In the early 1980s, then First Lady Nancy Reagan set about to create a new offensive in our society’s war on illegal drugs; in doing so, she popularized a now iconic phrase that was directed at young people across the country: “Just say ‘no’”. Inherent to her advocacy was the idea that all addictions begin with one bad choice and that the solution to the millennial problem of drug use in people is simply for them to say “no”. While this point of view may seem – at the surface – to be correct, the reality is that the pathways to addiction are much more complex and require an enormously more nuanced view. Consequently, I will argue that our efforts to prevent and intervene must be equally multi-faceted.
There is no one factor that triggers addiction. Instead, the pathway to it involves many influences that may each be necessary and yet not sufficient. Perhaps the clearest example of this is the choice to use the drug at all. Many people in our society misuse or abuse illegal drugs; in 2010, government statistics show that as many as 1 in 5 people aged 18-25 were using illegal drugs. What is more, many people use illegal drugs repeatedly over fairly prolonged periods of time. Yet only a surprisingly small fraction of all of these people develops what we refer to as a clinically significant substance use disorder (“addiction”) – a pattern of life-impairing, compulsive drug use. Yes, the choice to take an illegal drug is a necessary step in the pathway to becoming addicted to it, but it is not sufficient. Other factors are clearly in operation that alter the way a subset of people will respond once their drug experience has begun. A different way of saying this is that some people are vulnerable or susceptible to the development of a drug addiction, while others are resilient.
Their susceptibility results from a panoply of factors that arise long before the first “choice” to take the drug. Genetics are a major player. We know that a very large fraction of an individual’s propensity to develop an addiction is inherited in the genetic code. There is extensive evidence that susceptibility for addictions runs in families and that it is not simply the familial environment that causes this. Instead, the gene variants received from the parents are strikingly influential.
Biological age matters, as well. We know that the adolescent brain is highly vulnerable to social pressure to use drugs because of the difficulty they have with resisting their strong impulses and making effective life choices. As I discussed earlier, adolescents are neurobiologically disposed to acting on impulse because of the delayed development of brain systems required for good decision-making.
But it’s not all nature, nurture (life experiences) matters, too; for example, adversity during early childhood increases later risk for addictions, but the life experiences that place pressure on people to use drugs are not confined to the early years. For some, the ready availability of drugs in poor urban areas, coupled with the extreme hardship, adversity and life stress that often accompanies life in these areas, conspires to promote drug abuse. We all know that, for some, drug abuse begins with attempts to “medicate” the psychological distress caused by life stress. Each of these factors confers susceptibility and contributes to why some who use drugs develop addictions, while others do not.
To show that we can use this information about susceptibility to identify biological mechanisms, we can look to the effects of social stress on addiction. Substance abuse occurs at higher rates in young people who grew up in families with poor parental care/support and/or with extremely high levels of stress. Studies in monkeys were the amongst the first to show that a stressful social environment increases the susceptibility of individuals for drug use (monkeys that are socially subordinate are more likely to voluntarily take cocaine) and that this effect is related to the ability of social stress to diminish levels of a brain protein called the dopamine-D2 receptor in the brain’s reward system. More recently, researchers at Columbia verified this effect in humans; persons with poor social support exhibited the same decreased D2 levels that the socially subordinate monkeys did.
What does this change have to do with choosing to say “no”? Absolutely everything.
We know, from studies in rats, non-human primates and humans (including from my own research), that animals and persons with low D2 receptor levels in the brain’s reward system are at greater risk addiction precisely because this molecular dysfunction causes a relative inability to resist inappropriate impulses and to make effective decisions. It is important to note that having low levels of this receptor isn’t sufficient to cause addiction, but, as already argued, neither is using the drug itself. It’s a combination of factors that leads a subset of people down the pathway towards a potentially lethal disease that will ravage their lives and those of the people who care about them.
The value of such a discovery is that we now have a concept about how behavioral, biological and medical interventions can be targeted in an attempt to break the chain of events between the initial causes of susceptibility and the ultimate development of an addiction.
The common concept that the choice to use a drug is the key point of intervention is a myopic view that is ignorant of the real, multi-faceted influences on addiction. Instead, understanding and dissecting the biological pathways affected to cause susceptibility will almost certainly create a new and much more successful stage of the war against addictive disorders. That’s why it’s so important to support basic biological research on addictions, to embrace the concept that addiction is a disease of the brain and to carry on both animal and human research aimed at defeating this powerful foe.
“We know that the adolescent brain is highly vulnerable to social pressure to use drugs because of the difficulty they have with resisting their strong impulses and making effective life choices.”
Hmmm. Does that really make sense?
I’m with you on the relative difficulty for teens of ‘resisting impulses’, but it almost seems like you’re assuming that all teens will have the impulse to do drugs, because of social pressure. The level of perceived social pressure to use drugs is hugely variable though. Some individuals are luckier at choosing social groups, and some individuals make good ‘preliminary choices’ (like which friends to identify with).
I question the notion that teens are more biologically sensitive to social pressure- social learning is important across the lifespan, but our society has much more of an expectation of teens taking their cues from each other primarily than some other societies, and I think that has an impact as well.
You’re quite right that there are a variety of factors that influence choices to use and continue use of drugs, and will power models of behavior aren’t very illuminating… but I think it is worth examining where impulses come from.
I think the evidence for relatively delayed maturation of those brain circuits required for inhibiting motivated responses is pretty clear, as is the contribution of this phenomenon to the heightened propensity of the average adolescent to engage in high risk behaviors. Obviously, susceptibility for drug use and abuse is only one manifestation of this. But because one has no experience with how a drug will feel before its first consumed, most of the initial motivation to consume it is socially instructed. The desire to fit in, the desire to please others and the desire to share an experience are all examples of why a teenager may choose to use a drug, and it seems to me like it is clear that adolescents are more vulnerable, on average, to these influences than are adults, on average.
You are right that not all social influences and contexts are equal, which is something I tried to emphasize in my post. Those teens who have optimal social and familial environments are protected from drug abuse susceptibility for many reasons – including the impact of these influences on their dopamine receptors. We do definitely need to know more about this: both the functional aspects of environmental effects on vulnerability and the neurobiological pathways by which these effects have their influence.