Niacin is one of those supplements that everybody - a lot of people love
to hate and why is that? why the debate? Again, because you see some conflicts in
the (scientific) literature. We'll go into some of those conflicts and some of the
results in the second half of this video this video's on a -
on an article that was suggested by Dr. Angie Stones - Thank you again Dr. Stones.
One of our viewers and, again, it's incredible what you learn from
others if you just stop and listen. I'm glad I stopped and took a look at that
article. Without further ado, let's go ahead with part two of
the article. Part one actually went into this huge list of - of biomarkers that
they were looking at, and it started to talk a little bit about correlations.
I bogged down a little bit there, because, again, you can go back and look
at the last half of that last video, you see it gets somewhat tedious. Now, this
part of the video talks about the actual results and then it talks about - a
very interesting part - clusters; clusters of different components of the
biomarkers and one of my favorite clusters here has to do with macrocyte
function and you'll see why in this video. Again, pardon me - may be spending
too much time on that, let's go into some of the conclusions and discussions. So
all subjects, again, the nineteen of them had an atherogenic mix of dys -
lipedema and insulin resistance. Their ages - the mean was 47 with a
standard deviation of 13 years;
body mass index was 32 so, as I said, these were obese middle-aged men;
plasma triglycerides coming into it were two seventeen cholesterol LDL or bad
cholesterol was 125 so they had bad numbers coming into
it as well HDL was very low. HOMA IR, as I mentioned before, was 3
times normal. Now, this was only an 8 week study and the - the folks that are
major proponents of insulin (I mean niacin) and I'm a proponent of
niacin like everything - I don't see anything as black or white - I do think
there - there's more than just a signal in the literature which would indicate benefit..
There's a mixed bag of things going on in this study. Actually, that's what the -
this study does. It goes into the molecular reactions and says
there's clearly a mixed bag: you do get some increase in insulin resistance and
you get some improvement. A lot of other areas and, again, I think some of those
other areas are very, very interesting and very helpful. I would say this - I get
a lot of focus from viewers on the increase in insulin resistance. I think
John and I are both good examples.
We're both managing our insulin resistance very well at this point
and it's a pattern that I see typically - not within 8 weeks but within 6
months assuming you do the things you're supposed to do. The impact on insulin
resistance does not appear to be permanent. That's one of the questions
raised by this study, so yes it - it shows that you do have an increase in insulin
resistance but over the two months, well, we already knew all that. What it doesn't
show is the impact over at 6-month period. A couple of other things that it
does show that are very interesting - there are no changes on - on body mass
index, things like that. It improved the diyslipidemic profile. Here's a
couple of things that I thought were very interesting - adhesion molecules and
macrophage activation. Now why would they even look at that? Well,
remember - let's go back and think about the mechanism for inflammation. First of
all, it's not so much having high LDL that causes the problem, it's having
injury to the endothelium or intima so once you get those cuts, nicks, injury to
the endothelium, the lining of the artery - that's when LDL can get slipped through
there and lodge in the wall of the artery - the intima media space
adhesion model molecules; then it stands to reason and, again that's just one of
the theories that this hypotheses that that creates - does increase in adhesion
molecules cause some of this problem? - In other words, things sticking to that
slick endothelial lining of the wall due to cuts and things like that -
macrophage activation; why is that interesting? Well, again, let's think about
inflammation. Once you get this plaque in your artery walls, your immune system
does want to come in, absorb that LDL that's parked in that
artery wall, digest it and get it out of there. Well, how does it digest it?
Macrophages come in; they (I'm using a little non verbals here) - they grasp the
LDL, they bring it in there; Lysozymes release enzymes within that macrophage
to digest that LDL. Now, what happens with significant inflammation - you get so much
of this lysosomal activity - these digestive enzymes in the lysozymes being
released that it damages and even kills the macrophage. So, again, you - there
appears to be, at least in terms of hypothesis generation, a major component
of macrophage activation; to the extent that you have death of the macrophage
and spilling of those lysosomal contents. That's where you get the
liquid - hot liquid plaque and that - that again is what's dangerous. That's what
causes the climb and the clot causes the heart - the heart attack, the stroke, the
dementia and all those other bad things. So let's just go through here - like I
said, this article was gonna get geeky enough and detailed and long enough
without me going over a lot of the intro stuff so I've been very geeky. Those of
you who are starting to get bored, this is going to go get even more so. So you
may not want to watch the rest of it but for those of you who are interested in
again, deeper details around the biomarkers, I couldn't help but underline
some of these issues as you see on this page. I couldn't help but underline a lot
of them and why is that? Because this page is talking about clusters. Clusters
of those biomarkers and wanted to spend some time going over that. So at a
significance level of probability of .001 - what that means is with -
they found a lot of clusters of these biomarkers and if you looked at it from
a probability perspective, the probability was one in a thousand. So
there's probably significant correlation in these clusters. Now, what were the
clusters? There were 7 distinct clusters. The first one is a decrease in
triglycerides - was strongly (excuse me - negatively) correlated with
increments in those like hdl-c
Duh! if you haven't seen any of my videos on the triglyceride / HDL ratio, you need
to take a look at them. Those decreasing triglycerides, increasing HDL both have
an impact - very positive impact and - you know a high ratio of triglycerides over
HDL is my major tip-off. That's the first thing I look at when I look at a
cholesterol test because it shows the patient has
metabolic syndrome or insulin resistance. Insulin causes the body to shut down
triglyceride (fat) burning and it also tends to chew up HDL so that's why you tend to
see that with high insulin level levels. Now, furthermore, theHDL-C cholesterol
and apo a1 ratio is integral to that cluster. Significant thoughts in
terms of - okay what's going on here? reduction in total cholesterol and LDL
were the main - main drivers (bad English) of a cluster
integrating reductions in apoB & Lp(a); Apo a1 was significantly
associated with this cluster. So, again, John has told you a couple of times, he's
got what he considers to be significant Lp(a) when I think it's 120s,
130s, 150s, 180 is that kind of number like
I've mentioned before, I take care of several people that have 400
500. They - you know - they're - they have some of that French, Canadian gene
pool creating significant Lp(a) problems. Now, what does this mean? It's
just that Lp(a) is significantly associated with apoA 1 and apo b 1
I think what it's - again - more hypothesis-generating
given my experience, I think what that means is Lp(a) and again
given my experience with it, I think this is supportive
of the hypothesis that Lp(a) is really more of a reaction to things that
you'll see with apoA1 and apoB. In other words, getting insulin resistance
and damage to the - that intima back under control; we gets out of control and Lp(a)
appears to be something that increases to help patch that up.
The third cluster - insulin resistance HOMA IR insulin and il-6 levels. Now, what was
interesting, however, fasting glucose levels were independent of this cluster
despite significant elevation on treatment. So on treatment reduction in apo e levels did not correlate with changes in any lipids and he was (Tom
Decker, one of the viewers made a couple of
comments about that) but rather clustered with those circulating of mmp-9, it's a
matrix metalloprotease produced by - monocyte-derived macrophages. Again, we get back to
the role of macrophages in this inflammation process. Now, there's a
separate cluster elevation in adiponectin
on treatment correlated with non significant increment in cystatin C.
2 distinct clusters of inflammatory markers were identified, 1 with I cam
1 and 1 with TNF; TNF is tissue necrotic factor. Now, remarkably, and
despite a 20% decrease on treatment concomitant with those with athero-
genic lipoprotein lipids, changes in apo c3 levels were independent of all
other biomarkers. What does that mean? I have no clue. If - if you do, please comment
please fill us in with respect to biomarkers
associated with hepatic function and metabolism glucose tolerance levels
decreased independently while those of homocysteine increase. So there's a lot
of folks out there that love to focus on homocysteine and you'll go "Aha! that's
the problem with niacin. It increases homocysteine." Maybe you're right.
Again, I'm not stopping my niacin. NSC is a potential marker for
macrophage activation. It was independently reduced and, again, it goes
on into further components of inflammation. Here's another way of
looking at it. Here's the actual tables; I'm gonna zip through
these lipids and lipoproteins,
bad cholesterol, LDL 17% decrease; apoB - B which is the protein part of bad LDL
21% decrease; HDL 13% increased; so a lot of interesting things;
Lp(a) 21% decreased; and apo A 25% decreased; Again, we've had several people
focus on that. I don't think I'm smart enough to understand fully the impact of
apoE. Now, I've done several videos on apoE and I've had - obviously, I know
several facts about it but I think there's some more subtle theories going
around that I'm not sure that's significant. Anyway, HOMA IR increased;
insulin increased; and c-peptide increased. C-peptide is a part of the
original genetic structure of insulin before it gets cleaved into functioning
insulin - so what that basically means that - I don't think that's that
significant for this study, other than to mean that - you know - this was
endogenous or insulin made by the person and these people weren't getting insulin
so that's why I don't - I don't understand their desire to get that, other than just
to be complete but significant immediate insulin resistance, as I've said I'm not
surprised about that; My question is - Does it last six months or longer? and I don't
think that's the case. Look at some of these inflammatory markers: tissue
necrotic factors - three of them here; 12%, 12% and 14%
decrease; CRP took a nosedive - 36 - 40% decrease; homocysteine
26% increase; adhesion molecules (I haven't heard of those before, I've heard
obviously of the adhesion process) but, again, significant decrease in
adhesion. So, as we talked before, maybe that's helping; maybe that would help
decrease this process of plaque getting deposited because first the theory
is that - first. it has to get stuck or adhere to the lining of the artery
before it gets there. Now, as I have said many times, once I get going on the geeky
parts of some of this, I can go forever. As our friend, I don't even remember his
name now, said - there are always answers. Be careful when you start getting there
though because every answer creates a whole new set of questions. If you've
made it this far, thank you very much for your interest.