Obesity

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Obesity is a condition in which the natural energy reserve, stored in the fatty tissue of humans and other mammals, is increased to a point where it is associated with certain health conditions or increased mortality.

Although obesity is an individual clinical condition, it is increasingly viewed as a serious and growing public health problem: excessive body weight has been shown to predispose to various diseases, particularly cardiovascular diseases, diabetes mellitus type 2, sleep apnea and osteoarthritis.^[1][2]

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

Blood tests may be done to look for thyroid or hormone problems that could lead to weight gain.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Obesity is the nominal form of obese which comes from the Latin obēsus, which means “stout, fat, or plump.” Ēsus is the past participle of edere (to eat), with ob added to it. In Classical Latin, this verb is seen only in past participial form. Its first attested usage in English was in 1651, in Noah Biggs’s Matæotechnia Medicinæ Praxeos.^[1]

In several human cultures, obesity was associated with physical attractiveness, strength, and fertility. Some of the earliest known cultural artifact artifacts, known as Venus figurines, are pocket-sized statuettes representing an obese female figure. Although their cultural significance is unrecorded, their widespread use throughout pre-historic Mediterranean and European cultures suggests a central role for the obese female form in magical rituals, and suggests cultural approval of (and perhaps reverence for) this body form. This is most likely due to their ability to easily bear children and survive famine.

Obesity was considered a symbol of wealth and social status in cultures prone to food shortages or famine. It was viewed in the same manner well into the early modern period in European cultures as well, but as food security was realized, it came to serve more as a visible signifier of “lust for life”, appetite, and immersion in the realm of the erotic.

This was especially the case in the visual arts, such as the paintings of Rubens (1577–1640), whose regular depiction of fat women gives us the description Rubenesque. Obesity can also be seen as a symbol within a system of prestige. “The kind of food, the quantity, and the manner in which it is served are among the important criteria of social class. In most tribal societies, even those with a highly stratified social system, everyone – royalty and the commoners – ate the same kind of food, and if there was famine everyone was hungry. With the ever increasing diversity of foods, food has become not only a matter of social status, but also a mark of one’s personality and taste.”^[2]

In modern Western culture, the obese body shape is widely regarded as unattractive and many negative stereotypes are commonly associated with obese people. Obese children, teenagers and adults can also face a heavy social stigma. Obese children are frequently the targets of bullies and are often shunned by their peers. Although obesity rates are rising amongst all social classes in the West, obesity is often seen as a sign of lower socio-economic status.^[3] Most obese people have experienced negative thoughts about their body image, and some take drastic steps to try to change their shape including dieting, the use of diet pills, and even surgery. Not all contemporary cultures disapprove of obesity. There are many cultures which are traditionally more approving (to varying degrees) of obesity, including some African, Arabic, Indian, and Pacific Island cultures. Especially in recent decades, obesity has come to be seen more as a medical condition in modern Western culture even being referred to as an epidemic.^[4]

Recently emerging is a small but vocal fat acceptance movement that seeks to challenge weight-based discrimination. Obesity acceptance and advocacy groups have initiated litigation to defend the rights of obese people and to prevent their social exclusion.

Some notable figures within this movement, such as Paul Campos, argue that the social stigma surrounding obesity is founded in cultural anxiety, and that public concern over health risks associated with obesity are inappropriately used as a rationalization for this stigma.^[5]

Government agencies and private medicine have warned Americans for years of the adverse health effects associated with overweight and obesity. Despite the warnings, the problem is getting worse. In 2004, the CDC reported that 66.3% of adults in the United States were overweight or obese. The cause in most cases is a sedentary lifestyle; approximately 40% of adults in the United States do not participate in any leisure-time physical activity and less than 1/3 of adults engage in the recommended amount of physical activity.^[6] Overweight and obesity are easily determined by using Body Mass Index (BMI); this index uses your weight and height to determine body fat. An index A BMI range of 25 to 29.9 is considered overweight and anything over 30 obese. Individuals with a BMI over 30 increase the risk of several heath hazards.^[7]

Various stereotypes of obese people have found their way into expressions of popular culture. A common stereotype is the obese character who has a warm and dependable personality, or a jolly fat man like Santa Claus. Equally common is the obese vicious bully (such as Dudley Dursley from the Harry Potter book series, Eric Cartman from South Park, Nelson Muntz from The Simpsons).

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

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

A more unusual example of obesity-related humour is Bustopher Jones, from T. S. Eliot’s poem “Bustopher Jones: The Cat About Town” featured in Old Possum’s Book of Practical Cats, and the musical Cats derived from the poem. Bustopher’s claim to fame is that he is a regular visitor to many gentlemen’s clubs including Drones, Blimp’s and the Tomb. Due to his constant lunching at these clubs, he is remarkably fat, being described by others as “a twenty-five pounder… And he’s putting on weight everyday.” Another popular character, Garfield, a cartoon cat, is also obese for humor. When his owner, Jon, puts him on diets, rather than losing weight, Garfield slows down his weight gain.

It can be argued that depiction in popular culture adds to and maintains commonly perceived stereotypes, in turn harming the self esteem of obese people. On the other hand, obesity is often associated with positive characteristics such as good humor. In addition, some people are sexually attracted to obese people (see chubby culture and fat admirer).

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Karol Gema Hernandez, M.D. [2]

Obesity can be defined in absolute or relative terms. In practical settings, obesity is typically evaluated in absolute terms by measuring BMI (body mass index), but also in terms of its distribution through waist circumference or waist-hip circumference ratio measurements.^[1] In addition, the presence of obesity needs to be regarded in the context of other risk factors and comorbidities (other medical conditions that could influence risk of complications).^[2]

BMI, or body mass index, is a simple and widely used method for estimating body fat.^[3] BMI was developed by the Belgian statistician and anthropometrist Adolphe Quetelet.^[4] It is calculated by dividing the subject’s weight by the square of his/her height, typically expressed either in metric or US “Customary” units:

Metric: BMI = kg/m^2

Where kg is the subject’s weight in kilograms and m is the subject’s height in metres.

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

Where lb is the subject’s weight in pounds and in is the subject’s height in inches.

The current definitions commonly in use establish the following values, agreed in 1997 and published in 2000:^[5]

• A BMI less than 18.5 is underweight
• A BMI of 18.5–24.9 is normal weight
• A BMI of 25.0–29.9 is overweight
• A BMI of 30.0–39.9 is obese
• A BMI of 40.0 or higher is severely (or morbidly) obese
• A BMI of 35.0 or higher in the presence of at least one other significant comorbidity is also classified by some bodies as morbid obesity.^[6][7]

In a clinical setting, physicians take into account race, ethnicity, lean mass (muscularity), age, sex, and other factors which can affect the interpretation of BMI. BMI overestimates body fat in persons who are very muscular, and it can underestimate body fat in persons who have lost body mass (e.g. many elderly).^[2] Mild obesity as defined by BMI alone is not a cardiac risk factor, and hence BMI cannot be used as a sole clinical and epidemiological predictor of cardiovascular health.^[8] According to American Heart Association, when assessing and treating CVD, and obesity- related comorbilities, waist circumference indicating increased metabolic risk is as follows: ^[9]

• Women: >88 cm or >35 inches
• Men: >102 cm or >40 inches

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor-in-Chief: Salman J. Khan, M.D.

Most researchers have concluded that the combination of an excessive nutrient intake and a sedentary lifestyle are the main cause for the rapid acceleration of obesity in Western society in the last quarter of the 20th century. ^[1]

Despite the widespread availability of nutritional information in schools, doctors’ offices, on the internet and on groceries,^[2] it is evident that overeating remains a substantial problem. For instance, reliance on energy-dense fast-food meals tripled between 1977 and 1995, and calorie intake quadrupled over the same period.^[3]

However, dietary intake in itself is insufficient to explain the phenomenal rise in levels of obesity in much of the industrialized world during recent years. An increasingly sedentary lifestyle also has a significant role to play. More and more research into child obesity, for example, links such things as the school run, with the current high levels of this disease. ^[4]

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

As with many medical conditions, the calorific imbalance that results in obesity often develops from a combination of genetic and environmental factors. Polymorphisms in various genes controlling appetite, metabolism, and adipokine release predispose to obesity, but the condition requires availability of sufficient calories, and possibly other factors, to develop fully. Various genetic conditions that feature obesity have been identified (such as Prader-Willi syndrome, Bardet-Biedl syndrome, MOMO syndrome, leptin receptor mutations and melanocortin receptor mutations), but known single-locus mutations have been found in only about 5% of obese individuals. While it is thought that a large proportion of the causative genes are still to be identified, much obesity is likely the result of interactions between multiple genes, and non-genetic factors are likely also important.

A 2007 study identified fairly common mutations in the FTO gene; heterozygotes had a 30% increased risk of obesity, while homozygotes faced a 70% increased risk.^[5]

On a population level, the thrifty gene hypothesis postulates that certain ethnic groups may be more prone to obesity than others, and the ability to take advantage of rare periods of abundance and use such abundance by storing energy efficiently may have been an evolutionary advantage in times when food was scarce. Individuals with greater adipose reserves were more likely to survive famine. This tendency to store fat is likely maladaptive in a society with stable food supplies.^[6]

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

Medical illnesses that increase obesity risk include several rare congenital syndromes (listed above), hypothyroidism, Cushing’s syndrome, growth hormone deficiency.^[7] Smoking cessation is a known cause for moderate weight gain, as nicotine suppresses appetite. Certain medications (e.g. steroids, atypical antipsychotics, some fertility medication) may cause weight gain.

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

Flier^[8] summarizes the many possible pathophysiological mechanisms involved in the development and maintenance of obesity. This field of research had been almost unapproached until leptin was discovered in 1994. Since this discovery, many other hormonal mechanisms have been elucidated that participate in the regulation of appetite and food intake, storage patterns of adipose tissue, and development of insulin resistance. Since leptin’s discovery, ghrelin, orexin, PYY 3-36, cholecystokinin, adiponectin, and many other mediators have been studied. The adipokines are mediators produced by adipose tissue; their action is thought to modify many obesity-related diseases.

Leptin and ghrelin are considered to be complementary in their influence on appetite, with ghrelin produced by the stomach modulating short-term appetitive control (i.e. to eat when the stomach is empty and to stop when the stomach is stretched). Leptin is produced by adipose tissue to signal fat storage reserves in the body, and mediates long-term appetitive controls (i.e. to eat more when fat storages are low and less when fat storages are high). Although administration of leptin may be effective in a small subset of obese individuals who are leptin deficient, many more obese individuals are thought to be leptin resistant. This resistance is thought to explain in part why administration of leptin has not been shown to be effective in suppressing appetite in most obese subjects.

While leptin and ghrelin are produced peripherally, they control appetite through their actions on the central nervous system. In particular, they and other appetite-related hormones act on the hypothalamus, a region of the brain central to the regulation of food intake and energy expenditure. There are several circuits within the hypothalamus that contribute to its role in integrating appetite, the melanocortin pathway being the most well understood.^[8] 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.^[9]

The arcuate nucleus contains two distinct groups of neurons.^[8] 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.

Brain is actively involved in shaping eating behavior. Whenever food is consumed, brain gives a response to the nutrient intake. According to the latest research, the brain has an impaired response to nutrients in obese individuals as compared to lean people.

Several neurotransmitters have been studied for rewarding effects of food intake. These include dopamine, cannabinoids, opioids, serotonin, and neuropeptides.^[10][11] These neurotransmitters play a major role in homeostatic regulation of food intake.^[12] In a normal human being food consumption is followed by the release of these neurotransmitters from the brain to provide the feeling of satisfaction and reward. Dopamine is the thoroughly investigated and considered to be the primary neurotransmitter involved.^[13] Dopamine is a neurotransmitter that has an important role in motivation, processing of reward and behavior change through its projections from dorsal striatum, ventral tegmental area (VTA) and Nucleus accumbens (NAc). ^[14][15] Dopamine releases from dorsal striatum in response to the pleasure of food intake and activates many brain regions such as the midbrain, subcallosal cingulate and Prefrontal cortex.^[16] Furthermore, dopamine increases in VTA and NAc areas. The quantity of dopamine determines the pleasure arising from food, greater the magnitude greater will be the feeling of reward and pleasure.^[17] When dopamine activity reach a significant level and the feeling of reward is achieved, food intake is stopped.

In obesity, there is a decrease release of dopamine in response to food. This can be attributed to chronic food exposure and diminished dopamine activity.^[18][19] It occurs due to decrease in D2 receptors in the dorsal striatum.^[20] Consequently, this causes compensatory overeating to achieve the required feeling of reward.^[21][22] As per the clinical trial by Volkow et al using PET and multiple tracers, both drug addicts and individuals with morbid obesity have a smaller number of dopamine (D2) receptors in the striatum as compared to the healthy population.^[23] This shows the compulsive behavior in this population segment.

Wang and Haltia in their studies found out that lower D2 receptors are linked with higher Body Mass Index in individuals with obesity.^[24][25] These discoveries shows that impaired Dopamine receptor activity increases feeding and the risk for obesity.^[26] Guo et al. discovered that obesity and opportunistic eating were negatively associated with dopamine magnitude in ventromedial striatum, a region supporting reward and motivation.^[27]

This mechanism shows that brain has centers where changes occur in response to nutrient intake. In obese individuals, there is impaired mechanism towards food intake. These findings are critical as they might be the reasons behind eating disorders and failed weight loss efforts.

The role of bacteria colonizing the digestive tract in the development of obesity has recently become the subject of investigation. Bacteria participate in digestion (especially of fatty acids and polysaccharides), and alterations in the proportion of particular strains of bacteria may explain why certain people are more prone to weight gain than others. Human digestive tract are generally either members of the phyla of bacteroidetes or of firmicutes. In obese people, there is a relative abundance of firmicutes (which cause relatively high energy absorption), which is restored by weight loss. From these results it cannot yet be concluded whether this imbalance is the cause of obesity or an effect.^[28]

Some obesity co-factors are resistant to the theory that the “epidemic” is a new phenomenon. In particular, a class co-factor consistently appears across many studies. Comparing net worth with BMI scores, a 2004 study^[29] found obese American subjects approximately half as wealthy as thin ones. When income differentials were factored out, the inequity persisted—thin subjects were inheriting more wealth than fat ones. A higher rate of a lower level of education and tendencies to rely on cheaper fast foods is seen as a reason why these results are so dissimilar. Another study finds women who married into higher status are predictably thinner than women who married into lower status.

A 2007 study of more than 32,500 children of the original Framingham Heart Study cohort followed for 32 years indicated that BMI change in friends, siblings or spouse predicted BMI change in subjects irrespective of geographical distance. The association was strongest among mutual friends and lower among siblings and spouses (although these differences were not statistically significant). The authors concluded from the results that acceptance of body mass plays an important role in changes in body size.^[30]

While it may often appear obvious why a certain individual gets fat, it is far more difficult to understand why the average weight of certain societies have recently been growing. While genetic causes are central to understanding obesity, they cannot fully explain why one culture grows fatter than another.

This is most notable in the United States. In the years from just after the Second World War until 1960 the average person’s weight increased, but few were obese. In the two and a half decades since 1980 the growth in the rate of obesity has accelerated markedly and is increasingly becoming a public health concern.

There are a number of theories as to the cause of this change since 1980. Most believe it is a combination of various factors.

• Lack of activity: obese people are less active in general than lean people, and not just because of their obesity. A controlled increase in calorie intake of lean people did not make them less active; correspondingly when obese people lost weight they did not become more active. Weight change does not affect activity levels, but the converse seems to be the case.^[31]

• Lower relative cost of foodstuffs: massive changes in agricultural policy in the United States and Europe have led to food prices for consumers being lower than at any point in history. This can raise costs for consumers in some areas but greatly lower it in others. Current debates into trade policy highlight disagreements on the effects of subsidies. In the United States, production of corn, soy, wheat and rice is subsidized through the U.S. farm bill. Corn and soy, which are main sources of the sugars and fats in processed food, are thus cheap compared to fruits and vegetables.^[32]

• Increased marketing has also played a role. In the early 1980s in America the Reagan administration lifted most regulations pertaining to sweets and fast food advertising to children. As a result, the number of advertisements seen by the average child increased greatly, and a large proportion of these were for fast food and sweets.^[33]

• The changing workforce as each year a greater percent of the population spends their entire workday behind a desk or computer, seeing virtually no exercise. In the kitchen the microwave oven has seen sales of calorie-dense frozen convenience foods skyrocket and has encouraged more elaborate snacking.

• A social cause that is believed by many to play a role is the increasing number of two income households in which one parent no longer remains home to look after the house. This increases the number of restaurant and take-out meals.

• Urban sprawl may be a factor: obesity rates increase as urban sprawl increases, possibly due to less walking and less time for cooking.^[34]

• Since 1980 fast food restaurants have seen dramatic growth in terms of the number of outlets and customers served. Low food costs, and intense competition for market share, led to increased portion sizes—for example, McDonalds french fries portions rose from 200 calories (840 kilojoules) in 1960 to over 600 calories (2,500 kJ) today.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

• Cushing’s syndrome
• Drugs
• Diabetes
• Familial obesity
• Glucocorticoids
• Hypothyroidism
• Hyperandrogenism
• Metabolic Syndrome
• Overeating
• Physical inactivity
• Polycystic ovary syndrome

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]

United States

The prevalence of overweight and obesity in the United States makes obesity a leading public health problem. The United States has the highest rates of obesity in the developed world.^[1] From 1980 to 2002, obesity has doubled in adults and overweight prevalence has tripled in children and adolescents.^[2] From 2003-2004, “children and adolescents aged 2 to 19 years, 17.1% were overweight…and 32.2% of adults aged 20 years or older were obese.”^[2] The prevalence in the United States continues to rise.^[3]

United Kingdom

The Health Survey for England predicts that more than 12 million adults and 1 million children will be obese by 2010 if no action is taken.^[4][5]

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%.^[6]

Obesity is a public health and policy problem because of its prevalence, costs and burdens.^[7] The prevalence of obesity has been continually rising for two decades.^[8] This sudden rise in obesity prevalence is attributed to environmental and population factors rather than individual behavior and biology because of the rapid and continual rise in the number of overweight and obese individuals.^[9] The current environment produces risk factors for decreased physical activity and for increased calorie consumption. These environmental factors operate on the population to decrease physical activity and increase calorie consumption.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

The presence of risk factors and diseases associated with obesity are also used to establish a clinical diagnosis. Possible life-threatening risk factors that would indicate clinical treatment of obesity

• Coronary heart disease
• Type 2 diabetes
• Sleep apnea

Other risk factors

• Smoking
• Hypertension
• Age
• Family history

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]; Associate Editor(s)-in-Chief: Karol Gema Hernandez, M.D. [3] Usama Talib, BSc, MD [4]

Screening for obesity is recommended among children more than 6 years of age, and at least once a year among adults. Screening strategies include calculation of the body mass index (BMI), measurement of waist circumference, and measurement of body fat.

Screening for obesity should be performed at least once a year among adults. The cut-off values of BMI to define obesity and overweight among adults are as follows:

• Overweight: BMI >25.0-29.9 kg/m2
• Obesity: BMI≥30 kg/m2

Clinical practice guidelines and systematic review^[1][2] by the United States Preventive Services Task Force in 2010 stated:^[3][4]

• “Clinicians screen children aged 6 years and older for obesity and offer them or refer them to comprehensive, intensive behavioral intervention to promote improvement in weight status.”
• “Overweight = age- and gender-specific BMI at ≥85th to 94th percentile”
• “Obesity = age- and gender-specific BMI at ≥95th percentile”

The review included a meta-analysis of trials of weight management programs and concluded that weighted mean BMI decrease of 2.4 with comprehensive, medium- to high-intensity programs.^[2]

BMI does not take into account differing ratios of adipose to lean tissue; nor does it distinguish between differing forms of adiposity, some of which may correlate more closely with cardiovascular risk. Increasing understanding of the biology of different forms of adipose tissue has shown that visceral fat or central obesity (male-type or apple-type obesity) has a much stronger correlation, particularly with cardiovascular disease, than the BMI alone.^[5]

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)^[5] are both used as measures of central obesity.

In a cohort of almost 15,000 subjects from the National Health and Nutrition Examination Survey (NHANES) III study, waist circumference explained obesity-related health risk significantly better than BMI when metabolic syndrome was taken as an outcome measure.^[6]

An alternative way to determine obesity is to assess percent body fat. Doctors and scientists generally agree that men with more than 25% body fat and women with more than 30% body fat are obese. However, it is difficult to measure body fat precisely. The most accepted method has been to weigh a person underwater, but underwater weighing is a procedure limited to laboratories with special equipment. Two simpler methods for measuring body fat are the skinfold test, in which a pinch of skin is precisely measured to determine the thickness of the subcutaneous fat layer; or bioelectrical impedance analysis, usually only carried out at specialist clinics. Their routine use is discouraged.^[7]

Other measurements of body fat include computed tomography (CT/CAT scan), magnetic resonance imaging (MRI/NMR), and dual energy X-ray absorptiometry (DXA).^[8]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

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).^[1][2] 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.^[2]

Excessive body weight is associated with various diseases, particularly cardiovascular diseases, diabetes mellitus type 2, obstructive sleep apnea, certain types of cancer, and osteoarthritis.^[1] As a result, obesity has been found to reduce life expectancy.^[1]

Obesity increases the risk of many physical and mental conditions. These comorbidities are reflected predominantly in metabolic syndrome.^[1] Metabolic syndrome being a combination of medical disorders, which includes diabetes mellitus type 2, high blood pressure, high blood cholesterol, and high triglyceride levels.^[23]

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.^[24]

Obesity is one of the leading preventable causes of death worldwide.^{[25] [26][27]} 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/m^2[28] in non smokers and at a BMI of 24–27 kg/m² in current smokers and increases with changes in either direction.^[29][30] Obesity increases the risk of death in current and former smokers as well as in those who have never smoked.^[30] A BMI of over 32 has been associated with a doubled mortality rate among women over a 16-year period^[31] and obesity is estimated to cause an excess 111,909 to 365,000 death per year in the United States.^[27][1] Obesity on average reduces life expectancy by six to seven years.^[32][1] A BMI of 30–35 reduces life expectancy by two to four years^[28] while severe obesity (BMI > 40) reduces life expectancy by 20 years for men and five years for women.

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.^[33] The paradox was first described in 1999 in overweight and obese people undergoing hemodialysis,^[33] and has subsequently been found in those with heart failure, and peripheral artery disease (PAD).^[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 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.^[36][37] Even after cardiac bypass surgery, no increase in mortality is seen in the overweight and obese.^[38] One study found that the improved survival could be explained by the more aggressive treatment obese people receive after a cardiac event.^[39] Another found that if one takes into account chronic obstructive pulmonary disease (COPD) in those with PAD the benefit of obesity no longer exsists.^[34]

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