The ethics of social risk reduction in the era of the biological brain
Ted Schrecker [a, *], Lisa Acosta [b], Margaret A. Somerville [a], Harold
J. Bursztajn [c]
[a] McGill Centre for Medicine, Ethics and Law, 3690 Peel Street, Montreal,
Quebec, Canada H3A1W9
[b] Rush Medical College, 1524 West Harrison, #2A, Chicago, IL 60607,
USA
[c] Program in Psychiatry and Law, Harvard Medical School, Cambridge,
MA02138, USA
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 Congre´gation, Montre´al,
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), haroldbursztajn@hms.harvard.edu
(H.J. Bursztajn).
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 insufficient 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.
Keywords: Mental illness; Prevention; Public health; Methodology; Economics;
Ethics
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 fits
well with the commitments to nonmaleficence 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 reflects 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, Mun ˜ oz 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.
[2] Now, it is obviously worthwhile to know about the
effectiveness of initiatives like the one studied in San Francisco, which
are defined 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 significant
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 highrisk 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, defi nitions
are not necessarily given, nor are they neutral in their impact on research
outcomes and policy choices. We must, the refore, be methodologically
self-conscious in formulating and applying them. One approach to definition
adopts the familiar triad of primary, se condary 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, 199 2, 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), whi
ch 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 [3] 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
care requirements 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. [4] 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 different 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. [5] 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, emphasis added).
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 difficulties of conducting randomized controlled
trials for many kinds of interventions, should evidence of reduction
in risk factors be treated as sufficient 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 insufficient 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 affect
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 defined 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. [6]
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 affect 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'. [7] 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 al., 1993; McGuffin, 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, 1997a, 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 significance 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, is likely 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 identified 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 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 selfinterest, at least at the societal level.
This is likely to be more effective than invoking considerations of beneficence
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 difficulty of valuing suffering, 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 [8] 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 fisc 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 scientific 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
fulfil 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 valuefree. 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.
Footnotes
-
For an illustration of this omission, see
Coughlin and Beauchamp (1996).
-
Just over one-third (35.1%) were white, with
African Americans (23.7%) and Latinos (24.3%) comprising the next
two largest ethnic/racial groups. "Their mean age was 52.5 years,
mean income $11, 500, and mean years of education 12.1. Their unemployment
rate was very high (67.8%)." Thirty-nine of the unemployed subjects,
or 26% of the entire sample, were unemployed by reason of disability,
and another 21 (14% of the entire sample) were looking for work.
Ninety-three of the 150 participants, or almost two-thirds, were
female (Mun˜ oz et al., 1995, pp. 202–205).
-
We explain our preference for the terminology
of feedback loops in the section titled 'The biological plausibility
of prevention'.
-
The Epidemiologic Catchment Area (ECA) study
in the United States found that African-Americans suffered from higher
historical and current incidence of mental disorder than did whites
and Hispanics. "However, this difference in rates is confounded
by socioeconomic status (SES). When SES is controlled, rates for
African-Americans are no higher than for whites" (Regier & Kaelber,
1995, p. 143). This does not mean that race is unrelated to mental
disorder; it simply means that the effects of race may be mediated
by the all-too-familiar variable of race-related economic inequality.
The same may well be true for gender, disability, and age. In addition,
more sensitive and sophisticated indicators of economic situation
than conventional measures of SES are almost certainly needed for
purposes of further research.
-
Critiques of placebo-controlled trials of
antipsychotic medications can be found in Freedman, Weijer, and Glass
(1996b) and Freedman, Glass, and Weijer (1996a). For defences and
replies see Addington (1995) and Carpenter, Schooler, and Kane (1997).
-
As noted above (footnote 3) quarter of the
entire San Francisco sample were out of work because of disability.
On the circuitous and demanding procedure for obtaining federal disability
benefits see Gellhorn (1995).
-
Thus Kendler (1997, p. 7) has remarked on
geneticists' tendency "to define the environment as 'things
that get in the way of gene expression' ".
-
On the importance of "intuitive dissatisfaction" as
an ethical resource see Nagel (1991, p. 7).
References
-
Addington, D. (1995). The use of placebos in clinical trials for
acute schizophrenia. Canadian Journal of Psychiatry, 40, 171–176.
-
Albee, G. (1996). Revolutions and counterrevolutions in prevention.
American Psychologist, 51, 1130–11 33.
-
Avorn, J. (1984). Benefit and cost analysis in geriatric care: Turning
age discrimination into health policy. New England Journal of
Medicine, 310, 1294–1301.
-
Beauchamp, T., & Childress, J. (1994). Principles of biomedical
ethics (4th ed). New York: Oxford University Press.
-
Bebbington, P., & Kuipers, L. (1993). Social causation of schizophrenia.
In D. Bhugra, & J. Leff, Principles of social psychiatry (pp. 82–98).
Oxford: Blackwell.
-
Bowman, M. (1999). Individual differences in posttraumatic distress:
problems with the DSM-IV model. Canadian Journal of Psychiatry,
44, 21–33.
-
Breakey, W. (1996). Prevention. In W. Breakey, Community mental health
services (pp. 323–336). New York: Oxford University Press.
-
Bremner, J., Randall, P., Scott, T., Bronen, R., Seibyl, J., Southwick,
S., Delaney, R., McCar thy, G., Charney, D., &
Innis, R. (1995). MRI based measurement of hippocampal volume in
patients with combat-related PTSD. American Journal of Psychiatry,
152, 973–981.
-
Brenner, H., Hodel, B., Genner, R., Roder, R., & Corrigan, P. (1992).
Biological and cognitive vulnerability factors in schizophrenia:
Implications for treatment. British Journal of Psychiatry, 161(Suppl.
18), 154–163.
-
Brown, G. (1997). A psychosocial perspective on the aetiology of
depression. In A. Honig, & H. M. van Praag, Depression: Neurobiological,
psychopathological and therapeutic advances (pp. 343–362). Chichester:
Wiley.
-
Brown, S. (Ed.). (1998). Prenatal care: Reaching mothers, reaching
infants. Committee to Study Outreach for Prenatal Care, Institute
of Medicine. Washington, DC: National Academy Press.
-
Capponi, P. (1999). The war at home: An intimate portrait of Canada's
poor. Toronto: Viking.
-
Carpenter, W., Schooler, N., & Kane, J. (1997). The rationale and
ethics of medication-free research in schizophrenia. Archives of
General Psychiatry, 54, 401–407.
-
Cohen, C. (1993). Poverty and the course of schizophrenia: Implications
for research and policy. Hospital and Community Psychiatry, 44,
951–958.
-
Cooper, Z., & Paykel, E. (1993). Social factors in the onset and
maintenance of depression. In D. Bhugra, & J. Leff, Principles of
social psychiatry (pp. 99–121). Oxford: Blackwell.
-
Coughlin, S., Beauchamp, T. (Eds.). (1996). Ethics and epidemiology.
New York: Oxford University Press.
-
Dohrenwend, B., Levav, I., Shrout, P., Schwartz, S., Naveh, G., Link,
B., Skodol, A., & Stueve, A. (1992). Socioeconomic status and
psychiatric disorders: The causation-selection issue. Science,
255, 946–952.
-
Edin, K., & Lein, L. (1997). Making ends meet: How single mothers
survive welfare and low-wage work. New York: Russell Sage Foundation.
-
Ehrenreich, B. (1999). Nickel-and-Dimed: On (not) getting by in America.
Harper's Magazine, 298, 37–52.
-
Eisenberg, L. (1986). Mindlessness and brainlessness in psychiatry.
British Journal of Psychiatry, 148, 499–508.
-
Eisenberg, L. (1992). Child mental health in the Americas: A public
health approach. Bulletin of the Pan-American health Organization,
26, 230–241.
-
Eisenberg, L. (1995). The social construction of the human brain.
American Journal of Psychiatry, 152, 1563–1575.
-
Eisenberg, L. (1997). Psychiatry and health in low-income populations.
Comprehensive Psychiatry, 38, 69–73.
-
Eley, T., & Plomin, R. (1997). Genetic analyses of emotionality.
Current Opinion in Neurobiology, 7, 279–284.
-
Evans, R. (1993). Ethical ambiguities and economic consequences in
the allocation of health care. In B. Dickens, & M. Ouelette,
Health care, ethics and law (pp. 46–58). Montre´ al: Les Edition
Themis.
-
Evans, R., & Stoddart, G. (1990). Producing health, consuming health
care. Social Science and Medicine, 31, 1347–13 63.
-
Faraone, S. V., Tsuang, M. T., & Tsuang, D. W. (1999). Genetics
of mental disorders: Aguide for students, clinicians, and researchers.
New York: Guilford Press.
-
Farley, M., Baral, I., Kiremire, M., & Sezgin, U. (1998). Prostitution
in five countries: Violence and post-traumatic stress disorder. Feminism
and Psychology, 8, 405–426.
-
Farley, M., & Barkan, H. (1998). Prostitution, violence, and posttraumatic
stress disorder. Women and Health, 27, 37 –49.
-
Fleming, A. S., O'Day, D. H., & Kraemer, G. W. (1999). Neurobiology
of mother–infant interactions: Experience and nervous system plasticity
across development and generations. Neuroscience and Biobehavioral
Reviews, 23, 673–685.
-
Francis, D., Diorio, J., Liu, D., & Meaney, M. J. (1999). Nongenomic
transmission across generations of maternal behavior and stress responses
in the rat. Science, 286, 1155–1158.
-
Freedman, B., Glass, K., & Weijer, C. (1996a). Placebo orthodoxy
in clinical research II: Ethical, l egal and regulatory myths. Journal
of Law, Medicine and Ethics, 24, 252–259.
-
Freedman, B., Weijer, C., & Glass, K. (1996b). Placebo orthodoxy
in clinical research I: Empirical and methodological myths. Journal
of Law, Medicine and Ethics, 24, 243–251.
-
Funiciello, T. (1993). Tyranny of kindness. New York: Atlantic Monthly
Press.
-
Gellhorn, G. (1995). Disability and welfare reform. Fordham Urban
Law Journal, 22, 961–1008.
-
Greenfield, S., & Shore, M. (1995). Prevention of psychiatric disorders.
Harvard Review of Psychiatry, 3, 115–129.
-
Guy, K. (Ed.). (1997). Our promise to children. Ottawa: Canadian
Institute of Child Health.
-
Heller, K. (1996). Coming of age of prevention science. American
Psychologist, 51, 1123–1127.
-
Hertzman, C., & Wiens, M. (1996). Child development and long-term
outcomes: A population health perspective and summary of successful
interventions. Social Science and Medicine, 43, 1083–1095.
-
Hiday, V. (1997). Understanding the connection between mental illness
and violence. International Journal of Law and Psychiatry, 20,
399–417.
-
Hopper, K. (1996). Regulation from without: The shadow side of coercion.
In D. Dennis, & J. Monahan, Coercion and aggressive community
treatment (pp. 197–212). New York: Plenum.
-
Kamerman, S. (1995). Gender role and family structure changes in
the advanced industrialized west. In K. McFate, R. Lawson, & W.
J. Wilson, Poverty, inequality and the future of social policy
(pp. 231–256). New York: Russell Sage Foundation.
-
Kendler, K. (1995). Genetic epidemiology in psychiatry: Taking both
genes and environment seriously. Archives of General Psychiatry,
52, 895–899.
-
Kendler, K. (1997). The genetic epidemiology of psychiatric disorders:
A current perspective. Social Psychiatry and Psychiatric Epidemiology,
32, 5–11.
-
Kendler, K., Kessler, R., Walters, E., MacLean, C., Sham, P., Neale,
M., Heath, A., & Eaves, J. (1995). Stressful life events, genetic
liability and onset of an episode of major depression in women.
American Journal of Psychiatry, 152, 833–842.
-
Kraemer, G., & Clarke, S. (1996). Social attachment, brain function,
and aggression. Annals of the New York Academy of Sciences, 794,
121–135.
-
Krieger, N., & Zierler, S. (1996). What explains the public's health?.
Acall for epidemiologic theory. Epidemiology, 7, 107–109.
-
Kuhn, T. (1970). The structure of scientific revolutions (2nd ed).
Chicago: University of Chicago Press.
-
Longino, H. (1990). Science as social knowledge: Values and objectivity
in scientific inquiry. Princeton, NJ: Princeton University Press.
-
Lyons, M., Goldberg, J., Eisen, S., True, W., Tsuang, M., Meyer,
J., & Henderson, W. (1993). Do genes influence exposure to trauma?
A twin study of combat. American Journal of Medical Genetics,
48, 22–27.
-
Mann, J. (1997). Medicine and public health, ethics and human rights.
Hastings Center Report 27, no. 3, May–June, 6–13.
-
McGuffin, P., Owen, M., & Farmer, A. (1995). Genetic basis of schizophrenia.
The Lancet, 346, 678–682 .
-
McMichael, A. (1995). The health of persons, populations and planets:
Epidemiology comes full circle. Epidemiology, 6, 633–636.
-
Mrazek, P., & Haggerty, R. (Eds.). (1994). Reducing risks for mental
disorders: Frontiers for preventive intervention research. Committee
on Prevention of Mental Disorders, Institute of Medicine. Washington,
DC: National Academy Press.
-
Mun˜oz, R., Ying, Y., Bernal, G., Pe´rez-Stable, E., Sorensen, J.,
Hargreaves, W., Miranda, J., & Miller, L. (1995). Prevention
of depression with primary care patients: A randomized controlled
trial. American Journal of Community Psychology, 23, 199–222.
-
Myhrman, A., Rantakallio, P., Isohanni, M., Jones, P., &
Partanen, U. (1996). Unwantedness of a pregnancy and schizophrenia
in the child. British Journal of Psychiatry, 169, 537–540.
-
Nagel, T. (1991). Equality and partiality. New York: Oxford University
Press.
-
Nazroo, J., Edwards, A., & Brown, G. (1997). Gender differences
in the onset of depression following a shared life event: A study
of couples. Psychological Medicine, 27, 9–19.
-
Nelkin, D. M., & Lindee, S. (1995). The DNAmystique: The gene as
a cultural icon. New York: W.H. Freeman.
-
Nelson, C. A., & Bloom, F. E. (1997). Child development and neuroscience.
Child Development, 68, 970–987.
-
Norman, R., & Malla, A. (1993). Stressful life events and schizophrenia
I: A review of the research. British Journal of Psychiatry, 162,
161–166.
-
Offord, D., Kraemer, H., Kazdin, A., Jensen, P., & Harrington, R.
(1997). Lowering the burden of suffering from child psychiatric disorder:
Trade-offs among clinical, targeted and universal interventions.
Program in Human Development Working Paper No. 30, Canadian Institute
for Advanced Research, Toronto.
-
Paris, J. (1999). Does stress cause posttraumatic stress disorder?
(Editorial). Canadian Journal of Psychiatry, 44, 20.
-
Pearce, N. (1996). Traditional epidemiology, modern epidemiology,
and public health. American Journal of Public Health, 86, 678–683.
-
Pinker, S. (1997). How the mind works. New York: W.W. Norton.
-
Pitman, R. (1997). Overview of biological themes in PTSD. Annals
of the New York Academy of Sciences, 821, 1–9.
-
Regier, D., & Kaelber, C. (1995). The epidemiologic catchment area
(ECA) program: Studying the prevalence and incidence of psychopathology.
In M. Tsuang, M. Tohen, & G. Zahner, Textbook in psychiatric epidemiology
(pp. 135–155). New York: Wiley.
-
Remington, R. D. (Ed.) (1988). The future of public health, Committee
on the Future of Public Health, Institute of Medicine. Washington,
DC: National Academy Press.
-
Rutter, M., Dunn, J., Plomin, R., Simonoff, E., Pickles, A., Maughan,
B., Ormel, J., Meyer, J., & Eaves, L. (1997). Integrating nature
and nurture: Implications of person– environment correlations
and interactions for developmental psychopathology. Development
and Psychopathology, 9, 335–364.
-
Scarr, S. (1992). Developmental theories for the 1990s: Development
and individual differences. Child Development, 63, 1–19.
-
Scarr, S. (1993). Biological and cultural diversity: The legacy of
Darwin for development. Child Development, 64, 1333–1353.
-
Somerville, M. (1986). Should the grandparents die? Allocation of
medical resources with an aging population. Law, Medicine and
Health Care, 14, 158–163.
-
Somerville, M. (1989). Weaving 'birth' technology into the 'value
and policy web' of medicine, ethics and law: Should policies
on 'conception' be consistent?. Nova Law Review, 13, 515–608.
-
Somerville, M. (1993). The song of death: The lyrics of euthanasia.
Journal of Contemporary Health Law and Policy, 9, 1–76.
-
Somerville, M. (1999). The ethics and law of access to new cancer
treatments. Current Oncology, 6, 161–174.
-
Suomi, S. (1997a). Early determinants of behaviour: Evidence from
primate studies. British Medical Bulletin, 53, 170–184.
-
Suomi, S. (1997b). Long-term effects of different early rearing experiences
on social, emotional, and physiological development in nonhuman
primates. In M. Keshavan, &
R. Murray, Neurodevelopment and adult psychopathology (pp. 104–116).
Cambridge: Cambridge University Press.
-
Suomi, S., & Levine, S. (1998). Psychobiology of intergenerational
effects of trauma: Effects from animal studies. In Y. Danieli, International
handbook of multigenerational legacies of trauma (pp. 605–619). New
York: Plenum.
-
Tsuang, M., & Faraone, S. (1994). The genetic epidemiology of schizophrenia.
Comprehensive Therapy, 20, 130–135.
-
Valenstein, E. (1998). Blaming the brain: The truth about psychiatric
drugs. New York: Free Press.
-
van der Kolk, B. (1994). The body keeps the score: Memory and the
evolving psychobiology of posttraumatic stress. Harvard Review
of Psychiatry, 1, 253–265.
-
Ware, N., & Goldfinger, S. (1997). Poverty and rehabilitation in
severe psychiatric disorders. Psychiatric Rehabilitation Journal,
21, 3–9.
-
Yehuda, R., Giller, E., Southwick, S., Lowy, M., & Mason, J. (1993).
Hypothalamic pituitary adrenal dysfunction in posttraumatic stress
disorder. Biological Psychiatry, 30, 1031–1048.