Omega-3 for Inflammation & Performance Recovery - Dr Dan Plews x Dr Greg Peoples

[MUSIC] Hi guys and welcome back to the Pell Performance Podcast. On this podcast we sit down with leaders in their field of research and high performance as well as the founders and the builders of the companies that exist within the world of high performance sporting ecosystem. At Pell Art we are on a mission to get athletes to the start line in their best condition. We have a vision to shift micro nutrition from preventative into performance and we want to do this permanently. How we do that at Pell Art we enable athletes to get to the start line by developing clinical micro nutrition supplements across sleep, recovery, inflammation, energy and immunity. This is a great conversation today by our own Dr. Dan Pluse, our head of research. He is interviewing Dr. Gregory Peoples. Now Dr. Peoples is a premier expert in the physiological role of Omega-3 EPA and DHA and how it can optimize athletic performance and recovery. He has an academic career spanning over 20 years of Omega-3 research for athletes. Also in exercise physiology he has over 80 peer review publications. Now this is a fantastic episode. It is on the eve of our very own inclusion into our first medical research. This research paper has been done by Gregory and his team out of the University of Wollongong. It's an international Journal of Sports, Nutrition and Exercise and Metabolism. It aims to unlock really new novel insights into how rugby league players in Australia, professional rugby league players are engaging with Omega-3 fatty acid and also the supplementation advice in order to use these essential amino fatty acids as a nutritional tool to enhance performance and recovery. This study is an amazing example of what you can do and the potential benefit of Omega-3 for performance. Obviously Omega has some incredible attributes for overall health. But this particular study, one that we are very proud to have our very own Ultra-Mega product as the constant product used within the study to show the benefits of Omega. So Dan and Dr. Peoples are diving into this and I hope you guys enjoy. Great people, welcome to the Pillow Performance Podcast. It's really great to have you on here. I know that we first met when we came across your work where you contacted Asan, you know, we knew that you were doing some work using the Pillow Omega-3s and when CEO Damien asked me to do a podcast to start to have some people to come on at you or top of my list. So massive thanks for coming on. Yeah, look thanks Dan. I've, you know, apparently also followed your work around sort of heart because of that crossover with Omega-3s and heart. But that spot on, like we've been doing a range of work, particularly around contact athletes. And this opportunity that we had to work with a local group here in Moulinong, the St. George's World of Dragons was a great example of applying, putting in sports nutrition practice through a lot of the bariture work that we've done on Omega-3s. So yeah, hence reaching out to you guys and just letting you know that obviously the capsule has been used and also that opportunity with daily collection was occurring on side that. Yeah, and that's what, you know, we really want to talk about that study. But before we get there, would you be so kind of to give the listeners a little bit of a background of what you've come from in your research and your research interests? Yeah, it's been an interesting pathway. I initially studied biomedical science back in the day, but I was very fortunate to come across Professor Peter McLean, who had just moved to the University of Moulinong. This is going 20 years now and he offered me the opportunity to work in his laboratory and he'd been studying the role of Omega-3 in heart function for many years. A lot of his work had been in animal work and he said, "Look, we need to really sort of pull this across into examples where the human heart was being used." So I got to my honest under Peter and we looked at loading up Omega-3 into, I wouldn't say a leak cyclist, but they were very highly trained cyclists, as part of my honest project. And then I moved into a PhD with him after as well, looking at the the impacts of particularly DHA on contract offered to you and muscle function and putting muscle under stress, you know, conditions such as hypoxia and ischemia and having a look to how muscle sort of works under those conditions as well. So, you know, from there, I've sort of taken up my own personal laboratory, but I acknowledge a lot of Peter's training has put me in the position I am today, you know, sort of 20 years later and that constant theme of sort of continuing to sort of and you know how it is, probe that question on what's actually going on with the Omega-3 story. So did you look at the effects of hypoxia and how acute was the hypoxia you're talking, you know, altitude training hypoxia or? Yeah, I guess about back, back, one of my interesting areas and where I kind of differ to some other physiologists that worked in the area of Omega-3 is because I trained under Peter, we also have done animal work. So that particular work with hypoxia and muscle fatigue, I was part of my PhD, we actually had a controlled bypass surgery set up with contractile lymph, so I'm glad it's lymph. So we're able to do that. Yeah, we're able to manipulate the amount of oxygen that that lymph had and then we obviously had animals that were loaded up on DHA animals that were control animals and so. And quick, quick, quick finding, did the, did the Omega-3s that effects have good effects on? Yeah, so the interesting part about that is that the fatigue or the loss of contractile force during the hypoxic challenge was fairly similar. The difference was that when we went into the recovery stage, we actually then injected because we could inject direct into the arm and we injected caffeine directly into the arm and caffeine and then stimulates calcium release from the muscle. So what we noticed was that the animals that were loaded with DHA got a better contractile response during recovery. So could you take from that like a practical standpoint that if you're loading on Omega-3s and you're doing like, and you're training altitude, you could potentially recover faster from your efforts. Yeah, it's a take some caffeine post or could you draw that from that? Yeah, this is actually a bucket, this project in mind is to again, it's a common theme of our laboratories. We look at stuff either at cell at animal level and then we take it into the real world. So one of our bucket, this project is actually to look at some altitude, both responses. Without DHA loading in particular. It's not about anything that's really been done. I mean, no one really, I mean, when you talk about altitude, what nutrition is always talking about iron and ferritin and no one will mention Omega-3s when it comes to hypoxic or altitude training. It's not even in the discussion point. So it's quite, I mean, what you've discussed there, it's quite interesting, right? It could be, it could be something that's a real, a real good one. There's a couple of common themes. It really comes down to a lot of the work that Omega-3 does around cell integrity, cell durability is constantly sort of coming up around when cells are put into stress situations. So it's giving you an hypoxia, they're a good example. And really that backs back to the work that Omega-3 is a cardio protective and cardio protective means that when those my starts go into periods of a scheme, you know, those cells are loaded in DHA and less likely to experience aeridmias. So if you move that forward into sort of whole body situations, well, there's a high chance that's skeletal muscle war. So yeah, respond and cope better with hypoxic conditions too. So it's about this project. And then it obviously goes into more than just any type of environmental stress, right? Because I wouldn't do it then, you know, that what about the heat and what about all those, you know, and all those different environmental stresses that I mean, I remember my PhD supervisor always taught me is that he said, you know, well, one night in my PhD, it was very much in the practical, you know, I was working in Rome as it was, and it was very practically applied. And he is like, he says, we're in the business of useful, not interesting. And you know, what you did was very interesting. And then I guess it's the point of like now, it's like how to flip it onto the useful part, but there's got to be there definitely be something in there, it's fascinating. Everything has to start with interesting before it gets into the useful though you don't know. That's right. And it's also that ability to look and cross over information from other areas in it and look just to just sort of dwell on this for, you know, a short period of time, the concept of hypoxia and omega-3 is also not new when you look at areas like births at altitude. So if you look at the placental tissue of mothers that give birth at altitude, there was a very high amount of dHA in the placental tissue of those mothers, which also gives you the clue that dHA is to support during the schemic or hypoxic conditions. That's fascinating. Wow. So, I mean, I think to start off a conversation, I'd love, I think lots of listeners would like a bit of an overview of the differences between EPA and dHA and what it's doing in our physiology and I guess why is it even something that we should be interested in and be concerned about? Because I mean, even it's becoming increasingly popular and I like work for people like Ronda Patrick and they talk about omega-3s and omega-3 index and it's becoming increasingly something that people are talking about. talking about that's really important to kind of be on top of. So yeah, maybe just I think that might be a quite a good place to start. If you could start there perhaps. Yeah, yeah, sure. Look, it's a fascinating observation because as I said, I've sort of been working on it for 20 years and Peter, my supervisor, have been working on it for the 20 years before that. So we sort of have a chuckle sometimes that there's this sort of increased fascination in the last five years. Yeah, you have to be pleased to become, it's like, I mean, it's the same with loads of things, right? I would say HRV is the same. You know, it's been coming increasingly in popular and you know, been doing it since 2010, 2012. Yeah, yeah. And look, if we take it, just step back and answer that question about EPA and DHA and what's important. It's good to go back and remember, actually one of the first studies that looked at whether or not a megathrease broadly would have an impact on exercise performance was a paper in the late 80s by Alexander Leif. He actually considered whether or not there was any potential for megathrease in the diet to increase via two max. That was a question that he raised. But you know, without a lot of information behind him, the mechanism was somewhat true that he was looking at and was called membrane incorporation rather than circulating levels. But he was looking at it from the point of view of, well, when we consume a megathrease, EPA and DHA, which are along the chain of megathrease, they get taken up into the bloodstream. But then from there, like most fats, we sort of decide where they go. So there are, they become a post-issue intramuscular triglycerides. But for our purpose, it's about their role in the membrane. So in other words, they're taken up, they take up into the biolipid layer. So Alexander Leif observed that they were taken up into the red blood cell. So the red blood cell membrane was changing on the presentation of more megathrease in the diet. So he postulated that because the red blood cell was carrying oxygen, because the red blood cell had to squeeze through the capillary. And there was this story in the 1980s as well that was going on around the potential viscosity changes that were occurring in blood. And bleeding time was a good example of that. He postulated that potentially, you know, red blood cells would be able to deliver oxygen at a faster rate, more efficient rate. So he did come up with the outcome that the MAPS was increased. Now it's interesting that none of us, including our group, we've ever really been able to replicate that. And it's just fortunate that he showed that it did increase in the viscosity. Or I guess it was helped the flow, right? I'm assuming. Yeah. So if we go back to the 1980s, it was all about the news story coming through the megathrease with cardio protective. And a lot of that was around the eschemalizerating, a huge amount of the megathrease through the wild diets that they're beating and their bleeding time was longer. So this concept that it was something about the blood that was helping the cardio protective nature. So he postulated if that's the case, athletes might be able to benefit from an increased amount of blood flow, which is then delivering oxygen. And then he thought, well, there's maybe some question around the VR2 Max increasing. And as I said, he did report with the VR2 Max increased. It's just fortunate. And we don't do this so much these days is that he published the individual data of the athletes. So we actually get, if you go back to his paper, you can actually see, you know, VR2 Max participant one, pre-host and so on. Yeah. It's a classic example where one or two participants are driving the change. Yeah, right. So there's some pretty, yeah. So there's some kind of people who responded and some who didn't really respond. So what's interesting is fast forward, either my lab or other labs around the world have really never been able to replicate this idea that your VR2 Max, VR2 peak is increased. But sitting underneath that, there's been some interesting observations around in some maximal conditions. There's a potential for oxygen consumption to be a little bit lower for an external work right. So it comes back to the idea there seems to be a constant theme around oxygen efficiency, rather than the size of the oxygen engine getting any bigger, how we petition and use oxygen is part of the story. It looks like now. Yeah. So yeah, that's where it started. If we think about the EPA and DH, what's interesting there is that, yes, they're definitely too fatty acids that we shouldn't treat the same. One, there are different length chain in terms of the number of carbons. They've got, they've obviously got a different number of double bonds as well, despite both being the meatharies. The other reason why we shouldn't treat them as being the same is that when we talk about them being uptaken through our diet, put into the circulation, they then don't go and lodge themselves into the same memorized. So what we do know is that they have a preference for where they then go and eventually become phospholipid. So if you take EPA, we see it in the red blood cell. We also see it in platelets. We see it in endophilial cells. So EPA seems to have a stronger relationship with the vascular system, the blood system, the blood flow system, the anti-thrombotic type story that we see in that area. DH, on the other hand, is highly attracted to excitable cells, like skeletal muscle, heart, and now we also know in the last three decades brain. And where we look at those tissues, you don't really see a lot of EPA at all. So in other words, it's really important that both long-chain fatty acids and they have very different, even the, they're kind of like putting the same category DH and EPA, you know, just omega-3s, but they're distinctly different and they do, they have very distinctly different roles. So, is it, I mean, there's athletes then, which, which, you know, I know the answer that you're going to give me for this, but I think it's, I think it's a question that many people will be wanting to, or be on the tip of their tongue, for athletes, which ones are most important? Which one should we be most concerned about? EPA or DHA in terms of athletic populations? Yeah, that looked the way I'd like to, to treat it, is sort of looking at the athlete context and what type of physiological stride that they may be experiencing. So, you know, if it's something around skeletal muscle cardiac, it's going to be DHA, but equally there's some really strong roles for the anti-inflammatory process of EPA, and also as I mentioned, the concept that, you know, if EPA is also lodging into things like platelets and red blood cells and endothelial cells, there's certainly a vascular type theme that could come through. And I guess that vascular type theme could also help. I mean, I think we'll talk about how, you know, with the, with the EPA and the, you know, inflammation and recovery and whatnot. I'm guessing if it's helping on a vascular sense, it can also be helping with recovery as well, because if the flow is better, you know, the mitochondria will be working better, and I'm guessing that that would help in that respect as well. And look, it's a nice topic to address straightaway, because there's been some discussion over the last two decades that, you know, you look, take the example that you line up to go to surgery. One of the questions you're surging is asking, is, are you on fish or you need to, you know, you need to get off the fish or before I operate on you next week. And that's the concept or the fear that the, the amount of EPA that's been taken in is somehow going to prevent clotting. And so you're going to bleed out. Now, that is not true at all. In fact, the better way of looking at it is that restoring EPA into those tissues actually restores the normal homeostatic balance between clotting and antithromosis. And Bill Harris has looked at this time and time again, showing that actually if you then look at those that are on a megathrine fissure in the postoperative environment, there is evidence that they actually need less transfusions after surgery. So there's often a fear around particular parts of the a megathrine story that go right back to the 1970s because, you know, they're the estimates that they measured their bleeding time and the, it is extended. So the concept was that they're no, okay, well, if that extends, then there's potential that you could bleed out. And if I jump forward, the US military for a long time were actually preventing soldiers from taking a megathrine on the basis of the, you know, if you were injured, we can watch you to bleed out. Bill Harris would talk about it more is actually we're restoring the natural process. And if we were lying on evidence from 1970s where the S.E.M.O.s were eating whale diet, 50% fat, they hadn't anywhere near the EPA levels that those, those original studies were describing. So these normal dietary achievable supplemental doses that we're talking about today are actually just restoring normal homeostasis. I mean, that's quite amazing really that we can be so entrenched in, in almost traditional, all of the school's tradition that's not true really and they're still doing it to this day. And I guess that's a very, very good say where, you know, we're talking about the megathrine decks of Eskimo's. Talk about the megathrine decks of what most majority of people are today, but one of the recent papers that you did It was 24/26 rugby league players and you investigated the Omega 3 index of those players and then tried to supplement to help. One of the main findings at the start was that Omega 3 index was actually low, right? It was less than 8%. What surprised me by that was that in the reporting when you read the discussion, 46% of them said that they took a lot of fish and 8% of them said they still think about nearly all of them were low in the Omega 3 index. If you think there's a bit of taking that into account, there seems to be a little bit of the perception versus reality in athletes isn't really there. It's a really good translation of practice for sports dietitians that a lot of the time in those busy environments they have to rely on self-report. They have to rely on athletes giving them information about what they've eaten today, yesterday and tomorrow. But we're really fortunate that we've got now an Omega 3 index by a marker. Now just to step back on the Omega 3 index and what it does, again, we've been measuring that in the lab for many years. It's a process that I did personally myself. You would have to separate the red blood cells because the concept is you're using the red blood cell membrane as a reflection of all the other tissues. In other words, when the red blood cell membrane goes up, instead of having to take muscle biopsies and so on, we can be pretty assured that the presentation of the Omega 3's in the last three months has also gone up. The issue with self-report is that we know most people don't really tell the full story about what they're eating. But now in a situation where we can use a finger prick blood cell sample, we can actually go out into the field, we can actually follow athletes in the real world with a very quick sample. It obviously still goes off to the lab, but we get a full report back. The concept of the Omega 3 index then is that it is telling us how much EPA and how much DHA is actually in that red blood cell. If we look at the entire population, whether it's Australian, New Zealand or American, the general population as well, and look, this is actually just as a call out for your country. In New Zealand, there's an Omega 3 map that's now been updated regularly by stark and these colleagues. It's based on studies that occur. New Zealand is actually ahead of Australia and the US because it's just fractionally ahead in terms of population. What are those numbers? If we look at the Omega 3 index, we talk about numbers that are less than 4%, and what we're doing is adding up the percentage makeup of EPA and DHA. Most American data will be between 4% and 5% Australia seems to come out at the high falls to 5s, New Zealand, fractionally in front of around that 5.5. In terms of these targets, you always hear about targets about getting above 8% getting from 8 to 12%. A lot of that comes from the cutting of protective literature that once we get Omega 3 up, adding up to 8, 9, 10%, we know that the membranes are the heart and the muscle and the fact that brain are now really starting to drive up towards their plateau. We also know that 8% is the Omega 3 index. It's most associated with cutting of acetyl risk reduction. It's interesting that that number sort of then plays out into the other areas of topic whether it's delayed onset muscle so on us, whether it's heart rate reduction during exercise. We actually don't know whether it's thresholds are for all these other topics. All we know at the moment is the Omega 3 index is really useful for taking a player group and increasing it over time. When we first met online, we had a first conversation. I never knew about the Omega 3. I never knew about the fingertip capillary sample that you could take. It takes it to the next level of practical application. It's so good. I'm not sure you can get it that easily in New Zealand yet. This is just a call out to Bill Harris' group. As I said, I've personally run Omega 3 indexed from my own studies, which takes days and days in the land. What Bill's been able to do is take that out into a whole blood sample, put it onto a little blotting paper with some antioxidants and it's sent it off to his lab. In Australia, we have Layland Dome down here in Melbourne and he can run that analysis. Within seven days, you've got full-fat acid profile. Sporting teams can actually then make use of this kind of Omega 3 tracking through a competition cycle, off-season, on-season, all those types of environments. I mean, you're obviously, we were talking about rugby with this example, but the Omega 3 for endurance athletes is also just as important because of that. Particularly, my background is in Ironman Trafford and as soon as you said, the reduction is in sub-matte-small heart rate. That is the prerequisite of what you're trying to achieve in Ironman because it's not about how fast you go, it's about how easily you do it. No athletes will be thinking about, "I need to have Omega 3 indexed above 8%. They won't even have any clues." In the study with the rugby league, when you measured them, they started at 4.77%. These are obviously health-conscious individuals that they're reporting that they're trying to eat fish regularly, but they're still only at 4.77%. Then the supplementation came with three caps of the U.S. Epilop performance, Omega 3. Caps the day, which I think is just over 2,000 of the EPA and just over 1,500 of the DHA in that about, so you're talking nearly 4,000, I guess, or 3.5. Do you want to talk about what the findings were and what you. Yeah, it's a good point about the dose. The context to that was that the WNRL team was right on the eve of their. This is a variety of preseason. It's the idea that Omega 3 gets into the bloodstream as in the circulating bloodstream fairly quickly as in each day you take it. The reality is to turn those membranes over. That can take weeks if not months. This is this concept of consistency of presentation of Omega 3 on a daily basis. 10 days isn't it? Like a 10 day, you have to have at least a 10 day load before you actually start. Yeah, and we would. So it's all based on what dose. So if you go with a higher dose, you'll get to that plateau a bit quicker. If you come back down to a dose under a thousand milligrams, it actually might take about eight weeks. So we've done some dose responses in our way. And it comes down to the concept is how quickly do you need this to stop towards to get towards its plateau? And I would actually probably argue that four weeks is the minimum time. So we were within that four weeks. So we went with the higher dose. If we were working with the same team and they said, "Look, it's 12 weeks to our first game." Well, we could probably have been able to go down to maybe two capsules a day and we would have arrived there in about eight weeks. So it's all about this dose duration. In my mind, there's some magic numbers around a thousand milligrams is actually the minimum that an acidic. It's looking for and depending on how quickly they need to arrive there, they then need to go beyond the thousand milligrams if the timeline's coming under four weeks. So we went with the higher dose on the basis that we had to get there quickly and then sustain it for the season. And when you say like a thousand milligrams is a minimum, how would that. What's the ratio then? What's the ideal ratio of EPA versus D8? Yeah, the graph was only by 10 to bank towards the DHA. So I like to see two thirds, three quarters DHA and one third, one quarter EPA. Mainly because it gets back to that concessionary before about what are the membranes that we're trying to adjust. And so in the contact athletes, in the rugby league, rugby union AFL, we're looking at skeletal muscle. We're looking at how we're looking at brains. So we're trying to really present DHA and whenever we've gone in the lab and we've sampled muscle out, we really find literal no EPA in those tissues. So if the context is around those tissues, we opt towards the DHA. So not to say you shouldn't have EPA present at all. EPA is still really important, but you could probably afford to have that as the secondary failure acid on top of the EPA. Because yours was the opposite though. Yeah. Now that's it, classic. So just to put a bit of context on the study as well, we gave the sports digestion team and also the players sort of a free living environment. So we actually wanted to test the idea of uptake as well in terms of we gave them an education session. So explained why they should be taking these capsules. We gave them the dose responses. But then we treated it very differently to our traditional lab base where you're looking for high compliance in your constantly checking in with your participants. We actually just left them alone for the season and thought, "Well, this will be a good kind of translation to practice to say if we come back at the end of the season and we resample your blood, which of the athletes are optimised?" and which are the athletes have kind of stayed the same. And then we sort of probed around a little bit to say, well, if you're fully optimised, how consistent were you? Well, it was quite clear that they were the ones that stuck to the rules, followed the program. The ones at the bottom that were less optimised or didn't experience as much change, they weren't quite on board or they didn't really understand why they were needing a Megatree. Or there were also a couple of examples that they struggled. And this happens, people struggled to swallow tablets and capsules and a few things. And so the sports' dietics team had to sort of take the capsule and then try and incorporate it into some of their food products like a smoothie type environment, a protein shake. But that makes it a little bit more challenging and maybe their consistency then drops as well. But that's real life as well, isn't it? Exactly. And what I found interesting was that, I mean, after the intervention, it went from the Megatree and it's went from 4.7% to nearly 8%. But in Figure 1, that you've got the individual changes and it's like, it's massive. The individual-- Yes, some of them who are just straight up and there's one person who was total outlier. And I don't know how much they went up by, but it was a massive sense. So that was obviously the person who was the most compliant, right? And compliance is daily exposure. It's also how you take that Megatree. So what we know is if you take that on an empty stomach, that the chances that the enzymes then able to process, package, absorb, and uptake that Megatree into the circulation much lower, we gave them through that education process. You need to be taking these with food products, which means we're now presenting the Megatree's with a bolster food. So whether it's a breakfast or lunch at dinner, but that means that the Megatree's actually going with the bolster food, there's more chance than the enzymes that are responsible for breaking down their packaging and uptaking fats more generally. They're going to then work on those Megatree's. So we do know absorption's better when capsules are taken with food. They're not on an empty stomach. That's a good practical take if I'm just for anyone listening. I mean, I think people always take their supplements first thing in the morning, right? They're always on an empty stomach. It just appears to me. And there is a bit of confusion because some things are better on an empty stomach. But I always say that the Megatree's is a food. So you take it with food. A bit of a food isn't a food really. Well, it's kind of like it is in food obviously, but it's kind of. It's just. That's a good point because it's taking in that idea that when you're putting the capsules in, you are adding it on top of. We're all taking in a Megatree's. There are actually shorter chain Megatree's as well. I'll leave for example. But then if you take a contact athlete environment like we were studying, the chances are we did observed through our surveys that we did is they're eating canchun, for example. Now it's interesting that we're they're eating canchun, because of the protein. Yeah, butterly they're also getting a Megatree now. It has a bit of fear of canchun, too. Yeah, I'm going to say that would be a lot of canchun. Yeah, yeah. And just an interesting side note, we've got some other stuff coming up under review at the moment where we've got male and female data and the males are higher than the females. And it's not because of any sex related difference. It's just literally the boys eat more canchun than the girls. And I'm guessing, is there any relationship with that? Is that I'm guessing the males would eat more generally than the females? So is there a body weight? And then we get to ask the question, is there a body weight dose dependency here? And also, is it then possible to overdose on a Megatree's? Could you take too much? So look, the question of body weight has come up a lot of times. And there's some really good studies that are published at large population size that looks at the relative contribution of factors on a Megatree uptake. And what's interesting is body weight does have some role in it, but it seems to be a fairly minor role. And look, on a theoretical basis, it makes sense. If I take a 140 kilogram male front row proplanes for the Australian wallopies or our dragons and our local team here, you are putting the same dose into a larger vessel. It's a relatively impact to the smaller female. But it does seem like body weight, sex, a couple of other factors, physical activity, coming out less percent of the relative contribution. So that there is a small factor about body weight, but it doesn't seem to be a big factor. What comes out at 66, 67 percent of the relative contribution to whether someone uptakes a Megatree is just simply whether or not they're presenting it in the die or not. So that nutrition is always the first thing that comes to mind. It explains 66, 67 percent of the lead story uptake. That was a lot of. We don't have that sort of anything else. It's just. So we got this a body weight, we got this a physical activity, we got this kind of thing else. So the main thing is just take him. Got it taken. You got to take him, you got to present him. And I like to talk about it as preformed EPA in DHA, because there is a lot of chatter and talk around the idea that the body can convert that sort of chain of Megatree, ALA through to EPA, DHA. That we do have an enzyme in our body that's capable of doing it, but it's got a very, very low efficiency. Right. 10 percent. So I actually like to refer to it as preformed EPA, preformed. DHA, because that tells us that we're actually taking it through the diet as opposed to this concept and some how the body can convert a shorter chain into the longer chain. Otherwise, just. Does that conversion get. Does the efficiency get better as you take more? Because you would think the enzymes, right? They regulate in by the demand, really. That's what happens. So the more you take, do you actually. Does your conversion get better and better? Well, you spot on the enzymes, regulate. And so there's a lot of more basic studies that have looked at the background diet, whether it's hyanamegatory, hyanamegasix, and the presentation. And we've done some work here in the lab, again, using a rodent or animal model, where we manipulated the background diet in 12 different ways. So hyamegasix, low-megasix, hyanamegatory, low-megasix, and again, what was critical, it wasn't whether or not the background was hyanamegasix or not hyanamegasix, or ALA, it was actually whether or not you presented EPA or DHA in the diet. In other words, I'd like to think of the enzyme as kind of a baseline enzyme that just keeps a little bit rolling through if you're in a situation where you don't take any pre-finity. Yeah, yeah, yeah. It's like a backup mechanism almost, yeah. Very low. And there are examples, and we've published and data on this as well, where you take your vegan, you know, plant-based serious vegan plant-based athletes. Their omega-3 index will be lower than 3%, it's some of the lowest I've ever measured. So unless they're looking for other sources like ourbal sources, and we haven't talked about that. What's an interesting part is that we've talked about the marine fish-based sources, and it's in tunas and your salmons and those, but where do they get from in the food chain? They get from algae. So there are options for plant-based athletes and vegan athletes. It's going to be very much onto it. I mean, I always think that plant-based athletes are making the life very hard, right? The omega-3s, but then there's all the carnazine, the creatine, the so many things that are missing, the riboflavin, I mean, it's just. And I think. I was actually doing an interview with Dr. Tommy Wood. I don't know if he mentioned that the omega-3, the omega-3 uptake is actually almost dependent on lots of things that are in the carnazine and the creatine and some of the riboflavin and stuff. You actually need, especially in organ meats, for example, that some of the micronutrients in organ meats are very, very important in the uptake of omega-3. You really are running a losing battle list. It's so hard to do. They're digressing to that. Take her messages, very good athletes are very, very low in EPA and dairy. They're the last of it, the same. Yeah, which is a bit scary when you know what we're going to talk about what the roles of recovery and muscle-sonism is coming up. But one other thing in that study was you also mentioned the omega-6 to EPA, ratio and of course that went down because of the increase in the EPA, mainly, right? Yeah, because you want to, so why did you also measure that as well as the omega-3? Why was that of the problem? So in addition to just measuring the red blood cell EPA plus DHA percent, you can then look at the entire blood profile. In fact, the single finger prick will give you all of the fatty acids that are located in the whole blood at that time. If we then look at a few ratios, you can look at holistic omega-6 to omega-3, another which you can sum up, all your omega-6s and sum up, all your omega-3s. That gives you a more holistic look at the concept of how many of those two forms of polyunsaturated fatty acids there are. Now, it's not to say that reducing omega-6 out of the diet should be the absolute critical thing. Omega-6 also plays a really critical role in the diet too. What we should be looking at from that holistic omega-3 omega-6 is that a lot of the omega-6s that the modern diet gets is these kind of industrial. industrialized type foods and so if you look at the history of human diet our omega-6 levels have crawled up over time, particularly in the last 150 years. So you can call it a omega-6s is also in meats as well right there. That's right. But they're also hidden in a lot of processed foods. So typically if we were like say we were just eating a more whole whole food diet we would get the images of the omega-6s. But because of all the processed foods that are coming in like that omega-3s, omega-6s are just prepped up and open up and and the and also the lack of omega-3s has come down. So we're kind of. It spills it out. It spills it out but we want it to be the opposite way right. We want it to be kind of higher in the in the EPA. Yeah, you're all. So getting to the next ratio is picking two of those. So we look at the ratio between EPA as a representative omega-3 and a record-onc acid which is one of the key main omega-6s. And looking at that ratio gives you a little bit more insight and the reason why I look at those is important is they play a kind of an important opposite role in terms of pro-referencing. So you've got your record-onc acid side feeding down to some of your leukotreens and thrombocsines and your EPA also in opposite going down towards the anti-inflammatory thrombocsines and prostaglandins. So looking at those two are important because they can give you a feel for the holistic diet in what should be a balanced pathway between the both. So if we look at our rugby league players again they were up over we look at a number of around about 11 in other words there should be for every one EPA there should be about 11 a record-onc acid. We try and drive that down as low as possible under 11 just to give you a context we measured the same in a college NFL team a couple of years ago again had the monomega-3. So the reason that their ratio was 35 in the American diet so it was wow. I rocketing towards a mech 6 and you imagine in NCAA type college food American westernized diet through the roof and it's because their mech 6s was so hot we don't see that in the store so our rugby league. So just just to put into context when you did the recent study it started at 14% and it went down to 6.67% right so we like. The double the. That says a lot about the old sad you know the standard American diet. So we started at 35 in that group and again it was a preseason loading we had an opportunity to do we only managed to drive that down into the low 20s. So we would have needed another we would have needed another couple months to bring that particular work. What is some of the health consequences when you're up that high. Yeah look we know the concept of health is this dance between having healthy inflammation that we can resolve and not allowing that inflammation to spill out into some sort of chronic situation which just means our cells are always experienced to inflammatory products that can cause cell damage. So what we're trying to emphasize is if we can get this ratio down low we still have the this is really important point we still have the potential to create information which is a really important training response for. Yes still need to be able to. Many many many will argue that like those things are critical for adaptation right and you don't want to drive down information too much too often because it is part of the critical training response. We were just species and all of the social. Yeah yeah yeah yeah yeah right so. So so if you can get that ratio under 11 there's still a substantial amount a healthy amount of a record on a gas of that's that's available inside the cells and record on gas we know is really important for so function and structure and always. Inflammatory based pathways but equally your EPA is now brought up to be able to provide an. So they counter to that and anti inflammatory after an inflammatory process starts so in other words we can still experience those acute inflammation stimuli that we all need and that's really important for health adaptation strength of ourselves and at the same time we don't allow that information to to run out of control because our now our EPA is available and it's interesting we can bring to the end of the question as well. So both of them can play a role in terms of mopping up information up to the stimulus. So it's this idea of being able to inflame a cell but then also clean up and allow to recover afterwards so if athletes then if athletes went like just crazy on the omega three's and they were taking like you know they were had the pillow and they were taking like eight 10 caps a day. So you drive your omega six down to a danger well it's a dangerously low level but a level by which you're not you're almost affecting some of your training adaptation is that possible. So just in terms of the doses like the European safety. The authority will talk about sort of around 5,000 milligrams being the cover of the safety. I mean I certainly can six caps a day which is which is about the 5,000. So we don't see that equally come that it actually comes down a little bit and then plot out so in other words that cells then continue to hold the appropriate amount of a record on a gas. So it's a number one question I get from particularly coaches that I've discussed this with over time is this fear that the omega three's will be so anti-inflammatory that the training response will be lost and it's not the case. So if you look into the literature and it's an emerging thing around you know delayed onset muscle so on is there's not a lot of evidence for the cytokine response to be adjusted at all. So in other words you can load up on a omega three still perform damaging based eccentric exercise for example and still get the inflammatory base response it's it's the time period after that it's the cleanup that looks like to be the potential for where omega three's. Yeah going to play a role and what's interesting is that we we if you think about sort of the three elements of recovery in terms of muscle damage so you've got the actual soreness itself you got the inflammation and then you got the performance. The inflammation doesn't seem to be adjusted too much particularly in the first 24 48 hours in other words you get the response what we do start to notice in the pattern of activity that's occurring in the literature in the last 10 years is muscle soreness seems to be less so athletes will report that they're less sore when their omega three levels are up in relation to the omega six. And performance recovery is faster so if you get athletes to then do your classic isometric mid-thigh pulls counter movement jumps. Yeah it's it's able to return to force within 72 hours at a faster rate but it's not it's not because the inflammatory response has changed the inflammation still occurs. It opens up this real interesting question around is there other pathways that the omega three is are working on particularly after 24 hours once the inflammatory response occurs that that is going to be new and and a new term that we're getting used to is this term called resolves and resolves come particularly from DHA so DHA might actually now be also playing a role in producing the resolving element to inflammation. In other words we can all out to occur and then we can resolve the inflammation through these special products. So it allows you to come through but then the but then the amigas are actually speeding up the process once is come being as well and also like from some of my reading with the omega three reason. There's a little bit of evidence to suggest that you can potentially help with losing uptake as well so could that be helping with the recovery and I've you if you've got an athlete who's finishing the workout they've got higher than me goes to take the protein shake for recovery which the generally do helps with the losing uptake and and all the associated pathways are then associated with protein and recoveries is that something that could also be a play with the record. I've done in person work on it but from a theoretical point of view it gets us back to our original conversation that we're not talking about the circulating EPA. and DHA that's sitting within the plasma, we're talking about the membrane incorporated EPA, a DHA that are now. - We've got to be taking it a higher dose to get there. - Longer time, you've got to be sustained because you need to change the membranes. Now when we change membranes and we change phospholipid layers, we know that for example, transporters then change their activity. Self signaling is then sensitized or desensitized? - The losing will affect MTOR, right? And then the MTOR, MTOR is a cell signal for muscle growth and recovery and all that sort of thing. It's a fascinating, I mean, I mean, the implications are just so vast for sporting athletes. And I always get asked in it. I mean, I'm obviously, I can't be a bias 'cause I'm with the head of research for pillar, but the two, if anyone is looking for a self-managed athlete, it has to be a MEGA-3 magnesium because they're just the two that have the most, the most research behind them and have definitely shown to do to have a very positive effect. - Yeah, and it's a concept that each one of our cells has a membrane. Each one of those membranes has a phospholipid layer and we can modulate that phospholipid layer through MEGA-3 presentation. - Yeah. - Change the membranes, change the cell function. Is the theory. - Yeah, it's crazy. But like before we, I mean, I wanna get back more into the specifically recovery, muscle damage, muscle, muscle, I would love to talk about that a little bit more because there's been so much research to know, I don't know, you've been heavily involved in that. But I know also at the moment, you're currently doing some more research in a, obviously you've had the rapid communication that was recently published in European Journal of Nutrition and Metabolism. But you've also, and that was in '24, but now you're going and looking at the MEGA-3 index of a lot more athletes as well. So, do you wanna talk about that? Is there anything that you, is there any, because snippets like pre-published insights that we can get that you've found so far? - Yeah, look, and so again, the context it takes us back to the NCAA idea that all of the literature that we can't really see in terms of being able to describe the MEGA-3 profile, MEGA-3 index, very asset profile of athletes has come out of the college environments. And like we took before that, they're not reflective of elite athlete, professional athlete, training and supportive environments that also involve sports nutritionists and dietitians working alongside LL-LT teams. So, and again, a lot, it's American-based. So, we can't necessarily just translate all of that information across to New Zealand Australia, UK and so on. So, we're currently screening 500 Australian elite professional athletes. So, these are athletes that are full time working in sporting teams or Olympic-based teams and have appropriate allied health to say, well, one, we know there seems to be a difference globally around the world in terms of the different diets that our populations intake and two, that we'd likely be able to see also at difference in terms of whether or not you are getting supported through and maybe through a capsule, for example. So, we're close to 400 athletes so far. We're aiming between 500 and 600 across 30 different sports and what's interesting is that it's in Australian context. We're certainly coming at higher than the average NCAA American-based paper that's ever been published. But our median is going to be around the Australian median at low five. So, it's been a thousand Americans. And now we talked about the Amiga 6 to Amiga 3, being like 30% in the. What's the typical. What was the NCAA because I think we haven't discussed that. Yeah, it's the NCAA generally sort of comes out again around sort of high 18s, 19s, 20s. We're going to see sort of the ratio somewhere looks like it, you know, pretty good on the data. Somewhere a little bit higher than 11. So, in other words, even in the Australian air through context, we're going to have an opportunity in thing with Amiga 3's. What was the Amiga 3 index in the Amiga. In the NCAA? Yeah, Amiga 3 index so far for us is around 5.15.2. So, again, there's opportunity in to being. We see this kind of classic. It's not a build curve. We're seeing a classic cluster of Australian athletes between four and six and we're seeing a drag up. So, there are athletes presenting with 8s, 9s, 10s and 11s. But it's a real funnel that's occurring up at high level. And we're also taking survey data. And what's really evident is that the any athlete achieving a appropriate Amiga 3 index in excess of 8, if not as high as 10 and a low ratio of EPA and arachidonic acid, what we notice is that they're either consuming regular fish, but most often it's because they're taking a supplement. So, in other words, supplemental intake seems to be really critical. Is it possible to. Do you have any recommendations on supplements of Amiga 3? Is it possible. Are there any really not great ones out on the market that. Is it possible to buy some that. Obviously, in the study that you did, you used Pillar, and it was a very effective way to increase. Definitely worked, right? You took the Pillar, definitely increased the Amiga 3 indexes. Can you get supplements on the market that are hopeless or don't really too low? Yes, or. Yes, to be clear. What's critical is that the mix of EPA and DHA will differ as well as the amount. So, as we know, there's tens, if not, you know, hundreds of them are. 100% of them are. Exactly. And it gets back to the concept that the reflection of that Amiga 3 quality and the amount of each of those two fatty acids is going to be derived from where is that Amiga 3 source of marine fish driven that through? So, we've got tens of thousands of different variety of fish in the ocean. And so, it's natural that we're going to end up with a variety of different quality Amiga 3s. So, if you take, for example, just go back to fish, we know that, you know, tuner and salmon are very high in DHA, for example. So, it's all going to be down to the quality of the marine stock and the fish supply that's then formulating that Amiga 3. So, there is not a concept of walking in and just peaking up an Amiga 3 off the shelf. Consumers have to have to look at the back of the pack and see if you really can see some. Yeah, because otherwise, you're going to end up having to swallow 20 capsules to them. You know, you know, you know, another one for all of this type of capsule. I mean, with me, I always knew that Amiga 3 was great, but I never took it for most of my athletic career because I couldn't take the repeating of it. It's drove me mad, but with Pillar, it's the first time I've ever had a capsule that doesn't repeat on me. And I actually bite the capsules. I don't swallow them. I bite them and throw the capsules out. And I even, even my kids do it too. You know, I give them one capsule, one capsule down and they'll bite it and they'll like it. They actually really enjoy it. I mean, it feels like we're going to have kids on the same thing. My kids are dosed up to the eyeballs on Amiga 3 as well. Is that in terms of children? Is there a. I don't know if you're coming to talk about this, but as a parent, I'm kind of. I've got you here, I want to kind of know. Is there a dose that's optimal for my children? Yeah, look, it gets back down to the body mass. They are generally on average half the size of us, so you can afford to come down to it. Again, I operate on sort of the thousand milligrams for my kids. They're sort of in that early teenage type. But they're pretty lightweight, so around sort of 45 to 60 kilos. In terms of dosing kids, I don't think there's a lot of studies again, but you're done on it. I mean, with a pillow, if you were like one to two caps a day, you know, that two would be a max, right? One would be enough sort of thing. And look, it gets back to the point we're making. It's about constant presentation over. It's behaviour change. Rather than just seeing it as a sort of something I've got to take now and then. It's got to be behaviour change that we see it as. It's the same, but everything isn't it? You've got to make it a habit before. It's the same with what we record, HRV. We're just writing a book on HRV at the moment. One of the things we talked about, I was writing a chapter on it yesterday, is you know, you could probably get away with taking three readings a day. But you need to take it every day because if you take three readings a week, because if you don't, you need to take it every day. Because if you're thinking you're going to do it three times a week, you're not going to do it enough. You just need to make it into this like perpetual habit. But I mean, I am conscious of time and I really want to talk about the last thing we really want to talk about is mega-threase and recovery, muscle damage, inflammation. And definitely some of the. I mean, that's been a huge body of work that's come out in recent years. And obviously from an athletic standpoint, it's critical, right? It's what athletes are striving for. We've already talked about it a little bit, but maybe we can just delve into that a little bit more. I mean, I guess we can start off with some of the mechanisms that are still. why omega-3 is a helping in that regard? Yeah, so the damage literature really started turn the century. I think off the top, I had the first papers around 2002 and we saw probably a dozen papers over the next decade with some constant sort of theme around the idea that we'll soreness potentially is reduced a little bit in that first 48 hours recovery is a little bit fast and when we say recovery that's generally measured, as I said before through some sort of laboratory based activity like encountering the jumper of mid-thite pool representing dynamic or strength based activities. And then there's the idea that well if we've got a modulation then or potential theoretical modulation of information and anti-information studies have then looked at measuring some of the classic cytokine responses like I/O6 for example, 10 F alpha. If we progress forward we wrote a review on this about two or three years ago and tried to summarize what we're seeing in the literature for delayed onset muscle soreness and whether or not it was going to make an improvement. We looked at it from a very critical point of view of study design and when we looked at that body of work which encompassed off the time I had around about 12 papers, 14 papers at that time the study designs were at-hoc. We have some that have supplemented for three days and some that have supplemented for 21 days and the doses were all over the place. And what was also interesting and it's a really difficult part of recovery based research is that they were simply just nearly like cross-sectional studies where there was no baseline taken at all. You simply put your participants on that and make three for the decided amount of time with that dose and then you just randomly damage them in both directions. There's no guarantee that the randomisation process has just simply resulted in the two groups just being able to recover differently. That seems like the craziest study designs for me. So the problem and the trick with damaging based study is that just simply giving someone a damaging based activity is a preconditioning effect in itself. So the idea then is that if you can do a double blind placebo trial with a pre-imposed becomes challenging. As everyone knows you do one of those, you just do one or two of those damaging that we don't get to. You know where near a sore second third time. One of my, I have a PhD student doing this exact study at the moment and he's looking at he's got like a slow-reward to the sits on the chest and we're looking at changes in running gate to kind of predict muscle damage. So we're making him down here on the treadmill to induce muscle damage. And they're definitely getting buried sore but the reporting muscle sawdust after the first time compared to the third or fourth time is totally different. Yes, totally different. So we've just finished with a PhD student as well. So we took the approach that if we can extend the timeline between pre-imposed out far enough then that initial baseline assessment can sort of disappear into the background of the history of the muscles exposure. So we went on a trial for 12 weeks which was going to be the longest omega-3 trial in this literature so far. And we also did a randomisation process and followed a control through two to make sure that they then didn't change over the 12 weeks compared to our intervention. And so we've looked at it and the literature has looked at it in three ways. So we've looked at soreness, inflammation and that can be measured in a range of different markers that come out in the blood. And those markers being like, do you deal with ILC, CRP? Yeah, all the kinds of 10 FF. Yeah, so pro and anti-inflammatory top markers. Again, there's limitations to those as well in terms of the pathways. And as I mentioned, depending on whether you're loading fully up with DHA, the issue we've got at the moment is that the resolvings that DHA produce are really tricky to measure. They appear and disappear really quickly. There's not so many laboratory-based patients. But the most dynamic side you'd want, you'd be looking at more of the EPA though, right? To be. Yeah, we could go either way. So there's theories on both. We've actually interesting enough and this is where we probably potentially differ a little bit to your trial is weak, only supplemented on DHA. So this is unpublished at the moment. We have only supplemented on DHA on the basis of the resolvings, depending on part of the cleanup pathway afterwards. Yeah, okay. But if we back back into the literature, independent of the study design issues that we've identified around dose duration, damaging protocol, there still seems to be. You know when you look for that kind of theme that comes through, you know, you've got your head on and you just use your observational knowledge, you think that. See, the independent of the limitations, there's a constant theme that soreness is reduced. Yeah. That seems to be there, you know, despite the criticisms on how that was occurring. Now, interesting and again, it's unpublished. We've unveiled our results and long-for-hold soreness is down after being on DHA only. So we didn't have any EPA at all. We're actually just in just DHA, you know what I mean? The secondistically is not, I mean, it's not what is believed, right? It's not what's generally thought about mechanisms DHA, EPA. Do you think then that there's a study that could be a really great study? I mean, I'm thinking now about potentially a PhD topic, where you do a muscle-damaging protocol, well, you know, you do a long load, you do a good wash out, and you do only EPA, and then you do only DHA, and you look at. Has that ever been done? Do you think. Yeah, so it has, and this is a bit of a call out to Jeff in the US. So he's PhD was on this and it's just been published. He had that exact. He had an EPA group, a DHA group, and an EPA plus DHA group. His sample size was fairly small, but he did start to tease out a little bit of difference between the two of them, I would say. I haven't read them in full detail yet, and Jeff and I have catch ups now and then, and certainly it's a major topic that he's interested in going forward. For the exact point, can we split that up? Now, the issue then is you have to then come up with, because EPA and DHA are already in our diets, potentially. You have to come up, as you say, with wash out periods, and then supplementation options that will only then present. You'd have to very tightly regulate the habitual diet as well, wouldn't you? Yes, so it's very difficult. That's what we did with ours as well. So part of that is we've written a methods review recently too, and we've got a little infographic that sort of says that if you want to do studies relating to EPA plus DHA, you kind of need to follow these rules, because the issue is just like you saw in that regular e-paper, even when you do a control trial in the lab, you'll still get a variation response, you'll still get some people who will sort through the roof and to have them make through index or IIT, PIR, SIG coming down, and equally some don't change as much. The key is you've got to separate the group, so in other words, from a control grip point of view, you have to measure their pre-priced omega-3 profile and demonstrate that haven't changed. And you've got to move the entire group of the intervention outside of your control. Because otherwise you end up across those, you have some of the control group with the same omega-3 profile. The PIR season was called Jeff, is that what you said? So Jeff's the US PIR student, he wasn't one of my students, he's just a colleague now, but he's done his PIR-SIG. I've got Ryan Anthony here in the lab at Bullingall, and we did exactly that. We actually measured the omega-3 profile every four weeks, so we didn't just do baseline. We brought them back every four weeks and we continued to measure demonstrating that we not only separated the groups, but we reached a plateau as well. And did you find any, what did you find differences in when you loaded the DHTA EPA? And then the. Yes, now. Now with the EPA and the DHTA+ EPA? No, so we don't have any in-house, we don't have any EPA at all, we've only got DHTA. So we don't have to get in the States, or do you know anything about DHTA? Jeff in the States has teased out a little bit of difference, but I would say it's still not clear enough because he used very high doses, and again he didn't have a pre-post. He's only got a one-off, a comparison after being on the dose. We don't really know how those individuals would have responded, and we don't know what their status was before. So again, there's a limitation to Jeff's status at the same time. Maybe this is calling out when I get my PhD student going with, hello, maybe we can collaborate, and that could be a really great study for us to collaborate on. I think it would be excellent to. Yeah, look at the data out a little bit more. Yeah, absolutely. Look at what we've got is. It's probably another opportunity to revisit our literature review that we did where we sort of summed up all the studies. So as I said, we had about 14 at that point and we did it as kind of a classic SLR type metternalsus. We've got about another 14 papers that have appeared since then. So there's probably a good opportunity for another review down the year and I could potentially work on this. Yeah, right. And then add in some of these more recent studies like yours and eight hours that are just coming through. I still see it as we still have an answer to the question. I think we've been fumbling around in the area and everyone's had a bit of a go but no one's really, really solidified. It really needs to come up with and we're hoping we can have a better study design throughout study that we'll be publishing in the next 12 months. We're just I still see it as we're on a bit of a full front in terms of working on this area for the next sort of decade. I mean, I sit here talking to you and it's what I've come to really realize is that the area of Omega 3 research is so vast, there's so much to be done in the area in terms of the anabolic effects, the effects of even the protein uptake. And we even talked about sarcopenia in the elderly and all that sort of thing. You should come back another time. And that's what I wanted to say is that I think I need to have you back on because there's things that we haven't covered today like I wanted to talk about the athlete heart. I wanted to talk about some of the things in the arterial fibrillation, some of the myths around that. I want to talk about the evens for an incursion into that mix too. Concursion, anabolic effects. But I know we've been talking now for nearly an hour and ten minutes so we'll definitely, I mean, if you're happy to do it, we'll definitely try and get an impact. But before we do say goodbye, do you want to just tell anyone about where they can, if anyone's interested in a bit more of what you're lab doing and a bit more of your work, I guess, how can people find you, I guess, research, I guess you're in that. Yeah, so we're on the University of Wongong Graduate School of Medicine. So we've got sort of an ongoing research lab part of the campus here. So we're just an ourselves Sydney, always looking for new PhDs and postdoc opportunities, particularly as I said, probably the big topics for me will be concussion going forward. And again, it sort of brings in the role of mopping up that information after trauma, but this time it will be from a nerve perspective. But then as you and I are both sort of looking at, and I'm sure we can talk further the delayed onset muscle soreness, the muscle damage, the muscle recovery will be a key thing in our lab going forward as well, having those too. I mean, the concussion stuff is just another massive area. I interviewed Dr. Tommy, but it's not been published yet, but he specializes in neonatal brain injuries and he was big on the omega-3s for that. So it's just, it actually transcends into younger populations and way more than just athletes as well. Yeah, and look at that goes back to sort of the whole kind of brain opting for high levels of DHA being incorporated into their cells as well. So there's that concussion that just keeps coming through, the cells know what they want. They just go to present them with enough. Then the end of the day, you just have to give your body, I mean, there's that theory of nutrition, right, is that you just have to give your body the new chances. Knees and the ill do, it's hard to overdo a lot of nutrition, right? You just have to give it the nutrients and the ill. The problem comes when you don't, when you don't give it the new chance it needs, it will always search for more and you always hungry, you always want more. So, you know, I guess we can finish by saying that the average person in the population, including athletes, are not eating enough omega-3, if you're absolutely going to you. And we can see that from world maps of a megastore index. There is, there is not enough omega-3 out of it. And it does seem like the only way to really get it up is to supplement as well. Yeah. So, thanks, Greg. And yeah, let's do round two and thanks. Thanks very much. Thanks very much. Thanks very much. Much appreciated. Catch up.