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