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group_2_presentation_1-_obesity [2017/02/03 23:05]
gillr23
group_2_presentation_1-_obesity [2018/01/25 15:18] (current)
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 +=======Obesity Powerpoint=======
 +
 +{{:​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.
-<box 35% round right |>​{{:​bmi_formula.png|}}</​box|Figure 4: BMI Calculation Equation  +
-from http://​www.heartnewslinks.com/​editors-blog/​body-mass-index-bmi-bad>​+
  
 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>​
 +
 +
 +
 +{{:​bmi_formula.png|}}
 +
 +Figure 4: BMI Calculation Equation ​
 +from http://​www.heartnewslinks.com/​editors-blog/​body-mass-index-bmi-bad
  
  
 ==== BMI in children ==== ==== BMI in children ====
  
-Obesity is defined differently for children and teens compared to adults due to the fact that they are still growing (Figure 5). <box 70% round right |>​{{:​weight_status_category.png|}}</​box|Figure 5: BMI-for-Age Percentile Ranges for Children  +Obesity is defined differently for children and teens compared to adults due to the fact that they are still growing (Figure 5). BMIs for this cohort compare their height and weight against growth charts that take age and sex into account, since males and females in this cohort usually mature at different rates. ​
-from https://​www.cdc.gov/​healthyweight/​assessing/​bmi/​childrens_bmi/​about_childrens_bmi.html>​  +
-BMIs for this cohort compare their height and weight against growth charts that take age and sex into account, since males and females in this cohort usually mature at different rates. ​+
  
 Their BMI is referred to as BMI-for-age percentile, meaning the child’s BMI is compared with other children of the same sex and age who participated in national surveys that were conducted from 1963-65 to 1988-94.<​sup>​[4]</​sup>​ Their BMI is referred to as BMI-for-age percentile, meaning the child’s BMI is compared with other children of the same sex and age who participated in national surveys that were conducted from 1963-65 to 1988-94.<​sup>​[4]</​sup>​
 +
 +
 +{{:​weight_status_category.png|}}
 +
 +
 +Figure 5: BMI-for-Age Percentile Ranges for Children ​
 +from https://​www.cdc.gov/​healthyweight/​assessing/​bmi/​childrens_bmi/​about_childrens_bmi.html> ​
 +
 +
  
 ==== BMI Limitations ==== ==== BMI Limitations ====
 +
 +
 === Variance in Asian Populations === === Variance in Asian Populations ===
  
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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 ​45% round right |>{IMAGE}</​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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 A study conducted by Kazmi et al.(1996) investigated leptin concentrations in a sample of a  Rawalpindi population. There were three sampling groups—health obese, overweight and non-obese. According to the results, the mean serum leptin concentration for the obese group was 52.8 ug/mL and 6.3 ug/mL for the non-obese group. The results of this study concluded there is certainly a positive correlation between the Body Mass Index and leptin concentrations in individuals <​sup>​[21]</​sup>​. ​ A study conducted by Kazmi et al.(1996) investigated leptin concentrations in a sample of a  Rawalpindi population. There were three sampling groups—health obese, overweight and non-obese. According to the results, the mean serum leptin concentration for the obese group was 52.8 ug/mL and 6.3 ug/mL for the non-obese group. The results of this study concluded there is certainly a positive correlation between the Body Mass Index and leptin concentrations in individuals <​sup>​[21]</​sup>​. ​
  
-<box 45% round right |>{IMAGE}</​box|Figure 8: Human hormones and food intake>+<box 45% round right|>{{:​intake_final.png|}}</​box|Figure 8: Human hormones and food intake ​from http://​blog.naturessunshine.com/​wp-content/​uploads/​2015/​12/​Control_Food_Intake.jpg>
  
 **Ghrelin** **Ghrelin**
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 ==== Genetic Predisposition ==== ==== Genetic Predisposition ====
  
-<box 45% round right |>​{IMAGE}</​box|Figure 9: Human obesity gene map, updated in 2005. > 
 When assessing the heritability of obesity, it has a numerical association of 0.7, which is fairly high relative to heritability in schizophrenia (0.81) and autism (0.9). In the case of rare familial obesity, gene defects occur in appetite regulation. Variants in the leptin-melanocortin pathway result in about 5% of morbid human obesity. Common polygenic obesity is characterized by the human obesity gene map. When performing a closer analysis of some of the key factors involved in obesity, Pre-B cell colony enhancing factor (PBEF1), which is secreted by lymphocytes,​ is expressed by adipocytes. Presently, it is referred to as Visfatin <​sup>​[23]</​sup>​. ​ When assessing the heritability of obesity, it has a numerical association of 0.7, which is fairly high relative to heritability in schizophrenia (0.81) and autism (0.9). In the case of rare familial obesity, gene defects occur in appetite regulation. Variants in the leptin-melanocortin pathway result in about 5% of morbid human obesity. Common polygenic obesity is characterized by the human obesity gene map. When performing a closer analysis of some of the key factors involved in obesity, Pre-B cell colony enhancing factor (PBEF1), which is secreted by lymphocytes,​ is expressed by adipocytes. Presently, it is referred to as Visfatin <​sup>​[23]</​sup>​. ​
  
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 +{{:​genetics.gif}}
 +
 +
 +Figure 9: Human obesity gene map, updated in 2005. 
 +From http://​onlinelibrary.wiley.com.libaccess.lib.mcmaster.ca/​doi/​10.1038/​oby.2006.71/​full
  
 ===== Treatments ===== ===== Treatments =====
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 **Diet** **Diet**
  
-<​box ​45% round right |>{IMAGE}</​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  
 +>
 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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 **Cognitive Behaviour Therapy** **Cognitive Behaviour Therapy**
  
-<​box ​45% round right |>{IMAGE}</​box|Figure 11: The three main components of Cognitive Behaviour Therapy: thought, emotion and behaviour >+<​box ​30% round right  |>{{:cbt.png}}</​box|Figure 11: The three main components of Cognitive Behaviour Therapy: thought, emotion and behaviour ​ 
 +from http://​in8.uk.com/​wp-content/​uploads/​2016/​03/​CBT-image.png> 
 The third component of lifestyle modifications is to undergo cognitive behaviour therapy (CBT) to assess one’s current habits and identify factors, stressors or situations that may trigger one’s overeating habits and contribute to their obesity (Figure 11). With a CBT approach, patients suffering from obesity can get help through counseling, support groups, as well as adopt the family-based approach <​sup>​[25,​26]</​sup>​. ​ The third component of lifestyle modifications is to undergo cognitive behaviour therapy (CBT) to assess one’s current habits and identify factors, stressors or situations that may trigger one’s overeating habits and contribute to their obesity (Figure 11). With a CBT approach, patients suffering from obesity can get help through counseling, support groups, as well as adopt the family-based approach <​sup>​[25,​26]</​sup>​. ​
  
 The purpose of the CBT treatment is not to eliminate a psychiatric disorder but to change eating and exercise behaviours <​sup>​[36]</​sup>​. This intervention aims to educate individuals on how to change problematic behaviours. Firstly, CBT is based on the cognitive conceptualization of the processes that lead to overeating. Specifically,​ thoughts and thinking patterns that are considered central to the problem. Secondly, CBT is focused on altering the cognitive and behavioural mechanisms that maintain the problem behaviour. Lastly, CBT uses both cognitive and behavioural techniques to maintain healthy mechanisms <​sup>​[37]</​sup>​. The diagram here shows different components that contribute to CBT.  The purpose of the CBT treatment is not to eliminate a psychiatric disorder but to change eating and exercise behaviours <​sup>​[36]</​sup>​. This intervention aims to educate individuals on how to change problematic behaviours. Firstly, CBT is based on the cognitive conceptualization of the processes that lead to overeating. Specifically,​ thoughts and thinking patterns that are considered central to the problem. Secondly, CBT is focused on altering the cognitive and behavioural mechanisms that maintain the problem behaviour. Lastly, CBT uses both cognitive and behavioural techniques to maintain healthy mechanisms <​sup>​[37]</​sup>​. The diagram here shows different components that contribute to CBT. 
  
-Counseling ​is one way a patient can undergo CBT. It can either be delivered on a one-on-one basis, or in a group setting of approximately 10 participants with a trained healthcare professional <​sup>​[38,​39]</​sup>​. A study conducted by Renjilian and colleagues comparing the two treatment modalities concluded that participants who were randomized to receive group-based therapy lost more weight after 26 weekly sessions compared to those who were treated individually. Specifically,​ those receiving group therapy lost about 11 kg after 26 weekly sessions, in comparison to 9 kg for those who were individually treated <​sup>​[40]</​sup>​. ​+Counselling ​is one way a patient can undergo CBT. It can either be delivered on a one-on-one basis, or in a group setting of approximately 10 participants with a trained healthcare professional <​sup>​[38,​39]</​sup>​. A study conducted by Renjilian and colleagues comparing the two treatment modalities concluded that participants who were randomized to receive group-based therapy lost more weight after 26 weekly sessions compared to those who were treated individually. Specifically,​ those receiving group therapy lost about 11 kg after 26 weekly sessions, in comparison to 9 kg for those who were individually treated <​sup>​[40]</​sup>​. ​
  
-In addition to counseling, having a support network is important. This is  especially true if the individual is undergoing drastic changes. Receiving encouragement from family, friends and health care practitioners can be very motivating during challenging times of the weight loss and maintenance programs. Furthermore,​ patients can also join support groups with other people undergoing weight loss <​sup>​[25]</​sup>​. ​+In addition to counselling, having a support network is important. This is  especially true if the individual is undergoing drastic changes. Receiving encouragement from family, friends and health care practitioners can be very motivating during challenging times of the weight loss and maintenance programs. Furthermore,​ patients can also join support groups with other people undergoing weight loss <​sup>​[25]</​sup>​. ​
  
 Family-based obesity treatment has also been proven to be a very effective and sustainable approach, especially when treating pediatric obesity. The role of this treatment is to target eating and activity change in both child and parent. Programs using this approach teach parents behavioural skills to facilitate child behaviour change and utilize family resources to improve the efficacy of childhood obesity treatments. Simultaneously treating the child and parent helps create positive relationships between them as they both aim to reach their weight loss goal together <​sup>​[41,​42]</​sup>​. ​ Family-based obesity treatment has also been proven to be a very effective and sustainable approach, especially when treating pediatric obesity. The role of this treatment is to target eating and activity change in both child and parent. Programs using this approach teach parents behavioural skills to facilitate child behaviour change and utilize family resources to improve the efficacy of childhood obesity treatments. Simultaneously treating the child and parent helps create positive relationships between them as they both aim to reach their weight loss goal together <​sup>​[41,​42]</​sup>​. ​
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 **Pharmacotherapy** **Pharmacotherapy**
  
-<box 45% round right |>​{IMAGE}</​box|Figure 12: Orlistat, one of the pharmacological treatments for obesity > 
 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>​. ​
 +
 +<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>​
  
 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. ​ 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. ​
 +
  
 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**
 +
    
 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 ​45% round right |>{IMAGE}</​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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 **Summary of Treatment Options** **Summary of Treatment Options**
  
-<box 45% round right |>​{IMAGE}</​box|Figure 14: This chart shows a holistic approach to treating obesity. > 
 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. ​
  
 +{{:​flowchart_final.png|}}
 +
 +
 +Figure 14: A holistic approach to treating obesity.
  
 ===== References ===== ===== References =====
  
  
-  * A Timeline of HIV/AIDS. (n.d.). Retrieved October 17, 2016, from https://​www.aids.gov/​hiv-aids-basics/​hiv-aids-101/​aids-timeline/​index.html 
-  * AIDS.gov. (2015). HIV Test Types. Retrieved from https://​www.aids.gov/​hiv-aids-basics/​prevention/​hiv-testing/​hiv-test-types/​AIDS.gov. (2015). HIV Test Types. Retrieved from https://​www.aids.gov/​hiv-aids-basics/​prevention/​hiv-testing/​hiv-test-types/​ 
-  * AIDS.gov. (2015). Stages of HIV Infection. Retrieved from https://​www.aids.gov/​hiv-aids-basics/​just-diagnosed-with-hiv-aids/​hiv-in-your-body/​stages-of-hiv/​ 
  
-  * AIDSInfo(2016)HIV PreventionRetrieved from https://​aidsinfo.nih.gov/​education-materials/​fact-sheets/​20/​48/​the-basics-of-hiv-prevention +1     Ng, M., Fleming, T., Robinson, M., Thomson, B., GraetzN., & MargonoCet al(2014). Globalregionaland 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 Lancet384(9945)766-781http://dx.doi.org/10.1016/s0140-6736(14)60460-8
-  * AidsInfo. N.d. HIV Life Cycle. Retrieved from: https://​aidsinfo.nih.gov/​education-materials/​fact-sheets/​19/​45/​hiv-aids--the-basics +
-  * BergerE., GarrettL., MacGregorRR., VonmullerE., WeinerD2016HIV and AIDSAnnenberg Learner91-106.+
  
-  * Centers for Disease Control ​and Prevention. (2016). HIV/AIDS Testing. Retrieved from http://www.cdc.gov/hiv/​basics/​testing.html+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
  
-  * Global ​HIV/AIDS Overview. (2016, September 28). Retrieved ​October 20, 2016, from https://www.aids.gov/federal-resources/​around-the-world/​global-aids-overview/index.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
  
-  * Hall, H., Geduld, J., Boulos, D., Rhodes, P., An, Q., Mastro, T. et al. (2009). Epidemiology of HIV in the United States ​and Canada: Current Status and Ongoing ChallengesJAIDS Journal Of Acquired Immune Deficiency Syndromes, 51(Supplement ​1)S13-S20. http://dx.doi.org/10.1097/qai.0b013e3181a2639e+4     ​Child ​Teen BMI | Healthy Weight | CDC. (2017). Centers for Disease Control ​and PreventionRetrieved ​February 2017from https://www.cdc.gov/healthyweight/​assessing/​bmi/​childrens_bmi/about_childrens_bmi.html
  
-  * HollandK., & KrucikG(2013July 12)The History of HIVRetrieved October 172016from http://www.healthline.com/​health/​hiv-aids/​history#​EarliestCase1 +5.    JitnarinN., PostonW., Haddock, C., Jahnke, S., & TuleyB(2012)Accuracy of body mass index-defined overweight ​in fire fightersOccupational Medicine, 63(3)
-  * Large-Scale HIV Vaccine Trial to Launch ​in South Africa | NIH: National Institute of Allergy and Infectious Diseases. (2016, May 18). Retrieved November 04, 2016, from https://www.niaid.nih.gov/news-events/large-scale-hiv-vaccine-trial-launch-south-africa+227-230http://dx.doi.org/10.1093/occmed/kqs213
  
-  * NordqvistC(2016May 11). "​HIV/​AIDS:​ Causes, Symptoms ​and Treatments." Medical News Today. Retrieved 26 October 2016from http://www.medicalnewstoday.com/articles/​17131.php.+6.      SpiegelmanB& FlierJ. (2001). Obesity ​and the Regulation of Energy BalanceCell, 
 +104(4), 531-543. ​http://dx.doi.org/10.1016/​s0092-8674(01)00240-9
  
-  * Robinson, J. (2016)Understanding Treatment of AIDS/HIV. WebMD. Retrieved 26 October 2016from http://www.webmd.com/​hiv-aids/​guide/​understanding-aids-hiv-treatment?​page=3 +7.      Pietiläinen,​ K., Kaprio, J., Borg, P., Plasqui, G., Yki-JärvinenH., & KujalaUet al. (2008). Physical Inactivity ​and Obesity: A Vicious CircleObesity, 
-  * SharpP. M., & HahnBH. (2011). Origins of HIV and the AIDS pandemic. Cold Spring Harbor perspectives in medicine, 1(1), a006841.+16(2), 409-414. http://​dx.doi.org/​10.1038/​oby.2007.72
  
-  * Simon, V., Ho, D. D., Karim, QA2006HIV/AIDS Epidemiologypathogenesisprevention and treatment. The Lancet, 368: 489-504. +8 ​Cohen-ColeE& FletcherJ(2008)Is obesity contagious? Social networks vs environmental factors in the obesity epidemicJournal Of Health Economics27(5)
-  ​* ​  ​Surugue,​ L. (2016, November 2). First large-scale HIV vaccine trial in seven years to start in South Africa. International Business Times. Retrieved November 2, 2016, from http://www.ibtimes.co.uk/first-large-scale-hiv-vaccine-clinical-trial-seven-years-start-south-africa-1589468+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
  
-  * University ​of California San Francisco. (2006). HIV Antibody Assays. Retrieved from http://hivinsite.ucsf.edu/InSite.jsp?page=kb-02-02-01+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 
 + 
 +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 PopulationPLOS ONE, 10(4), e0123579http://​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 
 + 
 +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 
 + 
 +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 
 + 
 +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. 
 + 
 +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 
 + 
 +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 
 + 
 +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, 
 +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. 
 + 
 +26.  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. 
 + 
 +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. 
 + 
 +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. 
 + 
 +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/​ 
 + 
 +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. 
 + 
 +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. 
 + 
 +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. 
 + 
 +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. 
 + 
 +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 
 +& adolescent medicine, 158(4), 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 
 +Behavioral Medicine, 30(3),​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. 
 + 
 +44.  Finer, N. (2002). Sibutramine:​ its mode of action and efficacy. International Journal of Obesity, 26(S4), S29. 
 + 
 +45.  Davidson, M. H., Hauptman, J., DiGirolamo, M., Foreyt, J. P., Halsted, C. H., Heber, D., ... & Heymsfield, S. B. (1999). Weight control and risk factor reduction in obese subjects treated for 2 years with orlistat: a randomized controlled trial. Jama, 281(3), 235-242. 
 + 
 +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. 
 +  
 + 
  
  
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