Obesity
Obesity | |
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Specialty | Endocrinology |
Obesity is a condition in which excess body fat has accumulated to such an extent that health may be negatively affected.[1] It is commonly defined as a body mass index (BMI = weight divided by height squared) of 30 kg/m2 or higher.[1] This distinguishes it from being overweight as defined by a BMI of between 25–29.9 kg/m2.[1]
Excessive body weight is associated with various diseases, particularly cardiovascular diseases, diabetes mellitus type 2, obstructive sleep apnea, certain types of cancer, and osteoarthritis.[2][3] As a result, obesity has been found to reduce life expectancy.[3] The primary treatment for obesity is dieting and physical exercise. If this fails, anti-obesity drugs and (in severe cases) bariatric surgery can be tried.[2][4]
Rising rates of obesity seem to be a consequence of modern life, with access to large amounts of high calorie food and limited need for physical activity due to great technological advancements. However, this environment of plenty affects different people in different ways; some people are able to maintain a reasonable balance between energy input and energy expenditure whereas others have a chronic imbalance that favors energy input, which expresses itself as overweight and obesity. These differences could be due to genetic reasons, imbalance of the gut flora, or simple excess of intake compared with a person's basal metabolic rate and level of physical exercise. A combination of excessive caloric intake, lack of physical activity, and genetic susceptibility is thought to explain most cases of obesity, with a limited number of cases due solely to genetics, diet, medical reasons, or psychiatric illness.
With rates of adult and childhood obesity increasing, authorities view it as a serious public health problem.[4] Between 1980-2000, obesity among adults has more than doubled; obesity among adolescents has tripled and normal weight adults are in the minority. The obesity epidemic affects men and women of all ages, ethnic origin, races and educational attainment.[5] In the US, obesity is the second-leading cause of preventable death after smoking, but soon will overtake smoking.[5]
Although obesity is often stigmatized in the modern Western world, it has been perceived as a symbol of wealth and fertility at other times in history.[6]
Classification
Obesity, in absolute terms, is an increase of body adipose tissue (fat tissue) mass. In a practical setting it is difficult to determine this directly. Therefore obesity is typically assessed by BMI (body mass index) and in terms of its distribution via the waist circumference.[7] In addition, the presence of obesity needs to be evaluated in the context of other risk factors such as medical conditions that could influence the risk of complications.[2]
BMI
Body mass index or BMI is a simple and widely used method for estimating body fat mass.[8] BMI was developed in the 19th century by the Belgian statistician and anthropometrist Adolphe Quetelet.[9] BMI is an accurate reflection of body fat percentage in the majority of the adult population. It is less accurate in people such as body builders and pregnant women in whom body composition is affected.[2]
BMI is calculated by dividing the subject's weight by the square of his or her height, typically expressed either in metric or US "Customary" units:
- Metric:
where is the subject's weight in kilograms and is the subject's height in metres.
- US/Customary and imperial:
where is the subject's weight in pounds and is the subject's height in inches.
BMI | Classification |
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Less than 18.5 | underweight |
18.5–24.9 | normal weight |
25.0–29.9 is | overweight |
30.0–34.9 is | class I obesity |
35.0–39.9 | class II obesity |
Over 40.0 | class III obesity |
The most commonly used definitions, established by the WHO in 1997 and published in 2000, provide the values listed in the table at right.[1]
Some modifications to the WHO definitions have been made by particular bodies:[10][11]
- A BMI of 35.0 or higher in the presence of at least one other significant comorbidity is also classified by some bodies as class III obesity.
- For Asians, overweight is a BMI between 23 and 29.9 kg/m2 and obesity a BMI >30 kg/m2.
The surgical literature breaks down "class III" obesity into further catergories. [12]
- Any BMI > 40 is severe obesity
- A BMI of 40.0–49.9 is morbid obesity
- A BMI of >50 is super obese
Waist circumference and waist–hip ratio
In those with a BMI under 35, intra-abdominal body fat is related to negative health outcomes independent of total body fat.[13] Intra-abdominal or visceral fat has a particularly strong correlation with cardiovascular disease.[14] In a study of 15,000 subjects, waist circumference also correlated better with metabolic syndrome than BMI.[15] Women who have abdominal obesity have a cardiovascular risk similar to that of men.[16] In people with a BMI over 35, measurement of waist circumference however adds little to the predictive power of BMI as most individuals with this BMI have an abnormal waist circumferences.[2]
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) are both used as measures of central obesity.[14]
Body fat percentage
Body fat percentage is total body fat expressed as a percentage of total body weight. It is generally agreed that men with more than 25% body fat and women with more than 33% body fat are obese.[17] Body fat percentage can be estimated from a person's BMI by the following formula:
- where gender is 0 if female and 1 if male
This formula takes into account the fact that body fat percentage is 10% greater in women than in men for a given BMI. It recognizes that a person's percentage body fat increases as they age even if their weight remains constant. The results have an accuracy of 4%.[18]
Direct attempts to determine body fat percent are difficult and often expensive. One of the most accurate methods is to weigh a person underwater which is known as hydrostatic weighting. Two other simpler and less accurate methods for measuring body fat therefore have historically been used. The first is the skinfold test, in which a pinch of skin is precisely measured to determine the thickness of the subcutaneous fat layer. It has not, however, been adequately evaluated in obese subjects.[18] The other is bioelectrical impedance analysis which uses electrical resistance. Bioelectrical impedance however has not been shown to provide an advantage over BMI. Therefore the routine use of these tests are discouraged.[4]
Body fat percentage measurement techniques used mainly for research include computed tomography (CT scan), magnetic resonance imaging (MRI), and dual energy X-ray absorptiometry (DEXA).[13] These techniques provide very accurate measurements, but it may be difficult to scan the severely obese due to weight limits of the equipment and insufficient diameter of the CT or MRI scanner.[18]
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 complications that would indicate a need to commence or intensify treatment for obesity.[2] Smoking, high blood pressure, age and family history are other risk factors that, in combination with obesity, may indicate an additional reason for treatment.[2]
Childhood obesity
Obesity in children and adolescents is defined as a BMI greater then the 95th percentile.[19] Rates of obesity among this group have increased by 3 to 5 % from 1990 to the year 2000.[20] Rates have also increased in most other developed countries worldwide.[21]
A lot goes into why childhood obesity has been on the rise. One factor is heredity, it has been found that if one parent is obese, there would be a 50% chance their child will be the same, and 80% chance if both parents are obese.[5] Working parents play a factor into this as well as children would end up eating alone in front of the TVs and parents would compensate for their absence by giving the children fast food or sweets and chocolate. There has been an increase in snacking and soft drink consumption in children over the past years which play a major role as well. Over 50% of the commercials children view are based on food, generally sugary and unhealthy food, which would encourage them to purchase and consume.[5]
Effects on health
Mortality
Obesity is one of the leading preventable causes of death.[22][23][24] Mortality risk varies with BMI; the lowest risk is found at a BMI of 22–24 kg/m2 and increases with changes in either direction.[25] A BMI of over 32 is associated with a doubling of risk of death[26] and obesity is estimated to cause an excess 111,909 to 365,000 death per year in the United States.[27][3] Obesity on average reduces life expectancy by 6–7 years.[28][3] Severe obesity (BMIs >40) reduces life expectancy by 20 years for men and 5 years for women.[17]
Morbidity
A large number of physical and mental conditions have been associated with obesity.
Health consequences can be categorized by the effects of increased fat mass (osteoarthritis, obstructive sleep apnea, social stigmatization) or by the increased number of fat cells (diabetes, cancer, cardiovascular disease, non-alcoholic fatty liver disease).[3][29] Increases in body fat alter the body's response to insulin, potentially leading to insulin resistance. Increased fat also creates a proinflammatory state, increasing the risk of thrombosis.[29]
Central obesity, characterized by its high waist to hip ratio, is an important risk for metabolic syndrome. Metabolic syndrome is a combination of medical disorders which often includes diabetes mellitus type 2, high blood pressure, high blood cholesterol, and triglyceride levels.[30]
Obesity is related to a variety of other complications. Some of these are directly caused by obesity and others are indirectly related through mechanisms sharing a common cause such as poor diet or a sedentary lifestyle. The strength of the link between obesity and specific conditions varies. One of the strongest is the link with type 2 diabetes. Excess weight is behind 64% of cases of diabetes in men and 77% in women.[18]
Medical field | Condition | Medical field | Condition |
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Cardiovascular |
|
Gastrointestinal | |
Endocrine and reproductive |
|
Respiratory | |
Musculoskeletal |
|
Psychological |
|
Neurologic | Skin | ||
Cancer[36] | Genitourinary |
Obesity survival paradox
Although the negative health consequences of obesity in the general population are well supported by the available evidence, health outcomes in certain subgroups seem to be improved at an increased BMI, a phenomenon known as the obesity survival paradox.[40] The paradox was first described in 1999 in overweight and obese patients undergoing hemodialysis. Since then it has been found in a few other subgroups and explanations for its occurrence have been put forward.[40]
In people with heart failure, those with a BMI between 30.0–34.9 had lower mortality then those with a normal weight. This has been attributed to the fact that people often lose weight as they become progressively more ill.[41] Similar findings have been made in other types of heart disease. People with class I obesity and heart disease do not have greater rates of further heart problems than people of normal weight who also have heart disease. In people with greater degrees of obesity, however, risk of further events is increased.[42][43] Even after cardiac bypass surgery, no increase in mortality is seen in the overweight and obese.[44] One study found that the increased survival could be explained by the more aggressive treatment obese people receive after a cardiac event.[45]
Causes
Most researchers agree that a combination of excessive calorie consumption and a sedentary lifestyle are the primary causes of obesity.[46] In a minority of cases, increased food consumption can be attributed to genetic, medical, or psychiatric illness. Generally however the rising prevalence of obesity is attributed to the availability of an easily accessible and palatable diet,[47] car culture and mechanized manufacturing.[48][49] A 2006 review identifies ten other possible contributors to the recent increase of obesity: (1) insufficient sleep, (2) endocrine disruptors—food substances that interfere with lipid metabolism, (3) decreased variability in ambient temperature, (4) decreased rates of smoking as smoking 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.[50]
Diet
Despite the widespread availability of nutritional information in schools, doctors' offices, on the internet and on product packaging,[51] it is evident that overeating remains a substantial problem. In the period of 1971–2000, obesity rates in the United States increased from 14.5% to 30.9%.[52] During the same time period, an increase occurred in the average amount of calories consumed. For women, the average increase was 335 calories per day (1542 calories in 1971 and 1877 calories in 2004), while for men the average increase was 168 calories per day (2450 calories in 1971 and 2618 calories in 2004). Most of these extra calories came from an increase in carbohydrate consumption rather than an increase in fat consumption.[53] The primary sources of these extra carbohydrates are sweetened beverages, which now accounts for almost 25 percent of daily calories in young adults.[54] Dietary trends have changed with reliance on energy-dense fast-food meals tripling between 1977 and 1995, and calorie intake from fast food quadrupling over the same period.[55] In the early 1980s, the administration of Ronald Reagan lifted regulations limiting the advertising of sweets and fast food to children, and advertisement of these products directed towards children has increased.[56] Agricultural policy and techniques in the United States and Europe have led to lower food prices. In the United States, subsidization of corn, soy, wheat, and rice through the U.S. farm bill has made the main sources of processed food relatively cheap compared to fruits and vegetables.[57]
There is little evidence to support the commonly expressed view that some obese people eat little yet gain weight due to a slow metabolism. What has been found, however, is that some obese people underreport how much food they consume compared to those of normal weight.[18]
Sedentary lifestyle
A sedentary lifestyle plays a significant role in obesity.[18] Obese people are less active than those of normal weight. For example in Canada, 27.0% of sedentary men are obese as opposed to 19.6% of active men.[58] Normal weight people are more fidgety then their obese conterparts; this relationship is maintained even if normal weight people eat more or the obese person loses weight.[59]
In 2000 the CDC estimated that more than 40% of the US population was sedentary, another 30% was active but not sufficiently and less than 30% had an adequate level of physical activity.[54] There has been a trend toward decreased physical activity in part due to increasingly mechanized forms of work, changing modes of transportation, and increasing urbanization. A study from China found urbanization reduces daily energy expenditure by about 300–400 kcal and going to work by car or bus reduced it by a further 200 kcal.[49] Obesity rates have increased in relation to expanding suburbs. This has been attributed to increased time spent commuting, leading to less exercise and less meal preparation at home.[60] Driving one's children to school has become increasingly popular. In the USA the proportion of children who walk or bike to school declined between 1969 (42%) and 2001 (16%) resulting in less exercise.[54] Studies in children and adults have found an association between the number of hours of television watched and the prevalence of obesity.[61][62][63]
Genetics
Like many other medical conditions, obesity is the result of an interplay between genetic and environmental factors. Polymorphisms in various genes controlling appetite and metabolism may predispose to obesity when sufficient calories are present. Obesity is a major feature in a number of rare genetic conditions: Prader-Willi syndrome, Bardet-Biedl syndrome, MOMO syndrome, leptin receptor mutations, congenital leptin deficiency, and melanocortin receptor mutations. In a people with early-onset severe obesity (defined by an onset before ten years of age and body mass index over three standard deviations above normal), 7% harbor a single locus mutation.[64] Apart from the above syndromes, an association has been found between an FTO gene polymorphism and weight. The adults in the study who were homozygous for this allele weighed about 3 kilograms more and had a 1.6-fold greater rate of obesity than those who had not inherited this trait.[65] The association disappeared, though, when those with FTO polymorphisms participated in moderately intensive physical activity equivalent to 3 to 4 hours of brisk walking.[66] One study found that 80% of the offspring of two obese parents were obese, in contrast to less then 10% of the offspring of two parents who were of normal weight.[34][18]
The percentage of obesity that can be attributed to genetics varies from 6% to 85% depending on the population examined.[67] The thrifty gene hypothesis postulates that certain ethnic groups may be more prone to obesity in an equivalent environment. Their ability to take advantage of rare periods of abundance by storing energy as fat would be advantageous during times of varying food availability, and individuals with greater adipose reserves would be more likely survive famine. This tendency to store fat, however, would be maladaptive in societies with stable food supplies.[68] This is the presumed reason that Pima Indians, who evolved in a desert ecosystem, developed some of the highest rates of obesity when exposed to a Western lifestyle.[47]
Gut Flora
Our intestine is populated by a vast number of microflora which prove to be essential for our everyday life. It has been reported that gut flora for each individual has a specific metabolic efficiency. The difference in this aspect among individuals regulates the energy storage and the predisposition to obesity. It has been proven that the increase in obesity has an effect in the diversity of the gut flora as compared to lean people. The affect is specifically on two bacteria from the gut flora: Bacteroidetes and Firmicutes.
It was found that genetically obese (ob/ob) mice have 50% more Firmicutes and 50% fewer Bacteroidetes than genetically lean (+/+) mice. Based on this finding, an experiment was conducted on humans to investigate the relationship between these two bacteria and obesity. This experiment studied 12 obese people that were assigned low calorie diets. Their gut flora was tested for a year and it was found that the Bacteroidetes increased in number whereas the Firmicutes decreased in number as they lost weight ( there was a correlation between the weight loss and bacteria).[69] This change was division-wide, meaning the bacterial diversity remained the same without any blooms or extinctions of any bacterial species. These findings show a coexistence between the two bacteria which would imply that minimum competition for resources would occur by their cooperation or specialization. Therefore an obese gut has as yet an uncharacterized property which leads to an imbalance between the two bacteria; it tips towards the Firmicutes.[69]
Some studies are looking into the possible affects of different ratio of Bacteroidetes and Firmicutes forming in infants which may vary depending on type of delivery, choice of feeding, medication and hygiene that the infants undergo. The early colonization depending on these factors, may play a role with how much Bacteroidetes and Firmicutes one ends up with later.
Medical and psychiatric illness
Certain physical and mental illnesses and the pharmaceutical substances used to treat them can increase risk of obesity. Medical illnesses that increase obesity risk include several rare genetic syndromes (listed above) as well as some congenital or acquired conditions: hypothyroidism, Cushing's syndrome, growth hormone deficiency,[70] and the eating disorders: binge eating disorder and night eating syndrome.[3] However, obesity is not regarded as a psychiatric disorder, and therefore is not listed in the DSM-IVR as a psychiatric illness.[34]
Certain medications may cause weight gain or changes in body composition; these include insulin, sulfonylureas, thiazolidinediones, atypical antipsychotics, antidepressants, steroids, sulfonylureas, certain anticonvulsants (phenytoin and valproate), pizotifen, and some forms of hormonal contraception.[3]
Socioeconomic
While genetic influences are important to understanding obesity, they cannot explain the current dramatic increase seen within specific countries or globally.[47] Though it is accepted that calorie consumption in excess of calorie expenditure leads to obesity on an individual basis, the cause of the shifts in these two factors on the societal scale is much debated. There are a number of theories as to the cause but most believe it is a combination of various factors.
The correlation between social class and BMI varies globally. A review in 1989 found that in developed countries women of a high social class were less likely to be obese. No significant differences were seen among men of different social classes. In the developing world, women, men, and children from high social classes had greater rates of obesity.[71] An update of this review carried out in 2007 found the same relationships, but they were weaker. The decrease in strength of correlation was felt to be due to the effects of globalization.[72]
Many explanations have been put forth for associations between BMI and social class. It is thought that in developed countries, the wealthy are able to afford more nutritious food, they are under greater social pressure to remain slim, and have more opportunities along with greater expectations for physical fitness. In the developing world the ability to afford food, high energy expenditure with physical labor, and cultural values favoring a larger body size are believed to contribute to the observed patterns.[72] Attitudes toward body mass held by people in one's life may also play a role in obesity. A correlation in BMI changes over time has been found between friends, siblings, and spouses.[73]
Smoking has a significant effect on a individual's weight. Those who quit smoking gain an average of 4.4 kilograms for men and 5.0 kg for women over ten years.[74] Changing rates of smoking however have had little effect on the overall rates of obesity.[75]
Neurobiological mechanisms
Flier summarizes the many possible pathophysiological mechanisms involved in the development and maintenance of obesity.[76] 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, as well as 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, most obese individuals are thought to be leptin resistant and have been found to have high levels of leptin.[77] 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.[76]
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.[76] 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.[78]
The arcuate nucleus contains two distinct groups of neurons.[76] 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.[76]
Management
The main treatment for obesity consists of dieting and physical exercise. Diet programs may produce weight loss over the short term,[79] but keeping this weight off can be a problem. It often requires making exercise and a lower calorie diet a permanent part of a person's lifestyle.[80][81] In the general population only 20% are successful at long-term weight loss maintenance.[82] In a more structured setting, however, 67% of people who lost greater then 10% of their body mass maintained or continued to lose weight one year later.[83] An average maintained weight loss of more then 3 kg or 3% of total body mass could be sustained for five years.[84] There are significant benefits to weight loss. In a prospective study, intentional weight loss of any amount was associated with a 20% reduction in all-cause mortality.[85]
Diet
Diets to promote weight loss are generally divided into four categories: low-fat, low-carbohydrate, low-calorie, and very low calorie.[79] A meta-analysis of six randomized controlled trials found no difference between the main diet types (low calorie, low carbohydrate, and low fat), with a 2–4 kilogram weight loss in all studies.[79]
Low-fat diets
Low-fat diets involve the reduction of the percentage of fat in one's diet. Calorie consumption is reduced but not purposely so. Diets of this type include NCEP Step I and II. A meta-analysis of 16 trials of 2–12 months' duration found that low-fat diets resulted in weight loss of 3.2 kg over eating as normal.[79]
Low-carbohydrate diets
Low carbohydrate diets such as Atkins and Protein Power are relatively high in fat and protein. They are very popular in the press but are not recommended by the American Heart Association. A review of 94 trials found that weight loss was associated with decreased calorie consumption rather than any special properties of reduced carbohydrate consumption. No adverse affect from low carbohydrate diets were detected.[86]
Low-calorie diets
Low-calorie diets usually produce an energy deficit of 500–1000 calories per day, which can result in a 0.5 kilogram weight loss per week. They include the DASH diet and Weight Watchers among others. The National Institutes of Health reviewed 34 randomized controlled trials to determine the effectiveness of low-calorie diets. They found that these diet lowered total body mass by 8% over 3–12 months.[79]
Very low-calorie diets
Very low calorie diets provide 200–800 kcal/day while maintaining protein intake and limiting calories from both fat and carbohydrates. They subject the body to starvation and produce an average weekly weight loss of 1.5–2.5 kilograms. These diets are not recommended for general use as they are associated with adverse side effects such as loss of lean muscle mass, increased risks of gout, and electrolyte imbalances. People attempting these diets must be monitored closely by a physician to prevent complications.[79]
Exercise
With use, muscles consume energy derived from both fat and glycogen. Due to the large size of leg muscles, walking, running, and cycling are the most effective means of exercise to reduce body fat.[87][88] Exercise affects macronutrient balance. During exercise, there is a shift to greater use of fat as a fuel, post-exercise increases lipid oxidation to replenish glycogen. [5]
A meta-analysis of 43 randomized controlled trials by the Cochrane Collaboration found that exercising alone led to limited weight loss. In combination with diet, however, it resulted in a 1 kilogram weight loss over dieting alone. A 1.5-kilogram loss was observed with a greater degree of exercise.[89] Even though exercise as carried out in the general population has only modest effects, a dose response curve is found, and very intense exercise can lead to substantial weight loss. During 20 weeks of basic military training with no dietary restriction, obese military recruits lost 12.5 kg.[90]
A systematic review found that people who use pedometers, during on average an 18 week period, increased their physical activity by 27% and subsequently decreased their BMI by 0.38.[91]
Medication
Most drugs are anorexiants; appetite suppressants that act on either one or more neurotransmitters. They act by increasing secretion of the neurotransmitter(s) such as dopamine, norepinephrine, serotonin, or by inhibiting the reuptake, or by a combination of these mechanisms.[5] There are two commonly prescribed medications for obesity. One is orlistat, which reduces intestinal fat absorption by inhibiting pancreatic lipase; the other is sibutramine, which acts in the brain to inhibit deactivation of the neurotransmitters norepinephrine, serotonin, and dopamine (very similar to some anti-depressants), therefore decreasing appetite. Rimonabant, a third drug, works via a specific blockade of the endocannabinoid system. It has been developed from the knowledge that cannabis smokers often experience extreme hunger pangs, which cannabis smokers refer to as 'the munchies'. It has been approved in Europe for the treatment of obesity but has not yet received approval in the United States or Canada due to safety concerns.[92][93] Weight loss with these drugs is modest; over the longer term, average weight loss on orlistat is 2.9 kg, sibutramine is 4.2 kg and rimonabant is 4.7 kg. Orlistat and rimonabant lead to a reduced incidence of diabetes, and all drugs have some effect on cholesterol. There is little data on how these drugs affect the longer-term complications of obesity.[94] It is common for weight loss drugs to be tried and if there is little or no benefit from them to discontinue treatment.[4] A meta-analysis of randomized controlled trials by the Cochrane Collaboration concluded that in diabetic patients fluoxetine (Prozac), orlistat and sibutramine could achieve modest but significant weight loss over 12–57 weeks. The long-term health benefits remained unclear.[95]
Obesity may also influence the choice of drugs used to treat diabetes. Metformin may lead to mild weight loss in comparison to sulfonylureas and insulin. It has been show to reduce the risk of cardiovascular disease in obese type 2 diabetics.[96] The thiazolidinediones, on the other hand, may cause weight gain, but decrease central obesity and therefore can be used in obese diabetics.[97]
Ephedrine (Ma Huang) is a stimulant effective for weight loss; however it is not recommended due to potential side effects.[98]
Bariatric surgery
Bariatric surgery ("weight loss surgery") is the use of surgical interventions in the treatment of obesity. As every operation may have complications, surgery is only recommended for severely obese people (BMI >40) who have failed to lose weight with dietary modification and pharmacological treatment. 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.[99]
Surgery for severe obesity is associated with long-term weight loss and decreased overall mortality. A controlled prospective study carried out in Sweden involving 4,047 people found a weight loss of between 14% and 25% at 10 years depending on the type of procedure performed and a 29% reduction in all cause mortality when compared to standard weight loss measures.[100] A marked decrease in the risk of diabetes mellitus, cardiovascular disease and cancer has also been found after bariatric sugery.[101][102] Weight loss is marked in the first few months after surgery and is sustained in the long term. In one study there was an unexplained increase in deaths from accidents and suicide but this did not outweigh the benefit in terms of disease prevention. When comparisons are made between the procedures gastric bypass surgery is found to be about twice as effective as banding procedures.[102]
The effects of liposuction however are less well determined, with some small studies showing benefits[103] and others showing none.[104]
Clinical protocols
In a clinical practice guideline by the American College of Physicians, the following five recommendations are made:[105]
- 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 over 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.[106][107]
Behavioral Therapy
This involves changing diets, habits and physical activities to new behaviors that encourage weight loss. This program enables people to connect with a group of others that are attempting to loose weight so as to encourage and help each other out. This form of therapy helps provide realistic goals, partnership and frequent contact with health care provider, encourage self monitoring of diet and exercise to increase one's awareness of the activities and much more. Long term results are modest and can be done on the internet or in person by counseling. [5]
Epidemiology
The World Health Organization formally recognized the global nature of the obesity epidemic in 1997.[54] As of 2005 the WHO estimates that at least 400 million adults (9.8%) are obese, with higher rates among women than men.[1] The rate of obesity also increases with age at least up to 50 or 60 years old.[18] Once considered a problem only of high-income countries, obesity rates are rising worldwide. These increases have been felt most dramatically in urban settings.[1] The only remaining region of the world were obesity is not common is sub-Saharan Africa.[3]
- South Pacific
Many of the island nations of the South Pacific have very high rates of obesity. Nauru has the highest rates of obesity in the world (80%) followed by Tonga, the Federated States of Micronesia, and the Cook Islands. Being big has traditionally been associated with health, beauty, and status and many of these beliefs remain prevalent today.[109]
- Australia
Studies conducted in 2006 found that close to 52% of Australian women and up to 67% of Australian men aged 25 or over are overweight or obese.[110]
- China
Because the booming economy has increased average incomes, the population of China has since the 1980s taken up a more sedentary lifestyle and begun consuming more calorie-rich foods.[unreliable source?] From 1991 to 2004 the percentage of overweight or obese adults increased from 12.9% to 27.3%.[111]
- India
In India urbanization and modernization has been associated with obesity. As of 1999 in northern India 11% of urban women were found to be obese in contrast to 3.7% of rural women. Well women of high socioeconomic class had a rate of obesity of 10.4% as opposed to 0.9% in women of low socioeconomic class.[112] With people moving into urban centers and wealth increasing, concerns about an obesity epidemic in India are growing.
- European Union
Between the 1970s and the 2000s, rates of obesity in most European countries have increased. During the 1990s and 2000s the 27 countries making up the EU reported rates of obesity from 10–27% in men and from 10–38% in women.[113]
- United Kingdom
In the UK the rate of obesity has increased about fourfold over the last 25 years, reaching current levels of 22%.[18]
- Mexico
Mexico has the second-highest rate of obesity in the developed world, at 24.2% of the population.[108]
- United States
The United States has the highest rates of obesity in the developed world.[108] From 1980 to 2002, obesity rates have doubled, reaching the current rate of 32% of the adult population.[114] Rates of obesity vary by ethnicity and gender. In the US, 28% of men and 34% of women are obese, with rates rising to as high as 50% among African American women. [115] The prevalence of class III obesity (BMI ≥40) has increased the most dramatically from 0.78 percent in 1990 to 2.2 percent in 2000.[116]
- Canada
The number of Canadians who are obese has risen dramatically in recent years. In 2004, direct measurements of height and weight found 23.1% of Canadians older than 18 had a BMI greater than 30. When broken down into degrees of obesity, 15.2% were class I (BMI 30–34.9), 5.1% were class II (BMI 35–39.9), and 2.7%, class III (BMI > 40). This is in contrast to self-reported data the previous year of 15.2% and in 1978/1979 of 13.8%. The greatest increases occurred among the more severe degrees of obesity; class III obesity increased from 0.9% to 2.7% from 1978/1979 to 2004. Obesity in Canada varies by ethnicity; people of Aboriginal origin have a significantly higher rate of obesity (37.6%) than the national average.[58]
Public health
The World Health Organization ( WHO ) predicts that overweight and obesity may soon replace more traditional public health concerns such as undernutrition and infectious diseases as the most significant cause of poor health.[117]Obesity is a public health and policy problem because of its prevalence, costs, and health effects.[118] Public health efforts seek to understand and correct the environmental factors responsible for the increasing prevalence of obesity in the population. Solutions look at changing the factors that cause excess calorie consumption and inhibit physical activity. Efforts include federally reimbursed meal programs in schools, limiting direct junk food marketing to children,[119] and decreasing access to sweetened beverages in schools.[120] When constructing urban environments, efforts have been made to increase access to parks and to develop pedestrian routes.[121]
Many countries and groups have published reports pertaining to obesity. In 1998 the first US Federal guidelines were published, titled "Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults: The Evidence Report".[2] In 2006 the Canadian Obesity Network published the "Canadian Clinical Practice Guidelines (CPG) on the Management and Prevention of Obesity in Adults and Children". This is a comprehensive evidence-based guideline to address the management and prevention of overweight and obesity in adults and children.[122] In 2004, the United Kingdom Royal College of Physicians, the Faculty of Public Health and the Royal College of Paediatrics and Child Health released the report "Storing up Problems", which highlighted the growing problem of obesity in the UK.[123] The same year, the House of Commons Health Select Committee published its "most comprehensive inquiry [...] ever undertaken" into the impact of obesity on health and society in the UK and possible approaches to the problem.[124] 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.[4] 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.[125]
History and culture
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.[126]
Historical trends
Obesity has been recognized as a medical disorder at least since the time of Hippocrates when he stated that "Corpulence is not only a disease itself, but the harbinger of others".[3] It was known to the Indian surgeon Sushruta (6th century BCE), who related obesity to diabetes and heart disorder.[128] He recommended physical work to help cure it and its side effects.[128] For most of human history mankind struggled with food scarcity. With the onset of the industrial revolution it was realized that the military and economic might of nations were dependent on both the body size and strength of their soldiers and workers. Increasing the average body mass index from underweight to the normal range playied a significant role in the development of industrialized societies. Height and weight thus both increased though the 19th century in the developed world. During the 20th century, as populations reached their genetic potential for height, weight began increasing much more than height, resulting in obesity.[54] In the 1950s increasing wealth in the developed world decreased child mortality, but as body weight increased heart and kidney disease became more common.[54][129] During this time period insurance companies realized the connection between weight and life expectancy and increased premiums for the obese.[3]
Many cultures throughout history have viewed obesity as a flaw. The obesus or fat character in Greek comedy was a glutton and figure of mockery. During Christian times food was viewed as a gateway to the sins of sloth and lust.[6] In modern Western culture, excess weight is often regarded as unattractive, and obesity is commonly associated with various negative stereotypes. All ages can face social stigmatization and may be targeted by bullies or shunned by their peers. In Western culture obesity is once again seen as a sign off a low socio-economic status.[130] Obese people are less likely to be hired for a job and are less likely to be promoted.[34] Obese people are also paid less than their non-obese counterparts for an equivalent job. Obese women on average make 6% less and obese men make 3% less.[18]
The weight that is generally viewed as an ideal has become lower since the 1920s. The average height of Miss America pageant winners increased by 2% from 1922 to 1999, while their average weight decreased by 12%.[34]
Weight loss drugs
The first described attempts at producing weight loss are those of Soranus of Ephesus, a Greek physician, in the second century AD. He prescribed elixirs of laxatives and purgatives, as well as heat, massage, and exercise. This remained the mainstay of treatment for well over a thousand years. It was not until the 1920s and 1930s that new treatments began to appear. Based on its effectiveness for hypothyroidism, thyroid hormone became a popular treatment for obesity in otherwise healthy people. It had a modest effect but produced the symptoms of hyperthyroidism as a side effect, such as palpitations and difficulty sleeping. Dinitrophenol (DNP) was introduced in 1933; this worked by uncoupling the biological process of oxidative phosphorylation in mitochondria, causing them to produce heat instead of ATP. The most significant side effect was a dramatic rise in body temperature, frequently causing death. By the end of the 1930s DNP had fallen out of use.[47]
Amphetamines (marketed as Benzedrine) became popular for weight loss during the late 1930s. They worked primarily by suppressing appetite, and had other beneficial effects such as increased alertness. Use of amphetamines increased over the subsequent decades, culminating in the "rainbow pill" regime. This was a combination of multiple pills, all thought to help with weight loss, taken throughout the day. Typical regimens included stimulants, such as amphetamines and thyroid hormone, diuretics, digitalis, laxatives, and often a barbiturate to suppress the side effects of the stimulants. In 1967/1968 a number of deaths attributed to diet pills triggered a Senate investigation and the gradual implementation of greater restrictions on the market. This culminating in 1979 with the FDA banning the use of amphetamines, then the most effective of the diet drugs, in diet pills.[47]
Meanwhile, phentermine had been FDA approved in 1959 and fenfluramine in 1973. The two were no more popular then other drugs until in 1992 a researcher reported that the two caused a 10% weight loss which was maintained for over two years.[131] Fen-phen was born and rapidly became the most commonly prescribed diet medication. Dexfenfluramine (Redux) was developed in the mid-1990s as an alternative to fenfluramine with less side-effects, and received regulatory approval in 1996. However, this coincided with mounting evidence that the combination could cause valvular heart disease in up to 30% of those who had taken it, leading to withdrawal of Fen-phen and dexfenfluramine from the market in September 1997.[47]
Ephedra was removed from the US market in 2004 over concerns that it raises blood pressure and could lead to strokes and death.[34]
Non-medical effects
In addition to its health impacts, obesity leads to many problems including social stigmatization, disadvantages in employment, and increased business costs.[18] These effects are felt by all levels of society from individuals, to corporations, to governments.
Obesity and its health effects create sizable economic costs. In 1998 in the US, the medical costs attributable to obesity were $78.5 billion USD, or 9.1% of all medical expenditures.[132][133] Obesity prevention programs have been found to reduce the cost of treating obesity-related disease. Those reductions, however, are offset by medical costs incurred during the additional years of life gained. The authors therefore conclude that reducing obesity may improve the public's health, but it is unlikely to reduce overall health spending.[134]
Obese workers have higher rates absenteeism from work and take more disability leave, thus increasing costs for employers and decreasing productivity.[135] A study examining Duke University employees found that people with a BMI over 40 filed twice as many workers' compensation claims as those whose BMI was 18.5-24.9. They also had more than 12 times as many lost work days. The most common injuries in this group were due to falls and lifting, thus affecting the lower extremities, wrists or hands, and backs.[136] The US state of Alabama Employees' Insurance Board approved a controversial plan to charge obese workers $25 per month if they do not take measures to reduce their weight and improve their health. These measures are set to start Jan. 2010 and apply to those with a BMI of greater than 35 kg/m2 who fail to make improvements in their health after one year.[137]
Specific industries, such as the airline and food industries, have special concerns. Due to rising rates of obesity, airlines face higher fuel costs and pressures to increase seating width.[138] In 2000, the extra weight of obese passengers cost airlines US$275 million.[139] Costs for restaurants are increased by litigation accusing them of causing obesity.[140] In 2005 the US Congress discussed legislation to prevent civil law suits against the food industry in relation to obesity; however it did not become law.[140]
The arts
The first sculptural representations of the human body 20,000–35,000 years ago depict obese females. Some attribute the Venus figurines to the tendency to emphasize characteristics that portray fertility while others feel these could be actual representations of the people at the time.[citation needed] Corpulence is, however, absent in both Greek and Roman art, probably fitting with their ideals of moderation. This continued through much of Christian European history, with only those of low socioeconomic status being depicted as obese. During the Renaissance some of the upper class began flaunting their large size. This can be seen in portraits of Henry the VIII and Alessandro del Borro.[6] Rubens (1577–1640) regularly depicted full-bodied women in his pictures, from which derives the term Rubenesque. These women, however, still maintained the "hourglass" shape with its relationship to fertility.[88] During the 19th century, views on obesity changed in the Western world. After centuries of obesity being synonymous with wealth and social status, slimness began to be seen as the desirable standard.[6]
Fat acceptance and the obesity controversy
The main effort of the fat acceptance movement is to decrease discrimination against people who are overweight.[141] However some in the movement are also attempting to challenge the established relationship between obesity and negative health outcomes. The National Association to Advance Fat Acceptance (NAAFA) was formed in 1969 and describes itself as a civil rights organization dedicated to ending size discrimination.[142] Multiple books such as The Diet Myth by Paul Campos argue that the health risks of obesity are a conspiracy and the real problem is the social stigma facing the obese.[143] Similarly, The Obesity Epidemic by Michael Gard argues that obesity is a moral and ideological construct.[144] Other groups are also trying to challenge obesity's connection to poor health. The Center for Consumer Freedom, a organization partly supported by the restaurant and food industry, has run ads saying that obesity is not an epidemic but "hype".[145]
Some people are particularly attracted to the obese. Chubby culture[146] and fat admirers[147] have become recognized subcultures.
See also
References
- ^ a b c d e f World Health Organization (2000). Technical report series 894: Obesity: Preventing and managing the global epidemic (PDF). Geneva: World Health Organization. ISBN 92-4-120894-5.
- ^ a b c d e f g h National Heart, Lung, and Blood Institute. Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults (PDF). International Medical Publishing, Inc. ISBN 1-58808-002-1.
{{cite book}}
: CS1 maint: multiple names: authors list (link) - ^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa Haslam DW, James WP (2005). "Obesity". Lancet. 366 (9492): 1197–209. doi:10.1016/S0140-6736(05)67483-1. PMID 16198769.
- ^ a b c d e 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.
- ^ a b c d e f g Wexler Barbara, Gale Thomas. Weight in American: Obesity, Eating Disorders, and Other Health Risks. 2007
- ^ a b c d Woodhouse R (2008). "Obesity in art: A brief overview". Front Horm Res. 36: 271–86. doi:10.1159/000115370. PMID 18230908.
- ^ 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.
{{cite journal}}
: Check|doi=
value (help); Unknown parameter|doi_brokendate=
ignored (|doi-broken-date=
suggested) (help) - ^ Mei Z, Grummer-Strawn LM, Pietrobelli A, Goulding A, Goran MI, Dietz WH (2002). "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. 75: 978–85. PMID 12036802.
{{cite journal}}
: CS1 maint: multiple names: authors list (link) - ^ Quetelet LAJ (1871). Antropométrie ou Mesure des Différences Facultés de l'Homme. Brussels: Musquardt.
- ^ "NICE issues guidance on surgery for morbid obesity". National Institute for Health and Clinical Excellence. 19 July 2002. Retrieved 2007-03-08.
- ^ "Bariatric Surgery". USC Center for Colorectal and Pelvic Floor Disorders. University of Southern California. 2006. Retrieved 2007-03-08.
- ^ Gabriel I Uwaifo (June 19, 2006). "Obesity". Retrieved 2008-09-29.
- ^ a b U.S. Preventive Services Task Force Evidence Syntheses (2000). HSTAT: Guide to Clinical Preventive Services, 3rd Edition: Recommendations and Systematic Evidence Reviews, Guide to Community Preventive Services. ISBN url=http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=hstat3.section.36199.
{{cite book}}
: Check|isbn=
value: invalid character (help); Missing pipe in:|isbn=
(help) - ^ a b c 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. doi:10.1016/S0140-6736(04)17018-9. PMID 15364185.
{{cite journal}}
: CS1 maint: multiple names: authors list (link) - ^ 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. doi:10.1185/030079906X159489. PMID 14985210.
{{cite journal}}
: CS1 maint: multiple names: authors list (link) - ^ Larsson B, Bengtsson C, Björntorp P; et al. (1992). "Is abdominal body fat distribution a major explanation for the sex difference in the incidence of myocardial infarction? The study of men born in 1913 and the study of women, Göteborg, Sweden". Am J Epidemiol. 135 (3): 266–73. PMID 1546702.
{{cite journal}}
: Explicit use of et al. in:|author=
(help); Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ a b Schwarz, Steven (November 1, 2007). "Obesity". emedicine. Retrieved 2008-09-30.
- ^ a b c d e f g h i j k Peter G. Kopelman, Ian D. Caterson, Michael J. Stock, William H. Dietz (2005). Clinical obesity in adults and children: In Adults and Children. Blackwell Publishing. p. 493. ISBN 140-511672-2.
{{cite book}}
: CS1 maint: multiple names: authors list (link) - ^ "Healthy Weight: Assessing Your Weight: BMI: About BMI for Children and Teens".
{{cite web}}
: Text "CDC" ignored (help); Text "DNPAO" ignored (help) - ^ Ogden CL, Flegal KM, Carroll MD, Johnson CL (2002). "Prevalence and trends in overweight among US children and adolescents, 1999-2000". JAMA : the journal of the American Medical Association. 288 (14): 1728–32. PMID 12365956.
{{cite journal}}
: Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ "EU Platform on Diet, Physical Activity, and Health" (PDF). International Obesity Task Force.
- ^ Barness LA, Opitz JM, Gilbert-Barness E (2007). "Obesity: genetic, molecular, and environmental aspects". Am. J. Med. Genet. A. 143A (24): 3016–34. doi:10.1002/ajmg.a.32035. PMID 18000969.
{{cite journal}}
: Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ Mokdad AH, Marks JS, Stroup DF, Gerberding JL (2004). "Actual causes of death in the United States, 2000" (PDF). JAMA. 291 (10): 1238–45. doi:10.1001/jama.291.10.1238. PMID 15010446.
{{cite journal}}
: Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ Allison DB, Fontaine KR, Manson JE, Stevens J, VanItallie TB (1999). "Annual deaths attributable to obesity in the United States". JAMA. 282 (16): 1530–8. doi:10.1001/jama.282.16.1530. PMID 10546692.
{{cite journal}}
: Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ Calle EE, Thun MJ, Petrelli JM, Rodriguez C, Heath CW (1999). "Body-mass index and mortality in a prospective cohort of U.S. adults". N. Engl. J. Med. 341 (15): 1097–105. doi:10.1056/NEJM199910073411501. PMID 10511607.
{{cite journal}}
: Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ Manson JE, Willett WC, Stampfer MJ; et al. (1995). "Body weight and mortality among women". N. Engl. J. Med. 333 (11): 677–85. doi:10.1056/NEJM199509143331101. PMID 7637744.
{{cite journal}}
: Explicit use of et al. in:|author=
(help)CS1 maint: multiple names: authors list (link) - ^ Allison DB, Fontaine KR, Manson JE, Stevens J, VanItallie TB (1999). "Annual deaths attributable to obesity in the United States". JAMA. 282 (16): 1530–8. doi:10.1001/jama.282.16.1530. PMID 10546692.
{{cite journal}}
: Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ Peeters A, Barendregt JJ, Willekens F, Mackenbach JP, Al Mamun A, Bonneux L (2003). "Obesity in adulthood and its consequences for life expectancy: A life-table analysis" (PDF). Ann. Intern. Med. 138 (1): 24–32. PMID 12513041.
{{cite journal}}
: Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ 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.
- ^ 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.
- ^ Darvall KA, Sam RC, Silverman SH, Bradbury AW, Adam DJ (2007). "Obesity and thrombosis". Eur J Vasc Endovasc Surg. 33 (2): 223–33. doi:10.1016/j.ejvs.2006.10.006. PMID 17185009.
{{cite journal}}
: Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ a b c Poulain M, Doucet M, Major GC; et al. (2006). "The effect of obesity on chronic respiratory diseases: pathophysiology and therapeutic strategies". CMAJ. 174 (9): 1293–9. doi:10.1503/cmaj.051299. PMC 1435949. PMID 16636330.
{{cite journal}}
: Explicit use of et al. in:|author=
(help); Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ Choi HK, Atkinson K, Karlson EW, Curhan G (2005). "Obesity, weight change, hypertension, diuretic use, and risk of gout in men: the health professionals follow-up study". Arch. Intern. Med. 165 (7): 742–8. doi:10.1001/archinte.165.7.742. PMID 15824292.
{{cite journal}}
: Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ a b c d e f Kolata,Gina (2007). Rethinking thin: The new science of weight loss - and the myths and realities of dieting. Picador. ISBN 0-312-42785-9.
- ^ Beydoun MA, Beydoun HA, Wang Y (2008). "Obesity and central obesity as risk factors for incident dementia and its subtypes: A systematic review and meta-analysis". Obes Rev. 9 (3): 204–18. doi:10.1111/j.1467-789X.2008.00473.x. PMID 18331422.
{{cite journal}}
: Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ Calle EE, Rodriguez C, Walker-Thurmond K, Thun MJ (2003). "Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults". N. Engl. J. Med. 348 (17): 1625–38. doi:10.1056/NEJMoa021423. PMID 12711737.
{{cite journal}}
: Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ 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.
{{cite journal}}
: CS1 maint: multiple names: authors list (link) - ^ 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.
{{cite journal}}
: CS1 maint: multiple names: authors list (link) - ^ Makhsida N, Shah J, Yan G, Fisch H, Shabsigh R (2005). "Hypogonadism and metabolic syndrome: Implications for testosterone therapy". J. Urol. 174 (3): 827–34. doi:10.1097/01.ju.0000169490.78443.59. PMID 16093964.
{{cite journal}}
: Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ a b Schmidt DS, Salahudeen AK (2007). "Obesity-survival paradox-still a controversy?". Semin Dial. 20 (6): 486–92. doi:10.1111/j.1525-139X.2007.00349.x. PMID 17991192.
- ^ Habbu A, Lakkis NM, Dokainish H (2006). "The obesity paradox: Fact or fiction?". Am. J. Cardiol. 98 (7): 944–8. doi:10.1016/j.amjcard.2006.04.039. PMID 16996880.
{{cite journal}}
: Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ 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.
{{cite journal}}
: Explicit use of et al. in:|author=
(help)CS1 maint: multiple names: authors list (link) - ^ Oreopoulos A, Padwal R, Kalantar-Zadeh K, Fonarow GC, Norris CM, McAlister FA (2008). "Body mass index and mortality in heart failure: A meta-analysis". Am. Heart J. 156 (1): 13–22. doi:10.1016/j.ahj.2008.02.014. PMID 18585492.
{{cite journal}}
: Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ Oreopoulos A, Padwal R, Norris CM, Mullen JC, Pretorius V, Kalantar-Zadeh K (2008). "Effect of obesity on short- and long-term mortality postcoronary revascularization: A meta-analysis". Obesity (Silver Spring). 16 (2): 442–50. doi:10.1038/oby.2007.36. PMID 18239657.
{{cite journal}}
: Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ Diercks DB, Roe MT, Mulgund J; et al. (2006). "The obesity paradox in non-ST-segment elevation acute coronary syndromes: Results from the Can Rapid risk stratification of Unstable angina patients Suppress ADverse outcomes with Early implementation of the American College of Cardiology/American Heart Association Guidelines Quality Improvement Initiative". Am Heart J. 152 (1): 140–8. doi:10.1016/j.ahj.2005.09.024. PMID 16824844.
{{cite journal}}
: Explicit use of et al. in:|author=
(help); Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ Sara Bleich, David Cutler, Christopher Murray, Alyce Adams (2007). Working paper 12954: Why is the developed world obese?. National Bureau of Economic Research.
{{cite book}}
: Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ a b c d e f Pool, Robert (2001). Fat: Fighting the Obesity Epidemic. Oxford, UK: Oxford University Press. ISBN 0-19-511853-7.
- ^ Nestle M, Jacobson MF (2000). "Halting the obesity epidemic: A public health policy approach". Public Health Rep. 115 (1): 12–24. doi:10.1093/phr/115.1.12. PMC 1308552. PMID 10968581.
- ^ a b James WP (2008). "The fundamental drivers of the obesity epidemic". Obes Rev. 9 Suppl 1: 6–13. doi:10.1111/j.1467-789X.2007.00432.x. PMID 18307693.
{{cite journal}}
: Unknown parameter|month=
ignored (help) - ^ 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.
{{cite journal}}
: Explicit use of et al. in:|author=
(help)CS1 maint: multiple names: authors list (link) - ^ National Control for Health Statistics. "Nutrition For Everyone". Centers for Disease Control and Prevention. Retrieved 2008-07-09.
- ^ Flegal KM, Carroll MD, Ogden CL, Johnson CL (2002). "Prevalence and trends in obesity among US adults, 1999–2000". JAMA. 288: 1723–1727. doi:10.1001/jama.288.14.1723. PMID 12365955.
{{cite journal}}
: Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ Wright JD, Kennedy-Stephenson J, Wang CY, McDowell MA, Johnson CL (2004). "Trends in intake of energy and macronutrients—United States, 1971–2000". MMWR Morb Mortal Wkly Rep. 53 (4): 80–2.
{{cite journal}}
: Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ a b c d e f Caballero B (2007). "The global epidemic of obesity: An overview". Epidemiol Rev. 29: 1–5. doi:10.1093/epirev/mxm012. PMID 17569676.
- ^ Lin BH, Guthrie J and Frazao E (1999). "Nutrient contribution of food away from home". In Frazão E (ed.). Agriculture Information Bulletin No. 750: America's Eating Habits: Changes and Consequences. Washington, DC: US Department of Agriculture, Economic Research Service. pp. 213–239.
- ^ Brian Wansink and Mike Huckabee (2005), “De-Marketing Obesity,” California Management Review, 47:4 (Summer), 6–18.
- ^ Pollan, Michael (22 April 2007). "You Are What You Grow". New York Times. Retrieved 2007-07-30.
- ^ a b Tjepkema M (2005-07-06). "Measured Obesity–Adult obesity in Canada: Measured height and weight". Nutrition: Findings from the Canadian Community Health Survey. Ottawa, Ontario: Statistics Canada.
- ^ 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. doi:10.1126/science.1106561. PMID 15681386.
{{cite journal}}
: CS1 maint: multiple names: authors list (link) - ^ Lopez R (2004). "Urban sprawl and risk for being overweight or obese". Am J Public Health. 94 (9): 1574–9. PMID 15333317.
- ^ Gortmaker SL, Must A, Sobol AM, Peterson K, Colditz GA, Dietz WH (1996). "Television viewing as a cause of increasing obesity among children in the United States, 1986–1990". Arch Pediatr Adolesc Med. 150 (4): 356–62. PMID 8634729.
{{cite journal}}
: Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ Vioque J, Torres A, Quiles J (2000). "Time spent watching television, sleep duration and obesity in adults living in Valencia, Spain". Int. J. Obes. Relat. Metab. Disord. 24 (12): 1683–8. doi:10.1038/sj.ijo.0801434. PMID 11126224.
{{cite journal}}
: Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ Tucker LA, Bagwell M (1991). "Television viewing and obesity in adult females" (PDF). Am J Public Health. 81 (7): 908–11. PMC 1405200. PMID 2053671.
{{cite journal}}
: Unknown parameter|month=
ignored (help) - ^ Farooqi S, O'Rahilly S (2006). "Genetics of obesity in humans". Endocr. Rev. 27 (7): 710–18. doi:10.1210/er.2006-0040. PMID 17122358.
{{cite journal}}
: Unknown parameter|month=
ignored (help) - ^ 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.
{{cite journal}}
: Explicit use of et al. in:|author=
(help)CS1 maint: multiple names: authors list (link) - ^ Rampersaud E, Mitchell BD, Pollin TI; et al. (2008). "Physical activity and the association of common FTO gene variants with body mass index and obesity". Arch Intern Med. 16: 1791–97. doi:10.1001/archinte.168.16.1791. PMID 18779467.
{{cite journal}}
: Explicit use of et al. in:|author=
(help)CS1 maint: multiple names: authors list (link) - ^ Yang W, Kelly T, He J (2007). "Genetic epidemiology of obesity". Epidemiol Rev. 29: 49–61. doi:10.1093/epirev/mxm004. PMID 17566051.
{{cite journal}}
: CS1 maint: multiple names: authors list (link) - ^ 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.
- ^ a b Ley RE, Turnbaugh PJ, Klein S, Gordon JI. Microbial ecology: human gut microbes associated with obesity. Nature. 2006 Dec 21;444(7122):1022-3
- ^ 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. doi:10.1111/j.1365-2265.1993.tb00974.x. PMID 8435887.
{{cite journal}}
: CS1 maint: multiple names: authors list (link) - ^ Sobal J, Stunkard AJ (1989). "Socioeconomic status and obesity: A review of the literature". Psychol Bull. 105 (2): 260–75. doi:10.1037/0033-2909.105.2.260. PMID 2648443.
{{cite journal}}
: Unknown parameter|month=
ignored (help) - ^ a b McLaren L (2007). "Socioeconomic status and obesity". Epidemiol Rev. 29: 29–48. doi:10.1093/epirev/mxm001. PMID 17478442.
- ^ Christakis NA, Fowler JH (2007). "The Spread of Obesity in a Large Social Network over 32 Years". New England Journal of Medicine. 357 (4): 370–379. doi:10.1056/NEJMsa066082. PMID 17652652.
- ^ Flegal KM, Troiano RP, Pamuk ER, Kuczmarski RJ, Campbell SM (1995). "The influence of smoking cessation on the prevalence of overweight in the United States". N. Engl. J. Med. 333 (18): 1165–70. doi:10.1056/NEJM199511023331801. PMID 7565970.
{{cite journal}}
: Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ Chiolero A, Faeh D, Paccaud F, Cornuz J (2008). "Consequences of smoking for body weight, body fat distribution, and insulin resistance". Am. J. Clin. Nutr. 87 (4): 801–9. PMID 18400700.
{{cite journal}}
: Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ a b c d e Flier JS (2004). "Obesity wars: Molecular progress confronts an expanding epidemic". Cell. 116 (2): 337–50. doi:10.1016/S0092-8674(03)01081-X. PMID 14744442.
- ^ Hamann A, Matthaei S (1996). "Regulation of energy balance by leptin". Exp. Clin. Endocrinol. Diabetes. 104 (4): 293–300. PMID 8886745.
- ^ Boulpaep, Emile L.; Boron, Walter F. (2003). Medical physiologya: A cellular and molecular approach. Philadelphia: Saunders. ISBN 0-7216-3256-4.
{{cite book}}
: CS1 maint: multiple names: authors list (link) - ^ a b c d e f Strychar I (2006). "Diet in the management of weight loss". CMAJ. 174 (1): 56–63. doi:10.1503/cmaj.045037. PMC 1319349. PMID 16389240.
{{cite journal}}
: Unknown parameter|month=
ignored (help) - ^ Shick SM, Wing RR, Klem ML, McGuire MT, Hill JO, Seagle H (1998). "Persons successful at long-term weight loss and maintenance continue to consume a low-energy, low-fat diet". J Am Diet Assoc. 98 (4): 408–13. doi:10.1016/S0002-8223(98)00093-5. PMID 9550162.
{{cite journal}}
: Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ Tate DF, Jeffery RW, Sherwood NE, Wing RR (2007). "Long-term weight losses associated with prescription of higher physical activity goals. Are higher levels of physical activity protective against weight regain?". Am. J. Clin. Nutr. 85 (4): 954–9. PMID 17413092.
{{cite journal}}
: Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ "Science-Based Solutions to Obesity: What are the Roles of Academia, Government, Industry, and Health Care? Proceedings of a symposium, Boston, Massachusetts, USA, 10–11 March 2004 and Anaheim, California, USA, 2 October 2004". Am. J. Clin. Nutr. 82 (1 Suppl): 207S–273S. 2005. PMID 16002825.
{{cite journal}}
: Unknown parameter|month=
ignored (help) - ^ Weiss EC, Galuska DA, Kettel Khan L, Gillespie C, Serdula MK (2007). "Weight regain in U.S. adults who experienced substantial weight loss, 1999–2002". Am J Prev Med. 33 (1): 34–40. doi:10.1016/j.amepre.2007.02.040. PMID 17572309.
{{cite journal}}
: Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ Anderson JW, Konz EC, Frederich RC, Wood CL (2001). "Long-term weight-loss maintenance: A meta-analysis of US studies". Am. J. Clin. Nutr. 74 (5): 579–84. PMID 11684524.
{{cite journal}}
: Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ Williamson DF, Pamuk E, Thun M, Flanders D, Byers T, Heath C (1995). "Prospective study of intentional weight loss and mortality in never-smoking overweight US white women aged 40–64 years". Am. J. Epidemiol. 141 (12): 1128–41. PMID 7771451.
{{cite journal}}
: Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ Bravata DM, Sanders L, Huang J; et al. (2003). "Efficacy and safety of low-carbohydrate diets: A systematic review". JAMA. 289 (14): 1837–50. doi:10.1001/jama.289.14.1837. PMID 12684364.
{{cite journal}}
: Explicit use of et al. in:|author=
(help); Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ Gwinup G (1987). "Weight loss without dietary restriction: Efficacy of different forms of aerobic exercise". Am J Sports Med. 15 (3): 275–9. doi:10.1177/036354658701500317. PMID 3618879.
- ^ a b Fumento, Michael (1997). The Fat of the Land: Our Health Crisis and How Overweight Americans Can Help Themselves. Penguin (Non-Classics). p. 126. ISBN 0-14-026144-3.
- ^ 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.
{{cite journal}}
: CS1 maint: multiple names: authors list (link) - ^ Lee L, Kumar S, Leong LC (1994). "The impact of five-month basic military training on the body weight and body fat of 197 moderately to severely obese Singaporean males aged 17 to 19 years". Int. J. Obes. Relat. Metab. Disord. 18 (2): 105–9. PMID 8148923.
{{cite journal}}
: Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ Bravata DM, Smith-Spangler C, Sundaram V; et al. (2007). "Using pedometers to increase physical activity and improve health: a systematic review". JAMA : the journal of the American Medical Association. 298 (19): 2296–304. doi:10.1001/jama.298.19.2296. PMID 18029834.
{{cite journal}}
: Explicit use of et al. in:|author=
(help); Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ "Anti-obesity drug no magic bullet". CBC. January 2, 2007. Retrieved 2008-09-19.
- ^ "FDA Briefing Document NDA 21-888 Zimulti (rimonabant) Tablets, 20 mg Sanofi Aventis Advisory Committee" (PDF). FDA. June 13, 2007. Retrieved 2008-09-19.
- ^ Rucker D, Padwal R, Li SK, Curioni C, Lau DC (2007). "Long term pharmacotherapy for obesity and overweight: Updated meta-analysis". BMJ. 335 (7631): 1194–99. doi:10.1136/bmj.39385.413113.25. PMID 18006966.
{{cite journal}}
: Cite has empty unknown parameter:|unused_data=
(help); Text "http://www.bmj.com/cgi/content/full/335/7631/1194" ignored (help)CS1 maint: multiple names: authors list (link) - ^ 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.
{{cite journal}}
: CS1 maint: multiple names: authors list (link) - ^ 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.
- ^ Flanagan CM, Kaesberg JL, Mitchell ES, Ferguson MA, Haigney MC (2008). "Coronary artery aneurysm and thrombosis following chronic ephedra use". Int. J. Cardiol. doi:10.1016/j.ijcard.2008.06.081. PMID 18718687.
{{cite journal}}
: Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ 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.
{{cite journal}}
: CS1 maint: multiple names: authors list (link) - ^ 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.
{{cite journal}}
: Explicit use of et al. in:|author=
(help); Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ 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.
{{cite journal}}
: Explicit use of et al. in:|author=
(help)CS1 maint: multiple names: authors list (link) - ^ 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.
{{cite journal}}
: Explicit use of et al. in:|author=
(help)CS1 maint: multiple names: authors list (link) - ^ Giugliano G, Nicoletti G, Grella E; et al. (2004). "Effect of liposuction on insulin resistance and vascular inflammatory markers in obese women". Br J Plast Surg. 57 (3): 190–4. doi:10.1016/j.bjps.2003.12.010. PMID 15006519.
{{cite journal}}
: Explicit use of et al. in:|author=
(help); Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ Klein S, Fontana L, Young VL; et al. (2004). "Absence of an effect of liposuction on insulin action and risk factors for coronary heart disease". N. Engl. J. Med. 350 (25): 2549–57. doi:10.1056/NEJMoa033179. PMID 15201411.
{{cite journal}}
: Explicit use of et al. in:|author=
(help); Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ 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.
{{cite journal}}
: CS1 maint: multiple names: authors list (link) Fulltext. - ^ "Behavioral counseling in primary care to promote a healthy diet: Recommendations and rationale". Retrieved 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. doi:10.1016/S0749-3797(02)00580-9. PMID 12554027.
{{cite journal}}
: Explicit use of et al. in:|author=
(help)CS1 maint: multiple names: authors list (link) - ^ a b c Anon (2005). OECD Factbook: Economic, Environmental and Social Statistics. Organization for Economic Co-operation and Development. ISBN 9264018697.
- ^ "Obesity in the Pacific Too Big To Ignore" (PDF). Secretariat of the Pacific Community. WHO. 2002. Retrieved 2008-09-30.
- ^ "Childhood Obesity". Government of New South Wales. 2006-08-03. Retrieved 2008-06-22.
- ^ Popkin, Barry (September, 2007). "The World Is Fat". Scientific American. p. 94. ISSN 0036-8733.
{{cite news}}
:|access-date=
requires|url=
(help); Check date values in:|date=
(help); Cite has empty unknown parameter:|coauthors=
(help) - ^ Praween Kumar Agrawal (2002-05-23). "Emerging obesity in northern Indian states: A serious threat for health" (PDF). IUSSP Conference, Bankik, 10 June–12-2002. Retrieved 2008-07-24.
- ^ Tim Lobstein, Neville Rigby, Rachel Leach (2005-03-15). EU platform on diet, physical activity and health: International Obesity Task Force EU Platform Briefing Paper (PDF). International Obesity Task Force. Retrieved 2008-07-23.
{{cite book}}
: CS1 maint: multiple names: authors list (link) - ^ 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.
{{cite journal}}
: CS1 maint: multiple names: authors list (link) - ^ "International Obesity Task Force" (PDF). March 15 2005. Retrieved 2008-09-19.
{{cite web}}
: Check date values in:|date=
(help) - ^ Freedman DS, Khan LK, Serdula MK, Galuska DA, Dietz WH (2002). "Trends and correlates of class 3 obesity in the United States from 1990 through 2000". JAMA. 288 (14): 1758–61. doi:10.1001/jama.288.14.1758. PMID 12365960.
{{cite journal}}
: Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ Loscalzo, Joseph; Fauci, Anthony S.; Braunwald, Eugene; Dennis L. Kasper; Hauser, Stephen L; Longo, Dan L. (2008). Harrison's principles of internal medicine. McGraw-Hill Medical. ISBN 0-07-146633-9.
{{cite book}}
: CS1 maint: multiple names: authors list (link) - ^ Satcher D (2001). The Surgeon General's Call to Action to Prevent and Decrease Overweight and Obesity. U.S. Dept. of Health and Human Services, Public Health Service, Office of Surgeon General. ISBN 0-16051-005-8.
- ^ Brook Barnes (2007-07-18). "Limiting Ads of Junk Food to Children". New York Times. Retrieved 2008-07-24.
- ^ Tara McClair (2007-01-30). "Junk-food ban receives mixed reactions in schools". Retrieved 2008-07-24.
{{cite news}}
: Unknown parameter|publication=
ignored (help) - ^ Brennan Ramirez LK, Hoehner CM, Brownson RC; et al. (2006). "Indicators of activity-friendly communities: An evidence-based consensus process". Am J Prev Med. 31 (6): 530–32. doi:10.1016/j.amepre.2006.07.026. PMID 17169714.
{{cite journal}}
: Explicit use of et al. in:|author=
(help); Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ Lau DC, Douketis JD, Morrison KM, Hramiak IM, Sharma AM, Ur E (2007). "2006 Canadian clinical practice guidelines on the management and prevention of obesity in adults and children [summary]". CMAJ. 176 (8): S1–13. doi:10.1503/cmaj.061409. PMC 1839777. PMID 17420481.
{{cite journal}}
: Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ Storing up problems; the medical case for a slimmer nation (PDF). London: Royal College of Physicians. 2004-02-11. ISBN 1-86016-200-2.
- ^ Great Britain Parliament House of Commons Health Committee (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 2007-12-17.
{{cite book}}
: Unknown parameter|month=
ignored (help) - ^ Wanless, Sir Derek (2007). Our Future Health Secured? A review of NHS funding and performance. London, UK: The King's Fund. ISBN 185717562X. Retrieved 2007-12-17.
{{cite book}}
: Unknown parameter|coauthors=
ignored (|author=
suggested) (help) - ^ The Oxford English Dictionary (website)
- ^ Carol Gerten-Jackson. "The Tuscan General Alessandro del Borro".
- ^ a b "History of Medicine: Sushruta – the Clinician – Teacher par Excellence" (PDF). Dwivedi, Girish & Dwivedi, Shridhar. 2007. Retrieved 2008-09-19.
- ^ Breslow L (1952). "Public health aspects of weight control". Am J Public Health Nations Health. 42 (9): 1116–20. PMC 1526346. PMID 12976585.
{{cite journal}}
: Unknown parameter|month=
ignored (help) - ^ Critser, Greg (2004). Fat Land. London, England: Penguin Books Ltd. ISBN 0-14-101540-3.
- ^ Weintraub M (1992). "Long-term weight control: The National Heart, Lung, and Blood Institute funded multimodal intervention study". Clin. Pharmacol. Ther. 51 (5): 581–5. PMID 1445528.
{{cite journal}}
: Unknown parameter|month=
ignored (help) - ^ Finkelstein EA, Fiebelkorn IA, Wang G (2003). "National medical spending attributable to overweight and obesity: How much, and who's paying". Health Affairs. Online (May).
{{cite journal}}
: CS1 maint: multiple names: authors list (link) - ^ "Obesity and overweight: Economic consequences". CDC. Retrieved 2007-09-05.
{{cite web}}
: Unknown parameter|pubdate=
ignored (help) - ^ van Baal PH, Polder JJ, de Wit GA; et al. (2008). "Lifetime medical costs of obesity: Prevention no cure for increasing health expenditure". PLoS Med. 5 (2): e29. doi:10.1371/journal.pmed.0050029. PMC 2225430. PMID 18254654.
{{cite journal}}
: Explicit use of et al. in:|author=
(help); Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link) - ^ Chenoweth & Associates Inc. (2005). "The Economic Costs of Physical Inactivity, Obesity, and Overweight in California Adults" (PDF). Cancer Prevention and Nutrition Section, California Center for Physical Activity, California Department of Health Services, Sacramento, CA. Retrieved 2008-07-23.
- ^ 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.
{{cite journal}}
: CS1 maint: multiple names: authors list (link) - ^ "Extra pounds mean insurance fees for Ala. workers". Associated Press Writer. August 22 2008. Retrieved 2008-09-09.
{{cite web}}
: Check date values in:|date=
(help) - ^ Lisa DiCarlo (2002-10-24). "Why Airlines Can't Cut The Fat". Forbes.com. Retrieved 2008-07-23.
- ^ 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.
{{cite journal}}
: CS1 maint: multiple names: authors list (link) - ^ a b "109th U.S. Congress (2005–2006) H.R. 554: 109th U.S. Congress (2005–2006) H.R. 554: Personal Responsibility in Food Consumption Act of 2005". GovTrack.us. Retrieved 2008-07-24.
- ^ "WHAT IS NAAFA?". NAAFA. Retrieved 2008-09-29.
- ^ National Association to Advance Fat Acceptance (2008), We come in all sizes, NAAFA, retrieved 2008-07-29
- ^ Campos, Paul F. (2005). The Diet Myth. Gotham. ISBN 1-59240-135-X.
- ^ Gard, Michael (2005). The Obesity Epidemic: Science, Morality and Ideology. Routledge. ISBN 0415318963.
- ^ "Obesity: Time bomb or dud?". USA Today. 2005-05-25. Retrieved 2008-09-21.
- ^ Douglas Martin (1991-07-31). "About New York". New York Times. Retrieved 2008-07-24.
- ^ Areton (2002). "Factors in the sexual satisfaction of obese women in relationships". Electronic Journal of Human Sexuality. 5.
{{cite journal}}
: Unknown parameter|month=
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Further reading
- Fumento, Michael (1997). The Fat of the Land: Our Health Crises and How Overweight Americans can Help Themselves. New York: Penguin Books. ISBN 0-140261443.
- Kolata, Gina (2007). Rethinking Thin: The new science of weight loss - and the myths and realities of dieting. Picador. ISBN 0-312-42785-9.
- Kopelman, Peter G. (2005). Clinical obesity in adults and children: In Adults and Children. Blackwell Publishing. p. 493. ISBN 140-511672-2.
- Levy-Navarro, Elena (2008). The Culture of Obesity in Early and Late Modernity. Palgrave Macmillan. ISBN 0230601235.
- Pool, Robert (2001). Fat: Fighting the Obesity Epidemic. Oxford, UK: Oxford University Press. ISBN 0-19-511853-7.
External links
- World Health Organization - Obesity pages
- Diet, Nutrition and the prevention of chronic diseases (including obesity) by a Joint WHO/FAO Expert consultation (2003).
- Obesity at Endotext.org
- International Task Force on Obesity
- The Obesity Society (USA)
- National Obesity Forum (UK)
- Australasian Society for the Study of Obesity