Omega-3 & Brain and Spinal Cord Injuries
OmegaMatters: Episode 39
Hosts: Drs. Bill Harris & Kristina Harris Jackson
Guest: Dr. Adina Michael-Titus
About this episode:
In this episode Drs. Harris & Jackson are joined by Dr. Adina Michael-Titus, who is a professor of neuroscience at the Center for Trauma Sciences in Barts, the London School of Medicine and Dentistry. She is trained as both a neuroscientist and a pharmacologist and is interested in developing new therapies for traumatic spinal cord and brain injuries. And in this area of research, she’s been working extensively with omega-3s. For more information on OmegaMatters, visit: https://omegaquant.com/omegamatters-broadcasts/
SHOW TRANSCRIPT
Dr. Kristina Harris Jackson: Welcome to OmegaMatters, where we all talk all things Omegas. I’m Kristina Jackson. This is Bill Harris, my dad. And today we’re welcoming Dr. Adina, Michael-Titus, who is a professor of neuroscience at the Center for Trauma Sciences in Barts, the London School of Medicine and Dentistry. Is that said correctly? She is trained as both a neuroscientist and a pharmacologist and is interested in developing new therapies for traumatic spinal cord and brain injuries. And in this area of research, she’s been working with Omega-3s and so we decided to have her on Omega Matters today. Thank you for joining us.
Dr. Adina Michael-Titus: My pleasure. Thank you for inviting me.
Dr. Kristina Harris Jackson: Oh yes. So Bill, you guys are old friends, so if you’re going to get us started, you sure can.
Dr. Bill Harris: Yeah, sure. Again, thanks for joining us. I guess quickly for our audience, a little bit of your little history, how you got to where you are. Pharmacology and neuroscience is not exactly nutrition.
Dr. Adina Michael-Titus: Yes, no, and certainly not lipids. Some many years ago now, I got very interested in the various cellular processes that accompany brain aging. And we were working on lipids. I had a particular interest in omega-3 fatty acids and how they change in aging. So we had this project in the laboratory. And at the same time being a pharmacologist, I was aware that there were no treatments for spinal cord injury or traumatic brain injury (TBI). And I became aware of observations with alpha-linolenic acid (ALA) in a model of transient spinal cord ischemia. And these observations were reported in the group led by Michel Avstonsky and Catherine Artaud at the time. And they caught my attention. It was unusual to see a lipid showing a profile of neuroprotection very clearly, acute neuroprotection. And this is how it all started. Therefore, I thought well, we were very interested in docosahexaenoic acid (DHA) for obvious reasons. It’s so enriched in the brain and we were working in these aged animals, but we also had adult animals. Therefore, we decided to set up some experiments and investigate in parallel whether it was true that a single injection of this type of fatty acid could lead to some protection of the tissue after traumatic injury. And I can say the rest is history because…
Dr. Bill Harris: We just don’t know the history. You got to tell us.
Dr. Adina Michael-Titus: When they published the data, I think it would be kind to say the results were received with much skepticism because it was the very first time a lipid was shown to have very clear neuroprotective properties in a model of traumatic injury.
Dr. Bill Harris: And when was this?
Dr. Adina Michael-Titus: This work was happening in 2005, 2006.
Dr. Bill Harris: 20 years ago.
Dr. Adina Michael-Titus: Almost two decades ago. And there was disbelief, I can say it. Now with the perspective of time, you understand how people are reticent sometimes to walk into a new field. But there was still disbelief when we submitted the data. Although there had been the study in transient ischemia published by the French group. This was another level because it is true, traumatic injuries are very complex injuries even in animals where they can be made more homogeneous within a group of animals. It takes a lot to be able to rescue neuronal cells or non-neuronal cells. And there was no clear indication how this fit into the field because there was nothing in the field and there’s still nothing in the field to present. So we had to do a lot of, how should I say, more research. Of course we were ourselves taken aback when we saw the results, when we unblinded the data we were surprised. That’s why we only submitted after we repeated the whole set of experiments because we thought, is this right? It’s incredible.
Dr. Bill Harris: Can you describe for the people kind of what that experiment was that really got you started? How’d you do it?
Dr. Adina Michael-Titus: It was injecting basically, we took linolenic acid, which was reported by the French group, but also docosahexaenoic acid (DHA). And actually we took a non-omega-3, oleic acid, also part of the bunch of fatty acids tested and omega-6 fatty acids, arachidonic acid because we thought, well, what is it that makes omega-3 fatty acids special? If it’s true that they are special and they can offer neuroprotection. And we thought well, with this more comprehensive cover of different omega-3s and non-omega-6 completely different fatty acids, oleic acid. And the results were surprising
because we injected the bolus of fatty acid, whatever the fatty was, less than 0.1 milligram per kilo intravenously at half an hour after injury, which is a time… I must confess that I’m sometimes surprised when people test neuroprotectants immediately after injury because you’re never going to be with a casualty one minute after the injury.
So we always leave at least half an hour before we inject anything after an injury because if you look at time of intervention by trauma teams or emergency teams, that’s reasonable. If you are in a system, for example, we are in a level one trauma center and we know that our teams can deliver this type of intervention when they have a casualty in the civilian context. And it’s probably quite possible to do it also in the military context. So anyway, going back to the protocol, we injected 30 minutes after injury intravenously because again, this is relevant in patients. In animals, often people prefer routes which are a bit easier from the experimental point of view, like intraperitoneal administration or subcutaneous administration. So injected in a clinically relevant way. And then we looked at the animals over days after injury to see if neurologically they were better, because tissue protection is one thing, it’s good to have. But it has to have a correlation with some relevant clinical improvement. So that’s what we saw.
Dr. Bill Harris: Yeah. And how did you injure the animals? Is this a head bonk or a-
Dr. Adina Michael-Titus: The injury, you can injure the spinal cord in a variety of ways. For the first study, we started with a hemisection injury. So the animals had a profound damage on one side, this was a unilateral section and the contralateral side was intact. So this induces a very clear neurological impairment in terms of locomotion. And you can quantify this impairment and you can see how it evolves over time. And you can read effects. And this is a type of injury which may happen if you have a stabbing type of injuries and-
Dr. Bill Harris: This is not a stroke kind of thing.
Dr. Adina Michael-Titus: No, there’s no vascular component in this and the tissue has less vascular damage than in other types of injury. I’ll come back to this in a moment. So in terms of stabbing injuries, it’s a relevant injury. But it’s not enough in the field and that’s the next chapter. But in this model, the evidence was absolutely clear that there was a neuroprotective effect. We rescued neurons, we rescued non-neuronal cells, we had less neuroinflammation. And this was just one injection of fatty acid, ridiculously low dose. And it wasn’t even as a pharmacologist would look at it at the equilibrium conditions or steady state conditions, it was a bonus. So a bonus of fatty acids, which was by definition a non-equilibrium profile of availability of this type of agent. So this was truly surprising. But in the field of injury in general, traumatic injury of the brain or spinal cord there is much reticence first to accept effects without extensive validation of variety of models. And also in different laboratories…
Dr. Bill Harris: Yeah. I would think there would be maybe a lower hurdle, a lower level of evidence needed for something that’s completely safe.
Dr. Adina Michael-Titus: Yes. But there was already a lot of information on omega-3 fatty acids. You can take capsules and so on, but injected as a drug this was a paradigm shift.
Dr. Bill Harris: That’s different.
Dr. Adina Michael-Titus: And at the same time, another group in the world led by Nicholas Bazin was using a similar protocol in a stroke model. So completely different model of injury, but the same type of approach injecting intravenously. So all of a sudden we had evidence which started accumulating on how these fatty acids had a drug profile that you could inject acutely. It wasn’t a question of supplementing over days or weeks. It was conceptually quite important difference, I think. So the next step, the spinal cord injury community is very skeptical, I would say as a community because there hasn’t been any progress in neuroprotection over many, many years. And at present, there is no neuroprotection which can be offered to patients. So anyway, we did it ourselves.
So the next level was a compression injury, which is an element of… So you compress, again, by analogy we had stabbing in the first case. In the case of compression it’s as if you were, for example in a mine and you have a beam that falls on your cord, for example, in the neck region, cervical region, and compresses the cord. And this is a much more damaging type of injury and there is a much more of a hemorrhage component as well. So the destruction is more significant, the destruction of the cord. And we did a bilateral contusion injury. And again, we saw exactly the same things. And ultimately, last but not least, sorry, we did compression injury. Did I say compression or contusion?
Dr. Bill Harris: You said compression.
Dr. Adina Michael-Titus: Compression.
Dr. Bill Harris: Is it like a compression, like a rugby player in my head?
Dr. Adina Michael-Titus: Compression. And then also we did contusion. So contusion is where you have quite a speed not only you have something impacting the cord, but you have also the speed element which increases the destructive force on the tissue. And there again, we saw very clear evidence and we started doing, and these are heavy experiments and we did all this in rats and also in mice, because again, there is skepticism. Sometimes there is suspicion that some things you may see in rats or in mice, but they won’t apply for species. So we had a body, and this took us several years. But there is still a lot of reticence in the field in the first two, three years. Nonetheless, after we presented the data, other people started doing this. And now when we look at the literature on omega-3 fatty acids, especially the long-chain omega-3 fatty acids like DHA and traumatic injury, there are so many studies.
And of course, we and other authors started looking at traumatic brain injury. And again, we have now evidence that in a variety of models of traumatic brain injury, this paradigm of injecting a long-chain omega-3 fatty acid after injury, leads to significant tissue protection and also very clear neurological improvement.
Dr. Bill Harris: Yeah. And so this has all been done in animals. It’s been 20 years. I assume somebody’s trying this in humans.
Dr. Adina Michael-Titus: Well, there are two components here. So some experiments, and in our group we did this, in some experiments people have tried to combine the bolus with the diet as well to say, okay, we give a bolus where for example, the trauma team can give a bolus and maybe after that we can add more omega-3 in the diet as well. And in spinal cord injury in our compression study, we had clear evidence that for some parameters increasing the dietary intake was adding something. The effect was very strong with bolus. But for some parameters, whether it was inflammation or protection of oligodendrocytes to protect myelin ultimately, there was a plus offered by increasing the omega-3 in the diet.
So certainly there is some scope to increase omega-3s in the diet. There was an indication years ago, but the most important component is this use of something like docosahexaenoic acid (DHA)as a drug. And there were no preparations at the time that you could use as a drug. And we worked over many years with several partners, different partners from the private sector. And it was very difficult to convince people to continue to invest in this preparation as a drug, because the risk of attrition in generally the development of new drugs for neurological indications is very high. And for traumatic brain injury and traumatic spinal cord injury, it’s even higher because there isn’t even a single compound we can call first in class and then it shows that it can be done. So there were several attempts to create a formulation, which was going to be a drug type formulation. But it was a heavy financial investment. And several times we started and then we stopped because the investors became worried that perhaps this was going to be too high risk on operation.
Dr. Bill Harris: Really.
Dr. Adina Michael-Titus: And luckily as work was gaining momentum and in other fields, in neurology there were similar questions. For example, neonate hypoxic-ischemia encephalopathy, this is a condition which is due to ischemia which occurs very early in the neonate brain. And the person who has done a lot of work on this is Professor Richard Deckelbaum. So Richard was doing this amazing work himself with his group of Columbia students. And he did similar things to what we were doing. He injected DHA and he saw amazing protection this time in an immature brain. But exactly with the same approach, not giving to animals to eat something in the diet but an injectable approach. So like a drug type intervention. And luckily just very recently, I think Richard came across similar problems of convincing investors to develop formulation, but ultimately he created a spin-out deck therapeutics. And they have recently published their first results with an emulsion they are working on. And obviously this emulsion is destined to be used in phase one studies. Very likely it’ll take the typical drug development path. So it’ll be a phase one in healthy volunteers.
Dr. Bill Harris: And you say emulsion, so that implies kind of a triglyceride. Is it a free fatty acid? What is the form of the DHA?
Dr. Adina Michael-Titus: It’s a diglyceride, this new formulation they’re developing. They’ve published the data just a few months ago, and they’ve compared triglyceride with diglyceride forms and they show there is an advantage for the diglyceride form. So this becomes therefore proprietary formulation with which there is evidence at least in the experimental models of hypoxic-ischemia encephalopathy, that there is clearly efficacy. And some indication of efficacy superior to the triglyceride form. They show some data on bioavailability and also dynamics integration in membranes and so on. So it is very nice to see the first data indicating that it’s possible to develop something which could be used as both as a drug. But it has been an arduous journey because of the high risk associated with developing this type of intervention.
Dr. Bill Harris: And even Deckelbaum’s formulation has not been used in spinal cord injury or traumatic brain?
Dr. Adina Michael-Titus: Yeah, I think it’s still… They’ve just published their first paper and also confirmation in two independent labs in his group at Columbia and I believe the University of Bonn. And we are working very closely with Richard, we’re very excited to see that there is this development in the field because at the same time, because there was evidence that there was potential in using docosahexaenoic acid in traumatic brain injury. I think other groups have looked at it from a much more pragmatic perspective, in a different type of population. Now going back to brain injury, there is a whole spectrum of concussive injury or concussion. And of course now everybody accepts the high risk associated with contact sports and all the interesting characteristics of a distinct form of encephalopathy, which is chronic traumatic encephalopathy. So it’s a new chapter in a way in neurology.
But this has led people pragmatically to test supplementation, as I’m sure you know, supplementation with DHA this time as capsules of course over many months, to decrease the risk of negative consequences of injuries, especially repeated injuries. And I think this is a very nice development in the field because it is a different spectrum of injuries. It’s part of what we may describe as mild injuries, but I think it’s very promising because it’s started providing some indications using objective biomarkers of injury that for example, if you give docosahexaenoic acid at a certain level of two grams, three grams, you can decrease objective markers of injury. And the markers of injury you can use in concussion during a season of playing athletes in football as in American football or in rugby it’s the same, neurofilament L. It’s not only neurofilament L, but the neurofilament L form is very well consolidated now in neurology as a biomarker of injury in the peripheral compartment.
So this clearly indicates that there is a very specific beneficial change, which is the consequence of giving people this supplementation over months. It can be six months, eight months, without any deleterious consequences because that’s important too. It’s very important that young fit men and women who are involved in sports and contact sports, even more important when they go back to spinal cord injuries or traumatic brain injuries or spectrum.
Dr. Bill Harris: Right. So nobody’s infusing omega-3 on the sidelines in a football game yet after a concussion?
Dr. Adina Michael-Titus: No, there are preparations which are injectable, but they are part of parenteral nutrition. As you may know, there is an emulsion-
Dr. Bill Harris: OmegaVia
Dr. Adina Michael-Titus: OmegaVia for example. It’s not the only emulsion, but there are several emulsions where there is an omega-3 component. But this is a nutrition space. And I think this is one of the areas where there is still for some people, some confusion whether you take them because it’s good for you, it’s not specifically very good for your brain but it’s good to take them. And I think that we still need to do a lot of work on this because there is something very specific Omega-3s do beneficial in the brain and in the context of injury. And whereas in the field of cardiovascular protection, I think there is much more acceptance and much more evidence. I think we’re not quite the same place in the neuro field.
Dr. Kristina Harris Jackson: That’s his phone. We’ll cut that.
Dr. Adina Michael-Titus: So that’s where we are. And it’s very encouraging because this shows that it can be done and you can affect a parameter which is very objective.
Dr. Kristina Harris Jackson: Yeah. Has anybody tested EPA?
Dr. Adina Michael-Titus: Yes, I think indirectly EPA has been tested. EPA in spinal cord injury we’ve published a very small study where we showed as an injectable form like DHA, it did have some efficacy in animals, although not quite as strong as DHA. But we didn’t do an extensive dose response study and so on. And there is much less published with pure EPA. EPA is often part of fish oil interventions done even in mice or rats. And I think the evidence around EPA is we still need to do work on EPA. And there is, I think an impression that EPA at times may even be deleterious, may even lead to negative consequences. But it’s not clear yet. And I’m saying this very carefully because EPA and DHA can modulate inflammatory reaction, there is no doubt about it. And neuro inflammation in particular, but I don’t think we fully understand how different they are and where the differences lie.
And neuro inflammation in particular in the context of brain or spinal cord injury, is truly a double-edged sword because you need some of it but not too much. And you need to control it. So I think DHA and EPA are in this space where we still need to do a lot of work to understand differences between them. And also if you use mixed preparations, typical DHA, EPA almost one to one or 1.2 to one, whether you decrease the efficacy of DHA for example by mixing with EPA and what the ideal ratio is. So the work with EPA and even less with DPA because there isn’t enough out there. I think DHA is still the lead compound which has been studied by enough groups in the world and a variety of models of paradigms to say, well, there is something there which is very interesting.
Dr. Bill Harris: Yeah, right. You certainly hear anecdotes about people having traumatic brain injury and then being given seven, eight, 10 grams a day by mouth after. What do you think of that kind of work?
Dr. Adina Michael-Titus: Yes. Well, this goes back to some studies years ago when very high levels were given to, I remember a survivor of a mine-
Dr. Bill Harris: Oh, yeah. A survivor of, was it a mine accident?
Dr. Adina Michael-Titus: Yes, a mine accident. And at that time, certainly the doses were very high, I think higher than 10 grams even. And there have been more studies more recently using this approach in very severe traumatic brain injury, using very high levels of DHA administered to patients. The problem is that, again, we just don’t know how much should be given. I’m going back to the concussion studies in athletes, there is some indication you do need to be well above the 250 milligrams or 500 milligrams, well above that level, possibly well above two grams, three grams.
Dr. Bill Harris: Well, it’s that kind of study, obviously it’s just almost a series of case reports, that’s almost all you can do. You can’t randomize.
Dr. Adina Michael-Titus: No. And especially in severe traumatic brain injury, both spinal cord injury and traumatic brain injury are such tricky conditions because they’re so heterogeneous. It’s almost an equal one. In spinal cord injury, every patient is distinct. And in spinal cord injury you may rationalize a bit looking at the segmental level or cervical level, thoracic level, lumbar level. But in traumatic brain injury it’s even more heterogeneous. And there is a need for better stratification and understanding which patients would benefit from DHA. It’s far from clear the moment, whether it’s only the moderate and perhaps the mild end of the moderate injuries that would benefit. Or maybe we can hope to have improvement also in severe injuries. They’re completely different injuries in patients. And when you do studies, especially in very severely injured patients such as the studies that Professor Julian Bales has led I think over the last few years, it’s very difficult to have perfectly matched controls. And people will always object to these observations saying, “Well, there is no controls, not a randomized, double-blind.” It’s very hard to do that. And… Yeah.
Dr. Bill Harris: Yeah. Spinal cord injuries are so devastating. We all think of Christopher Reeves the Superman, and he’s kind of iconic for this. And could people have used Omega-3 right after that horse accident and saved him? It just seems like a low risk, high reward potential.
Dr. Adina Michael-Titus: Yes. But we do need a tool, and now that’s why it’s so encouraging to see the results from the Richard Deckelbaum’s lab and the initiative to create these emulsions. And they will allow us to move to man and test the hypothesis.
Dr. Bill Harris: Great.
Dr. Adina Michael-Titus: And it’ll require some thinking. Obviously Richard’s interest is still very much driven by neonate hypoxic-ischemic encephalopathy, which again is another example of injury of the brain where the outcome is dire for most neonates. And hypothermia which is the standard of care is without doubt helping some of the neonates, but not all of them. And many of them end up with lifelong major disability, cerebral palsy and so on. So these are indications where there is a long journey still that we need to continue and persevere I think, because now from a variety of perspectives there is evidence that these compounds have new protective potential. It was not a one-off bias by certain laboratory there type of methods or models or protocols.
Dr. Bill Harris: Yeah. Do you see a role for this in immediate post MI patient heart attack? Would there be-
Dr. Adina Michael-Titus: It’s an interesting question, Bill, and I think yes, cardiac arrest for example there’s clear evidence there are some changes in cardiac arrest people. And that this is fairly recent work where you can apply the same principle and injecting or giving omega-3 fatty acids may help patients. Another aspect of all this is to go back to something much more than anybody on is the Omega-3 index story. Now we have a tool which allows us to say, okay, I have some idea of this person is in a state of relative deficiency or not. And this is an incredibly important tool. In a study we have published fairly recently, we looked at patients admitted with trauma. And the first group of patients we published on is focused on traumatic brain injury. We also had some spinal cord injury patients, but it was a small study. It was part of a more comprehensive analysis of lipid changes. But we found that the typical adjunct patient arriving with a brain injury had an omega-3 index of around four.
And I’m not surprised because we know from various studies done in the last five, 10 years that there’s such variation worldwide in populations in dietary intake, dietary habits. There is this increased tendency to have an omega-6 rich diet, and we were surprised to see that the omega-3 index was fairly low. So this raises the question that the instinctive thing you would like to do immediately is also to improve that omega-3 index. And let alone all considerations which are more specific focused on your protection. The people who have major injuries and some of them have trauma of the brain but with additional physical trauma, other musculoskeletal trauma and other organs, they would be in a better place if they had slightly higher omega-3.
Dr. Bill Harris: Yeah. So have you or anybody looked at the sequela of TBI or spinal cord injuries in Japan versus a western country? You’ve got a higher omega-3 index population, are their injuries less severe?
Dr. Adina Michael-Titus: Yes. I’ve been asked this question, in I think at least 15 years, and I was talking about this with my trauma colleagues not so long ago, a month or so. Again, I asked her, I said, “I get asked this question.” It’s impossible to retrieve information which compares outcomes. It’s just impossible because the management of injuries is different. There are variations in different countries. So it’s like comparing plums and pears. It’s really difficult to extract good quality information, which would allow you to say, “Look, if a Japanese person in Osaka has a car accident and they have this omega-3 index, another person in Scotland or in the UK will have this outcome.” It’s difficult to extract this information. Nonetheless, what is interesting, I was looking not too long ago at a paper published in Japanese individuals with traumatic brain injury, not in the acute phase.
It was a while and I looked at their baseline omega index, it was close to seven, between six and seven. So it’s a different set point. Overall, I don’t think there is an impression that trauma or neurotrauma patients do amazingly differently in Japan because this would be known in the field if it were such a striking difference in outcome. So I guess this introduces an element of humility and perspective also in all this, because I think omega fatty acids certainly have a potential to induce a beneficial effect and an improvement. And for some patients it may be quite a meaningful improvement.
But also I think expectations need to be moderated by the reality of very complex conditions such as traumatic spinal cord injury or brain injury, where the severity of the impact on tissue is such that if you don’t manage expectations, people will just dismiss the whole thing. Just to give you an example, slightly different type of agent, as I said in spinal cord injury there’s nothing which can be offered routinely in the clinic now. But only a few months ago, finally a study was completed, much delayed by COVID of course among so many other clinical studies, showing that the compound Riluzole has some benefits.
Dr. Bill Harris: What is the compound?
Dr. Adina Michael-Titus: Riluzole, which is a compound that exists in medicine already. It is used in motor neuron disease. It gives patients a few extra months of life, very, very small effect but some effect in motor neurone disease. And it is a compound which act on glutamate release, there’s a lot of glutamate release in your degenerative diseases and in injury as well, while excessive glutamate release is not good news. And riluzole partly through an effect on specific potassium channel, family of the two poor domain potassium channels, riluzole appears to have an effect on glutamate dynamics, really decreases glutamate release. And there is this study which has been published only in a subgroup of patients with spinal cord injury within complete injuries, riluzole seems to induce an improvement. So it’s a Canadian study led by Michael Fehlings. And it’s interesting to know that riluzole shares with DHA at least one target, which is this family of two poor domain potassium channels like TREK-1, TREK-2 and TRAAK. So I guess the field now will pay attention to this. It’s not the end of the journey, it’s just-
Dr. Bill Harris: Having a pharmaceutical company behind it is going to drive research more than having a nutrition.
Dr. Adina Michael-Titus:
Riluzole is a small molecule, typical small molecule pharmacology and it’s already… But the effect was seen in a subgroup of patients. So that’s why I’m saying one needs to be very careful and to bear in mind this need to better stratify and understand when you go back to the clinical reality, which groups of patients would benefit from omega-3 fatty acids. And all the animal data so far don’t allow us to do predictions of this type. But the increased evidence that we have even in animals where we can measure the same biomarkers of injury, would allow us also to have outcomes which are a bit more translatable. So if you show that the DHA or a particular emulsion, for example, changes the level of a biomarker which goes up with injury in animals in the same way it goes up in humans, then you have direct equivalence with the clinic.
So you are getting closer to small bridges between rodents and humans because rodents do respond to injury in a different way, whether it’s spinal cord injury or brain injury. They have simpler nervous systems. So that’s the big caveat that needs to be kept in mind.
Dr. Bill Harris: Yeah. But you seem excited about the future.
Dr. Adina Michael-Titus:
I think Churchill said this, “Yes, it’s not the beginning of the end. It’s the end of the beginning.” So I think it’s an incredibly long time since that day when we unblinded the data and we couldn’t believe how strong the protection was used by fatty acids. But the whole field of the fatty acids research has moved incredibly in the last 20 years. And of course, nobody’s shocked anymore if you say, well, if you inject this lipid you’ll see something amazing. Or if you give it for two weeks, you’re going to see something amazing. Lipids have made it into therapeutics, and that’s so important. A chapter still needs to be written about neuroprotection in traumatic injuries, but I think omega fatty acids are much closer now to having a place in that chapter.
Dr. Bill Harris: That’s great.
Dr. Adina Michael-Titus: And I’m very excited to see that if we make progress with formulations which are translatable, then we can move to phase one. Now if these emulsions, for example, I mentioned a moment ago, if they’re fully validated in a few months to come, year to come, it shouldn’t take that much of a big leap to do the first phase one, phase two A in traumatic injuries and also in neonate hypoxic-ischemic encephalopathy.
Dr. Bill Harris: Yeah. Great. Well, this has been fascinating. Thank you very much for that tour you’ve given us of the history of this. It’s great. I think we probably need to wrap up. Tina, any final words from you?
Dr. Kristina Harris Jackson: No, you covered all the questions just seamlessly. It was beautiful. Yeah, thank you so much. I have nothing to add. That was fantastic. So thank you so much. We will have another OmegaMatters probably coming up soon, but this is a fascinating area and I am sure we’ll keep up with it and maybe come back to you in a little while to see where the field is at then. So thanks so much.
Dr. Adina Michael-Titus: Thank you so much for having me. And thank you for everything you are doing to promote Omega-3s in high quality research. Thank you.
Dr. Bill Harris: Thank you.
Dr. Kristina Harris Jackson: Yes, thanks.
Dr. Bill Harris: All right.
Dr. Adina Michael-Titus: Bye-bye.
Dr. Bill Harris: Bye-bye. Take care.