Hello! It’s been awhile. This is vacation time in the Netherlands. The kids are out of school for two weeks and we’re trying to do family-type things. I know, it’s a strange time to vacate, but the weather here is so spotty, this might be one of the few periods likely to get some sun and warmth.

So I thought! Last Saturday we rented a boat. A very large boat (11.5 meters/ about 38 feet) with cabins below deck and all that, and the four of us set off from a town called Sneek (pronounced Snake). Well named, because the waterways leading out of the harbour were so incredibly narrow and sinewy that we got lost before we ever got to the main canal. Ended up in some cul-de-sac where an irate man with a house on the water kept waving us away. That’s because we kept almost ramming his house, which was very close to the shore. We were trying to make a U-turn in a narrow spot — just about impossible, especially because I had not yet discovered the “bow-thrusters” among the many Dutch-named switches on the instrument panel. When he finally realized that we didn’t understand a word he was saying, he started again in English: “Practice!” he yelled. “Go on the lake and practice!”  Yes, yes, an obvious suggestion. If only we could find the lake.

Anyway, we had a lot of fun. Isabel and I mostly sitting up on the top deck sharing a big steering wheel, watching the cows and sheep going by, and the boys down below, playing cards, with occasional sojourns to the upper deck to help steer. As I am constantly reminded, seven-year-olds don’t want to watch; they want to do. But it was cold out! Polar winds blowing through us except when we were huddled under this massive flapping plastic tarp. Oh well, it was still great, and we didn’t hit a thing in four days. Well maybe just a few tiny bumps. Tiny!

Isabel and I are going to drive over to France in a couple of days. It’s only a few hours, and it’s worth it just for the food. But meanwhile I have two talks to prepare, and one of them is a TED talk. Yes, TED! I was invited to join this TEDx event held at my university, and I’m getting pretty jazzed about it. The theme of the conference is “trust,” so naturally my talk will be about trust and addiction.

At first, I wasn’t sure how to approach this topic. You can’t trust an addict, right? How do you know an addict is lying? Because his lips are moving… Hah hah. No, wait a minute, how about…addicts can’t trust the treatment community? We know that people are almost always let down by their experiences in rehab, whether in- or out-patient, and so much of the treatment world is dominated by 12-step philosophy, which is certainly not for everyone (right, Persephone?), and a 30-day stint of treatment is about as useful as a bath during a dust storm, and the revolving door of addicts coming in and out is closely matched by that of the treatment staff, who come and go at an alarming rate themselves, and most of whom really don’t have the knowledge or the credentials to help people in serious trouble. The general public can’t trust addicts, addicts can’t trust public institutions..etc, etc… Could that work?

But is seemed a bit superficial, a bit too obvious, no real bite to it. And then, about two weeks ago, it hit me: The main issue with trust and addiction is that addicts can’t trust themselves. Of course! You can’t trust yourself to take care of yourself. Because, when you tell yourself you’re going to stop, or at least slow down, or at least stop injecting, or whatever it is, and swear up and down that this time is the LAST time, and it will NOT happen again….you end up betraying yourself. Time and time again. Why would you trust yourself after you’ve let yourself down 50 or 500 times?! But it’s worse than that: you hardly even have a self to trust. You (or I) lose the sense of a grown-up conscientious self that can soothe you, hold you, get you through the rough times, tell you that it’s just craving and it will not last forever… That self is so damned hard to find after a while that you stop believing it exists. No, you can’t trust yourself. (And surely, as a consequence, no one else can trust you either.) So who/what do you end up trusting? Your addiction, of course! You trust that a hit of smack or a bottle of vodka or a few grams of coke or yet another roller-coaster ride of sex or gambling or that bowl of chocolate ice-cream or even the glazed eye of your computer screen will make you feel better. At least for a while. And it might. For a while. We put our trust in the thing we’re addicted to…because there is no one and nothing else to trust. And of course, of course, each time we do that, we lose even more ground with our self. The ability to trust ourself takes yet another soul-crushing hit. Vicious circle. And how.

This TED talk thing makes me nervous. I have to stand on a stage in front of 1,200 people, knowing that every move I make, every sound I utter, will appear on computer screens all over the world and become inscribed in the holy scrolls of YouTube for time immemorial. With no notes! No powerpoint slides at my fingertips to remind me of what I’m trying to say. Not even a podium to hide behind. Scary!

But I think I have a good talk. I’m going to present two psychological phenomena that make it particularly hard for addicts to trust themselves: ego fatigue (see previous posts) and delay discounting (the tendency to place way too much value on immediate rewards, at the expense of long-terms gains….like, oh, keeping your marriage or your job intact — a result of that dopamine/craving wave). I’ve got it down in my head, why these phenomena stack the deck against us. And why that makes it just so hard to quit. I’ve practiced it in the car. And once in front of Isabel. It’s going to be good.

And I’m going to practice it with you. Next post. Stay tuned.

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.

Yesterday I watched “Ben is Back” — a recently released feature film about a heroin-addicted young man (Lucas Hedges) and his heroic and tenacious mother (Julia Roberts) who tries her best to keep him “clean.” Ben is around 20 years old (at which age I too was also shooting heroin). He scams a trip home from his residential rehab so that he can spend Christmas with his family.

Ben seems to be trying with great determination to keep away from drugs. Yet the demon of addiction is doing pushups in the parking lot, just as they warn at the 12-step meeting he attends with his mom. He finds a bag of dope in the attic, but manages to avoid taking it and gives it to his mother instead. He looks the other way when dealers and drug buddies from his former life show up magically on elevators and at car windows. He bravely endures the cultural ambiguity of an American Christmas and tries his best to connect with his sibs and step-sibs. He’s a good guy, and he fights the good fight, but…well I don’t want to spoil it in case you decide to watch it.

I thought it was a pretty good movie (I love Julia Roberts) with a half-assed ending, but there were a few impressions I want to share with you — impressions that epitomize a lot of what’s wrong with the mainstream perception of drug addiction.

Although the subtext of the movie is clearly the overdose epidemic, there is hardly a wave at the real causes of overdose deaths: fentanyl in street drugs, drug/alcohol/drug interactions among pharmaceutical users, and impediments to getting methadone or suboxone when needed. (However, to its credit, the film provides a snapshot of the lunacy of pharmacies unwilling to dispense naloxone.) See Maia Szalavitz’s excellent synopsis of what we’re thinking and doing wrong.

Instead, the usual “Reader’s Digest” simplifications are offered. For example, Mom meets the doctor who first prescribed pain pills, which got Ben “hooked” years ago, and says she hopes he dies a horrible death. We know that the OxyContin surge in the 80’s and 90’s did increase exposure to opiates and fueled increased rates of addiction. But to continue to blame doctors is insane. As Maia Szalavitz (and I) have made clear with arguments and statistics, doctors aren’t the problem, and the result of blaming them is the cutback of pain meds for people who really need them, while driving addicts to the street — to heroin that’s laced or replaced with fentanyl.

The 12-step presence is portrayed somewhat accurately. Both the good (fellowship, honesty, and mutual respect) and the not-so-good (brain washing, propaganda, and the all-or-none trappings of the disease model) correspond well enough with reality.

There is some recognition that addicts have choices. Ben fights his impulses bravely, and he makes sensible choices to avoid contact with the people and places that serve as triggers. And yet there is this creepy sense of fatalism sneaking up on Ben and other addicts. As though whatever choices they think they’re making, they’re bound to succumb. By the way, addiction isn’t referred to as “a disease” in this movie. Yet the miasma of an alien presence or infection lurks behind much of the dialogue and plot.

Junkies are portrayed as zombies. They are the opposite of clean. They’re dirty. They hover in alleyways, under bridges, around trashcans brimming with burning litter. It’s a classic and grossly overdone stereotype. When I was shooting heroin or morphine in my twenties , garbage-strewn alleys and river banks were not my preferred home away from home.

Despite the biases, stereotypes, and omissions, the movie does portray the struggle to avoid temptation rather well. And despite the Hollywood heroism and unlikely confrontations between good and evil, the plot and characters are engaging. The movie may well be worth seeing.

But here’s my biggest beef. People who take drugs are shown to be occupied by some demonic force (or disease, or what have you) that makes them another species. They are not anything like normal people. They live in a different world, they’re not to be trusted, and they ought to be sent away to residential rehabs (where they won’t infect the rest of us) until the demon is exorcised — itself a rare event. This dichotomous “us vs them” perspective is the real message of the movie.

An alternative message, which I hope you’ve encountered in my posts and the comments and guest posts of others on this blog, is that people who use drugs are so crushed by emotional confusion and pain, much of which is served up by American culture itself, that they seek and sometimes find substances and activities that help them turn down the volume of their anxiety and depression and bring a semblance of balance to their lives — what I referred to as “substance” last post. The cause of addiction can be found in mall culture itself (portrayed in the movie as a sort of heaven on earth), the rampant commercialism that sucks meaning out of day-to-day life, the often immutable stamp of privilege vs. poverty and the stultifying dead-end lives of those who don’t make the cut. Not to mention the sheer hypocrisy of a society that proclaims Christian values but rewards self-serving, self-protective priorities. I wonder if Ben was infected by these horrors rather than a magical drug high, and whether that’s what made it so hard for him to quit.

By  Elizabeth from the blog….

I am very pleased to present a guest post, created by Elizabeth, who has been a member of this blog community for at least a year. Thanks, Elizabeth, for your contributions until now, and especially for this fascinating post–

The present “obesity epidemic” has given rise to public concern about the level of refined sugars, especially high-fructose corn syrup, in the North American diet.  While we can all agree that an excess amount of sugar is probably not good for anyone, more controversial questions about the “addictive nature” of such sugar intake have also emerged.  Public policy measures to curb access to this “addictive substance” (see NYC soda ban) are designed with intentions to prevent individuals from developing a “sugar dependency” and hopefully curb the rising rates of obesity.  But, is overconsumption of these sweet and calorie-dense foods really reflective of a widespread “addiction” to sugar?  Perhaps there is some truth to the matter, and perhaps we can understand this phenomenon better by looking at studies of drug intake.

Several years back, researcher Roy Wise argued that drug intake could be viewed as an “ingestive behavior.” He noted that animals who were limited to short periods of drug access at regular times throughout the day show signs of “regulated drug intake” to maintain a steady blood serum drug level similar to “regulated food intake” to maintain energy balance.  When the self-administration studies were halted, these animals displayed little, if any, signs of withdrawal.  Thus, they were probably not really addicted or dependent on the drug at all.

So what could make this regulated intake spiral out of control?

Marc has provided a wealth of information regarding the predictors of drug addiction, including the effects of stress, low feelings of self-worth, and the need to compensate by “self-medicating.”   I won’t belabor these points.  What is interesting to me is that these factors seem to aid the development of “addiction-like” drug intake in animals — when the self-administering rodents escalate their use over time, pursue the drug in the face of punishment, and show physiological withdrawal symptoms. In other words, when they seem to become addicted.

So, additional factors — beyond drug availability — may be necessary to make the “ingestion” of drugs more “addiction-like.”  Does this mean that the ingestion of foods can also be normal, versus addictive, depending on external factors?

Indeed, stress and negative self-worth also play major roles in the development of eating disordered behavior (e.g., excessive caloric restriction, binge food intake, purging, etc..).  Food and drug rewards act on the same neurotransmitter systems, so disruptions in reward circuitry can confer drug addiction and, likewise perhaps, change the meaning of food. Get this: If you want to get an animal to REALLY want to take a drug, you can deprive it of food.  This suggests that dysregulated food intake cross-sensitizes with dysregulated drug intake (kind of like how abuse of one substance can lead to abuse of another). Basically, since the brain interprets the value of both food and drug rewards through similar circuits, alterations in these circuits can cause EXCESSIVE pursuit of both.  The brain is saying “hey, I’m deprived of some necessary sustenance…give me more!  The next time I get that reward, it’s going to be REALLY reinforcing, so I will seek it harder and make SURE I get all I can!”  So, the next time drugs are encountered, we binge on them.  The next time we get access to a sweet treat, we are likely to binge on that as well.  In fact, there is a striking comorbidity between binge food intake and drug abuse.

What this means is that there can be addiction-like components to both binge eating and drug taking.  The super-sensitivity to both rewards appears to be greatly influenced by the individual’s history:  Have there been significant life stressors?  Has the individual been deprived? (Think of those with eating disorders who have excessively restricted their caloric intake in order to look or feel thin.) These factors come together to promote a sort of “super-craving” — for food, drugs, or both.

I’m not sure that these factors are widespread enough to completely explain the obesity epidemic, but they sure help put it in context.

I want to start unraveling the talks I heard, beginning with Kent Berridge’s talk. If you haven’t been following this blog or read my book, here’s some background: Berridge has made two major contributions to the study of addiction. The first is the idea that “wanting” and “liking” are independent neural systems. Wanting (or craving, as we understand it in addiction) is mostly fueled by dopamine, which is sent from the midbrain to the nucleus accumbens (NACC; or ventral striatum), a major center for goal-directed pursuit, lying in the middle of the brain, deep within the cortex and surrounded by the limbic structures. Here’s that slide once again. The NACC is represented by that yellow explosion, to convey the growth of craving over a matter of seconds or minutes. On the other hand, liking (or pleasure) is provided by — guess what? — opioids, whether they come from your local dealer or from the natural processes of your own brain (the hypothalamus produces opioids, which are critical for calming us down and relieving pain). The idea that wanting and liking are truly dissociable is pretty radical, both in psychology and in neuroscience. In the present post, I want to tell you about Kent’s recent research, as reported in Boston two weeks ago, where he demonstrates this independence — in that pristine way scientists have of breaking things down to their fundamental components.

Berridge’s other main contribution is the idea of incentive sensitization. This is the notion that particular cues or stimuli (whether out there in the world or generated from our own fantasies, memories, daydreams, etc) become strongly associated with our drug or drink of choice. And those cues — all by themselves — activate the wanting circuit. They directly release dopamine to the NACC, so that we find ourselves suddenly beset by craving, simply by exposure to a cue. The strength of that incentive sensitization obviously increases the more often we use, because the experience itself serves to reinforce the association with the cue. But I won’t discuss this further for now.

Okay, so Kent gets up in front of this group of 15 or so people, including only two other neuro people (Davidson and me). And he’s explaining his recent research with rats, in which he’s set out to show that wanting and liking truly are separate systems. He wants to get his message across to the group, of course, but the main goal is to develop a talk that will be of interest to you-know-who. He wants, we want, the Dalai Lama to say: Hey that’s really cool! Now I get how you can want something without even liking it! For Kent, and for me, this issue gets to the heart of the problem of desire — a problem which is as central to Buddhist psychology as it is to addiction psychology.

So here’s the experiment: The rat is “trained” to press a lever that delivers a sweet solution. This is a very typical “Skinnerian” learning paradigm. Rats love sweetness — don’t we all? — and it’s been shown that sugar speaks directly to those opioid-fueled cells in the NACC. So here’s a rat that has experienced liking which has led to wanting, in the very natural way that we are “trained” to go after rewarding experiences in life. So they are willing to press the lever many times over, as motivated by their wanting for the sweet taste — and as shown, through other studies, to depend on the flow of dopamine following that initial opioid rush.

But there’s another lever in the cage. When the rat presses it, just in the process of exploring its environment, it delivers a very salty taste. Kent is sitting in front of his computer, at the end of the table near the screen, and he looks up at us, wanting to get across how very nasty this liquid tastes to the poor rat. Imagine the taste of sea water, he says. Now imagine something that’s at least 10 times saltier — beyond the level of the Dead Sea. And I feel like I’m glimpsing the soul of this scientist. He is right there in the minds of his rats, trying to imagine — and communicate — what they are experiencing. Because that’s the necessary link here. The connection between experience and behavior. And if you’re studying it in rats rather than humans, you’d better be able to imagine what it’s like to be a rat. Anyway, the rats don’t need another trial to learn to stay away from lever #2. They hate what it gives them. There is no pleasure to be had there.

Now here comes the essence of being a good scientist: being clever enough to find the fracture point where you can split a phenomenon into its parts. We’ve got liking and wanting for lever #1. And zero liking or wanting for lever #2. Then the experimenter gives the rat a drug that reduces their blood level of sodium way below normal. They become salt-deprived. And now the punchline: The rats immediately go to lever #2 and start pressing like hell. Kent and his assistants have completely bypassed liking to get to wanting. There is clearly a high degree of wanting present, but there was never — not even once — an experience of liking that led to it.

Half the people in the room didn’t get it at all. So…the rats were salt-deprived. So they went after the salt lever? So what? Kent read their blank expressions and tried his best to convey what was so cool here. I sensed his disappointment. Who wants to go to all that trouble and have the punchline fall flat? The rats didn’t know they were salt-deprived, he explained. But the wanting circuit was immediately activated by something, some change in their biological state. It doesn’t really matter what activated it. The point is, wanting does not have to arise from liking. It’s an independent process, in mind and brain. It can arise from anything!

For me, the parallels with addiction were immediately striking. That sudden wanting, craving, compulsion that we experience for our drug of choice doesn’t have to depend on how much we liked it in the past — either the distant past or the recent past. You can crave something that you’ve never liked — just because, at some level, you need it. Granted, with drugs and booze, there is usually pleasure the first many times, then the pleasure fades, and after awhile there is no pleasure. Not even the anticipation of pleasure. The wanting comes from needing it, not from liking it. (Mind you, with tobacco, it seems you never have to experience any pleasure to graduate to craving.) So addiction is sort of like the rat experiment with a hunk of time subtracted out. After we become addicted, wanting has nothing to do with how much we do or did like it.

Following some questions and discussion, I think most of the group got it. You had to go right into Kent’s world — the world of a scientist as clever as he is determined. The point wasn’t what caused the sudden wanting. The point was simply that wanting and liking can be shown to be totally independent processes. Will the Dalai Lama get it? Will it help him, and the rest of us, understand something crucial about addiction?

Let’s hope so.