how long would it take someone to change their omega-3 index like if they were if I had never consumed fatty fish I wasn't taking an omega-3 supplement nothing like that and I started today is it one of those things like you see a pretty quick increase or is it as you're mentioning is sort of a lagging indicator where it's like okay take it for three months then we have to kind of go back and retroactively measure but then also as far as a benefit is concerned like or risk like if someone were to have a
low Omas omega-3 profile or index and they had that for 3 months is that potentially equivalent to 3 months of smoking how does it equivalent or how is it equivalent in terms of a time scale um well to address your first question it takes I would say about three month like about three months is a good time range like let's say you're now deciding I'm going to increase my omega-3 intake through supplementation through um maybe increasing sources of you know High um EPA and DHA like fatty fish um wild Alaskan salmon you would you would
wait about 3 months again because it takes about that long for your red blood cells to turn over so you have to wait that long before you can get an omega-3 index test done and um you know the question is well omega-3 index why do you want it to be higher well I mentioned the smoking right when I say higher most of the studies are like 8% omega-3 index or more and when I say low omega-3 index most studies are 4% or lower um average omega-3 index in in the United States is about 4 to
5% so we're really low compared that to Japan they're like 10 or 11% omega-3 index the average Japanese person on average has a 5-year increased life expectancy compared to the average American now um Bill Harris has done some some research looking at um huge pop you know huge sample sizes looking at the omega-3 index and life expectancy and people that have the 8% omega-3 index or higher have a five-year increased life expectancy compared to people with the low omega-3 index so 4% now how long does it you know how much omega3 would it take to
go from 4% to 8% right after today's video I put a link down below for element electrolytes they are not sweetened with arol element electrolytes are 1,000 milligram sodium 200 milligrams pottassium and 60 milligrams magnesium but that link down below gets you a free sample variety pack with any purchase of element electroly so whether you purchase their sparkling whether you purchase their stick packs or whatever you get a free sample variety pack and that's exclusively using my link down below that is drink lnt.com Thomas Again drink element.com Thomas really interesting stuff they curb my appetite
entirely but I also have them in a fasted State and I sip on them during my fasted workouts because I feel like I actually get replenished but I also get my Cravings satisfied so that link is down below in the description um obviously there's individual variation there's a you know Omega-3s are a you know compound that we make in our bodies from Ala we also have to get ala from our diet to make them but we have a lot of Gene variations that regulate the way we metabolize it with that said on average it takes
people about two grams of Omega-3 a day to go from a 4% to an 8% and those Studies have been done um so whether or not your omega-3 index is low for 3 months and then you go up to you know from 4% 4% to 8% like we don't like we don't know what effect that has right like you're asking a very complicated question in terms of like you know time kinetics and um you know oh I was low omega-3 during development and through my early adult life but then I you know at some point
would then go to randomized control trials yeah and that's where go you know we still we also have data where it's like okay people that are at high risks for let's say myocardial inunction so heart attack or people that have existing um cardiovascular disease they're taking you know Pharmaceuticals like statins for example to treat it um a lot of Studies have have taken these populations of people that presumably um do not take omega-3 unfortunately studies don't often measure the omega-3 index at the start of a trial I wish they did but they don't um it
costs more money and there's that's like the agal problem with randomized control trials is not measuring measuring nutrient levels in a person before the trial starts I think it really it's it's one of my my my pet peeves because um you know we have different Gene variations that regulate the way our body metabolites nutrients right it's not like a drug you don't have to measure someone's Baseline levels of let's say a Statin that you're going to give them at the start of a trial because nobody has statens at the start of a trial but people
have different you know intakes of fish they have different genes that regulate how much let's say they take eat a lot of walnuts or flax seeds which are high in ALA um the plant omega-3 that makes them either convert it well or not well like you know there's there's reasons why we need to to measure these you know nutrients at the start of a trial anyways not done but we do know for example there's been um the reduced trial that was the big trial that was that looked at um people with existing cardiovascular disease and
it was a 5-year trial where people were given a high dose of purified EPA so it was just one of the Omega-3s and it was in an ethylester form which we can talk about it's not very bioavailable and um or a placebo in this case the placebo was mineral oil and there's all sorts of controversy over that being actually pharmacologically active and not being a great Placebo regardless um after the five years people taking the EPA it was called it's called phipa it's a pharmaceutical um prescriptive form of Omega 3 that people are given for
example with high triglycerides or with existing cardiovascular disease um those people had a 25% decrease in heart attack or de actually was death from heart attack and death from heart disease compared to Placebo so that was quite robust um and regardless of all the arguments well the placebo was you know maybe the placebo was actively harmful even if you just look at the Baseline risk reduction it was very significant so and it was reducing triglyceride you know there was effects independent of looking and comparing to placeo group that were like wow this is unbelievable it's
taking like you were saying it's taking this unhealthy group of people giving them simply just a form of Omega-3 over the course of several years and it's like dramatically lowering their risk of dying from a heart attack which is the number one killer in the United States so in in your opinion if DHA had have been in the mix too do you think it would have even been more profound this is a great question Thomas um so another trial was then underway and began um I don't remember what year it started but the trial um
get gave EPA and DHA to people with existing cardiovascular disease that were on a Statin and um the form of this omega-3 was in free fatty acid form which is never given to anyone ever um so free fatty acids so typically the fatty acids the Omega the DHA EPA are bound to a triglyceride backbone okay and that's the way our bodies are best at metabolizing it okay it's the most bioavailable um ethylester is um is essentially when people uh are purifying the omega-3 getting away Mercury or pcbs things are you know unfortunately found in fish
they they they um take it off the triglyceride and they bind it to an ethanol backbone and they run it through this column that purifies it and it's just Cheaper to Keep It In This ethyl you know Esther backbone form um we still our bodies can metabolize those they're just not as uh bioavailable as triglyceride so for example if you are taking an ethylester form of Omega-3 like all the prescription forms are laasa which is DHA n EPA or fipa both of those are are ethylester you absolutely must take it with food and preferably with
a higher fat meal to absorb it like you would not absorb much at all of ethylester form of Omega-3 on an empty stomach free fatty acids are not bound to anything and anybody that has a chemistry background um or even just scientists in general like knows like free fatty acids act like a detergent they're licing cells they're um it's kind of like a soap almost in a way so why um I think the reason why that was that form was chosen because it can be highly bioavailable but it can also be very irritating because you're
giving your gut this like free fatty acid sort of detergent kind of form of Omega-3 um so that trial was ended early because there was basically it was not shown to have a beneficial effect on you know any of the outcomes and and so people this made the headlin people go oh it must be the DHA because they added DHA to the mix and this one I personally don't think that's true there's lots of other data they weren't as big of Trials like some out of Japan that also showed that you know D a plus
EPA dramatically you know reduces cardiovascular disease risk and also um heart attack risk in fact if you look at the other big trial vital the vital study this was a big trial at a Jo Joan Manson's group that used um both omega-3 vitamin D th those either alone or in combination or Placebo um and if we just look at the omega-3 group those people um had about a 28% reduction in in um heart attack or risk so that was a secondary outcome so the primary outcome of a trial is like okay we're going to design
this trial we're going to power the trial to get a statistically significant result based on you know this outcome and the outcome they based it on was all cardiovascular events not just heart attack everything okay in that case there was no effect of Omega-3 on all statistically significant by the way effect um it did there was a trend yeah um it wasn't statistically significant in reducing every single cardiovascular event right but if you then just looked at in isolation heart attack risk it was almost 30% lower in the group that was taking the omega-3 which
included DHA and EPA versus placebo so again one of those things were headlines oh there's no effect you know that's the that's the headline omega3 has no effect on on the um on cardiovascular health because of the primary outcome it just there's so much new Nuance when it comes to these randomized controls definitely and like and correct me if I'm wrong but even like as far as the mitochondria is concerned there's a higher concentration of DHA than EPA is am I mistaken no um so you know that it's interesting I personally think that both DHA
and EPA are very important to get from Diet also I I take personally take supplements and I think I think supplements are a great way to increase your omega-3 index as well so you know these these omega-3 fatty acids are well known for their quote unquote anti-inflammatory effects and a lot of that um there's a lot of metabolites from DHA and EPA that are different there's resolvin these resolve inflammation and so you're not getting that inflammatory cycle there's the marison they do something similar there's the specialized prom mediating um mediators the spms and these are
all involved in resolving inflammation and lowering inflammation and they're sort of different from EP EPA and DHA a lot of these are coming from DHA uh EPA also directly affects inflammation so it's decreasing the production of prostaglandins which are inflammatory mediators lucrin for example so so EPA also has a very direct role in inflammation and that's kind of this anti-inflammatory role of Omega-3 um however as you mentioned you know DHA accumulates in mitochondria um these are the energy producing organel inside of ourselves very important for you know energy they're important for aging important for muscle
function performance cognition everything right um but DHA also accumulates it's also very very highly found in all of our cell membranes so we're talking about in our neurons you know in you you know in cells and our muscle and what DHA is doing in that role is different than its anti-inflammatory role it's um it it's regulating what's called cell membrane fluidity the way our cells are you know sort of malleable and um the stiffness of them the flexibility of them why is this important I mean it's important for many many reasons we could go hours
and hours talking about this and I won't I'll spare you but just generally speaking sort of Thousand Mile High sort of um overview of it it's it's important for Transporters and receptors that are embedded in that cell membrane that are transporting nutrients like magnesium into our cells or you know glucose into our cells they're important for receptors like for example on neurons talking about serotonin receptors dopamine receptors when you don't have enough DHA if if it's deficient and these a lot of Studies have been done in animal studies with this looking at deficiency of DHA
you're you're you're you're screwing up neurotransmission um dopamine serotonin neurotransmission because the receptor structure and function is changed because of that cell it's stiffer it's stiffer it's not the right you know it doesn't have the right flexibility and so it affects um so many physiological processes and then glucose transports affected so you're not getting enough glucose into an across the bloodb brain barrier because the Transporters and this has been shown in animal studies the glucose Transporters are completely disrupted when there's a DHA deficiency at least in rodents so um it's very important I think dhha
is very important for for that reason and as we as we get into maybe talking a little bit more about some of the sort of Novel and I would say less well studied part of omega3 which is in the muscle the cardiovascular I mean there's omega-3 is one of the most well-studied nutrients like of all time I mean like there's we know so much about it you know there's so many people that have researched it over over the decades but um I think there's a really important role for DHA and and I do think some
of this has gotten a little bit lost in the headline you know where it's like oh the EPA is so important the EPA is what reduced the heart attack you know Risk by you know 25% or the death from a heart attack I guess from by 25% in that big study the redu a trial yeah looking at it in practically an echo chamber I mean it's not like factoring in like when we look at I mean cardiovascular function we look at longevity in the first place like a lot of roads lead back to mitochondria in
the first place and read back lead back to that membrane fluidity and all these things we're talking about so maybe in isolation when you look at it like that you can say yes EPA is is powerful and is important but it just seems like we're missing this whole piece yeah it's great so so mitochondria have two membranes and dhas accumulates in both of those membranes and those membranes are essential for the health of our mitochondria for how they're producing energy um for how things are like 99% of all the proteins in the mitochondria are not
made in the mitochondria we have a we have our own mitochondrial genome we make some mitochondrial proteins but the majority of them have to be transported into the mitochondria through a whole transport active transport mechanism which requires a functional membrane and DHA is part of that and DHA highly does highly um accumulates in mitochondrial membranes and so you know there's been tons and tons of animal research which is more pre-clinical stuff looking at you know function of mitochondria what happens when you make a um an animal deficient in DHA it's you know messes up mitochondrial
function and you know mitochondria is very important for the way we age it's important for our brain function it's important to produce energy you know just steady state energy but also like during exercise right so there's a lot of reasons why DHA are very important and I think the main thing also is avoiding that deficiency or insufficiency so as I mentioned um you know one of the top six preventable causes of death there's other data out there showing that like it's like 99% of people people in the United States have inadequate omega-3 intake 99 it's
like it's so high and like 80% globally or something like that where you know we're not getting we're not people are not eating enough fish or they're not supplementing enough with omega-3 like whatever you know there's you know you can find reasons why people don't want to take fish they might be afraid of the Mercury they might be afraid of contaminants but I'll tell you this like there was a huge push like decades ago by OBGYNs for pregnant women to avoid fish because of the contamination in the Mercury and I think that had just Rippling
effects negative Rippling effects you know because omega-3 is so important for brain development DHA is so important for brain development and women were just not eating fish and they weren't supplementing so they were essentially not getting much omega-3 in their diet um there's now been several studies that have come out that have found that the developing fetus um which is probably the most sensitive to Mercury toxicity actually benefits even more and the omega-3 is protective against the Mercury toxicity um in fact there's B there's been studies looking at development so um I think it was
like one year you know cing to development at one year and seven years or something like that where they do like they look at cognitive development over time of the child and they looked at the mother's omega-3 um status and they also looked at a biomarker which was Mercury the higher the mother's Mercury was the more intelligent or the the higher their child scored on intelligent tests now does that mean Mercury is increasing intelligence no Mercury was biomarking omega-3 and fish intake right so clearly the Mercury wasn't harming intelligence at all because you know it
was it was higher in the the mothers that had children with higher intelligent quo scores and stuff like that so wow right that's I mean it's it's like we've I've seen over the last like five years three years really like online this like I'm going to call it weird like a weird resistance to Omega-3s I'm not sure where it's coming from I'm not I've always kind of been in your Camp I've always been pretty high high dose relatively speaking two to three grams per day and especially when I was much lower carb then I would
probably go even higher just naturally just based on what I was consuming and it's been interesting to see I I don't know where it's coming from and every time I talk about it there's resistance from the heavy metal side there's this and that um I just I'm a little bit mind-boggled by it
