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Welcome to The Wellness Transcription Podcast,
the podcast that combines the power of Christian

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values with evidence based nutrition, fitness, and lifestyle content. I'm your host,

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doctor Patrick Early. Join me each
week as we explore the intersections of

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Christianity and wellness, offering you insights
to help nourish your body, mind,

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and soul. Whether you're looking to
improve your physical health or simply strengthen your

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personal relationship with Jesus, We've got
you covered. Stay tuned for inspiring discussions,

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expert guests, interviews, and practical
tips to help you live the life

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God calls us to live. All
right, guys, thank you for coming

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back to another episode of the Wall
This Transcription Podcast. It's been a while.

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I've had to revamp some things and
restart something, but I have a

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returning guest where I You're the first
returning guest on the show, So thanks

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for being Thank you guys. I
think it was episode two that we put

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out, or two or three actually, where I think me and Ryan were

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doing a real deep dive on cholesterol
and what all that looks like. And

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today I think we're going to talk
about an area that your healthcare provider most

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likely hasn't talked to you about yet, and that's not only just your typical

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cholesterol out to what we're going to
be talking about the risks and all that

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associated with something that's called remnant cholesterol. So if that's a new term for

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you guys, this is something that
I think you'll find pretty beneficial. Me

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and Ryan work pretty well together in
the s field that we're trying to really

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figure out a better way to educate
people about all the pieces of all this

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works together. So with that being
said, Ryan, I appreciate you being

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here. Thank you for taking time
out of your data to chat with me,

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and you know I can talk to
you for hours, So I just

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appreciate you being here and being so
willing to help educate people about stuff that's

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so important. Yeah, well thanks
for having me. Pat. You know

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how much Patrick, you know how
much I love to educate, So just

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whenever you're right into it. So
right, this was something that I wasn't

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very familiar with as a healthcare wrider. Now I have a little bit more

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extensive training and nutrition and other things. I've heard of these words before,

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but in practice, I just don't
really see it very often. So that's

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this concept of really focusing on remnant
cholesterol, and even if your cholesterol labs

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are good, so to speak,
that you may not necessarily be out of

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the woods as far as risk goes. For the audience listening, If you

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go to your doctor's office and you
get your typical cholesterol panal checked, you're

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looking at your total cholesterol HDL,
LDL and maybe treeglycerides. That's about it.

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And your doctor will either say it's
good or bad, and if it's

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bad, typically what they'll do is
they'll start what's called a statin medication that

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he would pick up from someone like
me at a pharmacy, and then we

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go from there. Usually it you're
usually ormostatic for a long period of time

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and then depending on how lads go
depends on if you go up or down

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in dose. But remnant cholesterol is
not something that's rarely ever checked, but

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it can be easily calculated, as
me and right are going to go into

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details about it. So, Ryan, what can you tell us just in

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generally what remnant cholesterol ends and why
we should be concerned about it. What's

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the literature say, because it's something
that's kind of hitting this hitten capturing researchers

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and clinicians attention as far as stuff
to put to pay attention for. Yeah,

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Patrick, For me, as a
practitioners well licensed pharmacists, we know

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that we focus on LDL and specifically
statins, and study after study has shown

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the benefit of statins in certain individuals. And what I mean by certain individuals

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is that there was a landmark study
published in two thousand and none where the

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investigators looked at several hundred thousand events
cardiovascular events across the nation, and what

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they were looking at was how many
of those folks had lipid panels, and

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they found that there were a little
over one hundred thousand of those folks had

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lipid panels. And what stood out
to them is that literally seventy five percent

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of those with cardiovascular events had quote
normal or target this is a better way

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to put it, target at LDL
levels. So it really started this conversation

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or really I guess it added momentum
to this conversation around Okay, if LDL

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lowering represents twenty to thirty percent and
pick your number, but it's still a

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minority of the overall risks. What
are the other factors that come into play

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when you're trying to assess your risk
factors. We're going to stay in the

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lipid space. We're not going to
talk today about about really interesting information markers.

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Right, we were familiar with reactive
protein. We'll maybe leave that for

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another day. We'll stay in the
lipid space, and specifically, what other

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information can we glean from a typical
lipid panel and move off of an LDL

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sort of centric interpretation of the panels. And so if we take a step

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back and we say total cholesterol,
what does total cholesterol represent? We know

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that total cholesterol obviously a component of
that is ld and most of your listeners

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are familiar with what we'll call the
LDL, right, the bad cholesterol,

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the villain, if you will.
And then we know that HDL is the

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so called good cholesterol. So now
you've got total cholesterol, which is comprised

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of LDL plus HDL. But there's
a third component of that total cholesterol that

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receives stray little airtime, if you
will, outside the research the clinical research

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community, and that are the triglyceride
rich remnant proteins okay, blip it proteins.

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So basically, the measure the difference
between total cholesterol LDL and HDL are

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the so called VLDLs. These VLDLs, again, as I said, carry

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a lot of our triglycerides, such
that if we compare VLDL levels to triglyceride

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direct cognasurement, they're pretty close.
There's an association, not a strict association.

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There are differences, but there's a
really good correlation. And so what

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this VLDL is triglyceride carrying cholesterol component
has become known as one name is remnant

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cholesterol. Those have been a lot
of research around what contribution is remnant cholesterol

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to that residual risk, and so
the research is showing that it actually contributes

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highly to the residual risk related to
cardiovascular events. And so this is important

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because now it starts to raise sort
of this idea about Okay, since they

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are triglyceride carrying, it brings triglycerides
back into the mix in terms of discussion

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about residual risks. We'll come back
that. But first to your listeners,

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say, okay, it's a real
simple number to calculate. So I have

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my total cholesterol that's equal to my
LDO plus my HDL plus my remnant cholesterol

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or VLDL these triglyceride carrying rocks.
So it's really that simple. If I

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know my total cholesterol, I can
subtract my OLDO, I can track my

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HDL, and the leftover. The
remaining the residual is that remnant cholesterol VLDL

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triglyceride carry So that's where a lot
of research is focusing now on remnant cl

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lestrol. That's how to calculate.
That's why it's important in terms of the

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residual. I think, yeah.
A couple important points that I like to

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make is there's it's a big part
of the equation which going back to that

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study you first alluded to where they
looked at over one hundred thousand patients and

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the rates of risk and events that
were going on. It says before admission.

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I'm looking at the paper now,
it says that only twenty one percent

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of patients had received some form of
lipid lowering medication before they were admitted for

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the event. That's important too,
is those labs may look fine, and

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a doctor may go, you don't
need a statin, or you don't need

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something right now. Just lifestyle changes
things like that, you'll be fine.

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Well from a patient perspective, you
hear okay, I mean doctor said,

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I'm good, I'm not at risk
for an event, when in reality you

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still could be. You just don't
really know. Another thing is that was

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done in two thousand and nine,
so I'd be hard pressed to think if

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you repeated that study now that those
numbers would probably be higher. I think

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the statin rate is pretty standard now. However, there are a lot of

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side effects that statins do bring about
that. It's definitely an impact compliance as

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far as that goes. And again
that statin may get that LDL quote bad

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cholesterol in range, but that doesn't
if you're not looking at the other pieces

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of the puzzle like you're talking about, we're not looking at remnant chosterol.

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We're not really factoring in the impact
trogly rides have in that whole process,

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where just we might be missing a
big piece of the puzzle as far as

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getting all that in check goes.
So, I mean, here's another part.

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It says almost half the LDL levels
we're less than one hundred milligrams per

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desolator. More than half the patients
have in minsioned HDL levels less than forty

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whereas less than ten percent have HDL
levels greater than sixty. What that means

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LDL looks okay. HDL is in
the majority of patients more than half,

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where subpar forty is for female.
I minimum would like it to be forty

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five to fifty, probably higher if
you can or females. Males can get

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away with a little bit less,
so forty five or higher for them is

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usually okay. But that's one part
of the pharmacological piece of at all is

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there's really not anything available behind the
counter, like prescription wise or even over

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the counter that really affects HGL to
any degree. The only thing that was

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used clinically for a long time was
diacin that did actually impact HBL levels a

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good bit, but you had to
take very high doses of it. And

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I can tell you as someone who's
taking too many B vitamins that once before

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that it is not fun. I
was driving home from or I was driving

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to work at the pharmacy when I
was in pharmacy school, and I had

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taken my settlements that morning, and
I'd forgotten I was doing something else,

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so I took my settlements again.
And normally that's not a problem, doeshn't

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to worry about. But I'm driving
to work and it's like a cold December

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day and I'm like, yeah,
I'm warm. What is happening? Like,

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I don't this doesn't feel right this. I'm like, I'm this is

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not good. I look in my
rear view. I look in my mirror,

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and I am I look like a
lobster, like I am here reared

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everywhere, and I'm like, that's
not good. Maybe I'm like, you

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know, something's wrong. Oh no, I took too much of my niosin,

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like too much of my bee vitamins
that I sense was causing this flushing.

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I got to work and to my
boss goes, do you go to

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the beach this weekend? And to
just stay there. So it's it's interesting

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because you can still use high to
his knives and there's a prescription, but

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again, it's so rough on the
system that a lot of times doctors are

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like, patients aren't gonna stick with
this. So there's really as far as

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getting HDL up, they just say
eat more fatty fish and kind of keep

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your you know, exercise and all
that and check and it might go up.

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But that's a whole other piece of
the puzzle too. I just thought

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that was interesting about that study because
it's it's really startling when you think about

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it, because I mean, if
your level can be that good and you

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still have events, I mean you're
talking about just about everybody at that point,

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is it risk for those things?
Yeah, So I think it's really

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important to understand the man and how
to calculate the vel. Also, to

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your listeners, I'll use VLDL and
rhymnet cholesterol interchangeably. I point that out

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because technically remnant cholesterol is your VLDL
the intermediate ditity so ideal, but I

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think your listeners need to know that
as well. So I am fluedging a

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little bit lumping in IDL and VLDL, but so your readers know that.

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But that's important because for two reasons. One is VLDL when it interacts with

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HDL. We'll talk about that in
a minute. To offload a lot of

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the bad lippets. As it decreases
in size, the VLDL, then that's

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what becomes the LDL. So said
differently, VLDL through interaction with HDL is

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turned into LDL. And so that's
important for two reasons. Is if you

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talk about LDL, we know that
they're really two proponents to that LDL.

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There's one that's non genetically determined and
one that's genetic determined. So you'll hear

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patients when practitioners talk about at L
little age. But basically, that's your

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portion of LDL that is bound to
another lip of protein app of protein eight

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and it's genetically to move for the
most part, and so it doesn't appear

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that SI statins impact that portion of
LDL to any great extent. So I

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always like to give patients rationale its
like you may be on a high those

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statin and you still have this stubbornly
high LDL. It could be that you

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have that genetic component of LDL that
just remains stubbornly high. So keep that

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in mind as you're talking about LDL. And where LDL comes from ultimately comes

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from VLDL remnant cholesterol. Okay,
So the other part of that in terms

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of relationships is we know that remnant
cholesterol is in balance with your HDL.

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Do they interact? So another words
of the LDL, it's carrying those triglycerides,

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it's carrying that free cholesterol, and
so through interacting with HDL VLDL all

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floats, does triglycerides st HDL,
it all floads that free cholesterol to HDL,

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and so that's the other reason why
you want to have higher HDL levels.

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You've got to have us think,
right, those clesterol and triblysterride molecules

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from vldal ideally go to HDL.
So if you look at numbers, typically

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what you'll see as an inverse relationship. If you have high rimnict cholesterol,

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you'll have low HDL, and vice
versa. These are generalizations, but if

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you're just looking at your numbers,
and that makes sense because HDL is that

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sync for those triblycerides and free cholesterol
that are coming from the remnant cholesterol.

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So that's the other really important reason
to understand what that remnant cholesterol number is.

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And then in relation to your HDL, it gives you some idea of

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how well you're clearing not only clearing
your clysterides, we're not, but what's

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the source to those triglyrods. Then
you get into the next step, which

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is really Okay, if I have
hot rimnedy cholesterol and I have low HDL,

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what options do I have? And
I think that's where I think your

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listeners might be interested to say,
Okay, First, where do those vo

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deals come from? And why might
I have an overload of those veils.

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I'll make two important points because I
would say, I want to say it's

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around twenty percent of the cholesterol and
is impacted by diets. So that's what's

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called exogenous cholesterol. So you've got
you eat something with that at it it

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gets broken down, it's terified and
then bile, and then it gets absorbed

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by things called kylum microns. Colum
Microns transport those across the intestinal barrier into

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the liver, where they're then packaged
and done. So that that is so

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if people say, oh, you
know, my doctor said that in order

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to get my cholesterol down, I
have to eat you know, less eggs

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or less cholesterol rich foods and vice
versa, you're all that stuff might be

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okay to do. I don't cast
you. Reducing it doesn't make much of

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a difference in my opinion, if
you eat foods that are hiring cholesterol.

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There's a lot of healthier foods that
are, it really doesn't move the needle

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there as much. So that's an
important piece to keep in mind is what

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we're really talking about with these risk
factors is more of a dodgenous production of

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cholesterol, which is your liver.
One of your liver's primary jobs is the

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production and packaging of these things.
An important thing. You mentioned ideal earlier

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too, and it's important for people
to go, Okay, well, let's

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say I coloculated my remnant, but
I don't know what my ideal is.

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Ideals intermediate for a reason, it's
halfleck. This is very short. It

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gets quickly converted to BLDL pretty fast. Yeah, or yeah ldld quickly,

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like both. It's a fast process. So it's really even if you were

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to able to measure it, it's
like it's not necessarily very useful because it's

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so hard to kind of catch.
You'd have to get the live measure stuff

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really quickly. But yeah, I
think for most people on statins, again,

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if we're only looking at one piece
of the puzzle, we're just for

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missing things. And then again it's
what else can you do to kind of

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affect the other things? Because the
reason HDL is oftentimes referred to as good

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cholesterol or it's very it helps a
lot with reverse cholesterol transport, which is

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what you mentioned, but without saying
reverse cholesterol transport. It helps take that

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cholestero back up, send it back
to the liver where it's recycled and reused.

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But again, if your HDL is
low, we're dumping off more l

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el in cholesterol rich things than we
are actually recycling it back, and then

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your triglysrids go up. And it's
always kind of this vicious cycle. So

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thank you for eloquently explaining that one. But those are those are some things

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that are important to keep in mind
to that. Yeah, so what do

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you want to do as a patient. As a healthcare practitioners, you know

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that statins are in your armamentarium for
lowering YELD. Great, it's if they

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work in your patients used, right, it's you know best in your patient.

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I think the other piece where we're
bringing up here these residual risk factors

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is okay, how do we reduce
remnant cholesterol and how do we increase our

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HDL? And so we said they're
related, so you can impact both in

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a decrease VLDAL increase HDL and have
an added potential synergistic effect. And so

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the other part of that is when
those VLDLs via IDL are converted to LDL,

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recognize that removes the triglycerides. In
other words, ldl's not carry triglycerides

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l els, right, And that's
the process of going from vld old id

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old lios. So that's the other
remnant cholesterol is that triglyceride carrying component lip

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protein LDL is not. So that's
the other reason to focus on those triglycerides.

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And you appropriately pointed out those triglycerides
are full initially in the liver.

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And we can talk for three podcasts
about how triglycerides excess triglytrides get into the

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liver, but whether say that for
another day. But the bottom line is

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to be able to impact rhymnic cholesterol, you've got to be able to impact

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synthesis of these remnant cholesterol, these
VLDL molecules in the liver. And this

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is where it gets really fascinating,
Patrick, because we really don't talk about

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this in pharmacy school, medical school, pharmacolleague, pharmacology in general. Excuse

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me it. For me, it's
most exciting because the first is the debt.

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Okay, if you're going to reduce
VLDL, what's the literal first step

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in the liver. The first step
begins with april lipoprotein B one hundred synthesis.

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So for the nerd listeners like myself
that you have today, right,

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it's called apo B one hundred simply
because because it uses one hundred percent of

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the amino acids in the gene for
an apole B. That's what it's called

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OB one hundred. It's one of
the largest proteins in the bodies, like

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over forty five hundred amino acids.
One hundred just means that when you synthesize

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VLDL and you create that first step
april B one hundred, it's using every

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one of those amino acids. But
that's important to distinguish because if you the

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first part of the translating that april
B one hundred in the hepatocyte, it

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only uses the first one hundred or
so amino acids to begin the process.

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While that's important is if you look
at the lipid composition of that april B

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one hundred beginning there in that patasite, it is seventy percent phosphatidocholiines. It

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only has twelve molecules a triblys ride, It only has six molecule us A

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cholesterol. It has fifty molecules of
phosphatidal colines. And so step one in

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synthesizing triglyceride rich VLDL that are ultimately
secreted into the bloodstream is comprised of phosphatidal

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colines. And so you've got to
really understand how phosphacidal colines play into that

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synthesis. Okay, so that's where
my interest is. As you know,

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Patrick, it says, all right, it's not just phosphatidal colines, because

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they're literally thousands of different species of
phosphidal colides that are produced by the liver.

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What's fascinating to me is this the
right ratio of polyensaturated fatty acid as

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well as saturated fatty acid containing phosphidal
colies. If you get a disruption in

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that balance, what happens is that
April B one hundred is degraded. It

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never gets converted, goes to the
next step where now you start piling on

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the triglycerides, and you start piling
on the cholesterols, and the cholesterol esters

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and it matures and then it is
secreted. And so if you mess up

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that first step with those spospitive coalings, then it degrades. Guess what happens.

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That means those triglycerides stay in the
liver, that cholesterol stays in the

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liver. But I know what that
means. That's the big BA de liver

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disease, right, those lipid droplets, and so you don't get those phosphatidal

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colings right on the front end,
you don't get efficient synthesis of VLDLs,

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you don't get efficient secretion of triglycerides
lipids from the liver, and you don't

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get them out there in the plasma
where they can interact with HDL molecules and

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thereby strip them of their triglycerides of
pre cholesterol. That's what HDO does.

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So that's component one why those spostatidal
coling molecules and metabolism in particular are so

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critical. But there's a second piece. So that's how I just now,

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it impacts the VLDL side of the
VLDL rhymnic chlesterol HDLs, But how does

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it affect HDL it self? And
we know that there's certain polysaturated fatty acid

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containing phosphat of colines that promote HDL
synthesis. Said differently, if you have

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the right mixture including polynsaturated fatty acids
EPA and DHA in particular. Then you

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promote synthesis of HDL in the plasma
through interaction with the enzyme l cat or

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lesser than cholesterol acetyl transformational can.
So now you start to see if rhemnic,

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cholesterol and HDL are critical and they
relate with each other. Right,

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one offlow strip glyceritis three cholesterol,
the others in exchange for cholesterol esters.

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Right, that's what's answered back to
VLDL. If you look at phosphide of

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colines, it impacts that GLDL synthesis
and secretions. It impacts the HDL,

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So it tends to decrease VLDL rhymnic
chlesterol and the increase HDL. That's where

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we are now in terms of the
conversation as as far as a new mechanism,

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No one to my knowledge besides us, are talking about that as the

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mechanism. Now what are we talking
about. We're talking about high dose synthetic

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EPA for triglycerides in patients that are
have high triglycerides that aren't impacted by statins.

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I don't know if you saw a
couple of weeks ago the EMA Medical

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Association, thank you, they came
out and stated strongly that looking at the

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evidence in Toto that you should really
watch your patients that are taking high dose

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EPA for triglycerides for increased instance of
a fit. Right, they said it

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is causing. So in other words, if you look back at all the

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meta analyses, if you're above one
grand per day of EPA, your risk

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of aphibs starts to increase. For
every grand per day. Above wearing one

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grand per day, you get about
a ten percent increase in risk. So

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that when you get up to four
grams per day, which was the reduce

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it tron, you see an increase
in aphib risk of almost fifty percent.

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And so now you start to say, well, okay, we really don't

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have a lot of great options.
You talked about NIS and when I say

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options, options are treating high triblycerides. And now you know why that's important

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rin the cholesterols in the contact,
particularly of low HDL. And so if

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we don't have a lot of options, we do a vibration. Again,

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I don't, I don't. I'm
sorry to interrupt, but I don't see

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a lot as a pharmacist, and
I view a lot of pharmacy stuff.

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Let's be honest, I feel a
lot of restrictions and a lot of different

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age grips and patient demographics, so
I see kind of what's archaeting, what's

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up? I rarely see fit of
five rates used anymore. Now is does

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that mean it's not used more frequently? No, But however it I just

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don't see it. They also come
with side effects too that are pretty rough.

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They are kind of hard on the
liver a little bit, and they

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do they have their own citizen.
Again, no drug is without side effects.

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So if you're stacking a stat and
have been a fibrite together, you

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know you can. Depending on which
ones they are, you may be helping

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yourself from a blood worker perspective,
but if you're causing, if you're increasing

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the likelihood for them to see adverse
effects, I'm just not going to be

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compliant with it. And then we're
back to squore one. It's a whole

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other important thing that I want to
interject one one more time, and I'll

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let you get back to go because
it's fascinating to me because, like you

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said, no one's talking about this, because no one really understands what's going

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on. I read a book a
long time ago and I'm pretty sure.

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Yeah, it was one of the
fasting books I remember. I think it

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was doctor Fun's fasting book I read
two years ago, and he made an

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offhand comment in the book that just
didn't It stuck with me, but I

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don't know why I remember it.
And he was talking about how you know,

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00:27:00.960 --> 00:27:03.440
when you eat too much you have
insular resistance, Like all these bats

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00:27:03.480 --> 00:27:07.960
get have to get deposited in different
tissues, so that's when then they go

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deliver first. And it's like,
that's what causes fat de liberties. In

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00:27:11.000 --> 00:27:14.839
my head of it's that's not that
simple, Like it's not just that part.

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00:27:14.960 --> 00:27:17.799
Now that may play in for sure, because a lot of times in

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diabetics we see insular resistance and all
these other issues, we're also going to

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00:27:22.119 --> 00:27:27.640
see cholesterol issues and those go hand
and hand. However, your mechanism and

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what I'm hearing, what we've talked
about for hours off my off recording,

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is this seems to make more sense
from a mechanistic standpoint of why we're seeing

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the fatt delivered disease rates. We're
seeing why these things are going up because

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they're all everything. It's important to
remember everything in the body is tied together,

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so as clinicians that they could for
in pharmacy school, we oftentimes tend

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to compartmentalize certain areas, so it'll
be like we're talking about cholesterol. We

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know that affects diabetes and stuff,
but then we're talking about other things.

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So AFM is never brought up as
far as I'm concerned with, like cholesterol

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and synthes works in the system and
if you get one of these off or

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others are just kind of compounds.
But that's really important that you mentioned that,

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because I think, go ahead,
yeah, well I'll pick up there

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right where you tee it up.
So right, doctor Phong nephrologists, Canadian

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00:28:25.640 --> 00:28:29.279
nefrogs right, big believer Internet facing
us. But I remember quickly the books

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00:28:29.279 --> 00:28:34.559
called a Unity Code, that really
fascinating ideas about how you change fatty acid

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metabolism in the liver. And I
think that's a really important point here because

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it ties into what we're talking about. So again, regardless of how you

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00:28:45.200 --> 00:28:49.799
get fatty acids formed, whether it's
coming from the adipocide right breakdown and fatty

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00:28:49.799 --> 00:28:53.680
acids are transporting pre fatty acid training
by transported back delivered, or we're talking

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about fruptosu blue coals that through donovol
lypogenesis are forming these fatty acid and then

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00:29:00.880 --> 00:29:06.000
combining them with glycerl molecules. Right, we know that those fatty acids combined

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00:29:06.079 --> 00:29:11.759
with glycols to form monoase oft prize
for glycrool. But why I painstakingly go

364
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through that step by step is at
the stage of diaso glycol the disoglyceol has

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00:29:19.480 --> 00:29:25.119
at least two pathways, two primary
pathways it can take. It can have

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an additional fatty acid attached and turn
into a triasy glycol right triblyceride. But

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what most people don't talk about is
that diaso glyceraol is also a precursor for

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phosphatidyl coline synthesis. And so if
you have properly operating phosphatidical coline synthesis,

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it's consuming a number of those diaso
glyceride molecules that are produced in the liver.

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Said differently, those diasoglyceride molecules that
are going into five through the coalings

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are not going into triblycerize and vice
versa. And so that's yet another reason

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in link between proper phosphattic coaling metabolism
and fat production and deposition in the liver.

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So the idea is this, if
you can figure out how to positively

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impact phosphitic coaling metabolism, you can
potentially impact remnant cholesterol and HDL and all

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the downstream things that are related.
Things pathophysiologies that are related that we know

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about and that we don't know about
that are we're just starting to appreciate and

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some of the things we're seeing anecdotally
in the patients that are taking this supplement

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that's been developed by my group over
the last few years. And so it's

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a unique mechanism. It focuses solely, not primarily, It focuses solely on

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00:31:00.200 --> 00:31:06.720
the nutritional deficiencies that we see in
patients that impact plastord to colding metabolism completely

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natural it will. Therefore, I
think that's why we're seeing some of the

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00:31:11.559 --> 00:31:17.960
really cool results that we're seeing in
patience when it comes to alterations in lipid

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00:31:18.039 --> 00:31:21.599
pms. Yeah, it's very important. Yeah, there's a piece that no

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00:31:21.680 --> 00:31:25.279
one's talking about, and the fact
that we that you've developed a potential answer

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00:31:25.359 --> 00:31:29.319
to that. I mean, it's
I've seen it work. It's very important.

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00:31:30.039 --> 00:31:34.279
I just it's my mind can go
on all sorts of different things.

387
00:31:34.319 --> 00:31:41.480
I'm looking at this. Yeah,
I mean there's really never been an answer

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00:31:41.559 --> 00:31:45.160
to how do we get those ratios
correct? You know, normally, And

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when I mentioned this before on the
last podcast I had you one, normally

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they'll go, okay, well,
EPA and DHA, we know we're good

391
00:31:52.559 --> 00:31:55.559
and the racious for what high quality
officials instead of so let's do that,

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00:31:55.759 --> 00:31:57.680
let's exercise, let's do some other
things, and you're kind of hoping at

393
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that point. You don't really know
how all that gets utilized. And I

394
00:32:02.119 --> 00:32:07.519
think that's so important. Where the
Sessamon component comes in is because I was

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00:32:07.559 --> 00:32:09.599
looking I was just curious. I
was looking into a lot of the studies

396
00:32:09.720 --> 00:32:15.000
just thought of sesame oil in general
and their effects on cardio metabolic risk factors

397
00:32:15.039 --> 00:32:16.759
and things like that. In time. Again, in all the papers,

398
00:32:16.799 --> 00:32:21.640
you see LDO goes down, HDO
goes up, Tragosa reds drop like it's

399
00:32:21.720 --> 00:32:25.640
over it up. You see in
multiple systematic reviews it's like people who utilize

400
00:32:25.680 --> 00:32:29.799
this and have this as a mainstay
of their diet, that there is marketing

401
00:32:29.920 --> 00:32:32.480
provements. And then every study that
I saw says they need to figure out

402
00:32:32.519 --> 00:32:37.240
mechanistically how this is going on and
why this is happening, because it just

403
00:32:37.400 --> 00:32:38.759
it looks good, but we just
don't know why. And I think that's

404
00:32:39.079 --> 00:32:43.880
you've kind of really teased that out, I think, and it's been it's

405
00:32:43.960 --> 00:32:46.880
that missing piece because a lot of
times when people see these changes happening in

406
00:32:46.920 --> 00:32:52.240
the liver and metabolism, they tend
to oversimplify what's actually going on. And

407
00:32:52.720 --> 00:32:57.640
to my knowledge, I never heard
of it before getting involved with you and

408
00:32:57.720 --> 00:33:00.519
talking about this and kind of getting
into the weeds. I have never heard

409
00:33:00.759 --> 00:33:05.640
of fosphitooch coolon being a part of
that to any great degree. Only on

410
00:33:05.720 --> 00:33:09.759
the handful of podcast as that mentioned, but it's never the mainstay of the

411
00:33:09.799 --> 00:33:15.400
conversation. So I think that's really
it's well, it's interesting, Patrick,

412
00:33:15.440 --> 00:33:20.359
because it's like anything else. The
literature is out there. There are some

413
00:33:20.680 --> 00:33:25.680
brilliant biochemists who have worked out VLDL
synthesis and the role of phosphit of coolies,

414
00:33:25.759 --> 00:33:29.519
the role of the ratio poster doth
that all means a hospital coli,

415
00:33:29.880 --> 00:33:34.599
the role of triglycerides, etc.
The are brilliant biochemists have worked out how

416
00:33:34.680 --> 00:33:40.920
sostitial colines impact the HDLs. But
that's been sort of in your silos where

417
00:33:42.039 --> 00:33:45.319
that's what you're funded to do as
a researcher, and you does some really

418
00:33:45.440 --> 00:33:50.599
interesting works, but no one to
my knowledge, at least outwardly and in

419
00:33:50.759 --> 00:33:53.480
podcasts like this, is talking about
how you call all that information together to

420
00:33:53.680 --> 00:34:01.839
provide a potential I keep emphasizing potential
solution for patients. And I was in

421
00:34:01.920 --> 00:34:06.359
the military for a number of years
and one of my favorite things that had

422
00:34:06.400 --> 00:34:08.639
a boss that always told me said, pedosciates, don't come to me with

423
00:34:08.760 --> 00:34:12.880
a problem, and you have a
solution. And so a lot of people

424
00:34:13.000 --> 00:34:17.079
have problems. But it's frustrating as
a practitioner if you know there's seventy five

425
00:34:17.199 --> 00:34:22.480
percent residual cardiovascular risk, but you
don't have anything to tell patients. And

426
00:34:22.559 --> 00:34:27.960
I'm not suggesting for one second that
this supplement of the UREAU or treatment mitigation

427
00:34:28.159 --> 00:34:31.480
whatever. Would never say that,
But what I would say is it begins

428
00:34:31.639 --> 00:34:37.480
to address the nutritional deficiencies. And
by definition, right in the course with

429
00:34:37.599 --> 00:34:45.440
the SHA dietary c health education now
is a supplement to diet which can positively

430
00:34:45.840 --> 00:34:52.559
impact fostered or coding metabolism and thus
through mechanisms that are completely I don't say

431
00:34:52.559 --> 00:34:57.679
complete, you're never perpleleg but are
really well characterized, will have an impact

432
00:34:57.800 --> 00:35:02.480
on these different lipid parameters. These
are known pathways. You just have to

433
00:35:02.559 --> 00:35:08.960
be able to impact them in a
positive way without causing horn. And when

434
00:35:09.039 --> 00:35:16.000
we take the reductionist approach of everything
is sort of a pharma. It's a

435
00:35:16.119 --> 00:35:21.440
one size fits all. Its EPA
is really good, and now we're going

436
00:35:21.519 --> 00:35:28.199
to give you four grams per day
of synthetic EPA, right extroversion, then

437
00:35:28.440 --> 00:35:30.920
that's going to be even better.
Well, the data are clear and the

438
00:35:31.039 --> 00:35:36.320
EMA is spoken, and cardiologists in
the world is spokens. That's not okay.

439
00:35:36.760 --> 00:35:38.559
There are side of that. So
when you take the reductionist approach,

440
00:35:38.920 --> 00:35:45.000
so why don't we do what nature
does, take a step back and say,

441
00:35:45.119 --> 00:35:50.000
this is a systems pharmacology. This
is a multifactorial process. I don't

442
00:35:50.239 --> 00:35:55.159
need to shove four grams of EPA
into somebody to ECHI is that I need

443
00:35:55.239 --> 00:36:00.880
to have some a way to impact
piland saturated fat as metabolism step once,

444
00:36:00.159 --> 00:36:07.159
and then those downstream events that augment
that proper diet. And believe me,

445
00:36:07.599 --> 00:36:12.400
I'm not here even advocating taking official
suppment. I'm here advocating eat your fatty's

446
00:36:12.559 --> 00:36:19.119
ish once a week twice. What
are I think the average recommendation from the

447
00:36:19.239 --> 00:36:22.559
USDA, the food organizations here as
well as an em A and all that

448
00:36:22.599 --> 00:36:27.719
stuff. I want to say it's
minimum two a week, if you can

449
00:36:27.960 --> 00:36:30.800
ideally three two to three. It
seems to be the sweet spot. Now

450
00:36:30.880 --> 00:36:35.280
again, if you eat every if
you're piscatarian and that's the only meat,

451
00:36:35.280 --> 00:36:39.360
so yeah, that's fine. Yeah, I guess my point is that it's

452
00:36:39.800 --> 00:36:45.079
yes, it always starts with eat
right and exercise, but in this case

453
00:36:45.159 --> 00:36:49.719
it stop there because that's what's the
frustrating things for patients sometimes is that's difficult

454
00:36:49.760 --> 00:36:52.480
to understand what it means right,
eat right, and exercise. Does it?

455
00:36:53.559 --> 00:36:59.239
It's gonna gives you nothing to go
off of. So yeah, if

456
00:36:59.320 --> 00:37:07.559
you can give your liver the dietary
ingredients it needs to process those proper dietary

457
00:37:07.760 --> 00:37:13.519
inputs, those essential fatty acids,
to me, that's a much better approach

458
00:37:14.000 --> 00:37:17.559
than inhibiting. I mean, I've
been in drug discovery for over twenty something

459
00:37:17.760 --> 00:37:23.239
years and the most common approach is
something is going to right. Let inhibit

460
00:37:23.679 --> 00:37:29.800
a basic process, whether it's beta
block. I mean again, I'm not

461
00:37:30.039 --> 00:37:34.679
cast throwing shade though those are important, but it's always block a process as

462
00:37:34.719 --> 00:37:38.639
opposed to how do we augmit what
we know to be a beneficial process to

463
00:37:39.159 --> 00:37:45.840
attack not the symptom, but rather
the ultimate cause for on pats of physiology,

464
00:37:45.880 --> 00:37:50.000
And that's what my you know,
I'm actually as a big proponent here.

465
00:37:50.760 --> 00:37:55.000
How do we augment what people are
doing from a prescription and dietary standpoint

466
00:37:55.119 --> 00:38:00.639
to achieve an even better There was
a point you made earlier about study with

467
00:38:00.760 --> 00:38:02.960
a FIB and EPA risk and stuff, and it's like, okay, let's

468
00:38:02.960 --> 00:38:06.719
say, I mean, if that's
well established in a load tried I think

469
00:38:06.760 --> 00:38:09.480
I went through that paper you sent
me on that one. That's very a

470
00:38:09.599 --> 00:38:13.920
very interesting link. I would have
you know, a normal practitioner would have

471
00:38:13.920 --> 00:38:16.039
never thought about that as being an
issue. But obviously there's pattern there,

472
00:38:16.079 --> 00:38:21.440
and if there's enough people saying this
is causative, then there's good data to

473
00:38:21.480 --> 00:38:24.920
back it up. However, if
you were doing that, let's say you

474
00:38:25.039 --> 00:38:30.719
had an imbalance there of fallen centric
botty acids and metabolism and stuff, and

475
00:38:30.840 --> 00:38:36.239
we've now progressed into an aphib situation. From a pharmacological standpoint, as a

476
00:38:36.280 --> 00:38:39.840
pharmacist, there's only really conductive medications
or beta blockers that can help with that.

477
00:38:40.440 --> 00:38:45.239
You're looking at your medications like amiodorones, paphnoones like other things for different

478
00:38:45.280 --> 00:38:51.519
aphibs and beta blockers, and that's
about it. Like they only touched the

479
00:38:51.599 --> 00:38:55.920
circuitry part of the cardiovascular issue that
they have because they need to get that

480
00:38:57.039 --> 00:39:01.760
under control immediately. But as far
as looking at the liver side of things,

481
00:39:01.800 --> 00:39:06.039
that's just not done, at least
in a hospital setting, and I

482
00:39:06.079 --> 00:39:07.840
don't think that's something that they need
to look at. I think that's something

483
00:39:08.000 --> 00:39:13.280
from a primary care of pharmacists standpoint, like, Hey, this is what

484
00:39:13.360 --> 00:39:17.239
my labs look like. What could
I do to impact these to minimize even

485
00:39:17.320 --> 00:39:22.360
having to go down that route in
the future. And all this ties back

486
00:39:22.440 --> 00:39:25.159
into remnant cholesterol risk because it's like
if you only go to your doctor,

487
00:39:25.679 --> 00:39:29.599
you know, maybe a year or
every six months or something, and you

488
00:39:29.719 --> 00:39:31.599
check everything and he just says,
all good, You're gonna keep going about

489
00:39:31.599 --> 00:39:35.480
your business. But if he says, hey, your labs look good,

490
00:39:35.639 --> 00:39:39.760
but your remnant cholesterol is looking a
little bit off the ratios off, then

491
00:39:39.880 --> 00:39:45.320
you can then have some additional guidance
as to how to control that to further

492
00:39:45.480 --> 00:39:51.320
minimize your risk. Because it's very
interesting the papers that you've sent me and

493
00:39:51.400 --> 00:39:54.599
that I've looked at myself, and
how all this would impact ASCBD scores because

494
00:39:54.679 --> 00:40:00.119
in the pharmacy world that is the
gold standard. What's their ASCBD risk and

495
00:40:00.199 --> 00:40:04.119
then what can we do to minimize
it? In pharmacy school, I heard

496
00:40:04.159 --> 00:40:07.480
this one hundred times. Calculate their
ASCVD risk score and then what would you

497
00:40:07.559 --> 00:40:12.760
do to you know, decrease the
risk. The answer was always this exercise

498
00:40:12.800 --> 00:40:15.760
and lifestyle change and if they're smoking, stop poking. That was the extent.

499
00:40:16.000 --> 00:40:21.079
That was the extent of it.
Very rarely until now, I would

500
00:40:21.119 --> 00:40:22.239
have never made the link to oh, well, we've got to make sure

501
00:40:22.280 --> 00:40:29.400
delivers metabolizing polyunsaturated batty acids correctly.
You know, those ratios are correct and

502
00:40:29.559 --> 00:40:31.960
we have to have a way to
get those in check and provide a solution.

503
00:40:32.159 --> 00:40:36.239
Otherwise you're just diagnosing another problem and
saying, well, we'll figure it

504
00:40:36.280 --> 00:40:39.400
out in ten years when the science
is there. So I think it's I've

505
00:40:40.320 --> 00:40:44.559
the product that you've developed and stuff
with the sessiment and all that and other

506
00:40:44.719 --> 00:40:49.280
in the extra mile, you guys
went to make sure we have enough methal

507
00:40:49.360 --> 00:40:52.360
donors in there and make sure we're
further facilitating that process and not just throwingame

508
00:40:52.679 --> 00:40:58.079
sessiment at it and seeing in real
time how all that plays into effect.

509
00:40:58.239 --> 00:41:04.480
It only solidifies mechanistically that what you're
saying makes the most sense. I mean,

510
00:41:04.599 --> 00:41:08.000
it's pretty obvious if when you lay
it out the way that it's laid

511
00:41:08.000 --> 00:41:12.760
out, that it works. And
again, I'm not saying like you were,

512
00:41:12.800 --> 00:41:15.280
I'm not saying that assessment is going
to be the end all be all,

513
00:41:15.679 --> 00:41:19.000
like cured anything. I don't like
using the word here because it's not

514
00:41:20.119 --> 00:41:23.199
that term gets thrown around all the
time and it's bothersome. But again,

515
00:41:24.480 --> 00:41:30.559
it's having a dietary supplement and nutrition
component that you can easily change with minimal

516
00:41:30.599 --> 00:41:37.519
side effects without having to go up
on that set and you're already on you

517
00:41:37.599 --> 00:41:39.800
know, it's say, there's just
so many implications there. I think it's

518
00:41:39.840 --> 00:41:45.559
just going to make it easier on
patience for clients purposes. It's I'm sorry,

519
00:41:45.599 --> 00:41:50.559
I'm rambling, but I think it's
very intriguing that we're finally get in

520
00:41:50.719 --> 00:41:54.000
some real answers to these problems that
people have been able to diagnose but not

521
00:41:54.119 --> 00:41:58.440
solved for a long time. Or
mitigate, I guess is a better word

522
00:41:58.480 --> 00:42:02.119
to say it. And the bottom
line is it's not a problem that has

523
00:42:02.199 --> 00:42:08.320
been solved. And so what I'm
suggesting through my approach is that we rethink

524
00:42:09.079 --> 00:42:15.480
how we approach these different parameters,
again without using these terms, et cetera,

525
00:42:15.800 --> 00:42:21.719
but how do we approach it from
a nutritional standpoint? And I think

526
00:42:21.880 --> 00:42:25.719
the other part we want to point
out is that there is a rare allergy

527
00:42:27.079 --> 00:42:35.199
to sessan And by allergy, it's
written. It's well known enough that the

528
00:42:35.239 --> 00:42:38.119
Food and Drug Administration points that out
to people. It just says, hey,

529
00:42:38.159 --> 00:42:43.840
if you have an allergy to sesame, then you shouldn't be using sentime

530
00:42:43.920 --> 00:42:47.039
seed all or you shouldn't be consuming
sesame seeds, right, which the old

531
00:42:47.079 --> 00:42:51.800
McDonald's right to all be patty special
software n sesame seed buns, right,

532
00:42:51.920 --> 00:42:58.280
So anything specimen. So nothing even
in nature, comes without risk. But

533
00:42:58.400 --> 00:43:00.199
as long as you're ware of what
that risk is, then you can make

534
00:43:00.320 --> 00:43:05.639
better decisions. And that's what I'm
saying with this lipid panel. There's so

535
00:43:05.960 --> 00:43:13.039
much more information baked into that lipid
panel that we have to grease out.

536
00:43:13.599 --> 00:43:19.840
I told you offline that I had
an individual who is highly trained and has

537
00:43:19.960 --> 00:43:24.639
a medical background who basically said that
the lipid panels really wasn't useful in his

538
00:43:24.840 --> 00:43:30.480
practice. And so we've just talked
about the sort of counterway to think about

539
00:43:30.559 --> 00:43:34.480
that, and we hope we've given
you guys something to think about and go

540
00:43:34.599 --> 00:43:37.480
out and read more. But a
lot of what we're talking about has occurred

541
00:43:37.480 --> 00:43:44.960
in the last ten to fifteen years, and that's sort of science and clinical

542
00:43:45.039 --> 00:43:46.880
science. That's the good, the
bad, and the ugly. So in

543
00:43:46.960 --> 00:43:51.320
other words, the good news is
is we're always living for we're always trying

544
00:43:51.360 --> 00:43:54.719
to improve opponents. The bad is
that well that the other good of that

545
00:43:55.039 --> 00:43:59.400
is, well, we'll talk about
bad. The bad is things changed very

546
00:43:59.559 --> 00:44:05.320
slow in terms of practice and research. And that's even though it's a bad

547
00:44:05.360 --> 00:44:07.119
thing, it changes slowly. It's
actually good because we don't want to be

548
00:44:07.239 --> 00:44:12.360
changing with the win. You don't
want to be changing practice guidelines hid in

549
00:44:12.400 --> 00:44:15.639
fifteen, probably even twenty years.
But you have to be aware of what

550
00:44:15.880 --> 00:44:21.599
cutting edge somebody it's the same and
say, how can I translate that to

551
00:44:21.880 --> 00:44:27.679
my patient? As the fiance catches
up with sort of the recommendations and it

552
00:44:27.760 --> 00:44:30.679
becomes and reaffirmed. So let's go
back to the a FIB with the EPA.

553
00:44:31.159 --> 00:44:37.519
This was a meta analysis published in
the journal Circulation of really High Profiles,

554
00:44:37.679 --> 00:44:43.880
highly respected journal that said that's their
conclusion after looking at the reduced trial,

555
00:44:44.360 --> 00:44:49.199
all the other trials and says there's
something to this. And for the

556
00:44:49.360 --> 00:44:52.559
EMA to come out and say something, right, that's what I mean by

557
00:44:52.920 --> 00:44:58.119
it takes years to really get something
to change practice guidelines. But that doesn't

558
00:44:58.199 --> 00:45:01.559
mean you have to wait or your
patience to try things that make kids.

559
00:45:04.679 --> 00:45:08.119
There's an important thing that I think
that I want to tease out as and

560
00:45:08.239 --> 00:45:12.360
I think as a patient. Again, it's really hard for me to take

561
00:45:12.519 --> 00:45:17.119
my scientist's credential hat off if I'm
thinking like a patient, and this can

562
00:45:17.199 --> 00:45:21.320
be applied just about anything medically.
It's like, well, I don't trust

563
00:45:21.480 --> 00:45:25.400
what these experts are telling me because
it seems like every ten to twenty years,

564
00:45:25.480 --> 00:45:30.679
like what they said was for sure
the way to go is not necessarily

565
00:45:30.719 --> 00:45:32.480
what they end up changing. And
I think science is meant to change.

566
00:45:32.519 --> 00:45:37.119
Otherwise it doesn't progress anywhere. So
as scientists and you have an expert telling

567
00:45:37.199 --> 00:45:39.559
you, well, I do not
know. The evidence isn't there yet,

568
00:45:39.599 --> 00:45:43.679
I'm not sure. That's not then
just saying I don't know what you're talking

569
00:45:43.719 --> 00:45:46.679
about. It's that this I can't
speak for the solidification of the science because

570
00:45:46.679 --> 00:45:50.760
you never know where it's going to
go, and you have to constantly adapt

571
00:45:50.840 --> 00:45:53.960
and change things. Now, as
far as treatment guidelines go for as CBD

572
00:45:54.119 --> 00:45:58.760
and things like that in cholesterol,
I don't see them changing very frequently.

573
00:45:59.000 --> 00:46:04.599
However, if you can come up
with an option nutritionally or from a supplement

574
00:46:04.719 --> 00:46:09.800
area that helps facilitate making those guidelines
work better. Because again I'm not saying

575
00:46:09.880 --> 00:46:15.519
that like this product that you've come
up with is going to magically get everyone

576
00:46:15.599 --> 00:46:19.960
off their status. That's not how
That's not how I see it going.

577
00:46:20.039 --> 00:46:25.159
There's too much of a benefit for
statin therapy in patients support disease that you

578
00:46:25.280 --> 00:46:30.119
can help augment to where we're not
dealing with just pushing this, just turning

579
00:46:30.199 --> 00:46:35.760
the stat and level from zero to
ten and hoping for the best. You're

580
00:46:35.800 --> 00:46:42.559
really helping all the other aspects of
this mechanism that aren't being impacted to be

581
00:46:42.679 --> 00:46:47.800
impacted, then you have to use
less medication potentially. Again, that's one

582
00:46:47.800 --> 00:46:51.920
of the hard things because people in
chylog don't trust. I don't trust the

583
00:46:51.920 --> 00:46:55.079
signist because it feels like there it's
always shady. It's what has to That's

584
00:46:55.119 --> 00:46:59.280
why I'm very careful to never speak
at absolutes, and you're not like that

585
00:46:59.400 --> 00:47:02.119
either. Very We'll see where this
goes. We'll tease this out, but

586
00:47:02.280 --> 00:47:07.639
it's never I hate setting the sites
to settle on the topic because as we

587
00:47:07.719 --> 00:47:10.679
continue to grow and learn more,
it's never going to be there. Well.

588
00:47:10.760 --> 00:47:15.159
But that's why we put back to
statins as a great examples is we

589
00:47:15.360 --> 00:47:21.920
knew for years that they benefit in
curtain patients. The studies showed that time

590
00:47:22.000 --> 00:47:27.159
and time again that there is benefit, but it took years to come back

591
00:47:27.239 --> 00:47:30.280
and say there is residual risk.
And that's what I keep coming back to.

592
00:47:30.760 --> 00:47:36.440
And it will take us years to
really hone in on what's the next

593
00:47:37.199 --> 00:47:40.079
uh SATIN if you will, in
terms of reducing that risk. But we

594
00:47:40.280 --> 00:47:45.000
have to be thinking about other markers
outside of the LDL sure to cover where

595
00:47:45.400 --> 00:47:50.920
those statins don't provide benefit to patients. And as you pointed out earlier,

596
00:47:51.039 --> 00:47:54.320
there are reasons that I mean,
we have to accept as health care practice,

597
00:47:54.360 --> 00:47:59.639
theirs that our patients aren't going to
take standard of care for some reasons,

598
00:47:59.800 --> 00:48:01.880
but for reasons that are their own. People. Some people don't want

599
00:48:01.880 --> 00:48:06.000
to take stabs. There may be
side effects, it maybe farm the natural

600
00:48:06.039 --> 00:48:10.400
approaches. So I think we have
to give patients the options that they want

601
00:48:10.599 --> 00:48:15.880
and provide them at the same time
with as much information and education as possible

602
00:48:15.000 --> 00:48:20.280
along with those options, and not
just throw things to get to the walls

603
00:48:20.880 --> 00:48:22.880
what sticks. Because at the end
of the day, that's why we have

604
00:48:23.159 --> 00:48:29.719
a license to practice, is you
have that is a responsibility to those patients

605
00:48:30.000 --> 00:48:32.880
as well, And so I approach
it in the pharmacy too. It's like

606
00:48:34.280 --> 00:48:37.199
I'm never gonna I tell this to
people all the time. I'm never going

607
00:48:37.280 --> 00:48:42.760
to recommend something to you from a
supplement or a nutrition stance. There isn't

608
00:48:42.880 --> 00:48:45.320
backed up by enough science for me
to go this might have benefit or it

609
00:48:45.440 --> 00:48:50.679
might not. You know, as
a if I got if I knew nothing

610
00:48:50.719 --> 00:48:53.760
about pharmacy and I was just an
average normal person walking around and I went

611
00:48:53.800 --> 00:48:55.920
to the doctor sett I need to
be on this stat And then I went

612
00:48:55.960 --> 00:48:59.679
to the store and picked it up
and they'll say I read the package insert,

613
00:48:59.760 --> 00:49:02.719
which a lot of people read now
when I was, you know,

614
00:49:02.840 --> 00:49:06.280
even in a couple of years,
I've seen more people reading the package in

615
00:49:06.760 --> 00:49:07.800
and they're like, oh my god, I read the side effect profile,

616
00:49:07.840 --> 00:49:09.559
and that's terrifying. I don't want
to be on that. It's like,

617
00:49:09.719 --> 00:49:14.079
okay, well they have to.
Legally, they have to put every possible

618
00:49:14.159 --> 00:49:16.840
thing on that package insert that could
happen so they don't get sued. That's

619
00:49:17.000 --> 00:49:21.280
basically how it works. They have
to tease it out. There's years of

620
00:49:21.320 --> 00:49:23.760
clinical trials, so they have to
be as upfront and honest with you with

621
00:49:23.920 --> 00:49:28.119
the information. Does that mean all
those bad things are going to happen to

622
00:49:28.159 --> 00:49:32.559
you? Probably not, but side
effects do happen, and they're not rare

623
00:49:32.639 --> 00:49:36.480
if they happen to you. I
had a professor at pharmacist school always tell

624
00:49:36.559 --> 00:49:38.159
us that he goes, it's not
rare if it happens to you, and

625
00:49:38.239 --> 00:49:43.880
I'm like, that's very good way
of looking at things. So I think

626
00:49:44.000 --> 00:49:46.599
if there's other answers to have to
where patients are like, look, I've

627
00:49:46.639 --> 00:49:52.559
tried satins felt terrible on them.
Probably some pharmacogenetic aspect to that, and

628
00:49:52.639 --> 00:49:58.199
that's been well established now too that
not many clinicians are aware of or that

629
00:49:58.280 --> 00:50:06.960
pharmacists advocate for, but they if
they've tried it, and then there's no

630
00:50:07.119 --> 00:50:12.000
other alternative option B that can help
facilitate that. They're just patients are just

631
00:50:12.039 --> 00:50:14.480
gonna get frustrated, like, well, I mean, okay, I want

632
00:50:14.519 --> 00:50:16.599
my cholesterol down so I don't have
a stroke or a heart attack, But

633
00:50:16.880 --> 00:50:21.559
I don't like the fact that my
legs feel like they're getting hit with baseball.

634
00:50:21.719 --> 00:50:24.079
That's because of this satin and I
don't know what to do. It's

635
00:50:24.079 --> 00:50:27.719
like I can't and if I get
off them, then my levels shoot way

636
00:50:27.760 --> 00:50:30.639
up. And it's just like they
get it's frustrating and it causes a lot

637
00:50:30.719 --> 00:50:35.119
of anxiety and other things along with
that, and it allows that sentiment to

638
00:50:35.199 --> 00:50:38.000
be created to where I don't know
who has my best interests at heart,

639
00:50:38.239 --> 00:50:43.400
Like I don't know why I'm not
getting any benefit there. And to be

640
00:50:43.559 --> 00:50:46.480
far and to be fair and balanced, Patricks, there are those patients that

641
00:50:46.679 --> 00:50:52.039
are perfectly happy with their statings.
It's doing exactly what it was supposed to

642
00:50:52.119 --> 00:50:55.760
do. It's lowering their LDL and
they're thrilled by their LDL levels, but

643
00:50:55.920 --> 00:51:00.719
they start to recognize again there's some
there could be and their specificus is something

644
00:51:00.800 --> 00:51:06.440
that is beyond meaning additive to statins. So you're right, we need to

645
00:51:06.480 --> 00:51:10.239
talk about candidly about those folks that
aren't satisfied with statins. But we also

646
00:51:10.360 --> 00:51:15.679
need to talk about candidly those folks
that really are pleased with what their statin

647
00:51:15.800 --> 00:51:19.559
is doing, but they're looking for
other things to address that residual risk.

648
00:51:19.679 --> 00:51:23.280
And I think we have to have
that curturation with patients for sure. Respect

649
00:51:23.320 --> 00:51:27.199
to that too. That is kind
of catching fire, especially like social media

650
00:51:27.280 --> 00:51:30.000
and stuff is they'll see there's proponents
that kind of go, oh, we

651
00:51:30.400 --> 00:51:34.400
LDL cholesterol is a terrible diagnostic marker
for heart disease, like don't pay attention.

652
00:51:35.039 --> 00:51:37.559
It's like, well, you can't
say that either, because patients that

653
00:51:37.679 --> 00:51:40.199
are responding really well on statins and
their levels are looking really good. Now

654
00:51:40.280 --> 00:51:44.119
you're telling me that the doctors don't
know what they're talking about, and then

655
00:51:44.119 --> 00:51:47.199
they shouldn't be looking at that.
So there's so many different goals for thought

656
00:51:49.000 --> 00:51:52.480
and again, it always goes back
to this who do I trust? Like?

657
00:51:52.800 --> 00:51:55.639
Who? Okay, one guy's telling
me that I need to take a

658
00:51:55.679 --> 00:51:59.440
stat and to help my LDL MYL
the olds improving. Then I hear another

659
00:51:59.480 --> 00:52:02.480
reputable source, supposedly over here saying
that Eliel's dumb, we don't need to

660
00:52:02.519 --> 00:52:06.559
look at it. And then we
have someone who you alluded to that goes

661
00:52:06.599 --> 00:52:09.000
to cholesterol labs are not beneficial in
my practice. So it's like you get

662
00:52:09.239 --> 00:52:14.519
three different schools of thought there,
and the patient's just caught. They're just

663
00:52:14.559 --> 00:52:17.199
spinning out of control and they can't
make sense in it. But again,

664
00:52:19.280 --> 00:52:22.760
it's never as easy and as simple
as it seems like if you get into

665
00:52:22.880 --> 00:52:27.639
the mechanisms, even further down the
rabbit hole where this goes, it's a

666
00:52:27.719 --> 00:52:31.079
bit overwhelming. But the body is
complex and overwhelming. So to say that

667
00:52:31.199 --> 00:52:36.000
it's black and white or cut and
dry a plus bak, we'll see mechanism.

668
00:52:36.079 --> 00:52:38.800
It's just usually not I try to
stay away from that kind of language

669
00:52:38.800 --> 00:52:43.920
because it's just not usedul Now I
do I have a couple other questions going

670
00:52:43.960 --> 00:52:45.840
back to Sessimon for you, and
then we'll kind of wrap it up a

671
00:52:45.880 --> 00:52:52.039
little bit. How we've talked about
how it helps with polyuncentury if iding have

672
00:52:52.199 --> 00:52:58.880
some metalloism, how we get that
EPA to DHA ratio of in fostituol colid

673
00:52:59.000 --> 00:53:02.079
rich dha go down the LCAT pathway
to help with HDL. We've also talked

674
00:53:02.079 --> 00:53:07.400
about the triglyz red lowing and then
the cholesterol remnant lowering piece of that.

675
00:53:07.159 --> 00:53:13.679
However, how exact I know you
alluded to this earlier about talking about inflammation

676
00:53:13.800 --> 00:53:16.239
and stuff too, which is another
big buzzword thing that I think we'd like

677
00:53:16.320 --> 00:53:21.840
to talk to touch on. Correct
me if I'm wrong, But like Sessamon

678
00:53:21.960 --> 00:53:25.599
and the papers I've looked at,
it helps with really decreasing or not really

679
00:53:25.639 --> 00:53:30.079
decreasing, but decreasing and balancing our
achdonic acid production. And it does that

680
00:53:30.280 --> 00:53:34.519
by is it? I think?
Is it the enzyme is a delta five

681
00:53:34.599 --> 00:53:37.199
desaturase that it helps. Yeah,
that's what I'm saying. It's an inhibitor

682
00:53:37.199 --> 00:53:44.599
of delta five dsaturase, which basically
lowers the amount of omega six conversions.

683
00:53:44.840 --> 00:53:47.639
Correct, Well, let's I think
this is I think this is fascinating for

684
00:53:49.400 --> 00:53:53.679
pharmacologists, pharmacists, which as most
of your listeners are many of your listeners

685
00:53:53.760 --> 00:54:00.639
are. Is the if you look
at pollen saturaated fatty as metabolism, we

686
00:54:00.840 --> 00:54:07.199
know that there are two groups Omega
six and omega three, so there is

687
00:54:07.599 --> 00:54:12.480
a single enzyme right in that past. So in other words, is a

688
00:54:12.639 --> 00:54:16.840
multi step process, multi inzomatic process. We metabolize essentral fatty ads as omega

689
00:54:16.880 --> 00:54:22.679
six and omega three. What's really
unique about that pathway is these enzymes.

690
00:54:22.719 --> 00:54:29.360
And you pointed out the rate limiting
step Delta five to saturates. It has

691
00:54:29.599 --> 00:54:36.440
an omega six input and it also
can process an omega three input, so

692
00:54:36.719 --> 00:54:42.760
it's the same enzyme, but it
can metabolize either omega six substrate or in

693
00:54:42.800 --> 00:54:47.880
a maja Maga three precursor. That's
important, really important when it comes to

694
00:54:49.119 --> 00:54:53.239
sessiment because as you know and as
your listeners know, on the omega six

695
00:54:53.360 --> 00:54:59.400
side, the output of that enzyme
is the rhachodonic acid. So now we're

696
00:54:59.440 --> 00:55:02.239
in a look at t we're into
a cyclop you know, it's all sorts

697
00:55:02.280 --> 00:55:08.199
of pro and anti inflammatory markers.
On the omega three side, the output,

698
00:55:08.599 --> 00:55:13.199
the metabolite, if you will,
is EPI. Okay, So when

699
00:55:13.239 --> 00:55:16.840
you think about delta five disat raates
the rate limiting steck. It kicks out

700
00:55:17.000 --> 00:55:21.760
a rackodonic acid on the omega six
side, and it kicks out EPA which

701
00:55:21.800 --> 00:55:25.320
is subsequently converted to DHA and further
downstream events. Right, So then it

702
00:55:25.400 --> 00:55:30.400
begs the question, well, how
can I inhibit or I mean, it

703
00:55:30.559 --> 00:55:34.559
would not be inhibiting. If I'm
inhibiting their enzyme would not be inhibiting racodonic

704
00:55:34.639 --> 00:55:39.199
acid formation in EPA formation simultaneously,
So it's a canceling out and the answer

705
00:55:39.280 --> 00:55:47.039
is no. This is what's fascinating
about Sessimon. Sessimon appears through mechanistic studies

706
00:55:47.119 --> 00:55:54.760
pharm acology studies in vitro and and
vivos to preferentially inhibit the omega six mechanism

707
00:55:54.960 --> 00:56:00.320
of delta five satur rates, meaning
it shuts down, not complete, but

708
00:56:01.000 --> 00:56:06.199
minimizes or mitigates a rackotonic acid formation, and we know that's good in the

709
00:56:06.239 --> 00:56:09.840
setting of high racotonic acid, so
that can be anti inflammatory, while at

710
00:56:09.880 --> 00:56:16.400
the same time it maintains or potentially
enhances the EPA formation subsequent downstream DHA.

711
00:56:16.880 --> 00:56:24.719
So that's how a single molecule in
sesame sidol extraction can impact inflammation significantly just

712
00:56:24.920 --> 00:56:31.000
through that single mechanism of action,
and then the other those folks interested in

713
00:56:31.079 --> 00:56:37.159
nutrogenomics, we know that there are
two types of individuals and it's race based,

714
00:56:37.239 --> 00:56:40.559
and we can go into this in
another call or a podcast. You're

715
00:56:40.599 --> 00:56:45.320
either a very rapid metabolizer, right, so let's go back to our P.

716
00:56:45.400 --> 00:56:47.880
Four fifty right, our drug metabolism. Language are a poor metabolizer extensive

717
00:56:47.880 --> 00:56:52.719
metabolism. You're either an extensive metabolizer, meaning you form a lot of a

718
00:56:52.800 --> 00:56:55.159
rackotonic acid in epa And that's the
term what your diet is, right,

719
00:56:55.760 --> 00:57:00.280
Mega six versus high and magas three
or vice versa. Okay, and there's

720
00:57:00.320 --> 00:57:07.400
another cobortive individuals for genetic reasons,
they're slow metabolizers, and so the impact

721
00:57:07.519 --> 00:57:12.639
of a bad diet is less than
those individuals. And how that sorts out

722
00:57:12.960 --> 00:57:22.639
from a racial standpoint is that the
more from a genealogical standpoint genetic standpoint,

723
00:57:22.239 --> 00:57:30.800
that African origin people have a much
higher chance of inheriting a rapid metabolism.

724
00:57:31.239 --> 00:57:37.360
So there have been numerous studies that
have said if you heat Omega six and

725
00:57:37.519 --> 00:57:42.159
you have an African descent, then
you're forming lots of araconomic aget that's related

726
00:57:42.159 --> 00:57:49.559
to obesity and inflammation in general the
non African origin. So now you're talking

727
00:57:49.599 --> 00:57:57.679
about your European Caucasians, they through
evolution have acquired a slower form of the

728
00:57:57.840 --> 00:58:05.800
gene, so now they metabolize those
EPA and arachdomic acid pre precurasors more slowly,

729
00:58:06.480 --> 00:58:10.920
and the bad the result of a
bad diet is manifest less in those

730
00:58:10.960 --> 00:58:16.480
who have slow metabolism. So that
starts to raise this interesting conversation around racial

731
00:58:16.599 --> 00:58:24.840
differences. So there is every potential
that this approach using cess received extract may

732
00:58:24.960 --> 00:58:30.599
have an impact that is differential or
differential impact based upon race. Those are

733
00:58:30.639 --> 00:58:34.800
all sorts of things that can be
looked at in the future. Right,

734
00:58:34.920 --> 00:58:37.760
But that's just one step on the
inflammation side, and I probably want a

735
00:58:37.760 --> 00:58:42.840
little deeper. That's you know,
that's a great way to think about the

736
00:58:43.199 --> 00:58:46.000
nation piece. Uh. Yeah.
Inflammation is a big buzzword, very important.

737
00:58:46.320 --> 00:58:49.960
It's one of those things that's like
you need, let's be honest,

738
00:58:50.000 --> 00:58:52.000
you need inflammation for things to work, do some other process you want to

739
00:58:52.119 --> 00:58:59.719
completely mitigate or whatever it is.
However, but here's the other important thing

740
00:58:59.760 --> 00:59:07.079
for a nutrition standpoint, is destiny
seed oil for thousands of years was the

741
00:59:07.599 --> 00:59:10.480
oil of choice. One of reasons, one of the reasons, my main

742
00:59:10.559 --> 00:59:15.679
reason is for stability. It's such
a high antioxidant oil that it was much

743
00:59:15.760 --> 00:59:22.159
more stable than less well more stable
than those oils that weren't as rich in

744
00:59:22.320 --> 00:59:25.679
antioxidants. And so now you've got
this. You know, we talked about

745
00:59:25.719 --> 00:59:30.280
cesciling, you talked about delta fied
to saturation and how that can impact inflammation,

746
00:59:30.599 --> 00:59:36.480
but we also know that those antioxidants
in this oil and the extract can

747
00:59:36.559 --> 00:59:42.760
also positively impact inflammation. Yeah,
and then man, there's so much cool

748
00:59:42.760 --> 00:59:45.960
stuff. And we didn't even get
to touch on the postitium component of like

749
00:59:45.079 --> 00:59:50.039
cognition improvement as well as skin improvements
too. That's another podcast rabbit Hole,

750
00:59:50.119 --> 00:59:53.039
want to go down on every want
to go down in, because that's a

751
00:59:53.119 --> 00:59:57.760
whole other interesting interlude. Like,
all these systems are interlinked, so it's

752
00:59:57.880 --> 01:00:00.880
very interesting when you start to tease
out why it's doing what it's doing,

753
01:00:00.440 --> 01:00:05.960
different aspects of it all. But
yeah, inflammation is a big one that

754
01:00:06.159 --> 01:00:10.360
I think a lot of people and
I've talked about information to a little bit

755
01:00:10.400 --> 01:00:14.159
of a degree on some other podcasts. I need to kind of recover it

756
01:00:14.239 --> 01:00:19.400
because I'm generalizing here, but I
think it's not a stretch for me to

757
01:00:19.480 --> 01:00:23.159
do this. What people here,
especially on social media or other platforms sell

758
01:00:23.199 --> 01:00:27.119
here inflammation they just think it's all
inflammation is the same, and it's not.

759
01:00:27.239 --> 01:00:30.320
In case, there's differences between acute
and systemic. And what I want

760
01:00:30.360 --> 01:00:35.119
to point out is when you're talking
about crp air lucan six, like other

761
01:00:35.239 --> 01:00:38.840
cytokines inflammatory cytokinds that are out there, that is systemic inflammation. And that's

762
01:00:38.960 --> 01:00:45.280
not usually something you see acutely raised
unless we're dealing with some other situation sepsis,

763
01:00:45.360 --> 01:00:47.920
other things like that. But when
you're talking about chronic inflammation, that's

764
01:00:47.960 --> 01:00:52.440
what most people are referring to.
As these systemic blood markers of inflammation that

765
01:00:52.519 --> 01:00:57.920
we see time and time again correlate
perfectly with these chronic diseases that we've seen

766
01:00:58.039 --> 01:01:01.840
on the rise. Well, now
let's bring these full circle, Patrick,

767
01:01:02.280 --> 01:01:07.800
And there's a fascinating paper that just
published I shared with you via text over

768
01:01:07.880 --> 01:01:16.800
the weekend that looks at independent risk
markers for ASCVD remnic cholesterol. Near the

769
01:01:16.840 --> 01:01:21.440
top of the list if not the
top of the list. An independent but

770
01:01:21.719 --> 01:01:30.760
equally important risk modifier for ASCVD is
see reactive protein. So this chronic inflammatory

771
01:01:30.920 --> 01:01:35.199
process, and you distinguish that that's
eloquently from acute right where you've got these

772
01:01:35.239 --> 01:01:38.239
pro inflammatory side of kinds in the
systemic inflammatory response centers. We're not talking

773
01:01:38.280 --> 01:01:43.639
about that. We're talking about chronic
inflammation. We're talking about he reactive protein

774
01:01:43.719 --> 01:01:51.079
CRP, and that is a very
important marker of risk that it gains independent

775
01:01:51.199 --> 01:01:54.800
of remnant cholesterols. But what this
paper shows is in this very large I

776
01:01:54.840 --> 01:02:00.679
think it was forty thousand plus patient
study, is when you can consider those

777
01:02:00.800 --> 01:02:06.800
as independent markers CRP and remnant cholesterol, that really starts to hone in on

778
01:02:06.960 --> 01:02:12.679
what your risk is from an ASCVD
standpoint. And that's the fascinating. Yes,

779
01:02:13.039 --> 01:02:17.239
that paper, three thousand patients,
I think they like that in that

780
01:02:17.440 --> 01:02:21.320
sea reacting for a team paper.
I've got it pulled up, I think

781
01:02:21.360 --> 01:02:25.440
yours, Yeah, thank you.
That was similar to the two thousand and

782
01:02:25.519 --> 01:02:30.920
nine paper where they looked at statins
and risk and a residual risk. But

783
01:02:30.119 --> 01:02:36.639
yes, the large study is the
bottom line, like thousands of people that

784
01:02:37.000 --> 01:02:45.599
looked at CRP and rhymney cholesterol independent
highly insignificant terms of predicting ASCVD risk.

785
01:02:47.599 --> 01:02:50.800
Yeah, I think I think we've
hit the nail on the head with it.

786
01:02:50.920 --> 01:02:52.719
It's just really cool how it all
kind of ties in and works together,

787
01:02:52.880 --> 01:02:55.519
and how you see that really Oh, here we go, I found

788
01:02:55.559 --> 01:03:00.760
it. Here we go. I
found out paper. Yeah, you're right,

789
01:03:00.039 --> 01:03:04.320
it's like forty thousand patients. And
then I was referring back to the

790
01:03:04.840 --> 01:03:07.400
other one we talked about where it
was over one hundred thousand, So started

791
01:03:07.400 --> 01:03:12.519
to get that mixed out there,
but still a lot of people right that

792
01:03:13.199 --> 01:03:17.880
it's not just one hundred person trials
and CRP. If you go to lab

793
01:03:17.960 --> 01:03:22.800
core for examples, and you look
at labport, what panel do they offer

794
01:03:22.920 --> 01:03:27.159
for inflammation? I mean, your
father and I run a phase one clinical

795
01:03:27.239 --> 01:03:30.480
center and one of the things we
look at is inflammation, and C reactive

796
01:03:30.519 --> 01:03:37.239
protein is what lab poor offers as
their general inflammatory marker. So that's a

797
01:03:37.360 --> 01:03:42.320
really solid marker, and it's neat
to see that it connects back to ASCVD

798
01:03:42.599 --> 01:03:49.199
risk and connects back to independently connects
back to the remnant cholesterol. So I

799
01:03:49.239 --> 01:03:52.719
think that's a great way to sort
of think about this one last aside I

800
01:03:52.800 --> 01:03:58.000
want to make because it's another popular
thing that's kind of catching win now because

801
01:03:58.519 --> 01:04:02.000
again this is a peo. I
feel like for the nutrition world, all

802
01:04:02.079 --> 01:04:06.199
of the world's problems have been thrown
in some sort of nutrition camp. Like

803
01:04:06.320 --> 01:04:11.320
for in the nineties, it was
like sugar most of the problem, and

804
01:04:11.400 --> 01:04:14.199
then before I would say the two
thousands, it was okay, sugar is

805
01:04:14.239 --> 01:04:17.639
the real cause of issues, and
then before that with it was hello,

806
01:04:17.800 --> 01:04:20.880
fat diets are the way to go. And now it's kind of the next

807
01:04:20.920 --> 01:04:24.840
one that's kind of catching win is, Oh, it's the seed oils that

808
01:04:24.920 --> 01:04:27.039
are causing all these issues that we
cook at it. It's like, I

809
01:04:27.119 --> 01:04:30.199
think if anyone gets anything out of
this podcast that we talked about sessamon as

810
01:04:30.239 --> 01:04:33.039
much as we've talked about that,
I think maybe the case can be made

811
01:04:33.320 --> 01:04:38.519
that seed oil it's fine and really
beneficial. So it's like, again,

812
01:04:38.559 --> 01:04:41.760
I think it's funny, how though, what all the seed oils together.

813
01:04:41.840 --> 01:04:45.760
It's like, you know, it's
funny you should say that, Patrick,

814
01:04:45.840 --> 01:04:48.920
because I literally had that question last
week. It says, oh, but

815
01:04:49.039 --> 01:04:54.400
I thought this, well, the
question was I thought sesame seed oil was

816
01:04:54.519 --> 01:04:56.800
banned, so I dug in a
little bit, well, well, because

817
01:04:56.840 --> 01:04:59.519
of reading about seed oils and things
like that, and to your point,

818
01:05:00.000 --> 01:05:02.679
we lumping things together. I mean, there's a reason why, to sess

819
01:05:02.760 --> 01:05:08.119
me, seed oil was the primary
cooking oil for thousands of years, and

820
01:05:08.679 --> 01:05:14.119
I'm not saying that it's not detrimental
in certain sceniar, but it's not something

821
01:05:14.280 --> 01:05:20.559
that science is pointing to as causative
for cardiovascular events, and at least from

822
01:05:20.599 --> 01:05:25.000
my reading, I shouldn't state that's
so sens aticate. I mean, another

823
01:05:25.039 --> 01:05:28.039
reason that they use sesame oil for
the longest time to cook with is because

824
01:05:28.079 --> 01:05:30.079
it's one of the oils to cook
with that has the highest smoke point,

825
01:05:30.159 --> 01:05:34.320
so you're less likely to have bubbling. And like if you cook with olive

826
01:05:34.360 --> 01:05:39.320
oil at really high temperatures, its
flashes everywhere. It's not fun to deal

827
01:05:39.400 --> 01:05:43.679
with. But I mean, as
far as a seed oil or an oil

828
01:05:43.840 --> 01:05:46.400
used for cooking that has a high
smoke point but yet actually it has flavor

829
01:05:46.480 --> 01:05:49.440
enhancing properties, selling me oil is
like I guess, like four hundred and

830
01:05:49.599 --> 01:05:54.760
ten or something like that. I'm
stretching because I had to dive into all

831
01:05:54.800 --> 01:05:57.800
of that when I was doing my
master's program. We were talking about oils

832
01:05:57.840 --> 01:06:02.320
and all sorts of stuff. But
again it yeah, and I'm a fonatology

833
01:06:02.559 --> 01:06:08.239
not a nutrition right, They've got
to be very I'm not a seed oil

834
01:06:08.280 --> 01:06:12.519
expert either, but I think and
then it goes back to the education piece

835
01:06:12.559 --> 01:06:15.199
of things, because people will go, oh, they're highly processed. It's

836
01:06:15.239 --> 01:06:19.239
like, okay, a lot of
foods that have any sort of packaging or

837
01:06:19.280 --> 01:06:24.960
shelf li for process to a degree. But they'll talk about using from a

838
01:06:25.039 --> 01:06:27.360
seed oil perspective, They'll say,
oh, well, you have to use

839
01:06:27.360 --> 01:06:30.320
all these different solvents to extract the
seed oils out, and you have to

840
01:06:30.599 --> 01:06:34.559
put them into this these big machines
to do all of that expel the oil

841
01:06:34.599 --> 01:06:40.920
out. Okay, Like I think
the big the big one now is oh

842
01:06:40.960 --> 01:06:44.360
they use he saye to like get
the oil separated. It's like, okay,

843
01:06:44.400 --> 01:06:46.039
well, if the final improduct has
zero hexane in it, they have

844
01:06:46.119 --> 01:06:51.719
to get all of it out,
so whoop to do? Yeah, you

845
01:06:51.760 --> 01:06:55.960
know, you raise an interesting point. I need to better educate myself on

846
01:06:56.519 --> 01:07:00.159
the pressing versus the use of organics. And I'm not certain, so I'm

847
01:07:00.199 --> 01:07:04.559
not saying one way or the other
how sesame seed oil is typically processed,

848
01:07:04.920 --> 01:07:12.079
but my reading is mainly through pretty
processing and not use of texting. But

849
01:07:12.440 --> 01:07:17.519
I need that however, I will. I'm pretty sure of the seed oils,

850
01:07:17.559 --> 01:07:23.760
like you have to do less less
expeller processing, and you don't have

851
01:07:23.880 --> 01:07:26.719
to do it at higher temperatures.
For sesame oil, it's very easy to

852
01:07:26.800 --> 01:07:30.400
coal press sesame oil out. As
far as sesame seeds in general, they

853
01:07:30.440 --> 01:07:35.400
have a higher concentration will in them
as opposed to say corn or canola oil

854
01:07:36.559 --> 01:07:41.960
or soybean oil that you have to
use higher temperature heating to kind of get

855
01:07:42.159 --> 01:07:45.639
in more of the product to get
that oil extracted out, whereas olive oil,

856
01:07:46.360 --> 01:07:51.320
peanut I think, and then sesame
oil that just there's more oil concentrated

857
01:07:51.400 --> 01:07:55.920
the seed itself, so it's easier
to coal press it out. So I

858
01:07:55.960 --> 01:07:58.880
think for sesame oil, I think
most of those are coal press, which

859
01:07:59.639 --> 01:08:01.559
most of your olive oil is cold
press for that exact reason. So it's

860
01:08:01.599 --> 01:08:03.960
one of the ones that if I'm
going to use, I like that one

861
01:08:04.039 --> 01:08:09.320
quite a bit. And again I
don't fry foods very much, and I've

862
01:08:09.400 --> 01:08:11.920
never heard of I mean, you
can saw tay things and sesame oil,

863
01:08:11.920 --> 01:08:17.439
but I don't think you rise like
anything. Yeah, and if you've got

864
01:08:17.479 --> 01:08:20.800
any listeners who really want to read, let me go back to AY Evading

865
01:08:21.079 --> 01:08:26.960
Medicine texts and read about sesame seedel
and AYE Evading medicine. There's a ton

866
01:08:27.119 --> 01:08:31.520
of information out there that's it's consistent
with what we're seeing anecdotally. It's fast.

867
01:08:31.640 --> 01:08:38.680
Last thing I wanted to mention there's
yeah, and we touched on I

868
01:08:38.720 --> 01:08:42.359
don't know if you're I want to
pose one question to you because I had

869
01:08:42.399 --> 01:08:45.520
a patient asked me this the other
day, literally, yes, Saturday,

870
01:08:45.239 --> 01:08:49.359
she came in and she was asking, she's wanting us to purchase the product

871
01:08:49.520 --> 01:08:54.439
that you've developed that we're that we
have in this pharmacy. And she was

872
01:08:54.560 --> 01:09:00.880
asking if there's any risk for lead
crimps or anything that you've seen with using

873
01:09:00.960 --> 01:09:06.000
something like sessimon in there. And
I didn't nothing that I've come across that

874
01:09:06.119 --> 01:09:10.000
really would make me think about that
to any certain degree. But have you

875
01:09:10.079 --> 01:09:13.880
seen that reported anywhere? Because I
know in some cell studies that I've found

876
01:09:14.680 --> 01:09:19.600
sessamon does have some hmg CoA reduct
tastes inhibiting a properties. So that's kind

877
01:09:19.640 --> 01:09:25.359
of working down that Staton pathway to
a degree. Have you seen anything in

878
01:09:25.439 --> 01:09:29.279
there of the you've reported with like
leg creeps or anything like that with Sessimon

879
01:09:29.359 --> 01:09:31.000
that because that was something that she
asked me about, but I was just

880
01:09:31.119 --> 01:09:38.760
curious across anything like that. So
I'd say two things. First, is

881
01:09:39.119 --> 01:09:42.199
ahe am not aware, which does
not mean it's not out there, But

882
01:09:42.359 --> 01:09:48.800
I am not aware of any muscle
related issues for Sessimon sesame seed oil extract

883
01:09:48.960 --> 01:09:54.960
or using it as a cooking oil. That's it. I will dig in

884
01:09:55.119 --> 01:09:58.039
and see if I can find anything
to be more definitive, But I've read

885
01:09:58.119 --> 01:10:01.000
quite a bit about sesame seed a
in Sesimon, and I am unaware of

886
01:10:01.159 --> 01:10:05.159
any side effect related to that.
And we have had no reports any dotally

887
01:10:08.359 --> 01:10:13.000
but always were but as always right
where pharmacants, we always have our ears

888
01:10:13.079 --> 01:10:15.720
open, right, what are some
things that are just sort of unexplainable.

889
01:10:16.359 --> 01:10:23.000
But the other thing that I want
to leave the listers with is that while

890
01:10:23.079 --> 01:10:29.680
this is natural, it is not
a pharmaceutical approach. There's a blurred line

891
01:10:29.920 --> 01:10:35.159
between natural and pharmaceutical, and that
blurred line is you're talking about small molecules,

892
01:10:35.239 --> 01:10:39.600
spider chemicals, in this case that
interact with processes in the body,

893
01:10:40.319 --> 01:10:47.520
and so for sesame seed oil and
specifically for sessimon, which is one of

894
01:10:47.600 --> 01:10:53.840
these actives in sesame cole extract.
There is in vitro work, much like

895
01:10:53.960 --> 01:10:59.760
you do for a prescription medication,
where you're looking at interactions between a molecule

896
01:11:00.119 --> 01:11:06.560
in cidercrop four fifties, there is
evidence that sessimon is able to modulate SIP

897
01:11:06.680 --> 01:11:15.119
to C nine activity, and so
the in vitro studies are more abundant than

898
01:11:15.199 --> 01:11:18.720
the in vivo studies. There was
one in vivo study done in humans that

899
01:11:18.880 --> 01:11:25.920
did not see an interaction, but
like got educated students for twenty something years,

900
01:11:26.720 --> 01:11:29.520
if it can interact, even at
the end vitro level, that's why

901
01:11:29.560 --> 01:11:32.640
the FDA mex pharmaceutical companies put that
information to packaging. Sir, Then you

902
01:11:32.880 --> 01:11:39.239
as a pharmacist need to be aware
that if you see something untoward then that

903
01:11:39.359 --> 01:11:44.520
could potentially be the reason. So
again that's the only not the only,

904
01:11:45.119 --> 01:11:50.399
well really the only thing that raises
my pharmacists awareness when I'm talking about this

905
01:11:50.479 --> 01:11:58.199
suthing beyond the sympomy. Yeah,
allergen for the but yeah, so stick

906
01:11:58.279 --> 01:12:01.039
two C nine so keep that in
mind. If you're a practitioner, or

907
01:12:01.079 --> 01:12:05.520
if you're patient and you're taking other
SIP two C nine, I check other

908
01:12:05.680 --> 01:12:12.239
if you're taking SIP two C nine
mediated metabolism interactions or excuse me, medicines,

909
01:12:13.159 --> 01:12:15.479
Yeah, that's it. Two C
nine is an interesting one. That's

910
01:12:15.520 --> 01:12:19.560
not one of the primary ones.
But I remember often, well, we

911
01:12:19.720 --> 01:12:24.359
know that SIP three A and four, right, they comprise the vast majority

912
01:12:24.439 --> 01:12:29.640
of metabolisms. SIP two C nine
is rare. But in terms of metalloism

913
01:12:29.720 --> 01:12:34.600
of prescription medical description, medications do
absolutely and you need to be aware in

914
01:12:34.720 --> 01:12:40.279
that when you're on these together,
right, and you know your dad could

915
01:12:40.359 --> 01:12:43.279
lectures for an hour on HERB drug
interactions, right, is the world's leading

916
01:12:43.319 --> 01:12:45.239
expert. But that's just something I
want to make sure he's pointed out to.

917
01:12:45.439 --> 01:12:48.520
Yeah, practitioners, I think patients. Common ones that come to my

918
01:12:48.640 --> 01:12:54.279
mind like colpidogrels one that is two
C nine A leapers als two C nine.

919
01:12:56.159 --> 01:13:00.960
The only other one I really see
this is flew with statin maybe a

920
01:13:01.039 --> 01:13:05.199
little bit, and then you know
phenotone. But I mean some of those

921
01:13:05.359 --> 01:13:09.760
you come across very often. But
again I guess I've said this on the

922
01:13:09.800 --> 01:13:13.319
podcast before. I always ask patients
whenever I have something, say to you,

923
01:13:13.399 --> 01:13:15.479
take any prescription medications. And one
patient when I asked her that,

924
01:13:15.560 --> 01:13:18.159
shecause You've asked me that every time
I've come in here, and I'm like,

925
01:13:19.239 --> 01:13:25.880
there's there's a reason I'm making my
job, so it's important, right.

926
01:13:26.319 --> 01:13:29.159
But that's what I wanted to point
out here as well, is just

927
01:13:29.680 --> 01:13:32.039
always be aware of the potential.
Now so I'm back in my pharmacy,

928
01:13:32.239 --> 01:13:38.159
you know, Professor days is always
be aware of the potential right for what

929
01:13:38.319 --> 01:13:41.079
is it? Forewarned, is forearmed
or whatever it is. But anyway,

930
01:13:41.199 --> 01:13:44.239
well keep that. Really appreciate you
coming on again. I'll have you on

931
01:13:44.520 --> 01:13:46.319
multiple times because there's multiple every time
I talk to you, there's like eight

932
01:13:46.359 --> 01:13:50.359
other areas I want to pick your
brain on because you're sharing a lot of

933
01:13:50.560 --> 01:13:55.840
the same interests and stuff like that. So I think we've got an interesting,

934
01:13:57.760 --> 01:14:00.600
really good backed mechanism or what way
for how we think's going on,

935
01:14:00.720 --> 01:14:05.359
and we'll continue to tease that out. But you've I really like the idea

936
01:14:05.560 --> 01:14:09.720
of really harping on the education piece
of all of this, because that's the

937
01:14:09.800 --> 01:14:13.880
key is making how can we take
these complex topics make them easier to understand,

938
01:14:14.039 --> 01:14:16.359
and how we can kind of take
all the pieces together and not look

939
01:14:16.439 --> 01:14:21.359
at it so compartmentalized, you know, and just that piece and that holistic

940
01:14:21.399 --> 01:14:27.279
approach I think is just a great
way of tackling complex issues, specifically around

941
01:14:27.319 --> 01:14:31.479
that cholesterol and risk and all that
stuff for heart disease. Well, all

942
01:14:31.560 --> 01:14:36.960
Blatt, we talked about a continuing
the education talk. It's right beyond LDL

943
01:14:38.199 --> 01:14:44.439
tackling residual risk and talking about these
things in a structured environment and continuing education.

944
01:14:44.720 --> 01:14:46.159
That would be a fascinating I think
people would get a lot of benefit

945
01:14:46.199 --> 01:14:48.439
out of that, and I definitely
want to pick your money and help out

946
01:14:48.479 --> 01:14:53.279
there. I think we can wrap
the episode up and then we'll go from

947
01:14:53.279 --> 01:14:56.279
there. I'll have you on again
soon, And like I said, I

948
01:14:56.399 --> 01:14:59.560
really appreciate your time and always enjoy
talking to you. You've been one of

949
01:14:59.600 --> 01:15:03.680
the best. You've been one of
the mentors that like its always really pushed

950
01:15:03.800 --> 01:15:09.920
me to kind of expand my horizons
as much as possible in ways of just

951
01:15:10.079 --> 01:15:12.800
continuing to stay on the forefront of
where all this is going. So I

952
01:15:12.840 --> 01:15:16.479
appreciate you with that for sure more
value to me than you want. Then

953
01:15:16.880 --> 01:15:21.199
it takes at effort. It takes
a lot of effort in reading. And

954
01:15:21.319 --> 01:15:25.720
my wife who's also a pharmacist of
twenty five plus years, that's what we

955
01:15:25.840 --> 01:15:31.000
talk about, is the difference maker
is the reading and staying apreast of what's

956
01:15:31.119 --> 01:15:35.560
new. And that's why the education
piece is so important. And why am

957
01:15:35.640 --> 01:15:41.000
I at this stage of my career
learning about the importance of remnant cholesterols.

958
01:15:41.359 --> 01:15:44.600
It blows my mind and I should
have known about it earlier. So yes,

959
01:15:44.680 --> 01:15:48.640
it's part of that passion just educating. Podcasts like yours and the motivations

960
01:15:48.680 --> 01:15:54.079
for doing that are really important.
And maybe we'll get some listeners that'll have

961
01:15:54.239 --> 01:15:58.239
questions that you know or want to
figure out how to help and educate as

962
01:15:58.319 --> 01:16:01.600
well and spread the words that's right, more people understand. I'd like to

963
01:16:01.640 --> 01:16:04.119
get that to it. I'd love
to get to a point because some of

964
01:16:04.199 --> 01:16:08.560
the podcasts I really enjoyed do have
like a live Q and a component,

965
01:16:08.680 --> 01:16:12.159
So it'd be interesting to see how
that I could factor that in later,

966
01:16:12.319 --> 01:16:14.800
or you know, just have people
send the questions to us and to see

967
01:16:14.800 --> 01:16:17.920
where and do like a ask me
anything kind of episode where we just kind

968
01:16:17.960 --> 01:16:20.239
of answer people's questions. I think
that would be a cool one to do,

969
01:16:20.600 --> 01:16:24.520
especially if you or my dad or
your guys groups. You're right,

970
01:16:24.680 --> 01:16:27.439
that would all definitely work on some
of that stuff. Ron, But I

971
01:16:27.760 --> 01:16:30.640
really appreciate you being here and thank
you for your time, and thank you

972
01:16:30.720 --> 01:16:49.720
guys for listening. Thank you for
joining us on today's episode of The Wellness

973
01:16:49.760 --> 01:16:55.640
Transcription Podcast. We hope you're inspired
to live a healthier, more purpose filled

974
01:16:55.720 --> 01:16:59.920
by Christ. Remember your well being
is a gift from God, and by

975
01:17:00.079 --> 01:17:02.680
taking care of your body, you
give him the glory. If you enjoy

976
01:17:02.760 --> 01:17:06.119
today's episode, please subscribe, share, and leave us a review. We'd

977
01:17:06.199 --> 01:17:11.319
love to hear from you guys.
Your continued support helps us spread this message

978
01:17:11.359 --> 01:17:15.520
of health and faith. Until next
time, may God's grace and good choices

979
01:17:15.720 --> 01:17:18.560
guide your path to a life soil
with joy, vitality, and a deeper

980
01:17:18.600 --> 01:17:21.840
connection with Jesus. God bless you
all, and we'll see you in the

981
01:17:21.920 --> 01:17:23.640
next episode.

