It's diabetes and more importantly prediabetes is the major cause
of plaque and inflammation it's the by far the major cause of heart
attack stroke blindness kidney disease all
those bad things that are associated with
chronic disease and a lot of folks don't know that that's one of the key
goals of this channel is to make people aware 90% of the people that
have prediabetes aren't even aware of it
so a couple of people have already responded saying oh this is an
interesting topic and again as often happens I learned a lot of stuff
I learned about a lot of things from you guys I think it was Bob Bell one of our
viewers that sent me this and sent me several other things as well
this again is a study that appeared in a journal called
Cell Reports it's a fairly deep scientific journal
again deep scientific title but we won't get too deep into that
Dysfunction of Persisting Beta Cells is a Key Feature
of Early Type 2 Diabetes Pathogenesis what does that mean here's the bottom
line here's what they did they happened to be in the belly of
a lot of surgical patients for other reasons
they had a mechanism and the patients gave prior agreement
they took some patients that had normal metabolism
some that had full-blown type 2 diabetes and some that had prediabetes they took
tiny biopsies out of the pancreas and the beta cells
to look at those beta cells and find out just
what's going on are you losing beta cell function or the beta cells actually
going away in other words going back to that
question of you can "grow your beta cells" back again
this for a spoiler I'll say look this would indicate what many of us
have thought for a long time it tends to provide a
lot of evidence a lot of proof that you don't lose those beta cells and
they're not shrinking they're not getting attacked they're not
being lost the size is still there now let me
clarify this is type 2 diabetes many of us know
type 1 diabetes is a whole different mechanism tends to happen
with very young people whereas type 2 diabetes
mostly hits us baby boomers with type 2 diabetes the original problem is
our receptors for insulin in our cell wall
get rusty they begin to become resistant to insulin so our beta cells
you can get my non-verbals here so the beta cells are having to push out more
insulin to get those faulty rusty dysfunctional insulin receptors in the
cell walls to work with type 1 diabetes it appears to be
for the most part immune activities inflammation actually
hitting the beta cells themselves usually
cross-reaction with something else a foreign body won't go
into that any deeper into that we'll talk a little bit more about the study
itself type 2 diabetes is a metabolic disorder
responsible for long-term complications decreased quality of life and premature
death type 2 diabetes is characterized by
insulin resistance and insufficient insulin release from
pancreatic islet beta cells to correct inadequate insulin
levels effective therapies target the correct
mechanism in other words why is this important
it's still debated whether insulin insufficiency is the result
of compromised beta cell function in other words the amount of insulin
released by each individual beta cell or reduced beta cell mass in other words
the number of beta cells within the pancreas have decreased
or a combination of both and again I'll keep giving you spoilers it was the
first one it's not a the second one and it's not a
combination of both at least according to this study
and again I think this study makes a heck of a lot of sense once you get
deeper into managing folks with prediabetes so prior to this
study their point was it's unclear whether the objective of
type 2 diabetes prevention and therapy should be
to protect and restore beta cell function or to prevent the death of beta
cells and increase their mass that was the study question researchers
used pancreas tissue slices from metabolically phenotype surgical
patients what does that mean I told you that they
took three groups of patients before the
surgery some were prediabetic some were
diabetic and some had neither problem so that's what they
mean by metabolically phenotype that's again
two dollar words for a 50 cent description
phenotype means what's their body function so they found out what was
going on with these folks and then they did
the biopsies surgical samples were the following four from non-diabetics
four from folks that had impaired glucose tolerance
IGT as you'll see in some of these images and
six from folks that had type 2 diabetes subjects were part of a larger cohort of
61 people with no diabetes 71 with impaired glucose tolerance and 88 with
type 2 diabetes prior to surgery subjects were
phenotyped based on hemoglobin A1c fasting glucose and these guys were
smart enough to do an OGTT oral glucose tolerance test and looking
at ADA guidelines valuable tissue slices were subsequently
used with again another technical term 3D
morphometric analysis as usual with these big words just break
it down morpho means your body shape and metrics means your measurement so
it's measurement of the shape of these
beta cells that's what that meant and they looked at kinetic
insulin secretion as well to quantify the endocrine cell content
beta alpha and gamma cells the researchers used this
3D morphometry in other words that's how they were able to tell
what type of cell is this is this the exocrine
pancreas cell exocrine means those are the the cells that
create enzymes for digestion or where is this the endocrine cells which
were the beta cells which were focused on here
in non-diabetics endocrine cells constitute about 0.48%
or plus or minus 0.09% let me clarify something 0.48
percent so about half of a percent of the pancreas volume
the distinct endocrine cell volume fractions of endocrine cells were not
significantly altered in the pancreas of non-diabetics
impaired glucose tolerance and type 2 diabetics
in other words what they're saying is you look at these
graphs and you look at the size and the portion of the mass of cells
made up by the insulin cells the beta cells
they were the same whether it was diabetic non-diabetic
or prediabetic neither the distribution or of endocrine object size nor their
contribution to the total volume was significantly changed thus
the 3D morphometry revealed no difference in
other words we're not losing the cells themselves
we're losing the function so speaking of function
that's what they did in the next series to address the beta cell function
researchers measured insulin secretion now you see that in this over here let
me go through what they found and then we'll talk
for a minute about this activity in the non-diabetic pancreas tissue
slices showed a typical you know the biphasic insulin secretory
pattern in other words secretion of that stored
insulin and then later on secretion of the
insulin that it made remember we were talking about that
earlier and we were talking about people with impaired glucose tolerance
prediabetes usually lose that stored insulin
function they looked at it on these cells when they took these cells out of
the pancreas and this was what was happening with the
cells in other words they were depleted in impaired glucose
tolerance samples showed a significantly increased basal insulin secretion in
other words it's what we see with an oral glucose tolerance test
these beta cells are working overtime they're not getting
a rest they're continuing to push out more insulin than a non-diabetic during
basal periods when we're fasting when we're asleep somebody with
prediabetes their beta cells are continuing to push
that insulin out because that insulin is not working
why is the insulin not working because those insulin receptors are resistant
that hopefully helps you connect some diets so in the type 2 diabetes the
baseline insulin secretion was similar to that of the non-diabetic in other
words nice low secretion it was significantly
lower than somebody with impaired glucose tolerance
and again that's what we tend to see as well especially with people
what happens is as your beta cells are continuing to try to
manage that glucose they have to put out more
during basal periods during fasting periods
they get worn out they're not able to store any for that first phase
and again as you continue to go into full-blown diabetes you start to get
depletion and fatigue of that beta cell it's no longer making
it can't respond to the first part and then when it gets
deeper it can't respond even to the second part
that gets into that discussion about the five stages of diabetes
both impaired glucose tolerance and type 2 diabetes patients
lacked the typical first phase peak prior to the second
phase plateau you see some of that here again it's a little bit difficult to
tell from this but what you see is look the
green you see that early storage phase that first phase and then
you get to 75 minutes and you get that second phase where the
beta cells are making insulin with the blue the impaired glucose
tolerance patients you see they're pushing along making insulin
even when they're supposed to be at rest so therefore once you get to that first
phase they don't have quite as much there
they're tired they haven't been able to store insulin
then they're still able though to get a little bit of a bump
in that second phase at 75 to 80 minutes this full-blown type 2 diabetic is down
in the orange as you see the beta cell has depleted
it's worn out it's not producing more during basal
periods at that point this is a diabetic
remember that person still has high blood sugars
the beta cells just not able to respond to it there's depletion so there's no
ability to respond to that first phase and then very minimal response
even at the second phase so you see what you've got there is that
what Joseph Kraft would call us and many others would call a stage five
insulinopenic insulinopenic patient type two diabetes patient a patient who
just doesn't have insulin anymore to put out so
to go back to the summary this helps us in terms of the image
let me read through again the text components beta cell mass and tissue
slices appears intact throughout the progression
from non-diabetes to prediabetes to type 2 in other words the cells are
still there in prediabetics impaired glucose
tolerant donor tissue the beta cell volume is unchanged but
beta cell function is significantly deteriorating
exhibiting increased basal release in other words
fasting release but loss of that first phase insulin
secretion in individuals with type 2 diabetes
function within the sustained beta cell volume
still further declines this means that beta cell dysfunction
develops early in prediabetes and deteriorates
further in type 2 diabetes these results indicate that the dysfunction
of persisting beta cells is the key factor not the loss of
mass not the loss of the cells themselves so as you begin to look
through this what you begin to see is again a good
visual impaired glucose tolerance they have
again normal glucose but it's taking a lot
more insulin to make that happen so you get
glucose values that are not that elevated but a lot of basal insulin to
keep it down then that first phase you've lost your
insulin you are not able to create a first phase
second phase and beta cell mass are still retained
in these prediabetics once you get into those
deeper stages of diabetes blood sugar is high
basal insulin has been depleted there's none of it for the first phase or second
phase but you still have that beta cell mass
there's a lot of promise in that because theoretically it should be easier to
restore function than it is to recreate new beta
cells so again got a little bit deep a couple
of our folks on our team got a little bit confused as we went through some of
this I hope that I didn't butcher that up too
much
why wait for a disease and hope for a cure I used to be an ER
doc my name is Ford Brewer I quit ER after a few years because it
was just so frustrating most of the things
bringing people into the ER are things that should have been
prevented including heart attack stroke number one cause of
death number one cause of permanent disability
people think that you're just gonna have those and that they're not predictable
both of those are wrong they are predictable
and you don't have to have them usually it's lifestyle lifestyle is more
important than supplements and even prescription drugs
and even stents and surgery but the current times
are tough major financial impact with the
lockdowns that most states have been going through
we've been working on a way to make this much more affordable with a subscription
process and that's exactly what we're announcing
today we've got two levels one is the Silver Membership
where you get access to our courses a private webinar each month and access
to our supplement store and supplement recommendations and
prescription or I would suggest even more so the Gold
Membership you can get a script for a Freestyle
Libre and find out what your blood sugar metabolism is doing on a daily
basis and you can get a lab order for
inflammation ogt and insulin survey you can also get a 30-minute one-on-one
with me so I'm looking forward to seeing you
cost is no longer an excuse so if you're interested go to
care.prevmedhealth.com/Membership or call us at 859-721-1414
859-721-1414 looking forward to seeing you
thank you