Obesity

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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

See Genetics of obesity

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]

  1. 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.
  2. 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.
  3. 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.
  4. 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.
  5. Those requiring bariatric surgery should be referred to high-volume referral centers, as the evidence suggests that surgeons who frequently perform these procedures have fewer complications.

A clinical practice guideline by the US Preventive Services Task Force (USPSTF) concluded that the evidence is insufficient to recommend for or against routine behavioral counseling to promote a healthy diet in unselected patients in primary care settings, but that intensive behavioral dietary counseling is recommended in those with hyperlipidemia and other known risk factors for cardiovascular and diet-related chronic disease. Intensive counseling can be delivered by primary care clinicians or by referral to other specialists, such as nutritionists or dietitians.[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

Diets

For more information, see: 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.[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

For more information, see: Drug treatments for obesity.


Bariatric surgery

For more information, see: 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

  1. ↑ 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.
  2. ↑ Ogden CL et al. (2006). "Prevalence of overweight and obesity in the United States, 1999-2004". JAMA 295: 1549–55. PMID 16595758.
  3. ↑ Ogden CL et al. (2008). "High body mass index for age among US children and adolescents, 2003-2006". JAMA 299: 2401–5. PMID 18505949.
  4. ↑ Goel MS et al. (2004). "Obesity among US immigrant subgroups by duration of residence". JAMA 292: 2860–7. PMID 15598917.
  5. ↑ 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.
  6. ↑ 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.
  7. ↑ Breier BH et al. (2001). "Fetal programming of appetite and obesity". Mol Cell Endocrinol 185: 73-9. PMID 11738796.
  8. ↑ 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.
  9. ↑ 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.
  10. ↑ 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
  11. ↑ 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.
  12. ↑ 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]
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  15. ↑ 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.
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  21. ↑ 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.
  22. ↑ 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.
  23. ↑ Galinier A et al. (2006). "Adipose tissue proadipogenic redox changes in obesity". J Biol Chem 281: 12682–7. PMID 16377639.
  24. ↑ 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.
  25. ↑ 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.
  26. ↑ 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.
  27. ↑ 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.
  28. ↑ Cani PD et al. (2007). "Metabolic endotoxemia initiates obesity and insulin resistance". Diabetes 56: 1761–72. PMID 17456850.
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  30. ↑ Behavioral counseling in primary care to promote a healthy diet: recommendations and rationale.. Retrieved on 2007-05-22.
  31. ↑ Pignone MP et al. (2003). "Counseling to promote a healthy diet in adults: a summary of the evidence for the U.S. Preventive Services Task Force". Am J Prev Med 24: 75-92. PMID 12554027.
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  33. ↑ Marteau T et al. (2004). "Psychological impact of genetic testing for familial hypercholesterolemia within a previously aware population: a randomized controlled trial". Am J Med Genet A 128: 285–93. PMID 15216550.
  34. ↑ Rief W et al. (2007). "Is information on genetic determinants of obesity helpful or harmful for obese people?-A randomized clinical trial". J Gen Intern Med 22: 1553–9. PMID 17879121.
  35. ↑ Svetkey LP, Stevens VJ, Brantley PJ, Appel LJ, Hollis JF, Loria CM et al. (2008). "Comparison of strategies for sustaining weight loss: the weight loss maintenance randomized controlled trial.". JAMA 299 (10): 1139-48. DOI:10.1001/jama.299.10.1139. PMID 18334689. Research Blogging. Review in: Evid Based Med. 2008 Aug;13(4):109 Review in: ACP J Club. 2008 Jul;149(1):4
  36. ↑ 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.
  37. ↑ Hunter CM et al. (2008). "Weight management using the internet a randomized controlled trial". Am J Prev Med 34: 119–26. PMID 18201641.
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  39. ↑ Pedersen SD et al. (2007). "Portion control plate for weight loss in obese patients with type 2 diabetes mellitus: a controlled clinical trial". Arch Intern Med 167: 1277–83. PMID 17592101. ACP Journal Club review
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  41. ↑ Volpp KG et al. (2008). "Financial incentive-based approaches for weight loss: a randomized trial". JAMA 300: 2631–7. PMID 19066383.
  42. ↑ 42.0 42.1 Nestle M (2010). "Health care reform in action--calorie labeling goes national.". N Engl J Med 362 (25): 2343-5. DOI:10.1056/NEJMp1003814. PMID 20375399. Research Blogging.
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  44. ↑ Dumanovsky T, Huang CY, Bassett MT, Silver LD (2010). "Consumer awareness of fast-food calorie information in New York City after implementation of a menu labeling regulation.". Am J Public Health 100 (12): 2520-5. DOI:10.2105/AJPH.2010.191908. PMID 20966367. Research Blogging.
  45. ↑ Bariatric Surgery. Centers for Medicare & Medicaid Services. Retrieved on 2008-06-26.
  46. ↑ Maggard MA et al. (2005). "Meta-analysis: surgical treatment of obesity". Ann Intern Med 142: 547–59. PMID 15809466.
  47. ↑ 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}}
  48. ↑ 48.0 48.1 Sjöström L et al. (2007). "Effects of bariatric surgery on mortality in Swedish obese subjects". N Engl J Med 357: 741-52. DOI:10.1056/NEJMoa066254. PMID 17715408. Research Blogging.
  49. ↑ 49.0 49.1 Adams TD et al. (2007). "Long-term mortality after gastric bypass surgery". N Engl J Med 357: 753-61. PMID 17715409.
  50. ↑ 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.
  51. ↑ 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)
  52. ↑ 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.
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