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Social Science & Medicine 60 (2005) 2673–2683

www.elsevier.com/locate/socscimed

The ‘geneticisation’ of heart disease: a network analysis of theproduction of new genetic knowledge

Edward Hall�

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

Available online 8 January 2005

Abstract

Genetic science is making ever-expanding claims about the (mal)functioning of the body. The ‘geneticisation’ of

health and medicine is extending from rare single gene conditions to more common multi-factorial disease, such as heart

disease. The dominant behavioural and socio-spatial explanations of heart disease are now being challenged by genetic

claims of deterministic biological causes. This paper builds an account of the transformation of heart disease in the new

genetics era, by applying actor network theory (ANT) to the production of genetic knowledge of one aspect of heart

disease—hypertension—within a medical genetics laboratory in Glasgow, Scotland. Using this approach, the paper

shows that there is no straightforward geneticisation of heart disease. Instead, there is a contested, complex and

uncertain understanding of heart disease as genetic, a product of the many people, technologies, natural elements and

spaces involved in the network of genetic science knowledge making. The paper concludes that a ‘critical’ ANT could be

developed that acknowledges the inherent unevenness of the network, and connects genetic and socio-spatial

explanations of heart disease.

r 2004 Elsevier Ltd. All rights reserved.

Keywords: Heart disease; Genetics; Actor network theory; Science

Introduction

The accelerating developments in genetic science are

beginning to transform the understanding of disease

causation and the practice of medicine (Conrad & Gabe,

1999). The established biomedical understanding of the

source of disease—within the organs, tissues and vessels

of the body—is being increasingly contested by a

conceptualisation of disease that traces its origin to the

genetic codes deep inside the cells. This deeply penetrat-

ing ‘medical gaze’ is being cast more widely from clearly

identified and determining rare ‘single gene’ conditions,

e front matter r 2004 Elsevier Ltd. All rights reserve

cscimed.2004.11.024

ing author. Tel.: +44 131 317 3601; fax:

04.

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

such as Cystic Fibrosis and Huntingdon’s disease, to

common multi-factorial diseases, including cancer,

stroke and coronary heart disease (Daily Telegraph,

2001; Observer, 2002). The challenge that this presents

to medical clinicians and to those who study health and

medicine is profound: dominant models of health, illness

and the body are being destabilised, patient health

beliefs are being challenged (Parrott, Silk, & Condit,

2003) and science and technology are taking an even

greater role in healthcare. Crucially, this is no idle

academic debate: the UK government is presently

investing £50 million in the ‘mainstreaming’ of genetic

testing and screening within NHS clinical practice for a

wide range of conditions (Lenaghan, 1998; Department

of Health, 2003). The pace of change is dramatic,

as genetics and the ‘geneticisation’ of health and

d.

ARTICLE IN PRESSE. Hall / Social Science & Medicine 60 (2005) 2673–26832674

disease—‘when genetic explanations gain ascendancy

and people are reduced to their DNA codes’ (Hedgecoe,

2003, p. 51)—envelop society and healthcare (Lippman,

1992); this paper offers a reflective pause to consider the

process of this transformation, focusing on coronary

heart disease (CHD).

CHD is the major cause of morbidity and mortality in

the West, with higher levels in the UK than most

developed countries (Department of Health, 1998). In

the UK, more than 1.4 million people experience

angina—the most common form of CHD—and around

300,000 people have a myocardial infarction or heart

attack every year. In Scotland, and particularly in

Glasgow, the problem is at its worst: an estimated half a

million people in Scotland have CHD and 12,500 die

each year (Scottish Executive, 2002). The dominant

explanation of CHD is of a condition of poor individual

lifestyle choices within the context of socio-economic

disadvantage. It has taken a steady drip-feed of media

announcements of ‘discoveries’ of ‘genes for’ particular

aspects of heart disease to provide a dynamic ‘genetic

tale’ to challenge this dominant ‘social story’ of heart

disease (for example, Guardian 2001; BBC News, 2003).

The transfer of genetic knowledge and techniques to

medical practice has been rather more rapid, with, for

example, a genetic test for Familial Hyperlipidaemia

(very high cholesterol) soon to become available in NHS

primary care (Department of Health, 2003). The

reimagining of heart disease as a genetic condition

seems to be well under way. The purpose of this paper is

to assess the nature and extent of this ‘geneticisation’.

Social scientists of health and medicine are increas-

ingly engaging with the ‘new’ genetics (see Conrad &

Gabe, 1999, for a fuller review), with studies settling

around three themes: patient responses to medical

genetic testing and counselling (Bosk, 1992; Cox &

McKellin, 1999; Taylor, 2004); lay interpretations of

genetics, particularly transformed perceptions of risk

(Kaufert, 2000); and broader concerns around the social

and healthcare implications of genetics (Shakespeare,

1999; Everett, 2003; Robins & Metcalfe, 2004). How-

ever, with a few exceptions—Cunningham-Burley and

Kerr (1999) and Hedgecoe (2003)—the facts and

technologies of genetics have been accepted as ‘true’

and complete. Little attention has been paid to the

ongoing production of genetic knowledge, whether in the

laboratory, in the broader networks of health policy or

in patient–clinician exchanges. This paper hopes to

disrupt this sense of genetic knowledge as given, by

looking inside the ‘black box’ of one particular aspect of

genetic knowledge making: the identification of ‘genes

for’ hypertension (high blood pressure, a key risk factor

for heart disease).

Within medical and health geographies there has been

very limited interest in human genetics (except, Hall,

2003). Much potential for critique is being lost, as

geography’s disciplinary spanning of the natural and

social worlds places it in a unique position to think

through the intertwining of biology, individual actions

and social understandings and structures that constitute

the new genetics (Castree, 1999). For health geogra-

phers, there is much to put our minds to: the ‘mapping’

of the interface of the social and the biological, the

possible reshaping of health inequalities, and the study

of the complex and contested production of genetic

knowledge within the spaces of science (and beyond). A

small group of geographers have applied ‘actor network

theory’ (ANT)—that views the world as being made up

of a multiplicity of interconnections between people,

objects, nature and spaces—to the twists and turns of

science and nature and society, and this paper will

follow their lead (Bingham, 1996; Whatmore, 1999).

The paper builds an account of the transformation of

heart disease in the new genetics era, by applying ANT

to the production of knowledge of the ‘genes for’

hypertension within a laboratory in Glasgow. Using this

theoretical approach, the paper shows how there is no

straightforward geneticisation of heart disease occur-

ring; instead there is a continually negotiated and

contested understanding of hypertension and heart

disease as genetic. This complexity is the product of

involvement of many people, things and contexts—

geneticists, laboratories, experimental rats, genetic

matter, computers, and funding bodies—that collec-

tively, though not equally, produce the ‘meaning’ of

hypertension and heart disease as genetic. The paper

draws upon empirical evidence—observation of and

interviews with a geneticist—gathered during 2003. The

paper begins by charting the seeming geneticisation of

heart disease, from an individual and social condition to

a genetic disease. The following section outlines and

then applies ANT to the identification of ‘genes for’

hypertension in the stages of a laboratory experiment.

The discussion and conclusion reflects on the nature and

extent of the geneticisation of hypertension and heart

disease.

Contested explanations of heart disease: from social to

genetic causation

Heart disease—incorporating the heart ‘events’ myo-

cardial infarction and sudden adult death syndrome,

and the heart ‘deterioration’ of angina and heart failure

(Gray, Dawkins, Simpson, & Morgan, 2002)—is the

major health issue in the UK and Scotland. It is also one

of the key drivers of health policy, not only because of

the high mortality and morbidity rates, and the severe

social and spatial inequalities, but also because heart

disease is understood as a largely preventable condition

through individual and social action (Department of

Health, 1998; Scottish Executive, 2002). This section

ARTICLE IN PRESSE. Hall / Social Science & Medicine 60 (2005) 2673–2683 2675

considers the individual and social ‘stories’ of heart

disease, and how genetic explanations are ‘folding into’

and challenging these dominant understandings in a

seeming geneticisation of the condition.

Risky behaviour

Health policy and popular discourse identify ‘lifestyle

behaviour’ as the primary cause of heart disease. In

particular, individual decisions to smoke, eat a high fat

diet, drink excessive alcohol, and do little physical

exercise, place people at risk of developing heart disease

prematurely. Crucially, the lifestyle risk factors empha-

sised are those within the (assumed) control and hence

responsibility of the individual. However, responses to

risk are not straightforward, for people’s understandings

of heart disease causation are complex. Davison,

Frankel, and Davey Smith (1992) study of lay under-

standings of heart disease in south Wales found that

while people recognised the risk factors that produced

‘coronary candidacy’, they also knew that some of those

who displayed these risk factors were not affected by

heart disease (in some cases living to an advanced age)

and others who adopted ‘healthy’ lifestyles were affected

(some dying young). These discrepancies are explained

by the participants in the study outwith the discourse of

risk, in terms of ‘fate’, ‘destiny’ and ‘chance’. The overall

observation of respondents that ‘it never seems to

happen to the people you expect it to happen to’ shows

the ‘limits of lifestyle’ explanations (Davison, Frankel, &

Davey Smith, 1992, p. 675) and hints at some element of

cause beyond the individual’s control. Further, there is

an awareness that people’s bodies respond differently to

the same lifestyle behaviours. This sense of uncertainty

and lack of control undermines a health policy centred

on reducing risky behaviours and opens up a space that

genetics, which can seemingly provide certainty and

explanation for these discrepancies, is beginning to fill.

A disease of inequality

The exhortations to improve individual lifestyle

behaviour dominate heart disease policy, yet it has long

been recognised that the incidence of the condition is

highly unequally distributed in a positive association

with a whole host of social categories, most significantly

social (or occupational) class (Marmot, Davey Smith, &

Stansfield, 1991; Bryce, Curtis, & Mohan, 1994); for

example, those in unskilled manual occupations (social

class V) are three times more likely to suffer from heart

disease than those in professional occupations (social

class I) (British Heart Foundation, 2002). The overall

decline in heart disease mortality has exacerbated this

inequality, with those groups experiencing the highest

levels of disease seeing the smallest falls in deaths

(National Heart Forum, 1998). The strong relationship

between social disadvantage and CHD has no straight-

forward explanation (Bryce et al., 1994; McLoone &

Boddy, 1994), but a combination of less knowledge

about risk factors (Foss et al., 1996), lower expectations

of health and healthcare, and poorer access to exercise

facilities, nourishing foodstuffs and healthcare, lock

many people on lower incomes into a vicious circle of

health neglect. Geographers and others have noted the

associated spatial patterning of heart disease (Sooman &

Macintyre, 1995) and have identified the specific role of

‘place’ in shaping health (Kearns & Gesler, 2002),

through physical environmental factors, social networks

(Cattell, 2003), access to healthcare, and shared socio-

cultural beliefs of health and risk behaviours (Macin-

tyre, MacIver, & Sooman, 1993; Hart, Ecob, & Davey

Smith, 1997). Understanding individual behaviour as

shaped by social and spatial contexts is a powerful

explanation of heart disease (Huff & Gray, 2001). The

seeming geneticisation of heart disease is a profound

challenge to this, as it both places the locus of cause

within an individual’s biology and removes it from their

behaviour and socio-spatial contexts. As a consequence,

heart disease is reimagined as a condition that affects a

body irrespective of context and, further, shifts respon-

sibility for heart disease from individuals and health

policy makers to medical geneticists and science.

Heart disease as a genetic condition

There is a powerful socio-cultural sense of heart

disease ‘running in families’ and medical research has

verified that family history is an ‘independent predictor’

of heart disease (Timmis & Nathan, 1997). However,

there has been less clarity about the mechanism of

inheritance, with the reproduction of ‘poor’ lifestyles in

families only partially satisfactory as an explanation

(Julian, Cowan, & McLenachan, 1998).

Medical genetic research, accelerated by the vast

‘library’ of gene codes generated by the Human Genome

Project (International Human Genome Mapping Con-

sortium, 2001), is filling this explanatory gap, rapidly

redefining the cause, manifestation and treatment of

health and illness, in the ‘geneticisation’ of health

(Lippman, 1992). A flurry of research announcements,

communicated through the media in an often confusing

mix of medical hope and ethical fear (Petersen, 2001),

has offered possible explanations for the major health

issues of the 21st century. Specifically, genes are

privileged with individual behavioural and especially

social and spatial causes marginalised. A marker of this

has been the significant expansion of genetic research

from the identification of single gene conditions, such as

Cystic Fibrosis, to multi-factorial conditions including

heart disease. Multi-factorial diseases involve many

elements—heart disease has many associated conditions

including hypertension, high cholesterol—and many

ARTICLE IN PRESSE. Hall / Social Science & Medicine 60 (2005) 2673–26832676

causes. While geneticists insist that, such is the condi-

tion’s complexity, a specific ‘gene for’ heart disease will

never be identified, several aspects of heart disease are

now being reimagined as ‘genetic’ (Lefkowitz & Will-

erson, 2001). For example, Familial Hyperlipidaemia, a

condition that affects 1 in 500 people, is directly

(although not automatically) inherited (Lyon & Gorner,

1996), and Long QT Syndrome is a rare disorder of the

heart’s ‘electrical system’ (British Heart Foundation,

2003). Both of these are rare and single-gene determi-

nate; more recent claims have broadened the scope of

the role of genetics in heart disease, implicating more

genes and more people, and furthering the implicit

geneticisation of heart disease. For example, the APOE

gene (on chromosome 19), in a specific mutation, is

involved in significantly raised cholesterol levels, and

affects 7% of people (Lucotte, Loirat, & Hazout, 1997);

a gene variant (known as PPAR@) found in 20% of the

population may be the cause of sudden and fatal heart

failure in some young people (Flavell et al., 2002); the

hormone angiotensinogen, an important determinant of

blood pressure, has been found to have a common

variation in a gene ‘promoter’ (on–off switch) (Day &

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). Such claims together build a ‘narra-

tive’ of heart disease that prioritises a genetic explana-

tion. While it is emphasised that there will never be a

deterministic ‘gene for’ for heart disease, the narrative

suggests that there must be genetic ‘predisposition’ for

the environment to then ‘trigger’ the development of the

condition (Hedgecoe, 2001).

Transforming heart disease in the new genetics era

The above suggests an ongoing transformation of

heart disease, from a disease of ‘external’ individual risk

behaviour, conditioned by social and spatial contexts, to

a disease of ‘internal’ genetic codes, in the ‘geneticisa-

tion’ of the condition. This paper offers a particular

analysis of this transformation, focusing on one

particular moment in the production of genetic knowl-

edge: the identification of potential ‘genes for’ hyperten-

sion. Through an engagement with ANT, this paper

explores the complexity of the process of this seeming

geneticisation.

Networks of social and natural ‘actors’

The theoretical collective of Callon (1986), Latour

(1987), Law (1992) and Serres and Latour (1995)

conceive of an ANT, in which people, objects and

places are involved in a multiplicity of interconnections

and, indeed, are produced by these interconnections.

ANT also represents a radically different understanding

of nature and society, rejecting the opposition that

characterises Western thinking (Whatmore, 1999), in-

stead considering natural and social actors in relation.

For thinking through the geneticisation of heart disease,

which involves the intertwining of the natural (genes,

disease and experimental rats) and the social (geneticists,

laboratories and funding bodies), such an interpretation

offers great potential. Further, the application of ANT

to studies of scientific knowledge ‘in the making’

(Latour, 1987) can be replicated for the study of the

contested process of identifying genes for hypertension

in the laboratory.

There is insufficient space here to fully review ANT,

and this is done very adequately elsewhere (Murdoch,

1997), but I will identify five aspects which will drawn

upon in the analysis of the geneticisation of hyperten-

sion and heart disease (below). Firstly, and most

importantly, ANT reimagines the world as made up of

social and natural ‘things’—people, buildings, animals,

plants, technologies—existing only in relation to one

another in a network of interconnections; it is the

connections that are crucial, rather than the things

themselves. Secondly, all things (known as ‘actors’),

human (e.g. geneticist), non-human (e.g. technologies)

and natural (e.g. genes), can exert agency in the network,

that is, they can have an effect, through their inter-

connections, on the overall outcome (Laurier & Philo,

1999). Thirdly, all of the actors, as has been hinted, can

only exert agency through their interconnections with

each other and as they do the outcome is built

collectively, yet unpredictably; all outcomes—meanings,

actions, objects—are ‘precarious’ and undergo constant

modification (Milligan, 2001). Fourthly, it is through the

continuous interconnections of messages—words, ideas,

objects, money and so on—between actors, that an

outcome is made or ‘stitched together’; these messages

(or ‘translations’) are all ‘inscribed’ with meaning and so

there are inevitable contestations in the making of the

outcome (Callon & Law, 1995). Fifthly, the production

of an outcome is collective, with no social or natural

actor wholly ‘directing’ the process. However, it is

recognised that some social actors attempt to ‘manage’

the network to stitch together a particular outcome,

enrolling or marshalling other actors and translations,

though, importantly, with no guarantee of success

(Bucchi, 2004). One significant technique of enrolment

is ‘strategic purification’, in which a social or natural

explanation or meaning is emphasised to gain support,

tapping into dominant binarist understandings (Castree

& MacMillan, 2001).

Drawing on the above, an ANT-inspired interpreta-

tion of the geneticisation of hypertension and heart

disease describes in detail the network of the making of

genetic knowledge, incorporating the agency of the

multiple social and natural actors, yet recognising the

ARTICLE IN PRESSE. Hall / Social Science & Medicine 60 (2005) 2673–2683 2677

marshalling of these actors, through the assertion

of particular meanings, by a small number of social

actors, in particular the geneticist running the experi-

ment. The outcome—the geneticisation of hyperten-

sion—is what is stitched together in the network, but the

result can in no way be accurately predicted or complete.

The analysis that follows reveals the contestation and

negotiation involved, and the necessary compromises

that produce a geneticisation that is uncertain and

cautionary.

The ‘geneticisation’ of heart disease: identifying ‘genes

for’ hypertension

The paper draws on evidence gathered during a study

in a medical genetics laboratory in Glasgow (based

within a university hospital) in May and June 2003. The

group of geneticists (18 research scientists and 9 support

staff) based there conduct a programme of research to

identify the multiple genes involved in the ‘expression’ of

hypertension. The study focused on a single experiment

in this broader programme of research. The experiment

used biological material from the kidneys of rats, long-

standing models for humans in medical research, bred to

exhibit different states of hypertension, in an attempt to

identify the genes (or more precisely ‘regions’ of multiple

genes) involved in these differences in blood pressure.

More specifically, a region of genes from rat chromo-

some 2, suspected of involvement in hypertension, was

transferred from rats with ‘normal’ blood pressure

(normotensive) to those with hypertension. The desired

‘outcome’ was the production of similar normal levels of

blood pressure in these new combined ‘cogenic’ strains

of rat—such a result would suggest that this region of

the chromosome is where the genes linked to hyperten-

sion lie. The experiment was carried out over a 4-week

period, undertaken by a single geneticist, with the

assistance of a laboratory technician and technical

support from scientists in another laboratory. The study

involved the observation of the complete experiment and

interviews (informally during the observation and more

formally at the end of the experiment period) with the

geneticist undertaking it. In addition, material from the

laboratory’s website and newspaper coverage of the

laboratory was gathered. Detailed notes were taken

throughout the observation and informal interviews; the

formal interview was tape-recorded and transcribed in

full. The transcripts were coded and common themes

identified and linked between observation and inter-

views. The quotes from the observation notes are as

close to verbatim as is possible.

At first sight the identification of (regions of) genes for

hypertension, as described above, and the broader

reformulation of heart disease as a genetic condition,

is easily explained: the geneticist, through the experi-

ment, analyses the biological material of the rats, and

identifies within them the genes responsible for hyper-

tension. The process of the experiment is clear and

the results certain, and the relations between the

social (the geneticist) and the natural (rats and genes)

clear and unmuddied. However, once we delve into the

‘black box’ of the experiment, the intricacies and

complexities of the many people, objects, interests and

epistemologies involved, and the negotiation and con-

testation that is inherent to a ‘certain’ scientific ‘fact’

being produced, become evident (Latour & Woolgar,

1979; Bucchi, 2004). In what follows, the four key

phases of the experiment—which I have termed ‘pre-

paration’, ‘extraction’, ‘digitisation’ and ‘reintegra-

tion’—are described and the network of making

geneticised knowledge of hypertension and heart disease

explored.

Phase 1: Preparation

The experiment, in many ways, begins long before the

geneticist enters the laboratory—a whole series of people

and objects need to be ‘enrolled’ and the network

managed for the outcome to become a possibility. The

experiment was funded (£15,000) by the British Heart

Foundation (BHF), as part of the charity’s long-

standing sponsorship of the laboratory. The professor

who directs the laboratory, her own post funded by the

BHF, has to secure and maintain this stream of

investment (and BHF’s overall support for genetic

research). This is achieved through regular reports

to the charity, emphasising the ‘progress’ in identi-

fying genes and potential clinical application. As

funding comes from other sources, such as the Wellcome

Trust, this maintenance of national and international

profile, in the highly competitive medical science

community, primarily through publishing papers in

medical journals and appearing at conferences, is an

ongoing issue:

We share our findings through journals and at

conferences, but wouldn’t tell other researchers of

our ‘candidate’ genes outwith this. There are other

research teams looking at the same gene regions – it’s

a competition and the Professor wants to win the race

y She will spend money to win (Observation,

17.06.03).

Another issue had to be negotiated by the director, as

a planning inquiry relating to the building of a major

new research facility to house the laboratory became a

source of intense debate, combining public fears of

genetic technologies with aesthetic objections to the

large buildings. The director offered a dual response in

the media coverage: an emphasis on the value of the

research to public health (particularly as Glasgow is a

centre of heart disease) and a threat of moving the

research centre (and its income, staff and prestige) to

ARTICLE IN PRESSE. Hall / Social Science & Medicine 60 (2005) 2673–26832678

another university. Headlines in a Glasgow newspaper

capture this:

Planning row threat to medical research: heart

experts may leave if protests delay new centre

(Herald, 25.02.03)

The heart of the matter: the fight over a world-

leading research centre is hotting up. But as coronary

capital of the world, Glasgow’s need seems great

(Herald, 29.05.03)

In addition, laboratory equipment including pipettes

and chemicals, computers, technical support staff, and

other scientists had to be ‘in place’ for the experiment to

begin, secured through funding, purchasing, and em-

ployment contracts. Finally, the rats used in the

experiment had to be bred (and genetically manipu-

lated), housed, and their biological material prepared for

the laboratory; the geneticist commented, ‘I have spent a

lot of time designing the rats’ (Observation, 12.06.03).

This is the building of the network, the incorporation

of the first set of natural and social actors, the

translation of the meaning of the laboratory in different

forms—reports, journal papers, media releases, employ-

ment contracts, rat breeding—for particular ends, and

the setting out of the intended outcome. In some ways,

there is an existing network, the ongoing research of the

laboratory, that is extended to include the new set of

social actors, meanings and outcome. The director,

marshalling resources for the existing network, is in a set

of interconnections with the charity, linked through the

medium of funding, which she maintains by asserting

the translation of research ‘success’ and value to the

aims of the BHF. To do this, and to attempt to achieve

the desired planning outcome, the director used ‘strate-

gic essentialism’, prioritising the role of genes in disease

in media coverage. The geneticist undertaking the

experiment shaped the network by incorporating the

rats and the biological material, employing a laboratory

assistant, and securing access to equipment and technol-

ogy. To achieve this, he had to convince all of these

actors—from the director, fellow scientists in the team

that will use the research results and the laboratory

assistant, to the rats and biological material—that the

outcome could be achieved and it was in their interests

to be enrolled. Different inscriptions are used to achieve

this, from personal contact to employment contracts,

and the care of the rats. Importantly, this is not a

smooth path, with some of the non-social actors exerting

agency:

The start of the experiment was delayed when some

of the samples from the rats were temporarily ‘lost’,

and others damaged as one of the freezers where

samples are kept broke down (Observation,

25.05.03).

The setting up of the experiment sees the first phase of

the ‘tension’ implicit in the network, amongst the many

actors being incorporated and the initial stitching

together, through various translations of meaning, of

the outcome. It is through these interconnections that

the laboratory, the geneticist and the experiment cannot

only be successful, but also can actually exist.

Phase 2: Extraction

The experiment took place during a narrow 4-week

window, defined by the research timetable of the

geneticist, the schedule of the laboratory’s research

programme, external research meetings where results

would have to be presented, and the geneticist’s planned

annual holiday. The preparation (described above) had

to be achieved to coincide with this time period. The

three types (normotensive, hypertensive and cogenic) of

rat kidneys were retrieved from the storage freezer’s

after some delay (see above) and taken to the laboratory

for ‘extraction’, described by the geneticist as:

The critical step, which I will only do myself or allow

the lab assistant to do (Observation, 23.05.03)

The biological material is put through a series of steps

to prepare it for the analysis (described below):

‘disruption’, where the kidneys are broken down to

destroy the cell structure, ‘homogenisation’, when the

samples are put in a larger volume of liquid to allow the

RNA (the active part of the genes) to be separated out,

‘spinning’ in the centrifuge to remove the remnants of

the cells, ‘washing’ with solutions to ‘build up’ the RNA

sample and ‘precipitation’, to concentrate the RNA.

Throughout these procedures, which stretched over

several days, the geneticist worked with the laboratory

assistant, following a series of methodological instruc-

tions or ‘protocols’ for the order of steps, the quantities

of liquids to use and the speed of the centrifugal spin. He

stressed that the ‘organisation is the crucial bit, once you

get going it is straightforward’ (Observation, 23.05.03).

The course of this phase was one of twists and turns,

however, with samples needing to be ‘located’, ‘getting

access to the centrifuge’, the difficulty of extracting some

of the rat material from a sample tube, contamination of

one sample with plastic, and the need to redo some of

the samples as they ‘failed quality control’ (Observation,

09.06.03). The geneticist was concerned that ‘so many

things going wrong’ (Observation, 23.05.03) would give

an inaccurate representation of science and commented,

‘you should have been here last week when everything

went smoothly’ (Observation, 09.06.03).

The geneticist (and science more broadly) has to

maintain the ‘integrity’ of the experimental method for

the outcome to be secured. The technological ‘protocols’

and repetition of procedures, the single use of pipette

tips to reduce contamination risk, and the wearing of

ARTICLE IN PRESSE. Hall / Social Science & Medicine 60 (2005) 2673–2683 2679

white coats and disposable latex gloves, are all transla-

tions of a meaning of science as powerful that together

‘convince’ and maintain the necessary enrolment of all

the key social actors—the laboratory assistant, other

scientists in the laboratory, the referees of medical

journals, and the BHF—in the network and so maintain

the stitching together of the desired outcome. Although

the geneticist is managing the network he is not in

complete control, as other actors (social and non-social),

from fellow scientists denying him access to equipment

to the protocols and chemicals produced by biotech

corporations, and from the rats genetic material being

difficult to extract to the timetable of the laboratory,

contest and complicate the supposedly straightforward

process of science.

Phase 3: Digitisation

The second phase of the experiment proper was the

transformation of the extracted biological material into

digital data, and its analysis using ‘microarray’ and

bioinformatics technologies. This process took place in a

different laboratory, a facility with specialist equipment

(that the main laboratory could not afford to purchase)

and expertise. A significant (but unstated) fee was paid

to use this facility and, further, the geneticist, when he

entered this laboratory had to negotiate the use of

machines, computers, liquids and knowledge. This was

far from straightforward: the facility undertakes analysis

for many scientists, so the geneticist had to compete for

time and space. He also had little expertise in this

technology—‘microarray is a little black boxy’, (Ob-

servation, 09.06.03)—and so relied on the laboratory

scientists for guidance (which they were not always

available to give). There was also an ongoing tension

between the geneticist and the main host scientist. Their

expectations of what the facility would do for the fee

were in conflict. In addition, he (jokingly) accused her of

‘being badly organised and having poor equipment’ and

complained of ‘working in an unfamiliar environment—

I can’t find anything; I have to use a pipette I don’t like’;

this caused him to make several mistakes (Observation,

09.06.03).

The extracted RNA samples were transferred between

the laboratories in a container of liquid nitrogen to

prevent degradation and once they were tested by the

host scientist for the level of concentration, a precondi-

tion for analysis. Enzymes were then added, and the

samples ‘incubated’ and spun, to convert or ‘synthesise’

the RNA to cDNA, the ‘expressive’ part of the gene; it

was in this process that the mistakes were made. This

prepared the genetic material for the ‘microarray

analysis’, a ‘cutting edge technology’ that scans the

cDNA samples for patterns of multiple gene expressions

(Observation, 12.06.03). The machine produces a

digitised image of these patterns, a mass of coloured

squares, that the geneticist describes as ‘qualitative data,

an impression’ of the multiple genes associated with

hypertension (Observation, 12.06.03). The ability to do

multiple gene analysis, however, compromises the

technology—the geneticist commented ‘with microarray

there is always uncertainty, it’s difficult to be absolutely

sure y we design the best experiments we can’

(Observation, 12.06.03). The microarray also produced

a large amount of ‘quantitative data’, tables of the gene

patterns, which the geneticist opened on the computer

screen once the first analysis was completed. He scanned

the results and exclaimed,

Yes! It’s bloody worked! This is absolutely amazing,

it blows me away! This completely validates all the

work we have done. Definitely a eureka moment,

which are few and far between

(Observation, 17.06.03)

He deemed the experiment a ‘success’: the cogenic and

normotensive samples shared the same patterns ‘prov-

ing’ that ‘moving a gene of interest’ is associated

with bodily state, and this meant ‘a causative link

for hypertension’ had been identified (Observation,

17.06.03).

More complex quantitative analysis, focusing on the

interactions between genes, involved the geneticist

negotiating with two further people: a ‘bioinformatics’

expert (also based in the facility), who ‘owns’ the

software and expertise and a research fellow from the

geneticist’s own laboratory who would undertake

the data analysis. The geneticist wanted the bioinforma-

ticist to ‘tell me what to do with the data’, but that

‘negotiating with him is quite difficult because I need

him to do things, but he has his own agenda’

(Observation, 17.06.03). Throughout this analysis the

geneticist was concerned about ‘running out of time’ as

his budget was restricted, results were needed for a

coming research meeting and he was due to go on leave,

‘I might have to cancel my holiday’ (Observation,

09.06.03).

This phase of the experiment saw the incorporation

into the network of a whole new set of social and natural

actors, and the (attempted) management of these to

secure the research outcome. The extracted genetic

material had to successfully translated, in the appro-

priate containers and concentrations, between labora-

tories, for the technical facility to be enrolled and

undertake the analysis. As noted above, this was a

problematic and contested process, with the geneticist

attempting to maintain control through negotiation—

with ‘uncooperative’ scientists, ‘uncertain’ microarray

technology and unstable enzymes, and restricted time

and budget—within a different scientific space. Further

social actors, the bioinformaticist and the research

fellow, had to be enrolled through the translation of

the genetic material from biological to digital data, but

ARTICLE IN PRESSE. Hall / Social Science & Medicine 60 (2005) 2673–26832680

there was no guarantee as one had ‘his own agenda’ and

‘owned’ the knowledge. The geneticist, through his

management of the network, stitched together the

outcome of a ‘causative genetic link for hypertension’.

However, as will be argued below, such was the nature

of the network of social and natural actors that this

result is contingent and not as ‘conclusive’ or certain as

it may seem.

Phase 4: Reintegration

While the procedures in the laboratories ended within

the 4-week period, the outcome of the experiment still

had to be secured within the main laboratory and the

broader scientific community. The geneticist’s first step

was to inform the director of the ‘success’ as soon as the

initial results had come through: she was, he commented

with a mixture of pleasure and relief, ‘very pleased to

hear about the results’ (Observation, 17.06.03). The

results were also communicated to the other scientists in

the laboratory who would use the data for their clinical

and human genetic research. The geneticist immediately

after the experiment had to rapidly write up the main

results for a prescheduled journal article and a national

meeting of researchers with Wellcome Trust funders.

This indicates the needs of the director and the

laboratory for successful results to secure continued

funding, maintain research prestige, and to make

possible the planned new facility for the laboratory.

The management of the network remained necessary

in this post-laboratory phase. The experimental results

had to be translated once again, in the form of reports to

others in the laboratory, journal articles for the broader

scientific community and through BHF media releases

to inform public understandings of hypertension and

heart disease (which would also help secure a favourable

planning decision). The key inscription here was one of

the ‘success’ and ‘certainty’ of the results, a necessary

meaning to secure the outcome. However, once the

‘successful’ outcome had been secured, the geneticist

began to describe the experiment in more nuanced

terms:

This is a work in progress, we still haven’t got an

answer. There never will be one answer. There are

very few things I can put my finger on and say these

are true or facts; everything is temporary or

cautionary, or ‘true at the moment’. The work will

never be finished

(Observation, 17.06.03)

The ‘success’ of the experiment becomes something

rather more uncertain and ‘cautionary’, the outcome

‘temporary’ rather than conclusive. He further commen-

ted that while the experiment began with a straightfor-

ward question, and a particular desired outcome, ‘Can

we identify the causative gene?, it ended up with a much

more complex set of answers’ (Interview, 25.07.03). He

explained these complexities in terms of a large number

of genes and their interactions, ‘hypertension is a

complex condition, with many genes working to-

gether’—and the ‘more subtle question’ of ‘pathways

of metabolism’ which place the genes within the

‘complex set of systems and contexts’ of the cell, body

and environment (Interview, 25.07.03).

The desired outcome in the experiment, the identifica-

tion of a genetic ‘causative link’ for hypertension, was

finally secured in the reintegration of the results into the

laboratory and medical science. However, this outcome

was for particular ends and asserted through inscrip-

tions of strategic essentialism, i.e. causative ‘genes for’

hypertension. The outcome was, however, rather more

uncertain, complex and open to further modification,

incorporating unknown gene interactions and acknowl-

edging environmental factors, particularly levels of salt

in the body (Interview, 25.07.03). The geneticisation of

hypertension at the end of a ‘successful’ experiment is

far from straightforward and complete.

Discussion and conclusion

The detailed description and analysis of the experi-

ment set out above reveals a cautionary, uncertain and

complex notion of the geneticisation of hypertension,

and more broadly heart disease, rather than the

straightforward transformation of an individual and

social to a genetic explanation. The incorporation and

interconnection of multiple actors—social, technological

and natural—in the network(s), produced knowledge or

knowledges of disease that are contested and incom-

plete. There were many competing interests and

epistemologies of the actors, from the funding and

planning priorities of the laboratory director and the

procedures and limitations of the technology, to the

occasional ‘deviance’ of the rat genetic material and the

unstable enzymes and the expectations of the other

scientists and the geneticist himself, all interconnected

within the network. The ANT analysis revealed the

agency of both the social and natural actors, with

scientists, technologies and animals exerting agency

through their connections, though recognised the key

roles of the geneticists and the laboratory director in

attempting to manage the network for a particular

purpose and outcome. Through the course of the four

phases of the experiment these competing interests

shaped the process and outcome, through messages or

translations of meaning, from funding applications and

media interviews to technology and equipment, and

from genetic material and data to the exchange of ideas

and jokes between scientists to journal articles. The

outcome, then, of the experiment, despite (and, indeed,

because of) the efforts of the geneticist, was a product of

ARTICLE IN PRESSE. Hall / Social Science & Medicine 60 (2005) 2673–2683 2681

the agency and translations of all of the social and

natural actors (to differing degrees). That the geneticist

began with a simple question and ended with a ‘complex

set of answers’ is, arguably, the product of this contested

network. The straightforward geneticisation of hyper-

tension was not possible and can never be so.

So what is the nature and extent of the geneticised

transformation of heart disease? The key social actors in

the network, the geneticist and the laboratory director,

frequently draw upon the dominant binary understand-

ing of genes and environment (and nature and society) in

a strategic essentialism to gain and maintain funding,

media attention and research profile. Further, it forms

the framework for their understanding of their purpose:

the ‘genes for’ hypertension and heart disease are there

to be found and the environment is minimised (Inter-

view, 25.07.03). The ANT interpretation challenges this

in several ways: firstly, by revealing the ‘messiness’ and

very social nature of the practice of science; secondly, by

stressing the impossibility of separating the effects of

social (environment) and natural (genes) actors; thirdly,

by showing how the ‘meaning’ of geneticisation becomes

translated into so many different forms (words, tech-

nologies, animals) that no ‘true’ or real genetic answer

can be identified; fourthly, by emphasising that no final

outcome can be reached and so no certain geneticised

conclusion can be reached (Bucchi, 2004). In sum, there

has not been a complete geneticisation of hypertension

and heart disease. Indeed, the geneticist in the study

stated that genes had to be understood in the contexts of

bodily and social environments. This can be understood

positively as a rejection of genetic determinism and an

acceptance of the central role of individual and social

factors in producing disease. However, Hedgecoe (2001)

sees such a development as part of a developing

‘enlightened geneticisation’ that while allowing the

environment (individual and social) a role, ‘constructs

it in such a way as to deny non-genetic factors decisive

control’ (p. 883, emphasis added). So, while it is

accepted, indeed emphasised, by geneticists that there

will never be a single ‘gene for’ heart disease, nor in fact

for specific conditions such as hypertension or hyperli-

pidaemia, the role of (unpredictable and non-specific)

environmental factors will always be within the context

of a (regular and specific) genetic ‘baseline’.

In conclusion, this paper has argued for the usefulness

of ANT in describing and understanding the complex-

ities of the making of scientific knowledge and in

critiquing the seeming geneticisation of heart disease.

However, ANT is limited in one crucial way: it does not

offer an explanation of these networks (Castree &

MacMillan, 2001). While the above analysis revealed the

motivations, interests and understandings of the many

actors, and the complex interconnections between them,

it said little about the politics of research, the inequal-

ities of funding and knowledge, the application of the

findings for other forms of research, the power and

financial interests involved and so on. There is a growing

unease implicit here: while it is fascinating and liberating

to reveal the social and natural actors involved, there is

no identification of the inequalities of interconnections,

the dominant role of certain social actors, the subjuga-

tion of natural actors and the broader social conse-

quences of the research outcomes, and indeed the

possibilities for change (Hetherington & Law, 2000).

Instead of dismissing ANT because of these weaknesses,

a ‘critical’ ANT could be developed that, while

recognising the many actors and networks, acknowl-

edged the powers and responsibilities of a few social

actors. Further, once the social unevenness of the

network is recognised then the uncertain and complex

nature of genetic knowledge can be reconnected to the

unequal social and spatial patterns of heart disease. As

noted at the outset of the paper, health geographers

have much to contribute to the ‘mapping’ of these

overlapping genetic and socio-spatial knowledges and

explanations of heart disease.

Acknowledgements

Many thanks to Martin, Anna, Katrina and all at the

laboratories for access, co-operation and interest. This

paper was first presented at the International Sympo-

sium of Medical Geography, in Manchester in July 2003.

The paper benefited from two excellent referees reports.

The research was funded by an Economic and Social

Research Council Research Grant R000223927.

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