How Omega-3 & Omega-6 Fatty Acids Impact Early-Onset Dementia
OmegaMatters: Episode 55
Hosts: Dr. Bill Harris & Kelly Patterson
Guest: Dr. Aleix Sala-Vila
About this episode: In this episode, Dr. Bill Harris and Kelly Patterson interview Dr. Aleix Sala-Vila about the relationship between omega-3 fatty acids, brain health, and dementia. Dr. Sala-Vila discusses recent research using UK Biobank data showing that people with higher blood levels of omega-3s—particularly DHA and other omega-3 fatty acids—had a lower risk of developing dementia, including early-onset dementia (before age 65). He emphasizes that these findings are observational, meaning they show associations rather than proof that omega-3s prevent dementia, but they add to growing evidence that maintaining higher omega-3 status may support long-term brain health.
The conversation also explores how omega-3s may help preserve brain function through mechanisms such as reducing inflammation, supporting blood flow, and improving the brain’s ability to use glucose—an important process that can become impaired years before Alzheimer’s symptoms appear. Dr. Sala-Vila notes that lifestyle factors including diet, physical activity, social engagement, and cognitive stimulation likely work together to influence dementia risk.
A second major topic is omega-6 fatty acids and dementia risk. Dr. Sala-Vila reviews research suggesting that linoleic acid—the primary omega-6 fat found in foods such as nuts, seeds, and seed oils—was associated with a lower risk of Alzheimer’s disease and all-cause dementia. He cautions against treating all omega-6 fats as the same, explaining that different omega-6 fatty acids may have different biological effects and that current evidence does not support demonizing linoleic acid.
The key takeaway for listeners is that higher omega-3 levels appear beneficial for brain health, healthy sources of omega-6 fats should not be avoided, and a comprehensive lifestyle approach—including a healthy diet rich in polyunsaturated fats—may help support healthy aging and potentially reduce dementia risk over time.
SHOW TRANSCRIPT
Kelly Patterson: Welcome to OmegaMatters, where we talk everything fatty acids. I’m Kelly Patterson along with Dr. Bill Harris and today our guest is Dr. Aleix Sala-Vila. Dr. Aleix Sala-Vila received his PhD in biomedicine from the University of Barcelona in 2004. His research has involved the role of bioactive compounds, especially omega-3 fatty acids from cellular biology to epidemiology, with the ultimate goal of reducing the incidence of chronic disease by optimizing omega-3 status. He has received four postdoctoral fellowships and has published over 45 papers on fatty acids. Alex, thank you so much for joining us today.
Aleix Sala-Vila: Thank you so much for invitation. So glad to be here.
Dr. Bill Harris: Good to be here. Hi. So did we mention Aleix is in Barcelona? Maybe we didn’t, but that’s where he is. And he has been one of the original FARI scientists to join our team. It’s been very, very productive. So Aleix, hi, good to see you.
Aleix Sala-Vila: Same.
Dr. Bill Harris: So we wanted to talk about a couple of things. Your bio talked about omega-3 and I think you got a wider interest than just omega-3, but let’s start with that. You’ve published a paper recently on omega-3 levels and a particular kind of dementia. You want to talk about that paper for us?
Aleix Sala-Vila: Yes. Well, I think that first of all, I think that we should make really clear that we don’t want to overstate any kind of findings in relation to dementia because I think that it’s a really concerning disease. And at this point, the main interest nowadays is just try to understand why this happens. So I truly think that lifestyle is a really powerful tool that we have to delay the onset and the progression of the disease. But at this point we cannot say omega-3 prevents Alzheimer’s, prevents dementia, cures Alzheimer’s or cures dementia because there are no randomized control trials. Because this would take too much time and this means too much money because it would be, I don’t know, years, decades of supplementation. So at this date, we just have observational data.
We have several observational studies, prospective cohort studies analyzing dietary intake of omega-3 or measuring both biomarkers of omega-3 and relating or examining the association with the incidents of dementia. Just to make that clear because okay, we cannot infer a causal effect. We cannot say omega-3 prevent dementia at this point. The maximum that we can say is people with higher levels of omega-3 have a lower risk of dementia.
Dr. Bill Harris: Do we have any treatments? Forget fatty acids for a moment. Any treatments for dementia yet or proven treatments to slow the progress of dementia?
Aleix Sala-Vila: No, not yet.
Dr. Bill Harris: Not really. So it’s just wide open field still?
Aleix Sala-Vila: Only some drugs approved for delaying the accumulation of the amyloid beta peptides, which is one of the hallmarks of Alzheimer’s disease. But there are some concerns in the sense that, okay, they are effective, but they are not really cost-effective.
Dr. Bill Harris: They don’t really change cognition?
Aleix Sala-Vila: No. No, not that much at this point. So before this, okay, we need to prevent rather than cure or slow down the progression.
Dr. Bill Harris: Great.
Aleix Sala-Vila: Lifestyle for sure. And I want to believe that maybe in 20 years we’ll be so sure that lifestyle has an impact like cardiovascular disease. I’m like to think that it’s similar to cardiovascular disease. Maybe 50 years later, no one said, “Okay, yeah, diet.” That’s not important. And nowadays, you go to the doctor on, “Okay, quit smoking, have some exercise and follow a healthy diet.” And I think that good for heart, good for brain will be pretty much the same for Alzheimer’s. It’s something that I want to believe that I will see, but not at this point. Maybe in 20 years.
Dr. Bill Harris: Yeah. Maybe toward the end, we can talk about other factors in the lifestyle besides fatty acids that might play a role here. So tell me the study you did.
Aleix Sala-Vila: So it’s good story because in 2023 we published a paper together with Bill and other scientists from FARI examining the associations between plasma omega-3 and incident dementia using the UK Biobank. And it was nice because it was the largest study to date. So we took advantage of the second release of metabolomics and we improved the papers that have been published in the UK Biobank because it was the largest data set ever. So I think it was an impact. And a few months later after that, we noticed that scientists call Hendrix, the surname is Hendrix, with an impressive track on early onset dementia published a really nice paper in JAMA Neurology, which is one of the best journals in the field, telling, “Okay, we identified using UK Biobank, lots of lifestyle related factors that associate with the onset of early dementia.” Early dementia by definition is diagnosis before 65 years old, so that’s it. That’s so simple.
So early onset dementia, also known as young-onset dementia, it’s diagnosis before 65. That’s so simple. So they identified some factors that could be related to lifestyle, and yeah, they looked at diet but not specifically at omega-3 fatty acids. So we said, “Oh, it’s a PT,” because, well, we just published a paper on any type of dementia, not distinguishing between late onset after 65 or early onset until 65. So we decided, “Okay, let’s try to replicate that study,” and we found, “Oh, that’s interesting.” So we decided, “Okay, let’s try to get another paper just dealing with this special outcome,” which was a part of the bigger outcome that we dealt before in our previous paper. And yeah, it was quite well received in the journals and yeah it’s until now.
Dr. Bill Harris: So how much effect… Go ahead, Kelly.
Kelly Patterson: How prevalent is early onset dementia? Do we know how many people have this? How big of an issue?
Aleix Sala-Vila: Yeah, that’s one of the reasons why early onset dementia is not so strict because, well, it’s much less prevalent compared to the late onset. Some people say that it’s around 5% of the cases of dementia, but in our population it was below 0.15%. So it’s tiny proportion. We were talking about trials because imagine the number of people that you would need to take into a trial just to get enough statistical power to get enough a significant or a meaningful effect because our case we were working with over 217,000 people and there were just 355 cases of early onset dementia.
Kelly Patterson: Wow. Wow.
Aleix Sala-Vila: Such a low number. So if you want to work with that, you need to work with some big data sets.
Dr. Bill Harris: Was the relationship between just DHA levels or was the total omega-3 levels were predicting?
Aleix Sala-Vila: It was total omega-3.
Dr. Bill Harris: Okay.
Aleix Sala-Vila: It was DHA and well, we worked with UK Biobank and one of the limitations of the UK Biobank is that fatty acids are measured using NMR— nuclear magnetic resonance—and it’s not the gold standard for measuring fatty acids. The best is gas chromatography. It’s by far the most common way to measure fatty acids. NMR, it’s good because it provides a huge snapshot of metabolites other than fatty acids and some fatty acids as well. But if you want to look at specific species of omega-3, you have limited information. You have, for instance, for omega-3, you have whole omega-3 and DHA, that’s all. You don’t have data for EPA, you don’t have data for DPA or ALA. So that’s it. So we ended up with three exposures of interest. One is DHA and it’s good because it’s the main omega-3 fatty acid that we have in brain.
The other one is omega-3 as a whole and the other one is one that we kind of created, so to speak, that is non-DHA omega-3 fatty acids. So it’s just maths, total omega-3 minus DHA. But this in this box goes EPA, DPA, ALA, so different omega-3 fatty acids, different origins, but well, this is a limitation, but this is what you have. You take it or you leave it. So that’s it. So we found really interesting associations or inverse associations for all omega-3 fatty acids for DHA. And interestingly, the associations were a little bit stronger for non-omega-3 fatty acids than for DHA, meaning that, “Okay, it’s good to increase your levels of DHA, which is the fatty acid, the omega-3 that you have in your brain, but other omega-3 fatty acids also have inverse associations.” Meaning that, “Okay, maybe DPA can be also helpful or we don’t know what happens with ALA because it was also here.” So also ALA could be helpful. It’s something that we cannot say at this moment.
Dr. Bill Harris: Mm-hmm. Yeah. Yeah. Interesting. So all the omega-3s, as far as we know, were favorably associated. Do you know what kind of intakes a person would have to have to have the levels of omega-3 that were associated with reduced risk for early onset? I should have prompted you with that question yesterday when we were planning this.
Aleix Sala-Vila: Yeah. I’m not sure, but I would say that in terms of omega-3, I think that around 500 milligrams per day would give enough omega-3 just to go to the top quartile, top quintile.
Dr. Bill Harris: Yeah. Sure.
Aleix Sala-Vila: I would go between 500 and 1,000 milligrams per day, something like that. I would go with three servings per week given or taken.
Kelly Patterson: Obviously it’s interesting that it makes sense DHA, because like you mentioned, I think we all associate DHA with the brain. Most people hear that and say, “Okay, if I want to do something healthy for my brain, I should take DHA.” Do you have a theory or a mechanism as to why the non DHA omega-3s seem to be so impactful, what they might be doing? Is it inflammation? It’s something else?
Aleix Sala-Vila: Yeah, definitely. I think that the vascular part is so important there because it’s so difficult. For instance, Alzheimer’s diseases are so related. They coexist. So I think that the vascular part, it’s so important and I think that it can be just misleading, just thinking on Alzheimer’s disease or dementia as something that it’s just a matter of the neurons or the brain membranes of the cells or I wouldn’t go that way. I think that it’s important to consider the blood flow, the neuroinflammation besides other classical mechanisms, the amyloid plaque aggregation, but I think that neuroinflammation and preservation of blood flow is so important.
And I think that EPA for sure contributes to brain health, maybe not impacting, I don’t know, the construction of the membranes because EPA is not that accumulated in our brain, but for sure decreases neuroinflammation, for sure promotes the blood flow in our brain. So the vascular part is so important and I think that EPA has a role on that.
Dr. Bill Harris: Yeah. And you published a paper earlier that looked at the importance of getting glucose into the brain and how that’s related to dementia as well. And was there an omega-3 connection with that as well?
Aleix Sala-Vila: Yes.
Dr. Bill Harris: I know that’s a long story.
Aleix Sala-Vila: I’m happy to go in that direction. So the brain is quite a small organ. It’s over two kilos, that’s it. It’s not that big, but it consumes the majority of our glucose. So brain needs glucose, lots of glucose. In absence of glucose can use ketonic bodies, but that’s exceptional. And when brain starts to use ketonic bodies, other organs, the liver, the heart. They have been deprived of glucose for a long, long, long time. So the brain is that the most important organ in terms of, okay, this is the last guide that we want to struggle without the glucose because glucose is so important for brain.
Dr. Bill Harris: Yeah.
Aleix Sala-Vila: So it has been seen that years, even decades before the onset of Alzheimer’s, some brain areas are starting to have difficulties to use this glucose just to get the glucose.
Dr. Bill Harris: Or to get it in or to get it into the brain?
Aleix Sala-Vila: Yeah. So maybe the glucose reaches the brain, but in some areas the cells cannot get the full amount. So they are, “Okay, we are not getting enough energy to behave, to work, to act in a normal way.” And that’s because some transporters are starting to be lost. It’s a membrane issue. And this is not happening in a random manner, not at all. It’s very consistent. We know that there are some areas that for sure are the first ones to struggle with this metabolic disturbance, so to speak. So we can track that because we have a glucose, you put a label, radioactive label, non-harmful, of course, and then you inject the glucose and you put the person into a minute of resonance and you can get pictures of how these labeled glucose is disappearing in the brain in the different ways. And you can see if your brain starts to having some traits of Alzheimer, you see that some areas are not using that…
Kelly Patterson: They’re not getting enough glucose.
Aleix Sala-Vila: Yeah.
Dr. Bill Harris: Is it because they have the Alzheimer’s or?
Aleix Sala-Vila: No, it’s because it’s something that it’s saying that maybe you are leaning towards Alzheimer, but you don’t have any clinical symptomatology.
Dr. Bill Harris: Oh, okay. So listen, yeah, before you…
Aleix Sala-Vila: The so called preclinical Alzheimer’s disease. So a few years later, sorry, a few years ago, Alzheimer was just a clinical construct. You have problems with your memory or you have lost your autonomy, your day-to-day ability to do normally, you have dementia or you have Alzheimer. Alzheimer is the most common type of dementia. Nowadays, there’s a different view. If you already have some load of amyloid, if you have some load of tau and you have some traits of Alzheimer, you have the so called preclinical Alzheimer. This doesn’t mean that you are going to have Alzheimer, but you have a high risk of having clinical Alzheimer. So thanks to biomarkers, magnetic resonance imaging, structural neuroimaging, all these kinds of new technology, which is rapidly evolving, we can see things happening in the brain years or even decades before Alzheimer’s, right? So we measured the omega-3 in the blood and we searched for associations with this ability or disability to use glucose in a population with brain working perfectly, cognitively perfect, but at a higher risk of Alzheimer because of genetics.
Kelly Patterson: Because of? Oh, okay.
Aleix Sala-Vila: And we observed that there was some nice associations in particular for ALA. So the higher levels of ALA, the better use of glucose. And in particular, with people with some amounts of amyloid, so that would be high risk of Alzheimer at the preclinical Alzheimer, but without symptomatology, but already with amyloid in the body, the higher levels of DHA, the better use of glucose. Meaning that, “Okay, if you want to do trials to preserve glucose using DHA, maybe if you are using the whole population, it’s not going to work. Maybe you need to select the people with already having some amounts of amyloid in the body.”
Dr. Bill Harris: Mm-hmm. So you’ve measured amyloid in the brain non-invasively?
Aleix Sala-Vila: Yeah. You can measure the amyloid in three different ways. So the classical ones is by using CSF that cerebral spinal fluid or by same inject a tracer that specifically links to the amyloid in the brain. So the CSF is better because well, okay, it’s more invasive, but it can give you earlier detection of what’s going on. Neuroimaging, it’s better because it gives you the pattern of the distribution of the amyloid, but both of them are, okay, they are invasive and they’re quite expensive. So we have a kind of paradigm shift with the emergence of blood-based biomarkers. And this is so helpful because it allows scalable, cheap, affordable measurements, not only in day-to-day clinical practice, but also in clinical settings in terms of research. So yeah we can measure the deposition of amyloid nowadays with minimally invasive and not really high cost.
Dr. Bill Harris: Okay. Okay, cool. So that’s cool. So we found, you said DHA and ALA were both linked inversely with…
Aleix Sala-Vila: So ALA in all the populations because we did some stratifications between men and women, APOE4 carriers and non-carriers. APOE4 carriership is the main genetic factor for late onset Alzheimer’s disease. So in terms of Alzheimer’s disease, there are two types. The one is so driven by genetics. So you have some specific mutations in some specific genes. So you are going to have Alzheimer. So period. It’s a family matter.
Dr. Bill Harris: Yeah. But it’s not APOE?
Aleix Sala-Vila: Yeah, that’s not APOE. That would be around one or 2% of Alzheimer’s. The most useful form, it’s late onset Alzheimer’s disease, meaning that okay, the peers, 60s, 70s, 80s, because aging is the most important risk factor. So the age almost and some risk factor. But in terms of genetics, APOE4 carriership increases your risk of having Alzheimer’s. So each of us have two alleles, so you can have zero copies of E4, one copy or two copies. So you’ll have one copy, you increase the risk by 40%. And if you have two copies, you increase the risk alleles…
Aleix Sala-Vila: Around 20% of the population carries at least one APOE4 allele and the 2% of the population carries both alleles of APOE4. So we stratify it for sex for APOE4 carriership and for the load of this amyloid and tau in the body. And ALA was related to better use of glucose in all types of populations, which is cool and DHA was related just in people with some preclinical Alzheimer. In other words, with people with some amounts of amyloid in the body.
Dr. Bill Harris: Oh, interesting.
Kelly Patterson: Okay.
Dr. Bill Harris: Interesting. Yeah. Cool. So omega-3 looks like it’s a healthy thing for the brain.
Aleix Sala-Vila: That’s for sure.
Dr. Bill Harris: For sure. We’ll come back to me.
Aleix Sala-Vila: We still don’t know what’s optimal dose, who could obtain the greatest benefits in terms of age, in terms of genetic makeup, in terms of gender, in terms of race, in terms of background, for instance, if you really have a supplement of omega-3 or consume three servings of fatty fish, does it make any sense to participate in a trial of supplementation of omega-3 to prevent this Alzheimer or dementia? I don’t know. We don’t know yet. So our main interest is trying to define who could obtain the greatest benefits. What’s the optimal dose? If we want to go with a supplementation with omega-3, what’s better? EPA, DHA, it doesn’t matter. What about ALA? It’s a matter just of these nutrients. It’s a matter of the food containing these nutrients. It’s a matter of something bigger diet, or even it’s a matter of a kind of lifestyle. Because for instance, last summer, a very important paper from a very important study from the United States called Pointer showed that, okay, diet is important, but it’s also important social engagement and cognitive training.
Dr. Bill Harris: Training.
Kelly Patterson: Activity and keeping your brain engaged.
Aleix Sala-Vila: So it’s a kind of multimodal approach. It’s not just diet. So once again, we’re not saying we’re going to cure Alzheimer just with eating fish or adding fish oil in our day-to-day. Maybe not, but for sure it will help. In the meantime, let’s go with omega-3. It will help your heart. If it doesn’t help your brain, it will help your heart. That’s for sure.
Dr. Bill Harris: Yeah, yeah. Well, since we’re on the omega train here, should we-
Aleix Sala-Vila: I think that maybe in 20 years we will say, “Yeah, it’s so clear that omega-3 helps our brain to get less dementia,” and I’m so convinced.
Dr. Bill Harris: Yeah. Well, should we hop over to the other side of the omega-3 story or the omega story, talk about omega-6, because you have another paper, another very interesting paper on the question of omega-6 and dementia. Tell us about that one.
Aleix Sala-Vila: This is also a cool story because well, in the terms of omega-6, as many of you know, so there’s some controversy, particularly in the States, because it states that the main source of oil, it’s seed oil. This doesn’t happen in Europe, in particular in Southern Europe. And so I’m from Barcelona, so we don’t have this kind of problem because we are soaked in olive oil. So this doesn’t concern us that much, but it’s a really important topic in the States. And for instance, I was in the American Oil Chemist Society last year and it was a specific session on that and the room was so crowded because it’s an important topic. Because some people say suddenly that seed oils are bad because they contain linoleic acid. That’s it. And linoleic acid is transformed to arachidonic acid and arachidonic acid is a bad for us.
So this is quite concerning and I know that you have been dealing with this topic, but it’s quite concerning because there is not much data on Omega-6 and dementia except for a meta-analysis from 2013 where Omega-6 was just used to calculate the Omega-6 to Omega-3 ratio. And Neil knows a lot about this ratio and some papers published, “Okay, you have higher levels of this ratio so you have higher risk of dementia.” And in some cases, in some cases Omega-6 have inverse association, Omega-3 have inverse association with stronger association. And this means that if you do the math, so both of them are protective, so to speak. I know that we cannot infer causality, but both of them have inverse associations, but just because omega-3 has stronger effect or stronger association, this means that the ratio has an inverse association.
Dr. Bill Harris: Right, right. It flips.
Kelly Patterson: Yeah.
Aleix Sala-Vila: It’s not biology, it’s just maths. And one of the concerns, and it’s a personal feeling that I have is that, “Okay, one thing is opinion and the other thing is science,” and it seems that, “Okay, I have an opinion,” I could say because I think that, “Okay, but I do science, you do science, so let’s talk in terms of science,” so it’s not what you think, it’s what you can prove. So in some cases, in the USA, okay, omega-6, maybe it’s not good for your brain, that’s it. So what? So we decide, “Okay, let’s go,” because in many force papers in which fatty acids have been involved, we observed divergent associations between different types of omega-6 and this age-related disease. We observed different associations between linoleic acid and other omega-6 fatty acids. So in some cases where if not protective, neutral, compared to arachidonic and compared to even longer omega-6.
So we decide, “Okay, let’s go. We have this data in the UK Biobank,” and it’s same here, same approach. We have data on linoleic acid, total omega-6, so we ended up creating these non-linoleic omega-6 fatty acids. And well, we were aiming at let’s identify neutral association for linoleic and it was so shocking because we observed actually that high levels of linoleic acid were so inversely associated with the risk of Alzheimer’s disease and the risk of all cause dementia. So it shocked us because we observed that linoleic acid behaved on one way and other omega-6 fatty acids were the totally opposite at high levels, high risk. So this is in response the message, we shouldn’t treat omega-6 equally. So it’s not the same, same chemical family. Okay, that’s fine. Same biological effects, not at all.
Kelly Patterson: So what might be for those non-linoleic… Well, and for linoleic as well too, the biggest sources of those in our diets. So obviously we’re both here in the U.S., Bill and I, and so that’s who we’re mostly talking to of people in the United States. If linoleic is okay, where are we getting that? And if non-linoleic omega-6s are potentially more risky, where are we usually getting those from?
Aleix Sala-Vila: Yeah. So linoleic is so abundant in your diet and the main sources could be seed oils, also nuts.
Kelly Patterson: So things like canola oil, corn oil, soybean oil? Yep.
Aleix Sala-Vila: And in plenty of nuts and seeds.
Kelly Patterson: Mm-hmm.
Aleix Sala-Vila: In the same time, some of these ingredients are used in some ultra-processed foods, which are not so good, but it’s not a matter of the nutrient per se or the source of their fatty acid per se. So it’s the food, not it’s the primary supply of the fatty acid. The other ones are not so abundant in our diet. For instance, you can find arachidonic acid in the egg yolk, but it’s marginal. We can find there because it’s a key component of the membranes, but it’s not such abundant fatty acid in the day-to-day.
Dr. Bill Harris: Yeah.
Aleix Sala-Vila: So if you have higher levels of arachidonic acid, adrenic acid, this long chain pollen situated omega-6 fatty acids, it’s due to metabolism.
Dr. Bill Harris: It’s not diet. It’s not from your diet. It’s metabolism, right?
Aleix Sala-Vila: It’s metabolism.
Kelly Patterson: You’re producing these. You’re not getting them from your diet, you’re being produced in your body. Okay.
Dr. Bill Harris: Right. That’s right.
Kelly Patterson: And do we know is that… Yeah, I was going to just ask, is that genetic? Do we know are some people producing more just genetically? Is there risk factors to that?
Dr. Bill Harris: Yeah.
Aleix Sala-Vila: I know that there are some genotypes that favor rapid metabolizers and some people don’t metabolize that fast, but it’s something that it’s just emerging. Some genes are really working so hard just to try to get a clue on this person to person differences because well, for sure, okay, arachidonic acid, it’s something that it’s needed in our body. For instance, it’s in our brain and if it’s in our brain, this means that it’s doing something there because other than that. So we wouldn’t have that in our brain. But if we have too much arachidonic acid, it’s a source of inflammatory biomarkers, it’s a source of lipid mediators that promote or amplify our vascular risk. So we don’t want to have too much arachidonic acid in our body.
So it seems that this is tightly controlled, but one thing that we should get so clear is that by increasing our levels of linoleic acid, we are not going to have just to increase the levels of linoleic. We’re not going to have high levels of arachidonic acid. Some people, some super metabolizers maybe will increase some levels, but I think that linoleic acid and all the healthy sources of linoleic acid shouldn’t be demonized just for that.
Kelly Patterson: Right.
Aleix Sala-Vila: Because actually a lot of stuff clinical research in animals, in cells have proved that linoleic acid is not bad. Actually it has been related to a kind of protection as long as it’s not oxidized. If it’s treated aggressively, if you have your bottle of canola oil for months and months and months, and then you consume that, okay, maybe it’s not going to be helpful for you. Maybe it’s going to harm you, but it’s not a problem of the linoleic acid or the canola oil, so to speak.
Dr. Bill Harris: Yeah. And I think it’s helpful from data perspective. I think the average U.S. intake of linoleic is somewhere in the 13, 14, 15 grams a day, something like that. So let’s say it’s 15 grams a day. The average arachidonic intake is like a hundred milligrams a day, very much like omega-3 intake, that low hundreds is about what people eat typically. So almost virtually a hundred percent of the omega-6 we eat is linoleic.
Kelly Patterson: It’s linoleic acid. Yep.
Aleix Sala-Vila: Right. And in addition, so many foods containing linoleic acid also contain other bioactives that could be helpful for your brain. I’m talking about particularly seeds and nuts, not that much for seed oils because seed oils undergo some processes that make losses in terms of antioxidants and this kind of stuff. But for instance, if you consume nuts, things like that, so you are getting linoleic acid, but at the same time, you are getting lots of antioxidants and phytosteroids and really good stuff for your body, for your heart, and for your brain.
Dr. Bill Harris: Do we know the food sources… When you look at a population like UK Biobank and we separate out into quintiles of linoleic acid blood levels, so 20%, 20%, do we know what the food sources are of linoleic acid for the highest group versus the lowest? I mean, are the high group people eating lots of nuts and seeds?
Kelly Patterson: Salad dressing versus processed stuff.
Dr. Bill Harris: Yeah. I mean, is any different or just different amount? I don’t know that we know it.
Aleix Sala-Vila: …In the UK, not much olive oil. I spent two years there and there was some of live oil in the supermarket, but they tell me that they didn’t like olive oil. They found olive oil to taste, the taste of olive oil was not good.
Dr. Bill Harris: Yeah. It’s not a great source of linoleic acid either.
Aleix Sala-Vila: No, no, no. Well, it contains some linoleic acid. So salad dressings, as you said, canola oil, sunflower oil besides some seeds, but I’m not sure whether someone has examined the associations of specific foods with specific fatty acids in the context of the UK Biobank. Maybe it’s something for them.
Dr. Bill Harris: Something for us to do, right? I know it’s new ideas all the time. So we have a happy story for the omega-3s in brain health and we have an emerging happy story with linoleic acid (omega-6) and brain health. So how would you advise the consumer to adjust his or her fatty acid intake to reduce risk for Alzheimer’s?
Aleix Sala-Vila: Okay. So far first message, the higher levels of omega-3, the better for your brain.
Dr. Bill Harris: Yeah.
Aleix Sala-Vila: At this point, we haven’t found any threshold saying, “Okay, above this point you are not going to have…”
Dr. Bill Harris: Yeah, the effect goes away, right?
Aleix Sala-Vila: Yeah. So far the higher, the better.
Kelly Patterson: Higher, the better.
Aleix Sala-Vila: So far, no evidence that men or women could get more benefits or APOE4 carriers, non-APOE4 carriers, at least using data from the UK Biobank. So the story is broad populations or broad effect. So both men and women carriers and non-carriers of APOE4. So anybody could get benefits of having higher levels of EPA and DHA.
Kelly Patterson: No, I was just going to ask just with populations, is there an age where it’s too late if somebody’s in their late 40s, early 50s and really starting to get concerned about their brain, is it too late to start?
Aleix Sala-Vila: No, not at all. So I would say it’s never too late or too early to start taking care of yourself. For instance, in the pregnant study, it was a landmark study testing effects of adding a Mediterranean diet in cardiovascular disease and it was in really old people in some cases. So all of them were in the 60s and in some cases were almost in the 70s in terms of prevention of cardiovascular disease. It seems that, “Okay, in the 70s, maybe I’m too old to get any kind of prevention because if I haven’t had any heart attack at this point, I’m not going to have heart attack.” And that’s not true. It’s never too late to start taking care of yourself and also in the opposite. If you’re a teenager saying, “Oh, that’s not going to happen to me.” Oh, that’s not true.
How you live in your 20s, it will have such an impact in your 40s and how you live in your 40s, 50s, it will have such an impact in your 60s, 70s and it’s never too late or too early to start taking care of yourself. So my advice, increase your levels of omega-3. If you’re not eating fish, add fish. If you don’t want to eat fish for several reasons because you don’t like the taste or because you are concerned about pollutants, because you are vegan or vegetarian, that’s fine. You have plenty of options. You have vegan supplements, you have fish oil, you have plenty of options. You have also some nutrients that contains omega-3, which are different ones from those found in fish. You have walnuts, you have canola, you have soybean that contain also omega-3 and they contain all the nutrients that maybe will be helpful for you. This, maybe, and I would like to highlight maybe, will help your brain because at this point we don’t know that yet. I hope so, but for sure will help your heart and the rest of your body.
In terms of omega-6, there’s no problem to eating or consuming food reaching omega-6 as long as they are not oxidized, as long as they are well-preserved. Try to avoid sources of omega-6, including junk food. That’s so easy. So it’s not a matter of the omega-6, it’s a matter of the food containing the omega-6, right?
Kelly Patterson: Yeah.
Dr. Bill Harris: Yeah.
Aleix Sala-Vila: So try to eat healthy, try to eat as much polyunsaturated fatty acids as you can, try to eat these fatty acids along with protection in terms of antioxidants, add vegetables, add foods that please to you and maybe this will help your brain, maybe, because we don’t know that much yet. I repeat, we are just starting to understand why some people have Alzheimer’s. So we are not at the point saying that we are going to beat Alzheimer just following a healthy diet. Be helpful for your brain, but for sure will be helpful for other parts of your body.
Kelly Patterson: Might help, definitely won’t hurt.
Dr. Bill Harris: Right.
Kelly Patterson: Yep.
Dr. Bill Harris: Good job. Okay. Nice overview. Very good. I think, Kelly, any last questions for Alex?
Kelly Patterson: I think I got all my questions answered. Thank you so much for joining us. That was so fascinating. I want to listen to learn more about your glucose brain metabolism and Alzheimer’s. I just think that’s fascinating. I’ve done some work with a lot of brain injury patients before in that it’s just very similar concerns and that’s so interesting.
Aleix Sala-Vila: It’s a really cool topic because we are getting more and more tools just to track these sublte changes that happen, I don’t know, maybe decades before the onset of the symptomatology. So in terms of FARI, we’re trying to get in contact with people having these resources or safety.
Dr. Bill Harris: Yeah. Yeah, exactly. Great.
Kelly Patterson: Awesome. Well, Bill, do you have any more questions?
Dr. Bill Harris: No, no, I think that’s great. I think we covered a lot of good stuff. Omega-3 is good for the brain. Omega-6, linoleic acid, it’s good for the brain. Don’t avoid it.
Kelly Patterson: Eat whole foods.
Dr. Bill Harris: Eat whole foods. Partners in prevention. That’s what we’ve got.
Kelly Patterson: Yeah.
Aleix Sala-Vila: It’s good to have these kinds of chats. Thank you so much for the invitations because, okay, as a scientist, they also want us not only to reach the scientific arenas, but also target as much people as possible and this type of podcasts and all these resources are so helpful just to reach all kind of people and deliver our message, not only to scientists, that it seems that we are living in our towers and we just communicate each other. But at some point it’s important to try to change society in a good way and this is so helpful. So thank you very much for giving me the opportunity to share the latest results that we have find.
Dr. Bill Harris: Great. Thank you.
Kelly Patterson: Great. So thank you and thank you for joining us. And everybody, thank you for joining us on OmegaMatters and we’ll see you next time.