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by Matt Field

Consider someone addicted to alcohol, drugs, or a behaviour like gambling. Why do they continue, even when they say they want to stop? It’s a question that highlights a fundamental disconnect: the gap between intention and action.

This apparent contradiction aligns with clinical definitions of addiction and with brain disease models, which suggest that repeated substance use changes brain function, making drug use compulsive and automatic, bypassing conscious decision-making. These brain adaptations help explain why addiction is so hard to overcome.

But there’s another important piece to the puzzle. People often use substances for reasons that make sense to them – to feel good, to relieve stress, or to connect socially. These motivations don’t disappear just because a substance becomes harmful.

Yet, over the past few decades, this insight has been sidelined in addiction science. Some critics have jumped on this gap to argue, reductively, that addiction is simply about people choosing pleasure: nothing more than “people take drugs because they enjoy it.”

Both the brain disease model and the “just say no” view contain partial truths. But both, on their own, are fundamentally flawed.

The brain disease model gained popularity in part because it seemed to offer two things: a foundation for developing new medical treatments and a way to reduce stigma. But it’s largely failed on both fronts. Despite billions invested in neuroscience, few new medications have emerged.Meanwhile, the most effective treatments remain psychosocial: talking therapies and harm-reduction strategies that have been around for decades. Worse, describing addiction as a chronic brain disease may increase stigma and pessimism, making recovery seem unlikely or out of reach.

Additionally, research shows that addiction is not entirely beyond voluntary control. People with addiction can and do reduce or stop their drug use in response to its consequences. This can be related to meaningful life changes — such as getting married, having children, or starting a new job — which may increase the costs or reduce the perceived benefits of continued use.

These findings challenge the view that addiction is purely compulsive, highlighting that people retain a degree of agency, even under difficult circumstances.

At the same time, these observations don’t justify the cynical view that addiction is just hedonism or bad choices. A more accurate, and more helpful, framework considers how people make decisions and how their environment shapes the value of different choice options.

Neuroeconomics
This is where insights from neuroeconomics – the study of how the brain makes value-based decisions – become useful. For example, one study found that when people are hungry, they pay more attention to how food tastes and less to how healthy it is, making unhealthy choices more likely.

Similarly, alcohol users who were craving alcohol and in a negative mood were shown to value alcohol more than food, shifting their choices accordingly. Other research has found that the set of available alternatives strongly influences how appealing (or not) a choice options becomes. As applied to addiction, when healthier or more rewarding options are limited, the relative value of drugs increases.

This suggests that addiction is less about losing the ability to choose and more about how context shapes choice. When someone is in treatment, they may genuinely want to stop using because the environment emphasises recovery, support and future goals. But once they return to a setting where drugs are easy to access and attractive alternatives are few, the relative value of drug use increases – and relapse becomes more likely.

This perspective also helps reconcile the role of brain changes in addiction. Neuroadaptations still matter: they can heighten cravings or make rewards harder to experience – but they don’t eliminate the ability to choose. Instead, these brain changes interact with a person’s environment to make certain choices more likely than others.

Crucially, this view also highlights why poverty is such a powerful driver of addiction. In deprived settings, alcohol, drugs and gambling outlets are often more accessible, while opportunities for meaningful alternatives – employment, education, stable housing – are scarce. These are deep-rooted structural issues, and they’re not easily fixed. But they matter.

On a more hopeful note, this model points to new pathways out of addiction. Rather than blaming individuals or pathologising them as brain-damaged, we can focus on reshaping environments to make non-drug alternatives more visible, available and valuable. This approach carries less stigma and more optimism: it views people not as broken, but as people who can make decisions and respond rationally to difficult situations.

Yes, the psychology of decision-making makes addiction tough to overcome. But by understanding how people weigh their options, and by improving the appeal and accessibility of alternatives to substance use, we can support real, lasting change. ■

Matt Field Professor of Psychology, University of Sheffield. This article is republished from The Conversation under a Creative Commons license.

by Pranoti Mandrekar, UMass Chan Medical School

Alcohol, whether consumed regularly or only on special occasions, takes a toll on your body. From your brain and heart, to your lungs and muscles, to your gastrointestinal and immune systems, alcohol has broad harmful effects on your health – including causing cancer.

Alcohol is the third-leading preventable cause of cancer in the U.S., responsible for about 100,000 cases of cancer and 20,000 cancer deaths annually. In comparison, alcohol-related vehicle crashes cause around 13,500 deaths each year in the U.S.

As early as the 1980s, researchers suspected that alcohol can cause cancer. Epidemiological studies have shown that alcohol is causally linked to cancer of the oral cavity, throat, voice box, esophagus, liver, colon and rectum, and breast. Another study reported an association between chronic and binge drinking and pancreatic cancer.

In 2000, the U.S. National Toxicology Program concluded that consuming alcoholic beverages is a known human carcinogen. In 2012, the International Agency for Research on Cancer, which is part of the World Health Organization, classified alcohol a Group 1 carcinogen, the highest classification indicating there is enough evidence to conclude a substance causes cancer in people. Both the Centers for Disease Control and Prevention and the National Institutes of Health concur that there is conclusive evidence that alcohol causes several types of cancer.

U.S. dietary guidelines state that even low amounts of alcohol – less than a single drink a day – increase cancer risk. Despite this, many Americans are not aware that alcohol causes cancer. A 2019 survey found that less than 50% of U.S. adults are aware of the cancer risks of alcohol consumption. The 2023 National Survey on Drug Use and Health found that over 224 million Americans ages 12 and older drank alcohol at some point in their lifetime – over 79% of people in this age group. Alcohol consumption was increasing even before the COVID-19 pandemic, reflecting an alarming public health issue.

I am a researcher studying the biological effects of moderate and long-term alcohol consumption. My team is working to uncover some of the mechanisms behind how alcohol increases cancer risk, including damage to immune cells and the liver.

How does alcohol cause cancer?
Cancer occurs when cells grow uncontrollably in the body. Alcohol may lead to tumor formation by damaging DNA, causing mutations that disrupt normal cell division and growth.

Researchers have identified several mechanisms associated with alcohol and cancer development. A 2025 report from the U.S. surgeon general highlights four distinct ways alcohol can cause cancer: alcohol metabolism, oxidative stress and inflammation, alterations in hormone levels, and interactions with other carcinogens such as tobacco smoke.

Alcohol metabolism is the process by which the body breaks down and eliminates alcohol. When alcohol breaks down, its first byproduct is acetaldehyde, a chemical that is itself classified as a carcinogen. Researchers have found that certain genetic mutations can lead the body to break down alcohol faster, resulting in increased levels of acetaldehyde.

There is also considerable evidence that alcohol can trigger the body to release harmful molecules called free radicals. These molecules can damage DNA, proteins and lipids in cells in a process called oxidative stress. My lab has found that free radicals formed from alcohol consumption can directly affect how well cells make and break down proteins, resulting in abnormal proteins that promote inflammation that favors tumor formation.

People who drink and smoke have an elevated risk of developing cancer of the mouth, pharynx and larynx. Alcohol makes it easier for the body to absorb the carcinogens in cigarettes and e-vapes. Smoking by itself can also cause inflammation and induce free radicals that damage DNA.

How much alcohol is safe?
You may be wondering how much alcohol you can safely drink and avoid harm. If you ask clinicians and scientists, you might not like the answer: none.

The Centers for Disease Control and Prevention and American dietary guidelines recommend consuming no more than one drink a day for women and no more than two drinks for men. The National Institute for Alcohol Abuse and Alcoholism and the U.S. surgeon general’s recent advisory have similar recommendations to limit alcohol consumption.

Alcohol consumption is a highly preventable cause of cancer. However, there isn’t currently a way to determine someone’s personal cancer risk from alcohol. Each person’s individual genetic background, lifestyle, diet and other health factors can all influence the effects of alcohol on tumor formation. Nevertheless, rethinking your alcohol drinking habits can help protect your health and reduce your cancer risk. ■

Note: The author of this piece Pranoti Mandrekar is Professor of Medicine, UMass Chan Medical School. This article is republished from The Conversation under a Creative Commons license. Read the original article.