This type of ‘reduction’ is different from theory-reduction of, for example, biology to physics and chemistry. Both types of ‘reduction’ are relevant to the relation between the BMM and the BPSM and both are in play in Engel’s 1977 paper. The BMM would predict scientific-explanatory reduction to primary biological causes only across the whole of health, like the biomedical models of infectious diseases (or of effects of lesions or of genes https://parliamentobserver.com/2024/05/27/top-5-advantages-of-staying-in-a-sober-living-house/ of major effect). A future application of clinical neuroscience may allow for more precise prediction of a neurogenetic vulnerability to addiction, lead to better understanding of pharmacokinetics and pharmacodynamics of drug use, and to bring greater precision to diagnosis than is currently possible. Realizing a neurobiological or genetic susceptibility to addiction could empower life planning and the avoidance of high-risk scenarios.
Box 1 What’s in a name? Differentiating hazardous use, substance use disorder, and addiction
The threats are based on emotional and moral attitudes towards the existence of the SIS and drug addicts generally, as opposed to empirical evidence (Des Jarlais, Arasteh, and Hagan 2008). Addictions research using heroin-assisted treatment (HAT) trials such as the North American Opiate Medication Initiative (NAOMI) and similar HAT studies and programs in Europe Sober House are a striking, if not controversial example of an effort to embody a biopsychosocial systems approach. The objective of these trials is to investigate the benefits and risks of administering medically supervised, pharmaceutical-grade injectable heroin to chronic opiate users where other treatment options, such as methadone maintenance therapy, have failed.
Ch. 1: Introduction to Psychological Models of Addiction
It thus seems that, rather than negating a rationale for a disease view of addiction, the important implication of the polygenic nature of addiction risk is a very different one. Genome-wide association studies of complex traits have largely confirmed the century old “infinitisemal model” in which Fisher reconciled Mendelian and polygenic traits [51]. A key implication of this model is that genetic susceptibility for a complex, polygenic trait is continuously distributed in the population. This may seem antithetical to a view of addiction as a distinct disease category, but the contradiction is only apparent, and one that has long been familiar to quantitative genetics.
Reciprocal Determinism as a Philosophical Model of Drug Addiction
This claim coincides with a recent emergence of a global advocacy movement that seeks to construct the use of drugs as a human right (Elliott, Csete, Wood, and Kerr 2005; Lines and Elliott 2007). The NAOMI trial raised significant scientific, legal, ethical and political concerns, which included issues of patient safety, the controversial use of placebo control therapy, lack of equipoise, treatment discontinuation, and compassionate access to treatment (Oviedo-Joekes, Nosyk, Marsh, et al. 2009). Reflecting on these concerns, the authors stated “we [had] to be clear in our ethics applications and in our informed consent process with participants that HAT will not be available outside the context of the study” (p. 267).
Anthropologists argue that humans first began consuming alcohol approximately 10,000 years ago after observing other animals selectively choosing fermented fruit over unfermented fruit when both were concurrently available. Our affinity for this inebriant was such that humans throughout most parts of the world had mastered the techniques of creating wine, beer, and distilled spirits 2000 years ago. Anthropological data further suggests that humans were using other psychoactive substances derived from natural sources for similar periods of time, with cocaine use dating to 2500 BC, cannabis use dating to 2700 BC, and opioid use dating to 5000 BC (Maisto et al., 2018). Perhaps most significantly, once these substances made their appearance in the archeological record, they did not vanish, but remained a permanent fixture of society. It is not trivial to delineate the exact category of harmful substance use for which a label such as addiction is warranted (See Box 1).
However, this criticism neglects the fact that neuroimaging is not used to diagnose many neurologic and psychiatric disorders, including epilepsy, ALS, migraine, Huntington’s disease, bipolar disorder, or schizophrenia. Even among conditions where signs of disease can be detected using brain imaging, such as Alzheimer’s and Parkinson’s disease, a scan is best used in conjunction with clinical acumen when making the diagnosis. Thus, the requirement that addiction be detectable with a brain scan in order to be classified as a disease does not recognize the role of neuroimaging in the clinic.
- Somatic markers are acquired by experience and are under control of a neural “internal preference system [which] is inherently biased to avoid pain, seek potential pleasure, and is probably pretuned for achieving these goals in social situations” (Damasio 1994, 179).
- Therefore, nutrition research has been constrained to reductionistic approaches, such as looking at single nutrients or single outcome measures such as changes in weight.
- The notion of addiction as a brain disease is commonly criticized with the argument that a specific pathognomonic brain lesion has not been identified.
- The NAOMI trial raised significant scientific, legal, ethical and political concerns, which included issues of patient safety, the controversial use of placebo control therapy, lack of equipoise, treatment discontinuation, and compassionate access to treatment (Oviedo-Joekes, Nosyk, Marsh, et al. 2009).
- For example, an individual’s socioeconomic status is correlated with increased negative consequences from substance use, such as increased sharing of used injecting equipment and higher prevalence rates of Human Immunodeficiency Virus (HIV) and hepatitis C (Strike, Myers, and Millson 2004).
- It has been shown that in the absence of the substance, negative moods (e.g., depression, anxiety) coupled with enhanced sensitivity to stress eventually create obsession-like preoccupation (brain becomes “hi-jacked”), a loss of executive functioning, and then relapse, reinitiating the cycle again (89).
What Exactly Is the Biopsychosocial Model of Addiction?
These dimensions, which operate at different levels, interact with one another to produce differences in drug use across individuals. In a similar fashion, a person’s current environment directly impacts the likelihood of using drugs by setting the contingencies that influence drug use. Of most importance, however, is the social environment, which acts to either encourage or discourage drug use. Indeed, one of the strongest prognosticators of drug use is the drug-use behavior of peers (Bahr et al., 2005; Walden et al., 2004), and numerous epidemiological studies have identified functional relationships between the behavior of peers and an individual’s drug use (Bot et al., 2005; Kelly et al., 2013).
- The authors outlined an agenda closely related to that put forward by Leshner, but with a more clinical focus.
- Converging research suggests that addiction and attachment have overlapping neural pathways.
- The late George Engel believed that to understand and respond adequately to patients’ suffering—and to give them a sense of being understood—clinicians must attend simultaneously to the biological, psychological, and social dimensions of illness.
- Even among conditions where signs of disease can be detected using brain imaging, such as Alzheimer’s and Parkinson’s disease, a scan is best used in conjunction with clinical acumen when making the diagnosis.
- While the biopsychosocial model has its place in the healthcare and mental healthcare systems, individuals might also implement tenants of this model in their own lives.
- An individual’s stress hormones (cortisol and adrenaline) are chronically elevated (Burke Harris, 2018; van der Kolk, 2014).
Life Course Perspective
- Paramount are the social determinants of health, particularly given associations between social disadvantage and the lifetime accumulation of stress and trauma, as well as how social factors impact opioid use (224, 225) and nutritional status (226, 227).
- Within that overall framework, diverse psychology specialty areas focused on personal processes – beliefs, about the world and their own agency, personal goals, emotions, and behavior – in interaction with biological and social processes.
- Simply put, alcohol or other drug use is more likely if positive outcomes are expected than if negative outcomes are expected.
Essential is the person’s perceptions and descriptions of their current situation regarding wellbeing, belonging to a community, and a positive sense of identity, including perceptions of a better life while living with core symptoms [44]. The person’s perceptions of the recovery process and their wellbeing constantly interplay with the relational, social, cultural and political surroundings as understood within a biopsychosocial approach [7, 9, 31, 41, 43]. The number of mechanisms by which the social environment can influence behavior is remarkable.
It is the integration of biological data and psycho-social, narrative, family information, and clinical phenomenology that will make way for more precise forecasting and earlier diagnosis than is possible today. This is one path to follow for new opportunities for treatment and intervention directed toward prevention. Accordingly, an analysis of the ethical, legal and social issues around other problems of addiction, such as prescription opiate misuse for pain management, may also be examined within the context of our proposed framework. Here, we examine some of the ethical challenges to research, service delivery, the philosophies and strategies of harm reduction, and clinical practice that HAT presents. For example, researchers have found a robust association between trauma and addiction (Dube et al., 2002, 2003; Giordano et al., 2016).