Health consequences of obesity/Bibliography: Difference between revisions
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(DHEAS)), estrogens (estrone and estradiol), sex hormone-binding globulin (SHBG), IGF-I and IGF- | (DHEAS)), estrogens (estrone and estradiol), sex hormone-binding globulin (SHBG), IGF-I and IGF- | ||
binding protein (IGFBP)-3, and the relationship between sex steroids, IGF-I and IGFBP-3..") | binding protein (IGFBP)-3, and the relationship between sex steroids, IGF-I and IGFBP-3..") | ||
#Bianchini F, Kaaks R, Vainio H. Overweight, obesity, and cancer risk. "Lancet Oncology." 3:9:565-574 | |||
("In addition to an increase in the risk of cardiovascular disease and type II diabetes, the evidence summarised here shows that excess body weight is directly associated with risk of cancer at several organ sites, including colon, breast (in postmenopausal women), endometrium, oesophagus, and kidney. In part, these associations with cancer risk may be explained by alterations in the metabolism of endogenous hormones-including sex steroids, insulin, and insulin-like growth factors-which can lead to distortion of the normal balance between cell proliferation, differentiation, and apoptosis. Avoidance of weight gain thus seems to be an important factor for cancer prevention..") | |||
==Primary Research Papers== | ==Primary Research Papers== | ||
#Terao S. ''et al.'' (2008) Inflammatory and injury responses to ischemic stroke in obese mice. Stroke, Journal of the American Heart Association. 39:943-950. The adhesion of leukocytes and platelets in cerebral venules, blood– brain barrier permeability, brain water content, and infarct volume were measured in wild-type, obese (ob/ob), and leptin-reconstituted ob/ob mice subjected to 30 minutes middle cerebral artery occlusion and reperfusion. Obesity worsens the inflammatory and injury responses to middle cerebral artery occlusion and reperfusion by a mechanism independent of leptin deficiency. Monocyte chemoattractant protein-1 appears to contribute to the exaggerated responses to ischemic stroke in obese mice. | #Terao S. ''et al.'' (2008) Inflammatory and injury responses to ischemic stroke in obese mice. Stroke, Journal of the American Heart Association. 39:943-950. The adhesion of leukocytes and platelets in cerebral venules, blood– brain barrier permeability, brain water content, and infarct volume were measured in wild-type, obese (ob/ob), and leptin-reconstituted ob/ob mice subjected to 30 minutes middle cerebral artery occlusion and reperfusion. Obesity worsens the inflammatory and injury responses to middle cerebral artery occlusion and reperfusion by a mechanism independent of leptin deficiency. Monocyte chemoattractant protein-1 appears to contribute to the exaggerated responses to ischemic stroke in obese mice. |
Revision as of 13:25, 12 October 2009
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Review Articles
- Magni P. et al. (2009) Feeding behavior in mammals including humans. Ann.N.Y.Acad.Sci. 1163:221-232. PMID 19456343
- Gaal L.F.V. et al. (2006) Mechanisms linking obesity with cardiovascular disease. Nature. 444:875-879. PMID 17167476 (“Obesity increases the risk of cardiovascular disease and premature death. Adipose tissue releases a large number of bioactive mediators that influence not only body weight homeostasis but also insulin resistance — the core feature of type 2 diabetes — as well as alterations in lipids, blood pressure, coagulation, fibrinolysis and inflammation, leading to endothelial dysfunction and atherosclerosis.”)
- Kopelman P.G. (2000) Obesity as a medical problem. Nature. 404:635-642. PMID 10766250
- Mathew B. et al. (2008) Obesity: effects on cardiovascular disease and its diagnosis. J Am Board Fam Med. 21:562-568. PMID 18988724 (“The higher prevalence of cardiovascular disease in obese individuals is indirectly mediated, to a large extent, by the increased frequency of various well known risk factors like hypertension, diabetes, and dyslipidemia, either individually or as part of the metabolic syndrome. However, there are several ways in which obesity directly affects the cardiovascular system; these will be discussed in detail.”)
5. Scott, K.M. et al. (2008). Obesity and Mental Disorders in the General Population: Results from the World Mental Health Surveys. Int J Obes, 32(1) 190-200. This paper reports on a globally-diverse study using 3rd world countries as well as developed, and identifies moderate associations between obesity and mental disorders (depressive and anxiety). In addition demographic variables such as sex, age and education are considered as mediators of any obesity-mental disorder relationship. Results show the associations to be strongest among those who are severely obese, and female (in the latter, statistical significance was reached in NZ and Lebanon). Results reveal differences between the countries, for example, in the US and Belgium there is a significant moderating role of education on the obesity-depressive disorder relationship, which is not seen elsewhere.
6. Puhl, R.M. (2007). Stigma, Obesity and the Health of the Nation’s Children. Psychological Bulleting, 133(4): 557-580. This paper focuses on childhood obesity, and the emotional and physical health consequences attached to the social stigma of obesity. Psychosocial and physical health consequences are also examined to investigate how they mediate negative health outcomes. The authors identify self-esteem, depression, body dissatisfaction and interpersonal relationships as the main psychosocial consequences.
7. Simon, G.E. (2008). Association between obesity and depression in middle-aged women. Gen Hosp Psychiatry, 30(1):32-39. This study focuses solely on American middle-aged females and reports a strong and consistent association between depression and obesity within this sub-group population. This study therefore lends support to Scott et al. (2008).
8. Rivenes, A.C. et al. (2009). The relationship between abdominal fat, obesity and common mental disorders: Results from the HUNT study. Journal of Pyschosomatic Research, 66:269-275. This extremely recent study uses a community-based sample and identifies abdominal fat distribution as the key mediator in the obesity-depressive disorder relationship. Further still, this study relates these findings to a hypothesis that links obesity and depression to metabolic disturbances involving the HPA axis.
9. Mather, A.A. et al. (2009). Associations of obesity with psychiatric disorders and suicidal behaviours in a nationally representative sample. Journal of Psychosomatic Research. 66:277-285. This Canadian study positively relates obesity with several lifetime psychiatric disorders (including depression, mania, panic attacks, social phobia, agoraphobia without panic disorder), any anxiety disorder, suicidal ideation and suicide attempts. Most of these associations were specific to women but some were present in men.
- Haslam, D.W. and James, W.P (2005) Obesity. Lancet. 366:1197-1209.
("Excess bodyweight is the sixth most important risk factor contributing to the overall burden of disease worldwide. 1·1 billion adults and 10% of children are now classified as overweight or obese. Average life expectancy is already diminished; the main adverse consequences are cardiovascular disease, type 2 diabetes, and several cancers. The complex pathological processes reflect environmental and genetic interactions, and individuals from disadvantaged communities seem to have greater risks than more affluent individuals partly because of fetal and postnatal imprinting.") This paper provides a brief overview of the various effects of obesity on an individual's health.
- Lukanova A, Lundin E, Zeleniuch-Jacquotte et al. (2004) Body mass index, circulating levels of sex-steroid hormones,IGF-1, and IGF binding protein-3: a cross-sectional study in healthy women. "Eur J Endocrinol." 150: 161-171.
("Excess weight has been associated with increased risk of cancer at several organ sites. In part, this ef fect may be modulated through alterations in the metabolism of sex steroids and IGF-I related peptides. The objectives of the study were to examine the association of body mass index (BMI) with circulating androgens (testosterone, androstenedione and dehydroepiandrosterone sulfate (DHEAS)), estrogens (estrone and estradiol), sex hormone-binding globulin (SHBG), IGF-I and IGF- binding protein (IGFBP)-3, and the relationship between sex steroids, IGF-I and IGFBP-3..")
- Bianchini F, Kaaks R, Vainio H. Overweight, obesity, and cancer risk. "Lancet Oncology." 3:9:565-574
("In addition to an increase in the risk of cardiovascular disease and type II diabetes, the evidence summarised here shows that excess body weight is directly associated with risk of cancer at several organ sites, including colon, breast (in postmenopausal women), endometrium, oesophagus, and kidney. In part, these associations with cancer risk may be explained by alterations in the metabolism of endogenous hormones-including sex steroids, insulin, and insulin-like growth factors-which can lead to distortion of the normal balance between cell proliferation, differentiation, and apoptosis. Avoidance of weight gain thus seems to be an important factor for cancer prevention..")
Primary Research Papers
- Terao S. et al. (2008) Inflammatory and injury responses to ischemic stroke in obese mice. Stroke, Journal of the American Heart Association. 39:943-950. The adhesion of leukocytes and platelets in cerebral venules, blood– brain barrier permeability, brain water content, and infarct volume were measured in wild-type, obese (ob/ob), and leptin-reconstituted ob/ob mice subjected to 30 minutes middle cerebral artery occlusion and reperfusion. Obesity worsens the inflammatory and injury responses to middle cerebral artery occlusion and reperfusion by a mechanism independent of leptin deficiency. Monocyte chemoattractant protein-1 appears to contribute to the exaggerated responses to ischemic stroke in obese mice.