With very few people given access to testing for covid-19, those of us experiencing mild symptoms are left wondering if we have the virus and just how concerned we should be. If it is coronavirus, the questions on all our minds are, what symptoms can you expect and for how long are you going to be ill? I am sharing with you my experience, what I have learnt from this and from other people (friends and family) who had covid-19, and adding a bit of the knowledge from scientific publications. As a scientist interested in the effects of inflammation on the brain and the body myself, I have also a professional interest in this topic! It was mid-March when I started to have a dry annoying cough. Being a psychiatrist, the first thing I thought was that I was nervous and worried about covid-19 and so I had developed a nervous cough… However, a couple of days later my temperature went up and I started to feel extremely fatigued — I quickly realized this could not possibly be just my anxiety. My temperature was not very high, and it has never gone above 38°C, but the extreme feeling of exhaustion and the aches I was experiencing reminded me of times when I had a very high fever. The glands in my neck felt very swollen for the few the first few days and I had a feeling of tightness in my chest. I remember at that time trying to read about the experience of other people who were suffering with covid-19 and coming across the interview of Dr Clare Gerada describing a very bad and painful sore throat in the first few days. After a few days, I developed strong nausea and for a couple of days I could hardly eat. At around days 5–6, I found myself so physically drained that I could hardly sit up in bed and I had the feeling I was fainting, even if I was just laying down on my bed. About 1 week after the first symptoms I completely lost my sense of smell, my nose was not blocked andI could breathe easily from my nose, but I could not smell anything at all, not even the strongest smells. This had never happened to me before and it felt very strange. The first 10–13 days were the toughest and although my temperature was not high, it was always about 37.1.-37.4 C so not really my normal temperature. The feeling of physical exhaustion and a feeling of tightness on my chest were the main issues during the second week. My cough was not very bad initially and it felt gradually improving in the first week but then became again worse around day 10; although gradually improving over time, it took nearly 5 weeks to get over it. Luckily my strength started to come back after 2 weeks and I started to go back very slowly to my routine, trying not to push myself too much. When trying to play football with my daughter in the third week, I could not last more than 2 minutes before becoming breathless and having to sit down. Now, I am not a very fit woman, but this was not normal for me, and it felt like my lungs still needed more time to recover. Another symptom I developed after 1–2 weeks was severe headaches and vertigo; however, I usually suffer with these symptoms so these may not be specific for everyone who is affected by covid-19 and it may just be that since your body is weakened by the virus, some symptoms you are more prone to experience are re-exacerbated. Other people tested positive for covid-19 experienced severe headache or dizziness for few days, and indeed from scientific publications these have also been reported in a small percentage of patients in China. In particular, in a paper published in JAMA Neurology, focusing on patients hospitalized in China for COVID-19, the most common neurological symptoms reported were dizziness (in 17% of their patients) and headache (in 13% of their patients). In another study, patients also reported gastro-intestinal symptoms such as diarrhoea which appears to be associated with longer duration of symptoms and viral clearance, which means the virus may stay in the body a bit longer than in those with only respiratory symptoms. Most of the people I have been in touch with and who were tested for covid-19 had high temperature which lasted sometimes over 1 week, in some cases until day 12–13, and this is also similar to what you see in publications from the data in China. From what you read from scientific publications, possible critical days go from day 6 to day 10 from the onset of the symptoms, as this is the range of days where people started to get admitted to hospital for breathing difficulties or in the worse cases transferred to the intensive care unit. The psychological pressure you feel while you develop these symptoms is very high as what you read from the newspaper is extremely scary. But, the truth is that the majority of people will get over this without ending up in hospital and by taking good care of yourselves, by resting, drinking plenty of water/fluids, and taking paracetamol even if your temperature is not extremely high. I extremely appreciate how difficult it is to understand when you should contact 111 or your GP as one of the main messages we get is to contact them if you have difficulty breathing. You also do not want to put pressure on the NHS with all we hear about the healthcare professionals being overwhelmed. That being said, GP practices are still working and GPs can do phone consultations that could be very helpful in this situation, so I would advise to contact your GP or 111 if you are struggling and if you are not sure whether you need to be seen or go to hospital. I think my message here is to try to not feel too anxious if you are starting to experience covid-19 symptoms and to take things one day at the time, knowing that it may take longer than a week to recover and maybe more than 2 weeks to get back to your normal self. Some recent newspaper articles have described symptoms lasting many weeks. But the most important thing is to take care of yourself and ask for help if you feel you are struggling. I have a little disclosure to make here… I have never been tested for covid-19 so I cannot say for sure that I had covid-19 and I guess most of you reading this will be probably in a similar situation. However, I hope that sharing my experience and what I have heard and read about it may help some of you struggling to find some answers and some reassurance about what you are experiencing. Let’s try to use this time to learn about taking better care of ourselves and of the world around us, and to bring with us what we have learnt to the future… a future world where covid-19 will be no more a threat to anyone. Header image source Freepik

As schools are shut across the UK and older people are particularly encouraged to isolate (including being discouraged them from caring for younger children), there will be very few people of working age who will not need to devote significant time to caring for friends, families and neighbours. The division between ‘carers’ and ‘others’ feels increasingly artificial. The care that we provide for each other is critical for holding our families, communities, and workplaces together — while that’s often overlooked in calmer times, it’s profoundly clear during the pandemic. We are in the early stage of understanding what coronavirus will mean for our health, our society, and the way that we relate to, and connect with, each other. I hope that we can not just respond and survive the current crisis but learn more about how we can and do support each other, which we can continue to acknowledge and appreciate once we get closer to returning to whatever longer-term ‘normal life’ will mean. Wellbeing and productivity are interdependent In February, I wrote about Wellcome’s burgeoning staff networks, and in particular our growing Parents and Carers network. That was written in another time, another age. We used to live in a world where we frequently asked each other to tuck in complex caring responsibilities around our work priorities so that we could maximise our productive working time. This will be nearly impossible for many over the next few months. Wellcome, like others, has become an all-remote organisation. We’re thinking a lot about new ways to enable ourselves to be as effective as possible as an organisation — for us measured in the positive impact we can have through supporting science to improve the health of humanity — while ensuring that we are each playing the best role we can as citizens as the pandemic progresses. The medical response to coronavirus will undoubtedly be key in bringing the risk level down and enabling many of the current social restrictions to loosen. Wellcome is funding work into new diagnostics, therapeutics and vaccines, and supporting our partners to do whatever they can to bring these products forward. At the same time, the more that we can all support each other to physically isolate ourselves and thereby reduce the spread and the burden on our healthcare systems — while nurturing our social connections through other means — the more effective the response will be and the flatter the epidemic curve. Over the year since we concluded our programme to look at the case for a four-day week I’ve been really keen to learn more about how we can maximise wellbeing and productivity as interdependent features of the modern workplace. One thing feels really true in these first weeks of the pandemic — our capacity and pace to burn through lots of work will get much slower and reduced, which will force us collectively both to prioritise even more; and to challenge with even more energy any drift towards presenteeism and overwork. I know that we’ll learn a huge amount from those who already work fully remotely, juggle caring responsibilities or manage significant adjustments to their daily life; and from those friends and colleagues in many Asian countries who have been working with these conditions (successfully) over the last few months. One thing is certain This will be a trying and testing time for everyone, in ways that we may not yet know. We also don’t know what the long term effects will be of this period; both through opportunities to work and live better as a society, and in new risks to our wellbeing. That uncertainty is OK — at this stage, we don’t need all of the answers. But it is clear that the way we care for each other over the coming months will determine the success of our response to this pandemic, and the way we emerge from it. NOTE FROM THE EDITORS: We are delighted to share this wonderful blog from Ed Whiting this week. Ed is the Director of Strategy at the Wellcome Trust and is also the Executive Leadership Team sponsor of Wellcome’s policy function, strategic partnerships and mental health priority area. With experience in public policy both inside and outside of Government, Ed has had a very impressive career so far! Thank you for letting us share your wonderful blog Ed! Header Image Source: Linkedin

In a famous episode reported in the book If this is a man, Italian writer Primo Levi recalls himself speaking with another prisoner in the nazi lager where he was confined and recalling some lines from Dante’s Inferno. “Considerate la vostra semenza:/ fatti non foste a viver come bruti /ma per seguir virtute e canoscenza Call to mind from whence we sprang: / Ye were not form’d to live the life of brutes / but virtue to purse and knowledge high” Suddenly, Levi writes, “they sounded like a trumpet blast, like the voice of God. For a moment, I forgot who I am and where I am”. The power of Poetry is here no doubt recognized as the ability of resonating verses to reconnect men and women with their own humanity. I do not imply of course any direct comparison between the times we are facing now and Levi’s atrocious conditions of life in a concentration camp during a war. Nevertheless, the confinement imposed by the coronavirus pandemic that we are experiencing, for several weeks now, is surely impacting on our sense of liberty, joy and fulfillment of life. It is an unprecedented experience putting all of us in direct confrontation with the challenges of an indefinite physical and psychological constraint. As a poet myself, I find that reading poetry, a genre that finds in the digital era a new and surprising outburst of consensus, can be regarded as a simple and sensible way to cope, through beauty, with the anguish and purposelessness engendered by present restrictions. It is not less interesting to point out, as a source of hope, that several poets in history have found profound inspiration in periods of isolation: the Russian writer Pushkin completed his novel Eugene Onegin while confined to a little Russian village by a cholera outbreak in 1830, the Italian author Torquato Tasso wrote notable poems while prisoner in the S. Anna Hospital in Ferrara, while Turkish poet Nazim Hikmet wrote in the 1940’s, during his imprisonment in Turkey, some of his best known poems, like “To life”. Here at a glance, I suggest some advantages of reading poetry in these days of forced at-home seclusion, and I include some advice on authors to approach. 1. Through poetry we are led towards pointing the attention to one’s inner self. We are taught to give new importance to solitude and imagination. I’d suggest reading “Daffodils” by William Wordsworth, “O solitude” by John Keats, and the book of poems Soledades by Antonio Machado. 2. Poetry tells us that through words we can cultivate hope and that it will always be within us. I’d suggest reading “Hope” by Emily Dickinson, “Blue bird” by Charles Bukovski, and Mottos for an harmonious life by Indian poet R. Tagore. 3. Poetry can be uplifting. In a moment of discomfort, it can sustain the spirit and enforce the will of reaction and self-empowerment. I’d suggest reading American activist and poet Maya Angelou, “Life does not frighten me”, the collection Leaves of Grass by Walt Whitman, and “Freedom” by Paul Eluard. 4. Poetry shows reality through new lenses. It allows us to go deep into the most normal things and give them a different meaning. I’d suggest reading “Butterfly” by Josif Brodskji, “The righteous” by J. L. Borges, and “The goat” by Umberto Saba. 5. Poetry expresses emotions, also those of anguish or anger, giving words to state of mind in which everyone could identify and feel understood. I’d read “Christmas” by G. Ungaretti, “S’i’ fosse foco” by Cecco Angiolieri, and “To me he seems like a God” by Greek poet Saffo. I’d go on, reporting that poetry can express the pleasures of meeting old friends or lovers (“Having a coke with you” by Frank O’Hara), can be fun (“The jabberwocky” by Lewis Carrol, the Calligrams by Apollinaire) and also that it can use metaphors and images that amaze our minds (“First light” by Giorgio Caproni, or “Moored boats” by Dino Campana); but I suppose I can stop here. I’d like though to leave you with a thoughtful invitation, offered by Portuguese poet Fernando Pessoa. This period of our lives can be dull and hard to endure, but “nothing I lost”, and if we really want it, we have the power to transform it in an unexpected opportunity for nurturing our souls and, also thank to poetry, to open the way to new paths for a future, deeper fulfillment. “I want, I will have – If not here, In a place I do not know yet. Nothing I lost. Everything I will be.” — F. PESSOA NOTE FROM THE EDITORS: We would like to say a huge thank you to Anna Maria for sharing this piece with our InSPIre the Mind readers. Anna Maria is an extremely talented poet and journalist and we are so grateful that she wanted to draw on her love of poetry to share with us all how we can use the art as a source of fulfilment during our current situation. Thank you again! Header image source Pixabay

A few months ago, I saw one of Yayoi Kusama’s installations, Gleaming Lights of the Souls. It is part of the permanent collection of the Louisiana Museum of Modern Art in Copenhagen. Today such a normal gallery visit feels like a treat that we will miss for a long time, due to the world-wide coronavirus lockdown. So, I thought it was the right time to write about it — to remember the emotions and the thoughts that I experienced at that time. And to offer some reading material that was not on coronavirus. I was in a small room surrounded by mirrors, the reflecting water of the floor and hundreds of lamps hanging from the ceiling. The lamps are changing their colours adding to the extraordinary experience. I looked at my own reflection and explored this new universe in relation to my own interior one. My everyday exterior environment was hectic and my interior one, shaken. For a second, I thought about me as if I were a neuron in the brain of a person suffering with depression surrounded by hundreds and thousands of other cells like microglia, astrocytes and oligodendrocytes. All these cells spoil me, the neuron. They talk perfectly with each other, interact with each other to protect me, feed me, cleaning ecologically after me and in many ways providing for me, the neuron. Besides neurons, there are other cells in the brain which are called glial cells. These cells are microglia, astrocytes and oligodendrocytes. Microglia is mainly involved in removing the aggressive agents. It can ingest these agents and produce inflammatory signals to call other microglia cells to help with the elimination of the agents. Astrocytes are star-shaped cells which play several roles, including to provide nutrients (food) to the neurons, to repair after an injury to neurons, to control the blood flow to the neurons, even to produce inflammatory signals. Oligodendrocytes are mainly responsible to produce the myelin sheaths, a substance which surround the axons of the neurons to insulate them. A. Neurons are in blue, microglia in green and astrocytes in red. Photography from Neurofit, Preclinical Research for CNS and PNS disorders B. Another Infinity Mirror Room of Yayoi Kusama entitled Brilliance of the Souls. Photography from Museum of Modern and Contemporary Art (Museum MACAN), Jakarta, Indonesia The crosstalk between microglia and other glial cells such as astrocytes and oligodendrocytes is essential in the protection of the neurons. What if in Kusama’s installation suddenly, the red colour gets slightly too bright disturbing my experience? What if the microglia become too active and I, the neuron, am exposed to sustained abnormal levels of inflammation? How will the other cells react to this new environment? Researchers try to understand how other cells in the brain communicate with themselves and provide the best surviving environment for the neurons. Thanks to many individuals suffering with depression who volunteer for research, a lot of studies are available on the role of different cells in the brain during a depressive episode. It seems that microglia are more active but are not increased numerically. This increased activity leads to a slightly increased and persistent production of inflammatory markers, which are responsible for recruiting more inflammatory markers from the body into the brain. In this environment, the astrocytes reduce their number, but not necessarily their function. So, the astrocytes continue to do their job in cleaning, feeding, maintaining the wellbeing of the neurons, but there are fewer of them able to do it. The number of oligodendrocytes is also reduced, mainly in the frontal lobe (key areas of the brain involved in depression). And then what happens to me, the neuron, the spoiled cell in the brain? A lot of questions remain unanswered. But it looks difficult to communicate with other neurons when you are living in a persistently inflamed environment. Neurons are susceptible to increased levels of toxins and reduced number of substances which support the growth, survival and differentiation of neurons. There are fewer synapses, places where neurons meet and exchange information between themselves. In this way high levels of inflammation may play a crucial role in initiating, maintaining and spreading the disease. Depression might begin in the brain and become a more systemic disease, later affecting your entire body and your everyday life. I, the observer of one of Yayoi Kusama’s infinity rooms, enjoyed the beauty of the installation together with my anxiety and sadness. Together we explored the feeling of infinite. It was difficult to concentrate and focus on the experience at some time. Ruminating thoughts invaded my mind. The art experience is influences by our mood and probably by the level of inflammation in our brain. Now, please have a close look at the picture below. Do you see the little snail? That’s pretty much me. I live in a wonderful world which I explore with curiosity and anxiety. I am curious and fascinated by its beauty, whilst also anxious to hurt its perfection. I make a living working as a trainee psychiatrist and occasionally as a researcher on depression and Alzheimer’s disease. Art and nature help me in my struggle to be authentic and honest with myself and my surroundings. HEADER Photo from Louisiana Museum of Modern Art Copenhagen

In 2008, Juliet Russell, Diccon Towns and I set up Salon London to get Londoners together with academics, experts, authors and their ideas in locations across London. Our thinking was that by presenting ideas in relaxed settings, our guests had a better chance of using up to the minute ideas from science and academia in their day to day lives. We had always been interested in psychology and psychiatry as keen observers — but our day jobs (as a writer, and as a musician) left us little time to find out what was happening in the worlds beyond our own disciplines. We wanted ideally to venture into the sciences and see what was happening in other people’s fields and if we could use that info in our own lives. When we launched Salon London we quickly found an audience that felt the same, and fairly soon psychology and neuroscience became a spine throughout our programming. This was because our audience (like us) didn’t want prescriptive ideas of ‘how to’ live their lives — they intuitively knew health and happiness can’t be hacked! — instead they were looking for the best information available to understand the world, themselves and their relationships and intuitively find their own ‘way’ through life. We found out years later that this was typical of more ‘eastern’ philosophical approach of how to live. We really liked this approach as it seemed to indicate that there were many different ways to live if you looked for them. In the decade that followed there certainly seemed to be a huge cultural shift, with more and more people seeking out different ideas for how to spend their time on the planet. Salon London attracted an interesting and interested audience, one keen to learn about new approaches and influences. Looking back, I really think we have played a tiny part in this cultural shift — being a signpost people could use to find their way to new ideas. And for me, a decade on it is that excitement of being able to connect people with an idea, an expert, a book that has the information they need for whatever they are facing in their life at that moment that still makes me happy. It’s just so joyful to connect people with the information they really need from an expert doing the research. Over the 12 years we’ve been in existence, we’ve worked with many brilliant academics, authors and experts: Carmine Pariante, Ian Robertson, Sophie Scott, David Nutt, Gustav Kuhn, Philippa Perry, Barbara Sahakian, Elaine Fox, Catherine Loveday and Gina Rippon and we discovered the huge joy of working with experts is the passion they have for their subjects. We also learned how to bring their ideas to life in an immersive and interactive way creating accessible Salons — and a number of PhD subjects were decided by people who’s interest in their subject was ignited by our Salons, including the relationship between nature and wellbeing, and where memory is held in the brain. But we began to realise it didn’t make sense to be exploring such big ideas only in the capital and so we started branching out to music festivals and soon we were packing out big stages with Salons on ‘stress’, ‘genetics’, and ‘false memories’. The work we’ve done as Salon London in festivals has been extraordinary — a kind of rock and roll public engagement, we have introduced thousands of people to new ideas from science and neuroscience at festivals such as Latitude, Wilderness, Blue Dot and Festival No 6. Working with serious academics in festivals has had its moments, it’s very disarming — you get to know someone very quickly when you’re sharing a dressing room, your stage suddenly floods or by answering a serious question by someone dressed as a badger! However, we began to see there was an increasing appetite for quality scientific information about mental health and on reflection we could see why. As the speed of our efficiency kept getting faster many of us were living our lives at such a pace and demanding so much of ourselves, without ever really giving ourselves the time to recover from the demands we put on ourselves. Living at such a relentless pace good mental health was tricky to maintain, but people wanted scientific evidence alongside their meditation or mindfulness. We also began to see that addressing this properly in a couple of hours in a field or in a London club was impossible. So seven years ago, to enable us to go deeper in to our subjects and to spend more time discussing the big ideas with the experts doing the research, we designed and set up our own ideas festival The Also Festival. This way we could take what we were doing in the city as Salon London (and now with Salon North) to a three-day setting in which we could go much further. The ALSO Festival sits in 50 acres of parkland sculpted by Capability Brown on the banks of a lake about an hour and a half from London. Here we had the ability to let ideas run wild — so we did — we rowed neuroscientists into the festival to rapturous applause, we put on midnight sessions on quantum theory, explored how sound works in the brain in immersive sessions in our disco bunker and even floated serious psychologists and their audience on a lake for guided meditations. In doing so we gave people a much bigger chance to come to spend a bit more time with the ideas in a relaxed setting and spend a bit more immersive time with the big ideas of our time. Seven years on we are now putting on a fully-fledged festival rated as one of the best boutique festivals in the world with over 250 sessions from gong baths to epigenetics to grime music. But our new extraordinary finding was not from one of our 7 stages; it was seeing how transformative our natural setting was to the mental health of our guests. Our audience arrives Friday stressed out from the working week- and yet after three days they left us relaxed and happy — even if they didn’t go to any of our sessions on mental health. So we decided to explore the relationship between nature and mental health by making it the theme for our 2019 Also Festival. Using data from Japan’s national public health program (in 1982, Japan made shinrin-yoku, or “forest bathing”, part of the national health program, and promoted topiary — the art or practice of clipping shrubs or trees into ornamental shape — as therapy) we brought many experts in to the festival to explore the relationship between our health and nature, including Tony Juniper, Mark Maslin, David Lindo and Shirley Gleeson. It was extraordinary to curate a three day programme around this theme and in doing so we enabled hundreds and hundreds of people to reconnect with nature in many different ways. This year we are building on the role nature plays in health by looking at the inter dynamic nature of health and mental health from nutrition and physical wellness. This is because it has not been joyful watching the health and wellness industry explode with social media being a useful tool for disseminating ideas but not necessarily by experts or those backed up by evidence. Food and exercise has become complicated and elitist ‘wellness’ is bound up with eating superfoods, and doing expensive exercise classes in sculpting leisure wear whilst posting it all on Instagram. This one image of health seems to be so, so prevalent it seems to be skewing the way we look at what it means to be well, and we really wanted to tackle that as a big theme of our programming in 2020. So, we’ll be drawing attention to the value of strong relationships and community and altruism. We’ll be talking up choirs and eating together and walking in nature and swimming in the wild and not even noticing you haven’t been on your phone for three days. We are currently programming hard as the festival is just over six months away : 3rd — 5th July 2020. Back in the city, we’ll be kicking off the new decade of Salon London on 16th January with InSPIre the Mind Editor, Prof Carmine Pariante, and Prof Catherine Loveday, who are going to be helping the Salon London crowd to understand the complicated subject of stress and the brain at the h Club in London’s Covent Garden. Two brilliant professors who not only can communicate their ideas very well but also want the audience to understand as much as they can so that they can take what they’ve learned and apply it to their own lives. This approach is Salon London GOLD. I’m hoping that in this way Salon London can help us all start the new decade with a measured approach to stress, one that helps us find the balance between enough to make life interesting but not enough to cause us any problems. NOTE FROM THE EDITORS: We would like to say a big thank you to Helen for writing this great piece. Helen has made great success of Salon London and the Also Festival and it is wonderful to get an insight into such a wonderful organisation. The Stress Salon takes place at 7pm on Thursday 16th January with Professor Carmine Pariante and Professor Catherine Loveday. Header Image Source Salon London

Attention deficit hyperactivity disorder (ADHD) is quite common. It affects about one in 20 children and is three or four times more common in boys than in girls. Children with ADHD, which is characterised by inattention, hyperactivity and impulsivity, are more likely to drop out of school. Fortunately, drugs to treat the condition work well for 60–80% of children who take them. But that leaves 20–40% of children who have a poor response to the drugs or who suffer from side effects. Some studies have shown that omega-3 fish oil may help with ADHD symptoms. What’s more, they’re safe and well-tolerated. However, the results of these studies have been mixed — some children get better, others get worse. We wanted to know whether these results were dependent on whether or not the children had enough omega-3 in their body to begin with. Omega-3 fatty acids, such as docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), are important for our brain, body, immune system and heart. We can only get them from food, such as oily fish, spinach and nuts. Previous studies have found that children with ADHD eat less omega-3-containing food and have less omega-3 in their bodies than children without ADHD, so they are also more likely to show symptoms indicating a lack of omega-3, such as eczema, brittle nails, and dry and scaly skin. But in previous studies, the way omega-3 fatty acids were given was not according to how much omega-3 was in their bodies in the first place. In our study, published in the journal Translational Psychiatry, we examined 92 children, aged 6 to 18, diagnosed with ADHD. Half were randomly assigned to a group taking omega-3, EPA. The other half (the control group) were given a placebo. The trial lasted 12 weeks. We measured the children’s progress with a continuous performance test (CPT), an objective cognitive assessment of attention, vigilance and impulsivity at the beginning and at the end of the trial. We found that children who are deficient in omega-3, measured in the blood, become more attentive and vigilant at the end of the 12 weeks when taking EPA. The difference was statistically significant, that is, unlikely to be the result of chance. However, we did not detect an improvement in ADHD symptoms based on the assessment by parents or teachers, perhaps because the trial was too short to affect these measures. One Can Have Too Much of Fish Oil Interestingly, we found that children who have the highest levels of omega-3 in their bodies have a worsening in some ADHD symptoms, especially impulsivity. This further suggests that you can have “too much of a good thing”, and that an adequate amount of omega-3 is needed for optimal results. Currently, there is no recommended dosage for pure EPA, but a panel of experts suggested that the patients who prefer omega-3 supplementation over stimulant medications (such as Ritalin), should take a combination of DHA and EPA at doses greater than or equal to 750mg a day for at least 12 weeks. However, no children should switch from medications to fish oil based on the results of our study — first, because we find an improvement in some symptoms of ADHD but not all symptoms; second, because we find that not all children benefit from fish oil, and some get worse; and third, because the relative small number of children in the study means that we (or other scientists) should repeat the study in a larger sample. Personalised Medicine Our study is the first to use the concept of personalised medicine (also known as “precision medicine”) applied to nutritional studies. It is also the first study to point out the omega-3 may not provide benefits for all children with ADHD, and in some cases, may even be detrimental. For this reason, children with ADHD should only take a supplement with omega-3 under the supervision of their doctors. And children shouldn’t switch from their medication to fish oil supplements, especially if they are doing well on their medication. But of course, eating more oily fish should be a priority for these children, too. Originally published at http://theconversation.com on November 21, 2019. header image source NutraIngredients

The debate over the psychological impact of violent gaming has been going on for years. If you ask worried parents, they might complain that the violent content is making children act more aggressively in the real world. If you ask the game producers, they might say that the social aspect of online games adds an extra dimension to peer relationships. The gamers themselves might say that playing games offers them ‘escapism’, a chance to escape the stresses of real life, or ‘catharsis’- that they play out all their anger in a safe way. Or they might just say that they enjoy them! But what is the truth? What does the science tell us about the impact of violent games on these adolescents? In May this year, the World Health Organisation (WHO) finalised their decision to include ‘gaming disorder’ in the International Classification of Diseases (ICD) for the first time. Many people laughed, or viewed this as a sad reflection of the addiction of ‘younger generations’ to technology. But gaming disorder is more than just a teen who won’t come to the dinner table unless shouted-at to turn their Xbox off. Although they don’t distinguish between types of video games, the WHO defines gaming disorder as: “a pattern of gaming behaviour characterised by impaired control over gaming, increasing priority given to gaming over other activities to the extent that gaming takes precedence over other interests and daily activities, and continuation or escalation of gaming despite the occurrence of negative consequences” For a person to be diagnosed with gaming disorder, these symptoms must be so severe that they significantly impair personal, family, social, educational or occupational functioning. This sounds scarily similar to the definition for other, more commonly-known addiction disorders, such as drug or gambling addiction. For the WHO to add this to their ICD reflects the fact that these behaviours have been identified all over the world, and that experts are having to develop treatments for them. Although only a small proportion of people who play games are affected by ‘gaming disorder’, it is clear that more people than ever are playing games, so it becomes more important than ever that we understand what the psychological impact of these games is, particularly those which include so much violent content. But, the WHO decision did not come out of nowhere. Scientists had been studying the effects of excessive game-playing long before. For example, five years ago, two researchers from Austria summarised 98 different studies on the effects of game play. They reported that there are social effects of most games, but that it depended on the type of game. Violent games (where the predominant aim is to harm other characters) were associated with increased aggression and reduced prosocial behaviour, whereas prosocial games (where the predominant aim is to help other characters) had the opposite effect. The problem with this is the classic chicken and egg conundrum (or, as we call it in science: ‘causality’). Do individuals with aggressive tendencies play more violent games, or does the playing of violent games increase aggressive tendencies in the people who play them? This is very difficult to work out, unless we start measuring children before they start playing violent games, and track them over time. Even if individuals are not showing any increases in aggressive behaviour, another concern might be desensitisation, where an individual becomes less emotionally affected or shocked by violent imagery. One review of the evidence has indeed reported that exposure to violent video games increases the risk of desensitisation to violence, which may lead to increased aggression or a reduction in prosocial behaviour. However, other studies, some using functional MRI scanning, have not shown any emotional desensitisation in the brains of adult males who play violent video games. So, more needs to be done to understand where there are any desensitisation effects. It is not such a bleak story though; a recent report found no link between aggressive video games and real-world aggression. In fact, some research even shows positive effects of video games. A large study in 2017, using data from 3195 children aged 6–11 in six EU countries reported that, once the figures were adjusted for many other aspects of the child’s environment, high usage of video games almost doubled the chance of a child having high intellectual functioning and school competence. There was no association with mental health problems, but those who used video games were less likely to have problems in peer relationships. However, this study did not describe the type or content of the games that these children were playing. Would the result have been different if they focused on games with violent content? Overall, much of what this research is telling us might seem like ‘common sense’, or may be consistent with what you have observed in your own life. Living with an adult ‘gamer’ myself (my fiancé, in fact!), who is as obsessed with gaming now as he was when he was a teenager, I have observed some of his most aggressive behaviour (and language!) when these games, both violent and non-violent, aren’t going his way. But, I also see him, with his headphones on, talking and laughing online with people he hasn’t seen in a long time. He communicates with friends and relatives who may not have easy access to other social interactions due to disability or social anxiety. Is gaming the best way to address this? No. But, it seems to me, that it is a relatively low-cost, enjoyable way of improving loneliness and social isolation in particularly difficult-to-engage groups of people. Perhaps, like so many other aspects of our lives such as healthy diet and drinking alcohol, it is a case of ‘consumption in moderation’. In this case, parental supervision and education is just as important. Parents need to be very aware of the level of game usage among their children, and of the level of violent content in these games. They also need to ensure that their children are aware and protected from the malicious or toxic behaviour that can often be found in forums where other players have anonymity. Gaming can have many positive effects, such as improving social interaction and may even help to build relationships, as players work together and share a common interest. They also allow players to ‘vent their frustrations’ by playing them out in the gaming world, which may be considered a more ‘safe’ environment. We must not forget that some games can be intellectually stimulating, and this, as we have seen in one of the studies, might even improve school performance. Like we have seen on the packets of sweet treats so many times before, maybe gaming needs to be ‘enjoyed as part of a healthy and balanced lifestyle’. header image source Photo by Sean Do on Unsplash

An old story I would like to start my blog by telling you an old story… It was a hot day in August 2008, when Tony Wyss-Coray sat in a conference room waiting for his lab’s weekly meeting to begin. Wyss-Coray, a professor of neurology at Stanford University, was leading a group of young researchers who studied brain cells degeneration. Sitting close to him was Saul Villeda, an emerging PhD student, who had spent the past year conducting research that aimed to understand how blood affects the brain. They thought that some molecules contained in blood might be able to reach the brain and cause detrimental changes. The hypothesis was not as absurd as it might sound. Villeda conducted pilot studies with mice: young mice received blood from old mice, and old mice received blood from young ones. Villeda wanted to see the effect on their brains. Something which could have never been done in a living human being. And what did Villeda find? Well, neurons in brains of young mice receiving old blood were unable to be regenerated, the neurons started to die, and ultimately young mice brains shrunk and became less functional. A region called the hippocampus, crucial for the process of brain cell generation, or neurogenesis, was one of the first to deteriorate, causing damage to mice’s memories and ability to process new information. Villeda immediately interrogated himself: “Why is this happening? What is it that “old blood” contains that is different from “young blood”?” The answer was simple: inflammation. Body inflammation is regulated by our immune system, the defensive response which protects us against threats, such as infections. Villeda found that some inflammatory proteins contained in the blood of old mice were responsible for the damage of brain cells of young mice. Most importantly, he found that young mice receiving old inflamed blood exhibited cognitive impairments, including memory and learning deficits, similar to those found in patients with neurodegenerative disorders, such as Alzheimer’s. A new story Now, you may wonder why I decided to tell you this story… well, interestingly enough Villeda’s findings could be of relevance for other types of brain and mental health conditions. Indeed, patients with neuropsychiatric disorders, like depression, are known to share similar inflammatory features with Alzheimer’s patients. Strikingly, at least a sub-group of depressed patients had a high level of inflammatory proteins in blood, a reduced number of new generated cells in the brain, and show cognitive impairments similar to those described above for patients with neurodegenerative conditions. This seems to suggest that in patients with depression, similarly to those with Alzheimer’s, blood inflammation is somehow involved in the changes occurring in the brain, and might also contribute to the development of the clinical symptoms of depression. We decided to investigate this hypothesis, and for this purpose we collected blood samples from patients with Hepatitis C virus (HCV), who received the inflammatory protein interferon-alpha (IFN-α) as standard treatment for their HCV infection. Interestingly, up to 35% of patients receiving this immunotherapy develop depression, and that is why this clinical model has been used for years to study the effect of inflammation in the context of depression. However, the exact brain mechanisms via which this happens are still unknown. Using a research model made up of human brain cells (not mice!), we exposed cells to blood from patients with and without depression, and we counted the number of new brain cells generated. Something which, again, could have never been done in a living human being! And findings were quite striking! From our investigations, recently published in the journal of Brain, Behavior and Immunity, we were able to demonstrate that blood from depressed patients can reduce the number of new generating brain neurons and increase the number of dying cells, when compared with blood from non-depressed patients. As Villeda did for his study, we immediately interrogated ourselves: “Why is this happening? What is it that IFN-α is doing to make the blood of some patients “depressed”?” The answer, again, was simple: inflammation. Although we were not able to detect any differences in the same inflammatory proteins reported by Villeda, we identified a novel group of blood molecules, like Mitogen-Activated Protein Kinases (MAPKs) and c-Jun N-terminal Kinases (JNKs), which are known to modulate the immune response, and to be potentially involved in the regulation of brain cells generation. Overall, this seems to suggest that depression, similar to other neurodegenerative disorders, is not an “all in the brain” condition, and that the complex inflammatory environment characterising our blood can affect the life and health of our brain cells, ultimately predisposing the individuals to the development of the symptoms associated with those pathologies. Of course, the story is much more complicated and there might be other factors contained in blood that, together with inflammation, can exert such detrimental consequences on our brain cells. These include other molecules, also detected in the blood of patients with neuropsychiatric or neurodegenerative disorders such as depression and Alzheimer’s, and belonging to the oxidative stress response, like Nuclear factor erythroid 2-related factor 2 (Nrf2) and Fos Proto-Oncogene, AP-1 Transcription Factor Subunit (FOS), which are also known to negatively affect brain cells generation. Although, evidence exists for other blood factors to regulate neurogenesis, ours and Villeda’s findings, unequivocally propose blood inflammation as among one of the major culprits. This, in turn, can have a crucial impact for patient’s therapeutic approaches. If we manage to develop new drugs targeting those blood factors, we might be able to prevent brain cells degeneration and ultimately improve patients’ symptoms. Currently, molecules that block the action of specific inflammatory proteins have been tested in clinical trials for depression (see, for example, ClinicalTrials.gov identifier NCT02473289), or as antiviral strategy, which could be re-purposed for psychiatric indication. One day, these new therapeutic interventions might become effective antidepressants, and will be prescribed to those patients having high levels of inflammation. Header image source: lightsource

Stress — it’s a hot topic for discussion. It seems that every day we are confronted with new information on managing it. The body has many ways to adapt to stress, but one of the most important is the production of cortisol. Each time we have a deadline to meet at work, a public presentation to give, or even have to face our greatest fear (spiders!), cortisol plays a behind-the-scenes role in allowing our body to successfully navigate the challenge ahead. We know the importance of cortisol to managing stress because a few people, those with a disease that prevents them from producing it, cannot live normally without taking replacement hormones that fill the role of their absent cortisol. On the flip side, cortisol that becomes elevated due to stress needs to return to a normal level to maintain health. Therefore, cortisol that is either too low or too high can be a problem. In several long-term illnesses such as rheumatoid arthritis and depression, cortisol levels can change from normal and stay at abnormal levels for a long-time. In depression, patients with long-term increases in the blood level of cortisol are also often found to have very severe depressive symptoms. At the same time, these depressed patients with high blood cortisol often show changes in the function of their immune systems. Generally, this is an over-activity of the immune system, leading immune cells to react like there is an infection in the body, but there isn’t. The presence of both increased blood cortisol and altered immune system function in depressed patients has led doctors to question whether there is a link between these two abnormalities: between problems with the way cortisol levels are controlled in depression and the over-activity of the immune system. Normally, increased cortisol is supposed to put the brakes on the immune system, so having high cortisol and increased immune system activity occurring at the same time in depression is puzzling. We are very interested in understanding how cortisol and the immune system relate to each in other depression, how this relationship might help us to better understand the causes of depression and how we might use a better understanding of this link between cortisol and the immune system to improve treatments for depressed patients. This is one of the areas of mental health research that we have extensively studied in our lab. Over the last 50 or so years, many research studies have looked at how cortisol relates to immune system function in depression. Overall, these studies tell a story that reads like this — cortisol becomes high in depression and this seems to be associated with increases in the activity of immune cells and the amounts of immune signals, called cytokines, that immune cells produce. The problem is that the results of these many studies differ from each other in many ways, often due to differences in the patients that were studied, the type of cytokine that was measured and/or the way in which the effects of increased cortisol were measured. To understand this situation better, we need to look at the overall effect across many studies, using a way to create large groups of patients using data already collected. This process is known as “meta-analysis”. What is a meta-analysis? It begins by finding all of the studies that have been published on the subject of interest, in this case measuring cortisol levels and immune system activity in the same depressed patients, and then using mathematical methods to combine all of the data from the many smaller studies into one large group of patients. Think of it like the democratic election process. Polls taken early in the campaign are like the small studies that report a specific result from a smaller number of patients. Polls ask a small number of the electorate who they think that they will vote for come election day. Since only a small percentage of the voter population is polled, it is possible that the results found by the pollsters may not truly represent how the election results will turn out. Only by examining the results on election night, or in a larger group of patients in meta-analysis, can the true underlying trends be identified. We chose to use meta-analysis to examine how cortisol levels relate to immune system function in depression, as it allowed us to determine an answer in a much shorter time frame than we would have if we designed and conducted a large study of our own. Furthermore, the results of meta-analysis can be used to identify important research questions or measurements that should be part of any future larger study. This helps to make the best use of the money needed to pay for the design and conduct of larger studies whilst also maximizing the potential benefits of these same studies. So, what did we do? Using meta-analysis, we combined patients from up to 32 individual studies into one larger group, totalling up to 1,850 depressed patients and 1,232 healthy controls. We identified a tendency for increased blood cortisol and other effects of increased blood cortisol to accompany increased immune system activity in depressed patients. We can tell this is so because meta-analysis generates a graph that shows how all of the data combined. In this typical picture of how meta-analysis results are presented, each horizontal line represents a study, and the black diamonds represent the combined groups of patients. The more to the right of the vertical line that the diamond falls, the more cytokines that the depressed patients produced when compared with non-depressed patients. In what is the key finding of our study, we found that patients with higher cortisol levels (represented by the top-most diamond) tended to produce the most cytokines, while patients with the lowest cortisol levels tended to produce lesser amounts of cytokines (bottom-most diamond). What’s next? When we began our meta-analysis, we found many individual studies that showed a strong association between increased blood cortisol and increased immune system activity in depression, but we also found other studies that did not find an association between increased blood cortisol and increased immune system activity in depression. By combining all of these studies into one larger group of patients, we found the trend that we discussed above. We also found that more studies need to be conducted, most certainly with very large groups of patients, to fully answer our question. This is important knowledge to have because it helps us to understand that more work in this area is necessary, and it showed us the real picture of the underlying data, a picture that we might have missed if we relied on only a few individual studies. There is still some way to go until our findings are directly applied to the development of new treatments for depression, but our work has taken important steps toward a better understanding of the link between increased cortisol and cortisol-related effects in depression and the function of the immune system. We hope that the answers that our study provides will help in the design of new, larger studies that examine this area further and push it toward directly impacting the suffering experienced by depressed patients. Header image source:welldoing.org

You might have seen the recent headlines. The Sun: The Mirror: Millions taking antidepressants ‘must be warned of dangerous side effects’ The Times: Antidepressants are effective but their use needs to be rationed and monitored The Guardian: I know antidepressant withdrawal symptoms are real. Why didn’t doctors? This news reflects a recently published document from the UK Royal College of Psychiatrists, the professional body responsible for education, for training, and for setting and raising standards in psychiatry. This Position Statement on Antidepressants and Depression describes a range of actions to promote optimal use and management of antidepressants, including, most notably, an updated appraisal of the risk of antidepressants ‘addiction’, i.e., the difficulty that some people have in stopping antidepressants because of ‘withdrawal’ symptoms experienced when they stop these drugs. The document is 29-pages long and you can read it here. Or you can read this blog: an enriched summary — enriched with my personal experience as a psychiatrist and extracts from other clinical guidelines, such as the 2018 Maudsley Prescribing Guidelines. Are antidepressants addictive? If you have ever had problems with tobacco, alcohol, opioids or other street drugs, you will know that taking such substance gives immediate pleasure, gratification and reward. Addictive substances are ‘mood-changing’. This is why people seek them out. Now, if you have ever taken an antidepressant, you know that there is no immediate pleasure. In fact, the only immediate effects of antidepressants are usually the adverse effects, such nausea, diarrhoea or increased agitation. In this sense, antidepressants are not addictive. Moreover, people can become ‘dependent’ on tobacco, alcohol, opioids or other street drugs, as they develop a compulsive desire to take the substances, and have difficulty controlling their use, despite evidence of harm. Again, people do not experience such a compulsive desire to take antidepressants. However, addictive substances have one important characteristic that can also be present with antidepressants. After you have taken the substance regularly, you suffer when you stop it, not only because you are missing the pleasurable effects, but because your body and brain now ‘require’ the substance, and you feel unwell if you do not take it. When you stop, you suffer from withdrawal symptoms. You go ‘cold turkey’. And antidepressants can do this. Not all antidepressants. Not in all patients. But some antidepressants can be very difficult to stop, for some patients. As the statement says, ‘Whilst the withdrawal symptoms which arise on and after stopping antidepressants are often mild and self-limiting, there can be substantial variation in people’s experience, with symptoms lasting much longer and being more severe for some patients.” This is what this blog is about. What do antidepressants withdrawal symptoms feel like? There are many types of symptoms, and not all patients experience all of them. Typical symptoms are: flu-like symptoms (shivering, excessive sweating, headache, nausea, vomiting); ‘shock-like’ sensations (brain zapping, as described by patients); insomnia and vivid dreams; irritability and crying spells; dizziness; and occasionally, movement problems and decreased concentration and memory. They usually start abruptly and within a few days of stopping the antidepressants. Thus, they are different from a return of the original anxiety and depression for which the antidepressants were prescribed in the first place, which is more gradual and can take weeks or months to reappear. The percentage of patients reporting withdrawal symptoms varies a lot in between studies, also because different antidepressants have different risk of withdrawal symptoms. An analysis of many studies, some including patients’ surveys– which may not be representative of the entire population of people taking antidepressants — find that more than half of patients who stop or reduce antidepressants experience withdrawal symptoms, with almost all of them reporting severe symptoms, and a significant proportion experiencing symptoms for several weeks, months, or longer. A stricter analysis only of studies that have a ‘placebo’ comparison– believe it or not, people can have withdrawal symptoms even when stopping an inert, dummy pill — brings the proportion of people who experience withdrawal symptoms at around 40%, with various levels of severity, from mild and self-limiting to prolonged and severe. In any case, it is a relevant proportion of people taking antidepressants. It is more than we used to think. And it is a good thing that new scientific evidence and patients’ voices have prompted the statement from the Royal College. And this blog. So, how can you minimise the risk of antidepressant withdrawal symptoms? First, do not take antidepressants unless you really need to take them. Most people who go through a difficult time in their lives should not be prescribed antidepressants. They should rely on the support of friends, family and the wider social support when going through a crisis. And, if they need professional help for coping, they should access psychological therapies first. In many countries, psychological therapies are rarely available in the public health services, but in the UK they are– another jewel in our NHS crown. Antidepressants should only be prescribed for people who suffer from clinical depression of significant intensity. These are people who have been suffering from sadness, tiredness, lack of hope and motivation, and thoughts about death, every day, for weeks or months. And who have a reduced quality of life because of their depression: they have stopped working; they no longer have social relationships; they have used more alcohol than before; they have been thinking about, or planning how, taking their own lives. Second, you should only take the antidepressants for as long as you need them, and not longer. Accepted clinical guidelines indicate that, for people who take an antidepressant for the first time, or only sporadically throughout their life, these drugs should be taken for a maximum of 6 to 9 months after people have started to be well again. Longer treatments, for 1–2 years or more, are only appropriate if there have been multiple, frequent and severe phases of depression. The decision to continue on an antidepressant should be regularly reviewed in discussion with the doctor. Third, if you decide to stop, do so slowly, and with the support of your doctor. People should never stop an antidepressant abruptly and without consulting their doctor. The dose should be reduced gradually, and the current advice of reducing and stopping over four weeks should be considered the minimum time, provided it is tolerable for the patient, but not the rule for everybody. For some people, it may be necessary to reduce over several months, especially if they have taken the antidepressants for years. The slower reduction should be toward the end, because this is when the proportional reduction of the dose is bigger. Of course, not everybody will experience the withdrawal symptoms in their more severe form. Longer duration of treatment, as mentioned above, and higher doses, increase the risk of severe withdrawal symptoms. Some antidepressants increase the risk more than others (for example, paroxetine, venlafaxine, amitriptyline, imipramine, all MOAIs). Children and adolescents are at a higher risk of severe withdrawal symptoms (and they should only receive antidepressants under the care of a specialist psychiatrist). People who are taking other medications affecting the brain (antihypertensive, antihistamine, antipsychotics) are a higher risk. People who experience a worsening of anxiety symptoms at the start of an antidepressant are a higher risk. And if you have experienced withdrawals symptoms when stopping an antidepressant before, you are likely to experience them again. If the symptoms do develop and cannot be tolerated, or do not improve spontaneously over 1–2 weeks, then there are steps that can be taken. The doctor should re-start the same antidepressant (or another antidepressant that is less likely to induce withdrawal symptoms) at the last dose before the withdrawal symptoms occurred, and the reduction should be slowed down. Slowed right down. What does the future hold? As the College statement says, ‘Depression is a condition that can affect people differently and cause a wide variety of distressing symptoms. It can lead to relationship and family breakdown, increase the likelihood of drug or alcohol addiction, reduce the ability to overcome serious illness and increase mortality rates — not just from the risk of suicide.’ Antidepressants are a recommended therapeutic option. And they do work — in fact they are more effective than many medications used for physical health problems (for example, than some drugs routinely prescribed for hypertension and chronic heart failure). But of course, we do need to understand more about these drugs. About ‘personalizing’ antidepressant treatment, in order to choose the antidepressant which is more likely to work best for an individual patient, or least likely to induce side effects. And, of course, as discussed here, we need to understand the best antidepressants to minimize the severity and duration of withdrawal symptoms. But we should not dismiss this important therapeutic tool, nor judge it more harshly than we judge other medications for physical disorders. Otherwise, we are simply perpetuating the stigma about mental health problems: not needing medications because they are ‘not real’ and are ‘all in the mind’. Disclaimer: My research work, and the work of our research group, is funded mostly by the UK National Health Service, and other governmental and charitable organisations. We also receive some research funding from pharmaceutical companies interested in the development of medications for depression; however, this blog, and similar blogs we post on these topics, are completely independent, and only based on the best scientific and clinical evidence.

Identifying women at risk could protect them and their infants. Perhaps not everyone knows that depression during pregnancy is as common as, or possibly more common, than postnatal depression. Contrary to what is commonly thought, women are not “hormonally protected” from mental health difficulties during pregnancy. Indeed, up to 20% of women will experience depression or anxiety at some point while they are pregnant. The whole perinatal period, i.e., pregnancy, birth and the first postnatal year, is associated with an increased vulnerability for the woman’s mental health. This increased vulnerability is because of the many changes and challenges, as well as the high levels of stress, associated with this particular time in a woman’s life. Whilst depression during pregnancy is common, many women are not currently identified as depressed by their doctors and midwives, thus they do not receive adequate treatment. Why is this important? There is extensive literature showing that an untreated episode of depression during pregnancy can be associated with negative long-term effects on the offspring’s development, not only in infancy but also through adolescence and young adulthood, even when taking the mother’s mental health outside of this period into account. We also know that antenatal depression is one of the strongest risk factors for developing postnatal depression, and that postnatal depression is itself often associated with difficulties in the mother-infant relationship, high levels of parenting stress (that is, the stress associated with the role of being a parent) and less optimal child development (for example, infants who have difficulties in speaking and in learning, or infants who show behavioural or emotional problems). https://womensmentalhealth.org/posts/partner_conflict_vulnerability_perinatal_depression/ The good news is that we can identify women who are at risk of suffering from depression and anxiety early on, when symptoms are only starting to emerge or even when they are not present yet. Understanding the risk factors can help more women to remain well. Indeed, the perinatal period represents a unique window of opportunity for intervention, as most women will have contact with health professionals, and they are usually highly motivated to engage in order to promote their own, as well as their infants’ wellbeing. Of course, it is important to highlight that feeling sad, tired and stressed during pregnancy does not necessarily mean that a woman is depressed. It can be completely normal to feel this way at times during pregnancy. What we are talking about is clinical depression — a pervasive and prolonged sadness that severely affects the woman’s ability to function everyday, to enjoy things in her life and to interact with people as she normally would. So, which women are at risk of developing depression and anxiety in pregnancy? In what is still one of the most read papers from our research group, published in Journal of Affective Disorders, I have discussed which factors increase the risk of depression and anxiety in pregnancy, ranging from the psycho-social aspects to the presence of obstetric and pregnancy-related difficulties. Perhaps not surprisingly, a previous history of mental disorders, and particularly a previous history of depression and anxiety, is one of the strongest risk factors. However, it is less known that high levels of stress also increase the risk of depression and anxiety in pregnancy. This includes stress during pregnancy (adverse experiences, such as the death of a relative or close friend, losing a job or experiencing a serious illness) but also, interestingly, stress early in life (for example, having been exposed to a difficult childhood because of violence or emotional neglect). Domestic violence, both current and previous, is another important risk factor, and women should be supported by health professionals in seeking help and refuge in such situations. There are also factors related to pregnancy, such as an unwanted pregnancy, as well as current or previous pregnancy complications or pregnancy loss. Some factors relate to social and economic circumstances: for example, experiencing economic difficulties, or a lack of social and partner support; not having a partner or experiencing problems in the marital relationship. Indeed, the experience of lack of support, particularly from the partner but also from family and friends, increases the woman’s vulnerability to depression and anxiety during pregnancy. On the other hand, protective factors have also been shown by research: being satisfied with the marital relationship; perceiving the partner and the social network as supportive and having a positive and active coping style. These protective factors are very important and can limit any potential negative impact of the risk factors. It is important to highlight that these are just “risk factors”, and do not cause these problems for every woman. Indeed, many women who have these risk factors will not develop depression and anxiety in pregnancy. Mental health during pregnancy depends on many different circumstances interacting and combining together in different ways, eventually increasing the risk that some women will become unwell while others remain well. Therefore, these are not causal and non-modifiable journeys, and they are not identical for all women. Photo by Heather Mount on Unsplash It is also important to say that not all episodes of depression during this period will be associated with negative consequences for the child. Once again, there are multiple factors that combine and interact together in different ways. For example, there are many factors that can protect the infant’s wellbeing when the mother is unwell, such as the presence of a supportive and caring partner. Nevertheless, correctly identifying the women most at risk of suffering from these disorders would offer the opportunity to provide preventative and supportive interventions and to monitor these women during pregnancy so that early symptoms could be recognised, and therapeutic interventions implemented in a timely manner. This is likely to have a long-term positive impact on both mother and infant.

The latest edition of the Diagnostic and Statistical Manual (DSM), a handbook used by healthcare professionals to diagnose mental illnesses, featured several new disorders. One was Gambling Disorder, the first and only behavioural addiction currently included in the manual. It was included on the basis that gambling activates the same parts of the brain as drugs like cocaine (specifically, parts of the brain related to reward and motivation). However, calls from the scientific community to recognise overeating as an addictive disorder were not applied, sparking controversy and debate amongst researchers. The idea of food being addictive is not a new one. In 1890, the word “addiction” was first used scientifically in one of the earliest medical journals on this topic (The Journal of Inebriety), in reference to chocolate. The term “food addiction” was later coined by Theron Randolph in 1956 but remained fairly unexplored in the following years. However, driven by rising rates of obesity and concern over the associated health and economic costs, the last decade has seen a rapid increase in interest in food addiction amongst scientists, the media and the public. As a relatively young field of research, many questions about food addiction remain unanswered: Can overeating become an uncontrollable medical condition? Is there enough evidence to include it as a mental disorder in the DSM? And if so, what are the potential consequences of such an important decision? What is the evidence for Food Addiction? Addiction? “My drug of choice is food. I use food for the same reasons an addict uses drugs: to comfort, to soothe, to ease stress.” — Oprah Winfrey To be diagnosed with an addictive disorder you must meet the following criteria: i) impaired control — difficulty controlling your use of the substance, ii) social impairment — experiencing social problems due to the addiction, iii) risky use — continuing to use the substance despite physical or mental health problems (or both),and iv) pharmacological criteria — such as withdrawal symptoms (symptoms like sweating or shaking as a result of stopping opioids suddenly). These have been shown in animal models in relation to foods high in fat or sugar. One study found that rats were willing to tolerate painful foot shocks to acquire a supply of Oreo cookies, which was interpreted as evidence of risky use. Other studies have documented intense withdrawal symptoms, such as teeth chattering, head shaking, anxiety and aggression shortly after a diet high in sugar was removed. In humans, the evidence is less clear. There is plenty of evidence from online forums and clinical case studies showing signs of craving, lack of control and withdrawal in people trying to cut down on processed food such as bread, sweets and crisps. But this type of evidence can be subjective and is often based on small numbers of participants. Scientists need much more than this to prove that food addiction exists. “Over the years, I needed to consume more calories for longer periods to achieve the same sense of control, emotional numbness, and euphoria” — Hansen (2016) More recently, scientists have shown that the same brain areas are activated by drugs like alcohol, cocaine, heroin and by processed foods. These are brain areas involved in reward, motivation, stress and self-control. Of course, we expect some overlap in brain areas relevant to both food and pleasure, but there is more and more evidence suggesting that they share brain processes which, when hijacked, result in binging and loss of control. One such brain imaging study found that individuals who tend to score higher on a specific scale that measures “food addiction” (for example, that eat to the point of feeling physical ill or that avoid professional or social situations where certain foods are available for fear of overeating) have increased activity in reward and motivation parts of the brain when they were told to expect a chocolate milkshake, and decreased activity in self-control parts of the brain when actually given the chocolate milkshake to drink. Interestingly, this can be found in both people of normal weight and with obesity. So if evidence shows that processed food activates the same reward and motivational parts of the brain as drugs and gambling do, why has food addiction not been officially recognised yet? Critics of food addiction argue that food is necessary for survival and therefore cannot be addictive. But think for a moment about water, a substance that is essential for survival. Water can become addictive when certain ingredients are added. Beer, for example, can be up to 97% water but becomes an addictive substance when ethanol is added. Supporters of the notion that food addiction does exist are not arguing that foods such as vegetables are addictive. It is the refined ingredients such as sugar and fats, specifically added to processed food, that make the food addictive. A recent BBC documentary “Why are we getting so fat?” featuring Dr Giles Yeo, a geneticist from Cambridge University, emphasises the importance of studying combinations of nutrients that do not occur naturally, but when combined can “pack a punch” to brain motivation circuits and change our normal eating behaviour. Yeo quotes a study where food items that containedbothfat and carbohydrate were valued more highly than food items high in just fat or carbohydrate alone. These “double-whammy” food items also had a greater effect on brain reward areas than the food items that were high in just fat or carbohydrate alone. It might seem obvious to some people that foods high in carbohydrates and fat would be more addictive, but as a recent Guardian article noted there is a certain hysteria surrounding food in today’s mainstream media. On a daily basis, we are bombarded with contradictory advice about what to eat and what not to eat. It is no wonder than many of us feel alienated and confused. A task for future research will be to work out exactly which combinations of nutrients have the potential to become addictive and to communicate this in a clear way to the public. What would be the potential repercussions of including food addiction in the DSM? Classifying overeating as an addiction would have far-reaching effects. It will undoubtedly impact public health, healthcare provision, economics, public opinion and governmental policy. Valuable lessons can be learned from looking back at the history of the tobacco industry. For many years the tobacco industry framed smoking addiction as a problem of self-control, blaming individuals rather than the companies supplying the cigarettes. Person-centered treatments, where the individual addicted to smoking was helped in finding their way of reducing or stopping, were the only accepted approach for a long time. This was before any effective policy interventions were considered due to lobbying from smoking companies. Luckily, things have changed now. Smoking rates in the UK are at an all-time low because of population-level changes to taxation, shop displays and laws on smoking indoors. Currently, much of society blames individuals with obesity for their excess weight, with common misunderstandings that individuals with obesity are entirely responsible for their condition. This mirrors what happened to smokers 50 years ago. These views are prevalent and exist even in those making critical decisions for the health of the UK. In a recent speech Health Secretary, Matt Hancock, said the following: “Prevention is about ensuring that people take greater responsibility for managing their own health. It’s about people choosing to look after themselves better…making better choices by limiting alcohol, sugar, salt and fat.” However, if the concept of food addiction is given support, we may see a shift towards more balanced, society-wide approaches to tackling the population’s diet. We have to make it easier for people to make healthy choices, across all social classes. Ideally, the price of processed foods should increase, the price of fresh, healthy produce should be subsidised, and advertising should be regulated more. Moreover, we could hope to see a reduction in weight-related discrimination targeted at individuals who are overweight or living with obesity, which would actually have positive consequences not only for their mental health, but also for their weight loss and maintenance of weight loss over time. However, not everybody shares this view. Opposing researchers theorise that it could offer individuals an excuse for unhealthy eating patterns and worsen the problem of obesity. Also, we could see the food industry try to contest research or block policy reforms, as has already occurred in the US with regard to menu labeling and restriction of junk food in schools. The food industry may also begin more aggressive marketing in developing countries, where laws are more relaxed (a trend we are already beginning to see). This issue will continue to be debated. As the field of food addiction moves into unknown territory, it important to truly understand if advocating a diagnosis of “food addiction” will have a more harmful or more beneficial net impact on health. Research, and more evidence, are urgently needed. The decision about this important question should not be left to the strongest lobbiers, it should be based on the populations’ health and wellbeing. We will need to work with the government and food producers to achieve this.