The Biology of Addiction Brain & Behavior Research Foundation

Women, on the other hand, have been found more susceptible to experience cravings or relapse. A gene may have all kinds of different biological possibilities but only actually “express” a few. But outside factors can act as catalysts, working to flip genetic switches that can turn other aspects of a gene’s DNA on and off.

It’s based on an understanding of how drugs work in the brain, along with an awareness of the genetic and environmental factors that affect each individual’s experience with addiction. 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]. 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].

Persistent impacts of smoking on resting-state EEG in male chronic smokers and past-smokers with 20 years of abstinence

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. 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.

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.

Ch. 1: Introduction to Biological Models of Addiction

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. Collectively, the data show that the course of SUD, as defined by current diagnostic criteria, is highly heterogeneous. Accordingly, we do not 5 Tips to Consider When Choosing a Sober Living House 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.

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.

Genetic and Biological Approaches to Addiction

It becomes more important to think about the constant activities with the help of which a person may achieve the required control and cope with the dependence that has genetic roots. Hazardous (risky) substance use refers to quantitative levels of consumption that increase an individual’s risk for adverse health consequences. 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]. 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.

• The sociocultural approach to substance use disorders says that family, society, and culture all play an important part in why people become addicts.
• The primary circuitry involves the prefrontal cortex, striatum (including the caudate and putamen), and thalamus.
• 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).
• This is in important ways different from the meaning of compulsivity as commonly used in addiction theories.
• In essence, the motivation of the behavior selection is determined by the desirability of the outcome.

But gender can impact almost every way alcohol and drug addiction manifests in a person, with everything from different body chemical compositions to different general body weights playing a role. 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.

This statement, while correct in pointing out broad heritability of behavioral traits, misses a fundamental point. The fact that normal anatomy shapes healthy organ function does not negate that an altered structure can contribute to pathophysiology of disease. 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”. However, as we will see below, in the case of addiction, it contributes to large, consistent probability shifts towards maladaptive behavior.