[EP.14] Why Omega 3 Accomplishes Longevity & Why Omega 6 isn’t the Almighty Devil?

Bill Harris_YT

Dr. Joel Rosen:
Hey guys, welcome back to another edition where I’m excited to announce our amazing guest Dr. Bill Harris as he’s been a leader and leading researcher in the omega-3 three fatty acid field for over 40 years. He has over 300 scientific papers on fatty acids and health, the vast majority on omega threes.

He has been on the faculty of three medical schools and has received five NIH grants to study omega threes. He was the co-author of three h A statements on fatty acid and heart health as the CO inventor of the Omega three index, which we’ll be getting into, and the Omega three blood tests and founder of mega quant analytics, Dr. Harris has been ranked among the top 2% of scientists worldwide based on the impact that he’s had with his research. Dr. Bill, thank you so much for being here today.

Dr. Bill Harris:
Great to be here. Yes.

Dr. Joel Rosen:
So I always like to do some research so that I can ask intelligent questions before we get here. I know that initially in the 70s, you were asked to study dietary fat and its effects on cholesterol. At that time, we knew that animal fats raised cholesterol, or at least now we know triglycerides and vegetable oils lowered cholesterol or triglycerides. But as you mentioned there we weren’t sure why. So potentially over the 40 years, I guess that’s a good starting point to know where we started from and where we are now. You know.

Dr. Bill Harris:
And so do we know why liquid oils, lower cholesterol, and saturated fats raise cholesterol? I think we know better. I think we know now that you’re changing membrane fatty acid composition with the different fats that we’re eating. and a high saturated fat diet does change the the way that the liver and liver cells process or remove LDL cholesterol LDL particles from the blood that’s of course, that’s the way statins work they upregulate the LDL receptors and remove more LDL from the blood.

And if you’re getting more saturated fat versus polyunsaturated fat, those LDL receptors are not as efficient at moving LDL out of circulation. So LDL levels go up. That’s kind of shorthand of what we know now but there is a physical selling biochemical reason for why different fats have different effects on cholesterol outs.

Dr. Joel Rosen:
Okay, great. So So then as far as springing forward from that we know so much about the Omega threes and the longevity studies and why they’re so important for human health. Maybe we can get into that.

Dr. Bill Harris:
Sure. Yeah. We’ve been interested in, of course, Omega Three for a lot of time. And until now, I don’t know maybe 10 or 15 years ago, nobody looked at total mortality or effects. They’ve looked and looked at people with cardiovascular disease and the effects of Omega three on those people typically lower the risk for cardiovascular events, which should translate into a longer lifespan.

You have fewer events. More recently we’ve been part of a group called Force fo RCE, which stands for Fatty Acid Outcomes Research Consortium, it’s a group that started at Tufts University in Boston. And it’s a collaboration of multiple individuals who have access to different research cohorts like the Framingham cohort, or like epic, or Mesa, or Eric, are these acronyms that we throw around the most people don’t know, but they’re fundamentally groups of people that have volunteered to be in a lifetime study.

You know, like in Framingham, they took like 4000 people out of the town of Framingham, Massachusetts, in the 1940s, when they started, and they did every test known to man in on these people, they’re all healthy people, you know, middle-aged people. And then they just followed him for years and looked for the relationship between some something, they measured either a sum, they developed the term risk factor, the Framingham group, there’s nobody used that term before.

And nobody knew it that nobody knew that smoking was related to a high risk for cancer or heart disease, they didn’t know high blood pressure was they didn’t know high cholesterol. So that’s how they discovered these risk factors. And so they’re like Framingham, there are cohorts like that all around the world. And so we have a collaboration with many of those cohorts, and the ones that have measured fatty acids in the blood and the ones we work together.

And we found when we asked the question, of all these cohorts and several, several 1000 people together, is there a relationship between the blood Omega three-level and your risk for dying over time? And of course, you know, the window, the average window of time between blood drawing and when we stopped following up on people, it’s like 16 years, 1316 years, something like that.

So it’s a, you know if you study Omega three levels and 10-year-olds, and ask, what’s the mortality in the next 10 years, you’re not going to find anything because nobody’s gonna die. You’ve got to study people toward the end of life, if you’re gonna look about look at prolonging life. We found that the higher the Omega three level, the lower the risk for death from not just total mortality, which was everything all in, but for cardiovascular disease, for cancer, and for non-cardiovascular, noncancer, whatever else is in that bucket, the whole thing.

So omega three, high omega three was associated with just a generalized slowing of the aging process. And we had been part of a study some years ago, where they looked at omega-three levels and how they predicted the rate of telomere shrinkage. And that was another study where we found that people who had the highest Omega three levels had the slowest rate of change over time in their telomeres, which is an anti-aging outcome.

And then the final one would be, look, just look at what we call ecological studies, or studies of this country versus that country, or this culture in that culture. And you look at Japan, which is a very high omega-three intake country, they also have, what a surprise, one of the longest lifespans on the planet, about four years longer than Americans on average. So we think we’re so great. Well, you know, so that’s, that’s also kind of a consistent story with the high omega three length with longer outcomes, longer excuse me lifespans,

Dr. Joel Rosen:
right. So mentioning risk risk factors, and the studies and the longevity studies that you’ve done. And have pretty clear consensus data that higher levels are correlated with longevity yet any any speculation as to when the FDA or whoever deems a risk factor variable to be a risk factor that omega three will become one as it isn’t at this time?

Dr. Bill Harris:
Yeah, that’s a great question. I’m not sure I’ll live to see it. I’d love to live longer than I would otherwise, because I’m taking all my omega threes might not be long enough, you know. So yeah, it’s not the FDA that determines that it would be medical societies. So like, a joint consensus conference by the American Heart Association and the American College of Cardiology, for example, that those guys get together periodically, and say, Hey, here’s a here’s a new risk factor. Let’s have a consensus conference on it and let’s make a decision and then advise our community that this is important. So that’s The way it would happen, that someone would have to bang on the door loud enough to get their attention. And the Omega three I mean, it’s, I know we’ve got 45 minutes here, but you

Dr. Joel Rosen:
no longer if we need it. Okay. Right, right.

Dr. Bill Harris:
I mean, it’s complicated because there have been many randomized trials with Omega three, many successful, but not, not a few that have been neutral, no, no benefit. And they’re, of course, they’re the when these studies are done, they’re done with the drug model in mind, you know, take people in their mid-60s, give them either a placebo, or give them Omega three, just like you’ve given them a placebo, or you give them a statin, and then wait 234 years and see if you’ve had any effect on heart disease rates.

Well, sometimes that doesn’t work with Omega three, and I would not expect it to work with Omega three, but the medical, because it’s on the Omega three benefits of life’s lifetime thing. It’s not a start when you’re already old and sick and on a bunch of drugs and trying to turn that battleship around with the nutrient.

They didn’t want it to happen. And so I’m not surprised, but the medical community doesn’t think that way. They think if you do what studies like that, and you don’t get an effective Omega three then Omega threes don’t work. And that’s the message that goes out to the community. They don’t work without any caveats without an A Yeah, but they don’t work. Well. They do work if you test them in the right way.

But nobody’s going to do a 40-year randomized trial, with a placebo and Omega Three to prove that they do have these effects. You can’t do it. So anyway, that’s because of that mindset in the cardiology community, particularly, most of them dismiss Omega three, as irrelevant. So back to your point about when are we going to get this test approved by the cardiovascular community? It’s gonna be a while because they have this idea that they don’t work.

Dr. Joel Rosen:
Right, gotcha. Yeah, thanks for sharing your insight on that. So as far as the mega Quan company and the company you founded, maybe tell us about exactly what an Omega quant test is? How would differ from an Omega three test that is being done through a different company, I know both tests aren’t necessarily created equal. So it’s a two-part question. No.

Dr. Bill Harris:
This raises yet another reason why testing is going to be hard to get into routine medical tests because there are different ways to do it. Right? There’s only one way to measure your serum cholesterol. Now, it is several things in the plasma or serum. With Omega three, you can measure fatty acids and all kinds of places in the blood, you can measure them in red blood cells, which is what we like to do because it’s a representative cell. But most clinical laboratories are and don’t think about red blood cells, they think about everything being measured in the serum or plasma.

And so all the methodologies are set up for that type that approach and, and so it’ll make it quant our laboratory, we, we measure whole blood Omega three levels, we measure red blood cell, we measure we can measure Plasma, we can do all that, and we do for different customers.

But our flagship test, we think is called the Omega three index, which is EPA plus DHA, the sum of those two in red blood cell membranes, we can get that number from either a direct red blood cell assay, which would be a blood sample would have to come in a tube. So we could isolate the red cells. Or we can do it from a dried blood spot, which is much more convenient, of course, to stay dried spot on a piece of paper. And so we get the Omega three index, that test we created, we developed, invented whatever you want to call it 20 years ago. Next year is our anniversary.

And we came up with it based on a lot of good scientific evidence at the time. And we proposed then back in 2004, that an Omega three index over 8% is the target value. That’s that’s what you want to go for. And that’ll make it three levels are not just a marker of how much fish you eat. They’re, in fact as much of a risk factor. As cholesterol is more than it’s a better risk factor, a better predictor of adverse outcomes. The lower it is. It goes the other way high.

Omega three is good. Low cholesterol is good, right? So yeah, it’s kind of like HDL cholesterol in that sense, the higher the better. So the Omega three index game was created, then we started the laboratory and around 2009. And now we’ve been just doing our thing and providing assays we, as you mentioned, there’s different ways of expressing it. And there are some labs, I think it’s Quest that does a plasma phospholipid Omega three level.

So that’s what they’re doing and that is different than the red blood cell, it gets a different number. The numbers are fair, I mean, the metrics are fairly highly correlated. So you can put on a graph the red blood cell level, and the plasma phospholipid level and make a nice line. So you can infer one from the other with an equation.

And we do that a lot to make sense of numbers that are not the red blood cell per se. So it gets confusing to be another lab, I believe it’s Boston, Boston Heart does whole plasma Omega three-level, some people. And to add to the confusion, if I might, we present our data as a percent of total fatty acids, Some labs will present their values as a concentration in like micromoles per mil, or micrograms per milliliter, things like that. When the numbers are completely hooey to me, You have no idea what one means relative to the other. So that’s part of the problem.

Again, by moving this thing into the clinic and making it a standardized test, we have to get everybody in the community together on one metric. And we’re that’s what we’re going to report. And then the doctors would know, we have one standard reference range, one target, healthy value, and then we can move forward. But unfortunately, it’s it’s more complicated. Yeah,

Dr. Joel Rosen:
thank you for sharing. And so I mean, you’re comparing apples, oranges, grapes, rains, when you have different units. But I’ve also heard you say that it’s a lot more noisier when you’re looking at plasma. So what is that extra noise bail wet that on top of those challenges that you’re getting these other information going on as well?

Dr. Bill Harris:
Yeah, yeah, exactly. Um, plasma eight levels of Omega three are noisier, they vary more day to day, it’s very much I mean, I’m sure your audience is very familiar with this serum glucose versus or plasma glucose versus hemoglobin a one c value was a monitoring glycemic status in patients.

And of course, hemoglobin eight, one C is a much, a much longer term more stable, and less noisy marker. That’s exactly what the Omega three index is a red blood cell. It’s measured also in like hemoglobin is measured in red cells. And it’s a long-term marker plasma, you know, if you have a high omega three meal last night, your tomorrow’s, your plasma level is going to be much higher.

And it’s going to misrepresent to the clinician what your general status is because it’s an aberration. You take big loads of fish oil pills, three hours before you go to have your blood drawn, your doctor is and you’re going to have a higher plasma level than you’d normally do. And we’ll look like you great, you know, but we look at the red cells, they tell a different story. So we prefer patient care. The most important thing for patient care is that you always use the same lab. I mean, I would love to say everybody needs to use Omega Quant it did not happen.

We’re not a big international conglomerate of laboratory stuff. So I know people are going to get omega-three testing in different different ways in different labs. And if you don’t want to be confused, just use the same metric all the time. And if you want to change your diet and you start taking supplements, you should watch that metric improve, it should improve. You know, and I’m thankful that anybody’s even caring to manage anything about Omega three in the blood. You know, there was 20 years ago, nobody gives a hoot, nobody. Now, even the big boys are starting to offer it. I don’t know how many doctors use it. But that I think is a step in the right direction and acknowledging the importance of Omega three in the blood panel.

Dr. Joel Rosen:
Yeah, no doubt. And I mean, the Omega Quan is so, so versatile. I mean, first, it’s affordable. And secondly, it can be sent all over which is great because it’s just a it’s a bloodspot. But you you mentioned before there’s a huge difference between taking it and then a huge difference between assimilating it, utilizing it, and having a subsequent increase in your percentage which we suggest that An RPC level should be a percent or higher. I guess there’s a lot of ways we can go.

And I know research is still getting into that. But, if you’re doing a plasma or serum level, it’s not indicating it’s giving you a better idea that there may be a lot more challenges going on. If you were to compare that to an A mega quant and see that the numbers are, are telling a different story, that it isn’t being utilized and getting into the red blood cell and being an elevating and increasing you’re, I guess, chances for longevity and reduction of inflammation, long-winded commentary, I guess, what would be some of the reasons if you would bill on why not all, not all people utilize and build up their Omega three levels, compared to everyone that does it? What are some of the differences in variations here?

Dr. Bill Harris:
Well, one is certainly going to be I guess, we’re going to assume the same intake, right? Not Omega three is going in the mouth? What explains the differences in blood levels and the differences in response to supplementation? So there are two different questions, right? Differences in chronic blood levels, just based on your standard diet are going to be more complicated than Why would there be a difference in Person A versus Person B taking 1000 milligrams a day? Right?

And, well, one thing is, what do you take the Omega threes with what kind of food or if you take Omega three, certain kinds of Omega three products, take them on an empty stomach, you’re not gonna get much absorption. Other forms are the triglyceride form, or five phospholipid form even if you take it on an empty stomach, it’s going to absorb pretty well. But the ethyl Ester form, which is the drug, the drug form, of Omega three, does not absorb well without other fat around it to stimulate the lipases and other pancreatic and biliary secretions to help digest fat and absorb fat. So it’s always best to take omega threes or whatever form it is, with with food.

And there’s almost always some fat in the food. So it’s, you don’t have to do this, you need dry toast and orange juice, there’s not much fat there, okay, but a standard meal, take the fish oil with that for best absorption. So that’s that’s one variability, one variance. But then you get into some of the few studies that looked like maybe your intake of choline might also affect how well you absorb or incorporate Omega-3 three into phospholipids. That’s, that needs to be developed further to be understood. Well, there are certainly some interactions with Omega three.

I mean, I’m jumping over to dementia at the moment here. However, there have been studies that have shown that for people who take Omega three with B vitamins or have good B vitamin status, the level of Omega three for them, does correlate with their risk for dementia. But if you got lousy beat B, vitamin status, the omega threes don’t relate. So there’s some interaction going on with B vitamins and Omega three that’s favorable? That’s not really, to your question.

And that’s not changing your blood levels, where your response is, and I think we don’t have too many good ideas, or good data to compare different responses in different people, partly because you need to do it in a lot of people. And you’d have to look at their genetic makeup. And you have to be sure they’re taking the stuff because noncompliance can screw that up in a minute. You know, people say they’re taking or they’re not. You know, they’re, of course, some products are probably poorly absorbed, because of an enteric coating kind of thing. And you got to know how much Omega Three you’re taking. You can’t just look at the front of the bottle and see 1000 milligrams and think you’re getting 1000 milligrams of EPA and DHA because you’re not. Hi, I

Dr. Joel Rosen:
hope you’re getting a lot of value from our podcast today. I know I had an excellent time interviewing Dr. Bill Harris, and the entire Omega quant information that he provided for us. If you’re frustrated that you’re not getting any information about your health challenges your blood tests are normal and you’re looking to do this test. I highly suggest it whether it’s the complete profile or just the basic profile. He’s been kind enough to give us a discount link if you click on the link below and use the discount code Dr. Joel, it will save you about 5% Something small but I still encourage you to do it. So now back to the interview. Right?

Oh, good, oh, good examples. But I think the importance is to have a baseline. People who are listening to this are typically taking, their health into their own hands. A good reason for a mega quant is because a lot of the people that I do work with personally hear about it, my blood tests are normal and nothing’s wrong with me, I feel awful. But when you have a baseline of an Omega quant that’s less than eight, or it’s in the threes or fours.

And you know that there’s some form of inflammatory cascade going on, and use yourself as a study of one and retest and see how that’s going. You know, I showed you the the genomic pyramid that we did before we began in that fatty acids section, they do have biosynthesis and utilization and pemt is one of those enzymes, but there are other CYP enzymes and other enzymes that are used for absorption and flow. And so that could that’s where I was thinking that could be helpful as well. You know, if that makes sense, right,

Dr. Bill Harris:
right. I mean, if you gotta if you’re looking at levels of anything in the blood, you got to consider the rate into the blood and the rate out of the blood. All right. And so some of those enzymes we were talking about earlier, are the synthetic side, on the synthesis of Omega three, the talk about the breakdown of or the use of the Omega threes throughout the body and what enzymes are, or genes produce enzymes are affected, that might affect that cascade, I think there’s a ton of work to be done. on just that very question. What are the genetic determinants of the Omega three-level? Right?

Dr. Joel Rosen:
Yeah. And where are the bees fit? And I mean, people just reduce Utley says I have MTHFR. And I can’t convert folic into folate, or methyl folate. What I explained to them is, that that’s a small income to the major expenses of histamine production, and other types of stressors, and that uses up the supply of that little income as well.

So now you’re getting very dynamic, but keeping it back to your test. As far as the complete go. So you have a basic profile, where you can look at just the Omega three index, and ideally looking to get it above 8%. I guess, before we move on to what’s on the complete test, maybe give us a little idea about the calculator, I think that a great tool that you guys have is the Omega three calculator. So let’s say you get that test result back here in the 5% range, and you have an Omega three calculator, where does that fit in? Yeah, so

Dr. Bill Harris:
, I’m glad you brought the calculator up. We did a paper with a gal named Rachel Walker at Penn State some years ago. We asked the question, how much Omega three dozen do you need to go from a 4% to 8% Omega three index, and we did it with a bunch of data that we had collected.

And we produced a calculator that is on our website now. And what you do is you put in your, your current Omega three index value, and then it’s sort of it’s it’s set the equation button, the background is set to tell you how much more omega three you need to take to go from your value update percent.

And for your example, 5%, you need roughly 1000 milligrams on average. I mean, that’s, again, coming from an equation from 1100 people, it’s a good place to start. Aim for 1000 additional grams of heat and milligrams of EPA and DHA per day and over three to four months, you should see an increase of up to 8%. And I think that’s a nice feature. But they’re always the caveat, and you’ve brought it up earlier, the response is different for different people.

So that’s why you would have to test and retest and see if you are the product you’re using your lifestyle and your jeans and your food and are you smoking I’m sure most people are not smoking who are doing this, but smoking lowers Omega three levels in the blood. So you have to take all that into account and test and retest.

Dr. Joel Rosen:
Right and not all you’ve talked about earlier not all Omega three sources are created equal. We have the triglyceride ethyl ester and the phospholipid. Maybe just touch upon that a little bit Bill because a lot of people ask the question what’s the best form or what why do I burp and get a fishy smell or why do I refrigerate it? What maybe we can get into that a little bit? Yeah,

Dr. Bill Harris:
so the forms the classic form is triglyceride, which is a standard fish oil. There is an ethyl Ester which is chemically produced or I mean biochemically produced from triglycerides. Everything starts with oil from fish. All the products do, I guess except crude Loyle which starts from krill, which is a little crustacean that’s at the base of the food chain. But the fish oils, it’s the crude fish oils from Peru where they usually come from anchovies sardines, they, the companies will take those then they will concentrate the Omega threes meaning they will remove another non-omega three fatty acids, throw them away, keep the Omega threes and keep concentrating and for different kept by different chemical processes. And one way to concentrate is just to make an ethyl ester. Instead of a glycerol Ester, which is triglycerides.

And the ethyl esters as I mentioned, they’re more concentrated per pill, typically, more molecules of EPA and DHA, but you have to be sure you’re taken with them to make them be absorbed. There are things called restructured triglycerides, reduce terrified triglycerides, where you prefer to start with the raw oil, cut off all the fatty acids from the glycerol backbone and triglyceride, throw away the non-omega threes, and then keep all the Omega threes and then re-esterified back to a glycerol backbone.

And again, now you’re back to triglyceride. It’s not exactly a natural triglyceride because they don’t exist like this in nature with all three fatty acids being omega threes on our triglycerides, usually, it’s one out of three, that’s the fatty acid Omega three. So anyway, it’s a good absorption form, the triglycerides are phosphor lipids which we get typically from krill oil, which is lower in the concentration of Omega three, but absorption is good. It’s it’s, it’s a good form.

And it’s kind of an expensive form. It’s it’s hard to hard to get right or to make. But it’s still a very effective form and learning rate for using Omega three levels. And there are a bunch of others that are coming out there as algebra, Algebra oils are primarily for vegans, and vegetarians, who don’t want any animal products, and those are fine. That’s an that’s a triglyceride-based oil. It just comes from originally from algae and I’m not talking seaweed, I’m talking about micro you know, single-celled algae that naturally make EPA naturally make DHA. They’ve been discovered by scientists and harvested and concentrated to produce oils that way. And I think you didn’t ask this. But that’s kind of what I think the future of Omega three supplements is going to be more and more. Well, we’re going to get into God go

Dr. Joel Rosen:
yeah, we can get into that right now. segue, because

Dr. Bill Harris:
there, the goal is, for many people, to have a land-based plant, like soybeans, like corn, corn is not being used. But that idea of something you can grow from the ground that will produce EPA and DHA and the oil. And they’ve done this and limited levels. And researchers around the world are still working on this. But they’ve had transplant genes into these into the seed crops, the seed oil crops, that will convert Omega six to Omega three, and then we’ll make EPA and DHA in the oil.

And so they can essentially there’s no you don’t have to kill any fish anymore. To make EPA DHA, they’re these molecules are very, very difficult to make chemically. Just like starting from raw materials in a chemistry factory. You can’t make them like drugs, many drugs are made, you know, but chemically synthesized from nothing up. Can’t do that for omega three, it’s just much too expensive. So we’ve got to have nature make them and then we isolate them and concentrate them. And I think I think we’re going to see over the next 1020 years, more and more profit-based if we can get past the GMO craziness. My opinion, right, yeah, that’s the paint. Everything is GMO is bad. Right, right. I mean, let’s think about this for a minute. So I think that one of the best uses of GMO technology is to increase omega-three, production so we don’t have to harvest fish to get it.

Dr. Joel Rosen:
Right. Right. Which, which I think opens the door, though, as far as a lot of people and you said before we began just battling the whole Omega six is bad. blanket statement, and I guess the skeptics would think, okay, GMO aside, how am I going to get the good without getting the bad? I guess that would be sort of the question or maybe we can start to tackle linoleic acid or omega sixes and the good is bad that you in your research of over 40 years have can distill down for us. Yeah, yeah,

Dr. Bill Harris:
I’ve, it seems like there is this idea that if you’re a fan of Omega three, you have to be, you have to hate Omega six, that you have to have a black hat and a white hat. And it’s just got to be that simple. Because the Omega sixes and omega threes compete for different pathways, yada, yada, yada.

And we eat a lot of linoleic acid and essential, it’s an essential fatty acid, everybody knows that. People are at one end, I think it’s poisoned. I think it’s good for you. I mean, the evidence we have from blood level. There are a lot of studies like this, though, we’re, we’ve published already, as part of this force research group, two studies, one looked at blood levels of linoleic acid 18 to omega six.

And then we looked at the risk of developing heart disease. And in another study, we looked at the risk of developing diabetes. And we found that maybe somewhat to someone’s surprise, the higher the level of linoleic acid, the lower the risk of developing heart disease or diabetes, so those aren’t the only diseases on the planet, God knows. But for those two major ones, higher linoleic acid levels predict better outcomes.

And I’ll just tell you, right now, we’re working on another paper, looking at omega six in a very large cohort, the UK Biobank, and we are seeing the same thing the higher the linoleic acid level, the lower the risk for death, from cardiovascular from cancer from everything else. It’s just so clear. So the folks that are squawking about Omega Little Lake acid being somehow poisoned.

They need to address those findings they need to what what I see people do is just to go, oh, this is just epidemiology. Wow. Come on. It’s life and death. I mean, we’re talking about human beings and do they live. Do they die? Do they get sick or not? And you gotta tell me why. high omega six in the plasma predicts better at Highland or lake predicts better outcomes. Tell me why that’s a poison. Right? You can’t just brush it off. You’ve got to address the issue if you’re gonna be scientific. And

Dr. Joel Rosen:
that’s, that’s the thing if you’re gonna be scientific about it. That’s right. And so as far as was there a difference between the form of the Omega six pill or was it was that

Dr. Bill Harris:
yeah, so arachidonic acids, the other one we typically measure in the blood. If we think about plasma levels, about 75% of the Omega six, family in plasma is linoleic acid. Of what’s left 75% of that is arachidonic acid. So those are the two big ones, but the little leg is much bigger. And what we’re seeing for the cardiovascular outcomes and diabetic outcomes, is there was no relationship between arachidonic acid levels and either of those outcomes, developing diabetes or developing heart disease.

So no signal there that Hi arachidonic I mean, that’s that is the if there’s a poster child, that’s it’s got a skull and crossbones across it, it’s, it’s arachidonic acid. But we haven’t seen any effect there. Now, I will say in this new analysis, we’re looking at total mortality, there are some outcomes, particularly the other causes of death were a high level of what we’ll call non-linoleic acid Omega six, we don’t know in this particular dataset, we don’t have the granularity.

We don’t know arachidonic acid levels per se, but we know the non la Omega six, which is mostly arachidonic we know and so for total deaths and non-cardiovascular noncancer outcomes, there’s a higher risk for death with higher levels of that non non la and six so I think that’s, that’s interesting, and it’s, it just tells you how nuanced you got to be.

And what it says to me It screams to me that people who want to lump all Omega sixes into one pot, and say they’re all the same thing are way off, that the evidence does not support that view. You got to be more careful and you got to talk about specific fatty acids. And some of them you can control some of them are dietary little leg is and to some extent arachidonic is we eat it anyway, but not very much. But the other Omega sixes are all metabolic. Fundamentally, they’re produced in the body from those But those precursors, and so to some extent are kind of hard to manipulate through changes in your ratios of some of the odd Omega sixes. So there’s a lot to learn here. And I think we don’t do a disservice to the field by just hanging all of them with a with a, a, they’re bad. All Omega sixes are bad.

Dr. Joel Rosen:
Right?

Dr. Bill Harris:
Maybe something to this the concern about, about seed oils, and diseases, you know, I hear people make that make that argument. And I’m not saying that’s not true. I haven’t studied it that well, I seed oil question, right? But to link it to linoleic acid, that’s wrong. Right?

Dr. Joel Rosen:
And also to not to necessarily have those ratios and I’ve, you know, that’s a good sort of next conversation is the complete test looks at the six to the three, which can be or can’t be useful information. But do not know, I mean, all things being equal the recommendation from a mega Kwan is to get those threes up, no matter what. The thing I was thinking about, though, before is that those other non-L A omega sixes are metabolic, I always look at it as if the pump is already primed.

And is that person already having smoke coming out of the chimney? if you will? Are they already having a problem with combining the food they eat with the air they breathe to produce ATP, CO2, and water? And typically, if that’s the case, then you’re already gonna have those Plinko chips going down the inflammatory pathways already? Anyways, if that makes sense. Does that make sense? Yeah,

Dr. Bill Harris:
yeah. I mean, it could be like, you’re you’re not sure what a Plinko chip is, though, you know, so do you remember the?

Dr. Joel Rosen:
I don’t know, he probably didn’t watch prices, right? So there was a game where they had to get into the $1,000. And it would go down the different ways, right? So based on inflammatory enzymes, up regulations and down regulations, they go down the wrong pathways and go down the Omega six and local trains and the prostaglandins and so forth. So, right.

Dr. Bill Harris:
I think to me, I mean, you’re kind of hinting around the Omega six Omega three ratio. Right, which we do provide in our complete analysis. Right. Right. So because people want it, you know, and we’ve got the data, so we give it to him, right? Am I a fan of it? No, you know, but I don’t call the shots of America. You know, just because I don’t like it doesn’t mean the whole world can’t see it, you know, right? So the problem with it is the number one thing I just mentioned, it’s assuming all Omega sixes are bad. Right?

And all omega threes are good. Yeah. Just very black, and white. Don’t think about it, look at a ratio. That’s a problem number two with that ratio, I think it’s not very actionable, because it leads people to think, Oh, well, I can fix my ratio by just eating less Omega six and not increasing my omega three, well, that’s not going to help at all, that’s gonna hurt twice, because you’re not increasing Omega three, and lowering your omega six is probably going to hurt you in the long run. So that would fix the ratio, the right way to fix the ratio is to increase your EPA DHA.

And that you can do based on the Omega three index, you learn that, and that will improve your ratio. But I don’t I may have another problem with the ratio you can have high levels of both EPA Omega three and Omega Six or low levels of Omega three and Omega Six and the same ratio. Right? So mathematically, it doesn’t make

Dr. Joel Rosen:
the sense that those studies ever do it going back to the ones that you were talking about, did they ever look at that high or low ratio are those ratios of six to three to see,

Dr. Bill Harris:
some of the ones we did, we did not in the forest group, but we’ve done it with a couple of with Women’s Health Initiative and with Framingham. And the omega, the Omega six Omega three ratio is driven by the Omega threes, or omega-six is quite pretty steady in the blood, and doesn’t vary very much between people but omega threes do and so that ratio is driven by so what the story that the low Omega three tells us the same is that high omega six Omega three ratio because the Omega threes driving the ratio.

Dr. Joel Rosen:
Right, gotcha. Yeah, I mean, I think the were that pervasive of the Omega six is the the oils that are that are hydrogenated or processed and high temperature used when you get a food that has a very high omega six Omega three ratio. I think that translates to the layman’s mind wanting to see what it looks like in the blood as well.

Dr. Bill Harris:
That’s it’s a great point because I think We labor under the illusion that what we eat all the fatty acids when saturated fats, monounsaturated fats, them all the Omega six, determine your blood pressure and fatty acid or your tissue fatty acid profile. And it isn’t that simple. You can’t control that much. I mean, your body has been designed to have so many checks and balances.

And you know, like, for example, the red blood cell, when it’s made in the bone marrow, it takes fatty acids from the blood and picks the ones that want and puts them in that membrane. So the membrane will have the properties it needs to, you know, squeeze through the capillaries and all that. You don’t you’re not in control. I mean, at one level, we do provide a complete report of all your fatty acids in the whole blood fatty acid profile. And it’s there we have the data, some people like to see it.

My question is, how actionable is it? From a physician’s point of view? Particularly, you know, what do you what are you going to do with, here’s some fatty acid that comprises, say, 1% of the total. And, you know, you’re in the 90th percentile or the 10th percentile, and we get phone calls from people saying, What do I do to fix that? I don’t know, you can’t do anything to fix that. It’s what it is. So I think there can be too much information. And I’m, you know I’m talking like a scientist, not a business business person.

But you know, that’s the way it is. Some people love that complete profile, and we’re happy to give it to him. And some people dig deeply into those fatty acids and try to make changes in their lifestyle, and you know, God bless them. That’s fine. Right? We just don’t know if it’s gonna work. That’s all right.

Dr. Joel Rosen:
No, it’s, you’re right, I think there’s a Goldilocks zone of too much and too little information, I do have a couple of friend practitioners who liked building the complete profile, because they’re looking at the saturated fatty acid component of it and trying to extrapolate the the membrane integrity, but then they also use the genomics that I was showing you earlier. But it’s good enough for a good area to start to talk about what’s your insight?

Or what could you tell the listener that more likely than not, is going to have some problems with listening to hearing about Omega six aren’t as bad as they originally put them in the category that they thought and heard about? But furthermore, on the other side of the switch, they’ve said that saturated fats are the only source of fats that I want. I guess, with the Omega Quan and all the studies that you’ve done, what would you be your insight on? Notwithstanding everything we’ve talked about before boosting up your Omega three ratio and having an above 8%? Where do saturated fats come in on this? Yeah,

Dr. Bill Harris:
well, it almost gets counterintuitive, because one of the ways there are two ways to raise your, saturated fat levels the primary saturated fat, is a fatty acid in the blood, and the membranes are palmitic acids and 16 carbon, with no double bonds. And the thing is, you can get that into your blood in two different ways.

One, you can eat it in saturated meat, you know, solid fats, butter, yada, yada, Crisco, or you can make it that’s not essential fatty acids, your body will make it from protein or carbohydrate. One way to raise levels of palmitic acid is to lower your fat intake and raise your carbohydrate intake, our high-carb diet will cause the liver to make more palmitic acid and put it out there. So when we’ve seen high palmitic acid levels, it’s like well, is it because you’re eating a lot of it, or because you’re on a high-carb diet, and you’re making a lot of it? And it’s, it’s a seesaw.

And it’s a little hard to counsel people on what to do about that. If they know they’re going out of their way to eat a really sad low-carb diet, which would be a low-carb diet typically a high-fat diet. And that may lower your levels of saturated fat. Because you’re not synthesizing as much,

Dr. Joel Rosen:
right? Yeah. Should be lower. Not higher. Yeah.

Dr. Bill Harris:
Hi. So Hi, Paul. Medic levels are one of the predictors of diabetes for example, right hallmarks are one of the whatever the word is predictors. Yeah. Right moving that, you know, do you do that by eating a high-fat diet or a low-fat diet? Wow. can go either way.

Dr. Joel Rosen:
Do you see their omega threes being low with those types of cohorts or

Dr. Bill Harris:
independent omega threes or not? Not even though it’s a percent of total fatty acids, and some people get a little wacky about, oh, my God is the if I change that one over there and raise it, then that’s going to lower the Omega three. Well, it doesn’t work that way in biology. If there is a, a, a seesaw, in any fatty acids, it’s all in the polyunsaturated.

The year when we looked at studies where people’s Omega three levels went way up because they took supplements, and what happened was their Omega 6 went down, but their saturates and monounsaturated stayed the same, unaffected. So there is a switching off of percent. percent, one goes up percent and the other one goes down. But it’s Omega six Omega three, that’s what switching naturally, because you make mistakes, no matter if you’re competing for different for the same spot on a membrane. saturates and models are not competing with those spots. Right. So anyway,

Dr. Joel Rosen:
it gets it gets complicated, but you know, it’s interesting. Yeah, yeah. I think that as far as the back to the original, will it ever be a risk factor? I think there are a lot of sacred cows in LDL is bad. HDL is good. And cholesterol is the overarching number that we need to look at. I think some doctors come out and say they’re not looking at cholesterol markers per se, in Ireland of its own, but they’re looking at triglycerides to HDL markers, or we’re looking at the small density particles and so forth. I guess the question would be Bill, how would that change around the recommendations or the inferences that you would have from the Omega quant?

Dr. Bill Harris:
Unrelated? I mean, I, you know, if you’re looking those are lipid lipid protein majors, right? I’m talking about TG HDL ratios, and LDL particle size ALP levels, right? Omega threes don’t well, to the extent that a fairly high dose of Omega three will lower your triglycerides, which it will, right, that will change your triglyceride ratio, right to the extent that that’s a predictor of metabolic syndrome, right should improve, right, mega threes aren’t going to do much for LDL cholesterol, right?

Values, particle numbers, or otherwise, they don’t play much in that in that sandbox. They otherwise, you know, unrelated to cholesterol, there’s a whole bunch of other things that affect risk. Reward, right? I mean, right? The last example is aspirin, you know, take a baby aspirin, you’ll reduce your risk for heart attacks doesn’t lower your cholesterol. All right, ladies in a different field.

Dr. Joel Rosen:
Right. And that pay there’s a play because of the controversy, or at least what I’ve been studying, and I said, I’d like to know a lot more than I know now to ask you better questions is that the polyunsaturated fatty acids are a lot more combustible. And I believe it from an oxidative standpoint versus oxidizable. Yeah, oxidizable Sorry.

And so if your pump is already primed as I said, and you’re not combining the food, you eat in the air, you breathe, and you have these free radicals that you’re in this excessive state of reduction for and there’s all these ancient hydrogen bonds are looking for oxidants to get reduced. That can cause again, the shifting of those arachidonic acid pathways and so forth. I guess if there’s a question in there, where do you think the science is going?

I know you know, I remember reading on your website about the palmitic acid and higher reflection of carbohydrate intake, but there’s still yet more information to be gleaned from the way that all the Saudi saturated fatty acids play together. I guess, if there is a question in there, where do you think the science is going towards and how can your test be helpful in in seeing some of these patterns? Yeah,

Dr. Bill Harris:
it’s a good question. Yeah, and I’ll just jump back to the polyunsaturated being susceptible to oxidation, right? applies even more omega three. Because there are more double bonds in a given omega-three fatty acid, no, four, five, and six double bonds are supposed to recognize it with its four and little leg with its two.

Dr. Joel Rosen:
So it’s more it’s just for the person listening. It’s more oxidizable with more oxygen,

Dr. Bill Harris:
more bonds you have right? In a test tube, and a testing unit test tube, right, you’re more likely to the fatty acids going to break down due to oxygen, we call it per

Dr. Joel Rosen:
oxidation, oxidation, right?

Dr. Bill Harris:
So but the yet the Omega threes are good,

Dr. Joel Rosen:
but Right, the longevity studies and

Dr. Bill Harris:
there are a lot of antioxidant systems in the body that protect these things. Right. And so to take what happens in a test tube With the hype of high levels of double bonds polyunsaturated are more oxidizable. Therefore, Bab is right. Wait a minute. No, you can’t do that. It’s simple-minded thinking. But Becky, I think your question is what there’s more information in fatty acid profiles than we know

Dr. Joel Rosen:
that’s right, right? Yeah. Thank you for getting that out of my question. Thank

Dr. Bill Harris:
you. But yeah, so and I think that’s true. I think there’s, it’s like a fingerprint. Golly, 10 years ago, we did a study in the Framingham group we looked at, we looked at all the fatty acids in the red blood cell and asked which ones are predictive of who’s going to have a cardiovascular event or not. And we just told the computer.

So we had, we had the full fatty acid profile of, you know, 4000 people, and we knew who had developed heart disease in-app, you know, sometime, after we’ve measured their fatty acid levels. And we said, the computer hears, it’s almost like machine learning or AI, you know, that kind of thing. Tell us what fatty acid is most linked most highly correlated with a reduced risk for heart disease. And the first fatty acid picked was linoleic acid. Course, higher levels, better outcomes.

Okay. So then we told the computer, okay, put that aside. Now, of all the other fatty acids, which one is next most associated with beneficial outcomes? And we picked another one, and we did that 10 times over. So we get 10, fatty acids that together predict that as a fingerprint. And so some of them are high levels, good. Some of them are high levels bad, you know, but just knowing what the fingerprint is. So we published that, and that was a lot of fun. So now we’re taking that same idea. Oh, we just got two NIH grants to study this. These are called Small Business Innovation Research grants.

Dr. Joel Rosen:
There’s me, I’m so sorry. Yes. Go ahead.

Dr. Bill Harris:
So we just got two grants, one of them is to develop a red blood cell-based profile fingerprint that would predict the risk of developing diabetes. So you get basically, is there more information in that blood fatty acid pattern than we realize? Can we dig deeper, and then we have the say, another grant that’s doing the same idea, but looking for risk for dementia, Alzheimer’s disease, and dementia?

Because these are two profiles that we theoretically if we find something that’s predictive, instead of just one fatty acid, maybe they’re seven, right? That’s Sing Sing a song together, one of them’s not singing. If we find that, then we have we have a new product or our small business. That’s why the government likes to fund these things to stimulate new ideas in small businesses. So that’s cool. So yeah, we’ll see how that goes. Next. That’s

Dr. Joel Rosen:
what machine learning the being able to find that fingerprint. Yeah,

Dr. Bill Harris:
that’s yeah, that’s the cool name for it. Right. People biostatisticians have been doing this for years anyway, with the right multivariate analysis and things, but now it’s got a cool name, machine learning AI

Dr. Joel Rosen:
and right. Multivariate learning, though. That’s right. That’s great. That’s great. I like I like the complete test. But at the same time, the, the, like you said, the, the basic profile of looking at your Omega three index, which is a percentage of omega threes to your whole blood, right, based on your RBC, which correlates, what 9890 99%, right, and be able to test it over time, and be able to use a calculator. At the end of the day, there’s no refuting the fact that these studies are showing that omega threes that have more double bonds that are easily or potentially in a test tube more oxidizable extend your lifespan. So,

Dr. Bill Harris:
so much for the idea that just because it’s highly oxidizable it’s gonna be bad for you.

Dr. Joel Rosen:
Yeah, I mean, if you have, the thing is, it’s like saying, you know, you have a barn that has dry wood and if there’s a fire on the left side of the building, that right side is more burnable. Right? I mean, at the end of the day, if you have more inflammation in your body, and you know, the pumps already primed, then that’s the problem, I think so

Dr. Bill Harris:
then oxidized the ability of a fatty acid is a whole different thing than inflammation. Those are different questions completely. You’re buying the inflammatory response to typically a pathogen, you know, some foreign object that is mounting a response to that’s immune-based. I mean, it’s the mixture of the inflammatory system and the immune system. It’s right by complicated you thought fattier. super complicated. Oh my god. Yeah, I’d be,

Dr. Joel Rosen:
I’ve started to put my toe on that rabbit hole a little bit in terms of how exactly those cytokines and the inflammatory immune response, communicate back and forth with, the entire fatty acid profile as well, you

Dr. Bill Harris:
know, I it’s it’s a crazy complex mix and it’s we haven’t talked about the resolvins protections. The quick Yeah,

Dr. Joel Rosen:
let’s talk about that. So I was gonna ask you thank you for what is your feeling of that, is it? Can you should you take that? Or what are protections and resolvins? And I know you don’t like this specify that s PMS the names but uh, as far as Yeah, yeah.

Dr. Bill Harris:
So these are sometimes called PMS or specialized proinflammatory resulting molecules. They’re made from omega threes primary, some are made from arachidonic acid. And they’re good, healthy.

And another one of the reasons why Omega Six should not be considered bad. But primarily these protection resolvins are made from Omega three, EPA, and DHA. They are supposed to be a little controversial these days, but they’re supposed to actively suppress or rather reverse an inflammatory response that’s appropriately been initiated by some system but needs to be shut down after a while. And that’s what the resolvers do they resolve inflammation.

And that’s good if you haven’t got the Omega threes around, and there’s nothing to make the resolvins from. And so you don’t make them and so you’re Musa nice story. And so, your inflammation persists longer than it otherwise would have. Right? Part of the there’s its omega threes are anti-inflammatory at the front end they can slow the inflammatory response at the beginning, and they can accelerate the resolution of that response.

So those are good now whether you should take and some companies are selling SPM, or what I call the pro-inflammatory, or rather inflammation resolving molecules. IRM is what I’d call the whatever, whatever. I like that. Yeah. So you know, and they’ll sell a pill that’s got some of these and it’s got a lot of EPA DHA in it too. But there are some of these ESP PMS there.

To me, I mean, they’re like 100 of them, you know, and you pick two, you pick three, to put into your pill, or that just happened to be in the fish oil that you’re using, and you just decide to identify it. I prefer to let the body make the molecules it needs in each cell type each cell type is going to be a different molecule at once. Give it the precursors, give it the EPA and DHA, give it the food to do the work well, and then let your body make the molecules that are as much cheaper. I mean, there’s no, I haven’t I haven’t seen clinical evidence that it makes a difference.

Dr. Joel Rosen:
So no, it’s good. I want to show you when we’re done here some of the pathways that I look at so it connects that thought in terms of Furthermore, those SPMs are those resolving mediators, they can inhibit platelet aggregation as well if I’m correct, but I believe that the platelet aggregation can be I guess, backdoor stimulated through uncoupling of nitric oxide or too much of a histamine response or these inflammatory mediators that end up pulling on the platelets weak link of the chain right so that’s where some of those connections end up coming together.

But I agree with you at the end of the day you’re taking a finger prick analysis, just black and white Where are you we see studies show that keep it simple and maybe we’ve lost you along the way here but caviar percentage of red blood cells from a mega US EPA and DHA be at least 8%

And if you’re not getting that then go out of your way to get that and foods I guess we can talk about that before we go here but what am I mean what’s nice about your company is you give a detailed explanation of the different foods both plant-based and I guess there’s not really I guess the algae now base but where you can be getting just you don’t have to get it all in supplements, but you can go out of your way to get it from foods. What do we what are they typically looking at?

Dr. Bill Harris:
Yes, obviously. So we do have a table report that lists a bunch of seafood from the highest EPA and DHA per serving to the lowest and of course there some some fish that are quite popular. They have almost no Omega Three in them. Tilapia is the one that leaps to mind. Tastes like doesn’t taste like fish. Well, I wonder why. He’s like a chicken because you feed them like chickens anyway.

So, at the top of the list, we have what kind of acronym this kind of comes around to smash fish. So SMA sh if you’ve got sardines, or I like to start with salmon, anchovies, mackerel, herring, and anchovies, and maybe albacore tuna is in there somewhere to write macros. They’re the um, I think so those are oily fish. Those are the best sources and you can get all the Omega three you need just means you don’t have to take supplements. It can be done the diet just so it’s a rare American that will do that. Right?

Dr. Joel Rosen:
Yeah, no, that’s been awesome. I mean, I always learn on these on these shows that I say, selfishly, I just let everyone else listen in when I publish it, because it’s, it’s for my, for my benefit, I love I’d love to hear about the results of the new studies and the NIH grants that you got going forward and keep an open invitation.

One of the questions I always ask Bill of my guests is knowing kind of what you’ve known or learned over the research of 40 plus years and would have talked to the young, bright-eyed, and bushy-tailed Bill back in the day, what would you have told yourself, that would have helped slow your ad rate of aging? Or would have been good information for you?

Dr. Bill Harris:
Oh, what would I have done differently? I might have. I mean, I’ve been taking omega-three supplements for a long time, and trying to increase dog fish intake being from the Midwest now in South Dakota, but most of the time I was in Kansas, Missouri. And that’s where most of my original research was and not exactly a high fish-consuming area. And if it’s it is it’s you know, fried cat test, you know, or something like that.

Bass. So I would probably start taking omega-3 three earlier. I did do pretty well, though. Got my omega-three index around 10%. And I just tried to keep it there. And I take about 1400 milligrams of EPA DHA a day, encapsulated restructured triglyceride form, right? That’s it, that’s a good form. So you know, otherwise, I would have started exercising regularly earlier in my life. I didn’t have to quit smoking, so I’m good with that.

Anyway, it’s been a good run, I was blessed to be able to get into a research field that I had no idea where it was going. And to get on the Omega Three train early and be able to stay on it. And so getting more and more interesting all the time. So it’s been a fast, fast, and fun career.

Dr. Joel Rosen:
Yeah, and those are good and also just without you saying it is your continual flexing of the frontal lobe and, and the different parts of the brain and never losing that, lose it or use it or lose it mentality of, of keeping the brain and the neurons firing. So thank you so much for being here today. I enjoyed our conversation and look forward to maybe Part Two when you have some more juicy information to share with us

Dr. Bill Harris:
anytime Joel loved it, and I appreciate being on. Hi, thank

Dr. Joel Rosen:
you so much for watching our age-reversing blueprint podcast. If you’ve made it this far, we sincerely thank you for your attention and your interest in reversing your age. If you’re looking to get more information on today’s topic or other podcasts that we’ve had, be sure to check out the show notes and be sure to check out Dr. Joel rosen.com. Have an awesome day.

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