• Created by: Ikra Amin
  • Created on: 15-01-15 18:14

biological explanations:

  • Genetic
  • Neural
  • Evolutionary


Ventromedial hypothalamus associated with obesity in animals

Lateral hypothalamus associated with satiety in animals 

Ghrelin - hunger 

Leptin - satiety

Neural explanations focus on the role of the hypothalamus, as it is known to regulate eating. Therefore, faulty functioning of the hypothalamus may lead to obesity, especially in terms of the function of the satiety centre, the VMH. Much evidence for the role of the VMH comes from animal studies.

Lashley: after lesions to laterla hypothalamus animals stop eating spontaneously and reverse occured after lesions to VMH - causing rats to over eat.

Stellar: where lateral hypothalamus stimulated by electrodes led to feeding behaviour and ignoring food when VMH stimulated

Positive & negative of animal studies in understanding human obesity: positive; it's better than nothing so suggests ways you can prevent/treat obesity (practical application). negative; can't extrapolate findings from animals to humans (low generalisability)

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neural cont..

The role of the VMH: has also be supported by human studies. Revers and Plum (69) used the case study method, and performed a post mortem of an obese female, to see whethere there were any abnormalities in her brain. they found her VMH had actually been destroyed. (the damage=obese as doesn't know when to stop eating) however, its a case study so cannot generalise. 

Leptin (neural)

Information regarding the role of the VMH itself in humans is limited and further research has focused on the role of leptin in affecting the brain. Leptin is a hormone produced in the stomach which affects the neurones that regulate appetite. It is actually a ‘neuropeptide’, i.e a minute protein encoded by genes, which acts as a chemical messenger. 

One of the neurones leptin is known to have an effect on  is POMC. POMC is important in regulating appetite: Friedman (05) found that obese people do produce leptin, but its ability to suppress POMC is blocked. This means that their appetite remains high and so they eat to a point where their weight meets their genetic  ‘set point’. 

Carlson's study of mice showing role of leptin in obesity: in obesity leptin is not sufficiently produced to block the POMC. Missing leptin gene so obese as they continuously eat and become obese. injecting leptin and they stop eating and weight goes back to normal. 

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  •  is a hormone secreted from the stomach that  was shown by Cummings (2006) to have a direct effect on the hypothalamus.
  • It is secreted in direct proportion to the emptiness of the stomach, with high grehlin secretion being linked to feelings of hunger.
  • Injections of grehlin increase food intake and body weight in both animals and humans (Cummings 2006) and gastric bands reduce grehlin secretion. It therefore seems likely that obesity may be related to over secretion of grehlin.

Yildiz et al (04) found that, for thin people, grehlin levels increase not just as time between meals increases, but also show a general increase throughout the day, in a form of circadian rhythm. They suggest that obese individuals may have a flaw in their circadian rhythm. But there is no direct evidence for this.

A02 eval for neural 

  • reductionist - doesn't consider other factors than the 2 chemicals contributing to an individuals weight and eating behaviour. someone may be obese due to their culture.
  • unclear- not fully understood how ghrelin and leptin work and how they work together or alone
  • availability of food may influence obesity (less food = less likely to be obese) (LEDC's)
  • cognitive factors (we think when to eat and what we eat) therefore deterministic as it disregards our free will of our thoughts
  • animal research - low generalisability

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Genetic explanation

People may inherit a propensity to become obese: family studies certainly indicate a strong relationship between body mass of parents and their children. Garn et al found the following:

 1 obese parent = 40% chance child also being obese

2 obese parents = 80%

2 thin parents = 7% 

^ AO1

However, as with all family studies, the environment is also very similar (a02), therefore separated twin studies, and adoption studies  have been conducted with the following results (a02):

  •  Stunkard et al (90)  found genetic factors accounted for 66-70% of the variance in BMI of 93 pairs of MZ twins reared apart (ao1)
  • The relationship is stronger for low BMI than for high BMI however. (ao2)
  • Stunkard et al (86)  performed an adoption study of 540 adult adoptees, and found a strong relationship between weight category of the adoptee and their biological parents (thin, median weight, overweight, obese) but no relationship with the adoptive parents weight. The relationship was stronger with the biological  mother than with the biological  father. (ao2)
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Certain genes have been identified as associated with obesity:

  •  Frayling et al (07) found people with two copies of the fat mass can obesity gene FTO, had a 70% increased risk of becoming obese, while people with only one copy, had a 30 % risk (ao1)
  • if parents eat unhealthy children may too so become obese because of that (ao2)
  • although this shows a genetic component to obesity it also demonstrates the FTO gene is not the only cause of obesity. the increase isnt 100% it's onlu 70%. this suggests there's other factors (e.g. environmental) which would trigger the fat mass gene.


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evolutionary explanations

  • explains how storing fat and gaining weight would have been adaptive to ancestors and now we still do it even though we know obesity leads to many negative health effects

this area has been dominated by the 'thirfty gene' hypothesis originally proposed by neel (1962). neel suggested that in our ancient history genes which enabled us to get fat were advantageous because they facilitated the deposition of fat during periods between periodic famines. individuals that had such genes and were fat had sufficient energy resources to survive the famines, and therefore passed their fat deposition genes 'thrifty genes' to their offspring. in modern society however, these genes become disadvantageous because they prepare us for a famine that never comes and the result is widespread obesity and associated health risks. the 'thrifty gene' hypothesis has been weidely reiterated in many recent publications as a key factors causing obesity. 

support for the evolutionary explanation comes from DiMeglio & mates (00) who found that Ps given liquid calories rather than an equal amount of solid calories put on more weight, presumably as we haven’t evolved to cope with high calorie liquids, which didn’t exist in the EEA (other than breast milk).

Similarly, Bray et al (04) looked at the consequences of the huge increase in intake of a popular drinks sweetener, high-fructose corn syrup. Its consumption in the US increased by 1000% between 1970 and 1990; as a foodstuff we haven’t evolved to cope with it appears not to stimulate leptin, leading to weight gain.


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thrifty gene flaws: 

  • famines are too infrequent, have acted for too short a period and involve insufficient mortality to select for genes that predispose for obesity
  • there's no evidence that fat people survive famines better than thin people, and in fact mortality actually falls mostly on groups such as the very young and very old where differential mortality in relation to body composition is very unlikely
  • observations of modern hunter-gatherer populations don't indicate that in periods between famines they fatten up- and hence suggest they have not inherited thrifty genes 
  • fails to explain why so many people remain thin

considering weaknesses ^ an alternative theory, the "drifty gene hypothesis" has been put forward. this is based on the idea that early humans were under predation pressure. this probably meant that ancestral humans had a body weight regulation system that prevented them becoming too thin to avoid starvation risk, but also prevented them becoming too fat to avoid predation risk. the environment occupied by early hominids changed dramatically about 2 million years ago with the emergence of the homoerectus. homoerectus was social, invented fire and weaponry. these 3 factors removed predation risk, allowing the genes regulating the upper limits of our body weight to randomly drift - the 'drifty gene' hypothesis. some people would stay the same, some would drift down, but some would drift up, therefore some people would remain thin and others would gain weight. 

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BEHAVIOURIST explanation for obesity 

suggests some people may be obese because:

  • operant and classical conditioning
  • children copy parents eating behaviour (they may eat unhealthy food) social learning theory
  • cues associated with eating (tv and snacking)
  • fatty food/high calorie food given as treat when upset and tastes better so you enjoy it (operant)

behaviourism suggests 3 means by which obesity may occur:

  •   Classical conditioning: eating becomes associated with other behaviours, (often behaviours that are routine) and so the behaviour leads to eating when we are not hungry, eg snacking while watching TV. (Remember the success of the ‘Do Something Different’ non-diet diet!)
  • Operant conditioning: obesity is related to the use of food as a reward (high calorie food given as reward and tastes nice)
  • Social learning theory: Obesity is due to observing and imitating obese role models, in particular people we identify with in some way.


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evidence for behavioural explanation

Classical conditioning: It is clear that people can learn to associate food with other stimuli and such associations can then lead to excessive eating. The Fletcher et al  ‘do something different’ study shows how breaking such habitual associations prevents overeating, and so leads to weight loss, even for people who are not actually dieting.

Operant conditioning: People can turn to food and eat excessively through ‘comfort eating’ and using food as a reward, as seen in the Wansink et al (2008) study.  However, operant conditioning alone cannot explain obesity, as we know there are biological factors which affect how rewarding certain foods are. Most appropriate IDA for this point: incomplete explanation

Operant conditioning techniques have been very successful in reinforcing healthy eating practices. Devlin & Yanovski (95) found Ps  on a such a programme had an average weight loss of between 15 and 20 pounds after 5 months on the scheme. Presumably, such a technique would only work if conditioning is related to obesity. However, this notion,  that a treatment’s   effectiveness  means the underlying cause is revealed has been termed the treatment aetiology fallacy, as this is not necessarily the case. For eg, operant techniques are very effective in shaping the behaviour of schizophrenics, even though the cause of SZ is likely to be a genetic vulnerability paired with an environmental trigger.


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social learning theory (still same explanation)

If SLT is valid, we would expect a relationship to exist between parents weight and children’s weight as parents are such important role models. In fact, the relationship between obesity levels of parent and child is very strong, but of course this could be due to genetic reasons. Therefore we need to look at other models for eating behaviour and obesity, for eg peer groups.

 Christakis and Fowler (07), looked at whether there could be link between obesity and social networks – specifically, if someone in your social circle gains weight are you more likely to gain weight too

They proposed having obese social contacts might change a person's tolerance for being obese or might influence his or her adoption of specific behaviours that affect weight (e.g., smoking, eating, and exercising).

 Christakis and Fowler used data from the Framingham heart study, evaluating  a network of 12,067 people who underwent repeated measurements over a period of 32 years. Christakis and Fowler examined the existence of clusters of obese persons within the network, the association between one person's weight gain and weight gain among his or her social contacts, and the dependence of this association on the nature of the social ties (e.g., ties between friends of different kinds, siblings, spouses, and neighbours), and the influence of sex, smoking behaviour, and geographic distance between the contacts

A person's chances of becoming obese increased significantly (by 57%) if he or she had a friend who became obese in a given interval. Among pairs of adult siblings, if one sibling became obese, the chance that the other would become obese increased by 40%. If one spouse became obese, the likelihood that the other spouse would become obese increased by 37%. These effects were not seen among neighbours in the immediate geographic location. People  of the same sex had relatively greater influence on each other than those of the opposite sex, as SLT would predict

therefore this study suggests that a person has an increased chance of becoming obese if a friend becomes obese. if one persn someones close to or related to becomes obese the other does too. 

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2nd psychological explanation


From AS notes:

  • stages in childhood (oral, phallic, anal) 
  • conscious, preconscious, subconscious
  • ID, Ego, Supergo
  • childhood and early experiences

freud proposed adult problem behaviour is due to unresolved conflicts occuring during childhood development through the pscyhosexual stages. this might apply to over eating:

  • fixation in oral stage leads to over eating
  • ID is in control, wants fatty food
  • bad expereiences in childhood so you overeat - comfort food

Clearly the psychodynamic explanation will view obesity as being related to either emotional deprivation, or overindulgence during the oral stage, when the libido is fixated on the mouth. The adult personality is then characterised by oral gratification.

Oral gratification comes from smoking, nail biting and of course, eating. This gratification acts as compensation for negative experiences and can function as a way of

If this explanation is valid we would expect to find two things:

  • Ø  Obese people will share underlying childhood traumas
  • Ø  Psychodynamic therapy will be effective in tackling obesity


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psychodynamic theory proposes that behavious is determined by the unconscious mind. we are therefore not actually aware of the driving forces underlying our behaviour.

3 structures of the unconscious:

  • ID - works on the pleasure principle and is concerned with gratifying needs , e.g. hunger
  • Ego - works on the reality principle, realise we cannot have all our needs immediately gratified
  • Supergo - operates on morality priniciple, we no longer want to gratify certain needs if doing so has negative effects on others

these structures of develop in childhood - a babys unconscious is essentially all ID; ego develops at 2 and superego at 5. for 'normal' psyche, the ego will be dominant.

whether or not behaviour is normal depends on how children develop through psychosexual stages. the source of pleasure for the ID alters through these stages; 

oral 0-18 monts; gratification comes from oral satisfaction

anal stage 18-36 months etc

A01: relation to obesity : as food is a source of pleasure, over eating is thought to show oral fixation 

oral fixation is due to a lack of gratification in the oral stage OR over gratification, therefore either could lead to obesity. AO1

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research has focused n problems in childhood, or lack of gratification, leading to overeating as a substitue for affection. 1 particular issue is that of childhood neglect or abuse (both physical and sexual) with psychodynamic theorists proposing food is used to substitute for sexual satisfaction. people who have been sexually abused may avoid sexual interaction, or receive less gratification from sex, and therefore more vulnerable to using food as sexual substitution. 

grant and boersma (2007) conducted two 90 min interviews with 11 p's enrolled on a hospital weight loss programme, involving attendance at a support group. there were 7 females an 2 males.

interviews were information and conversational, and designed to elicit information about family an childhood experiences that may have impacted on attitudes to food. 

there were 2 main findings:

  • where parents had used food to control the childm the children learned that food is a tool that can be used for purposed other than physical nourishment. they would then use it to 'rebel, numb or sooth emotional pain'
  • adult loneliness was a key issue. some ps had experienced being brought up in a warm, nurturing environment where family mealtimes were associated with a sense of belonging. adult loneliness then led to ps turning to food as early memories of warmth, nurturing, belonging and human connection..were recreated with food and emotional hunger was misinterpreted as physiological hunger. abused ps were using food to numb the pain they had experienced, but again were over eating due to loneliness.  so basically people who live alone tend to be more obese as no ones there with them but remembering childrennhood they ate with family so now eat more for a substitute. 
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other research found link between childhood abuse and obesity.

rohde et al 2008 found child sexual abuse to be associated with a doubling of the odds of obesity in a telephone sample of 4631 women. although this is a gynocentric sample, similar findings have occurred with research involving both genders. e.g;

williamson et al (02) surveyed 13000 people with 66% reporting some form of abuse (before 18 yrs of age) from the following types of abuse:

  • verbal
  • physical
  • fear of physical abuse
  • sexual

there was a strong association found between experience of abuse and risk of obesity. obesity increased with a number and severity of each type of abuse.

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Kiesewetter et al (10) investigated Ps who volunteered to enrol in a year long weight reduction programme, part of which involved psychoanalytic interactional group therapy sessions (12 sessions, 60 – 90 minutes long). In this type of therapy, the therapist is active and does give advice. A repeated measure design was used; there was no control group.

Kieswetter differentiated between securely and insecurely attached Ps (54% vs 46% of the sample respectively). They proposed insecurely attached Ps would be using food due to an increased need to re-experience denied relationships from childhood, which were now impossible to reshape: these patients’ food intake is a substitute for relationship experiences and food is used to avoid social dependency.

Support for this comes from the observations that nearly all such Ps revealed a long lasting emotional deprivation experience in childhood. Many showed signs of repressed anger and Kieswetter suggested that the acts of chewing and swallowing represented this anger. 

However, one problem with the study is that although the programme was successful, with significant weight loss seen (judged as 5% loss), there was no significant difference in weight loss found between securely and insecurely attached Ps, as had been predicted.

insecure-avoidants may not be helped by such therapy as they 'avoid' relationships. insecure resistant more likely to be obese. Indeed, the programme involved multiple components, for eg, engagement in sport, medical attention, and cooking lessons. It is therefore impossible to say which factor was most important.

difficult to draw conclusions from this study because: insecure attached more prone to obesity and also retrospective data - experimenter doesn't know how good your attachment was it is subjective and lowers validity support for this explanation

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