This also suggests some awareness that the BPSM cannot properly be used for defining and explaining disease. In section two, I argue, consistent with others (Bolton and Gillett 2019; Ghaemi 2010, 2011; McLaren 1998; Quintner and Cohen 2019; Weiner 2008), that the BPSM is not a scientific or explanatory model. The BPSM cannot be used to distinguish disease from non-disease, define diseases, https://megapolisnews.com/top-5-advantages-of-staying-in-a-sober-living-house/ or identify genuine cause-effect relationships. (This is not to say the BPSM has no value. As I argue, it is still a useful tool for organizing and communicating information about the psychosocial determinants of health). Drawing on Engel’s seminal 1977 article and several BPSM illness literatures, I describe the patterns of specious argumentation that constitute wayward discourse.
Substance abuse: Implications of a biopsychosocial model for prevention, treatment, and relapse prevention.
As McLaren has argued (1998), for the BPSM to be a genuinely scientific model, it would have to go beyond merely positing that illness involves biological, psychological, and social factors. It would have to provide an integrating theory that explained exactly how these factors interact to cause illness in practice. The model could do this by, for example, defining its three domains clearly and explaining how social factors of type X cause biological events of type Y, which in turn produce symptoms of type Z, and so on. Engel hoped that general systems theory could be used to build this kind of scientific version of the BPSM (Engel 1977).
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- Mental health problems, such as anxiety and depression, may increase [29], and it may be difficult to maintain social relationships, everyday parenting responsibilities and work routines [18, 34].
- While making a decision is itself a mental act, a mental act or event does not cause behaviour alone, but is one part of the complex process between neuronal firing and action.
- Reciprocal determinism demands not only a multifaceted approach, but an approach with constantly changing decision trees, if-then statements, and go/no-go decisions.
- Moreover, the larger social network of former users – all of whom are in various stages of recovery – encourage one another via modeling and reinforcement to take “personal inventory” and to identify the personal factors that play a causal role in their drug use.
These causal neurogenetic attributions have led some authors to advocate for involuntary treatment in addiction, arguing that, paradoxically, autonomy must be denied, “in order to create it” (Caplan 2008). Gilllett argues that the causal model is based on a faulty account of human autonomy and consciousness and is scientifically Sober House and conceptually questionable. Gillett challenges the neurophilosophical model of human decision-making, which, as he has previously argued (2008a), emphasizes selfishness, and “constricts the scope of reason so that it is subject to any desire or disposition that one happens to endorse at the time one acts” (p. 1215).
Overview of the BPSM
This is consistent with the fact that moderate-to-severe SUD has the closest correspondence with the more severe diagnosis in ICD [117,118,119]. Nonetheless, akin to the undefined overlap between hazardous use and SUD, the field has not identified the exact thresholds of SUD symptoms above which addiction would be definitively present. A lot more is going on in clinical care than decisions as to what treatments to recommend, including personal, interpersonal, and institutional processes. Engel says a lot of interesting things about all these things in his 1997 paper and others around that time (Engel, 1980, 1982), and they can be considered as part of what is covered by the BPSM.
1. Socrates, Plato, Aristotle and the origin of knowledge
- Why do individuals choose the pathological choice of using drugs at the expense of taking care of oneself and loved ones, of sacrificing personal relationships, of destroying one’s social environment.
- In other words, addiction can be viewed as a chronically evolving biopsychosocial disorder, encompassing dimensions that are both internal and external to the individual.
- White (1996) draws attention to a set of individuals whom he calls “acultural addicts.” These people initiate and sustain their substance use in relative isolation from other people who use drugs.
- At the severe end of the spectrum, these domains converge (heavy consumption, numerous symptoms, the unambiguous presence of addiction), but at low severity, the overlap is more modest.
Comment on Heilig et al.: The centrality of the brain and the fuzzy line of addiction
- A common criticism of the notion that addiction is a brain disease is that it is reductionist and in the end therefore deterministic [81, 82].
- One example is drug craving that may be experienced as strong, intense urges for immediate gratification that may impair rational thought about future planning (Elster and Skog 1999).
- Second, the authors claim that the OPPERA findings support the proposition that TMD is a “complex disorder.” However, as discussed, this argument only works if we read the proposition into the empirical findings.
- Calling a problem “a disease” also generally brings it under the jurisdiction of physicians, whose primary expertise is in the body and its defects, thereby encouraging pursuit of characteristically medical modes of treatment and management.
