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Negotiating the Relationship Between Addiction, Ethics, and

Brain Science

Daniel Z. Buchman

1,*

, Wayne Skinner

2,3

, and Judy Illes

1,4

National Core for Neuroethics, The University of British Columbia, Vancouver, BC, Canada

Centre for Addiction and Mental Health, Toronto, ON, Canada

Department of Psychiatry, The University of Toronto, Toronto, ON, Canada

Division of Neurology, University of British Columbia, Vancouver, BC, Canada

Abstract

Advances in neuroscience are changing how mental health issues such as addiction are understood

and addressed as a brain disease. Although a brain disease model legitimizes addiction as a

medical condition, it promotes neuro-essentialist thinking, categorical ideas of responsibility and

free choice, and undermines the complexity involved in its emergence. We propose a

‘biopsychosocial systems’ model where psycho-social factors complement and interact with

neurogenetics. A systems approach addresses the complexity of addiction and approaches free

choice and moral responsibility within the biological, lived experience and socio-historical context

of the individual. We examine heroin-assisted treatment as an applied case example within our

framework. We conclude with a discussion of the model and its implications for drug policy,

research, addiction health care systems and delivery, and treatment of substance use problems.

Keywords

mental health; neuroethics; public health; sociology

Brain Biology and Addiction

Recent advances in neuroscience provide compelling evidence to support a medical

perspective of problematic substance use and addiction (Dackis and O’Brien 2005). Despite

these developments, the science is still in its early stages, and theories about how addiction

emerges are neither universally accepted nor completely understood. Current ethical and

legal debates in addiction draw upon new knowledge about the biological and neurological

modification of the brain (Ashcroft, Campbell, and Capps 2007). Clinically, substance use

disorders

are characterized by compulsive engagement or impaired control over behaviour,

evidence of both tolerance and withdrawal, relapse despite continued harm, impairments in

social and occupational functioning, and irritability or intense cravings when a particular

substance is not directly available (American Psychiatric Association 2004).

Functional brain changes occur in response to stress and other stimuli in people who have

substance use problems. Recent neuroimaging studies suggest that people living with a drug

Correspondence Daniel Z. Buchman, National Core for Neuroethics, The University of British Columbia, 2211 Wesbrook Mall,

Koerner S124, Vancouver, BC V6T 2B5 CANADA, Tel: 604.822.0748, Fax: 604.827.5229, [email protected].

The DSM-IV-TR differentiates between Substance Dependence and Substance Abuse. In this paper we use the term “substance use

disorder” or “addiction” to refer to both the complex nature of severe substance dependence and substance abuse.

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Published in final edited form as:

AJOB Neurosci

. 2010 January ; 1(1): 36–45.

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addiction have considerable decreases in dopamine D2 receptors and in dopamine release

(Volkow, Fowler, Wang, Baler, and Telang 2009), which may contribute to both the

rewarding properties of substances and difficulties in abstaining despite adverse

consequences. Brain areas such as the prefrontal cortex have been identified as being

directly involved in assessing the reward potential of decision-making (Bechara and

Damasio 2002; Dom, Sabbe, Hulstijn, and Van Den Brink 2005), and vulnerability to

relapse. Abnormal hippocampus and anterior cingulate functioning is associated with

challenges in the ability to cope with stress, in addition to problems in cognition (Kaufman,

Ross, Stein, and Garavan 2003) such as salience, inhibitory control, motivation, memory,

and learning (Hyman 2005). Increased activation of the dorsal striatum has been linked with

a vulnerability to strong cravings (Sinha and Li 2007). In addition to the recent studies that

are investigating neurogenetic contributions to a vulnerability to addiction (Uhl, Drgon,

Johnson, and Liu 2009), arguments have been made for a somatic marker theory of

addiction (Verdejo-Garcia and Bechara 2009).

A neurobiological perspective has the potential to provide many benefits to people with

addiction in terms of psychopharmacological and other treatment options. However purely

reductive, neurobiological explanations of addiction occlude a comprehensive understanding

of the added influence of psychological, social, political, and other factors. The view of

addiction as primarily a brain disease (Leshner 1997) disregards the extensive body of

research that suggests neurogenetic explanations of mental illness contribute to negative

perceptions towards people with mental illness and substance use problems (Dietrich,

Matschinger, and Angermeyer 2006; Read, 2007; Read, Haslam, Sayce, and Davies 2006).

This view is problematic as individuals living with an addiction are highly stigmatized. The

brain disease model further implies simplistic categorical ideas of responsibility, namely that

addicted individuals are unable to exercise any degree of control over their substance use

(Caplan 2006, 2008). This kind of “neuro-essentialism” (Racine, Bar-Ilan, and Illes 2005)

may bring about unintentional consequences on a person’s sense of identity, responsibility,

notions of agency and autonomy, illness, and treatment preference.

We argue therefore for a biopsychosocial systems model of, and approach to, addiction in

which psychological and sociological factors complement and are in a dynamic interplay

with neurobiological and genetic factors. As Hyman (2007) has written, “neuroscience does

not obviate the need for social and psychological level explanations intervening between the

levels of cells, synapses, and circuits and that of ethical judgments” (p.8). Since the so-

called brain disease model of addiction does not resolve the volitional nature of substance

use completely, a biopsychosocial systems approach attempts to contextualize the

individual, thus providing a model to better understand both responsibility and self in

addiction.

This paper builds on the conceptual foundations of Hyman’s (2007) contribution on

addiction and voluntary control, and extends the thinking to include perspectives that

include, but also go beyond, neuroscience.

Psycho-Social Systems

Psycho-social systems are concrete entities or groups whose members act in relation to each

other, such as families, religious organizations, and political parties (Bunge 2004). Social

processes in addiction are investigated by examining social categories such as networks,

groups, organizations and subcultures that alone cannot be explained by neurobiology.

Addiction consists of interacting biological and psychosocial mechanisms because the

mechanism (e.g., the behaviour) contributing to addiction involves action within a social

system. The larger societal structure either restricts or enhances interactions between agents

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in a social system (Bunge 1997). Such actions require explanations at both the systemic and

individual levels.

Every learned action, whether pro-social or anti-social, may be prompted by social

conditions such as a lack of resources, conflict, social norms, peer pressure, an underlying

drive (e.g., hunger, sex, craving), or a combination of these factors (Bunge 1997).

Addiction-related behaviours affect the health of both individuals and communities, either

protectively or harmfully. The behaviours influence the extent an individual is able to

mobilize and access resources to achieve goals and adapt to adverse situations (Raphael

2004). For example, an individual’s socioeconomic status is correlated with increased

negative consequences from substance use, such as increased sharing of used injecting

equipment and higher prevalence rates of Human Immunodeficiency Virus (HIV) and

hepatitis C (Strike, Myers, and Millson 2004).

There are several processes that actively contribute to substance use with inputs and outputs

on biological and psycho-social levels. One example is drug craving that may be

experienced as strong, intense urges for immediate gratification that may impair rational

thought about future planning (Elster and Skog 1999). Cravings can be cue-elicited by

environmental stimuli (Childress, Mozely, McElgin et al. 1999; Loewenstein 2000), and

continued exposures to environmental stimuli may instigate a perpetual cycle of cravings

and possibly irreversible brain changes that can occur long after an individual has become

abstinent. Factors such as drug availability within the environment can increase craving and

consequently the vulnerability for relapse (Weiss 2005). Recent research has suggested that

enriched environments produce long-term neural modifications that decrease neural

sensitivity to morphine-induced reward (Xu, Hou, Gao, He, and Zhang 2007). Accordingly,

the social environment can increase the frequency of cravings, which may contribute to

increased drug consumption, and thus increase the probability that affected individuals will

participate in a series of habituated behaviours that facilitate using (Levy 2007b).

Rates of substance use and dependence vary across, and even within, cultural and social

groups (Wallace 1999; Wallace, Bachman, O’Malley et al. 2002). Factors such as

availability and peer modeling account for the inter- and intra-group disparities (Thomas

2007). These factors may indicate a certain level of group risk for problematic substance

use, but cannot verify either the likelihood of substance use occurring within the group or

which individuals within the group are more likely to be affected. These factors are not

inherent in the composition of the social structure, are neither stable nor persistent, but are

governed by the social values and norms of that social system or group (Bunge 2003).

Social norms regulate behaviour and may act as informal mechanisms of social control.

Social groups construct norms that affect individual behaviour, prevalence, and substance

use patterns. Group membership in which substance use is socially acceptable, encouraged,

or perhaps coerced is significantly associated with patterns of use (Lauer and Lauer 2002).

Group norms around social acceptance of substance use dictate variance in consumption

rates among diverse ethnic and cultural groups (Caetano and Clark 1998). It is these

systemic features that give individuals, in part, motives for action.

Both social norms and laws influence attitudes, perceptions, and beliefs of the effects of

substances and considerably affect consumption rates (Babor, Caetano, Casswell et al. 2003;

Hawkins, Catalano, and Miller 1992). Proponents of a ‘war on drugs’, for example, believe

that laws and policies that are lenient towards substance use are linked with greater

prevalence of use and criminal activity. However, research findings have not confirmed this

claim. In one study comparing cannabis use in San Francisco (where cannabis is

criminalized) and Amsterdam (de facto decriminalization), there was no evidence to support

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claims that criminalization laws reduce use or that decriminalization increases use. In fact,

San Francisco reported a higher cannabis use rate than Amsterdam (Reinarman, Cohen and

Kaal 2004).

Shifts in norms and laws can propel changes in behaviours associated with substance use

and the prevalence of substance misuse (Hawkins et al. 1992). An example of a profound

shift that has occurred since the latter part of the 20th century is tobacco use and a dramatic

decline in smoking rates (Health Canada 2007). Progress in the understanding of the

pharmacokinetics and pharmacodynamics of nicotine addiction has led to interventions that

have helped many individuals curb smoking behaviour. However, the full understanding of

these normative shifts includes not just the development of medical interventions for

smoking cessation, but also the powerful social and public health efforts to destabilize

smoking behaviour. Therefore, smoking has become less acceptable as a normative method

of social interaction.

Neuroethics and the Brain Disease Model

Long-standing debates concerning the moral status of addiction have arisen from one of two

perspectives: either addiction is a disease of the brain, or addiction is a matter of weak will.

The former absolves responsibility and the latter condemns the person, and thus

distinguishes between deontological and utilitarian positions. Supporters of the brain disease

model cite recent neuroscience research wherein addiction is ontologically reducible to the

level of brain cells (Dackis and O’Brien 2005; Volkow and Li 2005). The claim is that a

brain disease paradigm will decrease stigma associated with addiction, which should

increase access to the health care system. Those inclined to the moral stance see drug use as

an intentional, often criminal, act: the “person, not his autonomous brain, is the instigator of

relapse and the agent of recovery” (Satel 1999, p.861). Other authors take a somewhat

different approach, and conceptualize addiction as a “pleasure-oriented desire” (Foddy and

Savulescu 2006, 2007), skeptical that the continued medicalization of addiction will obviate

all responsibility for behaviours associated with drug use.

Substance Use, Autonomy and Decision-making

Discussions on the relationship between autonomy and decision-making capacity in addicted

persons have received much attention recently in the neuroscience, law, and bioethics

literature (Andreou 2008; Burns and Bechara 2007; Caplan 2006, 2008; Carter and Hall

2008a, 2008b; Hall, Capps, and Carter 2008; Levy 2006, 2007a; Morse 2007). These

writings have raised questions about the autonomy of people with addictions, their ability to

make a free, un-coerced choice, and the extent to which they possess mental competence to

consent to research (Carter and Hall 2008a, 2008b; Charland 2002, 2003; Dehue 2002; Hall,

Carter and Morely 2003a, 2003b). The view that people with addictions lack decision-

making capacity is supported by research in both addiction neuroscience and the

neuroscience of decision-making. For example, in non-addicted persons, studies have

demonstrated that unconscious brain activation directs behaviour and, consequently, action

may not be consciously controlled (Haggard 2008; Soon, Brass, Heinze, and Haynes 2008;

Wegner 2002). This view, effectively, undermines intentional self-determination. For

addiction, a causal neuroscientific model reinforces notions of a diseased brain. The model

suggests that substance use hijacks voluntary brain mechanisms and renders individuals

incapable of making rational decisions (Miller and Carroll 2006). These perspectives imply

a causal neurophilosophical model of decision-making and action, one that has been

critiqued by Gillett (2009). He describes the following trajectory of S_ BE1 _ BE2 _

Output, where:

• “S is the stimulus conditions provoking a decision or action

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• BE1 is the unconscious brain events preceding an action/decision

• BE2 is the conscious brain event (complex) or intention causing an action/decision

• Output is a bodily movement or a decision” (p. 332).

Gilllett argues that the causal model is based on a faulty account of human autonomy and

consciousness and is scientifically and conceptually questionable. Gillett challenges the

neurophilosophical model of human decision-making, which, as he has previously argued

(2008a), emphasizes selfishness, and “constricts the scope of reason so that it is subject to

any desire or disposition that one happens to endorse at the time one acts” (p. 1215). Gillett

criticizes theories of decision-making that conceptualize choice as autonomous phenomenon

only if inner mental states or networks cause it.

While making a decision is itself a mental act, a mental act or event does not cause

behaviour alone, but is one part of the complex process between neuronal firing and action.

Once an intention has been formed for example, to use substances one is aware of the

intention, though intention itself does not sufficiently cause the individual to seek out or use

drugs. Other factors are at play. From a neuroscience perspective, it is difficult to see such

actions as completely free, particularly when explanations of natural phenomena are

understood as causally ordered. The notion of free choice becomes particularly troublesome

due to the conscious experience of acting freely. As Searle (2004) argues, “there is a striking

difference between the passive character of perceptual consciousness and the active

character of what we might call ‘volitional consciousness’“ (41).

Action, subjective experience of action, and consequently responsibility for action is

mediated by many factors, including psychological phenomenon such as an individual’s

emotional processes. As a point of illustration, Damasio’s (1994) somatic marker hypothesis

(SMH) provides a helpful perspective on integrating the neuropsychological domain of

decision-making and human interaction with the social environment. The SMH proposes a

mechanism where emotion guides or significantly influences behaviour, particularly

decision-making. Somatic markers are acquired by experience and are under control of a

neural “internal preference system [which] is inherently biased to avoid pain, seek potential

pleasure, and is probably pretuned for achieving these goals in social situations” (Damasio

1994, 179). The brain responds to particular social cues that may provide instant pleasure, or

regulate biological homeostasis, such as relief from withdrawal (Li and Sinha 2008). Brain

systems that moderate feeling, memory, cognition, and engage the individual with the world

influence the decision to consume or not consume a drug, or participate in a specific

behaviour or series of actions. Accordingly, this cybernetic brain-environment interaction

may trigger strong somatic signals such as desire, urge and anticipation (Verdejo-Garcia and

Bechara 2009). In effect, this process may limit autonomy as it allows for “preference

reversals” (Levy 2007a) to occur in situations where an individual would rather not use.

The degrees in which self-control is exerted, free choice is realized and desired outcomes

achieved are dependent on these complex interacting biopsychosocial systems. Many post-

modern theorists such as Christman (2004) have challenged the original Kantian privileging

and definition of autonomy. One claim is based on the fact that decisional autonomy, or

rationality, is not the most valuable human characteristic, and the individual-as-independent

does not adequately characterize human beings (Russell 2009). Accordingly, the matrix of a

person’s socio-historical context, life narrative, genetics, and relationships with others

influence intention, decision, and action, and thus shape the brain. Autonomy, therefore, is

not adequately defined just by the events in the brain or the “quality” of the decision being

made. As Gillett (2009) remarks, “a decision is…not a circumscribed event in neuro-time

that could be thought of as an output, and an intention is not a causal event preceding that

output, but both are much more holistically interwoven with the lived and experienced fabric

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of one’s life” (p. 333). Many individuals who have serious addictions live in impoverished

environments without suitable resources or opportunities. Thus it is the limited option for

choice that is one prevailing variable, not only the reduced ability to choose alternatively.

An individual living with an addiction is in-the-world-with-others and thus acts as a being-

among-others, such that the individual’s decisions and complex engagement with the world

may not be as automatic as the neurophilosophical model may suggest (Gillett 2008a,

2008b, 2009). For that reason, individuals who live with an addiction may not completely be

enslaved or forced by their brain in the way in which, as Levy (2007a) has previously

deferred to Aristotle (1999), “a wind or people have [an agent] in their control were to carry

him off” (p.30). Given the spectrum nature of substance use problems, decision-making

capacity is therefore neither completely present nor absent, but may be, at some times in

certain contexts, weakened. One area in particular in which these neuroethics notions of

addiction may have significant impact is in the clinical setting.

Addiction Neuroethics in the Clinical Context

A future application of clinical neuroscience may allow for more precise prediction of a

neurogenetic vulnerability to addiction, lead to better understanding of pharmacokinetics

and pharmacodynamics of drug use, and to bring greater precision to diagnosis than is

currently possible. Realizing a neurobiological or genetic susceptibility to addiction could

empower life planning and the avoidance of high-risk scenarios. Individuals involved in

treatment could learn effective coping strategies, modify proximal environmental triggers,

and achieve other social goals. Yet when neurogenetic attributions are made entirely

irrespective of their social context, individuals with mental health problems are viewed as

less responsible (Mehta and Farina 1997), and the individuals themselves may perceive a

limited control over their actions (Shiloh, Rashuk-Rosenthal, and Benyamini 2002). These

perceptions may greatly affect addiction recovery rates (Godin and Kok 1996). As Hall and

colleagues (2003a) remark, “A ‘disease’ that can be ‘seen’ in the many-hued splendor of a

PET scan carries more conviction than one justified by the possibly exculpatory self-reports

of individuals who claim to be unable to control their drug use” (p.1485).

When neurogenetic attributions are presented in the clinic, pharmacological treatments are

often believed to be a more effective option over psychotherapy (Phelan, Yang, and Cruz-

Rojas 2006). This attribution could sway those who assign the cause of their addiction to be

exclusively neurological or genetically based, and not necessarily evaluate the risks and

benefits of pharmacotherapy, psychotherapy, or receiving both as combination. These causal

neurogenetic attributions have led some authors to advocate for involuntary treatment in

addiction, arguing that, paradoxically, autonomy must be denied, “in order to create it”

(Caplan 2008). In these extreme examples, a Ulysses contract (Andreou 2008) may be more

respectful of autonomy, and relevant harm reduction approaches in the clinical setting may

help empower a person to be more autonomous in their treatment decisions, pursue what is

meaningful to him or her, and accept the accompanying responsibilities (Buchman and

Russell 2009).

Notions of a pathologized self, deeply enmeshed with personal identity, may lead an

individual to internally negotiate a relationship between the self and the brain (Dumit 2003).

It may further challenge understandings of “accepted” identities, such as health seeking and

rational, as opposed to “contested” identities, such as addict, intoxicated, and at-risk (Fry

2008). The latter may compromise an individual’s sense and experience of free will, being-

in-the-world, perceptions of personal responsibility, and view abnormalities in dopamine

pathways as fatalistic.

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Guiding an individual’s behaviour are brain processes, somatic mechanisms, the ethical

rules and norms that govern society, and the nature of the interaction. The complex

combination of biological, psycho-social and systemic factors may explain why it is so

difficult for some individuals to refuse drugs in the face of increasingly negative

consequences. An underlying feature of these interacting systems is the human subjective

experience of free voluntary actions, which problematizes laws within the natural world that

every event has a cause with causally sufficient explanations.

Biopsychosocial Systems Approach

The biopsychosocial model of addiction (Figure 1) posits that intersecting biological,

psycho-social and systemic properties are fundamental features of health and illness. The

model includes the way in which macro factors inform and shape micro systems and brings

biological, psychological and social levels into active interaction with one another. It is a

model based on Engel’s original biopsychosocial model (Engel 1977) for which he argued

that to develop a scientific and comprehensive description of mental health, theories that

promote biological reductionism should be dismissed in favour of those that adhere to

general systems theory. The contemporary model, adapted for addiction, reflects an

interactive dynamic for understanding substance use problems specifically and addressing

the complexity of addiction-related issues. The empirical foundation of this model is thus

interdisciplinary, and both descriptive and applied.

The biopsychosocial systems model is grounded in systems theory in which knowledge

occurs at the intersection of the subjective and the objective, and not as an independent

reality. This is a radical departure from the traditional positivist epistemology, which relies

on empirical study and material proof (Bunge 1979; Heylighen, Cilliers, and Gerschenson

2007). Such new iterations of systems theory concentrate on the cognitive and social

processes wherein the construction of subjective knowledge occurs. Each element of a

system may be a complex system in its own right. The dynamic within these relationships

can contribute to or inhibit the emergence of a complex behaviour such as problematic

substance use, while regulating both inputs and outputs from changing internal and external

environments. The complex behaviour contributes both positive and negative feedback, and

thus affects how the complex behaviour emerges. Systems theory, therefore, balances

reductionism and the intrinsic heterogeneity within systems.

The actual social component of the biopsychosocial model is limited, however. The social

domain tends to account only for proximal environmental and social properties. The social

does not necessarily include macrosocial circumstances, such as governmental social

policies, drug policy or drug ‘strategy’ that has a direct effect on substance use rates and

patterns. A systems approach strives to achieve a unification of disciplines neuroscience,

biology, psychology, sociology, philosophy, economics, politics and law by examining

interacting and emerging patterns from each discipline, rather than focusing on common

material components (Heylighen et al. 2007). In this light, the addition of systems to the

prototype biopsychosocial model allows for the inclusion of macrosocial systems as well as

smaller components, such as cells and genes. Together they shape individual actions and

behaviours. A systems approach allows for the inclusion of psycho-social and socially

systemic explanations of addiction, which extend well beyond neurobiology while still

interacting with it (Bunge 1991).

The biopsychosocial systems model implicitly calls for an integrative discussion in the

ethics debate on substance use, decision-making, and responsibility. The model avoids a

forced choice between brain disease and condition of a weak will, and thus provides a useful

framework for overcoming a neuro-essentialist trap. Instead of focusing entirely on causal,

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reductive neurobiology and difficulties in decision-making, the biopsychosocial systems

model places the individual in his or her social environment and integrates his or her life

narrative. The model contextualizes the responsibility placed on the individual and further

allows for individual members of society to reflect on their own contributions in facilitating

substance misuse (Levy 2007b). The model, therefore, allows for diverse and

multidimensional aspects of knowledge to be drawn upon depending on the concern to be

addressed, and the tools available to address them (Cochrane 2007).

A biopsychosocial systems approach does not portray people as only controlled by the state

of their brains. Addictive behaviours are neither viewed as controlled or uncontrolled but as

difficult to control a matter of degree. Further, the clinically observed defining feature of

addiction a loss of control is understood as a socially normative notion. Thus the claim that

“an addict cannot be a fully free autonomous agent” (Caplan 2008, p.1919) is debatable.

While it assumes that people are usually fully free and autonomous, contemporary

discussions about autonomy as a hyper-value or hypergood (Frank 2004; Gaylin and

Jennings 2003; Taylor 1989) and conceptions of relational autonomy (Sherwin 1998)

necessitate a contextualized discussion of autonomy in debates about addictions (Buchman

and Russell 2009). Because of a tendency to focus on extreme pathological states, the wide

range of normal is often forgotten.

Heroin-Assisted Treatment: An Applied Case Example

Advances in addiction research are increasingly being applied to gain deeper knowledge

about the impact of drug use on brain structure and functioning, capacity, autonomy, free

choice and decision-making, behaviour, treatment, and symptom reduction. While research

of this kind raises important issues about identity, and notions of health and illness, the

outcomes have implications for drug policy, health care systems and delivery, and treatment

for substance use problems.

Addictions research using heroin-assisted treatment (HAT) trials such as the North

American Opiate Medication Initiative (NAOMI) and similar HAT studies and programs in

Europe are a striking, if not controversial example of an effort to embody a biopsychosocial

systems approach. The objective of these trials is to investigate the benefits and risks of

administering medically supervised, pharmaceutical-grade injectable heroin to chronic

opiate users where other treatment options, such as methadone maintenance therapy, have

failed.

The NAOMI trial raised significant scientific, legal, ethical and political concerns, which

included issues of patient safety, the controversial use of placebo control therapy, lack of

equipoise, treatment discontinuation, and compassionate access to treatment (Oviedo-

Joekes, Nosyk, Marsh, et al. 2009). Reflecting on these concerns, the authors stated “we

[had] to be clear in our ethics applications and in our informed consent process with

participants that HAT will not be available outside the context of the study” (p. 267).

Although a full discussion is warranted pertaining to these challenges, these ethical concerns

raised by Oviedo-Joekes et al. (2009) resonate with our present discussion.

Properties of the biopsychosocial systems model are reflected in the case example of HAT.

Here, we examine some of the ethical challenges to research, service delivery, the

philosophies and strategies of harm reduction, and clinical practice that HAT presents.

Integrating Cells and Society

Semi-synthetic opiates such as heroin mainly activate mu opioid receptors in the central

nervous system (Koob, Sanna, and Bloom 1998). Mu receptors activate analgesia,

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respiratory depression, miosis, euphoria, and reduced gastrointestinal motility. Frequent and

chronic opioid exposure may lead to a significant amount of neuroadaptations, which are

believed to contribute to tolerance, withdrawal, and other mechanisms contributing to the

cycle of compulsive use and relapse (Christie 2008).

Heroin is lipid soluble, which leads to fast penetration of the blood-brain barrier and high

abuse potential (Julien 2001). The reinforcing and euphoric properties of opiates arise from

increased amounts of extracellular dopamine in the ventral tegmental area and nucleus

accumbens. Individuals experiencing withdrawal may suffer severe symptoms that include

sweating, nausea, vomiting, abdominal pain and irritability (Koob and Le Moal 2005). The

risk of mortality is increased due to overdoses; there is an increased risk of acquiring

bacterial infections, and other blood-borne pathogens such as HIV and HCV, as described

earlier. Concurrent mental illness and addiction the norm rather than exception further

characterize individuals with severe opiate addiction (Rush, Urbanoski, Bassani, et al.

2008).

Chronic opioid dependence is associated with a high prevalence of health and psychosocial

issues (Oviedo-Joekes et al 2009), such as high rates of underemployment and

unemployment, involvement with the legal system, unstable housing, and street-involvement

(Fischer, Rehm, Brissette, et al 2005). Research from Europe suggests that chronic heroin-

injection users, who received heroin under supervision in tandem with drug treatment, were

less likely to be involved in criminal activities (Killias, Aebi, and Ribeaud 1998), had better

treatment retention (Haasen, Verthein, Degkwitz et al. 2007), improved social functioning,

and had reduced mortality (Rehm and Fischer 2008). Data from Canadian trials (Oviedo-

Joekes, Nosyk, Brissette et al., 2008), show a greater percentage of female participants

compared to the European trials and a high percentage more than 70% of participants

residing in precarious housing.

Additionally, a recent study by Lasnier, Brochu, Boyd, and Fischer (2009) did not find any

evidence of an increase or decrease in community-based crime associated with HAT clinics

in Canada.

The deontological principle of respect for persons is a characteristic feature of harm

reduction efforts such as HAT. This ethical principle is justified and framed as a matter of

human rights, which maintains that injection drug users, for example, have the right, like

other less stigmatized members of society, to access medical and social services. This claim

coincides with a recent emergence of a global advocacy movement that seeks to construct

the use of drugs as a human right (Elliott, Csete, Wood, and Kerr 2005; Lines and Elliott

2007).

Hunt (2004) takes the rights-based notion further and identifies and characterizes two ethics

of harm reduction. First, he describes a “weak” rights ethic, wherein individuals have the

right to access good healthcare. Second, Hunt identifies a “strong” rights account that

acknowledges a basic right to use drugs. Based on this definition, we believe that HAT falls

into both camps HAT seeks to promote the right to access good health care, and the basic

right as an individual asserting sovereignty over his or her body to inject heroin.

Stigma, Heroin Assisted Treatment, and the Biopsychosocial Systems Model

Whether or not drug use is recognized or constructed as a basic right, individuals living with

an addiction are amongst the most stigmatized members of society. Although stigma is

entrenched in all levels of social fabric, including health care services, it is important to

understand how individuals who participate in clinical trials or treatment may perceive the

supervised injecting of heroin. In a recent study examining stigma and supervised

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methadone maintenance therapy, Anstice, Strike, and Brands (2009) found that convenient

access to services, relationships with pharmacists and dispensing staff, and characteristics of

where the methadone was distributed were intimately linked with the client’s experiences of

being stigmatized. Moreover, the authors noted that some methadone dispensing locations

helped clients mitigate a stigmatized identity of “a drug user”; while other dispensing

locations exposed or perhaps did not take adequate steps to limit or minimize this effect.

Building on the findings from Anstice et al., future studies can examine ways in which

treatment outcomes can be improved by reducing stigma associated with supervised

treatment such as HAT.

The social burden of illicit drug addiction is estimated at billions of dollars per year (Fisher,

Oviedo-Joekes, Blanken, et al. 2007). Research that involves providing drugs to individuals

living with an addiction must negotiate between science, ethics, politics, law, and evidence-

based medicine. For instance, despite its cost-effectiveness and ease on burden of disease,

the supervised injection site (SIS) in the Downtown Eastside area of Vancouver, Canada has

been repeatedly threatened with closure by politicians. The threats are based on emotional

and moral attitudes towards the existence of the SIS and drug addicts generally, as opposed

to empirical evidence (Des Jarlais, Arasteh, and Hagan 2008).

The structural systems of society have a significant effect not only on the provision of

service delivery, but also on the design of randomized controlled trials like NAOMI, which

seek to minimize the health and social burden of drug addiction. Social justice demands that

politicians permit, and researchers and health care providers scientifically evaluate, more

controversial methods to treat stigmatized conditions such as addiction, where other

methods have either failed or provided limited benefit for the most marginalized members of

society. Accordingly, Oviedo-Joekes et al (2009) describe the systems approach to heroin-

assisted treatment:

“HAT is not simply a pharmacotherapy; it is a treatment approach that is situated

within a context involving neighborhood factors, the local drug scene, housing,

policing, medical care, and other treatment services. Its role and effectiveness is

entangled with the ancillary services available, drug policies, and treatment

philosophy” (p.262).

The biopsychosocial systems approach provides the impetus for a benevolent view of

individuals who have a serious addiction, such as heroin, and the data to date suggest that,

however unorthodox, the intervention appropriately address addiction related issues,

including stigma, at both the individual and societal level.

Conclusions

Robert K. Merton observed that, “In the modern world, the visibly practical

accomplishments of a science largely affect the social value placed upon it” (Merton 1961,

697). Media headlines such as “Brain’s Addiction Centre Found” (BBC 2007) speak to the

power of neuroscience and its ability to construct images of the brain, such that it has

become easy to defer to its account of the complex phenomena that constitute addiction.

Neuroethics challenges arise when knowledge exclusively from neuroscience is deemed

adequate to obtain a full understanding of a mental health disorder as complex as addiction.

While the practicality of biopsychosocial systems model may allow for a more integrative

explanation for addiction, it does not explain addiction entirely. Indeed, there is no single

theory or approach that can offer a complete explanation for the existence of any social

problem (Merton 1961). Moreover, the model does not solve the problem of free choice, as

the model still, even at the systems (macro) level, has causally sufficient preceding

conditions.

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It is the integration of biological data and psycho-social, narrative, family information, and

clinical phenomenology that will make way for more precise forecasting and earlier

diagnosis than is possible today. This is one path to follow for new opportunities for

treatment and intervention directed toward prevention. Accordingly, an analysis of the

ethical, legal and social issues around other problems of addiction, such as prescription

opiate misuse for pain management, may also be examined within the context of our

proposed framework.

The application of a multi-dimensional model like the model proposed here is not

revolutionary. As a rule, mental health workers are familiar with an integrative

understanding of addiction, and would not recommend a treatment intervention based on

biological information alone. However the rapid developments in neuroscience are moving

bio-psychiatry away from the mind, and towards actions in the brain. Mind once was the

place of mediation between person and situation, between the biological and the social. How

these advances will impact the ethical relationship between our brains and our selves in

addiction, is yet to be seen.

Acknowledgments

This paper is based on a thesis in fulfillment of the requirements for a Master of Social Work in the Collaborative

Program in Addiction Studies at the University of Toronto. Special thanks to Dr. Barbara Russell and Dr. Marilyn

Herie at both the Centre for Addiction and Mental Health and the University of Toronto who advised on earlier

versions of the manuscript; Neil Chahal and Sofia Lombera at the National Core for Neuroethics at the University

of British Columbia; the two anonymous reviewers for their thoughtful remarks. Supported by NIH/NIMH (#MH

R01MH84282-04A1), the Canadian Institutes for Health Research (CNE #85117), the Michael Smith Foundation

for Health Research, and the Vancouver Coastal Health Research Institute.

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Figure 1.

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