Health consequences of obesity/Bibliography

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A list of key readings about Health consequences of obesity.
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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.”)

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.

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.

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).

Rivenes, A.C. et al. (2009). The relationship between abdominal fat, obesity and common mental disorders: Results from the HUNT study. Journal of Psychosomatic 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.

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.)

Bianchini F, Kaaks R, Vainio H. (2002) 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.")

Bates G.W, Whitworth N.S. (1982) Effects of obesity on sex steroid metabolism" 35:(12):893-6. PMID: 7174771 (" This study was designed to compare plasma andorgens in obese, anovulatory women with non-obese, ovulatory women. The aouthors found a statistically significant increase in plasma androstenedione and testosterone in obese, anovulatory women.")

Bray G.A. (1997) Obesity and reproduction" 12: (1) 26-32. (" Obesity produces a variety of alterations in the reproductive system and, similarly, manipulations of the hypothalamic-pituitary gonadal axis produces changes in food intake, body weight and fat ditribution. This review focuses on the relationship between obesity and reproduction.")

Purohit A, Reed MJ. Regulation of oestrogen synthesis in postmenopausal women. Steroids 2002: 67; 979-983 ("The decrease in ovarian estrogen production that occurs at the menopause may lead to an increase in peripheral aromatase activity. Understanding the role of endogenous estrogen metabolites in regulating estrogen synthesis may give rise to new strategies for the prevention or treatment of breast cancer.")

Simpson ER. Role of aromatase in sex steroid action. Journal of Molecular Endocrinology (2000);25: 149-156 ("Our understanding of the role of oestrogens in both males and females have expanded greatly in recent years. Considerable emphasis has been placed on the regulation of extragonadal oestrogen biosynthesis, in particular that which occurs in adipose tissue.")

Hammoud AO, Gibson M, Peterson CM et al. Obesity and Male Reproductive Potential. Journal of Andrology: 27; 619 – 625 ("It is believed that with increasing prevalence of sedentary life styles and dietary changes, obesity is emerging as an important cause of adverse health outcomes, including male infertility. Findings suggest a possible link between life style changes, obesity, semen quality and possibly male ferility.")

Lukanova A, Lundin E et al. Body mass index, circulating levels of sex steroid hormones, IGF-1 and IGF-binding protein-3: a cross-sectional study in healthy women. European Journal of Enodcrinology 2004; 190: 161-171

Metwally M, Li TC, Ledger L. The impact of obesity on female reproductive function. Obesity Reviews 2007; 8: 515-523 (" A more and more women become obese, the reproductive problems associated with obesity present an ever-growing challenge to physicians involved in their fertility care. We aim to discuss the impact of obesity on the various aspect of females reproductive function with focus on clinical aspects of fertility problems in obese women.")

Key TJ, Pike MC. The dose-effect relationship between ‘unopposed’ oestrogens and endometrial mitotic rate: its central role in explaining and predicting endometrial cancer risk. British Journal of Cancer 1988: 57; 205-12 ("The "unopposed estrogen hypothesis" for endometrial cancer maintains that risk is increased by exposure to endogenous or exogenous estrogen that is not opposed simultaneously by a progestagen, and that this increased risk is due to the induced mitotic activity of the endometrial cells. ")

Strauss JF, Dunaif A. Molecular Mysteries of Polycystic Ovary Syndrome. Molecular Endrocinology 1999: 13; 800-805 ("Polycystic ovary syndrome (PCOS) is the most common endocrine disorder of women of reproductive age, affecting from 5–10% of women in this age group. Insulin resistance and pancreatic ß-cell dysfunction, both independent of obesity and unrelated to the actions of androgens on insulin dynamics, are strongly associated with PCOS (3, 4). Physicians have only recently come to appreciate the potential long-term consequences of PCOS, which include type 2 diabetes mellitus, hypertension, and cardiovascular disease. ")

Paul Angulo. Fatty Liver Disease. New England Journal of Medicine, vol 346, No.16, April 18 2002, 1221-1231 Obesity type 2 (non insulin dependant) diabetes mellitus, and hyperlipidaemia are coexisting conditions frequently associated with non-alcoholic fattyl liver disease.

Paul Angulo. Obesity and Nonalcoholic Fatty Liver Disease, Nutrition Reviews, vol 65, no 6 s57-s63, June 2007 Nonalcoholic fatty liver disease comprises a spectrum of liver pathology including bland steatosis, stetohepatisis, cirrhosis, and hepatocellular carcinoma. Nonalcoholic fatty liver disease affects a substantial proportion of the general population from several countries. The prevalence of NAFLD is expected to increase worldwide as the global obesity epidemic spreads and the trend in developing countries toward the Western lifestyle continues.

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.

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..")

Kirsi Hannele Pietilainen, Aila Rissanen, Jaakko Kaprio, Sari Makimattila, Anna-Maija Hakkinen, Jukka Westerbacka, Jussi Sutinen, Satu Vehkavaara and Hannele Yki-Jarvinen. Acquired Obesity is associated with increased liver fat, intra-abdominal fat, and insulin resistance in young adult monozygotic twins. American journal of Physiology: Endocrinology and metabolism, vol 228, E768-E774, 2005

Acquired obesity is associated with increased liver fat, intra-abdominal fat, and insulin resistance in young adult monozygotic twins.

Juraj Koska, Norbert Stefan, Paska A Permana, Christian Weyer, Mina Sodona, Clifton Bogardus, Steven R Smith, Denis R Joanisse, Tohru Funahashi, Jonathon Krakoff and Joy C Bunt. Increased fat accumulation in liver may link insulin resistance with suncutaneous adipocyte enlargement, visceral adiposity, and hypoadiponectinemia in obese individuals. American journal of clinical nutrition. Vol 87, 295-302 2008.

Enlargement of adipocytes from subcutaneous abdominal adipose tissue (SAT) , increased intrahepatic lipid content (IHL), intramyocellular lipid content (IMCL), and low circulating adiponectin concentrations are associated with insulin resistance. Because adiponectin increases fat oxidation in skeletal muscle and liver, and the expression of the adiponectin gene in SAT is inversely associated with adipocyte size, we hypothesised that hypoadiponectinemia links hypertrophic obesity with insulin resistance via increased IMCL and IHL.