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| + | =======Obesity Powerpoint======= | ||
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| + | {{:obesity_presentation.pptx|}} | ||
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| ====== Obesity ====== | ====== Obesity ====== | ||
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| <box 50% round right |>{{:bmi_classification_final.png}}</box|Figure 3: WHO standardized BMI categories in adults (Seidell & Halberstadt, 2015)> | <box 50% round right |>{{:bmi_classification_final.png}}</box|Figure 3: WHO standardized BMI categories in adults (Seidell & Halberstadt, 2015)> | ||
| - | Body Mass Index (BMI)is an index of weight-for-height that is commonly used to classify weight in adults (Figure 3).The BMI was created to estimate the individual’s level of body fat and therefore assesses an individual’s risk of disease. | + | Body Mass Index (BMI) is an index of weight-for-height that is commonly used to classify weight in adults (Figure 3).The BMI was created to estimate the individual’s level of body fat and therefore assesses an individual’s risk of disease. |
| BMI is measured standardly as weight in kilograms divided by the square of the height in meters (Figure 4). The values of the BMI are age and sex dependent as body composition varies between sexes and at different ages. The values are then assessed by looking at a BMI table or chart.<sup>[3]</sup> | BMI is measured standardly as weight in kilograms divided by the square of the height in meters (Figure 4). The values of the BMI are age and sex dependent as body composition varies between sexes and at different ages. The values are then assessed by looking at a BMI table or chart.<sup>[3]</sup> | ||
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| The secretory activity of adipocytes plays a huge role in regards to hormonal and metabolic activity that takes place. Adipose cells are increased in size and number in obese conditions, which initiate an immune response. The fat cells release pro-inflammatory adipokines that recruit macrophages to the site. Following this, Tumour Necrosis Factor- alpha (TNF-α) is released and additional immune cells are brought to the site. This constant state of inflammation causes insulin resistance. This is why diabetes is often comorbid with obesity <sup>[17]</sup>. This sequence of events is depicted in Figure 7. | The secretory activity of adipocytes plays a huge role in regards to hormonal and metabolic activity that takes place. Adipose cells are increased in size and number in obese conditions, which initiate an immune response. The fat cells release pro-inflammatory adipokines that recruit macrophages to the site. Following this, Tumour Necrosis Factor- alpha (TNF-α) is released and additional immune cells are brought to the site. This constant state of inflammation causes insulin resistance. This is why diabetes is often comorbid with obesity <sup>[17]</sup>. This sequence of events is depicted in Figure 7. | ||
| - | <box 35% round left |>{{:adipose_finalllll.png|}}</box|Figure 7:This figure is a visual depiction of the secretory pathway and function of adipokines in conditions where excessive adipocyte buildup occurs > | + | <box 35% round left |>{{:adipose_finalllll.png|}}</box|Figure 7:This figure is a visual depiction of the secretory pathway and function of adipokines in conditions where excessive adipocyte buildup occurs from http://www.the-scientist.com/images/December2012/Obese_Infograph.jpg> |
| When analyzing other inflammatory factors, it is evident that increased concentrations of the adipokine Interleukin-6 (IL-6) are positively correlated with increased fat mass and BMI. Furthermore, IL-6 is increases post-exercise with increased NEFAs, thus proposing a correlation between the adipokine and lipid mobilization <sup>[16]</sup>.Monophosphate activated protein kinase (AMPK) enables the oxidation of fatty acids during muscle contraction. AMPK is regulated by the hormone adiponectin, which induces insulin-sensitivity. In individuals who are obese, the concentration of adiponectin is reduced, as individuals with symptoms of diabetes are resistant to insulin <sup>[16]</sup>. | When analyzing other inflammatory factors, it is evident that increased concentrations of the adipokine Interleukin-6 (IL-6) are positively correlated with increased fat mass and BMI. Furthermore, IL-6 is increases post-exercise with increased NEFAs, thus proposing a correlation between the adipokine and lipid mobilization <sup>[16]</sup>.Monophosphate activated protein kinase (AMPK) enables the oxidation of fatty acids during muscle contraction. AMPK is regulated by the hormone adiponectin, which induces insulin-sensitivity. In individuals who are obese, the concentration of adiponectin is reduced, as individuals with symptoms of diabetes are resistant to insulin <sup>[16]</sup>. | ||
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| **Diet** | **Diet** | ||
| - | <box 28% round right |>{{:meal.png|}}</box|Figure 10: Illustration of the ideal food plate including all food groups > | + | <box 25% round right |>{{:meal.png|}}</box|Figure 10: Illustration of the ideal food plate including all food groups from http://www.arthritis.org/images/slideshows/ra-diet/ra-diet-13-fill-your-plate.jpg |
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| The first component of lifestyle modifications to treating obesity is undergoing dietary therapy (Figure 10). When assessing diet management in obese patients, weight reduction is highly dependent upon energy intake in comparison to energy expenditure <sup>[27]</sup>. | The first component of lifestyle modifications to treating obesity is undergoing dietary therapy (Figure 10). When assessing diet management in obese patients, weight reduction is highly dependent upon energy intake in comparison to energy expenditure <sup>[27]</sup>. | ||
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| The Canadian Clinical Practice Guidelines on the Management and Prevention of Obesity in Adults and Children recommends that in addition to lifestyle modifications such as dietary changes, physical activity and behaviour therapy, overweight individuals with BMIs greater than 27 kg/m^2 but with life threatening diseases, or obese individuals with BMIs greater than 30 kg/m^2 can undergo pharmacotherapy <sup>[2]</sup>. | The Canadian Clinical Practice Guidelines on the Management and Prevention of Obesity in Adults and Children recommends that in addition to lifestyle modifications such as dietary changes, physical activity and behaviour therapy, overweight individuals with BMIs greater than 27 kg/m^2 but with life threatening diseases, or obese individuals with BMIs greater than 30 kg/m^2 can undergo pharmacotherapy <sup>[2]</sup>. | ||
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| - | A meta analysis investigated 21 randomized control trials (RCT) that involved a total of 11 533 participants using either one of the two drugs: orlistat or sibutramine, or a placebo. These RCTs had a follow-up period of at least 1 year in obese and overweight adults. | ||
| <box 35% round right |>{{:orlistat.jpg|}}</box|Figure 12: Orlistat, one of the pharmacological treatments for obesity | <box 35% round right |>{{:orlistat.jpg|}}</box|Figure 12: Orlistat, one of the pharmacological treatments for obesity | ||
| from https://www.medexpress.co.uk/javax.faces.resource/treatments/335x335xorlistat-120mg-pills.jpg.xhtml,qln=img.pagespeed.ic.3lJxOPoYEm.jpg> | from https://www.medexpress.co.uk/javax.faces.resource/treatments/335x335xorlistat-120mg-pills.jpg.xhtml,qln=img.pagespeed.ic.3lJxOPoYEm.jpg> | ||
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| + | A meta analysis investigated 21 randomized control trials (RCT) that involved a total of 11 533 participants using either one of the two drugs: orlistat or sibutramine, or a placebo. These RCTs had a follow-up period of at least 1 year in obese and overweight adults. | ||
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| Olistat functions as a gastrointestinal lipase inhibitor and reduces fat absorption by approximately 30% (Figure 12). Patients can use it for up to two years <sup>[43]</sup>. On the other hand, sibutramine functions as a serotonin and noradrenaline reuptake inhibitor which induces weight loss through enhanced satiety and increased basal energy expenditure. Sibutramine is approved for clinical use for up to 1 year <sup>[44]</sup>. | Olistat functions as a gastrointestinal lipase inhibitor and reduces fat absorption by approximately 30% (Figure 12). Patients can use it for up to two years <sup>[43]</sup>. On the other hand, sibutramine functions as a serotonin and noradrenaline reuptake inhibitor which induces weight loss through enhanced satiety and increased basal energy expenditure. Sibutramine is approved for clinical use for up to 1 year <sup>[44]</sup>. | ||
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| **Maintenance of weight loss** | **Maintenance of weight loss** | ||
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| Studies that assessed orlistat therapy for at least 2 years and up to 5 years showed that weight loss attained by year 1 was better maintained over the subsequent 3 years in patients who received ongoing drug therapy. Specifically, Davidson et al. showed that patients who had ongoing treatment of orlistat for 2 years were associated with less regain of weight loss (32%) compared with diet only therapy (63%) <sup>[45]</sup>. | Studies that assessed orlistat therapy for at least 2 years and up to 5 years showed that weight loss attained by year 1 was better maintained over the subsequent 3 years in patients who received ongoing drug therapy. Specifically, Davidson et al. showed that patients who had ongoing treatment of orlistat for 2 years were associated with less regain of weight loss (32%) compared with diet only therapy (63%) <sup>[45]</sup>. | ||
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| **Bariatric Surgery** | **Bariatric Surgery** | ||
| - | <box 30% round left |>{{:surgical_procedures.png|}}</box|Figure 13: Four highly used surgical procedures used to treating obesity > | + | <box 30% round right |>{{:surgical_procedures.png|}}</box|Figure 13: Four highly used surgical procedures used to treating obesity from http://www.cmaj.ca/content/suppl/2007/09/04/176.8.S1.DC1/obesity-lau-onlineNEW.pdf> |
| Bariatric surgery is a treatment method that is considered for adult patients who have a BMI over 35kg/m^2 with severe comorbid diseases such as life-threatening cardiopulmonary problems, severe sleep apnea, or severe diabetes mellitus, or for those in the severely obese category with a BMI greater than 40 kg/m2. For teenagers, the Canadian Clinical Practice Guidelines on the Management and Prevention of Obesity in Adults and Children recommends that bariatric surgery be limited to an appropriately trained and experienced surgical team. After 6 months of using lifestyle modifications, healthcare practitioners assess the health of the patient and evaluate whether a satisfactory progress of weight loss or goal of 10% of body weight has been reached. In the case that satisfactory progress or goal has not been achieved, physicians will consider the eligibility of patients to undergo bariatric surgery. This is only considered if other nonsurgical weight loss attempts have failed. The goal of bariatric surgery is to relieve a patient suffering from obesity from his or her morbid body weight, improve their comorbidity and improve their quality of life. There are different surgical procedures (Figure 13). It is important to note that this treatment option requires lifelong medical surveillance <sup>[26]</sup>. | Bariatric surgery is a treatment method that is considered for adult patients who have a BMI over 35kg/m^2 with severe comorbid diseases such as life-threatening cardiopulmonary problems, severe sleep apnea, or severe diabetes mellitus, or for those in the severely obese category with a BMI greater than 40 kg/m2. For teenagers, the Canadian Clinical Practice Guidelines on the Management and Prevention of Obesity in Adults and Children recommends that bariatric surgery be limited to an appropriately trained and experienced surgical team. After 6 months of using lifestyle modifications, healthcare practitioners assess the health of the patient and evaluate whether a satisfactory progress of weight loss or goal of 10% of body weight has been reached. In the case that satisfactory progress or goal has not been achieved, physicians will consider the eligibility of patients to undergo bariatric surgery. This is only considered if other nonsurgical weight loss attempts have failed. The goal of bariatric surgery is to relieve a patient suffering from obesity from his or her morbid body weight, improve their comorbidity and improve their quality of life. There are different surgical procedures (Figure 13). It is important to note that this treatment option requires lifelong medical surveillance <sup>[26]</sup>. | ||
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| As seen in figure 14, there are different approaches to treating obesity. First, it is important to set a weight loss goal to reduce body weight by approximately 10% from baseline during the first six months of treatment. Healthcare practitioners typically recommend their patients to first undergo lifestyle modifications: proper nutrition, physical fitness, and cognitive behaviour therapy. After six months of treatment, healthcare practitioners will assess the patient’s progress and determine whether satisfactory progress or weight loss goal has been reached. In the case that it has been reached, the patient would be closely monitored on a regular basis to make sure that their weight is maintained. In the event that satisfactory progress is not attained, physicians will assess the patient’s eligibility to either undergo pharmacotherapy or bariatric surgery. Physicians typically opt for bariatric treatment in the event that nonsurgical treatments have failed. It is important to note that best weight loss and maintenance results are achieved when pharmacotherapy or bariatric treatment is used in conjunction with lifestyle modifications. | As seen in figure 14, there are different approaches to treating obesity. First, it is important to set a weight loss goal to reduce body weight by approximately 10% from baseline during the first six months of treatment. Healthcare practitioners typically recommend their patients to first undergo lifestyle modifications: proper nutrition, physical fitness, and cognitive behaviour therapy. After six months of treatment, healthcare practitioners will assess the patient’s progress and determine whether satisfactory progress or weight loss goal has been reached. In the case that it has been reached, the patient would be closely monitored on a regular basis to make sure that their weight is maintained. In the event that satisfactory progress is not attained, physicians will assess the patient’s eligibility to either undergo pharmacotherapy or bariatric surgery. Physicians typically opt for bariatric treatment in the event that nonsurgical treatments have failed. It is important to note that best weight loss and maintenance results are achieved when pharmacotherapy or bariatric treatment is used in conjunction with lifestyle modifications. | ||
| - | <style float-right> | + | {{:flowchart_final.png|}} |
| - | {{:treatment_options.png|}} | + | |
| Figure 14: A holistic approach to treating obesity. | Figure 14: A holistic approach to treating obesity. | ||
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| ===== References ===== | ===== References ===== | ||
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| 1. Ng, M., Fleming, T., Robinson, M., Thomson, B., Graetz, N., & Margono, C. et al. (2014). Global, regional, and national prevalence of overweight and obesity in children and adults during 1980–2013: a systematic analysis for the Global Burden of Disease Study 2013.The Lancet, 384(9945), 766-781. http://dx.doi.org/10.1016/s0140-6736(14)60460-8 | 1. Ng, M., Fleming, T., Robinson, M., Thomson, B., Graetz, N., & Margono, C. et al. (2014). Global, regional, and national prevalence of overweight and obesity in children and adults during 1980–2013: a systematic analysis for the Global Burden of Disease Study 2013.The Lancet, 384(9945), 766-781. http://dx.doi.org/10.1016/s0140-6736(14)60460-8 | ||
| - | 2. Seidell, J. & Halberstadt, J. (2015). The Global Burden | + | |
| - | of Obesity and the Challenges of Prevention. Annals Of Nutrition And Metabolism, 66(2), 7-12. http://dx.doi.org/10.1159/000375143 | + | 2. Seidell, J. & Halberstadt, J. (2015). The Global Burden of Obesity and the Challenges of Prevention. Annals Of Nutrition And Metabolism, 66(2), 7-12. http://dx.doi.org/10.1159/000375143 |
| 3. WHO: Global Database on Body Mass Index. (2017). Apps.who.int. Retrieved 1 February 2017, from http://apps.who.int/bmi/index.jsp?introPage=intro_3.html | 3. WHO: Global Database on Body Mass Index. (2017). Apps.who.int. Retrieved 1 February 2017, from http://apps.who.int/bmi/index.jsp?introPage=intro_3.html | ||
| + | |||
| 4. Child & Teen BMI | Healthy Weight | CDC. (2017). Centers for Disease Control and Prevention. Retrieved 1 February 2017, from https://www.cdc.gov/healthyweight/assessing/bmi/childrens_bmi/about_childrens_bmi.html | 4. Child & Teen BMI | Healthy Weight | CDC. (2017). Centers for Disease Control and Prevention. Retrieved 1 February 2017, from https://www.cdc.gov/healthyweight/assessing/bmi/childrens_bmi/about_childrens_bmi.html | ||
| + | |||
| 5. Jitnarin, N., Poston, W., Haddock, C., Jahnke, S., & Tuley, B. (2012). Accuracy of body mass index-defined overweight in fire fighters. Occupational Medicine, 63(3), | 5. Jitnarin, N., Poston, W., Haddock, C., Jahnke, S., & Tuley, B. (2012). Accuracy of body mass index-defined overweight in fire fighters. Occupational Medicine, 63(3), | ||
| 227-230. http://dx.doi.org/10.1093/occmed/kqs213 | 227-230. http://dx.doi.org/10.1093/occmed/kqs213 | ||
| + | |||
| 6. Spiegelman, B. & Flier, J. (2001). Obesity and the Regulation of Energy Balance. Cell, | 6. Spiegelman, B. & Flier, J. (2001). Obesity and the Regulation of Energy Balance. Cell, | ||
| 104(4), 531-543. http://dx.doi.org/10.1016/s0092-8674(01)00240-9 | 104(4), 531-543. http://dx.doi.org/10.1016/s0092-8674(01)00240-9 | ||
| + | |||
| 7. Pietiläinen, K., Kaprio, J., Borg, P., Plasqui, G., Yki-Järvinen, H., & Kujala, U. et al. (2008). Physical Inactivity and Obesity: A Vicious Circle. Obesity, | 7. Pietiläinen, K., Kaprio, J., Borg, P., Plasqui, G., Yki-Järvinen, H., & Kujala, U. et al. (2008). Physical Inactivity and Obesity: A Vicious Circle. Obesity, | ||
| 16(2), 409-414. http://dx.doi.org/10.1038/oby.2007.72 | 16(2), 409-414. http://dx.doi.org/10.1038/oby.2007.72 | ||
| + | |||
| 8. Cohen-Cole, E. & Fletcher, J. (2008). Is obesity contagious? Social networks vs environmental factors in the obesity epidemic. Journal Of Health Economics, 27(5), | 8. Cohen-Cole, E. & Fletcher, J. (2008). Is obesity contagious? Social networks vs environmental factors in the obesity epidemic. Journal Of Health Economics, 27(5), | ||
| 1382-1387. http://dx.doi.org/10.1016/j.jhealeco.2008.04.005 | 1382-1387. http://dx.doi.org/10.1016/j.jhealeco.2008.04.005 | ||
| + | |||
| 9. Masuo, K. (2000). A family history of obesity, a family history of hypertension and blood pressure levels. American Journal Of Hypertension, 13(6), S164. http://dx.doi.org/10.1016/s0895-7061(00)01125-0 | 9. Masuo, K. (2000). A family history of obesity, a family history of hypertension and blood pressure levels. American Journal Of Hypertension, 13(6), S164. http://dx.doi.org/10.1016/s0895-7061(00)01125-0 | ||
| + | |||
| 10. Weaver, J. (2008). Classical Endocrine Diseases Causing Obesity. Obesity And Metabolism, 212-228. http://dx.doi.org/10.1159/000115367 | 10. Weaver, J. (2008). Classical Endocrine Diseases Causing Obesity. Obesity And Metabolism, 212-228. http://dx.doi.org/10.1159/000115367 | ||
| + | |||
| 11. Schwartz, T., Nihalani, N., Jindal, S., Virk, S., & Jones, N. (2004). Psychiatric medication-induced obesity: a review. Obesity Reviews, 5(2), 115-121. http://dx.doi.org/10.1111/j.1467-789x.2004.00139.x | 11. Schwartz, T., Nihalani, N., Jindal, S., Virk, S., & Jones, N. (2004). Psychiatric medication-induced obesity: a review. Obesity Reviews, 5(2), 115-121. http://dx.doi.org/10.1111/j.1467-789x.2004.00139.x | ||
| + | |||
| 12. Dare, S., Mackay, D., & Pell, J. (2015). Relationship between Smoking and Obesity: A Cross-Sectional Study of 499,504 Middle-Aged Adults in the UK General Population. PLOS ONE, 10(4), e0123579. http://dx.doi.org/10.1371/journal.pone.0123579 | 12. Dare, S., Mackay, D., & Pell, J. (2015). Relationship between Smoking and Obesity: A Cross-Sectional Study of 499,504 Middle-Aged Adults in the UK General Population. PLOS ONE, 10(4), e0123579. http://dx.doi.org/10.1371/journal.pone.0123579 | ||
| + | |||
| 13. Vermeulen, A. (2005). The epidemic of obesity: Obesity and health of the aging male. The Aging Male, 8(1), 39-41. http://dx.doi.org/10.1080/13685530500049037 | 13. Vermeulen, A. (2005). The epidemic of obesity: Obesity and health of the aging male. The Aging Male, 8(1), 39-41. http://dx.doi.org/10.1080/13685530500049037 | ||
| + | |||
| 14. Schumann, N., Brinsden, H., & Lobstein, T. (2014). A review of national health policies and professional guidelines on maternal obesity and weight gain in pregnancy. Clinical | 14. Schumann, N., Brinsden, H., & Lobstein, T. (2014). A review of national health policies and professional guidelines on maternal obesity and weight gain in pregnancy. Clinical | ||
| Obesity, n/a-n/a. http://dx.doi.org/10.1111/cob.12062 | Obesity, n/a-n/a. http://dx.doi.org/10.1111/cob.12062 | ||
| - | 15. Why Is Sleep Important? - NHLBI, NIH. (2017). National Heart, Lung and Blood Institute. | + | |
| - | Retrieved 1 February 2017, from https://www.nhlbi.nih.gov/health/health-topics/topics/sdd/why | + | 15. Why Is Sleep Important? - NHLBI, NIH. (2017). National Heart, Lung and Blood Institute. Retrieved 1 February 2017, from https://www.nhlbi.nih.gov/health/health-topics/topics/sdd/why |
| 16. Gurevich-Panigrahi, T., Panigrahi, S., Wiechec, E., & Los, M. (2009). Obesity: pathophysiology and clinical management. Current Medical Chemistry, 16, 506-521. Retrieved from http://liu.diva-portal.org/smash/get/diva2:583167/FULLTEXT01.pdf | 16. Gurevich-Panigrahi, T., Panigrahi, S., Wiechec, E., & Los, M. (2009). Obesity: pathophysiology and clinical management. Current Medical Chemistry, 16, 506-521. Retrieved from http://liu.diva-portal.org/smash/get/diva2:583167/FULLTEXT01.pdf | ||
| - | 17. Odegaard, J., & Chawla, A. (2012). Adipose tissue metabolism in the obese. TheScientist. | + | |
| - | Retrieved 18 January 2017, from http://www.the-scientist.com/?articles.view/articleNo/33653/title/adipose-tissue-metabolism-in-the-obese/ | + | 17. Odegaard, J., & Chawla, A. (2012). Adipose tissue metabolism in the obese. TheScientist. Retrieved 18 January 2017, from http://www.the-scientist.com/?articles.view/articleNo/33653/title/adipose-tissue-metabolism-in-the-obese/ |
| 18. Kahn, B. B., & Flier, J. S. (2000). Obesity and insulin resistance. Journal of Clinical Investigation, 106(4), 473–481. | 18. Kahn, B. B., & Flier, J. S. (2000). Obesity and insulin resistance. Journal of Clinical Investigation, 106(4), 473–481. | ||
| + | |||
| 19. Després, J., & Marette, A. (1999). Obesity and Insulin Resistance. Insulin Resistance, 51-81. doi:10.1007/978-1-59259-716-1_4 | 19. Després, J., & Marette, A. (1999). Obesity and Insulin Resistance. Insulin Resistance, 51-81. doi:10.1007/978-1-59259-716-1_4 | ||
| + | |||
| 20. Klok, M. D., Jakobsdottir, S., & Drent, M. L. (2007). The role of leptin and ghrelin in the regulation of food intake and body weight in humans: a review. Obesity Reviews, 8(1), 21-34. doi:10.1111/j.1467-789x.2006.00270.x | 20. Klok, M. D., Jakobsdottir, S., & Drent, M. L. (2007). The role of leptin and ghrelin in the regulation of food intake and body weight in humans: a review. Obesity Reviews, 8(1), 21-34. doi:10.1111/j.1467-789x.2006.00270.x | ||
| + | |||
| 21. Kaszmi, A., Sattar.A., Hashim, R., Khan., S.P.., Younus, M., Khan, F.A. (2013). Serum Leptin values in the healthy obese and non-obese subjects of Rawalpindi. J Pak Med Assoc. 63(2), 245-8 | 21. Kaszmi, A., Sattar.A., Hashim, R., Khan., S.P.., Younus, M., Khan, F.A. (2013). Serum Leptin values in the healthy obese and non-obese subjects of Rawalpindi. J Pak Med Assoc. 63(2), 245-8 | ||
| + | |||
| 22. Tschop, M., Weyer, C., Tataranni, P. A., Devanarayan, V., Ravussin, E., & Heiman, M. L. (2001). Circulating Ghrelin Levels Are Decreased in Human Obesity. Diabetes, 50(4), 707-709. doi:10.2337/diabetes.50.4.707 | 22. Tschop, M., Weyer, C., Tataranni, P. A., Devanarayan, V., Ravussin, E., & Heiman, M. L. (2001). Circulating Ghrelin Levels Are Decreased in Human Obesity. Diabetes, 50(4), 707-709. doi:10.2337/diabetes.50.4.707 | ||
| + | |||
| 23. Walley, A.J., Blakemore, A.I.F. & Froguel, P. (2006). Genetics of obesity and the prediction of risk for health. Human Molecular Genetics. Retrieved 27January, 2017, from https://academic.oup.com/hmg/article/15/suppl_2/R124/626082/Genetics-of-obesity-and-the-prediction-of-risk-for | 23. Walley, A.J., Blakemore, A.I.F. & Froguel, P. (2006). Genetics of obesity and the prediction of risk for health. Human Molecular Genetics. Retrieved 27January, 2017, from https://academic.oup.com/hmg/article/15/suppl_2/R124/626082/Genetics-of-obesity-and-the-prediction-of-risk-for | ||
| 24. Rankinen, T., Zuberi, A., Chagnon, Y.C., Weisnagel, S.J., Argyropoulos, G., Walts, B., Perusse, L., & Bouchard, C. (2006). The human obesity gene map: the 2005 update. Obesity, | 24. Rankinen, T., Zuberi, A., Chagnon, Y.C., Weisnagel, S.J., Argyropoulos, G., Walts, B., Perusse, L., & Bouchard, C. (2006). The human obesity gene map: the 2005 update. Obesity, | ||
| 14(4), 529-644. | 14(4), 529-644. | ||
| + | |||
| 25. Pi-Sunyer, F. X., Becker, D. M., Bouchard, C., Carleton, R. A., Colditz, G. A., Dietz, W. H., ... & Higgins, M. (1998). Clinical guidelines on the identification, evaluation, and treatment of overweight and obesity in adults. American Journal of Clinical Nutrition, 68(4), 899-917. | 25. Pi-Sunyer, F. X., Becker, D. M., Bouchard, C., Carleton, R. A., Colditz, G. A., Dietz, W. H., ... & Higgins, M. (1998). Clinical guidelines on the identification, evaluation, and treatment of overweight and obesity in adults. American Journal of Clinical Nutrition, 68(4), 899-917. | ||
| Line 356: | Line 381: | ||
| 27. Poirier, P., & Després, J. P. (2001). Exercise in weight management of obesity. Cardiology clinics,19(3),459-470. | 27. Poirier, P., & Després, J. P. (2001). Exercise in weight management of obesity. Cardiology clinics,19(3),459-470. | ||
| + | |||
| 28. Hey, H., Petersen, H. D., Andersen, T., & Quaade, F. (1987). Formula diet plus free additional food choice up to 1000 kcal (4.2 MJ) compared with an is energetic conventional diet in the treatment of obesity. A randomised clinical trial. Clinical Nutrition,6(3),195-199. | 28. Hey, H., Petersen, H. D., Andersen, T., & Quaade, F. (1987). Formula diet plus free additional food choice up to 1000 kcal (4.2 MJ) compared with an is energetic conventional diet in the treatment of obesity. A randomised clinical trial. Clinical Nutrition,6(3),195-199. | ||
| + | |||
| 29. Lau, D. C., Douketis, J. D., Morrison, K. M., Hramiak, I. M., Sharma, A. M., Ur, E., & members of the Obesity Canada Clinical Practice Guidelines Expert Panel. (2007). 2006 Canadian clinical practice guidelines on the management and prevention of obesity in adults and children [summary]. Canadian Medical Association Journal, 176(8), S1-S13. | 29. Lau, D. C., Douketis, J. D., Morrison, K. M., Hramiak, I. M., Sharma, A. M., Ur, E., & members of the Obesity Canada Clinical Practice Guidelines Expert Panel. (2007). 2006 Canadian clinical practice guidelines on the management and prevention of obesity in adults and children [summary]. Canadian Medical Association Journal, 176(8), S1-S13. | ||
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| 30. Toubro, S., & Astrup, A. (1997). Randomised comparison of diets for maintaining obese subjects' weight after major weight loss: ad lib, low fat, high carbohydrate diet fixed energy intake. Bmj,314(707329. | 30. Toubro, S., & Astrup, A. (1997). Randomised comparison of diets for maintaining obese subjects' weight after major weight loss: ad lib, low fat, high carbohydrate diet fixed energy intake. Bmj,314(707329. | ||
| + | |||
| 31. 9 Popular Weight Loss Diets Reviewed by Science. (2016, October 04). Retrieved January 27, 2017, from https://authoritynutrition.com/9-weight-loss-diets-reviewed/ | 31. 9 Popular Weight Loss Diets Reviewed by Science. (2016, October 04). Retrieved January 27, 2017, from https://authoritynutrition.com/9-weight-loss-diets-reviewed/ | ||
| + | |||
| 32. Poirier, P., & Després, J. P. (2001). Exercise in weight management of obesity. Cardiology clinics, 19(3), 459-470. | 32. Poirier, P., & Després, J. P. (2001). Exercise in weight management of obesity. Cardiology clinics, 19(3), 459-470. | ||
| + | |||
| 33. Tremblay, A., Nadeau, A., Despres, J. P., St-Jean, L., Theriault, G., & Bouchard, C. (1990). Long-term exercise training with constant energy intake. 2: Effect on glucose metabolism and resting energy expenditure. International journal of obesity, 14(1), 75-84. | 33. Tremblay, A., Nadeau, A., Despres, J. P., St-Jean, L., Theriault, G., & Bouchard, C. (1990). Long-term exercise training with constant energy intake. 2: Effect on glucose metabolism and resting energy expenditure. International journal of obesity, 14(1), 75-84. | ||
| + | |||
| 34. Gwinup, G. (1987). Weight loss without dietary restriction: efficacy of different forms of aerobic exercise. The American journal of sports medicine, 15(3), 275-279. | 34. Gwinup, G. (1987). Weight loss without dietary restriction: efficacy of different forms of aerobic exercise. The American journal of sports medicine, 15(3), 275-279. | ||
| + | |||
| 35. Pate, R. R., Pratt, M., Blair, S. N., Haskell, W. L., Macera, C. A., Bouchard, C., ... & Kriska, A. (1995). Physical activity and public health: a recommendation from the Centers for Disease Control and Prevention and the American College of Sports Medicine. Jama, 273(5), 402-407. | 35. Pate, R. R., Pratt, M., Blair, S. N., Haskell, W. L., Macera, C. A., Bouchard, C., ... & Kriska, A. (1995). Physical activity and public health: a recommendation from the Centers for Disease Control and Prevention and the American College of Sports Medicine. Jama, 273(5), 402-407. | ||
| + | |||
| 36. Nozaki, T., Sawamoto, R., & Sudo, N. (2013). Cognitive behavioral therapy for obesity. Nihon rinsho. Japanese journal of clinical medicine, 71(2), 329-334. | 36. Nozaki, T., Sawamoto, R., & Sudo, N. (2013). Cognitive behavioral therapy for obesity. Nihon rinsho. Japanese journal of clinical medicine, 71(2), 329-334. | ||
| + | |||
| 37. Cooper, Z., Fairburn, C. G., & Hawker, D. M. (2003). Cognitive-behavioral treatment of obesity: A clinician's guide. Guilford Press. | 37. Cooper, Z., Fairburn, C. G., & Hawker, D. M. (2003). Cognitive-behavioral treatment of obesity: A clinician's guide. Guilford Press. | ||
| + | |||
| 38. Diabetes Prevention Program (DPP) Research Group. (2002). The diabetes prevention program (DPP). Diabetes care, 25(12), 2165-2171. | 38. Diabetes Prevention Program (DPP) Research Group. (2002). The diabetes prevention program (DPP). Diabetes care, 25(12), 2165-2171. | ||
| - | 39. Look AHEAD Research Group. (2003). Look AHEAD (Action for Health in Diabetes): design and methods for a clinical trial of weight loss for the prevention of cardiovascular disease in type 2 diabetes. Controlled clinical trials, | + | |
| - | 24(5), 610-628. | + | 39. Look AHEAD Research Group. (2003). Look AHEAD (Action for Health in Diabetes): design and methods for a clinical trial of weight loss for the prevention of cardiovascular disease in type 2 diabetes. Controlled clinical trials,24(5), 610-628. |
| 40. Renjilian, D. A., Perri, M. G., Nezu, A. M., McKelvey, W. F., Shermer, R. L., & Anton, S. D. (2001). Individual versus group therapy for obesity: effects of matching participants to their treatment preferences. Journal of consulting and clinical psychology, 69(4), 717. | 40. Renjilian, D. A., Perri, M. G., Nezu, A. M., McKelvey, W. F., Shermer, R. L., & Anton, S. D. (2001). Individual versus group therapy for obesity: effects of matching participants to their treatment preferences. Journal of consulting and clinical psychology, 69(4), 717. | ||
| + | |||
| 41. Wrotniak, B. H., Epstein, L. H., Paluch, R. A., & Roemmich, J. N. (2004). Parent weight change as a predictor of child weight change in family-based behavioral obesity treatment. Archives of pediatrics | 41. Wrotniak, B. H., Epstein, L. H., Paluch, R. A., & Roemmich, J. N. (2004). Parent weight change as a predictor of child weight change in family-based behavioral obesity treatment. Archives of pediatrics | ||
| - | & adolescent medicine, 158(4), | + | & adolescent medicine, 158(4), 342-347. |
| - | 342-347. | + | |
| 42. Epstein, L. H., Roemmich, J. N., Stein, R. I., Paluch, R. A., & Kilanowski, C. K. (2005). The challenge of identifying behavioral alternatives to food: clinic and field studies. Annals of | 42. Epstein, L. H., Roemmich, J. N., Stein, R. I., Paluch, R. A., & Kilanowski, C. K. (2005). The challenge of identifying behavioral alternatives to food: clinic and field studies. Annals of | ||
| - | Behavioral Medicine, 30(3), | + | Behavioral Medicine, 30(3),201-209 |
| - | 201-209 | + | |
| 43. Guerciolini, R. (1997). Mode of action of orlistat. International journal of obesity and related metabolic disorders: journal of the International Association for the Study of Obesity, 21, S12-23. | 43. Guerciolini, R. (1997). Mode of action of orlistat. International journal of obesity and related metabolic disorders: journal of the International Association for the Study of Obesity, 21, S12-23. | ||
| Line 383: | Line 421: | ||
| 46. James, W. P. T., Astrup, A., Finer, N., Hilsted, J., Kopelman, P., Rössner, S., ... & STORM Study Group. (2000). Effect of sibutramine on weight maintenance after weight loss: a randomised trial. The Lancet, 356(9248), 2119-2125 | 46. James, W. P. T., Astrup, A., Finer, N., Hilsted, J., Kopelman, P., Rössner, S., ... & STORM Study Group. (2000). Effect of sibutramine on weight maintenance after weight loss: a randomised trial. The Lancet, 356(9248), 2119-2125 | ||
| + | |||
| 47. Sjöström, L., Lindroos, A. K., Peltonen, M., Torgerson, J., Bouchard, C., Carlsson, B., ... & Sullivan, M. (2004). Lifestyle, diabetes, and cardiovascular risk factors 10 years after bariatric surgery. New England Journal of Medicine, 351(26), 2683-2693. | 47. Sjöström, L., Lindroos, A. K., Peltonen, M., Torgerson, J., Bouchard, C., Carlsson, B., ... & Sullivan, M. (2004). Lifestyle, diabetes, and cardiovascular risk factors 10 years after bariatric surgery. New England Journal of Medicine, 351(26), 2683-2693. | ||
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