Top Omega-3s Research Explains What You Need to Know

In this 2026 YouTube interview, host Nick Norwitz talks with Professor William Harris, a leading researcher on omega‑3 and omega‑6 fatty acids. The conversation begins with a basic biochemical overview: omega‑3s (ALA, EPA, DHA) and omega‑6s (linoleic acid, arachidonic acid) differ by the position of the first double bond, are poly‑unsaturated, and must be obtained from the diet. Harris explains that the shape of these molecules determines how they fit into cellular receptors and become signaling hormones. The pair then moves to measurement, describing the Omega‑3 Index – the percentage of EPA + DHA in red‑blood‑cell membranes – and the omega‑6:omega‑3 ratio. Normal U.S. levels are ~5.5 %, optimal >8 % (8‑12 % sweet spot). The ratio is deemed misleading because it is driven mainly by omega‑3 levels and ignores the distinct biological actions of individual fatty acids. They discuss why short‑term randomized controlled trials (RCTs) often fail to show cardiovascular benefit: modern patients receive statins, antihypertensives, and rapid acute care, making it hard for a modest nutrient dose (≈1 g EPA/DHA) to demonstrate an effect. Long‑term observational data linking higher Omega‑3 Index to lower all‑cause mortality and reduced heart disease are presented as stronger evidence. A high‑dose EPA trial (4 g/day) showed benefit, illustrating dose‑response considerations. Practical dosing guidance is offered: 1,000‑1,500 mg EPA + DHA daily for most adults to reach an ~8 % index; higher doses (2‑3 g) may be reasonable for high‑risk groups such as APOE4 carriers or those with a strong family history of Alzheimer’s. Harris notes the lack of RCTs for decades‑long outcomes like dementia, but observational studies (e.g., Framingham) show a ~50 % lower Alzheimer’s risk in the highest Omega‑3 quartile (~6.5‑7 % index). The interview also touches on the misconception that omega‑6 is inherently harmful; higher blood linoleic acid is associated with better outcomes, and reducing omega‑6 intake can be counterproductive. Finally, Harris shares personal habits (≈1.5 g EPA/DHA daily, regular fish consumption, moderate calories, exercise) and mentions his Fatty Acid Research Institute (FARI) as a resource for further reading.
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But it sounds like you're pretty convinced that omega-3s are beneficial for heart health.
Unfortunately, nutrition normal doesn't necessarily mean optimal.
Have you seen a ceiling on benefits?
Do people who have high blood levels of omega-3 have any different health outcomes?
How these different fats are processed into what really is a universe unto itself.
Matrix of life as a human is a much more complicated thing. And so we need to follow all those people that you've convinced to go on this sardine diet, and we can do some studies on it.
Sign my emails now, and PGP for professional guinea pig. All right, everybody, I'm back with another exciting conversation and I want to frame this one up with— I have been really astonished by how fascinated people are on this broad topic that is encapsulated in the idea of omega-3 and omega-6 fats, everything from sardine diets, seed oils, to just best forms of omega-3 for your brain. So I decided to get a world expert here to talk with me, Professor William Harris. If you don't know him already, he's a leading expert on omega-3 fatty acids and omega-6s. Particularly as relates to cardiovascular disease and neurological health. His resume is extensive. I'm not going to go through all of it, but it includes publishing hundreds of peer-reviewed papers, developing the widely used Omega-3 Index. And in this two-part conversation, we're going to cover all things omega-3 and omega-6s. So with that, I'm just going to jump into it. Professor Harris, welcome.
Thank you, Nick. Great to be here.
Well, I want to start with some information that people might know, but to get everybody up to speed, can you review for us What are these omega-3 and omega-6 fatty acids and why are they important to human physiology?
Great question. So omega-6 and omega-3, these are our fatty acids. Fatty acids are parts of fats and oils that we eat every day in our diets. Butter, vegetable oil, you know, beef tallow, whatever. Those are all fundamentally fatty acids. The omega part has to do with, from a chemical point of view, the omega-6 and omega-3 fatty acids have multiple double bonds in the most saturated fatty acids have just chemically single bonds, no double bonds. I'm gonna assume I'm not gonna explain what double bonds are, but we'll leave it at that. Chemically they're double bonds because they're called polyunsaturated. And when you have unsaturation, you have double bonds in molecules. The omega-3s are family fatty acids that have the first double bond 3 positions from the end. From the, what we call the omega carbon, not the alpha carbon, which is the front end. The back end is the caboose, is the omega carbon. And the omega-3s all have the first double bond there. Omega-6s have their first double bond 6 positions in. We can't, mammals cannot convert one to the other, so they're separate families. You have to consume them in your diet because we can't make them and they're essential fatty acids. Omega-3 fatty acids are typically we call There's 3 of them: ALA, which comes from plants, and EPA and DHA, which come from seafood primarily. On the omega-6 side, the ones— there's 2 that we care about. One's linoleic acid, which is a— is by far the predominant omega-6 fatty acid in our diets and in our, in our bodies, in our tissues. And arachidonic acid, which is a longer chain version of, of linoleic acid that's very bioactive as well. So the, again, the omega-3s are primarily from fish, the omega-6s are primarily from seed oils, vegetable oils, and they're very interesting. You're right, that's all over the place these days.
It's a great summary. I think one thing people often overlook, and I certainly did early on in my, my medical education, is the profound consequence of, you know, we're talking about these like chemical structures and it can go over people's heads like, okay, where— why does it matter where a double bond is? But it doesn't just impact the, like, let's say, physical properties of, say, how closely you can pack fats, but how these different fats are processed into what really is a universe unto itself of signaling molecules. So these things just aren't fuel. They can be turned into like a potent suite of hormones and how they do so depends on what fatty acids you're intaking and interactions with the host, which is why someone like you can build a whole career on it because it truly is an area of nutritional physiology where I feel like we have barely even seen the tip of the iceberg.
Yeah, yeah. You make a good point. It does seem like, you know, who cares where this double bond is? Well, your body cares a lot because the shapes of molecules are determined by the bonds that are in the molecules and that the shapes are what fit into receptors. And as you say, signaling molecules, these are of course things that come from outside of cells and tell cells what to do. And if there's nobody home, if the cells can't hear the signal, they're not gonna do what they're supposed to do. And the shape of these fatty acids and the hormones that are made from them are very important for, human physiology.
Well, we'll get into a lot of specifics in a bit, but I, I wanna remain high level for a moment. And your expertise are omega fats and cardiovascular and neuropsychological health. So to start with the cardiovascular health, I was interested, there's my understanding, discrepancies in the literature and some people pointing towards certain short-term trials and, and saying omega-3s don't have benefits for cardiovascular health. What do you think of that?
I think it's almost a category error in the sense that when— just to back up, there are omega-3 drugs, which is kind of crazy because omega-3s are nutrients. But some pharmaceutical companies have purified them and jammed a whole bunch of them into one capsule and give them to lower— primarily to lower blood triglyceride levels, which is a medical treatment. And they do that. They lower triglyceride levels. So they're treated as drugs by some pharmaceutical companies. The reason the pharmaceutical companies want to make it into a drug is that they can get reimbursed for the being prescribed these products. You can't get— a doctor can't get, or rather the insurance company doesn't get reimbursed for dietary supplements, which are also omega-3 products encapsulated. But they do for drugs. So there have been drug trials, and in order to get approval as a, as a drug, you have to do studies, of course. And some of these studies, um, over the last 10, 15 years have been what we'll call neutral, have not been— have not shown an effect. Omega-3 and reducing cardiovascular events, whereas 25, 30 years ago, studies, very similar studies, were showing great benefit in reducing risk for heart disease. So what happened? Partly what happened is medical science advances and treatments, treatments for heart disease advance. And people's— when they tip nowadays, when you have a heart attack, you usually get to the hospital quick and they usually reopen the blood vessels to feed your heart blood right away. And that never used to happen in the '90s. So the heart attacks were more severe in those days. And patients who got into studies, people who survived a heart attack and now we're going to do a study of Can fish oil prevent a second heart attack? For example, they— the omega-3s were very beneficial because these people's hearts were more damaged and the omega-3s had a bigger impact. Nowadays, hearts are not so damaged. We have statin drugs, we have blood pressure drugs, we have all kinds of blood thinning drugs that can— that people are on now. And when you do a study nowadays and you give omega-3 on top of all those other drugs, and you only do it for maybe 4 or 5 years and you pick people who are in their mid-60s to do the study and you then expect this fairly small, typically small doses of omega-3 with one exception, small, you know, 1-ish grams of omega-3 to be beneficial and prevent heart attacks in that context, it's very difficult to show it. And then so the doctor— doctors will say, oh well, that study, Study X didn't show any benefit of omega-3, therefore omega-3s don't do anything. That's a huge mistake because omega-3s are not intended to be drugs. They're intended to be nutrients that we take over our lifetime. And in that context, omega-3s are very effective in terms of reducing risk for lots of diseases. But it's very hard to show in the standard drug medical model of a short-term randomized controlled placebo trial. And now I mentioned an example of a— there is one recent study that gave 4 grams a day of EPA only, one of the two omega-3s. And it was very effective in reducing risk, partly because of very high dose, a higher dose, highest dose has ever been tested. So that's probably why that was helpful. But in, in general, I think the, the fact that these are nutrients, not drugs, they shouldn't be tested like drugs, and our assessment of whether they're beneficial or not should not be dependent on a randomized placebo-controlled trial in old sick people.
Also because of the limitations of just like the studies you can do. My favorite example is always Alzheimer's disease because I think we can speculate about like what nutritional interventions might be beneficial for Alzheimer's disease, then people are like, well, show me the double-blind RCT. Well, first of all, you can't blind diet. Second of all, you're never going to do like the 20 to 30-year study power for outcome. So it makes it difficult to make, you know, these strong claims based on nutrients for preventing what are decades-long diseases. But it sounds like you're pretty convinced that omega-3s now just focusing on the heart and then we'll get to the brain, are beneficial for heart health?
I'm convinced. Yeah, absolutely. We've done studies. What we primarily focus on nowadays is studies where we measure blood levels of omega-3 fatty acids in people. We don't necessarily do dietary frequent food frequency questionnaires or tell me what you ate yesterday studies where people can't remember what they ate. Even for lunch today, you know, never mind yesterday or last week. So we'd measure blood levels of omega-3 fatty acids, which is a much better marker of how much omega-3 you're eating.
Yeah, you can't—
and then we asked the question, okay, over time, do people who have high blood levels of omega-3 compared to those who have low have any different health outcomes? I mean, most cardiovascular disease is one of them, but the thing we've studied most recently is, is death from any cause, just death.
Probably very easy. Before we get into the outcomes, I just want to define for people what you're actually measuring. So, there's an omega-3 index and omega-6 to 3 ratio, I think, are the two big buckets. Can you distinguish what those are for us?
Sure. Yeah. The omega-3 index is a blood test that we came up with about 20 years ago. That's the amount of EPA and DHA in red blood cell membranes. So we isolate red blood cells from the, from the blood. Of course, the omega-3s and the omega-6s live their lives, do their stuff in membranes as a part of a membrane. And membranes are far more complicated than we need. That's where the action is. So we measure the amount of EPA and DHA in cell membranes. It's expressed as a percent of the total fat fatty acids in the membrane. So somewhere between 3% and 12% is kind of the, the range of possibilities for how much EPA and DHA is in a red cell. That's the omega-3 index. It's, it's red blood cell focused and it's EPA and DHA focused specifically.
People are going to ask like, what are the range targets? And they're going to want to know how they measure. So I'll just say for you, you do have a company that we're not here to plug, but you can get your omega-3 index measured, all that via OmegaQuant. I'll put the link below. That aside, what are target levels for this index that you think people should be trying to hit?
Yeah, let's start with what we think is normal. Well, normal, unfortunately, in nutrition, normal doesn't necessarily mean optimal. Normal omega-3 index levels in the US, for example, are around 5.5%. We've seen low levels of omega-3 in vegans, for example, are down around 3.5%. Which we think is pretty low. The optimal levels are over 8%. And that we see in populations like Japan where the fish intake is very common and they have very high omega-3 levels and they coincidentally don't have much heart disease at all and they live about 4 years longer than Americans do. I can't necessarily attribute all that to omega-3, but their omega-3 index, 8, 9% is kind of above that. 8 to 12 is what we think is a sweet spot., for omega-3 index.
Is that because there are harms above 12, or it's just really hard to get above 12? Another way to put that is, have you seen a ceiling on benefits that either plateau or you see a dip?
No. Well, we, we don't say it's 8 to 12 because above 12 is harmful. We don't know that. There are so few people on this planet that have omega-3 index over 12 that we really can't study it. We can't really study the question. If you had a whole whole bunch of people who had an omega-3 index of 15 and another group that had an omega-3 index of 10, and you had 1,000 people in each group, and you could follow them over time, then you could ask— answer the question, does having a 15 serve you better or worse than a 10? It's just a fog bank out there really beyond 12 because we really just don't know. We don't— there is a little bit of evidence from Japan that Even within Japan, people with higher, higher levels than the 8% seem to have reduced risk for heart attacks. But that's the only place you'd ever be able to do a study like that. Well, we don't see harm up there. I mean, we've known people that are up in the 10, 12, 15% and we don't see any harm there.
Yeah, I might be able to source you some more. As I'll tease in our second discussion, I got my levels measured via OmegaQuant and they came back around 16. And I know, you know, I tell people to do this, but as soon as I do something, people are gonna wanna replicate it. So there's a bunch of people doing sardine dieting and it's not just me, it's actually like a whole thing now. Anyway, we'll get into crazy diet fads later, but there might be a, a natural experimental opportunity. We'll just leave it at that.
Yeah, good, good. And so you need to follow all those people that you've, that you've convinced to go on this sardine diet and we can do some studies on it.
No, I know. Sign my emails now, MP PhD. PGP for Professional Guinea Pig. So, if you ever want to buy off these samples or anything, I'm your guy. But, that aside, we think it's a good omega-6 to 3 ratio. So, omega-3 index, percent of EPA and DHA in red blood cells, omega-6 to 3 ratio.
Kind of tell. Right. And, that has been another way of looking at omega-3 status or omega status, I guess you would say. Basically takes, as it says, it's the ratio of all the omega-6 fatty acids divided by the sum of all the omega-3 fatty acids. It's an idea that grew up in the '80s that this was meaningful and we could go into why, but I think there are many reasons not to attend to that particular ratio. First of all, we— it's completely unclear which fatty acids go— I mean, if you're measuring blood, there are at least 4 omega-3 fatty acids and there are at least 7 omega-6 fatty acids. And which ones you put in those ratios make a difference, and they never tell you which ones are in the ratio. Number 2, it presumes that all the omega-6 fatty acids have the same physiologic effects. As each other and all the omega-3s are equivalent, which is not true on both ends. There's some omega-6s that are beneficial, some that are linked with adverse outcomes. With omega-3s, the plant omega-3 level is not predictive of much in terms of health, but the EPA and DHA are. So if you just say omega-3 and you don't say which omega-3s, you've got a problem.
I think this is really, really important for people to understand because based on having my finger on the pulse of what people are talking about in the omega fat realm, the omega-6:3 ratio is what gets bandied about the most as like the marker to track. And as you pointed out, well, one, there's a problem with— there's a lot of like opacity with respect to that, what is really the numerator and what's really the denominator. And also you can get, I think, some pretty misleading outcomes. So, you know, Yeah. And one thing I found very interesting is I was reading some of your work and work of colleagues looking at omega-6 levels in the blood, but also in tissue, including like fat tissue. So like stored in the body. Now the common narrative, and I'll be honest, my understanding was I predicted higher omega-6 would be worse for you because higher omega-6 to 3 ratio associates with worse outcomes. And what you tend to see, and you can correct me if I'm wrong, but what I was finding when I looked at the data is there was this apparent paradox where higher omega-6 levels and a higher, higher omega-6 levels tended to correlate with better outcomes, but a lower omega-6 to 3 ratio did. And what seems to explain that at a high level, and I realize we're lumping here a bit, is that both can be beneficial, but if omega-3 are more beneficial, say for cardiovascular outcomes, that the whole omega-6 to omega-3 ratio is going to be driven by the denominator, the omega-3, and you're going to end up with this skewed perception and potentially— and this is what I see happening— people saying try to drop your omega-6 as low as you can in your diet, like straight up avoid walnuts because it will increase your ratio and that's bad reaction.
That's exactly the problem. By and large, the omega-6 omega-3 ratio is driven by your omega-3 level. Now, you— as the omega-3 goes up, the ratio goes down. And if you want to fix a bad omega-6, omega-3 ratio, take EPA and DHA. That will do it. That will improve a ratio. But I, I, I think you pointed— I mean, there's a recent paper I think you're thinking about where a higher level of omega-6 linoleic acid was beneficial, higher level of omega-3 EPA, DHA was beneficial, Yeah, but you do the ratio and it's, it's adverse, it goes the other way. So it's so confusing, you don't know what to do. And the idea of reducing your omega-6 intake in order to help your ratio is going to hurt your body because there's lower levels of omega-6 have consistently been associated with higher risk for death, higher risk for heart disease, higher risk for diabetes. So don't lower your omega-6 intake.
I'm going to show a graph of omega-6 to 3 ratio and outcomes. And what you'll see as the omega-6 to 3 ratio goes down, outcomes improve. Now I'm going to show another graph, which is a 3D bar graph. And on two of the axes are omega-6 and omega-3 independently. And what you're going to see in this graph, which is basically the same data, just looking at it a little bit more finely, is as omega-3 levels improve,, then outcomes improve. As omega-6 levels also go up, outcomes improve, and they compound. And this seems paradoxical, but understanding the distinction is huge because what it's saying is exactly what we just said. It's not that omega-6 are bad per se, it's that omega-3 are more good. So if you just look at the ratio, you end up with a misleading picture when in fact the benefits probably compound. So, you know, like a meal of like walnuts for a snack, let's say raw walnuts so they're not oxidized or anything, and salmon is going to be better than just the salmon alone if you're translating into real-world outcomes or situation.
Yeah. Right. Another problem is simply you can have a high level of omega-3 and a high level of omega-6 and have exactly the same ratio as if you have a low omega-6 and low omega-3. So, the ratio doesn't tell you anything about what to do. Many organizations now are saying ignore the ratio. That's not the way to look at it. Look at your actual blood levels of omega-3. That's where the problem is. We're low in omega-3. Don't worry about the omega-6s.
I would tend to agree with one caveat, and, and that is, do you feel people can overconsume, like, processed industrialized vegetable oils and seed oils? We'll get into this more, but do you think that can be overconsumed?
Well, in principle, I suppose anything could be overconsumed. That's true. And the whole seed oil thing is a complicated story as I'm sure we'll get into. But I think I'm not advocating that people take tablespoons of corn oil or soybean oil per se. I'm saying that this effort to reduce omega-6 I think is what's harmful. Let's just not worry about the omega-6s. Don't spend your time worrying about them. Recognize that there's good data that higher levels, blood levels of linoleic acid, the primary omega-6 in our diet and our blood, are— have been strongly linked to beneficial outcomes. Leave that aside. That's great. And anti-inflammatory for that matter. But recognize that in America, our problem is the lack of EPA and DHA. You raise that, get that one focused. That's why the Omega-3 Index focuses only on EPA and DHA. That's the problem.
Yeah. So simple focus on the Omega-3 Index. Don't worry about your linoleic acid intake per se, although I will promise we will parse seed oils versus like omega-6 linoleic acid because they are distinct. But from a practical point of view, what general dietary advice would you recommend for optimizing omega fatty acid balance? Like, if people aren't going to get their levels measured, what should they be targeting in terms of intake, either from whole foods and/or supplementation?
Yeah, I think a, a good target intake for EPA and DHA, particularly in America, is somewhere in the 1000 to 1500 milligrams a day. That would be a— so 1, 1.5 grams of EPA, DHA, not, not of fish oil. That can be achieved with fish, and I'm sure you're doing that with a sardine diet completely. But most people will use supplements to get that level. Then that should give you roughly about an 8% omega-3 index. Everybody's different, need to test yourself, but that would be the target. You don't need to go 2, 3, 4, 7 grams a day of EPA/DHA. That's completely unphysiologic. I don't think any population's really ever eaten that level of omega-3, except maybe some Eskimos.
And now, I'm going to add in another layer. And this is going to sound esoteric, but I know there are a lot of people very interested. Can you imagine subpopulations who would benefit from those higher levels, say 4 grams? In particular, I'm thinking about, say, people with— at high risk for Alzheimer's, APOE4 carriers or homozygotes. I happen to know I'm at high risk on APOE4 homozygote. And I've looked at some of the literature and shows, for example, that my brain has higher turnover of DHA. Maybe there are other conditions, but do you think if people who are particularly concerned about, say, Alzheimer's risk, family history, there could be benefits to higher doses than 1.5 grams EPA?
I completely agree. I completely agree. Most people don't know their ApoE genotype. I'm sure— good to know you do. I'm sorry to hear it's a homozygous for— it is what it is, right?
Yeah.
No one can change that.
Knowing that it works, it gives me the power to act. And there's a lot of evidence.
That's right.
I'm quite optimistic.
Yes, right, right. So I agree. Yeah, higher doses, probably twice what I was talking about would be— if I, if I was in your boat, I would do the same thing. I'd take 2 or 3 grams a day of EPA/DHA. We haven't got randomized trial evidence to prove that, but there's a lot of circumstantial evidence that supports it, and it's safe and probably helpful for a variety of other things too.
Before we end this first part of the conversation, I want to— we kind of touched on cardiovascular disease. We haven't really gotten into outcome data with respect to neuropsychological health broadly. So we alluded to dementia, Alzheimer's. But can you give us a picture of what the data say for omega-3 and brain health, be that mental health and/or neurological health?
Again, the kinds of studies we do where we look at blood levels of omega-3 in populations and then look to see who gets what diseases. When we look at the question of dementia, specifically Alzheimer's disease, dementia. We find that people who are at the highest levels of the omega-3 index have— in one study we did with the Framingham research group, we found that about 50% lower risk for developing Alzheimer's disease if you had highest— the highest levels of omega-3.
You remember what that number was, that threshold? Kind of, it's usually broken up into like quartiles or something.
It's in quartile. Yeah, in Framingham, the particular cohort that I'm sure you're well familiar with since you're in Boston, in that cohort, the, you know, people are not supplementing, it's all dietary. So the highest quintile or the 20th percentile is somewhere 6.5%, 7%. So it's not over 8% on average. Right. So even with that compared to reference. Even with that.
50% reduction. So, 50% reduction is very achievable with pretty mild supplementation if we're assuming the supplementation translating into a change in blood levels is possible.
And it does. Yeah. It always does. I think to be fair, we have to say the people that are having higher omega-3 levels without supplementation who are doing it fundamentally with fish.
Yeah.
They're eating a lot of other good things in fish. Yeah, I mean, there's great quality protein, uh, as you know, there's selenium, important minerals in, in fish, iodine is in fish, uh, things that— vitamin D is in fish, uh, we can— oily fish, all those are good in oily fish. And so we can't with ironclad certainty say it's the omega-3s because a high omega-3 level in a person who's not really taking supplements, uh, probably means more fish intake. And so it may just be a a surrogate marker of fish intake and the fish is really what's doing the job. I mean, we have to be careful that we don't jump too far into cause and effect when we can't do these trials.
But I also want to emphasize— so I think my audience is pretty scientifically literate and they understand this idea that correlation doesn't equal causation and there can be confounders. But I think there's another layer of nuance that I really want to pull out. We touched on it earlier, which is that when you're trying to figure out what you should do and how you should act as a person in life, you need to know what data you can actually collect to make that determination. And as we mentioned, there are certain— like, we can't do randomized controlled trials for 30 years for Alzheimer's. So then it comes down to what data do you have? And what I like to think is, well, you know, what are the associations and what is the biological plausibility? The preclinical models, all that, do they come together and tell a story? And then I guess the key thing, if there's a correlation, what's the size? And also what's the risk of intervention? So for example, for some drugs, you know, you might see a tiny little benefit and then you have to weigh it off against cons. What I'm seeing here, the way I think through this, is even if I don't have the 30-year RCT showing fish oil prevents Alzheimer's disease, what do I know? A large effect size correlation, very solid biological plausibility, clear mechanistic evidence. And then what's the risk of, say, eating more fish or supplementing with fish oils? Basically nil with a lot of upside. So just in determining how I make these decisions, and, and, and probably you too, I wanted to add in that layer because I don't think it's fair to just say, you know, we don't have perfect causative evidence, therefore don't act.
Right. I, I completely agree with you. I, I think that's exactly the way to think about in this particular situation. Your risks, probably if there's any even a whisper of benefit and there's no risk, the risk-benefit ratio is favorable.
My last question or two for you is, um, people always love to know how the experts live, what they do. So do you have any— I'm just going to say broadly— health staples, non-negotiables in your life, omega-3 or otherwise, that you're willing to share?
It's not particularly exotic. I do take about 1,500 milligrams a day of EPA and DHA. I make sure I do that routinely. And I have an omega-3 index of around 10. And I've been there for a long time and hope to keep it that way. Try to eat fish a couple times a week. But otherwise, I just not overeat. My wife and I, when we go out, we always split a meal. It— total calorie intake is a big deal, and we try to keep that down. And so I don't really have any, you know, fancy or particularly clever health, at least dietary patterns that I stick to. I exercise, you know, maybe 5 times a week, try to stay active. I'll be 77 next month, so I'm happy with the way it's going and want to keep going that way. Yeah.
It's funny when we're talking about longevity, if you'll indulge me in a quick mini rant and then we'll get on to part 2 is I love dorking out about metabolism, potential impacts on healthspan, longevity, looking at the survival curves in mice done all sorts of interesting interventions. But you can set the human data. There's not really like a clear theme once you have a baseline level of metabolic health for what predicts longevity other than maybe social connection. I just wanna give the eye perspective point of view because I've been thinking a lot about it as a lot of longevity stuff's been coming out. And then, yeah, you know, you juxtapose that to like the human being living. You're talking about eating dinner with your wife. I recently did a, a piece of short form content about making a particular sandwich, which didn't appear particularly healthy for my girlfriend. This hot honey blueberry sandwich I'm about to make is a health hack. Bear with me while I explain, because this isn't going where you think. This is about like social connection and the neurobiological and hormonal systems that are being activated in my body by virtue of just interacting socially with someone, doing a nice thing that goes beyond obsessing over very little numbers here or there. Not to say that it's not important. I think we both think these things are important, but always take a step back and just say, "This is fun to learn about. It should be an exciting journey, but at the same time, not to get too obsessive." So, Dr.
Nick Norwitz. Yeah, yeah. Great advice. Great advice. There is even the little topic we're talking about here of omega-3, they're not a silver bullet by any means. The matrix of life as a human is a much more complicated thing. And, Your social networking is— you're right, that's a powerful predictor of longevity.
Well, before we get into part 2, I'm going to cut part 1 here. Is there anything or anywhere you want to direct people to learn more about you, the work you do, anything like that?
Sure. About 5 years ago, we started a thing called the Fatty Acid Research Institute, FARI, F-A-R-I, and we have a website. And the purpose of our institute really is to do the kind of research I've been talking about here using large-scale databases, long-term outcome in human populations. We really don't do any animal work. I just have a— I have a distrust of animal studies in the omega-3 space because it seems like investigators always feed them far more omega-3 than any human could ever eat. And then they draw a conclusion and I think, oh, wait a minute, Is that true in people too? And in any event, we study humans and we study important human diseases. And we can learn a lot about me at the Fatty Acid Research Institute, our website, and look at the About Us type tab. And all my publications are linked there.
We'll drop in the links below. With that, thank you so much, Professor Harris, and everybody should come back for part 2.
Great, thanks.










