smoking cessation: trying hard; but could do better
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Smoking cessation: trying hard; but could do better
Stopping smoking is one of the most
important things an individual can do
to benefit health – at any stage of dis-
ease. In this issue of IJCP, Han et al.
(1) demonstrate the value of clinicians
continuing to encourage patients to
give up smoking, even if they have
relapsed several times already.
Smoking cessation can extend life
and it can improve the quality of life.
This comes at very low cost compared
with medical interventions. Economic
analysis has shown that using nicotine
replacement, the cost per life year
saved is small – somewhere between
£159 and £658 (2).
However, giving up smoking is not
easy. Smoking is an addictive beha-
viour and the habit dies hard. Around
between 10% and 40% of smokers
manage to quit at their first attempt,
while some groups such as the elderly
or pregnant mothers quit more suc-
cessfully (3,4). Nevertheless, despite
very best intentions, between 60%
and 90% of smokers who enter first
cessation programmes will relapse
(4,5). At this point, it is not uncom-
mon for physicians to lower their
expectations and to be less than ful-
some in their subsequent support.
Yet this may not be reasonable.
Smoking is an addictive behaviour
and as with all addictions, to be a suc-
cessful quitter, the patient must want
to change. Motivation is most import-
ant and at their first attempt not all
smokers may be maximally motivated.
The Stages of Change model (6) pos-
tulates that when people deliberately
make behavioural changes such as
stopping smoking, they go through a
series of changes. Each stage is associ-
ated with a different frame of mind
about the behaviour concerned and
each stage with a different kind of
motivation. There are five stages: pre-
contemplation in which the individual
sees no problem even though others
disapprove; contemplation (in which
the patient is weighing up the pros
and cons); active change; maintenance;
and relapse. In many cases, after
relapse the patient cycles back to a
stage of precontemplation. This model
suggests that people must be in the
stage of precontemplation or contem-
plation if they are to engage in active
change such as smoking cessation.
The cyclical nature of the process
also explains why almost two-thirds of
relapsed smokers are interested in try-
ing again within 30 days (7) and why
smokers who have made more
attempts to quit in the past continue
to try to do so. Han et al. (1) demon-
strate that success with relapsers can
be high, even outside the confines of a
strict clinical trial. In their study,
between 20% and 23% of those who
relapsed were abstinent at 26 weeks
on each consecutive quit attempt. This
is a large community study which
involved some 1745 patients. Those
who returned for subsequent treat-
ments tended to be heavy smokers
and more likely to have a history of
treatment for mental health problems.
Han et al.’s reported cessation success
of 20–23% for relapsed smokers is
somewhat higher than that reported in
many other studies which leads one to
ask how success can be made more
certain.
We know that trigger factors for
quitting smoking include personal
health, the cost of cigarettes, financial
pressures and pressure from family
and friends (7,8,9). We also know
that at the time they are likely to
relapse, patients are often aware of the
danger they are in (10) – knowledge
which could lead them to seek further
support from outside agencies if this
was available. Nevertheless, there are
few studies which have identified fac-
tors which can reduce the tendency to
relapse. Skills training to identify and
negate tempting situations, extended
treatment contact and pharmacotherapy
have been cited, but a recent system-
atic review concluded that most stud-
ies had limited power to differentiate
between interventions (11).
Despite best endeavours, smoking
remains one of the main challenges to
public health, especially in the devel-
oping world. Most people who cease
smoking will relapse at some point or
other and numerically, prevention of
relapse is at least as important as help-
ing first-time quitters. At the level of
the individual everyday consultation,
clinicians have an important part to
play, not only in helping first time
quitters but also in supporting those
addicts who have previously relapsed.
Peter Stott
Primary Care Physician
R E F E RE N C E S
1 Han E et al. Characteristics and smo-
king cessation outcomes of patients
returning for repeat tobacco depend-
ence treatment. Int J Clin Pract 2006;
60: 1068–74.
2 Parrott S, Godfrey C. Economics of
smoking cessation. BMJ 2004; 328:
947–9.
3 Whitson HE, Heflin MT, Burchett
BM. Patterns and predictors of smo-
king cessation in an elderly cohort.
J Am Geriatr Soc 2006; 54: 466–71.
4 Suplee PD. The importance of provi-
ding smoking relapse counselling dur-
ing the postpartum hospitalisation.
J Obstet Gynecol Neonatal Nurs 2005;
34: 703–12.
5 Austoker J, Sanders D, Fowler G. Can-
cer prevention in primary care: smo-
king and cancer: smoking cessation.
BMJ 1994; 308: 1478–82.
6 DiClemente CC, Prochaska JO, Fair-
hurst SK, Velicer WF, Velasquez MM,
Rossi JS. The process of smoking cessa-
tion: an analysis of precontemplation,
contemplation and preparation states of
change. J Consult Clin Psychol 1991;
59: 295–304.
EDITORIAL 1025
ª 2006 The AuthorsJournal compilation ª 2006 Blackwell Publishing Ltd Int J Clin Pract, September 2006, 60, 9, 1021–1027
7 Fu SS, Partin MR, Snyder et al. Pro-
moting repeat tobacco dependence
treatment: are relapsed smokers interes-
ted? Am J Manag Care 2006; 12: 235–
43.
8 Yang T, Fisher KJ, Li F, Danager BG.
Attitudes to smoking cessation and
triggers to relapse among Chinese male
smokers. BMC Public Health 2006; 6:
65.
9 Siahpush M, Carlin JB. Financial stress,
smoking cessation and relapse: results
from a prospective study of an Austra-
lian national sample. Addiction 2006;
101: 121–7.
10 Gwaltney CJ, Shiffman S, Balabanis
MH, Paty JA. Dynamic self-efficacy
and outcome expectancies: prediction
of smoking lapse and relapse. J Abnorm
Psychol 2005; 114: 661–75.
11 Lancaster T, Hajek P, Stead LF, West
R, Jarvis MJ. Prevention of relapse after
quitting smoking: a systematic review
of trials. Arch Intern Med 2006; 166:
828–35.
Diabetic neuropathy – a further indication for phosphodiesterasetype 5 inhibitors?
In this issue of the Journal, Hackett
and Cottage (1) present a series of five
cases in which regular phosphodiest-
erase type 5 (PDE5) inhibitors
appeared to improve diabetic neuropa-
thy. This observation potentially adds
to the already fascinating story of this
class of drugs.
The PDE5 inhibitors manipulate
vascular nitric oxide (NO) signalling.
NO is produced in the endothelium
and enters vascular smooth muscle
where it stimulates the production of
guanosine 3¢,5¢-cyclic monophosphate
(cGMP) which, in turn, causes relaxa-
tion and vasodilatation. cGMP is
degraded by PDE5 and, as a result,
inhibitors of PDE5 promote NO-
mediated vasodilatation.
The first PDE5 inhibitor, sildenafil,
was initially conceived as a potential
treatment of angina. In early clinical
trials, it did not show much promise
for this indication, but did appear to
promote penile erection, a physiologi-
cal process that is dependent on local
NO release. These observations
prompted a change of direction in the
clinical development of sildenafil and
it was later shown to be an effective
treatment for male erectile dysfunction
(ED) of various aetiologies (2). Two
further PDE5 inhibitors, vardenafil
and tadalafil, are also now available
for ED.
Sildenafil, marketed as Viagra�, was
the first widely available, convenient
and effective treatment of ED. As a
treatment for a disorder of sexual
function, it rapidly became known
throughout the world and is estab-
lished as an icon of the early 21st cen-
tury. Following its introduction, ED
was transformed from a condition that
was barely spoken about to one that
was widely acknowledged and treated.
Viagra has been the subject of count-
less jokes and cartoons, and has even
sparked debate on the potential conse-
quences of medicalising sexual func-
tion (3), and on the nature and
funding of the so-called ‘lifestyle
drugs’ and how healthcare systems
should deal with them (4).
Sildenafil is also a vasodilator in the
pulmonary circulation and reduces
pulmonary blood pressure in pulmon-
ary arterial hypertension (PAH) (5).
This physiological effect translates into
improved functional capacity when sil-
denafil is taken regularly for PAH (6),
and it has recently been licensed for
this indication. PDE5 inhibitors may
also be effective in Raynaud’s phe-
nomenon. A recent study found that
regular sildenafil reduced the fre-
quency and duration of acute attacks
(7). Moreover, there is emerging evi-
dence that regular PDE5 inhibition
effectively reduces blood pressure in
patients with systemic hypertension
(8).
Shortly after its introduction into
clinical practice, case reports of myo-
cardial infarction in patients who had
recently taken sildenafil prompted
concerns over its safety. However, it
was recognised that patients with ED
often have increased cardiovascular
risk (9) and also that sexual inter-
course itself is associated with a small
increased risk of myocardial infarction
(10). Reassuringly, pooled clinical trial
data (11,12) and prescription event
monitoring data (13,14) have found
no increased risk with sildenafil or
tadalafil use. More recently, there have
been case reports of non-arteritic
anterior ischaemic optic neuropathy, a
cause of sudden onset, untreatable and
irreversible visual loss, occurring after
PDE5 inhibitor use (15). While a
cause and effect relationship has not
been, and is unlikely to be, estab-
lished, patients are advised to stop tak-
ing these drugs immediately if they
experience sudden deterioration in
vision.
Could diabetic peripheral and auto-
nomic neuropathy be yet further indi-
cations for PDE5 inhibitors?
Microvascular dysfunction causing
ischaemic injury to peripheral nerves
is thought to play a central role in the
development of diabetic peripheral
neuropathy (16). Therefore, it is cer-
tainly possible that PDE5 inhibitors
might improve neural blood flow and,
as a result, also improve neural func-
tion. Studies on the effects of chronic
PDE5 inhibition on neurophysiologi-
1026 EDITORIAL
ª 2006 The AuthorsJournal compilation ª 2006 Blackwell Publishing Ltd Int J Clin Pract, September 2006, 60, 9, 1021–1027
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