On Naked Neuroscience, James Tytko learns about the traits shared by extremist individuals with the help of political neuroscientist Leor Zmigrod. Also, how the genetic predispositions of your peers could change your risk of developing certain psychiatric conditions. Plus, how a new sleep therapy could be about to revolutionise how we help people recover from PTSD...
In this episode
- Sleep sounds reencode traumatic memories for PTSD patients
Sleep sounds reencode traumatic memories for PTSD patients
Hein van Marle, Amsterdam UMC
Post traumatic stress disorder, PTSD, is a psychiatric condition where, upon suffering a traumatic event (a car accident, for example) a portion of people form traumatic memories which continually resurface. They may get intrusions during the day, or in nightmares, where they re-experience the same event with similar levels of fear and arousal as when it actually happened.
Hein van Marle is a psychiatrist and neuroscientist at the University Hospital in Amsterdam. He uses psychotherapy to treat PTSD patients, helping them reencode their traumatic memories so they’re less troublesome. He’s working on an innovative new method to improve treatment using the neuroscience of sleep and its role in memory storage.
One of the methods of treating PTSD involves using auditory clicks to help patients reprogramme traumatic memories. It’s called eye movement desensitisation and reprocessing (EMDR.) By playing targeted clicks to patients while they sleep, at times when the parts of the brain associated with memory formation are most active, it’s thought they could make the therapy sessions more impactful.
James Tytko started by asking Hein how the current gold standard treatment - EMDR - works…
Hein - It's a form of exposure based psychotherapy where the first step is that you reactivate the traumatic memory. The patient revisits their traumatic event and then different things can happen, but with EMDR, technically, we tax the working memory of the patient by giving them all kinds of sensory stimulations.; they have to follow a light that goes from left to right, or they listen to clicks, audio clicks, or they have to do maths. The effect of that is that the normal fear and arousal that they experience when they have a flashback, or even a nightmare, that doesn't get any room to happen because their brain is very much occupied with all the things that you let them do. That results in the fact that the memory gets re-encoded again in the brain in a more neutral form, in a form that is associated with less fear and arousal.
James - I guess it must be pretty draining for the patients to go through this therapy and to live through the source of this trauma over and again if they're having repeat sessions.
Hein - Yes, that's definitely true. On the one hand, you can say that psychotherapy in PTSD is to a certain level quite effective. On the other hand, it's also very demanding for the patient because basically every cell in their body says, 'I don't want to go back to that specific moment,' and then they have to. Our research is focused on ways to augment the trauma treatment and for this we use the time window of sleep. Sleep has a very important function in the long term storage of memories. What we do with this experiment is that we try to use a new technique from neuroscience that is called targeted memory reactivation. It works that if people form a new memory during the day, they learn something, then you pair that learning experience with a sensory stimulus like a sound or a smell maybe. Then, when people are asleep, then you again present that same sensory stimulus, the smell or the sound, and that biases the brain to process that associated memory in a prioritised way. This therapy called EMDR that we just explained, we use an auditory click that is already part of the normal standard therapeutic procedures, but for us the click can also be used at nighttime to present again and to use as a cue in order to strengthen the consolidation of the treatment memory.
James - Did you have concerns, with the limits that exist in our understanding of memory, the brain and sleep, that, by inducing the re-encoding of these memories while the patients were sleeping, you might see unintended consequences?
Hein - On the neuroscience side, people were very hesitant to use this in real patients with real traumatic memories. Nobody knew what was going to happen. Are you going to trigger nightmares? Are patients going to get more symptoms? But I think we had a very strong team of both hardcore sleep scientists and psychiatrists. We felt safe enough to do this. Then we saw that it was actually a safe procedure. We didn't induce any extra nightmares, we didn't induce any extra symptoms. Also it was technically feasible to do.
James - That's obviously a very positive step, the fact that this innovative treatment is safe and feasible. What about the findings, though, more concerned with what you were looking for, which is the brain activity involved with memory formation while the patients were sleeping conjured up by the triggers, the noises, that you'd worked on with them in previous therapy sessions?
Hein - We had two groups. All the patients got the EMDR session at nighttime, then they all went to sleep in the sleep lab. Half of the patients got the TMR cue during the night and the other half patients did not get any cue during the night. Then, when we looked at the brain activity, because we measured their EEG during sleep, we saw that the TMR cue induced an enhancement in the brainwave activity that is mostly related with this process of memory consolidation. These physiological sleep phenomena are very much linked to the process of memory consolidation. We saw that by giving the TMR cue during sleep we evoked the sleep phenomena in a more profound way than in the control group. Then we saw, within the TMR group itself, a correlation with these induced sleep phenomena and the reduction in PTSD symptom level. But we didn't see, however, that is important to mention, a clear difference between the TMR group and the control group. So the TMR by itself didn't result in less PTSD symptoms than the only EMDR group.
James - How do you assess that final finding? Is this a case of you need to go back and tweak the experiments to time the targeted therapy differently or to do more of it to see a greater benefit?
Hein - This effect that we saw the TMR induce, the sleep physiology changes that are related to consolidation, is basically a sign for us that we're on the right track. We're doing something that does something in the memory processing up to a level that it reduces the PTSD symptoms. Our next step will be that we're going to basically have a repeated application of the TMR and we are hoping that by this repeated application that we get a cumulative effect and that we'll be able to really create a difference and a benefit of TMR as opposed to the control group.
00:56 - Peering into the brains of political extremists
Peering into the brains of political extremists
Leor Zmigrod, University of Cambridge
The fatal stabbing of three young girls at a Taylor Swift dance class in the seaside town of Southport in the North of England has prompted some of the worst unrest the UK has seen in more than a decade. The violence, in towns and cities across England and in Northern Ireland, was fuelled, in part, by online misinformation, and was perpetrated largely by far-right and anti-immigrant groups. But what exactly causes extremism in the first place?
Leor Zmigrod is a researcher who explores the complex biological and environmental factors which contribute to why some people hold extreme views. A ‘political neuroscientist’, she explores these themes in her upcoming book ‘The Ideological Brain.’ I caught up with her to discuss her work, putting it in the context of recent events…
Leor - One of the challenges that we have when we think about extremism is we're very dependent on people's words and people's reports. That's usually how scientists or social scientists measure what makes people likely to hold extremist views, it's by asking them to tell us what they feel, why they feel it. But what neuroscience can offer us is the chance to explore what they don't tell us, what they can't tell us about themselves, the kind of cognitive processes that are taking place maybe while they're thinking about their ideologies or while they're not thinking about politics at all, but can give us a sense of how they approach the world, how their brains process information stimuli. Through that we can get an insight into these invisible processes that we wouldn't be able to tell with other methods.
James - We're talking in the wake of some civil unrest in the UK that's been perpetrated by right wing political movements. Is what you're going to tell me about the characteristics of extremist brains applicable across the spectrum?
Leor - What we're finding when we're looking at the traits that make people susceptible to holding extremist views is that there are some traits that predict what might predispose someone to any extremist ideology regardless of its mission. Those can include factors like people's cognitive rigidity, that's how inflexibly they process information about the world. We test that by looking at how adaptably they behave in response to changing environments or changing rules. We can give them neuropsychological tasks that measure how well they adapt when the rules of the game change and we see, across a huge set of ideological persuasions, that people who are more cognitively rigid tend to hold ideological views more extremely: they're more willing to endorse violence in the name of their ideology regardless of what it is. There are also traits that predispose someone more towards a conservative view, a more liberal view, or different kinds of ideologies. There are traits that also affect the tilt of whether you're leaning to the left or to the right.
James - Interesting. Let's stick for now with those traits that are more applicable across the board. Rigidity you mentioned, what other traits are part of the broader picture here of extremism?
Leor - Cognitive rigidity is one factor that we see when we look at how people reason and make decisions, but we can also look at their emotions. What we find is that people who tend to endorse violence in support of their ideology tend to actually be quite emotionally dysregulated. They tend to be more impulsive in their decisions, they tend to be more seeking of thrills and sensations that are new to them. When we measure this, we're not looking at their political emotions, we're looking just at their emotional habits in everyday life. Someone who tends to generally be more emotionally impulsive, seeking those thrills, also tends to search for them in the political realm.
James - Risk taking, thrill seeking, impulsivity. These are things we might associate more with men?
Leor - We find that men are more likely to endorse violence in the name of their ideological group, so they hold more violent extremist group views in general. Whether that's mediated through differences in risk taking, I don't know if we have evidence for that, but there is a gender component.
James - How powerful are psychological factors related to collective action and group think in extremism?
Leor - Studies that have looked at what motivates people who have been convicted for ideologically driven crimes or terrorist acts in the US, whether those are for the far left, far right or Islamist ideologies, all of them are united by the fact that in their recent history they'd experienced some kind of isolation or alienation or they'd been rejected, whether that's romantically, financially they'd had some kind of trouble; and so we do see that the way in which people experience their private lives leaks into their collective action decisions very, very strongly. Sometimes those psychological factors are stronger predictors than demographic factors that we might think of such as age, education level, gender, which is why we need a psychological lens on this rather than just breaking things down according to demographics.
James - Another very pertinent feature of recent extremist riots and so on has been the social media component. Is the way those platforms are designed, does they facilitate the extremist brain?
Leor - When we look at the way that social media platforms are designed, those algorithms that facilitate the circulation of information, we see that the information that gets most circulated is emotionally dysregulating information, either incredibly positive or incredibly negative. That facilitates this very bizarre and scary situation in which the most vulnerable minds psychologically, when they encounter misinformation online, are likely to encounter the kind of misinformation that is most likely to trigger them towards extremist thinking and rigid thinking. That's why we have to think very carefully about how our social media platforms and how information is propagated when we're thinking about the intersection between vulnerability and technology.
James - How does your work, your research into understanding cognitive rigidity, emotional dysregulation, etc., these extremist traits, lead us to be able to reduce the harms perpetrated by extremist ideologies?
Leor - Through this research, we're also learning about the kind of characteristics that make people resilient in the face of misinformation, in the face of dogmatic ways of thinking. What we're learning is about the value of flexibility, of emotional resilience, and to think about how we can nudge people or help those traits get expressed in people who are more vulnerable. In many ways, although this is a cognitive psychological, somewhat biological lens, it does not assume that things are fixed. People can and do change their levels of flexibility, of openness, and that's what we as a society need to think about: well, how do we open people up so that they can evaluate information in the most flexible, balanced, evidence accepting way?
08:10 - Genes of school friends may influence your psychiatric fate
Genes of school friends may influence your psychiatric fate
They say you can’t choose your family, but you can pick your friends. Research from Rutgers University suggests that secondary school aged children best choose wisely.
Jessica Salvatore works in the burgeoning field of socio-genomics. Flipping the nature/nurture debate on its head, it argues that we can think of the environment we grow up in as having a genotype of its own. This, she argues, is a much ignored determinant in our risk of developing psychiatric conditions in particular.
The new study, published in the American Journal of Psychiatry, found that the genetic makeup of adolescent peers may have long term consequences for individual risk of anxiety, depression, and substance use disorders…
Jessica - We know that from a number of studies peers play a particularly important influence on the risk of developing psychiatric and substance use disorders. What we were doing in this study was bringing a genetic perspective to this question: how do our peers, their genetic predispositions, influence risk above and beyond the peers' behaviour itself? What our collaborative research team did was we used Swedish national data to define schools that people attended as well as the neighbourhoods that they lived in growing up. We were able to characterise then the genetic risk carried by one's peers across these both geographical and school-based levels in adolescents
James - With these conditions it's a complicated picture to put it mildly with regard to what specific genes are associated with them. So how did you index someone's genetic risk for you to then study how this related to health outcomes for their peers?
Jessica - Using what we call pedigree based information. Individuals risk for disorder based on the number of people in their extended families who were affected by these disorders, so an individual who has a number of first degree relatives who are affected by, say, drug use disorder, alcohol use disorder, that person would have what we call a higher family genetic risk score, and then mapping individuals to peer groups to look at peer social genetic effects.
James - We know substance use disorder, for example, has genetic and environmental risk factors, so I trust you controlled for family socioeconomic factors when drawing your conclusions, given that you had access to their address and so on to go off?
Jessica - Absolutely. What we found was, in fact, the genetic predispositions of peers in adolescence was associated with a target individual's likelihood of developing alcohol use disorder, drug use disorder, major depression, or anxiety disorder later on in adulthood. One thing that I also want to mention is that these peer social genetic effects were statistically robust even after we controlled for whether or not the peers were themselves affected by these disorders. So of course, one natural explanation for how peers' genetic predispositions might influence our own outcomes is that the peers at higher genetic risk might also be more likely to develop these disorders themselves, which is in fact correct. But even after we statistically control for whether or not the peers were affected, we still see an association between peers, genetic predispositions, and our target individual's likelihood of developing disorder in adulthood.
James - And were your findings consistent across the conditions you studied: depression, anxiety, substance use disorder?
Jessica - That's actually one of the interesting nuances in these data, which is that we did find peer social genetic effects across all of these disorders, but the effects were stronger for what we call our externalising disorders: that's alcohol and drug use disorder, compared to what we call our internalising disorders: major depression and anxiety disorder. This finding is actually quite consistent with the broader peer influence literature where other research groups have found that there are stronger peer socialisation effects for these externalising disorders compared to internalising disorders.
James - Interesting. So the question becomes, how do we intervene using this information to bring down levels of these unfortunate afflictions in the population?
Jessica - What this study is really underscoring is that our environments have a genotype and that the genotype of these environments matter for our behavioural outcomes. A lot of times when we think about, ‘how do genes influence our behaviour,’ and what can we do about that, it's really thought of at an individual level: how do my genetic predispositions influence my risk? Ergo, intervention should be at the individual level. But what we demonstrate, as we've done in this study, we're going to get the strongest effects for prevention and intervention efforts when we consider social groups and implement the prevention and intervention efforts at the level of socialising units, that that tamps down on some of that disruptive behaviour that we know is an early precursor to disorders like alcohol use disorder and drug use disorder.
14:21 - Sleep sounds reencode traumatic memories for PTSD patients
Sleep sounds reencode traumatic memories for PTSD patients
Hein van Marle, Amsterdam UMC
Post traumatic stress disorder, PTSD, is a psychiatric condition where, upon suffering a traumatic event (a car accident, for example) a portion of people form traumatic memories which continually resurface. They may get intrusions during the day, or in nightmares, where they re-experience the same event with similar levels of fear and arousal as when it actually happened.
Hein van Marle is a psychiatrist and neuroscientist at the University Hospital in Amsterdam. He uses psychotherapy to treat PTSD patients, helping them reencode their traumatic memories so they’re less troublesome. He’s working on an innovative new method to improve treatment using the neuroscience of sleep and its role in memory storage.
One of the methods of treating PTSD involves using auditory clicks to help patients reprogramme traumatic memories. It’s called eye movement desensitisation and reprocessing (EMDR.) By playing targeted clicks to patients while they sleep, at times when the parts of the brain associated with memory formation are most active, it’s thought they could make the therapy sessions more impactful.
James Tytko started by asking Hein how the current gold standard treatment - EMDR - works…
Hein - It's a form of exposure based psychotherapy where the first step is that you reactivate the traumatic memory. The patient revisits their traumatic event and then different things can happen, but with EMDR, technically, we tax the working memory of the patient by giving them all kinds of sensory stimulations.; they have to follow a light that goes from left to right, or they listen to clicks, audio clicks, or they have to do maths. The effect of that is that the normal fear and arousal that they experience when they have a flashback, or even a nightmare, that doesn't get any room to happen because their brain is very much occupied with all the things that you let them do. That results in the fact that the memory gets re-encoded again in the brain in a more neutral form, in a form that is associated with less fear and arousal.
James - I guess it must be pretty draining for the patients to go through this therapy and to live through the source of this trauma over and again if they're having repeat sessions.
Hein - Yes, that's definitely true. On the one hand, you can say that psychotherapy in PTSD is to a certain level quite effective. On the other hand, it's also very demanding for the patient because basically every cell in their body says, 'I don't want to go back to that specific moment,' and then they have to. Our research is focused on ways to augment the trauma treatment and for this we use the time window of sleep. Sleep has a very important function in the long term storage of memories. What we do with this experiment is that we try to use a new technique from neuroscience that is called targeted memory reactivation. It works that if people form a new memory during the day, they learn something, then you pair that learning experience with a sensory stimulus like a sound or a smell maybe. Then, when people are asleep, then you again present that same sensory stimulus, the smell or the sound, and that biases the brain to process that associated memory in a prioritised way. This therapy called EMDR that we just explained, we use an auditory click that is already part of the normal standard therapeutic procedures, but for us the click can also be used at nighttime to present again and to use as a cue in order to strengthen the consolidation of the treatment memory.
James - Did you have concerns, with the limits that exist in our understanding of memory, the brain and sleep, that, by inducing the re-encoding of these memories while the patients were sleeping, you might see unintended consequences?
Hein - On the neuroscience side, people were very hesitant to use this in real patients with real traumatic memories. Nobody knew what was going to happen. Are you going to trigger nightmares? Are patients going to get more symptoms? But I think we had a very strong team of both hardcore sleep scientists and psychiatrists. We felt safe enough to do this. Then we saw that it was actually a safe procedure. We didn't induce any extra nightmares, we didn't induce any extra symptoms. Also it was technically feasible to do.
James - That's obviously a very positive step, the fact that this innovative treatment is safe and feasible. What about the findings, though, more concerned with what you were looking for, which is the brain activity involved with memory formation while the patients were sleeping conjured up by the triggers, the noises, that you'd worked on with them in previous therapy sessions?
Hein - We had two groups. All the patients got the EMDR session at nighttime, then they all went to sleep in the sleep lab. Half of the patients got the TMR cue during the night and the other half patients did not get any cue during the night. Then, when we looked at the brain activity, because we measured their EEG during sleep, we saw that the TMR cue induced an enhancement in the brainwave activity that is mostly related with this process of memory consolidation. These physiological sleep phenomena are very much linked to the process of memory consolidation. We saw that by giving the TMR cue during sleep we evoked the sleep phenomena in a more profound way than in the control group. Then we saw, within the TMR group itself, a correlation with these induced sleep phenomena and the reduction in PTSD symptom level. But we didn't see, however, that is important to mention, a clear difference between the TMR group and the control group. So the TMR by itself didn't result in less PTSD symptoms than the only EMDR group.
James - How do you assess that final finding? Is this a case of you need to go back and tweak the experiments to time the targeted therapy differently or to do more of it to see a greater benefit?
Hein - This effect that we saw the TMR induce, the sleep physiology changes that are related to consolidation, is basically a sign for us that we're on the right track. We're doing something that does something in the memory processing up to a level that it reduces the PTSD symptoms. Our next step will be that we're going to basically have a repeated application of the TMR and we are hoping that by this repeated application that we get a cumulative effect and that we'll be able to really create a difference and a benefit of TMR as opposed to the control group.
22:05 - Brain to Z: D is for dementia
Brain to Z: D is for dementia
D is for dementia.
Dementia is an umbrella term for a group of symptoms that affect our cognitive abilities.
People are mostly familiar with its impact on memory, but dementia can also change the way someone thinks and behaves: someone may start experiencing hallucinations, for example, or lose interest in socialising.
It’s normal for our cognitive abilities to change as we age, but dementia is more severe than occasionally forgetting something. People with dementia can’t carry out ordinary tasks of the day without help, and their symptoms are progressive, which means they will get worse over time.
Dementia is not a disease itself. Instead, it is caused by diseases that damage the brain. 55 million people worldwide are thought to be affected.
Alzheimer’s disease is cited as being responsible for 70% of dementia cases. Its causes are complex, but a key element is the build-up of misfolded proteins in the brain, one of these a form of amyloid. If these substances clump together, they form plaques and tangles which disrupt the normal functions of brain cells.
In 2022, putting an end to decades of failure, the first drug treatment for Alzheimer’s showed success in slowing cognitive decline in large scale trials. Lecanemab works by attaching itself to sticky beta amyloids which have collected around the neurons of Alzheimer’s patients. Then, it attracts the body's immune cells to break down the harmful clumps.
While the effect of lecanemab was recorded as statistically significant, it is still relatively small.
There are also those who say the benefits of lecanemab do not counterbalance the risk of serious side effects like bleeding and swelling in the brain. It’s also extremely expensive, costing about £20,000 per patient per year in the US.
Writing in The Journal of the Alzheimer's Association, Carol Brayne, Professor of Public Health Medicine from the University of Cambridge says that, “While the current amyloid immunotherapies may show a glint of promise for very selected groups, it’s clear these drugs will not address dementia risk at scale.”
A sobering conclusion, and recently The European Medicines Agency has rejected a licence for the drug, but the US Food and Drug Administration has licenced lecanemab, and another amyloid immunotherapy, donenemab.
Despite this, the fact that it works at all has been seen as a huge step forward in treating Alzheimer’s by some. Here’s Will McEwan from Cambridge University’s UK Dementia Research Institute speaking on the Naked Scientists…
'These are not the ideal drugs. These are not the drugs that will be prescribed in 20 or 30 years, but they will be the turning point. They'll be seen as the moment where we know that this is ultimately a treatable disease.'
Comments
Add a comment