Obesity is a chronic, relapsing, progressive disease characterised by excess or dysfunctional adipose tissue that impairs health. It is not a behavioural failing and it is not defined by appearance. Excess adiposity acts through mechanical loading, ectopic lipid deposition, chronic low-grade inflammation and altered adipokine and incretin signalling to increase the risk of type 2 diabetes mellitus, hypertension, dyslipidemia, coronary artery disease, heart failure with preserved ejection fraction, obstructive sleep apnea, metabolic dysfunction-associated steatotic liver disease, chronic kidney disease, osteoarthritis and at least a dozen cancers.

Historically obesity was defined by body mass index alone. Contemporary frameworks retain BMI as a screening tool but no longer accept it as a diagnosis on its own, because BMI cannot distinguish fat mass from lean mass, cannot localise adiposity, and performs differently across ancestries. Current practice therefore combines BMI with a confirmatory measure of adiposity such as waist circumference or waist-to-height ratio, followed by clinical staging that separates people who already have organ dysfunction attributable to adiposity from those who carry excess adiposity with preserved organ function. This distinction, expressed as clinical versus preclinical obesity, determines both the urgency and the intensity of treatment.

Management is complication-centric rather than weight-centric. Structured lifestyle intervention remains the foundation and is sufficient for some patients, but the therapeutic landscape has changed fundamentally with the incretin-based agents. Semaglutide and tirzepatide now produce mean weight reductions in the range historically achievable only with surgery, and, more importantly, have demonstrated benefit on hard outcomes including major adverse cardiovascular events, heart failure symptoms, sleep apnoea severity, kidney endpoints and liver histology. Oral small-molecule and combination amylin-based agents have entered practice. Metabolic and bariatric surgery remains the most durable intervention and is associated with substantially longer life expectancy, particularly in patients with type 2 diabetes mellitus.

The single most important principle for the clinician is chronicity. Weight regain after discontinuation of pharmacotherapy is the rule rather than the exception, and randomised evidence now supports continued therapy, with dose reduction as an intermediate option, rather than treatment cessation once a weight target is reached. Weight bias and stigma are themselves barriers to care and should be addressed explicitly in the clinical encounter.

• Depictions of obesity appear in Palaeolithic figurines, and physicians from Hippocrates onward recorded associations between corpulence, sudden death and infertility.
• For most of recorded history, adiposity signalled prosperity in food-scarce societies. The epidemiological reversal, in which obesity became concentrated in lower socioeconomic groups in high-income countries, is a twentieth century phenomenon.
• The body mass index derives from the Quetelet index described in the nineteenth century as a population statistic, not as a clinical diagnostic instrument. Its later adoption as a diagnostic threshold is the source of much of the current controversy about its use.
• Life insurance actuarial tables in the early twentieth century provided the first large-scale quantitative link between excess weight and mortality.
• The Swedish Obese Subjects study, initiated in 1987, was the first large prospective controlled study to demonstrate that surgically induced weight loss reduces mortality.^[1]
• The Diabetes Prevention Program established in 2002 that modest weight loss achieved by intensive lifestyle intervention prevents progression to type 2 diabetes mellitus.^[2]
• Recognition of obesity as a disease by major medical bodies, and the arrival of incretin-based pharmacotherapy in the 2020s, shifted obesity care from a behavioural counselling model to a chronic disease management model.
• In 2025 an international commission proposed formal diagnostic criteria separating clinical obesity, in which excess adiposity has caused organ or tissue dysfunction, from preclinical obesity, in which it has not.^[3]

Historical Perspective

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]

Contemporary Culture

In modern Western culture, the obese body shape is widely regarded as unattractive and many negative stereotypes are commonly associated with obese people. Obese children, teenagers and adults can also face a heavy social stigma. Obese children are frequently the targets of bullies and are often shunned by their peers. Although obesity rates are rising amongst all social classes in the West, obesity is often seen as a sign of lower socio-economic status.^[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]

Popular Culture

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

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

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

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

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

References

1. ↑ The Oxford English Dictionary (website)
2. ↑ Powdermaker H. “An anthropological approach to the problem of obesity.” In: Food and Culture: A Reader. Ed. Carole Counihan and Penny van Esterik. New York: Routledge, 1997;206. ISBN 0-415-91710-7.
3. ↑ Greg Critser, Fat Land. Houghton Mifflin, NY, 2003. ISBN 0-14101-540-3.
4. ↑ Phillips, Stone (2006-08-18). “Who’s to blame for the U.S. obesity epidemic?”. MSNBC. Retrieved 2007-06-03.
5. ↑ Paul Campos, The Diet Myth. Gotham Books, NY, 2004. ISBN 1-59240-135-X.
6. ↑ Centers for Disease Control and Prevention, National Center for Health Statistics, Fast Facts A to Z. Available at: http://www.cdc.gov/nchs/fastats/overwt.htm . Accessed July 15, 2007
7. ↑ 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 The Surgeon General; Washington, D.C. Available at: http://www.surgeongeneral.gov/topics/obesity/calltoaction/CalltoAction.pdf. Accessed July 12, 2007

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

Body mass index is calculated as weight in kilograms divided by the square of height in metres. It remains the recommended initial screening measure but should be confirmed by a measure of central adiposity before a diagnosis is assigned.^[4]

Ancestry matters. Because visceral adiposity and cardiometabolic risk occur at lower BMI values in several populations, particularly individuals of Asian ancestry, current standards recommend race- and ethnicity-specific BMI thresholds supplemented by waist-based measures rather than a single universal cutoff.^[4] Applying uncorrected European-derived thresholds systematically underdiagnoses obesity in these groups.

Waist circumference thresholds are those of the joint cardiovascular society guideline and should be interpreted with ancestry-specific adjustment.^[5]

This framework was proposed to prevent both overdiagnosis in people with high BMI and preserved health, and underdiagnosis in people with organ dysfunction from adiposity at BMI values below conventional thresholds.^[3]

• The Edmonton Obesity Staging System grades patients from stage 0 (no apparent risk factors, physical symptoms or functional limitation) through stage 4 (severe, potentially end-stage disability from obesity-related comorbidity), and predicts mortality more accurately than BMI alone.^[6]
• The European framework stages obesity by aetiology, degree of adiposity and associated complications, and formally incorporates psychological and functional domains.^[7]
• Adiposity-based chronic disease (ABCD) is a complication-centric nomenclature that classifies patients by the presence and severity of adiposity-related complications rather than by BMI, and directs the intensity of therapy accordingly.^[8]
• Sarcopenic obesity, the coexistence of excess adiposity with low skeletal muscle mass and function, is a distinct entity diagnosed by screening, then assessment of muscle function, then body composition, and is staged I or II according to the presence of complications.^[9]

• Body weight is defended by a hypothalamic control system rather than set by conscious choice. Peripheral signals of energy status, including leptin from adipocytes, insulin from the pancreas, and gut-derived peptides such as glucagon-like peptide-1, glucose-dependent insulinotropic polypeptide, amylin and ghrelin, converge on the arcuate nucleus and the melanocortin pathway.^[10]
• Most obesity is associated with leptin resistance rather than leptin deficiency, which is why exogenous leptin is ineffective except in the rare monogenic deficiency states.^[10]
• The pharmacological efficacy of incretin receptor agonists derives from engagement of these same central circuits, which is the mechanistic reason they achieve weight loss that behavioural intervention alone cannot.

• After weight loss, circulating levels of appetite-regulating hormones shift in a direction that favours weight regain, and these changes persist for at least one year after the intervention ends.^[11]
• Resting metabolic rate falls disproportionately to the loss of lean mass, and this metabolic adaptation can persist for years after substantial weight loss.^[12]
• These two observations together explain why obesity behaves as a relapsing disease and provide the physiological rationale for indefinite rather than time-limited therapy.

• Common obesity is highly polygenic. Genome-wide association studies have identified numerous loci influencing BMI, with strong enrichment for genes expressed in the central nervous system rather than in adipose tissue, reinforcing the neurobehavioural basis of energy balance.^[13]
• Monogenic obesity results from disruption of the leptin-melanocortin pathway, including biallelic variants in LEP, LEPR, POMC and PCSK1, and heterozygous MC4R variants, the commonest monogenic cause.^[14]
• Identification of these variants is clinically actionable, because melanocortin-4 receptor agonism produces substantial weight reduction in affected individuals.^[15]

• Adipose tissue functions as an endocrine organ. With expansion it becomes hypoxic and infiltrated by macrophages, producing a low-grade inflammatory state with elevated interleukin-6 and C-reactive protein and reduced adiponectin.
• Once subcutaneous storage capacity is exceeded, lipid is deposited ectopically in liver, skeletal muscle, pancreas, epicardium and kidney, producing insulin resistance, metabolic dysfunction-associated steatotic liver disease and myocardial remodelling.
• These pathways are pharmacologically reversible. In a randomised biomarker analysis, tirzepatide reduced high-sensitivity C-reactive protein by 54.6%, interleukin-6 by 30.2%, leptin by 61.4% and plasminogen activator inhibitor-1 antigen by 44.3%, and increased adiponectin by 47.7% at the 15 mg dose over 72 weeks.^[16]

Pathophysiology

Lifestyle

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

Genetics

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

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

Medical Illness

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

Medical illnesses that increase obesity risk include several rare congenital syndromes (listed above), hypothyroidism, Cushing’s syndrome, growth hormone deficiency.^[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).

Neurobiological Mechanisms

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.

Impaired Brain Response to Nutrients in Obese Individuals: A Link to Compulsive Eating behavior

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.

Microbiological Aspects

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

Social Determinants

Some obesity co-factors are resistant to the theory that the “epidemic” is a new phenomenon. In particular, a class co-factor consistently appears across many studies. Comparing net worth with BMI scores, a 2004 study^[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]

Environmental Factors

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

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

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

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

References

1. ↑ Sara Bleich, David Cutler, Christopher Murray, Alyce Adams. Why is the Developed World Obese? National Bureau of Economic Research Working Paper No. 12954. Issued in March 2007.
2. ↑ Centers for Disease Control and Prevention. Nutrition For Everyone. National Control for Health Statistics. Accessed July 15, 2007.
3. ↑ Lin BH, Guthrie J and Frazao E (1999). “Nutrient contribution of food away from home”. In: Frazao E (Ed). America’s Eating Habits: Changes and Consequences. Agriculture Information Bulletin No. 750, US Department of Agriculture, Economic Research Service, Washington, DC, pp. 213–239. Fulltext index.
4. ↑ http://politics.guardian.co.uk/publicservices/story/0,,2147839,00.html
5. ↑ Frayling TM, Timpson NJ, Weedon MN; et al. (2007). “A common variant in the FTO gene is associated with body mass index and predisposes to childhood and adult obesity”. Science. 316 (5826): 889–94. doi:10.1126/science.1141634. PMID 17434869.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
6. ↑ Chakravarthy MV, Booth FW (2004). “Eating, exercise, and “thrifty” genotypes: connecting the dots toward an evolutionary understanding of modern chronic diseases”. J. Appl. Physiol. 96 (1): 3–10. doi:10.1152/japplphysiol.00757.2003. PMID 14660491.
7. ↑ Rosén T, Bosaeus I, Tölli J, Lindstedt G, Bengtsson BA (1993). “Increased body fat mass and decreased extracellular fluid volume in adults with growth hormone deficiency”. Clin. Endocrinol. (Oxf). 38 (1): 63–71. PMID 8435887.CS1 maint: Multiple names: authors list (link)
8. ↑ ^{8.0 8.1 8.2} Flier JS (2004). “Obesity wars: molecular progress confronts an expanding epidemic”. Cell. 116 (2): 337–50. PMID 14744442.
9. ↑ Boulpaep, Emile L.; Boron, Walter F. (2003). Medical physiology: a cellular and molecular approach. Philadelphia: Saunders. ISBN 0-7216-3256-4.CS1 maint: Multiple names: authors list (link)
10. ↑ Cota, D. et al. (2006) Cannabinoids, opioids and eating behavior: the molecular face of hedonism? Brain Res. Rev. 51, 85–107
11. ↑ Atkinson, T. (2008) Central and peripheral neuroendocrine peptides and signalling in appetite regulation: considerations for obesity pharmacotherapy. Obes. Rev. 9, 108–120
12. ↑ Cason, A.M. et al. (2010) Role of orexin/hypocretin in reward-seeking and addiction: implications for obesity. Physiol. Behav. 100, 419– 428
13. ↑  Wise, R. (2006) Role of brain dopamine in food reward and reinforcement. Philos. Trans. R. Soc. Lond. B. Biol. Sci. 361, 1149– 1158
14. ↑ Wang, G.J.; Volkow, N.D.; Thanos, P.K.; Fowler, J.S. Imaging of brain dopamine pathways: Implications for understanding obesity. J. Addict. Med. 2009, 3, 8–18.
15. ↑ Abizaid, A.; Liu, Z.W.; Andrews, Z.B.; Shanabrough, M.; Borok, E.; Elsworth, J.D.; Roth, R.H.; Sleeman, M.W.; Picciotto, M.R.; Tschop, M.H.; et al. Ghrelin modulates the activity and synaptic input organization of midbrain dopamine neurons while promoting appetite. J. Clin. Investig. 2006, 116, 3229–3239.
16. ↑  Wise, R. (2006) Role of brain dopamine in food reward and reinforcement. Philos. Trans. R. Soc. Lond. B. Biol. Sci. 361, 1149– 1158
17. ↑ Rothemund, Y.; Preuschhof, C.; Bohner, G.; Bauknecht, H.C.; Klingebiel, R.; Flor, H.; Klapp, B.F. Differential activation of the dorsal striatum by high-calorie visual food stimuli in obese individuals. Neuroimage 2007, 37, 410–421.
18. ↑ Tang-Christensen, M.; Vrang, N.; Larsen, P.J. Glucagon-like peptide containing pathways in the regulation of feeding behaviour. Int. J. Obes. Relat. Metab. Disord. 2001, 25, S42–S47.
19. ↑ Steele, K.E.; Prokopowicz, G.P.; Schweitzer, M.A.; Magunsuon, T.H.; Lidor, A.O.; Kuwabawa, H.; Kumar, A.; Brasic, J.; Wong, D.F. Alterations of central dopamine receptors before and after gastric bypass surgery. Obes. Surg. 2010, 20, 369–374.
20. ↑ Geiger, B.M. et al. (2009) Deficits of mesolimbic dopamine neurotransmission in rat dietary obesity. Neuroscience 159, 1193– 1199
21. ↑ Lenard, N.R.; Berthoud, H.R. Central and peripheral regulation of food intake and physical activity: Pathways and genes. Obesity (Silver Spring) 2008, 16, S11–S22.
22. ↑ Arora, S.; Anubhut. Role of neuropeptides in appetite regulation and obesity—A review. Neuropeptides 2006, 40, 375–401.
23. ↑ Volkow, N.D.; Wang, G.J.; Fowler, J.S.; Telang, F. Overlapping neuronal circuits in addiction and obesity: Evidence of systems pathology. Philos. Trans. R. Soc. Lond. B Biol. Sci. 2008, 363, 3191–3200.
24. ↑ McFarland, K.; Ettenberg, A. Haloperidol does not affect motivational processes in an operant runway model of food-seeking behavior. Behav. Neurosci. 1998, 112, 630–635.
25. ↑ Wang, G.J.; Volkow, N.D.; Logan, J.; Pappas, N.R.; Wong, C.T.; Zhu, W.; Netusil, N.; Fowler, J.S. Brain dopamine and obesity. Lancet 2001, 357, 354–357.
26. ↑ Haltia, L.T.; Rinne, J.O.; Merisaari, H.; Maguire, R.P.; Savontaus, E.; Helin, S.; Nagren, K.; Kaasinen, V. Effects of intravenous glucose on dopaminergic function in the human brain in vivo. Synapse 2007, 61, 748–756.
27. ↑ Restaino, L.; Frampton, E.W.; Turner, K.M.; Allison, D.R. A chromogenic plating medium for isolating Escherichia coli O157:H7 from beef. Lett. Appl. Microbiol. 1999, 29, 26–30.
28. ↑ Ley RE, Turnbaugh PJ, Klein S, Gordon JI (2006). “Microbial ecology: human gut microbes associated with obesity”. Nature. 444 (7122): 1022–3. doi:10.1038/4441022a. PMID 17183309.CS1 maint: Multiple names: authors list (link)
29. ↑ Zagorsky JL. Is Obesity as Dangerous to Your Wealth as to Your Health? Res Aging 2004;26:130-152. PDF fulltext.doi:10.1177/0164027503258519.
30. ↑ Christakis NA, Fowler JH (2007). “The Spread of Obesity in a Large Social Network over 32 Years”. 357 (4): 370–379. doi:10.1056/NEJMsa066082. PMID 17652652.
31. ↑ Levine JA, Lanningham-Foster LM, McCrady SK, Krizan AC, Olson LR, Kane PH, Jensen MD, Clark MM (2005). “Interindividual variation in posture allocation: possible role in human obesity”. Science. 307 (5709): 584–6. PMID 15681386 doi:10.1126/science.1106561.CS1 maint: Multiple names: authors list (link)
32. ↑ Pollan, Michael (April 22, 2007). “You Are What You Grow”. New York Times. Retrieved 2007-07-30.
33. ↑ Brian Wansink and Mike Huckabee (2005), “De-Marketing Obesity,” California Management Review, 47:4 (Summer), 6-18.
34. ↑ Lopez R (2004). “Urban sprawl and risk for being overweight or obese”. Am J Public Health. 94 (9): 1574–9. PMID 15333317.

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

• Chronic positive energy balance operating on a susceptible polygenic background
• Obesogenic food environment, in particular the availability of energy-dense ultra-processed foods. In an inpatient randomised crossover trial with diets matched for presented macronutrients, sugar, sodium and fibre, an ultra-processed diet led to greater ad libitum energy intake and weight gain than an unprocessed diet^[17]
• Sedentary occupational and transport patterns
• Short or disrupted sleep and circadian misalignment including shift work
• Psychosocial stress, socioeconomic deprivation and food insecurity

Medication review is a mandatory part of the obesity assessment. A meta-analysis of 257 randomised trials covering 54 drugs and 84,696 patients quantified the effect of commonly prescribed agents on body weight.^[18]

Where a weight-inducing medication cannot be substituted, obesity pharmacotherapy remains effective. In a post hoc analysis of three randomised trials, approximately one fifth of participants used at least one weight-inducing medication concurrently and achieved weight reduction comparable to the primary trial results.^[19]

• Hypothyroidism
• Cushing’s syndrome
• Polycystic ovary syndrome
• Growth hormone deficiency
• Insulinoma
• Hypothalamic obesity following craniopharyngioma, cranial irradiation, traumatic brain injury or hypothalamic surgery
• Monogenic obesity of the leptin-melanocortin pathway^[14]
• Syndromic obesity including Prader-Willi syndrome and Bardet-Biedl syndrome

Primary obesity is a diagnosis reached after excess adiposity is confirmed and secondary causes have been considered. Secondary causes are uncommon but are disproportionately important because several are specifically treatable. Features suggesting a secondary cause include very early onset, rapid or discordant weight gain, hyperphagia out of proportion to context, disproportionate central fat distribution, developmental delay, hypogonadism, or dysmorphic features.^[4][8]

• A pooled analysis of 3663 population-based studies documented rising obesity prevalence in most countries between 1990 and 2022, with the global burden shifting from a predominance of underweight to a predominance of obesity in most regions.^[20]
• Global burden analyses estimate that more than two billion adults were living with overweight or obesity in 2021, with continued increases forecast through 2050 in the absence of major policy change.^[21]
• Child and adolescent overweight and obesity are projected to rise in parallel, with important implications for the future adult disease burden.^[22]

• During August 2021 to August 2023 the prevalence of obesity among adults aged 20 and over was 40.3%, with a prevalence of 39.2% in men and 41.3% in women and no significant difference between sexes.^[23]
• The prevalence of severe obesity was 9.4%, and was higher in women than in men in each age group.^[23]
• Over the preceding decade the age-adjusted prevalence of obesity did not change significantly, whereas the age-adjusted prevalence of severe obesity increased from 7.7% to 9.7%.^[23]
• Age-adjusted estimates for August 2021 to August 2023 were 40.3% for obesity, 9.7% for severe obesity and 31.7% for overweight, giving a combined overweight and obesity prevalence of 72.4%.^[24]
• Among children and adolescents aged 2 to 19 years, obesity prevalence was 21.1% and severe obesity 7%.^[24]
• Modelling studies had projected that severe obesity would become the most common BMI category in several population subgroups, a projection consistent with the observed rise in severe obesity despite the plateau in overall obesity prevalence.^[25]

Note for editors: the figure of 42.4%, derived from the 2017 to 2018 survey cycle, is frequently quoted but has been superseded by the estimates above.

• Family history of obesity and polygenic susceptibility^[13]
• Early-onset obesity in childhood or adolescence
• Female sex for severe obesity specifically^[23]
• Lower educational attainment and socioeconomic deprivation^[23]
• Ultra-processed dietary pattern^[17]
• Physical inactivity and prolonged sedentary time
• Short sleep duration, obstructive sleep apnea and shift work
• Weight-inducing medications^[18]
• Pregnancy with excessive gestational weight gain and postpartum weight retention
• Menopause and age-related decline in lean mass
• Smoking cessation
• Psychiatric illness, chronic stress and adverse childhood experiences
• Weight stigma, which is independently associated with disordered eating, avoidance of health care and worse metabolic outcomes^[26]

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

• Screen for excess adiposity at least annually in adults using BMI, and monitor for consistent increases in weight over time so that early intervention can prevent progression.^[4]
• Confirm an abnormal BMI with a measure of central adiposity before assigning a diagnosis, using ancestry-appropriate thresholds.^[4]
• Perform a comprehensive clinical evaluation including risk stratification and staging in all adults diagnosed with overweight or obesity.^[4]
• Offer or refer adults with BMI 30 kg/m² or greater to intensive, multicomponent behavioural interventions. This is a grade B recommendation of the United States Preventive Services Task Force.^[27]
• Measure weight and height with privacy and with equipment appropriate to body size, and seek permission before discussing weight. Anthropometric measurement is a recognised source of stigmatisation.^[26]

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]

• Untreated obesity is typically progressive, with weight gain continuing through middle age before plateauing or falling in late life.
• Weight loss achieved by any modality provokes counter-regulatory hormonal and metabolic adaptations that promote regain, so that the untreated natural history after successful weight loss is one of relapse.^[11][12]
• Complication burden accumulates with duration as well as with degree of adiposity, which is why early-onset obesity carries disproportionate lifetime risk.

• All-cause mortality is lowest at a BMI of approximately 20.0 to 25.0 kg/m² and rises progressively above that range, in an individual-participant analysis of 239 prospective studies.^[30]
• In a collaborative analysis of 57 prospective studies involving 900,000 adults, median survival was reduced by two to four years at BMI 30 to 35 kg/m² and by eight to ten years at BMI 40 to 45 kg/m² compared with the reference range.^[31]
• Prognosis is determined more accurately by functional and complication-based staging than by BMI alone.^[6]
• Prognosis is modifiable. Sustained weight reduction of 5% or more improves several cardiometabolic parameters, and reduction of 10% or more is required to modify many obesity-related complications.^[32]

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

History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | Chest X Ray | CT | MRI | Echocardiography or Ultrasound | Other Imaging Findings | Other Diagnostic Studies

• Weight trajectory including age of onset, maximum and minimum adult weight, and periods of rapid change
• Structured medication review for weight-inducing agents^[18]
• Dietary pattern, meal timing, eating behaviour and symptoms suggesting binge eating
• Physical activity, occupational activity and functional limitation
• Sleep duration, snoring, witnessed apnoea and daytime somnolence
• Symptoms of secondary causes including cold intolerance, proximal weakness, easy bruising, menstrual irregularity, visual disturbance and headache
• Reproductive history, gestational weight gain and gestational diabetes
• Previous weight management interventions, response and reasons for discontinuation
• Psychosocial history including mood, stress, food security and experience of weight stigma

• Height, weight, BMI and waist circumference measured with appropriate technique and privacy
• Blood pressure measured with a correctly sized cuff, since an undersized cuff overestimates pressure
• Acanthosis nigricans and skin tags suggesting insulin resistance
• Features of Cushing’s syndrome such as violaceous striae, facial plethora, dorsocervical fat pad and proximal myopathy
• Features of hypothyroidism including bradycardia and delayed relaxation of reflexes
• Hirsutism, acne and androgenic alopecia suggesting polycystic ovary syndrome
• Dysmorphic features, polydactyly, retinal changes, hypogonadism or developmental delay suggesting syndromic obesity
• Assessment of mobility, gait speed and grip strength where sarcopenic obesity is suspected^[9]
• Signs of complications including elevated jugular venous pressure, hepatomegaly, peripheral oedema and joint findings

• Fasting plasma glucose and glycated hemoglobin
• Fasting lipid profile
• Liver function tests with non-invasive fibrosis scoring where indicated
• Thyroid stimulating hormone
• Renal function with urine albumin-to-creatinine ratio
• Uric acid where clinically indicated
• Targeted testing for Cushing’s syndrome, polycystic ovary syndrome or hypopituitarism only when clinical features suggest them
• Genetic testing for monogenic or syndromic obesity in early-onset severe obesity with hyperphagia or syndromic features^[14]
• Preoperative and postoperative micronutrient panel in patients undergoing metabolic and bariatric surgery

• Low QRS voltage, leftward or vertical axis shift and non-specific repolarisation change may be seen. An electrocardiogram is used to evaluate comorbid coronary artery disease, left ventricular hypertrophy and atrial fibrillation rather than to diagnose obesity.

• Chest x ray may show cardiomegaly or basal atelectasis, and image quality is often limited by body habitus.
• Echocardiography is used to assess left ventricular hypertrophy, diastolic function and pulmonary pressures, particularly where heart failure with preserved ejection fraction is suspected.
• Hepatic ultrasound or transient elastography is used to evaluate metabolic dysfunction-associated steatotic liver disease.
• Computed tomography and magnetic resonance imaging can quantify visceral and ectopic fat but are not required for routine diagnosis. Magnetic resonance imaging of the brain is indicated when hypothalamic obesity is suspected.
• Dual-energy x-ray absorptiometry or bioelectrical impedance analysis is used for body composition assessment, and is central to the diagnosis of sarcopenic obesity.^[9]
• Polysomnography is indicated where obstructive sleep apnea is suspected.

Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

• Frame treatment around health outcomes and complications rather than weight alone, and set goals collaboratively.^[8]
• Aim for sustained reduction of 5% or more of baseline body weight for some clinically meaningful benefit, and 10% or more to modify many obesity-related complications.^[32]
• Deliver intensive, multicomponent behavioural intervention comprising dietary change, physical activity and behavioural therapy, either directly or by referral.^[27]
• Intensive lifestyle intervention reduced the incidence of type 2 diabetes mellitus by comparison with placebo and with metformin in adults at high risk.^[2]
• In established type 2 diabetes mellitus, intensive lifestyle intervention produced durable weight loss and improved fitness but did not reduce cardiovascular events over a median of 9.6 years, which is an important expectation-setting point when counselling patients.^[33]
• Primary care-led total diet replacement achieved remission of type 2 diabetes mellitus in a substantial proportion of participants, with remission strongly related to the magnitude of weight loss.^[34]
• Macronutrient composition matters less than adherence. A healthy low-fat and a healthy low-carbohydrate diet produced no significant difference in 12-month weight change, and neither genotype pattern nor insulin secretion predicted which diet suited whom.^[35]
• A Mediterranean dietary pattern supplemented with extra-virgin olive oil or nuts reduced major cardiovascular events in people at high cardiovascular risk, supporting diet quality as a target independent of weight.^[36]
• Address weight bias explicitly, use person-first non-judgemental language, and ensure the clinical environment is equipped appropriately.^[26]

• Pharmacotherapy is indicated as an adjunct to lifestyle intervention in adults with BMI 30 kg/m² or greater, or 27 kg/m² or greater with a weight-related complication.^[37]
• Prescribe obesity medications only alongside behavioural and lifestyle intervention, after a comprehensive pre-treatment evaluation, and using a person-centred shared decision-making approach.^[32]

Guidance differs in strength but not in direction, and both positions should be presented to patients.

• A joint society guidance statement made strong recommendations for bupropion-naltrexone, semaglutide, tirzepatide and setmelanotide on moderate-certainty evidence, and conditional recommendations for the remaining approved agents and for specific complications including obstructive sleep apnea, heart failure with preserved ejection fraction, steatotic liver disease, osteoarthritis, major adverse cardiovascular events and type 2 diabetes mellitus.^[38]
• A living clinical guideline issued conditional recommendations with a line-of-therapy structure: semaglutide and tirzepatide first line on moderate-certainty evidence, phentermine-topiramate second line, liraglutide third line and naltrexone-bupropion fourth line, each on low-certainty evidence. For BMI 27 to 30 kg/m² with a listed comorbidity, only semaglutide, tirzepatide and liraglutide were recommended.^[39]
• A systematic review and network meta-analysis provides comparative estimates across agents where head-to-head trials are unavailable.^[40]

Tirzepatide produced greater weight reduction than semaglutide in the only large head-to-head randomised comparison, with mean reductions of 20.2% versus 13.7% at 72 weeks.^[51]

Multi-agonist agents including triple hormone receptor agonists remain investigational and are not approved for clinical use. See Obesity future or investigational therapies.

• Gastrointestinal adverse effects predominate with incretin-based agents, are usually mild to moderate, and cluster during dose escalation.^[48]
• Withhold or adjust GLP-1 receptor agonists before elective procedures according to multisociety perioperative guidance, because of concerns regarding delayed gastric emptying and aspiration risk.^[61]
• An association between semaglutide and nonarteritic anterior ischaemic optic neuropathy has been reported in a single-centre retrospective matched cohort, with hazard ratios of 4.28 in type 2 diabetes mellitus and 7.64 in overweight or obesity. The authors state that causality is not established and that further study is required.^[62]
• In a post hoc analysis of three randomised trials in participants without known major psychopathology, tirzepatide was not associated with increased depressive symptoms, and suicidal ideation was reported in 0.6% of participants in each group.^[63]
• If a medication becomes unavailable, switching to another approved agent is recommended, with reassessment when supply is restored.^[32]

• Metabolic and bariatric surgery is recommended for individuals with BMI 35 kg/m² or greater regardless of the presence or severity of comorbidity, and should be considered for individuals with BMI 30 to 34.9 kg/m² with metabolic disease. Thresholds are adjusted downward in Asian populations, with surgery considered above BMI 27.5 kg/m².^[64]
• These criteria supersede the 1991 consensus thresholds that required BMI 40 kg/m², or 35 kg/m² with comorbidity.^[64]

• Sleeve gastrectomy and Roux-en-Y gastric bypass are the dominant contemporary operations. One anastomosis gastric bypass and biliopancreatic diversion with duodenal switch are performed in selected cases. Adjustable gastric banding has largely been abandoned because of poor durability and high reoperation rates.
• Endoscopic sleeve gastroplasty is an option for patients with class I or class II obesity who decline or are ineligible for surgery, and produced significantly greater weight loss than lifestyle intervention alone in a randomised trial.^[65]

• Bariatric surgery reduced overall mortality compared with usual care in the first large prospective controlled study.^[1]
• Median life expectancy was longer after bariatric surgery than after usual obesity care in long-term follow-up of the same cohort.^[66]
• In a one-stage meta-analysis of 174,772 participants with 7712 deaths over 1.2 million patient-years, metabolic and bariatric surgery was associated with a 49.2% reduction in the hazard of death and a median life expectancy 6.1 years longer than usual care. The gain was 9.3 years in patients with diabetes and 5.1 years in those without, with numbers needed to treat over 10 years of 8.4 and 29.8 respectively.^[67]
• Surgery was superior to intensive medical therapy for glycaemic control at five years in type 2 diabetes mellitus.^[68]
• Pooled long-term randomised data confirmed superior glycaemic outcomes with surgery compared with medical and lifestyle management.^[69]
• Weight loss after gastric bypass was largely sustained at 12 years, establishing durability well beyond that achievable with lifestyle intervention alone.^[70]

• Lifelong micronutrient supplementation and monitoring, including iron, vitamin B12, folate, calcium, vitamin D, and thiamine where vomiting occurs
• Surveillance for internal hernia, marginal ulceration, dumping syndrome, post-bypass hypoglycaemia, nephrolithiasis and metabolic bone disease
• Screening for alcohol use disorder and for psychological difficulty after surgery
• Structured long-term follow-up, since weight regain and recurrence of comorbidity occur in a proportion of patients

Obesity requires indefinite management. The evidence on withdrawal is now unambiguous.

• Withdrawal of semaglutide and lifestyle intervention after 68 weeks resulted in regain of approximately two thirds of the lost weight by week 120, with cardiometabolic improvements reverting toward baseline for most variables.^[71]
• Continued weekly semaglutide maintained weight loss whereas switching to placebo led to regain.^[72]
• In a randomised maintenance trial, weight change from baseline to week 112 was -21.9% with continued maximum tolerated dose tirzepatide, -16.6% with dose reduction to 5 mg and -9.9% with placebo. Rescue therapy for regain of at least half the lost weight was required by 8% on maximum tolerated dose, 25% on 5 mg and 67% on placebo. Dose reduction is therefore a reasonable alternative to discontinuation but is not equivalent to continuation.^[73]
• Continuing obesity medication during the weight maintenance phase carries a strong recommendation.^[38]
• Monitor weight, waist circumference, blood pressure, glycaemia, lipids, renal and hepatic parameters, nutritional adequacy, muscle mass and function, and quality of life at defined intervals.
• Maintain resistance training and adequate protein intake during and after weight loss to limit loss of lean mass, particularly in older adults.^[9]

• Children and adolescents. Evaluate and treat obesity promptly rather than adopting watchful waiting, using intensive health behaviour and lifestyle treatment as the foundation, with pharmacotherapy and surgery considered in appropriate candidates.^[74] Once-weekly semaglutide plus lifestyle intervention produced significantly greater reduction in BMI than placebo in adolescents with obesity.^[75]
• Older adults. Screen for sarcopenic obesity, prioritise preservation of muscle mass and physical function, and pair any weight reduction with resistance training and adequate protein.^[9]
• Pregnancy and preconception. Obesity pharmacotherapy is not recommended in pregnancy. Phentermine-topiramate requires monthly pregnancy testing because of teratogenicity, and contraceptive counselling should accompany any prescription in people who can become pregnant.^[39]
• Perioperative period. Follow multisociety guidance on withholding or adjusting GLP-1 receptor agonists before elective procedures.^[61]
• Type 2 diabetes mellitus. Select agents with demonstrated glycaemic and cardiorenal benefit, and anticipate somewhat smaller weight reduction than in people without diabetes.^[76][77]
• Patients requiring weight-inducing medications. Substitute where clinically possible, and where it is not, proceed with obesity pharmacotherapy, which retains efficacy in this group.^[19]
• Monogenic and syndromic obesity. Refer for genetic confirmation and consider melanocortin-4 receptor agonist therapy in eligible patients.^[15]

Case #1

• Body image
• Healthy diet
• Human weight
• Junk food
• National Weight Control Registry
• Physical exercise
• Pickwickian syndrome
• Obesity in the United States
• Obesity in India
• Overeaters Anonymous
• Metabolic syndrome
• Type 2 diabetes mellitus
• Metabolic dysfunction-associated steatotic liver disease
• Obstructive sleep apnea
• Bariatric surgery
• Prader-Willi syndrome
• Bardet-Biedl syndrome

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