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- Herausgeber: John Wiley & Sons
- Kategorie: Fachliteratur
- Sprache: Englisch
Practical Manual of Clinical Obesity provides practical, accessible and expert advice on the clinical diagnosis and management of obesity and will be your perfect go-to tool in the management of your patients.
Information is clear, didactic and attractively presented, with every chapter containing plenty of engaging text features such as key points, pitfall boxes, management flowcharts and case studies to enable a rapid
understanding of obesity diagnosis and management. Key clinical trials and major international society guidelines are referred to throughout.
Topics covered include:
• Assessment of the patient, including patient history, examination and investigations
• Patterns, risks and benefits of weight loss
• Evaluation of management options: diet, exercise, drugs, psychological treatments, and surgery
• Management of obesity related co-morbidities
Practical Manual of Clinical Obesity is ideal reading for endocrinologists of all levels, as well as all other health professionals who manage obese patients such as specialist nurses, dieticians, and GP’s with an interest in obesity management.
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Seitenzahl: 301
Veröffentlichungsjahr: 2013
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Contents
Preface
PART 1 The Biology of Obesity—Why It Occurs
CHAPTER 1 Energy Balance and Body Weight Homeostasis
Introduction
Basic concepts and principles in human energetics
Components of energy expenditure
Mechanisms of thermogenesis
Inter-individual variability in metabolic adaptation
Key web links
Further reading
CHAPTER 2 The Genetic Basis of Obesity
Introduction
Evidence for the heritability of fat mass
Gene–environment interactions
Molecular mechanisms involved in energy homeostasis
Human monogenic obesity syndromes
Fat mass and obesity-associated gene (FTO)
Pleiotropic (“syndromic”) obesity
Summary
Key web links
Further reading
CHAPTER 3 Adipocyte Biology
Introduction
TAG storage and release
Secretory function of WAT
Brown adipose tissue (BAT)
Conclusion
Key web links
Further reading
CHAPTER 4 Fetal and Infant Origins of Obesity
Introduction
Measurement
Conceptual framework of early origins of obesity
Modifiable developmental disease determinants
Summary
Key web links
Further reading
CHAPTER 5 Metabolic Fuels and Obesity
Introduction
Physiological conditions in weight-stable individuals
Exercise
Summary
Key web links
Further reading
PART 2 Clinical Management of the Obese Individual
CHAPTER 6 Practical Guide to Clinical Assessment and Treatment Planning
Setting up a clinic
Broaching the topic of obesity
Taking an obesity-focused history
Physical examination of the obese patient
Identifying the high-risk obese patient
Key web links
Further reading
CHAPTER 7 Stages of Obesity and Weight Maintenance
Stages of obesity
Factors affecting weight loss maintenance
The successful weight maintainer
Further reading
CHAPTER 8 Dietary Management
Specific strategies to help patients reduce calories
Key web links
Further reading
CHAPTER 9 Physical Activity and Exercise
Exercise and weight reduction
Exercise and obesity-related CVD
Key web links
Reference
Further reading
CHAPTER 10 Behavior Therapy
Principles of behavior therapy
Components of behavioral treatment
Key web links
Further reading
CHAPTER 11 Pharmacotherapy
The legacy of anti-obesity medications
Drugs that reduce food intake primarily by acting on the CNS
Drugs that reduce fat absorption
Weight-gaining medications
Key web links
Further reading
CHAPTER 12 Surgery
Weight loss procedures
Weight loss and complications
Effect on co-morbid conditions
Changes in QOL after bariatric surgery
Patient selection and pre-operative management
Post-operative management
Key web links
References
Further reading
PART 3 Clinical Management of Obesity-Related Co-morbidities
CHAPTER 13 Diabetes and Metabolic Diseases
Principles guiding management
Management algorithm
Key web links
References
Further reading
CHAPTER 14 Obesity and Reproductive Health
Obesity and reproductive health
Managing PCOS
Obesity and assisted reproduction therapy (ART)
Managing the pregnant obese woman
Key societies
Key web links
Further reading
CHAPTER 15 Gastro-intestinal and Hepatobiliary Disease
Non-alcoholic fatty liver disease (NAFLD)
Gallbladder disease
Gastritis and GERD
Other GI disorders
Key web links
Further reading
CHAPTER 16 Respiratory Disease
Obesity and lung function
Common respiratory diseases associated with obesity
Obstructive sleep apnea (OSA)
Obesity hypoventilation syndrome (OHS)
Management algorithm for OSA
Key web links
Further reading
CHAPTER 17 Obesity and Cardiovascular Disease
Introduction
Obesity and CVD risk
Physical fitness and cardiovascular risk in obesity
Obesity and hypertension
Obesity and stroke
Obesity and CHF
Obesity and sudden death
Management of cardiovascular risk in obesity
Key web links
Reference
Further reading
CHAPTER 18 Obesity: Mental Health and Social Consequences
Principles for management
Obesity and mental illness
Obesity and major psychiatric diseases
Obesity and mental well-being in children
Management
Key web link
Further reading
CHAPTER 19 Obesity and Musculo-skeletal Disease
Obesity and musculo-skeletal disease
Obesity and osteoarthritis
Obesity and gout
Obesity and low back pain
Management algorithms
Key web link
Further reading
CHAPTER 20 The Obese Patient in Hospital
The obese patient in hospital
Specialist equipment for the morbidly obese
Emergency care
Managing the severely obese in hospital
Key web links
Further reading
Conversion Table
Index
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Preface
According to the World Health Organization (WHO), obesity is one of the greatest public health challenges of the 21st century. In 2008, more than 1.4 billion adults, 20 years and older, were found to be overweight. Of these, over 200 million men and nearly 300 million women were obese. In the 27 member states of the European Union, approximately 60% of adults and over 20% of school-age children are overweight or obese. The prevalence of overweight and obesity in the USA is even more distressing, affecting over 68% of adults and 33% of children and adolescents. Overweight and obesity are now linked to more deaths worldwide than underweight. The cause for the rapid increase in the prevalence of obesity is multifaceted, brought about by an interaction between predisposing genetic and metabolic factors and a rapidly changing “modern” environment.
The health risks of excess weight have been demonstrated in multiple population studies. Obesity significantly increases a person’s risk of developing numerous non-communicable diseases (NCDs), including cardiovascular disease, cancer, diabetes, sleep disturbance, and other disabilities. The risk of developing more than one of these diseases (co-morbidity) also increases with increasing body weight. Accordingly, obesity-related health-care costs are soaring and contribute to an increasing percentage of total health-care expenditures. These data suggest that halting and reversing the obesity epidemic will require involvement of multiple stakeholders, including the medical profession.
Regardless of which health-care area a provider is working, clinicians are being called upon to provide care for persons affected by obesity. It is no longer sufficient to simply advise our patients to “eat less and move more.” Obesity is now considered a complex disease determined by genetic, physiological, behavioral, psychosocial, cultural, economic, and societal factors. The etiological mechanisms underlying obesity-related co-morbidities, for example, hemodynamic alterations, insulin resistance, hormonal abnormalities, ectopic fat, and secretion of adipokines, continue to be clarified. Research over the past decade has also elucidated the metabolic and genetic control systems that govern regulation of body weight and energy expenditure, leading to the development of novel pharmacological and surgical interventions. Each year new intervention trials demonstrate the beneficial effect of weight loss on a myriad of obesity-related co-morbidities.
In an effort to translate the emerging science and practice of obesity care for clinicians, the Practical Manual of Clinical Obesity has been written as a practical, evidence-based companion guide to the textbook Clinical Obesity in Adults and Children, edited by P.G. Kopelman, I.D. Caterson, and W.H. Dietz. The manual is intended for physicians, nurses, allied health professionals, and students who care for overweight and obese individuals. The 20 concise chapters of the manual are divided into three major sections: The Biology of Obesity—Why It Occurs, Clinical Management of the Obese Individual, and Clinical Management of Obesity-Related Co-morbidities. Each chapter includes features that are directly intended to improve its readability and usefulness for the busy clinician—key points, case studies, boxed figures, pitfalls, key web links, and references. A collective effort has been made by the three editors to write all chapters with “one voice.” We hope that we have succeeded in publishing a manual that will be a valuable resource for the care of patients affected by obesity.
R.F. KushnerV. LawrenceS. Kumar
PART 1
The Biology of Obesity—Why It Occurs
Victor Lawrence, Section Editor
CHAPTER 1
Energy Balance and Body Weight Homeostasis
Case study 1
Case study 2
Introduction
In most individuals, body weight remains relatively stable over years to decades despite wide variations in energy intake and expenditure. This would seem to suggest that body weight is rigorously defended by homeostatic mechanisms. However, whilst a useful defense against the development of obesity, any tendency to defend a set point once obesity is established may act as a barrier to the achievement and maintenance of planned weight loss.
Many individuals seeking professional help in relation to their own obesity become confused or frustrated by what appears to be inability to lose weight (or a tendency to gain weight) despite behaviors that might appear no less healthy than other individuals who do not appear to have a weight problem. Some will have developed counterproductive health beliefs that may act as barriers to weight loss (e.g., that they must have a slow metabolism and that this is genetically programmed or is the result of some undiagnosed metabolic disorder and therefore beyond their control). These misunderstandings can rapidly evolve into a sense of “learned helplessness” and all too often result in disengagement and failure to achieve goals.
Clear and accurate explanations of the complexities of energy balance regulation are often of practical help, particularly where such frustration or despondency exists.
Basic concepts and principles in human energetics
Energy balance and laws of thermodynamics
According to the first law of thermodynamics,
The chemical energy obtained from food is used to perform a variety of work, such as
synthesis of new macromolecules (
chemical work
)
muscular contraction (
mechanical work
)
maintenance of ionic gradients across membranes (
electrical work
)
If the intake and expenditure of energy are not equal, then a change in body energy content will occur, with negative energy balance resulting in the degradation of the body’s energy stores (glycogen, fat, and protein) or positive energy balance resulting in an increase in body energy stores, primarily as fat.
The second law of thermodynamics makes a distinction between the potential energy of food, useful work, and heat. It states essentially that
and describes the fact that when food is utilized in the body, these processes must be accompanied inevitably by some loss of heat. In other words, the conversion of available food energy is not a perfectly efficient process: about 75% of the chemical energy contained in foods may be ultimately dissipated as heat because of the inefficiency of intermediary metabolism. The energy “wasted” as heat may be calculated as the sum of BMR and adaptive thermogenesis. Adaptive thermogenesis refers to the increase in resting energy expenditure in response to stimuli such as food intake, cold, stress, and drugs.
Figure 1.1 Principles of energy balance within a schematic framework that depicts the transformation of energy from food to heat throughout the body. Note that on diets typically consumed in developed countries, the total energy losses in feces and urine are small (about 5%) so that the metabolizable energy available from these diets is around 95%. Reproduced from Kopelman et al. (eds). Clinical Obesity in Adults and Children, 3rd edn, Blackwell Publishing, Oxford, 2010, with permission from Blackwell Publishing.
Components of energy expenditure
It is customary to consider human energy expenditure as being made up of three components:
Energy spent on basal metabolism (BMR)
Energy spent on physical activity (work done plus exercise- or non-exercise-associated thermogenesis)
The increase in resting energy expenditure in response to stimuli such as food, cold, stress, and drugs (adaptive thermogenesis).
These three components are depicted in Figure 1.1 and are described in the following text.
Basal (or resting) metabolic rate (BMR)
This is the largest component of energy expenditure for most individuals. Typically, BMR accounts for 60–75% of daily energy expenditure. It is measured under standardized conditions, that is, in an awake subject lying in the supine position, in a state of physical and mental rest in a comfortable warm environment, and in the morning in the post-absorptive state, usually 10–12 h after the last meal.
By far the most important determinant of BMR is body size, in particular lean (fat-free) body mass which is influenced by weight, height, age, and gender. Lean body mass is increased in obese individuals, although to a lesser extent than fat mass. This means that, counter to many obese subject’s expectations, their BMR is almost certainly higher than that of their lean counterparts, and a low BMR is, with the debatable exception of hypothyroidism, virtually never a direct cause of obesity. On the contrary, a higher BMR in obese subjects tends to oppose further weight gain, although its fall with weight loss may act as a barrier to successful weight management.
Measurement of BMR by indirect calorimetry is a non-invasive test used in a number of obesity clinics often as a means of demonstrating to an individual that their BMR lies within the range expected for body composition, age, and sex.
In addition to increasing BMR, there appears to be a decrease in metabolic efficiency in obese subjects, which also acts to favor a return to the previous “set point.” Subjects made under experimental conditions to maintain body weight at a level 10% above their initial body weight show a compensatory change in resting energy expenditure (approximately 15%), which reflects changes in metabolic efficiency that oppose the maintenance of a body weight that is above or below the set or preferred body weight.
Energy expenditure due to physical activity
Physical activity can represent up to 70% of daily energy expenditure in an individual involved in heavy manual work or competition athletics, although values of 10–25% are more usual in modern Westernized civilizations.
Energy expended in physical activity may be thought of as being spent either on deliberate “exercise” or on all other “non-exercise” activities. Non-exercise activities may be deliberate and consciously modifiable (e.g., daily tasks such as work, shopping, cooking), may be related to posture and balance, or may be involuntary purposeless movements (e.g., fidgeting, movements during sleep), the latter being termed spontaneous physical activity (SPA). The energy dissipated as heat through such forms of “non-exercise” activities is called non-exercise activity thermogenesis (NEAT).
Levels of SPA are regulated in part by the SNS. Losses in body weight are accompanied by a major reduction in SPA, which can persist for several months after weight recovery and favor disproportionate recovery of fat mass. Twenty-four-hour energy expenditure attributed to SPA may vary between 100 and 700 kcal/day between individuals and can predict subsequent weight gain after a period of caloric restriction. In one study, more than 60% of the increase in total daily energy expenditure in response to overfeeding could be attributed to SPA, variability of which was the best predictor of individual weight gain.
Other components of NEAT also differ between obese and lean individuals. One study showed that obese participants were seated, on average, for 2 h longer per day than lean participants. This difference (corresponding to about 350 kcal/day) was not altered after weight gain in lean individuals or weight loss in obese individuals, suggesting that it might be biologically determined. Increased skeletal muscle work efficiency after experimentally induced weight loss has also been reported.
It seems likely that such mechanisms form a barrier to the effectiveness of planned weight loss regimens and are subject to as yet largely unknown genetic influences.
Energy expenditure in response to various thermogenic stimuli
Exertion, whether as exercise or as NEAT, generates heat as a by-product and contributes to thermogenesis. However, several non-exertional thermogenic stimuli with relevance to body weight regulation also exist. These include the following.
Diet-induced thermogenesis or the “thermic effect of food”
The thermic effect of food refers to heat production due to the mechanical and chemical consequences of food ingestion. This process dissipates some 7–9% of the energy content of a typical mixed meal and is affected by meal size, meal composition, meal frequency, thermogenic ingredients such as caffeine, and the individual subject’s insulin sensitivity.
Psychological thermogenesis
Psychological thermogenesis refers to heat dissipation over baseline in response to states such as anxiety or stress. Thermogenesis in this setting may depend on both changes in physical activity (e.g., SPA) and via central (e.g., endocrine) mechanisms.
Cold-induced thermogenesis
Energy is spent on maintaining temperature homeostasis through “shivering” (muscular activity) and “non-shivering” (SNS activity, partly via BAT) responses to cold. The extent to which maintenance of warm environments through modern central heating may contribute to obesity is at present unknown, although average temperature settings continue to rise steadily and there is some evidence that a lack of need to respond to “mild thermogenic stress” may lead to a long-term loss of BAT.
Drug-induced thermogenesis
Caffeine, alcohol, nicotine, and other prescription or “recreational” drugs may stimulate the dissipation of energy as heat. Of these, the most clinically relevant is probably the effect of smoking cessation on body weight with some 7 kg (15.4 lb) weight gained on average, partly through changes in food intake and partly through a reduction in thermogenesis. Discouraging the abuse of tobacco for weight control purposes remains a considerable practical challenge for clinicians.
Mechanisms of thermogenesis
The SNS, through its neurotransmitter norepinephrine (NE), acts via α- and β-adrenoceptors to influence heat production by either increasing the use of ATP (e.g., ion pumping and substrate cycling) or by reducing the efficiency of ATP synthesis. These actions induce metabolic inefficiency, which has the potential to oppose any change from the body weight set point.
The recent realization that brown fat exists in adult humans has rekindled interest in pharmacologic activation of BAT in anti-obesity therapy.
Leptin is a cytokine whose principal role is thought to be to defend minimum fat stores in the longer term. As fat stores fall, leptin levels also fall, with the net result being that of reduced thermogenesis and increased metabolic efficiency. This action is an example of a “lipostatic” model of weight defense: the set point is for body fat stores, and homeostatic regulation (e.g., by leptin pathways) acts to defend this set point (Box 1.1).
Inter-individual variability in metabolic adaptation
A striking feature of virtually all experiments of human overfeeding (lasting from a few weeks to a few months) is the wide range of individual variability in the amount of weight gain per unit of excess energy consumed. Some of these differences in the efficiency of weight gain could be attributed to inter-individual variability in the gain of lean tissue relative to fat tissue (i.e., variability in the composition of weight gain), but mostly lie in the ability to convert excess calories to heat, that is, in the large inter-individual capacity for diet-induced (and other forms of adaptive) thermogenesis.
Over-and under-feeding experiments suggest that in addition to the control of food intake, changes in the composition of weight (via partitioning between lean and fat tissues) and in metabolic efficiency (via adaptive thermogenesis) both play an important role in the regulation of body weight and body composition. Evidence from identical-twin studies suggests that the magnitude of these adaptive changes is strongly influenced by the genetic makeup of the individual.
Current evidence suggests the existence of two distinct but overlapping control systems underlying adaptive thermogenesis.
One control system responds rapidly to attenuate the impact of changes in food intake on changes in body weight through alterations in the activity of the SNS which is suppressed during starvation and increased during overfeeding.
The other control system, exemplified by leptin, has a slower time-constant since it operates as a feedback loop between the size of the fat stores and thermogenesis. Its suppression during weight (and fat) losses serves to restore body fat to its set or preferred level.
These autoregulatory control systems operating through adjustments in heat production or thermogenesis play a crucial role in attenuating and correcting deviations of body weight from its set or preferred value. The extent to which these adjustments through adaptive thermogenesis are brought about is dependent upon the environment (e.g., diet composition) and is highly variable from one individual to another. In societies where food is plentiful all year round and physical activity demands are low, the resultant subtle variations among individuals in adaptive thermogenesis can, in dynamic systems and over the long term, be important in determining long-term constancy of body weight in some and in provoking the drift toward obesity in others.
Key web links
Weight Control Information Network (National Institute of Diabetes and Digestive and Kidney Diseases). http://win.niddk.nih.gov/resources/ [accessed on December 29, 2012].
Association for the Study of Obesity. http://www.aso.org.uk/ [accessed on December 29, 2012].
National Institutes of Health. http://health.nih.gov/topic/Obesity [accessed on December 29, 2012].
Further reading
Garland, T., Jr., Schutz, H., Chappell, M.A. et al. (2011) The biological control of voluntary exercise, spontaneous physical activity and daily energy expenditure in relation to obesity: Human and rodent perspectives. Journal Experimental Biology, 214 (Pt 2), 206–229.
Gautron, L. & Elmquist, J.K. (2011) Sixteen years and counting: An update on leptin in energy balance. Journal of Clinical Investigation, 121, 2087–2093.
King, N.A., Hopkins, M., Caudwell, P., Stubbs, R.J. & Blundell J.E. (2008) Individual variability following 12 weeks of supervised exercise: Identification and characterization of compensation for exercise-induced weight loss. International Journal of Obesity, 32, 177–184.
Li, M.D. (2011) Leptin and beyond: An odyssey to the central control of body weight. Yale Journal of Biology and Medicine, 84, 1–7.
van Marken Lichtenbelt, W.D. & Schrauwen, P. (2011) Implications of nonshivering thermogenesis for energy balance regulation in humans. American Journal of Physiology – Regulatory Integrative and Comparative Physiology, 301, R285–R296.
van Marken Lichtenbelt, W.D., Vanhommerig, J.W., Smulders, N.M. et al. (2009) Cold-activated brown adipose tissue in healthy men. New England Journal of Medicine, 360, 1500–1508. Erratum in New England Journal of Medicine (2009), 360, 1917.
Richard, D. & Picard, F. (2011) Brown fat biology and thermogenesis. Frontiers in Bioscience, 16, 1233–1260.
Rosenbaum, M., Hirsch, J., Gallagher, D.A. & Leibel, R.L. (2008) Long-term persistence of adaptive thermogenesis in subjects who have maintained a reduced body weight. American Journal of Clinical Nutrition, 88, 906–912.
Schoeller, D.A. (2009) The energy balance equation: Looking back and looking forward are two very different views. Nutrition Review, 67, 249–254.
Sharma, A.M., Pischon, T., Hardt, S., Kunz, I. & Luft, F.C. (2001) Hypothesis: ß-adrenergic receptor blockers and weight gain—a systematic analysis. Hypertension, 37, 250–254.
