Motivation and The Brain Paper

Abstract

This paper examines the motivation behind eating healthy within a structure of biological and environmental variables, acting upon the mechanism of choice. The factors of intrinsic and extrinsic are covered as well as the various components of anorexia nervosa and obesity. Also, an analysis of the neurological structures involved in hunger and satiety is included, centering on research concerning hypothalamic lesions in rats.  

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Motivation and the Brain

Motivation is at its core potential in nature, only finding a kinetic outlet when behavior is facilitated. Motivation can be likened to a large boulder being suspended on a hill by the small, wooden peg of choice. The boulder stores only potential energy while withheld on top of the hill, but by acting upon the small, wooden peg of choice motivation can be translated into kinetic energy—behavior (i.e. the boulder rolling down the hill). Achievement motivation theory dictates that incentive value, the attractiveness of an incentive as determined by number or amount, is mediated by the tendency to succeed (Ts) and the tendency to avoid failure (Taf) (Deckers, 2005). The actual inclination to exhibit the potential energy of motivation as the kinetic energy of behavior is the sum of the tendency to succeed and the tendency to avoid failure (Ts + Taf). Thus, the motivation to eat healthily is suspended in potential energy, pending a choice arbitrated by the sum of Ts and Taf, and finding expression as behavior—kinetic energy. Furthermore, important to the discussion of the motivation to eat healthily is the underlying neurological structures involved in the sensation of hunger and satiety, intrinsic and extrinsic factors, and the environmental and biological basis of anorexia nervosa and obesity. 

Neurological Structures of Hunger and Satiety

In the 1930s, 40s, and 50s experiments on rats, concerning lesions to the ventromedial hypothalamus (VMH) and the lateral hypothalamus (LH), seemed to explain the neurological mechanisms of hunger and satiety (Pinel, 2007). It was hypothesized that these areas in the brain acted collectively as an on/off switch (VMH/LH) for the initiation of hunger and the consummation of satiety. Implicated as evidence for this supposed neurological on/off switch were experiments in which bilateral electrolytic lesions to the VMH caused hyperphagia (excessive eating) and lesions to the LH caused aphagia (complete cessation of eating) (Wickens, 2005). However, it was quickly realized that the hyperplasia of rats with lesioned VMH was only temporary, resulting in nothing more than an eventual higher static, set-point body weight. It has been suggested that the new set-point is due to the instrumental role that the VMH and LH play in the regulation of adipose tissue accumulation. It is also necessary to note that lesions to the VMH and LH damage the paraventricular nuclei and the ventral noradrenergic bundle, which contribute to blood glucose management. The VMH and LH seem to regulate adipose tissue concentrations in the body, which in turn moderate the sensations of hunger and satiety through the medium of blood glucose levels. In sum, the hypothalamus regulates the conversion of energy into fat, thereby creating an incentive for increased caloric intake when sections of the hypothalamus are lesioned. Coached in motivational psychology terms, the hypothalamus controls the physiological need for energy, through the psychological drive for hunger, by controlling the rate of fat storage.    

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Intrinsic and Extrinsic Factors

The objective incentive value, or physical properties of an incentive, differs from the utility, the subjective pleasure or usefulness of an incentive, as to the satisfaction rendered. For instance, the economic cost of food does not always translate into increased subjective satisfaction. As an example, a pricey meal at a nice restaurant has a high objective incentive, due to the high price, but might have low utility because it can cause heartburn, indigestion, and weight gain. Therefore, it is important to remember that more expensive food does not always translate into healthier eating. The motivation to eat healthily should be grounded in the utility of food as it pertains to the nourishment of the body, rather than any economic or social advantage. Furthermore, subjectively speaking losses are more dissatisfying than gains are satisfying. As applied to the subject of eating healthy, it is more essential to minimize binge eating, representing a setback or loss, than to maximize progress in dietary inhibition. In this way, frustration from losses can be marginalized affording the opportunity for continued healthy eating habits. All told, the intrinsic factors of utility and the subjective experience of losses and gains defy objective value and actual losses in a way that highlights the significance of perception on motivation. 

Anorexia and Obesity

The motivation behind eating disorders is not always clear but appears to be grounded in a complex interaction between genetic, neurological, hormonal, and environmental factors. For instance, anorexia nervosa has been linked to Type A personality traits—such as anxiety, perfectionism, and rigidity—and androgenic action during puberty (Sohn, 2002). The family environment also seems to have a substantial impact on the inception of anorexia during puberty. Families who report being less supportive and less encouraging of the open expression of feelings are particularly prone to producing adolescents afflicted by eating disorders (Dixon et. al., 1989). It is also necessary to mention that computerized axial tomography (CT) scans of teens exhibiting signs of anorexia show decreased size and functionality of the thalamus, hypothalamus, and other neurological structures (Chowdhury & Lask, 2000). As abovementioned, the hypothalamus plays a critical role in blood glucose levels and adipose accumulation. It is not clear whether food deprivation causes neurological abnormalities or if the abnormality causes food deprivation. Moreover, severe obesity has been directly linked to the fat mass and obesity-associated gene (FTO) in several genome-wide studies (Bouchard & Loos, 2008). These studies have uncovered that those with this risk allele are 1.67 times more likely to suffer from obesity than controls. However, the effect of the environment acting on genetic predisposition cannot be overstated. For instance, Ford (2008) maintains that poor-quality retail food environments in disadvantaged areas, as compared to better quality restaurants in middle and upper-class neighborhoods, contribute to obesity. Hence, the motivation behind eating disorders encompasses a wide range of environmental incentives, psychological drives, and issues of social conformity.  

Conclusion

In conclusion, the neurological structures most implicated in the control of hunger and satiety are the ventromedial hypothalamus (VMH) and the lateral hypothalamus (LH), as evidenced by bilateral electrolytic lesion experiments with rats and hypothalamus abnormalities in anorexia nervosa patients. The motivation behind eating healthy is mediated by environmental factors, such as limited access to better quality food restaurants and family interactions; and biological factors, such as the fat mass and obesity-associated gene (FTO) and androgenic action during puberty. Furthermore, it is more important to limit losses, such as binge eating, than it is to maximize gains, such as lower caloric intake, because cognitively speaking losses loom larger than gains. Also, the utility of food does not always directly correlate to the objective incentive value of the food. Sometimes eating healthy is not about spending more money on better food, it is about parsimoniously allocating funds to the foods that have the highest utility for bodily health. The boulder of motivation, necessary for eating healthy, can only act in conjunction and concurrent with the mechanism of choice, within the aforementioned framework of biological and environmental variables.                              

References

Bouchard, C., Loos, R.J.F. (2008). FTO: The first gene contributing to common forms of human obesity. Obesity Reviews, 9(3), 246-250. Retrieved May 15, 2009, from EBSCOHost Database. 

Chowdhury, U., Lask, B. (2000). Neurological correlates to eating disorders. European Eating Disorders Review, 8(2), 126-133. Retrieved May 15, 2009, from EBSCOHost Database. 

Deckers, L. (2005). Motivation: Biological, psychological, and environmental, Second Edition. Boston, MA: Allyn and Bacon.

Dixon, K.N., Jones, D., Lake, M., Nemzer, E., Sansone, R., & Stern, S.L. (1989). Family environment in anorexia nervosa and bulimia. International Journal of Eating Disorders, 8(1), 25-31. Retrieved May 15, 2009, from EBSCOHost Database. 

Ford, P.B. (2008). Disparities in obesity prevalence due to variation in the retail food environment: Three testable hypotheses. Nutrition Reviews, 66(4), 216-228. Retrieved. May 15, 2009, from EBSCOHost Database. 

Pinel, J.J. (2007). Basics of biopsychology. Boston, MA: Allyn & Bacon.

Sohn, E. (2002). The hunger artists. U.S. News & World Report, 132(20), 44. Retrieved May 15, 2009, from EBSCOHost Database. 

Wickens, A. (2005). Foundations of biopsychology, 2e. Upper Saddle River, N.J.: Pearson Hall.

Paper Topic

  • Resources: Assigned readings, Electronic Reserve Readings, the Internet, and other sources
  • Select one of the following topics as the basis for this paper:
  • Eating healthy
    • Exercising
    • Quitting smoking
    • Quitting drinking
    • Refraining from using drugs
  • Write a 1,050- to 1,400-word paper in which you analyze the brain structures and functions associated with the motivation to engage in your selected behavior.
  • Evaluate the influence of extrinsic and intrinsic factors, including heredity and the environment, on the motivation to engage in your selected behavior.
  • Include at least five references from scholarly, peer-reviewed sources.
  • Format your paper according to APA standards.

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