Curr Allergy Asthma Rep (2017) 17: 53

DOI 10.1007/s11882-017-0719-9

ALLERGIES AND THE ENVIRONMENT (M HERNANDEZ, SECTION EDITOR)

Role of Obesity in Asthma: Mechanisms

and Management Strategies
Hayley A Scott 1,2,3 & Lisa G Wood 1,2 & Peter G Gibson 1,3

Published online: 20 June 2017

# Springer Science+Business Media New York 2017

Abstract understanding of the mechanisms driving this association

Purpose of Review Obesity is a commonly reported comor-
bidity in asthma, particularly in severe asthma. Obese asth-
matics are highly symptomatic with a poor quality of life,
despite using high-dose inhaled corticosteroids. While the
clinical manifestations have been documented, the aetiologies
of obese-asthma remain unclear.
Recent Findings Several potential mechanisms have been
proposed, including poor diet quality, physical inactivity and
consequent accrual of excess adipose tissue. Each of these
factors independently activates inflammatory pathways, po-
tentially exerting effects in the airways. Because the origins
of obesity are multifactorial, it is now believed there are mul-
tiple obese-asthma phenotypes, with varied aetiologies and
clinical consequences.
Summary In this review, we will describe the clinical impli-
cations of obesity in people with asthma, our current
This article is part of the Topical Collection on Allergies and the
Environment
* Peter G Gibson
peter.gibson@hnehealth.nsw.gov.au
and describe recently proposed obese-asthma phenotypes.
We will then discuss how asthma management is complicated
by obesity, and provide graded recommendations for the man-
agement of obesity in this population.
Keywords Asthma . Asthma management . Asthma
mechanisms . Obesity . Phenotype . Weight loss
Introduction
Obesity is increasingly recognised as a common condition that
accompanies asthma. While both are common in westernised
countries, there is evidence that obesity contributes to an in-
crease in asthma prevalence [1]. According to a meta-analysis
of 333,102 adults, obesity almost doubles the odds of incident
asthma [2]. When obesity occurs with asthma, it is associated
with an increased asthma severity, with poorer asthma control
and increased asthma exacerbation risk [1, 35]. These effects
are consistently seen and indicate that obesity contributes to
an increased illness burden in asthma.

Hayley A Scott
Hayley.Scott@newcastle.edu.au
Clinical Complexities of Obese-Asthma
Lisa G Wood
Lisa.Wood@newcastle.edu.au
Asthma diagnosis can be confounded by obesity. This is be-
1
Priority Research Centre for Healthy Lungs, Hunter Medical
cause symptoms of exercise intolerance may occur in obesity
Research Institute, The University of Newcastle, New Lambton and mimic those of asthma. In addition, obesity is associated
Heights, NSW 2305, Australia with an increased perception of dyspnoea and this can mimic
2
School of Biomedical Sciences and Pharmacy, The University of asthma [6]. These findings underscore the need for objective
Newcastle, Callaghan, NSW 2308, Australia assessment of lung function and airway inflammation in order
3
School of Medicine and Public Health, The University of Newcastle, to establish a diagnosis of asthma and determine a treatment
Callaghan, NSW 2308, Australia approach.
53 Page 2 of 10
Monitoring Asthma
Asthma is a chronic condition that displays marked var-
iation in clinical severity. Monitoring asthma is impor-
tant to detect deterioration, assess severity and to aid in
treatment selection. Common monitoring tools include
spirometry and fractional exhaled nitric oxide (FeNO),
and both of these can be impacted by obesity. Asthma
results in an obstructive ventilatory defect. Obesity also
leads to changes in ventilatory function, including a
restrictive defect from extrapulmonary chest wall restric-
tion leading to a reduction in vital capacity. This can
limit the usefulness of the FEV1/VC ratio in assessing
asthma in obese patients. In a patient with confirmed
asthma and coexisting obesity, the FEV1 may be a bet-
ter measure to monitor asthma [7].
Obesity can cause late-onset adult asthma, and this
phenotype is associated with a reduced FeNO. There
is an inverse association between increasing body mass
index (BMI) and reduced exhaled NO [8, 9]. This may
be explained by uncoupling of nitric oxide synthase
(NOS) in the airway epithelium, which in turn occurs
because of an imbalance between L-arginine (NOS sub-
strate) and its endogenous inhibitor, asymmetric di-
methyl arginine (ADMA) [8]. This effect may limit the
usefulness of FeNO as a monitoring tool in obese-
asthma.
Obesity-Related Factors that Modulate
Inflammation
Asthma is now recognised as a heterogeneous condition, with
various phenotypes being described to characterise this het-
erogeneity. Hypothesis-free approaches have been used to
identify asthma phenotypes in adults and, using cluster anal-
ysis, studies consistently identify a phenotype that exists in
women and is associated with obesity [1013]. This predom-
inantly female population has late-onset asthma, a high symp-
tom expression despite complex medication regimes, and an
airway inflammatory pattern that is either neutrophilic or
mixed granulocytic in nature [10, 14].
Difficulty in establishing the mechanisms driving the
association between obesity and asthma likely stems
from the varied origins of both obesity and asthma.
Obesity is a multifactorial condition often involving a
poor-quality diet, a low exercise level and an excess of
adipose tissue. It is also a condition that is progressive
and relapsing, and may begin either early or later in
life. Each of these factors has the potential to interact
and contribute to the existence of multiple aetiologies of
obese-asthma.
Curr Allergy Asthma Rep (2017) 17: 53
Excess Adipose Tissue
Obesity results when energy homeostasis is dysregulated and
energy intake exceeds energy expenditure. Adipose tissue pro-
duces and secretes adipokines such as leptin and adiponectin,
and inflammatory mediators such as IL-6 and TNF- [15]. It
is characterised by Th1 inflammation, with neutrophils in-
creased in both the circulation [16] and adipose tissue [17]
of obese adults, and it is possible that this inflammation may
impact upon the airways of susceptible individuals. Indeed,
we have previously demonstrated an increase in neutrophilic
airway inflammation in obese adults with asthma [18].
Poor Diet Quality
Diet directly impacts the immune system and may therefore
influence both susceptibility to, and severity of, asthma.
Obese adults are more likely to consume a diet that is high
in fat and low in fruits and vegetables, with both these dietary
factors exerting pro-inflammatory effects, both systemically
and in the airways of people with asthma [19, 20, 21, 22].
This dietary pattern has been associated with more severe
asthma [23, 24].
High-Fat Diet
Both the quantity and type of dietary fat consumed modulates
the inflammatory response. We have demonstrated that a high-
fat meal increases sputum neutrophils and upregulates the
expression of TLR4 in airway cells, which is an innate im-
mune receptor that initiates NF-B-mediated inflammation
[20]. This is particularly relevant to obese individuals who
habitually consume a high-fat diet. While there is limited data
in people with asthma, saturated fats have been shown to be
associated with increased asthma risk [25, 26], airway
hyperresponsiveness [27] and sputum neutrophils [18].
Low Fruit and Vegetable Diet
Both asthma [28] and obesity [29] are conditions characterised
by oxidative stress, which is associated with increased airway
inflammation and airway hyperresponsiveness [30].
Antioxidants assist in maintaining the oxidant-antioxidant bal-
ance by neutralising reactive oxygen species (ROS). Fruits
and vegetables are the primary exogenous source of antioxi-
dants, and it is believed that low intake of these foods, which
is also common in obesity, may be contributing to an in-
creased prevalence of asthma [31]. In a 3-month randomised
controlled trial, we found that adults who consumed 5 serves
of vegetables and 2 serves of fruits/day had a 2.2-fold lower
risk of an asthma exacerbation compared with those
randomised to consume 2 serves of vegetables and 1 serve
of fruit/day [21]. Similarly, a 10-day low antioxidant diet
Curr Allergy Asthma Rep (2017) 17: 53
increased sputum neutrophils and was associated with poorer
asthma control and lung function in adults with asthma [22]. In
a murine model, OVA-sensitised mice were supplemented with
tomato extract for 14 days and had a significantly reduced
influx of eosinophils, IL-4 and IL-5 into the airways [32].
These studies suggest that short-term reductions in fruit and
vegetable intake exert a negative impact on asthma outcomes.
Physical Activity
Physical activity is lower in people who have asthma [33, 34]
and in people who are obese [35]; hence, obese asthmatics
have an increased likelihood of having a significantly reduced
physical activity level. In people with asthma, physical activ-
ity is associated with improved quality of life, lung function
and asthma control, reduced wheeze and fewer asthma exac-
erbations and emergency room presentations [36, 37, 38, 39].
While the literature supports a clear clinical benefit of phys-
ical training for people with asthma, the mechanisms respon-
sible for these improvements require further investigation. In a
review of OVA-sensitised murine models, exercise training
reduced broncholveolar IL-4, IL-5 and eosinophils, and in-
creased IL-10 [40]. Both Vieria et al. [41] and Silva et al.
[42] have demonstrated that part of this effect is mediated by
a reduced expression of NF-B. We have observed that
10 weeks of exercise training reduces sputum eosinophils by
50% in adults with asthma [43], while Mendes et al. [44]
also demonstrated a reduction in sputum eosinophils and ex-
haled nitric oxide (eNO) following aerobic training.
Obese-Asthma Phenotypes
Given the varied causes of obesity, it appears the origins of the
obese-asthma association are complex and highly variable be-
tween individuals. There are therefore a number of obese-
asthma phenotypes that have been recently proposed, with
further research needed to better define their clinical features
and establish their aetiologies, as well as describe additional
phenotypes which have yet to be defined.
Neutrophilic Obese-Asthma Phenotype
We have previously demonstrated an association between
BMI and sputum neutrophils [18]. Interestingly, this associ-
ation was only evident in women, with neutrophilic asthma
present in almost three times as many obese compared with
non-obese women (43 versus 16%, p = 0.017) [18]. Our
findings have since been confirmed by several studies.
Telenga [45] observed increases in both sputum and blood
neutrophils in obese women but not men with asthma.
Similarly, Marijsse [46] also observed an increase in sputum
neutrophils in obese compared with healthy weight adults
Page 3 of 10 53
with asthma. More recently, Chen [47] found this obesity-
induced increase in sputum neutrophils was associated with
increases in sputum IL-17, even after adjustment for BMI.
Sputum IL-17 was also associated with poorer asthma control
and lung function [48]. It is therefore possible that IL-17 is
promoting the neutrophilic obese-asthma phenotype.
It is unknown whether the neutrophilic obese-asthma phe-
notype is dependent on age of asthma onset; however, cluster
analysis has revealed an obese cluster with late-onset asthma
that is characterised by either neutrophilic or a mixed pattern of
airway inflammation [14]. Furthermore, obese children with
asthma do not have elevated sputum neutrophils compared
with their non-obese counterparts [49]. This suggests that the
neutrophilic obese-asthma phenotype is more common in
women with late-onset asthma. This phenotype may therefore
be the result of increased susceptibility to environmental expo-
sures related to ageing [50] or hormonal influences [51].
It is important to note that a number of studies have ob-
served no association between obesity and neutrophilic airway
inflammation in adults with asthma [5254]. This is likely due
to the varied manifestations of the obese-asthma association
and would be dependent on the cohort of subjects recruited. It
is possible that the neutrophilic obese-asthma phenotype
varies geographically due to environmental exposures and is
also dependent on the age, sex, degree of obesity, dietary
behaviours (including dietary fat and fruit and vegetable in-
take) and the age of asthma onset of the patients being studied.
We therefore propose the existence of a neutrophilic obese-
asthma phenotype that exists in a subset of the asthmatic pop-
ulation with late-onset asthma (Fig. 1). It is likely that this
phenotype may also include patients that have a mixed airway
inflammatory pattern. Further research is required to better
define this phenotype and establish its clinical characteristics.
Late-Onset Obese-Asthma Phenotype
Age of asthma onset has been used to define two obese-
asthma phenotypes, including a late-onset obese-asthma phe-
notype which is believed to develop as a direct result of obe-
sity [50, 55]. This phenotype is associated with a greater
prevalence of severe asthma, higher asthma medication use,
poorer lung function and older age at asthma diagnosis, com-
pared with lean adults with late-onset asthma [55]. It has been
proposed to also be associated with little or no eosinophilic
airway inflammation, but rather is believed to be driven by
changes in airway structure and function (Fig. 1) [13, 50]. An
important consideration is that a large proportion of adults
with late-onset asthma actually have neutrophilic asthma.
There is therefore a need to distinguish people with late-
onset obese-asthma from those with neutrophilic obese-asth-
ma. We propose that airway inflammation should be measured
in future studies of obesity, in order to distinguish and better
define these phenotypes.
53 Page 4 of 10
Fig. 1 This figure depicts three obese-asthma phenotypes, each of which
appears to be associated with a high prevalence of severe asthma: early-
onset obese-asthma, late-onset obese-asthma and neutrophilic obese-
Early-Onset Obese-Asthma Phenotype
Early-onset obese-asthma is a phenotype characterised by pre-
existing asthma that is complicated by the development of
obesity (Fig. 1) [50]. It is associated with more severe airway
obstruction and airway hyperresponsiveness, when compared
with lean asthmatics who also have early-onset asthma [55].
It has been proposed to be associated with eosinophilic airway
inflammation [50].
The mechanisms through which obesity complicates pre-
existing asthma are uncertain. A potential factor could be glu-
cocorticoid insensitivity, resulting in a reduced efficacy of
inhaled corticosteroid medications [56]. Another factor may
be physical inactivity, which has a large impact both on asth-
ma symptoms and airway inflammation. As an example, we
conducted a small study of overweight and obese asthmatics
who completed 10 weeks of exercise training [43]. Before
the intervention, 50% of patients had eosinophilic asthma;
however, following exercise training, only 20% of patients
were eosinophilic. This suggests that physical inactivity was
driving sputum eosinophilia in more than half of these over-
weight and obese patients with eosinophilic asthma.
Describing the inflammatory pattern of early-onset obese-
asthma as eosinophilic in nature is complicated by a recently
published study of 2450 Taiwanese children in fourthsixth
grades [57]. Children with long-standing obesity had an in-
creased prevalence of asthma that was associated with an ab-
sence of eosinophilic airway inflammation, measured by
FeNO. Conversely, children who had a rapid gain in fat mass
had an increased prevalence of asthma that was associated with
an elevated FeNO. This research suggests that while rapid
weight gain may predispose to an early-onset obese phenotype
that is characterised by eosinophilic asthma, longer standing
Curr Allergy Asthma Rep (2017) 17: 53
asthma. Triggers and airway inflammatory patterns appear to differ
between phenotypes. Further research is needed to better define each of
these phenotypes including their origins and clinical consequences
childhood obesity appears to drive a paucigranulocytic early-
onset obese-asthma phenotype.
Another factor complicating our understanding of the
early-onset obese-asthma phenotype is the impact that mater-
nal obesity has on asthma risk in offspring. In a meta-analysis
including 108,321 mother-child pairs, maternal obesity during
pregnancy increased the odds of asthma in the child by 21%,
with each 1 unit increase in BMI associated with a 23%
increase in the risk of developing early-onset asthma [58].
Interestingly, it appears maternal obesity has no effect on the
development of childhood hayfever or atopic eczema, sug-
gesting that this early-onset obesity-driven asthma is non-
allergic in nature and may therefore also represent early-
onset paucigranulocytic asthma [59]. However, whether this
inflammatory phenotype carries through to adulthood is
unknown.
We also do not know whether early-onset paucigranulocytic
asthma differs from late-onset obese-asthma, which is also
thought to be associated with a paucigranulocytic pattern of
airway inflammation. It may represent its own distinct pheno-
type or, conversely, these patients may be similar upon clinical
presentation. It is therefore apparent that a great many patients
do not currently fit within the three identified obese-asthma
phenotypes, highlighting that much more research is needed.
The Management of Asthma in People who are
Obese
Treatment Effects
The presence of obesity can have significant implications for
the treatment of asthma.
Curr Allergy Asthma Rep (2017) 17: 53
Bronchodilators
2-agonists are used for immediate symptom relief, and for
bronchoprotection against asthma triggers such as exercise.
Obesity is associated with a reduced response to 2-agonists
[60, 61], which means that patients report more symptoms,
and less effect of their bronchodilator. One possible mecha-
nism relates to the impact of a high-fat meal on 2-agonist
responses in asthma. It is observed that when people with
asthma ingest a high-fat meal, rich in stearic and palmitic
acids, the duration of bronchoprotection is significantly re-
duced [20]. This has serious clinical implications, consider-
ing the role of short-acting 2-agoinsts as rescue medications,
as well as their role in protecting against exercise-induced
bronchospasm.
Inhaled Corticosteroids
Obesity is also associated with a reduced response to inhaled
corticosteroids and montelukast [56, 60, 61]. Studies of the
molecular mechanism of glucocorticosteroid insensitivity in
obese-asthma identify impaired mitogen-activated protein ki-
nase phosphatase-1 (MKP-1) expression after stimulation
with dexamethasone [56]. This effect is seen in both periph-
eral blood mononuclear cells and airway cells, suggesting it is
a systemic, as well as an airway, problem. There is also en-
hanced expression of TNF- in both peripheral and lung im-
mune cells as body mass increases, and this profile is known
to be associated with reduced corticosteroid responsiveness in
asthma.
Biologics
Biologics such as monoclonal antibody therapy are an increas-
ing part of asthma management. At present, these agents are
used in severe refractory asthma. Examples include
omalizumab which targets immunoglobulin E (IgE) and leads
to reductions in asthma exacerbations, and a range of agents,
including mepolizumab, that are either available or in devel-
opment for eosinophilic asthma and act by blocking IL-5 or its
receptor.
Omalizumab dosing is determined by an individual patients
serum IgE and body weight. The product recommendations for
omalizumab recommend against dosing a patient with severe
refractory allergic asthma whose IgE/weight combination is
outside the recommended dosing table. This may have impli-
cations for obese-asthma. Obesity is very common in severe
asthma and this may contribute to a patient being denied
omalizumab according to the dosing recommendations.
Data from the Australian Xolair Registry investigated dos-
ing of patients outside the dosing table and found that these
patients had a similar response to omalizumab as those within
the dosing table [62, 63]. This registry also investigated the
Page 5 of 10 53
effect of obesity on response to omalizumab and found that a
clinical response (change in asthma control score >0.5 units)
was less frequent in obese patients compared to non-obese
patients (41% in obese-asthma vs. 66% in non-obese-asthma,
p = 0.017), but that when obese-asthma patients did respond,
the average improvement in asthma control score was highly
significant (1.4 units), and similar to non-obese responders.
These data challenge the restriction on the use of omalizumab
and suggest that treatment may be beneficial for obese patients
with refractory allergic asthma.
Obesity-Related Comorbidities and Asthma
Obesity is associated with a range of comorbid diseases that
may impact on asthma and its treatment [64]. Obesity and
comorbidities may interact in several ways. Obesity may po-
tentiate the severity of these conditions, and this can then
impact on asthma such that the obesity-related comorbidity
may reduce quality of life in asthma. Obesity may lead to
symptom misattribution where symptoms are mistakenly be-
lieved to be due to asthma, leading to asthma treatment esca-
lation without clinical benefit. Additionally, the obesity-
related comorbidity may interact with asthma to increase asth-
ma severity.
Obesity is associated with obstructive sleep apnoea which
can impact on asthma symptomatology by each of the above
mechanisms [65]. Obesity is associated with gastroesophageal
reflux disease. This can lead to symptom misattribution where
proximal reflux causes laryngeal symptoms that mimic asth-
ma [64].
Obesity-related comorbidities may interact with asthma
treatment. For example, obesity can potentiate diabetes
mellitus, which itself is worsened by oral corticosteroid use
in asthma [66]. Comorbidity treatment may interact with asth-
ma. Obesity is associated with cardiovascular diseases such as
ischaemic heart disease and hypertension. Treatment of these
conditions needs to be modified in a patient with asthma.
Specifically, aspirin [67] and -blockers [68] are contraindi-
cated in asthma.
Susceptibility to viral infection is also an important consid-
eration. Asthma is associated with an increased susceptibility
to respiratory viral infection, such as influenza and rhinovirus,
leading to asthma exacerbation. Obesity is also a risk factor for
severe influenza illness resulting in increased ICU admissions.
These potentiating risks underscore the need for annual influ-
enza vaccination in asthma, particularly severe asthma.
A new approach to asthma management can be used to
address these issues of obesity-related comorbidity in asthma.
This approach, termed multidimensional assessment [69] or
treatable traits [70], seeks to identify and treat multiple prob-
lems that co-occur in asthma. These treatable traits are
grouped into airway, extrapulmonary and risk factor domains.
This management approach identifies treatable components of
53 Page 6 of 10
the obese-asthma phenotype and then targets treatments to
each of these components. This may be a promising way to
manage obese-asthma from a clinical perspective, and address
the many interacting issues that occur.
The Management of Obesity in People who Have
Asthma
In people who are obese, the management of asthma should
include the management of obesity. The recommended ap-
proaches to weight loss vary according to the degree of obe-
sity. An additive approach is recommended, with more inva-
sive interventions only being considered as BMI category in-
creases [71].
Lifestyle Interventions
Lifestyle interventions are the most appropriate first line
of defence for all overweight and obese asthmatics
(BMI 25kg/m2). These include dietary, physical activi-
ty and/or behavioural therapy. Dietary therapy should
involve reducing caloric intake to create an energy def-
icit and support/education on how to modify the diet to
achieve this goal. Increased physical activity can also
contribute to creating an energy deficit, playing a key
role in weight loss because it increases energy expendi-
ture, as well as improving body composition by reduc-
ing body fat and preventing the decrease in muscle
mass often found during weight loss. In addition, there
are potential benefits such as increased cardiorespiratory
fitness. Behaviour therapy, such as development of self-
monitoring strategies, can be included in order to im-
prove compliance to planned adjustments in food intake
and physical activity [71].
Several studies have suggested that dietary restriction can
improve clinical aspects of asthma; however, few randomised
controlled trials have been conducted. One study employed a
14-week dietary restriction programme, resulting in a weight
loss of 14.5% and improvements in FEV1 and FVC [72].
Subjects in the weight loss group had significantly reduced
dyspnoea and rescue medication usage compared with con-
trols, and in the year following the intervention had signifi-
cantly fewer asthma exacerbations [72]. Another 10-week
randomised weight loss intervention in overweight and obese
asthmatic adults compared the effects of dietary intervention
(low-calorie diet, two meal replacements per day and dietetic
counselling), exercise intervention (group personal training
session once per week, plus gymnasium membership and dai-
ly step target) and a combination of both [43]. Both groups
that included the dietary component achieved significant
weight loss over 10 weeks. Improvements in quality of life
were observed for all groups, while asthma control and plasma
Curr Allergy Asthma Rep (2017) 17: 53
leptin improved in the diet and combined groups only [43].
Importantly, the study showed that weight loss of just 510%
induced a clinically significant improvement in asthma control
and asthma-related quality of life in the majority of patients
[43], suggesting that even small weight losses should be
advocated in the clinical management of this population.
More recently, a study in 330 obese uncontrolled asthmatic
adults, which used a 12-month behavioural intervention in-
volving dietary restriction, increased physical activity and
counselling on self-management skills, achieved a greater
weight loss in the intervention group (mean SD,
4.0 0.8 kg) compared to the control group
(2.1 0.8 kg). This small difference in weight loss did not
lead to a between-group difference in asthma control, lung
function or exacerbation rates [73]. However, interestingly,
participants with 5% weight loss achieved statistically sig-
nificantly improved ACQ scores compared with those who
lost 3% body weight. Non-randomised trials have also dem-
onstrated that dietary restriction improves clinical asthma out-
comes such as FEV1 [48, 74], FVC [74], quality of life [48],
dyspnoea [74] and asthma control [75].
Pharmacotherapy
Pharmacotherapy is recommended as an add-on therapy for
patients who have a BMI 30kg/m2 (or BMI 27kg/m2 if
concomitant obesity-related comorbidities exist), where life-
style changes have not achieved weight loss after 6 months
[71]. Pharmacotherapies should only be used in the context of
a treatment programme that includes elements of lifestyle
change as described above. Sibutramine and orlistat are ap-
proved by the FDA for long-term use in weight loss, yet have
side effects that need to be managed. Sibutramine is a
serotonin-reuptake inhibitor which acts as an appetite suppres-
sant and may induce side effects such as increased blood pres-
sure and tachycardia. Orlistat is a pancreatic enzyme inhibitor,
which inhibits fat absorption from the intestine and may also
reduce the absorption of fat-soluble vitamins and nutrients.
Only one study to date has examined the efficacy of weight
loss pharmacotherapy in asthma. Dias-Junior et al. [76] con-
ducted an RCT in 33 severe asthmatics, with the intervention
group using dietary restriction combined with sibutramine and
orlistat for 6 months. Subjects lost 7.5% of their initial body
weight, ACQ and FVC and symptoms were improved and
rescue medication use decreased.
Weight Loss Surgery
Bariatric surgery uses a physical barrier to reduce energy in-
take. Surgery is an option for patients with extreme obesity,
with BMI 40kg/m2, or BMI 35kg/m2 with serious obesity-
related comorbidities. Weight loss surgery is the most effec-
tive approach for achieving large weight changes and is
Curr Allergy Asthma Rep (2017) 17: 53
sustained for more than 5 years in most people. Clearly, there
are risks associated with surgery; hence, this approach should
only be considered when less invasive weight loss strategies
have proven unsuccessful and the patient is at high risk for
obesity-associated morbidity or mortality [71].
A number of studies have demonstrated an improve-
ment in asthma outcomes following bariatric surgery.
These studies have ranged from 1 to 7 years in follow-
up, achieved weight loss of 520 kg/m2 and shown im-
provements in lung function, quality of life, symptoms,
airway hyperresponsiveness and medication use [7780,
81]. While clinical improvements are consistently seen
following bariatric surgery, few studies have examined
changes in airway inflammation. In a study by Dixon
et al., 12 months after bariatric surgery, there were no
changes in bronchoalveolar lavage (BAL) neutrophils or
eosinophils, but there were increases in BAL lympho-
cytes, BAL and serum adiponectin concentrations and an
increase in peripheral blood lymphocyte function [81].
More recently, this group has reported no difference in
BAL cytokines and cytokine production from alveolar
macrophages, at 12 months post-bariatric surgery, in asth-
matic versus control subjects [82].
Conclusions
Obesity is a major risk factor for asthma and is associated with
a more severe clinical course of disease. It is also associated
with a poor diet quality, physical inactivity and excess adipose
tissue. Obesity can be long-term, relapsing or the result of
rapid weight gain. Each of these factors have been shown to
independently impact asthma outcomes and therefore should
be targeted as part of the management of obesity in asthma
using multidimensional assessment. For more than a decade,
research has attempted to establish the mechanisms linking
obesity with asthma incidence and severity. There are a num-
ber of distinct obese-asthma phenotypes that are now being
recognised and characterised. Because obesity is a common
comorbidity of severe asthma, obtaining a better understand-
ing of the aetiologies and management implications of the
many subtypes of obese-asthma is needed, to better manage
this increasingly prevalent population.
Compliance with Ethical Standards
Conflict of Interest Dr. Wood reports personal fees from Boehringer
Ingelheim and grants from NSA LLC, and DSM Nutraceuticals. Drs.
Scott and Gibson declare no conflicts of interest relevant to this
manuscript.
Human and Animal Rights and Informed Consent This article does
not contain any studies with human or animal subjects performed by any
of the authors.
Page 7 of 10 53
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