It’s late 2018 and I’m clutching the box of antidepressants (that belong to a group of drugs called selective serotonin reuptake inhibitors (SSRIs)) that my doctor has just prescribed for me. At 23 years of age, I’ve battled with anxiety and low mood for many years and just experienced one of the lowest points in my life. You’d think I would be feeling relieved and happy that I am finally getting the help I need and I’m on the road to recovery. Instead, I feel like I’ve failed. I feel ashamed. I feel weak and like I’m not strong enough to deal with my emotions on my own. If you can relate to or have experienced similar feelings, you’ll want to continue reading. And, if you are interested in this topic, you may want to come back to Inspire The Mind tomorrow for a blog written by Carmine Pariante, the blog editor and professor of Psychiatry at King’s College London, presenting some of the clinical and scientific evidence that underpins my (and perhaps your) personal experience. Fast-forward to today and I realise I couldn’t have been more wrong. I recognise that the moment I swallowed my first antidepressant pill is when my life changed for the better. I’ve spent over three years feeling better because of these very antidepressants and I’ve started to question: “Why did I feel like this?”, “Why did I let things get so bad?”, “Why did I leave it so long before getting the help I needed?” And, the answer lies within society and the huge amount of stigma that’s still around surrounding taking antidepressants. It’s only now, at 26-years-old, that I am writing about this because I have realised that I am a better version of myself for taking antidepressants and I feel the complete opposite of how this stigma made me think I’d feel —  strong, not weak. I feel responsible to use my platform as a freelance journalist to share my story, show others that they are not alone, help them to overcome and challenge this potentially damaging stigma and remind people to be kind. I hope that opening up discussions on this topic and reassuring people that it is not a weakness to take antidepressants will help to save lives now and in the future. Stigma struggles Hands up if you’ve ever heard antidepressants being referred to as a “quick fix” or “happy pills?” I thought so. Well, it’s terms like these and their negative connotations that influence us to create potentially harmful stereotypes about antidepressants; sometimes these stereotypes are passed down through generations and ingrained in our minds without us realising. For instance, my Dad advised me to try and avoid taking medication if I could help it. And, even my former hypnotherapist warned that I might struggle to come off them or they would just mask over the real problem. Further, the #ShowUsYourMeds campaign that launched in summer 2020, to show people there’s no shame in taking medication for mental illness, proves there are myths and misconceptions about taking antidepressants that are fuelling this stigma to exist. Among waiting times and costs, this stigma could be contributing to the 75% of people with mental health problems who were not receiving the treatment they needed in 2014. This percentage is now likely to have significantly increased with the number of people experiencing mental health problems having risen during the coronavirus pandemic. This stigma could be harmful by stopping people, like myself, from getting the life-saving help they need sooner. It forces people, like myself, to suffer in silence. This stigma made me leave it too long before I accepted medication for my mental health. I let it get to the point where I was crying uncontrollably in the middle of a high street, anxious and awake late into the night, not able to function at home or work, missing deadlines and sitting in my GP’s consulting room feeling hopeless. I left it until the point I felt I couldn’t cope. I fought so hard not to be put on antidepressants; I’d tried hypnotherapy, cognitive behavioural therapy (CBT), counselling, meditation, breathing techniques, yoga, you name it. While all of these helped, I was kidding myself that they were enough to help me on their own. I’d even had a prescription for antidepressants sitting on my bedside table for six months, but refused to actually get the medication for fear of being seen as weak. Of course, having therapy alongside taking medication can be beneficial. Combined treatment of antidepressant medication and psychological interventions is more effective than treatment with antidepressant medication alone in major depression, panic disorder, and OCD, evidence has found. I’m currently having counselling and hypnotherapy alongside taking my medication, but I’m also proud to be one of the six million-plus people on antidepressants across England. A sign of strength These days, I feel more myself than I had done in a long time. Yes, I still experience low days and wobbles, but these are fewer and further between and I have my antidepressants to thank for that. I’m not ashamed tosay that I wouldn’t be doing as well at my (often demanding) job or in my social life without these little round masses of solid medicine that I take each day. I do intend to come off them one day but for now, they are helping me to thrive. I’ve since realised that taking antidepressants is actually a sign of success, not failure; a sign of strength, not weakness. Those of us taking medication should feel proud that we are actively taking a positive step towards improving our mental health rather than letting it take over us. With around 10 million people in England predicted to need mental health support in the coming years, due to the pandemic, I want to remind anyone who is struggling of this point. If you are feeling as desperate, hopeless and out of your depth as I was, then I urge you: please, please go to your GP and ask for help. Don’t leave it as long as I did. Think about the number of happier, less worrisome years you could gain. Just as some need glasses to read and others need medication for migraines, some of us need medication for our mental health and that’s no bad thing! And, as the co-founder of the positive lifestyle brand Power of Positivity, Kristen Butler says: “Never be ashamed of yourself. Be proud of who you are, and don’t worry about how others see you.”

A recent article in The Guardian highlighted the urgent need for research into sex-related differences in asthma mortality, claiming that the influence of sex hormones (like testosterone and oestrogen) on treatment response is being ignored. It is the latest example of women’s disadvantages in health, compounded by the national shortage of hormone replacement therapy or HRT. Here I will present our recent findings on the same theme showing that there are important differences between men and women in the prognosis (outcomes) for epilepsy that have not been recognised until now. I am a paediatric neurologist with a research lab at King’s College London. We study the causes of epilepsy and the mechanisms of co-occurring conditions like behaviour and mood changes. We’re particularly interested in sleep and mental health. Find out more about our research here. What is Epilepsy? It’s the most common brain disorder in the world directly affecting 65 million people. People affected by epilepsy experience temporary interruptions in brain function, known as seizures, that may result in loss or impairment of consciousness, sensation, or control of movements. For most, it’s a chronic (long-lasting) condition incompletely treated with drugs that suppress seizures by reducing the electrical activity of the brain. At a personal level, epilepsy can have effects on mental health, social life, learning, work and relationships. One particular common type of epilepsy starts in adolescence, known as juvenile myoclonic epilepsy or JME. In our group we are studying the genetic causes of JME. Like many neuropsychiatric conditions, we believe that a combination of genes and environment result in susceptibility to this type of epilepsy. And like many psychiatric conditions, about one in three people don’t respond to conventional anti-seizure drugs and so are termed “drug-resistant”. To date, the dominant theory about drug resistance is that it is thought to be caused by genetic variants influencing how drugs are transported into the brain. However, there has been little scientific support for this theory over the past two decades. Instead, we hypothesised that there are probably different explanations of drug resistance for different groups of people with epilepsy. Our research We were lucky to have the world’s largest dataset of people recruited for research into JME. Because JME is more common in women, we had the idea from the outset of analysing factors that might affect drug resistance separately for men and for women — the first time anyone had thought to do this. What we found was astonishing. From previous studies, we knew that having absence seizures (brief blank spells lasting a few seconds) increased the risk of drug resistance , and we found this association in our dataset equally for men and for women. But what was really interesting was the relationship to stress. Stress is a well-known trigger for seizures and can take various forms: mental, physical or emotional. Common triggers for seizures include not sleeping well, drinking alcohol, mental stress or the hormonal changes of menstruation. In our study, around a half of both men and women reported that their seizures were triggered by stress, and one in five told us that all their seizures were triggered by stress. What came as a surprise was that stress triggers made the prognosis of epilepsy worse in women but had no effect on men’s long-term outcomes. Menstrual cycle triggers increased the risk of drug resistance 15-fold, and other stress triggers increased the risk of drug resistance five-fold in women. What this tells us in no uncertain terms is that the factors underlying drug resistance are different for women and men, and the data strongly suggest that mechanisms linking hormonal changes and stress response to brain activity are key to solving the problem of drug resistance. Future work This is a great opportunity to investigate how the menstrual cycle and stress response interact with seizure susceptibility. There are no current evidence-based interventions targeting stress or the menstrual cycle that reduce seizures. Perhaps this could be a stimulus to think about dedicated women’s epilepsy clinics? A forum for different therapies to come together to solve the challenges of stress reduction, sleep hygiene, sex and contraception, diet and drinking. But what is it about women’s response to stress that makes their seizures worse? The answer is not very clear. Surprisingly, what we know about the classic descriptions of the fight or flight responses to stress, orchestrated by the sympathetic nervous system, are based exclusively on experiments on male rodents. Why? Because the old assumption in science was that variability in sex hormones would have made the interpretation of results in female animals “too confusing”! So things haven’t really changed much in a century. Later work from the Stanford neuroscientist Shelley Taylor suggests that women may have alternative responses to stress mediated by the parasympathetic nervous system and the neurotransmitter (chemical messenger) oxytocin. Perhaps this is a clue to the sex difference in stress response and how it affects seizures. If we can unravel this mechanism, it may help many women experiencing conditions that vary with stress, like migraine, inflammatory bowel disease and depression. Another interesting avenue of research is the role of inflammation in chronic epilepsy. Already a well-known link in depression, the concept that brain or peripheral (outside the central nervous system) inflammation may also affect response to anti-seizure drugs is slowly gaining ground. And as we know, chronic stress can result in a maladaptive inflammatory response. We hope to be able to investigate the connections between stress, inflammation and drug resistance in women with epilepsy in the near future.

On the 24th of February 2022, my life was split into “before” and “after”. Guess which country I am from? Ukraine. Living through the war from far away is a disjointed experience. On one hand, my own life seems normal and sometimes even beautiful. On the other hand, every day I get news that someone I know has died or another place I have loved does not exist anymore. It is almost impossible to start processing this trauma since it keeps occurring. For the last 7 years, I have been researching and engaging with topics of mental health and art, two disciplines that inspire me and have such a clear social relevance. It is not easy for me to work in mental health research now, as I realize that on some days I also experience depressive symptoms. However, every crisis is also an opportunity for unforeseen growth. I have been stunned by the number of powerful stories from people around me, stories that need to be shared. So, I decided to interview three Ukrainian projects related to mental health and showcase their amazing work and resilience in times of war. This is the first blog in the series. In this blog, I interviewed Stanislav Turina, an artist, curator, and co-founder of atelienormalno, a studio space, where artists with Down’s Syndrome (which we would consider neuroatypical, individuals with atypical neurological development or functioning) collaborate with neurotypical artists and help each other develop professional skills to build a career. How did atelienormalno start out? Stanislav Turina: In 2018, myself and Katya Libkind got invited by Goethe Institute Ukraine to teach “art as a hobby” to adults with Down’s Syndrome. At the time, it was impossible to find an artist with Down Syndrome in Ukraine that had a public platform. In Germany, on the other hand, there are a lot of artists with Down’s Syndrome that have flourishing careers — personal exhibitions, big sales, and collaborations with museums. A German research institute with a focus on Down syndrome, Touchdown 21, provided us with a methodology for structuring the interactions and resolving conflicts. German magazine Ohrenkuss, where every edition is created by people with Down’s Syndrome, offered to publish the results in a special Ukrainian edition. The first class was an amazing eye-opening experience. It was our first contact with Down’s Syndrome. We noticed that one participant, Zhenya Golubentsev, has managed to create a deeply touching masterpiece. His paintings were exceptional, better than anything I have seen created at similar workshops. We asked ourselves — could art be his life’s calling? More on his story later… Our sessions culminated in an exhibition “What is important?”. However, we did not want to stop. The feedback was overwhelmingly good and we realized that we are getting exposed to something really important that does not exist in our country yet — inclusive artistic exchange. We never conceived of our work as “charity”, since we had no connection to the syndrome, we were genuinely interested in a permanent space, where neurotypical artists can come and exchange ideas with artists with Down’s Syndrome, on equal footing, to the benefit of both. In Ukraine, we are very self-organized. We do not wait; we create places and events we want to attend. A “Do It Yourself” (DIY) project atelienormalno was underway. Why painting? Painting is very relaxing. To paint is to be silent. People get together, they help each other, and they collaborate. It is a very nourishing interaction. We also use other materials — ceramics, play dough, and objects from the street. Art helps to reflect — a finished piece is something material left behind, and the topics that emerge tell a story. To see what you and others have painted is to enter a dialogue with the art and the artist. What were some of your main challenges and victories? At first, it was challenging to establish physical boundaries and define with participants which type of touch is appropriate. Then there were differences in character. Some artists were constantly late, some were reluctant to leave the studio. However, our German research partners had strategies at hand; most of our problems were not unique and usually, there was a solution or a way to prevent them. Another issue was funding and finding a permanent space. We operated with almost no budget. In our first year, we used the materials left from the art classes and the yearly budget was around thirty euros. We used discarded carpets to save on canvas! However, passion inspires and attracts. More and more people saw how much we care and came to volunteer or help in another way. The pandemic was a challenge but also brought progress. We helped our artists set up home studios and use digital tools. It is important to teach artists with Down’s Syndrome to be autonomous. We encouraged them to use social media, send texts, and get on Zoom. Together, at this point, we have exhibitions in major art spaces like Khanenko Museum or The Naked Room, sell works, give interviews, and win prizes. What happened with the project since the beginning of the Russian invasion? The war crushed all our plans. The majority of us were in Kyiv when everything started. I and a few other people are still here. Most others have decided to evacuate, the last of them just yesterday. One girl went on vacation with her parents and never came back. One guy escaped through the shelling but made it alive… The participant I mentioned earlier, Zhenya Holubentsev was out of Kyiv, when everything started, near a small village called Vablya, next to Borodyanka — a name that resonates throughout the world now. Borodyanka had even more victims than Bucha. He went there with his mother to be in nature and paint, a little en plein air. All of a sudden, the windows in their house blew up from a mine. Outside of the broken window — a convoy of Russian tanks, there must have been six hundred of them encircling the city! For a long time, they were sort of lucky, if I can use that word. Zhenya was allowed to paint throughout. His creed is painting every day, like all the great artists! The main shock came when they were allowed to return to Kyiv: they had no idea how badly the city had suffered but in the news, they saw the mass graves, dead bodies on the street, their neighbours shot in the head, the whole town completely ruined. After Zenya and his family returned, he really closed himself off. Now his family is in Germany, we hope he will get better soon. It is not easy to keep in touch nowadays. Crossing town can be unsafe: the air raid sirens happen all the time and we need to stay close to the bomb shelters. Nevertheless, we are all painting daily to keep our regularity. Everyone has a home studio, a relic of the pandemic, everyone knows how to use Zoom. Some artists have found this time very fruitful, and our work has been a big source of reflection, hope, and mental health support. Not having an opportunity to come together physically, we also started to exchange little bits of our daily life: photographs of what we are doing, little poems, and music we listen to. It really helps to find some beauty to counteract the horrors. And, I think, we all still firmly believe in our project and that after the war, we can have a better, brighter future — with a permanent space, secure funding, exciting collaborations, and my personal dream — a big public library dedicated to neurodivergent art and human rights. Note from the Author: Members of atelienormalno are volunteering in Kyiv in Pavlovskiy hospital for people with severe neuropsychological disorders. They would be very happy to receive any donations to the hospital to support their work in these tough times. Paypal: atelie.normalno@gmail.com

Disclaimer :  I am not a scientist nor a psychologist with a deep understanding about this topic, but merely a psychology student interested on how our own self-worth can affect many areas of our lives. — — — Over several years, research has shown how self-worth can affect our motivation and mental health. Recent research has also highlighted that self-esteem can affect motivation and job performance, and has been strongly linked to happiness and academic performance. So let’s understand the meaning of ‘self-worth’. Self-worth refers to how you view and describe yourself. It can be affected by several factors like, for instance, how others perceive you, your perceived weaknesses, and relationships at home or work. The self-worth theory The self-worth theory, proposed by Covington and Beery, states that individuals’ worth often comes to depend on the ability to achieve competitively, meaning that individuals strive to give value to their lives by constantly seeking the approval of others. This may mean accomplishing deeds or providing services which are valued by the group that one hopes to belong to. You are probably wondering, well, how can low self-worth and esteem affect our mental health and motivation? Recent research has shown that if you have a low self-worth, you may tend to focus more on previous mistakes and weaknesses. If you have good self-worth, you will feel good about yourself and more positive about life. If you have low self-worth, you may choose to focus on your negative traits as opposed to practicing positive affirmations and focussing on the positive qualities in yourself. Moreover, those with low self-worth are more prone to mental health problems, such as addiction, depression and anxiety, as well as difficulties with relationships. — — — There are many ways in which we can begin to improve our self-worth and have a healthy view of ourselves, and I want to spend some time with this blog to talk a little bit about these. Some may seem really obvious, but it’s often these simple things that we need reminding about. Be kind to yourself This means being gentle to yourself, especially at times when you feel like being self-critical. A good example of this would be trying to think of what you would say to a friend in a similar situation; we tend to give better advice, and to be far more forgiving, to others than to ourselves. Look after yourself Have a good night sleep — Sleep plays a big factor in how we feel and act throughout the day. Many studies have highlighted how poor sleep quality can affect not only your physical health but also your mental health! Think about your diet — Eating regularly and healthy meals can help make a big difference to your mood and energy levels. This is important as recent research has shown poor nutrition to affect mental wellbeing. Physical exercise — Exercise can be helpful for your mental wellbeing and make you feel better. This is because exercise can help improve mental health by reducing anxiety, depression and negative mood by improving self-worth and cognitive function. Give yourself a challenge At some point in life, we all feel nervous and afraid to do things. However, we shouldn’t stop us from trying new things and challenges. Perhaps consider setting weekly challenges which allows you to step out of your comfort zone! This could be simple things such as working out or doing the laundry. Achieving your goals will help increase your self-esteem! Build positive relationships Try focus on those relationships which are positive and contribute to your growth. If you find some relationships affect you negatively, you should try spending less time with that individual, or tell them how you feel and try to improve the relationship. Recognise what you are good at We are all good at something whether it is dancing, singing or cooking. We also enjoy things which we are good at. Therefore, it is important you find something you enjoy doing, which can help boost your mood and how you feel about yourself. This blog overall has described how self-worth can affect how we feel about ourselves and ways in which we could help increase our self-worth too. I hope you enjoyed reading this blog!

Trigger Warning: The following blog discusses graphic content shown in various horror films which some readers may find distressing. — — — I had always, at first jokingly and later, in the vein of exasperation, with an eye roll attached, been referred to as a hypochondriac. The definition of a hypochondriac, “a person often worried about their health”, always felt like a great misunderstanding of the illness. I wasn’t abnormally anxious, at least not to me. To me, it felt like I was the only sane one around. The term was first used to denote a form of melancholy; this made sense to me. The anxiety seemed to stem from a sadness above all, a depressive feeling that I didn’t really deserve to exist, that other people were the lucky ones, and I was not. My first breakdown had occurred during the night of a school play that I was starring in, at age 15. My throat started to close up; I thought I was having an allergic reaction. After multiple hospital visits, the GP told my mother that “panic attacks often plague high achievers”. The label of “hypochondriac” was often muttered in the same breath as “neurotic”, and “overly-sensitive”, and how I was “too smart for my own good”. My family often touted me as their golden prize, because I was the one who had surpassed the others in our family with my grades, voted most likely to be a famous author three times in the yearbook, my mother telling me that a psychic told her that I would be on TV in a few years promoting a novel. But I was a broken prize; an anxious over worrier that would have panic attacks if I couldn’t sleep without a night light, for instance. In the archives of my iPhone, buried within neon yellow notes, lives a collection of banal and serious sounding symptoms and the diagnoses I’d assigned to them: bloating stomach is ovarian cancer, a rash is Lyme disease, numb tingling skin is multiple sclerosis or maybe a stroke. A lump on the temples is surely going to burst and cause an aneurysm. My face is looking rounder, so I must have Cushing’s disease. I wonder if I should look into genetic testing to find out the chances of cardiac arrest occurring. Or perhaps Alzheimer’s disease. All of it reads like manic pleading with — who? Myself? One of my earliest memories is watching John Carpenter’s 1978 Halloween with my dad. I was young, definitely far too young to be watching. Within the fear that I felt, lay a tranquil veneer of calm, that my dad was revealing to me a truth of life, allowing me see the other side. What I, even then, as my needy and anxious child-self knew was that these horrors seemed to always be an invasion from the inside: inside a suburb, inside the house or, more relatable, from inside your own body or mind. Horror films became the catharsis for me, and death became the world I couldn’t face unless it was on a TV screen. My love of horror, the macabre, and the morbid, was as integral to my identity as my health neuroses. They seemed to validate the flighty and irrational worries I had. I was a child who loved Stephen King novels, Giallo horror films, slasher movies, and art house films like Hellraiser, Haus, Hour of the Wolf, Alice, Sweet Alice, Suspiria and Brian De Palma’s 1976 Carrie, which I later ‘remade’ on a shitty camcorder with friends, at the age of 12. I loved horror because it felt real, and it seemed to take the world and the body as seriously as I took it. Bad things happened, and horror wouldn’t sugarcoat that fact. For the first time in my life, I felt validated. These fantastical stories allowed me to stare death in the face, like exposure therapy. It was the summer, three years to the date of my dad’s stage four cancer diagnosis. A strange tight tugging on the right side of my abdomen and bloating became sinister seeming when it wouldn’t go away. The thing that had been living inside of me, this preoccupation with my body and my demise, reared its tantalisingly gruesome head. Like all good breakdowns, I lived in fear of what had already happened. I was unaware that I seemed, for lack of a better word, ‘crazy’. I stopped eating. I cried hysterically in 6 separate emergency doctors’ meetings, with permanent marker etched all over my body, circles ingraining themselves into my flesh. I told them with a giggle that this was “just to show them where the pain was”. Of course, they would all wonder how there could possibly be this much pain. “How could there not?”, I wanted to scream. Deep down, I knew that it wasn’t just the physical kind of pain I was talking about. I trawled cancer forums for hours every single night, staying up to read about brain cancer, colon cancer, erratic heartbeats in the stomach, corneal ulcers. Slowly, I pushed my boyfriend away. The imagined tumour became more important than him. It was summer, and I was in love, but I was afraid to speak of any goodness out loud in case I was punished for it by having it taken away. At night I closed my eyes and wouldn’t sleep, instead forcing myself to imagine what nothingness felt like, how it would feel for my friends and boyfriend going on with their lives when I was dead; an exercise in masochism. I wouldn’t be able to sit still for too long and would cry out like a wounded animal in pain. One night, I woke my father up calling 999 and begging for an ambulance to check my heart, certain that I was having a heart attack. Test after test showed that the only thing inside of me that was scary and wrong was in my head. I wanted rules to follow that would promise me results. I knew smoking and not wearing sunscreen and red meat could cause cancer. But what about my father, a health advocate, cycling nut, with no family history of cancer, contracting stage 4 prostate cancer? I didn’t like that you could follow the rules and still be punished. It felt biblical. What it did was feed into my OCD, governed by a system of irrational rules and consequences. My OCD told me that if I didn’t Google things, I didn’t care about my health, and cancer would be the outcome. It told me that if I didn’t seek reassurance 10 times a day from friends and family, I would suffer. If I didn’t force myself to think the same thoughts in the exact same way, I would lose my life. The only thing that soothed me that summer was watching 1970s slasher films, far removed from reality and life — or so I thought. Gritty and imbued with over stimulus, slasher films sing the body electric with red blood that is beating, ice shattering screams, flesh raw and visceral, soft and easily bitten into, broken into. Tobe Hooper’s 1974 masterpiece, the Texas Chainsaw Massacre, was my favourite to rewatch. From my childhood and my love affair with exploitation films that began in earnest at university, I knew the beats of every line of dialogue, every scorching yellow scratch on celluloid. Heat, revenge, the Final Girl. In the film, carcasses are interchangeable with live bodies, and flesh is hot and rotting in the Texan August sun. Seeing bodies in the state of distress and decay had an oddly calmative effect. I was taken out of my body but also mindful of how I, sat there, a spectator, was safe. My body was not in shreds: there was no live threat. It brought my fears out of the shadow and into broad daylight, validating them for all to witness. Just like my intruding thoughts about illness and death, the horror of the film doesn’t wait for the disguise or safety of darkness to make us scared. It leers at you while you squint in the bright fireball orange sun, making itself known, no discrimination for time of day or where you are in your life. This is what my illness felt like, a dread that didn’t go away with sunrise, but billowed like waves, ready to cause a panic attack or demand an emergency doctor appointment. It steamrolled my entire life in the process, at a time when I was meant to be young, free and in love. For me, these films were both extreme methods of exposure therapy, and although the situations were unlikely to happen to me, they validated the core truth behind the axe-wielding killers: that death is inevitable, and the one reality we all can’t avoid. Horror films helped me accept that simple truth, allowing me to feel a semblance of control, not over the outcome, but what I choose to spend my time doing. Now, I know I can maintain control over my mental health: I can choose to put a film on instead of reaching for Doctor Google.

Trigger Warning: This article includes references, graphics, images, and pieces of texts about sexual violence, rape and trauma. Definitions of conflict-related sexual violence and international’s responses are discussed. Some might find it distressing. In April 2022, the world woke up to a picture of the bodies of a naked man and some women partially burned on the roadside of a highway 20km outside the capital Kyiv, Ukraine. This distressing image, taken by the photographer Mikhail Palinchak, contributed to the mounting evidence of executions, rape, and torture that had been used against civilians since the initiation of the invasion of Ukraine. — — — I am a Core Trainee Psychiatrist, passionately advocating for human rights and mental health. I am part of the executive committee for the Royal College of Psychiatrists’ Women’s Mental Health Special Interests Group. I am a leader of Geopsychiatry, an NGO (non-governmental organisation) which studies the impact of war conflict, climate change, public health issues, globalisation, and foreign policy on mental health. I have written articles, such as the need for women's leadership in the UN, and how COVID-19 unmasked the ongoing pandemic of gender-based violence. Similarly, I have written a blog titled, “Mental health of women and children in conflict zones: Their bodies and health are the battlefields of war”. — — — As Christina Lamb says in her book Our Bodies, Their Battlefield: Through the Lives of Women, “Rape, is “the cheapest weapon [of war] known to man”, aiming to intimidate, degrade, and put fear into individuals and communities. This is often a planned, intended outcome of sexual violence, and in some cultures, it ensures that victims are rejected by their families and socially shamed. It is also a method of “ethnic cleansing, as it is deployed as strategically and deliberately as one would with bombs and bullets. Laura Shepherd also highlighted in her book Gender Matters in Gender Politics, that mass rape is the most common type of rape associated with war, usually committed in public. The perpetrators are usually men, soldiers or citizens, and the sexually violent act can be part of a military and/or political strategy. For example, rape camps were set up by Serbian soldiers during the Balkan wars, where victims were raped and forced to bear Serbian babies. In Iraq, ISIS sexually enslaved and trafficked women from the Yazidi minority as part of a campaign to destroy the community, fully acknowledging that children born of rape would be deemed Muslims and not Yazidi. Ukraine’s human rights ombudsman, Lyudmyla Denisova, has already collected several cases of sexual violence by Russian soldiers. In one case, 25 girls and women (aged 14 to 24) had been held in a basement by Russian soldiers. The soldiers threatened to “rape them to the point where they wouldn’t want sexual contact with any man, and to prevent them from having Ukrainian children”; reports from Bucha say 9 of them are now pregnant. Meanwhile, Ukrainian children from occupied cities are being forcibly fast-tracked for adoption by Russian families across the border. This will make it harder for Ukrainian families to track these children in the post-war future, especially when they grow up and forget their birth parents and heritage. This systematic propaganda aims to eradicate the very idea of being Ukrainian. Rape methodology has always been used in wars, even in ancient times. What’s shocking is that it still prevails. The United Nations (UN) Secretary, General Antonio Guterres, and the International Criminal Court have stated that conflict-related sexual violence is widely recognised as a war crime, that is preventable and punishable. These crimes and the perpetrators rightly deserve prosecution under International Criminal Law. However, threats of criminal accountability on an international level may preclude peaceful settlement, therefore making it harder to eliminate sexual violence in conflict. Terminology The term “conflict-related sexual violence” refers to rape, sexual slavery, forced pregnancy, forced abortion, enforced sterilization, forced marriage, and any other form of sexual violence of comparable gravity perpetrated against women, men, girls, or boys that is directly or indirectly linked to a conflict. Women are either killed or die of their wounds shortly after being raped, including the presence of HIV/AIDS increasing the chances that women will die consequently. Sexual violence is a serious violation of human rights—a problem of legal, social, and a public health concern. It is considered one of the worst traumas experienced by a person. What doesn’t result in death, predisposes the victim to acute and chronic mental illness, as well as other comorbidities and repercussions on physical health and mortality. Sex traffickers are preying on vulnerable women and girls on the borders between Ukraine and neighbouring countries. This is a form of slavery, and the mental and physical health effects of sex trafficking are dire. The UN had even asked the British government to ban single men from housing female refugees, as the unguarded moments for women and children are providing opportunities to those who seek to exploit them. How did the world respond to these grievous horrors? Over the centuries, laws and customs of war have navigated a broader understanding of sexual violence, the impacts and the need to protect potential victims. After World War I, the War Crimes Commission was established, and forced prostitution and rape were seen as a grave violation of the laws and customs of war. After World War II, under the International Military Tribunal at Nuremberg (IMT) and the International Military Tribunal for the Far East at Tokyo (IMTFE), the spectrum of sexual violence as a “war crime” was widened. However, rape was not explicitly mentioned in final verdicts. The trauma and violent acts towards these victims were not being acknowledged in these rulings; the victims felt ignored and shamed. In 2014, then UK Foreign Secretary William Hague and Special Envoy of the UN High Commission on Refugees Angelina Jolie hosted the Global Summit on Sexual Violence in Conflict. Hague stated that sexual violence in conflict is “the slave trade of our generation”; Jolie declared that sexual violence victims are “the forgotten victims of war; responsible for none of the harm, but bearing the worst of the pain”. Although women are generally thought of as victims of sexual violence in conflict, we should acknowledge that rape and sexual violence are used against women, girls, men and boys. In April 2019, the UN Security Council, via the adoption of resolution 2467, recognised the need for a survivor-centred approach to prevent and address sexual violence in conflict and post-conflict situations. Subsequently, the UN released the 11th annual report on Conflict-Related Sexual Violence, which spanned 19 countries covering the period of January to December 2019. Focusing on sexual violence as both a tactic of war and terrorism, the report calls for the reinforcement of a vision based on empowering women as agents for change, as well as amplifying the voices of survivors. For example, The UN Assistance Mission in Afghanistan (UNAMA) documented 102 cases of sexual violence — women, girls and 13 boys –attributed to members of the Taliban, Afghan National Defence and Security Forces, and a pro-government militia. During the 6-years of civil war in Yemen, many women have faced high levels of male violence, as armed men take advantage of the lck of security and lack of safe spaces for the vulnerable 83% of displaced women and children. On 13th April 2022, Lord Tariq Ahmed of Wimbledon debated at the UN Security Council on ending the perpetuating cycles of sexual violence in war conflicts — highlighting that impunity is still continuing as a norm for the perpetrators. Simultaneously, he stated that the UK has launched the Murad Code, a global code of conduct, to be used for the collection of information and evidence from survivors of conflict-related sexual violence. The code is named after Nadia Murad, the Nobel peace prize-winning Yazidi woman who survived capture by ISIS, and is hoped to become “the gold standard for any Non-Governmental Organization (NGO), government agency or human rights institution in the field”. By putting the survivors at the heart of the investigations, hopefully this would strengthen international actions and call for criminal prosecutions against the perpetrators. Proposed actions to help the victims of sexual violence A number of mental disorders are associated with sexual violence. The long-lasting consequences, such as physical injury, mental health deterioration, and social stigma place survivors of sexual violence at significantly high risk of adversities. Female refugees and immigrants are more likely to show higher levels of fear, more isolation, have greater trauma and have more mental health needs than other victims of crime. They may also misuse alcohol or drugs to cope with their situation. Their health needs span is associated with Sexual Transmitted Infections (STIs), pregnancy, injuries from physical and sexual assault, suicidality and other behavioural problems. Along with these challenges, female refugees and immigrants may remain silent, due to threats or fears of being deported or losing custody of their children. Primary care practitioners can play a key role in the recognition and management of mental disorders in immigrants and refugees, as they under-utilize formal mental health services. An integrated treatment approach is often required for extreme traumas, such as torture and rape. Clinicians should be alert for unexplained physical complaints, sleep disorders, panic disorder and somatoform disorder, severe dissociation mimicking brief reactive psychosis, and psychotic depression. Key elements to look out for include the level of psychological distress, the impairment associated with the symptoms for the patient and her family, substance abuse and suicidality. — — — Rape constitutes the worst harm in war due to the shame it brings to both the individuals and the communities. Shame might thrive on silence, but it also thrives on narratives that make certain acts or experiences shameful. It should be recognised that current international accountability and deterrence isn’t doing enough. Eradication of sexual violence should be seen as an achievable goal, and considered a priority by feminists and society at large. Perpetrators and “monstrous leadership” must be held accountable and be prosecuted. Otherwise, the hurt and damage of war will forever live through the civilians and communities deeply affected.

I have lived with an eating disorder since around the age of 12 and it has slowly destroyed my life up until my age now of 22. My illness has worked its way into every crevice. My eating disorder has identified all the aspects of my personality, what I love and what makes me tick, and burned them down to the ground. My eating disorder turned me into a shell of a human being for a really long time. A ghost of my former lively self. My eating disorder has caused destruction to relationships with those I love, my self-esteem, and my zest for life. There has been nothing romantic or glamorous about it. So, why are romantic portrayals of eating disorders still so pervasive? I wish my eating disorder was romantic like many films and TV shows paint them out to be. I wish my eating disorder was jolly and funny like Cassie’s in Skins, who would offer tips to her friends on how to not eat and remain bubbly and outgoing in the face of her struggles. I wish my eating disorder had a romantic subplot like Ellen’s in To the Bone, as she befriends Luke while in treatment, kisses him, then leaves viewers to believe they skipped off into the sunset together. I would love to sit here and type a heartfelt poem about all the life lessons my eating disorder taught me, or gush over how it helped me find my soulmate. I would love to say my eating disorder made me the centre of attention like Hannah in Hollyoaks, whose best friend worshipped her for her disordered behaviours. Or, it made me part of the ‘it’ crowd like Hanna in Pretty Little Liars, who was considered a better friend only when she was skinnier. I would love to say my eating disorder had a beautiful, poignant and purposeful ending like in Black Swan, the haunting ballet film in which Natalie Portman finds purpose after shrinking herself and squeezing every ounce of happiness from her life to play a role. I would love to tell you the recovery journey is always beautiful and inspiring, and it helps you find your true self beneath the rubble of what is left of your earlier life. But, the recovery process doesn’t mean your eating disorder just ceases to exist overnight like Blair’s in Gossip Girl, who had an eating disorder one day before it was never mentioned again. I can’t say all those positive things about eating disorders and I won’t, because it is damaging and unrealistic ideas like that which warp society’s views on how evil eating disorders are and keep those struggling trapped. Eating disorders have the highest mortality rate of all mental disorders and 20% of people with anorexia die — that’s 1 in 5. That’s going out for dinner with a group of four other friends and losing one of them. That’s having a movie night with your parents and siblings and there being an empty space on the sofa. So why, when these disorders are leaving parents without children, lovers without partners, and friends without shoulders to cry on, are we acting like they are aspirational? We live in a society that tends to promote under eating and suggests surviving on as little food as possible is a badge of honour. Our society also suggests eating less and in a disordered fashion is not only normal but the key to eternal happiness in success. We have influencers and reality stars promoting weight loss pills and flat tummy shakes. We walk into clothes stores and see mannequins that are all a size 4. We are demonised and body shamed within our own households for eating “too much” because our mothers and grandmothers have been taught over decades that enjoying food is sinful. Therefore, it is not surprising to me when I open Twitter or press play on a movie and I see eating disorders portrayed as some quest for love or self-discovery. It does, however, anger and upset me. One person dies every hour from an eating disorder. For those of us who recover, we have to live with lifelong damage to our health. How can the world live with itself, continuing to pretend eating disorders are far more joyous and aspirational than they are? We cannot carry on acting as though an eating disorder is merely a mission towards self-acceptance while people destroy their bodies in the hope that they will learn to love themselves when they look a certain way. We cannot pretend that recovery is a process of finding your true purpose. No one should have to hit rock bottom in order to realise that life is worth living. Just recently, I looked in the mirror with such immense shock, because I realised how much my hair had grown and how shiny it was. That’s because my body was starved for such a long time that my hair was weak, limp, lifeless and reflective of how I felt on the inside. I had accepted it as such and never believed it would look glossy or healthy ever again. That is reflective of how severely my eating disorder demolished my well-being, as are the arguments I’ve had with my mum, the days on end I’ve spent in bed crying because I don’t want to be seen, and the panic attacks I’ve had in supermarkets. The reality of living with an eating disorder is bleak and depressing. It is riddled with anxiety, fear, guilt, shame, and violent loneliness. Life with an eating disorder is not a pursuit of one’s true self or a pilgrimage. Life with an eating disorder is not a step in the pursuit of one’s happiness. This is why we need realistic portrayals of eating disorders, as well as encouragement to recover that doesn’t sugarcoat the hard work and effort that must go into it. The healing process from an ED is never plain sailing, but you can come out the other side into a richer, more fruitful life. My eating disorder turned me into someone I did not recognise and did not like. It did not find me love or joy or make me feel fulfilled. We need to stop glorifying disordered eating and such monstrous illnesses as if anything good can ever come from them. The only positive impact an eating disorder can have on our lives is recovery and letting it die.

I, like so many other students in the field of Neuroscience, spent the vast majority of my graduate training studying neurons — the primary information transmitting cells of the brain. It is the intricate circuits of neurons in the brain that give rise to all animal behaviors — from very basic things like breathing, eating, and drinking, to the most complex human thoughts such as moral reasoning and falling in love. But neurons are not the only cell type in the brain. Nor are they the only cells in the body that are responsible for shaping how we think, feel, and act. In recent years, my own personal scientific interest has mirrored that of the field of Neuroscience in general — turning attention towards another, often overlooked cell type in the brain — microglia. The prefix ‘micro’ comes from the ancient Greek word for ‘small’. Microglia are the tiniest cells that reside within the brain. Santiago Ramon y Cajal (1852–1934), a Spanish pathologist who is widely considered to be the father of neuroscience, famously overlooked microglia, thinking they were unlikely to be of any important consequence. It was not until his student Pio del Rio-Hortega (1882–1945) that someone began to take notice of this tiny cell type. I am an incoming Assistant Professor at Boston College, and my lab will study microglia, their role in development, and their interactions with the gut microbiome — which is the topic of this blog post. Microglia help to build the developing brain Microglia are a kind of immune cell called a ‘macrophage’ which comes from the Greek for big (macro) eaters (phages). As such, their job is to “eat” things within the brain — mainly the debris of other cells. However, work in recent decades has shown that microglia also eat synapses, the connections between neurons, during their development, a process called pruning. This ‘pruning’ of synapses is critical to the proper wiring of neural connections during development. What happens when microglial developmental pruning goes array? Why is it so important that we understand the role of microglia in sculpting the brain? The reason this is such a critical question is that indicators of abnormal microglial function, such as eating away at synapses, have been found in brain tissue from human patients with neurodevelopmental and neuropsychiatric conditions ranging from autism spectrum disorder to schizophrenia. Impaired social behavior is a symptom of these conditions. Studies in mice show that getting rid of microglial genes, such as P2Y12 and CX3CR1, reduces synaptic pruning. Furthermore, these mice display abnormal patterns of social interaction — reminiscent of disorders in humans such as autism. These findings, and others, suggest that a better understanding of microglial sculpting of the developing brain may be key to finding treatments and therapeutic interventions for neurodevelopmental disorders such as autism. Microbiota play important roles during development Microglia are not the only ‘micro’ cells with big impacts on brain development. The term ‘microbiota’ refers to the bacteria that live on and within our bodies. While it is common to view all bacteria as dangerous pathogenic invaders, many bacteria actually help us in a variety of sometimes surprising ways. For example, species of bacteria that live within our gut help us by breaking down foods that would be otherwise indigestible, communicating with our immune system and sensory nerves, and even by killing more dangerous microbes and viruses! During development, bacteria also train our immune systems and help shape brain organization. Microbiota in neuropsychiatric disorders As with microglia, gut microbiota are shifted in human neuropsychiatric disorders including autism, depression, and anxiety. But just because the microbiome is different, doesn’t necessarily mean that it causes the changes in brain function and behavior in these conditions. However, experimental manipulation of the gut microbiome has shown promising results so far. For instance, transferring typical microbiota to the guts of human patients with autism reduces their behavioral symptoms. Conversely, transferring microbiota from human autism patients into mice induces social behavior impairments in those animals. The term ‘Psychobiotics’ has been coined by John Cryan and colleagues to refer to bacteria with the potential to positively impact mental health. How do microglia and microbiota interact with one another? There are many outstanding questions as to how microbiota and microglia sculpt the brain during development. For example, microglia appear to be uniquely responsive to signals from the gut microbiome. How are those signals conveyed? There are many potential routes. For instance, when bacteria break down the food we ingest, there are byproducts of this process called metabolites. Studies have shown that these metabolites are often secreted into the bloodstream and can enter the brain. Another potential route is via the vagus nerve. This nerve relays information from the gut, as well as other parts of the body, to the brain. Importantly, bacteria within the gut function as part of a complex ecosystem of bacterial species. Not all bacterial changes are for the better. Therefore, it is essential that we more completely understand the complex interplay within the bacterial communities inside and around us. Much of the work to date has been done in male mice. However, in many cases when females have been studied, the results are not the same. How sex-specific are these findings? This is critically important as many disorders are more commonly diagnosed in males (autism spectrum disorder) or in females (anxiety and depression). Finally, many environmental exposures such as air pollution, pesticides, and even stress, are associated with a higher risk of many of these disorders. How do such environmental exposures impact microglia and the microbiome? Exciting work is currently being done to address these questions. Hopefully, the next decades will see significant advances in our ability to treat neuropsychiatric disorders. Better understanding of microglia, microbiota, and their interactions with one another may hold the key to some of these advances.

Hygge (pronounced “hoo-gah”) is a concept that originated in Danish culture that focuses on living with a sense of comfort, coziness, and peace. It has often been described as creating a warm atmosphere and enjoying the good things that life has to offer with as much positive energy surrounding oneself as possible. Happiness researchers continually find Denmark to have some of the happiest people on Earth, which Danes attribute to the practice of hygge. The increased feelings of happiness and inner peace, and the emotional, physical, and relationship benefits that are key components of the hygge lifestyle, made me interested in finding out more about it. So, I read a book by Meik Wiking’s The Little Book of Hygge: Danish secrets to Happy Living which discusses positive aspects of this type of lifestyle, and I was “hooked”. Then and there I knew I wanted to share what I learned in this blog. I am a mental health and wellness writer and have been incorporating Hygge living in my life for the past year and a half. Cultivating a practice like this has made me more in tune with my thoughts and feelings, thereby enabling me to live more calmly in the present most of the time. Of course, it is still a practice, and far from perfect, but I wholeheartedly embrace the imperfection of this style of living. Some of the emotional benefits of a hygge practice lifestyle may include less depression and anxiety, a greater sense of control over certain areas of one’s life, and increased self-compassion, with less self-judgment and inner criticism, as well as a greater awareness of mindfulness and gratitude. A Hygge-style environment promotes an atmosphere of safety and comfort, where our minds and bodies can feel more relaxed. This means we are more likely to reach out to build and nurture connections with others. In a hygge-centered lifestyle, there is an emphasis on connecting with family, friends, and loved ones. Having strong social support (more emphasis on quality of support as opposed to quantity) and spending time with those who are most important to us creates a sense of belonging and connection that research continuously shows impacts our health and well-being. Examples of possible social benefits may include a focus on togetherness, and feeling safe, increased trust and intimacy, improved existing relationships, (platonic or otherwise), the fostering of new social connections, and less reliance on social media, with more face-to-face connections sans technology. So how is it done? Warm Lighting — Lighting is an essential part of hygge living space. The use of warm, soft white light creates an inviting and comfortable space compared to harsh, bright white bulbs or fluorescent lighting. Texture — Hygge is all about things that feel soft and cozy. Soft accessories like blankets, throws, and pillows create a warm, relaxing, and inviting space. The soft textures can be calming when anxieties run high. Conversations can also seem calmer and more open in this type of space. A coffee break, aka a Fika — This may include baking or buying some sweet treats, and enjoying them in moderation. A hygge nook, aka a Hyggekrog — The designation of a stress-free space or corner in one’s home whereby one can relax and be themselves. Hosting a hygge get together — Hygge-style activities typically involve things that help us feel peaceful, cozy, and connected with others. Gatherings with friends in the home are a primary activity and are focused on the connection built with others, not how big or small one’s home is. Reading as a distraction — Even a short amount of time spent reading can help reduce stress, and anxiety. Along with Hygge’s theme, it can make one feel more present and engaged. Powering down of electronics — When screen time is limited, and all the distractions that come with it, burdens may seem less, as one is more in tune with the present. Intentional Lingering — This involves savouring the moment just a little longer, whatever chore one may be doing, however mundane, with no plans to rush on to the next thing. Minimal (but impactful) décor with less clutter — The utilization of pieces that have special meaning like pictures of family and loved ones. Hygge is about warmth and connection, so clutter free meaningful decor may serve to draw people in and create good meaningful conversation(s) around memories, which in and of itself can be a natural stress reliever. Colour — The colours chosen for a hygge living space are a significant part of setting a cozy stage for reflection and peace of mind. Neutral colours are often chosen, particularly whites, soft whites, beiges, blushes, soft browns, light pinks, and greys. The use of neutral colour palettes may help to calm one’s mind and ease worries and anxieties, which all fit in with this particular style of living. Child’s Play — This typically involves engaging one’s inner child by playing childlike games, thereby stimulating one’s sense of curiosity. Activities may include getting lost in a colouring book, playing hide and seek, exploring a new trail, or playing peek-a-boo with young children. To bring it to a closure, I would like to highlight that a Hygge-focused lifestyle alone might not cure one’s depression or anxiety. However, personally, it has helped me build an intuitive space that’s designed for my personal comfort, peace, and feelings of safety. I am better able to foster deeper connections within myself, as well as with loved ones around me. The benefits of implementing some of these elements go beyond my emotional, physical and social health, as I noticed it being a boon to my overall mental health and wellbeing. Just as Meik Wiking let me in on Danish secrets of happy living, I hope that this blog will do the same for you, my reader.

When I was a clinical psychology trainee at Temple University in the United States, one of the most common complaints I heard from people battling depression was how much they struggled to think clearly, and how much these cognitive difficulties interfered with their ability to live their life. I am now in the final stage of my clinical psychology training at Massachusetts General Hospital and, unfortunately, our understanding of cognitive difficulties in depression is still quite limited. I will soon start as a postdoc at Massachusetts General Hospital’s Depression Clinical & Research Program and my goal is to advance our understanding of why cognitive difficulties emerge in depression so that we can develop effective treatments for this debilitating symptom of depression. When people think about what depression entails, they usually think of states of ‘profound sadness’, ‘disengagement’ or ‘despondency’. Most people believe that they can, at least somewhat, understand how depression might feel — either because they happen to be one of the ‘one-in-five’ people with lived experience of depression or because they have had moments in their lives filled with sadness, disengagement, or despondency (albeit potentially without the severity and/or duration needed to meet formal criteria for depression). This focus on affect, such as sadness and despondency, as the defining features of depression, is, however, a relatively modern trend and prior to the 1850s, depression was considered “primarily a disorder of intellect, often — but not always — accompanied by sadness.” It is only in the last 20 years that researchers have, once again, seriously begun to consider why depressed people experience cognitive problems. Is cognitive functioning really disrupted in depression? That depressed people experience cognitive difficulties is well known. In fact, two of the nine diagnostic criteria that are used to establish a depression diagnosis are reflective of cognitive difficulties (diminished ability to think or concentrate, indecisiveness; psychomotor agitation/retardation) and between 30% and 80% of depressed individuals report cognitive problems, depending on the strictness of the criteria used. When evaluated, depressed individuals tend to display a broad range of cognitive problems, particularly on tests assessing: the capacity to rapidly process information; sustain attention; retain and recall information from memory; and executive functions (e.g., holding information in mind, impulse control, flexibly switching between different ways of responding). And yet, throughout the twentieth century, these cognitive deficits were considered to be ‘epiphenomena’ of depressed mood that simply waxed and waned with the severity of depressed mood. During the last 20 years, researchers have started to focus on cognition in depression — not simply because of growing reason to believe that individuals who experience cognitive problems are more likely to experience impairment in their professional and interpersonal functioning — but because of mounting evidence those cognitive problems persist when depression is in remission. A landmark 2019 review paper that pooled data from 11,882 individuals with remitted depression and 8,533 healthy controls found that individuals with remitted depression performed worse than their non-depressed peers across a wide range of tasks assessing processing speed, memory, attention, and executive function. Of even greater concern, there is growing reason to suspect that depression may increase the risk for neurodegenerative disorders. A review in this area found that, in a majority of studies, a history of depression is associated with a two- to five-fold increased risk of developing dementia. This mounting body of evidence underscores the clinical importance of understanding why cognitive problems persist in remitted depression and the reason why depression increases the risk for dementia. Is inflammation the link between depression and cognitive difficulties?' One plausible reason for why depressed individuals may experience persistent difficulties in cognitive function and increased risk for dementia is that their immune system is dysregulated. The immune system acts — mobilizing immune and non-immune cells — to protect the body from threats from pathogens, like bacteria and viruses, and to promote healing when we are injured. In the process of destroying the invading pathogen, the immune response can sometimes cause a lot of collateral damage to nearby healthy tissue and so, it is critically important that the immune response is time-limited. However, some individuals experience chronic, low-grade inflammation (where parts of the immune system become persistently overly activated) in the absence of a pathogenic threat. This type of chronic, low-grade inflammation is associated with worse immune function and greater susceptibility to disease. Not only is chronic inflammation linked with cancer, cardiovascular disease, and neurodegenerative disorders, but 50% of all deaths are attributable to inflammation-related diseases. Beyond the direct impact of chronic inflammation on human health, low-grade inflammation is known to affect brain regions and disrupt neurotransmission in ways that could explain why cognition is disrupted in depression. When the blood of depressed individuals is compared with non-depressed individuals, researchers consistently find that a sizeable minority — approximately 27% — of depressed individuals exhibit elevated levels of immune biomarkers (e.g., increased C reactive protein) that are indicative of chronic, low-grade inflammation (an important topic that has been discussed previously in Inspire the Mind before, here and here). Some of my own research has sought to shine a light on how inflammation could be linked with cognitive problems in depression. In a population-representative sample of almost 44,000 Dutch adults, we found that it was depressed individuals who also exhibited inflammation (based on blood levels of C reactive protein) who performed worse on a test of executive function. Of concern, a similar pattern of results was also evident in two independent studies of U.S. and Dutch adolescents, suggesting that a deleterious effect of inflammation on cognitive abilities can even be detected early in life. A limitation of this research is that it is associational in nature, meaning that it is difficult to know whether inflammation is causally related to cognitive problems in depression. For instance, there are multiple risk factors for depression — dysregulated sleep, poor diet, stress, physical inactivity, increased weight, and substance abuse — that are also risk factors for inflammation and cognitive difficulties. And so, is it inflammation that causes cognitive problems in depression, or is it simply a risk marker for poor diet, which is the true cause? Or are all of the above caused by poor sleep? More research, especially research using experimental designs that are better equipped to make causal claims, is needed to identify the true cause(s) underlying cognitive problems in depression. What can we do to treat these cognitive difficulties? Treatment options for depressed individuals seeking relief from cognitive problems, such as poor concentration, are extremely limited, although a range of treatments are currently being explored. Physical exercise, brain training exercises, and repetitive transcranial magnetic stimulation are non-pharmacological treatments that have some initial support for their pro-cognitive effects. There is currently one pharmacological treatment (vortioxetine) that has been approved by the United States Food and Drug Administration for the treatment of cognitive problems in depression and initial results suggest that it may help deliver pro-cognitive effects for depressed individuals. However, mixed results so far have been observed and the capacity of vortioxetine to exert persistent benefits beyond the short windows of clinical trials (the majority of which lasted 8 weeks) is unknown. Novel pharmacological treatments are currently being developed and trialled (excellent review available here) but the speed by which new efficacious treatments are discovered may be limited by a lack of mechanistic insight as to treatment targets. In conclusion, there has been considerable progress over the last 20 years in recognizing the cognitive difficulties depressed individuals experience. We now have a better understanding of how they disrupt all dimensions of people’s social and professional life and there is mounting evidence that not only do these difficulties persist when depression is in remission, but depression is linked with an increased risk for neurodegenerative disorders. Now that we recognize that these cognitive problems exist in depression, we must work to understand why they emerge so that we can develop tools to treat them. There is strong reason to believe that a dysregulated immune system could be responsible for these cognitive difficulties in depression and experimental research is now needed to offer mechanistic insight as to the origins of cognitive dysfunction in depression so that they can be used as potential targets for treatment development.

Is Our Immune System Conscious? I’m glad this title got your attention — it caught mine, too, when I realised it was possible! Though I trained as a Child and Adolescent Psychiatrist, I’ve always had an interest in the interface between psychology and philosophy. I was a founder member (and am still part of) the Philosophy Special Interest Group of the Royal College of Psychiatrists. I had phenomenology (which I describe below) drummed into me as a 1980s Manchester trainee, and still believe in its value, as my phenomenological approach contributed to correcting the under-diagnosis of ADHD in the UK in the late 1990s and early 2000s. Furthermore, I had moved toward infant and perinatal mental health, having spotted that infant psychiatry was, astonishingly, underserved. Here, my phenomenology seemed not to fit with the scaled hierarchy of the mother-child dyad. My attempts to combine these managed to catch Karl Friston’s attention, as he spotted that I was groping my way towards Active Inference, which he invented. What follows is where I’m up to, in what I hope is a digestible form. I’m hoping both to make Active Inference accessible and show how its application might radically transform how we should think of ourselves. Consciousness and Phenomenology Explaining consciousness remains the El Dorado of both psychology (the study of mind or behaviour) and cognitive neuroscience (the study of mental phenomena through neuronal structure and function). Descartes famously described us as being made of two kinds of substances, mind and matter, with consciousness being a defining principle of the former. Whether this distinction is genuine or illusory haunts everyone in the field. Meanwhile, for most of us, our everyday experience continues to assert that we are ghosts in the machinery of our bodies, living somewhere behind our eyes. However, what if our bodies support multiple kinds of consciousness, and the consciousness we know is only one type? As my example of our immune system shows, I’m not referring to psychological ideas of the “unconscious mind”, “altered states of consciousness” however caused, or rare psychopathological states where people segregate their consciousness into multiple personalities. Instead, I’m claiming that other systems in our Cartesian machines, far from being mere contextual influences on our experiential selves, have their own orders of consciousness, as subjective and inaccessible as the one we’re used to. The Dimensions of Consciousness For my proposal to make sense, we need some definition of consciousness that does not tie it irrevocably to brain function, but nonetheless says what we mean by it. I’ll therefore approach consciousness through what is called phenomenology. It’s a vast subject, but Figure 2 below summarises its essentials. So, we’re considering what it’s like to be conscious, not what kind of substrate is needed to support consciousness. To keep a very complex topic simple, I’m going to assume that self-consciousness is essential to consciousness (we’ll see why below) and we can describe our everyday experience sufficiently well in three dimensions 1. Awareness. This is our level of consciousness, from fully awake to comatose. 2. Identity. This is our recognition that we are different from our environment. 3. Subjectivity. This is the world we experience. The Free Energy Principle and Active Inference These describe an intellectual apparatus we can use to embody the phenomenological consciousness I’ve just described in a biologically plausible form. Being part of computational neuroscience, they are best described mathematically. However, their overall architecture can be summarised in three segments that don’t require complex maths to grasp. The Markov Blanket of Identity Let’s start (relatively) simply, with a single-celled organism living in some water. It’s an example of a (hierarchically stacked) Non-Equilibrium Steady State (NESS). To survive, these need stuff to keep them going, and to avoid stuff that will end them. We can describe that mathematically, by saying that the stuff it needs for survival forms its Markov Blanket. So long as it keeps its Markov blanket, the harmful stuff in its environment can’t touch it, and it can get to the stuff it needs. However, in all environments stuff moves around, so our organism needs to adapt to maintain its Markov blanket. Put another way, it identifies itself though its Markov blanket, and if it fails to correctly identify itself, it will end and dissolve into equilibrium. So, before we can identify anything else, we must identify ourselves within our environment. Active Inference & Subjectivity Our organism has a dilemma: how can it know what’s out there without breaching its Markov blanket? If it has an idea of what might be out there, it can try some action, and see if the outcome is as it hopes. Any prediction error can then be corrected by further actions. It’s behaving like an investor: it respires hoping its environment will afford oxygen; or eats hoping that what it ingests is nourishing. While we think of sensation as something passively receptive, it is anything but, with both internal and external sensations being inferred from prediction & error correction. As Figure 4 shows, sensory states are in a feedback loop with internal states, while action states crate a similar loop with external ones, enabling iterative error correction. So, we represent our world accurately but indirectly, using subjective representation. Free Energy & Well-Being Across Scale. Confusingly, the “free energy” being talked about here is informational free energy. This quantity is high when the probability of different outcomes is similar, low when a single outcome dominates. Our organism must find the “right” guess about its environment to survive, so it wants to reduce free energy as much as possible. Its success is a measure of its well-being. Fortunately, it can model informational free energy thermodynamically, so it can embody well-being in its metabolism. However, environments differ dramatically with scale, so estimates of well-being must vary with them. Consider our blood. What looks like a thick red liquid to us is a fluid home to a whole range of differently specialised cells, whose well-being must be nurtured to keep us healthy. We are to those cells as our world is to us, but measuring their well-being compared to ours means using tools as different as a telescope and a ruler. While both can measure length, their output is so different we need qualitatively different dimensions to capture them. Putting all this together, we have ended up with a subjective, dimensional space, wherein are represented estimates of our well-being in terms of our world at various scales, obtained from our guesses about it, and our actions upon it. We’ve described two of our conscious dimensions, subjectivity, and identity, as it’s our world. Let’s regard degree of awareness as a function of scale, as we have room for more complexity as scale increases. What is it like to be an immune system? Like our brains, our immune systems’ functioning can be described by FEP/AI. From what’s just been argued, they will also express our dimensions of consciousness. Unfortunately, I can no more prove that the immune system is conscious than I can prove that you are not an unconscious zombie, but we can look for suggestive signs, such as intentionality and choice. Intentionality and teleology is well-recognised in the immune system; indeed, philosophy has focused on trying to remove any implication of consciousness from them. That may be mistaken. Unsurprisingly, studies of the immune system’s impact on choices such as mate selection do not assess agency, but it does influence them, and its responsiveness to social environments is well-established. However, as our consciousness comes from a different system, immunological consciousness is inconceivable to us, so we will not notice it even when present. Despite this, a common need to ensure our bodies’ well-being will coordinate their actions. Does having a conscious immune system matter? It is tempting, particularly from a conventionally materialist position, to say that immune consciousness is as irrelevant as everyday consciousness; they simply reflect a particular point of view about our mechanistic selves. However, most think intention is an important component of cause, and FEP/AI embodies it in our biology. If so, our “psychological” accounts of our behaviour are incomplete, as they only address consequences of being a single type of agent, when it could be that we embody multiple, hierarchically arranged ones, working in cooperation to ensure our well-being and survival across different scales. Maybe it is time for behavioural science to move beyond the brain. Unlike Bataille and his colleagues, we no longer need to abandon reason to do so.

Antipsychotic Medications: Women are different from Men I am a psychiatrist working at the University Medical Center in Groningen, Netherlands and my research focuses on finding optimal treatments for schizophrenia-spectrum disorders. In this blog, I will specifically discuss the relationship between sex and antipsychotic treatment. Although some patients prefer treatment without medication, acute psychosis (that is, the onset or relapse of disorders such as schizophrenia) is usually treated with antipsychotic medication, such as haloperidol and olanzapine. You can learn more about psychosis and antipsychotics in a previous InSPIre the Mind blog written by ITM Deputy Editor, Melisa Kose. When the acute psychosis has passed, many patients are prescribed antipsychotics for a longer period of time to prevent a new psychosis (maintenance treatment). Classical antipsychotics such as haloperidol are still used, while second-generation antipsychotics such as olanzapine and amisulpride are often preferred because of their better balance of efficacy and side effects. In most countries, including the United Kingdom, antipsychotics are prescribed in a rather similar way to both men and women. That is, there is little difference in which antipsychotic is chosen and in what dose it is prescribed. Recent research from Prof. Paola Dazzan and our group in the Netherlands, however, suggests that it is time to make a distinction. The female body is not the same as the male body. Also, the female brain is not the same as the male brain. Sex hormones, such as testosterone and estrogen, have a significant impact on our brains and behaviour. That is why in the Netherlands the Alliance Gender and Mental Health Care (GGZ) was founded in 2021 and supported by our Queen Maxima, which will put tailor-made treatment for men and women on the map. For now, let’s focus on estrogens, the female hormones. Men also produce estrogens, but in women of reproductive age (between puberty and menopause) the production of estrogens is at least twice as high as in men. In these so-called “fertile years”, women generally have a menstrual cycle with a low estrogen period during menstruation and a high estrogen period in the other part of the menstrual cycle. For people with psychotic disorders, these estrogens can be an important support. Estrogens are beneficial for mental health in general, and for psychotic disorders in particular. During periods of high estrogen production, women are relatively protected against negative symptoms (lack of energy and motivation) and intellectual problems (difficulty concentrating and remembering). This means that, during the menstrual period, these symptoms may become a bit more intense, as some women do notice. This also means that after menopause, the symptoms can worsen considerably because the protection by natural estrogens is then permanently lost. Indeed, the level of professional and social functioning of women with a psychotic disorder goes down on average after menopause. But what does all this have to do with antipsychotics? Well, actually, a lot. The effects of antipsychotics on sex hormones First, most antipsychotics are broken down by an enzyme in the liver called CYP1A2. This enzyme breaks down antipsychotics so that they are no longer active. With a few exceptions (quetiapine, amisulpride, paliperidone, and lurasidone), all antipsychotics depend on this enzyme for their breakdown and eventual clearance from the body. However, estrogens slow down this enzyme. As a result, women during the fertile period will have a less active enzyme, which means that the breakdown of most antipsychotics is slower. Thus, when women in their fertile period receive a comparable amount of haloperidol, olanzapine, risperidone or most other antipsychotics as normally given to men, the concentrations in their bodies will become higher than in men. This can lead to side effects. The way I approach this is that I measure the antipsychotic blood levels in women at least annually. That measurement must then be done in the fertile phase of the cycle, so not during menstruation. Sometimes, it turns out that the amount of medication in the blood is very high and the dose can be somewhat reduced. For women who are already receiving a very low dose, such measurements are not necessary. The role of prolactin Many antipsychotics, such as risperidone, haloperidol, and amisulpride, increase another hormone called prolactin. This hormone is an important player after the birth of a baby as it enables breast development and milk production of the mother. Outside the postpartum period, however, the prolactin level should be quite low. Unfortunately, many antipsychotics have the side effect of increasing the production of prolactin. Only the antipsychotics aripiprazole and brexpiprazole do not have this side effect. Quetiapine does cause some prolactin increase, but much less than most other antipsychotic drugs. In contrast, some of the older antipsychotics like haloperidol and risperidone, increase prolactin quite a lot. What does high prolactin production mean? It may mean that the breasts feel a bit tense and become slightly larger. In some cases, there may even be a little milk production. But there’s another thing: you may have heard that breastfeeding women don’t get pregnant again easily? This is because prolactin inhibits the production of estrogens. That is a nice natural mechanism to ensure that a woman does not have the babies too quickly so that she can nurse them quietly. But in women with psychotic disorders, these estrogens had such an important protective role! With the increase of prolactin by antipsychotics, the production of estrogens is inhibited. What you can notice in some of the women who take an antipsychotic, especially those that raise prolactin the most, is that menstruation does not occur, and that women no longer have regular menstrual cycles. In addition, it can actually lead to a worsening of the symptoms that are kept at low levels by the estrogens, due to the reduced estrogens, such as the so-called “negative symptoms” (for example, motivation, and energy to get involved in work or social activities) and problems with thinking, concentration, and memory. This can lead to a greater need for in-patient care or for help with daily living. What can we do about this? Several things. For women of childbearing age who are taking an antipsychotic for a longer period of time (i.e., years rather than months), it would be good to check blood levels of that antipsychotic from time to time. People who use clozapine already do this; the blood levels of that drug are in any case checked annually, as recently discussed in InSPIre the Mind, but we do not do that as standard for the other drugs. With longer use of antipsychotics, it would also be good to use an antipsychotic that does not increase prolactin, or if that’s not possible for any reason, then to use an antipsychotic that causes minimal prolactin increase, such as aripiprazole, brexpiprazole or quetiapine. If someone is well on another antipsychotic, it may be helpful to take a low supplemental dose of aripiprazole, which will help get rid of the unwanted prolactin increase. We can also think of extra estrogens. This can be done via a contraceptive pill, such as the combination pill for women who are of childbearing age but do not want to have children. For women after menopause, Hormone Substitution Therapy is possible, which is the area of expertise of the gynaecologist. However, these hormone treatments come at a price, as they can increase the risk of blood clotting and even breast cancer alongside their benefits such as birth control and preventing a worsening of the psychotic disorder for postmenopausal women. An alternative is the drug raloxifene, of which we see favourable results in research, especially in women after menopause. This drug mimics the effect of estrogens but does not increase the risk of breast cancer. A gynaecologist is probably the most appropriate person to inform women about this and help them decide. Both psychiatrists and people with lived experience of psychosis should be more aware of the sex-specific differences in psychosis and its treatment, so as to optimize success and minimize side effects.