Three posts ago, I discussed the personality traits that make us most vulnerable to addiction. And I promised to say more about them.

Most experts agree that the two biggees are….

(1) an impulsive or risk-taking personality style

(2) an anxious, oversensitive personality style

Note once again that there is nothing like a standard “addictive personality” — contrary to popular belief. In fact, these traits are almost perfect opposites. In her upcoming (excellent!) book, Maia Szalavitz emphasizes a third gateway: an insidious combination of the two. Maia says this was the recipe for her own addiction, and I think that was it for me as well. So let’s call this third personality pathway…

(3) an impulsive or risk-taking style combined with oversensitivity

How do each of these trait structures predispose us to addiction?

Most experts emphasize the link between impulsivity and addiction. That’s pretty straightforward, but it’s especially problematic in adolescence, when every kid gets somewhat impulsive (except for the real nerds) because evolution designed us that way. Now trait impulsivity becomes a risk factor for all sorts of things: shop-lifting, uprotected sex, preventable accidents, etc. But when you’re an impulsive person at an impulsive stage of life, you’re especially likely to hold out your hand when powders or pills get passed around. “Hey, I want to try that!” Drugs and booze are risky, and risk-takers are first in line.

But there’s another, subtler, causal connection. Research links the impulsive/risk-taking trait package with inborn differences in the dopamine system, and this path to addiction was touted by Kenneth Blum as the reward deficiency syndrome. Due to normal genetic variability, some people have fewer or less sensitive dopamine receptors of a particular type (e.g., the D2 receptor in the nucleus accumbens, the brain region underlying reward seeking). According to Blum, these people need more dopamine to feel excited or engaged. I’ve written about this in detail elsewhere, but the idea is simple. If you need more dopamine to satisfy your underpopulated D2 receptor system, the easiest way to get it is to take drugs.

Now, if you know (maybe unconsciously) that you need more of a charge than others to feel good, then it makes sense to train yourself to seek and find risky situations. So, you may end up “hypersensitive” to high-impact rewards because that’s really what you live for. People who are extreme in their impulsivity also lack normal levels of social anxiety. So they don’t care much about how others react to their excesses. Then we are verging on the antisocial/psychopathic personality style. And those people can be bad news in all kinds of ways.

What about the anxious, oversensitive person? We become anxious about how others react to us, sensitive to rejection, and perhaps obsessively concerned about how we are acting, not only based on genetic patterns (e.g., not enough serotonin) but also based on our family environment. If you are raised by parents who are unpredictable, touchy, volatile, or anxious themselves, then you have every reason to become anxious in social situations — and a genetic blueprint that favours anxiety will help you get there. Why would such people be more likely to find drugs appealing and, eventually, addictive?

I can speak to that personally. My mom was volatile and somewhat of a perfectionist. There was a lot of love between us, but I learned to worry about how I was behaving — and my behaviour was far from perfect. What looks like social anxiety from the outside can feel like self-criticism and self-doubt on the inside. That was me, and like many others who feel this way, it led me to depression even before I got to boarding school — where I learned just how nasty life could get. Depression and anxiety are highly correlated with addiction for good reason: drugs make you feel different, either calmer or more uplifted, they give you the sense that you can control your mood by ingesting something, and you become less reliant on social approval because you’re standing right next to the feel-good tap. Particular drugs help (“self-medicate”) in particular ways. For me, it was the soothing caress of opiates; for others it can be the bright reassurance of meth or coke. For some, it’s both.

What about #3, the combo? Maia Szalavitz speculates that being a risk-taker and an anxious perfectionist was the recipe for her addiction. Same with me. From the age of 3 or 4, I was the kid who would climb up the rose trellis and stand on the roof, crowing. I was constantly cajoling my cousin, Nancy, to explore the ravine with me, though it was strictly off limits. To present my mom with the nicest possible bouquet, I picked every flower in our neighbour’s backyard. I slid down the ice slide right in front of my teacher, because I’d literally forgotten that she’d just told me never to do it again. That sent me on my first visit to the principal’s office — in Grade One! Then, as a teen, I wanted to try booze, and weed, as soon as they were offered. And I spent my last year of boarding school dreaming about our upcoming move to San Francisco, where the streets were said to be awash in LSD and other exciting chemicals.

But I think this is the most interesting part: my penchant for anxiety, depression, and self-criticism joined forces with a deeply rooted attraction to risk-taking. Take the pill, try the needle, why not? And then, wham! I suddenly feel like I’m the conductor of the symphony of my moods. Depression, be gone! With the help of my allies in the chemical kingdom, I’m the one in charge.

What this shows is that personality development brings divergent traits and proclivities to a point. Development takes the parts and welds them into a whole. And if that whole starts to coalesce around the attractions of substance use, there’s going to be a rough road ahead.

Will a developmental-learning model of addiction (e.g., Maia Szalavitz, Gabor Maté , Stanton Peele, and me) ever make peace with the disease model? That would be a happy ending! Nora Volkow and I could eat muffins together…or maybe have a glass of wine. We could establish a space for sharing data and ideas, working together toward an explanation that incorporates the best of both worlds.

Yet I don’t think it’s in the cards. Not because the disease model is so far off base scientifically. In fact, where the brain in concerned, the distinction between learning and pathology isn’t always obvious, as epitomized by ADHD, autism, bipolar disorder, even schizophrenia. There’s got to be some allowance for overlap — doesn’t there?

It’s not that the disease model is so wrong, it’s that the baggage it carries may never fit in the same home as the learning model. Here’s what I mean:

Society’s understanding of addiction can be seen as advancing through three stages.

First, beginning in the Victorian era, addicts were considered morally flawed and indulgent. We could call that the “sin” model. Consequently, the appropriate response to addiction was to punish the addict through scorn, isolation, and maybe even jail time. Through shame and retribution, the addict might, with luck, go back to being good.

The second stage was the era of the disease model, beginning in the middle of the 20th century. The change was driven by the emphasis on helplessness in Alcoholics Anonymous, beginning in the 30s, and the evolution of residential treatment centers that stressed obedience to therapeutic regimes, beginning in the 50s. Finally, the proliferation of neuroscience in the 80s and 90s put a seal on the package by pointing to a diseased organ, namely the brain. Now specific neural changes could be pinpointed as the source of addiction, and the disease model ruled the roost.

According to the disease model, the appropriate solution to addiction was medicine. Specifically, addicts were to be urged to follow the advice handed down by medical practitioners. Rather than confess to being immoral, addicts were advised to confess to being incapable. The only hope to control addiction was to accept a regime imposed by an authority. In other words, to subdue a problem located on the inside, you needed to take orders from the outside. It is this baggage that seems destined to clash with the mindset of a third, more progressive view of addiction.

The third stage in our understanding of addiction is the learning model: a developmental sequence of events that gives rise to habitual patterns of thinking and feeling. This view of addiction admits the potency of social factors, like isolation and dislocation, as catalogued by Bruce Alexander. It makes sense of the impact of adversity in early development, as emphasized by Gabor Maté and Maia Szalavitz. And it allows for the influence of societal and cultural issues, as portrayed by Carl Hart and Johann Hari.

According to a developmental-learning definition, the appropriate response to addiction is neither shame and isolation nor submission to a therapeutic regime. Rather, it is further growth. The solution to addiction can’t be a medical regime that returns the addict to some previous level of normality. Nor can it be disempowerment, intended to counter built-in character flaws. Rather, people emerge from addiction through ongoing development. In this light, addiction can be viewed as a stage of individual development, and it must therefore be addressed through individual efforts based on individual perspectives, goals, and capacities. A developmental-learning model of addiction suggests that positive change must be pursued from within.

The final two stages in our understanding of addiction, the disease model and the learning model, have both achieved some of their plausibility on the basis of brain research. But the role of neuroscience in these two stages of conceptualization could not be more different. Neuroscience helped shore up the disease model by identifying deviations from what is considered standard neural architecture, a project we could call “neuronormativity.” Remember: the target was a cure. In contrast, the developmental-learning model of addiction embodies an emerging understanding of neuroplasticity. This replaces the search for normality with an emphasis on the brain’s capacity to change.

Thus, both models borrow something from the brain—a detailed breakdown of measurable biological events. But they are fundamentally different in orientation, and they perceive the brain in such very different ways that it’s hard to imagine how they might be reconciled. It’s the same problem that’s appeared in the tension between developmental psychology and mainstream psychiatry over many decades. The brain is either a normative thing that can go wrong and then be repaired, or it is an open system that can develop along diverse trajectories, integrating the meaning of experience according to its own expertise.

Addiction is one of those trajectories, but then so is progress beyond addiction.

NOTE TO READERS: I do try to respond to most of the comments in the comment section following each post, unless there is already a dialogue going and/or I have little or nothing to add.  But I can’t always keep up with the volume of comments (volume = GOOD!) I’ll have an easier time responding, and so will others, if you keep your comments relatively succinct. Try for two or three paragraphs, max. Longer “essays” can be very thoughtful and informative, but they take time to consider and respond to intelligently. That’s the trade-off.

It’s been a while since my last post. I did some relaxing, hung out with my kids, but mostly I spent my time writing a long, dense article summarizing my book — an invited article for a journal. I found myself back in the ring, fighting the Disease Model of Addiction… Round 17.

Is this some imaginary nemesis? Am I some demented Batman doing battle with hidden enemies? My dear cousin, Karen, who’s given me advice on all matters of personal deportment, diplomacy, table manners, and proper toilet practices since the age of three (she even instructed me to wipe after peeing, which turned out not to be necessary for boys) …Karen tells me to put down my slingshot. Goliath is more imaginary than real, and I should try to be nice and get along with others.

And then my knowledgeable email buddy, Sally Satel, sends me an issue of the New England Journal of Medicine, published only last month, in which the disease model is centre stage once again. The title of the article is…

Neurobiologic Advances from the Brain Disease Model of Addiction

The second sentence says it all:  “In the past two decades, research has increasingly supported the view that addiction is a disease of the brain.” Nothing new there. In a nutshell…

Addiction is a chronic, relapsing brain disease, evidenced by changes in the brain, especially alterations in the striatum (the brain part that underlies goal-seeking) and in the prefrontal cortex (responsible for cognitive control). These regions become partially disconnected with ongoing drug use. (my summary)

The argument hasn’t changed in years. (For a detailed account, read my book.) But the next sentence takes a new tack: “Although the brain disease model of addiction has yielded effective preventive measures, treatment interventions, and public health policies to address substance-use disorders, the underlying concept of substance abuse as a brain disease continues to be questioned…”

Indeed it does, more and more, and the appendix to the article spells out some of the criticisms leveled by writers such as Maia Szalavitz, Carl Hart, Sally Satel, Bruce Alexander, our cantankerous and relentless Stanton Peele, and yours truly. (Gabor Maté and Johann Hari will agree if you ask them.)

As you might expect, the appendix also includes a brief counter-argument posed against each of these criticism. Here I’m going to review just two of these arguments/counterarguments and tell you why I think we should keep the slingshot loaded.

“1. Most people with addiction recover without treatment, which is hard to reconcile
with the concept of addiction as a chronic disease. This reflects the fact that the
severity of addiction varies, which is clinically significant for it will determine the type
and intensity of the intervention. Individuals with a mild to moderate substance use
disorder, which corresponds to the majority of cases, might benefit from a brief
intervention or recover without treatment whereas most individuals with a severe
disorder will require specialized treatment.”

So are they saying that most people with addictions don’t have a disease, and only those with severe addictions do? But you wouldn’t say that people with mild cases of cancer, pneumonia, tuberculosis, malaria, or even diabetes don’t have the disease. You’d say they do have the disease but it’s not too bad…yet. So maybe they’re saying that most people with a mild to moderate level of the brain disease of addiction don’t need intensive treatment? That might make sense, except that it doesn’t. This majority of addicts start using more than they should for a few months or even a few years, and then most of them just stop, without treatment. (The statistics on that are indisputable, so it’s good that the disease folks are finally acknowledging it.) But that doesn’t sound like a disease at all. It sounds like a bad habit that most people recognize is unhealthy and learn how to control. Then is there a threshold at which addiction goes from an overlearned habit to a disease? If there were, it would be measurable. But no one has ever succeeded in measuring it. Few would even try.

“3. Gene alleles associated with addiction only weakly predict risk for addiction, which
is hard to reconcile with the importance of genetic vulnerabilities in the Brain Disease
Model of Addiction. This phenomenon is typical of complex medical diseases with high
heritability rates for which risk alleles predict only a very small percentage of variance in
contrast to a much greater influence of environmental factors (i.e., cirrhosis, diabetes,
asthma, cardiovascular disease). This reflects, among other things, that the risk alleles
mediate the response to the environment; in the case of addiction, the exposures to drugs and stressful environments.”

My last post covered the genetics issue in some detail (and I’ll get back to it in a later post). But here’s the crux of the issue. Yes, weak genetic predictors may be typical of many diseases with high heritability. But they’re also typical of a bunch of other stuff…like personality! Personality outcomes fall into distinct categories: extrovert, anxious-neurotic, sociable, suspicious, dependent, etc, etc. (Should we add “addict” to the list?) And all of these “types” have weak genetic predictors (though high concordance between, say, identical twins). The reason is because people become the way they become based on what happens to them in life — the environment shapes them while they shape their environment. So the whole “genetics issue” — which has been a holy cow for disease model advocates — ends up saying nothing at all about whether addiction is a disease.

I’ll end by saying that holy cows get my goat (that actually means something in American). Next post, I’m going to tell you why I think it’s so hard (though it would be nice, Karen) to actually reconcile the disease and learning models of addiction.

Hi all. I haven’t written anything since New Year’s, and I guess it’s time to crank up the blog machine. I can see that we have a lot of new readers. I want to welcome you newcomers as well as ye olde and faithful — I hope there’s something here for you and I hope you’ll join in the dialogue with comments.

I just got an email from someone confused about the genetic roots of addiction. I get questions like this all the time. It’s a big issue that nobody’s very clear on. To be honest, I’ve been somewhat confused about the heritability of addiction too. One of the things I’ve found most confusing is that the heritability estimate keeps showing up in the 40 – 60% range, for drug addiction and alcoholism. How can it be that high, when most experts agree that the idea of an “addictive personality” is just plain wrong?

Over the past month I’ve been reading an advance copy of Maia Szalavitz’s latest book, Unbroken Brain: A Revolutionary New Way of Understanding Addiction (St. Martin’s Press, upcoming). Maia is one of today’s brightest, most insightful commentators on addiction and related issues. She’s been writing articles for the popular press (e.g., The Fix) as well as scientific publications (e.g., Nature) for years. In her new book she explains addiction as a learned style of thinking, a coping style that isn’t working, or a developmental disorder — a rigid system of behaviours and beliefs cemented together over development. Her focus is mainly on trauma — hurtful, often devastating events impacting on the lives of children/adolescents and/or their families. Yet despite (or maybe because of) this emphasis on environmental forces, her explanation of genetic factors is as smart and as accurate as they come.

The Big Three.

There are really just THREE things to keep in mind:

1. Yes, heritability can be in the 50% range for many different addictions. That means that identical twins (with the same genetic makeup) share a strong inherited tendency to become addicted. Specifically, if one twin becomes addicted, there’s a 50% probability that the other one will too, and the commonality has to come from their parents’ DNA (and possible “epigenetic” influences too). The rest of that 100% is made up of environmental factors.
2. This 50% figure is actually very typical of personality traits in general, such as the famous “Big Five” traits, like sociability or extroversion.
3. And yet the 50% figure for a genetic influence on addiction does NOT come from any single trait. There is no such thing as an addiction trait or addictive personality!!!

So how do we explain that 50%?!

Let’s say you and your brothers have big noses, or bad teeth, or muddy coloured eyes… And let’s say that this tendency comes from your shared DNA — which would not be surprising if it’s a trait you all share. Because you all carry the “big nose” gene, your chances of getting hot dates in college are diminished. You each have a strike against you.

Now let’s say that another set of brothers (or sisters) is congenitally shy, or has poor colour vision and thus poor taste in clothes. These are other genetic factors that might increase the risk of sitting home alone on Saturday night.

So we’ve got at least two radically different genetically-loaded traits that predict the same outcome. If we were doing a study on genetic factors that contribute to a diminished social life, both traits would show up as predictive. And if each one correlated 50% with its appearance in a twin brother, then it wouldn’t matter that we pool them together in our study, because genetic studies always pool individual traits and add up how much of any outcome is shared by family members (specifically,  family members living apart, since that’s the only way to isolate the contribution of genetics).

The last thing to note is that, if you were unfortunate enough to carry the colour-blindness gene and the big nose gene, then you and your sibs would have an even higher chance of a disappointing sex life, unless these traits happened to work together in a particularly charming combination (Leonard Cohen?) And even though that’s very possible, it wouldn’t matter much. Genetics is sort of a dumb science and all it cares about are averages.

So what traits predict addiction?

Several. The strongest predictors are (1) an impulsive or antisocial personality style, and (2) an anxious, overly-sensitive, perhaps OCD personality style. Note that these personality clusters are almost perfect opposites: the brash, uncaring person vs. the anxious, neurotic person. In fact, they may be based on opposite extremes of certain ingredients in the chemical recipe of personality: too much dopamine or too little serotonin for the anxious kid; too little dopamine or too much serotonin for the impulsive thrill-seeker (who needs to try harder to feel excited). Yet both these traits increase your odds of becoming an addict, and both are (partly) heritable. Which is to say they are shared between parents and children and between siblings (who carry much of the same DNA).

According to Maia Szalavitz in her new book, there’s a third heritable package that strongly predicts addiction: a combination of  reckless drive on the one hand and sensitivity to failure or loss on the other. Maia says that this disposition was her royal road to addiction, and I believe it was mine too. And by “royal road” I don’t mean a direct cause but a causal contributor — one variable among many. Like me, Maia is a developmental thinker, and she sees these genetic predictors as early conditions that can lead down many different roads, depending on environmental circumstances.

Next post I’m going to go into a lot more detail on how these very different personality styles can make one more vulnerable to addiction, and how other personality (and environmental!) factors can make one more resilient. And I’m going to remind you that these factors can interact with each other in all kinds of interesting ways.

Hello my lovelys! I’ve been thinking of you. Actually I thought of you mostly last night, New Year’s Eve, when my own addictive tendencies and my self-concept as someone who can drink alcohol safely (and socially) growled at each other for a little while.

I feel grateful that I’m no longer at the cliff edge that once defined my existence. We’re all at various distances from that scary place, some on the brink, caught by sudden vertigo when we look over the edge, others living on the flatlands, far from the escarpments that were so familiar. But we recognize each other as members of the same tribe, connected through experiences that others view as ugly, perverse, or mythical.

I feel particular empathy for those who are torn by temptation and confusion at a time when everyone around you seems to be having a good time. If there’s anything I can say to all my readers, some kind of ad-hoc post-modern blessing that would make sense to all of you no matter where you’re at, it’s this:

Accept and forgive yourself for wherever you are. You got to where you are through a sequence of events and experiences that no one else has encountered. Wherever you are and whatever you’re doing, enjoy, be safe, and see who you are now as a natural product of where you’ve been, en route to where you’re going. If sadness and loneliness are part of the picture today or tonight, take them in stride, with some humour and some optimism. If you’re with others, take stock of that magic — it doesn’t all have to come from you. This is probably not the last day of your life, but it’s an important day — the bridge between where you’ve been and where you’re going. Give yourself a warm hug whether or not you’ve got others to second the motion.

Happy New Year to all of you!