The Neuroscience of Relapse
RELAPSE PART 1: ROMANTICISING ALCOHOL
One question I see asked a lot within the recovery community is, “How long does it take for your brain to return to normal when you quit drinking/drugging?”. The answer I see given most often is one year, but like anything to do with the brain, the answer isn’t that simple. The truth of the matter is, some recovery of normal function will occur within 24 hours, whereas some synaptic pathways laid down during addiction may never change within a lifetime. This isn’t reason to despair – remember that every time we learn something/make a memory, there are changes in the brain that accompany that. So all the learning that occurs in addiction, such as all the associations between relaxing and drinking for example, or even between the label on your favourite brand of beer and getting drunk, those associations might potentially last for a lifetime. This is why you might hear old-timers 20 years into recovery suddenly reporting a craving after catching sight of a beer they used to drink, or the thought or drinking seeming to randomly pop into their head when celebrating an occasion or milestone.
I say this isn’t reason to despair, because we do a lot of learning in recovery too. We form new associations, new coping mechanisms, and new habits that counteract the old ones. All of these changes are also associated with plastic changes in the brain, such as new synaptic pathways, and the increased/decreased likelihood of an existing pathway firing. So what I’m saying is, we can and do change our brains for the better as we go through sobriety. Unfortunately, however, this learning isn’t always enough to prevent a relapse, although I do believe that through relapse we also learn, as I will explain.
As I mentioned in my first blog post, I have had a few relapses since I made the decision to quit drinking for good, perhaps 4 or 5. Perhaps 2 of these relapses have involved drinking over a few days, whereas the others were only a single day. In the recovery community it is often stated that relapsing is part of the journey, and I think that this is one area in which the science and recovery wisdom match up. Before I explain why, I want to say that I really don’t want anyone reading this to use this information as an excuse to relapse. I can’t have that on my conscience!! I am JUST talking about what I have learned from the relapses I have already had. I DO NOT intend on relapsing again ever.
In fact, whilst I was writing the first draft of this blog, something happened that really drove home to me how dangerous relapse can be. One of the lovely men in one of my online recovery groups relapsed after many, many years of sobriety, and he died. It actually makes me really sad to write that sentence, because although there are around 5,000 people in this particular group so it’s hard to know everyone, I had had some really lovely chats with this man. A lot of us had, and he had written a book as well as given an interview for a podcast, so a lot of us felt like we knew him. So of us did actually know him.
So PLEASE don’t read this and relapse! Don’t do it. OK? OK good thanks for that.
What does it mean to say relapse is a part of your journey?
When it is said that relapse is a part of your journey, it’s hard to know exactly what is meant. Like anything in recovery, it probably means different things to different people. I think part of it is probably intended to take the shame out of relapse. I see in the groups that people seem to suffer great shame when they relapse, and are very hard on themselves. If they can turn around and take the positives out of the experience, then it removes some of the shame. Also the identification of the fact that relapse is something most of us experience helps remove some of the shame. Personally I have never felt shame about my relapses, because I focus on how much sobriety I have had over the last year. A hell of a lot more than I had the year before that, that’s for sure! But I’ve also learned a lot from each and every incidence of relapse.
Incubation of craving – otherwise known as ‘romanticising of drinking/drugging’
My first relapse was a glass of wine I drank at a wedding, and it was because I was hungry. I was also angry, or “hangry” more accurately, and “Hungry, Angry, Lonely, Tired” are the common signs to watch out for in relapse. I was suffering two of them. OK, don’t to to weddings hungry. Lesson learned. My second relapse was at a 40th birthday. I didn’t start drinking until 10pm. I was stressed, and anxious, and lonely and wanted to hang out with my friends. Next time go home, post online, write. Wait until the morning and give my husband and daughter cuddles. Lesson learned.
The third time was different. I was stressed and working far too much, but that wasn’t the reason for the relapse. I had started romanticising drinking in my mind. I would see a glass of wine and I could almost taste it on my tongue, and it tasted like heaven, like nothing I’d ever had before. I started imagining this ‘old’ world in which I could drink and escape from all my problems for a few hours (never mind that alcohol was the thing causing a lot of these problems, and never mind that for the last few years it didn’t offer much of an escape anyway).
*Warning sciencey bit*
In the behavioural neuroscience literature this romanticising of drinking/drugging is known as ‘incubation of craving’. We can model this in rats. Of course we don’t know what the rats are actually thinking or feeling, but if a rat or mouse are trained to press a lever for ethanol (alcohol) or cocaine for example, and when the animal receives the drug, a light in the box will also turn on. If you then don’t give the animal the drug for 24 hours, then allow them to press the lever for the light they will press less than if it had been 3 weeks since they last had the drug. Similar effects have been shown when animals are tested 6 months later, which is a quarter of the lifetime of a rat or mouse, so these are long-lasting associations.
From this work we know that within the nucleus accumbens, there are changes in the way that neurons communicate with each other via synapses, and even the way in which particular neurons receive messages from other neurons, after long periods of withdrawal from drug. These are long-term plastic changes in the nucleus accumbens; specifically the way in which various types of glutamate receptors respond to neuronal inputs (see diagram of gluatamatergic synapse below). In this way it has been shown that addiction involves more than just dopamine as is commonly thought, but also involves changes in glutamate transmission, glutamate being main excitatory neurotransmitter of the brain.
What is especially exciting about this research is the possibility of developing medication that could specifically target these (metabotropic) receptors that have specific effects in incubation of craving weeks and weeks after withdrawal to prevent relapse. But that is still a way off into the future.
*End Sciencey bit*
Similarly, in my personal experience I found that after getting over the initially strong cravings, I honestly didn’t think about drinking that much. I thought I was cured! Yet at around the 4 month mark suddenly I would walk along the street and see someone in a café drinking a glass of wine out of the corner of my eye and it was like everything else in my vision went dark and I could only see the wine. I could almost taste it in my mouth and it tasted like heaven. I could feel the warmth as the wine trickled down my throat into my stomach, and I missed it. A lot.
I resisted these cravings for a long time, but then came a particularly stressful time at work and I couldn’t resist any longer. I needed a mental escape from my life. So I drank.
RELAPSE PART 2: WHEN REALITY DOESN’T MEET EXPECTATION
When I gave in and drank, surprise surprise, it was not as good as I had imagined. It didn’t taste as good, it didn’t make all my problems magically disappear, even for a little while (duh) and it just made me feel a bit fuzzy in my brain! After 6 or so months of being relatively clear-headed, I really did not like this feeling at all. I experienced what, in behavioural neuroscience, is known as ‘prediction error’ – the ‘error’ between predicted and actual outcomes. In other words, the reality of the alcohol I drank did not match up to the romanticised representation of drinking alcohol I had been imagining in my mind.
Of course like a trouper I didn’t stop drinking there and then, but instead I drank for a few more days, then stopped again, then repeated the whole pattern again a couple of weeks later. Unbelievably, it STILL didn’t match my expectations, and still didn’t cure all of my problems! I know, shocking right?
*Warning Sciencey bit*
In science, the common wisdom is that when there is an ‘error’ between predicted and actual outcomes, learning occurs. In fact, this is the process that has been shown to be most closely aligned to phasic (i.e. ‘quick’) dopamine firing. In my case, I experienced negative prediction error, meaning that the outcome (alcohol) I predicted was more valuable than the alcohol I actually experienced. When there is negative prediction error, we start to unlearn associations between stimuli/contexts/internal stimuli and alcohol, and I’m pretty sure this is what happened with me. I realised that the outcome was not as valuable as I had expected, so when I saw things/thought things that had previously triggered me to drink, that triggering was now vastly reduced. So much so that my last relapse honestly ended with me leaving half of the bottle of wine I was drinking halfway through because I just wasn’t into it. Something that NEVER would have happened a year ago.
*End Sciencey Bit*
So I think this process worked, because since then I have not craved alcohol. Glasses of wine have stopped jumping out at me when I am around them. I have been to several dinners with people drinking and haven’t even paid attention to their drinks. This is progress!
However, although I can be pretty arrogant, I am not so arrogant to believe that I will never experience a craving ever again, or begin to romanticise alcohol in a way that is not realistic. In fact, science also supports the notion that these associations between cues and alcohol are still there lurking underneath (it makes sense for the brain to retain information about things that predict reward, as I’ve talked about previously). Also of course there’s the possibility that the craving will incubate again, or that times of very high stress will cause cravings again. But I am hoping that I have learned enough to remember that alcohol doesn’t really provide an escape, or taste like heaven, or solve world hunger. It just makes me feel fuzzy in the head.
*Warning Sciencey bit*
As mentioned, it is this process (prediction error) that is linked to dopamine firing, although more recent research suggests that this function is confined to a subset of dopamine neurons. However, I have also mentioned that dopamine doesn’t straightforwardly represent a ‘reward’ pathway as many people believe. This is because if outcomes are perfectly predicted, there is no (phasic) dopamine response. You can see this below (from Schultz, 1998, J Neurophysiol), where the dopamine response is strongest (i.e. where the dots are closest together on the rasta plot) for the ‘CS’, i.e. ‘conditioned stimulus – in addiction this could be the pub, sight of glass of wine etc. When the reward is actually delivered, where it is labelled ‘R’, there is no phasic dopamine responses (i.e. the dots are the same as before and after reward delivery).
In real life terms, this means that if you are an alcoholic and you walk past a pub, then your dopamine will fire to the pub, and other cues (e.g. beer label/taps etc) that predict alcohol. When you drink the alcohol itself, however, because it is perfectly predicted by these cues, there is no dopamine firing. If dopamine was a straightforward ‘reward’ circuitry, it should spike whether alcohol was predicted or not. Rather, it is thought that dopamine in fact ‘teaches’ other parts of the brain about what stimuli to associate with reward, and therefore provides motivation or incentive to seek out those stimuli in future to maximise reward.
*End Sciencey Bit*
So as you can see, the neural circuitry of addiction is far, far more complicated than simply having a ‘reward’ circuitry or a ‘pleasure’ circuit. We still have so much to learn about addiction even in rats or mice, whose brains are far less complex than humans.
Having said all that, I really don’t recommend relapsing just so that you can learn to like drugs/alcohol less! It is not a good idea. There were a couple of times in my relapses I really felt out of control and had to email friends/my recovery coach/others and beg for help. Luckily I was able to get it back under control and get sober again, this time. Perhaps next time I won’t be so lucky and perhaps the consequences will be severe. So why play with fire? I have seen relapse lead to so many bad consequences for so many people. It just isn’t worth it.
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This post was shared to the FIX through Boozemusings Community by a Neuroscientist in Recovery https://neuroscientistinrecovery.blog/
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