The addiction trap | Aeon

Josh and Dawn, who were then dependent on heroin, at Union Square, New York in 2007. Photo by Brian Shumway/Redux


The addiction trap

Our inability to treat substance use disorders stems from a narrow-minded view that brains and genes are their real cause

by Judith Grisel + BIO

Josh and Dawn, who were then dependent on heroin, at Union Square, New York in 2007. Photo by Brian Shumway/Redux

By the time I realised that my drug use was killing me, I was institutionalised deep in the woods of Minnesota, at least a three-day drive from home, and without a car. My 1983 Corolla, including all my stuff, had been repossessed several months earlier. I was in a treatment centre at the unripe age of 23 as a result of one more half-baked decision in a long string: I deserved a break from my deranged life, I thought, and treatment, which was something like an educational spa, might be just the thing. Another way to put it is that I was lost.

As I gradually ‘came to’, any hope I’d had for a restful hiatus, or for learning expert tips on how to use drugs successfully, withered. Despair took its place: my life was a mess, and the suggestion unanimously endorsed by staff – that I should quit using if I wanted to live – seemed entirely unreasonable. Abstinence was never part of my plans. I felt like a passenger on a cruise ship duped into disembarking on a desert island – stranded without resources.

Denial is one of the core attributes of addictions, and the reason that I saw drugs as the solution, rather than the cause, of my problems. In fact, they were pretty much my only coping tool. Loneliness, failure, disappointment, shame – regular fare by this time – were solid reasons for turning to substances to escape. ‘You’d use too, if you had my life’ has been uttered countless times by people like me, often right up until they take their last wasted breath.

But using psychoactive drugs to enhance experience is at least as old as humanity itself, and the majority of people who do so don’t self-destruct. It seems that the drive to amend reality is baked into our neurobiology by evolutionary forces aimed at maximising flourishing. Had we lacked the proclivity to pass a pipe or a kava bowl, to sample bubbly brews or magic mushrooms, we’d also have been less likely to discover new vistas, or to break new ground in communication, art or engineering.

In fact, the same tendencies that led me for most of the 1980s to embrace the maniacal lifestyle of a stimulant abuser, in the 1990s attracted me to a career as a neuroscientist. Both are full of surprise and convey a sense of trailblazing. Desire for something other than what is leads us to reach beyond our grasp, leveraging curiosity and industry toward personal developmental goals (like those that impel kids to leave the nest) as well as collective achievements that benefit the population (exploiting RNA to quash a virus!).

So, for much of our history, the urge toward else has been a very good thing, not only enabling us to survive, but to thrive. However, perhaps beginning with the Industrial Revolution but certainly in recent history, the tendency to reach beyond our known grasp has become a liability for many. Two primary developments turned this source of evolutionary fitness into an Achilles heel: a dearth of developmentally appropriate opportunities for breaking new ground, and easy access to a surfeit of potent chemicals with which to medicate dis-ease.

Where an adventurous spirit was once the surest capital for realising big payoffs, prospects for novel and risky experiences, aside from drugs, are scarce today – especially for young people. Unfortunately, the drive to try new things, associated with independence in our evolutionary past, is now mis-timed toward the start of an extended adolescence, around puberty. Coincidently, there is a growing supply of addictive chemicals, readily available in more and more potent formulations. For too many of us, seeking a way to make life worth living, these become a quick fix by activating neurocircuitry responsible for encoding meaning, that few, if any, natural stimuli can compete with.

Addiction results as the brain changes, or adapts, to counteract the effects of drugs that masquerade as meaning and manipulate neurochemistry to convey mystery and hope. The more frequently someone takes a drug, the more profoundly the brain adapts but, because adolescent brains are so malleable, this population is especially vulnerable.

I first began drinking and using other drugs around 13, an age that, in another time and place, might have been associated with riveting occupations such as starting a family, homesteading or just struggling to stay alive. Instead, I was ‘safely’ ensconced in suburbia, and mostly bored out of my mind. My first drink released a racehorse from the gate. A constant sense of restlessness – as if I was in some urgent hurry but lacked any idea of what I should be doing – evaporated as I felt myself at last in sync with time and space. The drug seemed to speak to my soul: You! Belong! Here! Suddenly my life had both promise and purpose.

At the time, I didn’t realise that intoxication, in and of itself, wasn’t much of a purpose to organise one’s existence around, and when this finally dawned on me many years later, it was almost too late. But it is precisely this capacity that makes addictive drugs addictive – the shining star they light in our psyches is the impetus for regular use, and dependence simply the natural consequence of our habits.

Just over one in five of those who use addictive substances develop disordered use. ‘Why me?’ began as a personal quest to explain and hopefully repair my broken bits, but gradually the query broadened into a philosophical and scientific koan, evoking deeper and deeper wondering about what it means to be normal or abnormal; ordered or disordered. The scientific focus of these musings is anything but academic. Instead, they get to the heart of real-world matters related to diagnosis, treatment, prevention, and perhaps even a cure. In fact, it is a central concern in the study of any disorder to decide whether it is possible to separate people into clear-cut camps, such as sick or well. Are people who have depression or ADHD, for example, distinct from those who do not, or does the increasingly complicated binning simply reflect our need to impose order on chaos?

The case in point: does one use mind-altering drugs socially or does one use them addictively, and is there a slippery slope between the two? (From a scientific perspective, those who don’t use at all are theoretical outliers.) A simple answer would represent a breakthrough for scientists, policymakers and insurance companies, making our hypotheses, laws and actuarial predictions so much cleaner. Unfortunately, the question is still unresolved, which is to say, scientists aren’t entirely clear what it is they are attempting to study or cure.

Researchers do agree that irrational consumption, in which the costs of using drugs outweigh the benefits, is at the heart of substance use disorders. This pathology is driven by craving, tolerance and dependence, telltale signs of addiction that develop as the brain adapts to regular drug exposure in order to maintain homeostasis, and in particular as it becomes desensitised to the pleasurable sensations produced by a drug. At issue, though, is whether the separation between addicted and nonaddicted individuals is clear, and if so, what is responsible for the delineation? The messy alternative is that behaviours, feelings and brain states associated with addiction exist on a continuum, probably normally distributed, with pathology found toward the tail of multiple bell curves. In this case, there is no bright line, clear diagnostic criteria or defective brain chemical to demarcate those who are sick from those who are well. Instead, we are all more or less susceptible along a continuum in which fitness is a moving target contingent upon an ever-changing context.

It should have been obvious that genes don’t cause complex behaviours such as those underlying addiction

Given our inability to identify smoking guns, or, relatedly, to develop effective cures, the complicated scenario seems more in line with reality, though the question has not been settled. Alcoholics Anonymous, arguably the most effective treatment for the ‘disease’ of alcoholism, asserts it’s an ‘allergy’ that compels some of us to use despite mounting consequences. This perspective is also endorsed, though less definitely, by medical bodies such as the National Institutes of Health and the American Medical Association, as inscribed in their handbooks, the Diagnostic and Statistical Manual of Mental Disorders (5th ed, 2013) and the International Classification of Diseases (11th ed, 2019). Perhaps the best support for this view is that there is little evidence of formerly addicted individuals successfully transitioning to social use.

My own wish for a simple explanation stemmed from a strong desire to find a palatable alternative to a lifetime of sobriety, and the overblown optimism of behavioural genetics around the turn of the century. I began a postdoctoral fellowship in 1997 in the laboratory of one of the world’s experts on the genetics of addiction, John Crabbe, at the Oregon Health and Science University, fully aware that about half the risk for addictive disorders is inherited. Like hundreds of groups around the world, we seemed poised to explain this liability as geneticists and robots were closing in on the monumental task of sequencing the human genome.

We figured we’d simply need a group of people who had clearly trespassed the line beyond social use, and a control group who definitely hadn’t, and pick out whatever snippets of DNA distinguished the two groups of genomes. Unfortunately, more than anything else, such exercises helped us realise how much we didn’t know we didn’t know.

Of the relatively few discoveries linking DNA sequences to substance use disorders, the biggest hits turn out to code for liver enzymes. Though these might be statistically significant, I’m pretty sure my problems had more to do with what drugs did above my neck, than below. In retrospect, it should have been obvious that genes don’t cause complex behaviours such as those underlying addiction. Instead, as we now know, genes tip scales of sensitivity to shape a range of responses to our environment. It’s nature via nurture, as Matt Ridley put it in 2003, not one or the other.

It turns out there are many catalysts for substance use disorders and they interact with each other, making it nearly impossible to disentangle the cause, including those from our genome. Still, it might be fruitful to shine a spotlight on to three critical and interwoven threads: biological factors including innate tendencies and developmental vulnerabilities; experiences, especially stressful conditions during childhood; and the social and cultural contexts within which biology and personal experiences unfold.

As it did with me, addiction begins for the vast majority of people while the brain is undergoing dramatic developmental restructuring, particularly during adolescence. Studies suggest that up to 90 per cent of people with a substance use disorder begin using mind-altering chemicals before they turn 18. For example, the likelihood of developing alcohol abuse or dependence is seven times higher in those who begin drinking by age 14, as I did, than in those who wait until they are at least 21. The same is true of other drugs: one in four Americans who use any addictive substance before age 18 develop an addiction, compared with only one in 25 who start using at age 21 or later. This is because developing brains actually are like sponges – especially adept at absorbing experiences, and also expert at translating these experiences into long-term patterns. Early drug use alters the brain to generate habits and compulsions associated with drug addiction.

Unfortunately, those developmental years are precisely the time that drug experimentation is most likely to take place, underpinned by a biologically inveigled orientation toward risky behaviour and proscribed experiences, along with an impaired capacity to reason abstractly about the consequences of those choices. Both explorers and teenagers, for the same reasons, advance humanity’s interests as they risk themselves like hungry sheep searching for greener grass that might lead the way to a new field – or get them picked off by a wolf. These biases are by evolutionary design, because a group of young people emphasising potential over punishment living alongside more conservative folks helps to ensure an overall balance between change and stability.

The addiction pandemic doesn’t result from a single entity, and therefore won’t be solved by one either

For this reason, it doesn’t take much for some adolescents to realise that substances provide relief for a host of ills aside from boredom. Those who were or are subject to psychological, physical or sexual abuse, as well as general household dysfunction in the form of substance abuse by family members, mental illness or violence, are particularly likely to appreciate the capacity of substances to provide emotional relief from stressors. Just one of these adverse childhood experiences (ACEs) doubles the risk of developing alcohol dependency, and four or more increase the chances 10-fold. Childhood adversity is especially impactful for the same reason that early drug use is – developing brains are primed to translate experiences into structural changes in neural circuits, and changes to structure produce changes in function. A sensitive neurobiology is why young people learn much more efficiently than those who are older, a talent that works for ill as well as for good.

Beside early trauma, the bulk of experiential impact comes from ‘nonshared environmental factors’, which is a biostatistician’s way of saying that it could be anything. Though we might assume that growing up in a particular family or in a specific region would have major impacts, most environmental influence for most traits is nonshared, and therefore buried under so much noise that it is unlikely to rise to the surface of any scientific analysis. Prenatal perturbations, experiences with siblings, interactions with particular people, accidents or illnesses – often the result of happenstance – turn out to have significant impact.

In the decades that have been spent trying to unravel the knot of factors that predispose toward addiction, we’ve learned quite a lot, though truth be told, it’s not nearly enough. I began studying neuroscience to understand differences in my own brain that caused me to use drugs so self-destructively, and in the late 1980s to ’90s was not alone in believing that there would be a specific malfunction at the root. Unfortunately, understanding, treating and preventing substance use disorders have been so elusive because a tangled heap of genetic and developmental liabilities combines with opportunity and despair to promote destructive behaviour in ways that might be unique for each case. In contrast to COVID-19, the addiction pandemic doesn’t result from a single entity, and therefore won’t be solved by one either; and we’re going to have to do more than just hunker down and be patient. As T S Eliot noted, ‘What we call the beginning is often the end,’ and while it is beyond discouraging that neuroscience hasn’t helped alleviate the burden of substance use disorders, we might finally be off to a good start by recognising the mistake of focusing so narrowly on biomedical causes.

The brain is, by far, our most complex organ, making mental disorders among the most inscrutable of diseases. Moreover, our inability to identify neural causes (and cures) for substance use disorders might reflect a longstanding confusion around cause and effect. It’s looking less and less to be the case that addictive disorders result from aberrant brain activity, and more that early use, facilitated by genetic predispositions that often mix with early trauma, leads to alterations in brain circuitry that tip the scales toward the core attributes of addiction: drug craving, tolerance and dependence.

Humanity’s complexity is due to our capacity to respond in diverse ways to countless interacting influences; the broad range of response options within, and between, individuals is possible only in the absence of simple causes. Gregor Mendel’s pea plant seeds were brown or white, and this dichotomous trait was determined by a single gene. Unlike pea plants, human behaviour, including that associated with substance use disorders, results from a vast array of internal and external factors. These especially include genetic tendencies toward stress sensitivity, risk taking, novelty seeking and tolerance for punishment when it comes with reward, as well as early trauma, opportunity and random chance. All of these factors affect the brain’s structure and function to produce behaviour associated with addiction. As a result, our biology is decidedly not black (or brown) and white. In other words, although drug-disordered states are undoubtedly expressed through our brain circuitry, they are not of it. And if the brain doesn’t cause disordered use, it doesn’t really make sense to look there to explain it or to cure it.

There are many reasons why we have been stuck on the ‘brain causes behaviour’ hypothesis for addiction, all the while failing to appreciate that behaviour, and so much else, changes the brain. Thinking that a solution is just waiting to be discovered lets many of us off the hook. If the explanation was inside individual skulls rather than out there, in the rich milieu that gives rise to the people we are, the puzzle would be easier to solve.

The brain is a conduit, rather than a cause, of substance use disorders

It used to be that people studied the brain to gain a better understanding of the brain itself, hoping for some clinical benefit along the way. But this changed in the latter half of the 20th century as those in charge of funding such work decided that science for science’s sake wasn’t providing a fast enough return on investment; one had to make strides in the clinic to garner support. This seemed cockamamie to me at the time – the majority of scientists I knew worked long hours for mediocre pay. It wasn’t that they didn’t want to find a cure, or that this had been held up by a lack of legislative oversight: it’s just that human behaviour is complicated! Moreover, basic science aimed at understanding, more than application, was and is responsible for most clinical progress. The research behind innovation usually builds slowly, one tedious experiment at a time, motivated more by a desire to explain than by bureaucratic edicts.

Whether or not neuroscience will come up with a magic bullet for treating substance use disorders is itself an empirical question, awaiting convincing data. Just because we haven’t yet developed brain-based causal models to facilitate successful treatments does not mean we won’t sometime in the future. However, I’m not holding my breath, as it seems increasingly likely that the brain is a conduit, rather than a cause, of substance use disorders. Rather than directing our thoughts, feelings and behaviours, the brain, shaped by evolutionary as well as personal history, translates experiences into us; this means it is necessary, but not sufficient, to explain disordered substance use. Because the environmental context plays at least as big a role as biology, it doesn’t really make sense to target molecules over experiences.

In the broadest strokes, addictive disorders develop in vulnerable individuals who are bored or in pain. Though challenging for any of us, these feelings rub particularly hard against the adolescent grain because teen neurobiology is especially primed for tuning into, and generating, personally meaningful experiences. It’s not that addressing these factors will be any easier than developing brain-based interventions – in fact, changing culture and systems to address these states might be even more ambitious than engineering brains – but they are likely to be more effective. Another possible advantage to this outward-looking strategy is that recent research in developmental neuroscience suggests that, for the same reasons that childhood is such a vulnerable period, it might also represent an especially ripe time for effective interventions. So, while it is crystal clear that factors from our genes to challenging incidents in the middle-school lunchroom influence our brain structure and function, despair during adolescence is a better predictor of many disorders, including addiction.

The brain is more cart than horse. It seems increasingly likely that our inability to explain, prevent and treat substance use disorders stems from having too narrow a scope, one that myopically views the brain, as I once did, as the critical causal element.

It could be that substance use disorders develop when normal biology is diverted by developmental adversity and early use. In order to reverse the rising incidence of addiction, we need to reduce trauma in children by investing in healthy development from conception to independence. This obviously requires promoting peace and prosperity in kids’ caretakers and neighbourhoods. And we must also provide meaningful alternatives for teens to explore the edges of their own existence. As in my own case, drives toward risk and novelty peak during adolescence, and these tendencies can find an outlet in addictive drugs. The American Families Plan proposed by the US president Joe Biden would be a good start by investing billions of dollars into programmes such as childcare, paid family leave and education. But whatever we do, it’s clear that reversing the addiction pandemic depends upon prioritising childhood wellbeing and opportunity for a hopeful future.

To read more about addiction, visit Psyche, a digital magazine from Aeon that illuminates the human condition through psychology, philosophical understanding and the arts.

AddictionChildhood and adolescenceNeuroscience

Aeon is not-for-profit and free for everyone

Make a donation

Get Aeon straight to your inbox

Join our newsletter