Negotiating the Relationship Between Addiction, Ethics, and Brain Science PMC

One of the most generally cited problems with the BPS model is that its inclusiveness results in an unscientific, “fluffy,” pluralistic approach where, in the words of the dodo bird in Alice in Wonderland, all perspectives have won and deserve prizes. The goal of science is analytic understanding and that understanding requires intelligible frames http://www.degilden.info/levitan/nesterov-under-blagovest/ that break the world into its component parts. In contrast to this, the BPS model potentially justifies a morass of “anything goes” in medicine and health. To get a flavor of the difference in emphasis between a biomedical and biopsychosocial view, consider the hypothetical case of Joe, an overweight 60-year-old man who rarely exercises.

biopsychosocial theory of addiction

Fundamentally, we consider that these terms represent successive dimensions of severity, clinical “nesting dolls”. Not all individuals consuming substances at hazardous levels have an SUD, but a subgroup do. Not all individuals with a SUD are addicted to the drug in question, but a subgroup are. At the severe end of the spectrum, http://www.allsouthpark.ru/index.php?option=com_content&task=blogcategory&id=18&Itemid=39 these domains converge (heavy consumption, numerous symptoms, the unambiguous presence of addiction), but at low severity, the overlap is more modest. The exact mapping of addiction onto SUD is an open empirical question, warranting systematic study among scientists, clinicians, and patients with lived experience.

What causes addiction?

They found12 that there were over 400 locations in the genome and at least 566 variants within these locations that influence smoking or alcohol use, bringing science closer to identifying clusters of genes that could play a part in addiction. The study even identified new genes and functions not expected http://www.belushka-info.ru/worldnews/lenta_621.html to be important in addiction. Three of the genetic locations (identified as CUL3, PDE4B, PTGER3) mapped to all of the smoking and alcohol phenotypes measured. The clinical community has a growing array of psychosocial interventions with a strong evidence base available for the treatment of SUDs.

The latter may compromise an individual’s sense and experience of free will, being-in-the-world, perceptions of personal responsibility, and view abnormalities in dopamine pathways as fatalistic. Underlying the analysis of power in the clinical relationship is the issue of how the clinician handles the strong emotions that characterize everyday practice. On the one hand, there is a reactive clinical style, in which the clinician reacts swiftly to expressions of hostility or distrust with denial or suppression. Taken together, the findings from these studies suggest that there is growing support for relations among child BMI, social environment variables (media, peer, and parent), and psychological variables and body dissatisfaction in young children.

Psycho-Social Systems

In dismissing the relevance of genetic risk for addiction, Hall writes that “a large number of alleles are involved in the genetic susceptibility to addiction and individually these alleles might very weakly predict a risk of addiction”. He goes on to conclude that “generally, genetic prediction of the risk of disease (even with whole-genome sequencing data) is unlikely to be informative for most people who have a so-called average risk of developing an addiction disorder” [7]. It is true that a large number of risk alleles are involved, and that the explanatory power of currently available polygenic risk scores for addictive disorders lags behind those for e.g., schizophrenia or major depression [47, 48].

For instance, based on data from the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC) study [27], it has been pointed out that a significant proportion of people with an addictive disorder quit each year, and that most afflicted individuals ultimately remit. These spontaneous remission rates are argued to invalidate the concept of a chronic, relapsing disease [4]. The factors that increase an individual’s risk for addiction are numerous, yet they all find their place in the biopsychosocial model of addiction (Marlatt & Baer, 1988). Taken together, this model provides a holistic conceptualization of addiction that acknowledges the complexity of the disorder and provides guidance toward a solution, which must necessarily be multifaceted and holistic as well. The more we know about the biopsychosocial model, the more we can foster accurate empathy for those with addiction and work toward effective treatment and prevention efforts.

Biopsychosocial Systems Approach

Social learning theory and Bandura’s model of reciprocal determinism provide a framework to integrate the critical dimensions that play causal roles in the addictive process. This model has unique advantages in that it acknowledges that each component not only plays a direct and causal role in addiction but interacts directly with each of the other two components to increase or decrease the likelihood of addiction. Consequently, interventions that target one component impact all other components of the model, which in turn feedback in a reciprocal manner to impact the original component targeted by the intervention. This model is a dynamic model that recognizes that addiction is a continually evolving disorder whose critical features are constantly being modified and reorganized in response to a continuously changing environment and organism. Social norms, availability, accessibility, legality, modeling, expectancies, societal approval, visibility, targeting practices, and cultural beliefs all influence the experience of addiction.

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