Asthma diagnosis and treatmentDoes obesity weigh heavily on the health of the human airway?
Section snippets
Strength of association
A strong association, such as a 5- to 10-fold increase in risk, as is seen between cigarette smoking and lung cancer, is more likely to be causal than a weak association. A weak association is more likely to be spurious, arising from bias, confounding, or chance, although it does not rule out causality. The association between asthma and obesity is modest, with measures of relative risk described ranging from 1.5 to 3.0 in most studies, which raises concerns that it might not be causal.
Consistency of association
If the association is repeatedly observed in different populations in different settings, it is more likely to be causal than an isolated observation. The obesity-asthma association has been observed in both children and adults, in various races and ethnic groups, as well as in different parts of the world. In most studies asthma was clinically defined as a physician diagnosis of asthma, presence of asthma symptoms, use of asthma medications and hospitalizations, or emergency department visits
Specificity of association
This relates to a single cause leading to a single effect. This might be a holdover from infectious disease thinking and does not necessarily apply to complex disease traits, such as asthma (which more often than not have multifactorial causation). Such effect specificity is clearly lacking in this association because obesity has also been shown to cause various diseases other than asthma, such as Type II diabetes mellitus and coronary heart disease.
Temporality of association
This postulates that a cause must precede an effect in time. It was previously argued that asthma leads to physical inactivity and subsequent weight gain and obesity. Several prospective studies have now found a positive association between weight gain and subsequent development of (incident) asthma, thereby providing considerable support for the thesis that obesity in fact antecedes the development of asthma.7
Biologic gradient
The presence of a dose-response gradient (ie, more of a dose leads to more of an effect) supports the idea of causality. A modest dose-response relationship has in fact been described in various studies whereby the risk of asthma increases with the severity of overweight-obese status. However, several studies have also described another interesting observation that the association between BMI category and asthma risk might have a U- or J-shaped curve whereby the underweight category (or those
Plausibility of association
According to this postulate, the idea of causation must be biologically plausible. A host of mechanistic pathways have been suggested to explain this association, and these are summarized in Fig 1.8, 9, 10 However, these pathways might not be mutually exclusive, and the dominant mechanism among them is yet to be singled out.10 Some believe that asthma-like symptoms in obese patients might be due to reasons other than BHR, such as increased work of breathing associated with thoracic restriction,
Coherence of association
The idea of causation must accord with other relevant observations. For instance, there is at least one article examining data from the National Health and Nutrition Examination Survey that suggests that unadjusted prevalence of atopy increases significantly with increasing obesity.11
Experimental evidence for association
Supporting data for this association from animal experiments are limited. Fredberg and Shore,10 in their review in this journal, have quite rightly commented that “the majority of studies published on this topic are epidemiological investigations; the paucity of basic research on the possible role of adipose tissue in modulating asthma susceptibility and symptoms is quite striking.” It has now been shown that ozone-induced BHR and airway inflammation in mice that are obese (ob/ob) is higher
Analogy
Like obesity, other environmental factors are also associated with asthma. An example of such a factor is the popular hygiene hypothesis that has been described in the rostrum by Platts-Mills.15 This hypothesis proposes that decreased exposure to infections, decreased exposure to farm animals-endotoxin, or increased antibiotic use in early life results in dominance of TH2 responses, which might also partly explain the increase in asthma prevalence.
So is the association between obesity and
References (15)
- et al.
The asthma and obesity epidemics: the role played by the built environment—a Public Health perspective
J Allergy Clin Immunol
(2005) The epidemiology of obesity and asthma
J Allergy Clin Immunol
(2005)Adipose tissue, adipokines, and inflammation
J Allergy Clin Immunol
(2005)- et al.
Obesity, smooth muscle, and airway hyperresponsiveness
J Allergy Clin Immunol
(2005) - et al.
Effect of leptin on allergic airway responses in mice
J Allergy Clin Immunol
(2005) - et al.
Physical activity and exercise in asthma: relevance to etiology and treatment
J Allergy Clin Immunol
(2005) - et al.
Prevalence of overweight and obesity among US children, adolescents, and adults, 1999-2002
JAMA
(2004)
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Disclosure of potential conflict of interest: A Sood has consultant arrangements with Wyeth-Ayerst and GlaxoSmithKline; has received grants–research support from the American Lung Association; and is on the speakers' bureau for Actelion Pharmaceuticals.