Episode Transcript
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William Davis, MD (00:00):
Let's discuss
many of the facts and fictions
surrounding omega-3 fatty acids.
Because there have been severaldecades of confusion,
misinformation,misinterpretation, and it but
it's become very clear now howand when we should supplement
omega-3 fatty acids for actuallyvery significant benefits, even
(00:20):
though that was not clear in theearlier years.
Let's also be clear on whatwe're talking about.
We're talking about the EPA andDHA that come mostly from fish.
We're not talking about thelinolenic acid that comes mostly
from plant sources.
And I point that out becauseyou'll see a lot of misleading
marketing.
That's a lot of the source ofmisinformation here, is the
(00:43):
misleading marketing, peopletrying to grab a portion of a
very significant market foromega-3 fatty acids.
So for instance, you'll seeproducts that say, or like grain
products that say rich inomega-3 fatty acids.
That means it's rich inlinolenic acid, not EPA and DHA.
Now there's nothing wrong withlinolenic acid, it actually has
(01:03):
its own collection of benefits,separate and distinct from the
EPA and DHA.
But it's the EPA and DHA thathave, and we'll discuss this in
a moment, greater cardiovascularand brain health benefits that
linolenic acid does not have.
So don't fall for the misleadingmarketing that many food
companies will use, andsometimes supplement companies,
(01:26):
that are hawking their linoliticacid sources.
It's fine to get linolitic acid,but it has nothing to do with
EPA and DHA.
So the excitement over omega-3fatty acids, EPA, and DHA got
its start when epidemiologicstudies suggested that
fish-consuming cultures, likethe Inuit, the Eskimos, the
(01:48):
Japanese, and some othercultures had fewer
cardiovascular events comparedto Western cultures.
So studies were performed, mostfamously the GISI Prevenzioni,
Italian trial, 11,000participants, and people who got
what we would regard as a verymodest dose of 1,000 milligrams
of EPA and DHA per dayexperienced a marked reduction
(02:11):
in cardiovascular events likeheart attack, but especially
sudden cardiac death, a 45%reduction in sudden cardiac
death.
So that launched a lot ofenthusiasm for omega-3 fatty
acid supplementation.
Unfortunately, that study wasfollowed by a series of
relatively smaller studies thatwere came up with uneven
results.
Some showed benefit, some didnot.
(02:34):
One of the reasons for the greatuncertainty that was introduced
by some of these smaller trialsfrom a few years ago was that
there are numerousmethodological problems that
were not addressed.
For instance, one glaringproblem is that there was no
weight adjustment.
So here's an issue.
Just like vitamin D, verydependent on weight.
(02:56):
That is, let's say I hadsomebody with a very low
starting level, blood level of25 hydroxyvitamin D.
Let's say 17 nanograms permilliliter, which is very low.
We're aiming for 60 or higher.
So that person, let's say, takes8,000 units of an oil-based gel
cap of vitamin D.
And that person's slender.
Maybe they're 170-pound guy,right?
(03:18):
And his 25 hydroxy vitamin Dblood level goes from 17 to 63.
Okay, perfect, right?
Just where we want it.
What if that guy was 270 poundsand he started with a 25 hydroxy
vitamin D blood level of 17?
He takes the very same 8,000unit dose and his blood level
(03:39):
goes to 37, much reduced becausefat sequesters vitamin D.
Well, the very same phenomenonoccurs with omega-3 fatty acids.
So if you have a lot ofoverweight people, which is the
case in most of these clinicaltrials, right?
Because most Americans and otherpeople, other countries, are
overweight or obese.
So when you give people astandard fixed dose of omega-3
(04:02):
fatty acids, many people willnot have much of a rise in their
blood levels of omega-3s.
Now, one of the great things toknow is a test called an RBC,
red blood cell omega-3 index.
This is a test invented by Dr.
William Harris, who haspublished dozens and dozens of
studies validating this measure.
(04:24):
It's very, very helpful.
We know that the averageAmerican has an RBC, omega-3
index of 2.3% or thereabouts,meaning only 2.3% of all the
fatty acids in the membrane, thecell membrane of the red blood
cell, is our EPA and DHA.
If you consume fish on occasion,you might go to 3.5, 4.1%.
(04:48):
We're aiming for 10% in myprograms.
We're aiming for an RBC omega-3index of 10% or greater because
that's where we're confident weachieve effects like a reduction
in sudden cardiac death,reduction in heart attack, and
even maximum protection of brainhealth from dementia.
(05:08):
But more recently, largerstudies using higher doses.
Now recall that omega-3 fattyacid are a component of food,
right?
They're in fish and shellfishmostly.
And whenever we're talking aboutfood, we need to talk about
larger quantities.
In other words, if I said toyou, uh beef is good for you,
let's just say, right?
(05:29):
And I said you can have 50 gramsor 50,000 milligrams, that would
be a teensy weensy little piece.
So when we talk about food, weneed to talk about larger
quantities, especially gram oreven kilogram quantities.
So when we talk about omega-3fatty acids, a natural fat
component of foods, we need totalk about gram quantities,
(05:52):
several grams.
But that was not recognizeduntil recently.
And so more recently, largerstudies have been performed that
have indeed shown dramaticreduction in cardiovascular
events, stroke and heart attack.
That even better.
That argument has gainedterrific momentum, thank
goodness, for several studiesusing CT carony angiography.
(06:16):
And all that means, these areCAT scan CT devices using 3D
reconstruction of the variouscomponents of arteries.
I tried to do that study 18years ago, but the software we
had 18 years ago wasinsufficient, was not enough to
measure what are called voxelsor 3D pixels in space.
(06:36):
But now that technology hasadvanced, and several studies,
three studies, have used CT,quantitative CT coronary
angiography, not just to look atthe detail in the coronary
arteries, that is the arteriesof the heart, but also break
down how much soft plaque, thatis fatty plaque, fibrous plaque,
(06:57):
and calcium you have.
So it breaks the components ofartery of uh of carneur artery
atherosclerotic plaque into itsvarious components.
And in these three studies, suchas the hearts or the evaporate
trial, in which higher doses ofomega-three fatty acid were
used, and then baseline, andthen a follow-up CT
(07:17):
cardioranticram was performed,showed not only was there a
reduction in cardiovascularevents, but there was actual
regression, shrinkage, reductionof the fatty elements.
That's important because it'sthe fatty elements in the
coronary arteries that ruptureand cause heart attack.
That's how heart attack iscaused.
(07:38):
People think heart attacks arecaused by the progressive
worsening of a blockage.
30%, 50%, 70%, 100%.
No, most of the time it's therupture of a small plaque, maybe
only 35% reduction in thediameter of the artery, but it
erupts suddenly, closes off theartery.
That's how most heart attacksoccur.
Well, we now know with very goodevidence provided to us by these
(08:02):
CT carnearandrographic studies,that it's the fatty
rupture-prone components thatregress with omega-3 fatty
acids.
And interestingly, in all thesethree trials, because statin
cholesterol drugs are felt to bethe prevailing standard, they
thought it was unethical to usea placebo group.
So everybody's on statin, allthree of these trials.
(08:25):
And some had the addition ofomega-3s, some did not.
And only the people who got theomega-3 fatty acids experienced
regression of plaque, mostlyfatty plaque.
The people on statin drug aloneall experience progression,
worsening.
So the real pivotal finding hereis that omega-3 fatty acids not
(08:48):
only reduce heart attack andsudden cardiac death, also
reduce the fatty components ofcarneur atherosclerosis and
achieve regression of carneuratheroscleron plaque.
So for that reason alone, we areusing, I advocate, 3,600
milligrams or more of EPA andDHA total per day.
(09:11):
There are some subsets of peoplelike lipoprotein A people where
we use higher doses.
But for the most part, 3600milligrams in those studies,
3,000 to 3,300 milligrams of EPAand DHA were used.
I've been using higher doses formany, many years.
That works very, very well.
So we use 3,600 milligrams totalEPA and DHA.
(09:31):
Not 3,600 milligrams of fishoil, but 3,600 milligrams of the
EPA and DHA combined.
Now another area where theevidence is good that omega-3
fatty acids as EPA and DHA, notlenolinic acid, are beneficial
is in preservation of cognitivehealth.
So let me make this issuebecause it's very confusing and
(09:54):
it's leading to a lot ofmisinformation.
There are two groups ofbeneficial supplements or drugs
for brain health.
There are things that arenootropic, and there are things
that are neurotrophic.
And that's a big difference.
Something that's nootropic issomething that improves memory
(10:16):
or creativity or your ability tolearn and concentrate or recall
data temporarily.
Caffeine would be a goodexample.
You have a cup of coffee andyou're a little bit faster on
your feet, your concentration isa little bit better, energy is a
little higher for a few hours,and then you're back to normal.
Is your brain actually anyhealthier?
(10:37):
No.
That's a nootropic effect.
There's a long list of factorsthat are nootropic, such as uh
these are things you might nothave heard of, like uh dimethyl
aminoethanol or hooperzine orvinposetine or paracetam, uh
many ginkgo bloba, long list ofthings that improve your brain
(10:59):
function temporarily by boostingvarious neurotransmitters like
acetylcholine, epinephrine, ordopamine, but then your bet your
brain physiology reverts back tonormal.
Your brain's not healthier,you're not protected from
dementia.
You're just transiently a littlebit smarter, a little bit better
able to learn, be creative,recall lists of information,
(11:19):
etc.
To be distinguished, somethingthat is neurotrophic, that is,
factors that have been shown toactually benefit brain health
and physiology in a long-termway.
And these effects can bemeasured.
For instance, if you did an MRI,for instance, of the brain, you
can show that the hippocampus,the part of the brain that
(11:39):
transac near-term memory intolong-term memory, hippocampus
shrinks with cognitiveimpairment and dementia.
So if something is neurotrophic,it will protect the hippocampus
and preserve its volume.
Something that has neurotrophiceffects will preserve the volume
of the temporal or parietallobes of the brain and prevent
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atrophy of the brain.
Something with a neurotrophiceffect will have beneficial
effects on what are calledtrophic hormones, things that
encourage brain growth, BDNF,brain-derived neurotrophic
factor, IgF-1 alpha, and othergrowth factors.
In other words, there areclear-cut benefits that we can
(12:21):
list as neurotrophic thatactually benefit the brain long
term.
In that short list of thingsthat do that, omega-3 fatty
acids are neurotrophic.
So don't fall for all the claimsfor things that people say are
good for brain health, likecreatin, for instance, is
nootropic.
It does not actually improvebrain health, does not protect
(12:44):
you.
At least no one's shown thatfrom dementia.
But omega-3 fatty acids athigher doses appear to protect.
And just like the protect thedoses used to protect from
cardiovascular death and heartattack, that is north of 3,300
milligrams EPA and DHA per day,same thing with brain health,
preservation of brain health.
(13:04):
Higher doses because it's acomponent of food, right?
So we want doses of at least3,300 milligrams EPA and DHA per
day.
Let's talk for a moment aboutthe form of omega-3 fatty acids
that are important.
So if you were to eat a piece offish, let's say a piece of
salmon, you're going to get thetriglyceride form.
And all that means is that thereare three fatty acids on a
(13:28):
backbone of glycerol.
Triglyceride form, triglyceride,three tri fatty acids on a
glyceride or glycerol backbone.
That's how it occurs in fish,normally and naturally.
When fish oil is produced, it'ssubjected to alcohol extraction,
and those fatty acids areseparated from the glyceride,
(13:49):
the glycerol backbone, and youhave so-called ethyl ester
forms.
And that's a perfectly fineform.
It's just a little less wellabsorbed than the triglyceride
form.
So you can either get thetriglyceride form, typically in
liquid form, or the ethyl esterform, more common capsule form.
Both work perfectly fine.
And if you're tracking, say yourRBC omega-3 index, you can
(14:12):
always adjust your dose.
If let's say you're getting3,600 milligrams of EPADHA in
the ethyl ester form, but yourRBC omega 3 index is only 8.9%,
boost the dose a little bit,right?
So the the form in this case isnot that important if you're
tracking the blood levels ofomega-3s.
Now, many marketing claims aremade for the phospholipid form.
(14:36):
That's the form in krill oil.
Well, the problem with that iswhile the phospholipid form is a
very nicely absorbed form, it'sbetter absorbed than the
triglyceride form, betterabsorbed than the ethylester
form.
Problem is, most products likeacrill oil, the quantity of EPA
and DHA is so small as to bekind of useless.
(14:56):
You'd literally have to take theentire bottle or more every day
to even approach the intake, theRBC omega-3 index target of
regular fish oil.
So take krill oil if you wantthe astraxanthin carotenoid.
Don't take krill oil if you wantto achieve a truly beneficial
(15:18):
level of RBC omega-3 index thatprotects you from cardiovascular
events and from dementia.
So put aside all that you'veheard over the years, driven by
poor science, sloppy science,methodological flaws, and know
that the science has advanced,and we now know with confidence
that supplementation of omega-3fatty acids at a dose of at
(15:40):
least 3,300 milligrams EP andDHA per day is the dose that
provides maximum benefit.
Now, of course, you can adjustyour dose if you happen to eat
some fish every uh every sooften.
But of course, eating fish islimited by the fact that we've
tainted our oceans with mercury,shellfish with cadmium.
And if you eat a lot of fish,you're going to get mercury
(16:02):
toxicity, which has its own setsof concerns.
So we use the well, I it's bestto get it from the original
source, like fish and seafood.
We can't do that ad lib becauseof this mercury issue.
And so we resort to supplementsthat have negligible amounts of
mercury.
Now, if you learned somethingfrom this video, I invite you to
see my other videos on thisYouTube channel, my Define
(16:25):
Health Podcasts, my thousands ofblog posts, on my William
DavisMD.com.
And if you'd like support indoing these kinds of things,
join my conversations that wehave most weeks on my inner
circle.dr Davisinfinite Healthdot com.