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Primary care physicians are often in the best position to identify and treat patients with AUD.
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Despite decades of research into the neurobiology of alcohol use disorder (AUD), many patients still face stigma, dismissal or delayed treatment. In the United States, an estimated 29.5 million people had AUD in 2022, yet only 7.6% received any treatment for it, and even fewer were offered Food and Drug Administration-approved medications that could curb cravings or reduce relapse risk. This treatment gap persists not because of a lack of effective options but because we still fail to treat AUD as the medical condition science has shown it to be.
The American medical system is still treating AUD like a moral failing or a character flaw, when in reality, it’s a medical disorder involving the brain and behavior. Because of that stigma, people often don’t get the medical help they need, including help from primary care physicians and other clinicians who are often in the best position to intervene early.
The sedative pathway: Alcohol is a central nervous system depressant. Its initial sedative effect primarily targets the frontal lobe, the part of the brain responsible for judgment, planning and impulse control. That’s why people often feel more relaxed or disinhibited after a few drinks. For individuals who struggle with anxiety or inhibition, that effect can feel especially rewarding. Some people even use alcohol to self-medicate for sleep, unaware that while it might help them fall asleep faster, it significantly disrupts sleep quality, leading to fragmented rest and early wake-up.
Joseph R. Volpicelli, MD, PhD
© The Institute of Addiction Medicine
Over time, this sedative pathway becomes dangerously altered. The brain compensates for alcohol’s depressive effects by upregulating excitatory neurotransmitters like glutamate, gradually building up tolerance. Eventually, three drinks don’t make the person tired anymore but rather give a sensation of restoring the baseline. Then, when someone stops drinking, that balance is disrupted. Without alcohol’s dampening effect, the brain becomes hyperactive, triggering symptoms the alcohol masked, such as anxiety, restlessness and insomnia. So, what does that person do? They drink again to fix the feelings. And that’s how the addictive cycle begins.
The reward pathway: For some people, especially those with a strong genetic component of addiction, alcohol doesn’t just relax them — it makes them feel euphoric. This is because alcohol stimulates the release of endogenous opioids, which in turn increase dopamine in the brain’s reward pathway. When that dopamine surge hits, it directs a person’s attention and motivation toward the source: in this instance, alcohol. That’s what drives the craving to continue drinking. Within a single drinking session, people can quickly experience impaired control — one drink creates the desire for another, and another, until they’ve lost count.
Over time, both the sedative and euphoric effects of alcohol trap people in a cycle that’s hard to break. Some start drinking to feel good and get a dopamine high but eventually find themselves continuing to drink to maintain the status quo. The motivation shifts toward avoiding withdrawal. At that point, alcohol stops being a reward and instead becomes something the person needs to function.
The convergence of the high pulling a person in and the withdrawal keeping them in is what makes AUD so powerful. It’s a double bind: chasing the high and running from the crash. That is the addictive cycle in a nutshell.
The good news is this cycle can be interrupted. One of the most effective tools is naltrexone, an opioid antagonist that blocks the release of dopamine triggered by alcohol. When people consume alcohol while taking naltrexone, they don’t get the euphoric high, so they can still have a drink or two, but they’re much less likely to want the third or fourth. It works by cutting off the reinforcement loop, removing the neurochemical reward that drives binge episodes. That makes it especially useful for people who struggle with impaired control during a single drinking session.
Elation, however, is only one contributor to excessive drinking. Some people drink because they’ve developed a physical dependence due to years of building tolerance that has rewired their system. When they stop, they feel anxious, irritable and unable to sleep. The priority in these cases is managing the symptoms associated with withdrawal. That means helping the brain reestablish equilibrium, often using medications that either enhance GABA activity or calm the overactive glutamate system. Once balance is restored and acute symptoms have subsided, longer-term treatment should be considered — research tells us that the most effective long-term treatment plans combines medication, such as naltrexone (available as a daily oral pill or a long-acting monthly injection known as VIVITROL), with psychosocial supports to reduce the risk of relapse.
Despite evidence demonstrating the efficacy of FDA-approved medications to treat AUD, they are underutilized in clinical practice. The reason often comes down to how society and the health care system think about the disease. In medicine, there are still two competing models surrounding addiction: One views it as a treatable medical condition, and the other sees it as a moral failing or lack of willpower. With opioid use disorder, the medical model has largely taken hold, and prescribing medications like methadone, buprenorphine and naltrexone is now considered good clinical practice. But with alcohol, we still tend to fall back on the idea that people just need to exercise willpower. As a result, there’s been much more resistance to using medications as part of treatment.
Identifying the signs of and formally screening for AUD as a diagnosable condition can importantly begin at the level of primary care. Primary care physicians and other clinicians are in a unique position to identify problematic drinking behaviors early because they often see patients more frequently than specialists, and many of the issues that bring patients into the clinic, such as insomnia, anxiety, elevated blood pressure or gastrointestinal symptoms, can be directly linked to alcohol use. But recognizing and treating AUD in primary care isn’t always straightforward. Most providers genuinely want to help their patients, but the system isn’t always set up to make that easy. There is often limited time during appointments and the focus understandably shifts to addressing the most immediate concerns. In many cases, underlying alcohol use may not be obvious at first and, without sufficient exposure to addiction medicine during clinical training, it’s easy to overlook as a contributing factor.
When addiction is perceived as outside the scope of routine care or as something best handled by specialists, opportunities for early intervention can be missed. But with greater support, more integrated education and practical tools, primary care physicians and other clinicians can confidently address alcohol use as part of comprehensive patient care. In fact, many of the tools already exist, they’re just underutilized. Medications are safe, well studied and effective. Outpatient detox, too, is more accessible than many health care providers think, and ambulatory detoxification is safe and manageable. And when these approaches help someone enter recovery, it’s one of the most rewarding parts of medical practice.
There’s also a broader system benefit. Patients with untreated AUD often require more frequent and costly care for comorbid health conditions. By treating the addiction itself, we make it easier to manage those comorbid conditions, which ultimately saves the health care system money. When we intervene early and appropriately, everybody wins — the patient, the provider and the system.
Medication is a powerful tool, but it only works if patients are willing to take it, and that starts with how we talk with them. Too often, conversations about alcohol use are laced with judgment or discomfort, which only reinforces stigma and drives people away from care.
I always suggest the BRENDA approach, a patient-centered framework for discussing substance use without judgment. It’s designed to foster trust, encourage openness and align treatment with each patient’s unique goals and values. The process begins by gathering a full picture of how alcohol use is impacting the patient’s health, relationships and overall functioning. Then I share those findings in a neutral, nonconfrontational way, approaching the conversation with compassion and understanding. I identify what the patient wants to change and why and offer evidence-based advice tailored to the individual. Finally, I assess their readiness to change and work collaboratively from there.
When we follow this model, we build trust. Patients feel heard and understood. They are far more likely to engage with treatment because the conversation isn’t about judgment, it’s about support.
AUD is treatable, and health care providers, including those in primary care, have a critical role to play. With the right tools and mindset, we have an opportunity to help patients reclaim their health and their lives. Every day we delay treating AUD as the medical condition it is, we unnecessarily extend suffering that could be relieved with existing evidence-based treatments. The science is clear; only our willingness to use it remains the barrier.
Joseph R. Volpicelli, MD, PhD, is a scientist-clinician with over 40 years of experience specializing in addiction psychiatry. He is executive director of the Institute of Addiction Medicine. His early work led to the approval of naltrexone to treat alcohol dependence; it was the first new medication to be FDA approved for this condition in nearly 50 years.