Why We Drink Too Much
What neuroscience and biology say about alcohol—and why the New Year is a natural moment to ask better questions.
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After a long and possibly overindulgent holiday season, a lot of us are trying a Dry January, or at least rethinking our relationship with booze. This is the time of year when we might notice how much alcohol has woven itself into our social lives, our stress management, our celebrations. Charles Knowles is a Professor of Surgery at Queen Mary University of London and Chief Academic Officer at the Cleveland Clinic London, and his new book is called Why We Drink Too Much: The Impact of Alcohol on Our Bodies and Culture. Below, he joins us to explain why problematic drinking isn't defined by how much we consume, and what we really need to know if we want to change our relationship with alcohol.
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1. Why do humans consume alcohol?
A necessary starting point to understanding why some humans drink too much is understanding why humans consume alcohol at all. Our hominid ancestors evolved to metabolize alcohol over 10 million years ago, pushed by the need to safely consume rotting fruit from the forest floor. We have been deliberately manufacturing alcohol for over 15,000 years, and today it remains our most popular drug, despite many well-acknowledged downsides. Why do we continue to drink it? We can’t still claim this as a nutritional necessity.
The vervet monkey on the island of Saint Kitts in the Caribbean is one example of many animal species that consume alcohol, with individuals showing variable enthusiasm for doing so. This attests to a fundamental biological driver. It cannot simply come down to clever advertising, peer pressure, or the price being right at the liquor store.
The brain lies at the heart of this. If we ask most people, they will tell us that drinking alcohol makes them feel good and that they have fun drinking it. This is because alcohol is a primary reward; it can chemically alter the levels of certain neurotransmitters in our brains. The combined effects of alcohol on dopamine, but also on endorphins and GABA, lead to psychostimulatory and relaxant effects, in fact, mimicking the effects chemically of cocaine, opioids, and Valium. It is these positive effects of alcohol on the brain that are the fundamental basis of why we and other animals consume alcohol.
2. The drinking scales.
Although some people may find it hard to resist, ultimately, we consciously choose to drink. This is a cognitive process that takes information from our senses—the time of day, where we are, who we are with—and processes this information against what we know, using our ability to think intelligently before acting. The positive effects we get from drinking are based on alcohol’s psychostimulatory and relaxant effects. We then come to balance these pros against the common negative effects (hangover, cost, embarrassment, etc.). This balance of the pros and cons is what I call the drinking scales. Everyone has a slightly different balance depending on their positive and negative experiences of alcohol. And this balance changes throughout life with societal norms and values.
If the drinking scales worked perfectly to provide a logic-based decision all the time, I wouldn’t be writing this book. The problem is that all around us are people for whom the evident harm of drinking should have been sufficient years ago to outweigh any positives, but still they drink. In such people, we can think of the scales as being broken or bypassed. This happens because the brain is wired to allow it to happen. Survival programs deep in the ‘old’ parts of our brain, based around the reward pathway and memory, promote behavior that once aided our survival in the jungle but which now leads to serious consequences rather than any useful purpose. This is the basis of addiction. The question then becomes: why does this happen to some people and not to others?
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3. Problematic drinking is not defined by how much we consume.
“Why can’t he drink like a normal person?” We hear this said. Many people see problematic drinking as a black-and-white issue. There are normal drinkers, and then those who have a problem. But there is quite a lot of gray. The term gray area drinking has now become popular in community groups. But what do we mean by this compared to medical terms like alcohol dependence or alcohol use disorder?
I would recommend that anyone reviewing their relationship with alcohol should look at what I call the three Cs: consumption, consequences, and control.
While long-term consumption level may have some important ramifications for health or finances, consequences and control are much more important angles for looking at the problem.
Consequences from alcohol range from common downsides (like a hangover) through to serious harms (car accidents, criminality) and chronic health problems affecting the body and brain.
Control, however, is perhaps the most important. After all, if we could control our consumption, we could just stop when consequences started occurring. And this brings us back to considering a spectrum where white might be neutrality, a “take it or leave it” approach to drinking, and black is dependence. But what then is gray?
I define gray area drinking as someone who relies on alcohol in a way that is making them concerned about the amount they consume and their ability to control it. And it brings in a new concept called alcohol reliance, a state of mind where consumption of alcohol has become a regular habit that is hard to give up, but has not yet led to the behaviors that define alcohol dependence.
4. Bad genes.
It seems unfair. Why was I, of all my hard-drinking college buddies, singled out to develop alcohol dependence? This is what I call the “why me” question. Loss of control has very little to do with consumption. Although alcohol is clearly required, we don’t actually drink our way to having a problem. It therefore poses the question of whether there is something biologically different between individuals, and this has been debated since alcoholism became studied as a disease in the 1930s.
Twin and adoption studies show that alcoholism has a heritability of about 50 percent, meaning that about half of the risk of developing dependence falls at the door of genetics. Studies of mice breeds show that tolerance to, stimulatory response from, and therefore preference for alcohol can be genetically conferred. In fact, you can genetically engineer mice that mimic several behaviors of dependence. We also know that people with intolerance for alcohol (such as Asian flushing, caused by specific gene variants in liver enzymes) very rarely develop alcohol problems because the experience of drinking is deeply unpleasant.
The sort of experiments performed in mice based on stimulation from alcohol can also be performed in humans. An example is the San Diego cohort study. Measured doses of alcohol were given to young adults who were alcohol naïve, and the amount of stimulation they got from it was measured. Those who were more stimulated went on to have a higher risk of problems later in life. We can define humans who biologically find it fun to drink versus those that rapidly slump in the corner. The latter are relatively protected while the former are at greater risk of alcohol dependence.
But this doesn’t mean there is a single bad gene variant. Alcohol related disorders are what we call complex diseases or traits. They’re a mixture of nature and nurture, and the nature is a consequence of hundreds or thousands of subtle variations in our DNA spread across the two billion base pairs of our genome, and not just in the genes themselves. This means we’re looking for a needle in a haystack. In fact, one could say we’re looking for thousands of needles in a haystack, some of which look very much like hay.
The results of this exercise are disappointing at the current time. Most genes found overlap with major mental health disorders and ADHD. Some newer discoveries are in taste and in the way our brains rewire throughout life. We do find some genes associated in mice with increased stimulation related to GABA. However, overall, we are a long way off having predictive genetic testing.
5. Bad luck.
Despite the scientific fashion for all things genomic, how we turn out in life—our success, happiness, hopes, and dreams—generally has very much to do with the environment we grow up in and the effects of human interactions on our psyche. What we are exposed to during childhood, especially during the critical period of attachment, plays into the sort of later diagnoses that come from a psychiatrist, such as anxiety and depression, but also important personality traits like self-esteem and our social fitness.
Many psychological traits create a double weighting on the pros side of the drinking scales. Alcohol doesn’t just seem fun, it also provides relief by its relaxant and, if we drink enough, sedative effects. These dissociative properties can suppress negative feelings, thoughts, and memories; this is particularly true when suppressing the barrage of thoughts that comes with problems like ADHD and neurotic personality.
But there is another twist here which returns us to thinking about how the drinking scales can be bypassed or broken by the fundamental survival-biased wiring led from our reward pathway. Survival for our ancestors had a great deal to do with social fitness: how we relate to other humans for protection, reciprocal behavior such as hunting, and romantic desirability. If, when we are young, we find a profound solution to fear and social difficulties by using alcohol, we may come to falsely associate these rewards with a survival advantage.
Despite the illusion, our brain is still working from the ancestral jungle script. This is perhaps why disorders characterized by problems both of social interaction as well as negative thoughts are so strongly associated with alcohol dependence. Also, it may be no coincidence that the 15,000 years of deliberate alcohol manufacture quickly followed when humans started to live and cooperate in groups.