Obesity

Classification

Main article: Classification of obesity

Obesity is typically defined as a substantial accumulation of body fat that could impact health. The U.S. Centers for Disease Control and Prevention (CDC) further subdivides obesity based on BMI, with a BMI 30 to 35 called class 1 obesity; 35 to 40, class 2 obesity; and 40+, class 3 obesity.

For children, obesity measures take age into consideration along with height and weight. For children aged 5–19, the WHO defines obesity as a BMI two standard deviations above the median for their age (a BMI around 18 for a five-year old; around 30 for a 19-year old). For children under five, the WHO defines obesity as a weight three standard deviations above the median for their height.

Some modifications to the WHO definitions have been made by particular organizations.

• Any BMI ≥ 35 or 40 kg/m2 is severe obesity.
• A BMI of ≥ 35 kg/m2 and experiencing obesity-related health conditions or ≥ 40 or 45 kg/m2 is morbid obesity.
• A BMI of ≥ 45 or 50 kg/m2 is super obesity.

As Asian populations develop negative health consequences at a lower BMI than Caucasians, some nations have redefined obesity; Japan has defined obesity as any BMI greater than 25 kg/m2

The preferred obesity metric in scholarly circles is the body fat percentage (BF%) – the ratio of the total weight of person's fat to his or her body weight, and BMI is viewed merely as a way to approximate BF%. According to American Society of Bariatric Physicians, levels in excess of 32% for women and 25% for men are generally considered to indicate obesity.

BMI is now viewed as outdated in some countries because it ignores variations between individuals in amounts of lean body mass, particularly muscle mass. Individuals involved in heavy physical labor or sports may have high BMI values despite having little fat. For example, more than half of all NFL players are classified as "obese" (BMI ≥ 30), and 1 in 4 are classified as "extremely obese" (BMI ≥ 35), according to the BMI metric. However, their mean body fat percentage, 14%, is well within what is considered a healthy range. Similarly, Sumo wrestlers are typically categorized by BMI as "severely obese" or "very severely obese"; but one study of college-aged Sumo wrestlers found that 40% of them were no longer categorized as obese when body fat percentage (with a cutoff of

Canada utilises BMI sparingly within their method of defining levels of obesity through use of the Edmonton Scale (for adult obesity). This scale also introduces factors such as Quality of Life, Mental Health & Mobility amongst others. In recent years, Canada chose to allow both Chile & Ireland to adapt their obesity guidelines to suit both countries' health systems. In Ireland, obesity is now defined as "a Complex, Chronic & Relapsing Disease".

Effects on health

Obesity increases a person's risk of developing various metabolic diseases, cardiovascular disease, osteoarthritis, Alzheimer disease, depression, and certain types of cancer. High BMI is a marker of risk for, but not a direct cause of, diseases caused by diet and physical activity.

Mortality

Obesity is one of the leading preventable causes of death worldwide. The mortality risk is lowest at a BMI of 20–25 kg/m2 This appears to apply in at least four continents. Other research suggests that the association of BMI and waist circumference with mortality is U- or J-shaped, while the association between waist-to-hip ratio and waist-to-height ratio with mortality is more positive. In Asians the risk of negative health effects begins to increase between 22 and 25 kg/m2. In 2021, the World Health Organization estimated that obesity caused at least 2.8 million deaths annually. On average, obesity reduces life expectancy by six to seven years, a BMI of 30–35 kg/m2 reduces life expectancy by two to four years, while severe obesity (BMI ≥ 40 kg/m2) reduces life expectancy by ten years.

Morbidity

Main article: Obesity-associated morbidity

Obesity increases the risk of many physical and mental conditions. These comorbidities are most commonly shown in metabolic syndrome, a combination of medical disorders which includes: diabetes mellitus type 2, high blood pressure, high blood cholesterol, and high triglyceride levels. A study from the RAK Hospital found that obese people are at a greater risk of developing long COVID. The CDC has found that obesity is the single strongest risk factor for severe COVID-19 illness.

Complications may be 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.

Health consequences fall into two broad categories: those attributable to the effects of increased fat mass (such as osteoarthritis, obstructive sleep apnea, social stigmatization) and those due to the increased number of fat cells (diabetes, cancer, cardiovascular disease, non-alcoholic fatty liver disease). Increases in body fat alter the body's response to insulin, potentially leading to insulin resistance. Increased fat also creates a proinflammatory state, and a prothrombotic state.

Metrics of health

Main article: Metabolically healthy obesity

Newer research has focused on methods of identifying healthier obese people by clinicians, and not treating obese people as a monolithic group. Obese people who do not experience medical complications from their obesity are sometimes called (metabolically) healthy obese, but the extent to which this group exists (especially among older people) is in dispute. The number of people considered metabolically healthy depends on the definition used, and there is no universally accepted definition. There are numerous obese people who have relatively few metabolic abnormalities, and a minority of obese people have no medical complications. The guidelines of the American Association of Clinical Endocrinologists call for physicians to use risk stratification with obese patients when considering how to assess their risk of developing type 2 diabetes.

In 2014, the BioSHaRE–EU Healthy Obese Project (sponsored by Maelstrom Research, a team under the Research Institute of the McGill University Health Centre) came up with two definitions for healthy obesity, one more strict and one less so:

To come up with these criteria, BioSHaRE controlled for age and tobacco use, researching how both may effect the metabolic syndrome associated with obesity, but not found to exist in the metabolically healthy obese. Other definitions of metabolically healthy obesity exist, including ones based on waist circumference rather than BMI, which is unreliable in certain individuals.

Another identification metric for health in obese people is calf strength, which is positively correlated with physical fitness in obese people. Body composition in general is hypothesized to help explain the existence of metabolically healthy obesity—the metabolically healthy obese are often found to have low amounts of ectopic fat (fat stored in tissues other than adipose tissue) despite having overall fat mass equivalent in weight to obese people with metabolic syndrome.

Survival paradox

Although the negative health consequences of obesity in the general population are well supported by the available research evidence, health outcomes in certain subgroups seem to be improved at an increased BMI, a phenomenon known as the obesity survival paradox. The paradox was first described in 1999 in overweight and obese people undergoing hemodialysis

In people with heart failure, those with a BMI between 30.0 and 34.9 had lower mortality than those with a normal weight. This has been attributed to the fact that people often lose weight as they become progressively more ill. 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, the risk of further cardiovascular events is increased. Even after cardiac bypass surgery, no increase in mortality is seen in the overweight and obese. One study found that the improved survival could be explained by the more aggressive treatment obese people receive after a cardiac event. Another study found that if one takes into account chronic obstructive pulmonary disease (COPD) in those with PAD, the benefit of obesity no longer exists.

Causes

The "a calorie is a calorie" model of obesity posits a combination of excessive food energy intake and a lack of physical activity as the cause of most cases of obesity. A limited number of cases are due primarily to genetics, medical reasons, or psychiatric illness. Increasing rates of obesity at a societal level are felt to be due to an easily accessible and palatable diet, increased reliance on cars, and mechanized manufacturing.

Some other factors have been proposed as causes towards rising rates of obesity worldwide, including insufficient sleep, endocrine disruptors, increased usage of certain medications (such as atypical antipsychotics), increases in ambient temperature, decreased rates of smoking, Baum, Charles L. "The effects of cigarette costs on BMI and obesity." Health Economics 18.1 (2009): 3-19. APA demographic changes, increasing maternal age of first-time mothers, changes to epigenetic regulation from the environment, increased phenotypic variance via assortative mating, social pressure to diet, among others. According to one study in 2006, factors like these may play as big of a role as excessive food energy intake and a lack of physical activity; however, the relative magnitudes of the effects of any proposed cause of obesity is varied and uncertain, as there is a general need for randomized controlled trials on humans before definitive statement can be made.

According to the Endocrine Society, there is "growing evidence suggesting that obesity is a disorder of the energy homeostasis system, rather than simply arising from the passive accumulation of excess weight" and that "obesity pathogenesis involves two related but distinct processes: (1) sustained positive energy balance (energy [caloric] intake energy expenditure) and (2) resetting of the body weight "set point" at an increased value." In other words, the fundamental cause of obesity is consuming more calories than are used by the body, and the body adapting to a heavier weight as the standard for the individual.

Diet

Main article: Diet and obesity

1961 2001–03 Map of dietary energy availability per person per day in 1961 (left) and 2001–2003 (right) Calories per person per day (kilojoules per person per day)

Excess appetite for palatable, high-calorie food (especially fat, sugar, and certain animal proteins) is seen as the primary factor driving obesity worldwide, likely because of imbalances in neurotransmitters affecting the drive to eat, as well as changes to the duodenum impacting nutrient sensing and signaling. Dietary energy supply (the amount of calories in available food) per capita varies markedly between different regions and countries. It has also changed significantly over time. Total food energy consumption has been found to be related to obesity.

The widespread availability of dietary guidelines has done little to address the problems of overeating and poor dietary choice. From 1971 to 2000, obesity rates in the United States increased from 14.5% to 30.9%. During the same period, an increase occurred in the average amount of food energy consumed. For women, the average increase was 335 Cal per day (1542 Cal in 1971 and 1877 Cal in 2004), while for men the average increase was 168 Cal per day (2450 Cal in 1971 and 2618 Cal in 2004). Most of this extra food energy came from an increase in carbohydrate consumption rather than fat consumption. The primary sources of these extra carbohydrates are sweetened beverages, which now account for almost 25 percent of daily food energy in young adults in America, and potato chips. Consumption of sweetened beverages such as soft drinks, fruit drinks, and iced tea is believed to be contributing to the rising rates of obesity and to an increased risk of metabolic syndrome and type 2 diabetes. Vitamin D deficiency is related to diseases associated with obesity.

As societies become increasingly reliant on calorie-dense, big-portions, and fast-food meals, the association between fast-food consumption and obesity becomes more concerning. In the United States, consumption of fast-food meals tripled and food energy intake from these meals quadrupled between 1977 and 1995.

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. Calorie count laws and nutrition facts labels attempt to steer people toward making healthier food choices, including awareness of how much food energy is being consumed.

Obese people consistently under-report their food consumption as compared to people of normal weight. This is supported both by tests of people carried out in a calorimeter room and by direct observation.

Sedentary lifestyle

A sedentary lifestyle may play a significant role in obesity. Worldwide there has been a large shift towards less physically demanding work, and currently at least 30% of the world's population gets insufficient exercise. World trends in active leisure time physical activity are less clear. The World Health Organization indicates people worldwide are taking up less active recreational pursuits, while research from Finland found an increase and research from the United States found leisure-time physical activity has not changed significantly. Physical activity in children may not be a significant contributor.

In both children and adults, there is an association between television viewing time and the risk of obesity. Increased media exposure increases the rate of childhood obesity, with rates increasing proportionally to time spent watching television.

Genetics

Main article: Genetics of obesity

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 food energy is present. As of 2006, more than 41 of these sites on the human genome have been linked to the development of obesity when a favorable environment is present. People with two copies of the FTO gene (fat mass and obesity associated gene) have been found on average to weigh 3–4 kg more and have a 1.67-fold greater risk of obesity compared with those without the risk allele. The differences in BMI between people that are due to genetics varies depending on the population examined from 6% to 85%.

Obesity is a major feature in several syndromes, such as Prader–Willi syndrome, Bardet–Biedl syndrome, Cohen syndrome, and MOMO syndrome. (The term "non-syndromic obesity" is sometimes used to exclude these conditions.) 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 point DNA mutation.

Studies that have focused on inheritance patterns rather than on specific genes have found that 80% of the offspring of two obese parents were also obese, in contrast to less than 10% of the offspring of two parents who were of normal weight. Different people exposed to the same environment have different risks of obesity due to their underlying genetics.

The thrifty gene hypothesis postulates that, due to dietary scarcity during human evolution, people are prone to obesity. 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 to survive famine. This tendency to store fat, however, would be maladaptive in societies with stable food supplies. This theory has received various criticisms, and other evolutionarily-based theories such as the drifty gene hypothesis and the thrifty phenotype hypothesis have also been proposed.

Other illnesses

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, and some eating disorders such as binge eating disorder and night eating syndrome. The risk of overweight and obesity is higher in patients with psychiatric disorders than in persons without psychiatric disorders. Obesity and depression influence each other mutually, with obesity increasing the risk of clinical depression, and also depression leading to a higher chance of developing obesity.

Drug-induced obesity

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.

Social determinants

Main article: Social determinants of obesity

While genetic influences are important to understanding obesity, they cannot completely explain the dramatic increase seen within specific countries or globally. Though it is accepted that energy consumption in excess of energy expenditure leads to increases in body weight 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. Research 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. In 2007 repeating the same research found the same relationships, but they were weaker. The decrease in strength of correlation was felt to be due to the effects of globalization. Among developed countries, levels of adult obesity, and percentage of teenage children who are overweight, are correlated with income inequality. A similar relationship is seen among US states: more adults, even in higher social classes, are obese in more unequal states.

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. Stress and perceived low social status appear to increase risk of obesity.

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. However, changing rates of smoking have had little effect on the overall rates of obesity.

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. This could be partly explained by the fact that having dependent children decreases physical activity in Western parents.

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%. In part, this may be because of urban design issues (such as inadequate public spaces for physical activity). Time spent in motor vehicles, as opposed to active transportation options such as cycling or walking, is correlated with increased risk of obesity.

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

Gut bacteria

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 people. There is an indication that gut flora can affect the metabolic potential. This apparent alteration 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. The use of antibiotics among children has also been associated with obesity later in life.

An association between viruses and obesity has been found in humans and several different animal species. The amount that these associations may have contributed to the rising rate of obesity is yet to be determined.

Other factors

Not getting enough sleep is also associated with obesity. Whether one causes the other is unclear.

Some have proposed that chemical compounds called "obesogens" may play a role in obesity.

Certain aspects of personality are associated with being obese. Loneliness, neuroticism, impulsivity, and sensitivity to reward are more common in people who are obese while conscientiousness and self-control are less common in people who are obese. Because most of the studies on this topic are questionnaire-based, it is possible that these findings overestimate the relationships between personality and obesity: people who are obese might be aware of the social stigma of obesity and their questionnaire responses might be biased accordingly. Similarly, the personalities of people who are obese as children might be influenced by obesity stigma, rather than these personality factors acting as risk factors for obesity.

In relation to globalization, it is known that trade liberalization is linked to obesity; research, based on data from 175 countries during 1975–2016, showed that obesity prevalence was positively correlated with trade openness, and the correlation was stronger in developing countries.

Pathophysiology

Main article: Pathophysiology of obesity

Two distinct but related processes are considered to be involved in the development of obesity: sustained positive energy balance (energy intake exceeding energy expenditure) and the resetting of the body weight "set point" at an increased value. The second process explains why finding effective obesity treatments has been difficult. While the underlying biology of this process still remains uncertain, research is beginning to clarify the mechanisms.

At a biological level, there are many possible pathophysiological mechanisms involved in the development and maintenance of obesity. This field of research had been almost unapproached until the leptin gene was discovered in 1994 by J. M. Friedman's laboratory. 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. 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.

The arcuate nucleus contains two distinct groups of neurons. 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.

Management

Main article: Management of obesity

The main treatment for obesity consists of weight loss via lifestyle interventions, including prescribed diets and physical exercise. Although it is unclear what diets might support long-term weight loss, and although the effectiveness of low-calorie diets is debated,

Although 87% of participants in the National Weight Control Registry were able to maintain 10% body weight loss for 10 years, the most appropriate dietary approach for long term weight loss maintenance is still unknown. In the US, intensive behavioral interventions combining both dietary changes and exercise are recommended. Intermittent fasting has no additional benefit of weight loss compared to continuous energy restriction. Adherence is a more important factor in weight loss success than whatever kind of diet an individual undertakes.

Several hypo-caloric diets are effective. In the short-term low carbohydrate diets appear better than low fat diets for weight loss. In the long term, however, all types of low-carbohydrate and low-fat diets appear equally beneficial. Heart disease and diabetes risks associated with different diets appear to be similar.

Promotion of the Mediterranean diets among the obese may lower the risk of heart disease. Decreased intake of sweet drinks is also related to weight-loss. Success rates of long-term weight loss maintenance with lifestyle changes are low, ranging from 2–20%. Dietary and lifestyle changes are effective in limiting excessive weight gain in pregnancy and improve outcomes for both the mother and the child. Intensive behavioral counseling is recommended in those who are both obese and have other risk factors for heart disease.

Health policy

Obesity is a complex public health and policy problem because of its prevalence, costs, and health effects. As such, managing it requires changes in the wider societal context and effort by communities, local authorities, and governments. 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 food energy consumption and inhibit physical activity. Efforts include federally reimbursed meal programs in schools, limiting direct junk food marketing to children, and decreasing access to sugar-sweetened beverages in schools. The World Health Organization recommends the taxing of sugary drinks. When constructing urban environments, efforts have been made to increase access to parks and to develop pedestrian routes. Efforts also exist to address the occurrence of food swamps, or areas with an overabundance of convenient or fast food options, as these has been found to be strongly predictive of obesity rates.

Mass media campaigns seem to have limited effectiveness in changing behaviors that influence obesity, but may increase knowledge and awareness regarding physical activity and diet, which might lead to changes in the long term. Campaigns might also be able to reduce the amount of time spent sitting or lying down and positively affect the intention to be active physically. Nutritional labelling with energy information on menus might be able to help reducing energy intake while dining in restaurants. Some call for policy against ultra-processed foods.

Medical interventions

Medication

Main article: Anti-obesity medication

Since the introduction of medicines for the management of obesity in the 1930s, many compounds have been tried. Most of them reduce body weight by small amounts, and several of them are no longer marketed for obesity because of their side effects. Out of 25 anti-obesity medications withdrawn from the market between 1964 and 2009, 23 acted by altering the functions of chemical neurotransmitters in the brain. The most common side effects of these drugs that led to withdrawals were mental disturbances, cardiac side effects, and drug abuse or drug dependence. Deaths were reportedly associated with seven products.

Six medications for long-term use are: liraglutide, naltrexone/bupropion, orlistat, semaglutide, tirzepatide and phentermine/topiramate. There is no information on how these drugs affect longer-term complications of obesity such as cardiovascular disease or death, although studies on semaglutide have shown cardiovascular benefits.

In 2019 a systematic review compared the effects on weight of various doses of fluoxetine (60 mg/d, 40 mg/d, 20 mg/d, 10 mg/d) in obese adults. When compared to placebo, all dosages of fluoxetine appeared to contribute to weight loss but lead to increased risk of experiencing side effects such as dizziness, drowsiness, fatigue, insomnia and nausea during period of treatment. However, these conclusions were from low certainty evidence. When comparing, in the same review, the effects of fluoxetine on weight of obese adults, to other anti-obesity agents, omega-3 gel and not receiving a treatment, the authors could not reach conclusive results due to poor quality of evidence.

Among antipsychotic drugs for treating schizophrenia clozapine is the most effective, but it also has the highest risk of causing the metabolic syndrome, of which obesity is the main feature. For people who gain weight because of clozapine, taking metformin may reportedly improve three of the five components of the metabolic syndrome: waist circumference, fasting glucose, and fasting triglycerides.

Surgery

The most effective treatment for obesity is bariatric surgery. Surgery for severe obesity is associated with long-term weight loss, improvement in obesity-related conditions, and decreased overall mortality; however, improved metabolic health results from the weight loss, not the surgery. One study found a weight loss of between 14% and 25% (depending on the type of procedure performed) at 10 years, and a 29% reduction in all cause mortality when compared to standard weight loss measures. Complications occur in about 17% of cases and reoperation is needed in 7% of cases.

Epidemiology

Main article: Epidemiology of obesity

In earlier historical periods obesity was rare and achievable only by a small elite, although already recognised as a problem for health. But as prosperity increased in the Early Modern period, it affected increasingly larger groups of the population.

In 1997, the WHO formally recognized obesity as a global epidemic. The global prevalence of obesity more than doubled between 1980 and 2014. In 2014, more than 600 million adults were obese, equal to about 13 percent of the world's adult population, with that figure growing to 16% by 2022, according to the World Health Organization. The percentage of adults affected in the United States as of 2015–2016 is about 39.6% overall (37.9% of males and 41.1% of females). In 2000, the World Health Organization (WHO) stated that overweight and obesity were replacing more traditional public health concerns such as undernutrition and infectious diseases as one of the most significant cause of poor health.

The rate of obesity also increases with age at least up to 50 or 60 years old and severe obesity in the United States, Australia, and Canada is increasing faster than the overall rate of obesity. The OECD has projected an increase in obesity rates until at least 2030, especially in the United States, Mexico and England with rates reaching 47%, 39% and 35%, respectively.

Once considered a problem only of high-income countries, obesity rates are rising worldwide and affecting both the developed and developing world. These increases have been felt most dramatically in urban settings. In 2021, nearly half the global adult population - a billion men and 1.11 billion women aged 25 or older - were overweight or obese. It was predicted that if these trends continue about 57.4% of men and 60.3% of women would be overweight or obese by 2050.

Sex- and gender-based differences influence the prevalence of obesity. Globally there are more obese women than men, but the numbers differ depending on how obesity is measured.

History

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. The Oxford English Dictionary documents its first usage in 1611 by Randle Cotgrave.

Historical attitudes

Ancient Greek medicine recognizes obesity as a medical disorder and records that the Ancient Egyptians saw it in the same way. Hippocrates wrote that "Corpulence is not only a disease itself, but the harbinger of others". For most of human history, mankind struggled with food scarcity. Obesity has thus historically been viewed as a sign of wealth and prosperity. It was common among high officials in Ancient East Asian civilizations. In the 17th century, English medical author Tobias Venner is credited with being one of the first to refer to the term as a societal disease in a published English language book.

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. During this time period, insurance companies realized the connection between weight and life expectancy and increased premiums for the obese.

Many cultures throughout history have viewed obesity as the result of a character flaw. The obesus or fat character in Ancient 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.

Public perceptions in Western society regarding healthy body weight differ from those regarding the weight that is considered ideal – and both have changed since the beginning of the 20th century. 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%. On the other hand, people's views concerning healthy weight 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. These changes are believed to be due to increasing rates of adiposity leading to increased acceptance of extra body fat as being normal.

Obesity is still seen as a sign of wealth and well-being in many parts of Africa. This has become particularly common since the HIV epidemic began.

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 fertility while others feel they represent "fatness" in the people of the time. Corpulence is, however, absent in both Greek and Roman art, probably in keeping with their ideals regarding 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, as can be seen in portraits of Henry VIII of England and Alessandro dal Borro. 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.

Society and culture

Economic impact

In addition to its health impacts, obesity leads to many problems, including disadvantages in employment and increased business costs.

In 2005, the medical costs attributable to obesity in the US were an estimated $190.2 billion or 20.6% of all medical expenditures, while the cost of obesity in Canada was estimated at CA$2 billion in 1997 (2.4% of total health costs). The total annual direct cost of overweight and obesity in Australia in 2005 was A$21 billion. Overweight and obese Australians also received A$35.6 billion in government subsidies. The estimated range for annual expenditures on diet products is $40 billion to $100 billion in the US alone.

The Lancet Commission on Obesity in 2019 called for a global treaty—modelled on the WHO Framework Convention on Tobacco Control—committing countries to address obesity and undernutrition, explicitly excluding the food industry from policy development. They estimate the global cost of obesity $2 trillion a year, about or 2.8% of world GDP.

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. Sin taxes such as a sugary drink tax have been implemented in certain countries globally to curb dietary and consumer habits, and as an effort to offset the economic tolls.

Obesity can lead to social stigmatization and disadvantages in employment. When compared to their ideal weight counterparts, workers with obesity, on average have higher rates of absenteeism from work and take more disability leave, thus increasing costs for employers and decreasing productivity. A study examining Duke University employees found that people with a BMI over 40 kg/m2 filed twice as many workers' compensation claims as those whose BMI was 18.5–24.9 kg/m2. 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. The Alabama State Employees' Insurance Board approved a controversial plan to charge obese workers $25 a month for health insurance that would otherwise be free unless they take steps to lose weight and improve their health. These measures started in January 2010 and apply to those state workers whose BMI exceeds 35 kg/m2 and who fail to make improvements in their health after one year. This becomes a Catch 22 position as many insurance companies will refuse to pay for treatment methods for workers living with obesity.

Some research shows that people with obesity are less likely to be hired for a job and are less likely to be promoted. People with obesity are also paid less than their counterparts who do not live with obesity for an equivalent job; women with obesity on average make 6% less and men with obesity make 3% less.

Specific industries, such as the airline, healthcare and food industries, have special concerns. Due to rising rates of obesity, airlines face higher fuel costs and pressures to increase seating width. In 2000, the extra weight of passengers with obesity cost airlines US$275 million. The healthcare industry has had to invest in special facilities for handling patients with class III obesity, including special lifting equipment and bariatric ambulances. Costs for restaurants are increased by litigation accusing them of causing obesity. In 2005, the US Congress discussed legislation to prevent civil lawsuits against the food industry in relation to obesity; however, it did not become law.

With the American Medical Association's 2013 classification of obesity as a chronic disease,

In 2014, The European Court of Justice ruled that morbid obesity is a disability. The Court said that if an employee's obesity prevents them from "full and effective participation of that person in professional life on an equal basis with other workers", then it shall be considered a disability and that firing someone on such grounds is discriminatory.

In low-income countries, obesity can be a signal of wealth. A 2023 experimental study found that obese individuals in Uganda were more likely to access credit.

Size acceptance

The principal goal of the fat acceptance movement is to decrease discrimination against people who are overweight and obese. However, some in the movement are also attempting to challenge the established relationship between obesity and negative health outcomes.

A number of organizations exist that promote the acceptance of obesity. They have increased in prominence in the latter half of the 20th century. 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.

The International Size Acceptance Association (ISAA) is a non-governmental organization (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. 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.

Industry influence on research

In 2015, the New York Times published an article on the Global Energy Balance Network, a nonprofit founded in 2014 that advocated for people to focus on increasing exercise rather than reducing calorie intake to avoid obesity and to be healthy. The organization was founded with at least $1.5M in funding from the Coca-Cola Company, and the company has provided $4M in research funding to the two founding scientists Gregory A. Hand and Steven N. Blair since 2008.

Reports

Many organizations 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". In 2006, the Canadian Obesity Network, now known as Obesity Canada 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.

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. 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. 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. A 2007 report produced by Derek Wanless for the King's Fund warned that unless further action was taken, obesity had the capacity to debilitate the National Health Service financially. In 2022 the National Institute for Health and Care Research (NIHR) published a comprehensive review of research on what local authorities can do to reduce obesity.

The Obesity Policy Action (OPA) framework divides measure into upstream policies, midstream policies, and downstream policies. Upstream policies have to do with changing society, while midstream policies try to alter behaviors believed to contribute to obesity at the individual level, while downstream policies treat currently obese people.

Childhood obesity

Main article: Childhood obesity

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. 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. Childhood obesity has reached epidemic proportions in the 21st century, with rising rates in both the developed and the developing world. Rates of obesity in Canadian boys have increased from 11% in the 1980s to over 30% in the 1990s, while during this same time period rates increased from 4 to 14% in Brazilian children. In the US, the percentage of overweight and obese children increased to 16% in 2008, a 300% increase over the prior 30 years.

As with obesity in adults, many factors contribute to the rising rates of childhood obesity. Changing diet and decreasing physical activity are believed to be the two most important causes for the recent increase in the incidence of child obesity. Advertising of unhealthy foods to children also contributes, as it increases their consumption of the product. Antibiotics in the first 6 months of life have been associated with excess weight at age seven to twelve years of age. Because childhood obesity often persists into adulthood and is associated with numerous chronic illnesses, children who are obese are often tested for hypertension, diabetes, hyperlipidemia, and fatty liver disease.

Treatments used in children are primarily lifestyle interventions and behavioral techniques, although efforts to increase activity in children have had little success. In the United States, medications are not FDA approved for use in this age group. Brief weight management interventions in primary care (e.g. delivered by a physician or nurse practitioner) have only a marginal positive effect in reducing childhood overweight or obesity. Multi-component behaviour change interventions that include changes to dietary and physical activity may reduce BMI in the short term in children aged 6 to 11 years, although the benefits are small and quality of evidence is low.

Statistics

The CDC reported that this prevalence of obesity among U.S. adults 20 and over was 41.9% during 2017–March 2020 in which during the same time, the prevalence of severe obesity among U.S. adults was 9.2%. The prevalence of obesity was lowest among non-Hispanic Asian adults (17.4%) compared with non-Hispanic white (42.2%), non-Hispanic black (49.6%), and Hispanic (44.8%) adults.

Other animals

Main article: Obesity in pets

Obesity in pets is common in many countries. In the United States, 23–41% of dogs are overweight, and about 5.1% are obese. The rate of obesity in cats was slightly higher at 6.4%. The risk of obesity in dogs is related to whether or not their owners are obese; however, there is no similar correlation between cats and their owners.

References

Citations

References

1. (February 29, 2024). "Worldwide trends in underweight and obesity from 1990 to 2022: a pooled analysis of 3663 population-representative studies with 222 million children, adolescents, and adults". The Lancet.
2. (May 2021). "Obesity and Cardiovascular Disease: A Scientific Statement From the American Heart Association". Circulation.
3. CDC. (21 March 2022). "Causes and Consequences of Childhood Obesity".
4. "Policy Finder". American Medical Association (AMA).
5. (2005). "Nutrition and Fitness: Obesity, the Metabolic Syndrome, Cardiovascular Disease, and Cancer".
6. (October 2005). "Obesity". Lancet.
7. "Obesity - Symptoms and causes".
8. (August 2020). "Endocrine-disrupting chemicals: economic, regulatory, and policy implications". The Lancet. Diabetes & Endocrinology.
9. (2008). "Why is the developed world obese?". Annual Review of Public Health.
10. (15 July 2009). "Consequences of Weight Cycling: An Increase in Disease Risk?". International Journal of Exercise Science.
11. (August 2014). "Surgery for weight loss in adults". The Cochrane Database of Systematic Reviews.
12. (July 2008). "Safety and effectiveness of the intragastric balloon for obesity. A meta-analysis". Obesity Surgery.
13. (2015). "Encyclopedia of Mental Health". Academic Press.
14. (1 March 2024). "One in eight people are now living with obesity".
15. (January 2015). "Obesity and overweight Fact sheet N°311".
16. (2008). "Obesity in art: a brief overview".
17. (2023). "The implications of defining obesity as a disease: a report from the Association for the Study of Obesity 2021 annual conference - eClinicalMedicine". eClinicalMedicine.
18. (18 June 2013). "A.M.A. Recognizes Obesity as a Disease". The New York Times.
19. (21 June 2013). "The Facts About Obesity". [[American Hospital Association]].
20. (2005). "The SuRF Report 2". World Health Organization.
21. (9 June 2021). "Obesity and overweight". World Health Organization.
22. (7 June 2021). "Defining Adult Overweight and Obesity". U.S. Centers for Disease Control and Prevention.
23. (July 2007). "Increases in morbid obesity in the USA: 2000–2005". Public Health.
24. (December 2002). "Predictive values of body mass index and waist circumference for risk factors of certain related diseases in Chinese adults: study on optimal cut-off points of body mass index and waist circumference in Chinese adults". Asia Pac J Clin Nutr.
25. (1997). "Assessing obesity: classification and epidemiology". British Medical Bulletin.
26. (2017-12-23). "Impact of Misclassification of Obesity by Body Mass Index on Mortality in Patients With CKD". Kidney International Reports.
27. "Regular Exercise: How It Can Boost Your Health".
28. "NFL Players Not at Increased Heart Risk: Study finds they showed no more signs of cardiovascular trouble than general male population".
29. (2004). "Body composition and resting metabolic rate of Japanese college Sumo wrestlers and non-athlete students: are Sumo wrestlers obese?". Anthropological Science.
30. (May 2019). "Obesity: global epidemiology and pathogenesis". Nature Reviews. Endocrinology.
31. (October 2018). "Why causality, and not prediction, should guide obesity prevention policy". The Lancet. Public Health.
32. (December 2007). "Obesity: genetic, molecular, and environmental aspects". American Journal of Medical Genetics. Part A.
33. (March 2004). "Actual causes of death in the United States, 2000". JAMA.
34. (October 1999). "Annual deaths attributable to obesity in the United States". JAMA.
35. (May 2016). "BMI and all cause mortality: systematic review and non-linear dose-response meta-analysis of 230 cohort studies with 3.74 million deaths among 30.3 million participants". BMJ.
36. (March 2009). "Body-mass index and cause-specific mortality in 900 000 adults: collaborative analyses of 57 prospective studies". Lancet.
37. (October 1999). "Body-mass index and mortality in a prospective cohort of U.S. adults". The New England Journal of Medicine.
38. (November 2008). "General and abdominal adiposity and risk of death in Europe". The New England Journal of Medicine.
39. (August 2016). "Body-mass index and all-cause mortality: individual-participant-data meta-analysis of 239 prospective studies in four continents". Lancet.
40. (June 2013). "General and abdominal obesity parameters and their combination in relation to mortality: a systematic review and meta-regression analysis". European Journal of Clinical Nutrition.
41. (January 2004). "Appropriate body-mass index for Asian populations and its implications for policy and intervention strategies". Lancet.
42. "Obesity".
43. (June 2004). "Obesity, metabolic syndrome, and cardiovascular disease". The Journal of Clinical Endocrinology and Metabolism.
44. (12 August 2021). "Obesity linked to long Covid-19, RAK hospital study finds". Khaleej Times.
45. (July 2021). "Underlying Medical Conditions and Severe Illness Among 540,667 Adults Hospitalized With COVID-19, March 2020 – March 2021". Centers for Disease Control and Prevention.
46. (2005). "Clinical obesity in adults and children: In Adults and Children". Blackwell Publishing.
47. (June 2004). "Medical consequences of obesity". The Journal of Clinical Endocrinology and Metabolism.
48. (May 2007). "Obesity, inflammation, and insulin resistance". Gastroenterology.
49. (July 2006). "Inflammation and insulin resistance". The Journal of Clinical Investigation.
50. (July 2009). "The metabolic syndrome as a risk factor for venous and arterial thrombosis". Seminars in Thrombosis and Hemostasis.
51. (March 2014). "Metabolic mediators of the effects of body-mass index, overweight, and obesity on coronary heart disease and stroke: a pooled analysis of 97 prospective cohorts with 1·8 million participants". Lancet.
52. (February 2016). "Body Mass Index, Abdominal Fatness, and Heart Failure Incidence and Mortality: A Systematic Review and Dose-Response Meta-Analysis of Prospective Studies". Circulation.
53. (February 2007). "Obesity and thrombosis". European Journal of Vascular and Endovascular Surgery.
54. (June 2007). "Obesity and the skin: skin physiology and skin manifestations of obesity". Journal of the American Academy of Dermatology.
55. (June 2006). "An overview of dermatological conditions commonly associated with the obese patient". Ostomy/Wound Management.
56. (June 2008). "Obesity in pregnancy: pre-conceptional to postpartum consequences". Journal of Obstetrics and Gynaecology Canada.
57. (July 2013). "Role of the gastroenterologist in managing obesity". [[Expert Review of Gastroenterology & Hepatology]].
58. (2007). "Meralgia paresthetica: diagnosis and management strategies". Pain Medicine.
59. (January 2008). "Obesity and chronic daily headache". Current Pain and Headache Reports.
60. (February 2008). "Assessment of body mass index and hand anthropometric measurements as independent risk factors for carpal tunnel syndrome". Folia Morphologica.
61. (May 2008). "Obesity and central obesity as risk factors for incident dementia and its subtypes: a systematic review and meta-analysis". Obesity Reviews.
62. (March 2008). "Idiopathic intracranial hypertension (pseudotumor cerebri)". Current Neurology and Neuroscience Reports.
63. (November 2009). "Body size and risk of MS in two cohorts of US women". Neurology.
64. (February 2011). "Obesity and cancer risk: recent review and evidence". Current Oncology Reports.
65. (April 2006). "The effect of obesity on chronic respiratory diseases: pathophysiology and therapeutic strategies". CMAJ.
66. (5 February 2021). "Obesity and Mortality Among Patients Diagnosed With COVID-19: A Systematic Review and Meta-Analysis". Frontiers in Medicine.
67. (December 2014). "Body mass index and the risk of gout: a systematic review and dose-response meta-analysis of prospective studies". European Journal of Nutrition.
68. (March 2009). "Overweight and health problems of the lower extremities: osteoarthritis, pain and disability". Public Health Nutrition.
69. (November 2008). "[Considerable comorbidity in overweight adults: results from the Utrecht Health Project]". Nederlands Tijdschrift voor Geneeskunde.
70. (2014). "Erectile dysfunction and central obesity: an Italian perspective". Asian Journal of Andrology.
71. (2008). "A systematic review of overweight and obesity as risk factors and targets for clinical intervention for urinary incontinence in women". Neurourology and Urodynamics.
72. (June 2006). "Obesity and risk for chronic renal failure". Journal of the American Society of Nephrology.
73. (September 2005). "Hypogonadism and metabolic syndrome: implications for testosterone therapy". The Journal of Urology.
74. (October 2009). "Management of "buried" penis in adulthood: an overview". Plastic and Reconstructive Surgery.
75. (October 2013). "Healthy obese persons: how can they be identified and do metabolic profiles stratify risk?". Current Opinion in Endocrinology, Diabetes, and Obesity.
76. (May 2020). "Metabolically Healthy Obesity". Endocrine Reviews.
77. (October 2019). "Metabolically healthy obesity: facts and fantasies". The Journal of Clinical Investigation.
78. (July 2016). "American Association of Clinical Endocrinologists and American College of Endocrinology Comprehensive Clinical Practice Guidelines for Medical Care of Patients with Obesity". Endocrine Practice.
79. (February 2014). "The prevalence of metabolic syndrome and metabolically healthy obesity in Europe: a collaborative analysis of ten large cohort studies". [[BioMed Central]] ([[Springer Nature]]).
80. (26 November 2013). "The Healthy Obese Project (HOP)". BioSHaRE Newsletter.
81. (March 2018). "Calf muscle density is independently associated with physical function in overweight and obese older adults". Hylonome Publications.
82. (October 2008). "Metabolically healthy but obese individuals". [[The Lancet]].
83. (2007). "Obesity-survival paradox-still a controversy?". Seminars in Dialysis.
84. U.S. Preventive Services Task Force. (June 2003). "Behavioral counseling in primary care to promote a healthy diet: recommendations and rationale". American Family Physician.
85. (October 2006). "The obesity paradox: fact or fiction?". The American Journal of Cardiology.
86. (August 2006). "Association of bodyweight with total mortality and with cardiovascular events in coronary artery disease: a systematic review of cohort studies". Lancet.
87. (July 2008). "Body mass index and mortality in heart failure: a meta-analysis". American Heart Journal.
88. (February 2008). "Effect of obesity on short- and long-term mortality postcoronary revascularization: a meta-analysis". Obesity.
89. (July 2006). "The obesity paradox in non-ST-segment elevation acute coronary syndromes: results from the Can Rapid risk stratification of Unstable angina patients Suppress ADverse outcomes with Early implementation of the American College of Cardiology/American Heart Association Guidelines Quality Improvement Initiative". American Heart Journal.
90. (April 2007). "2006 Canadian clinical practice guidelines on the management and prevention of obesity in adults and children [summary]". CMAJ.
91. (1995). "A satiety index of common foods". Eur J Clin Nutr.
92. (January 2004). "Poverty and obesity: the role of energy density and energy costs". The American Journal of Clinical Nutrition.
93. (2000). "Halting the obesity epidemic: a public health policy approach". Public Health Reports.
94. (March 2008). "The fundamental drivers of the obesity epidemic". Obesity Reviews.
95. Masand PS. "Weight gain associated with psychotropic drugs". ''Expert opinion on pharmacotherapy.'' 2000;1:377–389.
96. (September 2020). "Have Our Attempts to Curb Obesity Done More Harm Than Good?". Cureus.
97. (November 2006). "Putative contributors to the secular increase in obesity: exploring the roads less traveled". International Journal of Obesity.
98. (2009). "Ten Putative Contributors to the Obesity Epidemic". Critical Reviews in Food Science and Nutrition.
99. "EarthTrends: Nutrition: Calorie supply per capita".
100. (15 February 2016). "Can We Selectively Reduce Appetite for Energy-Dense Foods? An Overview of Pharmacological Strategies for Modification of Food Preference Behavior". Current Neuropharmacology.
101. "USDA: frsept99b".
102. "Diet composition and obesity among Canadian adults".
103. FAO. (2025). "World Food and Agriculture – Statistical Yearbook 2025". FAO.
104. National Control for Health Statistics. "Nutrition For Everyone". Centers for Disease Control and Prevention.
105. (March 2008). "A call for higher standards of evidence for dietary guidelines". American Journal of Preventive Medicine.
106. (October 2002). "Prevalence and trends in obesity among US adults, 1999–2000". JAMA.
107. (February 2004). "Trends in intake of energy and macronutrients—United States, 1971–2000". MMWR. Morbidity and Mortality Weekly Report.
108. (2007). "The global epidemic of obesity: an overview". Epidemiologic Reviews.
109. (June 2011). "Changes in diet and lifestyle and long-term weight gain in women and men". The New England Journal of Medicine.
110. (August 2006). "Intake of sugar-sweetened beverages and weight gain: a systematic review". The American Journal of Clinical Nutrition.
111. (January 2009). "Intake of calorically sweetened beverages and obesity". Obesity Reviews.
112. (November 2010). "Sugar-sweetened beverages and risk of metabolic syndrome and type 2 diabetes: a meta-analysis". Diabetes Care.
113. (December 2015). "Causes of Vitamin D Deficiency and Effect of Vitamin D Supplementation on Metabolic Complications in Obesity: a Review". Current Obesity Reports.
114. (November 2008). "Fast food consumption and increased caloric intake: a systematic review of a trajectory towards weight gain and obesity risk". Obesity Reviews.
115. (1999). "Agriculture Information Bulletin No. 750: America's Eating Habits: Changes and Consequences". US Department of Agriculture, Economic Research Service.
116. (22 April 2007). "You Are What You Grow". The New York Times.
117. (2005). "Clinical obesity in adults and children: In Adults and Children". Blackwell Publishing.
118. "Metabolism alone doesn't explain how thin people stay thin". The Medical Post.
119. "Obesity and overweight".
120. "WHO | Physical Inactivity: A Global Public Health Problem".
121. (February 2006). "Diet modification for treatment and prevention of obesity". Endocrine.
122. (2007). "Pediatric Fitness".
123. (June 2008). "Thirty-year trends of physical activity in relation to age, calendar time and birth cohort in Finnish adults". European Journal of Public Health.
124. (2005). "Declining rates of physical activity in the United States: what are the contributors?". Annual Review of Public Health.
125. (February 2011). "Objectively measured physical activity and fat mass in children: a bias-adjusted meta-analysis of prospective studies". PLOS ONE.
126. (April 1996). "Television viewing as a cause of increasing obesity among children in the United States, 1986–1990". Archives of Pediatrics & Adolescent Medicine.
127. (December 2000). "Time spent watching television, sleep duration and obesity in adults living in Valencia, Spain". International Journal of Obesity and Related Metabolic Disorders.
128. (July 1991). "Television viewing and obesity in adult females". American Journal of Public Health.
129. (2008). "Media + Child and Adolescent Health: A Systematic Review". Common Sense Media.
130. "Case Study: Cataplexy and SOREMPs Without Excessive Daytime Sleepiness in Prader Willi Syndrome. Is This the Beginning of Narcolepsy in a Five Year Old?". European Society of Sleep Technologists.
131. (September 2017). "The contribution of genetics and environment to obesity". British Medical Bulletin.
132. (May 2006). "Obesity and cardiovascular disease: pathophysiology, evaluation, and effect of weight loss". Arteriosclerosis, Thrombosis, and Vascular Biology.
133. (May 2008). "FTO: the first gene contributing to common forms of human obesity". Obesity Reviews.
134. (2007). "Genetic epidemiology of obesity". Epidemiologic Reviews.
135. (July 2009). "The genetic contribution to non-syndromic human obesity". Nature Reviews. Genetics.
136. (December 2006). "Genetics of obesity in humans". Endocrine Reviews.
137. (2007). "Rethinking thin: The new science of weight loss – and the myths and realities of dieting". Picador.
138. (July 2009). "The genetic contribution to non-syndromic human obesity". Nature Reviews. Genetics.
139. (January 1993). "Increased body fat mass and decreased extracellular fluid volume in adults with growth hormone deficiency". Clinical Endocrinology.
140. (2010). "Psychiatric aspects of the obesity crisis". Psychiatr Times.
141. (March 2010). "Overweight, obesity, and depression: a systematic review and meta-analysis of longitudinal studies". Archives of General Psychiatry.
142. (January 2006). "Epidemiologic and economic consequences of the global epidemics of obesity and diabetes". Nature Medicine.
143. (March 1989). "Socioeconomic status and obesity: a review of the literature". Psychological Bulletin.
144. (2007). "Socioeconomic status and obesity". Epidemiologic Reviews.
145. (2009). "The Spirit Level: Why More Equal Societies Almost Always Do Better". Allen Lane.
146. (July 2007). "The spread of obesity in a large social network over 32 years". The New England Journal of Medicine.
147. (May 2001). "Do stress reactions cause abdominal obesity and comorbidities?". Obesity Reviews.
148. (August 2003). "Impact of objective and subjective social status on obesity in a biracial cohort of adolescents". Obesity Research.
149. (November 1995). "The influence of smoking cessation on the prevalence of overweight in the United States". The New England Journal of Medicine.
150. (April 2008). "Consequences of smoking for body weight, body fat distribution, and insulin resistance". The American Journal of Clinical Nutrition.
151. (2004). "Number of children associated with obesity in middle-aged women and men: results from the health and retirement study". Journal of Women's Health.
152. (February 2008). "A birth of inactivity? A review of physical activity and parenthood". Preventive Medicine.
153. "Obesity and Overweight". [[World Health Organization]].
154. (September 2014). "Driving towards obesity: a systematized literature review on the association between motor vehicle travel time and distance and weight status in adults". Preventive Medicine.
155. (March 2017). "What Is Driving Obesity? A Review on the Connections Between Obesity and Motorized Transportation". Current Obesity Reports.
156. (March 2001). "Introduction. Symposium: Obesity in developing countries: biological and ecological factors". The Journal of Nutrition.
157. (April 2008). "Gut microbiota and its possible relationship with obesity". Mayo Clinic Proceedings.
158. (2018). "Antibiotics: repeated treatments before the age of two could be a factor in obesity". Prescrire International.
159. (July 2006). "Obesity and infection". The Lancet. Infectious Diseases.
160. (May 2008). "Meta-analysis of short sleep duration and obesity in children and adults". Sleep.
161. (April 2018). "Sleep duration and incidence of obesity in infants, children, and adolescents: a systematic review and meta-analysis of prospective studies". Sleep.
162. (May 2011). "Obesity and short sleep: unlikely bedfellows?". Obesity Reviews.
163. (January 2015). "Personality traits and obesity: a systematic review". Obesity Reviews.
164. (May 2006). "A comparison of health behaviours in lonely and non-lonely populations". Psychology, Health & Medicine.
165. (April 2013). "Association of personality with the development and persistence of obesity: a meta-analysis based on individual-participant data". Obesity Reviews.
166. (July 2019). "Trade openness and the obesity epidemic: a cross-national study of 175 countries during 1975-2016". Annals of Epidemiology.
167. (2017). "Obesity Pathogenesis: An Endocrine Society Scientific Statement.". Endocr Rev.
168. (January 2004). "Obesity wars: molecular progress confronts an expanding epidemic". Cell.
169. (December 1994). "Positional cloning of the mouse obese gene and its human homologue". Nature.
170. (2003). "Medical physiology: A cellular and molecular approach". Saunders.
171. (June 2014). "2013 AHA/ACC/TOS guideline for the management of overweight and obesity in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and The Obesity Society". Circulation.
172. (2017). "2015–2020 Dietary Guidelines for Americans - health.gov". Skyhorse Publishing Inc..
173. (September 2019). "2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines". Circulation.
174. (January 2006). "Diet in the management of weight loss". CMAJ.
175. (April 1998). "Persons successful at long-term weight loss and maintenance continue to consume a low-energy, low-fat diet". Journal of the American Dietetic Association.
176. (April 2007). "Long-term weight losses associated with prescription of higher physical activity goals. Are higher levels of physical activity protective against weight regain?". The American Journal of Clinical Nutrition.
177. (January 2014). "Weight-loss maintenance for 10 years in the National Weight Control Registry". American Journal of Preventive Medicine.
178. (March 2019). "Dietary modifications for weight loss and weight loss maintenance". Metabolism.
179. (September 2018). "Behavioral Weight Loss Interventions to Prevent Obesity-Related Morbidity and Mortality in Adults: US Preventive Services Task Force Recommendation Statement". JAMA.
180. (July 2017). "Strategies to Improve Adherence to Dietary Weight Loss Interventions in Research and Real-World Settings". Behavioral Sciences.
181. [[Swedish Agency for Health Technology Assessment and Assessment of Social Services]] (SBU). (1987). "Dietary treatment of obesity". Annals of the New York Academy of Sciences.
182. (September 2014). "Comparison of weight loss among named diet programs in overweight and obese adults: a meta-analysis". JAMA.
183. (2014). "Low carbohydrate versus isoenergetic balanced diets for reducing weight and cardiovascular risk: a systematic review and meta-analysis". PLOS ONE.
184. (July 2005). "Long-term weight loss maintenance". The American Journal of Clinical Nutrition.
185. (May 2012). "Effects of interventions in pregnancy on maternal weight and obstetric outcomes: meta-analysis of randomised evidence". BMJ.
186. (October 2014). "Behavioral counseling to promote a healthful diet and physical activity for cardiovascular disease prevention in adults with cardiovascular risk factors: U.S. Preventive Services Task Force Recommendation Statement". Annals of Internal Medicine.
187. FAO. (2025). "World Food and Agriculture – Statistical Yearbook 2025". FAO.
188. FAO. (2025). "World Food and Agriculture – Statistical Yearbook 2025". FAO.
189. Satcher D. (2001). "The Surgeon General's Call to Action to Prevent and Decrease Overweight and Obesity". U.S. Dept. of Health and Human Services, Public Health Service, Office of Surgeon General.
190. (18 July 2007). "Limiting Ads of Junk Food to Children". The New York Times.
191. "Fewer Sugary Drinks Key to Weight Loss".
192. "WHO urges global action to curtail consumption and health impacts of sugary drinks".
193. (December 2006). "Indicators of activity-friendly communities: an evidence-based consensus process". American Journal of Preventive Medicine.
194. (2017-11-14). "Food Swamps Predict Obesity Rates Better Than Food Deserts in the United States". International Journal of Environmental Research and Public Health.
195. (May 2019). "Mass media to communicate public health messages in six health topic areas: a systematic review and other reviews of the evidence". Public Health Research.
196. (February 2018). "Nutritional labelling for healthier food or non-alcoholic drink purchasing and consumption". The Cochrane Database of Systematic Reviews.
197. (June 2022). "Regulating the Food Industry: An Aspirational Agenda". American Journal of Public Health.
198. (2023-04-20). "How did ultra-processed foods take over, and what are they doing to us?". the Guardian.
199. (November 2016). "Post-marketing withdrawal of anti-obesity medicinal products because of adverse drug reactions: a systematic review". BMC Medicine.
200. (28 November 2023). "Obesity Management in Adults: A Review". JAMA.
201. (2025-10-02). "A systematic review and meta-analysis of the efficacy and safety of pharmacological treatments for obesity in adults". Nature Medicine.
202. (2025-05-28). "Weight Regain After Liraglutide, Semaglutide or Tirzepatide Interruption: A Narrative Review of Randomized Studies". Journal of Clinical Medicine.
203. (October 2019). "Fluoxetine for adults who are overweight or obese". The Cochrane Database of Systematic Reviews.
204. (15 June 2016). "Metformin for Clozapine Associated Obesity: A Systematic Review and Meta-Analysis". PLOS ONE.
205. (January 2017). "Mechanisms, Pathophysiology, and Management of Obesity". The New England Journal of Medicine.
206. (March 2014). "The effectiveness and risks of bariatric surgery: an updated systematic review and meta-analysis, 2003–2012". JAMA Surgery.
207. (19 August 2020). "Effects of Diet versus Gastric Bypass on Metabolic Function in Diabetes". New England Journal of Medicine.
208. (August 2007). "Effects of bariatric surgery on mortality in Swedish obese subjects". The New England Journal of Medicine.
209. (2018). "The Double Burden of Malnutrition in Countries Passing through the Economic Transition". Ann Nutr Metab.
210. "Obesity and overweight".
211. FAO, IFAD, UNICEF, WFP and WHO. 2017.The State of Food Security and Nutrition in the World 2017. Building resilience for peace and food security. Rome, FAO
212. "Obesity and overweight".
213. (October 2017). "Prevalence of Obesity Among Adults and Youth: United States, 2015–2016". NCHS Data Brief.
214. World Health Organization. (2000). "Obesity: preventing and managing the global epidemic". World Health Organization.
215. (March 2008). "Severe obesity: Investigating the socio-demographics within the extremes of body mass index". Obesity Research & Clinical Practice.
216. Tjepkema M. (6 July 2005). "Nutrition: Findings from the Canadian Community Health Survey". Statistics Canada.
217. "Obesity Update 2017". Organisation for Economic Co-operation and Development.
218. (April 2008). "Management of obesity in adults: European clinical practice guidelines". Obesity Facts.
219. (4 March 2025). "Over 50% of adults worldwide predicted to be obese or overweight by 2050". BBC News.
220. (May 2014). "Systematic reviews of and integrated report on the quantitative, qualitative and economic evidence base for the management of obesity in men". Health Technology Assessment.
221. (10 May 2016). "Managing obesity in men".
222. "Online Etymology Dictionary: Obesity".
223. "Obesity, n".
224. (November 2003). "Prevention of obesity and diabetes". Diabetes Care.
225. (March 2007). "Obesity: a medical history". Obesity Reviews.
226. (2006). "Adipose Tissue And Adipokines in Health And Disease (Nutrition and Health)". Humana Press.
227. (2008). "Encyclopedia of Obesity". Sage Publications, Inc.
228. (December 2001). "Bias, discrimination, and obesity". Obesity Research.
229. (2000). "Is Miss America an undernourished role model?". JAMA.
230. (July 2008). "Changing perceptions of weight in Great Britain: comparison of two population surveys". BMJ.
231. (2005). "Clinical obesity in adults and children: In Adults and Children". Blackwell Publishing.
232. (March 2009). "Obesity and labour market success in Finland: the difference between having a high BMI and being fat". Economics and Human Biology.
233. (January 2012). "The medical care costs of obesity: an instrumental variables approach". Journal of Health Economics.
234. (1 January 2003). "National medical spending attributable to overweight and obesity: How much, and who's paying". Health Affairs.
235. (22 May 2007). "Obesity and overweight: Economic consequences". [[Centers for Disease Control and Prevention]].
236. (March 2010). "The cost of overweight and obesity in Australia". The Medical Journal of Australia.
237. (5 February 2003). "The diet business: Banking on failure". BBC News.
238. (27 January 2019). "Public health experts call for global food treaty". Financial Times.
239. (February 2008). "Lifetime medical costs of obesity: prevention no cure for increasing health expenditure". PLOS Medicine.
240. (2007). "Bariatric furniture: Considerations for use". Int J Ther Rehabil.
241. (January 2009). "Obesity status and sick leave: a systematic review". Obesity Reviews.
242. (April 2007). "Obesity and workers' compensation: results from the Duke Health and Safety Surveillance System". Archives of Internal Medicine.
243. "Alabama "Obesity Penalty" Stirs Debate".
244. (24 October 2002). "Why Airlines Can't Cut The Fat".
245. (October 2004). "Economic and environmental costs of obesity: the impact on airlines". American Journal of Preventive Medicine.
246. (2 July 2009). "Who Should Pay for Obese Health Care?". ABC News.
247. "109th U.S. Congress (2005–2006) H.R. 554: 109th U.S. Congress (2005–2006) H.R. 554: Personal Responsibility in Food Consumption Act of 2005". GovTrack.us.
248. (20 June 2013). "A changing battlefield in the fight against fat". The Washington Post.
249. (18 December 2014). "Obesity can be deemed a disability at work – EU court". Reuters.
250. (2023). "Worth Your Weight: Experimental Evidence on the Benefits of Obesity in Low-Income Countries". American Economic Review.
251. (January 31, 2022). "Fat Shaming im Netz: Ricarda Lang, die Angegriffene".
252. "What is NAAFA".
253. "ISAA Mission Statement".
254. (2007). "An Imperfect Fit: Obesity, Public Health, and Disability Anti-Discrimination Law". Social Science Electronic Publishing.
255. (March 1999). "The weight dilemma: a range of philosophical perspectives". International Journal of Obesity and Related Metabolic Disorders.
256. National Association to Advance Fat Acceptance. (2008). "We come in all sizes". NAAFA.
257. "International Size Acceptance Association – ISAA".
258. (9 August 2015). "Coca-Cola Funds Scientists Who Shift Blame for Obesity Away From Bad Diets". The New York Times.
259. (November 2016). "Food Industry Funding of Nutrition Research: The Relevance of History for Current Debates". JAMA Internal Medicine.
260. ((National Heart, Lung, and Blood Institute)). (1998). "Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults". International Medical Publishing, Inc.
261. (11 February 2004). "Storing up problems; the medical case for a slimmer nation". Royal College of Physicians.
262. Great Britain Parliament House of Commons Health Committee. (May 2004). "Obesity – Volume 1 – HCP 23-I, Third Report of session 2003–04. Report, together with formal minutes". TSO (The Stationery Office).
263. (2006). "Obesity: guidance on the prevention, identification, assessment and management of overweight and obesity in adults and children". [[National Health Services]] (NHS).
264. (2007). "Our Future Health Secured? A review of NHS funding and performance". The King's Fund.
265. (19 May 2022). "How can local authorities reduce obesity? Insights from NIHR research". National Institute for Health and Care Research.
266. (January 2009). "Obesity Policy Action framework and analysis grids for a comprehensive policy approach to reducing obesity". Obesity Reviews.
267. "Healthy Weight: Assessing Your Weight: BMI: About BMI for Children and Teens". [[Center for disease control and prevention]].
268. (June 2001). "Prevalence of overweight in US children: comparison of US growth charts from the Centers for Disease Control and Prevention with other reference values for body mass index". The American Journal of Clinical Nutrition.
269. (February 2005). "Childhood obesity". British Journal of Perioperative Nursing.
270. (January 2008). "Confronting Childhood Obesity". The Annals of the American Academy of Political and Social Science.
271. (December 2005). "Evidence for secular trends in children's physical activity behaviour". British Journal of Sports Medicine.
272. (April 2019). "The effect of screen advertising on children's dietary intake: A systematic review and meta-analysis". Obesity Reviews.
273. (March 2015). "Antibiotics in early life and obesity". Nature Reviews. Endocrinology.
274. (September 2012). "Effectiveness of intervention on physical activity of children: systematic review and meta-analysis of controlled trials with objectively measured outcomes (EarlyBird 54)". BMJ.
275. (February 2006). "Reducing obesity and related chronic disease risk in children and youth: a synthesis of evidence with 'best practice' recommendations". Obesity Reviews.
276. (October 2016). "Brief Primary Care Obesity Interventions: A Meta-analysis". Pediatrics.
277. (June 2017). "Diet, physical activity and behavioural interventions for the treatment of overweight or obese children from the age of 6 to 11 years". The Cochrane Database of Systematic Reviews.
278. CDC. (2025-03-25). "Adult Obesity Facts".
279. (2020-06-26). "Products - Data Briefs - Number 360 - February 2020".
280. (2006). "Prevalence and Risk Factors for Obesity in Adult Dogs from Private US Veterinary Practices". Intern J Appl Res Vet Med.
281. (May 2005). "Prevalence of obesity in dogs examined by Australian veterinary practices and the risk factors involved". The Veterinary Record.
282. (January 2010). "Overweight in dogs, but not in cats, is related to overweight in their owners". Public Health Nutrition.