Obesity is a disease in which excess body fat has accumulated to such an extent that health may be negatively affected.^[1] It is commonly defined as a body mass index (weight divided by height squared) of 30 kg/m² or higher.^[1] This distinguishes it from being overweight as defined by a BMI of between 25-29.9 kg/m².^[1] Many studies show an association between excessive body weight and various diseases, particularly cardiovascular diseases, diabetes mellitus type 2, sleep apnea, certain types of cancer, and osteoarthritis.^[2][3] As a result, obesity has been found to reduce life expectancy.^[3] With rates of adult and childhood obesity increasing, authorities view it as a serious public health problem. Attempts to address it include population-wide measures to improve dietary choices and increase physical exercise.^[4]

Classification

Obesity, in absolute terms, is an increase of body adipose tissue (fat tissue) mass. In a practical setting it is difficult to determine this directly. Therefore obesity is typically assessed by BMI (body mass index) and in terms of its distribution via the waist circumference.^[5] In addition, the presence of obesity needs to be evaluated in the context of other risk factors such as medical conditions that could influence the risk of complications.^[2]

BMI

An obese male. Weight 146 kg/322 lbs, height 177 cm/5 ft 10 in. The body mass index is 46 kg/m².

Body mass index or BMI is a simple and widely used method for estimating body fat mass.^[6] BMI was developed in the 19th century by the Belgian statistician and anthropometrist Adolphe Quetelet.^[7] BMI is an accurate reflection of body fat percentage in the majority of the adult population, but is less accurate in situations that affect body composition such as in body builders and pregnancy.^[2]

BMI 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: BMI = kg/m^2

where kg is the subject's weight in kilograms and m is the subject's height in metres.

US/Customary and imperial: BMI=lb*703/in^2

where lb is the subject's weight in pounds and in is the subject's height in inches.

The most commonly used definitions, established by the WHO in 1997 and published in 2000, provide the following values:^[1]

• 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?34.9 is class I obesity
• A BMI of 35.0-39.9 is class II obesity
• A BMI of > 40.0 is class III obesity

Some modifications to the WHO definitions have been made by particular bodies:^[8][9]

• 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.
• For Asians, overweight is a BMI between 23 and 29.9 kg/m² and obesity a BMI >30 kg/m².

The surgical literature breaks down "class III" obesity into further catergories.^[10]

• Any BMI > 40 is severe obesity
• A BMI of 40.0-49.9 is morbid obesity
• A BMI of >50 is super obese

Waist circumference and waist hip ratio

In those with a BMI under 35, intra-abdominal body fat is related to negative health outcomes independent of total body fat.^[11] Intra-abdominal or visceral fat has a particularly strong correlation with cardiovascular disease.^[12] In a study of 15,000 subjects, waist circumference also correlated better with metabolic syndrome than BMI.^[13] Women who have abdominal obesity have a cardiovascular risk similar to that of men.^[14] In people with a BMI over 35, measurement of waist circumference however adds little to the predictive power of BMI as most individuals with this BMI have an abnormal waist circumferences.^[2]

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.^[12]

Body fat percentage

On the left an abdominal CT of a person of normal weight. On the right an abdominal CT of an obese person. Note is made of 3.6 cm of subcutaneous fat.

Body fat % = 1.2*BMI+0.23*age-5.4-10.8*gender

where gender is 0 if female and 1 if male

This formula takes into account the fact that the body fat percent of women is 10% greater in men then women for a given BMI and that a persons percentage body fat increases as they age even if their weight remains constant.^[16]

Direct attempts to determine body fat percent are difficult and often expensive. One of the most accurate methods is to weigh a person underwater which is known as hydrostatic weighting. Two other simpler and less accurate methods for measuring body fat therefore have historically been used. The first is the skinfold test, in which a pinch of skin is precisely measured to determine the thickness of the subcutaneous fat layer. It has not, however, been adequately evaluated in obese subjects.^[16] The other is bioelectrical impedance analysis which uses electrical resistance. Bioelectrical impedance however has not been shown to provide an advantage over BMI. Therefore the routine use of these tests are discouraged.^[4]

Body fat percent measurements techniques which are used mainly for research include computed tomography (CT/CAT scan), magnetic resonance imaging (MRI/NMR), and dual energy X-ray absorptiometry (DEXA).^[11] These techniques provide very accurate measurements, although it may be difficult to scan the severely obese due weight limits of the equipment and insufficient diameter of the CT/MRI scanner.^[16]

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 complications that would indicate a need to commence or intensify treatment for obesity.^[2] Smoking, high blood pressure age and family history are other risk factors that, in combination with obesity, may indicate an additional reason for treatment.^[2]

Effects on health

Mortality

Obesity is one of the leading preventable causes of death.^[17] Mortality risk varies with BMI. The lowest risk is found at a BMI of 22-24 kg/m² and increases with changes in either direction.^[18] A BMI of over 32 is associated with a doubling of risk of death^[19] and obesity is estimated to cause an excess 111,909 to 365,000 death per year in the United States.^[20][3] Obesity on average reduces ones life expectancy by 6-7 years.^[21][3] For subjects with severe obesity (BMIs >40) life expectancy is reduced by 20 years in men and 5 years in women.^[22]

Morbidity

A large number of physical and mental conditions have been associated with obesity. Health consequences can be categorized by the effects of increased fat mass (osteoarthritis, obstructive sleep apnea, social stigmatization) or by the increased number of fat cells (diabetes, cancer, cardiovascular disease, non-alcoholic fatty liver disease).^[3][23] Increases in body fat alter the body's response to insulin leading to insulin resistance and creates a proinflammatory state and an increased risk of thrombosis.^[23]

Central obesity, characterized by its high waist to hip ratio, is an important risk for metabolic syndrome. Metabolic syndrome is a combination of medical disorders which often includes diabetes mellitus type 2, high blood pressure, high blood cholesterol, and triglyceride levels.^[24]

Obesity is related to a variety of other complications. Some of these are directly caused by obesity and others are indirectly related threw mechanisms such as sharing a common cause ie. poor diet or sedentary lifestyle. The strength of the link between obesity and specific conditions is variable. One of the strongest is the link with type 2 diabetes: 64% of diabetes in men and 77% of diabetes in women can be attributed to excess weight.^[16]

Obesity survival paradox

Although the negative health consequences of obesity in the general population are well supported by the available evidence, health outcomes in certain subgroups seem to be improved at an increased BMI, thus leading to the obesity survival paradox.^[34] The paradox was first described in 1999 in overweight and obese patients undergoing hemodialysis. Since then it has been found in a few other subgroups and explanations for its occurrence have been put forwards.^[34]

In people with heart failure, those with a BMI between 30.0-34.9 had lower mortality then those with a normal weight. This has been attributed to the fact that people often lose weight as they become progressively more ill.^[35] Similar findings have been make in other types of heart disease. People with class I obesity and heart disease do not have greater rates of further heart problems than people of normal weight who also have heart disease. In people with greater degrees of obesity, however, risk of further events is increased.^[36][37] Even after cardiac bypass surgery, no increase in mortality is seen in the overweight and obese.^[38] One study found that the increased survival could be explained by the more aggressive treatment obese people receive after a cardiac event.^[39]

Causes

Most researchers agree that a combination of excessive calorie consumption and a sedentary lifestyle are the primary causes of obesity.^[40] In a minority of cases, increased food consumption can be attributed to genetic, medical, or psychiatric illness, but in general the rising prevalence of obesity is attributed to the availability of an easily accessible and palatable diet,^[41] car culture, and mechanized manufacturing. A 2006 review identifies ten other possible contributors to the recent increase of obesity: (1) insufficient sleep, (2) endocrine disruptors - food substances that interfere with lipid metabolism, (3) decreased variability in ambient temperature, (4) decreased rates of smoking, which suppresses appetite, (5) increased use of medication that leads to weight gain, (6) increased distribution of ethnic and age groups that tend to be heavier, (7) pregnancy at a later age, (8) intrauterine and intergenerational effects, (9) positive natural selection of people with a higher BMI, (10) assortative mating, heavier people tending to form relationships with each other.^[42]

Dietary

USDA chart shows the increase in soda consumption and the decrease in milk consumption.

There is little evidence to support the commonly expressed view that some obese people eat little yet gain weight due to a slow metabolism. What has been found, however, is that some obese people underreport how much food they consume compared to those of normal weight.^[16]

Sedentary lifestyle

A sedentary lifestyle plays a significant role in obesity.^[16] In 2000 the CDC estimated that more than 40% of the US population was sedentary, another 30% was active but not sufficiently and less than 30% had an adequate level of physical activity.^[46] There has been a trend toward decreased physical activity in part due to increasingly mechanized forms of work, changing modes of transportation, and increasing urbanization. Studies in children and adults have found an association between the number of hours of television watched and the prevalence of obesity.^[50][51][52] Driving one's children to school decreases the amount of exercise that they get. This is reflected in the decline in the proportion of children who walk or bike to school which occurred between 1969 (42%) and 2001 (16%) in the USA.^[46] Obese people are less active than those of normal weight. For example in Canada, 27.0% of sedentary men are obese as opposed to 19.6% of active men.^[53] Normal weight people are also more fidgety then those who are obese. This relationship is maintained even if normal weight people eat more or the obese person loses weight.^[54] Obesity rates have increased in relation to expanding suburbs. This has been attributed to increased time spent commuting, leading to less exercise and less meal preparation at home.^[55]

Genetics

Like many other medical conditions, obesity is the result of an interplay between genetic and environmental factors. Polymorphisms in various genes controlling appetite and metabolism may predispose to obesity when sufficient calories are present. Obesity is a major feature in a number of rare genetic conditions: Prader-Willi syndrome, Bardet-Biedl syndrome, MOMO syndrome, leptin receptor mutations, congenital leptin deficiency, and melanocortin receptor mutations. In a people with early-onset severe obesity (defined by an onset before ten years of age and body mass index over three standard deviations above normal), 7% harbor a single locus mutation.^[56] Apart from the above syndromes, an association has been found between an FTO gene polymorphism and weight. The 16% of adults in the study who were homozygous for this allele weighed about 3 kilograms more then those who had not inheireted this trait and subsequently had a 1.6 fold greater rate of obesity.^[57] One study found that 80% of the offspring of two obese parents were obese in contrast to less then 10% of the offspring of two parents who were of normal weight.^[28][16] The percentage of obesity that can be attributed to genetics varies from 6% to 85% depending on the population examined.^[58]

On a population level, the thrifty gene hypothesis postulates that certain ethnic groups may be more prone to obesity when exposed to an equivalent environment. Their ability to take advantage of rare periods of abundance by storing energy as fat would be advantagious during times of varying food availability. Individuals with greater adipose reserves would be more likely survive famine. This tendency to store fat however would be maladaptive in societies with stable food supplies.^[59] This is the presumed reason why Pima Indians, who evolved in a desert ecosystem, developed some of the highest rates of obesity when exposed to a Western lifestyle.^[41]

Medical and psychiatric illness

Certain physical and mental illnesses and the pharmaceutical substances used to treat them can increase one's risk of obesity. Medical illnesses that increase obesity risk include several rare genetic syndromes (listed above) as well as some congenital or acquired conditions: (1) hypothyroidism, (2) Cushing's syndrome, (3) growth hormone deficiency,^[60] and (4)eating disorders: binge eating disorder and night eating syndrome.^[3] However, obesity is not regarded as a psychiatric disorder, and therefore is not listed in the DSM-IVR as a psychiatric illness.^[28]

Certain medications may cause weight gain and or negative changes in body composition, such as insulin, sulfonylureas, thiazolidinediones, atypical antipsychotics, antidepressants, steroids, sulfonylureas, certain anticonvulsants (phenytoin and valproate), pizotifen, and some forms of hormonal contraception.^[3]

Socioeconomic

While genetic influences are important to understanding obesity, they cannot explain the current dramatic increase seen within specific countries or globally.^[41] Though it is accepted that calorie consumption in excess of calorie expenditure leads to obesity on an individual basis, the cause of the shifts in these two factors on the societal scale is much debated. There are a number of theories as to the cause but most believe it is a combination of various factors.

The correlation between social class and BMI varies globally. A review in 1989 found that in developed countries women of a high social class were less likely to be obese. No significant difference were seen among men of different social classes. In the developing world, women, men, and children from high social classes had greater rates of obesity.^[61] An update of this review was carried out in 2007 and found the same relationships but they were less strong. The decrease in strength of correlation were felt to be due to the effects of globilization.^[62]

Many explanations have been put forth for associations between BMI and social class. It is thought that in developed countries, the wealthy are able to afford more nutricious food, they are under greater social pressure to remain slim, and have more opportunities along with greater expectations for physical fitness. In the developing world the ability to afford food, high energy expenditure with physical labor, and cultural values favoring a larger body size are believed to contribute to the observed patterns.^[62] The acceptance of body mass by people in one's life may also play a role in obesity. A correlation in BMI changes over time has been found between friends, siblings, and spouses.^[63]

Smoking has a significant affect on weight. Those who quit smoking gain on average 4-5 kilograms over ten years. One sixth of the rise in obesity in North Americans can be attributed to falling rates of smoking, although the health benefits of quitting smoking are considered undeniable.^[64]

Neurobiological mechanisms

On the left a mouse unable to produce leptin resulting in obesity. On the right a normal mouse for comparison.

Flier summarizes the many possible pathophysiological mechanisms involved in the development and maintenance of obesity.^[65] 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, as well as 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, most obese individuals are thought to be leptin resistant and have been found to have high levels of leptin.^[66] 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.^[65]

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.^[65] 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.^[67]

The arcuate nucleus contains two distinct groups of neurons.^[65] 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.^[65]

Management

The main treatment for obesity consists of eating less and exercising more. Diet programs may produce weight loss over the short term,^[68] but keeping this weight off can be a problem. It often requires making exercise and a lower calorie diet a permanent part of a person's lifestyle.^[69][70] In the general population only 20% are successful at long-term weight loss maintenance.^[71] In a more structured setting, however, 67% of people who lost greater then 10% of their body mass maintained or continued to lose weight one year later.^[72] An average maintained weight loss of more then 3 kg or 3% of total body mass could be sustained for five years.^[73] There are significant benefits to weight loss. In a prospective study, intentional weight loss of any amount was associated with a 20% reduction in all-cause mortality.^[74]

Diet

Diets to promote weight loss are generally divided into four categories low-calorie, low-fat, low-carbohydrate, and very low calorie.^[68]

Low calorie diets usually produce an energy deficit of 500?1000 calories per day, which can result in a 0.5 kilogram weight loss per week. They include the DASH diet and Weight Watchers among others. The National Institutes of Health reviewed 34 randomized controlled trials to determine the effectiveness of low-calorie diets. They found that these diet lowered total body mass by 8% over 3-12 months.^[68]

Low fat diets involve the reduction of the percentage of fat in ones diet. Calorie consumption is reduced but not purposely so. Diets of this type include NCEP Step I and II. A meta-analysis of 16 trials of 2?12 months duration found that low-fat diets resulted in weight loss of 3.2 kg over eating as normal.^[68]

Low carbohydrate diets are relatively high in fat and protein. They are very popular in the press however are not recommenced by the American Heart Association. Diets of this type include Atkins and Protein Power. A review of 94 trials found that weight loss was associated with decreased calorie consumption rather than any special properties of reduced carbohydrate consumption. No adverse affect from low carbohydrate diets were detected.^[75]

A further meta-analysis of 6 randomized controlled trials found no difference between the main diet types (low calorie, low carbohydrate, and low fat), with a 2?4 kilogram weight loss in all studies.^[68]

Very low calorie diets maintain protein intake while limiting calories from both fat and carbohydrates. They subject the body to starvation and produce average weekly weight loss of 1.5?2.5 kilograms. These diets are not recommended for general use as they are associated with adverse side effect such as loss of lean muscle mass, increased risks of gout, and electrolyte imbalances. People attempting these diets must be monitored closely by a physician to prevent complications.^[68]

Exercise

With use, muscles consume energy derived from both fat and glycogen. Due to the large size of leg muscles walking, running, and cycling are the most effective means of exercise to reduce body fat.^[76][77]

A meta-analysis of 43 randomized controlled trials by the Cochrane Collaboration found that exercising alone led to limited weight loss. In combination with diet, however, it resulted in a 1 kilogram weight loss over dieting alone. A 1.5 kilogram loss was observed with a greater degree of exercise.^[78] Even though exercise as carried out in the general population has only modest effects a dose response curve is found and very intense exercise can lead to substantial weight loss. During 20 weeks of basic military training with no dietary restriction obese military recruit lost 12.5 kg.^[79]

Medication

There are two commonly prescribed medications for obesity. One is orlistat, which reduces intestinal fat absorption by inhibiting pancreatic lipase; the other is sibutramine, which is a specific inhibitor of norepinephrine, serotonin, and dopamine in the brain,therefore decreasing appetite. Rimonabant, a third drug, works via a specific blockade of the endocannabinoid system. It has been approved in Europe for the treatment of obesity but has not yet received approval in the United States due to concerns about its safety.^[80] Weight loss with these drugs is modest, and over the longer term average weight loss on orlistat is 2.9 kg, sibutramine is 4.2 kg and rimonabant is 4.7 kg. Orlistat and rimonabant lead to a reduced incidence of diabetes, and all drugs have some effect on cholesterol. There is little data on how these drugs affect the longer-term complications of obesity.^[81] It is common for weight loss drugs to be tried and if there is little or no benefit from them to discontinue treatment.^[4]

A meta-analysis of randomized controlled trials by the Cochrane Collaboration concluded that in diabetic patients fluoxetine, orlistat and sibutramine could achieve modest but significant weight loss over 12-57 weeks. The long-term health benefits remained unclear.^[82]

Obesity may also influence the choice of drugs used to treat diabetes. Metformin may lead to mild weight loss in comparison to sulfonylureas and insulin. It has been show to reduce the risk of cardiovascular disease in type 2 diabetics who are obese.^[83] The thiazolidinediones on the other hand may cause some weight gain, but decrease central obesity and therefore can be used in obese diabetics.^[84]

Ephedrine(Ma Huang) is a stimulant effective for weight loss however it is not recommended due to potential side effects.^[85]

Bariatric surgery

Bariatric surgery (or "weight loss surgery") is the use of surgical interventions in the treatment of obesity. As every operation may have complications, surgery is only recommended for those with more severe obesity ( BMI > 40 ) who has failed to loss weight with dietary modification and pharmacological treatment. 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.^[86]

Surgery for severe obesity is associated with long-term weight loss and decreased overall mortality. A controlled prospective study carried out in Sweden involving 4,047 people found a weight loss of between 14% and 25% at 10 years depending on the type of procedure performed and a 29% reduction in all cause mortality when compared to standard weight lose measures.^[87] A marked decrease in the risk of diabetes mellitus, cardiovascular disease and cancer has also been found after bariatric sugery.^[88][89] Weight loss is marked in the first few months after surgery and is sustained in the long term. In one study there was an unexplained increase in deaths from accidents and suicide but this did not outweigh the benefit in terms of disease prevention. When comparisons are made between the procedures gastric bypass surgery is found to be about twice as effective as banding procedures.^[89]

The effects of liposuction however are less well determined with some small studying showing no benefits^[90] and others showing benefits.^[91]

Clinical protocols

In a clinical practice guideline by the American College of Physicians, the following five recommendations are made:^[92]

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.^[93][94]

Epidemiology

Obesity rates as a percentages of total population in OECD member countries in the years 1996-2003.^[95]

Australia

Studies conducted in 2006 found that close to 52% of Australian women and up to 67% of Australian men aged 25 or over are overweight or obese.^[96]

Canada

The number of Canadians who are obese has risen dramatically in recent years. In 2004, direct measurements of height and weight found 23.1% of Canadians older then 18 had a BMI greater then 30. When broken down into degrees of obesity 15.2% were Class I (BMI 30?34.9), 5.1% were Class II (BMI 35?39.9), and 2.7%, Class III (BMI > 40). This is in contrast to self reported data the year previous of 15.2% and in 1978/1979 of 13.8%. The greatest increases occurred among the more severe degrees of obesity, Class III obesity increased from 0.9% to 2.7% from 1978/1979 to 2004. Obesity in Canada varies by ethnicity with people of Aboriginal origin having a significantly higher rate of obesity rate (37.6%) then the national average.^[53]

European Union

Between the 1970s and the 2000s, rates of obesity in most European countries has increased. During the 1990s/2000s the 27 countries making up the EU reported rates of obesity from 10% to 27% in men and from 10% to 38% in women.^[97]

India

In India urbanization and modernizations has been associated with obesity. As of 1999 in northern Indian 11% of urban women were found to be obese in contrast to 3.7% of rural women. Well women of high socioeconmic class had a rate of obesity of 10.4% as oppose to a rate of 0.9% in women of low socioeconomic class.^[98] With people moving into urban centers and wealth increasing, concerns about an obesity epidemic in India are growing.

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%.^[99]

Mexico

Mexico has the second highest rate of obesity in the developed world at 24.2% of the population.^[95]

South Pacific

Many of the island nations of the South Pacific have very high rates of obesity. Nauru has the highest rates of obesity in the world (80%) followed by Tonga, the Federated States of Micronesia, and the Cook Islands. Being big has traditionally been associated with health, beauty, and status and many of these beliefs remain prevalent today.^[100]

United Kingdom

In the UK the rate of obesity has increased about fourfold over the last 25 years reaching current levels of 22%.^[16] 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.^[101][102]

United States

Percentage of the US population classified as obese according to the CDC, as of April 17, 2007.

The United States has the highest rates of obesity in the developed world.^[95] From 1980 to 2002, obesity rates have doubled reaching the current rate of 32% of the adults population.^[103] Rate of obesity vary by ethnicity and gender. In the USA 28% of men and 34% of women are obese with rates rising to as high as 50% among African American women.^[104] The prevalence of class 3 obesity (BMI ?40) has increased the most dramatically from 0.78 percent in 1990 to 2.2 percent in 2000.^[105]

Public health

Obesity is a public health and policy problem because of its prevalence, costs, and health effects.^[106] Public health efforts seek to understand and correct the environmental factors responsible for the increasing prevalence of obesity in the population. Solutions look at changing the factors that cause excess calorie consumption and inhibit physical activity. Efforts include federally-reimbursed meal programs in schools, limiting direct junk food marketing to children,^[107] and decreasing school time access to sweetened beverages.^[108] When constructing urban environments effort have been made to increase access to parks and develop pedestrian routes.^[109]

Many countries and groups have published reports pertaining to obesity. In 1998 the first US Federal guidelines were published the "Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults: The Evidence Report".^[2] In 2006 the Canadian Obesity Network published the "Canadian Clinical Practice Guidelines (CPG) on the Management and Prevention of Obesity in Adults and Children". This is a comprehensive evidence-based guideline to address the management and prevention of overweight and obesity in adults and children.^[110]

In 2004, the United Kingdom Royal College of Physicians, the Faculty of Public Health and the Royal College of Paediatrics and Child Health released the report "Storing up Problems", which highlighted the growing problem of obesity in the UK.^[111] The same year, the House of Commons Health Select Committee published its "most comprehensive inquiry [...] ever undertaken" into the impact of obesity on health and society in the UK and possible approaches to the problem.^[112] 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.^[4] 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.^[113]

Non-medical effects

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

Obesity and its health effects create sizable societal economic costs, with medical costs attributable to obesity rising to US$78.5 billion, or 9.1% of all medical expenditures in the U.S. as of 1998.^[114][115] One recent study, however, found that while obesity prevention programs reduce the cost of treating diseases related to obesity, those reductions are offset by medical costs during the additional years of life gained. The authors conclude that reducing obesity may improve public health, but is unlikely to reduce overall health spending.^[116]

Worker costs rise and productivity is impaired, as measured by usage of disability leave and absenteeism at work.^[117] 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.^[118]

Due to obesity airlines face higher fuel costs, as well as pressure to increase seating width. In 2000, the extra weight of obese passengers cost airlines and consumers US$275 million.^[119] Costs are also increased by litigation by obese persons suing restaurants (for causing obesity)^[120] and airlines (over airline seating width).^[121] In 2005 the US Congress discussed legislation to prevent civil law suit being brought against the food industry in relation to obesity. It however did not become law.^[120]

The US state of Alabama Employees' Insurance Board approved a controversial plan to charge obese workers $25 per month if they do not take measures to reduce their weight and improve their health. These measured are set to start Jan. 2010 and apply to those with a BMI of greater then 35 kg/m^2 who fail to make improvements in their health after one year.^[122]

Obese employees are paid less then their non obese counterparts for the equivalent job. Obese women on average make 6% less well obese men make 3% less.^[16]

History and culture

Etymology

Obesity is the nominal form of obese which comes from the Latin ob?sus, which means "stout, fat, or plump." ?sus 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 Matćotechnia Medicinć Praxeos.^[123]

Historical trends

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Obesity was a status symbol in renaissance culture: "The Tuscan General" Alessandro del Borro, 1645.^[124]

Many cultures through out history have viewed obesity as a flaw. The obesus or fat character in Greek comedy was a glutton and figure of mockery. During Christian times food was viewed as a gateway to the sins of sloth and lust.^[126] In Western culture, excess weight is often regarded as unattractive, and obesity is commonly associated with various negative stereotypes. All ages can face social stigmatization and may be targeted by bullies or shunned by their peers. In Western culture obesity is once again seen as a sign off a low socio-economic status.^[127] Obese people are less likely to be hired for a job, make less money when they are hired, and are less likely to be promoted.^[28]

The weight that is viewed by many as an ideal has become less over the last 75 years. The average heights of Miss America pageant winners increased by 2 % from 1922 to 1999 well at the same time her weight decreased by 12%.^[28]

Weight loss drugs

The first described attempts at producing weight loss are those of Soranus of Ephesus, a Greek physician, in the second century AD. He prescribed elixirs of laxatives and purgatives, as well as heat, massage, and exercise. This remained the mainstay of treatment for well over a thousand years. It was not until the 1920s and 1930s that new treatments began to appear. Based on its effectiveness for hypothyroidism, thyroid hormone became a popular treatment for obesity in otherwise healthy people. It had a modest effect but produced the symptoms of hyperthyroidism as a side effect, such as palpitations and difficulty sleeping. Dinitrophenol (DNP) was introduced in 1933; this worked by uncoupling the biological process of oxidative phosphorylation in mitochondria, causing them to produce heat instead of ATP. The most significant side-effect was a dramatic rise in body temperature, frequently causing death. By the end of the 1930s DNP had fallen out of use.^[41]

Amphetamines (marketed as Benzedrine) became popular for weight loss during the late 1930s. They worked primarily by suppressing appetite and had other beneficial effects such as increased alertness. Use of amphetamines increased over the subsequent decades, culminating in the "rainbow pill" regime. This was a combination of multiple pills, all thought to help with weight loss, taken throughout the day. Typical regimens included stimulants, such as amphetamines and thyroid hormone, diuretics, digitalis, laxatives, and often a barbiturate suppress the side effects of the stimulants. In 1967/1968 a number of deaths attributed to diet pills triggered a Senate investigation and the gradual implementation of greater restrictions on the market. This culminating in 1979 with the FDA banning the use of amphetamines, then the most effective of the diet drugs, in diet pills.^[41]

Meanwhile, phentermine had been FDA approved in 1959 and fenfluramine in 1973. The two were no more popular then other drugs until in 1992 a researcher reported that the two caused a 10% weight loss which was maintained for over two years.^[128] Fen-phen was born and rapidly became the most commonly prescribed diet medication. Dexfenfluramine (Redux) was developed in the mid-1990s as an alternative to fenfluramine with less side-effects, and received regulatory approval in 1996. However, this coincided with mounting evidence that the combination could cause valvular heart disease in up to 30% of those who had taken it, leading to withdrawal of Fen-phen and dexfenfluramine from the market in September 1997.^[41]

Ephedra was removed from the US market in 2004 over concerns that it raises blood pressure and could lead to strokes and death.^[28]

The arts

Venus of Willendorf created 24,000?22,000 BC

Fat acceptance movement

A small vocal fat acceptance movement is attempting to challenge the established relationship between obesity, diet and exercise, and the negative health outcomes that result. The National Association to Advance Fat Acceptance (NAAFA) was formed in 1969 and describes itself as a civil rights organization dedicated to ending size discrimination.^[129] Multiple books such as The Diet Myth by Paul Campos argue that the health risks of obesity are a conspiracy and the real problem is social stigma facing the obese.^[130] Similarly, The Obesity Epidemic by Michael Gard argues that obesity is a moral and ideological construct.^[131] Some people are attracted to the obese. Chubby culture^[132] and fat admirers^[133] have become recognized subcultures during the last few decades.

See also

References

Further reading

External links

• World Health Organization - Obesity pages
• Diet, Nutrition and the prevention of chronic diseases (including obesity) by a Joint WHO/FAO Expert consultation (2003).
• Obesity at Endotext.org
• International Task Force on Obesity
• The Obesity Society (USA)
• National Obesity Forum (UK)
• Australasian Society for the Study of Obesity

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