Please confirm that you would like to log out of Medscape.
If you log out, you will be required to enter your username and password the next time you visit.
Log outCancel
Obesity: How to Diagnose and Treat an Epidemic
Author: Harold Bays MD, FTOS, FACC, FACE, FNLA | November 28, 2017
| Contributor Information
Swipe to advance
Image data from Ogden CL, Carroll MD, Kit BK, et al. Prevalence of childhood and adult obesity in the United States, 2011-2012. JAMA. 2014;311(8):806-14.
Obesity: How to Diagnose and Treat an Epidemic
Author: Harold Bays MD, FTOS, FACC, FACE, FNLA | November 28, 2017 | Contributor Information
In the United States, obesity is both an epidemic and a substantial public health crisis, resulting in many metabolic and biomechanical adverse consequences, such as type 2 diabetes, high blood pressure, dyslipidemia, cardiovascular disease, arthritis, and sleep apnea. According to the American Society of Bariatric Physicians, "Obesity is defined as a chronic, relapsing, multi-factorial, neurobehavioral disease, wherein an increase in body fat promotes adipose tissue dysfunction and abnormal fat mass physical forces, resulting in adverse metabolic, biomechanical, and psychosocial adverse consequences."[1] More than one third of adults (36.5%) and 17% of children and adolescents in the United States are considered obese based on body mass index. The World Health Organization defines obesity as a body mass index (BMI) greater than 30 kg/m2.[2] In 2015, the Endocrine Society released guidelines on the treatment of obesity in various populations, including patients with type 2 diabetes, patients with hypertension, and women of childbearing age.[3]
Image adapted from Bays HE, Seger JC, Primack C, et al. Obesity Algorithm, presented by the Obesity Medicine Association. www.obesityalgorithm.org. 2016-2017. Accessed November 21, 2017.
Obesity: How to Diagnose and Treat an Epidemic
Author: Harold Bays MD, FTOS, FACC, FACE, FNLA | November 28, 2017 | Contributor Information
The etiology of obesity and its complications are due to many factors; thus, the adverse consequences of obesity are more complex than simply being an imbalance between energy intake and energy output.[4] Obesity is a multifactorial disease with genetic, environmental, and medical factors, interfacing with immune, endocrine, and neurobehavioral elements. Genetic factors may help explain 40-70% of the variance in obesity, within a limited range of a BMI between 18 and 30 kg/m2.[4] Studies on monozygotic twins indicate that genetic factors are significantly involved in obesity in terms of how energy is stored as either fat or lean tissue.[5,6] Extragenetic factors that influence nutritional and physical activity habits may play a large role in obesity, as evidenced by the increase in the prevalence of obesity and its complications with changes in environment (eg, work schedules, oversized food portions, lack of access to healthy foods, food advertising, lack of neighborhood sidewalks).[1,5]
Image from Ogden CL, Carroll MD, Fryar CD, Flegal KM. Prevalence of obesity among adults and youth: United States, 2011–2014. NCHS data brief, no 219. Hyattsville, MD: National Center for Health Statistics. 2015.
Obesity: How to Diagnose and Treat an Epidemic
Author: Harold Bays MD, FTOS, FACC, FACE, FNLA | November 28, 2017 | Contributor Information
In the United States, about 79 million adults older than 20 years (37 million men and 42 million women) and over 12 million children and adolescents are obese.[7] In 2011-2012, the prevalence of obesity among adult men and women was almost 35%.[2] The prevalence in children and adolescents has increased to 17.2%. Obesity also has a strong prevalence among non-Hispanic black women, with 26.8% of deaths in such patients associated with a BMI of 25 kg/m2 or higher.[1]
Obesity: How to Diagnose and Treat an Epidemic
Author: Harold Bays MD, FTOS, FACC, FACE, FNLA | November 28, 2017 | Contributor Information
Body fat percentage measures may be helpful for patients with extremes in muscle mass, such as increases in muscle mass for muscular individuals, or decreases in muscle mass (sarcopenia) in geriatric patients who may have a BMI in the normal range but may be likely to develop diabetes.[8]
Image adapted from Bays HE, Seger JC, Primack C, et al. Obesity Algorithm, presented by the Obesity Medicine Association. www.obesityalgorithm.org. 2016-2017. Accessed November 21, 2017.
Obesity: How to Diagnose and Treat an Epidemic
Author: Harold Bays MD, FTOS, FACC, FACE, FNLA | November 28, 2017 | Contributor Information
BMI is used more commonly than body fat percentage to define obesity. An individual's BMI is calculated as weight/height2. According to the WHO, overweight is defined as a BMI of 25-29.9 kg/m2, and obesity is defined as a BMI greater than 30 kg/m2. In children, overweight is commonly defined as a BMI above the 85th percentile, and obesity as a BMI above the 95th percentile.[9,10] When mapped, epidemiologic studies suggest a J-shaped curve relating weight distribution to mortality/morbidity, since along with high BMI, very low BMI is also associated with increased mortality risk.[11]
Image from Bays HE, Seger JC, Primack C, et al. Obesity Algorithm, presented by the Obesity Medicine Association. www.obesityalgorithm.org. 2016-2017. Accessed November 21, 2017.
Obesity: How to Diagnose and Treat an Epidemic
Author: Harold Bays MD, FTOS, FACC, FACE, FNLA | November 28, 2017 | Contributor Information
Waist circumference and body fat percentage are also used in conjunction with BMI to screen for possible health risks. Waist circumference provides information regarding adipose tissue function. Waist circumference is a measure of abdominal obesity; abdominal adiposity is a risk factor for cardiovascular disease, high blood glucose, high blood pressure, and dyslipidemia. Abdominal obesity is defined in men as a waist circumference greater than 40 inches, and in women as a waist circumference greater than 35 inches.
Image from Dreamstime.
Obesity: How to Diagnose and Treat an Epidemic
Author: Harold Bays MD, FTOS, FACC, FACE, FNLA | November 28, 2017 | Contributor Information
Obesity has a multitude of adverse metabolic health consequences. Obesity increases the prevalence of type 2 diabetes mellitus, hypertension, dyslipidemia, and metabolic syndrome.[12] The metabolic syndrome is a constellation of cardiometabolic risk factors (eg, abdominal obesity, high glucose levels, high blood pressure, elevated triglycerides, and reduced levels of high-density lipoprotein cholesterol) that reflect underlying adiposopathic complications of obesity. Obesity and the metabolic syndrome are risk factors for atherosclerotic cardiovascular disease, metabolic diseases, fatty liver, and several cancers. More than 80% of people with type 2 diabetes are overweight or obese, and the risk of hypertension increases in patients with upper body and abdominal obesity (apple shaped body configuration).[13]
Image from Dreamstime.
Obesity: How to Diagnose and Treat an Epidemic
Author: Harold Bays MD, FTOS, FACC, FACE, FNLA | November 28, 2017 | Contributor Information
During positive caloric balance, adipocytes are increased in size and possibly in number. If limitations exist on the ability to proliferate new fat cells, then the excessive energy may be stored by further hypertrophy of existing fat cells (promoting their dysfunction) or may be stored in ectopic fat depots such as pericardiac fat, perivascular fat, and visceral fat. Thus, an increase in visceral adiposity may be considered a reflection of global fat dysfunction. Adiposopathy, or "sick fat," is defined as anatomic and functional abnormalities of the adipocyte and adipose tissue caused by adiposity, resulting in imbalances in the endocrine and immune systems. These endocrine and immune imbalances directly and indirectly lead to hyperglycemia, high blood pressure, dyslipidemia, and cardiovascular disease.[14-16]
Image (left and upper) from Dreamstime. Image (inset) courtesy of David Goodsell/Wikimedia Commons.
Obesity: How to Diagnose and Treat an Epidemic
Author: Harold Bays MD, FTOS, FACC, FACE, FNLA | November 28, 2017 | Contributor Information
Many hormones impact appetite and food intake. An illustrative example is leptin, which is a peptide hormone secreted from fat cells and involved in the regulation of fat metabolism.[17] When a person gains weight, leptin secretion is increased. Leptin signals satiety to the hypothalamus, which promotes a reduction in dietary intake and fat storage while modulating energy expenditure and carbohydrate metabolism. Mutations resulting in defects of the leptin receptor in the hypothalamus may result in early onset obesity and hyperphagia despite normal or elevated leptin levels. Administration of leptin to leptin-deficient patients with obesity can be remarkably effective in reducing obesity. However, most individuals who are overweight or obese and have elevated leptin levels are sometimes described as leptin resistant. Administration of leptin to such individuals has not yet proven to substantially improve obesity or its complications. Attenuation of leptin secretion during the night or a change in other circadian satiety hormones lead to a situation called "night eating syndrome" in some individuals.[18]
Image from Bays HE, Seger JC, Primack C, et al. Obesity Algorithm, presented by the Obesity Medicine Association. www.obesityalgorithm.org. 2016-2017. Accessed November 21, 2017.
Obesity: How to Diagnose and Treat an Epidemic
Author: Harold Bays MD, FTOS, FACC, FACE, FNLA | November 28, 2017 | Contributor Information
Complicating obesity clinical management is the obesity paradox. One of the most challenging aspects of obesity is the presence of more than one obesity paradox. For example, not all patients who are overweight have excessive fat-related metabolic disease (EFRMD), and not all patients with EFRMD are significantly overweight.[19-21] Other layers of the obesity paradox include anatomic, demographic, therapeutic, and cardiovascular event paradoxes, such as reports of more favorable cardiovascular event outcomes in overweight and obese patients.
Image from Dreamstime.
Obesity: How to Diagnose and Treat an Epidemic
Author: Harold Bays MD, FTOS, FACC, FACE, FNLA | November 28, 2017 | Contributor Information
Because visceral adiposity may reflect global fat dysfunction and is an anatomic manifestation of adiposopathy, an increase in abdominal waist circumference is associated with increased cardiovascular and metabolic disease.[22] Body fat distribution can also be affected by age, sex, ethnicity, hormonal factors, diet, sedentary lifestyle, pharmacologic agents, and other environmental and lifestyle factors such as smoking and stress.[22] Visceral obesity–related cardiometabolic risks are influenced by physiologic characteristics of abdominal adipose tissues, such as adipocyte size and number, lipolytic responsiveness, lipid storage capacity, and inflammatory cytokine production.[23]
Visceral fat is an active endocrine gland that produces hormones and pro-inflammatory cytokines that have direct impact on insulin sensitivity and increased risk for type 2 diabetes and cardiovascular disease.[24,25]
Image from Bays HE, Seger JC, Primack C, et al. Obesity Algorithm, presented by the Obesity Medicine Association. www.obesityalgorithm.org. 2016-2017. Accessed November 21, 2017.
Obesity: How to Diagnose and Treat an Epidemic
Author: Harold Bays MD, FTOS, FACC, FACE, FNLA | November 28, 2017 | Contributor Information
A number of physiologic and environmental reasons help explain eating habits and include specific physiologic factors; eating on the basis of timing or emotions; environmental factors; and information gaps. Lack of proper nutritional education and proper nutritional information can contribute to unintended increased caloric consumption. Another important influence is the reward system, wherein eating occurs for reasons other than hunger. Some patients with overweight or obesity may have eating disorders such as binge eating disorder, bulimia nervosa, and night eating syndrome. Binge eating disorder affects 2-3% of US adults and is classified as frequent episodes of consuming large amounts of foods at least once a week for a period of 3 months and may occur in up to 50% of patients with severe obesity. Bulimia is categorized as a cycle of recurrent binge eating and compensatory purging. Laxative and diuretic abuse are also aspects of bulimia. Bulimia occurs in about 1% of adults, mostly women. The Russell sign (ie, calluses and abrasions on the dorsum of the hands from self-purging) points to bulimia, as does laboratory tests for hypokalemia due to hypomagnesemia. Night eating syndrome is when at least 25% of daily food consumption occurs after the evening meal. Eating is often required to return to sleep after recurrent awakenings.
Image from Bays HE, Seger JC, Primack C, et al. Obesity Algorithm, presented by the Obesity Medicine Association. www.obesityalgorithm.org. 2016-2017. Accessed November 21, 2017.
Obesity: How to Diagnose and Treat an Epidemic
Author: Harold Bays MD, FTOS, FACC, FACE, FNLA | November 28, 2017 | Contributor Information
Adiposity-relevant blood testing includes a fasting lipid panel, liver function studies, thyroid function tests, and fasting glucose and hemoglobin A1c (HbA1c). These initial laboratory studies are suggested to routinely screen for type 2 diabetes mellitus, dyslipidemia and fatty liver disease. Lipid panel testing is recommended for children and adolescents with a BMI at or above the 85th percentile for age and sex beginning at 10 years of age. Fasting glucose is recommended for all children and adolescents with a BMI at or above the 95th percentile beginning at 10 years of age. Clinicians should also assess for a family history of overweight and related complications.[26]
Image (left) from Dreamstime. Image (right) from Bays HE, Seger JC, Primack C, et al. Obesity Algorithm, presented by the Obesity Medicine Association. www.obesityalgorithm.org. 2016-2017. Accessed November 21, 2017.
Obesity: How to Diagnose and Treat an Epidemic
Author: Harold Bays MD, FTOS, FACC, FACE, FNLA | November 28, 2017 | Contributor Information
Patients with overweight or obesity may benefit from individualized testing. Individualized testing should be based on medical history, symptoms, signs, and overall health risk, such as evidence of central nervous system or endocrine causes of obesity, or other risk factors for cardiopulmonary diseases.
Image from Bays HE, Seger JC, Primack C, et al. Obesity Algorithm, presented by the Obesity Medicine Association. www.obesityalgorithm.org. 2016-2017. Accessed November 21, 2017.
Obesity: How to Diagnose and Treat an Epidemic
Author: Harold Bays MD, FTOS, FACC, FACE, FNLA | November 28, 2017 | Contributor Information
While almost all patients with obesity should be screened for diabetes, some clinicians find clinical use in assessing for insulin resistance, which may include measures of increased serum levels of fasting insulin and C-peptide. Prediabetes may be suggested by impaired fasting glucose (fasting plasma glucose levels of 100-125 mg/dL [5.6-6.9 mmol/L]) or impaired glucose tolerance (2-hour oral glucose tolerance test values of 140-199 mg/dL [7.8-11.0 mmol/L]) or A1C between 5.7-6.4%. Patients with these findings are at relatively high risk for the future development of diabetes. Type 2 diabetes is diagnosed when 2 successive fasting glucose levels are 126 mg/dL or greater or HbA1c is 6.5% or higher.[27]
Image from Bays HE, Seger JC, Primack C, et al. Obesity Algorithm, presented by the Obesity Medicine Association. www.obesityalgorithm.org. 2016-2017. Accessed November 21, 2017.
Obesity: How to Diagnose and Treat an Epidemic
Author: Harold Bays MD, FTOS, FACC, FACE, FNLA | November 28, 2017 | Contributor Information
Treatment options for patients who are overweight or obese often include coordination of a patient's nutrition and physical activity, along with behavior therapy, as well as potential pharmacotherapy and/or bariatric surgery. Therapies that decrease body fat will often improve adipocyte and adipose tissue function (thus improving metabolic disease) and improve fat mass disease.[11] Multidisciplinary programs that include a physician, a psychologist or psychiatrist, physical and exercise therapists, dietitians, and other subspecialists may often result in long-term modest weight loss, typically between 5% and 10%,[28] although this may be highly variable depending on the patient, provider, and program. Long-term weight loss was also achieved with multidisciplinary intervention in patients with diabetes in real-world clinical practice.[29]
Image from Bays HE, Seger JC, Primack C, et al. Obesity Algorithm, presented by the Obesity Medicine Association. www.obesityalgorithm.org. 2016-2017. Accessed November 21, 2017.
Obesity: How to Diagnose and Treat an Epidemic
Author: Harold Bays MD, FTOS, FACC, FACE, FNLA | November 28, 2017 | Contributor Information
Caloric restriction, self-monitoring, patient preference, and program adherence may be more important than any specific "diet." A low-calorie diet is categorized as an intake of 800-1800 kcal/day. A very low calorie diet is categorized as an intake of less than 800 kcal/day.[11] According to the National Weight Control Registry (NWCR), patterns that are associated with successful weight loss maintenance include maintaining a low-calorie, low-fat diet or low carbohydrates; self-monitoring one's weight; 60 minutes of physical activity daily; minimal sedentary activities (eg, minimal TV watching); and eating breakfast every day.[30]
Image from Bays HE, Seger JC, Primack C, et al. Obesity Algorithm, presented by the Obesity Medicine Association. www.obesityalgorithm.org. 2016-2017. Accessed November 21, 2017.
Obesity: How to Diagnose and Treat an Epidemic
Author: Harold Bays MD, FTOS, FACC, FACE, FNLA | November 28, 2017 | Contributor Information
While an increase in physical activity may contribute to weight loss, negative caloric balance is generally the most effective intervention. However, perhaps the main advantage of a routine increase in physical activity is maintaining long-term weight loss.[31] Prolonged sitting is associated with harmful health risks regardless of an individual's level of physical activity.[32] Technologies available that can help track and assess nutritional and physical activity include wearable bracelets that track an individual's number of steps per day to help decrease the amount of sedentary time.
Exercise should include stretching, aerobic and strength training. Short bouts of exercise of 10 minutes each may be preferred when prescribing exercise to obese adults. Short bouts of exercise may enhance exercise adherence, enhance weight loss and produce similar changes in cardiorespiratory fitness when compared to long bouts of exercise.[33]
Image from Bays HE, Seger JC, Primack C, et al. Obesity Algorithm, presented by the Obesity Medicine Association. www.obesityalgorithm.org. 2016-2017. Accessed November 21, 2017.
Obesity: How to Diagnose and Treat an Epidemic
Author: Harold Bays MD, FTOS, FACC, FACE, FNLA | November 28, 2017 | Contributor Information
Adult patients with overweight or obesity who have not had successful weight loss through appropriate nutritional and physical activity intervention may be considered for weight management pharmacotherapy. Weight management pharmacotherapy should be used in tandem with nutritional approaches, increased physical activity, and behavioral therapies. Prescription weight-loss drugs are approved for patients with a BMI of 30 kg/m2 or more and for patients with a BMI of 27 kg/m2 or more having adverse consequences of being overweight, such as hypertension, type 2 diabetes, or dyslipidemia.[31] Studies show that a 5-10% weight loss may improve metabolic and fat mass diseases,[11] improve endothelial function and reduce inflammation.[34,35]
Image from Bays HE, Seger JC, Primack C, et al. Obesity Algorithm, presented by the Obesity Medicine Association. www.obesityalgorithm.org. 2016-2017. Accessed November 21, 2017.
Obesity: How to Diagnose and Treat an Epidemic
Author: Harold Bays MD, FTOS, FACC, FACE, FNLA | November 28, 2017 | Contributor Information
Orlistat, approved by the FDA in 1999, blocks the action of intestinal lipase, which reduces fat absorption by the gastrointestinal tract. Phentermine, approved for decades, has an indicated use for short-term treatment of obesity (8-12 weeks).[31] Lorcaserin, approved by the FDA in 2012, selectively activates 5-HT2C receptors on anorexigenic pro-opiomelanocortin neurons in the hypothalamus to promote satiety. The combination of phentermine HCl and extended-release topiramate, approved by the FDA in 2012, may also increase satiety. Two other approved anti-obesity agents include (1) extended-release naltrexone (opioid antagonist)/bupropion (antidepressant) and (2) liraglutide (glucagon-like peptide-1 agonist).
Image from Dreamstime.
Obesity: How to Diagnose and Treat an Epidemic
Author: Harold Bays MD, FTOS, FACC, FACE, FNLA | November 28, 2017 | Contributor Information
Candidates for bariatric surgery include patients with obesity having a BMI >40 kg/m2, or a BMI ≥35 kg/m2 (sometimes ≥30 kg/m2) in the presence of significant obesity complications, such as type 2 diabetes, hypertension, and obstructive sleep apnea. Bariatric surgery, in carefully selected patients within a multidisciplinary support team, can substantially improve morbidities associated with severe obesity, such as obstructive sleep apnea, type 2 diabetes, hypertension, and heart failure.
Image from Dreamstime.
Obesity: How to Diagnose and Treat an Epidemic
Author: Harold Bays MD, FTOS, FACC, FACE, FNLA | November 28, 2017 | Contributor Information
Bariatric procedures are increasingly being performed laparoscopically, and a number of procedures are available. Preoperative considerations include prior efforts of nonsurgical methods toward weight loss, evaluation and management by a clinician trained in obesity medicine, and a willingness of the patient to commit to and comply with postoperative medical surveillance. Preoperative evaluations also usually involve overall assessment by a clinician trained in obesity medicine (perhaps board certified) and a trained bariatric surgeon, as well as a comprehensive evaluation of the cardiac, pulmonary, gastrointestinal, and mental health status of the patient. Both preoperatively and postoperatively, patients undergoing bariatric surgery should also maintain interactions with specialized health care professionals such as dietitians, as well as exercise and behavioral specialists. Several nutrition deficiencies may occur after gastric bypass surgery and will require life-long replacements.
Obesity is a substantial public health crisis in the United States and in the rest of the industrialized world. The prevalence is increasing rapidly in numerous industrialized nations worldwide.Diseases/Conditions, November 2017
Commenting is limited to medical professionals. To comment please Log-in.
Comments on Medscape are moderated and should be professional in tone and on topic. You must declare any conflicts of interest related to your comments and responses. Please see our Commenting Guide for further information. We reserve the right to remove posts at our sole discretion.
Comments on Medscape are moderated and should be professional in tone and on topic. You must declare any conflicts of interest related to your comments and responses. Please see our Commenting Guide for further information. We reserve the right to remove posts at our sole discretion.
Close
Contributor Information
Author
Harold Bays MD, FTOS, FACC, FACE, FNLA Medical Director / President
Louisville Metabolic and Atherosclerosis Research Center
Disclosure: Harold E. Bays, MD, has disclosed the following relevant financial relationships: Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: Amarin; Amgen; Astra Zeneca; Bristol Meyers Squibb; Catabasis; Daiichi Sankyo; Eisai; Eli Lilly; Isis; Merck; Novartis; NovoNordisk; Omthera; Regeneron; Sanofi; VIVUS; WPU Pharmaceuticals Serve(d) as a speaker or member of a speakers bureau for: Amarin; Amgen; Astra Zeneca; Bristol Meyers Squibb; Catabasis; Daiichi Sankyo; Eisai; Eli Lilly; Isis; Merck; Novartis; NovoNordisk; Omthera; Regeneron; Sanofi; VIVUS; WPU Pharmaceuticals Received research grant from: Amarin; Amgen; Ardea; Arisaph; California Raisin Marketing Board; Catabasis; Cymabay; Eisai; Elcelyx; Eli Lilly; Esperion; Gilead; Hanmi; Hisun; Hoffman La Roche; Home Acces; Janssen; Johnson and Johnson; Merck; Necktar; Novartis; NovoNordisk; Omthera; Orexigen; Pfizer; Pronova; Regeneron; Sanofi; Takeda; TIMI; VIVUS; WPU Pharmaceuticals
Reviewer
Osama Hamdy, MD, PhD
Medical Director
Obesity Clinical Program
Director of Inpatient Diabetes Program
Joslin Diabetes Center;
Associate Professor of Medicine
Harvard Medical School
Osama Hamdy, MD, PhD, has disclosed the following relevant financial relationships: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: on advisory panel of Astra-Zeneca Inc.
Received research grant from: USDA Dairy Council
Have a 5% or greater equity interest in: HealthyMation LLC
Received consulting fee from Merck Inc. for speaking and teaching
Received consulting fee from Abbott Nutrition for consulting
Close
References
Masters RK, Reither EN, Powers DA, et al. The Impact of Obesity on US Mortality Levels: The Importance of Age and Cohort Factors in Population Estimates. Am J Public Health. Aug 15, 2013.
Ogden CL, Carroll MD, Kit BK, et al. Prevalence of childhood and adult obesity in the United States, 2011-2012. JAMA. 2014;311(8):806-14.
Bouchard C, Tremblay A, Després JP, et al. The response to long-term overfeeding in identical twins. N Engl J Med. May 24 1990;322(21):1477-82.
Go AS, Mozaffarian D, Roger VL, et al. Heart disease and stroke statistics-2013 update: a report from the American Heart Association. Circulation. 2013;127:e6-e245.
Seger JC, Horn DB, Westman EC, et al. Obesity Algorithm, presented by the American Society of Bariatric Physicians, 2014-2015. Available at: www.obesityalgorithm.org.
Dietz WH, Economos CD. Progress in the control of childhood obesity. Pediatrics. 2015 Feb 9. 2014-972. [Epub ahead of print].
Després JP. Body fat distribution and risk of cardiovascular disease. Circulation. 2012; 126: 1301-13.
Nguyen NT, Magno CP, Lane KT, et al. Association of hypertension, diabetes, dyslipidemia, and metabolic syndrome with obesity: findings from the National Health and Nutrition Examination Survey, 1999 to 2004. J Am Coll Surg. 2008;207(6):928.
National Institute of Diabetes and Digestive and Kidney Diseases. Weight-control Information Network. Do You Know Some of the Health Risks of Being Overweight? Available at: http://win.niddk.nih.gov/publications/health_risks.htm.
Bays HE. Adiposopathy: Is sick fat a cardiovascular disease? JACC. 2011; 57: 2461-73.
Bays HE. Adiposopathy, diabetes mellitus, and primary prevention of atherosclerotic coronary artery disease: treating "sick fat" through improving fat function with antidiabetes therapies. Am J Cardiol. 2012;110: 4B-12B.
Bays H: Central obesity as a clinical marker of adiposopathy; increased visceral adiposity as a surrogate marker for global fat dysfunction. Curr Opin Endocrinol Diabetes Obes. 2014 21:345-351.
Zhang Y, Proenca R, Maffei M, et al. Positional cloning of the mouse obese gene and its human homologue. Nature. 1994;372: 425-32.
Birketvedt GS, Geliebter A, Florholmen J, et al. Neuroendocrine Profile in the Night Eating Syndrome. Curr Obes Rep. 2014 Mar;3(1):114-9.
Bays HE. "Sick Fat," metabolic disease, and atherosclerosis. Am J Med. 2009;122:S26-37.
Bays HE, Blonde L, Rosenson R. Adiposopathy: how do diet, exercise and weight loss drug therapies improve metabolic disease in overweight patients? Expert Rev Cardiovasc Ther. 2006;4(6):871-95.
Bays HE. Adiposopathy, "sick fat," Ockham's razor, and resolution of the obesity paradox. Curr Atheroscler Rep. 2014 May;16(5):409.
Shungin D, Winkler TW, Croteau-Chonka DC, et al. New genetic loci link adipose and insulin biology to body fat distribution. Nature. 2015;518:187-96.
Tchernof A, Després JP. Pathophysiology of human visceral obesity: an update. Physiol Rev. 2013;93:359-404.
Hamdy O. The role of adipose tissue as an endocrine gland. Curr Diab Rep. 2005 Oct;5(5):317-9.
Ahima RS, Flier JS. Adipose tissue as an endocrine organ. Trends Endocrinol Metab. 2000 Oct;11(8):327-32.
Barlow SE. Expert committee recommendations regarding the prevention, assessment, and treatment of child and adolescent overweight and obesity: summary report. Pediatrics. 2007;120(Suppl 4):S164-92.
Diagnosis and classification of diabetes mellitus. Diabetes Care. Jan 2010;33 Suppl 1:S62-9.
Jensen MD, Ryan DH, Apovian CM, et al. 2013 AHA/ACC/TOS guideline for the management of overweight and obesity in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and The Obesity Society. J Am Coll Cardiol. 2014; 63: 2985-3023.
Hamdy O, Mottalib A, Morsi A, et al. Long-term effect of intensive lifestyle intervention on cardiovascular risk factors in patients with diabetes in real-world clinical practice: a 5-year longitudinal study. BMJ Open Diabetes Res Care. 2017;5(1):e000259.
McKinney L. Diagnosis and Management of Obesity. Leawood, KS. American Academy of Family Physicians. 2013.
Biswas A, Oh PI, Faulkner GE, et al. Sedentary time and its association with risk for disease incidence, mortality, and hospitalization in Adults: a systematic review and meta-analysis. Ann Intern Med. 2015;162(2):123-32.
Jakicic JM, Wing RR, Butler BA, et al. Prescribing exercise in multiple short bouts versus one continuous bout: effects on adherence, cardiorespiratory fitness, and weight loss in overweight women. Int J Obes Relat Metab Disord. 1995;19(12):893-901.
Hamdy O, Ledbury S, Mullooly C, et al. Lifestyle modification improves endothelial function in obese subjects with the insulin resistance syndrome. Diabetes Care. 2003;26(7):2119-25.
Monzillo LU, Hamdy O, Horton ES, et al. Effect of lifestyle modification on adipokine levels in obese subjects with insulin resistance. Obes Res. 2003;11(9):1048-54.
Please do not use this form to submit personal or patient medical information or to report adverse drug events. You are encouraged to report adverse drug event information to the FDA.
Comments