Video summary
Recent research highlights a powerful synergy between dietary intake, specific nutrients, and lifestyle habits in slowing biological aging, with Omega-3 fatty acids playing a central role when combined with Vitamin D and resistance training. While Omega-3 supplementation alone can slow epigenetic aging, the addition of Vitamin D reduces age acceleration by approximately 3.3 months, and incorporating resistance training further increases this benefit to about 3.8 months. These physiological improvements translate into significant health outcomes, including a 40% reduction in prefrailty, a 61% decrease in invasive cancer risk, fewer infections, and a notable decline in falls among older adults. This protective effect is particularly critical given that low dietary intake of EPA and DHA ranks as one of the top six preventable causes of death, comparable to trans fats but often overlooked by the public.
The mechanisms behind these benefits involve both cellular integrity and systemic inflammation reduction; Omega-3s increase cell membrane fluidity while producing specialized pro-resolving mediators that counteract the stiffening associated with aging or high consumption of trans fats. This is especially vital for brain health, where a higher Omega-3 Index correlates with a 50% lower risk of Alzheimer's disease and larger hippocampus volumes that delay memory-related atrophy. Furthermore, these fatty acids support executive function in individuals with mild cognitive impairment by boosting neuronal autophagy and aiding neurotransmitter transporters like dopamine and serotonin receptors. Beyond the brain, Omega-3s are crucial for preventing disuse atrophy during periods of immobility caused by surgery or illness, addressing "anabolic resistance" where aging muscles fail to respond adequately to amino acids without proper support.
To maximize these protective effects against conditions such as sudden cardiac death and cognitive decline, experts recommend achieving an Omega-3 Index of 8% through a combination of diet, such as wild Alaskan salmon, and supplementation, with two grams daily often cited as a safe target for cardiovascular and brain benefits. This approach also addresses gut health by mitigating the risks associated with lipopolysaccharide (LPS) release from dying bacteria after meals; Omega-3s help suppress this post-meal LPS spike and degrade it within the gut, thereby preventing LDL particles from becoming small, dense, and atherogenic while reducing links to depressive symptoms. Although concerns exist regarding microplastics in fish or oxidation at very high doses, studies suggest that even large amounts can be safe short-term if membranes are not overfilled with DHA, and the health benefits generally outweigh potential mercury risks when choosing appropriate sources like sliced sardines rather than whole ones.
Ultimately, maintaining optimal levels of Omega-3s requires a consistent strategy because their anti-inflammatory effects last only about 24 hours, necessitating regular intake to sustain protection against heart attacks, infections, and cognitive decline. While the ideal ratio of EPA to DHA may vary based on individual needs—such as prioritizing DHA for Alzheimer's prevention or balancing both for general health—the focus should remain on reaching a target index rather than relying solely on dosage calculations from different supplement forms like ethyl esters versus triglycerides. By combining dietary sources with targeted supplementation and maintaining an active lifestyle, individuals can leverage the full potential of Omega-3s to slow biological aging, preserve muscle mass without exercise in some cases, and significantly extend life expectancy by up to five years compared to those with lower indices.
Read the full video transcript
And what it was found is that people
with a higher omega-3 intake
slowed their age acceleration. So, you
know, you're accelerating, your aging is
happening at a certain rate. If you're
smoking, it's happening at an
accelerated rate. If you're taking
omega-3, it's slowing that rate of
acceleration. But what was really
fascinating is that there was synergy.
So, when you looked at omega-3 plus
vitamin D, it slowed epigenetic aging
even further than just omega-3 alone. it
slowed it by about 3.3 months. When you
looked at all three combined, resistance
training, omega-3, and vitamin D, it
slowed it by about 3.8 months. So
really, it was like these lif these
healthy lifestyle factors converging
with omega-3 being the thing that's
really moving the lever. So excited to
be here, Expo West. I had no idea how
big of an event this was until I was
driving here in traffic and I thought
everyone was walking to Disneyland and
I'm like, this is this is not the
Disneyland crew. Um, so as Harmony
mentioned, I am a huge advocate of
omega-3. I mean, this started from gosh,
when I was a graduate student, I
started, you know, supplementing with
omega-3 back in 2007.
Um, just reading the scientific
literature and realizing how important
it was. And then when I went on to do my
posttock with Dr. Bruce Ames, the late
Dr. Bruce Ames um in in he's a UC
Berkeley professor but I was at
Children's Hospital Oakland Research
Institute and I was researching omega-3
in his lab as well. So it's it's been
not only a passion of mine at the
personal level but also something that I
research and I continue to research as
an associate scientist at the Omega-3
fatty acid institute that was founded by
Dr. Bill Harris. So today I'm going to
be talking about how we can all optimize
our longevity with the power of omega-3
delay of age related disease and through
the delay of the molecular events that
lead to age related disease. And we're
talking about cardiovascular disease
being a big one, cancer, Alzheimer's
disease. These diseases that not only
shorten our life expectancy but also
decrease the quality of our life, right?
We don't want to live the rest of our
life with Alzheimer's disease. You know,
the last 10 years with Alzheimer's
disease or with cancer.
This is a standard disclaimer here. I am
a scientific researcher and so what I'm
presenting here today is not medical
advice. It doesn't represent any omega-3
supplement company's views. It is my
views. These are my slides. This is what
I present when I go around and do
presentations. So, just keep that in
mind as forformational purposes only.
It's not meant to be prescri
prescriptive.
Okay. So, just to give you an overview
of what we're going to talk about today.
First, we're going to talk about the
role of omega-3 and cardiovascular
health. We're going to talk about
cardiovascular events. We're going to
talk about all cause mortality. Um, and
then we're going to talk about some of
the mechanisms like inflammation and
changing what's called selfu cell
fluidity, and we'll talk about what that
means. We're going to talk about how
omega-3 slows the aging process. It
slows biological aging. We're going to
talk about how it synergizes with other
micronutrients and lifestyle factors
like vitamin D and exercise. We're going
to talk about the role of omega-3 in
delaying age related neurodeenerative
disease like Alzheimer's disease. We're
going to talk about how it plays a role
in preventing brain atrophy as we age
and also improving cognitive function.
And then we're going to get into the
muscle and talk about disuse atrophy
when we're not using our muscles and how
omega-3 plays a very unique role in
helping prevent some of that disuse
atrophy and why that's so relevant. And
then we're going to talk about the gut.
We're going to we're going to finish on
the gut, which is actually a major
source of inflammation. And so we're
going to talk about a unique way that
omega-3 is actually playing a role in
inhibiting leaky gut.
So, I want to just get started with the
first slide here, which really
highlights the prevalence of omega-3
insufficiency and deficiency. People are
not getting omega-3 fatty acids from
their foods. So, about 90% of the US
population does not eat enough seafood
and about 80% globally of the population
not getting enough omega-3 from their
diet. Which leads me to this really
important study that was published out
of Harvard several ye several years ago
that identified low omega-3 intake as
one of the top six preventable causes of
death. So there are three types of
omega-3 fatty acids. There's alphal
leninoleic acid ALA that is found in
plant foods like walnuts like flax
seeds, chia seeds. And then there's the
marine type of omega-3 fatty acids
iicosa pentaeninoic acid EPA and
docahexaoyic acid DHA. And those are
found primarily in seafood. And so what
this Harvard study identified was that
people weren't eating enough of the EPA
and DHA from seafood. And why is that
important? What am I what do I mean by
top six preventable causes of death?
Well, what these researchers did was
they looked at all the different things
that people have control of in their
life and diseases that increase early
mortality. And top six of those were
things like smoking. So, if you avoided
smoking, you would, you know, live
longer. If you didn't, you would shorten
your life expectancy. Hypertension, type
two diabetes, cardiovascular disease,
and not getting enough omega-3 from your
diet. Right? Nobody is thinking about
that. Everyone's thinking about all
these other disease. they're not
thinking about what they're not getting
from their food. It was actually found
that 84,000 deaths a year were
attributed to people not getting enough
omega-3 and by people I mean in the
United States were not getting enough
omega-3 from their diet. And um compare
this to people eating trans fats. So
trans fats, everyone knows it's terrible
for cardiovascular health. Um it leads
to cardiovascular disease and that was
attributed to 82,000 deaths per year.
And when anyone walks into a grocery
store, you know, you can pull into any
aisle and pick up, you know, food and
it'll say zero trans fat, zero trans
fat. It's marketed everywhere.
Everyone's thinking about not consuming
trans fat because it leads to early
mortality. But nobody's walking into a
grocery store and thinking, am I getting
enough omega-3? Am I getting my fatty
salmon? Am I am I getting enough
seafood? Nobody's thinking about that.
But they should be. It's very important
for our health.
So, let's talk about, you know, how we
can measure omega-3 and how we know it's
important for health. Well, there's
large large studies that have been done,
longitudinal studies, Framingham cohort
being being a big one, where lots of
different blood biomarkers have been
measured in individuals, including the
omega-3 index. So, the omega-3 index is
a marker of your omega-3 fatty acid
levels in in blood cells. So, it's a
long-term marker because your red blood
cells take about 120 days to turn over.
So, it's nice to have more of a
long-term marker of omega-3 versus just
looking at omega-3 and plasma
phospholipids, which to some degree
could be reflective more of what your,
you know, recent diet was versus more of
your long-term omega-3 status. So, Dr.
Bill Harris um and his and his colleague
Clemens Van Shaki had identified this
omega-3 index back in I think it was
like 2002 2004 something like that and
so um when they when they measured you
know thousands of people's omega-3 index
what they found was that those people
with a high omega-3 index that's
indicated as 8% or more so 8% of the
fatty acids in the cell in the red blood
cell membranes were composed of these
omega-3 fatty acids s um they had a 90%
lower risk of sudden cardiac death
compared to people with a low omega-3
index being 4% or below. 90% lower risk
of sudden cardiac death. That means, you
know, if someone had a heart attack and
they had a high omega-3 index, they were
90% less likely to die from that heart
attack than someone who had a heart
attack that had a low omega-3 index.
That's a big difference. And if you
think about heart attacks, I mean, every
30 seconds, somebody in the United
States is having a heart attack. So this
is a this is a really important finding,
but it's not only important for reducing
the risk of sudden cardiac death, it's
also been linked to our life expectancy.
So yet again, looking at the omega-3
index in people um I think this was
maybe the Framingham, yeah, this is the
Framingham cohort. Again, this is a very
large population of people where a
variety of different biomarkers have
been measured. Those individuals with a
high omega-3 index of 8% or higher had a
5year increased life expectancy compared
to people with a low omega-3 index of 4%
or lower. I mean, 5 years is a big
difference in life expectancy. And
really, all we're talking about here is
the difference between having a high
omega-3 index and a low omega-3 index.
If you think about other countries that
actually do eat a lot of seafood, like
Japan for example, in Japan, their
average omega-3 index is 10%. So they're
in that high omega-3 index range. In the
United States, our omega-3 index on
average is about 5%. So we're pretty
close to that 4% which is the low range.
And if you look at the difference in
life expectancy between people that are
in the United States versus people that
live in Japan, it's about 5year
difference. So people in Japan have a
5-year increased life expectancy
compared to people in the United States
from that same Framingham cohort. And
this is the data that I find so
compelling. Um and I really you may have
heard me speak about this before and I
really like to talk about it and I like
people to see the graph because visually
it's it's just so clear. So what Bill
and his colleagues did was they took
this Framingham cohort and they took the
people with the high omega-3 and the low
omega-3 index and they said, "Okay, I
want to look at these individuals and I
want to specifically look at smokers
versus non-smokers with a high and low
omega-3." Because we know that smoking,
one of the worst things you can do for
your cardiovascular health is smoke
cigarettes. A lot of people associate
cancer, lung cancer with smoking when in
fact, you know, lung cancer increases in
a sort of dose dependent manner. The
more cigarettes that you smoke, you
know, the higher the risk of lung cancer
and that sort of compounds over time.
When it comes to cardiovascular disease
risk, that's an exponential increase.
Like you, it doesn't take much. And that
is because, you know, the damage that
the tobacco smoke is doing to the
endothelial cells and the inflammation
that's being generated really really bad
for cardiovascular health. Um, and so if
you look at individuals that have the
highest life expectancy, that would be
in green, they were non-smokers with a
high omega-3 index. They live the
longest. Big surprise. People that live
the shortest life expectancy is what you
would expect. Smokers with a low omega-3
index. That's red. So, they're dying
sooner. But what's so fascinating is
that when you take the smokers that
actually have a high omega-3 index, they
have the exact same life expectancy as
the non-smokers with a low omega-3
index. And really, you can look at this
data and go, "Wow, I don't smoke, but
it's like I smoke." You know, low
omega-3 is like smoking when it comes to
at least our overall life expectancy.
Um, of course, all the smokers when I
present this data think, "Oh, yes, I got
to take omega-3." Of course, that's the
wrong way to look at it, right? Because
you want to be that green curve. You
want to be the non-smoker with a high
omega-3 index. But it really just
highlights, you know, we know, and we're
going to talk a lot about this today,
that omega-3 fatty acids play a very,
very important role in cardiovascular
health. And that is why one, I think
they're really similar, not getting
enough of that in your diet is very
similar to consuming trans fats. We're
always worried about the things that
we're, you know, the toxins that we're
getting when also we should be worrying
about what we're not getting because
what we're not getting, our body needs
certain nutrients to function normally
and optimally. And what we're not
getting is also like a toxin. We're we
we are we're smoking when we're not
getting enough omega-3.
So let's talk about cardiovascular
health and the gold standard for
cardiovascular health which would be
randomized placeboc control trials of
which there have been quite a few
omega-3 fatty acid trials that have
looked at cardiovascular health. So the
first one is that I think has probably
one of the most robust effects is the
reduce it trial. This was about a
five-year randomized controlled trial
where individuals were separated. These
are individuals with high risk for
cardiovascular disease. Many of them are
already on some kind of firstline
standard of care treatment like statins
for example and others and they were
given either four grams of vipa this is
a pharmaceutical grade prescription form
of purified EPA or they were given a
placebo control for five years and after
the five years a variety of different
outcomes were looked at right and what
was found was that the people that were
given this vipa this high dose EPA and
it was four grams. They actually had
about a 25% lower um risk of all sorts
of cardiovascular events, death,
eskeemic events. So, we're talking a
pretty big effect here on lowering the
risk of heart attacks and strokes and
eskeemic, you know, es schemic events.
The next trial that had positive results
was the vital study. And the vital study
was a really big trial and it's still
ongoing and people are still harvesting
data from this trial. Um, and it there's
a lot of components to the trial, but
I'm going to talk about the omega-3
component where individuals were given a
very low dose of omega-3 fatty acids.
Actually, they were given LVA. This is
another prescription form of omega-3. In
this trial, they were only given 840
milligrams of Levvesa, which is a
combination of both EPA and DHA, or they
were given a placebo control. And this
was also a 5-year trial. After the five
years, some of the secondary outcomes
that were looked at were actually
improved with respect to cardiovascular
health. So individuals that were given
the the prescription in Luvvesa had a
28% lower heart attack risk and they had
a 17% lower coronary artery disease risk
compared to those given a placebo and
that was at a pretty low dose. I mean
we're talking less than a gram a day. So
pretty compelling data. There's also the
strength trial. Um this was four grams
of EPA and DHA. This was Epanova. Um,
Epanova was and is omega-3 fatty acids
in free fatty acid form. So, usually
these fatty acids are asterified.
Both of these that I'm talking about
here, prescription form, vipa and
lubevesa are in a ethylster form, which
is not quite as bioavailable as being in
a triglyceride form, which is what you
find naturally if you're getting omega-3
from fish. Um, and so free fatty acids
are actually very harsh on the gut. I
remember this is something that I was
looking at when I was a posttock in uh
Bruce Aim's lab and my colleague at the
time Mark Shagnaga was doing some of
these experiments. He's a gut health
expert and he was basically um looking
at you know free fatty acids and free
fatty acids can actually be very hard on
the gut almost like a detergent. So um
I'm not sure that Epino has gone
anywhere since then but it's it's kind
of um researchers are looking into the
the impacts of actually taking free
fatty acid form of omega-3 maybe being a
little bit hard on the gut. So that
trial was actually ended early because
it wasn't really showing any positive
results. But the take-home here is that
the the reduce it trial and the vital
study really gold standard showing, you
know, compared to placebo that if you
take omega-3 fatty acids, even at a
lower dose, it is reducing the
cardiovascular events that occur with
age.
And there's many reasons why omega-
omega-3 fatty acids are beneficial for
cardiovascular health. At the top of the
list would be inflammation. So, you
know, inflammation is a driver of heart
disease. It's a driver of
atheroscerosis.
And omega-3 fatty acids are in my view
the most potent naturally occurring
dietary compound that has
anti-inflammatory effects and it has it
through a variety of ways. So both EPA
and DHA, they get metabolized and their
metabolites help resolve inflammation.
So if we're looking at EPA, they make
resolins, the E the E series of resol
resolins. DHA makes the D series, but it
also makes the protectins and the
neuroprotectins. And these molecules,
they're not blunt force stopping
inflammation. Like you need
inflammation, right? We there's a reason
why our immune system is active. You
want it to be active, but you want it to
shut off when it's supposed to shut off.
And that's what these omega-3s are
really doing. They're keeping
inflammation in check.
The other way that omega-3 fatty acids
are cardioprotective
have to do with the cells and the
fluidity of them. And I I told you we'd
talk about this. So both DHA and EPA get
incorporated into our cell membranes.
They're a very important part of our
cell membranes. These are lipid
billayers that surround our cell and
they really change the way our cells
are, you know, moving. So what they do
is they make them more flexible instead
of really stiff. So trans fats make cell
membranes really stiff and omega-3 fatty
acids are the exact opposite. And it's
very important like if you're talking
about the endothelial cells that are
lining your vascular system, your
arteries, if you're talking about the
cells that are surrounding your
mitoardium, your paricardium, you know,
you know, surrounding your heart, those
you want all those cells to be flexible
and not stiff. And in fact, the
stiffening of our heart with age has to
do with that paricardium and myocardium
stiffness. And so omega-3 fatty acids
are really doing the opposite of what
the stiffening is. It's making them more
fluid. And that's another mechanism by
which omega-3 fatty acids are very
protective for the heart. So
cardoprotective.
Okay, I want to shift gears and talk
about some data that I'm super excited
about. This data has been emerging now
for I don't know the past eight or nine
years. And by emerging, what I mean is
we've had continual studies coming out
where it's just one after the other
validating confirming what has been
shown, which is that omega-3 fatty acids
slow biological aging. And what I mean
about that is, you know, we all all of
us sitting in this room, we're born, we
have our birthday, we have our age,
right? So I'm 47 and a half. And you
know, that's my chronological age. That
doesn't necessarily mean that if you
look at the age of the cells in my
organs, in my blood, in my liver, that
they're going to look 47 years old.
Depending on a variety of both genetic,
but also lifestyle factors. Importantly,
you know, your your cells in your body
can actually be either, you know, much
younger or much older than your
chronological age. And it really depends
on how you're living your life. And so
biological age, typically, we measure
this through epigenetic aging. And these
epigenetic aging clocks were developed
by Dr. Steve Horvath when he was at
UCLA. And there's a a variety of
different clocks that are used. There's
the DNA grimage, the DNA pheno age. Um,
and those are two of the major ones. And
then there's some other ones as well.
So, we're going to talk a little bit
about these epigenetic clocks. And what
these are are essentially just looking
at DNA methylation patterns. And these
methylation patterns are exactly that.
They're a pattern that change with age.
And the changing of these patterns
really seems to pre be a precursor to
the phenotype of aging into the outcomes
of aging. Right? to the phenotype being
frail, you know, having diseases, then
the outcomes, dying from heart,
cardiovascular disease, dying from
cancer, right? So, so the the epigenetic
aging clocks are very sensitive to the
molecular events that are causing aging.
And that's why we can measure these
clocks and make an estimation about what
our biological age is. So, one of the
first studies here, this was in 2019,
showed that omega-3 does slow biological
aging. was this was a prospective study
looking at people that um basically
reported their omega-3 intake and the
DNA grimage clock was used in this this
um study and the DNA grimage clock is a
very very accurate clock um that can
predict when someone is going to die. It
predicts like your your time to death
basically. And what it was found is that
people with a higher omega-3 intake
slowed their age acceleration. So, you
know, you're accelerating, your aging is
happening at a certain rate. If you're
smoking, it's happening at an
accelerated rate. If you're taking
omega-3, it's slowing that rate of
acceleration. So, it's slowing age
acceleration.
Another study that actually published
pretty recently in 2024.
This study also looked at omega-3
intake, both, you know, dietary,
supplemental intake, and found that
omega-3 did slow biological aging, and
it really mattered. The dose really
mattered, and this was based on gender.
So, for women, it took about at least
one gram of omega-3 to start to slow
biological aging in women, whereas for
men, it actually happened at a lower
dose. It happened at around 461
milligrams a day. So, um, it seems like
men men must probably must have more
inflammation going on because they were
they were really they seem to to be able
to have an effect even at a lower dose.
Um, but this is really interesting
because you see like once you hit that
one gram mark, that dotted line, this is
this is, you know, age acceleration.
You see that it slows, right? You're
slowing your age acceleration after that
one gram mark for for women and then a
little bit sooner than that for men.
Yeah. Another study showing that. But
even more what I'm even more excited
about is the randomized control trial
because that really is, you know, it's
it's it gets rid of the confounding
factors because at the end of the day, a
correlation study is is just that you're
correlating things and you try to, you
know, take in take into account all the
potential other confounding factors. But
when you have a randomized control
trial, then you can really definitively
say this is actually slowing aging. And
so what this trial did was it this was
in in Switzerland and um these people
were very healthy to start. So I'll say
this
aging epigenetic aging wasn't found to
be slowed by vitamin D alone which other
studies starting with vitamin D
deficient populations have found that
vitamin D does supplementation does slow
it. In this study they only took 2,000
IUs a day. If you're deficient it takes
about 4,000 IUs a day to bring you up to
a sufficient status. So in this study
they didn't didn't see any effect on
sewing of biological aging in you know
the vitamin D group exercise alone. So
this exercise was resistance training.
It was 30 minutes of resistance training
three days a week. Keep in mind that 90%
of the participants in Switzerland at
the at the start of this study were
already physically active which is
outrageous. So these are clearly
physically active people. These are
healthy adults. Okay? You would never
find that in the United States, but they
were already physically active. So there
was really wasn't much, you know,
slowing of epigenetic aging after
they're already being physically active,
adding, you know, the resistance
training on top of that. But adding the
omega-3 alone did slow epigenetic aging
in this population. So this was the only
thing that really had a profound effect.
But what was really fascinating is that
there was synergy. So when you looked at
omega-3 plus vitamin D, it slowed
epigenetic aging even further than just
omega-3 alone. It slowed it by about 3.3
months. When you looked at all three
combined, resistance training, omega-3,
and vitamin D, it slowed it by about 3.8
months. So really, it was like these
lifesy lifestyle factors converging with
omega-3 being the thing that's really
moving the lever. And you might look at
me and go, well Rhonda, I mean 3.8
months, what does that mean? like that
doesn't matter. I'm not talking about
extending your life expectancy by 3.8
months. I'm talking about slowing aging.
So, we're talking about a cumulative
effect, right? This is going to keep
compounding year after year. And what I
love about this study is they looked at
that. So, so the 3.8 months um of
epigenetic aging slowing that was the
combined omega-3 vitamin D and strength
training that also reduced prefrailty by
40%. So even though it was only about a
four-month slowing of epigenetic aging,
it reduced frailty by 40%. And it
reduced invasive cancer by 61%.
Wow. Exactly. I mean, this is this is
pretty exceptional. The omega-3 alone
without any other, you know, vitamin D
or resistance training reduced
infections by 13%. And it decreased
falls by 13%. So what the point I want
to make here is that I know Steve
Horvath who developed these epigenetic
aging clocks you know over a decade ago.
He's a friend of mine. I talked to him
the other day about this. I was so
excited about this data. Um you know he
he says that these these epigenetic
agent clocks are very sensitive to
inflammation. In fact it's one of the
things that really accelerates the aging
process inflammation. And we know that
omega-3 is as I mentioned it has very
powerful anti-inflammatory effects. I
talked about resolving inflammation. EPA
also can sort of directly affect
inflammation through the lucatryins and
the prostaglandins. It can reduce a
little bit of of those as well. So the
the fact that omega-3 is really having a
profound effect on biological aging in
my mind is very important. We know we
have the omega-3 index data and we know
the outcomes are also affected. we know
cardiovascular death, you know, is
lower. We know that you're increasing
life expectancy. And here we have, you
know, in real time, it's actually
slowing the aging process. So, um, this
trial, by the way, was a two-year trial.
So, I think that it's really important
to keep in mind that you can have an
outsiz effect by something as little as
in this study, you know, taking, let's
see, what was the dose? Um,
in this study, the dose was it was one
gram. It was one gram, as little as one
gram a day had an effect on slowing
aging. I mean, that's pretty profound.
And so, as I mentioned, these epigenetic
clocks are very sensitive to aging.
Sorry, to inflammation. And inflammation
is at the core of aging. I mean, this is
known. It is really, really one of the I
would say molecular processes that is
driving all these hallmarks of aging. It
is driving, you know, damage to your DNA
that leads to cancer. It's driving
damage to proteins that's leading to
them aggregating and not being degraded.
And you're getting these aggregates in
your brain leading to Alzheimer's
disease and in your cardiovascular
system leading to cardiovascular
disease, atheroscerosis. You know, it is
fundamentally driving cancer. I mean,
inflammation is at the heart of cancer.
It's really at the core of every age
related disease. And we now know it's
literally just accelerating the way our
DNA is changing with time, right? This
is the epigenetic clock data. It's
really just at the at the fundamental
level changing our DNA and accelerating
that. And so, you know, I remember there
was a study that was published, you
know, about 10 years ago. This was out
of Japan. And in Japan, they have a high
percentage of the centinarians, people
that live to be 100. And the semi super
centinarians, this is people live to be
105. And also the cent the super
centinarians that would be 110. And this
Japanese studies looked at you know all
these biomarkers to see you know if I
look at older adults if I look at the
centinarians and the semi and the super
centinarians like what what sort of
patterns arise what can I what can I
tell from these biomarkers that's going
to predict whether or not they're going
to live to be you know the next stage.
And the only thing that was able to
predict whether or not someone was going
to go from being an older adult to
someone that lives to be 100 and someone
that lives to be 100 to 105 and so on
was suppressing inflammation. Nothing
else predicted it. Not low blood
glucose, not lipids, not kidney
function, liver function. Nothing else
predicted it except for the ability to
suppress inflammation. And not only did
that predict the ability to live to the
next, you know, 105 or 110 being really
old, but it also predicted cognitive
function. So people were more
cognitively aware and they didn't have
neurogenerative disease as well if they
were able to have low inflammation.
And again, you know, omega-3 fatty acids
are doing just that. They are
suppressing inflammation. They're
resolving inflammation. They are doing
it through a variety of mechanisms. They
have these specialized pro-resolving
mediators that are really keeping the
immune response in check. And that is
important because our our immune system
is going to be activated every day.
We're being exposed to all kinds of
things in addition to pathogens when you
want it to be activated. I mean, just
air pollution that we're breathing in
constantly. Right now, you know, just
normal, you know, diet, you know, try
you try to eat as healthy as you can.
Inflammation's being generated in the
gut is constantly being generated. And
so, you really want to have something
that keeps that in check. Um, it also
plays a role in increasing the cellular
cleanup inside of ourselves, autophagy,
and that is also very important for
aging as well as helping reprogram
cells. But we're not going to get into
all that today.
Okay, I want to shift gears and talk
about another really important area with
omega-3 fatty acids and how it basically
affects our brain aging, cognition, and
the way our brain is aging. Omega-3
plays a very important role in the brain
throughout the lifespan from we're
talking in uterero development when
you're inside of your your mom's belly
and and your you're developing from that
point even preconception I mean it's
it's it plays an important role at every
life stage right now we're going to talk
about more of the end type we're going
to talk about neurodeenerative disease
but I just want you to keep in mind that
it's every stage is very important for
brain health
so Bill and his colleagues have also
published some studies is looking at the
Framingham cohort looking at omega-3
index and Alzheimer's disease. And so
again, what Bill found is that
individuals that had a high omega-3
index had about a 50% reduced risk of
Alzheimer's disease compared to people
with a low omega-3 index. So again, this
is correlative data. We're going to talk
about strengthening that with um some
some intervention and randomized control
trials as well. But I mean 50% reduction
is really really a big deal when it
comes to Alzheimer's disease.
Well, other studies have actually looked
at um omega-3 fatty acid levels and
reducing Alzheimer's disease risk and
found a dose dependent decrease. And
this always strengthens data when you
can find something that is dose
dependent. So for every increase in so
100 millgram per day increase in omega-3
fatty acids that was associated with
lowering the risk of Alzheimer's disease
and cognitive decline by 10%. So as you
kept going up 100 milligrams more you
had a 10% lower risk of Alzheimer's
disease and you went up 10% 100
milligrams more of omega-3 fatty acid
again an additional 10% decrease in
Alzheimer's disease risk again. And so
that's probably why when you get up to
that high omega-3 index, which we'll
talk about, it takes about two grams a
day to get to that high omega-3 index.
If you have a low omega-3 index, you
could see where that 50% reduction comes
into play because you keep going up in a
dose dependent manner. And this is an
analysis of multiple different studies
here showing that omega-3 reduces
Alzheimer's disease risk in a dose
dependent manner.
We also know that higher omega-3 index
is associated with a larger hippocample
brain volume. So as we reach older
adulthood and I mean the age of about 65
we start to lose 1 to 2% of our
hippocampus per year. So our brain our
hippocampus our brain is atrophying and
specifically our hippocampus is
atrophing and our hippocampus is very
important for a lot of different brain
functions. learning and memory being two
of the most important. And so you don't
want to lose 1 to 2% of your your
hippocample brain mass per year because
that's going to affect your memory. It's
going to affect your cognition, your
your executive function. It's going to
affect everything, right? So there are
studies that have found that a higher
omega-3 index is associated with larger
hypocample brain volume. And um and that
was also something that was found to be
dose dose dependent as well. And so it
was delaying it's it's basically staving
off that losing of the hippocample
volume. So you're basically you're going
against what happens naturally with age
because inflammation plays a role in
hippocample atrophy. And so if you can
if you can negate some of that
inflammation, you're going to keep some
of your brain mass. And of course that's
probably partly why you see a lower risk
of Alzheimer's disease as well.
And there's also been some studies
looking at omega-3 fatty acid
supplementation in individuals with mild
cognitive decline and how that can help
improve cognition um after taking
omega-3 fatty acids versus placebo. So
there have been a few studies. This is
this is a metaanalysis of multiple
studies as well. Um
sorry though this is this is one study
that did it was a two-year trial. These
patients had uh mild cognitive
impairment and they took two grams a day
of omega-3 for two years and after the
two years they had improvements in
cognitive function, executive function
um and importantly they actually had
lower plasma biomarkers of Alzheimer's
disease. So they had lower amaloid beta
in their in in their plasma but they
also had increased markers of neuronal
autophagy. So what that means so neurons
are they're not constantly make you're
not constantly making new neurons.
They're called post postmotic. So
basically what you have is you know
pretty much what what you're going to
get. And so our our our brain has ways
to to get rid of you know bad stuff that
is accumulated in them and that is
through a process called autophagy. Um
and so autophagy is very active in the
brain because it's very important to to
keep our neurons healthy. And so there's
biomarkers in the blood that are showing
that that's going up in people that
supplemented with omega-3 compared to
the placebo. So I think that um this is
alo also just strengthening the whole
picture here that I'm that I'm trying to
present to you, which is that omega-3
fatty acids are very important for brain
health. They're very important for
preventing inflammation in the brain,
which does lead to brain atrophy and
also lead to neurogenerative diseases
like Alzheimer's disease, you know,
dementia. And so, um, it's it's
something to keep in mind. As I
mentioned, 90% of the US population does
not get enough omega-3 from their diet.
So, there's a variety of reasons why
omega-3 is improving brain health,
inflammation being at the core, we
talked about that. Um, but also the the
cell membranes. It's it's in our in our
neurons, the cell membranes are very
important. And the fluidity, much like
in our cardiovascular system, the
fluidity is extremely important because
all of our transporters and receptors
for neurotransmitters, they're all in
that cell membrane. It's very important
for the structure and function of our
receptors and transporters. And so, it's
globally affecting neurotransmission.
When you have a cell membrane that's not
getting omega-3 and uh in the in the
brain, what happens is and there's
studies that have shown if for example
you take animals like mice and you make
them omega-3 deficient, their glucose
transporters aren't functioning right
because they're structurally like the
membranes too stiff and so the
transporter is not right and so glucose
can't get into the brain. And so this
over time, yeah, it's going to affect
your cognition in the short term. You're
going to feel brain foggy. It's not
going to you're not going to feel sharp.
But over time, what's going to happen is
low glucose in the brain affects a lot
of different processes, right?
Neurotransmission. It also leads to the
accumulation of tow tangles. This is a
hallmark of Alzheimer's disease as well.
And so you really it's really essential
for their cell membranes as well um as
boosting neurotransmission. So there
have been studies also showing that EPA
and DHA are important for dopamine,
serotonin. you know, when you have high
inflammation, it stops the release of
serotonin. You're not able to release
serotonin from the from the preynapse.
And so, um, it's really just globally
affecting neurotransmission,
neuroplasticity. It's affecting the
transporters, and it's affecting
inflammation. So, there's a lot of ways
that omega-3 is really behind the scenes
improving the way your brain is aging.
And when you don't have omega-3 there,
you know, not only is it not countering
the inflammation, but it's affecting
just global nutrient transport into your
brain and global neurotransmission.
Okay, we're going to shift gears now
again and talk about omega-3 um briefly
in the muscle. And this is something
that not a lot of people are aware of
and I think it's an important topic. So
um that you know some of these studies
that we're going to talk about come from
Stu Phillip and Chris Mclo when he was a
postoc in Stu Phillips's lab at McMaster
University. Chris Mclo now has gone on
he has his own lab and he's continuing
to research this topic but let's take a
a step back for a moment and just talk
about muscle mass and you know during
the aging process because it's important
to understand this to understand how
omega-3 is impacting it. So muscle mass
is very important for how we're aging.
Obviously frailty, you know, if you have
a fall, I mean the more muscle mass you
have, the less likely you are going to
fall. And if you do fall, you're going
to you're going to bounce back quicker,
right? So as you know, throughout our
life, you know, we reach our peak muscle
mass at around the age 20 to 30, then we
start to lose on average about 8% per
decade after that. Now, this is when I
say on average, I mean the average
person that's probably not really
physically active. If you add in
resistance training to that mix, you're
probably not losing 8% per decade.
The average person then when they hit
the age of 70 starts to lose 15% per
decade. And as people get older, they
become less physically active. Right?
As someone reaches the age of 70 to 80
years old, they have about 60 to 80% of
the muscle mass they had when they were
30. I mean, it's really, really a
profound decrease. And so you really
want to try to increase your muscle mass
as much as you can, you know, before you
get to that point. And it's important to
realize that as we age, so what's
important for increasing muscle mass?
Amino acids and resistance training,
right? The training is the phys the
mechanical force helps you increase
muscle mass. So um those are the two
most important signals for increasing
muscle mass. Um as we age, we become
less responsive to amino acids. So, it
doesn't have the same anabolic effect
that it does when you're younger. Amino
acids are much more anabolic in a
30-year-old than they are in a
70-year-old, unless they're training.
Physical activity and particularly
resistance training reensitizes the
muscles to amino acids so that it's
almost like you're younger again. And
that's really, really important. Um,
because most people are not training.
And so, this is this is called anabolic
resistance. You're basically when you
get older and you're not physically
active, your body is not responding to
amino acids. Your muscle is not
responding to amino acids the same. And
so you're not building muscle the same
way you did when you were 30, for
example.
Why is this important? This is important
because disuse atrophy events happen.
They happen because they're planned. So
surgeries, when you undergoing any kind
kind of surgery, you're going to have a
period of time when you are not mobile.
You are not using your muscles. And when
you're not using your muscles, you lose
them. You lose them. They atrophy. Um,
this could happen because you fell, you
had a fall. Uh, so you're not going to
be mobile for a period of time while
you're recovering. This could happen
because you have the flu or some other
respiratory disease, and you're not
moving around, right? So, there's a lot
of reasons why particularly older adults
have disuse atrophy events, planned or
not planned. And when they lose that
muscle, it is catastrophic because they
can never gain it back like they had
before they lost it. And um it's very
very hard for them. And anyone here that
has grandparents, parents that are aging
that have had these disuse events,
you'll see they start to compound. They
have one and then another and the next
thing you know they're they can barely
walk to their car. I mean, they just
they're they lose it quickly. It's a
very accelerated downhill trajectory.
So disuse atrophy is a problem and
anything that you can do to slow disuse
atrophy is hugely important. Hugely
important and this is where Chris and
Stu Phillips came in. So they were
looking at omega-3 fatty acids and their
effect on disuse atrophy. And you can't
do this experiment in older adults. It
would be unethical because they do lose
a lot of muscle mass and it's really
hard to gain it back. So they did this
study in younger women and um they gave
these women for four weeks ahead of
time. They gave them five grams of
omega-3. It's a high dose of omega-3.
Remember prescription forms of omega-3
are about four grams a day. So they were
going above that but they were doing it
for a month. And the reason they did the
high dose is because as in any
experiment whether we're talking about
creatine or omega-3 there's a loading
phase where there where um in this case
both both the researchers Stu and U
Chris Mclo were trying to get omega-3
fatty acids to accumulate in the cell
membranes in the muscle because it takes
about one month for that to happen. So
take so that's why they preloaded them
for one month with with five grams of
omega-3 and then they immobilized their
leg. So you put like a cast, you know,
around the leg so that they're basically
not using one leg. And you're looking at
muscle mass loss over that period of
time. And what was found was that the
the women that were given this omega-3
fatty acid supplement, it cut their
disuse atrophied in half. So they lost
only they lost, you know, only 50% of
what they would have lost if they didn't
have the omega-3. I mean, it's a huge
effect. And um I think this is really
really important because again, you
know, if you can do if you can give
older adults
an omega-3 supplement and make it where
they cut their disuse atrophy in half is
going to have a profound effect on these
events because that really does
eventually affect their trajectory and
into into their mortality risk. Right.
So, um, some follow-up studies by by
Chris Mcluri have found that actually it
doesn't really even seem to be the
inflammation that's playing a role in
this disuse atrophy. It's the
accumulation of the omega-3 in the
muscle cell membranes. And we've been
talking about transporters, right? Well,
amino acids are transportered through a
transporter. And what it seems to be
going on is that these the omega-3 in
the cell membrane is sensitizing the
amino acids in the muscle tissue like
they were young, like what exercise
does, right? So, um, very interesting
new data coming out of Chris Mcllor's
lab. I would say then, you know, in the
in the case of someone who's
supplementing with omega-3, then maybe
you would imagine that they would have
more muscle mass, like an older adult,
and that's exactly what's been shown. So
there's metaanalyses of studies that
have found that if you supple if older
adults supplement with two grams of
omega-3 per day, they actually have
higher muscle mass. They have improved
walking speed. And um I think this is
very important because you know and it's
not even necessarily in the context of
exercising. they they they just have
increased muscle mass likely because all
their sedentarism, the disuse events,
they're not losing as much muscle mass
from them because they have that
omega-3.
So, pretty powerful data. Um, and then
we're going to move on to the last part
of the talk here. I've got six minutes
left. That's perfect. We're going to
talk about the role omega-3 plays in
what is kind of known as leaky gut or
what I like to call gut permeability.
And um this is also very interesting
data because we've been talking a lot
about the role of omega-3 and
inflammation. Um it seems as though
there's multiple layers to this. So our
gut is the home of like trillions of
bacteria, right? We've got like
trillions of bacteria in our gut. Many
of many of them at the distal end of our
gut in the colon. Some of these bacteria
are good, the probiotic kind, and some
are bad pathogenic kind. But regardless,
bacteria in our gut, particularly the na
the gram negative bacteria, have a
component to their outer membrane. And
the bacteria have a component called
lipopolysaccharide. It's also referred
to endotoxin. They're kind of the same
thing, lipopolyaccharide. We have about
a gram of this lipopolyaccharide in our
guts at any given moment. It's a lot of
it just sitting around. And you know,
that's because bacteria are often dying
in our gut, right? And so when they die,
you still have those those dead cells
there.
And when we eat a meal, even if it's a
healthy meal, we have a transient
opening of the epithelial, you know,
cells and the and and the junctions that
are that are connecting our epithelial
cells lining our gut. There's a
transient opening of it and then closes.
Um, but when you have that opening,
guess what comes out? LPS. LPS comes
out. And this is kind of part of what's
called the postprandial
inflammatory response. You may have
heard of the postprandial gl glycemic
response, right? Or glucose response
where you're, you know, your blood
glucose levels go up after a meal
because you're eating carbohydrates.
Well, guess what else goes up?
Inflammation goes up after a meal
because LPS is being released into your
bloodstream after a meal. Now, the the
degree of how much LPS is released
depends on the meal that you're eating.
It also depends on whether or not you
have celiac, for example. CE people with
celiac, you know, if they have any
exposure to any sort of gluten, those
those junctions are open and the
floodgates are out and inflammation LPS
is going into their bloodstream. If you
eat a high high fat, high refined sugar,
you know, ultrarocessed foods, the the
the standard here, um that's really
going to cause a lot of leaky gut. It's
going to make your your intestines are
going to become permeable and LPS gets
released into the the bloodstream. I'm
going somewhere with this. So the LPS,
this is, you know, in your body. It gets
it's in your circulation now where all
your immune cells are. Okay? And it sees
LPS and it thinks this is bacteria
because it's part of a me bacterial cell
membrane. So it's ready. It's primed to
fire away to fight fight the invader,
right? It's not really an invader. It's
just something that was released
because, you know, we ate a meal. Um
part of the adaptive response here is
that we start to increase our
lipoprotein production. we make more
VLDLDL and LDL and that binds to LPS and
sequesters it and prevents it from, you
know, actually causing a lot of harm.
So, um, that's one of the reasons why
you never want to go get your LDL
measured right after you've been sick or
if you've had some kind of really
stressful event because inflammation,
stress causes inflammation and
inflammation will make your LDL number
go up. Just FYI, always do an N of two.
Um, but that's a that's a little side
note here. So the the binding of LPS to
these LDL particles, what's happening
now is um it's binding to a certain
region. It's binding to the region
called APOB. And the apo part of the LDL
particle is very important because that
is the part of the LDL particle that
gets recycled back to the liver so that
your LDL levels aren't staying around
forever in your bloodstream.
But LPS is obscuring that apo and so it
does not get recycled and so it stays
around in circulation longer. And what
happens is as it stays around it's
delivering triglycerides. What
lipoproteins are doing is they're
delivering triglycerides and cholesterol
mostly triglycerides fatty acids to your
other cells and for repair. You need
them for repair and things. But um now
this LDL particle can't go back to the
liver. It's got to stick around longer.
It's it's smaller in size. is it becomes
what's called a small dense LDL particle
and what happens is that small antel LDL
particle lodges itself in your arterial
wall and because the LPS is a signal for
the immune system hey bacterial invader
here the first line of defense is
macrofasages it's a type of immune cell
that come and engulf bacteria they eat
bacteria up so that it doesn't kill you
well they come thinking it's bacteria
but really it's a small dense LDL
particle lodged in your artery you got
this macroof phase it tries to eat it
only it can't because it's stuck to an
LDL particle and so now you have the
beginnings of what's called a foam cell
it's like a macrofase there and it's you
know making cytoines and stuff and now
bringing more and so you have the the
start of atheroscerosis
all coming from gut permeability all
coming from LPS leaking out into
circulation
why am I getting to this point um well
the other thing is also that this LP LPS
is affecting the brain and you know so
I'm talking about cardiovascular health
I'm talking about now that the LPS is
increasing you know inflammation and
that inflammation is affecting the brain
and I will just say this that there have
been studies that have injected LPS at a
normal level that you would find being
released in the circulation after a meal
into after a bad meal we'll say um
they've injected it into healthy
patients either LPS or a saline control
and injecting the LPS into those
individuals increases their inflammatory
biomarkers, but it also increases
depressive symptoms. It it increases um
you know social withdrawal as well.
Within that same study, if individuals
were given an omega-3 supplement before
they were injected with LPS, their
inflammatory markers weren't going up as
much and they weren't getting the
depressive symptoms. But that's a whole
other story. um in terms of like studies
have shown that actually inflammation is
a major part of depression and omega-3
particularly EPA seems to be very
powerful at reducing depressive symptoms
in people with major depressive
disorders. Um I'm unfortunately not
going to get into that today. It was
kind of a side note here because it's
all back to the LPS, right? LPS is
affecting cardiovascular health. LPS
being generated from the gut is
affecting your brain. This is why you
hear a lot of people talking about gut
health. Gut health is at the core of our
health in general. And it really is
true.
Why am I telling you this? Because
omega-3 actually in um decreases LPS
release after a meal. So in this study
here, there is a low fat and a highfat
meal. Typically higher fat fat meals do
increase more LPS because fat can kind
of lice this the gut cells and be an
irritant on the gut. But omega-3 in the
green at at every point um at the
baseline it seems as though the omega-3
group actually had a higher LPS. But
after the meal, you can see it's it's
suppressing the release of LPS and
endotoxin into your bloodstream. And um
which is kind of why I like to spread my
omega-3 intake out throughout the day.
It's very powerful um and important here
because now we're talking about not only
is omega-3 fatty acids reducing
inflammation at the level we already
discussed with these specialized
pro-resolving mediators and the
protectins and the resolins. But even at
the level of the gut, and we know this,
we know that from animal studies looking
at mechanism that omega-3 fatty acids in
the gut, when you take the omega-3 fatty
acids, they're working on site. They're
working at the first, you know, organ
that sees it, which is your gut. And
it's increasing the level of a protein
called IAP that degrades LPS in the gut.
It degrades LPS in the gut. It also
kills the bacteria that are producing
LPS. And so what what I'm getting at
here is there's so much to omega-3 when
it comes to inflammation. We're just
scratching the surface and of
understanding how it is so powerful at
reducing inflammation. Everything from
cardiovascular health to inflammation in
the brain to muscle to the gut, the
originator of a lot of inflammation in
our body. And I and I so I'm going to
end with that because I think it's very
important. Um and in conclusion, what
can you do? What what are the takehomes
here? In my opinion, one, everyone needs
to measure their omega-3 fatty acid
levels. You don't know what you you
don't measure. And so, you want to you
want to get this omega-3 index test,
which I heard may be in a little baggie
floating around um today, which is kind
of cool. Um the omega-3 index test, you
want to be at that 8% range. How do you
get to that 8% range? Well, a lot of
people can try to consume, you know,
fatty fish that are high in omega-3
fatty acids, low in contaminants, um,
like mercury, salmon, wild Alaskan
salmon is my favorite. Not everyone
likes to eat salmon and certainly
doesn't want to eat three to four, I
don't know how many servings a week it
will take. You have to measure your
omega-3 index to see um, not everyone
likes to to eat that fish because one,
unfortunately, our fish are contaminated
with microplastics and they're
contaminated with mercury and PCBs and
all kinds of environmental toxins.
Um, and some people just don't like the
taste. So, so Bill Harris has done some
studies also looking at what it takes to
get someone from a low omega-3 index of
4% to a high omega-3 index. If they
supplement, it seems as though if
they're taking a triglyceride form, a
little bit, maybe 1.5 to two grams a
day. Um, I like to say two grams a day
is really to be safe, but um, two grams
a day of omega-3 fatty acids seem to get
people from a low to a high omega-3, you
know, index level. And that's really
where you want to be. And that's where
you want to be for the brain benefits.
That's where you want to be for the
cardiovascular benefits, for the
reducing, you know, aging. It seems like
it's a a pretty good sweet spot and
that's what I take. Um, so with that
said, thank you so much for listening. I
hope you learned something today and I
think I have some time for questions.
Thank you so much, Dr. Rhonda Patrick.
We're going to do Q&A. We do have the
room until 12:15, so we do have a little
time here. If you do need to leave and
you're hopping over to another session,
make sure to get your gift bag in the
back with your complimentary omega-3
index test kit. Since I'm right here,
I'm going to go with you first.
>> Thank you so much. Great talk. I see
that you recommended two grams a day.
What is the ratio that you generally
recommend of the DHA and EPA?
>> Yeah, that's a great question. What is
the ratio of EPA to DHA? And I think
that really depends on what outcomes
that you're looking for. I think that,
you know, if you're looking the the data
really shows for cardiovascular health,
EPA is very important. DHA is as well.
It's very it's an important it's it's
it's the cell membrane component. D
mostly DHA is getting into cell
membranes. EPA too, but to a to a lesser
extent. Um, if you're if you're looking
for a lot of the brain benefits,
Alzheimer's disease, DHA really shines
there again, probably because that cell
membrane component. Same with the the
muscular effects. So, uh, personally,
you know, I like to go for closer to a 2
to1 ratio. I actually like DHA. I like a
little bit higher DHA for me.
>> For me, yeah. But, you know, other
people might want to go the opposite
direction,
>> right? Yeah. Perfect. I'm going to
continue in this row and I'm going to
hop over here.
>> We know there's been great studies on
the efficacy of supplements. Have you
seen any or done any work on consuming
through whole fish consumption verse
supplementation? What are your thoughts
on that in terms of efficacy and and
effectiveness?
>> Yeah, I mean, so several of the studies
that I presented, even some of the
initial omega-3 slowing biological
aging, um the omega-3 index, you know,
studies looking at 90% reduced, you
know, sudden cardiac death. Those were
really omega-3 intake and it was it was
people that were eating fish andor
supplementing. So, it's really kind of a
com combination. Um, and so there's
definitely like if if you can get your
omega-3 index up to that level from from
diet, it seems to be protective as well.
>> Perfect.
>> Is that your question?
>> Yes.
>> So,
>> comparing one or the other, not
directly.
>> Good. Okay. Perfect. I'm going to hop
over to you.
>> So, how many gel capsules would that be
for two grams?
>> It depends. It depends on how
concentrated the supplement you're
taking is. For me, it's four, but um you
know, you know, I like to find a more
concent. It's hard to get like one gram
of omega-3 into just one capsule. So,
generally, I would say two grams on, you
know, in general would probably be be
about four capsules.
>> Um my name is Ati Hakeim. I'm a family
medicine physician. It's the first time
I've attended this conferences. That was
outstanding you guys. That was
absolutely outstanding. And
cardiovascular disease is our number one
killer for every single person in this
room. Please listen to everything she
said. That was absolutely outstanding.
So my question is, we are working in a
sick care system in our country. We wait
for people to get sick. We work
backwards. That's not my goal. So how
soon can I start doing this for my
people? Cuz I have kiddos, right, that
already have hypertension, diabetes.
Yeah, we live in a sick care model and
I'd rather practice health care. How
soon can I start doing it? Can I start
reversing things for people that already
have it? I I personally think that
omega-3s are important starting, like I
said, from you know, you're in the womb
in uterero developing. I give my son um
my son is 8 years old and right now he's
getting about
a gram of omega-3 a day. Um, so you
know, I I I do recommend that, you know,
kids who some kids like to eat fish,
mine doesn't. So, omega-3
supplementation is only real omega-3
fatty acid source. But I think it's
important starting as soon as you can.
And the data really supports it. Also,
data supports it for cognitive health in
in children as well. And there are
studies showing that a gram a day is
safe in children and it lowers ADHD. It
improves cognition. I mean, there's all
sorts of in addition to cardiovascular
benefits, just brain benefits for
children.
Autoimmune. I mean, yeah. I mean, we
could have talked for hours about every
possible disease. It's pretty
ubiquitous.
>> Uh, I'm I'm a biochemist myself, but um,
is there like an upper tolerable limit?
Are there people getting too much?
Because I know um DHA has a bunch of
double bonds and it's eas easily
oxidized, prone to lipid proxidation and
if you have too much in your membrane,
it can be deletarious. Did they do any
studies showing like, oh, this person's
has way too much omega-3, he's probably
going to get sick or anything like that?
Um there's been studies like like Bill
did studies gosh back in a long time ago
maybe the 1980s um giving people 30
grams of omega-3 a day and there was no
negative effects and I don't remember
how long I'm not saying that that that
there aren't I'm just saying that he had
for the short amount of time that he did
it there was not I think that you know
we know that prescription forms are four
grams a day um and this is this is vipa
and lvesa so you know yeah I I think it
all depends on the person and there's
there's always an upper limit and so
it's better to kind of stay within that
safer range and talk about that with
your physician. But oxidation um your
your cell membranes only take up so much
like if you're if you if you're
overflooding the system with DHA, you
start to metabolize it like through
fatty acid oxidation. So that's that's
what happens.
>> One more over here and then I'm going to
jump to that side.
Um, first off, I think uh I don't work
for uh Nordic Naturals, but they do have
a 2X that gives you one gram in a a soft
gel.
>> Oh, nice. And one capsule.
>> Yeah. And all liquids uh give you more
than that in the liquid. Yep. So, um
>> but would you speak to the difference
between athaler and triglyceride? I know
I I listen I've listened about 20 times
to your conversation with Dr. Harris
>> from 22. So, found my fitness for people
who want the long form.
>> She does a great talk with Dr. Harris.
But, um,
>> thank you.
>> And all kinds of citations which you can
read.
>> Um, but if you would speak because on
the his Omegaquant website, he has a
calculation how much triglyceride you'd
have to take to get to that 2.2 grams
and how much uh how much ethylster you
would take.
>> Yeah. So, the difference between and I'm
going to just give a very general
overview here. Um, you know, the
ethylester versus triglyceride. So, when
omega-3 fatty acids are isolated from
fish and they're purified,
um they're oftent times run on a column
to purify away things like PCBs and
mercury. And so, um the the triglyceride
backbone is removed and they're
basically run through this alcohol
column. And so, it has a you know,
basically an an ethylster backbone to
run it through the column to purify. And
I think a lot of you know supplement
companies will leave it in that purified
form ethylester form that's not a
naturally occurring form. So when we
metabolize when we're taking an
ethylester form um it it's very
different in terms of like the enzymes
that are cleaving things and how much we
absorb. So we absorb far less of omega-3
in ethylsterform than if someone were
that were to then take that omega-3
that's been purified and then resterify
it on a triglyceride backbone which is
the I would say more of the gold
standard in my in my opinion because you
actually you get you're you're absorbing
so much more of that omega-3 from the
triglyceride form. So Dr. Dr. Harris on
his site does have a calculation that's
done and I think that the calculation
shows that if you're taking triglyceride
form you may not need you may not need
five sorry two grams you may need like
1.7 or something like that grams versus
the two if you're taking ethylester form
at the end of the day I don't think you
should just go off the calculation you
should take the omega-3 index test you
know before and maybe like you know a
few months after you're supplementing
right so 120 days at least wait before
you take the test again. Um, I would
wait a little bit longer and and see if
that dose is right for you because I've
I've seen people that have taken um two
three grams of ethylstroform and still
not raise their omega-3 index. So,
really testing is important part of this
equation here.
>> Amazing. You had a question here, right?
Perfect. And then I'm seeing we're back.
>> Uh, Dr. Patrick, thank you. Excellent,
excellent presentation. What do you make
of the recent three recent FARE papers
that all showed better avoided risk from
things like um early onset dementia, uh
anxiety, depression, lifetime history
with the nondha
component and the uh the the other
omega-3 in plasma?
>> You're talking about EPA?
Well, the the the studies found um that
the sum of ALA, EPA, and DPA had better
avoided risk for those um for those
eventualities than the DHA component,
which ties most heavily to the omega-3
index.
>> Um I haven't seen that study, but I mean
I've I've seen a lot of other studies
showing that DHA and EPA are very very
important. I mean, in terms of their
metabolites as well. So, I'll have to
look that study up.
I had a couple questions up here. Yes,
you've been waiting. Thank you.
>> Thank you so much. I have a question. I
really love eating seafood, but
considering all the impurities in the
seafood these days, like the
microplastics, heavy metals,
antibiotics, do you think it's still
worth eating seafood for omega-3s or
should we just take the supplements? And
are those supplements tested for heavy
metals and microplastics? And question
number two, would you have time to come
on my podcast in Australia to talk about
this more in detail? It's online. Um, so
the question is like, do do I think it's
safe to eat seafood? I eat salmon like
two or three times a week. Very small 4
ounce piece wild Alaskan salmon. Um, I,
you know, it it does have the the lowest
amount of of mercury contamination, but
you know, the microplastics are a
concern. I will say this about
microplastics, they do accumulate in the
intestines. And so eating like shellfish
or fish that have the full intact or
like a sardine, like the full sardine,
that's the worst thing you can do
because if if you're eating the intact
digestive tract, that's where all the
microplasters are accumulating. So, but
there's still probably some in the
muscle flesh of the of the salmon. I
still think it's healthy. There's so
many studies out there showing that
salmon is correlated, you know, eating
salmon is correlated with so many health
benefits. So, at the end of the day,
even with the contaminants, in fact,
there was a study, you remember that,
you know, that you're probably too
young, but like for a long time, um,
OBGYNS were recommending pregnant women
to not eat fish because of the
contaminants and the mercury and how it
was going to have a negative effect on,
you know, brain development in in in
udo. And so all these women stopped
eating fish and it was really terrible
because that was like their only source
of omega-3. And it turns out that um
newer studies have come out since then
that show that even women eating a lot
of fish in fact um the omega-3 fatty
acids were protecting against the
mercury toxicity. And there was even one
study that was published a few years ago
that showed higher levels of mercury
which was indicative of higher omega-3
intake because people that were taking
in fish had higher mercury actually was
a biioarker for intelligence and they
and the children had higher um
intelligence quotient scores. So IQ
scores if they had higher mercury not
because mercury is improving brain
function but because they were getting
omega-3 fatty acids. So in other words,
obviously, and this is kind of why I
want people to think about food in a
way. I want them to think about food not
so much about what you have to avoid,
but what you need. And you need
omega-3s, and they are so powerful. So,
I do a combination of both because I
still am not able to get my omega-3
index up to where it needs to be with
just eating salmon.
Just a quick follow on because she asked
my qu half of my question. Uh between
farmraised and wild caught besides the
detriments of uh contamination. Is that
from a strictly omega-3 perspective? Is
there one that's preferred or like get
it in however you can?
>> Yeah. Um, it's it's an interesting
question because, you know, it depends
on like some of the farm-raised sa
salmon, they're not eating the right
foods that normal salmon are eating in
the wild. So, a big a big part of that
would be like the little um the little
tiny fish that have aanthin in it.
Aanthin is a carotenoid that gives
salmon its pink color and it's also very
beneficial as well. So in in the
farmraised salmon, they're feeding them
other I hate to say maybe even corn um
stuff like it's not really great. Uh and
so they have to inject the salmon with
actual an asisanthin and they do that
like farmra salmon or they're basically
albino.
So, you know, there's a little bit of
like, well, there might be a higher
omega6 ratio in those types of salmon,
but the omega-3, as long as there's
enough omega-3 there, it's probably
fine. And I used to I've changed my mind
somewhat on this. I used to kind of been
like, oh, only wild, like don't don't do
the farm. And then some newer studies
have come out showing that farm salmon
raise like raises omega-3 fatty acid
levels like just as good in some cases.
So, um, don't sweat it too much.
>> Yeah, I I definitely eat it when I'm
out. I know at the restaurants it's
probably farmed, right? So, I eat wild
at home. When I'm out at a restaurant,
I'll do the farmed and I'm not like
dying over it, you know?
>> Yeah.
>> This is my 13th expo, and I have to tell
you, this is my favorite talk I've ever
done. So, thank you.
>> That's amazing.
>> Um, can you speak to the omega-3 content
of canned fish?
>> Sure. Um, it depends on the kind of
fish. I would say that there are
sardines that are very high in omega-3.
In fact, I mean, I can't there was I
used to eat sardines that had like 500
milligrams of DHA in them, which is
pretty high. The only um I think now is
the microplastics. They have to be like
the sliced sardines. I don't want to eat
the whole digestive tract. And then
there's the canned aspect. I think tin
cans don't they're not lined with
plastic so there shouldn't be as many
plastics leeching into them but I do
think they're again a good source and
I'm not as concerned about their mercury
because if if if a developing fetus
which is very very sensitive to mercury
way more sensitive than we are as adults
if they're okay and protected by the
omega-3 fatty acids I feel a lot better
about eating some some sardines and
getting some mercury in
Hey, uh, right here. Thank you so much
for being here. Thanks for Found My
Fitness, your recipes, all the tools
that you have on your websites and
everything. Um, I'm actually a fish
farmer, uh, an aquaponic farmer, so
raising fish to produce plants. Um,
um, so yeah, in an environment that's
recirculating with no heavy metals, no
microplastics, things like that, and
where we can actually tailor the diets,
add supplements to the diets, things
like that. I was curious if but you kind
of answered it if you have an opinion on
that but um on from that do you see
market shifts or uh potential products
coming from microbial sources whether
it's um you know bacteras being able to
generate these things or if you have
>> yeah I'm excited about all that research
that you know we can I some people are
really scared of genetic engineering I'm
not one of those people I mean it
depends on the context right but when it
comes to you know generating omega-3 in
a more sustainable way I'm very excited
about that possibility. I think we will
eventually head there actually quite
soon.
>> Yeah.
>> But I have a question for you.
>> Sure.
>> Um, have you seen any studies that have
compared microplastic levels in farmed
raised fish versus wild fish? Has that
been done yet?
>> Studies? Not necessarily. I'm part of
the aquaponics association. We're a
multinational aquaponics focused
association. Um, I've got colleagues at
universities and small farms, large
farms. It's something that we talk
about, but the way that we design our
systems is with generally PVC pipes and
then um
>> I'm trying to remember the acronym for
the the plastics used for the tanks, but
it's all food safe plastics. Um so
generally we like to think that our
microplastics are a lot lower.
>> The only inputs are filtered water, the
feed, and the supplements, calcium
carbonates, and things like that. So
>> I'm going to look that up when I'm done.
Yeah. Thank you so much. All right, we
actually have to slowly well quickly
actually leave this room. We have one
one last one I'll ask on your behalf.
When's the best time to take your
omega-3 supplements as our grand finale?
>> I think the best time to take them is
when you're going to consistently form a
habit to take them. And don't worry
about like I Yeah, it it really is the
day because like there's studies showing
that if you take an omega-3 fatty acid,
these SPM molecules, they're resolving
inflammation stay in your stay in
circulation for 24 hours. So, you're
good. You're covered today. So much Dr.
Rhonda Patrick.