educator's guide - xplore health · 2019-01-23 · however, for people of asian origin, ......
TRANSCRIPT
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BACKGROUND INFORMATION
Educator's guide
“A crisis of fat?”
DEVELOPED BY:
UPDATED BY:
www.xplorehealth.eu
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A crisis of fat? - 2 - Background information
TABLE OF CONTENTS
1. Introduction 3
2. State of the art 3
2.1. What is obesity 3
2.1.1 How common is obesity and whom does it affect? 4
2.1.2. Is obesity the same as body fat? 6
2.2. Causes of obesity 6
2.2.1 Genes 7
2.2.2 Environment 9
2.2.3 Epigenetics: genes and environment working together 12
2.3. Physiological processes affecting energy balance and weight regulation 13
2.4. Consequences of obesity 16
2.5. Obesity treatment 19
2.5.1 Treatment approaches 19
3. Ethical, Legal and Social Aspects (ELSA) 22
3.1. Introduction 22
3.2. Is Obesity a health problem? 22
3.3. The causes of obesity 23
3.4. Treatment of Obesity 25
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A crisis of fat? - 3 - Background information
1. Introduction
These teacher guidelines will give you information on the Xplore Health module “A crisis of
fat?”. It will first introduce the topic to enable you to prepare your lesson using the different
multimedia tools that you will find on the website. The guidelines provide information on the
state of the art in this research field and on the ethical, legal and social aspects surrounding
this topic.
2. State of the art
A rising prevalence of obesity is seen around the world. Worried about the long-term threat to
health from obesity, doctors and researchers are trying to understand what makes people
become obese so that they can design treatments and prevention strategies.
2.1. What is obesity?
Obesity is a disease characterized by an increase in the percentage of adipose tissue. It is
defined in terms of Body Mass Index (BMI), a simple measurement that takes into account a
person’s height and weight. To calculate BMI (kg/m2), the weight in kilograms is divided by
the square height in metres.
The definitions of overweight and obesity for most people are:
Overweight: BMI greater than or equal to 25kg/m2
Obesity: BMI greater than or equal to 30kg/m2
However, for people of Asian origin, lower cut-offs have been suggested due to their higher
percentage of body fat:
Overweight: BMI greater than or equal to 23kg/m2
Obesity: BMI greater than or equal to 25kg/m2
Defining obesity and overweight in children is harder due to their changing body mass during
growth. Similar growth charts to those that define normal height and weight at different ages
during childhood have been produced to define obesity and overweight in children.
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A crisis of fat? - 4 - Background information
2.1.1 How common is obesity and whom does it affect?
Key facts from WHO on obesity and overweight (fact sheet online, 16 February 2018):
- Worldwide obesity has nearly tripled since 1975.
- In 2016, 1.9 billion adults, 18 years and older, were overweight. Of these, over 650
million were obese.
- 39% of adults, 18 years and older, were overweight in 2016 and 13% were obese.
- Most of the world's population live in countries where overweight and obesity kills
more people than underweight.
- 41 million children under the age of five were overweight or obese in 2016.
- Over 340 million children and adolescents, aged 5-19, were overweight or obese in
2016.
Obesity and overweight are increasing in Spain and across the world. Currently, the OECD
countries with the highest rate of overweight or obese in adulthood include the USA (71%),
Mexico (72.50%), Chile (74.2%), New Zealand (66.6%) and Hungary (62.30%). In Spain,
51.5% of men and women have overweight or obesity. Combined data on obesity and
overweight prevalence show several countries where less than 40% of the adult population
have normal weight.
Figura 1. Rising overweight (including obesity) rates in adults aged 15-74
years [from OECD Obesity Update 2017]
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A crisis of fat? - 5 - Background information
Data on the prevalence of obesity from the World Health Organization (Noncommunicable
Diseases (NCD) Country Profiles, 2018) in adolescents aged 10-19 show that in Spain 11%
of boys and 6% of girls have obesity. These data show that these problems begin as early as
childhood. According to OECD latest Obesity Update 2017, in England, 12.35% of boys and
10.75% of girls aged 3-17 years have obesity; in the United States, these figures are 20.71%
and 18.97%.
Data from countries with rapidly enlarging populations and economies, such as India and
China, show a prevalence of childhood overweight and obesity. In China, 22% of boys and
15% of girls have obesity; these figures are 21% of boys and 18% of girls in India. These
global trends are studied closely by international organisations, such as the World Obesity
Figure 2. Obesity among adults, 2015 or nearest year [from OECD Obesity Update 2017]
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A crisis of fat? - 6 - Background information
Federation, who describe obesity as a ‘global epidemic’ and are concerned by the negative
impact it is having on health and disease and economic growth. Data on these trends is also
collected on a local level, and collated into health profiles for different regions by the Public
Health Observatories.
2.1.2 Is obesity the same as body fat?
All body fat stores contribute to body mass index; however, research has shown that not all
fat stores have the same impact on a person’s health. Visceral fat describes the fat located
around bodily organs such as the liver, kidneys and heart, and is thought to be metabolically
active and associated with insulin resistance (associated with the development of type 2
diabetes), and high levels of cholesterol. People with excess visceral fat also have an
increased risk of heart disease and stroke.
People with excess visceral fat tend to hold their extra weight around the middle of the body,
causing a so-called ‘apple-shaped’ appearance. This is also sometimes known as central
adiposity or obesity, and can be defined by the ratio of a person’s waist to hip ratio. Men tend
to have more visceral fat and be more centrally obese than pre-menopausal women (who
tend to have more subcutaneous fat and be ‘pear-shaped’). People from different ethnic
groups also have a varying risk of increased visceral fat: people of Asian origin are
particularly at risk, and this may underlie their increased risk of disorders such as type 2
diabetes. The lower BMI cut-offs for overweight and obesity in Asian people is to take into
account these differences.
Body fat is difficult to measure, but can be measured using DEXA (dual energy X-ray
absorptiometry) as well as MRI and CT scans. Bioelectrical impedance analysis is a simple,
non-invasive technique, often performed in pharmacies and gyms, but is rarely accurate.
2.2. Causes of obesity
Obesity is a so-called ‘complex disease’ where it is known that several different factors play a
role in causing the disease. These causes include a person’s environment (e.g. what they
eat, how much exercise they do, their sleep habits, etc.) and their genes. A person’s genes
and environment are thought to work together to predispose someone to obesity.
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A crisis of fat? - 7 - Background information
2.2.1 Genes
Evidence that a person’s genetic make-up plays a role in their risk of becoming obese comes
from many different types of research study. In their clinics, doctors often see that patients
with overweight and obesity have family members who have the same pattern of bodyweight.
This can often imply a genetic link, but as patterns of eating and exercise often also run in
families, this does not make it easy for researchers to decide whether a family is sharing
similar obesity genes, or whether they are sharing similar ‘obesogenic’ environments.
Studies of twins have helped clear up this uncertainty. Monozygotic (identical) twins share
the same genes but dizygotic twins do not, and neither type of twins has the same
environment. Estimates of how ‘heritable’ obesity is can be calculated from looking at the
intra-pair correlation of weight: monozygotic twins have a higher heritability of weight and
obesity than dizygotic twins, suggesting a genetic influence on weight (see below). Further
evidence of the importance of genetics over environment comes from adoption studies,
where twins and siblings were reared apart, as was sometimes normal practice in the 1940s.
Researchers found that a familial tendency towards obesity was still apparent in twins and
siblings reared separately, suggesting an overriding influence on obesity from genetics,
despite different environments.
Figure 3. Body Mass in twins [Borjeson, Acta Paediatr Scand, 1976]
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A crisis of fat? - 8 - Background information
Finding obesity genes
The last few decades of genetic research have taken many approaches to discover genes
that could cause obesity. These genetic studies have taken two main approaches: (i)
identification of common genetic variants (or single nucleotide polymorphisms) using
genome-wide association studies (GWAS), and (ii) identification of rare gene defects (such
as mutations and deletions) with candidate gene studies. These two approaches highlight the
complexity of understanding genetic factors in obesity as they study two very different
aspects of obesity: the common causes of obesity (using GWAS) and the rare causes of
obesity (using candidate gene studies). Identification of common genetic variants associated
with obesity helps researchers to understand the risk to large numbers of people, but these
variants are only associated with a small increase in risk (e.g. each copy of the FTO risk
allele is associated with a 0.45kg/m2 increase in body mass index). In contrast, identification
of a rare variant may yield insight into some unusual forms of obesity, such as congenital
leptin deficiency, but these are unlikely to be present in the majority of people with obesity.
Many people have questioned whether these recent genetic insights are worth the
considerable financial investment put into them. Understanding common variants may enable
doctors to build up ‘risk profiles’ for patients to help inform them more accurately about their
own genetic risk of developing obesity. It may also be possible to use this genetic information
to tailor treatments and lifestyle interventions that are known to be more or less effective for
certain risk groups according to their genetic make-up. For those people with rare forms of
obesity, understanding the exact gene defect causing their condition may enable them to use
prenatal screening in the future to prevent the same condition being present in offspring.
Single gene defects may also be targeted by gene therapies or specific tailored treatments,
such as the administration of leptin treatment to the few sufferers of congenital leptin
deficiency. For any genetic researcher, the ‘translation’ of their genetic insights to clinical
practice is important to justify their study. Genetic researchers also need to consider the
ethical aspects of their work and the potential for genetic information to be misused.
Type of genetic variation Rare single gene variants Multiple common gene variants
Effect on body weight Account for a lot of extra weight
in very few people
Account for a little bit of extra
weight in a lot of people
Examples Ob gene, MC4R gene FTO gene, TMEM18 gene
Association with other Can be associated with rare One of many ‘normal’ varied
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A crisis of fat? - 9 - Background information
clinical conditions diseases, e.g. congenital leptin
deficiency, MC4R deficiency
human characteristics, but can
also associate with other
common diseases, e.g. type 2
diabetes
How are these found? Candidate gene studies, animal
studies, exome sequencing
Genome-wide association studies
Potential relevance Prenatal genetic testing and
gene therapy
Understanding risk of disease
and tailoring disease prevention
strategies.
2.2.2 Environment
The environment can contribute significantly to a person’s weight, irrespective of their genetic
make-up. The environment is a loose definition that can take into account a range of factors
that affect (a) energy intake, such as the quantity, cost and type of food that is available, their
appetite and behaviour towards food, and (b) energy expenditure, including physical activity
levels and patterns of sedentary behaviour.
In simplistic terms, a balance exists between the energy intake and energy expenditure, such
that if the former exceeds the latter, there will be net weight gain. For an ‘average’ person,
the excess energy intake required to cause weight gain may be as little as 100 calories per
day to cause a 5kg weight gain over a 1-year period. Although calculations such as this help
us to understand how small amounts of excess energy intake can influence a person’s
weight, they do not take into account the range of other factors that affect propensity to
weight gain.
Energy intake Energy expenditure
Food intake Basal metabolic rate (depends on body
stores and contribution from
fat/carbohydrates/protein)
Individual behaviours – hunger and
appetite, habits, comfort, sleep, etc.
Thermogenesis, e.g. from food intake and
muscle activity
Societal and economic influences
e.g. cost and availability of food
Physical activity (e.g. volitional exercise or
normal activities such as sitting, working,
fidgeting, transportation, posture)
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A crisis of fat? - 10 - Background information
Energy intake
Over the last century, improving economic circumstances in developed countries have
enabled the production of cheap, high-energy food that can be transported around the world.
The increased accessibility of calorific food, and a food industry that promotes certain eating
patterns, are thought to underlie the rapid increase in obesity amongst the world’ population
over the last few decades. In contrast, economic difficulties facing the world’s poorest
nations, as well as famine cycles, prevent many populations from suffering the epidemics of
overweight and obesity that much of the global population is experiencing. Migration patterns
of certain ethnic groups highlight the importance of the external environment and
accessibility to food, such as that seen when Asian people move from a rural to urban
settings in Asia, or to a more ‘Westernised’ country such as the UK. The focus on population-
wide influences on energy intake, such as the role of the food industry, is key to prevention
strategies in obesity.
Individual determinants of energy intake are also important to the development of overweight
and obesity. A range of factors influences an individual’s energy intake, and this ranges from
hunger and appetite leading a person to eat, the satiety, satisfaction and comfort derived
from eating (whether as meals or snacks), as well as patterns of habitual eating. The
neurobehavioural mechanisms underlying all of these factors are increasingly understood,
and explain the complex relationship between all of these factors, many of which are
physiologically and genetically regulated.
Energy expenditure
The basal metabolic rate (BMR) of an individual accounts for 60-75% of their daily energy
expenditure. The BMR refers to the amount of energy the body requires to maintain normal
body functions in a normal environment, e.g. homeostatic cellular processes that keep the
body alive. The BMR itself is determined by a person’s body size and composition, and in
particular, their fat-free mass. The fat-free mass of a person is composed of their most
metabolically active tissues, such as the heart, brain, kidneys and liver. Fat, or adipose
tissue, contributes 20-30% of body weight, but only 3-5% of resting metabolic rate. It is
therefore understandable that a person with excessive body fat content is relatively
‘inefficient’ in their overall basal metabolic efficiency, with less calories used to keep their
body fat stores in a metabolic equilibrium. This inefficiency is one reason in which overweight
and obese people find it difficult to lose weight, as they have to increase their energy
expenditure significantly to overcome this net energy surplus.
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A crisis of fat? - 11 - Background information
Thermogenesis, or heat production by the body, is another important determinant of energy
expenditure. The body produces heat in many different contexts: in response to food
consumption, from muscle activity during exercise, during a stress response when hormones
such as adrenaline are produced, and finally in low temperature conditions when the body
shivers to produce heat.
The processes regulating basal metabolic rate and thermogenesis are not voluntary, and
therefore individuals have little ability to change these should they be trying to lose weight.
However, it is hoped that research into these processes may yield some novel methods of
pharmacological treatment for obesity in the future.
Physical activity is a significant component of energy expenditure, and one that is modifiable
through individual behaviour such as exercise. Large studies show the benefits of regular
physical activity on weight and risk of diseases, including type 2 diabetes, cardiovascular
disease, stroke and premature death. Regular, intensive physical activity, and achieving a
negative energy balance can be a successful means to weight loss, and in particular can
result in the loss of abdominal fat. However, an increase in physical activity may be
insufficient for an obese person to achieve significant weight loss; and only when this is
coupled with dietary change may the necessary weight loss ensue. The WHO
recommendations on physical activity (see below) are based on the knowledge that regular
physical activity is required to maintain weight in normal, healthy people. Societal and
behavioural factors play a significant role in activity levels, with increasing car use and
sedentary behaviour, playing an important role in increasing rates of obesity and overweight.
Children, aged 5-17 years Adults, aged 18-64 years Older adults, aged 65 +
Moderate-vigorous physical
activity for at least 60 minutes
per day
150 minutes of moderate intensity
activity (at least 10 minutes at a
time), e.g. 30 minutes 5 days per
week
Any amount of physical activity
that their abilities and conditions
allow will provide health
benefits.
Vigorous intensity activities,
such as those that strengthen
muscle and bone, at least 3
days per week
Or, 75 minutes of vigorous activity
per week
Aim to be active daily, and if
possible, aim for the same
amount of physical activity as
younger adults
Obese adults should aim for 60-
90 minutes of moderate intensity
physical activity on most days.
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A crisis of fat? - 12 - Background information
Moderate physical activity means that you get warm, mildly out-of-breath, and mildly sweaty,
and can include brisk walking, jogging, cycling, swimming, dancing or heavy housework or
DIY. Vigorous physical activity will include more intensive sports that result in being more
out-of-breath, sweaty or an increased heart rate.
2.2.3 Epigenetics: genes and environment working together
Epigenetics is an emerging area of science that is uncovering the link between our genes
and the environment they function in. Humans, mammals, and many other species, have an
epigenetic ‘landscape’ across the genome, composed of a range of different chemical and
structural modifications. This landscape varies according to the genetic architecture, forming
certain patterns in gene promoters, introns, exons and outside of genes. One commonly
studied epigenetic mark, DNA methylation, occurs predominantly at CpG dinucleotides
across the genome and can affect the machinery of gene transcription and whether a gene
gets switched on or off (gene expression). Other epigenetic marks, such as histone
modifications, can affect the structure and function of proteins with wide-ranging downstream
effects. From these descriptions, it can be seen that epigenetic modifications interact with our
genetic make-up very closely. To understand this better, some researchers have used an
analogy of an orchestra conductor (the epigenetic modification) in charge of many musicians
(the DNA code) to create music (gene functioning).
The environment in which an organism lives may also have a significant effect on its
epigenetic profile. In this context, the ‘environment’ of an organism might include certain
nutritional deficiencies, a high calorie food intake, smoking, or exposure to drugs and toxins.
These adverse environmental conditions can directly affect epigenetic marks with
downstream effects on gene expression and resulting in a change in phenotype, such as
onset of disease. Mammalian epigenetic profiles are thought to have particular susceptibility
to changes in environment during development as their epigenetic marks are erased and
replaced when an embryo is formed. This area of research is called ‘fetal programming’, and
describes how the maternal in utero environment may ‘programme’ an individual fetus to
develop obesity and type 2 diabetes in adulthood.
Understanding the role of epigenetic processes in mediating gene-environment interactions
is giving exciting insight into the causes of complex diseases such as obesity and type 2
diabetes. Researchers at the Blizard Institute, Queen Mary University, London (Finer,
Rakyan, Hitman) have identified that the presence of a genetic polymorphism associated
with increased risk of obesity at the FTO gene changes the epigenetic state of that gene
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A crisis of fat? - 13 - Background information
region. A different methylation pattern in the FTO gene in people carrying the obesity risk
allele may affect how the gene works and could provide a route to understand the
mechanisms underlying obesity. Epigenetic changes have also been found in fetal
programming studies such as the Dutch Winter Hunger Study that identifies higher rates of
type 2 diabetes in the adult offspring who were born to famine-exposed mothers during the
1940s. Another study has shown that mothers in India who are deficient in vitamin B12 (due
to the lacto-vegetarian diet that many Hindu Indians follow) have children who are at
increased risk of obesity and type 2 diabetes by the age of 6 years. These findings are
thought to underlie the concept of the ‘thrifty’ phenotype, in which there is an adaptation
towards an environment of nutritional deprivation, set down in early life. Other researchers
think that there may also be a ‘thrifty’ genotype in populations that have evolved to cope with
nutritional deprivation. It is thought that the ‘mismatch’ between these thrifty developmental
origins, and an actual environment of nutritional excess in later life, may be a high-risk
situation for individuals to become obese and develop type 2 diabetes. Many researchers
have suggested that this theory may explain the recent Asian epidemic of obesity and type 2
diabetes as populations have changed rapidly over recent generations from living in rural
areas (with nutritional deprivation and high physical activity levels) to urban areas where food
is in excess and physical activity levels drop.
2.3. Physiological processes affecting energy balance and weight regulation
As described above, obesity comprises a complex clinical condition, with numerous
underlying genetic and environmental triggers. These influences are now understood to
affect a wide range of physiological processes in the regulation of overall energy balance.
Such processes include neurobehavioral pathways and gut-brain signalling pathways that
work together to achieve homeostasis in the body. An expanding knowledge of these
complex pathways is yielding significant insights into the factors that control body weight,
such as appetite, satiety and eating behaviours.
The homeostatic control of energy balance (and therefore body weight) requires the brain to
act as the chief regulator, coordinating metabolic signals from peripheral tissues, paracrine
and endocrine hormone signalling, and feedback from the nervous system.
Metabolic signals, e.g. glucose and free fatty acids
Ingestion of food and the peripheral metabolic processes in the body is central to the
production and utilisation of fuel for energy metabolism. Variation in levels of these
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A crisis of fat? - 14 - Background information
metabolites, such as after a meal, will set off a cascade of peripheral metabolic processes
designed to achieve homeostasis. These processes include glycogenolysis (obtainment of
glucose from the degradation of glycogen), glycolysis (breakdown of glucose to extract
energy for cellular processes) and glycogenesis (conversion of excess glucose to glycogen
for storage). Like glucose, free fatty acids (from circulating trigylcerides) provide a rapid
energy source for metabolism and cellular processes (from storage in adipose tissue) and
can readily turn into fuel stores. These metabolic signals, as well as others, are the trigger to
more complex signalling within the body that not only keeps body systems working efficiently,
but also is responsive to states of energy influx, or extra requirement. The signalling that is
required comes from a combination of processes, driven mainly by hormonal and nervous
systems.
Hormonal signals
These function on both a local (paracrine) and systemic (endocrine) level, and include
numerous peptide hormones with wide-ranging effects. Leptin is one such important
hormone, produced peripherally by adipose cells according to the current size of fat stores in
the body. It is the main message to the brain, via other circulating hormones such as insulin,
on what is happening in the peripheries of the body and therefore how the brain should
regulate overall energy balance (e.g. to try and achieve a negative energy balance if fat
stores are excessive). On the other hand, there is Adiponectin, a hormone whose levels are
inversely proportional to the BMI, which, among other effects, increases insulin sensitivity
and promotes the uptake of glucose. It is thought that abnormalities in this process of leptin,
adiponectin and insulin signalling may predispose an individual to obesity and may offer a
therapeutic target in the future. Other important signalling hormones include gut peptides,
such as glucagon-like peptide 1 (GLP1) and cholecystekinin (CCK). These peptide hormones
are produced in the gastrointestinal tract in response to food ingestion, and provide an
efficient and responsive feedback system to other hormones to regulate the metabolic
environment (e.g. via insulin to normalise post-meal glucose levels) and to the brain to
control appetite and induce a feeling of fullness after a meal. In obesity and type 2 diabetes,
this efficient gut peptide response to a meal can be blunted, and newer drug therapies are
designed to restore the efficient functioning of this system. Other important hormone
regulators of energy balance include the more commonly-known hormones produced in
response to hypothalamic-pituitary signalling to peripheral endocrine organs such as the
adrenal gland (corticosteroids and sex hormones) and thyroid gland (thyroxine) as well as
the production of growth hormone by the pituitary itself. These endocrine hormones can
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A crisis of fat? - 15 - Background information
affect the basal metabolic rate (e.g. thyroid and sex hormones), insulin sensitivity
(corticosteroids), fat mass (growth hormone) as well as providing a complex interaction
between many of the circulating metabolic signals and paracrine signals already discussed.
Nervous system signals
The autonomic nervous system, which includes both sympathetic and parasympathetic
nerves, carries homeostatic feedback signals to and from the brain from peripheral tissues in
the body in relation to energy balance. Peripheral effects of these neural stimuli include the
production of insulin and catecholamines (e.g. adrenaline and noradrenaline) that in turn
regulate peripheral processes of energy balance. The vagus nerve carries important nerve
signals back to the brain from mechanoreceptors in the stomach in response to their being
stretched by ingestion of a meal.
Within the brain, several important structures receive the feedback signals outlined above
and provide a responsive signal back to the peripheries. The key neuroanatomical regions
are in the hypothalamus and brainstem, and importantly, these areas lack an effective blood-
brain-barrier, allowing easy recognition of signalling molecules and metabolites in the
systemic circulation. Within these brain regions, several specific neuropeptides communicate
and coordinate the complex messaging that is required to achieve optimal energy balance.
Important neuropeptides include neuropeptide-Y (NPY), which stimulates food intake and
decreases energy expenditure, the alpha-melanocyte stimulating hormone (a-MSH),
responsible for suppressing food intake, amines (e.g. serotonin, acetylcholine, adrenaline,
noradrenaline) and amino acids (e.g. glutamate and GABA).
In addition to the hypothalamus and brainstem, other brain regions are emerging as
important players in subtle neurobehavioral responses to food, such as reward behaviours,
motivation, and the hedonistic aspects of food intake. These brain regions include the
nucleus accumbens, and amygdala and contain many dopaminergic neurons. These brain
regions interact closely with the cortical function of the brain, including that of taste and visual
recognition of food, and a conscious understanding of food, appetite and hunger.
Understanding the complexities of these neurobehavioral mechanisms, and their relationship
to the homeostatic control of energy balance is crucial to develop a deeper understanding of
obesity. At the present time, many researchers are studying these brain processes to try to
understand whether in some people they malfunction and predispose to obesity. Animal
models, and studies of humans with rare monogenic forms of obesity is providing significant
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A crisis of fat? - 16 - Background information
insights, and this is being applied to larger studies of obesity to see if they may have a role in
common obesity. It is hoped that a detailed understanding of this pathophysiology will result
in targeted therapies that treat the higher control of food intake and appetite.
2.4. Consequences of obesity
Obesity and overweight predispose to a number of related ‘metabolic’ disorders that can
increase a person’s risk of morbidity and mortality. The risk of death is increased in people
with obesity mainly due to the excess risk of cardiovascular disease and cancer. Even when
adjusting for overall activity levels, smoking and other relevant factors, obesity is known to be
an independent risk factor for premature death.
Obesity-related complications relate to the complex pathophysiological problems associated
the disorder, and are wide-ranging. In relation to the obesity itself, the onset of these
complications is often silent or delayed, but provides an important focus for intervention as
they underlie the morbidity and mortality of obesity.
Figure 4. Estimated Hazard Ratios for Death
from Any Cause According to Body-Mass Index
for All Study Participants and for Healthy
Subjects Who Never Smoked [from A.
Berrington, P. Hartgede, J.R. Cerhan, et al.
(2010) Body-Mass Index and Mortality among
1.46 Million White Adults. The New England
Journal of Medicine 363;23, 2211-2219]
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A crisis of fat? - 17 - Background information
Mechanisms Associated risk
Metabolic disorders
Type 2 diabetes
High cholesterol and
triglycerides
(dyslipidaemia)
Fatty liver disease
Polycystic ovarian
syndrome
Adipocytes in excessive visceral fat stores
are large and produce excessive amounts
of pro-inflammatory cytokines, such as IL-1,
IL-6 and TNF-alpha. Suppression of
adiponectin production reduces the body’s
sensitivity to insulin. The overall result of
these factors is to increase insulin
resistance, one of the main features of type
2 diabetes.
An increase in free fatty acids passing
through the portal venous circulation also
results in excessive production of certain
lipid particles (e.g. VLDL) that further
increases the production of insulin into the
systemic circulation, compounding the
effects of peripheral insulin resistance.
Chronically high levels of insulin (due to
insulin resistance), as well as changes to
sex hormone metabolism can result in
polycystic ovarian syndrome, which is
manifest by chronic anovulation and raised
androgen concentrations.
Individuals with a BMI of
25-29.9 are twice as likely
to develop type 2
diabetes, and for a BMI of
30 or greater, the risk is
sixfold.
Cardiovascular disease
Hypertension
Ischaemic heart
disease
Strokes
Adipocytes produce hormones, such as
angiotensinogen, that can increase blood
pressure by direct effects on the vascular
endothelium. Obese people also have a
raised total circulating blood volume and
this raises the viscosity (thickness) of blood
as well as increasing its clotting ability (via
production of pro-thrombotic factors). These
factors all increase the risk of hypertension,
but also play a role in the development of
atherosclerosis. The dyslipidaemia
associated with obesity also predisposes to
the development of atherosclerosis, a
product of the accumulation of lipids in the
vascular endothelium. When this
The risk of high blood
pressure is 5 times higher
in people who are obese.
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A crisis of fat? - 18 - Background information
Mechanisms Associated risk
pathological process affects coronary
arteries, it can result in angina and heart
attacks; in the cerebrovascular circulation, it
results in TIAs and strokes.
Cancer
e.g breast, colon,
endometrial, kidney,
prostate, oesophageal
cancers
The excess risk of cancer in people who
are obese is thought to be due to many
different factors, including the pro-
inflammatory state, changes in metabolism
of sex hormones, and insulin resistance.
At least 10% of cancer
deaths are thought to be
due to obesity
Bone and joint disease
arthritis
osteoporosis
disability
Increased mechanical stress on joints from
excessive body weight can cause arthritis.
Arthritis is common in obesity, and is often
manifest as back pain, knee and hip
problems, and chronic disability. Reduced
bone density can also occur, due to vitamin
D deficiency and higher bone turnover due
to sex steroid hormone imbalance.
Reduced bone density, or osteoporosis,
can lead to fractures and further disability.
Respiratory disease
obstructive sleep
apnoea
obesity
hypoventilation
syndrome
These disorders result from the restriction
to breathing function due to excessive body
fat, fatty tissue in the neck and nasal polyps
obstructing the upper airways, and
hypothalamic disturbance of breathing
patterns.
Psychological problems
depression
anxiety
Mood disturbances, such as depression
and anxiety, are more common in people
with obesity. This is thought to be due to a
range of factors, including behavioural
disturbances associated with trying to lose
weight, dissatisfaction with body image, and
social stigma.
Women in the US who are
obese have a 37%
increased risk of
depression.
Pregnancy
complications
Obesity in pregnancy is increasingly
common due to the increased prevalence of
obesity in young people. Obesity in
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A crisis of fat? - 19 - Background information
Mechanisms Associated risk
pregnancy puts both mother and baby at
risk, due to higher rates of gestational
diabetes, pre-eclampsia and fetal
macrosomia.
2.5. Obesity treatment
The benefits of weight loss in obesity and overweight people are significant. The
Counterweight Programme has estimated that for an obese person with a BMI of >32.5
kg/m2, the benefits of 10% weight loss include a 9-fold decrease in type 2 diabetes, 6-fold
decrease in dyslipidaemia and hypertension and a 4-fold reduction in cardiovascular disease.
The question is how to achieve this weight loss. The view held by many to just “eat less and
exercise more” is correct in that these are the best strategies to achieve a negative energy
balance, but is overly simplistic. The neurobehavioral mechanisms in energy regulation and
the knowledge that individuals with a high fat mass are ‘energy inefficient’, highlights the
complexity of the underlying pathophysiological processes in obesity that are difficult to
overcome to achieve weight loss.
2.5.1 Treatment approaches
Lifestyle intervention, including diet and exercise
Many studies show the effectiveness of lifestyle interventions in both the prevention and
treatment of obesity. Lifestyle interventions can include a range of different approaches, but
their cornerstone is to achieve a negative energy balance through dietary change and
increased physical activity. For those people who are able to adopt significant lifestyle
changes and maintain them in the long-term, the effects on obesity and the development of
obesity-related complications also last into the long-term. In contrast, ‘quick fix’ interventions
such as crash diets, whilst they may achieve short-term weight loss, rarely produce medium-
or long-term effects on body weight. An understanding of the neurobehavioral mechanisms
that control energy balance, as well as the role of higher brain functions, such as reward
behaviour and motivation, that can malfunction in obesity give an insight into why a ‘lifestyle
approach’ to achieving weight loss is difficult.
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A crisis of fat? - 20 - Background information
Drug treatments
Over recent years, several different drug therapies have been trialled and used in the
treatment of obesity. Large clinical trials of some drugs have shown the beneficial effects on
weight loss from drugs such as sibutramine and rimonabant that work mostly centrally on
appetite and energy regulation. However, with increasing use in obese populations, side
effects of these drugs became apparent, including an increase in cardiovascular risk with
sibutramine, or mood disturbance and suicide with rimonabant, and have led to the
withdrawal of both of these drugs. Pharmaceutical companies are continuing to work on
these types of compounds, trying to exploit their potential benefits in newer drugs without the
associated risk of side effects. The mainstay of drug therapy at the present time is orlistat, a
drug that inhibits pancreatic and gastric lipases, preventing the breakdown of triglycerides in
the gut and therefore reducing their absorption and contribution to energy intake. The
benefits of this drug are modest, achieving on average 2-3kg of weight loss over a 1-year
period of taking the drug. However, the concern raised by many patients who take this drug
is that it causes gastro-intestinal side effects due to the rapid passage of high fat foods
through the GI tract, resulting in flatulence and diarrhoea. These side effects stop many
people from taking the drug, but for those who can tolerate them, the drug can be helpful in
the management of obesity.
Newer drug therapies available to treat obesity and type 2 diabetes include the GLP-1
agonists, such as liraglutide and exenetide, which stimulate the action of insulin and promote
weight loss. This drugs work on gut peptide, signalling cascade that is blunted in type 2
diabetes and obesity. As described earlier, these gut peptides, such as GLP-1, are
responsive to food intake in the stomach, producing a cascade of effects to metabolise
glucose and signal to the brain to reduce further food intake and appetite. The drugs used in
this category mimic the natural GLP-1 response in normal individuals. These drugs are
relatively new, and their mechanisms of action are not fully understood, but they seem to be
effective in producing modest weight loss as well as diabetes control over 1 year. Longer-
term studies to test their efficacy in maintaining this weight loss as well as reducing obesity-
related complications are awaited. Furthermore, these long-term follow-up studies will also
provide vital information about their safety and incidence of side effects.
Bariatric (weight-loss) surgery
Currently, bariatric surgery is the most successful means to achieve significant and long-term
weight loss in obese individuals and prevent or treat obesity-related complications. Several
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A crisis of fat? - 21 - Background information
different surgical approaches exist, including gastric banding and bypass operations. These
operations are thought to induce weight loss through a variety of different means, including
the restriction of food into the stomach, promoting early satiety and reduced appetite, as well
as malabsorption from the gut and therefore reduced energy intake. Large studies show that
these operations, and especially gastric bypass, can achieve significant weight loss of 10-
30%, as well as a significant reduction in mortality of up to 40%. These beneficial effects are
thought to outweigh the potential risks of performing surgery in obese individuals, and
studies also show that these operations are highly cost-effective as they reduce the expense
associated with long-term treatment of obesity-related complications such as disability and
type 2 diabetes. At the present time, surgery is an option for individuals with a BMI
>40kg/m2, or >35kg/m2 if associated with obesity-related complications such as type 2
diabetes or obstructive sleep apnoea. In the UK, these criteria are suggested by the National
Institute of Clinical Excellence, based on extensive research and evaluation of their cost-
effectiveness, however on a local level, access to these operations is sometimes restricted
due to short-term budgetary concerns of local health care organisations.
Psychological therapies
The neurobehavioral processes underlying obesity, including systems that promote ‘reward’
and ‘motivation’ from eating can be targeted through specific psychological techniques such
as cognitive-behavioural therapy. This treatment approach can also be useful due to the high
rates of psychological problems, such as depression and anxiety, in people with obesity.
Most specialist obesity services offer tailored psychological support and treatment for
patients. In children with obesity, such approaches often include family-based interventions,
understanding that the tendency towards obesity may be driven by familial eating patterns
and behaviours at home.
Novel therapies
Newer drug therapies are hoped to provide safe and effective non-surgical treatments for
obesity, and this is an area of rapid development by pharmaceutical companies. With
increasing understanding of the pathophysiology of obesity, new therapeutic targets are
suggested, such as those that work on gut-brain signalling pathways and the more complex
behavioural aspects of food intake.
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A crisis of fat? - 22 - Background information
3. Ethical, Legal and Social Aspects (ELSA)
In this section you will find a number of opinions and incentives for discussion in class on
ethical, legal and social aspects (ELSA) related to “A crisis of fat?”:
3.1. Introduction
Obesity is a growing problem for global health, both in the developed world and in newly
industrialising countries. How we think about, and tackle, obesity will have a significant
impact on rates of diabetes, heart disease, joint problems, and many other health conditions.
Obesity is a complex social and medical problem, and public and professional attitudes to
obesity contribute to this complexity.
3.2. Is obesity a health problem?
One initial reaction to the public health challenge of obesity is to argue that overweight or
obesity are not health problems, except in the most extreme cases. Many people who would
be considered clinically obese do not consider themselves to be overweight (and many
people who are not clinically obese consider themselves to be overweight – not simply
people who suffer from anorexia nervosa or bulimia, but people who are in the normal range
of “body-consciousness”).
A commonsense view sees variation in human body size as to be expected, and thus normal
rather than pathological. This is not to say that body size does not attract judgement and
comment – it does. Societies have complex cultural attitudes to body size to do with how
people understand beauty, fitness, and care over personal appearance, signals of prosperity
and so on.
One of the most difficult challenges for health promotion is how to educate people about
what, from a clinical point of view, obesity is (which may not match the commonsense
perception of being “heavy” or “fat” or “big-boned” or, for babies, “bonny”), without trading on
or exaggerating the stigma which attaches to some forms of obesity. Attitudes to obesity are
linked quite strongly to social expectations and comparisons with near neighbours and family
members: someone is not likely to consider themselves as overweight if they see themselves
as typical of their own family and friendship network.
Apart from the extreme cases, people do not often experience obesity directly, or, in the
short term, experience health problems caused by obesity. Even where they do, they may
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A crisis of fat? - 23 - Background information
consider shortness of breath, for instance, as just a sign that they are not very fit, and this
may not bother them, or indeed be a source of humour. In most cases, the consequences of
obesity materialise over time, and people are either unaware of them, or discount their
importance rather heavily. Therefore, while tackling obesity is important both for population
health and for individual health, it can be hard to persuade people of this, without appearing
to be moralistic or bullying. By the time a serious health consequence of obesity has
materialised, it may be too late to do much more than control the symptoms and repair the
damage as best may be.
3.3. The causes of obesity
Personal behaviour
One of the challenges of obesity from a health promotion point of view is that once the
person has accepted that obesity may be a health problem in general, and that it may be (or
become) one for them personally, lay theories of the causes of obesity come into focus.
People’s understanding of the behaviours which lead to obesity, or which can control or
move away from obesity, are complex, and may rest on mistaken or partial understandings
about eating patterns, the nutritional contents of different kinds of food, the amount of food
that constitutes a healthy intake, the efficacy of dieting in different ways, the role of exercise,
and so on. In addition to their “health beliefs”, it is also well known that changing old habits
and acquiring new ones is hard, and the “cognitive biases” which make changing present
behaviour to achieve long term but remote benefits are deeply entrenched in human
psychology.
On the other hand, it is also evident that there is a difference between how we judge our own
behaviour and how we judge that of others. While some of the time we might be more
forgiving or tolerant of others behaviour, much of the time we are all too willing to believe that
others’ behaviours are due to idleness, greed, fecklessness, or lack of willpower, whereas
our own behaviours are either rational, sensible and indeed no one’s business but our own or
hard to change because of “real” difficulties which are “genuine” barriers to behaviour change
(unlike those faced by the idle, feckless, etc. other person who is just weak-willed).
Nowhere is this inconsistency in thinking about behaviour more obvious than in debates
about personal responsibility for ill health (or obesity as a precursor to ill health). Because
obesity is often attributed to moral failings like greed or irresponsibility, a common view is
that the obese person should not receive the same level of help and support than someone
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A crisis of fat? - 24 - Background information
whose diabetes or heart disease is caused by some factor we are more willing to consider
independent of personal conduct. And even within obesity, someone whose overweight is
attributed to a “hormone problem” may receive more sympathy than someone whose
overweight is attributed to a lack of self-control.
Not only do these debates influence the public attitude to treatment of obesity itself, they are
even more influential in debates about the treatment of the health consequences of obesity
(heart disease, diabetes and so on) where a persistent theme seems to be that “self-
incurred” health problems should be a lower priority than “no-fault” health problems.
Genetics and physiology
From the ethical point of view, the main issue raised by the genetics and physiology of
obesity is in informing public attitudes to obesity and the perceived contribution of personal
behaviour. The genetics and physiology of obesity are intricate, and there is not likely to be a
simple genetic test, or set of tests, which could act as a screening test for the risk of obesity,
or obesity-related illness.
The main contribution of genetics and physiology to the clinical medicine of obesity is likely to
be in understanding causal pathways which can lead to medical treatments (considered
below). To the extent that genetics and physiology provide a partial explanation of why some
people are obese, and others are not, these partial explanations fit into the debates we have
just reviewed about the role of personal responsibility. In many ways, these will simply be
new versions of the older explanations of the type “I am not fat, I just have an underactive
thyroid” (meaning – I am overweight, but it’s not my fault) or “My family are all big-boned”
(meaning, I am overweight, but I was born this way, this is my natural shape).
Structural explanations
Although the personal behaviour and personal responsibility accounts of obesity are probably
dominant, there has been a growing interest in public debates about food in the ethics of the
food industry, and in the role of the government in shaping the environment.
The role of the food industry has increasingly been criticised. Concerns are raised about the
content of low quality fat and high energy density products along with the salt and sugar
content of common foodstuffs; while the added salt content of processed foods has long
been a concern, recent interest has broadened to encompass concern about the added
sugar content of processed foods. Not only are consumers unaware of the salt and sugar
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A crisis of fat? - 25 - Background information
contents of what they eat (notwithstanding more explicit food labelling), they are also
unaware of the way salt and sugar influence the desire to eat more of the same, thus
inducing over-eating.
Criticism has been levelled at portion sizes in fast-food outlets, at the marketing of high-
energy foods to children (including in some countries sponsorship of school activities and
sporting events to underscore an apparent link between consumption of high-energy foods
with active lifestyles), and so on. Either incomplete or misleading information, and pro-
consumption “nudges” which increase consumption and divert from healthier options are
increasingly widely criticised.
Another problem concerns the way food is retailed; while the widespread availability of
supermarkets and chains of small shops has made a big difference to the convenience of
urban life and in many rural communities as well, the marketing practices of the chains have
been criticised for undermining the diversity of products available, presenting relatively
unhealthy (high fat, high energy processed foods) in more convenient and lower cost forms
than fresh foods, and the discounting of bulk purchases in ways that induce higher rates of
consumption (notoriously in the case of alcohol, but also for sweets and biscuits, carbonated
drinks, and so on). If the marketing practices and dominant market position of the highstreet
retailers make healthy eating more difficult and more expensive, then there is a clear case for
government intervention through fiscal policy, product regulation, and licensing, as well as
the currently popular “nudges”, “responsibility deals” and voluntary agreements with the food
industry.
3.4. Treatment of obesity
The main approaches to obesity include education and information; behaviour change;
medication; and surgery.
Education and information involve identifying (possibly through screening programmes, more
likely through discussion at routine medical appointments, and possibly through referral to
specialist weight-loss services) people who are obese or at risk of becoming obese, and
educating them about the dangers of obesity and about what can be done to overcome
obesity.
This educational approach has certain hazards: it can enhance stigma; it may focus more on
the “worried well” than on the “genuinely” obese; it may not translate into actual behaviour
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A crisis of fat? - 26 - Background information
change. However, most governments and health services are now taking a more active
approach to raising public and individual awareness of the problems of, and caused by,
obesity.
Mere education and information alone may influence some people to change their behaviour
by taking up more intense physical activity, dieting, and deliberate attempts to eat a more
varied diet or a diet that has a higher proportion of fresh foods or lower fat or lower energy
content. However, many people will require further advice or assistance. Some private sector
initiatives, such as “Weightwatchers”-style programmes seem to have some success, and
public sector initiatives involving “prescriptions for exercise”, cognitive behaviour therapy,
and other means have also been tried with some success. Unfortunately, the evidence base
for interventions to reduce obesity involving personal behaviour change is not particularly
reliable, and further controlled trials are certainly needed.
Another strategy for personal behaviour change, involving “nudges” which “change the
defaults” for personal behaviour without needing direct and deliberate action on the part of
the consumer him or herself, is also receiving a lot of attention now. Some critics of this style
of intervention worry that because “nudges” do not involve autonomous choice they are
unfair or manipulative. However, the natural response to that is to point to the widespread
use of these types of behaviour modifying strategy by supermarkets and other retailers in
encouraging people to buy more, or certain kinds of, products already. To harness these
techniques to promote health would at least (a) have some chance of success and (b)
advance a personally and publicly beneficial, rather than a purely commercial, goal.
A different set of criticisms looks at the activity patterns of modern life, which encourage
sedentary work and long-distance commuting in cars or vehicles, which do not involve
exercise (but may involve boredom and boredom-induced comfort eating and drinking). The
role of government in providing open spaces for exercise (especially in schools, but for the
community at large) and in regulating transportation to make cycling and walking easier,
safer and more attractive, is important, and increasingly recognised.
All of these structural issues are currently the topic of much discussion in the West. However
it is clear that they are now, and will continue to be, just as important in the newly
industrialising countries, which are beginning to go through the “demographic transition”, and
where regulation of the food and drinks industries may be limited or only nascent.
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A crisis of fat? - 27 - Background information
Medical Treatment
Over the years, many different medical treatment strategies have been tried to treat obesity
directly, or to modify behaviour. Medicines, which boost the consumption of energy by the
body (such as amphetamines), were popular at one time. There was a vogue for appetite
suppressants. Recent approaches, which involve persuading the brain that the stomach is
full, when a smaller amount of food has actually been consumed, have been heavily invested
in by the pharmaceutical industry. So too have drugs which inhibit the uptake of fats or
energy from food consumed.
Aside from the medical question of how far these drug-based approaches are successful in
practice, and what side effects they have, the ethical questions here are challenging. First, it
is questionable whether a medical treatment, which permits the consumer to eat large
amounts of food without putting on weight, is morally acceptable: it may encourage waste or
greed, and it entrenches a high consumption habit, which will probably persist once the
medical treatment is discontinued. Second, there is a challenge along the lines that it is
morally preferable to change one’s behaviour through one’s own efforts, rather than through
taking a pill.
This type of criticism is of long-standing; similar debates arise in psychiatry about the relative
ethical standing of drug-based treatments for depression or low mood and cognitive
behavioural or psychotherapeutic interventions. It might reasonably be argued that where
someone cannot successfully change their diet or activity patterns, then a pill might be just
the intervention they need. And it may also be that the pill gets them started and makes
behaviour change easier, and thus more sustainable. Outside careful clinical trials we are
simply speculating and moralising.
Surgical treatment
In extreme cases, surgery to reduce the digestive tract so as to reduce appetite and the
ability to consume large quantities of food and drink has a good track record. But it is unlikely
to be a useful tool in large scale public health, dealing with mild to moderate obesity. In
addition, it has to overcome public scepticism about how far obesity is the fault of the obese
person. A standard complaint that surgery for obesity is a poor use of public (or insurance)
money has more to do with the view that the obese person is at fault than it has to do with
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A crisis of fat? - 28 - Background information
objective evidence about cost-effectiveness of the surgery, or the relative ineffectiveness of
other interventions in the most obese patient.
Authors:
The State of the Art document was drafted by Sarah Finer, Specialist Registrar & Clinical
Research Fellow in Diabetes & Endocrinology, Queen Mary University, London. The ELSA
document was drafted by Richard Ashcroft, Professor of Bioethics at Queen Mary,
University of London.
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A crisis of fat? - 29 - Background information
AUTHORS OF THIS DOCUMENT:
Sarah Finer i Richard Ashcroft
TEACHING CONSULTANTS:
Cristina Andrés-Lacueva, Rosina Malagrida i Josep Carreras
COORDINATION:
Rosina Malagrida
DATA: 26 d'octubre de 2018
DEVELOPED BY:
UPDATED BY: