William H. Miller III Department of Philosophy & Berman Institute of Bioethics, Johns Hopkins University, 281 Gilman Hall, 3400 N. Charles Street, Baltimore, MD, 21218, USA.
Psychopharmacology (Berl). 2022 Apr;239(4):993-1007. doi: 10.1007/s00213-021-06013-4. Epub 2021 Nov 26.
Although increasingly subject to criticism, the brain disease model of addiction (BDMA) remains dominant within addiction science. Yet few advocates or critics of the BDMA have provided an account of what a brain disease is. The aim of this review is to conceptually clarify what it would mean for the BDMA to be true, rather than to argue decisively for or against it.
Conceptual clarification of the BDMA requires consideration of possible models of disease and their relationship to the BDMA. A barrier to such consideration is belief that the BDMA is necessary to combatting addiction stigma. To address this barrier, I begin with discussion of what we know about the effects of the brain disease label on addiction stigma, and why labelling effects should have no bearing on the validity of the BDMA. I then distinguish strong, minimal, network, and mismatch models of disease, and I argue that the BDMA aligns with a strong disease model. This means that underlying brain pathology is hypothesized to be the cause of the personal-level observable signs and experienced symptoms characteristic of addiction. Evaluation of the BDMA therefore requires analysis of the concepts of brain dysfunction and causation, and their application to addiction science.
Brain dysfunction cannot be analyzed merely as brain changes or brain differences; nor can it be inferred merely from the presence of personal-level signs and symptoms. It is necessary to have an account of normal brain function by which to measure it. The theoretical and empirical challenges to developing such an account are not insurmountable, but they are substantial. Although there exist competing analyses of causation, there is a relatively standard method used to establish it within experimental science: intervention. Using this method, the causal significance of brain states, such as, e.g., extensive gray matter loss and/or neuroadapations in the mesocorticolimbic dopamine system, is not yet fully demonstrated. Further studies are necessary to determine their effect compared with other possible variables, such as, e.g., alternative reinforcers.
Conceptual clarification and preliminary empirical assessment of the BDMA recommends agnosticism about its validity and an openness to heterogeneity; in some cases addiction may be a brain disease, in others not. Either way, addiction stigma can be combatted by fighting moralism about drugs and moralistic drug policies directly, as opposed to resting hopes on the brain disease label.
尽管成瘾的大脑疾病模型（BDMA）越来越受到批评，但它仍然在成瘾科学中占据主导地位。然而，BDMA 的拥护者或批评者很少有人解释什么是大脑疾病。本综述的目的是从概念上澄清 BDMA 为真意味着什么，而不是对其进行果断的支持或反对。
BDMA 的概念澄清需要考虑可能的疾病模型及其与 BDMA 的关系。这种考虑的一个障碍是相信 BDMA 对于对抗成瘾污名是必要的。为了解决这个障碍，我首先讨论了我们对大脑疾病标签对成瘾污名的影响的了解，以及为什么标签效应不应影响 BDMA 的有效性。然后，我区分了强、最小、网络和不匹配的疾病模型，并认为 BDMA 与强疾病模型一致。这意味着，假设潜在的大脑病理学是导致个人层面可观察到的迹象和经历的成瘾特征的原因。因此，对 BDMA 的评估需要分析大脑功能障碍和因果关系的概念，以及它们在成瘾科学中的应用。
大脑功能障碍不能仅仅作为大脑变化或大脑差异来分析；也不能仅仅从个人层面的迹象和症状的存在来推断。有必要对正常的大脑功能有一个解释，以便对其进行测量。发展这样一个解释的理论和经验挑战并不是不可逾越的，但它们是实质性的。虽然存在因果关系的竞争分析，但在实验科学中有一种相对标准的方法来建立因果关系：干预。使用这种方法，大脑状态的因果意义，例如，广泛的灰质损失和/或中脑边缘多巴胺系统的神经适应，尚未得到充分证明。需要进一步的研究来确定它们与其他可能的变量（例如，替代强化物）相比的影响。
BDMA 的概念澄清和初步的经验评估建议对其有效性保持不可知论，并对异质性持开放态度；在某些情况下，成瘾可能是一种大脑疾病，而在其他情况下则不是。无论哪种情况，都可以通过直接对抗关于毒品的道德主义和道德主义的毒品政策来对抗成瘾污名，而不是将希望寄托在大脑疾病标签上。
