Obesity is an excess storage of fat and can affct any mammal. It is a condition in which the natural energy reserve of a mammal (such as a human), which is stored in fat, is expanded far beyond usual levels to the point where it causes health stress. Obesity in wild animals is relatively rare, but it is common in domestic animals like pigs and household pets who may be overfed and underexercised.
Obesity is a concept that is being continually redefined. In humans, the most common statistical estimate of obesity is the body mass index (BMI).
A person with a BMI over 25.0 kg/m2 is considered overweight; a BMI over 30.0 kg/m2 is considered obese. A further threshold at 40.0 kg/m2 is identified as urgent morbidity risk. The American Institute for Cancer Research considers a BMI between 18.5 and 25 to be an ideal target for a healthy individual (although several sources consider a person with a BMI of less than 20 to be underweight). The BMI was created in the 19th century by the Belgian statistician Adolphe Quetelet. The cut-off points between categories are occasionally redefined, and may differ from country to country. In June 1998 the NIH brought official US category definitions into line with those used by the WHO, moving the American 'overweight' threshold from BMI 27 to BMI 25. About 30,000,000 Americans moved from "ideal" weight to being 1–10 pounds (0.5–5 kg) "overweight" as a result.
The BMI cannot offer a complete diagnosis, in that it ignores fat distribution within the body (see central obesity), and the relative fat-muscle-bone contributions to total body weight. A powerful athlete may be classified as obese by the BMI due to heavy musculature, while a false 'normal' may be diagnosed in the case of an elderly person with very low lean mass, which masks excess adiposity. On its own, a BMI score is therefore inadequate as a diagnostic tool. In practice, in most examples of overweight that may be harmful to health, both doctor and patient can see 'by eye' that fat is an issue. In these cases, BMI thresholds provide simple targets all patients can understand. Doctors may also use a simple measure of waist circumference (which is a better predictor of complications such insulin resistance due to visceral fat - see Janssen et al, 2004); the skinfold test, in which a pinch of skin is precisely measured to determine the thickness of the subcutaneous fat layer; or bioelectrical impedance analysis, usually only carried out at specialist clinics.
Such clinical data is rarely available in the statistical raw materials required for large public health studies, however - whereas height and weight is commonly recorded. For this essential reason, BMI remains the most commonly-used approach for public health studies, and the most useful for cross-border, longitudinal and other types of comparative analysis.
Obesity is the nominal form of obese which comes from the Latin obsus, which means "stout, fat, or plump." sus is the past participle of edere (to eat), with ob added to it. In Classical Latin, this verb is seen only in past participial form. Its first attested usage in English was in 1651, in N. Biggs' Matæotechnia Medicinæ Praxeuus.
Obesity is generally a result of a combination of factors:
- Genetic predisposition
- Energy-rich diet
- Limited exercise and sedentary lifestyle
- Underlying illness (e.g. hypothyroidism)
- An eating disorder (such as binge eating disorder)
- Stressful mentality (debated)
- Insufficient sleeping (debated)
Although there is no definitive explanation for the recent epidemic of obesity, the evolutionary hypothesis comes closest to providing some understanding of this phenomenon. In times when food was scarce, the ability to take advantage of rare periods of abundance and use such abundance by storing energy efficiently was undoubtedly an evolutionary advantage. This is precisely the opposite of what is required in a sedentary society, where high-energy food is available in abundant quantities in the context of decreased exercise. Although many people may have a genetic propensity towards obesity, it is only with the reduction in physical activity and a move towards high-calorie diets of modern society that it has become widespread. Significant proportions (up to 30%) of the population in wealthy countries are now obese, and seen to be at risk of ill health.
Eating disorders can lead to obesity, especially binge eating disorder (BED). As the name indicates, patients with this disorder are prone to overeat, often in binges. A proposed mechanism is that the eating serves to reduce anxiety, and some parallels with substance abuse can be drawn. An important additional factor is that BED patients often lack the ability to recognize hunger and satisfaction, something that is normally learnt in childhood. Learning theory suggests that early childhood conceptions may lead to an association between food and a calm mental state.
Some recent research has suggested that some human obesity may be caused by a viral infection. The virus adenovirus vectors AD-36 and AD-37 have been identified as a cause of obesity in animals and as potential stimulants on human preadipocytes (Vangipuram et al 2004). While these viruses occur in humans, there is no clear evidence that their presence leads to in increased risk of obesity.
Flier (2004) 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 proposed that participate in the regulation of appetite and food intake, storage patterns of adipose tissue, development of insulin resistance and possible ways of interfering with these mechanisms. Since leptin, ghrelin, orexin, PYY 3-36, cholecystokinin, adiponectin and numerous 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 the stomach producing ghrelin when relatively empty and leptin being produced by adipose tissue when satiated with nutrients. Resistance to the leptin signal and causes for this resistance have been implicated in dysregulation of appetite, although administration of leptin has not proven to be a feasible way of suppressing appetite.
Neuroscientific approaches hinge on the action of the aforementioned hormones and mediators on the hypothalamus, the part of the brain that is thought to produce hunger signals for higher centers and induce food intake behavior.
While it is often quite 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 who is obese, they cannot 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 1960 almost the entire population was well fed, but not overweight. 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.
- One of the most important is the much lower relative cost of foodstuffs: massive agricultural subsidies in the United States and Europe have led to food prices for consumers being lower than at any point in history. Sugar and corn syrup, two huge sources of food energy, are some of the most subsidized products by the United States government.
- Increased marketing has also played a role. In the early 1980s the Reagan administration lifted most regulations pertaining to advertising to children. As a result the number commercials seen by the average child increased greatly, and a large proportion of these were for fast food and candy.
- Changes in the price of mineral oil and petrol are also believed to have had an effect, as unlike during the 1970s it is now affordable in the United States to drive everywhere - at a time when public transit goes underused. At the same time more areas have been built without sidewalks and parks.
- 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 has seen sales of generally unhealthy frozen meals 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 where 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 (Lopez 2004).
- Since 1980 both sit-in and 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.
- Increased food production is a likely factor. The U.S. produces three times more food than U.S. citizens eat.
- Increasing affluence itself (including many of the above factors as accompaniments of affluence) may be a cause, or contributing factor since obesity tend to flourish as a disease of affluence in countries which are developing and becoming westernised. (http://www.iotf.org/)
Interestingly the vast increase in the number of Americans who exercise and diet occurred before the increase in obesity, and some scholars have even argued that these trends actually encouraged obesity. Most diets fail, ending in binge eating and an overall increase in weight. Similarly those who workout but then stop can end up being fatter than those who never exercised.
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 2002 study  (http://roa.sagepub.com/cgi/content/abstract/26/1/130) found obese subjects approximately half as wealthy as thin ones. When income differentials were factored out, the inequity persisted - thin subjects were inheriting more wealthy than fat ones. Another study finds women who marry into higher status predictably thinner than women who married into lower status.
Obesity is correlated (in population studies) with a variety of complications. For many of these complaints, it has not been clearly established to what extent they are caused directly by obesity itself, or have some other cause (such as limited exercise) that causes obesity as well. Most confidence in a direct cause is given to the mechanical complications in the following list:
Additonal correlations are said to include:
- enlarged heart and its associated arrhythmia and dizziness
- high blood cholesterol and triglyceride levels (combined hyperlipidemia)
While being severely obese has many health ramifications, those who are somewhat overweight face little increased mortality or morbidity. Some studies suggest that the somewhat "overweight" tend to live longer than those at their "ideal" weight.
The mainstay of treatment for obesity is an energy-limited diet and increased exercise. Although adherence to this regimen can cure obesity, many patients are unable to make the required sacrifices. There might be an additional behavioral factor at the brain level "forbidding" obesity patients from losing too much weight.
Much research focuses on new drugs to combat obesity, which is seen as the biggest health problem facing developed countries. Some nutritionists feel that these research funds would be better devoted to advice on good nutrition, healthy eating and promoting a more active lifestyle.
Medication prescribed for diet/exercise-resistant obesity is orlistat (Xenical®, reduced intestinal fat absorption by inhibiting pancreatic lipase) and sibutramine (Reductil®, Medaria®, an anorectic).
In the presence of diabetes mellitus, there is evidence that the anti-diabetic drug metformin (Glucophage®) can assist in weight loss - rather than sulfonylurea derivatives and insulin, which often lead to further weight gain. The thiazolidinediones (rosiglitazone or pioglitazone) can cause slight weight gain, but decrease the "pathologic" form of abdominal fat, and are therefore often used in obese diabetics.
Increasingly, bariatric surgery is being used to limit stomach capacity (and thus food intake); this can happen laparoscopically. Ileal bypass reduces the length of the intestine and hence absorbing surface, but has more complications.
There is continuous debate over obesity, at several levels. The scientific evidence informing these debates is more contradictory than most simple arguments assume. Statistics demonstrating correlations are typically misinterpreted in public discussion as demonstrating causation, a fallacy known as the spurious relationship.
Causes of obesity
Conventional wisdom holds that obesity is caused by over-indulgence in fatty or sugary foods, portrayed as either a failure of will power or a species of addiction. Various specialists strongly oppose this view. For example, Professor Thomas Sanders, the director of the Nutrition, Food & Health Research Centre at King's College London, emphasises the need for balance between activity and consumption:
- In trials, there is no evidence suggesting that reducing fat intake has an effect on obesity. As long as your expenditure equals what you eat, you won't put on weight, regardless of how high the fat content is in your diet (The Times, London, 10 March 2004).
Medicalisation of obesity
Controversy also exists as to whether the concept of "obesity" is a valid one. These critics assert that physically active people are healthier than the sedentary regardless of their body weight. The focus on weight and body mass is fed, in their view, by a diet promotion industry, drug companies, and segments of the medical profession for profit purposes, by promoting a vision that equates health with slenderness, and makes extreme slenderness of a sort that is quite difficult for most people to achieve an ideal. In The Obesity Myth, Paul Campos writes that:
- . . . (F)rom the perspective of a profit-maximising medical and pharmaceutical industry, the ideal disease would be one that never killed those who suffered from it, that could not be treated effectively, and that doctors and their patients would nevertheless insist on treating anyway. Luckily for it, the American health care industry has discovered (or rather invented) just such a disease. It is called "obesity". Basically, obesity research in America is funded by the diet and drug industry - that is, the economic actors who have the most to gain from the conclusion that being fat is a disease that requires aggressive treatment. Many researchers have direct financial relationships with the companies whose products they are evaluating.  (http://society.guardian.co.uk/publichealth/story/0,11098,1203533,00.html)
More militant 'fat acceptors' reject any attempt to present obesity as a problem: Conventional wisdom, assuming obesity to be a health problem, is to be considered a prejudice, directly equivalent to the medicalisation of homosexuality in the 19th Century, and the consequent persecution of this minority.
Health effects of obesity
Opposing Campos are voices such as Greg Critser, who writes in Fat Land that the statistics such campaigners use are based on a selective sample of research data - a selection designed to emphasise obesity co-factors such as poor fitness, rather than obesity itself. Critser notes that advocates of the Obesity Myth position typically rely heavily on a study by Dr. Steven Blair at the Cooper Institute, Texas, which seemed to show that fit, fat subjects were healthier than unfit, skinny subjects:
- . . . Taking out the fitness variable and looking at body weight only, Blair admitted: "Men with a BMI of >30 were generally less physically fit and had more unfavorable risk factors than men in the lower BMI groups". Lower weight men had higher good cholesterol, lower bad cholesterol, and higher treadmill times than fatter men. "The highest death rate," he added, "was observed among those men in the highest BMI category and correspondingly lower death rates were observed in each subsequently lower BMI category." And when one looks at the difference between low fit men in all categories - which one might think would be most useful since most obese people are not fit - Blair's upbeat message fades: Normal weight nonfit men had an age-adjusted death rate (the number of excess deaths in the studied group) of 52.1; unfit fat men had the higher rate of 62.1. More: Unfit lean men were half as likely to have a history of hypertension than unfit fat men. In the real world, even according to Blairism, the fat are more likely to die early - and to live precariously - than the lean.
Medical responses to obesity
Conventional wisdom recommends that the obese adopt strategies to lose weight in order to mitigate the health risks associated with obesity. There is controversy both over what those strategies realistically include, and also whether such a goal does actually result in better health outcomes.
Weight reduction strategies include dietary changes, exercise regimes, weight loss drugs, and surgical interventions (see Therapy, above, for complete list). Of these, 'miracle diets' are most contested, with several studies suggesting that short-term weight loss typically results in metabolic adjustments leading to weight gain in the longer term.
Prevalence and Public Interest
What qualifies a medical condition as a matter of public interest, rather than a private health issue between doctor and patient, are its social costs. The estimation or measurement of the social cost of obesity is an extraordinarily hazardous statistical task, for two separate reasons.
Firstly, the collation of evidence concerning the prevalence of obesity, or especially changing rates of prevalence, is open to several types of distortion (see, for one example, this critique of health statistics on the topic compiled in the UK in 2003  (http://www.spiked-online.com/Articles/0000000CA8D9.htm)).
Secondly, since obesity is the correlate of a long list of factors which have significant health consequences in their own right, there may be no fact of the matter about which costs to attribute to obesity per se, and which are more properly costed to these co-factors. For one example, the proven relationship between obesity and low social status means that any group of obese persons' health outcomes will be significantly lowered by their average access to medical care, as a socioeconomic class, which will be, on average, lower than that of any non-obese control group.
Researchers from the US Centers of Disease Control and Prevention in Atlanta (Mokdad et al 2004) reported that approximately 400,000 US deaths annually were associated with poor diet and little exercise, and that if the trend continued, this would be 500,000 in 2005, overtaking smoking as the leading cause of death. These statistics are fiercely contested  (http://server1.consumerfreedom.com/article_detail.cfm/article/141), and error was admitted by the CDC in November 2004  (http://www.cbsnews.com/stories/2004/11/24/health/main657636.shtml). In particular, studies of this nature are normally unable to distinguish causes of death, so include many accidental deaths, murders etc, which ought not to be costed to obesity.
Canada and Europe are generally considered to be somewhat behind the United States in the trend towards overweight, with the rest of the world mixed. Some nations like Egypt and Mexico have also suffered from greatly increasing rates of obesity.
Policy responses to obesity
On top of controversies about the causes of obesity, and about its precise health implications, come policy controversies about the correct policy approach to obesity. The main debate is between 'personal responsibility' advocates, who resist regulatory attempts to intervene in citizen's private dietary habits, and 'public interest' advocates, who promote regulations, on the same public health grounds as the restrictions applied to tobacco products. In the USA, a recent bout in this controversy involves the so-called Cheeseburger Bill, an attempt to indemnify food industry businesses from frivolous law suits by obese clients.
'Personal responsibility' advocates work on the basis that, as the microbiologist Rene Dubos once said, health ought not to be considered an end in itself, but 'the condition best suited to reach goals that each individual formulates for himself'  (http://www.spiked-online.com/Articles/0000000CA7A4.htm). Any other definition permits authorities to curtail the autonomy of the self-determining individual, imposing quantity over quality of life onto them, undermining their civil liberties. As much as principled doctors, personal responsibility arguments have also been offered by food producer lobbies. In 1961, for example, as President John F Kennedy raised concerns about a lack of fitness in American society, a spokesman for the US Dairy industry, Frank R. Neu, wrote advertorials warning We May Be Sitting Ourselves To Death  (http://www.theatlantic.com/issues/61nov/neu.htm). Not food regulation, but personal exercising, is moved as the solution.
The 'public interest' advocate John Banzhaf has found a way to harness personal responsibility arguments to the public interest side of the debate in the USA, via recent changes  (http://banzhaf.net/docs/fatrates) to HMO regulations which enable health insurance providers to differentiate between obese and regular customers in their pricing. The 'public interest' objective is that obese people will have to pay extra for their health maintenance, bringing 'personal responsibility' to bear on their consumption choices. This new tactic is controversial itself - if a causal link pertains from low social status to obesity  (http://en.wikipedia.org/wiki/Obesity#Poverty_link.3F), the net effect will be increased costs for low income members of HMOs, particularly ethnic minorities, and reduced costs for slim, middle class white members.
On July 16, 2004, the US Department of Health and Human Services officially classified obesity as a disease. Speaking to a Senate committee, Tommy Thompson, the Secretary of Health and Human Services, stated that Medicare would cover obesity-related health problems. However, reimbursement would not be given if a treatment was not proven to be effective.
- Fat acceptance movement
- Fat admirer
- Pickwickian syndrome
- Healthy eating
- Body mass index
- Obesity, BMI and Calorie assessment Calculators (http://www.thedoctorslounge.net/centers/nutrition/calculators/index.htm)
- Body Mass Index Calculator (http://www.nutri.info/body_mass_index_download.htm)
- Obesity advice / FAQs (http://web4health.info/en/answers/life-obesity-menu.htm)
- International Task Force on Obesity (http://www.iotf.org/)
- Childhood Obesity (http://www.ericdigests.org/pre-9218/obesity.htm)
- Argument that the concern for obesity is overwrought (http://www.guardian.co.uk/weekend/story/0,3605,1200549,00.html)
- BMJ Article on Obesity and Public policy (http://bmj.bmjjournals.com/cgi/content/full/328/7452/1327)
- Economics of Obesity (http://www.thepublicinterest.com/current/article3.html)
- The Worldwide Obesity Epidemic (http://www.hsph.harvard.edu/symposium/sacks_files/v3_document.htm) by Frank Sacks MD
- Bruch H. Eating Disorders, Obesity, Anorexia Nervosa and the Person Within. New York: Basic Books, 1973.
- Janssen I, Katzmarzyk PT, Ross R. Waist circumference and not body mass index explains obesity-related health risk. Am J Clin Nutr 2004;79:379-84 PMID 14985210
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- Lopez R. Urban sprawl and risk for being overweight or obese. Am J Publ Health 2004;94:1574-9. PMID 15333317.
- Mokdad AH, Marks JS, Stroup DF, Gerberding JL. Actual causes of death in the United States, 2000. JAMA 2004;291:1238-45. PMID 15010446
- Roberts SB, Savage J, Coward WA, Chew B, Lucas A. Energy expenditure and intake in infants born to lean and overweight mothers. N Engl J Med 1988;318:461-6. PMID 3340127
- Ross JG, Pate RR. The National Children and Youth Fitness Study II: A summary of findings. J Phys Educ Recr Dance 1987;58:51-6.
- Tillotson JE. America's Obesity: Conflicting Public Policies, Industrial Economic Development, and Unintended Human Consequences. Annu Rev Nutr 2004;24:617-43. PMID 15189134
- Vangipuram SD, Sheele J, Atkinson RL, Holland TC, Dhurandhar NV. A human adenovirus enhances preadipocyte differentiation. Obes Res 2004;12:770-7. PMID 15166297.
- Wolf MC, Cohen KR, Rosenfeld JG. School-based interventions for obesity: Current approaches and future prospects. Psychology in the Schools 1985;22:187-200.
- The Oxford English Dictionary (website) (for the etymology)