Biological Research on Addiction 1st Edition

Still, about 25-50% of people with a substance use problem develop a severe, chronic disorder. For them, addiction is a disease that requires intensive treatments and continuing aftercare, monitoring and family or peer support to manage their recovery. People with a substance use disorder can still reduce their use or abstain — it’s just much harder than it is for others. Just like any other disease people need to be able to get quality, evidence-based treatment and care. This is why physiology of addiction supports the biological model due to its functions and abilities to investigate the chosen phenomenon as a complex mechanism that has to work accordingly.

• One model posits that there are “allostatic” changes (that is, alterations in baseline set-points) that may occur upon repeated exposure to drugs or stressors [97, 100].
• While the first use (or early use) may be by choice, once the brain has been changed by addiction, most experts believe that the person loses control of their behavior.
• Not only does our genetic blueprint make us more susceptible to addiction, but the ways our brains are wired make us more vulnerable to substance-abuse problems, as the use of these substances alters the way our brain functions and further cements the foundations for addiction.
• In my research, I’ve found four main “camps” that attempt to explain addictive behaviors.
• They can be responsible for about half of a person’s risk of developing a substance use disorder.

People have been fighting about which of these is the true cause of addiction for decade. In isolation, each of these camps tells us something interesting about human behavior, but together they give us a complete picture of why someone becomes addicted in the first place and how addiction is maintained. Multiple biological models have been proposed to understand addictions and addiction vulnerability, and many of these models are complementary and not mutually exclusive.

Rhesus Monkeys and Biological Addiction

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.

The addict’s choice of drug is a result of the interaction between the psychopharmacologic properties of the drug and the affective states from which the addict was seeking relief. In addiction research, it’s believed that people misuse alcohol and drugs because of the the chemical reactions these produce in the brain. Most substances increase dopamine release in sober house areas that have become known as our biological “reward” pathways (some people still mistakenly call these our “pleasure centers”). Repeated substance use can cause long-term changes in these reward pathways, altering responses and making future substance use more likely. In my research, I’ve found four main “camps” that attempt to explain addictive behaviors.

Genetics of addiction

Early reward-centric models focused on pleasurable aspects of taking drugs and proposed that drugs may “hijack” brain circuits involved in responses to “natural” rewards like sex or food [35, 36]. A central component in this circuitry is the nucleus accumbens located in the ventral striatum and receiving dopaminergic innervation from the ventral tegmental area (termed the mesolimbic dopamine system). This nucleus accumbens has at times been termed the brain’s “reward center” given that all known drugs with abuse potential, as well as natural rewards, lead to dopamine release in this structure [37, 38]. Consistent with a role for rewarding effects of drugs in addictive processes and a role for dopamine in this process, an incentive salience model of drug addiction proposes that “liking” a drug may be separated from “wanting” [42, 43]. Another reward-based model suggests a “reward deficiency syndrome” in which individuals with addictions seek out and engage in addictive behaviors to compensate for hypo-functioning reward signals in the mesolimbic dopamine pathway [44].

Many of these models have not been tested or applied to every specific type of addiction. Nevertheless, scientists and practitioners assume it is reasonable to apply these models to other addictions. As research in this area continues, we may learn that some models are more applicable to specific addictions.

Understanding the Biological Model of Addiction: What You Need to Know

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]. This volume is especially effective in presenting current knowledge on the key neurobiological and genetic elements in an individual’s susceptibility to drug dependence, as well as the processes by which some individuals proceed from casual drug use to drug dependence. He starts thinking about how much more fun he has when he drinks and how boring his life is without alcohol and drugs.

While Khantzian takes a psychodynamic approach to self-medication, David Duncan proposed a self-medication model that focuses on behavioral factors. While earlier behavioral formulations of drug dependence using operant conditioning maintained that positive and negative reinforcement were necessary for drug dependence, Duncan maintained that drug dependence was not maintained by positive reinforcement, but rather by negative reinforcement. Duncan applied a public health model to drug dependence, where the agent (the drug of choice) infects the host (the drug user) through a vector (e.g., peers), while the environment supports the disease process through stressors and lack of support. A crucial determinant of whether a drug user develops drug abuse is the presence or absence of negative reinforcement, which is experienced by problematic users, but not by recreational users. According to Duncan, drug dependence is an avoidance behavior, where an individual finds a drug that produces a temporary escape from a problem, and taking the drug is reinforced as an operant behavior. 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].