Here’s a little postscript. Some of you have questioned the liking vs. wanting paradigm, because these states are imputed by the experimenter. Where’s the evidence that the rat is actually feeling liking — or not feeling it, as was the case with the salt-delivery lever? Who’s to say what rats are feeling, anyway? I mean we don’t ask them to report on their inner states or to fill out questionnaires following the experiment.
So here’s a little video provided by Kent Berridge. It shows facial movements that are thought to correspond with liking — mainly based on the assumption that sugar is a natural and fundamental source of pleasure, for rats and humans both. But also based on similarities between rodent and human facial movements.
Berridge has used rat facial expressions to impute pleasure in a number of experiments. And the second expression shown — displeasure — would be what the rats showed to the salt solution, despite their strong attraction to the lever that delivered it.
Informed by unparalleled neuroscientific insight and written with his usual flare, Marc Lewis’s The Biology of Desire effectively refutes the medical view of addiction as a brain disease. A bracing and informative corrective to the muddle that now characterizes public and professional discourse on this topic.” —Gabor Maté, M.D., author of In The Realm of Hungry Ghosts: Close Encounters With Addiction
Hi Marc
Managed to catch up reading your latest posts and comments. I too love KB’s work and think it really explains a lot about addictive disorders. I think if we look at the very controversial Holmes experiments on patient B-19 we see that liking and wanting are very different! Most experiences of addiction will bare this out.
As one of the comments pointed out, and I know you agree, addiction cannot be simply explained by a single model – it is indeed a confluence of confounding factors that meet in a perfect storm to result in an addictive disorder in a particular individual. This is why I am working on a multidimensional cumulative model of addictive disorders.
Of course, all of this knowledge is only really helpful if we can translate it into treatment.
Anyway, I am hugely envious of your experience and am truly grateful that you share them in this forum, so I too may benefit.
P.S. This paper may truly turn things on their head, showing that DA may not be the only important factor, especially in the case of opioid use disorders, if it finds further research support! It concludes “The absence of detectable increased dopamine levels to both the expectation and delivery of a heroin-related reward may have been due to the impact of substitute medication. It does however contrast with the changes seen in abstinent stimulant users, suggesting that striatal dopamine release alone may not play such a pivotal role in opioid-maintained individuals.”
The paper can be found at:http://onlinelibrary.wiley.com/doi/10.1111/adb.12073/full
Hi Shaun. Good to have you back!
I’ve now read this article very thoroughly. What you emphasize in your comment is the idea that dopamine (DA) is not necessary as part of the reward mechanism underlying opiate pleasure. I think you and I would easily agree on this, and of course so would Kent Berridge, the guy who got it on the charts.
But let’s go the next step. We would still expect DA levels to rise in this study, prior to the first and especially the second heroin shot — simply on the basis of a learned expectancy. And clearly the authors tested exactly that: the role of DA in anticipation, based on previous experience. Whether we call it anticipation, or wanting, or craving, doesn’t seem all that important — or does it?! The effect should be there — and it’s not. So….why not?
The four probable explanations of the null finding (the absence of an effect) are presented by the authors, though not with much guidance as to how to think about them.
1.The heroin shots were passive — the subject knew that he didn’t have to do a thing to get his shot. So maybe DA only gets activated when drug-taking is active, not passive.
2. The PET methodology is simply too insensitive to pick up DA differences at this scale.
3. Despite what looks like sufficient statistical power, ten subjects just weren’t enough to get the effect.
4. Methadone blunts the system enough to quash or even reverse differences in DA.
It seems to me that any of these explanations would suffice. Putting together 2 and 3 is probably the simplest and most obvious. And we could throw in #4 for good measure.
But I think that explanation #1 is by far the most interesting. Could the DA system really just remain “disengaged” when you know you don’t have to do anything? When you don’t have to act — just sit on your butt and wait to be shot up. These guys are reporting feeling “high” after getting the drug, but more importantly, there was a significant drop in their “expectation” score following the disappointing second shot (of a very low dose). So that would mean that the DA signal is even more specific than we might have thought. Not only don’t you need DA to feel “high” or “pleasure” (as amply demonstrated by Berridge), but you don’t even need it to feel (what I assume would be EXCITED) anticipation of a nice big fat shot of pharmaceutical heroin. And remember, these folks have been on methadone for awhile. Pharmaceutical heroin would be a real treat!
So, an important next step would be to test this specificity hypothesis with a more reliable experimental method — not using PET, and moving beyond the small-N weakness and also beyond the possible methadone confound. If we could confirm that the DA signal is specific to having to ACT– having to DO — and that it’s really about “wanting” or yearning or craving, not just “anticipation”… then we’d be that much closer to a fine-tuned biological model of the particular urge that turns us into addicts.
Thanks for this video, it helps those of us who are interested in the human condition but not familiar with how rat research is relevant to homo sapiens. I went to hear Joseph LeDoux a couple of years ago, who spoke about fear, and his research on rats, and found it much harder to relate to than Steven Suomi’s research on rhesus monkeys.
Hi Robin. I see your point. The lower we go down the evolutionary ladder, the harder it is to imagine what animals may actually be feeling. But then there are marvelous researchers like Jaak Panksepp, who swears up and down that even rodents have emotions that are not much different from ours — plus a highly sophisticated research program to explain why.
Thanks for the detailed response Marc. As we discussed previously, my immediate thought was that the results showed that the agonist (or partial agonist in some) therapy was doing its work and blunting the effect was due to this – for me this would be a great explanation because it would show that these therapies do work by reducing expectation, and that even with the sensitised stimulus (visual and the DOC), there is a muted response.
Option 1 for me is less likely because of the visual stimulus they used. But what would be really interesting for me, if we could replicate these results in individuals who are not on substitution therapy, would be that maybe we have this whole “common reward pathway” thing wrong – that would mean that we would have to re-write the whole book on addiction and that maybe we need more specific interventions based on the class of drugs used.
I am just thinking out aloud here, but I would like to have a closer look at this and any similar studies (if there are any). I read that they could only get ethical approval for patients on OST – pity!
As for options 2 and 3, they are far less interesting!