PSYA3 Eating Behaviour

A major factor that influences eating behaviour between different cultures is the availability of food. Our attitudes are based around the food which is readily available to our cultures.

Research to support:

• Wardle et al. - studied diets of 16,000 young adults across Europe and found that warmer countries (Spain, Italy) ate more fruit and colder countries (UK, Sweden) ate more fibre. Shows availability affects eating choices. 

:) High population validity - 16,000 participants, easily generalised - 21 european countries, further generalisability

:( Only carried out on European countries - Ethnocentric, assumes behaviour is the same around the world

Research against:

• Leshem - compared diets of Beduin women in city, beduin wome in desert and jewish women in city and found similiarities between culture and not area. Shows that culture has an affect and not availability

:) useful in questioning the reliability of Wardle's findings

:( gender bias - only women used, cannot generalise to men, behaviours/attitudes may be different

Social factors have an impact on food preference when looking at attitudes towards food in cultures. For example, religion may have an impact, or family structures.

• Religion - behaviour is affected through processes such as lent or fasting, attitudes are affected through rules (e.g. Hindus are not allowed beef)
• Family structures - a single parent family may have one parent which works so there will be a lot of takeaways and ready meals, whilst if mum is at home to cook then there may be more cooked meals
• Laws/policies - Jamie Oliver (no sugar in schools/school vending machines)
• Employment - low paid job = more fattening foods which are cheap to buy, high paid job = healthier options which can also be influenced by fitness

Determinism v free will - deterministic, ignores the role of free will, can make conscious decisions about our food choices by ourselves, not shaped by where we live

Nature v nurture - ignores the role of nature, suggests that we are nurtured to have attitudes and behaviours, evolution play a part?

How we feel affects how we ear and what we think about eating. A negative modd may lead to comfort eating, where we eat food to temporarily escape a negative mood (e.g. ice cream after a break-up)

Research on the effects of mood on food:

• Garg et al - looked at how mood affects food consumption and whether this was influenced by nutritional information and product type, found people in a positive mood ate more healthy foods (grapes) whilst people in a bad mood ate more calorific food (popcorn).

:) lab environment - high levels of control, extraneous variables eliminated, cause and effect can be repeated

:( operationalisation - varaibles happy and sad were operationalised through videos, problems with individual differences, some people may think a happy movie is sad, some people may prefer one food type to another, validity comes into question.

Verplanken - carried out a correlational analysis which found that those with low self esteem were more likely to impulse buy and consume snacks.

Issues with correlation - cannot establish cause and effect as it only shows the relationship between two variables, mayble impulse buying causes a lower mood.

Gender bias - most participants were female, cannot generalise to men. Beta bias happens - minimises differences between sexes so doesnt recognise that there could be a difference

Contradictory findings:

Popper - found that marines had a decrease in food consumption during combat situations (stress doesn't result in overeating)

:) high ecological validity - real life situation

:( marines may have little time to eat and would normally eat less than an average person when in combat

Restrained eating aims to put a cognitive limit on food intake by not eating as much. However, it is that this in fact has negative consequences on the success of dieting because attempting to not eat actually increases the probability of over eating. Therefore, restraint contributes to the cause of over eating.

Research to support:

Ruderman & Wilson - studied 27 obese women through 3 conditions; exercise, dieting and non-treatment. The women were tested agianst a pre-load taste test after 4 weeks and against a stressful situation after 6 weeks. It was found that the dieting group ate more in both conditions. Therefore, dieting in fact caused individuals to over eat.

:) Methodology - researchers could manipulate each group and draw comparisons, also able to ensure that all groups experienced the same stressful situation making research replicable

:( Lacks population validity - only uses obese women, makes it difficult to generalise to others beyond the research situation

:( Beta bias - over generalises results to women, men may have a different response

The model suggests that hunger keeps the consumption of food above a minimum level and satiety (feeling full) keeps the consumption of food below a maxiumum level. This is different in dieters as they have a larger rasnge between hunger and satiety so it takes them longer to feel satieted/full as the boundary makes the body feel like it is constantly empty.

:) This supports the fact that overeating may be the consequence of being told to restrain, suggesting why diets do not work for obese people

:( Fails to explain anorexics, anorexics can starve themselves, model does not apply to all people, unrepresentative

:( Deterministic approach - ignores free will, ability to chose must play a role, individual differences in terms of mood, psychological factors must play a role

The role of denial is a cognitive approach which suggests that our attempts to suppress or deny thoughts have the opposite effect to what we want. This is sometimes called the theory of ironic processes of mental control and is central to diets because it is the decision to not eat certain foods in a diet which makes us eat because the forbidden food becomes the food we want to eat.

:) This offers an alternative to the boundary model, shows how individuals thought process may play a role in dieting

:) Many of the findings reflect peoples expereinces of trying to loose weight

:( Anecdotal evidience - issues with reliability, variables not controleed unlike in a lab, based on past experiences, might not be a reliably theory for the failure of diets. Biological explanation could be a reason as to why denial happens.

Ogden interviews three groups of obese participants; wight loss maintainers, gainers and those who remained stable. He concluded that weight loss maintainers had a psychological model in terms of obesity and therefore had psychological motivations to loose weight as it was associated with depression and low self esteem. 

On the other hand, those who put weight on tended to assign to the medical model, the model that states it is not our fault. Therefore to loose weight, ogden states that you must see yourself in a new light and for a diet to work, it must work with what YOU believe.

Other factors include; motivation, social support (e.g. weight watchers), operant conditioning

:) supported through successful Cognitive Behavioural Therapy (CBT) techniques. Dieting is fast being replaced by healthy eating, making people aware of comfort eating and food avoidance

:( Too much emphasis on free will, ignoring the idea we may be overweight genetically, genetically predisposed to being overweight

Our bodies have developed 2 systems, one that turns eating on and one that turns eating off. The hypothalamus is central to these systems and helps to regulate hunger and eating.

Lateral Hypothalamus - turns eating on (hunger), Ventromedial Hypothalamus - turns eating off (satiation)

Eating > Increase in blood glucose > Ventromedia hypothalamus activated> Satiety > Eating stops > Decrease in blood glucose > Lateral hypothalamus activated > Hunger > Eating (Process starts again)

Research evidence found that damage to the hypothalamus in rats caused the absense of eating. It was also found that stimulation of the lateral hypothalamus elicited feeding behaviour in rats. Neuropeptide Y (NPY) was injected into the rats, they began to feed. This occured when rats were satiated and then became obese. Provides support - shows the roles of the hypothalamus plays in eating behaviour, shows that turning off one system can lead to over (lateral) or under (ventormedial) eating 

Research Evaluation

:) Research provides support to the models

:( Outdated, cannot be generalised to humans, unethical

Hypothalamus Evaluation

:( cannot be explained by evolution, is NPY's normal function to influence feediong behaviour?

Ghrelin is a hormone secreted by the mucos membrane of an empty stomach and travels to the brain to indicate we are hungry (controls hunger). Our body produces extra amounts of Ghrelin when we are stressed - part of the body's natural defense as it reduces anxiety and depressive behaviours but also boosts appetite (comfort eating). Blocking Ghrelin controls weight but not stress.

Research evidence - Lutter et al. - starved mice for 4 days, found increase level of ghrelin in the mice. Therefore shows that Ghrelin exists in the process of hunger due to the fact that mice had empty stomachs, showing it plays a role

:( mice - cannot generalise to humans - humans are more physiollogically complex

:( mice had not had anything to eat - stress which exerted Ghrelin

:( shows more Ghrelin is used in the process, it doesnt show that Ghrelin caused hunger

Leptin is a hormone that is secreted by fat cells and released into the bloodstream. Leptin reacts upon receptors in the hypothalamus and inhibits hunbger by counteracting the effects of NPY. It leads to decreased appetite and signals to the brain that the body hashad enough to eat. Does not make us feel dull but moderates the effects of other signals. 

Increase in fat cells = increased Leptin = eat less, satiety signals make us fuller sooner

Decrease in fat cells = reduced Leptin = stimulates motivation centres in the brain so we are more interested in food

Absense of Leptin = uncontrolled intake = obesity

Research Evidence - Zhang et al - Injected mice who had the obesity gene with Leptin and found that injecting the rats made the mice lose weight dramatically. Therefore when Leptin is introduced into the body, mice became satieted as NPY was turned off, so they lost weight as they were not feeling hungry.

:) - evidence shows that the hypothalamus - especially in the VMH - particularly sensitive to Leptin

:) Trauma or tumors of the VHM can cause hyperphagia and obesity

Our ancestors ate what existed in their environment such as animals and plants. They had a preference for fatty foods as they needed energy for hunting to stay alive. When their was a decline in plants they ate meat which was high in minerals and nutrients. They preferred to eat foods which wee high in glucose. Therefore as we have food which is readily available to us, we do not have to go and hunt for our meals so we are more likely to gain weight which leads to obesity. 

:) Gibson & Wardle - examined the eating behaviour of 4 - 5 year olds and found that the best way to predict what fruit and veg was prefered was how dense they were in calories (bananas and potatos were likely to be chosen). Therefore this shows an evolved preference for calorie rich food

:( Many food preferences can be traced back but not all of them can be - majority of likes and dislikes appear not to be predetermined (Nature v Nurture debate)

:( Our evolved preferences may no longer be adaptive (e.g. low cholesterol foods and now needed) - contrast to our ancestors needs for saturated fats 

Neophobia - fear of new stimuli, including food. Due to this fear we have evolved to prefer the foods that we are familiar with. Ancestors eating behaviour was controlled by the environment which meant that our innate preferences had to quickly develop to our environment and we stick to what we know as familiarity offers security.

Birch - infancy = no neopobia - eat what is given to us, childhood = neophobia - we become more independent and decide what we eat, adulthood = no neophobia - open to trying new things

:) face validity - observed in eating behaviour

:( individual differences

:( free will v determinism - we do not have to be fearful of new foods and lots of people will eat new foods

Taste Aversion states that we avert from foods which may be new to us. Again, our ancestors survived eating poisonous foods by not eating them again due to the fact that they were poisonous. Taste aversion serves the function of keeping us alive. Anecdotal evidence came from farmers who observed that rats only take a small amount of any new food as this serves a function - of they become ill they lean to avoid it. This is also known as "bait shyness".

Bernstein & Webster - found that when giving cancer patients ice cream during treatment, taste aversion was formed as they associated the treatment (which made them ill) to the ice cream.

:) shows the advice that should be given to cancer patients

:( no control group for comparisons - possibility of affecting extraneous variables

:( individual differences/person preferences

:( low population validity

Genetic research shows higher rates of Anorexia Nervosa (AN) in individuals who are related to a sufferer of AN. It also shows higher rates of AN in monozygotic (identical) twins than dizygotic twins. This has led to an estimate of 76% influence of genetics in AN. 

Family Studies - Lilenfield et al - found relatives of AN sufferers are 7 to 12x more likely to develop forms of AN, so will have AN tendencies but will not meet the DSM criteria.

:( pop validity - only 26 people used - generalisations from this sample?

:( must be other factors - shows a vunerability to develop forms of AN - not the eating disorder

Twin Studies - Holland et al - found that 56% of MZ twins both had AN and 5% of DZ twins did. Therefore genetics provide a predisposition to AN as you cannot say its the sole cause

:) reliable finding - found in other countries such as USA, Australia & Denmark

:( research does not tell us how genetics increase the liklihood - just statistics

Serotonin is a neurotransmitter and disturbances in the levels of serotonin is thought to be characteristic of AN sufferers. This is based on the observed similarities between AN and OCD sufferers. Serotonin influnece symptoms of OCD as both disorders focus on specific control over something (AN = loosing weight/excersice, OCD = specific feature).

Animal research - shown that when serotonin is released into the VMH or LH, animals stopped eating. If high levels stop eating behaviour and high levels lead to AN = the absense of eating

:( animal research - how can we generalise to humans?

Human research - Bailer aet al - examined serotonin activity in women recovering from AN and found significantly higher activity in those recovering from AN, especially those who showed anxiety. Therefore persistent disruption if serotonin levels may lead to increased anxiety which triggers AN.

:( cause of effect? - serotonin could be a consequence of AN and not a cause of it - further research required

:) genetic and neural explanations of AN offer treatment implications (e.g. drug therapies)

:( Gender bias - research predominantly focussed on women

Adapted to feel famine (AFFH). Guisinger said that the typical symptoms of AN (restriction of food, denial of starvation) reflect a once ideal mechanism to feel famine. Our ancestors lived as nomads and these behaviours were adaptive. 

Ancestors - extreme weight loss due to lack of resources > restrict food intake > increased chances of survival to migrate to an environment with resources.

This exists now as we no longer have to migrate, ANs are simply hyperactive and although it is not adaptive anymore, if you are vunerable to developing AN and lose weight then these mechanisms are triggered.

:( difficult to prove or disprove - no scientific evidence for or against the explanation, it is impossible to test our ancestors and make comparisons

:( can it be suggested that AN is adaptive? - stats are still in the rise - why are the geners being naturally selected?

:( does not explain AN prevalence in females - surely everbody would have AN - unreliable

Reproductive Suppression Hypothesis (RSH). Surbey attempts to explain why AN is a characteristic of adolescents and why girls show stronger desires to control weight. This links to amenorrhoea and the fact girls choose to be AN to stop puberty.

Our ancestors delayed the onset of sexual maturation in response to cues about poor reproductive success. This is adaptive as we will not give birth when there is a low chance of survival (ours + genetic)

NOW - reach teenage years > still dependent on parents > continue with studies > own resources gained > more chance of a successful mate > start a family

AN is a varient of this adaptive behaviour. When girls feel unable to cope with adulthood they restict their diet to delay the onset.

:) Animal research shows hat when other species go through periods of stress puberty is suppressed.

:( why is AN prevelent in men? - men do not have periods and still get AN

AN does not exist univerally. This is thought to be due to the fact that other cultures do not admire thinness at the same level. Western standards of attractiveness are an important factor that contributes to AN and the media is a massive source of influence for body images in young adolecesnts. This is through influences such as TV, magazines and the internet

:) studies have shown that many teens are dissatisfied with their weight and many have a distorted view of their body image

:( is this really down to culture and the mass media?

:( individual differences? - media does not influence everyone in the same way - cannot explan every cause of AN

:( does not account for free will - variation exists within cultures - highlighting thinness does not mean that people will internalise these values - provides a deterministic account

It is an individual difference that it thought to determine susceptibility to the development of AN. Perfectionists focus on achieving perfection and avoiding failure. There is no middle ground do you are either perfect or a failure. AN is seen as a product of the drive to achieve perfection.

Research Evidence - Stober at al - found high levels of perfectionism in personality traists for teenage boys & girls - girls = 73%, boys = 50%

:( retrospective data - demand charactersistic, aware of research

:( population validity - only teenagers

:( Is perfectionism alone enough? - research to suggest that it needs to be paired with other personality traits - reductionist account of AN - too simplistic for complex behaviour

:( what comes first, perfectionism or AN? - Keys et al found that traits and behhaviour of soilders after WW2 changed as a result of starvation - cause and effect is unclear

Cognitive factors suggest that sociocultural factors are seen in behaviour due to cognitive processes that can be linked to AN. Sufferers of AN report experiencing obsessive thoughts about food, eating, body weight and body shape. They state they try to supress the thoughts but they are not successful and have little control.

Research Evidence - Cooper - found that in a modified version of the Stroop test, women with AN were slower to name the colour of the ink for food and body related words such as sausage, thighs or hips. Therefore the women had an attential bias for food and body related stimuli and not being able to control thoughts leads to obsessive thought and behaviour leading to AN

:) standardised - easily replicated - reliability can be checked, same findings found with other groups

:( demand characteristics - reduced validity, straight forward to pinpoint difference between lists, may guess they had to take longer

:( reductionist (A03) - only considers psychological causes, what about biological causes?