The Journal of Allergy and Clinical Immunology
Volume 115, Issue 5 , Pages 1102-1104, May 2005

Obesity, allergy and immunology

  • Celine Bergeron, MD, MSc

      Affiliations

    • From Meakins-Christie Laboratories, McGill University, Montreal, Canada
    • ,
  • Louis-Philippe Boulet, MD

      Affiliations

    • Centre de recherche en pneumologie, Hopital Laval, Universite Laval, Quebec city, Canada
    • ,
  • Qutayba Hamid, MD, PhD (Editors)

      Affiliations

    • From Meakins-Christie Laboratories, McGill University, Montreal, Canada
    • Corresponding Author InformationReprint requests: Qutayba Hamid, MD, PhD, McGill University, Meakins-Christie Laboratories, 3626 St Urbain St, Montreal, QC H2X 2P2, Canada.

Received 24 February 2005; accepted 10 March 2005.

Article Outline

 

Asthma, allergy, and obesity are common health problems, and their prevalence is increasing (Fig 1).1 Obesity is defined by a body mass index of greater than 30. Over the last few years, a number of studies have described an association between obesity and asthma (Fig 2).2, 3, 4, 5, 6, 7 In a large population of white Australian girls, a higher body mass index was reported to be a risk factor for atopy and wheeze.8 As a corollary, weight loss, as after bariatric surgery, has consistently been shown to improve asthma severity and control (Fig 3).9

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  • Fig 1. 

    Prevalence of obesity in the United States. A significant increase was observed in the 1990s throughout the United States. Mokdad AH, Serdula MK, Dietz WH, Bowman BA, Marks JS, Koplan JP. The spread of the obesity epidemic in the United States, 1991-1998. JAMA 1999;282:1519-22.

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  • Fig 2. 

    Association of high body mass index with asthma. In female subjects asthma is more prevalent in overweight and obese individuals. Reproduced with permission from Hancox et al.2

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  • Fig 3. 

    A, Asthma severity among morbidly obese asthmatic subjects before bariatric surgery. B, Changes in asthma severity after bariatric surgery. Close to 70% of obese asthmatic subjects have moderate-to-severe asthma. Two years after the bariatric surgery, 80% of obese asthmatic subjects have considerably improved their asthma symptoms and control. Reproduced with permission from Obesity Surgery 2004;14:1381-8.

Changes in airway structure and function have been associated with obesity. For example, it is common to observe an atypical obese airway pattern in morbidly obese persons at bronchoscopy (Fig 4). This pattern is believed to be attributed to fat infiltration and might be responsible for airway narrowing. In regard to physiologic changes, Boulet et al10 recently reported that obese subjects had lost the protective effect of deep inhalation to methacholine-induced bronchoconstriction that was observed in nonobese individuals (Fig 5).

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  • Fig 4. 

    Airways of a morbidly obese person (A) and of a nonobese person (B). In morbidly obese individuals it is common to observe widening of the bifurcation and a less-defined cartilage ring. BMI, Body mass index.

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  • Fig 5. 

    Absence of a protective effect of deep inhalation to methacholine-induced bronchoconstriction in obese subjects. For a similar dose of methacholine, avoidance of deep inspiration for a 20-minute period before methacholine challenge increased the decrease in FEV1 compared with nonavoidance in nonobese subjects (blue circles, body mass index [BMI] <30; P=.0003), whereas no difference was observed in obese subjects (red circles, body mass index ≥30; P>.05).

Fat tissue in obese persons is a source of inflammatory mediators (Table I)11 that might be implicated in asthma pathophysiology. Leptin is of particular interest because it has been found to be present in higher levels in obese asthmatic subjects compared with in obese nonasthmatic subjects (Fig 6).12 Leptin, an adipocyte-derived hormone, has been suggested to upregulate the inflammatory immune response. In an animal model of asthma, Shore et al13 recently showed that the allergen airway response is increased in the presence of leptin. They found that airway hyperresponsiveness, the number of BAL eosinophils and lymphocytes, and IL-4, IL-5, and IL-13 levels are all increased in leptin-treated animals compared with control animals.

Table I. Inflammatory mediators produced by fat tissue
Mediators releaseVisceral fatSubcutaneous fat
Leptin+++
TNF-α++
IL-6+++
Plasminogen activator inhibitor 1+++
Insulin-like growth factor 1++

Modified with permission from Wajchenberg.12

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  • Fig 6. 

    High levels of leptin in overweight children with asthma. High levels of serum leptin are present in overweight children, and even higher levels are found in asthmatic overweight children. Reproduced with the permission of Blackwell Publishing from Mai XM, Bottcher MF, Leijon I. Leptin and asthma in overweight children at 12 years of age. Pediatr Allergy Immunol 2004;15:523-30.

However, despite the animal, epidemiologic, and physiologic evidence to date, there have been no reports yet of a comprehensive study that shows a substantial difference in the pathology of asthma in obese compared with nonobese patients.

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References 

  1. Mokdad AH, Serdula MK, Dietz WH, Bowman BA, Marks JS, Koplan JP. The spread of the obesity epidemic in the United States, 1991-1998. JAMA. 1999;282:1519–1522
  2. Hancox RJ, Milne BJ, Poulton R, Taylor DR, Greene JM, McLachlan CR, et al. Sex differences in the relation between body mass index and asthma and atopy in a Birth Cohort. Am J Respir Crit Care Med. 2005;171:440–445
  3. Wickens K, Barry D, Friezema A, Rhodius R, Bone N, Purdie G, et al. Obesity and asthma in 11-12 year old New Zealand children in 1989 and 2000. Thorax. 2005;60:7–12
  4. Tantisira KG, Litonjua AA, Weiss ST, Fuhlbrigge AL. Association of body mass with pulmonary function in the Childhood Asthma Management Program (CAMP). Thorax. 2003;58:1036–1041
  5. Hedberg A, Rossner S. Body weight characteristics of subjects on asthma medication. Int J Obes Relat Metab Disord. 2000;24:1217–1225
  6. Guerra S, Sherrill DL, Bobadilla A, Martinez FD, Barbee RA. The relation of body mass index to asthma, chronic bronchitis, and emphysema. Chest. 2002;122:1256–1263
  7. Chinn S, Jarvis D, Burney P. Relation of bronchial responsiveness to body mass index in the ECRHS. European Community Respiratory Health Survey. Thorax. 2002;57:1028–1033
  8. Schachter LM, Peat JK, Salome CM. Asthma and atopy in overweight children. Thorax. 2003;58:1031–1035
  9. Simard B, Turcotte H, Marceau P, Biron S, Hould FS, Lebel S, et al. Asthma and sleep apnea in patients with morbid obesity: outcome after bariatric surgery. Obes Surg. 2004;14:1381–1388
  10. Turcotte H, Simard B, Boulay ME, Boulet LP. Influence of body mass index (BMI) on the effect of deep inspiration avoidance (DIA) on airway response to methacholine (M). Am J Respir Crit Care Med. 2004;169:A246
  11. Wajchenberg BL. Subcutaneous and visceral adipose tissue: their relation to the metabolic syndrome. Endocr Rev. 2000;21:697–738
  12. Mai XM, Bottcher MF, Leijon I. Leptin and asthma in overweight children at 12 years of age. Pediatr Allergy Immunol. 2004;15:523–530
  13. Shore SA, Schwartzman IN, Mellema MS, Flynt L, Imrich A, Johnston RA. Effect of leptin on allergic airway responses in mice. J Allergy Clin Immunol. 2005;115:103–109

PII: S0091-6749(05)00590-7

doi:10.1016/j.jaci.2005.03.018

The Journal of Allergy and Clinical Immunology
Volume 115, Issue 5 , Pages 1102-1104, May 2005

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