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Justifying our Present Doctrines of Moral and Legal Excuse

Neuroscientific research has the potential to advance our understanding of addiction in two dimensions. One, it can change our explanation of addiction.

This it can do in a variety of ways: (1) It can deepen our folk psychological ex-

planations by showing how the variables in such explanations are underlain by

the mechanisms of brain function; (2) it can precisify the folk explanations by

making the folk psychological states more precise in their boundaries or more

precise in the modes of their combination; (3) it can correct mistakes in the folk

psychological explanation; and/or (4) it can broaden those explanations by sup-

plementing them with explanations couched in the terms and variables of cogni- tive psychology, genetics, and neuroscience. Secondly, such research has the po- tential to change how we evaluate the behavior of addicts. It might show that we should excuse where currently we do not or that we should not excuse when currently we do. Alternatively, our present evaluations of excuse could remain unchanged but they could be supported and justified by neuroscientific explana- tions, showing us that addicts are incapacitated to the point of excuse just where and to the extent that we currently think that they are.

I shall assess each of these potentials for neuroscientific research in this, the fifth part of this Article; but the beginning of wisdom here is to keep the

potential explanatory work done by neuroscience, separate from the potential

excusing work done by neuroscience. These two uses of neuroscientific research

can be related—for a true excuse does depend on a certain form of explanation (of the behavior being excused) being true—yet they are not related in the sim- ple-minded ways that are so rampant in the neuroscience literature and that we have discussed before.

One of these simple-minded ways (of moving too quickly from explanation to excuse) is that of the incompatibilist. Such a person believes that mechanistic, causal explanations necessarily excuse because they show the actor had no free-

dom to do other than he did, such as take drugs.172 On such a view, to show how

unusually large releases of dopamine in certain areas of the brain cause early drug use, or to show how decreased releases of dopamine cause continued drug

use by addicts, is to show such drug usages to be excused.173 On such a view

there is no break between explaining and excusing: to (causally) explain is ipso

facto to excuse. We all need to be more patient here, asking what neuroscience

adds to the explanation of addiction, and then asking whether the explanations given by neuroscience shows there to be the kind of incapacity that excuses.

172. Ingo Willuhn et al., Excessive Cocaine Use Results from Decreased Phasic Dopamine Signaling of the Striatum, 17(5) NATURE NEUROSCIENCE 704, 710 (2014).

More insidiously present in the literature in neuroscience explaining addic- tion, is a second of the confusions that we explored before in Part II. This confu- sion is evident in the way that such neuroscientific literature orients neuroscien- tific research findings around the verification of “the disease model of addiction.” This may be fine as a bit of medical science, but as we saw in Part II such orientation is without import for questions of moral and legal excuse. Thus, the leading researchers in this area may well set for themselves the medical-sci- entific task of reviewing “recent advances in the neurobiology of addiction to clarify the link between addiction and brain function and to broaden the under-

standing of addiction as a brain disease.”174 _{And it may be good medical science}

to conclude “that neuroscience continues to support the brain disease model of

addiction”175 _{because this may well advance the medical goals of finding “new}

opportunities for the prevention and treatment of substance addictions.”176 _What

such medical characterization of the research (as “addictions are brain diseases”) does not do, is to call into question “deeply ingrained values about self-determi-

nation and personal responsibility.”177 _{Moralists and lawyers thus have no reason}

to join medical researchers in organizing neuroscientific findings by whether or not they support the view that addictions are diseases of the brain.

Part and parcel of the disease-orientation in characterizing neuroscientific research into addiction, is the characterization of the findings of that research into the disease criteria of dysfunction and disability that we discussed in Part II. One might (with apologies to Nancy Andreasen) call this the “broken-brain” way

of characterizing the findings of neuroscience.178 Thus, some statistically domi-

nant mode of functioning is characterized as “normal” and “proper,” and addic- tion is presented as dysfunctional and improper. Thus: “we have learned that ad-

diction is characterized by an expanding cycle of dysfunction in the brain.”179

More specifically, “we introduce the key brain circuits that are affected by the chronic abuse of drugs and then present a coherent model [in terms of four such

circuits] according to which addiction emerges as the net result of imbalanced

information processing in and among these circuits,”180 each of which changes

in ways characterized as “faltering.”181 One of these circuits is the reward circuit,

where a decrease in sensitivity to reward caused by abuse of drugs is character-

ized as a “dysfunction”182 a “disruption”183 and a “repeated perturbation.”184

174. Volkow et al., supra note 35, at 363.

175. Id.; see also Nora D. Volkow & Marisela Morales, The Brain on Drugs: From Reward to Addiction, 162 CELL 712, 720 (2015) (“In conclusion, uncovering the neurobiology underlying drug abuse has led to the recognition of addiction as a chronic disease of the brain.”).

176. Volkow et al., supra note 35, at 363. 177. Id. at 364.

178. See generally NANCY ANDREASEN,THE BROKEN BRAIN (1984) (dealing with mental disease generally, not addiction specifically).

179. Nora D. Volkow et al., Addiction: Decreased Reward Sensitivity and Increased Expectation Sensitivity Conspire to Overwhelm the Brain’s Control Circuit, 32 BIOESSAYS 748, 748 (2010) (emphasis added). 180. Id. at 748–49 (emphasis added).

181. Id. at 748. 182. Id. 183. Id. 184. Id. at 750.

Likewise, the disconnect between normal patterns of dopamine release in the synapses of the ventral striatum is characterized as an “unrestrained hyperacti-

vation of the motivation/[reward] circuit”185 _{and as an “improper regulation of}

brain activity by [those] prefrontal brain regions [part of the control circuit]”186

Again, there is nothing improper for medical purposes in characterizing the findings of neuroscience in terms of the dysfunction and disability that makes the disease classification plausible. The mistake is to infer from these criteria of disease being met by addiction, that such (medically classified) dysfunction “results in the compulsive drug intake that characterizes addiction” or that drug

use by addicts is “an automatic compulsive behavior.”187 The incapacities that

lead to the excuse of compulsion are not necessarily the same as, and do not necessarily follow on, the dysfunctions and disabilities that rightly characterize disease.

With these cautions in mind, I turn to the explanation of addiction offered up by the neuroscience of the last sixty-four years.