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Editor's note: the process addictions and the New ASAM definition of addiction.

As newly defined by the American Society of Addiction Medicine (ASAM 2011), the United States' addiction specialty society of physicians, addiction is a primary, chronic disease involving brain reward, motivation, memory and related circuitry. Dysfunction in these circuits leads to characteristic biological, psychological, social and spiritual manifestations. This is reflected in persons compulsively pursuing reward and/or relief by substance use and other behaviors. Addiction cannot be cured but can be brought into remission through a program of treatment, abstinence from all psychoactive substances, and supported recovery.

Alcohol and other drugs have long been recognized as addictive substances and addiction is now generally recognized as a chronic disease of the brain that involves relapse, progressive development, and the potential for fatality if not treated. Developing brain science has set the stage for inclusion of the process addictions, including food, sex, shopping and gambling, in this broader definition of addiction. The DSM-V Task Force, for example, has suggested a new category entitled Addictions and Related Disorders (Grant et al. 2010), which would include both substance-related and non-substance/behavioral addictions. This expansion of the addiction definition is based on an understanding that both psychoactive drugs and certain behaviors that produce a surge of dopamine in the midbrain are the biological substrate for addictive behavior. Individuals who are genetically predisposed to addiction are at higher risk for this "reward deficiency syndrome" due to the interplay of genetic and environmental factors (Smith 2011a).

Addiction is characterized by an inability to consistently abstain, impairment in behavioral control, craving, diminished recognition of significant problems with one's behaviors and interpersonal relationships, and a dysfunctional emotional response. Like other chronic diseases, addiction involves cycles of relapse and remission. Without treatment or engagement in recovery activities, addiction is progressive and can result in disability or premature death (ASAM 2011).

Addiction is a pathological process with characteristic signs and symptoms and a predictable prognosis if untreated. As a brain disease, it is characterized by the individual's inability to stop a dysfunctional behavior fueled by drugs or other repeated activities despite adverse consequences. The disease of addiction disrupts the areas of the brain responsible for modulating and controlling emotional, cognitive and social behaviors.

Acceptance of this medical model of addiction has allowed the field of addiction medicine to be viewed like those of other chronic diseases, which are influenced by genetic and environmental factors. As a result, addiction medicine is now a Board-certified medical specialty in the United States through the American Board of Addiction Medicine.

There is a strong genetic influence, with well-studied biological mechanisms, particularly for early onset addiction in adolescents. The expression of the addiction phenotype is based on a genetic predisposition or genotype that is influenced by environmental factors. If untreated, addiction follows a relapsing and remitting course, but treatment compliance is similar to other chronic medical conditions, such as diabetes, hypertension and asthma.

Addiction is most effectively managed as a chronic disease where both medical and psychosocial interventions are used. Large numbers of people will be exposed to psychoactive drugs but only a certain percentage, primarily the at-risk population, will progress to addictive disease. It is important to emphasize that the onset of addictive disease is an interplay between the psychological and physical characteristics of individuals, including their genetic makeup, the addictive potential of the psychoactive drugs they're exposed to, and the environment in which these variables interact.

Some of the key issues to understand about the patho-physiology of addiction are why and how people get addicted to drugs and why some psychoactive chemicals are addictive while others are not. The body has very precise mechanisms for maintaining biological homeostasis, for example pituitary hormones, thyroid, insulin/glucose. These mechanisms titrate neurochemicals within the body and brain to maintain this balance. The introduction of potent outside psychoactive drugs alters this neurochemical balance and disrupts the normal homeostatic system of craving and satiation for the biological functions necessary to sustain life, e.g. hunger, thirst, sex, sleep.

Many parts of the brain work together to maintain this homeostasis. The mid-brain or mesolimbic pathway uses reward, which is a sense of well-being or pleasure, to promote life sustaining and life fulfilling behaviors, e.g. eating, drinking, nurturing to sustain propagation of the species. Addiction occurs by disregulation of this natural process, such that the craving and drive focus on drugs or certain behaviors rather than natural life sustaining processes. All humans have this reward pathway but not all drugs are addicting, nor do all substance users become addicted.

The drugs of addiction are identifiable by their ability to stimulate dopamine secretion in this mesolimbic reward pathway. Genetically predisposed addicts are identifiable by their unique response to addictive substances that produce hypersecretion of dopamine in this mesolimbic reward pathway. Recent brain science studies using various types of neuroimaging support the concept that the process addictions also stimulate dopamine secretion, thus putting these behaviors on a parallel course with drug abuse as addictive diseases and leading to ASAM's including them in its new definition of addiction (Blum 2012; Oberg, Christie & Tata 2011; Potenza et al. 2011; Reynaud & Karila 2011; Zhang et al. 2011; El-Guebaly 2010; Han et al. 2010).

Repetitive drug taking begins to change into involuntary drug taking, at which point the behavior is driven by compulsion to use the drug without regard to adverse consequences. From a neurochemical point of view, crossing the line from homeostasis to allostasis can vary in time from the onset of drug use and is strongly influenced by the genetic predisposition of the individual. Frequent drug use in a person with genetic predisposition alters this hedonic set point and creates an earlier craving response for the drug despite adverse consequences. The drug or behavior loses its pleasurable effects at standard "doses" and tolerance develops such that high levels of usage are wanted or needed to feel normal. Cravings may continue or even increase despite cessation of drug use, leading to hedonic homeostatic dysregulation. This reward pathway is intimately connected via neural pathways to our judgment in emotional areas by way of projections to the prefrontal cortex (the thinking part of the brain) and the limbic system (the primitive part of the brain). Judgment becomes distorted and the brain begins to treat the drug as necessary for homeostasis and survival. With hedonic homeostatic dysregulation, addicts are logically aware that they do not need the drug, but survival drives tend to take precedence over logic. Continued substance use takes survival precedence over life goals, relationships, self-esteem, stability, safety, finances and health. Substituting "sex" or "food" or "gambling" for "drug" in the above presents an equally valid scenario.

The medical model focuses on addiction as a brain disease, emphasizing that drugs hijack the reward system, and alter the cognitive and reward processes, causing the person to think the drugs or processes are essential for survival. With the progression of addictive disease, addictive substances can alter the brain chemistry and mimic or aggravate comorbid psychological disorders including depression, anxiety and psychosis, complicating the treatment picture for such dual diagnosis patients.

THE NEW ASAM DEFINITION OF ADDICTION

The new ASAM definition of addiction emphasizes three broad areas.

Addiction is a primary, chronic disease of brain reward, motivation, memory and related circuitry. Addiction affects neurotransmission and interactions within reward structures of the brain, including the nucleus accumbens, anterior cingulate cortex, basal forebrain and amygdala, such that motivational hierarchies are altered and addictive behaviors, which may or may not include alcohol and other drug use, supplant healthy, self-care related behaviors. Addiction also affects neurotransmission and interactions between cortical and hippocampal circuits and brain reward structures, such that the memory of previous exposures to rewards (such as food, sex, alcohol and other drugs) leads to a biological and behavioral response to external cues, in turn triggering craving and/or engagement in addictive behaviors.

The neurobiology of addiction encompasses more than the neurochemistry of reward. The frontal cortex of the brain and underlying white matter connections between the frontal cortex and circuits of reward, motivation and memory are fundamental in the manifestations of altered impulse control, altered judgment, and the dysfunctional pursuit of rewards (which is often experienced by the affected person as a desire to "be normal") seen in addiction--despite cumulative adverse consequences experienced from engagement in substance use and other addictive behaviors. The frontal lobes are important in inhibiting impulsivity and in assisting individuals to appropriately delay gratification. When persons with addiction manifest problems in deferring gratification, there is a neurological locus of these problems in the frontal cortex. Frontal lobe morphology, connectivity and functioning are still in the process of maturation during adolescence and young adulthood, and early exposure to substance use is another significant factor in the development of addiction. Many neuroscientists believe that developmental morphology is the basis that makes early-life exposure to substances such an important factor.

Genetic factors account for about half of the likelihood that an individual will develop addiction. Environmental factors interact with the person's biology and affect the extent to which genetic factors exert their influence. Resiliencies the individual acquires (through parenting or later life experiences) can affect the extent to which genetic predispositions lead to the behavioral and other manifestations of addiction. Culture also plays a role in how addiction becomes actualized in persons with biological vulnerabilities to the development of addiction.

Other factors that can contribute to the appearance of addiction, leading to its characteristic bio-psycho-socio-spiritual manifestations, include:

a) The presence of an underlying biological deficit in the function of reward circuits, such that drugs and behaviors which enhance reward function are preferred and sought as reinforcers;

b) The repeated engagement in drug use or other addictive behaviors, causing neuroadaptation in motivational circuitry leading to impaired control over further drug use or engagement in addictive behaviors;

c) Cognitive and affective distortions, which impair perceptions and compromise the ability to deal with feelings, resulting in significant self-deception;

d) Disruption of healthy social supports and problems in interpersonal relationships which impact the development or impact of resiliencies;

e) Exposure to trauma or stressors that overwhelm an individual's coping abilities;

f) Distortion in meaning, purpose and values that guide attitudes, thinking and behavior;

g) Distortions in a person's connection with self, with others and with the transcendent (referred to as God by many, the Higher Power by 12-steps groups, or higher consciousness by others); and

h) The presence of co-occurring psychiatric disorders in persons who engage in substance use or other addictive behaviors.

Addiction is characterized by:

* inability to consistently Abstain;

* impairment in Behavioral control;

* Craving; or increased "hunger" for drugs or rewarding experiences;

* Diminished recognition of significant problems with one's behaviors and interpersonal relationships; and

* a dysfunctional Emotional response.

The above definition is quoted from ASAM's Public Policy Statement: Definition of Addiction (ASAM 2011).

SUMMARY

ASAM has now expanded into two new areas--the process addictions and the prescription drug problem, which are the focus of two special forums in this issue of the Journal of Psychoactive Drugs.

Each expansion of the definition of addiction by ASAM has been met with controversy. There was resistance to including drugs other than alcohol when ASAM was first founded in the 1950s and it wasn't until the 1980s that the disease model of addiction was applied to all drugs of addiction. Sex addiction was particularly controversial in the 1990s and was rejected by both ASAM and the AMA (Robinson 2011).

ASAM has addressed the prescription drug problem for more than a decade (ASAM 1989, rev. 2000). With the current escalating problems of prescription drugs and the nonmedical, sometimes lethal use of them by parts of society, much of the current overall drug problem emanates from the medical system. Prescription drug overdose, for example, is the leading cause of death in adolescents and young adults (Smith 2011b; DuPont 2010).

DOI: 10.1080/02791072.2012.662105

REFERENCES

American Society of Addiction Medicine (ASAM). 2011. Public Policy Statement: Definition of Addiction. Available at www.asam.org/research-treatment/definition-of-addiction

American Society of Addiction Medicine (ASAM). 1989, rev. 2000. Public Policy Statement: Measures to Counteract Prescription Drug Diversion. Available at www.asam.org/docs/publicy-policy-statements/ 1prescription-diversion--rev-400.pdf

Blum, K.; Garadner, E.; Oscar-Berman, M. & Gold, M. 2012. "Liking" and "wanting" linked to Reward Deficiency Syndrome (RDS): Hypothesizing differential responsivity in brain reward circuitry. Current Pharmaceutical Design January 9 [epub ahead of print].

DuPont, R.L. 2010. Prescription drug abuse: An epidemic dilemma. Journal ofPsychoactive Drugs 42 (2): 127-32.

El-Guebaly, N.; Mudry, T.; Zohar, J.; Tavares, H. & Potenza, M.N. 2011. Compulsive features in behavioral addictions: The case of pathological gambling. Addiction October 10 [epub ahead of print].

Grant, J.E.; Potenza, M.N.; Weinstein, A. & Gorelick, D.A. 2010. Introduction to behavioral addictions. American Journal ofDrug and Alcohol Abuse 36 (5): 233-41.

Han, D.H.; Kim, Y.S.; Lee, Y.S.; Min, K.J. & Renshaw, P.F. 2010. Changes in cue-induced, prefrontal cortex activity with video-game play. Cyberpsychology, Behavior, and Social Networking 13 (6): 655-61.

Oberg, S.A.; Christie, G.J. & Tata, M.S. 2011. Problem gamblers exhibit reward hypersensitivity in medial frontal cortex during gambling. Neuropsychologia 49 (13): 3768-75.

Potenza, M.N.; Walderhaaug, E.; Henry, S.; Gallezot, J.D.; Planeta-Wilson, B.; Ropchan, J. & Neumeister, A. 2011. Serotonin 1B receptor imaging in pathological gambling. World Journal of Biological Psychiatry September 22 [epub ahead of print].

Reynaud, M. & Karila, L. 2011. From substance dependence to addiction: Impact of a conceptual shift on therapeutic approaches? Current Pharmaceutical Design 17 (14): 1321-22.

Robinson, M. 2011. The wages of sexual-addiction politics. Psychology Today Available at www.psychologytoday.com/blog/cupidspoisoned-arrow/201112/the-wages-sexual- addiction-politics

Smith, D.E. 2011a. The evolution of addiction medicine as a medical specialty. Virtual Mentor 13 (12): 900-05. Available at http://virtualmentor.ama-assn.org/2011/12/mhst1-1112.html

Smith, D.E. 2011b. Integration of pharmacotherapy and psychosocial treatment in opiate-addicted youth. Journal ofPsychoactive Drugs 43 (3): 175-79.

Zhang, Y.; von Deneen, K.M.; Tian, J.; Gold, M.S. & Liu, Y. 2011. Food addiction and neuroimaging. Current Pharmaceutical Design 17 (12): 1149-57.

David E. Smith, M.D., FASAM, FAACT (a)

(a) Principal, David E. Smith, MD & Associates, San Francisco; Chair, Addiction Medicine, Newport Academy, Orange, CA; Medical Director, Center Point, San Rafael, CA; Member, Advisory Board, Dominion Diagnostics, North Kingstown, RI.

Please address correspondence to David E. Smith, M.D., David E. Smith, MD & Associates, 856 Stanyan Street, San Francisco 94117; phone: (415) 933-8759; fax: (415) 933-8674; email: DrSmith@DrDave.org
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Title Annotation:American Society of Addiction Medicine
Author:Smith, David E.
Publication:Journal of Psychoactive Drugs
Article Type:Editorial
Geographic Code:1USA
Date:Mar 1, 2012
Words:2396
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