 Okay, thank you very much. I'm delighted to be here and thank you very much to Stefan and Camilla and Matteo for inviting me to be part of this very exciting program. I'm really looking forward to today. So for the next 15 minutes or so I am going to talk about some of the work that we've been doing at Ulster in relation to personalized nutrition and set it in the context of non-communicable diseases. So first of all for the first few minutes just one slide on what is personalized nutrition and I know that we could spend the whole day discussing what exactly that is and then maybe to go through some of the aspects of personalized nutrition in the context of the work that we do at Ulster and focusing on riboflavin for today. So I'll talk about some work on gene-nutrient interactions, nutrient-nutrient interactions a little bit on health practitioners not much time and 15 minutes and just one slide on the challenges going ahead. So for this audience I don't think we need to spend a lot of time on what is personalized nutrition because really it means different things to different people and you know we've had lots of different definitions proposed that try to capture what it is we mean and understand. We've also had different levels proposed but I think for all of us really what the focus is is trying to target advice to support individuals to change and maintain a healthy balanced dietary intake that meets their personal requirement but what makes that very confusing is that we have very many things to consider within this. So there is individual variation and I know in the Stance for Health project you have been considering that and it's going to be very exciting to hear the data emerging today from the microbiome. So to talk through maybe some of these variations I am going to introduce you to my favorite nutrient riboflavin a somewhat overlooked nutrient and maybe more important than some people recognize and I will give two examples of how we can consider riboflavin in relation to personalized nutrition. The first example is gene nutrient example and it's in set in the context of hypertension which we know is one of the major non-communicable diseases. This is a paper sorry from the Lancet which shows us that despite everything we know about hypertension treatment and control rates are still far from optimal. So there are many other factors that must be going on in hypertension that we need to give our attention to and genetics are clearly one of them and this G was genome wide association study and eight separate loci were identified and one of those loci was around the empty hitch sorry I keep pressing the pointer the empty hitch for gene which I am going to focus on today and the prevalence of this polymorphism varies depending on where you live in the world so for example for some people it's virtually non-existent whereas if you live in Mexico one in three people carry this polymorphism which really is putting them at a much increased risk of hypertension and so what this graph tells us is that there are other factors impacting this polymorphism and those must be environmental factors if you think about that graph so we've been interested at Ulster in MTHF4 for many years and in order for MTHF4 to work effectively this is the folate cycle it's part of one carbon metabolism MTHF4 requires the B vitamin riboflavin and in people who carry this polymorphism that I'm talking about their ability to bind riboflavin is affected so they have an enzyme that works less efficiently so we looked at MTHF4 in relation to blood pressure in a cohort of premature cardiovascular disease patients and we reported what others have seen that if you carry this polymorphism both your systolic and diastolic blood pressure are significantly higher but what was very novel about the work that we did was we were the first people to show that if you gave riboflavin just at the dietary level that you were able to significantly lower your blood pressure but this was confined only to the people who carry this TT genotype so this is where the gene and the nutrient are interacting we went on to repeat this work in two separate studies and we can see that there is variation in the response we don't fully understand why but age may be a factor we were also able to look at this polymorphism in relation to blood pressure across the life cycle so we have a very nice large irish cohort of over 66 thousand adults and we showed that from as young as age 18 if you carry this TT genotype which is the red line your blood pressure is significantly higher than if you didn't when you start to get older other factors interfering with blood pressure come into play and the the waters get a little bit muckier but certainly your risk right throughout your life course is slightly higher and this would never be picked up because you're falling well below the cutoff for hypertension but you get to be hypertensive faster and this is true for systolic and diastolic blood pressure we then also were able in that cohort to look at the impact of riboflavin on that association and showed that in people who had poor riboflavin status this is observational data that their risk was three times higher if they carried this gene so there is clearly a gene nutrient effect going on here and when you give riboflavin the lowering that you see compares very well with other lifestyle factors that come into play so that's very important moving on then to my nutrient nutrient example riboflavin is also required in a separate metabolic pathway for the generation of active vitamin b6 or plp so what that means is that you can have a good vitamin b6 intake but if you don't have enough riboflavin there is a risk that you may not be able to convert it into its active form so that's where dietary intake alone won't tell you about your status so here we hypothesize that if you had a low riboflavin intake and this is based on a small randomized controlled trial we carried out many years ago that your vitamin b6 would also be lower again we looked in this large population of irish adults which we had biomarker data for and we demonstrated that if we subdivided them into classes of riboflavin status based on biomarker status and demonstrated that if you had low riboflavin status that this also resulted in a low concentration of vitamin b6 and this was irrespective of your gender or your age so this was right across the board that was interesting data the situation got worse if you superimposed the mth of four tt genotype onto that so if you had the tt and were deficient in riboflavin you have significantly lower plp this is observational we've got to prove it with randomized controlled trial but it does have implications for setting rda's for the likes of fsa and different bodies like that i can't talk much about attitudes of health practitioners but just to say that we did some work with general practitioners medical doctors across two jurisdictions so you know uniquely on the island of ireland we have the uk health service and the irish health service and we recruited gps and asked them some questions about personalized nutrition and what they told us overwhelmingly was that they were in favor of the concept however rather than just give riboflavin which has no upper limit it's not harmful they would prefer a targeted approach so as hosay said we need to work with industry to find nice ways point of care testing that we can help gps and medical practitioners to develop risk scores for diseases like hypertension and here you can see you know the very positive comments that the medical practitioners had in relation to the whole concept so in terms of the challenges and future directions we need accessible data and we need it to be harmonized we need to find out where the gaps are and in terms of the work that we do for with riboflavin you might be surprised to hear that this is actually quite difficult if you look across europe the uk and ireland are the only countries that report riboflavin status at a national level i think also germany might have some data but we have very little data and surprisingly you can see that unlike the developing countries where we have full-blown riboflavin deficiency and this is all measured in our laboratory back at ulster we have there is clear evidence of suboptimal status of riboflavin in different populations if that impacts it's not full-blown deficiency so people aren't worried about it but if we can show that it impacts on non-communicable diseases like hypertension then we should be worried about it and we should find a way to try and incorporate that into our personalized nutrition plans we were lucky enough to through a jpi funded project i led a project with colleagues from ubc in canada to really try and interrogate this a little bit and to try to develop some new accessible markers so there will be some nice data coming out on that in the near future and this is an example like stands for health how by coming together we can generate much better data we need to not just work as nutritionists we need to work with our industry partners we need to work with data analysts we need to work with artificial intelligence to try and develop our biomarkers and then work them into personalized plans so going forward i totally agree we need a multi-actor approach we need to work with industry our stakeholders our consumers we need innovative solutions we have to develop point of care testing we have to be able to find out where gaps are in the data and fill those gaps and we need education overwhelmingly when you look at um medical practitioners they embrace these concepts but they feel inadequate in terms of translating it to their patients and with that i would like to finish um and thank you for your attention and i'm really looking forward to the day and hearing all about the fantastic project that you've been working on for the past number of years thank you very much thank you Mary a lot of information very interesting information quick yeah you know because you have much more in your brain but we don't have too much time to explain about this any questions here in the room yes please just a minute they want to give you the microphone oh okay for the for the people at home or in the lab in the lab right yeah on your last slide so this was very interesting i understood the last slide best i have to admit because i'm more from the digital world than from food but the last the last slide said the very last point was education and you said that practitioners are interested in this but they're not educated on it do you have hypothesis on why that is i mean they have an interest but they don't know why is that well i think it's i think um if you look at there's actually i did some literature searching before i came and if you try and find out from dieticians or medical doctors what their attitudes are towards personalized nutrition the first thing is there isn't a huge amount of data because it's quite difficult to engage um health practitioners even in studies you know for us even to get the numbers that we got which were quite good for medical practitioner study was challenging um but if you look i found some nice work um that reported on dieticians attitudes and and really they don't feel that they have the confidence to give personalized nutrition to their patients so i think they just we need to develop work packages of how to educate them i think it's like cpd that type of activity that we can really engage with health practitioners because that's a really important part of the translation i think jose mentioned earlier you know we have to work together with our industry partners our digital technologies we also have to work with our health practitioners and give them the skills that they can then go on and translate to their patients yeah yeah don't expect for many clinicians to implement your findings unless there's a guideline a guideline from somewhere which will suggest that you have to do this absolutely clinicians are very busy and have too much things in their minds and i totally agree and i think that's why we have to try and influence clinical guidelines like the nice guidelines in the uk and similar guidelines so i think as scientists we should grab opportunities to get on those committees and to share our work because we can't expect clinicians to know about what's going on and all the scientific evidence but we have a responsibility to try and represent the scientific community by not turning away from nice committees and those kind of committees but get on them and try and spread the word and in that way you can influence the guidelines i think or try to testing the i don't need i think i have it for the people in the lab so here we go so i i repeated for the online people yes they're fun thanks um from uh biozoon i saw that you were testing uh riboflavine on uh on a different population group have you split it this population group by age and here my question is specifically interested on the effect of riboflavine on elderly people so are there any difference in the action with regard to decreasing the hypertension in elderly population or have you saw some kind of hints between that yeah when you measure hardly anybody in the world measures riboflavine status globally so our lab is one of the few we have been in you know we're working with uh different countries you know to try and explore that uh three different populations but what we know from our data is actually it's interesting as you age your riboflavine status doesn't get worse so for example with vitamin b6 you can see a decline in age but with riboflavin you don't in relation to the blood pressure lowering um older age becomes a little bit more complex because hypertension um there are a lot more determinants of hypertension in older age so your renal function starts to fall um your vessels become less elastic so there are many reasons why the effect of the gene maybe becomes a little less um of a it becomes less significant but we have conducted studies in the older adults and yes they respond the effect seems to be independent of the class of anti-hypertensive drug they take but this is an interesting question that we would like to address and I haven't got time today but we believe that um riboflavine's activity is via its effect on five methyl THF which is a folate co-factor which influences um nitric oxide which influences vasodilation so there is a mechanism uh you know that we have uh hypothesized um and again we're investigating that a little bit in a little bit more detail so it works in older people but there are other factors that impact hypertension in older people any more questions here in the room you can think that it's quite interesting because of we have different approaches to try to solve to cope with this deficiency in riboflavine exposure adding to different products but in the case we were testing because of we need to for clinicians to to give clear instructions about how to divide the people depending on the gut microbiota composition because depending on that the gut microbiome can produce synthesized riboflavine and so this could allow us to split the different patients exactly and to have different approaches for them okay so we'll see in the future I think the gut microbiota is really interesting we do not know how much the gut contributes to our riboflavine status and that going forward is so interesting to me how can we manage this yeah this could be another step that could be implemented also in the in the regular clinic exactly thank you any questions from the from the internet move on with the next speaker now but we will definitely take on the questions from the slido and inform them afterwards you're not doing the coffee break okay thank you thank you very so much thank you very much