychodynamic theories and measuring hypothetical constructs such as enmeshment. They are not easily to operationalise and pin down. As a result objective measures are almost impossible. Different researchers, using different techniques are going to come to different conclusions.
Practical Applications
Treatments based on FST have had some success in treating anorexia. It has been used to encourage greater cooperation within families and to encourage anorexics to seek out more interactions with people outside the family unit. Robin et al (1995) used the techniques on eleven anorexics for a period of 16 months. After that time six were reportedly recovered. A year later, a further three had recovered. However, this study was not blind. Those assessing recovery were aware of the patients who had been receiving the treatment. This introduces possible bias and reduces internal validity.
Social Learning Theory and Media
The approach is based on the portrayal of women in the media, particularly over the past forty years. In this time, the ideal shape has shifted from the rounded size 12/14 of the fifties and sixties, as exemplified by Jane Mansfield and Marilyn Monroe, to the emaciated, twig like form of today, for example Kate Moss and Posh. 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 slimmer’s disease.
The approach is based on the portrayal of women in the media, particularly over the past forty years. In this time, the ideal shape has shifted from the rounded size 12/14 of the fifties and sixties, as exemplified by Jane Mansfield and Marilyn Monroe, to the emaciated, twig like form of today, for example Kate Moss and Posh. 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 slimmer’s disease.
Modelling
A model is an iconic figure that provides a template for the behaviour of others. Models are particularly powerful if they are successful. The media portrayal of women and in particular their idea of ideal body shape has reset social norms and ideals. Size zero has become the acceptable and desirable norm in the eyes of many younger women.
Identification
As we saw in Approaches, identification is a powerful concept. If the model is the same gender, age, race or if they’re seen as glamorous and successful or has possessing traits that a young person desires in themselves they are far more likely to be imitated.
Vicarious Reinforcement
The hidden power behind SLT. Seeing a person being reinforced for their behaviour acts as a powerful reinforcer for the observer too. Thinness is reinforced by success in the music charts, sport, dancing. Those seen as slim get to marry footballers and actors (WAGS) making it far more likely that this characteristic (thin) will be imitated.
Evidence for the effects of media
Becker (1999) carried out a natural experiment as television was introduced to the island of Fiji in 1995. Three years after the introduction 65 girls were questioned about their attitude to eating and about their viewing habits. They had clearly been influenced by American TV programmes such as Friends, wanting to look like their television heroes. There was also a significant increase in girls reporting purging as a way to control weight. Rate of purging was positively correlated with hours watched. It’s worth mentioning that the affect is not just by direct observation of the programmes. In the days after watching programmes people would discuss what they’d seen and make the vicarious reinforcement more effective.
A model is an iconic figure that provides a template for the behaviour of others. Models are particularly powerful if they are successful. The media portrayal of women and in particular their idea of ideal body shape has reset social norms and ideals. Size zero has become the acceptable and desirable norm in the eyes of many younger women.
Identification
As we saw in Approaches, identification is a powerful concept. If the model is the same gender, age, race or if they’re seen as glamorous and successful or has possessing traits that a young person desires in themselves they are far more likely to be imitated.
Vicarious Reinforcement
The hidden power behind SLT. Seeing a person being reinforced for their behaviour acts as a powerful reinforcer for the observer too. Thinness is reinforced by success in the music charts, sport, dancing. Those seen as slim get to marry footballers and actors (WAGS) making it far more likely that this characteristic (thin) will be imitated.
Evidence for the effects of media
Becker (1999) carried out a natural experiment as television was introduced to the island of Fiji in 1995. Three years after the introduction 65 girls were questioned about their attitude to eating and about their viewing habits. They had clearly been influenced by American TV programmes such as Friends, wanting to look like their television heroes. There was also a significant increase in girls reporting purging as a way to control weight. Rate of purging was positively correlated with hours watched. It’s worth mentioning that the affect is not just by direct observation of the programmes. In the days after watching programmes people would discuss what they’d seen and make the vicarious reinforcement more effective.
|
Who’s a Barbie Girl?
Dittmar et (2006) studied 162 British girls aged between 5 and 8 years. The girls were exposed to either Barbie, a normal-shaped doll or to flowers and clothes etc. in series of storybooks. The DV, body esteem, was assessed by questionnaire and by the girls indicating their actual and ideal body shape using silhouettes. Those who had been expose to Barbie had significantly lower body esteem. The researchers believed that Barbie is a powerful role model because of her success and affluence. |
|
Cultures
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:
Findings. 12% of the London group developed an eating disorder during their course. None of the Cairo group did!
There has been a recent increase in reported incidence of anorexia in Japan. Again this has been attributed to changing portrayal of women by the media. Girls who regularly read magazines promoting thinness were most at risk.
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.
Other factors
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.
It seems that anorexics are more prone to media pressure. Hamilton and Waller (1993) showed photographs of ideal female bodies to a group of anorexics and a control group of no-anorexics. The control group were not affected however the anorexics subsequently over-estimated their own body size and weight even more after seeing the images. Cleary there is an issue her of cause and effect.
Nathanson (2000) writing for the BMA claimed that the media portrayal (and ‘obsession’ as she called it) with ‘stick thin women’ was related to increased incidence of anorexia in young British girls. She admitted that the causes of anorexia were many and varied and that many of the factors could not be controlled. However, media portrayal could be changed and this led to the Body Image Summit report that recommended magazines stopped using very thin models.
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!
There has been a recent increase in reported incidence of anorexia in Japan. Again this has been attributed to changing portrayal of women by the media. Girls who regularly read magazines promoting thinness were most at risk.
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.
Other factors
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.
It seems that anorexics are more prone to media pressure. Hamilton and Waller (1993) showed photographs of ideal female bodies to a group of anorexics and a control group of no-anorexics. The control group were not affected however the anorexics subsequently over-estimated their own body size and weight even more after seeing the images. Cleary there is an issue her of cause and effect.
Nathanson (2000) writing for the BMA claimed that the media portrayal (and ‘obsession’ as she called it) with ‘stick thin women’ was related to increased incidence of anorexia in young British girls. She admitted that the causes of anorexia were many and varied and that many of the factors could not be controlled. However, media portrayal could be changed and this led to the Body Image Summit report that recommended magazines stopped using very thin models.
Evaluation
Anorexia is a rare success story for the behaviourists. Their model can explain some of the patterns that we see:
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.
Interestingly, why do some blind women who have no access to these images sometimes develop eating disorders? There have been a number of cases reported.
When using the behaviourist model to explain any behaviour it is useful to adopt Mowrer’s Two Stage Approach. This explains how a given 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.
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!
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.
Interestingly, why do some blind women who have no access to these images sometimes develop eating disorders? There have been a number of cases reported.
When using the behaviourist model to explain any behaviour it is useful to adopt Mowrer’s Two Stage Approach. This explains how a given 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.
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!
|
Cognitive explanation
Distorted thinking Murphy et al (2010) suggest that all the symptoms of anorexia occur because of various cognitive distortions such as body dysmorphia, for example preoccupations with food, eating and weight and restrained eating. An overestimation of body weight and size does seem to be a common feature of anorexia nervosa. |
|
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.
Mackenzie et al (1993) asked patients with eating disorders about their actual and ideal weight and size and compared their responses with a control group. The anorexics tended to believe they were much larger and heavier than similar-sized controls and also believe that their ideal size should be much smaller than both. They were then given a chocolate bar and soft drink. Afterwards the perceptions of the control group had not altered but the anorexics estimated an increase in both size and weight.
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?
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.' This seems to suggest a possible causal role of the distortions as they still continue in the absence of the disorder.
Irrational Beliefs
Aaron T Beck outlined a number of irrational beliefs present in a range of psychological disorders such as awfulizing, catasphrophising and mustabation (I Kid you not!).
One of these relevant to anorexia is ‘all or nothing.’ Applying to anorexia… ‘If I’m not thin I’m fat/’ Essentially they see no shades of grey. Another is perfectionist personality:
Perfectionist personality
Many anorexics tend to be perfectionist; high achievers when it comes to sport, education, music, dance…
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.
Biological support
Sachdev et al (2008) carried out brain scans on anorexics and a control group of non-anorexics, while they watched images of either their own body or others.
When shown images of others there was no difference in levels of brain activity in areas known to be responsible for attention. However, when shown their own images anorexics showed far less activation than non-anorexics. This suggest that distortions only apply to their own body and not to the bodies of others.
Ethics
The cognitive model does however, raise ethical issues as it suggests that faulty thinking is responsible. Since we like to think we have some conscious control over our thoughts this could be seen as placing the blame on the individuals.
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.
The role of neural mechanisms in eating behaviour
The Board don't give us much to go on here:
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 too far from the norm there are noticeable behavioural changes within minutes and if no action is taken to address the issue coma can result.
The Board don't give us much to go on here:
- The role of neural mechanisms involved in controlling eating and satiation
- Evolutionary explanations of food preferences
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 too 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.
Note: 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
It is worth mentioning in an essay that most of us have a relatively stable body weight. To maintain this long term by diet alone it is estimated that we would need to vary our daily intake by no more than about ten calories from day to day. Clearly this does not happen which suggests biological mechanisms do the job instead!
The dual hypothalamic theory 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 in 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 of the body that were important. This would explain the hunger felt by diabetics. Although their 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 affect their eating behaviour, running counter to the research of others.
Lipostatic Hypothesis
Key elements: It involves fat levels, the ventromedial hypothalamus (VMH) and acts to make us feel sated (full). 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.
The role of leptin
Fat cells (adipose) produce a chemical called leptin (from the Greek leptos meaning thin). As fat levels increase so does the production of leptin that circulates in the blood and enters the brain. The VMH is particularly sensitive to circulating levels of leptin. As levels increase, appetite is suppressed and eating behavior ceases.
Research has shown that rats bred to be obese have a higher threshold in their sensitivity to leptin. That means fat levels need to be higher before hunger is switched off and eating ceases. This appears to be due to an issue with leptin receptors in the VMH. Crucially this seems to pre-date the development of obesity suggesting a causal relationship: the faulty receptors causing obesity rather than the other way around.
In addition, as we saw in diets, high levels of leptin in obese people leads to the brain becoming less sensitive so less likely to respond to rising fat levels and less likely to reduce appetite and eating.
Finally on leptin. Some rats are genetically predisposed to obesity (obesity prone) whereas others are obesity resistant. The offspring of obesity resistant parents are unlikely to become obese. With obesity prone rats the situation is more complex. If the mother is herself obese around the time of birth her offspring will almost certainly develop obesity. A slim mum with the gene will generally produce lean offspring. We therefore have an interaction between genes and perinatal environment needed to produce obesity. (Irani 2008).
Ghrelin
Produced in the stomach, levels of ghrelin increase as time since last eating increases. The arcuate nucleus of the hypothalamus detects the increase and at a certain point sends signals to the lateral hypothalamus which releases NPY and triggers hunger and eating behavior. The levels of ghrelin double in the build up to a meal but drop very quickly after eating.
Other hormones involved in eating behavior: Cholecystokinin
CCK is secreted by the duodenum (part of small intestine) following a meal. This stimulates receptors in the gastric-vagus nerve and messages are sent to the hypothalamus. When sufficient stimulation is received from the nerve the hypothalamus secretes anorexigenic peptides that stop eating. CCK injected directly into the brain is a powerful appetite suppressant.
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 (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.
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.
Obesity
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 biological and psychological explanations of obesity and considers the reasons why diets generally fail.
www.disclose.tv/action/viewvideo/152728/Why_Are_Thin_People_Not_Fat_Documentary/
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 biological and psychological explanations of obesity and considers the reasons why diets generally fail.
www.disclose.tv/action/viewvideo/152728/Why_Are_Thin_People_Not_Fat_Documentary/
Biological Explanations of Obesity
Genetic
Clearly there is a tendency for obesity to run in families. However, as you all know, as seasoned psychologists, that does not prove genetic causation. With obesity more than any other disorder it is easy to see why obese parents may have obese offspring. What a child eats is largely determined by what their parents eat. An unhealthy diet will therefore be common to both parents and their offspring.
Chaput et al (2014) reported that the concordance rate for obesity, for first degree relatives is between 20 and 50%. (First degree relatives being those with whom you share 50% of your genes: parents and siblings). This is described as a moderate concordance rate and could easily be explained by either genetic or environmental factors, or more likely than not a combination of both.
Twin studies
Nan et al (2012) studied 8000 MZ and 10,000 DZ twins and reported a concordance rate of between 61 and 80%, but the differences between MZ and DZ were not specified!
There is very obvious AO3 here:
- Shared environments
- MZ being treated more similarly than DZ
- A tendency for twin studies to over-estimate the genetic component.
See Appendix 1: how to get AO3 marks from twin studies
Polygenetic determination
If there was one single gene responsible for the ‘obesity pandemic’ scientists would have discovered it long ago. Clearly the genetic causes of obesity are complex and involve hundreds of genes.
Locke et al (2015) in a study of the genomes of 300,000 people, identified 97 possible genes that relate to BMI alone. This is just one measure of obesity. It is thought that those 97 genes only account for 3% of the genetic variation in BMI. Potentially there are thousands involved in obesity in general.
Neurochemical influences
Serotonin
There should be no surprises here. We saw earlier that the VMH triggers eating behavior. It is serotonin that closes down activity in the VMH when we’ve eaten enough.
There is a plethora of research that suggests some obese patients have lower than normal levels of serotonin. This would presumably make them less effective at switching off VMH activity and triggering the cessation of eating.
These low levels could be inherited or they could be associated with other disorders such as depression. Other causes may be periods of stress or low mood. We know that periods of stress and low mood can trigger comfort eating, especially of foods rich in carbohydrates. When we looked at anorexia, we saw that carbohydrate intake does increase levels of serotonin so there’s an obvious link there.
Dopamine
Dopamine operates in various pathways of the brain involved in the reward system. Locations include mesolimbic system (MLS), hippocampus and amygdala. Dopamine triggers the pleasure we feel when we engage in any enjoyable activity and that includes eating.
As humans we are aware of our mortality. We know that without food we will die. Animals are not so aware. Remove the ability to feel pleasure from rats and they will stop eating and starve to death!
Some forms of obesity are associated with a damaged dopamine system. The most likely fault is too few dopamine receptors making the brain (especially an area called the striatum) less sensitive to the effects of dopamine. Over-eating may therefore be an attempt to compensate for this lack of dopamine activity and pleasure from food. Eating more than usual will release more dopamine and provide normal levels of pleasure. This is thought to occur in addiction.
The DRD2 gene that encodes for D2 dopamine receptors has been most implicated in obesity (and in addiction).
Ritchie and Noble (2003) scanned the brains of people who had inherited the DRD2 variant. Typically they had up to 40% fewer D2 receptors. It is likely that these people would experience less pleasure from eating and other activities that people generally find pleasurable.
Why diets fail
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. At some time in their lifetime 90% of women in the UK we attempt to lose weight by reducing calorific intake.
Restraint Theory (Herman & Polivy 1975)
The idea that dietary restraint (cutting our calorific intake) eventually leads to an increase in the number of calories consumed and a subsequent weight gain. According to this theory, diets are counter-productive.
By attempting to cognitively control our food intake, rather than rely on biological systems, we label foods good, bad, forbidden. This results in a preoccupation with food and an eventual giving in to the inevitable hunger we face.
Disinhibition
This can be triggered by restraint. Inhibitions relating to food, for example ones that normally limit the amount we sit fit to eat become ignored and we eat as much as we want.
Disinhibitors are usually external factors such as stress, smells, behavior of those around us that in turn may affect our mood or self-esteem. They encourage us to eat and the whole process is then exacerbated by the ‘all or nothing’ effect in which we eat til full.
Obesity results from a combination of restraint and disinhibition.
Boundary theory
An attempt to explain restraint and disinhibition:
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. At some time in their lifetime 90% of women in the UK we attempt to lose weight by reducing calorific intake.
Restraint Theory (Herman & Polivy 1975)
The idea that dietary restraint (cutting our calorific intake) eventually leads to an increase in the number of calories consumed and a subsequent weight gain. According to this theory, diets are counter-productive.
By attempting to cognitively control our food intake, rather than rely on biological systems, we label foods good, bad, forbidden. This results in a preoccupation with food and an eventual giving in to the inevitable hunger we face.
Disinhibition
This can be triggered by restraint. Inhibitions relating to food, for example ones that normally limit the amount we sit fit to eat become ignored and we eat as much as we want.
Disinhibitors are usually external factors such as stress, smells, behavior of those around us that in turn may affect our mood or self-esteem. They encourage us to eat and the whole process is then exacerbated by the ‘all or nothing’ effect in which we eat til full.
Obesity results from a combination of restraint and disinhibition.
Boundary theory
An attempt to explain restraint and disinhibition:
|
Herman & Polivey (1984) believe that the physiological states of hunger and satiety (satisfied) set the lower and upper limits of the amount we eat. Below the lower limit we feel hungry and above the upper limit we feel bloated. This is the boundary model.
Between this lower and upper limit is the zone of biological indifference. Psychological factors determine the precise amount of food we eat in this zone. According to the model, dieters set a lower level for hunger (meaning it takes longer between meals for them to feel hungry) and set a higher level for satiety (meaning they can eat more before they feel full). In addition, dieters set a self-imposed DESIRED intake somewhere between the lower and upper boundary. This is their target intake amount. Once this is exceeded they continue to eat until they reach their upper satiety limit. |
Pre-load taste tests
A common measure used to determine how 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.
Ogden (2003) is a good example:
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.
However, pre-load tests like this are low in external (ecological) validity since they are such artificial tasks and laboratory based.
Media and disinhibition
Boyce & Kuijer (2014) compared restrained and unrestrained eaters.
They are then invited to take part in a taste test (favourite ploy) and given four bowls of unhealthy snack foods to eat. Again their grading of these items is ignored. The researchers just observe to see how much they eat.
Restrained eaters consumed significantly more after seeing the thin models. Both groups consumed similar amounts following neutral images.
Conclusion: media portrayal of thin models has a disinhibiting effect on dieters.
Evaluation of restraint theory
The overwhelming majority of low calorie, weight loss diets do ultimately fail, as this theory would predict. Wardle and Beale (1988) went further and found that restraint causes over-eating. 27 obese women were placed in one of three groups and tested at regular intervals for seven weeks:
They were checked for calorie intake during weeks four and six. It was 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.
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.
However, the model struggles to explain why some people are successful! If restricting eating always leads to eating more how can anorexics manage to lose so much weight? (Ogden 1994).
Restraint and success?
It’s not all negative. Sauvage et al (2009) carried out a longitudinal study of 163 women on a diet. Their progress was checked every two years for six years. Those showing the highest level of restraint were the ones who had lost the most weight.
These findings could possibly be explained by considering the different types of restraint.
Rigid restraint: all or nothing restraint usually results in disinhibition and weight gain
Flexible restraint: allows some consumption of forbidden fruits and tends to be associated with more successful dieting.
Psychological 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.
Adriaanse et al (2011) studied women attempting to curb their snacking behavior. They were presented with diet intentions in a negative form, for example ‘When I am sad I will not think of chocolate.’
Clearly thinking in these terms simply reinforces the association between ‘low mood’ and ‘chocolate’ via classical conditioning.
They found that such statements had an ironic rebound effect and increased the consumption of chocolate. The effect was therefore not only cognitive (thinking) but behavioural (eating chocolate).
However, according to Wegner himself, laboratory procedures like this seem to exaggerate the effect of ironic process. In real life it isn’t as noticeable.
Spiral Model (A model proposed by Heatherton & Polivy)
Body dissatisfaction resulting from media pressure lowers self-esteem and triggers dieting behavior.
Diet Hard 1:
Diet Hard 2: Diet Harder
Diet Hard 3: Diet Hard with a Vengeance…
Dieting is attempting to work against millions of years of adaptive evolution that has designed a body intent on remaining a certain weight, regardless of how big it is. Hunger, caused by dieting increases secretion of ghrelin, decreases levels of leptin and both trigger eating behavior.
Practical applications of the model
Basically the vicious cycle needs to be broken. Not experiencing weight gain will help preserve self-esteem and prevent disinhibition.
The conclusion is that restrained eating in the form of calorie controlled diets is best saved for weight maintenance than weight loss. There is no need for the body to deploy counter-measures to preserve body weight if weight is constant.
Finally on a more depressing note: Yagar et al (1988) believes constant disinhibition and repeated failure of diets can lead to substance abuse in an attempt to increase happiness.
A common measure used to determine how 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.
Ogden (2003) is a good example:
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.
However, pre-load tests like this are low in external (ecological) validity since they are such artificial tasks and laboratory based.
Media and disinhibition
Boyce & Kuijer (2014) compared restrained and unrestrained eaters.
- Some were shown images of thin models (advertising beauty products)
- Some were shown neutral images (furniture etc)
They are then invited to take part in a taste test (favourite ploy) and given four bowls of unhealthy snack foods to eat. Again their grading of these items is ignored. The researchers just observe to see how much they eat.
Restrained eaters consumed significantly more after seeing the thin models. Both groups consumed similar amounts following neutral images.
Conclusion: media portrayal of thin models has a disinhibiting effect on dieters.
Evaluation of restraint theory
The overwhelming majority of low calorie, weight loss diets do ultimately fail, as this theory would predict. Wardle and Beale (1988) went further and found that restraint causes over-eating. 27 obese women were placed in one of three groups and tested at regular intervals for seven weeks:
- Diet (restraint)
- Exercise (no restraint)
- Control (neither restraint nor exercise)
They were checked for calorie intake during weeks four and six. It was 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.
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.
However, the model struggles to explain why some people are successful! If restricting eating always leads to eating more how can anorexics manage to lose so much weight? (Ogden 1994).
Restraint and success?
It’s not all negative. Sauvage et al (2009) carried out a longitudinal study of 163 women on a diet. Their progress was checked every two years for six years. Those showing the highest level of restraint were the ones who had lost the most weight.
These findings could possibly be explained by considering the different types of restraint.
Rigid restraint: all or nothing restraint usually results in disinhibition and weight gain
Flexible restraint: allows some consumption of forbidden fruits and tends to be associated with more successful dieting.
Psychological 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.
Adriaanse et al (2011) studied women attempting to curb their snacking behavior. They were presented with diet intentions in a negative form, for example ‘When I am sad I will not think of chocolate.’
Clearly thinking in these terms simply reinforces the association between ‘low mood’ and ‘chocolate’ via classical conditioning.
They found that such statements had an ironic rebound effect and increased the consumption of chocolate. The effect was therefore not only cognitive (thinking) but behavioural (eating chocolate).
However, according to Wegner himself, laboratory procedures like this seem to exaggerate the effect of ironic process. In real life it isn’t as noticeable.
Spiral Model (A model proposed by Heatherton & Polivy)
Body dissatisfaction resulting from media pressure lowers self-esteem and triggers dieting behavior.
Diet Hard 1:
- There is initial weight loss until the body steps in and tries to restore its set point.
- Weight plateaus and may even start to rise.
- This causes demotivation and eventual disinhibition. The dieter assumes it’s down to a character defect or weak personality.
Diet Hard 2: Diet Harder
- However, they try again. This time being even stricter in their restraint.
- Initial success, but again the body fights back
- Weight is regained
- The dieter feels an even greater disappointment after trying so hard
- Even greater loss of self-esteem and greater self-blaming.
- And the process continues. All the time weight is increasing!
Diet Hard 3: Diet Hard with a Vengeance…
- Here we go again!
Dieting is attempting to work against millions of years of adaptive evolution that has designed a body intent on remaining a certain weight, regardless of how big it is. Hunger, caused by dieting increases secretion of ghrelin, decreases levels of leptin and both trigger eating behavior.
Practical applications of the model
Basically the vicious cycle needs to be broken. Not experiencing weight gain will help preserve self-esteem and prevent disinhibition.
The conclusion is that restrained eating in the form of calorie controlled diets is best saved for weight maintenance than weight loss. There is no need for the body to deploy counter-measures to preserve body weight if weight is constant.
Finally on a more depressing note: Yagar et al (1988) believes constant disinhibition and repeated failure of diets can lead to substance abuse in an attempt to increase happiness.
Theory of Planned Behaviour (TPB)
Assumption
A person’s decision to perform a particular behaviour (such as stopping smoking) can be predicted by their intentions. Immediately you can hopefully spot the weakness in this theory, nicely summed up by the saying
‘the road to hell is paved with good intentions.’
All too often our behaviour falls well short of our intentions
According to the theory, intentions are determined by three variables:
1. Individual Attitude (Personal perspective if you like)
This is our personal attitude towards the target behaviour. It is the sum of all our knowledge, attitudes, prejudices etc. that we think of when we consider the behaviour. For example, our individual attitude to weight loss might be that we would be healthier, less effort getting up the stairs, look better and fit into all those clothes we have in the wardrobe but is going to involve sacrifices and possible cravings. We weigh up the good and the bad and form an overall impression.
2. Subjective norms
Considers how we view the ideas of other people about the target behaviour. For example the attitude of family and friends to my losing weight. They want me to look better and be happier with my shape but know I might get grouchy and moody. The closer the friends the greater the influence of their attitudes upon us.
As this stands we have the theory of reasoned action (TRA). A vital component is missing:
3. Self efficacy
To become TPB we need to add ‘self-efficacy.’ In practice this means adding the extent to which you believe the change in behaviour is possible. So for example, if you have been trying for 28 years to stop eating kebabs (with chilli sauce) after a night out drinking, then you’re not going to rate your chances too highly this time.
This has two effects:
Assumption
A person’s decision to perform a particular behaviour (such as stopping smoking) can be predicted by their intentions. Immediately you can hopefully spot the weakness in this theory, nicely summed up by the saying
‘the road to hell is paved with good intentions.’
All too often our behaviour falls well short of our intentions
According to the theory, intentions are determined by three variables:
1. Individual Attitude (Personal perspective if you like)
This is our personal attitude towards the target behaviour. It is the sum of all our knowledge, attitudes, prejudices etc. that we think of when we consider the behaviour. For example, our individual attitude to weight loss might be that we would be healthier, less effort getting up the stairs, look better and fit into all those clothes we have in the wardrobe but is going to involve sacrifices and possible cravings. We weigh up the good and the bad and form an overall impression.
2. Subjective norms
Considers how we view the ideas of other people about the target behaviour. For example the attitude of family and friends to my losing weight. They want me to look better and be happier with my shape but know I might get grouchy and moody. The closer the friends the greater the influence of their attitudes upon us.
As this stands we have the theory of reasoned action (TRA). A vital component is missing:
3. Self efficacy
To become TPB we need to add ‘self-efficacy.’ In practice this means adding the extent to which you believe the change in behaviour is possible. So for example, if you have been trying for 28 years to stop eating kebabs (with chilli sauce) after a night out drinking, then you’re not going to rate your chances too highly this time.
This has two effects:
- The more control we believe we have over our behaviour, the stronger our intention to perform the behaviour.
- The person with the higher perceived level of control will try harder and longer to succeed.
Health concerns, mood, advertising and health information and culture, including parental choices, schooling etc. will all feed into determining subjective norms and individual attitudes.
Evaluation
At present this is the most widely used and applied model of social cognition used in health psychology. This would suggest it has a fair amount in its favour.
All three components (individual attitude, subjective norm and perceived behavioural control) correlate with intentions.
It has proved to be especially useful in predicting intentions relating to testicular self-examination, dieting and weight loss, smoking, alcohol consumption, increasing exercise and as the following study shows, intention to wear sun protection:
With regards to eating behaviour specifically, health does seem importsnt in determining intentions but is not so crucial as taste and desire for certain foods.
However, this is not always the case and its essential weakness is the same as TRA; intentions not being the nest predictors of eventual behaviour. Have I said this before?
Many see it as too rational, ignoring as it does, feelings, motivations and real-life pressures. Completing a questionnaire in the cold light of day is never likely to be a good predictor of eventual real-life behaviour.
Evaluation
At present this is the most widely used and applied model of social cognition used in health psychology. This would suggest it has a fair amount in its favour.
All three components (individual attitude, subjective norm and perceived behavioural control) correlate with intentions.
It has proved to be especially useful in predicting intentions relating to testicular self-examination, dieting and weight loss, smoking, alcohol consumption, increasing exercise and as the following study shows, intention to wear sun protection:
With regards to eating behaviour specifically, health does seem importsnt in determining intentions but is not so crucial as taste and desire for certain foods.
However, this is not always the case and its essential weakness is the same as TRA; intentions not being the nest predictors of eventual behaviour. Have I said this before?
Many see it as too rational, ignoring as it does, feelings, motivations and real-life pressures. Completing a questionnaire in the cold light of day is never likely to be a good predictor of eventual real-life behaviour.
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.
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.
