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  • 1. Biological explanations of eating behaviour Neural mechanisms and eating behaviour From a biological perspective, eating behaviour is usually referred to as ingestive behaviour which serves to maintain homeostasis via negative feedback. Homeostatsis:The mechanisms by which biological variables are regulated within defined limits.This is the Idea that the body is constantly striving to achieve an optimal physiological state (e.g. temperature/ satiety) Negative feedback:Assumption that any given bodily variable has a set point (or range) and the actual value of this variable is compared by the body to where it should be and adjusted accordingly. For example the 'lipostatic hypothesis' and the 'gluclosatic hypothesis' which suggest that when our fat stores are depleated or blood gluglose levels are low, we feel hungry, which makes us eat Resent evidence has indicated that a number of neural mechanisms are associated with eating; for example, the hypothalamus (including the paraventrial hypothalamus and the perifornical area) and neurotrasmitters (catecholamines, serotonin and peptides). Hypothalamus: Research into the role of neural areas associated with eating behaviour has indicated that the hypothalamus plays a significant role. Early research suggested that the hypothalamus was central to food intake: Medial hypothalamus- ‘satiety centre’: Activate when you are full to stop eating Lateral hypothalamus- ‘feeding centre’: Active when you are hungry to start eating More recent research has indicated, however, that there is a more complex system involving: • ParaventricularHypolthalamus/ Nucleus- Increases eating behaviour • Perifornical Area- Reduces eating behaviour Neurotrasmitters: Central to both the simple and more complex models are a number of neurotransmitters which are regarded as key to our understanding of the neurological basis of eating behaviour. These neurotransmitter pathways are situated in the central nervous system and the peripheral nervous system. These neurotransmitters are the catecholamines, serotonin and peptides.
  • 2. Neurotransmitters that increase food intake: 1. Norepinephrine (NE): This neurotransmitter is a catecholamine, and has been found to influence eating behaviour if injected into areas of the hypothalamus. If injected into the paraventricular nucleus, NE stimulates eating behaviour. If injected into the perifornical area, NE reduces eating behaviour. Leibowitz (1986) found that NE increases calorie intake, and increases the desire for carbohydrates 2. Neuropeptide Y: This neurotransmitter is a peptide, which is found in high concentrations in the paraventricular nucleus and the perifornical area. Research has found that when rats are injected with Neuropeptide Y, they will continue to consume large amounts of food, even if they are already ill. This suggests that they may be being driven to eat by the hedonic/ pleasurable qualities of the food, rather than a physiological need to eat. Leibowitz (1986) found that Neuropeptide Y increases the preference and desire for carbohydrates. 3. Galanin: This neurotransmitter is particularly found in the paraventricular hypothalamus Leibowitz (1986) injected Galanin into rats and found that it increased food intake and caused a preference for fats rather than carbohydrates. Neurotransmitters that decrease food intake: Rowland et al (1996) found that a number of neurotransmitters decrease food intake: 1. Cholecystokinin (CCK): This is a peptide which is released into the blood stream during meals If injected into rats, CCK causes a reduction in appetite and satiation. It also suppresses weight gain. 2. Corticotropin-releasing hormone (CRH): This is a peptide which is produced in the paraventricular hypothalamus. CRH has been found to reduce food intake. 3. Serotonin (5HT): Has been linked to suppressed appetite and reduced food intake. This could explain why patients with depression have a suppressed appetite and often lose weight, as they have higher levels of serotonin than is considered normal. Neurotransmitters, therefore, seem to function by either increasing or decreasing food intake. The role of neurotransmitters has also been investigated through research on the impact of drugs on eating behaviour.
  • 3. The impact of drugs on eating behaviour: If we understand the ways in which particular drugs make us want to eat more or less, and also how these drugs affect our brains, we can begin to comprehend how the chemicals in our brains influence what, how and when we eat and stop eating. 1. Nicotine-Has been found to decrease food intake Influences the activity of the neurotransmitter Acetylcholine Smokers generally weigh about seven pounds less than non-smokers (US Dept of Health and Human Services, 1990) Ogden and Fox (1994)- some dieters use smoking as a weight-loss strategy Ogden (1994)- Smoking cessation may result in increased consumption of calories (particularly from sweet foods) 2. Amphetamines-Amphetamines act on the catecholamines and some on serotonin pathway Have been found to have an impact on subjective hunger and food intake (Silverstone and Kyriackides, 1982).Have been used legally and illegally by dieters to increase success of diets 3. Alcohol- Hollister (1991) found that alcohol influences eating behaviour in different ways Looked at research into the effect of alcohol on eating behaviour and found that it sometimes increases food intake and sometimes deceased food intake Evaluation of neural explanations of eating behaviour: Reflection of people’s experience: People generally start eating when they are hungry and stop eating when they become full Insight into brain chemicals: Practical applications: medical / neurological treatments for eating disorders (e.g. obesity) could be suggested if they increase/ decrease eating behaviour Explanation of some differences: Explains why some people with different disorders or medical problems may eat more or less food than others Lab based research (involving animals): Although the research is controlled (IV and DV can be controlled), much of the research has been conducted on animals which reduces the generalizability of the findings Influence of social factors and social drives: Doesn’t explain why people eat differently in different situations, or why people eat in some situations when there is no physiological drive to eat Physiological drives can be overridden: Other factors play a role in how much food a person consumes (e.g. a desire to be thin will reduce the amount of food an individual consumes). People don’t just stop eating because they are full In summary: It has been suggested that the catecholamine, serotonin and peptide pathways influence eating behaviour in the following ways: The serotonin pathway: Influence feelings of fullness (satiety) during a meal, causing the person to stop eating. Catecholamines: Influence satiety between meals, thereby triggering hunger and determining the intervals between eating. Peptides: Influence the reward and pleasurable (sometimes referred to as ‘hedonic’) properties of food (Blundell et al, 1989).
  • 4. Ao3: This approach is reductionist because it assumes that all aspects of eating behaviour can be explained by biology (neurological factors) This approach argues from the nature perspective, as it assumes that eating behaviour is influenced by biological mechanisms rather than social or environmental cues This approach argues that eating behaviour is determined by physiological factors, meaning that the individuals eating behaviour is controlled by factors other than their own free will(in this sense it is deterministic) This approach is parsimonious as it explains eating behaviour from one point of view and ignores other possibilities such as psychological or environmental factors