The New Science of Alcohol and Health


By Professor David Nutt

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A world-renowned authority on the science of alcohol exposes its influence on our health, mood, sleep, emotions, and productivity — and what we can and should do to moderate our intake.

From after-work happy hour to a nightly glass of wine, we’re used to thinking of alcohol as a normal part of our daily lives. In Drink?, neuropharmacology professor David Nutt takes a fascinating, science-based look at drinking to unpack why we should reconsider our favorite pastime.

Using cutting-edge scientific research and years of hands-on experience in the field, Nutt delves into the long- and short-term effects of alcohol. He addresses topics such as hormones, mental health, fertility, and addiction, explaining how alcohol travels through our bodies and brains, what happens at each stage of inebriation, and how it effects us even after it leaves our systems. With accessible, easy-to-understand language, Nutt ensures that readers recognize why alcohol can have such a negative influence on our bodies and our society. In the vein of This Naked Mind,Drink? isn’t preachy; it simply gives readers clear, evidence-based facts to help them make the most informed choices about their consumption.



THE IMPACT OF alcohol on health is profound. Up to half of all people in beds in orthopedic wards are there because of an alcohol-related injury and on weekends the emergency departments of our hospitals are filled with people who are drunk. Alcohol and medicine are inextricably entwined in the same way as money and banking.

In the UK, most people know me as the UK government chief drugs advisor who was fired in 2009 for saying government drugs policy wasn’t evidence based. But I’m also a doctor, and all my professional life I, like all doctors, have been confronted with the challenge of alcohol in our patients and in our colleagues.

The real reason for my firing, I believe, was that I had the temerity to say on prime-time radio that alcohol was the most harmful drug in the UK. At that time alcohol wasn’t even allowed to be considered a drug by the UK Advisory Council on the Misuse of Drugs—the ACMD—despite every scientist in the country knowing that it most certainly was a drug.

The evidence on which I based my statement was the most sophisticated and detailed analysis of drug harms ever conducted. Since then, similar studies have been carried out in Europe and Australia, each coming to the same conclusion: that alcohol is the most harmful drug in their societies too.

The main reason why alcohol scores at the top of the harm scale is that so many of us like to drink it. Typically, in first world Western countries, alcohol is consumed by over 80 percent of all adults. Of that 80 percent, only about one-fifth get into problems with it. But there are so many of these people that their alcohol problems have a massive impact on the rest of us, especially their families and friends. Alcohol is linked to a lot of violence both within and outside the family, road traffic accidents, loss of work, and many illnesses. In the US, drinking costs $249 billion a year, of which $28 billion are health-care costs and $23 billion from crime.1

Yet most of us continue to drink, and most don’t get into serious difficulties with alcohol. This tells us that there are different biological and social factors that impact our relationship with alcohol. I believe that understanding these can help each of us, and our governments, make more rational and health-promoting decisions about how we all deal with alcohol. This book attempts to do this in a language every drinker can easily understand.

At a personal level, alcohol has been something I have been studying during my 40 years of medical research. For two years, in the late 1980s, I ran the inpatient research ward at the National Institute on Alcohol Abuse and Alcoholism (NIAAA) in the National Institutes of Health (NIH). Since then, back in the UK, I have continued to study the brain basis of alcohol enjoyment and problems, along with treating patients with alcohol problems.

Yet also, with one of my daughters, I own a wine bar in West London. My life encapsulates the good and bad of alcohol and pulls together my knowledge, experiences, and ideas in a way that I hope will explain why such a simple molecule as alcohol can give so much pleasure and pain at the same time.

Professor David Nutt is Professor of Neuropsychopharmacology at Imperial College London, Chair of DrugScience (drugscience.org.uk) and a former chair of the Advisory Council on the Misuse of Drugs.




LET’S TAKE A short tour through your brain and body on alcohol. Your first drink starts with a single mouthful, to bastardize a saying by Mao Zedong.

In fact, you would be surprised how difficult it is to get people to drink alcohol for the first time. Pure alcohol tastes repellent, and nobody—except perhaps an alcoholic—would drink it. Even in the various forms in which we buy it, it’s often bitter and tart, if not downright unpleasant, and needs a mixer. Some of the common flavors that alcohol comes in—wine-flavored, hops-flavored—are quite strange and so also have to be acquired.

One of the most effective ways to make alcohol more appealing to people is to add sweeteners. This holds true for rats too. When scientists use rats to study the effects of alcohol, it’s standard to sweeten it to ensure the rats drink it—a rat cooler, if you like. In fact, I’d say the main reason super-sweet (and often brightly colored) coolers like Smirnoff Ice are on sale is to appeal to entry-level consumers who don’t yet have the taste for alcohol, aka teenagers.

You may also be surprised to hear that we quickly acquire that taste. Very soon after the first mouthfuls, our brain learns that a few minutes after the difficult taste come good feelings of being warm, relaxed, maybe a little more sociable. And once those good feelings become associated with the taste, the smell, and the setting, routine, and/or ritual, we then start to like the taste. I’ve often heard people say things along these lines: “I love the taste of 1984 Château Latour/Whispering Angel/Pol Roger.” But I say to them: “If you gave that to your child, they would spit it out. You have acquired the love of that taste. And what has given you that love of the taste is the effect of the alcohol. And, of course, the knowledge that it’s really expensive.”

This learning effect holds true in rats too: once a rat has been made to drink enough alcohol, it will continue to drink it, even if it’s not flavored.

Another sensation many people learn to like is the hot feeling you get as alcohol goes down your throat, which will be familiar if you drink spirits and especially if you’ve ever done shots. It can become appealing because your brain knows you’re about to get the pleasurable hit from the alcohol. As spirits are a dilute form of alcohol, that hot feeling is not nearly as intense as if you were to put neat alcohol on your tongue or a cut. That would burn—and really hurt.

These two elements—the flavors and the mouthfeel as well as the look of your favorite drink and the place and time you usually drink—prompt your brain to get ready to experience the effects of alcohol.

As the liquid flows into your stomach, it begins to be absorbed through the walls of the stomach, then via the small intestine. The alcohol goes via the bloodstream into the liver, where it starts to be broken down, the main by-product being acetaldehyde. Then this alcohol and acetaldehyde mixture travels through the bloodstream and into the heart and also crosses the blood–brain barrier and enters your brain.

Alcohol is such a small molecule that absorption happens pretty quickly; within five or ten minutes of your first mouthful, you will start to feel the first effects in your body. You may begin to feel warmer, a little flushed, as alcohol allows the blood vessels of your skin to expand, which is called vasodilation.


When the alcohol mixture hits the brain, it starts to do the things that make us like it. I find it helpful to describe the brain as working like an electrochemical machine. This machine is made up of a web of around 200 billion neurons. All our thoughts and processes are mediated by messages between the neurons. Your machine’s outputs—being awake, asleep, storing memories, swallowing, and so on—are the results of these millions of messages, flying around the brain web.

Each message travels along the neuron via electricity, but the connection that bridges the gap between neurons—called the synapse—is chemical. The chemicals that bridge those gaps are called neurotransmitters.

What’s important to know for the story of how alcohol works is that it—like other drugs—works at the level of this chemical connection.

There are around 80 different types of neurotransmitters (chemical messengers). And there are even more types of the receptors that they slot into. Each receptor is triggered by a different neurotransmitter.

The two neurotransmitters that are the most common and the most powerful, because they are effectively the on–off switch of the brain, are gamma-aminobutyric acid (GABA) and glutamate. In essence these two neurotransmitters are the core of the brain. They do all the basic work such as sleeping, laying down memories, and thinking.

Glutamate turns on the brain and GABA turns it off. When glutamate is released and goes across the synapse, it turns on the next neuron, which makes the brain more active. GABA does the opposite.

The two work hand in hand, like yin and yang. You need GABA to control glutamate because if you have too much glutamate your system goes into overload; this leads to getting very anxious, or even to a seizure, and potentially to brain damage.

Your brain has evolved so that every time glutamate is released, GABA is released too. It’s a beautifully balanced system.

There’s another type of neurotransmitter, called a neuromodulator because it modifies the brain’s response rather than affects it directly. So, if you have a car accident, the memory of it will be laid down by glutamate—for example, that you were driving at 60 miles an hour, that you were on the highway—but the emotion will be encoded by a neuromodulator, noradrenaline. This adds extra information to the memory, but it’s not the core component.

Neuromodulators work like a backup to GABA and glutamate because most outputs of the brain use more than one neurotransmitter.

To explain with an example, we think there are at least four neurotransmitters that keep us awake: acetylcholine, orexin, histamine, noradrenaline—and at least four that put us to sleep: GABA, adenosine, serotonin, endocannabinoids. This means that if one fails, the others can back it up. So someone with narcolepsy, for example, has a deficiency in one neuromodulator, orexin. They’re not good at staying awake because the backups aren’t always powerful enough.

The names of some neuromodulators will be very familiar to you. As well as noradrenaline, serotonin and dopamine are involved in many processes, particularly emotional ones. Then there are the endorphins, which are actually a different type of molecule called a peptide, little pieces of protein.

All the various drugs and mind-altering substances that human beings take work on different combinations of neurotransmitter and neuromodulator systems. Alcohol is one of the most promiscuous of drugs, in that it affects a lot of different types of receptors and hence the majority, if not all, of the neurons. Which is why it can give us so many different kinds of effects and experiences.


As you can see, the brain is an incredibly evolved and finely balanced machine. And then you add in alcohol and that balance dissolves like a sugar cube in a hot cup of tea—or rather, a hot toddy.

The first thing alcohol does is to turn on the calming GABA system, so you start to feel relaxed. Valium works on the same system. This is why we drink. And it’s especially why a lot of us drink at parties.

Most of us have some level of social anxiety, and alcohol removes our fear and inhibitions. Alcohol’s calming effect is also the reason why, as soon as the seatbelt sign is turned off on an airplane, the beverage cart is wheeled down the aisle. It’s because many people are anxious about flying.

However, if you turn the GABA system on too much, it can switch off parts of the brain you don’t want switched off, for example, your judgment or even your consciousness. And if you drink a great deal of alcohol and the GABA system is maximally potentiated, it turns off your brain, in the same way as an anesthetic, so you stop breathing. That’s one way you can die from alcohol. This is what we call alcohol poisoning.

Going back to your judgment, do you ever intend to drink a couple of drinks but then lose control and end up bingeing? Why is that? One of the main reasons is that the part of the brain that tells you to stay in control—the frontal cortex—is the first part that’s switched off by alcohol.

In fact, the parts of the brain that are about retaining judgment and control are very sensitive to alcohol. You may find you lose judgment over other things too: your attractiveness, your ability to dance or to chat someone up.

Drink more, and as you go over the drunk-driving limit—which is 80 milligrams of alcohol per 100 milliliters of blood (a blood alcohol content [BAC] of 0.08 percent)—you begin to get the double whammy: as well as stimulating GABA, the alcohol starts to block your glutamate receptors. And remember, glutamate is the neurotransmitter that keeps you awake. As your level gets higher, you’re starting to become properly drunk. If you reach the point of 0.15 percent BAC, you’ll also start to lose the capacity to lay down memory. This is a blackout.

As your blood alcohol concentration rises, it affects new and different neuromodulators too. And each one will have its own specific influences in different parts of the brain.

There are three that are the most important. First, a rising blood alcohol level increases the effects of serotonin, a mood enhancer that also makes you more empathetic. Its pro-serotonin effect is also what makes other people seem more attractive—so-called “beer goggles.” In that way, it has a similar effect to MDMA, or ecstasy.

It’s the stimulation of a different serotonin receptor, one in the nerves of the stomach, that makes you sick.

We talk about throwing up from alcohol pretty casually, but, in fact, vomiting is crucial, as it stops you from dying. This survival mechanism is one of the reasons alcohol has survived in our culture for thousands of years. Vomiting gets rid of enough alcohol so you stay alive.

Second, drinking releases dopamine, which is involved in drive, motivation, and energy. This is a factor in alcohol’s stimulant effect, which makes you feel exhilarated, more active, and gives you feelings of energy and enthusiasm. Dopamine makes you louder—this is an effect people get from cocaine too.

Dopamine is one of the transmitters that also lays down behavioral patterns, so it’s important in addiction. Dopamine release may be the reason people get locked into habits that start off being fun, or at least not damaging, but then become so, for example, hair-twisting and nail-biting. Dopamine is also why you get into stupid arguments about irrelevant things when you’re drunk, but can’t stop yourself.

Third, the high you get from alcohol comes from endorphins. These are your body’s natural opioids, the brain’s natural pain-reducing system, also the source of the runner’s high. This reward system gives you a chilled sort of pleasure and, in some people, may also be a key factor in their addiction. Several studies have shown that when the effects of endorphins are blocked with the anti-drinking medication nalmefene, some addicts are able to stop drinking.1 Using sophisticated brain imaging, we have been able to see that this effect is related to the interactions between endorphins and dopamine in the brain.

It’s this cornucopia of effects that gives alcohol such a wide appeal. And as we are all different, it will slot into your personal brain chemistry in a different way to that of your friend. Perhaps you drink to reduce anxiety? Or after work as a valve to release stress? Or to get motivated to go out? Or for liquid courage to go fighting? A large part of alcohol’s appeal is that, for many people, it fills in the gaps in your personality, making you the person you want to be.


Keep drinking and, by this point, you are likely to be slurring. Your memory is shot due to the glutamate effect, so you’re repeating yourself, repeating yourself.

You may also be finding a lot of things funny, including the things you’re repeating, which may be due to your serotonin and GABA systems. And alcohol is dampening down the centers of the brain that control coordination, hence the UK slang “legless.”

With your dopamine up and your self-control down, you may be beginning to get argumentative. You may also do something stupid—smoking when you’ve given up, drunk driving, shopping-cart racing—because your judgment is impaired.

There was a really sad case of a 16-year-old girl, Natalie Dursley, who was picked up by an ambulance after collapsing at a nightclub. She was so confused, she opened the doors of the vehicle on the highway, fell out, and died. This is a perfect example of the complete loss of insight that can happen when you are drunk. At root, you’ve seriously disrupted the efficiency of your brain—an effect I like to compare to having a virus in your computer.

Keep on drinking, and you’re moving toward anesthesia, a system shutdown. In fact, medical anesthetics target the GABA and glutamate systems too. An anesthetic you’d have for a minor op would switch on GABA to put you to sleep. And for a major one, it’d switch off glutamate, which keeps you awake and alive. That is why you need to be ventilated, as you can no longer breathe on your own.

Before modern anesthetics existed, if a sailor had to have an injured limb removed, he’d be made legless first. There’s some good reason for this: alcohol does dampen down the pain—as well as the memory.

It’s the fact that alcohol affects both GABA and glutamate—the double whammy—that makes it dangerous. GABA and glutamate regulate not only being awake but also being alive. This is why people do die of alcohol poisoning. If you drink enough, you can stop breathing. Below is an at-a-glance guide to how drunkenness progresses.


Different people do have very different experiences under the influence, which comes from the setting and expectations more so than from any difference in the alcohol itself. The buzz from a warm can of gin and tonic on a packed commuter train will feel completely different from the same measure in a martini in a chic hotel bar, for example. And pregaming before clubbing is a world away from a glass of sherry with your parents at Christmas. People might drink at bedtime to relax or they might (though it’s best not to) drink before a business meeting for confidence.

Buckfast Tonic Wine is interesting as a social experiment (albeit inadvertent) and a great illustration of how alcohol’s effects interact with personal intention. Originally made by the monks of Buckfast Abbey in England as a pick-me-up, “Buckie” is a strong, fortified wine—15 percent alcohol—with lots of added caffeine. One bottle contains the equivalent of nearly five double espressos.

It was first sold as a tonic for people who needed energy, as the caffeine overcomes the sedative effects of the alcohol. You might know that Buckie has become the cult drink of soccer fans in Scotland (where it is also known as “wreck the hoose juice”); these fans down a bottle (or maybe more) before going out for a fight. In a Scottish survey of young offenders, 43 percent who’d drunk before their offense said their drink of choice was Buckfast.3

It’s the same wine as when it was marketed as a tonic but is now used for a completely different purpose. In 2014, the Scottish government debated whether Buckie should no longer be sold in glass bottles, as there were reports of them being used as weapons, according to the Scotsman newspaper.4 Although this law was not passed and Buckie still comes in a wine bottle, it is now—perhaps to reduce the risk of broken bottle violence—available in cans as well.

Of course, violence and alcohol are well-established bedfellows. It’s one reason most sporting venues and festivals no longer use glasses (the other is that drunk people are so clumsy).


The time of day you drink is also a factor. It makes sense that the sleepier you are, the more likely it is that alcohol will put you to sleep. That’s the reason people mix stimulants and alcohol as in Buckie; stimulants to keep you awake, sedatives to take away the anxiety. In fact, “uppers and downers” is the most popular combination in the history of drug taking.

Another example of this is cocaine and alcohol. Back in the 1890s, when cocaine was legal, a wine called Mariani from Italy contained both. And it was endorsed by the Pope, no less. And you don’t need to have seen Scarface to know that people mix cocaine and alcohol at parties. The reason why people might do this is in order to be able to drink more and for longer. Interestingly, when in the 1990s the Icelandic government passed a law to allow 24-hour drinking, there was subsequently an increase in amphetamine use.5

One of the issues with cocaine and alcohol is that they work together in the body to produce a new chemical, called coca-ethylene (CE). CE is a longer-acting form of cocaine that hangs around in the body for hours rather than minutes. And this makes it more toxic to the heart. That’s why there’s such a strong association between taking cocaine, drinking, and heart attacks.

The upper–downer effect accounts for the popularity of Red Bull and vodka too; it’s a mix that’s been shown in animal studies to have brain-altering effects.6 You might consider a red bull vodka terribly unsophisticated and prefer an espresso martini, but in reality, what you’re doing to your brain is not so different.

Alcohol with tobacco is probably the most common combination of all. A lot of people find that once they’ve gotten into the habit of having a cigarette with a drink, it’s hard to have one without the other. This may be due to the fact that smoking accentuates the impact of alcohol on dopamine. It may also be due to the fact that alcohol disinhibits you, so after a drink you lose the will not to smoke.

There is no doubt, either, that getting drunk faster—and so raising your blood alcohol levels faster—will mean you overcome your inhibitions more quickly. Drink fast, and you may find your insight has gone and you are overwhelmed by alcohol before you even realize you are drunk. The strength of the alcohol you’re drinking also matters in this respect; the faster you are able to get drunk, the more quickly bad things start to happen.

This is why the trend for drinks becoming stronger in the past 50 years or so is not a positive one. In the 1960s and ’70s, when I was a student, most lagers and ales in pubs were 3 to 4 percent. Then along came Stella at 5 percent. Now pub beers are routinely 4 to 5 percent. Wine’s strength has also generally gone up, from 11 or 12 percent to 13 or 14.

Some drinks have been shown to make your blood alcohol levels rise faster for other reasons too: champagne more than wine, for example. In fact, most people get drunk faster on fizzy drinks.



  • "[Drink?] offers an abundance of medical research without judgement."—Library Journal
  • "Professor Nutt both knows what he’s talking about, and isn’t afraid to say it. And Drink? is a very good book for anyone interested in what alcohol does to us, both mentally and physically, in both good and bad ways."—Club Soda

On Sale
Dec 22, 2020
Page Count
256 pages
Hachette Go

Professor David Nutt

About the Author

David Nutt is Professor of Neuropsychopharmacology and director of the Neuropsychopharmacology Unit in the Division of Brain Sciences at Imperial College, London.

After completing his medical training at Guy's Hospital London, continuing in neurology to MRCP, he went on to his psychiatric training in Oxford, he continued there as a lecturer and then later as a Wellcome Senior Fellow in psychiatry. He then spent two years as Chief of the Section of Clinical Science in the National Institute of Alcohol Abuse and Alcoholism in NIH, Bethesda, USA. On returning to England in 1988 he set up the Psychopharmacology Unit in Bristol University, an interdisciplinary research grouping spanning the departments of Psychiatry and Pharmacology before moving to Imperial College London in December 2008 where he leads a similar group with a particular focus on brain imaging especially PET.

David is currently Chair of DrugScience (formally the Independent Scientific Committee on Drugs (ISCD) and President of the European Brain Council. previously he has been President of the European College of Neuropsychopharmacology (ECNP), the British Neuroscience Association (BNA) and the British Association of Psychopharmacology (BAP). In addition, he is a Fellow of the Royal Colleges of Physicians and of Psychiatrists and a Fellow of the Academy of Medical Sciences. He is also the UK Director of the European Certificate and Masters in Affective Disorders Courses and a member of the International Centre for Science in Drug Policy. He has edited the Journal of Psychopharmacology for over two decades and acts as the psychiatry drugs advisor to the British National Formulary.

Previously he has been a member and then Chair of the Advisory Committee on the Misuse of Drugs (ACMD – 1998-2009), a member of the HEFCE/NHS Senior Lecturer Selection Panel and of the MRC Neuroscience Board. Other previous national contributions include serving as the medical expert on the Independent Inquiry into the Misuse of Drugs Act (2000 Runciman report), and membership of the Committee on Safety of Medicines, the Committee on NHS drugs and the Ministry of Defence Science Advisory Board. He was the clinical scientific lead on the 2004/5 UK Government Foresight initiative "Brain science, addiction and drugs" that provided a 25-year vision for this area of science and public policy.

David broadcasts widely to the general public both on radio and television including BBC science and public affairs programmes on therapeutic as well as illicit drugs, their harms and their classification. He also lecturers widely to the public as well as to the scientific and medical communities; he has presented three time at the Cheltenham Science Festival and several times for Café Scientifiques.

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