The ethics of social risk reduction in the era of the biological brain
Ted Schreckera, Lisa Acostab,Margaret A. Somervillea,
Harold J. Bursztajn McGill Centre for Medicine, Ethics and Law, 3690 Peel
Street, Montreal, Quebec, Canada H3A1W9 (This article is dedicated, with deep
respect and a sense of great loss,to the late Jonathan Mann. Among the many ways
he contributed to making the world a better place, his work in joining ethical
analysis and public health,both in theory and in practice,has given to us all a
legacy for the future. For this and much more,we are all in his debt.
*Correspondence address. 450,rue de la Congregation, Montreal, Quebec, Canada
H3K 2H7. Fax: 514-932-5230. E-mail addresses: tschrecker@sympatico.ca (T.
Schrecker), lacosta@rushu.rush.edu (L. Acosta),somerville @falaw.lan.mcgill. ca
(M.A. Somerville), harold_bursztajn@hms.harvard.edu (H.J. Bursztajn).
Rush Medical College, 1524 West Harrison, #2A, Chicago, IL 60607,
USA Program in Psychiatry and Law, Harvard Medical School, Cambridge, MA
02138, USA
Abstract
In keeping with our transdisciplinary orientation,in this article we
try to do several things at once. We address research on preventing mental
illness and its relation to existing conceptions of public health, a topic to
which insuficient attention has been paid in the era of the biological brain,
while using this case study to illustrate the limits of conventional approaches
in bioethics. After identifying the crucial need for methodological
self-consciousness in prevention research and policy, we explore the
implications as they relate to (i) the values embedded in the choice of research
designs and strategies, and (ii) contrasting intellectual starting points
regarding the biological plausibility of preventing mental illness. We then draw
attention to the need for more thoughtful analysis of the appropriate role and
limits of economics in making choices about prevention of mental illness. # 2001
Elsevier Science Ltd. All rights reserved.
Introduction
The chapter on prevention in a recent text on mental health planning
begins: ''The proposition that it is better to prevent illness than to allow it
to occur with its associated suffering, loss of function, and need for
treatment, is one of the basic premises of public health that requires no
justification'' (Breakey,1996,p. 323). Public health as a profession and a field
of inquiry is undeniably organized around the premise that prevention is
valuable; thus, the substance of public health has been defined as ''organized
community efforts aimed at the prevention of disease and the promotion of
health'' (Remington 1988,p. 41). Attaching high priority to prevention also its
well with the commitments to nonmalficence and beneficence that are widely
acknowledged as central principles of bioethics (Beauchamp & Childress,1994,
pp. 189-325). However, few propositions in public health or public policy
require no justification. This point is particularly evident in the literature
on preventing mental illness, where the case for preventive interventions is
often made primarily on economic grounds. Implicit in this argument, if seldom
acknowledged or defended, is the premise that allocations of resources to
prevention require justification,and some do not make the grade.
This is a normative proposition; it can be neither established nor
refuted on scientific grounds. In this respect as in several others,the
prevention of mental illness raises complex ethical issues at the interface of
science, public policy,law and clinical practice. Such issues have not been
fully addressed in contemporary bioethics because of the field's preoccupation
with two particular frames: the clinical frame, in which ethical analysis is
organized around physician-patient relationships, and the human subjects
research frame, in which analysis is organized around researcher-subject
relationships. In each case, the focus is on relations and transactions among
individuals. In this article we explore several clusters of issues surrounding
prevention, public health and mental illness, focusing not on individuals but
rather on how the biological and biomedical approaches that dominate research on
mental illness have distracted attention from public health as the project of
''assuring the conditions in which people can be healthy'' (Remington 1988,p.
40; Mann, 1997,p. 7). Our approach insists that ethical analysis must be
expanded to include issues and choices that arise in the choice of research
methodologies and strategies themselves. Although critiques of the ideal of
value-free research are nothing new,the implications of such critiques as
applied to research on the etiology and prevention of mental illness have not
been adequately explored.
Central to this argument is the importance of what Shrader-Frechette and
McCoy (1993,pp. 84-101), drawing on the work of Helen Longino (1990),have called
methodological value judgments. This concept re.ects the earlier insight of
Thomas Kuhn (1970,pp. 199-200) concerning the impossibility of any ''neutral
algorithm for theory-choice''. It does not mean there is anything unscientific
about such choices,and identifying them does not imply that the scientists who
make them are doing bad science,or conducting themselves unethically. Indeed, .
. . scientists make methodological value judgments whenever they follow one
methodological rule,rather than another. For example, whenever one uses a
particular research design because of available computer software,one is making
a methodological value judgment that the research design is adequate. . . . Even
collecting data requires use of methodological value judgments because one must
make evaluative assumptions about what data to collect and what to ignore,how to
interpret the data,and how to avoid erroneous interpretations. (Shrader-
Frechette and McCoy,1993,p. 84)
For example, a cross-sectional questionnaire survey used to study the
relation between homelessness and serious mental illness will yield a different
kind of result from that obtainable by way of a longitudinal ethnography, and
those differences will persist even if each study is a paragon of methodological
rigour on its own terms. Like the choice to make the case for preventive
interventions primarily on economic grounds, the choice of methodologies is not
exclusively a scientific one. Neither, however, is it merely a matter of
opinion; the value judgments embedded in the choice among possible research
designs and strategies must reflect the same intellectual rigour as the actual
conduct of research, whether conducted in the laboratory or in the field.
Central to our argument, as well, is the inadequacy of some conceptions of
prevention when assessed against the demands of ''assuring the conditions in
which people can be healthy''. An important,and increasingly widespread set of
methodological value judgments limits the universe of measures to achieve this
goal, as it applies to mental illness, by circumscribing the range of research
designs whose results are considered credible. Consequently, we suggest that
discussions of public health and mental illness should refer not only to
prevention,but also (and in some instances preferably) to social risk reduction.
This position reflects an increasingly broad acceptance of the importance of
social determinants of health (Evans & Stoddart,1990), but it is
controversial because it implies at least provisional acceptance of a connection
between the social environment and mental illness that some would view as
unproved,or even ideological (Heller,1996,p. 1124). Conversely,the provisional
rejection of that connection can likewise be regarded as ideological
(Albee,1996).
Our approach emphasizes the importance of transdisciplinarity and
methodological pluralism, but goes further in terms of identifying the central
importance of methodological self-consciousness. Certain background assumptions
(Longino,1990,pp. 59-61,108-112,117- 121,133-161) about how the world works are
unavoidably embedded in the choice of research designs and strategies, and in
other areas of the public health enterprise. These assumptions may have
significant ethical implications when they are embodied in research leading to
findings that are subsequently regarded as authoritative, whether in clinical
practice or in public policy. Our position also implies the need for engagement
with macro-level debates about at least some aspects of social
policy,particularly with respect to such initial presumptions
(Somerville,1989,p. 539; 1993,pp. 64-68) as those having to do with the
appropriate role of economic analysis in public health. Since interventions
aimed at reducing the incidence or the destructive consequences of mental
illness will probably involve substantial allocations of societal resources,as
they have historically done in other areas of public health,a direct encounter
between ethics and public policy is unavoidable, and indeed should be welcomed.
Prevention Research: Values in Research Design
Recent research on preventing mental illness reflects the drift in
contemporary epidemiology away from determinants of population health,and toward
a focus on individuals within a high-risk population. Lost in that shift are
important questions about why populations differ in health status (Krieger &
Zierler,1996; McMichael, 1995; Pearce, 1996), and about the connections between
those differences and the social determinants of health. The shift reflects an
important methodological value judgment,and underscores the importance of our
earlier discussion of this topic. In terms of the conclusions that follow for
purposes of trying to prevent mental illness, there is an important difference
between asking why certain individuals in a high-risk population suffer from a
particular disorder and asking why the incidence of the disorder is much higher
in particular populations.
An especially dramatic contrast emerges from two lines of research on
PTSD. Whereas research on PTSD among prostitutes documents an incidence that is
higher than some studies have found among combat veterans (Farley &
Barkan,1998; Farley,Baral, Kiremire,& Sezgin,1998), a recent article and an
accompanying editorial in the Canadian Journal of Psychiatry (Bowman, 1999;
Paris, 1999) ask instead why some people appear relatively invulnerable to PTSD,
and emphasize the potential significance of hereditary differences in
susceptibility. As in research on other potentially disabling mental disorders,
it is important to ask both why so many members of a population develop the
disorder and why some do not. Each set of questions is important, but the choice
to organize research primarily or exclusively around one or the other embodies a
methodological value judgment of some importance. The need to scrutinize such
choices with specific attention to their ethical and policy implications,and to
the initial presumptions they embody, is not adequately emphasized in existing
approaches to ethics in public health research.1
As another example, Munoz et al. (1995), reported qualified success in a
randomized controlled trial of ''a course on cognitive behavioural methods to
gain greater control of one's mood'' as an initiative to prevent major
depression among members of a high-risk population } patients of San Francisco
outpatient primary care clinics serving low-income and minority populations.
Along almost every dimension (class, race, gender, relatively advanced age,
relatively limited education, disability) the demographics of the sample
reflected the fault lines that define economic vulnerability and marginalization
in contemporary North America. Now, it is obviously worth while to know about
the effectiveness of initiatives like the one studied in San Francisco, which
are denied with reference to the responsibilities and budgets of mental health
professionals who must work within a particular institutional framework. An
alternative research perspective,on a different scale, might ask such questions
as: were vulnerability and marginalization depressogenic at the level of the
individual subjects? How might the life events associated with low income and
economic insecurity be involved? The answers to this set of questions might in
turn suggest quite different, albeit more ambitious and longer term, directions
for preventive intervention or, to use our preferred terminology, social risk
reduction.
Several points need to be made about this example before proceeding any
further. No criticism is intended of the San Francisco project researchers, who
were acutely aware both of the special vulnerabilities associated with their
study population and of the broader background conditions against which their
study took place. Depression may be a special case, since the social and
economic risk factors are probably better established than in the case of other
major mental illnesses (Mrazek & Haggerty,1994,pp. 165-171).
Nevertheless, such factors as poverty and social disorganization may be
relevant across the spectrum of severe mental illness, especially in terms of
opportunities for what would conventionally be described as secondary or
tertiary prevention (Cohen, 1993; Hiday, 1997; Ware & Goldfinger,1997). Some
of the questions asked in the preceding paragraph can only be answered by way of
qualitative methods, preferably undertaken longitudinally. (The underutilization
of qualitative methods in mental illness research deserves discussion in a
separate article.) Finally, the example suggests a contrast between what might
be called clinical and contextual foci for prevention research. The contrast is
generically important,and one can find numerous other illustrations.
For instance, low birth weight has been identified as a general risk
factor for a variety of adverse health outcomes, including those related to
mental illness (Mrazek & Haggerty, 1994, pp. 182-183). Improving the
adequacy of prenatal care appears to be important in reducing low birth weight,
and ''lack of prenatal care has important implications for mental disorders''
(Mrazek & Haggerty,1994,pp. 222-225). At least in the United
States,inadequate prenatal care is directly related to economic
vulnerability,particularly when combined with residence in ''geographic pockets
of need'' (Brown,1988, pp. 26-53). Financial factors such as lack of insurance
and inadequate insurance coverage are the most signi.cant barriers to access to
such care (Brown,1988,pp. 54-114). Interventions to improve the life chances of
low birth weight babies (as described by Hertzman & Wiens,1996,p. 1089) and
educational programs to improve the healthrelated behaviours of pregnant women
in certain high risk groups (Mrazek & Haggerty, 1994, p. 232) thus might
have significant effects in improving health outcomes. So, for that matter,
might national health insurance on the Canadian model. None of these measures
would eliminate all obstacles to adequate prenatal care, or even all the
obstacles unequivocally related to mothers' economic situations. Each, however,
could be a necessary (although not sufficient) condition for the effectiveness
of a range of other, more targeted interventions.
What does it mean to prevent mental illness? Here as elsewhere,
definitions are not necessarily given, nor are they neutral in their impact on
research outcomes and policy choices. We must, therefore, be methodologically
self-conscious in formulating and applying them. One approach to de.nition
adopts the familiar triad of primary, secondary and tertiary prevention: primary
prevention refers to efforts to reduce a disease's rate of occurrence; secondary
prevention refers to efforts to reduce prevalence, for example through more
effective case finding; and tertiary prevention refers to efforts to reduce
severity and adverse consequences or to prevent relapse (Eisenberg, 1992, pp.
231-232; Greenfield & Shore,199 5). An alternative view was adopted in 1994
by a committee of the US Institute of Medicine (IOM) (Mrazek & Haggerty,
1994), which defined prevention strictly in terms of avoiding the initial onset
of a disorder. All interventions contributing to recovery and rehabilitation or
reducing the probability of subsequent episodes were regarded instead as
elements of treatment protocols. The success of preventive initiatives was
thereby transformed into a dichotomous variable: mental illness in any specific
individual was prevented/not prevented.
This definition has the undeniable attraction of precision, but it may be
a false precision. The approach of the IOM committee can very easily have the
effect of shrinking the universe of potential preventive interventions, in
contrast to a separate body of interventions that qualify as treatment or
rehabilitation, and which are presumably well understood. Numerous interventions
may fit clearly into neither category, yet may still be extremely important in
affecting the course of mental illness and the associated suffering. It may be
more valuable, and more consistent with public health objectives as they have
been widely recognized outside the mental health field, to think in terms of a
continuum from primary prevention through treatment and other clinical
interventions, on which the location of various dividing lines is treated as a
matter of secondary importance.
For example, for purposes of designing interventions to weaken the
feedback loops that link economic situation and major depression, consider the
frustrations and adversities experienced on a daily basis by one adult member of
a household with two income earners. Each has a relatively secure job with
negotiated sick leave provisions that make possible the occasional 'mental
health day' (a wise and revealing phrase). Then compare his situation with that
of a single mother juggling child caqEÏequirements with the demands of a job in
retail or fast-food (cf. Ehrenreich,1999) ... or worse,dealing with the
sometimes capricious demands of a social service bureaucracy (Capponi,1999; Edin
& Lein,1997; Funiciello,1993). Should interventions that ameliorate the
adversities experienced by people in this second category be considered
effective if they 'only' improve chances of rehabilitation, facilitate
adaptation or reduce the likelihood of subsequent illness-related disability?
In order to constitute prevention as defined by the IOM
committee,interventions must be demonstrably associated with reduced incidence,
or initial occurrence, of mental illness. The problem is complicated because
economic situation may affect the risk of mental illness either directly or
through a variety of intervening variables,such as community disorganization or
levels of violence. Economic situation may also be a variable that mediates the
effects of other demographic characteristics on the incidence and course of
mental illness. Further,it may be difficult to separate income-related effects
on the mental health of children and adolescents from effects on that of their
parents. Indeed, it would be surprising if this were not the case.
As a general observation,by no means confined to interventions that
address variables related to economic situation,prevention may emerge as
possible at a variety of scales or levels,with di.erent actors,obligations,and
degrees of ethical and logistical complexity involved. An ethic of public health
as applied in the mental health field might regard the question 'is it
prevention?' as distinctly secondary to the question 'does it help?' Pointing
out the importance of this distinction is valuable,in and of itself.
Standards of Proof
Health economist Robert Evans has identified an important ''asymmetry of
onus'' in the evidentiary criteria applied to prevention. Many complicated and
expensive treatments have come into widespread use despite the lack of
conclusive evidence, specifically evidence from randomized clinical trials, that
shows their benefit in terms of such outcome measures as life expectancy and
quality of life. By contrast,''in preventive health care,if we do not know,we do
not do it'' (Evans,1993,p. 55).
This observation does not imply criticism of clinicians, who may have
several good reasons to make some treatments available even in the absence of
evidence from controlled trials. Many of the available outcome measures have
important limitations. Especially with respect to psychiatric medications,an
important ethical debate continues about (a) when placebos may justifiably be
used in controlled trials, and the ethical requirements governing the design of
trials that incorporate a placebo arm,and (b) when trials must be 'unblinded' }
in other words, when patients must be informed about the kind of treatment they
are receiving and about the results of the trial so far. These are major
questions that continue to demand ethical investigation. Finally, a ubiquitous
question about evidence-based medicine and the application of practice
guidelines is the extent to which even the best designed studies at the
population level can be used,on their own, to assess the appropriateness of a
clinical intervention with respect to any individual patient.
The IOM committee demonstrated the importance of Evans' insight when it
identified randomized controlled trials,ideally repeated to test the
intervention's generalizability, as the evidentiary gold standard in prevention
research (Mrazek & Haggerty,1994,pp. 373-376). The implications for
prevention policy of setting such a high standard of proof are evident from the
report's finding that: There are data that clearly show that preventive
interventions can reduce risk factors that are associated with the onset of many
mental disorders. However,as yet,there is no evidence that preventive
interventions reduce the incidence of mental disorders (Mrazek &
Haggerty,1994, p. 298).
How should this conclusion be used as the basis for making decisions
about prevention programs and strategies? In other words, how much evidence is
enough,and what values should bear on the choice of evidentiary standards?
Keeping in mind the dificulties of conducting randomized controlled trials for
many kinds of interventions, should evidence of reduction in risk factors be
treated as suficient to justify preventive interventions, or should evidence of
the link between reduction in risk factors and reduction in the incidence of
mental illness also be required? As in the case of results from clinical trials
of new or improved therapies are involved,what are the ethical implications of
waiting for more conclusive evidence? Somerville (1999) points out that this
issue has recently arisen in Canada,where provincial authorities have claimed in
several cases that the evidence is insu.cient to justify providing reimbursement
for leading-edge cancer treatments through public health insurance plans.
No scientist or social scientist can answer such questions on the basis
of professional competence. Instead, they demand explicit attention to the
various, potentially competing values at stake and the way they a.ect key
choices that are made about research designs: identifying outcome measures;
determining the appropriate standard of proof (how much evidence is enough);
assigning the burden of proof; and selecting an appropriate scale. On this last
point, consider the fact that the smaller the scale of the intervention and the
fewer the confounding variables, the more likely it is that a controlled trial
will result in a demonstration of success. Conversely,the larger the scale of
the intervention and the more events and situations that may affect the relation
(a) between the intervention and the risk factor and (b) between the risk factor
and the outcome measure,the harder it becomes to demonstrate success.
This point can be illustrated using two hypothetical examples.
First, consider an imaginary quantitative study designed to compare
incremental interventions like the San Francisco mood control course with
interventions to alter the depressogenic background conditions that de.ned the
high-risk population. Such a study might involve three,rather than two groups of
randomly assigned subjects,with the third group not receiving the course but
being offered access to relatively more generous unemployment benefits, or a
fast-track application procedure for a higher level of disability benefits.
Second, imagine a prospective longitudinal study designed to test the
ability of social policy interventions to prevent mental illness by altering
environmental variables that now a.ect exposure to risk factors in early
childhood. Such a study might recruit pregnant,lowincome single women in the
United States through intensive outreach and then assign them randomly to one of
two groups. The control group would receive only the income supports available
since the 1996 welfare reforms, and the uneven access to prenatal and postnatal
medical care of uncertain quality that goes along with their situation. The
treatment group would be offered universal first-dollar health care coverage, as
well as a Norwegian-style package of support measures for single mothers (as
outlined by Kamerman, 1995, pp. 247-251). The mental health of the children in
both groups, and of the mothers,would then be followed through at least until
the children's adolescence. To put it mildly,the barriers confronting such
studies are formidable; they involve numerous variables that are normally
outside the control of researchers. It would be all but impossible to control
for genetic variables in the study design,thus exposing results to criticism
from evolutionary psychologists.
Conversely, even such an ambitious study might understate the effects of
economic situation on mental health } for instance,because of its inability to
control for the effects of a past history of employment discrimination, or for
the effects of economic adversity on mothers' preconception health status. We
are left with the disquieting possibility that choosing certain research
strategies and standards of proof means the big questions about preventing
mental illness probably will not be studied in ways that demonstrate the
effectiveness of larger-scale,contextual interventions, and even the small
questions will be asked in ways that seriously circumscribe the set of possible
answers.
The Biological Plausibility of Prevention
An even more far-reaching illustration of the importance of
methodological self-consciousness in the choice of research designs and
strategies involves the biological focus that now dominates published
psychiatric research, at least in North America. That orientation arguably
engenders an attitude best described as biological fatalism with respect to the
prospects for preventing mental illness. The perils of biological fatalism are
especially important when genetic 'explanations' are being advanced,given the
role of ''the gene as cultural icon'' (Nelkin & Lindee,1995) and the
popularity of evolutionary explanations for patterns of human behaviour as
diverse as mate preferences, fondness for gossip and distaste for eating worms
(Pinker,1997).
At one level, to the extent that we are biological beings all our
behaviour (like that of any other organism) can be described in terms of 'gene
expression'. However, like most tautologies this one is of severely limited
explanatory value. It is important to recall that the most sophisticated
statistical calculations often show that heredity accounts for 50% or less of
the variance in outcomes as diverse as developing schizophrenia and volunteering
for combat in Southeast Asia (Jones & Cannon,1998; Lyons et a‚EÏ993;
McGufin, Owen, & Farmer,1995; Tsuang & Faraone,1994).
Although the influence of experience on brain structure and function is
perhaps particularly evident in childhood and adolescence, it is by no means
limited to early life (Nelson & Bloom,1997). Stressful life events and
situations throughout the life course appear to play an important role in the
onset of major depression (Brown, 1997; Cooper & Paykel,1993),and probably
in the severity of schizophrenic symptoms and the timing of onset (Bebbington
& Kuipers,1993; Norman & Malla, 1993).
Generalizations about environmental change and the prevention of mental
illness are thoroughly unwise: mental illness is an imprecise 'supercategory'
(Eisenberg, 1977, p. 903) and the environmental factors that interact with an
individual's genotype may be as diverse as oxygen deprivation or inadequate
nutrition during pregnancy, central nervous system infections in childhood
(Jones & Cannon,1998,p. 19) and unwanted pregnancy (Myhrman,Rantakallio,
Isohanni,Jones,& Partanen,1996) } all of which are at least potentially
implicated as risk factors for schizophrenia. Nevertheless, it is important to
reject the presumption,which may or may not be stated explicitly, that causal
linkages run primarily from the biological substrate to subjective or
psychological experience: in other words, primarily from brain to mind. Indeed,
as contemporary brain research deepens our understanding of the physiological
processes that can be initiated or intensified by changes in the social
environment, it undermines the viability of any dichotomy between mind and brain
(Eisenberg, 1986,1995; Valenstein, 1998). When environment and genetics interact
the direction of causation is often far from self-evident; and multiple feedback
loops,both positive and negative, are involved (Kendler, 1995; Rutter et
al.,1997). Indeed, the concept of a feedback loop is little used in mental
illness research although, because of its intrinsically dynamic orientation,it
may be more precise than the currently preferred vocabulary of risk and
protective factors in describing the actual interaction of environmental
variables in and with people's lives (Eisenberg,1997, p. 69; Brenner, Hodel,
Genner,Roder, & Corrigan,1992).
For purposes of research on prevention, it is important to recognize that
environmental characteristics of concern may be experienced by everyone, or
almost everyone, in a particular society or subgroup within a society. Thus,
Jones and Cannon (1998,pp. 14,15) remark that if everyone smoked, then the
incidence of lung cancer would appear to be genetically determined. Analogously,
the incidence of any specific mental illness will appear to be genetically
determined in subgroups within a particular society that share exposure to a
particular set of social risks.
The issue here is one of how the choice of an intellectual starting point
affects the conclusions that are plausible, or even possible. Research that does
not start by according a privileged position to the background assumptions of
evolutionary biology } leading to such manifestations of genetic determinism as
the claim that children and adolescents seek out, influence or even 'create'
their environments based on genetic predispositions (see e.g. Scarr,1992,1993) }
tends to generate findings that emphasize the significance of environmental
factors, broadly defined, and that undermine neat distinctions between the
biological and the behavioural. The example of PTSD is useful because of the
dramatic illustrations it provides of the interaction between psychology and
biology (Pitman,1997; van der Kolk, 1994).
For example,a variety of neuroendocrinal abnormalities as well as smaller
hippocampal size,as documented by brain imaging,have been associated with PTSD
(Bremner et al.,1995; Yehuda, Giller, Southwick, Lowy, & Mason, 1993).
Research on the relation between stress and behaviour more generally emphasizes
the perils of simplistically assuming that genetics provides the only meaningful
account of intergenerational transmission of illness. Stephen Suomi's work on
the effects of maternal rearing practices and social environment on infant
primates (Suomi, 1997a,b; see also Kraemer & Clarke, 1996) suggests that . .
. effects of early experiences are not limited to behavioural phenomena but
instead can encompass a wide range of biological functioning. Indeed,research
with monkeys has shown that even those behavioural and physiological processes
that have highly heritable features can be substantially modified by certain
early experiences (Suomi,1997,p.181).
Suomi hypothesized three distinct nongenetic pathways for the
intergenerational transmission of the effects of traumatic stress (Suomi &
Levine,1998). Fleming, O'Day and Kraemer (1999) have described at the molecular
level the various mechanisms by which such transmission might occur, and
Francis, Diorio, Liu, and Meaney (1999) have identified and demonstrated the
operation of one such mechanism across generations of rats. The implications for
the etiology of mental illness in human populations are, to say the least,
provocative when we consider the evidence for familial transmission of such
effects.
Apart from the specific case of PTSD, heredity's contribution to the risk
for such conditions as major depression and schizophrenia is well established,
as is the substantial genetic contribution to variability in individual
responses to stress (Eley & Plomin,1997; Kendler et al.,1995). However,the
etiological signi.- cance of stressful events and situations may be
underestimated in research designs that restrict their consideration to discrete
events occurring over a limited period of time, often less than a year, or fail
to take into account broader situational factors. For example,one British study
found that ''significant involvement in domestic roles'' by men in a household
apparently acted as a protective factor against depression when a shared crisis
involving ''children,housing and reproduction'' confronted both members of a
couple. When the household was characterized by a pronounced genderbased
division of labour, on the other hand, women were five times as likely as men to
experience a depressive episode (Nazroo,Edwards,& Brown,1997).
Adversities that are related to economic situation constitute another
broad category of such situational factors. It could be argued that such a
longer-range perspective invites confusion about causation. In other words, do
disorders like schizophrenia or depression result in a 'downward drift' into
life situations where adversities are more frequent? They almost certainly do,
although the relative plausibility of downward drift and an alternative
explanation,in which the environmental factors associated with social and
economic disadvantage result in increased incidence of mental illness, i kely
to vary not only with the disorder in question (Dohrenwend et al.,1992) but
also, perhaps, with the study population.
The ethics and economics of social risk reduction Here we return to an
issue identi.ed at the start of the article. Even when the effectiveness of
preventive interventions can be demonstrated, much of the contemporary
literature suggests that the desirability of undertaking them is not
self-evident. The IOM report refers to cost effectiveness or benefit-cost ratio
as a (T. Schrecker et al. / Social Science & Medicine 52 (2001) 1677-1687
1683) criterion that should be incorporated into the design of research on
preventive interventions (Mrazek & Haggerty, 1994, pp. 240, 285,405-409). A
Canadian study of the economics of preventing mental illness among children
cites ''a need to find the optimal combination of approaches to reduce the
burden of suffering that is affordable since the costs of interventions can be
enormous, yet are balanced by the cost of the illness itself'' (Offord, Kraemer,
Kazdin, Jensen,& Harrington, 1997,p. 3, see also pp. 14-16). Such approaches
are typical of the ''social investment model'' (Hertzman & Wiens,1996, p.
1092) adopted by many advocates of preventive interventions,yet they are a long
way from the broad vision of public health identified earlier in this article.
It is probably true that ''investing in high quality social and physical
environments makes good economic sense'' (Guy,1997,p. 21),at least some of the
time. Perhaps more importantly,any credible evidence to that effect gives
advocates of preventive intervention the tactical advantage of arguing from
enlightened self interest, at least at the societal level. This is likely to be
more effective than invoking considerations of bene.- cence or protecting the
vulnerable, since such themes seem to be increasingly peripheral to the main
concerns of government. Many health economists concede the malleability of
economic analysis with respect to such issues as the definition of relevant
costs,the choice of discount rates,and the di.culty of valuing su.ering,
disability,and reductions in longevity. Indeed, for purposes of economic
analysis no value at all may be attached to the reduction of suffering per se.
Unfortunately, it is not clear how thoroughly these uncertainties are
understood by the users of the resulting numbers. For purposes of ethical
analysis it is therefore critically important to ask under what conditions,and
for what reasons, the relevant decision-makers would be justified in refusing to
support programs or interventions on the basis that they will not pay for
themselves. One can readily think of situations in which defining the rationale
for preventive interventions in economic terms is intuitively troubling and we
normally recoil from such forms of triage, at least when they are presented
explicitly, for a variety of reasons. They imply the possibility, and perhaps
the inevitability, of age discrimination (Avorn,1984; Somerville,1986), as well
as the possibility that those already vulnerable for one of many reasons will be
further disadvantaged by moving to the end of the queue for resources that would
enable them to minimize their suffering and to cope as best they can with a
variety of reduced capacities. For instance, consider a hypothetical situation
in which (a) a randomized controlled trial demonstrates the effectiveness of a
package of measures to reduce the subsequent incidence of mental illness and
other adverse outcomes among severely disadvantaged children, but (b) a cost-
benefit analysis shows a higher cost-benefit ratio,as determined with reference
to subsequent outcomes,from spending the money that would finance those measures
on further improving the situation of middle-class children who are already
relatively comfortable? Many conceptions of distributive justice fail to provide
a convincing rationale for allocations of resources that effectively increase
inequalities of situation or opportunity.
By the same token informed consent considerations, which in the context
of psychiatric genetics have appropriately been called ''the cornerstone of
ethical research and practice,'' argue against a variety of public health
research designs and practices that leave the most disadvantaged worse off.
(Faraone,Tsuang,& Tsuang, 1999,p. 231).
It must also be acknowledged that research is carried out within a social
and economic context, and research directions may be shaped by economic or
professional interests. Valenstein (1998) emphasizes this point in his
discussion of the connections between the profitability of pharmacotherapy and
the ascendancy of biological psychiatry. More generally, as
universities,granting agencies and private sources of research funding alike
come to organize their priorities around the possibilities for
commercialization,prevention research is likely to be short-changed simply
because it is difficult, if not impossible, to envision a scenario in which
intellectual property rights in findings could be asserted in a way comparable
to the routine filing of patent applications for pharmaceutical compounds or
human genetic material.
Conversely, when research on interventions with a potential for social
risk reduction might strengthen the case for a new or additional commitment of
resources, institutional responses are likely to resemble those encountered in
the case of very expensive cancer treatments (Somerville, 1999). Kim Hopper
(1996, p. 205), whose particular concern is the tension between historical
conceptions of public health and the contemporary inadequacy of services for the
homeless mentally ill,warns of:
. . . the prospect that the public fis could substitute for the common
weal as the reference point for 'harm,' such that 'wasteful' or 'excess'
spending will be seen as the functional equivalent of assault on the body
politic.
As disturbing as this prospect may be, even more disturbing is the
possibility that the values of fiscal conservatism could be cloaked in the
superficially unexceptionable guise of scienti.c conservatism. Thus, as in the
example of cancer treatments, demanding (perhaps impossibly demanding) standards
of proof may be adopted as preconditions for institutional action, because they
increase the credibility of claims that 'no benefit has been demonstrated' or,
simply, that 'nothing works'. The economies achieved by asserting such claims
may be consistent with organizational objectives, whether they involve raising
share prices or lowering public expenditures,but such objectives cannot in
themselves claim any distinctive ethical status.
Conclusion
In keeping with our transdisciplinary orientation, in this article we
have tried to do several things at once. We have done so because of the urgent
need for those involved with research on mental illness, in any capacity, to
look beyond their own specific professional competence or institutional
responsibility. Specifically, ethical inquiry in this area needs to expand
beyond its present intellectual boundaries if it is to fulfill its proper
function of embedding ethics in our approaches to mental illnesses and people
suffering from them. We have identified a number of key methodological value
judgments in contemporary research on preventing mental illness, focusing on the
possibilities for its prevention, in order to demonstrate the need for
methodological self-consciousness on the part of researchers who may be too
ready to see both their choice of research designs and the findings that result
as value-free.
And we have suggested that efforts to prevent mental illness must draw on
approaches from other areas of public health practice,where the idea of social
risk reduction is more widely accepted even if not described in those words. In
mental health as elsewhere, we are on the brink of developing a far richer and
more paradigm for both conducting and applying research. It will take courage
and humility to pursue this paradigm, and to put it into practice.
Acknowledgements
An earlier version of this article was presented at the XXIVth
International Congress on Law and Mental Health, Toronto, June 1999. All views
expressed are exclusively those of the authors.