Latest / Hardiness with Dr Paul Taylor / All you need to know about omega 3 fatty acids, Part 1: Wisdom wednesdays

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All you need to know about omega 3 fatty acids, Part 1: Wisdom wednesdays · Hardiness with Dr Paul Taylor

• 0:05
  Speaker 1: Hey, everyone, welcome to another edition of Wisdom Wednesdays. So
• 0:11
  Speaker 1: this is going to be a two part series on
• 0:14
  Speaker 1: Amiga three fatty acids. So you may be taking one
• 0:18
  Speaker 1: right now, and particularly if you're health conscious and if
• 0:21
  Speaker 1: you are taking in a Mega three party acid. Maybe
• 0:23
  Speaker 1: you're doing it because of your brain health, maybe you're
• 0:26
  Speaker 1: doing it for your heart health, maybe you're doing it
• 0:28
  Speaker 1: because you've heard at santi inflammatory and it's good for
• 0:32
  Speaker 1: all of those things. But what we need to understand
• 0:35
  Speaker 1: is that depending on your goal, you might be taking
• 0:39
  Speaker 1: the wrong ratio of EPA to dita and it turns
• 0:43
  Speaker 1: out that there's a reasonable chance that your A mega
• 0:47
  Speaker 1: three supplement might be rancid before it even hits your gut. Now,
• 0:52
  Speaker 1: this two part series is designed to fix both of
• 0:55
  Speaker 1: those problems. So for part one, and we want to
• 0:58
  Speaker 1: talk about the impact on the so your body doesn't
• 1:01
  Speaker 1: see a meiga threes, it sees two very different molecules.
• 1:06
  Speaker 1: And the frustrating thing when you talk about amgia three,
• 1:09
  Speaker 1: thaty acids or a Mega three supplements is that everything
• 1:12
  Speaker 1: is just labeled A megia threes and that's as if
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  Speaker 1: EPA and DTA are the same molecule with the same job,
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  Speaker 1: and they're not not even close. So we need to
• 1:21
  Speaker 1: dig into the biology because it really does matter. Now DITA.
• 1:25
  Speaker 1: They're both pretty unpronounceable names, but DA is doco sehexionic acid,
• 1:31
  Speaker 1: and it's a structural compound. It's the most highly unsaturated
• 1:35
  Speaker 1: fatty acid in the human body, and it's what your
• 1:38
  Speaker 1: neural membranes in your brain and the retinal cells in
• 1:41
  Speaker 1: your eyes are literally built from. Now. The curled, flexible
• 1:45
  Speaker 1: shape of deita is actually a load burring structure. Your
• 1:51
  Speaker 1: brain and eyes depend on DTA being exactly that shape.
• 1:56
  Speaker 1: It is the fact that your nervous system is physically
• 1:59
  Speaker 1: construc structed from now. EPA ecosapenteonic acid is actually functional.
• 2:06
  Speaker 1: It works primarily at the level of your vasculature and
• 2:11
  Speaker 1: your immune system, and it competes with a rackodonic acid.
• 2:15
  Speaker 1: You may have heard of this. That's the Amiga six
• 2:18
  Speaker 1: arty acid that your body uses as the raw material
• 2:22
  Speaker 1: for what's called pro inflammatory ecosinoids, and it competes with
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  Speaker 1: Amiga six for the same enzymatic slots in the body.
• 2:32
  Speaker 1: So more EPA in your membranes means less a rachodonic
• 2:36
  Speaker 1: acid getting converted into the signaling molecules that drive inflammation.
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  Speaker 1: So we need some amiga sixes, we need some aracodonic acid,
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  Speaker 1: but too much actually drives inflammation and lots of people
• 2:49
  Speaker 1: are way out of balance in the ratio. Now, EPA
• 2:53
  Speaker 1: also stabilizes the membrane environment inside the artery wall. So
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  Speaker 1: DTA builds things, EPA modulates things. They're different tools for
• 3:04
  Speaker 1: different jobs, and critically the conversion between the two of
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  Speaker 1: them runs essentially one way. So let's i talk about
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  Speaker 1: a twenty nineteen randomized control trial. This was in what's
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  Speaker 1: called an isotope tracking trial by Methol and colleagues and
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  Speaker 1: was published in the American Journal of Clinical Nutrition, and
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  Speaker 1: it used compound specific isotobe analysis to track this, so
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  Speaker 1: basically it had little traces through the body that could
• 3:34
  Speaker 1: actually track it, and the finding was clear. EPA converts
• 3:38
  Speaker 1: forward into DA in the body, but DHA does not
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  Speaker 1: retro convert back into EPA in any meaningful quality. So
• 3:48
  Speaker 1: if you're taking a DHA heavy supplement hoping your body
• 3:52
  Speaker 1: will sort out its EPA needs, it won't. That's not
• 3:56
  Speaker 1: how the biochemistry works. So there's a new meta analysis
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  Speaker 1: that actually changes how we think about dose dosing. And
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  Speaker 1: it was a twenty twenty six just this year. It's
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  Speaker 1: a systematic review and meta analysis published by an author
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  Speaker 1: called Cabir and its colleagues and it was published in
• 4:13
  Speaker 1: Critical Reviews in Food Science and Nutrition and sort of
• 4:17
  Speaker 1: Macquari University in Australia, and it's nice to see Australian
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  Speaker 1: research leading the world. Now. What they did in this
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  Speaker 1: is they pulled the data from ninety six clinical trials
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  Speaker 1: on a Mega three supplementation and that's a really big
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  Speaker 1: evidence base and what they find is really important. When
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  Speaker 1: you look at the EPA, the DHA ratio in the supplement,
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  Speaker 1: not just a total dose. You get different biological outcomes
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  Speaker 1: depending on what you're trying to achieve. What they find
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  Speaker 1: is that supplements with the ratio below one, that's the
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  Speaker 1: EPA the DHA so ratio low one means it's DHA dominant.
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  Speaker 1: There's more DJA in your supplement that produced the GREA
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  Speaker 1: reductions in inflammatory side accounts things like c reactive protein TUMU,
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  Speaker 1: crosis factor alpha and interlook in six. These are very
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  Speaker 1: common inflammatory cidoknts now supplements with the ratio at are
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  Speaker 1: above one, so that we're EPA dominant, there's more EPA
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  Speaker 1: than dha, and the supplement they most effectively reis the
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  Speaker 1: EPA DHA blood ratio and lower that aracodonic acid that
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  Speaker 1: a Mega six that can become toxic in the body.
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  Speaker 1: Now we need to really think about this because these
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  Speaker 1: are actually different anti inflammatory mechanisms. Reducing the amount of
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  Speaker 1: CRP and interlooking six and T and f alpha in
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  Speaker 1: your body is working on inflammation systemically, but lowering aracodonic
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  Speaker 1: acid is about reducing the substrate for pro inflammatory or
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  Speaker 1: cosonoid production in the first place. So they're different pathways
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  Speaker 1: in different tools. So on dosing, the data was pretty
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  Speaker 1: clear in this research study one to three grams per
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  Speaker 1: day of combined EPA and DSA produce the most consistent
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  Speaker 1: reductions in crptnf ALF and interlooking six. Below one gram
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  Speaker 1: of it, you're likely not moving the data at all,
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  Speaker 1: and above three grams, the incremental benefit flattens out for
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  Speaker 1: most people, and we'll get into that in a moment.
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  Speaker 1: Higher doses also mean higher oxidation risk from your supplement
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  Speaker 1: if you're not careful about the quality, and this is
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  Speaker 1: why that there is basically different research around epas shows
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  Speaker 1: different outcomes because they don't look at the amount. Typically,
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  Speaker 1: they don't look at the oxidation of it and things
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  Speaker 1: like that. Now let's get let's back to the case
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  Speaker 1: in point. There's an important pape you should know about
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  Speaker 1: that complicates the story slightly, but all will become clear
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  Speaker 1: in the end. So this was a twenty twenty one study.
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  Speaker 1: It was a network meta analysis by Vores and colleagues,
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  Speaker 1: and it was published in Advances in Nutrition, and they
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  Speaker 1: pulled together the data from five head to head trials
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  Speaker 1: directly comparing DTA versus EPA in isolation, so not a
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  Speaker 1: combined AMGA three supplement, just pure dha or versus pure epa,
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  Speaker 1: and they found no significant difference between the two on
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  Speaker 1: crp interlut in six and ten and f alfa. Now
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  Speaker 1: that appears to be a bit of a contradiction to
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  Speaker 1: the paper I talked about earlier. The twenty twenty six
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  Speaker 1: analysis was looking at the ratio effects within combined EPA
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  Speaker 1: and DSA supplements across a much larger pool of trials.
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  Speaker 1: And the second one I talked about was comparing monotherapy
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  Speaker 1: pure DHA versus pure epa. Now they're different experimental questions,
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  Speaker 1: and they're both valid. But what it tells you is
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  Speaker 1: that the ratio story specifically about how you formulate combine supplements,
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  Speaker 1: not necessarily the DSA is intrinsically better and the inflammating
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  Speaker 1: molecule and EPA in isolation. Right, So this is cleared
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  Speaker 1: up a little, this apparent contradiction by a twenty twenty
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  Speaker 1: three review that was published in the General Nutrients, and
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  Speaker 1: they find that EPA and DHA regulate cellular function through
• 8:27
  Speaker 1: both shared and divergent molecular mechanisms, and the different pathways
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  Speaker 1: of EPA and DHA in the body ended up in
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  Speaker 1: different metabolic feits in what's called our lip protein system.
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  Speaker 1: So basically, the way that these molecules work kind of
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  Speaker 1: against each other in combined supplements may actually explain some
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  Speaker 1: of the conflicting trial data that we've seen over the years.
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  Speaker 1: EPA and DSA and combination don't simply add their effects,
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  Speaker 1: they actually interact with each other. Now, I want to
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  Speaker 1: spend a minute talking about the cardiovascar story. So this
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  Speaker 1: is where we get into what should you be taking
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  Speaker 1: for what outcome? Because it really is striking. So there
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  Speaker 1: were two large trials that actually looked at cardiovascular events.
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  Speaker 1: And they were called the Reduce It and the Jealous trials,
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  Speaker 1: and they both used EPA only. And the Jealous trial
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  Speaker 1: was published in a Lancet in two thousand and seven
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  Speaker 1: and that had over eighteen thousand patients with high cholesterol,
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  Speaker 1: and that showed a roughly nineteen percent reduction in major
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  Speaker 1: carnary events with one point eight crammed grams per day
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  Speaker 1: of pure EPA when added to statin therapy. Now, the
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  Speaker 1: Reduce A trial that was published in the New England
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  Speaker 1: Journal of Medicine in twenty nineteen that used four grams,
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  Speaker 1: so more than double the amount of highly purified APA
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  Speaker 1: in cardiov vascular risk patients on statins, and they showed
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  Speaker 1: a twenty five percent reduction in major cardiovascular events. And
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  Speaker 1: that's a pretty remarkable result. Now compare that to two
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  Speaker 1: other large studies, one called the Strength and the other
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  Speaker 1: one was called the Many Trials. These were two large
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  Speaker 1: trials that used mixed EPA and DHA formulation, which essentially
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  Speaker 1: came up flat on hard cardiovascular endpoints. And so what
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  Speaker 1: is going on there mechanistically? Why would EPA on its
• 10:32
  Speaker 1: own have a real impact on cardiovascar events. But when
• 10:35
  Speaker 1: you mix it with DTA essentially does nothing for cardiovascar events,
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  Speaker 1: so that the Micaeludes and colleagues suggest that EPA may
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  Speaker 1: have a stronger and more prolonged protective effect against LDL,
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  Speaker 1: that that's the nasty type of cholesterol LDL oxidation and
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  Speaker 1: also something technical called chrystal cholesterol crystal domain formation in
• 11:03
  Speaker 1: r walls, and they find that this is probably due
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  Speaker 1: to epa specific length of hydrocarbons and the position of
• 11:12
  Speaker 1: the double bonds. This is geeky biochemistry, but basically it
• 11:16
  Speaker 1: allows more efficient electron stabilization. So basically it is acting
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  Speaker 1: against oxidation of L d L, and we know that
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  Speaker 1: oxidation of LDL is a big driver of cardiovascar events
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  Speaker 1: and heart disease. So essentially EPA may be the better
• 11:34
  Speaker 1: molecule for your artery walls. Now this isn't fully settled science.
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  Speaker 1: It's all going debates about whether because there was a
• 11:43
  Speaker 1: there was a mineral oil placebo in the reduced trial,
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  Speaker 1: and some people think that artificially inflated the apparent benefit
• 11:51
  Speaker 1: of EPA by worsening the control groups outcomes. So this
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  Speaker 1: is why the science gets a little bit messy. But
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  Speaker 1: the direction of the evidence EPA focused for hard cardiovascar
• 12:03
  Speaker 1: endpoints is pretty consistent. So the practical takeaway here is
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  Speaker 1: that if you are trying to reduce your risk of
• 12:10
  Speaker 1: heart disease, if you've got that in the family, or
• 12:13
  Speaker 1: you're concerned about heart disease, you really want to be
• 12:17
  Speaker 1: looking at either an APA very dominant solution where there's
• 12:21
  Speaker 1: much more APA than DHA, or you just take a
• 12:25
  Speaker 1: pharmaceutical grade EPA on its own. And if your goal
• 12:30
  Speaker 1: is to manage inflammation, or if you're about brain health,
• 12:34
  Speaker 1: then we really want to be looking to DHA on
• 12:38
  Speaker 1: its own or something that is very much DHA dominant
• 12:42
  Speaker 1: in the ratios. Now, unless you're a biochemistry get your
• 12:46
  Speaker 1: head might be spinning right now. So I want to
• 12:51
  Speaker 1: leave the second part of this where we talk about
• 12:53
  Speaker 1: the ransidity problem until next week, because that is something
• 12:57
  Speaker 1: that genuinely shocked me. But the takeaway for this week
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  Speaker 1: is APA is the stuff you want to take for
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  Speaker 1: your heart, and DJA is the stuff that you want
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  Speaker 1: to take for your brain and your eyes. That's it
• 13:09
  Speaker 1: for this week, folks, Catch you next time.