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October 2015

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Biology of Addiction

Drugs and Alcohol Can Hijack Your Brain

Illustration of circuits and arrows inside a man’s brain.

People with addiction lose control over their actions. They crave and seek out drugs, alcohol, or other substances no matter what the cost—even at the risk of damaging friendships, hurting family, or losing jobs. What is it about addiction that makes people behave in such destructive ways? And why is it so hard to quit?

NIH-funded scientists are working to learn more about the biology of addiction. They’ve shown that addiction is a long-lasting and complex brain disease, and that current treatments can help people control their addictions. But even for those who’ve successfully quit, there’s always a risk of the addiction returning, which is called relapse.

The biological basis of addiction helps to explain why people need much more than good intentions or willpower to break their addictions.

“A common misperception is that addiction is a choice or moral problem, and all you have to do is stop. But nothing could be further from the truth,” says Dr. George Koob, director of NIH’s National Institute on Alcohol Abuse and Alcoholism. “The brain actually changes with addiction, and it takes a good deal of work to get it back to its normal state. The more drugs or alcohol you’ve taken, the more disruptive it is to the brain.”

Researchers have found that much of addiction’s power lies in its ability to hijack and even destroy key brain regions that are meant to help us survive.

A healthy brain rewards healthy behaviors—like exercising, eating, or bonding with loved ones. It does this by switching on brain circuits that make you feel wonderful, which then motivates you to repeat those behaviors. In contrast, when you’re in danger, a healthy brain pushes your body to react quickly with fear or alarm, so you’ll get out of harm’s way. If you’re tempted by something questionable—like eating ice cream before dinner or buying things you can’t afford—the front regions of your brain can help you decide if the consequences are worth the actions.

But when you’re becoming addicted to a substance, that normal hardwiring of helpful brain processes can begin to work against you. Drugs or alcohol can hijack the pleasure/reward circuits in your brain and hook you into wanting more and more. Addiction can also send your emotional danger-sensing circuits into overdrive, making you feel anxious and stressed when you’re not using the drugs or alcohol. At this stage, people often use drugs or alcohol to keep from feeling bad rather than for their pleasurable effects.

To add to that, repeated use of drugs can damage the essential decision-making center at the front of the brain. This area, known as the prefrontal cortex, is the very region that should help you recognize the harms of using addictive substances.

“Brain imaging studies of people addicted to drugs or alcohol show decreased activity in this frontal cortex,” says Dr. Nora Volkow, director of NIH’s National Institute on Drug Abuse. “When the frontal cortex isn’t working properly, people can’t make the decision to stop taking the drug—even if they realize the price of taking that drug may be extremely high, and they might lose custody of their children or end up in jail. Nonetheless, they take it.”

Scientists don’t yet understand why some people become addicted while others don’t. Addiction tends to run in families, and certain types of genes Stretches of DNA, a substance you inherit from your parents, that define characteristics such as your risk for certain disorders, such as addiction. have been linked to different forms of addiction. But not all members of an affected family are necessarily prone to addiction. “As with heart disease or diabetes, there’s no one gene that makes you vulnerable,” Koob says.

Other factors can also raise your chances of addiction. “Growing up with an alcoholic; being abused as a child; being exposed to extraordinary stress—all of these social factors can contribute to the risk for alcohol addiction or drug abuse,” Koob says. “And with drugs or underage drinking, the earlier you start, the greater the likelihood of having alcohol use disorder or addiction later in life.”

Teens are especially vulnerable to possible addiction because their brains are not yet fully developed—particularly the frontal regions that help with impulse control and assessing risk. Pleasure circuits in adolescent brains also operate in overdrive, making drug and alcohol use even more rewarding and enticing.

NIH is launching a new nationwide study to learn more about how teen brains are altered by alcohol, tobacco, marijuana, and other drugs. Researchers will use brain scans and other tools to assess more than 10,000 youth over a 10-year span. The study will track the links between substance use and brain changes, academic achievement, IQ, thinking skills, and mental health over time.

Although there’s much still to learn, we do know that prevention is critical to reducing the harms of addiction. “Childhood and adolescence are times when parents can get involved and teach their kids about a healthy lifestyle and activities that can protect against the use of drugs,” Volkow says. “Physical activity is important, as well as getting engaged in work, science projects, art, or social networks that do not promote use of drugs.”

To treat addiction, scientists have identified several medications and behavioral therapies—especially when used in combination—that can help people stop using specific substances and prevent relapse. Unfortunately, no medications are yet available to treat addiction to stimulants such as cocaine or methamphetamine, but behavioral therapies can help.

“Treatment depends to a large extent on the severity of addiction and the individual person,” Koob adds. “Some people can stop cigarette smoking and alcohol use disorders on their own. More severe cases might require months or even years of treatment and follow-up, with real efforts by the individual and usually complete abstinence from the substance afterward.”

NIH-funded researchers are also evaluating experimental therapies that might enhance the effectiveness of established treatments. Mindfulness meditation and magnetic stimulation of the brain are being assessed for their ability to strengthen brain circuits that have been harmed by addiction. Scientists are also examining the potential of vaccines against nicotine, cocaine, and other drugs, which might prevent the drug from entering the brain.

“Addiction is a devastating disease, with a relatively high death rate and serious social consequences,” Volkow says. “We’re exploring multiple strategies so individuals will eventually have more treatment options, which will increase their chances of success to help them stop taking the drug.”

To find publicly funded addiction treatment centers in your state, call 1-800-622-HELP, or visit https://findtreatment.samhsa.gov/ .

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  • Published: 22 February 2021

Addiction as a brain disease revised: why it still matters, and the need for consilience

  • Markus Heilig 1 ,
  • James MacKillop   ORCID: orcid.org/0000-0003-4118-9500 2 , 3 ,
  • Diana Martinez 4 ,
  • JĂŒrgen Rehm   ORCID: orcid.org/0000-0001-5665-0385 5 , 6 , 7 , 8 ,
  • Lorenzo Leggio   ORCID: orcid.org/0000-0001-7284-8754 9 &
  • Louk J. M. J. Vanderschuren   ORCID: orcid.org/0000-0002-5379-0363 10  

Neuropsychopharmacology volume  46 ,  pages 1715–1723 ( 2021 ) Cite this article

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The view that substance addiction is a brain disease, although widely accepted in the neuroscience community, has become subject to acerbic criticism in recent years. These criticisms state that the brain disease view is deterministic, fails to account for heterogeneity in remission and recovery, places too much emphasis on a compulsive dimension of addiction, and that a specific neural signature of addiction has not been identified. We acknowledge that some of these criticisms have merit, but assert that the foundational premise that addiction has a neurobiological basis is fundamentally sound. We also emphasize that denying that addiction is a brain disease is a harmful standpoint since it contributes to reducing access to healthcare and treatment, the consequences of which are catastrophic. Here, we therefore address these criticisms, and in doing so provide a contemporary update of the brain disease view of addiction. We provide arguments to support this view, discuss why apparently spontaneous remission does not negate it, and how seemingly compulsive behaviors can co-exist with the sensitivity to alternative reinforcement in addiction. Most importantly, we argue that the brain is the biological substrate from which both addiction and the capacity for behavior change arise, arguing for an intensified neuroscientific study of recovery. More broadly, we propose that these disagreements reveal the need for multidisciplinary research that integrates neuroscientific, behavioral, clinical, and sociocultural perspectives.

Introduction

Close to a quarter of a century ago, then director of the US National Institute on Drug Abuse Alan Leshner famously asserted that “addiction is a brain disease”, articulated a set of implications of this position, and outlined an agenda for realizing its promise [ 1 ]. The paper, now cited almost 2000 times, put forward a position that has been highly influential in guiding the efforts of researchers, and resource allocation by funding agencies. A subsequent 2000 paper by McLellan et al. [ 2 ] examined whether data justify distinguishing addiction from other conditions for which a disease label is rarely questioned, such as diabetes, hypertension or asthma. It concluded that neither genetic risk, the role of personal choices, nor the influence of environmental factors differentiated addiction in a manner that would warrant viewing it differently; neither did relapse rates, nor compliance with treatment. The authors outlined an agenda closely related to that put forward by Leshner, but with a more clinical focus. Their conclusion was that addiction should be insured, treated, and evaluated like other diseases. This paper, too, has been exceptionally influential by academic standards, as witnessed by its ~3000 citations to date. What may be less appreciated among scientists is that its impact in the real world of addiction treatment has remained more limited, with large numbers of patients still not receiving evidence-based treatments.

In recent years, the conceptualization of addiction as a brain disease has come under increasing criticism. When first put forward, the brain disease view was mainly an attempt to articulate an effective response to prevailing nonscientific, moralizing, and stigmatizing attitudes to addiction. According to these attitudes, addiction was simply the result of a person’s moral failing or weakness of character, rather than a “real” disease [ 3 ]. These attitudes created barriers for people with substance use problems to access evidence-based treatments, both those available at the time, such as opioid agonist maintenance, cognitive behavioral therapy-based relapse prevention, community reinforcement or contingency management, and those that could result from research. To promote patient access to treatments, scientists needed to argue that there is a biological basis beneath the challenging behaviors of individuals suffering from addiction. This argument was particularly targeted to the public, policymakers and health care professionals, many of whom held that since addiction was a misery people brought upon themselves, it fell beyond the scope of medicine, and was neither amenable to treatment, nor warranted the use of taxpayer money.

Present-day criticism directed at the conceptualization of addiction as a brain disease is of a very different nature. It originates from within the scientific community itself, and asserts that this conceptualization is neither supported by data, nor helpful for people with substance use problems [ 4 , 5 , 6 , 7 , 8 ]. Addressing these critiques requires a very different perspective, and is the objective of our paper. We readily acknowledge that in some cases, recent critiques of the notion of addiction as a brain disease as postulated originally have merit, and that those critiques require the postulates to be re-assessed and refined. In other cases, we believe the arguments have less validity, but still provide an opportunity to update the position of addiction as a brain disease. Our overarching concern is that questionable arguments against the notion of addiction as a brain disease may harm patients, by impeding access to care, and slowing development of novel treatments.

A premise of our argument is that any useful conceptualization of addiction requires an understanding both of the brains involved, and of environmental factors that interact with those brains [ 9 ]. These environmental factors critically include availability of drugs, but also of healthy alternative rewards and opportunities. As we will show, stating that brain mechanisms are critical for understanding and treating addiction in no way negates the role of psychological, social and socioeconomic processes as both causes and consequences of substance use. To reflect this complex nature of addiction, we have assembled a team with expertise that spans from molecular neuroscience, through animal models of addiction, human brain imaging, clinical addiction medicine, to epidemiology. What brings us together is a passionate commitment to improving the lives of people with substance use problems through science and science-based treatments, with empirical evidence as the guiding principle.

To achieve this goal, we first discuss the nature of the disease concept itself, and why we believe it is important for the science and treatment of addiction. This is followed by a discussion of the main points raised when the notion of addiction as a brain disease has come under criticism. Key among those are claims that spontaneous remission rates are high; that a specific brain pathology is lacking; and that people suffering from addiction, rather than behaving “compulsively”, in fact show a preserved ability to make informed and advantageous choices. In the process of discussing these issues, we also address the common criticism that viewing addiction as a brain disease is a fully deterministic theory of addiction. For our argument, we use the term “addiction” as originally used by Leshner [ 1 ]; in Box  1 , we map out and discuss how this construct may relate to the current diagnostic categories, such as Substance Use Disorder (SUD) and its different levels of severity (Fig.  1) .

figure 1

Risky (hazardous) substance use refers to quantity/frequency indicators of consumption; SUD refers to individuals who meet criteria for a DSM-5 diagnosis (mild, moderate, or severe); and addiction refers to individuals who exhibit persistent difficulties with self-regulation of drug consumption. Among high-risk individuals, a subgroup will meet criteria for SUD and, among those who have an SUD, a further subgroup would be considered to be addicted to the drug. However, the boundary for addiction is intentionally blurred to reflect that the dividing line for defining addiction within the category of SUD remains an open empirical question.

Box 1 What’s in a name? Differentiating hazardous use, substance use disorder, and addiction

Although our principal focus is on the brain disease model of addiction, the definition of addiction itself is a source of ambiguity. Here, we provide a perspective on the major forms of terminology in the field.

Hazardous Substance Use

Hazardous (risky) substance use refers to quantitative levels of consumption that increase an individual’s risk for adverse health consequences. In practice, this pertains to alcohol use [ 110 , 111 ]. Clinically, alcohol consumption that exceeds guidelines for moderate drinking has been used to prompt brief interventions or referral for specialist care [ 112 ]. More recently, a reduction in these quantitative levels has been validated as treatment endpoints [ 113 ].

Substance Use Disorder

SUD refers to the DSM-5 diagnosis category that encompasses significant impairment or distress resulting from specific categories of psychoactive drug use. The diagnosis of SUD is operationalized as 2 or more of 11 symptoms over the past year. As a result, the diagnosis is heterogenous, with more than 1100 symptom permutations possible. The diagnosis in DSM-5 is the result of combining two diagnoses from the DSM-IV, abuse and dependence, which proved to be less valid than a single dimensional approach [ 114 ]. Critically, SUD includes three levels of severity: mild (2–3 symptoms), moderate (4–5 symptoms), and severe (6+ symptoms). The International Classification of Diseases (ICD) system retains two diagnoses, harmful use (lower severity) and substance dependence (higher severity).

Addiction is a natural language concept, etymologically meaning enslavement, with the contemporary meaning traceable to the Middle and Late Roman Republic periods [ 115 ]. As a scientific construct, drug addiction can be defined as a state in which an individual exhibits an inability to self-regulate consumption of a substance, although it does not have an operational definition. Regarding clinical diagnosis, as it is typically used in scientific and clinical parlance, addiction is not synonymous with the simple presence of SUD. Nowhere in DSM-5 is it articulated that the diagnostic threshold (or any specific number/type of symptoms) should be interpreted as reflecting addiction, which inherently connotes a high degree of severity. Indeed, concerns were raised about setting the diagnostic standard too low because of the issue of potentially conflating a low-severity SUD with addiction [ 116 ]. In scientific and clinical usage, addiction typically refers to individuals at a moderate or high severity of SUD. This is consistent with the fact that moderate-to-severe SUD has the closest correspondence with the more severe diagnosis in ICD [ 117 , 118 , 119 ]. Nonetheless, akin to the undefined overlap between hazardous use and SUD, the field has not identified the exact thresholds of SUD symptoms above which addiction would be definitively present.

Integration

The ambiguous relationships among these terms contribute to misunderstandings and disagreements. Figure 1 provides a simple working model of how these terms overlap. Fundamentally, we consider that these terms represent successive dimensions of severity, clinical “nesting dolls”. Not all individuals consuming substances at hazardous levels have an SUD, but a subgroup do. Not all individuals with a SUD are addicted to the drug in question, but a subgroup are. At the severe end of the spectrum, these domains converge (heavy consumption, numerous symptoms, the unambiguous presence of addiction), but at low severity, the overlap is more modest. The exact mapping of addiction onto SUD is an open empirical question, warranting systematic study among scientists, clinicians, and patients with lived experience. No less important will be future research situating our definition of SUD using more objective indicators (e.g., [ 55 , 120 ]), brain-based and otherwise, and more precisely in relation to clinical needs [ 121 ]. Finally, such work should ultimately be codified in both the DSM and ICD systems to demarcate clearly where the attribution of addiction belongs within the clinical nosology, and to foster greater clarity and specificity in scientific discourse.

What is a disease?

In his classic 1960 book “The Disease Concept of Alcoholism”, Jellinek noted that in the alcohol field, the debate over the disease concept was plagued by too many definitions of “alcoholism” and too few definitions of “disease” [ 10 ]. He suggested that the addiction field needed to follow the rest of medicine in moving away from viewing disease as an “entity”, i.e., something that has “its own independent existence, apart from other things” [ 11 ]. To modern medicine, he pointed out, a disease is simply a label that is agreed upon to describe a cluster of substantial, deteriorating changes in the structure or function of the human body, and the accompanying deterioration in biopsychosocial functioning. Thus, he concluded that alcoholism can simply be defined as changes in structure or function of the body due to drinking that cause disability or death. A disease label is useful to identify groups of people with commonly co-occurring constellations of problems—syndromes—that significantly impair function, and that lead to clinically significant distress, harm, or both. This convention allows a systematic study of the condition, and of whether group members benefit from a specific intervention.

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 ). Challenges to diagnostic categorization are not unique to addiction, however. Throughout clinical medicine, diagnostic cut-offs are set by consensus, commonly based on an evolving understanding of thresholds above which people tend to benefit from available interventions. Because assessing benefits in large patient groups over time is difficult, diagnostic thresholds are always subject to debate and adjustments. It can be debated whether diagnostic thresholds “merely” capture the extreme of a single underlying population, or actually identify a subpopulation that is at some level distinct. Resolving this issue remains challenging in addiction, but once again, this is not different from other areas of medicine [see e.g., [ 12 ] for type 2 diabetes]. Longitudinal studies that track patient trajectories over time may have a better ability to identify subpopulations than cross-sectional assessments [ 13 ].

By this pragmatic, clinical understanding of the disease concept, it is difficult to argue that “addiction” is unjustified as a disease label. Among people who use drugs or alcohol, some progress to using with a quantity and frequency that results in impaired function and often death, making substance use a major cause of global disease burden [ 14 ]. In these people, use occurs with a pattern that in milder forms may be challenging to capture by current diagnostic criteria (See Box  1 ), but is readily recognized by patients, their families and treatment providers when it reaches a severity that is clinically significant [see [ 15 ] for a classical discussion]. In some cases, such as opioid addiction, those who receive the diagnosis stand to obtain some of the greatest benefits from medical treatments in all of clinical medicine [ 16 , 17 ]. Although effect sizes of available treatments are more modest in nicotine [ 18 ] and alcohol addiction [ 19 ], the evidence supporting their efficacy is also indisputable. A view of addiction as a disease is justified, because it is beneficial: a failure to diagnose addiction drastically increases the risk of a failure to treat it [ 20 ].

Of course, establishing a diagnosis is not a requirement for interventions to be meaningful. People with hazardous or harmful substance use who have not (yet) developed addiction should also be identified, and interventions should be initiated to address their substance-related risks. This is particularly relevant for alcohol, where even in the absence of addiction, use is frequently associated with risks or harm to self, e.g., through cardiovascular disease, liver disease or cancer, and to others, e.g., through accidents or violence [ 21 ]. Interventions to reduce hazardous or harmful substance use in people who have not developed addiction are in fact particularly appealing. In these individuals, limited interventions are able to achieve robust and meaningful benefits [ 22 ], presumably because patterns of misuse have not yet become entrenched.

Thus, as originally pointed out by McLellan and colleagues, most of the criticisms of addiction as a disease could equally be applied to other medical conditions [ 2 ]. This type of criticism could also be applied to other psychiatric disorders, and that has indeed been the case historically [ 23 , 24 ]. Today, there is broad consensus that those criticisms were misguided. Few, if any healthcare professionals continue to maintain that schizophrenia, rather than being a disease, is a normal response to societal conditions. Why, then, do people continue to question if addiction is a disease, but not whether schizophrenia, major depressive disorder or post-traumatic stress disorder are diseases? This is particularly troubling given the decades of data showing high co-morbidity of addiction with these conditions [ 25 , 26 ]. We argue that it comes down to stigma. Dysregulated substance use continues to be perceived as a self-inflicted condition characterized by a lack of willpower, thus falling outside the scope of medicine and into that of morality [ 3 ].

Chronic and relapsing, developmentally-limited, or spontaneously remitting?

Much of the critique targeted at the conceptualization of addiction as a brain disease focuses on its original assertion that addiction is a chronic and relapsing condition. Epidemiological data are cited in support of the notion that large proportions of individuals achieve remission [ 27 ], frequently without any formal treatment [ 28 , 29 ] and in some cases resuming low risk substance use [ 30 ]. For instance, based on data from the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC) study [ 27 ], it has been pointed out that a significant proportion of people with an addictive disorder quit each year, and that most afflicted individuals ultimately remit. These spontaneous remission rates are argued to invalidate the concept of a chronic, relapsing disease [ 4 ].

Interpreting these and similar data is complicated by several methodological and conceptual issues. First, people may appear to remit spontaneously because they actually do, but also because of limited test–retest reliability of the diagnosis [ 31 ]. For instance, using a validated diagnostic interview and trained interviewers, the Collaborative Studies on Genetics of Alcoholism examined the likelihood that an individual diagnosed with a lifetime history of substance dependence would retain this classification after 5 years. This is obviously a diagnosis that, once met, by definition cannot truly remit. Lifetime alcohol dependence was indeed stable in individuals recruited from addiction treatment units, ~90% for women, and 95% for men. In contrast, in a community-based sample similar to that used in the NESARC [ 27 ], stability was only ~30% and 65% for women and men, respectively. The most important characteristic that determined diagnostic stability was severity. Diagnosis was stable in severe, treatment-seeking cases, but not in general population cases of alcohol dependence.

These data suggest that commonly used diagnostic criteria alone are simply over-inclusive for a reliable, clinically meaningful diagnosis of addiction. They do identify a core group of treatment seeking individuals with a reliable diagnosis, but, if applied to nonclinical populations, also flag as “cases” a considerable halo of individuals for whom the diagnostic categorization is unreliable. Any meaningful discussion of remission rates needs to take this into account, and specify which of these two populations that is being discussed. Unfortunately, the DSM-5 has not made this task easier. With only 2 out of 11 symptoms being sufficient for a diagnosis of SUD, it captures under a single diagnostic label individuals in a “mild” category, whose diagnosis is likely to have very low test–retest reliability, and who are unlikely to exhibit a chronic relapsing course, together with people at the severe end of the spectrum, whose diagnosis is reliable, many of whom do show a chronic relapsing course.

The NESARC data nevertheless show that close to 10% of people in the general population who are diagnosed with alcohol addiction (here equated with DSM-IV “dependence” used in the NESARC study) never remitted throughout their participation in the survey. The base life-time prevalence of alcohol dependence in NESARC was 12.5% [ 32 ]. Thus, the data cited against the concept of addiction as a chronic relapsing disease in fact indicate that over 1% of the US population develops an alcohol-related condition that is associated with high morbidity and mortality, and whose chronic and/or relapsing nature cannot be disputed, since it does not remit.

Secondly, the analysis of NESARC data [ 4 , 27 ] omits opioid addiction, which, together with alcohol and tobacco, is the largest addiction-related public health problem in the US [ 33 ]. This is probably the addictive condition where an analysis of cumulative evidence most strikingly supports the notion of a chronic disorder with frequent relapses in a large proportion of people affected [ 34 ]. Of course, a large number of people with opioid addiction are unable to express the chronic, relapsing course of their disease, because over the long term, their mortality rate is about 15 times greater than that of the general population [ 35 ]. However, even among those who remain alive, the prevalence of stable abstinence from opioid use after 10–30 years of observation is <30%. Remission may not always require abstinence, for instance in the case of alcohol addiction, but is a reasonable proxy for remission with opioids, where return to controlled use is rare. Embedded in these data is a message of literally vital importance: when opioid addiction is diagnosed and treated as a chronic relapsing disease, outcomes are markedly improved, and retention in treatment is associated with a greater likelihood of abstinence.

The fact that significant numbers of individuals exhibit a chronic relapsing course does not negate that even larger numbers of individuals with SUD according to current diagnostic criteria do not. For instance, in many countries, the highest prevalence of substance use problems is found among young adults, aged 18–25 [ 36 ], and a majority of these ‘age out’ of excessive substance use [ 37 ]. It is also well documented that many individuals with SUD achieve longstanding remission, in many cases without any formal treatment (see e.g., [ 27 , 30 , 38 ]).

Collectively, the data show that the course of SUD, as defined by current diagnostic criteria, is highly heterogeneous. Accordingly, we do not maintain that a chronic relapsing course is a defining feature of SUD. When present in a patient, however, such as course is of clinical significance, because it identifies a need for long-term disease management [ 2 ], rather than expectations of a recovery that may not be within the individual’s reach [ 39 ]. From a conceptual standpoint, however, a chronic relapsing course is neither necessary nor implied in a view that addiction is a brain disease. This view also does not mean that it is irreversible and hopeless. Human neuroscience documents restoration of functioning after abstinence [ 40 , 41 ] and reveals predictors of clinical success [ 42 ]. If anything, this evidence suggests a need to increase efforts devoted to neuroscientific research on addiction recovery [ 40 , 43 ].

Lessons from genetics

For alcohol addiction, meta-analysis of twin and adoption studies has estimated heritability at ~50%, while estimates for opioid addiction are even higher [ 44 , 45 ]. Genetic risk factors are to a large extent shared across substances [ 46 ]. It has been argued that a genetic contribution cannot support a disease view of a behavior, because most behavioral traits, including religious and political inclinations, have a genetic contribution [ 4 ]. This statement, while correct in pointing out broad heritability of behavioral traits, misses a fundamental point. Genetic architecture is much like organ structure. The fact that normal anatomy shapes healthy organ function does not negate that an altered structure can contribute to pathophysiology of disease. The structure of the genetic landscape is no different. Critics further state that a “genetic predisposition is not a recipe for compulsion”, but no neuroscientist or geneticist would claim that genetic risk is “a recipe for compulsion”. Genetic risk is probabilistic, not deterministic. However, as we will see below, in the case of addiction, it contributes to large, consistent probability shifts towards maladaptive behavior.

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

However, a heritability of addiction of ~50% indicates that DNA sequence variation accounts for 50% of the risk for this condition. Once whole genome sequencing is readily available, it is likely that it will be possible to identify most of that DNA variation. For clinical purposes, those polygenic scores will of course not replace an understanding of the intricate web of biological and social factors that promote or prevent expression of addiction in an individual case; rather, they will add to it [ 49 ]. Meanwhile, however, genome-wide association studies in addiction have already provided important information. For instance, they have established that the genetic underpinnings of alcohol addiction only partially overlap with those for alcohol consumption, underscoring the genetic distinction between pathological and nonpathological drinking behaviors [ 50 ].

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. Viewing addiction susceptibility as a polygenic quantitative trait, and addiction as a disease category is entirely in line with Falconer’s theorem, according to which, in a given set of environmental conditions, a certain level of genetic susceptibility will determine a threshold above which disease will arise.

A brain disease? Then show me the brain lesion!

The notion of addiction as a brain disease is commonly criticized with the argument that a specific pathognomonic brain lesion has not been identified. Indeed, brain imaging findings in addiction (perhaps with the exception of extensive neurotoxic gray matter loss in advanced alcohol addiction) are nowhere near the level of specificity and sensitivity required of clinical diagnostic tests. 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.

For the foreseeable future, the main objective of imaging in addiction research is not to diagnose addiction, but rather to improve our understanding of mechanisms that underlie it. The hope is that mechanistic insights will help bring forward new treatments, by identifying candidate targets for them, by pointing to treatment-responsive biomarkers, or both [ 52 ]. Developing innovative treatments is essential to address unmet treatment needs, in particular in stimulant and cannabis addiction, where no approved medications are currently available. Although the task to develop novel treatments is challenging, promising candidates await evaluation [ 53 ]. A particular opportunity for imaging-based research is related to the complex and heterogeneous nature of addictive disorders. Imaging-based biomarkers hold the promise of allowing this complexity to be deconstructed into specific functional domains, as proposed by the RDoC initiative [ 54 ] and its application to addiction [ 55 , 56 ]. This can ultimately guide the development of personalized medicine strategies to addiction treatment.

Countless imaging studies have reported differences in brain structure and function between people with addictive disorders and those without them. Meta-analyses of structural data show that alcohol addiction is associated with gray matter losses in the prefrontal cortex, dorsal striatum, insula, and posterior cingulate cortex [ 57 ], and similar results have been obtained in stimulant-addicted individuals [ 58 ]. Meta-analysis of functional imaging studies has demonstrated common alterations in dorsal striatal, and frontal circuits engaged in reward and salience processing, habit formation, and executive control, across different substances and task-paradigms [ 59 ]. Molecular imaging studies have shown that large and fast increases in dopamine are associated with the reinforcing effects of drugs of abuse, but that after chronic drug use and during withdrawal, brain dopamine function is markedly decreased and that these decreases are associated with dysfunction of prefrontal regions [ 60 ]. Collectively, these findings have given rise to a widely held view of addiction as a disorder of fronto-striatal circuitry that mediates top-down regulation of behavior [ 61 ].

Critics reply that none of the brain imaging findings are sufficiently specific to distinguish between addiction and its absence, and that they are typically obtained in cross-sectional studies that can at best establish correlative rather than causal links. In this, they are largely right, and an updated version of a conceptualization of addiction as a brain disease needs to acknowledge this. Many of the structural brain findings reported are not specific for addiction, but rather shared across psychiatric disorders [ 62 ]. Also, for now, the most sophisticated tools of human brain imaging remain crude in face of complex neural circuit function. Importantly however, a vast literature from animal studies also documents functional changes in fronto-striatal circuits, as well their limbic and midbrain inputs, associated with addictive behaviors [ 63 , 64 , 65 , 66 , 67 , 68 ]. These are circuits akin to those identified by neuroimaging studies in humans, implicated in positive and negative emotions, learning processes and executive functions, altered function of which is thought to underlie addiction. These animal studies, by virtue of their cellular and molecular level resolution, and their ability to establish causality under experimental control, are therefore an important complement to human neuroimaging work.

Nevertheless, factors that seem remote from the activity of brain circuits, such as policies, substance availability and cost, as well as socioeconomic factors, also are critically important determinants of substance use. In this complex landscape, is the brain really a defensible focal point for research and treatment? The answer is “yes”. As powerfully articulated by Francis Crick [ 69 ], “You, your joys and your sorrows, your memories and your ambitions, your sense of personal identity and free will, are in fact no more than the behavior of a vast assembly of nerve cells and their associated molecules”. Social and interpersonal factors are critically important in addiction, but they can only exert their influences by impacting neural processes. They must be encoded as sensory data, represented together with memories of the past and predictions about the future, and combined with representations of interoceptive and other influences to provide inputs to the valuation machinery of the brain. Collectively, these inputs drive action selection and execution of behavior—say, to drink or not to drink, and then, within an episode, to stop drinking or keep drinking. Stating that the pathophysiology of addiction is largely about the brain does not ignore the role of other influences. It is just the opposite: it is attempting to understand how those important influences contribute to drug seeking and taking in the context of the brain, and vice versa.

But if the criticism is one of emphasis rather than of principle—i.e., too much brain, too little social and environmental factors – then neuroscientists need to acknowledge that they are in part guilty as charged. Brain-centric accounts of addiction have for a long time failed to pay enough attention to the inputs that social factors provide to neural processing behind drug seeking and taking [ 9 ]. This landscape is, however, rapidly changing. For instance, using animal models, scientists are finding that lack of social play early in life increases the motivation to take addictive substances in adulthood [ 70 ]. Others find that the opportunity to interact with a fellow rat is protective against addiction-like behaviors [ 71 ]. In humans, a relationship has been found between perceived social support, socioeconomic status, and the availability of dopamine D2 receptors [ 72 , 73 ], a biological marker of addiction vulnerability. Those findings in turn provided translation of data from nonhuman primates, which showed that D2 receptor availability can be altered by changes in social hierarchy, and that these changes are associated with the motivation to obtain cocaine [ 74 ].

Epidemiologically, it is well established that social determinants of health, including major racial and ethnic disparities, play a significant role in the risk for addiction [ 75 , 76 ]. Contemporary neuroscience is illuminating how those factors penetrate the brain [ 77 ] and, in some cases, reveals pathways of resilience [ 78 ] and how evidence-based prevention can interrupt those adverse consequences [ 79 , 80 ]. In other words, from our perspective, viewing addiction as a brain disease in no way negates the importance of social determinants of health or societal inequalities as critical influences. In fact, as shown by the studies correlating dopamine receptors with social experience, imaging is capable of capturing the impact of the social environment on brain function. This provides a platform for understanding how those influences become embedded in the biology of the brain, which provides a biological roadmap for prevention and intervention.

We therefore argue that a contemporary view of addiction as a brain disease does not deny the influence of social, environmental, developmental, or socioeconomic processes, but rather proposes that the brain is the underlying material substrate upon which those factors impinge and from which the responses originate. Because of this, neurobiology is a critical level of analysis for understanding addiction, although certainly not the only one. It is recognized throughout modern medicine that a host of biological and non-biological factors give rise to disease; understanding the biological pathophysiology is critical for understanding etiology and informing treatment.

Is a view of addiction as a brain disease deterministic?

A common criticism of the notion that addiction is a brain disease is that it is reductionist and in the end therefore deterministic [ 81 , 82 ]. This is a fundamental misrepresentation. As indicated above, viewing addiction as a brain disease simply states that neurobiology is an undeniable component of addiction. A reason for deterministic interpretations may be that modern neuroscience emphasizes an understanding of proximal causality within research designs (e.g., whether an observed link between biological processes is mediated by a specific mechanism). That does not in any way reflect a superordinate assumption that neuroscience will achieve global causality. On the contrary, since we realize that addiction involves interactions between biology, environment and society, ultimate (complete) prediction of behavior based on an understanding of neural processes alone is neither expected, nor a goal.

A fairer representation of a contemporary neuroscience view is that it believes insights from neurobiology allow useful probabilistic models to be developed of the inherently stochastic processes involved in behavior [see [ 83 ] for an elegant recent example]. Changes in brain function and structure in addiction exert a powerful probabilistic influence over a person’s behavior, but one that is highly multifactorial, variable, and thus stochastic. Philosophically, this is best understood as being aligned with indeterminism, a perspective that has a deep history in philosophy and psychology [ 84 ]. In modern neuroscience, it refers to the position that the dynamic complexity of the brain, given the probabilistic threshold-gated nature of its biology (e.g., action potential depolarization, ion channel gating), means that behavior cannot be definitively predicted in any individual instance [ 85 , 86 ].

Driven by compulsion, or free to choose?

A major criticism of the brain disease view of addiction, and one that is related to the issue of determinism vs indeterminism, centers around the term “compulsivity” [ 6 , 87 , 88 , 89 , 90 ] and the different meanings it is given. Prominent addiction theories state that addiction is characterized by a transition from controlled to “compulsive” drug seeking and taking [ 91 , 92 , 93 , 94 , 95 ], but allocate somewhat different meanings to “compulsivity”. By some accounts, compulsive substance use is habitual and insensitive to its outcomes [ 92 , 94 , 96 ]. Others refer to compulsive use as a result of increasing incentive value of drug associated cues [ 97 ], while others view it as driven by a recruitment of systems that encode negative affective states [ 95 , 98 ].

The prototype for compulsive behavior is provided by obsessive-compulsive disorder (OCD), where compulsion refers to repeatedly and stereotypically carrying out actions that in themselves may be meaningful, but lose their purpose and become harmful when performed in excess, such as persistent handwashing until skin injuries result. Crucially, this happens despite a conscious desire to do otherwise. Attempts to resist these compulsions result in increasing and ultimately intractable anxiety [ 99 ]. This is in important ways different from the meaning of compulsivity as commonly used in addiction theories. In the addiction field, compulsive drug use typically refers to inflexible, drug-centered behavior in which substance use is insensitive to adverse consequences [ 100 ]. Although this phenomenon is not necessarily present in every patient, it reflects important symptoms of clinical addiction, and is captured by several DSM-5 criteria for SUD [ 101 ]. Examples are needle-sharing despite knowledge of a risk to contract HIV or Hepatitis C, drinking despite a knowledge of having liver cirrhosis, but also the neglect of social and professional activities that previously were more important than substance use. While these behaviors do show similarities with the compulsions of OCD, there are also important differences. For example, “compulsive” substance use is not necessarily accompanied by a conscious desire to withhold the behavior, nor is addictive behavior consistently impervious to change.

Critics question the existence of compulsivity in addiction altogether [ 5 , 6 , 7 , 89 ], typically using a literal interpretation, i.e., that a person who uses alcohol or drugs simply can not do otherwise. Were that the intended meaning in theories of addiction—which it is not—it would clearly be invalidated by observations of preserved sensitivity of behavior to contingencies in addiction. Indeed, substance use is influenced both by the availability of alternative reinforcers, and the state of the organism. The roots of this insight date back to 1940, when Spragg found that chimpanzees would normally choose a banana over morphine. However, when physically dependent and in a state of withdrawal, their choice preference would reverse [ 102 ]. The critical role of alternative reinforcers was elegantly brought into modern neuroscience by Ahmed et al., who showed that rats extensively trained to self-administer cocaine would readily forego the drug if offered a sweet solution as an alternative [ 103 ]. This was later also found to be the case for heroin [ 103 ], methamphetamine [ 104 ] and alcohol [ 105 ]. Early residential laboratory studies on alcohol use disorder indeed revealed orderly operant control over alcohol consumption [ 106 ]. Furthermore, efficacy of treatment approaches such as contingency management, which provides systematic incentives for abstinence [ 107 ], supports the notion that behavioral choices in patients with addictions remain sensitive to reward contingencies.

Evidence that a capacity for choosing advantageously is preserved in addiction provides a valid argument against a narrow concept of “compulsivity” as rigid, immutable behavior that applies to all patients. It does not, however, provide an argument against addiction as a brain disease. If not from the brain, from where do the healthy and unhealthy choices people make originate? The critical question is whether addictive behaviors—for the most part—result from healthy brains responding normally to externally determined contingencies; or rather from a pathology of brain circuits that, through probabilistic shifts, promotes the likelihood of maladaptive choices even when reward contingencies are within a normal range. To resolve this question, it is critical to understand that the ability to choose advantageously is not an all-or-nothing phenomenon, but rather is about probabilities and their shifts, multiple faculties within human cognition, and their interaction. Yes, it is clear that most people whom we would consider to suffer from addiction remain able to choose advantageously much, if not most, of the time. However, it is also clear that the probability of them choosing to their own disadvantage, even when more salutary options are available and sometimes at the expense of losing their life, is systematically and quantifiably increased. There is a freedom of choice, yet there is a shift of prevailing choices that nevertheless can kill.

Synthesized, the notion of addiction as a disease of choice and addiction as a brain disease can be understood as two sides of the same coin. Both of these perspectives are informative, and they are complementary. Viewed this way, addiction is a brain disease in which a person’s choice faculties become profoundly compromised. To articulate it more specifically, embedded in and principally executed by the central nervous system, addiction can be understood as a disorder of choice preferences, preferences that overvalue immediate reinforcement (both positive and negative), preferences for drug-reinforcement in spite of costs, and preferences that are unstable ( “I’ll never drink like that again;” “this will be my last cigarette” ), prone to reversals in the form of lapses and relapse. From a contemporary neuroscience perspective, pre-existing vulnerabilities and persistent drug use lead to a vicious circle of substantive disruptions in the brain that impair and undermine choice capacities for adaptive behavior, but do not annihilate them. Evidence of generally intact decision making does not fundamentally contradict addiction as a brain disease.

Conclusions

The present paper is a response to the increasing number of criticisms of the view that addiction is a chronic relapsing brain disease. In many cases, we show that those criticisms target tenets that are neither needed nor held by a contemporary version of this view. Common themes are that viewing addiction as a brain disease is criticized for being both too narrow (addiction is only a brain disease; no other perspectives or factors are important) or too far reaching (it purports to discover the final causes of addiction). With regard to disease course, we propose that viewing addiction as a chronic relapsing disease is appropriate for some populations, and much less so for others, simply necessitating better ways of delineating the populations being discussed. We argue that when considering addiction as a disease, the lens of neurobiology is valuable to use. It is not the only lens, and it does not have supremacy over other scientific approaches. We agree that critiques of neuroscience are warranted [ 108 ] and that critical thinking is essential to avoid deterministic language and scientific overreach.

Beyond making the case for a view of addiction as a brain disease, perhaps the more important question is when a specific level of analysis is most useful. For understanding the biology of addiction and designing biological interventions, a neurobiological view is almost certainly the most appropriate level of analysis, in particular when informed by an understanding of the behavioral manifestations. In contrast, for understanding the psychology of addiction and designing psychological interventions, behavioral science is the natural realm, but one that can often benefit from an understanding of the underlying neurobiology. For designing policies, such as taxation and regulation of access, economics and public administration provide the most pertinent perspectives, but these also benefit from biological and behavioral science insights.

Finally, we argue that progress would come from integration of these scientific perspectives and traditions. E.O. Wilson has argued more broadly for greater consilience [ 109 ], unity of knowledge, in science. We believe that addiction is among the areas where consilience is most needed. A plurality of disciplines brings important and trenchant insights to bear on this condition; it is the exclusive remit of no single perspective or field. Addiction inherently and necessarily requires multidisciplinary examination. Moreover, those who suffer from addiction will benefit most from the application of the full armamentarium of scientific perspectives.

Funding and disclosures

Supported by the Swedish Research Council grants 2013-07434, 2019-01138 (MH); Netherlands Organisation for Health Research and Development (ZonMw) under project number 912.14.093 (LJMJV); NIDA and NIAAA intramural research programs (LL; the content is solely the responsibility of the author and does not necessarily represent the official views of the National Institutes of Health); the Peter Boris Chair in Addictions Research, Homewood Research Institute, and the National Institute on Alcohol Abuse and Alcoholism grants AA025911, AA024930, AA025849, AA027679 (JM; the content is solely the responsibility of the author and does not necessarily represent the official views of the National Institutes of Health).

MH has received consulting fees, research support or other compensation from Indivior, Camurus, BrainsWay, Aelis Farma, and Janssen Pharmaceuticals. JM is a Principal and Senior Scientist at BEAM Diagnostics, Inc. DM, JR, LL, and LJMJV declare no conflict of interest.

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National Research Council (US) and Institute of Medicine (US) Committee on Immunotherapies and Sustained-Release Formulations for Treating Drug Addiction; Harwood HJ, Myers TG, editors. New Treatments for Addiction: Behavioral, Ethical, Legal, and Social Questions. Washington (DC): National Academies Press (US); 2004.

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New Treatments for Addiction: Behavioral, Ethical, Legal, and Social Questions.

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1 Introduction and Background

Drug use is one of the nation's most expensive health problems, costing $109.8 billion in 1995 alone ( Harwood, Fountain, and Livermore, 1998 ). In addition to the financial costs, drug use also exacts a human cost with thousands of lives being damaged and forever changed by drug use and addiction. Prevention and treatment research, as well as clinical experience, have shown that it is often possible to intervene successfully in addiction. However, such interventions must be grounded solidly in research and must also provide long-term behavioral and sometimes pharmacological support to ultimately achieve abstinence.

As part of these research-based interventions, the National Institute on Drug Abuse (NIDA) is funding the development of new classes of medications to treat drug addiction. These medications include immunotherapies and sustained-release formulations. Immunotherapies involve products that are introduced into the body to stimulate an immune response either through active immunization (e.g., vaccines) or passive immunization (monoclonal antibodies). This immune response counteracts the effects of the target drug. Currently, immunotherapies are being developed to counteract the effects of cocaine (see Carerra et al., 2001 ; Fox et al., 1996 ; Kantak et al., 2001 ), methamphetamine (see Aoki, Hirose, and Kuroiwa, 1990 ); phencyclidine (“angel dust” or PCP) (see Proksch, Gentry, and Owens, 2000 ), and nicotine ( Hieda et al., 1997 ; Pentel et al., 2000 ; Tuncok et al., 2001 ). Sustained-release formulations, also known as depot medications, involve a slow, timed release of medications that counteract the effects of illicit drugs. Sustained-release preparations of naltrexone ( Kranzler, Modesto-Lowe, and Nuwayser, 1998 ) for opioid addiction and lofexidine ( Rawson et al., 2000 ) to treat nicotine addiction are currently being developed. All three therapies—vaccines, monoclonal antibodies, and sustained-release formulations—are long acting, but time limited, with durations from weeks to months.

The availability of these medications will raise a host of issues. Some of these issues will marry traditional vaccine concerns, such as establishing and monitoring safety, ensuring efficacy, and financing and distributing the medications, with traditional drug abuse treatment issues, such as ensuring patient adherence to treatment, using these therapies in a variety of settings, and dealing with coercive legal methods that are sometimes used to “motivate” treatment initiation. In addition, less traditional issues may also be raised, such as who should be immunized or treated with a depot medication and when, and who will decide.

  • COMMITTEE CHARGE AND REPORT

NIDA requested the advice of the National Research Council and the Institute of Medicine of the National Academies about behavioral, ethical, legal, and social issues likely to arise as a result of research they are funding to develop immunotherapies and sustained-release formulations. The Committee on Immunotherapies and Sustained-Release Formulations for Treating Drug Addiction was formed to identify and define the behavioral, ethical, legal, and social questions that will be raised in determining who should be given these medications and under what circumstances, given the major issue of therapeutic safety. This study was not intended to be a safety review of immunotherapies and sustained-release formulations, which are still under development, but safety forms a necessary backdrop for all of the issues the committee considered. Morover, the committee was not asked to evaluate the actual or potential efficacy of immunotherapies and depot medications for treating drug addiction. These therapies are still under development, and none has even been submitted to the Food and Drug Administration (FDA) for approval.

The committee was not expected to achieve consensus about how all of the issues should be resolved. Rather, the committee was expected to achieve consensus about what the issues are likely to be and which are likely to be the most pressing Indeed, the committee was charged with anticipating issues that may or may not bear upon the assessment of safety and efficacy of these medications. The committee has attempted to forecast issues that may arise in the therapeutic use of these medications if and when they are approved by the FDA for use. The committee believes that the nature and importance of many of these issues are such that NIDA may wish to encourage research into these issues in parallel with—if not integrated into—clinical trials that are done in order to test and demonstrate the safety and efficacy of medications. The committee suggests that some or all of these issues be examined during the FDA approval process.

This report reviews the behavioral, ethical, legal, and social issues likely to arise if, and when, immunotherapies and sustained-release formulations become available for treating drug addiction. It identifies the relevant issues and lays out a research agenda for NIDA. Because these therapies are still early in development, no literature exists that the committee could analyze or synthesize as a way of identifying and defining the behavioral, ethical, legal, and social issues. Rather, the committee reviewed similar, but related, literatures to better understand the potential implications of these new medications. This process required some creative thinking and use of judgment and members' expertise about what the issues are likely to be and which of them are most pressing.

The rest of this chapter provides a basic description of both immunotherapies and sustained-release formulations. In Chapter 2 the committee lays out considerations for clinical trials, focusing in particular on issues that are generally considered outside the usual FDA process.

Chapter 3 then considers a range of treatment issues, including the organization and delivery of care in alternative treatment settings, privacy, financing, and costs. Finally, in Chapter 4 the committee looks at potential adverse behavioral responses to the use of immunotherapies and at the difficult practical, ethical, and legal issues of consent, particularly for vulnerable populations.

  • MEDICAL BASIS OF IMMUNOTHERAPY

Vaccination (active immunization) for the prevention and treatment of human disease has a long and distinguished medical history dating back at least to the pioneering work of Jenner nearly 200 years ago. The World Health Organization (2003) suggests that clean water and vaccines have been the two greatest contributions to worldwide public health. Indeed, vaccines prevent illness or death in millions of individuals each year.

Vaccines work by stimulating an immune response to a disease-related organism or subunit(s). Over a period of weeks to months, immunization(s) lead(s) to the generation of protective antibodies in body fluids, which act as an early surveillance system to block or reduce the effects of an invading organism or substance, such as a toxin.

The next advance in immunotherapy came in the early 20th century. Before the advent of antibiotics, polyclonal antibodies in the form of a specific immune serum were used to treat infectious diseases. Although these antisera were highly effective in treating diseases, such as pneumococcal pneumonia and tetanus, they sometimes produce a serious adverse side effect called serum sickness ( Devi et al., 2002 ). This allergic reaction resulted from the administration of animal antisera to humans, so animal antisera could only be used as a last treatment option. Later, the technique of plasmapheresis and the development of specific vaccines provided the possibility of immunizing human donors and then collecting human immune globulin for the purpose of treatment ( Mallat and Ismail, 2002 ). Indeed, human immune globulins are still used under certain situations to treat hepatitis B, tetanus, and Varicella zoster (which causes chickenpox) ( Terada et al., 2002 ).

Advances in biotechnology and genetic engineering over the last 30 years have made it possible to generate the newest form of immunological medication, monoclonal antibodies. These antibodies are of uniform composition, well-characterized chemical properties (in terms of specificity, affinity, and amino acid composition) and can be produced by large-scale manufacturing techniques without the use of animals or animal proteins ( Smith, 1996 ; Demain, 2000 ). Because monoclonal antibodies are not produced from human blood, they do not carry the risk of transmission of human infectious agents, such as HIV and hepatitis B and C viruses, and so represent an intrinsically safer product in that regard.

The medical rational for using immunotherapies for treating or preventing drug abuse is similar in concept to more traditional immunological applications. However, the primary action of an antidrug antibody in the serum is to reduce drug levels in the brain by binding the drug before it enters the brain ( Pentel and Keyler, 2004 ). Because the drug binds with high affinity to the antibody, the rewarding as well as the medically harmful effects of the drug are reduced or blocked. And because these therapies target only the drug, they are potentially safer than treatment with small molecule drug agonists, which bind directly to important receptor systems in the brain and other organs (Pentel, this volume).

Current immunotherapies for drug abuse are of two types, active and passive. Although both treatments require highly specific, high-affinity antibodies, the medical use and the mechanisms of the therapies differ somewhat. In active immunizations, drug vaccines are used to stimulate the body to makes its own antibodies and to create a long-term immunological memory for a more rapid future response to the vaccine ( Kosten et al., 2002a , 2002b ) In passive immunotherapy, laboratory-generated antibodies (e.g., monoclonal antibodies) are injected: more antibody can be administered and the protection can be immediate, but it only lasts until the antibody is cleared, and there is no immunological memory against the drug ( Owens et al., 1988 ). Depot medications are variations of currently available medications that are designed to release a drug slowly, over a long period of time. They act by binding to the drug receptor (in the brain or elsewhere in the body), “locking out” the drug from the site of action.

In all cases, however, these medications only target the pharmacological effect of particular licit and illicit drugs. They do nothing to counteract the effects of craving and overlearned drug-seeking behavioral responses that frequently lead to relapse ( Robinson and Berridge, 2000 ; Berke and Hyman, 2000 ; O'Brien et al., 1998 ). Consequently, their use is expected to require the concomitant availability of psychosocial and behavioral treatment programs to maximize their effectiveness. We discuss these issues in more detail in Chapter 3 .

Active Immunotherapy

In active immunotherapy, a chemical derivative of the drug of abuse (called a hapten) is coupled to an antigenic protein carrier, which is then used as a vaccine (with or without an immune enhancing adjuvant) for immunization. Because stimulation of an immune response requires multiple interactions on the surface of an antibody-forming B lymphocyte, a single, small drug molecule (like cocaine or nicotine) cannot produce cross-linking of cell surface antibodies on a B cell to activate it to produce more antibodies. Consequently, drug haptens must be irreversibly bound to their large protein carriers for use as vaccines.

The molecular orientation and spacing of the drug haptens on the protein surface are critical factors that scientists must control for an optimal immune response. The antibody response will not increase if a vaccinated individual uses the small drug molecule itself; only the circulating antibody at the time of drug use will be protective. Because cross-linking of surface antibody on B cells is required to stimulate antibody production, the same drug hapten-protein vaccine must be used for boosting the immune response on later occasions. Periodic boosting with the vaccine is required to keep serum antibody levels high (Pentel, this volume).

The actual serum level of an antibody is affected by the quality of the drug-protein vaccine, the dose of the vaccine, the frequency of vaccinations, the time interval between immunizations, and poorly understood genetic variations among individuals (Pentel, this volume). On the basis of results from prior vaccine regimens, it is anticipated that the immune response will not be adequate for at least 3-6 weeks after the start of vaccination, and booster immunizations will be required every 1-6 months to maintain a sufficient level of drug-specific antibodies ( Cerny et al., 2002 ; Hieda et al., 2000 ; Byrnes-Blake et al., 2001 ; Kantak et al., 2001 ). Improper timing of vaccinations could result in a poor response or a significant reduction in the amount of circulating antibody. Thus, the timing and duration of vaccinations will need to be carefully coordinated with patient needs and other medical interventions, such as counseling or behavioral modification programs.

Passive Immunotherapy

In passive immunotherapy, rather than vaccinating an individual to stimulate his or her antibody response, preformed antidrug antibody medications are administered directly. Although this antibody medication could be a polyclonal serum or a purified immunoglobulin fraction from the serum of an individual who has been vaccinated against a drug of abuse, a monoclonal antibody is more likely to be used. Given today's technology for making and selecting monoclonal antibodies, it should be possible to make high-affinity antibodies to most drugs.

The monoclonal antibodies that have been safely used in humans are chimeric monoclonal antibodies (comprised of 34 percent mouse protein and 66 percent human protein), humanized monoclonal antibodies (comprised of more than 90 percent human protein), and fully human antibodies ( Villamor, 2003 ). All of these types of antibodies are currently made by advanced biotechnological techniques called antibody engineering. As of mid 2003 there are 10 FDA-approved therapeutic monoclonal antibodies and one FDA-approved monoclonal antibody approved. Of relevance to the therapeutic strategies for using immunotherapies for drugs of abuse is Synagis ® ( Simoes and Groothuis, 2002 ). This monoclonal antibody is approved for the prevention of serious lower respiratory disease caused by respiratory syncytial virus (RSV) in pediatric patients at high risk of the disease. This antibody is administered before and then monthly throughout the RSV season to maintain protective circulating antibody levels ( Simoes and Groothuis, 2002 ).

For treating drug abuse, monoclonal antibodies could be used in three clinical scenarios: to treat drug overdose, to prevent drug use relapse, or to protect certain at-risk populations who have not yet become drug dependent (e.g., adolescent children who have begun using cocaine). Other special populations, such as fetuses of drug-abusing mothers, might also warrant protective immunotherapy of the mother to prevent fetal exposure to the abused drug. Active vaccination could be used to prevent drug-use relapse or to protect at-risk individuals, though not for drug overdose. Depending on the particular situation, active vaccination or monoclonal antibody therapy (or a combination of the two) could be administered. For example, antibody fragments (of a size that would be cleared by the kidney) could be used to treat overdose so that not only would the antibody bind the drug and lower the amount in the brain, but also so the drug-antibody complexes would be cleared quickly from the body. In a drug abuse protection or relapse setting, where it would be desirable to have significant antibody present over a long period of time, one could envision administering a loading dose of an antibody medication with carefully timed periodic repeat doses to maintain the desired serum antibody concentrations. An example of a current successful medical therapy is Remicade ® for the treatment of rheumatoid arthritis ( Vizcarra, 2003 ). This chimeric monoclonal antibody is given at 0, 2, and 6 weeks as a loading dose and then every 8 weeks thereafter. Vaccinations with an antinicotine vaccine might be appropriate in patients who are attempting to stop cigarette smoking.

Advantages and Potential Disadvantages of the Therapies

Both active and passive immunotherapy require high-affinity antibody binding to be medically effective, and both have potential strengths and weaknesses.

  • Antibodies target the drug, not the drug's sites of action in the brain.
  • The binding of drug to antibody inactivates the drug.
  • An antibody can be highly specific for a drug or drug class.
  • Immunotherapies can complement conventional therapies (such as behavioral modification) for a more comprehensive medical approach.
  • The use of immunotherapy would not necessarily preclude the use of chemical agonist or antagonist, but an important exception is the combined use of a nicotine agonist therapy and antinicotine antibodies.
  • Immunotherapy has a different pattern of side effects (in theory, fewer) than treatment with chemical agonist or antagonist.
  • Antibodies are not addictive, as are some chemical agonists.

Potential Disadvantages

  • Monoclonal antibodies are time consuming and expensive to produce.
  • The production of a high-affinity antidrug antibody is sometimes difficult.
  • Vaccinations may lead to an inadequate response in some individuals.
  • Vaccinations may not produce antibodies in a timely fashion for proper integration with other medical interventions (e.g., drug overdose).
  • The beneficial effects of the therapy could be overcome by large amounts of drug.
  • The immunotherapy could lead to allergic reactions.

There are other potential problems with the use of antidrug antibodies for the treatment of drug abuse. Because in some cases the drugs of abuse are closely related in structure to either neurochemicals or approved medications (e.g., nicotine replacement therapy for cigarette smoking), it is possible that the therapies could lead to unexpected adverse reactions or reduced effectiveness of other medications. Some of these possible outcomes can be avoided or anticipated by careful screening of the antibodies for cross reactivity against known drugs and neurochemicals before they are used in humans. It is also possible that immunological responses against an antidrug of abuse antibody binding site (called an anti-paratype response) could lead to a second generation of antibodies, which are complementary to the antibody binding site and are capable of being druglike, thus, able to activate receptor systems just like the drug of abuse. It is known that monoclonal antibodies and other protein therapeutics do stimulate an immune response to the product in some individuals; therefore, they may not be suitable for life-long or even extended use in all individuals. Vaccines comprised of the drug-protein conjugate might also lead to entirely unexpected allergic reactions. However, it is expected that most of these potential problems would be anticipated, tested for, and dealt with during the clinical trails of new medications and the FDA approval process.

Finally, there are ethical considerations, however remote, for the use of vaccines. Active vaccination can stimulate long-lasting immunologic memory that could serve as a marker of past immunization and could stigmatize an individual for extended periods of time, or even over their entire life if tests were available for detecting memory immune cells. Monoclonal antibodies, however, have a finite life span, and after some period of time following treatment would no longer be detectable. Depot medications would similarly be undetectable following treatment because of their finite life span.

Depot therapies for opioid addiction pose a different set of advantages and challenges. A great deal is already known about the therapeutic agent (naltrexone) that is being developed for depot use because it has been used in non-depot form for more than 20 years. Naltrexone is known to be very effective as well as safe when patients adhere to the medication. For the depot versions, extensive work has been done by companies seeking to develop and obtain FDA approval for their products. Their primary advantage is expected to be in greater adherence, since dosing will only be about once every 30 days, instead of daily. One noteworthy issue is that patients on depot therapies who need treatment for acute pain (e.g., due to trauma) will present problems because naltrexone blocks opioid analgesics as well as illicit opioids. Special protocols (medications, dosing) will be required to treat pain for patients on naltrexone.

This consideration of the medical basis for immunotherapy and sustained-release formulations for treating drug addiction has led to one major recommendation by the committee, but several recommendations in subsequent sections are also related to the medical basis for these therapies.

Recommendation 1 The National Institute on Drug Abuse should support basic immunology studies on increasing the stability and longevity of antibody blood levels and on developing combination therapies to simultaneously treat a variety of abused drugs.
  • Cite this Page National Research Council (US) and Institute of Medicine (US) Committee on Immunotherapies and Sustained-Release Formulations for Treating Drug Addiction; Harwood HJ, Myers TG, editors. New Treatments for Addiction: Behavioral, Ethical, Legal, and Social Questions. Washington (DC): National Academies Press (US); 2004. 1, Introduction and Background.
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P. Blandina

International Research Journal Commerce arts science

In recent years India is facing a major problem with the illicit use of drug, drug trafficking, consuming and so on. It is a complex phenomenon which has various social, cultural, biological, geographical, historical and economic aspects. The processes of industrialization, urbanization and migration have led to loosening of the traditional method of social control. The spread and entrenchment of drug abuse needs to be prevented. The sole aim of the research is to find out the generic answer on it. The researcher believed that improvement in the systems can yet be made. Introduction – : A drug is a chemical substance whether or not obtained from natural sources which is taken for the pleasant effects it produces. It has to be understood that drugs in common use differ in their pharmacological effects. The word " drug " relates not to any one particular kind of drug but to various kinds of narcotic substances, which may differ from one another in its effects both qualitatively and quantitatively. The international convention on Drugs to which India is a signatory has classified drugs into two categories. Such as Narcotic drugs and Psychotropic substances. Drug abuse means taking a drug to reasons other than medical and amount strength, Frequency or manner that damages the physical and mental functioning. The researcher here states that the uses of drug damage the physical and mental health of the individual but also kills him. It ruins his family and social values. The main drugs of abuse in India are cannabis, heroin and opium. Mostly they are used for cultural and traditional reasons, because of easily availability and local cultivation. However there is reported increase in abuse of prescription drugs such as morphine ephedrine morphine, proxyvon, diazepam and codeine based cough syrups. The majority o f addicts are between 15 to 35 years of age and it is the most productive age group of the country. There is also increasing abuse of drugs and psychotropic substances among out of school children, street children. This problem is also spread in the rural areas. The abuse of inject able heroin is particularly widespread in the northeastern state of Manipur, Nagaland and Mizoram. Traditional abuse of opium still continues in the states of Rajasthan, Punjab, Madhya Pradesh, Utter Pradesh and Gujarat. With every addict, the life of a whole family is affected. Drug addiction is the compulsive use of psychoactive drugs, to the point where the user has no effective choice but to continue use. Drug addiction has 2 components Physical dependency and Psychological dependency. 1)Physical dependency occurs when a drug has been used habitually and the body has become accustomed to its effects. The person must then continue to use the drug in order to feel normal or its absence will trigger the symptoms of withdrawal.

Rajyasri Roy

ibuathu njati

Abstract:-Drug and substance abuse has been of great concern to institutions, families, employers and employees alike. However, these concerns have to be addressed through dissemination of relevant knowledge about drug use and abuse. Children, workers and managers need to know and understand the dangers of drug and substance abuse at home and work places. Drug and substance abuse weakens an individual working stability and by extension weakens firms output.

Azrah Hassan

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    1 KENDRIYA VIDYALAYA, AFS YELAHANKA,BANGALORE- 560063 BIOLOGY INVESTIGATORY PROJECT DRUG ADDICTION SUBMITTED BY: HARSHA VARDHAN S XII - A CBSE Roll No. - 2019-20 2 S.No. Content Page No. 1. Certificate 2 2. Acknowledgements 3 3. Aim/Objective 6 4. Project Report on Drugs Dependence 7 5. Introduction to "drugs addiction" 8 6.