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Obesity

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Obesity
SpecialtyEndocrinology Edit this on Wikidata

Obesity is a medical condition in which excess body fat has accumulated to the extent that it may have an adverse affect on health, leading to reduced life expectancy.[1][2] Body mass index (BMI), which compares weight and height, is used to define a person as overweight (pre-obese) when their BMI is between 25 kg/m2 and 30 kg/m2 and obese when it is greater than 30 kg/m2.[3]

Obesity is associated with many diseases, particularly heart disease, type 2 diabetes, breathing difficulties during sleep, certain types of cancer, and osteoarthritis.[2] Obesity is most commonly caused by a combination of excessive dietary calories, lack of physical activity, and genetic susceptibility, though a limited number of cases are due solely to genetics, medical reasons, or psychiatric illness.

The primary treatment for obesity is dieting and physical exercise. If this fails, anti-obesity drugs may be taken to reduce appetite or inhibit fat absorption. In severe cases, surgery is performed to reduce stomach volume and bowel length, leading to earlier satiation and reduced ability to absorb nutrients from food.[4]

Obesity is a leading preventable cause of death worldwide, with increasing prevalence in adults and children, and authorities view it as one of the most serious public health problems of the 21st century.[5] Obesity is stigmatized in the modern Western world, though it has been perceived as a symbol of wealth and fertility at other times in history, and still is in many parts of Africa.[2][6]

Classification

An obese male with a body mass index of 46 kg/m2: weight 146 kg (322 lb), height 177 cm (5 ft 10 in)

Obesity is a medical condition in which excess body fat has accumulated to the extent that it may have an adverse affect on health.[7] It is defined by body mass index (BMI) and further evaluated in terms of its distribution via the waist–hip ratio and total cardiovascular risk factors.[8][9] BMI is highly related to both percentage body fat and total body fat.[10]

BMI

Body mass index or BMI is a simple and widely used method for estimating body fat mass.[11] BMI was developed in the 19th century by the Belgian statistician and anthropometrist Adolphe Quetelet.[12] BMI is an accurate reflection of body fat percentage in the majority of the adult population. It however is less accurate in people such as body builders and pregnant women.[13]

BMI Classification
< 18.5 underweight
18.5–24.9 normal weight
25.0–29.9 overweight
30.0–34.9 class I obesity
35.0–39.9 class II obesity
> 40.0   class III obesity  

BMI is calculated by dividing the subject's mass by the square of his or her height, typically expressed either in metric or US "Customary" units:

Metric:
US/Customary and imperial:

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

The most commonly used definitions, established by the World Health Organization (WHO) in 1997 and published in 2000, provide the values listed in the table at right.[14]

Some modifications to the WHO definitions have been made by particular bodies. The surgical literature breaks down "class III" obesity into further categories.[15]

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

As Asian populations develop negative health consequences at a lower BMI than Caucasians, some nations have redefined obesity. The Japanese have defined obesity as any BMI greater than 25[16] while China uses a BMI of greater than 28.[17]

Waist circumference and waist–hip ratio

The waist circumference (>102 cm in men and >88 cm in women) and the waist–hip ratio (the circumference of the waist divided by that of the hips of >0.9 for men and >0.85 for women) are both used as measures of central obesity.[18]

In those with a BMI under 35, intra-abdominal body fat is related to negative health outcomes independent of total body fat.[19] Intra-abdominal or visceral fat has a particularly strong correlation with cardiovascular disease.[18] In a study of 15,000 people, waist circumference also correlated better with metabolic syndrome than BMI.[20] Women with abdominal obesity have a cardiovascular risk similar to that of men.[21] 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.[22]

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 (1.4 inches) of subcutaneous fat.

Body fat percentage is total body fat expressed as a percentage of total body weight. It is generally agreed that men with more than 25% body fat and women with more than 33% body fat are obese.[23] Body fat percentage can be estimated from a person's BMI by the following formula:

where gender is 0 if female and 1 if male

This formula takes into account the fact that body fat percentage is 10 percentage points greater in women than in men for a given BMI. It recognizes that a person's percentage body fat increases as they age even if their weight remains constant. The results of this formula have an accuracy of 4%.[24]

There are many other methods used to determine body fat percentage. Hydrostatic weighing, one of the most accurate methods of body fat calculation, involves weighting a person underwater. Two other simpler and less accurate methods have been used historically but are now not recommended.[25] The first is the skinfold test, in which a pinch of skin is precisely measured to determine the thickness of the subcutaneous fat layer.[26] The other is bioelectrical impedance analysis which uses electrical resistance. Bioelectrical impedance has not been shown to provide an advantage over BMI.[27]

Body fat percentage measurement techniques used mainly for research include computed tomography (CT scan), magnetic resonance imaging (MRI), and dual energy X-ray absorptiometry (DEXA).[19] These techniques provide very accurate measurements, but it can be difficult to obtain in the severely obese due to weight limits of most equipment and insufficient diameter of many CT or MRI scanners.[28]

Childhood obesity

An overweight child

The healthy BMI range varies with the age and sex of the child. Obesity in children and adolescents is defined as a BMI greater than the 95th percentile or to put it another way the 5% with the greatest BMI.[29] The reference data that these percentiles are based on is from 1963 to 1994 and thus has not been affected by the recent increases in rates of obesity.[30]

Childhood obesity has reached epidemic proportions in 21st century with rising rates in both the developed and developing world. Rates of obesity in Canadian boys have increased from 11% in 1980s to over 30% in 1990s, while during this same time period rates increased from 4 to 14% in Brazilian children.[31]

As with obesity in adults many different factors contribute to the rising rates of childhood obesity. Changing diet and decreasing physical activity are believed to be the two most important in causing the recent increase in the rate of obesity. Activities from self propelled transport, to school physical education, and organized sports has been declining in many countries.[32] Treatments used in children are primarily lifestyle interventions and behavioral techniques. Medications are not FDA approved for use in this age group.[31]

Effects on health

Excessive body weight is associated with various diseases, particularly cardiovascular diseases, diabetes mellitus type 2, obstructive sleep apnea, certain types of cancer, and osteoarthritis.[2] As a result, obesity has been found to reduce life expectancy.[2]

Mortality

Obesity is one of the leading preventable causes of death worldwide.[5][33][34] Large scale American and European studies have found that mortality risk varies with BMI; the lowest risk is found at a BMI of 22.5–25 kg/m2[35] in non smokers and at a BMI of 24–27 kg/m2 in current smokers and increases with changes in either direction.[36][37] Obesity increases the risk of death in current and former smokers as well as in those who have never smoked.[37] A BMI of over 32 has been associated with a doubled mortality rate among women over a 16-year period[38] and obesity is estimated to cause an excess 111,909 to 365,000 death per year in the United States.[34][2] Obesity on average reduces life expectancy by six to seven years.[39][2] A BMI of 30–35 reduces life expectancy by two to four years[35] while severe obesity (BMI > 40) reduces life expectancy by 20 years for men and five years for women.[23]

Morbidity

Obesity increases the risk of many physical and mental conditions. These comorbidities are reflected predominantly in metabolic syndrome.[2] Metabolic syndrome being a combination of medical disorders, which includes diabetes mellitus type 2, high blood pressure, high blood cholesterol, and high triglyceride levels.[40]

Complications are either directly caused by obesity or indirectly related through mechanisms sharing a common cause such as a poor diet or a sedentary lifestyle. The strength of the link between obesity and specific conditions varies. One of the strongest is the link with type 2 diabetes. Excess body fat underlies 64% of cases of diabetes in men and 77% of cases in women.[41]

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).[2][42] Increases in body fat alter the body's response to insulin, potentially leading to insulin resistance. Increased fat also creates a proinflammatory state, increasing the risk of thrombosis.[42]

Medical field Condition Medical field Condition
Cardiology Dermatology
Endocrinology and Reproductive medicine Gastrointestinal
Neurology Oncology[53]
Psychiatry Respirology
Rheumatology and Orthopedics Urology and Nephrology

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, a phenomenon known as the obesity survival paradox.[63] The paradox was first described in 1999 in overweight and obese people undergoing hemodialysis,[63] and has subsequently been found in those with heart failure, and peripheral artery disease (PAD).[64]

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.[65] Similar findings have been made 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.[66][67] Even after cardiac bypass surgery, no increase in mortality is seen in the overweight and obese.[68] One study found that the improved survival could be explained by the more aggressive treatment obese people receive after a cardiac event.[69] Another found that if one takes into account chronic obstructive pulmonary disease (COPD) in those with PAD the benefit of obesity no longer exsists.[64]

Causes

At an individual level, a combination of excessive caloric intake, lack of physical activity, and genetic susceptibility is thought to explain most cases of obesity, with a limited number of cases due solely to genetics, medical reasons, or psychiatric illness.[70] In contrast at a societal level increasing rates of obesity are felt to be due to an easily accessible and palatable diet,[71] increased reliance on cars, and mechanized manufacturing.[72][73]

A 2006 review identified ten other possible contributors to the recent increase of obesity: (1) insufficient sleep, (2) endocrine disruptors (environmental pollutants that interfere with lipid metabolism), (3) decreased variability in ambient temperature, (4) decreased rates of smoking, because smoking suppresses appetite, (5) increased use of medications that can cause weight gain (e.g., atypical antipsychotics), (6) proportional increases in ethnic and age groups that tend to be heavier, (7) pregnancy at a later age (which may cause susceptibility to obesity in children), (8) epigenetic risk factors passed on generationally, (9) natural selection for higher BMI, and (10) assortative mating leading to increased concentration of obesity risk factors (this would not necessarily increase the number of obese people, but would increase the average population weight).[74] There is substantial but not conclusive evidence for these mechanisms, and the authors specify that they are probably less influential than the ones discussed in the previous paragraph (but still important).

Diet

Map of dietary energy availability per person per day in 1979-1981 (kcal/person/day)[75]
  no data
  <1600
  1600–1800
  1800–2000
  2000–2200
  2200–2400
  2400–2600
  2600–2800
  2800–3000
  3000–3200
  3200–3400
  3400–3600
  >3600
Map of dietary energy availability per person per day in 2001–2003 (kcal/person/day)[75]
  no data
  <1600
  1600–1800
  1800–2000
  2000–2200
  2200–2400
  2400–2600
  2600–2800
  2800–3000
  3000–3200
  3200–3400
  3400–3600
  >3600

The per capita dietary energy supply varies markedly between different regions and countries. It has also changed significantly over time.[76] From the early 1970s to the late 1990s the average calories available per person per day (the amount of food bought) has increased in all part of the world except Eastern Europe. The United States had the highest availability with 3,654 calories per person in 1996.[77] This increased further in 2002 to 3,770.[78] During the late 1990s Europeans had 3394 calories per person, in the developing areas of Asia there were 2,648 calories per person, and in sub-Sahara Africa people had 2,176 calories per person.[77][79]

United States Department of Agriculture chart showing the increase in soda consumption and the decrease in milk consumption from 1947 to 2001[80]

The widespread availability of nutritional guidelines[81] have done little to address the problems of overeating and poor dietary choices.[82] In the period of 1971–2000, obesity rates in the United States increased from 14.5% to 30.9%.[83] During the same time period, an increase occurred in the average amount of calories consumed. For women, the average increase was 335 calories per day (1,542 calories in 1971 and 1,877 calories in 2004), while for men the average increase was 168 calories per day (2,450 calories in 1971 and 2,618 calories in 2004). Most of these extra calories came from an increase in carbohydrate consumption rather than an increase in fat consumption.[84] The primary sources of these extra carbohydrates are sweetened beverages, which now accounts for almost 25 percent of daily calories in young adults in America.[85] Consumption of sweetened drinks is believed to be contributing to the rising rates of obesity.[86][87]

A comparison of a cheeseburger 20 years ago (left) which had 333 calories with a modern cheeseburger (right) contains 590 calories

As societies become increasingly reliant on energy-dense, large portion, fast-food meals, the association between fast food consumption and obesity becomes more concerning.[88] In the United States consumption of fast food meal has tripled and calorie intake from fast food has quadrupled between 1977 and 1995.[89]

Agricultural policy and techniques in the United States and Europe have led to lower food prices. In the United States, subsidization of corn, soy, wheat, and rice through the U.S. farm bill has made the main sources of processed food cheap compared to fruits and vegetables.[90]

There is little evidence to support the commonly expressed view that some obese people eat little yet gain weight due to a slow metabolism. On average obese people have a greater energy expenditure than thin people.[91] This is because it takes more energy to maintain an increased body mass.[55] Obese people also under report how much food they consume compared to those of normal weight.[92] Tests of people carried out in a calorimeter support this conclusion.[93]

Sedentary lifestyle

A sedentary lifestyle plays a significant role in obesity.[94] Worldwide there has been a large shift towards less physically demanding work,[95][96][97] and currently at least 60% of the world's population does not get sufficient exercise.[96] This is primarily due to increasing use of mechanized transportation and a greater prevalence of labor saving technology in the home.[95][96][97] World trends in active leisure time physical activity are controversial. The World Health Organization indicates that worldwide people are taking up less active recreational pursuits however a study from Finland[98] found an increase and a study from the United States found leisure-time physical activity has not changed significantly.[99]

Studies in children and adults have found an association between the number of hours of television watched and the prevalence of obesity.[100][101][102] A 2008 meta analysis found that 63 of 73 studies (86%) showed an increased rate of childhood obesity with increased media exposure, and rates increasing proportionally to time spent watching television.[103]

Genetics

A 1680 painting by Juan Carreno de Miranda of a girl presumed to have Prader-Willi syndrome[104]

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 predispose to obesity when sufficient calories are present. As of 2006 more than 41 of these sites have been linked to the development of obesity when a favorable environment is present.[105]

Some of these include the FTO gene polymorphism and the NPC1 gene.[106] Adults who were homozygous for a particular FTO allele weighed about 3 kilograms more and had a 1.6-fold greater rate of obesity than those who had not inherited this trait.[107] This association disappeared, though, when those with FTO polymorphisms participated in moderately intensive physical activity equivalent to three to four hours of brisk walking.[108] Another study found that 80% of the offspring of two obese parents were obese, in contrast to less than 10% of the offspring of two parents who were of normal weight.[109]

The percentage of obesity that can be attributed to genetics varies from 6% to 85% depending on the population examined.[110] The thrifty gene hypothesis postulates that certain ethnic groups may be more prone to obesity in an equivalent environment. Their ability to take advantage of rare periods of abundance by storing energy as fat would be advantageous during times of varying food availability, and 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.[111] This is the presumed reason that Pima Indians, who evolved in a desert ecosystem, developed some of the highest rates of obesity when exposed to a Western lifestyle.[112]

Obesity is also 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 people with early-onset severe obesity (defined by an onset before 10 years of age and body mass index over three standard deviations above normal), 7% harbor a single locus mutation.[113]

Medical and psychiatric illness

Certain physical and mental illnesses and the pharmaceutical substances used to treat them can increase risk of obesity. Medical illnesses that increase obesity risk include several rare genetic syndromes (listed above) as well as some congenital or acquired conditions: hypothyroidism, Cushing's syndrome, growth hormone deficiency,[114] and the eating disorders: binge eating disorder and night eating syndrome.[2] However, obesity is not regarded as a psychiatric disorder, and therefore is not listed in the DSM-IVR as a psychiatric illness.[115]

Certain medications may cause weight gain or changes in body composition; these include insulin, sulfonylureas, thiazolidinediones, atypical antipsychotics, antidepressants, steroids, certain anticonvulsants (phenytoin and valproate), pizotifen, and some forms of hormonal contraception.[2]

Socioeconomic

While genetic influences are important to understanding obesity, they cannot explain the current dramatic increase seen within specific countries or globally.[116] 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 differences 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.[117] An update of this review carried out in 2007 found the same relationships, but they were weaker. The decrease in strength of correlation was felt to be due to the effects of globalization.[118]

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 nutritious food, they are under greater social pressure to remain slim, and have more opportunities along with greater expectations for physical fitness. In undeveloped countries 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.[118] Attitudes toward body mass held 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.[119]

Smoking has a significant effect on an individual's weight. Those who quit smoking gain an average of 4.4 kilograms (9.7 lb) for men and 5.0 kilograms (11.0 lb) for women over ten years.[120] Changing rates of smoking however have had little effect on the overall rates of obesity.[121]

In the United States the number of children a person has is related to their risk of obesity. A woman's risk increases by 7% per child, while a man's risk increases by 4% per child.[122] This could be partly explained by the fact that having dependent children decreases physical activity in Western parents.[123]

In the developing world urbanization is playing a role in increasing rate of obesity. In China overall rates of obesity are below 5% however in some cities rates of obesity are greater than 20%.[124]

Early malnutrition

Malnutrition in early life is believed to play a role in the rising rates of obesity in the developing world.[125] Endocrine changes that occur during periods of malnutrition may promote the storage of fat once more calories become available.[125]

Infectious agents

The study of the effect of infectious agents on metabolism is still in its early stages. Gut flora has been shown to differ between lean and obese humans. There is an indication that gut flora in obese and lean individuals can affect the metabolic potential. This apparent alteration of the metabolic potential is believed to confer a greater capacity to harvest energy contributing to obesity. Whether these differences are the direct cause or the result of obesity has yet to be determined unequivocally.[126]

An association between viruses and obesity has been found in humans as well as number of different animal species. The amount that these association may have contributed to the rising rate of obesity is yet to be determined.[127]

Pathophysiology

A comparison of a mouse unable to produce leptin thus resulting in obesity (left) and a normal mouse (right)

Flier summarizes the many possible pathophysiological mechanisms involved in the development and maintenance of obesity.[128] 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, insulin, 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.[129] 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 people.[128]

A graphic depiction of a leptin molecule

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.[128] 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.[130]

The arcuate nucleus contains two distinct groups of neurons.[128] 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.[128]

Management

The main treatment for obesity consists of dieting and physical exercise. Diet programs may produce weight loss over the short term,[131] but keeping this weight off can be a problem and often requires making exercise and a lower calorie diet a permanent part of a person's lifestyle.[132][133] Success rates of long-term weight loss maintenance are low and range from 2–20%.[134] In a more structured setting, however, 67% of people who lost greater than 10% of their body mass maintained or continued to lose weight one year later.[135] An average maintained weight loss of more than 3 kg (6.6 lb) or 3% of total body mass could be sustained for five years.[136] 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.[137]

The most effective, but also most risky treatment for obesity is bariatric surgery. Due to its cost and risk of complications, researchers are fervently searching for new obesity treatments.

Dieting

Diets to promote weight loss are generally divided into four categories: low-fat, low-carbohydrate, low-calorie, and very low calorie.[131] A meta-analysis of six randomized controlled trials found no difference between the main diet types (low calorie, low carbohydrate, and low fat), with a 2–4 kilogram (4.4–8.8 lb) weight loss in all studies.[131] At two years, all diet methods resulted in similar weight loss irrespective of the macronutrients emphasized.[138]

Low-fat diets

Low-fat diets involve the reduction of the percentage of fat in one's 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 (7.1 lb) over eating as normal.[131]

Low-carbohydrate diets

Low carbohydrate diets such as Atkins and Protein Power are relatively high in fat and protein. They are very popular in the press but are not recommended by the American Heart Association. A review of 107 studies did not find that low-carbohydrate diets cause weigh loss, except when calorie intake was restricted.[139] No adverse effects from low carbohydrate diets were detected.[140]

Low-calorie diets

Low-calorie diets usually produce an energy deficit of 500–1,000 calories per day, which can result in a 0.5 kilogram (1.1 lb) 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 diets lowered total body mass by 8% over 3–12 months.[131]

Very low-calorie diets

Very low calorie diets provide 200–800 kcal/day, maintaining protein intake but limiting calories from both fat and carbohydrates. They subject the body to starvation and produce an average weekly weight loss of 1.5–2.5 kilograms (3.3–5.5 lb). These diets are not recommended for general use as they are associated with adverse side effects 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.[131]

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.[141] Exercise affects macronutrient balance. During moderate exercise, there is a shift to greater use of fat as a fuel.[142]

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 (3.3 lb) loss was observed with a greater degree of exercise.[143] 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 recruits lost 12.5 kg (27.6 lb).[144] High levels of physical activity seem to be necessary to maintain weight loss.[145]

A systematic review found that people who use pedometers, during on average an 18-week period, increased their physical activity by 27% and subsequently decreased their BMI by 0.38.[146]

The city of Bogota, Colombia blocks off 113 kilometers (70 miles) of roads every Sunday and on holidays to make it easier for it citizens to get exercise. These pedestrian zones are part of an effort to combat chronic diseases, including obesity.[147]

Medication

Medication used to treat obesity: orlistat (Xenical) and sibutramine (Meridia)

Only two anti-obesity medications are currently approved by the FDA for long term use.[148] One is orlistat (Xenical), which reduces intestinal fat absorption by inhibiting pancreatic lipase; the other is sibutramine (Meridia), which acts in the brain to inhibit deactivation of the neurotransmitters norepinephrine, serotonin, and dopamine (very similar to some anti-depressants), therefore decreasing appetite. Rimonabant (Acomplia), a third drug, works via a specific blockade of the endocannabinoid system. It has been developed from the knowledge that cannabis smokers often experience hunger, which is often referred to as "the munchies". It has been approved in Europe for the treatment of obesity but has not yet received approval in the United States or Canada due to safety concerns.[149][150]

Weight loss with these drugs is modest; over the longer term, average weight loss on orlistat is 2.9 kg (6.4 lb), sibutramine is 4.2 kg (9.3 lb) and rimonabant is 4.7 kg (10.4 lb). Orlistat and rimonabant lead to a reduced incidence of diabetes, and all three drugs have some effect on cholesterol. There is however little data on how these drugs affect the longer-term complications or outcomes of obesity.[151]

There are a number of less commonly used medication. Some are approved for only short term use, others are used off label, and still others are used illegally. Most are appetite suppressants that act on either one or more neurotransmitters.[152] Phendimetrazine (Bontril), diethylpropion (Tenuate), and phentermine (Adipex-P) are approved by the FDA for short term use while bupropion (Wellbutrin), topiramate (Topamax), and zonisamide (Zonegran) are sometimes used off label.[148]

Certain drugs are useful depending on the comorbities present. Metformin (Glucophage) is preferred in overweight diabetics as it may lead to mild weight loss in comparison to sulfonylureas or insulin.[153] The thiazolidinediones, on the other hand, may cause weight gain, but decrease central obesity.[154] Diabetics also achieve modest weight loss with fluoxetine (Prozac), orlistat and sibutramine over 12–57 weeks. The long-term health benefits of theses treatments however remains unclear.[155]

Fenfluramine and dexfenfluramine were withdrawn from the market in 1997,[148] while ephedrine (Ma Huang) was removed from the market in 2004.[156] Dexamphetamines are not approve by the FDA for the treatment of obesity[157] due to concerns regarding addiction.[148] These drug are all not recommended due to potential side effects.[158] People however do occasionally use these drug illegally.[159]

Surgery

Bariatric surgery ("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 severely obese people (BMI > 40) who have failed to lose 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) and 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.[160]

Surgery for severe obesity is associated with long-term weight loss and decreased overall mortality. One study 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 loss measures.[161] A marked decrease in the risk of diabetes mellitus, cardiovascular disease and cancer has also been found after bariatric surgery.[162][163] 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.[163] When the two main techniques are compared gastric bypass procedures are found to lead to 30% more weight loss than banding procedures one year after surgery.[164]

The effects of liposuction on obesity are less well determined. Some small studies show benefits[165] while others show none.[166]

Clinical protocols

In a clinical practice guideline by the American College of Physicians, the following five recommendations are made:[167]

  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 person 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 (Adderall) may be used on a selective basis. Evidence is not sufficient to recommend sertraline, topiramate, or zonisamide.
  4. In people with a BMI over 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 person 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 people 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.[168][169]

Weight loss programs

Weight loss programs often promote lifestyle changes and diet modification. This may involves eating smaller meals, by cutting down on certain types of food, and making a conscious effort to exercise more. These program enables people to connect with a group of others that are attempting to loss weight in the hopes that they will encourage and help each other out.[170]

A number of different program exist including Weight Watchers, Overeaters Anonymous, and Jenny Craig. They appear to provide modest weight loss (2.9 kg, 6.4 lb) over dieting on ones own (0.2 kg, 0.4 lb) over a two year period.[171] Internet based programs appear to be ineffective.[172]

Epidemiology

World obesity prevalence among males[173]
  <5%
  5–10%
  10–15%
  15–20%
  20–25%
  25–30%
  30–35%
  35–40%
  40–45%
  45–50%
  50–55%
  >55%
World obesity prevalence among females[173]
  <5%
  5–10%
  10–15%
  15–20%
  20–25%
  25–30%
  30–35%
  35–40%
  40–45%
  45–50%
  50–55%
  >55%

For thousands of years obesity was rarely seen.[174] It was not until the 20th century that it became common, so much so that in 1997 the WHO formally recognized obesity as a global epidemic.[85] As of 2005 the WHO estimates that at least 400 million adults (9.8%) are obese, with higher rates among women than men.[175] The rate of obesity also increases with age at least up to 50 or 60 years old.[176] Once considered a problem only of high-income countries, obesity rates are rising worldwide. These increases have been felt most dramatically in urban settings.[175] The only remaining region of the world where obesity is not common is sub-Saharan Africa.[2]

Public health

The World Health Organization (WHO ) predicts that overweight and obesity may soon replace more traditional public health concerns such as undernutrition and infectious diseases as the most significant cause of poor health.[177] Obesity is a public health and policy problem because of its prevalence, costs, and health effects.[178] 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,[179] and decreasing access to sweetened beverages in schools.[180] When constructing urban environments, efforts have been made to increase access to parks and to develop pedestrian routes.[181]

Many countries and groups have published reports pertaining to obesity. In 1998 the first US Federal guidelines were published, titled "Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults: The Evidence Report".[182] 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.[183] 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.[184] 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.[185] 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.[186] 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.[187]

Comprehensive approaches are being looked at to address the rising rates of obesity. The Obesity Policy Action (OPA) framework divides measure into 'upstream' policies, 'midstream' policies, 'downstream' policies. 'Upstream' policies look at changing society, 'midstream' policies try to alter individuals behavior to prevent obesity, and 'downstream' policies try to treat currently afflicted people.[188]

Economic impact

In addition to its health impacts, obesity leads to many problems including disadvantages in employment[189] and increased business costs. These effects are felt by all levels of society from individuals, to corporations, to governments.

The estimate range for annual expenditures on diet products is $40 billion to $100 billion in the US alone.[190] Well in 1998, the medical costs attributable to obesity in the US were $78.5 billion USD, or 9.1% of all medical expenditures.[191][192]

Obesity prevention programs have been found to reduce the cost of treating obesity-related disease. However, the longer people live the more medical costs they incur. Researchers therefore conclude that reducing obesity may improve the public's health, but it is unlikely to reduce overall health spending.[193]

Obese people can require special equipment, including wide chairs.[194]

Obesity can lead to social stigmatization and disadvantages in employment.[195] Obese workers, on average when compared to their normal weight counterparts, have higher rates absenteeism from work and take more disability leave, thus increasing costs for employers and decreasing productivity.[196] A study examining Duke University employees found that people with a BMI over 40 filed twice as many workers' compensation claims as those whose BMI was 18.5–24.9. They also had more than 12 times as many lost work days. The most common injuries in this group were due to falls and lifting, thus affecting the lower extremities, wrists or hands, and backs.[197] 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 measures are set to start January 2010 and apply to those with a BMI of greater than 35 kg/m2 who fail to make improvements in their health after one year.[198]

Some research shows that obese people are less likely to be hired for a job and are less likely to be promoted.[199] Obese people are also paid less than their non-obese counterparts for an equivalent job. Obese women on average make 6% less and obese men make 3% less.[200]

Specific industries, such as the airline and food industries, have special concerns. Due to rising rates of obesity, airlines face higher fuel costs and pressures to increase seating width.[201] In 2000, the extra weight of obese passengers cost airlines US$275 million.[202] Costs for restaurants are increased by litigation accusing them of causing obesity.[203] In 2005 the US Congress discussed legislation to prevent civil law suits against the food industry in relation to obesity; however it did not become law.[203]

History and culture

Venus of Willendorf created 24,000–22,000 BC
During the renaissance the wealthy often were obese: The Tuscan General Alessandro del Borro, attributed to Charles Mellin, 1645[204]

Etymology

Obesity is from the Latin obesitas, which means "stout, fat, or plump." Ēsus is the past participle of edere (to eat), with ob (over) added to it.[205] The Oxford English Dictionary documents its first usage in 1611 by Randle Cotgrave in A Dictionarie of the French and English Tongues.[206]

The Greeks were the first to recognize obesity as a medical disorder.[174] Hippocrates states that "Corpulence is not only a disease itself, but the harbinger of others".[2] It was known to the Indian surgeon Sushruta (6th century BCE), who related obesity to diabetes and heart disorder.[207] He recommended physical work to help cure it and its side effects.[207] For most of human history mankind struggled with food scarcity. With the onset of the industrial revolution it was realized that the military and economic might of nations were dependent on both the body size and strength of their soldiers and workers. Increasing the average body mass index from underweight to the normal range played a significant role in the development of industrialized societies. Height and weight thus both increased through the 19th century in the developed world. During the 20th century, as populations reached their genetic potential for height, weight began increasing much more than height, resulting in obesity.[85] In the 1950s increasing wealth in the developed world decreased child mortality, but as body weight increased heart and kidney disease became more common.[85][208] During this time period insurance companies realized the connection between weight and life expectancy and increased premiums for the obese.[2]

Many cultures throughout 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.[6] In modern 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 a reason for discrimination.[199]

How weight is viewed has changed over the last 100 years. The weight that is viewed as an ideal has become lower since the 1920s. This is illustrated by the fact that the average height of Miss America pageant winners increased by 2% from 1922 to 1999, while their average weight decreased by 12%.[209] People's perceptions of what is a healthy weight however have changed in the opposite direction. In Britain the weight at which people considered themselves to be overweight was significantly higher in 2007 than in 1999.[210] These changes are believed to be due to increasing rates of adiposity leading to increased acceptance of extra body fat as being normal.[210]

In many part of Africa obesity is still seen as a sign of wealth and well being. This has become particularly common since the HIV epidemic began.[2]

The arts

The first sculptural representations of the human body 20,000–35,000 years ago depict obese females. Some attribute the Venus figurines to the tendency to emphasize characteristics that portray fertility while others feel these could be actual representations of the people at the time.[6] Corpulence is, however, absent in both Greek and Roman art, probably fitting with their ideals of moderation. This continued through much of Christian European history, with only those of low socioeconomic status being depicted as obese. During the Renaissance some of the upper class began flaunting their large size. This can be seen in portraits of Henry the VIII and Alessandro del Borro.[6] Rubens (1577–1640) regularly depicted full-bodied women in his pictures, from which derives the term Rubenesque. These women, however, still maintained the "hourglass" shape with its relationship to fertility.[211] During the 19th century, views on obesity changed in the Western world. After centuries of obesity being synonymous with wealth and social status, slimness began to be seen as the desirable standard.[6]

Size acceptance and the obesity controversy

The main effort of the fat acceptance movement is to decrease discrimination against people who are overweight and obese.[212][213] However some in the movement are also attempting to challenge the established relationship between obesity and negative health outcomes.[214]

A number of organizations exist that promote the acceptance of obesity. They have increased in prominence in the latter half of the 20th century.[215] The US based National Association to Advance Fat Acceptance (NAAFA) was formed in 1969 and describes itself as a civil rights organization dedicated to ending size discrimination.[216] The International Size Acceptance Association (ISAA) is an NGO which was founded in 1997. It has more of a global orientation and describes its mission as promoting size acceptance and helping to end weight-based discrimination.[217] These groups often argue for the recognition of obesity as a disability under the US Americans With Disabilities Act (ADA). The American legal system however has decided that the potential public health costs exceed the benefits of extending this anti-discrimination law to cover obesity.[214]

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 the social stigma facing the obese.[218] Similarly, The Obesity Epidemic by Michael Gard argues that obesity is a moral and ideological construct, rather than a health problem.[219] Other groups are also trying to challenge obesity's connection to poor health. The Center for Consumer Freedom, an organization partly supported by the restaurant and food industry, has run ads saying that obesity is not an epidemic but "hype".[220]

People are known to select potential partners based on a similar body mass.[221] The rising rates of obesity have therefore provided greater opportunities for overweight people to find partners. Certain subcultures also label themselves as particularly attracted to the obese. Chubby culture[222] and fat admirers[223] are examples.

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Bibliography

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