Obesity
Obesity is a condition in which the natural energy reserve, stored in the fatty tissue of humans and other mammals,
is increased to a point where it is associated with certain health conditions or increased mortality.
Obesity is both an individual clinical condition and is increasingly viewed as a serious public health problem. Excessive
body weight has been shown to predispose to various diseases, particularly cardiovascular diseases,
diabetes mellitus
type 2, sleep apnea, and
osteoarthritis.
Current Research
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Cultural and Social Significance
Etymology
Obesity is the nominal form of obese which comes from the Latin obēsus, which means "stout, fat, or plump." Ēsus is the
past participle of edere (to eat), with ob added to it. In Classical Latin, this verb is seen only in past participial
form. Its first attested usage in English was in 1651, in Noah Biggs's Matæotechnia Medicinæ Praxeos.
History
In several human cultures, plumpness was associated with physical attractiveness, strength, and fertility. Some of the
earliest known cultural artifacts, known as Venus figurines, are pocket-sized statuettes representing an obese female
figure. Although their cultural significance is unrecorded, their widespread use throughout pre-historic Mediterranean
and European cultures suggests a central role for the obese female form in magical rituals, and suggests cultural approval
of (and perhaps reverence for) this body form. This is most likely due to their ability to easily bear children and survive
famine.
A large, well-fed body was occasionally considered a symbol of wealth and social status in cultures prone to food shortages
or famine. Well into the early modern period in European cultures, it often served this role. But as food security was
realized, it came to serve more as a visible signifier of "lust for life", appetite, and immersion in the realm of the
erotic.
This was especially the case in the visual arts, such as the paintings of Rubens (1577–1640), whose regular use of the full
female figures gives us the description Rubenesque for plumpness. Obesity can also be seen as a symbol within a system of
prestige. "The kind of food, the quantity, and the manner in which it is served are among the important criteria of social
class. In most tribal societies, even those with a highly stratified social system, everyone - royalty and the commoners -
ate the same kind of food, and if there was famine everyone was hungry. With the ever increasing diversity of foods, food
has become not only a matter of social status, but also a mark of one's personality and taste."
Contemporary Culture
In modern Western culture, the obese body shape came to be widely regarded as unattractive. Many negative stereotypes are
commonly associated with obese people, such as the belief that they are lazy, stupid, or even evil, gluttony being the
second of the seven deadly sins. Obese children, teenagers and adults face a heavy social stigma. Obese children are
frequently the targets of bullies and are often shunned by their peers. Obesity in adulthood can lead to a slower rate of
career advancement. Most obese people have experienced negative thoughts about their body image, and many take drastic
steps to try to change their shape.
Not all contemporary cultures disapprove of obesity. There are many cultures which are traditionally more approving (to
varying degrees) of obesity, including some African, Arabic, Indian, and Pacific Island cultures. Especially in recent
decades, obesity has come to be seen more as a medical condition in modern Western culture.
Recently emerging is a small but vocal fat acceptance movement that seeks to challenge weight-based discrimination. Obesity
acceptance and advocacy groups have initiated litigation to defend the rights of obese people and to prevent their social
exclusion.
Popular Culture
Various stereotypes of obese people have found their way into expressions of popular culture. A common stereotype is the
obese character who has a warm and dependable personality, but equally common is the obese vicious bully. (Dudley Dursley
from the Harry Potter book series is a perfect example of this.) Gluttony and obesity are commonly depicted together in
works of fiction. In cartoons, obesity is often used to comedic effect, with fat cartoon characters having to squeeze
through narrow spaces, frequently getting stuck or even exploding.
A more unusual example of obesity-related humour is Bustopher Jones, the fat cat, from the musical Cats, whose claim to
fame is that he is a regular visitor to many gentlemen's clubs including Drones, Blimp's and the Tomb. Due to his constant
lunching at these clubs, he is remarkably fat, "a twenty-five pounder... And he's putting on weight everyday." Another
popular character, Garfield, a cartoon cat, is also obese for humor. When his owner, Jon, puts him on diets, rather than
losing weight, Garfield slows down his weight gain.
It can be argued that depiction in popular culture adds to and maintains commonly perceived stereotypes, in turn harming
self esteem of obese people. A charge of discrimination on the basis of appearance could be leveled against these
depictions.
On the other hand, obesity is often associated with positive characteristics such as good humor (the stereotype of the
jolly fat man like Santa Claus), and some people are more sexually attracted to obese people than to slender people (see
chubby culture, fat admirer).
Effects on Health
Obesity, especially central obesity (male-type or waist-predominant obesity), is an important risk factor for the
"metabolic syndrome" ("syndrome X"), the clustering of a number of diseases and risk factors that heavily predispose for
cardiovascular disease. These are
diabetes mellitus type 2,
high blood pressure,
high cholesterol, and triglyceride
levels (combined hyperlipidemia). An inflammatory state is present, which — together with the above — has been implicated
in the high prevalence of atherosclerosis (fatty lumps in the arterial wall), and a prothrombotic state may further worsen
cardiovascular risk.
Apart from the metabolic syndrome, obesity is also correlated (in population studies) with a variety of other
complications. For many of these complaints, it has not been clearly established to what extent they are caused directly
by obesity itself, or have some other cause (such as limited exercise) that causes obesity as well. Most confidence in a
direct cause is given to the mechanical complications in the following list:
- Cardiovascular: congestive heart failure, enlarged heart and its associated arrhythmias and dizziness, cor
pulmonale, varicose veins, and pulmonary embolism
- Endocrine: polycystic ovarian syndrome (PCOS), menstrual disorders, and infertility
- Gastrointestinal: gastroesophageal reflux disease (GERD), fatty liver disease, cholelithiasis (gallstones),
hernia, and colorectal cancer
- Renal and genitourinary: urinary incontinence, glomerulopathy, hypogonadism (male), breast cancer (female),
uterine cancer (female), stillbirth
- Integument (skin and appendages): stretch marks, acanthosis nigricans, lymphedema, cellulitis, carbuncles,
intertrigo
- Musculoskeletal: hyperuricemia (which predisposes to gout), immobility, osteoarthritis, low back pain
- Neurologic: stroke, meralgia paresthetica, headache, carpal tunnel syndrome, dementia
- Respiratory: dyspnea, obstructive sleep apnea, hypoventilation syndrome, Pickwickian syndrome, asthma
- Psychological: Depression, low self esteem, body dysmorphic disorder, social stigmatization
While being severely obese has many health ramifications, those who are somewhat overweight face little increased
mortality or morbidity. Some studies suggest that the somewhat "overweight" tend to live longer than those at their
"ideal" weight. This may in part be attributable to lower mortality rates in diseases where death is either caused or
contributed to by significant weight loss due to the greater risk of being underweight experienced by those in the ideal
category. Another factor which may confound mortality data is smoking, since obese individuals are less likely to smoke.
osteoporosis is known to occur less in slightly overweight people.
Metrics
In the clinical setting, obesity is typically evaluated by measuring BMI (body mass index), waist circumference, and
evaluating the presence of risk factors and comorbidities. In epidemiological studies, BMI alone is used to define
obesity.
BMI
BMI, or Body Mass Index, was developed by the Belgian statistician and anthropometrist Adolphe Quetelet. It is calculated
by dividing the subject's weight in kilograms by the square of his/her height in metres (BMI = kg / m2) or (BMI =
weight(lbs.) * 703 / height(inches)2).
The current definitions commonly in use establish the following values, agreed in 1997 and published in 2000:
- A BMI less than 18.5 is underweight
- A BMI of 18.5 - 24.9 is normal weight
- A BMI of 25.0 - 29.9 is overweight
- A BMI of 30.0 - 39.9 is obese
- A BMI of 40.0 or higher is severely (or morbidly) obese
- A BMI of 35.0 or higher in the presence of at least one other significant comorbidity is also classified by
some bodies as morbid obesity.
BMI is a simple and widely used method for estimating body fat. In epidemiology BMI alone is used as an indicator of
prevalence and incidence.
BMI as an indicator of a clinical condition is used in conjunction with other clinical assessments, such as waist
circumference. In a clinical setting, physicians take into account race, ethnicity, lean mass (muscularity), age, sex,
and other factors which can affect the interpretation of BMI. BMI overestimates body fat in persons who are very muscular,
and it can underestimate body fat in persons who have lost body mass (e.g. many elderly). Mild obesity as defined by
BMI alone is not a cardiac risk factor, and hence BMI cannot be used as a sole clinical and epidemiological predictor of
cardiovascular health.
Waist Circumference
BMI does not take into account differing ratios of adipose to lean tissue; nor does it distinguish between differing
forms of adiposity, some of which may correlate more closely with cardiovascular risk. Increasing understanding of the
biology of different forms of adipose tissue has shown that visceral fat or central obesity (male-type or apple-type
obesity) has a much stronger correlation, particularly with cardiovascular disease, than the BMI alone.
The absolute waist circumference (>102 cm in men and >88 cm in women) or waist-hip ratio (>0.9 for men and >0.85 for women)
are both used as measures of central obesity.
Body Fat Measurement
An alternative way to determine obesity is to assess percent body fat. Doctors and scientists generally agree that men
with more than 25% body fat and women with more than 30% body fat are obese. However, it is difficult to measure body fat
precisely. The most accepted method has been to weigh a person underwater, but underwater weighing is a procedure limited
to laboratories with special equipment. Two simpler methods for measuring body fat are the skinfold test, in which a pinch
of skin is precisely measured to determine the thickness of the subcutaneous fat layer; or bioelectrical impedance
analysis, usually only carried out at specialist clinics.
Other measurements of body fat include computed tomography (CT/CAT scan), magnetic resonance imaging (MRI/NMR), and dual
energy X-ray absorptiometry (DXA).
Gestalt
In practice, for most examples of overweight that may designate risk, both doctor and patient can see "by eye" whether
excess fat is a concern. In these cases, BMI thresholds provide simple targets all patients can understand.
Risk factors and Comorbidities
The presence of risk factors and diseases associated with obesity are also used to establish a clinical diagnosis. Coronary
heart disease,
type 2 diabetes, and sleep apnea are possible life-threatening risk factors that would indicate clinical
treatment of obesity. Smoking,
hypertension, age and family history are other risk factors that may indicate treatment.
Diabetes and heart disease are risk factors used in epidemiological studies of obesity.
Causes
Overeating
In its simplest conception, obesity is only made possible when the lifetime energy intake exceeds lifetime energy
expenditure by more than it does for individuals of "normal weight".
When food energy intake exceeds energy expenditure, fat cells (and to a lesser extent muscle and liver cells) throughout
the body take in the energy and store it as fat.
In all individuals, the excess energy utilized to generate fat reserves is minute relative to the total number of calories
consumed. This means that very fine perturbations in the energy balance can lead to large fluctuations in weight over
time. To illustrate, an obese 40 year old who carries 100 lb of adipose tissue has only consumed about 25 more calories
per day than he has burned on average - or the equivalent of an apple every three days. In comparison a very lean
40-year-old who carries only 15 lb of body fat will have exceeded his daily energy expenditure by about four calories a
day - the equivalent of an apple every 18 days.
Additional Factors
Factors that have been suggested to contribute to the development of obesity include:
- Genetic factors and some genetic disorders (e.g., Prader-Willi syndrome)
- Underlying illness (e.g., hypothyroidism)
- Eating disorders (e.g., binge eating disorder)
- Certain medications (e.g., atypical antipsychotics)
- Sedentary lifestyle
- A high glycemic diet (i.e., a diet that consists of meals that give high postprandial blood sugar)
- Weight cycling, caused by repeated attempts to lose weight by dieting
- Stressful mentality
- Insufficient sleep
- Smoking cessation
As with many medical conditions, the caloric imbalance that results in obesity often develops from a combination of
genetic and environmental factors. Polymorphisms in various genes controlling appetite, metabolism, and adipokine release
predispose to obesity, but the condition requires availability of sufficient calories, and possibly other factors, to
develop fully. Various genetic abnormalities that predispose to obesity have been identified (such as Prader-Willi
syndrome and leptin receptor mutations), but known single-locus mutations have been found in only about 5% of obese
individuals. While it is thought that a large proportion of the causative genes are still to be identified, much obesity
is likely the result of interactions between multiple genes, and non-genetic factors are likely also important.
Some eating disorders are associated with obesity, especially binge eating disorder (BED). As the name indicates, patients
with this disorder are prone to overeat, often in binges. A proposed mechanism is that the eating serves to reduce
anxiety,
and some parallels with substance abuse can be drawn. An important additional factor is that BED patients often lack the
ability to recognize hunger and satiety, something that is normally learned in childhood. Learning theory suggests that
early childhood conceptions may lead to an association between food and a calm mental state.
Tendencies of Ethnic Groups
Certain populations and individuals may be more prone to obesity than others, and the ability to take advantage of rare
periods of abundance and use such abundance by storing energy efficiently was undoubtedly an evolutionary advantage in
times when food was scarce. Individuals with greater adipose reserves were more likely to survive famine. This tendency
to store fat is likely maladaptive in a society with adequate and stable food supplies.
Neurobiological Mechanisms
Flier summarizes the many possible pathophysiological mechanisms involved in the development and maintenance of obesity.
This field of research had been almost unapproached until leptin was discovered in 1994. Since this discovery, many other
hormonal mechanisms have been elucidated that participate in the regulation of appetite and food intake, storage patterns
of adipose tissue, development of insulin resistance. Since leptin's discovery, ghrelin, orexin, PYY 3-36, cholecystokinin,
adiponectin, and many other mediators have been studied. The adipokines are mediators produced by adipose tissue; their
action is thought to modify many obesity-related diseases.
Leptin and ghrelin are considered to be complementary in their influence on appetite, with ghrelin produced by the stomach
modulating short-term appetitive control (i.e. to eat when the stomach is empty and to stop when the stomach is stretched).
Leptin is produced by adipose tissue to signal fat storage reserves in the body, and mediates long-term appetitive
controls (i.e. to eat more when fat storages are low and less when fat storages are high). Although administration of
leptin may be effective in a small subset of obese individuals who are leptin-deficient, many more obese individuals are
thought to be leptin-resistant, and this resistance has been implicated in obesity in some people, is thought to explain
in part why administration of leptin has not been shown to be effective in suppressing appetite in most obese subjects.
Neuroscientific approaches hinge on the action of the aforementioned mediators on the hypothalamus, the part of the brain
that is thought to process signals related to metabolic state and energy storage and to shift the energy balance in either
a positive or negative direction, primarily by acting on appetite and energy expenditure. Lesion studies in the 1940s and
1950s identified two regions of the hypothalamus — the lateral hypothalamus (LH) and ventromedial hypothalamus (VMH) — as
the brain's hunger and satiety centers, respectively. Specific lesions to a mouse's LH suppressed its appetite while
damaging the VMH caused overeating.
Studies of the distribution of the leptin receptor in the mid-1990s cast doubt upon this dual center theory of hunger and
satiety. Leptin's effect on the arcuate nucleus melanocortin system is now considered central to the regulation of feeding
and metabolism.
Poverty Link
Some obesity co-factors are resistant to the theory that the "epidemic" is a new phenomenon. In particular, a class
co-factor consistently appears across many studies. Comparing net worth with BMI scores, a 2004 study found obese
American subjects approximately half as wealthy as thin ones. When income differentials were factored out, the inequity
persisted — thin subjects were inheriting more wealth than fat ones. A higher rate of lack of education and tendencies to
rely on cheaper fast foods is seen as a reason why these results are so dissimilar. Another study finds women who married
into higher status are predictably thinner than women who married into lower status.
Therapy
The mainstay of treatment for obesity is an energy-limited diet and increased exercise. In studies, diet and exercise
programs have consistently produced an average weight loss of approximately 8% of total body mass on average (excluding
study drop-outs). While not all dieters will be satisfied with this outcome, studies have shown that a loss of as little
as 5% of body mass can create enormous health benefits.
A more intractable therapeutic problem appears to be weight loss maintenance. Of dieters who manage to lose 10% or more
of their body mass in studies, 80-95% will regain that weight within two to five years. It appears that the homeostatic
mechanisms regulating body weight are very robust (see leptin, for example), and vigorously defend against weight loss.
Much important research is now being devoted to determining what factors can improve the currently dismal weight loss
maintenance rates.
Recent scientific research has cast some doubt over whether or not dieting actually improves health, with some studies
indicating that dieting may in fact be more detrimental than remaining overweight.
In a clinical practice guideline by the American College of Physicians, the following five recommendations are made:
- People with a BMI of over 30 should be counseled on diet, exercise and other relevant behavioral
interventions, and set a realistic goal for weight loss.
- If these goals are not achieved, pharmacotherapy can be offered. The patient needs to be informed of the
possibility of side-effects and the unavailability of long-term safety and efficacy data.
- Drug therapy may consist of sibutramine, orlistat, phentermine, diethylpropion, fluoxetine, and bupropion.
For more severe cases of obesity, stronger drugs such as amphetamine and methamphetamine may be used on
a selective basis. Evidence is not sufficient to recommend sertraline, topiramate, or zonisamide.
- In patients with BMI > 40 who fail to achieve their weight loss goals (with or without medication) and who
develop obesity-related complications, referral for bariatric surgery may be indicated. The patient needs
to be aware of the potential complications.
- Those requiring bariatric surgery should be referred to high-volume referral centers, as the evidence
suggests that surgeons who frequently perform these procedures have fewer complications.
Much research focuses on new drugs to combat obesity, which is seen as the biggest health problem facing developed
countries. Nutritionists and many doctors feel that these research funds would be better devoted to advice on good
nutrition, healthy eating, and promoting a more active lifestyle.
Medication most commonly prescribed for diet/exercise-resistant obesity is orlistat (Xenical, which reduces intestinal fat
absorption by inhibiting pancreatic lipase) and sibutramine (Reductil, Meridia, an anorectic). In the presence of
diabetes
mellitus, there is evidence that the anti-diabetic drug metformin (Glucophage) can assist in weight loss — rather than
sulfonylurea derivatives and insulin, which often lead to further weight gain. The thiazolidinediones (rosiglitazone or
pioglitazone) can cause slight weight gain, but decrease the "pathologic" form of abdominal fat, and are therefore often
used in obese diabetics.
Increasingly, bariatric surgery is being used to combat obesity. The most common weight loss surgery in Europe and A
ustralia is the adjustable gastric band where a silicone ring is placed around the top of the stomach to help restrict
the amount of food eaten in a sitting. This surgery has been FDA approved in the United States since 2001 but has been
being used in other parts of the world since the early 1990s. It is considered the safest and least invasive of the
available weight loss surgeries such as Roux-en-Y gastric bypass surgery (RNY), biliopancreatic diversion, and stomach
stapling (also known as "vertical banded gastroplasty", VBG). Unlike those more invasive techniques the band surgery does
not cut into or reroute any of the digestive tract and is completely reversible. Removing the implant returns the stomach
to its pre-surgical norm. All of these surgeries can be done laparoscopically. The more invasive of the surgeries usually
bypass or remove some portion of the patient's intestines which causes malabsorption and dumping.
All of these surgeries come with risk to the patient. For instance a recent study by the U.S. Department of Health and
Human Service showed a 40% complication rate within 180 days of bariatric surgery. Moreover these surgeries do not
guarantee either successful weight loss or reduced morbidity and mortality. Patients are also required to make lifelong
changes to their diet if they are to keep the lost weight off in the long term. Therefore, as with any major surgery,
patients needs to carefully evalute the long term ramifications of their choice.
Public Health and Policy
Prevalence
United Kingdom
The Health Survey for England predicts that more than 12 million adults and 1 million children will be obese by 2010 if no
action is taken. The prime minister has urged people to take more responsibility for their fitness and diet.
United States
The prevalence of overweight and obesity in the United States makes obesity a leading public health problem. The United
States has the highest rates of obesity in the developed world. From 1980 to 2002, obesity has doubled in adults and
overweight prevalence has tripled in children and adolescents. From 2003-2004, "children and adolescents aged 2 to 19
years, 17.1% were overweight...and 32.2% of adults aged 20 years or older were obese." The prevalence in the United
States continues to rise. The prevalence of obesity has been continually rising for two decades. This sudden rise in
obesity prevalence is attributed to environmental and population factors rather than individual behavior and biology
because of the rapid and continual rise in the number of overweight and obese individuals. The current environment
produces risk factors for decreased physical activity and for increased calorie consumption. These environmental factors
operate on the population to decrease physical activity and increase calorie consumption.
Environmental Factors
While it may often appear obvious why a certain individual gets fat, it is far more difficult to understand why the
average weight of certain societies have recently been growing. While genetic causes are central to understanding obesity,
they cannot fully explain why one culture grows fatter than another.
This is most notable in the United States. In the years from just after the Second World War until 1960 the average
person's weight increased, but few were obese. In the two and a half decades since 1980 the growth in the rate of obesity
has accelerated markedly and is increasingly becoming a public health concern.
There are a number of theories as to the cause of this change since 1980. Most believe it is a combination of various
factors:
- Lack of activity: obese people appear to be less active in general than lean people, and not just because of
their obesity. A controlled increase in calorie intake of lean people did not make them less active;
correspondingly when obese people lost weight they did not become more active. Weight change does not
affect activity levels, but the converse seems to be the case.
- One of the most important is the much lower relative cost of foodstuffs: massive changes in agricultural
policy in the United States and Europe have led to food prices for consumers being lower than at any point
in history. Sugar and corn syrup, two huge sources of food energy, are some of the most subsidized products
by the United States government. This can raise costs for consumers in some areas but greatly lower it in
others. Current debates into trade policy highlight disagreements on the effects of subsidies.
- Increased marketing has also played a role. In the early 1980s in America the Reagan administration lifted
most regulations pertaining to sweets and fast food advertising to children. As a result, the number of
advertisements seen by the average child increased greatly, and a large proportion of these were for fast
food and sweets.
- Changes in the price of petrol (i.e. gasoline) are also believed to have had an effect, as unlike during the
1970s it is now affordable in the United States to drive everywhere — at a time when public transit goes
underused. At the same time more areas have been built without sidewalks and parks.
- The changing workforce as each year a greater percent of the population spends their entire workday behind a
desk or computer, seeing virtually no exercise. In the kitchen the microwave oven has seen sales of
calorie-dense frozen convenience foods skyrocket and has encouraged more elaborate snacking.
- A social cause that is believed by many to play a role is the increasing number of two income households in
which one parent no longer remains home to look after the house. This increases the number of restaurant
and take-out meals.
- Urban sprawl may be a factor: obesity rates increase as urban sprawl increases, possibly due to less walking
and less time for cooking.
- Since 1980 both sit-in and fast food restaurants have seen dramatic growth in terms of the number of outlets
and customers served. Low food costs, and intense competition for market share, led to increased portion
sizes — for example, McDonalds french fries portions rose from 200 calories (840 kilojoules) in 1960 to
over 600 calories (2,500 kJ) today.
- Increased food production is a probable factor. The U.S. produces three times more food than U.S. residents
eat.
- Increasing affluence itself (including many of the above factors as accompaniments of affluence) may be a
cause, or contributing factor since obesity tends to flourish as a disease of affluence in countries which
are developing and becoming westernised. This is supported by a dip in American GDP after 1990, followed
by a substantial increase. U.S. obesity statistics followed the same pattern, offset by two years.
- An aging population may also be a major factor, as the likelihood of becoming obese increases with age.
Beyond their twenties, the older a person becomes the slower their metabolism becomes, reducing the amount
of calories required to sustain the body, thus if a person does not reduce their intake of food with age,
they will become obese over time. As the average age of individuals within a society increases, the rate
of obesity also increases. This situation is exacerbated by the baby boom generation, which represents a
disproportionately large portion of the population in many countries and is currently nearing the latter
end of the typical lifespan in affluent nations, and therefore is in the high-risk zone for obesity.
Interestingly an increase in the number of Americans who exercise and diet occurred before the increase in obesity, and
some scholars have even argued that these trends actually encouraged obesity. Nearly all diets fail, with participants
resuming their previous eating habits or even engaging in binge eating. Many then see an overall increase in their weight.
If the diet is then repeated and abandoned again, a pattern of rising and falling weight is established, known as weight
cycling. Similarly those who work out but then stop can end up being heavier than those who never exercised.
Public Health and Policy Responses
On top of controversies about the causes of obesity, and about its precise health implications, come policy controversies
about the correct approach to obesity. The main debate is between "personal responsibility" advocates, who resist
regulatory attempts to intervene in citizen's private dietary habits, and "public interest" advocates, who promote
regulations, on the same public health grounds as the restrictions applied to tobacco products. In the U.S., a recent bout
in this controversy involves the so-called Cheeseburger Bill, an attempt to indemnify food industry businesses from what
some consider to be frivolous lawsuits by obese clients.
"Personal responsibility" advocates work on the basis that, as the microbiologist Rene Dubos once said, health ought not
to be considered an end in itself, but "the condition best suited to reach goals that each individual formulates for
himself." Any other definition permits authorities to curtail the autonomy of the self-determining individual,
imposing quantity over quality of life onto them, undermining his civil liberties. As much as principled doctors, personal
responsibility arguments have also been offered by food producer lobbies. In 1961, for example, as President John F
Kennedy raised concerns about a lack of fitness in American society, a spokesman for the U.S. Dairy industry, Frank R.
Neu, wrote advertorials warning We May Be Sitting Ourselves To Death. Not food regulation, but personal exercising, is
mooted as the solution.
When it comes to childhood obesity, personal responsibility also means parental responsibility. A survey by the nonpartisan
group Public Agenda found 68 percent of American parents said it was "absolutely essential" to teach their children good
eating habits, but only 40 percent believe they had succeeded. Fewer parents say it is essential to teach their children
about physical fitness (51 percent), but more believe they have succeeded (53 percent). Overall, parents said they found
it difficult to protect their children from negative social messages on a range of topics, including bad nutrition.
On July 15, 2004, the United States Department of Health and Human Services announced a new policy from HHS' Centers for
Medicare & Medicaid Services (CMS) removing language in the Medicare Coverage Issues Manual stating that obesity is not
an illness. According to the press release "This step allows members of the public to request that Medicare review medical
evidence to determine whether specific treatments related to obesity would be covered by Medicare. By law, Medicare covers
specified medically necessary services for illness and injury. The prior manual language, because it stated that obesity
was not an illness, could prevent Medicare from covering treatments for diseases related to obesity."
Non-Medical Consequences
Besides increases in disease and mortality there are other implications of the present world trend in obesity. Among
these are:
- Increased pressure on airline revenues (or increased fares) due to lobbying efforts to increase seating width
on commercial airplanes and due to higher fuel costs. (Extra weight of obese passengers is costing
airlines and consumers US$275,000,000 per annum.)
- Increased litigation by obese persons suing restaurants (over causation of obesity) and airlines (over
airline seating width). Note that the Personal Responsibility in Food Consumption Act of 2005 was motivated
by a need to reduce litigation from obesity activists.
- Sizeable societal economic costs attributable to obesity, with medical costs attributable to obesity rising
to 78.5 billion dollars or 9.1 percent of all medical expenditures in the U.S. as of 1998. However, such
studies do not necessarily consider that earlier mortality of obese people may save health costs associated
with aging.
(adapted from Wikipedia, the free encyclopedia http://en.wikipedia.org/wiki/Obesity)
OBJECTIVES: To examine whether high relative weight increases the risk of future sickness absence and to what extent any differences in short and long absence periods can be
explained by specific obesity-related disorders, general health, and working conditions. RESEARCH METHODS AND PROCEDURES: The study included 5386 female and 1452
male employees of the city of Helsinki surveyed in 2000 to 2002. Survey data were linked to sickness absence records until the end of 2004 (mean follow-up time 2.9 years).
RESULTS: Women and men with higher relative weight had clearly more short (1 to 3 days) and long (>3 days) periods of sickness absence during follow-up. The associations
were rather monotonic and stronger for long periods. In women, adjusting for arthrosis and
decreased the excess risk of long periods among those who were obese. In men,
arthrosis,
, and metabolic disease explained some of the excess risk for both short and long periods among the obese. Adjusting for physical functioning and self-rated health
decreased the excess risk for short and long periods of sickness absence among obese women and men. Working conditions had almost no effect on the association between
BMI and short or long periods of sickness absence. DISCUSSION: Obesity increases the risk of having short and long periods of sickness absence. This finding can be partly
explained by measures of general health and specific obesity-related disorders. Healthy weight maintenance is a crucial issue in promoting occupational functioning and minimizing
the costs associated with sickness absence.
Journal: Obesity (Silver Spring). 2007 Feb;15(2):465-72.
Authors: Vasilakopoulou A, le Roux CW.
Department of Metabolic Medicine, Hammersmith Hospital, Imperial College, London, UK Laiko General Hospital, Athens,
Greece.
Objective:Obesity is a serious public health problem associated with increased morbidity and mortality. Although the causes
for obesity are unclear, it seems that environmental, genetic, neural and endocrine factors contribute to its development.
However, the rapid global spread of obesity resembles epidemiologically the spread of an infectious disease. Thus far,
little consideration has been given to the possibility that the epidemic of obesity could be due to an infectious agent.
Seven viruses and a scrapie agent have been implicated in obesity.Design:This review evaluates the infectious pathogens and
the evidence that these viruses are associated with obesity and concludes that a strong evidence base is emerging that
associates certain viruses with obesity.Conclusion:More work is however required to elucidate the mechanisms of weight gain
after viral infection. In the mean time, discounting viruses as a contributing factor to obesity would deprive us of a
potential new avenue of investigating and treating the ever increasing epidemic of obesity.International Journal of Obesity
advance online publication, 10 April 2007; doi:10.1038/sj.ijo.0803623.
Journal: Int J Obes (Lond). 2007 Apr 10;
PURPOSE OF REVIEW: Obesity is the number one preventable risk factor for chronic kidney disease. Obesity is, however,
associated with improved survival in patients with end-stage renal disease (ESRD). RECENT FINDINGS: Multiple observational
studies have documented an association between obesity and risk of kidney disease even after adjustment for obesity-related
co-morbid conditions, including
. Prevalence of a body mass index of at least 35 kg/m among incident dialysis
patients has increased by 64% over the past decade, and if trends continue 20% of all patients will initiate dialysis with
this degree of obesity. Weight loss improves glomerular hemodynamics in morbidly obese adults and may retard progression of
chronic kidney disease. In contrast, once a patient reaches ESRD, the degree of adiposity correlates with survival, and
weight loss may not necessarily be beneficial. SUMMARY: Weight loss appears to be beneficial in obese patients both with and
without chronic kidney disease. The safety of intentional weight loss in obese ESRD patients, however, remains
questionable. The preclusion of obese ESRD patients from kidney transplantation needs to be readdressed and more studies
are needed to determine effective strategies for addressing the obesity epidemic in the chronic kidney disease and ESRD
populations.
Journal: Curr Opin Nephrol Hypertens. 2007 May;16(3):237-41
Authors: McLaughlin T, Abbasi F, Lamendola C, Reaven G.
Divisions of Endocrinology, Stanford University School of Medicine, Stanford, Calif.
BACKGROUND: The possibility that substantial heterogeneity in metabolic abnormalities exists in moderately obese individuals
has not been emphasized in studies of the effect of obesity on morbidity and mortality. We tested the hypothesis that risk
factors for
mellitus and cardiovascular disease vary dramatically in moderately obese individuals as a
function of differences in a specific measure of insulin sensitivity. METHODS: Participants included 211 apparently healthy,
obese (body mass index [calculated as weight in kilograms divided by height in meters squared], 30.0-34.9) volunteers for
weight loss studies. Main outcome measures included insulin-mediated glucose uptake as quantified by the insulin suppression
test and metabolic variables known to increase the risk for
and cardiovascular disease. RESULTS: Insulin
sensitivity varied 6-fold. When compared with the most insulin-sensitive third, the most insulin-resistant third of the
population had significantly higher (P<.001) systolic and diastolic
(139 +/- 20 vs 123 +/- 18 mm Hg, and
83 +/- 3 vs 75 +/- 10 mm Hg, respectively), higher fasting and 2-hour oral glucose load concentrations (103 +/- 11 vs 95
+/- 11 mg/dL [5.7 +/- 0.6 vs 5.3 +/- 0.6 mmol/L], and 139 +/- 30 vs 104 +/- 19 mg/dL [7.7 +/- 1.7 vs 5.8 +/- 1.1 mmol/L],
respectively), higher plasma triglyceride concentrations (198 +/- 105 vs 114 +/- 51 mg/dL [2.2 +/- 1.2 vs 1.3 +/- 0.6
mmol/L]), lower plasma high-density lipoprotein cholesterol concentrations (41 +/- 9 vs 50 +/- 13 mg/dL [1.1 +/- 0.2 vs 1.3
+/- 0.3 mmol/L]), and more prevalent impaired glucose tolerance (47% vs 2%). CONCLUSIONS: The magnitude of risk factors for
and cardiovascular disease varies markedly in moderately obese individuals as a function of differences in
degree of insulin sensitivity. Because not all moderately obese individuals are at similar risk for developing
and cardiovascular disease, intensive therapeutic interventions should be addressed to the insulin-resistant
subset of this population.
Journal: Arch Intern Med. 2007 Apr 9;167(7):642-8.
Authors: Razak F, Anand SS, Shannon H, Vuksan V, Davis B, Jacobs R, Teo KK, McQueen M, Yusuf S.
Population Health Research Institute, Department of Medicine, and Department of Clinical Epidemiology and Biostatistics,
McMaster University, Hamilton, Canada; Faculty of Medicine and Department of Medicine, University of Toronto, Toronto,
Canada; and Six Nations Health Services, Ohsweken, Ontario, Canada.
BACKGROUND: Body mass index (BMI) is widely used to assess risk for cardiovascular disease and
. Cut points
for the classification of obesity (BMI >30 kg/m(2)) have been developed and validated among people of European descent.
It is unknown whether these cut points are appropriate for non-European populations. We assessed the metabolic risk
associated with BMI among South Asians, Chinese, Aboriginals, and Europeans. METHODS AND RESULTS: We randomly sampled 1078
subjects from 4 ethnic groups (289 South Asians, 281 Chinese, 207 Aboriginals, and 301 Europeans) from 4 regions in Canada.
Principal components factor analysis was used to derive underlying latent or "hidden" factors associated with 14 clinical
and biochemical cardiometabolic markers. Ethnic-specific BMI cut points were derived for 3 cardiometabolic factors. Three
primary latent factors emerged that accounted for 56% of the variation in markers of glucose metabolism, lipid metabolism,
and blood pressure. For a given BMI, elevated levels of glucose- and lipid-related factors were more likely to be present
in South Asians, Chinese, and Aboriginals compared with Europeans, and elevated levels of the
-related factor
were more likely to be present among Chinese compared with Europeans. The cut point to define obesity, as defined by
distribution of glucose and lipid factors, is lower by approximately 6 kg/m(2) among non-European groups compared with
Europeans. CONCLUSIONS: Revisions may be warranted for BMI cut points to define obesity among South Asians, Chinese, and
Aboriginals. Using these revised cut points would greatly increase the estimated burden of obesity-related metabolic
disorders among non-European populations.
Journal: Circulation. 2007 Apr 9;
Treatment of obesity continues to rely upon the classical triad of nutritional advise, increase of physical activity and
use of drugs. However, in recent years, there have appeared novelties in both therapeutic targets and new molecules. With
regard to therapeutic targets of obesity, success does not consist of losing much weight but attaining a moderate yet
maintained weight lose (5-10% of initial weight) at the expense of visceral fat. In other words, instead of weight, what is
needed is a waist reduction, mainly to improve or prevent obesity-related metabolic and vascular complications. Regarding
drugs, a new molecules is about to appear in the international pharmaceutical market: rimonabant. A selective blocker of
the endocannabinoid receptor CB1, it has proven to be effective and safe in treating obesity and its comorbidities. Another
known agent, orlistat, has proven to be effective in the prevention of the development of
in obese patients
with or without glucose intolerance.
Journal: Med Clin (Barc). 2007 Apr 7;128(13):508-14.
Within the last decade an intensive research led to an identification of several genes which are involved in a regulation
of energy balance. In most cases, carriers of these gene mutations do not exhibit further characteristic phenotypic
features except for a severe obesity. Obesity based on mutation of one gene product is called monogenic obesity. Mutations
in genes for leptin, leptin receptor, proopiomelanocortin, prohormone convertase 1, melanocortin 4 and 3 receptor disrupt
the physiological humoral signalization between peripheral signals and the hypothalamic centres of satiety and hunger.
Defects of all above mentioned genes lead to phenotype of abnormal eating behaviour followed by a development of severe
early-onset obesity. Mutations of melanocortin 4 receptor gene represent the most common cause of monogenic obesity because
they are detected in almost 6 % children with early-onset severe obesity. Mutations of the other genes involved in energy
homeostasis are very rare. Although these mutations are sporadic we assume that further research of monogenic forms of
obesity might lead to our understanding of physiology and pathophysiology of regulation of the energy homeostasis and
eating behaviour. Additionally, they may open new approach to the management of eating behaviour and to the treatment of
obesity.
Journal: Cas Lek Cesk. 2007;146(3):240-5.
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