AUD is a medical condition that is characterized by the Diagnostic and Statistical Manual of Mental Disorders (DSM-5-TR), as “a problematic pattern of alcohol use leading to clinically significant impairment or distress.” AUD can be mild, moderate, or severe, depending on the number of symptoms a patient has experienced in the previous 12 months (see next section on symptoms of AUD). As AUD progresses in severity, alcohol-induced changes in the brain can make it very difficult to cut down or quit. With prolonged abstinence, however, at least some AUD-induced brain function changes may improve and even reverse as other neurocircuits compensate for those compromised by alcohol. Evidence-based treatment can help people achieve abstinence and facilitate these brain changes. (See Core articles on neuroscience and treatment.)

Previously, AUD has been referred to as alcohol abuse, alcohol dependence, alcohol addiction, and, colloquially, alcoholism. It is important to note that the terms “alcohol abuse” and “alcoholism” may increase stigma, whereas using the diagnostic term “alcohol use disorder” with patients may help reduce stigma. (See Core article on stigma.)

The term “addiction” is widely used but is not a diagnosis. When drinking becomes compulsive, it can be considered an addiction.8 In the context of addiction, compulsivity can be described as repetitive behaviors that persevere in the face of adverse consequences and are inappropriate to a particular situation. Individuals who suffer from compulsions often recognize that the behaviors are harmful, but they perform them nonetheless to temporarily reduce tension, stress, or anxiety.

An alcohol addiction aligns symptomatically with the former diagnosis of alcohol dependence (DSM-IV) and the current diagnoses of moderate or severe AUD (DSM-5-TR). Alcohol addiction can be framed as a three-stage cycle that serves as a model for translating the brain changes associated with AUD to the clinical domain. In this model, dysregulation occurs in three functional domains, including incentive salience, negative emotionality, and executive function, that overlap with the three stages of the addiction cycle.

• The first stage, called the binge/intoxication stage, is associated with the development of incentive salience neurocircuits, which link the pleasurable, rewarding experience of drinking with “cues” such that the cues gain motivational significance. These and other neurocircuits help develop and strengthen habitual drinking and may lay the groundwork for compulsive use of alcohol.
• The second stage, called the withdrawal/negative affect stage, is associated with states such as anxiety, dysphoria, and irritability. During this stage, the person feels alcohol is needed for relief from discomfort and emotional pain.
• The third stage, called the preoccupation/anticipation stage, is associated with executive function deficits.
  The three stages are hypothesized to be mediated by three major neurocircuitry elements: the basal ganglia, extended amygdala, and prefrontal cortex, respectively. People who drink heavily can enter the addition cycle at any of these stages. (See Core article on neuroscience.)...