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Health & Place 10 (2004) 311–318

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Spaces and networks of genetic knowledge making: the‘geneticisation’ of heart disease

Edward Hall�

School of Social Sciences, Media and Communication, Queen Margaret University College, Clerwood Terrace, Edinburgh EH12 8TS, UK

Abstract

The ‘geneticisation’ of health, medicine and the body is extending from single-gene to multi-factorial conditions such

as heart disease. Adopting ‘Actor Network Theory’, the paper argues that the making of genetic knowledge occurs in

spaces and networks where contested knowledges necessarily produce a geneticisation that is neither certain nor

complete. Drawing on empirical research in a coronary care unit in Glasgow, Scotland, the paper sets out the network

of consultants, rehabilitation nurses and people with heart disease and others who collectively, through contestation

and the marshalling of knowledges by prominent social actors, produce an understanding of the role of genes in heart

disease.

r 2004 Elsevier Ltd. All rights reserved.

Keywords: Geneticisation; Heart disease; Knowledges; Networks

Introduction

Knowledges of the body, health and illness are

undergoing a period of intense transformation, as

developments in human genetic science accelerate and

reshape medical and public understandings and prac-

tices (Conrad and Gabe, 1999). The ‘medical gaze’ is

penetrating deeper into the body (Philo, 2000), con-

structing a new spatial discourse of a ‘genetic body’ in

which an increasing number of health, illness and

behavioural conditions are being connected to, ex-

plained by and are indeed becoming particular sets of

gene sequences (Hall, 2003). From a small number of

relatively rare single-gene conditions, most notably

Cystic Fibrosis and Huntingdon’s Disease, the discourse

is now encompassing common complex illnesses such as

cancers and heart disease (Martin, 1999). This incor-

e front matter r 2004 Elsevier Ltd. All rights reserve

althplace.2004.08.006

1-317-3601; fax: +44-131-317-3604.

ess: ehall@qmuc.ac.uk (E. Hall).

poration of a multitude of conditions into a genetic

narrative has become known as ‘geneticisation’: ‘‘[De-

fining] most disorders, behaviours, and physiological

variations as wholly or in part genetic in origin’’

(Lippman, 1998, p. 64). This paper is an attempt to

assess the seeming ‘geneticisation’ of heart disease, the

major cause of mortality and morbidity in the West

(British Heart Foundation, 2002). Increasing research

claims and accompanying media coverage of the role of

the genes in several key aspects of heart disease,

particularly hypertension and high cholesterol, are

forming a significant challenge to the dominant ex-

planation of causation, that is, ‘poor’ lifestyle behaviour

in the context of social and spatial inequalities. The

paper maps the dynamics of one set of spaces where this

possible transformation is occurring: a hospital coron-

ary care unit in Glasgow, Scotland. It argues that the

process of geneticisation is anything but as straightfor-

ward as that imagined by Lippman (1998), as consultant

cardiologists, cardiac rehabilitation nurses, and people

d.

ARTICLE IN PRESSE. Hall / Health & Place 10 (2004) 311–318312

with heart disease collectively, through contested knowl-

edges and uneven power relations, form an under-

standing of the role of genes in heart disease.

A sense of a plurality of knowledges of genetics—in

particular, that such knowledge is not the preserve of

genetic science—is gradually emerging in social studies

of genetics. The bulk of medical sociologies of genetics

have assessed the impact of genetic knowledge as given,

with emphasis on genetic testing (Hallowell, 1999), ‘gene

therapy’ techniques (Stockdale, 1999) and fears for a

new eugenics (Shakespeare, 1999). In contrast, there has

been little concern with the (ongoing) production of

medical genetic knowledge, be it in the laboratory, in

health policy or in exchanges between health profes-

sionals and patients (except Cunningham-Burley and

Kerr, 1999; Hall, 2003; Hedgecoe, 2003). Unpacking

genetic knowledge outwith scientific spaces—for in-

stance, recognising lay constructions of genetics (Hunt

et al., 2001)—could destabilise the completeness and

certainty and hence unsettle the determinism and

inevitability of geneticisation. That sociologists of

science generally assume that the public know little or

nothing about genetics, needing guidance from scientists

and health professionals to understand the issues, makes

such an approach difficult, however (Kerr et al., 1997).

This paper attempts to do just this through an analysis

of the interconnections of lay and health professional

knowledges of the role of genes in heart disease within a

hospital setting.

Within geography, engagement with human genetics

has been very limited (Greenhough, 2002; Hall, 2003),

despite Parr’s (2002, p. 247) plea to health geographers

to ‘‘debate more rigorously’’ the social and biological

construction of bodies. Parr’s call draws on the

possibilities opened up by the post-structuralist ‘cultural

turn’, that is, the transformation of knowledge as

singular, absolute and universal into a recognition of it

as partial, uncertain and multiple. Geographers have

added an extra twist to this, asserting that knowledges

are intimately linked to spaces—of bodies and society—

to the extent that once a particular ‘imaginary’ or

knowledge of a space becomes dominant, then other

representations and ways of knowing become difficult or

even impossible to imagine (Massey, 1999). Hall (2003)

sets out how the increasing dominance of genetic

narratives of the body and health are dependent on

the spatialising of the genetic material (in particular, in

the form of genetic maps); once the genetic material has

been spatialised, it can be bounded, known and

exploited. Geneticisation is perhaps the inevitable out-

come of the making of spatial knowledge of the genes.

However, this is not the end of the story. The cultural

turn not only ‘lifted the lid’ on such dominant knowl-

edges, but also opened up the possibility of other,

contesting knowledges. The key theoretical manoeuvre

was the rethinking of knowledge as relational, that is, as

produced and known in networks of interconnections,

rather than as linear, i.e. issued from a singular,

objective and superior position (Massey, 1999). Again

this is intimately tied up with space: knowledge is

produced collectively from a number of locations—in

this instance, people with heart disease, hospital staff,

and the coronary care unit—rather than from a single

position—the medical genetics laboratory or the con-

sultant. In an attempt to capture the dynamics of these

multiple, competing strands of knowledge of the role of

genes in heart disease, the paper employs ‘Actor

Network Theory’ (Latour, 1987). While usually asso-

ciated with studies of scientific practice (see Hall, in

press), Actor Network Theory can be effectively applied

to the study of the multiple sources of interconnected

knowledge making in networks and within particular

socio-spatial contexts, sources that include not only

people, but also institutions and technology and further

genes, disease and bodies (Murdoch, 1997). I will

provide a fuller account of the theoretical approach

later in the paper.

The remainder of the paper begins with an explora-

tion of the seeming geneticisation of heart disease,

charting its transformation from individual and social

causes to genetic explanation. The Actor Network

Theory approach is then set out and used to analyse

the empirical data gathered in a coronary care unit in

Glasgow. The two spaces and networks of ‘diagnosis’

and ‘rehabilitation’ are described and discussed. The

paper concludes with an assessment of the nature of the

geneticisation of heart disease and identifies a distinct

role for geographies of health in research on the genetics

of health.

The geneticisation of heart disease

Coronary heart disease remains the major cause of

mortality and morbidity in the developed world, with

more than 1.4 million people experiencing angina and

around 300,000 people suffering a myocardial infarction

(heart attack) in the UK every year (British Heart

Foundation, 2002). As such, it dominates health policy,

with the focus on improving individual lifestyle beha-

viour, whilst acknowledging the significant socio-spatial

inequalities in incidence. Medical genetic claims and

associated media coverage are beginning to reimagine

heart disease as a condition ‘wholly or in part genetic in

origin’ (Lippman, 1998, p. 64). In this section, the paper

charts this seeming transformation of heart disease in

the context of medical genetic claims and practices.

Popular knowledges have always recognised that

heart disease ‘runs in families’ (Hunt et al., 2001) and

‘family history’ has always been part of cardiological

assessment (Gray et al., 2002). While inheritance has

been acknowledged as an ‘independent predictor’ of

ARTICLE IN PRESSE. Hall / Health & Place 10 (2004) 311–318 313

heart disease risk (Timmis and Nathan, 1997), the

detailed mechanisms have not been identified. In the

absence, until recently at least, of a genetic explanation,

the ‘cause’ of heart disease has been attributed directly

to individual behaviour and indirectly to social and

spatial inequalities (Huff and Gray, 2001).

Public health advice on heart disease centres on

individuals’ need to improve their lifestyle behaviours—

in particular, cease smoking, reduce alcohol consump-

tion, eat a low fat diet and increase levels of physical

exercise—and so reduce their ‘risk’. Central to this is the

assumption that individuals have the desire to change

and that it is within their control to do so (Petersen and

Lupton, 1996). However, Davison et al.’s (1992) study of

lay knowledges of heart disease causation in south

Wales exposes the weaknesses of this assumption: those

interviewed were fully aware of the behaviours that put

people at risk, but at the same time other knowledges—

of fate, destiny and chance—were drawn upon to

explain those of ‘coronary candidacy’ who did not

succumb to heart disease, i.e. people who lived to an

advanced age despite ‘unhealthy’ lifestyles and, con-

versely, individuals who died young yet lived ‘safely’

within the limits of risk. Such gaps in the dominant

explanation, and in individuals’ willingness to accept it,

provide possible ‘entry points’ for genetic narratives of

disease causation, seemingly replacing the uncertainty of

‘fate’ with the supposed certainty of medical science and

the gene.

The individualism of heart disease policy provides a

clear framework for geneticisation. A genetic explana-

tion sits more uneasily, however, with the significant

social and spatial inequalities in the incidence of heart

disease (Bryce et al., 1994). The evidence of inequality is

substantial (Huff and Gray, 2001), in particular for

social class—for example, those in manual occupations

are three times more likely to suffer from heart disease

than those in non-manual occupations—yet, an

explanation has been less straightforward to identify

(Marmot et al., 1991). It is thought, however, that less

knowledge about risk factors and lower expectations

about health, combined with limited access to exercise

facilities, nourishing food and addiction to nicotine and

alcohol, place some people in positions where ‘positive’

choices about lifestyle are much more limited (McLoone

and Boddy, 1994). Geographers argue that not only are

social contexts important in shaping health knowledges

and illness incidence, but also the physical and

social landscape and networks of the places where

people live (Kearns and Gesler, 2002). So, adopting

a risky behaviour, such as a high fat diet, is not simply

an individual decision, but is conditioned by local

knowledges and availability of food. Huff and

Gray (2001) argue that such a conceptualisation is the

closest we have got to identifying the cause of heart

disease.

A ‘family history’ of heart disease is perhaps therefore

a social rather than a biological inheritance, with the

sharing of socio-spatial environments reproducing dis-

ease through the passing on of behaviours and knowl-

edges of health (Julian et al., 1998). However, despite the

credibility of this explanation, medical genetics is

increasingly providing specific microbiological accounts

of the causation of many aspects of heart disease

(Lefkowitz and Willerson, 2001). Crucially for the

narrative of geneticisation, this has extended from

relatively well-known single-gene conditions, such as

‘Familial Hyperlipidaemia’ (very high cholesterol)

(Lyon and Gorner, 1996) and ‘Long QT Syndrome’

(a disorder of the heart’s ‘electrical system’) (British

Heart Foundation, 2003), to genetic ‘predictors’ of more

complex conditions that contribute to heart disease.

Amongst the many claims are the following examples: a

gene variant (PPAR@) that may cause ‘Sudden Adult

Death Syndrome’ is found within 20 per cent of the

population (Flavell et al., 2002); the hormone angio-

tensinogen, an important determinant of blood pressure,

has been found to have a common variation in a gene

‘promoter’ (on–off switch) (Day and Wilson, 2001); and

the E4 version of the APOE gene, found in a quarter of

the UK population, multiples by three times the risk of

heart disease for smokers (Guardian, 2001).

These medical science ‘discoveries’ and their publica-

tion in the popular media are seemingly generating a

progressive geneticisation of heart disease. Further, and

more powerfully, non-genetic factors, such as smoking,

are being incorporated within the genetic explanation.

By accepting the role of behavioural factors in disease,

geneticisation widens its explanatory claim from single-

gene to complex conditions. Importantly, however,

while apparently emphasising the interaction of ‘nature’

and ‘nurture’ (and rejecting genetic determinism), the

genetic factors remain the underlying cause of the

condition, the ‘predisposition’ that individual behaviour

or the environment then ‘triggers’ (Hedgecoe, 2001). In

other words, in this ‘enlightened geneticisation’ (Hedge-

coe, 2001), while medical genetics emphasises that there

will never be a ‘gene for’ heart disease, individual

behaviour and the environment do not have ‘decisive

control’ (Hedgecoe, 2001, p. 883). The outcome is a

‘geneticisation by stealth’ (Hedgecoe, 2002, p. 9), as

health conditions such as heart disease are gradually

interwoven with genetic ‘causes’. Eventually, merely

mentioning them in the same breath is sufficient, without

the need for scientific proof (Lippman, 1991).

Despite the seemingly unstoppable process of genet-

icisation, and the associated marginalisation of indivi-

dual and social factors, the geneticisation of heart

disease is neither uncontested nor inevitable (Hedgecoe,

2002). The reasons for this are: firstly, the growing

realisation, as genetic science transfers into medical

practice, that genetics will never deliver the promised

ARTICLE IN PRESSE. Hall / Health & Place 10 (2004) 311–318314

certainty, and that individual and socio-spatial factors

explain large swathes of heart disease incidence (Kerr,

2004); secondly, those on the ‘front line’ of medicine and

heart disease—health professionals and patients—‘work

out’ the meaning of the relationship between genes and

heart disease. As Hedgecoe (2002) argues, the key to

understanding the significance of geneticisation is to

investigate these socio-spaces: ‘‘What is needed is

detailed empirical research on how geneticisation is

taking place, carried out in as many different contexts as

possible’’ (23, emphasis added). In the following section,

one particular context—the coronary care unit of a

hospital in Glasgow—is the setting for the ‘working

out’, through a contested network of people, ideas and

technologies, of the meaning of the relation between

genes and heart disease.

Spaces and networks of genetic knowledge making

To conceptualise this network of contested knowl-

edges, the paper adopts Actor Network Theory

(ANT)—a theoretical framework developed by Callon

(1986), Law (1992) and Latour (1993)—which offers

several distinctive conceptual advantages over other

sociologies of genetic science (e.g. Martin, 1999; Hedge-

coe, 2002): it is a distinctly relational and ongoing (as

opposed to linear and complete) understanding of the

making of knowledge and objects; it acknowledges the

multiplicity of ‘actors’ in this collective making, includ-

ing non-human actors; and the networks are specific

(sets of) spaces, placing the knowledge-making within a

broad context of socio-spatial relations.

There is insufficient space here to fully explore Actor

Network Theory (see Murdoch, 1997), but there are five

key themes that will be drawn upon in the analysis.

Firstly, and most crucially, a claim, such as geneticisa-

tion, can only become a ‘fact’ if a collective of ‘actors’—

people, institutions and ‘things’—engage with the claim

and actively make it a fact (Bucchi, 2004). In other

words, the knowledge being made, and the agency that

the multiple actors have, is wholly dependent upon their

relations to one another; as such, the meanings being

constructed are always open to contestation (Milligan,

2001). Secondly, thinking relationally implies that all

actors are equal in their ability to influence the making

of knowledge, although ANT concedes that some,

especially social, actors have more say in the forming

of outcomes (Castree and MacMillan, 2001). Thirdly,

another outcome of imagining the world as a set of

relations, rather than opposites, is that natural as well as

social actors play a role in the network, so the outcome

can be influenced, for example, by people, institutions

and technologies and bodies, genes and emotions

(Laurier and Philo, 1999). This rejection of the

natural–social binary by ANT makes it extremely

applicable to cutting through a debate such as genet-

icisation, polarised around this dichotomy. Fourthly,

once natural as well as social, and non-human as well as

human, actors are embroiled in the network, then a wide

variety of forms of communication have to be recog-

nised in the ‘translation’ of meaning across the net-

work—not only language, but also the ‘inscription’ of

objects with meaning, e.g. technologies and practices.

Fifthly, once the number of actors has been multiplied,

and social actors decentred, then the possibilities for

democratic knowledge emerging and the options for

contesting dominant ideas and power open up.

Overall, Actor Network Theory provides a framework

for thinking through the becoming of knowledge,

acknowledging the many interests, voices and meanings

of those engaged in the process. However, it would be

wrong to assume that such a network just forms and an

outcome ‘just happens’—Latour (1987) stresses that this

collective process is always managed, to an extent at

least, by particular social actors, who Latour (1987,

p. 108) called ‘fact-builders’. These prominent actors

achieve the desired outcome by ‘enrolling’ or marshal-

ling other actors, ‘translating’ the desired outcome into

meanings that appeal to their different interests (Bucchi,

2004). Such marshalling is not guaranteed to produce

the ‘desired’ outcome—the results of a network are

always precarious and uncertain, open to reinterpreta-

tion and, as such, never complete.

The discussion that follows focuses on one particular

set of spaces and networks of knowledge-making about

genes and heart disease, analysing interviews with two

cardiology consultants and two cardiac rehabilitation

nurses, and focus groups with six groups of people with

heart disease. The interviews and focus groups took

place between May and July 2003; the sessions included

discussion of a selection of newspaper stories of claims

of links between heart disease and genes. Two key stages

of cardiac care can be identified, each involving a

particular set of actors and dynamics and within

particular spaces—the diagnosis of heart disease in the

consulting room and the rehabilitation of the person

with heart disease in clinics and exercise classes.

Diagnosis

Following a suspected myocardial infarction and

admission through the accident and emergency unit or

on referral from a GP for symptoms of angina, a person

enters into the coronary care unit and, once an initial

assessment and stabilisation has been undertaken, they

are diagnosed in a consulting room. In a medicalised

system of healthcare, diagnosis—when symptoms are

described, analysed and linked to a particular disease

category—is perhaps the critical moment for both the

individual and the consultant. The two consultants

stated that at the moment of diagnosis an attempt is also

ARTICLE IN PRESSE. Hall / Health & Place 10 (2004) 311–318 315

made to identify the cause, however problematic or

precautionary, to facilitate the start of the rehabilitation

process (see below). In his diagnosis, one consultant

identifies the cause(s) in the following way:

I go for the usual suspects: smoking, lipids [choles-

terol], family history, in that order (C1).

Drawing on his medical knowledge and experience, he

‘knows’ that the most probable causes will be individual

behaviour, such as smoking or diet. There is another

important reason for this focus, however—the need to

provide a ‘target’ and motivation for the individual in

rehabilitation. In the first hint of his understanding of

the role of genes in heart disease diagnosis, the

consultant adds:

I accept [the genetic component of heart disease], but

do not put it nearly as high in my priorities as

smoking and lipidsyHyperlipidaemia runs in fa-

milies, but I tend to take the reassuring line. I advise

them to look at any possible lifestyle risk factor (C1).

There is an acceptance of the role of genes, but the

emphasis is firmly on individual behaviour, on linking

the heart disease to something the individual has done,

has responsibility for and, crucially for rehabilitation,

has the ability to change. The second consultant sums up

his approach to people diagnosed with heart disease:

[I say to] patients, ‘this is down to you, you can

change your lifestyle, you change your diet, you can

exercise and all these things and you can protect

yourself from heart attack’ (C2).

There is an attempt to marginalise the perceived role

of genes in heart disease. The consultants believe that

there is so powerful an association between genes and

certainty of disease amongst patients (and the broader

public) that placing genetic causation on an equal

footing—rather than at the bottom of ‘the order’—

could potentially lead to health fatalism—as opposed to

‘hope’—which would limit the effectiveness of rehabili-

tation.

A lot of people in this city [Glasgow] believe that

they’re destined to die because their father died of

heart disease. yI think it is very important to give

people hope (C2).

One consultant, closely involved in medical genetic

research carried out elsewhere in the hospital (see Hall,

in press), privately at least, stressed the significant role

that genes played in heart disease. However, when asked

how he would translate such claims for patients he was

cautious:

You have to explain to patients that, ‘Yes, these

genes exist, but they may not necessarily function in

you and you may have protective genes, we don’t

know. What we do know though is that there are

benefits from an active lifestyle, and with an active

lifestyle you’ll enjoy it, you’ll feel better’. yIf people

are happier, they will take a much greater interest in

the treatments we have to offer (C2).

In the space of the consulting room the cause of the

individual’s condition is identified, emphasising lifestyle

behaviours and marginalising genes. Although this may

seem a straightforward process of linear knowledge, i.e.

the giving out of medical knowledge from the consultant

to the unknowledgeable patient, and a certain and fixed

outcome, i.e. the diagnosis, we can prise open the ‘black

box’ of the diagnosis and discover the complexity of the

network. Most importantly, we can recognise that the

consultants are ‘managing’ the outcome, or at least

attempting to. To do this—and indeed for the con-

sultants to secure their own identities and positions—a

whole host of other actors have to be enrolled to support

their attempt to secure the ‘fact’ of lifestyle as the cause.

The consultant’s white coat, language and terminology,

his reference to expert knowledge and experience and the

‘feel’ of the consulting room, all drawing on the power

of the medicalisation of health, ‘translate’ to the patient

the particular understanding of the cause of heart

disease. The consultant makes every effort to enrol the

patient to give the best chance of success, through

appealing to their sense of hope, connecting to their

lifestyles and by generating a notion of control by the

patient over their future. In addition, other actors—e.g.

patients’ families and nursing staff (see below)—have to

be convinced of the result to ensure the successful

outcome. However, this outcome is by no means certain

or secure. While the consultants employ ‘strategic

essentialism’ to marginalise the role of genes and place

lifestyle factors centre stage, some of the patients are not

wholly enrolled. As one commented in a focus group on

his diagnosis:

The consultant said some of the cause was in my

family and some was my own doing [smoking]. I

asked him [again] what the cause was, and he said

‘What do you think?’, implying that it was my fault,

never mind my family history (FG3).

The patient is resisting the consultant’s attempt at

enrolment—‘What do you think?’—by asserting, at least

in his thoughts, his understanding of the role of

inheritance his condition. Although the people with

heart disease acknowledged the role of lifestyle beha-

viours, they drew upon personal embodied experiences,

family histories and social contacts:

I think it’s important [lifestyle behaviour]. I don’t

knock it, it’s good advice. But I can’t get it out of my

own mind, when I think of people I know. Genes

ARTICLE IN PRESSE. Hall / Health & Place 10 (2004) 311–318316

don’t seem to get the publicity that smoking does

(FG3).

The patients—their bodies, emotions, histories and

experiences—disrupt the management of the network by

the consultants (and the many actors and translations

marshalled to support their desired outcome). Although

their contesting understandings are not expressed in the

space of the consulting room, they remain important in

the experience of their condition and rehabilitation.

There seems to be a gap opening up between what the

consultants (and their allies) understand they are

achieving, and what many people with heart disease

increasingly feel about the use of such strategic

essentialism to cut genes out of the explanatory picture.

Adopting a network approach allows us to see inside the

black box of diagnosis and the contestation of the

dominant knowledge by an assumed weak and un-

knowledgeable actor (the lay patient); the outcome of

the diagnosis is suddenly not as secure as it first seemed.

Rehabilitation

A patient’s stay in intensive care in the coronary care

unit usually lasts a few days; they are then discharged

and enter into the second phase (and set of spaces) of

coronary care—rehabilitation. Rehabilitation takes

place in a number of locations—including local clinics

and the coronary care unit—with rehabilitation nurses

providing the co-ordination role, the ‘‘first port of call’’

for the patient (RN1). This occurs as soon as the patient

is diagnosed (before discharge from the hospital) and

sees the marshalling of a network of people, places and

objects.

Once the diagnosis is made, that’s really when we

come in and approach the patient and facilitate their

care. They are enrolled in a programme and we

continue to follow them up in the community (RN1).

The programme on which they are enrolled is

encapsulated in ‘‘the wee white book’’ of diet and

exercise guidance, information about drugs, numbers for

advice and so on, which is ‘‘more or less gospel for the

first month, the do’s and don’ts’’ (RN2). The pro-

gramme includes a 12-week course of exercise and talks

on diet, cholesterol, blood pressure and coping, pro-

vided by a ‘‘multi-disciplinary team of nurses, dieticians

and clinical psychologists’’ (RN1). The rehabilitation

nurses see the programme as together providing clinical

care, ‘‘allaying any fears, any misconceptions which

have been identified’’ and ‘‘giving confidence’’ (RN1).

The rehabilitation nurses are, as with the consultant,

attempting to manage the network of patients, their

families (some of whom attend the rehabilitation

sessions), other health professionals, and spaces through

particular understandings or translations (the ‘wee white

book’, advice line and the exercise classes and talks) to

produce a particular outcome—the knowledge amongst

patients that they are actively responding to their heart

disease with the implicit assumption that it was caused

by their poor lifestyle behaviour. At all points through

the rehabilitation ‘fears’ and ‘misconceptions’—under-

standings that do not match onto the desired outcome—

are ‘identified’ and ‘allayed’, essential to maintain the

result. The nurses deal with genetic claims for causation

of heart disease with extreme caution, and any questions

or ‘fears’ regarding this are swiftly ‘quashed’. While they

acknowledge there are a ‘‘small percentage of people

who you can’t explain through normal risk factors’’

(RN1), when asked about the role of genes by patients,

perhaps in response to a newspaper article brought

along to a rehabilitation session, they respond very

carefully.

I would very much stick to the line that [genetics] is in

its infancy, we don’t know enough about it at the

moment. It’s something that’s being looked into, but

well just wait and see how it goes. There’s not enough

evidence to support it (RN2).

Importantly, the nurses note that patients are asking

about genetic causation of heart disease more now (and

‘‘have more knowledge on board’’ (RN1)), and the

nurses themselves are gaining more knowledge through

their reading of cardiology journals and most recently

by attending the British Cardiac Society conference held

in Glasgow in 2003. With these contestations in the

network, the nurses struggle to maintain their manage-

ment of lifestyle factors as primary cause, responding

to one newspaper story discussed in the interviews

(Guardian, 2001), linking specific genes to heightened

risk of heart disease from smoking, by stating that to

patients:

I would want to play down that down a wee bityI

would want to really quash it and deal with smoking

side of it (RN2).

Their concern is that of patient fatalism, in this

instance, that ‘‘people will say, ‘well, there’s no point in

me giving up [smoking]’’’ (RN2). Those patients that

attend the sessions—and importantly the majority do

not, in itself a significant contestation of the desired

outcome of rehabilitation—do not necessarily share this

fatalism. While some do see genes as ‘‘unknown, locked

inside, there is no warning of disease, it just happens’’

(FG2), more commonly patients have a sense of genes as

one element in the causation of their condition:

We have built in [genetic susceptibilities] and we can

make these worse by behaviour (FG2).

Many patients know, through their embodiedness,

family history and lay medical knowledge, that their

ARTICLE IN PRESSE. Hall / Health & Place 10 (2004) 311–318 317

condition can only be explained by a combination of

genetic and non-genetic factors; consequently, they tend

to be pragmatic rather than fatalistic, as the health

professionals fear.

Discussion and conclusion

This analysis of one set of spaces and network of

actors reveals a complex and contested understanding of

the role of genes in heart disease. The process of

attempting to secure a particular understanding—that of

heart disease as caused solely by individual behaviour—

by the consultants and rehabilitation nurses was

contested by the actions, words and embodied experi-

ences of many of the people with heart disease. Actor

network theory shows that while certain powerful social

actors use all the resources at their disposal, and all

forms of translations, they can only secure a precarious

and temporary outcome of heart disease as non-genetic.

Patients’ family knowledge, media coverage and the

unpredictability of the disease for themselves or people

they know, all pick away at that outcome and suggest a

greater complexity.

What does this mean for the seeming geneticisation of

heart disease? On the one hand, it could be argued that

the practices of the consultants and rehabilitation nurses

show clearly that genetic explanations are yet to get a

hold on the imaginations and practices of coronary care,

with genes only included when all possible lifestyle

behaviours have been accounted for. On the other hand,

the strategic essentialism of the consultants and nurses

could indicate a denial or nervousness about the power

of the gene, i.e. that the role of genes cannot be identified

or even discussed because of fears of patient fatalism. Is

this what Lippman (1991) was hinting at, i.e. that once a

disease condition and genes are mentioned in the same

breath they will be forever linked whatever the quality or

quantity of the scientific or medical evidence? The

geneticisation of heart disease, the consultants and

nurses seem to believe, is on the brow of the hill and

they see it as their responsibility to fight back any

advance. However, while this marginalisation is partially

successful, many patients desire an acknowledgement by

consultants and nurses of the role of genes and broader

biology in heart disease, while emphasising the central

role of lifestyle (Shostak, 2003).

In conclusion, there can never be a straightforward

and complete geneticisation of heart disease as imagined

by Lippman (1998), because of the contesting knowl-

edges of consultants, nurses, people with heart disease

and others. Instead of simply accepting or rejecting

geneticisation, we can perhaps refocus our research onto

a critical examination of the broader contexts within

which medical genetic knowledges are developing—

government genetic health policy (Department of

Health, 2003) and social and spatial inequalities in

health (Kelly, 2002)—areas where geographies of health

have much to contribute.

Acknowledgements

Many thanks to all those who participated in the

research, in particular the consultants, rehabilitation

nurses and people with heart disease. The paper was first

presented at the Annual Meeting of the American

Association of Geographers in New Orleans, March

2003; thanks to Gail Davis, Suzanne Williamson and

Rosie Day for organising both the session and this

collection. The three referees reports provided insightful,

thorough and constructive criticism. The research was

funded by Economic and Social Research Council

Research Grant R000223927. This paper is dedicated

to Rosina, who arrived as it was being completed.

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