Obesogenic environment/Bibliography: Difference between revisions
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<ref>Dallman M, Pecorano N, Akana S, La Fleur S, Gomez F, Houshyar H, Bhatnagar S, Laugero K and Manalo S. (2003) Chronic stress and obesity: a new view of "comfort food." PNAS (100): 11696-701.</ref> | <ref>Dallman M, Pecorano N, Akana S, La Fleur S, Gomez F, Houshyar H, Bhatnagar S, Laugero K and Manalo S. (2003) Chronic stress and obesity: a new view of "comfort food." PNAS (100): 11696-701.</ref> | ||
Another paper looking at the link between chronic stress and an increase in the consumption of “comfort food.” This paper attempts to apply some of the results found in experiments on rats to the human obesity epidemic. The main comparisons are made to eating disorders and depression rather than the general population. | Another paper looking at the link between chronic stress and an increase in the consumption of “comfort food.” This paper attempts to apply some of the results found in experiments on rats to the human obesity epidemic. The main comparisons are made to eating disorders and depression rather than the general population. | ||
[[User:Helen Martin|Helen Martin]] 12:00, 22 October 2011 (UTC) | |||
<ref>FossB, Drystad SM. (2011) Stress in obesity: cause or consequence? Med Hypotheses (77): 7-10.</ref> | |||
<ref>Seckl J. prenatal glucocorticoids and long term programming.(2004) European journal of endocrinology.(151):49-62</ref> | |||
<ref>Drake A and Reynolds R. Impact of maternal obesity on offspring obesity and cardiometabolic disease risk.(2010) Reproduction.(140): 387-398.</ref> | |||
<ref>Reynolds R et al. Stress responsiveness in adult life: Influence of mother’s diet in late pregnancy.(2007) The journal of clinical endocrinology and metabolism. (92): 2208-10.</ref> | |||
Revision as of 06:00, 22 October 2011
Helen Martin 11:48, 22 October 2011 (UTC)
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[1] An interesting article commenting on whether the changes in our behavior towards diet and physical activity are some of the reasons why obesity is such a rising problem within our society. In terms of diet, the composition and effect of dietary fat is discussed, the availability of energy dense foods which are generally high in fat and whether reporting of percentage of calories coming from fat is being underreported. The effect of physical activity as a protective mechanism countering the effects of a energy dense diet as a solution to the obesity epidemic, however this doesn’t really address the environment. In terms of environment, the authors suggest tackling obesity to start with prevention, thus targeting children to instill a healthy attitude towards food.
[2] This article suggests obesity is a product of a ‘normal response, by normal people, to an abnormal situation.’ Tackling obesity requires multiple approaches, the most successful and cost effective possibly being public health approaches which need to be widely implemented in order to have an impact on obesity.
[3] An in depth overview of the literature on obesity, looking into the composition of diet, calorie consumption and how this can be targeted by policies. The difficulties of imposing strict diet controls on obese people and the defense of the body to weight loss are all explored within this comprehensive overview.
[4] The classical view of the stress HPA axis is that the stress hormone, cortisol, negatively feeds back on the pituitary and hypothalamus to reduce its activity, thus limiting the stress response. However, from experiments done on rats it seems that these stress hormones may have an excitatory effect on these higher centres when the rat suffers chronic stress. This indicates that it may cause increased ingestion of “comfort food,” defined as food high in carbohydrate and fat, causing weight gain.
[5] Another paper looking at the link between chronic stress and an increase in the consumption of “comfort food.” This paper attempts to apply some of the results found in experiments on rats to the human obesity epidemic. The main comparisons are made to eating disorders and depression rather than the general population. Helen Martin 12:00, 22 October 2011 (UTC) [6] [7] [8] [9]
Wardle, J et al. (2008) Evidence for a strong genetic influence on childhood adiposity despite the force of the obesogenic environment. American Journal of Clinical Nutrition, Vol. 87, No. 2, 398-404.
Hinde, S. et al. (2005). Changing the obesogenic environment: insights from a cultural economy of car reliance. Transportation Research Part D: Transport and Environment Volume 10, Issue 1, Pages 31-53.
- ↑ Hill J and Peters J. (1998) Environmental contributions to the obesity epidemic. Science Mag. (208):1371-75
- ↑ Rutter H. (2011) Where next for obesity? Lancet. (378):745
- ↑ Swinburn B, Sacks G, Hall K, Finegood D, Moodie M and Gortmaker S. (2011) The global obesity pandemic: shaped by global drivers and local environments. Lancet (378): 804-14.
- ↑ Pecorano N, Reyes F, Gomez F, Bhargava A and Dallman M. (2004) Chronic stress promotes palatable feeding which reduces signs of stress: feedforward and feedback effects of chronic stress. Endocrinology (145): 3754-62.
- ↑ Dallman M, Pecorano N, Akana S, La Fleur S, Gomez F, Houshyar H, Bhatnagar S, Laugero K and Manalo S. (2003) Chronic stress and obesity: a new view of "comfort food." PNAS (100): 11696-701.
- ↑ FossB, Drystad SM. (2011) Stress in obesity: cause or consequence? Med Hypotheses (77): 7-10.
- ↑ Seckl J. prenatal glucocorticoids and long term programming.(2004) European journal of endocrinology.(151):49-62
- ↑ Drake A and Reynolds R. Impact of maternal obesity on offspring obesity and cardiometabolic disease risk.(2010) Reproduction.(140): 387-398.
- ↑ Reynolds R et al. Stress responsiveness in adult life: Influence of mother’s diet in late pregnancy.(2007) The journal of clinical endocrinology and metabolism. (92): 2208-10.