PSYA3-Eating-Behaviours Essay Answers.pdf

AQA A PsychologyPsya3:

Eating Behaviour

Model Essay Answers

AQA A

June 2015/16 Spec

Saj Devshi - www.loopa.co.uk - A* Psychology Revision

The A* Students Handbook (c)

Introduction..

1

Hello,Firstly thank you for purchasing my ebook for AQA Psychology Psya3 Eating Behaviour. A bit about me: My name is Saj Devshi and I was a private student that self-taught myself AQA Psychology from 2011-2012 and I received my certificate in January 2013 achieving an A* Grade. The certificate you can view on my website which I will post at the bottom - You can also get my other A* model essay answers from there too for the other topics for AQA Psychology. I achieved an A* grade overall scoring two As for Psya1 and Psya2 as well as 100% in both my A2 exams (Psya3 and Psya4). My final score was 373/400 ums points. (You only needed 90% in A2 and 320 ums for an A* grade). So basi-cally I didnt just beat the boundary - I absolutely smashed it. How did I do it? It wasnt easy and I am by no means some savant genius. I made great notes and essays that sim-plified things for me as I had no teachers and it is these notes I share with you now to help you with this topic. Self-teaching myself AQA Psychology from the ground up has given me a unique and strong foundation in grasping the concepts. I am by no means the oracle but I understood enough that I was able to work completely independently without sup-port and create such good, concise essays. Since 2012 thousands of students across the UK (as well as abroad where these exams are also taken) have downloaded my books to support their revision. These books will help cut down revision time as all the essays are made concisely and clearly for people to follow. Im confident these essays will serve you well as they did me for AQA Psychology.

If your curious to know more about me you can visit my website at http://www.loopa.co.ukThere it tells you more about me, how I self-taught myself as well as how to contact me di-rectly for help and advice and get books on the other topics and papers too.You can get plenty more free resources by liking my Facebook page and following me on twitter below - My Facebook page: http://www.facebook.com/aqapsychologyFollow me on twitter here too: https://twitter.com/SajDevshi

Again thank you for your support and I wish you the very best in your exams! Now - Lets get this show started..This book is subject to copyright and is not to be sold, shared, uploaded or distributed. It is for personal individual use only. If you are a school

or college and wish to distribute this for your students, you can earn distribution rights by placing a link to http://www.loopa.co.uk on your schools website within the psychology subject page. Any questions contact myself on: [email protected]

Eating Behaviours Specification Overview

2

Above is an extract from the AQA specification for the Eating Behaviour topic itself. This outlines exactly what the topic consists of but more importantly what the actual questions can be based on within the exam itself. Our job is then to break this down into possible essay questions that can be asked. We use a combination of past paper questions combined with the spec outline above and we then know exactly what the essay questions are.They are:

Factors influencing attitudes to food and eating behavior Explanations for the success and failure of dieting Neural mechanisms in controlling eating behaviour Evolutionary explanations of food preference Psychological explanations for Anorexia Nervosa Biological explanations for Anorexia nervosa

Just to note - you are required to only learn ONE eating disorder from a choice of anorexia ner-vosa, bulimia nervosa or obesity. I have taken a look at each and decided to focus on anorexia ner-vosa as I feel it has the most research available for it and seems easier to write about due to this.

We now know the possible essay questions - our next task is to source the informa-tion to write the essays for them. Thankfully thats where this book comes in. Ive done the hard part for you and sourced AO1 and AO2/AO3 and structured it in an easy to understand way. Your task is then to put the essays into your own words.

Before we do that - lets take a look at structuring and memorising your essays.

Structuring and Acronyms

Structuring the essays is exactly the same across all my books. We use the acronym method as well as the age old technique of writing and re-writing our final essay an-swers over and over until they stick. The essays that I give, you will be wise to put them into your own words as you dont want them to look the same as the other students who may purchase this book.

Use this information to create your own es-says as mentioned but the trick or aim is to format and structure them in a way thats nice and easy to remember.

I personally always try to write theory first followed by my evaluation points rather than mixing them together throughout the essays- Why do I do this? Imagine your an examiner sat for ages marking countless papers where students have mixed and matched their theory and evaluation points. Imagine now you see hundreds of these - It will likely drive you mad trying to decipher where the marks go. Now imag-ine you find an essay that lays out theory and evaluation distinctively and clearly - Like the picture across on the right - You can see the green is theory and blue is evaluation quite clearly there.

You can see exactly where the marks go and your able to give it better attention. Also your more likely to be happier about its formatting and structure too picking up those bonus marks.

This is why I propose you structure your es-says this way with all your theory first and then all your evaluation after a line of space from the theory section. Ultimately it is up to you but its what I did in my exams and I wanted to share it too.

Lets look at acronyms and how they work too now across on the next page.

3

Acronyms

In short acronyms are just a combination of letters you use to remember your es-says as they relate to the first letter of the researchers name. They are particularly helpful in memorising large amounts of in-formation by using triggers (the letters) to help you recall each element step by step. The way I use acronyms is I combined this method with the chunking strategy we learnt about in AS Psya1.

Acronyms act as markers that I used to trigger my memory to recall the rest of the essay. It is harder to remember a whole paragraph from memory than it is a few let-ters which can then lead me to remem-ber what those letters stand for and the actual studies themselves. This then trig-gers my memory to recall how each study is evaluated for strengths and weaknesses and so forth - a bit like a chain reaction.

Heres an example from my Aggression book across on the right. You see 4 letters I use to remember all my evaluation points. These 4 letters are MHBC.

I have used the acronym MHBC which stands for the researchers McGun, Hutchings, Brunner and Caspi et al.

As soon as I see the question I recall my acronym for this particular essay that I have memorised and write this at the top: MHBC. The green element is the Theory while the blue is the evaluation. Notice where I have put the letters. As soon as I finish writing my theory (the green element) I look at my acronym and recall M = McGun hence I recall his name and as I have practiced countless times writing this essay I recall his study too. By the time I finish writing about his study I recall how it was evaluated (again due to having written it hundreds of times before through prac-tice). I look at the next letter which is H = Hutchings and this triggers my memory for his study and findings as well as the evaluation points.

This is how memorising the essays with chunking and acronyms works. It takes

4

practice - Using this method WILL NOT WORK unless you have model essays cre-ated first and set up in a way that acro-nyms fit into them as I have done. Thats the bit that will require work on your half - structuring it in a way that suits you. Once done you employ this method to recall the essays.

I used this method across all 4 papers hav-ing first developed it in Psya1 after I pan-icked and looked at the vast amount of in-formation I needed to learn. I had to dumb it down for me and this is how I did it. I re-fined it to work even better at A2 level and gained full marks for both Psya3 and Psya4 using this method to memorise all my essays. You do need to start early how-ever in practicing and memorising your es-says as there is a lot to learn.

The theory element is the only element you should really try learn from memory word for word - a theory is simply a concept or explanation for something (although in some cases, dependent on how the ques-tion is worded it can also be research stud-ies). Theory you should really know from the top of your head as how can you evalu-ate something you don't fully understand or can explain? Thats the bit you need to grasp really as if you understand the the-

ory it is then far easier to oer evaluative commentary on it.

So thats structure and memorising your es-says covered as well as the overview. We know everything we need to know now so lets move on to the essay answers them-selves.

If you need further support you can get it here:

http://www.loopa.co.uk

Click on the Resources tab for further help and information - more is added con-stantly.

Right - On to the first essay..

5

Attitudes To Food And Eating BehaviourTheory AO1

One explanation for eating behavior is through Banduras social learning theory through observing modeled behavior from other people. Children may learn their atti-tudes to eating behavior through observing parents and their preferences and the satis-faction they receive and through this vicari-ous learning, they may come to model the behavior themselves. Children will identify with their parents closely and research by Brown et al found a consistent correlation between the eating habits of parents and their children around snack food intake, motivation to eat and dissatisfaction around their body. Parents also tend to shape childrens eating habits through their own as they also control the purchase of foods eaten within the home. If parents pur-chase food based on their own prefer-ences this will invariable aect childrens eating habits.

Social learning may also occur through the media with books and television highlight-ing dierent attitudes which people ob-serve and learn from. This may occur through celebrities people may identify with who may highlight particular food di-ets and the benefits gained (losing weight for example). People may also learn about

healthy eating this way and appropriate foods to eat. Macintyre et al found the me-dia did influence peoples food preferences however this may then be limited by a per-sons own personal circumstances such as income, family, culture or even age.

Cultural factors such as ethnicity may also aect eating behavior. For example Khan et al found white women were more prone to have body dissatisfaction and dis-orders such as bulimia nervosa than Asian or black women. Kennedy et al studied over 14000 women aged between 18-23 and found the longer the women were in Australia, regardless of ethnicity, they re-ported attitudes and eating behaviors simi-lar to women born in Australia. This is known as the acculturation eect. So-cial class may also be a factor; Dorn-busch et al surveyed 7000 american ado-lescents finding higher-class females wanted to be thinner more than those of lower social classes. Goode et al found such individuals were also more likely to achieve this and a positive correlation was found between income and healthy eating.

Mood may also aect peoples attitude to food and eating behavior. Research has found some individuals with bulimia ner-

6

vosa associate negative feelings of anxiety prior to binge eating (Davis et al). Wegner et al found similar results with students who recorded their eating patterns and mood over a two week period. The days they were found to binge saw them report more negative feelings compared to non-binge days. Interestingly students did not report feeling better after bingeing how-ever.

Garg et als study confirms a link between negative feelings and unhealthy eating. Par-ticipants watched either a sad movie or more happier upbeat movie and both were given the choice of consuming buttered popcorn (unhealthy) or seedless grapes (healthy). Those watching the sad movie consumed 36% more popcorn than those watching the happier movie. Gargs expla-nation for this was those who felt sad would seek unhealthy foods to make them-selves feel better while those already in a positive mood may turn to healthier foods to extend their positive feelings. When par-ticipants in another version of this study were given nutritional information prior to consumption the unhealthy food consump-tion dropped dramatically suggesting nutri-tional knowledge may aect peoples atti-tude to food and eating behavior.

Knowledge in regards to healthy foods may also aect peoples attitudes to food. Higher level education is linked with an in-creased awareness into healthy based eat-ing habits and this may also explain peo-ples attitude towards food however food availability, price and income likely aect whether this knowledge is acted on.

Evaluation AO2/AO3

Social learning theory is supported by re-search evidence. Gast et al surveyed boys and girls aged 10-12 finding a positive cor-relation between peer influence and disor-dered eating habits. An important element determining this correlation was the like-ability of peers inline with social learning theories idea that being able to identify with models would play a role in shaping behaviour. Fisher et al also found support-ing evidence of social learning influencing eating habits when studying mother daughter relationships. A good predictor for the daughters eating habits was found to be their mothers dietary restraint and how they perceived the risks of their daughters becoming overweight. This would suggest the daughters were learn-ing from their mothers behaviours and atti-tudes supporting social learning explana-tions.

7

Lawrence et al investigated aecting food choices for ethnic minority females through nationwide discussion groups. Women of Bangladeshi and Pakistani back-grounds learned cooking skills from family elders and took pride in traditional cooking practices but turned to western junk food when they had insucient preparation time. Zimbabwean women were found to have been influenced by western culture in their eating habits due to the pressure of being slim however this was not the case for women living in Zimbabwe. Healthy eat-ing was valued by all women however this did not necessarily translate into it aect-ing their behaviour. This suggested that eat-ing behaviour is influenced by time, avail-ability, cost, culture and even health fac-tors.

Stefansson et al found Copper Inuits dis-liked the taste of sugar and were repulsed by it. They had lived in isolation away from other people on a diet of roots and flesh with no experience of consuming anything dierent. This suggests that culture may in-fluence eating habits and preferences but also the cross-cultural preference for sweet tasting foods may not exist.

Xie et al found children and adolescents from high-income backgrounds were found to eat more healthy foods than

those from lower-income families. They consumed less saturated fats, more pro-tein, calcium and ate closer to daily guide-lines. This suggested income did aect eat-ing behaviour and attitudes to certain foods. However this is based on correla-tional findings and we cannot infer cause and eect for certain that better income relates to healthier eating habits. Their may well be confounding unknown variables contributing in between such as the stress of being poor actually contribut-ing to poor eating habits.

However De Almeida et al found informa-tion on health alone from unknown, unreli-able sources that is presented in a conflict-ing or confusing way was not usually acted on by people. This implies information on healthy eating alone may not be sucient in promoting healthy eating patterns from individuals and where it comes from and how it is presented may also impact eating behaviour and shape attitudes.

Steptoe et als study ranked factors taken into account by individuals when they chose their foods. Sensory qualities were highest above health concerns suggesting healthy eating was not the most important factor in determining attitudes to food.

8

Most studies have focused purely on women and their attitudes to eating behav-iour which suggests many theories may suer from gender bias and not necessar-ily generalise to men. Therefore explana-tions may lack population validity if their application is limited to only one gender. There may also be problems in generalis-ability as some studies are based on peo-ple who are diagnosed with eating disor-ders such as bulimia nervosa, some are based on people with sub-clinical condi-tions while others are based on people who may be experiencing temporary de-pressed moods. The issue here is we can-not generalise findings from such specific circumstances to other groups or even the wider population itself and hence the find-ings may lack external validity in the sense that the studies are not measuring how eating behaviour is aected in a way that can be generalised beyond that niche group of people.

Understanding how eating behaviour and attitude is aected has real world applica-tions. Information promoting healthy eat-ing can be used in advertising campaigns to utilise these points through providing positive role models from the media to pro-mote healthy consumption. This may help lower costs overall on the NHS budget for

obesity which has been recognised as a growing problem.

Research into cultural influences could also be argued to be culturally biased as the attitudes towards certain foods may be specific to that culture alone. Therefore what may be valid for one culture may not necessarily be true for another e.g. the western value of being thin and dieting and problems with obesity may not apply to cultures where the focus is on avoiding starvation.

A major weakness for such explanations is the role of free will people have is not fac-tored into explanations for peoples attitude towards food. Although exposure through social learning, culture and knowledge may influence them, there are always peo-ple who are unaected by such highlight-ing how free will also plays a role in shap-ing attitudes.

While explanations focusing on social learning, culture and media look at the nur-ture side of explaining peoples attitudes to food, evolutionary explanations look at how our preference for fatty foods, sweet foods and rejection of bitter tasting foods can be explained through nature and biol-ogy. Therefore eating behaviour is influ-enced by a complex mix of biological and

9

psychological mechanisms. Focusing only on psychological causes (nurture) is there-fore reductionist and over-simplified as a more complex process is evidently occur-ring with nature and nurture combining to shape peoples attitudes to food.

(Note to students - Its possible to bor-row some points from my essay on evolutionary explanations of food pref-erence for this section as there is clear overlap. That essay is further down - You may be able to use some AO1 points as AO1 points here as it also ex-plains peoples attitude towards food and eating behaviour (through sweet preference, fatty foods, meat products and our bitter/sour taste rejection mechanisms)

10

Success And Failure For Dieting

Theory AO1 (Reasons For Failure)

One explanation for the failure of dieting is Restraint theory. This is when people may consciously try to eat less and restrain their intake but this actually causes indi-viduals to overeat. A study by Wardles and Beales highlighted how dieting actu-ally contributed to overeating. 27 obese women were put either into a diet group which focused on restrained eating pat-terns, an exercise group or a non-treatment group for seven weeks. Assess-ments on food intake and appetite were made before and after they ate a snack at week four and again at week 6 but this was under stressful conditions. The study found the women in the dieting group ate more than the other groups at both peri-ods suggesting restrained eating actually increased food intake resulting in the fail-ure of dieting. The boundary model by Herman et al can explain why restrained eating may actually lead to over-eating. They suggested hunger kept the intake of food above a minimum level while satiety (feeling of satisfaction after eating) kept the intake of food below a maximum level. Psychological factors are believed to play a role between these two levels with those

dieting believed to have a larger range be-tween satiation and hunger. This may be due to it taking longer for dieters to feel hungry (lowering their minimum level away from their satiety level). Once restrained eaters do eat they may find themselves eat-ing more than they had planned as it takes longer for satiation to occur.

Another explanation looks at the role of de-nial which suggests when we deny or at-tempt to suppress certain thoughts this has the opposite eect and makes it even more prominent. Wagner et als study highlights the basis for this where partici-pants were asked to not think about a white bear but ring a bell every time they did. A control group was asked to actively think about it. Results found those asked not to think about it rang the bell more of-ten than the other group. Wagner called this The theory of ironic process of mental control as denial of a thought leads to it occurring more often. Applying this to diet-ing and restrained eating, when dieters at-tempt to not eat certain foods or less of them they would then become more tempt-ing and prominent in their minds leading to the failure of diets.

11

This book is subject to copyright and is not to be sold, shared, uploaded or distributed. It is for personal individual use only. If you are a school or college and wish to distribute this for your students, you can earn distribution rights by placing a link to http://www.loopa.co.uk on your

schools website within the psychology subject page. Any questions contact myself on: [email protected]

Theory AO1 - (Reasons For Success)

Reddan et al proposed successful dieting could be achieved through controlling cog-nitive thoughts such as focusing on the de-tails of what is being eaten rather than negative self-talk such as not another sandwich. He suggested that focusing on the specifics (ham, cheese, pineapple etc) people are less likely to get bored and thus maintain their diet. This was tested in a study that saw 135 people given a jelly bean. They were either described using a number (bean no.9) or through describing more detail about them (cherry flavored number 9). Participants were seen to be-come bored faster if they saw general infor-mation about the beans rather than more detail suggesting their may be a cognitive element to dieting that shapes attitude to-wards food and thus successful dieting.

Another explanation for successful dieting looks at relapse prevention. This would in-volve identifying times when lapses may occur for individuals and what they could do to refocus should they happen. This is to encourage individuals to not revert back to old eating habits and lose motivation should they have one lapse in their dieting. Other explanations suggest incentives or social support also aid successful dieting. Operant conditioning could be applied

through the use of praise or rewards acting as a positive reinforcement to maintain their progress e.g. buying clothes to suit their new body figure. Social learning the-ory may also explain successful dieting through role models that achieve such pro-gress and then individuals observing and learning this for themselves that it may be possible. This may be more realistic when its people they know themselves firsthand.

Evaluation AO2/AO3

For the most part research evidence sup-ports restrained theories predictions that restraining eating can lead to over-eating and thus diets fail due to this. However a weakness is it is unable to explain why some people are able to successfully lose weight through restrained eating or why anorexics may lose huge amounts of weight without overeating either. This is a weakness for Restraint theory as it sug-gests other factors may also be involved and the theory may be reductionist in fo-cusing only on people eating less as the sole cause for diets failing and this view may be too simplistic. It may well be their is a cognitive element too like Reddan et al suggested that goes hand in hand with restraint eating which may be the actual cause. We cannot therefore infer cause and eect between the research findings

12

into restrained eating resulting in over-eating and diets failing as this is based on correlational research. It may be other un-accounted variables like negative cognitive thoughts towards eating the same foods while dieting leads to this.

Herman and Polivy found supporting evi-dence of cognitive shifts occurring which led to a breakdown of self-control or moti-vation. Dieters reported to them that they could not be bothered to maintain their di-ets and it required too much eort suggest-ing cognitive shifts may also explain suc-cess and failure in dieting. Ogden found that the more dieters tried to suppress thoughts on forbidden foods the more they actually thought about them suggesting de-nial may actually create further pressure leading to the failure of diets.

Another weakness is many of the studies into successful dieting or failure have been based on anecdotal accounts of individu-als. These accounts are then used to ex-plain various dieting strategies however such anecdotal evidence is usually not 100% accurate, has a lack of controls in place and is dicult to replicate to verify reliability. Also many studies into success-ful dieting lack ecological validity due to their unnatural setup (labratory settings, be-ing monitored on food intake) and there-

fore findings cannot be generalised to the wider population which further undermines possible theories developed from such studies.

Another issue to consider is whether peo-ple actually have the free will to control their weight loss or whether it may be bio-logically determined. A number of geneti-cally related causes may determine weight control and this may be outside an individu-als own level of control. For example LPL (Lipoprotein lipase) is produced by fat cells to help store calories as fat. If a per-son produces too much they may regain lost weight much faster than others. Kern et al confirmed this in one study where 9 people had their LPL levels measured be-fore and after dieting and losing 90 pounds. The people who were fatter at the start were found to have higher levels of LPL levels suggesting the body was fight-ing harder in those individuals to regain the lost weight. The weight loss would have ac-tivated the production of this enzyme which may explain why some people find dieting easier while others struggle. This also undermines explanations for success-ful dieting and failures suggesting a more individualistic explanation likely exists for each persons own circumstances.

13

Another issue is that research into success-ful dieting is culturally biased as some cul-tural groups have been found to struggle with dieting with a natural inclination to-wards obesity. Adults from asian back-grounds have been found to be more prone to suer from obesity than european adults (Park et al) and Misra et al found a similar trend in asian children and adoles-cents compared to their european counter-parts. Therefore culture itself and biology (nature) may be an influencing factor as to whether diets may ultimately be successful or fail.

Individual dierences could also explain varying success rates for dieting. Low-restrainers find dieting easy while high-restrainers struggle. One explanation of-fered by Mensink et al for this is that high-restrainers are hypersensitive to food cues and therefore quit their diets more easily when exposed to such. Stirling et al found those more likely to give in to forbid-den chocolates were high-restrainers also supporting this explanation however there is no accounting for whether being a high or low restrainers is something that is learnt or innate.

One issue raised is that if dieting is likely to fail because of cognitive or biological factors then diet plans have little justifica-

tion. Evidence however has suggested a combined approach works best that in-volves dieting, trying to lose weight and group support which provides real-world applications into how we might help peo-ple trying to lose weight.

Research into dieting can also help lead to real-world strategies for successful diet-ing that could help towards addressing the growing problem of obesity in various west-ern cultures.

Diet plans represent the nurture side of the argument as people make environ-mental changes to influence their body shapes through restrictive/altered eating patterns. Peoples genetic predisposition towards certain body types and the dier-ences in progress between individuals could be explained through nature and their own biology. Therefore the success or failure for dieting may be down to a combi-nation of tackling the right foods through diet but also catering this for each individu-als own biology.

14

Neural Mechanisms In Eating BehaviourTheory AO1

The hypothalamus is a gland in the brain that is responsible for Homeostasis. This is when conditions within our body are kept constant such as body temperature, urine and sweat levels as well as the intake of food and drink. It is for this reason the hypothalamus is believed to play a role within eating behavior.

Two systems are believed to have evolved to control eating behavior with one de-signed to turn it on and the other to turn it o. Glucose levels play a huge role with hunger levels increasing as glucose levels within the blood decrease. Low glucose in the blood activates the lateral hypothala-mus (LH) which results in feelings of hun-ger. Once food is consumed glucose levels increase which then activates the ven-tromedial hypothalamus (VMH) which causes feelings of satisfaction or satia-tion which helps stop further feeding. There is a time lag between these two mechanisms and the bodies ability to rec-ognise an individual has eaten enough due to slow digestion and receptors having in-sucient data to turn o hunger initially.

Researchers found damage to the lateral hypothalamus in rats caused them to stop eating while stimulation to the lateral hypothalamus through the injection of a neurotransmitter known as neuropeptide Y (NPY) caused them to begin feeding and even overeat beyond satiation (Wickens 2000)

This suggests the neurotransmitter NPY plays a role in both stimulating the lateral hypothalamus and increasing eating behav-ior.

Research also found damage to the ven-tromedial hypothalamus (VMH) resulted in rats overeating as there was no stop signal for satiation onset leading to a con-dition known as hyperphagia which means excessive hunger and increased ap-petite. Stimulation of the Ventromedial Hy-pothalamus was also found to inhibit and stop feeding, again suggesting this neural mechanism controls eating behavior.

Another mechanism believed to be in-volved is the fat hormone Leptin which is neuropeptide produced by fat tissue and secreted into the bloodstream resulting in fat loss and decreased appetite. Leptin sig-

15

nals to the brain via the hypothalamus that calorie storage is high however when peo-ple do not eat enough this causes Leptin levels to drop. The hypothalamus detects this and interprets this as a lack of calories and begins to generate the sensation of hunger thus aecting eating behaviour.

Zhang et al found some rats were found to have defective genes where Leptin re-lease did not happen leading to obesity. In-jecting them with Leptin was found to cause them to lose weight suggesting defi-ciencies in genetics could also lead to im-balances in hormones and thus aect eat-ing behavior also.

Other neural explanations suggest the amygdala and inferior prefrontal cortex, which are are located within the brain, af-fect eating behavior through cognitive and neural factors. The Amygdala is believed to influence food choice through previous experience while the pre-frontal cortex re-ceives messages regarding smell which if damaged can aect the taste of food.

Evaluation AO2/AO3

One weakness for the homeostatic expla-nation is that the hunger mechanism should in theory be adaptive to anticipate and prevent deficits in energy rather than

simply reacting to them. The explanation that hunger and eating is triggered only due to low glucose levels does not fit in with the evolutionary perspective in which our biology has evolved. We should be able to promote levels of consumption which keep us above our optimum level to buer against future lack of food. However an argument in favor of the homeostatic ex-planation is it could be argued we con-sume only what we require for the short-term to keep us from storing fat and re-main agile and flexible to continue to gather food which could be sometimes strenuous and not possible if we are con-sistently carrying extra stored energy through fat.

Another weakness into the assumption the lateral hypothalamus is responsible for turning eating on is that damage to this area of the brain also caused deficits in thirst and sex drive. Recent studies have also found neural circuits running through-out the brain play a role in eating behavior and not simply just the hypothalamus. Therefore the view the lateral and ven-tromedial hypothalamus are alone responsi-ble is reductionist and over-simplistic as it appears there is a more complex proc-ess occurring that these explanations are unable to account for.

16

Other research has found that rats were able to reach satiety even when the Ven-tromedial Hypothalamus was removed while rats with their Lateral Hypothala-mus removed were still able to become hungry. This supports the argument that duel control theory (LH and VMH) is reduc-tionist as hunger and satiety were not af-fected.

Research into NPY has also found it may not influence eating behaviour as much as previously thought. Marie et al found that mice who were genetically manipulated not to produce NPY had no change in their eating behavior compared to normal mice. This suggests that NPY injections may sim-ply be an experimental side eect and cause behavior that may not translate into real world scenarios beyond the laboratory conditions. Due to this theories around NPY aecting eating behavior may lack ex-ternal validity when generalising the find-ings to real world settings. Also with ani-mal studies we can not be certain the re-sults translate into human subjects due to dierences in biology e.g. rats do not have a functioning prefrontal cortex like humans and this helps us make decisions. Therefore such studies may lack internal validity as any observations made in ani-

mals may not necessarily apply to human eating behavior.

This biological approach to explaining eat-ing behavior through neural mechanisms can be seen as an example of biological determinism as it focuses solely on the role of nature with no consideration for cul-tural or social factors. This theory cannot also account for the role of free-will and how this can shape attitudes towards food and override biological urges e.g. dieting behavior.

However research into neural mechanisms that may be responsible for aecting eat-ing behavior opens up real-world applica-tions that can be developed to treat obe-sity. For example drugs with Leptin may be developed to increase weight loss or drugs that inhibited the lateral hypothala-mus may help people reduce their cravings if it is biologically determined through neu-ral mechanisms.

Other research has shown hunger and eat-ing patterns may not necessarily be under the control of neural mechanisms. Lutter et al found the body produced extra ghre-lin when stressed and this has been associ-ated with a boost in appetite and comfort eating. The view that its neural mecha-nisms alone may therefore be reductionist

17

and over-simplified as there may be a combination of dierent processes in-volved in managing hunger.

Cognitive factors may play a bigger role in determining satiety and when a person is full. People are aware of when they have eaten and they could therefore conclude they are full leading to the feeling of satia-tion.

Various signals are sent to the hypothala-mus which are all part of a complex sys-tem in regulating the body and its quite possible other factors beyond neural mechanisms play a role such as biological rhythms. Rats for example are active and begin to eat as darkness descends and this is influenced by the Suprachiasmatic nucleus which is another part of the hypo-thalamus.

18

Evolutionary Explanations Of Food PreferenceTheory AO1

Humans originate from hunter-gatherers and their diet would have consisted of whatever was available in their environ-ment i.e. plants and animals.

A preference for fatty foods would have been adaptive as this provides valuable en-ergy resources which were vital during a time when eating the next meal is always uncertain. Calories were less available within the EEA and therefore it would have been adaptive for humans to develop a preference for high calorie foods as this would provide them with the longest pe-riod of energy compared to other nutrients.

Our preference for sweet foods would have had an evolutionary advantage as sweetness is associated with high-energy as well as being non-toxic and therefore beneficial for survival. In contrast our abil-ity to detect and reject bitter/sour tastes also make evolutionary sense as such tastes would have been indicative of poi-son or toxins which plants produce to dis-courage being eaten. Therefore us having a natural dislike to bitter and sour tastes make sense as this could have been dan-gerous if consumed. Humans possess around 30 genes coded for bitter taste re-

ceptors with each interacting with several compounds. The result is humans have a wider scope to recognise bitter tasting foods. In support of the evolutionary expla-nation for bitter/sour food development, children have been found to be more sensi-tive to bitter tastes and this fits in with evo-lutionary explanations. Children being young and lacking environmental experi-ence to know which foods are safe to eat suggests being more prone to bitter/sour foods helps in their survival while this knowledge develops.

Our preference for meat developing could be explained due to a decline in plants caused by receding forests. Also meat is full of nutrients which some argue was the catalyst for the growth of the brain as this provided important amino acids and minerals which vegetation alone would not have been able to provide. Meat is also rich in fat and high in energy and available all year round compared to sea-sonal plant life therefore making its prefer-ence more logical from an evolutionary per-spective. Therefore our preference for meat could also be explained due to shrink-ing plant supplies but also the nutritional value and developmental benefits it sup-plied for our brain.

19

Our ability to learn taste aversion to foods that are toxic can also be explained through evolutionary explanations. Taste aversion occurs when food is toxic and we subsequently develop a dislike towards it after consumption and illness. This would have helped us survive from an evolution-ary perspective as if we survived the initial consumption our body would adapt by learning to avoid the foods by developing a natural dislike for it. The opposite can oc-cur also with a preference for foods that may improve health. Garcia et al found that when a rat with a thiamine deficiency consumed food with a distinctive taste and then was followed by a thiamine injection, the rat would subsequently develop a pref-erence for this food. Developing such a preference would have an adaptive advan-tage from an evolutionary perspective as our body is likely to adapt to foods that it perceives as improving health. Salt prefer-ence could also be attributed to this as it is essential for maintaining neural and mus-cular activity as well as containing sodium chloride which is essential for keeping hy-drated and an adaptation for this would make sense to aid in survival.

Evaluation AO2/AO3

Support for the preference of sweet foods having an evolutionary basis comes

from a study by Desor and Steiner et al. They found neonates preferred sweet foods compared to bitter suggesting there was an innate preference. This was based on them judging their choice preferences and facial expressions.

The strength of this study is it helps rules out extraneous variables such as environ-mental and social learning factors as the neonates are too young to have learnt pref-erences giving these findings greater valid-ity. However interpreting preference using facial expressions from neonates is subjec-tive and can be easily misinterpreted and unreliable. Therefore expressions observed may not necessarily imply a sweet prefer-ence.

In support of sweet preferences having an evolutionary basis Logue et al found that the human tongue had specific recep-tors for recognising sweetness which was not true of other tastes. There are also more receptors for recognising sweetness than any other taste which suggests sweet preference have a preferred adaptive ad-vantage which is shaped by genetics and through evolution.

If sweet preference was determined by evo-lution it would be found across cultures which is generally true and supports evolu-

20

tionary explanations. However Stefansson found that Copper Inuits were disgusted at the taste of sugar when they first tried it which undermines evolutionary explana-tions of sweetness being universal through evolution. This could be explained due to a lack of exposure for such sweet foods how-ever from their environment.

Humans do not appear to display an in-nate preference for salt until about the age of 4 months and by age 2 children across cultures appear to show a universal predis-position towards salt. This implies that our preference for salty foods may be a matura-tional preference and our taste buds de-velop to detect salt in time for weaning which would be adaptive as children grow more independent in their food choice at this age allowing them to move away from liquid food diets completely.

Although our evolutionary desire for fat, sugar and salt could be argued to explain why hamburgers, sugary foods and pizzas sell so well it could also be argued that this is a product of advertising, availability and just convenience rather than evolutionary food preferences. Evolutionary theories for food preferences can rarely be conclu-sively proved either way and rely on post-hoc evidence (explaining behavior after its observed through evolution rather than pre-

dicting it before). Due to this Popper ar-gued evolutionary theories that could not be scientifically proven and remain specula-tive lacking validity.

Evidence for preference for meat comes from our study of chimpanzees in Tanza-nia. When coming close to starvation Stan-ford found chimpanzees will kill and eat the most fattiest parts such as the brain and bone marrow of colobus monkey's rather than more tender nutritious flesh. This highlights how our own behavior may have been shaped in the EEA (environ-ment of evolutionary adaptation) and supports explanations for how meat prefer-ence may have formed through lack of vegetation from the environment.

Support for our rejection of bitter tast-ing foods being adaptive comes from a study by Sandell et al. 35 adults were screened to test them for a gene that makes them more sensitive to bitter foods. They then consumed various vegetables some of which contained a mild toxin called Glucosinolates. Those with the sen-sitive version of the gene rated the vegeta-bles containing Glucosinates as 60% more bitter than those with an insensitive form of the gene. This suggests an adaptive abil-ity to detect and avoid toxic foods which would explain why such genes are more

21

widespread supporting evolutionary expla-nations for bitter food avoidance.

However such a study raises serious ethi-cal concerns when patients are being poi-soned (even mildly) as this could cause ad-verse reactions for some putting their lives at risk. It could be argued through a cost-benefit analysis the gains in understanding food preference outweigh the potential costs.

Understanding how taste aversion and preference works has real world applica-tions and can help understand why pa-tients develop an aversion to foods during cancer treatment. Patients have reported developing an aversion to food they con-sumed just prior to chemotherapy and this has resulted in the development of The scapegoat Technique to help patients con-tinue to enjoy their foods after treatment. This involves giving cancer patients a novel food along with something they are familiar with prior to treatment. Results have found patients form an aversion to the novel food instead of the familiar allow-ing them to continue to eat foods they are familiar with. This also explains how adap-tive avoidance of unfamiliar foods occurs to aid in survival when they produce dis-comfort as the body learns to avoid it due to health risks.

Evolutionary explanations for eating prefer-ences align themselves with the nature side of nature vs nurture as they see pref-erences as dictated by biology which is shaped through genes. However a weak-ness of this is nurture is completely ig-nored such as environmental learning and cultural factors which can aect eating be-havior also. Therefore evolutionary theories are deterministic as they assume our genes can completely dictate food prefer-ences as this is clearly not the case. Many people for example enjoy bitter foods or foods that are actually poisonous for us (al-cohol for example). Therefore evolutionary explanations ignore the role of free will and peoples ability for cognitive thoughts in choosing their own taste preferences thus overriding genetic predisposition which clearly is possible.

22

Psychological Explanations For Anorexia Nervosa (AN)

Theory AO1

One explanation for AN is the influence of cultural views of attraction. Within west-ern society beauty is equated to being slim and this western ideal of attraction is be-lieved to contribute heavily towards AN. The media then maintains this through the influence of television, magazines, fashion and celebrity lifestyle all of which consis-tently reinforce this cultural ideal within the population. The constant portrayal of slim models leads people to question their own body types causing them to strive to be thin. Gregory et al found up to 16% of 15-18 year old girls within the UK reported to be dieting. A possible reason for this could be girls internalize culturally defined stan-dards of female beauty which leads to un-happiness over their own body type not matching this ideal and an obsession with dieting and food leads to AN. Research has also found women are more at risk than men and other possible psychological factors that contribute could revolve around low self-esteem, OCD, perfection-ist tendencies or those with high social anxiety. Therefore personality factors may also explain AN through such traits.

Social learning theory can also be used to explain how culture and role-models can influence the onset of AN. Teenagers may observe and pay attention to celeb-rity role models who are extremely thin, re-tain this information and then reproduce this behavior through excessive dieting if they are motivated to do so. Observing models who are famous and rich may lead them to think being thin is what is re-quired to achieve success or even become accepted.

A persons ethnic group appears to also mitigate incidences of AN. Other cultural groups with dierent values that place less emphasis on the need for women to be slim have lower rates of AN. Within non-western cultures and black populations AN is seen to occur much less compared to white western cultures (e.g. Fiji and the Caribbean where there are more positive images of larger bodies)

Peer influences are also believed to play a role towards AN in some cases. Adoles-cents may be more susceptible to peer in-fluences such as disordered eating pat-terns within their group. One study by Eisenberg et al found unhealthy dieting such as the use of dieting pills or purging

23

(vomiting after eating, taking laxatives) was apparent within peer groups suggesting this too could contribute towards the devel-opment of AN.

Peers could contribute towards AN through the teasing of overweight girls or underweight boys. This would reinforce cul-tural ideals of what body types should be like and contribute towards shaping peo-ples attitudes towards food and develop-ing AN.

Bruchs psychodynamic explanation sug-gests AN has its origin within early child-hood and is caused by how parents re-spond to their childs needs. Eective par-ents would recognise their needs and feed them when hungry or comfort them when required. Ineective parents may respond incorrectly to this, comforting them when they needed feeding or feeding them when they required comforting or other needs. Due to this children may grow up confused about their own internal needs causing them to become overly reliant on their par-ents which makes it dicult for them to be-come autonomous when they become ado-lescents as they do not feel in control over their own bodies. The developing of abnor-mal eating patterns and body shape may then be a way for them to exercise control

over themselves which leads to eating dis-orders.

Evaluation - AO2/AO3

Hoek et al found evidence to suggest AN may not actually be caused due to culture undermining this explanation. Research-ers examined the records of over 44000 people admitted over 1987 to 1989 on the Caribbean island of Curacao. Within this culture it was acceptable to be overweight however results found only 6 cases of AN which actually falls within the range of rates reported within westernized coun-tries suggesting cultural influences may not explain this. However methodological problems with this study is it was based on a small sample of one islands inhabi-tants and therefore could be argued to be culturally biased as results may only ap-ply to this group of Carribean people. Also the measurements were only over a small window of 2 years and perhaps a longer timescale could be argued to be needed. This study also lacks external validity and generalisation due to these factors as the measurement of people on this island and its findings may not apply to the wider population. This means we cannot draw firm conclusions on whether culture miti-gates or causes AN.

24



However supporting the role of culture influencing AN, Lai et al found that the rate of anorexia began to increase for Chi-nese residents of Hong Kong as the cul-ture became more westernised suggesting culture does influence AN. However this is based on correllational findings and we cannot infer cause and eect for certain between western culture influencing AN. There may well be other confounding un-known variables such as personality fac-tors or individual dierences that are con-tributing. For example low self-esteem leading individuals to be influenced by western culture as they develop paraso-cial relationships with celebrities.

Medias influence towards AN has sup-porting evidence from Becker et al. Fijan adolescent girls and their eating attitudes and behaviours were examined prior to the introduction of television. Attitudes were seen to shift with a greater desire from them to lose weight and become more like western television characters highlighting how the media may contribute to the on-set of AN indirectly as viewers strive to change their body types. However again personality factors could be a confound-ing variable aecting the DV (attitudes and behaviours) as other explanations sug-gest those with low self-esteem or OCD

traits or obession with perfectionism are more susceptible to influence. Also this study could be argued to lack internal va-lidity as we cannot say for certain that a change in attitude towards image can di-rectly lead to the development of AN. It may well be other factors contribute as many people diet successfully without de-veloping such a eating disorder. Therefore the findings lack external validity when we try to generalise the findings as an ex-planation for how AN may develop.

Explanations that focus solely on culture, media or even psychodynamic explana-tions can also be argued to be reduction-ist and oversimplified as a more complex process beyond simply a single explana-tions appears to be occurring. This is where a combination of processes may be interacting such as media influence, cul-tural attitudes and even personality factors all combining for individuals to develop AN. This is supported by the mere fact not everyone who diets, lives in particular cul-tures or follows celebrity lifestyles develop AN or a eating disorder.

Such psychological explanations focus on the nurture side of the nature v nur-ture argument suggesting it is environ-mental factors that cause AN. However bio-logical explanations put forth a case for

25

neural or genetic causes which suggest na-ture may be the cause. A diathesis stress model may actually better explain how both play a role with some individuals hav-ing the genetic pre-disposition for the disor-der provided sucient environmental trig-gers cause the onset of AN. Therefore this may explain how both approaches (nature and nurture) interact.

Much of the research is also based on fe-males and how AN develops for them. Therefore explanations may suer from gender bias as the same psychological factors that aect women may not neces-sarily explain the onset of AN for men due to them perceiving environmental factors dierently. Therefore these explanations suer from gender bias and may only ex-plain AN developing for women.

26

Biological Explanations For Anorexia NervosaTheory AO1 (Evolutionary Explanation)

One biological explanation for AN is through Guisingers adapted to flee hy-pothesis (AFFH). This is an evolutionary explanation which suggests AN is a symp-tom of behaviours which were adaptive within the environment of evolutionary adaptation (EEA). Within the EEA there would have been prolonged periods of famine causing food restriction requiring hunter-gatherers to migrate in response. Therefore AN would have evolved to help people cope and respond with such envi-ronmental changes. This explains why many AN suerers report hyperactivity de-spite lack of energy. Hyperactivity is ex-plained as a form of migratory restless-ness to allow an increase in activity to aid in migration during food shortage. Within the EEA those who were able to move to areas of greater food availability were most likely to survive and this hyperactivity and denial of starvation would aid in this.

Under normal circumstances when people begin to lose weight biological mecha-nisms would begin conserving energy while increasing hunger however in times of famine or scarce food supply another mechanism is required to aid survival by

turning these biological mechanisms o. This is how AN is explained by Guisinger as she states being able to turn o hunger and provide energy (hyperactivity) in times of need is advantageous for survival to re-spond to such environmental pressures.

Theory AO1

(Neurotransmitter Explanation)

Another biological explanation suggests AN may have a physical cause through neurotransmitter imbalances. Bailer et al examined serotonin disturbances be-tween individuals with AN and binge-eating/purge type behaviours and com-pared them with a healthy control group. The highest serotonin activity was appar-ent within AN suerers and this is believed to suppress appetite and increase anxiety which are characteristics of AN. Therefore higher than normal levels of serotonin activ-ity may trigger anxiety and explain AN.

Another biological explanation into neuro-transmitters looks at dopamine overactiv-ity. Kaye et al compared 10 recovering AN suerers to 12 healthy women using pet scans to measure dopamine activity within the brain. The AN women were found to have overactivity within their dopamine re-

27

ceptors within the basal ganglia which is associated with interpreting pleasure and harm. This part of the brain may aect the way people interpret rewards or pleasur-able activities such as food and eating. Therefore higher than normal dopamine lev-els may explain AN as suerers find it di-cult to associate positive feelings with pleasurable acts such as the consumption of food.

Theory AO1

Hypothalamus dysfunction theory is an-other biological explanation and works on the idea that animals (and people) have a set weight for their bodies. As weight in-creases or decreases the body adapts making adjustments in food regulation to return the individual to this set weight.

The hypothalamus is believed to play a key role in hunger and satiation with the lateral hypothalamus (LH) seen as the feeding switch which turns on eating behaviour while the ventromedial hypothalamus (VMH) is seen as the satiation switch which makes an individual cease feeding. Garfinkel et al suggested it was a dis-turbed hypothalamus which may cause AN through the LH never sending a signal for an individual to eat or the VMH being over-activated with the individual receiving a

constant signal telling them they are full. This would then explain AN through biologi-cal explanations such as brain dysfunc-tion.

Evaluation AO2/AO3

A major problem with evolutionary explana-tions such as Gusinger et als AFFH is they are reliant on post-hoc evidence and drawing conclusions from behavior ob-served after its happened. Therefore this raises methodological problems as it is incredibly dicult to test scientifically to prove or disprove. Popper et al argued theories that cannot be scientifically proven or disproven remain speculative and lack validity as we have no direct evidence for this explanation.

A major weakness of AN being an evolu-tionary adaptation is the condition appears more maladaptive overall than adaptive especially during the harsh conditions of the EEA. AN leaves an individual weak, frail and vulnerable as well as a liability to the group and it seems unlikely any benefit could be achieved from such a weak state if it were adaptive. The basics for survival also become dicult such as hunting for food which is a necessity for all animals and this further undermines evolu-tionary explanations for the disorder. Alter-

28



native psychological approaches such as social learning and cultural explanations appear to oer a better explanation that have more supporting evidence through media influences which further undermines evolutionary explanations.

However twin studies provide strong ge-netic evidence for AN having a biological cause which may have been shaped by evolution. Holland et al examined identical twins (MZ) and non-identical twins (DZ) for AN finding that MZ twins shared much higher concordance rates of the disorder of up to 55% compared to DZ twins who shared only 7%. This provides strength for biological causes for AN however a weak-ness is we cannot be certain this is due to evolution. Another weakness of such find-ings is it also highlights the role nurture and the environment may play as if AN was caused purely by biological factors alone the concordance rates between twins would be 100%. This highlights how psychological and environmental factors clearly play a role too and in fact combine with biological elements for the onset of AN. The diathesis-stress model may bet-ter explain how nature and nurture com-bine with some people having a genetic predisposition for AN (possibly caused by evolution) but then this only being trig-

gered once the right environmental stres-sors are experienced.

A weakness for neurotransmitter re-lated explanations for AN are they are based on correlational findings where we cannot infer cause and eect for cer-tain. Serotonin or Dopamine increase may in fact be a symptom of AN rather than a cause and such explanations and studies lack internal validity as we cannot conclu-sively say either neurotransmitter is the cause for certain but merely present in indi-viduals with AN. Also with Bailer et als study the women were already recover-ing from AN and its impossible to establish whether any serotonin imbalance observed was the cause of AN or a symptom.

Also Kaye et als study into dopamine suf-fers from methodological problems such as gender bias and the fact that it was a small sample. The study focused only on women and we cannot say for certain im-balances in dopamine would be the same for men with AN. Also the sample size was incredibly small meaning we may struggle to generalise the findings to the wider population. For these reasons the studies lack external validity and it may be that they only oer an explanation for AN for women which fall within a small sample

29

range rather than everyone with the disor-der.

Supporting evidence for hypothalamus dysfunction theory comes from research by Brobeck et al. They found if the LH in rats were damaged it lead to a disorder known as aphagia which is a failure to eat when hungry. This provides support for the idea that damage or dysfunction of the hy-pothalamus could lead to reduced eating supporting biological explanations for AN.

Further supporting research comes from Stellar et al who found that stimulating the VMH inhibited feeding which again sup-ports the idea that possible over activation of the VMH could explain AN as this would result in dramatic weight loss.

A weakness of such explanations is they are reductionist in trying to explain a com-plex illness like AN down to one compo-nent such as the hypothalamus while ignor-ing other possible contributing factors such as environmental stressors or dicult life events which is usually seen to result in decreased food intake.

Such biological explanations are also de-terministic in assuming that people have no control over biology or AN which is evi-dently not true as highlighted by Holland

et als study into identical twins. The fact that they share identical genetic makeup yet concordance rates for AN are only 55% highlights the role of free will people have in being able to override their biologi-cal pre-dispositions if they wished and is a major weakness that biological explana-tions cannot account for.

Biological explanations oer the possibil-ity for treatments through drug therapies to bring neurotransmitter levels into bal-ance or even gene replacement therapy opening up possible routes for treating the disorder. Research into biological causes also has real world applications espe-cially in the world of insurance cover for psychiatric conditions. Within the US, AN treatment was restricted as it was not rec-ognised as having a biological cause how-ever research into biological explanations may lead insurance companies to question this assumption in much the same way schizophrenia is accepted as being more biologically determined. This would help open up treatment and cover for possibly millions highlighting the research value for people.

30

Thats It!

Thats all the essays covered! If you find this book helpful be sure to check out my other books on my website here covering the AS and A2 topics:

www.loopa.co.uk/shop

You can also get more free resources (which I am constantly updating over time) here:

http://www.loopa.co.uk/aqa-psychology-revision-resources/

If you have any questions about this book or have spotted an error you can message me here:

[email protected]

I periodically update all the books with mi-nor updates completely free for all those that purchase this book from my website. You can download the new versions from my website by simply logging in to your Loopa account through the My Account tab on my website and re-downloading the book as I replace the old version. It will

likely have v1.1 or v1.2 at the end of the file name signifying an update usually.

The spec is likely to change over time and provided its not a massive change my aim is to keep updating these books to give people the best value.

If you find this book helpful you can follow me here on my Facebook page here where I post all my updates:

www.Facebook.com/aqapsychology

My twitter handle is here if you wish to fol-low me too: https://twitter.com/SajDevshi

Lastly I wish you the best of luck in your ex-ams - if you have any questions you can drop me an email here and I will try my best to answer them:

[email protected]

=)

-Saj

31

Copyright Notice (c)

No part of this book has is to be reproduced, copies, shared, uploaded on the internet or shared without owners consent which is not given. This book is the culmination of many months of work, sourcing, re-writing and structuring essays to help students in their Psy-chology revision. If you found this book helpful, please show your support by encouraging other students to get their own books as this allows future updated versions to be re-leased inline with any spec changes.

If you are a school/college teacher and have found these books helpful ; please encourage your students to purchase their own copies or earn distribution rights for your students by placing a link to the Loopa website (http://www.loopa.co.uk) on your school websites Psy-chology section for other students to refer too.

xxxii

PSYA3-Eating-Behaviours Essay Answers.pdf

Documents

Transcript of PSYA3-Eating-Behaviours Essay Answers.pdf