Welcome to The Wellness Transcription Podcast, the podcast that combines the power of Christian
values with evidence based nutrition, fitness, and lifestyle content. I'm your host,
doctor Patrick Early. Join me each week as we explore the intersections of
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God calls us to live. All right, guys, thank you for coming
back to another episode of the Wall This Transcription Podcast. It's been a while.
I've had to revamp some things and restart something, but I have a
returning guest where I You're the first returning guest on the show, So thanks
for being Thank you guys. I think it was episode two that we put
out, or two or three actually, where I think me and Ryan were
doing a real deep dive on cholesterol and what all that looks like. And
today I think we're going to talk about an area that your healthcare provider most
likely hasn't talked to you about yet, and that's not only just your typical
cholesterol out to what we're going to be talking about the risks and all that
associated with something that's called remnant cholesterol. So if that's a new term for
you guys, this is something that I think you'll find pretty beneficial. Me
and Ryan work pretty well together in the s field that we're trying to really
figure out a better way to educate people about all the pieces of all this
works together. So with that being said, Ryan, I appreciate you being
here. Thank you for taking time out of your data to chat with me,
and you know I can talk to you for hours, So I just
appreciate you being here and being so willing to help educate people about stuff that's
so important. Yeah, well thanks for having me. Pat. You know
how much Patrick, you know how much I love to educate, So just
whenever you're right into it. So right, this was something that I wasn't
very familiar with as a healthcare wrider. Now I have a little bit more
extensive training and nutrition and other things. I've heard of these words before,
but in practice, I just don't really see it very often. So that's
this concept of really focusing on remnant cholesterol, and even if your cholesterol labs
are good, so to speak, that you may not necessarily be out of
the woods as far as risk goes. For the audience listening, If you
go to your doctor's office and you get your typical cholesterol panal checked, you're
looking at your total cholesterol HDL, LDL and maybe treeglycerides. That's about it.
And your doctor will either say it's good or bad, and if it's
bad, typically what they'll do is they'll start what's called a statin medication that
he would pick up from someone like me at a pharmacy, and then we
go from there. Usually it you're usually ormostatic for a long period of time
and then depending on how lads go depends on if you go up or down
in dose. But remnant cholesterol is not something that's rarely ever checked, but
it can be easily calculated, as me and right are going to go into
details about it. So, Ryan, what can you tell us just in
generally what remnant cholesterol ends and why we should be concerned about it. What's
the literature say, because it's something that's kind of hitting this hitten capturing researchers
and clinicians attention as far as stuff to put to pay attention for. Yeah,
Patrick, For me, as a practitioners well licensed pharmacists, we know
that we focus on LDL and specifically statins, and study after study has shown
the benefit of statins in certain individuals. And what I mean by certain individuals
is that there was a landmark study published in two thousand and none where the
investigators looked at several hundred thousand events cardiovascular events across the nation, and what
they were looking at was how many of those folks had lipid panels, and
they found that there were a little over one hundred thousand of those folks had
lipid panels. And what stood out to them is that literally seventy five percent
of those with cardiovascular events had quote normal or target this is a better way
to put it, target at LDL levels. So it really started this conversation
or really I guess it added momentum to this conversation around Okay, if LDL
lowering represents twenty to thirty percent and pick your number, but it's still a
minority of the overall risks. What are the other factors that come into play
when you're trying to assess your risk factors. We're going to stay in the
lipid space. We're not going to talk today about about really interesting information markers.
Right, we were familiar with reactive protein. We'll maybe leave that for
another day. We'll stay in the lipid space, and specifically, what other
information can we glean from a typical lipid panel and move off of an LDL
sort of centric interpretation of the panels. And so if we take a step
back and we say total cholesterol, what does total cholesterol represent? We know
that total cholesterol obviously a component of that is ld and most of your listeners
are familiar with what we'll call the LDL, right, the bad cholesterol,
the villain, if you will. And then we know that HDL is the
so called good cholesterol. So now you've got total cholesterol, which is comprised
of LDL plus HDL. But there's a third component of that total cholesterol that
receives stray little airtime, if you will, outside the research the clinical research
community, and that are the triglyceride rich remnant proteins okay, blip it proteins.
So basically, the measure the difference between total cholesterol LDL and HDL are
the so called VLDLs. These VLDLs, again, as I said, carry
a lot of our triglycerides, such that if we compare VLDL levels to triglyceride
direct cognasurement, they're pretty close. There's an association, not a strict association.
There are differences, but there's a really good correlation. And so what
this VLDL is triglyceride carrying cholesterol component has become known as one name is remnant
cholesterol. Those have been a lot of research around what contribution is remnant cholesterol
to that residual risk, and so the research is showing that it actually contributes
highly to the residual risk related to cardiovascular events. And so this is important
because now it starts to raise sort of this idea about Okay, since they
are triglyceride carrying, it brings triglycerides back into the mix in terms of discussion
about residual risks. We'll come back that. But first to your listeners,
say, okay, it's a real simple number to calculate. So I have
my total cholesterol that's equal to my LDO plus my HDL plus my remnant cholesterol
or VLDL these triglyceride carrying rocks. So it's really that simple. If I
know my total cholesterol, I can subtract my OLDO, I can track my
HDL, and the leftover. The remaining the residual is that remnant cholesterol VLDL
triglyceride carry So that's where a lot of research is focusing now on remnant cl
lestrol. That's how to calculate. That's why it's important in terms of the
residual. I think, yeah. A couple important points that I like to
make is there's it's a big part of the equation which going back to that
study you first alluded to where they looked at over one hundred thousand patients and
the rates of risk and events that were going on. It says before admission.
I'm looking at the paper now, it says that only twenty one percent
of patients had received some form of lipid lowering medication before they were admitted for
the event. That's important too, is those labs may look fine, and
a doctor may go, you don't need a statin, or you don't need
something right now. Just lifestyle changes things like that, you'll be fine.
Well from a patient perspective, you hear okay, I mean doctor said,
I'm good, I'm not at risk for an event, when in reality you
still could be. You just don't really know. Another thing is that was
done in two thousand and nine, so I'd be hard pressed to think if
you repeated that study now that those numbers would probably be higher. I think
the statin rate is pretty standard now. However, there are a lot of
side effects that statins do bring about that. It's definitely an impact compliance as
far as that goes. And again that statin may get that LDL quote bad
cholesterol in range, but that doesn't if you're not looking at the other pieces
of the puzzle like you're talking about, we're not looking at remnant chosterol.
We're not really factoring in the impact trogly rides have in that whole process,
where just we might be missing a big piece of the puzzle as far as
getting all that in check goes. So, I mean, here's another part.
It says almost half the LDL levels we're less than one hundred milligrams per
desolator. More than half the patients have in minsioned HDL levels less than forty
whereas less than ten percent have HDL levels greater than sixty. What that means
LDL looks okay. HDL is in the majority of patients more than half,
where subpar forty is for female. I minimum would like it to be forty
five to fifty, probably higher if you can or females. Males can get
away with a little bit less, so forty five or higher for them is
usually okay. But that's one part of the pharmacological piece of at all is
there's really not anything available behind the counter, like prescription wise or even over
the counter that really affects HGL to any degree. The only thing that was
used clinically for a long time was diacin that did actually impact HBL levels a
good bit, but you had to take very high doses of it. And
I can tell you as someone who's taking too many B vitamins that once before
that it is not fun. I was driving home from or I was driving
to work at the pharmacy when I was in pharmacy school, and I had
taken my settlements that morning, and I'd forgotten I was doing something else,
so I took my settlements again. And normally that's not a problem, doeshn't
to worry about. But I'm driving to work and it's like a cold December
day and I'm like, yeah, I'm warm. What is happening? Like,
I don't this doesn't feel right this. I'm like, I'm this is
not good. I look in my rear view. I look in my mirror,
and I am I look like a lobster, like I am here reared
everywhere, and I'm like, that's not good. Maybe I'm like, you
know, something's wrong. Oh no, I took too much of my niosin,
like too much of my bee vitamins that I sense was causing this flushing.
I got to work and to my boss goes, do you go to
the beach this weekend? And to just stay there. So it's it's interesting
because you can still use high to his knives and there's a prescription, but
again, it's so rough on the system that a lot of times doctors are
like, patients aren't gonna stick with this. So there's really as far as
getting HDL up, they just say eat more fatty fish and kind of keep
your you know, exercise and all that and check and it might go up.
But that's a whole other piece of the puzzle too. I just thought
that was interesting about that study because it's it's really startling when you think about
it, because I mean, if your level can be that good and you
still have events, I mean you're talking about just about everybody at that point,
is it risk for those things? Yeah, So I think it's really
important to understand the man and how to calculate the vel. Also, to
your listeners, I'll use VLDL and rhymnet cholesterol interchangeably. I point that out
because technically remnant cholesterol is your VLDL the intermediate ditity so ideal, but I
think your listeners need to know that as well. So I am fluedging a
little bit lumping in IDL and VLDL, but so your readers know that.
But that's important because for two reasons. One is VLDL when it interacts with
HDL. We'll talk about that in a minute. To offload a lot of
the bad lippets. As it decreases in size, the VLDL, then that's
what becomes the LDL. So said differently, VLDL through interaction with HDL is
turned into LDL. And so that's important for two reasons. Is if you
talk about LDL, we know that they're really two proponents to that LDL.
There's one that's non genetically determined and one that's genetic determined. So you'll hear
patients when practitioners talk about at L little age. But basically, that's your
portion of LDL that is bound to another lip of protein app of protein eight
and it's genetically to move for the most part, and so it doesn't appear
that SI statins impact that portion of LDL to any great extent. So I
always like to give patients rationale its like you may be on a high those
statin and you still have this stubbornly high LDL. It could be that you
have that genetic component of LDL that just remains stubbornly high. So keep that
in mind as you're talking about LDL. And where LDL comes from ultimately comes
from VLDL remnant cholesterol. Okay, So the other part of that in terms
of relationships is we know that remnant cholesterol is in balance with your HDL.
Do they interact? So another words of the LDL, it's carrying those triglycerides,
it's carrying that free cholesterol, and so through interacting with HDL VLDL all
floats, does triglycerides st HDL, it all floads that free cholesterol to HDL,
and so that's the other reason why you want to have higher HDL levels.
You've got to have us think, right, those clesterol and triblysterride molecules
from vldal ideally go to HDL. So if you look at numbers, typically
what you'll see as an inverse relationship. If you have high rimnict cholesterol,
you'll have low HDL, and vice versa. These are generalizations, but if
you're just looking at your numbers, and that makes sense because HDL is that
sync for those triblycerides and free cholesterol that are coming from the remnant cholesterol.
So that's the other really important reason to understand what that remnant cholesterol number is.
And then in relation to your HDL, it gives you some idea of
how well you're clearing not only clearing your clysterides, we're not, but what's
the source to those triglyrods. Then you get into the next step, which
is really Okay, if I have hot rimnedy cholesterol and I have low HDL,
what options do I have? And I think that's where I think your
listeners might be interested to say, Okay, First, where do those vo
deals come from? And why might I have an overload of those veils.
I'll make two important points because I would say, I want to say it's
around twenty percent of the cholesterol and is impacted by diets. So that's what's
called exogenous cholesterol. So you've got you eat something with that at it it
gets broken down, it's terified and then bile, and then it gets absorbed
by things called kylum microns. Colum Microns transport those across the intestinal barrier into
the liver, where they're then packaged and done. So that that is so
if people say, oh, you know, my doctor said that in order
to get my cholesterol down, I have to eat you know, less eggs
or less cholesterol rich foods and vice versa, you're all that stuff might be
okay to do. I don't cast you. Reducing it doesn't make much of
a difference in my opinion, if you eat foods that are hiring cholesterol.
There's a lot of healthier foods that are, it really doesn't move the needle
there as much. So that's an important piece to keep in mind is what
we're really talking about with these risk factors is more of a dodgenous production of
cholesterol, which is your liver. One of your liver's primary jobs is the
production and packaging of these things. An important thing. You mentioned ideal earlier
too, and it's important for people to go, Okay, well, let's
say I coloculated my remnant, but I don't know what my ideal is.
Ideals intermediate for a reason, it's halfleck. This is very short. It
gets quickly converted to BLDL pretty fast. Yeah, or yeah ldld quickly,
like both. It's a fast process. So it's really even if you were
to able to measure it, it's like it's not necessarily very useful because it's
so hard to kind of catch. You'd have to get the live measure stuff
really quickly. But yeah, I think for most people on statins, again,
if we're only looking at one piece of the puzzle, we're just for
missing things. And then again it's what else can you do to kind of
affect the other things? Because the reason HDL is oftentimes referred to as good
cholesterol or it's very it helps a lot with reverse cholesterol transport, which is
what you mentioned, but without saying reverse cholesterol transport. It helps take that
cholestero back up, send it back to the liver where it's recycled and reused.
But again, if your HDL is low, we're dumping off more l
el in cholesterol rich things than we are actually recycling it back, and then
your triglysrids go up. And it's always kind of this vicious cycle. So
thank you for eloquently explaining that one. But those are those are some things
that are important to keep in mind to that. Yeah, so what do
you want to do as a patient. As a healthcare practitioners, you know
that statins are in your armamentarium for lowering YELD. Great, it's if they
work in your patients used, right, it's you know best in your patient.
I think the other piece where we're bringing up here these residual risk factors
is okay, how do we reduce remnant cholesterol and how do we increase our
HDL? And so we said they're related, so you can impact both in
a decrease VLDAL increase HDL and have an added potential synergistic effect. And so
the other part of that is when those VLDLs via IDL are converted to LDL,
recognize that removes the triglycerides. In other words, ldl's not carry triglycerides
l els, right, And that's the process of going from vld old id
old lios. So that's the other remnant cholesterol is that triglyceride carrying component lip
protein LDL is not. So that's the other reason to focus on those triglycerides.
And you appropriately pointed out those triglycerides are full initially in the liver.
And we can talk for three podcasts about how triglycerides excess triglytrides get into the
liver, but whether say that for another day. But the bottom line is
to be able to impact rhymnic cholesterol, you've got to be able to impact
synthesis of these remnant cholesterol, these VLDL molecules in the liver. And this
is where it gets really fascinating, Patrick, because we really don't talk about
this in pharmacy school, medical school, pharmacolleague, pharmacology in general. Excuse
me it. For me, it's most exciting because the first is the debt.
Okay, if you're going to reduce VLDL, what's the literal first step
in the liver. The first step begins with april lipoprotein B one hundred synthesis.
So for the nerd listeners like myself that you have today, right,
it's called apo B one hundred simply because because it uses one hundred percent of
the amino acids in the gene for an apole B. That's what it's called
OB one hundred. It's one of the largest proteins in the bodies, like
over forty five hundred amino acids. One hundred just means that when you synthesize
VLDL and you create that first step april B one hundred, it's using every
one of those amino acids. But that's important to distinguish because if you the
first part of the translating that april B one hundred in the hepatocyte, it
only uses the first one hundred or so amino acids to begin the process.
While that's important is if you look at the lipid composition of that april B
one hundred beginning there in that patasite, it is seventy percent phosphatidocholiines. It
only has twelve molecules a triblys ride, It only has six molecule us A
cholesterol. It has fifty molecules of phosphatidal colines. And so step one in
synthesizing triglyceride rich VLDL that are ultimately secreted into the bloodstream is comprised of phosphatidal
colines. And so you've got to really understand how phosphacidal colines play into that
synthesis. Okay, so that's where my interest is. As you know,
Patrick, it says, all right, it's not just phosphatidal colines, because
they're literally thousands of different species of phosphidal colides that are produced by the liver.
What's fascinating to me is this the right ratio of polyensaturated fatty acid as
well as saturated fatty acid containing phosphidal colies. If you get a disruption in
that balance, what happens is that April B one hundred is degraded. It
never gets converted, goes to the next step where now you start piling on
the triglycerides, and you start piling on the cholesterols, and the cholesterol esters
and it matures and then it is secreted. And so if you mess up
that first step with those spospitive coalings, then it degrades. Guess what happens.
That means those triglycerides stay in the liver, that cholesterol stays in the
liver. But I know what that means. That's the big BA de liver
disease, right, those lipid droplets, and so you don't get those phosphatidal
colings right on the front end, you don't get efficient synthesis of VLDLs,
you don't get efficient secretion of triglycerides lipids from the liver, and you don't
get them out there in the plasma where they can interact with HDL molecules and
thereby strip them of their triglycerides of pre cholesterol. That's what HDO does.
So that's component one why those spostatidal coling molecules and metabolism in particular are so
critical. But there's a second piece. So that's how I just now,
it impacts the VLDL side of the VLDL rhymnic chlesterol HDLs, But how does
it affect HDL it self? And we know that there's certain polysaturated fatty acid
containing phosphat of colines that promote HDL synthesis. Said differently, if you have
the right mixture including polynsaturated fatty acids EPA and DHA in particular. Then you
promote synthesis of HDL in the plasma through interaction with the enzyme l cat or
lesser than cholesterol acetyl transformational can. So now you start to see if rhemnic,
cholesterol and HDL are critical and they relate with each other. Right,
one offlow strip glyceritis three cholesterol, the others in exchange for cholesterol esters.
Right, that's what's answered back to VLDL. If you look at phosphide of
colines, it impacts that GLDL synthesis and secretions. It impacts the HDL,
So it tends to decrease VLDL rhymnic chlesterol and the increase HDL. That's where
we are now in terms of the conversation as as far as a new mechanism,
No one to my knowledge besides us, are talking about that as the
mechanism. Now what are we talking about. We're talking about high dose synthetic
EPA for triglycerides in patients that are have high triglycerides that aren't impacted by statins.
I don't know if you saw a couple of weeks ago the EMA Medical
Association, thank you, they came out and stated strongly that looking at the
evidence in Toto that you should really watch your patients that are taking high dose
EPA for triglycerides for increased instance of a fit. Right, they said it
is causing. So in other words, if you look back at all the
meta analyses, if you're above one grand per day of EPA, your risk
of aphibs starts to increase. For every grand per day. Above wearing one
grand per day, you get about a ten percent increase in risk. So
that when you get up to four grams per day, which was the reduce
it tron, you see an increase in aphib risk of almost fifty percent.
And so now you start to say, well, okay, we really don't
have a lot of great options. You talked about NIS and when I say
options, options are treating high triblycerides. And now you know why that's important
rin the cholesterols in the contact, particularly of low HDL. And so if
we don't have a lot of options, we do a vibration. Again,
I don't, I don't. I'm sorry to interrupt, but I don't see
a lot as a pharmacist, and I view a lot of pharmacy stuff.
Let's be honest, I feel a lot of restrictions and a lot of different
age grips and patient demographics, so I see kind of what's archaeting, what's
up? I rarely see fit of five rates used anymore. Now is does
that mean it's not used more frequently? No, But however it I just
don't see it. They also come with side effects too that are pretty rough.
They are kind of hard on the liver a little bit, and they
do they have their own citizen. Again, no drug is without side effects.
So if you're stacking a stat and have been a fibrite together, you
know you can. Depending on which ones they are, you may be helping
yourself from a blood worker perspective, but if you're causing, if you're increasing
the likelihood for them to see adverse effects, I'm just not going to be
compliant with it. And then we're back to squore one. It's a whole
other important thing that I want to interject one one more time, and I'll
let you get back to go because it's fascinating to me because, like you
said, no one's talking about this, because no one really understands what's going
on. I read a book a long time ago and I'm pretty sure.
Yeah, it was one of the fasting books I remember. I think it
was doctor Fun's fasting book I read two years ago, and he made an
offhand comment in the book that just didn't It stuck with me, but I
don't know why I remember it. And he was talking about how you know,
when you eat too much you have insular resistance, Like all these bats
get have to get deposited in different tissues, so that's when then they go
deliver first. And it's like, that's what causes fat de liberties. In
my head of it's that's not that simple, Like it's not just that part.
Now that may play in for sure, because a lot of times in
diabetics we see insular resistance and all these other issues, we're also going to
see cholesterol issues and those go hand and hand. However, your mechanism and
what I'm hearing, what we've talked about for hours off my off recording,
is this seems to make more sense from a mechanistic standpoint of why we're seeing
the fatt delivered disease rates. We're seeing why these things are going up because
they're all everything. It's important to remember everything in the body is tied together,
so as clinicians that they could for in pharmacy school, we oftentimes tend
to compartmentalize certain areas, so it'll be like we're talking about cholesterol. We
know that affects diabetes and stuff, but then we're talking about other things.
So AFM is never brought up as far as I'm concerned with, like cholesterol
and synthes works in the system and if you get one of these off or
others are just kind of compounds. But that's really important that you mentioned that,
because I think, go ahead, yeah, well I'll pick up there
right where you tee it up. So right, doctor Phong nephrologists, Canadian
nefrogs right, big believer Internet facing us. But I remember quickly the books
called a Unity Code, that really fascinating ideas about how you change fatty acid
metabolism in the liver. And I think that's a really important point here because
it ties into what we're talking about. So again, regardless of how you
get fatty acids formed, whether it's coming from the adipocide right breakdown and fatty
acids are transporting pre fatty acid training by transported back delivered, or we're talking
about fruptosu blue coals that through donovol lypogenesis are forming these fatty acid and then
combining them with glycerl molecules. Right, we know that those fatty acids combined
with glycols to form monoase oft prize for glycrool. But why I painstakingly go
through that step by step is at the stage of diaso glycol the disoglyceol has
at least two pathways, two primary pathways it can take. It can have
an additional fatty acid attached and turn into a triasy glycol right triblyceride. But
what most people don't talk about is that diaso glyceraol is also a precursor for
phosphatidyl coline synthesis. And so if you have properly operating phosphatidical coline synthesis,
it's consuming a number of those diaso glyceride molecules that are produced in the liver.
Said differently, those diasoglyceride molecules that are going into five through the coalings
are not going into triblycerize and vice versa. And so that's yet another reason
in link between proper phosphattic coaling metabolism and fat production and deposition in the liver.
So the idea is this, if you can figure out how to positively
impact phosphitic coaling metabolism, you can potentially impact remnant cholesterol and HDL and all
the downstream things that are related. Things pathophysiologies that are related that we know
about and that we don't know about that are we're just starting to appreciate and
some of the things we're seeing anecdotally in the patients that are taking this supplement
that's been developed by my group over the last few years. And so it's
a unique mechanism. It focuses solely, not primarily, It focuses solely on
the nutritional deficiencies that we see in patients that impact plastord to colding metabolism completely
natural it will. Therefore, I think that's why we're seeing some of the
really cool results that we're seeing in patience when it comes to alterations in lipid
pms. Yeah, it's very important. Yeah, there's a piece that no
one's talking about, and the fact that we that you've developed a potential answer
to that. I mean, it's I've seen it work. It's very important.
I just it's my mind can go on all sorts of different things.
I'm looking at this. Yeah, I mean there's really never been an answer
to how do we get those ratios correct? You know, normally, And
when I mentioned this before on the last podcast I had you one, normally
they'll go, okay, well, EPA and DHA, we know we're good
and the racious for what high quality officials instead of so let's do that,
let's exercise, let's do some other things, and you're kind of hoping at
that point. You don't really know how all that gets utilized. And I
think that's so important. Where the Sessamon component comes in is because I was
looking I was just curious. I was looking into a lot of the studies
just thought of sesame oil in general and their effects on cardio metabolic risk factors
and things like that. In time. Again, in all the papers,
you see LDO goes down, HDO goes up, Tragosa reds drop like it's
over it up. You see in multiple systematic reviews it's like people who utilize
this and have this as a mainstay of their diet, that there is marketing
provements. And then every study that I saw says they need to figure out
mechanistically how this is going on and why this is happening, because it just
it looks good, but we just don't know why. And I think that's
you've kind of really teased that out, I think, and it's been it's
that missing piece because a lot of times when people see these changes happening in
the liver and metabolism, they tend to oversimplify what's actually going on. And
to my knowledge, I never heard of it before getting involved with you and
talking about this and kind of getting into the weeds. I have never heard
of fosphitooch coolon being a part of that to any great degree. Only on
the handful of podcast as that mentioned, but it's never the mainstay of the
conversation. So I think that's really it's well, it's interesting, Patrick,
because it's like anything else. The literature is out there. There are some
brilliant biochemists who have worked out VLDL synthesis and the role of phosphit of coolies,
the role of the ratio poster doth that all means a hospital coli,
the role of triglycerides, etc. The are brilliant biochemists have worked out how
sostitial colines impact the HDLs. But that's been sort of in your silos where
that's what you're funded to do as a researcher, and you does some really
interesting works, but no one to my knowledge, at least outwardly and in
podcasts like this, is talking about how you call all that information together to
provide a potential I keep emphasizing potential solution for patients. And I was in
the military for a number of years and one of my favorite things that had
a boss that always told me said, pedosciates, don't come to me with
a problem, and you have a solution. And so a lot of people
have problems. But it's frustrating as a practitioner if you know there's seventy five
percent residual cardiovascular risk, but you don't have anything to tell patients. And
I'm not suggesting for one second that this supplement of the UREAU or treatment mitigation
whatever. Would never say that, But what I would say is it begins
to address the nutritional deficiencies. And by definition, right in the course with
the SHA dietary c health education now is a supplement to diet which can positively
impact fostered or coding metabolism and thus through mechanisms that are completely I don't say
complete, you're never perpleleg but are really well characterized, will have an impact
on these different lipid parameters. These are known pathways. You just have to
be able to impact them in a positive way without causing horn. And when
we take the reductionist approach of everything is sort of a pharma. It's a
one size fits all. Its EPA is really good, and now we're going
to give you four grams per day of synthetic EPA, right extroversion, then
that's going to be even better. Well, the data are clear and the
EMA is spoken, and cardiologists in the world is spokens. That's not okay.
There are side of that. So when you take the reductionist approach,
so why don't we do what nature does, take a step back and say,
this is a systems pharmacology. This is a multifactorial process. I don't
need to shove four grams of EPA into somebody to ECHI is that I need
to have some a way to impact piland saturated fat as metabolism step once,
and then those downstream events that augment that proper diet. And believe me,
I'm not here even advocating taking official suppment. I'm here advocating eat your fatty's
ish once a week twice. What are I think the average recommendation from the
USDA, the food organizations here as well as an em A and all that
stuff. I want to say it's minimum two a week, if you can
ideally three two to three. It seems to be the sweet spot. Now
again, if you eat every if you're piscatarian and that's the only meat,
so yeah, that's fine. Yeah, I guess my point is that it's
yes, it always starts with eat right and exercise, but in this case
it stop there because that's what's the frustrating things for patients sometimes is that's difficult
to understand what it means right, eat right, and exercise. Does it?
It's gonna gives you nothing to go off of. So yeah, if
you can give your liver the dietary ingredients it needs to process those proper dietary
inputs, those essential fatty acids, to me, that's a much better approach
than inhibiting. I mean, I've been in drug discovery for over twenty something
years and the most common approach is something is going to right. Let inhibit
a basic process, whether it's beta block. I mean again, I'm not
cast throwing shade though those are important, but it's always block a process as
opposed to how do we augmit what we know to be a beneficial process to
attack not the symptom, but rather the ultimate cause for on pats of physiology,
And that's what my you know, I'm actually as a big proponent here.
How do we augment what people are doing from a prescription and dietary standpoint
to achieve an even better There was a point you made earlier about study with
a FIB and EPA risk and stuff, and it's like, okay, let's
say, I mean, if that's well established in a load tried I think
I went through that paper you sent me on that one. That's very a
very interesting link. I would have you know, a normal practitioner would have
never thought about that as being an issue. But obviously there's pattern there,
and if there's enough people saying this is causative, then there's good data to
back it up. However, if you were doing that, let's say you
had an imbalance there of fallen centric botty acids and metabolism and stuff, and
we've now progressed into an aphib situation. From a pharmacological standpoint, as a
pharmacist, there's only really conductive medications or beta blockers that can help with that.
You're looking at your medications like amiodorones, paphnoones like other things for different
aphibs and beta blockers, and that's about it. Like they only touched the
circuitry part of the cardiovascular issue that they have because they need to get that
under control immediately. But as far as looking at the liver side of things,
that's just not done, at least in a hospital setting, and I
don't think that's something that they need to look at. I think that's something
from a primary care of pharmacists standpoint, like, Hey, this is what
my labs look like. What could I do to impact these to minimize even
having to go down that route in the future. And all this ties back
into remnant cholesterol risk because it's like if you only go to your doctor,
you know, maybe a year or every six months or something, and you
check everything and he just says, all good, You're gonna keep going about
your business. But if he says, hey, your labs look good,
but your remnant cholesterol is looking a little bit off the ratios off, then
you can then have some additional guidance as to how to control that to further
minimize your risk. Because it's very interesting the papers that you've sent me and
that I've looked at myself, and how all this would impact ASCBD scores because
in the pharmacy world that is the gold standard. What's their ASCBD risk and
then what can we do to minimize it? In pharmacy school, I heard
this one hundred times. Calculate their ASCVD risk score and then what would you
do to you know, decrease the risk. The answer was always this exercise
and lifestyle change and if they're smoking, stop poking. That was the extent.
That was the extent of it. Very rarely until now, I would
have never made the link to oh, well, we've got to make sure
delivers metabolizing polyunsaturated batty acids correctly. You know, those ratios are correct and
we have to have a way to get those in check and provide a solution.
Otherwise you're just diagnosing another problem and saying, well, we'll figure it
out in ten years when the science is there. So I think it's I've
the product that you've developed and stuff with the sessiment and all that and other
in the extra mile, you guys went to make sure we have enough methal
donors in there and make sure we're further facilitating that process and not just throwingame
sessiment at it and seeing in real time how all that plays into effect.
It only solidifies mechanistically that what you're saying makes the most sense. I mean,
it's pretty obvious if when you lay it out the way that it's laid
out, that it works. And again, I'm not saying like you were,
I'm not saying that assessment is going to be the end all be all,
like cured anything. I don't like using the word here because it's not
that term gets thrown around all the time and it's bothersome. But again,
it's having a dietary supplement and nutrition component that you can easily change with minimal
side effects without having to go up on that set and you're already on you
know, it's say, there's just so many implications there. I think it's
just going to make it easier on patience for clients purposes. It's I'm sorry,
I'm rambling, but I think it's very intriguing that we're finally get in
some real answers to these problems that people have been able to diagnose but not
solved for a long time. Or mitigate, I guess is a better word
to say it. And the bottom line is it's not a problem that has
been solved. And so what I'm suggesting through my approach is that we rethink
how we approach these different parameters, again without using these terms, et cetera,
but how do we approach it from a nutritional standpoint? And I think
the other part we want to point out is that there is a rare allergy
to sessan And by allergy, it's written. It's well known enough that the
Food and Drug Administration points that out to people. It just says, hey,
if you have an allergy to sesame, then you shouldn't be using sentime
seed all or you shouldn't be consuming sesame seeds, right, which the old
McDonald's right to all be patty special software n sesame seed buns, right,
So anything specimen. So nothing even in nature, comes without risk. But
as long as you're ware of what that risk is, then you can make
better decisions. And that's what I'm saying with this lipid panel. There's so
much more information baked into that lipid panel that we have to grease out.
I told you offline that I had an individual who is highly trained and has
a medical background who basically said that the lipid panels really wasn't useful in his
practice. And so we've just talked about the sort of counterway to think about
that, and we hope we've given you guys something to think about and go
out and read more. But a lot of what we're talking about has occurred
in the last ten to fifteen years, and that's sort of science and clinical
science. That's the good, the bad, and the ugly. So in
other words, the good news is is we're always living for we're always trying
to improve opponents. The bad is that well that the other good of that
is, well, we'll talk about bad. The bad is things changed very
slow in terms of practice and research. And that's even though it's a bad
thing, it changes slowly. It's actually good because we don't want to be
changing with the win. You don't want to be changing practice guidelines hid in
fifteen, probably even twenty years. But you have to be aware of what
cutting edge somebody it's the same and say, how can I translate that to
my patient? As the fiance catches up with sort of the recommendations and it
becomes and reaffirmed. So let's go back to the a FIB with the EPA.
This was a meta analysis published in the journal Circulation of really High Profiles,
highly respected journal that said that's their conclusion after looking at the reduced trial,
all the other trials and says there's something to this. And for the
EMA to come out and say something, right, that's what I mean by
it takes years to really get something to change practice guidelines. But that doesn't
mean you have to wait or your patience to try things that make kids.
There's an important thing that I think that I want to tease out as and
I think as a patient. Again, it's really hard for me to take
my scientist's credential hat off if I'm thinking like a patient, and this can
be applied just about anything medically. It's like, well, I don't trust
what these experts are telling me because it seems like every ten to twenty years,
like what they said was for sure the way to go is not necessarily
what they end up changing. And I think science is meant to change.
Otherwise it doesn't progress anywhere. So as scientists and you have an expert telling
you, well, I do not know. The evidence isn't there yet,
I'm not sure. That's not then just saying I don't know what you're talking
about. It's that this I can't speak for the solidification of the science because
you never know where it's going to go, and you have to constantly adapt
and change things. Now, as far as treatment guidelines go for as CBD
and things like that in cholesterol, I don't see them changing very frequently.
However, if you can come up with an option nutritionally or from a supplement
area that helps facilitate making those guidelines work better. Because again I'm not saying
that like this product that you've come up with is going to magically get everyone
off their status. That's not how That's not how I see it going.
There's too much of a benefit for statin therapy in patients support disease that you
can help augment to where we're not dealing with just pushing this, just turning
the stat and level from zero to ten and hoping for the best. You're
really helping all the other aspects of this mechanism that aren't being impacted to be
impacted, then you have to use less medication potentially. Again, that's one
of the hard things because people in chylog don't trust. I don't trust the
signist because it feels like there it's always shady. It's what has to That's
why I'm very careful to never speak at absolutes, and you're not like that
either. Very We'll see where this goes. We'll tease this out, but
it's never I hate setting the sites to settle on the topic because as we
continue to grow and learn more, it's never going to be there. Well.
But that's why we put back to statins as a great examples is we
knew for years that they benefit in curtain patients. The studies showed that time
and time again that there is benefit, but it took years to come back
and say there is residual risk. And that's what I keep coming back to.
And it will take us years to really hone in on what's the next
uh SATIN if you will, in terms of reducing that risk. But we
have to be thinking about other markers outside of the LDL sure to cover where
those statins don't provide benefit to patients. And as you pointed out earlier,
there are reasons that I mean, we have to accept as health care practice,
theirs that our patients aren't going to take standard of care for some reasons,
but for reasons that are their own. People. Some people don't want
to take stabs. There may be side effects, it maybe farm the natural
approaches. So I think we have to give patients the options that they want
and provide them at the same time with as much information and education as possible
along with those options, and not just throw things to get to the walls
what sticks. Because at the end of the day, that's why we have
a license to practice, is you have that is a responsibility to those patients
as well, And so I approach it in the pharmacy too. It's like
I'm never gonna I tell this to people all the time. I'm never going
to recommend something to you from a supplement or a nutrition stance. There isn't
backed up by enough science for me to go this might have benefit or it
might not. You know, as a if I got if I knew nothing
about pharmacy and I was just an average normal person walking around and I went
to the doctor sett I need to be on this stat And then I went
to the store and picked it up and they'll say I read the package insert,
which a lot of people read now when I was, you know,
even in a couple of years, I've seen more people reading the package in
and they're like, oh my god, I read the side effect profile,
and that's terrifying. I don't want to be on that. It's like,
okay, well they have to. Legally, they have to put every possible
thing on that package insert that could happen so they don't get sued. That's
basically how it works. They have to tease it out. There's years of
clinical trials, so they have to be as upfront and honest with you with
the information. Does that mean all those bad things are going to happen to
you? Probably not, but side effects do happen, and they're not rare
if they happen to you. I had a professor at pharmacist school always tell
us that he goes, it's not rare if it happens to you, and
I'm like, that's very good way of looking at things. So I think
if there's other answers to have to where patients are like, look, I've
tried satins felt terrible on them. Probably some pharmacogenetic aspect to that, and
that's been well established now too that not many clinicians are aware of or that
pharmacists advocate for, but they if they've tried it, and then there's no
other alternative option B that can help facilitate that. They're just patients are just
gonna get frustrated, like, well, I mean, okay, I want
my cholesterol down so I don't have a stroke or a heart attack, But
I don't like the fact that my legs feel like they're getting hit with baseball.
That's because of this satin and I don't know what to do. It's
like I can't and if I get off them, then my levels shoot way
up. And it's just like they get it's frustrating and it causes a lot
of anxiety and other things along with that, and it allows that sentiment to
be created to where I don't know who has my best interests at heart,
Like I don't know why I'm not getting any benefit there. And to be
far and to be fair and balanced, Patricks, there are those patients that
are perfectly happy with their statings. It's doing exactly what it was supposed to
do. It's lowering their LDL and they're thrilled by their LDL levels, but
they start to recognize again there's some there could be and their specificus is something
that is beyond meaning additive to statins. So you're right, we need to
talk about candidly about those folks that aren't satisfied with statins. But we also
need to talk about candidly those folks that really are pleased with what their statin
is doing, but they're looking for other things to address that residual risk.
And I think we have to have that curturation with patients for sure. Respect
to that too. That is kind of catching fire, especially like social media
and stuff is they'll see there's proponents that kind of go, oh, we
LDL cholesterol is a terrible diagnostic marker for heart disease, like don't pay attention.
It's like, well, you can't say that either, because patients that
are responding really well on statins and their levels are looking really good. Now
you're telling me that the doctors don't know what they're talking about, and then
they shouldn't be looking at that. So there's so many different goals for thought
and again, it always goes back to this who do I trust? Like?
Who? Okay, one guy's telling me that I need to take a
stat and to help my LDL MYL the olds improving. Then I hear another
reputable source, supposedly over here saying that Eliel's dumb, we don't need to
look at it. And then we have someone who you alluded to that goes
to cholesterol labs are not beneficial in my practice. So it's like you get
three different schools of thought there, and the patient's just caught. They're just
spinning out of control and they can't make sense in it. But again,
it's never as easy and as simple as it seems like if you get into
the mechanisms, even further down the rabbit hole where this goes, it's a
bit overwhelming. But the body is complex and overwhelming. So to say that
it's black and white or cut and dry a plus bak, we'll see mechanism.
It's just usually not I try to stay away from that kind of language
because it's just not usedul Now I do I have a couple other questions going
back to Sessimon for you, and then we'll kind of wrap it up a
little bit. How we've talked about how it helps with polyuncentury if iding have
some metalloism, how we get that EPA to DHA ratio of in fostituol colid
rich dha go down the LCAT pathway to help with HDL. We've also talked
about the triglyz red lowing and then the cholesterol remnant lowering piece of that.
However, how exact I know you alluded to this earlier about talking about inflammation
and stuff too, which is another big buzzword thing that I think we'd like
to talk to touch on. Correct me if I'm wrong, But like Sessamon
and the papers I've looked at, it helps with really decreasing or not really
decreasing, but decreasing and balancing our achdonic acid production. And it does that
by is it? I think? Is it the enzyme is a delta five
desaturase that it helps. Yeah, that's what I'm saying. It's an inhibitor
of delta five dsaturase, which basically lowers the amount of omega six conversions.
Correct, Well, let's I think this is I think this is fascinating for
pharmacologists, pharmacists, which as most of your listeners are many of your listeners
are. Is the if you look at pollen saturaated fatty as metabolism, we
know that there are two groups Omega six and omega three, so there is
a single enzyme right in that past. So in other words, is a
multi step process, multi inzomatic process. We metabolize essentral fatty ads as omega
six and omega three. What's really unique about that pathway is these enzymes.
And you pointed out the rate limiting step Delta five to saturates. It has
an omega six input and it also can process an omega three input, so
it's the same enzyme, but it can metabolize either omega six substrate or in
a maja Maga three precursor. That's important, really important when it comes to
sessiment because as you know and as your listeners know, on the omega six
side, the output of that enzyme is the rhachodonic acid. So now we're
in a look at t we're into a cyclop you know, it's all sorts
of pro and anti inflammatory markers. On the omega three side, the output,
the metabolite, if you will, is EPI. Okay, So when
you think about delta five disat raates the rate limiting steck. It kicks out
a rackodonic acid on the omega six side, and it kicks out EPA which
is subsequently converted to DHA and further downstream events. Right, So then it
begs the question, well, how can I inhibit or I mean, it
would not be inhibiting. If I'm inhibiting their enzyme would not be inhibiting racodonic
acid formation in EPA formation simultaneously, So it's a canceling out and the answer
is no. This is what's fascinating about Sessimon. Sessimon appears through mechanistic studies
pharm acology studies in vitro and and vivos to preferentially inhibit the omega six mechanism
of delta five satur rates, meaning it shuts down, not complete, but
minimizes or mitigates a rackotonic acid formation, and we know that's good in the
setting of high racotonic acid, so that can be anti inflammatory, while at
the same time it maintains or potentially enhances the EPA formation subsequent downstream DHA.
So that's how a single molecule in sesame sidol extraction can impact inflammation significantly just
through that single mechanism of action, and then the other those folks interested in
nutrogenomics, we know that there are two types of individuals and it's race based,
and we can go into this in another call or a podcast. You're
either a very rapid metabolizer, right, so let's go back to our P.
Four fifty right, our drug metabolism. Language are a poor metabolizer extensive
metabolism. You're either an extensive metabolizer, meaning you form a lot of a
rackotonic acid in epa And that's the term what your diet is, right,
Mega six versus high and magas three or vice versa. Okay, and there's
another cobortive individuals for genetic reasons, they're slow metabolizers, and so the impact
of a bad diet is less than those individuals. And how that sorts out
from a racial standpoint is that the more from a genealogical standpoint genetic standpoint,
that African origin people have a much higher chance of inheriting a rapid metabolism.
So there have been numerous studies that have said if you heat Omega six and
you have an African descent, then you're forming lots of araconomic aget that's related
to obesity and inflammation in general the non African origin. So now you're talking
about your European Caucasians, they through evolution have acquired a slower form of the
gene, so now they metabolize those EPA and arachdomic acid pre precurasors more slowly,
and the bad the result of a bad diet is manifest less in those
who have slow metabolism. So that starts to raise this interesting conversation around racial
differences. So there is every potential that this approach using cess received extract may
have an impact that is differential or differential impact based upon race. Those are
all sorts of things that can be looked at in the future. Right,
But that's just one step on the inflammation side, and I probably want a
little deeper. That's you know, that's a great way to think about the
nation piece. Uh. Yeah. Inflammation is a big buzzword, very important.
It's one of those things that's like you need, let's be honest,
you need inflammation for things to work, do some other process you want to
completely mitigate or whatever it is. However, but here's the other important thing
for a nutrition standpoint, is destiny seed oil for thousands of years was the
oil of choice. One of reasons, one of the reasons, my main
reason is for stability. It's such a high antioxidant oil that it was much
more stable than less well more stable than those oils that weren't as rich in
antioxidants. And so now you've got this. You know, we talked about
cesciling, you talked about delta fied to saturation and how that can impact inflammation,
but we also know that those antioxidants in this oil and the extract can
also positively impact inflammation. Yeah, and then man, there's so much cool
stuff. And we didn't even get to touch on the postitium component of like
cognition improvement as well as skin improvements too. That's another podcast rabbit Hole,
want to go down on every want to go down in, because that's a
whole other interesting interlude. Like, all these systems are interlinked, so it's
very interesting when you start to tease out why it's doing what it's doing,
different aspects of it all. But yeah, inflammation is a big one that
I think a lot of people and I've talked about information to a little bit
of a degree on some other podcasts. I need to kind of recover it
because I'm generalizing here, but I think it's not a stretch for me to
do this. What people here, especially on social media or other platforms sell
here inflammation they just think it's all inflammation is the same, and it's not.
In case, there's differences between acute and systemic. And what I want
to point out is when you're talking about crp air lucan six, like other
cytokines inflammatory cytokinds that are out there, that is systemic inflammation. And that's
not usually something you see acutely raised unless we're dealing with some other situation sepsis,
other things like that. But when you're talking about chronic inflammation, that's
what most people are referring to. As these systemic blood markers of inflammation that
we see time and time again correlate perfectly with these chronic diseases that we've seen
on the rise. Well, now let's bring these full circle, Patrick,
And there's a fascinating paper that just published I shared with you via text over
the weekend that looks at independent risk markers for ASCVD remnic cholesterol. Near the
top of the list if not the top of the list. An independent but
equally important risk modifier for ASCVD is see reactive protein. So this chronic inflammatory
process, and you distinguish that that's eloquently from acute right where you've got these
pro inflammatory side of kinds in the systemic inflammatory response centers. We're not talking
about that. We're talking about chronic inflammation. We're talking about he reactive protein
CRP, and that is a very important marker of risk that it gains independent
of remnant cholesterols. But what this paper shows is in this very large I
think it was forty thousand plus patient study, is when you can consider those
as independent markers CRP and remnant cholesterol, that really starts to hone in on
what your risk is from an ASCVD standpoint. And that's the fascinating. Yes,
that paper, three thousand patients, I think they like that in that
sea reacting for a team paper. I've got it pulled up, I think
yours, Yeah, thank you. That was similar to the two thousand and
nine paper where they looked at statins and risk and a residual risk. But
yes, the large study is the bottom line, like thousands of people that
looked at CRP and rhymney cholesterol independent highly insignificant terms of predicting ASCVD risk.
Yeah, I think I think we've hit the nail on the head with it.
It's just really cool how it all kind of ties in and works together,
and how you see that really Oh, here we go, I found
it. Here we go. I found out paper. Yeah, you're right,
it's like forty thousand patients. And then I was referring back to the
other one we talked about where it was over one hundred thousand, So started
to get that mixed out there, but still a lot of people right that
it's not just one hundred person trials and CRP. If you go to lab
core for examples, and you look at labport, what panel do they offer
for inflammation? I mean, your father and I run a phase one clinical
center and one of the things we look at is inflammation, and C reactive
protein is what lab poor offers as their general inflammatory marker. So that's a
really solid marker, and it's neat to see that it connects back to ASCVD
risk and connects back to independently connects back to the remnant cholesterol. So I
think that's a great way to sort of think about this one last aside I
want to make because it's another popular thing that's kind of catching win now because
again this is a peo. I feel like for the nutrition world, all
of the world's problems have been thrown in some sort of nutrition camp. Like
for in the nineties, it was like sugar most of the problem, and
then before I would say the two thousands, it was okay, sugar is
the real cause of issues, and then before that with it was hello,
fat diets are the way to go. And now it's kind of the next
one that's kind of catching win is, Oh, it's the seed oils that
are causing all these issues that we cook at it. It's like, I
think if anyone gets anything out of this podcast that we talked about sessamon as
much as we've talked about that, I think maybe the case can be made
that seed oil it's fine and really beneficial. So it's like, again,
I think it's funny, how though, what all the seed oils together.
It's like, you know, it's funny you should say that, Patrick,
because I literally had that question last week. It says, oh, but
I thought this, well, the question was I thought sesame seed oil was
banned, so I dug in a little bit, well, well, because
of reading about seed oils and things like that, and to your point,
we lumping things together. I mean, there's a reason why, to sess
me, seed oil was the primary cooking oil for thousands of years, and
I'm not saying that it's not detrimental in certain sceniar, but it's not something
that science is pointing to as causative for cardiovascular events, and at least from
my reading, I shouldn't state that's so sens aticate. I mean, another
reason that they use sesame oil for the longest time to cook with is because
it's one of the oils to cook with that has the highest smoke point,
so you're less likely to have bubbling. And like if you cook with olive
oil at really high temperatures, its flashes everywhere. It's not fun to deal
with. But I mean, as far as a seed oil or an oil
used for cooking that has a high smoke point but yet actually it has flavor
enhancing properties, selling me oil is like I guess, like four hundred and
ten or something like that. I'm stretching because I had to dive into all
of that when I was doing my master's program. We were talking about oils
and all sorts of stuff. But again it yeah, and I'm a fonatology
not a nutrition right, They've got to be very I'm not a seed oil
expert either, but I think and then it goes back to the education piece
of things, because people will go, oh, they're highly processed. It's
like, okay, a lot of foods that have any sort of packaging or
shelf li for process to a degree. But they'll talk about using from a
seed oil perspective, They'll say, oh, well, you have to use
all these different solvents to extract the seed oils out, and you have to
put them into this these big machines to do all of that expel the oil
out. Okay, Like I think the big the big one now is oh
they use he saye to like get the oil separated. It's like, okay,
well, if the final improduct has zero hexane in it, they have
to get all of it out, so whoop to do? Yeah, you
know, you raise an interesting point. I need to better educate myself on
the pressing versus the use of organics. And I'm not certain, so I'm
not saying one way or the other how sesame seed oil is typically processed,
but my reading is mainly through pretty processing and not use of texting. But
I need that however, I will. I'm pretty sure of the seed oils,
like you have to do less less expeller processing, and you don't have
to do it at higher temperatures. For sesame oil, it's very easy to
coal press sesame oil out. As far as sesame seeds in general, they
have a higher concentration will in them as opposed to say corn or canola oil
or soybean oil that you have to use higher temperature heating to kind of get
in more of the product to get that oil extracted out, whereas olive oil,
peanut I think, and then sesame oil that just there's more oil concentrated
the seed itself, so it's easier to coal press it out. So I
think for sesame oil, I think most of those are coal press, which
most of your olive oil is cold press for that exact reason. So it's
one of the ones that if I'm going to use, I like that one
quite a bit. And again I don't fry foods very much, and I've
never heard of I mean, you can saw tay things and sesame oil,
but I don't think you rise like anything. Yeah, and if you've got
any listeners who really want to read, let me go back to AY Evading
Medicine texts and read about sesame seedel and AYE Evading medicine. There's a ton
of information out there that's it's consistent with what we're seeing anecdotally. It's fast.
Last thing I wanted to mention there's yeah, and we touched on I
don't know if you're I want to pose one question to you because I had
a patient asked me this the other day, literally, yes, Saturday,
she came in and she was asking, she's wanting us to purchase the product
that you've developed that we're that we have in this pharmacy. And she was
asking if there's any risk for lead crimps or anything that you've seen with using
something like sessimon in there. And I didn't nothing that I've come across that
really would make me think about that to any certain degree. But have you
seen that reported anywhere? Because I know in some cell studies that I've found
sessamon does have some hmg CoA reduct tastes inhibiting a properties. So that's kind
of working down that Staton pathway to a degree. Have you seen anything in
there of the you've reported with like leg creeps or anything like that with Sessimon
that because that was something that she asked me about, but I was just
curious across anything like that. So I'd say two things. First, is
ahe am not aware, which does not mean it's not out there, But
I am not aware of any muscle related issues for Sessimon sesame seed oil extract
or using it as a cooking oil. That's it. I will dig in
and see if I can find anything to be more definitive, But I've read
quite a bit about sesame seed a in Sesimon, and I am unaware of
any side effect related to that. And we have had no reports any dotally
but always were but as always right where pharmacants, we always have our ears
open, right, what are some things that are just sort of unexplainable.
But the other thing that I want to leave the listers with is that while
this is natural, it is not a pharmaceutical approach. There's a blurred line
between natural and pharmaceutical, and that blurred line is you're talking about small molecules,
spider chemicals, in this case that interact with processes in the body,
and so for sesame seed oil and specifically for sessimon, which is one of
these actives in sesame cole extract. There is in vitro work, much like
you do for a prescription medication, where you're looking at interactions between a molecule
in cidercrop four fifties, there is evidence that sessimon is able to modulate SIP
to C nine activity, and so the in vitro studies are more abundant than
the in vivo studies. There was one in vivo study done in humans that
did not see an interaction, but like got educated students for twenty something years,
if it can interact, even at the end vitro level, that's why
the FDA mex pharmaceutical companies put that information to packaging. Sir, Then you
as a pharmacist need to be aware that if you see something untoward then that
could potentially be the reason. So again that's the only not the only,
well really the only thing that raises my pharmacists awareness when I'm talking about this
suthing beyond the sympomy. Yeah, allergen for the but yeah, so stick
two C nine so keep that in mind. If you're a practitioner, or
if you're patient and you're taking other SIP two C nine, I check other
if you're taking SIP two C nine mediated metabolism interactions or excuse me, medicines,
Yeah, that's it. Two C nine is an interesting one. That's
not one of the primary ones. But I remember often, well, we
know that SIP three A and four, right, they comprise the vast majority
of metabolisms. SIP two C nine is rare. But in terms of metalloism
of prescription medical description, medications do absolutely and you need to be aware in
that when you're on these together, right, and you know your dad could
lectures for an hour on HERB drug interactions, right, is the world's leading
expert. But that's just something I want to make sure he's pointed out to.
Yeah, practitioners, I think patients. Common ones that come to my
mind like colpidogrels one that is two C nine A leapers als two C nine.
The only other one I really see this is flew with statin maybe a
little bit, and then you know phenotone. But I mean some of those
you come across very often. But again I guess I've said this on the
podcast before. I always ask patients whenever I have something, say to you,
take any prescription medications. And one patient when I asked her that,
shecause You've asked me that every time I've come in here, and I'm like,
there's there's a reason I'm making my job, so it's important, right.
But that's what I wanted to point out here as well, is just
always be aware of the potential. Now so I'm back in my pharmacy,
you know, Professor days is always be aware of the potential right for what
is it? Forewarned, is forearmed or whatever it is. But anyway,
well keep that. Really appreciate you coming on again. I'll have you on
multiple times because there's multiple every time I talk to you, there's like eight
other areas I want to pick your brain on because you're sharing a lot of
the same interests and stuff like that. So I think we've got an interesting,
really good backed mechanism or what way for how we think's going on,
and we'll continue to tease that out. But you've I really like the idea
of really harping on the education piece of all of this, because that's the
key is making how can we take these complex topics make them easier to understand,
and how we can kind of take all the pieces together and not look
at it so compartmentalized, you know, and just that piece and that holistic
approach I think is just a great way of tackling complex issues, specifically around
that cholesterol and risk and all that stuff for heart disease. Well, all
Blatt, we talked about a continuing the education talk. It's right beyond LDL
tackling residual risk and talking about these things in a structured environment and continuing education.
That would be a fascinating I think people would get a lot of benefit
out of that, and I definitely want to pick your money and help out
there. I think we can wrap the episode up and then we'll go from
there. I'll have you on again soon, And like I said, I
really appreciate your time and always enjoy talking to you. You've been one of
the best. You've been one of the mentors that like its always really pushed
me to kind of expand my horizons as much as possible in ways of just
continuing to stay on the forefront of where all this is going. So I
appreciate you with that for sure more value to me than you want. Then
it takes at effort. It takes a lot of effort in reading. And
my wife who's also a pharmacist of twenty five plus years, that's what we
talk about, is the difference maker is the reading and staying apreast of what's
new. And that's why the education piece is so important. And why am
I at this stage of my career learning about the importance of remnant cholesterols.
It blows my mind and I should have known about it earlier. So yes,
it's part of that passion just educating. Podcasts like yours and the motivations
for doing that are really important. And maybe we'll get some listeners that'll have
questions that you know or want to figure out how to help and educate as
well and spread the words that's right, more people understand. I'd like to
get that to it. I'd love to get to a point because some of
the podcasts I really enjoyed do have like a live Q and a component,
So it'd be interesting to see how that I could factor that in later,
or you know, just have people send the questions to us and to see
where and do like a ask me anything kind of episode where we just kind
of answer people's questions. I think that would be a cool one to do,
especially if you or my dad or your guys groups. You're right,
that would all definitely work on some of that stuff. Ron, But I
really appreciate you being here and thank you for your time, and thank you
guys for listening. Thank you for joining us on today's episode of The Wellness
Transcription Podcast. We hope you're inspired to live a healthier, more purpose filled
by Christ. Remember your well being is a gift from God, and by
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