Progression to chronic obstructive pulmonary 1

Progression to chronic obstructive pulmonary disease (COPD): Could it be
prevented by manual therapy and exercise during the ‘at risk’ stage
(stage 0)?

Roger M. Engel

, Subramanyam Vemulpad

Department of Health and Chiropractic, Macquarie University, Bldg E7A 222, Balaclava Road, Sydney, NSW 2109, Australia

a r t i c l e

i n f o

Article history:
Received 3 October 2008
Accepted 7 October 2008

s u m m a r y

A number of predisposing factors are recognised as increasing the risk of developing chronic pulmonary
obstructive disease (COPD). There is increasing recognition that COPD may be an inﬂammatory disease
with systemic consequences. However, the trigger for the transition from ‘at risk’ (stage 0) to COPD state
remains unclear. The current approach to intervention for the ‘at risk’ group is risk factor avoidance. We
propose that if interventions shown to improve chronic respiratory symptoms in COPD sufferers could be
applied to the ‘at risk’ group, then moderation or even reversal of the changes typical of this transition
becomes a possibility. Exercise training has been shown to be beneﬁcial at all stages of COPD. Mobility
of the chest wall inﬂuences lung function. We hypothesise that the application to ‘at risk’ individuals
(stage 0) of therapeutic interventions known to improve chronic respiratory symptoms and cardiovas-
cular function in mild/moderate COPD (stages 1 and 2) could delay progression of the disease (i.e. man-
ifestation of mild/moderate COPD). If the hypothesis were conﬁrmed, the potential to delay or even
prevent the onset of COPD would be feasible.

Introduction

Two large studies have recently documented a high prevalence

of COPD

[1,2]

. The situation is set to deteriorate as the condition is

projected to become the ﬁfth most frequent cause of death world-
wide by 2020

[3]

Cigarette smoking is recognised as the main predisposing factor

for increasing the risk of developing COPD

[4,5]

. However, only a

minority of heavy smokers develop chronic airﬂow limitation

[6–8]

. Other possible predisposing factors include a history of

childhood respiratory tract infections

[9,10]

, occupational expo-

sure

[11,12]

, low birth weight

[13]

, air pollution

[14,15]

and diets

low in anti-oxidants

[16]

There is increasing recognition that COPD may be an inﬂamma-

tory disease with systemic consequences

[17,18]

. COPD itself may

cause systemic inﬂammation

[19,20]

or inﬂammation in the respi-

ratory system may trigger airﬂow obstruction in susceptible indi-
viduals

[21]

. In the latter case, the inﬂammation precedes the

onset of symptoms of chronic lung disease

[18]

. It is possible that

adverse airway remodelling occurring as a result of childhood
respiratory infections could render the person more susceptible
to respiratory conditions such as COPD later in life

[6,22,23]

. In

summary it would appear that apart from smoking, the trigger

for the transition from non-diseased to COPD state remains
unclear.

Investigating the period when diagnosis can ﬁrst be conﬁrmed

and declining lung function begins to accelerate beyond what is
attributable to age alone could provide further insight into the ori-
gins of the condition and hence possible intervention.

Persons ‘at risk’ of developing COPD (stage 0) are often charac-

terised by normal spirometry in the presence of chronic symptoms
such as cough and sputum production

[4]

The current approach to intervention for people in this group is

risk factor avoidance. The recommended interventions are health
education, smoking cessation and inﬂuenza vaccination

[4,5]

. Exer-

cise training has been shown to beneﬁt all levels of COPD

[24,25]

by improving cardiovascular ﬁtness, muscle function, muscle
strength and endurance

[5]

. However, the role of exercise in pre-

venting COPD remains to be tested in the ‘at risk’ group

[4,5,26]

We propose that if interventions shown to improve chronic

respiratory symptoms in COPD sufferers could be applied during
the period when alterations in lung architecture associated with
COPD begin i.e. the ‘at risk’ or stage 0, then moderation or even
reversal of those changes becomes a possibility. If these interven-
tions were low risk, low cost, effective and amenable to implemen-
tation in all parts of the world

[27]

, considerable impact on the

future burden of the disease would result.

Hypothesis. It is hypothesised that the application to ‘at risk’
individuals (stage 0), of therapeutic interventions known to

0306-9877/$ - see front matter Crown Copyright Ó 2008 Published by Elsevier Ltd. All rights reserved.
doi:10.1016/j.mehy.2008.10.017

Corresponding author. Tel.: +61 2 9850 6387; fax: +61 2 9850 9389.
E-mail address:

rengel@els.mq.edu.au

(R.M. Engel).

Medical Hypotheses 72 (2009) 288–290

Contents lists available at

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Medical Hypotheses

j o u r n a l h o m e p a g e : w w w . e l s e v i e r . c o m / l o c a t e / m e h y

Author's personal copy

improve chronic respiratory symptoms and cardiovascular func-
tion in mild/moderate COPD (stages 1 and 2) could delay progres-
sion of the disease (i.e. manifestation of mild/moderate COPD).

Evaluation and discussion

The hypothesis has two parts: identiﬁcation of the therapeutic

interventions (part 1) and delaying disease progression (part 2).

A possible step-wise approach to evaluate this hypothesis is

outlined below, with steps (i)–(v) related to part 1 and step (vi) re-
lated to part 2 of the hypothesis.

Part 1

Step (i). Identify the interventions.
Step (ii) Test the interventions on healthy (normal) individuals

with normal spirometry and no history of respiratory disease.

Step (iii) Test the interventions on healthy individuals with nor-

mal spirometry and a history of respiratory disease.

Step (iv) Test the interventions on individuals with mild COPD.
Step (v) Test the interventions on individuals with moderate

COPD.

Part 2

Step (vi) Test the interventions on individuals with chronic

cough and phlegm, normal spirometry and a history of respira-
tory disease but no diagnosis of COPD i.e. at risk (stage 0) group.

In examining these steps a number of issues need to be consid-

ered. As only a minority of smokers develop chronic airﬂow limita-
tion, the interventions must have the potential to beneﬁt non-
smokers as well. They must be low risk, cost-effective and easily
implemented and must have the potential to improve the typical
pattern of lung function decline seen as part of the progression
of COPD.

Part 1

Step (i). Identifying the interventions: Exercise training has been

shown to beneﬁt all stages of COPD. It is accepted that it plays a
role in addressing skeletal muscle abnormalities (the most com-
mon co-morbidities described in association with COPD)

[28]

improving peripheral muscle strength and cardiovascular ﬁtness,
in turn relieving breathlessness and fatigue in the COPD patient

[5]

. As skeletal muscle abnormalities are common in people diag-

nosed with COPD, their presence in the ‘at risk’ stage (stage 0)
could, at least in part, be the cause of the accelerating decline in
lung function seen in typical early COPD.

One area that is often overlooked when investigating the source

of the improvements from exercise training in COPD is the role the
mobility of the chest wall has in inﬂuencing lung function. Mobility
of the chest wall includes the costo-transverse, costo-vertebral and
intervertebral joints and their associated muscles. These structures
are rarely assessed when evaluating lung function in the COPD pa-
tient. As an example of the relationship between chest wall mobil-
ity and lung function, mechanical restriction of the chest wall (by
chest strapping) during exercise induces severe dyspnoea even in
healthy individuals

[29]

. These ﬁndings lead to our hypothesis

and the following questions.

Could an intervention aimed directly at increasing chest wall

mobility deliver an improvement in lung function in the COPD pa-
tient? Could administering this type of intervention to the COPD
patient in conjunction with exercise return even greater beneﬁts
than exercise alone?

Step (ii) of the hypothesis has already been completed. A study

measuring the effect of administering a combination of interven-
tions (manual therapy directed at the posterior chest wall tissues
followed by exercise) on the respiratory function of normal, non-
smoking individuals found that short term lung function increased
following manual therapy to the posterior structures of the chest
wall. Interestingly, the study also showed that increased mobility
in these structures mitigated some of the negative short term
respiratory effects of exercise

[30]

. A study investigating the

changes in chest wall movements following the administration of
manual therapy (directed at the posterior chest wall tissues) fol-
lowed by exercise to non-smoking individuals with a history of
respiratory disease [step (iii) of the hypothesis] is in the ﬁnal plan-
ning stages and due to commence shortly. (authors’ work in
progress;

http://www.anzctr.org.au/ACTRN12608000518369.aspx

Two studies testing whether this combination of interventions
could have an impact on individuals already diagnosed with mild
and moderate COPD (steps (iv) and (v) of the hypothesis) are
underway (authors’ work in progress; the study design on mild
COPD participants can be viewed at

http://www.anzctr.org.au/

ACTRN12606000369527.aspx

; the study design on moderate COPD

participants

can

viewed

http://www.anzctr.org.au/

ACTRN12607000388415.aspx

Part 2 – Delaying disease progression

If application of this combination of interventions were to show

an improvement in lung function, respiratory symptoms and/or
cardiovascular ﬁtness across all stages of COPD beyond what is ex-
pected from current pulmonary rehabilitation programs, then it
should be included as part of standard COPD management. Delay
in disease progression for the ‘at risk’ (stage 0) group could then
be assessed via a longitudinal study comparing the beneﬁts of cur-
rent interventions such as health education, smoking cessation and
inﬂuenza vaccination with and without the addition of manual
therapy and exercise.

Testing this combination of interventions on the ‘at risk’ group

(step (vi)) of the hypothesis) is in the planning stage with the ﬁnal
design of the study dependent on the outcomes from the current
studies testing steps (iii)–(v).

Signiﬁcance

If the hypothesis were conﬁrmed, the potential to delay or even

prevent the onset of COPD would be feasible. The beneﬁt to indi-
viduals would be signiﬁcant and the impact on the burden of dis-
ease considerable. There would be a paradigm shift, from COPD
being considered a ‘progressive’ (once airﬂow limitation begins)
and ‘not fully reversible’ (once a diagnosis is made), to being a
‘reversible’ condition. This would have immense impact on future
projections for the disease, along with morbidity and mortality
rates.

References

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