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| Obesity Classification & external resources | ||
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|---|---|---|
| Silhouettes representing healthy, overweight, and obese. | ||
| ICD-10 | E66. | |
| ICD-9 | 278 | |
| DiseasesDB | 9099 | |
| MedlinePlus | 003101 | |
| eMedicine | med/1653 | |
| MeSH | C23.888.144.699.500 | |
Obesity is a condition in which the natural energy reserve, stored in the fatty tissue of humans and other mammals, is increased to a point where it is associated with certain health conditions or increased mortality.
Although obesity is an individual clinical condition, it is increasingly viewed as a serious and growing public health problem: excessive body weight has been shown to predispose to various diseases, particularly cardiovascular diseases, diabetes mellitus type 2, sleep apnea and osteoarthritis.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.
Contents |
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.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. 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).
BMI, or body mass index, is a simple and widely used method for estimating body fat.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. BMI was developed by the Belgian statistician and anthropometrist Adolphe Quetelet.Quetelet LAJ. (1871). Antropométrie ou Mesure des Différences Facultés de l\'Homme. Brussels: Musquardt. 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:
Where is the subject\'s weight in kilograms and is the subject\'s height in metres.
Where is the subject\'s weight in pounds and 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: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.
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). 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.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.
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) has a much stronger correlation, particularly with cardiovascular disease, than the BMI alone.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.
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.
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.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.
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.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.
Other measurements of body fat include computed tomography (CT/CAT scan), magnetic resonance imaging (MRI/NMR), and dual energy X-ray absorptiometry (DXA).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.
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. Smoking, hypertension, age and family history are other risk factors that may indicate treatment.
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).Bray GA (2004). "Medical consequences of obesity". J. Clin. Endocrinol. Metab. 89 (6): 2583-9. doi:10.1210/jc.2004-0535. PMID 15181027. Mortality is increased in obesity, with a BMI of over 32 being associated with a doubled risk of death.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. There are alterations in the body\'s response to insulin (insulin resistance), a proinflammatory state and an increased tendency to thrombosis (prothrombotic state).
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).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.
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.
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.
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. 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.
Despite the widespread availability of nutritional information in schools, doctors\' offices, on the internet and on groceries,Centers for Disease Control and Prevention. Nutrition For Everyone. National Control for Health Statistics. Accessed July 15, 2007. 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.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.
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. http://politics.guardian.co.uk/publicservices/story/0,,2147839,00.html
Less well established life style issues which may influence obesity include a stressful mentality and insufficient sleep[citation needed].
As with many medical conditions, the calorific imbalance that results in obesity often develops from a combination of genetic and environmental factors. Polymorphisms in various genes controlling appetite, metabolism, and adipokine release predispose to obesity, but the condition requires availability of sufficient calories, and possibly other factors, to develop fully. Various genetic conditions that feature obesity have been identified (such as Prader-Willi syndrome, Bardet-Biedl syndrome, MOMO syndrome, leptin receptor mutations and melanocortin receptor mutations), but known single-locus mutations have been found in only about 5% of obese individuals. While it is thought that a large proportion of the causative genes are still to be identified, much obesity is likely the result of interactions between multiple genes, and non-genetic factors are likely also important.
A 2007 study identified fairly common mutations in the FTO gene; heterozygotes had a 30% increased risk of obesity, while homozygotes faced a 70% increased risk.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.
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.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.
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.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. 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).
Scientists investigating the mechanisms and treatment of obesity may use animal models such as mice to conduct experiments.
FlierFlier JS (2004). "Obesity wars: molecular progress confronts an expanding epidemic". Cell 116 (2): 337-50. PMID 14744442. 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. 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.Boulpaep, Emile L.; Boron, Walter F. (2003). Medical physiology: a cellular and molecular approach. Philadelphia: Saunders. ISBN 0-7216-3256-4.
The arcuate nucleus contains two distinct groups of neurons. The first group coexpresses neuropeptide Y (NPY) and agouti-related peptide (AgRP) and has stimulatory inputs to the LH and inhibitory inputs to the VMH. The second group coexpresses pro-opiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART) and has stimulatory inputs to the VMH and inhibitory inputs to the LH. Consequently, NPY/AgRP neurons stimulate feeding and inhibit satiety, while POMC/CART neurons stimulate satiety and inhibit feeding. Both groups of arcuate nucleus neurons are regulated in part by leptin. Leptin inhibits the NPY/AgRP group while stimulating the POMC/CART group. Thus a deficiency in leptin signaling, either via leptin deficiency or leptin resistance, leads to overfeeding and may account for some genetic and acquired forms of obesity.
The role of bacteria colonizing the digestive tract in the development of obesity has recently become the subject of investigation. Bacteria participate in digestion (especially of fatty acids and polysaccharides), and alterations in the proportion of particular strains of bacteria may explain why certain people are more prone to weight gain than others. Human digestive tract are generally either members of the phyla of bacteroidetes or of firmicutes. In obese people, there is a relative abundance of firmicutes (which cause relatively high energy absorption), which is restored by weight loss. From these results it cannot yet be concluded whether this imbalance is the cause of obesity or an effect.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.
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 studyZagorsky JL. Is Obesity as Dangerous to Your Wealth as to Your Health? Res Aging 2004;26:130-152. PDF fulltext.doi:10.1177/0164027503258519. 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.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.
The main treatment for obesity is to reduce body fat by eating fewer calories and exercising more. A beneficial side effect of exercise is to increase muscle, tendon, and ligament strength, which helps to prevent injury from accidents and vigorous activity. 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. Certain nutrients, such as phenylalanine, are natural appetite suppressants which allow resetting of the body\'s set point for body weight.[citation needed]
In a clinical practice guideline by the American College of Physicians, the following five recommendations are made: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.
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.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.
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".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.
In general, dieting means eating less. Various dietary approaches have been proposed, some of which have been compared by randomized controlled trials:
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.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.
A meta-analysis of randomized controlled trials by the international Cochrane Collaboration in 2002 concludedPirozzo 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. 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 reviewSamaha 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. 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."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.
The Women\'s Health Initiative Randomized Controlled Dietary Modification TrialHoward 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. 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:
Additional recent randomized controlled trials have found that:
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. American Diabetes Association (2008). "Nutrition Recommendations and Interventions for Diabetes". Diabetes Care 31 suppl: S61-78. doi:10.2337/dc08-S061.
"The glycaemic 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."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.
The glycemic load is "the mathematical product of the glycemic index and the carbohydrate amount".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.
In a randomized controlled trial that compared four diets that varied in carbohydrate amount and glycemic index found complicated resultsMcMillan-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. :
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.Thomas DE, Elliott E, Baur L (2007). "Low glycaemic index or low glycaemic load diets for overweight and obesity". Cochrane database of systematic reviews (Online) (3): CD005105. doi:10.1002/14651858.CD005105.pub2. PMID 17636786.
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.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. 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.
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.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.
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.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
