Eating Behaviour - Food Preferences

  • Created by: KPountney
  • Created on: 22-03-18 12:15
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  • Eating Behaviour - Food Preferences
    • Evolutionary Explanations
      • Taste Aversion
        • We are genetically hard-wired to learn taste aversions that make us less likely to eat food that has gone bad or is toxic.
      • Neophobia
        • The reluctance to try new or unusual foods (innate). This is most pronounced in childhood between the ages of 2 and 6 years when they are exploring their environment.
          • Research to Support - Heritability of Neophobia - Knoapia (2007) - Measured food neophobia using the food neophobia scale questionnaire in a sample of 468 adult female twin pairs (211 MZ and 257 DZ) - The heritability estimate for food neophobia in this sample was found to be 67% - This suggests that two thirds of the variation in food neophobia is genetically determined - This lends support to the view that neophobia evolved among human beings because it protected them from potentially harmful food.
      • Preference for Sweet Food
        • In the EEA (Environment of Evolutionary Adaption) one source of sugar and therefore high in calories was ripe fruit which is high in fructose (a source of fast-acting energy) characterised by a sweet taste. Fruit provides vitamins and minerals that were very valuable to our ancestors so it would have been adaptive for them to develop a preference for sweet tasting food.
    • Social Learning Theory
      • Parental Influences
        • SLT emphasises the impact that observing other people (models) has on our own attitudes and behaviour. Other people often include parents with the implication here that children acquire their eating behaviour through modelling their parents' eating behaviour. Parental attitudes to food inevitably affect children as they control the foods bought and served in the home
        • Brown and Ogden report consistent correlations between parents and their children in terms of snack food intake, eating motivations and body dissatisfaction Parents may also manipulate the availability of certain foods as a reward; for example, the use of sweets or fatty foods as a treat for good behaviour. They may also use one food as a reward for eating another "you can't eat any ice cream unless you eat your fruit first." According to Birch et al, this is not a useful strategy as the preference for food used as a reward increases, the preference for the disliked food actually decreases.
          • Evaluation - Limitations of research into parental influences - Research in area is quite limited. Studies are typically on a small scale and carried out on a highly selective sample of white Americans.
      • Peer Influences
        • Other important influences in children are their peers (people of equal status), with research showing that children will model the eating behaviour of other children around them.
        • Birch arranged for participant children to be placed at school lunchtimes next to 3 or 4 other children who had different vegetable preferences from them. After 4 days, the participant children had changed their preferences more than the non-participant (they switched from carrots to peas or vice versa) in response to observing the other children. This change was still evident after several weeks.
    • Cultural Influences
      • Cultural Norms/the Context of Meals
        • A powerful cultural influence on food preference is what is seen as 'normal' eating behaviour within a culture. According to Rozin, cultural influences are the single most reliable predictor of food preference, such as family eating patterns. This is because, culture determines the food we put on the table and what our children are exposed to.
          • For example, what constitutes a 'proper' meal for the older generation in the UK is 'meat and two veg' and there is a general rule that the main meal on a Sunday is a roast dinner.
        • Also in societies such as the UK and USA, grazing and the desire for convenience food are increasingly common. As a result, reliance on takeaway food has become the norm for some people.
      • Media Effects
        • As children get older, models outside of the family become more important. A clear example of this is TV advertising as even children watching a moderate amount of TV will be exposed to numerous adverts, which are aimed at them. For example, foods which are linked to fun-related themes or promoted by characters which children can identify with.
        • In more recent years, the media has been used to educate people about more healthy ways to eat which take account of personal circumstances such as income. For example, Jamie Oliver has led campaigns about eating healthily aimed at the less-educated British public.
        • Research Support for Media Influence - Boyland et al. (2013) - Exposure to food advertising on TV influences on food preferences and actual food intake in children. However, they found that it influences children of different weight statuses differently with adverts for foods high in fat, salt and sugar having a strong influence on obese and overweight children.
        • Real-world Application: Implications of Media Influence on food preference - Obesity in children increases with the more hours they spend watching TV.
    • Neural Mechanisms in Eating and Satiation
      • The role of the Hypothalamus
        • Humans along with animals are homeostatic - they maintain balance. In terms of eating, homeostasis means detecting the state on the internal environment (e.g. whether the body has enough nutrients) and also correcting this to restore balance. The body has evolved two separate systems - one to turn eating 'on' - the lateral hypothalamus (LH) - and the other for turning it 'off' - the ventromedial hypothalamus (VMH).
          • Glucose levels are monitored and play a key role in activating these systems. Hunger increases as glucose levels decrease. A decline in the level of glucose activates the lateral hypothalamus resulting in feelings of hunger. This causes the individual to eat, which causes glucose levels to rise again. This rise in glucose activates the ventromedial hypothalamus which leads to satiation which in turn inhibits further eating.
            • Research on the LH - 1950's - Found that damage to the LH in rats caused them to stop eating (aphagia). The refused to eat and would starve to death unless force-fed. They also found that stimulation of the LH brings about feeding behaviour. This led to the belief that they found the 'on' switch for eating behaviour.
              • Furthermore, a neuro-transmitter called Neuropeptide Y (NPY) found in the hypothalamus is of particular importance. When injected into rats, they immediately began feeding, even when they had already eaten. Stanley (1986) found that repeated injections of NPY into the hypothalamus caused rats to become obese in a very short period of time.
                • Commentary on the role of the LH - Damage to the LH also causes a decrease in other behaviours, such as thirst and sex, so it is not exclusive to hunger. Further research suggests that eating behaviour is controlled by neural networks throughout the brain, not just in the hypothalamus. This implies that although it clearly plays a role, the LH may not be the brains 'eating centre.'
                • Commentary on the role of NPY - Recent research  suggests that NPY's normal function is not to do with eating behaviour. In support of this, Maine et al bred mice that did not produce NPY and did not find a decrease in their eating behaviour. It is more probable that the abnormally high levels of NPY injected in experiments stimulates hunger which is not usually produced by normal levels of the neuro-transmitter.
            • Research on the VMH - Found that damage to the VMH caused rats to overeat leading to hyperhagia. They also showed a preference for sweet tasting food, with some rats experiencing a 400% increase in body weight. Stimulation of this however, leads to inhibited feeding. This supports the belief that the VMH acts as an 'off' switch for eating and is responsible for satiation.
              • Commentary - Supported by research on humans that showed damage to the VMH which resulted in obesity. However, Gold found that damage to the VMH alone did not cause over-eating - only when other parts of the brain were also damaged (most notably the PVN). Despite this, Gold's research is not replicable.
      • The role of Leptin
        • In order for our body to control food intake and maintain a fairly constant weight, the hypothalamus needs to receive signals about body fat amount. It is thought that Leptin is the hormone responsible for this as it is released by fat cells around the body, travelling in the blood to the hypothalamus where it acts as a satiety signal. The more fat stored = the more Leptin = less eating.
          • Research Evidence - Experiments on mice - Some mice have 2 copies of the obesity gene and these ob/ob mice tend to over-eat foods high in fat and sugar. Zhang found that these mice also have defective genes for the production of Leptin, but that when injected with it they lose weight dramatically. This is because leptin sends messages to the brain about being full, so a lack of it can lead to over-eating.
            • Supported by research on humans, that shows that people lacking the Leptin gene are obese but will lose weight when given Leptin injections. However, high levels of Leptin do not always decrease hunger and most people with obesity do not have a problem producing it. It is clear that Leptin plays a role in controlling hunger but it may be more complex than first thought. For example, it could be more to do with genetic sensitivity, in that some people have fewer Leptin receptors, meaning that the message about being full is not getting to the brain.
      • The role of Ghrelin
        • Ghrelin is a hormonal marker of how long since we have last eaten. Known as the 'the hunger hormone,' its role in appetite control was noted when it was discovered that when injected into to the bloodstream of rats, food intake was stimulated. Produced in the stomach and pancreas, Ghrelin stimulates the appetite with the purpose of increasing the intake of food and promoting the storage of fat. So when Ghrelin levels are high, we feel hungry. After we eat, Ghrelin levels fall and we feel satisfied.
          • Research to Support the role of Ghrelin in appetite control - Wren et al. (2001) - Found that given intravenously, Ghrelin caused a  short-term increase in the amount of food eaten.

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