exploring the relationship between social science and software development methodologies: a blog by Pascal Belouin

  

I take the liberty of going off-subject a little bit by publishing this essay I wrote recently. Hope some will find it of interest!

Abstract
Neuroscientific discourses about addiction have greatly contributed to our understanding of the biological phenomena that accompany repeated, compulsive drug use. We now have a deep understanding of the mode of action of most psychoactive drugs on the brain, as well as of their short and long-term effects on areas responsible for managing high-order thinking, emotions and reward. However, they rely on a theoretical and methodological framework that could be challenged by approaches that emphasise the ‘constructed’ nature of social reality, and the singular role of the structure of language in this construction. Indeed, modern neuroscience relies on assumptions inherited from the empirical scientific tradition so pervasive in modern science in this day and age. However, some of the bases on which such a view of the world relies could be considered incompatible with a definition of addiction unavoidingly rooted in language.
The questioning of the neuroscientific discourse about addiction presented in this essay is thus decomposed in three main parts. After a brief exploration of the theoretical roots of neuroscience, an overview and critique of recent neuroscientific articles about addiction is made in the second part. Finally, the final part of this essay is dedicated to presenting a critique of neuroscientific discourse about ‘addictive behaviours’.

Introduction
One of the strongest appeals of neuroscientific accounts of addiction lies in the fact that they are part of a certain realist, objectivist, empirical tradition that has been very successful in what is commonly called the ‘hard’ sciences since Bacon and Newton. The modern scientific paradigm of knowledge production has had a revolutionary impact not only on our understanding of the world but also on our daily lives and on the way we perceive ourselves and others around us (Smith, 1998).
When applied to the functioning of the brain, the empirical scientific paradigm has provided us with great insight into the biological processes that accompany particular behavioural phenomena. Modern neuroscience has allowed us to understand the role of certain parts of the brain in for instance language processing (Bear et al., 2001), or the experience/anticipation of a reward (Berridge, 1993). Neurophysiology has allowed the discovery of new drugs for the treatment of ailments such as epilepsy or dementia, and will certainly be the source of great breakthroughs in the near future.

The empirical scientific paradigm has also been adopted in ‘softer’ sciences such as psychology, where it took the form of behaviourist and cognitivist approaches to the study of animal and human behaviour. These behaviourist and cognitivist approaches in psychology provide neurophysiologists with a way to interpret the physiological phenomena observed in the framework of empirical research, through what is commonly called a reductionist approach. Reductionists make the assumption that the correlative observation of particular phenomena on a molecular, structural/physiological, and ‘psychosocial’ level entails causal relations between the phenomena happening at these different levels of ‘objective truth’ (Bray, 1997). In this framework, the problematic notion of addiction has been in recent years framed as a ‘disease of the brain’, on the basis of a certain interpretation of the neurophysiological data gathered in the framework of experiments carried on animal models as well as human subjects. However, we would like to argue in this essay that, for a number of reasons, establishing the validity of the observation of a particular psychological (or sociological) phenomena could be considered much more problematic than it is generally acknowledged in neurophysiological-behaviouristic accounts.

Indeed, neurophysiologically oriented interpretations of animal behaviour (and, often, their extrapolation to explain human behaviour as well) rely on a theoretical framework that could be challenged by certain epistemological positions that acknowledge the central role of language in any account of an objective truth. Although rules of experimental design exist so as to allow behavioural neurophysiologist researchers to assert the legitimacy of their results, their conclusion still rely on certain definitions of addiction and are always ultimately grounded in a particular epistemological position in regards to what constitutes ‘objective truth’. We would therefore like to argue in this essay that exploring the epistemological roots of neurophysiologically-grounded accounts of addiction could be a salutary exploratory exercise which may pave the way to a more socially and culturally-aware understanding to the group of phenomena conceptualized under the highly-politicised notion of addiction.

The theoretical roots of neuroscientific accounts of addiction
The mechanical body
The current neuroscientific interpretation of animal (and human) behaviour, distributed amongst disciplines such as physiological psychology, or behavioural neurology, relies on theoretical and methodological bases which could be traced back to Hippocrates and his suggestion that “from nothing else but the brain come joys, delights, laughter and sports, and sorrows, griefs, despondency, and lamentations”. (Carlson, 2009). This opposition to the idea that the human mind is somewhat detached and of a different nature than the body, although not endorsed by Descartes, was nonetheless developed thanks to his work. His understanding of the body, and more particularly of the brain as a system responsible for the behaviour of the body to which it belongs, allowed for the birth of experimental physiology, which seek to adopt the scientific methods of enquiry established in sciences such as physics to the study of animal (and human) behaviour.

The application of the experimental paradigm used in the natural sciences to the study of neurophysiological phenomena through, for instance, the study of pathological cases as well as direct intervention on the functioning of the central nervous system of experimental subjects was, as it has been in most other disciplines, a phenomenal success. The work of, among others, Johannes Müller, Pierre Flourens and Paul Broca led the way to a revolutionary change in our understanding of neurophysiological phenomena, and in the identification of the role of certain parts of the brain in allowing high-level, human functions such as for instance the ability for language (Bear et al., 2001).
The validity of neurophysiological accounts of the behaviour of animals (and, by extension, and although much more problematically, of humans) relies on several bedrock epistemological assumptions. First, neurophysiologists rely on a strictly monist and realist standpoint: objective reality can be discovered and understood through the correct and rigorous use of the scientific method. In this framework, the conscious mind, as an intangible, ‘out-of-the-body’ object, disappears or at least becomes a ‘consequence’ (both causally and evolutionarily) of the body that ‘hosts’ or ‘produces’ it. One of the main consequences of this monist, functionalist and realist approach was the idea that what has been called the conscious mind, and even the soul in ancient times was the product of the activity of the nervous system of humans.

The commitment of neurophysiologically oriented psychologists to an empiricist, scientific methodological paradigm is also reflected in their stated goal to produce multi-level generalisable accounts of psychological phenomena and, as a consequence, of the behaviours they observe. One of the main rules for considering the general laws established by researchers as valid is their ability to predict in which conditions a particular phenomenon is to happen again. The design and implementation of experiments whose results could be considered as being able to predict a particular kind of behaviour thus became the main activity of researchers involved in the field of behavioural and, later on, cognitive psychology. The rapprochement with neurophysiology and, later on, genetics (with the sound grounding of Darwin’s evolutionary theory) made sense, and resulted in an explosion in the production of neurophysiological accounts of behaviour.
As we will see in the further parts of this essay, this approach therefore relies on the assumption that the working of the components of an observed phenomenon are identified, and that there exists a strict causal relationship between the phenomena observed at one level and the one observed at the level below.

The computer metaphor and the birth of a new science
According to neuroscientists, animals and humans are complex systems whose behaviours can be explained on different but causally related levels: Descartes’ central notion that the world could be understood in purely mechanistic terms resulted in what is now call reductionism. Reductionism could be understood as the process through which the observed behaviour of a complex system is defined as the product, or the cause, of the operation of its identified parts (Bray, 1997). Thus, a particular behaviour (smoking a cigarette) will be explained in terms of the consequence of the reception of a particular stimulus (let us say, watching somebody else smoking).

On a physiological level, the behaviour will be explained on the basis of the firing of particular neurons in particular parts of the brain (for instance, what is commonly called the reward system). This in turn can be explained on a biochemical level by the interaction of neurotransmitters and chemical signalling between neurons, which causes certain parts of the brain to be activated. Note that ideas such as the meaning of smoking at a particular moment by this particular person at this particular point in this particular culture is considered as irrelevant, and that it does not form a part of the ‘context’ in this account of the ‘behaviour of smoking’.

As higher levels of causal explanation are required, a more sophisticated theoretical framework is therefore needed to explain the influence of the environment on the subjects being studied. One could argue that this is where behaviouristic and cognitivist approaches to psychology are integrated into neurophysiological accounts of behaviour so as to provide a seemingly complete, objective account of a particular observed phenomenon. Thus, neurophysiologically-oriented psychological perspectives put forward the idea that a certain observed phenomena at what we could call the psychological or psychosocial level, such as, for instance, depression, can be explained (and therefore predicted) through their decomposition on the neurophysiological, neuropharmacological and even genetic levels.
Neurophysiological accounts of psychological phenomena thus often use the theoretical framework brought about by the behaviourist school in psychology, an approach noticeably introduced by the work of Ivan Pavlov and B.F Skinner (Carlson, 2009). Behaviourism considers behaviour as being solely the product of a reaction of humans and animals to stimuli present in the environment. Animal and human behaviour can then be explained through the reinforcing action of certain behaviours in relation to the environment. Purely behaviourist approaches to psychological phenomena can be challenged on a number of grounds, one of the strongest being that they do not acknowledge the existence of high-order thinking in humans. Indeed, behaviourist accounts of human behaviour through a process of reinforcement tend to fail to acknowledge or leave room for the fact that the behaviour of humans and animals is based on the representation they have of their environment and not on the environment itself (Baum, 2005).

No room for intentionality: challenging the computational/information processing model of the brain
The limits of behaviourism were sought to be overcome through the introduction of cognitivist accounts of human psychology. According to Neisser (1967), cognitive psychologists see the mind not as a ‘black box’ unavailable for scientific study as did behaviourists, but as a signal-processing system similar to a computer. Behaviours are thus understood as responses to external stimuli are thus understood as being the products of the processing of information available in the environment.
The fact that behaviourist and later on cognitivist approaches to psychology share with disciplines like biology the certainty of the discovery of an objective reality through empirical pursuits made this an ideal way to provide an integrated account of animal and human behaviour. However, as we will see in the further parts of this essay, this definition of ‘psychological’ phenomena could be challenged on various grounds, noticeably in regards to the nature of language itself and of its subjection to social, political and cultural values.
Not only the computer metaphor that underlies most neuroscientific accounts of addiction has been the subject of criticisms from the continental school of philosophy, but also from thinkers belonging to the analytic tradition such as John R. Searle, for example, challenged this purely ‘computational’ model of the brain on the grounds that it did not leave any room for intentionality.

More precisely, Searle argues that the purely formal manipulation of symbols which ultimately constitutes the activity of the brain as it is endorsed by researchers claiming a belonging to the cognitivist tradition does not account for our capability as human beings to attach meaning to the symbols we (unconsciously or consciously) manipulate in our brain. In this famous “Chinese room argument”, Searle makes a very strong case against views of the brain as a purely mechanistic tool for the manipulation of symbols by arguing that the sole manipulation of symbols is not enough for allowing understanding (Searle, 1990). In other words, although computational models of the brain are allowed to mimic the ‘signal processing’ that goes on within the brain, the presence of a ‘thinking being’ is required to give sense to the symbols and signals manipulated by a human brain. High-order thinking is only possible if the subject somehow ‘represents’ and attach meaning to sensory data.
Thus, cognitivist models of the brain could be seen as missing something, namely ‘what it feels like’ to experience the world as a subject. Although Searle’s argument has been the object of numerous attacks from researchers belonging to the cognitivist tradition (see for instance Chalmers, 1994), his definition of intentionality remains an interesting point of departure for an argument that would challenge the purely objectivist view of addiction as it is championed by recent accounts of addiction as a ‘brain disease’ such as for instance the one proposed by Volkow et al. (2010).
Neuroscience was therefore born out of the alliance of the study of the biology of the central nervous system and behaviourist-cognitivist accounts of the mind fused into an interdisciplinary whole, united both in the pursuit of a better understanding of animal and human behaviour and by a common epistemological view of the world through the empirical, scientific method of knowledge production. It provided a scientific license to the use of certain psychoactive substances to counteract the effect of ‘drugs of abuse’, and paved the way to behaviourist and pharmacological treatments to ‘addiction’.

Explaining addiction with the body: the neuroscientific understanding of addiction
Therapeutic expectations: neuroscience as a medical science, addiction as a illness
Unlike physics, neurophysiology and physiological psychology have a particular role for humans: they are framed as a part of medical science, the “science of dealing with the maintenance of health and the prevention and treatment of disease” (Princeton University, 2010). Thus, it could be argued that the attention of neuroscientists working on addiction and addictive behaviours has been directed from the start towards finding ways to ‘cure’ or to solve the problem of addiction, through means that correspond to each of the level at which they traditionally analyse their object of study. Thus, appeared chemically, behaviourally and psychologically based treatments based on neuroscientific research.

In this framework, it could be argued that neuroscientists were directed towards the study of addiction on the basis of a definition of the phenomena inferred from the ‘malfunctioning’ of individuals affected by it in society, and on the physiological consequences that the repeated use of certain substances have on the body of users. This particular aspect of the neuroscientific discourse of first addressing the issue of addiction as a social or societal problematic phenomenon is particularly salient in a short article by Nestler (2002), which starts with the following sentence: “In terms of lost lives and productivity, drug addiction remains one of the most serious threats to our nation’s public health” (Nestler, 2002, p. 1076).
In the same order of idea, the chapter dedicated to addiction in Physiology of Behaviour (Carlson, 2009), a widely used textbook covering the subject of the neurophysiology of behaviour starts by enumerating the “disastrous effects” of addictive substances such as drugs or alcohol. These, according to Carlson, include not only a range of physical ailments such as cirrhosis of the liver or strokes, but also social problems caused by illegal drug markets and the spread of infectious diseases amongst ‘addict populations’. One could argue that these statements help to highlight the need for a better understanding of addiction as a certain form of behaviour. However, this framing of addiction as problematic behaviour could also be seen as having a role in the definition of the very phenomena neuroscientists studying addiction are investigating.

The experimental bases of neuroscientific accounts of addiction
Our understanding of the neurophysiological mechanisms that underpin the behaviour of animals and humans has greatly increased over the course of the last three decades, thanks both to great technological advances in terms of neuroimaging and to the empirical scientific paradigm of knowledge production. In this framework, neuroscientists have been investing the notion of addiction over the course of the last 50 years. This resulted in a large amount of experimental data and literature now available on the subject (White, 2000).
In this sense, neuroscience is a very powerful tool for understanding the biological grounding and manifestation of drug use. The first biggest breakthrough was the discovery of neurotransmitters (Tansey, 2006), made by Henry Dale and Otto Loewi. Interestingly, Tansey even hints in this article at what might be the first mention of what is now commonly called an “addictive drug”, nicotine, as acting as a neurotransmitter (2006, p. 420).
The biological phenomena that underpin addiction where also investigated in the framework of experiments involving animal models such as mice, dogs, or monkeys. These experiments adopted a behaviourist approach to the study of drug self-administration in rodents, mostly relying on apparatuses borrowed from the behaviourist experimental toolkit, such as the ‘Skinner box’ or a T-maze.

Thompson (1965) traces the first behaviourist experiments on the reinforcing effect of drugs self-administration back to 1955 and the work of Nichols, Headlee and Coppock (Nichols et al., 1956). More animals such as monkeys or cats where subjected to such experiments over the years, and by the beginning of the 1980s a lot of data had been generated to show that model animals, in an experimental context, would self-inject large amounts of most known ‘drugs of abuse’ (Woods, 1978). These experiments paved the way for wider-ranging research endeavours where neurophysiological data and behavioural/phenomenological data would be correlated with more and more precision, thanks in part to advances in neuroimaging and computer science.

Current neuroscientific understandings of addiction
As illustrated by Hyman and Malenka (2001), Modern neuroscience allowed the discovery of the way psychoactive drugs act on the brain by disrupting the ‘normal’ action of certain neurotransmitters by either binding to specific receptors (agonists, like opiates), disrupting the binding potential of certain receptors (antagonists, such as ketamine) or by disrupting the reuptake of certain neurotransmitters (like, for instance, cocaine, amphetamine or SSRIs).

Furthermore, neuroscientific accounts of addiction provide great insight into the physiological mechanisms accompanying addictive behaviours. Carlson (2009) provides a useful overview of the quite large number of different brain areas and synaptic receptors that are particularly involved in behaviours and subjective sensations related to drug use. These include the forebrain circuits, and more precisely the prefrontal cortex ventral and dorsal striatum. Golstein et al (2002) present strong evidence that activity of the orbitofrontal cortex and the anterior cingulate gyrus is correlated to “intoxication, craving, and bingeing” in “addicted subjects”. As Golstein points out, neuroscientific research has linked these areas of the brain with high order thinking and, in behaviourist terms, in “the ability to track, update, and modulate the salience of a reinforcer as a function of context”. Addiction is therefore characterised by neuroscientists as the cause of craving, the decision of taking drugs ‘regardless of long-term negative consequences’, and relapse. The importance of environmental cues in relapse was also posited in, among others, the work of Childress et al. (1993).

It has also been shown that taking certain drugs for an extended period of time triggers long-time structural anomalies in the same regions and in the nucleus accumbens, involved according for instance to Carlson (2009, p.621) in the regulation of emotions. Thus, researchers such as Laura Peoples (2002) argue that the anterior cingulate cortex and related brain areas have a role in mediating reward expectancy and “willed control of actions”. Peoples therefore argue that abnormalities in these areas could impair addicts’ decision-making process regarding their drug use. Thus, the long-term effects of drug use on the structure of reward pathways are understood by neuroscientists as having a central role in compulsive behaviour.
On a lower level on the reductionist scale, the effects of psychoactive drugs at a molecular level have also been the objects of thorough neuroscientific investigations, and a short overview of the molecular and cellular sites of action of most psychoactive drugs is provided by Teesson et al. (2002). One of the most known illustrations of this is the discovery of the inhibitory action of cocaine on dopamine reuptake, which gave birth to what is now called the ‘dopamine hypothesis’. In contrast to the short-term effects of what could be called the mechanisms of intoxication, researchers such as Hyman and Malenka (2001) present some of the long-lasting effects of various psychoactive drugs on the expression of a number of genes and proteins within neurons. Supposedly drug-induced changes at the molecular, intra cellular level comprise a change in the activation of genes and proteins having a role in transcription, such as the Fos family, CdK5 and CREB, which have a role in the remodelling of neural processes. Furthermore, long-term use of certain drugs of abuse seems to have an effect on the expression of GLuR2, a protein involved in the normal functioning of the brain.

The evolution of the neuroscientific definition of addiction towards the notion of brain disease
The neurophysiological approach to an explanation of addictive, or compulsive behaviour reached its peak in the current understanding of addiction as a brain disease championed mostly (but not only) by the National Institute of Drug Abuse in the U.S. The fact that addiction to psychoactive substances as well as to the ‘high’ experienced by people addicted to gambling or the use of certain psychoactive substances has identical, long-lasting effects on brain chemistry and that, according to Volkow et al., “these studies have shown how repeated drug use can target key molecules and brain circuits, and eventually disrupt the higher order processes that underlie emotions, cognition and behaviour” (2010) seems to indicate that the mechanisms underlying the behaviour that accompany addiction are the same as in most rewarding experiences. In this framework, disorders such as over-eating (or food addiction), pathological gambling (Wareham and Potenza, 2010) and even romantic love (Reynauld et al, 2010) find their origin in brain chemistry imbalance. The role of the dopaminergic channels and more generally of the ‘reward system’ is thus put to the fore by proponent of the ‘brain disease’ paradigm as central in causing such behaviours (Volkow et al., 2010).

Thus, by focussing on brain chemistry, addiction researchers have come to the conclusion that addiction was a disease, as it modifies sometimes permanently the structure of the brain. As recent evidence seems to suggest that any type of activity, not necessarily pathological could potentially fit this profile, it could be argued that getting married, having a job and a couple of children also entail ever-lasting modifications in the structure of the brain, by, for instance, associating the view of one’s children with a strong sense of reward. Thus, the question arises: what is the difference between a lover on a date and a junkie enjoying a fix?
Although Goldstein (2002) mentions the involvement of parts of the brain involved in high-order thinking in behaviours considered as addictive, she does not acknowledge the fact that high order thinking may have itself a causal role in what could be described as the subjective sensations that play a central role in the neuroscientific understanding of addiction such as craving, or behaviours such as relapse.
These challenges to the idea that drugs had a specific, long-term action on the brain both at a structural and a molecular level has been sought to be overcome through a redefinition of the neuroscientific notion of addiction in the Diagnostic and Statistical Manual, as illustrated by Fascella et al. (2010). In the short extract presented below, Fascella et al. argue for a widening in the definition of ‘substance related disorders’ to include disorders which, although not related to the presence of extraneous psychoactive substances in the central nervous system, result in the same behavioural patterns.
Substance-related disorders were initially “carved in” under Sociopathic Personality for the first DSM, in 1952,3 and were still considered personality disorders for the next DSM revision, in 1968 (DSM-II4). They eventually were “carved out” for independent status in 1980 (DSM-III5) and have remained thus for nearly 30 years. But in each of these prior nosologic revisions, the substance-related disorders (whether “carved in” under broader categories or “carved out” to stand alone) together and defined by substance taking. In con- trast to prior revisions, DSM-V is considering whether addictions can be defined apart from drug taking—a fundamental shift in the way these disorders have previously been viewed.

Could it be incidental that the study of addiction led to the discovery of the reward system and of the dopaminergic pathways in learning and reward processing? It could be argued that the fact that addiction research has been at the forefront of ‘reward research’ enticed researchers to make the assumption that strong activation of the reward system was a phenomenon typical and limited to psychoactive substances, and that the subsequent discovery of the role of the same parts of the brain in a large range of human activities associated with strong rewards challenged this special status.

Alternatives to cognitivist & behaviourist interpretations of the physiological phenomena accompanying addiction
Towards a discursive approach to the notion of addiction
Cognitive scientists reject the dualist notion of the subject as introduced by Descartes in their analysis of the relationship between brain states and behaviour. However, dualist accounts of the mind, and particularly of the dichotomy between individual and society seem to still play an important role in their definition of addictive behaviours, and to what constitutes the context of such behaviours. While the mechanical metaphor may be plausibly retained in the analysis of model organisms in the framework of tightly controlled experiments, it could be argued that the notion of context, or environment, becomes central in the analysis of the human beings, importantly but not only due to the fact that both observer and observee are themselves part of a complex system of interrelationships between human subjects. Interesting in this regard is the work performed by Bruce Alexander et al. on the environmental factors of opiate self-administration in rodents (1981). In place of traditionally clinical, prison-like environment that characterises many of the experiments involving rats, Alexander placed his subjects in a ‘Rat Park’, where they could breed and form colonies, have nests: lead a normal rat life. He found that “colony males ingested much less morphine solution than isolated males though there was no difference in preference for sweet or bitter-sweet solutions.” Could such a finding be extrapolated to investigate drug self-administration in humans?
Neuroscientific notions of addiction such as the one provided by Nestler (2002), according to which “addiction can be defined as the loss of control over drug use, of the compulsive seeking and taking of drug regardless of the consequences” seem to make the assumption of an isolated, Cartesian subject independent of the historical, social and political context within which it inscribes itself into. Certain actions or behaviours are exhibited by the subject, of which the causes can be explained by the response of the central nervous system to a variety of external (and internal) stimuli.

Alternative epistemological positions, found for instance in the work of Marcel Mauss (1985), Max Weber (1930), Michel Foucault (1985), Louis Althusser (1964) and even Jacques Lacan seem to suggest that the notion of individual human subject, far from being an autonomous entity set apart from ‘society’, could be understood as a culturally-constituted phenomenon. Indeed, such a perspective hints towards a new conception of the subject as the direct product of particular “techniques of the self” which can be uncovered and understood through what Foucault calls the “genealogical method”. The work of Foucault on the creations of institutions such as the mental asylum (1972) highlighted the way certain types of ‘subject positions’ are made available within culture, such as for instance the evolution of the notion of ‘mad individual’. Could the notion of ‘addict’ be explained using such a theoretical apparatus? If human subjects are constituted through culture, and more particularly through the interplay of institutionalised, dominant forms of discourse, what signification does the notion of ‘context’ takes in regards to the explanation of the behaviour of these subjects?

The institutional role of neuroscientific discourse about addiction
An interesting illustration of the crucial epistemological problem posed by the delicate problem of the definition of addiction and addictive disorders is provided by Scott Vreko (2010): Vreko proposes that the recent emergence of different discourses about addiction which now labels behavioural compulsive disorders such as pathological gambling are, behind the mask of therapeutic legitimacy, part of what could be called ‘civilizing technologies’, used to produce “better citizens”.
Thus, neuroscientific discourses about addiction could also be understood as having an institutional role within western society, one of enforcing certain categories of classification of human subjects and of the biological explanation of phenomena which definition is by contrast rooted in the cultural, historical and political context within which they are produced. It could therefore be argued that, being a behaviour initially rooted in the reaction of the human central nervous system to particular psychoactive substances has become the perfect target for the use of very similar substances, but this time to ‘cure’ the subject of certain types of behaviour (or subjective conditions, such as depression) considered as pathological (Keane and Hamill, 2010). For instance, as illustrated by Acker (2002), it could be argued that the neurophysiological-behaviouristic orientated discourses about addiction participated in the construction of the ‘heroin junkie’.

Thus, the knowledge produced by neuroscientists has a strong social and societal impact but is interpreted differently by people holding very different and sometimes incommensurable views of the world, as they view the world with their own different sets of value, which is dependent on their social, historical and cultural context. That way, as a consequence not dissimilar to what Barthes called the “death of the author” (1977), the interpretation of the neuroscientific accounts of addiction has a very different impact on researchers in the field as opposed to members of the general public, and on policy makers.
The use of psychoactive substances seems therefore to be regulated along two axes:

  • A legal, medicalised channel through which access to psychoactive substances is regulated by professionals, including doctors, pharmacists, pharmaceutical companies financing the research producing the neurophysiological-behaviourist accounts of addiction, and policy makers which formulate policies on the basis of these accounts.
  • A discourse according to which addiction is constructed as a disorder of physiological origins, and drug addicts as the alienated victims of ‘substances of abuse’, finding its expression for example in the ‘war on drugs’ policies and ‘addiction as a brain disease’ paradigms in the neurosciences.

These two axes share a large number of similarities. Modes of consumption are in the same time different and share some commonalities. In these two different contexts, psychoactive substance can form the object of a structured market of distribution, and generate immense profits for those that are on top of the chain. The behaviour of ‘addicted’ drug users is problematised on the basis of a vocabulary relying on the notions of craving, compulsion and relapse, and informs repressive policies based on the idea that ‘access creates the addict’. On the other hand, the prescription and use of psychoactive substances by people suffering from an increasing number of disorders such as depression, anxiety, attention-deficit hyperactivity disorder and even period pains (Connor, 2010), which themselves could be seen as dependent to a certain extent to the social context within which they are defined, is regulated through channels of distribution legitimated by institutional neuroscientific discourse.

Conclusion
Neurosciences have proven the mode of action of most drugs of abuse, and their effect on brain structures. However, as we have seen, the problem of the definition (and to a greater extent of the treatment) of addiction is complex, as by nature this notion could be considered as socially constructed. Thus, we have tried to argue in this essay that using a strictly objectivist, empirical, experimental framework to gain insight into the causes of such a behaviour could be considered as insufficient, as it does not account for the constructed nature of the definitions used in the framework of such research. Indeed, neuroscientific accounts of addiction could be seen as almost ‘erasing’ the subject, or at least the subjective, reflexive account of one’s own behaviour and considers it as an epiphenomenon which has no impact on addictive behaviour.

In that sense, the notion of compulsion adopted by neuroscientist approaches the proverbial ‘irrational act’ and borders on folk psychology. The neuroscientific view of society as only the sum of the human subjects in comprises, could be seen as a by-product of the reductionist approach and is insufficient to get to analyse a phenomenon whose roots are themselves cultural, historical and more crucially political. In contrast to the purely objectivist, empiricist and reductionist accounts of addiction produced by neuroscientist, a discursive approach to the problem of addiction would therefore put a strong emphasis on the notion of cultural, historical, and even political context as deeply involved in the causes of ‘addictive behaviour’.

References
Acker, C.J. (2002) Creating the American Junkie—Addiction Research in the Classic Era of Narcotic Control, Baltimore: Johns Hopkins University Press.

Alexander, B. K., Beyerstein, B. L.. Hadaway, P. F. and Coambs, R. B. (1981) Effects of early and later colony housing on oral ingestion of morphine in rats, Pharmac. Biochem. Behav., 15(4) pp. 571-576.

Altman, J., Everitt, B. J., Glautier, S., Markou, A., Nutt, D., Oretti, R., Phillips, G. D. and Robbins, T. W. (1996) The biological, social and clinical bases of drug addiction: commentary and debate, Psychopharmacology, 125 pp. 285–345.

Althusser, L. (1969) Ideology interpellates individuals as subjects, in du Gay, P., Evans J. and Redman P. (eds) (2008) Identity: A Reader , London: Sage/The Open University, pp. 31-38.
Barthes, R (1977) Image-Music-Text, London: Fontana Press.

Baum W.M. Understanding behaviorism: Behavior, culture, and evolution (2nd ed.) Malden, MA: Blackwell, 2005.

Bear, M. F.; B. W. Connors, and M. A. Paradiso (2001) Neuroscience: Exploring the Brain. Baltimore: Lippincott.

Berridge, K.C (1996) Food reward: brain substrates of wanting and liking, Neurosci. Biobehav. Rev. 20 pp. 1-25.

Bray, D. (1997) Reductionism for biochemists: how to survive the protein jungle, Trends in Biochemical Sciences, 22, pp. 325–326.

Berridge, K. C. and Robinson, T. E. (1993) The neural basis of drug craving: an incentive-sensitization theory of addiction, Brain Res. Rev., 18 pp. 247–291.

Campbell, N. (2010) Towards a critical neuroscience of ‘addiction’, BioSocieties 5(1) pp. 89–104.

Carlson, N.R. (2007), Physiology of behavior, Boston: Allyn and Bacon.

Chalmers, D.J. (1994) A Computational Foundation for the Study of Cognition, PNP Technical Report, Washington University, pp. 94-103.

Childress AR, Hole AV, Ehrman RN, Robbins SJ, McLellan AT, O’Brien CP (1993) Cue reactivity and cue reactivity interventions in drug dependence. NIDA Res Monogr. , 137 pp. 73-95.

Connor, S. (2010) It’s official: A small dose of Prozac can help beat PMS, The Independent [online], http://www.independent.co.uk/life-style/health-and-families/health-news/its-official-a-small-dose-of-prozac-can–help-beat-pms-2082691.html, [Accessed 30 September 2010]

Courtwright, D. (2010) The NIDA brain-disease paradigm: History, resistance, and spinoffs. BioSocieties, 5(1) pp. 137–147.

Dick, D. and Foroud, T. (2003) Genetic Strategies to Detect Genes Involved in Alcoholism and Alcohol-Related Traits, National Institute on Alcohol Abuse and Alcoholism Publications [online], http://www.niaaa.nih.gov/publications/ [Accessed 30 September 2010]

Domjan, M.P. (2002) The Principles Of Learning And Behavior: 5th edition, Wadsworth Publishing.

Dunbara, D., Kushnera, H.I., b and Scott Vreckoc (2010) Drugs, addiction and society, BioSocieties 5(1) pp. 5.

Erickson, C. (2003) Addiction is a disease, Addiction Today, Jan./Feb.

Frascella, J., Potenza, M.N, Brown, L.L, Childress, A.R (2010) Shared brain vulterabilities open the way for nonsubstance addictions: carving addiction at a new joint? Annals of the new york academy of sciences, 1187 pp. 294-315.

Foucault, M. (1972) Histoire de la folie à l’âge classique, Gallimard

Foucault, M. (1985) ‘Preface to The History of Sexuality Vol. II’. Originally printed in The Use of Pleasure: The History of Sexuality Vol. II (trans. R. Hurley), Pantheon Books. Reprinted in Rabinow, P. (eds)

Goldstein RZ, Volkow ND. (2002) Drug addiction and its underlying neurobiological basis: neuroimaging evidence for the involvement of the frontal cortex. Am. J Psychiatry, 159 pp. 1642–1652.

Heyman, Gene M. (1996) Resolving the contradictions of addiction, Behavioral and Brain Sciences, 19(4) pp. 561-610.

Hyman, S. E. and Malenka, R. C. (2001) Addiction and the brain: the neurobiology of compulsion and its persistence, Nature Reviews Neuroscience, 2 pp. 695–703.

Kalant, H. (1999) Differentiating drugs by harm potential: the rational versus the feasible, Substance Use & Misuse, 34(1) pp. 25–34.

Keane, H., Hamill, K. (2010) Variations in addiction: The molecular and the molar in neuroscience and pain medicine, BioSocieties, 5(1) pp. 52-69.

Mauss, M. (1985) ‘A category of the human mind: The notion of “person”, the notion of “self”’, Chapter 26 in du Gay, P., Evans, J. and Redman, P. (eds) (2000). Originally given as a lecture in 1938 and first published in Carrithers, M., Collins, S. and Lukes, S. (eds) The Category of the Person: Anthropology, Philosophy, History, Cambridge, Cambridge University Press (trans. W.D Halls).

Neisser, U. (2009) Cognitive psychology, Grolier Multimedia Encyclopedia. [online] http://gme.grolier.com [Accessed 30/09/2010]

Nestler, E. J. (2002) From neurobiology to treatment: progress against addiction, Nature Neuroscience, Supplement 5 pp. 1076–1079.

Nichols, J.R., Headlee, C.P. and Coppock H. (1956) Drug addiction 1: Addiction by escape training, Journal of the American Pharmaceutical Association, 45 pp. 788–791.

Orford, J. (2001) Excessive Appetites: A Social–Behavioural–Cognitive–Moral Model, 2nd edn, Chapters 1, 2 and 15, John Wiley and Sons: Chichester.

Peoples, L. L. (2002) Will, anterior cingulate cortex, and addiction, Science, 296 pp. 1623–1624.

Princeton University (2010) Medical Science, Wordnet [online] http:// http://wordnet.princeton.edu/ [Accessed 30/09/2010]

Reynauld, M., Karila, L., Blecha, L., Benyamina, A. (2010) Is love passion an Addictive Disorder? The American Journal of Drug and Alcohol Abuse, 36 pp. 261-267.

Searle, J.R. (1990) Is the brain a digital computer? Proceedings and Addresses of the American Philosophical Association, 64 pp. 21-37.

Smith, M.J. (1998) Social Science In Question: Towards a Postdisciplinary Framework, London, Sage/The Open University.

Steeves, T. D. L., Miyasaki, J., Zurowski, M., Lang, A. E., Pellechia, G., Van Eimeren, T., Rusjan, P., Houle, S. and Strafella, A. P. (2009) Increased striatal dopamine release in Parkinsonian patients with pathological gambling: a [11C] raclopride PET study, Brain, 132 pp. 1376–85.

Tansey, C. R. (2006). Henry dale and the discovery of acetylcholine, Biologies, 329.

Teesson, M., Degenhardt, L. and Hall, W. (2002) Chapter 4, Theories of addiction: Causes and maintenance of addiction, Addictions, pp. 33–47, Psychology Press: Brighton.

Thompson, T. (1968) Drugs as Reinforcers: Experimental Addiction, Substance Use & Misuse, 3(1) pp. 199-206.

Volkow, N.D, Wang, G-J, Fowler, J.S, Tomasi, D, Telang, F and Baler, R (2010) Addiction: Decreased reward sensitivity and increased expectation sensitivitiy conspire to overwhelm the brain’s control circuit, BioEssays, 32 pp. 748–755.

Wareham, J.D, Potenza, M.N (2010) Pathological Gambling and Substance Use Disorders, The American Journal of Drug and Alcohol Abuse, 36 pp. 242-247.

Weber, M. (1930) ‘The religious foundations of worldly ascetism’. From The Protestant Ethic and the Spirit of Capitalism (London, Routledge, 1992).

White, W. (2000). Addiction as a disease: Birth of a concept. Counselor, 1(1) pp. 46-51,73.

Woods, J. H. (1978). Behavioral pharmacology of drug self-administration. In M.A. Lipton, A. DiMascio, and K.F. Killam (Eds.), Psychopharmacology: A generation of progress, New York: Raven.

Related posts:

  1. Research proposal : A Foucauldian analysis of the evolution of the discourse about software development methodologies
  2. An introduction to the genealogy of subjectification
  3. Applying social scientific concepts to domain definition: a short overview
  4. Intertextuality and User interfaces as Relational Systems of Representations
  5. LinkedIn, Facebook and Social Identity Theory

1 Comment to “Towards a Critical Discursive Analysis of Neuroscientific Accounts of Addiction”

Leave a Reply