Other Addictions
Addiction-related structural neuroplasticity
Addiction is a state characterized by compulsive engagement in rewarding stimuli, despite adverse consequences. The process of developing an addiction occurs through instrumental learning, which is otherwise known as operant conditioning.
In humans, addiction is diagnosed according to diagnostic models such as the Diagnostic and Statistical Manual of Mental Disorders, through observed behaviors. There has been significant advancement in understanding the structural changes that occur in parts of the brain involved in the reward pathway (mesolimbic system) that underlies addiction. Most research has focused on two portions of the brain: the ventral tegmental area, (VTA) and the nucleus accumbens (NAc).
The VTA is the portion of the mesolimbic system responsible for spreading dopamine to the whole system. The VTA is stimulated by ″rewarding experiences″.
The release of dopamine by the VTA induces pleasure, thus reinforcing behaviors that lead to the reward.1 Drugs of abuse increase the VTA’s ability to project dopamine to the rest of the reward circuit.2 These structural changes only last 7–10 days,3 however, indicating that the VTA cannot be the only part of the brain that is affected by drug use, and changed during the development of addiction.
The nucleus accumbens (NAc) plays an essential part in the formation of addiction. Almost every drug with addictive potential induces the release of dopamine into the NAc. In contrast to the VTA, the NAc shows long-term structural changes. Drugs of abuse weaken the connections within the NAc after habitual use, as well as after use then withdrawal.
Structural changes of learning
Learning by experience occurs through modifications of the structural circuits of the brain. These circuits are composed of many neurons and their connections, called synapses, which occur between the axon of one neuron and the dendrite of another. A single neuron generally has many dendrites which are called dendritic branches, each of which can be synapsed by many axons.
Along dendritic branches there can be hundreds or even thousands of dendritic spines, structural protrusions that are sites of excitatory synapses. These spines increase the number of axons from which the dendrite can receive information. Dendritic spines are very plastic, meaning they can be formed and eliminated very quickly, in the order of a few hours. More spines grow on a dendrite when it is repetitively activated. Dendritic spine changes have been correlated with long-term potentiation (LTP) and long-term depression (LTD). LTP is the way that connections between neurons and synapses are strengthened; LTD is the process by which synapses are weakened. For LTP to occur, NMDA receptors on the dendritic spine send intracellular signals to increase the number of AMPA receptors on the post synaptic neuron.
If a spine is stabilized by repeated activation, the spine becomes mushroom shaped and acquires many more AMPA receptors. This structural change, which is the basis of LTP, persists for months and may be an explanation for some of the long-term behavioral changes that are associated with learned behaviors, including addiction.
Research methodologies
Animal models
Animal models, especially rats and mice, are used for many types of biological research. The animal models of addiction are particularly useful because animals that are addicted to a substance show behaviors similar to human addicts. This implies that the structural changes that can be observed after the animal ingests a drug can be correlated with an animal’s behavioral changes, as well as with similar changes occurring in humans.
Administration protocols
Administration of drugs that are often abused can be done either by the experimenter (non-contingent), or by a self-administration (contingent) method. The latter usually involves the animal pressing a lever to receive a drug. Non-contingent models are generally used for convenience, being useful for examining the pharmacological and structural effects of the drugs. Contingent methods are more realistic because the animal controls when and how much of the drug it receives. This is generally considered a better method for studying the behaviors associated with addiction. Contingent administration of drugs has been shown to produce larger structural changes in certain parts of the brain, in comparison to non-contingent administration.
Types of drugs
All abused drugs directly or indirectly promote dopamine signaling in the mesolimbic dopamine neurons which project from the ventral tegmental area to the nucleus accumbens (NAc). The types of drugs used in experimentation increase this dopamine release through different mechanisms.
Opiates
Opiates are a class of sedative with the capacity for pain relief. Morphine is an opiate that is commonly used in animal testing of addiction. Opiates stimulate dopamine neurons in the brain indirectly by inhibiting GABA release from modulatory interneurons that synapse onto the dopamine neurons. GABA is an inhibitory neurotransmitter that decreases the probability that the target neuron will send a subsequent signal.
Stimulants
Stimulants used regularly in neuroscience experimentation are cocaine and amphetamine. These drugs induce an increase in synaptic dopamine by inhibiting the reuptake of dopamine from the synaptic cleft, effectively increasing the amount of dopamine that reaches the target neuron.
Addiction medicine
Physicians specializing in the field are in general agreement concerning applicability of treatment to those with addiction to drugs, such as alcohol and heroin, and often also to gambling, which has similar characteristics and has been well-described in the scientific literature. There is less agreement concerning definition or treatment of other so-called addictive behavior such as sexual addiction and internet addiction, such behaviors not being marked generally by physiologic tolerance or withdrawal.
Doctors focusing on addiction medicine are medical specialists who focus on addictive disease and have had special study and training focusing on the prevention and treatment of such diseases. There are two routes to specialization in the addiction field: one via a psychiatric pathway and one via other fields of medicine. The American Society of Addiction Medicine notes that approximately 40% of its members are psychiatrists (MD/DO) while the remainder have received primary medical training in other fields.
In several countries around the world, specialist bodies have been set up to ensure high quality practice in addiction medicine. For example, within the United States, there are two accepted specialty examinations.2 One is a Board Certification in Addiction Psychiatry from the American Board of Psychiatry and Neurology.3 The other is a Board Certification in Addiction Medicine from the American Board of Preventive Medicine. The latter approach is available to all physicians with primary Board certification, while the former is available only to board-certified psychiatrists. Doctors of Osteopathic Medicine may also seek board certification via the American Osteopathic Association (AOA). The Doctor of Osteopathic Medicine must have a primary board certification in Neurology & Psychiatry or Internal Medicine from the American Osteopathic Association and complete an AOA approved addiction medicine fellowship. Successful completion of a board examination administered via the AOA will grant a certificate of added qualification (CAQ) in addiction medicine.
Within Australia, addiction medicine specialists are certified via the Chapter of Addiction Medicine, which is part of the Royal Australasian College of Physicians. They may alternatively be a member of the Section of Addiction Psychiatry, Royal Australian & New Zealand College of Psychiatrists.
The International Society of Addiction Medicine also can provide certification of expertise.
Addiction psychology mostly comprises the clinical psychology and abnormal psychology disciplines and fosters the application of information obtained from research in an effort to appropriately diagnose, evaluate, treat, and support clients dealing with addiction. Throughout the treatment process addiction psychologists encourage behaviors that build wellness and emotional resilience to their physical, mental and emotional problems.
The basis of addiction is controversial. Professionals view it as a disease or a choice. One model is referred to as the Disease model of addiction. The second model is the Choice model of addiction. Researches argue that the addiction process is like the disease model with a target organ being the brain, some type of defect, and symptoms of the disease. The addiction is like the choice model with a disorder of genes, a reward, memory, stress, and choice.21 Both models result in compulsive behavior.
Cognitive Behavioral Therapy, Dialectal Behavior Therapy and Behaviorism are widely used approaches for addressing Process Addictions and Substance Addictions. Less common approaches are Eclectic, Psychodynamic, Humanistic, and Expressive therapies.1 Substance addictions are relate to drugs, alcohol, and smoking. Process addictions relate to non-substance related behaviors such as gambling, spending, sexual activity, gaming, internet, and food.
Addiction is a progressive disease and psychiatric disorder that is defined by the American Society of Addiction Medicine as "a primary, chronic disease of brain reward, motivation, memory and related circuitry. It is characterized by the inability to control behavior, it creates a dysfunctional emotional response, and it affects the users ability to abstain from the substance or behavior consistently. Psychology Today defines addiction as "a state that can occur when a person either consumes a substance such as nicotine, cocaine, or, alcohol or engages in an activity such as gambling or shopping/spending."
When a non-addict takes a drug or performs a behavior for the first time he/she does not automatically become an addict. Over time the non-addict chooses to continue to engage in a behavior or ingest a substance because of the pleasure the non-addict receives. The now addict has lost the ability to choose or forego the behavior or substance and the behavior becomes a compulsive action. The change from non-addict to addict occurs largely from the effects of prolonged substance use and behavior activities on brain functioning. Addiction affects the brain circuits of reward and motivation, learning and memory, and the inhibitory control over behavior.
There are different schools of thought regarding the terms dependence and addiction when referring to drugs and behaviors. One adopted belief is that "drug dependence" equals "addiction." The second belief is that the two terms do not equal each other. According to the DSM, the clinical criteria for "drug dependence" (or what we refer to as addiction) include compulsive drug use despite harmful consequences; inability to stop using a drug; failure to meet work, social, or family obligations; and, sometimes (depending on the drug), tolerance and withdrawal. The latter reflects physical dependence in which the body adapts to the drug, requiring more of it to achieve a certain effect (tolerance) and eliciting drug-specific physical or mental symptoms if drug use is abruptly ceased (withdrawal). Physical dependence can happen with the chronic use of many drugs—including even appropriate, medically instructed use. Thus, physical dependence in and of itself does not constitute addiction, but often accompanies addiction. This distinction can be difficult to discern, particularly with prescribed pain medications, where the need for increasing dosages can represent tolerance or a worsening underlying problem, as opposed to the beginning of abuse or addiction.
There are some characteristics of addiction that regardless of the type share commonalities. The behavior provides a rapid and potent means of altering mood, thoughts, and sensations of a person which occur because of physiology and learned expectations. The immediate precipitating factors of the relapse, the timing of the relapse and the rate of relapse following treatment is high.
Addiction as a Disease
It seems that wherever one finds intoxication, one likely will find addiction. Recently researchers have argued that the addiction process is like the disease model, with a target organ, a defect, and symptoms of the disease. In other accounts, addiction is a disorder of genes, reward, memory, stress, and choice.
The Disease Model in Addiction
According to the new disease model, rather than being a disease in the conventional sense, addiction is a disease of choice. That is, it is a disorder of the parts of the brain necessary to make proper decisions. As one becomes addicted to cocaine, the ventral tegmentum nucleus accumbens in the brain is the organ. The defect is stress-induced hedonic regulation.
Understanding the impact that genes, reward, memory, stress, and choice have on an individual will begin to explain the Disease Model of Addiction
Genetic
The genetic makeup of an individual determines how they respond to alcohol. What causes an individual to be more prone to addiction is their genetic makeup. For example, there are genetic differences in how people respond to methylphenidate (Ritalin) injections.
Reward
Increased dopamine is correlated with increased pleasure. For that reason, dopamine plays a significant role in reinforcing experiences. It tells the brain the drug is better than expected. When an individual uses a drug, there may be a surge of dopamine in the midbrain, which can result in the shifting of that individual’s pleasure “threshold”.
Memory
The neurochemical, glutamate is the most abundant neurochemical in the brain. It is critical in memory consolidation. When an addict discovers an addicting behavior, glutamate plays a role by creating the drug cues. It is the neurochemical in motivation which initiates the drug seeking, thus creating the addiction.
Stress
When under stress the brain is unable to achieve homeostasis. As a result, the brain reverts to allostasis, which in turn alters the brains ability to process pleasure, which is experienced at the hedonic “set point” (see figures one). Thus, previous pleasures may become no longer pleasurable. This is also known as anhedonia, or “pleasure deafness.” When stressed, the addict may experience extreme craving—an intense, emotional, obsessive experience.
Choice
An addict may incur damage to the orbitofrontal cortex (OFC), the anterior cingulate cortex (ACC), and the prefrontal cortex (PFC). This damage causes a tendency to choose small and immediate rewards over larger but delayed rewards, deficits in social responding due to decreased awareness of social cues, and a failure of executive function such as sensitivity to consequences.