A Breakdown of The Science Behind: Why We Drink

Humans are not the only species that consume alcohol. The Vervet monkeys of St Kitts in the Caribbean are one well-known example, but they are far from unique. What’s particularly interesting is that, just like humans, individuals within the same species vary widely in how much they seek out alcohol.

This strongly suggests a fundamental biological driver. Alcohol consumption cannot be explained solely by advertising, social pressure, or availability – something deeper is at play.

At the heart of alcohol use is the brain. Ask most people why they drink and they will tell you that alcohol makes them feel good and helps them relax or enjoy themselves.

Alcohol is what neuroscientists call a primary reward. Even without learning or social conditioning, it directly alters levels of key neurotransmitters – the chemicals that allow nerve cells to communicate. By affecting dopamine, endorphins, and GABA, alcohol produces both stimulating and relaxing effects.

Chemically, these effects overlap with those produced by drugs such as cocaine, opioids, and Valium. It is these pleasurable brain effects that form the fundamental reason why humans – and other animals – consume alcohol at all.

Although alcohol can be hard to resist for some, drinking usually begins as a conscious choice.

This decision-making process draws on information from our senses – where we are, who we are with, the time of day – and combines it with learning and memory. We weigh the anticipated positive effects of alcohol against the negatives, such as hangovers, cost, embarrassment, or regret.

I describe this balancing act as the drinking scales. Everyone’s scales are slightly different, shaped by personal experiences and cultural norms, and they change across the lifespan.

If the drinking scales always led to rational decisions, there would be little need for this book. The problem is that many people continue to drink even when the harms clearly outweigh any benefits.

In these cases, the scales can be thought of as being bypassed or broken. This happens because the brain is wired to prioritise survival. Ancient reward and memory systems – once essential for survival in the wild – can override conscious decision-making and promote behaviour that is no longer adaptive.

This is the biological basis of addiction, and it raises a crucial question: why does this happen to some people and not others?

Problematic drinking is often seen in black-and-white terms: either someone drinks “normally” or they have a problem. In reality, there is a wide grey area in between.

Rather than focusing only on consumption, I suggest looking at what I call the three Cs:

• Consumption

• Consequences

• Control

While long-term consumption matters for physical health, consequences and control are often more revealing. Consequences can range from hangovers and regret to serious injuries, illness, or legal problems. Control is perhaps the most important factor of all – if we could reliably control our drinking, we could simply stop when problems began.

Grey area drinking describes a state where alcohol has become something a person relies on, causing concern about both quantity and control, but without the behaviours that define alcohol dependence. I refer to this state as alcohol reliance.

Many people ask the “why me?” question when they develop alcohol problems while others around them do not.

Research suggests that genetics account for around 50% of the risk of alcohol dependence. Twin and adoption studies support this, as do animal studies showing that preference for alcohol and sensitivity to its effects can be inherited. In humans, people who experience unpleasant reactions to alcohol – such as facial flushing caused by certain liver enzyme variants – are far less likely to develop alcohol problems.

Studies also show that individuals who find alcohol particularly stimulating are at greater long-term risk than those who simply feel sedated.

Alcohol-related disorders are complex traits influenced by hundreds or thousands of small genetic variations, combined with environment and experience. Many of the genes identified overlap with those involved in mental health conditions and ADHD.

At present, we are a long way from being able to predict alcohol problems using genetic testing alone.

While genetics matter, environment and psychological development play an enormous role in shaping drinking behaviour.

Early life experiences, attachment, self-esteem, and social confidence all influence how alcohol is experienced later in life. For some people, alcohol does more than provide pleasure – it offers relief from anxiety, intrusive thoughts, or social discomfort.

In these cases, alcohol adds extra weight to the “pros” side of the drinking scales, making it more likely to be relied upon.

Our brains evolved to prioritise social connection as a survival strategy. If alcohol appears to solve social fear or emotional distress during formative years, the brain may falsely associate it with safety and belonging.

This may help explain why conditions involving social difficulty and negative thinking – such as ADHD – are so strongly linked to alcohol dependence. It may also be no coincidence that widespread alcohol production emerged alongside early human cooperation and group living.

In animal studies, GLP-1 drugs consistently reduce alcohol consumption in alcohol-preferring mice and Vervet monkeys. Small human trials and a large 2024 US study involving over 800,000 patients with alcohol use disorder also found lower rates of intoxication among those prescribed GLP-1 drugs.

However, caution is needed. These findings largely involve people with obesity who were already engaged in medical care. The drugs tend to reduce rather than eliminate drinking, and there are potential risks when alcohol is combined with these medications, including pancreatitis and kidney problems.

For people with severe alcohol dependence, GLP-1 drugs may help, but they are unlikely to be a complete solution on their own.