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MQ Mental Health Science Meeting Live Blog

 We’re swearing to take on mental illness through research – our Mental Health Science Meeting is at the heart of turning this promise into reality. Today in London, world-class scientists from across disciplines are coming together to find solutions to mental illness. This year, their talks and discussion are focused around the emergence of mental illness. 

Follow our live blog to keep up-to-date with the discussion and join in the conversation on Twitter with #MQScienceMeeting.

Dr Sophie Dix, Director of Research at MQ, explains why the meeting can transform mental health:

Friday 3 February

15:45 Closing words, Cynthia Joyce

Cynthia Joyce takes to the stage with some closing words - "Bringing everyone from different disciplines together has made our founders' and our supporters' dreams come true."

15:00 Keynote 3: “The social environment and the brain – implications for preventing and treating mental disorders”

Chair: Essi Viding (University College London) 

Andreas Meyer-Lindenberg (Central Institute of Mental Health, Mannheim) 

Our final talk comes from Andreas Meyer-Lindenberg, discussing the potential for social environments to impact the brain, enabling us to develop a better understanding for the ways we can treat and prevent mental illnesses.

Andreas is basing his talk around schizophrenia - he suggests that different enviromental factors like urbanicity, migration and social status could influence the liklihood of developing schizophrenia. 

He firstly focuses on social status and shows a study which details that the more you earn is directly correlated to how long you live. Andreas says across different spieces there is evidence that there is a link between your social status and life expectancy. So, how is status processed in the brain?

Andreas talks about an electronic game his team produced to try and find answers to this - featuring simulated people who were either better or worse than the player. He talks about the processes in the brain which change when people lose status in the game. 

Andreas' next area of exploration is the impact that city living has on the brain. 

"There is a relatively clear dark-side to city living on mental illness." Andreas Meyer-Lindenberg

If you are born in a big city, Andreas says, your risk of schizophrenia jumps up by a third. Andreas discovered that people who were born in the city had a structurally different brain than those who were not. 

So what are the risk factors of living in a city that cause this?

"Although everyone has an opinion on what makes a city healthy, there is limited data as to what a healthy city actually is. So we decided to go - gingerly as psychiatrists - into urban design." Andreas Meyer-Lindenberg

Andreas points at the rapid urbanisation in cities, he's producing an app that track people using GPS around cities, he worked with geographers and town planners and was able to grasp a good idea of the kind of environments people were walking around in. The algortihm they produced enabled push notifications to come through on people's smart phones asking them to measure how they were feeling and their stress levels - and sometimes they ran programmes that correlated more closely to psychosis. At the end of the experiement, they did brain imaging and were able to track  what's happening to the brain. 

Andreas goes onto look at the impact that 'green space' has on the brain - focusing on an experiment that sent people on a walk in the countryside, what they saw was that people's brain images changed and they were also cognitively better. They found that this was mainly due to ruminating less - a common mechanism that's seen in depression. In conclusion, there's a suprisingly strong effect for being around nature.

For the second part of his talk, Andreas focuses on ethnic minority migration

Andreas says findings have discovered that for first generation migrants, the risk of schizophrenia is higher - if you are a child of a migrant this creeps up even more. But this isn't due to the stress of migration. It also isn't about the pre-migration state. The evidence says that this is caused by living in a society which is different from the one you were born in, in second-generation it's due to your family being set up differently to the society you're in.

He found differences in the scans of brains of migrants and non-migrants. Interviewing them, he beleives that the perceived discrimination against the ethnic-minority group is the main risk factor that produced an increased risk of psychosis. 

To end his talk, Andreas ends on a more positive note, talking about how resilience against disorders can be increased. He draws upon the way social networks have been seen to increase resilience - and the same is true for Facebook friends. The increase in the size of your social network - both online and in real life - appears to have a beneficial effect. 

His next steps are trying to track these social interactions, there are two areas of potential, firstly he discusses the use of hyperscanning and watching brain imaging whilst two people interact. Secondly, he introduces the idea that the chips in smart phones that are used in contactless payments can actually offer a good indication of when people are interacting. 

14:00 Panel Discussion: What good is a diagnosis?

The expert panel takes to the stage for an exciting debate on a divisive question, chaired by Stuart Hughes, BBC Senior World Affairs Producer. 

The panel includes:

Megan Haste, Mental Health Blogger
Prof Ezra Susser, Professor of Epidemiology and Psychiatry at University of Columbia
Prof Sir Simon Wessely, President of the Royal College of Psychiatrists (a psychiatrist with a particular interest in unexplained symptoms and syndromes)
Prof Miranda Wolpert, Director of Evidence Based Practice and Research at University College London (whose work focuses on how services can promote resilience in children and young people)

  • To join in the conversation use #MQScienceMeeting and ask a question – Stuart will be checking Twitter throughout the discussion. If you’d like to view a live stream of the discussion, it’s happening on our Facebook now.

12:10 “Psychotic symptoms in young people – what do they mean?”
Mary Cannon

Not all children who experience psychotic symptoms will go onto have further difficulties, Mary explains. 

Mary Cannon makes the case that symptoms like hearing voices are actually quite common in young people – her study showed that almost one in five of 11-13 year olds report them. She then followed them up with interviews to cross-reference the surveys and gather more data. 

Auditory hallucinations were a common symptom young people reported. Mary found that children who ticked the box saying that they could hear voices that others couldn't were found to have psychotic symptoms when interviewed. She noticed that these symptoms tended to be more prevelant in younger children:

Ages 9 to 12: 17%.
Ages 13 to 18: 7.5%.
Whole population: 4/5%. 

Studies that followed children into adolescence with these symptoms showed they persisted years later. 

Mary goes onto draw attention to the dramatic statistic: 25% of children who had these strong level of psychotic symptoms when they were young went on to develop schizophrenia. 

So what is associated with these psychotic symptoms? 

  • Childhood trauma - bullying, maltreatment, being involved in an accident - the highest risk was a combination of bullying and maltreatment at home
  • Cannibis use

Mary goes onto offer some more "heartening" reports - if bullying or assaults stopped, the reports of psychotic experiences stopped too - giving evidence of some preventions. 

She’s interested in understanding which children who present these symptoms will then go onto struggle with more mental health problems later in life. She combines clinical interviewing, qualitative interviewing, through to genetics, brain imaging and neuropsychology to begin to find answers.

At the end she leaves the room with a question - is there a potential that we could go in too early when someone experiences mental health issues?

11:40 Three generations at high risk of depression

Myrna Weissman (Columbia University)

Myrna opens her talk by taking the room back to the 1970s and a lecture which posed the question: 'Does childhood depression exist?' which suggested that depression was a condition confounded in middle-age women, and couldn't start in adolesence.

She goes onto discuss her study which looked at individuals with depression and the next two generations after them.

The major finding for generation two (the children of the adults who had depression) continued to have almost a three-fold increase of any mood disorders, major depression and anxiety disorder. Generation three are now 18 years old and already 29% of them have high-risk of depression. 

One of the most upsetting findings was that 3.9% of generation two died by unnatural causes which includes suicide, accidents and overdose.

So how do we break the cycle of transmission for depression?

"Depression is a complex disorder, it's on-set and recurrance is precipitated by stressful events in vulnerable people. What could be more stressful than having a parent with depression?"  Myrna Weissman

So - Myrna's approach was to make the parents less depressed. Her study focused around a treatment programme called 'STAR*D'. After three months of treatment, she saw that if the mother remitted, the children got better. 

However, Myrna needed to prove that it was the treatment that caused the mother to get better - and not another factor - so she did a random assignment. She saw the same results - that if the mother's mental health bettered, the children also saw an improvement in their mental health. 

If you treat mothers for depression - shouldn't we try to get in as early as possible? Myrna asks: should we look at treating mothers during pregnancy? 

Myrna talks about the US Preventive Services Task Force which has become very interested in depression and has promoted that screening for depression should be routine for adults over the age of 18 and this includes during pregnancy.

However, we don't know the long-term impacts of taking antidepressants on the developing foetus. Can we use psychotherapy instead?

"The United States in psychotherapy is declining. Training in evidence-based psychotherapy is declining." Myrna Weissman

"What is being used in poor countries is too expensive in the United States. This is a paradox." Myrna Weissman

Myrna suggests that we know that depression is transmitted to children and now we need to look at the mechanisms and prevention methods. She believes that we should screen mothers during pregnancy for depression and we should be offering them psychotherapy. 

Myrna makes the point that we need to think about - what is a family? - taking on board that mental health is impacted by both biology and the environment.

11:10 “Bullying victimization and mental health: A longitudinal twin study”       

Jean-Baptiste Pingault (UCL) 

Our talks turn to focus on the risk factors for mental illness. First up, MQ Fellow, Jean-Baptiste Pingault speaks about his work on the impact that bullying has on mental health.

He’s interested in whether bullying causes mental illness, or whether factors – like genetics influences or home life – are more likely to explain the relationship. 

He’s using a longitudinal twin study to be able to reduce the variables and compare how much bullying in childhood can effect wellbeing.

Why twins?

  • They are matched on many of the confounders. Eg. same age, same family...
  • Also matched on many unknown confounders - share the same environment and genetic factors

Jean-Baptiste says, when there is a causal relationship - we expect the twin who has been exposed to the bullying is more at risk to mental health than the one who hasn't been bullied.  

Jean-Baptiste's study looks at 5,500 pairs of twins, looking at when a child was exposed to bullying at age 11, age 15 and age 22 - and the impact that had on mental their mental health. He goes onto show findings that there is a pattern that exposure to bullying seems to have a causal effect on mental health. That there is a casual effect on anxiety, but not on other mental health outcomes. 

Jean-Baptiste speaks about Louise's talk looking at risk factors on mental health - and says that this might be the correlation between having mental health problems and the liklihood that you will get bullied.

Jean-Baptiste says that his findings are quite consitent with previous studies. He says that longitudinal findings show that there is a decreasing impact of bullying victimization over time. This highlights the possibility of resilience in bullying.

Interventions can be approached in two ways:

1. Can we stop bullying from happening in the first place? If we can stop it happening - will this then stop anxiety and depression? Intervening early is really important, preventing longer-term mental health outcomes. 

2. It is unlikley that we can prevent bullying from happening - findings show that the possibility that mental health problems reduce over time due to resilience. So can we create interventions that aid resilience?

What's the future of Jean-Baptiste's fellowship?

  • Follow up studies into adulthood, looking particularly at self-harm
  • Extend to other cohorts with other methods to strengthen causal inference
  • Refine findings looking at different forms of bullying, including cyber-bullying
  • Understanding genetic influences in depression

Jean-Baptiste is taking an innovative statistical approach to explore the impact of bullying. By identifying those people most at risk of bullying, he asks, can we improve support for young people? 

10:50 Coffee break

The room is humming with lively conversation between researchers. 

We speak to Niall Boyce, from the The Lancet Psychiatry to see what he thinks about the meeting so far:

Symposium 3: Developmental neurocognitive models

Chair: Francesca Happé (King’s College London)

10:00 “Developmental neurocognitive perspectives on ADHD and schizophrenia” 
Graham Murray (University of Cambridge) 

Graham Murray takes to the stage and is asking some big questions: 

  • What happens to brain structure and functions when ADHD kids grow up?
  • What is the course of cognitive function in schizophrenia over the lifespan?
  • What cognitive processes underpin the emergence of delusions in schizophrenia?

Graham speaks about the Northern Finland Birth Cohort 1986, saying there are differences in brain structure in ADHD individuals.

Graham then goes onto discuss the cognitive ways we can access ADHD - he talks about how people who don't have ADHD  become more engaged in a task the more difficult it gets, whilst those with ADHD do not.

"There's more to mental disorder than whether or not you meet diagnositc criteria - but I appreciate that we don't have interventions to improve working memory or brain structure yet, but I think we need to remember these different aspects of mental disorder in our research and in our practice." Graham Murray

Graham goes onto make the case that difficulties in learning and decision-making could underpin the emergence of delusions. He says scans of the brain in people who have experienced delusions for the first time have abnormalities.

"Jumping to conclusions" in schzophrenia 

Most cognitive tasks that psychologists deliver give all the information to the participant and the individual has to make the best option on what they see. However, in real life, you're able to often make a decision after thinking about it for a while and this can be tested in a lab by giving individuals the option to gather more information before making a decision.

Studies show that on the whole, patients with schizophrenia gather less information than people without schizophrenia - a so called, "jumping to conclusions" bias.

Why do they do that? Is it because they make random decisions? Or is there other underlying cognitive process going on? Or do they attribute a greater cost to sampling information?  

Graham talks about the cost to gather information - such a the time it takes - and the suggestion that those people with schizophrenia attribute a higher cost to gathering information.

Graham goes onto talk about his work which suggests that people showing early signs of psychosis attribute a much higher cost to gathering experience, compared to those who don't have schizophrenia.

This result differs from studies which have looked at chronic schizophrenia, where it appears that there is no change in the amount of value attributed to gathering information - and the main difference is that people with chronic schizophrenia have "noisy" cognitive experience and that's why they did not want to gather more information. 

"There is value in studying individuals at different stages of a disorder" Graham Murray 

He’s taking an interdisplinary approach to find answers – working between psychologists, psychiatrists, paediatricans, neuroscientists, physicists and epidemiologists.

Finding answers to these questions has exciting potential for creating interventions – but Graham says it’s crucial to invest in studies that look at how mental illness develops over many years.

09:30 “Antecedents of adolescent depressive disorder and implications for prevention”

Frances Rice (Cardiff University) 

Can we predict if an adolescent will develop depression? Frances Rice draws the room’s attention to the potential that developmental pathways could play in finding answers.  

What do we know about early-onset depression?

  • Factors relating to family, such as depression in a parent is a common and potent risk factor. There are about 2 million children in the UK growing up with a depressed parent. We know that depression is moderately heritable, caused by genetic and environmental facts. 
  • Social factors like poverty and stressful life events are also highlighted as key risk factors to early-onset depression. 

These risks can co-occur.

Frances goes onto explore her piece of work, digging deeper into the discussion, asking which which clinical factors are worth focusing on to understand the risk of developing depression? How important is factors like low mood, anxiety, irritability and disruptive behavior in predicting first-onset depression?

She was interested in looking at young people with depressed parents who had experienced depression for the first time - excluding those who had experienced depression before. 

She compared the risk factors (like economic disadvantage) and clinical factors like low mood, fear and anxiety to see the pathways that could lead to depression. She says that the family and social risks were acting directing on developing depression and she found 6 pathways to major depression disorder.

This work can be used to influence how we prevent depression, she says it's worth considering:

  • There are multiple routes to depression
  • Prevention needs to consider how to tackle these social risks
  • Anxiety and irritability could be targted to prevent depression

Finally, she turns her attention to the potential for these risk factors to help us create better interventions, comparing different types of classroom prevention techniques she looked at whether depressive symptoms were changed. 

She focused on three cognitive factors that could be associated with depression:

  • Decision-making around rewards
  • Ability to recall specific memories
  • Looking at the speed in which someone endorses negative self beliefs 

She compared different techniques including different types of CBT and Mindfulness. The only group which showed a reduction in depression symptoms - was a type of CBT with 'behavioural activation' which focused on increasing reward-seeking behaviour.  

09:00 “Neuroplasticity and Prevention Neuroscience for Disorders of Impulse and Attention”
Edmund Sonuga-Barke (King’s College London)

Our first talk of the day comes from Edmund Sonuga-Barke who’s looking at how ‘extraordinary environments’ can cause mental disorders to develop, even when the genetic risk is low.

He argues that these extraordinary environments impact the learning processes in the brain (neuro-plastic responses). They can either cause the brain to ‘derail’, increasing the potential that someone will develop disorders like ADHD - or on the other hand, if these extraordinary environments are therapeutic - they can decrease the potential that someone will develop ADHD.

In effect, he says, these neuro-plastic responses are a "double-edged sword."

Edmund says his "big picture" talk will look at the potential for prevention neuroscience and whether therapies can have "extreme" neuroplastic effects that can promote the healing of the brain.

Genes are important in ADHD - but they are completely dependent on the type and range of experiences of the individual that is being studied.

"Genes say very little about the potential for extraordinary environments to influence ADHD." Edmund Songua-Barke

He draws upon the English and Romanian Adoptees Study by Michael Rutter to show how radical environmental change (exposure to severe deprivation during early development) had a devastating impact - one of the areas of impact was an increase in the chance of developing a neurodevelopment disorder, like depression and ADHD, despite there being low genetic risk. Around 50% showed depression, and the babies who had over 6 months of this severe deprivation were 7 times more likely to have ADHD. Edmund says his paper on this is coming out in two weeks in the Lancet. 

Edmund goes onto look at the biological mechanisms to support his argument, focusing on the potential of dopamine dysregulation. 

Now he asks whether therapies can increase extreme responses in the brain to heal the brain of ADHD - when the genetic risk is high?

Edmund draws upon Barkley's hypotheses which says that the "exectutive dysfunction", which affects the working memory, produces ADHD and therefore its a good area to base therapies on. However, he argues that 'working memory training' that has been produced to try and treat ADHD had no effect on people with ADHD.

"If you go in early - are you going to have better effects?" Edmund Sonuga.

Edmund says that the earlier you can intervene with ADHD the greater the benefit you can have.  

Next up, Edmund draws upon examples of 'computer-game' style programmes which encourage infants to hold their gaze rather than be distracted. This saw some promising results.

Edmund sums up his talk:

  • We are only just beginning to understand how genes can exploit neuroplasticity to alter the risk of developing disorders
  • Dopamine is an interesting focus 
  • Therapies could be based on neuroplasticity

08:30 Coffee talk

Researchers from around the world and across disciplines are back for another day of cutting-edge science. As they drink their morning coffee, they talk about which discussions excited them from the day before – and who they’re looking forward to hearing today.

Thursday 2 February 

17:00 – 19:00 Poster session 

The meeting moves out of the auditorium and into the poster session where over 50 up-and-coming scientists – including some of our very own MQ Fellows – are waiting to present their work. 

The posters range from design and methodology studies and systematic reviews, as well as novel scientific findings including many on mechanisms of risk and resilience.

16:15 Neurodevelopmental trajectories to psychopathology” 

Carmen Sandi (École Polytechnique Fédérale de Lausanne) 

Our final talk of the day comes from Carmen Sandi who’s offering insights into the understanding of how the effects of genes and stress may impact the trajectories to psychopathology. Her findings focus on the mechanisms of abnormal aggression and fear learning in development.  

Her talk draws upon two examples: 

  1. The genetic risk factors - in particular, the alteration of a gene that has been linked to schizophrenia, autism and bipolar
  2. The environmental factors - the detrimental effects that occur when stress and psychological trauma are experienced when the brain is still developing

Carmen explains that a gene called STX keeps popping up when looking at disorders like schizophrenia, autism and bipolar. The gene appears to alter cell adhesion processes, making connections in the brain "less sticky" - which is key to understanding its link to different disoders.

This is a crucial gene to look at during early development, and Carmen says that animals with changes in STX display schizophrenia-like behaviours, different aggressive behaviours (such as attacks on younger animals which didn't pose a threat, and attacking in specific areas of the body) and psychopathic traits, such as abnormally low levels of anxiety and fear.

Carmen wanted to see how these mechanisms in the brain changed when the animals were exposed to something which would cause them fear.  

This lead to work on ways to treat the animals from displaying the psychopathy-like behaviours. Giving the mice a certain drug (d-cycloserine), her results were remarkably positive - the mice displayed anxiety, were attacking less and demonstrated fear after being given the drug.

She also describes the importance of environmental factors and talks about how stressful experiences caused normally developing mice to become more aggressive. Adding: "Stress has a huge impact on the brain - especially when the exposure is during development."

Carmen looks to the future with her final slide asking, can we identify biomarkers that explain individual differences in abnormal agression induced by peripubertal stress? 

Her understanding of genes and the importance of stress can inform how we create new therapies. 

Symposium 2: Early mechanisms of mental illness

Chair: Matt Jones (University of Bristol)

15:00 “(Epi)genomic pathways to mental health: genes, environment and development”

Jonathan Mill (University of Exeter/King’s College London)

What are the causes and consequences of molecular variation in the brain? How do these link to mental health across a life time? 

Jonathan Mill’s talk turns to exploring how patterns in gene regulation are involved in the development of the brain, and how these are influenced by both genetics and the environment.

Jonathan follows on from Ezra's talk also suggesting the influence that diet can have an impact on prental brain development. He says genes can be influenced by different factors like diet, infection, medication, climate, hormones... The list goes on! When the foetus is developing, this is when these environmental exposures play a role - with the potential to influence the liklihood of developing conditions like schzophrenia. 

Jonathan talks about his exciting approach, looking at the genes of human brains of people who have been diagnsoed with schzophrenia, compared to those who haven't, in identical twins to reduce other factors that could influence the results. 

Jonathan makes it clear that you ‘can’t believe the hype’ around how much impact gene regulation can have on mental health, he draws upon some outlandish headlines from newspapers including: 'Darwin was wrong'. He talks about the number of limitations for studying epigenetics which are often done in very small numbers and often with a narrow type of tissue.

As a final comment - Jonathan makes the plea that we must invest in brain banking - as blood is not sufficient to study genes. 

14:30 Assembly of inhibitory circuitries and schizophrenia”

Beatriz Rico (King’s College London)

The symposium continues with Beatriz Rico, Professor of Developmental Neurobiology.

The discussion around the biological basis for schizophrenia is now being explored by Beatriz whose research focuses on understanding the cellular and molecular mechanisms that control the development of circuits in the cerebral cortex – the brain’s outer layer of tissue. 

Beatriz talks about how cells need a modulator - just like an orchestra needs a conductor - a modulator sychnoises different neurons to fine tune the information to produce a person's behaviour. So what happens if any of these processes fail? 

Beatriz says we have to look at what is going on when schizophrenia starts to development to understand what the brain processes are behind it. 

Beatriz says there is no treatment to have a reduction of the negative symptoms of schizophrenia - there have only been 8 out of 200 drugs that have been approved, and they're all for anti-psychotic symptoms. 

We know that has high heritablity - if you have no relatives wtih the condition there is a  1% chance you will develop it, compared to if your twin has the condition, when it rises 49%.

Beatriz says talks about the alterations in the frontal cortex for someone with schzophrenia. Her work aims to inform new treatments that can bring hope to people with schizophrenia. 

14:00 “Prenatal nutritional deficiencies and neurodevelopmental disorders:  where do we go from here?”

Ezra Susser (Columbia University)

Ezra opens his talk: "I'm going to talk about prevention. This is an old idea - but a new idea for research. We've got a long way to go but considering how new it is, we've come a long way."

Ezra’s interested in how we can prevent disorders like schizophrenia and autism. He’s been looking at the role that prenatal micronutrients like folic acid could play.

Ezra’s not shying away from the challenges in finding definitive results that suggest prenatal micronutrients could prevent these ‘complex’ disorders.

Ezra makes the point that we know that in some cases taking a nutrient in your diet reduces your risk of developing mental illness, but we must consider the side-effects - there might be adverse effects!

"Unexpected things could happen - but so far, so good." Ezra Susser

Ezra talks about the studies he did on the Dutch famine at the end of 1944 and another study he worked on surroudning The Chinese Famine after the Great Leap Forward (1958-1961). Both of these large studies show that starvation is linked to later schizophrenia - but we don't know why. 

What is the relevance of these famine studies if they don't show us the causes of schzophrenia? It generated an ongoing dialogue around people working at different levels of science. 

There are several mechanisms that have the potential for prevention of schzophrenia - "my favourite" says Ezra - is micronutrient defincieny. 

So, this is what we know... 

- Micronutrients can prevent brain disorders
- Folic accid supplements prevents neural tube defects
- Iodeine supplements prevents cretinism

Ezra talks about his studies on the potential of micronutrients like folic acid, choline, vitamin D, omega-3 fatty acids to prevent schzophrenia. He says: "There are no definitive results - yet!"

What are the challenges we have to overcome to get definitive findings? Ezra explains...

1. Relationships among neurodevelopmental disorders - conditions like schizophrenia and autism can't be neatly separated, there's a lot of overlap in the causes. The best way to confront this is to think about multiple disorders and outcomes. Ezra talks about a MoBa study which showed that women who took folic acid during pregnancy had children who had a reduced risk of autism-spectrum disorders - the children are now getting to the age when they'd develop schizophrenia so watch this space... 

2. There's relationships among micronutrients - the two micronutrients that may prevent schizophrenia - coline and folate - are fundamental in how the brain develops. They are also interelated - for example, you won't see an effect of coline if you have too much folate. Ezra argues that we should choose the sets that have an interplay with eachother, if you don't do that you could be mis-led as the effect that you see for one, is going to be dependent on the others. 

3. The trials. It's not clear whether it's ethical to run tests on folic acid in pregnancy as it's recommended that folic acid should be taken by all women who are expecting. We're also held back by the length of the trials which at the moment aren't long enough to gain definitive results. One way we can combat this is to fund these longer studies, he references Josh Roffman's work, an MQ Fellow, who's analysing whether the programme in the US in the 1990s required manufacturers to fortify food with folic acid had an impact on brain development and schizophrenia.

4. Discrepancies in evidence from different levels. People taking folic acid is increasing in a lot of countries - but at the same time, autism is also increasing. This challenges us to think about why we're getting different results at different levels. How do we tackle this? Consider biological explanations, Ezra says.

5. Translational science reciprocal not linear. There's a constant interplay between the findings at different levels. This has been true for micronutrients. We're drawing our findings on a global scale - from basic science, from animal models, epigenics. If you try and start with basic science and then more the next step, you're missing a point. 

Ezra envisons the future, saying that we can find answers - and we will get there. Adding that working together is crucial and "science has a lot to gain from globalisation" Ezra Susser

12:50 Lunchtime conversation

The speakers and attendees break for lunch and cluster together to discuss the talks from the day so far.

We caught up with two MQ Fellows to see what they think of the meeting so far, Patrick Rothwell said: "The meeting has a lot of potential to bring together people working across levels to develop a common vocabulary and communicate with one another that will lead to break-throughs down the road."

Sam Norton added: "It's a great opportunity to hear new ideas and network with some of the top scientists working in mental health research. I've enjoyed the breadth of research - although it was all on anxiety disorders, it really covered a whole range of approaches." 

We caught up with a delegate, Rachel Ryan from Imperial College University, to see what she thought of the day: 

Symposium 1: Anxiety and related behaviours        
Chair: Elaine Fox (University of Oxford)

12:00 “Repetitive Thought in Depression and Anxiety Disorders”

Michelle Moulds (University of New South Wales) 

Michelle Moulds follows on from Hugo and Susanne with a focus on repetitive thought and the role of rumination in depression and anxiety.

Rumination refers to the repetitive passive thinking - so thinking that's 'about me', 'about my problems' and about what's happening in the past. Michelle says we know that people who have a tendancy to respond to a sad mood are those people who are more likely to become depressed and stay depressed for longer. 

The problematic part of rumination is the fact you're thinking in a very abstract way, asking 'why' - instead of thinking in a logical way - 'what can I do to improve my mood'. 

Michelle is interested in the impact that rumination has on memory. She has been looking at how depressed people respond to negative memories compared to people who aren't depressed. She found that depressed individuals were more likely to dwel, ruminate and analyse the causes of the negative memories. 

"When depressed individuals were asked to bring positive memories to mind - it actually made their mood worse." Michelle Moulds. 

And rumination is not just a feature of depression - people with anxiety also engage in rumination, as well as those with PTSD who often go over the trauma they have experienced. Michelle says that worry and rumination are linked. 

In light of this, she makes the case for a transdiagnostic approach - and draws on studies which show how effective it can be.

This is why she thinks a transdiagnostic approach is useful:

1. We can shift from a disorder-specific focus - with a view to develop effective treatments regardless of what disorder someone has
2. There's clinical advantages - we can address the underlying processes in the brain rather than the symptoms and this helps us treat people who have more than one conditions, like people with anxiety and depression
3. There's theoretical advantages - it would allow us to gain a better understanding on whether rumination and worry share common underlying processes in the brain

She talks through a study where individuals were given a treatment to stop rumination who showed a reduction in developing disorders like general anxiety disorder and depression.


11:30 “Interoceptive processing as an intervention target for anxiety prevention: Application in Autism”

Hugo Critchley (University of Sussex)

Hugo Critchley, Chair of Psychiatry at Brighton and Sussex Medical School offers exciting potential for preventing anxiety and panic symptoms from escalating into anxiety disorders.

What is interoception? He asks. Hugo draws upone James-Lange, saying that what we're feeling has direct correlation in our body. Our feeling of the changes in our body is actually the emotion. 

Interoception is the "body-to-brain axis of sensation concerning the state of the internal body and its visceral organs" (Sherrington, 1948). So for example, Hugo says, there are receptors that tell the body how fast the heart is beating - this 'interoceptive information' comes up the spinal chord, interacting at multiple levels into the brain. 

Hugo has been focusing on mapping the brain changes when a person is under stress. 

How does the mind represent what is going on in the body? He points to some brain regions which are really sensitive to changes in the brain - like the amygdala. 

"Signals from heartbeats intensify processes of fear" Hugo Critchley

Hugo says there is an argument that interoception refers to a psychological process - people more sensitve to changes in their body are more likely to develop anxiety disorders. However, he says, the ability to be very sensitve to changes in the body could also make you more empathic and you may be better abled to regulate your emotions. 

Hugo asks the room if they can hear their own heartbeat. He goes onto explain that heartbeat detection tasks - where someone can track their own heartbeat - can be used to see whether 'interoception' links to anxiety. 

Hugo goes onto talk about his work being funded by MQ, which is making a software platform that enables the team to improve interoceptive processes, like an increased heartbeat, in people living with autism. 

11:00 “Using new technology to identify cortico-striatal activity changes underlying OCD-like behaviors”

Susanne Ahmari (University of Pittsburgh)

It’s Susanne Ahmari’s turn to take to the stage, opening the anxiety and related beahviours symposium.

She’s asking how the communication between the decision-making brain regions (prefrontal cortext) and the action-selecting brain regions (striatum) change as OCD-like behaviours develop?

OCD consists of either obsessions (recurrent, presistent intrusive thoughts, impulses or images) or compulsions (repetitive behaviours or mental acts). Ahmari says that despite OCD being incredibly common (2/3% of the population)  the treatment for it is extremely limited - SRI's are only effective in 10/15% of people. 

Susanne explains that patients end up engaging in these loops of obsessions and compulsions - but what's going on in the brain when you're having a compulsion? What does this look like - literally?

Susanne grounds her findings from studies in humans and then translates them to animal-models. Susanne speaks about her use of optogentics - enabling her to select and light-up certain cells in the brain, turn on and off particular circuits and look at what the impact this has on behaviour. 

But how do you access OCD-relevant behaviours in mice? This is a human condition, can it be linked to animals?

Susanne says one way we can answer this is through a type of excessive grooming seen in mice that has similarities to OCD behaviour.

Susanne Ahmari was able to study the brain patterns when the mouse was engaging in this activity using a tiny microscope inserted into the brain, this enabled her to determine how the brain processes change and develop in OCD-like behaviours. 

Susanne's goal is to develop "improved neuroscience-based treatments for OCD". 

Her work has the potential to inform new treatments for OCD – understanding these processes in the brain could inform new treatment approaches – whether it’s non-invasive brain stimulation or drugs based on exposure therapy.


10:15 Keynote 1: Pervasive and persistent impact of childhood bullying victimization”

Louise Arsenault (Kings College London)
Chair: Jeremy Hall (Cardiff University)

As the first talk of the day – Louise opens the discussion focusing directly on young people’s lived experience by looking at the impact of bullying.

Louise maps out the evidence that bullying is harmful for young kids.

Victims of bullying are a vulnerable group of people who are likely to face adversity or to face mental health problems - is this to do with bullying per se or are they vulnerable to start with?  

Why should we bother about bullying? Louise answers:

1. It's common among children and adolescents
2. It can be persistent across time
3. It is widespread across different settings
4. It can take various forms
5. It knows no boundaries - Susanne comments that this is a worldwide problem
6. It evolves with its time - Susanne calls on the emergence of cyber bullying, a form of bullying which never stops!

Susanne explains the factors that contribute to the liklihood that someone is going to be bullied, highlighting how being maltreated at home is the "saddest finding"

"If your twin has been bullied, you are more likely to be bullied as well. There are heritabile characteristics that make a child more likely to be bullied - but environment is also important." Louise Arsenault.

Susanne goes onto explain that in this line of research, finding the factors that are likely to cause someone to be bullied, is important as it enables us to intervene and prevent bullying.  

Being bullied leads to emotional problems, over and above the effect of family-wide factors including genes. Susanne draws attention to two cohorts of twins to prove her point. 

"If you stop bullying, you will reduce mental health problems" Louise Arsenault

Louise now goes onto discuss the long-lasting effect of being bullied. Susanne says - victims who were bullied were at a higher risk of developing depression disorders - but were not at risk of developing substance abuse problems. 

The outcomes of being bullied are not limited to mental health problems: there is also socio-economic outcomes seen later in life. Those who are bullied are under-represented in people who have higher degress, they are also less likely to have a spouse and women are more likely to be obese later in life. 

"It's possible that kids who get bullied do not achieve their full potential" Louise Arsenault

Important take-home messages from Louise:

1. You can predict who is more likely to get bullied
2. Being bullied in childhood is associated with mental health problems
3. Being bullied gets under the skin - the whole body seems to react to this problem
4. Bullying seems to effect other outcomes in people's lives

"We need to get the focus on getting families involved, but better than that we could have a public health approach. We know who is likley to be bullied so we could prevent kids getting bullied in the first place." Louise Arsenault

Questions are coming from the floor, including:

Ezra Susser:  "Bullying varies enormously across different contexts. You have so many contexts where bullying is institutionalised. Could this be a focus for intervention?"

Louise Arsenault: "As adults we have to reflect what messages we're sending to kids - if children see adults bullying each other in the public arena, obviously they think it's okay to bully. As a society we may want to think about these implications. Just focusing on the bullies is a good place to start - but we need to level-up."

10:00 Welcome

 Sophie Dix (MQ) & Jeremy Hall (Cardiff University)

The event kicks off with MQ’s Director of Research Sophie Dix and Neurosciences and Mental Health Research Institute’s Professor Jeremy Hall.

The meeting begins with swearing as Sophie introduces MQ’s commitment – swearing to take on mental health in young people.

Sophie explains the potential for research to increase understanding, improve treatments and bring hope of prevention. MQ’s We Swear campaign features celebrities like Gillian Anderson saying it’s to give a **** about mental illness in young people and a short video:

A big focus is made on the importance of taking a multi-disciplinary approach to research, resonating with the room filled with people from different disciplines.

Sophie explains how this is a crucial part of ensuring the success for Brighter Futures, the young people’s research programme that ties into the We Swear campaign.

Brighter Futures has a threefold approach to taking on mental illness in young people:

  1. Bring together world-leading experts in a major research consortium focused on the early development of mental illness
  2. Partnering on a wide range of projects to turn evidence into practice and improve support for young people.
  3. Creating a UK-led global network for young people’s mental health research.

"We can't do this alone" - Sophie Dix

09:45 Morning anticipation

Over 200 scientists, researchers, clinicians and service users are pouring through the doors at Amnenesty International in London eager to find solutions to the big issues in mental health. 

"My lab is very interested in early life stress and trauma and the consequences this has on brain development - in particular I'm looking forward to hearing from Louise Arsenault about the impact of bullying on childhood and Susanne Ahmari's talk on interoceptive processing."  Liat Levita, University of Sheffield. 

We spoke to Jeremy Hall from Cardiff University, who's chairing a session ahead of the meeting: 

Last updated: 6 February 2017

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