Peter R. Martin: Historical Vocabulary of Addiction, Vol. II

Akrasia

According to the electronic version of the Oxford English Dictionary (OED), the noun akrasia is a borrowing from ancient Greek ἀκρασία (“impotence, want of self-command”) and ἀκρατής (“powerless, without authority, without self-command, incontinent”).  This is a term used in Philosophy, defined in OED as: “Lack of physical or (especially in later use) mental strength; weakness of will. Also: the state of tending to act against one's better judgement.”  

The meaning of the word akrasia parallels ideas in Book VII of Nicomachean Ethics, wherein impediments, hindrances or obstructions to virtue are discussed in depth (Natali 2009) by the Ancient Greek philosopher Aristotle (384–322 BCE), known as the founder of the Peripatetic school of philosophy in the Lyceum in Athens.  This book is one of the best-known Aristotelian works on ethics (defined in OED as: “Moral principles, or a system of these”), the branch of knowledge Aristotle himself considered as a rational response to the question of how humans should best live their lives. 

The first use of the term akrasia in the English language is exemplified by an entry in Dictionary of the synonymous words and technical terms in the English language (Leslie, Moir, Creech et al. 1806): “An indisposition to motion arising from weakness, acracy, acrasy, or acrasia.”  In 1853, in a quotation from An expository lexicon of the terms, ancient and modern, in medical and general science, Robert Gray Mayne (1808–1868) seems to have confused the word akrasia with a similarly sounding term acrasia (Mayne 1860): “Acrāsia, incontinence, or intemperance in food, drink, or any other thing; excess; also applied to weakness, or inability to move; or to want of tone, and so like Acrateia.” 

The ancient Greek noun acrasia is partly a borrowing from the post-classical Latin acrasia (“intemperance”) and the ancient Greek ἀκρασία (“bad mixture”) and ἄκρατος (“unmixed, untempered, intemperate”).  The term acrasia is defined in OED as: “Intemperance, excess (in early use personified); irregular or disorderly behaviour; [equated with the noun acrasy.]”  

An example of the first use of acrasia in the English language is by the English poet Edmund Spenser (1552/53–1599) in his fantastical allegory The faerie queene celebrating the Tudor dynasty and Elizabeth I (Spenser 1931): “Here wonnes Acrasia, whom we must surprise, Els she will slip away, and all our drift despise.”  A later quotation, from the allegorical romance Bentivolio and Urania by Nathaniel Ingelo (c.1621–1683), an English clergyman, writer and musician, seems to more resemble the current use of the word (Ingelo 1660): “Here sate an overgrown Woman...; which by her excessive bulk, swollen out of all measure with intemperance, they guess'd to be Acrasia..” 

Since the use of acrasia for akrasia, the words have been used interchangeably despite some subtle distinctions between the two spellings as suggested by their definitions.  Both versions now typically mean the state of acting against one's better judgment or lacking self-control.  Akrasia/acrasia is characterized by knowing what one ought to do but succumbing to impulses or desires that go against one’s long-term goals or values or acting contrary to that knowledge due to weakness of will or irrational impulses.  It is the state of intending or believing one should do one thing, but then doing another (Messerli, Fink and Reuter 2022).  This notion is captured well by a quote from Real Ethics by John Michael Rist (1936—), a British/Canadian scholar of ancient philosophy and classics (Rist 2002):“We… are overpowered by one or other version of acrasia; we ‘know the better and do the worse’.” 

The term akrasia is relevant to the phenomenology of addiction but the degree to which concepts conveyed by this word are fully explanatory of the disorder has been debated for centuries.  Causally relating akrasia to addiction places an emphasis on the inability to meet one’s own expectations — a life not lived optimally or to one’s standards.  According to this perspective, addiction stems from an individual’s human characteristics, such as their moral weakness and the detrimental life decisions made because of personal shortcomings (Rise and Halkjelsvik 2019). 

The notion that personal traits and accompanying choices made by an individual may have a causal role in their developing addiction was generally accepted in history (Fisher 2022).  Despite the recent emphasis on brain research to explain addictive disorders (Berridge and Robinson 2016; Volkow, Koob and McLellan 2016), the accepted wisdom from the past is still accepted by some contemporary proponents (Heather, Best, Kawalek et al. 2018).  Analogously to the role of akrasia in the pathogenesis of addiction, it has been suggested that akrasia may be an important contributing factor to other disorders, e.g., sexually transmitted infections (Fontdevila 2006). 

Since the “Decade of the Brain,” a designation for the period of 1990–1999 by U.S. President George H. W. Bush (1924–2018) “to enhance public awareness of the benefits to be derived from brain research,” the neuroscience community came to hold distinctly opposing views to those who considered traits and choices as causal in pathogenesis of addiction.  The resulting focus on brain-based underpinnings of addictive disorders, characterized by pathological drives, appetites and desires, emerged during this period and has continued to the present (Leshner 1997; Heilig, MacKillop, Martinez et al. 2021).  This viewpoint is not unique to the present time, as the influential physicians Benjamin Rush (1746-1813) and Thomas Trotter (1760-1832) had proposed that alcoholism was a bone fidemedical disease and not a result of a weakness of personality (Rush, Thomas and Andrews 1790; Trotter 1804). 

As a result of these past and present influences, contemporary physicians are now taught that addiction is a brain disease with biopsychosocial underpinnings that may best be addressed from a pharmacopsychosocial perspective (Engel 1977; Martin, Weinberg and Bealer 2007; Heilig, Epstein, Nader et al. 2016).  The hope has been that a brain-disease model of addictive disorders will mitigate the stigma so very frequently experienced by patients with this disorder. Unfortunately, the disease model of addiction has not yet had this positive outcome on the attitudes of society (Heather 2017).

The leaders of the National Institute on Drug Abuse (NIDA) and National Institute on Alcohol Abuse and Alcoholism (NIAAA) have promulgated an investigative focus on neurobiological advances derived from the brain disease model of addiction (Volkow, Koob and McLellan 2016):

“…we review recent advances in the neurobiology of addiction to clarify the link between addiction and brain function and to broaden the understanding of addiction as a brain disease. We review findings on the desensitization of reward circuits, which dampens the ability to feel pleasure and the motivation to pursue everyday activities; the increasing strength of conditioned responses and stress reactivity, which results in increased cravings for alcohol and other drugs and negative emotions when these cravings are not sated; and the weakening of the brain regions involved in executive functions such as decision making, inhibitory control, and self-regulation that leads to repeated relapse. We also review the ways in which social environments, developmental stages, and genetics are intimately linked to and influence vulnerability and recovery.  We conclude that neuroscience continues to support the brain disease model of addiction.” 

            Much (though hardly all) of the knowledge referred to above comes from animal models which are not considered relevant to the human condition by all researchers (Field and Kersbergen 2020).  Harold Kalant (1923 –2021), a Canadian pharmacologist and physician who studied the effects of alcohol and drugs on the human body in addiction, has a much less sanguine viewpoint on the brain disease model of addiction (Kalant 2010):

“…a reductionist approach which attempts to analyse addiction at ever finer levels of structure and function, is inherently incapable of explaining what causes these mechanisms to be brought into play in some cases and not in others, or by self-administration of a drug but not by passive exposure.  There is abundant evidence that psychological, social, economic and specific situational factors play important roles in initiating addiction, in addition to genetic and other biological factors. Therefore, if we hope to be able to make predictions at any but a statistical level, or to develop effective means of prevention, it is necessary to devise appropriate integrative approaches to the study of addiction, rather than pursue an ever-finer reductive approach which leads steadily farther away from the complex interaction of drug, user, environment and specific situations that characterizes the problem in humans.”

Substance-related and addictive disorders manifest clinically as the loss-of-control over self-destructive behaviors.  It is easy to understand how akrasia might factor into the phenomenology of addiction (American Psychiatric Association 2022).  For example, the difficulty experienced by an individual in quitting problematic addictive behaviors, while at the same time recognizing the negative impact of continuing them, may be attributed to akrasia expressed as the reluctance and inability to resist the associated cravings.  Akrasia in an individual can also contribute to relapse after a period of abstinence.  Thus, individuals may give in to impulsive urges or triggers, even after having been taught the tools needed to resist them in psychotherapeutic treatment focused on recovery skills. 

Under each of these situations, akrasia is conceptualized as an aspect of the personality of the individual suffering from addiction, which enhances the likelihood that they will commit errorsof choice and/or judgement.  However, commission of these errors of choice are not necessarily attributable to having a structurally or functionally diseased brain.  Consequently, the brain disease model of addiction is not consistent with the notion of akrasia (Heather, Field, Moss et al. 2022). 

Research investigating whether and how childhood temperament and environment interact to produce behavioral disturbances later in life has been a rich source for psychiatric understanding of personality and psychopathology (Chess, Thomas, Rutter et al. 1963; Fan, Zang, Liu et al. 2023).  A related construct, compatible with the notion of akrasia, is that personality characteristics may be a predisposition and/or consequence of substance use disorders, an idea that has long been considered for alcoholism (Cox 1988).   Fruitful linkage of these concepts to the brain disease model of addiction, however, would require that neuroscience of the underpinnings of personality be more fully developed than it has been to date (Kennis, Rademaker and Geuze 2013; Allen, Hall, Schreiber et al. 2022). 

There are personality-based theories of addiction that may appropriately be adapted to the brain disease model of addiction.  For example, a neurogenetic and adaptive model of alcoholism is grounded in the notion that the age (or presumably developmental stage) at which the disorder begins, namely early onset versus late onset alcoholism, can greatly influence phenomenology of the disorder (Cloninger 1987).  The personality characteristics of late onset alcohol use disordered individuals are more compatible with having the characteristics of akrasia, presumably having had the opportunity to acquire enough self-regulation during adolescence and early adulthood to eventually be able to act against one’s better judgement and with reduced self-control.  

Another personality-based theory of addiction with potential implications for neuroscience is based on childhood temperament and personality expressed as aggression (Martin 2021) in the classroom environment (Kellam, Rebok, Ialongo et al. 1994).  Aggressive behaviors identified in childhood are highly predictive of development of substance use and related disorders.  The presence of this personality trait may have certain parallels with the above-mentioned early onset type of alcoholism, as those with early onset alcohol use disorder are typically the ones who demonstrate early aggressive behaviors.  However, aggressiveness seems quite incompatible with akrasia, which is based in passivity and a weakness of will. 

Scholarly examination of choice and judgment has led to emergence of interdisciplinary academic fields that study these issues related to normal brain functioning.  For example, relatively new domains in which psychological and other fields have amalgamated including, behavioral economics, neuroeconomics and picoeconomics among others.  These disciplines examine judgment and choice in terms of probabilistic determinations as part of decision-making and executive functions (Bickel and Yi 2010), motivational states (Ainslie 1992) as well as the normal range of brain functions as influenced by genetic and environmental determinants (Ross, Kincaid, Spurrett et al. 2010), respectively. 

The complexities of the human condition of addiction have led to several recent volumes in which scholars from a wide range of disciplines — neuroscience, philosophy, psychiatry, psychology, cognitive science, sociology, economics and law — have together explored how judgment and choice pertains to addiction (Ross, Kincaid, Spurrett et al. 2010; Heather, Field, Moss et al. 2022).

Of course, it is difficult to overlook the rapidly evolving findings that have emerged from the brain disease perspective of addiction (Berridge and Robinson 2016; Volkow, Koob and McLellan 2016).  The underlying hypothesis is that addiction is a consequence of identifiable pathological changes in brain function (and structure) which manifest clinically as dysfunctional behavior.  The development of addiction results from conditioned responses to the environment and/or to interoceptive cues which identifiably change relevant brain circuits.  

Fundamental neurobiological processes that contribute to development of pathological changes in brain structure and function, presumably causing addictive behaviors, include conditioning, reward, kindling, salience, self-medication and trauma/stress (see chapters on Conditioning, Reward, Kindling, Salience, Self-medication and Trauma in Historical Vocabulary of Addiction (Martin 2022)).  These neurobiological processes culminate in learning which forms the basis of addiction and accompanying rewiring of brain circuits.  In addition, neurotoxicity from repeated use of drugs of abuse may cause brain injury that compounds brain effects of neuroadaptation causing unpredictable changes in behavior possibly compatible with akrasia. 

A theoretical reconciliation of the brain disease model with addiction-associated personality characteristics such as impaired self-regulation in akrasia has been attempted within a dual-systems perspective (McClure and Bickel 2014; Heather 2020).  This perspective has a long and illustrious history with origins in Greek philosophy and contributions from many subsequent thinkers such as Freud (“ego” and “id”) and Adam Smith (“impartial spectator” and “the passions”) (Ashraf, Camerer and Loewenstein 2005).  

Within the field of psychology, as relevant to addiction, the opposing concepts within the dual-systems perspective are represented by the impulsive (automatic) decision system and the executive (deliberative) decision system (Bickel, Miller, Yi et al. 2007).  The first of these deals with implicit, automatic and mainly non-conscious decision processes and the latter with explicit, controlled and mainly conscious processes (Heather 2020).  The balance between these two decision systems is presumably disturbed in individuals who suffer from addiction, wherein automatic processes, like cue-elicited urges, attentional bias, automatic approach tendencies, implicit memory associations and cognitions promote the maintenance of out-of-control and dysfunctional behaviors.  The deliberative system becomes progressively impaired as poor goal-directed planning, limited self-control capacity and distorted judgements and evaluations undermine attempts to resist the pathological automatic decisions of addiction.   

Examination of the executive (deliberative) decision system in addiction provides an important contrast to the brain disease model.  Successful treatment of addiction focuses on the deliberative decision system rather than the automatic decision system.  Enhancement of the capacity of the individual to weigh pros and cons of a decision about whether to self-administer a drug or partake in a behavior is essential to recovery (Martin 2020). 

Treatment approaches directed at diminishing the reward value of a drug of abuse, namely the brain responses to drug-associated stimuli, predominantly address the impulsive (automatic) decision system.  Such changes in the impulsive decision system are typically a consequence of extinction due to long-term sobriety, not a means to achieve sobriety per se, although pharmacological treatments may be somewhat effective in this regard.  Therefore, psychosocial therapies of addiction, including cognitive-behavioral therapy (CBT), motivational enhancement, mindfulness practices and developing effective relapse prevention plans as in the 12-step mutual support programs, have focused on enhancing healthy decision making. 

Treatment of akrasia can lead the addicted individual to prioritize long-term well-being and rational choices over immediate gratification and, thereby, replace addictive with healthy behaviors and enhance efforts towards recovery.  Akrasia must be contained in treatment as it essentially leads to self-sabotaging recovery by engaging in actions that undermine their healing, such as seeking out triggers or risky situations despite knowing the potential harmful consequences. 

References:

Ainslie G. Picoeconomics: the strategic interaction of successive motivational states within the person. Cambridge: Cambridge University Press; 1992.

Allen TA, Hall NT, Schreiber AM, Hallquist MN. Explanatory personality science in the neuroimaging era: the map is not the territory. Curr Opin Behav Sci 2022; 43:236–41.

American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders: DSM-5-TR. Fifth edition, Text Revision. Washington, DC: American Psychiatric Association Publishing; 2022.

Ashraf N, Camerer CF, Loewenstein G. Adam Smith, Behavioral Economist. J Econ Perspect 2005;19(3):131–45.

Berridge KC, Robinson TE. Liking, wanting, and the incentive-sensitization theory of addiction. Am Psychol 2016;71(8):670–9.

Bickel WK, Miller ML, Yi R, Kowal BP, Lindquist DM, Pitcock JA. Behavioral and neuroeconomics of drug addiction: Competing neural systems and temporal discounting processes. Behav Econ Perspect Drug Abuse Res 2007;90: S85–91.

Bickel WK, Yi R. Neuroeconomics of Addiction: The Contribution of Executive Dysfunction. In: Ross D, Kincaid H, Spurrett D, Collins P, editors. What is Addiction? The MIT Press; 2010. pp. 1–25.

Chess S, Thomas A, Rutter M, Birch HG. Interaction of temperament and environment in the production of behavioral disturbances in children. Am J Psychiatry 1963;120(2):142–8.

Cloninger C. Neurogenetic adaptive mechanisms in alcoholism. Science 1987;236(4800):410–6.

Cox WM. Personality Theory. In: Chaudron CD, Wilkinson DA, editors. Theor Alcohol. Toronto, Canada: Addiction Research Foundation; 1988.

Engel G. The need for a new medical model: a challenge for biomedicine. Science 1977;196(4286):129.

Fan X, Zang T, Liu J, Wu N, Dai J, Bai J, Liu Y. Changes in the gut microbiome in the first two years of life predicted the temperament in toddlers. J Affect Disord 2023; 333:342–52.

Field M, Kersbergen I. Are animal models of addiction useful? Addiction 2020;115(1):6–12.

Fisher CE. The Urge: Our History of Addiction. New York: Penguin Press; 2022.

Fontdevila J. Phenomenologies of the akratic self: masculinity, regrets, and HIV among men on methadone. J Urban Health 2006;83(4):586–601.

Heather N. Q: Is addiction a brain disease or a moral failing? A: Neither. Neuroethics 2017;10(1):115–24.

Heather N. The concept of akrasia as the foundation for a dual systems theory of addiction. Behav Brain Res 2020; 390:112666.

Heather N, Best D, Kawalek A, Field M, Lewis M, Rotgers F, Wiers RW, Heim D. Challenging the brain disease model of addiction: European launch of the addiction theory network. Addict Res Theory 2018;26(4):249–55.

Heather N, Field M, Moss A, Satel S. Evaluating the Brain Disease Model of Addiction. 1st ed. Abingdon, Oxon: Routledge; 2022.

Heilig M, Epstein DH, Nader MA, Shaham Y. Time to connect: bringing social context into addiction neuroscience. Nat Rev Neurosci 2016;17(9):592–9.

Heilig M, MacKillop J, Martinez D, Rehm J, Leggio L, Vanderschuren LJMJ. Addiction as a brain disease revised: why it still matters, and the need for consilience. Neuropsychopharmacology 2021;46(10):1715–23.

Ingelo N. Bentivolio and Urania: in four bookes. London: Printed by J.G. for Richard Marriot and are to be sold at his shop...; 1660.

Kalant H. What neurobiology cannot tell us about addiction. Addiction 2010;105(5):780–9.

Kellam SG, Rebok GW, Ialongo N, Mayer LS. The course and malleability of aggressive behavior from early first grade into middle school: results of a developmental epidemiologically based preventive trial. J Child Psychol Psychiatry 1994;35(2):259–81.

Kennis M, Rademaker AR, Geuze E. Neural correlates of personality: An integrative review. Neurosci Biobehav Rev 2013;37(1):73–95.

Leshner AI. Addiction is a brain disease, and it matters. Science 1997;278(5335):45.

Leslie J, Moir J, Creech W, Hill P, Hope Trust, Bell & Bradfute. Dictionary of the synonymous words and technical terms in the English language. Edinburgh: Printed by John Moir, Royal Bank Close, for the author: And sold by Messrs Bell & Bradfute: W. Creech: P. Hill... [and 11 others]; 1806.

Martin PR. Historical Vocabulary of Addiction. Cordoba, Argentina: INHN Publisher; 2022.

Martin PR, Weinberg BA, Bealer BK. Healing Addiction: An Integrated Pharmacopsychosocial Approach to Treatment. Hoboken, New Jersey: John Wiley & Sons, Inc.; 2007.

Martin PR. Recovery. Historical Vocabulary of Addiction. inhn.org.ebooks. February 20, 2020.

Martin PR. Aggression. Historical Vocabulary of Addiction. inhn.org.ebooks. April 22, 2021.

Mayne RG. An expository lexicon of the terms, ancient and modern, in medical and general science; including a complete medico-legal vocabulary. London: J. Churchill; 1860.

McClure SM, Bickel WK. A dual-systems perspective on addiction: contributions from neuroimaging and cognitive training. Ann N Y Acad Sci 2014;1327(1):62–78.

Messerli M, Fink J, Reuter K. The varying rationality of weakness of the will: an empirical investigation and its challenges for a unified theory of rationality. Synthese 2022;200(5):365.

Natali C. Aristotle: Nicomachean ethics, Book VII: Symposium Aristotelicum. Oxford: Oxford Univ. Press; 2009.

Rise J, Halkjelsvik T. Conceptualizations of addiction and moral responsibility. Front Psychol 2019;10.

Rist JM. Real ethics: reconsidering the foundations of morality. Cambridge, U.K.: Cambridge University Press; 2002.

Ross D, Kincaid H, Spurrett D, Collins P. What Is Addiction? Cambridge MA: The MIT Press; 2010.

Rush B, Thomas I, Andrews ET. An inquiry into the effects of spirituous liquors on the human body: to which is added, a moral and physical thermometer. Printed at Boston: By Thomas and Andrews; at Faust’s Statue, no. 45, Newbury Street; 1790.

Spenser E. The Faerie Queene Disposed into Twelve Books Fashioning Twelve Moral Vertues. J.M. Dent & Sons Ltd.; E.P. Dutton; 1931. London & Toronto New York: J.M. Dent & Sons Ltd.; E.P. Dutton; 1931.

Trotter T. An essay, medical, philosophical, and chemical, on drunkenness, and its effects on the human body. London: Printed for T.N. Longman and O. Rees; 1804.

Volkow ND, Koob GF, McLellan AT. Neurobiologic advances from the brain disease model of addiction. N Engl J Med 2016;374(4):363–71.

August 10, 2023