Obesity E-Book

• Herausgeber: Festina Lente Ediciones
• Kategorie: Fachliteratur
• Sprache: Englisch

Seitenzahl: 206

Veröffentlichungsjahr: 2022

Beschreibung

Obesity is becoming one of the preeminent public health concerns, with prevalence increasing throughout the world. Covering many aspects of contemporary obesity research, this timely book by some of the leading experts in the field explores issues relating to the biology, diagnosis, treatment, and prevention of obesity, including childhood obesity. The work is attuned to the needs of those living with obesity, with a chapter devoted to the harm caused by weight stigma and false narratives around lifestyle choices. 'Obesity, the other pandemic of the 21st century' reviews the available evidence to prove that obesity should be considered not just as a key contributor towards other comorbidities, but as a disease by itself. Importantly, the effect of the COVID-19 pandemic on obesity is addressed, which raised the complexity and severity of the obesity and should be a call to action for the prevention and early treatment of this disease. This book has been developed by World Obesity Federation collaborators, and is aimed at healthcare practitioners, academics, policymakers, students, patients living with obesity and all those impacted by the issue. The research covered in these pages goes some way towards proving that obesity is quickly becoming 'the other pandemic' of the 21st century. Much like any major pandemic, the consequence of inaction is truly alarming.

Leseprobe

OBESITY:

THE OTHER PANDEMIC OF THE 21ST CENTURY

© 2022, Ada Cuevas, Donna Ryan

© Festina Lente, 2022

© World Obesity Federation, 2022

ISBN Printed edition: 978-956-6210-02-3

ISBN Digital edition: 978-956-6210-03-0

EDITION: Ada Cuevas, Donna Ryan.

DESIGN: Edith Cornejo, Carolina Zúñiga.

COVER DESIGN: Josefina Gajardo.

www.ebookspatagonia.com

All rights reserved

We want to express our sincere thanks to Claudia Batz and Julian Jones for their collaboration and hard work in the development of this book.

In addition, we thank Leonardo Farkas, who selflessly supported us in carrying out this educational project for the benefit of all people living with obesity.

We dedicate this book to all those patients who lived with obesity and who have passed away during the COVID-19 pandemic

CONTENTS

Prologue

1. Ancestral roots of obesity

Ada Cuevas | Alberto Maiz

2. The Impact of Two Pandemics on Human Health

Donna Ryan

3. Neuro-Hormonal Regulation of the Appetite And Metabolic Expenditure

María-Paz Marzolo

4. Child and adolescent obesity

Salesa Barja | Louise Alison Baur

5. Diagnosis and classification of obesity

Alex Valenzuela Montero

6. Therapeutic interventions in obesity

Ada Cuevas | Rodrigo Alonso

7. Comorbidities associated with obesity

Ada Cuevas | John Wilding

8. The impact and implications of obesity stigma and discrimination

Stuart W. Flint | Verónica Vázquez-Velázquez

9. Obesity, fertility and pregnancy

Verónica Alvarez | Alfredo M Germain

10. Policies in prevention of obesity: progress and gaps

T. Alafia Samuels | Daniela Godoy

11. Testimony of a patient living with obesity

Sarah Le Brocq

Prologue

The obesity epidemic is recognised as one of the most important public health problems facing the world today, affecting a rapidly increasing number of people worldwide. Once seen as a health concern in high-income countries only, the greatest rise and highest numbers of obesity are now seen in low-and middle-income countries. In many of these countries, undernutrition still prevails, and they are now experiencing the double burden of malnutrition.

The worldwide prevalence of obesity nearly tripled between 1975 and 2016. According to the World Health Organization, in 2016, 2 billion adults were considered overweight, of which 650 million were living with obesity. If current trends continue, it is estimated that 2.7 billion adults will be overweight, over 1 billion affected by obesity, and 177 million adults severely affected by obesity by 2025. The same trends apply to children and adolescents.

At the same time, great advances in research on factors that regulate body weight have increased recognition of obesity as a chronic and relapsing disease, and not only a consequence of poor habits associated with ‘lifestyle’. Instead, it is the result of the confluence and interaction of the multiple “roots of obesity”, such as genetic, biological, psychological factors, nutrition, physical inactivity, food availability, stress, among others. Unfortunately, despite this, patients living with obesity are frequently stigmatised and discriminated against by society and even healthcare professionals. This not only delays and hinders their treatment, but also negatively affects mental health and wellbeing.

Therefore, we have developed this new book with a broader and cross-sectional approach. We cover anthropological theories and causes of obesity, obesity across the life course, therapeutic alternatives, food systems, and stigma. We also include a chapter addressing the impacts of the COVID-19 pandemic on people living with obesity.

We hope in this way to contribute to the knowledge of all the actors involved, which enables the development of joint and multidisciplinary working strategies. Such strategies must involve not only health professionals but also authorities, educators, food producers, the media, patients, and their families, and in this way prevent and adequately treat this other global pandemic.

JOHANNA RALSTON,

CEO World Obesity Federation

ADA CUEVAS,

Editor

Introduction

The prevalence of obesity has increased dramatically over the past 30 years, currently being considered a global epidemic and one of the most important challenges for different health organisations. In 2008, for the first time in human history, the number of people living with obesity worldwide exceeded the number of people suffering from starvation and malnutrition. Currently, more than 1.9 billion adults are overweight, of whom more than 600 million have obesity. Moreover, obesity has also increased in the child population and 10% of children worldwide are living with overweight or obesity.

Obesity was initially a problem in more developed and affluent countries; however, it has now become increasingly common in low- and middle-income countries, often co-existing with undernutrition, leading to the dual burden of malnutrition in these countries.

The root causes of obesity are multifactorial, including genetic, biological, economic, environmental, psychological, and other factors. This chapter discusses the possible role of ancestral and evolutionary factors in the alarming rates of obesity in today’s world.

Obesity in human history

Venus de Willendorf (28.000-25.000 a.C.),Naturhistorisches Museum Wien, Viena.

In general, human history has been marked by periods of famine and undernutrition, which may lead us to think that obesity did not exist in ancient times. However, there is some evidence that obesity already existed in the Stone Age. Images and statues have been found from the Upper Palaeolithic era portraying corpulent bodies, with large amounts of adipose tissue in the abdomen and breasts, suggesting that the artists had seen these human Figures in real life (Figure: Venus of Willendorf ). However, obesity was a very uncommon condition until the mid-20th century, and was mainly observed in the more affluent classes. During the late 18th century, the industrial revolution brought with it major technological and agricultural developments that increased food production, and by the mid-19th century, Europe and the USA had sufficient food available for the majority of their populations, with malnutrition consequently decreasing and obesity increasing. However, due to the two World Wars and the Great Depression, the sharpest rise in obesity began in the second half of the twentieth century, when the richer and more developed countries had large amounts of energy-rich food readily available to nearly everybody. This generated the explosive rise in obesity that we have observed over the past three decades and which has expanded into developing countries.

Evolutionary bases for obesity

Thrifty Genotype Hypothesis

In 1960, JV Neel proposed the thrifty genotype hypothesis, which suggests that populations vary genetically in their predisposition to store energy as fat, according to their ancestral exposure to cycles of famine and abundance of foods. According to this hypothesis, people experiencing frequent periods of famine developed the thrifty genotype, which could increase survival and reproductivity as they were better able to save energy. This genotype allowed them to accumulate as much fat as possible during periods of food abundance so that they had reserves enabling them to survive and reproduce in times of food shortage. According to this theory, the mismatch between our ancestors’ way of life and modern lifestyles is the cause of the current obesity epidemic.

An alternative vision, put forward by Speakman in 2007 and known as the predation release or thrifty genotype hypothesis, holds that during the times when predation existed, genes that conferred speed, agility, and thinness prevailed, and by contrast, those linked to energy storage were cancelled out. Subsequently, once the threat of predation had disappeared, those genes that promoted the accumulation of energy and that could encourage obesity would have been expressed.

Barker’s Hypothesis (Thrifty Phenotype)

Another hypothesis claiming to explain the high rates of obesity in the modern day was put forward by Barker in the 1980s. This hypothesis states that negative environmental factors, primarily foetal malnutrition, can impact the development of obesity and diabetes in adult life. According to this theory, poor nutrition in the womb causes intrauterine growth retardation and low birth weight in newborns, who in utero will develop metabolic compensation mechanisms consisting of increased capacity for storage of adipose tissue and lower peripheral glucose oxidation.

The thrifty phenotype hypothesis is supported by epigenetics, which postulates that environmental factors during foetal life generate signals to the body to prepare itself for postnatal life. Therefore, a pregnant mother exposed to an adverse nutritional environment would cause the gestating foetus to adapt, enabling it to survive in similar adverse nutritional conditions, mainly through a greater ability to accumulate adipose tissue. However, the mismatch between this adaptive development and their actual environment will subsequently lead to an increased risk of obesity, diabetes, and cardiovascular disease.

Moreover, the mother’s nutritional status and metabolic health during pregnancy can affect the weight of children at birth; therefore, children of mothers with obesity or poorly-controlled gestational diabetes may have an increased risk of developing obesity and other metabolic diseases in their adult life.

Epigenetic programming works by DNA methylation and acetylation, modulation of histones, altering DNA replication time and processes. These can lead to changes in gene expression that could increase the risk of obesity transgenerationally.

Hypothesis of Adaptive Evolution in Humans

Another hypothesis regarding the obesity epidemic in modern life is based on the evolution of humans and natural selection. According to these principles, the current obesity epidemic would represent a mismatch between the current environment and the development of an adaptive capacity to store more adipose tissue.

This hypothesis states that early humans appeared around 1.8 to 2 million years ago in Africa, and that different evolutionary and adaptive processes brought about changes leading to greater energy availability. Therefore, brain development, increased body size, and migration to colder areas resulted in changes that would allow for greater energy reserve and availability. Homo sapiens, originally from Africa, were able to adapt and survive in different types of habitat with a great capacity for survival and reproduction, and achieving an effective system for storing energy was fundamental to this purpose.

In Palaeolithic times, when the ability to store energy was fundamental to survival and reproduction, humans were much more physically active and fed mainly on food obtained from hunting and gathering, with low fat consumption. This lifestyle pattern changed in Neolithic times, with the emergence of agriculture, domestication of animals, population growth, and dietary changes with significantly higher consumption of foods with higher carbohydrate content (rice, corn, potatoes, and barley), but with low protein consumption and a more sedentary lifestyle compared to the Palaeolithic era. There is evidence that it was a period of infectious diseases, famine, and malnutrition, and it has been proposed that it was during these times that the thrifty gene developed. Furthermore, the presence of diseases caused by infection and poor nutrition may also have played a role in the evolution of the thrifty genotype.

The 20th and 21st centuries have seen dramatic technological developments, urbanisation, and modernisation, with subsequent changes in our lifestyle, a reduction of infectious diseases, and an increase in chronic non-communicable diseases. In other words, over a short period, there has been a dramatic shift in our pattern of eating, characterised by the ready availability of highly caloric foods, mainly high in sugars and fats, and by very low physical activity, the consequence of huge technological advances that have led to a more sedentary lifestyle among the global population. This has led to environmental conditions that have promoted the explosive increase in obesity and associated metabolic complications.

While none of the hypotheses raised is absolutely accurate or absolute in explaining the current obesity epidemic, we might consider that they all may have some etiopathogenic role, whether in isolation or synergy. The thrifty genotype and/or adaptive evolution of humans may have produced long-term changes (over hundreds or thousands of years) that would genetically predispose us to obesity. In contrast, the thrifty phenotype or epigenetic changes would generate short-term adaptations that would promote the development of obesity and associated complications from one generation to the next. Likewise, the impact of epigenetic impairments on body weight would manifest itself in individuals genetically predisposed to develop obesity. Therefore, genetic and epigenetic variations can modify the phenotypes of body adiposity and generate variations between individuals. Moreover, hereditary factors related to obesity can be modulated by environmental factors, such as our diet, physical activity, sleep disturbances, stress and others.

Thus, obesity has reached epidemic proportions globally and has nearly tripled worldwide between 1975 and 2016. According to the World Health Organization, in 2016, more than 1.9 billion adults were overweight and of those, over 650 million were living with obesity. It is a consequence of a health-disruptive environment that promotes low levels of physical activity, sedentary behaviours and the high consumption of foods rich in energy (fat, sugar and starches). But like all chronic diseases, the root causes of obesity run much deeper. They can be genetic, psychological, sociocultural, and economic.

Hence, it is important to take into account all these elements when developing preventive and therapeutic strategies for obesity, which must be implemented very early and throughout the life course.

References

1.Barker DJP, Clark PM. Fetal undernutrition and disease in later life. Rev Reprod 1997; 2:105-112

2.Neel V. Diabetes mellitus: a thrifty genotype rendered detrimental by progress? Am J Hum Genet 1962;14:353-362

3.Kirchengast S. Diabetes and Obesity- An evolutionary Perspective. AIMS Medical Science 2017;4(1):28-51

4.Gluckman PD, Hanson MA. Developmental and Epigenetic Pathways to Obesity: An evolutionary Developmental Perspective. Int J Obesity 2008;32:S62-S71.

5.Qasim A, Turcotte M, J de Souza R, et al. On the origin of obesity: identifying the biological, environmental and cultural drivers of genetic risk among human populations. Obesity Reviews 2018;19:121-149.

Introduction and Background on Two Pandemics – Obesity and COVID-19

Two pandemics claimed global attention in 2020. When COVID-19 swept the globe that year, it quickly became clear that persons with obesity were more susceptible to poor outcomes if they became infected with the SARS Coronavirus 2. It has been said that the COVID-19 pandemic was like an X-ray for our health care systems – it exposed all the underlying problems and vulnerabilities. Indeed, it focussed attention on the obesity problem that had been too long ignored.

Epidemiology and Impact of Obesity – a Global Perspective

Dramatic increases in obesity prevalence rates, measured on a population basis as BMI >30 kg/m2, were first recognised in high income countries in the late 1980s. Since that time, rates of overweight and obesity have also risen dramatically in low– and middle-income countries, particularly in urban settings, and the chronic relapsing disease of obesity is now considered a pandemic. There are 2 billion people worldwide with obesity or its antecedent, overweight, including 124 million children and these numbers are projected to continue to increase. Globally, over 3 million people die each year because of overweight and obesity, surpassing the number who die of underweight.

Figure 1. Reduction in life expectancy in years due to overweight and obesity from 2020-2050 by country members of OECD, G20 or EU28.

It’s important to understand the impact of rising obesity rates around the world. The Organisation for Economic Cooperation and Development recently published a perspective on the impact of obesity among member countries, G20 countries and 28 EU countries. A dramatic result of the impact of rising obesity rates is a reversal of our gains in life expectancy. Figure 1 shows the reduction in life expectancy due to obesity in the countries projected for 2020 to 2050.

Obesity does not only affect life expectancy. The costs of obesity are economic and social, as this chronic disease has an adverse impact on global human capital. Because obesity is a driver of type 2 diabetes, cardiovascular diseases, cancer and other chronic diseases, the impact of obesity affects health care budgets. By 2050, treating the diseases caused by obesity will cost an average of 8.4% of total health care spending (net of spending for long-term care). The United States will spend nearly 14% of their health budget on obesity and overweight, while Estonia will spend less than 5%. But the impact of obesity is not only about money spent on health care. Obesity can also result in lost productivity, absenteeism, lower productivity at work, and increased risk for permanent disability. Furthermore, as the severity of obesity increases, the costs and indirect losses escalate similarly.

Given the global crisis in rising rates of obesity and its associated disability and health care costs, there is a need to understand why effective obesity prevention and treatment approaches have been so challenging. Indeed, no country has successfully reduced obesity rates in adults. Why can’t we just educate people to eat healthy meals and exercise more? The chief issue with our obesity challenge is that the physiology that governs body weight has been challenged by the modern environment. This is discussed in detail in Chapter 3.

When overweight and obesity develop in adults, it is very difficult to reverse. Successful weight loss is almost always accompanied by regain. The reason for this is the body’s physiological response to reduction in fat mass. The body defends its highest fat mass producing a “set point” for body weight. This is a formidable opponent in resisting weight loss and promoting weight gain after successful loss. In Figure 2, we see that “willpower” to eat less is in a tug of war with the physiologic signals that, once weight loss begins, promote hunger, reduce satiety and satiation and reduce energy expenditure. Thus, these powerful signals make it very difficult to reverse obesity.

We should not be discouraged about contending with the food and physical activity environment, however. If we can make healthy behaviours a default condition, we can be successful in preventing obesity. Indeed, as discussed in other chapters in this book, there have been successes in reducing childhood obesity rates by enacting comprehensive environmental measures including front-of-package nutrition labelling, preventing marketing unhealthy foods to children, reformulation of foods, increasing physical activity in schools and changes to the physical environment to promote more active lifestyles. These measures are proven useful obesity prevention measures. But we will also need health systems approaches if we are to successfully address obesity as a pathway to better health. Overcoming the biologic resistance to weight loss and propensity to regain can be overcome with special behavioural techniques, bariatric surgery, and newer medications.

Figure 2. Will Power versus Biologic Adaptations. A reduction in fat mass produces physiologic adaptations like starvation, where there a reduction in energy expenditure and a drive to increase food intake. This is termed metabolic or biologic adaptation to weight reduction.

Epidemiology and Impact of COVID-19

On December 31, 2019, pneumonia of unknown cause was reported in Wuhan China, and on January 12, 2020, China shared the genetic sequence of a novel coronavirus, now called SARS CoV2. It is thought that this virus, like earlier coronaviruses causing disease (MERS and SARS) moved from animals with bats being the major reservoir, to humans. Since then, the viral disease, termed COVID-19 (for COronaVIrus Disease 2019) has spread by human-to-human interaction across the world to 6 continents. As of late January 2022, there were more than 350 million confirmed cases globally and nearly 5.6 million deaths. Globally, more than 9.8 billion vaccine doses have been administered.This last has been good news; alpha, delta and omicron variants have circulated as of this writing, but the rate of severe disease is much less in fully vaccinated individuals.

Clinical Characteristics of COVID-19

While 40% or more of cases are asymptomatic, typical presentation of COVID-19 is as an influenza like illness, although loss of smell and taste, gastrointestinal symptoms or neurological symptoms may also be features of presentation. The 2021 report from the International Severe Acute Respiratory and Emerging Infections Consortium (ISARIC) on 60 109 hospitalised cases of COVID-19 across 43 countries found that the three most common symptoms at admission were history of fever (68.7% of patients), cough (68.5%), and/or shortness of breath (65.8%), and that 92% of those admitted experienced one or more of these. Additional COVID-19 symptoms at admission included fatigue (46.4%), confusion (27.3%), muscle pain (20.1%), diarrhoea (19.1%), nausea and vomiting (18.8%), headache (13.0%), sore throat (10.5%), loss or altered sense of taste (7.2%) or smell (6.2%). Adults over 60, children and women with COVID-19 are less likely to present with typical symptoms. Nausea and vomiting are common atypical presentations for those under 30 years. Confusion is a frequent atypical presentation of COVID-19 in adults over 60 years.

Risk for severe COVID-19

Older adults are at higher risk for adverse outcomes. In the United States, 8 of 10 COVID-19 deaths occurred in individuals >65 years old. The impact of age on risk for hospitalisation and death is depicted in Figure 3.

Figure 3.Age and Risk for hospitalisation and Death with COVID-19

(Rate ratios compared to 18-29 year old persons)

Hospitalisation

Death

18-29 years

Comparison Group

Comparison Group

30-39 years

2X higher

4X higher

40-49 years

3X higher

10X higher

50-64 years

4X higher

30X higher

65-74 years

5X higher

90X higher

75-84 years

8X higher

220X higher

85+ years

18X higher

630X higher

Certain underlying medical conditions can also increase risk for more severe outcomes with COVID-19. These include cancer, chronic kidney disease, chronic pulmonary disease, Down Syndrome, Heart conditions (heart failure, coronary artery disease or cardiomyopathies), immunocompromised state from solid organ transplant, pregnancy, sickle cell disease, smoking, type 2 diabetes and obesity (BMI >30 kg/m2)

Obesity and COVID-19 severity

Early during the COVID-19 pandemic, a meta-analysis quantified the impact of obesity (BMI >30 kg/m2) on adverse outcomes with COVID-19. In persons with obesity, risk for hospitalisation increased by 113%, for Intensive Care requirement by 74%, for mechanical ventilation by 66% and for death 48%, when compared to individuals of normal weight. Also, the higher the BMI, the greater the risk.These relationships are illustrated in Figure 4. Furthermore, while BMI is measuring body size and correlates on a population basis with total body fat, risk for adverse COVID-19 outcomes can be specifically tied to visceral and ectopic fat deposition. When Asian specific cut points are used to quantify obesity (BMI >25 kg/m2), the association holds that adverse COVID-19 outcomes occur in this population at the Asian-specific cut points.

The relationship between obesity and adverse COVID-19 outcomes is an independent one, and it exists in all age groups. Furthermore, the higher the BMI, the greater the risk for hospitalisation, invasive mechanical ventilation, ICU admission and death – across all age groups. This is illustrated in the Figure 5 with data from 231 US hospitals.

Figure 4. Relationship between Obesity (BMI>30kg/m2) and adverse outcomes with COVID-19. Results of a meta analysis of 75 papers evaluating the relationship between obesity and COVID-19.

Figure 5. Relationship between BMI and COVID-19 Outcomes (hospitalization, ICU admission, invasive mechanical ventilation and death) in 231 US hospitals 4/1/20 - 12/31/20

Underlying Biologic Mechanisms

The proposed hypothetical mechanisms that underlie this association between excess abnormal body fat and poor outcomes with COVID-19 are many. Stigma may be a factor, as persons with obesity are known to delay medical treatment. Other factors that may play a role in persons with increased body size are lack of access to diagnostic equipment because of size restrictions and difficulty achieving a prone position, which is used to improve pulmonary ventilation. ACE-2, the receptor that enables cell entry of the virus, is expressed in increased numbers in bronchial epithelium in obesity.Adipose tissue also expresses ACE-2 and therefore fat may serve as viral reservoir. Pulmonary lipofibroblasts have been implicated in the increased risk for pulmonary fibrosis and the increased numbers of these in obesity may play a role in respiratory failure. Persons with obesity have altered respiratory physiology with decreased expiratory reserve volume and functional residual capacity. There is also altered immune surveillance and response in obesity. Endothelial dysfunction and a proinflammatory and prothrombotic milieu have been associated with obesity. Figure 6 illustrates the host response to COVID-19. Obesity imparts problems with one’s ability to mount an initial response to the vaccine and then as the disease progresses, obesity produces an exaggeration of the pro-inflammatory and pro-thrombotic viral response.

Figure 6. Impact of Obesity on Viral Response in COVID-19. Obesity worsens the host’s ability to mount an early antiviral response and increases the host infla- mmatory and pro-thrombotic response in established infection.

Vaccination for individuals with obesity

There is concern that persons with obesity might have diminished protection from SARS CoV2 vaccination based on experience with influenza immunisation. A study of influenza vaccination showed that adults with obesity had two times greater incidence of influenza and/or influenza like illness despite being vaccinated. The mRNA vaccine developed by Pfizer and BioNTech showed 95% efficacy in preventing symptomatic COVID-19 and a subgroup analysis of the 12,003 participants with obesity (BMI >30 kg/m2) showed that there was no difference in efficacy compared to participants without obesity.This is reassuring. The mRNA vaccine developed by Moderna has been demonstrated to have similar efficacy in preventing symptomatic disease. In that trial, with >30,000 participants, “severe obesity” defined as BMI >40 kg/m2