Control, Can We Have Some?

Towards a Transdisciplinary Ecological Perspective

of Drug Consumption and Addiction*

Jean-Paul C. Grund, PhD 1,2,3

Trust is good, control is better - Vladimir Ilyich Lenin

*: Published in: Grazia Zuffa, Susanna Ronconi. (eds.) Drugs and control. Guidelines for self-regulation
– a blueprint for people who use drugs and drug service professionals. (in Italian)

Declaration of interests
I declare no competing interests.

Acknowledgements
Part of the ideas in this paper is drawn from my previous work, published in 1993 and I rewrote some
of the older text to match my current understanding of this topic (and the English language). In
examining the evidence for the brain disease model of addiction, I have relied heavily on the work of
Professor Wayne Hall and colleagues, University of Queensland and Professor Carl Hart, Columbia
University, New York.
1
: Addiction Research Centre, Utrecht, the Netherlands
2
: Department of Addictology, 1st Faculty of Medicine, Charles University & General University
Hospital, Prague, the Czech Republic
3
: Freudenthal Institute for Science and Mathematics Education, Utrecht, the Netherlands.

© J-P. Grund, 2017 (All rights remain with the author.)

Corrrespondence to jpgrund [at] drugresearch.nl

1
Introduction

“Addiction is progressive, chronic, and fatal! Addiction is a brain disease with a genetic
component. Addiction is a family disease.” (IAS, ND)

With several variations the conceptualization of (illicit) drug consumption and ‘addiction,’ epitomized
in this statement, is implicit in most, if not all, traditional drug research and drug treatment efforts. In
particular, the medical or disease model of addiction and the related Gateway (or Stepping Stone)
Theory have been important in propagating this perspective on the consumption of psychoactive
substances. According to the National Institute on Drug Abuse (NIDA), addiction is defined as “a
chronic, relapsing brain disease that is characterized by compulsive drug seeking and use, despite
harmful consequences” (Volkow, 2010). Likewise, the Gateway Theory presupposes that use of more
common drugs or less deleterious drugs precedes and may predict use of other, harder substances,
their harmful consumption and involvement in crime in the future (D. Kandel, 1975; D B Kandel,
Yamaguchi, & Chen, 1992a; Denise B. Kandel, 2003; Kirby & Barry, 2012; Vanyukov et al., 2012). The
disease model and the gateway theory have provided the justification for highly ideological
treatment approaches, such as the Minnesota Model, most drug free therapeutic communities and –
often in lieu of professional support – the 12-Steps Fellowship.

The rendering of drug consumption in largely negative terms and outcomes and, more in general, a
focus on its adverse consequences and associations with deviance or crime is not merely inherent in
the disease model and gateway theory. In essence it is equally implicit in other deficiency-oriented
theories, such as, neuroscientific, psychological and social theories (Stallwitz, 2012), albeit
formulated in different terms and proposing varying explanations. Indeed, the notions that “drugs
are addictive, unhealthy and dangerous” and addiction a perhaps irreversible brain disease (“once an
addict, always an addict”) are well entrenched in conventional wisdom (Galbraith, 1958) and most
mainstream drug treatment is nowadays based on these assumptions.

Not only do most traditional theories ignore the potential positive aspects of drug consumption in
their explanatory framework, there is equally little consideration for the wide variation in drug
consumption patterns and drug careers (Cohen, P. and Sas, 1993; Cohen & Sas, 1994; Decorte, T. and
Slock, 2005; Decorte, 2000; Jean-Paul Grund, Kaplan, & De Vries, 1993; Nabben, T., Benschop, A.,
Korf, 2011) or the spontaneous recovery from serious drug dependence (without treatment) (E.H.
Prins, 1995; Charles Winick, 1964) documented in empirical studies that are at odds with the medical
model’s underlying assumption of inevitable unidirectional progression and sequencing towards a
(final) stage of complete loss of control (Goldstein & Volkow, 2011; D B Kandel, Yamaguchi, & Chen,
1992b). Yet, the following observation suggests that even heavy drug consumers attempt to regulate
their drug intake. In this case, job considerations resulted in seriously cutting back cocaine use, even
terminating consumption for a while.

“Cor looks good. He wears a nice and clean shirt and clean jeans. He tells he is working as a
house painter again after a jobless period. … He says he is doing alright now. However about
two months ago he was not. He was in a period of intensive cocaine use. But he realized that
he had to cut back his cocaine use to an acceptable amount and although he says this has
cost much energy, he stopped taking cocaine for some time. He tells that he is using cocaine

2
 moderately now.” (cocaine and heroin consumer, Rotterdam, ± 1990 in (Jean-Paul Grund,
1993)

The disease model and other deficiency-oriented theories seem thus a poor fit with the experiences
of the average drug consumer and empirical epidemiological evidence, which suggest that success in
controlling drug consumption is not merely associated with the pharmacological properties
(addiction potential) of a substance. House painter Cor had realized (a conscious process) that he had
to cut back his cocaine use but his decision to step down coincided with his new job (a major life
event, strengthening his life structure).

Few researchers would disagree that the outcomes of drug use are somehow dependent on the
interaction of the pharmacological properties of the substance taken, the psychology of the
consumer and the environs and circumstances in which these are taken; what Zinberg termed, Drug,
Set and Setting (1984). But major differences remain over what proportion of the phenomenon is
explained by each of the three components, what value should be attributed to each or how these
influence one another (causality vs. contingency).

From Intradisciplinary1 to Transdisciplinary Explanations

Much research of psychoactive drug use and the models of drug use and ‘addiction’ these examine or
generate continue to be largely based on the hypotheses and explanations raised within a single
discipline, using the methodologies and instruments common in that discipline in studies of captured
samples that may not represent wider populations of people who use drugs2. These research
methods intend to exclude but actually generate and reinforce scientific bias – as they seek for clear-
cut unidirectional cause-effect relationships in a complex multidimensional world where there
actually are very few. Concretely, was it Cor’s realization that he had to cut back his cocaine use that
made him seek/accept a job? Or did the job offer generate his concerns over his cocaine
consumption? In this chapter, I propose that, in our complex social universe, there is no such thing as
clear-cut unidirectional causality.

As Stallwitz (2012) recently noted, psychological variables play an insignificant and subordinate role
in the disease model, and social or physical environmental variables no role at all (Stallwitz, 2012).
Medicine and neuroscience, psychology and sociology have all produced several such
intradisciplinary theories of drug consumption, inebriation and addiction, often with little
consideration for relevant work conducted in other disciplines. While psychological theories may
explain problematic individual drug careers, they do not detail why other individuals, raised and
living under equal conditions do not develop problematic drug consumption patterns. Conversely,
while sociological models, such as labelling and subculture theory, have pointed at important social
determinants of drug use and deviance, these tend to ignore differences between individuals,
personal motives and preferences, responsibility or autonomy (Adams et al., 2003; Soussan &
Kjellgren, 2016; Stallwitz, 2012). What all traditional intradisciplinary explanations of drug use and
addiction have in common is their focus on problematic drug use patterns that are deemed morally
unacceptable and socially deviant and their neglect of the wide variation in consumption patterns
that characterizes human drug consumption.

1
For the sake of argument (and space ) I refrain from discussing the differences in collaboration between
scientific disciplines.
2
For a discussion of the methodological limitations of such studies, see e.g. Stallwitz, 2012.

3
In the last 20 years, the (brain) disease model of addiction and ‘spin-off’ theories, such as the
gateway theory, have become the dominant theoretical framework in research, treatment and
(funding) policy, while recent theory development in psychology, sociology and other disciplines is
increasingly influenced by various assumptions of the medical model and of neuroscience in
particular.

In the following pages, I will therefore first critically examine some of the key characteristics of the
brain disease model of addiction and the gateway theory and juxtapose these with the findings from
epidemiological studies and qualitative research that looked into the drug consumption patterns and
experiences of various populations of drug consumers. Subsequently, I will lay out the contours of a
transdisciplinary model for comprehending the entire spectrum of drug use patterns – whether this
concerns youthful experimentation, sustained recreational consumption, festive mass inebriation or
heavy, out-of-control chronic use – that aims to address the shortcomings of intradisciplinary
theories. If there is one thing clear, the human consumption of psychoactive drugs in all its
manifestation transcends the reach of any single scientific discipline involved in the study of drug use
and ‘addiction.’ My aim is therefore to stimulate the development of a scientific framework for the
study of drug use in all its expressions. Practically, in the context of this volume, this paper outlines
the theoretical and research fundament of an innovative and alternative approach for people who
use drugs and drug service providers alike on managing personal drug consumption, preventing drug
related harms and overcoming these once a relationship with drugs has turned sour.

The Medical or Disease Model

Within the medical or disease model, addiction is conceptualized as a progressive and chronic illness,
inevitably brought about by the repeated self-administration of a psychoactive substance which
pharmacology is deemed extremely addictive. Next to their powerful lure on the brain, repeated
intake of such substances also causes tolerance to the psychoactive effects and, depending on the
class of drugs, physical dependence3. Tolerance requires increased dosing to attain the effects
pursued, while physical dependence dictates repeated administration to avoid withdrawal symptoms
and remain functional. This repetitive sequence turns into a vicious, downward spiral as dependence
progresses, successively altering a person’s objectives and values, leading him or her to engage in
socially undesirable behaviours only to avoid withdrawal, such as sex work or criminal activities.
Chronic indulgence in psychoactive substances will inexorably result in loss of control, physical and
psychological deterioration, social and moral decay (Cohen, 2009; Stallwitz, 2012).

Neuroscientific Explanations – the Brain Disease Model of Addiction

More recently, neurobiological models of addiction have focused on the (dis)function of certain
parts, systems and processes in the brain. Advances in neurobiology have contributed to our
understanding of the cellular and circuitry underpinnings of addiction (Kalivas & Volkow, 2005).
Receptor theory focuses on the interaction of endogenous (naturally produced by the human body)
endorphins and their receptors, their role in the brain’s reward system and the disrupting effect of
repeated administration of exogenous equivalent drugs (Gardner, 2011; Gerrits, Lesscher, & van Ree,
2003; Levy, 2013). Recent neuroimaging studies focusing on the loss of control over drug intake that
is seen in addiction have proposed a key role of the prefrontal cortex, which wields influence in the

3
E.g. with habitual use of alcohol, opioids, GHB or benzodiazepines; much less so with cannabis, cocaine or ATS

4
limbic reward regions and is involved in higher-order executive functions, such as, self-control,
salience attribution and awareness. These studies assert that chronic compulsive drug taking and
disadvantageous (socially unacceptable) behaviours associated with addiction are the result of
disruption of the prefrontal cortex, resulting in the erosion of free will (Goldstein & Volkow, 2011).

Several authors have criticized these neurobiological explanations and challenged the basic
assumptions and foundations of the brain disease model of addiction. Hall et al (2015) note that
addiction is not a chronic relapsing disorder, citing epidemiological evidence that most people with
addiction recover without treatment (Heyman, 2009; Kincaid & Sullivan, 2010; Satel & Lilienfeld,
2013). According to developmental neuroscientist Marc Lewis, the disease model does account
better for the neurobiology of addiction than other models and provides a framework for people to
explain their addiction and deal with the complex feelings involved – helplessness, guilt, shame, and
blame. But, citing natural recovery rates of 50-80% in alcoholics, Lewis argues that, even from the
perspective of neuroscience, the phenomenon of addiction does not lend itself to two (qualitatively)
different states: disease and non-disease (Lewis, 2013).

The internal inconsistency these authors point at is illustrated by numerous empirical social
epidemiological and qualitative studies of various drugs and consumer populations. From the
spontaneous recovery from heroin addiction among American G.I.s, returning from Viet Nam in the
1970s (Robins, L.N., Helzer, J.E., Hesselbrock, M. and Wish, 1979; Robins, 1993; Robins, Helzer, &
Davis, 1975) to the variations in consumption patterns, documented in the studies of cocaine use by
Cohen et al. in Amsterdam (Cohen, P. and Sas, 1993; Cohen & Sas, 1994), DeCorte et al. in Antwerp
(Decorte, T. and Slock, 2005; Decorte, 2000), Zuffa et al. in the Tuscan region in Italy (Meringolo P.,
Petrini F. Zuffa G., 2014) and Alves in São Paulo (D. Y. D. Alves, 2015), ecstasy (Nabben, T., Benschop,
A., Korf, 2011) and even heroin and crack-cocaine (Blackwell, 1983; Jean-Paul Grund, 1993; Stallwitz,
2012; Stallwitz & Shewan, 2004), these studies document a rich variety in both consumption patterns
and in the efforts people who use drugs undertake to regulate or control their intake of drugs.

Epidemiological studies suggest that addiction to various substances may carry over in subsequent
family generations (Kimura & Higuchi, 2011; Palmer et al., 2015; Reilly, Noronha, Goldman, & Koob,
2017). Nonetheless, while studies of the genetics of addiction have identified a number of ‘addiction
genes,’ many more are implicated in the genetic susceptibility to addiction (W. Hall et al., 2015). By
themselves, these genes are poor predictors of addictive behaviors (Ball, 2008; W. D. Hall, Gartner, &
Carter, 2008; Kendler et al., 2012). In various combinations they do predict the risk of addiction, but
as Hall et al. (2015) note, no better than a simple family history (Gartner, Barendregt, & Hall, 2009).

Likewise, animal models of addiction are often projected on human behavior, but in animals chronic
self-administration of drugs does not invariably lead to addictive behavioral patterns (W. Hall et al.,
2015). For example, rhesus monkeys with time limited unrestricted daily access to cocaine (four
hours a day; each lever press giving a dose of cocaine) developed remarkably regulated daily cocaine
intake patterns that were sustained over periods of months (Wilson, Hitomi, & Schuster, 1971). But
in increasingly restrictive experimental regimes, such as a progressive ratio schedule (which increases
the No. of lever presses required for a dose of cocaine) (Johanson, 1984) the same monkeys will
frenziedly press the lever more than 10.000 times (Yanagita, 1973).

As in most animal studies, animal models of addiction rely on specifically bred strains of rats and
standard experimental conditions in which the animals are housed that are a world apart from this

5
species natural habitat. Housed in more natural conditions or ‘enriched environments’, rats taught to
self-administer opiates respond different to this substance than those housed in standard laboratory
cages. Under more natural conditions of feeding, play, mating or nesting, rats might not completely
eschew addictive substances all the time, but they largely abstain, favoring these natural rewards
(Ahmed, Lenoir, & Guillem, 2013; B. Alexander, Hadaway, & Coambs, 1998; B. K. Alexander, Coambs,
& Hadaway, 1978).4 Thus, the results of animal studies largely rest on an ultimo reduction of normal
rat life into a high stress Ratu Graib, a matter generally underplayed by its proponents (Ahmed et al.,
2013) and poorly understood by the public and drug professionals alike (W. Hall et al., 2015).
Importantly, animal models of addiction do not consider spontaneous recovery (P Biernacki, 1990;
Patrick Biernacki, 1986; Engel H. Prins, 2008; C Winick, 1962; Charles Winick, 1964), implicitly
assuming that once addicted an animal (and, by analogy, a person) will remain addicted without
treatment and at high risk of relapse long thereafter (W. Hall et al., 2015).

Human neuroimaging studies of people addicted to drugs have received strong methodological
critique that question the ‘significant’ differences reported from small samples(Button et al., 2013;
Ioannidis, 2011), selective publication of positive results and further biased reporting (Ioannidis,
Munafò, Fusar-Poli, Nosek, & David, 2014). Even in more robust studies that report differences
between the brains of addicted people and controls, large overlaps are observed in structure (size),
activity and functionality (W. D. Hall, Carter, & Yücel, 2015). Such limitations are acknowledged by
those publishing these studies (Nutt, Lingford-Hughes, Erritzoe, & Stokes, 2015), but hardly ever
make it into the popular and media discourse (W. Hall et al., 2015). Other authors have argued that
neuroimaging bears no relevance on causality in addiction (Ersche, Williams, Robbins, & Bullmore,
2013), differences in brain activity between people who are ‘addicted’ and those not do mean that
drug use is an irresistible compulsion (Hyman, 2007; Kincaid & Sullivan, 2010). Likewise, the brain
disease model does not answer the question why people take drugs. It equates the neurology of drug
action with the neurology of motivated action (J. Davies, 2017). In other words, the desire to take
drugs is the same as the direct effect of drugs on specific brain functions. This equates cause and
effect, which, as Davies explains, is an(other) internal contradiction, or a ‘dualist delusion (J. Davies,
2017).

Without a doubt, all psychoactive substances temporarily change how specific neurons in people’s
brains behave (communicate with one another), but so far, studies have not been able to identify the
biological substrate of addiction, which would differentiate individual addicted to psychoactive
substances from those who are not (Hart, 2017; Hart, Marvin, Silver, & Smith, 2012). As Hart notes,
only very few people taking these substances become addicted (Csete et al., 2016; Mental Health
Services Administration, 2012; Warner, Kessler, Hughes, Anthony, & Nelson, 1995), while those that
do develop compulsive drug consumption patterns (a relatively small percentage) are often facing
coexistent mental health and socioeconomic problems (Hart, 2017).

As the neurobiology of addiction gets increasingly complex, neuroscientists have moved from one
area of interest to the next, perhaps driven more by the speed of medical technology than by solid
theoretical and empirical considerations. Pointing at the abundancy of evidence on psychological,
social, economic and situational factors in initiating addiction and their complex interplay with
genetic and other biological factors, Kalant noted that “a reductionist approach which attempts to

4
See the online comic “Rat Park” by Stuart McMillen (2013) for an accurate portrayal of the results and history
of the Rat Park studies by Alexander and colleagues [LINK].

6
analyse addiction at ever finer levels of structure and function, is inherently incapable of explaining
what causes these mechanisms to be brought into play in some cases and not in others, or by self-
administration of a drug but not by passive exposure” (Kalant, 2010).

The Gateway Theory

Other Studies have described a typical sequential progression of drug involvement, from the use of
legal substances, such as alcohol and/or cigarettes, to cannabis and onto other illicit and (diverted)
prescribed drugs over a lifespan (Baggio et al., 2015; Degenhardt et al., 2010; Fergusson, Boden, &
Horwood, 2006; D B Kandel et al., 1992a; Kirby & Barry, 2012). Significant associations between
earlier use of alcohol and cannabis and use of other illicit drugs later in life were reported (Denise B.
Kandel, 2003; Kirby & Barry, 2012). In particular, frequent cannabis use has been associated with use
of other illicit drugs, heavy drug use, dependence and poly drug use (Fergusson et al., 2006) Although
this typical sequence was observed in many studies (J. A. Andrews, Hops, Ary, Lichtenstein, &
Tildesley, 1991; Baggio et al., 2015; BLAZE-TEMPLE & LO, 1992; Degenhardt et al., 2010; Donovan &
Jessor, 1983; Fergusson et al., 2006; Fergusson & Horwood, 2000; D B Kandel et al., 1992a; Kirby &
Barry, 2012; Mills & Noyes, n.d.; Welte & Barnes, 1985), studies failed to find a relationship between
drug initiation profiles and current drug use (Ginzler, Cochran, Domenech-Rodríguez, Cauce, &
Whitbeck, 2003), only moderate effects that disappeared after adjustments for stress and life-course
variables (Van Gundy & Rebellon, 2010), a declining effect with increasing age (Fergusson et al.,
2006) and atypical sequencing of drug use initiation (Golub & Johnson, 2002; Mackesy-Amiti,
Fendrich, & Goldstein, 1997). These observations are at odds with a general causal model of
progression towards harder drugs, uncontrolled or harmful drug consumption patterns (Mayet,
Legleye, Beck, Falissard, & Chau, 2016). In particular the uniform and developmentally deterministic
sequencing in drug use initiation – from ‘softer’ to ‘harder’ drugs, the core element of the gateway
hypothesis – may be more variable and opportunistic than previously assumed (Ginzler et al., 2003;
Vanyukov et al., 2012).

Many studies focus on what overall is a minority of people who consume drugs – those who got into
serious problems with their relationship with drugs at some point in their life. But these worst case
scenarios are relatively rare, with e.g. 90% of people who drink alcohol consuming this “hard drug” in
moderation. Clearly, the rate of problem use may differ by substance. For example, in 2010, 1.4%
and 1.2% of people aged 15-64 years in the Netherlands (some 12 million people) used ecstasy or
cocaine in the last month (EMCDDA, 2011b). The estimated number of problem users was
respectively 600 and 45,000 (Ouwehand et al., 2011). Likewise, studies suggest that trauma and
neglect or other mental health problems are associated with problem drug use (National Institute on
Drug Abuse, 2010). Rates of problem drug use5furthermore vary between countries. With 3.1 (per
1000 inhabitants), this seems rather low in the Netherlands, and high in countries such as the United
Kingdom (9.8) and Italy and Spain (both 8.5) (Van Laar& Ooyen-Houben, 2009). Although these data

EMCDDA: Definitions of problem and recreational and integrated drug use:

‘Problem drug use’ is defined as ‘injecting drug use or long duration/regular use of opioids, cocaine and/or
amphetamines’ (EMCDDA, Statistical bulletin 2009). This definition specifically includes regular or long-term
use of prescribed opioids such as methadone, but does not include their rare or irregular use, or the use of
ecstasy or cannabis.
Recreational drug use … means the use of psychoactive substances to 'have fun' in nightlife (EMCDDA, 2002).

7
need to be interpreted with caution because of variations in method and definitions, these
differences are striking and pointing towards variations in the cultural assimilation of drug use
between countries and cultures.

Understanding the Ecology of Drug Consumption

Not a disease. Drug Use as part of the Human Condition

Critically examining the scientific evidence for the brain disease model of addiction or gateway
theory suggests that there is insufficient support for the concept as addiction as a disease (W. Hall et
al., 2015; Hart, 2017). Drug use is not a disease, whether this concerns occasional, recreational or
heavy, compulsive consumption and drugs should not be equated with infective microbe agents or
other pathogens. In contrast with bacteria or viruses (always on the look-out for a good host), drugs
are lifeless commodities. Nor should they be compared to e.g. environmental pollution, which may,
end up in our body unwittingly and unwanted. Drugs6 only become active and do what they do when
we put them into our bodies and people who use drugs (PWUD) generally do so voluntarily. What
matters therefore is, first of all, the relationship that we as humans develop with psychoactive
substances, how we bond with these substances and how we value these bonds (Cohen, 2009; Hari,
2014).7

The bonds humans develop with psychoactive substances could be described in terms of beneficial or
detrimental; healthy or unhealthy; controlled or compulsory, much, as Cohen (2009) argued, as any
other bond we develop. Using psychoactive substances in a manner in which the benefits prevail
over the costs and the potential harms are minimized could be termed a healthy relationship with
drugs. Conversely, when costs or harms outweigh the benefits the relationship may be termed
unhealthy. Noteworthy is that such opposite labels do not represent binary (0 or 1) states but the
extreme positions on a dynamic continuum – these are not static features. Over time the quality of
our bonds is subject to change, as is our appraisal of their utility. Furthermore, these labels represent
values; they cannot be dissociated from the culture, our system of values and beliefs and, indeed, the
entire Human Condition, which are equally subject to change over time.8

Finally and crucially, the human relationship with mind altering drugs is not an isolated 1-on-1
relationship, our bonding with drugs is contingent on what and how we do in the rest of our daily
lives and, as I discuss shortly, on a myriad of external influences. As all of these may change over
time, so may drug use patterns. Therefore, the bonds people develop with drugs; the effects of
psychoactive substances in humans are the outcome of a complex interaction between
pharmacology, brain chemistry and ecological influences – what the American psychiatrist Norman
Zinberg described as Drug, Set and Setting in his ground-breaking book with the same title (N.
Zinberg, 1984).

6
I refer here to the use of psychoactive drugs other than prescribed by a physician or other health care
provider.
7
It should, however, be noted that consumption of psychoactive substances is not an exclusively human
activity; it has been documented in many other animal species and in the Animal Kingdom we see similar
variations in consumption patterns as among human consumers(Siegel, 1989).
8
For a more exhaustive discussion, please see Cohen, 2009.

8
Drug, Set & Setting
The use of mind-altering drugs is a complex phenomenon influenced by various factors, which can
roughly be grouped into three groups of variables; drug, set and setting.

All psychoactive drugs affect the brain or the central nervous system (CNS) and accelerate, slow
down or alter the lived experience. Drug refers to the specific psychopharmacological properties of
the substance being consumed and their effect on the brain, which are traditionally classified in
stimulants (e.g. cocaine, amphetamine, nicotine), depressants (opioids, alcohol, benzodiazepines)
and hallucinogens (LSD, Psilocybin, 2CB, DMT). Not all psychoactive substances fit that easily in this
classification. Ecstasy has, for example, both stimulant and mild hallucinogenic (entactogenic or
empathogenic) effects, while ketamine, a dissociative anaesthetic has both depressant and
hallucinogenic effects. The effects of drugs both affect and are mediated through different brain
chemicals (neurotransmitters), such as dopamine or serotonin. These neurotransmitters act at the
synapses, the junctions where neurons (or nerve cell) exchange chemical or electrical impulses in an
effort to maintain homeostasis.9 Different (classes of) drugs affect the release of neurotransmitters
differently. For example, amphetamine increases dopamine release, while cocaine prevents its re-
uptake. A drug’s half-life, the body’s metabolism and individual physiology further contribute to the
outcomes of these brain processes. The route of administration and the dosing (amount and timing)
of the drug taken and its purity are also important determinants of the drug experience. Injected, the
effects of any drug are more rapid and stronger than when (in order of magnitude) inhaled via the
lungs (a close 2nd), snorted, anally inserted or swallowed. Just about all drugs mostly do what they
promise; providing pleasure, relief or other complex feelings that people seek. But they do so
differently for different people.

Zinberg proposed a rather general definition of Set, “the attitude of the person at the time of use,
including his personality structure” (N. Zinberg, 1984). Set is usually interpreted as including
individual psychological characteristics and personality factors, (unconscious) motivations, attitudes,
expectations and beliefs. Depressants, stimulants and sedatives may both affect and attract people
with different psychological profiles differently (G. Andrews, Tennant, Hewson, & Vaillant, 1978;
Martin & Otter, 1996; Soussan & Kjellgren, 2016). The emotional state before, during and after taking
a drug and the expectations and beliefs a person brings to a drug experience are important
predictors how the drug effect is experienced and the experience is labelled (Becker, 1953; Schachter
& Singer, 1962). Understanding and awareness of the acute drug effects facilitates interpreting the
resulting mental state as such and not (only) as the result of (unrelated) mental or bodily processes
or external cues. This influences the meaning and label attributed to the chemistry of a (lifeless)
drug. Peoples’ beliefs and expectancies of drugs are furthermore shaped by observation of drug
taking peers or previous use and how confident they feel in handling the experience, as well as by
information on the Internet and other media and health messages received from peers or
‘institutions’ (e.g. schools or drug prevention programs). Set is often discussed in terms of
psychological deficits or vulnerability and much less in terms of resilience. (Childhood) ADHD and
trauma, Post-Traumatic Stress Syndrome, Anxiety disorder, bipolar disorder, Borderline Personality
Disorder and other mental health problems have all been associated with compulsive drug use

9
Homeostasis refers to the self-regulating processes of biological systems (like the human body or an amoeba)
that aim at keeping the system parameters within a normal range of values in order to maintain equilibrium or
relatively stability within the system environment.

9
(National Institute on Drug Abuse, 2010). If we interpret Zinberg’s words as the personal attributes
an individual brings to the actual drug experience, then a person’s biological and/or genetic
predisposition, brain chemistry and actual physical condition are arguably part of set as well. These
are generally understood as personal attributes, as are gender, age and perhaps education. Set thus
presents a complex interaction of psychology and biology, while environmental factors, such as
traumatic events, may further influence its expression. Likewise, individual beliefs and expectations
are not entirely dissociated of social beliefs and conventions.

Figure 1. Drug, set and setting (Zinberg, 1984; Grund, 1993).

Setting finally involves all the environmental variables that may influence the outcome of drug use of
use. These include formal and informal social controls and other factors exogenous to the individual.
I will specify these below.

Although Zinberg’s model closely resembles the classical epidemiological triad of “pathogen, host &
environment,” he and his colleagues explicitly rejected the disease model of addiction and focused
on the determinants of “control” and self-regulation. Based on qualitative and quantitative research
among users of various illicit drugs, Zinberg suggested that environmental variables are the main
factors in distinguishing controlled, recreational, controlled substance use from the heavy
consumption patterns we generally associate with social and health harms (Zinberg, 1984; Zinberg &

10
Harding, 1979). Several studies subsequently replicated Zinberg’s findings, for example in people
who use heroin (Blackwell, 1983; Dalgarno & Shewan, 2005; Jean-Paul Grund, 1993; Lalander, 2003;
Stallwitz, 2012; Stallwitz & Shewan, 2004), cocaine (Cohen, P. and Sas, 1993; Cohen & Sas, 1994;
Decorte, T. and Slock, 2005; Decorte, 2000; Erickson, P.G., Adlaf, E.M., Smart, R.G. and Murray, 1994;
Meringolo P., Petrini F. Zuffa G., 2014) , ecstasy (Nabben, T., Benschop, A., Korf, 2011; Shewan,
Dalgarno, & Reith, 2000) or cannabis (Sifaneck, Kaplan, Dunlap, & Johnson, 2003). The setting, or
environment, is furthermore not a static condition, but a complex interactional arena where
individuals and groups actively interact with each other and with structural institutions. Rhodes
therefore speaks of a “risk environment” (Rhodes, 2002, 2009).

Control, Can We Have Some?

Use of psychoactive drugs is tied to formal and informal controls – rules and constraints. Legal drugs
such as tobacco and alcohol are controlled by formal rules and regulations – explicit commandment
provisions and partial prohibitions – that in themselves do not forbid their consumption when
certain conditions are met (such as taxing, quality control, licenced points of sale, opening hours, age
and traffic restrictions). Within this legal latitude, consumption of legal substances and preventing
their potential harms is a matter of individual responsibility, social control and, many would argue,
media and market forces. In the case of illegal drugs, the picture gets a bit more opaque. Not only
does legally banning (certain) drugs fail to meet its own goals and objectives, drug prohibition adds
to the ‘burden of disease’ associated with drug use and social injustice and diverts needed funding
from harm reduction, prevention and treatment (Csete et al., 2016; W. Hall et al., 2015; Hart, 2017).
In effect, prohibition means handing over control to unregulated market forces, while effectively
preventing (health) authorities using proven effective tools effectively. More recently, the rise of new
psychoactive substances (NPS) or legal highs and iDrugs (drugs, both scheduled and unscheduled,
sold online) has further muddied the idea of controlling drug consumption through criminal law and
enforcement. With 101 new Figure 2. Drug Policy and social & Health Harms (source: Global
psychoactive substances first notified Commission on Drug Policy
to the EMCDDA early Warning
System in 2014 and over 450 new
psychoactive substances under
scrutiny in 2015 (Evans-Brown et al.,
2015), the changing landscape of
intoxication and the digitalization of
drug markets is perhaps the greatest
challenge the international drug
control system is facing since the first
International Opium Convention in
The Hague in 1912. Figure 2
illustrates how both regimes result in
the absence of effective regulation
and contribute to high levels of social
and health harms.

Banning drugs also presents an obstacle to effective peer driven harm reduction, self-regulation and
social control in drug use. Many authors have described the pernicious role of stigma and social
exclusion that results from the punitive approach to drug use (Csete et al., 2016; W. Hall et al., 2015;

11
Hart, 2017) . But prohibition also presents an obstacle to the collective, peer-based accrual of
knowledge on non-problematic drug consumption patterns and obstructs knowledge transfer within
and between generations (Jean-Paul Grund, 1993). Indeed, one can observe “generational
forgetting” (Johnston et al., 2011) among new generations of drug users, policy makers and society
alike. Each new generation of illicit drug consumers is thrown back at itself in acquiring controlled
usage patterns. With the seemingly endless supply of “Mystery White Powders,” this may equally
apply to the unrestricted markets in NPS, although harm reduction is a major theme in online drug
forums (Móró & Rácz, 2013; Soussan & Kjellgren, 2014). Below, I further discuss the influence of
prohibition on peoples’ drug taking patterns.

Despite these considerable obstacles, self-regulation strategies are a common feature in most
people’s drug consumption; of any psychoactive substance – old, new, legal or not. A key question
therefore is what prevents people’s drug use from getting out of control – as is assumed to be
inevitable in the long run by the Gateway theory and other biomedical explanations of drug use and
addiction – or from resulting in drug related harm? How do people safeguard themselves from their
relationship with drugs going sour? What strategies do drug users apply to regulate intoxication and
the associated risks, the risk of dependence or habitual use in particular? What variables impact on
people’s ability to self-regulate their consumption? These are some of the questions that I aim to
address in the remaining pages of this chapter.

Social Controls: Rituals and Social Sanctions

In their detailed study of "controlled" and "compulsive" drug use, Zinberg and his colleagues found
that all drug users, to some extent, ritualize their drug intake, and that "controlled use of illicit drugs
is mainly supported by subcultures of drug using individuals by applying rituals and social sanctions"
(N. Zinberg, 1984).

Rituals are stylized, prescribed behaviour patterns surrounding substance use, including the methods
of acquisition and administration, the selection of the physical and social environment for use,
activities after the drug is administered, and methods to prevent unwanted effects of the drug or its
status (Agar, 1973; Jean-Paul Grund et al., 1993; Moore, 1993; N. E. Zinberg, Harding, & Winkeller,
1977).

The following two field notes10 give an impression of the ritualized behaviors involved in chasing
cocaine.

“He puts some pieces of base on the foil. From his pocket he takes a tube and starts to chase
the cocaine base. He follows the drug carefully on the foil. However, the cocaine follows a
very whimsical path on the foil. The drop splits up several times and when he stops heating
the foil it spreads into a large spot. After exhaling he starts again but he first chases the
offshoots of the spot making it one drop again.”

Smoking cocaine from tinfoil is not the easiest of tasks, requiring concentration and specific skills that
are honed through ritualized practice. The next note field note illustrates how these subcultural
rituals and the required knowledge are conveyed among people who use drugs. Note that even
regular cocaine smokers take an active interest in their health.

10
All field notes are drawn from my earlier work (Jean-Paul Grund, 1993); some were slightly edited.

12
 One of the [men] was explained a part of the cocaine chasing ritual. One of his friends put a
lump of base on the foil and then with a lighter ... he melted the lump from above until just a
little smoke came off. “This is what you do to take the ammonia rests out of it. It's better for
your lungs and you taste the difference,” one of his other friends said.

Social sanctions refer to the norms on how, or whether, a particular substance should be used. Social
sanctions include informal, often unspoken, values or rules of conduct, shared by a group, as well as
formal norms, as in legislation and policy.

The young man prepares the cocaine and shares it with his mate. One of the other men at the
table, who just finished his cocaine, asks him “Could you spare me a knife tip?” The young one
excuses himself for being not able to help him. But one minute later he grabs a knife from the
table and takes a little bit of cocaine base of his foil and puts it on the foil of the guy who had
previously asked, saying: "Sorry, I can't miss more; we already have to smoke from it both."

Although first excusing himself, the young man subsequently shares a part of his drugs with someone
he is not familiar with. By doing so, he complies with the almost universal peer norm that governs
the collective use of drugs, that of sharing some of your drugs with a fellow user that is in need and
also hints at its exceptions (Y. D. D. Alves & Delgado, 2016; Jean-Paul Grund, 1993; Lalander, 2003;
Stallwitz, 2012). As Marcel Maus explained, such is not a gratuitous gift (Mauss, 1925; Mauss & Halls,
2000). By giving some of his drugs the giver increases both his status as a credible community
member and the probability that his gift will be reciprocated when the roles are reversed.

Both rituals and social sanctions (rules) are aimed at managing the process of and around the use of
drugs. Important is that rituals and social sanctions surrounding drug use include both rational and
non-rational elements. Because the rituals of controlled and compulsive consumers are often very
similar, these two groups distinguish themselves mainly by the different social sanctions they abide
with. It is therefore important to clearly distinguish the two terms because "the distinction between
drug rituals and social sanctions is one of behaviour versus belief, or practice versus dogma" (Zinberg
& Harding, 1979). Zinberg and colleagues emphasized that drug, set and setting are not independent
influences, but represent an intricate interplay. The fit between pharmacology and personality may
thus differ between individuals and cultures, and between locations and times.

Modulating Contingencies: Drug Availability and Life Structure

Zinberg attributed particular importance to social rules and rituals in maintaining controlled drug
consumption patterns. Building on his work, I have argued that the effectiveness of these social
controls in controlling drug use is modulated by additional factors, such as the conditions under
which drugs are available and, what Faupel termed, ‘life structure’ (Faupel, 1987). Both the
availability of drugs and an individual’s life structure affect one’s ability to abide with these social
regulatory mechanisms (Jean-Paul Grund, 1993). Figure 3 presents a three cluster feedback model of
drug use self-regulation and details the factors in each cluster.

The availability of drugs does not only affect the extent, but also the nature of substance use, such as
the route of administration or the degree of secrecy surrounding it. Scarcer drugs are more often
administered by more efficient modes of administration (J.-P. C. Grund & Blanken, 1993), such as
injecting or smoking cocaine – potentially leading to greater health damage. When drugs are scarce
or novel, rituals increase in importance and become more rigid, while social sanctions are less well

13
developed and supported. In the late 1980s, when ecstasy hit the club scene of Amsterdam, patrons
on the drug switched en masse from alcohol to mineral water. Later on, when clubbers got better
acquainted with the drug’s effects, their alcohol drinking patterns returned to ‘normal’ again. They
did so in a relatively drug policy climate. When, however, a substance use is prohibited and strictly
enforced, and anonymity thus important, rituals and rules focus more at the preservation of
anonymity and avoiding contacts with law enforcement or other state agents than on safer use
(Jean-Paul Grund, 1993). Such concerns may quickly outweigh health concerns among people who
use drugs heavily (Connors, 1992).

Next to economic considerations, the life structure of people who use drugs and situational factors
play a role of significance in upholding rules and rituals, and thus also in the occurrence of drug
related problems. Faupel (1987) described successful addicted thieves who kept their use under tight
control until they made a big sting, making plenty of drugs available, subsequently axing the need for
regular (criminal) activities and thus eroding the importance of rituals and rules. Grund described
cocaine dealers in Rotterdam as small entrepreneurs with a full agenda, who smoked much cocaine,
but seemed to experience few mental health problems commonly associated with heavy cocaine use.
This was in contrast to the problematic, often homeless, users on the street he studied, who used
much less cocaine, but presented with much more cocaine-associated mental health problems
(Grund, 1993). Both authors emphasize the interplay of these environmental variables and Grund
suggests that the dynamics between these three clusters of environmental variables
(availability/access, rituals and rules, and life structure) largely determines the effectiveness of self-
regulation processes (Faupel, 1987; Jean-Paul Grund, 1993).

The Ecology of Risk: Conditional Causality in a Challenging 'Living World’

Self-regulation furthermore goes beyond limiting the quantities of drugs that one consumes. It also
concerns the prevention and control of drug related problems (Grund, 1993) and here we can again
distinguish multiple environmental factors exogenous to the individual that modulate the drug use
experience and the likelihood of social and health harms. The British sociologist Tim Rhodes first
introduced the term ‘risk environment’ in which he further detailed the environmental factors that
may impact on drug use and HIV risks in particular into four types of influences – physical, social,
economic and political – that may exercise their power on two-levels (Rhodes, 2002, 2009; Strathdee
et al., 2010).

The micro risk environment focuses on personal decision making and the influence of common
norms and practices, e.g. in networks of drug users. The macro risk environment aims to describe
structural factors, such as laws and their implementation, economic conditions and broader cultural
beliefs or practices (Rhodes, 2002; Rhodes, 2009). This framework is useful because it is shifts the
focus of attention from individuals to the social situations, processes and structures in which people
participate and communicate (Rhodes et al, 2009).

14
Figure 3. The Risk Environment of Psychoactive Drug Use At its core, the risk environment is
about complexity and contingent
causation (Glass &McAtee, 2006),
the phenomenon that in many
social and health problems
causation is conditional. The risk
environment puts particular
emphasis on the interaction
between the individual, his or her
immediate social environment and
the structural determinants of risk
behavior and drug-related
problems, such as the (drug)
economy and (drug) policy. The
concept allows for sufficient space
for exploration of how structural
forces influence the lived experience at local level differently (Duff, 2007) and it prevents that
individuals are put away as largely passive and therefore complicit in the structural determinants of
social problems and health damage (Fitzgerald , 2009). In other words, we react to and anticipate on
the forces in our environment and thereby we change her.

Discussion
In this paper I have examined the evidence for the brain disease model of addiction and the closely
associated gateway theory, relying on the critical review work of eminent researchers in this field (W.
Hall et al., 2015; Hart, 2017). I have presented evidence from various disciplines that casts serious
doubts on the rather unidirectional and unidimensional assertions of the brain disease model of
[Drugs + Brain = (eventually) Disease] and presented an alternative conceptualization of drug use.

Addiction as a Brain Disease

The biomedical sciences and neuroscience in particular are contributing considerable interesting and
useful knowledge to our understanding of the brain, not only on the biological substrate of addiction.
Nonetheless, truly understanding the brain is still in its infancy, as is understanding the role of brain
chemistry and wiring or genetics in the consumption of psychoactive substances. A critical
examination of the evidence base of the brain disease model of addiction suggests that the
neuroscience or biomedical sciences are far away from providing a conclusive explanation of
addiction, pointing at important shortcomings in reliability, validity and generalizability. Researchers
from within and outside the biomedical sciences have pointed at lack of scientific rigor in
neuroscientific studies of addiction (J. Davies, 2017; W. Hall et al., 2015; Hart, 2017; Lewis, 2013).
Discordant findings such as from the body of social scientific studies discussed in this paper, or
alternative explanations that question the reductionist/materialist biomedical explanation of
addiction, are routinely ignored. Many brain scientists take great liberty in interpreting their findings
and generalizing findings from small samples of ‘addicted brains’ to wider populations of people who
use psychoactive substances. Neuroscience may be describing the chemistry and circuitry involved in
the biology of intoxication, but not the reasons why people use drugs, whether in moderation or in

15
excess, or those for ceasing to do so. Furthermore, the humongous investments in the neuroscience
of addiction have yielded very little return in terms of new addiction treatments. In fact, Methadone
maintenance treatment and the principle of drug substitution predate the idea of addiction as a
brain disease (Leshner, 1997) over three decades (W. Hall et al., 2015). Carter & Hall (2010) called for
“more explanatory humility in addiction neurobiology.” Indeed, neuroscientists should be much
more reserved in communicating their results to wider audiences (J. Davies, 2017; W. D. Hall et al.,
2015).

Brain Disease as an Apologue

The unidimensional apologue of addiction as a brain disease does indeed matter, but the question is
to whom. Overblown interpretations of brain studies feed into the limited understanding of the
science of addiction among the “general and not-so-general public” (J. Davies, 2017). People fancy,
what Davies termed, scientistic explanations that offer absolvence – in the sense meant by Heidegger
(Richardson, 2013) – of the responsibility for disapproved-of behaviours and relabel them as
‘suffering from’ (imaginary) disease (J. B. Davies, 2013; Lewis, 2013). In other words, the disease
model provides people with a powerful cognitive dissonance reduction tool.

Brain Disease as an Instrument of Drug Policy

But perhaps a more relevant question is what explains its dominance in science, policy and drug
services at the expense of competing perspectives on drug use and addiction from the social
sciences, humanities, criminology or economical and other disciplines that looked at the
phenomenon of human drug consumption. The emphasis on the (diseased) brain did, for example,
not have much of an impact on ‘addiction rates,’ drug demand or drug supply in the last 20 years and
has done little to remove the stigma associated with drug use or addiction but, in contrast, breeds
disease, prejudice and social injustice and, importantly, detracts funding from evidence based public
health strategies (Csete et al., 2016; W. Hall et al., 2015; Hart, 2017). This has not prevented many of
the (unsubstantiated) assertions of the biomedical model becoming conventional wisdom, which, as
John Kenneth Galbraith explained, serves to maintain the status quo and the vested interests of
those in power (Galbraith, 1958). And, as Davies notes, the dominance of the bio-medical model is
not (solely) a matter of academic merit, but a power struggle over grants and status and the perks
that come with these; a “war” in which, since the idea was first coined (Leshner, 1997), the medium
continues to be the message (McLuhan & Fiore, 1967) but “in equipment terms, it’s asymmetric
warfare,” Davies writes (J. Davies, 2017). Albert Einstein reportedly first pencilled many of his
theories on the back of an old envelope or other scratch paper (Isaacson, 2007). Today, media savvy
celebrity brain researchers are “Trumpeting” oversimplified findings and interpretations in sleek
YouTube videos to the backdrop of large humming and flashing machines and alluringly colorized
(Hickman 2014) 3D renderings of the brain. With complex academic papers11, “disgruntled opinion
pieces” and two-dimensional PowerPoint renderings at scientific or drug policy conferences, the
proponents of competing perspectives are clearly outgunned (J. Davies, 2017).

Towards a Paradigm Shift

While this may be true, in the last years we are witnessing important changes in the balance with
interventions and policies that rely on competing perspectives. Important harbingers of change are
the growing number of countries and states that legalized cannabis for medical and/or recreational

11
Such as this one.

16
consumption; harm reduction measures, such as heroin prescription programs12, Naloxone
prescription and training or drug consumption rooms (Stone, 2016). The Dutch were perhaps the first
to embrace the (then pre-natal) idea of drug, set and setting (J-PC. Grund & Breeksema, 2017), but
meanwhile these are evident in a growing number of countries. Furthermore, neuroscience – with
the limitations discussed – is certainly part of the equation. In particular outside the
morally/politically tainted area of drug use and addiction we can find fascinating new research, which
may also bear on our understanding of drug in the brain. For example, memory reconsolidation
experiments have shown that the neuronal basis of memories is much more variable than previously
assumed (Dębiec, Bush, & LeDoux, 2011; Nader, 2015a, 2015b; Sara, 2000). In other words, each
time we recollect a memory, it changes (a bit) and so does our brain wiring. Based on this finding,
Dutch researchers are now exploring interesting new pharmaco-behavioral treatments for PTSD and
other anxiety related disorders (Kindt, Soeter, & Vervliet, 2009; Soeter & Kindt, 2010, 2012). Overall,
this may imply a larger degree of plasticity of the brain than the brain disease model assumes, which,
I suggest, offers openings towards collaboration with the behavioral, social and other relevant
sciences.

However, to gain a really comprehensive understanding of ‘addiction,’ it must be conceptualized

within the entire spectrum of human drug use and the multiple forces that shape drug using careers
over time. This requires a paradigm shift in drug research, policy and intervention towards an
ecological perspective on the use of psychoactive drugs and integrative transdisciplinary research
methodologies. The works presented in the previous section provide the rationale for this paradigm
shift and outline the theoretical fundaments of this new paradigm. At the core is a different way of
looking at drug use, not for (1 on 1) causality, but for contingencies (Rhodes, 2009). Although each of
these authors emphasizes different aspects, they unanimously stress the interaction between
pharmacology, psychology and environment that codetermine peoples’ patterns of substance use
and the potential for effective self-regulation (Jean-Paul Grund, 1993; Rhodes, 2009; N. Zinberg,
1984). In other words, human drug use is located in an ecology where these biological, psychological
and social factors meet and exercise mutual influence on its outcomes (MIOVSKY et al., 2016).

Meanwhile, the thinking about drugs continues to be largely unidirectional and unidimensional
among many academics, policy makers, the general and ‘not so general’ public alike. This is not
merely the outcome of asymmetric science wars. To many people, the ideas presented in this paper
and book may sound radical and it will take time for these to sink in. After all, it took the Vatican 350
Years to utter Galileo Was Right (COWELL, 1992). Indeed, Galileo’s ideas were long subject to similar
asymmetric warfare. And, with respect to the arsenal in the battle for the hearts and minds of the
public, it should be noted that, despite the emphasis on interaction in the works of Zinberg, Rhodes
and Grund, the graphical representation of their ideas is two dimensional (and thus no match with
the PR machine promoting the brain disease model). In thinking how to best graphically present the
complex idea of drug use as subject to multi directional and multidimensional contingencies in a way
that approaches this dynamic, I was very much inspired by the videos of the helical model of the
Galaxy by DjSadhu13, which suggests that the planets does not merely move in heliocentric motion
around the sun, but as a helix, subject to forces that vary with it’s the sun’s location in the universe.
Since these two videos appeared, they were followed by several online pieces pointing at several

12
Which I view as an 'availability intervention,' a social-economic intervention with a pharmacological agent.
13
See https://www.youtube.com/watch?v=C4V-ooITrws

17
(mathematical) in accuracies.14 But that is not my point. Whether the helical model represents the
universe mathematically accurate or not (forget the mathematics), I suggest that, in illustrating the
complexities involved in drug use, it provides a useful metaphor for visualizing both the social and
individual space of the human drug use experience (perhaps the entire human experience) and the
forces that shape its pathway15. I have tried to do so in figures 4 & 5.

Figure 4. A Helical view of Drug Use Pathways – The Helix of Self-Regulation (I. the Social Universe)

Figure 5. A Helical view of Drug Use Pathways – The Helix of Self-Regulation (II. the Set)

Attributing magnitude or direction

to the forces involved in the self-
regulation of drug use is beyond
the scope of this paper. Claims, like
“at least half of a person's
susceptibility to drug addiction can
be linked to genetic factors” (Price,
2008) are meaningless as they are
devoid of context. “Life is, after all,
a helix, not just rotation.” None of
these forces explains drug use by
itself, none of them is constant in
time or space, but they may all
influence a drug use career and
each other and may do so differently at different points on this journey. Explaining this complexity is
beyond the reach of any discipline.

14
See e.g.
http://www.slate.com/blogs/bad_astronomy/2013/03/04/vortex_motion_viral_video_showing_sun_s_motion
_through_galaxy_is_wrong.html
15
Without the suggestion of magnitude or direction of force.

18
This, I suggest, will require a transdisciplinary ecological research approach, which aims to promote
novel conceptual and methodological integrations of knowledge from biomedical, psychological,
social scientific and other relevant disciplines within an issue-driven research framework. A
collaborative scientific approach that transcends the theoretical insights and methodological
boundaries of the multiple disciplines involved in drug studies (Choi & Pak, 2006; Nicolescu & ERTAS,
2008; Stokols et al., 2003) – one that appreciates the various aspects of drug use as intimately
interconnected and explicable only by reference to the entire experience.

I propose that this should be an open research platform where researchers of different disciplines
meet and, collegially but critically examine and interpret their methodologies, data and findings
together against the collective body of knowledge their areas of expertise represent. A research
platform that, rather than neglecting these, embraces discordant data and methodological
challenges and aims to develop new, transdisciplinary methods for studying the human penchant for
intoxication (Siegel, 1989). An open and transparent platform that integrates the experiences of the
social actors and key populations involved – of people who use drugs (PWUD) and their families,
policy makers, service providers and other stakeholders. Such a transdisciplinary research effort will
build common paradigms, a shared language and, indeed, a new epistemology of drug use and
encourage the generation of new knowledge and theory towards meaningful progress in our
understanding of the complexities surrounding human drug consumption (MIOVSKY et al., 2016).

I am well aware that implementing this framework for drug science is ambitious and its
implementation will be a complicated and protracted process, but my hope is that such a framework
will contribute to a more comprehensive understanding of the entire landscape of intoxication and a
more solid evidence base for effective and humane drug policies.

Lessons for Drug Policy and Interventions

The current, prohibition based, approach to, what psychopharmacologist Ronald Siegel termed, our
“4th Drive” (Siegel, 1989) relies largely on a political ‘disease myth’ that is being sustained by the
brain disease and other deficiency based models of addiction. While evidence-based decision
making, evaluation and tailored regulation are making headway in every conceivable policy area,
drug policy seems much less bound by the rules of rationality, transparency or individual liberties. It
has not delivered on its own objectives at great human (lives lost; infectious diseases, incarceration,
stigma) and economic cost and cannot be trusted to do so anytime soon. Prohibition of drugs
effectively results in relinquishing the drug market to criminal entrepreneurs. Or, in its most recent
fall-out, the rise of NPS and (deep) web drug markets, to free marketers. Neither can be trusted to
act in the interest of the public and nor can a government that bases such consequential public
policies on mythology. In few other public policy areas, this would be an acceptable outcome. Public
policies rooted in the ecological perspective, on the other hand, do live up to their objectives (Colson
& Bergeron, 2017; Csete et al., 2016). They are simply better in sync with the playful nature of
humans (Huizinga, 2003) and allow for moving beyond the objective of rebalancing drug policies
from law enforcement to the health pillars. Indeed, effective regulation is better.

Not all drugs are the same. Different (classes of) drugs require different control regimes, both in
terms of formal control (tailored government regulation) and informal controls. Important is that the
(illegal) status of drugs, and the resources that a society employs to enforce this status, has not only
consequences for the potential for drug related harm, but also for the actual outcomes of drug use

19
itself and the ability to exercise control over one’s personal drug use. It was Sir Karl Popper in his
influential The Open Society and Its Enemies, who wrote that the role of the state is not to make
people happy, but to relieve avoidable suffering (Popper Karl, 1945). In an open society, creating
happiness ought not to be a task of the government and its agencies, but to support individuals and
their social associations in the prevention and reduction of problems they encounter in the pursuit of
happiness. In an open society, the government lays out the ground rules for transparent social and
economic relationships, equality and equivalence and aims to strike a balance between effective
government regulation and individual liberties and responsibility, good citizenship and self-
regulation. In the process, the government should do no harm. The definition of happiness and its
pursuit (e.g. free partner choice or substance use) should, according to Popper, be left to the
individual and his social associations.

Not all people are the same. The ecological perspective outlined in this paper helps to understand
the interaction of pharmacological drug effects, human psychology and environmental contingencies
that shapes the outcomes of psychoactive drug use and bears on individual’s susceptibility to ‘out-of-
control’ consumption and vulnerability to drug-related harms, including infectious diseases and
overdose. Certainly, people’s mental status impacts on their ability to self-regulate their
consumption of psychoactives or prevent other drug related harms. Therefore, decent screening for
co-morbid mental health problems at intake is a prerequisite for all drug treatment. But
vvulnerability to drug-related harm is closely related to more general inequalities in health, social
and material conditions (Hart, 2017; Rhodes, 2009) and telling people they have a chronic disease
does not help. An environmental approach exposes the parallels and linkages in how health,
vulnerability and resilience, drug use in general, and drug-related harm in particular, are influenced
by context and dovetails with calls for a paradigm shift in Public Health from behavioral to ecological
change strategies (Diez Roux, 2007; Susser & Susser, 1996). It seeks to move the focus of change
from the individual to the social situations and structures in which people participate and interact
(MIOVSKY et al., 2016; Rhodes, 2009). This shifts the focus of intervention strategies for drug or other
health problems to broader issues such as self-determination and emphasizes empowerment and the
importance of non-drug and non-health interventions to reduce such problems.

The contributions in the remainder of this book discuss the practical implications of the ecological
perspective for people who use drugs, service providers and policy makers. Concepts, such as self-
management and its relation to self-change, are discussed, as is taking people’s competencies as
resources; handles in support of resilience. The role of moderation management in therapeutic
communities is examined and, indeed, the consequences for the culture and mission of drug
prevention and treatment services. Finally, the book offers practical guidance for people who use
drugs and drug services providers and innovative examples of such approaches, both in the
community and online

Italy was on the forefront of a paradigm shift in psychiatry, moving the treatment of mental health
problems from institutions to community-based services. This book shows that Italians may, once
more, take the practical lead towards an equally momentous and much needed paradigm shift.

20
References
Adams, J. B., Heath, A. J., Young, S. E., Hewitt, J. K., Corley, R. P., & Stallings, M. C. (2003).
Relationships between personality and preferred substance and motivations for use among
adolescent substance abusers. The American Journal of Drug and Alcohol Abuse, 29(3), 691–
712.

Agar, M. (1973). Ripping and running: A formal ethnography of urban heroin addicts (Vol. 1).
Academic Press.

Ahmed, S. H., Lenoir, M., & Guillem, K. (2013, August). Neurobiology of addiction versus drug use
driven by lack of choice. Current Opinion in Neurobiology.
http://doi.org/10.1016/j.conb.2013.01.028

Alexander, B., Hadaway, P., & Coambs, R. (1998). Rat Park Chronicle (From Drugs: Should We
Legalize, Decriminalize or Deregulate? P 266-270, 1998, Jeffrey A. Schaler, ed.--See NCJ-
172364).

Alexander, B. K., Coambs, R. B., & Hadaway, P. F. (1978). The effect of housing and gender on
morphine self-administration in rats. Psychopharmacology, 58(2), 175–179.
http://doi.org/10.1007/BF00426903

Alves, D. Y. D. (2015). Jamais fomos zumbis : contexto social e craqueiros na cidade de.
UNIVERSIDADE FEDERAL DA BAHIA. Retrieved from
https://www.academia.edu/17469605/Jamais_fomos_zumbis_contexto_social_e_craqueiros_n
a_cidade_de_São_Paulo_Versão_final_

Alves, Y. D. D., & Delgado, Y. D. (2016). O uso do crack como ele é: o cachimbo, o “bloco” e o usuário.
Etnografica, (vol. 20 (3)), 495–515. http://doi.org/10.4000/etnografica.4640

Andrews, G., Tennant, C., Hewson, D. M., & Vaillant, G. E. (1978). Life event stress, social support,
coping style, and risk of psychological impairment. The Journal of Nervous and Mental Disease,
166(5), 307–16. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/650194

Andrews, J. A., Hops, H., Ary, D., Lichtenstein, E., & Tildesley, E. (1991). The Construction, Validation
and Use of a Guttman Scale of Adolescent Substance Use: An Investigation of Family
Relationships. Journal of Drug Issues, 21(3), 557–572.
http://doi.org/10.1177/002204269102100305

Baggio, S., Iglesias, K., Fournier, N., Studer, J., N’Goran, A., Deline, S., … Gmel, G. (2015). Prospective
pathways between heroin use and non-medical use of prescription opioids: Trajectories among
young Swiss men. Heroin Addiction and Related Clinical Problems, 17(1), 65–72. Retrieved from
http://www.scopus.com/inward/record.url?eid=2-s2.0-84931398196&partnerID=tZOtx3y1

Ball, D. (2008). Addiction science and its genetics. Addiction, 103(3), 360–367.

Becker, H. S. (1953). Becoming a marihuana user. American Journal of Sociology, 235–242.

Biernacki, P. (1986). Pathways from heroin addiction : recovery without treatment. Philadelphia:
Temple University Press.

Biernacki, P. (1990). Recovery from opiate addiction without treatment: A summary. The Collection
and Interpretation of Data from ….

Blackwell, J. S. (1983). Drifting, controlling and overcoming: Opiate users who avoid becoming
chronically dependent. Journal of Drug Issues. Retrieved from

21
 http://psycnet.apa.org.proxy.library.uu.nl/index.cfm?fa=search.displayrecord&uid=1984-
06662-001

BLAZE-TEMPLE, D., & LO, S. K. (1992). Stages of drug use: a community survey of Perth teenagers.
Addiction, 87(2), 215–225. http://doi.org/10.1111/j.1360-0443.1992.tb02695.x

Button, K. S., Ioannidis, J. P. A., Mokrysz, C., Nosek, B. A., Flint, J., Robinson, E. S. J., & Munafò, M. R.
(2013). Power failure: why small sample size undermines the reliability of neuroscience. Nature
Reviews Neuroscience, 14(5), 365–376. http://doi.org/10.1038/nrn3475

Carter, A., & Hall, W. D. (2010, May). The need for more explanatory humility in addiction
neurobiology: Commentaries on Kalant (2010). Addiction. http://doi.org/10.1111/j.1360-
0443.2009.02783.x

Choi, B. C. K., & Pak, A. W. P. (2006). Multidisciplinarity, interdisciplinarity and transdisciplinarity in

health research, services, education and policy: 1. Definitions, objectives, and evidence of
effectiveness. Clinical & Investigative Medicine, 29(6), 351–364. Retrieved from
http://search.ebscohost.com/login.aspx?direct=true&db=aph&AN=23637429&site=ehost-live

Cohen, P. and Sas, A. (1993). Ten Years of Cocaine. A Follow Up Study of 64 Cocaine Users in
Amsterdam. (U. of A. Department of Human Geography, Ed.).

Cohen, P. (2009). Die nackte Herrscherin. Die moderne Neurowissenschaft und das Konzept der
Abhängigkeit. Wiener Zeitschrift Für Suchtforschung, 32(3/4), 61–70.

Cohen, P., & Sas, A. (1994). Cocaine use in Amsterdam in non deviant subcultures. Addiction
Research, 2(1), 71–94. http://doi.org/10.3109/16066359409005547

Colson, R., & Bergeron, H. (2017). European drug policies : the ways of reform. Routledge. Retrieved
from https://www.routledge.com/European-Drug-Policies-The-Ways-of-Reform/Colson-
Bergeron/p/book/9781138915206

Connors, M. M. (1992). Risk perception, risk taking and risk management among intravenous drug
users: Implications for AIDS prevention. Social Science & Medicine, 34(6), 591–601.
http://doi.org/10.1016/0277-9536(92)90187-U

COWELL, A. (1992). After 350 Years, Vatican Says Galileo Was Right: It Moves. New York Times.
Retrieved from http://www.nytimes.com/1992/10/31/world/after-350-years-vatican-says-
galileo-was-right-it-moves.html

Csete, J., Kamarulzaman, A., Kazatchkine, M., Altice, F., Balicki, M., Buxton, J., … Beyrer, C. (2016).
Public health and international drug policy. The Lancet, 387, 1427–80.
http://doi.org/http://dx.doi.org/10.1016/S0140-6736(16)00619-X

Dalgarno, P., & Shewan, D. (2005). Reducing the risks of drug use: The case for set and setting.
Addiction Research & Theory.

Davies, J. (2017). Addiction is not a brain disease. Addiction Research & Theory, 1–2.
http://doi.org/10.1080/16066359.2017.1321741

Davies, J. B. (2013). Myth of Addiction. London & New York: Routledge.

Dębiec, J., Bush, D. E. A., & LeDoux, J. E. (2011). Noradrenergic enhancement of reconsolidation in
the amygdala impairs extinction of conditioned fear in rats—a possible mechanism for the
persistence of traumatic memories in PTSD. Depression and Anxiety, 28(3), 186–193.

22
Decorte, T. and Slock, S. (2005). The Taming of Cocaine II. (B. VUB, University Press, Ed.).

Decorte, T. (2000). The taming of cocaine: cocaine use in European and American cities. VUB Press.
Retrieved from https://biblio.ugent.be/publication/122998

Degenhardt, L., Dierker, L., Chiu, W. T., Medina-Mora, M. E., Neumark, Y., Sampson, N., … Kessler, R.
C. (2010). Evaluating the drug use “gateway” theory using cross-national data: consistency and
associations of the order of initiation of drug use among participants in the WHO World Mental
Health Surveys. Drug and Alcohol Dependence, 108(1–2), 84–97.
http://doi.org/10.1016/j.drugalcdep.2009.12.001

Diez Roux, A. V. (2007). Integrating Social and Biologic Factors in Health Research: A Systems View.
Annals of Epidemiology, 17(7), 569–574. http://doi.org/10.1016/j.annepidem.2007.03.001

Donovan, J. E., & Jessor, R. (1983). Problem drinking and the dimension of involvement with drugs: a
Guttman scalogram analysis of adolescent drug use. American Journal of Public Health, 73(5),
543–552. http://doi.org/10.2105/AJPH.73.5.543

Erickson, P.G., Adlaf, E.M., Smart, R.G. and Murray, G. F. (1994). The Steel Drug. Cocaine and Crack in
Perspective, Lexington Books, New York, NY. - Cerca con Google. (N. Lexington Books, New York,
Ed.).

Ersche, K. D., Williams, G. B., Robbins, T. W., & Bullmore, E. T. (2013). Meta-analysis of structural
brain abnormalities associated with stimulant drug dependence and neuroimaging of addiction
vulnerability and resilience. Current Opinion in Neurobiology, 23(4), 615–624.
http://doi.org/10.1016/j.conb.2013.02.017

Evans-Brown, M., Gallegos, A., Francis, W., Christie, R., Cunningham, A., Sekula, J., … European
Monitoring Centre for Drugs and Drug Addiction. (2015). New psychoactive substances in
Europe : an update from the EU Early Warning System, March 2015. Publications Office.
Retrieved from http://www.emcdda.europa.eu/publications/rapid-communications/2015/new-
psychoactive-substances

Faupel, C. E. (1987). Drug Availability, Life Structure, and Situational Ethics of Heroin Addicts. Journal
of Contemporary Ethnography, 15(3–4), 395–419.
http://doi.org/10.1177/089124168701500305

Fergusson, D. M., Boden, J. M., & Horwood, L. J. (2006). Cannabis use and other illicit drug use:
testing the cannabis gateway hypothesis. Addiction (Abingdon, England), 101(4), 556–69.
http://doi.org/10.1111/j.1360-0443.2005.01322.x

Fergusson, D. M., & Horwood, L. J. (2000). Does cannabis use encourage other forms of illicit drug
use? Addiction, 95(4), 505–520. http://doi.org/10.1046/j.1360-0443.2000.9545053.x

Galbraith, J. K. (1958). The Affluent Society. Boston: Houghton Mifflin Harcourt.

Gardner, E. L. (2011). Addiction and Brain Reward and Antireward Pathways. In Chronic Pain and
Addiction (Vol. 30, pp. 22–60). Basel: KARGER. http://doi.org/10.1159/000324065

Gartner, C. E., Barendregt, J. J., & Hall, W. D. (2009). Multiple genetic tests for susceptibility to
smoking do not outperform simple family history. Addiction, 104(1), 118–126.

Gerrits, M. A. F. ., Lesscher, H. B. ., & van Ree, J. M. (2003). Drug dependence and the endogenous
opioid system. European Neuropsychopharmacology, 13(6), 424–434.
http://doi.org/10.1016/j.euroneuro.2003.08.003

23
Ginzler, J. A., Cochran, B. N., Domenech-Rodríguez, M., Cauce, A. M., & Whitbeck, L. B. (2003).
Sequential Progression of Substance Use Among Homeless Youth: An Empirical Investigation of
the Gateway Theory. Substance Use & Misuse. Retrieved from
http://www.tandfonline.com/doi/abs/10.1081/JA-120017391

Goldstein, R. Z., & Volkow, N. D. (2011). Dysfunction of the prefrontal cortex in addiction:
neuroimaging findings and clinical implications. Nature Reviews. Neuroscience, 12(11), 652–69.
http://doi.org/10.1038/nrn3119

Golub, A., & Johnson, B. D. (2002). The misuse of the “Gateway Theory” in US policy on drug abuse
control: A secondary analysis of the muddled deduction. International Journal of Drug Policy,
13(1), 5–19. http://doi.org/10.1016/S0955-3959(01)00111-6

Grund, J.-P. (1993). Drug use as a social ritual : functionality, symbolism and determinants of self-
regulation. Retrieved from http://repub.eur.nl/res/pub/39132/

Grund, J.-P., & Breeksema, J. (2017). Drug Policy in The Netherlands. In R. Colson & H. Bergeron
(Eds.), European drug policies : the ways of reform (pp. 128–148). Routledge. Retrieved from
https://www.routledge.com/European-Drug-Policies-The-Ways-of-Reform/Colson-
Bergeron/p/book/9781138915206

Grund, J.-P. C., & Blanken, P. (1993). From “Chasing the Dragon” to “Chinezen”: the Diffusion of
Heroin Smoking in the Netherlands. Addiction Research Institute (IVO), Rotterdam. Retrieved
from http://www.drugtext.org/pdf/grund02.pdf

Grund, J.-P., Kaplan, C. D., & De Vries, M. (1993). Rituals of regulation: controlled and uncontrolled
use in natural settings”. In Heather, N., Wodak, A., Nadelmann, E. and O’Hare, P. (Eds),
Psychoactive Drugs and Harm Reduction: From Faith to Science (pp. 77–90). Whurr Publishers,
London.

Hall, W., Carter, A., & Forlini, C. (2015). The brain disease model of addiction: is it supported by the
evidence and has it delivered on its promises? The Lancet. Psychiatry, 2(1), 105–10.
http://doi.org/10.1016/S2215-0366(14)00126-6

Hall, W. D., Carter, A., & Yücel, M. (2015). Ethical Issues in the Neuroprediction of Addiction Risk and
Treatment Response. In Handbook of Neuroethics (pp. 1025–1044). Dordrecht: Springer
Netherlands. http://doi.org/10.1007/978-94-007-4707-4_69

Hall, W. D., Gartner, C. E., & Carter, A. (2008). The genetics of nicotine addiction liability: ethical and
social policy implications. Addiction, 103(3), 350–359. http://doi.org/10.1111/j.1360-
0443.2007.02070.x

Hari, J. (2014). Chasing the scream. Best Books.

Hart, C. L. (2017). Viewing addiction as a brain disease promotes social injustice. Nature Human
Behaviour, 1(3), 55. http://doi.org/10.1038/s41562-017-0055

Hart, C. L., Marvin, C. B., Silver, R., & Smith, E. E. (2012). Is cognitive functioning impaired in
methamphetamine users? A critical review. Neuropsychopharmacology : Official Publication of
the American College of Neuropsychopharmacology, 37(3), 586–608.
http://doi.org/10.1038/npp.2011.276

Heyman, G. M. (2009). Addiction: A disorder of choice. Harvard University Press.

Huizinga, J. (2003). The sociology of culture: in 9 volumes. 3. Homo ludens: a study of the play-

24
 elements in culture. Routledge.

Hyman, S. E. (2007). The Neurobiology of Addiction: Implications for Voluntary Control of Behavior.
The American Journal of Bioethics, 7(1), 8–11. http://doi.org/10.1080/15265160601063969

Ioannidis, J. P. A. (2011). Excess Significance Bias in the Literature on Brain Volume Abnormalities.
Archives of General Psychiatry, 68(8), 773. http://doi.org/10.1001/archgenpsychiatry.2011.28

Ioannidis, J. P. A., Munafò, M. R., Fusar-Poli, P., Nosek, B. A., & David, S. P. (2014). Publication and
other reporting biases in cognitive sciences: detection, prevalence, and prevention. Trends in
Cognitive Sciences, 18(5), 235–241. http://doi.org/10.1016/j.tics.2014.02.010

Isaacson, W. (2007). Einstein His Life and Universe. New York: Simon and Schuster.

Johanson, C. E. (1984). Assessment of the dependence potential of cocaine in animals. Cocaine:

Pharmacology, Effects, and Treatment of Abuse, 54–71.

Kalant, H. (2010). What neurobiology cannot tell us about addiction. Addiction (Abingdon, England),
105(5), 780–9. http://doi.org/10.1111/j.1360-0443.2009.02739.x

Kalivas, P. W., & Volkow, N. D. (2005). The neural basis of addiction: a pathology of motivation and
choice. The American Journal of Psychiatry, 162(8), 1403–13.
http://doi.org/10.1176/appi.ajp.162.8.1403

Kandel, D. (1975). Stages in adolescent involvement in drug use. Science, 190(4217), 912–914.
http://doi.org/10.1126/science.1188374

Kandel, D. B. (2003). Does Marijuana Use Cause the Use of Other Drugs? JAMA, 289(4), 482.
http://doi.org/10.1001/jama.289.4.482

Kandel, D. B., Yamaguchi, K., & Chen, K. (1992a). Stages of progression in drug involvement from
adolescence to adulthood: further evidence for the gateway theory. Journal of Studies on
Alcohol, 53(5), 447–457. http://doi.org/10.15288/jsa.1992.53.447

Kandel, D. B., Yamaguchi, K., & Chen, K. (1992b). Stages of progression in drug involvement from
adolescence to adulthood: further evidence for the gateway theory. Journal of Studies on
Alcohol, 53(5), 447–457. http://doi.org/10.15288/jsa.1992.53.447

Kendler, K. S., Chen, X., Dick, D., Maes, H., Gillespie, N., Neale, M. C., & Riley, B. (2012). Recent
advances in the genetic epidemiology and molecular genetics of substance use disorders.
Nature Neuroscience, 15(2), 181–9. http://doi.org/10.1038/nn.3018

Kimura, M., & Higuchi, S. (2011). Genetics of alcohol dependence. Psychiatry and Clinical
Neurosciences, 65(3), 213–225. http://doi.org/10.1111/j.1440-1819.2011.02190.x

Kincaid, H., & Sullivan, J. A. (2010). Medical Models of Addiction. In D. Ross, H. Kincaid, D. Spurrett, &
P. Collins (Eds.), what is addiction? (p. 353). MIT, Cambridge, MA.

Kindt, M., Soeter, M., & Vervliet, B. (2009). Beyond extinction: erasing human fear responses and
preventing the return of fear. Nature Neuroscience, 12(3), 256–258.

Kirby, T., & Barry, A. E. (2012). Alcohol as a gateway drug: a study of US 12th graders. The Journal of
School Health, 82(8), 371–9. http://doi.org/10.1111/j.1746-1561.2012.00712.x

Lalander, P. (2003). Hooked on heroin : drugs and drifters in a globalized world. Berg. Retrieved from
http://www.diva-portal.org/smash/record.jsf?pid=diva2%3A415600&dswid=-8563

25
Leshner, A. I. (1997). Addiction is a brain disease, and it matters. Science (New York, N.Y.), 278(5335),
45–7. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/9311924

Levy, N. (2013). Addiction is Not a Brain Disease (and it Matters). Frontiers in Psychiatry, 4, 24.
http://doi.org/10.3389/fpsyt.2013.00024

Lewis, M. (2013). Why Addiction is NOT a Brain Disease | Mind the Brain. Retrieved April 23, 2013,
from http://blogs.plos.org/mindthebrain/2012/11/12/why-addiction-is-not-a-brain-disease/

Mackesy-Amiti, M. E., Fendrich, M., & Goldstein, P. J. (1997). Sequence of drug use among serious
drug users: typical vs atypical progression. Drug and Alcohol Dependence, 45(3), 185–96.
Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/9179520

Martin, C., & Otter, C. (1996). Locus of Control and Addictive Behaviour. In Addictive Behaviour:
Molecules to Mankind (pp. 121–134). London: Palgrave Macmillan UK.
http://doi.org/10.1007/978-1-349-24657-1_8

Mauss, M. (1925). The gift, trans. I. Cunnison. London: Cohen and West.

Mauss, M., & Halls, W. D. (2000). The gift: The form and reason for exchange in archaic societies. WW
Norton & Company.

Mayet, A., Legleye, S., Beck, F., Falissard, B., & Chau, N. (2016). The Gateway Hypothesis, Common
Liability to Addictions or the Route of Administration Model A Modelling Process Linking the
Three Theories. European Addiction Research, 22(2), 107–17.
http://doi.org/10.1159/000439564

McLuhan, M., & Fiore, Q. (1967). The medium is the message. New York, 123, 126–128.

Mental Health Services Administration. (2012). Results from the 2011 National survey on drug use
and health: summary of national findings, NSDUH series H-44, HHS publication no.(SMA) 12-
4713. Substance Abuse and Mental Health Services Administration, Rockville, MD.

Meringolo P., Petrini F. Zuffa G. (2014). Cocaine users and self regulation mechanisms. Drugs and
Alcohol Today, vol 14(4), 194–206.

Mills, C. J., & Noyes, H. L. (n.d.). Patterns and correlates of initial and subsequent drug use among
adolescents.

MIOVSKY, M., GABRHELÍK, R., LIBRA, J., POPOV, P., PAVLOVSKA, A., KALINA, K., … GRUND, J. P. C.
(2016). The Prague Comprehensive Model of Academic Addictology (Addiction Science)
Education. EDUCATION, 16, 1.

Moore, D. (1993). Social controls, harm minimisation and interactive outreach: the public health
implications of an ethnography of drug use. Australian Journal of Public Health, 17(1), 58–67.

Móró, L., & Rácz, J. (2013). Online drug user-led harm reduction in Hungary: a review of “Daath”.
Harm Reduction Journal, 10(1), 18. http://doi.org/10.1186/1477-7517-10-18

Nabben, T., Benschop, A., Korf, D. (2011). Antenne 2011 - Trends In Alcohol, Tabak En Drugs Bij jonge
Amsterdammers. Amsterdam: Rozenberg Publishers.

Nader, K. (2015a). Emotional Memory. In Handbook of experimental pharmacology (Vol. 228, pp.
249–270). http://doi.org/10.1007/978-3-319-16522-6_9

Nader, K. (2015b). Reconsolidation and the Dynamic Nature of Memory. Cold Spring Harbor

26
 Perspectives in Biology, 7(10), a021782. http://doi.org/10.1101/cshperspect.a021782

National Institute on Drug Abuse. (2010). Comorbidity: Addiction and Other Mental Illnesses, 12.
Retrieved from https://www.drugabuse.gov/sites/default/files/rrcomorbidity.pdf

Nicolescu, B., & ERTAS, A. (2008). Transdisciplinary theory and practice. Creskill: Hampton Press.

Nutt, D. J., Lingford-Hughes, A., Erritzoe, D., & Stokes, P. R. A. (2015). The dopamine theory of
addiction: 40 years of highs and lows. Nature Reviews Neuroscience, 16(5), 305–312.
http://doi.org/10.1038/nrn3939

Palmer, R. H. C., Brick, L., Nugent, N. R., Bidwell, L. C., McGeary, J. E., Knopik, V. S., & Keller, M. C.
(2015). Examining the role of common genetic variants on alcohol, tobacco, cannabis and illicit
drug dependence: genetics of vulnerability to drug dependence. Addiction, 110(3), 530–537.
http://doi.org/10.1111/add.12815

Popper Karl, R. (1945). The open society and its enemies. London, Routledge & Sons, 2, 268–352.

Price, M. (2008). Genes matter in addiction. Retrieved May 10, 2017, from
http://www.apa.org/monitor/2008/06/genes-addict.aspx

Prins, E. H. (1995). Maturing Out: An empirical study of personal histories and processes in hard-drug
addiction. Retrieved from http://repub.eur.nl/res/pub/21449/

Prins, E. H. (2008, January 31). “Maturing Out” and the Dynamics of the Biographical Trajectories of
Hard Drug Addicts. Forum Qualitative Sozialforschung / Forum: Qualitative Social Research.
Retrieved from http://www.qualitative-research.net/index.php/fqs/article/view/322/705

Reilly, M. T., Noronha, A., Goldman, D., & Koob, G. F. (2017). Genetic studies of alcohol dependence
in the context of the addiction cycle. Neuropharmacology.
http://doi.org/10.1016/j.neuropharm.2017.01.017

Rhodes, T. (2002). The “risk environment”: a framework for understanding and reducing drug-related
harm. International Journal of Drug Policy, 13(2), 85–94. http://doi.org/10.1016/S0955-
3959(02)00007-5

Rhodes, T. (2009). Risk environments and drug harms: a social science for harm reduction approach.
The International Journal on Drug Policy, 20(3), 193–201.
http://doi.org/10.1016/j.drugpo.2008.10.003

Richardson, W. J. (2013). Heidegger: Through phenomenology to thought. Springer.

Robins, L.N., Helzer, J.E., Hesselbrock, M. and Wish, E. (1979). Vietnam veterans three years after
Vietnam: how our study changed our view on heroin”, in , Hum. In N. Y. Human Sciences Press
(Ed.), Brill, L. andWinick, C. (Eds), The Yearbook of Substance Use and Abuse.

Robins, L. N. (1993). The sixth Thomas James Okey Memorial Lecture. Vietnam veterans’ rapid
recovery from heroin addiction: a fluke or normal expectation? Addiction (Abingdon, England),
88(8), 1041–54. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/8401158

Robins, L. N., Helzer, J. E., & Davis, D. H. (1975). Narcotic use in southeast Asia and afterward. An
interview study of 898 Vietnam returnees. Archives of General Psychiatry, 32(8), 955–61.
Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/1156114

Sara, S. J. (2000). Retrieval and reconsolidation: toward a neurobiology of remembering. Learning &
Memory, 7(2), 73–84.

27
Satel, S., & Lilienfeld, S. O. (2013). Brainwashed: The seductive appeal of mindless neuroscience. Basic
Books.

Schachter, S., & Singer, J. (1962). Cognitive, social, and physiological determinants of emotional state.
Psychological Review, 69(5), 379.

Shewan, D., Dalgarno, P., & Reith, G. (2000). Perceived risk and risk reduction among ecstasy users:
The role of drug, set, and setting. International Journal of Drug Policy.

Siegel, R. K. (1989). Intoxication: Life in pursuit of artificial paradise. EP Dutton.

Sifaneck, S. J., Kaplan, C. D., Dunlap, E., & Johnson, B. D. (2003). BLUNTS AND BLOWTJES: CANNABIS
USE PRACTICES IN TWO CULTURAL SETTINGS AND THEIR IMPLICATIONS FOR SECONDARY
PREVENTION. Free Inquiry in Creative Sociology, 31(1), 3–14. Retrieved from
http://ojs.library.okstate.edu/osu/index.php/FICS/article/view/1484

Soeter, M., & Kindt, M. (2010). Dissociating response systems: erasing fear from memory.
Neurobiology of Learning and Memory, 94(1), 30–41.

Soeter, M., & Kindt, M. (2012). Stimulation of the noradrenergic system during memory formation
impairs extinction learning but not the disruption of reconsolidation.
Neuropsychopharmacology, 37(5), 1204–1215.

Soussan, C., & Kjellgren, A. (2014). Harm reduction and knowledge exchange-a qualitative analysis of
drug-related Internet discussion forums. Harm Reduction Journal, 11(1), 25.
http://doi.org/10.1186/1477-7517-11-25

Soussan, C., & Kjellgren, A. (2016). The users of Novel Psychoactive Substances: Online survey about
their characteristics, attitudes and motivations. International Journal of Drug Policy, 32, 77–84.
http://doi.org/10.1016/j.drugpo.2016.03.007

Stallwitz, A. (2012). The Role of Community-mindedness in the Self-regulation of Drug Cultures: A

Case Study from the Shetland Islands. Springer Science+ Business Media.

Stallwitz, A., & Shewan, D. (2004). A qualitative exploration of the impact of cultural and social
factors on heroin use in Shetland (Scotland). Journal of Psychoactive Drugs, 36(3), 367–78.
http://doi.org/10.1080/02791072.2004.10400036

Stokols, D., Fuqua, J., Gress, J., Harvey, R., Phillips, K., Baezconde-Garbanati, L., … Trochim, W. (2003).
Evaluating transdisciplinary science. Nicotine & Tobacco Research, 5(6), 21–39.
http://doi.org/10.1080/14622200310001625555

Stone, K. (2016). The Global State of Harm Reduction 2016. London. Retrieved from
https://www.hri.global/files/2016/11/14/GSHR2016_14nov.pdf

Strathdee, S. A., Hallett, T. B., Bobrova, N., Rhodes, T., Booth, R., Abdool, R., & Hankins, C. A. (2010).
HIV and risk environment for injecting drug users: the past, present, and future. Lancet,
376(9737), 268–84. http://doi.org/10.1016/S0140-6736(10)60743-X

Susser, M., & Susser, E. (1996). Choosing a future for epidemiology: II. From black box to Chinese
boxes and eco-epidemiology. American Journal of Public Health, 86(5), 674–7.
http://doi.org/10.2105/AJPH.86.5.674

Van Gundy, K., & Rebellon, C. J. (2010). A Life-course Perspective on the “Gateway Hypothesis”.
Journal of Health and Social Behavior, 51(3), 244–59.

28
 http://doi.org/10.1177/0022146510378238

Vanyukov, M. M., Tarter, R. E., Kirillova, G. P., Kirisci, L., Reynolds, M. D., Kreek, M. J., … Ridenour, T.
A. (2012). Common liability to addiction and “gateway hypothesis”: theoretical, empirical and
evolutionary perspective. Drug and Alcohol Dependence, 123 Suppl, S3-17.
http://doi.org/10.1016/j.drugalcdep.2011.12.018

Volkow, N. D. (2010). Drugs, brains, and behavior-the science of addiction. Retrieved on March, 23,
2011.

Warner, L. A., Kessler, R. C., Hughes, M., Anthony, J. C., & Nelson, C. B. (1995). Prevalence and
correlates of drug use and dependence in the United States: Results from the National
Comorbidity Survey. Archives of General Psychiatry, 52(3), 219–229.

Welte, J. W., & Barnes, G. M. (1985). Alcohol: The gateway to other drug use among secondary-
school students. Journal of Youth and Adolescence, 14(6), 487–98.
http://doi.org/10.1007/BF02139522

Wilson, M. C., Hitomi, M., & Schuster, C. R. (1971). Psychomotor stimulant self administration as a
function of dosage per injection in the rhesus monkey. Psychopharmacologia, 22(3), 271–281.

Winick, C. (1962). “Maturing out of narcotic addiction.” US Bulletin on Narcotics, Vol. 14 No(1), 1–17.

Winick, C. (1964). The life-cycle of the narcotic addict and of addiction. Bulletin on Narcotics, 16(1),
1–11.

Yanagita, T. (1973). An experimental framework for evaluation of dependence liability of various

types of drugs in monkeys. Bull Narc, 25(4), 57–64.

Zinberg, N. (1984). Drug, Set, and Setting. The Basis for Controlled Intoxicant Use. New Haven: Yale
University Press. Retrieved from http://yalepress.yale.edu/book.asp?isbn=9780300036343

Zinberg, N. E., Harding, W. M., & Winkeller, M. (1977). A Study of Social Regulatory Mechanisms in
Controlled Illicit Drug Users. Journal of Drug Issues, 7(2), 117–133.
http://doi.org/10.1177/002204267700700203

29