Search Results

Addictive disorders may best be described as attribution of salience to drug-associated cues and drug consumption at the expense of other reinforcers. Dopamine and serotonin dysfunction can contribute to these states due to drug-associated neuroadaptation and alterations in bottom-up and top-down information processing. Relevant findings are described with respect to their computational and behavioral implications.

This chapter analyzes the extent to which addictive disorders are heritable. It is a fact that alcoholism and other addictions run in families. This does not, on its own, prove that there is a substantial genetic component to the risk for developing these disorders. It could well be that the risk, for the most part at least, instead comes from growing up in a family affected by addictive disorders. Other shared environmental factors, outside the family, could also contribute. Addiction is after all strongly associated with growing up and living in poverty, being exposed to violence, or having a low level of education. Each or all of these factors could theoretically contribute to addiction risk. Whether most of the risk comes from genes, the shared environmental factors, or a combination of both is an empirical question.

This chapter identifies a gap between the science of addiction and the treatment of addictive disorders. It also sets out three overarching questions. First, can we tolerate that a large proportion of the treatment and recovery community ignores the modern science of addiction and the evidence for new treatments simply because it contradicts their interpretation of principles conceived three quarters of a century ago? Second, if addiction is a chronic, relapsing disorder, then, whatever tools we use based on the evidence, its management has to be the work of a lifetime. Combine that with the insight that most people with addictive disorders largely lack financial resources, and another set of unavoidable questions presents itself. Can a traditional twenty-eight-day residential program, with its cost somewhere in the range of $40,000 and up, continue to be justified under those circumstances, in particular when data show that outpatient-based treatments that apply modern behavioral and pharmacological treatments can achieve equally good or even better outcomes? Third, how can we get rid of the quacks?

In the introduction, a philosophically informed concept of mental disorders is presented. In order to define a clinically relevant mental malady, it suggests to focus on functional impairments relevant for human survival and the individually harmful consequences resulting from these dysfunctions. While this approach generally defines what can count as a mental disorder, it does not help to understand the neurobiological underpinnings of specific disorders. Traditional disease categories, on the other hand, do not reflect current neurobiological research. With respect to neurobiological lay based disease classifications, it is suggested to assess alterations of basic mechanisms of decision making and reward related learning, which cut across established nosological boundaries. For example, dopamine-dependent reinforcement learning is altered in psychotic, affective and addictive disorders.

This chapter focuses on the link between stress and the risk of relapse to addiction. Various studies have confirmed that exposure to stress induces cravings in patients with addictive disorders. Animal experiments also demonstrate that stress triggers resumption of drug and alcohol seeking. By studying the brain circuits that produce stress-induced relapse in animals, scientists hope to discover new ways through which medications can help prevent relapse in patients with addictive disorders. Based on this type of research, several promising mechanisms are undergoing clinical evaluation. Perhaps the most important among these are blockers of a receptor for the main brain mediator of stress responses, corticotropin releasing factor (CRF). CRF blockers are promising as a future alcoholism treatment. Studies are ongoing and answers are expected within the next couple of years.

This chapter begins by discussing the common elements of effective treatments for addiction. First, they all specifically focus on drug seeking and taking. Second, methods that focus on practicing changing specific behaviors do a better job than methods that talk about these behaviors, try to dissect intrapsychic conflicts thought to underlie them, or apply other complicated psychological constructs. The chapter then considers techniques to manage withdrawal and initiate abstinence, and argues that safely and humanely detoxifying people and initiating abstinence makes sense only if accompanied by a well thought out, long-term plan for managing addiction. It sets out steps that patients can take to deal with relapse. It also considers the recent wave of psychological approaches broadly covered by the umbrella term of “mindfulness” or “third-wave cognitive behavioral therapies”.

This chapter begins with a discussion of people's lack of sympathy and compassion for the plight of alcohol or drug addicts. It explains how most people think that addiction is self-inflicted and how they consciously distance themselves from those with addictive disorder. It then sets out the book's purpose, namely to share some of the amazing advances the neuroscience of addiction has made over the years. The book presents the author's personal take on what addiction is: a malfunction of some of the most fundamental brain circuits that make us tick, and a disease that is not much different from other chronic, relapsing medical conditions. The chapter emphasizes that addiction is not a moral failing, an inability to say no, or a condition that can be cured by mystic incantations. The book also shows that scientific advances have improved, in major ways, the lives of people with addiction, and that they hold out considerable hope for further progress.

This chapter asks: Is there really any important difference between people who develop a destructive relationship with a drug and those who do not? Is there a line, however bright, the crossing of which signifies it an important transition and justifies distinguishing those who have crossed it from those who have not? Or is all substance use in principle equal, and harmful in varying degrees that depend only on the amounts used and the social, economic, or medical circumstances of the individual? It is argued that whether there is a difference between people who develop a destructive relationship with a drug and those who do not needs to be determined by clinical utility. If there are certain characteristics that tend to occur together in people with particular treatment needs, or in whom similar mechanisms are at play that could be targeted by current or future treatments, then it is practical to have a specifically labeled category (or group of categories) for those people.

The notion that people take drugs to alleviate emotional pain rings intuitively true with patients, treatment providers, and many others. Often referred to as a “self-medication” view of addiction, this notion has had interesting ups and downs through the years. This chapter follows this notion through these cycles to obtain a better understanding of the flaws inherent in a naive, original version of the theory. It also paves the way for a better informed and more useful modern interpretation. The chapter then considers the notion that prolonged drug use triggers long-term changes, or “adaptations,” in brain function. These adaptations would come online when addictive drugs cause excessive activity of brain reward circuitry and would attempt to counter the rewarding drug actions.

Addiction can be likened to a state of temporary blindness, wherein addicts are prevented from seeing how to make better choices by the deep-seated biological and psychological mechanisms that contribute to the formation of an addictive disorder. This chapter aims to provide readers with a deep appreciation of the physical and mental implications of an addiction, and offers advice on how best to understand and help someone whose decision-making is impaired by their disorder. The author argues that an addict’s choice to recover can only be realized if the treatment they receive is tailored to their problem and targets the susceptibilities, circumstances, cognitive and visceral biases, and co-occurring mental health concerns that seem to combine to cause addiction. The author offers specific tools and strategies to help remove the blindfold of addiction so that addicts can clearly see the path to recovery and become capable of making self-respecting, constructive choices.

This chapter first considers medications to treat heroin addiction. These include methadone, buprenorphine, and naltrexone. All three bind tightly to opioid receptors but without activating them at all. Because the receptors are now occupied by an inactive molecule, patients can inject as much heroin as they wish but will not experience a high no matter what. The chapter then turns to medications for the treatment of alcoholism. Disulfiram, discovered in the 1920s, continues to be marketed under the trade name Antabuse. Disulfiram works by blocking a step along the sequence through which alcohol is broken down and eliminated from the body. As a result of this blockade, the toxic substance acetaldehyde accumulates in the bloodstream. What that means is that if alcohol is consumed while a patient is on disulfiram, the accumulation of acetaldehyde results in facial flushing, as well as an extremely unpleasant and potentially dangerous reaction that includes a pounding heart and elevated blood pressure. This is intended to deter alcohol use, but does not reduce cravings for alcohol. Naltrexone was approved for alcoholism treatment in 1994 under the name Revia. It works by blocking the reward from alcohol, thus preventing a relapse to heavy drinking.

This chapter discusses studies on the critical role of drug-associated cues for relapse. Both patients and clinicians have long known that individuals with addictive disorders report craving and relapse when exposed to stimuli associated with their drug use. Understanding how these stimuli start playing an important role for triggering craving and relapse is one of the most important questions facing addiction research. Imaging studies have provided support for an involvement of a network of brain structures in cue-induced cravings; that is in good agreement with available animal studies. Based on the developing understanding of how drug cues cause relapse, attempts have also been made to develop behavioral treatments.

The second chapter focuses on basic learning mechanisms and specifically on Pavlovian conditioning and its relevance for mental disorder. Pavlovian conditioning has been implicated in addictive disorders, but may also play a role in affective and psychotic experiences. Influences of Pavlovian cues on instrumental behavior are explained with respect to their clinical consequences.

This chapter assesses treatments for addiction. It argues that any effective treatment must reflect a marriage of two perspectives. One is the perspective focused on building a relationship that allows the treatment provider to walk beside the patient. This perspective boils down to caring about and respecting the fellow human who also happens to be a patient. Clearly this is the domain of words spoken, but even more, of words listened to. The other perspective is about the specific, scientifically based methods for helping guide the course of this walk in a desired direction and actually getting there. That is the domain of science that provides specific tools and techniques to put at the disposal of our patients. Among useful tools, there are both those that are behavioral and those that are pharmacological. But in the end, it all has to come together.

This chapter considers the spiritual aspects of treatment for addiction. It argues that achieving recovery from addiction is a daunting task. To date, treatments that have emerged are, with a few exceptions, only modestly effective. Even as these treatments improve, people will continue to need support outside the professional treatment setting in order to live lives that are both worthwhile and free of alcohol and drugs. Alcoholics Anonymous (AA) is a major resource where countless patients find support for a drug-free life. However, because of its spiritual focus, AA is not for everyone. Other options may be a better match. The chapter also describes the Minnesota Model which has become most widespread model for addiction treatment worldwide.

This chapter presents the author's account of his early lessons about the destructive force of addiction. He describes one of his previous patients named Eric, an alcoholic and diabetic who refused treatment for his addiction and died shortly after his release from the hospital. The author believes that he still remembers Eric's story because it freed him of some of his innocence and naïveté. But it also captured several elements from which a journey into the landscape of addiction should start: that addiction makes people continue to use a drug even if they know it causes them severe harm and is likely ultimately to cost them their life. That nice people who might be perfectly able to contribute to society still may end up using drugs until they die. That the potential for denial, both from the patient and from everyone else, until it is too late exceeds most people's imagination.

This chapter argues that addiction is inherently a chronic, relapsing disease, not much different from diseases such as hypertension, diabetes, or asthma. Similar to those diseases, the risk for developing addiction has a strong genetic component. Likewise, the development and course of addiction are determined by an intricate interplay among genetic risk factors, environmental influences, and behavioral choices. Addiction cannot currently be cured but can be managed with a degree of success that is sufficient to allow patients to live a good life. If not managed, it disables, kills, and leads to significant costs and suffering. For these conditions, long-term disease management that combines pharmacological and behavioral approaches is an undisputed norm, and success is hardly assessed by the number of people completely cured of their ailment. At the same time, we continue to debate whether addiction really is a medical condition; focus on short-term fixes such as detoxification or twenty-eight-day residential programs; see anything other than complete abstinence as a failure; and frequently view the harm caused by addiction as self-inflicted.

This chapter focuses on a fundamental tenet of addiction medicine: reexposing the brain of an addicted person to a small amount of drug is one of the most powerful triggers for relapse. The phenomenon, called priming, is simply striking in countless clinical histories. Anyone can stop taking drugs with relative ease. In fact, people with addiction do it all the time. In contrast, staying sober and eliminating or at least minimizing relapse in the long run is a tremendous challenge. To successfully treat addiction, there is a need to understand what triggers relapse, what mechanisms are involved when it happens, and how we can intervene in those mechanisms to prevent relapse.

This chapter argues that the processes most obviously relevant for the clinical problems of addiction are also the hardest to measure in an objective and reliable manner. Until we have a more integrated understanding of how basic processes and complex behaviors are linked, we need to find a pragmatic level of simplification. On one hand, this simplified view should come close enough to the phenomena of drug seeking and relapse to help us make clinically useful predictions. On the other hand, this simplified view must be firmly grounded in what we currently know about basic molecular and cellular processes of the brain. It is not immediately obvious where this just-right amount of simplification lies. Useful guidance can, however, be obtained from a somewhat surprising source: evolution. A perspective on human behavior from the vantage point of our history as a species and the evolution of the brain is useful in learning how brain circuitry produces feelings, decisions, and behaviors that are at play every day of our lives. Yet it is that same circuitry and the same processes that make an addicted patient engage in the seemingly incomprehensible behaviors of addiction.