Discuss Factors Leading to Overeating and Obesity
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Factors that lead to obesity are split into 2 main areas – nature and nurture. Nature and nurture can be argued for almost everything that exists today: for example, our behaviour, actions, and appearance. Nurture can be seen as cognitive thoughts on dieting and societys views on our food preferences, while nature is the biological theory of breaking down overeating to neurons and chemicals in our body, as well as evolutionary theories that suggest obesity is due to our mal-adaptation of eating environments.
Evolutionary factors suggest that obesity is the maladaptive product of changes that took place in the environment of evolutionary adaptation thousands of years ago. Food preferences and eating habits have developed so that we are advised to eat high fats, carbohydrates, sugars and so on, that contribute to our daily survival. But as these adaptive behaviours thousands of years ago meets the needs and society of today, the same mechanism becomes maladaptive and may lead to obesity.
If this evolutionary explanation of eating behaviour is correct, then such behaviour is universal, present in young children before cultural or social learning takes place, which can be mirrored in the animal kingdom. A study that shows such preferences are universal is the Eskimo study by Bell (1973), in which sweet foods were introduced to an Alaskan community previously lacking them. Sweets were not rejected, and a preference was shown to be developed, proving that eating behaviour is not learnt, but innate. This supports the evolutionary theory because we have a “built in” system where we have a liking for sweet foods, and everyone around the world is the same, and culture does not affect our preferences for foods.
The liking for calorie snacks seems to be innate and therefore passed down through genes from our ancestors. This is seen in the study by Birch and Deysher (1985) in which preschool children learn to eat smaller meals of a taste associated with a high calorie snack and larger meals of low calorie associated tastes. This study supports evolutionary explanations because preschool children (2-4yrs) are too young to understand nutrition, so the associations they have with high calorie and low calorie snacks must be inherited from our ancestors.
Nature has given us preferences for different foods that may help us survive, as we can see in the Alaskan study, as well as the preschool children study. Preferences from our ancestors have also decided the amount of calories or sugar that we need to feel full. However, all these studies can be criticised because they do not take into account different cultures and environments. It also rejects the idea of free will, as we can choose what we want to eat normally, not just high sugar/fat foods. Furthermore the theory can be criticised in general because it is reductionist since it is based on adaptation and mal-adaptation, but has nothing to do with our social changes. It can also be deterministic because we can choose our diet, or can go against our diets, but does not take into account that we have a limited number of choices.
Although there are some elements of our eating behaviour that may be due to adaptation, it does seem likely that there are other, more individualised, factors which explain why some people become obese and others do not. This leads to the other naturalistic case of obesity caused by biological forms, such as different neurons, hormones and brain structures.
Biological psychologists suggest that obesity is the product of different neurons and brain structures that make us who we are. They say that food preferences and eating habits developed to promote survival such as binge eating, as it is a basic survival instinct that we are born with. Hunger is activated by signals in our brain, such as homeostasis, in which mechanisms exist to detect imbalances in the equilibrium of our body, whether it is sugar levels, water, temperature etc.
Studies done on rats led to discovery of the role of the hypothalamus in obesity. The neurotransmitter NPY was injected to the hypothalamus to trigger eating behaviours (Wickens 2000). The eating behaviour was shown even when the rats were full, but on the other hand, eating behaviour is also produced by abdominal fat (Yang et al 2008) creating a vicious circle effect, thus showing that eating behaviour is only partially down to the neurotransmitters in the brain.
The role of leptin proteins has also been investigated in rats. Obese rats seem to have defective genes for producing leptin, which is responsible for weight loss. When injected with leptin, obese rats seem to lose weight rapidly. Ghrelin is another hormone that is produced under stress, which seems to boost appetite, hence the binge “comfort eating” that some people have. But both the hormones can be dismissed as partial theories that could be possible, as we can cognitively over ride these signals by dieting and choosing whether we want to eat or not.
Brain areas involved in are the amygdala, and the inferior frontal cortex. The amygdala is involved in food selection which stops us from eating novel foods, thus avoiding the risk of obesity. Rolls & Rolls 1973 did an experiment where they removed the amygdala from rats, resulting in the rats eating anything that is given to them. The inferior frontal cortex gets messages from the olfactory system (smell) where if damaged, shows a reduction in eating behaviours (Kolb & Whishaw 2006).
A study that showed the spatial awareness networks in our limbic system is the Krispy Kreme study (Mohanty et al, 2008). Participants were split into 2 groups, one fasted for 8 hours, the other ate as many doughnuts they could (up to 8). MRI scans were made while participants viewed images of doughnuts or screwdrivers (as far from food as possible). Eaters hunger centres did not activate on doughnut images, so they didnt show food seeking behaviours. This shows that the centres only activate when necessary, not automatically, suggesting that we do not eat every time we pass a bakery, even if it is attractive. This also explains why everything becomes a food cue when were hungry, but ignored when we are full.
This theory does not take into the account how