Obesity is a condition in which the natural energy reserve, stored in the fatty tissue of humans and other mammals, exceeds healthy limits. It is commonly defined as a body mass index (weight divided by height squared) of 30 kg/m2 or higher.
Although obesity is an individual clinical condition, some authorities view it as a serious and growing public health problem. Some studies show that excessive body weight has been shown to predispose to various diseases, particularly cardiovascular diseases, diabetes mellitus type 2, sleep apnea and osteoarthritis.[1][2]
Classification
Obesity can be defined in absolute or relative terms. In practical settings, obesity is typically evaluated in absolute terms by measuring BMI (body mass index), but also in terms of its distribution through waist circumference or waist-hip circumference ratio measurements.[3] In addition, the presence of obesity needs to be regarded in the context of other risk factors and comorbidities (other medical conditions that could influence risk of complications).[1]
BMI
BMI, or body mass index, is a simple and widely used method for estimating body fat.[4] BMI was developed by the Belgian statistician and anthropometrist Adolphe Quetelet.[5] It is calculated by dividing the subject's weight by the square of his/her height, typically expressed either in metric or US "Customary" units:
- Metric: BMI = kg / m2
Where kg is the subject's weight in kilograms and m is the subject's height in metres.
- US/Customary: BMI = lb * 703 / in2
Where lb is the subject's weight in pounds and in is the subject's height in inches.
The most commonly used definitions, established by the WHO in 1997 and published in 2000, provide the following values:[6]
- A BMI less than 18.5 is underweight
- A BMI of 18.5–24.9 is normal weight
- A BMI of 25.0–29.9 is overweight
- A BMI of 30.0–39.9 is obese
- A BMI of 40.0 or higher is severely (or morbidly) obese
- A BMI of 35.0 or higher in the presence of at least one other significant comorbidity is also classified by some bodies as morbid obesity.[7][8]
In a clinical setting, physicians take into account race, ethnicity, lean mass (muscularity), age, sex, and other factors which can affect the interpretation of BMI. BMI overestimates body fat in persons who are very muscular, and it can underestimate body fat in persons who have lost body mass (e.g. many elderly).[1] Mild obesity as defined by BMI alone is not a cardiac risk factor, and hence BMI cannot be used as a sole clinical and epidemiological predictor of cardiovascular health.[9]
Waist circumference
-
BMI does not take into account differing ratios of adipose to lean tissue; nor does it distinguish between differing forms of adiposity, some of which may correlate more closely with cardiovascular risk. Increasing understanding of the biology of different forms of adipose tissue has shown that visceral fat or central obesity (male-type or apple-type obesity, also known as "belly fat") has a much stronger correlation, particularly with cardiovascular disease, than the BMI alone.[10]
The absolute waist circumference (>102 cm in men and >88 cm in women) or waist-hip ratio (>0.9 for men and >0.85 for women)[10] are both used as measures of central obesity.
In a cohort of almost 15,000 subjects from the National Health and Nutrition Examination Survey (NHANES) III study, waist circumference explained obesity-related health risk significantly better than BMI when metabolic syndrome was taken as an outcome measure.[11]
Body fat measurement
An alternative way to determine obesity is to assess percent body fat. Doctors and scientists generally agree that men with more than 25% body fat and women with more than 30% body fat are obese. However, it is difficult to measure body fat precisely. The most accepted method has been to weigh a person underwater, but underwater weighing is a procedure limited to laboratories with special equipment. Two simpler methods for measuring body fat are the skinfold test, in which a pinch of skin is precisely measured to determine the thickness of the subcutaneous fat layer; or bioelectrical impedance analysis, usually only carried out at specialist clinics. Their routine use is discouraged.[12]
Other measurements of body fat include computed tomography (CT/CAT scan), magnetic resonance imaging (MRI/NMR), and dual energy X-ray absorptiometry (DXA).[13]
Risk factors and comorbidities
The presence of risk factors and diseases associated with obesity are also used to establish a clinical diagnosis. Coronary heart disease, type 2 diabetes, and sleep apnea are possible life-threatening risk factors that would indicate clinical treatment of obesity.[1] Smoking, hypertension, age and family history are other risk factors that may indicate treatment.[1]
Effects on health
A large number of medical conditions have been associated with obesity. Health consequences are categorised as being the result of either increased fat mass (osteoarthritis, obstructive sleep apnea, social stigma) or increased number of fat cells (diabetes, cancer, cardiovascular disease, non-alcoholic fatty liver disease).[14] Mortality is increased in obesity, with a BMI of over 32 being associated with a doubled risk of death.[15] There are alterations in the body's response to insulin (insulin resistance), a proinflammatory state and an increased tendency to thrombosis (prothrombotic state).[14]
Disease associations may be dependent or independent of the distribution of adipose tissue. Central obesity (male-type or waist-predominant obesity, characterised by a high waist-hip ratio), is an important risk factor for the metabolic syndrome, the clustering of a number of diseases and risk factors that heavily predispose for cardiovascular disease. These are diabetes mellitus type 2, high blood pressure, high blood cholesterol, and triglyceride levels (combined hyperlipidemia).[16]
Apart from the metabolic syndrome, obesity is also correlated with a variety of other complications. For some 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.
- Cardiovascular: congestive heart failure, enlarged heart and its associated arrhythmias and dizziness, varicose veins, and pulmonary embolism
- Endocrine: polycystic ovarian syndrome (PCOS), menstrual disorders, and infertility[17]
- Gastrointestinal: gastroesophageal reflux disease (GERD), fatty liver disease, cholelithiasis (gallstones), hernia, and colorectal cancer
- Renal and genitourinary: erectile dysfunction,[18] urinary incontinence, chronic renal failure,[19] hypogonadism (male), breast cancer (female), uterine cancer (female), stillbirth
- Integument (skin and appendages): stretch marks, acanthosis nigricans, lymphedema, cellulitis, carbuncles, intertrigo
- Musculoskeletal: hyperuricemia (which predisposes to gout), immobility, osteoarthritis, low back pain
- Neurologic: stroke, meralgia paresthetica, headache, carpal tunnel syndrome, dementia,[20] idiopathic intracranial hypertension
- Respiratory: obstructive sleep apnea, obesity hypoventilation syndrome, asthma
- Psychological: Depression, low self esteem, body dysmorphic disorder, social stigmatization
While being severely obese has many health ramifications, those who are somewhat overweight face little increased mortality or morbidity. Osteoporosis is known to occur less in slightly overweight people.
Causes and mechanisms
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. [21]
Despite the widespread availability of nutritional information in schools, doctors' offices, on the internet and on product packaging,[22] 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.[23]
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. [24]
Less well established and possibly underinvestigated life style issues that may influence obesity include (1) insufficient sleep, (2) endocrine disruptors - food substances that interfere with lipid metabolism, (3) decreased variability in ambient temperature, (4) decreased rates of smoking, which suppresses appetite, (5) increased use of medication that leads to weight gain, (6) increased distribution of ethnic and age groups that tend to be heavier, (7) pregnancy at a later age, (8) intrauterine and intergenerational effects, (9) positive natural selection of people with a higher BMI, (10) assortative mating, heavier people tending to form relationships with each other.[25]
Genetics
As with many medical conditions, the calorific imbalance that results in obesity is probably the result of 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. It is thought that a large proportion of the causative genes are still to be identified. Studies in over 5000 identical twins demonstrated that childhood obesity has a strong (77%) inherited component.[26]
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.[27]
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.[28]
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.[29] 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
Scientists investigating the mechanisms and treatment of obesity may use
animal models such as
mice to conduct experiments.
Flier[30] 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.[30] 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.[31]
The arcuate nucleus contains two distinct groups of neurons.[30] 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.
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 bacteria 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.[32]
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[33] 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.[34]
Treatment
-
Main article: Weight loss
The main treatment for obesity is to reduce body fat by eating fewer calories and exercising more. Diet and exercise programs produce an average weight loss of approximately 8% of total body mass (excluding program drop-outs). Not all dieters are satisfied with these results, but a loss of as little as 5% of body mass can create large health benefits.[citation needed]
Much more difficult than reducing body fat is keeping it off. Eighty to ninety-five percent of those who lose 10% or more of their body mass by dieting regain all that weight back within two to five years. The body has systems that maintain its homeostasis at certain set points, including body weight.[citation needed] Therefore, keeping weight off generally requires making exercise and eating right a permanent part of a person's lifestyle.[citation needed]
Clinical protocols
In a clinical practice guideline by the American College of Physicians, the following five recommendations are made:[35]
- People with a BMI of over 30 should be counseled on diet, exercise and other relevant behavioral interventions, and set a realistic goal for weight loss.
- If these goals are not achieved, pharmacotherapy can be offered. The patient needs to be informed of the possibility of side-effects and the unavailability of long-term safety and efficacy data.
- Drug therapy may consist of sibutramine, orlistat, phentermine, diethylpropion, fluoxetine, and bupropion. For more severe cases of obesity, stronger drugs such as amphetamine and methamphetamine may be used on a selective basis. Evidence is not sufficient to recommend sertraline, topiramate, or zonisamide.
- In patients with BMI > 40 who fail to achieve their weight loss goals (with or without medication) and who develop obesity-related complications, referral for bariatric surgery may be indicated. The patient needs to be aware of the potential complications.
- Those requiring bariatric surgery should be referred to high-volume referral centers, as the evidence suggests that surgeons who frequently perform these procedures have fewer complications.
A clinical practice guideline by the US Preventive Services Task Force (USPSTF) concluded that the evidence is insufficient to recommend for or against routine behavioral counseling to promote a healthy diet in unselected patients in primary care settings, but that intensive behavioral dietary counseling is recommended in those with hyperlipidemia and other known risk factors for cardiovascular and diet-related chronic disease. Intensive counseling can be delivered by primary care clinicians or by referral to other specialists, such as nutritionists or dietitians.[36][37]
Exercise
Exercise requires energy (calories). Calories are stored in body fat. The body breaks down its fat stores in order to provide energy during prolonged aerobic exercise. The largest muscles in the body are the leg muscles, and naturally these burn the most calories, which make walking, running, and cycling among the most effective forms of exercise for reducing body fat.
A meta-analysis of randomized controlled trials by the international Cochrane Collaboration found that "exercise combined with diet resulted in a greater weight reduction than diet alone".[38]
Dieting
-
In general, dieting means eating less. Various dietary approaches have been proposed, some of which have been compared by randomized controlled trials:
- "all 4 diets resulted in modest statistically significant weight loss at 1 year, with no statistically significant differences between diets"
- "The higher discontinuation rates for the Atkins and Ornish diet groups suggest many individuals found these diets to be too extreme"
Low carbohydrate versus low fat
-
Many studies have focused on diets that reduce calories via a low-carbohydrate (Atkins diet, Zone diet) diet versus a low-fat diet (LEARN diet, Ornish diet). The Nurses' Health Study, an observational cohort study, found that low carbohydrate diets based on vegetable sources of fat and protein are associated with less coronary heart disease.[41]
A meta-analysis of randomized controlled trials by the international Cochrane Collaboration in 2002 concluded[42] that fat-restricted diets are no better than calorie restricted diets in achieving long term weight loss in overweight or obese people.
A more recent meta-analysis that included randomized controlled trials published after the Cochrane review[43][44][40] found that "low-carbohydrate, non-energy-restricted diets appear to be at least as effective as low-fat, energy-restricted diets in inducing weight loss for up to 1 year. However, potential favorable changes in triglyceride and high-density lipoprotein cholesterol values should be weighed against potential unfavorable changes in low-density lipoprotein cholesterol values when low-carbohydrate diets to induce weight loss are considered."[45]
The Women's Health Initiative Randomized Controlled Dietary Modification Trial[46] found that a diet of total fat to 20% of energy and increasing consumption of vegetables and fruit to at least 5 servings daily and grains to at least 6 servings daily resulted in:
- no reduction in cardiovascular disease[47]
- an insignificant reduction in invasive breast cancer[48]
- no reductions in colorectal cancer[49]
Additional recent randomized controlled trials have found that:
- The choice of diet for a specific person may be influenced by measuring the invididual's insulin secretion:
- In young adults "Reducing glycemic [carbohydrate] load may be especially important to achieve weight loss among individuals with high insulin secretion."[51] This is consistent with prior studies of diabetic patients in which low carbohydrate diets were more beneficial.[52][53]
The American Diabetes Association released for the first time a recommendation for a low carbohydrate diet to reduce weight for those with or at risk of Type 2 diabetes. The American Diabetes Association released its 2008 Clinical Practice Recommendations for physicians in January 2008. [54]
Low glycemic index
"The glycemic index factor is a ranking of foods based on their overall effect on blood sugar levels. Low glycaemic index foods, such as lentils, provide a slower more consistent source of glucose to the bloodstream, thereby stimulating less insulin release than high glycaemic index foods, such as white bread."[55][56]
The glycemic load is "the mathematical product of the glycemic index and the carbohydrate amount".[57]
In a randomized controlled trial that compared four diets that varied in carbohydrate amount and glycemic index found complicated results[58]:
- Diet 1 and 2 were high carbohydrate (55% of total energy intake)
- Diet 1 was high-glycemic index
- Diet 2 was low-glycemic index
- Diet 3 and 4 were high protein (25% of total energy intake)
- Diet 3 was high-glycemic index
- Diet 4 was low-glycemic index
Diets 2 and 3 lost the most weight and fat mass; however, low density lipoprotein fell in Diet 2 and rose in Diet 3. Thus the authors concluded that the high-carbohydrate, low-glycemic index diet was the most favorable.
A meta-analysis by the Cochrane Collaboration concluded that low glycemic index or low glycemic load diets led to more weight loss and better lipid profiles. However, the Cochrane Collaboration grouped low glycemic index and low glycemic load diets together and did not try to separate the effects of the load versus the index.[55]
Drugs
-
Medication most commonly prescribed for diet/exercise-resistant obesity is orlistat (Xenical, which reduces intestinal fat absorption by inhibiting pancreatic lipase) and sibutramine (Reductil, Meridia, an anorectic). Weight loss with these drugs is modest, and over the longer term average weight loss on orlistat is 2.9 kg, sibutramine 4.2 kg and rimonabant 4.7 kg. Orlistat and rimonabant lead to a reduced incidence of diabetes, and all drugs have some effect on lipoproteins (different forms of cholesterol). There is little data, however, on longer-term complications of obesity such as heart attacks. All drugs have side-effects and potential contraindications.[59] It is common for weight loss drugs to be tried for a period of time (e.g. 3 months), and to discontinue them or change to another agent if no benefit is achieved, such as weight loss less than 5% the total body weight.[12]
A meta-analysis of randomized controlled trials by the international Cochrane Collaboration concluded that in diabetic patients fluoxetine, orlistat and sibutramine could achieve significant but modest weight loss over 12-57 weeks, with long-term health benefits being unclear.[60]
Obesity may also influence the choice of drug treatment for diabetes. Metformin may lead to mild weight reduction (as opposed to sulfonylureas and insulin), and has been demonstrated to reduce the risk of cardiovascular disease in type 2 diabetics who are obese.[61] The thiazolidinediones may cause slight weight gain, but decrease the "pathologic" form of abdominal fat and may therefore be used in diabetics with central obesity.[62]
Bariatric surgery
-
Bariatric surgery (or "weight loss surgery") is the use of surgical interventions in the treatment of obesity. As every surgical intervention may lead to complications, it is regarded as a last resort when dietary modification and pharmacological treatment have proven to be unsuccessful. Weight loss surgery relies on various principles; the most common approaches are reducing the volume of the stomach, producing an earlier sense of satiation (e.g. by adjustable gastric banding and vertical banded gastroplasty) while others also reduce the length of bowel that food will be in contact with, directly reducing absorption (gastric bypass surgery). Band surgery is reversible, while bowel shortening operations are not. Some procedures can be performed laparoscopically. Complications from weight loss surgery are frequent.[63]
Two large studies have demonstrated a mortality benefit from bariatric surgery. A marked decrease in the risk of diabetes mellitus, cardiovascular disease and cancer.[64][65] Weight loss was most marked in the first few months after surgery, but the benefit was sustained in the longer term. In one study there was an unexplained increase in deaths from accidents and suicide that did not outweigh the benefit in terms of disease prevention. Gastric bypass surgery was about twice as effective as banding procedures.[65]
Counseling
A meta-analysis of randomized controlled trials concluded that "compared with usual care, dietary counseling interventions produce modest weight losses that diminish over time."[66]
Cultural and social significance
Etymology
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.[67]
History
Obesity was a status symbol in European culture: "The Tuscan General" by Alessandro del Borro, 17th century.
In several human cultures, obesity was associated with physical attractiveness, strength, and fertility. Some of the earliest known cultural 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."[68]
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.[69] 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.[70]
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.[71]
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.[72] 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.[73]
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[weasel words]. 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).
Public health and policy
Graphic chart comparing obesity percentages of the total population in
OECD member countries.
Prevalence
- United Kingdom
The Health Survey for England predicts that more than 12 million adults and 1 million children will be obese by 2010 if no action is taken.[74][75]
- United States
The prevalence of overweight and obesity in the United States makes obesity a leading public health problem. The United States has the highest rates of obesity in the developed world.[76] From 1980 to 2002, obesity has doubled in adults and overweight prevalence has tripled in children and adolescents.[77] From 2003-2004, "children and adolescents aged 2 to 19 years, 17.1% were overweight...and 32.2% of adults aged 20 years or older were obese."[77] Currently, about 119 million, or 64.5%, of US adults are either overweight or obese.[78] The prevalence in the United States continues to rise.[79]
- China
Because of the booming economy increasing average incomes, the population of China has recently begun a more sedentary lifestyle and at the same time begun consuming more calorie-rich foods. From 1991 to 2004 the percentage of adults who are overweight or obese increased from 12.9% to 27.3%.[80]
Obesity is a public health and policy problem because of its prevalence, costs and burdens.[81] The prevalence of obesity has been continually rising for two decades.[82] This sudden rise in obesity prevalence is attributed to environmental and population factors rather than individual behavior and biology because of the rapid and continual rise in the number of overweight and obese individuals.[83] The current environment produces risk factors for decreased physical activity and for increased calorie consumption. These environmental factors operate on the population to decrease physical activity and increase calorie consumption.
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[78]
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.[84]
- 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.[85]
- 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.[86]
- 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[citation needed].
- Urban sprawl may be a factor: obesity rates increase as urban sprawl increases, possibly due to less walking and less time for cooking.[87]
- 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[citation needed].
Public health and policy responses
Public health and policy responses to obesity seek to understand and correct the environmental factors responsible for shifts in the prevalence of overweight and obesity in a population. Obesity and overweight are, currently, primarily policy problems in the United States.[citation needed] Policy and public health solutions look to change the environmental factors that promote calorie dense, low nutrient food consumption and that inhibit physical activity.[citation needed]
In the United States, policy has focused primarily on controlling childhood obesity which has the most serious long-term public health implication. Efforts have been underway to target schools. There are efforts underway to reform federally-reimbursed meal programs, limit food marketing to children, and ban or limit access to sugar sweetened beverages. In Europe, policy has focused on limiting marketing to children. There has been international focus on sugar policy and the role of agriculture policy in producing food environments that produce overweight and obesity in a population. To confront physical activity, efforts have examined zoning and access parks and safe routes in cities.[citation needed]
In the United Kingdom, a 2004 report by the Royal College of Physicians, the Faculty of Public Health and the Royal College of Paediatrics and Child Health, titled "Storing up Problems",[88] was followed by a report by the British House of Commons Health Select Committee - the "the most comprehensive inquiry" ever by that body - on the impact of obesity on health and society in the UK and possible approaches to the problem.[89] 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.[12] A 2007 report produced by Sir Derek Wanless for the King's Fund warned that unless further action was taken, obesity had the capacity to cripple the National Health Service financially.[90]
Non-medical consequences
Besides increases in disease and mortality there are other implications of the present world trend in obesity. Among these are:
- Increased pressure on airline revenues (or increased fares) due to lobbying efforts to increase seating width on commercial airplanes, and due to higher fuel costs: in 2000, extra weight of obese passengers cost airlines and consumers US$275,000,000.[91]
- Increased litigation by obese persons suing restaurants (for causing obesity)[92] and airlines (over airline seating width)[2] [3]. The Personal Responsibility in Food Consumption Act of 2005 was motivated by a need to reduce litigation from obesity activists.
- Sizable societal economic costs attributable to obesity, with medical costs attributable to obesity rising to 78.5 billion dollars or 9.1 percent of all medical expenditures in the U.S. as of 1998[93][94] One recent study, however, found that while obesity prevention programs reduce the cost of treating diseases related to obesity, those reductions are offset by medical costs during the additional years of life gained. The authors conclude that reducing obesity may improve public health, but is unlikely to reduce overall health spending.[95]
- Decreased worker productivity as measured by usage of disability leave and absenteeism at work.[96]
- A study examining Duke University employees found that those with a BMI>40 filed twice as many workers compensation claims as workers whose BMI was 18.5-24.9, and had more than 12 times as many lost work days. The most common injuries were due to falls and lifting, and affected the lower extremities, wrists or hands, and backs.[97]
See also
References
- ^ a b c d e National Heart, Lung, and Blood Institute. Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults. International Medical Publishing, Inc. ISBN 1-58808-002-1.
- ^ Haslam DW, James WP (2005). "Obesity". Lancet 366 (9492): 1197–209. doi:10.1016/S0140-6736(05)67483-1. PMID 16198769.
- ^ Sweeting HN (2007). "Measurement and definitions of obesity in childhood and adolescence: a field guide for the uninitiated". Nutr J 6: 32. doi:10.1186/1475-2891-6-32. PMID 17963490.
- ^ Mei Z, Grummer-Strawn LM, Pietrobelli A, Goulding A, Goran MI, Dietz WH. Validity of body mass index compared with other body-composition screening indexes for the assessment of body fatness in children and adolescents. Am J Clin Nutr 2002;75:978-85. PMID 12036802.
- ^ Quetelet LAJ. (1871). Antropométrie ou Mesure des Différences Facultés de l'Homme. Brussels: Musquardt.
- ^ World Health Organization Technical report series 894: "Obesity: preventing and managing the global epidemic.". Geneva: World Health Organization, 2000. PDF. ISBN 92-4-120894-5.
- ^ NICE issues guidance on surgery for morbid obesity. National Institute for Health and Clinical Excellence (19th July 2002). Retrieved on 2007-03-08.
- ^ Bariatric Surgery. USC Center for Colorectal and Pelvic Floor Disorders. University of Southern California (2006). Retrieved on 2007-03-08.
- ^ Romero-Corral A, Montori VM, Somers VK, et al (2006). "Association of bodyweight with total mortality and with cardiovascular events in coronary artery disease: a systematic review of cohort studies". Lancet 368 (9536): 666–78. doi:10.1016/S0140-6736(06)69251-9. PMID 16920472.
- ^ a b Yusuf S, Hawken S, Ounpuu S, Dans T, Avezum A, Lanas F, McQueen M, Budaj A, Pais P, Varigos J, Lisheng L, INTERHEART Study Investigators. (2004). "Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study.". Lancet 364: 937-52. PMID 15364185.
- ^ Janssen I, Katzmarzyk PT, Ross R (2004). "Waist circumference and not body mass index explains obesity-related health risk". Am. J. Clin. Nutr. 79 (3): 379–84. PMID 14985210.
- ^ a b c National Institute for Health and Clinical Excellence. Clinical guideline 43: Obesity: the prevention, identification, assessment and management of overweight and obesity in adults and children. London, 2006.
- ^ Vanhecke TE, Franklin BA, Lillystone MA, Sandberg KR, deJong AT, Krause KR, Chengelis DL, McCullough PA. Caloric expenditure in the morbidly obese using dual energy X-ray absorptiometry. J Clin Densitomet 2006;9:438-444. PMID 17097530.
- ^ a b Bray GA (2004). "Medical consequences of obesity". J. Clin. Endocrinol. Metab. 89 (6): 2583-9. doi:10.1210/jc.2004-0535. PMID 15181027.
- ^ Manson JE, Willett WC, Stampfer MJ, et al (1995). "Body weight and mortality among women". N. Engl. J. Med. 333 (11): 677-85. PMID 7637744.
- ^ Grundy SM (2004). "Obesity, metabolic syndrome, and cardiovascular disease". J. Clin. Endocrinol. Metab. 89 (6): 2595-600. doi:10.1210/jc.2004-0372. PMID 15181029.
- ^ van der Steeg JW, Steures P, Eijkemans MJ, et al (2008). "Obesity affects spontaneous pregnancy chances in subfertile, ovulatory women". Hum. Reprod. 23 (2): 324–8. doi:10.1093/humrep/dem371. PMID 18077317.
- ^ Esposito K, Giugliano F, Di Palo C, Giugliano G, Marfella R, D'Andrea F, D'Armiento M, Giugliano D (2004). "Effect of lifestyle changes on erectile dysfunction in obese men: a randomized controlled trial". JAMA 291 (24): 2978-84. doi:10.1001/jama.291.24.2978. PMID 15213209.
- ^ Ejerblad E, Fored CM, Lindblad P, Fryzek J, McLaughlin JK, Nyrén O (2006). "Obesity and risk for chronic renal failure". J. Am. Soc. Nephrol. 17 (6): 1695-702. doi:10.1681/ASN.2005060638. PMID 16641153.
- ^ Whitmer RA, Gunderson EP, Barrett-Connor E, Quesenberry CP Jr, Yaffe K (2005). "Obesity in middle age and future risk of dementia: a 27 year longitudinal population based study". BMJ 330 (7504): 1360. PMID 15863436.
- ^ 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.
- ^ Centers for Disease Control and Prevention. Nutrition For Everyone. National Control for Health Statistics. Accessed July 15, 2007.
- ^ 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.
- ^ Caroline Bennett and agencies (August 13, 2007). Call to ban cars nears schools to tackle obesity. Retrieved on 2008-03-24.
- ^ Keith SW, Redden DT, Katzmarzyk PT, et al (2006). "Putative contributors to the secular increase in obesity: exploring the roads less traveled". Int J Obes (Lond) 30 (11): 1585-94. doi:10.1038/sj.ijo.0803326. PMID 16801930.
- ^ Wardle J, Carnell S, Haworth CM, Plomin R (2008). "Evidence for a strong genetic influence on childhood adiposity despite the force of the obesogenic environment". Am. J. Clin. Nutr. 87 (2): 398-404. PMID 18258631.
- ^ 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.
- ^ 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.
- ^ 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.
- ^ a b c Flier JS (2004). "Obesity wars: molecular progress confronts an expanding epidemic". Cell 116 (2): 337-50. PMID 14744442.
- ^ Boulpaep, Emile L.; Boron, Walter F. (2003). Medical physiology: a cellular and molecular approach. Philadelphia: Saunders. ISBN 0-7216-3256-4.
- ^ 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.
- ^ 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.
- ^ 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.
- ^ Snow V, Barry P, Fitterman N, Qaseem A, Weiss K (2005). "Pharmacologic and surgical management of obesity in primary care: a clinical practice guideline from the American College of Physicians". Ann Intern Med 142 (7): 525-31. PMID 15809464. Fulltext.
- ^ Behavioral counseling in primary care to promote a healthy diet: recommendations and rationale.. Retrieved on 2007-05-22.
- ^ Pignone MP, Ammerman A, Fernandez L, et al (2003). "Counseling to promote a healthy diet in adults: a summary of the evidence for the U.S. Preventive Services Task Force". American journal of preventive medicine 24 (1): 75-92. PMID 12554027.
- ^ Shaw K, Gennat H, O'Rourke P, Del Mar C (2006). "Exercise for overweight or obesity". Cochrane database of systematic reviews (Online) (4): CD003817. doi:10.1002/14651858.CD003817.pub3. PMID 17054187.
- ^ Truby H, Baic S, deLooy A, et al (2006). "Randomised controlled trial of four commercial weight loss programmes in the UK: initial findings from the BBC "diet trials"". BMJ 332 (7553): 1309-14. doi:10.1136/bmj.38833.411204.80. PMID 16720619.
- ^ a b Dansinger ML, Gleason JA, Griffith JL, Selker HP, Schaefer EJ (2005). "Comparison of the Atkins, Ornish, Weight Watchers, and Zone diets for weight loss and heart disease risk reduction: a randomized trial". JAMA 293 (1): 43-53. doi:10.1001/jama.293.1.43. PMID 15632335.
- ^ Halton TL, Willett WC, Liu S, et al (2006). "Low-carbohydrate-diet score and the risk of coronary heart disease in women". N. Engl. J. Med. 355 (19): 1991-2002. doi:10.1056/NEJMoa055317. PMID 17093250.
- ^ Pirozzo S, Summerbell C, Cameron C, Glasziou P (2002). "Advice on low-fat diets for obesity". Cochrane database of systematic reviews (Online) (2): CD003640. PMID 12076496.
- ^ Samaha FF, Iqbal N, Seshadri P, et al (2003). "A low-carbohydrate as compared with a low-fat diet in severe obesity". N. Engl. J. Med. 348 (21): 2074–81. doi:10.1056/NEJMoa022637. PMID 12761364.
- ^ Foster GD, Wyatt HR, Hill JO, et al (2003). "A randomized trial of a low-carbohydrate diet for obesity". N. Engl. J. Med. 348 (21): 2082–90. doi:10.1056/NEJMoa022207. PMID 12761365.
- ^ Nordmann AJ, Nordmann A, Briel M, et al (2006). "Effects of low-carbohydrate vs low-fat diets on weight loss and cardiovascular risk factors: a meta-analysis of randomized controlled trials". Arch. Intern. Med. 166 (3): 285-93. doi:10.1001/archinte.166.3.285. PMID 16476868.
- ^ Howard BV, Manson JE, Stefanick ML, et al (2006). "Low-fat dietary pattern and weight change over 7 years: the Women's Health Initiative Dietary Modification Trial". JAMA 295 (1): 39-49. doi:10.1001/jama.295.1.39. PMID 16391215.
- ^ Howard BV, Van Horn L, Hsia J, et al (2006). "Low-fat dietary pattern and risk of cardiovascular disease: the Women's Health Initiative Randomized Controlled Dietary Modification Trial". JAMA 295 (6): 655-66. doi:10.1001/jama.295.6.655. PMID 16467234.
- ^ Prentice RL, Caan B, Chlebowski RT, et al (2006). "Low-fat dietary pattern and risk of invasive breast cancer: the Women's Health Initiative Randomized Controlled Dietary Modification Trial". JAMA 295 (6): 629-42. doi:10.1001/jama.295.6.629. PMID 16467232.
- ^ Beresford SA, Johnson KC, Ritenbaugh C, et al (2006). "Low-fat dietary pattern and risk of colorectal cancer: the Women's Health Initiative Randomized Controlled Dietary Modification Trial". JAMA 295 (6): 643-54. doi:10.1001/jama.295.6.643. PMID 16467233.
- ^ Gardner CD, Kiazand A, Alhassan S, et al (2007). "Comparison of the Atkins, Zone, Ornish, and LEARN diets for change in weight and related risk factors among overweight premenopausal women: the A TO Z Weight Loss Study: a randomized trial". JAMA 297 (9): 969-77. doi:10.1001/jama.297.9.969. PMID 17341711.
- ^ Ebbeling CB, Leidig MM, Feldman HA, Lovesky MM, Ludwig DS (2007). "Effects of a low-glycemic load vs low-fat diet in obese young adults: a randomized trial". JAMA 297 (19): 2092-102. doi:10.1001/jama.297.19.2092. PMID 17507345.
- ^ Stern L, Iqbal N, Seshadri P, et al (2004). "The effects of low-carbohydrate versus conventional weight loss diets in severely obese adults: one-year follow-up of a randomized trial". Ann. Intern. Med. 140 (10): 778–85. PMID 15148064.
- ^ Garg A, Bantle JP, Henry RR, et al (1994). "Effects of varying carbohydrate content of diet in patients with non-insulin-dependent diabetes mellitus". JAMA 271 (18): 1421–8. PMID 7848401.
- ^ American Diabetes Association (2008). "Nutrition Recommendations and Interventions for Diabetes". Diabetes Care 31 suppl: S61-78. doi:10.2337/dc08-S061.
- ^ a b Thomas D, Elliott E, Baur L (2007). "Low glycaemic index or low glycaemic load diets for overweight and obesity" 3: CD005105. doi:10.1002/14651858.CD005105.pub2. PMID 17636786.
- ^ Jenkins DJ, Wolever TM, Taylor RH, et al (1981). "Glycemic index of foods: a physiological basis for carbohydrate exchange". Am. J. Clin. Nutr. 34 (3): 362-6. PMID 6259925.
- ^ Brand-Miller JC, Thomas M, Swan V, Ahmad ZI, Petocz P, Colagiuri S (2003). "Physiological validation of the concept of glycemic load in lean young adults". J. Nutr. 133 (9): 2728-32. PMID 12949357.
- ^ McMillan-Price J, Petocz P, Atkinson F, et al (2006). "Comparison of 4 diets of varying glycemic load on weight loss and cardiovascular risk reduction in overweight and obese young adults: a randomized controlled trial". Arch. Intern. Med. 166 (14): 1466-75. doi:10.1001/archinte.166.14.1466. PMID 16864756.
- ^ Rucker D, Padwal R, Li SK, Curioni C, Lau DC (2007). "Long term pharmacotherapy for obesity and overweight: updated meta-analysis". BMJ 335 (7631): 1194–9. doi:10.1136/bmj.39385.413113.25. PMID 18006966.
- ^ Norris SL, Zhang X, Avenell A, Gregg E, Schmid CH, Lau J (2005). "Pharmacotherapy for weight loss in adults with type 2 diabetes mellitus". Cochrane database of systematic reviews (Online) (1): CD004096. doi:10.1002/14651858.CD004096.pub2. PMID 15674929.
- ^ UK Prospective Diabetes Study (UKPDS) Group (1998). "Effect of intensive blood-glucose control with metformin on complications in overweight patients with type 2 diabetes (UKPDS 34)". Lancet 352 (9131): 854–65. doi:10.1016/S0140-6736(98)07037-8. PMID 9742977.
- ^ Fonseca V (2003). "Effect of thiazolidinediones on body weight in patients with diabetes mellitus". Am. J. Med. 115 Suppl 8A: 42S–48S. doi:10.1016/j.amjmed.2003.09.005. PMID 14678865.
- ^ Encinosa WE, Bernard DM, Chen CC, Steiner CA (2006). "Healthcare utilization and outcomes after bariatric surgery". Medical care 44 (8): 706-12. doi:10.1097/01.mlr.0000220833.89050.ed. PMID 16862031.
- ^ Sjöström L, Narbro K, Sjöström CD, et al (2007). "Effects of bariatric surgery on mortality in Swedish obese subjects". N. Engl. J. Med. 357 (8): 741-52. doi:10.1056/NEJMoa066254. PMID 17715408.
- ^ a b Adams TD, Gress RE, Smith SC, et al (2007). "Long-term mortality after gastric bypass surgery". N. Engl. J. Med. 357 (8): 753-61. doi:10.1056/NEJMoa066603. PMID 17715409.
- ^ Dansinger ML, Tatsioni A, Wong JB, Chung M, Balk EM (2007). "Meta-analysis: the effect of dietary counseling for weight loss". Ann. Intern. Med. 147 (1): 41-50. PMID 17606960.
- ^ The Oxford English Dictionary (website)
- ^ 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.
- ^ Greg Critser, Fat Land. Houghton Mifflin, NY, 2003. ISBN 0-14101-540-3.
- ^ Phillips, Stone. "Who's to blame for the U.S. obesity epidemic?", MSNBC, 2006-08-18. Retrieved on 2007-06-03. (English)
- ^ Paul Campos, The Diet Myth. Gotham Books, NY, 2004. ISBN 1-59240-135-X.
- ^ 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
- ^ 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
- ^ BBC England to have 13m obese by 2010 25 August 2006
- ^ Forecasting obesity to 2010
- ^ According to circa 2005 OECD data. See §3.3, Overweight and obesity, Health at a Glance 2007: OECD Indicators, SourceOECD (accessed on line January 12, 2008.)
- ^ a b Ogden CL, Carroll MD, Curtin LR, McDowell MA, Tabak CJ, Flegal KM (2006). "Prevalence of overweight and obesity in the United States, 1999-2004". JAMA 295 (13): 1549-55. doi:10.1001/jama.295.13.1549. PMID 16595758.
- ^ a b BBC NEWS | Health | US people getting fatter, fast
- ^ The rapid epidemic of obesity in individual U.S. states from 1985-2004 can be seen here and here
- ^ Popkin, Barry. "The World Is Fat", Scientific American, September, 2007, pp. 94. ISSN 0036-8733.
- ^ U.S. Dept. of Health and Human Services, Public Health Service, Office of Surgeon General, The Surgeon General's Call to Action to Prevent and Decrease Overweight and Obesity 2001 (2001)
- ^ Centers for Disease Control and Prevention, U.S. Obesity Trends 1984 - 2002 [1].
- ^ Morrill A, Chinn C. The obesity epidemic in the United States. J Public Health Policy 2004;25:353-366. PMID 15683071.
- ^ 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.
- ^ Pollan, Michael. "You Are What You Grow", New York Times, April 22, 2007. Retrieved on 2007-07-30.
- ^ Brian Wansink and Mike Huckabee (2005), “De-Marketing Obesity,” California Management Review, 47:4 (Summer), 6-18.
- ^ Lopez R (2004). "Urban sprawl and risk for being overweight or obese". Am J Public Health 94 (9): 1574-9. PMID 15333317.
- ^ (2004-02-11) Storing up problems; the medical case for a slimmer nation (PDF), London: Royal College of Physicians. ISBN 1-86016-200-2.
- ^ 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. London, UK: TSO (The Stationery Office). ISBN 0-21501-737-4. Retrieved on 2007-12-17.
- ^ Wanless, Sir Derek; John Appleby, Anthony Harrison, Darshan Patel (2007). Our Future Health Secured? A review of NHS funding and performance. London, UK: The King's Fund. ISBN 185717562X. Retrieved on 2007-12-17.
- ^ Dannenberg AL, Burton DC, Jackson RJ (2004). "Economic and environmental costs of obesity: the impact on airlines". American journal of preventive medicine 27 (3): 264. doi:10.1016/j.amepre.2004.06.004. PMID 15450642.
- ^ 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
- ^ Finkelstein EA, Fiebelkorn IA, Wang G (2003). "National medical spending attributable to overweight and obesity: how much, and who’s paying". National medical spending attributable to overweight and obesity: how much, and who's paying Online (May).
- ^ Obesity and Overweight: Economic Consequences. CDC. Retrieved on 2007-09-05.
- ^ van Baal PHM, Polder JJ, de Wit GA, Hoogenveen RT, Feenstra TL, et al. "Lifetime medical costs of obesity: Prevention no cure for increasing health expenditure," Public Library of Science: Medicine, 2008
- ^ The Economic Costs of Physical Inactivity, Obesity, and Overweight in California Adults, report by Chenoweth & Associates Inc. for the Cancer Prevention and Nutrition Section, California Center for Physical Activity, California Department of Health Services, Sacramento, CA, 2005.
- ^ Ostbye T, Dement JM, Krause KM (2007). "Obesity and workers' compensation: results from the Duke Health and Safety Surveillance System". Arch. Intern. Med. 167 (8): 766-73. doi:10.1001/archinte.167.8.766. PMID 17452538.
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other vitamins: A: Vitamin A deficiency/Bitot's spots, C: Scurvy,
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| Hyperalimentation | Obesity - Vitamin poisoning (Hypervitaminosis A, Hypervitaminosis D, Hypervitaminosis E) |
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