Heroin Addiction and Crime

Heroin Addiction and Crime
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Heroin is an opiate and breaks down into morphine in the brain. When heroin is taken, an initial dose of hedonic pleasure washes over the person as heroin binds to the various mu-opiod receptors in the limbic, cingulate, orbito-frontal, pre-frontal cortex and brainstem causing an initial euphoria followed by a sedative, detached, tranquil state [1]. In addition to such hedonic effects, heroin also binds to the mu-opiod receptors in the Ventral Tegmental Area (VTA) of the reward mediating mesodopaminergic pathway [2], and causes an increased dopamine release in the nucleus accumbens in the striatum to mediate an intense drug-induced reward [3]. Instrumentally learned behavior such as heroin abuse can take on two forms; goal directed impulsive (S-R-O) actions and non-purposeful, automatic compulsive (S-R) habits. Following the feeling of the first heroin mediated reward and euphoria, an addict learns that the outcome of heroin abuse is positive and heroin abusing for the addict then takes on the goal directed action located in the posterior dorsomedial striatum (pDMS) [4]. However, over time, the increased dopamine release in the striatum causes the goal directed heroin abuse action to change over to become an uncontrollable compulsive habit [5] located in the dorsolateral striatum (DLS) [4]. However, things become even worse when the increased dopamine release in the striatum also causes the drug addict to pathologically ‘want’ not just heroin but everything that looks like heroin through the incentive salience theory [6], whereby now the addict becomes primitively motivated to obtain anything that is related to heroin and commits acquisitive crimes of robbery [7] and sometimes even violent crimes [8] to obtain the heroin they so crave. Heroin addicts also have extensive orbitofrontal and prefrontal cortex damage which causes a dampened behavior inhibition, decreased appraisal of the future [9] and this, compounded with the increased scores of aggression seen in heroin addicts [10]; makes for a dangerous heroin addicted criminal in society.

Spider - A Day In The Life Of A Heroin Addict
Incy Wincy Spider (heroin) went up the water sprout (your veins!)

1.1) Mechanism of Heroin Action in the Brain

1.1 a) Nucleus Accumbens Shell and Ventral Pallidum Mediated Hedonic Liking

Heroin Addiction and Crime
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Heroin, upon intake binds to the various mu-opiod receptors in the limbic structures, cingulate, orbitofrontal, pre-frontal cortex, and brainstem and lowers pain sensitivity and activates the parasympathetic system to provide hedonic pleasure. There are five components of the reaction to heroin intake: a euphoric rush of intense pleasure, often characterized by analogy to sexual orgasm, followed by a general feeling of well-being due to a warm peripheral flushing, followed then by a detached, separated state which can include virtual unconsciousness, and finally, a fade back to an appearance of normality. This is then followed by a fifth, highly dysphoric withdrawal state [11] .

Earlier theories postulated that the release of dopamine from the Ventral Tegmental Area into the nucleus Accumbens as part of the mesodopaminergic pathway is what mediated the hedonic pleasure felt by a heroin addict through its reward producing properties [12]. However, evidence had been accumulated against it and today, even though we can see that intra Accumbens dopamine agonists are reinforcing, and dopamine is released in excess in the Accumbens for appetitive reinforcers [13], such a release does not mediate hedonic ‘liking’ in animals and reinforcement does happen in its absence as well. Dopamine in the nucleus Accumbens is released not just in response to positive reinforcers, but is also released in response to unconditioned and salient stimuli that predict them, as seen through micro dialysis techniques [14].

The hedonic ‘liking’ of heroin therefore is not a result of the dopamine release in the nucleus Accumbens but is due to heroin binding to the various mu-opiod receptors on the nucleus Accumbens shell and areas in the ventral pallidum [47]. A study by Peciña and Berridge has shown that injection of DAMGO; a mu-opiod receptor agonist in the nucleus Accumbens shell increases the experiences pleasantness or ‘liking’ experienced following tasting something sweet [15]. Similarly, in electrophysiological studies, given oral infusion of a sweet sucrose taste, the neuronal firing rates of ventral pallidum seemed to increase dramatically correlating with ‘liking’ reactions [16].

In a recent case study illuminating the effects of bilateral damage to the ventral pallidum shows how this affects hedonic mechanisms in the brain [17]. Bilateral damage to the ventral pallidum caused anhedoinia in the patient whereby the patient lost 20 lbs and described being in depression. What is remarkable is that the patient was a previous drug addict and following the lesion, “reported the disappearance of all drug cravings and remained abstinent from all recreational drugs other than an occasional glass of wine with dinner” (p 786) [18]. However, pleasure magnification requires unanimity and cooperation among all opioid hotspots in nucleus Accumbens and ventral pallidum [19].

1.1 b) Locus Coeruleus Mediated Negative Withdrawal

Opiate drugs produce powerful physical withdrawal effects. Heroin also binds to the mu-opiod receptors on neurons in the locus coeruleus (LC) and inhibits the production of cAMP and nor adrenaline, which then fails to arouse the brain sufficiently under the influence of heroin, allowing for heroin's sedative intoxication effects. However, according to the 'opponent process theory' [20], [21] whereby a long-lasting unpleasant process opposes the euphoric effects of drugs, with increasing heroin abuse, the brain desensitizes to the effects of heroin and develops tolerance, whereby the increased dopaminergic release in the nucleus Accumbens is lowered while production and release of nor adrenaline in the LC is up regulated for the same dose of heroin. The positive reward then decreases over time as dopamine release decreases over time, while negative withdrawal symptoms increase as more nor adrenaline is released and uncomfortable symptoms including aggression, intense craving, stomach cramps, runny nose, sneezing, and diarrhea result [1]. Such drastic withdrawal effects promotes incentive learning in the drug addict and just as hunger increases the hedonic impact of food [47], in the presence of withdrawal, heroin's value also increases, whereby heroin intake also becomes a negative reinforcement for the addict [23].

1.2) Hijacking of the Mesodopaminergic Pathway by Heroin

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In addition to such hedonic effects, heroin also binds to the mu-opiod receptors in the Ventral Tegmental Area (VTA) of the mesodopaminergic pathway originally designed to mediate rewards to natural stimuli such as sex, food and mates[2], and hyperpolarizes nearby GABAergic neurons to indirectly cause an increased dopamine release in the nucleus accumbens in the striatum, several key cortical loci, including the anterior cingulate cortex (ACC), orbitofrontal cortex (OFC) and prefrontal cortex (PFC) and mediates an intense drug-induced reward [3]. This drug induced reward is far greater than the reward produced through stimuli such as sex, food, and mates [24].

Consistent with this hypothesis:

  1. Garzon and Pickel [25]and Svingos et al. [26] found that the mu-opiod receptors in the VTA are located mainly on the axon terminals of inhibitory neurons that mainly synapse onto dopaminergic neurons causing an increased dopamine release.
  2. Opiods have been found to only hyperpolarize GABAergic interneurons and not affect the dopaminergic neurons in any way [27].
  3. Administration of mu-opiod receptor agonists like heroin in the VTA causes the activation and firing of dopaminergic neurons [28].
  4. It has been proven that administration of opiates in the VTA causes dopamine release in the nucleus Accumbens [29].
  5. Lastly, application of a GABAergic agonist into the VTA causes a dampening of the dopamine release into the nucleus Accumbens [30].

1.3) Dopamine Release in the nucleus Accumbens and Resultant Instrumental Learning

Dopamine neurons in the nucleus Accumbens usually fire in response to unexpected rewards, or to unexpected stimuli that predict reward [12] and this signal is used by the posterior dorsomedial striatum and the Prefrontal cortex (prelimbic region) and the Orbitofrontal cortex (OFC) to learn about reward providing goal driven actions [31]. Since the PFC underlies working memory , release of dopamine in this area from the VTA facilitates the learning of reward related information so future actions can be learned, encoded, selected and performed [32]. Neurons in the OFC evaluate the value of potential choices [34], [35] and as such increased release of dopamine from the VTA into the OFC functions to allow a person to assess the subjective value of the reward of the action and integrate it with the consequences of such a behavior done to attain it [35]. This is how goal directed behavior is learnt.

However the most important structure that learns from the increased drug mediated dopamine release is the nucleus Accumbens. Normally if presynaptic and postsynaptic neurons are paired together repetitively, synaptic depression results, however if such synapses are accompanied by a pulse of dopamine, they are strengthened [36] and as such, targets of dopaminergic innervations such as nucleus Accumbens become involved in instrumental learning. In the nucleus Accumbens glutamatergic NMDA receptors and dopamine have been implicated in acquiring food motivated, goal directed behavior and blockade of NMDA receptors in this area has been related to retardation of instrumental learning for food [37]. However, this blockade only works during the learning phase of a behavior, once the response has been learned; blocking the NMDA receptor has no effect on the learned behavior [38].

However, the nucleus Accumbens is not just needed for learning instrumental behavior, but is also needed for providing extra motivation for behavior especially those triggered by Pavlovian conditioned stimuli (see Incentive salience theory), and also when rewards are hard to obtain or are delayed. This can be seen with the fact that rats with lesions to this trained to acquire lever pressing responses, do so at randomly normal or even below normal reinforcement schedules [39], even though they are fully sensitive to the changes in the action-outcome contingency [40]. Therefore, this increased dopamine release in the nucleus Accumbens facilitates to not just provide supraphysiological reward, but also functions as a neuromodulator to change the motivational systems in the brain.

1.3 a) Transition from Goal directed heroin abuse in the pDMS to Habitual Heroin Abuse in DLS

Baxter and Murray's (2002) Monkey Experiment
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Monkey solves two discrimination tasks then undergoes Outcome devaluation

Instrumentally learned behavior such as substance abuse can take on two forms: goal directed impulsive (Stimulus-Response-Outcome: S-R-O) actions and non-purposeful, automatic compulsive (Stimulus-Response: S-R) habits. We explore goal driven (S-R-O) actions and automatic and unconscious (S-R) habits because initially when a drug addict takes a drug, the stimulus is the drug, the response is taking it and the drug addict not only understands the value of the reward or hedonic pleasure due to the drug but knows that taking it leads up to this outcome. The increased dopamine release in the nucleus accumbens discussed above facilitates to teach the pDMS, OFC and PFC to calculate the value of the reward and about the action-outcome contingency leading to a goal mediated action of drug taking [31]. Goal directed (S-R-O)actions is mediated by the prefrontal dorsomedial striatum (pDMS). Therefore given value to an outcome, a goal directed response towards it should emerge as an (S-R-O) action, whereas habits should be automatic and should not be contingent on the value of the outcome and should be a S-R behavior. Reward devaluation strategies using satiation have been used by researchers to explore goal-directed actions and distinguish it from (S-R) habits. In one experiment by Baxter and Murray [41] a monkey was trained to solve two discrimination tasks. In the first task, the right choice was a cone and the reward underneath it was a grape. In the second task, the right choice was a cube and the reward was a peanut. Following this, the monkey is given either a large bowl of peanuts or grapes and then both correct responses of a cube or a cone are presented again and after the devaluation of one reward through satiation, the monkey’s responses are recorded. Typically monkeys choose the reward they had not been given earlier and this is a goal-directed action, where the monkey is aware of the slightly higher value of the novel food and therefore performs an appropriate response to obtain it instead of the satiated one. In another experiment, Yin et a. [4] did pre-training, post-training as well as reversible inactivation of the pDMS along with action–outcome learning variables such as the rats’ sensitivity to degradation of the instrumental contingency, and outcome devaluation to show that pre-training lesions caused the animals to be deficient in acquiring the action-outcome contingency, that post training lesions caused a disruption in the acquisition and the expression of instrumental actions, while the reversible inactivation of the pDMS caused a loss in the expression of goal directed actions but did not affect its acquisition.

However with increased drug abuse, the goal mediated (S-R-O)action of drug taking slowly changes to being an unconscious, habitual, outcome non-contingent (S-R) behavior, whereby the addict starts taking the drug not to avoid its negative withdrawal effects or to experience its hedonic "liking' effects, but rather takes it out of sheer compulsion. In the beginning during the goal directed (S-R-O) action of drug intake, the increased dopamine release in the nucleus Accumbens strengthens the synaptic S-R and R-O connections, however as time passes, this same excess dopamine release starts to entrench the S-R connection, while the R-O connection gets lost. This causes the goal driven action of drug taking to transfer over to an automatic, unconscious and reflexive (S-R) drug abuse habit mediated by the dorsalateral striatum (DLS). This habitual, automatic drug abuse behavior is inflexible, unconscious and extremely potent [5] as shown in rats, whereby, when taught to inhibit responding to a previously rewarding to select a newly rewarding or previously unrewarded stimulus [42],[43], the show cognitive inflexibility at doing so [44], [45].

1.3 b) Incentive Sensitization Theory of Drug motivated Behaviour

Incentive Sensitization :Drug Associated Stimuli
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All drug related stimuli cause pathological 'wanting' and elicit irrational behaviours

The incentive-sensitization theory of addiction focuses on how drug related cues trigger excessive incentive motivation for drugs, leading to compulsive drug seeking approach behaviors and drug taking [46], [6]. The increased dopamine release in the nucleus Accumbens not just causes the turning over of goal directed heroin intake to compulsive heroin abuse, but also causes the development of hypersensitivity within the addict for all drug-associated stimuli [46]. There are three fundamental characteristics to the incentive sensitization theory [47], [47] (i) Drug related stimuli can elicit approach towards them (through excessive 'wanting'), acting as ‘motivational magnets’ (Pavlovian conditioned approach behavior)(ii) Drug-related stimuli can fuel already occurring actions by eliciting cue-triggered 'wanting' for their associated unconditioned rewards. (iii) Drug-related stimuli can cause the acquisition of new instrumental behaviors themselves by acting as reinforcers. The most evident research for incentive sensitization theory shows that drug-associate stimuli facilitates all three features of incentive stimuli: Pavlovian conditioned approach behavior [48]; Pavlovian instrumental transfer [49]; and conditioned reinforcement [50], [51].

Therefore, when the neural circuits of motivation become increasingly sensitized to the drug (Conditioned Stimulus: CS) and all drug related stimuli (Unconditioned Stimulus: US), any drug- related stimulus such as money, environment, needles, etc. become as strongly associated with the rewarding outcome of the drug (US) as the drug itself, and coming into contact with any of these cues elicits a pathological “wanting” and irrational approach behavior [52]. This implicit “wanting” is similar to implicit memory and to unconscious perception (e.g., blindsight), which can occur and motivate and influence behavior without conscious awareness [53], [54]. Furthermore in addicts already high on a drug, if the dose it too low to produce any conscious experience of pleasure, implicit “wanting” can also be compulsively activated leading to further irrationally motivated unconscious drug-seeking behavior [55], [56].

Furthermore in addicts already high on a drug, if the dose it too low to produce any conscious experience of pleasure, implicit “wanting” can also be compulsively activated leading to further irrationally motivated unconscious drug-seeking behavior [57].

1.4) Contributing factors to Heroin Related Crime

1.4 a) Heroin abuse and OFC and PFC Damage

The prefrontal and other cortical areas primarily mediate cognitive forms of desire and act-outcome representations, whereas nucleus Accumbens related circuitry (especially dopamine-related systems) play a more important role in unconsciously motivated Pavlovian-guided attributions of incentive salience [58], [47],[60],[59] and with the cognitive deficits in the behavioral inhibitory control, decision making and mental flexibility of the PFC and the OFC [9] as found by Rogers et al. [61] in opiate addicts, the cue-triggered “wanting,” might momentarily override more rational and stable life priorities [62] and may lead to unconscious impulsive, dangerous decisions and behaviour with no rational brake” of cognitive regulatory processes to inhibit it [63], [64].

1.4 b) Heroin abuse and aggression

Heroin causes Aggression
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Opiate (heroin) abuse has traditionally been linked to non-aggressive behavior in abusers due to its causation of ‘euphoria, relaxation, drowsiness, and lethargy’ [65]. However, other studies claim that opiate abuse in fact does increase aggression, as seen by the increased measures of hostility in opiate abusers in self-report [67], observer report questionnaires [8], and in laboratory based measures as that argued by Gerra et. al (2004) whereby heroin dependant patients were more aggressive than controls. Recent studies claim that after drug tolerance occurs, the aggression that a heroin addict experiences is usually directed to perform acquisitive crime to secure more drugs than violent crime [69], [70] and this finding has been confirmed by another study conducted in Spain [7]whereby after reviewing 578 arrested individuals, heroin abuser arrestees were seen to have performed acquisitive crimes such as shoplifting, stealing and robbery more than fatal violent interpersonal crimes such as murder, rape, etc. However, these measures of aggression show the acute effects of heroin abuse, over the long term, heroin abuse produces complex neurobiological changes that lead to a variety of different violent consequences.

1.4 c) Heroin abuse and Voilition

Puppets of their addiction?
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Volition consists of a series of decisions regarding whether to act, what action to perform and when to perform it. When we wish to perform an action, our brain unconsciously elicits the behavior and sends it for approval to the pre-supplementary motor area [71], the parietal cortex [72], and the dorsal frontal median cortex [73] (dFMC) 10 seconds before the actual elicitation of the behavior [74] so that it may be inhibited, shaped and elicited appropriately in accordance with one’s will and social consequences. Given this model of the basis of behavior, the concept of free will is nothing but a predetermined action, inhibited, shaped and elicited by the mechanism of the brain, and as such, if the cortices regulating such a behavior are damaged as they are in the brain of heroin addicts, their behavior shall be the unconsciously motivated irrational behaviors from the nucleus Accumbens which doesn’t truly reflect their free will or personality and is not under their conscious control. Therefore, for such actions that have not been consciously regulated or performed, addicts must not be asked to assume personal responsibility to them.

1.5) Types of heroin related crimes

It all comes down to this
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Criminality in heroin addicts is a partial correlate of their aggressiveness. Offenses committed by heroin addicts can be classified into three categories: crimes against 1) people (interpersonal crime), 2) property, and 3) against self. Heroin addiction has been commonly related to crimes against property with the highest reports of crime being offenses of shoplifting, burglary and robbery. As the addiction progresses, the instances of interpersonal violence and crimes against the self decrease, however those crimes against property decrease in a much slower rate . In terms of criminal trends. although the European Union average for heroin related crime decreased by 39% from 2003-2008, starting in the year 2009 forward, there instead became an increase in such heroin related crimes in the European Union countries. Also in terms of interpersonal violence, heroin addicts do not usually commit crimes of homicide, but a preference for female victims is seen in heroin addicts with long term abuse history, and heroin abuse has also been linked with non-homicidal interpersonal violence. In terms of violence against the self, such as suicidal behavior, heroin addicts are 7 times more likely to commit suicide compared to the general population and 14 times more likely compared to age matched controls. What’s remarkable is that 40% of heroin abusers claim to have attempted suicide. Moreover, these attempters are more likely female, reported parallel addictions with heroin and cocaine, childhood abuse, trauma, treatment with antidepressants [75].

1.5 a) Motivation to commit heroin related crimes

What is their motivation to commit crime?
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It cannot be simply said that heroin addicts commit crimes of robbery, stealing, property theft, etc. to obtain money so that they may buy heroin due to solely heroin mediated hedonic pleasure or heroin withdrawal mediated negative reinforcement. This is because, excessive drug seeking motivation has also been found in heroin addicts who continue to use the drug despite the absence of withdrawal symptoms [32], and in those who work for doses they cannot subjectively distinguish from a placebo despite no positive reinforcement [55]. Upon further examination, one can see that the slow progression of heroin abuse goes from being a goal mediated action to a compulsive habit and involves a diminished influence of the PFC and the cortical systems in decision making to a greater involvement of sub cortical structures such as the dorsalateral striatum (DLS) implicated in the habit based (S-R) behaviors [5]. Such motivated crimes could be also attributed to the incentive salience theory whereby the excessive 'wanting' of a drug like substance or a secondary reinforcer such as money to obtain the drugs can cause such an overwhelming primitive motivation to obtain it and when this combines with the OFC and PFC damage in heroin addicts, their excessive bouts of aggression, and loss of volition, crimes of acquisition and even interpersonal violence can result.

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Written by Aishwarya Lakshmanan from the University of Toronto, HMB300H1 S 2013

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