The science behind addiction

By Sandra Sarr, MFA

May 01, 2026

Dr. Ethan Anderson discusses his research on addiction on KLSU “Tiger Talk” podcast.

Dr. Ethan Anderson with KLSU host in the studio

WATCH THE INTERVIEW

KLSU: What do you do at the vet school?

Dr. Ethan Anderson: I’m primarily a scientist studying addiction. My lab uses animal models to understand how drugs of abuse change the brain over time and, importantly, how we might prevent or reverse those changes. The goal is to identify ways to restore the brain to a healthier state after prolonged drug use.

KLSU: What led you to study addiction?

Dr. Anderson: Like many people, I’ve seen how addiction affects others’ lives. That made me curious about how substances can so profoundly alter behavior. I wanted to understand what’s happening in the brain and ultimately find ways to intervene.

KLSU: Why do drugs of abuse affect the brain’s reward system so strongly?

Dr. Anderson: These drugs interact with receptors that are heavily concentrated in reward-related areas of the brain. Think of it like a lock-and-key system—certain compounds just happen to fit. When those receptors are activated, the brain interprets the experience as highly rewarding and reinforces the behavior. Interestingly, studying drugs has also helped scientists understand how normal brain function works, since these systems evolved for natural rewards like food and social interaction.

KLSU: Is that an evolutionary adaptation?

Dr. Anderson: Not really. It’s more of a biological coincidence. Many animals have these same receptors but don’t seek out drugs the way humans do. I don’t think there’s a clear evolutionary advantage to drug use. That said, once humans began using substances, it may have had some subtle influence on populations over time—but we didn’t evolve to take drugs.

KLSU: Could research on drug cravings help treat other types of cravings, like for sugar?

Dr. Anderson: Yes, to a degree. Modern addiction research focuses heavily on craving, which is often what drives relapse. Even if someone becomes physically sober, the craving can persist. The same brain systems underlie many types of craving, including food. So if we understand how drug cravings work, we may learn how to address other compulsive behaviors as well.

That said, we have to be careful. A treatment that eliminates all reward would be harmful—you’d risk making someone depressed. The goal is to selectively reduce intense, pathological cravings without affecting normal enjoyment.

KLSU: Are there any promising developments in that area?

Dr. Anderson: One interesting example is GLP-1 agonists—drugs originally developed for diabetes that are now widely used for weight loss. They reduce food cravings, and recent studies suggest they may also reduce cravings for alcohol and other substances. It’s still an active area of research, but it highlights how interconnected these systems are.

KLSU: How do you prevent treatments themselves from becoming addictive?

Dr. Anderson: That’s a critical concern. History gives us clear lessons—heroin was once marketed as a treatment for morphine addiction, which obviously created bigger problems. Today, we carefully test new compounds in animal models and human trials to ensure they don’t have addictive properties. We look for drugs that reduce craving without activating the same reward pathways in harmful ways.

KLSU: Could social support help reduce addiction risk?

Dr. Anderson: Absolutely. Strong social networks can be protective. Addiction often leads to isolation—people withdraw from relationships and prioritize substance use. Reversing that pattern can help. Social connection is itself a powerful reward, so strengthening those bonds can mitigate early signs of addiction.

KLSU: Is addiction genetic?

Dr. Anderson: It is partially heritable—about 50%. If someone has a family history of addiction, they’re at higher risk. But environment plays a huge role. You can have a strong genetic predisposition, but if you’re never exposed to a substance, you won’t develop addiction. Access and environment are critical factors.

KLSU: You study epigenetics. How does that factor in?

Dr. Anderson: Epigenetics refers to changes in how genes are expressed, rather than changes to the DNA itself. Life experiences—like stress or trauma—can alter gene expression in lasting ways. Drugs of abuse do something similar. They change how the brain functions at a molecular level, effectively rewiring it over time.

What’s promising is that while we can’t change our genes, we may be able to target these epigenetic changes and reverse some of their effects.

KLSU: How do stereotypes about addiction affect people?

Dr. Anderson: Stigma is a major barrier. Many people recognize they have a problem but don’t seek help because they don’t want to be labeled. Reframing addiction as a treatable brain disease—not a moral failing—is essential. When people feel less judged, they’re more likely to pursue treatment.

KLSU: Why are drug cravings so much stronger than cravings for things like food?

Dr. Anderson: A key factor is dopamine. It’s often misunderstood as a “pleasure chemical,” but it’s really about signaling importance—it tells your brain to pay attention. Natural rewards increase dopamine modestly. Drugs can increase it dramatically—sometimes hundreds or even thousands of times more.

That exaggerated signal makes the brain prioritize drug use above other needs. Over time, that can override normal motivations like eating or socializing.

KLSU: Why do people keep using substances even after negative experiences?

Dr. Anderson: The brain tends to strongly encode the initial rewarding effects while downplaying the negative ones. For example, alcohol might feel good at first but cause illness later. The early positive experience is often more memorable and reinforcing, which drives repeated use.

KLSU: What progress has been made in treatment?

Dr. Anderson: There are already effective treatments. Naloxone (Narcan) can reverse opioid overdoses and save lives. Medications like methadone help people manage opioid dependence. But many existing treatments don’t address craving directly, which is a major gap.

Future therapies will ideally reduce the desire to use substances, making recovery more sustainable.

KLSU: Why don’t more people seek treatment?

Dr. Anderson: Motivation is a big challenge. Many individuals still find drugs rewarding and don’t want to stop, even when they recognize the harm. That’s why targeting craving is so important—if we can reduce that reinforcement, people may be more willing to seek help.

KLSU: Are there differences between alcohol and other drugs?

Dr. Anderson: Yes. Many drugs act on very specific receptor systems—opioids on opioid receptors, cannabinoids on cannabinoid receptors, and so on. Alcohol is less selective. It affects multiple systems, including GABA receptors, and requires larger quantities to produce effects. That makes its impact broader and somewhat less targeted compared to other drugs.

KLSU: What are you working on now in your lab?

Dr. Anderson: We’re studying how drugs change the brain at a molecular level—particularly through epigenetic mechanisms. We’re also developing new compounds designed to reverse those changes.

In our models, some of these compounds reduce alcohol intake and drug-seeking behavior without affecting normal rewards like food. That’s important because it suggests we can target addiction specifically without disrupting overall well-being.

KLSU: When might we see treatments like that available?

Dr. Anderson: Drug development takes time, but I’m optimistic that within the next decade we could see new therapies that directly target craving. There’s a lot of exciting work happening—not just in my lab, but around the world—and I think we’re moving in a very promising direction.

KLSU: Anything else you’d like to add?

Dr. Anderson: Just that addiction is complex, but it’s also treatable. The more we understand about how the brain changes, the better equipped we are to develop effective therapies. There’s real reason for optimism about where this field is headed.