Week 2 - Overweight and Obesity - Part 1 PDF

WEEK 2: OVERWEIGHT AND OBESITY – PART I EHR522: EXERCISE FOR METABOLIC AND MENTAL HEALTH CONDITIONS Subject Coordinator: Tim Miller [email protected] 02 6338 4442 Clinical Exercise Physiology, 5th Edition - Chapter 9 OVERWEIGHT & OBESITY  Overweight and obesity is an epidemic associated with, if...

WEEK 2: OVERWEIGHT AND OBESITY – PART I EHR522: EXERCISE FOR METABOLIC AND MENTAL HEALTH CONDITIONS Subject Coordinator: Tim Miller [email protected] 02 6338 4442 Clinical Exercise Physiology, 5th Edition - Chapter 9 OVERWEIGHT & OBESITY  Overweight and obesity is an epidemic associated with, if not the principal cause of, much disease and disability  Short-term intervention – limited effectiveness  Long-term success – rare without ongoing medical efforts  Obesity – a chronic illness, often with co- morbidities that need to be considered  Significant weight loss has far-ranging positive health effects and can often control or eliminate comorbidities  Exercise and dietary changes are the main contributors OVERWEIGHT & OBESITY  WHO reports that obesity (BMI > 30) has tripled worldwide since 1975  In 2016, it was estimated that at least 2.5 billion people were either overweight or obese, with 600 million categorised as obese  Overweight and obesity causes more death than does being underweight  Obesity has led to discrimination in more recent years  Many view obesity as a moral or social issue, stigmatising its management. This can add to the barriers related to understanding and treating the condition OVERWEIGHT & OBESITY  Obesity and extreme obesity are associated with an increased rate of death from all causes, particularly from cardiovascular disease  Obesity and sedentary lifestyle is considered the second leading cause of preventable death in the USA, and may overtake tobacco abuse within the next decade  For obese individuals, life expectancy decreases by about 7 years compared with normal-weight individuals OVERWEIGHT & OBESITY IN AUSTRALIA – A GROWING PROBLEM OVERWEIGHT AND OBESITY  In Australia, per capita spending is approximately $830 more for an obese individual versus someone of normal body weight  Obesity reduces life expectancy and this effect is more powerful in those who develop obesity earlier in life  Obesity and sedentary lifestyle is considered the second leading cause of preventable death in the United States and may overtake tobacco abuse within the next decade  In 2016 life expectancy fell slightly for the first time, reflecting the effects of obesity-related chronic illness on society OVERWEIGHT & OBESITY OVERWEIGHT & OBESITY OVERWEIGHT & OBESITY  Exercise, diet modifications and lifestyle changes are the foundation of a behavioural-based approach to the management of obesity  There is merit for utilising effective multidisciplinary teams, though there are practical limitations to this, particularly in the private sector  A long-term-horizon approach is imperative to success  Using a behaviour change approach is critical OVERWEIGHT & OBESITY  Overweight and Obesity  An abnormal or excessive fat accumulation that presents a risk to health  An excess of subcutaneous fat in proportion to lean body mass  Body Mass Index (BMI)  Indicates overweight for height, but does not discriminate between fat mass and lean tissue  Significant correlation with total body fat  Acceptable clinical measure of overweight and obesity  Most successful in large cohorts OVERWEIGHT & OBESITY  Australia (WHO, USA, Canada and Europe):  Overweight: 25.0 to 29.9  Obesity: ≥ 30  Inaccuracies in some individuals  Is a given BMI ‘unhealthy’?  Is body fat percentage actually elevated?  The diagnostic accuracy of a BMI > 30 to diagnose obesity is limited (low sensitivity), but does well to identify those who are not obese (high specificity) OVERWEIGHT & OBESITY OVERWEIGHT & OBESITY OVERWEIGHT & OBESITY  BMI thresholds vary internationally by race  In Japan  Overweight: 23.0 to 24.9  Obese: ≥ 24.9  Higher incidence of diseases associated with weight and body fat occurring at lower BMI values in Asian populations OVERWEIGHT & OBESITY OVERWEIGHT & OBESITY  Other methods for the assessment of body composition  Skinfolds  Bioelectrical impedance  Water or air displacement  Dual-energy x-ray absorptiometry (DEXA)  Possible barriers  Technical skill  Patient cooperation  Time  Cost  Space CHILDHOOD OBESITY  70% of all obesity begins in adulthood  There is, however, a strong association between childhood obesity and the risk of adulthood obesity. This association is affected by:  Severity of childhood obesity  Age of onset  Whether the parents are also obese  Most obese children will carry their obesity into adulthood  Increasing childhood obesity is a worldwide issue CENTRAL ADIPOSITY  BMI > 30 carries increased health risk for obesity- related comorbidities  Heart disease  Diabetes  Hypertension  Dyslipidaemia  Sleep apnoea  Gasto-oesophageal reflux disease (GORD)  The pattern of fat distribution also affects risk. Abdominal (central or android) obesity is more closely related to elevated cardiometabolic risk than is gluteofemoral (gynoid or lower body) obesity CENTRAL ADIPOSITY  The enzyme lipoprotein lipase, which regulates the storage of fats as triglycerides, is more active in abdominal obesity and therefore increases fat storage  Central obesity can be grossly estimated by waist- to-hip ratio. Increased health risk when  Women > 0.8  Men > 1.0  Alternately, just waist circumference. Increased health risk when  Women > 80cm  Men > 94cm WAIST AND HIP MEASUREMENT  Accurate measurement of waist and hip circumferences is important  Waist: With the subject standing, arms at the sides, feet together, and abdomen relaxed, a horizontal measure is taken at the narrowest part of the torso (above the umbilicus and below the xiphoid process)  Hip: With the subject standing, legs slightly apart (10cm), a horizontal measure is taken at the maximal circumference of the hips (the proximal thighs), just below the gluteal fold VISCERAL VS. SUBCUTANEOUS ADIPOSITY  Visceral fat – Lies deep within the body cavities, surrounding internal organs including the liver, pancreas and intestines  Visceral fat can be stored within the liver and lead to non-alcoholic fatty liver disease (NAFLD)  Visceral fat accumulation is associated with a higher cardiometabolic risk than subcutaneous fat because of its metabolic characteristics, which include insulin resistance and glucose intolerance VISCERAL VS. SUBCUTANEOUS ADIPOSITY  Visceral fat is best measured by MRI, U/S or CT  A more practical measure is sagittal diameter  Patient lies on their back with knees bent, feet flat on the surface and arms in a relaxed position  Distance from floor/plinth to a horizontal level at anterior abdomen at the level of the iliac crest  Taken during a normal exhalation (tidal breathing)  A promising technique that’s the best practical predictor of visceral fat  > 30cm is related to an increase cardiovascular disease risk and insulin resistance VISCERAL VS. SUBCUTANEOUS ADIPOSITY OVERWEIGHT & OBESITY PATHOPHYSIOLOGY OF OBESITY  Obesity results from longstanding positive energy balance  Average daily calorie intake has increased by over 200 kcal over the last several decades as food costs have fallen dramatically and as more calories are consumed outside the home  At the same time, physical activity has fallen because of advances in equipment and ergonomics in the workplace PATHOPHYSIOLOGY OF OBESITY  Recent research has identified an ever-increasing number of genetic and physiologic factors pointing to a large array of neurological and peripheral endocrine messengers that influence food intake and nutrient utilisation and that regulate weight in a way that often frustrates patients’ weight loss efforts  Advanced neuroimaging research has recently shown similar patterns of brain activation between addictive-like eating and substance abuse PATHOPHYSIOLOGY OF OBESITY  Leptin is secreted by fat cells  Humans produce leptin in proportion to their weight and girth  Exogenous leptin administration has limited benefit for weight reduction except in the rarest of cases of human obesity because of a genetic absence of this fat cell hormone PATHOPHYSIOLOGY OF OBESITY  Genetic causes of obesity are a feature of rare disorders such as Prader-Willi syndrome, but are thought to be a factor in at least half of human obesity based on studies of twins raised separately or children who were adopted  Body fat distribution is also genetically determined and gender specific, and predictable changes throughout life may confound patients’ efforts at weight control  Increasing age reduces growth hormone and gonadal hormone secretion, which may predispose to greater visceral fat storage PATHOPHYSIOLOGY OF OBESITY  Set-Point Theory  Weight loss decreases total and resting energy expenditure, which slows further weight loss  Weight gain through overfeeding is associated with an increase in energy expenditure, which slows further weight gain  After weight loss, individuals require 15% fewer calories to maintain their lower weight  This tendency causes weight loss patients to return to higher weights unless they restrict calories over the long term or expend calories through greater physical activity PATHOPHYSIOLOGY OF OBESITY  Efforts to augment energy expenditure through medications have been complicated by adverse effects of increased blood pressure and heart rate  This area will remain a target for ongoing pharmaceutical research because resting metabolic activity accounts for about 70% of energy expenditure  The metabolic cost of food digestion accounts for about 10% of energy expenditure. The remainder is physical activity PATHOPHYSIOLOGY OF OBESITY  An interesting observation in patients following gastric bypass weight loss surgery is the dramatic reduction in ghrelin, a potent appetite-increasing gut hormone, which may explain, in part, the success of this surgical procedure  Ghrelin, produced as the stomach empties, triggers the central nervous system appetite stimulant neuropeptide Y (NPY), growth hormone and norepinephrine  Neuropeptide Y and norepinephrine predominantly stimulate carbohydrate intake.  Weight loss can increase serum ghrelin levels, which may explain part of the process that makes sustaining weight loss difficult PATHOPHYSIOLOGY OF OBESITY  Cholecystokinin, serotonin and peptide YY are among a group of central nervous system and gut peptides involved in satiety and reduced food intake  Serotonin has been targeted in the treatment of depression with selective serotonin reuptake inhibitors such as fluoxetine, but these medications have had limited effect in weight loss treatment  Nutrient selection during weight loss treatment may be a factor because appetite-reducing peptide YY is increased during high protein diets. This may partially explain the appetitereducing effect of high protein diets CLINICAL CONSIDERATIONS IN OVERWEIGHT & OBESITY  Although medically significant obesity exists in most patients who seek medical care, only a minority present requesting medical help with weight reduction  Compassion and understanding coupled with flexible and practical weight loss recommendations are essential to building rapport with obese patients  Most individuals seeking professional help with weight loss have a BMI of 38 or more, and invariably they have attempted to lose weight several times in the past  Proper assessment of the barriers to, and benefits of, weight loss should be the initial step in the clinical evaluation of the obese patient CLINICAL CONSIDERATIONS IN OVERWEIGHT & OBESITY CLINICAL CONSIDERATIONS IN OVERWEIGHT & OBESITY  Establishing where the patient is located on the Stages of Change Model can be useful in helping to approach and commence your treatment plan  One of the major barriers is that obesity and its common comorbidities are often silent  Readiness to change (ie. to lose weight) should be used to develop a tailored plan for the individual. For instance, patients who are not intending to lose weight (precontemplators) might simply be educated about the health risks of being overweight and the benefits of losing weight. CLINICAL CONSIDERATIONS IN OVERWEIGHT & OBESITY  Medical causes of obesity, including illnesses, medications and lifestyle changes known to increase weight, should be identified  Diabetes mellitus  Polycystic ovarian syndrome (PCOS)  Cushing’s syndrome  Many medications (neuroleptics, psychotropics, anticonvulsants, hypoglycaemic agents, B-blockers, ACEinhibitors and hormone therapies)  Smoking cessation  Job changes  Injuries  Sleep habits  Life stressors CLINICAL CONSIDERATIONS IN OVERWEIGHT & OBESITY  History of obesity should be obtained where possible, including  Age of onset of obesity  Weight gain since adolescence  Changes in weight distribution  Peak and lowest maintained adult weight  Any history of weight loss, be it intentional or not  Methods used to lose weight  Assessment of readiness for weight loss, social support, weight control skills, and history of any past or present eating disorders (binge eating disorder, bulimia nervosa, or, rarely, anorexia nervosa) should be considered CLINICAL CONSIDERATIONS IN OVERWEIGHT & OBESITY  An exercise history should identify current intentional exercise or opportunities for increased lifestyle activities, evaluate any exercise barriers and patient-specific benefits to help in the assessment of any contraindications to moderate or vigorous exercise, and develop a comprehensive exercise plan.  Exercise testing may be appropriate for the assessment of cardiovascular disease or to explain dyspnoea on exertion, which is common in obese patients