Obesity: Difference between revisions
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'''Obesity''' is the medical condition associated with excessive stores of body fat, to the extent that it causes serious health | '''Obesity''' is the medical condition associated with excessive stores of [[adipocyte|body fat]], to the extent that it causes serious health risks. Physical problems include [[hypertension|high blood pressure]], heart disease, some cancers and [[Diabetes mellitus type 2]]; emotional problems include low self esteem, and depression. More than a billion people are classed as obese worldwide, and by 2025, 300 million people are expected to suffer from [[Diabesity|obesity-related diabetes]]. | ||
There are many ways of measuring body fat, but the most common measures the relationship between weight and height by the [[body mass index]] (BMI). A BMI of 30 or more puts you in the category of ''obese''. This method is simple, but imprecise; people with well-developed muscle may have a high BMI yet a low proportion of body fat. | |||
==Prevalence and epidemiology== | |||
Obesity is increasing in Europe.<ref name="pmid19286092">{{cite journal |author=Kotseva K ''et al.''|title=Cardiovascular prevention guidelines in daily practice: a comparison of EUROASPIRE I, II, and III surveys in eight European countries |journal=Lancet |volume=373 |pages=929–40 |year=2009 |pmid=19286092 |url=http://linkinghub.elsevier.com/retrieve/pii/S0140-6736(09)60330-5}}</ref> In the U.S.A., obesity is increased through 2004<ref name="pmid16595758">{{cite journal |author=Ogden CL ''et al.''|title=Prevalence of overweight and obesity in the United States, 1999-2004 |journal=JAMA |volume=295 |pages=1549–55 |year=2006 |pmid=16595758 |url=http://jama.ama-assn.org/cgi/pmidlookup?view=long&pmid=16595758}}</ref> but has been stable since<ref name="pmid18505949">{{cite journal |author=Ogden CL ''et al.'' |title=High body mass index for age among US children and adolescents, 2003-2006 |journal=JAMA |volume=299 |pages=2401–5 |year=2008|pmid=18505949 |url=http://jama.ama-assn.org/cgi/pmidlookup?view=long&pmid=18505949}}</ref>. Among immigrants, the incidence of obesity increases with the duration of living in the U.S.A..<ref name="pmid15598917">{{cite journal |author=Goel MS ''et al.'' |title=Obesity among US immigrant subgroups by duration of residence |journal=JAMA |volume=292|pages=2860–7 |year=2004 |pmid=15598917|url=http://jama.ama-assn.org/cgi/pmidlookup?view=long&pmid=15598917}}</ref> | |||
==Causes/etiology== | |||
'' See [[Genetics of obesity]]'' | |||
The proximate cause of obesity is a mix of environmental and genetic factors.<ref name="pmid2336075">{{cite journal |author=Stunkard AJ ''et al.''|title=The body-mass index of twins who have been reared apart |journal=N Eng J Med |volume=322 |pages=1483–7 |year=1990 |pmid=2336075}}</ref><ref name="pmid17652652">{{cite journal |author=Christakis NA, Fowler JH |title=The spread of obesity in a large social network over 32 years |journal=N Engl J Med |volume=357 | |pages=370–9 |year=2007 |pmid=17652652}}</ref> In only very few cases can obesity in humans be attributed to a single gene defect, but many genes have been found that have (usually rare) variants associated with an increased risk of obesity. | |||
Obesity is generally associated with a state of [[leptin]] resistance, that is analogous to the [[insulin resistance]] seen in [[diabetes mellitus type 2 ]]. Leptin is a [[hormone]] that is secreted into the blood from fat tissues (adipocytes); it acts on the appetite-regulating centres of the [[hypothalamus]] to suppress [[appetite]], and it is secreted at high levels in most obese individuals. However, in these obese individuals, the [[hypothalamus]] does not respond appropriately to leptin. | |||
== | The role of fetal programming,<ref name="pmid11738796">{{cite journal| author=Breier BH ''et al.''| title=Fetal programming of appetite and obesity|journal=Mol Cell Endocrinol|year= 2001|volume= 185| pages= 73-9|pmid=11738796| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&email=badgett@uthscdsa.edu&retmode=ref&cmd=prlinks&id=11738796}}</ref> <ref name="pmid11479129">{{cite journal| author=Vickers MH ''et al.''| title=Dysregulation of the adipoinsular axis - a mechanism for the pathogenesis of hyperleptinemia and adipogenic diabetes induced by fetal programming|journal=J Endocrinol|year= 2001| volume=170| pages= 323-32|pmid=11479129 | ||
|url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&email=badgett@uthscdsa.edu&retmode=ref&cmd=prlinks&id=11479129}} </ref><ref name="pmid10893326">{{cite journal| author=Vickers MH ''et al.''|title=Fetal origins of hyperphagia, obesity, and hypertension and postnatal amplification by hypercaloric nutrition|journal=Am J Physiol|year=2000|volume=279|pages=E83-7|pmid=10893326 | |||
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&email=badgett@uthscdsa.edu&retmode=ref&cmd=prlinks&id=10893326}} </ref> perhaps operative in the higher risk of obesity in offspring of older and/or very lean women. | |||
''' | ===Environment and lifestyle=== | ||
The increase in overweight and obesity that has taken place during the 20<sup>th</sup> century is likely to be due to environmental changes (in the widest sense), including especially lifestyle changes that affect diet and exercise habits. While a sedentary lifestyle is involved in the development of a wide range of physical and mental ills, and obesity is associated with a more sedentary lifestyle, it is not obvious that lack of exercise is a ''major'' factor in the present obesity epidemic. In a 5.6 years follow-up study of 393 middle-aged healthy subjects, Cambridge epidemiologists demonstrated that carrying excess weight predicted a sedentary lifestyle, but that sedentary time did not predict weight gain.<ref>Ekelund U ''et al.''(2008) Time spent being sedentary and weight gain in healthy adults: reverse or bidirectional causality? ''Am J Clin Nutr'' 88:612-7</ref> Failure of sedentary time to predict weight gain might conceivably reflect insufficient sample size to reveal a significant prediction, as might greater errors in estimating sedentary time than measuring weight change. | |||
Many other changes in environment and lifestyle may be involved in the increasing prevalence of obesity. In one multi-center review of the literature, 10 other factors, including epigenetic changes were found to be equally plausible etiologic factors contributing to the epidemic.<ref name="pmid16801930">{{cite journal |author=Keith SW ''et al.''|title=Putative contributors to the secular increase in obesity: exploring the roads less traveled|journal=Int J Obes|volume=30|pages=1585–94|year=2006|pmid=16801930 |url=http://www.uab.edu/images/shrp/shrp06/Putative%20contributors%20to%20the%20secular%20increase%20in%20obesity%20-%20exploring%20the%20roads%20less%20traveled.pdf}}</ref><ref name="pmid19221391">{{cite journal| author=Wansink B, Payne CR| title=The joy of cooking too much: 70 years of calorie increases in classic recipes. | journal=Ann Intern Med | year= 2009 | volume= 150 | issue= 4 | pages= 291-2 | pmid=19221391 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19221391 }} </ref> | |||
Stress and depression (and associated disruptions of sleep) can lead to obesity.<ref name="pmid19808765">{{cite journal|author=Kivimäki M ''et al.''|title=Common mental disorder and obesity: insight from four repeat measures over 19 years: prospective Whitehall II cohort study| journal=BMJ|year=2009|volume=339|pages=b3765|pmid=19808765 | |||
|url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=19808765}}</ref> <ref name="pmid18253159">{{cite journal| author=Vgontzas AN ''et al.''| title=Short sleep duration and obesity: the role of emotional stress and sleep disturbances| journal=Int J Obes|year= 2008|volume=32|pages=801-9|pmid=18253159 | |||
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&email=badgett@uthscdsa.edu&retmode=ref&cmd=prlinks&id=18253159}}</ref><ref name="pmid16801930"/>; changes in eating patterns may contribute<ref>{{Cite journal | |||
| doi = 10.1161/CIR.0b013e31823ac046 | |||
| issn = 0009-7322, 1524-4539 | |||
| last = Roger | |||
| first = V. L. | |||
| coauthors = A. S. Go, D. M. Lloyd-Jones, E. J. Benjamin, J. D. Berry, W. B. Borden, D. M. Bravata, S. Dai, E. S. Ford, C. S. Fox, H. J. Fullerton, C. Gillespie, S. M. Hailpern, J. A. Heit, V. J. Howard, B. M. Kissela, S. J. Kittner, D. T. Lackland, J. H. Lichtman, L. D. Lisabeth, D. M. Makuc, G. M. Marcus, A. Marelli, D. B. Matchar, C. S. Moy, D. Mozaffarian, M. E. Mussolino, G. Nichol, N. P. Paynter, E. Z. Soliman, P. D. Sorlie, N. Sotoodehnia, T. N. Turan, S. S. Virani, N. D. Wong, D. Woo, M. B. Turner, on behalf of the American Heart Association Statistics Committee and Stroke Statistics Subcommittee | |||
| title = Heart Disease and Stroke Statistics--2012 Update: A Report From the American Heart Association | |||
| journal = Circulation | |||
| accessdate = 2011-12-16 | |||
| date = 2011-12-15 | |||
| url = http://circ.ahajournals.org/citmgr?gca=circulationaha;CIR.0b013e31823ac046v1 | |||
}}</ref><ref name="pmid21738451">{{cite journal| author=Duffey KJ, Popkin BM| title=Energy density, portion size, and eating occasions: contributions to increased energy intake in the United States, 1977-2006. | journal=PLoS Med | year= 2011 | volume= 8 | issue= 6 | pages= e1001050 | pmid=21738451 | doi=10.1371/journal.pmed.1001050 | pmc=PMC3125292 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21738451 }} </ref><ref>{{Cite journal|volume=337|pages= a2002|last = Maruyama|first = K|coauthors = et al.| title = The joint impact on being overweight of self reported behaviours of eating quickly and eating until full : cross sectional survey |journal = BMJ|date = 2008-10-21| url = http://www.bmj.com/cgi/content/abstract/337/oct21_2/a2002}}</ref> and cultural changes in perceptions of overweight<ref name="pmid18617488">{{cite journal |author=Johnson F ''et al.'' |title=Changing perceptions of weight in Great Britain: comparison of two population surveys |journal=BMJ |volume=337|pages=a494 |year=2008 |pmid=18617488}}</ref> Smoking cessation has a well known effect to increase caloric intake. | |||
=== Evolutionary perspectives of obesity=== | |||
To fully understand the causes and prevalence of obesity, evolutionary factors may need integration into the mix of environmental and genetic proximate causes of obesity. [[Evolutionary medicine]] suggests we get fat because of built-in encouragements to eat heartily when we have plenty to eat and to restrict energy expenditures in preparation for inevitable food shortages. It may also suggest we consider the effect of the types of food we eat compared to those evolution adapted us to eat. We’ve only recently, on an evolutionary timescale, begun to eat readily absorbable carbohydrates in disproportionate amounts. Our hunter-gatherer ancestors had little access to such food items, with the exception of a bit of honey. Now we have so-called refined carbohydrates readily available and much consumed. Those include granulated sugar and sucrose dissolved in soft drinks; syrups and candies; milled cereal grain flours and their host pastries, pastas and breads; and many other processed ‘high glycemic’ foods. Those foods stimulate the secretion of insulin as control for glucose homeostasis, and induce other hormonal changes that influence appetite and efficiency of energy utilization. Science writer Gary Taubes summarizes the argument: | |||
<blockquote> | <blockquote>“There is considerable evidence that the obesity epidemic is caused by a hormonal phenomenon, specifically by the consumption of refined carbohydrates, starches and sugars, all of which prompt (sooner or later) excessive insulin secretion. Insulin is the primary regulator of fat storage. When insulin levels are elevated, fat accumulates in our body tissue; when they fall, fat is released and we use it for fuel. By stimulating insulin secretion, carbohydrates make us fat; by driving us to accumulate fat, they increase hunger and decrease the energy we expend in metabolism and physical activity. In short, obesity is caused not by overeating or sedentary behaviour, but by hormonal malfunctioning triggered by the consumption of particular types of carbohydrate-containing foods.”<ref name=taubesns08>Taubes G. (2008) The great diet delusion: It is time for nutrition researchers and health authorities to wake up to the fact that people do not get fat simply because they overeat. ''New Scientist'' 19 January 2008, page 17</ref></blockquote> | ||
== Pathophysiology == | |||
'''The response to a meal in obesity: the insulin paradox''' | '''The response to a meal in obesity: the insulin paradox''' | ||
All consumers of refined starches, soft drinks, high-fructose corn syrups and other energy-replete products are not born equal. Obese persons, after a meal, appear to burn carbohydrates less efficiently and fat even more poorly.<ref name="pmid11771681">{{cite journal |author=Lopes IM ''et al.''|title=Effects of leptin resistance on acute fuel metabolism after a high carbohydrate load in lean and overweight young men |journal=J Am Coll Nutr |volume=20 |pages=643–8 |year=2001 |pmid=11771681 |url=http://www.jacn.org/cgi/content/full/20/6/643}}</ref> A contribution of leptin resistance was suggested, as circulating concentrations of leptin were higher in the obese men that were the least efficient metabolisers of fat. However, the arrow of causality may be oriented in the other direction. In persons with a family history of obesity, the earliest obesogenic changes are not related to leptin, but to metabolic efficiency and to insulin status and responsiveness: subjects at increased risk of obesity oxidize carbohydrates more quickly and fat more slowly, and have lower insulin, consistent with a greater insulin sensitivity.<ref name="pmid14970841">{{cite journal |author=Giacco R ''et al.'' |title=Insulin sensitivity is increased and fat oxidation after a high-fat meal is reduced in normal-weight healthy men with strong familial predisposition to overweight |journal=Int J Obes Relat Metab Disord|volume=28|pages=342–8 |year=2004 |pmid=14970841 |url=http://www.nature.com/ijo/journal/v28/n2/abs/0802589a.html}}</ref> These findings contrast with those implicating obesity with the development, over the long term, of the opposite of insulin sensitivity, i.e. insulin resistance. | |||
'''Magnesium''' | '''Magnesium''' | ||
Obese subjects, like type II diabetics, are magnesium deficient.<ref name="pmid12701060">{{cite journal |author=Takaya J ''et al.'' |title=Intracellular magnesium of platelets in children with diabetes and obesity |journal=Metab Clin Exp|volume=52 |pages=468–71 |year=2003 |pmid=12701060}}</ref> This deficiency is intracellular, and measuring intracellular magnesium requires techniques not yet available in routine clinical settings. Magnesium is required in more than 300 enzymatic reactions, including several that are rate-limiting in carbohydrate utilization. Insulin action depends on magnesium availability in cells and high glucose exposure leads to magnesium depletion and insulin resistance. In obese children, magnesium deficiency precedes insulin resistance<ref name="pmid12701060"/>, but how the heightened responsivity of cells to insulin, that is characteristic of the pre-obese state,<ref name="pmid14970841"/> relates to magnesium deficiency is not known. | |||
'''Oxidative stress and reductant stress''' | '''Oxidative stress and reductant stress''' | ||
At the scale of the | At the scale of the adipocyte, we are facing a paradox similar to the one involving insulin. Obesity may present associated with a range of abnormalities: insulin resistance, chronic inflammation, oxidative stress and a range of ills aggregating in what has been called the metabolic syndrome. It thus appears reasonable to assume that adipocytes, in obesity, are in a state of oxidative stress. However, studying obesity in isolation, it became apparent that obesity at the adipocyte level required the opposite of oxidative stress, e.g. a balance between oxidants and reductants tilted in favour of the latter.<ref name="pmid16377639">{{cite journal |author=Galinier A ''et al.'' |title=Adipose tissue proadipogenic redox changes in obesity |journal=J Biol Chem|volume=281 |pages=12682–7|year=2006 |pmid=16377639 |url=http://www.jbc.org/cgi/content/full/281/18/12682}}</ref> | ||
'''Omega-6 vs. omega-3 unsaturated fatty acids''' | '''Omega-6 vs. omega-3 unsaturated fatty acids''' | ||
The amount of fat to which | The amount and type of fat to which adipocytes are exposed conditions their development. The amount of omega-6 fatty acids in the diet, in absolute terms as well as relative to the amounts of omega-3 fatty acids, have risen sharply since 1945 due to novel techniques to extract fat from vegetable sources. Omega-6 fatty acids, as a [[prostacyclin]] precursors, enhance [[cyclic AMP]]-dependent signaling pathways in preadipocytes and promote the development of mature adipocytes. Only by modulating the proportion of omega-6 fatty acids in the diet (without increasing total caloric intake), it is possible to cause in animals a 50% increase in body mass.<ref name="pmid12576509">{{cite journal |author=Massiera F ''et al.'' |title=Arachidonic acid and prostacyclin signaling promote adipose tissue development: a human health concern? |journal=J Lipid Res |volume=44 |pages=271–9 |year=2003 |pmid=12576509 |url=http://www.jlr.org/cgi/content/full/44/2/271}}</ref> | ||
'''''Starving in a sea of plenty''''' | '''''Starving in a sea of plenty''''' | ||
In | In 2008, a [[twin study]] was published which carefully selected, from 2,453 young healthy twin pairs, 14 pairs that were discordant for obesity (one twin being obese, and the other not).<ref name="pmid18336063">{{cite journal |author=Pietiläinen KH ''et al.''|title=Global transcript profiles of fat in monozygotic twins discordant for BMI: pathways behind acquired obesity |journal=PLoS Med|volume=5|pages=e51 |year=2008 |pmid=18336063 |url=http://medicine.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pmed.0050051&ct=1#toclink5}}</ref> This study ruled out all genetic factors, as well as intrauterine influences and several environmental factors commonly shared amongst siblings of similar ages. The most significant changes in adipocytes were a sharp decrease in the number of mitochondria, the power plants of the cells that are involved in fat burning, and a specific decrease in their ability to oxidize (burn) three amino acids called [[branched-chain amino acids]], that are the first amino acids to be used as fuel when other sources are unavailable. These amino acids, being poorly catabolized, were higher in the circulation; this signalled the release of higher amounts of more insulin, possibly leading to a vicious cycle. Considering metabolic pathways that were, on the contrary, up-regulated, the researchers found that numerous inflammatory cascades were overactive. The decline in the number of mitochondria remains the most important finding, which will help to design therapies addressing the fact that, in the disease of affluent civilisations ''par excellence'', adipocytes and their energy-producing organelles, the mitochondria, are "starving in a sea of plenty". | ||
'''The gut flora of the obese: the enemy within''' | '''The gut flora of the obese: the enemy within''' | ||
The gut flora, which fulfills an essential symbiotic role in animal metabolism, is probably the first victim of a high-fat diet. Before one becomes obese due to dietary excesses, the trillions of micro-organisms which inhabit our intestines have already transformed into a pro-inflammatory, obesogenic organ.<ref name="pmid18326589">{{cite journal |author=Kalliomäki M | The gut flora, which fulfills an essential symbiotic role in animal metabolism, is probably the first victim of a high-fat diet. Before one becomes obese due to dietary excesses, the trillions of micro-organisms which inhabit our intestines have already transformed into a pro-inflammatory, obesogenic organ.<ref name="pmid18326589">{{cite journal |author=Kalliomäki M ''et al.'' |title=Early differences in fecal microbiota composition in children may predict overweight |journal=Am J Clin Nutr|volume=87|pages=534–8 |year=2008|pmid=18326589}}</ref><ref name="pmid18305141">{{cite journal |author=Cani PD ''et al.'' |title=Changes in gut microbiota control metabolic endotoxemia-induced inflammation in high-fat diet-induced obesity and diabetes in mice |journal=Diabetes |year=2008 |pmid=18305141}}</ref><ref name="pmid17456850">{{cite journal|author=Cani PD ''et al.'' |title=Metabolic endotoxemia initiates obesity and insulin resistance|journal=Diabetes|volume=56 |pages=1761–72|year=2007|pmid=17456850 |url=http://diabetes.diabetesjournals.org/cgi/content/full/56/7/1761}}</ref> | ||
==Treatment== | ==Treatment== | ||
''See also [[Bariatric surgery]], [[Drug treatments for obesity]] and [[Exercise and body weight]]'' | |||
In a [[clinical practice guideline]] by the [[American College of Physicians]] | The mainstay of treatment for obesity is an energy-limited [[dieting|diet]] and increased [[Physical exercise|exercise]]. In studies, diet and exercise programs have consistently produced an average weight loss of approximately 8% of total body mass (excluding study drop-outs). While not all dieters will be satisfied with this outcome, a loss of as little as 5% of body mass can create large health benefits. A more intractable [[Sociotherapy|therapeutic]] problem appears to be weight loss maintenance. Of dieters who manage to lose 10% or more of their [[body mass]] in studies, 80-95% will regain that weight within two to five years, supporting the finding that the body has various mechanisms that maintain weight at a certain set point. | ||
# People with a BMI | |||
A [[clinical practice guideline]] issued by the [[American College of Physicians]] in 2005 made five recommendations:<ref name=Snow2005>{{cite journal | author=Snow V ''et al.''| title=Pharmacologic and surgical management of obesity in primary care: a clinical practice guideline from the American College of Physicians| journal=Ann Intern Med | year=2005| pages=525-31| volume=142|id=PMID 15809464}} [http://www.annals.org/cgi/content/full/142/7/525].</ref> | |||
# People with a BMI above 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 [[Adverse effect (medicine)|side-effects]] and the unavailability of long-term safety and efficacy data. | # If these goals are not achieved, pharmacotherapy can be offered. The patient needs to be informed of the possibility of [[Adverse effect (medicine)|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]]. | # 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]]. | ||
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# 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. | # 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 [[ | A [[clinical practice guideline]] by the [[U.S. 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.<ref>{{cite web |url=http://www.ngc.gov/summary/summary.aspx?ss=15&doc_id=3494 |title=Behavioral counseling in primary care to promote a healthy diet: recommendations and rationale. |accessdate=2007-05-22}}</ref><ref name="pmid12554027">{{cite journal |author=Pignone MP ''et al.'' |title=Counseling to promote a healthy diet in adults: a summary of the evidence for the U.S. Preventive Services Task Force|journal=Am J Prev Med|volume=24|pages=75-92|year=2003|pmid=12554027}}</ref> | ||
===Counseling=== | ===Counseling=== | ||
A [[meta-analysis]] of [[randomized controlled trial]]s concluded that "compared with usual care, dietary counseling interventions produce modest weight losses that diminish over time."<ref name="pmid17606960">{{cite journal |author=Dansinger ML | A [[meta-analysis]] of [[randomized controlled trial]]s concluded that "compared with usual care, dietary counseling interventions produce modest weight losses that diminish over time."<ref name="pmid17606960">{{cite journal |author=Dansinger ML ''et al.'' |title=Meta-analysis: the effect of dietary counseling for weight loss|journal=Ann Intern Med |volume=147|pages=41-50 |year=2007 |pmid=17606960}}</ref> | ||
The role of genetic counseling is unclear<ref name="pmid15216550">{{cite journal |author=Marteau T ''et al.'' |title=Psychological impact of genetic testing for familial hypercholesterolemia within a previously aware population: a randomized controlled trial |journal=Am | The role of genetic counseling is unclear<ref name="pmid15216550">{{cite journal|author=Marteau T ''et al.'' |title=Psychological impact of genetic testing for familial hypercholesterolemia within a previously aware population: a randomized controlled trial |journal=Am J Med Genet A|volume=128 |pages=285–93 |year=2004 |pmid=15216550 }}</ref>; but based on a study done of hypercholesterolemia, it is possible that genetic counseling might lead to patients preferring medication over diet therapy.<ref name="pmid17879121">{{cite journal |author=Rief W ''et al.''|title=Is information on genetic determinants of obesity helpful or harmful for obese people?-A randomized clinical trial |journal=J Gen Intern Med|volume=22|pages=1553–9|year=2007|pmid=17879121}}</ref> | ||
==== | ====Delivery method for counseling==== | ||
* Personal contact may better sustain weight loss<ref name="pmid18334689">{{cite journal| author=Svetkey LP, Stevens VJ, Brantley PJ, Appel LJ, Hollis JF, Loria CM et al.| title=Comparison of strategies for sustaining weight loss: the weight loss maintenance randomized controlled trial. | journal=JAMA | year= 2008 | volume= 299 | issue= 10 | pages= 1139-48 | pmid=18334689 | doi=10.1001/jama.299.10.1139 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18334689 }} [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18667668 Review in: Evid Based Med. 2008 Aug;13(4):109] [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18624372 Review in: ACP J Club. 2008 Jul;149(1):4] </ref> | |||
* The [[Internet]] may increase [[patient participation]] in their health care.<ref name="pmid12684363">{{cite journal| author=Tate DF, Jackvony EH, Wing RR| title=Effects of Internet behavioral counseling on weight loss in adults at risk for type 2 diabetes: a randomized trial. | journal=JAMA | year= 2003 | volume= 289 | issue= 14 | pages= 1833-6 | pmid=12684363 | doi=10.1001/jama.289.14.1833 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12684363 }} </ref><ref name="pmid18201641">{{cite journal|author=Hunter CM ''et al.''|title=Weight management using the internet a randomized controlled trial|journal=Am J Prev Med|volume=34|pages=119–26|year=2008 |pmid=18201641}}</ref> | |||
* High-frequency [[telephone]] contact may help.<ref name="pmid19221377">{{cite journal| author=Digenio AG, Mancuso JP, Gerber RA, Dvorak RV| title=Comparison of methods for delivering a lifestyle modification program for obese patients: a randomized trial. | journal=Ann Intern Med | year= 2009 | volume= 150 | issue= 4 | pages= 255-62 | pmid=19221377 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19221377 }} </ref> | |||
The [[Internet]] | |||
===Diets=== | ===Diets=== | ||
{| | {{main|Diet (weight loss)}} | ||
====Portion control==== | |||
A randomized controlled trial found that patients using portion control plates and log books had more weight loss and less use of hypoglycemic drugs.<ref name="pmid17592101">{{cite journal |author=Pedersen SD ''et al.''|title=Portion control plate for weight loss in obese patients with type 2 diabetes mellitus: a controlled clinical trial |journal=Arch Intern Med|volume=167|pages=1277–83 |year=2007|pmid=17592101}}[http://www.acpjc.org/Content/147/3/issue/ACPJC-2007-147-3-068.htm ACP Journal Club review]</ref> | |||
==== | ====Drink more water==== | ||
Encouraging more water drinking may help.<ref name="pmid19336356">{{cite journal|author=Muckelbauer R ''et al.''|title=Promotion and provision of drinking water in schools for overweight prevention: randomized, controlled cluster trial|journal=Pediatrics|volume=123|pages=e661–7|year=2009|pmid=19336356|url=http://pediatrics.aappublications.org/cgi/pmidlookup?view=long&pmid=19336356}}</ref> | |||
====Financial incentives==== | |||
Financial incentives may help.<ref name="pmid19066383">{{cite journal |author=Volpp KG ''et al.''|title=Financial incentive-based approaches for weight loss: a randomized trial|journal=JAMA |volume=300 |pages=2631–7|year=2008 |pmid=19066383|url=http://jama.ama-assn.org/cgi/pmidlookup?view=long&pmid=19066383}}</ref> | |||
===Food labeling=== | |||
The Nutrition Labeling and Education Act (NLEA) of 1990 went into effect in 1994 to require labeling on on packaged foods. | |||
New York City required labeling by restaurants with 15 or more outlets to post caloric content starting July, 2008.<ref name="pmid20375399">{{cite journal| author=Nestle M| title=Health care reform in action--calorie labeling goes national. | journal=N Engl J Med | year= 2010 | volume= 362 | issue= 25 | pages= 2343-5 | pmid=20375399 | doi=10.1056/NEJMp1003814 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20375399 }} </ref> The New York law may increase awareness of calories.<ref name="pmid19808705">{{cite journal| author=Elbel B, Kersh R, Brescoll VL, Dixon LB| title=Calorie labeling and food choices: a first look at the effects on low-income people in New York City. | journal=Health Aff (Millwood) | year= 2009 | volume= 28 | issue= 6 | pages= w1110-21 | pmid=19808705 | doi=10.1377/hlthaff.28.6.w1110 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19808705 }} </ref><ref name="pmid20966367">{{cite journal| author=Dumanovsky T, Huang CY, Bassett MT, Silver LD| title=Consumer awareness of fast-food calorie information in New York City after implementation of a menu labeling regulation. | journal=Am J Public Health | year= 2010 | volume= 100 | issue= 12 | pages= 2520-5 | pmid=20966367 | doi=10.2105/AJPH.2010.191908 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20966367 }} </ref> | |||
Public Law 111-147, the Patient Protection and Affordable Care Act, mandates that restaurants with 20 or more outlets nationwide post caloric information “in a clear and conspicuous manner.”<ref name="pmid20375399">{{cite journal| author=Nestle M| title=Health care reform in action--calorie labeling goes national. | journal=N Engl J Med | year= 2010 | volume= 362 | issue= 25 | pages= 2343-5 | pmid=20375399 | doi=10.1056/NEJMp1003814 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20375399 }} </ref> | |||
===Medications=== | |||
{{main|Drug treatments for obesity}} | |||
=== | |||
===Bariatric surgery=== | ===Bariatric surgery=== | ||
{{main|Bariatric surgery}} | |||
''[[Bariatric surgery]]'' (or "weight loss surgery") is the use of surgical interventions in the treatment of obesity. As every surgical intervention may lead to complications, it is regarded as a last resort when dietary modification and pharmacological treatment have proven to be unsuccessful. | ''[[Bariatric surgery]]'' (or "weight loss surgery") is the use of surgical interventions in the treatment of obesity. As every surgical intervention may lead to complications, it is regarded as a last resort when dietary modification and pharmacological treatment have proven to be unsuccessful. | ||
In the U.S.A.,[[Medicare]] will only only pay for procedures performed at approved facilities.<ref name="urlBariatric Surgery">{{cite web |url=http://www.cms.hhs.gov/MedicareApprovedFacilitie/BSF/|title=Bariatric Surgery |publisher=Centers for Medicare & Medicaid Services|accessdate=2008-06-26}}</ref> | |||
In the | |||
* '''Predominantly restrictive procedures'''. The most common approaches are reducing the volume of the stomach, producing an earlier sense of satiation (e.g. by [[adjustable gastric band]]ing and [[Vertical banded gastroplasty surgery|vertical banded gastroplasty]]). | * '''Predominantly restrictive procedures'''. The most common approaches are reducing the volume of the stomach, producing an earlier sense of satiation (e.g. by [[adjustable gastric band]]ing and [[Vertical banded gastroplasty surgery|vertical banded gastroplasty]]). | ||
* '''Predominantly malabsorptive procedures''' Others procedures also reduce the length of bowel that food will be in contact with, directly reducing absorption ([[gastric bypass surgery]]). | * '''Predominantly malabsorptive procedures''' Others procedures also reduce the length of bowel that food will be in contact with, directly reducing absorption ([[gastric bypass surgery]]). | ||
Band surgery is reversible, while gastric bypass surgery is not. In general, gastric bypass surgery leads to more weight loss than band surgery. A [[meta-analysis]] by the [[American College of Physicians]] reports the following weight loss at 36 months:<ref name="pmid15809466">{{cite journal |author=Maggard MA ''et al.''|title=Meta-analysis: surgical treatment of obesity|journal=Ann Intern Med|volume=142|pages=547–59|year=2005|pmid=15809466}}</ref> | |||
In general, | |||
* Biliopancreatic diversion - 53 kg | * Biliopancreatic diversion - 53 kg | ||
* Roux-en-Y gastric bypass | * Roux-en-Y gastric bypass - 41 kg (Open - 42 kg; Laparoscopic - 38 kg) | ||
* Adjustable gastric banding - 35 kg | * Adjustable gastric banding - 35 kg | ||
* Vertical banded gastroplasty - 32 kg | * Vertical banded gastroplasty - 32 kg | ||
This analysis does not include a more recent [[randomized controlled trial]].<ref>Nguyen NT ''et al.'' (2009)[http://journals.lww.com/annalsofsurgery/Abstract/2009/10000/A_Prospective_Randomized_Trial_of_Laparoscopic.14.aspx A prospective randomized trial of laparoscopic gastric bypass versus laparoscopic adjustable gastric banding for the treatment of morbid obesity: Outcomes, quality of life, and costs] ''Ann Surg'' 250:631-41}}</ref> | |||
===== | Two studies report decreases in mortality from bariatric surgery.<ref name="pmid17715408">{{cite journal|author=Sjöström L ''et al.''|title=Effects of bariatric surgery on mortality in Swedish obese subjects |journal=N Engl J Med|volume=357|pages=741-52|year=2007|pmid=17715408 |doi=10.1056/NEJMoa066254}}</ref><ref name="pmid17715409">{{cite journal |author=Adams TD ''et al.'' |title=Long-term mortality after gastric bypass surgery |journal=N Engl J Med |volume=357|pages=753-61 |year=2007 |pmid=17715409 }}</ref> In the Swedish [[randomized controlled trial]], patients with a BMI of 34 or more for men and 38 or more for women underwent various types of bariatric surgery and were followed for a mean of 11 years. Surgery patients had 5% mortality while control patients had 6.3% mortality. <ref name="pmid17715408"/> In a Utah retrospective [[cohort study]] that followed patients for a mean of 7 years after various types of gastric bypass, surgery patients had 0.4% mortality while control patients had 0.6% mortality.<ref name="pmid17715409"/> | ||
Bariatric surgery remits [[diabetes mellitus type 2]] in more than 1 of every two people after 2 years if they are similar to the patients in the [[randomized controlled trial | |||
Bariatric surgery remits [[diabetes mellitus type 2]] in more than 1 of every two people after 2 years if they are similar to the patients in the [[randomized controlled trial]] by Dixon ''et al.''.<ref name="pmid18212316">{{cite journal |author=Dixon JB ''et al.'' |title=Adjustable gastric banding and conventional therapy for type 2 diabetes: a randomized controlled trial |journal=JAMA |volume=299 |pages=316–23 |year=2008 |pmid=18212316 |url=http://jama.ama-assn.org/cgi/pmidlookup?view=long&pmid=18212316}}</ref> In this trial, 73% of the patients remitted their diabetes versus 13% of the patients in the control group. | |||
==Prevention== | ==Prevention== | ||
Display of calorie information on the menus or menu boards of restaurants has been proposed by the city of New York.<ref name="nyt">Rivera R | Display of calorie information on the menus or menu boards of restaurants has been proposed by the city of New York.<ref name="nyt">Rivera R (2007) “New York City Reintroduces Calorie Rule,” The New York Times, October 25, 2007, http://www.nytimes.com/2007/10/25/nyregion/25calories.html (accessed October 26, 2007)</ref> | ||
Eating breakfast may reduce weight gain by adolescents<ref name="pmid18310183">{{cite journal |author=Timlin MT | Eating breakfast may reduce weight gain by adolescents<ref name="pmid18310183">{{cite journal |author=Timlin MT ''et al.'' |title=Breakfast eating and weight change in a 5-year prospective analysis of adolescents: Project EAT (Eating Among Teens) |journal=Pediatrics |volume=121 |pages=e638-45 |year=2008 |pmid=18310183 |url=http://pediatrics.aappublications.org/cgi/pmidlookup?view=long&pmid=18310183}}</ref> | ||
==References== | ==References== | ||
{{Reflist|2}}[[Category:Suggestion Bot Tag]] | |||
[[Category: |
Latest revision as of 16:00, 27 September 2024
Obesity is the medical condition associated with excessive stores of body fat, to the extent that it causes serious health risks. Physical problems include high blood pressure, heart disease, some cancers and Diabetes mellitus type 2; emotional problems include low self esteem, and depression. More than a billion people are classed as obese worldwide, and by 2025, 300 million people are expected to suffer from obesity-related diabetes.
There are many ways of measuring body fat, but the most common measures the relationship between weight and height by the body mass index (BMI). A BMI of 30 or more puts you in the category of obese. This method is simple, but imprecise; people with well-developed muscle may have a high BMI yet a low proportion of body fat.
Prevalence and epidemiology
Obesity is increasing in Europe.[1] In the U.S.A., obesity is increased through 2004[2] but has been stable since[3]. Among immigrants, the incidence of obesity increases with the duration of living in the U.S.A..[4]
Causes/etiology
The proximate cause of obesity is a mix of environmental and genetic factors.[5][6] In only very few cases can obesity in humans be attributed to a single gene defect, but many genes have been found that have (usually rare) variants associated with an increased risk of obesity.
Obesity is generally associated with a state of leptin resistance, that is analogous to the insulin resistance seen in diabetes mellitus type 2 . Leptin is a hormone that is secreted into the blood from fat tissues (adipocytes); it acts on the appetite-regulating centres of the hypothalamus to suppress appetite, and it is secreted at high levels in most obese individuals. However, in these obese individuals, the hypothalamus does not respond appropriately to leptin.
The role of fetal programming,[7] [8][9] perhaps operative in the higher risk of obesity in offspring of older and/or very lean women.
Environment and lifestyle
The increase in overweight and obesity that has taken place during the 20th century is likely to be due to environmental changes (in the widest sense), including especially lifestyle changes that affect diet and exercise habits. While a sedentary lifestyle is involved in the development of a wide range of physical and mental ills, and obesity is associated with a more sedentary lifestyle, it is not obvious that lack of exercise is a major factor in the present obesity epidemic. In a 5.6 years follow-up study of 393 middle-aged healthy subjects, Cambridge epidemiologists demonstrated that carrying excess weight predicted a sedentary lifestyle, but that sedentary time did not predict weight gain.[10] Failure of sedentary time to predict weight gain might conceivably reflect insufficient sample size to reveal a significant prediction, as might greater errors in estimating sedentary time than measuring weight change.
Many other changes in environment and lifestyle may be involved in the increasing prevalence of obesity. In one multi-center review of the literature, 10 other factors, including epigenetic changes were found to be equally plausible etiologic factors contributing to the epidemic.[11][12] Stress and depression (and associated disruptions of sleep) can lead to obesity.[13] [14][11]; changes in eating patterns may contribute[15][16][17] and cultural changes in perceptions of overweight[18] Smoking cessation has a well known effect to increase caloric intake.
Evolutionary perspectives of obesity
To fully understand the causes and prevalence of obesity, evolutionary factors may need integration into the mix of environmental and genetic proximate causes of obesity. Evolutionary medicine suggests we get fat because of built-in encouragements to eat heartily when we have plenty to eat and to restrict energy expenditures in preparation for inevitable food shortages. It may also suggest we consider the effect of the types of food we eat compared to those evolution adapted us to eat. We’ve only recently, on an evolutionary timescale, begun to eat readily absorbable carbohydrates in disproportionate amounts. Our hunter-gatherer ancestors had little access to such food items, with the exception of a bit of honey. Now we have so-called refined carbohydrates readily available and much consumed. Those include granulated sugar and sucrose dissolved in soft drinks; syrups and candies; milled cereal grain flours and their host pastries, pastas and breads; and many other processed ‘high glycemic’ foods. Those foods stimulate the secretion of insulin as control for glucose homeostasis, and induce other hormonal changes that influence appetite and efficiency of energy utilization. Science writer Gary Taubes summarizes the argument:
“There is considerable evidence that the obesity epidemic is caused by a hormonal phenomenon, specifically by the consumption of refined carbohydrates, starches and sugars, all of which prompt (sooner or later) excessive insulin secretion. Insulin is the primary regulator of fat storage. When insulin levels are elevated, fat accumulates in our body tissue; when they fall, fat is released and we use it for fuel. By stimulating insulin secretion, carbohydrates make us fat; by driving us to accumulate fat, they increase hunger and decrease the energy we expend in metabolism and physical activity. In short, obesity is caused not by overeating or sedentary behaviour, but by hormonal malfunctioning triggered by the consumption of particular types of carbohydrate-containing foods.”[19]
Pathophysiology
The response to a meal in obesity: the insulin paradox
All consumers of refined starches, soft drinks, high-fructose corn syrups and other energy-replete products are not born equal. Obese persons, after a meal, appear to burn carbohydrates less efficiently and fat even more poorly.[20] A contribution of leptin resistance was suggested, as circulating concentrations of leptin were higher in the obese men that were the least efficient metabolisers of fat. However, the arrow of causality may be oriented in the other direction. In persons with a family history of obesity, the earliest obesogenic changes are not related to leptin, but to metabolic efficiency and to insulin status and responsiveness: subjects at increased risk of obesity oxidize carbohydrates more quickly and fat more slowly, and have lower insulin, consistent with a greater insulin sensitivity.[21] These findings contrast with those implicating obesity with the development, over the long term, of the opposite of insulin sensitivity, i.e. insulin resistance.
Magnesium Obese subjects, like type II diabetics, are magnesium deficient.[22] This deficiency is intracellular, and measuring intracellular magnesium requires techniques not yet available in routine clinical settings. Magnesium is required in more than 300 enzymatic reactions, including several that are rate-limiting in carbohydrate utilization. Insulin action depends on magnesium availability in cells and high glucose exposure leads to magnesium depletion and insulin resistance. In obese children, magnesium deficiency precedes insulin resistance[22], but how the heightened responsivity of cells to insulin, that is characteristic of the pre-obese state,[21] relates to magnesium deficiency is not known.
Oxidative stress and reductant stress
At the scale of the adipocyte, we are facing a paradox similar to the one involving insulin. Obesity may present associated with a range of abnormalities: insulin resistance, chronic inflammation, oxidative stress and a range of ills aggregating in what has been called the metabolic syndrome. It thus appears reasonable to assume that adipocytes, in obesity, are in a state of oxidative stress. However, studying obesity in isolation, it became apparent that obesity at the adipocyte level required the opposite of oxidative stress, e.g. a balance between oxidants and reductants tilted in favour of the latter.[23]
Omega-6 vs. omega-3 unsaturated fatty acids
The amount and type of fat to which adipocytes are exposed conditions their development. The amount of omega-6 fatty acids in the diet, in absolute terms as well as relative to the amounts of omega-3 fatty acids, have risen sharply since 1945 due to novel techniques to extract fat from vegetable sources. Omega-6 fatty acids, as a prostacyclin precursors, enhance cyclic AMP-dependent signaling pathways in preadipocytes and promote the development of mature adipocytes. Only by modulating the proportion of omega-6 fatty acids in the diet (without increasing total caloric intake), it is possible to cause in animals a 50% increase in body mass.[24]
Starving in a sea of plenty
In 2008, a twin study was published which carefully selected, from 2,453 young healthy twin pairs, 14 pairs that were discordant for obesity (one twin being obese, and the other not).[25] This study ruled out all genetic factors, as well as intrauterine influences and several environmental factors commonly shared amongst siblings of similar ages. The most significant changes in adipocytes were a sharp decrease in the number of mitochondria, the power plants of the cells that are involved in fat burning, and a specific decrease in their ability to oxidize (burn) three amino acids called branched-chain amino acids, that are the first amino acids to be used as fuel when other sources are unavailable. These amino acids, being poorly catabolized, were higher in the circulation; this signalled the release of higher amounts of more insulin, possibly leading to a vicious cycle. Considering metabolic pathways that were, on the contrary, up-regulated, the researchers found that numerous inflammatory cascades were overactive. The decline in the number of mitochondria remains the most important finding, which will help to design therapies addressing the fact that, in the disease of affluent civilisations par excellence, adipocytes and their energy-producing organelles, the mitochondria, are "starving in a sea of plenty".
The gut flora of the obese: the enemy within
The gut flora, which fulfills an essential symbiotic role in animal metabolism, is probably the first victim of a high-fat diet. Before one becomes obese due to dietary excesses, the trillions of micro-organisms which inhabit our intestines have already transformed into a pro-inflammatory, obesogenic organ.[26][27][28]
Treatment
See also Bariatric surgery, Drug treatments for obesity and Exercise and body weight
The mainstay of treatment for obesity is an energy-limited diet and increased exercise. In studies, diet and exercise programs have consistently produced an average weight loss of approximately 8% of total body mass (excluding study drop-outs). While not all dieters will be satisfied with this outcome, a loss of as little as 5% of body mass can create large health benefits. A more intractable therapeutic problem appears to be weight loss maintenance. Of dieters who manage to lose 10% or more of their body mass in studies, 80-95% will regain that weight within two to five years, supporting the finding that the body has various mechanisms that maintain weight at a certain set point.
A clinical practice guideline issued by the American College of Physicians in 2005 made five recommendations:[29]
- People with a BMI above 30 should be counseled on diet, exercise and other relevant behavioral interventions, and set a realistic goal for weight loss.
- If these goals are not achieved, pharmacotherapy can be offered. The patient needs to be informed of the possibility of side-effects and the unavailability of long-term safety and efficacy data.
- Drug therapy may consist of sibutramine, orlistat, phentermine, diethylpropion, fluoxetine, and bupropion. For more severe cases of obesity, stronger drugs such as amphetamine and methamphetamine may be used on a selective basis. Evidence is not sufficient to recommend sertraline, topiramate, or zonisamide.
- In patients with BMI > 40 who fail to achieve their weight loss goals (with or without medication) and who develop obesity-related complications, referral for bariatric surgery may be indicated. The patient needs to be aware of the potential complications.
- Those requiring bariatric surgery should be referred to high-volume referral centers, as the evidence suggests that surgeons who frequently perform these procedures have fewer complications.
A clinical practice guideline by the U.S. 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.[30][31]
Counseling
A meta-analysis of randomized controlled trials concluded that "compared with usual care, dietary counseling interventions produce modest weight losses that diminish over time."[32]
The role of genetic counseling is unclear[33]; but based on a study done of hypercholesterolemia, it is possible that genetic counseling might lead to patients preferring medication over diet therapy.[34]
Delivery method for counseling
- Personal contact may better sustain weight loss[35]
- The Internet may increase patient participation in their health care.[36][37]
- High-frequency telephone contact may help.[38]
Diets
Portion control
A randomized controlled trial found that patients using portion control plates and log books had more weight loss and less use of hypoglycemic drugs.[39]
Drink more water
Encouraging more water drinking may help.[40]
Financial incentives
Financial incentives may help.[41]
Food labeling
The Nutrition Labeling and Education Act (NLEA) of 1990 went into effect in 1994 to require labeling on on packaged foods.
New York City required labeling by restaurants with 15 or more outlets to post caloric content starting July, 2008.[42] The New York law may increase awareness of calories.[43][44]
Public Law 111-147, the Patient Protection and Affordable Care Act, mandates that restaurants with 20 or more outlets nationwide post caloric information “in a clear and conspicuous manner.”[42]
Medications
Bariatric surgery
Bariatric surgery (or "weight loss surgery") is the use of surgical interventions in the treatment of obesity. As every surgical intervention may lead to complications, it is regarded as a last resort when dietary modification and pharmacological treatment have proven to be unsuccessful. In the U.S.A.,Medicare will only only pay for procedures performed at approved facilities.[45]
- Predominantly restrictive procedures. 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).
- Predominantly malabsorptive procedures Others procedures also reduce the length of bowel that food will be in contact with, directly reducing absorption (gastric bypass surgery).
Band surgery is reversible, while gastric bypass surgery is not. In general, gastric bypass surgery leads to more weight loss than band surgery. A meta-analysis by the American College of Physicians reports the following weight loss at 36 months:[46]
- Biliopancreatic diversion - 53 kg
- Roux-en-Y gastric bypass - 41 kg (Open - 42 kg; Laparoscopic - 38 kg)
- Adjustable gastric banding - 35 kg
- Vertical banded gastroplasty - 32 kg
This analysis does not include a more recent randomized controlled trial.[47]
Two studies report decreases in mortality from bariatric surgery.[48][49] In the Swedish randomized controlled trial, patients with a BMI of 34 or more for men and 38 or more for women underwent various types of bariatric surgery and were followed for a mean of 11 years. Surgery patients had 5% mortality while control patients had 6.3% mortality. [48] In a Utah retrospective cohort study that followed patients for a mean of 7 years after various types of gastric bypass, surgery patients had 0.4% mortality while control patients had 0.6% mortality.[49]
Bariatric surgery remits diabetes mellitus type 2 in more than 1 of every two people after 2 years if they are similar to the patients in the randomized controlled trial by Dixon et al..[50] In this trial, 73% of the patients remitted their diabetes versus 13% of the patients in the control group.
Prevention
Display of calorie information on the menus or menu boards of restaurants has been proposed by the city of New York.[51]
Eating breakfast may reduce weight gain by adolescents[52]
References
- ↑ Kotseva K et al. (2009). "Cardiovascular prevention guidelines in daily practice: a comparison of EUROASPIRE I, II, and III surveys in eight European countries". Lancet 373: 929–40. PMID 19286092.
- ↑ Ogden CL et al. (2006). "Prevalence of overweight and obesity in the United States, 1999-2004". JAMA 295: 1549–55. PMID 16595758.
- ↑ Ogden CL et al. (2008). "High body mass index for age among US children and adolescents, 2003-2006". JAMA 299: 2401–5. PMID 18505949.
- ↑ Goel MS et al. (2004). "Obesity among US immigrant subgroups by duration of residence". JAMA 292: 2860–7. PMID 15598917.
- ↑ Stunkard AJ et al. (1990). "The body-mass index of twins who have been reared apart". N Eng J Med 322: 1483–7. PMID 2336075.
- ↑ Christakis NA, Fowler JH (2007). "The spread of obesity in a large social network over 32 years". N Engl J Med 357: 370–9. PMID 17652652.
- ↑ Breier BH et al. (2001). "Fetal programming of appetite and obesity". Mol Cell Endocrinol 185: 73-9. PMID 11738796.
- ↑ Vickers MH et al. (2001). "Dysregulation of the adipoinsular axis - a mechanism for the pathogenesis of hyperleptinemia and adipogenic diabetes induced by fetal programming". J Endocrinol 170: 323-32. PMID 11479129.
- ↑ Vickers MH et al. (2000). "Fetal origins of hyperphagia, obesity, and hypertension and postnatal amplification by hypercaloric nutrition". Am J Physiol 279: E83-7. PMID 10893326.
- ↑ Ekelund U et al.(2008) Time spent being sedentary and weight gain in healthy adults: reverse or bidirectional causality? Am J Clin Nutr 88:612-7
- ↑ Jump up to: 11.0 11.1 Keith SW et al. (2006). "Putative contributors to the secular increase in obesity: exploring the roads less traveled". Int J Obes 30: 1585–94. PMID 16801930.
- ↑ Wansink B, Payne CR (2009). "The joy of cooking too much: 70 years of calorie increases in classic recipes.". Ann Intern Med 150 (4): 291-2. PMID 19221391. [e]
- ↑ Kivimäki M et al. (2009). "Common mental disorder and obesity: insight from four repeat measures over 19 years: prospective Whitehall II cohort study". BMJ 339: b3765. PMID 19808765.
- ↑ Vgontzas AN et al. (2008). "Short sleep duration and obesity: the role of emotional stress and sleep disturbances". Int J Obes 32: 801-9. PMID 18253159.
- ↑ Roger, V. L.; A. S. Go, D. M. Lloyd-Jones, E. J. Benjamin, J. D. Berry, W. B. Borden, D. M. Bravata, S. Dai, E. S. Ford, C. S. Fox, H. J. Fullerton, C. Gillespie, S. M. Hailpern, J. A. Heit, V. J. Howard, B. M. Kissela, S. J. Kittner, D. T. Lackland, J. H. Lichtman, L. D. Lisabeth, D. M. Makuc, G. M. Marcus, A. Marelli, D. B. Matchar, C. S. Moy, D. Mozaffarian, M. E. Mussolino, G. Nichol, N. P. Paynter, E. Z. Soliman, P. D. Sorlie, N. Sotoodehnia, T. N. Turan, S. S. Virani, N. D. Wong, D. Woo, M. B. Turner, on behalf of the American Heart Association Statistics Committee and Stroke Statistics Subcommittee (2011-12-15). "Heart Disease and Stroke Statistics--2012 Update: A Report From the American Heart Association". Circulation. DOI:10.1161/CIR.0b013e31823ac046. ISSN 1524-4539 0009-7322, 1524-4539. Retrieved on 2011-12-16. Research Blogging.
- ↑ Duffey KJ, Popkin BM (2011). "Energy density, portion size, and eating occasions: contributions to increased energy intake in the United States, 1977-2006.". PLoS Med 8 (6): e1001050. DOI:10.1371/journal.pmed.1001050. PMID 21738451. PMC PMC3125292. Research Blogging.
- ↑ Maruyama, K; et al. (2008-10-21). "The joint impact on being overweight of self reported behaviours of eating quickly and eating until full : cross sectional survey". BMJ 337: a2002.
- ↑ Johnson F et al. (2008). "Changing perceptions of weight in Great Britain: comparison of two population surveys". BMJ 337: a494. PMID 18617488.
- ↑ Taubes G. (2008) The great diet delusion: It is time for nutrition researchers and health authorities to wake up to the fact that people do not get fat simply because they overeat. New Scientist 19 January 2008, page 17
- ↑ Lopes IM et al. (2001). "Effects of leptin resistance on acute fuel metabolism after a high carbohydrate load in lean and overweight young men". J Am Coll Nutr 20: 643–8. PMID 11771681.
- ↑ Jump up to: 21.0 21.1 Giacco R et al. (2004). "Insulin sensitivity is increased and fat oxidation after a high-fat meal is reduced in normal-weight healthy men with strong familial predisposition to overweight". Int J Obes Relat Metab Disord 28: 342–8. PMID 14970841.
- ↑ Jump up to: 22.0 22.1 Takaya J et al. (2003). "Intracellular magnesium of platelets in children with diabetes and obesity". Metab Clin Exp 52: 468–71. PMID 12701060.
- ↑ Galinier A et al. (2006). "Adipose tissue proadipogenic redox changes in obesity". J Biol Chem 281: 12682–7. PMID 16377639.
- ↑ Massiera F et al. (2003). "Arachidonic acid and prostacyclin signaling promote adipose tissue development: a human health concern?". J Lipid Res 44: 271–9. PMID 12576509.
- ↑ Pietiläinen KH et al. (2008). "Global transcript profiles of fat in monozygotic twins discordant for BMI: pathways behind acquired obesity". PLoS Med 5: e51. PMID 18336063.
- ↑ Kalliomäki M et al. (2008). "Early differences in fecal microbiota composition in children may predict overweight". Am J Clin Nutr 87: 534–8. PMID 18326589.
- ↑ Cani PD et al. (2008). "Changes in gut microbiota control metabolic endotoxemia-induced inflammation in high-fat diet-induced obesity and diabetes in mice". Diabetes. PMID 18305141.
- ↑ Cani PD et al. (2007). "Metabolic endotoxemia initiates obesity and insulin resistance". Diabetes 56: 1761–72. PMID 17456850.
- ↑ Snow V et al. (2005). "Pharmacologic and surgical management of obesity in primary care: a clinical practice guideline from the American College of Physicians". Ann Intern Med 142: 525-31. PMID 15809464. [1].
- ↑ Behavioral counseling in primary care to promote a healthy diet: recommendations and rationale.. Retrieved on 2007-05-22.
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- ↑ Tate DF, Jackvony EH, Wing RR (2003). "Effects of Internet behavioral counseling on weight loss in adults at risk for type 2 diabetes: a randomized trial.". JAMA 289 (14): 1833-6. DOI:10.1001/jama.289.14.1833. PMID 12684363. Research Blogging.
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- ↑ Bariatric Surgery. Centers for Medicare & Medicaid Services. Retrieved on 2008-06-26.
- ↑ Maggard MA et al. (2005). "Meta-analysis: surgical treatment of obesity". Ann Intern Med 142: 547–59. PMID 15809466.
- ↑ Nguyen NT et al. (2009)A prospective randomized trial of laparoscopic gastric bypass versus laparoscopic adjustable gastric banding for the treatment of morbid obesity: Outcomes, quality of life, and costs Ann Surg 250:631-41}}
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- ↑ Dixon JB et al. (2008). "Adjustable gastric banding and conventional therapy for type 2 diabetes: a randomized controlled trial". JAMA 299: 316–23. PMID 18212316.
- ↑ Rivera R (2007) “New York City Reintroduces Calorie Rule,” The New York Times, October 25, 2007, http://www.nytimes.com/2007/10/25/nyregion/25calories.html (accessed October 26, 2007)
- ↑ Timlin MT et al. (2008). "Breakfast eating and weight change in a 5-year prospective analysis of adolescents: Project EAT (Eating Among Teens)". Pediatrics 121: e638-45. PMID 18310183.