Motivation and emotion/Book/2016/Eating disorders and motivation: Difference between revisions
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==Overview== |
==Overview== |
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Understanding |
Understanding the motivations to eat is complex and involves both short- and long-term biological factors as well as psychological and environmental factors, but what motivates people to do the opposite? What motivates an individual to impose rigid restrictions on their eating to the point where they are essentially not eating at all? What drives a person to go on a food binge, consuming overly large amounts of food in a small period of time? These are actions carried out by many people suffering from eating disorders, which is an increasing issue in today's society, with much of the research focused on the treatment of eating disorder. However, the first step should be in understanding the motivation behind the development of an eating disorder and how that motivation can be turned around to aid in its treatment. This chapter will introduce the current theories on why we eat and what motivates a range of eating disorder to develop. |
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==Why do we eat?== |
==Why do we eat?== |
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The body has certain biological needs which, when fulfilled, allow people to function and maintain '''''[[w:Homeostasis|homeostasis]]'''''. One such need is hunger. Unlike some other needs (e.g., thirst and sex), hunger is more motivationally complex (Weingarten, 1985). To understand hunger three factors must be considered: short-term appetite, long-term energy balance and cognitive-social-environmental factors (Weingarten, 1985). |
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=== Short-term appetite === |
=== Short-term appetite === |
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Short-term appetite is explained by the '''''glucostatic hypothesis'''''. The glucostatic hypothesis states that hunger occurs when blood-sugar levels drop, |
Short-term appetite is explained by the '''''[https://www.ncbi.nlm.nih.gov/pubmed/19002144 glucostatic] hypothesis'''''. The glucostatic hypothesis states that hunger occurs when blood-sugar levels drop, causing feelings of hungry and wanting to eat (Campfield, Smith, Rosenbaum, & Hirsch, 1996). Once enough food has been consumed to increase blood-glucose levels back to the required levels, hunger decreases and feelings of satiety take over (Campfield, et al., 1996). |
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=== Long-term energy balance === |
=== Long-term energy balance === |
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Long-term energy is monitored via |
Long-term energy is monitored via fat cells within the body (Cummings et al., 2002). According to the '''''[[citizendium:Lipostatic_hypothesis|lipostatic]] hypothesis''','' as masses of fat stored within the body drop below its homeostatic balance, fat (adipose tissue) releases hormones into the bloodstream causing hunger, and in turn, as fat stores reach or go above homeostatic levels satiety takes place (Cummings et al., 2002). |
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=== Set-point theory === |
=== Set-point theory === |
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An alternative to the lipostatic hypothesis is '''''set-point theory'''''. Set-point theory argues that each individual has a different biologically determined "fat thermostat" which has set-points to determine energy levels. Hunger is produced by declines in energy levels with satiety being reached once energy levels are at or above the set-point (Pinel, Assanand, & Lehman, 2000). |
An alternative to the lipostatic hypothesis is '''''[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2990627/ set-point] theory'''''. Set-point theory argues that each individual has a different biologically determined "fat thermostat" which has set-points to determine energy levels. Hunger is produced by declines in energy levels with satiety being reached once energy levels are at or above the set-point (Pinel, Assanand, & Lehman, 2000). |
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Set-point theory dominates much of the current literature and is often the preferred view taken by health professionals, despite a strong lack of evidence supporting its major predictions (Pinel, Assanand, & Lehman, 2000). |
Set-point theory dominates much of the current literature and is often the preferred view taken by health professionals, despite a strong lack of evidence supporting its major predictions (Pinel, Assanand, & Lehman, 2000). |
||
=== Positive incentive theory === |
=== Positive incentive theory === |
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'''''Positive incentive theory''''' suggests that the primary inducement of hunger and eating is the positive incentive value food holds. People are driven to eat by the anticipation of pleasure eating will provide (Pinel, Assanand, & Lehman, 2000). |
'''''[https://www.verywell.com/the-incentive-theory-of-motivation-2795382 Positive incentive] theory''''' suggests that the primary inducement of hunger and eating is the positive incentive value food holds. People are driven to eat by the anticipation of pleasure eating will provide (Pinel, Assanand, & Lehman, 2000). |
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=== Cognitive-social-environmental factors === |
=== Cognitive-social-environmental factors === |
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Other motivations for eating included time of day, stress, sight and smell of food, and the taste of food itself. Eating is often a social experience and frequently occurs with other people, for example: catching up with friends at a cafe, family gatherings (religious holidays, family dinners, parties etc.). This does not mean, however, that the only time we eat is when we socialise or when we are hungry. |
Other motivations for eating included time of day, stress, sight and smell of food, and the taste of food itself. Eating is often a social experience and frequently occurs with other people, for example: catching up with friends at a cafe, family gatherings (religious holidays, family dinners, parties etc.). This does not mean, however, that the only time we eat is when we socialise or when we are hungry. |
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Phan and Chambers (2016) surveyed 198 people about their motivations for eating and found that the main drive for eating meals (breakfast, lunch and dinner) was a combination of need (hunger), convenience, habits, and price. They also found that dinner differed slightly from breakfast and lunch motivations in that people were often driven to have dinner to provide variety within their diet and to be social. Snacking was also looked at in the survey |
Phan and Chambers (2016) surveyed 198 people about their motivations for eating and found that the main drive for eating meals (breakfast, lunch and dinner) was a combination of need (hunger), convenience, habits, and price. They also found that dinner differed slightly from breakfast and lunch motivations in that people were often driven to have dinner to provide variety within their diet and to be social. Snacking was also looked at in the survey with results showing that motives for daytime snacking revolved around health and weight control, whereas late night snacking was purely for pleasure (Phan & Chambers, 2016). Food preference is also a major drive for our eating behaviors with many people initially driven to high sugar and fat content foods which are highly prevalent in developed countries today (Berridge, 2009). |
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[[File:Peanut Butter, The Binges.jpg|thumb|''Figure 1''. Eating disorders are characterised by patterns of disturbance in eating or eating related behaviours.]] |
[[File:Peanut Butter, The Binges.jpg|thumb|''Figure 1''. Eating disorders are characterised by patterns of disturbance in eating or eating related behaviours.]] |
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Revision as of 01:21, 12 January 2017
What motivates eating disorders?
Overview
Understanding the motivations to eat is complex and involves both short- and long-term biological factors as well as psychological and environmental factors, but what motivates people to do the opposite? What motivates an individual to impose rigid restrictions on their eating to the point where they are essentially not eating at all? What drives a person to go on a food binge, consuming overly large amounts of food in a small period of time? These are actions carried out by many people suffering from eating disorders, which is an increasing issue in today's society, with much of the research focused on the treatment of eating disorder. However, the first step should be in understanding the motivation behind the development of an eating disorder and how that motivation can be turned around to aid in its treatment. This chapter will introduce the current theories on why we eat and what motivates a range of eating disorder to develop.
Why do we eat?
The body has certain biological needs which, when fulfilled, allow people to function and maintain homeostasis. One such need is hunger. Unlike some other needs (e.g., thirst and sex), hunger is more motivationally complex (Weingarten, 1985). To understand hunger three factors must be considered: short-term appetite, long-term energy balance and cognitive-social-environmental factors (Weingarten, 1985).
Short-term appetite
Short-term appetite is explained by the glucostatic hypothesis. The glucostatic hypothesis states that hunger occurs when blood-sugar levels drop, causing feelings of hungry and wanting to eat (Campfield, Smith, Rosenbaum, & Hirsch, 1996). Once enough food has been consumed to increase blood-glucose levels back to the required levels, hunger decreases and feelings of satiety take over (Campfield, et al., 1996).
Long-term energy balance
Long-term energy is monitored via fat cells within the body (Cummings et al., 2002). According to the lipostatic hypothesis, as masses of fat stored within the body drop below its homeostatic balance, fat (adipose tissue) releases hormones into the bloodstream causing hunger, and in turn, as fat stores reach or go above homeostatic levels satiety takes place (Cummings et al., 2002).
Set-point theory
An alternative to the lipostatic hypothesis is set-point theory. Set-point theory argues that each individual has a different biologically determined "fat thermostat" which has set-points to determine energy levels. Hunger is produced by declines in energy levels with satiety being reached once energy levels are at or above the set-point (Pinel, Assanand, & Lehman, 2000).
Set-point theory dominates much of the current literature and is often the preferred view taken by health professionals, despite a strong lack of evidence supporting its major predictions (Pinel, Assanand, & Lehman, 2000).
Positive incentive theory
Positive incentive theory suggests that the primary inducement of hunger and eating is the positive incentive value food holds. People are driven to eat by the anticipation of pleasure eating will provide (Pinel, Assanand, & Lehman, 2000).
Cognitive-social-environmental factors
Other motivations for eating included time of day, stress, sight and smell of food, and the taste of food itself. Eating is often a social experience and frequently occurs with other people, for example: catching up with friends at a cafe, family gatherings (religious holidays, family dinners, parties etc.). This does not mean, however, that the only time we eat is when we socialise or when we are hungry.
Phan and Chambers (2016) surveyed 198 people about their motivations for eating and found that the main drive for eating meals (breakfast, lunch and dinner) was a combination of need (hunger), convenience, habits, and price. They also found that dinner differed slightly from breakfast and lunch motivations in that people were often driven to have dinner to provide variety within their diet and to be social. Snacking was also looked at in the survey with results showing that motives for daytime snacking revolved around health and weight control, whereas late night snacking was purely for pleasure (Phan & Chambers, 2016). Food preference is also a major drive for our eating behaviors with many people initially driven to high sugar and fat content foods which are highly prevalent in developed countries today (Berridge, 2009).
What is an eating disorder?
An eating disorder is characterised by a disturbance in eating or eating related behaviour resulting in altered food intake, which significantly impairs physical health and psychological well being (American Psychological Association, 2013). The Diagnostic and Statistical Manual of mental disorders 5 (DSM-5, 2013) currently lists a range of eating and feeding disorders (see Table 1). Anorexia Nervosa, Bulimia Nervosa and Binge-Eating Disorder are the most common out of all the eating disorders and are diagnosed mostly in females (Sharan & Sundar, 2015). Eating disorders have a lifetime prevalence between 0.9% and 3.5% depending on the disorder (Sharan, & Sundar, 2015). The etiology of eating disorders is very complex and involves a range of factors including biological, psychological and environmental.
| Eating Disorder | Definition |
|---|---|
| Pica | The eating of one of more nonnutritive, nonfood substance on a regular basis over a period of at least one month. |
| Rumination Disorder | The repeated regurgitation of food after feeding or eating over a period of at least one month. |
| Avoidant/Restrictive Food Intake Disorder | Avoidance or restriction of food intake manifested by clinically significant failure to meet nutrition requirements or insufficient energy intake through oral intake of food. |
| Anorexia Nervosa | Persistent restriction of energy intake, intense fear of gaining weight or of becoming fat, persistent behaviour that interferes with weight gain (e.g. excessive exercise, purging) and a disturbance of self perceived weight or shape. |
| Bulimia Nervosa | Three essential features: recurrent episodes of binge eating, recurrent inappropriate compensatory behaviours to prevent weight gain, and self-evaluation that is unduly influenced by body shape and weight. |
| Binge-eating Disorder | Recurrent episodes of binge-eating that must occur on average, at least once per week for three month. |
| Other Specified Feeding or Eating Disorder | Presentation of symptoms characteristic of an eating disorder that cause clinically significant distress or impairment in social, occupational, or other important areas of functioning but do not meet the full criteria for any of the above listed feeding or eating disorders. Used when the clinician does want to specify why the full criteria are not met. |
| Unspecified Feeding of Eating Disorder | Applies to presentations of symptoms characteristic of feeding or eating disorder that cause clinically significant distress but do not meet the full criteria for any of the above eating disorders and the clinician does not want to specify the reason why the full criteria are not met. |
(American Psychological Association, 2013)
Drive behind an eating disorder
Many eating disorders such as anorexia nervosa are marked by strict eating restrictions and excessive exercise, but how does one go from eating for a biological drive and social or environmental factors listed to eating on an incredibly restricted diet or not eating at all?
The etiology of eating disorders, especially anorexia nervosa, are very complex involving biological, psychological, and environmental factors. They are still not fully understood, with much of how they develop still being debated today (Sharan & Sundar, 2015). Certain personality traits such as perfectionism, rigidity, and being rule-bound have frequently be found as risk factors for the development of eating disorders. The influences from the media which place a high value on slenderness, with most beauty icons being thinner than the average person and magazines publishing articles on weight loss saw a rise in eating disorders among young women in the later half of the 20th century, with these 'ideals' held by many Western countries now being a main precipitating factor in the development of eating disorders (Keating, 2010; Pinel, Assanand, & Lehman, 2000).
Biological Perspectives
The current biological perspective on eating disorders states that "Eating disorders represent a distortion and overriding of the normal neuro-biologically regulated eating behaviours in response to the continued drive for thinness and a fear conditioning about normal weight" (Sharan & Sundar, 2015, p. ). Bergh and Sodersten (1996) suggested that eating disorders develop because it is initially rewarding for sufferers to eat less food and the behaviour then becomes maintained through conditioning to situations which provide them with positive rewards. Berridge and colleagues (2010) expanded on Bergh and Sodersten's (1996) theory, stating that eating disorders are caused by reward dysfunction, an overactivation or suppression of some parts in the brain which causes an excessive liking (in terms of binge-eating behaviour) or an excessive disliking (in terms of food restriction) in food. This view on eating disorder continues to gain traction, since people with eating disorders, especially anorexia, have been found to have a greater degree of anhedonia - the reduced capacity to experience reward or pleasure (Keating, 2010).
Positive Incentive Theory
Linking into theories of reward dysfunction is positive incentive theory, which centers around the positive incentive value of food, driving people to eat because of the anticipated pleasure they will receive through eating. It stems from reward dysfunction with the pleasure usually received from eating (reward) causing us to want to eat more and from the more recent desire we have for our food to look and taste appealing (Berridge, 2009).
In eating disorders, positive incentive theory suggests that eating declines as a consequence of a decline in positive incentive value. This is especially seen in the presence of palatable food when the positive incentive value is no longer sufficient to motivate consumption (Pinel, Assanand, & Lehman, 2000). This theory is often overlooked with eating disorder motivation because many sufferers show a high level of interest in food itself - frequently talk and thinking about food and will often prepare it for others. However, positive incentive value for interacting with food does not equal positive incentive value of eating food itself (Pinel, Assanand, & Lehman, 2000).
Self-determination Theory
Another theory proposed for the motivation behind eating disorders is self-determination theory. This theory is often used to explain a patient's motivation to change in the treatment of eating disorders but may also be flipped to explain why they develop. In self-determination theory, a number of different forms of motivation are in play.
Controlled motivation
Controlled motivation is the external reasons a person has to change, which are environmentally influenced. For example: expectations held by others (the media, family and friends), rewards, and punishments.
Introjected motivation
Introjected motivation reflects feelings of guilt, shame, anxiety, and internal compulsions about one's body image and self-esteem.
Autonomous and Intrinsic motivations
Autonomous motivation refers to the personal values and commitment displayed by sufferers to maintain their disordered eating behaviours. Intrinsic motivation relates to the individual's enjoyment, pleasure, and interests which may also influence their choices in their eating disorder behaviour.
All these different types of motivation combine together to develop and maintain the individual's eating disorder behaviour, reinforcing itself as it continues and creating a stronger drive for thinness (Keating, 2009; Vansteenkiste et al., 2005).
Summary
- Our bodies have a biological drive for eating based on feelings of hunger and satiety using complex mechanisms to maintain homeostasis.
- Three main factors should be considered in the motivation for eating: short-term appetite, long-term energy balance, and environmental factors.
- The glucostatic hypothesis explains short-term appetite as motivation for eating caused by increases and decreases in blood glucose levels.
- The lipostatic hypothesis explains motivation for eating as trying to maintain levels of fat stores for long term energy releases.
- Set-point theory argues that each person has individual biological set-points which maintain homeostasis by motivating hunger when energy levels fall below the set-points within bodily systems.
- Positive incentive theory explains the main drive for eating is from the anticipated pleasure of eating food.
- A variety of cognitive, social, and environmental factors need to be considered for eating motivations.
- Eating disorders are marked by disorder eating behaviour which results in altered food intake, significantly impacting physiological and psychological health and well-being.
- Motivation behind eating disorders is just as complex as motivation for eating itself and constitutes psychological, biological, and environmental factors.
- Biological perspectives on eating disorder development emphasise reward dysfunction in certain areas of the brain.
- Positive incentive theory states that eating disorders are the result of a decrease in the positive incentive value of food.
- Self determination theory is made up of different forms of motivation (controlled, introjected, autonomous, and intrinsic motivations) which interplay to develop and maintain eating disorders.
Glossary
Homeostasis: the body's tendency to maintain a stable internal state.
Glucostatic hypothesis: hunger occurs when blood-sugar levels drop.
Lipostatic hypothesis: masses of fat stored within the body drop below its homeostatic balance, fat (adipose tissue) releases hormones into the bloodstream causing hunger.
Set-point theory: hunger is produced by declines in energy levels with satiety being reached once energy levels are at or above the set-point.
Positive incentive theory: the primary inducement of hunger and eating is the positive incentive value food holds.
Eating disorder: a disturbance in eating or eating related behaviour resulting in altered food intake, which significantly impairs physical health and psychological well being.
Etiology: the cause, set of causes, or manner of causation of a disease or condition.
Reward dysfunction: an overactivation or suppression of some parts in the brain which causes an excessive liking (in terms of binge-eating behaviour) or an excessive disliking (in terms of food restriction) in food.
Self-determination theory: concerned with the motivation behind choices people make without external influence and interference.
See also
- Anorexia nervosa and extrinsic motivation (Book chapter, 2016)
- Eating disorder recovery and Mmotivation (Book chapter, 2014)
- Self determination theory (Book chapter, 2011)
References
Bergh, C., & Sodersten, P. (1996). Anorexia nervosa, self-starvation and the reward of stress. Nature Medicine 2(1), 21–22
Berridge, K. C. (2009). 'Linking' and 'wanting' food rewards: Brain substrates and roles in eating disorders. Physiology & Behaviour, 97, 537-550. http://dx.doi.org/10.1016/j.physbeh.2009.02.044
Berridge, K. C., Ho, C., Richard, J. M., & DiFeliceantonio, A. G. (2010). The tempted brain eats: Pleasure and desire circuits in obesity and eating disorders. Brain Research, 1350, 43-64. http://dx.doi.org/10.1016/j.brainres.2010.04.003
Campfield, L. A., Smith, F. J., Rosenbaum, M., & Hirsch, J. (1996). Human eating: Evidence for a physiological basis using a modified paradigm. Neuroscience and Behavioural Reviews, 20, 133-137.
Cummings, D. E., Weigle, D. S., Frayo, R. S., Breen, P. A., Ma, M. K., Dellinger, E. P., et al. (2002). Plasma ghrelin levels after diet-induced weight loss or gastric bypass surgery. New England Journal of Medicine, 246, 1623-1630.
Keating, C. (2010). Theoretical perspective on anorexia nervosa: The conflict of reward. Neuroscience and Biobehavioral Reviews, 34, 73-79. http://dx.doi.org/10.1016/j.neubiorev.2009.07.004
Phan, U. T. X., & Chambers, E. (2016). Application of an eating motivation survey to study eating occasions. Journal of Sensory Studies, 31, 114-123. http://dx.doi.org/10.1111/joss.12197
Pinel, J. P. J., Assanand, S., & Lehman, D. R. (2000). Hunger, eating and ill health. American Psychologist, 55(10), 1105-1116. http://dx.doi.org/10.1037//0003-066X.55.10.1105
Sharan, P., & Sundar, A. S. (2015). Eating disorders in women. Indian Journal of Psychiatry, 57(2), 286-295. http://dx.doi.org/10.4103/0019-5545.161493
Vansteenkiste, M., Soenens, B., & Wandereycken, W., (2005). Motivation to change in eating disorder patients: a conceptual clarification on the basis of self-determination theory. International Journal of Eating Disorders, 37(3), 207–219.
Weingarten, H. P. (1985). Stimulus control of eating: Implications for a two-factor theory of hunger. Appetite, 6, 387-401.