Obesity

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Overview

Template:DiseaseDisorder infobox

WikiDoc Resources for Obesity

Articles

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List of terms related to 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.

Although obesity is an individual clinical condition, it is increasingly viewed as a serious and growing 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.[1][2]

Obesity is characterized as a state of excess adipose mass with abnormal increase of fat on the subcutaneous connective tissue. Obesity is generally gauged by the Body Mass Index(BMI). A high BMI is associated with a higher risk for potentially lethal medical problems.

BMI (kg/m2)
Appropriate Weight 18.5-25
Overweight >25
Obesity >30

Classification

Obesity can be defined in absolute or relative terms. In practical settings, obesity is typically evaluated in absolute terms by measuring BMI (body mass index), but also in terms of its distribution through waist circumference or waist-hip circumference ratio measurements.[3] In addition, the presence of obesity needs to be regarded in the context of other risk factors and comorbidities (other medical conditions that could influence risk of complications).[1]

BMI

BMI, or body mass index, is a simple and widely used method for estimating body fat.[4] BMI was developed by the Belgian statistician and anthropometrist Adolphe Quetelet.[5] It is calculated by dividing the subject's weight by the square of his/her height, typically expressed either in metric or US "Customary" units:

Metric: <math>BMI = kg/m^2</math>

Where <math>kg</math> is the subject's weight in kilograms and <math>m</math> is the subject's height in metres.

US/Customary: <math>BMI=lb*703/in^2</math>

Where <math>lb</math> is the subject's weight in pounds and <math>in</math> is the subject's height in inches.

The current definitions commonly in use establish the following values, agreed in 1997 and published in 2000:[6]

  • 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.[7][8]

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).[1] 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.[9]

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.[10]

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)[10] are both used as measures of central obesity.

In a cohort of almost 15,000 subjects from the National Health and Nutrition Examination Survey (NHANES) III study, waist circumference explained obesity-related health risk significantly better than BMI when metabolic syndrome was taken as an outcome measure.[11]

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. Their routine use is discouraged.[12]

Other measurements of body fat include computed tomography (CT/CAT scan), magnetic resonance imaging (MRI/NMR), and dual energy X-ray absorptiometry (DXA).[13]

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.[1] Smoking, hypertension, age and family history are other risk factors that may indicate treatment.[1]

Differential Diagnosis

Contributory Factors

Genetic factors

Hypothalamic Dysfunction

Endocrine

Lipomatosis

  • Andler's Disease
  • Launois-Bensaude Syndrome
  • Madelung's Disease
  • Multiple lipomas

Effects on health

A large number of medical conditions have been associated with obesity. Health consequences are categorised as being the result of either increased fat mass (osteoarthritis, obstructive sleep apnea, social stigma) or increased number of fat cells (diabetes, cancer, cardiovascular disease, non-alcoholic fatty liver disease).[14] Mortality is increased in obesity, with a BMI of over 32 being associated with a doubled risk of death.[15] There are alterations in the body's response to insulin (insulin resistance), a proinflammatory state and an increased tendency to thrombosis (prothrombotic state).[14]

Disease associations may be dependent or independent of the distribution of adipose tissue. Central obesity (male-type or waist-predominant obesity, characterised by a high waist-hip ratio), is an important risk factor for the metabolic syndrome, 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 blood cholesterol, and triglyceride levels (combined hyperlipidemia).[16]

Apart from the metabolic syndrome, obesity is also correlated with a variety of other complications. For some 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.

While being severely obese has many health ramifications, those who are somewhat overweight face little increased mortality or morbidity. Osteoporosis is known to occur less in slightly overweight people.

Causes and mechanisms

Lifestyle

Most researchers have concluded that the combination of an excessive nutrient intake and a sedentary lifestyle are the main cause for the rapid acceleration of obesity in Western society in the last quarter of the 20th century. [21]

Despite the widespread availability of nutritional information in schools, doctors' offices, on the internet and on groceries,[22] it is evident that overeating remains a substantial problem. For instance, reliance on energy-dense fast-food meals tripled between 1977 and 1995, and calorie intake quadrupled over the same period.[23]

However, dietary intake in itself is insufficient to explain the phenomenal rise in levels of obesity in much of the industrialized world during recent years. An increasingly sedentary lifestyle also has a significant role to play. More and more research into child obesity, for example, links such things as the school run, with the current high levels of this disease. [24]

Less well established life style issues which may influence obesity include a stressful mentality and insufficient sleep.

Genetics

As with many medical conditions, the calorific 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 conditions that feature obesity have been identified (such as Prader-Willi syndrome, Bardet-Biedl syndrome, MOMO syndrome, leptin receptor mutations and melanocortin 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.

A 2007 study identified fairly common mutations in the FTO gene; heterozygotes had a 30% increased risk of obesity, while homozygotes faced a 70% increased risk.[25]

On a population level, the thrifty gene hypothesis postulates that certain ethnic groups 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 may have been 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 stable food supplies.[26]

Medical illness

Certain physical and mental illnesses and particular pharmaceutical substances may predispose to obesity. Apart from the fact that correcting these situations may improve the obesity, the presence of increased body weight may complicate the management of others.

Medical illnesses that increase obesity risk include several rare congenital syndromes (listed above), hypothyroidism, Cushing's syndrome, growth hormone deficiency.[27] Smoking cessation is a known cause for moderate weight gain, as nicotine suppresses appetite. Certain medications (e.g. steroids, atypical antipsychotics, some fertility medication) may cause weight gain.

Mental illnesses may also increase obesity risk, specifically some eating disorders such as bulimia nervosa, binge eating disorder, and compulsive overeating (also known as food addiction).

Neurobiological mechanisms

Scientists investigating the mechanisms and treatment of obesity may use animal models such as mice to conduct experiments.

Flier[28] 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, and 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. This resistance is thought to explain in part why administration of leptin has not been shown to be effective in suppressing appetite in most obese subjects.

While leptin and ghrelin are produced peripherally, they control appetite through their actions on the central nervous system. In particular, they and other appetite-related hormones act on the hypothalamus, a region of the brain central to the regulation of food intake and energy expenditure. There are several circuits within the hypothalamus that contribute to its role in integrating appetite, the melanocortin pathway being the most well understood.[28] The circuit begins with an area of the hypothalamus, the arcuate nucleus, that has outputs to the lateral hypothalamus (LH) and ventromedial hypothalamus (VMH), the brain's feeding and satiety centers, respectively.[29]

The arcuate nucleus contains two distinct groups of neurons.[28] The first group coexpresses neuropeptide Y (NPY) and agouti-related peptide (AgRP) and has stimulatory inputs to the LH and inhibitory inputs to the VMH. The second group coexpresses pro-opiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART) and has stimulatory inputs to the VMH and inhibitory inputs to the LH. Consequently, NPY/AgRP neurons stimulate feeding and inhibit satiety, while POMC/CART neurons stimulate satiety and inhibit feeding. Both groups of arcuate nucleus neurons are regulated in part by leptin. Leptin inhibits the NPY/AgRP group while stimulating the POMC/CART group. Thus a deficiency in leptin signaling, either via leptin deficiency or leptin resistance, leads to overfeeding and may account for some genetic and acquired forms of obesity.

Microbiological aspects

The role of bacteria colonizing the digestive tract in the development of obesity has recently become the subject of investigation. Bacteria participate in digestion (especially of fatty acids and polysaccharides), and alterations in the proportion of particular strains of bacteria may explain why certain people are more prone to weight gain than others. Human digestive tract are generally either members of the phyla of bacteroidetes or of firmicutes. In obese people, there is a relative abundance of firmicutes (which cause relatively high energy absorption), which is restored by weight loss. From these results it cannot yet be concluded whether this imbalance is the cause of obesity or an effect.[30]

Social determinants

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[31] 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 a lower level 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.

A 2007 study of more than 32,500 children of the original Framingham Heart Study cohort followed for 32 years indicated that BMI change in friends, siblings or spouse predicted BMI change in subjects irrespective of geographical distance. The association was strongest among mutual friends and lower among siblings and spouses (although these differences were not statistically significant). The authors concluded from the results that acceptance of body mass plays an important role in changes in body size.[32]

Treatment

Main article: Weight loss

The main treatment for obesity is to reduce body fat by eating fewer calories and exercising more. A beneficial side effect of exercise is to increase muscle, tendon, and ligament strength, which helps to prevent injury from accidents and vigorous activity. Diet and exercise programs produce an average weight loss of approximately 8% of total body mass (excluding program drop-outs). Not all dieters are satisfied with these results, but a loss of as little as 5% of body mass can create large health benefits.

Much more difficult than reducing body fat is keeping it off. Eighty to ninety-five percent of those who lose 10% or more of their body mass by dieting regain all that weight back within two to five years. The body has systems that maintain its homeostasis at certain set points, including body weight. Therefore, keeping weight off generally requires making exercise and eating right a permanent part of a person's lifestyle. Certain nutrients, such as phenylalanine, are natural appetite suppressants which allow resetting of the body's set point for body weight.

Clinical protocols

In a clinical practice guideline by the American College of Physicians, the following five recommendations are made:[33]

  1. 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.
  2. 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.
  3. 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.
  4. 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.
  5. 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.

A clinical practice guideline by the US Preventive Services Task Force (USPSTF) concluded that the evidence is insufficient to recommend for or against routine behavioral counseling to promote a healthy diet in unselected patients in primary care settings, but that intensive behavioral dietary counseling is recommended in those with hyperlipidemia and other known risk factors for cardiovascular and diet-related chronic disease. Intensive counseling can be delivered by primary care clinicians or by referral to other specialists, such as nutritionists or dietitians.[34][35]

Exercise

Exercise requires energy (calories). Calories are stored in body fat. The body breaks down its fat stores in order to provide energy during prolonged aerobic exercise. The largest muscles in the body are the leg muscles, and naturally these burn the most calories, which make walking, running, and cycling among the most effective forms of exercise for reducing body fat.

A meta-analysis of randomized controlled trials by the international Cochrane Collaboration found that "exercise combined with diet resulted in a greater weight reduction than diet alone".[36]

Dieting

Main article: Dieting

In general, dieting means eating less. Various dietary approaches have been proposed, some of which have been compared by randomized controlled trials:

"all 4 diets resulted in modest statistically significant weight loss at 1 year, with no statistically significant differences between diets"
"The higher discontinuation rates for the Atkins and Ornish diet groups suggest many individuals found these diets to be too extreme"

Low carbohydrate versus low fat

Main article: Medical research related to low-carbohydrate diets

Many studies have focused on diets that reduce calories via a low-carbohydrate (Atkins diet, Zone diet) diet versus a low-fat diet (LEARN diet, Ornish diet). The Nurses' Health Study, an observational cohort study, found that low carbohydrate diets based on vegetable sources of fat and protein are associated with less coronary heart disease.[39]

A meta-analysis of randomized controlled trials by the international Cochrane Collaboration in 2002 concluded[40] that fat-restricted diets are no better than calorie restricted diets in achieving long term weight loss in overweight or obese people.

A more recent meta-analysis that included randomized controlled trials published after the Cochrane review[41][42][38] found that "low-carbohydrate, non-energy-restricted diets appear to be at least as effective as low-fat, energy-restricted diets in inducing weight loss for up to 1 year. However, potential favorable changes in triglyceride and high-density lipoprotein cholesterol values should be weighed against potential unfavorable changes in low-density lipoprotein cholesterol values when low-carbohydrate diets to induce weight loss are considered."[43]

The Women's Health Initiative Randomized Controlled Dietary Modification Trial[44] found that a diet of total fat to 20% of energy and increasing consumption of vegetables and fruit to at least 5 servings daily and grains to at least 6 servings daily resulted in:

  • no reduction in cardiovascular disease[45]
  • an insignificant reduction in invasive breast cancer[46]
  • no reductions in colorectal cancer[47]

Additional recent randomized controlled trials have found that:

  • The choice of diet for a specific person may be influenced by measuring the invididual's insulin secretion:
In young adults "Reducing glycemic [carbohydrate] load may be especially important to achieve weight loss among individuals with high insulin secretion."[49] This is consistent with prior studies of diabetic patients in which low carbohydrate diets were more beneficial.[50][51]

Low glycemic index

"The glycaemic index factor is a ranking of foods based on their overall effect on blood sugar levels. Low glycaemic index foods, such as lentils, provide a slower more consistent source of glucose to the bloodstream, thereby stimulating less insulin release than high glycaemic index foods, such as white bread."[52][53]

The glycemic load is "the mathematical product of the glycemic index and the carbohydrate amount".[54]

In a randomized controlled trial that compared four diets that varied in carbohydrate amount and glycemic index found complicated results[55]:

  • Diet 1 and 2 were high carbohydrate (55% of total energy intake)
    • Diet 1 was high-glycemic index
    • Diet 2 was low-glycemic index
  • Diet 3 and 4 were high protein (25% of total energy intake)
    • Diet 3 was high-glycemic index
    • Diet 4 was low-glycemic index

Diets 2 and 3 lost the most weight and fat mass; however, low density lipoprotein fell in Diet 2 and rose in Diet 3. Thus the authors concluded that the high-carbohydrate, low-glycemic index diet was the most favorable.

A meta-analysis by the Cochrane Collaboration concluded that low glycemic index or low glycemic load diets led to more weight loss and better lipid profiles. However, the Cochrane Collaboration grouped low glycemic index and low glycemic load diets together and did not try to separate the effects of the load versus the index.[52]

Drugs

Main article: Anti-obesity drug

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). Weight loss with these drugs is modest, and over the longer term average weight loss on orlistat is 2.9 kg, sibutramine 4.2 kg and rimonabant 4.7 kg. Orlistat and rimonabant lead to a reduced incidence of diabetes, and all drugs have some effect on lipoproteins (different forms of cholesterol). There is little data, however, on longer-term complications of obesity such as heart attacks. All drugs have side-effects and potential contraindications.[56] It is common for weight loss drugs to be tried for a period of time (e.g. 3 months), and to discontinue them or change to another agent if no benefit is achieved, such as weight loss less than 5% the total body weight.[12]

A meta-analysis of randomized controlled trials by the international Cochrane Collaboration concluded that in diabetic patients fluoxetine, orlistat and sibutramine could achieve significant but modest weight loss over 12-57 weeks, with long-term health benefits being unclear.[57]

Obesity may also influence the choice of drug treatment for diabetes. Metformin may lead to mild weight reduction (as opposed to sulfonylureas and insulin), and has been demonstrated to reduce the risk of cardiovascular disease in type 2 diabetics who are obese.[58] The thiazolidinediones may cause slight weight gain, but decrease the "pathologic" form of abdominal fat and may therefore be used in diabetics with central obesity.[59]

Bariatric surgery

Main article: bariatric surgery

Bariatric surgery (or "weight loss surgery") is the use of surgical interventions in the treatment of obesity. As every surgical intervention may lead to complications, it is regarded as a last resort when dietary modification and pharmacological treatment have proven to be unsuccessful. Weight loss surgery relies on various principles; the most common approaches are reducing the volume of the stomach, producing an earlier sense of satiation (e.g. by adjustable gastric banding and vertical banded gastroplasty) while others also reduce the length of bowel that food will be in contact with, directly reducing absorption (gastric bypass surgery). Band surgery is reversible, while bowel shortening operations are not. Some procedures can be performed laparoscopically. Complications from weight loss surgery are frequent.[60]

Two large studies have demonstrated a mortality benefit from bariatric surgery. A marked decrease in the risk of diabetes mellitus, cardiovascular disease and cancer.[61][62] Weight loss was most marked in the first few months after surgery, but the benefit was sustained in the longer term. In one study there was an unexplained increase in deaths from accidents and suicide that did not outweigh the benefit in terms of disease prevention. Gastric bypass surgery was about twice as effective as banding procedures.[62]

Counseling

A meta-analysis of randomized controlled trials concluded that "compared with usual care, dietary counseling interventions produce modest weight losses that diminish over time."[63]

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.[64]

History

Obesity was a status symbol in European culture: "The Tuscan General" by Alessandro del Borro, 17th century.

In several human cultures, obesity was associated with physical attractiveness, strength, and fertility. Some of the earliest known cultural artifact 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.

Obesity was considered a symbol of wealth and social status in cultures prone to food shortages or famine. It was viewed in the same manner well into the early modern period in European cultures as well, 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 depiction of fat women gives us the description Rubenesque. 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."[65]

Contemporary culture

In modern Western culture, the obese body shape is widely regarded as unattractive and many negative stereotypes are commonly associated with obese people. Obese children, teenagers and adults can also face a heavy social stigma. Obese children are frequently the targets of bullies and are often shunned by their peers. Although obesity rates are rising amongst all social classes in the West, obesity is often seen as a sign of lower socio-economic status.[66] Most obese people have experienced negative thoughts about their body image, and some take drastic steps to try to change their shape including dieting, the use of diet pills, and even surgery. 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 even being referred to as an epidemic.[67]

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. Some notable figures within this movement, such as Paul Campos, argue that the social stigma surrounding obesity is founded in cultural anxiety, and that public concern over health risks associated with obesity are inappropriately used as a rationalization for this stigma.[68]

Government agencies and private medicine have warned Americans for years of the adverse health effects associated with overweight and obesity. Despite the warnings, the problem is getting worse. In 2004, the CDC reported that 66.3% of adults in the United States were overweight or obese. The cause in most cases is a sedentary lifestyle; approximately 40% of adults in the United States do not participate in any leisure-time physical activity and less than 1/3 of adults engage in the recommended amount of physical activity.[69] Overweight and obesity are easily determined by using Body Mass Index (BMI); this index uses your weight and height to determine body fat. An index A BMI range of 25 to 29.9 is considered overweight and anything over 30 obese. Individuals with a BMI over 30 increase the risk of several heath hazards.[70]

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, or a jolly fat man like Santa Claus. Equally common is the obese vicious bully (such as Dudley Dursley from the Harry Potter book series, Eric Cartman from South Park, Nelson Muntz from The Simpsons).

Gluttony and obesity are commonly depicted together in works of fiction.

In cartoons, obesity is often used to comedic effect, with fat animal characters (such as Piggy, Porky Pig, Tummi Gummi, and Podgy Pig) having to squeeze through narrow spaces, frequently getting stuck or even exploding.

A more unusual example of obesity-related humour is Bustopher Jones, from T. S. Eliot's poem "Bustopher Jones: The Cat About Town" featured in Old Possum's Book of Practical Cats, and the musical Cats derived from the poem. Bustopher's 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, being described by others as "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 the self esteem of obese people. On the other hand, obesity is often associated with positive characteristics such as good humor. In addition, some people are sexually attracted to obese people (see chubby culture and fat admirer).

Public health and policy

Graphic chart comparing obesity percentages of the total population in OECD member countries.

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.[71][72]

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.[73] From 1980 to 2002, obesity has doubled in adults and overweight prevalence has tripled in children and adolescents.[74] 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."[74] The prevalence in the United States continues to rise.[75]

China

Because of the booming economy increasing average incomes, the population of China has recently begun a more sedentary lifestyle and at the same time begun consuming more calorie-rich foods. From 1991 to 2004 the percentage of adults who are overweight or obese increased from 12.9% to 27.3%.[76]

Obesity is a public health and policy problem because of its prevalence, costs and burdens.[77] The prevalence of obesity has been continually rising for two decades.[78] 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.[79] 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 are 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.[80]
  • 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. 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. In the United States, production of corn, soy, wheat and rice is subsidized through the U.S. farm bill. Corn and soy, which are main sources of the sugars and fats in processed food, are thus cheap compared to fruits and vegetables.[81]
  • 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.[82]
  • 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.[83]
  • Since 1980 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.

Public health and policy responses

Some U.S. Kaiser Permanente facilities now provide oversized chairs such as this one at Richmond Medical Center, for obese patients.

Public health and policy responses to obesity seek to understand and correct the environmental factors responsible for shifts in the prevalence of overweight and obesity in a population. Obesity and overweight are, currently, primarily policy problems in the United States. Policy and public health solutions look to change the environmental factors that promote calorie dense, low nutrient food consumption and that inhibit physical activity.

In the United States, policy has focused primarily on controlling childhood obesity which has the most serious long-term public health implication. Efforts have been underway to target schools. There are efforts underway to reform federally-reimbursed meal programs, limit food marketing to children, and ban or limit access to sugar sweetened beverages. In Europe, policy has focused on limiting marketing to children. There has been international focus on sugar policy and the role of agriculture policy in producing food environments that produce overweight and obesity in a population. To confront physical activity, efforts have examined zoning and access parks and safe routes in cities.

In the United Kingdom, a 2004 report by the Royal College of Physicians, the Faculty of Public Health and the Royal College of Paediatrics and Child Health, titled "Storing up Problems",[84] was followed by a report by the British House of Commons Health Select Committee - the "the most comprehensive inquiry" ever by that body - on the impact of obesity on health and society in the UK and possible approaches to the problem.[85] In 2006, the National Institute for Health and Clinical Excellence (NICE) issued a guideline on the diagnosis and management of obesity, as well as policy implications for non-healthcare organizations such as local councils.[12] A 2007 report produced by Sir Derek Wanless for the King's Fund warned that unless further action was taken, obesity had the capacity to cripple the National Health Service financially.[86]

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: in 2000, extra weight of obese passengers cost airlines and consumers US$275,000,000.[87]
  • Increased litigation by obese persons suing restaurants (for causing obesity)[88] and airlines (over airline seating width)[5] [6]. The Personal Responsibility in Food Consumption Act of 2005 was motivated by a need to reduce litigation from obesity activists.
  • Sizable 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[89][90]
  • Decreased worker productivity as measured by usage of disability leave and absenteeism at work.[91]
  • A study examining Duke University employees found that those with a BMI>40 filed twice as many workers compensation claims as workers whose BMI was 18.5-24.9, and had more than 12 times as many lost work days. The most common injuries were due to falls and lifting, and affected the lower extremities, wrists or hands, and backs.[92]

See also

References

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  88. ↑ 109th U.S. Congress (2005-2006) H.R. 554: 109th U.S. Congress (2005-2006) H.R. 554: Personal Responsibility in Food Consumption Act of 2005
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  92. ↑ Ostbye T, Dement JM, Krause KM (2007). "Obesity and workers' compensation: results from the Duke Health and Safety Surveillance System". Arch. Intern. Med. 167 (8): 766–73. doi:10.1001/archinte.167.8.766. PMID 17452538.

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