It hurts to have to say that the standards of medicine for prevention of
heart attack and stroke are basically very simple and based on cholesterol
levels. If you have a closed low cholesterol level, they recommend a
lifestyle, of course, with statins and it's simple but wrong. Well, why do I say
wrong? Half of people that have heart attacks and strokes have normal
cholesterol levels so not only does that hurt to have to say that it kills people
on a regular - every minute of every day. So, what's even more unfortunate is that
we know what else is going on. The science has shown us that the cause is
cardiovascular inflammation. The science has also shown us how to treat and
prevent cardiovascular inflammation. Now, regarding how to detect cardiovascular
inflammation, I've done a full - did digital course on how to do it. It is
simple, there - there's a simple series of tests - cardiovascular inflammation
screening - you can get those, John and I developed a course and that course is
still free at this point. You can look on our website, look on the YouTube channel
and John can help - help you if you still can't find it, we've got plenty of videos
on it. What's even more unfortunate, again, as I
said is that we know how to treat and prevent cardiovascular inflammation - the
major cause of heart attack and stroke. Well, how do you treat it? Of course,
number one is lifestyle. Obviously, decrease smoking, get your weight where
it needs to be. What people - one of the key things about lifestyle that people
do not understand is that insulin resistance - high insulin and high blood
sugar are the most common cause of plaque in the arteries due to
damaging the slick inner lining, the intima or endothelium of the artery.
So that's one thing that a lot of this channels about - helping people understand
the specifics and the focus and the importance of high blood sugar. Now, there
are people that - that control those things and still need help and you can't
get to this part of heart attack and stroke prevention without talking about
drugs and statins. I know I get a lot of haters telling me that I'm paid by the -
by the big pharma. Now, the answer - No, I'm not. I'm not paid by Big Pharma. I'm paid
by my patients to help them not have a heart attack and stroke so if patients
do have the cardiovascular inflammation process going on, they do have plaque. I
do recommend statins. Now, there are a lot of patients that are at the level of
sophistication who - that understand that some statins are better than others for
helping treat cardiovascular inflammation. That's exactly right. When
you look at our - our discussion channels, look up Elbert Kong, E-L-B-E-R-T K-O-N-G
He's making some comments about that. Matt Kelly is as well, and I see that John
Lorscheider, as us- as usual, is doing a great job in terms of helping them
through this. Some of the questions are "Hey Doc, I um - I'm on lipitor. I wanted to
switch to rosuvastatin because I heard it was better for cardiovascular
inflammation. I actually brought it up with my doc and he's skeptical. Do you
have any any research - any science that - any articles that show that?" And the
answer is - Yes I do. That's what this video is about actually because John
talked about the Jupiter study - Jupiter was the classic study showing that not
only does inflammation cause heart attacks and strokes - that statins and
specifically rosuvastatin does help decrease. It, actually,
takes a major chunk out of the heart attack and stroke risk that you have
from cardiovascular inflammation so - let's go to this study and talk about
differences in statins and a couple of other things, you know - How the statins
work. This is 2017 - that Jupiter study that
we'll talk about later was in the New England Journal, back in '08 because
it was a major - should have been a major standards changer.
It wasn't. And we can talk about that a little bit later, as well. But, again, let's
go to this article - it was in current cardiology reviews in 2017: The
Anti-inflammatory Effects of statins on coronary artery disease and updated
review in the literature. In other words, there - there's two different ways of
articles that might review literature. One is a lit review, like you see here,
that is reviewing conclusions that have been seen in other studies on the topic.
It's different from a meta-analysis because with a meta-analysis, you get
deeper. You try to actually compare the data in one study to another and pool
that data you got to have a lot of - a lot of similarities. A lot of ability to
compare. Now, this is not a meta-analysis. This is just an updated review of the
literature but it gets into some very interesting things in this area of
differentiating statins and, mostly, the pleiotropic effects of statins. Now, what
do I mean by pleiotropic effects? Pleio- just means multiple, -tropic
means going after so when you hear the term pleiotropic effects of statins,
here's what they're talking about. Everybody and their dog knows that statins
lower cholesterol but what was interesting and what they showed with
Jupiter and some other studies that Paul Ridker at Harvard did - was that
statins actually helped even if somebody has inflammation but they don't have
high cholesterol. That's that 50% of people that have heart attack and
stroke but had normal cholesterol. Statins still helped anyway and some
statins help more than others and, again, it's through that pleiotropic - they have
another effect on something else. What is the other effect and what is that
something else? Well, let's talk about it. As you see on the highlighted area,
they're close. Their beneficial effect, apart from cholesterol reduction,
relies in their pleiotropic properties. Emerging evidence - lab and clinical
trials have pointed out the pivotal role of inflammation in- in initiation
exacerbation of atherosclerosis. To - to get a little bit more graphic - what
happens most often is that it's either elevated insulin or elevated sugar
causes damage to the intima, the endothelial - the slick lining - the slick
lining of the artery. Once you get damaged, it really doesn't matter so much
what level your cholesterol value is. Cholesterol will seep through that
damaged membrane and lodge in the artery wall. Once you get that -
that's called plaque, by the way, - once you get that plaque in the artery wall then
you get your own immune system - immune cells start going through that into that
damaged endothelial lining as well. They begin to attack. They release enzymes
meant to absorb - digest the cholesterol. Those enzymes can cause a heart attack
and clot or they cause a clot. And, so, there you go. Now, let's go - a couple more
details on this - Introduction then they talk about, again, those pleiotropic
effects. The beneficial effects lie in their anti-inflammatory properties which
are exhibited by a reduction in the release of c-reactive peptide chemokines
and chemo ("-kines" means attract, so chemicals that
attract. Cytokines - cells that attract, again, immune system properties; and
adhesion molecules. Those are molecules that are used by immune cells to attach
or adhere to the damaged slick endothelial lining or intima of the
artery wall. They also modulate t-cell activities, in other words, immune cell
activities. Furthermore, statins inhibit the trans-thelial - trans endothelial
migration of leukocytes due to a decrease in expression of adhesion
molecules such as Icam1 - so, they actually even know now the adhesion
molecules that are being impacted and how the statins impact them. Lymphocyte
function associated antigen-1, monocyte chemotactic protein-1. Statins further
prevent inflammation by emit - inhibiting chemokine release and Th-1
type chemokine receptors so if that didn't get geeky enough for you, I'm
sorry because that might be about as geeky as we get for this video. The next
statement that - or the next page goes into table 1 which is just a series of
the - some of the studies they looked at and studies that many of you have
probably already heard about; Jupiter which John mentioned in those comments,
PROVE IT-TIME, WOSCOPS (that stands for West of Scotland Trial), TNT, IDEAL trial -
and these are also in things like - look, in case you can't read that - we will move
that over a little bit and - Simvastatin reduced this and major coronary artery
events; Rosuvastatin reduce the risk of coronary artery events; Atorvastatin
reduced risk - Atorvastatin does work, it just doesn't work as effectively
as Pravastatin, Semistatin, and especially Rosuvastatin, or Patavastatin,
the new medication; And we'll talk about those, again, a little bit more a
little bit later. Prevostatin reduced coronary events,
Retorvastatin, etc. I will leave this
- the link to this article under the video as I usually do. Now, let's go and check
and see some of the other highlighted information here. First comments on the
pleiotopic effects are made after researchers had observed the overall use
or benefits of the use of statins were larger than what one would expect based
on decreasing statins - I mean decreasing LDL or cholesterol
alone. Jupiter, in fact, was a study designed
specifically to look at this. Paul Ridker, one of the major proponents of
this concept of cardiovascular information at Harvard actually was the
principal investigator for the Jupiter study and, basically, what they did was
they showed that these people that had normal cholesterol values but elevated
CRP (c-reactive protein) - if you gave them a rosuvastatin or crestor, you cut
their heart attack and stroke risk in half - so much so that they had to stop
the study early because they knew these people needed - needed that treatment.
What's unfortunate about that study - the Jupiter study and we'll cover it a
little bit more in detail in other - other videos - is that the medical community did
not respond. We did not change our standards based on that. Anyhow, that's
another video - another topic. Well, let's go back and talk a little bit more about
anti-inflammatory effects. Now, I said I wasn't going to get more geeky in terms
of biochemistry. I will just make a couple of other points here. Many of the
pleiotropic effects are mediated by the inhibition of isoprenoids which act as
intracellular signaling and, again, you see translational modifications of
proteins such as nuclear laminins, Ras, Rho, Rac, and Rap; and frankly, I'm not an
expert on any of those but, again, I mentioned that just to get the point
that at this point in time - 2017, 2018, and now 2019 - it's becoming really clear how
statins decrease cardiovascular inflammation. Now, in this next section
they - they go systematically through this. What is the evidence? had it - how was it
built? Here's section number 3: Is
anti-inflammatory impacts - now, I will - again, this is probably repetitive unless
you're just way at a deep level and I'm going to jump over this next couple of
sections. Furthermore, statins have shown to decrease number of inflammatory cells
in atherosclerosis plaques apart from the 37%
reduction of CRP in the jupiter trial. A significant reduction in incidence of
major cardiovascular events occurred. Furthermore, other studies have revealed
CRP adversely affects the endothelial function by reducing the expression of
nitric oxide in cultivated endothelial cells. In other words, we're also
beginning to realize that once you get that elevated CRP (c-reactive protein)
that c-reactive protein appears to be part of the mechanism for damaging that
lining of the artery. CRP has been used to predict heart attack and stroke death
and has been used effectively to do that. Unfortunately, it's still not a part of
the standards of medicine. I use it - that's one of the key parts of this - of
this channel - this YouTube channel: To make other people aware. Preclinical
evidence of statins and their - their effect, again, more studies - more looking
at reduce inflammation within the lesion. Anti-inflammatory activity of that first
one was for Patavastatin - the next 3 were
simvastatin. The next two actually had to do with inflammation within lung tissue.
It's a different - it's a different issue. Now I - pardon me - those of you who wanted
to bottom-line it and get straight to the issue about which statins have
better power for cardiovascular inflammation, here's where that is - it's
over on the left hand side. The yellow stuff that I have. The yellow
highlighting that I've provided. However, it seems that not all statins have the
same effect on inflammation. Nakagomi and associates examined where the
different statins exert differing effects on inflammation, insulin
resistance, and the progression of carotid atherosclerosis in patients with
dyslipidemia. As far as the inflammatory markers are concerned,
Petivastatin caused a greater reduction in levels of TNF (tissue necrotic factor),
MCP, TNF and some others compared to atorvastatin. So Petivastatin does help.
it's a great medication and, two years ago, I had patients that were starting on
it. Unfortunately, at that time, I had to tell them - we don't know yet. Now, we do
know it is very good at decreasing inflammation but pitavastatin or
llevarlo, I still don't use a lot and let me tell you why. It's incredibly
expensive. The best that you can do with good RX is to get it down to about $300
per month from its normal average retail price of 350. It is - it's a great
medicationl it doesn't increase insulin resistance like the most of the other
statins but it is very expensive. I don't use it. I use crestor. If you do - if you
manage your lifestyle well, manage your insulin resistance, watch the carbs, keep
your blood sugar down, you can do well with a very inexpensive statins. Again,
Simvastatin, Pravastatin are great. I tend to use
rosuvastatin, for the most part. It has less of effect on insulin resistance and
you can go in very, very low doses. I have a lot of patients that are on 2.5 of
Crestor twice a week. I, personally, that's actually what I'm taking - 2.5
milligrams of Crestor twice a week. Now, again, back to this study. The author
suggested that treatment with Pitavastatin may be more beneficial
than atorvastatin for reducing inflammation in patients with dyslipidemia.
Similarly, Khoruna and associates compared the anti-inflammatory effects
of atorvastatin or lipitor and rosuvastatin or crestor in
patients with acute coronary syndrome. They found that even though both statins
lowered the CRP level, the use of rosuvastatin was more effective in terms
of events. So, again, there you have it. There's science out there and you know
if your doc wants, he and I can - he or she and I can go look up these studies and
actually decide how much and how geeky we want to get on that and how much
we want to debate that issue but the bottom line is the vet - to me, the problem
is not so much debating with Docs which statin to use. The problem is getting
docs and patients to understand that it's cardiovascular inflammation, it's
not cholesterol level, unless you have familial hypercholesterolemia and once
you get sophisticated enough to look at cardiovascular information, we're talking
about insulin resistance here more than anything else and yes,
priorities: Number 1, 2 and 3 for insulin resistance are lifestyle,
lifestyle, and lifestyle but there are still people that need other help
medications after that. Thank you for your interest.