Psychoactive Addiction Definition Essay

"Addictive" redirects here. For other uses, see Addiction (disambiguation) and Addictive (disambiguation).

Addiction and dependence glossary[1][2][3][4]
  • addiction – a brain disorder characterized by compulsive engagement in rewarding stimuli despite adverse consequences
  • addictive behavior – a behavior that is both rewarding and reinforcing
  • addictive drug – a drug that is both rewarding and reinforcing
  • dependence – an adaptive state associated with a withdrawal syndrome upon cessation of repeated exposure to a stimulus (e.g., drug intake)
  • drug sensitization or reverse tolerance – the escalating effect of a drug resulting from repeated administration at a given dose
  • drug withdrawal – symptoms that occur upon cessation of repeated drug use
  • physical dependence – dependence that involves persistent physical–somatic withdrawal symptoms (e.g., fatigue and delirium tremens)
  • psychological dependence – dependence that involves emotional–motivational withdrawal symptoms (e.g., dysphoria and anhedonia)
  • reinforcing stimuli – stimuli that increase the probability of repeating behaviors paired with them
  • rewarding stimuli – stimuli that the brain interprets as intrinsically positive and desirable or as something to approach
  • sensitization – an amplified response to a stimulus resulting from repeated exposure to it
  • substance use disorder – a condition in which the use of substances leads to clinically and functionally significant impairment or distress
  • tolerance – the diminishing effect of a drug resulting from repeated administration at a given dose

Addiction is a brain disorder characterized by compulsive engagement in rewarding stimuli despite adverse consequences.[8] Despite the involvement of a number of psychosocial factors, a biological process – one which is induced by repeated exposure to an addictive stimulus – is the core pathology that drives the development and maintenance of an addiction.[1][9] The two properties that characterize all addictive stimuli are that they are reinforcing (i.e., they increase the likelihood that a person will seek repeated exposure to them) and intrinsically rewarding (i.e., they are perceived as being inherently positive, desirable, and pleasurable).[1][3][7]

Addiction is a disorder of the brain's reward system which arises through transcriptional and epigenetic mechanisms and occurs over time from chronically high levels of exposure to an addictive stimulus (e.g., eating food, the use of cocaine, engagement in sexual intercourse, participation in high-thrill cultural activities such as gambling, etc.).[1][10][11]ΔFosB, a gene transcription factor, is a critical component and common factor in the development of virtually all forms of behavioral and drug addictions.[10][11][12][13] Two decades of research into ΔFosB's role in addiction have demonstrated that addiction arises, and the associated compulsive behavior intensifies or attenuates, along with the overexpression of ΔFosB in the D1-typemedium spiny neurons of the nucleus accumbens.[1][10][11][12] Due to the causal relationship between ΔFosB expression and addictions, it is used preclinically as an addiction biomarker.[1][10][12] ΔFosB expression in these neurons directly and positively regulates drug self-administration and reward sensitization through positive reinforcement, while decreasing sensitivity to aversion.[note 1][1][10]

As described by two groups of researchers, addiction exacts an "astoundingly high financial and human toll" on individuals and society as a whole through the direct adverse effects of drugs, associated healthcare costs, long-term complications (e.g., lung cancer with smoking tobacco, liver cirrhosis with drinking alcohol, or meth mouth from intravenous methamphetamine), the functional consequences of altered neural plasticity in the brain, and the consequent loss of productivity.[14][15][16] Classic hallmarks of addiction include impaired control over substances or behavior, preoccupation with substance or behavior, and continued use despite consequences.[17] Habits and patterns associated with addiction are typically characterized by immediate gratification (short-term reward), coupled with delayed deleterious effects (long-term costs).[18]

Examples of drug and behavioral addictions include: alcoholism, amphetamine addiction, cocaine addiction, nicotine addiction, opiate addiction, food addiction, gambling addiction, and sexual addiction. The only behavioral addiction recognized by the DSM-5 and the ICD-10 is gambling addiction. The term addiction is misused frequently to refer to other compulsive behaviors or disorders, particularly dependence, in news media.[19] An important distinction between drug addiction and dependence is that drug dependence is a disorder in which cessation of drug use results in an unpleasant state of withdrawal, which can lead to further drug use.[20] Addiction is the compulsive use of a substance or performance of a behavior that is independent of withdrawal.

Neuropsychology[edit]

This section needs expansion. You can help by adding to it.(February 2016)

Cognitive control and stimulus control, which is associated with operant and classical conditioning, represent opposite processes (i.e., internal vs external or environmental, respectively) that compete over the control of an individual's elicited behaviors.[21] Cognitive control, and particularly inhibitory control over behavior, is impaired in both addiction and attention deficit hyperactivity disorder.[22][23] Stimulus-driven behavioral responses (i.e., stimulus control) that are associated with a particular rewarding stimulus tend to dominate one's behavior in an addiction.[23]

Stimulus control of behavior[edit]

See also: Stimulus control

Cognitive control of behavior[edit]

See also: Cognitive control

Behavioral addiction[edit]

Main article: Behavioral addiction

The term behavioral addiction correctly refers to a compulsion to engage in a natural reward – which is a behavior that is inherently rewarding (i.e., desirable or appealing) – despite adverse consequences.[6][11][13] Preclinical evidence has demonstrated that marked increases in the expression of ΔFosB through repetitive and excessive exposure to a natural reward induces the same behavioral effects and neuroplasticity as occurs in a drug addiction.[11][24][25][26]

Reviews of both clinical research in humans and preclinical studies involving ΔFosB have identified compulsive sexual activity – specifically, any form of sexual intercourse – as an addiction (i.e., sexual addiction).[11][24] Moreover, reward cross-sensitization between amphetamine and sexual activity, meaning that exposure to one increases the desire for both, has been shown to occur preclinically and clinically as a dopamine dysregulation syndrome;[11][24][25][26] ΔFosB expression is required for this cross-sensitization effect, which intensifies with the level of ΔFosB expression.[11][25][26]

Reviews of preclinical studies indicate that long-term frequent and excessive consumption of high fat or sugar foods can produce an addiction (food addiction).[11][13]

Gambling is a natural reward which is associated with compulsive behavior and for which clinical diagnostic manuals, namely the DSM-5, have identified diagnostic criteria for an "addiction".[11] There is evidence from functional neuroimaging that gambling activates the reward system and the mesolimbic pathway in particular.[11][27] Similarly, shopping and playing videogames are associated with compulsive behaviors in humans and have also been shown to activate the mesolimbic pathway and other parts of the reward system.[11] Based upon this evidence, gambling addiction, video game addiction and shopping addiction are classified accordingly.[11][27]

Risk factors[edit]

There are a range of genetic and environmental risk factors for developing an addiction that vary across the population.[1][28] Roughly half of an individual's risk for developing an addiction is derived from genetics, while the other half is derived from the environment.[1] However, even in individuals with a relatively low genetic loading, exposure to sufficiently high doses of an addictive drug for a long period of time (e.g., weeks–months) can result in an addiction.[1] In other words, anyone can become an addict under the right circumstances.

Genetic factors[edit]

It has long been established that genetic factors along with environmental (e.g., psychosocial) factors are significant contributors to addiction vulnerability. Epidemiological studies estimate that genetic factors account for 40–60% of the risk factors for alcoholism. Similar rates of heritability for other types of drug addiction have been indicated by other studies.[29] Knestler hypothesized in 1964 that a gene or group of genes might contribute to predisposition to addiction in several ways. For example, altered levels of a normal protein due to environmental factors could then change the structure or functioning of specific brain neurons during development. These altered brain neurons could change the susceptibility of an individual to an initial drug use experience. In support of this hypothesis, animal studies have shown that environmental factors such as stress can affect an animal's genotype.[29]

Overall, the data implicating specific genes in the development of drug addiction is mixed for most genes. One reason for this may be that the case is due to a focus of current research on common variants. Many addiction studies focus on common variants with an allele frequency of greater than 5% in the general population, however when associated with disease, these only confer a small amount of additional risk with an odds ratio of 1.1–1.3 percent. On the other hand, the rare variant hypothesis states that genes with low frequencies in the population (<1%) confer much greater additional risk in the development of disease.[30]

Genome-wide association studies (GWAS) are a recently developed research method which are used to examine genetic associations with dependence, addiction, and drug use. These studies employ an unbiased approach to finding genetic associations with specific phenotypes and give equal weight to all regions of DNA, including those with no ostensible relationship to drug metabolism or response. These studies rarely identify genes from proteins previously described via animal knockout models and candidate gene analysis. Instead, large percentages of genes involved in processes such as cell adhesion are commonly identified. This is not to say that previous findings, or the GWAS findings, are erroneous. The important effects of endophenotypes are typically not capable of being captured by these methods. Furthermore, genes identified in GWAS for drug addiction may be involved either in adjusting brain behavior prior to drug experiences, subsequent to them, or both. [31]

A study that highlights the significant role genetics play in addiction is the twin studies. Twins have similar and sometimes identical genetics. Analyzing these genes in relation to genetics has helped geneticists understand how much of a role genes play in addiction. Studies performed on twins found that rarely did only one twin have an addiction. In most cases where at least one twin suffered from an addiction, both did, and often to the same substance.[32]

Environmental factors[edit]

Environmental risk factors for addiction are the experiences of an individual during their lifetime that interact with the individual's genetic composition to increase or decrease the his or her vulnerability to addiction.[1] A number of different environmental factors have been implicated as risk factors for addiction, including various psychosocial stressors;[1] however, an individual's exposure to an addictive drug is by far the most significant environmental risk factor for addiction.[1] The National Institute on Drug Abuse cites lack of parental supervision, the prevalence of peer substance use, drug availability, and poverty as risk factors for substance use among children and adolescents.[33]

Adverse childhood experiences (ACEs) are various forms of maltreatment and household dysfunction experienced in childhood. The Adverse Childhood Experiences Study by the Centers for Disease Control and Prevention has shown a strong dose–response relationship between ACEs and numerous health, social, and behavioral problems throughout a person's lifespan, including those associated with substance abuse.[34] Children's neurological development can be permanently disrupted when they are chronically exposed to stressful events such as physical, emotional, or sexual abuse, physical or emotional neglect, witnessing violence in the household, or a parent being incarcerated or suffering from a mental illness. As a result, the child's cognitive functioning or ability to cope with negative or disruptive emotions may be impaired. Over time, the child may adopt substance use as a coping mechanism, particularly during adolescence.[34] A study of 900 court cases involving children who experienced abuse found that a vast amount of them went on to suffer from some form of addiction in their adolescence or adult life.[35] This pathway towards addiction that is opened through stressful experiences during childhood can be avoided by a change in environmental factors throughout an individuals life and opportunities of professional help.[35]

Age[edit]

Adolescence represents a period of unique vulnerability for developing addiction.[36] In adolescence, the incentive–rewards systems in the brain mature well before the cognitive control center. This consequentially grants the incentive–rewards systems a disproportionate amount of power in the behavioral decision making process. Therefore, adolescents are increasingly likely to act on their impulses and engage in risky, potentially addicting behavior before considering the consequences.[37] Not only are adolescents more likely to initiate and maintain drug use, but once addicted they are more resistant to treatment and more liable to relapse.[38][39] Statistics have shown that those who start to drink alcohol at a younger age are more likely to become dependent later on. About 33% of the population tasted their first alcohol between the ages of 15 and 17, while 18% experienced it prior to this. As for alcohol abuse or dependence, the numbers start off high with those who first drank before they were 12 and then drop off after that. For example, 16% of alcoholics began drinking prior to turning 12 years old, while only 9% first touched alcohol between 15 and 17. This percentage is even lower, at 2.6%, for those who first started the habit after they were 21.[40]

Most individuals are exposed to and use addictive drugs for the first time during their teenage years.[41] In the United States, there were just over 2.8 million new users of illicit drugs in 2013, or about 7,800 new users per day.[41] Over half (54.1 percent) were under 18 years of age.[41]

Comorbid disorders[edit]

Individuals with comorbid (i.e., co-occurring) mental health disorders such as depression, anxiety, attention-deficit/hyperactivity disorder (ADHD) or post-traumatic stress disorder are more likely to develop substance use disorders.[42][43][44] The National Institute on Drug Abuse cites early aggressive behavior as a risk factor for substance use.[33]

Transgenerational epigenetic factors[edit]

See also: Transgenerational epigenetic inheritance

Epigenetic genes and their products (e.g., proteins) are the key components through which environmental influences can affect the genes of an individual;[28] they also serve as the mechanism responsible for the transgenerational epigenetic inheritance of behavioral phenotypes, a phenomenon in which environmental influences on the genes of a parent can affect the associated traits and behavioral phenotypes of their offspring (e.g., behavioral responses to certain environmental stimuli).[28] In addiction, epigenetic mechanisms play a central role in the pathophysiology of the disease;[1] it has been noted that some of the alterations to the epigenome which arise through chronic exposure to addictive stimuli during an addiction can be transmitted across generations, in turn affecting the behavior of one's children (e.g., the child's behavioral responses to addictive drugs and natural rewards).[28][45] More research is needed to determine the specific epigenetic mechanisms and the nature of heritable behavioral phenotypes that arise from addictions in humans.[28][45] Based upon preclinical evidence with lab animals, the addiction-related behavioral phenotypes that are transmitted across generations may serve to increase or decrease the child's risk of developing an addiction.[28][45]

Mechanisms[edit]

Transcription factor glossary
  • gene expression – the process by which information from a gene is used in the synthesis of a functional gene product such as a protein
  • transcription – the process of making messenger RNA (mRNA) from a DNA template by RNA polymerase
  • transcription factor – a protein that binds to DNA and regulates gene expression by promoting or suppressing transcription
  • transcriptional regulationcontrolling the rate of gene transcription for example by helping or hindering RNA polymerase binding to DNA
  • upregulation, activation, or promotionincrease the rate of gene transcription
  • downregulation, repression, or suppressiondecrease the rate of gene transcription
  • coactivator – a protein that works with transcription factors to increase the rate of gene transcription
  • corepressor – a protein that works with transcription factors to decrease the rate of gene transcription
  • response element – a specific sequence of DNA that a transcription factor binds to

Signaling cascade in the nucleus accumbens that results in psychostimulant addiction
v·t·e

This diagram depicts the signaling events in the brain's reward center that are induced by chronic high-dose exposure to psychostimulants that increase the concentration of synaptic dopamine, like amphetamine, methamphetamine, and phenethylamine. Following presynaptic dopamine and glutamateco-release by such psychostimulants,[46][47]postsynaptic receptors for these neurotransmitters trigger internal signaling events through a cAMP-dependent pathway and a calcium-dependent pathway that ultimately result in increased CREB phosphorylation.[46][48][49] Phosphorylated CREB increases levels of ΔFosB, which in turn represses the c-Fos gene with the help of corepressors;[46][50][51]c-Fosrepression acts as a molecular switch that enables the accumulation of ΔFosB in the neuron.[52] A highly stable (phosphorylated) form of ΔFosB, one that persists in neurons for 1–2 months, slowly accumulates following repeated high-dose exposure to stimulants through this process.[50][51] ΔFosB functions as "one of the master control proteins" that produces addiction-related structural changes in the brain, and upon sufficient accumulation, with the help of its downstream targets (e.g., nuclear factor kappa B), it induces an addictive state.[50][51]

Chronic addictive drug use causes alterations in gene expression in the mesocorticolimbic projection.[13][53][54] The most important transcription factors that produce these alterations are ΔFosB, cAMP response element binding protein (CREB), and nuclear factor kappa B (NF-κB).[13] ΔFosB is the most significant biomolecular mechanism in addiction because the overexpression of ΔFosB in the D1-typemedium spiny neurons in the nucleus accumbens is necessary and sufficient for many of the neural adaptations and behavioral effects (e.g., expression-dependent increases in drug self-administration and reward sensitization) seen in drug addiction.[13] ΔFosB expression in nucleus accumbensD1-typemedium spiny neurons directly and positively regulates drug self-administration and reward sensitization through positive reinforcement while decreasing sensitivity to aversion.[note 1][1][10] Specific drug addictions in which ΔFosB has been implicated in addictions to alcohol, amphetamine, cannabinoids, cocaine, methylphenidate, nicotine, phenylcyclidine, propofol, opiates, and substituted amphetamines, among others.[10][13][53][55][56]ΔJunD, a transcription factor, and G9a, a histone methyltransferase, both oppose the function of ΔFosB and inhibit increases in its expression.[1][13][57] Increases in nucleus accumbens ΔJunD expression (via viral vector-mediated gene transfer) or G9a expression (via pharmacological means) reduces, or with a large increase can even block, many of the neural and behavioral alterations seen in chronic drug abuse (i.e., the alterations mediated by ΔFosB).[12][13]

ΔFosB also plays an important role in regulating behavioral responses to natural rewards, such as palatable food, sex, and exercise.[13][58] Natural rewards, like drugs of abuse, induce gene expression of ΔFosB in the nucleus accumbens, and chronic acquisition of these rewards can result in a similar pathological addictive state through ΔFosB overexpression.[11][13][58] Consequently, ΔFosB is the key transcription factor involved in addictions to natural rewards (i.e., behavioral addictions) as well;[13][11][58] in particular, ΔFosB in the nucleus accumbens is critical for the reinforcing effects of sexual reward.[58] Research on the interaction between natural and drug rewards suggests that dopaminergic psychostimulants (e.g., amphetamine) and sexual behavior act on similar biomolecular mechanisms to induce ΔFosB in the nucleus accumbens and possess bidirectional cross-sensitization effects that are mediated through ΔFosB.[11][25][26] This phenomenon is notable since, in humans, a dopamine dysregulation syndrome, characterized by drug-induced compulsive engagement in natural rewards (specifically, sexual activity, shopping, and gambling), has also been observed in some individuals taking dopaminergic medications.[11]

ΔFosB inhibitors (drugs or treatments that oppose its action) may be an effective treatment for addiction and addictive disorders.[59]

The release of dopamine in the nucleus accumbens plays a role in the reinforcing qualities of many forms of stimuli, including naturally reinforcing stimuli like palatable food and sex.[60][61] Altered dopamine neurotransmission is frequently observed following the development of an addictive state.[11] In humans and lab animals that have developed an addiction, alterations in dopamine or opioid neurotransmission in the nucleus accumbens and other parts of the striatum are evident.[11] Studies have found that use of certain drugs (e.g., cocaine) affect cholinergic neurons that innervate the reward system, in turn affecting dopamine signaling in this region.[62]

Summary of addiction-related plasticity[edit]

Reward system[edit]

Main article: Reward system

This section needs expansion. You can help by adding to it.(August 2015)

Mesocorticolimbic pathway[edit]

Understanding the pathways in which drugs act and how drugs can alter those pathways is key when examining the biological basis of drug addiction. The reward pathway, known as the mesolimbic pathway, or its extension, the mesocorticolimbic pathway, is characterized by the interaction of several areas of the brain.

  • The projections from the ventral tegmental area (VTA) are a network of dopaminergicneurons with co-localized postsynaptic glutamate receptors (AMPAR and NMDAR). These cells respond when stimuli indicative of a reward are present. The VTA supports learning and sensitization development and releases DA into the forebrain.[64] These neurons also project and release DA into the nucleus accumbens,[65] through the mesolimbic pathway. Virtually all drugs causing drug addiction increase the dopamine release in the mesolimbic pathway,[66] in addition to their specific effects.
  • The nucleus accumbens (NAcc) is one output of the VTA projections. The nucleus accumbens itself consists mainly of GABAergicmedium spiny neurons (MSNs).[67] The NAcc is associated with acquiring and eliciting conditioned behaviors, and is involved in the increased sensitivity to drugs as addiction progresses.[64] Overexpression of ΔFosB in the nucleus accumbens is a necessary common factor in essentially all known forms of addiction;[1] ΔFosB is a strong positive modulator of positively reinforced behaviors.[1]
  • The prefrontal cortex, including the anterior cingulate and orbitofrontal cortices,[68] is another VTA output in the mesocorticolimbic pathway; it is important for the integration of information which helps determine whether a behavior will be elicited.[69] It is also critical for forming associations between the rewarding experience of drug use and cues in the environment. Importantly, these cues are strong mediators of drug-seeking behavior and can trigger relapse even after months or years of abstinence.[70]

Other brain structures that are involved in addiction include:

  • The basolateral amygdala projects into the NAcc and is thought to also be important for motivation.[69]
  • The hippocampus is involved in drug addiction, because of its role in learning and memory. Much of this evidence stems from investigations showing that manipulating cells in the hippocampus alters dopamine levels in NAcc and firing rates of VTA dopaminergic cells.[65]

Role of dopamine and glutamate[edit]

Dopamine is the primary neurotransmitter of the reward system in the brain. It plays a role in regulating movement, emotion, cognition, motivation, and feelings of pleasure.[71] Natural rewards, like eating, as well as recreational drug use cause a release of dopamine, and are associated with the reinforcing nature of these stimuli.[71][72] Nearly all addictive drugs, directly or indirectly, act upon the brain's reward system by heightening dopaminergic activity.[73]

Excessive intake of many types of addictive drugs results in repeated release of high amounts of dopamine, which in turn affects the reward pathway directly through heightened dopamine receptor activation. Prolonged and abnormally high levels of dopamine in the synaptic cleft can induce receptor downregulation in the neural pathway. Downregulation of mesolimbic dopamine receptors can result in a decrease in the sensitivity to natural reinforcers.[71]

Drug seeking behavior is induced by glutamatergic projections from the prefrontal cortex to the nucleus accumbens. This idea is supported with data from experiments showing that drug seeking behavior can be prevented following the inhibition of AMPA glutamate receptors and glutamate release in the nucleus accumbens.[68]

Reward sensitization[edit]

Target
gene
Target
expression
Neural effectsBehavioral effects
c-FosMolecular switch enabling the chronic
induction of ΔFosB[note 2]
dynorphin
[note 3]

What is Addiction?: A Perspective


by Howard J. Shaffer, Ph.D., C.A.S.

Acknowledgements:The author extends thanks to Chrissy Thurmond, Chris Reilly, Richard LaBrie, Debi LaPlante and Adrian Charles for their contributions to earlier versions of this article.

Addictive behaviors represent confusing and complex patterns of human activity (Shaffer, 1996, 1997). These behaviors include drug and alcohol abuse, some eating disorders, compulsive or pathological gambling, excessive sexual behaviors, and other intemperate behavior patterns. These behaviors have defied explanation throughout history. In this essay, I will attempt to clarify the nature of addiction and provide an introduction to the field of addictive behaviors.

The field of addictions rests upon a variety of disciplines. Medicine, psychology, psychiatry, chemistry, physiology, law, political science, sociology, biology and witchcraft have all influenced our understanding of addictive behavior. Most recently, biological explanations of addiction have become popular. These approaches seek to understand alcoholism, for example, by identifying the genetic and neurochemical causes of this problem. It is interesting to recognize that as we understand more about the biology of addiction, social and cultural influences become more—not less—important. To illustrate, not everyone who is predisposed genetically to alcoholism develops the disorder. Some people who are not prone bio-genetically to alcoholism or other addictions will acquire the condition. Therefore, social and psychological forces will remain very important in determining who does and who does not develop addictive behaviors.

Now it is common to think of drugs as "addictive." Warning labels inform us that tobacco is an addictive substance. We think of heroin and cocaine as addictive. Yet, addiction is not simply a property of drugs, though drugs are highly correlated with addiction. Addiction results from the relationship between a person and the object of their addiction. Drugs certainly have the capacity to produce physical dependence and an abstinence syndrome (e.g., neuroadaptation). New evidence suggests that neuroadaptation also results from addictive behaviors that do not require ingesting psychoactive substances (e.g., gambling).

Altlhough neuroadaptation (i.e., tolerance and withdrawal) can result from a variety of repetitive behaviors, neuroadaption is not the same as addiction. If neuroadaptation and its common manifestation of physical dependence were the same as addiction, then it would be incorrect to consider pathological gambling as an addictive behavior. It would be inaccurate to talk about sex and love addicts. Many people who use narcotics as post-operative pain medications never display addictive behavior even though they have became dependent physically on these psychoactive substances. Stopping drug abuse will not end addiction, since addictive behavior patterns (e.g., gambling) can exist in the absence of drug abuse. Addiction is not simply a qualitative shift in experience, it is a quantitative change in behavior patterns: things that once had priority become less important and less frequent behaviors become dominant. Addiction represents an intemperate relationship with an activity that has adverse biological, social, or psychological consequences for the person engaging in these behaviors.

Conceptual Confusion About the Definition of Addiction

Absent a clear definition of addiction, researchers will continue finding it very difficult to determine addiction prevalence rates, etiology, or the necessary and sufficient causes that stimulate recovery. Absent a working definition of addiction, clinicians will encounter diagnostic and treatment matching difficulties (e.g., Havens, 1982; Marlatt, 1988; Shaffer, 1987, 1992; Shaffer & Robbins, 1995). Satisfactory treatment outcome measures will remain elusive. Without a functional definition of addiction, social policy makers will find it difficult to establish regulatory legislation, determine treatment need, establish health care systems, and promulgate new guidelines for health care reimbursement.

Scientists and treatment providers are not the only ones with a problem when the meaning of addiction is fuzzy. The average citizen will find that, without a clear definition of addiction, the distinctions among an array of human characteristics (e.g., interest, dedication, attention to detail, craving, obsession, compulsion and addiction) will remain blurred. Finally, the contemporary conceptual chaos surrounding addiction must be resolved to clarify the similarities and differences—if these exist—between process or activity addictions (e.g., pathological gambling, excessive sexual behavior) and psychoactive substance using addictions (e.g., heroin or alcohol) (Shaffer, 1997).

Paradigms Serve Both Organizing and Blinding Functions

In response to my preceding comments, some clinicians, researchers and policy makers may argue that they indeed have an explicit definition of addiction. Since these individuals have a model, they incorrectly assume that they also have the truth; they assume that their model is accurate. In addition, they incorrectly assume that their model will work for the rest of us if only we could see the light (cf., Shaffer, 1994). However, this is the problem with worldviews in general and scientific paradigms (Kuhn, 1962) in particular: as a conceptual schema organizes one person’s thoughts, simultaneously, it blinds that person to alternative considerations (Shaffer & Gambino, 1983). Rigid thinking sets in and science fails to progress until anomalies challenge the conventional wisdom.

Distinctions Among Use, Abuse, Dependence, and Addiction

Absent a consensual definition of addiction, clinicians and social policy makers often are left to debate whether patients who use drugs also "abuse" drugs. Treatment programs regularly mistake drug users and "abusers" for those who are drug dependent. Too often the result is unnecessary hospitalization, increased medical costs, and patients who learn to distrust health care providers; alternatively, absent a precise definition of addiction, some patients fail to receive the care they require. As a result of these complex conditions, practice guidelines in the addictions are equivocal and health care systems experience management and reimbursement chaos. [Although a full discussion of this matter is beyond the scope of this essay, it also is important to note that not all people with addiction are impaired in every aspect of their daily life. Despite some exceptions, substance addictions tend to be more broad-spectrum disorders while pathological gambling tends to be a more narrow-spectrum disorder.]

Even under most established constructions of addiction, not all drug dependent patients evidence addictive behavior. For example, in most civilized countries, under nearly all traditional circumstances, people who are nicotine dependent do not evidence addiction with its attendant anti-social behavior pattern. When tobacco is recast as a socially or legally illicit substance, however, these antisocial aspects of addictive behavior have emerged (e.g., Reuters News Service, 1992).

Complicating matters, neuroadaptation and physical dependence can emerge even in the absence of psychoactive drug use. For example, upon stopping, pathological gamblers who do not use alcohol or other psychoactive drugs often reveal physical symptoms that appear to be very similar to either narcotics, stimulants, or poly-substance withdrawal (e.g., Shaffer, Hall, Walsh, & Vander Bilt; 1995; Wray & Dickerson, 1981). Perhaps repetitive and excessive patterns of emotionally stirring experiences are more important in determining whether addiction emerges than does the object of these acts.

Addiction with Dependence and Without Dependence: Substances and Process

If addiction can exist with or without physical dependence, then the concept of addiction must be sufficiently broad to include human predicaments that are related to both substances and activities (i.e., process addictions). Although it is possible to debate whether we should include substance or process addictions within the kingdom of addiction, technically there is little choice. Just as the use of exogenous substances precipitate impostor molecules vying for receptor sites within the brain, human activities stimulate naturally occurring neurotransmitters (e.g., Hyman, 1994; Hyman & Nestler, 1993; Milkman & Sunderwirth, 1987). The activity of these naturally occurring psychoactive substances likely will be determined as important mediators of many process addictions.

The Neurochemistry of Addiction: Shifting Subjective States

We may be able to advance the field by considering the objects of addiction to be those things that reliably and robustly shift subjective experience. The most reliable, fast-acting and robust "shifters" hold the greatest potential to stimulate the development of addictive disorders. In addition, the strength and consistency of these activities to shift subjective states vary across individuals. Currently, we cannot predict with precision who will become addicted. Nevertheless, psychoactive drugs and certain other activities like gambling, exercising, and meditating will correlate highly with shifting subjective states because these activities reliably influence experience—and therefore neurochemistry. Consequently, psychoactive drug use and other activities (e.g., gambling) that can potently and reliably influence subjective state shifts will tend to be ranked high among the full range of activities that can associate with addictive behaviors.

Objects of Addiction: Cause, Consequence, or Relationship

To this point, I have implied tacitly that simply using drugs or engaging in certain activities do not cause addiction. Now let me be explicit: from a logical perspective, the objects of addiction are not the sole cause of addictive behavior patterns. The teleological aspects of addiction theory and practice contribute much to contemporary conceptual chaos. If drug using were the necessary and sufficient cause of addiction, then addiction would occur every time drug using was present. Similarly, if drug using was the only cause of addiction, addictive behaviors would be absent every time drug using was missing. However, as I described before, neuroadaptation and pathological gambling are often present when drug using is absent. Therefore, either drug using is not a necessary and sufficient cause to produce addiction or gambling disorders are not representative of addictive behaviors. Furthermore, using psychoactive drugs may not be a primary cause of addiction. Even though drug using is highly correlated with addiction—because psychoactive substances reliably shift subjective experiences—drug taking is neither a necessary nor a sufficient cause of addiction. Pathological gambling and excessive sexual behaviors that do not fall within the domain of obsessive compulsive disorders reveal that addiction can exist without drug taking. These observations serve to remind us that the objects of addiction do not fully explain the emergence of addiction. Consequently, scientists need to develop a model of addiction that can better account for a more complex relationship between a person who might develop addiction and the object of their dependence. One strategy for developing a new model is to emphasize the relationship instead of either the attributes of the person struggling with addiction or the object of their addiction.

To emphasize the relationship between the addicted person and the object of their excessive behavior serves to remind us that it is the confluence of psychological, social and biological forces that determines addiction. No single set of factors adequately represents the multi-factorial causes of addiction (e.g., Shaffer, 1987, 1992; Zinberg, 1984). Unfortunately, the parameters of this unique relationship also are difficult to define. Therefore, until experience provides more insight into the synergistic nature of these factors and helps us determine the interactive threshold(s) that may apply, we are forced to operationalize addiction so that researchers, clinicians and policy makers can share a common perspective (Shaffer, 1992; Shaffer & Robbins, 1991; 1995).

Using an Operational Definition: A Simple Behavioral Model:

In the field of addictions, workers need precise operational definitions. To avoid confusion, researchers and clinicians have developed handy operational schemes to reduce inconsistency. One simple model for understanding addiction is to apply the three Cs:

  • Behavior that is motivated by emotions ranging along the Craving to Compulsion spectrum

  • Continued use in spite of adverse consequences and

  • Loss of Control.

Vague definitions of addiction, encouraged Vaillant (1982) to note that recognizing alcoholism (and perhaps other addictions) ultimately was similar to identifying a mountain or season; when confronted with these situations, we know these things implicitly. However useful, tacit knowledge is insufficient architecture upon which to rest the advancement of a science.

As a young science, the addictions represents a growing body of knowledge and a variety of emerging biological and social science methodologies—with all of the attendant rules and regulations of science—for expanding and verifying the emerging knowledge base. If the field of addictions is to mature, as have other domains of science, we must diligently work toward conceptual clarity. To develop theoretical precision, the field of addictions must escape from the cloak of partisan ideas. Conceptual clarity does not require that clinicians, researchers and social policy makers agree. However, it does require that as addiction specialists we define our concepts and work precisely and operationally. Under these conditions, treatments and research become replicable. The full tapestry of addiction patterns begins to emerge. The freedom to explore important issues develops. Conceptual chaos diminishes and, with all of its inherent debates, science progresses (e.g., Shaffer, 1986).

References

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