Helena Davies Hi, my name is Helena Davies. I’m  a Postdoctoral Researcher based at the Psychiatric   Centre in Ballerup, Copenhagen, and my research  has focused on the genetics of eating disorders.   In this video, I’ll talk about what we know about  the genetic component of eating disorders, why   it’s important to study this, and where research  is going next. I’ll also touch on the how,   how do we study eating disorder genetics and what  do we mean by terms like heritability [pause]? This is a question I get asked a lot when I  talk about my job and my research. The simple   answer is yes, eating disorders do have  a genetic component, but I really want to   stress that this does not mean that they’re caused  entirely by genetics. So, if we go back in time,   historically, eating disorders were seen as  largely caused by social and cultural influences,   but this all changed around the 1990s,  with the first publications of twin   studies of eating disorders, which  demonstrated this genetic component. Twin studies compare the level of  similarity between identical twins   with that of non-identical twins. And given  that identical twins share 100% of their DNA   and non-identical twins share 50%, this  gives an estimate of heritability. So,   in other words, how much of the differences  between people can be attributed to genetics? And from these twin studies and the many  published since, we know that eating disorders   are approximately 50% heritable. So, about  half of the differences between people can   be attributed to genetics, and this is actually  comparable with other illnesses, such as type 2   diabetes and depression. And actually, given the  longstanding historical focus on the environmental   aspects of causality within the field of eating  disorders, these findings were actually somewhat   controversial. But it’s now widely accepted,  amongst the scientific community, that genetics   does indeed play a role eating disorders and,  in fact, in all psychiatric disorders [pause]. This is a really great question because it’s  understandably quite a misunderstood term.   My original training was actually in psychology,  not in genetics, and so, it also took me a while   to get my head around this. But heritability is  a measure of how much the differences between   us can be attributed to genetics. And there  are some points that I think are important   to understand when we’re thinking about what  heritability means and what it does not mean. So, first, it’s a population level  measure, which means you cannot   interpret it on an individual level. So,  for example, if a trait is 30% heritable,   this does not mean that the causes of the illness  or trait within an individual is 30% due to their   genetics and 70% due to their environment. What  it does mean is that the differences in the trait   between people in a population can, on average,  be attributed to 30% genetics and 70% environment. The second point I’d like to highlight is that  heritability is not a measure of the proportion of   a trait that’s due to genetics, but the proportion  of the differences in the trait that are due to   genetics. So, for example, if every single person  in the population under study had the trait or   illness you were studying, your heritability  would actually be estimated at 0% in a twin study,   because there are no differences between people  and therefore, there’s nothing to estimate. The third and final point I’d like to highlight  is that there are no fixed or true heritability   estimates for a trait. The estimates are specific  to a particular population at a particular time,   and it also depends on how you measure the  trait itself. So, this means that research   that’s based on different groups of people  at different times, using different measures,   can actually give a really wide range  of heritability estimates [pause]. So, yes, there are many ways to study genetic  differences between people without looking at   twins. And actually, whilst twin studies are  able to estimate the contribution of genetics   without actually having to look at people’s  DNA, molecular genetics research looks for   differences in people’s actual DNA. So, if we use  eating disorders as an example, we can compare   the DNA of people with an eating disorder to  the DNA of people without an eating disorder,   and any genetic differences between the two groups  might be causally related to the eating disorder. What’s important to mention here is that we’re not  looking at a handful of pre-selected genes. These   types of studies, known as genome-wide  association studies, scan across the   entire genome, looking for really, really small  differences in the DNA that each have a really,   really small effect. I should also mention  that these genome-wide association studies   look at common differences between  people, and what do I mean by this?   I mean that differences in our genetic  information that affect less than 1% of   the population are considered rare and other  methods are used to study these differences. So far, we’ve only conducted, or mostly only  conducted, genome-wide association studies on   anorexia nervosa, but this will be changing soon,  so do watch this space. But from these studies,   we’ve learned that anorexia nervosa may be  best thought of as a psychiatric and metabolic   disorder, and this is because of findings that  showed the genetic basis of anorexia nervosa   overlapped with metabolic traits. And the authors  of the study that found this speculated that this   might help to answer some of the many perplexing  questions we have about anorexia nervosa. So,   for example, how people with the illness  can lose so much weight in the first place,   when weight loss is so difficult for  the majority of people in the world. Overall, findings from molecular genetics research  have really complemented those from twin studies,   in that they both show that eating disorders  do, indeed, have a genetic component [pause]. The short answer is no, absolutely not. There  is no single gene for an eating disorder.   Genetic risk is made up of hundreds, maybe  even thousands, of very small differences in   DNA that each contribute a very small amount  to overall risk. This means that genetics is   only ever part of the story and that no-one  is destined to experience an eating disorder. A really useful way to think about genetic risk  was designed by Professor Jehannine Austin,   and it’s known as the “mental health jar analogy.”  In this analogy, you can think of your risk for an   eating disorder as a jar, and in this jar, you  have your genetic risk for an eating disorder,   which doesn’t change from birth. So, for some  people, this might mean that their jar is a   third full, whilst for others it might only be 10%  full. And throughout your life, you’ll experience   environmental factors that may increase your risk  for an eating disorder and you can think of each   one as adding more to your jar. So, in order to  experience an eating disorder, your jar has to   be full. However, and this is really important,  protective factors, such as a good sleep pattern   or social support, make your jar bigger, which  means you can experience more environmental   risk factors, without your jar becoming full and  without experiencing an eating disorder [pause]. Eating disorders are extremely complex  and studying their genetics helps to   shed some light on how they come about and  therefore, how we might be able to treat them.   Knowing more about their biology means  we are one step closer to the ultimate   goal of developing drugs that target the  disorders. And this is really important,   because currently, there are no drugs that have  been developed specifically for eating disorders. Learning about genetics can also, perhaps  counterintuitively, teach us about the role   of the environment. And a useful way of thinking  about this is that within a group of people who   are all exposed to the same environment, which  includes the same societal pressure to conform to   certain body standards, and all the other factors  that we associate with eating disorders, only a   minority will actually go on to develop an eating  disorder or disordered eating. So, in this way,   genetics can help us to understand why some people  respond differently to the same environment. And finally, Jehannine Austin and their  team’s work has also nicely shown the   many benefits associated with knowing that  psychiatric disorders have a genetic component,   which can, for example, help  to address feelings of guilt   or shame that are tied up with misconceptions  about the causes of their disorder [pause]. So, as I mentioned, we have so far, focused  largely on anorexia nervosa. So, a first step,   which we’re already working on, will be  exploring the genetics of other eating   disorders, like bulimia nervosa and binge eating  disorder. So, in general, eating disorders are   often overlooked in research, even though they  have one of the highest mortality rates of all   psychiatric disorders, and therefore, they lag  behind slightly in psychiatric genetic discovery.   But some eating disorders fare worse than others  and bulimia nervosa and binge eating disorder   are examples of this. And in fact, they’re  actually more common than anorexia nervosa,   but have significantly less research dedicated  to them, but we’re really hoping to change that. I also mentioned that in genome-wide association  studies what we’re looking for are these really   small differences in the DNA, that each  contribute a really small amount to overall   risk. And in order to detect these really small  differences, we need really, really large samples,   ideally in the hundreds of thousands. And this  is where worldwide collaborative efforts come in,   such as the Psychiatric Genomics Consortium. So,  this is an initiative where Researchers from all   over the world come together and contribute  data, which we then analyse collectively. Moving forward, we’ll need continued  collaboration of the consortium,   as well as continued recruitment effort across  the globe, with a particular focus not only on   recruiting people with eating disorders that are  often overlooked, such as binge eating disorder,   but also those with other characteristics  that are also currently underrepresented in   our samples, such as males, people  of non-European genetic ancestry,   and people with a broader range of educational  and socioeconomic backgrounds. Overall,   it’s a really exciting time for  eating disorders genetics research.